Environmental health
INeal
A126348-9781118984765.pdf
Table of Contents Title Page Copyright Dedication Tables, Figures, Text Boxes, and Tox Boxes The Editor The Contributors Acknowledgments Potential Conflicts of Interest in Environmental Health: From Global to Local
References Part 1: Methods and Paradigms
Chapter 1: Introduction to Environmental Health What Is Environmental Health? The Evolution of Environmental Health Spatial Scales, from Global to Local The Forces that Drive Environmental Health Key Terms Discussion Questions References For Further Information
Chapter 2: Ecology and Ecosystems as Foundational for Health
Environment as Ecology: Ecology as the Study of Our Home Population Ecology Community Ecology Ecosystem Ecology Systems Thinking: From Ecology to Human Health Features of Our Home: Ecological Characteristics as Foundational for Health
2
Toward Ecological Approaches to Health and Home Summary Key Terms Discussion Questions References For Further Information
Chapter 3: Sustainability and Health Historical Considerations of Sustainability Sustainable Human Well-Being and the Three-Legged Stool Drivers of Nonsustainability, Limits to Growth, and Collapse What Should Concern Us More: Population Growth Or Consumerism? Limits to Growth Human Societal Collapse? Prevention Through Systems Thinking and Early Action The Importance of Scale The Way Forward Summary Key Terms Discussion Questions References For Further Information
Chapter 4: Environmental and Occupational Epidemiology A Primer on Epidemiology Environmental and Occupational Epidemiology Epidemiology and Risk Assessment Future Directions Summary Key Terms Discussion Questions
3
References For Further Information
Chapter 5: Geospatial Data for Environmental Health Components of Georeferenced Data Basic GIS Operations Mapping and Spatial Analysis of Exposure Mapping and Spatial Analysis of Disease Risk What Makes Good Maps of Good Data? What Can We Do with GIS? Are There Any Limitations? Summary Key Terms Discussion Questions References For Further Information
Chapter 6: Toxicology Introduction to Toxicology Toxicology and Environmental Public Health Toxicant Classifications Testing Compounds for Toxicity From Regulatory Toxicology to Public Health Policy Summary Key Terms Discussion Questions References For Further Information
Chapter 7: Genes, Genomics, and Environmental Health Fundamental Concepts of Genetics and Genomics Approaches for Identifying Gene-Environment Interactions Examples of Gene-Environment Interactions in the Real World
4
Summary Key Terms Discussion Questions References For Further Information
Chapter 8: Exposure Science, Industrial Hygiene, and Exposure Assessment
Anticipation, Recognition, Evaluation, and Control Exposure Science Summary Key Terms Discussion Questions References For Further Information
Chapter 9: Environmental Psychology Environmental Psychology and Toxicology Environmental Psychology Processes So What? Interventions That Work Summary Key Terms Discussion Questions References For Further Information
Chapter 10: Environmental Health Ethics Defining Ethics and Morals The Modern Philosophical Background Professionalism Expanding Horizons and Challenges Implications for Professional Ethics Concluding Discussion Summary Key Terms
5
Discussion Questions References For Further Information
Chapter 11: Environmental Justice and Vulnerable Populations
The Roots of Environmental Justice Elements of Environmental Justice From Research to Action on Environmental Justice Social Inequality and Environmental Quality Summary Key Terms Discussion Questions References For Further Information
Part 2: Environmental Health on the Global Scale Chapter 12: Climate Change and Human Health
Greenhouse Gases A Warming Earth: From Past to Future Earth System Changes Food and Malnutrition Weather Extremes and Disasters Air Pollution Infectious Diseases Mental Health Effects The Public Health Response to Climate Change Climate Change as a Public Issue Summary Key Terms Discussion Questions References For Further Information
Part 3: Environmental Health on the Regional Scale
6
Chapter 13: Air Pollution History of Air Pollution Types of Ambient Air Pollution Studies of Air Pollution and Health Sources and Effects of Outdoor Pollutants Air Pollution Prevention and Control Larger Effects of Regional Air Pollution Summary Key Terms Discussion Questions References For Further Information
Chapter 14: Energy and Human Health Household Energy Fossil Fuels Nuclear Energy Renewable Sources of Energy Energy Conservation and Efficiency Summary Key Terms Discussion Questions References For Further Information
Chapter 15: Healthy Communities The History of Cities Poverty and Industrialization in Cities The Modern Metropolis: Consumption and Urban Sprawl Community Design and Health Cities as Healthy Human Habitats Summary Key Terms Discussion Questions
7
References For Further Information
Chapter 16: Water and Health The Role of Water in Life Regulatory Framework Risk Characterization for Water Contaminants Emerging Issues Summary Key Terms Discussion Questions References For Further Information
Part 4: Environmental Health on the Local Scale Chapter 17: Solid and Hazardous Waste
Solid Waste Solid Waste Management Strategies Primary Prevention of Waste Waste Treatment and Disposal Health Concerns Summary Key Terms Discussion Questions References For Further Information
Chapter 18: Pest Control and Pesticides Insect Pests Vertebrate Pests Pesticides Integrated Pest Management Summary Key Terms Discussion Questions
8
References For Further Information
Chapter 19: Food Systems, the Environment, and Public Health
What Is the Food System? Food Production: Industrial Agriculture Industrial Food Animal Production Sustainable Agriculture Food Consumption and Food Environments Food Safety and Environmental Health: A Systems Perspective Making Change: Food System Policy Summary Key Terms Discussion Questions References For Further Information
Chapter 20: Buildings and Health The Range of Buildings Key Elements of a Healthy Building Toward Safe, Healthy Buildings Architecture, Environment, and Human Health Summary Key Terms Discussion Questions References For Further Information
Chapter 21: Work, Health, and Well-Being The Interaction of Work and Health Protecting Safety and Health on the Job Workers' Compensation Sustainability
9
Globalization Summary Key Terms Discussion Questions References For Further Information
Chapter 22: Radiation Nonionizing Radiations Ionizing Radiation: The Basics Sources of Ionizing Radiation Exposure Cellular and Biological Effects of Ionizing Radiation Human Health Effects of Ionizing Radiation Radiation Protection Assessing Radiation Risks Summary Key Terms Discussion Questions References For Further Information
Chapter 23: Injuries Injury Prevention and Control Policy for Injury Prevention and Control Injury Prevention in Practice Injury Control in Special Settings Summary Key Terms Discussion Questions References For Further Information
Chapter 24: Environmental Disasters Scope of the Problem The Public Health Consequences of Environmental
10
Disasters Disaster Risk and Its Determinants Managing Disaster Risk Summary Key Terms Discussion Questions References For Further Information
Chapter 25: Nature Contact The Links Between Nature and Human Health Domains of Nature Contact The Greening of Environmental Health Summary Key Terms Discussion Questions References For Further Information
PART 5: The Practice of Environmental Health Chapter 26: Environmental Public Health: From Theory to Practice
Concepts of Environmental Health Prevention Principles of Prevention in Environmental Public Health Core Functions of Environmental Public Health Environmental Public Health Systems Summary Key Terms Discussion Questions References For Further Information
Chapter 27: Risk Assessment in Environmental Health History Risk Assessment
11
Risk Management and Communication Summary Key Terms Discussion Questions References For Further Information
Chapter 28: Communicating Environmental Health Communication, Social Marketing, and Environmental Health Environmental Risk Communication Summary Key Terms Discussion Questions References For Further Information
Index End User License Agreement
12
List of Illustrations Chapter 1: Introduction to Environmental Health
Figure 1.1 Title Page of Chadwick's Groundbreaking 1842 Report
Figure 1.2 A Victim of Minamata Disease Being Bathed: Photograph by W. Eugene Smith
Figure 1.3 The Need for Primary Prevention: An Early 20th- Century View
Figure 1.4 The DPSEEA Model
Chapter 2: Ecology and Ecosystems as Foundational for Health
Figure 2.1 A Food Web in a North American Terrestrial Food Ecosystem
Figure 2.2 Invasive Species and Their Impacts
Figure 2.3 A Classical Model of Ecological Succession in a North American Forest Ecosystem
Figure 2.4 The Phosphorus Cycle
Figure 2.5 Transactions Between Atmosphere, Geosphere, and Hydrosphere Provide a Basis for the Earth's Capacity to Support Life
Figure 2.8 Ecosystems as Settings for Human Health and Well-Being
Figure 2.6 Linear Thinking Versus Systems Thinking
Figure 2.7 A Systems Map of U.K. Land Use and the Domains That Influence It
Figure 2.9 The Life Cycle and Transmission of Leptospira Bacteria
Figure 2.10 The MA Conceptual Framework
Figure 2.11 The Social Ecological Model
Chapter 3: Sustainability and Health
Figure 3.1 The Great Acceleration
13
Figure 3.2 Nested Model of Sustainability
Figure 3.3 A Safe Operating Space for Humanity
Chapter 4: Environmental and Occupational Epidemiology
Figure 4.1 Area of PFOA Contamination
Chapter 5: Geospatial Data for Environmental Health
Figure 5.1 Hypothetical Example of the Layering GIS Operation
Figure 5.2 Examples of Buffers Around Point, Line, and Area Features
Figure 5.3 Map of Genesee County, Michigan, Block Groups (1990 Census) Showing Proportions of Respondents Self- Identifying Race as “Black”
Chapter 6: Toxicology
Figure 6.1 Toxicology: From Populations to Molecules
Figure 6.2 Examples of Dose-Response Curves
Figure 6.3 Metabolic Transformations of Benzo(a)pyrene
Figure 6.4 Structures of Some Suspected Endocrine- Disrupting Chemicals
Figure 6.5 Key Steps in Toxicokinetics
Figure 6.6 The Metabolism of Acetaminophen
Figure 6.7 Molecular Structure and LD50 for Eight Chemicals
Chapter 7: Genes, Genomics, and Environmental Health
Figure 7.1 The Human Genome
Figure 7.2 The Basic Structural Elements of a Gene
Figure 7.3 The Cystic Fibrosis Mutation
Figure 7.4 Chromatin Dynamics in Response to Epigenetic Modification
Figure 7.5 Schematic of the Agouti Gene and How Its Methylation Status Affects Phenotype in Mice
Figure 7.6 Primary Biotransformation Pathway for Alcohol
14
Chapter 8: Exposure Science, Industrial Hygiene, and Exposure Assessment
Figure 8.1 An Air Pollution Monitoring Station for Ozone and Particulate Matter, in Atlanta
Figure 8.2 Personal Protective Equipment
Figure 8.3 Assessing Exposure in an Occupational Setting
Chapter 9: Environmental Psychology
Figure 9.1 Long Waits and Crowded Buses at a School in Singapore
Figure 9.2 Effects of Noise Exposure on Reading Acquisition, Mediated by Poor Auditory Discrimination
Figure 9.3 Illustration of Convenience, Attractiveness, and Normativeness in a School Cafeteria
Figure 9.4 A Waste Setup That Provides a Physical Cue to Encourage Recycling
Figure 9.5 The Five Oaks Neighborhood Following the Defensible Space Intervention
Figure 9.6 Location of Hand Cleaner Dispenser in Patient Room: In Line of Sight (left) and Inside the Door (right)
Figure 9.7 A Utility Bill Employing Social Norms to Encourage Energy Conservation
Chapter 11: Environmental Justice and Vulnerable Populations
Figure 11.1a Distribution of Major Industrial Facilities by Racial Composition of Census Tracts, Southern California
Figure 11.1b Distribution of Major Industrial Facilities by Proportion of Census Tract Residents Living Below the Federal Poverty Line, Southern California
Figure 11.2 The Four Elements of Cumulative Impacts
Figure 11.3 Children in Los Angeles Playing Soccer Near an Oil Refinery
Figure 11.4 Explanations for the Effect of Social Inequality on the Environment
15
Figure 11.5 Members of Clean Up Green Up, an L.A. Environmental Justice Advocacy Group, Hold a Press Conference in Support of Their Goals
Chapter 12: Climate Change and Human Health
Figure 12.1 Components of Radiative Forcing
Figure 12.2 The Melting of Arctic Sea Ice
Figure 12.3 Processes and Pathways Through Which Climate Change Influences Human Health
Figure 12.4 Number of Days in June, July, and August When Daytime Maximum Temperatures Exceed a Given Threshold (indicated by a vertical line)
Figure 12.5 Urban Heat Island Profile
Figure 12.6 The Relationship Between Temperature and Ozone Levels in Santiago, Chile
Figure 12.7 Satellite Photo of a Harmful Algal Bloom in Lake Erie in 2011
Figure 12.8 The Association Between Temperature and Childhood Diarrhea, Peru, 1993–1998
Figure 12.9a Alternative Emission Pathways
Figure 12.9b Climate Stabilization Wedges
Figure 12.10 The CDC's BRACE Framework
Figure 12.11 No-Regrets Solutions
Figure 12.12 Global Warming's Six Americas: Arraying the U.S. Population Along a Continuum of Belief, Concern, and Motivation
Figure 12.13 A Comparison of Cumulative CO2 Emissions (1950–2000) (upper panel) with the Burden of Four Climate- Related Health Effects (Malaria, Malnutrition, Diarrhea, and Inland Flood-Related Fatalities (lower panel)
Chapter 13: Air Pollution
Figure 13.1 Children Wear Masks in the Thick Haze on Tiananmen Square in Beijing, China, January, 2013.
16
Figure 13.2 The Distribution of PM2.5 Levels in Cities in India, China, Europe, and the United States
Figure 13.3 Mortality and Air Pollution Levels During the 1952 London Fog
Figure 13.4 The Respiratory System
Figure 13.5 Particulate Matter Mass Distribution in an Urban Area
Chapter 14: Energy and Human Health
Figure 14.1 The Fuel Ladder
Figure 14.2 Association Between Energy Use and Health, by Nation
Figure 14.3 Pathways Linking Energy and Health
Figure 14.4 World Energy Consumption
Figure 14.5 Indoor Air Pollution from Traditional Cooking
Figure 14.6 Products Made from a 42-Gallon Barrel of Crude Oil (in gallons)
Figure 14.7 An Oil Refinery
Figure 14.8 Renewable Energy
Chapter 15: Healthy Communities
Figure 15.1 World Population: Urban and Rural, 1950–2050
Figure 15.2 Nearly 1 Billion People Live in Urban Slums, Such as This One in Nairobi
Figure 15.3 Heavy Traffic, as Shown Here in Delhi, Brings Pollution, Injury Risks, Noise, and Mental Stress, and Inhibits Physical Activity
Figure 15.4 Schematic Comparison of Street Networks and Land Use in a Traditional Neighborhood and in an Area of Sprawl
Figure 15.5 Percentage of Self-Reported Obesity in Adults in the United States, by State, 2013
Figure 15.6 An Example of Complete Streets in Copenhagen, Where Many Streets Are Designed to Accommodate
17
Pedestrians, Bicyclists, Transit, and Automobiles
Figure 15.7 Access to Healthy Food Options
Figure 15.8 Overlapping Frameworks for Healthy Community Design
Figure 15.9 Relationship Between Growth of Bicycle Infrastructure and Amount of Cycling in Portland, Oregon
Chapter 16: Water and Health
Figure 16.1 The Hydrological Cycle
Figure 16.2 Schematic of the Interconnections Between Water and Health
Figure 16.3 Pesticide Movement in the Hydrological Cycle, Including Movement to and from Sediment and Aquatic Biota in a Stream
Figure 16.4 Sanitation Options
Figure 16.5 An Idealized Wastewater Treatment System, Based on Boston's Deer Island System
Figure 16.6 Carrying Water
Figure 16.7 Basic Drinking-Water Treatment Process
Figure 16.8 A Multibarrier Approach to Maximize Microbiological Water Quality
Chapter 17: Solid and Hazardous Waste
Figure 17.1 Chemical Drums at Love Canal
Figure 17.2 Composition of the 251 Million Tons of Municipal Solid Waste Produced in the United States (Before Recycling), 2012
Figure 17.3 Total Amount and Per Capita Generation Rate of Municipal Solid Waste Produced in the United States (Before Recycling), 1960–2012
Figure 17.4 Total Amount and Percentage of Municipal Solid Waste Recycled in the United States, 1960–2012
Figure 17.5 Glass and Paper Recycling in Industrial Nations
Figure 17.6 Waste Tires
18
Figure 17.7 Generalized Depiction of a State-of-the-Art Sanitary Landfill
Figure 17.8 Generalized Diagram of Incineration Material and Process Flow
Figure 17.9 Mine Tailings Pile: The Legacy of Sixty Years of Lead and Zinc Mining in Ottawa County, Oklahoma
Chapter 18: Pest Control and Pesticides
Figure 18.1 Application of Lead Arsenate in the Early 1900s
Figure 18.2 Modern Pesticide Application Equipment
Figure 18.3 A Corn Borer, an Example of an Insect Pest, Causing Damage in the Stalk of a Corn Plant
Figure 18.4 Farmers Applying Organophosphate Insecticides in Thailand
Chapter 19: Food Systems, the Environment, and Public Health
Figure 19.1 Selected Components of the Food System
Figure 19.2 Applying Herbicide to a North Carolina Cornfield
Figure 19.3 Potential Pathways for the Spread of Antibiotic- Resistant Bacteria from Animals to Humans
Figure 19.4 Manure Cesspit Outside Hog CAFO in Duplin County, North Carolina
Figure 19.5 Ducks in One of Takao Furuno's Rice Paddies in Japan
Figure 19.6 The EPA Food Recovery Hierarchy Prioritizes Actions to Prevent and Divert Wasted Food
Figure 19.7 Contribution of Different Food Categories to Estimated Domestically Acquired Illness and Death, United States, 1998–2008
Figure 19.8 A Health Inspector Tests the Temperature of Refrigerated Meat at a Restaurant
Figure 19.9 A 1993 Outbreak Caused by E. Coli 0157 in Undercooked Beef at Jack in the Box Restaurants Sickened 732 People and Killed 4 Children
19
Figure 19.10 An Example of Improper Grain Storage
Figure 19.11 A U.S. Department of Agriculture Food Safety Inspection Service Inspector at a Poultry Processing Facility in Accomac, Virginia, Testing for Cleanliness and the Avian Influenza (AI) Virus
Chapter 20: Buildings and Health
Figure 20.1 Housing Can Take Many Forms and Vary Greatly in Desirability and Safety
Figure 20.2 Trailer Provided by FEMA after Hurricane Katrina
Figure 20.3 School Design
Figure 20.4 Mold-Damaged Building in New Orleans Following Hurricane Katrina
Figure 20.5 Concentrations of PBDE in Breast Milk, Stockholm, 1972–1997
Chapter 21: Work, Health, and Well-Being
Figure 21.1 From July 1906 Through June 1907, 526 Workers Were Killed on the Job in Allegheny County, Pennsylvania
Figure 21.2 Who Bears the Cost of Worker Injuries?
Chapter 22: Radiation
Figure 22.1 The Electromagnetic Spectrum
Figure 22.2 Cell phones Are Virtually Ubiquitous, and Entail Exposure to Radiofrequency Radiation
Figure 22.3 A Basal Cell Carcinoma of the Skin of Twenty Years, Duration in a Fifty-Eight-Year-Old Man
Figure 22.4 Nuclear Transformation Mechanisms That Release Radioactivity
Figure 22.5 Using X-Rays for Fitting Shoes
Figure 22.6 The Chernobyl Disaster
Chapter 23: Injuries
Figure 23.1 The Injury Pyramid
20
Figure 23.2 Typology of Violence
Chapter 24: Environmental Disasters
Figure 24.1 Annual Incidence of Natural and Technological Environmental Disasters—Worldwide, 1964–2013
Figure 24.2 Comparison of the Public Health Impacts of Natural and Technological Disaster Events, 1964–2013
Figure 24.3 Key Public Health Impacts for Natural and Technological Disasters, 1964–2013
Figure 24.4 Three Conceptual Frameworks for Disaster Risk Management
Figure 24.5 The Four Elements of a Resilience Framework
Chapter 25: Nature Contact
Figure 25.1 John Muir ({–1914) Was a Naturalist and Conservationist Whose Writings Had a Profound Influence on American Attitudes Toward Nature
Figure 25.2 The Human-Animal Bond
Figure 25.3 A Community Garden
Figure 25.4 Robert Taylor Homes, Chicago: An Aerial View, the Buildings Without Nearby Trees, and the Buildings with Nearby Trees
Figure 25.5 A Sunday Afternoon on the Island of LaGrande Jatte, 1884–1886, by Georges Seurat
Figure 25.6 Green Exercise
Figure 25.7 Frank Lloyd Wright's Fallingwater
Chapter 27: Risk Assessment in Environmental Health
Figure 27.1 The Multitude of Factors Affecting Risk of Disease
Figure 27.2 Timeline of Milestones in the History of Risk Assessment
Figure 27.3 The Process of Using Environmental Health Risk Assessment to Protect Public Health
Figure 27.4 Threshold Compared to Nonthreshold Dose-
21
Response Models
Figure 27.5 Approach to Carcinogen and Noncarcinogen Dose-Response Assessment
Figure 27.6 Some Common Exposure Pathways
Chapter 28: Communicating Environmental Health
Figure 28.1 Social Amplification of Risk Framework
22
List of Tables Chapter 2: Ecology and Ecosystems as Foundational for Health
Table 2.1 Scale in Ecology, and Some Disciplines That Contribute at Each Level
Table 2.2 Type of Relationship Between Different Species
Table 2.3 Links Between Ecology and Systems Thinking as a Basis for Health
Chapter 3: Sustainability and Health
Table 3.1 Metrics of Sustainability
Chapter 6: Toxicology
Table 6.1 Carcinogen Classification of Chemicals: IARC Results as of March 2015
Chapter 9: Environmental Psychology
Table 9.1 Contrasting Toxicology and Environmental Psychology
Table 9.2 Examples of Convenience, Attractiveness, and Normativeness Applied to a School Cafeteria
Chapter 12: Climate Change and Human Health
Table 12.1 The Main Greenhouse Gases
Table 12.2 Temperature and Precipitation Effects on Selected Vectors and Vector-Borne Pathogens
Table 12.3 Co-Benefits of Climate Mitigation and Adaptation Activities
Chapter 13: Air Pollution
Table 13.1 Major Ambient Air Pollutants: Sources, Health Effects, and Regulations
Chapter 14: Energy and Human Health
Table 14.1 Energy Use in Selected Countries, 2005–2009
Chapter 15: Healthy Communities
23
Table 15.1 Stages of Urban Evolution and Characteristic Environmental Conditions and Health Issues
Table 15.2 Comparison of Sprawl and Smart Growth
Chapter 16: Water and Health
Table 16.1 Hot Spots of Current and/or Potential Water Conflicts
Table 16.2 Examples of Large-Scale Human Impacts on Aquatic Systems
Table 16.3 Classes of Chemical Contaminants in Water
Table 16.4 Examples of Studies of Possible Links Between Exposure to Chemicals in Drinking Water and Increased Health Risk
Table 16.5 Pathogens in or Related to Water, Diseases They Cause, and Approaches to Prevention and Treatment
Table 16.6 Global Challenges in Water and Sanitation, Particularly in Low- and Middle-Income Countries
Table 16.7 The Indicator Approach to Monitoring Water Quality
Table 16.8 Simple, Low-Cost Water Treatment Options
Table 16.9 Approaches to Disinfection
Chapter 18: Pest Control and Pesticides
Table 18.1 Pesticides Classified by Target or Mode of Action
Chapter 19: Food Systems, the Environment, and Public Health
Table 19.1 HACCP Principles
Table 19.2 Jurisdiction over Food Safety in the United States
Table 19.3 Some of the Many Policies Shaping the U.S. Food System
Chapter 20: Buildings and Health
Table 20.1 Average Exposure Concentrations of Formaldehyde and Contribution of Various Atmospheric Environments to Exposure to Formaldehyde
24
Table 20.2 Hazardous Ingredients of Cleaners (Partial Listing)
Table 20.3 Approaches to Protecting Health and Safety in Buildings
Chapter 21: Work, Health, and Well-Being
Table 21.1 The Public Health Impact of OSHA Regulations
Chapter 22: Radiation
Table 22.1 Units of Radiation Exposure and Dose
Table 22.2 Average Amounts of Ionizing Radiation Received Annually by a U.S. Resident
Table 22.3 Representative Radiation Doses in Select Medical Procedures Performed in the United States
Table 22.4 Major Forms and Features of Acute Radiation Syndromes
Table 22.5 Estimated Lifetime Risks of Fatal Cancer AttribuTable to 0.1 Sv Low-Dose-Rate Whole-Body Irradiation
Chapter 23: Injuries
Table 23.1 The Haddon Matrix Applied to Motor Vehicle Crashes
Table 23.2 Options Analysis in Injury Control
Table 23.3 Countermeasures for Intentional Injuries
Table 23.4 Countermeasures for Burns
Table 23.5 Countermeasures for Poisoning
Table 23.6 Countermeasures for Falls
Table 23.7 Countermeasures for Drowning
Table 23.8 Countermeasures for Road Injuries
Table 23.9 Countermeasures for Playground Injuries
Table 23.10 Countermeasures for Home Injuries
Chapter 24: Environmental Disasters
25
Table 24.1 A Typology of Environmental Disasters
Table 24.2 The Ten Deadliest Environmental Disasters— Worldwide, 1964–2013
Table 24.3 Major Causes of Death During Environmental Disasters
Table 24.4 Public Health Consequences and Capabilities Associated with All Disasters
Chapter 26: Environmental Public Health: From Theory to Practice
Table 26.1 Essential Services of Environmental Public Health
Table 26.2 The Protocol for Assessing Community Excellence in Environmental Health (PACE-EH) Process
Chapter 28: Communicating Environmental Health
Table 28.1 Factors Important in Risk Perception
26
Environmental Health
From Global to Local Third Edition
Howard Frumkin, Editor
27
Copyright © 2016 by John Wiley & Sons, Inc. All rights reserved.
Published by Jossey-Bass
A Wiley Brand
One Montgomery Street, Suite 1000, San Francisco, CA 94104-4594— www.josseybass.com
No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400, fax 978-646-8600, or on the Web at www.copyright.com. Requests to the publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, 201-748-6011, fax~201-748-6008, or online at www.wiley.com/go/permissions.
Limit of Liability/Disclaimer of Warranty: While the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional where appropriate. Neither the publisher nor author shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages. Readers should be aware that Internet Web sites offered as citations and/or sources for further information may have changed or disappeared between the time this was written and when it is read.
Jossey-Bass books and products are available through most bookstores. To contact Jossey- Bass directly call our Customer Care Department within the U.S. at 800-956-7739, outside the U.S. at 317-572-3986, or fax 317-572-4002.
Wiley publishes in a variety of print and electronic formats and by print-on-demand. Some material included with standard print versions of this book may not be included in e-books or in print-on-demand. If this book refers to media such as a CD or DVD that is not included in the version you purchased, you may download this material at http://booksupport.wiley.com. For more information about Wiley products, visit www.wiley.com.
Library of Congress Cataloging-in-Publication Data Environmental health (Frumkin)
Environmental health : from global to local / [edited by] Howard Frumkin. — Third edition.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-118-98476-5 (paperback), ISBN 978-1-118-98807-7 (pdf), ISBN 978-1-118- 98806-0 (epub)
I. Frumkin, Howard, editor. II. Title.
[DNLM: 1. Environmental Health. 2. Environmental Exposure—prevention & control. 3. Environmental Medicine–methods. WA 30.5]
RA565
28
616.9'8—dc23
2015036497
Cover design by Wiley
Cover image: © Top Image: © Cultura/Mischa Keijser/Getty; Bottom Image: © Auffret Cline/EyeEm/
29
Dedication
I dedicate this book to my wife, Joanne, and to my children, Gabe and Amara.
Joanne–lover of truth, of science, and of narrative, who walks the talk, who is incapable of pretense or malice, and whose love is an
incalculable gift.
Gabe and Amara–dedicated environmentalists, great lovers of the outdoors, hard-headed idealists, change agents, and two of the
most wonderful people I know. They will make giant contributions to a safer, healthier, more sustainable, and more just world.
30
Tables, Figures, Text Boxes, and Tox Boxes
Tables 2.1 Scale in Ecology, and Some Disciplines That Contribute at
Each Level 2.2 Type of Relationship Between Different Species 2.3 Links Between Ecology and Systems Thinking as a Basis for
Health 3.1 Metrics of Sustainability 6.1 Carcinogen Classification of Chemicals: IARC Results as of
March 2015 9.1 Contrasting Toxicology and Environmental Psychology 9.2 Examples of Convenience, Attractiveness, and
Normativeness Applied to a School Cafeteria 12.1 The Main Greenhouse Gases 12.2 Temperature and Precipitation Effects on Selected Vectors
and Vector-Borne Pathogens 12.3 Co-Benefits of Climate Mitigation and Adaptation Activities 13.1 Major Ambient Air Pollutants: Sources, Health Effects, and
Regulations 14.1 Energy Use Within Selected Countries, 2005–2009 15.1 Stages of Urban Evolution and Characteristic Environmental
Conditions and Health Issues 15.2 Comparison of Sprawl and Smart Growth 16.1 Hot Spots of Current and/or Potential Water Conflicts 16.2 Examples of Large-Scale Human Impacts on Aquatic
Systems 16.3 Classes of Chemical Contaminants in Water 16.4 Examples of Studies of Possible Links Between Exposure to
Chemicals in Drinking Water and Increased Health Risk 16.5 Pathogens in or Related to Water, Diseases They Cause, and
Approaches to Prevention and Treatment
31
16.6 Global Challenges in Water and Sanitation, Particularly in Low- and Middle-Income Countries
16.7 The Indicator Approach to Monitoring Water Quality 16.8 Simple, Low-Cost Water Treatment Options 16.9 Approaches to Disinfection 18.1 Pesticides Classified by Target or Mode of Action 19.1 HACCP Principles 19.2 Jurisdiction over Food Safety in the United States 19.3 Some of the Many Policies Shaping the U.S. Food System 20.1 Average Exposure Concentrations of Formaldehyde and
Contribution of Various Atmospheric Environments to Exposure to Formaldehyde
20.2 Hazardous Ingredients of Cleaners (Partial Listing) 20.3 Approaches to Protecting Health and Safety in Buildings 21.1 The Public Health Impact of OSHA Regulations 22.1 Units of Radiation Exposure and Dose 22.2 Average Amounts of Ionizing Radiation Received Annually
by a U.S. Resident 22.3 Representative Radiation Doses in Select Medical Procedures
Performed in the United States 22.4 Major Forms and Features of Acute Radiation Syndromes 22.5 Estimated Lifetime Risks of Fatal Cancer Attributable to 0.1
Sv Low-Dose-Rate Whole-Body Irradiation 23.1 The Haddon Matrix Applied to Motor Vehicle Crashes 23.2 Options Analysis in Injury Control 23.3 Countermeasures for Intentional Injuries 23.4 Countermeasures for Burns 23.5 Countermeasures for Poisoning 23.6 Countermeasures for Falls 23.7 Countermeasures for Drowning 23.8 Countermeasures for Road Injuries 23.9 Countermeasures for Playground Injuries 23.10 Countermeasures for Home Injuries
32
24.1 A Typology of Environmental Disasters 24.2 The Ten Deadliest Environmental Disasters—Worldwide,
1964–2013 24.3 Major Causes of Death During Environmental Disasters 24.4 Public Health Consequences and Capabilities Associated
with All Disasters 26.1 Essential Services of Environmental Public Health 26.2 The Protocol for Assessing Community Excellence in
Environmental Health (PACE-EH) Process 28.1 Factors Important in Risk Perception
33
Figures 1.1 Title Page of Chadwick's Groundbreaking 1842 Report 1.2 A Victim of Minamata Disease Being Bathed: Photograph by
W. Eugene Smith
1.3 The Need for Primary Prevention: An Early 20th-Century View
1.4 The DPSEEA Model 2.1 A Food Web in a North American Terrestrial Food Ecosystem 2.2 Invasive Species and Their Impacts 2.3 A Classical Model of Ecological Succession in a North
American Forest Ecosystem 2.4 The Phosphorus Cycle 2.5 Transactions Between Atmosphere, Geosphere, and
Hydrosphere Provide a Basis for the Earth's Capacity to Support Life
2.6 Linear Thinking Versus Systems Thinking 2.7 A Systems Map of U.K. Land Use and the Domains That
Influence It 2.8 Ecosystems as Settings for Human Health and Well-Being 2.9 The Life Cycle and Transmission of Leptospira Bacteria 2.10 The MA Conceptual Framework 2.11 The Social Ecological Model 3.1 The Great Acceleration 3.2 Nested Model of Sustainability 3.3 A Safe Operating Space for Humanity 4.1 Area of PFOA Contamination 5.1 Hypothetical Example of the Layering GIS Operation 5.2 Examples of Buffers Around Point, Line, and Area Features 5.3 Map of Genesee County, Michigan, Block Groups (1990
Census) Showing Proportions of Respondents Self- Identifying Race as ``Black''
6.1 Toxicology: From Populations to Molecules
34
6.2 Examples of Dose-Response Curves 6.3 Metabolic Transformations of Benzo(a)pyrene 6.4 Structures of Some Suspected Endocrine-Disrupting
Chemicals 6.5 Key Steps in Toxicokinetics 6.6 The Metabolism of Acetaminophen 6.7 Molecular Structure and LD$_{50}$ for Eight Chemicals 7.1 The Human Genome 7.2 The Basic Structural Elements of a Gene 7.3 The Cystic Fibrosis Mutation 7.4 Chromatin Dynamics in Response to Epigenetic Modification 7.5 Schematic of the Agouti Gene and How Its Methylation
Status Affects Phenotype in Mice 7.6 Primary Biotransformation Pathway for Alcohol 8.1 An Air Pollution Monitoring Station for Ozone and
Particulate Matter, in Atlanta 8.2 Personal Protective Equipment 8.3 Assessing Exposure in an Occupational Setting 9.1 Long Waits and Crowded Buses at a School in Singapore 9.2 Effects of Noise Exposure on Reading Acquisition, Mediated
by Poor Auditory Discrimination 9.3 Illustration of Convenience, Attractiveness, and
Normativeness in a School Cafeteria 9.4 A Waste Setup That Provides a Physical Cue to Encourage
Recycling 9.5 The Five Oaks Neighborhood Following the Defensible Space
Intervention 9.6 Location of Hand Cleaner Dispenser in Patient Room: In
Line of Sight (left) and Inside the Door (right) 9.7 A Utility Bill Employing Social Norms to Encourage Energy
Conservation 11.1a Distribution of Major Industrial Facilities by Racial
Composition of Census Tracts in Southern California 11.1b Distribution of Major Industrial Facilities by Proportion of
35
Census Tract Residents Living Below the Federal Poverty Line in Southern California
11.2 The Four Elements of Cumulative Impacts 11.3 Children in Los Angeles Playing Soccer Near an Oil Refinery 11.4 Explanations for the Effect of Social Inequality on the
Environment 11.5 Members of Clean Up Green Up, an L.A. Environmental
Justice Advocacy Group, Hold a Press Conference in Support of Their Goals
12.1 Components of Radiative Forcing 12.2 The Melting of Arctic Sea Ice 12.3 Processes and Pathways Through Which Climate Change
Influences Human Health 12.4 Number of Days in June, July, and August When Daytime
Maximum Temperatures Exceed a Given Threshold (indicated by a vertical line)
12.5 Urban Heat Island Profile 12.6 The Relationship Between Temperature and Ozone Levels in
Santiago, Chile 12.7 Satellite Photo of a Harmful Algal Bloom in Lake Erie in 2011 12.8 The Association Between Temperature and Childhood
Diarrhea, Peru, 1993–1998 12.9a Climate Stabilization Wedges 12.9b Climate Stabilization Wedges 12.10 The CDC's BRACE Framework 12.11 No-Regrets Solutions 12.12 Global Warming's Six Americas: Arraying the U.S.
Population Along a Continuum of Belief, Concern, and Motivation
12.13 A Comparison of Cumulative CO$_{2}$ Emissions (1950– 2000) (upper panel) with the Burden of Four Climate- Related Health Effects (Malaria, Malnutrition, Diarrhea, and Inland Flood-Related Fatalities (lower panel)
13.1 A Group of Children Wear the Masks on Tiananmen Square in Thick Haze in Beijing, China. 3-Jan-2013
36
13.2 The Distribution of PM$_{2.5}$ Levels in Cities in India, China, Europe, and the United States
13.3 Mortality and Air Pollution Levels During the 1952 London Fog
13.4 The Respiratory System 13.5 Particulate Matter Mass Distribution 14.1 The Fuel Ladder 14.2 Association Between Energy Use and Health, by Nation 14.3 Pathways Linking Energy and Health 14.4 World Energy Consumption 14.5 Indoor Air Pollution from Traditional Cooking 14.6 Products Made from a 42-Gallon Barrel of Crude Oil (in
gallons) 14.7 An Oil Refinery 14.8 Renewable Energy 15.1 World Population: Urban and Rural, 1950–2050 15.2 Nearly 1 Billion People Live in Urban Slums, Such as This
One in Nairobi 15.3 Heavy Traffic, as Shown Here in Delhi, Brings Pollution,
Injury Risks, and Mental~Stress, and Inhibits Physical Activity
15.4 Schematic Comparison of Street Networks and Land Use in a Traditional Neighborhood and in an Area of Sprawl
15.5 Percentage of Self-Reported Obesity in Adults in the United States, by State, 2013
15.6 An Example of Complete Streets in Copenhagen, Where Many Streets Are Designed to Accommodate Pedestrians, Bicyclists, Transit, and Automobiles
15.7 Access to Healthy Food Options 15.8 Overlapping Frameworks for Healthy Community Design 15.9 Relationship Between Growth of Bicycle Infrastructure and
Amount of Cycling in Portland, Oregon 16.1 The Hydrological Cycle 16.2 Schematic of the Interconnections Between Water and
37
Health 16.3 Pesticide Movement in the Hydrological Cycle, Including
Movement to and from Sediment and Aquatic Biota in a Stream
16.4 Sanitation Options 16.5 An Idealized Wastewater Treatment System, Based on
Boston's Deer Island System 16.6 Carrying Water 16.7 Basic Drinking-Water Treatment Process 16.8 A Multibarrier Approach to Maximize Microbiological Water
Quality 17.1 Chemical Drums at Love Canal 17.2 Composition of the 251 Million Tons of Municipal Solid
Waste Produced in the United States (Before Recycling), 2012
17.3 Total Amount and Per Capita Generation Rate of Municipal Solid Waste Produced in the United States (Before Recycling), 1960–2012
17.4 Total Amount and Percentage of Municipal Solid Waste Recycled in the United States, 1960–2012
17.5 Glass and Paper Recycling in Industrial Nations 17.6 Waste Tires 17.7 Generalized Depiction of a State-of-the-Art Sanitary Landfill 17.8 Generalized Diagram of Incineration Material and Process
Flow 17.9 Mine Tailings Pile: The Legacy of Sixty Years of Lead and
Zinc Mining in Ottawa~County, Oklahoma 18.1 Application of Lead Arsenate in the Early 1900s 18.2 Modern Pesticide Application Equipment 18.3 A Corn Borer, an Example of an Insect Pest, Causing Damage
in the Stalk of a Corn Plant 18.4 Farmers Applying Organophosphate Insecticides in Thailand 19.1 Selected Components of the Food System 19.2 Applying Herbicide to a North Carolina Cornfield
38
19.3 Potential Pathways for the Spread of Antibiotic-Resistant Bacteria from Animals to Humans
19.4 Manure Cesspit Outside Hog CAFO in Duplin County, North Carolina
19.5 Ducks in One of Takao Furuno's Rice Paddies in Japan 19.6 The EPA Food Recovery Hierarchy Prioritizes Actions to
Prevent and Divert Wasted Food 19.7 Contribution of Different Food Categories to Estimated
Domestically Acquired Illness and Death, United States, 1998–2008
19.8 A Health Inspector Tests the Temperature of Refrigerated Meat at a Restaurant
19.9 A 1993 Outbreak Caused by E. Coli 0157 in Undercooked Beef at Jack in the Box Restaurants Sickened 732 People and Killed 4 Children
19.10 An Example of Improper Grain Storage 19.11 A U.S. Department of Agriculture Food Safety Inspection
Service Inspector at a Poultry Processing Facility in Accomac, Virginia, Testing for Cleanliness and the Avian Influenza (AI) Virus
20.1 Housing Can Take Many Forms and Vary Greatly in Desirability and Safety
20.2 Trailer Provided by FEMA after Hurricane Katrina 20.3 School Design 20.4 Mold-Damaged Building in New Orleans Following
Hurricane Katrina 21.1 From July 1906 Through June 1907, 526 Workers Were
Killed on the Job in Allegheny County, Pennsylvania 21.2 Who Bears the Cost of Worker Injuries? 22.1 The Electromagnetic Spectrum 22.2 Cell Phones Are Virtually Ubiquitous, and Entail Exposure to
Radiofrequency Radiation 22.3 A Basal Cell Carcinoma of the Skin of Twenty Years Duration
in a Fifty-Eight-Year-Old Man 22.4 Nuclear Transformation Mechanisms That Release
39
Radioactivity 22.5 Using X Rays for Fitting Shoes 22.6 The Chernobyl Disaster 23.1 The Injury Pyramid 23.2 Typology of Violence 24.1 Annual Incidence of Natural and Technological
Environmental Disasters—Worldwide, 1964–2013 24.2 Comparison of the Public Health Impacts of Natural and
Technological Disaster Events, 1964–2013 24.3 Key Public Health Impacts for Natural and Technological
Disasters, 1964–2013 24.4 Three Conceptual Frameworks for Disaster Risk
Management 24.5 The Four Elements of a Resilience Framework 25.1 John Muir (1838–1914) Was a Naturalist and
Conservationist Whose Writings Had a Profound Influence on American Attitudes Toward Nature
25.2 The Human-Animal Bond 25.3 A Community Garden 25.4 Robert Taylor Homes, Chicago: An Aerial View, the Buildings
Without Nearby Trees, and the Buildings with Nearby Trees 25.5 A Sunday Afternoon on the Island of La Grande Jatte, 1884–
1886, by Georges~Seurat 25.6 Green Exercise 25.7 Frank Lloyd Wright's Fallingwater 27.1 The Multitude of Factors Affecting Risk of Disease 27.2 Timeline of Milestones in the History of Risk Assessment 27.3 The Process of Using Environmental Health Risk Assessment
to Protect Public Health 27.4 Some Common Exposure Pathways 27.5 Threshold Compared to Nonthreshold Dose-Response
Models 27.6 Carcinogen and Noncarcinogen Dose-Response
Relationships
40
28.1 Social Amplification of Risk Framework
41
Text Boxes 1.1 Definitions of Environmental Health 1.2 Environmental Health: Common Good or Nanny State? 1.3 A Prevention Poem: A Fence or an Ambulance 2.1 Food Webs 2.2 Biological Invasions 2.3 Conservation Biology 2.4 Ecosystem Services 2.5 Restoration Ecology: The Practical Application of Ecological
Literacy and Systems Thinking 2.6 Infectious Disease as an Ecological and Social Process: The
Example of Leptospirosis 3.1 Planetary Health 3.2 Sustainability in Health Care 4.1 Example of a Community Cohort Study 4.2 An Interview Study to Improve Sanitation 6.1 Dose-Response Curve 6.2 Transporting Vital, Yet Dangerous Chemicals 6.3 Chemical Carcinogenesis 6.4 Endocrine Disruptors 6.5 The Microbiome and Toxicology 6.6 LD50 for Various Compounds
6.7 Replace, Reduce, Refine: Laboratory Animals in Toxicology 7.1 Liver Cancer from Moldy Corn and Peanuts: Aflatoxin and the
Role of GSTM1 Polymorphism 7.2 Genetic Susceptibility to Environmental Mercury 8.1 Assessing an Electronics Manufacturing Facility: The Role of
Anticipation 8.2 Understanding Concentration, Exposure, and Dose 8.3 Assessing Exposure to Carbon Monoxide 10.1 Selected Ethics Approaches
42
10.2 The Art of Ethics 10.3 Professionalism and Ethics 10.4 Typical Elements in Professional Codes of Ethics 10.5 Environmental Responsibility Principles in Ethics Codes 10.6 Environmental Responsibility 11.1 Roots of Environmental Justice in Warren County, North
Carolina 11.2 Children Are Not Small Adults 11.3 Environmental Justice Meets Urban Forestry 12.1 Some Effects of Weather and Climate on Vector- and Rodent-
Borne Diseases 12.2 The CDC's BRACE Framework 13.1 Air Pollution in the World's Dirtiest Cities 13.2 London 1952: One of the World's Worst Air Pollution
Disasters 13.3 The Clean Air Act: Environmental Regulation for Public
Health Protections 14.1 Health Impacts of the Dublin Coal Ban 14.2 Peak Petroleum and Public Health 14.3 Health Co-Benefits of Energy Conservation and Efficiency 15.1 Urbanization Versus Urbanism 15.2 Policies That Regulate Land Use 15.3 Impacts of Community Design on Health 15.4 Safe Walking and Cycling 15.5 Health Impact Assessment: A Tool for Land-Use and
Transportation Decision Making 15.6 Smart Growth Principles to Promote Equitable, Healthy, and
Sustainable Communities 15.7 Principles of Universal Design 15.8 LEED for Neighborhood Development Certification Program 16.1 Water as a Nutrient 16.2 A Gross Inequity 16.3 Antibiotic Resistance
43
16.4 Chronology of Events During the Walkerton, Ontario, E. coli O157 Outbreak in 2000
16.5 Risk Factors and the Changing Burden of Disease 16.6 Water Treatment More Than a Century Ago (1881) 16.7 The Contaminant Candidate List 17.1 U.S. Solid and Hazardous Waste Laws and Policy 17.2 The Challenge of Medical Waste 17.3 e-Waste 17.4 Tire Reuse and Recycling 17.5 International Trafficking in Hazardous Wastes 18.1 Insect Repellants 18.2 Who Is Responsible for Applying Pesticides? 18.3 Pesticide Toxicity Categories and Labeling Requirements 19.1 Policy Approaches to Antibiotic Use in Animal Agriculture 19.2 Organic Agriculture: What Does It Mean? 19.3 The Environmental Impacts of Wasted Food 19.4 Globalization, Seafood, and Food Safety 19.5 Mycotoxins 20.1 Manufactured Structures 20.2 Homelessness: An Environmental Health Problem? 20.3 Chemical Safety in Buildings 20.4 Sick Building Syndrome 20.5 Building Design for the Elderly 21.1 “Statistics Are People with the Tears Wiped Away” 21.2 Mine Disasters, Miner Protections 21.3 Core Elements of All Safety and Health Management Systems 22.1 Is Cell Phone Use Linked to Cancer? 22.2 What Are Isotopes? 22.3 What Happens During Most Nuclear Power Plant Accidents? 23.1 Fatal Occupational Injury at a Gun Range 23.2 Texting and Driving 23.3 Engineering the Driver Out of the Equation
44
23.4 Firearm Policy 24.1 Disaster Resilience 24.2 The 11 E's of Public Health Preparedness 24.3 A Case Study of Haiti's Troubled Recovery 25.1 Getting Kids Outside: A Public Health Strategy? 25.2 Community Gardens 25.3 Nature Contact in the Inner City 25.4 Parks and Public Health 25.5 Green Exercise 25.6 Nature Contact, Poverty, and Health: A Connection? 25.7 Biophilic Design 26.1 Keeping Track in Environmental Health 26.2 Careers in Environmental Health 27.1 Example of Problem Formulation: Assessing a New
Incinerator 27.2 Example of Hazard Identification: Evaluating Methylmercury 27.3 Technical Terminology in Risk Assessment 27.4 Risk Characterization for a Methylmercury Risk Assessment 27.5 Risk Management for Methylmercury in Seafood 28.1 Risk Communication: A Two-Way Process 28.2 Elements of a Comprehensive Risk and Crisis Communication
Plan 28.3 Overcoming Psychological, Cultural, and Sociological Barriers
to Risk Communication 28.4 Questions Frequently Asked During an Emergency or Crisis
45
Tox Boxes 2.1 Polychlorinated Biphenyls (PCBs) 6.1 Bisphenol A (BPA) 6.2 Polycyclic Aromatic Hydrocarbons 6.3 Phthalates 7.1 Benzene 11.1 Lead (Pb) 13.1 Carbon Monoxide 13.2 Mercury (Hg) 16.1 Arsenic 16.2 Disinfection By-Products 18.1 Organophosphates 18.2 Organochlorine Pesticides 19.1 Dioxins 20.1 Volatile Organic Compounds (VOCs): The Case of
Formaldehyde 20.2 Radon 20.3 Asbestos 20.4 Polybrominated Diphenyl Ethers (PBDEs)
An instructor's supplement is available at www.wiley.com/go/frumkin3e. Additional materials such as videos, podcasts, and readings can be found at www.josseybasspublichealth.com. Comments about this book are invited and can be sent to [email protected].
46
The Editor Howard Frumkin has been dean, and professor of environmental and occupational health sciences, at the University of Washington School of Public Health since 2010. From 2005 to 2010, he held leadership roles at the U.S. Centers for Disease Control and Prevention, first as director of the National Center for Environmental Health and Agency for Toxic Substances and Disease Registry (NCEH/ATSDR), and later as special assistant to the CDC director for climate change and health. From 1990 to 2005, he was professor and chair of environmental and occupational health at Emory University's Rollins School of Public Health and professor of medicine at the Emory School of Medicine.
Dr. Frumkin trained in internal medicine, epidemiology, and occupational and environmental medicine. His research interests include public health aspects of the built environment, climate change, energy policy, and nature contact; toxic effects of chemicals; and environmental health policy. He is the author or coauthor of over 200 scientific journal articles and chapters, and his books, in addition to this one, include Urban Sprawl and Public Health (Island Press, 2004, coauthored with Lawrence Frank and Richard Jackson), Emerging Illness and Society (Johns Hopkins University Press, 2004, co-edited with Randall Packard, Peter Brown, and Ruth Berkelman), Safe and Healthy School Environments (Oxford University Press, 2006, co-edited with Robert Geller, Leslie Rubin, and Janice Nodvin), Green Healthcare Institutions: Health, Environment, Economics (National Academies Press, 2007, co- edited with Christine Coussens), and Making Healthy Places: Designing and Building for Health, Well-Being, and Sustainability (Island Press, 2011, co-edited with Andrew Dannenberg and Richard Jackson).
Dr. Frumkin has worked with many organizations active at the interface of human health and the environment. He has served on the boards of the Bullitt Foundation, the Children & Nature Network, the Seattle Parks Foundation, the Pacific Northwest Diabetes Research Institute, the U.S. Green Building Council, the Washington Global Health Alliance, Physicians for Social Responsibility, the Association of Occupational and Environmental
47
Clinics, the American Public Health Association, and the National Environmental Education Foundation. He has served on the Executive Committee of the Regional Open Space Strategy for Central Puget Sound, on Procter & Gamble's Sustainability Expert Advisory Panel, on the National Toxicology Program Board of Scientific Counselors, on the National Research Council Committee on Sustainability Linkages in the Federal Government, on the Washington Department of Ecology Toxics Reduction Strategy Group, and on Seattle's Green Ribbon Commission. He has served on advisory boards for the Yale Climate and Energy Institute, the Wellcome Trust Sustaining Health initiative, the National Sustainable Communities Coalition, and the Center for Design and Health at the University of Virginia School of Architecture. As a member of the EPA's Children's Health Protection Advisory Committee, he chaired the Smart Growth and Climate Change work groups. A graduate of the Institute for Georgia Environmental Leadership, he was named 2004 Environmental Professional of the Year by the Georgia Environmental Council.
Dr. Frumkin was born in Poughkeepsie, New York. He received his AB degree from Brown University, his MD degree from the University of Pennsylvania, his MPH and DrPH degrees from Harvard University, his internal medicine training at the Hospital of the University of Pennsylvania and Cambridge Hospital, and his environmental and occupational medicine training at Harvard. He is board certified in internal medicine and in environmental and occupational medicine, and is a Fellow of the American College of Physicians, the American College of Occupational and Environmental Medicine, Collegium Ramazzini, and the Royal College of Physicians of Ireland. He is an avid cyclist, paddler, and hiker. He is married to radio journalist Joanne Silberner, and has two children—Gabe, a political campaign worker, and Amara, a health worker.
48
The Contributors Michelle L. Bell, PhD
Mary E. Pinchot Professor of Environmental Health
School of Forestry & Environmental Studies
Yale University
New Haven, Connecticut
Pamela Rhubart Berg, MPH
Education Program Manager
Center for a Livable Future
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Thomas A. Burke, PhD, MPH
Jacob I. and Irene B. Fabrikant Professor and Chair in Health Risk and Society
Director, Risk Sciences and Public Policy Institute
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Anthony G. Capon, MBBS, PhD, FAFPHM
Professor and Director
International Institute for Global Health
United Nations University
Kuala Lumpur, Malaysia
Megan Cartwright, BS
PhD Candidate, Environmental and Occupational Health Sciences
School of Public Health
University of Washington
49
Seattle, Washington
Kristin Aldred Cheek, BA, MS
PhD Candidate, Department of Design and Environmental Analysis
College of Human Ecology
Cornell University
Ithaca, New York
Vincent T. Covello, PhD
Founder and Director, Center for Risk Communication
New York, New York
Andrew L. Dannenberg, MD, MPH
Affiliate Professor, Environmental and Occupational Health Sciences, and Urban Design and Planning
School of Public Health and College of Built Environments
University of Washington
Seattle, Washington
David L. Eaton, PhD
Dean, Graduate School and Professor, Environmental and Occupational Health Sciences
School of Public Health
University of Washington
Seattle, Washington
Anna Engstrom, BS
PhD Candidate, Environmental and Occupational Health Sciences
School of Public Health
University of Washington
Seattle, Washington
Gary W. Evans, PhD
50
Elizabeth Lee Vincent Professor of Human Ecology
Departments of Design & Environmental Analysis and of Human Development
College of Human Ecology
Cornell University
Ithaca, New York
Henry Falk, MD, MPH
Carter Consulting, Inc.
Consultant to Office of Noncommunicable Disease, Injury and Environmental Health (ONDIEH)
Centers for Disease Control and Prevention
Atlanta, Georgia
Timothy Ford, PhD
Dean, School of Health Professions
Shenandoah University
Winchester, Virginia
Lynn R. Goldman, MD, MS, MPH
The Michael and Lori Milken Dean of Public Health and Professor of Environmental and Occupational Health
Milken Institute School of Public Health
The George Washington University
Washington, DC
George C. Hamilton, PhD
Professor and Chair
Department of Entomology
Rutgers University
New Brunswick, New Jersey
Jeremy J. Hess, MD, MPH
Associate Professor of Medicine, Division of Emergency
51
Medicine
School of Medicine
Associate Professor, Environmental and Occupational Health Sciences
School of Public Health
University of Washington
Seattle, Washington
Jason R. Holmes, MD
Resident Physician, Emergency Medicine
Emory University
Atlanta, Georgia
Leo Horrigan, MHS
Food Systems Correspondent
Center for a Livable Future
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Pierre Horwitz, PhD
Professor of Environmental Science
School of Natural Sciences
Edith Cowan University
Joondalup, Western Australia
Andrew Jameton, PhD
Professor Emeritus, Health Promotion, Social and Behavioral Health
College of Public Health
University of Nebraska Medical Center
Omaha, Nebraska
Mark E. Keim, MD, MBA
Owner, DisasterDoc™, LLC
52
Lawrenceville, Georgia
Juleen Lam, PhD
Assistant Research Scientist
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Dave Love, PhD, MSPH
Assistant Scientist
Center for a Livable Future
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Edward Maibach, MPH, PhD
University Professor, Department of Communication
Director, Center for Climate Change Communication
George Mason University College of Humanities and Social Sciences
Fairfax, Virginia
David Michaels, PhD, MPH
Assistant Secretary of Labor for Occupational Safety and Health
Washington, DC
Professor of Environmental and Occupational Health
Milken Institute School of Public Health
The George Washington University
Washington, DC
Gary W. Miller, PhD
Professor and Associate Dean for Research
Department of Environmental Health
Rollins School of Public Health
Emory University
53
Atlanta, Georgia
Christine L. Moe, PhD
Eugene J. Gangarosa Professor of Safe Water and Sanitation
Director, Center for Global Safe Water, Sanitation, and Hygiene at Emory University
Hubert Department of Global Health
Rollins School of Public Health
Emory University
Atlanta, Georgia
Rachel Morello-Frosch, PhD, MPH
Professor, Department of Environmental Science, Policy & Management
School of Public Health
University of California, Berkeley
Berkeley, California
Matthew P. Moeller, MS, CHP
Chief Executive Officer
Dade Moeller & Associates
Richland, Washington
Keeve Nachman, PhD, MHS
Assistant Professor and Program Director
Food Production & Public Health Program
Center for a Livable Future
Johns Hopkins Bloomberg School of Public Health
Baltimore, MD
Roni Neff, PhD
Assistant Professor, Environmental Health Sciences
Program Director, Food System Sustainability and Public Health
Center for a Livable Future
54
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Cindy L. Parker, MD, MPH
Assistant Professor, Departments of Environmental Health Sciences, and Krieger School of Arts and Sciences
Associate Director, Environment, Energy, Sustainability & Health Institute
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Margot W. Parkes, MBChB, MAS, PhD
Canada Research Chair in Health, Ecosystems and Society
Associate Professor, School of Health Sciences, Cross Appointed, Northern Medical Program
University of Northern British Columbia
Prince George, British Columbia, Canada
Manuel Pastor, PhD
Professor, Departments of Sociology and of American Studies & Ethnicity
Director, Program on Environmental and Regional Equity
University of Southern California
Los Angeles, California
Jonathan A. Patz, MD, MPH
Professor and John P. Holton Chair in Health and the Environment
Director, Global Health Institute
University of Wisconsin
Madison, Wisconsin
Héctor Luis Maldonado Pérez, BS
Research Assistant and Graduate Student
School of Public Health
55
Rutgers University
New Brunswick, New Jersey
Junaid A. Razzak, MD, PhD
Professor, Department of Emergency Medicine
Johns Hopkins School of Medicine
Department of International Health
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Jessica D. Rhodes, MD, MPH
Family Medicine Resident
Sutter Santa Rosa Family Medicine Residency
Santa Rosa, California
Mark Gregory Robson, PhD, MPH, DrPH
Distinguished Service Professor and Chair
Department of Plant Biology and Pathology
Rutgers University
New Brunswick, New Jersey
Sven E. Rodenbeck, ScD, PE, BCEE
Rear Admiral (retired), U.S. Public Health Service
Senior Service Fellow
Agency for Toxic Substances and Disease Registry
Centers for Disease Control and Prevention
Atlanta, Georgia
P. Barry Ryan, PhD
Professor, Exposure Science and Environmental Chemistry
Department of Environmental Health
Director of Laboratories
Rollins School of Public Health
56
Emory University
Atlanta, Georgia
Jonathan Samet, MD, MS
Director, USC Institute for Global Health
Distinguished Professor and Flora L. Thornton Chair
Department of Preventive Medicine
Keck School of Medicine
University of Southern California
Los Angeles, California
Christopher M. Schaupp, BS
Graduate Student, Environmental and Occupational Health Sciences
School of Public Health
University of Washington
Seattle, Washington
Brian S. Schwartz, MD, MS
Professor, Departments of Environmental Health Sciences and Epidemiology
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Mary C. Sheehan, MALD, MPH, PhD
Faculty Associate
Johns Hopkins Bloomberg School of Public Health
Baltimore, Maryland
Wattasit Siriwong, PhD
Associate Professor and Deputy Dean
College of Public Health Sciences
Chulalongkorn University
Bangkok, Thailand
57
Marissa N. Smith, MS
PhD Candidate, Environmental and Occupational Health Sciences
School of Public Health
University of Washington
Seattle, Washington
Kyle Steenland, PhD, MS
Professor, Departments of Environmental Health and Epidemiology
Rollins School of Public Health
Emory University
Atlanta, Georgia
Gregory R. Wagner, MD
Senior Advisor to the Director, National Institute for Occupational Safety and Health
Centers for Disease Control and Prevention (CDC/NIOSH), Washington, DC
Adjunct Professor, Harvard T. H. Chan School of Public Health
Boston, Massachusetts
Lance A. Waller, PhD
Rollins Professor and Chair, Department of Biostatistics and Bioinformatics
Rollins School of Public Health
Emory University
Atlanta, Georgia
Nancy M. Wells, PhD
Associate Professor, Department of Design and Environmental Analysis
College of Human Ecology
Cornell University
58
Ithaca, New York
James S. Woods, PhD, MPH, MS
Research Professor Emeritus
Department of Environmental and Occupational Health Sciences
School of Public Health
University of Washington
Seattle, WA
Anna Q. Yaffee, MD, MPH
Resident Physician
Department of Emergency Medicine
School of Medicine
Emory University
Atlanta, Georgia
Michael G. Yost, PhD
Chair and Professor, Department of Environmental Health and Occupational Health Sciences
School of Public Health
University of Washington
Seattle, Washington
59
Acknowledgments In many religions and cultures teachers are revered. I honor that tradition, as well I should: I have been blessed with more superb teachers than I had any right to expect when I first marched off to school. They didn't know it, but they were all preparing me to envision this book and pull it together. One of the sweetest privileges of an editor—and there have been many—is the chance to thank them.
I express my deep and lasting gratitude to my high school teacher Barbara Leventer, who taught me that writing a research paper means specifying a hypothesis, organizing an outline, finding the right sources, and writing clearly (yes, that was all possible before the Internet!); my college teachers the late Ed Beiser, who taught me that there is no excuse for muddled thinking and unclear expression, and Steve Lyons and the late Hunter Dupree, who taught me the majesty and endless relevance of history; my medical school teachers Paul Stolley, who taught me the power of epidemiological data and who set a standard for principled advocacy, and the late John Eisenberg, who modeled a formidable combination of clinical excellence, astute policy analysis, and great kindness; my residency chief Bob Lawrence, who taught me that primary care extends from the bedside to the global commons; and my graduate school teachers Richard Monson, the late John Peters, and David Wegman, who taught me the interface of public health and the environment. Dick Jackson has been a mentor, thought partner, and friend since he arrived at the CDC 20 years ago.
I thank Dean Jim Curran and my colleagues and students at Emory University's Rollins School of Public Health, where I had the great good fortune to serve as a faculty member from 1990 to 2005, and where I edited the first edition of this textbook. I also thank my colleagues at the U.S. Centers for Disease Control and Prevention, where I directed the National Center for Environmental Health (NCEH) and the Agency for Toxic Substances and Disease Registry (ATSDR) from 2005 to 2010, and where I edited the second edition. And I thank my colleagues at the University of Washington School of Public Health, where I have served as dean since 2010. Two great universities and a great government agency have offered a
60
wonderful career path, marked by intellectual stimulation, hard- working, dedicated colleagues, and dear friends. I thank my colleagues at other agencies, such as the Environmental Protection Agency and the National Institute of Environmental Health Sciences, and at organizations ranging from environmental and community groups to law firms to manufacturing companies, who have taught me more than I can say about the many facets of environmental health. Over the years I have especially appreciated my friends and colleagues at Physicians for Social Responsibility; the Institute of Medicine Roundtable on Environmental Health, Research, and Medicine; Atlanta's Clean Air Campaign; the EPA's Children's Health Protection Advisory Committee; the Association of Occupational and Environmental Clinics; the American Public Health Association; Sustainable Atlanta; the Children & Nature Network; the Bullitt Foundation; the Washington Global Health Alliance; the U.S. Green Building Council; the American Institute of Architects; and the Seattle Parks Foundation. Special gratitude to the members of my Green Reading Groups, first in Atlanta, and later in Seattle—perfect blends, both, of close friendship, intellectual curiosity, and environmental learning.
Thank you to Karla Armenti, Kathlyn Barry, Darrell Norman Burrell, William Daniel, J. Aaron Hipp, Peter LaPuma, Susan West Marmagas, Camille Martina, Mary Kay O'Rourke, Anne Riederer, Lauren Savaglio, and Alfredo Vergara, who provided valuable feedback on the previous edition of this book, which helped greatly in designing changes for this edition.
I thank the chapter authors of this book, all of them highly expert and exceedingly busy people. They willingly shared their expertise and time (and gracefully tolerated my prodding and editing) to help compile the kind of book that we would all want to use in our own teaching. I am especially pleased that the authors include several graduate students and trainees, whose skill and energy bode well for the future of our field. I thank my editors at Jossey-Bass. The late Andy Pasternack, who edited the first two editions, was a friend, supporter, and mentor; his premature loss leaves a hole in the universe. Seth Schwartz ably succeeded Andy, bringing the same belief in this project, generous tolerance of delays, and discipline. Melinda Noack and Justin Frahm rounded out an all-star team at Jossey-Bass. And I thank copyeditor Elspeth MacHattie, a
61
consummate professional, a pleasure to work with, and an enormous asset to this book.
I thank the staff who supported the preparation of the first and second editions of this book: Hope Jackson, Robin Thompson, Adrienne Tison, Erica Weaver, Rachel Wilson, and Suzanne Mason at Emory, and Cheryl Everhart at NCEH/ATSDR. And special thanks to JeShawna Schmidt, who supported me at the University of Washington in preparing this third edition, with her extraordinary combination of organizational skills, work ethic, grace, dedication, kindness, and optimism.
I had an unforgettable opportunity while preparing the third edition: a two-week academic residency at Villa Serbelloni, the Rockefeller Foundation's center in Bellagio, Italy. This sojourn exemplified the power of a physical setting—the indescribable beauty of Lake Como and of the facility itself—to inspire good work and to promote well-being. More importantly, it also exemplified the magic that occurs when people from diverse backgrounds and disciplines come together. My fellow residents hailed from South Africa, Kenya, India, and across the United States, and were working on housing, transportation, NGO governance, urban resiliency, literature, visual art, and dance—but all, in a real sense, were working on social change, dedicated to making the world a better place. I made lifelong friends, I learned from each of them, and they are all reflected in this book. I thank the Rockefeller Foundation for the privilege.
Finally, I acknowledge my beloved wife, best friend, and trusted consultant, Joanne Silberner, who silently, eloquently raised her eyebrows when I told her I had committed to another edition of this book, then supported me unstintingly throughout. Without her, nothing.
62
Potential Conflicts of Interest in Environmental Health: From Global to Local In recent years, increasing attention has been focused on integrity in scientific publishing. Much of this concern has grown out of pharmaceutical research; in that arena, conflicts of interest are widespread (Friedman & Richter, 2004) and consequential; funding sources have been shown to predict research findings (Kjaergard & Als-Nielsen, 2002; Lexchin, Bero, Djulbegovic, & Clark, 2003; Smith, 2005; Lundh, Sismondo, Lexchin, Busuioc, & Bero, 2012). But pharmaceutical research is not the only vulnerable area; in environmental health, private interests may also collide with public good, so conflicts of interest must be recognized as a real concern in this field too (Michaels & Monforton, 2005; Sutton, Woodruff, Vogel, & Bero, 2011). In 2015, disclosures about an allegedly conflicted climate change researcher on the front page of the New York Times—nobody's ideal venue for such matters—reinforced this fact (Gillis, 2015; Gillis & Schwartz, 2015).
Conflicts of interest have been defined as “conditions in which professional judgment concerning a primary interest (such as a patient's welfare or the validity of research) tends to be unduly influenced by a secondary interest (such as financial gain)” (Thompson, 1993). Conflicts of interest, real or perceived, can derail the quest for truth, have a corrosive effect on scientific data (Bekelman, Li, & Gross, 2003; Rennie, 2010), and undermine public faith in science (Friedman, 2002; Kennedy, 2004; Lo & Field, 2009).
Importantly, the bias resulting from conflicts of interest may be subconscious, reflecting neither malfeasance nor even intent. Bias is a normal part of human cognition, and people are often unaware of their biases (Cain & Detsky, 2008; Young, 2009).
Conflicts of interest may be financial or nonfinancial. The financial variety is intuitively clear; as former JAMA editor Drummond Rennie wrote, “numerous studies have confirmed what we all know: money talks” (Rennie, 2010). The nonfinancial variety is not always as clear. These conflicts may be personal, political, religious, ideological, or careerist (Levinsky, 2002). The editors of PLoS
63
Medicine described two examples (The PLoS Medicine Editors, 2008): the peer reviewer who disapproves of a particular research method for religious reasons, and who obstructs the publication of research using that method; and the editor who remains close to her former advisor, and who tilts toward accepting the advisor's paper.
Those who publish or report on science have increasingly tackled the challenge of conflicts of interest (Maurissen et al., 2005; Lo & Field, 2009). Transparency is a leading solution, recalling Justice Louis Brandeis's adage that “sunshine is the best disinfectant”— even if it is not always sufficient (Bero, Glantz, & Hong, 2005; Resnik & Elliott, 2013). The Committee on Publication Ethics (COPE, 2011), a forum for peer-reviewed journal editors and publishers, in its Code of Conduct, requires that “[r]eaders should be informed about who has funded research or other scholarly work and whether the funders had any role in the research and its publication and, if so, what this was.” Similarly, the International Committee of Medical Journal Editors (ICMJE, 2014) expects authors to disclose both “financial relationships with entities in the bio-medical arena that could be perceived to influence, or that give the appearance of potentially influencing,” and “other [nonfinancial] relationships or activities that readers could perceive to have influenced, or that give the appearance of potentially influencing” an author's work. Accordingly, most medical journals now require disclosures of potential conflicts of interest when publishing papers. Such disclosures serve a purpose; they inform readers' views of what they read (Chaudhry, Shroter, Smith, & Morris, 2002; Kesselheim et al., 2012).
Disclosure has moved beyond the publication of research findings in journals. Many (but not enough) reports of scientific results in the popular media now mention funding sources (Cook, Boyd, Grossman, & Bero, 2007). Many universities require faculty to report potential conflicts of interest (Boyd & Bero, 2000). Disclosure is especially important in review papers (Michaels, 2009; Viswanathan et al., 2014). “Because analysis, interpretation, and synthesis, often of conflicting data, are important aspects of these papers,” wrote one journal editor, “they are particularly susceptible to suspicions of bias, subconscious or otherwise” (DeMaria, 2004). The same, of course, is true for textbook chapters. But it is rare for textbooks to disclose potential conflicts of interest. This omission is
64
curious given the wide readership of textbooks, the tendency of textbook chapters to present broad conclusions, and the fact that student readers, at an early stage of their training, may be more impressionable than discerning.
This third edition of Environmental Health: From Global to Local, continuing a practice begun in the second edition, has addressed this concern by asking each chapter author to report both real and perceived conflicts of interest. Following guidelines from a Natural Resources Defense Council workshop (Sass, 2009) and from the ICMJE (2014), each author was asked to disclose relationships occurring during the last three years, currently active, or reasonably anticipated to occur in the foreseeable future “with companies that make or sell products or services discussed in the chapter, companies that make or sell related products or services, and other pertinent entities with an interest in the topic, specifying the type of relationship.” These relationships were defined as including (but not limited to)
Grant support
Employment (past, present, or firm offer of future)
Stock ownership or options
Payment for serving as an expert witness or giving testimony
Personal financial interests on the part of the author, immediate family members, or institutional affiliations that might gain or lose financially through publication of the chapter
Other forms of compensation, including travel funding, consultancies, honoraria, board positions, and patent or royalty arrangements
Employment by a for-profit, nonprofit, foundation, or advocacy group
If it is important for authors to offer these disclosures to readers, it is even more important for the editor—who selects and curates all material in the book—to do so. During the three years prior to starting work on this book, and while doing the editing, in addition to my work as dean at the University of Washington School of Public Health, I held the following positions:
Board member of the U.S. Green Building Council, which
65
promotes green, healthy buildings (uncompensated)
Board member of the Bullitt Foundation, a regional environmental grantmaker in the Pacific Northwest (uncompensated)
Board member of the Seattle Parks Foundation, which promotes parks and park access in Seattle (uncompensated)
Member of the American Institute of Architects Design & Health Leadership Group, which promotes healthy building design (uncompensated)
Member of the American Association for the Advancement of Science Climate Science Panel, which provides public information on climate science (uncompensated)
Member of the Yale Climate and Energy Institute External Advisory Board (uncompensated)
Member of the Procter & Gamble Sustainability Expert Advisory Panel (honorarium paid to University of Washington)
Member of several editorial boards, all uncompensated (American Journal of Industrial Medicine, Salud Pública de México, Environmental Health Perspectives, American Journal of Preventive Medicine, ECOHEALTH, Annual Review of Public Health, and Ecopsychology)
Each author's employment is shown in the author identification section, and disclosures of potential conflicts of interest appear at the bottom of the first text page of his or her chapter. I am not aware of another major textbook that has implemented such a policy. I hope this helps to ensure the integrity of every chapter in this book and becomes more common in scientific textbooks in coming years.
Howard Frumkin Editor
66
References Bekelman, J. E., Li, Y., & Gross, C. P. (2003). Scope and impact of financial conflicts of interest in biomedical research: A systematic review. JAMA, 289, 454–465.
Bero, L. A., Glantz, S., & Hong, M. K. (2005). The limits of competing interest disclosures. Tobacco Control, 14(2), 118–126.
Boyd, E., & Bero, L. (2000). Assessing faculty financial relationships with industry. JAMA, 284, 2209–2214.
Cain, D. M., & Detsky, A. S. (2008). Everyone's a little bit biased (even physicians). JAMA, 299(24), 2893–2895.
Chaudhry, S., Shroter, S., Smith, R., & Morris, J. (2002). Does declaration of competing interests affect readers' perceptions? A randomized trial. BMJ, 325, 1391–1392.
Committee on Publication Ethics. (2011). Code of conduct and best practice guidelines for journal editors. Retrieved from http://publicationethics.org/files/Code_of_conduct_for_journal_editors_Mar11.pdf
Cook, D. M., Boyd, E. A., Grossman, C., & Bero, L. A. (2007). Reporting science and conflicts of interest in the lay press. PLoS ONE, 2(12), e1266.
DeMaria, A. N. (2004). Authors, industry, and review articles. Journal of the American College of Cardiology, 43(6), 1130–1131.
Friedman, L. S., & Richter, E. D. (2004). Relationship between conflicts of interest and research results. Journal of General Internal Medicine, 19(1), 51–56.
Friedman, P. (2002). The impact of conflict of interest on trust in science. Science and Engineering Ethics, 8, 413–420.
Gillis, J. (2015, March 3). Climate change researcher offers a defense of his practices. New York Times, p. A19. Retrieved from http://www.nytimes.com/2015/03/03/science/climate-change- researcher-wei-hock-soon-offers-a-defense-of-his-practices.html? _r=0
67
Gillis, J., & Schwartz, J. (2015). Deeper ties to corporate cash for doubtful climate researcher. New York Times, February 22, p. A1. Retrieved from http://www.nytimes.com/2015/02/22/us/ties-to- corporate-cash-for-climate-change-researcher-Wei-Hock- Soon.html
International Committee of Medical Journal Editors. (2014). Recommendations for the conduct, reporting, editing, and publication of scholarly work in medical journals. Retrieved from http://www.icmje.org/icmje-recommendations.pdf
Kennedy, D. (2004). Disclosure and disinterest. Science, 303, 15.
Kesselheim, A. S., Robertson, C. T., Myers, J. A., Rose, S. L., Gillet, V., Ross, K. M.,…Avorn, J. (2012). A randomized study of how physicians interpret research funding disclosures. New England Journal of Medicine, 367(12), 1119–1127.
Kjaergard, L. L., & Als-Nielsen, B. (2002). Association between competing interests and authors' conclusions: Epidemiological study of randomised clinical trials published in the BMJ. BMJ, 325(7358), 249–249.
Levinsky, N. G. (2002). Nonfinancial conflict of interest. New England Journal of Medicine, 347(10), 759–761.
Lexchin, J., Bero, L. A., Djulbegovic, B., & Clark, O. (2003). Pharmaceutical industry sponsorship and research outcome and quality. BMJ, 326, 1167–1170.
Lo, B., & Field, M. J. (2009). Institute of Medicine Committee on Conflict of Interest in Medical Research, Education, and Practice. Conflict of interest in medical research, education, and practice. Washington, DC: National Academies Press.
Lundh, A., Sismondo, S., Lexchin, J., Busuioc, O. A., & Bero, L. (2012). Industry sponsorship and research outcome. Cochrane Database of Systematic Reviews, 12, MR000033. doi:10.1002/14651858.MR000033.pub2
Maurissen, J. P., Gilbert, S. G., Sander, M., Beauchamp, T. L., Johnson, S., Schwetz, B. A.,…Barrow, C. S. (2005). Workshop proceedings: Managing conflict of interest in science: A little
68
consensus and a lot of controversy. Toxicological Sciences, 87, 11– 14.
Michaels, D. (2009). Addressing conflict in strategic literature reviews: Disclosure is not enough. Journal of Epidemiology and Community Health, 63(8), 599–600.
Michaels, D., & Monforton, C. (2005). Manufacturing uncertainty: Contested science and the protection of the public's health and environment. American Journal of Public Health, 95(Suppl. 1), S39–48.
The PLoS Medicine Editors. (2008). Making sense of non-financial competing interests. PLoS Medicine, 5(9), e199.
Rennie, D. (2010). Integrity in scientific publishing. Health Services Research Journal, 45(3), 885–896.
Resnik, D. B., & Elliott, K. C. (2013). Taking financial relationships into account when assessing research. Accountability in Research, 20(3), 184–205.
Sass, J. (2009). Effective and practical disclosure policies: NRDC paper on workshop to identify key elements of disclosure policies for health science journals. Natural Resources Defense Council. Retrieved from http://www.nrdc.org/health/disclosure
Smith, R. (2005). Medical journals are an extension of the marketing arm of pharmaceutical companies. PLoS Medicine, 2, e138. doi:10.1371/journal.pmed.0020138
Sutton, P., Woodruff, T. J., Vogel, S., & Bero, L. A. (2011). Conrad and Becker's “10 Criteria” fall short of addressing conflicts of interest in chemical safety studies. Environmental Health Perspectives, 119(12), A506–507.
Thompson, D. F. (1993). Understanding financial conflicts of interest. New England Journal of Medicine, 329, 573–576.
Viswanathan, M., Carey, T. S., Belinson, S. E., Berliner, E., Chang, S. M., Graham, E.,…White, C. M. (2014). A proposed approach may help systematic reviews retain needed expertise while minimizing bias from nonfinancial conflicts of interest. Journal of Clinical
69
Epidemiology, 67(11), 1229–1238.
Young, S. N. (2009). Bias in the research literature and conflict of interest: An issue for publishers, editors, reviewers and authors, and it is not just about the money. Journal of Psychiatry and Neuroscience, 34(6), 412–417.
70
Part 1 Methods and Paradigms
71
Chapter 1 Introduction to Environmental Health
Howard Frumkin
Dr. Frumkin's disclosures appear in the front of this book, in the section titled “Potential Conflicts of Interest in Environmental Health: From Global to Local.”
72
Key Concepts Environmental health is the field of public health that addresses physical, chemical, biological, social, and psychosocial factors in the environment. It aims both to control and prevent environmental hazards and to promote health and well-being through environmental strategies.
People have always been concerned with environmental health, but the nature of their concerns has evolved with the transition from prehistoric, to agricultural, to industrial, to postindustrial life.
Many disciplines contribute to environmental health: epidemiology and toxicology, psychology and communications, urban planning and food science, law and ethics, and more.
Environmental health utilizes the geographic concept of spatial scales, from the global (with issues such as climate change), to the regional (air quality), to the local (neighborhood design), to the hyperlocal (ergonomics).
Environmental health thinking takes a systems approach, embracing complexity, and focusing on “upstream” factors as well as on “downstream” health impacts.
Please stop reading.
That's right. Close this book, just for a moment. Lift your eyes and look around. Where are you? What do you see?
Perhaps you're in the campus library, surrounded by shelves of books, with carpeting underfoot and the heating or air-conditioning humming quietly in the background. Perhaps you're home—a dormitory room, a bedroom in a house, a suite in a garden apartment, maybe your kitchen. Perhaps you're outside, lying beneath a tree in the middle of campus, or perhaps you're on a subway or a bus or even an airplane. What is it like? How does it feel to be where you are?
Is the light adequate for reading? Is the temperature comfortable?
73
Is there fresh air to breathe? Are there contaminants in the air—say, solvents off-gassing from newly laid carpet or a recently painted wall? Does the chair fit your body comfortably?
If you're inside, look outside. What do you see through the window? Are there trees? Buildings? Is the neighborhood noisy or tranquil? Are there other people? Are there busy streets, with passing trucks and busses snorting occasional clouds of diesel exhaust?
Now imagine that you can see even farther, to a restaurant down the block, to the nearby river, to the highway network around your city or town, to the factories and assembly plants in industrial parks, to the power plant in the distance supplying electricity to the room you're in, to the agricultural lands and forests some miles away. What would you see in the restaurant? Is the kitchen clean? Is the food stored safely? Are there cockroaches or rats in the back room? What about the river? Is your municipal sewage system dumping raw wastes into the river, or is there a sewage plant discharging treated, clean effluent? Are there chemicals in the river water? What about fish? Could you eat the fish? Could you swim in the river? Do you drink the water from the river?
As for the highways, factories, and power plant…are they polluting the air? Are the highways clogged with traffic? Are people routinely injured and killed on the roads? Are workers in the factories being exposed to hazardous chemicals or to noise or to machines that may injure them or to stress? Are trains pulling up to the power plant regularly, off-loading vast piles of coal? And what about the farms? Are they applying pesticides, or are they controlling insects in other ways? Are you confident that you're safe eating the vegetables that grow there? Drinking the milk? Are the farmlands shrinking as residential development from the city sprawls outward?
Finally, imagine that you have an even broader view. Floating miles above the Earth, you look down. Do you notice the hundreds of millions of people living in wildly differing circumstances? Do you see vast megacities with millions and millions of people, and do you see isolated rural villages three days' walk from the nearest road? Do you see forests being cleared in some places, rivers and lakes drying up in others? Do you notice that the Earth's surface temperature is slightly warmer than it was a century ago? Do you see cyclones forming in tropical regions, glaciers and icecaps
74
melting near the poles?
OK, back to the book.
Everything you've just viewed, from the room you're in to the globe you're on, is part of your environment. And many, many aspects of that environment, from the air you breathe to the water you drink, from the roads you travel to the wastes you produce, may affect how you feel. They may determine your risk of being injured before today ends, your risk of coming down with diarrhea or shortness of breath or a sore back, your risk of developing a chronic disease in the next few decades, even the risk that your children or your grandchildren will suffer from developmental disabilities or asthma or cancer.
75
What Is Environmental Health? Merriam-Webster's Collegiate Dictionary first defines environment straightforwardly as “the circumstances, objects, or conditions by which one is surrounded.” The second definition it offers is more intriguing: “the complex of physical, chemical, and biotic factors (as climate, soil, and living things) that act upon an organism or an ecological community and ultimately determine its form and survival.” If our focus is on human health, we can consider the environment to be all the external (or nongenetic) factors— physical, nutritional, social, behavioral, and others—that act on humans.
A widely accepted definition of health comes from the 1948 constitution of the World Health Organization: “A state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity.” This broad definition reaches well beyond blood pressure readings and X-ray results to include many dimensions of our lives: well-being, comfort, even happiness.
Environmental health has been defined in many ways (see Text Box 1.1). Some definitions evoke the relationship between people and the environment—a systems-based, ecological approach—while others focus more narrowly on addressing particular environmental conditions. Some focus on controlling hazards, while others focus on promoting health-enhancing environments. Some focus on physical and chemical hazards, while others extend more broadly to aspects of the social and built environments. In the aggregate the definitions in Text Box 1.1 make it clear that environmental health is many things: an interdisciplinary academic field, an area of research, and an arena of applied public health practice.
76
Text Box 1.1 Definitions of Environmental Health “Environmental health comprises those aspects of human health, including quality of life, that are determined by physical, chemical, biological, social and psychosocial factors in the environment. It also refers to the theory and practice of assessing, correcting, controlling, and preventing those factors in the environment that can potentially affect adversely the health of present and future generations.” (World Health Organization)
“Environmental health is the branch of public health that protects against the effects of environmental hazards that can adversely affect health or the ecological balances essential to human health and environmental quality.” (Agency for Toxic Substances and Disease Registry)
“Environmental health includes both the direct pathological effects of chemicals, radiation and some biological agents, and the effects (often indirect) on health and well-being of the broad physical, psychological, social and aesthetic environment, which includes housing, urban development, land use, and transport.” (European Charter on Environment and Health)
“Environmental health focuses on the health interrelationships between people and their environment, promotes human health and well-being, and fosters a safe and healthful environment.” (National Association of City and County Health Officials)
Source: U.S. Department of Health and Human Services, 1998.
77
The Evolution of Environmental Health Human concern for environmental health dates from ancient times, and it has evolved and expanded over the centuries.
Ancient Origins The notion that the environment could have an impact on comfort and well-being—the core idea of environmental health—must have been evident in the early days of human existence. The elements can be harsh, and we know that our ancestors sought respite in caves or under trees or in crude shelters they built. The elements can still be harsh, both on a daily basis and during extraordinary events; think of the Indian Ocean earthquake and tsunami of 2004, Hurricanes Katrina and Rita in 2005 and Sandy in 2012, the Sichuan earthquake of 2008, the Nepal earthquake of 2015, and the ongoing droughts in Australia and California.
Our ancestors confronted other challenges that we would now identify with environmental health. One was food safety; there must have been procedures for preserving food, and people must have fallen ill and died from eating spoiled food. Dietary restrictions in ancient Jewish and Islamic law, such as bans on eating pork, presumably evolved from the recognition that certain foods could cause disease. Another challenge was clean water; we can assume that early peoples learned not to defecate near or otherwise soil their water sources. In the ruins of ancient civilizations from India to Rome, from Greece to Egypt to South America, archeologists have found the remains of water pipes, toilets, and sewage lines, some dating back more than 4,000 years (Rosen, 1958/1993). Still another environmental hazard was polluted air; there is evidence in the sinus cavities of ancient cave dwellers of high levels of smoke in their caves (Brimblecombe, 1988), foreshadowing modern indoor air concerns in homes that burn biomass fuels or coal.
An intriguing passage in the biblical book of Leviticus (14:33–45) may refer to an environmental health problem well recognized today: mold in buildings. When a house has a “leprous disease” (as the Revised Standard Version translates this passage),
…then he who owns the house shall come and tell the priest,
78
“There seems to me to be some sort of disease in my house.” Then the priest shall command that they empty the house before the priest goes to examine the disease, lest all that is in the house be declared unclean; and afterward the priest shall go in to see the house. And he shall examine the disease; and if the disease is in the walls of the house with greenish or reddish spots, and if it appears to be deeper than the surface, then the priest shall go out of the house to the door of the house, and shut up the house seven days. And the priest shall come again on the seventh day, and look; and if the disease has spread in the walls of the house, then the priest shall command that they take out the stones in which is the disease and throw them into an unclean place outside the city; and he shall cause the inside of the house to be scraped round about, and the plaster that they scrape off they shall pour into an unclean place outside the city; then they shall take other stones and put them in the place of those stones, and he shall take other plaster and plaster the house. If the disease breaks out again in the house, after he has taken out the stones and scraped the house and plastered it, then the priest shall go and look; and if the disease has spread in the house, it is a malignant leprosy in the house; it is unclean. And he shall break down the house, its stones and timber and all the plaster of the house; and he shall carry them forth out of the city to an unclean place.
Can we conclude that mold grew within warm, damp ancient dwellings? And what was that “unclean place outside the city”—an early hazardous waste site? Who hauled the wastes there, and did that work undermine their health?
Still another ancient environmental health challenge, especially in cities, was rodents. European history was changed forever when infestations of rats in fourteenth-century cities led to the Black Death (Zinsser, 1935; Herlihy and Cohn, 1997; Cantor, 2001; Kelly, 2005). Modern cities continue to struggle periodically with infestations of rats and other pests (Sullivan, 2004), whose control depends in large part on environmental modifications.
Industrial Awakenings Modern environmental health further took form during the age of industrialization. With the rapid growth of cities in the seventeenth
79
and eighteenth centuries, sanitarian issues rose in importance. “The urban environment,” wrote one public health historian, “fostered the spread of diseases with crowded, dark, unventilated housing; unpaved streets mired in horse manure and littered with refuse; inadequate or nonexisting water supplies; privy vaults unemptied from one year to the next; stagnant pools of water; ill- functioning open sewers; stench beyond the twentieth-century imagination; and noises from clacking horse hooves, wooden wagon wheels, street railways, and unmuffled industrial machinery” (Leavitt, 1982, p. 22).
The provision of clean water became an ever more pressing need, as greater concentrations of people increased both the probability of water contamination and the impact of disease outbreaks. Regular outbreaks of cholera and yellow fever in the eighteenth and nineteenth centuries (Rosenberg, 1962) highlighted the need for water systems, including clean source water, treatment including filtration, and distribution through pipes. Similarly, sewage management became a pressing need, especially after the provision of piped water and the use of toilets created large volumes of contaminated liquid waste (Duffy, 1990; Melosi, 2000; also see Chapter 16 and Text Box 4.2 in Chapter 4).
The industrial workplace—a place of danger and even horror—gave additional impetus to early environmental health efforts. Technology advanced rapidly during the late eighteenth and nineteenth centuries, new and often dangerous machines were deployed in industry after industry, and mass production became common. In communities near industrial facilities, the air, water, and soil could become badly contaminated in ways that would be familiar to modern environmental professionals (Tarr, 1996, 2002), but the most abominable conditions were usually found within the mines, mills, and factories themselves. Workers became the proverbial canaries in the coal mines.
Charles Turner Thackrah (1795–1833), a Yorkshire physician, became interested in the diseases he observed among the poor in the city of Leeds. In 1831, he catalogued many work-related hazards in a short book with a long title: The Effects of the Principal Arts, Trades and Professions, and of Civic States and Habits of Living, on Health and Longevity, with Suggestions for the Removal of Many of the Agents which Produce Disease and Shorten the
80
Duration of Life. In it he proposed guidelines for preventing certain diseases, such as eliminating lead as a glaze in the pottery industry and using ventilation and respiratory protection to protect knife grinders. Public outcry and the efforts of early Victorian reformers such as Thackrah led to passage, in the U.K., of the Factory Act in 1833 and the Mines Act in 1842. Occupational health did not blossom in the United States until the early twentieth century, pioneered by the remarkable Alice Hamilton (1869–1970). A keen firsthand observer of industrial conditions, with a powerful social conscience, she documented links between toxic exposures and illness among miners, tradesmen, and factory workers, first in Illinois (where she directed that state's Occupational Disease Commission from 1910 to 1919) and later from an academic perch at Harvard (as that university's first female professor). Her books, including, in 1925, Industrial Poisons in the United States and, in 1934, Industrial Toxicology, helped to establish that workplaces could be dangerous environments for workers.
A key development in the seventeenth through nineteenth centuries was the quantitative observation of population health—the beginnings of epidemiology. With the tools of epidemiology, observers could systematically attribute certain diseases to particular environmental exposures (as explored in Chapter 4). John Graunt (1620–1674), an English merchant and haberdasher, realized that London's weekly death records—the “bills of mortality”—were a treasure trove of information. He analyzed them, and published his findings in 1662 as Natural and Political Observations Upon the Bills of Mortality. Graunt's work was a pioneering example of demography. Almost two centuries later, when the British Parliament created the Registrar-General's Office (now the Office of Population Censuses and Surveys) and William Farr (1807–1883) became its compiler of abstracts, the link between vital statistics and environmental health was forged. Farr made observations about fertility and mortality patterns, identifying rural-urban differences, variations between acute and chronic illnesses, and seasonal trends, and implicating certain environmental conditions in illness and death. Farr's 1843 analysis of mortality in Liverpool led the British Parliament to pass the Liverpool Sanitary Act of 1846, which created a sanitary code for Liverpool and a public health infrastructure to enforce it.
81
If Farr was a pioneer in applying demography to public health, his contemporary Edwin Chadwick (1800–1890) was a pioneer in combining social epidemiology with environmental health. At the age of 32, Chadwick was appointed to the newly formed Royal Commission of Enquiry on the Poor Laws, and helped reform Britain's Poor Laws. Five years later, following epidemics of typhoid fever and influenza, he was asked by the British government to investigate sanitation. His classic 1842 report, Sanitary Conditions of the Labouring Population (Figure 1.1), drew a clear link between living conditions—in particular overcrowded, filthy homes, open cesspools and privies, impure water, and miasmas—and health, and made a strong case for public health reform. The resulting Public Health Act of 1848 created the Central Board of Health, with power to empanel local boards that would oversee street cleaning, trash collection, and water and sewer systems. As sanitation commissioner, Chadwick advocated such innovations as urban water systems, toilets in every house, and transfer of sewage to outlying farms where it could be used as fertilizer (Hamlin, 1998). Chadwick's work helped establish the role of public works— essentially sanitary engineering—in protecting public health.
82
Figure 1.1 Title Page of Chadwick's Groundbreaking 1842 Report
83
Source: Wellcome Trust, Wellcome Images.
These achievements are profoundly important to public health. As eloquently pointed out by Thomas McKeown (1979) more than a century later, environmental health interventions were to do far more than medical care to improve public health and well-being during the industrial era. A recent economic analysis (Cutler & Miller, 2005) notes that from 1900 to 1940, infant mortality rates fell by 62%, total mortality fell by 40%, and life expectancy rose from 47 to 63 years—and that clean water alone accounted for three quarters of the decline in infant mortality, and over 40% of the decline in total mortality. Another analysis (Lee, 2007) attributes much of the decline in infant mortality during the same era to pasteurization of milk. These victories are well worth remembering at a time when some public health actions, including those in environmental health, are tinged with ideological controversy (see Text Box 1.2).
The physician John Snow (1813–1858) was, like William Farr, a founding member of the London Epidemiological Society. Snow gained immortality in the history of public health for what was essentially an environmental epidemiology study. During an 1854 outbreak of cholera in London, he documented a far higher incidence of disease among people who lived near or drank from the Broad Street pump than among people with other sources of water. He persuaded local authorities to remove the pump handle, and the epidemic in that part of the city soon abated. (There is some evidence that it may have been ending anyway, but this does not diminish the soundness of Snow's approach.) Environmental epidemiology was to blossom during the twentieth century (see Chapter 4), supplemented by the development of geospatial information late in the century (see Chapter 5), and was to provide some of the most important evidence needed to support effective preventive measures.
Finally, the industrial era led to a powerful reaction in the worlds of literature, art, and design. In the first half of the nineteenth century, Romantic painters, poets, and philosophers celebrated the divine and inspiring forms of nature. In Germany painters such as Caspar David Friedrich (1774–1840) created meticulous images of the trees, hills, misty valleys, and mercurial light of northern Germany, based on a close observation of nature, and in England Samuel
84
Palmer (1805–1881) painted landscapes that combined straightforward representation of nature with religious vision. His countryman John Constable (1776–1837) worked in the open air, painting deeply evocative English landscapes. In the United States, Hudson River School painters, such as Thomas Cole (1801–1848), took their inspiration from the soaring peaks and crags, stately waterfalls, and primeval forests of the northeast. At the same time, the New England transcendentalists celebrated the wonders of nature. “Nature never wears a mean appearance,” wrote Ralph Waldo Emerson (1803–1882) in his 1836 paean, Nature. “Neither does the wisest man extort her secret, and lose his curiosity by finding out all her perfection. Nature never became a toy to a wise spirit. The flowers, the animals, the mountains, reflected the wisdom of his best hour, as much as they had delighted the simplicity of his childhood.” Henry David Thoreau (1817–1862), like Emerson a native of Concord, Massachusetts, rambled from Maine to Cape Cod and famously lived in a small cabin at Walden Pond for two years, experiences that cemented his belief in the “tonic of wildness.” And America's greatest landscape architect, Frederick Law Olmsted (1822–1903), championed bringing nature into cities. He designed parks that offered pastoral vistas and graceful tree- lined streets and paths, intending to offer tranquility to harried people and to promote feelings of community. These and other strands of cultural life reflected yet another sense of environmental health, arising in response to industrialization: the idea that pristine environments were wholesome, healthful, and restorative to the human spirit. This dimension is explored in Chapter 25.
85
Text Box 1.2 Environmental Health: Common Good or Nanny State? Political scientists, economists, and other scholars have long noted the tension between individualism and collectivism. Individualists emphasize personal independence, autonomy, and liberty, while collectivists emphasize the value of group norms and action—not only in promoting the common good but also in achieving social justice and in providing social support and identity. In recent years political discourse in the United States (dating from the presidency of Ronald Reagan), Great Britain (dating from Margaret Thatcher's time as prime minister), and other countries, has tilted toward individualism, signaling a mistrust of collective action and especially of government action. President Reagan famously declared, in his first inaugural speech, “Government is not the solution to our problem; government is the problem.”
In environmental health, as in many fields of public health, collective action is essential—so much so that public health has been defined as “collective action for sustained population-wide health improvement” (Beaglehole, Bonita, Horton, Adams, & McKee, 2004). Zoning for healthy neighborhoods, fuel efficiency and air quality regulations for clean air, and food inspections and standards for wholesome food are examples of concerted government action that protects public health. Critics regard some such government actions as paternalistic and restrictive of individual liberty. They warn of the nanny state (Calman, 2009; Wiley, Berman, & Blanke, 2013).
There are strong moral and practical arguments for collective action in environmental health, not least the fact that preventing disease and promoting health often require action well beyond the scope of personal behavior (Minkler, 1999; Chokshi & Stine, 2013). Individuals cannot on their own achieve clean air, clean water, safe roads, walkable neighborhoods, or reduced carbon emissions. A rich legal
86
tradition in the United States supports the role of government in promoting public health; examples include Jacobson v. Massachusetts (1905), in which the U.S. Supreme Court upheld a city's right to compel smallpox vaccination (Parmet, Goodman, & Farber, 2005), and Euclid v. Ambler (1926), in which the Supreme Court upheld a local zoning ordinance, based in part on protecting public health (Schilling & Linton, 2005). More generally, environmental health efforts are embedded in the larger concept of the common good—a concept with a lengthy history and a compelling contemporary role (Etzioni, 2004, 2015). Balancing the common good with individual rights remains a fascinating challenge in public health and public policy.
The Modern Era The modern field of environmental health dates from the mid- twentieth century, and no landmark better marks its launch than the 1962 publication of Rachel Carson's Silent Spring. Silent Spring focused on DDT, an organochlorine pesticide that had seen increasingly wide use since World War II. Carson had become alarmed at the ecosystem effects of DDT; she described how it entered the food chain and accumulated in the fatty tissues of animals, how it indiscriminately killed both target species and other creatures, and how its effects persisted for long periods after it was applied. She also made the link to human health, describing how DDT might increase the risk of cancer and birth defects (see Text Box 6.4 in Chapter 6). One of Carson's lasting contributions was to place human health in the context of larger environmental processes. “Man's attitude toward nature,” she declared in 1963, “is today critically important simply because we have now acquired a fateful power to alter and destroy nature. But man is a part of nature, and his war against nature is inevitably a war against himself… [We are] challenged as mankind has never been challenged before to prove our maturity and our mastery, not of nature, but of ourselves” (New York Times, 1964).
The recognition of chemical hazards was perhaps the most direct legacy of Silent Spring. Beginning in the 1960s, Irving Selikoff (1915–1992) and his colleagues at the Mount Sinai School of Medicine intensively studied insulators and other worker
87
populations and showed that asbestos could cause asbestosis (a fibrosing lung disease), lung cancer, mesothelioma, and other cancers. Outbreaks of cancer in industrial workplaces—lung cancer in a chemical plant near Philadelphia due to bis-chloromethyl ether (Figueroa, Raszkowski, & Weiss, 1973; Randall, 1977), hemangiosarcoma of the liver in a vinyl chloride polymerization plant in Louisville (Creech & Johnson, 1974), and others— underlined the risk of carcinogenic chemicals. With the enormous expansion of cancer research, and with effective advocacy by such groups as the American Cancer Society (Patterson, 1987), environmental and occupational carcinogens became a focus of public, scientific, and regulatory attention.
But cancer was not the only health effect linked to chemical exposures. Herbert Needleman (1927–), studying children in Boston, Philadelphia, and Pittsburgh, showed that lead was toxic to the developing nervous system, causing cognitive and behavioral deficits at levels far lower than had been appreciated. When this recognition finally helped to achieve the removal of lead from gasoline, population blood lead levels plummeted, an enduring public health victory—and one that may even have helped reduce crime levels twenty years later (Nevin, 2007). Research also suggested that chemical exposures could threaten reproductive function. Wildlife observations such as abnormal genitalia in alligators in Lake Apopka, Florida, following a pesticide spill (Guillette et al., 1994) and human observations such as an apparent decrease in sperm counts (Swan, Elkin, & Fenster,1997) suggested that certain persistent, bioaccumulative chemicals (persistent organic pollutants, or POPs) could affect reproduction, perhaps by interfering with hormonal function. Emerging evidence showed that chemicals could damage the kidneys, liver, and cardiovascular system and immune function and organ development.
Some knowledge of chemical toxicity arose from toxicological research (see Chapter 6) and other insights resulted from epidemiological research (see Chapter 4). But catastrophes— reported first in newspaper headlines and only later in scientific journals—also galvanized public and scientific attention. The discovery of accumulations of hazardous wastes in communities across the nation—Love Canal in Niagara Falls, New York (Gibbs, 1998); Times Beach, Missouri, famous for its unprecedented dioxin
88
levels; Toms River, New Jersey (Fagin, 2013); Woburn, Massachusetts (Harr, 1996), where municipal drinking water was contaminated with organic chemicals; “Mount Dioxin,” a defunct wood treatment plant in Pensacola, Florida; Anniston, Alabama, where residents (especially black residents) were exposed to intolerable levels of PCBs (Spears, 2014); and many others—raised concerns about many health problems, from learning disabilities to immune dysfunction to cancer to birth defects. Mercury contamination of Minamata Bay, Japan, and the resulting burden of neurological illness riveted world attention, spurred by the heart- wrenching photographs of Eugene Smith (Smith & Smith, 1975) (Figure 1.2). And acute disasters, such as the isocyanate release that killed hundreds and sickened thousands in Bhopal, India, in 1984, made it clear that industrialization posed real threats of chemical toxicity (Dhara & Dhara, 2002; Lapierre & Moro, 2002).
Figure 1.2 A Victim of Minamata Disease Being Bathed: Photograph by W. Eugene Smith
In tandem with the growing awareness of chemical hazards, environmental health during the second half of the twentieth century was developing along another promising line: environmental psychology. As described in Chapter 9, this field arose as a subspecialty of psychology, building on advances in perceptual and cognitive psychology. Scholars such as Stephen
89
Kaplan and Rachel Kaplan at the University of Michigan carried out careful studies of human perceptions and of reactions to various environments. An important contribution to environmental psychology was the theory of biophilia, first advanced by Harvard biologist E. O. Wilson in 1984. Wilson defined biophilia as “the innately emotional affiliation of human beings to other living organisms.” He pointed out that for most of human existence, people have lived in natural settings, interacting daily with plants, trees, and other animals. As a result, Wilson maintained, affiliation with these organisms has become an innate part of human nature (Wilson, 1984). Other scholars extended Wilson's concept beyond living organisms, postulating a connection with other features of the natural environment—rivers, lakes, and ocean shores; waterfalls; panoramic landscapes and mountain vistas (Kellert & Wilson, 1993; see Chapter 25). Environmental psychologists studied not only natural features of human environments but also such factors as light, noise, and way-finding cues to assess the impact of these factors. They increasingly recognized that people responded to various environments, both natural and built, in predictable ways. Some environments were alienating, disorientating, or even sickening, whereas others were attractive, restorative, and even salubrious.
A third development in modern environmental health was the continued integration of ecology with human health, giving rise to a field called ecohealth. Ancient wisdom in many cultures had recognized the relationships between the natural world and human health and well-being. But with the emergence of formal complex systems analysis and modern ecological science, the understanding of ecosystem function advanced greatly (see Chapter 2). As part of this advance the role of humans in the context of ecosystems was better and better delineated. On a global scale, for example, the concept of carrying capacity (Wackernagel & Rees, 1995) helped clarify the impact of human activity on ecosystems and permitted evaluation of the ways ecosystem changes, in turn, affected human health and well-being (Aron & Patz, 2001; McMichael, 2001; Alcamo et al., 2003; Waltner-Toews, 2004; Brown, Grootjans, Ritchie, & Townsend, 2005; Rayner & Lang, 2012). Ecological analysis was also applied to specific areas relevant to human health. For example, there were advances in medical botany (Lewis & Elvin- Lewis, 2003; van Wyk & Wink, 2004), in the understanding of
90
biodiversity and its value to human health (Chivian & Bernstein, 2008), and in the application of ecology to clinical medicine (Aguirre, Ostfeld, Tabor, House, & Pearl, 2002; Ausubel, 2004). These developments, together, reflected a progressive synthesis of ecological and human health science, yielding a better understanding of the foundations of environmental health.
A fourth feature of modern environmental health was the expansion of health care services related to environmental exposures. Occupational medicine and nursing had been specialties in their respective professions since the early twentieth century, with a traditional focus on returning injured and ill workers to work and, to some extent, on preventing hazardous workplace exposures. In the last few decades of the twentieth century, these professional specialties incorporated a public health paradigm, drawing on toxicological and epidemiological data, using industrial hygiene and other primary prevention approaches, and engaging in worker education (see Chapter 21). In addition, the occupational health clinical paradigm was broadened to include general environmental exposures. Clinicians began focusing on such community exposures as air pollutants, radon, asbestos, and hazardous wastes, emphasizing the importance of taking an environmental history, identifying at-risk groups, and providing both treatment and preventive advice to patients. Professional ethics expanded to recognize the interests of patients (both workers and community members) as well as those of employers, and in some cases even the interests of unborn generations and of other species (see Chapter 10). Finally, a wide range of alternative and complementary approaches—some well outside the mainstream—arose in occupational and environmental health care. For example, an approach known as clinical ecology postulated that overloads of environmental exposures could impair immune function, and offered treatments including “detoxification,” antifungal medications, and dietary changes purported to prevent or ameliorate the effects of environmental exposures (Rea, 1992– 1998).
Environmental health policy also emerged rapidly. With the promulgation of environmental laws beginning in the 1960s, federal and state officials created agencies and assigned them new regulatory responsibilities. These agencies issued rules that aimed
91
to reduce emissions from smokestacks, drainpipes, and tailpipes; control hazardous wastes; and achieve clean air and water. Although many of these laws were oriented to environmental preservation, the protection of human health was often an explicit rationale as well. (Indeed, the mission of the U.S. Environmental Protection Agency, or EPA, is “to protect human health and the environment.”) Ironically, the new environmental regulations created a schism in the environmental health field. Responsibility for environmental health regulation had traditionally rested with health departments, but this was now transferred to newly created environmental agencies. At the federal level, the EPA assumed some of the traditional responsibilities of the Department of Health, Education, and Welfare (now Health and Human Services), and corresponding changes occurred at the state level. Environmental regulation and health protection became somewhat uncoupled from each other.
Environmental regulatory agencies increasingly attempted to ground their rules in evidence, using quantitative risk assessment techniques (see Chapter 27). This signaled a sea change in regulatory policy. The traditional approach had been simpler; dangerous exposures were simply banned. For example, the 1958 Delaney clause, an amendment to the 1938 Federal Food, Drug, and Cosmetic Act, banned carcinogens in food. In contrast, emerging regulations tended to set permissible exposure levels that took into account anticipated health burdens, compliance costs, and technological feasibility. Moreover, regulations tended to assign the burden of proof of toxicity to government regulators. As the scientific and practical difficulties of this approach became clear in the late twentieth century, an alternative approach emerged: assigning manufacturers the burden of proving the safety of a chemical. Based philosophically in the precautionary principle (see Chapter 26), this approach was legislated in Europe as part of the European Union's REACH (Registration, Evaluation, Authorization and Restriction of Chemicals) initiative, which entered into force in 2007 (European Commission, 2009). It has not, for the most part, been implemented in U.S. toxics law (see Chapter 6).
In the twenty-first century, then, while traditional sanitarian functions remain essential, the environmental health field has
92
expanded well beyond its origins. Awareness of chemical toxicity has advanced rapidly, fueled by discoveries in toxicology and epidemiology. At the same time, the complex relationships inherent in environmental health—the effects of environmental conditions on human psychology, and the links between human health and ecosystem function—are better and better recognized. In practical terms, clinical services in environmental health have developed, and regulation has advanced through a combination of political action and scientific evidence.
Emerging Issues Environmental health is a dynamic, evolving field. Looking ahead, we can identify at least five trends that will further shape environmental health: environmental justice, a focus on susceptible groups, scientific advances, global change, and moves toward sustainability.
Beginning around 1980, African American communities identified exposures to hazardous waste and industrial emissions as matters of racial and economic justice. Researchers documented that these exposures disproportionately affected poor and minority communities, a problem that was aggravated by disparities in the enforcement of environmental regulations. The modern environmental justice movement was born, a fusion of environmentalism, public health, and the civil rights movement (Bullard, 1994; Cole & Foster, 2000; see also Chapter 11). Historians have observed that environmental justice represents a profound shift in the history of environmentalism (Gottlieb, 1993; Shabecoff, 1993; Dowie, 1995). This history is commonly divided into waves. The first wave was the conservation movement of the early twentieth century, the second wave was the militant activism that blossomed in 1970 on the first Earth Day, and the third wave was the emergence of large, “inside-the-beltway” environmental organizations such as the Environmental Defense Fund, the League of Conservation Voters, and the Natural Resources Defense Council, which had gained considerable policy influence by the 1980s. Environmental justice, then, represents a fourth wave, one that is distinguished by its decentralized, grassroots leadership, its demographic diversity, and its emphasis on human rights and distributive justice. The vision of environmental justice—
93
eliminating disparities in economic opportunity, environmental exposures, and health—is one that resonates with public health priorities. It emphasizes that environmental health extends well beyond the control of hazardous exposures to include human rights and equity as well. This vision will be an increasingly central part of environmental health in coming decades.
Environmental justice is one example of a broader trend in environmental health—a focus on susceptible groups. For many reasons, specific groups may be especially vulnerable to the adverse health effects of environmental exposures. In the case of poor and minority populations, these reasons include disproportionate exposures, limited access to legal protection, limited access to health care, and in some cases compromised baseline health status. Children make up another susceptible population, for several reasons; they eat more food, drink more water, and breathe more air per unit of body weight than adults do and are therefore more heavily exposed to any contaminants in these media (Landrigan & Etzel, 2014). Children's behavior—crawling on floors, placing their hands in their mouths, and so on—further increases their risk of exposure. With developing organ systems and immature biological defenses, children are less able than adults to withstand some exposures. And with more years of life ahead of them, children have more time to manifest delayed toxic reactions. These facts have formed the basis for research and public health action on children's environmental health.
Women bear some specific environmental exposure risks, both in the workplace and in the general environment, due both to disproportionate exposures (e.g., in health care jobs) and to unique susceptibilities (e.g., to reproductive hazards). Elderly people also bear some specific risks, and as the population ages, this group will attract further environmental health attention. For example, urban environments will need to take into account the limited mobility of some elderly people and provide ample sidewalks, safe street crossings, and accessible gathering places to serve this population. People with disabilities, too, require specific environmental health attention to minimize the risks they face. In coming decades environmental health will increasingly take account of susceptible groups as the risks they face and their needs for safe, healthy environments become better recognized.
94
A third set of emerging issues in environmental health grows out of scientific advances. In toxicology better detection techniques have already enabled us to recognize and quantify low levels of chemical exposure and have supported major advances in the understanding of chemical effects (see Chapter 6). Innovative toxicological approaches, including physiologically based pharmacokinetic modeling (PBPK) and high-throughput computational techniques, offer rapid insights into chemical toxicity. Advances in data collection and analysis techniques have supported innovative epidemiological analyses. In particular the use of geographic information systems (GISs) has yielded new insights on the spatial distribution of environmental exposures and diseases (see Chapter 5). The use of large databases—the “big data” revolution—has also enabled highly innovative analyses. Perhaps the most promising scientific advances are occurring at the molecular level, in the linked fields of genomics, toxicogenomics, epigenetics, and proteomics (see Chapter 7). New genomic tools such as microarrays (or gene chips) have enabled scientists to characterize the effects of chemical exposures on the expression of thousands of genes. Databases of genetic responses, and the resulting protein and metabolic pathways, will yield much information on the effects of chemicals and on the variability in responses among different people. Big data are also increasingly available from other data sources— smartphones that track travel patterns, social media, online searches, customer loyalty cards, charge card purchases, wearable devices that track activity and health parameters, and more. While these sources raise profound privacy concerns, reality mining can provide unprecedented insights into exposures, preferences, behaviors, and health outcomes across populations (Pentland, Lazer, Brewer, & Heibeck, 2009; Eagle & Greene, 2014). Scientific advances related to environmental health—from molecular biology to information science—will have profound effects on the field in coming decades.
Moving from the molecular scale to the global scale, a fourth set of emerging environmental health issues relates to global change. This broad term encompasses many trends, including population growth, climate change, urbanization, changing patterns of energy use, and the increasing integration of the world economy (Friedman, 2008). These trends will shape environmental health in many ways.
95
The global population now exceeds 7 billion and is expected to plateau at roughly 9 to 10 billion during the twenty-first century (see Chapter 3). Most of this population growth will occur in developing nations, and much of it will be in cities. Not only this population growth but also the increasing per capita demand for resources such as food, energy, and materials will strain the global environment (Heinberg, 2007; Brown, 2011), in turn affecting health in many ways. For example, environmental stress and resource scarcity may increasingly trigger armed conflict, an ominous example of the links between environment and health (Homer-Dixon, 1999; Klare, 2001). Global climate change, which results in large part from increasing energy use (see Chapter 14), will threaten health in many ways, from infectious disease risks to heat waves to severe weather events (see Chapter 12). As more of the world's population is concentrated in dense urban areas, features of the urban environment—noise, crowding, processed foods, vehicular and industrial pollution—will increasingly shape health (see also Chapter 15). And with integration of the global economy—through the complex changes known as globalization— hazards increasingly cross national boundaries, trade agreements and market forces challenge and possibly undermine national environmental and health policies (Gleeson & Friel, 2013; Walls, Smith, & Drahos, 2015), and global solutions to environmental health challenges will increasingly be needed (Labonté, Schrecker, Packer, & Runnels, 2009).
Sustainability has been a part of the environmental health vernacular since the 1980s. In 1983, the United Nations formed the World Commission on Environment and Development to propose strategies for sustainable development. The commission, chaired by then Norwegian prime minister Gro Harlem Brundtland, issued its landmark report, Our Common Future, in 1987. The report included what has become a standard definition of sustainable development: “development that meets the needs of the present without compromising the ability of future generations to meet their own needs.” In 1992, several years after the publication of Our Common Future, the United Nations Conference on Environment and Development (UNCED), commonly known as the Earth Summit, convened in Rio de Janeiro. This historic conference produced, among other documents, the Rio Declaration on Environment and Development, a blueprint for sustainable
96
development. The first principle of the Rio declaration placed environmental health at the core of sustainable development: “Human beings are at the centre of concerns for sustainable development. They are entitled to a healthy and productive life in harmony with nature” (United Nations, 1992).
Like environmental justice the concept of sustainable development blends environmental protection with notions of fairness and equity. As explained on the Web site of the Johannesburg Summit, held ten years after the Earth Summit:
The Earth Summit thus made history by bringing global attention to the understanding, new at the time, that the planet's environmental problems were intimately linked to economic conditions and problems of social justice. It showed that social, environmental and economic needs must be met in balance with each other for sustainable outcomes in the long term. It showed that if people are poor, and national economies are weak, the environment suffers; if the environment is abused and resources are over consumed, people suffer and economies decline. The conference also pointed out that the smallest local actions or decisions, good or bad, have potential worldwide repercussions [United Nations Department of Economic and Social Affairs, 2006].
The concept of sustainability has emerged as a central theme, and challenge, not only for environmentalism but for environmental health as well. In the short term, sustainable development will improve the living conditions and therefore the health of people across the world, especially in the poor nations. In the long term, sustainable development will protect the health and well-being of future generations. As described in Chapter 3, some of the most compelling thinking in environmental health in recent years offers social and technical paths to sustainable development (Hawken, Lovins, & Lovins, 1999; Brown, 2001; McDonough & Braungart, 2002; Brown et al., 2005; Institute of Medicine, 2013). These approaches build on the fundamental links among health, environment, technological change, and social justice. Ultimately, they will provide the foundation for lasting environmental health.
97
Spatial Scales, from Global to Local The concept of spatial scale is central to many disciplines, from geography to ecology to urban planning. Some phenomena unfold on a highly local scale—ants making a nest, people digging a septic tank. Some phenomena spread across regions—the pollution of a watershed from an upstream factory, the sprawl of a city over a 100- mile diameter. And some phenomena, such as climate change, are truly global in scale. Al Gore, in describing environmental destruction in his 1992 book, Earth in the Balance, borrowed military categories to make this point, distinguishing among “local skirmishes,” “regional battles,” and “strategic conflicts.”
Spatial scale is important not only in military and environmental analysis but also in environmental health. Some environmental factors that affect health operate locally, and the environmental health professionals who address these factors work on a local level; think of the restaurant and septic tank inspectors who work for the local health department or the health and safety officer at a manufacturing facility. Other environmental factors affect health at a regional level, and the professionals who address these problems work on a larger spatial scale; think of the state officials responsible for enforcement of air pollution or water pollution regulations. Global problems such as climate change require responses on the national and international scales. These responses are crafted by professionals in organizations such as the World Health Organization and the Intergovernmental Panel on Climate Change. So useful is the concept of spatial scales in environmental health that it provides the framework for this book. After introducing the methods and paradigms of environmental health in the first eleven chapters, this book addresses specific issues, beginning with global scale problems in Chapter 12, moving to regional scale problems in Chapters 13 to 16, and ending with local problems in Chapters 17 to 25. The final three chapters (Chapters 26 to 28) describe the practice of environmental health, focusing on such efforts as risk assessment and communication.
It is clear that environmental health professionals work on different spatial scales, but it is not always so clear who is an environmental health professional. Certainly, the environmental health director at
98
a local health department; the director of environment, health, and safety at a manufacturing firm; an environmental epidemiology researcher at a university; or a physician working for an environmental advocacy group would self-identify and be recognized by others as an environmental health professional. But many other people work in fields that have an impact on the environment and human health. The engineer who designs power plants helps to protect the respiratory health of asthmatic children living downwind if she plans for effective emissions controls. The transportation planner who enables people to walk instead of drive also protects public health by helping to promote physical activity and clean up the air. The park superintendent who maintains urban green spaces may contribute greatly to the well-being of people in his city. In fact much of environmental health is determined by “upstream” forces that seem at first glance to have little to do with environment or health.
99
The Forces that Drive Environmental Health Public health professionals tell the emblematic story of a small village perched alongside a fast-flowing river. The people of the village had always lived near the river, they knew and respected its currents, and they were skilled at swimming, boating, and water rescue. One day they heard desperate cries from the river and noticed a stranger being swept downstream past their village. They sprang into action, grabbed their ropes and gear, and pulled the victim from the water. A few minutes later, as they rested, a second victim appeared, thrashing in the strong current and gasping for breath. The villagers once again performed a rescue. Just as they were remarking on the coincidence of two near drownings in one day, a third victim appeared, and they also rescued him. This went on for hours. Every available villager joined in the effort, and by mid-afternoon all were exhausted. Finally, the flow of victims stopped, and the villagers collapsed, exhausted, along the waterfront.
Just at that moment another villager strode whistling into town, relaxed and dry. He had not been seen since the first victims were rescued and had not helped with any of the rescues. “Where were you?” his neighbors demanded of him. “We've been pulling people out of the river all day! Why didn't you help us?”
“Ah,” he replied. “When I noticed all the people in the river, I thought there must be a problem upstream. I walked up to that old footbridge, and sure enough, some boards had broken and there was a big hole in the walkway. So I patched the hole, and people stopped falling through.” (See Text Box 1.3.)
100
Text Box 1.3 A Prevention Poem: A Fence or an Ambulance Like the story of the villagers who saved drowning victims, this poem emphasizes that prevention may lie with root causes. These root causes are often environmental, like the hole in the village's bridge or, in this case, an unguarded cliff edge (See Figure 1.3).
101
102
Figure 1.3 The Need for Primary Prevention: An Early 20th- Century View
Source: Iowa Public Health Association, 1912.
'Twas a dangerous cliff, as they freely confessed,
Though to walk near its crest was so pleasant;
But over its terrible edge there had slipped
A duke, and full many a peasant;
So the people said something would have to be done,
But their projects did not at all tally.
Some said: “Put a fence round the edge of the cliff;”
Some, “An ambulance down in the valley.”
But the cry for the ambulance carried the day,
For it spread through the neighboring city.
A fence may be useful or not, it is true,
But each heart became brimful of pity
For those who slipped over that dangerous cliff;
And dwellers in highway and alley,
Gave pounds or gave pence, not to put up a fence,
But an ambulance down in the valley.
“For the cliff is all right if you're careful,” they said,
“And if folks ever slip and are dropping,
It isn't the slipping that hurts them so much
As the shock down below when they're stopping.”
So day after day as those mishaps occurred,
Quick forth would those rescuers sally,
To pick up the victims who fell off the cliff
With the ambulance down in the valley.
Then an old sage remarked, “It's a marvel to me
103
That people gave far more attention
To repairing results than to stopping the cause,
When they'd much better aim at prevention.
Let us stop at its source all this mischief,” cried he;
“Come, neighbors and friends, let us rally;
If the cliff we will fence, we might also dispense
With the ambulance down in the valley.”
“Oh he's a fanatic,” the others rejoined;
“Dispense with the ambulance? Never!
He'd dispense with all charities too if he could.
No, no! We'll support them forever!
Aren't we picking up folks just as fast as they fall?
And shall this man dictate to us? Shall he?
Why should people of sense stop to put up a fence
While their ambulance works in the valley?”
But a sensible few who are practical too,
Will not bear with such nonsense much longer.
They believe that prevention is better than cure;
And their party will soon be the stronger.
Encourage them, then, with your purse, voice, and pen,
And (while other philanthropists dally)
They will scorn all pretense and put a stout fence
On the cliff that hangs over the valley.
Better guide well the young than reclaim them when old,
For the voice of true wisdom is calling;
To rescue the fallen is good, but it's best
To prevent other people from falling;
Better close up the source of temptation and crime
104
Than deliver from dungeon or galley;
Better put a strong fence 'round the top of the cliff,
Than an ambulance down in the valley. Joseph Malins (1895)
Upstream thinking has helped to identify the root causes of many public health problems, and this is nowhere more true than in environmental health. Environmental hazards sometimes originate far from the point of exposure. Imagine that you inhale a hazardous air pollutant. It may come from motor vehicle tailpipes, from power plants, from factories, or from any combination of these. As for the motor vehicle emissions, the amount of driving people do in your city or town reflects urban growth patterns and available transportation alternatives, and the pollutants generated by people's cars and trucks vary with available technology and prevailing regulations. As for the power plants, the amount of energy they produce reflects the demand for energy by households and businesses in the area they serve, and the pollution they emit is a function of how they produce energy (are they coal, nuclear, or wind powered?), the technology they use, and the regulations that govern their operations. Hence a full understanding of the air pollutants you breathe must take into account urban growth, transportation, energy, and regulatory policy, among other upstream determinants. This book contains chapters on many of the upstream forces that affect environmental health, including community design, transportation, and energy.
These ideas are at the core of a useful model created by the World Health Organization (Briggs, 1999). The DPSEEA (driving forces- pressures-state-exposure-effects-actions) model was developed as a tool both for analyzing environmental health hazards and for designing indicators useful in decision making (Figure 1.4). The driving forces are the factors that motivate environmental health processes. In our air pollution example, these factors might include population growth; consumer preferences for energy-consuming homes, appliances, and vehicles; and sprawl that requires traveling over long distances. The driving forces result in pressures on the environment, such as the emission of oxides of nitrogen, hydrocarbons, particulate matter, and other air pollutants. These emissions, in turn, modify the state of the environment,
105
accumulating in the air and combining to form additional pollutants such as ozone. However, this deterioration in the state of the environment does not invariably threaten health; human exposure must occur. In the case of air pollutants, exposure occurs when people are breathing when and where the air quality is low. (Some people, of course, sustain higher exposures than others; an outdoor worker, an exercising athlete, or a child at play receives relatively higher doses of air pollutants than a person in an air-conditioned office.) The hazardous exposure may lead to a variety of health effects, acute or chronic. In the case of air pollutants, these effects may include coughing and wheezing, asthma attacks, heart attacks, and even early death.
Figure 1.4 The DPSEEA Model Source: Briggs, 1999.
Finally, to eliminate or control environmental hazards and protect human health, society may undertake a wide range of actions, targeted at any of the upstream steps. For example, protecting the public from the effects of air pollution might include encouraging energy conservation to reduce energy demand and designing live-
106
work-play communities to reduce travel demand (addressing driving forces), providing mass transit or bicycle lanes to reduce automobile use, requiring emissions controls on power plants or investing in wind turbines to reduce emissions from coal-fired power plants (addressing pressures), requiring low-sulfur fuel (addressing the state of the environment), warning people to stay inside when ozone levels are high (addressing exposures), and providing maintenance asthma medications (addressing health effects). However, as discussed in Chapter 26, the most effective long-term actions are those that are preventive, aimed at modifying the forces that drive the system. This theme is universal in public health, applying both to environmental hazards and to other health hazards, and it is the central message of this book.
107
Key Terms biophilia
“The innately emotional affiliation of human beings to other living organisms,” as defined by E.O. Wilson.
collectivism An approach emphasizing shared solutions, group norms and action, social justice, and social support and identity.
common good The shared interests of an entire group or population, as distinct from the interests of individuals or special interests.
DPSEEA An acronym for a conceptual model, developed by the World Health Organization, that describes environmental factors relevant to health: driving forces-pressure-state-exposure- effects-actions.
environment The complex of physical, chemical, biotic, and social factors that surround an organism.
environmental health The field of public health that addresses physical, chemical, biological, social, and psychosocial factors in the environment. It aims both to control and prevent environmental hazards and to promote health and well-being through environmental strategies (see Text Box 1.1 for additional definitions).
environmental justice Both equal protection for all communities from environmental hazards and equal access for all communities to environmental, social, and economic assets that promote health and well-being, such as clean air, safe drinking water, green space, public transit, and economic opportunity.
health A state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity.
individualism An approach emphasizing personal independence, autonomy, and liberty.
108
nanny state Used as a derogatory term to describe government actions seen as overprotective or as undermining personal choice.
precautionary principle The concept articulated in Principle 15 of the Rio Declaration, “Where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be used as a reason for postponigng cost-effective measures to prevent environmental degradation.”
reality mining The collection and analysis of data, usually from electronic sources such as smartphones, social media posts, or credit card records, to identify patterns of behavior.
sanitarian The field that emerged, and an individual with expertise in that field, food protection, hazardous substances, product safety, housing, institutional health and safety, radiation protection, recreational areas and waters, solid waste management, vector control, water quality, wastewater technology and management, hazardous waste management or industrial hygiene.
sanitary issues The subset of environmental health concerns, dating from historical times, that includes provision of clean water, sewage management, and safe food.
spatial scale A concept important in fields from geography to urban planning to public health; it refers to the physical extent of a process or place. A small spatial scale might be a room in a building; a large spatial scale might be an entire river system.
sustainability The ability of a system to continue functioning without depleting or damaging the things it needs to function.
109
Discussion Questions 1. Name three ways in which your environment affects your health,
three ways in which your environment affects your short-term mood, and three ways in which your environment affects your long-term well-being.
2. Imagine you were the health commissioner of your city or town in 1866, 150 years before this textbook was published. What would have been the most pressing environmental health concerns? Now imagine you are the health commissioner of your city or town today. What are the most pressing environmental health concerns?
3. The environment affects health in many ways, but most doctors and nurses receive very little training in environmental health. What environmental health topics do you think health care providers should learn about?
4. Environmental health relates to many upstream factors. Select any cabinet department of the U.S. government other than the Department of Health and Human Services, and describe how its work affects health.
110
References Aguirre, A. A., Ostfeld, R. S., Tabor, G. M., House, C., & Pearl, M. C. (Eds.). (2002). Conservation medicine: Ecological health in practice. New York: Oxford University Press.
Alcamo, J., Bennett, E. M., Millennium Ecosystem Assessment. (2003). Ecosystems and human well-being: A framework for assessment. Millennium Ecosystem Assessment. Washington, DC: Island Press.
Aron, J. L., & Patz, J. A. (Eds.). (2001). Ecosystem change and public health: A global perspective. Baltimore: Johns Hopkins University Press.
Ausubel, K., with Harpignies, J. P. (Eds.). (2004). Ecological medicine: Healing the Earth, healing ourselves. San Francisco: Sierra Club Books.
Beaglehole, R., Bonita, R., Horton, R., Adams, O., & McKee, M. (2004). Public health in the new era: Improving health through collective action. Lancet, 363(9426), 2084–2086.
Briggs D. (1999). Environmental health indicators: Framework and methodologies. Geneva: World Health Organization. Retrieved from http://whqlibdoc.who.int/hq/1999/WHO_SDE_OEH_99.10.pdf
Brimblecombe, P. (1988). The Big Smoke: A history of air pollution in London since medieval times. London: Routledge.
Brown, L. R. (2001). Eco-economy: Building an economy for the Earth. New York: Norton.
Brown. L. R. (2011). World on the edge: How to prevent environmental and economic collapse. New York: Routledge.
Brown, V. A., Grootjans, J., Ritchie, J., & Townsend, M. (2005). Sustainability and health: Supporting global ecological integrity in public health. London: Earthscan.
Bullard, R. D. (1994). Dumping in Dixie: Race, class, and
111
environmental quality (2nd ed.). Boulder, CO: Westview Press.
Calman, K. (2009). Beyond the “nanny state”: Stewardship and public health. Public Health, 123(1), e6–10.
Cantor, N. (2001). In the wake of the plague: The Black Death and the world it made. New York: Free Press.
Chivian, E., & Bernstein, A. (2008). Sustaining life: How human health depends on biodiversity. New York: Oxford University Press.
Chokshi, D. A., & Stine, N. W. (2013). Reconsidering the politics of public health. JAMA, 310(10), 1025–1026.
Cole, L. W., & Foster, S. R. (2000). From the ground up: Environmental racism and the rise of the environmental justice movement. New York: New York University Press, 2000.
Creech, J. L., & Johnson, M. N. (1974). Angiosarcoma of the liver in the manufacture of polyvinyl chloride. Journal of Occupational Medicine, 16, 150–151.
Cutler, D., & Miller, G. (2005). The role of public health improvements in health advances: The twentieth-century United States. Demography, 42(1), 1–22.
Dhara, V. R., & Dhara, R. (2002). The Union Carbide disaster in Bhopal: A review of health effects. Archives of Environmental Health, 57, 391–404.
Dowie, M. (1995). Losing ground: American environmentalism at the close of the twentieth century. Cambridge, MA: MIT Press.
Duffy, J. (1990). The sanitarians: A history of American public health. Urbana: University of Illinois Press.
Eagle, N., & Greene, K. (2014). Reality mining: Using big data to engineer a better world. Cambridge, MA: MIT Press.
Etzioni, A. (2004). The common good. Cambridge, MA: Polity.
Etzioni, A. (2015). The new normal: Finding a balance between individual rights and the common good. New Brunswick, NJ: Transaction.
112
European Commission. (2009). What is REACH? Retrieved from http://ec.europa.eu/environment/chemicals/reach/reach_intro.htm
Fagin, D. (2013). Toms River: A story of science and salvation. New York: Bantam.
Figueroa, W. G., Raszkowski, R., & Weiss, W. (1973). Lung cancer in chloromethyl methyl ether workers. New England Journal of Medicine, 288, 1096–1097.
Friedman, T. (2008). Hot, flat, and crowded: Why we need a green revolution and how it can renew America. New York: Farrar, Straus & Giroux.
Gibbs, L. M. (1998). Love Canal: The story continues. Gabriola Island, BC: New Society.
Gleeson, D., & Friel, S. (2013). Emerging threats to public health from regional trade agreements. Lancet, 381(9876), 1507–1509
Gore, A. (1992). Earth in the balance. Boston: Houghton Mifflin.
Gottlieb, R. (1993). Forcing the spring: The transformation of the American environmental movement. Washington, DC: Island Press.
Guillette, L. J., Jr., Gross, T. S., Masson, G. R., Matter, J. M., Percival, H. F., & Woodward, A. R. (1994). Developmental abnormalities of the gonad and abnormal sex hormone concentrations in juvenile alligators from contaminated and control lakes in Florida. Environmental Health Perspectives, 102, 680– 688.
Hamlin, C. (1998). Public health and social justice in the age of Chadwick: Britain, 1800–1854. New York: Cambridge University Press.
Harr, A. (1996). A civil action. New York: Vintage.
Hawken, P., Lovins, A., & Lovins, L. H. (1999). Natural capitalism: Creating the next industrial revolution. Boston: Little, Brown.
Heinberg, R. (2007). Peak everything: Waking up to a century of declines. Gabriola Island, BC: New Society.
113
Herlihy, D., & Cohn, S. K. (1997). The Black Death and the transformation of the west. Cambridge, MA: Harvard University Press.
Homer-Dixon, T. F. (1999). Environment, scarcity and violence. Princeton, NJ: Princeton University Press.
Institute of Medicine, Roundtable on Environmental Health Sciences, Research, and Medicine. (2013). Public health linkages with sustainability. Washington, DC: National Academies Press.
Iowa Public Health Association (1912). The fence or the ambulance. Reprinted in Iowa Public Health Association. (2015). Public health history in Iowa. Retrieved from http://www.iowapha.org/Resources/Documents/PHM+Winter+2011– 2012+The+Fence+or+the+Ambulance.pdf.
Kellert, S. R., & Wilson, E. O. (Eds.). (1993). The biophilia hypothesis. Washington, DC: Island Press.
Kelly, J. (2005). The great mortality: An intimate history of the Black Death, the most devastating plague of all time. New York: HarperCollins.
Klare, M. T. (2001). Resource wars: The new landscape of global conflict. New York: Henry Holt.
Labonté, R., Schrecker, T., Packer, C., & Runnels, V. (Eds.). (2009). Globalization and health: Pathways, evidence and policy. New York: Routledge.
Landrigan, P. J., & Etzel, R. A. (Eds.). (2014). Textbook of children's environmental health. New York: Oxford University Press.
Lapierre, D., & Moro, J. (2002). Five past midnight in Bhopal: The epic story of the world's deadliest industrial disaster. New York: Warner Books.
Leavitt, J. W. (1982). The healthiest city: Milwaukee and the politics of health reform. Princeton, NJ: Princeton University Press.
Lee, K. S. (2007). Infant mortality decline in the late 19th and early 20th centuries: The role of market milk. Perspectives in Biology and Medicine, 50(4), 585–602.
114
Lewis, W. H., & Elvin-Lewis, M.P.F. (2003). Medical botany: Plants affecting human health (2nd ed.). Hoboken, NJ: Wiley.
McDonough, W., & Braungart, M. (2002). Cradle to cradle: Remaking the way we make things. New York: North Point Press.
McKeown, T. (1979). The role of medicine: Dream, mirage, or nemesis? Princeton, NJ: Princeton University Press.
McMichael, T. (2001). Human frontiers, environments and disease. New York: Cambridge University Press.
Melosi, M. V. (2000). The sanitary city: Urban infrastructure in America from colonial times to the present. Baltimore: Johns Hopkins University Press.
Minkler, M. (1999). Personal responsibility for health? A review of the arguments and the evidence at century's end. Health Education & Behavior, 26(1), 121–140.
Nevin, R. (2007). Understanding international crime trends: The legacy of preschool lead exposure. Environmental Research, 104(3), 315–336.
New York Times. (1964). Rachel Carson dies of cancer; “Silent Spring” author was 56. New York Times, April 15. Retrieved from http://www.nytimes.com/learning/general/onthisday/bday/0527.html (Statements quoted originally aired on CBS Reports, April 3, 1963)
Parmet, W. E., Goodman, R. A., & Farber, A. (2005). Individual rights versus the public's health—100 years after Jacobson v. Massachusetts. New England Journal of Medicine, 352(7), 652– 654.
Patterson, J. T. (1987). The dread disease: Cancer and modern American culture. Cambridge, MA: Harvard University Press.
Pentland, A., Lazer, D., Brewer, D., & Heibeck, T. (2009). Using reality mining to improve public health and medicine. Studies in Health Technology and Informatics, 149, 93–102.
Randall, W. (1977). Building 6: The tragedy at Bridesburg. Boston: Little, Brown.
115
Rayner, G., & Lang, T. (2012). Ecological public health: Reshaping the conditions for good health. New York: Earthscan.
Rea, W. J. (1992–1998). Chemical sensitivity (4 vols.). Boca Raton, FL: Lewis.
Rosen, G. (1993). A history of public health (Exp. ed.). Baltimore: Johns Hopkins University Press. (First edition published 1958)
Rosenberg, C. (1962). The cholera years: The United States in 1832, 1849, and 1866. Chicago: University of Chicago Press.
Schilling, J., & Linton, L. S. (2005). The public health roots of zoning: In search of active living's legal genealogy. American Journal of Preventive Medicine, 28(2, Suppl. 2), 96–104.
Shabecoff, P. (1993). A fierce green fire: The American environmental movement. New York: Hill & Wang.
Smith, W. E., & Smith, A. M. (1975). Minamata. New York: Holt, Rinehart & Winston.
Spears, E. (2014). Baptized in PCBs: Race, pollution, and justice in an all-American town. Chapel Hill: University of North Carolina Press.
Sullivan, R. (2004). Rats: Observations on the history and habitat of the city's most unwanted inhabitants. New York: Bloomsbury.
Swan, S. H., Elkin, E. P., & Fenster, L. (1997). Have sperm densities declined? A reanalysis of global trend data. Environmental Health Perspectives, 105, 1228–1232.
Tarr, J. A. (1996). The search for the ultimate sink: Urban pollution in historical perspective. Akron, OH: University of Akron Press.
Tarr, J. A. (2002). Industrial waste disposal in the United States as a historical problem. Ambix, 49, 4–20.
United Nations. (1992). Report of the United Nations Conference on Environment and Development: Annex I: Rio Declaration on Environment and Development. Retrieved from http://www.un.org/documents/ga/conf151/aconf15126- 1annex1.htm
116
United Nations Department of Economic and Social Affairs. (2006). Johannesburg Summit 2002. Retrieved from http://www.un.org/jsummit/html/basic_info/unced.html
U.S. Department of Health and Human Services. (1998). An ensemble of definitions of environmental health. Retrieved from http://web.health.gov/environment/DefinitionsofEnvHealth/ehdef2.htm
van Wyk, B.-E., & Wink, M. (2004). Medicinal plants of the world: An illustrated scientific guide to important medicinal plants and their uses. Portland, OR: Timber Press.
Wackernagel, M., & Rees, W. (1995). Our ecological footprint: Reducing human impact on the Earth. Gabriola Island, BC: New Society.
Walls, H. L., Smith, R. D., & Drahos, P. (2015). Improving regulatory capacity to manage risks associated with trade agreements. Global Health, 11(1), 14.
Waltner-Toews, D. (2004). Ecosystem sustainability and health: A practical approach. New York: Cambridge University Press.
Wiley, L. F., Berman, M. L., & Blanke, D. (2013). Who's your nanny? Choice, paternalism and public health in the age of personal responsibility. Journal of Law, Medicine & Ethics, 41(Suppl. 1), 88– 91.
Wilson, E. O. (1984). Biophilia: The human bond with other species. Cambridge, MA: Harvard University Press.
World Commission on Environment and Development. (1987). Our common future. New York: Oxford University Press.
Zinsser, H. (1935). Rats, lice and history: Being a study in biography, which, after twelve preliminary chapters indispensable for the preparation of the lay reader, deals with the life history of typhus fever. Boston: Little, Brown.
117
For Further Information There is a rich literature describing the history of environmental health. In fact much of this history is identical with the larger history of public health! While historical accounts of specific topics, such as chemical contaminants, appear at the end of later chapters in this book, some of the best general books include four that are listed in the References above—Duffy, 1990; Melosi, 2000; Rosen, 2015; and Tarr, 1996—and also D. Porter, Health, Civilization and the State: A History of Public Health from Ancient to Modern Times (New York: Routledge, 1999).
Many agencies address environmental health issues. They include
European Commission: http://ec.europa.eu/health/healthy_environments/policy/index_en.htm
U.S. Centers for Disease Control and Prevention, National Center for Environmental Health and Agency for Toxic Substances and Disease Registry: http://www.cdc.gov/nceh and http://www.atsdr.cdc.gov
U.S. Environmental Protection Agency: multiple EPA sites pertain to health; two good starting points are http://www2.epa.gov/communityhealth and http://www2.epa.gov/healthresearch
U.S. National Institutes of Health, National Institute of Environmental Health Sciences: http://www.niehs.nih.gov
World Health Organization: http://www.who.int/topics/environmental_health/en
Similarly, many organizations address environmental health issues, some as a part of a larger public health agenda, and some because they are specifically focused on environmental health. Leading examples include
American Public Health Association: https://www.apha.org/topics-and-issues/environmental-health
Association of State and Territorial Health Officials: http://www.astho.org/programs/environmental-health
118
International Society for Environmental Epidemiology: http://www.iseepi.org
International Society of Exposure Science: http://www.isesweb.org
National Association of City and County Health Officials: http://www.naccho.org/topics/environmental/index.cfm
National Environmental Health Association: http://www.neha.org
There are many academic programs of environmental health, at schools of public health, schools of medicine, and other institutions. Too numerous to list here, they are easily accessible through Web searches.
119
Chapter 2 Ecology and Ecosystems as Foundational for Health
Margot W. Parkes and Pierre Horwitz
The authors acknowledge Cindy L. Parker, Jessica Rhodes, and Brian S. Schwartz for their contributions to the systems section of this chapter, and Howard Frumkin for his editing assistance. Margot Parkes acknowledges support from her appointment as a Canada Research Chair in Health, Ecosystems, and Society (CRC 950-230463). During the preparation of this chapter Dr. Parkes received research funding from the Canadian Institutes for Health Research, the International Development Research Centre, and the Public Health Agency of Canada. Dr. Parkes has held (uncompensated) positions with the International Association for Ecology and Health (IAEH), the journal EcoHealth, the Canadian Public Health Association Working Group on Ecological Determinants of Health, the Canadian Community of Practice in Ecosystem Approaches to Health, and the Network for Ecosystem Sustainability and Health. During the preparation of this chapter Dr. Horwitz received research funding from the Wildlife Conservation Society, Rio Tinto, the Australian Government, and the State Government of Western Australia. He has held (uncompensated) positions with the International Association for Ecology and Health, the journals EcoHealth and BioScience, the Scientific and Technical Review Panel for the Ramsar Convention on Wetlands, and Bush Heritage Australia. Disclosures by Dr. Frumkin, who wrote Tox Box 2.1, appear in the front of this book, in the section titled “Potential Conflicts of Interest in Environmental Health: From Global to Local.”
120
Key Concepts Ecology is a scientific discipline that focuses on interactions of living things in relation to their environment, and encourages understanding of the environment as our home.
An ecosystem is a complex system of organisms, their environment, and the interactions that connect them.
Ecosystems provide a range of ecosystem services and constitute the life support systems that are foundational for human health.
Ecological literacy helps us to interpret the consequences of our actions and the influence of the environment on our lives, and to make predictions about the future of life on this planet; it applies across spatial scales, from the subcellular, through the local and the regional, to the global.
Subfields of ecology include population ecology, community ecology, and ecosystem ecology.
Systems thinking is central to ecology and, indeed, to much of human health.
An ecological approach to public health views humans as nested within ecosystems, calls for integrated consideration of environmental and social factors, and highlights system characteristics such as complexity, emergence, and feedback loops.
The German physician and zoologist Ernst Haeckel coined the word ecology in the 1860s, but it would be almost a century—in the 1950s —before the science of ecology began to flourish. Ecology focuses on the interactions of living things in relation to their environment. This emerging science drew on critical strands of thought, including population dynamics, systems theory, and a strong environmental ethic. It was informed by, yet contrasted sharply with, a tendency of biology to deconstruct systems into component parts and to focus narrowly on these component parts.
The word ecology (like the word economy) is derived from the
121
Greek word oikos meaning household, home, or place to live. Thinking of the environment as our home expands the scope of environmental health science and practice well beyond simply controlling harmful exposures. An ecosystem is a complex system of organisms and their environment, including both living (biotic) and nonliving (abiotic) components, and the interactions that connect them. These relationships support all of life and profoundly shape the health of the organisms within our shared home. The biological unit we recognize most readily is a species, which is a group of living organisms consisting of similar individuals capable of exchanging genes or interbreeding (known as the biological species concept). Species are held in assemblages (ecological communities); one or more ecological communities makes an ecosystem, and one or more ecosystems are found in a biome.
Understanding our homes in ecological terms has become more important as societies have become more modern, urbanized, cosmopolitan, and technology-dependent—and in many cases more separated from exposure to the “elements” (air, soil, water, and weather). Together these trends shift our experiences away from the living systems around us and from what is local. They diminish our ability to read, interpret, and understand the system of which we are a part—to know what is likely to occur and to be appropriate locally, given the constraints and opportunities presented by human habitat —contributing to a loss of ecological literacy.
The ecological concepts in this chapter provide a series of foundational principles to help us understand the links between environment and health, and their individual, community, and societal implications.
122
Environment as Ecology: Ecology as the Study of Our Home Ecology is attentive to the world around us, the world to which we belong. It is attentive to the parts that make up our surroundings— the abiotic components that are physical and chemical and the biotic components that live, reproduce, and grow. These parts influence one another, and have interrelationships and interdependencies that are so important that the whole that comes from these interactions is said to be more than the sum of its parts. In fact, some properties of ecosystems are emergent, meaning that they don't exist in isolation in individual parts of the system but arise when components interact (more about this later). Accordingly, ecology never deviates from the principle of holism, the all-encompassing approach of focusing on or investigating wholes rather than parts and seeking to see as many connections as possible, rather than eliminating some connections to see components parts more clearly. The corollary is that reducing an environment to its component parts only, and seeing the world as a machine, or as a series of linear cause-effect relationships (reductionism), is inconsistent with ecological understandings and approaches. Ecologists recognize the system—how it is organized (structure), what processes it uses (process), and what it does (function)—and on that basis seek to make sense of a complex and uncertain world. Accordingly, an ecologist is trained to observe and measure, and to do something that is somewhat intuitive for humans—to explore patterns across space (e.g., geographic distribution) and across time (e.g., aging, growth, and succession).
A starting point in ecological thought is the question of scale; the analytical approach described above applies from the very smallest level of the living world (such as the tiniest microbes) to the very largest (the planet). A hierarchy is a way of organizing according to levels of scales. These organizational levels are central to ecology, and some of the corresponding disciplines are shown in Table 2.1. Other examples of hierarchies in ecology include food webs (organized according to trophic levels), systems (where all systems are made of smaller systems, and are part of larger systems), and
123
the organizational units of ecology themselves.
Table 2.1 Scale in Ecology, and Some Disciplines That Contribute at Each Level
Level of scale Disciplines Focal studies Molecules Molecular
biology, genetics
Inheritance
Cells Cell biology, biochemistry
Infection
Tissues/organs Anatomy, physiology
Individual function
Organism/individual Embryology, morphology
Reproduction, behavior, and life history
Populations (of single species)
Population ecology
From demography and migration to speciation and evolution
Communities (assemblages of species)
Community ecology
Landscapes
Ecosystems (and biomes)
Ecosystem sciences
Interdisciplinarity
Planet Sustainability Transdisciplinarity
Some patterns repeat across scales. Taking the planet as an example, ecosystems can be thought of as the tissues of the planet and individuals as the cells; the powerful metaphor here is that each level, including the planet, can be considered living. Importantly, any ecological level (not just the ecosystem level) can function as a system, in which the whole is greater than the sum of the parts; one individual animal or plant can be the host “environment” to countless other individuals, even populations, of other species, and thereby function as a system of interacting life forms. With hundreds of species of archaea, bacteria, and fungi in the human gut, and hundreds more on the skin, in the mouth, and elsewhere on our bodies, each of us can be considered a walking ecosystem!
Our language can become complicated around questions of scale
124
too. When we humans talk of communities, we are often speaking about interactions among humans defined by location or special interest. To an ecologist such a community is technically a subpopulation. When we expand our notion of human communities to explicitly consider social and ecological interactions, the term community becomes more consistent with the ecologist's view— interactions among different species (the focus of community ecology, as described below)—and becomes more relevant for humans and their health. An even broader notion of the human community is the assemblage of life on Earth with which we live communally within a shared home, our planet. This notion lies at the heart of both an environmental ethic and the discipline of human ecology, the study of the reciprocal relationship between humans and their environments, including urban, rural, regional, and other habitats.
Each level in Table 2.1 contributes to biodiversity. Biodiversity (or biological diversity) is the degree of variation of life, encompassing genetic variation, phenotypic variation, different life history stages (from spores to cells, or seeds to juveniles to adults, or eggs to larvae/pupae to adults), species, communities, and ecosystems. Biodiversity has become central to ecological thought and is increasingly recognized as a pillar of human health (see Bernstein, 2014, and also Discussion Question 1 later). Much of the effort in ecology is directed toward measuring and understanding the distribution, diversity, and abundance of life, and the factors that influence them. These factors are also considered at different levels, discussed here in relation to population ecology, community ecology, and ecosystem sciences.
A special case of scale and hierarchy in ecology is the food web: the sequence, from tiny organisms to top predators, through which food is produced and consumed. Text Box 2.1 describes food webs, exploring an example from a North American terrestrial ecosystem (also see Discussion Question 2).
125
Text Box 2.1 Food Webs A food web consists of the pathways through which food energy and nutrients are captured, incorporated into living matter, consumed, and transmitted through the ecosystem. At the bottom of the food web, almost all food energy derives ultimately from the sun. Autotrophs (or primary producers)—for the most part plants, algae, and some bacteria—harness solar energy through photosynthesis, reducing inorganic carbon (in forms such as CO2) to organic carbon (such as carbohydrates) whose chemical bonds contain energy. These organisms are then consumed by heterotrophs (or consumers). In simple terms, the first level of heterotrophs consists of herbivores, which eat plants. Primary predators eat the herbivores, secondary predators eat the primary predators, and so on. For example, in many grassland ecosystems, grass is a primary producer, grasshoppers are primary consumers, rats that eat the grasshoppers are primary predators, and snakes that eat the rats are secondary predators. This predation sequence can continue; hawks that eat snakes are tertiary (or apex) predators. These trophic levels exemplify hierarchic scales, a recurring theme in ecology (and also illustrate the maxim of interrelatedness that “everybody is somebody else's lunch”). Throughout the process, when organisms die they are consumed by decomposers (or detritivores) such as fungi or earthworms, which recycle energy and materials back into the food web. These relationships are depicted in Figure 2.1.
126
Figure 2.1 A Food Web in a North American Terrestrial Food Ecosystem
Energy flow is a key feature of the food web. At each trophic level, energy is used for metabolic processes and is released back to the environment. Therefore energy transfer is incomplete, and the biomass of each trophic level is substantially less than that of the level below. Put differently, a consumer at any trophic level typically consumes far more than its own mass from the trophic level below. This is highly relevant to environmental health, since it explains why persistent pollutants such as mercury and polychlorinated biphenyls (PCBs; see Tox Box 2.1) undergo not only bioaccumulation but also biomagnification (or bioamplification) as they move up the food web. This helps explain why such pollutants can reach high concentrations in the tissues of animals high on the food web, such as raptors, killer whales, sea lions, salmon, and even humans.
127
Population Ecology Population ecology deals with the dynamics of species populations, how these populations interact with their surroundings, and how they change over time and space. All populations can be characterized by their age structure, sex ratio, reproductive strategies (such as how many offspring they produce, and how much parental care is needed), and migration rates (emigration and immigration). Demography is the study of these characteristics; they can be presented in life tables so that survival, breeding, and migration rates for any species can be explored to make predictions about the fate of a population.
The size of a population, measured as the number of individuals, grows whenever the reproduction rate (plus immigration) exceeds the death rate (plus emigration). These periods of growth occur when resources—energy in such forms as food or light, needed nutrients, water, shelter, habitat (the physical space occupied by a species, including everything within it)—are sufficiently plentiful to enable individuals in the population to grow, mature, reproduce, and in some cases raise their young. Under hypothetical circumstances with no constraints, individuals will continue to reproduce, and a population will undergo exponential growth: that is, geometric growth, with the rate of growth proportional to population size rather than linear or occurring at a fixed rate. But growth can continue only as long as resources are sufficient to sustain it. When a limit is reached the population is said to equilibrate at a certain size: the carrying capacity or the maximum population that can be sustained indefinitely by its supporting ecosystems. (For more on sustainability and carrying capacity and their relevance to human health, see Chapter 3.)
Populations rarely achieve this carrying capacity because other important ecological processes intervene. As the numbers of a single species increase in a population so, soon after, will the numbers of their predators. In this sense predation (and also herbivory, where animals graze on a plant population) is said to regulate population growth, in other words, to keep it in check. A similar process occurs for parasitism, where a parasite makes the host less fit and less able to reproduce rapidly. In both cases the
128
numbers of the prey and the host are regulated, and the numbers of the predators and the parasites are similarly limited by the availability of prey and hosts.
Still another mechanism may regulate population numbers: competition. This occurs when similar species have overlapping distributions and depend on the same resources for their survival and growth. The closer species are in this regard, the more they are likely to compete for the same resources; they are said to have overlapping niches. A niche is the multidimensional ecosystem space in which a species exists (its habitat) and also what it does (its ecological role, both structurally and functionally). The resulting deprivation of resources for one or the other species diminishes its fitness or survival in the presence of the competitor.
129
Tox Box 2.1 Polychlorinated Biphenyls (PCBs)
What Are They? PCBs are a group of 209 isomers of a synthetic organic chemical. Each isomer of PCB consists of a pair of benzene rings, with various configurations of chlorine atoms attached. PCBs are generally liquids, and as the chlorine content increases, they become more oily and viscous. PCBs don't dissolve well in water but are very soluble in oils and fats. They are very stable and persist in the environment—an example of persistent organic pollutants.
How Are They Used? PCBs were manufactured in high quantities from the 1930s through the 1970s for use as insulating and dielectric fluids in electrical equipment such as capacitors and transformers. They were also used as coolants and lubricants and found many other industrial uses—as a component of carbon paper, in hydraulic oil, as plasticizers in paints, in adhesives, and more.
How Are People Exposed? At the time PCBs were being manufactured, people might have been exposed at work, while manufacturing PCBs or
130
PCB-containing products, and also might have been exposed in the general environment, following leaks or spills or by exposure to PCB-containing wastes. Fires or leaks in transformers were a common means of exposure. Extensive PCB contamination occurred near industrial facilities, such as in Anniston, Alabama, the site of a major PCB manufacturing plant, or along the Hudson River, due to dumping at General Electric capacitor manufacturing facilities in the towns of Fort Edward and Hudson Falls, New York. When PCBs enter the environment, they may remain in soil or river sediment for many years. In water, small organisms can absorb PCBs, which bioaccumulate as they move up the food web (Box 2.1), reaching very high levels in predator species. Fatty fish can contain substantial levels of PCBs, and fish consumption is now the leading route of human exposure—an illustration of the links between ecosystem function and human health. Other sources of exposure persist, even years after PCB manufacturing ended; these include old fluorescent light ballasts, old caulking, and other residual materials. In addition to ingestion, people can absorb PCBs by inhalation or through their skin. Ongoing population blood testing by the Centers for Disease Control and Prevention shows that many people carry a body burden of PCBs, although population PCB levels are declining over time.
What Are the Toxic Effects? High-level PCB exposure can cause a skin condition called chloracne and other acute symptoms. However, the far more common scenario is long-term, lower-dose exposure, say, from eating contaminated fish. The effects are far-reaching, if not fully understood. Toxicological data, and some epidemiological data, suggest that certain PCBs (a subset with dioxin-like activity) increase the risk of cancer, and the International Agency for Research on Cancer (IARC) in 2013 classified these PCBs as carcinogenic to humans. PCBs are also considered endocrine disrupters and developmental neurotoxins. They can interfere with hormone function, especially estrogens. Animal and human evidence suggests
131
that maternal PCB exposure may lead to reduced conception rates, fertility, and birth weights. Children exposed to PCBs in utero and early in life may be at risk of behavioral, cognitive, and psychomotor abnormalities. PCB exposure is also associated with immune dysfunction.
How Are People Protected? PCB production was banned in the United States in 1979, and many other countries banned PCB production at about the same time. Residual PCBs in equipment and the general environment break down very slowly. People can reduce their exposure by reducing their consumption of fish that are high in PCBs, and by avoiding contact with such potential sources as old transformers.
Want to Learn More? The Agency for Toxic Substances and Disease Registry Toxicological Profile for PCBs dates from 2000, but a 2011 update provides more current information; these are available at www.atsdr.cdc.gov/toxprofiles. The most recent IARC review of PCBs may be found at monographs.iarc.fr/ENG/Monographs/vol107 and is summarized in B. Lauby-Secretan et al., “Carcinogenicity of Polychlorinated Biphenyls and Polybrominated Biphenyls,” Lancet Oncology, 2013, 14(4), 287–288. Another recent review focusing on carcinogenicity is C. Zani, G. Toninelli, B. Filisetti, and F. Donato, “Polychlorinated Biphenyls and Cancer: An Epidemiological Assessment,” Journal of Environmental Science and Health: Part C, Environmental Carcinogenesis & Ecotoxicology Reviews, 2013, 31(2), 99– 144. A recent review focusing on developmental toxicity is N. El Majidi, M. Bouchard, and G. Carrier, “Systematic Analysis of the Relationship Between Standardized Prenatal Exposure to Polychlorinated Biphenyls and Mental and Motor Development During Follow-up of Nine Children Cohorts,” Regulatory Toxicology and Pharmacology, 2013, 66(1), 130–146.
In addition to these technical sources, a book-length account of PCB exposure in Anniston, Alabama, with attention to
132
health and social impacts and environmental justice, is Ellen Griffith Spears's Baptized in PCBs: Race, Pollution, and Justice in an All-American Town (Chapel Hill: University of North Carolina Press, 2014).
Contributed by Howard Frumkin
The principles of population ecology give us considerable insight into the roles that populations of a single species play with respect to other species and throughout ecosystems (see Table 2.1). Patterns emerge in life history strategies across these levels, with two distinct patterns apparent. Some species, such as many weeds, are opportunists; they grow rapidly, mature quickly, and produce many progeny. These characteristics are associated with r-selected species. They are characteristically found in disrupted or unstable environments, such as after a fire, landslide, volcanic eruption, or similar disturbance. Other species, typically in more stable environments, grow to be larger individuals, take longer to reach maturity, live longer, produce fewer progeny, and invest considerably more parental energy. These species are referred to as K-selected species.
A special case of population dynamics occurs when a species moves to a place where it has never occurred before, becoming an established and successful colonist. Biological invasions are explored further in Text Box 2.2.
133
Text Box 2.2 Biological Invasions The term biological invasions implies a large-scale movement of animals or plants into areas where they were previously absent or uncommon (in other words, beyond their historical or known geographic distribution). All living things have the potential to move into new areas, if environmental conditions are suitable and if the opportunity presents itself, which means that biological invasions are common occurrences. But human actions often facilitate such invasions, and the results can damage ecosystems, threaten human health, and be costly. One example is zebra mussels, (Figure 2.2, left side), which were discovered in the Great Lakes in the late twentieth century, probably having arrived via the ballast tanks of ships from Europe. These mussels have proliferated, clogging the intakes of municipal water supplies and power plants, contributing to the growth of harmful algal blooms, and displacing other food sources in the aquatic food web. Another example is the red imported fire ant, (Figure 2.2, right side), a species native to South America that has spread across much of the southeast United States since the mid-twentieth century. These ants attack humans and wild and domestic animals, inflicting painful stings, and because they are attracted to electromagnetic fields, can disrupt electrical machinery. Some invasive species, such as the gypsy moth and the emerald ash borer, can cause considerable damage to forests and crops. Still others can be vectors of human disease; examples include the Asian tiger mosquito, a vector of encephalitis and the West Nile virus that arrived in North America in imported tires in around 1985, and fresh water snails, intermediate hosts for schistosomiasis that have been introduced into many regions in Africa, the Middle East, Latin America, and the Caribbean. (See Figure 2.2.)
134
Figure 2.2 Invasive Species and Their Impacts The zebra mussel (upper left), and the inside of a pipe packed with zebra mussels (lower left), disrupting water flow. The red imported fire ant (upper right), and the hand of a victim of the ant's stings (lower right). Sources: TexasInvasives.org (upper left); TN Department of Agriculture Upper right); Science Photo Library (lower left); Photo by Bart Drees (lower right).
Ecosystem disturbances such as land clearing or too frequent or intense fires can pave the way for invasive species. Characteristics that enable an introduced species (sometimes known as an exotic or alien species) to establish itself in a new environment include a capacity to disperse into an area; suitable environmental conditions for its establishment, survival, and growth; the absence of predators and parasites that regulate its growth in other parts of its range; and the ability to grow, mature, and reproduce rapidly. These features together help it to outcompete other species with similar ecological requirements.
Why worry about biological invasions? As the examples above suggest, invaders may compete with native species for space or food, by aggressiveness or by predation. Invasive species can also significantly alter the habitats for other species, and they can significantly restructure food webs.
135
Invasive species may bring unwanted passengers—other symbionts, parasites, or pathogens. The action of moving and releasing species into an area has the potential to move and release other biotic material; moving soil with a plant will introduce soil organisms, transporting fish or other species in water will introduce waterborne microbes, plants, or animals. Many such examples of accidental introductions have occurred in all parts of the world.
So far we have been concerned with population growth, and the factors that limit the apparently inexorable potential for populations to increase in size. But populations do not always grow. Population decline occurs when the death rate (plus emigration rate) exceeds the birthrate (plus immigration rate)—caused by such factors as habitat changes, lack of resources, disease, and predation. Unless these population pressures are removed, fewer and fewer individuals reach maturity and reproduce. At the extreme, breeding can eventually cease, and the last individuals die off. If all populations of one species suffer the same demise, the species is said to be extinct. At this point extinction is irreversible; the unique assemblages of genes, and unique genes themselves, that make up the species are lost from ecosystems, and the planet, forever. Extinction, in geological time frames, is quite rare, although major episodes have occurred in the geological past (such as the mass extinction event that defines the end of the Cretaceous geological epoch and the beginning of the Tertiary, some 66 million years ago). The suggestion that the actions of humans, a single species, might be responsible for another extinction event of planetary magnitude with geological implications (Kolbert, 2014) is proving to be a source of profound concern. Conservation biology is one of the human responses to this prospect and is explored in Text Box 2.3.
136
Text Box 2.3 Conservation Biology Where human activity is implicated in the decline of a population and in the possibility of the extinction of a species, the field of conservation biology seeks to intervene to prevent this irreversible loss. Intervention is costly, so criteria for setting priorities are needed. These criteria are based on the size of the population, the rate of population loss, the distribution range (extent of occurrence of a species), and the area of the habitat that the species occupies in that range. A species or subspecies meeting the criteria can then be placed into a category of threat, according to the Red List scheme adopted by the International Union for Conservation of Nature (IUCN).
Extinct (EX) There is no reasonable doubt that the last individual has died.
Extinct in the wild (EW)
A species is known to survive only in cultivation, in captivity, or as a naturalized population (or populations) well outside its past range.
Threatened, including
Critically endangered (CR)
Endangered (EN)
Vulnerable (VU)
Best available evidence indicates that a species faces a high to extremely high risk of extinction in the wild.
Near threatened (NT)
A species has been evaluated and does not meet the criteria but is close to qualifying or likely to qualify for a threatened category in the near future.
137
(LC) under a higher category of threat (for widespread and abundant species).
Data deficient (DD)
There is inadequate information to assess risk of extinction based on species distribution and/or population status.
In many countries laws have been established to protect endangered or threatened species and prevent extinctions. To gain legal protection under such laws, a species must be formally recognized by the government (by gazettal, or formal listing), often using the categories promoted by the IUCN. Once a species is listed, the government can ban or regulate the processes known to threaten the species.
138
Community Ecology A core focus in ecology is identifying characteristic assemblages of species. Populations of a number of species aggregate either because they have the same habitat requirements or because they are developing at the same rate and are affected by the same things at the same time. They can also evolve together over much longer periods of time, and even become dependent on one another. These assemblages are known as ecological communities. Examples are everywhere: the highly idiosyncratic communities of insects, arachnids, and crustaceans found in caves; the plants and animals found in the riparian zone of a lake; and even the assemblage of species with which humans regularly find themselves living—pets (dogs and cats), rats and mice, cockroaches, seagulls, particular weeds, productive plants, and so on.
Ecologists search for underlying reasons why these assemblages stay together and become so identifiable. They ask, What structures a community?, and ground their answers in biotic processes (predation, competition, disease, and parasite-host relationships, which are said to be density dependent) and in abiotic processes (disturbances such as fire, cyclones, drought, and flood, which are density independent).
Succession (Figure 2.3) is the sequence by which ecological communities develop over time. According to classic ecological theory, disturbances enable colonizers to establish themselves. Over time they provide sustenance and improve the habitat for other species. Gradually communities shift from being dominated by r- selected species to being dominated by K-selected species. Climax communities eventually develop, and remain until disturbances occur and the process begins again. Local species diversity is maximized when ecological disturbances are neither too rare nor too frequent (the so-called intermediate disturbance hypothesis). When disturbances are too rare then only species associated with climax communities will persist; when they are too frequent then only colonizing opportunist species will be encouraged. Our understanding of ecological succession has been updated and informed by the experience of restoration ecology, which is explored in Text Box 2.5.
139
Figure 2.3 A Classical Model of Ecological Succession in a North American Forest Ecosystem
Over time, a predictable sequence of species unfolds, with K-selected species replacing r-selected species.
Symbiosis is another key concept in community ecology—a particular set of long-term interactions between different biological species where at least one species in the relationship can receive benefit. Table 2.2 describes three types of symbiosis (parasitism, mutualism, and commensalism) as well as two other types of relationships between species: competition and predation.
Table 2.2 Type of Relationship Between Different Species
Relationship type
Species A
Species B
Example
Competition Benefit Harm Lion and hyena compete for same prey.
Predation Benefit Harm Polar bear feeds on seal. Symbiosis: parasitism
Benefit Harm Tapeworm lives in intestines of host, harming host.
Symbiosis: mutualism
Benefit Benefit Bee gains nectar from a flower and in the process pollinates flower.
Symbiosis: commensalism
Benefit Neither benefit
Cattle egrets live near cows, to eat insects found near the
140
nor harm cows.
141
Ecosystem Ecology At the larger spatial scale of the ecosystem, ecologists study energy and matter cycles. In addition to energy, critical cycles are the hydrological (water) cycle, carbon cycle, nitrogen cycle, and phosphorus cycle (key nutrients required for life) and food webs. Elements cycle through different states and chemical configurations, through both biotic and abiotic pathways. Cycles of important or dominant elements (both energy and materials) demonstrate how ecosystems function, by illustrating how they change form. Parts of a cycle can be extremely slow and occur over very long geological time frames, while other parts can be brisk, seemingly occurring in the blink of an eye.
The hydrologic cycle, pictured in Figure 16.1 (see Chapter 16), is a familiar part of our daily experience, through rainfall, evaporation, condensation, the flows of rivers and streams, and the retention of water in ice sheets, extensive wetland systems and ground water. Human land use and water use have a profound effect on the distribution of surface water and ground water and the ecosystems dependent on them. These ongoing disruptions to the hydrological cycle are also being influenced by climate change in new and, increasingly, unpredictable ways. On the one hand, when the atmosphere warms up it retains more water, along with more energy—the perfect ingredients for severe storms, with heavy rainfall and resulting floods that threaten people and property. On the other hand, in some regions climate change means far less rain. Prolonged droughts and fires in Australia, the American southwest, and other places have proven a huge challenge for farming communities and forest and park managers in terms of water resource management, as well as for other species living in affected ecosystems. Discussion Question 3 encourages consideration of how the hydrological cycle varies across regional and global scales. For more on how climate change affects the hydrological cycle, and through it human health and well-being, see Chapter 12.
The phosphorus cycle (Figure 2.4), in contrast, is less evident to a casual observer. Phosphorus is an essential nutrient for cell growth and maintenance. Phosphorus occurs in rocks, and when the rocks weather and erode to form soils the phosphorus becomes available
142
for uptake by microbes and plants. It can then be returned to the soil with dead and decaying material, where decomposition and soil formation processes make it available again. Or it can be consumed when herbivores graze on plants, becoming incorporated into the food chain and eventually excreted into water or soil. Eventually soils form sedimentary rocks and the cycle starts again. An interesting loop in the phosphorus cycle occurs when it is excreted in a concentrated form by bats (after they have been eating insects) and sea birds (after eating fish). Over long periods of time these concentrated deposits, called guano, build up, and people who discover them can mine them for the phosphorus they contain—an extremely valuable fertilizer (through which the phosphorus enters the soil and is incorporated into plants, and the cycle goes on!).
Figure 2.4 The Phosphorus Cycle
Soil, formed by the interaction of biotic and abiotic environments, is a wonderful example of an ecological process. Soil is produced steadily over time, serving both as a setting for and a product of ecosystem interactions and energy and nutrient cycles. Fertile soil requires the presence of eroded rock substrate, nutrients, and organic matter; the latter two depend in turn on plant and animal
143
life that flourished, died, and was decomposed by insects and microorganisms into organic and nutrient components. Soil formation is therefore a result of complex ecosystem transactions linking the geosphere, atmosphere, hydrosphere, and biosphere (Montgomery, 2007) and is foundational to the earth's capacity to support life (Figure 2.5).
Figure 2.5 Transactions Between Atmosphere, Geosphere, and Hydrosphere Provide a Basis for the Earth's Capacity to Support Life
Source: Adapted from Parkes & Weinstein, 2004.
Life occurs in the relatively thin “carpet” covering the surface of our large planet, where it is both a product of and contributes to the character of earth, air, and water (hence the double arrows).
Ecological cycles illustrate that ecosystems perform functions—from relatively simple ones, such as eroding, absorbing, and evaporating, to extraordinarily complex ones, such as decomposing. Ecosystem functions are made up of ecological processes and their component species, particularly microbes and invertebrates that “do most of the doing” in ecosystems. The richness of an ecological community reflects its level and complexity of ecosystem functions.
144
Assuming that each species occupies a different niche, and is therefore capable of doing different things, then ecosystems that contain more species should be capable of fulfilling more functional roles. Increased diversity stabilizes the functioning of the total ecosystem by increasing its resilience to disturbances, thus providing “insurance” against potentially disruptive events (more about resilience later).
Many of the processes, functions, and “products” discussed here— rainfall, soil, natural fertilizer—are enormously useful to people. In economic terms, what they provide has great value to people— including a role in promoting human health. This value is captured in the idea of ecosystem services (Text Box 2.4).
145
Text Box 2.4 Ecosystem Services Ecosystem services are defined simply as “the benefits people obtain from ecosystems” (Millennium Ecosystem Assessment, 2003, p. 49). But ecosystem services are often taken for granted and overlooked, with their value “externalized” from the market economy. Everyone recognizes that products and services such as a university course, a bicycle repair, or a pizza have value, as reflected in their market prices, but these prices exclude the “real” cost, because they all, in some way, depend on the services that ecosystems provide. Explicitly identifying the value of ecosystem services can lead to better decision making and more sustainable societies (see Chapter 3).
The Millennium Ecosystem Assessment (2005b), one of the largest international initiatives seeking to understand ecosystems in relation to human well-being, has classified ecosystem services into four groups:
Provisioning services provide or produce goods such as food, fiber, fuel, genetic resources, biochemicals, natural medicines and pharmaceuticals, ornamental resources, and fresh water.
Regulating services include the benefits gained from regulating such ecosystem features as air quality, climate, water quality, erosion, disease transmission, pest proliferation, pollination, and natural hazard occurrence.
Cultural services include nonmaterial benefits such as cultural diversity, spiritual and religious values, knowledge systems, educational values, inspiration, aesthetic values, social relations, sense of space, cultural heritage values, and recreation and ecotourism.
Supporting services are those that underpin the other services such as soil formation, photosynthesis, primary production, nutrient cycling, and water cycling.
Ecosystem services are underpinned by, and utterly dependent
146
upon, biodiversity (Sandifer et al., 2015). Attention to the benefits people obtain from ecosystems can directly inform decision making: for example, by communicating the implications of planning, implementation, and assessment efforts for integrated land and water management (UNU-IHDP, 2014).
Ecological integrity is maintained when the structure, composition, and function of an ecosystem operate within natural or historic bounds—when human activity has not unduly stressed the ecosystem or undermined long-standing ecological processes. Ecological integrity is not just a feature of a sustainable ecosystem; it also indicates that the ecosystem can continue to provide human benefits, as depicted in Figure 2.8.
Figure 2.8 Ecosystems as Settings for Human Health and Well- Being
A broad conceptual model showing the relationship between ecological integrity, ecosystem services, and the benefits that humans derive. The biodiversity of ecosystems, the structure of ecosystems, and the processes used and functions performed within ecosystems, all supply the foundational conditions under which ecosystem services are provided. Humans then derive and demand these ecosystem services for their well-being. Feedback loops show that there are consequences of humans deriving these services.
147
Systems Thinking: From Ecology to Human Health Systems thinking is a core feature of ecology. A systems thinker sees the world as a web of interrelated, interacting components, and not simply as an assembly of linear relationships. Systems have several features. They are composed of parts that are related to each other, in relationships that are often nonlinear and bidirectional. Systems have temporal and spatial boundaries, and can interact with the larger environment by receiving inputs and by generating outputs. Boundaries are the places where values are exposed and disagreements are highlighted. In complex systems, boundary setting is explicitly a social construct, an acknowledgment that a system is not “real.”
Systems can be nested within larger systems, they can contain smaller subsystems (recall the issues of scale and hierarchy introduced in relation to Table 2.1), and they can overlap with other systems. Systems can be characterized by flows of energy, material, and information. They are dynamic, meaning that they undergo constant change, and while they often tend toward an equilibrium, they can change according to predictable patterns or in random, chaotic ways. Feedback loops, repeating chains or circuits of cause and effect, are a common and important feature of systems. These loops may be either positive (self-reinforcing) or negative (self-cancelling). Systems can be self-organizing, using numerous interactions or feedback loops among their components to establish a pattern or arrive at a state. They can also be adaptive in response to altered circumstances, leading to new equilibrium states. Sometimes change can be abrupt, if the system passes a tipping point, or a system threshold. The simplest demonstration of this phenomenon might be a chemical titration. The Resilience Alliance describes a tipping point in social-ecological systems as a sequence of events in which eventually, through successional processes, all the resources become conserved and committed, competition for them is intense, and the system becomes tightly bound. At this tipping point, a critical event could trigger a release of the resources and allow reorganization and recolonization to occur (see Walker & Salt, 2006). At other times, systems can
148
demonstrate resilience, defined as “the capacity…to absorb disturbance; to undergo change and still retain essentially the same function, structure, and feedbacks” (Walker & Salt, 2006, p. 32). Resilience is characterized by persistence, adaptiveness, variability, and unpredictability (evolutionary, developmental, and sustainable). Figure 2.6 shows a schematic comparison of systems thinking with linear thinking.
Figure 2.6 Linear Thinking Versus Systems Thinking The model on the left consists of simple, unidirectional relationships, while the model on the right demonstrates more complexity, with system boundaries, reciprocal relationships, and feedbacks.
There are countless examples of systems. Many of these come from the world of ecology—a colony of ants, a hurricane forming in the Caribbean and moving over North America, a patch of forest or desert, the microbiome in our intestines. Systems thinking is indispensable not only in ecology but in many other arenas, from engineering to information technology, from epigenetics to neuroscience, from politics to social structure. Not surprisingly, systems thinking is key in environmental health, because it helps us to understand the links between natural systems and human systems, and it underscores that all actions and decisions have consequences in a complex system.
Application of systems thinking to humans' interactions with their environment is demonstrated by increasing attention to such concepts as social-ecological systems (Berkes, Colding, & Folke, 2003; Walker & Salt, 2006) and coupled human-natural systems (Liu et al., 2007). The concept of coupled human-natural systems offers an integrated approach to systems that does not seek to separate human or social systems from their environmental settings. (Some people prefer the term coupled human-
149
environment system, because the word natural implies that humans are not part of natural systems and this implication undermines the point of integrated systemic thinking.) The social- ecological systems approach to systems thinking and analysis is explicit in its coupled human-environment view and does not seek to separate humans from ecological analysis. Social-ecological systems acknowledge the consequences of social actors and institutions, the biotic and abiotic responses of the ecosystem to human actions, whereby both social and ecological characteristics influence the trajectory of the system (in the way they co-evolve) and the degree of system resilience.
An integrated understanding of both social and ecological dynamics helps elucidate people's interactions with such diverse settings as watersheds, fisheries, forests, and even urban areas. This is exemplified by the interactions depicted in Figure 2.7, which shows a systems map of land use in the United Kingdom. While land use may seem a simple issue, the systems map depicts just how many factors may influence, and be influenced by, the use of land and water for residential, agricultural, or commercial purposes as well as for non-use or indirect ecosystem services. The systems map also depicts well-being as being influenced by a range of these interactions, reflecting diverse relationships among biophysical and social processes, and the emergent characteristics of complex systems.
150
Figure 2.7 A Systems Map of U.K. Land Use and the Domains That Influence It
Source: Foresight Land Use Futures Project, 2010.
Complexity is a feature of almost every system relevant to human health. What is complexity? Consider the differences between the simple and often replicable task of following a recipe, the complicated and highly technical task of sending a rocket ship to the moon, and the complex task of raising a child in a society, which is highly variable and not replicable and for which past experience of success does not necessarily translate to the next situation (Glouberman & Zimmerman, 2002).
Complex systems are made up of a large number of heterogeneous elements, some simple and others complex and even chaotic. The elements of a complex system interact with each other through positive and negative feedbacks. These interactions can result in unpredictable and unexpected phenomena, a property known as emergence (Meadows, 2008)—the idea introduced earlier, that the whole becomes more than the sum of its parts. Emergence arises from the ways in which the parts of a system influence one another, expressing consequences and leading to
151
outcomes that would not have occurred if the components had not been interacting. The effects of interactions persist over time and adapt to changing circumstances (Hammond, 2009; Meadows, 2008). Small changes in initial conditions can have large and unpredictable effects (Pearce & Merletti, 2006). Not surprisingly, emergent properties can result in surprises. A surprise in an ecological system would be an unexpected discrete event (e.g., a town records its highest daily rainfall); abrupt, nonlinear, discontinuous behavior (e.g., a sharp change is noted—from 1985 onward a town has received half the annual rainfall it received prior to that year); or genuine novelty (e.g., for the first time anywhere, silver nitrate was sprayed into the atmosphere to trigger a massive rainfall event). Surprises can prove challenging when trying to manage complex systems to further societal objectives such as sustainability. These ideas are developed further in Chapter 3.
Many of the fundamentals of ecology can be understood in systems terms. Table 2.3 shows the well-known laws of ecology proposed by ecologist Barry Commoner in 1971, and corresponding system attributes for each. Application of these “laws” and attributes reinforces recognition of social-ecological systems as complex adaptive systems, for which “understanding how their component parts function doesn't mean you can predict their overall behavior” (Walker & Salt, 2006, p. 38).
Table 2.3 Links Between Ecology and Systems Thinking as a Basis for Health
Barry Commoner's laws of ecology
Corresponding systems attributes
Everything is connected to everything else.
Interconnectedness and complexity. Emergence and emergent properties.
There is no such thing as a free lunch.
Interrelationships and reciprocity.
Nature knows best. Integration. Knowing comes from the whole as much as the parts. Feedbacks and self-organization.
Everything must go somewhere.
Nestedness: nothing exists outside its ecology.
152
Interdependence, cycling, nonlinearity, and uncertainty. Rethinking of waste as a part of ecological processes.
Source: Adapted from Commoner, 1971; Parkes and Horwitz, 2009.
153
Features of Our Home: Ecological Characteristics as Foundational for Health Ecosystems are settings for human health (Figure 2.8). An understanding of ecology and some of its component perspectives— on populations, communities, and ecosystems—together with a systems perspective enables us to consider the role of ecological dynamics in maintaining the integrity of our home. In addition, ecological principles help us to identify pathways by which the ecosystems on which we depend set the context for health.
The interrelationships depicted in Figures 2.7 and 2.8 remind us that ecosystems, as settings for human health and well-being, are best understood as a combination of ecological and social interactions. These include economic, cultural, political, and institutional components. This holistic systems orientation leads to perspectives on interconnectedness and reciprocity that have a long history among Indigenous knowledge systems around the planet, and have become increasingly central to such fields as restoration ecology (Text Box 2.5), human ecology, and sustainability science (Chapter 3).
154
Text Box 2.5 Restoration Ecology: The Practical Application of Ecological Literacy and Systems Thinking The field of restoration ecology is founded on the recognition that ecosystems can be seriously degraded or damaged, as signaled by diminished richness of species (local extinctions of populations) and reduced ecosystem functions, depriving recipients of the ecosystem services that were once available. This degradation might result from overexploitation, serious pollution events, or deconstructive land-use activities such as mining, forest removal, or land clearing for agriculture; or it might be a consequence of a serious disturbance like an intense fire or flood. The practice of restoration ecology builds on knowledge of the species assemblages that are local and endemic in order to reintroduce them, based on knowledge of the physical characteristics of the site. It must also seek to reverse or eliminate the disturbances that led to the ecosystem degradation in the first place, a task that is sometimes both ecologically and politically challenging. In restoration work considerable attention is devoted to invasive species and how to strategically control their proliferation. In theory, restoration ecology recognizes that ecosystems are nonequilibrial and that alternative stable states (alternative end points depending on an ecosystem's trajectory) are possible. Restoration goals must therefore be set, and the effort may be deemed to have failed unless the desired ecological functions and ecosystem services, including local biodiversity characteristics, have been recovered. Since ecosystems are dynamic, an adaptive approach is mandatory, including monitoring to determine the trajectory of the efforts and ensuring the resources to undertake interventions where necessary. Restoration ecology is therefore an intentional, political process and an explicitly social- ecological endeavor (see Discussion Question 6).
155
An ecological orientation emphasizes the environment as a dynamic, living system and as a context for health. Accordingly, the concept of environmental health expands its focus beyond the environment as a source of hazardous exposures (e.g., through soil, water, and air) to the environment as human habitat, nested within the landscapes, ecosystems, and social-ecological systems on which human survival, livelihood, and well-being depend. This requires an inclusive and interactive view of the environment, with features of the physical environment (such as water quality in a river) seen as embedded within larger features (such as the land, surface water, and groundwater interactions of watersheds). Indeed, an ecological perspective makes clear that all features of ecosystems reflect interactions among multiple living and nonliving components.
Ecological relationships commonly demonstrate reciprocity, a principle that extends to the human relationship with the environment. Because of its importance for health and well-being, the Ottawa Charter for Health Promotion (World Health Organization [WHO], 1986) identified reciprocal maintenance as a fundamental component of creating supportive environments for health:
The inextricable links between people and their environment constitutes the basis for a socioecological approach to health. The overall guiding principle for the world, nations, regions and communities alike, is the need to encourage reciprocal maintenance—to take care of each other, our communities and our natural environment. The conservation of natural resources throughout the world should be emphasized as a global responsibility [WHO, 1986].
The integrative, socioecological approach of the Ottawa Charter may not have been fully realized over recent decades, but it recalls long- held Indigenous approaches to health and well-being (Stephens, Parkes, & Chang, 2007), and it offers a compelling and practical approach to promoting human health (Hancock, 2011) (also see Discussion Question 5). An example from the ecology of infectious disease, leptospirosis, is presented in Text Box 2.6, with an emphasis on the interaction of ecological and social processes that influence health in an ecosystem setting.
156
Text Box 2.6 Infectious Disease as an Ecological and Social Process: The Example of Leptospirosis The disease ecology of leptospirosis demonstrates many of the concepts and approaches outlined in this chapter. Bacteria responsible for the disease (Leptospira) are very common in mammal hosts such as rats and other rodents, maintaining their numbers by multiplying in the host's kidneys, which provide the conditions for “breeding” of the bacteria (although we don't usually use this term in relation to bacteria). These maintenance or reservoir hosts are not necessarily, or are only mildly, debilitated by the “infection” because the host and the bacteria have evolved a type of commensalism (see Table 2.2). The bacteria are shed in the urine of the individual hosts, passing to the environment, where they encounter and infect new individual hosts, maintaining their populations in a population of mammals in the environment. This is a positive feedback cycle of infection: growth in the host, passage to the environment, infection in a new host, and so forth.
Humans—and some other mammals, such as cattle and goats —become accidental hosts when they come in contact with bacteria-containing animal urine in the environment and are infected; several types of these bacteria (serovars) are pathogenic to humans, so here the relationship is more like parasitism, in which the parasite benefits and the host is harmed. In humans the infections can produce a wide range of clinical syndromes, including nonspecific fever, kidney and liver failure, and pulmonary hemorrhage. Infection of accidental hosts is obviously undesirable, lowering the host's reproductive fitness and possibly causing death. Some medical or veterinary attention is required in the form of antibiotics. This might control the infection in an individual, but addressing the disease more definitively requires attention to the environmental conditions in which the infection occurs. (See Figure 2.9.)
157
Figure 2.9 The Life Cycle and Transmission of Leptospira Bacteria
An infected reservoir host such as a rat releases the bacteria to the environment through its urine. If the urine contaminates water or soil, livestock or domestic animals may ingest it and become secondary Leptospira hosts. People may be exposed by ingesting contaminated water or by bringing contaminated soil or water into contact with broken skin or their eyes. Leptospirosis may affect different organs and cause a range of symptoms.
Indeed there is a complex interaction between humans, animal reservoirs, Leptospira, and the environment in which they coexist. There are distinct epidemiological patterns of leptospirosis, depending on the ecosystem setting and closely associated with the hydrological cycle, where animal urine is passed directly into or runs off into surface waters. In rural areas transmission is usually associated with farming and livestock; risk of exposure rises during the warm and rainy months. In urban areas infection is associated with overcrowding, poor hygiene, inadequate sanitation, and poverty, all of which typically occur in urban slums in developing countries. In developed countries infection is now increasingly being associated with outdoor recreational exposure and international travel. A common explanation for outbreaks of leptospirosis is the ecological disturbance of land-use change. Deforestation in rural areas and impermeable surfaces (rooftops and roadways) in urban areas cause faster rainfall runoff into places where rodents may live, driving them toward greater human contact and
158
resulting in infection. Upstream interventions include minimizing exposure during periods of risk, controlling rodent populations, restoring the ecological functions in watersheds, and addressing the social-economic circumstances that contribute to the changed hydrological conditions. Each of these interventions, antibiotics included, seeks to initiate negative feedback in the system.
The example of leptospirosis illustrates that ecosystems and social systems interact, and that humans are part of the ecological community—one of an assemblage of species interacting within their environment. In addition to the host-agent-environment model of understanding infectious disease processes, the ecological concepts exemplified by leptospirosis demonstrate the importance of complex interactions, including positive and negative feedbacks loops, as core characteristics of relations between environment and health (Wilcox, Aguirre, & Horwitz, 2012).
This ecological perspective is relevant not only to infectious diseases. The interacting spheres depicted in Figure 2.5 can, for example, provide extremely helpful guidance in understanding the source, fate, distribution, and impact of many environmental contaminants, noting especially the interactions between abiotic contaminants and biotic living systems. For more on the concept of ecotoxicology, see Chapter 3.
159
Toward Ecological Approaches to Health and Home Public health and environmental health have not always succeeded in incorporating the ecologically-oriented and systems-based perspective outlined in this chapter. This limits and constraints that include a preoccupation with proximate risk factors, a focus on individual-level versus ecosystem-level influences on health, a time- window (rather than life-course) view of how risks operate, and the unfamiliar challenge of scenario-based forecasting of health consequences of future, large-scale social and environmental changes (McMichael, 1999). Complexity can be overwhelming, so clear conceptual pathways from ecosystems to health are useful.
A well-established example is provided by the Millennium Ecosystem Assessment (MA). The MA not only defined and classified ecosystem services (Text Box 2.4); it also identified how these services underpin well-being by providing a foundation for health, basic material for a good life, good social relations, security, and freedom of choice and action (MA, 2003, 2005a). These relationships are depicted within local, regional, and global contexts in the conceptual framework of the Millennium Ecosystem Assessment (Figure 2.10). This framework can be used to explore and demonstrate many of the ecological characteristics introduced in this chapter. The framework also encourages recognition that changes to ecosystems influence health through pathways that are direct (e.g., floods and heat waves), ecosystem-mediated (e.g., altered infectious disease risks, reduced food yields), and also indirect, deferred and displaced (e.g., population displacement, livelihood loss) (MA, 2005a). All of these pathways may also be influenced by the other components of well-being depicted in Figure 2.10, and are affected by drivers of change operating over short- and long-term time frames.
160
Figure 2.10 The MA Conceptual Framework Source: MA, 2005b, Figure SDM1.
Changes in drivers that indirectly affect ecosystems, such as population, technology, and lifestyle (upper right corner) can lead to changes in drivers that directly affect ecosystems, such as fisheries' catches or fertilizer applications to increase food production (lower right corner). The resulting changes in the ecosystem (lower left corner) cause ecosystem services to change and thereby affect human well-being. These interactions can take place at more than one scale and can cross scales. For example, a global timber market may lead to regional loss of forest cover, increasing flood magnitude along a local stretch of river. Similarly, interactions can take place across different time scales. Actions to respond to negative changes or to enhance positive changes can be taken at almost all points in this framework (crossbars).
The MA is just one example of applying ecological concepts to health and well-being. A range of related approaches encourage a systemic understanding of environmental impacts and health using
161
ecological principles. The field of ecohealth adopts systems approaches to promote the health of people, animals, and ecosystems in the context of social and ecological interactions (Parkes, Horwitz, & Waltner-Toews, 2014). Related frameworks include ecosystem approaches to health (Charron, 2012; Webb et al., 2010), ecological public health (Rayner & Lang, 2012), and human-animal-ecosystem approaches including conservation medicine and One Health (Wilcox et al., 2012; Zinsstag, Schelling, Waltner-Toews, & Tanner, 2011). By recognizing ecosystems as foundational for health and well-being, each of these approaches offer new insights for the field of environmental health, and present new opportunities to both understand and respond to contemporary health challenges.
162
Summary An ecologically oriented approach to public health views humans as nested within ecosystems, calls for integrative consideration of environmental and social factors, and highlights system characteristics such as complexity, emergence, and feedback loops. Recognizing ecology and ecosystems as foundational for health enhances our understanding of the determinants of health, and also our capacity to respond to evolving health challenges now and into the future. This chapter presents ecological literacy as an essential prerequisite for environmental health, creating an increased awareness of ecosystems as settings for health, in contexts ranging from cities to agricultural lands, from parks to wetlands to oceans, and on land, in water, or in air. Ecological approaches affirm the realization that the environment is our home.
163
Key Terms abiotic
Physical or chemical; used of the properties of an ecosystem (cf. biotic).
abundance Number of individuals in a species population.
assemblage of species The characteristic collection of species that make up an ecological community.
autotroph Autotrophs (literally, “self-feeders”) use inorganic molecules and an external energy source to manufacture their own organic molecules (biomass).
bioaccumulation A process in which an organism takes up a chemical pollutant, such as DDT or mercury, and retains it in its tissues during its lifetime rather than expelling the pollutant as waste.
biodiversity Degree of variation of life in all its forms (also known as biological diversity).
biological invasion Large-scale movement of animals or plants into areas where they were previously absent or uncommon.
biomagnification (bioamplification) A process in which a chemical pollutant occurring in an organism's tissues is retained and, when the organism is consumed by a predator, becomes more concentrated in the predator's tissues. This process continues at every level of consumption; so by the time the top predator consumes its prey, the pollutant is substantially more concentrated (and potentially more toxic).
biotic Living; used of the biological features of an ecosystem (cf. abiotic).
boundaries
164
System boundaries differentiate between what is “in” and what is “out”: what is deemed relevant and what is irrelevant, important and unimportant, worthwhile and not worthwhile, and who benefits and who is disadvantaged.
carrying capacity The maximum population that can be sustained indefinitely by its supporting ecosystems.
climax community The assemblage of species that occurs once the effects of a disturbance have diminished, when colonizing and early successional species have been replaced by K-selected species able to persist in more stable conditions.
commensalism A symbiotic relationship in which one species derives a benefit from another without affecting the fitness or survival of the other species.
community ecology The branch of ecology that considers assemblages of species and particularly the interactions among them.
competition A relationship in which two or more species must share scarce or limited resources.
complex system A system made up of a large number of heterogeneous elements, some simple and others complex and even chaotic. These elements interact with each other through positive and negative feedbacks.
conservation biology The study of the biological characteristics of species that are important for their conservation.
consumers Organisms, almost always animals, that eat other organisms; primary consumers are herbivores that eat producers (like plants) or detritivores; secondary consumers are predators or carnivores that eat primary consumers.
coupled human-natural systems An integrated approach to systems that does not seek to separate human or social systems from their environmental settings.
165
cycle A cycle (hydrological, carbon, nitrogen, phosphorus) is a sequence of events that repeats itself.
decomposer (detritivore) An organism that derives its energy from consuming the dead or dying matter or products from other life.
demography The study of the characteristics and structure of populations.
distribution The geographic occurrence (in range and extent) of a species.
disturbance Temporary physical, chemical, or biological disruptions to an ecosystem. Disturbances dictate the character of the ecosystem, and in this sense, under some circumstances, ecosystems need disturbances.
dynamic A term applied to systems to convey the idea that they undergo constant change: constancy comes from the fixed rules that operate in a system and give it a recognizable state; change comes from feedback loops, self-organization, and emergence, with novelty generated by the system.
ecological community See assemblage of species.
ecological integrity The condition or quality of the whole of a successful ecosystem. This integrity has four attributes: (1) system “health” (continued successful functioning), (2) capacity to withstand stress, (3) undiminished optimum capacity for ongoing developmental options, and (4) continued capacity for change and development, unconstrained by human interruptions.
ecological literacy A learned ability to read, interpret, and understand the environment.
ecological processes The “how” of ecosystem functions; the cycling of water, nutrients, and energy.
ecology
166
A scientific discipline that focuses on interactions of living things in relation to their environment.
ecosystem A complex system of organisms and their environment, and the interactions that connect them.
ecosystem functions What ecosystems are doing (embracing ecological processes).
ecosystem services “The benefits people obtain from ecosystems” (MA, 2003, p. 49). This construct allows ecosystems, which provide the basis for life on Earth, to be more clearly and overtly included in economics and decision making.
emergent Not existing in isolation in individual parts of the system but arising when components interact. Emergent properties characterize complex systems and uncertainty (see surprise).
equilibrium A self-regulated stable state in which negative feedback will operate to bring a changing parameter back to its original condition so the ecosystem maintains its state. Contemporary ecological thinking considers ecosystems to be nonequilibrial, so that multiple states are possible rather than one stable state.
exponential growth Geometric growth, with the rate of growth proportional to population size rather than linear or occurring at a fixed rate.
extinction Extinction occurs when there are no living individuals of a species.
feedback loop A repeating chain or circuit of cause and effect in which the events and parameters are of the system itself.
flow Transfer of material or energy or information in an ecosystem.
food web The pattern of relationships among ecosystem species as defined by who eats whom, who is feeding on what, and who is making their own food, usually arranged in trophic levels of producers,
167
consumers, and decomposers. habitat
The physical space occupied by a species, characterized by physical (rocks, soils, landforms, water depth, etc.), chemical (air and water quality), and biological (vegetation, animals, microbes, etc.) features.
herbivores Plant eaters.
heterotroph An organism that cannot make its own energy and must rely on organic molecules made by other organisms.
hierarchy Something structured according to levels or scales.
holism An all-encompassing approach of focusing on or investigating wholes rather than parts.
human ecology The study of the reciprocal relationship between humans and their environments. Such study is necessarily interdisciplinary, drawing on social, natural, cultural, political, and technical disciplines and dimensions.
introduced species (alien or exotic species) A species that moves to a place where it has never occurred before, becoming an established and successful colonist.
K-selected species Species, typically found in stable environments, in which individuals grow to be larger, take longer to reach maturity, live longer, produce fewer progeny (“expensive offspring”), and invest considerably more parental energy than r-selected species individuals do.
Millennium Ecosystem Assessment The MA “assessed the consequences of ecosystem change for human well-being. From 2001 to 2005, the MA involved the work of more than 1,360 experts worldwide. Their findings provided a state-of-the-art scientific appraisal of the condition and trends in the world's ecosystems and the services they provide, as well as the scientific basis for action to conserve and use them sustainably” (www.millenniumassessment.org).
168
mutualism A form of symbiosis in which both species derive a benefit from each other.
nested How complex systems are organized; they are composed of systems, and they themselves are found wholly within systems.
niche The multidimensional ecosystem space where a species exists and also what it does. Arguably, no two species can have the same niche. This concept is paralleled in economics where a product is said to have a “niche” in the market.
parasitism A relationship in which an individual of one species derives a benefit directly from an individual of another species, and in the process negatively affects the fitness and possibly even the survival of the (infected) individual.
patterns Observable regularities repeated in space and or time.
population decline Reduction in population size. occurring when the death rate (plus emigration) exceeds the reproduction rate (plus immigration).
population ecology The study of populations of species, including their biology, demography, habitat, and specific interactions.
population growth Increase in population size, occurring when the reproduction rate (plus immigration) exceeds the death rate (plus emigration).
predator An animal that eats another animal (prey). Such predation is one way in which population numbers are regulated: when prey are abundant, predators can increase and vice versa. Constant rates of predation can suppress population growth among prey.
primary producer See autotroph; primary producers are almost always photosynthesizing organisms.
reciprocity (reciprocal maintenance)
169
A state of mutual dependence or action or influence. Reciprocal maintenance—taking care of each other, our communities, and our natural environment so they will take care of us—is a guiding principle of the Ottawa Charter.
regulation of population growth Constraint of population growth by resource availability, disease, predation, or some other factor that prevents a population from breeding to its maximum capacity.
resilience The “capacity [of an ecosystem]…to absorb disturbance; to undergo change and still retain essentially the same function, structure, and feedbacks” (Walker & Salt, 2006).
restoration ecology A field of practice that builds on knowledge of the species assemblages that are local and endemic in order to reintroduce them, based on knowledge of the physical characteristics of the site.
richness A measure of population numbers and of biodiversity, usually dependent on the size of the area sampled and the number of samples taken.
r-selected species Species such as weeds that are opportunists, capitalizing on spare resources (such as extra light, space, or nutrients) to grow rapidly, mature quickly, and produce many progeny (“cheap offspring”) (cf. K-selected species).
scale A spatial, temporal, quantitative, or analytical dimension (e.g., small to large or short-term to long-term) used to measure and study a phenomenon.
self-organizing Able to establish a pattern or arrive at a state. In a system this ability is a product of numerous interactions among system components, often taking the form of feedback loops (positive or negative) that are entirely internal to the system.
social-ecological systems An approach to systems thinking and analysis that does not separate humans from ecological analysis, whereby both social
170
and ecological dynamics influence the trajectory of the system, and its degree of resilience.
species A group of living organisms consisting of similar individuals capable of exchanging genes or interbreeding.
succession Following a disturbance, the gradual, orderly, and progressive replacement of one ecosystem community by another until a stable climax community is established.
surprise Any of three properties of an ecological system: (1) an unexpected discrete event; (2) abrupt, nonlinear, discontinuous behavior; or (3) genuine novelty. Ecologist Lance Gunderson (2003) considers a crisis to be the consequence of surprises that leads to an unambiguous policy failure.
symbiosis A term meaning “living together” that describes certain relationships between species; these relationships are often intimate and highly evolved.
systems thinking An approach that assumes the issue under investigation is occurring in a complex and uncertain system, and cannot be seen in isolation from its context (cf. holism).
tipping point A system threshold, the “straw that broke the camel's back.” Systems are “buffered” and can often absorb change and retain the same state. At some point, however, even a slight change is too much, and the system responds.
trophic levels The levels that make up a food web. Classically, in terrestrial ecosystems, they form a pyramid of layers, with producers at the bottom, primary consumers in the next layer, secondary consumers next, and an apex predator at the top.
171
Discussion Questions 1. Recognition of the links between biodiversity and health is said
to be increasing (Bernstein, 2014; MA, 2005a; Sandifer et al., 2015). What do you think has changed in our understanding of both health and biodiversity to create this new interest? Can you provide an example of a biodiversity and health connection that is relevant to your own life? Can you think of another example that might become more relevant two generations from now?
2. Figure 2.1 presents a food web in a North American ecosystem. What features of this figure make it possible to identify the geographic location this food web.? How might you depict a food web from a different part of the world or a different biome (e.g., sub-Saharan Africa or Australia or the Pacific Ocean)? Consider the implications of swapping a species in Figure 2.1 with a species from another part of the world. How would the idea of biological invasion (Text Box 2.2) influence this?
3. The hydrological cycle is shown in Figure 16.1 (Chapter 16). Draw the hydrological cycle for the region of the planet in which you live, including in your diagram evaporation, evapotranspiration, cloud formation, rain/precipitation, infiltration, soil moisture, runoff, surface water flow (rivers), other surface water bodies on land (like lakes and swamps), aquifers, and then oceans and seas, glaciers, and ice caps (whichever are relevant to your region).
Now draw the cycle again but at the global scale. Consider the ways the hydrological cycle may be different in the different regions of the planet.
How different are these cycles? How similar are they? What are the points of connection between them? How is your understanding of the regional scale enhanced by understanding the global scale, and vice versa? What could you gain and lose by trying to understand the hydrological cycle at the scale of your neighborhood or the area where you spend most of your time?
4. Scales are important in ecology, and in environmental health. This can be illustrated by a “zoom in, zoom out” mental exercise.
172
Think of your current home, and identify a small living thing there. Maybe a potted-plant? Maybe your cat? If you are not able to identify something else alive inside your home, use yourself as an example of a living creature.
Now start to zoom out. Look down on this living thing with a view of the room it is in, and the house or building in which the room is situated. Do you notice more living (biotic) parts or more nonliving (abiotic) parts of the environment interacting with your living thing? Do you see any evidence of the living and nonliving things interacting? How do social dynamics influence this?
Continue to zoom out farther to the street block and the neighborhood? Do you see more life yet? What other species do you see that make up this ecological community? What species do you not see? What things move and interact the most? Do you see cars, buses, and trucks? What are they carrying? Where are these things coming from and going to? Consider the kinds of energy being used and the ecological and social influences on these energy flows. Consider the same questions for water: where is it flowing from and flowing to? What are the ecological influences on how your living thing can access this water?
Zoom out farther, more quickly now. Zoom out to the borders of the region in which you are currently located. Does what you are seeing look more or less alive? Do you visualize this view as a roadmap or as a satellite image? Which of these two views looks more alive? Why? Would you prefer to describe what you see as an environment or an ecosystem? Can you see evidence of ecological cycles from this vantage point?
Stop! Once you have a large-scale (regional or even statewide) view in your mind's eye, consider three questions:
How would this view have looked different 5 years ago? 50 years ago? 1,000 years ago?
Identify two positive and three negative influences on health for each of these time frames at this scale.
Give three examples of where you can see (imagine?) the
173
atmosphere (air), geosphere (rock, land), and hydrosphere (water) interacting to support life within the view you see.
Web sites that can help you experience these features of zooming in and out through social and ecological contexts include scaleofuniverse.com and www.ecologicalfootprint.com
5. The social ecological model (Figure 2.11) (also see Bronfenbrenner, 1977) is commonly invoked in public health to clarify the hierarchical role of social determinants of health, and the way health is grounded in the settings in which people live, work, learn, and play (WHO, 1986). While Figure 2.11 and ones like it are common depictions, they place little emphasis on ecosystems. Do you think this is an important omission? How would you redraw this figure to show the role of ecosystems? Could you adapt the figure to better reflect the “socioecological approach” proposed by the Ottawa Charter (WHO, 1986), which encourages reciprocal maintenance—taking care of each other, our communities, and our natural environment? More recently, “social-ecological systems” have been described as another way to understand the links between humans and their environment, with an emphasis on the concept of resilience (Berkes et al., 2003). How does the idea of resilience influence how you view the social ecological model in Figure 2.11?
174
Figure 2.11 The Social Ecological Model Source: Bronfenbrenner, 1977.
6. Text Box 2.5 describes restoration ecology. Please give an example of a restoration ecology effort. In what ways does such an effort need to take account of similarities to, and differences from, the classical ecological succession model? Why is it important for restoration ecology to address the social and environmental determinants of health?
175
References Berkes, F., Colding, J., & Folke, C. (2003). Navigating social- ecological systems: Building resilience for complexity and change. New York: Cambridge University Press.
Bernstein, A. S. (2014). Biological diversity and public health. Annual Review of Public Health, 35(1), 153–167.
Bronfenbrenner, U. (1977). Toward an experimental ecology of human development. American Psychologist, 32(7), 513–531.
Charron, D. F. (Ed.). (2012). Ecohealth research in practice: Innovative applications of an ecosystem approach to health. New York: Springer.
Commoner, B. (1971). The closing circle: Confronting the environmental crisis. London: Cape.
Glouberman, S., & Zimmerman, B. (2002). Complicated and complex systems: What would successful reform of Medicare look like? (Discussion Paper No. 8). Commission on the Future of Healthcare in Canada.
Gunderson, L. (2003). Adaptive dancing: Interactions between social resilience and ecological crises. In F. Berkes, J. Colding, & C. Folke (Eds.), Navigating social-ecological systems: Building resilience for complexity and change (pp. 33–52). New York: Cambridge University Press.
Hammond, R. A. (2009). Complex systems modeling for obesity research. Preventing Chronic Disease, 6(3), A97.
Hancock, T. (2011). It's the environment, stupid! Declining ecosystem health is THE threat to health in the 21st century. Health Promotion International, 26(Suppl. 2), ii168–172.
Kolbert, E. (2014). The sixth extinction: An unnatural history. New York: Holt.
Liu, J., Dietz, T., Carpenter, S. R., Alberti, M., Folke, C., Moran, E., …Taylor, W. W. (2007). Complexity of coupled human and natural
176
systems. Science, 317(5844), 1513–1516.
McMichael, A. J. (1999). Prisoners of the proximate: Loosening the constraints on epidemiology in an age of change. American Journal of Epidemiology, 149(10), 887–897.
Meadows, D. H. (2008). Thinking in systems: A primer. White River Junction, VT: Chelsea Green.
Millennium Ecosystem Assessment. (2003). Ecosystems and human well-being: A framework for assessment. Washington, DC: Island Press. Summary available online at http://www.millenniumassessment.org
Millennium Ecosystem Assessment. (2005a). Ecosystems and human well-being: Health synthesis. Geneva: World Health Organization. Retrieved from http://www.millenniumassessment.org/en/index.aspx
Millennium Ecosystem Assessment. (2005b). Living beyond our means: Natural assets and human well-being. Statement from the board. Washington, DC: World Resources Institute. Full report available at http://www.millenniumassessment.org
Montgomery, D. Dirt: The erosion of civilizations. Berkeley: University of California Press, 2007.
Parkes, M. W., & Horwitz, P. (2009). Water, ecology and health: Ecosystems as settings for promoting health and sustainability. Health Promotion International, 24, 94–102.
Parkes, M. W., Horwitz, P., & Waltner-Toews, D. (2014). Ecohealth. In A. C. Michalos (Ed.), Encyclopedia of quality of life and well- being research (pp. 1770–1775). Heidelberg: Springer-Verlag.
Parkes, M. W., & Weinstein, P. (2004). An ecosystems approach to environmental health. In N. Cromar, S. Cameron, & H. Fallowfield (Eds.), Environmental health in Australia and New Zealand (pp. 45–65). Melbourne: Oxford University Press.
Pearce, N., & Merletti, F. (2006). Complexity, simplicity, and epidemiology. International Journal of Epidemiology, 35(3), 515– 519.
177
Rayner, G., & Lang, T. (2012). Ecological public health: Reshaping the conditions for good health. London: Routledge.
Sandifer, P. A., Sutton-Grier, A. E., & Ward, B. P. (2015). Exploring connections among nature, biodiversity, ecosystem services, and human health and well-being: Opportunities to enhance health and biodiversity conservation. Ecosystem Services, 12, 1–15. doi:10.1016/j.ecoser.2014.12.007
Stephens, C., Parkes, M., & Chang, H. (2007). Indigenous perspectives on ecosystem sustainability and health. EcoHealth, 4, 369–370.
UNU-IHDP. (2014). Land, water, and people: From cascading effects to integrated flood and drought responses. Summary for decision-makers. Bonn: UNU-IHDP.
Walker, B., & Salt, D. (2006). Resilience thinking: Sustaining ecosystems and people in a changing world. Washington, DC: Island Press.
Webb, J., Mergler, D., Parkes, M. W., Saint-Charles, J., Spiegel, J., Waltner-Toews, D.,…Woollard, R. F., (2010). Tools for thoughtful action: The role of ecosystem approaches to health in enhancing public health. Canadian Journal of Public Health, 101, 439–441.
Wilcox, B. A., Aguirre, A. A., & Horwitz, P. (2012). Connecting ecology, health, and sustainability. In A. A. Aguirre, R. S. Ostfeld, & P. Daszak (Eds.), New directions in conservation medicine: Applied cases of ecological health (pp. 17–32). New York: Oxford University Press.
World Health Organization. (1986). Ottawa Charter for Health Promotion. First International Conference on Health Promotion, Ottawa, Canada, 17–21 November 1986. Retrieved from http://www.who.int/healthpromotion/conferences/previous/ottawa/en
Zinsstag, J., Schelling, E., Waltner-Toews, D., & Tanner, M. (2011). From “one medicine” to “one health” and systemic approaches to health and well-being. Preventive Veterinary Medicine, 101, 148– 156.
178
For Further Information Books Aguirre, A. A., Ostfeld, R. S., & Daszak, P. (Eds.). (2002) New directions in conservation medicine: Applied cases of ecological health. New York: Oxford University Press.
Aron, Joan L., & Patz, J. A. (2001). Ecosystem change and public health: A global perspective. Baltimore: Johns Hopkins University Press.
Collinge, S. K., & Ray, C. (Eds.). (2006). Disease ecology: Community structure and pathogen dynamics. New York: Oxford University Press.
Daily, G. C. (Ed.). (1997). Nature's services: Societal dependence on natural systems. Washington, DC: Island Press.
Hallström, L. K., Guehlstorf, N. P., & Parkes, M. W. (2015). Ecosystems, society, and health: Pathways through diversity, convergence, and integration. Montreal: McGill Queens University Press.
Hancock, T., Spady, D. W., & Soskolne, C. L. (Eds.). (2015). Global change and public health: Addressing the ecological determinants of health: The report in brief. Available at http://www.cpha.ca/uploads/policy/edh-brief.pdf
Horwitz, P., Finlayson, C. M., & Weinstein, P. (2012). Healthy wetlands, healthy people: A review of wetlands and human health interactions (Ramsar Technical Report No. 6). Gland and Geneva: Ramsar and WHO. Available at http://www.ramsar.org/sites/default/files/documents/pdf/lib/rtr6- health.pdf
Mayer, K. H., & Pizer, H. F. (Eds.). (2008). The social ecology of infectious diseases. Burlington, MA: Academic Press.
Millennium Ecosystem Assessment. (2005). Ecosystems and human well-being: Biodiversity synthesis. Washington, DC: World
179
Resources Institute. Full report available at http://www.millenniumassessment.org
Parkes, M. W. (2011). Ecohealth and Aboriginal health: A review of common ground. Prince George, BC: National Collaborating Centre for Aboriginal Health. Available at http://www.nccah- ccnsa.ca/docs/Ecohealth_MargotParkes2011-EN.pdf
Ostfeld, R. S., Keesing, F., & Eviner, V. T. (Eds.). (2008). Infectious disease ecology: Effects of ecosystems on disease and of disease on ecosystems. Princeton, NJ: Princeton University Press.
Waltner-Toews, D. (2004). Ecosystem sustainability and health: A practical approach. New York: Cambridge University Press.
Waltner-Toews, D., Kay, J. J., & Lister, N.-M. E. (2008). The ecosystem approach: Complexity, uncertainty, and managing for sustainability. New York: Columbia University Press.
Wackernagel, M., & Rees, W. (1996). Our ecological footprint: Reducing human impact on the Earth. Gabriola Island, BC: New Society.
Waldrop, M. M. (1993). Complexity: The emerging science at the edge of chaos. New York: Simon & Schuster.
Zinsstag, J., Schelling, E., Whittaker, M., Tanner, M., & Waltner- Toews, D. (Eds.). (2015). One Health: The theory and practice of integrated health approaches. Wallingford, UK: CABI.
Programs, Organizations, Web Sites Future Earth: http://www.futureearth.org
International Association for Ecology & Health, and its journal, EcoHealth: http://www.ecohealth.net
Learning for Sustainability: http://learningforsustainability.net
Millennium Ecosystem Assessment: http://www.millenniumassessment.org
Resilience Alliance: http://www.resalliance.org
The Rockefeller Foundation–Lancet Commission on Planetary
180
Health: https://www.rockefellerfoundation.org/planetary-health
181
Chapter 3 Sustainability and Health
Cindy L. Parker, Jessica D. Rhodes, and Brian S. Schwartz
During the preparation of this chapter Dr. Parker served on the Boards of Physicians for Social Responsibility and the Chesapeake Climate Action Network, as a Fellow of the Post- Carbon Institute, and as co-chair of the Climate Communication Consortium of Maryland coordinating committee, all uncompensated positions. Dr. Rhodes and Dr. Schwartz report no conflicts of interest related to the authorship of this chapter.
182
Key Concepts Sustainability refers to the ability of a system to continue functioning without depleting or damaging the things it needs to function. The term has come to be used in many ways. Almost all are relevant to human health and well- being.
Human activity over recent centuries—a growing population and growing energy and resource use—has altered many Earth systems in patterns that are not sustainable.
Sustainability is a feature of complex systems, so systems thinking is required to address it.
Sustainability has traditionally been considered to involve three domains—environmental, social (including health), and economic.
Neo-sustainability refers to the ability of an activity to sustain a system by improving its quality and operating within its limits. This may imply innovative ideas of prosperity, growth, and quality of life.
There are many approaches to measuring progress toward sustainability, on all levels, from global to local.
Moving toward sustainability is necessary not only as a basis for long-term human health and equity but also as a basis for the continued viability of civilization as we know it.
Did you know that you're living in an era called the Anthropocene? Geologists call the era in which modern civilization evolved the Holocene, an era characterized by relatively stable conditions on Earth. The Anthropocene represents a change. Popularized by atmospheric chemist Paul Crutzen at the dawn of the twenty-first century, this term identifies an era in which human influence has altered many fundamental Earth processes: the climate, the extent of photosynthesis (a key part of primary production, the basis of most food chains; see Chapter 2), land cover, river flows, ocean food webs, the cycling of materials such as nitrogen and phosphorus, and the likelihood of species extinctions,
183
to name a few. The Anthropocene began during the industrial revolution when fossil fuel use rose dramatically. Carbon dioxide levels in the atmosphere climbed from preindustrial levels of around 270 parts per million (ppm) to 310 ppm by the mid- twentieth century, and with the Great Acceleration after World War II (Steffen, Grinevald, Crutzen, & McNeill, 2011)—with steeply increasing population, industrialization, fossil fuel extraction, agricultural activity (including mechanization, clearing of forests, and fertilizer use), and consumption of goods—these levels have risen to more than 400 ppm today. This has led to complex changes: accelerating rates of species extinction, increasing amounts of reactive nitrogen in the environment, and massive swaths of natural ecosystems being converted for human use.
The most recent stage of the Anthropocene, the twenty-first century, is characterized by the rapid economic development of countries, including China, India, Brazil, and Indonesia, continuing the Great Acceleration. Figure 3.1 shows some indicators of this acceleration— more people, more economic activity, bigger impacts on the environment. These changes have occurred very quickly, which is cause for both pride and concern. But clearly this kind of geometric growth cannot go on for long in a finite world without serious consequences. The systems we have altered are in a very real sense life support systems, not only for our planet's plant and animal life but for humans as well. The air we breathe, the water we drink, the materials we use, the crops we grow, all depend on them. Sustainability must be a matter of deep human concern.
184
185
Figure 3.1 The Great Acceleration Source: Steffen et al., 2004.
The twenty-first century has also seen an increasing awareness of the global scale of human impact on planet Earth. Attempts at global governance to manage and mitigate the damage have begun. What will it take for the Anthropocene to become an age of sustainability? What would a sustainable society look like? This chapter introduces some foundations of the concept of sustainability, discusses the core elements of sustainability, reviews ways to measure progress toward sustainability, and describes a path forward, including the concept of neo-sustainability.
186
Historical Considerations of Sustainability Many disciplines have used the term sustainability, often defined in different ways. We begin our discussion with a simple definition: according to Merriam-Webster online, sustainable means “able to be used without being completely used up or destroyed,” “involving methods that do not completely use up or destroy natural resources,” and “able to last or continue for a long time.” In the twenty-first century, sustainability has become part of our modern lexicon but means widely different things to different people. Most agree it is a positive concept, and thus it is widely embraced. But where did the term sustainability originate? Why is it important? What does it have to do with the Great Acceleration? And what does it have to do with health?
Many Indigenous peoples have lived by the philosophy of sustainability for generations (Sveiby, 2009), but modern uses of the term date to the environmental movement of the 1960s and 1970s. People began to realize that industrialization and economic development—vehicles for improving living conditions for people worldwide—were seriously damaging the environment. Initially, sustainability was a concept grounded in conservation. In 1970, an International Union for Conservation of Nature (IUCN) report emphasized the importance of conservation, defined as “management of the resources of the environment—air, water, soil, minerals and living species including man—so as to achieve the highest sustainable quality of human life.” Notably, human well- being was at the center of this framework.
At the United Nations Conference on the Human Environment in 1972 in Stockholm, a declaration was issued acknowledging how economic and social development had improved quality of life throughout the world but also noting that this development had simultaneously damaged the Earth's ecosystems—calling into question the staying power of the benefits. The declaration called on society to protect the Earth's natural resources for the benefit of present and future generations. Shortly after, in 1980, the IUCN released its World Conservation Strategy, which challenged human society on its “quest for economic development and enjoyment of the riches of nature” to recognize “resource limitation and carrying
187
capacities of ecosystems” and take into account “the needs of future generations” (IUCN, 1980). The report also argued that economic growth and development are compatible with conservation, and that conservation must be integrated with them to make development sustainable (IUCN, 1980), without clearly explaining how necessary trade-offs might be achieved.
Sustainability became popularized with the United Nations' 1987 Brundtland Report, Our Common Future. However, the Brundtland Report focused not on sustainability but on sustainable development, defined as economic development that “meets the needs of the present without compromising the ability of future generations to meet their own needs” (World Commission on Environment and Development, 1987). The report is written at a high level; it does not specify how current development that does not affect future generations is to be measured and tracked. While the report acknowledges that sustainable development implies limits, it declares that these are “not absolute limits but limitations imposed by the present state of technology and social organization on environmental resources and by the ability of the biosphere to absorb the effects of human activities” (World Commission on Environment and Development, 1987). By suggesting that technology and innovation could overcome limits to growth (which in practical terms meant economic growth), the Brundtland Report avoided the vexing problem of limits.
Even though virtually every environmental impact could also affect human health, health did not formally enter the sustainable development discussion until 1989, when then World Health Organization (WHO) director Dr. Hiroshi Nakajima prioritized the linkages among health, economic development, and the environment (Institute of Medicine [IOM], 2013). The WHO Commission on Health and the Environment was soon launched, and issued reports on the arenas of food and agriculture, energy, industry, and urbanization (IOM, 2013). These reports influenced discussions at the landmark 1992 United Nations (UN) Conference on Environment and Development in Rio de Janeiro, Brazil (the Rio Conference). Principle 1 of the Rio Declaration on Environment and Development states, “Human beings are at the centre of concerns for sustainable development. They are
188
entitled to a healthy and productive life in harmony with nature” (United Nations, 1992a), while Agenda 21, the action plan that arose from the Rio Conference, devotes a chapter to “protecting and promoting human health” (United Nations, 1992b). Through both the Rio Declaration and Agenda 21, the international community endorsed the idea of sustainable development, with human health an integral consideration. Even though health is certainly a fundamental need, some argue a right, of human society, sustainability is not about the health of individuals, although that result flows from it. Rather it is about the health of the global population—all of us. This idea is developed in Text Box 3.1, which examines planetary health.
189
Text Box 3.1 Planetary Health Unsustainable practices are threatening health on an unprecedented scale. In 2014, a team from the Lancet, the University of Auckland, the Auckland University of Technology, Umeå University, and the London School of Hygiene and Tropical Medicine proposed a broad framework for addressing this challenge, calling their concept planetary health. They argued powerfully for the need to act, based on the same sustainability considerations introduced in this chapter:
Our patterns of overconsumption are unsustainable and will ultimately cause the collapse of our civilization. The harms we continue to inflict on our planetary systems are a threat to our very existence as a species. The gains made in health and wellbeing over recent centuries, including through public health actions, are not irreversible; they can easily be lost, a lesson we have failed to learn from previous civilizations. We have created an unjust global economic system that favors a small, wealthy elite over the many who have so little [Horton et al., 2014].
Planetary health, according to these authors, aims “to protect and promote health and wellbeing, to prevent disease and disability, to eliminate conditions that harm health and wellbeing, and to foster resilience and adaptation.” They propose “a new principle of planetism and wellbeing for every person on this earth—a principle that asserts that we must conserve, sustain, and make resilient the planetary and human systems on which health depends by giving priority to the wellbeing of all.” This is more than a public health agenda; it is “an attitude toward life and a philosophy for living,” requiring “urgent transformation…in our values and our practices.” In this transformation, health professionals would serve as an “independent conscience,” deploying traditional public health values of social justice and fairness for all, and working through “collective actions of
190
interdependent and empowered peoples and their communities” (Horton et al., 2014).
191
Sustainable Human Well-Being and the Three-Legged Stool In the decades since, the idea of sustainable development has continued to evolve and recognition of the importance of health has grown. The UN's Millennium Development Goals, adopted by all UN member states in 2000, all incorporated health, either explicitly (through setting targets for reducing child mortality, improving maternal health, and combating infectious diseases, etc.) or implicitly (through setting targets for eradicating extreme poverty and hunger, achieving universal primary education, promoting gender equality, and ensuring environmental sustainability, etc.).
The 2002 UN World Summit on Sustainable Development in Johannesburg introduced the idea that sustainable development rests on three interdependent and mutually reinforcing pillars— economic development, social development, and environmental protection—a three-legged stool that requires all legs to be of equal importance and thus the same length (United Nations, 2002). Critics, however, have argued that the three pillars are not equivalent because the environment underpins both economy and society (Adams, 2006), and they have proposed a nested model of sustainability (see Figure 3.2). In this view the environment represents an outer bound to human activity, implying the existence of limits, and furthering thinking about the underlying complex relationships (Adams, 2006).
192
Figure 3.2 Nested Model of Sustainability Source: Adapted from Adams, 2006.
Where does health fit in? Health—defined by the WHO (1948) as “a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity”—is at the core of the social dimension, so much so that some have argued that achieving well-being in a sustainable manner ought to guide sustainability efforts (Holdren, 2008). The dependence of health on the larger environmental context is captured in the concept of ecosystem services, such as purification of air and water, protection from some natural disasters, and pollination of crops (Millennium Ecosystem Assessment, 2005). As described in Chapter 2, many of these services are essential for human well-being, although they are typically undervalued by conventional economic reckoning (Summers, Smith, Case, & Linthurst, 2012). When ecosystem damage compromises these services, disease and suffering can follow, in both predictable and unpredictable ways (Myers et al., 2013). In fact, while failure in any of the three domains—economic, social, or environmental—can trigger human suffering on a large scale, and all are interrelated, Diamond (2005) and others have argued that in human history, serious environmental problems are a recurring primary cause of societal collapse.
A closely related core component of the social dimension is equity. Since the Rio conference, there has been broad agreement that deep inequities—between rich nations and poor nations and also within nations—are not only unfair, they are a barrier to sustainability
193
(Ehrlich, Kareiva, & Daily, 2012). Equity considerations also extend across time, which is no surprise given that sustainability intrinsically considers long-term outcomes. The concept of intergenerational equity posits that we have a moral requirement to leave a livable world to future generations (Padilla, 2002). These concepts correspond closely to the idea of environmental justice (see Chapter 11).
The Brundtland Report's definition of sustainable development can thus be seen, in retrospect, as both holistic and vague. This may have served a useful purpose in 1987 to appeal to a broad audience and garner acceptance of the general concept, but such vagueness has allowed governments, environmentalists, policymakers, and businesses to act in the name of sustainability and sustainable development in widely different ways that conveniently suited their needs (Adams, 2006). Recent decades have seen an explosion of interest in sustainability. Sustainable is now a catchword in green business, and many corporations, universities, and cities have offices of sustainability. Ironically, despite such interest and action, human destruction of the environment continues at an accelerated pace. This failure may be in part due to the way each entity has defined sustainability. If sustainability can mean anything to anyone, it is no longer a useful term (Farley & Smith, 2014).
194
Drivers of Nonsustainability, Limits to Growth, and Collapse Humans place demands on the environment through our numbers (population size), but also by how we use, produce, and/or distribute land, food, water, consumer goods, and energy. Many of these activities use finite natural resources (e.g., ores to make metals; petroleum to make plastics; ancient groundwater aquifers, which are not rechargeable on human time scales, to irrigate crops), while others rely on renewable resources (e.g., wind, sun, rechargeable aquifers). These drivers are captured in the equation I = PAT where I is society's impact on the Earth's systems (and therefore, as we have seen, on human health and well-being), P is population, A is affluence (a measure of per capita consumption), and T is a technology factor reflecting the efficiency of production and consumption (Ehrlich & Holdren, 1971). This is a reminder that both population and the intensity of how people live are drivers of sustainability.
The remarkable growth of the P and T parts of the equation is evident in Figure 3.1. Consumerism encourages, and relies on, the acquisition of goods and services in ever-greater amounts; it has been estimated that 70% of the U.S. economy and 20% of the world economy is based on the purchasing decisions of the U.S. consumer (United Nations Environment Programme, 2012).
The P part of the equation, population, has been the subject of robust debate since the eighteenth century. In his Essay on the Principle of Population, Thomas Malthus argued that the human population could not continue to grow exponentially because the natural resources that provided human subsistence, namely the products of agriculture, were limited and could grow only arithmetically. When the population exceeded the ability of the Earth's resources to provide subsistence, he argued, war, pestilence, famine, and death would inevitably result to restore the population into balance with natural resource limits (Malthus, 1798). Some contemporary scholars, such as Jean-Jacques Rousseau, disagreed with Malthus and thought human ingenuity would provide for unlimited social improvement and endless growth (Farley & Smith,
195
2014). The global exploitation of fossil fuels and technological improvements leading to the agricultural revolution of the twentieth century seemed, for a time, to have proven Malthus wrong. Dramatically increased agricultural productivity fed a growing population. But in the decades since, with continued population growth and concomitant environmental degradation, Malthus's basic premise that there are limits to ecosystem services has emerged as relevant to any discussion of sustainability.
196
What Should Concern Us More: Population Growth Or Consumerism? In the 1960s, as the world awoke to the environmental impacts of industrialization and economic growth, the concept of limits was reexplored. In 1968, in Tragedy of the Commons, Garrett Hardin posited limits to human consumption through the concept of carrying capacity. In population biology, as noted in Chapter 2, carrying capacity refers to the maximum species population that an ecosystem can continuously support, and Hardin effectively applied the concept to the human population. He argued that when there are resources shared in common, individual users benefit directly from their use but share only indirectly in the cost of overuse. This encourages individuals to exploit the resource for private gain at the expense of the common good, and ultimately leads to degradation of the resource (Hardin, 1968). Hardin's example was a shared pasture, on which each herder has an incentive to maximize the number of his or her own livestock grazing. But if all herders acted on that incentive, overgrazing would result. For the pasture, as for other common pool resources, exceeding the limit or carrying capacity would result in ecosystem degradation and collapse. In the same year, Paul Ehrlich revived the Malthusian debates with his book Population Bomb (1968), in which he predicted that population growth would continue to outpace agricultural growth, leading to global famine and starvation as early as the 1970s. While his predictions certainly did not pan out in the time frame suggested, he made an important contribution to the discussion of whether there is a limit to the human population the Earth can sustain. And given current population projections of almost 10 billion people by 2050 (United Nations Department of Economic and Social Affairs, Population Division, 2015), and the mounting threat of climate change to agricultural production, Malthus and his neo-Malthusian counterparts may, in the end, turn out to be correct.
There has been a longstanding tension between those who view population as the primary driver of environmental degradation and those who point instead to consumerism. While population can be directly measured, and has been for a long time, progress toward
197
measuring the environmental impact of technology and consumption has only more recently developed. The concept of the ecological footprint emerged in the early 1990s from the attempt to measure these impacts while moving beyond a focus on economic indicators and looking through the lens of ecosystem services (Rees, 2013). The ecological footprint of a population is defined as “the total area of land and water ecosystems required to produce the resources that the population consumes, and to assimilate the wastes that the population generates, wherever on earth the land/water are located” (Rees, 2013). Thus the ecological footprint approximates the area of earth needed to sustain the consumption and absorb the waste of a society. Another component of the footprint is biodiversity loss, which inevitably accelerates as a society's ecological footprint grows.
Today's global ecological footprint is 2.6 global hectares (gha) per person—substantially higher than what is available—just 1.8 gha per person (Borucke et al., 2013). Wealthy consumers, on average, use 4 to 10 gha per person of productive ecosystems to support their lifestyles, up to five times their fair share of global biocapacity. Even at current average levels of economic production and consumption, we are already exceeding the long-term carrying capacity of the Earth. To support the current global population of 7 billion at the average standard of living of a North American would require in excess of four more planet Earths. The global population is living and developing in part by “depleting essential natural capital and overcharging vital waste sinks” (Rees, 2013). This stark finding allows us to grasp the concept that our present lifestyles and resource use are unsustainable and inequitable.
198
Limits to Growth In 1972, an international scientific think tank convened to analyze the impacts of human population growth on the environment by using computer systems models to explore the question of whether the Earth has finite limits. In its report, Limits to Growth, the Club of Rome predicted that if human population and consumption continued to grow unabated, human carrying capacity on Earth would be exceeded, resulting in widespread ecosystem collapse (Meadows, Meadows, Randers, & Behrens, 1972). The report firmly claimed that there are limits to human economic and population growth. It attracted plenty of detractors. Some, such as economist Julian Simon, rejected the neo-Malthusian view of limits to growth, and challenged the model used in the Club of Rome report. He argued that human population growth is itself a source of human ingenuity and intellectual capital that can yield solutions to environmental problems and overcome resource scarcity (Simon, 1981).
In 2004, the Club of Rome's Limits to Growth: 30-Year Update was released. This report discussed the degraded state of the global environment, from which resources are being extracted and exploited faster than they can be restored and into which pollutants and wastes are being released faster than they can be absorbed. It warned that humanity is in a dangerous state of overshoot: that is, of exceeding carrying capacity (Meadows, Meadows, & Randers, 2004). In retrospect, the 1972 “business as usual” scenario turned out to have projected accurately the consumption, population growth, and greenhouse gas emissions over the subsequent four decades, validating the think tank's original model and conclusions (Farley & Smith, 2014). However, the growing evidence of overshoot and its associated risks has not yet spurred fundamental changes in how we live. In the words of sustainability experts, “the predominant paradigm of social and economic development remains largely oblivious to the risk of human-induced environmental disasters at continental to planetary scales” (Rockström et al., 2009a).
Recent work has also addressed signals of limits to growth (Rockström et al., 2009a, 2009b). A team based at the Stockholm
199
Resilience Centre and the Stockholm Environment Institute has proposed a safe operating space for humanity within nine key planetary boundaries (Rockström et al., 2009b) (Figure 3.3). For seven of these nine, they proposed quantitative limits that, if exceeded, could trigger abrupt, nonlinear environmental change, with potentially catastrophic consequences for human civilization (Table 3.1). This approach offers insights into humanity's predicaments (Rockström et al., 2009b).
Figure 3.3 A Safe Operating Space for Humanity Source: Rockström et al., 2009b.
There are nine planetary limits, represented by the green inner circle. Each limit, surpassed, takes humanity into potentially unsafe territory. The diagram suggests that this has occurred with respect to climate change, biodiversity loss, and the nitrogen cycle.
Table 3.1 Metrics of Sustainability
Ecological footprint (Borucke et al., 2013)
200
Living Planet Index (Loh et al., 1998) City Development Index (United Nations Commission on Human Settlements, 2001) Human Development Index (United Nations Development Programme, 1990) Environmental Sustainability Index (Esty, Levy, Srebotnjak, & de Sherbinin, 2005) Environmental Performance Index (Esty et al., 2006) Environmental Variability Index (South Pacific Applied Geoscience Commission, 2005) Index of Sustainable Economic Welfare (Cobb, 1989) Environmental adjusted domestic product (Hanley, 2000) Genuine progress indicator (Cobb, Halstead, & Rowe, 1995)
Unfortunately, three of these nine boundaries have already been crossed. First, we have already surpassed the boundary of 350 ppm of carbon dioxide (1 watt/m2 of radiative forcing above preindustrial levels) and now risk irreversible climate change, such as the melting of ice sheets and major sea level rise (Rockström et al., 2009b) (see Chapter 12). Second, the rate of biodiversity loss is now 100 to 1,000 times the natural background rate, well beyond the boundary of 10 times, and equivalent to the rates of the last major extinction (Rockström et al., 2009b). Biodiversity is the cornerstone of stable ecosystems (see Chapter 2), and even though little is known about the exact rate of species loss that would lead to ecosystem collapse, we are pushing the edge. Third, we have surpassed the safe boundaries of the nitrogen and phosphorus cycles. Mainly through fertilizer production and legume cultivation, humans convert over 120 million tons per year of atmospheric nitrogen to its reactive forms, well beyond the estimated safe limit of 35 million tons per year, and more than all of Earth's natural nitrogen fixation systems combined. Humans mine vast amounts of phosphorus from rock and 8.5 to 9.5 million tons flows into the oceans annually, more than eight times the natural background rate. High concentrations of nitrogen and phosphorus cause large-scale algae blooms that grow quickly and then die and sink to the ocean's bottom. The decay process depletes the available oxygen from the water, resulting in oxygen levels too low to support life (eutrophication), and killing
201
any marine life unable to exit the area (Rockström et al., 2009b).
The fact that we have crossed three of nine planetary boundaries means we are clearly not in a safe operating space for humanity and a sustainable future is not in sight. To make matters worse, the Earth's dynamic system means that the boundaries may interact, and transgression of one boundary may fundamentally lower the safe thresholds for others (Rockström et al., 2009a). Although there have been some global efforts to curb human impact on the environment, such as the Convention on Biological Diversity and the United Nations Framework Convention on Climate Change, progress has been minimal, as increasing rates of biodiversity loss and carbon dioxide emissions continue unabated.
202
Human Societal Collapse? Prevention Through Systems Thinking and Early Action The idea of environmental limits and the possibility that we have exceeded them has spurred contemplation about the fate of modern human society. Some believe surpassing environmental limits will lead to the collapse of modern society, as it has contributed to the decline of past civilizations. In his book Collapse (2005), evolutionary biologist Jared Diamond identified major environmental problems facing humanity today, and noted that many of them—deforestation; soil erosion, salinization, and fertility loss; water management problems; overhunting; overfishing; invasive species; population growth; and populations' increased per capita impact—have contributed to the collapse of past societies. Additional problems, including anthropogenic climate change, environmental toxicants, and energy scarcity, threaten modern society (Diamond, 2005). Others writers, such as Thomas Homer- Dixon (2001), have argued that resource scarcity (another way of thinking about humans surpassing environmental limits) will contribute to a future of violence and conflict. Still others have taken an economic approach to environmental limits. Both Richard Heinberg (2011) and Jeff Rubin (2012) have discussed a plateauing of economic growth, imposed by environmental limits and our overuse of some of Earth's most important natural resources, namely fossil fuels.
If humans are now facing environmental limits to growth, and collapse is one possible outcome of these environmental limits, perhaps our previous discussion of the three pillars of sustainable human well-being needs revision, designating the environmental pillar as the most important one after all. This idea of the primacy of the environment is gaining increasing attention (Farley & Smith, 2014). Humanity's basic needs derive from healthy ecosystems and planetary systems (e.g., the climate system), therefore human health and well-being depend on the sustainability of healthy environments and ecosystems. The limits to growth are limits to the well-being of healthy environments and ecosystems.
Human society, the climate, ecosystems, the economy, food
203
production and distribution, and other such components form an interconnected, dynamic, complex system. Such systems can be difficult to understand and characterize. If health depends on sustainability, and if sustainability is a function of complex dynamic systems, then achieving sustainability depends on systems thinking. (Systems thinking is described in Chapter 2.) Viewing the world as a complex, dynamic, interconnected system yields several lessons with regard to achieving sustainability and avoiding collapse. First, managing a complex system—involving in this case matching resource use to limits, across spatial scales, under diverse government jurisdictions and cultural traditions, under changing circumstances, and without full information, while working toward fair and equitable social arrangements—is enormously challenging: a classic example of a wicked problem. A wicked problem is one that has no clear solution, in large part owing to complexity compounded by organizational, political, and cognitive barriers (Rittel & Webber, 1973). While originally described in the context of social policy, wicked problems confront us in many aspects of environment, health, and sustainability, from setting energy policy to managing fisheries to tackling climate change.
Second, and relatedly, complex systems are policy resistant because the features of complexity can overwhelm our ability to understand and respond (Hammond, 2009). The more complex the system, the more daunting the challenge. Effective sustainability efforts under such circumstances require structured analysis of problems, embracing and harnessing complexity rather than oversimplifying (Ostrom, 2009), taking innovative and flexible approaches, working across organizational and disciplinary boundaries, constantly incorporating new information and adapting to it, and effectively engaging stakeholders (Folke, Hahn, Olsson, & Norberg, 2005; Plummer & Armitage, 2007; Waltner-Toews, 2008).
Lastly, systems thinking helps anticipate some of the challenges inherent in moving toward sustainability. In complex systems, small changes can lead to large and unexpected results; abrupt changes may occur if tipping points are reached; and systems can self- organize and reach new equilibrium states, some of which may be far less hospitable to humans than the Holocene has been. Environmental scientist and pioneering systems thinker Donella Meadows (2008) has pointed out that “because of feedback delays
204
within complex systems, by the time a problem becomes apparent it may be unnecessarily difficult to solve” (p. 3).
To address the challenge of managing complex systems, the idea of adaptive management arose in ecology in reference to natural resource management. This is a structured, iterative approach to decision making in the face of uncertainty and complexity, in which observations over time feed learning and become the basis of ongoing course corrections. Adaptive management is pertinent not just to natural resources; for example, as described in Chapter 12, climate change adaptation relies on very similar principles. In public health more generally, and in sustainability efforts, systems science is widely applicable, and tools such as systems dynamics models, network analysis, and agent-based modeling (Luke & Stamatakis, 2012) help address complex challenges.
These observations suggest that early action is preferable to delayed action, that resiliency of systems is a critical goal, and that critical thresholds define priorities for action—with special urgency when we are approaching or exceeding them.
205
The Importance of Scale A major challenge to date in moving toward sustainability has been that many drivers are global in scale; greenhouse gas emissions on the other side of the globe contribute to climate change regardless of what we do to reduce our own emissions. In contrast, climate change, energy scarcity, water scarcity, food production, land use, and the connections among them require local responses. This has implications for community resilience; as energy gets more expensive, the production of food and clean water will be impacted (Neff, Parker, Kirschenmann, Tinch, & Lawrence, 2011), the transportation of food and other goods over great distances will be curtailed, and more generally, the idea that localities can overcome local ecological and environmental limits by using cheap and plentiful fossil energy will be constrained. It is a paradox that a set of profoundly global problems—climate change, ecological degradation, energy scarcity, water scarcity, species and biodiversity losses—must be addressed with local responses.
Consideration of scale is thus critical to any discussion of sustainability. Policy responses must be developed at all scales, from local to regional, national, and global. These responses can build on the observation that grassroots efforts at the local level can be very effective not only in engaging the local populace but also in motivating change at larger scales (e.g., local food production efforts may create momentum toward changes in the national Farm Bill). The issue of scale has also been inherent in the Intergovernmental Panel on Climate Change's thinking about responses to climate change. Mitigation efforts to reduce greenhouse gas emissions generally require effort at larger scales, whereas adaptation efforts, to reduce the impacts of climate change that are already built in and oncoming, generally require effort at smaller scales. Building community resilience in many ways is just a comprehensive and forward-looking set of adaptation responses.
206
The Way Forward Health in All Policies and Sustainability in All Policies During the recent decades many public health practitioners have come to realize that intersectoral action is needed to protect the public's health—a practical application of systems thinking. Policies promulgated in other sectors, such as agriculture, housing, urban planning, or environmental protection, have public health implications, both positive and negative. In 1972, the Finnish government, in an effort to reduce high rates of cardiovascular mortality, adopted the concept of healthy policies in working with meat and dairy producers, schools, and the media. The program was so successful that Finland became a model for intersectoral action to improve the public's health. The idea of health in all policies (HiAP) gained popularity in 2006, during the Finnish presidency of the European Union. Other countries, recognizing that a healthy population is central to most other societal activities, are adopting HiAP as a core principle in all public policy making.
While this has been a welcome development, the focus may still be too narrow to ensure that human well-being can be sustained into the future. The inability of society or an economy to exist without a healthy environment providing our most basic needs suggests that the sustainability of healthy environments may need to be an essential component of all policy considerations; that is, we need sustainability in all policies (SiAP). Accordingly, the Sustainable Development Goals (sustainabledevelopment.un.org), successors to the Millennium Development Goals, embed health progress in the framework of sustainability.
A New Definition of Sustainability For the word sustainability to be as meaningful and useful as possible, a precise and measurable definition is essential. As we have discussed, sustainability was initially oriented toward development in less developed countries, but it now must apply to everyone, everywhere on the planet. One approach is the concept of neo-sustainability, defined as “the ability of an activity to sustain a system by improving its quality and operating within its limits.”
207
This definition is built on three premises, or rules, of sustainability, that link our prior discussions:
1. There are natural limits to growth, as dictated by the carrying capacity of the environment.
2. Environmental concerns must be given primacy, because without healthy ecosystems societal well-being will not be sustainable.
3. A systems approach must be used, because the economy, society, and the environment are nested systems and decisions made in one arena impact all others (Farley & Smith, 2014).
Although neo-sustainability makes concrete the decades of thinking on and experience with our environmental challenges, there are still major questions that local and global societies must tackle. We still have to consider:
What are our individual and collective needs?
How much is enough?
What factors and resources are under our control?
How much control do we actually have and how best can we exercise it?
What is the best way to allocate resources?
How do we balance the needs of the present against the needs of future generations?
What is it exactly that we want to sustain?
Various methods have been recommended to motivate action with these sustainability principles in mind. One is to seek equity, including intergenerational equity, international equity, and equity across communities. Another is to set limits, meaning requiring that resources be used more sparingly and more fairly. Another is to minimize environmental harms, and if they are unavoidable, to ensure they are equitably distributed. If society decides it cannot do without wind turbines or incinerators, these cannot be located only in poor areas. Neo-sustainability principles, systems thinking, and considerations of scale would lead to the conclusion that actions must not exceed environmental limits at any scale: local, regional, or global. We cannot shift environmental harms from one region to
208
another (e.g., through use of consumer electronics in the United States that leads to exposure to toxic by-products of recycling in West Africa, or through deep well injection from across state lines— where environmental regulations may be more lax—of the flowback of contaminated water from hydraulic fracturing). Only if we considered our stewardship of the environment in unconnected pieces rather than in reference to scale and systems thinking could we conclude that shifting environmental harms from one location to another is a reasonable policy option (Farley & Smith, 2014).
What is to be sustained? After an extensive literature review the Board on Sustainable Development of the U.S. National Academy of Sciences offered a three-part answer (U.S. National Research Council, Policy Division, Board on Sustainable Development, 1999):
Nature, including the Earth, biodiversity, and ecosystems
Life support, including ecosystem services, resources, and environment
Community, including cultures, groups, and places
Using the nested approach of describing the relationships of economy, society, and environment, each of these realms would require metrics to gauge progress toward sustainability.
Measuring Progress Toward Sustainability So that responsible parties, including governments, non- governmental organizations, and the private sector, can know whether sustainability by any definition is being achieved, sustainability metrics must be tracked over time. Optimal metrics have a number of attributes: they are credible; specific; actionable; relevant; consistent and comparable over time and space; scalable from the local to the global; robust to minor changes in methodology, scale, or data; accurate; unbiased; explicit; understandable; cost effective; helpful for prioritizing key issues in need of action; and available in a timely manner (Hambling, Weinstein, & Slaney, 2011).
Perhaps the most widely influential set of sustainability metrics comes from the UN Commission on Sustainable Development (CSD) (United Nations Department of Economic and Social Affairs, 2007). CSD issued indicators to track progress in sustainable
209
development following the adoption of Agenda 21 in Rio in 1992, and has subsequently refined them, most recently in 2007. The CSD indicators are distributed across fourteen theme areas (poverty, governance, health, education, demographics, natural hazards, atmosphere, land, oceans/seas/coasts, freshwater, biodiversity, economic development, global economic partnership, and consumption and production patterns) with multiple subthemes for each, leading to a total of ninety-six indicators, of which fifty are “core” indicators. The health indicators include mortality (both childhood mortality and life expectancy), health care delivery (access, and penetration of specific services), nutritional status, and health status (morbidity from certain diseases, tobacco use prevalence, and suicide rate). Many cities and regions have identified their own sustainability metrics.
Measuring the state of ecosystems is key for sustainability indicators. Extensive data regarding the health of ecosystems around the world and their continued ability to meet human needs were gathered in 2005, in an initiative called the Millennium Ecosystem Assessment (www.millenniumassessment.org/en/index.html). These findings provide a useful baseline for subsequent measures of sustainability.
The most widely used measure of economic performance is the gross domestic product (GDP), but economists have discussed alternative metrics more suited to measuring sustainability. Although the GDP is widely used (including in the CSD metrics discussed above) and standardized across countries, it is a poor measure of sustainability for at least two major reasons. First, it assumes that more economic activity is invariably better. However, there is a very high correlation between GDP and energy inputs into economies—and energy inputs account in large part for the environmental limits we are now facing (Warr & Ayres, 2010). Second, GDP calculations are indifferent to the type of economic activity counted; they do not subtract for economic activity that impedes societal and environmental sustainability, such as coal mining, or for the results from such activity, such as treating disease resulting from air pollution (Daly, 2013).
The ecological footprint has many advantages as a metric, including its widespread familiarity and use; the availability of online “quizzes” that enable people to assess their own ecological
210
footprints and compare themselves to others near and far; and its ability to be used at different scales to help with decision making about priorities and to track progress (Borucke et al., 2013). Many other metrics for sustainability and societal progress exist (see Table 3.1). No metrics are perfect; many do not incorporate dynamic changes over time, systems thinking, feedbacks, scale, or interconnections among the various domains of sustainability. More accurate metrics of sustainability will require the use of complex systems models.
Can Sustainability Be Achieved? What Might It Look Like? Several authors have written about what sustainability might look like if we could achieve it. Heinberg (2011) has written that our concept of growth must transition from economic expansion to human development. Both Heinberg (2011) and Rubin (2012) have argued that we are about to experience not only limits to growth but the end of growth. One framework, contraction and convergence, promotes an overall reduction of resource use (and greenhouse gas emissions), together with sharing of the contraction across nations and subpopulations, to promote equity (Stott, 2012).
Scholars have variously imagined futures that are highly local (Heinberg, 2011) and highly urban, with smaller homes, less “stuff,” less driving, and greatly reduced per capita carbon footprints (Owen, 2009), perhaps as eco-cities incorporating urban agriculture and other forms of nature (Wong & Yuen, 2011). Some have argued that we won't achieve sustainability by simply replacing our current consumer culture with a new consumer culture based on solar panels, electric cars, and vegetable-based plastics (Heinberg, 2011). Others have focused on the role of the food system, our approach to providing food, and our dietary habits. Pollan's proposed solution to the obesity epidemic and other food challenges—“eat food, not too much, mostly plants”—would also yield sustainability benefits (Pollan, 2008). Climate and food system connections have also been made explicit in solutions; for example, contraction and convergence on meat is similar to what must be done across countries on greenhouse gas emissions (Friel et al., 2009).
The health sector has a broad and varied role to play in achieving
211
sustainability. Health professionals can use the health co-benefits from reduced resource use, healthier ecosystems, cleaner air from reduced greenhouse gas emissions, and a sense of community that derives from sustainable community design principles to motivate these transitions. Opportunities for sustainability within the health care delivery system are described in Text Box 3.2. Including health professionals in policymaking could encourage full recognition of the health co-benefits of sustainability efforts.
212
Text Box 3.2 Sustainability in Health Care Where should sustainability happen? For the most part the sustainability focus has been anywhere energy and resources are created and used—in energy generation, in manufacturing, in transportation, in agriculture, and in the design and operation of cities and buildings. Health professionals may feel that sustainability initiatives have little relevance to their work. But the health care sector is an important setting in which to encourage sustainability efforts, for at least four reasons. First, health facilities are highly energy intensive (second only to the food industry in energy use per square foot) (Energy Information Administration, 2009). In fact the health care sector accounts for 8% of all U.S. greenhouse gas emissions (Chung & Meltzer, 2009). Second, reducing the use of energy and resources can yield substantial economic benefits—an important consideration in an industry whose costs have been rising rapidly. Third, sustainable practices are often also healthy practices, advancing the central mission of health care facilities. Finally, many health care organizations strive to be leaders in their communities, and sustainability offers an opportunity to play this role.
In response to such thinking, a set of efforts known collectively as green health care (or sustainable health care) has emerged in recent years and is slowly spreading. Green health care advances sustainability by
Reducing energy use in health care facilities through energy conservation and the use of renewable energy sources
Reducing materials use through efficiency efforts
Reducing the health-related transportation footprint by encouraging walking, cycling, and transit use by employees, patients, and visitors, and by encouraging telecommuting and teleconferencing when feasible
213
Reducing water use through conservation
Reducing the waste stream through efficiency, reuse, and recycling
Supporting local agriculture through preferential purchasing
Leading community resilience efforts by preparing for emergencies such as heat waves
Reducing the use of persistent, bioaccumulative, and/or toxic chemicals by preferentially purchasing safer materials
Efforts across the health care sector are being led by such organizations as Health Care Without Harm (noharm.org), Practice Greenhealth (practicegreenhealth.org), and the Healthier Hospitals Initiative (healthierhospitals.org). Health care organizations such as Kaiser Permanente have set a high standard of practice and serve as a model for the industry (share.kaiserpermanente.org/article/environmental- stewardship-overview).
The signs of unsustainability are all around us. Having already crossed three of nine planetary boundaries is an ominous indication that the time to change course is short if we want a sustainable future for humanity and other life on planet Earth. Scholars have provided some specific instructions for how to get started, and there is already much we can do, while additional research may continue to provide new ideas and means to achieve our goals. There is much work to do; the future may be bright with possibilities, but we must get to work now.
214
Summary Sustainability refers to the ability of a system to continue functioning without depleting or damaging the things it needs to function. In the context of environmental health, sustainability applies to three interdependent aspects of human existence: the environment, society, and the economy (including equity). Population growth and patterns of resource use have created threats to both sustainability and human health: alterations of earth systems, excessive use of materials and energy, and production of waste faster than ecosystems can absorb it. Measures such as the ecological footprint help quantify these pressures. Trends in climate, biodiversity loss, and nitrogen cycling may indicate that humanity is exceeding planetary limits; this poses large-scale public health risk. Sustainable practices maintain, or better yet improve, the systems upon which human well-being depends, and therefore promote human health. Emerging conceptual frameworks, such as contraction and convergence, and emerging implementation approaches and metrics, are driving action toward long-term sustainability.
215
Key Terms adaptive management
A process of structured, iterative decision making in the setting of complexity and uncertainty. Information is continually gathered, supporting frequent and iterative course corrections. The goal is to reduce uncertainty over time, continually improve decision making, and yield better outcomes.
Anthropocene The current era, in which humans have altered many fundamental Earth processes, such as the chemistry of the soil, water, and atmosphere, with substantial, largely negative consequences for ecosystems and biodiversity; in short, the era in which humans control the climate.
Brundtland Report The 1987 report of the UN's World Commission on Environment and Development (chaired by Gro Harlem Brundtland, former prime minister of Norway), titled Our Common Future.
carrying capacity The maximum number of organisms that an ecosystem can support and sustain without degrading the ability of that ecosystem to maintain that abundance in the future.
co-benefits Collateral outcomes of policies or programs that offer benefits beyond those primarily intended. For example, shifting from single-occupancy vehicle use to walking, cycling, and transit use, in an effort to reduce energy use, also yields cleaner air and more physical activity and reduces road traffic injuries.
collapse Throughout history and prehistory, once thriving human civilizations have experienced gradual or at times rapid declines, eventually ending in failure, as, for example, the Mayan, Anasazi, and Easter Island civilizations did.
consumerism A culture of valuing the ever-increasing acquisition and consumption of goods and services. (Not to be confused with the ecological term consumer, referring to heterotrophs.)
216
contraction and convergence A suggested framework for achieving sustainability. It promotes an overall reduction of resource use—thus reducing waste production, including greenhouse gas emissions—shared across nations and all populations equitably.
ecological footprint “The total area of land and water ecosystems required to produce the resources that the population consumes, and to assimilate the wastes that the population generates, wherever on earth the land/water are located” (Rees, 2013, p. 701).
ecosystem services Essential benefits to humans provided by ecosystems, such as pollination of food crops, purification of air and water, and protection against some natural disasters.
Great Acceleration A period of time following World War II when population, industrialization, and resource use increased exponentially.
green health care Health care delivery that achieves better environmental performance, including reduced energy and resource use, reduced waste generation, local sourcing of food and supplies, and related activities.
Health in all policies A model for intersectoral action to improve the public's health by thoughtfully developing all policies so as to minimize negative public health consequences.
intergenerational equity The concept that future generations are no less important or valuable than present generations and therefore future generations have a right to a livable world.
limits to growth A concept popularized by the 1972 book of the same name (Meadows et al., 1972), which described the consequences of various computer-simulated population and economic growth scenarios in the face of finite resources.
Malthusian Referring to the theory proposed by Thomas Malthus in 1798 that population growth would always eventually outstrip
217
available food resources, condemning the growing population to starvation and disease, and thereby reducing the population.
Millennium Development Goals Eight international development goals that emerged from the United Nations Millennium Summit in 2000 to focus efforts to improve people's well-being, especially in developing countries.
neo-sustainability A new concept of sustainability built on the three critical premises of limits to growth, environmental primacy, and the need to employ a systems approach.
overshoot Exceed the carrying capacity of the environment in relation to population size.
population growth In this chapter, a reference to the ever-increasing human population.
primacy of the environment The concept that without a healthy environment, there can be no human society or functional economic system, and therefore protecting the environment is the first priority.
resilience The “capacity of a system to absorb disturbance; to undergo change and still retain essentially the same function, structure, and feedbacks” (Walker & Salt, 2006, p. 32).
Rio Declaration A product of the United Nations Conference on Environment and Development that took place in Rio de Janeiro in 1992, meant to direct future sustainable global development.
safe operating space for humanity A framework of planetary boundaries within which, humanity can develop without causing environmental change that would unacceptably jeopardize future life on the planet.
scale Geographic size or level, as in local, regional, national, or global.
sustainability The ability of a system to continue functioning without depleting or damaging the things it needs to function.
218
sustainability metrics (or indicators) Standards or statistics for measurement of sustainability. With these metrics a baseline of the sustainability of practices or activities can be ascertained and progress toward sustainability goals can be measured and tracked.
sustainable development Economic development that “meets the needs of the present without compromising the ability of future generations to meet their own needs” (World Commission on Environment and Development, 1987).
Sustainable Development Goals A new set of development goals, created to replace the Millennium Development Goals when they sunset in 2015, addressing similar concerns of health, poverty, education, and equity but in a sustainability framework.
systems thinking An approach to considering a coupled human-natural system that recognizes the interlinkages among the many parts of the system and their ability to change, adapt, and evolve.
tipping point The point at which an object or system is displaced from its state of equilibrium. Often used to describe a climate threshold that, when surpassed, will push the Earth's climate irreversibly out of a stable state.
219
Discussion Questions 1. Was the early thinking of Thomas Malthus at all relevant to
humanity's current predicament? Why or why not?
2. What are the key drivers of our nonsustainability? How are they connected to one another?
3. What happened during the Great Acceleration?
4. Does your city have sustainability metrics? If so, what do you think of them? If not, find a city that does, and comment on whether these metrics would be applicable to your city.
5. Can human intellectual development, ingenuity, and technology overcome limits to growth and concerns about societal collapse?
6. What is systems thinking, and how can it allow us to come to a better understanding of our sustainability challenges?
7. Consider your own lifestyle—where you live, how you travel, what you eat, and so on. Is your lifestyle sustainable? Is it healthy? Could you make changes that would promote both sustainability and health?
8. How do you think public health should incorporate sustainability into its mission?
220
References Adams, W. N. (2006). The future of sustainability: Re-thinking environment and development in the twenty-first century (Report of the IUCN Renowned Thinkers Meeting, 29–31 January 2006). Morges, Switzerland: IUCN.
Borucke, M., Galli, A., Iha, K., Lazarus, E., Mattoon, S., Morales, J. C.,…Wackernagel, M. (2013). The national footprint accounts, 2012 edition (Working Paper). Oakland, CA: Global Footprint Network.
Chung, J. W., & Meltzer, D. O. (2009). Estimate of the carbon footprint of the U.S. health care sector. JAMA, 302(18), 1970–1972.
Cobb, C., Halstead, T., & Rowe, J. (1995). The genuine progress indicator: Summary of data and methodology. Washington, DC: Redefining Progress.
Cobb, C. W. (1989). The Index of Sustainable Economic Welfare. In H. Daly, & J. B. Cobb. (Eds.), For the common good: Redirecting the economy toward community, the environment, and a sustainable future (pp. 401–457). Boston: Beacon Press.
Daly, H. (2013). A further critique of growth economics. Ecological Economics, 88, 20–24.
Diamond, J. (2005). Collapse: How societies choose to fail or succeed. New York: Viking/Penguin.
Ehrlich, P. R. (1968). The population bomb. Cutchogue, NY: Buccaneer Books.
Ehrlich, P. R., & Holdren, J. P. (1971). Impact of population growth. Science, 171, 1212–1217.
Ehrlich, P. R., Kareiva, P. M., & Daily, G. C. (2012). Securing natural capital and expanding equity to rescale civilization. Nature, 486(7401), 68–73.
Energy Information Administration. (2009). U.S. commercial buildings energy intensity (Table 6b). Retrieved from http://www.eia.gov/emeu/efficiency/cbecstrends/cbi_html/cbecs_trends_6b.html
221
Esty, D. C., Levy, M., Srebotnjak, T., & de Sherbinin, A. (2005). 2005 Environmental Sustainability Index: Benchmarking national environmental stewardship. New Haven, CT: Yale Center for Environmental Law & Policy.
Esty, D. C., Levy, M., Srebotnjak, T., de Sherbinin, A., Kim, C. H., & Anderson, B. (2006). Pilot 2006 Environmental Performance Index. New Haven, CT: Yale Center for Environmental Law & Policy.
Farley, H. M., & Smith, Z. A. (2014). Sustainability: If it's everything, is it nothing? New York: Routledge.
Folke, C., Hahn, T., Olsson, P., & Norberg, J. (2005). Adaptive governance of social-ecological systems. Annual Review of Environment and Resources, 30(1), 441–473.
Friel, S., Dangour, A. D., Garnett, T., Lock, K., Chalabi, Z., Roberts, I.,…Haines, A. (2009). Public health benefits of strategies to reduce greenhouse-gas emissions: Food and agriculture. Lancet, 374, 2016–2025.
Hambling, T., Weinstein, P., & Slaney, D. (2011). A review of frameworks for developing environmental health indicators for climate change and health. International Journal of Environmental Research and Public Health, 8(7), 2854–2875.
Hammond, R. A. (2009). Complex systems modeling for obesity research. Preventing Chronic Disease, 6(3), A97.
Hanley, N. (2000). Macroeconomic measures of “sustainability.” Journal of Economic Surveys, 14(1), 1–30.
Hardin, G. (1968). The tragedy of the commons. Science, 162(3859), 1243–1248.
Heinberg, R. (2011). The end of growth: Adapting to our new economic reality. Gabriola Island, BC: New Society.
Holdren, J. P. (2008). Science and technology for sustainable well- being. Science, 319(5862), 424–434.
Homer-Dixon, T. F. (2001). Environment, scarcity, and violence. Princeton, NJ: Princeton University Press.
222
Horton, R., Beaglehole, R., Bonita, R., Raeburn, J., McKee, M., & Wall, S. (2014). From public to planetary health: A manifesto. Lancet, 383(9920), 847.
Institute of Medicine. (2013). Public health linkages with sustainability: A workshop summary. Washington, DC: National Academies Press.
International Union for Conservation of Nature. (1970). Tenth General Assembly, New Delhi, 24 November–1 December 1969: Vol. 2. Proceedings and summary of business. Morges, Switzerland: Author.
International Union for Conservation of Nature. (1980). World conservation strategy: Living resource conservation for sustainable development. Morges, Switzerland: Author.
Loh, J., Randers, J., MacGillivray, A., Kapos, V., Jenkins, M., Groombridge, B., & Cox, N. (1998). Living planet report. Gland, Switzerland: WWF.
Luke, D. A., & Stamatakis, K. A. (2012). Systems science methods in public health: Dynamics, networks, and agents. Annual Review of Public Health, 33, 357–376.
Malthus, T. (1798). An essay on the principle of population. London.
Meadows, D. H. (2008). Thinking in systems: A primer. White River Junction, VT: Chelsea Green.
Meadows, D. H., Meadows, D. L., & Randers, J. (2004). Limits to growth: The 30-year update. White River Junction, VT: Chelsea Green.
Meadows, D. H., Meadows, D. L., Randers, J., & Behrens, W. W., III. (1972). The limits to growth; A report for the Club of Rome's project on the predicament of mankind. Milford, CT: Universe.
Millennium Ecosystem Assessment. (2005). Ecosystems and human well-being: Synthesis. Washington, DC: Island Press.
Myers, S. S., Gaffikin, L., Golden, C. D., Ostfeld, R. S., Redford, K. H., Ricketts, T. H.,…Osofsky, S. A. (2013). Human health impacts of
223
ecosystem alteration. Proceedings of the National Academy of Sciences of the United States of America, 110(47), 18753–18760.
Neff, R. A., Parker, C. L., Kirschenmann, F. L., Tinch, J., & Lawrence, R. S. (2011). Peak oil, food systems, and public health. American Journal of Public Health, 101(9), 1587–1597.
Ostrom, E. (2009). A general framework for analyzing sustainability of social-ecological systems. Science, 325(5939), 419–422.
Owen, D. (2009). Green metropolis: Why living smaller, living closer, and driving less are the keys to sustainability. New York: Riverhead Books.
Padilla, E. (2002). Intergenerational equity and sustainability. Ecological Economics, 41(1), 69–83.
Plummer, R., & Armitage, D. (2007). A resilience-based framework for evaluating adaptive co-management: Linking ecology, economics and society in a complex world. Ecological Economics, 61(1), 62–74.
Pollan, M. (2008). In defense of food: An eater's manifesto. New York: Penguin.
Rees, W. E. (2013). Ecological footprint, concept of. In S. Levin (Ed.), Encyclopedia of biodiversity (Vol. 2, 2nd ed., pp. 701–713). Amsterdam: Elsevier.
Rittel, H.W.J., & Webber, M. M. (1973). Dilemmas in a general theory of planning. Policy Sciences, 4, 155–169.
Rockström, J., Steffen, W., Noone, K., Persson, Å., Chapin, F. S., III, Lambin, E.,…Foley, J. (2009a). Planetary boundaries: Exploring the safe operating space for humanity. Ecology and Society, 14(2), 32.
Rockström, J., Steffen, W., Noone, K., Persson, Å, Chapin, F. S., III, Lambin, E.,…Foley, J. (2009b). A safe operating space for humanity. Nature, 461(7263), 472–475.
Rubin, J. (2012). The end of growth. Toronto: Random House Canada.
Simon, J. (1981). The ultimate resource. Princeton, NJ: Princeton
224
University Press.
South Pacific Applied Geoscience Commission. (2005). Building resilience in SIDS: The Environmental Vulnerability Index. Suva, Fiji: Author.
Steffen, W., Grinevald, J., Crutzen, P., & McNeill, J. (2011). The Anthropocene: Conceptual and historical perspectives. Philosophical Transactions: Series A, Mathematical, Physical, and Engineering Sciences, 369, 842–867.
Steffen, W., Sanderson, R. A., Tyson, P. D., Jäger, J., Matson, P. A., Moore, B., III,…Wasson, R. J. (2004). Global change and the Earth system: A planet under pressure. New York: Springer.
Stott, R. (2012). Contraction and convergence: The best possible solution to the twin problems of climate change and inequity. BMJ, 344.
Summers, J. K., Smith, L. M., Case, J. L., & Linthurst, R. A. (2012). A review of the elements of human well-being with an emphasis on the contribution of ecosystem services. Ambio, 41(4), 327–340.
Sveiby, K. (2009). Aboriginal principles for sustainable development as told in traditional law stories. Sustainable Development, 17(6), 341–356.
United Nations. (1992a). Rio Declaration on Environment and Development. Nairobi: United Nations Environment Programme.
United Nations. (1992b). United Nations Conference on Environment & Development, Rio de Janeiro, Brazil, 3 to 14 June 1992, Agenda 21. Nairobi: Author Retrieved from https://sustainabledevelopment.un.org/content/documents/Agenda21.pdf
United Nations. (2002). Report of the World Summit on Sustainable Development, Johannesburg, South Africa, 26 August– 4 September 2002. New York: Author.
United Nations Commission on Human Settlements. (2001). The state of the world's cities report 2001. Nairobi: UN-Habitat.
United Nations Conference on the Human Environment. (1972). Declaration of the United Nations Conference on the Human
225
Environment. Retrieved from http://www.unep.org/Documents.Multilingual/Default.asp? documentid=97&articleid=1503
United Nations Department of Economic and Social Affairs. (2007). CSD indicators of sustainable development (3rd ed.). New York: Author. Retrieved from www.un.org/esa/sustdev/natlinfo/indicators/guidelines.pdf
United Nations Department of Economic and Social Affairs, Population Division. (2015). World population prospects: The 2015 revision. New York: United Nations.
United Nations Development Programme. (1990). Human development report 1990. New York: Oxford University Press.
United Nations Environment Programme. (2012). GEO 5: Global environment outlook: Environment for the future we want. Nairobi: Author.
U.S. National Research Council, Policy Division, Board on Sustainable Development. (1999). Our common journey: A transition toward sustainability. Washington, DC: National Academies Press.
Walker, B., & Salt, D. (2006). Resilience thinking: Sustaining ecosystems and people in a changing world. Washington, DC: Island Press.
Waltner-Toews, D. (2008). The ecosystem approach: Complexity, uncertainty, and managing for sustainability. New York: Columbia University Press.
Warr, B. S., & Ayres, R. U. (2010). Evidence of causality between the quantity and quality of energy consumption and economic growth. Energy, 35(4), 1688–1693.
Wong, T., & Yuen, B. (Eds.). (2011). Eco-city planning: Policies, practice and design. New York: Springer.
World Commission on Environment and Development. (1987). Report of the World Commission on Environment and Development: Our common future. New York: United Nations.
226
World Health Organization. (1948). Preamble to the Constitution of the World Health Organization. Geneva: Author.
227
For Further Information Books and Articles Brown, L. R. (2011). World on the edge: How to prevent environmental and economic collapse. New York: Norton.
Heinberg, R., & Lerch, D. (Eds.). (2010). The post carbon reader: Managing the 21st century's sustainability crisis. Healdsburg, CA: Watershed Media.
Hopkins, R. (2008). The transition handbook: From oil dependency to local resilience. White River Junction, VT: Chelsea Green.
Nelson, D. R. (2011). Adaptation and resilience: Responding to a changing climate. Wiley Interdisciplinary Reviews. Climate Change, 2(1), 113–120.
Organizations International Institute for Environment and Development (IIED): www.iied.org. Promotes sustainable patterns of world development through collaborative research, policy studies, networking, and knowledge dissemination.
International Institute for Sustainable Development (IISD): www.iisd.ca. Publishes the Earth Negotiations Bulletin: http://www.iisd.ca/enbvol/enb-background.htm
Sustainable Communities Online (formerly Sustainable Communities Network): http://www.sustainable.org. An online clearinghouse for information on sustainability.
Transition Network: https://www.transitionnetwork.org. Promotes the “transition model,” creating initiatives that rebuild resilience and reduce CO2 emissions.
Worldwatch Institute: www.worldwatch.org. Dedicated to fostering the evolution of an environmentally sustainable society —one in which human needs are met in ways that do not threaten the health of the natural environment or the prospects
228
of future generations.
229
Chapter 4 Environmental and Occupational Epidemiology
Kyle Steenland and Christine L. Moe
Dr. Steenland and Dr. Moe report no conflicts of interest related to the authorship of this chapter.
230
Key Concepts Epidemiology is the study of the distribution and determinants of health and disease in human populations.
Environmental epidemiology and occupational epidemiology study the role of exposures in the general environment and in the workplace, respectively. They employ many similar methods.
In environmental and occupational health, epidemiological data complement other kinds of data, such as toxicological data.
There are many kinds of epidemiological study designs. The optimal study design depends on the features of the population being studied, the exposure of interest, the disease of interest, and other factors.
The strongest epidemiological conclusions come from studies that use large populations and accurate and precise measurements of exposure and disease.
Epidemiologists work to achieve results that are free of bias (confounding, selection bias, and information bias).
Epidemiological data can both identify a harmful exposure and quantify the amount of harm due to the exposure. Hence they are invaluable in risk assessment, standard setting and other policymaking, and dispute resolution in environmental and occupational health. Epidemiological data can also determine the degree to which an intervention to change exposure, and improve health outcomes, is effective.
231
A Primer on Epidemiology Epidemiology is the study of the distribution and determinants of health and disease in human populations. Epidemiologists seek to determine whether a given exposure, or set of exposures, causes a certain disease. Obviously, if we can show that an exposure causes disease, we have a chance to intervene and prevent disease occurrence, which is our ultimate goal.
Epidemiology can give us the tools, the techniques of study design and analysis, to determine whether a given exposure is associated with a given disease, and sometimes to determine whether an intervention to change exposure, and improve health outcomes, is effective. How do we judge that an association is causal (a process sometimes called causal inference)?
A general philosophical framework for judging causality, accepted by most epidemiologists, stems from the writings of the philosopher Karl Popper (for a good discussion of causal inference, see Rothman & Greenland, 2008). This framework posits that observations (especially repeated observations) that one event (A) is followed by another (B) enable the epidemiologist to form a hypothesis; that is, a proposition that A causes B. The key to Popperian philosophy is that all hypotheses (or theories of causation) are tentative and may be disproved by further testing. Hypotheses that are tested many times and hold up tend to become accepted as scientific facts (e.g., we now accept that cigarettes cause lung cancer), but over the course of time many accepted hypotheses are overthrown by new scientific insights (e.g., we now know that miasma, or foul air, does not cause cholera).
On the practical level a famous set of criteria set out by Austin Bradford Hill (1965) is commonly used by epidemiologists to judge whether a particular causal hypothesis is plausible, that is, whether the observed association between A and B supports the conclusion that in fact A causes B. Hill set out nine criteria. Only one—the proper temporal relationship—is absolutely required: the exposure must precede the disease. Although it seems this should always be easy to know, sometimes it is not clear; in cross-sectional studies, for example, one generally does not know this. Other
232
commonly used Hill criteria that favor causality are consistency (the association is repeated in many studies), a large effect size (the exposed have much more disease than the nonexposed), a positive dose-response relationship (more exposure causes more disease), and biological plausibility (some biological explanation makes it reasonable that A causes B).
Regulators and risk assessors must conclude from the weight of the epidemiological evidence, applying criteria such as these, whether an association is likely to be causal. A number of agencies, such as the International Agency for Research on Cancer (IARC), the National Toxicology Program (NTP), the Institute of Medicine (IOM) (a part of the National Academies of Sciences, Engineering, and Medicine), and the U.S. Environmental Protection Agency (EPA), regularly review epidemiological evidence and publish summaries in which they evaluate whether associations are likely to be causal. Epidemiology has provided evidence judged as causal for many exposures and diseases, including evidence associating lead with cognitive impairment in children, trihalomethanes (in water) with bladder cancer, particulate air pollution with cardiorespiratory disease, radon gas with cancer, and ergonomic stress with low back pain, to name just a few.
Kinds of Epidemiological Studies Epidemiological studies can be divided into categories that reflect their design.
Descriptive Studies At the simplest level are the descriptive studies, which characterize a disease by factors such as age, sex, time, and geographic region. These studies do not formally test a hypothesis that a specific exposure (or risk factor) is associated with a disease but rather describe patterns in disease occurrence in terms of broad demographic and other variables. These studies are often first steps and may provide clues about factors that cause disease. For example, the fact that malaria occurs mainly in tropical areas provides a clue that a warm climate may play a role in its transmission. The fact that heart disease occurs at a later age in women than men may provide a clue that endogenous estrogen plays a protective role.
233
Descriptive studies can sometimes perform an important role in public policy by determining which diseases are responsible for the greatest burden in different countries. One of the most important efforts in this regard in recent years is the Global Burden of Disease Study (Lim et al., 2012), a large international effort based on using existing data from a variety of sources, to estimate which diseases in different countries were responsible for the most death and disability. This is done with a measure called disability-adjusted life years (DALYs), a sum of years lived with disability and years lost due to premature death. Going further, Lim et al. used existing estimates of the effects of major known risk factors for disease to estimate the relative importance of major known risk factors in causing disability and premature death, using DALYs. The major environmental exposures causing the most burden of disease were indoor and outdoor air pollution, ranked third and ninth, respectively, among all major risk factors. The high number of DALYs from indoor air pollution is due to the common use of biofuel (e.g., wood, dung) for cooking and heating in large parts of the world, as discussed in Chapters 14 and 20, causing not only chronic disease among adults (lung cancer, heart disease) but also pneumonia in children.
Correlational, or Ecological, Studies Descriptive studies are a close cousin to correlational studies, or ecological studies, which examine the correlation between some specific exposure and disease rates, at the level of groups rather than individuals. For example, one can correlate breast cancer rates in countries around the world with degree of socioeconomic development; breast cancer incidence is higher in richer, more urbanized countries. Like descriptive studies, ecological studies often provide clues about possible risk factors for disease, factors that can then be examined further in studies of individuals. Generally, ecological studies are viewed as weaker than studies of individuals, because across a population, individuals with the risk factors are not necessarily the same individuals who contract the disease. As a result, ecological studies are often called hypothesis- generating studies. However, in some instances an ecological design is the design of choice. One example is time series studies of air pollution, in which pollution levels are correlated with disease rates on a day-to-day basis. Such studies have the advantage of
234
looking at a population that is presumably stable over time (eliminating most confounding). The only variables changing on a daily basis are the exposure variable of interest (air pollution levels) and the outcome of interest (daily disease rates), although seasonal variation in temperature also needs to be taken into account.
Etiologic, or Analytical, Studies Etiologic studies, or analytical studies, are generally studies of individuals in which the investigators seek to test a specific hypothesis about exposure and disease: for example, whether pesticide exposure is associated with Parkinson's disease. These studies are often undertaken after descriptive and correlational studies have indicated that they are worth doing: that is, after a plausible hypothesis has emerged that needs to be tested.
Analytical studies can in turn be divided into two types, clinical trials and observational studies.
Clinical Trials Clinical trials, usually called randomized clinical trials, are in a sense the model for rigorous epidemiological studies. They are often done to compare one medication or treatment to another. They are controlled experiments, because they assign treatment (or exposure) randomly to one group and not another. The treated and untreated groups are therefore likely to be comparable with regard to other variables (such age, weight, sex, and education) that might affect the disease outcome; therefore any difference in subsequent disease rates can be assumed to be due to exposure. Both treated and untreated groups are followed prospectively over time.
Randomized clinical trials in medicine are usually used to compare a treatment hypothesized to be beneficial to a conventional treatment or to no treatment. In environmental/occupational epidemiology the “treatment” is the exposure of interest. Clinical trials are generally impractical in this setting for ethical reasons. One cannot ethically expose half of a population to a toxin, such as inhaled silica, and not expose the other half in order to evaluate the effect of exposure. Therefore the epidemiologist interested in studying suspected occupational and environmental toxins often needs to conduct observational studies. However, randomized intervention trials can used to measure the effect of lowering
235
exposures. For example, it is common to use randomized trials to determine whether improving water quality or sanitation can reduce childhood diarrhea (as discussed in Text Box 4.2). Another possibility could be determining whether a new keyboard could reduce carpal tunnel syndrome resulting from typing at a computer (O'Connor, Page, Marshall, & Massy-Westropp, 2012).
Observational Studies Observational studies are uncontrolled studies, or natural experiments, of which the epidemiologist takes advantage. For example, the epidemiologist wants to study the effect of lead on cancer risk, so he or she observes a cohort of lead-exposed workers over time and compares their cancer rates to those of the general population. However, the workers and the general population may differ in some important respects, such as smoking habits or diet, that may in turn affect cancer rates (such variables are called confounders). The epidemiologist may be able to adjust or control for the effects of such confounders, but if he or she cannot, these effects may distort the findings about the effect of exposure on disease. For this reason observational studies are viewed as less definitive than clinical trials.
The three principal designs for observational studies are cohort, case-control, and cross-sectional. Cohort studies start with an exposed group and a nonexposed group, both disease free, and follow them forward in time to observe disease incidence or mortality rates. Disease rates in the exposed and nonexposed groups can be then compared using a rate ratio or a rate difference. The observation period in cohort studies may start in the past and move forward to the present (retrospective studies), or start in the present and move into the future (prospective studies). The former is quicker and usually less expensive. For example, to study lung cancer among welders and nonwelders one can identify a cohort as of 1950 and trace its members' lung cancer mortality until the present. The disadvantage of the retrospective approach is having to depend on historical information about exposure levels and about potential confounders (e.g., smoking habits). Although prospective studies take a long time and are often expensive, they are more appropriate when one wants to measure exposure levels and confounding variables at baseline, or when
236
biological samples such as blood tests are required. Prospective studies may also be needed to study diseases that are difficult to ascertain in retrospect, such as spontaneous abortions (whose occurrence and date of occurrence may be difficult to remember accurately). Cohort studies can consider disease events per person (cumulative incidence, or risk) or disease events per person- time (rates, such as incidence rate or mortality rate). The former are appropriate for short follow-up periods and fixed cohorts, in which everyone can be followed for the whole follow-up period. The latter are appropriate for long follow-up periods and dynamic cohorts, in which individuals may enter follow-up at different times and be lost to follow-up at any time and are therefore followed for different periods of time. Cohort studies are good for rare exposures and common diseases, because one begins with assembling an exposed group and hence can readily assemble an adequate number of exposed subjects (e.g., welders); conversely, when the disease is rare, a very large number of subjects may need to be assembled to yield an appreciable number of cases. (Text Box 4.1 presents an example of a cohort study.)
237
Text Box 4.1 Example of a Community Cohort Study Perfluorooctanoic acid (PFOA, also known as C8), a synthetic chemical created during World War II, is an 8-carbon fluorocarbon useful for the polymerization of longer chain fluorocarbons. It is present at background levels of about 4 ng/ml in the blood of virtually everyone in the U.S. population, as well as everyone in other industrialized countries, although the exact route of exposure is not clearly known. PFOA has been used in making commercial products such as Teflon, Scotchgard, and Gore-Tex, although such use has been cut back or eliminated since the mid-2000s. PFOA causes tumors in animals (liver, testicular, and pancreatic) and causes neonatal death in mice. PFOA biopersists indefinitely and has a half-life in humans of about 3.5 years, so it is likely to be an environmental contaminant for a long time to come.
Operations at a Dupont plant making Teflon in Parkersburg, West Virginia, resulted in PFOA contamination of drinking water in nearby parts of West Virginia and Ohio (Figure 4.1). Approximately 70,000 residents living in six water districts near the plant had their blood levels measured in 2005 and 2006 as part of the settlement of a class action lawsuit against Dupont; blood levels averaged 80 ng/ml (with a very wide range for which the median was 28 ng/ml). In addition, approximately 1,000 workers at the chemical plant had been measured in 2004 and had displayed blood levels on the order of 500 ng/ml at that time.
238
Figure 4.1 Area of PFOA Contamination
As part of the class action settlement, the C8 Science Panel was created. The three-person panel was charged with determining whether PFOA was “probably linked” to any disease in the mid-Ohio valley. The C8 Science Panel was guaranteed independence from either side in the lawsuit. A finding of a probable link would trigger court-ordered surveillance for the diseases implicated. Note that the
239
probable link standard is a lower bar than epidemiologists usually use to determine causality; the panel simply had to decide whether PFOA was more probably than not associated with a given disease. The panel was made up of three persons so that there would be no possibility of a tie vote.
The panel embarked on a six-year epidemiological effort consisting of eleven studies with a cost of $35 million, far more than is available in typical federal grant funding by the U.S. National Institutes of Health; this funding was supplied by Dupont but was administered by the West Virginia court.
One of these studies was a cohort study of 32,000 adults, a subset of the 70,000 people tested in 2005 and 2006. Among these 32,000 were approximately 3,000 workers who had worked at the Dupont plant.
This cohort had many advantages for an epidemiological study. It was a very large cohort, enabling study of relatively rare diseases. Most of these subjects had been tested in the mid-2000s and their PFOA blood levels at that time were known. Some cohort members lived far from the plant and had low PFOA levels, whereas those close to the plant had very high levels. This large exposure contrast was ideal for an epidemiological approach, enabling a determination of whether higher exposure was associated with higher disease. The cohort was relatively homogeneous, living within a confined region, with limited potential for the confounding that can occur when studying diverse widespread populations. Furthermore, data were available to study the cohort members' exposure back in time, critical for estimating the effect of exposure on chronic disease, which might occur many years after exposure. Interviews with the cohort were likely to be possible, enabling study of disease incidence, a stronger end point than mortality, as many serious diseases are not necessarily fatal. (However, the C8 Science Panel also assessed mortality in the cohort, using the National Death Index.)
Data on plant emissions of PFOA over time were available. The C8 Science Panel used a fate-transport model to estimate the spread of PFOA into the groundwater system,
240
which was the source of the contaminated public drinking water. The fate-transport model estimated how far the PFOA traveled in the air before settling to the ground, and how much went into the Ohio River directly. Then the model estimated how long it took the PFOA to get into the groundwater and estimated groundwater levels over time. Finally, a second model estimated how much PFOA a study participant might have absorbed from drinking water, and what his or her likely serum levels were in any given year. These models were linked with residential history so that the C8 Science Panel was able to estimate the PFOA serum levels of all study participants for each year from 1950 through 2011. The additional exposure of workers was also modeled, using over 2,000 serum PFOA estimates available from Dupont from the 1970s to 2004. Overall the model performed well. The correlation between modeled exposures and PFOA serum levels measured in 2005 and 2006 was 0.71 (Winquist, Lally, Shin, & Steenland, 2013).
The C8 Science Panel conducted interviews with the 32,000- person cohort (representing 80% of the target adult population) from 2008 to 2011, in which residential and medical history was collected. Self-reported medical history for serious chronic disease was then verified by medical histories from doctors and hospitals. Approximately 60% of participants reported a chronic disease for which medical records were sought. Approximately 75% of these people consented to medical record review; among those who consented, at least one record was obtained for 92% of them, and about 77% of these records validated the self-report. The C8 Science Panel then conducted a cohort analysis of verified medical disease for fifty-five different diseases. The cohort study consisted of a retrospective cohort incidence follow-up, internal to the cohort, in which incidence rates of disease were calculated for different levels of cumulative serum levels (summed across all years since birth). This study was unusual in having an internal estimate of dose rather than an external estimate of exposure.
Of the fifty-five diseases studied, the C8 Science Panel concluded that six were “probably linked” to PFOA (kidney
241
cancer, testicular cancer, ulcerative colitis, thyroid disease, high cholesterol, and pregnancy-induced hypertension). Of these, only one (testicular cancer) had been implicated in animal studies. Ulcerative colitis, an autoimmune disease, had perhaps the strongest evidence. Based on 151 observed cases, rate ratios increased steadily by quartile of cumulative PFOA serum level, from 1.00 (the lowest quartile referent group), to 1.76 (1.04, 2.99), 2.63 (1.56, 4.43), and 2.86 (1.65, 4.96), with a p value for a positive trend of <0.0001 (Steenland, Zhao, Winquist, & Parks, 2013).
The PFOA studies by the C8 Science Panel were unusual for a class action suit. In the United States, such suits usually result in negotiated settlements between the community and polluter, with no scientific study to determine whether the community pollution actually caused disease (Steenland, Savitz, & Fletcher, 2014).
Case-control studies use an opposite approach to that of cohort studies. Here, the epidemiologist begins with diseased and nondiseased groups and looks backward in time. For example, bladder cancer patients (cases) and people free of bladder cancer (controls) can be asked about their past consumption of water treated with chlorine, which results in trihalomethane formation (trihalomethanes are suspected bladder carcinogens). The investigator determines the odds of exposure in each group and compares them—if a is the number exposed, and b is the number nonexposed, then a / b is the odds of exposure. If the odds of exposure are higher among the cases than among the controls, then one judges that the exposure is associated with the disease. The usual measure of effect is the odds ratio. Case-control studies are more subject to bias than cohort studies because it is sometimes difficult to choose cases and controls who are representative of the overall diseased and nondiseased populations (this is particularly true for the controls) and because it is often difficult to measure past exposure accurately. Recall bias, for example, can occur if cases tend to remember more about past exposures than controls do. However, if cases and controls are chosen properly, a case- control study should give the same answer as would a cohort study about the exposure-disease relationship.
242
Case-control studies are useful for rare diseases and common exposures, the opposite of cohort studies. Case-control studies can be carried out in the general population or in hospitals or can be nested within cohort studies.
Cross-sectional studies, or prevalence studies, tend to measure exposure and disease at the same time. For example, lead exposure in relation to performance on tests of intelligence in children may be studied by measuring lead in blood at the time of the neurological testing, or cadmium levels in the urine of smelter workers can be measured at the same time as small protein in the urine (a measure of kidney damage). Cross-sectional studies are often done when the outcome of interest is subclinical or asymptomatic disease. In the workplace, cross-sectional studies will miss symptomatic cases if workers with the disease have left work.
A typical problem with cross-sectional studies is determining whether exposure in fact preceded the health outcome. For example, in the case of the smelter workers, if those with higher levels of cadmium in the urine were also excreting more small protein, it would not be known whether the protein excretion preceded or followed the presence of cadmium in the urine. The same would be true for neurological tests in relation to lead levels in children. Interpretation of positive findings in the latter study would be made even more difficult by the fact that socioeconomic status (SES) is an important confounder that is difficult to control; children of low SES have higher lead exposure and perform worse on neuropsychological tests. Cross-sectional studies tend to be seen as a somewhat weaker design than cohort and case-control studies, although they are often the only possible design and can provide valid results, which can then be confirmed in cohort or case-control studies.
Bias Bias refers to the distortion of the true relationship between exposure and disease. The most important sources of bias are selection bias, confounding, and information bias.
Selection bias occurs when the relationship between exposure and disease in the study population is not representative of the true relation between exposure and disease in the general population
243
because the investigator has selected the study population in a nonrepresentative way. For example, in a study of ethylene oxide (a sterilant gas) and breast cancer, suppose only 20% of the individuals in the target population answer a questionnaire about breast cancer occurrence. These self-selected study participants may differ from the rest of the target population: they may, for example, have more breast cancer (motivating them to participate) and higher exposures (making them concerned that exposure may have caused their disease and again motivating participation). This would result in demonstrating an association between exposure and disease that might not have been found if the entire target population had participated. This kind of bias generally cannot be corrected. In fact, one cannot even be sure of the direction of such a bias based on the 20% of the population studied, because the rate of occurrence of breast cancer in the remaining 80% of subjects cannot be known. The study conclusions will thus be suspect. The healthy worker effect is another kind of selection bias, occurring when workers are compared to the general population. Workers are healthier than the general population, so study results will be biased against finding adverse health effects among the workers. This is another example of a selection bias that cannot be readily fixed at the analysis stage.
Confounding refers to the distortion of the exposure-disease relationship by a third variable that is associated both with exposure and with disease. For example, in the study of welders in relation to lung cancer, if the welders smoke more than nonwelders do, then smoking (strongly associated with lung cancer) would act as a confounder. Adjustment for the effect of smoking can be made during analysis by stratification, separating the groups into smokers and nonsmokers, determining the exposure-disease relationship in each group, and then forming a weighted average of the exposure-disease relationship across both groups. Adjustment can also be accomplished using one of several statistical approaches that involve multivariate analysis. However, this can be done only when adequate data on smoking have been collected in both exposed and nonexposed groups.
The welding–lung cancer relationship might also differ between smokers and nonsmokers. One could imagine, for example, that only smokers show a welding effect, because smoking injures the
244
lung epithelium, permitting a carcinogenic effect from the metal fumes. This situation is called effect modification because the third variable (smoking) modifies the effect of the exposure variable of interest (welding). Effect modification is different from confounding. In this circumstance the investigator cannot calculate the weighted average of exposure-disease associations across both strata of the third variable and instead must report results for each stratum separately. No adjustment for confounding is possible, as no weighted average of exposure effect across levels of the confounder should be conducted.
Finally, once the study population has been selected, information bias can occur when information obtained about either exposure or disease is incorrect. One of the main sources of information bias in epidemiological studies is mismeasurement or misclassification of exposure. When exposure is measured incorrectly (for a continuous exposure variable) or misclassified (for a categorical exposure variable), one can expect the exposure- disease association to be distorted. When exposure is measured or classified equally poorly for both diseased and nondiseased groups (called nondifferential error or misclassification), then the effect is usually to bias the finding toward the null hypothesis (toward finding no exposure-disease association). Conversely, if the mismeasurement or misclassification is greater for either the diseased or the nondiseased, bias away from the null can occur. This problem is typical of retrospective exposure assessment in case- control studies, when cases may recall past exposures more often than controls do (recall bias), biasing the study toward finding an association (away from the null).
Data Analysis Methods of analysis in epidemiology typically depend on whether the exposure variable and the disease variable are continuous variables or categorical variables. Most of the approaches described previously consider disease to be a categorical (yes/no) variable (often called a dichotomous variable). This is typically true of a specific disease: you either get the disease or you don't. However, many studies consider a continuous disease variable, such as blood pressure or the concentration of small protein in the urine. In some instances these variables can be transformed into
245
categorical variables (e.g., high blood pressure might be defined as a systolic pressure greater than 140), especially when there are medical guidelines for such cut points. Exposure variables may also be continuous (e.g., cadmium in the urine) or categorical (welder or nonwelder).
When both exposure and disease variables are dichotomous, then one usually calculates the measures referred to previously, such as a rate ratio or an odds ratio. These categorical analyses may be stratified to control for confounding, as indicated earlier. However, when both the disease and the exposure are continuous variables (e.g., blood pressure as the outcome, and age and weight as predictors), typically a regression analysis (e.g., linear regression) is conducted in which the outcome is a measure associated with disease and the predictors include exposure and any other confounder variables about which the investigator has data. One seeks to know whether the exposure is a significant predictor of disease, as reflected by a regression coefficient for the exposure variable that differs significantly from the null value of zero.
In addition, mixtures of these situations can arise. A linear regression analysis for a continuous outcome may also be calculated with the exposure variable categorized in the regression. Furthermore, even when the disease variable is dichotomous, one can employ a type of regression called logistic regression, in which the measure of interest remains the odds ratio and either categorical or continuous variables may be included among the predictors.
One important feature of any data analysis is the precision of the estimate of effect (e.g., the rate ratio, the odds ratio, or the regression coefficient for the exposure variable). Large sample sizes confer greater statistical power to detect associations, and lead to high precision. Precision is often presented by a confidence interval, which represents a range of plausible values for the measure of effect. For example, an odds ratio in a case- control study of bladder cancer and water supply (public water versus private wells) might be 2.00, indicating that those who use public water (more trihalomethanes) versus private wells (fewer trihalomethanes) have a doubling of bladder cancer risk. If the study is based on 20 cases and 20 controls, it will have low precision and the 95% confidence interval for the odds ratio of 2.00 might be
246
0.50 to 8.00, indicating a wide range for plausible values. If the study were based on 2,000 cases and 2,000 controls, the 95% confidence interval might be 1.90 to 2.30, indicating a narrow range of plausible values. The precision of the estimate is a reflection of what is called random error, the error likely to result from choosing a sample of the total population of interest (in this case, all users of water).
Precision is related to statistical significance. Statistically significant usually means that the estimate of effect is different from the null value and that the difference is unlikely to have occurred by chance. Typically, a finding is judged to be statistically significant when the difference from the null value has less than a 1 in 20 likelihood of having occurred by chance (usually stated as a p value of less than .05). A 95% confidence interval that excludes the null value (e.g., the null value of 1.00 for an odds ratio, which indicates no difference in risk of disease between exposed and nonexposed), corresponds to a p value of less than .05. Epidemiologists now prefer to express the precision of study results with confidence intervals rather than with p values and tests of statistical significance, partly because a range of plausible values is more informative than a single test of statistical significance.
Drawing Epidemiologic Conclusions Two dimensions of epidemiologic results are important in drawing conclusions. Validity (sometimes called internal validity) refers to whether the results of a study are “true”—whether the investigators reached correct conclusions about the population studied. Validity depends on having used appropriate study methods and data analysis. Generalizability (sometimes called external validity) is the extent to which the conclusions of a study in one population can be applied to other populations. The results of a study of U.S. university student volunteers, for instance, may not be applicable to a population of retirees or to a rural population in a developing nation with different biological and social circumstances.
247
Environmental and Occupational Epidemiology Environmental and occupational epidemiology uses few truly unique epidemiological techniques and is simply an area of epidemiology defined by the exposures it studies.
Environmental epidemiology concerns environmental agents to which large numbers of people are exposed involuntarily. This area of concern usually excludes voluntary exposures such as alcohol, cigarettes, and medications. However, it usually does include environmental (“secondhand”) tobacco smoke and infectious or chemical agents in water supplies. Although this definition is a bit arbitrary, and although environmental epidemiology thus defined may overlap with other areas of epidemiology, nonetheless it is useful. Some examples of environmental agents (and their associated outcomes) are radon in homes in relation to lung cancer, environmental tobacco smoke in relation to lung cancer, arsenic in water in relation to low birth weight, chlorination by-products in water supplies in relation to bladder cancer, pesticide residues in food in relation to cancer, particulate matter in the air in relation to cardiovascular disease, and lead in soil in relation to neurological deficits. On the positive side, access to parks and physical activity may be associated with better health, interventions to limit secondhand smoke may lower the risk of cardiovascular disease, and use of bicycle helmets may decrease head trauma. Many environmental exposures are low level and relatively homogeneous across large numbers of people, making them difficult to study. The differences in risk between those with more exposure and those with less exposure are usually small and therefore hard to detect reliably, often requiring large sample sizes.
Environmental exposures can be thought of as contributing either to epidemics or to endemic diseases. Epidemics are unusual outbreaks of disease clearly above a normal level and often caused by known agents, although sometimes the agent is initially unknown. For example, the cholera outbreaks in Peru in 1991 had a known cause. However, causes of other recent disease outbreaks have not been initially known, including the cause of the 1981
248
outbreak of neuropathy in Madrid (eventually found to be due to an oil contaminant), of the 1993 gastrointestinal illness outbreak in Milwaukee (due to cryptosporidium), and of the 1976 pneumonia outbreak in Philadelphia (due to Legionnaires' disease). In contrast, endemic diseases exist at constant, low (or background) levels and may or may not have an environmental cause. Examples are lung cancer and the radon in homes, cardiovascular disease and low-level air pollution, and neurological deficits in children and lead in the environment. Other examples are motor vehicle deaths and the varied factors contributing to them, and obesity related to sugar in foods. Possible associations between low-level environmental agents and background levels of disease are more and more often the subject of environmental epidemiology, especially in developed countries, and these associations are difficult to detect.
Occupational epidemiology is the epidemiological study of illness or injury associated with workplace exposures. Examples include the association of stressful repetitive motion and carpal tunnel syndrome, welding and lung cancer, silica exposure and kidney disease, and shift work and breast cancer. Occupational epidemiology often involves relatively high exposures in relatively small numbers of people, often geographically isolated at a worksite. This context makes for easier studies from a scientific standpoint (the workplace exposure is a natural experiment). However, workplace studies also involve vested economic interests and are sometimes politically controversial. It may be difficult to gain access to the workers or their worksite, for example.
Historically, occupational studies were carried out in the context of very high exposures. Early studies revealed silicosis and asbestosis resulting from silica and asbestos exposure, respectively. Occupational studies have also been responsible for the discovery of many carcinogens, including asbestos, aniline dyes, silica, nickel, cadmium, arsenic, dioxin, beryllium, acid mists, radon gas, and diesel fumes (Rom & Markowitz, 2006). Most of these agents occur in the general environment as well, where people are exposed at much lower levels. Whether associations seen in the workplace also occur in the general environment may be a difficult question. However, diesel fumes in ambient air, radon in homes, and arsenic in water are known to be environmental carcinogens.
Today, workplace exposures to suspected toxins are much lower
249
than in the past, at least in industrialized countries, and they are less often the focus of occupational epidemiology. Occupational studies today often involve issues more difficult to study, such as possible relationships between job stress and heart disease, lifting and back strain, or shift work and breast cancer.
Understanding Clusters One aspect of both environmental and occupational epidemiology that deserves special mention is the occurrence of clusters. A cluster is an apparently elevated number of cases of disease in a limited area over a limited period of time, suggesting some common cause (Rothman, 1990); typically the number of cases in the cluster is small, on the order of ten or twenty rather than hundreds. Clusters typically come to the attention of public health authorities, who must first determine whether a cluster in fact represents an unusually high occurrence of disease. This is more difficult than it might seem, particularly for environmental clusters whose geographic and temporal boundaries are not clear. For example, three cases of childhood leukemia on the same street might be unusual if the denominator at risk is taken to be all the children on that street, but might not appear excessive if the boundary is the local neighborhood composed of a dozen streets. Assuming that investigators can determine that a cluster does in fact represent a high rate of disease, the next step is to determine whether there is a common cause. (Some clusters will occur simply as random events.) A common cause is more likely when the cases of disease are restricted to a specific diagnosis, such as childhood leukemia, rather than a general category, such as childhood cancer; cancer includes many diseases with many different causes. But even when the cases represent a narrow and specific diagnosis, they will often have many possible causes, and an epidemiological study will often not be able to pinpoint a specific cause. One reason for this is that such a study is typically restricted to a small number of cases (often using a case- control design), and the power to detect an association is low, even when that association is quite strong. For the reasons given above, most investigations of clusters do not results in identification of a common cause (Caldwell, 1990).
Nonetheless, despite the long odds, cluster investigations have from time to time provided important clues that have later been
250
confirmed in larger studies. Among the famous clusters that have led to discovery of new associations are the 1976 cluster of Legionnaires' disease cases in a hotel in Philadelphia (environmental), the clusters of asthma cases in Barcelona in the early 1980s that were eventually tied to soybean dust (environmental), the 1973 cluster of angiosarcoma cases among workers in a single vinyl chloride plant (occupational), and the 1977 cluster of infertility in a plant making a pesticide called dibromochloropropane (DBCP) (occupational). Studies of clusters have more chance of leading to the discovery of a specific cause when the disease in question is extremely rare. Occupational clusters have somewhat more of a chance than environmental clusters do of representing a common cause because they have a natural boundary (the worksite) and therefore avoid the boundary problem inherent in environmental clusters. Recent examples of such occupational clusters include the occurrence of a rare gall bladder tumor among printers using dichloroethane in Japan (Kumagai, Kurumatani, Arimoto, & Ichihara, 2013), and the occurrence of a rare lung disease (bronchiolitis obliterans) among workers at a microwave popcorn plant (Kreiss et al., 2002).
Measuring Exposure Measuring exposure with as much accuracy as possible is key to valid epidemiological studies (for a fuller discussion see Chapter 8). Accurate exposure assessment is essential to detecting and quantifying a dose-response relationship, for example, which is one of the key elements supporting a causal relationship. Mismeasured exposure (as a continuous variable) usually leads to flattening, or attenuating, a true dose-response. Misclassification of dichotomous exposure status (exposed versus nonexposed) can severely bias results toward the null.
In cross-sectional or prospective studies current exposure can be measured more or less easily, depending on the agent of interest. However, it is often difficult to assess exposure accurately when exposure must be estimated in the past, as in case-control studies, in retrospective cohort studies, and in cross-sectional studies of the impact of past exposures on current outcomes.
In case-control studies of bladder cancer and drinking water, for example, subjects may be trying to remember their pattern of
251
drinking-water consumption over the past fifty years. In cross- sectional studies of lead and neurological deficits in children, one may wish not only to measure current lead levels via the blood but also to assess prior exposure to lead via its measurement in bone. In retrospective cohort studies, investigators may be estimating past silica exposure for workers in a specific plant. As can be seen in these examples, in some instances investigators attempt to measure external exposure (water drinking patterns, silica in workers' breathing zone), and in others they seek a biomarker of internal exposures (blood and bone lead). We discuss both these scenarios.
First, let us consider more thoroughly the example of assessment of past exposure to silica among workers in a retrospective cohort study. Suppose there are some existing silica exposure measurements made during the past twenty years for some workers in some jobs. Such a relatively short record is typically the case, as exposure measurements were not often made until somewhat recently. However, the cohort may have been employed over the past forty or fifty years, and because investigators seek to conduct an exposure-response analysis, they require an estimate of past exposure for all workers across all jobs at all points in time. This may not be possible at all in many retrospective cohort studies. However, in some instances it may be possible to construct a job- exposure matrix (JEM), which is simply a cross classification of jobs and exposure levels across time. This can be done if industrial hygienists can extrapolate beyond more recent exposure data to make a good guess about exposure further back in time, based on process changes at the plant. Typically plants were dirtier further back in time. A JEM will enable an estimate of cumulative exposure to silica for each worker. Cumulative exposure is often the measure of interest for chronic disease outcomes such as silicosis, lung cancer, or kidney disease.
An alternative to estimating external exposure is to use a biomarker of exposure. Examples of such biomarkers are dioxin in blood, cotinine (a metabolite of nicotine) in blood, and lead in bone. Such biomarkers can be useful because they measure internal dose rather than external exposure. They may therefore take into account variation in absorption and metabolism of the external dose, possibly providing a more accurate estimate of the biologically relevant dose that can cause disease. However, there are many
252
problems that may make a measure of the internal dose less desirable than a measure of the external exposure, including wide individual variation, difficulty in obtaining accurate laboratory measurements of the biomarker, and possibly choosing the wrong biomarker in a metabolic pathway that features several candidate toxins. Perhaps more important in the case of retrospective exposure assessment, few biomarkers of exposure persist long enough to be useful for such a study.
For example, in a case-control study of Parkinson's disease in which serum from the cases is available, it would be ideal to measure past exposure to pesticides (organophosphates and organochlorines) as well as other organochlorines, such as polychlorinated biphenyls (PCBs). Generally, some time must pass between the first exposure and subsequent development of symptomatic chronic disease (the latency period), so the epidemiologist is often interested in past not recent exposures. However, organophosphate pesticides, thought to play a role in chronic neurological disease partly because of their acute effects on the nervous system, are rapidly metabolized. Therefore blood levels of these compounds cannot be used to measure exposure beyond a few days in the past. Organochlorine pesticides and PCBs are also of interest because they have been shown to decrease dopamine levels in the brain in animal studies, and dopamine loss is the hallmark of Parkinson's disease. Organochlorines have half-lives that are measured in years. Some may be measured in the serum long after exposure has ceased, and therefore may be more useful in detecting exposures above background levels.
Another important example is lead, often measured in the blood, where it reflects exposure over the previous two or three months. However, lead also accumulates in the bone where it provides a good indicator of cumulative exposure over time, even long after exposure ceases. This has been important in measuring the association between lead and neurological deficits in children. This association has been controversial for several reasons. Most studies are cross-sectional, and current blood lead levels may not reflect past exposure. Lead exposure and SES are closely related, and SES in turn is closely related to performance on cognitive tests. Lead in teeth shed by children has been useful in establishing prior lead exposure and can act as a measure of the level of exposure in groups
253
that are identical in SES. Similarly, bone lead measured by radiographic techniques has been important in studies of past lead exposure in adults in relation to blood pressure and other long-term effects of lead. (See Text Box 4.2 for an example of the use of environmental epidemiology.)
254
Text Box 4.2 An Interview Study to Improve Sanitation Few environmental health problems are more global and fundamental than the provision of safe water and sanitation. Although the need for safe water has typically received more attention, lack of access to improved sanitation is far more widespread than lack of access to improved water (an estimated 2.5 billion people, or more than one third of the global population, lack improved sanitation, compared to an estimated 700 million lacking improved water) (World Health Organization and UNICEF, 2014). This highlights the importance of sanitation. Indeed, the Millennium Development Goals included halving the proportion of the world's population without access to improved water and sanitation by 2015—a goal that was met for water in 2012 but was not achieved for sanitation by the target date of 2015. Water and sanitation are discussed in detail in Chapter 16. Here, we consider some of the issues environmental epidemiologists confront when studying sanitation.
Studies of Sanitation and Health Epidemiological studies of sanitation are challenging for a number of reasons. Sanitation involves very private behavior that is difficult to assess and to change. There are multiple health outcomes (diarrhea, intestinal helminth infections, schistosomiasis, trachoma, stunting, environmental enteropathy) that may be affected by sanitation but that are also influenced by other, confounding factors. When children are the focus of study, caregivers are asked to recall episodes of pediatric diarrhea; these data are notoriously difficult to interpret, especially in low-income settings where caregivers may be looking after many young children and juggling many responsibilities (Arnold et al., 2013). Most epidemiological studies of sanitation are observational rather than randomized controlled trials, and these studies confront many confounders and sources of bias. The few intervention
255
trials that have been conducted have had serious methodological weaknesses.
Intervention studies usually take one of two approaches. The first is to compare rates of health outcomes before and after a sanitation intervention. The second is to compare health outcomes in households (or communities) with a sanitation intervention to outcomes in households (or communities) without the intervention. While household-level sanitation interventions can sometimes be randomized, with control households receiving the intervention later, it is generally not possible to randomize the implementation of urban sanitation projects, for both technical and political reasons.
In addition, owing to people's personal and cultural preferences, providing a sanitation intervention doesn't guarantee that everybody will use it (Barnard et al., 2013). When assessing “exposure” to improved sanitation, investigators need to consider both the extent of sanitation coverage in a community and the actual use of the sanitation intervention. Some studies have only measured access to improved sanitation (such as the presence of a household toilet or latrine). More recent studies have attempted to document use of latrines by noting the presence of feces or anal cleansing materials or by using electronic devices to monitor movement within the latrine structure (Clasen et al., 2012).
To make matters more complex, it has recently been recognized that the benefits of improved sanitation may extend beyond the intervention households to neighboring households as well, because better containment of fecal contamination at the household level ultimately reduces communal exposure to fecal pathogens in the environment (Root, 2001). The greater the proportion of households using improved sanitation, the greater the subsequent reduction in excreta entering the public environment, and thus the greater the likelihood of a health benefit to the whole community. This is similar to the concept of increasing herd immunity (through providing vaccinations) or reducing exposure to secondhand smoke (through instituting smoking bans). Failure to account for the effect of communal exposure can
256
lead to an underestimate of the impact of a sanitation intervention.
Barreto et al. (2007) reported a landmark study of the impact of a large-scale, urban sanitation intervention on child health. The city of Salvador (population approximately 2.5 million) is in the poorest part of Brazil. In 1996, this city embarked on a citywide sewerage intervention that took eight years to complete. Over 2,000 km of sewer pipes were installed, and more than 300,000 households were connected to the sewer network, raising the proportion of the population connected to the sewer system from 26% to 80%. Barreto and colleagues conducted two longitudinal studies, at the beginning of the intervention (1997–1998) and at its end (2003–2004), to assess the health impacts.
Twenty-four study areas (each consisting of about 600 households) were randomly selected from low-income parts of the city that initially lacked sewerage. In the preintervention phase, a cohort of 841 children (0–36 months of age at the time of recruitment) was recruited from randomly selected households in these study areas, and was followed for up to eight months. In the postintervention phase, 1,007 children in the same age range were recruited from the same twenty-four study areas and followed for up to eight months. For both cohorts, baseline data collection from each study household included information on socioeconomic status, living and sanitation conditions, child health, and anthropometric measurements. Each study household was visited twice weekly to monitor child health and the hygiene behavior of child and caregiver and to collect a fecal specimen from the child for pathogen testing. The health outcome studied was “longitudinal prevalence” of diarrhea, defined as the ratio of days with diarrhea to total days observed.
In the data analysis a series of models took into account various confounding and mediating variables. The potential confounders were factors that could affect the risk of diarrhea but were independent of the sanitation intervention, such as socioeconomic status, child age and sex, breastfeeding, and housing conditions. The potential
257
mediators were those that were related to the sanitation intervention but could also change independently of the intervention, such as open sewage near the house, presence of an indoor toilet, and excreta disposal practices.
The investigators found that the sewerage intervention was associated with an overall 22% reduction in diarrhea prevalence, after adjusting for baseline sewer coverage and potential confounding variables. Diarrhea reduction was greater (43%) in areas with higher baseline diarrhea rates. Comparison of statistical models with different sets of variables indicated that the diarrhea reduction could be completely explained by the increased sewer coverage, and not by factors such as hygiene behavior or the presence of an indoor toilet. These latter variables changed very little between the preintervention and postintervention assessments, suggesting that they were either not affected by the sanitation program or had little effect on the risk of diarrhea in this context.
Discussion Large-scale sanitation interventions are complex, usually occur over a long period of time, and may affect many environmental and sociobehavioral factors. This large intervention took eight years to complete, so it was not possible to study the impact of the intervention on the original cohort of young children. Instead, after the intervention, the investigators recruited a second cohort of children in the same age range and from the same sentinel areas in order to compare health outcomes. For both cohorts the investigators needed a follow-up time long enough to collect numbers of diarrhea days sufficient for comparing the estimates of diarrhea prevalence in the two cohorts with adequate statistical power while controlling for potential confounders. The study team had also to ensure that both follow-up periods covered the same time of year, to account for potential seasonality of diarrheal disease. Frequent household visits helped minimize difficulty with recalling and reporting diarrheal episodes.
Over eight years, infrastructure and economic conditions can
258
change. The investigators had no control over where the sanitation intervention was built, and the study was not randomized. However, the investigators did examine the relationship between the intervention and the health outcome in a range of neighborhoods with varying degrees of sanitation coverage, and they observed that the before-after prevalence ratios ranged from 0.15 to 3.02. The sophisticated analytical strategy considered a large set of individual and ecological potential confounders.
At the household level, introduction of a toilet or latrine may reduce fecal contamination in the immediate household area. However, if this on-site sanitation does not safely contain or treat the fecal waste, there is still a potential for fecal contamination to move into the surrounding neighborhood and pose a health risk to others. Barreto et al. (2007) explain that, in Brazil, indoor toilets are often installed without any connection to a sewer. This study demonstrated the health impact of a sewerage intervention that did not change household sanitation access or hygienic behavior. The observed diarrhea reduction was attributed to a reduction of fecal contamination in the public domain, but this was not directly measured.
The magnitude of reduction of diarrhea prevalence reported here is similar to the pooled estimates of effect from meta- analyses of other sanitation studies (e.g., Esrey, Potash, Roberts, & Shiff, 1991; Fewtrell et al., 2005; Waddington et al., 2009). Replication is important in confirming epidemiological results.
259
Epidemiology and Risk Assessment The results of occupational and environmental epidemiological studies can affect public health by alerting policymakers to new hazards and possibly by triggering regulations about permissible levels of exposure. Sometimes a single large and definitive study is deemed sufficient to change public policy, but in other instances regulators want to see a study's results replicated (recall Hill's criterion of consistency). When a number of studies point in the same direction, public authorities are more likely to act.
In the past, qualitative literature reviews were used to summarize the evidence across many studies. Today, one is more likely to see a meta-analysis that provides a weighted average of quantitative results across studies. Originally used with clinical trials, meta- analyses have been used extensively in the last decade with observational studies. They can combine results from different study designs, such as rate ratios from cohort studies and odds ratios from case-control studies. For example, a meta-analysis may give a weighted average of lung cancer rate ratios or odds ratios across many studies of silica and lung cancer (more specifically, the logarithms of the ratio measures are used, and then results are converted back to the original scale at the end). The weights are typically the inverse of the variance of each study's result; this means that the largest studies with the narrowest confidence intervals, those that are estimated more precisely, will have the lowest variance and be accorded the most weight.
Meta-analyses do not require access to the original study data; they can use results from the published literature. Meta-analyses are most often performed to determine a common ratio measure of disease rates (e.g., a rate ratio) in the exposed versus the nonexposed. However, they may also be done to determine a common exposure-response coefficient across a number of exposure-response analyses.
Exposure-response analyses are of particular interest to public health authorities who seek to determine a permissible exposure level for the public or for workers. The determination of a permissible exposure level is based on risk assessment (and is
260
discussed in detail in Chapter 27). Risk assessment may be based on animal data or human data. The former requires extrapolation from animals to humans and hence involves a considerable amount of uncertainty. For this reason, human (epidemiological) data are preferred, but they may not exist for the agent in question. When epidemiological data do exist, results giving the increased rate of disease per unit of exposure (exposure-response data) for an exposed population must typically be converted to the excess risk of disease over a lifetime for an individual who received a specific exposure. The exposure associated with a specific level of excess lifetime risk, typically somewhere in the range of 1 in 100,000 to 1 in 1,000, is then determined to be permissible or not. For workers, the U.S. Occupational Safety and Health Administration (OSHA) typically seeks to limit excess risk to 1 in 1,000, a higher risk than is usually accepted by the EPA, under the assumption that workers voluntarily accept a somewhat higher risk. Rates can be converted to risk using simple formulas.
Two issues of concern arise for risk assessors working with epidemiological exposure-response models. The first is the shape of the exposure-response curve. When data are sparse, and sometimes even when they are not, it may be difficult to choose among competing models for setting permissible limits because these models can have very different consequences. Typical questions involving model selection might be whether the exposure-response shows a linear increase in disease rates per unit of exposure, whether there is a threshold below which there is no risk followed by an increase, or conversely, whether there is a cut point above which disease risk begins to flatten out or even decrease. A second question typical of risk assessment is the nature of the exposure- response relationship in the low-dose region, where there may be few data. This question often arises when occupational epidemiological studies (of worksites with comparatively high exposure) are used for risk assessment for general environmental exposures such as diesel fumes, dioxin, or asbestos.
An example in which both these issues occurred is a risk assessment for cancer subsequent to dioxin exposure, based on a study of 3,538 workers (Steenland, Deddens, & Piacitelli, 2001). Most of these workers were exposed to dioxin several orders of magnitude above typical environmental levels, raising the issue of whether results
261
could be extrapolated to low-dose levels. However, there were some data in the low-dose range, yielding more confidence in such extrapolation. The model using the logarithm of cumulative exposure produced estimated risks from low-dose exposure that were ten times higher than the risks predicted by the linear model, and fit the data significantly better than the linear model.
262
Future Directions Occupational epidemiology is becoming less and less concerned with exposures to toxins, which are becoming less prevalent in the workplace in developed countries, although they continue to be present in many developing countries. Instead, in more developed countries, interest is now focusing more on other types of exposures that affect a large number of workers. One such exposure is job stress, which is difficult to measure but which may have large consequences via increasing blood pressure or cardiovascular disease, or both. Results to date for a link between job stress and blood pressure are tantalizing but far from conclusive; potential confounding by socioeconomic status is a major issue in studies of job stress. A noisy workplace is an exposure that may result in stress and increased blood pressure (and there is an overlap here with environmental exposures to noise; recent studies of those living near noisy airports have showed increased in blood pressure). Another related exposure is loss of employment, which may in turn increase stress and predict poor health in other ways. Yet another area of much recent research is whether shift work, which causes disruption of circadian rhythms and possible alteration of estrogen hormones, is related to breast cancer.
When toxins do continue to be of concern in the workplace, epidemiologists are increasingly concerned with risks of subclinical outcomes among the exposed workers, outcomes that may or may not have long-term consequences. Examples of these outcomes are excess small protein in the kidney (future kidney disease?), and the presence of autoantibodies in the serum (future autoimmune disease?).
Another trend is the assessment of gene-environment interactions. For example, subjects exposed to pesticides in the past may be at risk for Parkinson's disease only if they have a certain genetic polymorphism. (This possibility and its implications for public health are discussed in Chapter 7.)
One problem, which often affects occupational studies, is the increasing difficulty of conducting workplace studies at all. In many instances permission from the employer is required, and the spread
263
of market economies, coupled with the weakness of organized labor, has meant less emphasis on workplace health and safety and more barriers to conducting occupational studies.
As for environmental epidemiology, low-level exposure to common toxins continues to be of interest in determining whether such exposure contributes to background endemic disease rates. Arsenic in the water, mercury in the air, and small particulates in the air are just a few of the agents of interest.
In addition to these classic problems, newer issues are demanding attention. Global climate change is now accepted as a real trend by the scientific community (see Chapter 12). However, the health effects of climate change are challenging to study and have yet to be fully documented. Indeed, the end points for such studies are not always clear, and the appropriate study designs may not be apparent. Other issues are even newer, such as how to measure the health effects of urban environment features such as parks, pedestrian infrastructure, and pavement (see Chapter 15).
Other future directions that affect all epidemiological studies involve new types of data collection using new technology. For data collection from individuals, web-based interviews are becoming more common, along with daily recording on cell phones of data like diet diaries. Other innovations include small mobile devices that measure either exposure or outcome continuously and that can be carried or worn by study participants in order to record data on a continuous basis—examples are blood pressure monitors that can be worn for twenty-four hours, and monitors of heart rate variability. At the same time that these data collection techniques for individuals in field studies are becoming more sophisticated, there is a parallel trend toward using big data to detect trends and tease out associations for large populations. For example, electronic medical records can be used to measure medication use among large populations and to determine if such use is associated with future adverse health events. Under the U.S. Affordable Care Act, newly available, large-scale data sets are being used to evaluate the efficacy of different treatments and procedures in the effort to increase use of evidence-based medicine.
Genome-wide association studies (GWAS) have become common, replacing studies of candidate genes, and have been accompanied by
264
the development of statistical techniques that attempt to sort out the meaningful signals from the noise (false positives). Similarly, proteomics data are increasingly used to supplement genomic data. Most recently, some investigators are now working on exposomics, the search via environment-wide association studies (EWAS) in large databases for associations between biomarkers and environmental toxins (Vineis, van Veldhoven, Chadeau-Hyam, & Athersuch, 2013; Brunekreef, 2013). All these new “omics” analyses, which are explored in Chapter 7, are big data analyses, and require caution regarding the occurrence of false positive findings due to the large number of associations analyzed (i.e., a multiple comparison problem, typically requiring an adjustment of the p value for what is considered noteworthy or “significant”). In the past, positive findings in many of these large data sets have been difficult to replicate in other data.
However, it is worth noting that these future directions are occurring primarily in developed industrialized countries (where the practice of epidemiology is more common). In less developed countries, large numbers of people still sustain very high levels of exposure to the classic occupational and environmental toxins. In many of these cases, what is needed is hazard surveillance and control rather than new epidemiological studies.
265
Summary Epidemiology is the study of the distribution and determinants of health and disease in human populations, and epidemiologists are dedicated to studying whether a given exposure or set of exposures causes a certain disease. Environmental epidemiology and occupational epidemiology study the role of exposures in the general environment and in the workplace, respectively. Investigators in these two fields use many similar methods.
There are many kinds of epidemiological study designs. Examples include ecological studies, cohort studies, and case-control studies. In each case, epidemiologists work to define and measure exposures, to define and measure the health outcomes of interest, and to define and measure other factors that may bear on the association of interest. They also work to eliminate or control sources of bias that may skew their findings, including confounding, selection bias, and information bias.
Epidemiological data are invaluable in risk assessment, in standard setting and other policymaking, and in dispute resolution in environmental and occupational health.
266
Key Terms analytical studies
Studies at the level of individuals in which investigators seek to test a specific hypothesis, such as a possible association between exposure and disease, or a possible therapeutic benefit of an intervention.
attributable fraction The proportion of disease in either an exposed group or the general population for which the exposure was responsible; equivalently, the proportion of disease that could be prevented by eliminating the exposure.
bias Distortion of the true relationship between exposure and disease. The most important sources of bias are selection bias, confounding, and information bias.
big data A general term for structured, partly structured, or unstructured data sets that have the potential to be mined for useful information but are so large that traditional data management and analytical techniques are inadequate.
biological plausibility The consistency of the hypothesized association with biological theory (one of the Hill criteria).
biomarker of exposure A cellular, biochemical, analytical, or molecular measure obtained from biological media such as tissues, cells, or fluids and indicative of exposure to an agent of interest.
case-control studies Studies in which the investigator begins with diseased and nondiseased groups and looks backward in time to assess and compare their exposures.
categorical variable A variable such as sex or smoking status that can take on only discrete values, often a limited number of values (current, former, or never).
causal inference
267
The process of judging whether an association is causal, a central task in epidemiology and other sciences.
causal relationship An association in which an exposure is causally related to an outcome.
clinical trials Experiments that test the effects of a therapeutic intervention such as a medication by comparing its effects in groups that receive different treatments or different dose levels of a treatment. Individuals are usually randomly assigned to the treatment groups to avoid confounding (see randomized clinical trials).
cluster A group of cases, in time or in space, or both, in excess of expectation.
cohort studies Studies that start with an exposed group and a nonexposed group, both disease free, and follow them forward in time to observe disease incidence or mortality rates.
confidence interval A range of plausible values for a measure of effect. The ends of the range are called the confidence limits.
confounder See confounding.
confounding Distortion of the exposure-outcome relationship by a factor associated with the exposure of interest and with the outcome of interest but not through the causal pathway being studied (i.e., not an intermediate variable).
consistency The finding of an association in many studies (one of the Hill criteria).
continuous variable A variable such as weight or blood pressure that can take on any value between its minimum and its maximum. Compare to categorical variable.
correlational studies
268
See ecological studies. cross-sectional studies
Studies that measure exposure and disease at the same time. cumulative incidence
See risk. DALYs (disability-adjusted life years)
A measure of burden of disease across a population, consisting of the sum of years lived with disability and years lost due to premature death.
descriptive studies Studies that characterize a disease by factors such as age, sex, time, and geographic region but do not formally test a hypothesis (cf. analytical studies).
dichotomous variable A form of categorical variable with only two possible values (e.g., diseased/nondiseased).
dose-response In epidemiology, toxicology, and clinical medicine, the quantitative relationship, in a test system, an individual, or across a population, between the magnitude of exposure and the magnitude of outcome. The presence of a dose-response relationship adds weight to the possibility of a causal relationship (one of the Hill criteria).
ecological studies Studies of the correlation between an exposure and disease rates, at the level of groups rather than individuals.
effect modification A situation in which a third variable modifies the effect of the exposure variable of interest on an outcome of interest.
effect size The strength of the association between a hypothesized cause and an outcome. A stronger association adds weight to the possibility of a causal relationship (one of the Hill criteria).
endemic disease A disease with long-term presence within a given geographic area or population group.
environmental epidemiology
269
Epidemiology that focuses on exposures in the general environment, such as air pollutants, and their health outcomes.
epidemic The rapid spread of disease among a large number of people in a given population.
epidemiology The study of the distribution and determinants of health and disease in human populations.
etiologic studies See analytical studies.
generalizability The extent to which the conclusions of a study in one population can be applied to other populations (sometimes called external validity).
healthy worker effect A type of selection bias occurring when workers are compared to the general population. Workers are healthier than the general population, so study results will be biased against finding adverse health effects among the workers.
Hill criteria Criteria originally elaborated by A. Bradford Hill and used by epidemiologists to judge whether a particular causal hypothesis is plausible: that is, whether the observed association between A and B can be interpreted to mean that it is likely that in fact A causes B.
incidence rate An outcome measure: the rate of onset of new cases of disease per unit of person-time.
information bias The bias that occurs when information obtained about either exposure or disease is incorrect.
job-exposure matrix (JEM) A cross-classification of jobs and workplace exposure levels across time that assigns typical exposures according to common job classifications and work practices. Used for imputing past workplace exposures (known as exposure reconstruction).
latency period
270
The elapsed time between an exposure and the onset of symptoms of resulting disease.
linear regression A form of analysis (usually multivariate) that examines the relationship between a continuous dependent variable and independent variables (which may be either continuous or categorical), based on the assumption that there is a linear relationship between the dependent variable and the set of predictor variables.
logistic regression A form of (often multivariate) analysis that examines the relationship between a categorical dependent variable and one or more independent variables, which may be either categorical or continuous. The outcome variable is usually dichotomous (e.g., diseased or not diseased).
measure of effect A measure of the association between exposure and outcome. Examples are ratio measures such as rate ratios, relative risks, odds ratios, and difference measures such as the rate or risk difference.
meta-analysis An analysis that combines the quantitative results (measures of effect) across different studies and provides a single overall average of the measure of effect, usually via weighting the measures of effect of various studies according to their size.
misclassification A source of information bias, occurring when a categorical exposure is classified incorrectly.
mismeasurement A source of information bias, occurring when a continuous exposure variable is measured incorrectly.
mortality rate An outcome measure: the rate of deaths per unit of person-time.
multivariate analysis A data analysis that considers more than one independent and/or dependent variable.
National Death Index (U.S.A.) A centralized database of death record information maintained
271
by the National Center for Health Statistics (NCHS), dating from 1979, and available for epidemiological research. Provides both vital status (dead or not), and cause of death if dead.
natural experiment A study in which individuals or groups are exposed to a factor of interest, not through the action of the investigator (as in a controlled trial) but by circumstance, in a manner that resembles random assignment (see observational studies).
nondifferential error When exposure is measured or classified equally poorly for both diseased and nondiseased groups, or disease is measured or classified equally poorly for both exposed and nonexposed groups. Generally biases affect measures to the null.
null hypothesis The notion that an exposure and an outcome are not associated, the counterpoint to a hypothesized association between the two.
observational studies Studies in which the investigator does not manipulate variables of interest (as in an experiment) but simply observes exposures and/or outcomes of interest.
occupational epidemiology Epidemiology that focuses on exposures in the workplace and their health outcomes.
odds ratio An outcome measure: the odds that an outcome occurs given a particular exposure compared to the odds that the outcome occurs in the absence of that exposure.
p value The probability that an observed association occurred by chance, assuming that the null hypothesis is true.
precision An estimate of the accuracy or variance of a measure of effect. In epidemiology, as in other sciences, a larger sample is likely to yield a more precise measurement, signaled by narrower confidence intervals.
prevalence The proportion of a population with a particular condition at a point in time.
272
prospective studies Studies that move forward in time, observing outcomes (usually disease or death) that occur during the study period (cf. retrospective studies).
randomized clinical trials Controlled experiments in which a treatment (or exposure) of interest is randomly assigned to one group and not to another.
rate An outcome measure: events (such as disease onset or deaths) per unit of person-time.
rate ratio An outcome measure formed by the ratio of disease rates in exposed and unexposed groups.
recall bias A form of information bias in which cases tend to remember more about past exposures than controls do.
regression analysis A statistical process for estimating associations among variables, usually to quantify the effect of an independent variable (exposure) upon a dependent variable (outcome). Typically used when multiple variables are in play, and some need to be “controlled” to observe an association of interest.
relative risk See risk.
retrospective studies Studies that look backward and observe outcomes (usually disease or death) that have already occurred (cf. prospective studies).
risk An outcome measure: events per person over a defined period of time. Equivalent to cumulative incidence in a cohort study. A ratio of two risks is called a relative risk, although this term is sometimes used generically to include all ratio measures (e.g., rate ratios and odds ratios).
risk assessment A stepwise process of organizing information about a hazard or agent of concern. The steps include problem formulation, hazard identification, exposure assessment, dose-response assessment,
273
and risk characterization. sample size
The number of observations in a study. A larger sample size generally produces results that are more statistically stable (more precise, with smaller variance) and informative.
selection bias The bias that occurs when the relationship between exposure and disease in the study population is not representative of the true relation between exposure and disease in the general population because the investigator has selected the study population in a nonrepresentative way.
statistical power The likelihood that a study will detect an association when there is a true association to be detected. High statistical power corresponds to low probability of a type II (false negative) error.
statistical significance A feature of an observed association, indicating that the observed association was unlikely to have occurred by chance, if the null hypothesis is true.
stratification An analytical approach involving subdividing a study population into distinct groups (strata) according to some parameter such as age, and calculating a weighted average of measures of effect across these strata. Useful as a way of avoiding confounding.
temporal relationship The relationship, in time, between a hypothesized cause and a hypothesized effect. When judging whether a causal association is plausible, this is the only Hill criterion that is required: a cause must precede an effect.
validity The “truth” of study results—whether the investigators reached correct conclusions about the population studied (sometimes called internal validity).
274
Discussion Questions 1. In the Lim et al. (2012) study of the global burden of disease,
one measure of the burden of disease was the attributable fraction (AF). The AF is defined as the number of cases of a given disease due to a particular exposure, and it is calculated as AF = [(RR − 1)p]/[(RR − 1)p + 1], where RR is the relative risk (or rate ratio or odds ratio) of disease for the exposed versus the nonexposed, and p is the proportion of the population exposed. If 5% of the U.S. population is exposed occupationally to diesel fumes, and the RR for lung cancer due to occupational diesel fumes is 1.5, calculate the AF. There are about 150,000 lung cancer deaths per year in the United States. What percentage of these deaths do you estimate is due to occupational exposure to diesel fumes? In addition, virtually the entire U.S. population is exposed environmentally to diesel fumes, with an estimated RR of 1.05 compared to a hypothetical nonexposed population. What percentage of U.S. lung cancer deaths may be due to environmental diesel fume exposure?
2. Suppose you want to study whether global warming is likely to increase human disease. With increased global temperature, one issue is the extension of areas in which mosquitos can live, which in turn can extend the range of malaria and dengue fever. Can you suggest one or more study designs that could be used to determine whether climate change has resulted in more malaria in specific geographic areas? Is it too soon to do such a study? What data would you need?
3. We rely on both human evidence (from epidemiology) and animal evidence (from toxicology) to clarify the health effects of toxic exposures. Each provides valuable information, and each has both advantages and disadvantages. Please compare and contrast the two kinds of evidence, and explain their relative merits.
4. In a cross-sectional study of PFOA and kidney function (as measured by the glomerular filtration rate, or GFR), the data suggest that serum PFOA is higher when the GFR is lower, suggesting that PFOA may decrease kidney function. Can you
275
think of an alternative association? Consider that PFOA is excreted primarily via the kidneys.
5. You conduct a case-control study of breast cancer, and you find that higher SES is a risk factor for breast cancer. It is known that having any children is associated with lower breast cancer risk, and that having more children is associated with lower risk than having fewer children. Do you think that the finding of more risk in women of higher SES might be due to confounding? How would you address this question in your analysis?
276
References Arnold B. F., Galiani, S, Ram, P. K., Hubbard, A. E., Briceño, B., Gertler, P. J., & Colford, J. M. (2013). Optimal recall period for caregiver-reported illness in risk factor and intervention studies: A multicountry study. American Journal of Epidemiology, 177(4), 361–370.
Barnard, S., Routray, P., Majorin, F., Peletz, R., Boisson, S., Sinha, A., & Clasen, T. (2013). Impact of Indian Total Sanitation Campaign on latrine coverage and use: A cross- sectional study in Orissa three years following programme implementation. PLoS One, 8(8), 71438.
Barreto, M. L., Genser, B., Strina, A., Teixeira, M. G., Assis, A. M., Rego, R. F.,…Cairncross, S. (2007). Effect of city-wide sanitation programme on reduction in rate of childhood diarrhoea in northeast Brazil: Assessment by two cohort studies. Lancet, 370, 1622–1628.
Brunekreef, B. (2013). Exposure science, the exposome, and public health. Environmental and Molecular Mutagenesis, 54(7), 596– 598.
Caldwell, G. (1990). Twenty-two years of cancer cluster investigations at the Centers for Disease Control. American Journal of Epidemiology, 132(Suppl. 1), S43–S62.
Clasen, T., Fabini, D., Boisson, S., Song, J., Aichinger, E., Bui, A.,… Nelson, K. (2012). Making sanitation count: Developing and testing a novel device for assessing latrine use in low-income settings. Environmental Science & Technology, 46(6), 3295–3303.
Esrey, S. A., Potash, J. B., Roberts, L., & Shiff, C. (1991). Effects of improved water supply and sanitation on ascariasis, diarrhoea, dracunculiasis, hookworm infection, schistosomiasis, and trachoma. Bulletin of the World Health Organization, 69(5), 609–621.
Fewtrell, L., Kaufmann, R. B., Kay, D., Enanoria, W., Haller, L., & Colford, J. M., Jr. (2005). Water, sanitation, and hygiene interventions to reduce diarrhoea in less developed countries: A systematic review and meta-analysis. Lancet: Infectious Diseases,
277
5(1), 42–52.
Hill, A. B. (1965). The environment and disease: Association or causation? Proceedings of the Royal Society of Medicine, 58, 295– 300.
Kreiss, K., Gomaa, A., Kullman, G., Fedan, K., Simoes, E. J., & Enright, P. L. (2002). Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. New England Journal of Medicine, 347, 330–338.
Kumagai, S., Kurumatani, N., Arimoto, A., & Ichihara, G. (2013). Cholangiocarcinoma among offset colour proof-printing workers exposed to 1,2-dichloropropane and/or dichloromethane. Occupational and Environmental Medicine, 70(7), 508–510.
Lim, S. S., Vos, T., Flaxman, A. D., Danaei, G., Shibuya, K., Adair- Rohani, H.,…Memish, Z. A. (2012). A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380, 2224– 2260.
O'Connor, D., Page, M. J., Marshall, S. C., & Massy-Westropp, N. (2012). Ergonomic positioning or equipment for treating carpal tunnel syndrome. Cochrane Database of Systematic Reviews, 18(1), CD009600.
Rom, W., & Markowitz, S. (Eds.). (2006). Environmental and occupational medicine (4th ed.). Philadelphia: Lippincott Williams & Wilkins.
Root, G. P. (2001). Sanitation, community environments, and childhood diarrhoea in rural Zimbabwe. Journal of Health, Population, and Nutrition, 19(2), 73–82.
Rothman, K. (1990). A sobering start for the Cluster Busters' Conference. American Journal of Epidemiology, 132(Suppl. 1), S6– S13.
Rothman, K., & Greenland, S. (2008). Causation and causal inference. In K. Rothman & S. Greenland, Modern epidemiology (3rd ed., pp. 5–31). Philadelphia: Lippincott-Raven.
278
Steenland, K., Deddens, J., & Piacitelli, L. (2001). Risk assessment for 2,3,7,8-p-dioxin (TCDD) based on an epidemiologic study. American Journal of Epidemiology, 154, 451–458.
Steenland, K., Savitz, D. A., & Fletcher, T. (2014). Commentary: Class action lawsuits: Can they advance epidemiologic research? Epidemiology, 25(2), 167–169.
Steenland, K., Zhao, L., Winquist, A., & Parks, C. (2013). Ulcerative colitis and perfluorooctanoic acid (PFOA) in a highly exposed population of community residents and workers in the mid-Ohio valley. Environmental Health Perspectives, 121(8), 900–905.
Vineis, P., van Veldhoven, K., Chadeau-Hyam, M., & Athersuch, T. J. (2013). Advancing the application of omics-based biomarkers in environmental epidemiology. Environmental and Molecular Mutagenesis, 54(7), 461–467.
Waddington, H., & Snilstveit, B. (2009). Effectiveness and sustainability of water, sanitation, and hygiene interventions in combating diarrhoea. Journal of Development Effectiveness, 1(3), 295–335.
Winquist, A., Lally, C., Shin, H. M., & Steenland, K. (2013). Design, methods, and population for a study of PFOA health effects among highly exposed mid-Ohio valley community residents and workers. Environmental Health Perspectives, 121(8), 893–899.
World Health Organization and UNICEF. (2014). Progress on drinking water and sanitation: 2014 update. Geneva: Authors.
279
For Further Information Textbooks Many excellent epidemiology textbooks are available, some providing a general overview of the field and others focusing on environmental and occupational epidemiology. Here are some examples.
General Epidemiology Gordis, L. (2013). Epidemiology (5th ed.). Philadelphia: Saunders.
Rothman, K. J. (2012). Epidemiology: An introduction. New York: Oxford University Press.
Rothman, K. J., Lash T. L., & Greenland, S. (2012). Modern epidemiology (4th ed.). Philadelphia: Lippincott Williams & Wilkins.
Szklo, M., & Nieto, F. K. (2014). Epidemiology: Beyond the basics (3nd ed.). Sudbury, MA: Jones & Bartlett.
Weiss, N. S., & Koepsell, T. D. (2014). Epidemiologic methods: Studying the occurrence of illness. New York: Oxford University Press.
Environmental and Occupational Epidemiology Baker, D., & Nieuwenhuijsen, M. J. (Eds.). (2008). Environmental epidemiology: Study methods and application. New York: Oxford University Press.
Checkoway, H., Pearce, N., & Kriebel, D. (2004). Research methods in occupational epidemiology (2nd ed.). New York: Oxford University Press.
Friis, R., & Sellers, T. (2008). Epidemiology for public health practice (4th ed.). Sudbury, MA: Jones & Bartlett.
Merrill, R. M. (2007). Environmental epidemiology: Principles and methods. Sudbury, MA: Jones & Bartlett.
280
Smith, T., & Kriebel, D. (2014). A biologic approach to environmental assessment and epidemiology. New York: Oxford University Press.
Journals Many journals publish epidemiological research. These include general medical and public health journals and also specialty journals such as the following:
American Journal of Epidemiology: http://aje.oxfordjournals.org
Annals of Epidemiology: http://www.annalsofepidemiology.org
Epidemiologic Reviews: http://epirev.oxfordjournals.org
Epidemiology: http://journals.lww.com/epidem
International Journal of Epidemiology: http://ije.oxfordjournals.org
Journal of Epidemiology and Community Health: http://jech.bmj.com
Organizations American College of Epidemiology: http://www.acepidemiology.org. A professional organization dedicated to continuing education and advocacy for epidemiologists in support of their efforts to promote public health.
Conference of State and Territorial Epidemiologists: http://www.cste.org. A professional association of public health epidemiologists working in states, local health agencies, and territories.
International Society for Environmental Epidemiology: http://www.iseepi.org. A group with members from over fifty countries that provides a professional forum for discussing problems unique to the study of health and the environment.
Society for Epidemiologic Research: http://www.epiresearch.org. A forum in which professionals can share epidemiological research.
281
Chapter 5 Geospatial Data for Environmental Health
Lance A. Waller
During the preparation of this chapter Dr. Waller served on the National Academies Committee on Applied and Theoretical Statistics (uncompensated), and as an expert witness for Pope McGlamry, Attorneys at Law.
282
Key Concepts Data relevant to environmental health are often place-based and may be georeferenced, that is, associated with particular geographic locations.
These data may include environmental exposures, health outcomes, and other information.
Geographic information systems (GIS) allow mapping of these data, which in turn allows a range of useful analyses.
A range of operations, such as layering, buffering, and spatial queries, are used in these analyses.
GIS analyses are limited by data quality and availability and by other technical and methodological issues.
Georeferenced data, that is, data measurements associated with particular geographic locations, often play a critical role in environmental health. In fact the phrase “global to local,” used in the title of this book, builds on a fundamental geographic concept, the notion of spatial scale. The spatial extent of a phenomenon— say, levels of a chemical exposure from an industrial spill—may in turn define the spatial extent of resulting health impacts and of potential remediation or other intervention efforts. Mapping spatially referenced exposure, populations at risk, and environmental factors (e.g., stream flow, wind speed and direction, emissions locations, or monitoring sites) allows us to manage data geographically, identify the linkages across multiple indicators measured by different agencies over the same study area, and acquire valuable background information for interpreting the environmental context of public health data.
To begin to build ideas, consider the following key components of an environmental health response to an accidental release of a toxic agent: responders need to know, where is the exposure of interest and where is the population at risk? The greatest concern arises when areas of high exposure overlap areas of high population density. Although neither a quantitative exposure assessment nor an analytical epidemiological study, the simple act of overlaying a
283
map of exposure with a map of population density provides a valuable exploratory tool for identifying areas of greatest immediate concern.
The role of maps in public health extends back at least to physician John Snow's famous maps of cholera mortality in London (Snow, 1853, 1855/1936). Most students of public health have encountered the story of Snow, who mapped cholera deaths during the 1854 outbreak in London, noted an aggregation near a public water pump on Broad Street, and petitioned for the removal of the pump handle in the interest of public health. The story provides a powerful motivator for the potential of geographically linking data sets (in Snow's case, victims' homes and the locations of public pumps). Such a brief summary of the incident minimizes some of the nuances of the story and the role of maps plotted by Snow and others in the public health response, and Brody, Rip, Vinten- Johansen, Paneth, and Rachman (2000), Koch (2005), and Johnson (2007) all provide insightful historical discussions regarding the variety of maps considered in the public health response to the 1854 epidemic.
The dramatic impact of the story of Snow's map often serves as a call for increased use of maps and mapping in environmental health, with the goal of identifying previously unknown connections between environmental exposures and public health problems. Indeed, if Snow could accomplish his study with little more than time, ink, and paper, many wonder what tools today's computers offer for such explorations. In this chapter we consider two elements of geospatial analysis in public health: geographic information systems and spatial analysis.
A geographic information system, or GIS, is a computer software system (or more accurately, a set of linked software packages) that enables the collection, management, linkage, display, and analysis of georeferenced data. The first formal GISs arose out of the Canada Geographic Information System, devised in the 1960s to aid in the Canada Land Survey (Longley, Goodchild, Maguire, & Rhind, 2001, pp. 10–11). Since then, GISs have developed and evolved to address a wide spectrum of applications, grown to accommodate vast stores of georeferenced data, and advanced in both usability and versatility.
284
Spatial analysis involves the application of quantitative methods (including statistical analysis) to georeferenced data to address spatial research questions such as these:
Are health outcomes clustered in space?
Where are exposures highest?
Are there associations between exposures, demographics, and health outcomes?
This chapter provides an introductory overview of the use of georeferenced data, geographic information systems, and spatial analysis within the field of environmental health. Important considerations include a general discussion of the role of maps in environmental health, the role of cartographic principles in an age of computer-generated maps, the basic features and operations of GISs, classification of basic spatial questions of interest, illustrations of the types of geospatial analysis encountered in environmental health analyses enabled by GISs, and some limiting factors in such analyses.
285
Components of Georeferenced Data Georeferenced data consist of location, attributes, and support. Location refers to the geographic location where a data measurement is taken. An attribute is a measurement taken at a given location. Note that several attributes may exist at a single location. For example, levels of particulate matter, oxides of nitrogen, and ozone may all be measured in one place. Support denotes the type of location associated with the attribute measurement. Geographic support is often classified in terms of points (single locations), lines (collections of segments such as roads or rivers), and areas (typically, political divisions such as states, counties, or census tracts, but also watersheds or ecologically defined zones). Support provides a context for interpreting attribute values and a reference location for mapping. Data with point support are located as points on a map. Data with line support are associated with lines or curves on the map. Examples of the latter are traffic density on a particular road segment or contaminant levels in a stream. Data with area support are often represented via choropleth maps with areas shaded or colored to represent attribute values.
To further understand these components it is helpful to think of a data set as consisting of a table of values (as in a spreadsheet) linked to a map of data locations. Suppose each row in the data table corresponds to the set of attribute measurements associated with a single location. Each column corresponds to a particular type of attribute measurement across locations: for example, levels of particulate matter at each of a number of air sampling sites. The linkage between the table and map is such that selecting a location on the map results in selection of the associated row of attribute values in the table, and the selection of a row of the table corresponds to selection of the associated location on the map.
The multiple components of georeferenced data imply multiple components of data accuracy. In particular, quality assessments of georeferenced data must consider location accuracy and support accuracy as well as attribute accuracy. A precisely measured attribute value associated with the wrong location can be as misleading as a mismeasured attribute value.
286
Basic GIS Operations A variety of GIS packages is available, with a range of features, interfaces, and interoperability. However, all GISs contain certain core features allowing basic operations on spatial data, and we review three of these here: layering, buffering, and spatial queries.
As its name implies, layering refers to linking two or more separate databases by their underlying geography. For example, suppose we have a census database providing summary information on population demographics for census tracts in a given county. Suppose we obtain a second database providing the location and flow levels for a stream network in the same county. Finally, suppose we have a third database providing a point location for the residence of each case of a particular disease reported in the county for a given year and also concentration values for contaminant levels in tap-water samples from these homes. We now have three different data sets, but we can overlay the respective maps of locations by layering the data in a GIS. Conceptually, this corresponds to overlaying transparent maps of each set of locations so that we may view them together (see Figure 5.1). More important, we may now reference elements of one layer by their proximity to elements in another layer; for example, we can identify which streams are near homes with high tap-water concentration values.
287
Figure 5.1 Hypothetical Example of the Layering GIS Operation
Buffering involves selection of data items by their position relative to other locations. For example, suppose we wish to identify the census tracts falling within 1 km of a selected stream segment. We select the particular stream segment on our stream map, then define a buffer zone of the prescribed distance around it. Most GISs implement equidistant buffers around points, lines, and areas (see
288
Figure 5.2 for examples), but some GISs allow the user to adjust for preferred directions corresponding to wind direction and the like.
Figure 5.2 Examples of Buffers Around Point, Line, and Area Features
At its heart, any GIS either implements or accesses a relational database system allowing sorting, combining, and selecting of data values. In addition to standard database queries, such as, “Find all records with concentrations above 5 ppm,” a GIS can also conduct spatial queries, such as, “Display all homes within 1 km of a selected stream segment.” For example, suppose we wish to identify case residences within 1 km of the dashed stream segment in Figure
289
5.1. Layering our map of residences with our map of streams places the case residence data in geographic context with the stream data, and buffering identifies which case residences are within the prescribed distance (e.g., the darker houses in Figure 5.1). One may also conduct combined queries incorporating both location and attribute data, such as, “Display all records with concentrations above 5 ppm [an attribute value] and within 1 km of the selected stream segment [a relative location value].”
Combining all three operations (layering, buffering, and spatial queries) allows complex queries, such as, “Display all census tracts with disease rates above 5 cases per 100,000 person-years at risk, which are within 1 km of the selected stream segment and have concentration values above 5 ppm.” This query requires layering to combine the stream, health, and population databases, buffering to identify census tracts within the prescribed distance of the stream, and a combined spatial and data query to identify the desired records.
290
Mapping and Spatial Analysis of Exposure Having defined the basic structure of georeferenced data and basic GIS operations, we next consider the role of geography in environmental health science. Building on the earlier example of considering an appropriate public health response to an accidental toxic release, we find that spatial questions abound: Where was the release? Which way was the wind blowing? What streams are nearby? Where are exposures the highest? Where do we expect high exposures to accumulate over time? Who lives in that area? Who works in that area? What are the possible evacuation routes? Can the spill be contained? How can responders best reach the spill site? Expanding to other environmental health research scenarios, we find similar sets of questions: for example, Where are pesticides applied? Which pesticides were applied where? How much? Who lives nearby? Who works nearby? Are environmental hazards sited in neighborhoods with high concentrations of minority residents? How many children live near a proposed landfill? Are residences of cases closer to waste sites than residences of controls? An accurate map of exposure values would seem to answer, in whole or in part, many of these questions.
Several basic issues are involved in planning and creating exposure maps. To start, consider what information might be contained in a map of exposure. First, most exposure maps are maps of ambient exposures, the level of a contaminant existing at a given location. Note that the ambient exposure is only one component of the personal exposure sustained by a person at a given location. Other factors influencing a person's exposure include his or her respiratory rate, use of protective equipment, and behaviors such as smoking, among others, suggesting that two different people at the same location may sustain very different personal exposures from the same ambient exposure (see Chapter 8).
With our spatial questions in place, we next consider what data are required to map ambient exposures. In the case of airborne exposures, we might use point monitoring stations, which provide detailed ambient levels at those specific points. Construction of a map requires interpolation to all points within the study area, based on the observed data. The accuracy of the monitoring data
291
combined with the accuracy of the interpolation method will affect the accuracy of the overall exposure map. A GIS can place the point locations in context, but we need to use spatial analysis to fill in (interpolate) exposure values between measurement locations. The basic idea in spatial interpolation is intuitive; we seek to predict values for new locations based on a weighted average of the observed data values, with observations near the prediction location receiving more weight than observations farther away. Some methods use distance-decay weights, while an approach known as kriging bases prediction on optimal weights based on statistical estimation of the amount of spatial correlation between observations as a function of the distance and direction between them. Many statistical techniques are used for spatial interpolation, and Webster and Oliver (2001) and Waller and Gotway (2004) provide details and additional references.
In the absence of measured exposure values, it is common to use geographic proximity as a surrogate for relative exposure; that is, we generally assume that individuals residing or working closer to a source of contamination receive a higher exposure than individuals farther away. Even though proximity alone rarely (if ever) provides an accurate surrogate for exposure values, the relative ranking may be sufficiently accurate for some exploratory classifications, for example, into “high” and “low” exposure regions. Accurate exposure assessments strengthen the accuracy of any measured associations between exposure and health; however, the use of proximity may be acceptable for pilot studies, preliminary classifications, and other exploratory uses.
292
Mapping and Spatial Analysis of Disease Risk Just as maps of exposure suggest answers to questions of interest in environmental health, maps of disease incidence and prevalence also provide insight into patterns and trends in the data. Questions of interest include these: Where is disease incidence or prevalence highest? Where is it lowest? Is the highest (or lowest) observed local incidence more extreme than we would expect if all people were at the same level of risk? How do observed local incidences or prevalences, or both, correspond to a map of exposure?
Maps of disease may be dot maps, with point locations of each case, or choropleth maps, indicating counts or estimated rates from nonoverlapping regions such as states, counties, or census tracts. Choropleth maps are more common than point maps due to confidentiality restrictions; reporting aggregate counts of cases from census regions reveals less individual information than a map of case residence addresses does. Although not particularly cartographically progressive, choropleth maps summarize information and are easily created and (more important) easily interpreted by public health professionals and the general public (Pickle, Herrman, Kerwin, Croner, & White, 1994).
As with exposure, many factors complicate the construction of maps of health outcomes. First, most people move about during the day, making it difficult to assign individuals to fixed locations on a map. Especially important in environmental health is the difference between residential location (where one sleeps), and occupational location (where one works). The location of interest corresponds to the relevant exposures, but these are often unknown and under study. In addition, data on residential location may be more readily available (from billing or other mailing records) than data on occupational location are. Another complication arises from increasing geographic resolution; choosing geographically small regions often results in smaller local sample sizes that erode the statistical precision of the local estimates within each region.
Spatial analysis of local disease risk estimates involves stabilizing local risk/rate estimates for area-support data, and investigating
293
whether local rates are higher (or lower) than expected based on the demographics of the local population (e.g., age, race, and sex). A variety of statistical methods exist for stabilizing local estimates from small sample sizes (Lawson & Williams, 2001; Waller & Gotway, 2004), but few are widely available in standard statistical software. Methods for assessing potential clusters of high risk also exist but, again, are rarely part of standard statistical training or software. Waller and Gotway (2004) provide an overview of such methods, and the R statistical package (R Core Team, 2014) contains several user-developed packages providing new spatial analysis tools to users (Bivand, Pebesma, & Gómez-Rubio, 2013).
294
What Makes Good Maps of Good Data? The preceding sections suggest that mapping exposure and health data may provide answers to relevant questions. However, the discussion has also raised some worries regarding the accuracy of mapped values, such as ambient versus personal exposures and the statistical precision of rate estimates from small areas. One of the greatest strengths of GIS is the ability to link disparate data sets collected over the same study area. For instance, we may wish to link exposure, health, and demographic data over the same region. These three data sets are likely to have been collected separately by different agencies, perhaps over different time periods, and for different reasons. As a result, the primary strength of GIS also entails an important weakness: the accuracy of any conclusions we draw from a map critically depends on the quality of the individual data components. Unlike a designed study in which a single research team is in charge of collecting, processing, analyzing, and interpreting the data, most GIS applications draw heavily from existing data sources for both location and attribute data such as census counts, stream locations, and the like, and as a result, these data almost always involve varying levels of quality and accuracy.
Once the data are connected, a second challenge is the selection and application of appropriate statistical methods to provide quantitative answers to components of the questions of interest. This can be challenging in the spatial setting, since many of the familiar assumptions of statistics are questionable or inappropriate in spatial public health data. For instance, outcomes are often binary or counts and do not follow Gaussian distributions. Nearby observations are often correlated rather than independent, since they occur in a similar environment. Due to these complications, it is important to incorporate collaborators with expertise in spatial statistics in most geographic studies of environmental health.
In addition to quality data and appropriate analysis, creating a good map also requires careful thought about and selection of cartographic symbols, colors, and other features. For instance, the standard order of hues in the spectrum (red, orange, yellow, green, blue, indigo, violet) may strike the novice mapmaker as a sensible way to display ordered categories in a map, but shifts from light to
295
dark versions of the same hue (light red to dark red, for instance) are actually much easier for map readers to interpret as representing increasing values. As a test, try to decide quickly, without referencing the entire spectrum, whether green is “bigger” than orange. Now, try to sort “light red” and “medium red” in terms of increasing value. (Monmonier, 1996, provides a readable introduction to important cartographic concepts and is essential reading for anyone planning to make wide use of GIS techniques or mapping in general.)
296
What Can We Do with GIS? The previous discussion outlines data structures and operations in a GIS setting, and how these feed into spatial analyses. Next, we briefly consider three examples of GIS applications addressing different types of questions in environmental health.
A Study of Physical Activity Among Park Users The first example is a comparison of physical activity levels between users and nonusers of parks in DeKalb County, Georgia. This is a case-control design, but rather than comparing people with and without a disease, we want to compare people who do and do not use parks. As with any case-control study, we want the cases and controls to come from the same base population—in this case, to be drawn from neighborhoods that are demographically similar and roughly equidistant from parks, to remove transportation time and demographics as potential confounders. The initial study design proposes to sample park users by encountering and interviewing them in the park. But how should nonusers be sampled?
We might use a two-stage approach. First, the sample of park users provides data regarding the geographic distribution of residences of park users, in effect defining a catchment area for the park. By mapping the sampled park users' homes onto a street map layer in our GIS and then layering census block groups (subdivisions of census tracts), we assign each park user's home to its associated census block group. The U.S. Census provides summary demographic information for each block group, allowing us to identify additional block groups within the park's catchment area having demographics similar to the park users' and from which we can draw nonusers. More specifically, by buffering around park boundaries and applying a spatial query, we can identify the subset of the demographically matched block groups that are within the same geographic catchment area as the park users.
Note that this proposed study employs all three GIS operations. It is an unconventional use of GIS; it identifies proximity-based exposure surrogates to insert into a statistical model measuring links between the (surrogate) exposure and outcome.
297
An Analysis of Environmental Justice Second, we consider the application of GIS operations and local demographic summaries as part of an assessment of an environmental justice claim. In June of 1998, Father Schmitter and Sister Chiaverini of the St. Francis Prayer Center in Flint, Michigan, alleged environmental justice violations, under Title VI of the U.S. Civil Rights Act of 1964, relating to the siting of a new steel recycling minimill proposed by the Select Steel Corporation of America. In August of 1998, the U.S. Environmental Protection Agency (EPA) agreed to investigate the claim. (A full collection of the EPA documents relating to the case appears on the Web page of the EPA's Office of Civil Rights: www.epa.gov/civilrights/index.html.)
The proposed minimill was to produce up to 43 tons per hour of specialty metals and, according to the EPA's review, had the potential to emit 100 tons per year of criteria pollutants, including particulate matter, lead, carbon monoxide, and oxides of nitrogen. The complaint filed with the EPA alleged that “the vast majority of the people within 3 miles of the proposed site are minority Americans and will be burdened with a disparate impact of pollution in an already deeply polluted area.” In reaction the Detroit News reported its own study, describing the “overwhelmingly white makeup of the surrounding neighborhood's demographics” based on data for the neighborhood within a one-mile radius around the proposed site. The EPA reported demographic data based on one-, two-, three-, and four-mile radii and yielding 13.8%, 37.2%, 51.1%, and 55.2% minority populations, respectively.
How can a GIS help clarify the situation? Figure 5.3 displays a map of census block groups for the 1990 U.S. Census (the most recent census at the time of the EPA investigation), indicating the proposed minimill location and associated one-, two-, and three- mile buffers. We shade block groups according to the proportion of census responders who self-identified their race as “black” (the most common nonwhite racial classification for this county). The map immediately clarifies the discrepancies between reports. The proposed location is northeast of the city of Flint, and a large proportion of the county's nonwhite population resides within the city. Within one mile, the population is predominantly white (as claimed in the newspaper reports), while the three-mile buffer
298
begins to include the more densely populated block groups with higher proportions of nonwhite (predominantly black) residents. Although similar information is revealed in the EPA's report in the form of a table, a GIS quickly provides the same table accompanied by a map clarifying the initially confusing results (Figure 5.3). As a result, the EPA has added tools to its Web sites linking EPA, U.S. Census, and U.S. Geological Survey (USGS) data and enabling users to create similar maps online.
299
Figure 5.3 Map of Genesee County, Michigan, Block Groups (1990 Census) Showing Proportions of Respondents Self-Identifying Race as “Black”
The location of the proposed steel recycling minimill is also indicated, accompanied by one-, two-, and three-mile buffers.
Characterizing the Built Environment
300
As described in Chapter 15, modern software and applications now permit many uses of GIS techniques for characterizing community features. One example is Walk Score (www.walkscore.com). This initiative layers information on amenities such as schools and stores, transit access, crime rates, and many other features. It summarizes this information to permit people to rate individual addresses—a useful tool when you're apartment hunting. Walk Score can also be linked with georeferenced health data in public health research, to test, for instance, whether a more walkable neighborhood is associated with greater social capital (Rogers, Halstead, Gardner, & Carlson, 2011), more physical activity among children (Larouche, 2013), or reduced stroke risk among elders (Qureshi et al., 2014).
301
Are There Any Limitations? Many introductions to the use of GIS and spatial analysis in public health offer long lists of advantages but often provide little discussion of limitations or complications. The examples offered here illustrate several compelling reasons to incorporate a GIS into the environmental health toolbox, and it is only fair to discuss the other side of the coin.
First and foremost, as mentioned earlier, the ability to combine multiple data sets collected by different agencies for different reasons is both a strength and a potential weakness of a GIS, because assessments of data quality often become murky when multiple data sets of differing quality are combined. In addition, we must consider data quality of locations as well as data quality of attributes.
Second, by their nature, most GIS studies are observational rather than experimental. That is, measures of associations are based on observed data, and epidemiological concepts of the different types of bias, confounding, and effect modification should always define the suitable context for interpretation of results.
Third, as already noted, typical statistical assumptions often do not hold for georeferenced data. Spatial data often include spatial correlations between observations (nearby observations being more similar than those taken far apart). Such correlations violate many standard statistical assumptions and require specialized statistical techniques for analysis, many of which are not currently available in either GIS or standard statistical software packages (Cromley & McLafferty, 2002; Waller & Gotway, 2004).
Fourth, data availability (both location and attribute) varies widely. Some studies may require development of a base map of locations before any study data can be assigned locations on the map. The use of global positioning systems (GPSs) and aerial and satellite imaging aid in the development of such base maps, and relatively recent developments such as Google Earth provide growing access to base map imagery worldwide. That said, linking freely available images with GIS-based data can sometimes be a delicate task, and adding the standard GIS operations to Google Earth images is often
302
not as straightforward as many users would like it to be.
Finally, basic GIS operations such as layering and buffering can be complicated when based on layers using different projections of the Earth's surface to the map plane or on layers with different levels of resolution. For example, if we zoom in on the Mississippi River in a national map we may find a river defined by only a few line segments at the county level. For another example, consider that we may have population demographics for census block groups and hospital discharge data for hospital catchment areas whose borders do not coincide with block group boundaries. Combining data from such “misaligned” data often requires additional assumptions and calculations above and beyond standard GIS operations.
303
Summary In summary, geographic information systems and spatial analysis provide a valuable set of tools for managing, merging, querying, and displaying geographically referenced data relevant to environmental health issues. The basic operations outlined in this chapter may be combined in myriad ways to address public health questions of interest, resulting in a broad set of tools for exploring, summarizing, and displaying such data.
However, as noted in the previous section, the use of GISs still requires appreciation of common limitations in both public health and geography. There is much to be gained by training public health professionals to “think spatially” and similarly much to be gained by training GIS professionals to “think epidemiologically.” Innovative applications of GIS and spatial analysis in environmental health most often occur as the result of collaboration between individuals familiar with GIS capabilities and individuals trained in public health research. A final consideration is that it is always helpful to frame research goals in terms of questions to be answered and analytical methods in terms of the questions they answer, and then to carefully match capabilities.
304
Key Terms attribute
A measurement taken at a given location. buffering
Selection of data items by their position relative to other locations.
choropleth map A map in which areas are shaded or patterned according to the value of an attribute, such as population density or disease incidence.
geographic information system (GIS) A computer software system (or more accurately, a set of linked software packages) that enables the collection, management, linkage, display, and analysis of georeferenced data.
georeferenced data Data associated with particular locations (also called spatial data, geospatial data, or geographic information). Usually stored as coordinates, and can be mapped.
interpolation Prediction of values for new locations based on a weighted average of observed data values. In this process, observations near the prediction location are weighted more heavily than observations farther away.
kriging A form of data interpolation that models the interpolated values using a Gaussian statistical process. Kriging is designed to characterize the error of predictions, to minimize this error, and to optimize the smoothness of the fitted values.
layering Linking two or more separate databases by their underlying geography.
location A unique place, often identified by GIS coordinates.
spatial analysis The application of quantitative methods (including statistical
305
analysis) to georeferenced data to address spatial research questions.
spatial query An “interrogation” of a database with reference to location (e.g., “Display all homes within 1 km of a hazardous waste site”).
spatial scale A fundamental concept of geography, referring to the size of a geographic unit, either relative or absolute. Scale has at least three common usages: cartographic scale (the size of a feature on a map relative to its true size); analysis scale (the unit size at which an analysis is carried out—e.g., census block, metro area); and phenomenon scale (the size of an entity, regardless of how it is studied or represented).
spatial statistics The field of study that quantitatively analyzes spatial data and the statistical modeling of spatial variability and uncertainty.
support The type of location associated with the attribute measurement.
306
Discussion Questions 1. The issue of data quality is always important in environmental
health research, but do the structure and operations of a GIS raise particular issues that might not arise in a controlled laboratory setting?
2. How might the basic operations of a GIS and spatial analysis tools help to meet each of the following research needs?
Investigate the health impact of an accidental release of a toxic agent into a stream.
Design a mosquito spraying program targeting control of the spread of West Nile virus.
Develop a sampling plan for controls in an environmental case-control study.
Evaluate and prioritize potential locations for new air monitoring stations.
Define commuting patterns relating to various real estate developments, and project the impact of lane blockages in various parts of the street network.
In each case, discuss the data layers needed, the questions that various GIS operations might answer, and how close those questions are to the questions of primary interest in environmental health.
307
References Bivand, R. S., Pebesma, E., & Gómez-Rubio, V. (2013). Applied spatial data analysis with R (2nd ed.). New York: Springer.
Brody, H., Rip, M. R., Vinten-Johansen, P., Paneth, N., & Rachman, S. (2000). Map-making and myth-making in Broad Street: The London cholera epidemic, 1854. Lancet, 356, 64–68.
Cromley, E. K., & McLafferty, S. L. (2002). GIS and public health. New York: Guilford Press.
Johnson, S. (2007). The ghost map: The story of London's most terrifying epidemic—and how it changed science, cities, and the modern world. New York: Riverhead Books.
Koch, T. (2005). Cartographies of disease: Maps, mapping, and medicine. Redlands, CA: ESRI Press.
Larouche, R. (2013). Assessing the health-related outcomes and correlates of active transportation in children and youth. Applied Physiology, Nutrition, and Metabolism, 39(3), 403.
Lawson, A. B., & Williams, F. L. (2001). An introductory guide to disease mapping. Hoboken, NJ: Wiley.
Longley, P. A., Goodchild, M. F., Maguire, D. J., & Rhind, D. W. (2001). Geographic information: Systems and science. Hoboken, NJ: Wiley.
Monmonier, M. (1996). How to lie with maps (2nd ed.). Chicago: University of Chicago Press.
Pickle, L. W., Herrman, D., Kerwin, J., Croner, C., & White, A. (1994). The impact of statistical graphic design on interpretation of disease rate maps. In Proceedings of the American Statistical Association's Section on Statistical Graphics (pp. 111–116). Alexandria, VA: American Statistical Association.
Qureshi, A. I., Adil, M. M., Miller, Z., Suri, M., Rahim, B., Gilani, S. I., & Gilani, W. I. (2014). Walk Score and risk of stroke and stroke subtypes among town residents. Journal of Vascular and
308
Interventional Neurology, 7(3), 26–29.
R Core Team. (2014). R: A language and environment for statistical computing. Vienna: R Foundation for Statistical Computing.
Rogers, S., Halstead, J., Gardner, K., & Carlson, C. (2011). Examining walkability and social capital as indicators of quality of life at the municipal and neighborhood scales. Applied Research in Quality of Life, 6(2), 201–213.
Snow, J. (1936). Snow on cholera. New York: Oxford University Press. (Papers by Snow originally published 1853 and 1855)
Waller, L. A., & Gotway, C. A. (2004). Applied spatial statistics for public health data. Hoboken, NJ: Wiley.
Webster, R., & Oliver, M. A. (2001). Geostatistics for environmental scientists. Hoboken, NJ: Wiley.
309
For Further Information Longley and others (2001), cited above in the References, provide many, many examples of the use of GISs in a broad array of disciplines, and Cromley and McLafferty (2002), also cited in the References, explore public health applications in detail. In addition, see the following:
Albert, D. P., Gesler, W. M., & Levergood, B. (Eds.). (2000). Spatial analysis, GIS, and remote sensing applications in the health sciences. Chelsea, MI: Ann Arbor Press.
Kahn, O., & Skinner, R. (Eds.). (2002). Geographic information systems and health applications. Hershey, PA: Idea Group.
Kurland, K. S., & Gorr, W. L. (2007). GIS tutorial for health (2nd ed.). Redlands, CA: ESRI Press. For those interested in hands-on examples, this tutorial workbook provides many examples and a time-limited version of ArcGIS by ESRI, one of the most common GIS packages in use.
Lawson, A. B. (2006). Statistical methods in spatial epidemiology (2nd ed.). Hoboken, NJ: Wiley.
Melnick, A. L., & Fleming, D. (2002). Introduction to geographic information systems for public health. Sudbury, MA: Jones & Bartlett.
Mitchell, A. (1999). The ESRI guide to GIS analysis: Vol. 1. Geographic patterns and relationships. Redlands, CA: ESRI Press. This text and the next provide many examples of the types of spatial analysis enabled by GIS.
Mitchell, A. (2005). The ESRI guide to GIS analysis: Vol. 2. Spatial measurements and statistics. Redlands, CA: ESRI Press.
310
Chapter 6 Toxicology
Gary W. Miller
The author would like to thank his colleague Dr. Jason Richardson, who coauthored the first two versions of this chapter. Dr. Miller reports no conflicts of interest related to the authorship of this chapter. Marissa Smith reports no conflicts of interest related to the authorship of the tox boxes.
311
Key Concepts Toxicology is an interdisciplinary field that examines the adverse effects of chemicals on biological systems.
Toxicology provides the biological foundation for suspected associations between chemicals and disease.
The basic tenet of toxicology—that “the dose makes the poison”—often implies there is a corresponding increase of toxicity with an increase of dose. Recent data suggest that some chemicals may exert their maximal effects at lower levels.
Data from toxicity testing are essential to assessing the risk of environmental chemicals.
Much toxicological research focuses on individual chemicals, but in the real world, people are exposed to complex mixtures—an ongoing challenge for science and policy.
Emerging high-throughput technologies promise to greatly expand our knowledge of the potential adverse effects of thousands of untested compounds.
Public health policy to protect people from harmful chemicals is complex, and in many ways fails to incorporate current science.
312
Introduction to Toxicology Toxicology (from the Greek toxinos, meaning “poison”) is the study of the adverse effects of chemicals on biological systems. These adverse effects can range from mild skin irritation to liver damage, birth defects, and even death. Chemicals of natural origin are referred to as toxins, while chemicals that result from synthetic processes are referred to as toxicants. The breadth of topics in toxicology requires the field to take an interdisciplinary approach, borrowing techniques and methods from numerous scientific fields including chemistry, pharmacology, pathology, physiology, biochemistry, and more recently, bioinformatics and computational biology. The term biological system can be broadly defined, and so a toxicologist might study the effects of pesticides on insect physiology, of herbicides on plant development, of antibiotics on bacterial growth, or of pollution on an entire ecosystem (the latter has evolved into a separate discipline termed ecotoxicology; see Walker, Sibly, Hopkin, & Peakall, 2012). However, most work in the field of toxicology as it relates to public health is focused on the adverse effects of chemicals on human health. Toxicology is a dynamic field that examines toxic interactions from the level of the molecule all the way to populations (Figure 6.1). This chapter explores how these adverse effects are determined, with an emphasis on the impact of environmental contaminants on human health and the ways in which modern scientific approaches are being applied to ongoing and emerging concerns.
313
Figure 6.1 Toxicology: From Populations to Molecules Toxicological effects can be observed at levels ranging from large human populations to specific organs or molecules. The skills and approaches needed to examine each level vary considerably, which necessitates the collaboration of investigators with various areas of expertise.
A basic tenet of toxicology is that all substances have the potential to be toxic, not just the poisons that come readily to mind such as strychnine, cyanide, or nerve gas. Paracelsus (born Philippus Aureolus Theophrastus Bombastus von Hohenheim), considered the father of toxicology, was the first to articulate this concept, in the1500s. Of course, all compounds are not equally toxic; some have effects at minuscule doses and others require very high doses (see Figure 6.7 for lethal dose examples). Moreover, while Paracelsus's dictum that “the dose makes the poison” is frequently quoted and often true, new insights suggest a more complex reality—that for some chemicals the maximal toxicity and adverse health effects may occur at very low doses and not increase with increasing dose (as discussed further next).
314
Figure 6.7 Molecular Structure and LD50 for Eight Chemicals
For example, table salt (sodium chloride) used in moderation is fine in the human diet, but consuming half a cup of salt a day would eventually cause significant electrolyte and kidney problems and possibly death. Conversely, ingestion of even a small amount of potassium cyanide (one gram) can kill a human. It is the job of the toxicologist to determine the relative toxicity of various compounds within the context of anticipated human exposures. This information, when combined with information about the potential utility of a compound and the mechanisms and frequency of exposure, aids regulatory bodies in deciding whether a compound is acceptable for a particular use and what levels of exposure are
315
permissible. For example, the general public (and regulatory agencies) would not tolerate a cold remedy that caused mild liver or kidney damage in 10 percent of users or a food additive that caused cancer in 1 in 1,000 consumers. However, if a new chemotherapeutic agent cured cancer in 80% of the cases, some mild liver or kidney damage might be considered acceptable. Toxicology helps researchers to characterize the adverse effects that form part of the risk-benefit balance for a given chemical, and defining the dose-response relationship is perhaps the most critical aspect of this process (Text Box 6.1).
316
Text Box 6.1 Dose-Response Curve Increasing the dose of a medication increases the therapeutic effect until a maximal response is achieved (Figure 6.2). Adverse effects typically follow a similar trend. Ideally, the maximal therapeutic effects occur at a dose that is lower than the dose at which toxic effects are observed. One half of the maximal effect, whether it be therapeutic or toxic, can be used to compare the potency of different compounds. In Figure 6.2, Drug A has its maximal effect before toxic effects are observed, while Drug B exerts toxic effects at a dose lower than its maximal therapeutic effect. The vast majority of environmental chemicals have no direct beneficial effect on human health; thus the focus is on their toxic effects.
Figure 6.2 Examples of Dose-Response Curves
The dose-response relationship is a quantitative description of the association between exposure to a compound and the toxic effects produced by that exposure. In order for a chemical to exert a toxic effect, the chemical or its active metabolite must reach the site in
317
the body where it can exert its adverse actions, it must do so at a concentration sufficient to cause an effect, and it must persist at this site long enough to exert the effect. In order to assess the toxicity of a given chemical, we need to know not only about the toxic effects it produces but also how an individual might be exposed to the compound and how frequently that exposure occurs (exposure is examined further in Chapter 8). In adults, dermal exposure, ingestion, and inhalation are the major routes by which individuals can be exposed to chemicals. There are also some unusual exposure routes, such as through broken skin or through the eyes.
For the developing embryo or fetus the primary route of exposure is via the placenta. Given the inherent vulnerability of the fetus, in utero exposures via the placenta are of major concern. Major research efforts are under way to better understand the role of the placenta in human health (National Institute of Child Health and Human Development, 2015). After birth, the nutrient-rich breast milk on which infants rely represents another unique source of exposure.
The timing and route of administration can have a significant effect on the toxicity of certain chemicals. For example, the pesticide chlorpyrifos, an organophosphate (see Text Box 6.7), is ten times more toxic via oral administration than via dermal application, and in utero exposures that occur during critical windows of development can have greater overall effects on the health of the developing child than exposures that occur during adolescence.
318
Tox Box 6.1 Bisphenol A (BPA)
WHAT IS IT? Bisphenol A (BPA) is an organic chemical composed of two benzene rings with one hydroxyl group on each ring and two methyl groups between the rings. BPA is soluble in organic solvents but has poor water solubility.
HOW IS IT USED?
BPA is a building block of polycarbonate plastic, a rigid plastic used to make many products, including reusable water bottles and other drink containers, compact discs, auto parts, toys, medical devices, and eyeglasses. BPA used to be used in baby bottles, sippy cups, and other products for
319
babies and young children, but (as described below) that use has ended. The second largest use of BPA is in epoxy resins used in the linings of metal cans used for food storage, water pipes, and beverage bottle caps, and in thermal paper products such as shopping receipts. BPA meets the U.S. Environmental Protection Agency's definition of a high production volume chemical—one that is produced or imported in quantities greater than 1 million pounds.
HOW ARE PEOPLE EXPOSED? Of the three main routes of toxicant exposure (oral, inhalation, and dermal), oral ingestion of BPA is most common. BPA used in food and drink packaging leaches into the contents and is ingested. Leaching occurs at a greater rate when packaging that contains BPA is heated or when the food is acidic. BPA is frequently present in the polymer linings of metal food cans that may be stored for months prior to consumption. During this period, BPA can leach from the can lining into the food. The 2009 to 2010 National Health and Nutrition Examination Survey (NHANES) found that 90% of Americans had detectible exposure to BPA. This widespread exposure to BPA has raised concerns over its effects at a population level.
WHAT ARE THE TOXIC EFFECTS? For BPA, as for most toxicants, high-level exposure is associated with different health impacts than low-level exposure is. While BPA has been in consumer products since the 1950s, concern over its low-dose toxicity only recently arose. The potential for low-dose impacts was first discovered by accident. Scientists at Western Case Reserve University studying reproduction using animal models noticed that a high proportion of their animals were failing to reproduce. This led the scientists to carefully examine every piece of laboratory equipment for a possible cause. Eventually, they discovered that the janitor was cleaning the cages and water bottles using a harsh soap that damaged the plastic surfaces, allowing BPA to leach out (Hinterthuer, 2008). This finding catalyzed concern over exposure to BPA
320
in people.
The biggest concerns from low-level BPA exposure are endocrine disruption and reproductive and developmental toxicity. Animal and cell culture studies show that BPA mimics the hormone estrogen and interferes with the endocrine system. Endocrine disruption can lead to adverse developmental, reproductive, neurological, and immune effects in humans and animals. A detailed 2008 review of BPA literature by the National Toxicology Program (listed in the final section of this Tox Box) found grounds for concern over developmental toxicity for fetuses, infants, and children exposed to BPA. The parts of the body found to be most susceptible included the brain and prostate gland. BPA was also found to be associated with behavioral problems. Other research suggests that, as an endocrine disruptor, BPA may be associated with a risk of obesity, adult reproductive health problems, and specific cancers.
HOW ARE PEOPLE PROTECTED?
The reduction of BPA exposure in the United States is a unique and interesting example of consumer power. The potential toxicity of BPA led many consumers to reduce their use of BPA products. In response, industries began using alternative chemicals. Unfortunately, most of these chemical replacements have not been proven to be safer than BPA. The Food and Drug Administration, largely in response to the
321
National Toxicology Program's 2008 report, banned BPA in baby bottles and cups designed for toddlers in 2012. Practical recommendations to reduce exposure, such as not heating plastic food containers, also help to protect people from the potential toxicity associated with BPA exposure.
WANT TO LEARN MORE? Several government agencies have issued assessments of BPA. The Food and Drug Administration has released a series of reports; the latest, in 2014, was Updated Review of Literature and Data on Bisphenol A (www.fda.gov/downloads/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/UCM424071.pdf In 2008, the National Toxicology Program released its Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol A (NIH Publication No. 08-5994) (ntp.niehs.nih.gov/ntp/ohat/bisphenol/bisphenol.pdf). BPA toxicity is a highly contested topic. An industry point of view is presented at factsaboutbpa.org and an environmental point of view is presented at www.nrdc.org/living/chemicalindex/bisphenol-a.asp.
Contributed by Marissa Smith
Several issues must be considered when evaluating a dose-response relationship. First and foremost, it must be known that the response observed is due to the exposure to the compound. Second, the magnitude of the response is generally a function of the dose administered, although these relationships are not necessary linear. Some dose-response curves are very steep, while others resemble an inverted U where maximal toxicity does not occur at the maximal dose or exposure. There also needs be a quantitative method for measuring the response, as discussed in Chapter 8. An additional layer of complexity is that one must consider windows of susceptibility. For example, a particular dose considered to be safe during adulthood could have more deleterious effects during pubertal development. Also, during embryogenesis and fetal development there are particular points in time when chemicals have a much more detrimental effect. Thus “the dose makes the poison” concept needs to take into consideration the temporal and
322
relational aspects that can significantly modify the relationship.
Decades ago many compounds could be detected in the environment or in the body only at relatively high concentrations; for example, in parts per million. Today's detection systems, such as gas and liquid chromatography, mass spectrometry, and atomic absorption spectrometry, are up to a million times more sensitive. As a result, dangerous chemicals are now routinely detected in environmental and human samples, even though present at extremely low levels. It is essential to remember that the biological dose, and not the mere presence of a toxicant in a sample, is the key driver of toxicity. If it takes a concentration of 10 parts per billion of a particular compound to cause any toxicity and if that compound is detected at 1 part per trillion, it is very unlikely to cause an effect. There are several critical questions to ask: How much of the chemical is in the environment? How much of the chemical is in sufficient proximity to a human population to cause exposure? How much of the chemical actually enters the human body? What level of the chemical is necessary to cause an adverse biological effect? As described in Chapter 8, this is the domain of an exposure assessment professional, often working in conjunction with a toxicologist or chemist. The toxicologist is primarily focused on the effects of the chemical of interest once it is in the body.
323
Toxicology and Environmental Public Health Toxicology plays a key role in the field of environmental health and public health in general. By focusing on biological mechanisms of action and physiological pathways perturbed by various chemicals, toxicology provides a biological anchor for association studies. This foundation helps to connect environmental concerns to biomedical or clinical strategies for preventing or treating certain conditions. The field of toxicology helps to determine the conditions under which a given compound may cause adverse effects, so it is important for public health professionals to understand key concepts that toxicologists use to make these determinations. Once exposure has occurred, through what routes does the compound enter the body? How much of the compound enters? Where in the body does it go? What does it do once it reaches a particular organ? What physiological effects follow, and if appropriate, what forms of treatment exist? How does the body handle the compound? Does it persist in particular organs? Is it metabolized and excreted in the urine? Armed with the scientific principles of toxicology, the public health professional can find answers to these questions and make prudent decisions on how to manage a particular exposure.
Toxicology is integrated into public health practice in several ways. For example, in providing safe drinking water to a community, it is important to understand both the adverse effects of organisms found in the water and the adverse effects of chemicals used to kill the organisms. As discussed in Chapter 16, chlorination is an effective means of reducing microbiological contamination in water, but chlorine is a dangerous chemical to transport, as explored in Text Box 6.2, and once in drinking water, chlorine can form chlorinated organic compounds known as disinfection by-products. Toxicology can help in identifying these compounds, assessing the risk they pose, and balancing that risk against the risk of microbiological contaminants. In risk assessment as in many areas of health, collaboration between professionals in related disciplines becomes critical in protecting the public.
324
Text Box 6.2 Transporting Vital, Yet Dangerous Chemicals Chlorine is the primary means of water disinfection in many countries. Large volumes of the chemical must be transported across the country in train cars and tanker trucks. There have been several accidents that have led to the release of large amounts of chlorine, from a train accident in Graniteville, South Carolina, to an incident at a water park in White Lake Township, Michigan, and a storage tank rupture in Cocoa Beach, Florida. The properties that make chlorine an excellent disinfectant also make it a potentially hazardous human health threat. Chlorine is a yellow-greenish gas with intermediate water solubility. It can combine with water to form hydrochloric acid and hypochlorous acid:
Thus, when chlorine gas is inhaled, it can react with the moisture in a person's eyes, mouth, and airways to form corrosive acids. The initial symptoms include irritation and pain in the eyes, throat, and lungs. The irritation of the airway mucosa leads to inflammation and swelling in the lungs. When the reaction is severe, pulmonary edema can occur, with the lungs filling with fluid, impairing breathing. Even after the initial acute irritant inhalation exposures have subsided, more persistent problems can occur, such as a condition called reactive airways dysfunction syndrome.
From a historical perspective the incident at Graniteville stands out as one of the worst chlorine gas releases in the United States. Over 5,000 people were evacuated, 250 people were injured, and 9 people died (Wenck et al., 2007). Those who were injured may continue to have breathing difficulties for years. This incident illustrates the acute toxicity of irritating inhaled materials and how this exposure may occur both in the workplace and in the general environment. It also illustrates the trade-offs inherent in environmental health; although chlorine gas is highly toxic, chlorine has an
325
important, and arguably essential, public health role in water purification.
Another reason that a student in any discipline, but especially environmental health, should develop an appreciation for toxicology is that it is highly relevant to his or her own health. We are exposed to myriad chemicals every day. We ingest chemical residues in the food we eat and we inhale particles in the air we breathe. Many people voluntarily ingest pharmaceutical and recreational drugs, with little or no knowledge of the potential adverse effects. An understanding of toxicology can clarify some of these issues and help us make healthy and informed choices. For example, a student who has a basic understanding of toxicology will realize that a claim that a product—whether a vitamin, a herbal supplement, an agricultural chemical, a medication, or an illegal drug—has no side effects is erroneous and misleading. No agent is completely free of adverse effects, given sufficient doses and circumstances. Similarly, a student who thinks in terms of toxicological action will realize that natural is not the same as safe. Nature produces some highly toxic compounds, such as arsenic, snake venoms, and the carcinogenic toxins produced by some molds. Many psychogenic compounds are completely natural but can have dramatic and long-term adverse effects on brain chemistry. Natural is not necessarily safe.
326
Toxicant Classifications Toxic compounds are categorized in three major ways: by chemical class, by source of exposure, and by effects on human health, or more specifically, on specific organ systems. A knowledge of each category helps in understanding toxicology.
Examples of chemical classes are heavy metals, alcohols, and solvents. In essence, the rules of chemistry create the classes, based on such features as functional groups, the presence of metallic elements, and physical properties, such as vapor pressure. Chemical classification may also address physical state; that is, whether a toxicant exists as a liquid, solid, gas, vapor, dust, or fume.
The second system of categorization is functional and is based on the source of exposure. Examples are industrial pollutants, waterborne toxicants, air pollutants, and pesticides. These categories are useful in identifying the source of a problem and are commonly used by environmental health professionals. However, chemicals used in similar ways may vary greatly in their mechanism of toxicity. Because this categorization system groups together chemicals with little chemistry in common, it can obscure connections based on molecular structure. To the toxicologist this system ignores the biological mechanisms that underlie toxicity, even though it is quite relevant when attempting to reduce exposures.
The third system of categorization looks at the organ system in which toxic effects are most pronounced (the target organ). For example, chemicals may target the liver (hepatotoxic), the kidney (nephrotoxic), or the nervous system, whether peripheral or central (neurotoxic). Chemicals that disrupt DNA structure or function are classed as genetic toxicants, mutagens, or carcinogens, depending on their specific effects; carcinogenicity has been a central focus of toxicology, as discussed in Text Box 6.3.
327
Text Box 6.3 Chemical Carcinogenesis For more than two centuries it has been known that chemical exposure can cause cancer. The International Agency for Research on Cancer (IARC) is a division of the World Health Organization. IARC serves as the arbiter of human carcinogen classification. Determining whether compounds are carcinogens is a complicated process. That said, it is problematic that fewer than 1,000 compounds have IARC designations, a mere fraction of the estimated 80,000 chemicals in commerce. Toxicology plays an important role in determining whether or not chemicals are classified as carcinogens (Table 6.1).
Table 6.1 Carcinogen Classification of Chemicals: IARC Results as of March 2015
Number of categorized chemicals
Group 1
Carcinogenic to humans 116
Group 2A
Probably carcinogenic to humans
73
Group 2B
Possibly carcinogenic to humans
287
Group 3
Not classifiable as to its carcinogenicity to humans
503
Group 4
Probably not carcinogenic to humans
1
Cancer is pathologically defined as uncontrolled cell growth, growth that reflects alterations in the cell's genome or gene expression (or both). Chemically induced carcinogenesis has classically been thought to proceed in stages: initiation, promotion, progression, and metastasis. Some chemicals may directly damage DNA during initiation. Promotion
328
involves factors that facilitate cell growth and replication, such as dietary and hormonal factors. An example of a promoting agent is the hormone estrogen, which activates gene expression pathways in target organs such as the breast and thereby promotes tumor growth. Progression is irreversible and involves morphological alterations in the genomic structure and growth of altered cells. In the final stage, metastasis, the affected cell population spreads from its immediate microenvironment to invade other tissues. Many of the known environmental chemical carcinogens must be bioactivated in order to exert their damaging effects. An example is benzo[a]pyrene, which must be converted to its epoxide metabolite in order to damage DNA (Figure 6.3). Other chemical carcinogens include metals (such as arsenic, chromium, and nickel), minerals (such as asbestos), aliphatic compounds (such as formaldehyde and vinyl chloride), and aromatic compounds (such as coke oven emissions and naphthylamines). Over the past few years many suspected chemical carcinogens have been found to exert their actions through epigenetic modification, as discussed in Chapter 7. Rather than causing overt mutations of key regulatory genes, chemicals can modify gene function epigenetic changes, such as methylation, to impact key stages of carcinogenesis. This area of research could greatly change the way we think about cancer causation.
Figure 6.3 Metabolic Transformations of Benzo(a)pyrene This simplified diagram shows metabolic transformations yielding a carcinogen, involving the enzymes cytochrome P450 (CYP) and epoxide hydrolase (EH).
Although many chemicals have the potential to induce cancer, a number of defense mechanisms can mitigate cell damage. Many enzyme systems can detoxify reactive toxicants before they can interact with their target molecules.
329
DNA repair mechanisms can often repair damage caused by toxicants. If DNA is not repaired, the cell may undergo programmed cell death before the altered DNA can be replicated. Finally, the immune system can seek out and destroy transformed cells that have escaped the other mechanisms of defense.
Other organ systems that can be the targets of toxicity include the respiratory system, cardiovascular system, skin, reproductive system, endocrine system, immune system, and blood. Endocrine disruption has been of special interest in recent years, as described in Text Box 6.4. Fetal development is more a process than an organ system, but it too is often viewed as a target of toxic exposures.
330
Text Box 6.4 Endocrine Disruptors Over the past several years, toxicologists have been observing that chemicals in the environment may act in a manner analogous to that of endogenous hormones in wildlife and humans. Such chemicals are termed endocrine disruptors and can be defined as exogenous substances or mixtures that alter the function of the endocrine system. Although this concept has received heightened attention in recent years, it is not new. Rachel Carson's book Silent Spring, published in 1962, is widely considered to have foreshadowed the current interest in endocrine disruption. Carson suggested that widespread and heavy use of the insecticide DDT was causing problems in bird reproduction, and that if not stopped, DDT use would devastate bird populations and lead to a “silent spring.”
The endocrine disrupters that have gained the most attention mimic endogenous estrogen; they are often termed environmental estrogens or xenoestrogens (Dickerson & Gore, 2007). Estrogen is the predominant female reproductive hormone. It exerts its physiological actions by binding to nuclear receptors and activating gene transcription in target tissues such as the breast, uterus, and brain. Environmental estrogens may disrupt normal estrogen function by binding to these same receptors and eliciting a response similar to, although usually smaller than, the response elicited by the endogenous hormone. Alternatively, environmental estrogens may block normal estrogen binding to these receptors. Chemicals that may act this way include the pesticide DDT (Tox Box 18.2, in Chapter 18) and polychlorinated biphenyls (PCBs) (Tox Box 2.1, in Chapter 2). There is some evidence linking human trends such as menarche at younger ages and declining sperm counts with environmental estrogens, although this finding remains controversial.
In addition to man-made chemicals that may act as estrogen mimics, there are also naturally occurring estrogen mimics,
331
such as the isoflavones that are synthesized by plants as a defense against pathogens and herbivores. Indeed, high levels of isoflavones in clover have been linked to the infertility in sheep termed clover disease. High levels of isoflavones have also been found in soy milk. Excretion of natural hormones, the use of estrogen-containing pharmaceuticals, and the use of veterinary medication may also contribute to the levels of estrogens in the environment.
Estrogens are not the only hormones whose action may be disrupted by environmental chemicals. The androgenic pathway has also been suggested to be a target for a variety of environmental toxicants, including phthalates (see Tox Box 6.3 later in the chapter), vinclozolin, and DDE (dichlorodiphenyldichloroethylene), a metabolite of DDT. These chemicals may interfere with androgen-mediated events such as formation of the male genitalia during embryogenesis. Indeed, recent animal studies have demonstrated that exposure to vinclozolin results in transgenerational toxicity (Crews et al., 2012).
The thyroid system is another major endocrine target of environmental toxicants. Various chemicals have been demonstrated to interfere with thyroid function, primarily in laboratory tests. For example, PCBs, polybrominated diphenyl ethers, and perchlorate have all been demonstrated to affect thyroid function. Because thyroid hormones are critical in neurodevelopment and metabolic control, there is increasing concern over the effects such chemicals might have on the human population and whether such exposures might contribute to cognitive dysfunction, decreased IQ, obesity, or diabetes (Meeker, 2012). Figure 6.4 shows the structures of six suspected endocrine-disrupting chemicals. An exciting development in toxicity testing is the use of high- throughput screens that are making it possible to test tens of thousands of chemicals for their ability to interact with key endocrine targets.
332
Figure 6.4 Structures of Some Suspected Endocrine- Disrupting Chemicals
The organ system classification of toxicants is commonly used in teaching graduate toxicology, but studying the compounds by chemical class and source has considerable value. When working to protect human health, one needs to consider how a chemical will affect a particular physiological function, whether it be blood pressure, respiration, memory, or urine production. Because each of these functions is controlled by a particular organ system (or systems), organ system classification provides a logical framework for toxicologists; indeed, toxicologists often specialize in the actions of compounds on a specific organ system. Also, even though compounds that affect a specific system may differ in their chemical composition, they often share the features that lead them to target that system. A public health professional should not be satisfied with knowing that a particular substance is toxic, but should ask, What does it do to the body? What system is it disrupting? What are the expected effects? The organ system approach is especially helpful in answering such questions, but if one is trying to determine how a mixture of endocrine-disrupting compounds is impacting reproduction, one also needs to evaluate the chemical
333
characteristics and source of exposures.
To evaluate the toxic effects of a chemical on a particular organ system, one needs a general understanding of how that system works. For example, the main function of the kidneys is to maintain fluid and electrolyte homeostasis in the body. This is accomplished by the reabsorption of material filtered from the blood, including water, ions, and nutrients, and by the excretion of waste material. The kidneys receive a disproportionate amount of the body's blood flow, approximately 20% of cardiac output, considering that they represent less than 1% of the total body weight. This high blood flow, in combination with the numerous transport mechanisms within the kidney designed to reclaim water and nutrients and excrete waste, renders the kidneys exquisitely sensitive to damage by blood-borne toxicants. Of all the cell types in the kidney, one of the most common targets of toxicant-induced injury is the proximal tubule. The proximal tubule is divided into three morphologically distinct segments that vary in structure and function. The proximal tubule reabsorbs 99% of the filtered material. The numerous transport mechanisms in the proximal tubule allow reabsorption of amino acids, sugars, proteins, many electrolytes, and other solutes. Damage to the proximal tubules by toxicant exposure can lead to deterioration of renal function and ultimately renal failure. Exposure to mercury, for example, is known to damage one particular segment of the proximal tubule due to its specific complement of enzymes (see Tox Box 6.2). A toxicologist interested in identifying how mercury alters renal function might isolate proximal tubules in the laboratory, perform toxicity tests on these isolated cellular sections, and compare these animal results with human urine clearance studies and postmortem examination.
334
Tox Box 6.2 Polycyclic Aromatic Hydrocarbons
WHAT ARE THEY? Polycyclic aromatic hydrocarbons (PAHs) are a group of semivolatile organic compounds consisting of multiple aromatic rings. Their nonpolar structure makes them highly lipophilic and thus more soluble in fats and oils than in water. The larger PAHs (more than six aromatic rings) are the least water soluble. PAHs accumulate in the environment and in the human body. Of the hundreds of PAHs found in the environment, seventeen have been identified by the U.S. Agency for Toxic Substances and Disease Registry as having the greatest potential for adverse human health effects. They are listed below.
Seventeen PAHs with Potential for Adverse Human Health Impacts
Acenaphthene
Acenaphthylene
Anthracene
Benz(a)anthracene
Benzo(a)pyrene
Benzo(e)pyrene
335
Benzo(b)fluoranthene
Benzo(ghi)perylene
Benzo(j)fluoranthene
Benzo(k)fluoranthene
Chrysene
Dibenz(ah)anthracene
Fluoranthene
Fluorene
Indeno(1,2,3-cd)pyrene
Phenanthrene
Pyrene
HOW ARE THEY USED? PAHs are usually not produced intentionally but are released into the environment as combustion by-products, industrial waste, and chemical spills. Most PAHs are released into the air as a by-product of fossil fuel combustion, but smaller quantities of PAHs are also released from natural volcanic activity. Once in the air, PAHs disperse, sometimes across great distances, before settling in soil or water bodies. Coke ovens release PAHs into the air as coal is burned to create the pure carbon used in producing aluminum, steel, graphite, and electronics. The residues not released into the air are termed coal-tar pitch. Coal-tar pitch is a component of coal- tar sealants that are used to seal asphalt paving, parks, and playgrounds. PAHs also enter the environment as discharge from industrial and wastewater treatment plants. Finally, PAHs may enter the environment through chemical spills. The Deepwater Horizon oil spill in 2010 greatly increased PAHs, among other contaminants, in the Gulf of Mexico. Once in the water, PAHs generally adhere to sediment, where they can be ingested and metabolized by microorganisms.
HOW ARE PEOPLE EXPOSED? The most common route of exposure to PAHs is through
336
inhalation of contaminated air. Inhalation exposure to PAHs occurs whenever people are in close proximity to busy roads, waste incinerators, and agricultural burning. People living in rural regions tend to be exposed to lower air concentrations of PAHs than those living in urban areas. Indoor air may also contain PAHs from wood and tobacco smoke. People who work in plants that produce coal tar, asphalt, or aluminum; in municipal waste incinerators; or in close proximity to vehicle exhaust inhale higher levels of PAHs than the general public.
Oral exposure to PAHs, though minor when compared to inhalation exposure, occurs through ingestion of contaminated food. PAHs are found in food that is grown in contaminated soil or cooked by grilling or charring. In developing countries, cooking and heating in poorly ventilated spaces with wood, dung, or agricultural residues and also household use of coal drastically increase PAH exposure. Some Superfund Sites in the United States have exceedingly high levels of PAHs in the soil that result in community exposures. This exposure route is particularly relevant for children, who may ingest soil as they play outdoors.
WHAT ARE THE TOXIC EFFECTS? The primary health impact of concern following PAH exposure is carcinogenesis, though reproductive and immune system disorders have also been reported. Laboratory animals exposed to PAH mixtures develop tumors, and similar evidence of carcinogenicity exists in humans. People who have experienced long-term exposures to high concentrations of PAHs are at an increased risk of developing cancer. IARC has classified benz[a]anthracene and benzo[a]pyrene as probable human carcinogens. Though evidence for noncarcinogenic impacts is less conclusive, prenatal exposure to PAHs in animals resulted in birth defects including decreased body weight, reproductive problems, and immune system disorders. Whether these impacts occur in humans is unknown.
337
HOW ARE PEOPLE PROTECTED? People are protected from PAH exposure through international efforts and the efforts of federal agencies such as the Occupational Safety and Health Administration (OSHA) and the Environmental Protection Agency (EPA). Internationally, the World Health Organization is working to reduce indoor air pollutant exposure in developing countries by supporting the transition to cleaner fuels and distribution of improved indoor cooking stoves. The European Union limits the concentration of specific PAHs in car and truck tires because, as tires wear, the rubber disintegrates and PAHs are released into the environment. In the United States, various federal laws and regulations limit PAH exposure. OSHA has set an occupational exposure limit that prevents workers from inhaling more than 0.2 milligrams of PAHs per cubic meter of air over the course of an eight-hour workday. The EPA limits the concentration of PAHs in drinking water under the Safe Drinking Water Act and limits seven specific PAHs under the Clean Air Act. Lifestyle choices, such as avoiding cigarette and wood smoke and moderating consumption of charred or grilled foods can also protect people from PAH exposures.
WANT TO LEARN MORE? The ATSDR Toxicological Profile on PAHs is available at www.atsdr.cdc.gov/toxprofiles/tp69.pdf. A recent review article on the effects of PAHs is K.-H. Kim, S. A. Jahan, E. Kabir, and R.J.C. Brown, “A Review of Airborne Polycyclic Aromatic Hydrocarbons (PAHs) and Their Human Health Effects,” Environment International, 2013, 60, 71–80. To learn more about the measurement of PAHs in the environment, and how this supports risk assessment, see J. Wickliffe et al., “Evaluation of Polycyclic Aromatic Hydrocarbons Using Analytical Methods, Toxicology, and Risk Assessment Research: Seafood Safety After a Petroleum Spill as an Example,” Environmental Health Perspectives, 2014, 122(1), 6–9.
Contributed by Marissa Smith
338
Toxicokinetics It is a useful exercise to track a potentially toxic compound from the environment (from water, air, soil, or food) into and then through the body all the way to its molecular site of action. This study of this process is referred to as toxicokinetics. Suppose that a given compound is generated as a by-product of a particular industrial process. Whereas an exposure assessor measures the concentrations of the compound in the air and an epidemiologist studies the incidence of certain diseases in the surrounding community, the toxicologist is concerned with how the compound gets into the body and what it does once it is there. For example, the compound may be inhaled into the lungs. Once there, it rapidly crosses the alveolar membrane and enters the pulmonary circulation. It travels through the pulmonary vein to the left side of the heart and then circulates throughout the entire body. A large proportion of the compound goes to the liver, where it is activated into a reactive epoxide. This metabolite then finds its way to the kidneys, where it is reabsorbed along with salts and other polar compounds and transported across the cellular membrane of the proximal tubule. There it accumulates and damages cellular macromolecules.
If the toxicologist can show that this compound damages the kidney and if the epidemiologist identifies an exposure-related increase in the incidence of renal failure in a population, regulatory steps may be taken to eliminate or limit the use of this compound. Toxicology helps researchers to provide biological plausibility to association studies conducted in large human populations. Toxicology can also be very useful in monitoring the development of new compounds. If a toxicologist shows that a new compound has an effect in rats or mice similar to the effect of a known toxicant, the new compound is likely to show the same toxicity in humans, so a manufacturer would be wise to discontinue development of that compound. Thus the understanding of mechanisms can lead to the development of safer chemicals and drugs. In fact, toxicology can inform developments in green chemistry, the design of chemical products and processes that reduce or eliminate the use or generation of hazardous substances.
After a person is exposed to a particular chemical (the term xenobiotic is used to describe chemicals that are foreign to the
339
body), a sequence of steps determines the response to the chemical: absorption into the body, distribution throughout the body, metabolism, and excretion (Figure 6.5). Each of these steps can impact the toxicity of the chemical by influencing where it goes, how it can be chemically modified, and how long it stays in the body. This toxicokinetic sequence is described in the following sections.
Figure 6.5 Key Steps in Toxicokinetics
Absorption Once a person has come in contact with a toxic compound, that compound may gain access to the body. It is not enough for this compound to contact the skin, be inhaled into the lungs, or enter the intestinal track; it must actually traverse the biological barrier. Each of these pathways exhibits characteristics that affect absorption. One of the most important characteristics affecting the entire process of toxicokinetics is solubility. Compounds that readily dissolve in water are called hydrophilic (meaning “water loving”), and compounds that dissolve in lipids instead are called hydrophobic (“water hating”) or lipophilic (“fat loving”). Recall from chemistry the terms polar and nonpolar used to describe chemicals. Asymmetric molecules, such as water or chemicals with long side chains and functional groups, are often polar, whereas symmetric molecules with minimal added groups, such as benzene, are nonpolar. Salad dressing illustrates this property; the oil (hydrophobic) and the vinegar (hydrophilic) don't readily mix. The octanol:water coefficient (termed Kow) is a way chemists measure the relatively solubility of chemicals. Urine is composed primarily of water, explaining how water-soluble chemicals can be excreted in
340
urine. Furthermore, if one considers that most of the biological barriers that exist in our bodies are composed of lipids, the ability of chemicals to traverse these barriers has much to do with whether or not they are fat soluble.
The gastrointestinal system is designed for nutrient absorption, and it has a large surface area with numerous transport mechanisms. The presence of gut bacteria (the microbiome) can affect absorption (see Text Box 6.5). Many toxicants can take advantage of this system to enter the body. Toxicants can also be absorbed through the pulmonary alveoli. The alveoli are the functional units of the lung and the sites of gas exchange between the air and the blood supply. The skin represents a third key route of toxicant exposure. Many occupational exposures occur via this route. Although intact skin offers an effective barrier against water-soluble toxicants, fat-soluble toxicants can readily penetrate the skin and enter the bloodstream.
341
Text Box 6.5 The Microbiome and Toxicology Humans provide a home to microorganisms that reside within our intestines, oral and nasal mucosa, and urogenital system and on our skin. While these microbes are very small, the number of microbes that reside in one person is estimated to be over 100 trillion. That outnumbers the number of human cells in a given person by a factor of 10. Once thought to be mere parasites or pathogens, many of these microbes are now recognized as playing important roles in the processing of nutrients and environmental chemicals. Microbes in our intestines can influence the uptake of chemicals (and nutrients) in our food, and the chemicals to which we are exposed can alter the composition of the microbes themselves, creating a complex series of feed forward and feedback mechanisms that can have major effects on health. Through efforts such as the Human Microbiome Project (www.hmpdacc.org), scientists are learning more about what roles these microbes play in human health.
A recent paper provides a wonderful illustration of how the microbiome fits into toxicology. The study focused on two groups, a group that regularly consumed meat products and a group of vegetarians. The researchers had both groups consume a steak meal and then measured the formation of trimethylamine N-oxide, a compound associated with cardiovascular disease. The meat eaters generated much higher levels of trimethylamine N-oxide than the vegetarians even though they consumed the same meal. The increased production of the carcinogen was shown to be the result of the different gut microbiomes present in the two groups. This study shows that diet can alter the composition of one's gut microbiome and that this can, in turn, alter the potential adverse effects of subsequent exposures that occur from ingestion of food (Tang et al., 2013).
342
Distribution Once in the bloodstream a toxicant can be distributed throughout the body. If the toxicant is fat soluble, it is often carried through the aqueous environment of the bloodstream in association with blood proteins, such as albumin. Toxicants generally follow the laws of diffusion, moving from areas of high concentration to areas of low concentration. Chemicals absorbed in the intestine are shunted to the liver through the portal vein, in a first-pass process, and may undergo metabolism promptly. A limited number of chemicals may be excreted unchanged into bile or by the kidneys into urine.
Metabolism Once in the body most toxicants undergo metabolic conversion, or biotransformation, a process mediated by enzymes. The majority of biotransformation reactions occur in the liver, which is rich in metabolic enzymes. However, nearly all cells in the body have some capacity for metabolizing xenobiotics. In general, metabolic transformations lead to products that are more water soluble and less fat soluble. The metabolic product is therefore more soluble in urine, which facilitates its excretion. For example, benzene is oxidized to phenol (see Tox Box 7.1, in Chapter 7), and glutathione combines with halogenated aromatics to form nontoxic and more polar mercapturic acid metabolites. However, metabolic transformations sometimes yield increasingly toxic products. One example is the oxidation of methanol (a relatively nontoxic compound in its native form) to formaldehyde and formic acid (a compound that is quite toxic to the optic nerve and causes blindness).
Traditionally, metabolic transformations are divided into four categories: oxidation, reduction, hydrolysis, and conjugation. Transformations in the first three of these reaction categories, known as phase I reactions, generally increase the polarity of substrates and can either increase or decrease toxicity by revealing functional sites. Many compounds undergo bioactivation at this stage. In conjugation, the only phase II reaction, polar groups are added to the products of phase I reactions. Most chemicals pass sequentially through these two phases, as illustrated by acetaminophen (Figure 6.6), although some
343
are directly conjugated. Many examples of each type of reaction can be found in standard toxicology textbooks (such as Klaasen, 2013).
Figure 6.6 The Metabolism of Acetaminophen Acetaminophen (or paracetamol, as it is known in Europe) is one of the most commonly used over-the-counter medications. The drug can undergo hydroxylation (phase I) followed by glutathione conjugation (phase II), or also directly undergo glucuronidation or sulfation (phase II). When insufficient levels of glutathione are available, a very toxic metabolite can build up in the liver and lead to significant toxicity.
As mentioned earlier, various combinations of these reactions may be assembled in response to the same toxicant. Metabolic strategies for a particular toxin may vary widely among species, so an animal study, to be applicable to humans, should use a species with pathways similar to those of humans. The most prominent enzyme system for performing phase I reactions is the cytochrome system. These enzymes are found in the endoplasmic reticulum of hepatocytes and other cells. In recent years, advances in molecular biology have greatly expanded our understanding of a particular enzyme complex, cytochrome P450. Dozens of distinct P450 genes have been identified and sequenced. They have been grouped into eight distinct families, and for many, specific functions have been identified. For example, the enzyme CYP1A1 metabolically activates polycyclic aromatic hydrocarbons (PAHs); the enzyme
344
CYP2D6 is responsible for metabolizing such medications as beta- blockers and tricyclic antidepressants, while the enzyme CYP2E1 bioactivates vinyl chloride, methylene chloride, and urethane. Polymorphism in the genes that code for various P450 proteins results in different metabolic phenotypes, explaining why people may vary widely in their responses to similar medications or chemical exposures. Chapter 7 explores this key principle in detail.
Disruption of enzymatic function is a common mechanism of toxicity, as when organophosphate pesticides compete with acetylcholine for the binding sites on cholinesterase molecules (see Tox Box 18.1, in Chapter 18), or when metals such as beryllium compete with magnesium and manganese for enzyme ligand binding. For example, methyl alcohol is oxidized first by the enzyme alcohol dehydrogenase to formaldehyde, and then, by aldehyde dehydrogenase, to formic acid, which is toxic to the optic nerve. This process can be blocked by large doses of ethanol, which competes for enzyme binding sites and slows the formation of the toxic metabolite. The drug fomepizole acts in the same way, by selectively inhibiting alcohol dehydrogenase. This drug has been used to treat ethylene glycol poisoning, preventing the formation of the toxic metabolites glycolic acid and oxalic acid.
345
Tox Box 6.3 Phthalates
WHAT IS IT?
Like many groups of organic compounds, phthalates are a diverse group of individual chemicals with unique uses and toxic effects. As a group, phthalates are comprised of dialkyl or alkyl aryl esters of phthalic acid. The basic structure of a phthalate is shown here, with the carbon backbone and two variable groups (represented by OR and OR′). As with many organic compounds, the toxicity of a particular phthalate is determined by its molecular properties. Phthalates are classified as having either low or high molecular weights. Low molecular weight phthalates have between three and six carbons and high molecular weight phthalates have between seven and thirteen carbons on their backbones. The most common phthalates are diethylhexyl phthalate (DEHP), diisononyl phthalate (DINP), butyl benzyl phthalate (BBP), diethyl phthalate (DEP), di-n-butyl phthalate (DnBP), di-n- octyl phthalate (DnOP), dimethyl phthalate, (DMP), and dimethyl-terephthalate (DMT).
346
HOW IS IT USED? Phthalates are produced on a massive scale due to their wide use in consumer products. In fact, the EPA classifies phthalates as high production volume chemicals, meaning they are produced or imported in quantities greater than 1 million pounds per year in the United States. Most commonly, phthalates are used as plasticizers to increase the flexibility and durability of plastics. Consequently, they are found in most plastic products, including children's toys, clothing, cosmetics, food packaging, and even construction materials. Phthalates are also found in products used in medical care, such as intravenous fluid bags, blood transfusion bags, and other plastic tubing. Lower molecular weight phthalates are used in perfumes and solvents.
HOW ARE PEOPLE EXPOSED? People are exposed to phthalates through all three of the main exposure routes: oral, inhalation, and dermal. Uniquely, people can also be exposed to phthalates by intravenous injection, since phthalates are present in IV bags and tubing. Oral ingestion of phthalates represents the largest portion of total phthalate exposures. Oral exposure to phthalates occurs through ingestion of contaminated food, mouthing of plastic products, and ingestion of house dust. Phthalates found in food packaging can leach into and contaminate the food people eat. Children's toys also contain phthalates that are ingested when children put the toys in their mouths and chew them. Phthalates are also found in products designed directly for oral use in adults and children, such as toothbrushes, dishes, and food preparation items. Consumer products containing phthalates tend to disintegrate over time. These particles end up in house dust where detectable concentrations of phthalates can be found. This presents an additional risk of exposure to children, who spend more time on and near the ground where they are more likely to interact with house dust. Children inhale and ingest this house dust, leading to higher exposures to phthalates (relative to body weight) than adults sustain. Adult inhalation of phthalates is less common, though the
347
presence of phthalates in beauty products, such as fragrances, does lead to some exposure. The potential for dermal exposure is high; however, the phthalates that are absorbed through skin are thought to be less toxic. The most unique exposure route for phthalates is intravenous injection of phthalates that leach from the plastic tubing and fluid bags used in medical settings—a special concern for neonates in the intensive care unit, due to the increased susceptibility of neonates to the toxic effects of phthalates. Leaching from blood transfusion bags is also problematic because some phthalates, such as DEHP, are more slowly detoxified when injected directly into the bloodstream.
WHAT ARE THE TOXIC EFFECTS? Like most groups of chemicals, phthalates have different acute and chronic toxic effects. Most phthalates have low acute toxicity. However, chronic low-dose exposures are associated with reproductive and developmental toxicity, endocrine disruption, carcinogenicity, and asthma. These end points are not consistent across all phthalates because this is a diverse group with complex metabolism pathways. Once in the body, some phthalates can be metabolized into other bioactive phthalates. DEHP, for example, is metabolized into four different monophthalates. One of the monophthalates, mono-(2-ethylhexyl) phthalate, has been shown to be developmentally toxic in animals. DEHP, BBP, DBP, and DEP are toxic to animal fetuses. Animal offspring experimentally exposed prenatally to these phthalates developed birth defects including cleft palates and lung abnormalities. Male offspring had reproductive abnormalities including undescended testes, hypospadias, and hormonal disruptions. The International Agency for Cancer Research classifies BBP and DBP as possible human carcinogens and DEHP as a probable human carcinogen. In humans, DEHP is associated with asthma.
HOW ARE PEOPLE PROTECTED? Phthalates are regulated both internationally and nationally. The European Chemical Agency classifies five phthalates as
348
“substances of very high concern.” Substances in this classification are candidates for further regulation. In the United States the Consumer Product Safety Commission has banned manufacturers from using several phthalates (DEHP, DBO, BBP, DIDP, and DnOP) in concentrations greater than 0.1% (for an individual phthalate) in children's products. Some hospitals have adopted practices to decrease the phthalates in blood transfusion bags used for neonates. Because the phthalates leach over time, some hospitals prioritize fresh blood donations for neonates or use bags that do not contain phthalates. More research is currently being conducted to better understand the impacts of phthalate co- exposures on human health, because people are commonly exposed to mixtures of phthalates.
WANT TO LEARN MORE? A general review of phthalates, including regulatory issues, is P. Ventrice, D. Ventrice, E. Russo, and G. De Sarro, “Phthalates: European Regulation, Chemistry, Pharmacokinetic and Related Toxicity,” Environmental Toxicology and Pharmacology, 2013, 36(1), 88–96. A useful review of phthalate exposure and toxicity, with a focus on the food supply, is S. E. Serrano, J. Braun, L. Trasande, R. Dills, and S. Sathyanarayana, “Phthalates and Diet: A Review of the Food Monitoring and Epidemiology Data,” Environmental Health, 2014, 13(1), 43.
The special concerns of children's health with respect to phthalates are discussed in J. M. Braun, S. Sathyanarayana, and R. Hauser, “Phthalate Exposure and Children's Health,” Current Opinion in Pediatrics, 2013, 25(2), 247–254.
An emerging field of interest is the role of endocrine disrupters in promoting obesity, a topic discussed in M. Goodman, J. S. Lakind, and D. R. Mattison, “Do Phthalates Act as Obesogens in Humans? A Systematic Review of the Epidemiological Literature,” Critical Reviews in Toxicology, 2014, 44(2), 151–175.
Contributed by Marissa Smith
349
The enzyme systems that metabolize xenobiotics are not static. When the demand is high, their synthesis can be enhanced in a process called enzyme induction. The resulting increase in enzyme activity helps the organism respond to subsequent exposures, not only to the original xenobiotic but to similar substances as well. DDT and methylcholanthrene are examples of substances known to induce metabolic enzymes. People vary in their capacity for biotransformation in several ways. Two mechanisms of variation have already been mentioned: genetic factors and enzyme induction. Other factors that account for interindividual differences in metabolism are general health, nutritional status, and concurrent medications.
Excretion Biotransformation tends to make compounds more polar and less fat soluble; the beneficial outcome of this process is that toxins can be more readily excreted from the body. The major route of excretion of toxins and their metabolites is through the kidneys. Serum is filtered through the kidneys, key nutrients and most of the water are reclaimed, and some chemicals are actively secreted during this process. The daily volume of filtrate produced is about 200 liters—five times the total body water—in a remarkably efficient and thorough filtration process.
A second major organ of excretion is the liver. The liver occupies a strategic position because the portal circulation promptly delivers compounds to it following gastrointestinal absorption. Furthermore, the generous perfusion of the liver and the discontinuous capillary structure within it facilitate filtration of the blood. Thus excretion into the bile is potentially a rapid and efficient process. Toxicants that are secreted with the bile enter the gastrointestinal tract and, unless reabsorbed, are secreted with the feces. Materials ingested orally and not absorbed and materials carried up the respiratory tree and swallowed are also passed with the feces. All of this may be supplemented by some passive diffusion through the walls of the gastrointestinal tract, although that is not a major mechanism of excretion.
Volatile gases and vapors are excreted primarily by the lungs. The process is one of passive diffusion, governed by the difference between plasma and alveolar vapor pressure. Volatiles that are
350
highly fat soluble tend to persist in body reservoirs and take some time to migrate from adipose tissue to plasma to alveolar air. Less fat-soluble volatiles are exhaled fairly promptly, until the plasma level has decreased to that of ambient air. Ethanol is amphipathic, meaning that it has both lipophilic and hydrophilic properties, allowing it to dissolve readily in liquids and to partition into lipid membranes, resulting in accumulation in lipid stores. As it slowly but predictably moves out of lipid stores, it is liberated into exhaled breath. This is the premise behind the use of the Breathalyzer to determine one's level of intoxication. Interestingly, the alveoli and bronchi can sustain damage when a vapor such as gasoline is exhaled, even when the initial exposure occurred percutaneously or through ingestion.
Other routes of excretion, although of minor significance quantitatively, are important for a variety of reasons. Excretion into mother's milk obviously introduces a risk to the infant, and because milk is more acidic (pH 6.5) than serum, basic compounds are concentrated in milk. Moreover, owing to the high fat content of breast milk (3% to 5%), fat-soluble substances such as DDT can also be passed to the infant. Some toxins, especially metals, are excreted in sweat or laid down in growing hair, which may be of use in diagnosis. Finally, some materials are secreted in the saliva and may then pose a subsequent gastrointestinal exposure hazard.
351
Testing Compounds for Toxicity How does a toxicologist determine that one compound is more toxic than another? Several decades ago toxicologists used a rather crude method for determining the relative toxicity of compounds. By exposing laboratory animals to compounds and determining the dose that killed half the animals, they calculated the “lethal dose for 50%,” or LD50, an index that allowed comparisons among several unrelated compounds (Text Box 6.6).
352
Text Box 6.6 LD50 for Various Compounds The LD50, or lethal dose for 50%, is the dose of a chemical that kills 50% of those exposed to it in a defined time frame. A low LD50 for a chemical indicates that, compared to other compounds, less of this chemical is needed to cause toxicity— that it is more potent, or in common terms, that it is more poisonous. Figure 6.7 displays the LD50s and the structures for several chemicals; LD50s are expressed in terms of dose per kilogram of body weight.
Although crude, the LD50 has some important scientific strengths. The exposure is well defined (unlike the exposure in most human situations), the outcome is unambiguous, the measure can be applied across different compounds, and it can lead to a useful practical conclusion: if a compound is lethal at very low doses then human exposures should be prevented or strictly controlled. In today's modern laboratories, toxicologists focus more on how chemicals exert their toxic effects, such as through DNA mutation, enzyme inhibition, or altered nerve firing. This allows much of the testing to occur in test tubes, petri dishes, and 96- or 384-well trays. Experiments can focus on the effects of numerous chemicals on specific molecular or cellular targets. Such insight allows scientists to focus efforts when more complex experimental models like isolated organs or intact animals are needed. In recent years, questions about animal testing have been raised, and alternative methods are being actively pursued, as discussed in Text Box 6.7.
353
Text Box 6.7 Replace, Reduce, Refine: Laboratory Animals in Toxicology Laboratory animal research has long been a mainstay in the field of toxicology. Currently, ethical considerations, biological necessity, and costs are driving the trend to use fewer animals in toxicology research. There have been several initiatives in the United States and Europe to decrease reliance on laboratory animals; however, animal studies are required by many regulatory agencies, and there are many biological processes that cannot be effectively modeled in cell culture or test tubes. As countries strive to collect data on more chemicals, the push has been to focus on strategies that do not use animals. Toxicology in the 21st Century (Tox21) (www.ncats.nih.gov/research/reengineering/tox21/tox21.html) is a program that involves several U.S. federal agencies with a goal of systematically testing tens of thousands of chemical for their potential toxicity. These programs focus on high- throughput technologies that use cell lines and robotics to evaluate the toxicity of thousands of chemicals. Ideally, results from these studies can identify important physiological pathways of concern and mine data from previous animal studies to predict adverse effects. When the field is armed with data from thousands of chemicals and can derive structure activity relationships (that can be validated from the toxicity testing) on a computer, it becomes possible to predict which compounds will exert adverse effects without ever moving to the stage of animal testing. For example, if a chemical is structurally similar to a known carcinogen and exerts many of the same actions in a high- throughput screen, it may be possible to restrict its use (or halt its development) without ever entering animal testing. Of course chemicals that are destined for human use, either as pharmaceutical agents or as food additives, would still be subject to the animal testing required by the Food and Drug Administration (FDA) or other regulatory bodies. The Center
354
for Alternatives to Animal Testing is an excellent resource for strategies to reduce the number of animals used in research (caat.jhsph.edu).
355
From Regulatory Toxicology to Public Health Policy Toxicology can generate vast amounts of data on how chemicals affect human health, but in order to protect public health this information must be integrated into public policy. These issues fall into the domain of regulatory toxicology, which is closely aligned with the field of risk assessment (see Chapter 27). The basic principles of the dose-response relationship described earlier in this chapter are a critical part of that process. Through evaluation of dose-response curves generated during laboratory testing, several values can be determined that can be a basis for regulatory decisions. One of the most important values determined in such studies is the no-observed-adverse-effect level, or NOAEL. This is the highest dose administered for which no harmful effects are observed. The NOAEL is used by the Environmental Protection Agency in establishing the reference dose (RfD), which is an estimate of the daily oral dose of a chemical that is likely to be without appreciable risk for an individual over a lifetime of exposure. Results from toxicology studies directly impact a variety of regulatory and other policy approaches.
Public health policy to protect people from harmful chemicals is distributed across a series of agencies, defined by a range of laws, and as described below, far from complete. Policies are implemented according to the domains of exposure, including the workplace, the general environment, consumer goods, foods, and water.
Some of the highest exposures to chemicals occur in the workplace. In that setting, OSHA has regulatory responsibility. OSHA's approach to protecting workers from chemicals is explored in Chapter 21.
For nonworkplace exposures, the major piece of protective legislation in the United States is the Toxic Substances Control Act (TSCA) of 1976, which authorizes the EPA to regulate chemical substances and mixtures. Under TSCA, the EPA has three major responsibilities: gathering information on new and existing chemicals being manufactured in the United States, assembling
356
data on chemical risks, and regulating chemicals that present an “unreasonable risk of injury to health or the environment.” The EPA had a formidable job when it first implemented the TSCA. More than 60,000 chemicals were already in commercial use, and the law required no testing, so these chemicals were presumed to be safe and were grandfathered in. With chemicals innocent until proven guilty, the EPA bears the burden of proof that a chemical poses an “unreasonable risk.” Nor does the TSCA require premarket testing for new chemicals; it only requires manufacturers to provide basic chemical information, along with any toxicity information they have. This is in sharp contrast to pharmaceutical regulation, which requires evidence of safety before a product is brought to market. The EPA can regulate only when the available data demonstrate toxicity—providing a strong incentive for manufacturers not to conduct toxicity testing.
Critics charge that under the TSCA, the EPA cannot require toxicity testing unless it knows that a chemical is toxic, but without such testing, a determination of toxicity is impossible—a regulatory Catch-22. And regulation has proven as difficult as data collection. When the EPA did try to regulate a well-established hazard, asbestos, in the 1980s, a court struck down the EPA's action, ruling that the agency had failed to meet TSCA's high burden of proof (“substantial evidence” of an “unreasonable risk”) and had not proposed the “least burdensome” approach to regulation. Consequently, the EPA has regulated only five chemicals under the TSCA in the decades since that law passed—decades during which over 20,000 new chemicals were brought to market. The law is widely considered ineffective (U.S. Government Accountability Office [GAO], 2005, 2007; Markell, 2010; Vogel & Roberts, 2011).
During the first decade of the twenty-first century, European nations developed a comprehensive approach to chemical management called REACH (Registration, Evaluation, Authorization and Restriction of Chemicals). A key feature of REACH is the requirement for premarket testing of chemicals, placing the burden of proof of safety on manufacturers (GAO, 2005, 2007; Williams, Panko, & Paustenbach, 2009). Moreover, some U.S. states began regulating chemicals on their own; examples include Washington State's Children's Safe Products Act and Maine's Toxic Chemicals in Children's Products Act; both passed in
357
2008. These developments have spurred calls for TSCA reform from across the political spectrum (Applegate, 2008; Denison, 2009; Vogel & Roberts, 2011), including from the EPA itself (www.epa.gov/oppt/existingchemicals/pubs/principles.html). Key provisions of TSCA reform include expanded safety reviews and testing of chemicals, increased access to information regarding chemical toxicity, and protection of vulnerable populations (Applegate, 2008); by late 2015, Congress was close to passing such a bill, the Lautenberg Act.
Other laws regulate chemical exposures in other ways. As described in Chapter 18, the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) provides the basis for the EPA to regulate pesticides, principally through issuing registration—in effect a license for a particular pesticide to be used in particular ways. FIFRA has stronger provisions than TSCA for premarket evaluation, data generation, product labeling, and the EPA's ability to suspend or cancel a pesticide's registration—four key features of regulatory strategy. Under another law, the Federal Food, Drug, and Cosmetic Act (FFDCA), the EPA sets maximum residue levels, or tolerances, for pesticides used in or on foods or animal feed. The regulatory framework under FFDCA is health based (“reasonable certainty of no harm”), with far less emphasis on risk- benefit analysis, a sharp contrast with the TSCA. Of note, FFDCA is also the law that enables the FDA to regulate the safety of foods, food additives, medications, and cosmetics. A third law, the Food Quality Protection Act (FQPA), amended FIFRA and FFDCA in 1996, setting tougher safety standards for new and old pesticides and creating uniform requirements regarding processed and unprocessed foods. FQPA includes several provisions that incorporate toxicological knowledge. First, assessment must include aggregate exposures including all dietary exposures, drinking water, and nonoccupational (e.g., residential) exposures. Second, when assessing a tolerance, EPA must consider cumulative effects and common modes of toxicity among related pesticides, the potential for endocrine disruption effects, and an appropriate safety factor. Third, EPA must incorporate a tenfold safety factor in setting tolerances, reflecting the special vulnerability of infants and children.
Still another law, the Emergency Planning and Community
358
Right-to-Know Act (EPCRA) of 1986, was passed in the aftermath of one of the world's worst chemical disasters: the 1984 release from a Union Carbide plant in Bhopal, India, of forty tons of methyl isocyanate (MIC), killing as many as 5,000 people and injuring ten times that number. EPCRA addressed emergency preparedness for chemical disasters, defining local-level responsibilities and procedures. It also required industry to report on the storage, use, and releases of hazardous chemicals to federal, state, and local governments, and created an important repository of data, the Toxics Release Inventory (TRI). The TRI is not a complete inventory of hazardous chemical use—for example, small users such as dry cleaners are not required to report—but it represents a key approach to chemical protection: namely that disclosure and transparency lead to accountability, and ultimately to the adoption of cleaner, safer practices (Khanna, Quimio, & Bojilova, 1998)
While these laws are in some respects complementary, there is also a fragmented quality to them—intensified by the fact that still other laws regulate specific media such as air (the Clean Air Act; see Chapter 13) and water (the Clean Water Act and the Safe Drinking Water Act; see Chapter 16). For instance, if a pesticide is found to contaminate a river that supplies a community's drinking water, is this a concern for FIFRA or the Safe Drinking Water Act (Franklin, 2011–2012)?
359
Summary Toxicology addresses the adverse effects of chemicals in terms of an exposure and effect sequence—from exposure to absorption to distribution to metabolism to excretion—and analyzes the end effects on organs and physiological systems that may occur during this process. Identifying mechanisms or pathways of toxicity can help to establish a biological basis for regulation. This knowledge is directly informative to regulators and others who work to identify the safest chemicals for our use and to set acceptable levels of exposure for chemicals that may be dangerous.
360
Key Terms absorption
The movement of a chemical across a biological barrier, such as skin, intestinal lining, or alveoli.
alcohol dehydrogenase An enzyme involved in the conversion of ethanol to acetaldehyde; the primary means of metabolizing ingested alcohol.
animal testing The process of modeling the toxic effects of chemicals by exposing laboratory species in a control setting.
bioactivation A metabolic process that alters a chemical in a way that increases its reactivity.
biotransformation A metabolic process that changes the properties of a given chemical.
carcinogenesis The process of cancer development, which typically includes a series of mutations to tumor-promoting and tumor-suppressing genes.
carcinogens Chemicals that can induce cancer.
conjugation The addition of chemical entities to increase the solubility and excretion of a given compound.
cytochrome P450 Enzymes involved in the metabolism of chemicals, found at high levels in the liver.
dermal exposure The process by which a chemical gains entry to the body via the skin.
distribution The movement of a chemical throughout the body.
dose-response relationship
361
The graphical representation of increasing exposure to a chemical compared to the biological effects.
ecotoxicology The study of the adverse effects of chemicals on the environment or an ecosystem.
Emergency Planning and Community Right-to-Know Act (EPCRA)
A 1986 law aimed at preparing local communities and governments for potential exposures to toxic chemicals by providing access to information on the nature of the health risks posed by the chemicals.
endocrine disruptors Exogenous agents that interfere with the production, release, transport, metabolism, binding, action, or elimination of natural hormones, such as estrogen, androgens, and the thyroid hormone, that are responsible for the maintenance of homeostasis and the regulation of developmental processes.
enzyme induction A process that results in an increased expression of proteins involved in metabolizing a particular class of chemicals.
epigenetic A term describing modifications to DNA that do not involve a change in the primary sequence of nucleotides.
excretion The process by which a chemical exits the body.
Federal Food, Drug, and Cosmetic Act (FFDCA) A law initially passed in 1938 and designed to protect consumers from hazards found in ingested or applied products.
Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA)
A law initially passed in 1910 to protect users, consumers, and the environment from risks associated with pesticide use.
Food Quality Protection Act (FQPA) A law passed in 1996 that requires health assessment–based changes to the laws governing the use of pesticides.
genetic toxicants Chemicals that damage DNA or the machinery involved in
362
maintaining DNA integrity. green chemistry
A field devoted to the generation of materials in ways that focus on minimizing adverse effects on the environment and human health.
hepatotoxic Inducing adverse effects in the liver.
hydrolysis A chemical process that uses water to break apart chemical bonds.
hydrophilic Polar, or water soluble.
hydrophobic Nonpolar, or fat soluble.
ingestion The introduction of a compound into the digestive tract via the mouth.
inhalation The introduction of a gas or particle into the lungs via the airway.
initiation An early step in the process of carcinogenesis that typically involves DNA mutation.
LD50 The dose at which one half of the test group dies in a certain period of time. LD stands for “lethal dose.”
metabolism The processing of chemicals within the body; it can involve activation, inactivation, breakdown, or conjugation with other constituents.
metastasis Movement of cancerous cells from the original site of the tumor or growth, typically involving distribution within the bloodstream or lymphatic system.
microbiome The compilation of microbial organisms that live within the intestines, on the skin, and within various mucus membranes.
363
mutagens Chemicals that can induce physical alterations in the structure of DNA.
nephrotoxic Inducing adverse effects in the kidney.
neurotoxic Inducing adverse effects in the central or peripheral nervous system.
no-observed-adverse-effect level The highest exposure at which there are no discernable negative biological effects of a certain chemical.
oxidation A metabolic process that involves the introduction of molecular oxygen to alter a chemical.
phase I reaction A metabolic process that modifies a chemical; hydroxylation, oxidation, and reduction are common mechanisms.
phase II reaction A metabolic process that generally involves the addition of side chains or functional groups (glucoronide, glutathione, methyl groups).
progression A step in carcinogenesis that involves the acquisition of traits that increase the aggressive nature of a tumor.
promotion A step in carcinogenesis that involves the expansion of the cells containing a particular mutation.
REACH (Registration, Evaluation Authorization, and Restriction of Chemicals)
The European approach to chemical management, entered into force in 2007. REACH includes many precautionary provisions such as the requirement for premarket testing of chemicals.
reduction A metabolic process that involves the gain of an electron.
reference dose (RfD) A level of daily oral exposure to a chemical, such as a pesticide, that has no apparent adverse effects on humans; the RfD is used
364
in setting regulatory guidelines. registration (of pesticides)
The process that industries must follow to inform the EPA of any intended use of chemicals to control unwanted species in agricultural or consumer settings.
regulatory toxicology The subspecialty that focuses on the use of laboratory and epidemiological data to guide the development and enforcement of laws aimed at protecting consumers and the environment from chemicals.
target organ The specific physiological system affected by a given toxicant.
tolerance An EPA-set limit on the amount of residual pesticide that can be present in foods and consumer goods.
Toxic Substances Control Act (TSCA) The 1976 law that governs the uses of chemicals, excluding drugs, cosmetics, and food.
toxicant A synthetic compound that exerts notable adverse effects on a biological system.
toxicokinetics The study of the movement of toxic compounds from the environment into and within a target organism.
toxicology A field of science dedicated to the study of the adverse effects of chemicals on biological systems.
Toxics Release Inventory (TRI) A database maintained by the EPA that provides information on incidents involving the introduction of hazardous chemicals into the environment.
toxin A compound of natural origin that exerts notable adverse effects on a biological system.
xenobiotic A chemical that is foreign to a given organism.
365
Discussion Questions 1. Historically, toxicology testing has been focused on one chemical
at a time, yet we are rarely exposed to chemicals in isolation. Why do you think this approach to testing has been taken? What challenges may be involved in studying mixtures of chemicals?
2. If a company claims that its product is “all natural,” does that mean it is safe? Why or why not?
3. What chemicals do you think are most harmful to your own health? How are you exposed? How could you go about determining whether or not each of these chemicals was harmful to you?
4. The REACH legislation mandates a reduced reliance on animal testing, and Europe has long banned animal testing for cosmetics. Are there any potential negative consequences that could occur with the move away from animal testing?
5. Manufacturers removed bisphenol A from most of their products over the past few years. What replaced it? What type of testing did the replacement chemical undergo?
366
References Applegate, J. S. (2008). Synthesizing TSCA and REACH: Practical principles for chemical regulation reform. Ecology Law Quarterly, 35(4), 721–770.
Carson, R. (1962). Silent spring. Boston: Houghton Mifflin.
Crews, D., Gillette, R., Scarpino, S. V., Manikkam, M., Savenkova, M. I., & Skinner, M. K. (2012). Epigenetic transgenerational inheritance of altered stress responses. Proceedings of the National Academy of Sciences of the United States of America, 109(23), 9143–9148.
Denison, R. A. (2009). Ten essential elements in TSCA reform. Environmental Law Reporter, 39, 10020–10028.
Dickerson, S. M., & Gore, A. C. (2007). Estrogenic environmental endocrine-disrupting chemical effects on reproductive neuroendocrine function and dysfunction across the life cycle. Reviews in Endocrine & Metabolic Disorders, 8(2), 143–159.
Franklin, C. (2011–2012). FIFRA v. the courts: Redefining federal pesticide policy, one case at a time. Natural Resources & Environment, 26, 18.
Hinterthuer, A. (2008). Safety dance over plastics. Scientific American, 299(3), 108, 110–111. Retrieved from http://www.scientificamerican.com/article/just-how-harmful-are- bisphenol-a-plastics
Khanna, M., Quimio, W., & Bojilova, D. (1998). Toxic release information: A policy tool for environmental protection. Journal of Environmental Economics and Management, 36(3), 243–266.
Klaasen, C. D. (Ed.). (2013). Casarett and Doull's Toxicology: The basic science of poisons (8th ed.). New York: McGraw-Hill.
Markell, D. (2010). An overview of TSCA, its history and key underlying assumptions, and its place in environmental regulation. Washington University Journal of Law and Policy, 32(1), 333–375.
367
Meeker, J. D. (2012). Exposure to environmental endocrine disruptors and child development. Archives of Pediatrics & Adolescent Medicine, 166(6), E1–7.
National Institute of Child Health and Human Development. (2015). The Human Placenta Project. Retrieved from http://www.nichd.nih.gov/research/HPP
Tang, W. H., Wang, Z., Levison, B. S., Koeth, R. A., Britt, E. B., Fu, X.,…Hazen, S. L. (2013). Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk. New England Journal of Medicine, 368, 1575–1584.
U.S. Government Accountability Office. (2005). Chemical regulation: Approaches in the United States, Canada, and the European Union (GAO-06-217R). Washington, DC: Author.
U.S. Government Accountability Office. (2007). Comparison of U.S. and recently enacted European Union approaches to protect against the risks of toxic chemicals (GAO-07-825). Washington, DC: Author.
Vogel, S. A., & Roberts, J. A. (2011). Why the Toxic Substances Control Act needs an overhaul, and how to strengthen oversight of chemicals in the interim. Health Affairs, 30(5), 898–905.
Walker, C. H., Sibly, R. M., Hopkin, S. P., & Peakall, D. B. (2012). Principles of ecotoxicology (4th ed.). Boca Raton, FL: CRC Press.
Wenck, M. A., Van Sickle, D., Drociuk, D., Belflower, A., Youngblood, C., Whisnant, M. D.,…Gibson J. J. (2007). Rapid assessment of exposure to chlorine released from a train derailment and resulting health impact. Public Health Reports, 122(6), 784– 792.
Williams, E. S., Panko, J., & Paustenbach, D. J. (2009). The European Union's REACH regulation: A review of its history and requirements. Critical Reviews in Toxicology, 39(7), 553–575.
368
For Further Information Books and Monographs Anastas, P. T., & Warner, J. C. (2000). Green chemistry: Theory and practice. New York: Oxford University Press.
International Agency for Research on Cancer. (2015). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans (Web site). http://monographs.iarc.fr/ENG/Classification
Roberts, S. M., James, R. C., & Williams, P. L. (Eds.). (2015). Principles of toxicology: Environmental and industrial applications (3rd ed.). Hoboken, NJ: Wiley.
Organizations Agency for Toxic Substances and Disease Registry (ATSDR): http://www.atsdr.cdc.gov. ATSDR maintains data on hazardous chemicals at http://www.atsdr.cdc.gov/toxfaq.html and http://www.atsdr.cdc.gov/toxpro2.html
Center for Alternatives to Animal Testing (CAAT) at Johns Hopkins University: http://caat.jhsph.edu
Society of Toxicology: http://www.toxicology.org. The Society of Toxicology is a professional organization that promotes the use of toxicology to improve human health.
369
Chapter 7 Genes, Genomics, and Environmental Health
David L. Eaton and Christopher M. Schaupp
Dr. Eaton and Mr. Schaupp report no conflicts of interest related to the authorship of this chapter. Disclosures by Dr. Frumkin, who wrote Tox Box 7.1, appear in the front of this book, in the section titled “Potential Conflicts of Interest in Environmental Health: From Global to Local.” Dr. Woods reports no conflicts of interest related to the authorship of Text Box 7.2.
370
Key Concepts DNA, as the “blueprint of life,” is the principal biological template that allows all living organisms to reproduce and pass on their fundamental attributes to offspring. Understanding how DNA functions in a cell and organism is important to understanding how environmental factors can contribute to both human disease and well-being.
Although DNA is critically important in determining many of the attributes that make one individual different from another, other factors, called epigenetics, can modify how genes are expressed, and thus have important impacts on individual characteristics.
Environmental factors, including diet, chemical exposures, and lifestyle (e.g., smoking and alcohol consumption), may interact with both genetic and epigenetic processes to alter the etiology and progression of many chronic diseases of public health importance.
Interindividual differences in susceptibility to environmental pollutants may be determined by both genetic and epigenetic processes. One common source of variability in genetic susceptibility is genetic and epigenetic differences in how the body processes exogenous chemicals (absorption, metabolism/biotransformation, and excretion).
Molecular tools (so-called omics technologies) that can quickly and cheaply acquire millions of biological data points have transformed how scientists study the causal relationships between environmental exposures and disease outcomes. These tools include genomics (e.g., DNA sequencing and single nucleotide polymorphism, or SNP, analysis), transcriptomics (measuring gene expression at the messenger RNA, or mRNA, level), proteomics (measuring the amount and nature of proteins in a cell or tissue), and metabolomics (measuring the array of small molecules in a cell or tissue). These molecular tools have made the study of gene-environment interactions in populations possible. The
371
analysis of such large amounts of data requires sophisticated mathematical, statistical, and computational approaches (bioinformatics).
Understanding the fundamental processes that dictate how an individual responds to environmental challenges has important regulatory and public health policy implications, and also raises important ethical, legal, and social questions regarding how such information should be used.
“Why me, Doc?” is not an uncommon question when you or a family member has been diagnosed with a dreaded but all too common disease, such as cancer or Alzheimer's disease. “Was it something bad in my genes?” “Something I ate?” “Perhaps something I was exposed to in my workplace?” The answers to these very personal questions have their roots in the age-old debate over whether nature or nurture makes us who and what we are. Today, with the entire human genome sequence available and a plethora of modern techniques ready to probe it, the answer to this nature versus nurture question should be at hand. However, as is commonly the case, it is not that simple.
In this chapter you will learn about what it is that nature (your genes) contributes to your life as well as some ways in which the world around you (your environment) has an impact on your health. Importantly, you will also learn how various genes and environmental factors interact in complex ways to increase or decrease your risk of developing some unwanted outcome, such as a disease, an adverse drug reaction, or an allergic response to something in your food, air, or water. So in the rest of this chapter you will learn from numerous examples about gene-environment interactions (GxE interactions). But first, you need some fundamental understanding of how genes operate, and how environmental exposures can modify your health either directly (see Chapter 6, on toxicology) or by interacting with your genes.
372
Fundamental Concepts of Genetics and Genomics Basic Components of a Gene and a Genome Every living organism uses an elegant and seemingly simple string of chemicals, called bases, hooked together end to end to form deoxyribonucleic acid, or DNA. Just four different bases make up DNA: thymine (T), guanine (G), cytosine (C), and adenine (A). Each of these bases has a 5-carbon sugar molecule, called deoxyribose, attached to it. When the sugar is attached to the base, the combined molecule is called a nucleotide. But in the cell, this string of nucleotides called DNA is actually two complementary strands of DNA woven together in the famous double helix first described by Watson and Crick in 1954. The elegance of DNA is that the four bases pair up in a specific way: A always pairs with T, and G always pairs with C. So, if one strand of DNA has the nucleotide sequence CGTCCGAT, you can immediately deduce that the corresponding strand that pairs with this has the sequence GCAGGCTA. The order of bases is what determines an individual's genetic code. Approximately 3 billion base pairs constitute a human genome. If you were to grab one end of a single molecule of DNA and stretch it out, those 3 billion base pairs that make up your genome would be over 1 meter long! And every cell in your body has an exact copy of all 3 billion base pairs in the exact same order. Imagine a single book, 600,000 pages long (with each base representing 1 character, and 5,000 characters on a single- spaced page). But even more amazing than packaging a 600,000 page book of code into each cell is that only a small fraction of that information is actually used in any given cell or tissue. A liver cell expresses a different set of genes than a brain cell or kidney cell.
So what is a gene? A gene is a specific sequence of nucleotides that contains information and that controls some function in the cell, such as forming a protein. Within the continuous 3 billion base pairs (nucleotides) in a molecule of DNA are “start” and “stop” signals that constitute the boundaries of each gene. There are approximately 24,000 genes in the human genome. That is a startlingly small number of genes, given the complexity of human
373
life! The genome and the genes within it, however, are not packaged as a single long chain of DNA, but rather in discrete units called chromosomes, and every chromosome is part of a matched set of two. There is a total of forty-six chromosomes. Forty-four of these are present as duplicates; thus there are twenty-two autosomes and two more chromosomes that are sex-specific—the X chromosome (female) and the Y chromosome (male) (Figure 7.1). One chromosome in each of the twenty-two autosomes comes from the mother and one comes from the father. Females also receive an X chromosome from both mother and father, whereas males also receive an X chromosome from the mother and a Y chromosome from the father.
Figure 7.1 The Human Genome The genome consists of 3 billion base pairs of nucleotides, packaged in discrete units
374
called chromosomes. There are 23 pairs of chromosomes—22 pairs are autosomes, and 2 consist of sex chromosomes (XX or XY). Chromosomes vary in size (chromosome 1 being the largest with about 4,000 genes, and the Y chromosome being the smallest, with 458 genes).
Within each of these chromosomes are packaged hundreds to thousands of individual genes. Since a child receives half of his or her chromosomes from the mother and the other half from the father, every child has two copies of every gene, a fifty-fifty mixture from the two parents. Since you have two copies of every gene, it is convenient to have a term that refers to just one of these copies. The term allele is used to identify the single gene from each parent. So while the two chromosomes of a pair carry very similar DNA, the two alleles of any given gene are not necessarily identical in sequence. If one of these alleles is different in sequence from the common form, it is called the variant allele. The reason why two people don't look, act, or sound exactly alike is in part the result of small differences in the sequence of genes, and in how much of the gene is expressed. We will discuss how the regulation of gene expression occurs later.
The basic structure of a gene is shown in Figure 7.2. The core function of most genes is to make proteins, which are the business end of biology. Almost all the cellular work in an organism is done by proteins. Proteins are constructed by linking amino acids together in a specific order. There are twenty-one different amino acids that make up the proteins in the body. The order of the amino acids is determined explicitly by the order of the bases in DNA.
375
Figure 7.2 The Basic Structural Elements of a Gene
But there is an intermediary between the sequence of DNA in a gene and the protein product that is coded by that gene. That intermediary is ribonucleic acid, or RNA. Like DNA, RNA is made up of four bases, each coupled with a sugar (ribose). The bases in RNA include three of the same bases found in DNA: guanine (G), adenine (A), and cytosine (C). But RNA uses the base uracil (U) in place of thymine. Thus RNA is copied from DNA based on the same base-pairing principles as apply in double-stranded DNA. This process is known as gene transcription (Figure 7.2). There are several different types of RNA, each with its own function. The RNA that codes directly for proteins is called messenger RNA (mRNA). You may have noticed that there are only four different nucleotides in DNA and in RNA, yet there are twenty-one different amino acids in proteins. The genetic code is conferred by the fact that sequences of three consecutive nucleotides (e.g., TCG, or ATT), called codons, represent a signal for a specific amino acid. Since there are four nucleotides in three possible positions (first, second, or third) there are sixty-four unique combinations of bases, more than enough to code for the twenty-one amino acids, as well as start and stop codons. Indeed, there is some redundancy in the genetic code such that most amino acids have more than one triplet codon.
When a gene is transcribed into an mRNA molecule, portions of the
376
gene are spliced out of the sequence, such that the mature mRNA molecule is much shorter than the sequence of the gene (Figure 7.2). Most genes contain noncoding DNA interspersed between segments of coding DNA. The coding DNA sequences are referred to as exons, and the interspersed noncoding DNA segments are called introns. All of the DNA sequence is initially transcribed into RNA, but enzymes that recognize splice junctions (specific nucleotide sequences at the boundary between an intron and an exon) cut out the noncoding DNA and reassemble the parts into mature mRNA that contains only the complementary sequence of coding DNA from the gene (plus a little bit of noncoding RNA at the beginning and end of the mRNA). Metabolic machinery in the cell then utilizes the triplet codon sequence information in the mature mRNA molecule to assemble amino acids in exactly the correct order. This process is referred to as translation (Figure 7.2). It follows that a small difference from the reference DNA sequence in a particular gene can result in a different protein being formed by that gene.
Types of Genetic Variability Differences in single nucleotides in the same position of the same gene are the most common type of genetic variability and are referred to as single nucleotide polymorphisms (SNPs). It is estimated that there are approximately 3 million SNP differences between any two individuals' genomes. In other words, any two people's genomes are roughly 99.9% identical. But variability is not randomly distributed across the genome. Genes that code for critically important functions have very few SNP differences, and are considered to be highly conserved. Most of the SNP variability in the human genome is scattered throughout the large part of the genome that is not part of a gene (intergenic regions), or located in noncoding (intronic) sequences within genes. In fact only about 5% of the 3 billion nucleotides in the human genome are actually in exons (the coding parts of genes), and even then, not all changes in nucleotide sequences within an exon actually change the protein. When there is a change in the nucleotide sequence but the different sequence does not result in a different amino acid (recall that there are usually two or three different codons for the same amino acid), that change is referred to as a synonymous cSNP. The “c” stands for coding, recognizing that most of the DNA sequence in the
377
genome does not even code for proteins. If a SNP in an exon of a particular gene results in a change in the triplet codon for a particular amino acid, resulting in a changed protein, the cSNP is referred to as a non-synonymous cSNP. A substantial amount of the remaining 95% of the genome still provides important information, such as the switching mechanism that determines when genes are or are not expressed, as well as coding for RNA genes, a relatively newly discovered way in which the cell controls its own growth. Even certain intronic sequences have been shown to have a functional role in partially determining the level of expression of a gene or the stability of the mRNA that is formed from the gene.
Although SNPs are by far the most common type of genetic variability in the human genome, many other types of differences exist. For example, there can be small (a few nucleotides) or even large (hundreds or thousands of nucleotides) insertions or deletions (so-called indels) in genes. Depending on where the indel occurs, it may have no effect or a little effect, or it may completely eliminate the function of a gene. For example, the genetic disease known as cystic fibrosis can result from a simple three base pair deletion across codons in a gene that codes for a protein that helps to regulate chloride ion flux across cell membranes (Figure 7.3). Because of the three-nucleotide deletion, the protein from the defective gene is missing one amino acid, and that in turn makes the protein ineffective. This is an example of a disease gene. Genetic variants that directly cause a disease are rare (generally occurring in less than 1% of the population), and thus such variants are usually referred to as mutations, rather than polymorphisms.
Figure 7.3 The Cystic Fibrosis Mutation Note: NT = nucleotide, AA = amino acid.
This figure shows the mRNA sequence for a protein that gives rise to cystic fibrosis, when mutated a certain way (there are other mutations that can also give rise to cystic
378
fibrosis). In this example, three nucleotides (CUU) in the disease gene are deleted, resulting in three missing nucleotides in the corresponding mRNA. This deletion results in one missing amino acid in the protein, an amino acid critical to the protein's function. It is this loss of function that gives rise to the disease characteristics.
Another form of genetic variability occurs when an entire gene is either missing (deletion polymorphism) or occurs more than once in the same genome (gene duplication). One of the most widely studied genetic variants in the human genome is the human glutathione S-transferase M1 (GSTM1) polymorphism, in which about 50% of the human population is homozygous null, meaning that the gene is completely absent from their genome (Text Box 7.1). The form of genetic variability in which someone has inherited multiple copies of the same gene is referred to as copy number variation (CNV). CNVs are actually quite common in the human genome, amounting to an estimated 13% of human genomic DNA, and accounting for about 0.4% of the variability between any two genomes. In rare circumstances, such as with Down's syndrome (Trisomy 21), an entire chromosome can exist with three copies (triploid), instead of the normal two copies (diploid).
379
Text Box 7.1 Liver Cancer from Moldy Corn and Peanuts: Aflatoxin and the Role of GSTM1 Polymorphism In parts of Jiangsu province in China, liver cancer (hepatocellular carcinoma, or HCC) was for many years the leading cause of death in males under the age of 50, yet in many other parts of the world, liver cancer in men is relatively rare. What is going on? Epidemiological studies in this and other regions of the world with high incidence of HCC have identified two important risk factors: endemic Hepatitis B virus (HBV) infections and the presence of a dietary contaminant called aflatoxin B1 (AFB1). While each factor alone increases the risk of HCC, the two together exhibit synergism; in one study, HBV infection increased the risk about fifteenfold, AFB1 exposure about three-fold, and both risk factors together sixtyfold! This illustrates how two different environmental factors can interact to produce toxicity or disease at a rate much higher than either alone.
Early studies of aflatoxin-induced liver cancer in animal models led to the discovery of a remarkable species difference in susceptibility to AFB1. Nearly all laboratory rats given AFB1 in their diets, even at low concentrations, developed HCC, while laboratory mice given AFB1 in their diets, even at extremely high concentrations, remained free of liver cancer. Perhaps understanding the molecular basis for this species difference could reveal genetic differences, and lead to a better understanding of human risk from AFB1. In fact, such studies have been completed, with fascinating results. As it turns out, mice are highly resistant to the cancer-causing effects of AFB1 because they express in their liver a specific form of an enzyme known as glutathione S- transferase (GST). GSTs are a multigene family of enzymes, with fifteen different genes in the human genome coding for GSTs. In the mouse, one specific form, mGSTA3, has a remarkably high ability to detoxify the epoxide of AFB1. A
380
GST enzyme normally expressed in the rat liver, rGSTA3, is 85% similar in its gene and protein sequence to mGSTA3, yet has less than 1% of the activity of the mouse form toward the carcinogenic AFB-epoxide. So mice are resistant and rats are highly sensitive to the potent liver carcinogen owing to only a few amino acid differences in one enzyme! As it turns out, human GSTs have even less activity toward AFB1-epoxide than rat GSTs. Thus, on a biochemical basis, humans should be even more sensitive to the cancer-causing effects of AFB1 than rats. In fact, of the fifteen human genes that code for GSTs, only one, called hGSTM1, has any measurable AFB1 detoxifying ability.
The human GSTM1 gene is interesting, because, as noted previously, approximately 50% of the human population is homozygous null for it, meaning that neither copy of the GSTM1 gene is present in the genome. This is an example of a gene deletion polymorphism. Obviously, if half the human population lacks the gene, it was not very important for normal human function in evolutionary terms. Yet GSTM1 protein is involved in the detoxification of a variety of environmental pollutants, including AFB1, so one might hypothesize that people who lack GSTM1 might be more susceptible to AFB1-induced liver cancer. Indeed, that appears to be the case. Several epidemiological studies have suggested that the GSTM1 deletion polymorphism is associated with about a twofold increase in risk of liver cancer in people who live in areas of the world where AFB1 is present in the diet. One study in human liver cells showed that the same dose of AFB1 generated three times more DNA damage in liver cells that lacked the GSTM1 gene, compared to liver cells that had one or two functional GSTM1 alleles.
How Gene Expression Is Regulated
Transcription Factors and Promoter Regions of Genes While the structure of the human genome is elegant in its design, equally remarkable are the processes that determine when a gene is expressed in a given cell and how much of it is expressed. As noted previously, every cell has the entire genome but only a small part of
381
it is used to determine the phenotype of a cell, tissue, or individual. What specifically signals a gene to begin the process of transcription, and then translation? Much of this is determined by specific sequences of DNA in the 5′-flanking region of a gene, sometimes called the promoter (or regulatory) region (Figure 7.2). Located at the very “front end” of a gene, these switching signals are represented by unique DNA sequences, from five to over twenty nucleotides long, that provide binding sites for specific proteins that uniquely recognize only that sequence of DNA. By binding to the DNA sequence, these proteins, called transcription factors, initiate the process of transcription. Generally the transcription factor proteins do not act alone but manage to recruit other critical proteins in the process, such that it is actually a complex of proteins that bind to the transcription factor binding site in DNA. In some instances, transcription factor proteins need a small molecule to bind to the protein before they can recruit other proteins, move to the nucleus of the cell, and bind to the binding site on a gene. Such proteins are called ligand-activated nuclear transcription factors. A good example of this is hormonal signaling by such molecules as estrogen, testosterone, and thyroid hormone. Estrogen —either produced normally in the body (endogenous) or from an exogenous synthetic estrogen (such as a birth control pill)—is recognized by a specific protein called the estrogen receptor. When the ligand (estrogen) binds to its receptor, the complex moves to the nucleus, and binds to estrogen receptor binding sites on certain genes, which are then turned on to express the gene (make the specific protein). Thus it is transcriptional activation via estrogen of a whole host of genes involved in the female reproductive function that provides the phenotype associated with endogenous production of estrogen. Likewise, some chemicals in the environment, called endocrine disruptors, can also affect estrogen signaling, either by mimicking estrogen and activating the estrogen receptor (an estrogen receptor agonist) or by blocking estrogen from binding to the receptor (an estrogen receptor antagonist). (See Text Box 6.4, in Chapter 6.)
Epigenetic Regulation of Gene Expression Although ligand-activated transcription factors represent an important pathway for regulation of gene transcription, there are many other cellular processes involved in regulating gene
382
expression. An exciting new area of discovery is epigenetic regulation of gene expression (Figure 7.4). It was discovered many decades ago that some of the nucleotides in regulatory regions of genes could exist in two forms—with a methyl group attached to certain bases in certain positions or in a normal, unmethylated state. It is now recognized that early in life, during embryonic and fetal development, and throughout life, when cells are undergoing replication, regulatory regions of genes across the entire genome manifest differing states of DNA methylation. In general, genes with more methylated bases in the regulatory region (hypermethylation) are underexpressed (mostly switched off), whereas genes with fewer methylated bases in the regulatory region (hypomethylation) tend to be overexpressed (switched on). Modulation of gene expression via changes in DNA methylation is one form of epigenetic regulation of genes.
Figure 7.4 Chromatin Dynamics in Response to Epigenetic Modification
Source: Johnstone, 2002.
In this figure, methylation induces a closed chromatin state, while removal of methyl groups (Me) and addition of acetyl (Ac) groups results in an opened chromatin state, allowing easier access for transcriptional machinery. Also involved in nucleosome structure are phosphorylation (P), the enzymes histone acetyltransferases (HATs) and histone deacetylases (HDACs), and methyl-binding proteins (MECP2).
The elegant switching on and off of genes during embryonic and fetal development is what allows the amazing development of a fertilized egg into a healthy baby. And complex regulation of gene expression through methylation of DNA continues to occur throughout early development and into adulthood. Obviously,
383
interference with or perturbations of DNA methylation could have grave consequences for a developing embryo or for the successful growth and development of a young child into a healthy adult. Changes in DNA methylation are a common characteristic of many neoplasms (benign and cancerous tumors). Changes in gene expression, because of altered epigenetic regulation, and/or the accumulation of mutations in DNA in somatic cells in the body are what cause a normal stem cell to veer into cancerous growth.
Although methylation is one of the most important and best understood mechanisms of epigenetic regulation of gene expression, there are other epigenetic modes of alteration of gene expression. For example, a group of proteins known as histone deacetylases (HDACs) have the unique function of changing how histone proteins are folded. Histones facilitate the proper winding of DNA into chromosomes in the nucleus. In order for a gene to be expressed, it has to be unwound from the histones to allow DNA and RNA synthesis machinery to read the DNA sequence (transcription and translation). The addition of an acetyl group (two carbons and one oxygen) to a histone will affect its ability to wind and unwind DNA and thereby affect the efficiency of transcription. Thus alterations in histone acetylation and deacetylation, like alterations in DNA methylation and demethylation, can affect transcriptional efficiency of a gene.
Lastly, epigenetic regulation of gene expression can also be determined in part by the binding of a relatively newly discovered class of RNA, called microRNA (miRNA), to the 3′-terminal ends of mRNA molecules. These miRNAs are derived from non-protein- coding genes (so-called RNA genes). Once fully formed, miRNAs are twenty-one to twenty-three nucleotides long, and function by recognizing specific sequences in the 3′ end of a mature mRNA molecule (Figure 7.2). The miRNA binds to the mRNA where it inhibits the efficient translation of that mRNA and/or targets the mRNA for degradation, such that the level of gene expression is decreased.
As described earlier, changes in DNA—mutations—have a role in many diseases. However, many (perhaps most) environmental diseases are not the result of mutations; instead, the epigenetic mechanisms just described are responsible. The epigenome responds dynamically to cues from the environment, including the
384
drugs you take, the air you breathe, the food you eat, how stressed you are, and what toxicants you are exposed to.
To get a better sense of the epigenetic regulation of gene expression, consider the example of identical twins. Although they are genetically identical (they are from the same embryo), they become phenotypically divergent; they look different from one another as they age and they act differently. This is the result of differences in diet, exercise, lifestyle, and so forth, which change the methylation and acetylation patterns in their epigenomes. The more we learn about epigenetics, the more apparent it has become that epigenetic changes can influence health, not only of directly affected people but also of subsequent generations. The choices a person makes in his or her lifetime can affect his or her own epigenome and also that of his or her offspring. This hereditary transmission of environmental information is known as transgenerational epigenetic inheritance.
Experiments in mice highlight the important of maternal diet in shaping the epigenome of offspring. For example, all mammals have a gene called the agouti gene. The product of this gene is a 131 amino acid peptide that causes the pigment cells in hair follicles to synthesize a yellow pigment instead of black or brown pigment. But the same agouti peptide also binds to certain receptors in the brain, causing changes in metabolism that result in obesity. Thus, when a mouse's agouti gene is demethylated, its coat is yellow, and the mouse is obese and prone to diabetes and cancer. When the agouti gene is methylated (as it is in normal mice), the coat color is brown and these mice have a low obesity risk. Fat yellow mice and skinny brown mice are genetically identical (Figure 7.5). The fat yellow mice have an altered phenotype because of epigenetic modifications that simultaneously change hair color and fat metabolism (Duhl, Vrieling, Miller, Wolff, & Barsh, 1994). When researchers fed pregnant yellow mice (those that have the demethylated agouti gene) a diet rich in methyl group precursors, such as Vitamin B12 or betaine, most of the pups were brown and stayed healthy for life. The results of this experiment show that the environment in the womb influences adult health, and support the fetal origins of adult disease hypothesis, which states that early developmental exposures involve epigenetic modifications that influence disease susceptibility as an adult.
385
Figure 7.5 Schematic of the Agouti Gene and How Its Methylation Status Affects Phenotype in Mice
Source: Hudson Alpha Institute for Biotechnology, 2009.
Chemicals and additives that enter our bodies can also affect the epigenome. Bisphenol A (BPA), a synthetic chemical with endocrine-disrupting properties, is a plasticizer previously used in many consumer products, including water bottles and tin cans (as described in Tox Box 6.1 in Chapter 6). But in recent years its use has been phased out following studies suggesting health hazards, especially in infants and children. Perhaps the most striking evidence for BPA's toxicity came from a study of the agouti gene in lab mice (Dolinoy, Huang, & Jirtle, 2007). When pregnant yellow mothers were fed BPA, more yellow, unhealthy babies were born than normal. Exposure to BPA during early development had resulted in decreased methylation of the agouti gene. However, when BPA-exposed, pregnant yellow mice were fed food supplemented with methyl donors (e.g., vitamin B12 and folic acid), the offspring were predominantly brown (methylated agouti gene). Thus the maternal nutrient supplementation had counteracted the negative effects of exposure. Taken together, these studies suggest that our health is not only determined by what we eat and to what we are exposed but also by what our parents ate and perhaps their
386
environmental exposures when they were young.
Omics Technologies The suffix -omics first came into widespread use in association with genetics. The complete set of genes contained in an organism's DNA was referred to as the genome, so the study of the genome was called genomics. Following suit has been a host of similar terms used to describe the study of particular aspects of genomics. For example, the entire complement of mRNA molecules (gene transcripts) in a given cell is referred to as that cell's transcriptome, and the study of the entire set of transcripts in a particular cell or tissue at a particular point in time is referred to as transcriptomics. Since most transcripts (mRNA) in a cell can be converted to proteins, the entire population of proteins within a cell or tissue is referred to as the proteome, and the study of the proteome is proteomics. Likewise, all parts of a cell that are involved in the cell's complex metabolism, such as the substrates, cofactors, and products of each of the thousands of enzymatic reactions carried out by the proteome, are referred to as the metabolome, and the study of metabolomes is thus metabolomics. Not surprisingly, similar terminologies have arisen to describe the study of the global process by which epigenetic factors influence gene expression—epigenomics. One subset of the epigenome is the global pattern of methylation of nucleotides throughout an entire genome, and it is referred to as the methylome. New tools and technologies in molecular biology now make it possible to acquire not only the entire sequence of someone's genome but also his or her transcriptome, proteome, metabolome, and methylome. However, it is important to note that the genome of an individual is identical in every cell, whereas the transcriptome, proteome, metabolome, and methylome are unique to each tissue, and even to the time the sample from that tissue was collected! Thus, although genomes are highly stable across tissues and time, all of the other omics outputs are tissue and time specific. Given that there are about 24,000 genes, probably more than 100,000 different proteins, and literally millions of potential measurement values across tissues and time in a single individual, managing such a huge amount of information is very challenging and requires sophisticated mathematical and computational
387
approaches.
Fortunately, new computing approaches and hardware, software programs, and robust statistical analyses are continuously being developed and improved to collect, organize, and analyze DNA and protein sequences, transcriptomes, metabolomes, and other sources of large data generated by modern biological and health sciences research. This growing field, known as bioinformatics, is an essential component of all omics technologies. One of the biggest challenges scientists face when confronted with literally hundreds of thousands to millions of comparisons is the so-called false discovery rate. Recall the familiar statistical concept of comparing two variables to determine whether one is significantly different from the other, often using simple tests such as the t-test. One of the first decisions in applying any such test is to decide on a level of significance. For example, a common choice of p value is 0.05; when p < .05, there is less than a 5% probability that an observed difference between two values occurred by chance, suggesting that some factor—perhaps the independent variable under study—is truly associated with the difference. However, accepting this 5% threshold implies that in 5% of observations, what seems statistically significant is in fact a chance occurrence (assuming that the data are normally distributed). Now imagine doing 1 million different comparisons, having set the p value at 0.05. This means that 50,000 of the comparisons would show statistically significant differences just as a result of random variation rather than of true, functional differences. This is referred to as the multiple comparisons problem, and the erroneous positive associates are called false discoveries. Thus statistical approaches that utilize far more rigorous comparison thresholds than p < 0.05 are required to identify changes that are truly significant. For this reason, modern biostatistical analyses increasingly include a bioinformatics perspective, to help researchers analyze and interpret the huge amounts of data that are becoming commonplace in molecular biology laboratories around the world. This is especially important in the study of gene- environment interactions, where many comparisons of different gene polymorphisms with respect to environmental factors can lead to spurious associations that arise just by chance (false discoveries).
388
Approaches for Identifying Gene- Environment Interactions The early concepts that genes and environment could somehow interact to produce disease came from pioneering studies over 100 years ago on the origins of metabolic diseases. Sir Archibald Garrod (1857–1936), a distinguished English physician, was the first to describe familial “inborn errors of metabolism,” including the conditions known as alkaptonuria and albinism. Although he did not use the term genetics, Garrod clearly described the concept of individual susceptibility, and envisioned the role of genetic factors in diseases: “In every case of every malady there are two sets of factors at work in the formation of the morbid picture, namely internal or constitutional factors, inherent in the sufferer and usually inherited from his forebearers and external ones which fire the train” (Omenn & Motulsky, 2006). One of Garrod's coworkers, William Bateson (1861–1926), coined the term genetics, to describe the occurrence of these metabolic disorders in families (parents and siblings). Bateson noted that these metabolic diseases often occurred in marriages among first cousins whose parents did not display the disease, an occurrence that we now know is consistent with a recessive Mendelian trait.
In the early years of genetic discovery, research focused solely on the effect of an individual organism's genes or genome on that organism's health. However, variations in single genes that cause disease (Mendelian disorders) are quite rare, and thus relatively few individuals benefit from identification of these genes. Common afflictions such as type 2 diabetes and obesity, which have great public health significance, are far too complex to be explained by the action of a variant in a single gene. Instead, such conditions result from gene-environment interactions. For the purposes of this discussion, environment refers to anything outside the body that can affect one's health. Such a broad definition is necessary, given that virtually any type of exposure (e.g., climate, food, drugs, radiation, chemicals) can be associated with a health outcome in an individual or population, possibly resulting in a diseased state. Elucidating the interactions between genes and also between genes and the environment in the context of multifactorial diseases such
389
as obesity, is extremely important in reducing the burden they impose on society.
There is a distinction between an environmental response gene and a disease gene. An environmental response gene dictates a person's response to certain environmental exposures, but without such an exposure this gene generally has no health consequence. One example is a polymorphism in a gene called N-acetyltransferase 2 (NAT2), which is discussed later in this chapter. (Note also that an environmental response gene may be responsive to many different exposures if that gene encodes for a protein in a common metabolic pathway.) Conversely, a disease gene is one that causes a disease irrespective of environmental cues. Cystic fibrosis, a terribly debilitating disease, is caused by mutations in the CFTR gene, which encodes for the cystic fibrosis transmembrane conductance regulator protein. Many different mutations within the CFTR gene may result in this disease, most resulting in an amino acid substitution or deletion (see Figure 7.3) that causes the CFTR protein to malfunction or be degraded. Many other disorders are caused by heritable disease genes, including Huntington's disease, Duchenne muscular dystrophy, and sickle-cell anemia, as well as certain types of Parkinson's disease. However, very rarely are diseases the result of mutations in a single gene; more often disease results from the interactions of multiple genes, all or some of which may have uncommon genetic variants. A final point to keep in mind is that environmental exposures can affect the severity or progression of a disease even when the disease itself is not caused by an exposure per se. For example, cystic fibrosis is not caused by exposure to smoke or airborne pollutants but is certainly aggravated by these exposures.
Although significant strides have been made in understanding the genetic bases of disease, this knowledge remains incomplete. As we have already discussed, many factors can influence disease and the risk of disease; however, there are now specific types of studies that aim to parse the genetic components underlying disease. They are termed genetic association studies. Genetic association is the co- occurrence, more frequently than would occur by chance, of a genetic characteristic and some other trait(s). There are two main approaches used in genetic association studies. The first, the candidate gene approach, is hypothesis driven, building on a
390
detailed understanding of biochemical pathways. Given a gene's known role in a pathway important to a disease of interest, scientists can advance an educated guess as to what might occur if that gene's functionality were altered in some way. Researchers then sequence the gene of interest in patients with a particular disease, and determine whether a mutation is more common among them than among people without that disease. An example is the LMNA gene responsible for Hutchinson-Gilford progeria syndrome (Eriksson et al., 2003).
Technical advances have allowed for a newer, so-called agnostic approach to genetic association studies, one that is much broader in scope. Instead of focusing on one or a few genes, a genome-wide association study (GWAS) scans a wide range of genes, seeking associations between particular genes and traits of interest. Proponents of this approach consider it less inherently biased than candidate gene studies. However, GWAS require much larger sample sizes and more complex statistical analyses, and due to the sheer amount of data, such studies may result in spurious positive results. Nonetheless, GWAS studies are particularly relevant to environmental health because they can integrate environmental exposure data with genetic analysis. For example, a GWAS might compare a group of diseased factory workers with nondiseased workers from the same factory, genotyping them all for common SNPs, and stratifying them according to their workplace exposures. Sophisticated statistical analysis can then be employed to reveal genes or GxE interactions that may be associated with the disease outcome. This powerful technique can be harnessed together with candidate gene approaches to understand more completely the genetic underpinnings of disease.
391
Examples of Gene-Environment Interactions in the Real World Drug Responses Much of what we know today about GxE interactions stems from early discoveries related to individual, or in some instance racial/ethnic, differences in response to drugs given to treat a disease. One of the first observations of a clinically relevant drug response that differed between racial groups occurred during World War II. When U.S. troops were fighting in parts of the world where malaria was common, it was noticed that some but not all soldiers developed a blood disease called hemolytic anemia following treatment with the antimalarial drug primaquine. Moreover, nearly all those who developed this adverse effect from the drug were African American (Earle, Bigelow, Zubrod, & Kane, 1948), which strongly suggested that some genetic difference conferred susceptibility. Today we know that this response is due to a variant in a gene for the protein, glucose-6-phosphate dehydrogenase (G6PDH), and that the variant allele is much more common in people of African and Mediterranean ancestry than it is in Caucasians.
One of the most dramatic early examples of a drug-gene interaction involves a drug that is widely used to cause local muscle paralysis during surgery. This drug, succinylcholine, is a very effective inhibitor of the neurotransmitter acetylcholine, released at the neuromuscular junction. When the brain signals a muscle fiber to contract, that electrical signal is converted to a chemical signal, the neurotransmitter acetylcholine, which binds to a receptor in the muscle fiber, causing it to contract. Succinylcholine is an inhibitor of the acetylcholine receptor, thereby blocking the stimulation of the muscle fiber. Normally succinylcholine is rapidly broken down in the bloodstream by an enzyme called pseudocholinesterase (also called butyrylcholinesterase). Because it is so quickly broken down, physicians normally just drip the drug into an IV to maintain paralysis. Once the surgery is complete, the drip is stopped, and the patient quickly regains muscle function as the drug is eliminated from the body. As the name suggests, pseudocholinesterase doesn't
392
participate in the normal breakdown of acetylcholine, so there are no serious physiological consequences if the enzyme is deficient. Indeed, there is a genetic polymorphism that is present in a small percentage of the population that results in a pseudocholinesterase enzyme with little or no activity—ordinarily a harmless trait, even in people who are homozygous for the defective enzyme. But if these people receive a normal therapeutic dose of succinylcholine, they remain paralyzed for hours or even days, because it is not promptly broken down and continues to block excitation of muscle fibers (Omenn & Motulsky, 2006).
The term pharmacogenetics was first used in 1959, by Vogel, to describe such phenomena. Other investigators utilized studies comparing drug responses in identical and fraternal twin pairs. Such studies revealed that identical twins had much more similar plasma levels and elimination rates of common drugs than did fraternal twins (Omenn & Motulsky, 2006). However, it was also discovered that some drugs have a bimodal or trimodal distribution of pharmacological effects, toxicity, and plasma levels across populations, suggesting a simple pattern of Mendelian inheritance (Omenn & Motulsky, 2006). Numerous drugs have such profiles, indicating important single gene differences in how these drugs are metabolized.
Dietary, Occupational, and Environmental Exposures Medications provide revealing examples of GxE interactions, but the same principles can be seen in dietary, workplace, and general environmental exposures as well. This section offers three more examples in which multiple genes are involved in modulating risk: one involving alcohol, a dietary exposure; a second involving beryllium, a workplace exposure, and the third involving exposure to pesticides, which can occur as either an occupational or a nonoccupational exposure. Additional examples appear in Tox Box 7.1, on benzene, and in Text Box 7.2, on mercury. These examples illustrate the complexity of many GxE interactions.
393
Tox Box 7.1 Benzene
WHAT IS IT? Benzene is the simplest of the aromatic, or ring-shaped, organic chemicals, with the chemical formula C6H6. It occurs naturally as a component of petroleum, in coal tar, and in other fossil fuels. It is a colorless liquid with a sweet odor.
HOW IS IT USED? Benzene is widely used in chemical manufacturing, to make polymers, plastics, resins, adhesives, and a variety of other products. It is also used as a solvent. Because of these many uses, benzene is one of the top twenty industrial chemicals in terms of production volume.
HOW ARE PEOPLE EXPOSED? The main route of benzene exposure is inhalation, although other exposure pathways, such as oral and dermal, may contribute. Benzene comprises a small percentage of gasoline, so people pumping gasoline may inhale it. Benzene is a component of tobacco smoke, so smokers are regularly exposed. Benzene is present in motor vehicle exhaust, and in such products as glues, paints, and furniture wax. When benzene contaminates groundwater—say, from leaking underground gasoline storage tanks—it may enter an aquifer that is used for drinking water and thus be ingested. For members of the general public, benzene exposure is generally
394
quite low, but workers in certain industries, such as the petrochemical and tire manufacturing industries, may sustain much higher exposures.
WHAT ARE THE TOXIC EFFECTS? As with many chemicals, the acute effects of high-level exposure differ from the long-term effects of chronic low- level exposure. High-level exposure (in the hundreds or thousands of parts per million, or ppm) can cause headaches, confusion, and even unconsciousness and death. In the case of long-term, lower levels of exposure, the main target organ is the bone marrow, where blood is formed. Benzene may impair the production of blood cells, causing anemia, and is a risk for cancer, especially acute myeloid leukemia. (It is classified as a Group 1 carcinogen by the International Agency for Research on Cancer [IARC].) Benzene is also a reproductive toxicant; animal studies show that prenatal exposure is associated with low birth weight, delayed bone formation, and bone marrow damage.
In understanding benzene toxicity, both toxicology and genetics offer important insights. Once absorbed, benzene is metabolized through well-defined pathways. Some of the metabolites are more toxic and others less toxic than benzene itself. Eventually, the metabolites are excreted. Some of these metabolic pathways are illustrated in the accompanying figure, which shows benzene oxidized to benzene oxide, then to either phenol or catechol, and then to a range of other metabolites. Not shown are a number of additional metabolic pathways, called conjugation reactions, that further detoxify many of the benzene metabolites and facilitate their excretion in the urine.
395
Source: Rothman et al., 1997.
Three major proteins, each coded by a gene, are involved in the biotransformation of benzene: cytochrome P450 2E1 (CYP2E1), myeloperoxidase (MPO), and NAD(P)H quinone oxidoreductase 1 (NQO1). All three of these enzymes are polymorphic, meaning that there are different forms, or DNA sequence variants, in the genes that encode them. External variables (e.g., concurrent chemical exposures) can also affect the biotransformation processes. CYP2E1 is responsible for the initial activation of benzene, and increased expression of CYP2E1, or mutations that make the enzyme more active, can lead to increased formation of the
396
toxic metabolites benzene oxide and hydroquinone. The same is true for MPO, which acts to produce more toxic metabolites, such as 1,4-benzoquinone.
Benzene oxide is particularly toxic, because it can bind DNA and damage genetic material directly—an action that is part of the carcinogenic pathway. NQO1 is a detoxifying, antioxidant enzyme that serves to reduce the production of toxic metabolites. Genetic variants of NQO1 can lead to less active NQO1, allowing more toxic metabolites to build up. In fact, the risk of hematological malignancy following benzene poisoning is significantly higher in people with a particular NQO1 mutation compared to people with the normal genotype. Deleterious genetic variants in some or all three of these genes can be synergistic, conferring even higher risk of disease following benzene exposure.
HOW ARE PEOPLE PROTECTED?
Protection from benzene involves interrupting exposure. The two major sources of exposure are cigarette smoke and gasoline. Smokers can reduce their benzene exposure by quitting smoking, and nonsmokers by avoiding secondhand
397
smoke. Similarly, avoiding breathing gasoline fumes is an effective preventive strategy; the familiar vapor recovery systems at gas stations (as shown here), and not “topping off” after refueling has automatically stopped are effective practices.
More broadly, benzene exposure can be limited through regulation. Workplace regulation of benzene set important precedents in regulatory law (Feitshans, 1989). In 1971, the newly formed Occupational Safety and Health Administration (OSHA) adopted a 10 ppm threshold limit value (TLV) for benzene exposure, as part of a large group of consensus standards drawn from then-prevailing voluntary industry limits. In 1978, based on evidence of benzene carcinogenicity, OSHA proposed to lower the workplace exposure limit to 1 ppm. However, this rule was challenged by industries that used benzene, as well as by labor unions, and was vacated by the Supreme Court in 1980. OSHA had based its approach on the notion that there was no safe threshold for exposure to a carcinogen and so exposure must be held to the “lowest feasible level.” However, the industries argued that feasible should include not only technical but also economic constraints, and that OSHA had failed to demonstrate “appreciable benefits” from the more stringent regulation. The court sided with the challengers, invalidating the proposed rule. The court held that OSHA had not supported its approach with “substantial evidence” of “significant risk,” and had failed to show that the proposed regulation was “reasonably necessary.” In effect, this established a far-reaching legal requirement that regulatory agencies ground their actions in risk assessment (see Chapter 27). Notably, the court did not require cost-benefit analysis of the regulation. In 1987, based on newly available quantitative epidemiological data, OSHA again imposed the 1 ppm standard, and that regulation remains in place.
WANT TO LEARN MORE? A thorough (if slightly dated) review of benzene toxicity is ATSDR's Toxicological Profile for Benzene, last updated in 2007, available at www.atsdr.cdc.gov/ToxProfiles/TP.asp?
398
id=40&tid=14. The IARC evaluation of benzene was most recently updated in 2012; see IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Vol. 100F. Chemical Agents and Related Occupations, available at monographs.iarc.fr/ENG/Monographs/vol100F/index.php
Contributed by Howard Frumkin
Alcohol Drinking excessive amounts of alcohol can lead over time to multiple pathologies in the liver, including cirrhosis, or fibrotic hardening of the liver, and liver cancer. There are also acute effects that can be modulated by genotype. As with many chemical exposures, these effects are related primarily to biotransformation of the parent compound. In this metabolic pathway, ethanol is converted to acetaldehyde by an enzyme called alcohol dehydrogenase (ADH), which is most active in the liver and stomach, and then to acetate by a second enzyme, aldehyde dehydrogenase (ALDH) (see Figure 7.6).
Figure 7.6 Primary Biotransformation Pathway for Alcohol
Although acetate is relatively nontoxic, acetaldehyde is toxic, and it is therefore important to keep circulating levels of acetaldehyde low. A relatively common polymorphism, seen primarily in Asian populations, exists in the ALDH2 gene. This variant, known as ALDH2*2, results in reduced function of the ALDH2 enzyme, leading to a buildup of acetaldehyde in the blood following consumption of alcohol, and causing severe flushing and very unpleasant “hangover-like” symptoms (Crabb, Matsumoto, Chang, & You, 2004). For people harboring the ALDH2*2 variant, even very small amounts of alcohol can result in a severe reaction. Interestingly, based on an understanding of this mechanism of action, a drug called disulfiram, or Antabuse, that inhibits the ALDH2 enzyme was developed for the treatment of alcoholism and remains an effective approach. People who take Antabuse know that
399
they will become very ill if they drink alcohol, so it provides a strong and usually effective means of discouraging alcohol consumption.
Chronic Beryllium Disease A unique example of workplace exposure and risk of disease involves beryllium, the fourth element in the periodic table. Beryllium is most commonly used to make metal alloys that are exceptionally strong, light, and flexible and are used in settings such as the aerospace industry. Although beryllium is present in microgram quantities in our bodies, it is highly toxic. Like many other metals, beryllium's toxicity is related to its ability to displace metal ions (in this case, primarily magnesium) in enzymes, thereby impairing their function. Not only is beryllium classified as a Group I carcinogen by IARC but beryllium poisoning can also lead to debilitating, incurable lung illnesses, including acute beryllium disease and chronic berylliosis. While dermal and oral exposure can occur, the most common route of exposure is inhalation, especially among workers manufacturing beryllium alloy– containing products, and the pathology related to beryllium exposures manifests primarily in the lungs.
Chronic berylliosis is notable for a few reasons. First, workers who develop berylliosis may not display symptoms until many years after exposure. This is because the immune response elicited by beryllium exposure first requires sensitization, or priming, of the immune system. A person who is sensitized to beryllium may, when reexposed, mount an immune response that recognizes beryllium as a threat and activates a unique group of scavenging cells called macrophages. This is usually a helpful process, but in people who develop berylliosis, the macrophages begin to cluster after repeated exposures, forming granulomas in the lung that eventually impair lung function.
Interestingly, sensitivity to beryllium seems to be governed primarily by variation in a single gene, HLA-DPB1, which encodes human leukocyte antigen class II histocompatibility antigen, DP(W2) beta chain, a cell surface receptor responsible for eliciting a particular immune response. The SNP called HLA-DBP1*0201 results in an amino acid substitution of a glutamate instead of the normal lysine at amino acid position 69. Although this variant is quite common, present in about 33% of the general population, only
400
about 5% of beryllium-exposed workers develop chronic berylliosis. Thus the variant is not necessarily a specific predictor of berylliosis risk (in epidemiological terms, the positive predictive value is low). However, between 75% and 97% of beryllium-exposed workers who develop chronic berylliosis harbor the Glu69 variant, compared to only 30% to 45% of workers who do not develop berylliosis (Silver & Sharp, 2006). Thus the negative predictive value is high. These facts raise fascinating ethical, social, and legal issues, which are explored in the discussion questions at the end of this chapter.
401
Text Box 7.2 Genetic Susceptibility to Environmental Mercury
James S. Woods
Mercury (Hg) is a neurotoxic metal, and people are exposed from a variety of relatively common environmental sources, from dental amalgam tooth fillings to fish consumption. Children are particularly susceptible to mercury neurotoxicity. A current major challenge is identifying children who may be genetically susceptible to Hg toxicity. Recent gene-Hg interaction studies have identified some common genetic variants that exacerbate the adverse effects of Hg. Two examples of single gene polymorphisms that affect mercury neurotoxicity are genetic variants in coproporphyrinogen oxidase (CPOX) and catechol-O-methyl transferase (COMT).
CPOX is an enzyme of the heme biosynthetic pathway. It catalyzes formation of the heme precursor, protoporphyrin, into which iron is incorporated to form heme. Heme plays an essential role in a wide range of neurological processes, and heme deficiency is associated with a number of neurodevelopmental and neurodegenerative disorders. About 28% of people have a SNP in exon 4 of the CPOX gene that encodes a variant form of CPOX, called CPOX 4, which substantially reduces heme synthesis. This variant doesn't necessarily compromise heme-dependent neurological processes, but it does lower the threshold for Hg toxicity. Children with the CPOX4 variant, when exposed to Hg, show substantially worse neurobehavioral function than exposed children without the variant (called wild type, or CPOX WT). The effects are wide ranging, including attention, visual- spatial acuity, executive function, learning and memory, and motor function issues. Interestingly, modification of Hg neurotoxicity by CPOX4 in children is restricted almost exclusively to boys, suggesting differential sensitivity to Hg toxicity based on gender as well as on genetic predisposition (Woods et al., 2012).
402
Dopamine (DA) is the principal neurotransmitter affecting the integration of cognitive functions in humans, and methylation of DA by catechol-O-methyl transferase (COMT) is the principal mechanism by which this DA activity is regulated. Polymorphisms of COMT are associated with a number of neuropsychiatric and affective disorders, especially in children. One polymorphism of particular interest is COMT rs4680, which is found in about half of children, and which independently predisposes them to many of the same disorders of attention, learning, and memory as does Hg exposure. Accordingly, one might expect children genotyped with COMT rs4680 to be especially susceptible to the neurobehavioral effects of Hg, and this is exactly what is observed. Thus, while either COMT rs4680 or Hg has a limited impact on children's neurobehavioral performance, children with both the gene variant and Hg exposure show greater deficits in tests of attention, learning and memory, and visual-spatial acuity, in a gene-dose response manner, compared to Hg-exposed children genotyped as COMT WT. As with CPOX4, the effect of COMT rs4680 on Hg toxicity is restricted almost exclusively to boys, demonstrating differential sensitivity to Hg toxicity based on gender as well as on genetic predisposition (Woods et al., 2014).
Pesticides One of the most complicated examples of a GxE interaction involves organophosphate (OP) pesticides and the serum enzyme paraoxonase 1 (PON1). As described in Tox Box 18.1, OP compounds elicit nearly all of their toxic effects by inhibiting the action of acetylcholinesterase (AChE), an enzyme that breaks down the important neurotransmitter acetylcholine. When the action of AChE is blocked, acetylcholine is allowed to continue stimulating neuromuscular junctions. As a result, OP poisoning can result in excessive stimulation of the nervous system, leading to a constellation of symptoms summarized as SLUDGE (salivation, lacrimation, urination, defecation, gastrointestinal movement, and emesis). PON1 hydrolyzes some OP compounds to prevent their toxic effect on AChE, and variations in PON1 can modify these toxic
403
effects.
Two polymorphisms in PON1 are usually considered: PON1 a nonsynonymous cSNP called Gln192 and a non-coding variant called PON1 108C → T. Substituting the wild type arginine at codon 192 for a glutamine increases the catalytic efficiency of PON1, while the PON1 108C → T variant affects the expression of the gene and thus decreases the serum levels of PON1. Only by examining the genotype for both of these alleles can one make an accurate assessment of a person's susceptibility to OP toxicity. Factors other than OP exposure can also modulate PON1 activity, including alcohol, smoking, certain drugs, diet, and certain physiological and pathological conditions (Costa, Vitalone, Cole, & Furlong, 2005).
These examples illustrate the ways in which genes and environmental exposures interact to affect people's responses to exposures, and they also highlight some of the challenges public health professionals must consider when investigating gene- environment interactions.
404
Summary Most of the chronic diseases of greatest public health importance, such as cancers, heart disease, degenerative neurological diseases (e.g., Parkinson's, Alzheimer's), and diabetes and other metabolic disorders, arise from complex interactions between a person's inherited biology (both genetic and epigenetic in origin) and his or her environment. While the genetic and epigenetic deck of cards you are dealt at birth is not readily modifiable, many environmental factors are. Thus there is great interest and value in understanding gene-environment interactions, to permit interventions such as environmental control measures that can reduce disease burden. In this chapter, we have discussed the tools, technologies, and approaches used by public health scientists to tease apart these complex interactions. The wonderful discoveries made possible through advances in genomics, transcriptomics, proteomics and metabolomics—coupled with advances in computational and statistical approaches to managing the massive amounts of data derived from these tools (bioinformatics), and large, novel population-based study designs (e.g., genome-wide association studies, GWAS)—hold great promise. This field will increasingly help to identify modifiable environmental factors that can reduce the incidence of environment-related diseases, and improve both early diagnosis and treatment.
405
Key Terms 5′ flanking region
Region of DNA adjacent to the 5′ region, or beginning of the gene, in contrast to the 3′ region, which is at the end of a gene.
adenine A nitrogenous purine base (abbreviated “A”) found in DNA and RNA; pairs with thymine in DNA and uracil in RNA.
aflatoxin B1 (AFB1) Mycotoxin produced by the mold Aspergillus flavus, which grows commonly on corn and peanuts. This B1 form is among the most potent liver carcinogens yet discovered.
agonist A chemical that binds and activates a receptor, eliciting a biochemical response.
allele One of a number of alternative forms of a gene or DNA sequence that can occupy a genetic locus on a chromosome. Different alleles produce variation in inherited characteristics, and one form of an allele may be expressed more than another form in an individual (dominant versus recessive alleles).
amino acid Organic molecule containing both an amine (-NH2) and carboxyl (-COOH) group. There are twenty-one amino acids that link together to form peptides (fewer than ≈50 amino acids) and proteins (more than ≈50 amino acids).
antagonist Chemical that blocks agonist-mediated responses rather than eliciting a biological response itself upon binding to a receptor.
autosome Any chromosome other than a sex chromosome. Humans have twenty-two pairs of autosomes and one pair of sex chromosomes (XX in females and YY in males).
berylliosis A lung disease resulting from exposure to beryllium or beryllium alloys; it involves an immune response and may persist irrespective of exposure level.
406
bioinformatics A field that uses computer science, mathematics, and statistics to collect, organize, and analyze complex biological data.
candidate gene A gene located on a chromosome region suspected of being involved in a disease and producing a protein that could contribute to the development of the disease in question.
chromosome A structure composed of long, threadlike packages of DNA and associated proteins that carries all the information of an organism.
codon A three-base sequence in DNA that is transcribed into mRNA and specifies a single amino acid to be added into a polypeptide chain or causes termination of translation.
copy number variation (CNV) Differences between individuals in the number of copies of a particular gene. Although every gene in a genome typically has two alleles, it is not unusual for multiple copies of one or the other allele to be present in the gene region.
cytosine A nitrogenous pyrimidine base (abbreviated “C”) found in DNA and RNA; pairs with guanine in DNA and RNA.
deoxyribonucleic acid (DNA) The chemical in the cell nucleus that carries genetic instructions for an organism's structure and function.
deoxyribose Pentose (5-carbon) sugar present in a nucleotide subunit of DNA, with only one hydroxyl group on the sugar (in contrast to ribose, which has two hydroxyl groups on the pentose sugar).
diploid Containing two sets of homologous chromosomes (i.e., a “double” genome) and hence two copies of each gene or genetic locus. The diploid number in humans is 46.
disease gene A gene or gene variant that results in a disease state, irrespective of environmental cues.
407
double helix The structural arrangement of DNA, resembling a spiraling ladder and created by the specific base pairing of individual nucleotides through hydrogen bonding.
endocrine disruptor An exogenous agent that interferes with the production, release, transport, metabolism, binding, action, or elimination of natural hormones, such as estrogen, androgens, and the thyroid hormone.
endogenous Originating within an organism.
environmental factors Abiotic or biotic factors that influence living organisms.
environmental response gene A gene that dictates a person's response to certain environmental exposures but that without such an exposure generally does not confer injury or advantage.
epigenetic Involving heritable, phenotypic changes in gene expression that do not involve changes in gene sequence; often these changes are controlled by methylation of cytosine bases in DNA and/or modification of histone proteins.
epigenome All the chemical modifications (e.g., methylation, histone acetylation) accrued to the entirety of one's genome, other than changes in the core composition of DNA (mutations).
epigenomics The study of heritable, phenotypic changes in gene expression that do not involve changes in gene sequence.
exogenous Originating outside an organism.
exon Segment of a gene consisting of a sequence of nucleotides that will be represented in mRNA. In protein-coding genes, exons encode the amino acids in the protein. Exons are usually adjacent to introns.
false discovery rate
408
The expected percentage of false predictions based on chance alone in a set of predictions.
fetal origins of adult disease The concept that events during early development (e.g., malnutrition) have a profound impact on a person's risk for development of certain chronic diseases as an adult. Also referred to as the Barker hypothesis.
gene The basic unit of heredity. A chromosomal segment that carries information for a discrete hereditary characteristic, usually corresponding to an RNA sequence or protein.
gene-environment interaction Differential effect of a particular environmental exposure on disease risk in people with different genotypes. Ecogenetics is the study of genetic determinants that define susceptibility to environmentally influenced adverse health effects.
genetic association The co-occurrence, more often than can be explained by chance, of two or more traits in a population of individuals and where at least one trait is known to be genetic.
genetic code The complete set of triplet codons in DNA that signals for protein production, including start and stop codons, and multiple triplet codons specific for each of the 21 amino acids used to construct peptides and proteins from mRNA.
genome A single complete set of genetic information (i.e., the genes plus all the noncoding information) contained in an organism's or cell's DNA.
genome-wide association study (GWAS) Investigation of many common genetic variants in different individuals to determine whether any genetic variant is associated with a particular trait or phenotype.
genomics The comprehensive study of whole sets of genes and their interactions, rather than single genes.
genotype The allelic constitution, which does not show directly as outward
409
characteristics. The genotype is dictated by the specific nucleotide sequences within genes.
guanine A nitrogenous pyrimidine base (abbreviated “G”) found in DNA and RNA; pairs with cytosine in DNA and RNA.
Hepatitis B virus (HBV) A virus that primarily manifests its effects in the liver, resulting in chronic hepatitis. HBV is a major risk factor for hepatocellular carcinoma.
hepatocellular carcinoma (HCC) A type of liver cancer arising from the epithelium, which can result from a number of preventable factors, such as Hepatitis B and C infection, chronic alcohol consumption, aflatoxin ingestion, and diabetes.
histones Small, positively charged proteins that fold to form nucleosome cores around which DNA is wrapped in chromosomes. Histones can be important in epigenetic regulation (see epigenetic).
histone deacetylase (HDAC) Enzyme that removes acetyl groups from core histones.
homozygous Possessing two identical forms of a particular gene (allele), one inherited from each parent.
indel A region in a gene where a small segment of nucleotides (from two to several hundred) has been inserted in or deleted from the normal sequence of the gene.
intergenic region A length of DNA sequence located between defined genes.
intron A noncoding region of a gene that is transcribed into an RNA molecule but then excised by RNA splicing. Although often considered to have no biological function, introns may encode other regulatory RNAs, such as miRNAs, or include recognition motifs that control transcription and/or RNA stability.
ligand-activated nuclear transcription factor Transcription factor activated by the binding of a specific
410
substrate, which may induce a conformational change in the transcription factor or facilitate its transit into the nucleus.
locus In genetics, the place on a gene where a specific gene is located.
messenger RNA (mRNA) Template for protein synthesis that binds to ribosomes. The sequence of a strand of mRNA is complementary to the cognate sequence of DNA from which it is transcribed.
metabolome The complete set of small molecules in a biological sample; they reflect biochemical processes occurring within the cells or tissue of interest. The metabolome may be altered in response to an environmental exposure or disease state.
metabolomics The systematic study of metabolites or suites of metabolites within a given cell or tissue.
methylation Addition of methyl (CH3-) groups to DNA. Methylation of certain cytosine bases in a gene's DNA often results in silencing that gene's expression. Chemical perturbations and certain disease states may result in or from hypo- and hypermethylated genes.
methylome Set of methylation modifications to DNA in an organism's genome.
microRNA (miRNA) Short (21 to 23 nucleotides) RNA molecule encoded by a gene that can regulate gene expression through complementary base- pairing with mRNA.
multiple comparisons problem The problem inherent in a data analysis with a large enough number of comparisons to raise the risk of false positive findings.
mutation A permanent structural alteration in DNA. In most cases, mutations either have no effect or cause harm, but they can occasionally confer an advantage to the organism. The concept
411
of natural selection is based on the theory that random mutations can give rise to beneficial changes that provide a selection advantage over other organisms that do not have the mutation.
non-synonymous cSNP A SNP in the coding region of a gene (e.g., in an exon) that produces a change in the translated sequence, resulting in an altered amino acid sequence being translated from the mRNA transcript of the gene of interest.
nucleotide A structural component of DNA and RNA that is composed of a 5-carbon sugar (ribose in RNA and deoxyribose in DNA), at least one phosphate group, and a nitrogenous base.
phenotype The observable characteristics, including physical appearance and behavior, of a cell or organism. Phenotype can be defined at the level of the organism or at discrete levels of function, such as at the enzyme activity level.
polymorphism A change in the nucleotide sequence of a specific region of DNA in one DNA sample when compared to the sequence in many samples. Polymorphism can exist in many different forms, including gene deletions, gene duplications, indels, or single nucleotide polymorphisms.
promoter Nucleotide sequence in DNA to which RNA polymerase binds to begin transcription; most often upstream of the transcriptional initiation site.
proteome The entirety of proteins expressed in a cell, tissue, or organism at any given moment in time.
proteomics Study of all the proteins produced by a cell, tissue, or organism. Proteomics often investigates changes in the proteome caused by changes in the environment or by extracellular signals.
receptor Any protein that binds to a specific signaling molecule (ligand) and initiates a cellular response; receptors may be present on the
412
cell surface or within the cell. ribonucleic acid (RNA)
A polymer formed from covalently linked ribonucleotide monomers. In RNA, uracil is substituted for thymine in the genetic code.
single nucleotide polymorphism (SNP) A SNP arising through a single base pair change in a specific region of DNA compared to the same region in a population of DNA samples. To be classified as a SNP, the allele frequency (variant form) must be present in a population of at least 1% of the alleles; if it occurs at a lower rate, it is considered a rare variant or a mutation.
splice junctions Sites at which introns and exons join and the exons are then ligated following removal of the intronic sequences during transcription.
splicing Linking two RNA exons together while removing the intronic DNA sequence that lies between them.
synergism An instance in which the combined effects of two chemicals are greater than the sum of the effects of each agent alone.
synonymous cSNP A SNP in the coding region of a gene (e.g., in an exon) that results in no change in the translated sequence (cf. non- synonymous SNP).
thymine A nitrogenous purine base (abbreviated “T”) found in DNA. Thymine pairs with adenine in DNA. In RNA, thymine is replaced with uracil.
transcription Copying of one strand of DNA into a complementary RNA sequence by RNA polymerase.
transcription factor Sequence-specific DNA binding protein that binds to gene promoters and other regulatory elements (transcription factor binding sites) and initiates gene-specific transcription.
413
transcriptome The entire complement of RNA molecules in a given cell.
transcriptomics The study of the transcriptome.
transgenerational epigenetic inheritance The passing of epigenetic alterations to the genome (and associated phenotypic alterations) to subsequent generations. Most, but not all, epigenetic modifications are cleared and reestablished during each generation. Environmental factors may modify the extent of transgenerational epigenetic inheritance.
translation The process by which ribosomes decode an RNA message (mRNA) to synthesize a protein.
triploid Possessing three sets of a particular chromosome or chromosomes. Whole organism triploidy would result in 69 chromosomes. Trisomy 21, in which a third copy of chromosome 21 results in the phenotype described as Down syndrome, is the best known triploid disease.
uracil A nitrogenous purine base (abbreviated “U”) found in RNA. Uracil pairs with adenine in RNA.
variant (allele) An alteration in the normal sequence of a gene. Hundreds of variants may exist for a single gene. Whether the sequence variability is considered the common form (sometimes called wild type) or the variant form (sometimes called mutant) may depend on the reference population, since variant alleles are heritable and will be enriched in populations with many carriers.
414
Discussion Questions 1. Almost all workers who develop chronic berylliosis harbor the
Glu69 variant, compared to only 30% of workers who do not develop berylliosis. At least three approaches to the use of genotyping for the Glu69 variant might be considered:
Employers that use beryllium require all potential employees to be genotyped prior to hiring, and reject applicants based on a positive finding.
Employers that use beryllium require all potential employees to be genotyped prior to hiring, provide a detailed explanation of the risks involved for Glu69-positive workers, then allow each applicant to decide whether to accept employment, and ask hired workers to sign a waiver taking full responsibility for any adverse outcomes.
Employers do not use genetic testing.
Which approach do you favor, and why? How would your answer change if the predictive value of genetic testing were 100%?
2. As you read in Text Box 7.2, genetic variants in CPOX and COMT genes can increase susceptibility to mercury (Hg) exposure (e.g., from fish consumption or dental amalgams), especially in boys. However, fish are also a leading dietary source of omega fatty acids, which are important for neurological development. How would you frame this issue for public education, and how would you present possible testing options for children who may be at risk of increased mercury exposure?
415
References Costa, L. G., Vitalone, A., Cole, T. B., & Furlong, C. E. (2005). Modulation of paraoxonase (PON1) activity. Biochemical Pharmacology, 69(4), 541–550.
Crabb, D. W., Matsumoto, M., Chang, D., & You, M. (2004). Overview of the role of alcohol dehydrogenase and aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology. Proceedings of the Nutrition Society, 63, 49–63.
Dolinoy, D. C., Huang, D., & Jirtle, R. L. (2007). Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proceedings of the National Academy of Sciences of the United States of America, 104, 13056– 13061.
Duhl, D.M.J., Vrieling, H., Miller, K. A., Wolff, G. L., & Barsh, G. S. (1994). Neomorphic agouti mutations in obese yellow mice. Nature Genetics, 8(1), 59–65.
Earle, D. P., Bigelow, F. S., Zubrod, C. G., & Kane, C.A. (1948). Studies on the chemotherapy of the human malarias: IX. Effect of pamaquine on the blood cells of man. Journal of Clinical Investigation, 27, 121–129.
Eriksson, M., Brown, W. T., Gordon, L. B., Glynn, M. W., Singer, J., Scott, L.,…Collins, F. S. (2003). Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature, 423, 293–298.
Feitshans, I. L. (1989). Law and regulation of benzene. Environmental Health Perspectives, 82, 299–307.
Hudson Alpha Institute for Biotechnology. (2009). Epigenetics. Retrieved from http://archive.hudsonalpha.org/education/outreach/basics/epigenetics
Johnstone, R. W. (2002). Histone-deacetylase inhibitors: Novel drugs for the treatment of cancer. Nature Reviews: Drug Discovery, 1(4), 287–299.
416
Omenn, G. S., & Motulsky, A. G. (2006). Ecogenetics: Historical perspectives. In D. L. Eaton & L. G. Costa (Eds.), Gene-environment interactions: Fundamentals of ecogenetics (chap. 1). Hoboken, NJ: Wiley.
Rothman, N., Smith, M. T., Hayes, R. B., Traver, R. D., Hoener, B., Campleman, S.,…Ross, D. (1997). Benzene poisoning, a risk factor for hematological malignancy, is associated with the NQO1 609C → T mutation and rapid fractional excretion of chlorzoxazone. Cancer Research, 57, 2839–2842.
Silver, K., & Sharp, R. R. (2006). Ethical considerations in testing workers for the -Glu69 marker of genetic susceptibility to chronic beryllium disease. Journal of Occupational and Environmental Medicine, 48(4), 434–443.
Woods, J. S., Heyer, N. J., Echeverria, D., Russo, J. E., Martin, M. D., Bernardo, M. F.,…Farin, F. M. (2012). Modification of neurobehavioral effects of mercury by a genetic polymorphism of coproporphyrinogen oxidase in children. Neurotoxicology and Teratology, 34, 513–521.
Woods, J. S., Heyer, N. J., Russo, J. E., Martin, M, D., Pillai, P, B., Bammler, T. K., & Farin, F. M. (2014). Genetic polymorphisms of catechol-O-methyl transferase modify the neurobehavioral effects of mercury in children. Journal of Toxicology and Environmental Health: Part A, 77, 293–312.
417
For Further Information Costa, L. G., & Eaton, D. L. (Eds.). (2006). Gene-environment interactions: The fundamentals of ecogenetics. Hoboken, NJ: Wiley.
Kari, E., North, K. E., & Martin, L. J. (2008). The importance of gene-environment interaction implications for social scientists. Sociological Methods & Research, 37(2), 164–200.
Kelada, S. N., Eaton, D. L., Wang, S. S., Rothman, N. R., & Khoury, M. J. (2003). The role of genetic polymorphisms in environmental health. Environmental Health Perspectives, 111, 1055–1064.
National Institute for Environmental Health Sciences. (2014). Gene-environment interaction. Available at http://www.niehs.nih.gov/health/topics/science/gene-env
418
Chapter 8 Exposure Science, Industrial Hygiene, and Exposure Assessment
Michael G. Yost and P. Barry Ryan
Dr. Yost and Dr. Ryan report no conflicts of interest related to the authorship of this chapter.
419
Key Concepts Assessing environmental exposures to chemical, physical, and biological agents is a key step in identifying hazards, understanding the risks that hazards pose to human health, controlling exposures, and monitoring the success of control efforts.
Industrial hygiene is a discipline that involves the anticipation, recognition, evaluation, and control of workplace hazards.
Industrial hygiene uses many measurement techniques, such as air sampling and biomonitoring.
Industrial hygiene uses a hierarchy of control strategies, such as substitution, ventilation, and personal protective equipment.
Exposure science is an emerging discipline involving the study of human contact with chemical, physical, and biological agents occurring across diverse environments. Exposure scientists apply many of the tools of traditional industrial hygiene both to workers and to the general population.
This chapter introduces concepts and activities that are at the core of environmental health: recognizing, measuring, and ultimately controlling human exposures to harmful agents. Our account begins with industrial hygiene, a technical field that historically evolved in industrial workplaces. It then moves beyond industrial hygiene to describe exposure science, a modern field focused on exposure assessment in both the workplace and the general environment.
Industrial hygiene and exposure science share a common task: quantifying exposures. This task is relevant both to public health practice and to research. In public health practice, quantifying exposures helps us to assess potential problems, direct preventive efforts and monitor their success, and check compliance with regulations. Quantifying exposures is also essential for research, because it allows investigators to quantify the association
420
between the exposures and health outcomes. For example, knowing that carbon monoxide is an asphyxiant is only partially useful. Knowing how much carbon monoxide exposure is dangerous, and knowing how to measure the exposures where and when they occur, enables us to understand the biological effects more completely, identify acceptable levels and set standards accordingly, and monitor environments to be sure they are safe.
Industrial hygiene has moved beyond its traditional approach of measuring exposures to controlling them. Typically, an industrial hygienist in a factory is called upon to, say, monitor air levels of a hazardous agent such as a chemical solvent. If the exposures are excessive in a particular part of the factory, the hygienist will implement controls: for example, by substituting a safer solvent, upgrading the ventilation system, or providing personal protective equipment for affected workers.
In contrast, exposure scientists usually focus only on measuring and quantifying exposures in the general population (often in a research setting); the results of the exposure assessment then become the inputs for risk assessment and decisions by public health policymakers. Responsibility for controlling the excessive exposures rests with these other professionals.
421
Anticipation, Recognition, Evaluation, and Control Industrial hygiene (referred to as occupational hygiene outside the United States) has been defined as “the discipline of anticipating, recognizing, evaluating and controlling health hazards in the working environment with the objective of protecting workers health and well-being, and safeguarding the community at large” (International Occupational Hygiene Association, 2009). Industrial hygienists are professionals trained to manage workplace risks, in collaboration with allied professionals such as occupational physicians and nurses who treat work-related illness. Industrial hygiene has been practiced in the United States for about one hundred years. Industrial hygienists work to predict and then recognize workplace hazards, quantify the exposures, and implement appropriate control strategies.
Koren and Bisesi (2002, pp. 563–565) have developed concise definitions of each part of this paradigm. They define anticipation of hazards as “proactive estimation of health and safety concerns that are commonly, or at least potentially, associated with a given occupational or environmental setting.” Recognition of occupational hazards is the “identification of potential and actual hazards in a workplace through direct inspection,” a definition that emphasizes that empirical observation is at the heart of industrial hygiene. Evaluation includes measuring exposures through “visual or instrumental monitoring of a site.” Finally, control is the “reduction of risk to health and safety through administrative or engineering measures.” Industrial hygienists spend much of their time in real workplaces, observing, measuring, and problem solving to improve worker health and safety.
Anticipation Anticipation is the first step before conducting a field assessment. The hygienist typically obtains information such as the site history, a manufacturing processes diagram, worker job titles, and material safety data sheets for the chemicals in use. The hygienist uses this information and practical knowledge to develop a preliminary list of
422
potential workplace hazards, including safety hazards that pose a risk of injury and health hazards that pose a risk of disease. This anticipation process may also uncover environmental hazards that can impact nearby communities, rivers, woodlands, or other sensitive environments.
Examples of safety hazards include insufficient emergency egress; moving machinery or vehicles, such as fork lifts; slippery, elevated, or uneven surfaces contributing to trips and falls; and inappropriate chemical storage posing risk of fires or explosions. Although these concerns are the domain of a related profession, safety engineering, many industrial hygienists handle safety concerns as part of their job, especially at smaller facilities.
Examples of health hazards in the workplace include physical hazards, or agents, such as high noise levels, elevated temperatures and humidity, and radiation. Physical agents have in common high levels of energy or force on parts of the body. Physical hazards also include repetitive motion such as occurs in typing or hand tool use, which can increase the risk of musculoskeletal injuries such as back pain or carpal tunnel syndrome. Exposure to chemical hazards, or agents, can occur in many workplace processes and may present an acute or chronic hazard. Acute, high- level exposures to certain highly toxic chemicals, such as chlorine gas, may result in both acute and chronic health effects, disability, and even death. Such events must be clearly anticipated and controlled. More commonly, long-term exposures can lead to chronic effects, such as neurological damage from solvent exposures. For example, long-term exposure to benzene increases the risk of bone marrow dysfunction and aplastic anemia, a blood disease; inhaling asbestos fibers can lead to lung disease and cancers; inhaling crystalline silica contributes to silicosis in foundry workers; and radon increases the risk of lung cancer in uranium miners.
Some workplaces can also present biological hazards. For example, in health care settings workers may be exposed to blood- borne pathogens, such as hepatitis A, B, or C or HIV, that can be contracted due to mishandling of needles or other instruments that come into contact with body fluids. In these workplaces strict disinfection protocols, personal protective equipment such as gloves and masks, and secure disposal of biohazard wastes are used to
423
prevent the spread of infections.
Industrial hygienists often are called upon to anticipate environmental hazards as well as workplace hazards. Environmental hazards may endanger public safety (as when a chlorine tank ruptures and neighbors are exposed to toxic gas), health (as when organic solvents from improper storage or disposal contaminate groundwater or drinking water), or welfare (as when smokestack emissions damage nearby trees or homes). Environmental effects also include ecological damage (such as killing fish by reducing the oxygen-carrying ability of lakes or streams) and economic damage (such as contaminating nearby land with heavy metals, industrial solvents, or pesticides that diminish the land's value for residential or recreational purposes). The industrial hygienist should anticipate such possibilities and review the site history. For example, a review of records or employee interviews may suggest that solvents have seeped into the ground and migrated off-site, contaminating groundwater. A hygienist who suspects such widespread contamination may consult with an environmental specialist to assess nearby groundwater.
Text Box 8.1 presents an example of an industrial hygiene evaluation, emphasizing hazard anticipation. The example shows that even with minimal information, the hygienist can anticipate hazards prior to visiting a facility. This assessment strategy depends on examining a range of information before visiting the site: the industrial process description, the job titles of workers, the chemicals in use at the facility (often found on the material safety data sheets required by law), and the history of the site. Using this information the hygienist develops a list of potential health and safety hazards, perhaps in checklist form, to enhance observations during the walk-through visit.
424
Text Box 8.1 Assessing an Electronics Manufacturing Facility: The Role of Anticipation An industrial hygienist is asked to evaluate an electronic manufacturing facility and to focus on occupational hazards. Several operations with potential health impacts are performed at this workplace. Solvents such as trichloroethylene, acetone, and Stoddard solvent are used extensively for degreasing in industry. Most facilities have a single room in which these materials are used. The prudent hygienist anticipates possible spillage, respiratory exposure (perhaps due to inadequate ventilation), and skin contact (perhaps due to improper handling or inadequate personal protective equipment). On-site solvent storage may result in exposure and environmental contamination. The hygienist plans a close inspection of solvent use and storage areas in this facility.
During her walk-through visit, the hygienist notices that some workers perform repetitive operations as part of their jobs. She observes the repetitive activities to assess potential musculoskeletal damage. Similarly, she inspects machinery for electrical safety, unguarded belts, risks of crush injury, and so on. The hygienist also looks for hazards not identified in the initial request, for example, blocked fire exits, noise, and potential for trips and falls.
She also reviews administrative procedures, such as worker safety training, job injury records, and tracking of chemical inventories to assess possible workplace risks. Only direct inspection (or evaluation, as discussed later in this chapter) can lead to a direct conclusion about control strategies.
The initial recognition phase is usually accomplished during a site visit or walk-through, where the hygienist conducts a visual inspection of the facility to assess both qualitative and quantitative information about hazards. The hygienist inspects processes and
425
procedures at the facility, observes workers in various job categories, and reviews any health and safety programs in place at the plant. During a walk-through the hygienist looks for a wide range of issues: physical, chemical, and biological exposures; ergonomic, mechanical, and psychological factors; safety hazards such as exposed machinery or slippery surfaces; high noise levels; and the presence of chemicals. A similar on-site review may look for environmental hazards, with an emphasis on off-site emissions.
Another important purpose of the walk-through is recognition of special subpopulations in the facility that are at elevated risk. Some workers may perform lifting or repetitive movements in their jobs, exposing them to ergonomic hazards. Work in a high-temperature area may subject other workers to heat stress. During a walk- through the hygienist notes these subpopulations and may evaluate hazards differently for different groups. The hygienist concludes the recognition phase with a detailed picture of the manufacturing processes, a list of the associated hazards, and a written hazard evaluation plan. From this plan a detailed protocol is developed for the next phase, the evaluation of the hazards.
Evaluation After the walk-through the hygienist will have a list of potential hazards but no quantitative information about worker exposures. For example, if a metalworking facility uses toxic degreasing solvents, the risk of exposure may be minimal with proper storage, personal protective gear, and appropriate ventilation. The evaluation phase actually begins during the walk-through, and there is a smooth transition from the recognition of hazards to their evaluation.
Evaluation focuses on quantifying the degree of exposure. Exposures can be assessed in several ways: area sampling collects measurements in a room in the vicinity of some workers; personal sampling collects contaminants in the breathing zone of individuals, using small portable samplers; biological sampling collects body fluids or breath samples to measure contaminants or specific metabolites.
Population Sampling for Exposure Assessment
426
The starting point when conducting an exposure study is the identification of the study population to be sampled. This involves enumerating all the people who could be sampled. In a workplace the focus is usually on certain workers with specific job titles—those identified during the anticipation phase as having a potential for high exposures. Other selection criteria may also apply, based on concerns raised by workers or their union, consultants, or regulatory authorities.
The next choice is the sampling strategy to be applied to the population. In small workplaces (e.g., a dozen or fewer employees) a simple census of all individuals may be taken. This ensures that all exposures are monitored. In larger facilities this approach can be too costly, so a statistically representative sample is needed. A common approach here is stratified sampling.
In stratified sampling the population is divided into subgroups (strata), and each individual monitored represents a known number of individuals in the subgroup. For example, if a trucking company has 5,000 drivers serving a state, it may be impractical to monitor all of them for exposure to diesel exhaust during trips. The hygienist may subdivide the drivers into groups according to the type of route (say, long-haul or delivery) and destination city, creating, say, fifty groups of roughly 100 individuals each. The hygienist then selects some members from each group (usually at random) to create a statistically representative sample of the full 5,000. Although stratified sampling is subject to error because not all the exposed people are monitored, it can be an efficient way to characterize an entire population when differences between groups have an effect on exposures. Techniques are available to estimate the size of the error. Statistical colleagues can help the hygienist to determine the number of samples needed from each group to characterize exposures for the entire population.
A third strategy is the so-called convenience sample. Often such a strategy consists of monitoring volunteers or individuals with a particular complaint. Convenience sampling can be subject to bias; those who volunteer or have complaints are not likely to represent all members of the group. This sampling strategy should be avoided in favor of randomly selecting individuals. However, a related sampling strategy may have a role and is used in regulatory settings. The hygienist may choose worst-case sampling—selecting workers
427
at highest risk of exposure or measuring at times when exposures are highest. The assumption in worst-case sampling is that if these workers' exposures are acceptable, then all the remaining workers are also unlikely to be overexposed.
Exposure Evaluation Instruments Two general types of devices are used for measuring environmental exposures: direct reading devices and sample collection devices. Direct reading devices provide near real-time measurements of the exposure of interest, and sample collection devices store or trap samples for later analysis.
Direct reading instruments are available for measuring many physical hazards, such as temperature, noise, and radiation. These instruments typically have a digital readout and the ability to store data over a period of time for later downloading. Common examples are digital thermometer-hygrometers to measure temperature and humidity, noise monitors, and ultraviolet radiation monitors. Other direct reading instruments can measure various pollutants, including gases, vapors, and airborne particles. For example, fine particles can be measured with a device called an optical particle counter. These instruments are usually portable, battery operated, lightweight, and enclosed in a rugged case for field surveys.
Sample collection instruments are often used when multiple airborne pollutants are present or further laboratory analysis is needed. The collection device draws in a known volume of air, including whatever contaminants are in it, and traps the contaminants on an absorbing medium. The absorbing medium is used to stabilize and store the contaminant so the sample can be taken later to a laboratory where the mass of the contaminant stored in the medium is determined. The air concentration of the contaminant in the sample can then be quantified in units of mass per volume, by dividing the mass of contaminant collected on the absorbing medium by the volume of air that was sampled. These air concentrations typically have units of micrograms per cubic meter (µg/m3). By increasing the volume of air sampled, more contaminant mass can be collected, thereby increasing the sensitivity for detecting low levels of contamination.
Sample collection instruments can be either active or passive.
428
Active sampling devices draw air through the absorbing medium using an electric pump. The pump's airflow rate can be varied, and the total volume of air sampled is calculated by multiplying the flow rate by the duration of sampling. The sampling time period can sometimes be shortened by increasing the pump flow rate, thereby delivering the same volume of air in less time. This can be useful when exposures occur over short time periods or are highly variable. Conversely, the flow rate can be decreased if longer sample times are needed.
Active sampling is highly versatile, sensitive, and specific for the contaminant of interest because sophisticated laboratory analysis methods (such as mass spectrometry) can be used to analyze the samples. However, running the pump requires a battery or electricity and the pump may be bulky or noisy and have limited run time. These drawbacks make such devices unsuitable for some kinds of personal sampling, although area sampling is more feasible. In Figure 8.1, both the sampling devices (for ozone and particulate matter) and the pump are located inside the box at the bottom of the apparatus. The vertical pipe with the metal cone on top collects the fine particle sizes that can be inhaled deeply into the lungs. Ozone is sampled off the same airstream.
429
Figure 8.1 An Air Pollution Monitoring Station for Ozone and Particulate Matter, in Atlanta
Passive sampling devices use diffusion, rather than a pump, to collect the air sample. This method requires an absorbing medium that removes the compound of interest from the air by reaction or absorption at the surface of the medium. The concentration gradient between the air to be sampled and the surface of the absorbing medium causes the contaminant of interest to diffuse from the air to the surface where it is trapped. The mass collected in the medium is then analyzed in a laboratory, as in active sampling analysis. The flow rate of the air delivered to the surface during sampling is computed using Fick's law of diffusion; the volume sampled is this sampling rate multiplied by the sampling time. The concentration is then calculated in the same way as for an active sample, by dividing the mass collected by the volume of air sampled.
Although passive devices do not require a pump, their diffusion method generates low sampling rates; often these flow rates are 1,000-fold slower than rates in active sampling devices. Thus the contaminant mass sampled in a given time is correspondingly lower. However, in occupational settings concentrations are often sufficiently high that passive devices can still achieve excellent results. Further, laboratory analysis has substantially improved, reducing the amount of material needed for accurate quantification. When available and of sufficient precision and accuracy, passive sampling devices can be the method of choice. Passive devices for particulate matter are not yet of sufficient precision and accuracy to merit their use in typical occupational settings.
Biomonitoring (also called biological monitoring) involves the collection of body fluids or tissue such as saliva, blood, hair, or urine. These are analyzed for either the contaminant or a metabolite of that contaminant. Biomonitoring is discussed later in this chapter.
Control Control of workplace hazards is an important element of industrial hygiene practice that corresponds, in public health terms, to primary prevention (as discussed in Chapter 26). Several approaches are used to modify the workplace environment:
430
substitution, isolation, ventilation, administrative changes, and personal protection. Substitution involves replacing a hazardous material or process with a less hazardous one. For example, benzene (a bone marrow toxin) might be replaced by less toxic toluene. Isolation involves containing or limiting human access to the hazardous materials, usually through engineering controls. For example, a metal casing may be may be used to enclose a solvent washer. For certain hazards, most notably chemical and heat- related hazards, ventilation provides a viable control strategy. For example, the introduction of fresh air or use of a local exhaust hood may significantly reduce exposure to these hazards. Administrative controls consist of policies and procedures that reduce risks. For example, maintenance workers place a lock and signed tag on machinery controls to prevent unintended operation during repairs, a standard injury prevention strategy called lockout tag-out. Rotating workers to limit the time spent by any individual in a high-exposure location may have a role as well (an approach used, for example, with radiation workers).
Protective devices are often used to control safety hazards. For example, a cutting machine may be designed so that the worker needs to push two buttons, one with each hand, to initiate a cut; this guarantees that the worker's hands cannot be in the cutting zone during operation.
Personal protective equipment (PPE), such as respirators, gloves, safety glasses, hardhats, safety harnesses, and steel-toed boots may be recommended, although this approach is less preferable than the environmental changes described previously. Figure 8.2 shows an example of personal protective equipment in use. Working at a degreasing tank, a worker may inhale vapors or absorb solvent that splashes on bare skin. This worker wears personal protective equipment consisting of gloves and a face shield to protect the hands and face from splashed solvent and a respirator to prevent vapors from being inhaled.
431
Figure 8.2 Personal Protective Equipment Source: Courtesy of Phillip L. Williams, University of Georgia College of Public Health.
This worker is positioned over a solvent bath. Note the sampling apparatus on the worker's belt, and the hose running from the breathing zone.
432
Exposure Science Exposure science is broadly defined as the study of human contact with chemical, physical, or biological agents occurring in the environment. It focuses on the mechanisms and dynamics of events either causing or preventing adverse health outcomes (National Research Council, 2012). Exposure scientists quantify exposures in both occupational settings (as do industrial hygienists) and in community settings where people may encounter hazards as they go about their daily activities. Exposure science often focuses on evaluating exposure determinants, which are the factors and conditions that influence these exposures. Exposure assessment, one aspect of exposure science, aims to quantify exposures in both occupational and environmental settings. These assessments focus on key concepts such as concentration, exposure, and dose (as discussed in Text Box 8.2).
Frequency, Intensity, and Duration of Exposure An important aspect of exposure is its time course, sometimes referred to as the exposure profile, which can be graphed as the concentration present in a person's breathing zone (or, less typically, in other media such as in drinking water or during dermal exposure) over a period of time. The term total exposure is sometimes used to describe the area under this exposure-time curve. Different exposure profiles can yield similar total exposures. For example, one worker may weld for 15 minutes in an enclosed space and sustain a concentration of metal fumes of 40 mg/m3, receiving a total exposure of (40 mg/m3)(0.25 hr) = 10 mg/m3 × hr. After finishing his task, he experiences no further exposure to welding fumes. A coworker, working in the same area but not exposed directly to the fumes, remains for the entire 8-hour shift. Over the course of the day, the coworker experiences a concentration of 1.25 mg/m3. The coworker receives an identical total exposure [(1.25 mg/m3)(8 hr)= 10 mg/m3 × hr], but the exposure profile is different. In some circumstances, different exposure profiles may have different health effects, even with equivalent total exposures.
433
Text Box 8.2 Understanding Concentration, Exposure, and Dose Exposure assessment asks, how much of a contaminant is available to a person? For example, how much carbon monoxide is in the air inside a warehouse, or how much pesticide contamination is in food? The answer to “how much” is usually measured as a concentration, expressed in units of mass per mass, volume per volume, or mass per volume. Air contaminants such as particulate matter are quantified in units of mass per volume: micrograms (µg) of contaminant per cubic meter of air (µg/m3). For gases, concentrations are often stated as units of a mixing ratio: the volume fraction of the contaminant per total volume of air. Typical units are parts per million (ppm) or parts per billion (ppb).
Suppose an exposure scientist measures a carbon monoxide (CO) concentration of 1 ppm in a skating rink (where ice resurfacers sometimes cause elevated CO levels). This means that in any given volume of air, if it were divided into 1 million portions of equal volume, 1 part would be CO and the other 999,999 parts would be clean air. So in 1 cubic meter (m3) of air, 1 cubic centimeter (cm3, or cc) would be pure CO and the remainder would be air (the nitrogen and oxygen would represent about 780,000 cc and 210,000 cc, respectively). Of course, all of these parts are mixed together so the CO molecules are dispersed throughout the entire cubic meter. Although 1 ppm seems a tiny concentration, for many air contaminants it represents a significant health concern (also see Text Box 8.3).
Concentrations in other environmental media, such as water, soil, and food, are stated in similar units. Contaminant concentrations in water can be expressed as either mass per volume (µg/m3) or mass per mass (µg/g). (Concentrations in µg/g are analogous to a volume mixing ratio in air because 1 microgram of contaminant per gram of water corresponds to
434
8.1
1 ppm.) Similarly, contaminants in soil or food can be described either way.
But concentration is different from exposure. For people to be exposed, they must come into contact with the contaminant. Exposure for human populations is defined as contact between the contaminant and a boundary interface of the person with the environment. The boundaries of interest are tissues such as skin, alveolar surfaces, and the gastrointestinal tract lining, which separate the “inside” of a human body from the “outside” environment. Exposure requires the simultaneous presence of a contaminant in the environment and contact at the interface with a human receptor.
Exposure is a function of both the concentration (exposure intensity) and time. Therefore exposures are expressed as units of concentration multiplied by time duration, such as micrograms per cubic meter multiplied by hours (µg/m3 × hr). For ingestion, the time factor may appear as the number of meals or the total mass taken into the body during a day, year, or other period.
Dose is conceptually different from concentration and exposure. Dose refers to the mass of contaminant that crosses the tissue barrier and gets inside the body. Suppose a person inhales a concentration of 2 µg/m3 of dust for a period of 8 hours. The inhalation exposure is (2 µg/m3) (8 hr) = 16 (µg/m3 × hr). To compute the dose, additional information is needed. The dose is delivered to the lungs through breathing. A typical breathing rate (depending on the person's size, activity, and other factors) might be approximately 1 m3 of air per hour. So during an 8-hour period, this person would breathe in 8 m3 of air. The potential dose is the product of the concentration, the duration of exposure, and the rate at which the material reaches the appropriate boundary:
In this case, 16 µg of contaminant has reached the body
435
boundary. This is called the potential dose and represents the maximum dose, assuming all the material crosses the boundary. But let's say that only 50% of the dust can cross the boundary and be absorbed inside the body. This absorption factor of 50% is multiplied by the potential dose to compute the absorbed dose, which would be (0.5)(16 µg) = 8 µg. Note that the units correspond to the mass delivered across the boundary. There is no explicit time dimension.
For exposure assessment, evaluators often stop at the potential dose. However, absorption is typically incomplete, and the absorbed dose or target organ dose (the fraction reaching a particular organ) generally is lower than the potential dose. Toxicologists, physicians, and other health scientists may focus on the absorbed dose to understand the relationship between exposure and health effects (see Chapter 6).
Applying the concepts of exposure and dose can require a detailed understanding of how material actually gets inside the body. For example, if a worker wears a respirator, calculations of inhalation exposure must account for the lower concentrations inside the respirator. One also needs information regarding the efficiency of transfer across the alveolar membranes in the lungs to estimate absorbed dose. Similarly, estimates of ingestion combine information about the concentration in food or water, the amount consumed, and the efficiency of absorption. To combine these routes, a biomarker of exposure—say, blood levels of the contaminant or urinary levels of its metabolite—would provide an integrated estimate of dose.
Figure 8.3 illustrates exposure measurements on a worker performing sandblasting to remove silica-containing material. Silica inhalation can cause severe respiratory disease. The worker is protected by an airline respirator that supplies fresh air through a hose, preventing exposure to the harmful dust. However, noise from the sandblaster could still damage hearing so the worker wears a noise monitor to assess this hazard (the small box on the worker's lower back).
436
Figure 8.3 Assessing Exposure in an Occupational Setting Source: Courtesy of Phillip L. Williams, University of Georgia College of Public Health.
The shape of the exposure profile matters because some contaminants are easily cleared at low exposure levels but toxic at higher levels. In this case, the dose rate may affect the health outcome. Exposure assessors focus on the intensity of exposure, frequency of exposure, and duration of exposure, asking questions such as: What is the peak concentration in the monitoring period? How much variability occurs from minute to minute or hour to hour? Do exposures recur regularly or episodically? Is the duration of exposure short followed by no exposure, or does exposure occur at moderate levels for a long period? Such information can prove invaluable in addressing potential effects and control strategies.
Three basic scenarios, defined by the U.S. Environmental Protection Agency (U.S. EPA), are used by scientists to distinguish exposures across different time periods (U.S. Environmental Protection Agency, Office of Research and Development, National Center for Environmental Assessment, 2015). Acute exposure occurs by ingestion, skin absorption, or breathing for twenty-four hours or
437
less. Chronic exposure consists of repeated episodes that occur by the same routes for more than approximately 10% of the life span in humans. Subchronic exposure is repeated exposure by one or more of these routes for more than thirty days, up to approximately 10% of the life span in humans. When acute exposures occur at high levels, poisoning or other immediate responses may follow. Chronic exposures at lower levels may be linked to health outcomes such as cancer, chronic lung damage, or similar effects. Subchronic exposures are between these two and also may be episodic or recurring.
438
Text Box 8.3 Assessing Exposure to Carbon Monoxide Carbon monoxide is a common toxic exposure, described in Tox Box 13.1. Exposure to CO can be measured in two ways. Simple CO air samplers are available that operate either actively or passively. Personal monitoring devices can determine exposure in real time and even sound an alarm when dangerous levels are present. An alternative strategy is to measure carboxyhemoglobin in the blood, a biological marker formed by the CO adduct to hemoglobin. Small amounts of CO are produced endogenously, so unexposed people typically have about 1% carboxyhemoglobin. Smokers have a higher percentage, up to 4%, from CO inhaled in cigarette smoke. Most people experience symptoms such as headaches at levels above about 10%, and levels above 40% are life threatening.
Measuring total exposure as defined previously does not tell the full story with respect to carbon monoxide's effects. Many scenarios could give rise to the same total and aggregate exposure. Exposure to 1 ppm of CO for 10,000 hours would give the same exposure as 10,000 ppm of CO for 1 hour. However, these two scenarios would yield completely different effects. The long-term, low-level exposure would cause no problems at all, whereas the brief, intense exposure would surely result in death. In addition, CO binds tightly to hemoglobin, so that even after ambient concentrations are reduced, elimination of CO from the body proceeds slowly. Thus the adverse impact of CO may persist for some time after the exposure ends.
This example illustrates the importance of considering the intensity and duration of the exposure in estimating health effects. In this case, limiting both peak exposures and exposure duration is necessary to protect health. Further, this example emphasizes the importance of understanding the toxicology of the effect. CO binds reversibly to hemoglobin but with a very long half-life. At low CO
439
exposures a person still has plenty of hemoglobin left to bind oxygen. However, high CO exposures displace so much oxygen from hemoglobin that asphyxiation can result.
Routes and Pathways of Exposure There are three principal routes of exposure for people: inhalation exposure, ingestion exposure, and dermal exposure. These routes of exposure are different from the exposure pathway, or the path by which the contaminant moves from a source to a human receptor. For example, pesticide exposures in children may come from several pathways. Children may ingest pesticides from residues present on food (a dietary pathway); they may get pesticides on their skin from their parents' contaminated clothing if the parents work on a farm (a take-home pathway); if spraying takes place close to their home, they may inhale pesticide particles or vapors (a drift pathway). These pathways differ substantially and each requires entirely different assessment and control strategies to reduce exposure.
Exposure Assessment Methods Ideally, an exposure assessment method quantifies the mass of contaminant reaching the target organ in each exposed person. Of course this is generally not feasible, but four broad assessment method categories approximate this ideal to increasing degrees: imputing or modeling exposures, measuring environmental exposures, measuring personal exposures, and measuring biomarkers. In general these methods become increasingly expensive, and increasingly accurate, as one moves up this continuum.
Imputing or Modeling Exposures Exposure scientists use indirect exposure assessment methods to impute exposures when they lack direct measurements or only have partial data. Indirect approaches are usually substantially simpler and less costly than direct measurements. Additionally, for retrospective studies, in which it is impossible to take measurements, indirect approaches are the only methods available.
Air pollution studies provide one example. In a study of inhalation
440
exposure to air pollution, researchers might use a time-location study to identify various microenvironments (home, work, travel, etc.) in which people spend a significant portion of their day. The researchers then measure pollutant concentrations in representative microenvironments, and have subjects record or estimate the amount of time spent in the microenvironments. From these data, the scientists could multiply the concentrations by the amount of time spent in each microenvironment and sum the results for an estimate of each person's exposure. A similar approach can be used, for example, for ingestion. Concentrations of contaminants can be measured in many different foods; people can record the types and amounts of foods they eat, using a food diary; and dietary exposures can be estimated by summing over all the foods eaten.
A related strategy that uses exposure scenarios constructs estimates without direct measurement by assuming activity patterns for typical individuals (children, adult men, adult women, etc.). Available monitoring data for each activity and location can then be combined to model estimates of individual exposures. This approach is inexpensive because no individuals are measured or activities recorded. Exposure scenarios are used extensively in risk assessment.
A special case of indirect exposure assessment is the job-exposure matrix (JEM) (see Chapter 4). Suppose an exposure assessment is needed for a retrospective study of silica exposures in a worker cohort. Consulting old employment records, the exposure scientist identifies ten job categories, each with characteristic tasks, and fifteen work zones, each with silica concentrations derived from historical industrial hygiene monitoring or by using estimates from a panel of experts. The exposure scientist then constructs a JEM, assigning an exposure level to each worker based on his or her job assignment and work zone location. If the workplace changes over time, as is typical, then a JEM, for each time period is created to account for the differences. A JEM is often the only way to assess exposures in retrospective studies. However, JEM creation can be time consuming, and accurate records may not be available to complete the assessment.
Measuring Environmental Exposures
441
Direct exposure measurements are typically done at fixed locations (area sampling) or on individual subjects (personal sampling). In air pollution monitoring in most major cities, fixed-site sampling has been commonly used over many years. Daily and hourly measurements of O3 (ozone), NOx (nitrogen oxides), SOx (sulfur oxides), and PM (particulate matter) track compliance with regulations. These measurements also provide information used to warn the public of dangerous peaks and to support health research.
Measuring Personal Exposures Personal exposure monitoring generally involves placing a small, portable sampling device on a person to collect a sample within his or her breathing zone during daily activities. Personal monitoring started in the workplace in the early 1960s and has become routine practice in industrial hygiene assessments. Personal sampling is considered a reference method for assessment because it accounts for time, location, and the person's behavior; all of these can have a profound effect on exposures.
The breathing zone air sample can be analyzed for the contaminant of interest, either in real time or with a time-integrated sample collection device. With direct reading, real-time methods, a person's exposure profile can be observed and synchronized with a video recording. The video is overlaid with a bar graph or other indicator from the real-time monitor, demonstrating how specific activities contribute to exposures. This technique, known as video exposure monitoring (VEM), is a powerful training tool and aid for developing control strategies. Similarly, real-time monitors can be wirelessly paired with smartphones or GPS devices to evaluate time- activity contributions to exposure.
While the focus here is on inhalation exposures, generalization to other personal exposures is possible. For example, duplicate diet sampling, in which identical meals are collected from each individual in a study, is a method of quantifying ingestion exposures from food.
Aggregate and Cumulative Exposure Assessment The Food Quality Protection Act of 1996 expanded the single contaminant approach to exposure assessment and introduced new
442
concepts of aggregate exposure and cumulative exposure (also see Chapter 27). Aggregate exposure refers to assessing simultaneously all routes and exposure pathways involved for a single compound. An agricultural worker may have exposure to a single pesticide through both inhalation and skin absorption while picking crops. In addition, he may ingest food containing residues of the same pesticide. The clothing he wore at work and brought home may also carry residual contamination. Counting only one route and pathway, such as inhalation during spraying, underestimates his total exposure, perhaps substantially. Aggregate exposure assessment over all routes and pathways simultaneously is necessary in order to quantify the hazard accurately.
The concept of cumulative exposure extends this approach to multiple compounds that have similar biological mechanisms. Cumulative exposure is defined as aggregate exposure to a series of compounds (or nonchemical exposures) that affect health through similar mechanisms. A common example of cumulative exposure focuses on organophosphate (OP) pesticides such as chlorpyrifos, malathion, and diazinon (see Tox Box 18.1, in Chapter 18). These compounds share a common biological mechanism of toxicity: inhibition of the enzyme acetylcholinesterase, which is necessary for normal transmission of nerve signals. OP pesticides interfere with this process, resulting in continued firing of the neuron. A cumulative exposure assessment for all OP pesticides is needed to understand the impact of exposure not just to a single OP but rather to all pesticides operating through acetylcholinesterase inhibition. This requires measurement either of all the compounds simultaneously or of some biological effect, such as acetylcholinesterase inhibition in exposed people, that integrates over all exposures. Naturally such assessments are complex, especially when extended to nonchemical exposures, such as stress or malnutrition, that may compound the effects of chemical exposures.
Measuring Biomarkers So far we have focused on sampling environmental media from places where people are likely to contact a contaminant. However, it is possible to measure contaminant levels in humans themselves, and thereby verify that exposures occurred. Biological markers
443
(sometimes referred to as biomarkers) of exposure are used for this purpose. Biomarkers are collected by sampling body fluids or tissues such as exhaled breath, urine, blood, feces, or hair. These biosamples are analyzed for the contaminants of interest (called the parent compound) or a related compound (usually a metabolite), or a biological response known to reflect exposure. For example, cotinine (a metabolite of nicotine) can be measured in urine to quantify exposure to tobacco smoke, and carboxyhemoglobin levels in blood are measured to quantify exposure to carbon monoxide. Pesticides provide another example. Blood samples can be analyzed for OP parent compounds, urine samples can be analyzed for OP metabolites such as dialkyl phosphates, or acetylcholinesterase enzyme activity in serum can provide a measure of the biological effect.
Biomarkers of exposure have important advantages and disadvantages. Detection of an exposure biomarker proves that absorption of the compound has occurred. Other environmental measurements cannot confirm this conclusion. Furthermore, biomarkers account for bioavailability, which describes the ability of a compound to pass across the contact boundary into the body through, for example, ingestion. Biomarkers also integrate over all routes of exposure and therefore are useful for aggregate assessments. For these reasons, biomonitoring has been called the “gold standard” for exposure assessment (Sexton, Needham, & Pirkle, 2004).
Biomonitoring has evolved rapidly to consider biological indicators not only of exposure but also of biological response to the exposures. Many of these approaches are called omics because they draw on a suite of molecular biology techniques with that suffix: genomics, proteomics, and metabolomics (as explored in Chapter 7). These techniques employ large-scale array technology to screen for hundreds or thousands of genes, proteins, and metabolites that are associated with particular exposures or in some cases correlate with disease risk.
Patterns or features associated with clusters of these proteins and biological molecules can be derived with bioinformatics and multivariate statistical analysis to provide insights into how an organism dynamically responds to environmental exposures. These responses may persist over various time scales: days, months, or
444
years. Together, these biomolecular features, reflecting gene expression, cellular functions, and metabolism, become part of a person's exposome (the totality of exposure events that affect the person) (Wild, 2005). For example, exposures to OP pesticides can cause a nonspecific, short-term depression in enzyme activity that may last a few days; however, this exposure can also give rise to pesticide-protein adducts that persist in the blood for more than a month and that can identify the specific pesticides (Marsillach, Costa, & Furlong, 2013). Some exposures may also induce epigenetic changes that persist for years or become permanent (Kyrtopoulos, 2013). For example, smoking and exposure to tobacco smoke both result in epigenetic changes that revert to normal over time, and changes that can persist over decades (Bossé et al., 2012).
However, interpreting measurements of biomarkers in relation to the timing of the actual exposure events can be complex. Some compounds produce long-lived biomarkers that reflect months or years of exposure; other compounds produce short-lived biomarkers that may correspond only to exposures that occurred a few minutes ago. In addition, there are usually multiple metabolic pathways that influence biomarkers, and these may behave similarly for several related chemicals, or become saturated if multiple exposures use the same pathway. This may make it difficult to know what specific chemical caused the exposure. To understand and apply biomarkers properly, the exposure scientist should be well versed in the pharmacokinetics of the compound: that is, how it is processed in the body (see Chapter 6). Collaboration with a toxicologist can be helpful for understanding such problems.
The ability of biomarkers to integrate exposure over all routes and pathways, a major strength, also can be a major shortcoming. For example, once a molecule such as a pesticide enters the body and is metabolized, the source is no longer identifiable. The exposure may have come from inhalation, dermal contact, or through ingestion of residues in the food supply. A related problem occurs when individuals have different abilities to metabolize a contaminant, due to a genetic polymorphism (see Chapter 7). This can mean that identical exposures can generate different observed metabolite levels in individuals and also convey different risks of health effects. Failure to recognize these genetic differences may lead to misclassification of exposures and the risk of harm to the individual.
445
Given the valuable insights from such assessments, the use of biomarkers of exposure and effect is likely to increase in the future. New, more accurate biomarkers of exposure are being developed and are appearing in the literature. Current research suggests that panels of biomarkers, measuring multiple markers at once, may be able to overcome some of the shortcomings listed here while giving new and powerful insights into mechanisms of toxicity and control strategies for exposure (Ryan et al., 2007; Cohen Hubal et al., 2010; Cochran & Driver, 2012).
Ingestion and Skin Absorption: Challenges for Exposure Assessment Ingestion and skin absorption are important routes of exposure in many circumstances. These two routes also pose special challenges for exposure assessment. A duplicate diet study is a direct approach to assessing ingestion exposure. Duplicate portions of the food eaten by test subjects are collected and analyzed for contaminant levels. Typically all of the food eaten is weighed and homogenized to create a single bulk sample. An aliquot of the sample is analyzed for contaminant concentration (mass/mass). The exposure is computed by multiplying this concentration by the amount eaten.
Dietary diaries offer another and indirect approach for assessment of ingestion exposures. Each subject keeps a food diary listing foods eaten and portion sizes. The researcher purchases these foods at local grocery stores for later analysis. A data set is compiled listing each type of food and the contaminant concentrations. The food diary data from each participant can be combined with the concentration data to estimate the amount of contaminant ingested.
Food diaries are much easier to administer than duplicate diet studies and so can be implemented on a large scale. Fewer food samples have to be analyzed because once all the individual food items have been assessed, no further analysis is needed. However, because the foods consumed are never measured, they may differ from what is analyzed. This causes error in the exposure estimates due to the variability in concentrations in various food items.
Dermal exposures can present unique challenges. Patch sampling is one direct assessment technique; an adsorbent material patch is
446
placed on the skin or outer garments. The subject then carries out normal activities, creating exposure to the contaminant. The patches intercept the contaminant of interest before it reaches the skin. Following exposure the patches are removed and analyzed for contaminant mass. Knowing the area of the patch relative to the total exposed skin surface area, one can estimate overall skin exposure to the arms, legs, torso, and so forth. The total exposure is estimated by summing over all exposed areas of the body. Tape stripping is another technique. A special adhesive tape is applied to a known area of the skin, and then stripped away to remove a single layer of exposed skin cells. The tape samples are analyzed like the patch samples described previously, and used to compute total exposure over the skin area. Tape stripping has the advantage that it measures what gets on the skin; repeated stripping in the same area can measure the depth of contaminant penetration.
A limitation of both the patch and tape stripping methods is that they sample only a small portion of the overall exposed skin area. This makes it possible, indeed likely, that some exposed areas will be missed. This can lead to underestimation of exposure. The fluorescent tracer method used in pesticide sampling is an alternative that samples all skin areas. A nontoxic fluorescent tracer is added to the pesticide spray mix, and later the worker is video- imaged under ultraviolet light, revealing areas where the tracer deposited on the skin. The tracer technique can be very useful for both field studies and training simulations; it also has been used to assess potential biological contamination and hand-washing effectiveness.
447
Summary The paradigm of industrial hygiene, based on the anticipation, recognition, evaluation, and control of workplace hazards, provides a framework for more general exposure assessment. Many tools of traditional industrial hygiene are transferable to exposure science, which spans both occupational and community settings. But exposure science requires some new tools as well. Sampling strategies, compliance with monitoring protocols, and field implementation are often more difficult in community exposure assessment studies. Community studies also call for statistical sampling techniques much like those used in epidemiological studies. Exposure science is a rapidly growing area, ripe for contributions from professionals in many areas of environmental health.
448
Key Terms absorbed dose
The amount of a substance penetrating across the absorption barriers (the exchange boundaries) of an organism, via either physical or biological processes.
absorption factor The ratio of the mass of the material crossing the absorption barrier to the mass of the material applied to the barrier.
active sampling Using a mechanical pump, fan, syringe, or other device to draw an environmental sample into a collection medium or vessel for the purpose of capturing an agent.
acute exposure A contact event between an agent and a target occurring over a short time, generally less than a day. (Other terms, such as short-term exposure and single dose, are also used.)
administrative controls Methods used to modify or control exposures based on changing work practices or procedures, such as hours worked, location of work, and rest-work rotation schedules.
aggregate exposure The simultaneous assessment of all routes and exposure pathways into an organism for a single compound (cf. cumulative exposure).
anticipation The ability to expect the presence of a hazard based on common work practices and knowledge of similar exposure scenarios.
area sampling Collecting environmental samples at fixed locations, rather than near moving individuals.
bioavailability The ability or tendency, rate, and extent to which an agent can cross an exposure barrier, be absorbed by an organism, and be available for metabolism or interaction with biologically significant receptors. Bioavailability involves both release from a medium (if present) and absorption by an organism.
449
biological hazard A biological substance (such as a bacterium or virus) capable of causing harm to an organism, or a material (such as medical waste) or process (such as cleaning health care facilities) that may entail exposure to such a substance.
biological sampling Collecting biological specimens.
biomarkers Indicators of changes or events in biological systems; also called biological markers.
biomarkers of exposure cellular, biochemical, analytical, or molecular measures obtained from biological media such as tissues, cells, or fluids, indicative of exposure to an agent of interest.
biomonitoring Collecting biological specimens, such as blood, urine, breath, saliva, or other materials, to detect the presence and amount of exposure to a potentially harmful agent.
chemical hazard A chemical agent capable of causing harm to an organism.
chronic exposure A continuous or intermittent long-term contact between an agent and a target. (Other terms, such as long-term exposure, are also used.)
concentration The amount of contaminant present in an environmental medium, generally expressed in mass per volume (µg/m3) or as fractional dilution ratio (ppmv or ppbv).
control The ability to modify or limit exposures to harmful agents through intentional modification of exposure pathways.
cumulative exposure The simultaneous assessment of aggregate exposures to multiple compounds (or nonchemical exposures) that affect organism health through similar mechanisms (cf. cumulative impacts, in Chapter 11).
dermal exposure
450
Exposure to a contaminant through contact with the skin. direct reading instruments
Exposure monitoring devices capable of measuring an agent in a sampled medium and providing a direct indication of the agent concentration to the operator through a display or other output.
dose The amount of agent that enters a target after crossing an exposure surface.
dose rate Dose per unit of time.
duplicate diet study A method of sampling ingestion exposures that collects meals identical to those eaten by subjects over a period of time in order to measure the presence of an agent in their food.
duration of exposure The length of time over which continuous or intermittent contacts occur between an agent and a target. For example, if an individual is in contact with an agent for 10 minutes per day for 300 days over a 1-year time period, the exposure duration is 1 year.
environmental hazard An agent present in the environment capable of causing harm to an organism.
evaluation The collection of data in the form of records, interviews, photographs, samples, or other empirical indicators of exposure, and the synthesis of this data into a consistent representation of the health hazard presented by an agent.
exposome The measure of all a person's exposures, beginning in utero and extending over a lifetime, and how those exposures relate to health.
exposure Contact between an agent and a target. Contact takes place at an exposure surface over an exposure period.
exposure assessment The process of estimating or measuring the magnitude,
451
frequency, and duration of exposure to an agent, along with the number and characteristics of the population exposed. Ideally, it describes the sources, pathways, routes, and uncertainties in the assessment.
exposure pathway The course an agent takes from its source to the target receptor.
exposure scenarios Combinations of facts, assumptions, and inferences that define a discrete situation where potential exposures may occur. These scenarios may include the source, the exposed population, the time frame of exposure, microenvironment(s), and activities. They often are created to aid in estimating exposure.
exposure science The application of scientific methods to study human contact with chemical, physical, or biological agents occurring in the environment and to determine the mechanisms and dynamics of events either causing or preventing adverse health outcomes.
frequency of exposure The number of exposure events in an exposure duration.
health hazard A potential adverse change in health status.
indirect exposure assessment Assessment that relies on estimated values (or self-reported values) for the frequency, intensity, and duration of exposure events, rather than on directly observed or measured quantities.
industrial hygiene The science and professional practice of anticipation, recognition, evaluation, and control of workplace and environmental hazards.
ingestion exposure Exposure to an agent through eating or swallowing contaminated media.
inhalation exposure Exposure to an agent through breathing in contaminated air or gases.
intensity of exposure Generally refers to the magnitude or amount (how much) of
452
contact between the agent and the barrier; can be expressed in quantitative terms (e.g., a concentration) or qualitative terms (high, medium, or low).
isolation The containing of or limiting of access to hazardous materials (e.g., by placing a physical barrier such as a container between a hazardous agent and the worker).
job-exposure matrix (JEM) A cross classification of jobs and workplace exposure levels across different agents or time, which assigns typical exposures according to common job classifications and work practices. Used for imputing past workplace exposures (known as exposure reconstruction).
modeling exposures Creating a physical or a conceptual mathematical representation of the exposure process, including events and outcomes.
passive sampling Sampling an agent without using a mechanical pump, fan, syringe, or other device to draw an environmental sample into a collection medium or vessel. Typically passive sampling collects samples by diffusion or gravitational sedimentation.
peak concentration The maximum concentration experienced during an exposure event.
personal protective equipment Clothing, eyewear, respiratory protection devices, or any other items worn by a person and designed to prevent injury or harm from an agent present in the environment.
personal sampling Collecting a sample with a portable sampler affixed in the immediately breathing zone of a mobile individual.
pharmacokinetics A branch of science dedicated to determining the internal fate and distribution of substances administered to a living organism.
physical hazard An agent that presents a hazard due to its ability to deposit excessive energy (e.g., mechanical, acoustic, thermal,
453
electromagnetic, or nuclear) in an organism. protective devices
Barriers, guards, or other equipment placed between a person and a hazard, designed to prevent injury or harm (also see personal protective equipment).
recognition Appropriate identification and classification of hazardous agents in the workplace or environment.
safety engineering A discipline of applied science that seeks to minimize potential health hazards through the application of process design and testing standards that reduce the likelihood of injury or adverse outcomes.
safety hazard A set of circumstances or agents that can increase the likelihood of injury or adverse outcomes for a person.
sample collection instruments Devices designed to probe environmental media and capture or record agents for analysis.
subchronic exposure A contact between an agent and a target of intermediate duration between acute and chronic. (Other terms, such as less- than-lifetime exposure, are also used.)
substitution Replacing a hazardous agent with another and less hazardous alternative.
target organ dose The amount or fraction of a harmful agent that reaches an organ or tissue in the body that is the site where the adverse health outcome originates.
ventilation Movement of air, through the use of fans or other means, so as to provide sufficient clean or uncontaminated air to maintain health.
walk-through A site survey technique used by hygienists and exposure scientists to observe potential hazards; generally it consists of a
454
planned traverse of the (work) site, accompanied by people familiar with the work processes, along with forms, photographic equipment, or other methods of documenting the conditions.
455
Discussion Questions 1. What are the three primary routes of exposure for people?
2. Which routes of exposure are most important for workplaces? Which routes are more important in the community setting than they are in the workplace? Which are less important?
3. How are the routes of exposure different from exposure pathways? Which one is more important for the purpose of controlling exposures? Provide an example of an exposure pathway and describe how it applies to exposure control.
4. Name three key advantages of exposure biomonitoring compared to other types of exposure assessment. Are there any disadvantages to using biomonitoring?
5. Provide an example of a direct exposure assessment method and an indirect exposure assessment method for dietary exposures. What are the strengths and limitations of each? Which type of assessment applies to a duplicate diet study?
6. What are the differences between cumulative assessments and aggregate exposure assessments?
456
References Bossé, Y., Postma, D. S., Sin, D. D., Lamontagne, M., Couture, C., Gaudreault, N.,…Laviolette, M. (2012). Molecular signature of smoking in human lung tissues. Cancer Research, 72, 3753–3763.
Cochran, R. C., & Driver, J. H. (2012). Estimating human exposure: Improving accuracy with chemical markers. Progress in Molecular Biology and Translation Science, 112, 11–29.
Cohen Hubal, E. A., Richard, A. M., Shah, I., Gallagher, J., Kavlock, R., Blancato, J., & Edwards, S. W., (2010). Exposure science and the U.S. EPA National Center for Computational Toxicology. Journal of Exposure Science & Environmental Epidemiology, 20(3), 231–236.
International Occupational Hygiene Association. (2009). What is occupational hygiene? Retrieved from http://ioha.net/objectives.html
Koren, H., & Bisesi, M. (2002). Handbook of environmental health and safety: Principles and practices (2 vols., 4th ed.). Boca Raton, FL: CRC Press.
Kyrtopoulos, S. A. (2013). Making sense of OMICS data in population-based environmental health studies. Environmental and Molecular Mutagenesis, 54(7), 468–479.
Marsillach, J., Costa, L. G., & Furlong, C. E. (2013). Protein adducts as biomarkers of exposure to organophosphorus compounds. Toxicology, 307, 46–54.
National Research Council. (2012). Exposure science in the 21st century: A vision and a strategy. Washington, DC: National Academies Press.
Ryan, P. B., Burke, T. A., Cohen Hubal, E. A., Cura, J. J., & McKone, T. E. (2007). Using biomarkers to inform cumulative risk assessment. Environmental Health Perspectives, 115(5), 833–840.
Sexton, K., Needham, L. L., & Pirkle, J. L. (2004). Human biomonitoring of environmental chemicals: Measuring chemicals in human tissues is the “gold standard” for assessing people's exposure
457
to pollution. American Scientist, 94(1), 38–45.
U.S. Environmental Protection Agency, Office of Research and Development, National Center for Environmental Assessment. (2015). Integrated Risk Information System (IRIS): IRIS glossary. Retrieved from http://www.epa.gov/ncea/iris/index.html
Wild, C. P. (2005). Complementing the genome with an “exposome”: The outstanding challenge of environmental exposure measurement in molecular epidemiology. Cancer Epidemiology, Biomarkers & Prevention, 14(8), 1847–1850.
458
For Further Information Books and Articles
Standard References in Industrial Hygiene
Plog, B. A., & Quinlan, P. J. (Eds.). (2012). Fundamentals of industrial hygiene (6th ed.). Itasca, IL: National Safety Council.
Ramachandran, G. (2005). Occupational exposure assessment for air contaminants. Boca Raton, FL: CRC Press.
Rose, V. E., & Cohrssen, B. (Eds.). (2011). Patty's industrial hygiene (4 vols., 6th ed.). Hoboken, NJ: Wiley.
Overviews of Exposure Assessment
Butt, T. E., Clark, M., Coulon, F., & Oduyemi, K. O. (2009). A review of literature and computer models on exposure assessment. Environmental Technology, 30(14), 1487–1501.
Cohen Hubal, E. A., Sheldon, L. S., Burke, J. M., McCurdy, T. R., Berry, M. R., Rigas, M. L.,…Freeman, N. C. (2000). Children's exposure assessment: A review of factors influencing children's exposure, and the data available to characterize and assess that exposure. Environmental Health Perspectives, 108(6), 475–486.
Cordioli, M., Ranzi, A., De Leo, G. A., & Lauriola, P. (2013). A review of exposure assessment methods in epidemiological studies on incinerators. Journal of Environmental and Public Health, 129470.
Poole, A., van Herwijnen, P., Weideli, H., Thomas, M. C., Ransbotyn, G., & Vance, C. (2004). Review of the toxicology, human exposure and safety assessment for bisphenol A diglycidylether (BADGE). Food Additives and Contaminants, 21(9), 905–919.
Rezagholi, M., & Mathiassen, S. E. (2010). Cost-efficient design of occupational exposure assessment strategies—a review. Annals of Occupational Hygiene, 54(8), 858–868.
Reviews of Exposure Biomarkers
459
Corradi, M., Goldoni, M., & Mutti, A. (2015). A review on airway biomarkers: Exposure, effect and susceptibility. Expert Review of Respiratory Medicine, 9(2), 1–16.
DeMarini, D. M. (2013). Genotoxicity biomarkers associated with exposure to traffic and near-road atmospheres: A review. Mutagenesis, 28(5), 485–505.
Liu, K. S., Hao, J. H., Zeng, Y., Dai, F. C., & Gu, P. Q. (2013). Neurotoxicity and biomarkers of lead exposure: A review. Chinese Medical Sciences Journal, 28(3), 178–188.
In addition, the Centers for Disease Control and Prevention maintains a Web site with useful information on biomonitoring: http://www.cdc.gov/biomonitoring
The Exposome In addition to Kyrtopoulos (2013), listed in the References, see the following:
Bonvallot, N., Tremblay-Franco, M., Chevrier, C., Canlet, C., Debrauwer, L., Cravedi, J. P., & Cordier, S. (2014). Potential input from metabolomics for exploring and understanding the links between environment and health. Journal of Toxicology and Environmental Health, Part B: Critical Reviews, 17(1), 21–44.
Verma, M. (2012). Epigenetic biomarkers in cancer epidemiology. Methods in Molecular Biology, 863, 467–480.
Wild, C.P., Scalbert, A., & Herceg, Z. (2013). Measuring the exposome: A powerful basis for evaluating environmental exposures and cancer risk. Environmental and Molecular Mutagenesis, 54(7), 480–499.
Reviews of Job-Exposure Matrices
Burstyn, I. (2011). The ghost of methods past: Exposure assessment versus job-exposure matrix studies. Occupational and Environmental Medicine, 68(1), 2–3.
Lavoue, J., Labreche, F., Richardson, L., Goldberg, M., Parent, M. E., & Siemiatycki, J. (2014). 0382 CANJEM: A general population job exposure matrix based on past expert assessments of exposure
460
to over 250 agents. Occupational and Environmental Medicine, 71(Suppl. 1), A48.
Peters, S., Kromhout, H., Portengen, L., Olsson, A., Kendzia, B., Vincent, R.,…Vermeulen, R. (2013). Sensitivity analyses of exposure estimates from a quantitative job-exposure matrix (SYN-JEM) for use in community-based studies. Annals of Occupational Hygiene, 57(1), 98–106.
Organizations
Information on Industrial Hygiene
American Conference of Governmental Industrial Hygienists (ACGIH): http://www.acgih.org
American Industrial Hygiene Association (AIHA): http://www.aiha.org
Information on Exposure Assessment
International Society of Exposure Science (ISES): http://www.iseaweb.org
U.S. Environmental Protection Agency, Exposure assessment tools and models (2014): http://epa.gov/opptintr/exposure
461
Chapter 9 Environmental Psychology
Nancy M. Wells, Gary W. Evans, and Kristin Aldred Cheek
Dr. Wells, Dr. Evans, and Ms. Aldred Cheek report no conflicts of interest related to the authorship of this chapter.
462
Key Concepts Environmental psychology marshals both theory and empirical evidence to understand human-environment relations.
Environmental psychologists recognize that behavior, like physical health, is affected by the immediate social and physical environment as well as by the broader sociocultural context in which daily life unfolds.
Environmental psychology focuses on a broad variety of environmental exposures and circumstances, such as features that encourage (or discourage) socializing, wayfinding cues, crowding, noise, light and color, and housing quality. Only some of these fall within the scope of traditional environmental health sciences, so the two fields are highly complementary.
Environmental psychology focuses on a broad variety of outcomes, including health, social interactions, stress, and happiness. Again, only some of these fall within the scope of traditional environmental health sciences, so the two fields are highly complementary.
Environmental psychology offers valuable insights into promoting attitudes and behaviors that are health promoting and environmentally friendly.
How does crowding affect human health, well-being, and functioning? How about environmental stressors such as noise or chaos? How about housing quality? Natural or technological disasters?
How do people's attitudes toward the environment form? What makes people adopt pro-environment, health-promoting behaviors such as recycling, conserving water, using public transportation, and reducing energy consumption? What are the most effective ways to “nudge” or motivate such behavior change?
Questions such as these are central to environmental psychology—a problem-driven field that marshals both theory and empirical
463
research to understand human-environment relations in order to improve environmental conditions and to promote health, comfort, safety, satisfaction, and productivity across a variety of contexts (Gifford, 2014). Like public health professionals, environmental psychologists are eclectic in their methodologies, borrowing from many different sciences. Most environmental psychology research occurs in the field, rather than in the laboratory, because environmental psychologists pay close attention to context. They recognize that behavior, like physical health, is affected by the immediate social and physical environment as well as by the broader sociocultural context in which daily life unfolds.
Environmental psychology emerged as a field in the1960s, growing out of the work of social psychologists who recognized that the physical environment played a role in social phenomena such as aggression and cooperation, and the work of cognitive psychologists interested in how context affected perception and cognition. More recently, environmental psychology has developed increased synergies with public health. Attention has turned to the role of both small- and large-scale environmental features, in both nature and the built environment, in promoting health (Wells, Evans, & Yang, 2010) as well as in encouraging health behaviors, such as physical activity and healthy dietary intake, and reducing risky behaviors (e.g., forgetting to wash one's hands in health care settings). Environmental psychology and public health also share a focus on social inequalities, because harmful environmental exposures such as childhood poverty and housing quality are associated with low socioeconomic status (SES).
In this chapter we present an overview of environmental psychology. We begin by examining parallels and distinctions between environmental psychology and biomedical sciences, especially environmental toxicology. We then summarize key principles of environmental psychology that have particular relevance to public health. Environmental psychology concerns both the built and natural environment. In this chapter we focus primarily on the built environment; the natural environment is discussed in Chapter 25.
464
Environmental Psychology and Toxicology Environmental psychology has some commonalities with toxicology, such as their shared focus on influences of the physical environment on human health and well-being. However their approaches differ in important ways. In this section we consider six differences between environmental psychology and the more traditional biomedical perspectives of toxicology. First, a few specific scenarios illustrate how these perspectives both intersect and differ:
Minamata Bay. In 1956, it was discovered that methylmercury, released by the Chisso Corporation's nearby chemical factory, was bioaccumulating in fish and shellfish in Minamata Bay and the Shiranui Sea in southern Japan, resulting in mercury poisoning among people living in the area. Minamata disease, a neurological syndrome, has affected more than 2,000 of these victims, who experience numbness of hands and feet; narrowing of visual field; damaged hearing and speech; and in some cases, paralysis, coma, and death (see figure 1.2 in Chapter 1).
Sound in daily life. John has worked in a furniture factory for the last thirty years. Prolonged exposure to excessive noise can result in hearing loss. OSHA regulations limit workplace exposure to noise to 90 decibels (dB) for an eight-hour period or 105 dB for one hour. Workers are also required to wear hearing protection when using equipment that generates sounds above 85 dB. However, John doesn't always wear the hearing protection (in part, because he wants to be able to communicate with coworkers if they get injured or have a problem). Consequently, he has some hearing loss.
Housing hazards. The Valdez family—Charlotte and her three children—live in a two-bedroom apartment in the Anacostia neighborhood of Washington, DC. The apartment is rent subsidized but has various physical problems. Lead paint chips from the windowsills, the heat and humidity cannot be controlled, and cigarette fumes from a neighbor who smokes heavily seep through the ventilation system into the Valdezes' apartment. As a result, the Valdez children suffer from various health ailments, including asthma.
465
Ecological Perspective Biomedical models, such as those used in toxicology, tend to focus on direct relations between a particular environmental exposure and an outcome of interest, such as lead and children's IQ, whereas environmental psychology models are more likely to consider a broader, bioecological context. This perspective means that both factors in the immediate setting and factors more remote from the individual influence how that individual responds to the physical environment. These factors can be other physical characteristics of the environment as well as psychosocial characteristics, including individual factors such as personality, culture, or SES, or even biological variables such as genetics or sex. As an illustration, the traditional biomedical perspective would largely conceptualize density or crowding in terms of disease vectors and influences on pathogen exposure and transmission. An environmental psychologist would also be interested in whether the density was proximate, at a small spatial scale—say, a house or a classroom—or whether it was on a larger spatial scale, such as the neighborhood, because the former threatens interpersonal relationships whereas the latter may facilitate positive social interactions. Furthermore, the influences of density tend to be exacerbated among low-income families and vary with personality as well as gender (Bilotta & Evans, 2013).
Outcomes of Interest The fields of toxicology and environmental psychology tend to focus on somewhat different outcomes, even when considering the same environment or exposure (Table 9.1). Toxicology focuses on how poisons trigger physical dysfunction, from inflammation to cancer to neurotoxicity; whereas environmental psychology broadens the range of effects experienced by victims of poisoning beyond physiology, including their moods and emotion, social interactions, and stress. For example, residents suffering from Minamata disease likely also experienced anxiety and possibly depression, as well as stigma, and ostracization. Edelstein (1988), in a study of families living near a hazardous waste site, found multiple indices of psychological distress and heightened family conflict, along with elevated feelings of loss of control and helplessness.
466
Table 9.1 Contrasting Toxicology and Environmental Psychology
Toxicology Environmental Psychology
Ecological perspective
Direct relations Broader, ecological context
Outcomes of interest
Singular focus, typically physiological
Broader focus, including mental health, social interaction, stress
Health promotion
Pathogenesis Pathogenesis and salutogenesis
Exposure Singular effects, ambient environmental exposure
Synergistic effects, built environment, movement between settings
Humans as dynamic organisms
Biological effects on passive organisms
Coping strategies used by humans
Direct/indirect effects
Predominantly direct effects, few indirect path models or consideration of moderators
Predominantly indirect effects, consideration of moderator models
Health Promotion Another distinction between toxicology and environmental psychology concerns the extent of their focus on health promotion. Toxicology examines pathogenesis—the origins of disease or dysfunction—while environmental psychology tends to focus equally on pathogenesis and salutogenesis, aiming to understand what environmental features enhance functioning, promote health, and bolster resilience. For example, although addressing housing hazards is important for health, the home is also a refuge providing restoration or recovery from the demands of the outside world. Understanding how the design of housing can foster positive personal growth and interpersonal and familial relationships is a major area of research on housing and behavior (Hartig & Lawrence, 2003). The home is also a place where routines and
467
rituals happen that are critical for the healthy development of children (Evans, 2006).
Exposure The field of environmental health has traditionally focused primarily on ambient environmental exposures, often at the metropolitan or regional scales. In contrast, most environmental psychology research focuses on the built environment at the building to neighborhood scale. This occurs in part because that is where people spend the most time, and in part because the promotion of wellness is often more readily accomplished at the smaller scale. Furthermore, the intensity and the duration of exposure to physical environments are often greater in interior than in exterior environments. Like other environmental health scientists, environmental psychologists are sensitive to the importance of both the intensity and the duration of exposures. As an illustration, in a study of children's household crowding, Solari and Mare (2012) demonstrated stronger detrimental effects of household crowding on children's health and academic achievement in Los Angeles than in a national sample, a finding possibly explained by more variable levels of crowding over time, particularly at the higher end of the density distribution. They also found that long-term crowding predicted adverse outcomes better than a one-time exposure estimate. These findings illustrate the role of intensity and duration in environmental psychology research.
Another aspect of exposure that interests environmental psychologists is movement across space. When people go in and out of buildings, for example, their exposure to air quality, noise, density, light, and temperature can be dramatically altered. Estimates of environment-response functions that do not take this into account likely underestimate environmental impacts.
Environmental psychologists, like other social and biomedical scientists, often attempt to isolate the effect of a single environmental factor. But increasingly environmental psychologists are examining the synergistic impacts of many environmental agents—what is sometimes called cumulative risk (a topic explored in Chapter 11; see Figure 11.2). For example, in the vignette about the Valdez family's challenges in dealing with housing hazards, respiratory health is compromised by multiple structural
468
deficiencies such as inadequate heating and also exposure to secondary cigarette smoke. As a second illustration of the importance of multiple exposures, substandard housing in lower quality neighborhoods had more adverse mental health sequelae than substandard housing in moderate quality neighborhoods (Jones-Rounds, Evans, & Braubach, 2013). Moreover this pattern of worse mental health in relation to multiple environmental risk exposures was similar across eight European countries, including both Western and former Eastern bloc societies. One of the reasons certain occupations may be associated with adverse health outcomes is the confluence of risk precipitated by those work environments—including chemicals, physical hazards, changing job schedules, and psychosocial conditions such as lack of control. Multiple exposure estimation is important for several reasons. First, it more closely approximates the ecological context in which most risk factors occur. Many environmental risks co-occur, and this especially happens among disadvantaged populations. Second, exposure to an accumulation of risk factors usually has substantially greater adverse effects on human health and well-being than a singular risk exposure has (Evans, Li, & Whipple, 2013).
Humans as Dynamic Organisms The traditional toxicological model of environmental health essentially portrays the organism as a vessel that passively absorbs insults with internal, biological processes. Despite exceptions, such as recognition of the role of immune tolerance or epigenetic adaptation (Chapter 7), this view appears not to appreciate sufficiently that human beings are active, dynamic organisms that use various strategies to cope with environmental demands. These coping strategies can directly alter exposure or can marshal resources to mitigate adverse exposures once they occur. Earlier we described an example of hearing loss in a work environment and noted that the decision of the individual, John, on whether or not to use hearing protection significantly influenced his exposure to noise. Instead of using hearing protection to modify noise, another possible coping strategy might be to try to ignore the noise. However, as we point out later on, this strategy not only forfeits auditory protection but may also inadvertently lead to other, unintended effects, such as not paying attention to the speech of
469
others. In many situations, people make efforts to try to deal with substandard environmental conditions. These coping strategies can directly and indirectly influence health and well-being.
Direct/Indirect Effects Toxicological models typically posit a direct, one-to-one function between exposure and outcome. But because human beings are embedded in an ecological context and because they are dynamic, coping organisms, many environmental impacts on human beings are indirect. Parents in crowded homes can socially withdraw as a way to reduce unwanted social interaction. A by-product of this withdrawal is fewer socially supportive interactions with their families (Evans, 2001). Another illustration of indirect effects is that the effects of a particular environmental factor vary according to situational or personal variables. Personal characteristics such as personality, gender, or SES can moderate environmental impacts. For example, the adverse impacts of PCBs on early cognitive development can be attenuated somewhat by more sensitive, responsive parenting. This type of parenting means the caregiver is attuned to the needs of the child and responds to the child's needs in a consistent and predictable manner.
470
Environmental Psychology Processes The field of environmental psychology is quite broad— encompassing children's environments, design for older adults, universal design, and design for dementia; cutting across setting types, from schools to homes to workplaces; and including a wide variety of theories. It is beyond the scope of this chapter to describe all aspects of environmental psychology in detail. To present an overview of the field of environmental psychology, we focus on five underlying processes that exemplify transactions between people and physical settings: these processes involve physical layout, stress and coping, diet and physical activity, pro-environment behavior, and light and color.
Physical Layout Environmental psychologists have examined aspects of physical layout across varied contexts such as homes, hospitals, schools, and streetscapes and across scales from room to city. Among the earliest environmental psychology studies is research investigating how the configuration of physical elements within a mental hospital affects patient behavior (Evans & McCoy, 1998; Gifford, 2014). By rearranging furniture and otherwise intervening in the physical space, researchers discovered that certain seating configurations facilitate social interaction, whereas others impede it. The former configurations, termed sociopetal, consist of moveable seating that can be configured for face-to-face interaction across comfortable interpersonal distances. The latter, sociofugal configurations, are inflexible and do not facilitate eye contact or a comfortable interpersonal distance. Sociofugal seating often takes the form of straight rows of seating, each facing away from the row behind, or shoulder-to-shoulder seats. The concepts of sociopetal and sociofugal arrangements can be used to guide designers to ensure that spaces facilitate behavior that is context appropriate. In settings such as cafés or meeting rooms, social interaction and social connection are desired, so sociopetal configurations are appropriate. However, in contexts such as a church or library, a sociofugal arrangement may be appropriate, to discourage interaction. Social capital comprises community cohesion (e.g.,
471
shared values, social support) as well as informal social control (e.g., monitoring youth behaviors, taking part in crime watch programs), and operates at the more macro scale, such as the neighborhood or streetscapes. Social capital can directly support physical and psychological well-being and may also buffer some of the adverse effects of other risks (Kawachi & Berkman, 2000). Some of the physical variables associated with greater social capital are well- maintained surroundings; parks and other green spaces; low traffic congestion; well-functioning social spaces such as plazas, shopping nodes, restaurants, and cafés; high external density; pedestrian- oriented design; and elements that inhibit criminal behavior (as discussed on the next page).
Related to layout is proxemics, the study of how people use space to communicate nonverbally. One important aspect of proxemics is personal space, the area or bubble around our body that we maintain between ourselves and others. One of the critical factors influencing personal space is the interpersonal relationship we have or might desire to have with others. Hall (1966) noted that in multiple cultures one can identify an intimate distance for embracing and touching, a personal distance for interactions among close friends and family, a social distance used with acquaintances, and a public distance used for public speaking. Although these four zones appear to be universal, the specific amount of distance associated with each varies with the culture. For example, Middle Eastern and Latin cultures prefer a relatively smaller personal space, reflecting a preference for higher levels of social interaction (Hall, 1966). There are also cultural differences in how people use the physical environment to communicate nonverbally. For example, acoustic privacy is as important as visual privacy in Germany, whereas in Japan visual privacy is prioritized. Thus one sees heavy, opaque doors and well-insulated walls in the former culture, and moveable, lightweight, translucent screens and partitions in the latter (Hall, 1966). Focal points are areas that facilitate social interaction. Well-designed focal points are activity generators (e.g., a coffee pot or the mailroom), are centrally located near multiple circulation paths, function as neutral territories (e.g., between departments), include sociopetal furnishings, and provide a visual prospect (Evans & McCoy, 1998). Having a visual prospect means that one can see who is in a space prior to making a behavioral commitment to that space.
472
In workplaces and schools, researchers have examined the different impacts of physical layouts, including open-plan layouts and closed-plan layouts. Open-plan layouts have the advantage of flexibility, while closed-plan layouts are fixed and rigid. Proponents of open-plan office systems suggest that open layouts increase communication among coworkers. Research suggests a more nuanced view. Task-related as well as nonwork communication may increase, but the nature of one's job plays a critical role; those needing to concentrate or engage in private interactions find open- plan layouts unsatisfactory (Becker & Steele, 1995). Similarly, in school environments, open-plan configurations may support spontaneous engagement and intrinsic motivation but are also associated with high levels of distraction (Evans, 2006). Younger children and those with less executive function ability perform worse and have greater adjustment problems in open-classroom configurations. Schools with a modified open layout—one that incorporates activity pockets and stimulus shelters—can balance the pros and cons of open and closed floorplans.
Layout also affects people's experience of wayfinding. Signage systems are actually one of the least critical factors in wayfinding inside buildings or in a city. Probably the most fundamental contributor to getting lost is the inability to form a legible mental map or image of the space one is in. Even long-term employees in health care facilities, let alone visitors and patients, can get disoriented because the basic footprint or layout of many hospitals is unintelligible. Simple, regular shapes contribute to legibility and facilitate the development of a cognitive map, or mental representation, of a building, thus facilitating wayfinding. Building features that facilitate wayfinding not only enhance feelings of comfort and ease but also can reduce the experience of stress when navigating a novel environment (e.g., a medical complex) and can help to ensure a safe exit in case of a fire or other emergency. A more subtle impact is the reduction in staff time required to provide directions to disoriented users. Other building characteristics that enhance occupants' ability to find their way include enabling people to see from the interior to the outdoors, locating interior landmarks at decision points, and ensuring that circulation paths are aligned with building facades (Evans & McCoy, 1998).
Considering layout issues on a larger scale brings us to the concept
473
of defensible space. Defensible space (Newman, 1972, 1996) and crime prevention through environmental design (CPTED) (Casteel & Peek-Asa, 2000; Taylor & Harrell, 1996) have their origins in the (in)famous Pruitt Igoe public housing complex in Saint Louis, Missouri. This housing project, comprising thirty-three eleven-story buildings, was acclaimed as an architectural marvel for its “vertical neighborhoods” created by “skip-stop elevators” that stopped only on the first, fourth, seventh, and tenth floors (“Slum Surgery in St. Louis,” 1951). And yet, just a decade after its occupation, the complex had high vacancy rates and was plagued by crime, violence, and fear. Finally, in the early 1970s, the entire complex was demolished. Analysis of Pruitt Igoe and other crime- ridden residential areas indicates that various aspects of the layout of both the interior and exterior of the complex likely contributed to residents' lack of territoriality and, ultimately, to high rates of crime. Human territoriality refers to our sense of spatial ownership and its nonverbal expression or delineation in the physical environment. For example, a fence around a home expresses territoriality, suggesting monitoring and control and signaling a transition from the public domain to the private. Plantings, decorations, and other signs of maintenance and care also serve as territorial markers. Signals and symbols of territoriality are inversely associated with crime rates. Conversely, incivilities such as litter and vandalism communicate that a place is not cared for or “owned” and are also linked to crime rates. The broken windows hypothesis suggests that once a place is slightly degraded, people will regard litter and disrepair as the norm and will further degrade the area. Furthermore, such incivilities incur a cycle of fear and withdrawal from public spaces, further emboldening intruders and would-be criminals to victimize the neighborhood. This in turn increases incivilities and, according to the broken windows hypothesis, creates a downward spiral of reduced defensible space and escalating crime.
The principles of defensible space, developed by architect and city planner Oscar Newman (1972, 1996) include the following:
Enhance a sense of territoriality and create social legibility with communal spaces and entries that are shared by only a few families. Social legibility confers the ability to recognize who belongs, or not, in a particular building or space. When a large
474
number of people share a communal space, people tend not to have a feeling of ownership or control. It is also easier for outsiders to gain access.
Use environmental design elements to create a continuum of spaces from public to semipublic to semiprivate to private. Without a gradation of spaces, residents' sense of territoriality is undermined, limiting their ability to control the space. Group or secondary territorial spaces are particularly important to facilitate the development of social capital.
Limit the scale of buildings to three to five floors. Large-scale complexes have a feeling of anonymity and interfere with a sense of ownership and control over property.
Increase visual surveillance. Facilitate “eyes on the street.” When residents can see the areas in and around their residences it deters crime, because residents can see when intruders are present. Moreover, criminals perceive that they can be monitored and so choose easier targets.
Foster an ambience of caring. Consistent with the broken windows hypothesis, criminals are attracted to areas with poor maintenance and upkeep. Abandoned buildings, vandalism, graffiti, and poorly maintained grounds connote a lack of investment and absence of pride in place.
Stress and Coping Stress occurs when environmental demands exceed personal coping resources. Thus stress is fundamentally a transactional process between person and environment. In this definition, stress is equivalent to strain and refers to the organism's responses when the balance between demands and resources becomes dysregulated. These responses can include physiological changes in bodily response systems, such as the hypothalamic-pituitary-adrenal axis (HPA) or elevated sympathetic nervous system activity, as well as behavioral responses such as anxiety, perceived distress, or diminished ability to sustain task performance at a high level. The environment can be a source of stress (i.e., a stressor) in several ways. Our focus here is on physical stressors, but note that both physical and psychosocial characteristics of environments can be stressors. First, the physical environment can directly increase
475
demands on the individual. For example, crowding and noise can increase levels of stimulation sufficiently to overwhelm the organism. If a person needs to concentrate at work, assignment to an open-plan office may be stressful. Second, the physical setting can create stress by engendering anxiety or worry, as in the case of exposure to hazardous waste. (See Chapter 28 for a discussion of factors that affect people's level of anxiety with environmental exposures.) Or environmental conditions may directly cause negative affect; high levels of perceptible pollutants or extreme temperatures can make people feel nervous, anxious, overwhelmed, irritable, hostile, upset, distressed, and/or sad. Third, traffic congestion and other environmental stressors can interfere with goal achievement, engendering frustration and (if chronic) high levels of fatigue and helplessness. Fourth, sometimes the coping strategies people use to respond to a stressor can create physical or psychological health problems. As noted earlier, coping with the overload of social interaction produced by crowding reliably leads children and adults to withdraw socially, thus weakening social support resources. For further reading on the meaning and measurement of stress, as well as strain, see Cohen, Kessler, and Gordon (1997).
Environmental stress is one of the most active areas of research within environmental psychology (Bilotta & Evans, 2013; Evans, 2001). Research on crowding, noise, and housing and neighborhood physical quality provides examples of stress and its impacts.
Crowding Both laboratory and field studies reveal that crowding is a stressor, as indicated by increases in such physiological markers as blood pressure and cortisol. The most salient index of crowding is people per room. Consider the following college dorm room choices: a moderately large double room or a small single room. Which would you prefer, and what do you think the implications of your choice might be for studying in your room, sleeping, or engaging in interpersonal relationships with people on your hallway? A few studies have also shown that people who live in denser residences handle stress less well—that is, when exposed to an acute stressor (e.g., giving a speech to an audience), they show elevated cardiovascular reactivity and slower recovery to baseline. The daily
476
experience of crowding appears to create elevated chronic stress. Baseline cardiovascular and neuroendocrine indices of stress are elevated among those living in more crowded homes. These physiological outcomes of crowding are more robust for males. Crowded individuals also have difficulty completing complex tasks —those that require multi-tasking or extensive information processing—although simple tasks are largely unaffected (unless the crowding is extreme). The interplay between stressors and task performance reliably produces this pattern of outcomes. One reason may be that at least for a short period of time, individuals can still manage to process information well even when under high levels of stress. However, when task demands are ratcheted up, then performance suffers. This is a good example of the dynamic transactions between people and the environment. Several studies have also linked residential crowding to poorer cognitive achievement in children, and one interesting study showed that preschoolers in crowded nursery schools fared worse when they were also from more crowded homes (Maxwell, 1996). These findings are a nice illustration of the role of multiple exposures in human response. The effects on health or well-being of exposure to one environmental setting can be conditioned by exposure in another setting as well.
Crowding also influences social relationships. People find it difficult to maintain positive social relationships with those with whom they live or work when the home or the workplace is crowded. For example, families living in more crowded homes experience greater conflict and less cohesion. Environmental psychologists have shown that crowding effects in the laboratory generalize to the field, and a few field experiments (e.g., random assignment to public housing) as well as prospective, longitudinal studies have yielded comparable results.
Whereas most of the data on crowding and human health and behaviors emanate from North America and Europe, levels of crowding are much more extreme in some other cultures (see, e.g., Figure 9.1), especially in low-income countries. The few studies that have been conducted in these settings find stronger adverse outcomes than do studies from wealthy countries (Bilotta & Evans, 2013; Evans, 2001; Gifford, 2014). Recall the similar pattern of data uncovered in the United States by Solari and Mare (2012) when
477
comparing samples with different amounts of variation in household density. Furthermore, although there is cultural variation in how people perceive crowding, high-density housing causes similar, negative psychological distress sequelae across ethnic groups (Evans, Lepore, & Allen, 2000).
Figure 9.1 Long Waits and Crowded Buses at a School in Singapore
Source: Tan, 2012.
Noise Noise levels are typically assessed in decibels on a logarithmic scale, with each increase of 10 decibels perceived as twice as loud as the prior level. There is some evidence that both the frequency and the periodicity of noise influence human responses, with aperiodic, high-frequency sounds producing more stress. Similar to crowding, noise reliably produces elevated physiological stress, and there is some evidence that this is especially likely as the duration of exposure lengthens and that it can be exacerbated by high task demands (Bilotta & Evans, 2013; Evans, 2001). The latter finding illustrates the dynamic nature of human responses to environmental conditions. When task demands are low,
478
performance can be maintained, at least for a moderate duration, without considerable effort. However, when task demands are high (e.g., dual tasks versus a single task), then performance can be maintained only with extensive effort that elevates physiological stress. If complex task performance is allowed to degrade under noise or some other environmental stressor, then little physiological cost is apparent.
One of the most widely found effects of noise is delayed reading acquisition among children. This has been found in cross-sectional, longitudinal, and noise attenuation studies (Evans, 2006). One theory about these effects illustrates how coping with environmental conditions may be a cause of adverse outcomes. Children without hearing loss (having a normal audiogram) who are chronically exposed to noise have worse auditory discrimination abilities on standard assessment instruments than do unexposed children. The ability to perceive sounds accurately is a fundamental building block for reading. Thus noise exposure leads to poor auditory discrimination that in turn leads to delay in children's reading acquisition (see Figure 9.2). Why might this occur? As noted, this happens in children with normal hearing capabilities. This cognitive effect likely reflects an unintended side effect of human dynamic responses to suboptimal environmental conditions. If you live in a noisy apartment building, you may cope with it by tuning out the noise. Unfortunately, you may also tune out a multitude of auditory stimuli, including speech. This model also reminds us of the dangers of overreliance on self-reports of environmental effects, which is, unfortunately, too common in environmental psychology. Some environmental conditions that are harmful are imperceptible, and as indicated, people may adapt to chronic exposures, becoming less aware or threatened even though adverse impacts still occur.
Figure 9.2 Effects of Noise Exposure on Reading Acquisition, Mediated by Poor Auditory Discrimination
When people have to live or work in noisy settings, they may over time learn that there is little they can do to control their exposure. An organism that chronically experiences uncontrollable stimuli, such as chronic noise, may be more susceptible to learned
479
helplessness. One of the key features of learned helplessness is diminished motivation. In a classic series of experiments, Glass and Singer (1972) showed that when adults were exposed to uncontrollable noise, they were less likely to persist on challenging puzzles. This has been replicated outside the laboratory, including among children attending schools near airports. Interestingly, teachers in noisy school settings also report more difficulties in motivating their students to work, as well as greater deficiencies in students' abilities to pay attention and stay on tasks (Evans, 2006).
These environmental psychology studies on crowding and noise illustrate how the range of health outcomes from environmental exposures can be expanded considerably beyond the toxicological approach. They also illustrate another important point from a policy and practice perspective. At levels of density far below those likely to enhance disease transmission or levels of noise capable of producing hearing damage, several serious adverse outcomes are apparent. Many of the stress effects of environmental conditions will be overlooked if environmental health is defined strictly as physical morbidity. Furthermore, a subset of people are noise sensitive, and they respond with greater annoyance and physiological stress to noise stimuli.
Housing and Neighborhood Conditions As a final illustration of stress as a model of environment-health relationships, housing and neighborhood conditions can also be conceptualized as stressors. There are several reasons why suboptimal housing may be stressful. Housing is a symbol of status and identity, and inadequate housing may lead to stigmatization and diminished self-esteem. Poor quality housing engenders concerns about safety and health, and when children or frail elderly individuals are present, these issues can be life threatening. Poorly designed housing can damage coping resources. For example, low- income, single female heads of households residing in the upper levels of high-rise buildings consistently report social isolation and difficulties managing young children (Evans, Wells, & Moch, 2003). When housing quality is poor, instead of housing serving as a refuge, providing a space to relax and recover from a difficult job or other demands, the place where one lives itself adds to the strains of daily life (Hartig & Lawrence, 2003). As an illustration, children
480
living in poor quality housing accompanied by high levels of density and noise have elevated levels of stress hormones. These effects are independent of SES (Bilotta & Evans, 2013). Housing quality has been linked to elevated physiological stress among adolescents and adults, as well as to psychological distress (Evans et al., 2003). Although too many of these data are cross-sectional, longitudinal studies and a few natural experiments with random assignment to housing show similar trends. For example, several longitudinal studies have shown improvements in housing satisfaction and psychological well-being among residents moving to better quality housing and residents whose housing stock has been improved by renovations (Braubach, Jacobs, & Ormandy, 2011). Although much of this work has been conducted in the United Kingdom and the United States, consistent findings emerge in other economically developed countries. Much less is known, however, about housing and psychological reactions among residents in less economically developed countries. Given the wider range of housing quality in such countries, one would expect to see (similar to the research on crowding) even stronger adverse responses to substandard housing among children and their families in poorer countries.
Aspects of neighborhood quality salient for stress include low quality municipal and retail services (e.g., sporadic trash pickups, slow emergency response times, unavailability of healthy food choices, poor or absent public transit), minimal recreational opportunities, high street traffic volume, high residential instability, and incivilities such as abandoned buildings, vandalism, graffiti, and exposure to pollutants. Children and adults in such neighborhoods show elevated psychological distress (Rollings, Wells, & Evans, 2015). Although we are unaware of any work on neighborhood physical quality and physiological stress in adults or children, there is some indirect evidence. There is a large literature documenting that lower SES neighborhoods have poorer physical conditions on a wide array of variables, including housing stock (Evans, 2004). There is also evidence that residence in such neighborhoods, independent of household SES, is related to higher levels of physiological stress in adults (G. D. Smith, Hart, Watt, Hole, & Hawthorne, 1998) and adolescents (McGrath, Matthews, & Brady, 2006).
Diet and Physical Activity
481
The rapid onset of the obesity pandemic has increased attention in the fields of public health, urban planning, nutrition, and environmental psychology to the potential role of obesogenic conditions that encourage sedentary lifestyles and poor diets (Story, Kaphingst, Robinson-O'Brien, & Glanz, 2008; Wells, Ashdown, Davies, Cowett, & Yang, 2007). This paradigm shift occurred in the late 1990s and early 2000s, and was characterized by movement away from individually focused interventions toward more broad- brush strategies targeting communities and populations through environment and policy (Sallis, Bauman, & Pratt, 1998; Story et al., 2008). While these research efforts originated primarily in the United States and Australia, the International Physical Activity and Environment Network (IPEN), a twelve-country collaboration, has more recently formed to examine environmental and policy influences on physical activity internationally (Kerr et al., 2013).
Much of the research and many of the intervention efforts examining the influence of the environment on physical activity and dietary intake have been framed by an ecological perspective emphasizing the influence of factors across multiple contexts and scales ranging from microlevel elements such as sidewalks and benches to macrolevel factors such as urban land-use policies (Dannenberg, Frumkin, & Jackson, 2011) (see also Chapter 15). Various research efforts have increased our understanding of the ways in which the environment can foster or impede health behaviors. Here, we provide a brief overview of this evidence, considering two examples related to physical activity—child care outdoor learning environments and the commuter environment— and two examples related to dietary intake—the neighborhood food environment and the school cafeteria.
Child Care Outdoor Learning Environments In an effort to understand how the physical environment might bolster levels of physical activity early in life, researchers have examined child care outdoor learning environments. Time outdoors is among the strongest predictors of physical activity, and specific characteristics of the outdoor environment may promote physical activity. Studies of child care center outdoor learning environments illustrate the utility of two concepts in ecological studies of physical activity and diet: behavior setting and affordances. Behavior
482
settings are physical and social contexts in which behaviors occur (Gifford, 2014). Research focused on behavior settings allows examination of the physical areas within which certain activities occur (e.g., wheeled locomotion, imaginative play, climbing), recognizing that the physical boundaries of space do not always correspond to the functional boundaries. Characteristics of the setting may promote or deter specific activities. A key concept in environmental psychology is affordances—the possible uses or functions that the arrangement of physical features in the environment conveys to the user (Gifford, 2014). By signaling what the environment can do for the occupant, affordances can encourage certain behaviors such as physical activity. This perspective can be contrasted with environmental determinism, which implies that the physical environment directly causes certain human responses. In some cases, such as behavioral toxicology or repetitive strain with a poorly positioned keyboard, this can occur, but more typically the physical environment acts as a stimulus that (dis)encourages or facilitates (inhibits) certain behaviors and responses.
In a child care outdoor learning environment a wide, circular pathway for wheeled toys is a potent affordance for physical activity (Moore & Cosco, 2014). Green outdoor child care play areas with trees, shrubbery, and broken ground are associated with both more physical activity and lower ultraviolet (UV) exposure (Moore & Cosco, 2014). Thus, the design of the green, outdoor learning environments of child care centers can contribute to children's health by promoting physical activity and by reducing sunburn risk. In addition, a pre-post intervention study revealed that the introduction of activity-friendly, manipulatable play equipment in preschool environments reduced the time spent in sedentary behavior and increased light, moderate, and vigorous physical activity (Hannon & Brown, 2008). Moreover, considering the overall layout of child care centers, researchers have found that behavior settings that are centrally located and those that are immediately adjacent to other behavior settings are most associated with physical activity among young children (Smith et al., 2014).
The Commuting Environment and Physical Activity The transportation environment has been identified as a fertile
483
domain for promoting physical activity through the concept of active living. In fact, while physical activity has historically been designated as either utilitarian (e.g., laying bricks) or recreational (e.g., playing basketball), its focus now includes active transport (e.g., biking or walking as transportation; see Chapter 15). Researchers have examined environmental influences on travel behavior in general and on active transport specifically. With Americans averaging more than 100 hours per year on their daily commute (the equivalent of 2.5 work weeks of time), active transport merits focus (Wener & Evans, 2007). Pedestrian-oriented neighborhoods that support active transport have a high degree of mix of residential and commercial land uses, a relatively high density or compactness of development, highly connected street network patterns, and human-scale features (Dannenberg, Frumkin, & Jackson 2011).
Lower levels of regular physical activity seem to be directly related to increases in the number of vehicle miles traveled per year (Wener & Evans, 2007). In fact train commuters, compared to automobile commuters, walk 30% more steps per day and are four times more likely to achieve the 10,000 steps per day recommended by the Centers for Disease Control and Prevention (CDC) (Wener & Evans, 2007). Moreover, in a prospective study examining the effects of light rail being added to a neighborhood, a new rail stop was associated with increased ridership. In addition, walks to light rail were associated with more bouts of moderate physical activity (Brown & Werner, 2008).
The Neighborhood Food Environment The association of the food environment and diet has been documented at a variety of scales, from grocery store shelf to the home kitchen cupboard to the neighborhood (see Chapter 19). Although the evidence is somewhat mixed (Caspi, Sorensen, Subramanian, & Kawachi, 2012), supermarket availability has been linked to both obesity rates and dietary intake. For example, the presence of a supermarket within a census tract has been associated with a 32% greater likelihood of consuming the recommended number of daily fruit and vegetable serving (Morland, Wing, & Diez Roux, 2002). In a rare natural experiment, Wrigley, Warm, and Margetts (2003) found that following the construction of a
484
supermarket in a retail-poor area of the United Kingdom, mean daily intake of fruit and vegetables increased only marginally; however, among those with poor diets prior to the opening of the store, 60% significantly increased their fruit and vegetable consumption. Moreover, proximity was important. The effect of the new store was strongest among those living closest. This pattern of findings is another illustration of indirect effects of the environment on human health and behavior. Individual differences in dietary habits moderate the impact of the availability of access to healthy food on vegetable and fruit consumption. Furthermore, the impact of gaining access to healthy food choices is accentuated by residential proximity to the newly introduced neighborhood market. Introduction of the supermarket alone mattered some, but consideration of context, both environmental and personal, provides a richer understanding of the influence of a neighborhood design change on human health and behavior.
Research evidence also suggests that availability of healthy food underlies, in part, poor dietary patterns among low-income individuals. Lower SES households typically have less access to healthy food. Low-SES neighborhoods have fewer retail stores, including fewer large grocery stores and supermarkets. In a study of several metropolitan areas, Morland, Wing, Diez Roux, and Poole (2002) found that the wealthiest neighborhoods have nearly four times more supermarkets than the poorest neighborhoods—an average of twenty-seven versus an average of seven.
The association of the neighborhood food environment with (un)healthy habits reveals the powerful influence of food availability and accessibility. It also illustrates racial and economic disparities, a pattern seen with many other environmental features, both positive, such as green space (Wells & Jimenez, in press) and recreational facilities, and negative, such as substandard housing, crowding, noise, lack of neighborhood services, and pollutants (Evans, 2004; Evans, Wells, & Schamberg, 2010). The issue of environmental justice is discussed in detail in Chapter 11.
School Cafeterias as Food Environments Schools are increasingly recognized as a promising context for health intervention strategies that promote healthy habits, including healthy eating. Researchers have begun to examine how
485
features of the school cafeteria influence dietary intake. For example, children choose and eat more fruits and vegetables when a salad bar is provided (Slusser, Cumberland, Browdy, Lange, & Newmann, 2007). Other characteristics of the cafeteria environment can affect meal choices by influencing perceived accessibility of those choices. Availability and accessibility are sometimes conflated; typically, availability refers to the presence of the food (e.g., fruit and vegetables) in the environment (e.g., home, school, or neighborhood), and accessibility captures whether the food is in a form and location that makes consumption easy. Availability and accessibility are predictors of dietary intake across settings and scales, from the neighborhood to the cupboard. Moreover, in the school cafeteria, inefficient layout, unattractiveness, noise, and crowding, combined with short lunch periods and long lines, can pressure students to select faster food options and may compel students to choose off-campus options (Gorman, Lackney, Rollings, & Huang, 2007).
Conversely, thoughtful food presentation and layout, attractive produce displays, and opportunities to try new foods can be effective in promoting increased fruit and vegetable consumption at school (Story et al., 2008). With the aim of nudging children toward healthier choices, the principles of convenience, attractiveness, and normativeness appear to be effective in increasing healthy food consumption in school cafeterias (see Table 9.2 and Figure 9.3).
Table 9.2 Examples of Convenience, Attractiveness, and Normativeness Applied to a School Cafeteria
Convenience Improve the convenience of fruits and vegetables:
Provide a “healthy convenience line,” with only submarine sandwiches and healthy sides.
Locate fruit next to cash register.
Provide salad in see-through takeout containers.
Place juice boxes near ice cream.
Attractiveness Improve the attractiveness of fruits and vegetables:
Post lunch menu with color photos of fruits and
486
vegetables served.
Label vegetables with descriptive names.
Display fruit in nice bowls or on tiered stands.
Normativeness Make the selection of fruits and vegetables seem normative:
Use verbal prompts from cafeteria staff: “Would you like to try…?”; “No veggie? How about…?”; “You can have another side…how about a piece of fruit?”
Use visual prompts: “Last chance for fruit” displayed next to fruit basket at cash register.
Source: Hanks, Just, & Wansink, 2013, p. 868.
Figure 9.3 Illustration of Convenience, Attractiveness, and Normativeness in a School Cafeteria
Source: Cornell University BEN Center, used with permission.
Implementing these principles in two school cafeterias yielded an 18% increase in fruit consumption and a 25% increase in vegetable consumption (Hanks et al., 2013). An environment that provides easy, visual access to healthy foods affords healthy eating. Similarly, placing less healthy options in less salient locations can discourage unhealthy choices.
487
Pro-Environment Behavior With growing concerns about finite natural resources, environmental degradation, and the impacts of climate change on human health, there is interest in how to encourage people to engage in pro-environment behaviors (which are in most cases also pro-health behaviors, directly or indirectly). Various behaviors can help to alleviate environmental problems, including engaging in environmental activism, supporting public policy changes, and performing specific personal behaviors such as recycling, riding public transportation, purchasing goods that have fewer environmental impacts, and curtailing the use of resources (Stern, 2000). What factors influence whether a person engages in pro- environment behavior? People's fundamental values, such as concern for the natural environment, do play a role, as do attitudes toward environmental problems and toward pro-environment behaviors (Gifford, 2014). However, there is often a gap between attitudes and behavior, and changing someone's attitude does not necessarily lead to behavior change (Winter & Koger, 2004). Environmental psychologists have identified a number of factors in the social, physical, and political environments that account for this gap or act as barriers to behavior change. Successful interventions leverage what we know about the complex systems in which behaviors occur.
488
Figure 9.4 A Waste Setup That Provides a Physical Cue to Encourage Recycling
Source: UW Recycling, University of Washington, n.d.
Several strategies to induce pro-environment behavior focus on social phenomena, such as personal and social norms, to influence behavior. For example, social norms have been used effectively to increase energy conservation behavior (Allcott, 2011). Social modeling, including demonstrating desired behaviors, has been effective in water conservation and recycling behaviors (Osbaldiston & Schott, 2012). Goal setting and commitments—specific and written—have been effective as well. Other strategies focus on altering environmental cues or on the nature of reinforcements (i.e., reward and punishment). For example, prompts that are specific and close to where and when the behavior occurs—such as well- designed instructions on a recycling bin—can influence behavior (Winter & Koger, 2004) (see Figure 9.4). Feedback on energy use (e.g., electricity or gas consumption), particularly if it is frequent, can increase conservation (Osbaldiston & Schott, 2012). While pro- environment behavior can be reinforced through incentives, rewards, and feedback, these effects often do not persist after the reinforcement is removed (Winter & Koger, 2004). One possible reason for this is that extrinsic rewards, while sometimes effective
489
in the short run, have a less durable impact than intrinsic motivations (De Young, 2000). In addition to focusing on intrinsic motivations (such as behavioral competence, frugal consumption, or participation in maintaining a community), removing barriers, increasing convenience, and generally making behaviors easier to engage in can create situations that are more supportive of pro- environment behaviors (Osbaldiston & Schott, 2012; Winter & Koger, 2004). The connection here with attitudes and values is useful to consider. When it is relatively easy, effortless, or not unduly expensive to behave more ecologically, attitudes predict behavior reasonably well. However, when the constraints or costs are high, the concordance between attitudes and behaviors is weak. The role of social marketing in affecting behavior, based on many of the principles described here, is discussed in Chapter 28.
No one strategy is singularly effective in promoting pro- environment behavior. The effectiveness of an intervention can vary depending on the type of behavior being targeted, whether that behavior takes place at home or in public, how much effort or forethought the behavior requires, the existence of individual as well as collective efficacy to engage in the behavior(s), and other factors, including financial cost. As with promoting health behaviors such as physical activity, there is general agreement that educational strategies (intended to increase environmental concern, change attitudes, or instruct people how to change behavior), while beneficial, are not sufficient to promote pro-environment behaviors. Indeed, many strategies work better in combination—such as specific instructions on how to engage in the desired behavior combined with goals, or prompts combined with reconfiguring the environment to make a behavior easy (Osbaldiston & Schott, 2012).
Light and Color Most psychological research on light and color focuses on aesthetic preference. However, there is also some evidence relating to health and behavior.
Aesthetic Preference People universally prefer natural light, and most people dislike fluorescent light relative to incandescent lighting or daylight. As any theatergoer or movie buff can attest, lighting is also a powerful
490
contributor to mood. With respect to color, people vary more, with some evidence of preference for the blue-green part of the spectrum. With regard to facial color, people universally prefer redder skin hues, perhaps because this connotes health, and red clothing on a potential mate is seen as sexually attractive, particularly among male viewers (Elliot & Maier, 2014). In contrast, with regard to objects, some market research suggests that blue attracts attention. Other than facial color, the cross-cultural extent of these preferences is unclear. Consistent with an environmental psychology perspective on indirect effects, gender, immediate context (say, fighting or flirting), and culture may moderate the impacts of color on human behavior.
Health and Behavior Light affects comfort, health, and well-being in several ways, ranging from transient symptoms to more troubling ailments. Eye strain results when fluorescent lights flicker at a slow rate, and glare is a reliable cause of physical discomfort. Text legibility is a function of luminance (brightness), contrast, font size, and the age of the viewer. Gender and culture do not appear to matter for the influence of light on performance. Age, however, is a powerful factor. As individuals age they need more luminance and contrast to maintain comparable legibility relative to a younger person, but regardless of age, there is a nonlinear relation between legibility and performance, with diminishing gains as luminance and contrast increase. Another major health impact of inadequate lighting is falls, particularly among older people (Gifford, 2014; Veitch, 2006). Eyestrain at work, particularly with the widespread use of visual displays, is epidemic, with close to half of all office workers reporting visual discomfort from their work settings.
The visual system consists of two major components. Up to now we have focused on aspects of light and color in relation to retinal photoreceptors (rods and cones). A second visual pathway links the eye with the hypothalamus and regulates the hormone melatonin. During the hours of daylight, melatonin is low, and as the sky becomes darker, melatonin increases. This process of the entraining or setting of the biological clock by melatonin happens in an approximate twenty-four-hour, circadian cycle, and is ubiquitous in animals, including human beings. The visual spectrum also affects
491
melatonin, with blue light increasing and red light suppressing melatonin (Gifford, 2014; Veitch, 2006). Circadian rhythms are critical for sleep quality, mood, human performance, and as described next, mental health.
The activating properties of light are well documented in relation to a form of depression, seasonal affective disorder (SAD). Insufficient exposure to daylight can cause feelings of negative affect, low energy, and anxiety or worry among some people. Experimental work and epidemiological studies provide converging evidence for SAD. Exposure to full spectrum lighting at high intensity reduces SAD. One example of field research findings is that seasonal variability in depressive symptoms occurs in both the northern and southern hemispheres and is more dramatic farther from the equator. In studies of populations near the equator, with minimal annual fluctuation in hours of daylight, rates of SAD are close to zero. Children in Swedish nursery schools, however, show predictable changes in exposure to daylight, melatonin, and the stress hormone cortisol during the winter compared to the spring and fall. One open question remains why some people appear to be more vulnerable than others to these effects of luminance on affect and mental health. There is also good evidence for reduced pain symptoms, use of medications, and recovery time in postsurgical patients whose hospital rooms have more daylight (Gifford, 2014). The potential interplay between daylight exposure, circadian rhythms, and the hypothalamic-pituitary-adrenal axis and psychological stress is a topic worthy of future research. Cortisol, one of the major stress hormones, also follows a circadian rhythm and has important health consequences. Research described in Chapter 25 also indicates that not only the amount of daylight but also access to the natural environment, and the qualities of views, matter for mental well-being and pain recovery.
At this point we know much less about the effects of color on human health and behavior than we do about the effects of light. The red end of the visual spectrum increases brain activity, indicative of higher physiological arousal or wakefulness (Elliot & Maier, 2014). Until recently, little reliable impact of color on human behavior was discernable, despite media claims to the contrary. There is emerging evidence that, on the one hand, red is a cue for dominance, particularly among males, and thus can enhance competitive
492
performance in sports as well as games. Red also evokes avoidance motivation and can undermine performance on tasks requiring cognitive flexibility (e.g., analogies, reasoning, creativity). Blue, on the other hand, may facilitate performance on such tasks, particularly those requiring creativity. The evidence for adverse red effects on challenging, complex tasks is stronger than for beneficial blue impacts on creative tasks. Blue, in contrast to red, may evoke motivations to connect and socially bond with those around us. As Elliot and Maier (2014) note, context is critical in understanding how color can influence human behavior. Red in one context may heighten attraction and desire and in another increase avoidance and feelings of danger or threat.
493
So What? Interventions That Work Environmental Psychology Reduces Crime: Creation of Mini-Neighborhoods in Five Oaks The Five Oaks neighborhood in Dayton, Ohio, was in crisis. Violent crime had increased by 77%, robberies by 76%, vandalism by 38%, and overall crime by 16%. In addition, drug dealers, pimps, and prostitutes had taken over the streets, and gunshots were heard at all hours, day and night (Newman, 1996, pp. 31–32). The value of homes in the neighborhood had dropped by 11% in one year, at the same time that regional values had increased by 6%. Analysis indicated that of the neighborhood's total traffic volume, 35% was cutting through the neighborhood, rather than going to a destination in the neighborhood. Through a collaborative process with city planners and citizens, Oscar Newman, an architect and planner, developed a plan to create mini-neighborhoods within Five Oaks. This was accomplished by restructuring the streets through the installation of gates that closed off selected streets (Figure 9.5). These changes limited vehicular access and enabled residents to regain control of their streets. With means of entrance and egress limited to one side of each mini-neighborhood, drug dealers and their clients would think twice about doing business there.
494
Figure 9.5 The Five Oaks Neighborhood Following the Defensible Space Intervention
Source: Newman, 1999–2009.
Within a year of the intervention creating mini-neighborhoods, cut- through traffic was reduced by 67%, overall traffic volume dropped by 36%, and traffic accidents declined by 67%. Moreover, a survey of residents revealed that 73% thought there was less traffic. Overall crime dropped by 26% and violent crime dropped by 50%, and 53% of residents perceived that there was less crime. Housing values were up by 15% in Five Oaks in the first year, compared to 4% regionally (Newman, 1996). A survey of defensible space interventions found a 30% to 84% reduction of robberies following the design changes (Casteel & Peek-Asa, 2000).
Environmental Psychology Reduces Infections in Hospitals: Design and Hospital Hand Washing One in twenty-five patients in U.S. hospitals acquires an in-hospital infection, resulting in approximately 75,000 deaths annually (CDC, 2015). A simple, proven strategy to reduce infection rates is hand washing. However, despite considerable effort to educate medical
495
staff about the essential role of hand hygiene in combatting nosocomial infections, compliance rates have proven resistant to change, leading researchers to consider design interventions that might lead to greater compliance. Two examples demonstrate how environmental design interventions can address this serious public health challenge.
David Birnbach and colleagues (2010) randomly assigned fifty-two physicians to examine a patient in one of two full-scale, simulated patient rooms differing only in the location of the alcohol rub dispenser. As shown in Figure 9.6, in one condition the dispenser was directly in the health care provider's line of vision when examining the patient. In the other condition the dispenser was immediately adjacent to the door upon entering the room and not in the direct line of vision either upon entry or when examining the patient. The placement of the dispenser adjacent to the doorway is typical for many patient rooms. When the dispenser was directly in their line of sight, 54.8% of physicians sanitized their hands. When it was in the typical location, the rate was 11.5%.
Figure 9.6 Location of Hand Cleaner Dispenser in Patient Room: In Line of Sight (left) and Inside the Door (right)
Source: Left-hand photo appears courtesy of D. J. Birnbach et al., used with permission. Right-hand photo is from Munro, 2013.
In another study, Venkatesh and colleagues (2008) compared the use of hand sanitation devices located, similar to one room in the Birnbach study, adjacent to the doorway entry. Over several intermittent, four-day periods, during day and night shifts, and across twelve different hospital patient rooms, medical staff compliance was monitored automatically, comparing the traditional
496
hand sanitizing dispenser to the same dispenser with an added auditory alarm. Inclusion of the alarm raised hand hygiene compliance rates from 36.3% to 70.1%. Infections with vancomycin- resistant Enterococcus, a primary cause of nosocomial infections, dropped from 4.7 per month in the six-month period without alarms to 1.0 during the six-month period with alarmed hand sanitation dispensers. Of additional interest, when the patient room was in direct visual sight of a nurses station, compliance was also higher. Furthermore, the alarmed hand sanitizer dispenser was twice as effective in patient rooms not directly visible from a nurses station.
Environmental Psychology Saves Energy Electricity use is associated with a range of environmental impacts, from air pollution to climate change, that in turn threaten health. Energy conservation programs have the potential to reduce environmental and health impacts, as well as to avoid construction of costly new electricity generation plants to meet demand. While there have been some gains in energy conservation from the adoption of more efficient equipment, the number of appliances and electronics using electricity is growing. Rebates and other incentive programs to encourage conservation can be expensive. Governments and utilities have sought low-cost ways to motivate residential electricity users to conserve.
Working with software firm OPOWER, twelve utilities in several regions of the United States participated in large, randomized field experiments, with 600,000 households assigned to treatment or control groups (Allcott, 2011). Households in the treatment group received a monthly or quarterly home energy report that included two modules: social comparison and action steps (Figure 9.7). The social comparison module used descriptive norms to compare a customer's energy use to mean household energy use and to a comparison group of 100 similar homes nearby. Residents were told their energy usage was great (accompanied by two smiley faces), good (one smiley face), or more than average. The action steps module comprised three categories: quick changes (e.g., reduce brightness on televisions), purchases with some cost (e.g., occupancy sensors), and longer-term investments (e.g., a high- efficiency washing machine). On average, residents in the treatment
497
group reduced monthly electricity consumption by 2%, a number comparable to other energy conservation programs, and the reductions were durable over a two-year testing period. The experiment was based in part on research by Robert Cialdini and others demonstrating the effective use of social norms to bring about pro-environment behavior relative to littering, theft in national parks, and recycling (Cialdini, 2003)—an approach that aligns with the heuristic presented in Chapter 28: “Make the behavior you are promoting easy, fun, and popular.”
Figure 9.7 A Utility Bill Employing Social Norms to Encourage Energy Conservation
Source: Xcel Energy, 2015.
498
Summary Our environment has profound effects on our behavior and our health. In this chapter we have considered ways in which environmental psychology and environmental toxicology, the traditional environmental health model, differ in their approaches when considering similar fundamental questions. Environmental psychology tends to employ a broader ecological perspective, often looking across contexts. Outcomes in environmental psychology research are often psychological rather than physiological. Environmental psychologists, like contemporary public health researchers, focus on both pathogenesis and salutogenesis, while toxicologists are mostly interested in the origins of disease. Environmental psychologists consider synergistic effects of the environment, while toxicologists usually study singular effects. The dynamic coping strategies employed by humans are often represented in environmental psychology models whereas environmental toxicologists tend to view humans as largely passive organisms. Similarly, environmental psychologists often examine indirect effects of the environment as well as the moderating effect of people's personal characteristics, while most toxicological models examine one-to-one direct functions.
More broadly, environmental psychology and public health also have a great deal in common and in the past two decades have converged in their approaches to research and practice. Both fields recognize the sometimes subtle, sometimes overt influence that the built, natural, and social environments can have on human health and well-being. Both environmental psychology and public health increasingly employ an ecological perspective, examining complex, dynamic systems across time and space. Both are concerned about rigorous examination of causal links between environmental characteristics and human health and welfare, but they also recognize some of the serious challenges to validity when single causes are isolated and considered apart from the natural ecological web in which environment-human relations are typically embedded. In addition, both fields are prevention oriented, with a focus on health promotion as much as disease prevention.
499
Key Terms accessibility
The ability to be used easily; healthy foods have accessibility when they are in a form and location that makes consumption easy (cf. availability).
active transport A means of travel that entails physical activity, such as walking or cycling.
affect Emotion, feeling.
affordance A potential use or function that resides in the relationship between a person and an environmental feature. For example, stairs offer many people the affordance of walking from one floor to another.
availability The quality of being present in the environment: for example fruits and vegetables being present at home, at school, or in the neighborhood (cf. accessibility).
behavior settings Physical and social contexts in which behaviors occur.
broken windows hypothesis The idea that decay and disorder (e.g., litter, vandalism) will lead to more decay and disorder.
cognitive map A mental representation of the physical world: for example, of a building, campus, or city. Characteristics of the environment can foster or hinder the development of a cognitive map.
crime prevention through environmental design (CPTED) Use of physical design to deter criminal behavior (closely related to defensible space).
crowding A psychological phenomenon, when a person feels “crowded”; differs from density which can be objectively measured as the number of people per square foot or per acre.
500
defensible space A type of space created through the use of environmental characteristics that promote safety and deter crime. The idea was developed by Oscar Newman and is closely related to crime prevention through environmental design (CPTED).
environmental stress The response that occurs when environmental demands exceed a person's coping resources. Stress can result in physiological changes as well as behavioral responses such as anxiety, perceived distress, and diminished ability to stay on task.
focal points Areas or objects that draw people together and foster social interaction (e.g., in a workplace, a coffee pot or the mailroom).
layout In an open-plan layout, large spaces are shared and flexible partitions may be used to delineate activity zones; a closed-plan layout uses permanent walls and doors to divide space into rooms.
learned helplessness The belief that no amount of effort will succeed in overcoming difficult circumstances.
legibility A quality of built environment characteristics that are “readable” and that facilitate the creation of a cognitive map and are thus easy to navigate.
normative Typical; the usual, customary practice or behavior.
personal space A portable territory people carry with them.
proxemics The study of the ways space is used to communicate nonverbally.
recreational A term applied to physical activity carried out for fun or exercise, such as going for a jog (cf. utilitarian).
seasonal affective disorder (SAD) Depression that varies by season and is due to lack of sunlight exposure.
501
social capital The aggregate social relationships and networks that serve as the “glue” among people, featuring shared values and behavioral norms such as trust and reciprocity, and that promote mutually advantageous social cooperation.
social comparison An approach to motivating behavior change that provides people with information about what others, such as neighbors, are doing.
sociofugal Describes physical spaces that discourage social interaction; encourage solitary activity. (cf. sociopetal).
sociopetal Describes physical spaces that foster social interaction (cf. sociofugal).
territoriality A sense of spatial ownership made visible (e.g., a fence around one's home or an article of clothing used to “reserve” a chair in a public space). It may apply to personal territory, group territory (i.e., space used by a subset of qualified users), and public territory.
utilitarian A term applied to physical activity that is incidental to completing a task, such as laying bricks (cf. recreational).
wayfinding Navigation, or finding one's way through an environment such as a building, campus, or city.
502
Discussion Questions 1. Think back to your first day on your campus. Was it difficult to
navigate? How did that feel? What helped you learn your way around and feel more oriented in getting from place to place? What cues or features might have made you feel more oriented, and also have made it easier to navigate initially?
2. Consider the route you take most often from home to school. Is your commute stressful or relaxing? Why? What kind of information do you absorb along the way? Do you isolate yourself from others (say, by listening to music), or do you interact with others? What options are available to you on this route (fast food restaurants, nature views, and so on)? How does each of these contextual factors affect your mood, your expectations about the day ahead, your readiness to learn, and your overall health?
3. In what settings do you usually interact with classmates and friends? Do those settings facilitate socializing? Why or why not?
4. Think of a recent incident in which you felt excessively exposed to crowding, noise, or poor lighting. How did you react? How do you think others around you reacted? Can you think of environmental interventions that would have made that setting less stressful?
5. What environmental cues affect your choices of food? Nutritional content labels? Displays on store shelves? Seeing what other people are eating? Serving size? Others? Please describe a recent food choice you made that was affected by one or more of these factors.
503
References Allcott, H. (2011). Social norms and energy conservation. Journal of Public Economics, 95(9), 1082–1095.
Becker, F. D., & Steele, F. (1995). Workplace by design: Mapping the high-performance workscape. San Francisco: Jossey-Bass.
Bilotta, E., & Evans, G. W. (2013). Environmental stress. In A. E. Steg, A. van den Berg, & J.I.M. deGroot (Eds.), Environmental psychology (pp. 27–35). London: BPS Blackwell.
Birnbach, D., Nevo, I., Scheinman, S., Fitzpatrick, M., Shekhter, I., & Lombard, J. (2010). Patient safety begins with proper planning: A quantitative method to improve hospital design. Quality and Safety in Health Care, 19(5), 462–465.
Braubach, M., Jacobs, D. E., & Ormandy, D. (Eds.). (2011). Environmental burden of disease associated with inadequate housing: Methods for quantifying health impacts of selected housing risks in the WHO European region. Summary report. Copenhagen: WHO Regional Office for Europe.
Brown, B. B., & Werner, C. M. (2008). Before and after a new light rail stop: Resident attitudes, travel behavior, and obesity. Journal of the American Planning Association, 75(1), 5–12.
Caspi, C. E., Sorensen, G., Subramanian, S., & Kawachi, I. (2012). The local food environment and diet: A systematic review. Health & Place, 18(5), 1172–1187.
Casteel, C., & Peek-Asa, C. (2000). Effectiveness of crime prevention through environmental design (CPTED) in reducing robberies. American Journal of Preventive Medicine, 18(4), 99– 115.
Centers for Disease Control and Prevention. (2015). Healthcare- associated infections (HAIs). Retrieved from http://www.cdc.gov/HAI/surveillance/index.html
Cialdini, R. B. (2003). Crafting normative messages to protect the environment. Current Directions in Psychological Science, 12(4),
504
105–109.
Cohen, S., Kessler, R. C., & Gordon, L. U. (1997). Measuring stress: A guide for health and social scientists. New York: Oxford University Press.
Dannenberg, A. L., Frumkin, H., & Jackson, R. J. (2011). Making healthy places: Designing and building for health, well-being, and sustainability. Washington, DC: Island Press.
De Young, R. (2000). New ways to promote proenvironmental behavior: Expanding and evaluating motives for environmentally responsible behavior. Journal of Social Issues, 56(3), 509–526.
Edelstein, M. R. (1988). Contaminated communities: The social and psychological impacts of residential toxic exposure. Boulder, CO: Westview Press.
Elliot, A. J., & Maier, M. A. (2014). Color psychology: Effects of perceiving color on psychological functioning in humans. Annual Review of Psychology, 65, 95–120.
Evans, G. W. (2001). Environmental stress and health. In T. Baum, T. Revenson, & J. E. Singer (Eds.), Handbook of health psychology (pp. 365–385). Hillsdale, NJ: Erlbaum.
Evans, G. W. (2004). The environment of childhood poverty. American Psychologist, 59(2), 77.
Evans, G. W. (2006). Child development and the physical environment. Annual Review of Psychology, 57, 423–451.
Evans, G. W., Lepore, S. J., & Allen, K. M. (2000). Cross-cultural differences in tolerance for crowding: Fact or fiction? Journal of Personality and Social Psychology, 79(2), 204–210.
Evans, G. W., Li, D., & Whipple, S. S. (2013). Cumulative risk and child development. Psychological Bulletin, 139(6), 1342–1396.
Evans, G. W., & McCoy, J. M. (1998). When buildings don't work: The role of architecture in human health. Journal of Environmental Psychology, 18(1), 85–94.
Evans, G. W., Wells, N. M., & Moch, A. (2003). Housing and mental
505
health: A review of the evidence and a methodological and conceptual critique. Journal of Social Issues, 59(3), 475–500.
Evans, G. W., Wells, N. M., & Schamberg, M. A. (2010). The ecological context of SES and obesity. In L. Dube, A. Bechara, A. Dagher, D. Drewnowski, J. LeBel, J. P. James,…R. Y. Yada (Eds.), Obesity prevention: The role of brain and society on individual behavior. New York: Elsevier.
Gifford, R. (2014). Environmental psychology: Principles and practice (5th ed.). Colville, WA: Optimal Books.
Glass, D. C., & Singer, J. E. (1972). Urban stress. New York: Academic Press.
Gorman, N., Lackney, J. A., Rollings, K., & Huang, T.T.K. (2007). Designer schools: The role of school space and architecture in obesity prevention. Obesity, 15(11), 2521–2530.
Hall, E. T. (1966). The hidden dimension. Garden City, NY: Doubleday.
Hanks, A. S., Just, D. R., & Wansink, B. (2013). Smarter lunchrooms can address new school lunchroom guidelines and childhood obesity. Journal of Pediatrics, 162(4), 867–869.
Hannon, J. C., & Brown, B. B. (2008). Increasing preschoolers' physical activity intensities: An activity-friendly preschool playground intervention. Preventive Medicine, 46, 532–536. doi:10.1016/j.ypmed.2008.01.006
Hartig, T., & Lawrence, R. J. (2003). Introduction: The residential context of health. Journal of Social Issues, 59(3), 455–473.
Jones-Rounds, M. L., Evans, G. W., & Braubach, M. (2013). The interactive effects of housing and neighbourhood quality on psychological well-being. Journal of Epidemiology and Community Health, 68(2), 202–431.
Kawachi, I., & Berkman, L. (2000). Social cohesion, social capital, and health. In L. F. Berkman & I. Kawachi (Eds.), Social epidemiology (pp. 174–190). New York: Oxford University Press.
Kerr, J., Sallis, J. F., Owen, N., De Bourdeaudhuij, I., Cerin, E.,
506
Sugiyama, T.,…Mitás, J. (2013). Advancing science and policy through a coordinated international study of physical activity and built environments: IPEN adult methods. Journal of Physical Activity and Health, 10(4), 581–601.
Maxwell, L. E. (1996). Multiple effects of home and day care crowding. Environment and Behavior, 28(4), 494–511.
McGrath, J. J., Matthews, K. A., & Brady, S. S. (2006). Individual versus neighborhood socioeconomic status and race as predictors of adolescent ambulatory blood pressure and heart rate. Social Science & Medicine, 63(6), 1442–1453.
Moore, R. C., & Cosco, N. G. (2014). Growing up green: Naturalization as a health promotion strategy in early childhood outdoor learning environments. Children, Youth and Environments, 24(2), 168–191.
Morland, K., Wing, S., & Diez Roux, A. (2002). The contextual effect of the local food environment on residents' diets: The Atherosclerosis Risk in Communities study. American Journal of Public Health, 92(11), 1761–1768.
Morland, K., Wing, S., Diez Roux, A., & Poole, C. (2002). Neighborhood characteristics associated with the location of food stores and food service places. American Journal of Preventive Medicine, 22(1), 23–29. doi:10.1016/S0749-3797(01)00403-2
Munro, M. (2013). Nightmare microbes could end the “antibiotic miracle.” Retrieved from https://margaretmunro.wordpress.com/2013/12/02/nightmare- microbes-could-end-the-antibiotic-miracle/#more-918
Newman, O. (1972). Defensible space. New York: Macmillan.
Newman, O. (1996). Creating defensible space. U.S. Department of Housing and Urban Development (HUD), Office of Policy Development and Research. Retrieved from http://www.huduser.org/publications/pdf/def.pdf
Newman, O. (1999–2009). Defensible space (Web site). http://www.defensiblespace.com/book/cases.htm
507
Osbaldiston, R., & Schott, J. P. (2012). Environmental sustainability and behavioral science: Meta-analysis of proenvironmental behavior experiments. Environment and Behavior, 44, 257–299.
Rollings, K. A., Wells, N. M., & Evans, G. W. (2015). Neighborhood quality review. Manuscript in preparation.
Sallis, J. F., Bauman, A., & Pratt, M. (1998). Environmental and policy interventions to promote physical activity. American Journal of Public Health, 15(4), 379.
Slum surgery in St. Louis. (1951). Architectural Forum, 94(4), 128– 136.
Slusser, W. M., Cumberland, W. G., Browdy, B. L., Lange, L., & Newmann, C. (2007). A school salad bar increases frequency of fruit and vegetable consumption among children living in low-income households. Public Health Nutrition, 10(12), 1490–1496.
Smith, G. D., Hart, C., Watt, G., Hole, D., & Hawthorne, V. (1998). Individual social class, area-based deprivation, cardiovascular disease risk factors, and mortality: The Renfrew and Paisley Study. Journal of Epidemiology and Community Health, 52(6), 399–405.
Smith, W. R., Moore, R. C., Cosco, N. G., Wesoloski, J., Danninger, T., Ward, D. S.,…Ries, N. (2014). Increasing physical activity in childcare outdoor learning environments: The effect of setting adjacency relative to other built environment and social factors. Environment and Behavior. Advance online publication. doi:10.1177/0013916514551048
Solari, C. D., & Mare, R. D. (2012). Housing crowding effects on children's wellbeing. Social Science Research, 41(2), 464–476.
Stern, P. C. (2000). New environmental theories: Toward a coherent theory of environmentally significant behavior. Journal of Social Issues, 56(3), 407–424.
Story, M. T., Kaphingst, K. M., Robinson-O'Brien, R., & Glanz, K. (2008). Creating healthy food and eating environments: Policy and environmental approaches. Annual Review of Public Health, 29, 253–272.
508
Tan, M. (2012). Long waiting time for buses causes displeasure in TP students. Red Dot Gazette, February 9. Retrieved from https://reddotgazette.wordpress.com/2012/02/09/long-waiting- time-for-buses-cause-displeasure-in-tp-students
Taylor, R. B., & Harrell, A. (1996). Physical environment and crime. Washington, DC: U.S. Department of Justice, Office of Justice Programs, National Institute of Justice.
UW Recycling, University of Washington. (n.d.) MiniMax. Retrieved from http://www.washington.edu/facilities/building/recyclingandsolidwaste/minimax
Veitch, J. (2006). Lighting for high quality workplaces. In D. J. Clemets-Croome (Ed.), Creating the productive workplace (2nd ed., pp. 206–222). London: Taylor & Francis.
Venkatesh, A. K., Lankford, M. G., Rooney, D. M., Blachford, T., Watts, C. M., & Noskin, G. A. (2008). Use of electronic alerts to enhance hand hygiene compliance and decrease transmission of vancomycin-resistant Enterococcus in a hematology unit. American Journal of Infection Control, 36(3), 199–205.
Wells, N. M., Ashdown, S. P., Davies, E.H.S., Cowett, F. D., & Yang, Y. (2007). Environment, design and obesity: Opportunities for interdisciplinary collaborative research. Environment and Behavior, 39(1), 6–33.
Wells, N. M., Evans, G. W., & Yang, Y. (2010). Environments and health: Planning decisions as public health decisions. Journal of Architectural and Planning Research, 27(2), 124–143.
Wells, N. M., & Jimenez, F. E. (In press). Nature's impact on children's health. In W. Bird & M. Van den Bosch (Eds.), Oxford Textbook of Nature and Public Health.
Wener, R. E., & Evans, G. W. (2007). A morning stroll: Levels of physical activity in car and mass transit commuting. Environment and Behavior, 39(1), 62–74.
Winter, D., & Koger, S. (2004). The psychology of environmental problems (2nd ed.). Mahwah, NJ: Erlbaum.
509
Wrigley, N., Warm, D., & Margetts, B. (2003). Deprivation, diet, and food-retail access: Findings from the Leeds “food deserts” study. Environment and Planning A, 35(1), 151–188.
Xcel Energy. (2015). Conservation by peer pressure (Web log post). http://connect.xcelenergy.com/minnesota/conservation-by-peer- pressure
510
For Further Information Textbooks In addition to Gifford (2014), listed in the References, see the following:
Bell, P. A., Greene, T. C., Fisher, J. D., & Baum, A. (2005). Environmental psychology. Hove, U.K.: Psychology Press.
Clayton, S. D. (2012). The Oxford handbook of environmental and conservation psychology. New York: Oxford University Press.
Koger, S. M., & Winter, D. D. (2010). The psychology of environmental problems: Psychology for sustainability (3rd ed.). New York: Taylor & Francis.
Steg, L., van den Berg, A. E., & de Groot, J.I.M. (Eds.). (2012). Environmental psychology: An introduction. Hoboken, NJ: Wiley- Blackwell.
Journals Environment and Behavior: http://eab.sagepub.com
Health & Place: http://www.journals.elsevier.com/health-and- place
Journal of Environmental Psychology: http://www.journals.elsevier.com/journal-of-environmental- psychology
Organizations and Web Sites Environmental Design Research Association: http://edra.org. An international, interdisciplinary association of design professionals, social scientists, and others, focused on social aspects of the environment.International Association for People- Environment Studies: http://iaps-association.org. An international, interdisciplinary association of social scientists, geographers, design professionals, and others, focused on people's interaction with their environment.
511
Society for Environmental, Population and Conservation Psychology: http://www.apa.org/about/division/div34.aspx. This society is Division 34 of the American Psychological Association.
512
Chapter 10 Environmental Health Ethics
Andrew Jameton and Howard Frumkin
During the preparation of this chapter Dr. Jameton served as a board member of Physicians for Social Responsibility, and of City Sprouts, a community gardening project in Omaha. Dr. Frumkin's disclosures appear in the front of this book in the section entitled “Potential Conflicts of Interest in Environmental Health: From Global to Local.”
513
Key Concepts Principles of ethics and morals go beyond empirical concerns; they establish normative values to guide judgment, decisions, and conduct.
Three central ethics concepts are scientific integrity, justice, and human welfare.
Many professions publish a code of ethics outlining the main ethical ideals and standards of the profession.
Environmental health ethics responsibilities are growing in parallel with the profession's expanding scope.
Measures indexing public health benefits to environmental costs can provide ethically appropriate data for setting priorities.
Environmental health practitioners play an increasingly fundamental role in mediating between the current and long- term health needs of humans and the natural world.
Environmental health professionals have an important responsibility to advocate the sustainability of human and environmental health in all activities.
514
Defining Ethics and Morals Ethics can be defined most conveniently in contrast with morals. The term morality, or morals, refers to a person's or a society's core beliefs regarding what is most important, valuable, or right with regard to conduct and character. The term ethics refers to a more formal version of morality. Ethics can mean
A reasoned or systematic approach to figuring out what is the right or wrong action or position.
Professional morality, as expressed in widely accepted codes and statements, in contrast to personal morality.
The scholarly study of morality by philosophers.
When ethical challenges arise in professional life, people may need to make use of any of these formal concepts of morality. Because ethics is mostly discussed when making decisions, ethics is not simply about describing the morality of a person, association, or culture. Instead, it is a normative process of deciding what we ought to do or not do.
Ethics is intrinsically social and not individual. Beginning students of ethics often think of moral beliefs as essentially private, and consider it inappropriate to make moral judgments about the conduct of others. However, people are social creatures, and most environmental health decisions involve and affect many people and the environment. Accordingly, what is “right” in environmental health can never be simply the opinion of a single individual.
When we make decisions we always go beyond the bare facts and use language and ideas that cannot be resolved entirely by scientific methods. Nevertheless we can think objectively to some degree in ethics. Thinking objectively in ethics is usually characterized by
Being reasonable and not doctrinaire
Listening actively to others
Letting the best reasons determine judgments
Remaining calm and optimistic in the face of controversy
Being realistic about the situations and choices that we face
515
Considering the approaches of other cultures involved in the situation
Ethics can be challenging in that its statements and discussions are less precise than the language of scientific discussion and are open to persistent controversies. Nevertheless, we all need to have a sense of integrity and meaning in our daily lives, and there is no way to achieve this without considering our actions in a broad moral context.
516
The Modern Philosophical Background Philosophical Ethics Principles and Consensus In their study of ethics, philosophers generate theories and ideas useful in resolving disagreements. These resources vary widely in style and origin, with a rich and nuanced vocabulary of concepts, principles, and values. To simplify things, philosophical ethics typically follows a format that emphasizes a small number of core values or principles. Some approaches get by with just one central idea, such as utilitarianism or the Golden Rule, but most include roughly half a dozen central ideas.
Followers of such systems embrace and interpret the remaining moral ideas in terms of the central ones. So a community that holds hospitality as central might extend that notion to imply ecosystem protection. In contrast, a system with respect for individuals at the center might uphold hospitality as a secondary consequence. Then a community generally relates a history or narrative that explains the importance and coherence of the central values and helps to interpret them in specific cases.
Ethics has its roots in ancient philosophy, but in complex, modern societies, with technology posing dilemmas that would have been unimaginable to ancient philosophers, traditional morality may provide little guidance. Moreover, our contemporaries are more than just citizens; they often have professional identities—nurse, lawyer, scientist, public health professional—that entail specialized knowledge, defined roles in society, and consequent responsibilities. These developments have given rise to modern ethics. Modern ethics holds that people and societies generally share certain attributes: they uphold key rules that value human life, promote reciprocity, set conditions of praise and blame, control access to resources, define kinship structures, and promote caring for the sick and educating the young (D. E. Brown, 1991). Modern ethics acknowledges that religions and cultures vary in how they handle these concerns and which ones they make central, but also holds that if we follow human reason and strive to be culturally neutral, we can achieve substantial agreement among cultures and nations.
One narrative element is that human history is so full of violent
517
societal and religious conflicts that we must rise above local cultures to find agreement on an increasingly crowded globe. The hope is that human reason and the best side of our natures will prevail.
Modernity has limits. Philosophers disagree about which modern principles to make central, and different formulations of principles generate inconsistent decisions. Text Box 10.1 mentions a few prominent moral theories. As we shall see, many of these contribute to environmental ethics thinking, and are applicable to environmental public health.
518
Text Box 10.1 Selected Ethics Approaches
Deontology: The position that individual autonomy is key, but that responsible choice requires obedience to a common moral law.
Utilitarianism: The position that the right act is that which maximizes the likely balance of happiness over unhappiness.
Bioethics: A set of principles for health care ethics, emphasizing beneficence, nonmaleficence (avoiding harm), respect for patient autonomy, and justice.
Feminist ethics: An approach to modern ethics based on principles of equality and justice, with a critique of patriarchy, gender stereotypes, and dominance.
Care ethics: The principle of care, emphasizing that process and relationships, not abstract principles, should dominate ethics.
Religious ethics: Traditions of belief and community practices that base morality on the authority of spiritual entities, a supreme being, or a cosmic order.
Unlike older traditions that carry with them an extensive history of precedents, modern ethics is often too general and vague to determine decisions about hard cases. The two world wars of the last century and the persistent violence of our own time testify that modern ethics has not prevented violent conflict. Another difficulty is that elites in the West have dominated the formation of modern ethics, resulting in an unbalanced picture from a global perspective. As environmental health concerns become more global, the hoped- for universal ethics looks more parochial. Broad modern ethics principles overlook such traditional moral concepts as hospitality, reciprocity, loyalty, kinship, material modesty, democracy, solidarity, collective planning, piety, and a spiritual view of nature.
Despite disagreement, there are certain points to which we can give
519
durable answers. First, morality and ethics are universal among societies, natural to humans, and an important part of the normal personality. As Socrates said, “No one knowingly does wrong.” Morality performs an important species function in upholding idealism and cooperation in balance against our tendencies toward envy, violence, and shortsightedness.
Philosophers also agree that ethics needs organizations to back it up. Organizations provide education in basic principles, flexible responses to change, processes for resolving disputes and defining membership, and ways to reward the deserving and punish wrongdoers. Since people are social creatures, ethics is intrinsically social and speaks to individuals with the voice of the community. As a result, most ethicists hold that “we are not made for ourselves alone”—altruism is part of human nature. Purely egoistic theories fit professional ethics poorly because ideals of service are essential for practice. Meanwhile, few theories support pure altruism; instead, they balance care for self and care for others and expect organizations to support this balance. For instance, professionals need to protect their own welfare and that of their organizations if they are to serve others.
Because ethical thinking is inevitably complex and nuanced, it is helpful to consider how to participate gracefully in controversies. Text Box 10.2 offers some ideas.
520
Text Box 10.2 The Art of Ethics Be flexible in appealing to resources and authorities. Modern moral theory, professional ethics, religion, and traditional cultural beliefs are all potentially helpful.
Accept that consensus is not inevitable. Even if a small group of people agree, a larger may not.
Remember that ethics does not determine decisions. Ethics is interpretive, not deductive.
Express key moral concepts briefly, clearly, and gently.
Ethics is on its best behavior when organizing the facts of the issue. Though key, clarifying ethical issues need occupy only a small portion of effort.
Look to prevent disputes from straying into larger doctrinal questions likely to delay resolving the issue at hand.
Always keep service to the communities to whom we are responsible foremost.
Key Modern Ethics Principles Three modern principles of ethics are primary to environmental health: scientific integrity, justice, and welfare.
Scientific Integrity Because public health is grounded in science and evidence, a commitment to scientific integrity is essential. Scientific integrity is closely related to more general notions of honesty and truth- telling (Bok, 1999). Disclosing scientific evidence sometimes stands in tension with such concerns as sharing health data harmful to the reputation of a community, disclosing the health hazards of profitable businesses, and identifying risks not readily apparent to individuals. Where a risk is discovered that needs public attention, honesty requires environmental health professionals to advocate their concerns to each other and the public.
521
Justice In public health, justice is usually framed as social justice, which highlights differences among people that affect health status unfairly or inequitably. Thus discussions of public health often refer to the poorer health statistics for such vulnerable subpopulations as the poor, people with disabilities, and racial and ethnic minorities. One important analysis notes that social justice emphasizes equal treatment across all economic classes, in contrast to market justice, which privileges the well-off (Beauchamp, 1976). Social justice is becoming increasingly salient in light of rising economic inequality within nations and globally (Milanovic, 2011; Piketty, 2014).
Another application of justice is to emphasize basic human rights, defining activities and legal conditions that ensure the basic liberties and material goods needed for a decent life. The United Nations Universal Declaration of Human Rights set the standard for these definitions (United Nations, 1948). The main sections of the declaration are foundational to each of the major organizational divisions of the United Nations.
Welfare Ethics underlies how public health typically gathers, analyzes, and presents data. These standard practices reflect a commitment to a public welfare economics perspective. The statistical approach to public health and welfare is derived from nineteenth-century utilitarianism, the moral theory that each person or organization should choose what, among the various available options, will likely lead to the most human happiness and the least suffering—that is, will maximize expected value.
One of the beauties of utilitarian theory is that it includes justice; each person's happiness or welfare counts, and because there is no reason to think that anyone is capable of much more happiness than another, no one person's happiness outweighs another's (Bentham, 1790/2007).
In line with utilitarian thinking, defined data on health and environment can be combined to help evaluate and guide our approach to public health problems. For example, the Global Burden of Disease project compares the amount of misery caused by a key list of health conditions. The project then uses these estimates
522
to calculate such figures as disability-adjusted life years (DALYs) and healthy life expectancy (HALE) (Murray et al., 2012). These figures are useful globally in identifying the main causes of health problems, committing resources where they are needed, and measuring progress and decline.
523
Professionalism The environmental health professions grew along with the many scientifically based professions of the twentieth century; during that time hundreds of professional and occupational associations in health, environment, and related fields were founded. Establishing ethical principles for professional practice formed an integral part of these professional developments. Text Box 10.3 lists some reasons why professions and ethics intertwine.
524
Text Box 10.3 Professionalism and Ethics Members of Professions…
Provide a socially valued service.
Possess a high degree of independence on the job as a result of their special expertise, and are not easily supervised by others.
Have a skill or craft that if incompetently conducted would be harmful.
Depend on the trust and confidence of clients to function effectively.
Cooperate with members of other disciplines and organizations toward common goals.
The twentieth century marked a period of great achievement in population health. Average global life expectancy grew substantially. The health and environmental professions played active roles in these developments, spurred in part by ideals of progress and a moral commitment to promote health. Professions state their commitments in several formats: some appear as lists in ethics codes, some professional organizations declare themselves simply in an oath or mission statement, and some publish interpretive statements on significant issues affecting their members and their clientele. Text Box 10.4 displays some typical principles.
525
Text Box 10.4 Typical Elements in Professional Codes of Ethics
Dedication to service to communities and populations
Respect for other professionals
Assurance of high levels of competence
Scientific integrity and transparency
Advocacy of sound health principles
Protection of confidentiality
Honesty and integrity in conduct
Disclosure of conflicts of interest
Informed consent and cooperation with clients
Promotion of the profession itself
Association leadership or an ethics committee usually submits its consensus on principles to the membership for approval. The principles simultaneously express idealism and define minimum standards of conduct. Codes are not static; associations continually revise them to clarify their meaning and to respond to new situations, controversies, and technologies. Though not lively reading, codes are valuable and should be read carefully.
Societal, technological, and economic change generate many controversies around environmental health ethics. As time passes, issues open up, settle down for a while, and reopen. A few examples appear in the following paragraphs, and more appear in the discussion questions at the chapter's end. Because codes seldom neatly resolve these questions, we often need to study, and refer to, the background ethics.
Public Regulation of Behavior Versus Individual Freedom A persistent issue facing health professionals has been the extent to which government (and employers) may appropriately manage health behavior and factors affecting health. Motorcyclists who
526
disdain helmets, firearm enthusiasts who loath regulations, smokers uninterested in quitting, and lovers of large soft drinks, together with businesses that profitably encourage these attitudes, have opposed public health interventions in these areas, extolling individual liberty and deriding the “nanny state” (see Text Box 1.2 in Chapter 1). Deciding what to do in particular cases involves complex considerations of respect for individuals, the capacity of communities to avoid exposure, the soundness of the science establishing risks, the level of damage and risk, and the costs of preventing and managing harm.
Nondisclosure Versus the Right to Know Sometimes, professionals are privy to information that an employer or client wants to keep confidential, and they must weigh this against the potential public benefit of disclosing it. Imagine a toxicologist at a chemical company who discovers that one of her employer's products poses a particular danger, or a state health department epidemiologist who discovers an increased risk of birth defects in one county; in both cases the employer might direct the professional not to share this information.
Scientific Research and Public Health Advocacy Because scientists and academics need to maintain their objectivity, and their reputation for it, they are rightly cautious in making claims about the implications of data for behavior and policy. Between “There are some indications this might be dangerous,” and “Wow, this is really dangerous and we should have done something about it years ago,” are sometimes decades of research, data collection, hypothetical explanation, and controversy. Filtered through commerce, media, and politics, advocacy and eventual policymaking may be highly effective, or this process may distort the science and do more harm than good.
Environmental Justice Some policies and practices tend to harm certain groups unfairly. As described in Chapter 11, vulnerable populations may be deprived of access to such assets and services as health care, jobs, education, family planning, transportation, and green space. Politics, economics, and discrimination may result in siting a trash-burning
527
power plant or a bus depot in a low-income community, placing the poor and vulnerable at higher risk than those who are better off.
Common Resources The material conditions of a region may be limited and resources for maintaining basic welfare scarce. Poorly managed common resources may become quickly depleted (Hardin, 1968; Ostrom, 2012). Any arrangement for managing commons is likely to arouse controversy over fairness, prudence, and the authority of the decision makers.
528
Expanding Horizons and Challenges The Role of Fundamental Causes The scope and importance of environmental health expanded during the last century, driven in part by the commitment of the scientific professions to expose the fundamental causes of health problems. As the first principle of the ethics code of the American Public Health Association says, “Public health should address principally the fundamental causes of disease and requirements for health” (Public Health Leadership Society, 2002). Some features of this expanded scope are discussed in the following paragraphs.
Peoples and Cultures Increasing global interconnectedness through technology, communication, organizations, migration, and transboundary health projects has helped to obviate discriminatory assumptions about cultural differences. Rather than accepting cultural relativism (“when in Rome, do as the Romans do”), ethicists interpret local morality within the framework of modern ethics. Regions that discriminate on the basis of race, ethnicity, religion, wealth, sex, disability, or sexual preference don't receive a clean bill of ethics health.
Global Health Ethics Enough universal health challenges have arisen that many issues are best managed globally. Many needed resources that were once in a global commons are becoming scarce or polluted and/or are falling under private ownership. Ethics offers principles for sustainably managing such commons as bodies of water, the atmosphere, and the biosphere (Kinzig et al., 2013; Kolstad et al., 2014). Because the situation is global, so must ethics be global.
Time Frame As issues become globalized, the time frame of environmental health expands, reaching forward and back in time over multiple generations. Looking back, regional differences affecting health status have centuries-long histories. Looking ahead, present
529
practices will have multigenerational consequences. Accordingly, ethics must address such multigenerational issues as our responsibility for future generations (Weston, 2008).
Global Ecosystem The vision of environmental health is coming to embrace the entire planetary ecosystem (see Chapters 2 and 3). This global health vision returns us to the ancient anthropological concept of humanity's situation as expressed in the fourth-century bce work of Hippocrates: We are a species with natural and social needs that maintains itself in a natural context. Ethics must therefore address such issues as our responsibility for stewardship of ecosystem integrity and toward other species.
Sustainability and Resilience As we enter the Anthropocene, a fresh conception of environmental health is emerging. The commitment of environmental health to protect environmental human health is merging with protecting the health of the environment. Chapter 3 describes the concepts of sustainability and resilience—both their origins in environmental functions and their application to human health and equity.
Modern societies generally place a high priority on economic growth, correctly assuming that this usually enhances public health (World Bank, 1993). However, through consumption, expanding population, and pollution, growth is veering into ranges that damage environmental integrity and threaten human health. Public health professionals, including those in environmental health, need to ask how important it is at this point to incorporate the health of the environment into their work. Four main ethical themes arise around this question: our view of the future, our concern for future generations, the ethical standing of nonhuman nature and animals, and how holistic we ought to be as environmental health professionals.
Our View of the Future Since the future is uncertain, we tend to discount our expectations. Many discount the future heavily. In business there is enough uncertainty in the next five years that longer term worries sink to
530
zero. The public health viewpoint differs. Life expectancy and public health infrastructure are multidecadal, and the determinants of health are multigenerational. So, public health concerns extend over many generations. A public health approach to the proper degree of discounting might sometimes be not to discount; what is good for people's health now, such as clean air or biodiversity, will continue to serve into the indefinite future. Moreover, the precautionary principle (see Chapter 26) offers a reminder of how to consider the uncertainty associated with such future projections; it suggests that we should be cautious about taking risks with irreversible consequences.
Next Generations Some argue that since future people can't speak to us, we should not take their views into account. However, we still can and should consider their needs. Moreover, some future generations are already alive. If we add the next two generations to the expected life span of people alive now, we readily encompass over a century of compassion and concern. Some argue that our great-grandchildren are likely to be better off and better able to pay our debts; the counterargument is that in fairness, those who did not incur our costs should not be responsible for paying them (Caney, 2009). Some accept an obligation to no more than their own children and grandchildren; however, given the broad scale of environmental degradation, we cannot safely maintain a legacy for our own offspring without mitigating threats to all children.
The Moral Standing of Nature Well into the twentieth century, philosophical thought distinguished humans sharply from animals. Unlike animals, it was said, we are the reasoning beings; we are conscious; we have a moral nature. However, evidence contradicts this perspective. Our feelings and cognition have evolutionary roots in species with psychological phenomena like ours. Clearly, mammals are capable of pain, intention, social membership, attraction, and in at least some, a sense of morality (Hearne, 1986). We love and care for pets and charismatic wild animals, and contemporary concern for the welfare of farm animals has grown. Moreover, animals and humans have mutual interests. What poisons animals tends to poison humans. As
531
species go extinct, biomes that support human health are degraded. Some argue further that if we are to treat each other empathetically, we need the capacity to care for animals and nature and include them in our community.
Holism and Interconnection To decide whether environmental health should concern itself with the natural world or leave it to the ecologists and engineers, we have to ask how much humans depend on the health of the planet. Why not say that as long as we can kill off natural enemies of humans without hurting ourselves, doing so is all to the good? We could celebrate an end to mosquitoes (the second most dangerous animal), harmful bacteria, and marginally habitable wilderness areas, such as rain forests and deserts. We could terraform the world for total human occupation in towns and cities with our gardens, windmill farms, and animal husbandry.
Biologists and ecologists hold that this analytical view is unrealistic. Collapsing environmental systems are likely to destroy ecological networks supporting us. If so, then environmental health professionals must also respect nature's welfare, including plants and microorganisms that lack evident consciousness but are essential for the ecosystem as a whole, such as plankton, fungi—and even mosquitoes. Under this view, the “safe operating space for humanity” (Steffen et al., 2015), described in Chapter 3, is not only a physical description of limits; it also asserts an ethical mandate.
Climate Change Climate change poses an enormous, and unprecedented, set of environmental health challenges—and consequently, ethical challenges (Garvey, 2008; Gardiner, 2011; D. A. Brown, 2012). These are captured in our three key principles: scientific integrity, justice, and welfare. As for scientific integrity, there is widespread consensus that the planet is warming due to human activity, especially the burning of fossil fuels, as explained in Chapter 12. As for welfare, projected warming will devastate civilizations and public health. And climate change violates justice. The human right to a livable environment will become unattainable, and the poorest of the world and future generations, who have contributed the least to the problem, are being and will be most harmed.
532
Parallel religious principles of stewardship and care reach the same conclusion, and where key ethics principles converge, the main ethical judgment is clear: we must halt climate change. However, ethical examination reveals some remaining issues.
Future Generations What of risks to our great-grandchildren and to the generations that follow? From a scientific perspective, any level of warming reached during this century is likely to persist for thousands of years. At warming rates current from 2015 to 2020, most of the globe could become uninhabitable for mammals by 2300 (McMichael & Dear, 2010). For evolutionary biologists, this is the blink of an eye, but in conventional public health terms, 2300 is far off. We need longer time horizons to address long-range ethical imperatives (Weston, 2008). How long is the time frame that should shape our commitment of public health resources?
Discounting Climate change requires us to reassess discounting (Beckerman & Hepburn, 2007; Stern, 2007). Discounting usually involves specifying a steady annual rate over an interval. But it is essential to bring climate change under control during present decades. So a more discrete and nonlinear approach is needed for valuing future risks. The decades from now into the middle of the century are crucial, especially up front.
Technological Prospects The prospects of technological solutions are not merely a question of prediction but also a philosophical matter of optimism and faith in progress. There are reasons for pessimism: most technological progress in the last few centuries has relied on fossil fuels; it often takes generations for new technologies to spread, and there is much more fuel in the ground than can safely be burned (Meinshausen et al., 2009). But the future is not here yet, and we can't know what surprises lie ahead. Many economists project that the costs of scaling up existing alternative energy technologies while phasing out fossil fuels will be manageable (Mountford, 2014).
Meanwhile, there is philosophical disagreement over what alternatives are safe. Some analysts are skeptical about the safety of
533
nuclear power and geoengineering and the manageability of associated risks (Katz, Light, & Thompson, 2003), while others see these technologies as necessary, manageable, and profitable.
Global Justice International climate negotiators are increasingly aware that no agreement is possible without addressing global inequities. Needed equity elements include every nation playing a role in coping with the problem (United Nations Framework on Climate Change [UNFCC], 2014), and nations bearing burdens related to their current contribution to the problem and, more controversially, their past contribution (Athanasiou & Kartha, 2007), their ability to respond, and their ability to help others to cope (UNFCC, 2009). Concern is growing for nations already affected, such as island nations, low-lying countries such as Bangladesh, and arid regions.
How should we view these international inequities? One side holds that we should establish equity among nations without considering equity within them. The contrasting view, reflecting the utilitarian idea that each person counts for one, thinks in terms of equal energy access for each person. For energy-rich individuals, this involves reducing and limiting energy consumption, while for the poor more energy is needed (Cox, 2013; Lichtenberg, 2013) (also see Chapter 14). The related concept of contraction and convergence is discussed in Chapter 3.
Consumption Although the estimated financial costs of converting the world to alternative energy are small relative to the overall economy, more materially and ecologically oriented economists take the environmental costs of consumption into account and conclude that we need to limit consumption. Many people have taken this message to heart and are adopting more modest and healthier lifestyles, and many religious and philosophical traditions recommend the same (Thomas, 2011; Francis, 2015).
Can we maintain good health and well-being at low levels of consumption? A few countries maintain high levels of public health at low levels of consumption and environmental cost (Caldwell, 1986; Dwyer, 2009). Their life expectancies approximate the maximum life expectancies in wealthier economies, while their
534
average consumption levels are about a third that of countries with the largest per capita economies. This suggests that ethics and practicality may coexist comfortably, especially if population growth is limited.
Raw Utility University of Chicago professor David Archer asks us to consider this challenge: suppose that my car burns a gallon of gasoline to carry me to work. The drive emits a certain amount of CO2 into the atmosphere. Most of that CO2 leaves the atmosphere in the next few years, but some of it remains for 10,000 years and beyond. During its lifetime in the atmosphere, that CO2 traps 40 million times more harmful atmospheric energy than the amount of energy benefit I get from driving to work (Archer, 2009, pp. 173–174). Now, no utilitarian calculation of expected value can justify my producing 40 million units of harm for each unit of benefit. Of course, Archer's ratio is an energy calculation, not a welfare calculation. But any plausible translation of the energy calculation into utilitarian terms is likely to come down on the side of more harm than good—so my job better be important.
535
Implications for Professional Ethics Climate change exemplifies the large-scale challenges confronted by environmental health professionals—who care about them both in their capacity as citizens and in their professional capacity. How might professional ethics and professional actions evolve in response?
Association Ethics Codes and Statements Association ethics codes are in some cases silent about such challenges as sustainability and global environmental change. Statements of responsibility can be incorporated into such codes. Text Box 10.5 offers samples.
536
Text Box 10.5 Environmental Responsibility Principles in Ethics Codes
We recognize the importance of the natural environment and its long-term stability to human health.
We accept an obligation to work with other professions, disciplines, the public, businesses, and governments to maintain the planet in a condition that affords adequate and equitable levels of human health over the next several generations.
We protect the fundamental right of people and communities to a safe planetary system.
Universities, organizations, and services may also include similar clauses in their mission statements and objectives. Meanwhile, many organizations and associations are publishing specific statements on climate and sustainability.
Environmental Indexing Since it helps to optimize both justice and welfare, setting priorities is not only an operational imperative but also advances ethical practice. Priority setting can be accomplished by evaluating health interventions based not only on their impact on health status and their cost, but also on their environmental impact and their distributional characteristics—the extent to which they reduce social inequities.
Some health interventions are costly in economic and/or environmental terms. Cleaning up toxic materials in the environment requires substantial amounts of energy; water-based sewage systems are more costly than latrine systems; fertilizer- intensive, industrial agriculture contributes to the geochemical flow of nitrogen and phosphorus. Other health interventions may aggravate disparities; for instance, reviving an urban neighborhood with green, transit-oriented development may lead to gentrification that displaces low-income residents. Incorporating these
537
dimensions explicitly may help achieve more ethically sound decisions, including—importantly—environmental protection.
Text Box 10.6 notes some areas in which environmental health is already playing an ethically significant role in exercising environmental responsibility.
538
Text Box 10.6 Environmental Responsibility
Identifying, quantifying, predicting, and publishing the environmental health risks of biodiversity loss.
Analyzing both the health and environmental impacts of various energy policies.
Promoting healthy practices that help to reduce environmental damage, such as the co-benefits of active transportation and local food production.
Promoting environmentally sound practices in the organizations in which we work.
Advocacy There is considerable debate about the propriety of scientists acting as advocates (Nelson & Vucetich, 2009). Some argue that scientists should “stick with the science” and leave policy implementation to policymakers, while others argue that scientists should engage fully in translating science into policy, undertaking advocacy and even activism. Several lines of ethical reasoning support the role of advocacy for professionals in public health: the fact that they are citizens with a right to advocate; the fact that they possess special expertise that qualifies them to weigh in; and the fact that advocacy need not mean abandoning objectivity or scientific integrity (Maccarone, 2005). In advocating for needed changes in public policy, environmental health professionals can advocate directly in policy settings, to other health professionals, and to the public (McCally & Cassel, 1990; Weed & McKeown, 2003). Environmental health advocacy frequently dovetails with advocacy in other sectors; for example, health professionals may find common ground with those who support biodiversity, parks and recreation infrastructure, or green building, and joint advocacy may yield wide-ranging solutions with co-benefits. Advocacy may also appropriately begin “at home,” in health science schools, by supporting the incorporation of global change content into health curricula and promoting institutional conservation of fossil fuels and other
539
resources.
Optimism, Pessimism, and Hope Activists debate how strongly to present the problems and how optimistically to portray plans for action. Gloomy pessimism ensures paralysis, but overenthusiastic optimism seems inauthentic. A cliché in this area is the assertion that “I am not optimistic, but I am hopeful.” In the words of environmental educator David Orr, “Hope, authentic hope, can be found only in our capacity to discern the truth about our situation and ourselves and summon the fortitude to act accordingly” (Orr, 2007, p. 1395), a reminder that environmental health insights, collected and reported with scientific integrity, can be deployed in the service of hope. Indeed, some argue that we have a moral obligation to maintain hope both in ourselves and others (McKinnon, 2014).
540
Concluding Discussion Let us conclude by reviewing the role of ethics in environmental health. Shared philosophical concepts and ethical values provide basic motives for what people generally do, especially in organizations and communities. Philosophy draws on traditions extending over a wide range of cultures over thousands of years. Many of these older societies struggled, as we do now, to maintain their health and stability under changing and dangerous conditions and so have thought about many of the same ethical principles we consider here.
This global conception of environmental health defines a meaningful philosophy grounded in fundamentals: in our planetary biosphere we survive as a species in an environment, on this we build our infrastructure, on that our health, and on that our culture. Atop this pyramid rests an ethical high ground for all environmental health concerns, from global to local. The most basic human right is to a thriving global ecology, and it is the job of environmental health to protect it.
Students just completing their professional degrees and entering public health practice have a likely forty-year span in which to champion environmental health. As it happens, these are the same key decades in which the ethical issues brought forward in this chapter need to be resolved. Thus, these years constitute a special and ethically important time to join the profession.
541
Summary Morality is the set of core beliefs or commitments held by a person or society; ethics is the systematic study and exercise of morals. Ethical issues arise regularly in environmental health. Environmental health ethics rests on a background of comprehensive modern moral theories. Three key ethics principles are scientific integrity, justice, and human welfare. Like other professions, environmental health features codes of professional ethics that enunciate the profession's ethical ideals and standards. During the last century, the scope of environmental health expanded greatly, and new areas of concern, especially sustainability and climate, are raising ethical controversies. Public health and environmental health professions are finding ways to respond ethically to these challenges. Ethically, protection of human environmental health is central to civilizations.
542
Key Terms activism
Vigorous and persistent advocacy for change in politics and organizations.
advocacy Expressing public support for a position, set of facts, or point of view.
autonomy Acting on the basis of choices guided by values and principles that one accepts as one's own.
bioethics The study of ethics in biology and medicine. Also, a set of principles for health care ethics, emphasizing beneficence, nonmaleficence (avoiding harm), respect for patient autonomy, and justice.
care ethics The principle of concern for others, with a priority on process and relationships, not abstract principles.
consumption Individuals' and industries' use of goods, materials, and energy that have environmental costs.
deontology The ethical theory that individual autonomy is key to ethics, but that responsible choice requires obedience to a common moral law.
discount Calculate the importance to present decisions of future consequences by reducing the calculated costs and benefits by a percentage over time.
environmental ethics The study of moral values and principles as they apply to the biosphere and humanity's place in it.
ethics A set of formal approaches to morality, especially, the branch of philosophy dealing with theories of right, wrong, and moral
543
responsibility. expected value
The reduction of the value of a result of an action in proportion to the probability that it will occur.
feminist ethics An approach to modern ethics based on principles of equality and justice, with a critique of patriarchy, gender stereotypes, and dominance.
fundamental cause The most basic and stable explanation of the occurrence of an event or trend.
justice A family of concepts related to fairness, human rights, equity, and equality, applied to individual actions, organizations, and situations.
modern ethics A family of approaches to ethics dominant in Western philosophy since the eighteenth century and emphasizing reasoning and well-defined principles and de-emphasizing appeals to authority.
morality A person's or a society's core beliefs regarding what is most important, valuable, or right with regard to conduct and character.
normative Setting standards and making moral and ethical judgments that go beyond the facts to include goals and choices.
objectivity Adhering closely to observed facts, and in ethics, being reasonable rather than doctrinaire, letting the best reasons determine judgment, being realistic, and maintaining calm in disputes.
precautionary principle As articulated in Principle 15 of the Rio Declaration on Environment and Development, “Where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be used as a reason for postponing cost-effective measures to prevent environmental degradation.”
544
professionalism An organized approach to an occupation that emphasizes high levels of competence and dedication to service to clients and the public.
religious ethics Traditions of belief and community practices that base morality on the authority of spiritual entities, a supreme being, or a cosmic order.
responsibility What one is accountable for, such as an area of concern within one's actions, decisions, or role; assigning praise or blame to other individuals, organizations, and causes acknowledges their accountability.
scientific integrity Maintenance of high standards of research methodology together with fair and honest assessment of authorship, results, conflicts of interest, and the limitations of methods and interpretation.
utilitarianism The position that morally right acts are those that maximize the likelihood of happiness over unhappiness.
welfare A combination of concerns having to do with basic human well- being, health, economic capacity, and life satisfaction.
545
Discussion Questions 1. During environmental health grand rounds, a student new to
public health heard some roughly equivalent terms: population, community, group, society, culture, neighborhood, collectivity, humans, humanity, our species, people, and more. How much difference does using one or another of these terms make to ethics? Is there a best term to use for environmental health? And by the way, what does environmental mean in environmental health?
2. A student working in a village family-planning clinic has learned that a woman in this region must have her husband's permission to obtain family-planning services and that such permission is not likely to be forthcoming. She wants to tell the donor agency about the problem, but the instructor recommends that she be quiet about the issue. What should she do?
3. A city in the U.S. Southwest is planning to restore some wetlands in a park running along its downtown river. A question has been raised about mosquitoes. Some think that mosquitoes will promote the bird population and that the natural beauty of the project will outweigh the risks. Others are worried that the mosquitoes might bring such diseases as malaria, especially as more people migrate from the South. How should city planners balance these concerns?
4. What are some analogies between human health and the health of the environment? What are some ways in which they are dissimilar? How might healthy environments be unhealthy for humans, and vice versa? What ideas in our religious traditions help us to make concern for environmental health paramount and meaningful?
5. Your friend lives in a large city in a developed country. He greatly admires technological marvels, the conveniences, the wealth, the literature, and the splendid art museum. He is completely disinterested in suffering and poverty in the rest of the world. He just sees that as the normal and ancient background of the human condition. For him, only the achievements matter. Can he be a good public health
546
professional?
6. In some developed countries, many of the poorest live at an income near the global economic mean. By some estimates, that is the highest level of income the globe can afford for everyone. Should everyone else in the developed country strive for a level of consumption and an ecological footprint that match those of the poorest?
7. To create wilderness areas around the globe, millions of people have been displaced from their homes. And where threatened animals such as tigers are being hunted, poachers are shot. What does this mean about the value of people in relationship to other species?
8. Indoor air conditioning makes people more productive and comfortable; it also protects vulnerable people, such as the elderly and the sick. Some public health officers say that people have a right to air conditioning. But it is energy costly. Is there some way to balance its health benefits with its costs?
9. As the world warms, more people are likely to migrate from the girdle of the Earth poleward, especially toward the north. Given that they are environmental refugees, and that population growth has economic advantages, should public health professionals in the United States, Canada, and Europe champion immigration, despite widespread political opposition?
10. Do you have some personal values that harmonize well with the professional ethics of environmental health? Do you have some that make you less comfortable here?
11. Small, local community gardens and farmers' markets have been sprouting up in your city. The public health department is worried about possible lead in the soil, infections from leafy crops, perishable foods, and the like. The department is proposing a tax, a licensing fee, and inspections for gardens and markets. The proposed rules appear to gardeners to be designed to suppress competition with larger grocers and farms. Where should environmental health stand on this?
12. A new chemical preservative is being used on vegetables in salads served at fast food restaurants. Chemically, it is similar to some compounds listed by the EPA as carcinogenic, but so far
547
only a few studies of marginal statistical significance have been published. A public advocacy group is protesting the use of the new preservative. You have been asked to contribute your public health expertise to the protest. Do you want to take this on? Would you contact the researchers who have done the studies?
13. A major foundation, supported primarily by the irrigation industry, is promoting projects in developing countries to make agricultural water use more efficient. Indeed, the millions of smallhold farms in the world could use water much more efficiently, but they lack the technology, capital, and organization. Water will be increasingly critical for nutrition in future decades. The foundation's projects tend to undermine local communities and put farming into the hands of international corporations. How should environmental health practitioners participate ethically in these projects?
548
References Archer, D. (2009). The long thaw: How humans are changing the next 100,000 years of Earth's climate. Princeton, NJ: Princeton University Press.
Athanasiou, T., & Kartha, S. (2007). The Greenhouse Development Rights framework: The right to development in a climate constrained world. Washington, DC: Heinrich Böll Foundation.
Beauchamp, D. E. (1976). Public health as social justice. Inquiry, 13(1), 3–14.
Beckerman, W., & Hepburn, C. (2007). Ethics of the discount rate in the Stern Review on the Economics of Climate Change. World Economics, 8(1), 187–210.
Bentham, J. (2007). An introduction to principles of morals and legislation. Mineola, NY: Dover. (Originally published 1790)
Bok, S. (1999). Lying: Moral choice in public and private life (2nd ed.). New York: Random House.
Brown, D. A. (2012). Climate change ethics: Navigating the perfect moral storm. New York: Routledge.
Brown, D. E. (1991). Human universals. Philadelphia: Temple University Press.
Caldwell, J. C. (1986). Routes to low mortality in poor countries. Population and Development Review, 12(2), 171–220.
Caney, S. (2009). Climate change and the future: Discounting for time, wealth, and risk. Journal of Social Philosophy, 40(2), 163– 186.
Cox, S. (2013). Any way you slice it: The past, present, and future of rationing. New York: New Press.
Dwyer, J. (2009). How to connect bioethics and environmental ethics: Health, sustainability, and justice. Bioethics, 23(9), 497– 502.
549
Francis. (2015). Laudato si' [Praise be to you]: On care for our common home. Retrieved from http://w2.vatican.va/content/francesco/en/encyclicals/documents/papa- francesco_20150524_enciclica-laudato-si.html
Gardiner, S. M. (2011). A perfect moral storm: The ethical tragedy of climate change. New York: Oxford University Press.
Garvey, J. (2008). The ethics of climate change: Right and wrong in a warming world. New York: Continuum.
Hardin, G. (1968). The tragedy of the commons. Science, 162, 1243– 1248.
Hearne, V. (1986). Adam's task: Calling animals by name. New York: Knopf.
Katz, E., Light, A., & Thompson, W. (Eds.). (2003). Controlling technology: Contemporary issues (2nd ed.). Amherst, NY: Prometheus Books.
Kinzig, A. P., Ehrlich P. R., Alston, L. J., Arrow, K., Barrett, S., Buchman, T. G.,…Saari, D. (2013). Social norms and global environmental challenges: The complex interaction of behaviors, values, and policy. Bioscience, 63, 164–175.
Kolstad, C., Urama, K., Broome, J., Bruvoll, A., Carińo Olvera, M., Fullerton, D.,…Kverndokk, S. (2014). Social, economic and ethical concepts and methods. In Intergovernmental Panel on Climate Change, Climate change 2014: Mitigation of climate change. Contribution of Working Group III to the Fifth Assessment Report of the Intergovernmental Panel on Climate Change (pp. 207–282). New York: Cambridge University Press.
Lichtenberg, J. (2013). Distant strangers: Ethics, psychology, and global poverty. New York: Cambridge University Press.
Maccarone, E. M. (2005). The ethics of advocacy: Scientists and environmental policy. Environmental Philosophy, 2, 44–53.
McCally, M., & Cassel, C. K. (1990). Medical responsibility and global environmental change. Annals of Internal Medicine, 113(6), 467–473.
550
McKinnon, C. (2014). Climate change: Against despair. Ethics & the Environment, 19(1), 31–48.
McMichael, A. J., & Dear, K.B.G. (2010). Climate change: Heat, health, and longer horizons. Proceedings of the National Academy of Sciences of the United States of America, 107, 9483–9484.
Meinshausen, M., Meinshausen, N., Hare, W., Raper, S.C.B., Frieler, K., Knutti, R.,…Allen, M. R. (2009). Greenhouse-gas emission targets for limiting global warming to 2°C. Nature, 458(7242), 1158–1162.
Milanovic, B. (2011). The haves and the have-nots: A brief and idiosyncratic history of global inequality. New York: Basic Books.
Mountford, H. (2014). Better growth, better climate: The new climate economy. London: Global Commission on the Economy and Climate.
Murray, C.J.L., Vos, T., Lozano, R., Naghavi, M., Flaxman, A. D., Michaud, C.,…Memish, Z. A. (2012). Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990–2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380, 2197–2223.
Nelson, M. P., & Vucetich, J. A. (2009). On advocacy by environmental scientists: What, whether, why, and how. Conservation Biology, 23(5), 1090–1101.
Orr, D. W. (2007). Optimism and hope in a hotter time. Conservation Biology, 21(6), 1392–1395.
Ostrom, E. (2012). Future of the commons: Beyond market failure and government regulation. London: Institute of Economic Affairs.
Piketty, T. (2014). Capital in the twenty-first century. Cambridge, MA: Harvard University Press.
Public Health Leadership Society. (2002). Principles of the ethical practice of public health. Retrieved from http://phls.org/CMSuploads/Principles-of-the-Ethical-Practice-of- PH-Version-2.2-68496.pdf
Steffen, W., Richardson, K., Rockström, J., Cornell, S. E., Fetzer, I.,
551
Bennett, F. M.,…Sörlin, S. (2015). Planetary boundaries: Guiding human development on a changing planet. Science, 347(6223). doi:10.1126/science.1259855
Stern, N. (2007). The economics of climate change: The Stern Review. Cambridge, U.K.: Cambridge University Press.
Thomas, L. (Ed.). (2011). Religion, consumerism and sustainability: Paradise lost? London: Palgrave Macmillan.
United Nations. (1948). The Universal Declaration of Human Rights. Retrieved from http://www.un.org/en/documents/udhr/index.shtml#a2
United Nations Framework Convention on Climate Change. (2009). Copenhagen Accord. Retrieved from http://unfccc.int/resource/docs/2009/cop15/eng/l07.pdf
United Nations Framework Convention on Climate Change. (2014). Lima call for climate action (Advance unedited version). Retrieved from http://newsroom.unfccc.int/media/167536/auv_cop20_lima_call_for_climate_action.pdf
Weed, D. L., & McKeown, R. E. (2003). Science and social responsibility in public health. Environmental Health Perspectives, 111, 1804–1808.
Weston, B. H. (2008). Climate change and intergenerational justice: Foundational reflections. Vermont Journal of Environmental Law, 9, 375–430.
World Bank. (1993). World development report 1993: Investing in health. New York: Oxford University Press.
552
For Further Information Bayer, R., Gostin, L. O., Jennings, B., & Steinbock, B. (Eds.). (2007). Public health ethics: Theory, policy, and practice. New York: Oxford University Press.
Beauchamp, T. L., & Childress, J. F. (2013). Principles of biomedical ethics (7th ed.). New York: Oxford University Press.
Boylan, M. (Ed.). (2008). International public health policy and ethics. Dordrecht, Netherlands: Springer Science.
Coughlin, S. S. (2009). Case studies in public health ethics (2nd ed.). Washington, DC: American Public Health Association.
Farmer, P. (2003). Pathologies of power: Health, human rights, and the new war on the poor. Berkeley: University of California Press.
Gorz, A. (1980). Ecology as politics. Boston: South End Press.
Holland, S. (2014). Public health ethics (2nd ed.). Cambridge, U.K.: Polity Press.
Mill, J. S. (1998). Utilitarianism (R. Crisp, Ed.). New York: Oxford University Press.
Rachels, J., & Rachels, S. (2007). The elements of moral philosophy (5th ed.). Boston: McGraw-Hill.
Resnik, D. (2012). Environmental health ethics. New York: Cambridge University Press.
Sandel, M. J. (2010). Justice: What's the right thing to do? New York: Farrar, Straus and Giroux.
553
Chapter 11 Environmental Justice and Vulnerable Populations
Rachel Morello-Frosch and Manuel Pastor
Funding was provided by the W.K. Kellogg Foundation, the William and Flora Hewlett Foundation, and the National Institute of Environmental Health Sciences P01 (RD83543301). Dr. Morello-Frosch and Dr. Pastor report no conflicts of interest related to the authorship of this chapter. Anna Engstrom reports no conflicts of interest related to the authorship of the tox box.
554
Key Concepts Certain populations are uniquely vulnerable to the adverse health effects of hazardous environmental exposures, due to multiple and higher exposures, susceptibility to harmful effects related to social conditions or underlying biological factors, or both.
Vulnerable groups include communities of color and the poor, linguistically isolated and immigrant groups, and people with biologically determined susceptibilities due to age (e.g., children), disability, or other underlying chronic health conditions.
Environmental justice (EJ) addresses the disproportionate impact of environmental hazards on vulnerable groups, particularly communities of color, the poor, and other populations. EJ also promotes enhanced access to environmental, social, and economic assets such as good air quality, safe drinking water, green space, and public transit.
Environmental justice advocates have catalyzed scientific research on environmental equity and have also sought to transform regulatory science and policymaking to address the cumulative impacts of environmental and social stressors faced by vulnerable groups.
Part of what has made this movement from research to action possible is community-based participatory research (CBPR), which brings together academics and advocates to collaborate in new ways to investigate key environmental justice questions and advance environmental health science.
Environmental health researchers, practitioners, advocates, and policymakers are increasingly concerned about the origins and persistence of health disparities in the United States. Scientific research indicates that the inequitable distribution of health is linked to environmental and social conditions combined with underlying vulnerability factors that put people at “risk of risks” (Phelan, Link, & Tehranifar, 2010). This combination of environmental hazard exposures and socioeconomic stressors has
555
been described as a form of double jeopardy (Institute of Medicine, 1999) that disproportionately impacts vulnerable groups, particularly communities of color and the poor, immigrants and linguistically isolated groups, and children and the disabled.
The environmental justice movement emerged in the late 1980s from deep roots in the civil rights and the labor, indigenous peoples, and farmworker rights movements. It has sought to transform environmentalism, policymaking, and more recently, environmental health science in order to address the disproportionate impact of environmental hazards on communities of color and the poor. As articulated by sociologist Robert Bullard (1996), environmental justice is the principle that “all people and communities are entitled to equal protection of environmental and public health laws and regulations.” The U.S. Environmental Protection Agency's Office of Environmental Justice elaborates on this equity principle, including equal protection, defining environmental justice as
the fair treatment and meaningful involvement of all people regardless of race, color, national origin, or income with respect to the development, implementation, and enforcement of environmental laws, regulations, and policies. EPA has this goal for all communities and persons across this Nation. It will be achieved when everyone enjoys the same degree of protection from environmental and health hazards and equal access to the decision-making process to have a healthy environment in which to live, learn, and work [U.S. Environmental Protection Agency, 2015].
This chapter provides an overview of the topic of environmental justice; its emergence in the realms of environmental health science, policymaking, and regulation; and its implications for improving the health of vulnerable communities. The first section provides a brief history of the emergence of the environmental justice movement in the United States. The second section outlines the basic elements of the environmental justice framework, stressing the key role of precautionary strategies. The third section highlights the evolution of environmental justice research, with a focus on cumulative impacts, children's health, and climate change. The fourth section looks at emerging work on the relationship between social equity and overall environmental quality. The chapter concludes with a discussion of the implications for future
556
environmental justice research and policy.
557
The Roots of Environmental Justice Concern about the inequitable impact of environmental problems on vulnerable and socially marginalized groups has a long history in the field of public health. For example, during the Great Depression of the 1930s, workers digging a tunnel through silica-laden rock for a hydroelectric project for the New Kanawha Power Company, a subsidiary of the Union Carbide Corporation, at Gauley Bridge, West Virginia, were sickened with silicosis, a debilitating lung disease, due to the company's refusal to provide appropriate safeguards. An estimated 700 workers died, 500 of whom were African American, in large part because they were relegated to the most hazardous jobs with the highest silica exposures. Efforts by advocates to compensate workers and their families for this occupational disaster were successful, yet the allocation of funds was based on race, with unmarried African American men receiving the lowest level of compensation compared to their white, married counterparts (Cherniack, 1986). Similarly, the United Farm Workers, a union of farmworkers in the United States, founded in the 1960s, sought to improve wages and working conditions for disenfranchised, immigrant agricultural laborers in California and other parts of the Southwest through unionization campaigns and regulations that strengthened field sanitation rules and restricted or banned the use of organochlorine pesticides, such as DDT, and acutely toxic organophosphates (Harrison, 2011; Pulido, 1996).
The “modern” environmental justice movement emerged in 1982 when a predominantly African American community in Warren County, North Carolina, protested the siting of a landfill slated to receive over 60,000 tons of soil contaminated with toxic polychlorinated biphenyls (PCBs; see Tox Box 2.1 in Chapter 2). This incident brought together the environmental and civil rights communities and attracted national attention, including the support of members of the Congressional Black Caucus, who joined the protests (Bullard, 1990). Over 500 people were arrested at one such protest (Text Box 11.1)
558
Text Box 11.1 Roots of Environmental Justice in Warren County, North Carolina “[E]ven in 1982 we knew that where we lived, where we worked, and where we played was really our environment. When the state of North Carolina decided that it was going to put PCB into a community that was 65 percent African Americans, we said ‘No.’ We said we will put our lives on the line.
“And we did it by laying our bodies in front of the trucks, but as we lay there we knew that we were neither politically or economically empowered enough to stop the trucks… As we lay our bodies in front of the trucks and were hauled off to jail by the bus load, we didn't know that the media was going to publicize [our plight]… We didn't know that hundreds of people were going to come and demonstrate with us.
“We only knew in our hearts that we were doing the right thing. We knew in our hearts that God required of us to do justice. We hoped and prayed that our going to jail would not be in vain. And we feel that it was not in vain because many good things happened as a result of our going to jail. For the first time, blacks and whites in Warren County united. African Americans determined that henceforth and forever more we will have some say in the government that was controlling our destiny.”
Source: Burwell, 1992.
The Warren County struggle inspired other grassroots groups across the country to organize around environmental justice concerns affecting communities of color, the poor, and working-class white communities throughout the United States (Bullard, 1990; Gottlieb, 1993). Since those early days, these place-based movements have mobilized against industrial contamination, mining on indigenous land, and the location of hazardous facilities; pushed for chemicals policy reform and stronger regulation of pollution from ports,
559
railroads, and other goods movement emission sources; and advocated for enhanced participation in environmental and land- use decision making (Edelstein, 1988; Freudenberg & Steinsapir, 1992; Hricko, 2008; Lerner, 2005; Levine, 1982).
Environmental justice activism—which highlighted the links among sustainability, social justice, discrimination, environmental degradation, and public health—spurred government action. In 1992, the U.S. Environmental Protection Agency (U.S. EPA) published a groundbreaking report, Environmental Equity: Reducing Risk for All Communities, which supported the claims of environmental injustice and laid out the first set of policy proposals by a federal agency to address EJ issues. The report led to the creation of the National Environmental Justice Advisory Council; the establishment of the Office of Environmental Equity (later renamed the Office of Environmental Justice) within the EPA; and an Executive Order, from then president Bill Clinton, titled “Federal Actions to Ensure Environmental Justice in Minority Populations and Low-Income Populations,” which directed all federal agencies to consider the environmental and human health effects of federal actions on minority and low-income populations with the goal of achieving environmental protection for all communities (Executive Order No. 12898, 1994).
560
Elements of Environmental Justice Over the last three decades the environmental justice movement has redefined environmentalism in ways that make community health and well-being and their connection to place a central focus of activism and policy advocacy; it rejects the historical anti-urban bias of the traditional environmental movement and embraces the notion that the environment consists of the places where communities live, work, and play (Principles of Environmental Justice, 1991). Most important, the EJ movement promotes a framework for social change that upholds the rights of all individuals to be protected from environmental degradation and its attendant health impacts, pushes for precautionary approaches partly because of the recognition that less powerful groups need to be protected, and demands that regulatory agencies proactively redress disproportionate and cumulative health risk burdens through targeted action and resources (Brulle & Pellow, 2006).
The precautionary principle is key: it holds that in the face of uncertain but suggestive evidence of adverse environmental or human health effects, regulatory action should prevent harm from environmental hazards, particularly for vulnerable populations (Morello-Frosch, Pastor, & Sadd, 2002). Children, for example, are more susceptible to the effects of environmental pollution than adults are—because of fundamental differences in their physiology, metabolism, and absorption and exposure patterns—and research indicates that children of color often bear the highest burden of exposures to environmental hazards and their potentially adverse health effects. For example, although lead exposures in the general U.S. population have steadily declined due to regulatory action to remove lead from paint and gasoline, poor children of color, particularly African Americans, have persistently higher exposure levels than their wealthier, white counterparts, due to their higher likelihood of living in older, substandard housing with peeling lead paint (Jacobs et al., 2002) (see Tox Box 11.1).
561
Tox Box 11.1 Lead (Pb)
WHAT IS IT? Lead is a naturally occurring heavy metal and a ubiquitous environmental contaminant.
HOW IS IT USED? Lead and lead compounds have been used since ancient times for a wide range of applications. Metallic (elemental) lead is very rare; most lead alloys and compounds that people use are either inorganic or organic lead. Tetraethyl and tetramethyl lead, the best known organic lead compounds, were once added to gasoline as antiknock agents; in the United States, the combustion of leaded gas released approximately 4 million metric tons of lead into the environment over the course of the twentieth century. Inorganic lead compounds, such as lead chromate (“chrome yellow”) and lead carbonate (“white lead”), were once used as pigments in ceramic glazes, dyes, and paints. In addition, lead alloys and lead compounds are used in fishing weights, lead-acid batteries, ammunition, pipes, and in radiation shielding materials. Lead crystal glass may contain 25% to 40% lead oxide.
HOW ARE PEOPLE EXPOSED?
562
Historically, the workplace was a significant source of human lead exposure due to the intensive use of organic and inorganic lead in a variety of industries. Workers involved with the production (lead miners, dye and paint makers, metal refiners), application (painters, ceramic and pottery makers, explosives makers, plumbers, solderers, welders), or recycling (lead smelters, scrap metal workers) of leaded materials were at risk of significant, chronic lead exposure. The primary sources of nonoccupational lead exposure used to be from leaded gasoline and leaded paint. While these products have been banned in the United States, lead can persist in the environment for decades, and lead exposure is still a problem for people in older homes and in urban areas. For example, leaded paint chips and peels over time, so people in older homes with leaded paint may be exposed to lead in household dust or during home renovations. High lead levels in soil are also a problem in urban areas, due to the combustion of leaded gasoline, flaking of lead paint, and subsequent deposition of lead into the soil. Childhood lead exposure is still an important concern because young children ingest more dust and soil than do adults. This is an environmental justice issue, presumably because of disparate exposures; data show that black children have substantially higher blood lead levels than white children (Wheeler & Brown, 2013). Recreational lead exposure may occur among individuals who use lead glazes or paints, leaded fishing weights, or lead ammunition. Importantly, the inorganic form of lead is the focus of most human health-related concerns, because the combustion of leaded gasoline (organic lead) results in the release and deposition of inorganic lead in
563
the environment, and organic lead is also converted to inorganic lead in the human body.
WHAT ARE THE TOXIC EFFECTS? While lead can affect multiple organ systems, most of the adverse health effects associated with both acute and chronic lead exposure are due to the effects of lead on the nervous system. Importantly, children are the most susceptible to lead toxicity. Children are at risk of proportionately higher lead body burdens because they eat more dust and soil, which may be contaminated with lead. In addition, the blood-brain barrier in young children is not fully developed, so more lead can reach the child's brain. Finally, children absorb lead from their digestive tracts more efficiently than adults do, so more of the lead they ingest can reach the bloodstream and eventually the brain. Blood lead levels (BLLs) are used as a biomarker of recent or current lead exposure. Importantly, there is no threshold for lead toxicity; adverse health effects, including cognitive impairment, can occur at BLLs below U.S. regulatory standards.
Acute lead poisoning is rare. In both children and adults, acute, high-level lead exposure (high BLL) is associated with severe neurological toxicity, including peripheral nerve damage and brain damage (encephalopathy).
Chronic, low-level lead exposure is the primary public health concern for lead. In children, elevated BLLs, even relatively mild elevations, are associated with decreased IQ, hyperactivity, behavioral deficits, learning disabilities, hearing loss, and anemia. In adults, elevated BLLs are associated with cardiovascular effects (hypertension, increased blood pressure), impaired kidney function, and reproduction problems.
HOW ARE PEOPLE PROTECTED? The keystone of public health actions to protect people from lead is prevention of exposure—ending the use of lead in consumer products and industrial settings. To protect the public, numerous policies have been enacted to regulate lead
564
in the air (Clean Air Act), in the water (Clean Water Act and Safe Drinking Water Act), and at hazardous waste sites (Superfund). In addition, the EPA provides guidelines on how to safely remove and dispose of residential lead-based paint to limit exposure to lead dust. The Centers for Disease Control and Prevention recommends public health intervention for children with BLLs above the reference level of 5 µg/dL. In addition, the Occupational Safety and Health Administration and the National Institute for Occupational Safety and Health have established standards and surveillance programs to limit occupational lead exposure. The phasing out of leaded paint and leaded gasoline, along with these various policy measures, has contributed to a significant decline in the ambient lead levels and median BLLs in the United States. However, lead can persist in soil for decades and it is still a major public health concern. For example, nearly 35% of American homes still have lead- based paint, and leaded gasoline and paint are still widely used in developing countries.
WANT TO LEARN MORE? The ATSDR Toxicological Profile for Lead, current as of 2007, is at www.atsdr.cdc.gov/toxprofiles/tp.asp? id=96&tid=22
A useful review of the effects of lead on children is D. C. Bellinger, “Very Low Lead Exposures and Children's Neurodevelopment,” Current Opinion in Pediatrics, 2008, 20, 172–177.
Three books that provide in-depth accounts of lead toxicity in social context are C. Warren, Brush with Death: A Social History of Lead Poisoning (Baltimore: Johns Hopkins University Press, 2001); L. Denworth, Toxic Truth: A Scientist, a Doctor, and the Battle over Lead (Boston: Beacon Press, 2009); and G. Markowitz and D. Rosner, Lead Wars: The Politics of Science and the Fate of America's Children (Berkeley: University of California Press, 2013).
Contributed by Anna Engstrom
565
More recently, EJ advocates have expanded the environmental health discourse to address multiple, cumulative, and potentially synergistic risks from environmental and social stressors; promoted a new paradigm of community-driven science; and enhanced public participation and accountability in formulating environmental policy. Environmental justice advocacy has also broadened its focus to engage with a wide array of environmental and social equity issues, such as climate change, transit justice, community development and land-use planning, food security, and access to parks, green space, and other amenities.
566
From Research to Action on Environmental Justice The Warren County protests not only spawned an environmental justice movement but also led to a new field of research on the question of environmental inequity. The first major salvo was the landmark 1987 report by the United Church of Christ (UCC) titled Toxic Wastes and Race in the United States, the first national study examining demographic disparities in the location of hazardous waste sites (Lee, 1987). The UCC study found that race was the most significant variable in differentiating between areas with and without waste treatment, storage, and disposal facilities. A follow- up analysis found persistent racial and economic disparities in waste facility siting (Mohai & Saha, 2007).
While some critics of the environmental justice perspective have cast doubt on the ubiquity of inequity, most (although not all) of the research evidence has pointed to a pattern of disproportionate exposures to toxics and associated health risks among communities of color and the poor (and increasingly among linguistically isolated immigrants), with racial and ethnic disparities often persisting across economic strata (Ringquist, 2005). Moreover, these locational studies documented inequities for a variety of environmental hazards, including waste sites, industrial facilities, transportation thoroughfares, garbage transfer stations, concentrated animal feeding operations, and other types of so- called locally undesirable land uses (LULUs). (See, for example, the maps in Figures 11.1a and 11.1b, which relate demographic and economic aspects of neighborhoods and the distribution of facilities with toxic emissions in Southern California.)
567
Figure 11.1a Distribution of Major Industrial Facilities by Racial Composition of Census Tracts, Southern California
Note: The distribution of the industrial facilities, represented by dots on the map, is based on data from the U.S. EPA's Toxic Release Inventory (TRI).
568
Figure 11.1b Distribution of Major Industrial Facilities by Proportion of Census Tract Residents Living Below the Federal Poverty Line, Southern California
Note: The distribution of the industrial facilities, represented by dots on the map, is based on data from the U.S. EPA's Toxic Release Inventory (TRI).
Most locational studies are cross-sectional and raise the question of whether environmental hazards are being sited in communities of color and low income or whether these populations are simply moving into neighborhoods that already host emissions sources due to lower housing prices and other market dynamics. This “which came first” question has been examined using longitudinal analysis. Two such temporal studies concluded that inequities in the location of environmental hazards were driven primarily by the disparate siting of facilities in existing communities of color, rather than geographic movement of these populations. In short, contrary to the minority move-in hypothesis, hazardous facilities tend to be sited in particularly vulnerable communities (Pastor, Sadd, & Hipp, 2001; Saha & Mohai, 2005).
Recognizing the limitations of proximity studies, scientists have
569
sought to better characterize inequities in human exposures to toxicants and their health implications. New methods include exposure studies based on modeling, biomonitoring, or other approaches that better elucidate inequalities in exposures to pollutants in different media, including air, dust, and water. For example, studies on air quality have found a disproportionate burden of exposures and associated cancer and respiratory health risks for communities of color and poor residents (Jerrett et al., 2001; Morello-Frosch, Pastor, & Sadd, 2001; Woodruff, Parker, Kyle, & Schoendorf, 2003). A handful of studies have examined inequities in access to safe drinking water and found that compared to wealthier areas with fewer residents of color, areas with higher poverty and greater proportions of people of color are more likely to have drinking water with higher levels of arsenic and nitrates (Balazs, Morello-Frosch, Hubbard, & Ray, 2011, 2012; Cory & Rahman, 2009). Biomonitoring studies that measure chemicals and their metabolites in human tissues, such as blood and urine, have found higher levels of certain compounds among communities of color and the poor, including endocrine-disrupting chemicals such as pesticides; flame retardants; perfluorinated compounds, which are used to make nonstick coatings and stain repellants; and bisphenol A, a chemical used in plastic containers and the lining of food cans (Cox, Niskar, Narayan, & Marcus, 2007; Dewailly et al., 1994; Nelson, Scammell, Hatch, & Webster, 2012).
Cumulative Impacts Vulnerable populations are often simultaneously impacted by multiple environmental stressors, and therefore a source-by-source and pollutant-by-pollutant regulatory paradigm fails to adequately protect them. Moreover, chronic social stressors, such as poverty, discrimination, and poor housing quality, disproportionately impact these same communities. Research is beginning to show how social and environmental stressors can combine additively or synergistically to produce health disparities. Together, these stressors are recognized as contributing to cumulative impacts. Four key concepts underlie emerging scientific knowledge about cumulative impacts:
1. Health disparities between racial/ethnic and socioeconomic groups are significant and exist for conditions such as asthma,
570
heart disease, and low birth weight that are linked to social and environmental factors.
2. Inequalities in exposures to environmental hazards are significant and are linked to increased risk of adverse health outcomes.
3. Intrinsic biological and physiological factors can modify the effects of environmental factors and contribute to differences in the frequency and severity of environmentally mediated disease.
4. Extrinsic social vulnerability factors at the individual and community levels may amplify the effects of environmental hazards and can contribute to health disparities.
These four concepts have complex interrelationships and feedback loops (Figure 11.2). For instance, health disparities resulting from heightened environmental exposures and social vulnerability increase rates of preexisting health conditions, in turn heightening biological susceptibility to further environmental exposures (Morello-Frosch, Zuk, Jerrett, Shamasunder, & Kyle, 2011).
571
Figure 11.2 The Four Elements of Cumulative Impacts Source: Based on Morello-Frosch et al., 2011.
Work to develop more sophisticated methods for assessing cumulative impacts and environmental health disparities is in its infancy, and uncertainties remain over the appropriate way to cumulate and deal with interactions and their overlapping components or pathways. Fundamental to the utility of the cumulative impacts framework is taking the steps needed to incorporate vulnerability into environmental health research, assessments, policies, and actions. While current risk assessment methods address differential susceptibility for certain intrinsic biological factors, such as age, by adding safety or default factors to protect these biologically sensitive populations (e.g., children), factors that increase vulnerability of disadvantaged communities (e.g., neighborhood poverty, food insecurity, and other psychosocial
572
stressors) are not currently considered in the environmental risk assessment process. Researchers have established, however, that many dimensions of social vulnerability, such as human capital, political capital, discrimination, and features of the built environment, matter to outcomes and should be taken into account in risk assessment practices.
Health impact assessment (HIA) provides a promising approach for incorporating cumulative impacts into assessments to guide decision making (see Text Box 15.5, in Chapter 15). HIA is an interdisciplinary method for assessing the health impacts of proposed policies, plans, and projects and for explicitly addressing socially excluded or vulnerable populations by using a combination of quantitative, qualitative, and participatory techniques (Cole et al., 2004; Corburn & Bhatia, 2007). By considering the baseline environmental factors and social conditions, such as health status and vulnerabilities, of the communities potentially impacted by decisions, HIAs have the potential to address the complex causal pathways through which decisions can affect health. Compared to risk assessment, which is a quantitative approach, HIA employs a diverse array of evidence for analysis (e.g., epidemiological evidence along with qualitative observations of neighborhood social conditions and physical environments). This may result in more efficient and precautionary actions than risk assessments, which rely heavily on a toxicological evidence base.
Another approach is cumulative impact screening assessments that highlight vulnerable communities that should be prioritized for interventions that improve existing conditions and prevent future harm (Sadd, Pastor, Morello-Frosch, Scoggins, & Jesdale, 2011). This is in keeping with a precautionary approach: rather than maintain a system in which disadvantaged neighborhoods are only considered when they organize for regulatory action, cumulative impact screening removes this burden from vulnerable communities and increases the likelihood that disadvantaged neighborhoods will get focused regulatory attention. Several environmental agencies in the United States, such as the EPA and the California Environmental Protection Agency, are developing such tools to inform regulatory programs in ways that advance environmental justice goals (Office of Environmental Health Hazard Assessment, 2014; U.S. EPA, n.d.).
573
Generational Equity Children bear a disproportionate burden of the adverse health effects of toxic environmental exposures. Complex and highly sensitive developmental processes that occur during the prenatal period and continue throughout childhood and adolescence can be disrupted by environmental chemical exposures (Figure 11.3 and Text Box 11.2). In these windows of vulnerability (Barker, 2004), perturbations due to chemical exposures can disrupt organ formation and cause both adverse effects during early childhood and an increased risk of diseases throughout the life course. For example, both animal and human studies have linked prenatal chemical exposure to adverse health effects at birth (e.g. preterm birth, low birth weight, and birth defects) and to diseases and mortality later in life (e.g., neurodevelopmental defects, cancer, and cardiovascular disease) (Stillerman, Mattison, Giudice, & Woodruff, 2008). Pregnant women in the United States are exposed to numerous chemicals, such as polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), perfluorinated compounds (PFCs), phenols, polybrominated diphenyl ethers (PBDEs), phthalates, polycyclic aromatic hydrocarbons (PAHs), and perchlorate (Woodruff, Zota, & Schwartz, 2011). Maternal exposures are of concern because chemicals can cross the placenta, putting the developing fetus at risk for adverse health outcomes.
574
Figure 11.3 Children in Los Angeles Playing Soccer Near an Oil Refinery
Proximity of some neighborhoods to sources of pollution poses an exposure risk, often disproportionately affecting poor children and children of color.
Understanding how children are uniquely vulnerable to environmental hazards requires consideration of the timing of exposure to environmental hazards during the life course (i.e., whether it occurs during the prenatal years, infancy, adolescence, or adulthood) and of socioeconomic, political, cultural, and gender dynamics. For example, the lack of child care for agricultural workers often forces families, mostly mothers, to take their children to the fields while they work, thereby increasing young children's exposures to pesticides. Many of these pesticides are known neurotoxicants and carcinogens, and the potential long-term effects of childhood and prenatal exposures are just now being explored and understood.
575
Text Box 11.2 Children Are Not Small Adults Scientific consensus that children are uniquely sensitive to environmental hazards emerged after the publication in 1993 of a milestone National Academies report, Pesticides in the Diets of Infants and Children, which evaluated the evidence indicating that children are dramatically different from adults in their sensitivity to chemicals (National Research Council, 1993). The report highlighted that compared to adults, children are disproportionately exposed to environmental chemicals in air, food, and water per unit of body weight. Pound for pound, children eat more food, drink more water, and breathe more air than adults. Further, children's hand-to-mouth behaviors and activities that involve a lot of time playing on the ground magnify exposures, and children's ability to metabolize chemicals also differs from that of adults, because they often lack the capacity to effectively break down and remove toxic chemicals from the body. By virtue of their young age, children have a longer life expectancy than adults, and therefore they have more time to develop diseases with long latency periods, such as cancer, that are linked to early environmental exposures (Landrigan & Goldman, 2011).
More recent research has documented the adverse neurodevelopmental and health consequences for children who grow up under extremely adverse socioeconomic conditions (Danese & McEwen, 2012). These early childhood experiences related to poverty, chronic psychosocial stress, exposure to violence, and other forms of hardship can become biologically embedded or “get under the skin” in ways that enhance lifetime susceptibility to disease from childhood on through adulthood. Therefore, when combined with environmental chemical exposures, such as lead exposure from living in old, substandard housing, these forms of early childhood social adversity can amplify the risks of permanent neurodevelopmental damage over the life
576
course.
Finally, the contribution of environmental pollutants to the incidence, prevalence, and costs of disease and to mortality among U.S. children is significant. An examination of this burden for four categories of illness—lead exposure, asthma, cancer, and neurobehavioral disorders, some of which disproportionately affect low-income children and children of color—found that the costs of these environmentally related diseases amount to $54.9 billion annually, approximately 2.8% of the total cost of illness in the United States (Landrigan, Schechter, Lipton, Fahs, & Schwartz, 2002). Scientific recognition of and public concern about children's unique vulnerability to environmental chemicals has influenced policy, beginning with President Clinton's Executive Order No. 13045, issued in 1997, which directs federal agencies to consider the particular vulnerability of children to environmental health risks. In addition, the Food Quality Protection Act of 1996, which governs the use of pesticides, is the first federal environmental statute to contain explicit provisions for protecting children's health.
The Climate Gap Climate change is an issue of great importance for environmental justice because of both its overall consequences, as explored in Chapter 12, and its disparate impact on vulnerable and socially marginalized populations. While climate disparities also have a global dimension—with those countries most threatened by the risks of global warming frequently lacking resources to adapt and build resilience—the term climate gap refers to the disproportionate impact of climate change and climate change mitigation on certain social groups, such as people of color and the poor (Shonkoff, Morello-Frosch, Pastor, & Sadd, 2011). As discussed in Chapter 24, vulnerability to climate change is determined by the ability of a community or household to anticipate, cope with, resist, and recover from the direct and indirect impacts of extreme weather events and geophysical shifts, such as sea level rise, hurricanes and floods, heat waves, air pollution, and infectious diseases.
Consider, for example, the situation of older adults and the
577
disabled. The elderly are particularly vulnerable to the health effects of weather extremes such as heat waves due to a higher prevalence of chronic disease, functional and cognitive limitations, greater sensitivity to extreme heat, potential for social isolation, and limited financial resources that make responding to heat events more difficult and costly (Balbus & Malina, 2009). Long-term increases in temperature variability are predicted to increase mortality risks in older people with chronic conditions, particularly those suffering from diabetes and congestive heart failure (Zanobetti, O'Neill, Gronlund, & Schwartz, 2012). Respiratory problems experienced by older adults will be exacerbated by worsening air quality (especially greater levels of ozone and fine particulate matter), increased aeroallergen levels, and wildfire smoke due to climate change (Richardson, English, & Rudolph, 2012). Although the climate change health risks experienced by people with disabilities have not been extensively studied, the “invisibility” of these risks to decision makers and disaster planners is of great concern. During extreme weather events, the elderly and people with cognitive or physical disabilities will experience greater difficulty in responding, and relocating to safer areas. For example, electricity loss in multistory buildings with elevators makes it extremely difficult for those with disabilities to evacuate (Haq, Whitelegg, & Kohler, 2008).
But it is not just intrinsic factors such as age or disability that increase climate-related risks: low-income urban communities and communities of color are especially vulnerable to heat waves and higher temperatures because they are often segregated in neighborhoods in the inner city (Schulz, Williams, Israel, & Lempert, 2002) that are more likely to experience heat island effects (Harlan et al., 2008). As explained in Chapter 12, heat islands occur in urban areas when lighter-colored (higher albedo) materials such as grass, trees, and soil are replaced by darker- colored (lower albedo) materials such as roads, buildings, and other surfaces, leading to increased absorption of sunlight, and when the loss of vegetation leads to a loss of cooling through evapotranspiration. This phenomenon decreases the dissipation of heat, and makes cities—and particular neighborhoods within them —especially hot. A recent national land cover analysis found persistent racial and ethnic disparities in heat risk–related land cover characteristics of neighborhoods, disparities that persisted even after adjusting for biophysical factors that influence tree
578
growth (Jesdale, Morello-Frosch, & Cushing, 2013). Studies indicate that technological adaptation is another critical extrinsic factor in heat-associated health outcomes; lack of access to air conditioning is correlated with risks of heat-related morbidity and mortality among communities of color and low income as well as among the urban elderly and disabled in the United States (Semenza et al., 1996). One study using heat-wave data from Chicago, Detroit, Minneapolis, and Pittsburgh found that African Americans had a 5.3% higher prevalence of heat-related mortality than whites and that 64% of this disparity was potentially attributable to disparities in prevalence of air conditioning (O'Neill, Zanobetti, & Schwartz, 2005).
With the eighth largest economy in the world, California has taken unprecedented steps to address climate change through enactment of a comprehensive climate change law, the Global Warming Solutions Act of 2006 (Assembly Bill 32, or AB 32), which established a binding reduction of the state's greenhouse gas emissions to 1990 levels by 2020 and to 80% of 1990 levels by 2050. Environmental justice organizations successfully ensured that AB 32 included language mandating consideration of procedural, geographic, and social equity. In 2012, the state enacted two Climate and Community Revitalization bills—Senate Bill 535 and Assembly Bill 1532—that direct revenues from California's market- based system of auctioning greenhouse gas allowances (in the form of emission permits) into less advantaged communities. Specifically, these bills require that at least 25% of cap-and-trade revenue be invested in projects that provide benefits to disadvantaged communities and that 10% be directly invested in projects within those communities, with the sort of cumulative impact screening tools discussed earlier being used to identify these communities based on a combination of environmental exposure and social vulnerability factors. Ultimately, the goals of this legislation are to advance mitigation, adaptation, and equity strategies that address the climate gap (Text Box 11.3).
579
Text Box 11.3 Environmental Justice Meets Urban Forestry It's nearly 100 degrees outside and there's no shade in sight. The intensity of the heat radiating from the streets and sidewalks is stifling. Known as the heat island effect, this uncomfortable, and dangerous, situation has become all too common for residents in urban areas. Urban forests and residential tree plantings can alleviate heat islands while also contributing to climate change adaptation and mitigation. Despite the economic, public health, and environmental benefits that trees provide to communities, many neighborhoods across the nation—particularly low-income neighborhoods of color—are bare expanses of cement and asphalt without protective tree canopies (Jesdale et al., 2013). Urban Releaf, an urban forestry nonprofit based in Oakland, California, has planted roughly 20,000 trees in low-income neighborhoods since its launch, but has consistently relied on a shoestring budget and a staff of volunteers (Kersten, Morello-Frosch, Ramos, & Pastor, 2012). However, California, as part of its climate change law (the Global Warming Solutions Act) that mandates ambitious reductions in greenhouse gas emissions and that directs a portion of cap-and-trade revenues to communities affected by environmental hazards and social vulnerability factors, has allocated a large portion of urban forestry money exclusively to disadvantaged communities plagued by pollution. Advocates for Urban Releaf, which has applied for the forestry dollars as part of an ongoing statewide grant process, expect that the new program will support their efforts to add much-needed tree canopy to historically neglected Oakland neighborhoods.
580
Social Inequality and Environmental Quality Social inequality has been growing steadily during the past three decades (Organisation for Economic Co-operation and Development, 2014), with the degree of inequality and its rate of increase in the United States outpacing similar changes in other countries. This trend has important implications for population health because of the growing evidence of an adverse effect of income inequality on overall health and mortality (Kondo et al., 2009; Wilkinson & Pickett, 2006). Emerging evidence also suggests that unequal societies may be more likely to pollute or otherwise degrade their environments (Cushing, Morello-Frosch, Wander, & Pastor, 2015). Why would this be so? Three possible mechanisms are outlined in Figure 11.4. The first pathway is through the asymmetry in power between the privileged and the poor (Boyce, 1994). In this view the wealthy accrue more of the economic benefits of polluting activities both as producers (e.g., shareholders of polluting industries) and consumers (because consumption increases with wealth), even as they are better able to avoid the harmful effects of pollution, for example, by moving away from industrial areas or wielding political influence to keep polluting activities from being sited in their neighborhoods. Given this imbalance, higher pollution levels are likely to result.
581
Figure 11.4 Explanations for the Effect of Social Inequality on the Environment
Source: Cushing et al., 2015.
These explanations relate to (1) asymmetries in political power, (2) the relationship between inequality and the environmental intensity of consumption, and (3) the erosion of social cohesion and cooperation.
The second pathway involves the ways in which inequality leads people to consume more because of a desire to emulate the privileged. When consumption levels of the wealthiest set the standard for what constitutes a good life and when society is highly unequal, consumers must stretch further to meet that standard by spending more. The recent growth in income inequality in the United States has been accompanied by rising household debt across the entire income spectrum as well as by longer work hours (Frank, 2011; Wisman, 2011). Increases in work hours, in turn, result in greater stresses on the environment because (1) they increase overall economic production, a primary driver of environmental degradation, and (2) longer work hours are thought to induce changes in the environmental intensity of lifestyles, such as driving to work. Additionally, as income inequality rises, the economic elite (and even the upper middle class) often increasingly isolate themselves in terms of where they live and send their children to school (Lasch, 1996). This physical separation between relatively privileged members of society and those who are disadvantaged, as exemplified by racial residential segregation, may lead to longer commutes, intensifying the transportation-related environmental footprint.
The third pathway builds on this issue of separation and involves the ways in which inequality erodes social cohesion and trust (Kemp-Benedict, 2013). This increases competition and insecurity about the future and makes cooperation appear more risky. These trends may erode investments in public services, such as education and public transit, that can lessen a society's impact on the environment (Wisman, 2011). More fundamentally, reduced trust makes it difficult to overcome the barriers to environmental stewardship of common-pool resources (Ostrom, 1998). Studies showing that unequal societies invest less in pro-environmental policies, monitoring, and research (Magnani, 2000; Tonn, 2007) do suggest that inequality undermines the willingness to cooperate to
582
protect the environment.
While the theory and the empirical evidence on the relationship between equality and sustainability are still emerging (Ash, Boyce, Chang, & Scharber, 2013), early findings indicate that in some contexts, social inequality is linked to greater environmental degradation, such as air pollution and water contamination. This suggests that environmental justice is not just about helping or empowering specific disadvantaged groups; failing to tackle the disparities built into our environmental riskscapes (Morello-Frosch & Lopez, 2006) can undermine the health and well-being of everyone.
583
Summary The persistence of health disparities has placed the field of environmental health sciences at a crossroads. Achieving environmental justice requires innovative scientific and regulatory strategies that look “upstream” to address the social determinants of health, including the cumulative impacts of social and environmental stressors that combine to keep vulnerable communities less healthy than others (Pastor & Morello-Frosch, 2014; Wilson, Hutson, & Mujahid, 2008). Proactive screening tools that can efficiently identify communities in order to better target resources are likely to be an important part of the future for this field.
Another key element for the field will be community-based participatory research (CBPR). This term describes a range of community-academic partnerships that forge new lines of scientific inquiry and translate knowledge into policy action; this style of collaborative work has been a key part of environmental justice research from the earliest days of the movement. CBPR requires power sharing among partners in all aspects of the research process —doing the research, interpreting the findings, and then acting on the science. The benefits are several. The involvement of communities that directly experience exposures and diseases of concern can bring both their firsthand knowledge and their commitment to the task of translating results into change (Freudenberg, Pastor, & Israel, 2011) (Figure 11.5). Over the last two decades, CBPR in the area of environmental justice has gained wider recognition and funding support, largely through the many projects funded by the National Institute of Environmental Health Sciences, the EPA, and private foundations.
584
Figure 11.5 Members of Clean Up Green Up, an L.A. Environmental Justice Advocacy Group, Hold a Press Conference in Support of Their Goals
Most fundamentally, what is needed is a shift in the basic paradigm of environmental health. Addressing the concerns of the least advantaged is sometimes seen in both social science and public policy as an afterthought: we need to fix the economy, then we can help the poor; we need to constrain inflation in the health system, then we can expand care; we need to tackle climate change, then we will worry about disparities. But if environmental health advocates want to maximize improvements in health conditions, surely addressing the most exposed and most vulnerable—including children, the elderly, communities of color, the poor, and linguistically isolated immigrants—is one way to yield the highest returns for our society as a whole. Addressing environmental justice, in short, is good for everyone.
585
Key Terms climate gap
The disproportionate impact of climate change and climate change mitigation on certain social groups, such as people of color and the poor.
community-based participatory research A collaborative method for conducting research that involves community members, nongovernmental organizations, and academic researchers as partners. These partners share decision making and ownership of the research process and translate study results into action through interventions and policy change aimed at improving community health.
cumulative impacts The aggregate health effects of hazardous exposures from diverse sources in different media (air, water, food, or soil), and of social and other factors. Of special concern with regard to populations that are uniquely vulnerable due to adverse social conditions or are sensitive because of biological factors (such as underlying chronic health conditions), or both (cf. cumulative exposure, in Chapter 8).
environmental justice Both equal protection for all communities from environmental hazards and equal access for all communities to environmental, social, and economic assets that promote health and well-being, such as clean air, safe drinking water, green space, public transit, and economic opportunity.
health impact assessment An evaluation that combines quantitative and qualitative methods to assess the health impacts of proposed policies, plans, and projects and to explicitly address impacts on socially excluded or vulnerable populations.
precautionary principle A policy framework in which actions are undertaken when scientific evidence suggests that an activity raises a threat of harm to the environment or human health. Precautionary action is warranted even when cause-and-effect relationships are not
586
fully established. sensitivity
Possessing intrinsic biological and physiological factors—for example, age or underlying chronic health conditions—that can enhance the effects of environmental factors and contribute to differences in the frequency and severity of environment-related disease.
social determinants of health The socioeconomic conditions that shape individual and group differences in health status through their unequal distribution among diverse population groups.
vulnerability Extrinsic factors at the individual and community level—such as race, gender, and socioeconomic status—that may amplify the adverse effects of environmental hazards and contribute to health disparities.
587
Discussion Questions 1. What is the state of the scientific research on inequalities in
exposures to environmental hazards?
2. How can social and environmental stressors combine to disproportionately affect the health and well-being of vulnerable communities?
3. What are the mechanisms by which social inequality can adversely affect environmental health and well-being for everyone?
4. Describe examples of an environmental justice concern in your community. What is the environmental issue, who is affected, and how?
5. What strategies should regulatory agencies take to achieve environmental justice goals in your state?
6. “Children are not just small adults.” Why are children especially susceptible to environmental hazards?
7. What environmental justice issues may disproportionately impact children's health or the health of the elderly?
588
References Ash, M., Boyce, J. K., Chang, G., & Scharber, H. (2013). Is environmental justice good for white folks? Industrial air toxics exposure in Urban America. Social Science Quarterly, 94(3), 616– 636.
Balazs, C., Morello-Frosch, R., Hubbard, A., & Ray, I. (2011). Social disparities in nitrate-contaminated drinking water in California's San Joaquin Valley. Environmental Health Perspectives, 119(9), 1272.
Balazs, C., Morello-Frosch, R., Hubbard, A., & Ray, I. (2012). Environmental justice implications of arsenic contamination in California's San Joaquin Valley: A cross-sectional, cluster-design examining exposure and compliance in community drinking water systems. Environmental Health, 11, 84.
Balbus, J. M., & Malina, C. (2009). Identifying vulnerable subpopulations for climate change health effects in the United States. Journal of Occupational and Environmental Medicine, 51(1), 33–37.
Barker, D. J. (2004). The developmental origins of chronic adult disease. Acta Paediatrica, 93(446, Suppl.), 26–33.
Boyce, J. K. (1994). Inequality as a cause of environmental degradation. Ecological Economics, 11(3), 169–178.
Brulle, R. J., & Pellow, D. N. (2006). Environmental justice: Human health and environmental inequalities. Annual Review of Public Health, 27, 103–124.
Bullard, R. D. (1990). Dumping in Dixie: Race, class, and environmental quality. Boulder, CO: Westview Press.
Bullard, R. D. (1996). Symposium: The legacy of American apartheid and environmental racism. St. John's Journal of Legal Commentary, 9, 445–474.
Burwell, D. (1992). Reminiscences from Warren County, North Carolina. In C. Lee (Ed.), Proceedings of the First National People
589
of Color Environmental Leadership Summit. New York: United Church of Christ Commission for Racial Justice.
Cherniack, M. (1986). The Hawk's Nest incident: America's worst industrial disaster. New Haven, CT: Yale University Press.
Cole, B. L., Wilhelm, M., Long, P. V., Fielding, J. E., Kominski, G., & Morgenstern, H. (2004). Prospects for health impact assessment in the United States: New and improved environmental impact assessment or something different? Journal of Health Politics, Policy and Law, 29(6), 1153–1186.
Corburn, J., & Bhatia, R. (2007). Health impact assessment in San Francisco: Incorporating the social determinants of health into environmental planning. Journal of Environmental Planning and Management, 50(3), 323–341.
Cory, D. C., & Rahman, T. (2009). Environmental justice and enforcement of the Safe Drinking Water Act: The Arizona arsenic experience. Ecological Economics, 68(6), 1825–1837.
Cox, S., Niskar, A. S., Narayan, K. V., & Marcus, M. (2007). Prevalence of self-reported diabetes and exposure to organochlorine pesticides among Mexican Americans: Hispanic Health and Nutrition Examination Survey, 1982–1984. Environmental Health Perspectives, 115(12), 1747–1752.
Cushing, L., Morello-Frosch, R., Wander, M., & Pastor, M. (2015). The haves, the have-nots, and the health of everyone: The relationship between social inequality and environmental quality. Annual Review of Public Health, 36, 193–209.
Danese, A., & McEwen, B. S. (2012). Adverse childhood experiences, allostasis, allostatic load, and age-related disease. Physiology & Behavior, 106(1), 29–39.
Dewailly, E., Ryan, J. J., Laliberté, C., Bruneau, S., Weber, J.-P., Gingras, S., & Carrier, G. (1994). Exposure of remote maritime populations to coplanar PCBs. Environmental Health Perspectives, 102(Suppl. 1), 205.
Edelstein, M. R. (1988). Contaminated communities: The social and psychological impacts of residential toxic exposure. Boulder,
590
CO: Westview Press.
Executive Order No. 12898, 59 Fed. Reg. 32 (1994). Retrieved from http://www.archives.gov/federal-register/executive- orders/pdf/12898.pdf
Executive Order No. 13045, 62 Fed. Reg. 78 (1997). Retrieved from http://www.gpo.gov/fdsys/pkg/FR-1997-04-23/pdf/97-10695.pdf
Frank, R. H. (2011). The Darwin economy: Liberty, competition, and the common good. Princeton NJ: Princeton University Press.
Freudenberg, N., Pastor, M., & Israel, B. (2011). Strengthening community capacity to participate in making decisions to reduce disproportionate environmental exposures. American Journal of Public Health, 101(Suppl. 1), S123–130.
Freudenberg, W., & Steinsapir, C. (1992). Not in our backyards: The grassroots environmental movement. In Riley E. Dunlap & Angela G. Mertig (Eds.), American environmentalism (pp. 27–35). Philadelphia: Taylor & Francis.
Gottlieb, R. (1993). Forcing the spring: The transformation of the American environmental movement. Washington, DC: Island Press.
Haq, G., Whitelegg, J., & Kohler, M. (2008). Growing old in a changing climate: Meeting the challenges of an ageing population and climate change. Stockholm: Stockholm Environment Institute. Retrieved from http://www.sei- international.org/mediamanager/documents/Publications/Future/climate_change_growing_old.pdf
Harlan, S. L., Brazel, A. J., Jenerette, G. D., Jones, N. S., Larsen, L., Prashad, L., & Stefanov, W. L. (2008). In the shade of affluence: The inequitable distribution of the urban heat island. Research in Social Problems and Public Policy, 15, 173–202.
Harrison, J. L. (2011). Pesticide drift and the pursuit of environmental justice. Cambridge, MA: MIT Press.
Hricko, A. (2008). Global trade comes home: Community impacts of goods movement. Environmental Health Perspectives, 116(2), A78–81.
591
Institute of Medicine. (1999). Toward environmental justice: Research, education, and health policy needs. Washington, DC: National Academies Press. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/23035313
Jacobs, D. E., Clickner, R. P., Zhou, J. Y., Viet, S. M., Marker, D. A., Rogers, J. W.,…Friedman, W. (2002). The prevalence of lead-based paint hazards in U.S. housing. Environmental Health Perspectives, 110(10), A599–606.
Jerrett, M., Burnett, R. T., Kanaroglou, P., Eyles, J., Finkelstein, N., Giovis, C., & Brook, J. R. (2001). A GIS-environmental justice analysis of particulate air pollution in Hamilton, Canada. Environment and Planning A, 33(6), 955–974.
Jesdale, B. M., Morello-Frosch, R., & Cushing, L. (2013). The racial/ethnic distribution of heat risk–related land cover in relation to residential segregation. Environmental Health Perspectives, 121(7), 811–817.
Kemp-Benedict, E. (2013). Inequality and trust: Testing a mediating relationship for environmental sustainability. Sustainability, 5(2), 779–788.
Kersten, E., Morello-Frosch, R., Ramos, M., & Pastor, M. (2012). Facing the climate gap. Retrieved from https://dornsife.usc.edu/assets/sites/242/docs/FacingTheClimateGap_web.pdf
Kondo, N., Sembajwe, G., Kawachi, I., van Dam, R. M., Subramanian, S. V., & Yamagata, Z. (2009). Income inequality, mortality, and self rated health: Meta-analysis of multilevel studies. BMJ, 339, b4471.
Landrigan, P. J., & Goldman, L. R. (2011). Children's vulnerability to toxic chemicals: A challenge and opportunity to strengthen health and environmental policy. Health Affairs, 30(5), 842–850.
Landrigan, P. J., Schechter, C. B., Lipton, J. M., Fahs, M. C., & Schwartz, J. (2002). Environmental pollutants and disease in American children: Estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities. Environmental Health Perspectives, 110(7), 721–728.
592
Lasch, C. (1996). The revolt of the elites and the betrayal of democracy. New York: Norton.
Lee, C. (1987). Toxic wastes and race in the United States: A national study on the racial and socio-economic characteristics of communities surrounding hazardous waste sites. Retrieved from http://d3n8a8pro7vhmx.cloudfront.net/unitedchurchofchrist/legacy_url/13567/toxwrace87.pdf? 1418439935
Lerner, S. (2005). Diamond: A struggle for environmental justice in Louisiana's chemical corridor. Cambridge, MA: MIT Press.
Levine, A. (1982). Love Canal: Science, politics, and people. Lexington, MA: Lexington Books.
Magnani, E. (2000). The environmental Kuznets curve, environmental protection policy and income distribution. Ecological Economics, 32(3), 431–443.
Mohai, P., & Saha, R. (2007). Racial inequality in the distribution of hazardous waste: A national-level reassessment. Social Problems, 54(3), 343–370.
Morello-Frosch, R., & Lopez, R. (2006). The riskscape and the color line: Examining the role of segregation in environmental health disparities. Environmental Research, 102(2), 181–196.
Morello-Frosch, R., Pastor, M., & Sadd, J. (2001). Environmental justice and southern California's “riskscape”: The distribution of air toxics exposures and health risks among diverse communities. Urban Affairs Review, 36(4), 551–578.
Morello-Frosch, R., Pastor, M., & Sadd, J. (2002). Integrating environmental justice and the precautionary principle in research and policy making: The case of ambient air toxics exposures and health risks among schoolchildren in Los Angeles. Annals of the American Academy of Political and Social Science, 584(1), 47–68.
Morello-Frosch, R., Zuk, M., Jerrett, M., Shamasunder, B., & Kyle, A. D. (2011). Understanding the cumulative impacts of inequalities in environmental health: Implications for policy. Health Affairs, 30(5), 879–887.
593
National Research Council. (1993). Pesticides in the diets of infants and children. Washington, DC: National Academies Press. Retrieved from http://site.ebrary.com/lib/berkeley/Doc? id=10055284
Nelson, J. W., Scammell, M. K., Hatch, E. E., & Webster, T. F. (2012). Social disparities in exposures to bisphenol A and polyfluoroalkyl chemicals: A cross-sectional study within NHANES 2003–2006. Environmental Health, 11(10).
Office of Environmental Health Hazard Assessment. (2014). CalEnviroScreen 2.0. Sacramento: California Environmental Protection Agency, Office of Environmental Health Hazard Assessment. Retrieved from http://oehha.ca.gov/ej/ces2.html
O'Neill, M. S., Zanobetti, A., & Schwartz, J. (2005). Disparities by race in heat-related mortality in four US cities: The role of air conditioning prevalence. Journal of Urban Health, 82(2), 191–197.
Organisation for Economic Co-operation and Development. (2014). United States: Tackling high inequalities and creating opportunities for all. Paris: Author. Retrieved from http://www.oecd.org/unitedstates/Tackling-high-inequalities.pdf
Ostrom, E. (1998). A behavioral approach to the rational choice theory of collective action: Presidential address, American Political Science Association, 1997. American Political Science Review, 92(01), 1–22.
Pastor, M., & Morello-Frosch, R. (2014). Integrating public health and community development to tackle neighborhood distress and promote well-being. Health Affairs, 33(11), 1890–1896. Retrieved from http://doi.org/10.1377/hlthaff.2014.0640
Pastor, M., Sadd, J., & Hipp, J. (2001). Which came first? Toxic facilities, minority move-in, and environmental justice. Journal of Urban Affairs, 23(1), 1–21.
Phelan, J. C., Link, B. G., & Tehranifar, P. (2010). Social conditions as fundamental causes of health inequalities: Theory, evidence, and policy implications. Journal of Health and Social Behavior, 51(1, Suppl.), S28–40.
594
Principles of environmental justice. (1991). Retrieved from http://www.ejnet.org/ej/principles.html
Pulido, L. (1996). Environmentalism and economic justice: Two Chicano struggles in the Southwest. Tucson: University of Arizona Press.
Richardson, M. J., English, P., & Rudolph, L. (2012). A health impact assessment of California's proposed cap-and-trade regulations. American Journal of Public Health, 102(9), e52–58.
Ringquist, E. J. (2005). Assessing evidence of environmental inequities: A meta-analysis. Journal of Policy Analysis and Management, 24(2), 223–247.
Sadd, J. L., Pastor, M., Morello-Frosch, R., Scoggins, J., & Jesdale, B. (2011). Playing it safe: Assessing cumulative impact and social vulnerability through an environmental justice screening method in the South Coast Air Basin, California. International Journal of Environmental Research and Public Health, 8(5), 1441–1459.
Saha, R., & Mohai, P. (2005). Historical context and hazardous waste facility siting: Understanding temporal patterns in Michigan. Social Problems, 52(4), 618–648.
Schultz, A. J., Williams, D. R., Israel, B. A., & Lempert, L. B. (2002). Racial and spatial relations as fundamental determinants of health in Detroit. Milbank Quarterly, 80(4), 677–707.
Semenza, J. C., Rubin, C. H., Falter, K. H., Selanikio, J. D., Flanders, W. D., Howe, H. L., & Wilhelm, J. L. (1996). Heat-related deaths during the July 1995 heat wave in Chicago. New England Journal of Medicine, 335(2), 84–90.
Shonkoff, S. B., Morello-Frosch, R., Pastor, M., & Sadd, J. (2011). The climate gap: Environmental health and equity implications of climate change and mitigation policies in California—a review of the literature. Climatic Change, 109(1), 485–503.
Stillerman, K. P., Mattison, D. R., Giudice, L. C., & Woodruff, T. J. (2008). Environmental exposures and adverse pregnancy outcomes: A review of the science. Reproductive Sciences, 15(7), 631–650.
595
Tonn, B. (2007). Determinants of futures-oriented environmental policies: A multi-country analysis. Futures, 39(7), 773–789.
U.S. Environmental Protection Agency. (1992). Environmental equity: Reducing risk for all communities. Washington, DC: Author. Retrieved from http://www.epa.gov/environmentaljustice/resources/reports/annual- project-reports/reducing_risk_com_vol1.pdf
U.S. Environmental Protection Agency. (2015, January 15). What is environmental justice? (Web page). Washington, DC: Environmental Protection Agency, Office of Environmental Justice. Retrieved from http://www.epa.gov/environmentaljustice
U.S. Environmental Protection Agency. (n.d.). EJSCREEN: Environmental justice screening and mapping tool. Retrieved from http://www2.epa.gov/ejscreen
Wheeler, W., & Brown, M. J. (2013). Blood lead levels in children aged 1–5 Years—United States, 1999–2010. Morbidity and Mortality Weekly Report, 62(13), 245–248.
Wilkinson, R. G., & Pickett, K. E. (2006). Income inequality and population health: A review and explanation of the evidence. Social Science & Medicine, 62(7), 1768–1784.
Wilson, S., Hutson, M., & Mujahid, M. (2008). How planning and zoning contribute to inequitable development, neighborhood health, and environmental injustice. Environmental Justice, 1(4), 211–216.
Wisman, J. D. (2011). Inequality, social respectability, political power, and environmental devastation. Journal of Economic Issues, 45(4), 877–900.
Woodruff, T. J., Parker, J. D., Kyle, A. D., & Schoendorf, K. C. (2003). Disparities in exposure to air pollution during pregnancy. Environmental Health Perspectives, 111(7), 942.
Woodruff, T. J., Zota, A. R., & Schwartz, J. M. (2011). Environmental chemicals in pregnant women in the United States: NHANES 2003–2004. Environmental Health Perspectives, 119(6), 879.
596
Zanobetti, A., O'Neill, M. S., Gronlund, C. J., & Schwartz, J. D. (2012). Summer temperature variability and long-term survival among elderly people with chronic disease. Proceedings of the National Academy of Sciences of the United States of America, 109(17), 6608–6613.
597
For Further Information There is a rich literature on environmental justice and vulnerable populations. In addition to the report of the Institute of Medicine (1999) that is listed in the References, see these key sources.
Environmental Justice Agyeman, J. (2005). Sustainable communities and the challenge of environmental justice. New York: NYU Press.
Bullard, R. D. (2005). The quest for environmental justice: Human rights and the politics of pollution. Berkeley, CA: Counterpoint Press.
Pellow, D. N., & Brulle, R. J., (Eds.). (2005). Power, justice, and the environment: A critical appraisal of the environmental justice movement. Cambridge, MA: MIT Press.
Rechtschaffen, C., Gauna, E., & O'Neill, C. (Eds.). (2009). Environmental justice: Law, policy & regulation (2nd ed.). Durham, NC: Carolina Academic Press.
Sandler, R., & Pezzullo, P. C. (Eds.). (2007). Environmental justice and environmentalism: The social justice challenge to the environmental movement. Cambridge, MA: MIT Press.
Taylor, D. (2014). Toxic communities: Environmental racism, industrial pollution, and residential mobility. New York: NYU Press.
Walker, G. (2012). Environmental justice: Concepts, evidence and politics. New York: Routledge.
Book-length accounts of environmental justice issues in specific places provide special insights. Examples include the following:
Checker, M. (2005). Polluted promises: Environmental racism and the search for justice in a southern town. New York: NYU Press. This book focuses on Augusta, Georgia.
Klinenberg, E. (2003). Heat wave: A social autopsy of disaster in
598
Chicago. Chicago: University of Chicago Press.
Spears, E. G. (2014). Baptized in PCBs: Race, pollution, and justice in an all-American town. Chapel Hill: University of North Carolina Press. This book focuses on Anniston, Alabama.
Children's Environmental Health Grandjean, P. (2013). Only one chance: How environmental pollution impairs brain development—and how to protect the brains of the next generation. New York: Oxford University Press.
Landrigan, P. J., & Etzel, R. A. (Eds.). (2013). Textbook of children's environmental health. New York: Oxford University Press.
599
Part 2 Environmental Health on the Global Scale
600
Chapter 12 Climate Change and Human Health
Jonathan A. Patz and Howard Frumkin
Dr. Patz reports no conflicts of interest related to the authorship of this chapter. Dr. Frumkin's disclosures appear in the front of this book, in the section titled “Potential Conflicts of Interest in Environmental Health: From Global to Local.”
601
Key Concepts According to the United Nations Intergovernmental Panel on Climate Change (IPCC), by 2100 average global temperatures are projected to increase between 1.5°C and 4.0°C, sea levels will rise, and hydrological extremes (floods and droughts) will intensify.
Climate change can directly threaten health in several ways: through heat-related morbidity and mortality and through flooding and storms with associated trauma and mental health impacts.
Climate change can also threaten health through many indirect pathways, including compromised food production, air pollution, infectious diseases, mental health problems, population dislocation, and civil conflict.
Climate-related health risks must be assessed in the context of concurrent environmental stressors, such as urbanization (creating urban heat islands) and land cover changes (modifying the dynamics of mosquito-borne diseases).
Risk management of climate change ranges from primary mitigation of greenhouse gas emissions to a number of adaptations. Both co-benefits and unintended consequences of policy changes in the energy, transportation, agriculture, and other health-relevant sectors must be considered in any comprehensive public health approach to global climate change.
Climate change, whether resulting from natural variability or from human activity, depends on the overall energy budget of the planet, the balance between incoming (solar) shortwave radiation and outgoing longwave radiation. This balance is affected by the Earth's atmosphere, in much the same way that the glass of a greenhouse or a car's windshield on a hot day allows sunlight to enter and then traps heat (infrared) energy inside. An atmosphere with higher levels of so-called greenhouse gases will retain more of this heat and will result in higher average surface temperatures than will an atmosphere with lower levels of these gases.
602
A major source of information on climate change is the work of the United Nations Intergovernmental Panel on Climate Change (IPCC), which was established by the World Meteorological Organization (WMO) and the United Nations Environment Programme (UNEP) in 1988. Approximately every five years since 1990, most recently in 2014, the IPCC has conducted assessments of current scientific work on climate change, the potential impacts of this change, and various prevention options. Several national assessments have also been conducted; the third and most recent U.S. National Climate Assessment was published in 2014.
603
Greenhouse Gases The composition of the Earth's atmosphere has changed since preindustrial times. These changes, which began around the mid- 1700s, include increases in the atmospheric levels of carbon dioxide (CO2), methane (CH4), and nitrous oxide (N2O) that far exceed any changes occurring in the preceding 10,000 years. Historical levels of these gases are known from analyses of air trapped in bubbles in Antarctic ice cores. For example, the concentration of CO2 has risen by approximately 35%, from about 280 parts per million by volume (ppmv) in the late eighteenth century to about 400 ppmv at present.
These gases are known as greenhouse gases. They contribute to warming of the Earth—an effect called positive radiative forcing—by absorbing and then re-emitting infrared radiation toward the lower atmosphere and the Earth's surface. (Figure 12.1 summarizes the principal components of radiative forcing, and Table 12.1 shows today's concentrations of these greenhouse gases.)
604
Figure 12.1 Components of Radiative Forcing Source: IPCC, 2013.
This figure shows the extent to which various factors—levels of certain gases, changes in land use, and so on—contribute to radiative forcing (as of 2005, relative to the start of the industrial era, in about 1750). Most of these factors result from human activity; the only exception was a natural increase in solar irradiance. Positive forcings lead to warming of the climate and negative forcings (principally aerosol particles that reflect and absorb solar energy and alter cloud properties) lead to cooling. The black line over each bar represents the range of uncertainty for the respective value.
Table 12.1 The Main Greenhouse Gases
Greenhouse gases
Chemical formula
Preindustrial concentration (ppbv)
Concentration in 2012–2013 (ppbv)
Atmospheric lifetime (years)
Carbon dioxide
CO2 278,000 395,000 Variable
605
Methane CH4 700 11,762–1,893 12.2 ± 3
Nitrous oxide N2O 275 325 120
CFC-12 CCl2F2 0 0.527 102
HCFC-22 CHClF2 0 0.210–231 12.1
Sulfur hexafluoride
SF6 0 0.007 3,20
Note: ppbv = parts per billion by volume; CFC-12 = dichlorodifluoromethane; HCFC-22 = chlorodifluoromethane (both are used as refrigerants).
a GWP for 100-year time horizon.
b No single lifetime for CO2 can be defined because different sink processes have different rates of uptake.
c Includes indirect effects of tropospheric ozone water vapor production.
d Net global warming potential (i.e., including the indirect effect due to ozone depletion).
Sources: Carbon Dioxide Information Analysis Center, 2014.
606
A Warming Earth: From Past to Future Long-term climate change, whether from natural sources or from human activity, can be observed as a signal against a background of natural climate variability. To help detect the meaning of this signal, we need to estimate natural variability using historical climate data. Because instrument records are available only for the recent past (a period of less than 150 years), previous climates must be deduced from paleoclimatic records, including tree rings, pollen series, faunal and floral abundances in deep-sea cores, isotope analyses of coral and ice cores, and for the more recent historical period, diaries and other documentary evidence. Results of these analyses show that surface temperatures in the mid- to late twentieth century appear to have been warmer than they were during any similar period in the last 600 years in most regions and in at least some regions warmer than in any other century for several thousand years.
About half of the anthropogenic greenhouse gas (GHG) emissions that occurred between 1750 and 2010 occurred after 1970. Growth in emissions has been greatest in the first decade of the twenty-first century (2.2% per year, compared with 1.3% from 1970 to 2000). Emissions continue to increase; 2011 emissions exceeded those in 2005 by 43% (IPCC, 2013), although 2014 may have marked a plateau. CO2 from fossil fuels and industrial processes accounted for ≈ 78% of the total increase from 1970 to 2010. Economic and population growth contribute most to increases in emissions globally and have outpaced improvements in energy efficiency.
607
Earth System Changes Although the average effect across the Earth's surface is a warming, changing temperatures tell only part of the story. Higher temperatures evaporate soil moisture more quickly (contributing to severe droughts), but warm air can also hold more moisture than cool air, resulting in heavy precipitation events; such hydrological extremes (floods and droughts) are very much a part of climate change scenarios and of substantial concern to public health professionals. Additionally, the Arctic and Antarctic ice caps are melting, releasing vast amounts of water into the oceans, raising ocean levels, and potentially altering the flow of ocean currents. The weather patterns that result from these and other changes vary greatly from place to place and over short periods of time, emphasizing the importance of climate variability. For these reasons the term climate change is more accurate than global warming and is the accepted term for this set of changes.
Accordingly, the accelerating temperature changes noted earlier have been associated with corresponding Earth system changes. Since 1961, sea levels have risen on average by approximately 2 millimeters per year, and snow cover and glaciers have diminished in both hemispheres. Most striking is the extent to which the Arctic ice cap has melted in the past thirty years—by about 7.4% per decade (Figure 12.2). These trends are expected to continue. According to the IPCC, over the course of the twenty-first century, sea levels will rise between 26 and 98 centimeters, and floods and droughts will continue to intensify.
608
Figure 12.2 The Melting of Arctic Sea Ice Adapted from: National Snow & Ice Data Center, 2015.
This map—a view from above the North Pole—shows the extent of Arctic sea ice in October 2012 compared with the average over the preceding three decades. It shows a dramatic decrease in sea ice concentration, the fraction of the ocean covered by sea ice. (The grey circle centered over the North Pole indicates where the central Arctic is not visible to the satellite instruments used to generate these maps.) The loss of arctic sea ice is an example of a feedback loop. During the summer months, sea ice can reflect as much as 70% of incoming solar radiation back to space. When sea ice disappears, the dark ocean surface absorbs much of the incoming radiation, reflecting less than 10%. This extra energy increases the ocean temperature and the temperature of the overlying atmosphere, contributing further to global warming.
Ocean Temperatures and Hurricanes Records indicate that sea surface temperatures have increased steadily over the last one hundred years, and more sharply over the last thirty-five years. Recent decades have repeatedly set records for sea surface temperatures, with 2014 the warmest year on record (www.ncdc.noaa.gov/sotc/global).
Uncertainty exists over whether hurricane frequency will increase, but evidence points to more extreme hurricanes (categories 4 and 5)
609
(Bender et al., 2010; IPCC, 2013). Sea level rise will continue to exacerbate storm surges, worsen coastal erosion, and inundate low- lying areas. Salinization of aquifers likely will augment challenges to coastal cities and towns.
Sea Level Rise Sea level has risen approximately 20 cm over the last 100 years, far more than in the two previous millennia, an increase associated with thermal expansion of sea water and with melting glaciers. While sea level is likely to rise between 26 and 98 cm by 2100, more extreme estimates that envision catastrophic melting events reach as high as >200 cm. (This is called a tail risk—the extreme end of the distribution of probabilities for a particular outcome.)
One expected effect of sea level rise is an increase in flooding and coastal erosion in low-lying coastal areas. This will endanger large numbers of people; fourteen of the world's nineteen current megacities are situated at sea level. Coastal regions at risk of storm surges will expand and the population at risk will increase from the current 75 million to 200 million (McCarthy, Canziani, Leary, Dokken, & White, 2001). For Bangladesh, a 1.5 meter rise is projected to have even more catastrophic consequences. Countries such as Egypt, Vietnam, Bangladesh, and small island nations are especially vulnerable, for several reasons. Coastal Egypt is already subsiding due to extensive groundwater withdrawal, and Vietnam and Bangladesh have heavily populated, low-lying deltas along their coasts.
Rising sea levels may affect human health and well-being indirectly, in addition to direct effects through inundation or heightened storm surges. Rising seas, in concert with withdrawal of freshwater from coastal aquifers, could result in saltwater intruding into those aquifers and could also disrupt stormwater drainage and sewage disposal.
Particularly Vulnerable Regions Certain regions and populations are more vulnerable than others to the health impacts of climate change (Hess, Malilay, & Parkinson, 2008). These vulnerable areas include
Areas or populations within or bordering regions with a high
610
endemicity of climate-sensitive diseases (such as malaria)
Areas with an observed association between epidemic disease and weather extremes (e.g., El Niño–linked epidemics)
Areas at risk from combined climate impacts relevant to health (e.g., stress on food and water supplies or risk of coastal flooding)
Areas at risk from concurrent environmental or socioeconomic stresses (e.g., local stresses from land-use practices or an impoverished or undeveloped health infrastructure) and with little capacity to adapt
These Earth system changes have complex direct and indirect implications for human health, as illustrated in Figure 12.3. This figure, crafted by Dr. Tony McMichael, a seminal thinker regarding the health impacts of global change, reflects the ecological approach presented in Chapter 2. It depicts the interacting physical, social, and economic processes that determine health. The following sections of this chapter address major categories of anticipated health effects of climate change. These include malnutrition (possibly the largest problem); risks from weather extremes and disasters such as heat and cold, storms and flooding, and drought and wildfires; air pollution and aeroallergens; infectious diseases, including those that are waterborne, foodborne, and vector-borne; mental health effects; and the effects of armed conflict and dislocation. The last section of the chapter addresses the public health response to climate change, from preparedness to greenhouse gas mitigation. Co-benefits of mitigation are considered, as well as the ethical dimensions of climate change and health.
611
Figure 12.3 Processes and Pathways Through Which Climate Change Influences Human Health
Source: McMichael, 2013.
612
Food and Malnutrition Malnutrition is one of the most pressing health concerns in the context of the changing climate. Three mechanisms affect food security: reduced crop yields, increased crop losses, and decreased nutrient content.
On average, climate change is projected to reduce global food production by up to 2% per decade, even as demand increases by 14% (Porter et al., 2014). More than 800 million people currently experience chronic hunger, concentrated in areas where productivity could likely be most affected (Food and Agriculture Organization of the United Nations [FAO], 2013; Wheeler & von Braun, 2013). Major contributors to reduced yields will be water shortages (especially for glacial melt–dependent regions in Asia, Europe, and South America) and hotter temperatures (because most cultivars are already growing close to their thermal optimum). Wheat, maize, sorghum, and millet yields are estimated to decline by approximately 8% across Africa and South Asia by 2050 (Porter et al., 2014). By 2050, around 25 million more children might be undernourished as the result of climate change, and rates of growth stunting could increase substantially (Nelson et al., 2009; Lloyd, Sari Kovats, & Chalabi, 2011). Climate change-related price shocks (rapid rises in food prices), especially for staples such as corn and rice, could more than double by mid-century, placing impoverished populations at further risk (Bailey, 2011).
Plant diseases caused by fungi, bacteria, viruses, and oomycetes, already responsible for a 16% global crop loss, may substantially increase with climate change (Chakraborty & Newton, 2011). In addition, climate change favors the growth of many weeds, which compete with crops (Ziska & McConnell, 2015). Also, the nutrient value of some crops may diminish. CO2 “fertilization” can reduce the protein content in wheat and rice, and the iron and zinc content in crops such as rice, soybeans, wheat, and peas (S. S. Myers et al., 2014).
Adaptive measures range from drought- or salt-resistant crops to improved technology such as drip irrigation and hoop houses (inexpensive greenhouses). Other potential adaptation strategies
613
include changing planting dates, increasing crop diversity, reducing waste, increasing cropping efficiency, and changing diets.
An indirect pathway by which climate change may affect crops is biofuel production. Some crops and cropland will be diverted from food to fuel. While the impacts are controversial, this diversion may have unintended consequences, contributing to food shortfalls and rising food prices (Tirado, Cohen, Aberman, Meerman, & Thompson, 2010; Harvey & Pilgrim, 2011; HLPE, 2013).
In addition to reducing crop production, climate change will affect food availability in another way: through its effects on fisheries and aquaculture. According to the FAO (2013), 540 million people globally depend on wild fisheries and aquaculture as sources of protein and income. For the poorest 80% of these, fish represents at least half of their animal protein and dietary minerals. Climate change will affect river and marine ecosystems and threaten fish availability, through many pathways. A key issue is ocean acidification; oceans have absorbed about 30% of anthropogenic CO2, their surface pH has become 0.1 units more acidic since the beginning of the industrial era, and IPCC scenarios predict a further drop in global surface ocean pH of between 0.14 and 0.35 units over the twenty-first century (IPCC, 2013). Ocean acidification threatens marine shell-forming organisms (such as corals) and their dependent species. Other challenges to fisheries include altered river flows, destructive coastal storms, and the spread of pathogens (Cochrane, De Young, Soto, & Bahri, 2009; Porter et al., 2014).
614
Weather Extremes and Disasters Extreme temperatures, severe storms, rising sea levels, and floods, droughts, and wildfires are all threats to public health. Although slight changes in the average blood pressure or cholesterol level across a population can represent a health risk, in the case of climate it is the extremes of temperature and in the water cycle that threaten human health.
Heat Waves Extremes of both hot and cold temperatures are associated with higher morbidity and mortality compared to the intermediate, or comfortable, temperature range (Kilbourne, 2008). The relationship between temperature and morbidity and mortality is J- shaped, with a steeper slope at higher temperatures.
The body's thermoregulatory mechanisms can cope with a certain amount of temperature rise through control of perspiration and vasodilation of cutaneous vessels. The ability to respond to heat stress is thus limited by the capacity to increase cardiac output as required for greater cutaneous blood flow. Over time, people can adapt to high temperatures by increasing their ability to dissipate heat through these mechanisms. Heat-related illnesses range from heat exhaustion to kidney stones (which increase with dehydration).
Epidemiologists quantify heat-related mortality in two ways: tabulating death certificates that cite heat as a cause, and tracking mortality increases across populations during heat waves— periods of unusually hot weather, defined by the World Meteorological Organization as more than five consecutive days with temperatures at least 5°C above the average maximum temperature during the 1961 to 1990 baseline period. The first approach typically leads to underestimates, because heat-related deaths are routinely attributed to cardiovascular and other causes without citing heat as the underlying factor. In the United States, an average of 658 deaths are certified as heat-related each year, representing more fatalities than all other weather events combined (Luber & McGeehin, 2008; Centers for Disease Control and Prevention [CDC], 2013). More accurate risk estimates compare
615
observed versus expected mortality during heat events; for example, 70,000 excess deaths were estimated for the 2003 European heat wave and 15,000 for the 2010 Russian heat wave (Robine et al., 2008; Matsueda, 2011).
Heat waves have been growing more frequent, more intense, and longer in duration over recent decades (Habeeb, Vargo, & Stone, 2015), and this trend is expected to continue, especially in the high latitudes of North America and Europe (Goodess, 2013). “Mega” heat waves (as have occurred in Europe and Russia) are projected to increase in frequency by five- to tenfold within the next forty years (Barriopedro, Fischer, Luterbacher, Trigo, & García-Herrera, 2011). Figure 12.4 shows the projected number of extremely hot days each year in Milwaukee, Atlanta, New York City, and Dallas (defined as above 32°C [90°F] in the first three cities, and above 38°C [100°F] in Dallas). Each city will confront a marked increase in hot days— for example, a tripling in New York (Patz, Frumkin, Holloway, Vimont, & Haines, 2014). These trends will have serious public health consequences. While air conditioning and preparedness have reduced heat-related deaths and illness in the United States (Kalkstein, Greene, Mills, & Samenow, 2011), climatic and demographic trends (such as the aging population) suggest that risks may persist. One estimate, focusing on a set of twelve U.S. cities, projected over 200,000 excess heat-related deaths during the twenty-first century (Petkova et al., 2014). While the reduction of extremely cold days will avoid some cold-related deaths, this reduction is not expected to balance the increase in heat-related deaths (Luber et al., 2014).
616
Figure 12.4 Number of Days in June, July, and August When Daytime Maximum Temperatures Exceed a Given Threshold (indicated by a vertical line)
Source: Patz et al., 2014.
The solid-line curves show observations from 1960–1999, and the dotted-line curves, shifted to the right, show projected distributions for 2046–2065 under a business-as - usual emissions scenario. A relatively small shift can lead to a substantial change in the area under the steep portion of the curve.
The epidemiology of heat waves has been well studied, and vulnerability and protection factors are well known. People who are most vulnerable include the poor, the elderly, those who are socially isolated, those who lack air conditioning, and those with certain medical conditions that impair the ability to dissipate heat. A particular risk factor is living in cities, especially in hot parts of cities, because of the heat island effect.
An urban heat island is an urban area that generates and retains heat as a result of buildings, human and industrial activities, and other factors (Figure 12.5). Black asphalt and other dark surfaces (on roads, parking lots, and roofs) have a low albedo (reflectivity); they absorb and retain heat, reradiating it at night, when the area
617
would otherwise cool down. In addition, urban areas are relatively lacking in trees, so they lose the cooling effect associated with evapotranspiration.
Figure 12.5 Urban Heat Island Profile Source: WikiMedia Commons, 2011.
The urban heat island results from dark surfaces, loss of tree canopy, and concentrated generation of heat. Some neighborhoods in a city are far warmer than others, due to local factors such as topography and building types.
An interesting aspect of heat, and one with both health and economic consequences, is its impact on people at work. Outdoor workers such as farmworkers and construction workers, and those in facilities without air conditioning, such as garment factories in poor nations, are most directly affected by heat. The reduction in their work capacity can be substantial, with serious economic consequences. One study estimates that ambient heat stress has reduced global labor capacity by 10% at summer's peak over the past few decades (Dunne, Stouffer, & John, 2013), and by mid- century, workdays lost due to heat could reach 15% to 18% in Southeast Asia, West and Central Africa, and Central America (Kjellstrom, Holmer, & Lemke, 2009). These regions contain some fragile economies, which could be particularly susceptible to reduced labor capacity.
Climate-Related Disasters
618
Floods, droughts, and extreme storms have claimed millions of lives during recent years and have adversely affected the lives of many more millions of people and caused billions of dollars in property damage. According to the International Federation of Red Cross and Red Crescent Societies (IFRC), an average of 114,992 people died each year due to natural disasters during the period from 2003 to 2012 (Vinck, 2013). (The IFRC's World Disasters Report draws from the EM-DAT International Disaster Database at the Centre for Research on the Epidemiology of Disasters [CRED] at the University of Louvain, which is cited extensively in Chapter 24.) The number of people affected by natural disasters is two orders of magnitude greater than the number killed (CRED, 2015). In addition to causing acute deaths and injuries, disruption of health care, and lasting health impacts such as mental health disorders, disasters can halt or reverse economic growth and profoundly disrupt social structures.
Floods and Heavy Rain Floods are the most common type of natural disaster worldwide, with between 150 and 200 major floods occurring annually (Vinck, 2013). Increased severe rainstorms are one contributor. In the United States, the amount of precipitation falling in the heaviest 1% of rain events increased by 20% during the past century, and total precipitation increased by 7%. Over the last century the upper Midwest experienced a 50% increase in the frequency of days with precipitation of over four inches (Kunkel, Easterling, Redmond, & Hubbard, 2003). Other regions, notably the South, have also seen marked increases in heavy downpours, with most of these events coming in the warm season and almost all of the increase coming in the last few decades.
Heavy rains can increase the risk of waterborne diseases, a risk discussed below in the section on infectious diseases. They can also result in flooding that kills, injures, and displaces people. Population concentrations in high-risk areas such as floodplains and coastal zones increase vulnerability to floods. Degradation of the local environment can also contribute significantly to vulnerability. For example, Hurricane Mitch, the most deadly hurricane to strike the Western Hemisphere in the last two centuries, caused 11,000 deaths in Central America, with thousands
619
more people recorded as missing. Many fatalities occurred during mudslides in deforested areas (National Climatic Data Center, 1999).
Wildfires The incidence of extensive wildfires (those burning over 400 hectares each) in the Western United States rose fourfold between the period from 1970 to 1986 and the period from 1987 to 2003 (Westerling, Hidalgo, Cayan, & Swetnam, 2006). Several climate- related factors may have played a role in this increase: droughts that dried out forests; higher springtime temperatures that hastened spring snowmelt and thereby lowered soil moisture; and the rise of some tree pest species (Running, 2006; Westerling et al., 2006). Forecasts call for an increased risk of wildfires in many (but not all) areas over the course of the twenty-first century (Moritz et al., 2012).
Wildfires threaten health both directly and through reduced air quality. Fire smoke carries a large amount of fine particulate matter that exacerbates cardiac and respiratory problems such as asthma and chronic obstructive pulmonary disease (COPD). A study on worldwide mortality estimated 339,000 premature deaths per year (with a possible range of 260,000–600,000 deaths) attributable to pollution from forest fires, especially particulates (Johnston et al., 2012).
620
Air Pollution Climate change may affect exposure to air pollutants in many ways because it can influence both the levels of pollutants that are formed and the ways in which these pollutants are dispersed. Air quality is likely to suffer with a warmer, more variable climate (Bernard, Samet, Grambsch, Ebi, & Romieu, 2001).
Ozone Ozone is an example of a pollutant whose concentration may increase with a warmer climate. As explained in Chapter 13, higher temperatures increase ozone formation from precursors—a relationship demonstrated in many cities, and shown graphically in Figure 12.6. Accordingly, the ozone season in affected cities occurs during the summer, when warmer temperatures promote ozone formation. (Particulate matter formation can also increase at higher temperatures, due to increased gas-phase reaction rates.) This suggests that hotter summers will worsen air quality. However, air pollution chemistry is complex, and other factors—from changing vegetation to policies that reduce methane emissions—will also play a role, leading to variability from place to place (Fiore, Naik, & Leibensperger, 2015).
621
Figure 12.6 The Relationship Between Temperature and Ozone Levels in Santiago, Chile
Source: Rubio & Lissi, 2014.
This graph shows the association between measured maximum temperature, and the average eight-hour ozone level, measured in Santiago's O'Higgins Park. In studies in cities around the world, hot days feature higher ozone levels.
The role of vegetation is especially interesting. As explained in Chapter 13, many species of trees emit volatile organic compounds (VOCs) such as isoprenes, which are precursors of ozone. Isoprene production is highly responsive to leaf temperature and light. Under the right circumstances, higher levels of isoprenes result in higher levels of ozone (Squire et al., 2015).
The relationship between climate change and air pollution is complex. Many feedback loops operate, some helpful and others harmful. On the one hand, some particles in the air reflect radiant energy and can help to cool the atmosphere; the best-known example is the cooling that follows major volcanic eruptions. On the other hand, a warmer climate will mean more demand for energy to power air conditioners, resulting in more air pollution (if fossil fuel
622
plants supply the power). Overall, for air pollution, as for many other aspects of climate change, the impacts are not fully understood, but potential threats to public health deserve careful attention.
Aeroallergens Pollen is another air contaminant that may increase with climate change. Higher levels of carbon dioxide promote growth and reproduction by some plants, including many that produce allergens. Ragweed plants experimentally exposed to high levels of carbon dioxide can increase their pollen production several-fold. Over half the U.S. population (55%) tests positive for allergens, and over 34 million have asthma (Allergy USA, 2014). In recent decades the allergy season has lengthened with earlier flowering of some species, such as oaks, and levels of allergens such as ragweed (Ambrosia) pollen have risen, a predictable effect of higher temperatures and CO2 levels (Zhang et al., 2015). Ragweed season has been lengthening since the mid-1990s, particularly at higher latitudes along a 1,600-mile north-south sampling of monitoring stations through mid-North America (Ziska et al., 2011).
Aeroallergens are not the only allergens to become more troublesome with climate change. With higher levels of carbon dioxide, poison ivy grows more exuberantly, and its allergen, urushiol, becomes more allergenic. Unhappily, poison ivy seems to enjoy a special advantage compared to other plants; its vines grow twice as much per year in air with doubled preindustrial carbon dioxide levels as in unaltered air, a fivefold greater increase than reported for other plant species (Mohan et al., 2006). Emerging evidence suggests that other allergenic species respond to climate change by becoming more harmful; researchers have observed enhanced growth of weeds such as stinging nettle and leafy spurge, which cause rashes following skin contact (Ziska, 2003), greater allergenicity of Aspergillus (Lang-Yona et al., 2013), and extended ranges and active seasons for some stinging insects.
623
Infectious Diseases A range of infectious diseases can be influenced by climate conditions. The diseases most sensitive to influence by ambient climate conditions are those spread not by person-to-person pathways but directly from the source: the waterborne and foodborne diseases as well as vector-borne diseases (which involve insects and/or rodents in the pathogen's life cycle). For each of these infectious diseases, climate factors interact with a range of other factors: land-use patterns (deforestation, road construction, urbanization, dam construction), disease control programs, and others. Accordingly, these diseases, and the ways in which climate change affects them, are best considered through the lens of ecological thinking (see Chapter 2).
Waterborne Diseases Waterborne diseases are likely to become a greater problem as climate change continues and affects both freshwater and marine ecosystems. In freshwater systems, both water quantity and water quality can be affected by climate change. In marine waters, changes in temperature, ph, and salinity will affect coastal ecosystems in ways that may increase the risk of certain diseases.
Freshwater Ecosystems Waterborne diseases are particularly sensitive to changes in the hydrological cycle. Many community water systems are already overwhelmed by extreme rainfall events. Flooding can contaminate drinking water with runoff from sewage lines, containment lagoons (such as those used in animal feeding operations), or nonpoint source pollution (such as agricultural fields) across watersheds. Runoff can exceed the capacity of the sewer system or treatment plants, which then discharge the excess wastewater directly into surface water bodies. Urban watersheds sustain more than 60% of their annual contaminant loads during storm events (Fisher & Katz, 1988).
Thus it is no surprise that outbreaks of such diseases as cryptosporidiosis and giardiasis are associated with prior heavy rainstorms (Curriero, Patz, Rose, & Lele, 2001; Cann, Thomas,
624
Salmon, Wyn-Jones, & Kay, 2013). Childhood gastrointestinal illness in the United States (Uejio et al., 2014) and India (Bush et al., 2014) has been linked to heavy rainfall. A Dutch study showed a 33% increase in gastrointestinal illness associated with sewage overflow following heavy rain; flood waters contained Campylobacter, Giardia, Cryptosporidium, noroviruses, and enteroviruses (De Man et al., 2014). An infamous example of heavy rain contributing to an outbreak was the 1993 Milwaukee cryptosporidiosis outbreak (Rose, 1997), which sickened over 400,000 and killed over 100.
With climate change projected to result in more severe and frequent precipitation events, the risk of waterborne diseases is expected to rise (Patz & Hahn, 2013). Using 2.5 inches (6.4 cm) of daily precipitation as the threshold for initiating a combined sewer overflow (CSO) event, the frequency of such events in Chicago is expected to rise by 50% to 120% by the end of this century (Patz Vavrus, Uejio, & McLellan, 2008), posing increased risks to drinking and recreational water quality.
Intense rainfall can also contaminate recreational waters and increase the risk of human illness (Schuster et al., 2005). For example, heavy runoff leads to higher bacterial counts in rivers in coastal areas and at coastal beaches, especially at the beaches near river outflows (Dwight, Semenza, Baker, & Olson, 2002). This suggests that the risk of swimming at some beaches increases with heavy rainfall, a predicted consequence of climate change.
Marine Ecosystems Warm water and nutrient loading (primarily with nitrogen and phosphorus) favor blooms of marine algae, including two groups, dinoflagellates and diatoms, that can release toxins into the marine environment. These harmful algal blooms (HABs)—previously called red tides—can cause acute paralytic, diarrheic, and amnesic poisoning in humans, as well as extensive die-offs of fish, shellfish, and marine mammals and birds that depend on the marine food web. Over recent decades the frequency and global distribution of harmful algal blooms appear to have increased, along with more human intoxication from algal sources (Anderson, Cembella, & Hallegraeff, 2012). These have occurred both in marine settings and in freshwater lakes, such as Lake Erie (Figure 12.7). For example, in
625
the summer of 2012, a group of seven vacationers on the Washington coast harvested mussels, prepared them in a soup, and ate them; within hours they experienced paresthesias, a “floating” sensation, nausea, vomiting, ataxia, and other symptoms. They were diagnosed with paralytic shellfish poisoning, a condition caused by eating fish or shellfish contaminated by saxitoxin, an algal product more toxic than sodium cyanide (Hurley, Wolterstorff, MacDonald, & Schultz, 2014). Of note, the number of cases reported in 2012 was substantially higher than in previous years; this was attributed to an unusually warm, sunny summer. Climate change is predicted to increase the frequency of such episodes, and in addition, ocean acidification may increase the toxicity of some algal species (Fu, Tatters, & Hutchins, 2012; Glibert et al., 2014). Ciguatera, a form of poisoning caused by ingesting fish that contains toxins from any of several dinoflagellate species, could also expand its range. This condition has been linked to sea surface temperatures, and as these warm, according to one projection, ciguatera fish poisoning could increase by two- to fourfold over the coming century (Gingold, Strickland, & Hess, 2014).
Figure 12.7 Satellite Photo of a Harmful Algal Bloom in Lake Erie in 2011
Source: National Oceanic and Atmospheric Administration, 2014.
This was the worst bloom in recent history, impacting over half the lake shore.
Some bacteria, especially Vibrio species, also proliferate in warm
626
marine waters (Pascual, Rodó, Ellner, Colwell, & Bouma, 2000). Copepods (or zooplankton), which feed on algae, can serve as reservoirs for V. cholerae and other enteric pathogens. For example, in Bangladesh, cholera follows seasonal warming of sea surface temperatures, which can enhance plankton blooms (Colwell, 1996). Other Vibrio species have expanded in northern Atlantic waters in association with warm water (Thompson et al., 2004). For example, in 2004 an outbreak of V. parahaemolyticus shellfish poisoning was reported from Prince William Sound in Alaska. This pathogenic species of Vibrio had not been isolated from Alaskan shellfish previously due to the coldness of the Alaskan waters. What could have caused the species' expanded range? Water temperatures during in the 2004 shellfish harvest remained above 15°C, and mean water temperatures were significantly higher than they had been during the previous six years (McLaughlin et al., 2005). Such evidence suggests the potential for warming sea surface temperatures to increase the geographic range of shellfish poisoning and Vibrio infections into temperate and even arctic zones.
The incidence of diarrhea from other pathogens also shows temperature sensitivity, which may in turn signal sensitivity to changing climate. During the 1997 and 1998 El Niño event, winter temperatures in Lima, Peru, increased more than 5°C above normal, and the daily hospital admission rates for diarrhea more than doubled compared to rates over the prior five years (Checkley et al., 2000) (Figure 12.8)—a pattern that has been confirmed in multiple settings (Vezzulli, Colwell, & Pruzzo, 2013). Long-term studies of the El Niño–Southern Oscillation, or ENSO, have confirmed this pattern. ENSO refers to natural year-to-year variations in sea surface temperatures, surface air pressure, rainfall, and atmospheric circulation across the equatorial Pacific Ocean. This cycle provides a model for observing climate-related changes in many ecosystems. Sea surface temperature has had an increasing role in explaining cholera outbreaks in recent years (Vezzulli et al., 2013), as has ENSO, perhaps because of concurrent climate change (Rodó, Pascual, Fuchs, & Faruque, 2002). Overall there is growing evidence that climate change can contribute to the risk of waterborne diseases in both marine and freshwater ecosystems.
627
Figure 12.8 The Association Between Temperature and Childhood Diarrhea, Peru, 1993–1998
Source: Checkley et al., 2000.
Daily time series between January 1, 1993, and November 15, 1998, for admissions for diarrhea and for mean ambient temperature in Lima, Peru. Shaded area represents the 1997–1998 El Niño event.
Foodborne Diseases More frequent warm days, greater humidity, and other climate- related factors can affect the persistence and dispersal of foodborne pathogens in many ways, and can increase the risk of foodborne infectious diseases (Hellberg & Chu, 2015). (As described in Chapter 16, waterborne and foodborne diseases can be hard to distinguish from each other, because contaminated water often contaminates food.) Data from many parts of the world show a strong association
628
between temperature and the incidence of food poisoning with various pathogens—Campylobacter, Salmonella, Cryptosporidium, Shigella, and Giardia—showing different time lags between peak temperature and the peak in infections, and with the effect most pronounced at especially high temperatures (Kovats et al., 2004; Naumova et al., 2007). Not surprisingly, modeling suggests a sharp increase in foodborne illness with continued climate change. For example, one study, focusing on Beirut, projected a 16% to 28% increase by mid-century, and an increase of up to 42% by 2100 (El- Fadel, Ghanimeh, Maroun, & Alameddine, 2012). Improved food- handling practices, which play a major part in prevention, are therefore an important aspect of climate change adaptation (Lake et al., 2009).
Vector-Borne Diseases Vector-borne diseases are infectious diseases, caused by protozoa, bacteria, and viruses, that are spread by organisms such as mosquitoes and ticks. The life cycle of these pathogens involves much time outside the human host and therefore much exposure to and influence by environmental conditions. The term tropical diseases is a reminder that each pathogen or vector species thrives in a limited range of climatic conditions.
The incubation time of a vector-borne infectious agent within its vector organism is typically very sensitive to changes in temperature and humidity (Patz et al., 2003). Many other mechanisms govern the impact of climate change on vector-borne diseases, as shown in Text Box 12.1 geographic shifts of vectors or reservoirs; changes in rates of development, survival, and reproduction of vectors, reservoirs, and pathogens; and increased biting by vectors and prevalence of infection in reservoirs or vectors (Medlock & Leach, 2015). All affect transmission to humans, such that exposure to vector-borne disease will likely worsen in a warmer world (Mills, Gage, & Khan, 2010; Patz & Hahn, 2013).
629
Text Box 12.1 Some Effects of Weather and Climate on Vector- and Rodent- Borne Diseases Vector-borne pathogens spend part of their life cycle in cold- blooded arthropods that are subject to many environmental factors. Changes in weather and climate that can affect transmission of vector-borne diseases include variations in temperature, rainfall, wind, extreme flooding or drought, and sea level rise. Rodent-borne pathogens can be affected indirectly by ecological determinants of food sources, affecting rodent population size, and floods can displace them and lead them to seek food and refuge. These effects are summarized in Table 12.2.
Table 12.2 Temperature and Precipitation Effects on Selected Vectors and Vector-Borne Pathogens
Temperature effects
Vector Survival can decrease or increase depending on the species.
Some vectors have higher survival at higher latitudes and altitudes with higher temperatures.
Changes in susceptibility of vectors to some pathogens (e.g., higher temperatures reduce the size of some vectors but reduce the activity of others).
Changes in the rate of vector population growth.
Changes in feeding rate and host contact (which may alter the survival rate).
Changes in the seasonality of populations.
Pathogen Decreased extrinsic incubation period in
630
vector at higher temperatures.
Changes in the transmission season.
Changes in distribution.
Changes in viral replication.
Precipitation effects
Vector Increased rain may increase larval habitat and vector population size by creating a new habitat.
Excess rain or snowpack can eliminate habitat by flooding, thus decreasing the vector population size.
Low rainfall can create habitat by causing rivers to dry into pools (dry season malaria).
Decreased rain can increase container- breeding mosquitoes by forcing increased water storage.
Epic rainfall events can synchronize vector host seeking and virus transmission.
Increased humidity increases vector survival; decreased humidity decreases vector survival.
Pathogen Few direct effects but some data on humidity effects on malarial parasite development in the anopheline mosquito host.
Vertebrate host
Increased rain can increase vegetation, food availability, and population size.
Increased rain can also cause flooding and decrease population size but increase contact with humans.
Decreased rain can eliminate food and force rodents into housing areas, increasing human contact, but it can also decrease
631
population size.
Increased sea level
Can alter estuary flow and change existing salt marshes and associated mosquito species, decreasing or eliminating selected mosquito breeding sites (e.g., reduced habitat for Culiseta melanura).
Source: Adapted from Gubler et al., 2001.
Mosquito-Borne Diseases Malaria and arboviruses are transmitted to humans by mosquitoes. Because insects are cold-blooded, climate change can shift the distribution of mosquito populations, affect mosquito biting rates and survival, and shorten or lengthen pathogen development time inside the mosquito, factors that ultimately determine infectivity.
Malaria remains a scourge in many parts of the world. Despite considerable progress in fighting this disease in recent decades, it still accounts for over a million deaths each year, about 90% of these in Africa (Murray et al., 2012). Malaria risk is complex, and varies with demographic shifts, control measures, and other factors (Parham et al., 2015). However, malarial mosquito populations can be exquisitely sensitive to warming; an increase in temperature of just half a degree centigrade can translate into a 30% to 100% increase in mosquito abundance, an example of biological amplification by temperature effect (Pascual, Ahumada, Chaves, Rodó, & Bouma, 2006). Accordingly, most models forecast global increases in malaria risk over the next century, especially in highland regions of Africa, Asia, and Latin America (with some reduction of risk in tropical regions) (Caminade et al., 2014), emphasizing the importance of malaria control measures as a part of climate adaptation.
Arboviruses include the causative agents of dengue fever, West Nile virus, chikungunya, and Rift Valley fever. Dengue and chikungunya are transmitted by Aedes mosquitoes, West Nile virus by Culex mosquitoes, and Rift Valley fever usually through contact with the blood or organs of infected animals but also by Aedes mosquitoes. The four diseases differ clinically and epidemiologically, and have
632
distinct geographic ranges. For example, Rift Valley fever has generally been confined to east Africa, although it has recently spread to other parts of Africa and to the Arabian peninsula, while dengue fever is widespread across south Asia, Africa, and Latin America. However, the four diseases also share important features, all relevant to climate change. First, there is evidence that climatic conditions, such as temperature and rainfall, can affect their spread. Second, the geographic range of all four diseases has expanded in recent decades. Third, modeling projects the potential for further spread with continued climate change. Finally, for each disease, infection reflects complex interplays of behavior, land use, mosquito control strategies, and other factors, so controlling these diseases in the face of climate change will be a complex challenge (Martin et al., 2008; Dhiman, Pahwa, Dhillon, & Dash, 2010; Weaver & Reisen, 2010; Morin et al., 2013; Campbell et al., 2015; Paz, 2015).
Tick-Borne Disease Lyme disease is a tick-borne disease that was first described in the 1970s and has since become prevalent in North America, Europe, and Asia. The ecology and infectivity of this disease are related to many factors, such as habitat fragmentation and increased human contact with the mammals (deer, mice, and others) that carry the vector, the Ixodes tick. However, the tick life cycle is strongly influenced by temperature and other weather factors; for example, cold weather is limiting (Ostfeld & Brunner, 2015). The tick range has been expanding, and warming temperatures are projected to shift the range limit for this tick northward by 200 km by the 2020s and 1,000 km by the 2080s (Ogden et al., 2006).
Rodent-Borne Diseases Rodent populations can be affected by weather, raising the potential for the diseases they transmit to be climate responsive. Examples of these diseases include hantavirus infection, leptospirosis, and plague.
Hantavirus infections are transmitted largely by exposure to infectious excreta from rodents and may cause serious disease and a high fatality rate in humans. Hantavirus pulmonary syndrome emerged in the southwestern United States in 1993, after an El Niño brought heavy rains, which in turn led to a growth in rodent
633
populations (Glass et al., 2000). Leptospirosis, a bacterial disease that can feature pulmonary hemorrhage, meningitis, and kidney failure, is transmitted through the urine of infected rodents and other mammals. Events that increase exposure to rodents, such as extreme flooding, can greatly increase the risk of contracting this disease (Lau, Smythe, Craig, & Weinstein, 2010). Finally, plague is caused by the bacteria Yersinia pestis, which is transmitted by fleas, whose primary reservoir host is rodents. Plague also varies with weather and across seasons (Ben Ari et al., 2011). In fact, historical tree-ring data suggest that during the major plague epidemics of the Black Death period (1280 to 1350), climate conditions were becoming both warmer and wetter (Stenseth et al., 2006).
634
Mental Health Effects Mental health disorders such as depression and anxiety cause major morbidity worldwide (Whiteford et al., 2013). Climate change may threaten mental health in several ways (Fritze, Blashki, Burke, & Wiseman, 2008; Berry, Bowen, & Kjellstrom, 2010; Doherty & Clayton, 2011).
Mental Health Impacts of Climate-Related Disasters Following disasters such as floods and wildfires, mental health consequences such as post-traumatic stress, depression, and anxiety are common, and may represent a major part of the resulting health burden (North & Pfefferbaum, 2013; Goldmann & Galea, 2014). Several months after Hurricane Katrina, 49.1% of those surveyed in New Orleans, and 26.4% in other affected areas, had developed anxiety-mood disorder, as defined in the DSM-IV, and one in six had post-traumatic stress disorder (PTSD) (with considerable overlap between the two) (Galea et al., 2007). Researchers have documented similar patterns after floods, dam collapses, heat waves, droughts, and wildfires—all disasters likely to increase with climate change. Mental health typically improves over time following disasters, but distress may persist for years, especially among vulnerable groups (Norris, Tracy, & Galea, 2009). Risk factors for mental disorders following disasters include low social capital or support, physical injury, property loss, witnessing others with illness or injury or in pain or dying during the disaster, loss of family, displacement, and a preexisting history of psychiatric illness. Children may be at special risk. These risk factors suggest a variety of protective strategies, including strengthening social support both before and after disasters, providing postdisaster mental health services, and prompt insurance compensation for loss.
Slow-moving climate disasters may also threaten mental health. In Australia during the recent decade-long drought, increases were found in anxiety, depression, and possibly suicidality among rural populations (Berry, Hogan, Owen, Rickwood, & Fragar, 2011). Strategies to reduce this burden included raising mental health literacy, building community resilience through social events, and disseminating drought-related information (Oldham, 2013).
635
Mental Health Impacts of Displacement Climate change may degrade familiar environments, causing a sense of loss, stress, and mental distress. In Arctic settings, where climate change has led to rapid environmental degradation and where indigenous peoples place high cultural value on place attachment, this phenomenon has been documented (Brubaker, Berner, Chavan, & Warren, 2011). In addition, climate change may force populations to relocate, either after an acute disaster or because needed resources (such as fresh water) become increasingly scarce (United Nations High Commissioner for Refugees, 2009). This relocation may create a considerable mental health burden (Loughry, 2010). An important protective strategy is keeping families, even entire communities, united (Jacob, Mawson, Payton, & Guignard, 2008).
Anxiety and Despair Related to Climate Change Climate change may exacerbate feelings of despair, anxiety, and hopelessness (Fritze et al., 2008; Doherty & Clayton, 2011). As discussed later in this chapter, effective communication and empowering people to take constructive actions may be useful strategies.
Heat and Mental Illness Hot weather may pose special hazards for people with underlying mental illness (Bulbena, Sperry, & Cunillera, 2006; Bouchama et al., 2007). Four categories of ailments are relevant: depression and suicide, dementia, psychotic illness, and substance abuse.
Suicide has long been observed to vary in seasonal patterns, with increases in the spring and early summer in northern latitudes, and to increase with hot weather. A study of suicides in the United Kingdom between 1993 and 2003 (Page, Hajat, & Kovats, 2007) showed a 3.8% increase in suicide for each degree Celsius of temperature rise above 18 degrees. Could a warming climate increase the risk of suicide?
Dementia is an established risk factor for hospitalization and death during heat waves (Basu & Samet, 2002). Contributing factors may include impaired cognitive ability to recognize risk and to respond appropriately, and the effects of medications and age.
636
For patients with psychotic illness such as schizophrenia, extremely hot weather has been associated with increased risk of disease exacerbation, as measured by increased hospital admissions (Sung, Chen, Lin, Lung, & Su, 2011). Three reasons may operate: illness- associated defects in thermoregulation, medication-related defects in thermoregulation, and impaired cognitive ability to recognize risk and to respond appropriately.
Substance abuse may increase risk during severe heat because of the dehydration associated with alcohol and opioid use, and the elevation of body temperature induced by sympathomimetic drugs, such as amphetamine, cocaine, and MDMA (Martinez, Devenport, Saussy, & Martinez, 2002).
Adaptation measures include increased special attention to people with mental illness in heat wave preparedness planning, increased monitoring of such patients during heat waves, and training of health care providers (Cusack, de Crespigny, & Athanasos, 2011).
War, Refugees, and Population Dislocation Climate-related disasters may trigger broad population dislocations, often to places ill prepared for the quantity and needs of refugees overwhelmed by undernutrition and stress. Even with baseline refugee support, displaced groups commonly experience a range of public health threats, including violence, sexual abuse, and mental illness (McMichael, McMichael, Berry, & Bowen, 2010).
A growing body of evidence links climate change and violence, from self-inflicted and interpersonal harm to armed conflict (Levy & Sidel, 2014). A meta-analysis by Hsiang, Burke, and Miguel (2013) found that each standard deviation of increased rainfall or warmer temperature increases the likelihood of intergroup conflict by 14% on average. Strategic analyses by military authorities—both the Center for Naval Analysis Military Advisory Board, a group of retired generals (CNA Military Advisory Board, 2014), and the U.S. Department of Defense (2014)—have warned that climate change could catalyze instability and conflict.
637
The Public Health Response to Climate Change The links between human health and climate change are complex, diverse, and not always discernible, especially over short time spans. Understanding and addressing these links requires systems thinking, with consideration of many factors, ranging beyond health to such sectors as energy, transportation, agriculture, and development policy (Frumkin & McMichael, 2008). Interdisciplinary collaboration is critical. A wide range of tools is needed, including innovative public health surveillance methods, geographically based data systems, classical and scenario-based risk assessment, and integrated modeling.
Mitigation and Adaptation Two kinds of strategies, both familiar to public health professionals, are relevant in responding to climate change. The first, known as mitigation, corresponds to primary prevention, and the second, known as adaptation, corresponds to secondary prevention (or preparedness).
Mitigation aims to stabilize or reduce the production of greenhouse gases (and perhaps to sequester those greenhouse gases that are produced). Key mitigation strategies include more efficient energy production and reduced energy demand. For example, sustainable energy sources, such as wind and solar energy, do not contribute to greenhouse gas emissions (see Chapter 14). Similarly, transportation policies that rely on walking, bicycling, mass transit, and fuel-efficient automobiles result in fewer greenhouse gas emissions than are produced by the current U.S. reliance on large, fuel-inefficient automobiles (see Chapter 15). Much energy use occurs in buildings, and green buildings that emphasize energy efficiency, together with electrical appliances that conserve energy, also play a role in reducing greenhouse gas emissions (see Chapter 20). Some mitigation strategies aim not to reduce the production of greenhouse gases but to accelerate their removal from the atmosphere. Carbon dioxide sinks such as forests are effective in this regard, so land-use policies that preserve and expand forests
638
are an important tool in mitigating global climate change.
An important concept in mitigation is stabilization wedges. This concept is explained in Figure 12.9. Figure 12.9 graphs annual carbon emissions over time. It shows two possible pathways during the twenty-first century: the current path, which is a steep continued rise in emissions, and a flat path, which represents stabilization of current emissions. (Of course, this is a simplified schematic; other paths are possible, such as stabilization at some different emission level, or a downward path representing reduced emissions.) The triangle between the current path and the flat path is called the stabilization triangle, and it represents the reductions needed to reach stabilization. Figure 12.10 divides that triangle into wedges, each corresponding to a strategy that reduces carbon emissions by 1 billion tons per year. These strategies include energy efficiency, waste reduction, replacing coal with natural gas, increasing reliance on nuclear energy, switching to renewable energy sources, and land-use and agricultural changes. In 2004, when this concept was introduced, seven wedges were needed to achieve stabilization; at present, because emissions have continued to rise since then, eight or nine wedges would be required. To surpass stabilization, and reduce carbon emissions enough to avoid dangerous climate change, as many as nineteen wedges could be needed (Davis, Cao, Caldeira, & Hoffert, 2013). Most of these strategies are technically feasible and currently available (Pacala & Socolow, 2004; Socolow, 2011, September 27).
639
Figure 12.9a Alternative Emission Pathways Source: Princeton Environmental Institute, Carbon Mitigation Initiative, 2015.
Figure 12.9b Climate Stabilization Wedges Source: Princeton Environmental Institute, Carbon Mitigation Initiative, 2015.
Adaptation aims to reduce the public health impact of climate change. For example, if we anticipate severe weather events such as
640
hurricanes, then preparation by emergency management authorities and medical facilities can minimize morbidity and mortality. This presupposes rigorous vulnerability assessment efforts, to identify likely events, at-risk populations, and opportunities to reduce harm (Ebi, Smith, & Burton, 2005; Kirch, Menne, & Bertollini, 2005; Menne & Ebi, 2006; Schipper & Burton, 2009).
Improving essential infrastructure could help communities adapt to climate change. For example, vegetation, building placement, white roofs, and architectural design can reduce the urban heat island effect and therefore electricity demands for air conditioning. These efforts can involve complicated trade-offs. For example, a recent study found that waste heat from air conditioning can warm outdoor air more than 1°C, so an important adaptation to urban heat islands—the use of air conditioning—can actually contribute to urban heat islands (Salamanca, Georgescu, Mahalov, Moustaoui, & Wang, 2014)! Other examples of adaptation measures include heat wave early warning systems (Lowe, Ebi, & Forsberg, 2011) and switching from surface water to groundwater sources to reduce the risk of contamination (Ebi, Lindgren, Suk, & Semenza, 2013). Optimal adaptation strategies achieve multiple objectives in tandem, taking advantage of co-benefits, as discussed on the next page.
A holistic, ecological approach to climate change adaptation, rather than engineering single solutions, may better build resiliency and secure the multiple potential benefits and cost savings associated with these improvements. As sea level rises, seawalls have frequently served to stabilize shorelines. But planting mangroves for storm surge protection incurs a fraction of the cost of building and maintaining seawalls or dikes for this purpose, while also preserving wetlands and marine food chains that support local fisheries (Arkema et al., 2013).
Public Health Action Public health action related to climate change is based on many of the core public health functions, and utilizes many of the standard tools in the public health toolbox (Frumkin, Hess, Luber, Malilay, & McGeehin, 2008). For instance, public health surveillance is needed to detect the emergence or range expansion of infectious diseases, and public health communication helps people recognize hazards
641
and take appropriate precautionary actions. Forecasting and modeling, which are relatively new to public health, are also central to tackling climate change. In this endeavor, public health professionals collaborate with climate scientists, demographers, and others to build scenarios predicting how climate change will affect human health. Because the effects of climate change vary from place to place, scenarios are developed for specific locations (Moss et al., 2010; Ebi et al., 2014). This in turn enables planning and implementing strategies to protect the public.
Several frameworks for public health action on climate change have been proposed. A leading example is Building Resistance Against Climate Affects, or BRACE, described in Text Box 12.2.
642
Text Box 12.2 The CDC's BRACE Framework The Building Resilience Against Climate Effects (BRACE) framework, developed at the U.S. Centers for Disease Control and Prevention (CDC), is an approach to anticipating and managing the health effects of climate change (Marinucci, 2014). Designed to be used by state and local public health officials, it is implemented through the CDC's Climate-Ready States & Cities Initiative (www.cdc.gov/climateandhealth/climate_ready.htm). The BRACE framework consists of five steps, as shown in Figure 12.10.
Figure 12.10 The CDC's BRACE Framework Source: CDC, 2015.
643
Several aspects of the BRACE framework are notable. First, it embodies adaptive management—an iterative, learning- based approach to the design, implementation, and evaluation of interventions in complex, changing systems, as expressed by the cyclical structure of Figure 12.10. Second, the framework requires integrating climate data and health data, which in turn requires collaboration across disciplines. Third, priority setting is built into the framework, as agencies move sequentially through the steps. This is an important aspect when public health agencies face scarce resources and competing demands, and need to focus on the most important challenges.
Co-Benefits An important theme in both mitigation and adaptation is co- benefits. Although the steps needed to address climate change may appear formidable, some of them—reducing greenhouse gas emissions, shifting to renewable energy sources, shifting transportation patterns, shifting diets toward less meat, and others —yield many benefits (Jack & Kinney, 2010; Cheng & Berry, 2013; Thurston, 2013; West et al., 2013; Balbus, Greenblatt, Chari, Millstein, & Ebi, 2014), making them especially attractive, cost effective, and politically feasible. Examples of such co-benefits are shown in Table 12.3. Many of these co-benefits have been carefully investigated and quantified. For example, the production of meat is highly carbon intensive, accounting for as much as 18% of global greenhouse gas emissions (FAO, 2006). A British study found that lowering the consumption of red and processed meat in that country could reduce its greenhouse gas emissions by 3%, while cutting risks of coronary heart disease, diabetes, and colorectal cancer by fractions ranging up to 12% (Aston, Smith, & Powles, 2012). Similarly, a study in the Midwestern United States found that replacing short automobile trips by bicycling could reduce regional PM2.5 and ozone levels, and increase physical activity, enough to avoid 1,295 deaths per year in a region of 31.3 million people, and save approximately $3.8 billion a year from avoided mortality and reduced health care costs (Grabow et al., 2012). Such opportunities are referred to as no-regrets solutions, as suggested in Figure 12.11.
644
Table 12.3 Co-Benefits of Climate Mitigation and Adaptation Activities
Climate strategies Mitigation Shift From Single- Occupancy Vehicles Toward Cycling, Walking, Transit
Shift Diets Toward Less Meat, More Fruits and Vegetables
Shift Energy Sources From Fossil Fuels to Renewable Energy Sources
Benefits Direct Indirect
↑ Physical activity
↓ Cardiovascular disease, cancer, depression, etc.
↑ Air quality ↓ Cardiovascular & respiratory disease
Healthier diets
↓ Cardiovascular disease, stroke
↑ Nature contact
↑ Mental health, ↑ physical activity, ↑ property values
↑ Social capital
↑ Overall health and well-being
↓ Urban heat ↓ Heat-related
645
island morbidity
Improved stormwater management
↓ Flooding
Economic benefits
Figure 12.11 No-Regrets Solutions Source: Pett, 2009.
Joel Pett Editorial Cartoon used with the permission of Joel Pett and the Cartoonist Group. All rights reserved.
646
Climate Change as a Public Issue Public Belief in Climate Change Perspectives on and responses to climate change vary widely. Two decades of polling suggest that about two thirds of Americans believe that climate change is occurring; of these about two thirds (or about 40% of the total) believe humans cause it, and about half (or about one in three overall) believe it will pose a serious threat in their lifetimes (Jones, 2014; Pew Research, 2014; Leiserowitz et al., 2015). Americans tend to view climate change as remote in time and space—a problem for the next generation or people in faraway countries—and rank it as a low priority, well behind concerns such as jobs, health care, or even other environmental issues (Pew Research, 2014). In other wealthy nations, climate change tends to elicit greater public concern (Pugliese & Ray, 2009; Lee, Markowitz, Howe, Ko, & Leiserowitz, 2015).
The U.S. population may be segmented along a spectrum from “alarmed” (≈16%) to “dismissive” (≈10%), according to climate change beliefs, concerns, and motivations (Roser-Renouf et al., 2014) (Figure 12.12). Many factors shape views of climate change (Brulle, Carmichael, & Jenkins, 2012): economic trends, cultural norms, the beliefs of family and friends, and values and political ideology. People often form and reinforce their beliefs using cognitive shortcuts called heuristics, which bypass evidence (Pidgeon & Fischoff, 2011). Media coverage matters (Boykoff, 2011). Deliberate, well-funded attempts to deceive the public and sow confusion have succeeded (Oreskes & Conway, 2010; Brulle, 2014); despite robust scientific consensus on climate change, there is widespread perception that scientists disagree, which in turn fuels public disbelief (Lewandowsky, Gignac, & Vaughan, 2013). Many people also are unduly influenced by personal experience, such as short-term weather perturbations. A heat wave may strengthen belief in climate change, and a snowy winter may undermine it. Interpretation of weather rests heavily on prior beliefs and social cues (T. A. Myers, Maibach, Roser-Renouf, Akerlof, & Leiserowitz, 2013; Zaval, Keenan, Johnson, & Weber, 2014).
647
Figure 12.12 Global Warming's Six Americas: Arraying the U.S. Population Along a Continuum of Belief, Concern, and Motivation
Source: Roser-Renouf et al., 2014.
As discussed in Chapter 28, effective communication may shift knowledge, attitudes, and behavior toward reducing risks and promoting health. This is as true for climate change as it is for other health-relevant exposures (Maibach, Roser-Renouf, & Leiserowitz, 2008), and climate communication has become a focus of research and practice in both public health and other fields (Moser & Lisa, 2007; Moser, 2010; Whitmarsh, O'Neill, & Lorenzoni, 2011; Bostrom, Böhm, & O'Connor, 2013). The salient principles are those used in environmental health communication more generally: two- way communication, gearing messages to the audience, limiting use of fear-based messages (Feinberg & Willer, 2011), frequently repeating simple, clear messages from trusted sources, and making health-promoting choices easy and appealing.
For communicating climate change, health may be a compelling frame (Maibach, Nisbet, Baldwin, Akerlof, & Diao, 2010; Myers, Nisbet, Maibach, & Leiserowitz, 2012), reflecting the fact that substantial numbers of people believe that climate change threatens health (Akerlof et al., 2010). Although further research is needed to define the role of health in climate communication, practical communication resources are becoming available (Maibach, Nisbet, & Weathers, 2011). Moreover, health care providers are a highly trusted source, ranking significantly higher than mainstream media (Leiserowitz et al., 2015), implying an important role for health professionals in climate communication.
Climate Change Policy International efforts to address climate change are carried out
648
under the United Nations Framework Convention on Climate Change (UNFCCC). Adopted in 1992, the UNFCCC sets out a framework that aimed to stabilize atmospheric concentrations of greenhouse gases at a level that would prevent dangerous interference with the climate system. The UNFCCC has carried out its business through regular meetings called the Conferences of Parties (COP). Perhaps the best known was the third meeting, in 1997 in Kyoto. This resulted in the Kyoto Protocol, which committed developed countries and emerging market economies to reduce their overall emissions of six greenhouse gases by at least 5% below 1990 levels over the period between 2008 and 2012, with specific targets varying from country to country. However, the United States, at the time the largest greenhouse gas emitter (China has since surpassed it), did not sign the Kyoto Protocol.
By 2007, it was clear that many signatory nations were not on track to achieve their anticipated emission reductions, even though the protocol required relatively modest emissions reductions, far below those required to stabilize greenhouse gases at any level below 700 ppm. Barriers to robust international agreements have included the unwillingness of some wealthy countries (including the United States) to accept binding limits, and tension between wealthy countries (which have caused most greenhouse gas emissions) and low- and middle-income countries (which are eager for economic development, and believe that wealthy countries should shoulder much of the responsibility).
Market mechanisms could play a powerful role in reducing carbon emissions. This involves putting a price on carbon, to correct a market failure that contributes to ongoing emissions: the fact that the costs of these emissions are not borne by the individuals and firms that benefit but instead are externalized. There are two major approaches to increasing the price of carbon, both designed to guide decision making, reduce high-carbon practices, and incentivize the development and use of low-carbon technologies. In the first, cap and trade, government sets a ceiling (or cap) on total greenhouse gas emissions and distributes emissions permits (say, through an auction) among companies that emit. Companies then buy and sell these permits at prevailing market prices, as government progressively lowers the cap to reach stated goals. The United States successfully used a cap-and-trade system to reduce sulfur dioxide
649
and nitrous oxide emissions beginning in the 1980s, and greenhouse gas cap-and-trade systems are in place in the European Union, California, Tokyo, and other jurisdictions. The second mechanism is a carbon tax, in which government places a tax on carbon emissions. Carbon taxes are in use in Sweden and Ireland, in the Canadian provinces of British Columbia and Quebec, in Boulder, Colorado, and other jurisdictions. Economists and policy experts debate the relative merits of these two approaches (Aldy & Stavins, 2012; Goulder & Schein, 2013). While the debate may sound far removed from public health, the role of carbon pricing in preventing illness and injury makes the subject very much a matter of health policy (Howden-Chapman, Chapman, Capon, & Wilson, 2011).
However, both approaches require legislative action, and both meet stiff political opposition from such interests as fossil fuel companies (Jenkins, 2014). This political reality has prevented action at the federal level in the United States, and in Australia led to the repeal of a carbon tax in 2014, just two years after it was adopted. The alternative, then, is executive action. In the United States, this means regulation by the U.S. Environmental Protection Agency (EPA). Regulation of greenhouse gases dates to the Massachusetts v. EPA Supreme Court ruling in 2007, which found that greenhouse gases met the definition of air pollutants under the Clean Air Act. The EPA was then required to make a scientific determination—an endangerment finding—that greenhouse gas emissions were “reasonably anticipated to endanger public health or welfare.” The EPA made this determination in 2009—a striking example of climate regulation being grounded in public health. This finding, in turn, required the EPA to regulate motor vehicle greenhouse gas emissions.
Since then, the EPA has initiated a series of regulatory actions, both for mobile sources and for stationery sources, designed to reduce greenhouse gas emissions, as well as to yield other benefits. These include stricter vehicle emission standards for both light-duty vehicles (called Corporate Average Fuel Efficiency, or CAFE, standards) and trucks, and stricter emissions standards for power plants and factories.
In November, 2014, U.S. President Barack Obama and Chinese President Xi Jinping, whose nations together account for more than
650
a third of the world's greenhouse gas emissions, announced a joint commitment on climate change. President Obama agreed to cut US CO2 emissions 28% below 2005 levels by the year 2025, and President Xi pledged that by 2030, China's CO2 emissions would peak and its share of renewable energy would rise by 20 percent. These commitments set the stage for the twenty-first COP, in Paris, in December, 2015. At that convening, nearly 200 nations agreed on the goal of limiting global warming to two degrees Centigrade, each nation agreed to set Nationally Determined Contributions toward that goal, wealthy nations agreed to help fund climate adaptation actions by poor nations, and provisions for transparency and verification were adopted. While critics noted that these steps would not suffice to avoid serious risks, most observers celebrated COP21 as a turning point and a major step forward.
Ethical Considerations Climate change raises ethical concerns in several ways. First, on the global scale, the nations responsible for the lion's share of carbon emissions to date account for a small proportion of the world's population and are relatively resilient to the effects of climate change. In contrast, the large population of the global south—the poor countries—accounts for a relatively small share of cumulative carbon emissions, and a very low per capita emission rate (although total emissions from developing nations are growing rapidly, with China surpassing the United States in 2006). The United States, with 5% of the global population, produces 25% of total annual greenhouse gas emissions. This discrepancy exemplifies the ethical implications posed by climate change on a global scale, shown graphically in Figure 12.13. Poor populations in the developing world have little by way of industry, transportation, or intensive agriculture; they contribute only a fraction of the greenhouse gases per capita that the developed countries produce, and their capacity to protect themselves against the adverse consequences of what are mostly others' greenhouse gases is quite limited (Shue, 2014). Of course, if developing nations do not choose energy-efficient development pathways, global climate change trends will intensify even as the imbalance of equity decreases (Patz & Kovats, 2002).
651
Figure 12.13 A Comparison of Cumulative CO2 Emissions (1950– 2000) (upper panel) with the Burden of Four Climate-Related Health Effects (Malaria, Malnutrition, Diarrhea, and Inland Flood- Related Fatalities (lower panel)
Source: Patz, Gibbs, Foley, Rogers, & Smith, 2007.
Note the mismatch between the countries that have contributed most to climate change, and the countries that are suffering its consequences the most.
Within the United States, and within many other nations, a similar disparity exists. Poor and disadvantaged people in many cases bear the brunt of climate change impacts, including health impacts—a pattern reflecting broader inequities in environmental health, as discussed in Chapter 11. This was graphically demonstrated in the aftermath of Hurricane Katrina, a disaster typical of those expected to increase with climate change. The poor populations of New Orleans and the nearby Gulf region were disproportionately likely to
652
fail to evacuate, to suffer catastrophic disruption following the storm, and to be unable to recover (Pastor et al., 2006; Dyson, 2007). The realization of inequities in risk and recovery resources has given rise to the concept of climate justice, a subset of environmental justice (Schlosberg & Collins, 2014).
Finally, an ethical issue arises with respect to intergenerational justice. Climate change has enormous potential impacts on the health and well-being of future generations (Page, 2007; Gardiner, 2011). As discussed in Chapter 10, ethical and religious thinkers have argued that we in the present owe a moral obligation to those who will follow to reverse climate change. For economists, the discount rate is a means of expressing value with regard to future generations. For example, the Stern report, a prominent economic analysis of climate change, used a 1.4% discount rate (Stern, 2006), whereas other economists have applied a several-fold higher discount rate (Broome, 2008). The higher discount rate implies to policymakers that the current generation should spend less on mitigating climate change, whereas the lower discount rate suggests more spending on mitigating climate change now, to avoid future harm. Policy decisions on how much the current generation should spend to mitigate climate change for the benefit of yet unborn people involve both an ethical issue and an economic issue.
653
Summary Climatologists now state with high certainty that global climate change is real, occurring more rapidly than expected, and caused by human activities, especially through fossil fuel combustion and deforestation. Environmental public health researchers assessing future projections for global climate have concluded that, on balance, adverse health outcomes will dominate under these changed climatic conditions. The number of pathways through which climate change can affect the health of populations makes this environmental health threat one of the largest and most formidable of the new century. Conversely, the potential health co- benefits from moving beyond our current fossil fuel–based economy may offer some of the greatest health opportunities in recent history.
654
Key Terms adaptation
Adjustments in ecological, social, or economic systems in response to observed or expected climate impacts. More particularly, changes in processes, practices, and structures to reduce potential harm or to exploit beneficial opportunities associated with climate change.
adaptive management An iterative, learning-based approach to the design, implementation, and evaluation of interventions in complex, changing systems.
albedo Reflectivity; the fraction of incident energy (such as light) reflected by a surface without being absorbed.
cap and trade An environmental policy tool designed to limit emissions of a pollutant such as carbon dioxide or sulfur dioxide. The cap is a limit on emissions set by a regulatory authority; the limit is lowered over time to reduce emissions. The trade is a market for permits to emit. Using this trading, emitters able to reduce their emissions can sell their allocated permits to other emitters. This approach creates incentives to innovate to reduce emissions (cf. carbon tax).
carbon tax An environmental policy tool designed to reduce carbon emissions by placing a tax on carbon emissions, generally upstream (say, at the point of fossil fuel production). By increasing the price of carbon-based fuels, a carbon tax would reduce demand (cf. cap and trade).
climate change Global-scale changes resulting from higher concentrations of greenhouse gases, land-use changes such as deforestation, and other drivers. Features Earth system changes such as changes in rainfall patterns, greater ocean acidification, and more frequent heat waves. These effects vary from place to place.
climate justice
655
The concept of fairness and equity in bearing the risks of climate change and benefiting from protection against that change. A form of environmental justice.
climate variability Fluctuations of climate over seasons and years relative to long- term average patterns.
co-benefits Benefits that flow from an action in addition to the primary benefits that motivated the action (also called collateral benefits). For example, shifting travel from automobiles to walking, cycling, and transit is a climate mitigation strategy that also yields benefits through improved air quality, increased physical activity, and reduced road traffic fatalities.
dangerous interference “Dangerous anthropogenic interference with the climate system” is the term of art used by the UNFCCC to characterize human actions that have driven earth system changes beyond a threshold of safety and stability.
El Niño–Southern Oscillation (ENSO) Natural year-to-year variations in sea surface temperatures, surface air pressure, rainfall, and atmospheric circulation across the equatorial Pacific Ocean.
endangerment finding The EPA's 2009 determination, under the Clean Air Act, that greenhouse gas emissions were “reasonably anticipated to endanger public health or welfare.” This finding triggered EPA regulation of greenhouse gases.
global warming The increase in average surface temperature on a global scale. Climate change is a preferred term because, while warming refers only to one parameter (temperature) and one direction of change (hotter), climate change takes in the complex changes in many earth systems.
greenhouse gases Atmospheric gases that increase radiative forcing: carbon dioxide, water vapor, methane, and others.
harmful algal blooms Overgrowths of algae in bodies of water, usually following excess
656
loading of nutrients into the water, and often harming aquatic ecosystems and posing health risks to people.
heat wave A period of extremely hot days, defined by the World Meteorological Organization as more than five consecutive days with temperatures 5°C above the average maximum during the 1961–1990 baseline period.
Kyoto Protocol A 1997 international treaty, negotiated under the UNFCCC, that committed nations to reduce greenhouse gas emissions.
mitigation Actions that aim to stabilize or reduce the production of greenhouse gases (and perhaps to sequester those greenhouse gases that are produced), corresponding to the public health concept of primary prevention.
ocean acidification The ongoing trend toward lower pH in the oceans, resulting from absorbing carbon dioxide.
radiative forcing The difference between solar energy absorbed by the Earth and energy radiated from it.
stabilization wedges Mitigation strategies that contribute to reducing greenhouse gas emissions, and that—in aggregate—achieve a designated goal.
tail risk The extreme end of a distribution of probabilities for a particular outcome. In the context of climate change, tail risk corresponds to low-probability, high-consequence events such as extreme sea level rise.
United Nations Framework Convention on Climate Change (UNFCCC)
A framework adopted internationally in 1992 that aimed to stabilize greenhouse gases at a level that would prevent “dangerous interference” with the climate system.
urban heat island An urban area that is routinely hotter than surrounding areas.
vulnerability assessment
657
Systematic, place-based evaluation of degree of exposure to hazards (susceptibility) and capacity to cope with or recover from consequences of disasters (resilience).
658
Discussion Questions 1. Climate change has been called the major environmental health
challenge of the twenty-first century. Do you agree or disagree? Explain your reasoning.
2. Identify three current environmental health problems likely to be exacerbated by climate change. How might existing public health practices be altered to anticipate these effects of climate change? What other key sectors (beyond health) should be engaged?
3. What are some of the major driving forces behind both the risks of climate change and our vulnerabilities to that change? Which scientific experts would be best able to assemble a comprehensive assessment of climate change risks? What types of policymakers should be involved, and at what levels (local, regional, international)?
4. What are three potential co-benefits and three potential unintended consequences of mitigating greenhouse gas emissions?
5. How large is your carbon footprint? Online calculators are available at these sites: www.carbonfootprint.com/calculator.aspx; www3.epa.gov/carbon-footprint-calculator; www.nature.org/greenliving/carboncalculator; and www.terrapass.com/carbon-footprint-calculator
6. A substantial minority of Americans do not believe that climate change is occurring or that humans play a role. Why do you think these beliefs persist despite scientific evidence to the contrary?
7. Suppose your local health department hired you to oversee climate change planning and preparedness. What steps would you take in your first sixty days on the job? In your first year?
659
References Akerlof, K., Debono, R., Berry, P., Leiserowitz, A., Roser-Renouf, C., Clarke, K. L.,…Maibach, E. W. (2010). Public perceptions of climate change as a human health risk: Surveys of the United States, Canada and Malta. International Journal of Environmental Research in Public Health, 7, 2559–2606.
Aldy, J. E., & Stavins, R. N. (2012). Using the market to address climate change: Insights from theory & experience. Daedalus, 141(2), 45–60.
Allergy USA. (2014). Allergy facts and figures. Retrieved from http://allergyusa.com/allergy-resources/providers/allergy-facts- figures
Anderson, D. M., Cembella, A. D., & Hallegraeff, G. M. (2012). Progress in understanding harmful algal blooms: Paradigm shifts and new technologies for research, monitoring, and management. Annual Review of Marine Science, 4(1), 143–176.
Arkema, K. K., Guannel, G., Verutes, G., Wood, S. A., Guerry, A., Ruckelshaus, M.,…Silver, J. M. (2013). Coastal habitats shield people and property from sea-level rise and storms. Nature Climate Change, 3(10), 913–918.
Aston, L. M., Smith, J. N., & Powles, J. W. (2012). Impact of a reduced red and processed meat dietary pattern on disease risks and greenhouse gas emissions in the UK: A modelling study. BMJ Open, 2(5). doi:10.1136/bmjopen-2012-001072
Bailey, R. (2011). Growing a better future: Food justice in a resource-constrained world. Oxford, U.K.: Oxfam. Retrieved from https://www.oxfam.org/en/growing-better-future
Balbus, J. M., Greenblatt, J. B., Chari, R., Millstein, D., & Ebi, K. L. (2014). A wedge-based approach to estimating health co-benefits of climate change mitigation activities in the United States. Climatic Change, 127(2), 199–210.
Barriopedro, D., Fischer, E. M., Luterbacher, J., Trigo, R. M., &
660
García-Herrera, R. (2011). The hot summer of 2010: Redrawing the temperature record map of Europe. Science, 332, 220–224.
Basu, R., & Samet, J. M. (2002). Relation between elevated ambient temperature and mortality: A review of the epidemiologic evidence. Epidemiologic Reviews, 24(2), 190–202.
Ben-Ari, T., Neerinckx, S., Gage, K. L., Kreppel, K., Laudisoit, A., Leirs, H., & Stenseth, N. C. (2011). Plague and climate: Scales matter. PLoS Pathogens, 7(9).
Bender, M. A., Knutson, T. R., Tuleya, R. E., Sirutis, J. J., Vecchi, G. A., Garner, S. T., & Held, I. M. (2010). Modeled impact of anthropogenic warming on the frequency of intense Atlantic hurricanes. Science, 327, 454–458.
Bernard, S. M., Samet, J. M., Grambsch, A., Ebi, K. L., & Romieu, I. (2001). The potential impacts of climate variability and change on air pollution–related health effects in the United States. Environmental Health Perspectives, 109(Suppl. 2), 199–209.
Berry, H. L., Bowen, K., & Kjellstrom, T. (2010). Climate change and mental health: A causal pathways framework. International Journal of Public Health, 55, 123–132.
Berry, H. L., Hogan, A., Owen, J., Rickwood, D., & Fragar, L. (2011). Climate change and farmers' mental health: Risks and responses. Asia-Pacific Journal of Public Health, 23(2, Suppl.), 119S–132.
Bostrom, A., Böhm, G., & O'Connor, R. E. (2013). Targeting and tailoring climate change communications. Wiley Interdisciplinary Reviews: Climate Change, 4(5), 447–455. doi:10.1002/wcc.234
Bouchama, A., Dehbi, M., Mohamed, G., Matthies, F., Shoukri, M., & Menne, B. (2007). Prognostic factors in heat wave related deaths: A meta-analysis. Archives of Internal Medicine, 167(20), 2170– 2176.
Boykoff, M. (2011). Who speaks for the climate? Making sense of media reporting on climate change. Cambridge, U.K.: Cambridge University Press.
Broome, J. (2008). The ethics of climate change. Scientific
661
American, 298, 96–102.
Brubaker, M., Berner, J., Chavan, R., & Warren, J. (2011). Climate change and health effects in northwest Alaska. Global Health Action, 4.
Brulle, R. (2014). Institutionalizing delay: Foundation funding and the creation of U.S. climate change counter-movement organizations. Climate Change, 122, 681–694.
Brulle, R., Carmichael, J., & Jenkins, J. C. (2012). Shifting public opinion on climate change: An empirical assessment of factors influencing concern over climate change in the U.S., 2002–2010. Climate Change, 114, 169–188.
Bulbena, A., Sperry, L., & Cunillera, J. (2006). Psychiatric effects of heat waves. Psychiatric Services, 57(10), 1519.
Bush, K. F., O'Neill, M. S., Li, S., Mukherjee, B., Hu, H., Ghosh, S., & Balakrishnan, K. (2014). Associations between extreme precipitation and gastrointestinal-related hospital admissions in Chennai, India. Environmental Health Perspectives, 122, 249.
Caminade, C., Kovats, S., Rocklov, J., Tompkins, A. M., Morse, A. P., Colon-Gonzalez, F. J.,…Lloyd, S. J. (2014). Impact of climate change on global malaria distribution. Proceedings of the National Academy of Sciences of the United States of America, 111(9), 3286– 3291.
Campbell, L. P., Luther, C., Moo-Llanes, D., Ramsey, J. M., Danis- Lozano, R., & Peterson, A. T. (2015). Climate change influences on global distributions of dengue and chikungunya virus vectors. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 370(1665).
Cann, K., Thomas, D. R., Salmon, R., Wyn-Jones, A., & Kay, D. (2013). Extreme water-related weather events and waterborne disease. Epidemiology and Infection, 141, 671–686.
Carbon Dioxide Information Analysis Center. (2014). Recent greenhouse gas concentrations. doi:10.3334/CDIAC/atg.032. Retrieved from http://cdiac.ornl.gov/pns/current_ghg.html
662
Centers for Disease Control and Prevention. (2013). Heat-related deaths after an extreme heat event—four states, 2012, and United States, 1999–2009. Morbidity and Mortality Weekly Report, 62(22), 433–436.
Centers for Disease Control and Prevention. (2015). The CDC's Building Resilience Against Climate Effects (BRACE) framework. Retrieved from http://www.cdc.gov/climateandhealth/brace.htm
Centre for Research on the Epidemiology of Disasters. (2015). The human cost of natural disasters: A global perspective. Brussels: Université Catholique de Louvain. Retrieved from http://reliefweb.int/sites/reliefweb.int/files/resources/PAND_report.pdf
Chakraborty, S., & Newton, A. C. (2011). Climate change, plant diseases and food security: An overview. Plant Pathology, 60, 2–14.
Checkley, W., Epstein, L. D., Gilman, R. H., Figueroa, D., Cama, R. I., Patz, J. A., & Black, R. E. (2000). Effects of El Niño and ambient temperature on hospital admissions for diarrhoeal diseases in Peruvian children. Lancet, 355, 442–450.
Cheng, J. J., & Berry, P. (2013). Health co-benefits and risks of public health adaptation strategies to climate change: A review of current literature. International Journal of Public Health, 58(2), 305–311.
CNA Military Advisory Board. (2014). National security and the accelerating risks of climate change. Alexandria, VA: CNA Corporation.
Cochrane, K., De Young, C., Soto, D., & Bahri, T. (2009). Climate change implications for fisheries and aquaculture. Rome: Food and Agriculture Organization. Retrieved from http://www.fao.org/docrep/012/i0994e/0994e00.htm
Collins, W. D., Ramaswamy, V., Schwarzkopf, M. D., Sun, Y., Portmann, R. W., Fu, Q.,…Zhong, W. Y. (2006). Radiative forcing by well-mixed greenhouse gases: Estimates from climate models in the Intergovernmental Panel on Climate Change (IPCC) Fourth Assessment Report (AR4). Journal of Geophysical Research— Atmospheres, 111, D14317. doi:10.1029/2005JD006713
663
Colwell, R. R. (1996). Global climate and infectious disease: The cholera paradigm. Science, 274, 2025–2031.
Curriero, F., Patz, J. A., Rose, J., & Lele, S. (2001). The association between extreme precipitation and waterborne disease outbreaks in the United States, 1948–1994. American Journal of Public Health, 91, 1194–1199.
Cusack, L., de Crespigny, C., & Athanasos, P. (2011). Heatwaves and their impact on people with alcohol, drug and mental health conditions: A discussion paper on clinical practice considerations. Journal of Advanced Nursing, 67(4), 915–922.
Davis, S. J., Cao, L., Caldeira, K., & Hoffert, M. I. (2013). Rethinking wedges. Environmental Research Letters, 8(1).
De Man, H., van den Berg, H., Leenen, E., Schijven, J. F., Schets, F. M., van der Vliet, J. C.,…de Roda Husman, A. M. (2014). Quantitative assessment of infection risk from exposure to waterborne pathogens in urban floodwater. Water Research, 48, 90–99.
Dhiman, R. C., Pahwa, S., Dhillon, G. P., & Dash, A. P. (2010). Climate change and threat of vector-borne diseases in India: Are we prepared? Parasitology Research, 106(4), 763–773.
Doherty T. J., & Clayton S. (2011). The psychological impacts of global climate change. American Psychologist, 66, 265–276.
Dunne J. P., Stouffer, R., & John, J. G. (2013). Reductions in labour capacity from heat stress under climate warming. Nature Climate Change, 3, 563–566.
Dwight, R. H., Semenza, J. C., Baker, D. B., & Olson, B. H. (2002). Association of urban runoff with coastal water quality in Orange County, California. Water Environment Research, 74(1), 82–90.
Dyson, M. E. (2007). Come hell or high water: Hurricane Katrina and the color of disaster. New York: Basic Books.
Ebi, K. L., Hallegatte, S., Kram, T., Arnell, N., Carter, T., Edmonds, J.,…Zwickel, T. (2014). A new scenario framework for climate change research: Background, process, and future directions.
664
Climatic Change, 122(3), 363–372.
Ebi, K. L., Lindgren, E., Suk, J. E., & Semenza, J. C. (2013). Adaptation to the infectious disease impacts of climate change. Climatic Change, 118(2), 355–365.
Ebi, K. L., Smith, J., & Burton, I. (Eds.). (2005). Integration of public health with adaptation to climate change: Lessons learned and new directions. London: Taylor & Francis.
El-Fadel, M., Ghanimeh, S., Maroun, R., & Alameddine, I. (2012). Climate change and temperature rise: Implications on food- and water-borne diseases. Science of the Total Environment, 437, 15– 21.
Feinberg, M., & Willer, R. (2011). Apocalypse soon? Dire messages reduce belief in global warming by contradicting just-world beliefs. Psychological Science, 22(1), 34–38.
Fiore, A. M., Naik, V., & Leibensperger, E. M. (2015). Air quality and climate connections. Journal of the Air & Waste Management Association, 65(6).
Fisher, G. T., & Katz, B. G. (1988). Urban stormwater runoff: Selected background information and techniques for problem assessment with a Baltimore, Maryland, case study (U.S. Geological Survey Water-Supply Paper 2347). Reston, VA: U.S. Geological Survey.
Food and Agriculture Organization of the United Nations. (2006). Livestock's long shadow: Environmental issues and options. Rome: Author. Retrieved from http://www.fao.org/docrep/010/a0701e/a0701e00.HTM
Food and Agriculture Organization of the United Nations. (2013). The state of food insecurity in the world 2013: The multiple dimensions of food security. Rome: Author.
Fritze, J. G., Blashki, G. A., Burke, S., & Wiseman, J. (2008). Hope, despair and transformation: Climate change and the promotion of mental health and wellbeing. International Journal of Mental Health Systems, 2(1), 13.
665
Frumkin, H., Hess, J., Luber, G., Malilay, J., & McGeehin, M. (2008). Climate change: The public health response. American Journal of Public Health, 98, 435–445.
Frumkin, H., & McMichael, A. J. (2008). Climate change and public health: Thinking, communicating, acting. American Journal of Preventive Medicine, 35, 403–410.
Fu, F. X., Tatters, A. O., & Hutchins, D. A. (2012). Global change and the future of harmful algal blooms in the ocean. Marine Ecology Progress Series, 470, 207–233.
Galea, S., Brewin, C. R., Gruber, M., Jones, R. T., King, D. W., King, L. A.,…Kessler, R. C. (2007). Exposure to hurricane-related stressors and mental illness after Hurricane Katrina. Archives of General Psychiatry, 64, 1427–1434.
Gardiner, S. M. (2011). A perfect moral storm: The ethical tragedy of climate change. New York: Oxford University Press.
Gingold, D. B., Strickland, M. J., & Hess, J. J. (2014). Ciguatera fish poisoning and climate change: Analysis of National Poison Center data in the United States, 2001–2011. Environmental Health Perspectives, 122(6), 580–586.
Glass, G. E., Cheek, J. E., Patz, J. A., Shields, T. M., Doyle, T. J., Thoroughman, D. A.,…Bryan, R. (2000). Using remotely sensed data to identify areas of risk for hantavirus pulmonary syndrome. Emerging Infectious Diseases, 63(3), 238–247.
Glibert, P. M., Icarus Allen, J., Artioli, Y., Beusen, A., Bouwman, L., Harle, J.,…Holt, J. (2014). Vulnerability of coastal ecosystems to changes in harmful algal bloom distribution in response to climate change: Projections based on model analysis. Global Change Biology, 20(12), 3845–3858.
Goldmann, E., & Galea, S. (2014). Mental health consequences of disasters. Annual Review of Public Health, 35, 169–183.
Goodess, C. M. (2013). How is the frequency, location and severity of extreme events likely to change up to 2060? Environmental Science & Policy, 27, S4–14.
666
Goulder, L. H., & Schein, A. (2013). Carbon taxes vs. cap and trade: A critical review. Cambridge, MA: National Bureau of Economic Research.
Grabow M. L., Spak, S. N., Holloway, T., Stone, B., Mednick, A. C., & Patz, J. A. (2012). Air quality and exercise-related health benefits from reduced car travel in the midwestern United States. Environmental Health Perspectives, 120, 68–76.
Gubler, D. J., Reiter, P., Ebi, K. L., Yap, W., Nasci, R., & Patz, J. A. (2001). Climate variability and change in the United States: Potential impacts on vector- and rodent-borne diseases. Environmental Health Perspectives, 109(Suppl. 2), 223–233.
Habeeb, D., Vargo, J., & Stone, B. (2015). Rising heat wave trends in large US cities. Natural Hazards, 76(3), 1651–1665.
Harvey, M., & Pilgrim, S. (2011). The new competition for land: Food, energy, and climate change. Food Policy, 36(Suppl. 1), S40– 51.
Hellberg, R. S., & Chu, E. (2015). Effects of climate change on the persistence and dispersal of foodborne bacterial pathogens in the outdoor environment: A review. Critical Reviews in Microbiology, 1–25. Advance online publication.
Hess, J. J., Malilay, J. N., & Parkinson, A. J. (2008). Climate change: The importance of place. American Journal of Preventive Medicine, 35, 468–478.
HLPE. (2013). Biofuels and food security. A Report by the High Level Panel of Experts on Food Security and Nutrition of the Committee on World Food Security. Rome: Committee on World Food Security.
Howden-Chapman, P. L., Chapman, R. B., Capon, A. G., & Wilson, N. (2011). Carbon pricing is a health protection policy. Medical Journal of Australia, 195(6), 311–312.
Hsiang, S. M., Burke, M., & Miguel, E. (2013). Quantifying the influence of climate on human conflict. Science, 341.
Hurley, W., Wolterstorff, C., MacDonald, R., & Schultz, D. (2014).
667
Paralytic shellfish poisoning: A case series. Western Journal of Emergency Medicine, 15(4), 378–381.
Intergovernmental Panel on Climate Change. (2013). Climate change 2013: The physical science basis. Contribution of Working Group I to the Fifth Assessment Report of the Intergovernmental Panel on Climate Change. New York: Cambridge University Press.
Jack, D. W., & Kinney, P. L. (2010). Health co-benefits of climate mitigation in urban areas. Current Opinion in Environmental Sustainability, 2, 172–177.
Jacob, B., Mawson, A. R., Payton, M., & Guignard, J. C. (2008). Disaster mythology and fact: Hurricane Katrina and social attachment. Public Health Reports, 123, 555–566.
Jenkins, J. D. (2014). Political economy constraints on carbon pricing policies: What are the implications for economic efficiency, environmental efficacy, and climate policy design? Energy Policy, 69, 467–477.
Johnston F. H., Henderson, S. B., Chen, Y., Randerson, J. T., Marlier, M., Defries, R. S.,…Brauer, M. (2012). Estimated global mortality attributable to smoke from landscape fires. Environmental Health Perspectives, 120, 695–701.
Jones, J. (2014). In U.S., most do not see global warming as serious threat: Nearly two in three believe global warming will happen during their lifetimes. Retrieved from http://www.gallup.com/poll/167879/not-global-warming-serious- threat.aspx
Kalkstein, L. S., Greene, S., Mills, D. M., & Samenow, J. (2011). An evaluation of the progress in reducing heat-related human mortality in major U.S. cities. Natural Hazards, 56(1), 113–129.
Kilbourne, E. M. (2008). Temperature and health. In R. B. Wallace (Ed.), Maxcy-Rosenau-Last public health and preventive medicine (15th ed., pp. 725–734). New York: McGraw-Hill Medical.
Kirch, W., Menne, B., & Bertollini, R. (Eds.). (2005). Extreme weather events and public health responses. New York: Springer.
668
Kjellstrom, T., Holmer, I., & Lemke, B. (2009). Workplace heat stress, health and productivity—an increasing challenge for low and middle-income countries during climate change. Global Health Action, 2. doi:10.3402/gha.v2i0.2047
Kovats, R. S., Edwards, S. J., Hajat, S., Armstrong, B. G., Ebi, K. L., & Menne, B. (2004). The effect of temperature on food poisoning: A time-series analysis of salmonellosis in ten European countries. Epidemiology and Infection, 132(3), 443–453.
Kunkel, K. E., Easterling, D. R., Redmond, K., & Hubbard, K. (2003). Temporal variations of extreme precipitation events in the United States: 1895–2000. Geophysical Research Letters, 30, 1900.
Lake, I. R., Gillespie, I. A., Bentham, G., Nichols, G. L., Lane, C., Adak, G. K., & Threlfall, E. J. (2009). A re-evaluation of the impact of temperature and climate change on foodborne illness. Epidemiology and Infection, 137(11), 1538–1547.
Lang-Yona, N., Levin, Y., Dannemiller, K. C., Yarden, O., Peccia, J., & Rudich, Y. (2013). Changes in atmospheric CO2 influence the allergenicity of Aspergillus fumigatus. Global Change Biology, 19(8), 2381–2388.
Lau, C. L., Smythe, L. D., Craig, S. B., & Weinstein, P. (2010). Climate change, flooding, urbanisation and leptospirosis: Fuelling the fire? Transactions of the Royal Society of Tropical Medicine and Hygiene, 104(10), 631–638.
Lee, T. M., Markowitz, E. M., Howe, P. D., Ko, C.-Y., & Leiserowitz, A. A. (2015). Predictors of public climate change awareness and risk perception around the world. Nature Climate Change, 5. Advance online publication. doi:10.1038/nclimate2728
Leiserowitz, A., Maibach, E., Roser-Renouf, C., Feinberg, G., & Rosenthal, S. (2015). Climate change in the American mind: March 2015. Yale University and George Mason University. New Haven, CT: Yale Project on Climate Change Communication. Retrieved from http://environment.yale.edu/climate- communication/files/Global-Warming-CCAM-March-2015.pdf
Levy, B. S., & Sidel, V. W. (2014). Collective violence caused by climate change and how it threatens health and human rights.
669
Health and Human Rights International Journal, 16, 32–40.
Lewandowsky, S., Gignac, G. E., & Vaughan, S. (2013). The pivotal role of perceived scientific consensus in acceptance of science. Nature Climate Change, 3(4), 399–404.
Lloyd, S. J., Sari Kovats, R., & Chalabi, Z. (2011). Climate change, crop yields, and undernutrition: Development of a model to quantify the impact of climate scenarios on child undernutrition. Environmental Health Perspectives, 119, 1817–1823.
Loughry, M. (2010). Climate change, human movement and the promotion of mental health: What have we learnt from earlier global stressors? In J. McAdam (Ed.), Climate change and displacement: Multidisciplinary perspectives (pp. 221–238). Oxford, U.K.: Hart.
Lowe, D., Ebi, K. L., & Forsberg, B. (2011). Heatwave early warning systems and adaptation advice to reduce human health consequences of heatwaves. International Journal of Environmental Research and Public Health, 8(12), 4623–4648.
Luber, G., Knowlton, K., Balbus, J., Frumkin, H., Hayden, M., Hess, J.,…Ziska, L. (2014). Human health. In J. M. Melillo, T. C. Richmond, & G. W. Yohe (Eds.), Climate change impacts in the United States: The third national climate assessment (pp. 220– 256). U.S. Global Change Research Program. Washington, DC: U.S. Government Printing Office.
Luber G., & McGeehin M. (2008). Climate change and extreme heat events. American Journal of Preventive Medicine, 35, 429–435.
Maibach, E. W., Nisbet, M., Baldwin, P., Akerlof, K., & Diao, G. (2010). Reframing climate change as a public health issue: An exploratory study of public reactions. BMC Public Health, 10, 299.
Maibach, E., Nisbet, M., & Weathers, M. (2011). Conveying the human implication of climate change: A climate change communication primer for public health professionals. Fairfax, VA: George Mason University Center for Climate Change Communication. Retrieved from http://www.climatechangecommunication.org/report/new-climate- change-communication-primer-public-health-professionals
670
Maibach, E. W., Roser-Renouf, C., & Leiserowitz, A. (2008). Communication and marketing as climate change–intervention assets: A public health perspective. American Journal of Preventive Medicine, 35(5), 488–500.
Marinucci, G. D., Luber, G., Uejio, C. K., Saha, S., & Hess, J. J. (2014). Building resilience against climate effects—a novel framework to facilitate climate readiness in public health agencies. International Journal of Environmental Research and Public Health, 11(6), 6433–6458.
Martin, V., Chevalier, V., Ceccato, P., Anyamba, A., De Simone, L., Lubroth, J.,…Domenech, J. (2008). The impact of climate change on the epidemiology and control of Rift Valley fever. Revue Scientifique et Technique, 27(2), 413–426.
Martinez, M., Devenport, L., Saussy, J., & Martinez, J. (2002). Drug-associated heat stroke. Southern Medical Journal, 95(8), 799–802.
Matsueda, M. (2011). Predictability of Euro-Russian blocking in summer of 2010. Geophysical Research Letters, 38(6). doi:10.1029/2010GL046557
McCarthy, J., Canziani, O. F., Leary, N. A., Dokken, D. J., & White, K. S. (Eds.). (2001). Climate change 2001: Impacts, adaptation, and vulnerability. Contribution of Working Group II to the Third Assessment Report of the Intergovernmental Panel on Climate Change. New York: Cambridge University Press.
McLaughlin, J. B., DePaola, A., Bopp, C. A., Martinek, K. A., Napolilli, N. P., Allison, C. G.,…Middaugh, J. P. (2005). Outbreaks of Vibrio parahaemolyticus gastroenteritis associated with Alaskan oysters. New England Journal of Medicine, 353(14), 1463–1470.
McMichael, A. J. (2013). Globalization, climate change, and human health. New England Journal of Medicine, 369(1), 96.
McMichael, A. J., McMichael, C., Berry, H., & Bowen, K. (2010). Climate-related displacement: Health risks and responses. In J. McAdam (Ed.), Climate change and population displacement: Multidisciplinary perspectives (pp. 191–220). Oxford, U.K.: Hart.
671
Medlock, J. M., & Leach, S. A. (2015). Effect of climate change on vector-borne disease risk in the UK. Lancet: Infectious Diseases, 15(6), 721–730.
Menne, B., & Ebi, K. L. (Eds.). (2006). Climate change and adaptation strategies for human health. Darmstadt, Germany: Steinkopff-Verlag.
Mills, J. N., Gage, K. L., & Khan, A. S. (2010). Potential influence of climate change on vector-borne and zoonotic diseases: A review and proposed research plan. Environmental Health Perspectives, 118, 1507–1514.
Mohan, J.,E., Ziska, L. H., Schlesinger, W. H., Thomas, R. B., Sicher, R. C., George, K., & Clark, J. S. (2006). Biomass and toxicity responses of poison ivy (Toxicodendron radicans) to elevated atmospheric CO2. Proceedings of the National Academy of Sciences of the United States of America, 103(24), 9086–9089.
Morin, C. W., Comrie, A. C., & Ernst, K. (2013). Climate and dengue transmission: Evidence and implications. Environmental Health Perspectives, 121(11–12), 1264–1272.
Moritz, M. A., Parisien, M.-A., Batllori, E., Krawchuk, M. A., Van Dorn, J., Ganz, D. J., & Hayhoe, K. (2012). Climate change and disruptions to global fire activity. Ecosphere, 3(6), art49.
Moser, S. C. (2010). Communicating climate change: History, challenges, process and future directions. Wiley Interdisciplinary Reviews: Climate Change, 1(1), 31–53.
Moser, S. C., & Lisa, D. (2007). Creating a climate for change: Communicating climate change and facilitating social change. Cambridge, U.K.: Cambridge University Press.
Moss, R. H., Edmonds, J. A., Hibbard, K. A., Manning, M. R., Rose, S. K., van Vuuren, D. P.,…Wilbanks, T. J. (2010). The next generation of scenarios for climate change research and assessment. Nature, 463(7282), 747–756.
Murray, C.J.L., Rosenfeld, L. C., Lim, S. S., Andrews, K. G., Foreman, K. J., Haring, D.,…Lopez, A. D. (2012). Global malaria mortality between 1980 and 2010: A systematic analysis. Lancet,
672
379(9814), 413–431.
Myers, S. S., Zanobetti, A., Kloog, I., Huybers, P., Leakey, A. D., Bloom, A. J.,…Usui, Y. (2014). Increasing CO2 threatens human nutrition. Nature, 510, 139–142.
Myers, T. A., Maibach, E. W., Roser-Renouf, C., Akerlof, K., & Leiserowitz, A. A. (2013). The relationship between personal experience and belief in the reality of global warming. Nature Climate Change, 3(4), 343–347.
Myers, T. A., Nisbet, M., Maibach, E., & Leiserowitz, A. (2012). A public health frame arouses hopeful emotions about climate change. Climate Change, 113(3–4), 1105–1112.
National Climatic Data Center. (1999). Mitch: The deadliest Atlantic hurricane since 1780. Retrieved from http://www.ncdc.noaa.gov/ol/reports/mitch/mitch.html
National Oceanic and Atmospheric Administration. (2014). NOAA, partners predict significant harmful algal bloom in western Lake Erie this summer. Retrieved from http://www.noaanews.noaa.gov/stories2014/20140710_erie_hab.html
National Snow & Ice Data Center. (2015). Sea ice: More information. Retrieved from http://nsidc.org/soac/sea-ice-more- information
Naumova, E. N., Jagai, J. S., Matyas, B., DeMaria, A., Jr., MacNeill, I. B., & Griffiths, J. K. (2007). Seasonality in six enterically transmitted diseases and ambient temperature. Epidemiology and Infection, 135(2), 281–292.
Nelson, G. C., Rosegrant, M. W., Koo, J., Robertson, R. D., Sulser, T., Zhu, T.,…Lee, D. R. (2009). Climate change: Impact on agriculture and costs of adaptation. Washington, DC: International Food Policy Research Institute. Retrieved from http://www.ifpri.org/publication/climate-change-impact- agriculture-and-costs-adaptation
Norris, F. H., Tracy, M., & Galea, S. (2009). Looking for resilience: Understanding the longitudinal trajectories of responses to stress. Social Science & Medicine, 68, 2190–2198.
673
North, C. S., & Pfefferbaum, B. (2013). Mental health response to community disasters: A systematic review. JAMA, 310, 507–518.
Ogden, N. H., Maarouf, A, Barker, I. K., Bigras-Poulin, M., Lindsay, L. R., Morshed, M. G.,…Charron, D. F. (2006). Climate change and the potential for range expansion of the Lyme disease vector Ixodes scapularis in Canada. International Journal for Parasitology, 36(1), 63–70.
Oldham R. L. (2013). Mental health aspects of disasters. Southern Medical Journal, 106, 115–119.
Oreskes, N., & Conway, E. M. (2010). Merchants of doubt. New York: Bloomsbury.
Ostfeld, R. S., & Brunner, J. L. (2015). Climate change and Ixodes tick-borne diseases of humans. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 370(1665).
Pacala, S., & Socolow, R. (2004). Stabilization wedges: Solving the climate problem for the next 50 years with current technologies. Science, 305(5686), 968–972.
Page, E. A. (2007). Climate change, justice and future generations. Northampton, MA: Elgar.
Page, L. A., Hajat, S., & Kovats, R. S. (2007). Relationship between daily suicide counts and temperature in England and Wales. British Journal of Psychiatry, 191, 106–112.
Parham, P. E., Waldock, J., Christophides, G. K., Hemming, D., Agusto, F., Evans, K. J.,…Michael, E. (2015). Climate, environmental and socio-economic change: Weighing up the balance in vector-borne disease transmission. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 370(1665).
Pascual, M., Ahumada, J. A., Chaves, L. F., Rodó, X., & Bouma, M. (2006). Malaria resurgence in the east African highlands: Temperature trends revisited. Proceedings of the National Academy of Sciences of the United States of America, 103(15), 5829–5834.
674
Pascual, M., Rodó, X., Ellner, S. P., Colwell, R., Bouma, M. J. (2000). Cholera dynamics and El Niño–Southern Oscillation. Science, 289, 1766–1769.
Pastor, M., Bullard, R., Boyce, J., Fothergill, A., Morello-Frosch, R., & Wright, B. (2006). In the wake of the storm: Environment, disaster, and race after Katrina. New York: Russell Sage Foundation.
Patz, J. A., Frumkin, H., Holloway, T., Vimont, D. J., & Haines, A. (2014). Climate change: Challenges and opportunities for global health. JAMA, 312(15), 1565–1580.
Patz, J. A., Gibbs, H. K., Foley, J. A., Rogers, J. V., & Smith, K. R. (2007). Climate change and global health: Quantifying a growing ethical crisis. EcoHealth, 4, 397–405.
Patz, J. A., Githeko, A. K., McCarty, J. P., Hussein, S., Confalonieri, U., & de Wet, N. (2003). Climate change and infectious diseases. In A. J. McMichael, D. H. Campbell-Lendrum, C. F. Corvalán, K. L. Ebi, A. Githeko, J. D. Scheraga, & A. Woodward (Eds.), Climate change and human health: Risks and responses (pp. 103–132) Geneva: World Health Organization.
Patz, J. A., & Hahn M. B. (2013). Climate change and human health: A One Health approach. In J. S. Mackenzie, M. Jeggo, P. Daszak, & J. A. Richt (Eds.), One Health: The human-animal-environment interfaces in emerging infectious diseases (pp. 141–171). New York: Springer.
Patz, J. A., & Kovats, R. S. (2002). Hotspots in climate change and human health. BMJ, 325, 1094–1098.
Patz, J. A., Vavrus, S. J., Uejio, C. K., & McLellan, S. L. (2008). Climate change and waterborne disease risk in the Great Lakes region of the U.S. American Journal of Preventive Medicine, 35, 451–458.
Paz, S. (2015). Climate change impacts on West Nile virus transmission in a global context. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 370(1665).
Petkova, E. P., Bader, D. A., Anderson, G. B., Horton, R. M.,
675
Knowlton, K., & Kinney, P. L. (2014). Heat-related mortality in a warming climate: Projections for 12 U.S. cities. International Journal of Environmental Research and Public Health, 11(11), 11371–11383.
Pett, J. (2009). [Editorial cartoon by Joel Pett]. USA Today, December 13.
Pew Research. (2014). Climate change: Key data points from Pew Research. Retrieved from http://www.pewresearch.org/key-data- points/climate-change-key-data-points-from-pew-research
Pidgeon N., & Fischhoff, B. (2011). The role of social and decision sciences in communicating uncertain climate risks. Nature Climate Change, 1, 35–41.
Porter, J. R., Xie, L., Challinor, A. J., Cochrane, K., Howden, M., Iqbal, M. M.,…Travasso, M. I. (2014). Food security and food production systems. In C. B. Field, V. R. Barros, D. J. Dokken, K. J. Mach, M. D. Mastrandrea, T. E. Bilir,…L. L. White (Eds.), Climate change 2014: Impacts, adaptation and vulnerability. Part A: Global and sectoral aspects. Contribution of Working Group II to the Fifth Assessment Report of the Intergovernmental Panel on Climate Change (pp. 485–533). New York: Cambridge University Press.
Princeton Environmental Institute, Carbon Mitigation Initiative. (2015). Princeton, NJ: Princeton University. Retrieved from http://cmi.princeton.edu/wedges/slides.php
Pugliese, A., & Ray, J. (2009). A heated debate: Global attitudes toward climate change. Harvard International Review, 31, 64–68.
Robine, J.-M., Cheung, S. L., Le Roy, S., Van Oyen, H., Griffiths, C., Michel, J. P., & Herrmann, F. R. (2008). Death toll exceeded 70,000 in Europe during the summer of 2003. Comptes Rendus Biologies, 331, 171–178.
Rodó, X., Pascual, M., Fuchs, G., & Faruque, A. S. (2002). ENSO and cholera: A nonstationary link related to climate change? Proceedings of the National Academy of Sciences of the United States of America, 99(20), 12901–12906.
676
Rose, J. B. (1997). Environmental ecology of cryptosporidium and public health implications. Annual Review of Public Health, 18(1), 135–161.
Roser-Renouf, C., Maibach, E., Leiserowitz, A., Feinberg, G., Rosenthal, S., & Kreslake, J. (2014). Global warming's six Americas, October 2014: Perception of the health consequences of global warming and update on key beliefs. Yale University and George Mason University. New Haven, CT: Yale Project on Climate Change Communication.
Rubio, M. A., & Lissi, E. A. (2014). Temperature as thumb rule predictor of ozone levels in Santiago de Chile ground air. Journal of the Chilean Chemical Society, 59, 2427–2431.
Running, S. W. (2006). Is global warming causing more, larger wildfires? Science, 313, 927–928.
Salamanca, F., Georgescu, M., Mahalov, A., Moustaoui, M., & Wang, M. (2014), Anthropogenic heating of the urban environment due to air conditioning. Journal of Geophysical Research: Atmospheres, 119, 5949–5965.
Schipper, E. L., & Burton, I. (Eds.). (2009). The Earthscan reader on adaptation to climate change. London: Earthscan.
Schlosberg, D., & Collins, L. B. (2014). From environmental to climate justice: Climate change and the discourse of environmental justice. Wiley Interdisciplinary Reviews: Climate Change, 5(3), 359–374.
Schuster, C. J., Ellis, A. G., Robertson, W. J., Charron, D. F., Aramini, J. J., Marshall, B. J., & Medeiros, D. T. (2005). Infectious disease outbreaks related to drinking water in Canada, 1974–2001. Canadian Journal of Public Health, 96(4), 254–258.
Shue, H. (2014). Climate justice: Vulnerability and protection. New York: Oxford University Press.
Socolow, R. (2011, September 27). Wedges reaffirmed [Web log post]. Retrieved from http://www.climatecentral.org/blogs/wedges-reaffirmed
677
Squire, O. J., Archibald, A. T., Griffiths, P. T., Jenkin, M. E., Smith, D., & Pyle, J. A. (2015). Influence of isoprene chemical mechanism on modelled changes in tropospheric ozone due to climate and land use over the 21st century. Atmospheric Chemistry and Physics, 15(9), 5123–5143.
Stenseth, N. C., Samia, N. I., Viljugrein, H., Kausrud, K. L., Begon, M., Davis, S.,…Chan, K. S. (2006). Plague dynamics are driven by climate variation. Proceedings of the National Academy of Sciences of the United States of America, 103(35), 13110–13115.
Stern, N. H. (2007). The economics of climate change: The Stern review. New York: Cambridge University Press.
Sung, T.-I., Chen, M.-J., Lin, C.-Y., Lung, S.-C., & Su, H.-J. (2011). Relationship between mean daily ambient temperature range and hospital admissions for schizophrenia: Results from a national cohort of psychiatric inpatients. Science of the Total Environment, 410–411, 41–46.
Thompson, J. R., Randa, M. A., Marcelino, L. A., Tomita-Mitchell, A., Lim, E., & Polz, M. F. (2004). Diversity and dynamics of a North Atlantic coastal Vibrio community. Applied and Environmental Microbiology, 70(7), 4103–4110.
Thurston, G. D. (2013). Mitigation policy: Health co-benefits. Nature Climate Change, 3(10), 863–864.
Tirado, M. C., Cohen, M. J., Aberman, N., Meerman, J., & Thompson, B. (2010). Addressing the challenges of climate change and biofuel production for food and nutrition security. Food Research International, 43(7), 1729–1744.
Uejio, C. K., Yale, S. H., Malecki, K., Borchardt, M. A., Anderson, H. A., & Patz, J. A. (2014). Drinking water systems, hydrology, and childhood gastrointestinal illness in central and northern Wisconsin. American Journal of Public Health, 104, 639–646.
United Nations High Commissioner for Refugees. (2009). Climate change, natural disasters and human displacement: A UNHCR perspective. Retrieved from http://www.unhcr.org/refworld/docid/4a8e4f8b2.html
678
U.S. Department of Defense. (2014). 2014 Climate change adaptation roadmap. Retrieved from http://www.acq.osd.mil/ie/download/CCARprint_wForeword_c.pdf
Vezzulli, L., Colwell, R. R., & Pruzzo, C. (2013). Ocean warming and spread of pathogenic vibrios in the aquatic environment. Microbial Ecology, 65(4), 817–825.
Vinck, P. (2013). World disasters report: Focus on technology and the future of humanitarian action. Geneva: International Federation of Red Cross and Red Crescent Societies. Retrieved from http://worlddisastersreport.org/en
Weaver, S. C., & Reisen, W. K. (2010). Present and future arboviral threats. Antiviral Research, 85(2), 328–345.
West, J. J., Smith, S. J., Silva, R. A., Naik, V., Zhang, Y., Adelman, Z.,…Lamarque, J.-F. (2013). Co-benefits of mitigating global greenhouse gas emissions for future air quality and human health. Nature Climate Change, 3, 885–889.
Westerling, A. L., Hidalgo, H. G., Cayan, D. R., & Swetnam, T. W. (2006). Warming and earlier spring increase western U.S. forest wildfire activity. Science, 313, 940–943.
Wheeler, T., & von Braun, J. (2013). Climate change impacts on global food security. Science, 341, 508–513.
Whiteford, H. A., Degenhardt, L., Rehm, J., Baxter, A. J., Ferrari, A. J., Erskine, H. E.,…Vos, T. (2013). Global burden of disease attributable to mental and substance use disorders: Findings from the Global Burden of Disease Study 2010. Lancet, 382, 1575–1586.
Whitmarsh, L., O'Neill, S., & Lorenzoni, L. (Eds.). (2011). Engaging the public with climate change: Behavior change and communication. London: Earthscan.
WikiMedia Commons. (2011). Urban heat island profile. Retrieved from http://commons.wikimedia.org/wiki/File:Urban_heat_island_profile.gif
Zaval, L., Keenan, E. A., Johnson, E. J., & Weber, E. U. (2014). How warm days increase belief in global warming. Nature Climate
679
Change, 4(2), 143–147.
Zhang, Y., Bielory, L., Mi, Z., Cai, T., Robock, A., & Georgopoulos, P. (2015). Allergenic pollen season variations in the past two decades under changing climate in the United States. Global Change Biology, 21(4), 1581–1589.
Ziska, L. H. (2003). Evaluation of the growth response of six invasive species to past, present and future atmospheric carbon dioxide. Journal of Experimental Botany, 54(381), 395–404.
Ziska L., Knowlton K., Rogers C., Dalan, D., Tierney, N., Elder, M. A.,…Frenz, D. (2011). Recent warming by latitude associated with increased length of ragweed pollen season in central North America. Proceedings of the National Academy of Sciences of the United States of America, 108, 4248–4251.
Ziska, L. H., & McConnell, L. L. (2015). Climate change, carbon dioxide, and pest biology: Monitor, mitigate, manage. Journal of Agricultural and Food Chemistry. doi:10.1021/jf506101h
680
For Further Information Review Articles McMichael, A. J. (2013). Globalization, climate change, and human health. New England Journal of Medicine, 368(14), 1335–1343.
Patz, J. A., Frumkin, H., Holloway, T., Vimont, D. J., & Haines, A. (2014). Climate change: Challenges and opportunities for global health. JAMA, 312(15), 1565–1580.
Reports Intergovernmental Panel on Climate Change (IPCC): http://www.ipcc.ch. IPCC reports represent some of the most authoritative and exhaustive synthesis assessments. Its fifth assessment report was published in 2014. Full and summary reports and downloadable graphs and figures are available from the IPCC Web site.
U.S. Centers for Disease Control and Prevention: http://www.cdc.gov/climateandhealth. This site focuses specifically on health aspects of climate change, including public health actions in response.
U.S. Environmental Protection Agency (EPA): http://www.epa.gov/climatechange/effects/health.html. This informative EPA site covers the many sectors affected by climate change.
U.S. Global Change Research Program: This initiative publishes periodic National Climate Assessments under the title Climate Change Impacts in the United States. The most recent assessment was published in 2014. It is available at http://nca2014.globalchange.gov
World Health Organization (WHO): http://www.who.int/globalchange/climate/en. The WHO has been assessing the health risks of climate change for nearly two decades, and this Web site contains links to WHO reports and ongoing projects.
681
Books Butler, C. D. (Ed.). (2014). Climate change and global health. Boston: CABI.
Epstein, P., & Ferber, D. (2011). Changing planet, changing health: How the climate crisis threatens our health and what we can do about it. Berkeley: University of California Press.
Griffiths, J., Rao, M., Adshead, F., & Thorpe, A. (Eds.). (2009). The health practitioner's guide to climate change: Diagnosis and cure. London: Earthscan.
Levy, B. S., & Patz, J. A. (Eds.). (2015). Climate change and public health. New York: Oxford University Press.
Luber, G., & Lemery, J. (Eds.). (2015). Global Climate change and human health: From Science to Practice. San Francisco: Jossey- Bass.
Blogs Dot Earth: http://dotearth.blogs.nytimes.com. An interactive blog that explores trends and ideas with readers and experts. World-renowned reporter Andrew C. Revkin carefully follows and reports on climate change science and policy.
RealClimate: http://www.realclimate.org. A blog containing commentaries by climate scientists that sort out the often polarizing or conflicting stories in the mainstream press. Discussions are restricted to climate science topics (and not political or economic implications). Postings are signed by the author(s) so you know exactly from where the information comes.
Materials for Teachers EcoHealth: http://ecohealth101.org. A source of useful information and student exercises for middle and high school teachers and students. Topics (and lesson plans) include human health effects of climate change, ozone depletion, biodiversity and land-use change, mechanized intensive agriculture, and globalization.
682
GRID-Arendal: http://www.grida.no. A collaborating center of UNEP. The mission of this site (established in 1989 by the government of Norway) is to communicate environmental information to policymakers and facilitate environmental decision making for change.
683
Part 3 Environmental Health on the Regional Scale
684
Chapter 13 Air Pollution
Michelle L. Bell and Jonathan Samet
Dr. Bell and Dr. Samet report no conflicts of interest related to the authorship of this chapter. Anna Engstrom and Marissa Smith report no conflicts of interest related to the authorship of the tox boxes.
685
Key Concepts Air pollution is a major contributor to adverse human health conditions, from asthma to cardiovascular disease to premature death.
Air pollution is not just a modern phenomenon; it has been recognized as a problem for thousands of years.
Air pollution is a growing concern for developing areas of the world with expanding transportation and industry.
Air pollution is not a single entity; it consists of distinct, identifiable components (such as ozone and particulate matter), each with its own sources, chemistry, and toxic effects.
Air pollution emissions come from many sources; these can be natural sources or human activities.
The ambient concentration of an air pollutant in a particular location depends on many factors, including emissions sources, weather, and land patterns.
Air quality management strategies include controlling emissions at the source, reducing emissions, and decreasing population exposure.
This chapter discusses the relationship between outdoor (ambient) air pollutants and human health. These environmental contaminants differ from many others in that exposure is unavoidable and affects all segments of the population. For example, when point source water contamination occurs, the natural resource needed (water) can be retrieved from another location or treated, but outdoor air pollution affects everyone. Indoor air pollution is also a health concern; this is discussed in Chapter 20.
The discussion begins with a brief history of air pollution, which has been recognized to some extent as a health problem for centuries. Various study designs used to assess the health effects of air pollution are discussed, as each has key strengths and weaknesses.
686
Our understanding of how air pollution affects health is based on a synthesis of research over multiple disciplines and research designs. This chapter reviews the general sources and health effects of major outdoor air pollutants. It concludes with a discussion of the links between air pollution and other environmental health concerns.
687
History of Air Pollution Air pollution has long been a contributor to ill health. With the discovery of fire, humans began to pollute air in the places they lived and the outside air. As urban areas developed, pollution sources, such as chimneys and industrial processes, were concentrated, leading to visible and damaging pollution dominated by smoke. Nearly 2,500 years ago, Hippocrates noted that health could be affected by the air we breathe and that the quality of the air differed by area (Hippocrates, 1849). In thirteenth-century London air pollution was so severe that abatement strategies were developed (Brimblecombe, 1986). At that time, air pollution was generally a local issue, generated from kilns, hearths, and furnaces. Since then, the nature of air pollution has changed along with growing populations, industrialization, and fossil fuel–based transportation. High-volume production and transport of pollution across large distances mean that the effects of air pollution can occur far from sources. Air pollution problems now range from the local to the global scale.
Modern-day recognition of the dangers of air pollution can be traced to several extreme episodes during the last century. In 1930, in the Meuse Valley in Belgium, more than sixty people died during such an episode, over ten times the underlying mortality rate (Firket, 1936; Nemery, Hoet, & Nemmar, 2001). The original investigators warned that should such an air pollution episode occur in a city with a larger population, such as London, thousands would die. In October 1948, industrial pollution settled on Donora, a small town in southwestern Pennsylvania (Schrenk, Heimann, Clayton, Gafafer, & Wexler, 1949; Davis, 2002). Twenty people died, about six times the typical mortality rate. Perhaps the most severe such event took place in London in December 1952 (see Text Box 13.2 and Figure 13.3 later in the chapter). In these and similar episodes, pollution levels and subsequent health effects were so severe that the connection between air pollution and health was readily apparent.
In response to severe air pollution episodes such as those in Donora and London, many governments, particularly those of the United States and the United Kingdom, enacted legislation to improve air
688
quality and initiated research on air pollution and health. Despite control measures that have lowered concentrations, air pollution continues to harm health in developed areas and is a growing concern in regions of the world with rapidly developing industry and transportation systems (see Text Box 13.1). The Global Burden of Disease initiative estimated that ambient particulate matter, one type of air pollution, alone caused over 3.2 million premature deaths in 2010 (Lim et al., 2012).
689
Text Box 13.1 Air Pollution in the World's Dirtiest Cities Air pollution levels in the fast-growing cities of low- and middle-income countries can be extreme. The combination of vehicular traffic and industry—with ineffective regulation and uncontrolled emissions—has led to some of the highest pollution levels on the Earth. In China, where air quality can be poor (Chan & Yao, 2008), urban air pollution levels routinely exceed World Health Organization (WHO) standards by an order of magnitude (Figure 13.1). The Chinese government launched a “war on pollution” in 2013, and in 2014, the Chinese Environmental Protection Ministry announced that only eight of the nation's seventy-four large cities had met official air quality standards (up from three the previous year). There were also 471 “environmental emergencies” in 2014, due to especially high air pollution levels (“Air in 90% of China's cities…,” 2015). As shown in Figure 13.2, Indian cities have even higher particulate matter levels than do Chinese cities. Many other cities of Asia, Africa, and Latin America are similarly afflicted, and air pollution continues to rise in many regions of the world.
690
Figure 13.1 Children Wear Masks in the Thick Haze on Tiananmen Square in Beijing, China, January, 2013.
Source: Xinhua News Agency, 2014.
Lou Linwei / Alamy Stock Photo.
Figure 13.2 The Distribution of PM2.5 Levels in Cities in India, China, Europe, and the United States
Source: Greenstone et al., 2015.
In each panel, the vertical dotted line corresponds to the WHO standard, and the vertical solid line corresponds to the relevant nation's standard.
The health impacts of this pollution are severe. The 2010 Global Burden of Disease Study attributed over 3.2 million deaths, 3.1% of global disability-adjusted life years (DALYs),
691
and 22% of ischemic heart disease DALYs to particulate matter (Lim et al., 2012); most of these occurred in the cities of developing nations. By one calculation the average Indian in a polluted city would gain 3.2 years of life if urban pollution were reduced to legal standards (Greenstone et al., 2015). A study of Mexico City, Santiago, and São Paulo estimated that air pollution control would avert over 156,000 deaths, 4 million asthma attacks, 300,000 children's medical visits, and almost 48,000 cases of chronic bronchitis in those cities over a twenty-year period (Bell, Davis, Gouveia, Borja- Aburto, & Cifuentes, 2006).
Some notable progress has been achieved. For example, Mexico City was the most polluted city on the planet in 1992, according to the United Nations, due to a combination of a large population, vehicular and industrial sources, practices such as trash burning, and challenging geographic and meteorological conditions. (The city lies in the high-altitude crater of an extinct volcano, where low atmospheric oxygen levels cause incomplete fuel combustion, intense sunlight drives ozone formation, and the topography helps form inversion layers that trap pollutants.) Months would go by without a single day of acceptable air quality. In the 1990s, the city initiated its PROAIRE program, combining regulatory, economic, technological, and behavioral approaches. Air quality has improved dramatically, and health benefits are expected to follow (Riojas-Rodríguez, Álamo-Hernández, Texcalac-Sangrador, & Romieu, 2014).
692
Types of Ambient Air Pollution The concentration of an air pollutant depends on many factors, including emissions, weather, and land patterns. During conditions of stagnant winds and a temperature inversion, pollution does not disperse, leading to higher pollutant concentrations. Pollution in a given area can vary by season or day depending on weather and sources, such as traffic and wood burning. Some pollutants, such as ozone and small particles with long residence times in the atmosphere, can travel large distances, causing damaging effects far from the pollution sources.
Air pollutants can be categorized by source or by physical and chemical characteristics. Table 13.1 summarizes the characteristics of several major air pollutants, their sources and health effects, and their pertaining regulations and guidelines, including the National Ambient Air Quality Standards (NAAQS) established under the U.S. Clean Air Act and the guidelines of the World Health Organization (2006). An air pollutant may be directly emitted (a primary pollutant) or formed in the atmosphere through physical and chemical conversion of precursors (a secondary pollutant). For example, carbon monoxide (CO) emitted from a car tailpipe is a primary pollutant; however, ozone, a secondary pollutant, is formed in the atmosphere when sunlight chemically converts other pollutants into ozone and other oxidant species.
Table 13.1 Major Ambient Air Pollutants: Sources, Health Effects, and Regulations
Source types and major sources
Health effects Regulations and guidelines
Lead Primary Anthropogenic Leaded fuel (phased out in some locations such as the United States), lead batteries,
Accumulates in organs and tissues. Learning disabilities, cancer, damage to the nervous system.
U.S. NAAQS Quarterly average: 0.15 µg/m3
WHO guidelines Annual: 0.50
693
metal processing
mg/m3
Sulfur dioxide
Primary Anthropogenic Combustion of fossil fuel (power plants), industrial boilers, household coal use, oil refineries Biogenic Decomposition of organic matter, sea spray, volcanic eruptions
Lung impairment, respiratory symptoms. Precursor to PM. Contributes to acid precipitation.
U.S. NAAQS 1-hour average: 75 ppb (196 µg/m3) 3-hour average: 0.5 ppm (1300 µg/m3)
WHO guidelines 10-minute average: 500 µg/m3 Annual: 20 µg/m3
Carbon monoxide
Primary Anthropogenic Combustion of fossil fuels (motor vehicles, boilers, furnaces) Biogenic Forest fires
Interferes with delivery of oxygen. Fatigue, headache, neurological damage, dizziness.
U.S. NAAQS 1-hour average: 35 ppm (40 mg/m3) 8-hour average: 9 ppm (10 mg/m3)
WHO guidelines 15-minute average: 100 mg/m3 30-minute average: 60 mg/m3 1-hour
694
average: 30 mg/m3
Particulate matter
Primary and secondary Anthropogenic Burning of fossil fuel, wood burning, natural sources (e.g., pollen), conversion of precursors (NOx, SOx, VOCs) Biogenic Dust storms, forest fires, dirt roads
Respiratory symptoms, decline in lung function, exacerbation of respiratory and cardiovascular disease (e.g., asthma), mortality. Effects can vary by particle size and composition.
U.S. NAAQS PM10: 24- hour average 150 µg/m3: PM2.5: Annual arithmetic mean: 12 µg/m3: 24-hour average: 35 µg/m3
WHO guidelines PM10: Annual: 20 µg/m3 24-hour average: 50 µg/m3 PM2.5: Annual: 10 µg/m3 24-hour average: 25 µg/m3
Nitrogen oxides
Primary and secondary Anthropogenic Fossil fuel combustion (vehicles, electric utilities, industry), kerosene
Decreased lung function, increased respiratory infection. Precursor to ozone. Contributes to PM and acid precipitation.
U.S. NAAQS (NO2) Annual arithmetic mean: 53 ppb (100 µg/m3) 1-hour average: 100 ppb (188
695
heaters Biogenic Biological processes in soil, lightning
µg/m3) Related to compliance with NAAQS for ozone
WHO guidelines (NO2) 1-hour average: 200 µg/m3 Annual: 40 µg/m3
Tropospheric ozone
Secondary Formed through chemical reactions of anthropogenic and biogenic precursors (VOCs and NOx) in the presence of sunlight
Decreased lung function, increased respiratory symptoms, eye irritation, bronchoconstriction.
U.S. NAAQS 8-hour average: 0.075 ppm (147 µg/m3)
WHO guidelines 8-hour average: 100 µg/m3
Toxic pollutants (hazardous pollutants) (e.g., asbestos, mercury, dioxin, some VOCs)
Primary and secondary Anthropogenic Industrial processes, solvents, paint thinners, fuel
Cancer, reproductive effects, neurological damage, respiratory effects.
EPA rules on emissions for more than 80 industrial source categories (e.g., dry cleaners, oil refineries, chemical plants) EPA and state rules on vehicle
696
emissions Volatile organic compounds (e.g., benzene, terpenes, toluene)
Primary and secondary Anthropogenic Solvents, glues, smoking, fuel combustion Biogenic Vegetation, forest fires
Range of effects, depending on the compound: irritation of respiratory tract, nausea, cancer. Precursor to ozone. Contributes to particulate matter.
EPA limits on emissions EPA toxic air pollutant rules Related to compliance with NAAQS for ozone
Biological pollutants (e.g., pollen, mold, mildew)
Primary Anthropogenic Systems, such as central air conditioning, that create conditions that encourage production of biological pollutants Biogenic Trees, grasses, ragweed, animals, debris
Allergic reactions, respiratory symptoms, fatigue, asthma.
Note: This table lists only a sample of the sources and health effects associated with each pollutant. Additionally, health effects may be the result of characteristics of a pollutant mixture rather than of a single pollutant. Additional legal requirements often apply, such as state regulations.
Another important feature of air pollution is whether the emissions are natural (biogenic) or from human activity (anthropogenic). Naturally occurring pollutants include volatile organic compounds (VOCs) from vegetation, pollens, volcanic gases, and dust from deserts.
697
Text Box 13.2 London 1952: One of the World's Worst Air Pollution Disasters By the 1950s, high air pollution levels in London were common. In fact London's characteristic fogs had long been noted by tourists, authors such as Charles Dickens, and painters such as Claude Monet. However from December 5 to 9, 1952, an unprecedented air pollution event took place.
Several factors contributed to the episode: the use of coal as a primary method of home heating; a particularly cold winter, meaning even more coal burning; and stagnant atmospheric conditions preventing pollution from dispersing. Pollution became so thick that visibility was reduced to near zero. Traffic came to a virtual standstill.
The sharp increase in air pollution was immediately followed by a sharp increase in sickness and death, with mortality rates three times normal levels. Mortuaries did not have enough room and undertakers ran out of coffins. Indicators of morbidity, such as hospital admissions, rose with air pollution concentrations. Later analysis of archived autopsy lung tissue found soot and an excess of other particles (Hunt, Abraham, Judson, & Berry, 2003).
Mortality rates did not return to normal levels until several months after the fog. The initial government report (U.K. Ministry of Health, 1954) hypothesized that influenza accounted for the extra deaths during these months. However, more recent analysis has shown that the true death toll from the episode was 10,000 to 12,000 deaths, rather than the 3,000 to 4,000 typically reported, and that only a fraction of those could be attributed to influenza (Bell & Davis, 2001; Bell, Davis, & Fletcher, 2004) (Figure 13.3).
698
Figure 13.3 Mortality and Air Pollution Levels During the 1952 London Fog
Source: Adapted from Bell & Davis, 2001.
In physical form, air pollutants can be gases or particles. Pollutants that are aerosols consist of small, solid or liquid particles suspended in air. A pollutant's physical form and chemical composition and characteristics (e.g., its solubility if it is a gas) affect the pollutant's ability to penetrate the respiratory system. Other factors that affect respiratory penetration are the pollutant's ambient concentration and the exposed individual's ventilation rate (that is, rate of inhalation of air). For example, exercise increases the breathing rate, and oral breathing enables pollutants to bypass the nasal passages, where they might be prevented from entering the lungs. Gaseous pollutants that are highly soluble in water, such as sulfur dioxide (SO2), are largely removed by the upper airway, whereas less water-soluble gases, such as ozone, penetrate deeper into the lungs (Figure 13.4).
699
Figure 13.4 The Respiratory System This figure shows the lung structure as well as the fraction of particles of different sizes deposited in the various parts of the lung. Very large particles are stopped at the nose, while very small particles reach the alveoli and deposit there.
Source: Oberdörster, Oberdörster, & Oberdörster, 2005. Reproduced with permission from Environmental Health Perspectives. Drawing courtesy of J. Harkema.
Finally, air pollutants can also be classified by the way they are legally regulated. A commonly used term in the United States is criteria pollutants, a group of key outdoor air pollutants defined by the Clean Air Act (CO, lead, nitrogen dioxide, ozone, particulates, and SO2) and for which the U.S. Environmental Protection Agency (EPA) promulgates NAAQS to protect human health and welfare. (Welfare in this context includes such public goods as crops and livestock, air and ground transportation, and visibility.) Another regulatory category, hazardous air pollutants (HAPs), established by the Clean Air Act Amendments of 1990, includes a number of volatile organic chemicals, pesticides, herbicides, and radionuclides. This category does not include all known hazardous air pollutants and does include some pollutants for which the hazard level is unknown.
700
Studies of Air Pollution and Health The health effects of air pollution have been extensively studied through diverse research methods, including epidemiological, human exposure, and animal and other toxicological studies. Each approach has strengths and weakness, and results from complementary research designs are needed to paint a complete picture of the many ways air pollution affects health.
Epidemiological studies investigate air pollution and health outcomes in the real world, typically in large populations. Air monitoring data are often used as surrogates for individual exposure. That is, one or more monitors placed in a city are assumed to represent citywide exposures. In reality, people's activity patterns (the ways they spend their time in different environments, such as work and home) also determine their individual exposures. Adverse health outcomes can be assessed through public health databases, questionnaires, or tests of pulmonary function. For example, a landmark study of air pollution and mortality in six U.S. cities used outdoor monitors in each city to estimate exposure. People in the city with the highest air pollution levels had a 26% higher mortality rate than those in the least polluted city (Dockery et al., 1993). Another epidemiological study, the American Cancer Society's Cancer Prevention Study II (CPSII), tracked about 500,000 adults in 151 U.S. metropolitan areas, and used aggregate exposure data based on monitor measurements) and individual-level health information. The investigators found that participants in the most polluted areas had a 17% higher mortality rate than those in the least polluted areas (Pope et al., 1995, 2002; Krewski et al., 2009).
A key advantage of epidemiological studies is the investigation of real-world populations and air pollution conditions. However, potential weaknesses of epidemiological studies are the often limited ability to control for other factors—referred to as confounding factors, such as population characteristics and pollutants other than those being investigated—and the difficulty of accurately estimating personal exposure (see Chapter 8).
Controlled human studies involve exposure of volunteers to a
701
specified concentration of a pollutant or pollutant mixture in a laboratory setting and measurements of health responses (Sandstrom, 1995). Exposure studies can control for many potential confounding factors, carefully characterize exposure, and incorporate detailed outcome assessment. To protect participants' safety, such research examines health effects that are mild, acute, and reversible. For example, human exposure studies can investigate heart rate variability, lung function changes and the fraction of particles deposited in the lung. Exposures are typically of short duration and at low concentrations. Human exposure studies are particularly useful for characterizing mechanisms of injury and assessing threshold concentrations for short-term effects.
Animal studies involve exposures on a short- or long-term basis to a pollutant or pollutant mixture under well-characterized conditions. Animals are sometimes even placed at sites of particular interest, such as along roadways. Generally rodents are used, but dogs and primates have also been studied. For example, animal exposure studies of air pollution have been used to research respiratory and heart rates in rats, DNA damage in mice, brain damage in dogs, and myocardial ischemia in dogs.
Animal studies sometimes incorporate invasive assessment procedures, such as lung biopsies. Biological samples can be collected for detailed studies of mechanisms of injury. Various animal models are used that mimic human diseases, such as asthma, coronary heart disease, and congestive heart failure. However, evidence from animal studies may not apply to people, and responses to a particular pollutant sometimes vary even among animal species.
Cellular and molecular studies are increasingly important, particularly for investigating mechanisms of disease. Elegant mechanistic studies may assess gene expression in response to air pollution exposure. Emerging technologies (so-called omics approaches, as discussed in Chapter 7) are expected to deepen mechanistic understanding and to provide useful biomarkers of exposure.
702
Sources and Effects of Outdoor Pollutants The health consequences of air pollution are wide-ranging, extending from effects on comfort and well-being to respiratory symptoms and premature death.
This section reviews the sources and health impacts of several common outdoor air pollutants; they are summarized in Table 13.1. Much human health research aims to investigate a particular pollutant, while controlling for potential confounding by other pollutants. Indeed, some pollutants, such as CO, appear to have individual, specific health effects. However, air pollution is actually a complex mixture of multiple pollutants. Damage from air pollution may result from the combined effects (interaction) of several pollutants. Programs for air pollution control generally provide individual standards for each pollutant, although the adverse health effects of different pollutants may be related and a number of pollutants have common sources. Some key ambient air pollutants are discussed in Tox Boxes in other chapters: benzene in Chapter 7, lead in Chapter 11 and VOCs in Chapter 20.
Particulate Matter Particulate matter (PM) refers to a class of pollution rather than an individual pollutant with a specified chemical structure, such as SO2. PM consists of solid or liquid particles suspended in air, regardless of their chemical composition. PM can be either primary (directly emitted) or secondary (formed in the atmosphere through gaseous precursors such as nitrogen oxides [NOx], sulfur oxides [SOx], and VOCs). PM results from the burning of fuel (e.g., emissions from power plants), driving on unpaved roads, industrial activity, and wood-burning stoves, and from natural sources such as pollen, dust, salt spray, erosion, and mold. PM concentrations can vary within a region or even a city (e.g., concentrations can be higher near major highways).
The composition of PM can differ by location, season, source, and meteorology (Bell, Dominici, Ebisu, Zeger, & Samet, 2007). In the eastern United States, PM often has a substantial sulfate component, reflecting the contributions of emissions from power
703
plants. In the western United States, transportation emissions contribute a larger fraction of PM, creating a substantial nitrate component. Variation can also exist at the subregional level.
Particles are generally categorized by size, using a measure called aerodynamic diameter, which is determined by a particle's shape and density and permits comparison of particles having irregular shapes and different sizes and densities. PM10 refers to particles with an aerodynamic diameter of 10 µm or less, whereas PM2.5, or fine PM, has an aerodynamic diameter up to 2.5 µm, and ultrafine PM particles have an aerodynamic diameter up to 0.1 µm. Coarse PM (PM10–2.5) refers to particles with an aerodynamic diameter between 2.5 and 10 µm. Total suspended particles (TSP) refers to almost all particles in the air and is typically measured as particles up to about 45 µm in aerodynamic diameter. Figure 13.5 depicts the typical mass distribution of particles in an urban area, showing two modes, one of fine particles, which tend to be of secondary origin, and the other of coarse particles, which are more likely to be primary. There is often a third mode of very small particles in the nano size range (below 0.1 µm), which have been generated freshly by combustion.
704
Figure 13.5 Particulate Matter Mass Distribution in an Urban Area
A particle's size is related to its source and determines how it is transported in the atmosphere and where it is deposited in the environment and in the respiratory system. Smaller particles penetrate more deeply into the lung. Such particles are typically generated through combustion processes. Diesel exhaust, a combination of gases and particles, is of particular concern because the particles are extremely small (<1 µm) (Kagawa, 2002).
Ambient levels of PM, as indicated by PM10, PM2.5, or other measures, have been associated with health effects including increased hospital and emergency room admissions, respiratory symptoms, decline in pulmonary function, exacerbation of chronic respiratory and cardiovascular diseases, and premature mortality (U.S. EPA, 2003, June; Pope & Dockery, 2006). Laboratory animals exposed to PM show a range of responses including inflammation and pulmonary injury. Time series studies—tracking day-to-day variation in PM levels and in health outcomes—have shown that acute PM exposure is associated with higher risk of mortality,
705
reminiscent of the London and Donora episodes but occurring at modern levels of PM exposure (summarized in Shang et al., 2013; Atkinson, Kang, Anderson, Mills, & Walton, 2014). Longitudinal studies, such as the Six Cities study and CPSII (described above), also demonstrate a link between long-term PM exposure and mortality (summarized in Hoek et al., 2013).
Regulations for controlling PM have evolved in response to a greater understanding of how PM affects human health. The first U.S. NAAQS was established for TSP, in 1971, but this standard was replaced with one for PM10 when it became clear that these smaller particles were more closely associated with health effects. Later evidence demonstrated that even smaller particles, PM2.5, were responsible for adverse health effects, and a PM2.5 standard was added in 1997. The World Health Organization has set air quality guidelines for PM10 and for PM2.5 (WHO, 2006), and many countries have promulgated PM limits as well.
Although the health risks of PM have been studied extensively, much remains unknown. For example, the health risk of PM may depend on the particulates' content of metals, acidity, organics, or sulfates, or on specific combinations of these. Identifying the aspects of PM that are harmful is a critical research need (Lippmann, Chen, Gordon, Ito, & Thurston, 2013). Similarly, the biological mechanisms by which PM causes premature mortality are not fully understood. Leading hypotheses focus on reflexes in the lung that lead to autonomic nervous systems changes, perhaps predisposing to arrhythmias, and on inflammation that in turn predisposes to thrombosis or related changes (Brook et al., 2010).
Sulfur Dioxide Sulfur dioxide, SO2, a water-soluble gas, was a primary component of the 1952 London fog. Sulfur oxides are produced from the combustion of sulfur-containing fuels and materials, such as coal and metal ores. Some coal, such as that from the eastern United States, has particularly high sulfur content. Power plants are the main source of SO2 emissions in the United States. Other sources are industrial boilers, trains, ships, and metal-processing facilities. Household use of coal can contribute significant amounts of SO2 as well. In some areas, such as parts of China, coal is the
706
primary fuel for cooking and heating and causes high levels of SO2 indoors. Natural sources of SO2 include volcanoes.
SO2 can be converted to sulfuric acid and therefore contributes to acid deposition, which harms vegetation, other materials, and wildlife. SO2 also contributes to the formation of particulate matter. Sulfate aerosols, a major component of fine particulate matter, can travel far from their sources. The tall stacks of power plants often release pollution above the inversion layer, which reduces local pollution but allows pollutants to migrate long distances and undergo chemical transformation.
Because SO2 is highly soluble in water, most inhaled SO2 is absorbed by the mucous membranes of the upper airways with little reaching the lung; however, increased ventilation and oral breathing, such as from exercise, can raise the dose delivered to the lung. SO2 has been associated with reduced lung function, bronchoconstriction (increased airway resistance), respiratory symptoms, hospitalizations from cardiovascular and respiratory causes, eye irritation, adverse pregnancy outcomes, and mortality. However, it is difficult to attribute these reported associations to SO2 itself, because it is a precursor to particulate matter and generally exists as a component of a complex, combustion-related pollutant mixture. Experimental studies suggest that some people with asthma may be particularly sensitive to SO2 itself. Controlled exposure studies have shown that effects can occur with very short- term exposure (e.g., ten minutes) in some people with asthma, whereas epidemiological research has shown that effects are also associated with long-term exposure (e.g., yearly levels).
Nitrogen Oxides Nitrogen oxides, NOx, make up a category of highly reactive gases containing nitrogen and oxygen, such as nitrogen dioxide (NO2) and nitrogen oxide (NO). NOx are produced through combustion, including fossil fuel combustion, when the nitrogen that constitutes almost 80% of air is oxidized. Sources of NOx therefore include car and truck engines, electric utilities, and industries. Indoor sources can also contribute to NO2 through kerosene heaters, nonvented gas stoves and heaters, and tobacco smoke. NOx have natural sources
707
such as stratospheric intrusion (when NOx enter the troposphere from the stratosphere) and biological processes in soil, forest fires, and lightning, but the principal sources are power plants and motor vehicles.
NO2 is nearly insoluble in water and can reach the lower respiratory tract. Health effects of NO2 include irritation of the eyes, nose, and throat at higher concentrations; short-term decreases in lung function; and possibly increased respiratory infections and symptoms for children. It is difficult to separate the effects of NO2 from the effects of related air pollutants such as ozone and particulate matter. Both NO and NO2 are toxic gases, and NO2 is regulated in the United States as a criteria pollutant under the Clean Air Act. Nitrogen oxides also have indirect but important roles as precursors of tropospheric ozone and secondary particulate matter, and play a crucial role in the formation of acid precipitation. NO is a greenhouse gas, and thus contributes to global warming (see Chapter 12). NOx and the pollutant species formed as NOx undergo chemical reactions can travel long distances, so health effects may take place far from sources. Emissions have declined in recent decades, by just over 50% from 1980 to 2013 (see www.epa.gov/airtrends/aqtrends.html to track air quality trends since 1980).
Volatile Organic Compounds Volatile organic compounds (VOCs) are a category of organic chemicals with a high vapor pressure, so they readily evaporate at normal temperature and pressure. They include benzene, chloroform, formaldehyde (see Tox Box 20.1, in Chapter 20), isoprene, methanol, monoterpenes, and hundreds of additional compounds. VOCs originate from natural sources (primarily vegetation such as oak and maple trees); industrial processes such as chemical production, use of solvents, and power generation; and transportation, including motor vehicles and off-road sources (e.g., aircraft, construction equipment, and lawn mowers). Transportation accounts for nearly half of VOCs, and motor vehicle emissions (especially from older, poorly maintained vehicles) represent about 75% of that amount. In many locations biogenic sources contribute more to VOCs than anthropogenic emissions do.
708
In fact, the natural appearance that gives the Blue Ridge mountains and the Great Smoky Mountains their names results from biogenic VOCs (mostly isoprene) that form aerosols. VOCs are precursors of ozone but also have independent health effects, including irritation of the respiratory tract, headaches, and carcinogenicity.
709
Tox Box 13.1 Carbon Monoxide
WHAT IS IT? Carbon monoxide (CO) is an odorless, tasteless, and colorless gas, formed by the incomplete combustion of carbon- containing molecules.
HOW IS IT USED? CO is not “used”; it is a by-product of the combustion of such materials as gasoline, natural gas, propane, oil, wood, coal, charcoal, and tobacco. Motor vehicles and other equipment with internal combustion engines (power generators, lawn movers) are the largest source of outdoor CO emissions. In some regions, wood burning also contributes significantly to outdoor CO levels. Indoor sources of CO include gas-powered stoves, space heaters, water heaters, generators, and fireplaces as well as leaking chimneys, tobacco smoke, and exhaust from attached garages. Volcanoes, forest fires, and photochemical reactions in the atmosphere are natural sources of CO.
HOW ARE PEOPLE EXPOSED? People are exposed to CO through inhalation; CO is rapidly absorbed into the bloodstream through gas exchange in the lungs. A common pathway for CO exposure is cigarette smoking; regular smokers can have blood CO levels over twenty times higher than background atmospheric CO levels. Indoor exposure to CO occurs mainly through the use of gas- powered appliances or internal combustion engines in confined or unventilated areas. For example, the incidence of CO poisoning often rises immediately following a snowstorm or after a weather-related power outage when people use gas-
710
powered generators and propane heaters in their homes. Outside, people are exposed to CO in the ambient air, and CO levels are particularly high near heavily trafficked city streets, in areas with large numbers of wood-burning stoves, and during temperature inversions (cold weather). The measurement of carbon monoxide exposure provides a good example of exposure assessment, as explored in Text Box 8.3, in Chapter 8.
WHAT ARE THE TOXIC EFFECTS? Both the acute and chronic health effects of CO exposure are primarily due to the disruption of oxygen transport to tissues in the body. Normally, the protein hemoglobin binds oxygen and transports it to heart, brain, muscles, and other tissues. However, when CO enters the bloodstream, it binds to hemoglobin, displacing oxygen, and forms carboxyhemoglobin (COHb). With rising COHb levels, the ability of hemoglobin to deliver oxygen to the tissues is disrupted. The tissues most sensitive to hypoxia are those most affected, leading to cardiovascular, respiratory, and neurological toxicity. People exposed to low CO levels for a short time may experience fatigue, headaches, nausea, dizziness, disorientation, and visual and coordination impairment. At higher levels or longer exposures, CO can cause angina (chest pain), severe impairments in vision and cognition, and even death. People with preexisting heart or lung conditions as well as pregnant women may be more susceptible to CO toxicity. (This diagram shows health effects associated with particular CO inhalation times and concentration levels.)
711
HOW ARE PEOPLE PROTECTED? The EPA has established National Ambient Air Quality Standards to regulate CO ambient air levels. In most areas vehicles are still the major source of CO emissions, but the introduction and widespread use of catalytic converters, which reduce CO emissions by converting CO to CO2, have reduced CO emissions from vehicles. In addition, preventive measures, including the widespread installation of CO detectors and public education campaigns focusing on safe operation of gas-powered equipment and proper ventilation, are also important means of protecting people from CO toxicity.
WANT TO LEARN MORE? The ATSDR Toxicological Profile for Carbon Monoxide is at www.atsdr.cdc.gov/toxprofiles/tp.asp?id=1145&tid=253
The clinical management of CO poisoning is reviewed in J. A. Guzman, “Carbon Monoxide Poisoning,” Critical Care Clinics, 2012, 28, 537–548. This is an interesting area for public health, as the evidence base for a standard treatment, hyperbaric oxygen, is incomplete. It is reviewed in N. A.
712
Buckley, D. N. Juurlink, G. Isbister, M. H. Bennett, & E. J. Lavonas, “Hyperbaric Oxygen for Carbon Monoxide Poisoning,” Cochrane Database of Systematic Reviews, 2011 (4), CD002041.
The public health approach to preventing and managing CO toxicity is reviewed in S. Iqbal, J. H. Clower, S. A. Hernandez, S. A. Damon, & F. Y. Yip, “A Review of Disaster-Related Carbon Monoxide Poisoning: Surveillance, Epidemiology, and Opportunities for Prevention,” American Journal of Public Health, 2012, 102(10), 1957–1963.
Contributed by Anna Engstrom
Tropospheric Ozone Ozone (O3), a gas, is present in the troposphere, the lowest atmospheric layer—which extends from the Earth's surface to the stratosphere, a distance of approximately 10 to 15 km—and in the stratosphere, which extends from the troposphere to about 45 to 55 km above the Earth's surface. Stratospheric ozone forms the naturally occurring ozone layer that protects us from ultraviolet radiation, whereas tropospheric ozone, sometimes called ground-level ozone, is a harmful pollutant. To communicate the difference between stratospheric and tropospheric ozone, the EPA introduced the slogan “Good up high—bad nearby.”
Tropospheric ozone is a colorless gas and a photochemical oxidant formed through complex, nonlinear chemical reactions involving the precursors VOCs and NOx in the presence of sunlight. Because of this process, pollution involving ozone is sometimes referred to as photochemical smog. Stratospheric ozone can also intrude into the troposphere.
Due to ozone's complex chemistry, decreased emissions of either NOx or VOCs could potentially result in higher ozone levels, depending on the initial concentrations of the two main categories of precursors, among other factors. In some areas, referred to as NOx-limited, reductions of NOx may be the most effective way to reduce ozone levels, whereas in VOC-limited areas, reducing VOC emissions may be more effective.
713
Concentrations of ozone are highly seasonal, with higher levels during the hotter months, and also show strong diurnal patterns, following sunlight and transportation emissions patterns. After ozone precursors are emitted they can travel downwind and contribute to the formation of ozone, which can itself travel with wind patterns. Thus, elevated concentrations can result from the transport of ozone and its precursors at distances of up to hundreds of miles away. Ozone problems tend to be more regional than localized. Ozone levels are lower indoors than outdoors, because ozone adsorbs to indoor surfaces and rapidly breaks down.
Ozone is not highly soluble in water and can thus reach the lower respiratory tract. Because of its oxidant properties, ozone can break molecular bonds and rapidly damage human tissue. Short-term exposure to ozone for healthy adults has been associated with temporarily decreased lung function, increased airway resistance, and increased respiratory symptoms, such as coughing and wheezing. These changes are reflected by increases in clinic visits, emergency room visits, school absenteeism, and hospitalizations following high-ozone days. Short-term exposure to ozone has been associated with daily mortality (Bell, McDermott, Zeger, Samet, & Dominici, 2004).
People with asthma are especially susceptible because ozone inflames the airway linings and can trigger asthmatic attacks. However, healthy people can also be affected (U.S. EPA, 2013). Children, with their narrow caliber airways, are also susceptible (see Chapter 11). People who spend time outdoors, such as outdoor exercisers or workers, are susceptible because of their greater exposure. Long-term ozone exposure may contribute to the development of chronic lung diseases, such as asthma and bronchitis, and accelerate aging of the lungs. Ozone has also been associated with impaired lung development in children and the onset of asthma.
714
Tox Box 13.2 Mercury (Hg)
WHAT IS IT?
© Cerae | Dreamstime.com – Mercury (Hg) Photo.
Mercury is a heavy metal found in the environment in three forms, elemental, inorganic, and organic, each with unique chemical and toxicological properties. Elemental mercury can be obtained from mining inorganic mercury (mercuric sulfide) in the form of cinnabar ore. Elemental mercury is familiar to many people as a silvery liquid; it readily vaporizes at room temperature. When elemental mercury combines with sulfur, oxygen, or chlorine, it forms inorganic salts. The most significant toxic exposure in humans comes from mercury in its organic form. Organic mercury is formed when mercury and carbon combine. The most common of
715
the many forms of organic mercury is methylmercury. Microorganisms in the environment convert elemental and inorganic mercury into methylmercury by adding one carbon atom and three hydrogen atoms. Dimethylmercury is a highly toxic form of organic mercury that, although rare in the environment, has been found in highly contaminated Superfund sites.
HOW IS IT USED? The chemical properties of elemental, inorganic, and organic mercury make these substances suitable for many commercial applications. Throughout the nineteenth and early twentieth centuries, mercury nitrate was used in the production of the felt used by milliners. Today, mercury is used in electronics, batteries, thermometers, and medical equipment. The torr, a common unit of pressure measured in millimeters of Hg, derives its units from the use of mercury in early pressure gauges. Mercury is used in certain industrial processes (alkali and metal processing), and in artisanal gold mining. Mercury also has medical applications, including its use in dental amalgams and as a component of thimerosal, a preservative that is sometimes used in vaccines. (Since 2001, all vaccines in the United States recommended for children under age 6 contain no or only trace amounts of thimerosal.)
HOW ARE PEOPLE EXPOSED? Mercury naturally contaminates fossil fuels, especially coal, so fossil fuel combustion releases mercury into the environment. Coal-fired power plants account for about half of airborne mercury emissions in the United States and globally—the largest source. It is estimated that the concentration of mercury in the air has increased three- to sixfold since the industrial revolution began. After atmospheric deposition, mercury enters the ecosystem and is widely circulated (its sources and paths are displayed in the illustration below). People are exposed to mercury through oral, inhalation, and dermal exposure. The most common route is oral exposure, through the ingestion of contaminated
716
food, a result of deposition of airborne mercury in water and on farmland. However, inhalation and dermal exposures can be high among people who work with mercury. Inorganic mercury can be methylated by microorganisms in the air, water, and soil. Once methylated, the mercury can enter the food chain, bioaccumulating as it is consumed at higher trophic levels. This concept is particularly relevant to seafood consumption. When people eat large, predatory fish such as tuna, swordfish, and king mackerel from contaminated bodies of water, they ingest mercury. Inhalation and dermal exposures are most commonly associated with workplace exposure in electronics manufacturing, the automotive industry, and chemical processing. In some cases, dermal exposures can occur when people touch contaminated soil; however, this route contributes the least to overall mercury exposure.
WHAT ARE THE TOXIC EFFECTS? Like many toxicants, mercury has toxic effects following high, acute exposures that are different from the effects of low, chronic exposures. High-level exposure to mercury is rare; however, it can lead to severe neurological impacts,
717
including loss of senses, unconsciousness, and even death. More common are low-level, chronic exposures. These types of exposures are most concerning in young children, pregnant women, and women of childbearing age. Because mercury remains in the body for years following exposure, mercury exposures that occur prior to conception affect the developing fetus. Exposure to low levels of mercury during development is associated with neurological disorders including developmental delays. High-level prenatal exposure to mercury is associated with mental retardation, deafness, blindness, cerebral palsy, and congenital malformations. Much of our understanding of the impacts of high-level mercury exposure comes from the tragic poisoning that occurred in Minamata, Japan, in the1950s and '60s. Industrial pollution of Minamata Bay released mercury into the water, where it was organified and bioconcentrated in the food chain. Fish consumers were exposed to high levels of mercury that led to many of the health impacts discussed above. These symptoms are collectively termed Minamata disease (see Figure 1.2). The term mad hatter syndrome has been used to describe the symptoms of inorganic mercury toxicity in adults, in reference to the afflictions of nineteenth- century milliners who developed tremors, mood shifts, and other neurological abnormalities following long-term occupational exposure (also known as erethism). A milder syndrome, generally characterized by tremors, manifests in dentists exposed to mercury through the application of dental amalgams.
HOW ARE PEOPLE PROTECTED? People are protected from mercury exposure through international action, federal laws, and public health recommendations. In 2005, the United Nations Environment Programme established the Global Mercury Partnership as a primary exposure prevention strategy. The program aims to reduce mercury emissions, research the environmental transport and fate of mercury pollution, and improve management strategies for mercury storage and waste treatment. The United States has participated in the Global
718
Mercury Partnership by implementing the Mercury Export Ban Act of 2008, which aims to reduce the amount of mercury on the global market.
Because of its multiple exposure routes, mercury in the United States is regulated by multiple federal agencies, including the EPA, the Occupational Safety and Health Administration (OSHA), and the Food and Drug Administration (FDA). OSHA protects workers by regulating workplace mercury vapor levels. The EPA regulates environmental concentrations of mercury pursuant to the Clean Air Act, Clean Water Act, and the Safe Drinking Water Act. However, the complex ecosystem transport and bioaccumulative nature of mercury make this a complex task. Therefore the FDA prohibits the sale of commercial fish with greater than 1 part per million of mercury.
Local and state authorities create public health advisories to help prevent recreational or subsistence consumption of fish from areas known to have high concentrations of mercury. Specific fish consumption advisories have been created for pregnant women and young children to help them avoid exposure to mercury by eating fish from less contaminated sources that are lower on the food chain. These advisories are particularly important because they allow pregnant women and young children to still obtain the nutritional benefits of seafood consumption.
WANT TO LEARN MORE? ATSDR's Toxicological Profile for Mercury (www.atsdr.cdc.gov/toxprofiles/tp46.pdf) dates from 1999, but a 2013 addendum (www.atsdr.cdc.gov/toxprofiles/mercury_organic_addendum.pdf provides current information on organic mercury compounds.
More recent reviews of mercury toxicity include J. D. Park & W. Zheng, “Human Exposure and Health Effects of Inorganic and Elemental Mercury,” Journal of Preventive Medicine and Public Health, 2012, 45(6), 344–352; and K. M. Rice, E. M. Walker Jr., M. Wu, C. Gillette, & E. R. Blough,
719
“Environmental Mercury and Its Toxic Effects,” Journal of Preventive Medicine and Public Health, 2014, 47(2), 74–83.
A review that focuses on a major exposure pathway in low- income countries is A. K. Kristensen, J. F. Thomsen, & S. Mikkelsen, “A Review of Mercury Exposure Among Artisanal Small-Scale Gold Miners in Developing Countries,” International Archives of Occupational and Environmental Health, 2014, 87(6), 579–590.
A classic book, by W. Eugene Smith and Aileen M. Smith, is Minamata: The Story of the Poisoning of a City, and of the People Who Chose to Carry the Burden of Courage (Holt, Rinehart & Winston, 1975). It includes moving photographs of the victims of Minamata disease.
Contributed by Marissa Smith
Air Toxics Hundreds of other ambient air pollutants exist besides those just described. They include hydrochloric acid, mercaptan, parathion, naphthalene, biphenyl, vinyl bromide, methyl bromide, dioxin, and cadmium, to name a few. Exposure to these pollutants can occur through inhalation, but they also enter other environmental media such as water and food. Therefore exposure can occur through eating foods, drinking water, or coming into contact with soil contaminated by atmospheric deposition. Health effects of these air toxics include damage to the neurological, immune, respiratory, and reproductive systems (e.g., reduced fertility), as well as developmental problems and some cancers. Like humans, animals may experience health problems if exposed to sufficient quantities of air toxics. Some air toxics bioaccumulate in tissues, so that the concentrations in aquatic or marine animals can rise to levels far above those in the surrounding air and water. The concentrations increase higher in the food chain, for example, as larger fish eat contaminated smaller fish. This can result in humans being exposed to elevated levels through eating seafood. Polychlorinated biphenyls (PCBs) are one example of such a pollutant (see Tox Box 2.1).
720
Air Pollution Prevention and Control There are many approaches to improving air quality. Air quality management is a topic that is too diverse for full treatment here, but we note that strategies are based on a foundation of evidence that builds from sources of air pollution to patterns of population exposure and then to associated health risks. Approaches include controlling emissions at the source, such as with scrubbers at coal- fired power plants; reducing emissions, such as through increased public transportation or emissions controls for automobiles; and decreasing exposure, such as through attending to the EPA's Air Quality Index, which provides a health warning on high air pollution days to encourage sensitive individuals to avoid the outdoors. These strategies reflect the preventive approaches described in Chapter 26.
Reduction of the health effects of air pollution comes from actions at multiple spatial and institutional levels, ranging from personal decisions by individuals, to community and state plans, and to multigovernment agreements. In the United States, the federal policy framework is defined by the Clean Air Act (Text Box 13.3). Due to the transport of pollution across state boundaries, many pollutants, such as ozone, are addressed through multistate consortiums. Because air pollution also crosses political boundaries, agreements between national governments may be needed. Actions by individuals may also contribute to improved air quality; use of mass transit instead of private automobiles and lessened use of wood-burning fireplaces may enhance air quality locally.
721
Text Box 13.3 The Clean Air Act: Environmental Regulation for Public Health Protections The Clean Air Act is the major piece of federal legislation that addresses air quality in the United States. Congress passed the original Clean Air Act in 1963, when memories of the air pollution disasters in Donora, Pennsylvania, and London, England (Text Box 13.2), were still fresh. The law was greatly expanded in 1970, the same year Congress created the U.S. Environmental Protection Agency. The new EPA was assigned responsibility for implementing the Clean Air Act. Later amendments further expanded the Act's scope.
One approach to regulation is to limit the air concentrations of certain pollutants. Under the Clean Air Act, the EPA set National Ambient Air Quality Standards (NAAQS) for six criteria pollutants (carbon monoxide, lead, nitrogen dioxide, ozone, particulates, and sulfur dioxide). These standards include primary standards, designed to protect public health, including the health of sensitive subpopulations, with an adequate margin of safety, and secondary standards, designed to avert damage to soil, water, crops, and buildings. The EPA is required to consider revisions of the NAAQS based on updated scientific review.
Areas that fail to meet national air quality standards are called nonattainment areas. States have a major role in achieving and maintaining acceptable air quality, including remedying nonattainment. They develop state implementation plans (SIPs), based on air quality measurements, inventories of sources, and projections of future emissions. SIPs may limit emissions from stationary sources such as power plants and factories or from mobile sources (vehicles) through such means as state emissions inspection and maintenance programs. An interesting feature of the Clean Air Act is its linkage with other federal spending, including highway funds; if the EPA does not
722
approve of a SIP for a nonattainment area, the federal government may withhold highway funding—a strong motivator for state and local officials.
A second approach to air quality regulation is to limit emissions. The Clean Air Act requires the EPA to regulate sources such as power plants and factories, both when they are newly constructed and when they are modified. The EPA is also authorized to regulate emissions from mobile sources (mostly vehicles), and to regulate motor vehicle fuels, if the pollutants in question “may reasonably be anticipated to endanger public health or welfare.” The EPA utilized this authority to require the removal of lead from gasoline during the 1990s, a major public health victory, and twenty years later (after a prolonged legal battle that reached the Supreme Court), to regulate CO2 emissions from motor vehicles.
Under the Clean Air Act, EPA limited sulfur dioxide emissions from power plants using a cap-and-trade approach. Beginning in the 1990s, the agency issued emissions allowances to power plants. A plant could then match its emissions to its allowances either by reducing emissions or by purchasing unneeded allowances from other plants. This market-based approach has successfully lowered SO2 emissions nationally, and is considered a possible model for reducing CO2 emissions as well (Chan, Stavins, Stowe, & Sweeney, 2012).
Other provisions of the Clean Air Act include regulations on emissions of 190 “hazardous air pollutants” using maximum achievable control technology (MACT), provisions that limit interstate pollution, and provisions that phase out chlorofluorocarbons that deplete the stratospheric ozone layer.
Air quality regulation is a complex undertaking, with a variety of policy approaches. Other countries have legal frameworks that share some features of the U.S. Clean Air Act and that differ in other respects.
723
Larger Effects of Regional Air Pollution Many atmospheric pollutants affect air quality and human health through multiple pathways. For example, NO2 affects health directly but also contributes to the formation of ozone, and SO2 contributes to the formation of particulate matter. Ambient air pollutants also figure into many other environmental problems. NOx and SOx are the primary causes of acid precipitation. Indoor air pollution levels are related to indoor sources and the penetration of outdoor air. PM and ozone both reduce visibility. The same fossil fuel–burning processes that generate ambient air pollutants also produce greenhouse gases, such as CO2 and methane (CH4), which contribute to global warming. In fact, the U.S. EPA has legal authority to regulate emissions of greenhouse gases under the Clean Air Act. Many technologies and policies to mitigate ambient air pollution could also reduce production of greenhouse gases, and vice versa (West et al., 2013). Thus the control of regional air pollution and of the related health consequences is intertwined with ecological health and climate change.
724
Summary Although the link between air pollution and human health has been known for centuries, research in recent decades has shown the full scope of the continued serious threat posed to public health. Findings from a broad range of research, including both epidemiological and toxicological studies, provide scientific evidence on how air pollution affects health. Collectively, these complementary research approaches, each having particular strengths and weaknesses, provide a more complete understanding of the health risk posed by air pollution.
Ambient air pollution results from a variety of natural and anthropogenic sources. Particulate matter pollution is unique in that it is defined without regard to chemical composition, whereas other air pollutants are defined based on chemical structure (e.g., carbon monoxide). Health responses to ambient air pollution range from an increased risk of respiratory symptoms such as coughing and wheezing to increased risk of mortality. Many air pollutants have common sources, and some primary pollutants contribute to the formation of other, secondary pollutants. Many of the same sources that produce pollution of local concern also contribute to the greenhouse gases that are causing global climate change.
725
Key Terms aerodynamic diameter
A measure of particulate matter based on size and how the particle moves through air, determined by a particle's shape and density, permits comparison of particles having irregular shapes and different sizes and densities.
cap and trade An environmental policy tool designed to limit emissions of a pollutant such as carbon dioxide or sulfur dioxide. The cap is a limit on emissions set by a regulatory authority; the limit can be lowered over time to reduce emissions. The trade is a market for permits to emit. Using this trading, emitters able to reduce their emissions can sell their allocated permits to other emitters. This approach creates incentives to innovate to reduce emissions, but can also result in redistribution of health effecrts, in which some people are worse off.
coarse PM (PM10–2.5) Particulate matter with an aerodynamic diameter between 2.5 and 10 µm.
criteria pollutants A group of key outdoor air pollutants defined by the Clean Air Act (CO, lead, nitrogen dioxide, ozone, particulates, and SO2) for which the U.S. EPA promulgates National Ambient Air Quality Standards (NAAQS) to protect human health and welfare.
fine PM (PM2.5) Particulate matter with an aerodynamic diameter no larger than 2.5 µm.
ground-level ozone See tropospheric ozone.
hazardous air pollutants (HAPs) A category of pollutants established by the Clean Air Act Amendments of 1990; it includes a number of volatile organic chemicals, pesticides, herbicides, and radionuclides.
nitrogen oxides (NOx) A category of highly reactive gases containing nitrogen and
726
oxygen, such as nitrogen dioxide (NO2) and nitrogen oxide (NO).
ozone (O3) A gas consisting of three oxygen atoms. A secondary air pollutant, it is chemically unstable, oxidizing, and irritating when inhaled.
ozone layer Stratospheric ozone (O3), ozone about 45 to 55 km above the earth's surface. It is naturally occurring and protects us from ultraviolet radiation.
particulate matter (PM) A class of pollution consisting of solid or liquid particles suspended in air, regardless of their chemical composition.
PM10 Particulate matter with an aerodynamic diameter no larger than 10 µm.
PM2.5 Fine PM, particulate matter with an aerodynamic diameter no larger than 2.5 µm.
primary pollutant A pollutant directly emitted from sources.
secondary pollutant A pollutant formed through chemical and physical transformation of precursors in the atmosphere.
smog Tropospheric ozone (O3), sometimes called photochemical smog.
sulfur dioxide (SO2) A water-soluble gas formed from sulfur oxides, which are produced from combustion of sulfur-containing fuels and materials, such as coal and metal ores; it contributes to acid deposition.
total suspended particles (TSP) Almost all particle matter in the air, typically measured as particles up to about 45 µm in aerodynamic diameter.
tropospheric ozone The ground-level ozone, at earth's surface layer; it is harmful to
727
human health. ultrafine PM
Particulate matter with an aerodynamic diameter up to 0.1 µm. volatile organic compounds (VOCs)
A category of organic chemicals with a high vapor pressure, which readily evaporate at normal temperature and pressure; examples include benzene, chloroform, isoprene, and hundreds of additional compounds.
728
Discussion Questions 1. What are the primary air pollution problems in your
community? What are the main sources?
2. How do your everyday activities contribute to air pollution?
3. How is regional air pollution related to other health and environmental issues?
4. Air pollution is a complex mixture of multiple contaminants; however, air pollutants are often regulated and studied individually. Why is this the case? What are the consequences of this separation? Insofar as this creates difficulties, how can they be addressed?
5. What actions can be taken to lower air pollution emissions? Consider possibilities at multiple levels: the individual, the community, the government, and so forth.
6. In metro areas with high ground-level ozone, ozone levels tend to vary during the day, peaking in the late afternoon and early evening—the very time of day when school sports teams are practicing. As a result, student athletes may be exposed to high levels of ozone. This is a special concern since they may breathe hard while practicing, increasing their exposure. How would you advise school officials to handle this situation? Consider the need to balance two health-promoting strategies: encouraging physical activity and minimizing exposure to unwholesome air.
729
References Air in 90% of China's cities still not safe for breathing, despite “war on pollution.” (2015, February 2). RT.com. Retrieved from http://rt.com/news/228579-china-air-standards-pollution
Atkinson, R. W., Kang, S., Anderson, H. R., Mills, I. C., & Walton, H. A. (2014). Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions: A systematic review and meta- analysis. Thorax, 69(7), 660–665.
Bell, M. L., & Davis, D. L. (2001). Reassessment of the lethal London fog of 1952: Novel indicators of acute and chronic consequences of acute exposure to air pollution. Environmental Health Perspectives, 19(Suppl. 3), 389–394.
Bell, M. L., Davis, D. L., & Fletcher, T. (2004). A retrospective assessment of mortality from the London smog episode of 1952: The role of influenza and pollution. Environmental Health Perspectives, 112, 6–8.
Bell, M. L., Davis, D. L., Gouveia, N., Borja-Aburto, V. H., & Cifuentes, L. A. (2006). The avoidable health effects of air pollution in three Latin American cities: Santiago, São Paulo, and Mexico City. Environmental Research, 100(3), 431–440.
Bell, M. L., Dominici, F., Ebisu, K., Zeger, S. L., & Samet, J. M. (2007). Spatial and temporal variation in PM2.5 chemical composition in the United States for health effects studies. Environmental Health Perspectives, 115, 989–995.
Bell, M. L., McDermott, A., Zeger, S. L., Samet, J. M., & Dominici, F. (2004). Ozone and short-term mortality in 95 US urban communities, 1987–2000. JAMA, 292, 2372–2378.
Brimblecombe, P. (1986). The Big Smoke: A history of air pollution in London since medieval times. New York: Methuen.
Brook, R. D., Rajagopalan, S., Pope, C. A., 3rd, Brook, J. R., Bhatnagar, A., Diez-Roux, A. V.,…Kaufman, J. D. (2010). Particulate matter air pollution and cardiovascular disease: An update to the
730
scientific statement from the American Heart Association. Circulation, 121(21), 2331–2378.
Chan, C. K., & Yao, X. (2008). Air pollution in mega cities in China. Atmospheric Environment, 42(1), 1–42.
Chan, G., Stavins, R., Stowe, R., & Sweeney, R. (2012). The SO2 allowance trading system and the Clean Air Act Amendments of 1990: Reflections on 20 years of policy innovation. National Tax Journal, 65(2), 419–452.
Chen T.-P. (2015). Beijing quietly curbs discussion of documentary on air pollution. Online environmental film soars in popularity, and government steps in to tamp down the buzz. Wall Street Journal, March 2. Retrieved from http://www.wsj.com/articles/beijing- quietly-curbs-discussion-of-documentary-on-air-pollution- 1425312297
Davis, D. L. (2002). When smoke ran like water: Tales of environmental deception and the battle against pollution. New York: Basic Books.
Dockery, D. W., Pope, C. A., 3rd, Xu, S., Spengler, J. D., Ware, J. H., Fay, M. E.,…Speizer, F. E. (1993). An association between air pollution and mortality in six U.S. cities. New England Journal of Medicine, 329, 1753–1759.
Firket, J. (1936). Fog along the Meuse Valley. Transactions of the Faraday Society, 32, 11927.
Greenstone, M., Nilekani, J., Pande, R., Ryan, N., Sudarshan, A., & Sugathan, A. (2015). Lower pollution, longer lives: Life expectancy gains if India reduced particulate matter pollution. Economic & Political Weekly, 50, 40–46.
Hippocrates. (1849). The genuine works of Hippocrates (F. Adams, trans.). London: Sydenham Society.
Hoek, G., Kirshnan, R. M., Beelen, R., Peters, A., Ostro, B., Brunekreef, B., & Kaufman, J. D. (2013). Long-term air pollution exposure and cardio-respiratory mortality: A review. Environmental Health, 12(1), 43.
731
Hunt A., Abraham, J. L., Judson, B., & Berry, C. L. (2003). Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues. Environmental Health Perspectives, 111, 1209–1214.
Kagawa, J. (2002). Health effects of diesel exhaust emissions: A mixture of air pollutants of worldwide concern. Toxicology, 27, 349–353.
Krewski, D., Jerrett, M., Burnett, R. T., Ma, R., Hughes, E., Shi, Y.,… Tempalski, B. (2009). Extended follow-up and spatial analysis of the American Cancer Society study linking particulate air pollution and mortality (Research Report 140). Cambridge, MA: Health Effects Institute.
Lim, S. S., Vos, T., Flaxman, A. D., Danaei, G., Shibuya, K., Adair- Rohani, H.,…Memish, Z.A. (2012). A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380, 2224– 2260.
Lippmann, M., Chen, L. C., Gordon, T., Ito, K., & Thurston, G. D. (2013). National Particle Component Toxicity (NPACT) initiative: Integrated epidemiologic and toxicologic studies of the health effects of particulate matter components (Research Report 177). Cambridge, MA: Health Effects Institute. Retrieved from http://pubs.healtheffects.org/view.php?id=410
Nemery, B., Hoet, P.H.M., & Nemmar, A. (2001). The Meuse Valley fog of 1930: An air pollution disaster. Lancet, 357, 704–708.
New Mexico Department of Health. (2014). Contaminants of concern: Mercury. Retrieved from https://nmtracking.org/environ_exposure/contaminants/mercury
Oberdörster, G., Oberdörster, E., & Oberdörster, J. (2005). Nanotoxicology: An emerging discipline evolving from studies of ultrafine particles. Environmental Health Perspectives, 113, 823– 839.
Pope, C. A, 3rd, Burnett, R. T., Thun, M. J., Calle, E. E., Drewski, D., Ito, K., & Thurston, G. D. (2002). Lung cancer, cardiopulmonary
732
mortality, and long-term exposure to fine particulate air pollution. JAMA, 287, 1132–1141.
Pope, C. A., 3rd, & Dockery, D. W. (2006). Health effects of fine particulate air pollution: Lines that connect. Journal of the Air and Waste Management Association, 56, 709–742.
Pope, C. A., 3rd, Thun, M. J., Namboodiri, M. M., Dockery, D. W., Evans, J. S., Speizer, F. E., & Heath, C. W., Jr. (1995). Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. American Journal of Respiratory and Critical Care Medicine, 151, 669–674.
Riojas-Rodríguez, H., Álamo-Hernández, U., Texcalac-Sangrador, J. L., & Romieu, I. (2014). Health impact assessment of decreases in PM10 and ozone concentrations in the Mexico City Metropolitan Area: A basis for a new air quality management program. Salud Pública de México, 56(6), 579–591.
Sandstrom, T. (1995). Respiratory effects of air pollutants: Experimental studies in humans. European Respiratory Journal, 8, 976–995.
Schrenk, H. H., Heimann, H., Clayton, G. D., Gafafer, W. M., & Wexler, H. (1949). Air pollution in Donora, PA: Epidemiology of the unusual smog episode of October 1948, preliminary report. Public Health Bulletin No. 306. Washington, DC: U.S. Public Health Service.
Shang, Y., Sun, Z., Cao, J., Wang, X., Zhong, L., Bi, X.,…Huang, W. (2013). Systematic review of Chinese studies of short-term exposure to air pollution and daily mortality. Environment International, 54, 100–111.
U.K. Ministry of Health. (1954). Mortality and morbidity during the London fog of December 1952. Report on Public Health and Medical Subjects No. 95. London: Author.
U.S. Environmental Protection Agency. (2003, June). Fourth external review draft of air quality criteria for particulate matter (EPA/600/P-99/002aD). Research Triangle Park, NC: National Center for Environmental Assessment, RTP Office, Office of Research and Development.
733
U.S. Environmental Protection Agency. (2013). Final report: Integrated science assessment of ozone and related photochemical oxidants (EPA/600/R-10/076F). Washington, DC: Author.
West, J. J., Smith, S. J., Silva, R. A., Naik, V., Zhang, Y., Adelman, Z.,…Lamarque, J.-F. (2013). Co-benefits of mitigating global greenhouse gas emissions for future air quality and human health. Nature Climate Change, 3(10), 885–889.
World Health Organization. (2006). Air quality guidelines: Global update 2005—particulate matter, ozone, nitrogen dioxide and sulfur dioxide. Copenhagen: Author.
Xinhua News Agency. (2014). China focus: China fights air pollution as smog persists. Retrieved from http://news.xinhuanet.com/english/china/2014- 02/23/c_133137096.htm
734
For Further Information Books Ayres, J., Maynard, R. L., & Richards, R. (2006). Air pollution and health. Hackensack, NJ: World Scientific.
Jacobson, M. Z. (2012). Atmospheric pollution: History, science and regulation (2nd ed.). New York: Cambridge University Press.
National Research Council, Committee on Air Quality Management in the United States. (2004). Air quality management in the United States. Washington, DC: National Academies Press.
Vallero, D. (2014). Fundamentals of air pollution (5th ed.). San Diego: Academic Press.
Agencies and Organizations American Lung Association (ALA): http://www.lungusa.org (click on “air quality”). Information on both indoor and outdoor air quality and a link to the periodic ALA report State of the Air, summarizing recent research, are available at this agency Web site.
Centers for Disease Control and Prevention (CDC): http://www.cdc.gov/nceh/airpollution. General information on air pollution and health, information on asthma epidemiology, and information on specific subtopics such as carbon monoxide can be found on this Web site.
U.S. Environmental Protection Agency (EPA): http://www.epa.gov/ebtpages/air.html. A wide range of articles on air quality, addressing various pollutants, their sources and effects, and how to monitor and control them, including information on the Air Quality Index, is available from this Web site.
In addition, most state environment departments provide information on current air quality levels on their Web sites.
735
Chapter 14 Energy and Human Health
Howard Frumkin
This chapter draws heavily on K. R. Smith, H. Frumkin, K. Balakrishnan, C. D. Butler, Z. A. Chafe, I. Fairlie, and others' “Energy and Human Health,” in Annual Review of Public Health, 2013, 34, 159–188, and on Jeremy Hess's “Energy Production,” which was Chapter 13 in the second edition of this textbook. Dr. Frumkin's disclosures appear in the front of this book, in the section titled “Potential Conflicts of Interest in Environmental Health: From Global to Local.”
736
Key Concepts Energy is essential for human health, well-being, and comfort.
The ways in which people make and use energy correlate closely with human development, both over historical time and across today's world.
Greater prosperity is associated with increased energy use, cleaner energy sources, greater distance between energy production and end use, and deferment of health impacts over time.
There are several energy sources on Earth. The sun is primary among them, as direct sunlight, as energy for plant growth, and as stored solar energy in fossil fuels. Other energy sources include geothermal energy, hydropower, and nuclear energy.
Each source of energy has a profile of health impacts.
Life cycle analysis—from “harvesting” and transporting raw materials, to fuel production, to energy transmission and consumption, to waste generation and management— clarifies the full health impacts each form of energy.
Major changes in energy patterns may be imminent, driven by such forces as petroleum depletion and global climate change. These changes will have important health consequences.
Energy policy is health policy. Rigorous analysis, using scientific evidence and tools such as health impact assessments, can help us identify the most health-protective energy policies.
Energy use is central to human activity. We need energy to prepare our food, warm our homes, power our travel, produce our goods, and for countless other purposes. “The history of human culture,” wrote one historian, “can be viewed as the progressive development of new energy sources and their associated conversion
737
technologies.” (Hall, Tharakan, Hallock, Cleveland, & Jefferson, 2003, p. 318). Early humans relied on their own muscles, and later on burning wood and other biomass, starting perhaps 300,000 years ago (Roebroeks & Villa 2011). Indeed, the control of wood fires for cooking is arguably the fundamental transformation that made humans distinct from other primates (Wrangham, 2010). Still later our ancestors learned to harness water and wind. Burning animal products, such as whale oil, was important for a time. Modern history brought the use of coal and, later, natural gas, oil, and nuclear power (Nye, 1998). Contemporary societies mirror that history. Depending upon the level of economic development in an area, today's energy sources range from human and animal exertion, to harvested or scavenged biomass (wood, dung, peat), to more processed biofuels (charcoal), to commercial fossil fuels and electricity.
Energy use is correlated with population growth (Fröling, 2011) and economic output (Cleveland, Costanza, Hall, & Kaufmann, 1984; Hall et al., 2003). As shown in Table 14.1, energy use varies dramatically across countries. Not only the amount of energy used but also the quality of that energy drive economic productivity, with more efficient and flexible energy sources (liquid fuels and especially electricity) associated with higher productivity (Schurr, 1984; Toman & Jemelkova, 2003). This notion is reflected in the concept of the fuel ladder (or energy ladder) (Figure 14.1)—the idea that increasing development and wealth are marked by the use of progressively cleaner fuels, processed farther from the point of use (Grübler, 2004; Hosier, 2004). Of course, energy availability is not the only driver of development; education and labor markets, women's rights, financial institutions, physical infrastructure, and other factors play central roles as well.
Table 14.1 Energy Use in Selected Countries, 2005–2009
Country Per capita energy use, 2005–2009 (kg of oil equivalent per year)
Bangladesh 205 Haiti 320 Ethiopia 381 Philippines 426
738
India 614 Vietnam 697 Nigeria 721 Indonesia 857 Brazil 1371 Argentina 1,967 China 2,029 South Africa 2,742 United Kingdom 2,973 Germany 3,811 France 3,870 Australia 5,501 United States 7,029 Canada 7,333 Kuwait 10,408 Qatar 17,419
Source: Data from World Bank, 2015.
739
Figure 14.1 The Fuel Ladder With greater prosperity and technological development comes a shift toward cleaner, more efficient, and more convenient energy sources, with the energy generated farther from the point of use.
As with economic development, greater energy use is also associated with better health, at least up to a point (Figure 14.2). Metrics such as infant mortality and life expectancy improve up to levels of about 2,000 to 3,000 kg of oil equivalent per person per year, but beyond that point, rising energy use is not associated with further health improvement (Wilkinson et al., 2007; Gohlke et al., 2011). Energy availability is also associated with health at the household level, as captured in the terms energy security and energy poverty. Energy security, at the household level, refers to a family's probability of having enough energy to cook food, heat the home during cold weather, and cool the home during warm weather—a matter of energy availability, affordability, and capacity (Pachauri & Spreng, 2011). Energy poverty (or fuel poverty), conversely, refers to financial hardship that makes it difficult to afford energy for these basic uses (Boardman, 1991, 2010). Energy poverty is associated
740
with many of the afflictions of poverty, including poor health and social outcomes (Cook et al., 2008; Howden-Chapman et al., 2011).
Figure 14.2 Association Between Energy Use and Health, by Nation
Source: Wilkinson, Smith, Beevers, Tonne, & Oreszczyn, 2007.
The measures of health are infant mortality (upper panel) and life expectancy (lower panel). Each circle represents a country, with the size proportional to the country's population.
741
While supporting health in many ways, all forms of energy also have negative consequences. From early times, technical advances in harnessing energy, from fire (that burned people) to steam engines (that exploded), made clear that intense exposure to energy could be injurious (Schivelbusch, 1986, p. 131). The well-known Haddon injury matrix (Chapter 23) exemplifies this concept, classifying the kinetic energy of a moving automobile (derived from fossil fuel combustion) as the vector of injury (Haddon, 1980).
But energy does not harm people only through sudden injuries. Throughout the energy life cycle, from initial fuel collection to energy production to disposal of waste products, adverse consequences may arise—emphasizing the importance of life cycle analysis. Figure 14.3 shows pathways linking energy and health. It distinguishes primary energy sources—and the fuel cycles through which they are gathered and used to generate energy—from secondary energy forms, such as electricity, that are essentially energy “carriers.” It also shows how the energy provides “services,” such as transportation—the end uses. Each stage has associated adverse health impacts. Energy is a health issue.
742
Figure 14.3 Pathways Linking Energy and Health Source: Wilkinson et al., 2007.
This chapter describes the public health consequences of major forms of energy. For perspective, Figure 14.4 depicts world energy consumption in recent years. The largest sources of energy are the fossil fuels—petroleum, coal, and natural gas—so named because they were formed over millions of years from organic matter such as plants (and therefore represent stored solar energy). Biomass, such as peat and wood, represents a quantitatively smaller source of energy, but serves the needs of much of the world's population. Electricity does not appear in Figure 14.4 because it is a secondary energy source, formed from combustion of fossil fuels, from nuclear reactions, and from falling water (in hydroelectric plants). Figure 14.4 also shows the ongoing rise in global energy use, a reminder that energy is not only a health concern, it is a growing health concern.
743
Figure 14.4 World Energy Consumption ***Includes geothermal, solar, wind, etc.
**In these graphs, peat and shale oil are aggregated with coal.
*World includes international aviation and international marine bunkers.
Note: Mtoe = million tons of oil equivalent.
Source: International Energy Agency, 2014, p. 6.
One of the principal health effects of energy use is mediated by
744
climate change, a result, in large part, of burning fossil fuels. Climate change is explored in detail in Chapter 12. In this chapter, we focus on the other ways in which energy use affects health.
745
Household Energy Patterns of Household Fuel Use The Global Energy Assessment estimates that in 2005 about 2.8 billion people, mostly in the poorest countries, relied on solid fuels such as biomass (wood, agricultural residues, and animal dung), charcoal, and coal for cooking and other household energy needs (Smith et al., 2012). India and China together account for about half the global population that uses solid fuels for cooking (27% and 25%, respectively); sub-Saharan Africa also accounts for a significant share (United Nations Development Programme, 2009). Wood is the predominant solid fuel used. Household fuel patterns vary across countries: for example, charcoal in sub-Saharan Africa, coal in China, dung in India, kerosene in Djibouti, and electricity in South Africa (Smith et al., 2012). Within a country, both household poverty and rural location predict the use of solid fuels. Rising income, however, does not assure a smooth transition to cleaner fuels; availability, pricing policies, education, and cultural preferences play a role (Masera, Saatkamp, & Kammen, 2000). In the United States, over 2.5 million households, many in areas of rural poverty, rely on solid fuel for home heating, with potential exposures to high levels of indoor air pollutants (Rogalsky, Mendola, Metts, & Martin, 2014).
Exposure to Household Fuel Combustion Products Poor households often burn fuel in inefficient, poorly vented combustion devices, resulting in considerable waste of fuel energy, and emission of toxic products of incomplete combustion (Figure 14.5). The use of traditional stoves in small, poorly ventilated kitchens, in close daily proximity to household members, leads to significant exposures, particularly to women and children, who spend the most time in or near the kitchen. Very young children are at special risk, as they are highly exposed during vulnerable developmental periods (see Chapter 11).
746
Figure 14.5 Indoor Air Pollution from Traditional Cooking Source: Kang, 2011.
Cooking arrangements like the one pictured here (in Guatemala) result in prolonged, high-level exposure to particulate matter, carbon monoxide, and other pollutants, especially for women and children.
The concentrations and composition of the various pollutants generated by solid fuel combustion depend on a number of factors, including fuel type and moisture content, household layout and kitchen location, stove technology, and behaviors (such as where children play) (Jetter et al., 2012; Smith et al., 2012). Scientists have studied a range of pollutants in households that burn solid fuels, especially particulate matter (PM). The highest PM levels are found in homes burning dung, followed by charcoal and wood; PM levels in households using kerosene, other liquid fuels, gas, and/or electricity are roughly an order of magnitude lower (Smith et al., 2012).
In addition to PM, products of incomplete combustion include gases such as carbon monoxide, oxides of nitrogen, phenols, quinones or semiquinones, chlorinated acids such as methylene chloride, and
747
dioxins. A typical solid fuel stove converts 6% to 20% of its fuel into toxic substances. At least twenty-eight pollutants present in solid fuel smoke have been shown to be toxic in animal studies, including some fourteen carcinogens and four cancer-promoters (Naeher et al., 2007). The International Agency for Research on Cancer (IARC) classifies emissions from household coal combustion as “carcinogenic to humans” (i.e., a Group 1 carcinogen), and emissions from household combustion of biomass fuel (mainly wood) as “probably carcinogenic to humans” (i.e., a Group 2A carcinogen) (IARC, 2010).
Health Effects of Household Fuel Combustion Household use of solid fuel increases the risk of pneumonia (especially in children), chronic obstructive pulmonary disease (COPD), and lung cancer, and likely the risk of ischemic heart disease, cerebrovascular disease, cataracts, and tuberculosis as well. Globally, the impact is high. In the 2010 Global Burden of Disease study, household air pollution from solid fuels accounted for 3.5 million deaths per year and 4.3% of global DALYs, behind only high blood pressure and tobacco smoking as risk factors (Lim et al., 2012). This burden is disproportionately felt in poor nations. The International Energy Agency (IEA) projects that by 2030, premature deaths from indoor use of biomass will exceed those due to HIV/AIDS (IEA, 2010).
Interventions to Protect Health Household energy interventions to date have largely centered on improving fuel efficiency, through improved fuels and/or improved stoves (Smith et al., 2012). The ideal improved biomass stove would be energy efficient, effective at reducing pollutant emissions, locally produced, inexpensive, easily maintained, and well accepted by households. However, technical and social barriers have made it difficult to achieve all these goals. Current innovations aim both for cleaner burning stoves, and for behavioral innovations such as social marketing and market-based incentives (Ruiz-Mercado, Masera, Zamora, & Smith, 2011; Lewis & Pattanayak, 2012). When families use improved stoves, substantial health gains, such as reduced child pneumonia, follow (Smith et al., 2011). Replacing solid fuels altogether, with cleaner fuels such as gas or electricity, is
748
also a highly promising approach and part of broader development strategies.
749
Fossil Fuels Fossil fuels were formed over millions of years. Organic material that was deposited on the Earth's surface was buried, subjected to pressure and temperature in the Earth's crust, and converted into energy-dense forms. Fossil fuels derive their energy from the chemical bonds created during photosynthesis. Depending on where the organic matter was deposited and the geological forces that operated, it became coal, oil, natural gas, or one of a variety of other less common materials. Fossil fuels now comprise over 80% of the world's energy supply (Figure 14.1), with oil and coal being the two leading sources, followed by natural gas.
The health impacts of fossil fuels occur across those fuels' life cycle, from mining or extraction to transport to combustion to waste management. Impacts manifest on spatial scales from local to global, both nearby and remotely, and both promptly and after substantial delay.
All fossil fuels contribute to global climate change, as their combustion releases greenhouse gases, principally carbon dioxide, methane, and oxides of nitrogen. The health impacts of climate change are explored in Chapter 12.
Coal Coal is a combustible, sedimentary rock composed of the fossilized remains of prehistoric vegetable matter preserved from biodegradation by water and mud. Peat is its precursor. It is composed primarily of carbon and hydrogen but may include small amounts of other elements, such as sulfur and mercury (which may have important consequences when the coal is burned).
Coal is a major energy source, constituting approximately 25% of energy consumption and 40% of electricity generation worldwide (IEA, 2014). (In the United States the use of coal has declined, beginning in about 2010, as increasingly available natural gas has displaced it.) Coal accounts for roughly 40% of CO2 emissions and is therefore a major contributor to climate change—one of the principal health impacts of any energy source.
750
Coal is produced through surface or underground mining—both dangerous operations for workers. Injuries occur as a result of falling rocks, falls into mine shafts, machinery, gas inhalation, explosions, floods, and cave-ins. Respiratory hazards arise from silica dust and coal dust, placing miners at risk of silicosis and coal workers' pneumoconiosis (Laney & Weissman, 2014), also known as black lung disease, as well as lung cancer (Graber, Stayner, Cohen, Conroy, & Attfield, 2014). Since 1900, in the United States alone, over 100,000 coal miners have been killed at work, and over 200,000 have succumbed to coal workers' pneumoconiosis (Epstein et al., 2011). Other occupational hazards include heat and noise.
Many modern coal mines involve mountaintop removal and strip mining, processes that result in ecological damage, stress nearby communities, increase the risk of mudslides, and contaminate water sources with waste emissions (National Research Council [NRC], Committee on Coal Waste Impoundments, Committee on Earth Resources, 2002; Palmer et al., 2010; Holtzman, 2011). Appalachian counties near such coal mining operations depend on the employment they generate, but suffer from widespread poverty and elevated rates of cancer and cardiovascular, pulmonary, and kidney diseases (Hendryx & Ahern, 2008; Hendryx, 2010; Ahern & Hendryx, 2012).
After being mined, coal is processed and transported to power stations, factories, and other points of use. About 70% of coal is transported by train, representing about 44% of U.S. train freight tonnage (Association of American Railroads, 2011). Consequences of this freight traffic include noise and dust exposure and also injuries and fatalities from crashes and other incidents (averaging 762 fatalities each year from 2006 to 2014) (Federal Railroad Administration, 2015). Processing results in occupational hazards that include dust exposure (in such operations as forming briquettes for residential use), noise, ergonomic hazards, and exposure to carcinogens (in converting coal to derivative fuels such as coke or coal gas). Coal gasification was widely used to produce fuel gas from coal during the nineteenth and early twentieth centuries; while no longer common, it left a legacy of over 50,000 manufactured gas plants across the United States. These sites are commonly contaminated with aromatic organic compounds, metals, and other toxics, posing community health risks and high cleanup costs
751
(Hatheway, 2012).
Combustion is the stage of the coal life cycle with the heaviest health burden (Gaffney & Marley, 2009). Primary products of coal combustion include carbon dioxide, carbon monoxide, oxides of sulfur, oxides of nitrogen, a range of solid and vapor-phase organic compounds, particulate matter, mercury, and other metals. Secondary pollutants—those formed in the air from precursors emitted from smokestacks—include ozone, some components of PM (sulfates, nitrates, elemental carbon), and organic vapors. These exert their effects downwind from where the precursors are emitted, sometimes hundreds of miles away, as they form in moving air masses.
Carbon dioxide is the most significant pollutant in the context of climate change; its health impacts are discussed in Chapter 12. The remaining pollutants exert health effects directly. Landmark episodes—in Belgium's Meuse River Valley in 1930, Donora, Pennsylvania, in 1948, and London in 1952—resulted from intensive coal combustion, with human exposure enhanced by local geography and weather. These episodes highlighted the acute fatal potential of coal combustion. Less dramatic effects, and less acute effects, have been intensively studied in recent years and are in many cases relatively well characterized (Brook et al., 2010; Künzli, Perez, & Rapp, 2010) (also see Chapter 13). Both particulate matter (PM) and ozone derive from coal combustion (although other sources, such as motor vehicles, are important as well). So does mercury; in fact coal combustion is the largest source of anthropogenic mercury emissions globally, accounting for about half of such emissions (with artisanal and small-scale gold mining the next largest source) (Rafaj, Bertok, Cofala, & Schöpp, 2013). Dublin, Ireland, eliminated coal combustion in 1990, providing a dramatic example of public health impact (Text Box 14.1).
752
Text Box 14.1 Health Impacts of the Dublin Coal Ban In 1990, Dublin banned the sale of bituminous coal, which had long been a primary source of energy for household heating. Alert investigators in Dublin recognized a natural experiment on the health effects of coal combustion. To study this association, they compared measures of air pollution and several health outcomes for six years before and after the ban. Adjusting their time series data for weather, respiratory epidemics, and death rates in the rest of Ireland, they evaluated the effect of the ban on age-standardized death rates in Dublin. The results were dramatic. Pollution, as indicated by average black smoke concentrations, declined by 35.6 mg/m3 (a 70% reduction) after the ban, and nontrauma death rates decreased by 5.7% (95% CI 4–7, p <0.0001). Most of the prevented deaths would previously have been due to respiratory and cardiovascular causes; the city saw approximately 116 fewer respiratory deaths and 243 fewer cardiovascular deaths each year after the ban (reductions of 15.5% and 10.3% respectively), an even steeper drop than prior studies had projected (Clancy, Goodman, Sinclair, & Dockery, 2002). A later study looked at lung cancer mortality associated with the coal ban—a challenging study since smoking rates in Dublin were falling fast at the time of the ban. But after controlling for smoking, the reduced air pollution was found to account for a modest reduction of lung cancer deaths as well (Kabir, Bennett, & Clancy, 2007).
Coal combustion waste (CCW), the final step in the coal life cycle, has received less attention in the health literature, but huge spills in recent years—near Kingston, Tennessee, in 2008 and near Eden, North Carolina, in 2014—highlight the potential hazards. CCW, including fly ash from smokestacks and bottom ash and boiler slag from furnaces, represents the second largest solid waste stream in the United States after municipal solid waste—115 million tons in 2013, according to the American Coal Ash Association (2014), or
753
over 700 pounds per person (although these data are based on only 60% of coal burned, so the true figure is probably substantially higher). Coal ash contains toxic metals such as arsenic, lead, mercury, cadmium, and chromium, as well as radioactivity (Hvistendahl, 2007). The leading methods of managing CCW are surface impoundment, landfilling, and disposal in abandoned mines. The impoundments are large “lakes,” often behind dams, and many of them pose hazards in the event of dam failure (Manuel, 2009). About 43% of CCW finds industrial use (recycling) as structural fill and in manufacturing such products as cement, asphalt, wallboard, and bricks (Tenenbaum, 2009). Industrial use of CCW offers indirect health benefits, because it reduces the need to use energy (and contribute to climate change) in primary manufacturing, but there is potential human exposure from leaching of toxic components. This exposure pathway has not been well studied.
Studies of the health costs of coal-derived electricity in the United States have yielded estimates ranging from $62 billion to $523 billion annually, or from 3.2 cents to 28.9 cents per kilowatt-hour— at the upper extreme, several times the cost of electricity itself in the United States (National Research Council, Committee on Health, Environment, and Other External Costs and Benefits of Energy Production and Consumption, 2009; Levy et al., 2009; Epstein et al., 2011).
Petroleum Petroleum is a liquid mixture of aliphatic and aromatic hydrocarbons. When refined, petroleum yields a variety of products, from lubricants to plastics to asphalt, but the majority—in the range of 85%—becomes fuel. Petroleum accounts for about one third of primary energy consumption and more than 90% of transportation fuel—principally gasoline, diesel fuel, and jet fuel. When refined, as shown in Figure 14.6, a forty-two-gallon barrel of crude oil yields about nineteen gallons of gasoline, eleven gallons of diesel fuel and heating oil, four gallons of jet fuel, and smaller amounts of other products, such as liquefied petroleum gas and propane, some of which goes to heating and power generation. A small but important part of the petroleum produced serves as feedstock for petrochemicals.
754
Figure 14.6 Products Made from a 42-Gallon Barrel of Crude Oil (in gallons)
Source: Energy Information Administration [EIA], 2014.
The petroleum life cycle begins with exploration, drilling, and extraction. Workplace hazards at this stage include injury risk, ergonomic hazards, noise, vibration, and chemical exposures, and for offshore oil well workers, long-term shift work. Large-scale spills during extraction, such as the 2010 Deepwater Horizon spill (Solomon & Janssen, 2010; Diaz, 2011; Grattan et al., 2011), and during transport by pipeline or ship, such as the 1989 Exxon Valdez spill (Palinkas, Petterson, Russell, & Downs, 1993) and the 1998 pipeline leak and subsequent explosion in northern Nigeria (Aroh et al., 2010), can cause considerable ecological damage, as well as human health impacts ranging from acute injuries and fatalities to food contamination to mental health disorders (Aguilera, Méndez, Pásaro, & Laffon, 2010). In some places, such as Iraq, Colombia, and Nigeria, refineries and pipelines have been targets of intentional attacks, resulting in some of the same risks (Onuoha, 2008).
Petroleum refining (Figure 14.7) entails extensive potential exposure to chemicals, many of them carcinogenic, among both refinery workers and people living nearby. The petroleum industry conducted or funded a series of occupational epidemiological studies in the 1990s and 2000s, which revealed few consistent patterns of illness (Wong & Raabe, 2000; Tsai & Wendt, 2001; Satin, Bailey, Newton, Ross, & Wong, 2002; Tsai, Wendt, Cardarelli, & Fraser, 2003; Sorahan, 2007). Critics identified sources of
755
negative bias (Egilman, Scout, Kol, Hegg, & Bohme, 2007). Communities near refineries may also be exposed to a range of air toxics (Brody et al., 2009).
Figure 14.7 An Oil Refinery Source: Center for Land Use Interpretation, n.d.
Refineries are large industrial complexes. Petroleum arrives by ship or rail, and products from gasoline to diesel fuel to petrochemicals are manufactured. Some refineries are located near residential areas.
Advances in technology have permitted oil production from unconventional sources, principally oil sands and oil shale. These processes are more energy intensive than producing conventional petroleum, resulting in substantially higher greenhouse gas emissions (Cai et al., 2015; Nduagu & Gates, 2015), and can cause considerable local ecological disruption (Schindler, 2014). A review by the Royal Society of Canada, focusing on Alberta's extensive oil sands industry, found adverse health effects related to “boom town” social disruption, such as violence and substance abuse, but no increase in cancer or other chemical-related outcomes (Gosselin et al., 2010; Weinhold, 2011).
As with coal, combustion of petroleum products yields a range of air pollutants, including carbon dioxide, carbon monoxide, oxides of nitrogen, hydrocarbons, particulate matter, and metals, with secondary ozone formation also important. The health effects have
756
been best characterized with regard to transportation-related emissions (Health Effects Institute, 2010).
While petroleum is associated with health hazards, its use also confers many benefits—so much so that, ironically, a scarcity of petroleum may also threaten health and well-being. The concept of peak petroleum is explored in Text Box 14.2.
757
Text Box 14.2 Peak Petroleum and Public Health Petroleum is a pillar of the current world economy. It has a central role as a transportation fuel, and it is a key ingredient in a wide range of synthetic processes, such as the production of fertilizers, plastics, resins, textiles, pesticides, and pharmaceuticals. Approximately 85% of petroleum, by volume, is converted to fuel. Petroleum has important roles in public health and medicine both as a transportation fuel for patients, health workers, and supplies and as a synthetic precursor for a wide range of medical devices and pharmaceuticals.
The world's oil deposits are limited resources; they were formed over millennia and are not being replenished on any meaningful human time scale. Production must at some point be limited by resource depletion and fall short of demand. Peak petroleum is the point of maximum production, after which production inexorably falls.
M. King Hubbert, an American oil geologist, introduced the peak petroleum concept and term in the 1950s (Hubbert, 1956). He hypothesized that if the total quantity and production rates of a finite resource such as petroleum were known, then its production timeline, including peaking and declining, could be accurately predicted. Using formulas originally developed for bacterial colony growth, he accurately predicted that oil field production in the contiguous United States would peak in the early 1970s. His methods have since been used to predict the point of peak production in other oil fields around the globe, as well as the point of global peak production.
The idea of peak petroleum has been widely discussed since Hubbert's time (e.g., Campbell & Laherrèrre, 1998). Analyses are complicated by uncertainties in reserves estimates, differing reporting protocols, and incentives for oil- producing nations to skew estimates of total reserves
758
(Deffeyes, 2003). Hubbert projected the global peak would arrive between 1996 and 2006. With recent technical advances—principally horizontal drilling and hydraulic fracturing—and the exploitation of unconventional sources, the peak has been deferred.
Regardless of the precise date, global peak oil production will occur at some point, and the transition to a post-peak world is likely to be challenging. At present there is no transportation fuel that is as economical, portable, and energy-dense as petroleum, so demand will continue to rise as populations grow and become more prosperous. Prices for petroleum-based fuels and products made from oil precursors are likely to rise steadily in the long run, though the period of the peak may show significant price fluctuations as high prices reduce demand.
The effects of this transition on health care and public health will be felt in at least four areas: medical supplies and equipment, including pharmaceuticals; medical transport; food production; and energy generation (Frumkin, Hess, & Vindigni, 2009; Schwartz, Parker, Hess, & Frumkin, 2011). Indirect health effects could result from a persistent economic downturn, with associated social disruption, and possibly armed conflict (Klare, 2002, 2012).
The health sector has only just begun to confront this challenge. Important activities include scenario building and contingency planning, addressing the areas noted earlier that are most likely to be affected. Although public health functions and health services will face a considerable challenge, there will also likely be health benefits, such as improvements in cardiovascular health from reduced vehicular travel and increased walking and bicycling, increased efficiency, less consumption of meat (whose production is highly petroleum intensive), and localization (Frumkin et al., 2009). As with any public health preparedness activity, anticipation and planning will help in managing health impacts.
Gas
759
Natural gas has grown in importance in recent years as technical advances—precision drilling of deep wells and hydraulic fracturing —have boosted production, most notably in North America. Natural gas has been considered a promising bridge energy source because the combustion of methane, its main component, generates about half the carbon dioxide per unit of energy released as the combustion of coal, and fewer other air pollutants. However, methane is a powerful greenhouse gas, and even small amounts of leakage during natural gas production, transport, and use may undermine the climate change advantage of this energy source. Such issues have been the subject of life cycle analyses (Howarth, Santoro, & Ingraffea, 2011; Skone et al., 2014). A second health concern arises from hydraulic fracturing (fracking), which entails high-pressure injection of a mixture of water, sand, and chemicals into underground rock formations (and subsequent reinjection of waste chemicals from fracking operations). There is potential for contamination of water tables both by methane (Osborn, Vengosh, Warner, & Jackson, 2011) and by fracking chemicals, although data on the magnitude of this problem are scarce (Colborn, Kwiatkowski, Schultz, & Bachran, 2011; Finkel & Law, 2011; Mitka, 2012). Fracking also has the potential to induce earthquakes (NRC, 2012). Finally, contamination of air and soil near drilling sites may be associated with adverse health effects (Rabinowitz et al., 2014). As natural gas becomes an increasingly important energy source in the United States, research on its health consequences will need to continue (Penning, Breysse, Gray, Howarth, & Yan, 2014; Tuller, 2015).
760
Nuclear Energy Nuclear energy is an important and controversial source of electricity. Proponents note that it is carbon-free—that, compared to fossil fuels, it contributes little to climate change and could play a vital role in meeting the world's energy needs while battling climate change (e.g., Brook et al., 2014; Freed, 2014). Opponents cite potential dangers: radiation exposure during nuclear power plant operations, the challenges of storing nuclear waste, the potential for catastrophic accidents at nuclear power plants, and the potential for terrorists or others to weaponize nuclear fuel. All these considerations bear directly on human health.
Nuclear energy accounted for approximately 11% of global electricity production in 2012. Three countries draw over half their electricity from nuclear plants (France leads at 77%, followed by Slovakia at 57% and Hungary at 54%), and ten additional countries, all but one in Europe, draw over 25% from this source. In the United States, 19% of electricity comes from nuclear plants (Nuclear Energy Institute, 2011). Japan generated more than 30% of its electricity from nuclear until 2011, but the Fukushima disaster that year turned Japanese public opinion sharply against nuclear power, and the nation closed its nuclear plants. By late 2015, two had reopened. Time will tell to what extent Japan resumes using nuclear energy.
A full description of the nuclear fuel cycle is beyond the scope of this chapter. Each step in nuclear energy production, from uranium mining to radioactive waste disposal (with reprocessing sometimes included) leads to specific radioactive and chemical emissions and waste streams.
For nuclear workers the major occupational health concern is radiation-induced cancer (reviewed in Wakeford, 2009). Among uranium miners the risk probably stems from exposure to radon gas in underground mines; various studies have documented significant excesses in lung cancer among these workers (e.g., NRC, 1999). Uranium may also have endocrine-disrupting activity (Raymond- Whish et al., 2007). The largest available study of nuclear power workers (over 400,000 workers in fifteen countries, contributing
761
over 5 million person-years of observation) found increased risks of solid cancers and leukemia (Cardis, Vrijheid, & Gilbert, 2005), consistent with prior studies of low-dose radiation health effects (Chapter 22).
Uranium mining, the first step in the nuclear power life cycle, generates very large amounts of waste material (tailings and rock) and contaminated process water, which may contain low-level radioactivity, metals, and acids. These can cause considerable ecological damage, and may contaminate drinking water and food chains in nearby communities.
During normal operation, nuclear reactors routinely release radioactive gases to the atmosphere and radioactive liquids to the sea or rivers. In addition, when reactors are depressurized for refueling, larger gaseous emissions occur over short time periods. The main radioactive releases are tritium (half-life about 12 years), carbon-14 (5,700 years), krypton-85 (11 years), argon-41 (1.8 hours), and a number of iodine isotopes (including iodine-129, with a half-life of 16 million years). Reprocessing plants, which are found mostly in France and the United Kingdom, release radioactive substances at higher rates than do power plants.
The health consequences among populations living downwind of nuclear power plants remain controversial. In the 1990s, several studies found increased incidences of childhood leukemia near UK nuclear facilities. However, official estimated doses from released nuclides were too low, by two to three orders of magnitude, to explain the increased leukemia. Recent epidemiological studies have reopened the debate, suggesting childhood leukemia excesses in association with living near nuclear plants (Baker & Hoel, 2007; Hoffmann, Terschueren, & Richardson, 2007; Kaatsch, et al., 2008; Spix, et al., 2008). One hypothesis (Fairlie, 2009) proposes that infant leukemia is mainly a teratogenic effect of in utero radiation exposures, due to maternal radionuclide intake during pregnancy. Research is ongoing on this important question (National Research Council, Committee on the Analysis of Cancer Risks in Populations Near Nuclear Facilities, 2012).
After use in a nuclear reactor, “spent” fuel comprises high-level radioactive waste. Fission of uranium atoms yields radioactive isotopes such as cesium-137 and strontium-90, which account for
762
most of the heat and radiation in high-level waste. Another by- product is transuranic elements—heavier elements such as plutonium that have assimilated neutrons from fissioning uranium atoms. These produce less heat and radiation than fission products, but they persist for far longer (plutonium-239 has a half-life of 24,000 years, compared to about 30 years for strontium-90 and cesium-137), therefore accounting for most of the long-term radioactive hazard in high-level waste.
The health risk of high-level waste relates to its high radiation levels. There is at present no strategy or facility for long-term disposal or storage of high-level radioactive waste; this unresolved problem represents an ongoing threat to health and the environment (Lee, Ojovan, & Jantzen, 2013).
Additional health risks relate to the possibility that fuel may be diverted to nuclear weapons production, by states and/or by non- state entities (Case, 2011). The magnitude of this risk is difficult to quantify.
In addition to the routine risks of nuclear power, accidents pose health risks (Christodouleas et al., 2011). Major accidents to date include those at Three Mile Island in 1979, Chernobyl in 1986, and Fukushima in 2011. Four types of radiation exposure may occur during and after a nuclear plant accident. First, plant workers or cleanup crews in close proximity to a radiation source may sustain total or partial body exposure. These doses may be quite high, to the point of acute fatality. Second, external contamination may occur when fission products settle on people's skin. Third, internal contamination may occur when people ingest or inhale fission products such as radioactive iodine and cesium isotopes—the mechanism of widespread population exposure. Iodine-131 tends to settle to the ground, enter the food chain, and accumulate in the thyroid, where it releases beta radiation. Finally, large quantities of radioactive water were released into the ocean at Fukushima, and impacts on the marine food chain have not been fully characterized.
The short-term death toll of nuclear accidents related to radiation exposure has been low: twenty-eight at Chernobyl, and none at Three Mile Island or Fukushima (United Nations Scientific Committee on the Effects of Atomic Radiation, 2012). Physical trauma, heat stress, and related causes accounted for some acute
763
fatalities among workers and community residents; while precise counts are unavailable, these probably numbered in the dozens following Chernobyl and Fukushima (Tanigawa, Hosoi, Hirohashi, Iwasaki, & Kamiya, 2012). Following Chernobyl there were 134 confirmed cases of acute radiation illness (International Atomic Energy Agency [IAEA], 2002) among emergency workers.
Long-term outcomes have been studied after the Chernobyl and Three Mile Island accidents. With respect to cancer, the Three Mile Island accident was followed by approximately a doubling of leukemia risk among men in the highest radiation exposure category, but not women, in nearby counties, representing an excess of five cases during thirteen years of follow-up (Talbott, Youk, McHugh-Pemu, & Zborowski, 2003; Han, Youk, Sasser, & Talbott, 2011), and an equivocal increase in thyroid cancer (Levin, 2008; Goyal, Camacho, Mangano, & Goldenberg, 2012). Following the Chernobyl accident, populations in Ukraine, Belarus, and Russia showed a substantial increase in thyroid cancer incidence, especially among people exposed during childhood and adolescence (Shibata, Yamashita, Masyakin, Panasyuk, & Nagataki, 2001; Shakhtarin et al., 2003; Ron, 2007; Hatch et al., 2009; Cardis & Hatch, 2011), with very low mortality from this cause. There was roughly a doubling of leukemia incidence in the most heavily exposed emergency and recovery operations workers (“liquidators”) during the first decade after the accident (Romanenko et al., 2008; Ivanov et al., 2012). No other consistent increases in cancer have been documented to date (Cardis et al., 2006; Balonov, 2007; Howe, 2007; Cardis & Hatch, 2011). The impacts of the Fukushima disaster on cancer incidence will become clear when sufficient time has elapsed.
Perhaps the larges noncancer impact of nuclear plant disasters relates to mental health. The Chernobyl accident resulted in the initial evacuation of about 116,000 people, and the later relocation of 220,000 people, from affected parts of Belarus, Russia, and Ukraine, with enormous social and economic consequences (IAEA, 2002). Substantial and persistent mental health burdens have been documented among cleanup workers, people who were relocated, and people who remained in contaminated areas (Bromet, Havenaar, & Guey, 2011; Bromet, 2012). Following the Three Mile Island disaster, similar mental health consequences were
764
documented (Dew & Bromet, 1993). Other noncancer effects following Chernobyl included increases in cataracts (Worgul et al., 2007) and possibly in cardiovascular disease (Ivanov, 2007) among emergency and recovery workers, and possibly an excess in congenital abnormalities in populations in nearby areas (Nussbaum, 2007; Wertelecki, 2010).
Nuclear energy arouses considerable public and policy concern. The main health effect of routine nuclear plant operation appears to be the increased incidence of childhood leukemia. The main burden of disease following nuclear accidents has been thyroid cancer and mental illness in exposed populations, with additional impacts on cleanup workers. Further concerns include the environmental effects of uranium mining and milling, the management of nuclear waste, and the potential for weaponization, which are often excluded from assessments of nuclear power. It is difficult to weigh the health consequences of nuclear power against those of fossil fuels, since one aspect of nuclear power is the possibility of low- probability, high-consequence events. However, to date, the health impacts of biomass and of fossil fuels have substantially exceeded the health impacts of nuclear power (Kharecha & Hansen, 2013).
765
Renewable Sources of Energy Renewable energy sources offer several potential advantages. First, finite resources are not irreversibly depleted when they are used. Second, they may have a smaller carbon footprint than fossil fuels, implying less contribution to climate change. Third, they may pollute less than fossil fuels. Fourth, they may provide social and economic benefits and promote equity. Each of these potential benefits corresponds to health benefits. However, whether the benefits are realized depends heavily upon how the energy is produced. Moreover, no energy source is free of health and environmental impacts. Issues of land use, maintenance, materials inputs, and energy storage raise concerns about environmental, occupational, and community health impacts.
Solar Three technologies are used to generate electricity from solar radiation: photovoltaic (PV) cells, which generate electricity directly; concentrating solar power thermal systems, which use a liquid to transfer absorbed heat to a steam generator that drives a turbine; and solar towers, which are effectively chimneys where rising hot air powers turbine generators. Solar energy has been deployed in both small-scale (mainly rooftop) applications and in large-scale electricity production.
The major health concern from solar power relates to the life cycle of photovoltaic cells. These are typically made with crystalline silicon; depending on the technology used, other compounds used may include copper indium diselenide (CIS), copper indium gallium diselenide (CGS), gallium arsenide (GaAs), and cadmium telluride (CdTe). Silica mining is associated with risk of silicosis, a pneumoconiosis (Leung, Yu, & Chen, 2012). PV manufacturing, like semiconductor manufacturing, may entail exposure to toxic metals (cadmium, arsenic, chromium, and lead) and gases (arsine, phosphine, and silane) (Fthenakis, 2003; Fthenakis, Kim, & Alsema, 2008; Taylor, 2010). Little information is available on workplace exposures; available data suggest that environmental emissions are generally low (Fthenakis et al., 2008), although waste management and end-of-life product disposal remain challenges
766
(Silicon Valley Toxics Coalition, 2009). Overall, solar power is likely to be far less hazardous than any of the fossil fuels or household energy approaches discussed earlier.
Biofuels Biofuels are fuels derived from recently formed biomass (as opposed to the ancient biomass that makes up fossil fuels). Ethanol and biodiesel, the two principal modern biofuels, are used mainly as liquid transportation fuels. Ethanol is made from food crops such as corn, sorghum, barley, sugar beets, and sugarcane or from cellulosic plant matter such as trees, grasses, and crop waste; it is blended with petroleum-based gasoline. Biodiesel is made from vegetable or animal fats; it is used either in pure form or as a blend with conventional diesel fuel. First-generation biofuels, such as corn ethanol, are made by fermenting sugars from high-sugar or high- starch plants such as corn. Second-generation biofuels come from plants that are not otherwise used as foods or grown on productive cropland, and even from such sources as algae, and use advanced production processes; the goals are to avoid competing with food production, to reduce fossil fuel and water use, and to protect water quality and wildlife habitat.
Global biofuel production grew from 16 billion liters in 2000 to more than 110 billion liters in 2013, reaching about 3.5% of the transportation fuel produced globally. Some countries rely heavily on biofuels; for example, 25% of Brazil's transportation fuel is biofuel (IEA, 2011). In the United States, ethanol replaced about 10% of gasoline use in 2014, a doubling in less than a decade (EIA, 2015). Subsidies and other policy incentives have supported the growth of the biofuel industry.
A principal potential health benefit of biofuels is the reduction of greenhouse gas emissions relative to fossil fuel use (Hill, Nelson, Tilman, Polasky, & Tiffany, 2006; Field, Campbell, & Lobell, 2007). However, life cycle analyses that account for fossil fuel inputs, land- use changes, and other factors, suggest that biofuels are not always advantageous in climate terms (Searchinger et al., 2008; Earley & McKeown, 2009; Sheehan, 2009). For example, corn-derived ethanol has a low net energy balance because much energy is required to produce corn and convert it into ethanol (Hill et al., 2006). An analysis in Brazil, where biofuel production is divided
767
between sugar cane ethanol and soybean biodiesel, concluded that land-use changes from growing these crops could fully offset the carbon savings (Lapola et al., 2010). Second-generation biofuels may optimize the climate equation (Eisentraut, 2010).
A second potential health benefit of biofuels is reduced air pollution. Biodiesel vehicles, in particular, have substantially lower emissions of particulate matter, carbon monoxide, volatile organic compounds, and oxides of sulfur compared to conventional diesel vehicles (Morris et al., 2003). A third potential health benefit flows from the potential for economic development, especially in rural areas (Leistritz & Hodur, 2008; Eisentraut, 2010), if market arrangements allow farmers to profit from growing and selling these crops (Vanwey, 2009).
However, biofuels may incur health and environmental costs. One issue is the diversion of farmland to grow biofuel feedstock instead of food, the so-called food versus fuel dilemma. By 2012, roughly 40% of U.S. corn production was directed to ethanol production. Rising food prices may result, threatening the nutritional status of at-risk populations (Runge & Senauer, 2007), a problem that hits developing nations especially hard (Rosenthal, 2013). However, food prices are determined by a complex web of causal factors, and debate remains about the role of biofuels (Congressional Budget Office, 2009; Babcock, 2011; Mueller, Anderson, & Wallington, 2011). In addition, biofuel production may lead to intensified agriculture, contributing to many of the problems described in Chapter 19—freshwater depletion; water pollution; loss of forest, wildlife habitat, and ecosystem services (Fargione, Hill, Tilman, Polasky, & Hawthorne, 2008; Demirbas, 2009; Scovronick & Wilkinson, 2014); and even antibiotic resistance (Olmstead, 2009). Occupational health threats in the biofuel industry have not been well studied, but there is evidence from a Danish study of elevated worker exposure to dust, endotoxin, fungi, and aspergillus (Schlünssen, Madsen, Skov, & Sigsgaard, 2011). Optimizing biofuel use, including health benefits, will require careful life cycle analyses, development of efficient crops and production technologies, use of crop waste and of marginal rather than productive agricultural land to the extent possible, more attention to health impacts (Ridley et al., 2012), and policies that advance these goals (Childs & Bradley, 2007; Robertson et al., 2008).
768
Hydroelectric Hydroelectric power is produced when falling or flowing water strikes the blades of turbines that in turn generate electricity. Dams may be as large as China's Three Gorges Dam, which generates approximately 20,000 megawatts, or as small as microprojects that generate up to 100 kilowatts—enough to power individual homes or farms or even small villages. Larger hydroelectric plants typically feature dams that form reservoirs. In addition to electric power generation, dams often serve other purposes, including flood control; water storage for domestic, industrial, and agricultural use during droughts, and irrigation; and the provision of recreational opportunities. Hydroelectric power represents about 16% of the world's electricity supply, and about one in four of the world's 36,000 registered dams is used for hydropower generation (International Commission on Large Dams, n.d.).
Hydroelectric generation is widely considered a clean source of energy because it does not involve combustion (Kosnik, 2008). However, dams may disrupt river ecosystems considerably, changing water flow and temperature, and causing sedimentation, reduced water quality, loss of wetlands, disruption of fish migration, and even species extinction (Rosenberg, McCully, & Pringle, 2000). Large hydroelectric facilities, especially in warm climates, may also contribute to greenhouse gas emissions (Gunkel, 2009; Electric Power Research Institute, 2010) due to release of carbon during initial flooding of reservoirs and to ongoing formation of methane from deep anaerobic decomposition.
There are three potential health hazards related to hydropower: population displacement, infectious disease risk, and disaster risk. First, large dam construction has in some cases displaced substantial numbers of people who had been living in areas flooded to form reservoirs (World Commission on Dams, 2000), with profound social and health consequences (Scudder, 2006; McDonald-Wilmsen & Webber, 2010). Construction of China's Three Gorges Dam, for example, completely or partially flooded 13 cities and towns, 365 townships, and 1,711 villages; inundated about 26,000 hectares of farmland; and displaced at least 1.3 million people, resulting in unemployment, dismantling of social support networks, homelessness, depression, and poor self-rated health
769
(Hwang, Cao, & Xi, 2011; Xi & Hwang, 2011). Second, hydroelectric projects, by altering local hydrology and expanding the habitat of infectious organisms and/or vectors, can increase the risk of certain infectious diseases (Jobin, 1999). Schistosomiasis exemplifies this problem, as dam construction can expand the snail vector's habitat (in the aquatic weeds that flourish in reservoirs), prolong the breeding periods (functionally eliminating the dry season that would otherwise reduce snail populations), and prolong human contact with wet environments and therefore with snails (Steinmann, Keiser, Bos, Tanner, & Utzinger, 2006). Some hydroelectric projects appear to have increased malaria risk, although this is a less consistent finding (Keiser et al., 2005). Third, dam failures may occur because of poor construction, military or terrorist attack, earthquakes, or other causes, with catastrophic consequences for downstream communities. For example, in 1975, torrential rainfall during a typhoon caused the failure of the Banqiao Dam on the Ru River in Henan Province, China, together with nearby smaller dams; an estimated 171,000 people were killed and 11 million lost their homes.
Policy on dams needs to balance the considerable health benefits of available energy with both local adverse health and social impacts and remote impacts related to climate change contributions. Health impacts can be mitigated through equitable resettlement policies (World Bank, 2004), infectious disease control programs (Zhu, Xiang, Wu, & Zhou, 2008), and perhaps capturing methane generated in reservoirs and using it as an energy source (Lima, Ramos, Bambace, & Rosa, 2008).
Wind Wind power provides a small but growing segment of electrical energy, reaching 4.4% in the United States by 2015 (10% in the state of Texas), and 3.1% globally (with several countries, including Denmark, Nicaragua, Portugal, and Spain generating more than 20% of their electricity from wind) (REN21, 2015). Wind has the potential to supply a significant portion of the world's energy needs (Zhou, Luckow, Smith, & Clarke, 2012). Wind energy offers promising health benefits: the absence of greenhouse gases and other pollutant emissions during operation (although there are emissions associated with manufacturing the equipment) and the
770
absence of a waste stream. Health concerns center around the swishing, whistling, or throbbing noise that results from the motion of gear trains and turbine blades (Harrison, 2011). People living near wind turbines, especially those who can see the turbines and/or dislike them, have reported annoyance, sleep disturbance, and reduced quality of life (e.g., Shepherd, McBride, Welch, Dirks, & Hill, 2011). Protective strategies involve noise reduction and increased distance between wind turbines and people. Overall, the population health impacts appear to be far lower than for equivalent energy generation by fossil fuel combustion (Colby et al., 2009; Knopper & Ollson, 2011). (Figure 14.8 illustrates three types of renewable energy.)
771
772
Figure 14.8 Renewable Energy Sources: Pure Energies, n.d.; Xiabo Chan/Alamy; The Fiber School, 2015.
Solar panels on a home, China's Three Gorges dam, and wind turbines on a wind farm, all generate renewable energy.
773
Energy Conservation and Efficiency Energy conservation and energy efficiency are closely related. Energy conservation refers to reducing the use of energy (say, by reducing demand), while energy efficiency refers to getting more service from each unit of energy used. Both strategies reduce the amount of energy that needs to be produced and distributed. To the extent that energy production has adverse health effects, reducing energy use may reduce those health effects. For instance, reducing production by coal-fired power plants, all things being equal, should decrease the risks associated with the coal fuel cycle, such as black lung disease, particulate air pollution, and contributions to climate change. Conservation and efficiency are potentially the most efficient, economical, healthful, and environmentally friendly approaches to energy. The health benefits of conservation and efficiency are explored in Text Box 14.3.
Two major caveats apply. First, about 2.4 billion people lack access to clean fuels for cooking and heating, and about 1.6 billion people lack access to electricity (Smith et al., 2012). Most of these people are in low-income countries, but some are poor people in wealthy countries. For these people, adequate access to energy is a more pressing health need than energy conservation. Second, energy efficiency may have paradoxical effects, such as increasing overall consumer demand for energy (Smil, 2005) and/or reducing healthy physical activity. Energy conservation may have complex effects and requires thorough analysis.
774
Text Box 14.3 Health Co-Benefits of Energy Conservation and Efficiency Energy efficiency and conservation are pillars of climate change mitigation, so public health thinkers about climate change have worked to document the health co-benefits of these strategies (Haines et al., 2007). Opportunities lie in energy policy, transportation policy, food and agriculture policy, and building design.
A broad energy policy approach is to reduce the carbon intensity of economic activity. A specific example is increasing the efficiency of coal plants. More efficient plants offer direct benefits in energy efficiency; they also offer health co-benefits such as cleaner air, leading to reduced cardiovascular and pulmonary disease, as discussed in Chapter 13 (Smith & Haigler, 2008; West et al., 2013).
Transportation policy approaches include both more efficient vehicles and reduced vehicle use. Efficient vehicles, in turn, deliver both greater fuel efficiency (meaning less fuel burned) and lower emissions from tailpipes, with health benefits that include reduced cardiovascular and pulmonary disease, fewer motor vehicle crashes, and more physical activity. For example, according to one analysis, implementing California's Advanced Clean Car Program, with standards that include both energy efficiency and emissions reductions, would avoid 400 to 420 deaths, 390 to 405 heart attacks, 8,075 to 8,440 exacerbations of asthma and lower respiratory symptoms, and $7.2 to 8.1 billion in health care costs each year in California (American Lung Association in California, 2011, 2012). When efficiency strategies include smaller vehicles, increased crash risk is a trade-off.
In addition to more efficient vehicles, energy conservation and efficiency in transportation entail reducing travel demand and shifting from motor vehicles to walking, cycling, and mass transit (see Chapter 15; also see Woodcock, Banister, Edwards, Prentice, & Roberts, 2007; Giles-Corti,
775
Foster, Shilton, & Falconer, 2010; Xia, Zhang, Crabb, & Shah, 2013), with concomitant redesign of the built environment (Younger, Morrow-Almeida, Vindigni, & Dannenberg, 2008; Hankey & Marshall, 2010). Conserving energy by reducing automobile travel (in effect substituting human exertion for vehicular engines as the energy source) has a range of health co-benefits related to improved air quality, increased physical activity, reduced car crashes, and reduced noise, as explored in Chapter 15.
With regard to food, energy conservation and efficiency are achieved at many stages, from agricultural practices to consumer choices of what to eat, as discussed in Chapter 19. Many of these strategies offer health co-benefits. For example, because food contains embedded energy, reducing food waste is a form of energy conservation—and by increasing the supply of available food, represents a strategy for feeding people who are food insecure. Similarly, because livestock production is energy intensive, diets that contain less meat are a form of energy conservation, and also a strategy for reducing cardiovascular disease and many cancers (Sabaté & Soret, 2014; Tilman & Clark, 2014).
Finally, energy-efficient buildings offer a promising approach as buildings account for a substantial proportion of energy use. As described in Chapter 20, design features of energy- efficient buildings include advanced heating and cooling systems; tight construction, including high-performing insulation, to reduce outside air exchanges and attendant energy loss; highly efficient appliances, lights, and other equipment; smart infrastructure that turns off lights, heat, and appliances when not in use; green roofs, shades, and other features to prevent overheating in hot weather; and other conservation and efficiency techniques. Care is needed to avoid potential health impacts that might result from reduced air exchange in buildings. Reduced use of energy in buildings offers “upstream” health benefits such as less coal combustion, and immediate benefits such as enhanced well- being and protection from winter cold. Wilkinson et al. (2009) calculated that energy-efficient homes in the United Kingdom would save 850 disability-adjusted life years
776
(DALYs), and reduce carbon emissions by 0.6 megatons per million people each year.
777
Summary Energy is essential to human welfare —a key underpinning of health, comfort, and well-being. In fact, providing energy to the billions who lack it is a pressing priority in global health. At the same time, however, energy systems contribute substantially to the global burden of disease. Much of this impact derives from the contributions of fossil fuels to climate change. In addition, according to the Global Energy Assessment (Smith et al., 2012), household air pollution from solid fuels was responsible for 2.2 million premature deaths in 2005 and generalized outdoor air pollution (in part from fossil fuel combustion) was responsible for about 2.7 million premature deaths in the same year. Including energy's indirect role in toxic chemical exposures, occupational risks, road traffic accidents, and physical inactivity would increase these values substantially. Such calculations have some uncertainties, but the direct effects alone rank energy systems above the global health impact of all other risk factors except malnutrition and unsafe sex and roughly equal to the global impacts of tobacco, alcohol, and high blood pressure based on WHO estimates for 2000. The vast part of the direct impact comes from the poor management of biomass and fossil fuel combustion, at both the household scale and the global scale. Clearly, energy is a health issue.
Other energy sources, such as nuclear power, carry some risk as well, although a quantitative comparison to the major energy risks is difficult because of the role of low-probability, high-consequence disasters in nuclear power settings. Health impacts from renewable energy sources are likely to be much smaller, but vigilance is needed to be sure these energy sources are managed carefully. Energy efficiency measures are generally desirable.
Energy exemplifies the challenging and fascinating trade-offs that arise in environmental public health. Tools such as life cycle analysis help us to fully understand the health, environmental, and economic costs and benefits across production, storage, transport, and end-use processes. This approach enables both full cost and full benefit accounting (National Research Council, Committee on Health, Environment, and Other External Costs and Benefits of
778
Energy Production and Consumption, 2009) and supports the healthiest energy decisions.
779
Key Terms biodiesel
A biofuel derived from vegetable oils or animal fats, intended to be used in place of conventional diesel fuel.
biofuels Fuels, such as biogas and biodiesel, derived from recently formed biomass—raw materials such as cellulose, animal fats, or algae.
biomass Organic materials, such as wood, peat, and dung, that may be used as fuel.
coal A fossil fuel—combustible sedimentary rock composed of the fossilized remains of prehistoric vegetable matter. Plentiful and commonly burned to generate electricity.
coal gasification The production of synthetic gas—a mixture of methane and other components—by heating coal under pressure in relatively anaerobic conditions.
energy In physics, the capacity to do work; more generally, the capacity to move objects, heat food or spaces, and perform other tasks necessary for health and well-being.
energy conservation In thermodynamics, the principle that the total energy of a closed system remains fixed. More generally, reducing the use of energy, say, by reducing demand or eliminating waste.
energy efficiency Getting more service from a given amount of energy.
energy poverty Financial hardship that prevents buying enough energy for basic uses (also known as fuel poverty).
energy security Having enough energy to cook food, heat the home during cold weather, and cool the home during warm weather—a matter of
780
availability, affordability, and capacity (in contrast to energy poverty).
fossil fuels Fuels formed over millions of years from organic matter such as plants (e.g., coal, petroleum, and natural gas).
fuel ladder The idea that increasing development and wealth are marked by the use of progressively cleaner fuels, processed farther from the point of use (also called an energy ladder).
hydroelectric power Electricity generated through the use of moving water (also called hydropower).
life cycle analysis An analysis that addresses all steps from initial fuel collection (say, coal mining) through transport, use (say, combustion in power plants), and waste disposal.
natural gas A fossil fuel occurring in underground deposits (often in association with petroleum), composed of hydrocarbons (mostly methane, with propane, butane, and others), and used as a fuel.
nuclear energy Energy released during controlled nuclear fission or fusion reactions, used to generate electricity (also called nuclear power).
peak petroleum The point of maximum production of petroleum, after which production will decline. Applied to the life cycle of an individual oil well, an entire oil field, or by extension, a nation's or the world's oil supply. More broadly, the concept that petroleum supplies are finite and petroleum will become an increasingly scarce resource.
petroleum A fossil fuel: a liquid mixture of hydrocarbons that can be extracted and refined into liquid fuels such as gasoline and diesel. The major source of transportation fuel.
power In physics, the rate of doing work or using energy; more generally, the resource in various forms (e.g., electricity,
781
gasoline) needed to do work. renewable energy sources
Sources of energy such as solar, hydropower, and biofuels that do not deplete a finite supply when used. Conversely, nonrenewable energy sources, such as coal and petroleum, are finite and are depleted when used.
solid fuels Fuels in solid form, such as coal, charcoal, wood, or dung, commonly used in households in poor countries.
782
Discussion Questions 1. Describe three ways in which energy use promotes health and
well-being.
2. List all the different types of energy you use over the course of a typical day. Create a table that lists each activity and describes the energy type and source, the alternatives available to you for each activity, where the energy is produced (at the point of consumption or more remotely), and the health effects of the energy source. Be sure to consider energy embedded in food as well.
3. Pick a technical innovation that reduces work and thus improves energy efficiency, such as a smaller, more fuel-efficient car or a well—insulated building with little air circulation. Write a paragraph that outlines the resulting co-benefits to energy and health and the potential trade-offs (such as the increased risk of injuries from driving a smaller car or increased exposure to respiratory pathogens in a building with little ventilation). How might a health impact assessment determine the ultimate value of the innovation?
4. Nuclear energy is essential in the fight against climate change. Please make a health-based argument for or against this position. Use evidence!
5. Conservation is not only the least expensive source of energy, it is the healthiest. Please make a health-based argument for or against this position. Use evidence!
783
References Aguilera, F., Méndez, J., Pásaro, E., & Laffon, B. (2010). Review on the effects of exposure to spilled oils on human health. Journal of Applied Toxicology, 30, 291–301.
Ahern, M., & Hendryx, M. (2012). Cancer mortality rates in Appalachian mountaintop coal mining areas. Journal of Environmental and Occupational Science, 1(2), 63–70.
American Coal Ash Association. (2014). 2013 Coal combustion product (CCP) production & use survey report. Retrieved from http://www.acaa- usa.org/Portals/9/Files/PDFs/2013ReportFINAL.pdf
American Lung Association in California. (2011). The Road to Clean Air study. Retrieved from www.lungusa.org/california-cleancars
American Lung Association in California. (2012). The Road to Clean Air II—a zero emission future: Public health and societal benefits, zero emission fleet in California. Retrieved from www.calcleancars.org/resources-studies.html
Aroh, K. N., Ubong, I. U., Eze, C. L., Harry, I. M., Umo-Otong, J. C., & Gobo, A. E. (2010). Oil spill incidents and pipeline vandalization in Nigeria: Impact on public health and negation to attainment of Millennium development goal: The Ishiagu example. Disaster Prevention and Management, 19, 70–87.
Association of American Railroads. (2011, July). Railroads and coal. Washington, DC: Author. Retrieved from http://www.aar.org/ ∼/media/aar/Background-Papers/Railroads-and-Coal.ashx
Babcock, B. A. (2011). The impact of US biofuel policies on agricultural price levels and volatility (International Centre for Trade and Sustainable Development Issue Paper No. 35). Geneva: ICTSD. Retrieved from http://ictsd.org/downloads/2011/12/the- impact-of-us-biofuel-policies-on-agricultural-price-levels-and- volatility.pdf
Baker, P. J., & Hoel, D. G. (2007). Meta-analysis of standardized
784
incidence and mortality rates of childhood leukaemia in proximity to nuclear facilities. European Journal of Cancer Care, 16(4), 355– 363.
Balonov, M. (2007). Third annual Warren K. Sinclair keynote address: Retrospective analysis of impacts of the Chernobyl accident. Health Physics, 93(5), 383–409.
Boardman, B. (1991). Fuel poverty: From cold homes to affordable warmth. London: Belhaven Press.
Boardman, B. (2010). Fixing fuel poverty: Challenges and solutions. London: Earthscan.
Brody, J. G., Morello-Frosch, R., Zota, A., Brown, P., Pérez, C., & Rudel, R. A. (2009). Linking exposure assessment science with policy objectives for environmental justice and breast cancer advocacy: The Northern California Household Exposure Study. American Journal of Public Health, 99(Suppl. 3), S600–609.
Bromet, E. J. (2012). Mental health consequences of the Chernobyl disaster. Journal of Radiological Protection, 32(1), N71–75.
Bromet, E. J., Havenaar, J. M., & Guey, L. T. (2011). A 25 year retrospective review of the psychological consequences of the Chernobyl accident. Clinical Oncology, 23(4), 297–305.
Brook, B. W., Alonso, A., Meneley, D. A., Misak, J., Blees, T., & van Erp, J. B. (2014). Why nuclear energy is sustainable and has to be part of the energy mix. Sustainable Materials and Technologies, 1– 2, 8–16.
Brook, R. D., Rajagopalan, S., Pope, C. A., 3rd, Brook, J. R., Bhatnagar, A., Diez-Roux, A. V.,…Kaufman, A. D. (2010). Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation, 121(21), 2331–2378.
Cai, H., Brandt, A. R., Yeh, S., Englander, J. G., Han, J., Elgowainy, A., & Wang, M. Q. (2015). Well-to-wheels greenhouse gas emissions of Canadian oil sands products: Implications for U.S. petroleum fuels. Environmental Science & Technology, 49(13), 8219–8227. doi:10.1021/acs.est.5b01255
785
Campbell, C. J., & Laherrèrre, J. H. (1998). The end of cheap oil. Scientific American, 278, 78–83.
Cardis, E., & Hatch, M. (2011). The Chernobyl accident—an epidemiological perspective. Clinical Oncology, 23(4), 251–260.
Cardis, E., Howe, G., Ron, E., Bebeshko, V., Bogdanova, T., Bouville, A.,…Zvonova, I. (2006). Cancer consequences of the Chernobyl accident. Journal of Radiological Protection, 26, 127–140.
Cardis, E., Vrijheid, M., & Gilbert, E. (2005). Risk of cancer after low doses of ionising radiation—retrospective cohort study in 15 countries. BMJ, 331(7508), 77–81.
Case, S. C., Rapporteur; Nuclear and Radiation Studies Board, Division on Earth and Life Studies, National Research Council. (2011). Proliferation risk in nuclear fuel cycles: Workshop summary. Washington, DC: National Academies Press.
Center for Land Use Interpretation. (n.d.) Cherry Point Refinery [Photo]. Retrieved from http://clui.org/ludb/site/cherry-point- refinery
Childs, B., & Bradley, R. (2007). Plants at the pump: Biofuels, climate change, and sustainability. Washington, DC: World Resources Institute.
Christodouleas, J. P., Forrest, R. D., Ainsley, C. G., Tochner, Z., Hahn, S. M., & Glatstein, E. (2011). Short-term and long-term health risks of nuclear-power-plant accidents. New England Journal of Medicine, 364(24), 2334–2341.
Clancy, L., Goodman, P., Sinclair, H., & Dockery, D. W. (2002). Effect of air-pollution control on death rates in Dublin, Ireland: An intervention study. Lancet, 360(9341), 1210–1214.
Cleveland, C. J., Costanza, R., Hall, C.A.S., & Kaufmann, R. (1984). Energy and the U.S. economy: A biophysical perspective. Science, 225, 890–897.
Colborn, T., Kwiatkowski, C., Schultz, K., & Bachran, M. (2011). Natural gas operations from a public health perspective. Human and Ecological Risk Assessment, 17(5), 1039–1056.
786
Colby, W. D., Dobie, R., Leventhall, G., Lipscomb, D. M., McCunney, R. J., Seilo, M. T., & Søndergaard, B. (2009). Wind turbine sound and health effects: An expert panel review (Prepared for American Wind Energy Association and Canadian Wind Energy Association). Retrieved from http://www.canwea.ca/pdf/talkwind/Wind_Turbine_Sound_and_Health_Effects.pdf
Congressional Budget Office. (2009). The impact of ethanol use on food prices and greenhouse-gas emissions. Washington, DC: Author.
Cook, J. T., Frank, D. A., Casey, P. H., Rose-Jacobs, R., Black, M. M., Chilton, M.,…Cutts, D. B. (2008). A brief indicator of household energy security: Associations with food security, child health, and child development in US infants and toddlers. Pediatrics, 122, e867–875.
Deffeyes, K. S. (2003). Hubbert's peak: The impending world oil shortage. Princeton, NJ: Princeton University Press.
Demirbas, A. (2009). Political, economic and environmental impacts of biofuels: A review. Applied Energy, 86, S108–117.
Dew, M. A., & Bromet, E. J. (1993). Predictors of temporal patterns of psychiatric distress during 10 years following the nuclear accident at Three Mile Island. Social Psychiatry and Psychiatric Epidemiology, 28(2), 49–55.
Diaz, J. H. (2011). The legacy of the Gulf oil spill: Analyzing acute public health effects and predicting chronic ones in Louisiana. American Journal of Disaster Medicine, 6(1), 5–22.
Earley, J., & McKeown, A. (2009). Red, white, and green: Transforming U.S. biofuels. (Worldwatch Report 180). Washington, DC: Worldwatch Institute.
Egilman, D., Scout, Kol, L., Hegg, L. A, & Bohme, S. R. (2007). Manipulated data in Shell's Benzene Historical Exposure Study. International Journal of Occupational and Environmental Health, 13, 222–232.
Eisentraut, A. (2010). Sustainable production of second-generation biofuels: Potential and perspectives in major economies and
787
developing countries. Paris: International Energy Agency. Retrieved from http://www.iea.org/publications/freepublications/publication/second_generation_biofuels.pdf
Electric Power Research Institute. (2010). The role of hydropower reservoirs in greenhouse gas emissions (EPRI Publication 1017971). Palo Alto, CA: Author.
Energy Information Administration. (2014). Oil (petroleum) basics. Retrieved from http://www.eia.gov/KIDS/energy.cfm? page=oil_home-basics
Energy Information Administration. (2015). How much ethanol is in gasoline and how does it affect fuel economy? Retrieved from http://www.eia.gov/tools/faqs/faq.cfm?id=27&t=10
Epstein, P. R., Buonocore, J. J., Eckerle, K., Hendryx, M., Stout, B. M., III, Heinberg, R., et al. (2011). Full cost accounting for the life cycle of coal. Annals of the New York Academy of Sciences, 1219, 73–98.
Fairlie, I. (2009). Childhood cancers near German nuclear power stations: Hypothesis to explain the cancer increases. Medicine, Conflict and Survival, 25(3), 206–220.
Fargione, J., Hill, J., Tilman, D., Polasky, S., & Hawthorne, P. (2008). Land clearing and the biofuel carbon debt. Science, 319(5867), 1235–1238.
Federal Railroad Administration, Office of Safety Analysis. (2015). Ten year accident/incident overview. Retrieved from http://safetydata.fra.dot.gov/OfficeofSafety/publicsite/Query/TenYearAccidentIncidentOverview.aspx
The Fiber School. (2015). Fiber optics for wind turbines [Photo]. Retrieved from http://learnfiberoptic.com/training-industry/fiber- optics-wind-turbines
Field, C. B., Campbell, J. E., & Lobell, D. B. (2007). Biomass energy: The scale of the potential resource. Trends in Ecology & Evolution, 29, 65–72.
Finkel, M. L., & Law, A. (2011). The rush to drill for natural gas: A public health cautionary tale. American Journal of Public Health,
788
101, 784–785.
Freed, J. (2014). Back to the future: Advanced nuclear energy and the battle against climate change. Brookings Essay. Retrieved from http://www.brookings.edu/research/essays/2014/backtothefuture#
Fröling, M. (2011). Energy use, population and growth, 1800–1970. Journal of Population Economics, 24, 1133–1163.
Frumkin, H., Hess, J., & Vindigni, S. (2009). Energy and public health: The challenge of peak petroleum. Public Health Reports, 124, 5–19.
Fthenakis, V. M., Kim, H. C., & Alsema, E. (2008). Emissions from photovoltaic life cycles. Environmental Science & Technology, 42(6), 2168–2174.
Fthenakis, V. M. (2003). Overview of potential hazards. In T. Markvart & L. Castaner (Eds.), Practical handbook of photovoltaics: Fundamentals and applications (pp. 857–868). New York: Elsevier.
Gaffney, J. S., & Marley, N. A. (2009). The impacts of combustion emissions on air quality and climate—from coal to biofuels and beyond. Atmospheric Environment, 43, 23–36.
Giles-Corti, B., Foster, S., Shilton, T., & Falconer, R. (2010). The co- benefits for health of investing in active transportation. New South Wales Public Health Bulletin, 21(5–6), 122–127.
Gohlke, J. M., Thomas, R., Woodward, A., Campbell-Lendrum, D., Prüss-Ustün, A., Hales, S., & Portier, C. J. (2011). Estimating the global public health implications of electricity and coal consumption. Environmental Health Perspectives, 119, 821–826.
Gosselin, P., Hrudey, S. E., Naeth, M. A., Plourde, A., Therrien, R., Van Der Kraak, G., & Xu, Z. (2010). The Royal Society of Canada Expert Panel: Environmental and health impacts of Canada's oil sands industry. Ottawa: Royal Society of Canada. Retrieved from http://www.rsc.ca/documents/expert/RSC%20report%20complete%20secured%209Mb.pdf
Goyal, N., Camacho, F., Mangano, J., & Goldenberg, D. (2012). Thyroid cancer characteristics in the population surrounding Three
789
Mile Island. Laryngoscope, 122(6), 1415–1421.
Graber, J. M., Stayner, L. T., Cohen, R. A., Conroy, L. M., & Attfield, M. D. (2014). Respiratory disease mortality among US coal miners; Results after 37 years of follow-up. Occupational and Environmental Medicine, 71(1), 30–39.
Grattan, L. M., Roberts, S., Mahan, W. T., Jr., McLaughlin, P. K., Otwell, W. S., & Morris, J. G., Jr. (2011). The early psychological impacts of the Deepwater Horizon oil spill on Florida and Alabama communities. Environmental Health Perspectives, 119(6), 838– 843.
Grübler, A. (2004). Transitions in energy use. In C. J. Cleveland (Ed.), Encyclopedia of energy (Vol. 6, pp. 163–177). Boston: Elsevier.
Gunkel, G. (2009). Hydropower—A green energy? Tropical reservoirs and greenhouse gas emissions. Clean-Soil, Air, Water, 37, 726–734.
Haddon, W. J. (1980). Advances in the epidemiology of injuries as a basis for public policy. Public Health Reports, 95, 411–421.
Haines, A., Smith, K. R., Anderson, D., Epstein, P. R., McMichael, A. J., Roberts, I.,…Woods, J. (2007). Policies for accelerating access to clean energy, improving health, advancing development, and mitigating climate change. Lancet, 370(9594), 1264–1281.
Hall, C., Tharakan, P., Hallock, J., Cleveland, C., & Jefferson, M. (2003). Hydrocarbons and the evolution of human culture. Nature, 426, 318–322.
Han, Y. Y., Youk, A. O., Sasser, H., & Talbott, E. O. (2011). Cancer incidence among residents of the Three Mile Island accident area: 1982–1995. Environmental Research, 111(8), 1230–1235.
Hankey, S., & Marshall, J. D. (2010). Impacts of urban form on future US passenger-vehicle greenhouse gas emissions. Energy Policy, 38(9), 4880–4887.
Harrison, J. P. (2011). Wind turbine noise. Bulletin of Science, Technology & Society, 31, 256–261.
790
Hatch, M., Brenner, A., Bogdanova, T., Derevyanko, A., Kuptsova, N., Likhtarev, I.,…Tronko, M. (2009). A screening study of thyroid cancer and other thyroid diseases among individuals exposed in utero to iodine-131 from Chernobyl fallout. Journal of Clinical Endocrinology and Metabolism, 94, 899–906.
Hatheway, A. W. (2012). Remediation of former manufactured gas plants and other coal-tar sites. Boca Raton, FL: CRC Press.
Health Effects Institute. (2010). Traffic-related air pollution: A critical review of the literature on emissions, exposure, and health effects (Special Report 17). Boston: Author. Retrieved from http://pubs.healtheffects.org/view.php?id=334.
Hendryx, M. (2010). Poverty and mortality disparities in central Appalachia: Mountaintop mining and environmental justice. Journal of Health Disparities Research and Practice, 4(3), 44–53.
Hendryx, M., & Ahern, M. M. (2008). Relations between health indicators and residential proximity to coal mining in West Virginia. American Journal of Public Health, 98(4), 669–671.
Hill, J., Nelson, E., Tilman, D., Polasky, S., & Tiffany, D. (2006). Environmental, economic, and energetic costs and benefits of biodiesel and ethanol biofuels. Proceedings of the National Academy of Sciences of the United States of America, 103(30), 11206–11210.
Hill, J., Polasky, S., Nelson, E., Tilman, D., Huo, H., Ludwig, L.,… Bonta, D. (2009). Climate change and health costs of air emissions from biofuels and gasoline. Proceedings of the National Academy of Sciences of the United States of America, 106, 2077–2082.
Hoffmann, W., Terschueren, C., & Richardson, D. B. (2007). Childhood leukemia in the vicinity of the Geesthacht nuclear establishments near Hamburg, Germany. Environmental Health Perspectives, 115(6), 947–952.
Holtzman, D. C. (2011). Mountaintop removal mining: Digging into community health concerns. Environmental Health Perspectives, 119, a476–483.
Hosier, R. H. (2004). Energy ladder in developing countries. In C. J.
791
Cleveland (Ed.), Encyclopedia of Energy (Vol. 2, pp. 423–435). Boston: Elsevier.
Howarth, R. W., Santoro, R., & Ingraffea, A. (2011). Methane and the greenhouse-gas footprint of natural gas from shale formations. Climatic Change, 106, 679–690.
Howden-Chapman, P., Viggers, H., Chapman, R., O'Sullivan, K., Barnard, L. T., & Lloyd, B. (2011). Tackling cold housing and fuel poverty in New Zealand: A review of policies, research, and health impacts. Energy Policy, 49, 134–142.
Howe, G. R. (2007). Leukemia following the Chernobyl accident. Health Physics, 93(5), 512–515.
Hubbert, M. K. (1956). Nuclear energy and the fossil fuels. Paper presented at the Spring Meeting, Southern District, Division of Petroleum, American Petroleum Institute, San Antonio, Texas. Retrieved from www.hubbertpeak.com/hubbert/1956/1956.pdf
Hvistendahl, M. (2007). Coal ash is more radioactive than nuclear waste. Scientific American. Retrieved from http://www.scientificamerican.com/article.cfm?id=coal-ash-is- more-radioactive-than-nuclear-waste
Hwang, S. S., Cao, Y., & Xi, J. (2011). The short-term impact of involuntary migration in China's Three Gorges: A prospective study. Social Indicators Research, 101(1), 73–92.
International Agency for Research on Cancer. (2010). IARC monographs on the evaluation of carcinogenic risks to humans: Vol. 95. Household use of solid fuels and high temperature frying. Lyon: World Health Organization & International Agency for Research on Cancer.
International Atomic Energy Agency. (2002). Follow-up of delayed health consequences of acute accidental radiation exposure: Lessons to be learned from their medical management. IAEA- TECDOC-1300. Vienna: Author.
International Commission on Large Dams. (n.d.). World Register of Dams. Retrieved from http://www.icold- cigb.net/GB/World_register/world_register.asp
792
International Energy Agency. (2010). World energy outlook 2010. Paris: Author.
International Energy Agency. (2011). Biofuels can provide up to 27% of world transportation fuel by 2050. Retrieved from http://www.iea.org/topics/renewables/subtopics/bioenergy
International Energy Agency. (2014). Key world energy statistics. Geneva: Author. Retrieved from http://www.iea.org/publications/freepublications/publication/key- world-energy-statistics-2014.html
Ivanov, V. K. (2007). Late cancer and noncancer risks among Chernobyl emergency workers of Russia. Health Physics, 93(5), 470–479.
Ivanov, V. K., Tsyb, A. F., Khait, S. E., Kashcheev, V. V., Chekin, S. Y., Maksioutov, M. A., & Tumanov, K. A. (2012). Leukemia incidence in the Russian cohort of Chernobyl emergency workers. Radiation and Environmental Biophysics, 51(2), 143–149.
Jetter, J., Zhao, Y., Smith, K. R., Khan, B., Yelverton, T., DeCarlo, P., & Hays, M. D. (2012). Pollutant emissions and energy efficiency under controlled conditions for household biomass cookstoves and implications for metrics useful in setting international test standards. Environmental Science & Technology, 46(19), 10827– 10834.
Jobin, W. R. (1999). Dams and disease: Ecological design and health impacts of large dams, canals and irrigation systems. London: Spon Press.
Kaatsch, P., Spix, C., Schulze-Rath, R., Schmiedel, S., & Blettner, M. (2008). Leukaemia in young children living in the vicinity of German nuclear power plants. International Journal of Cancer, 122(4), 721–726.
Kabir, Z., Bennett, K., & Clancy, L. (2007). Lung cancer and urban air-pollution in Dublin: A temporal association? Irish Medical Journal, 100(2), 367–369.
Kang, E. (2011, December). Wood stove intervention can reduce childhood pneumonia. Environmental Factor. Retrieved from
793
http://www.niehs.nih.gov/news/newsletter/2011/december/science- woodstove
Keiser, J., De Castro, M. C., Maltese, M. F., Bos, R., Tanner, M., Singer, B. H., & Utzinger, J. (2005). Effect of irrigation and large dams on the burden of malaria on a global and regional scale. American Journal of Tropical Medicine and Hygiene, 72(4), 392– 406.
Kharecha, P. A., & Hansen, J. E. (2013). Prevented mortality and greenhouse gas emissions from historical and projected nuclear power. Environmental Science & Technology, 47(9), 4889–4895.
Klare, M. T. (2002). Resource wars: The new landscape of global conflict. New York: Holt.
Klare, M. T. (2012). The race for what's left: The global scramble for the world's last resources. New York: Metropolitan Books.
Knopper, L. D., & Ollson, C. A. (2011). Health effects and wind turbines: A review of the literature. Environmental Health, 10, 78– 87.
Kosnik, L. (2008). The potential of water power in the fight against global warming in the U.S. Energy Policy, 36, 3252–3265.
Künzli, N., Perez, L., & Rapp, R. (2010). Air quality and health. Lausanne: European Respiratory Society.
Laney, A. S., & Weissman, D. N. (2014). Respiratory diseases caused by coal mine dust. Journal of Occupational and Environmental Medicine, 56 (Suppl. 10), S18–22.
Lapola, D. M., Schaldach, R., Alcamo, J., Bondeau, A., Koch, J., Koelking, C., & Priess, J. A. (2010). Indirect land-use changes can overcome carbon savings from biofuels in Brazil. Proceedings of the National Academy of Sciences of the United States of America, 107(8), 3388–3393.
Lee, W. E., Ojovan, M. I., & Jantzen, C. M. (Eds.). (2013). Radioactive waste management and contaminated site clean-up: Processes, technologies and international experience. Oxford, U.K.: Woodhead.
794
Leistritz, F. L., & Hodur, N. M. (2008). Biofuels: A major rural economic development opportunity. Biofuels, Bioproducts and Biorefining, 2, 501–504.
Leung, C. C., Yu, I. T., & Chen, W. (2012). Silicosis. Lancet, 379(9830), 2008–2018.
Levin, R. J. (2008). Incidence of thyroid cancer in residents surrounding the Three Mile Island nuclear facility. Laryngoscope, 118(4), 618–628.
Levy, J. I., Baxter, L. K., & Schwartz, J. (2009). Uncertainty and variability in health-related damages from coal-fired power plants in the United States. Risk Analysis, 29(7), 1000–1014.
Lewis, J. J., & Pattanayak, S. K. (2012). Who adopts improved fuels and cookstoves? A systematic review. Environmental Health Perspectives, 120(5). doi:10.1289/ehp.1104194
Lim, S. S., Vos, T., Flaxman, A. D., Danaei, G., Shibuya, K., Adair- Rohani, H.,…Memish, Z. A. (2012). A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380(9859), 2224–2260.
Lima, I., Ramos, F., Bambace, L., & Rosa, R. (2008). Methane emissions from large dams as renewable energy resources: A developing nation perspective. Mitigation and Adaptation Strategies for Global Change, 13, 193–206.
Manuel, J. (2009). Balancing act: Creating the right regulation for coal combustion waste. Environmental Health Perspectives, 117, A498–503.
Masera, O. R., Saatkamp, B. D., & Kammen, D. M. (2000). From linear fuel switching to multiple cooking strategies: A critique and alternative to the energy ladder model. World Development, 28(12), 2083–2103.
McDonald-Wilmsen, B., & Webber, M. (2010). Dams and displacement: Raising the standards and broadening the research agenda. Water Alternatives, 3(2), 142–161.
795
Mitka, M. (2012). Rigorous evidence slim for determining health risks from natural gas fracking. JAMA, 307, 2135–2136.
Morris, R. E., Pollack, A. K., Mansell, G. E., Lindhjem, C., Jia, Y., & Wilson, G. (2003). Impact of biodiesel fuels on air quality and human health (NREL/SR-540-33793). Golden, CO: National Renewable Energy Laboratory. Retrieved from http://www.afdc.energy.gov/afdc/pdfs/33793.pdf
Mueller, S. A., Anderson, J. E., & Wallington, T. J. (2011). Impact of biofuel production and other supply and demand factors on food price increases in 2008. Biomass and Bioenergy, 36(5), 1623–1632.
Naeher, L. P., Brauer, M., Lipsett, M., Zelikoff, J. T., Simpson, C. D., Koenig, J. Q., & Smith, K. R. (2007). Woodsmoke health effects: A review. Inhalation Toxicology, 19(1), 67–106.
National Research Council. (1999). Health effects of exposure to radon: BEIR VI. Washington, DC: National Academies Press.
National Research Council. (2012). Induced seismicity potential in energy technologies. Washington, DC: National Academies Press. Retrieved from http://www.nap.edu/catalog.php?record_id=13355
National Research Council, Committee on Coal Waste Impoundments, Committee on Earth Resources. (2002). Coal waste impoundments: Risks, responses, and alternatives. Washington, DC: National Academies Press.
National Research Council, Committee on Health, Environment, and Other External Costs and Benefits of Energy Production and Consumption. (2009). Hidden costs of energy: Unpriced consequences of energy production and use. Washington, DC: National Academies Press.
National Research Council, Committee on the Analysis of Cancer Risks in Populations Near Nuclear Facilities—Phase I. (2012). Analysis of cancer risks in populations near nuclear facilities: Phase I. Washington, DC: National Academies Press.
Nduagu, E., & Gates, I. D. (2015). Unconventional heavy oil growth and global greenhouse gas emissions. Environmental Science & Technology, 49(14), 8824–8832. doi:10.1021/acs.est.5b01913
796
Nuclear Energy Institute. (2105). Nuclear energy around the world. Retrieved from http://www.nei.org/resourcesandstats/nuclear_statistics/worldstatistics
Nussbaum, R. (2007). The Chernobyl nuclear catastrophe: Unacknowledged health detriment. Environmental Health Perspectives, 115(5), A238–239.
Nye, D. E. (1998). Consuming power: A social history of American energies. Cambridge, MA: MIT Press.
Olmstead, J. (2009). Fueling resistance? Antibiotics in biofuel production. Minneapolis: Institute for Agriculture and Trade Policy. Retrieved from http://www.iatp.org/documents/fueling-resistance- antibiotics-in-ethanol-production
Onuoha, F. C. (2008). Oil pipeline sabotage in Nigeria: Dimensions, actors and implications for national security. African Security Review, 17(3), 99–115.
Osborn, S. G., Vengosh, A., Warner, N. R., & Jackson, R. B. (2011). Methane contamination of drinking water accompanying gas-well drilling and hydraulic fracturing. Procceedings of the National Academy of Sciences of the United States of America, 108, 8172– 8176.
Pachauri, S., & Spreng, D. (2011). Measuring and monitoring energy poverty. Energy Policy, 39, 7497–7504.
Palinkas, L. A., Petterson, J. S., Russell, J., & Downs, M. A. (1993). Community patterns of psychiatric disorders after the Exxon Valdez oil spill. American Journal of Psychiatry, 150(10), 1517–1523.
Palmer, M. A., Bernhardt, E. S., Schlesinger, W. H., Eshleman, K. N., Foufoula-Georgiou, E., Hendryx, M. S.,…Wilcock, P. R. (2010). Science and regulation: Mountaintop mining consequences. Science, 327(5962), 148–149.
Penning, T. M., Breysse, P. N., Gray, K., Howarth, M., & Yan, B. (2014). Environmental health research recommendations from the Inter-Environmental Health Sciences Core Center Working Group on unconventional natural gas drilling operations. Environmental Health Perspectives, 122(11), 1155–1159.
797
Pure Energies. (n.d.). Pure Energies [Web site.] Retrieved from http://pureenergies.com/us/community
Rabinowitz, P. M., Slizovskiy, I. B., Lamers, V., Trufan, S. J., Holford, T. R., Dziura, J. D.,…Stowe, M. H. (2014). Proximity to natural gas wells and reported health status: Results of a household survey in Washington County, Pennsylvania. Environmental Health Perspectives, 123, 21–26.
Rafaj, P., Bertok, I., Cofala, J., & Schöpp, W. (2013). Scenarios of global mercury emissions from anthropogenic sources. Atmospheric Environment, 79, 472–479.
Raymond-Whish, S., Mayer, L. P., O'Neal, T., Martinez, A., Sellers, M. A., Christian, P. J.,…Dyer, C. A. (2007). Drinking water with uranium below the U.S. EPA water standard causes estrogen receptor-dependent responses in female mice. Environmental Health Perspectives, 115(12), 1711–1716.
REN21 (Renewable Energy Policy Network for the 21st Century). (2015). Renewables 2015: Global status report. Paris: REN21 Secretariat. Retrieved from http://www.ren21.net/GSR-2015- Report-Full-report-EN
Ridley, C. E., Clark, C. M., LeDuc, S. D., Bierwagen, B. G., Lin, B. B., Mehl, A., & Tobias, D. A. (2012). Biofuels: Network analysis of the literature reveals key environmental and economic unknowns. Environmental Science & Technology, 46, 1309–1315.
Robertson, G. P., Dale, V. H., Doering, O. C., Hamburg, S. P., Melillo, J. M., Wander, M. M.,…Wilhelm, W. W. (2008). Agriculture: Sustainable biofuels redux. Science, 322(5898), 49–50.
Roebroeks, W., & Villa, P. (2011). On the earliest evidence for habitual use of fire in Europe. Procceedings of the National Academy of Sciences of the United States of America, 108(13), 5209–5214.
Rogalsky, D. K., Mendola, P., Metts, T. A., & Martin, W. J., 2nd. (2014). Estimating the number of low-income Americans exposed to household air pollution from burning solid fuels. Environmental Health Perspectives, 122(8), 806–810.
798
Romanenko, A. Y., Finch, S. C., Hatch, M., Lubin, J. H., Bebeshko, V. G., Bazyka, D. A.,…Zablotska, L. B. (2008). The Ukrainian- American study of leukemia and related disorders among Chornobyl cleanup workers from Ukraine: III. Radiation risks. Radiation Research, 170(6), 711–720.
Ron, E. (2007). Thyroid cancer incidence among people living in areas contaminated by radiation from the Chernobyl accident. Health Physics, 93(5), 502–511.
Rosenberg, D. M., McCully, P., & Pringle, C. M. (2000). Global-scale environmental effects of hydrological alterations: Introduction. BioScience, 50(9), 746–751.
Rosenthal, E. (2013). As biofuel demand grows, so do Guatemala's hunger pangs. New York Times, January 5, p. A6. Retrieved from http://www.nytimes.com/2013/01/06/science/earth/in-fields-and- markets-guatemalans-feel-squeeze-of-biofuel-demand.html
Ruiz-Mercado, I., Masera, O., Zamora, H., & Smith, K. R. (2011). Adoption and sustained use of improved cookstoves. Energy Policy, 39, 7557–7566.
Runge, C. F., & Senauer, B. (2007). How biofuels could starve the poor. Foreign Affairs, 86(3), 41–53.
Sabaté, J., & Soret, S. (2014). Sustainability of plant-based diets: Back to the future. American Journal of Clinical Nutrition, 100(Suppl. 1), 476S–482.
Saenko, V., Ivanov, V., Tsyb, A., Bogdanova, T., Tronko, M., Demidchik, Y, S., & Yamashita, S. (2011). The Chernobyl accident and its consequences. Clinical Oncology, 23(4), 234–243.
Satin, K. P., Bailey, W. J., Newton, K. L., Ross, A. Y., & Wong, O. (2002). Updated epidemiological study of workers at two California petroleum refineries, 1950–95. Occupational and Environmental Medicine, 59(4), 248–256.
Schindler, D. W. (2014). Unravelling the complexity of pollution by the oil sands industry. Procceedings of the National Academy of Sciences of the United States of America, 111(9), 3209–3210.
799
Schivelbusch, W. (1986). The railway journey: The industrialization of space and time. New York: Berg.
Schlünssen, V., Madsen, A. M., Skov, S., & Sigsgaard, T. (2011). Does the use of biofuels affect respiratory health among male Danish energy plant workers? Occupational and Environmental Medicine, 68(7), 467–473.
Schurr, S. H. (1984). Energy use, technological change, and productive efficiency: An economic-historical interpretation. Annual Review of Energy, 9, 409–425.
Schwartz, B. S., Parker, C. L., Hess, J., & Frumkin, H. (2011). Public health and medicine in an age of energy scarcity: The case of petroleum. American Journal of Public Health, 101(9), 1560–1567.
Scovronick, N., & Wilkinson, P. (2014). Health impacts of liquid biofuel production and use: A review. Global Environmental Change, 24, 155–164.
Scudder, T. (2005). The future of large dams: Dealing with the social, environmental and political costs. London: Earthscan.
Searchinger, T., Heimlich, R., Houghton, R. A., Dong, F., Elobeid, A., Fabiosa, J.,…Yu, T.-H. (2008). Use of U.S. croplands for biofuels increases greenhouse gases through emissions from land-use change. Science, 319(5867), 1238–1240.
Shakhtarin, V. V., Tsyb, A. F., Stepanenko, V. F., Orlov, M. Y., Kopecky, K. J., & Davis, S. (2003). Iodine deficiency, radiation dose, and the risk of thyroid cancer among children and adolescents in the Bryansk region of Russia following the Chernobyl power station accident. International Journal of Epidemiology, 32, 584–591.
Sheehan, J. J. (2009). Biofuels and the conundrum of sustainability. Current Opinion in Biotechnology, 20(3), 318–324.
Shepherd, D., McBride, D., Welch, D., Dirks, K. N., & Hill, E. M. (2011). Evaluating the impact of wind turbine noise on health- related quality of life. Noise & Health, 13(54), 333–339.
Shibata, Y., Yamashita, S., Masyakin, V. B., Panasyuk, G. D., & Nagataki, S. (2001). 15 Years after Chernobyl: New evidence of
800
thyroid cancer. Lancet, 358, 1965–1966.
Silicon Valley Toxics Coalition. (2009). Toward a just and sustainable solar energy industry. San Francisco: Author. Retrieved from http://svtc.org/our-work/solar
Skone, T. J., Littlefield, J., Marriott, J., Cooney, G., Jamieson, M., Hakian, J., & Schivley, G. (2014). Life cycle analysis of natural gas extraction and power generation. (DOE/NETL-2014/1646). Washington, DC: U.S. Department of Energy, National Energy Technology Laboratory, Office of Fossil Energy.
Smil, V. (2005). Energy at the crossroads: Global perspectives and uncertainties. Cambridge, MA: MIT Press.
Smith, K. R., Balakrishnan, K., Butler, C., Chafe, Z., Fairlie, I., Kinney, P.,…Schneider, M. (2012). Energy and health. In GEA Writing Team, Global Energy Assessment: Toward a sustainable future (pp. 255–324). Cambridge, U.K.: Cambridge University Press and International Institute for Applied Systems Analysis.
Smith, K. R., & Haigler, E. (2008). Co-benefits of climate mitigation and health protection in energy systems: Scoping methods. Annual Review of Public Health, 29, 11–25.
Smith, K. R., McCracken, J. P., Weber, M. W., Hubbard, A., Jenny, A., Thompson, L. M.,…Bruce, N. (2011). Effect of reduction in household air pollution on childhood pneumonia in Guatemala (RESPIRE): A randomised controlled trial. Lancet, 378, 1717–1726.
Solomon, G. M., & Janssen, S. (2010). Health effects of the Gulf oil spill. JAMA, 304(10), 1118–1119.
Sorahan, T. (2007). Mortality of UK oil refinery and petroleum distribution workers, 1951–2003. Occupational Medicine (London), 57(3), 177–185.
Spix, C., Schmiedel, S., Kaatsch, P., Schulze-Rath, R., & Blettner, M. (2008). Case-control study on childhood cancer in the vicinity of nuclear power plants in Germany 1980–2003. European Journal of Cancer, 44(2), 275–284.
Steinmann, P., Keiser, J., Bos, R., Tanner, M., & Utzinger, J. (2006).
801
Schistosomiasis and water resources development: Systematic review, meta-analysis, and estimates of people at risk. Lancet: Infectious Diseases, 6(7), 411–425.
Talbott, E. O., Youk, A. O., McHugh-Pemu, K. P., & Zborowski, J. V. (2003). Long-term follow-up of the residents of the Three Mile Island accident area: 1979–1998. Environmental Health Perspectives, 111, 341–348. [Erratum, Environmental Health Perspectives, 111, A453.]
Tanigawa, K., Hosoi, Y., Hirohashi, N., Iwasaki, Y., & Kamiya, K. (2012). Loss of life after evacuation: Lessons learned from the Fukushima accident. Lancet, 379(9819), 889–891.
Taylor, D. A. (2010). On the job with solar PV. Environmental Health Perspectives, 118(1), A19.
Tenenbaum, D. J. (2009). Trash or treasure? Putting coal combustion waste to work. Environmental Health Perspectives, 117, A490–497.
Tilman, D., & Clark, M. (2014). Global diets link environmental sustainability and human health. Nature, 515(7528), 518–522.
Toman, M. A., & Jemelkova, B. (2003). Energy and economic development: An assessment of the state of knowledge. Energy Journal, 24, 93–112.
Tours China. (n.d.). Three Gorges Dam [Photo]. Retrieved from http://www.tourschina.com/yangtze-river/three-gorges-dam.htm
Tsai, S. P., & Wendt, J. K. (2001). Health findings from a mortality and morbidity surveillance of refinery employees. Annals of Epidemiology, 11(7), 466–476.
Tsai, S. P., Wendt, J. K., Cardarelli, K. M., & Fraser, A. E. (2003). A mortality and morbidity study of refinery and petrochemical employees in Louisiana. Occupational and Environmental Medicine, 60(9), 627–633.
Tuller, D. (2015). As fracking booms, dearth of health risk data remains. Health Affairs, 34(6), 903–906.
United Nations Development Programme. (2009). The energy
802
access situation in developing countries: A review focused on least developed countries and Sub-Saharan Africa. Nairobi: United Nations.
United Nations Scientific Committee on the Effects of Atomic Radiation. (2012). UNSCEAR assessment of the Fukushima-Daiichi accident: Background information for journalists. Retrieved from http://www.unis.unvienna.org/pdf/2012/UNSCEAR_Backgrounder.pdf
Vanwey, L. (2009). Social and distributional impacts of biofuel production. In R. W. Howarth, & S. Bringezu (Eds.), Biofuels: Environmental consequences and interactions with changing land use (pp. 205–215). Proceedings of the Scientific Committee on Problems of the Environment (SCOPE), International Biofuels Project Rapid Assessment, 22–25 September 2008. Ithaca: Cornell University. Retrieved from http://cip.cornell.edu/biofuels
Wakeford, R. (2009). Radiation in the workplace—a review of studies of the risks of occupational exposure to ionising radiation. Journal of Radiological Protection, 29(2A), A61–79.
Weinhold, B. (2011). Alberta's oil sands: Hard evidence, missing data, new promises. Environmental Health Perspectives, 119, a126– 131.
Wertelecki, W. (2010). Malformations in a Chornobyl-impacted region. Pediatrics, 125(4), 836–843.
West, J. J., Smith, S. J., Silva, R. A., Naik, V., Zhang, Y., Adelman, Z.,…Lamarque, J.-F. (2013). Co-benefits of mitigating global greenhouse gas emissions for future air quality and human health. Nature Climate Change, 3(10), 885–889.
Wilkinson, P., Smith, K. R., Beevers, S., Tonne, C., & Oreszczyn, T. (2007). Energy, energy efficiency, and the built environment. Lancet, 370, 1175–1187.
Wilkinson, P., Smith, K. R., Davies, M., Adair, H., Armstrong, B. G., Barrett, M.,…Chalabi, Z. (2009). Public health benefits of strategies to reduce greenhouse-gas emissions: Household energy. Lancet, 374, 1917–1929.
Wong, O., & Raabe, G. K. (2000). A critical review of cancer
803
epidemiology in the petroleum industry, with a meta-analysis of a combined database of more than 350,000 workers. Regulatory Toxicology and Pharmacology, 32(1), 78–98.
Woodcock, J., Banister, D., Edwards, P., Prentice, A. M., & Roberts, I. (2007). Energy and transport. Lancet, 370, 1078–1088.
Worgul, B. V., Kundiyev, Y. I., Sergiyenko, N. M., Chumak, V. V., Vitte, P. M., Medvedovsky, C.,…Shore, R. E. (2007). Cataracts among Chernobyl clean-up workers: Implications regarding permissible eye exposures. Radiation Research, 167(2), 233–243.
World Bank. (2004). Involuntary resettlement sourcebook: Planning and implementation in development projects. Washington, DC: Author.
World Bank. (2015). Energy use (kg of oil equivalent per capita). Retrieved from http://data.worldbank.org/indicator/EG.USE.PCAP.KG.OE
World Commission on Dams. (2000). Dams and development: A new framework for decision-making. London: Earthscan.
Wrangham, R. (2010). Catching fire: How cooking made us human. New York: Basic Books.
Xi, J., & Hwang, S. S. (2011). Relocation stress, coping, and sense of control among resettlers resulting from China's Three Gorges Dam project. Social Indicators Research, 104(3), 507–522.
Xia, T., Zhang, Y., Crabb, S., & Shah, P. (2013). Cobenefits of replacing car trips with alternative transportation: A review of evidence and methodological issues. Journal of Environmental and Public Health. doi:10.1155/2013/797312
Younger, M., Morrow-Almeida, H. R., Vindigni, S. M., & Dannenberg, A. L. (2008). The built environment, climate change, and health: opportunities for co-benefits. American Journal of Preventive Medicine, 35(5), 517–526.
Zhou, Y., Luckow, P., Smith, S. J., & Clarke, L. (2012). Evaluation of global onshore wind energy potential and generation costs. Environmental Science & Technology, 46(14), 7857–7864.
804
Zhu, H. M., Xiang, S., Wu, X. H., & Zhou, X. N. (2008). Three Gorges Dam and its impact on the potential transmission of schistosomiasis in regions along the Yangtze River. Ecohealth, 5, 137–148.
805
For Further Information Good sources for learning more about the general role of energy in society include National Research Council, Committee on Health, Environmental, and Other External Costs and Benefits of Energy Production and Consumption (2010) and Nye (1999), both listed in the References, and the following:
Goldemberg, J., & Lucon, O. (2010). Energy, environment and development (2nd. ed.). London: Earthscan.
Johnson, B. (2014). Carbon nation: Fossil fuels in the making of American culture. Lawrence: University Press of Kansas.
Jones, C. F. (2014). Routes of power: Energy and modern America. Cambridge, MA: Harvard University Press.
Odum, H. T., & Odum, E. C. (1976). Energy basis for man and nature. New York: McGraw-Hill.
Yergin, D. (2011). The quest: Energy, security, and the remaking of the modern world. New York: Penguin Press.
There are also many sources for learning about specific forms of energy, such as these:
Freese, B. (2003). Coal: A human history. Cambridge, MA: Perseus.
Yergin, D. (1991). The prize: The epic quest for oil, money and power. New York: Simon & Schuster.
For a focus on health aspects of energy, reviews include Smith (2012), listed in the References, and the following:
Smith, K. R., Frumkin, H., Balakrishnan, K., Butler, C. D., Chafe, Z. A., Fairlie, I.,…Schneider, M. (2013). Energy and human health. Annual Review of Public Health, 34, 159–188.
Authoritative sources on energy use patterns include the following:
International Energy Agency: http://www.iea.org
U.S. Energy Information Administration: http://www.eia.gov
806
Chapter 15 Healthy Communities
Andrew L. Dannenberg and Anthony G. Capon
Dr. Dannenberg and Dr. Capon report no conflicts of interest related to the authorship of this chapter.
807
Key Concepts The design of neighborhoods, towns, and cities can affect people's health.
Modern public health is historically tied to urban planning and land-use policy.
Land-use and transportation decisions can either support or undermine routine physical activity, air quality, safety, social interaction, mental well-being, social equity, and other determinants of health.
Smart growth principles offer human health benefits and also support environmental sustainability and resiliency goals.
Health impact assessment is a tool that can assist decision makers in considering the potential impacts of proposed plans, projects, and policies on the health of populations.
Emerging research and trends in both community development and public health are conducive to increasing collaboration between land-use planners and public health professionals.
The built environment comprises the totality of the places and the infrastructure people create—buildings, neighborhoods, streets, parks, transportation systems, and more—almost all the settings in which we live, work, study, and play. The built environment affects health through various pathways: facilitating or impeding physical activity, providing or impeding access to healthy food and jobs, improving or degrading air quality, and promoting social interaction or aggravating social isolation. This chapter examines how features of community design affect public health.
We can consider the built environment and its effect on health from any of a number of spatial scales. A person's chair, for instance, is a component of the built environment on a small (or micro) scale, and chair design can certainly affect well-being; consider how a poorly designed chair can cause back pain—an example of ergonomics, a topic introduced in Chapter 21. On a somewhat bigger scale, buildings are important, because people spend most of
808
their time in buildings, as discussed in Chapter 20. In this chapter we focus on considerably larger spatial scales: the neighborhood, the town, the city, and the metro area. Although discussed individually, each of these scales is related to the others, and each affects health and well-being.
809
The History of Cities Early cities were established along trade routes or at points where the movement of goods shifted from one mode of transportation to another, such as at river and ocean ports. Early population hubs often developed around a central public plaza. The main form of travel was walking, so people needed to live near where they worked, traded, and prayed; compact, high-density settlement was the norm. The need to move goods and people locally led to the development of street networks for use by wagons and carriages.
Industrialization in nineteenth-century Europe, North America, and certain other places brought an influx of manufacturing jobs and workers into cities. By 1800, London's population had reached 1 million (rivalled only by Beijing, Tokyo, and Guangzhou); a century later it had surpassed 6 million. During that same interval, New York's population rose from 60,000 to almost 3.5 million. These fast-growing cities featured crowded, squalid conditions and inadequate infrastructure, facilitating the spread of diseases such as tuberculosis and typhoid. Successive waves of migration into cities —notably (in the United States) millions of immigrants from Europe between the 1880s and the 1920s, and the great migration of African Americans from southern states to northern and midwestern cities during the twentieth century—accelerated urban growth, with unprecedented concentrations of poverty in urban centers (see Text Box 15.1).
810
Text Box 15.1 Urbanization Versus Urbanism Urbanization is a dynamic process of growth and change in cities, generally featuring population growth, and often also featuring expanding urban boundaries, changes in density, and demographic changes such as greater heterogeneity. In contrast, urbanism (or urbanicity) refers to the characteristics of cities at particular points in time, and their impacts on the people who live there (Vlahov & Galea, 2002).
By the late nineteenth century, public health professionals on both sides of the Atlantic were coming to understand infectious disease transmission in cities, and they focused their attention on urban planning, public infrastructure, and housing quality (Melosi, 2000). This was a formative stage in public health history, and it is now referred to as the sanitary movement (Duffy, 1990; Halliday, 2007). In fact, many of the concepts and practices of modern public health developed in response to the challenges of urbanization. Public health professionals helped to develop potable water supplies, sewage systems, and waste management. An architect and an urban housing specialist were among the founding members of the American Public Health Association in 1873, illustrating the historical relationship between public health and cities.
Technological developments during the 1800s and 1900s enabled profound changes in urban form (Jackson, 1985). With the advent of electrification in the late nineteenth and early twentieth centuries, railroads and streetcars could be extended into the surrounding countryside. Automobile ownership became widespread during the 1920s. Construction techniques changed as well; for example, starting in the 1830s the balloon frame house (made with lighter studs rather than heavy timbers) enabled rapid, inexpensive construction of large numbers of private homes. Houses outside the city went from being second homes for the wealthy to being permanent residential alternatives to the gritty urban center for middle- and upper-class citizens who could now
811
easily commute greater distances to their jobs in the urban core. This trend—a pattern known as urban sprawl—accelerated rapidly in the decades after World War II, especially in North America and Australia, but also in Europe.
Meanwhile, over the course of the twentieth century and into the twenty-first, urbanization in wealthy countries was eclipsed by phenomenal urban growth in low- and middle-income countries. At present the world has nearly forty mega cities (with populations larger than 10 million); the list includes Shanghai, Beijing, Guangzhou, and Shenzhen in China; Delhi, Mumbai, Kolkata, Chennai, and Hyderabad in India; Jakarta, Karachi, Lahore, Bangkok, Dhaka, Tehran, and Manila in Asia and the Middle East; Lagos and Kinshasa in Africa; and Mexico City, Buenos Aires, and Rio de Janeiro in Latin America. Yet these cities taken altogether represent only a small fraction of the world's urban population; many more people live in cities of between 1 million and 10 million inhabitants. During the first decade of the twenty-first century, the world's urban population surpassed its rural population for the first time (Figure 15.1), and over 90% of urban growth is now occurring in developing countries.
Figure 15.1 World Population: Urban and Rural, 1950–2050 Source: United Nations, 2014, p. 7.
This trend is continuing. Each week, the global urban population grows by more than 1 million people, the equivalent of a new city the size of Tucson, Arizona. By the middle of the twenty-first century, the world's cities will contain more than 2 billion additional people. Most of this population growth will be in small and
812
medium-sized cities in low- and middle-income countries in Asia and Africa (Montgomery, 2008).
This brief historical account suggests that urban development proceeds in stages (Table 15.1). Of course, there is no neat sequence; cities typically exhibit characteristics of more than one stage at any one time. While the principal health concerns are generally different for each stage, chronic diseases are an increasing burden in both low- and high-income cities (Bygbjerg, 2012; Lozano et al., 2012). The final stage is an aspirational one: the healthy eco-city. Globally, a key question is how cities might move directly from poverty to healthy eco-city status, avoiding the pitfalls of the intermediate stages.
Table 15.1 Stages of Urban Evolution and Characteristic Environmental Conditions and Health Issues
Stage of urban evolution
Characteristic environmental conditions
Characteristic health issues
1. Poverty (e.g., New York in 1890; Lagos, Nigeria today)
Contaminated water, poor sanitation, poor housing
Infectious diseases, malnutrition, injury
2. Industrial (e.g., Pittsburgh in 1920; Chongqing, China today)
Air pollution and land contamination by chemicals and solid waste
Chronic respiratory disease, injury, heart disease
3. Consumption (e.g., Houston today)
High levels of consumption of water, energy, and other resources
Chronic diseases (obesity, diabetes, heart disease, cancer), injury, depression
4. Healthy eco-city (e.g., Copenhagen)
Conditions of life in balance with nature
Maximum health potential
Source: Adapted from Bai & Imura, 2000.
This chapter is organized around these stages. We begin by discussing the first two stages, urban poverty and industrialization (with its accompanying pollution), with a focus on contemporary developing nations—the modern counterpart of the nineteenth-
813
century cities described above. We then turn to consumption, with a focus on the typical sprawling metro areas of the United States during the last fifty years. Finally, we end with the healthy eco-city, a model that combines health, resiliency, prosperity, and sustainability.
814
Poverty and Industrialization in Cities As human habitats, cities offer many potential advantages. They are engines of innovation and economic growth. They are centers of productive activity and employment. They are the setting for many social advances—female labor force participation, literacy, social mobility, and cultural and artistic endeavors. Greater population density implies the ability to deliver services—from water, sanitation, and electricity to education and health care—more efficiently than in rural areas (Cohen, 2006). Accordingly, in most countries, urban dwellers enjoy better average health status than people who live in rural areas do (World Health Organization [WHO] and UN-HABITAT, 2010).
However, rapid urban growth throughout the developing world has outstripped the capacity of most cities to provide adequate basic services for their citizens (Cohen, 2006). Perhaps the major concern is the extreme concentration of poverty; one in three city dwellers in developing nations (above 80% in some cities) lives in a slum, with inadequate access to safe water, sanitation, and infrastructure; poor housing quality; overcrowding; and insecure residential status (Sverdlik, 2011; Fink, Gunther, & Hill, 2014) (Figure 15.2). In 2013, UN-Habitat estimated that 863 million people globally lived in urban slums—reflecting an increase of nearly 10 million each year over the preceding twenty-five years (UN-HABITAT, 2013).
815
Figure 15.2 Nearly 1 Billion People Live in Urban Slums, Such as This One in Nairobi
Source: Stroppa, 2012.
Such urban environments present a host of health hazards. Rural- urban migration disrupts social networks and support systems. The adjustment to new environments, often featuring noise, crowding, and privation, can create considerable stress, contributing to high rates of depression and anxiety, substance abuse, domestic violence,
816
and related outcomes. Unsustainable transport and land-use policies lead to heavy traffic congestion and high levels of air pollution in many cities (Figure 15.3). Industrial employment poses risks of workplace injuries and illnesses, as described in Chapter 21. Crowding and substandard sanitation increase the risk of infectious disease, even as reduced access to fresh foods and opportunities for physical activity contribute to obesity and related chronic diseases, fueling the “double burden” of disease (Bygbjerg, 2012; Eckert & Kohler, 2014). Cities are now confronting global epidemics of chronic diseases, including heart disease, diabetes, lung disease, and cancer.
Figure 15.3 Heavy Traffic, as Shown Here in Delhi, Brings Pollution, Injury Risks, Noise, and Mental Stress, and Inhibits Physical Activity
Source: “Air monitoring centre of INDIA freezes off the WHO report,” 2014.
These complex challenges recapitulate the urban health struggles of the nineteenth and twentieth centuries in what are now wealthy cities, albeit at a larger scale and with more rapid changes than ever seen before. The cities of developing nations will be at the center of global public health efforts in coming years.
817
The Modern Metropolis: Consumption and Urban Sprawl After World War II, for many U.S. families the American Dream consisted of a home in the suburbs with a yard, a car (or two) in the garage, and a white picket fence. The result was low-density development across large swaths of land outside traditional city boundaries, or urban sprawl—the expression of the American Dream for tens of millions of people during the second half of the twentieth century. The design of low-density development over large areas of land is called urban sprawl. This American Dream, manifested as urban sprawl, became a reality for tens of millions of people during the second half of the twentieth century. A similar pattern emerged in other wealthy nations with plenty of land, such as Canada and Australia. In recent years urban sprawl has also appeared around the traditionally compact cities of Europe (García- Palomares, 2010), and in rapidly developing nations such as China (Zhao, 2010, 2011), marking it as a truly global phenomenon. This pattern involves consumption of large amounts of land, and of other resources as well, such as fossil fuels to supply motor vehicles, water lost to runoff from extensive impermeable surfaces, consumer goods to fill large houses, and time spent in travel.
Land-use and transportation practices evolved rapidly. As farmland and forest at the urban edge were converted to residential use, standard housing densities declined to one or two households per acre, a radical departure from traditional city and town densities of five to ten or more per acre. Land-use mix declined; instead of co- locating residential, commercial, recreational, educational, and other uses, planners began separating distinct uses, often to comply with local zoning laws (Figure 15.4). As a result, long distances between destinations such as home, school, work, and shopping became the norm. With longer trip distances, walking and bicycling became less practical. Mass transit could not be supported in low- density communities because too few people were clustered near trip origins and destinations to justify transit stations. Transportation planners estimate a housing density of at least twelve dwelling units per acre is needed to support rapid rail service and seven units per acre to support local bus service every half hour
818
(Booth, Leonard, & Pawlukiewicz, 2002).
Figure 15.4 Schematic Comparison of Street Networks and Land Use in a Traditional Neighborhood and in an Area of Sprawl
Source: Courtesy of Thomas E. Low, DPZ, Charlotte, North Carolina.
The traditional town and city design in the upper panel features a gridlike arrangement of streets, high connectivity, placement of different land uses near each other, and high density. In the loop and lollipop arrangement of streets shown in the lower panel, different parcels of land are developed independently and not linked to each other, resulting in low connectivity, low-density land use, and separation of different land uses.
Many of the communities designed and built to support the post– World War II American Dream were subsequently found to have
819
unintended consequences for health. Features of such communities, reflecting both land-use and transportation decisions, are described in the following paragraphs and in Table 15.2.
Table 15.2 Comparison of Sprawl and Smart Growth
Sprawl Smart growth/New Urbanism/Transit- oriented development
Land-use mix Low High Density Low High Connectivity Low High Activity centers
Busy arterial roadways, automobile- oriented
Dense, pedestrian-friendly commercial centers
Design Designed for easy automobile passage
Designed for pedestrian legibility and aesthetics
Transportation Automobile-centered Balance of walking, cycling, transit, and use of automobiles
Parks and green space
Emphasis on private spaces (yards); parks reachable by car
Emphasis on public spaces (parks), parks reachable by foot
Per capita carbon footprint*
Higher Lower
* See Jones & Kammen, 2014.
Separation of Land Uses Through Zoning When planners make zoning decisions, they determine how specific parcels of land and areas within a community are used. Initially intended to protect people from harmful industrial exposures, zoning decisions now often separate residential neighborhoods from employment and services, and can encourage social isolation through the segregation of populations by age, family size, or income (Text Box 15.2).
820
Text Box 15.2 Policies That Regulate Land Use Land-use regulations are largely the domain of local governments. These regulations range from local building codes to larger scale zoning and subdivision regulations. They can either promote or hinder the development of healthy places. For example, a regulation that limits the number of alcohol outlets may enhance the quality of community life, whereas one that requires a minimum number of parking spaces may encourage automobile use and reduce walkability.
Building codes prescribe the bulk, scale, massing, and style of structures. For example, codes that require uniform setbacks of buildings from streets, and retail space on the first floors of urban buildings, contribute to a pedestrian- friendly realm at the street level. Appropriate scaling of buildings, continuity of building materials, and a coherent design vocabulary all help to establish a sense of place for a community, creating environments where people like to live, work, and play or to visit.
Zoning codes prescribe certain locations as appropriate for specific uses, such as residential, commercial, industrial, recreational, or open space, and regulate parameters such as density, lot coverage, and building setbacks. Zoning was begun in the early 1900s to protect public health, safety, and welfare and to enforce social norms (Schilling & Linton, 2005). Although zoning has helped communities to separate incompatible land uses, such as noxious industries and homes, it has not always delivered high-quality, livable environments. In fact the attractive old neighborhoods of Charleston, Annapolis, and Georgetown would violate the current zoning codes of many cities because of their narrow streets, mixed land uses, and other design features. Innovative zoning codes, such as the model codes developed by the American Planning Association (2006), can be used to promote healthy community design.
821
Subdivision regulations operate on a larger scale than zoning, governing the layout and form of entire communities. When a large parcel of land is being developed, it is typically subdivided into smaller parcels. Subdivision regulations control the process of subdividing, or platting, land and laying out streets, lots, and other land uses. Subdivision regulations are particularly critical to community design because they govern street network arrangements, open space placement, and connectivity both within the development and with adjacent developments.
Metropolitan planning organizations (MPOs) were created as a result of the Federal-Aid Highway Act of 1962, which required, as a condition of federal highway funding, that all urbanized areas with at least 50,000 people undertake “continuing, comprehensive, and cooperative” planning. MPOs are assemblies of local elected officials and state agency representatives responsible for planning the use of transportation funds in their metropolitan areas. Such work has direct implications for land use and economic development and, ultimately, for health. The large number of political jurisdictions in a typical MPO—often dozens of towns, cities, counties, law enforcement agencies, school systems, utility districts, and other entities—can stymie smooth functioning. Some MPOs are actively involved in planning for healthy communities (Federal Highway Administration [FHWA], 2012).
Comprehensive plans are official documents adopted by local governments that serve as guides for making land-use changes, preparing capital improvement programs, and determining the rate, timing, and location of future growth. They usually focus on land use, transportation, community facilities, parks , and recreation. Some comprehensive plans include detailed functional plans that address specific elements such as housing, educational campuses, public transit, parks and open space, streets and vehicle circulation, historic preservation, economic development, bicycle and pedestrian access and connectivity, and health and emergency services. Some comprehensive plans include a chapter focused on health aspects of planning (Ricklin &
822
Kushner, n.d.). Sources: Adapted from Frumkin, Frank, & Jackson, 2004, pp. 207–209; Dannenberg, Frumkin, & Jackson, 2011, pp. 22–23, 381.
Low-Density Development Planners in the nineteenth-century city responded to disease epidemics associated with crowding by establishing limits on the number of residences and buildings allowed per unit area. Limiting the density of development has become standard in suburban and rural land-use planning, contributing to urban sprawl.
Dispersion of Activity Centers In contrast to the compact downtown areas of traditional cities and towns, commercial and recreational activities in sprawling metropolitan areas are often arrayed along long stretches of busy roads, in strip malls, big-box stores, and office parks. Traditional gathering places such as parks, plazas, and sidewalks are rarely found in such areas.
Automobile-Oriented Transportation Systems Sprawling metropolitan areas have extensive roadway systems. Multilane freeways, divided highways, vast parking lots, drive- through opportunities for everything from food to banking to laundries, and a relative absence of sidewalks and bicycle paths define a mode share (the distribution of different modes of travel) that emphasizes the automobile over other modes, such as walking or bicycling. Various estimates suggest there are three to eight parking spaces per car in the United States, affecting millions of acres of land in terms of impervious surfaces and water runoff, and competing with land uses that are more beneficial to health such as parks, housing, community facilities, and businesses.
Disinvestment in Central Cities A key feature of urban history during the second half of the twentieth century was the flight of middle- and upper-class people, capital, and economic opportunities from central cities (Wilson, 1987, 1997). There was a prominent racial overlay in the United States; the racially unbalanced migration was dubbed white flight.
823
In many cities this left large swaths of concentrated poverty with large minority populations and high rates of unemployment, substandard housing, underfunded public schools, social breakdown, and poor health. In public health the term urban health became synonymous with “the health of poor people,” raising profound questions of equity and social justice (U.S. Environmental Protection Agency [U.S. EPA], 2013).
824
Community Design and Health The design of neighborhoods, towns, cities, and transportation systems can have wide-ranging effects on health (Text Box 15.3). As discussed in the following sections, these effects operate through the physical activity people get, the air they breathe, their risk of injuries, their access to healthy food, the noise they endure, and their contact with each other, which affects social capital and mental health. All of these effects, in turn, contribute to health disparities for vulnerable populations.
825
Text Box 15.3 Impacts of Community Design on Health
Looking out his bedroom window, Renaldo Ruiz sees a nearby park that has a playground, a soccer field, and shade trees that help him cool off in the summer. But he rarely goes to the park because there is a ten-lane freeway between his window and the park. With no safe pedestrian crossing, the freeway is an impenetrable barrier. His parents worry about traffic danger and seldom let him play outdoors by himself or walk to school. Most afternoons, Renaldo is driven home, plays video games with his siblings, and watches television. Renaldo's environment makes it difficult for him to be physically active.
In April 2010 in East Wenatchee, Washington, a 13-year- old girl and a 14-year-old boy suffered serious injuries when struck by an automobile near North Georgia Avenue and Grant Road. One vehicle had slowed for the pedestrians, but the car in the second lane failed to see the pedestrians and hit them. The crash occurred just east of an intersection where another 14-year-old pedestrian had been hit by a car four months earlier. The city's streets department reported plans to add a crosswalk, a pedestrian refuge island, and lighted signs to improve safety, acknowledging that crosswalk markings alone would be inadequate to protect pedestrians.
In New York City, Linda Lee's life revolves around four destinations within a few blocks. Drop off her children, ages 3 and 5, at Greenways Day Care Center. Make sure her 75-year-old grandmother, who uses a wheelchair, makes it to lunch at the Meridian Senior Center. Then, all too frequently, take her son, who has asthma, to the Jackson Children's Clinic. And as summer arrives, watch her children burn off limitless energy at the public swimming pool. The mayor is considering closing all four to combat a $650 million deficit. In making steep cuts to
826
dozens of agencies and programs, it was inevitable that some neighborhoods would suffer disproportionately.
Source: Adapted from Dannenberg, Frumkin, & Jackson, 2011, chaps. 2, 5, and 9.
Physical Activity and Obesity Land-use and transportation practices of the last century have had major impacts on physical activity levels (Durand, Andalib, Dunton, Wolch, & Pentz, 2011). Sedentary lifestyles have become the norm in the United States. Only 48% of adults in the United States meet the 2008 Physical Activity Guidelines of the Centers for Disease Control and Prevention (2014). A sedentary lifestyle increases the risk of cardiovascular disease, stroke, and all-cause mortality, whereas physical activity prolongs life. A low level of physical fitness is similar to hypertension, high cholesterol, diabetes, and smoking in elevating cardiovascular risk (Lee, 2012). Physical activity protects against cancers of the breast, colon, and other organs (Lemanne, Cassileth, & Gubili, 2013). Physical inactivity in children is of special concern because a physically inactive child is more likely than an active one to become a physically inactive adult (Tammelin, 2005).
Beyond its direct effects on health, physical inactivity is a risk factor for weight gain. Overweight and obesity are defined by body mass index (BMI), calculated by dividing a person's weight in kilograms by height in meters squared. A BMI between 25 and 30 indicates overweight, and a BMI of 30 or more signals obesity. Overweight and obesity are creating one of the most pressing and costly public health crises in the United States and globally (Figure 15.5). In 1960, one in four American adults was overweight; by the 2011 to 2012 period that proportion had increased to two in three (Ogden, Carroll, Kit, & Flegal, 2014). The prevalence of obesity has followed a similar trajectory, reaching one in three in the 2011 to 2012 period (Ogden et al., 2014). These trends have occurred in children as well as in adults, and disproportionately in poor and minority communities. Obesity is a risk factor for overall mortality, cardiovascular mortality, diabetes, hypertension, depression, and gall bladder disease. An analysis of overweight- and obesity-related medical costs found that between 5% and 10% (depending on the calculation methods used) of health care dollars in the United States
827
are spent on these largely preventable conditions (Tsai, Williamson, & Glick, 2011). Unforeseen societal costs of rising obesity range from increased fuel costs for airlines as the average weight of their passengers has risen (Dannenberg, Burton, & Jackson, 2004) to a need for larger beds in hospitals (Rundle, 2002) and increased load capacity for automobiles (Woodyard, 2007).
Figure 15.5 Percentage of Self-Reported Obesity in Adults in the United States, by State, 2013
Source: Centers for Disease Control and Prevention, 2015a.
Design for Physical Activity Land-use mix, density, connectivity, and design play a significant role in physical activity levels in communities (McCormack & Shiell, 2011). When different land uses (e.g., residential, offices, retail, and schools) are located close to one another, destinations are closer and trip distances shorter, enabling people to travel from place to place on foot or by bicycle (Transportation Research Board and Institute of Medicine [TRB and IOM], 2005). Such utilitarian physical activity becomes a part of the daily routine, and is better maintained over the long term than recreational physical activity.
828
Higher density development also has implications for physical activity. Higher density is associated both with increased walking and bicycling (TRB and IOM, 2005) and with increased transit use. In turn, people who use transit typically walk to and from transit stops, which adds a median of twenty-one minutes of physical activity to each day (Freeland, Banerjee, Dannenberg, & Wendel, 2013).
In sprawling cities, many employment centers, schools, and shopping malls are located in low-density exurban enclaves, far from urban centers or residential subdivisions and accessible only by automobile.
Certain features of street design, such as a highly connected grid or network of streets and the presence of sidewalks or paths, are associated with increased physical activity through walking and bicycling (TRB and IOM, 2005). Many suburban neighborhoods feature low connectivity, with design features such as cul-de-sacs and long block lengths. By increasing trip distances, these features discourage walking and bicycling. Urban planners typically use a quarter or a half of a mile as the longest distance most people are willing to walk to a destination.
Other community design features, including shade, safety, and natural amenities such as trees, scenery, and absence of hills, are also associated with increased walking trips (TRB and IOM, 2005). In addition, perceptions of neighborhood safety and crime affect decisions about outdoor activity, including walking (Frank & Engelke, 2000). High or low local temperatures, rain, snow, and poor air quality also may discourage outdoor physical activity.
More than 12% of commuters walk or bike to work in cities such as Boston, Washington, DC, and Seattle, where land-use mix, density, connectivity, and design are favorable. In contrast, fewer than 2% of commuters walk or bike to work in cities such Oklahoma City, Wichita, and Fort Worth, where the built environment is not conducive to active transportation (Alliance for Biking and Walking, 2014).
Parks and Green Space Public parks provide places in which people can be physically active, enjoy contact with nature and with other people, and relax.
829
Parks add substantially to the quality of life of a city's residents. Many great city parks, such as New York's Central Park or San Francisco's Golden Gate Park, were designed and built early in those cities' growth, while large tracts of land were still available. Other, often smaller, parks have been added to cities during urban redevelopment efforts, to make those cities more attractive and livable. A commonly used benchmark for city planners recommends 10 acres of parkland per 1,000 People. People use parks more when the parks are conveniently located, especially within safe walking distance of their homes (McCormack, Rock, Toohey, & Hignell, 2010). Urban planners typically try to create a mix of accessible, small, local parks, distributed throughout a city, and a few bigger parks with space for larger recreational facilities, such as ball fields and longer walking and biking trails. More information on parks appears in Chapter 25.
Air Quality Air pollution threatens health, as described in detail in Chapter 13, and patterns of urbanization and transportation have emerged as primary determinants of both local and global air quality. Air pollutants from the transportation sector include greenhouse gases that contribute to climate change, criteria air pollutants, and air toxics. The transportation sector accounts for between 25% and 30% of greenhouse gas emissions in the United States, for more than half of the oxides of nitrogen and carbon monoxide, and for substantial portions of ozone precursors and some air toxics.
Pollution exposure from cars and trucks is most marked near heavily trafficked roads or in places with particularly high emissions levels and/or physical properties (such as urban canyons) that impede air circulation and trap pollutants. Many of these pollution hot spots are in low-income neighborhoods that also face other environmental and social threats to health (see Chapter 11).
In cities, heavy traffic secondary to regional land-use patterns is a major source of air pollutants. This operates on a regional scale for air pollutants such as ozone, and on the small scale of city blocks for pollutants such as particulate matter, where denser neighborhoods may expose people to high levels of pollutants due to proximity to traffic. One solution is cleaner vehicles; for example, technological advances have reduced vehicle carbon monoxide emissions by at
830
least 80% in major urban areas of wealthy nations (McDonald, Gentner, Goldstein, & Harley, 2013). In contrast, traffic remains a major source of urban air pollution in the cities of low- and middle- income nations (Global Road Safety Facility at the World Bank and Institute for Health Metrics and Evaluation, 2014) (Figure 15.3).
In addition to cleaner technology, reducing vehicle miles traveled (VMT) in single-occupancy vehicles is a primary way to reduce air pollution and the resulting health consequences in both the local and global environments. This is a matter of transportation planning. After rising steadily for many decades, per capita VMT has been falling and total VMT has been leveling off in the United States since about 2007 (McCahill, 2014). This change is due to a number of factors including the 2008–2009 recession, a rise in telecommuting, and increasing preferences among young adults to live and work in areas that are less automobile dependent. This decline in per capita VMT contributes to less motor vehicle exposure and fewer motor vehicle–related injuries. This underscores the need for alternative modes of dependable and safe transportation as a goal for community design and transportation planning.
Injury Risk Community design has considerable influence on the risk of injuries, especially those related to transportation (see Chapter 23). Since the first recorded motor vehicle collision in 1896, in New York City, motor vehicle crashes and fatalities increased in the United States, peaking in the 1970s and 1980s. In 2012 in the United States, 33,561 people were killed on the roads (roughly 23,000 in vehicles, 5,000 on motorcycles, and 5,500 pedestrians and cyclists), and 2,362,000 were injured (National Highway Traffic Safety Administration [NHTSA], 2014). Traffic fatalities remain the leading cause of death in children and young adults through 44 years of age (CDC, 2015b). Globally, road injuries have risen to a leading position among causes of death—in fact they are the top cause of death among males ages 5 to 29 (Global Road Safety Facility at the World Bank and Institute for Health Metrics and Evaluation, 2014).
The sprawling communities that characterize many American cities, and increasingly cities around the world, encourage automobile use.
831
While vehicle speeds are constrained on crowded urban roadways, more vehicle miles traveled and higher speeds—meaning greater risk of injuries and fatalities—typify roads and highways farther from the urban core. States with lower population densities experience higher rates of traffic fatalities per vehicle mile traveled (Clark & Cushing, 2004). Similarly, communities with greater urban sprawl have higher road fatality rates, likely due to the higher “exposure” to VMT in these communities (Ewing, Schieber, & Zegeer, 2003). One approach to prevention, therefore, would be decreasing travel demand, because reducing miles driven would reduce the likelihood of collisions for all road users (Fuller & Morency, 2013). In fact, as expected, there is evidence that shifting from automobile travel to mass transit reduces road fatality rates (Stimpson, Wilson, Araz, & Pagan, 2014).
Another environmental approach to injury prevention focuses on the design of roadways. Interstate highways incorporate design features such as limited access interchanges and center medians that give them a relatively low rate of fatalities per VMT. Local roadway design uses traffic-calming techniques such as roundabouts, one-way streets, and speed bumps to alter driver behavior and reduce crash likelihood and severity (Bunn et al., 2003). This relatively low-cost approach is suitable for both low- income and high-income settings. For example, the simple installation of speed bumps on roads near schools in communities around Durban, South Africa, reduced serious pedestrian and vehicle collisions by more than 20%, and fatal collisions by more than 50% (Nadesan-Reddy & Knight, 2013). These environmental design strategies complement other public health approaches to road safety, including improved road and vehicle design and policies related to speed limits, alcohol-impaired driving enforcement, and teen licensure, which have successfully reduced traffic fatalities per VMT in the United States in recent decades (NHTSA, 2014) (see Text Box 15.4).
832
Text Box 15.4 Safe Walking and Cycling Walking and bicycling are known as active transportation because they entail physical activity. When physical activities are a part of a daily routine, such as commuting to work or school, they are more easily sustained than if they require the discipline of gym visits. Healthy community design facilitates active transportation.
It is essential that pedestrians and cyclists be safe on the streets—and if streets are primarily designed for vehicles, that goal can be elusive. Among those killed in motor vehicle crashes in the United States in 2012, 14% were pedestrians and 2% were bicyclists (NHTSA, 2014). While rates of pedestrian fatalities have generally declined over the past twenty years, this may be due at least in part to reduced walking—a Pyrrhic victory in a society suffering from sedentary lifestyles and the associated health consequences. Interestingly, pedestrian fatality rates vary greatly by city, suggesting that local circumstances can play a major causal role. After adjusting for walking rates, sprawling cities such as Jacksonville, Houston, and Phoenix, which have less pedestrian infrastructure, have the highest pedestrian fatality rates. Older, more compact cities, such as New York and Boston, have far lower pedestrian fatality rates (Alliance for Biking and Walking, 2014, p. 84). This is ironic, given that people walk much more in the latter cities! Similarly, pedestrian and bicyclist injury rates are lower in Holland and Germany than in the United States; in these countries, walking and bicycling are more common, and the pedestrian and cycling infrastructure far better developed (Pucher & Dijkstra, 2003). Good walking and cycling infrastructure—an environmental approach—can both encourage walking and cycling and make these activities safer.
What infrastructure is needed? For pedestrians, this includes ample sidewalks; clearly marked, visible, and well-lit crosswalks; and traffic signals timed to allow even slow walkers (such as children, the elderly, and people with
833
disabilities) time to get across the street. For cyclists, optimal infrastructure includes bicycle paths that are physically separated from traffic. When this is not possible, design strategies can minimize the risk of vehicle-bicycle encounters; examples of such strategies are bike boulevards that divert cyclists from major roads to small side streets, separate traffic signals for cyclists, and traffic-calming measures that greatly slow vehicles. The concept of complete streets holds that streets should serve all users— vehicles, transit riders, cyclists, and pedestrians—with a focus on multimodal accessibility and safety (McCann, 2013) (Figure 15.6). Such streets can trigger a virtuous cycle, making more people feel safe while walking and cycling and thus increasing the numbers of pedestrians and cyclists, thus increasing their safety, and so on (Jacobsen, 2003).
Figure 15.6 An Example of Complete Streets in Copenhagen, Where Many Streets Are Designed to Accommodate Pedestrians, Bicyclists, Transit, and Automobiles
Source: Pedestrian and Bicycle Information Center, Image Center, 2009.
At present, improving infrastructure for pedestrians and
834
bicyclists is a low priority in U.S. transportation policy. Although pedestrians and bicyclists accounted for 16% of roadway fatalities in 2012, pedestrian and bicycle infrastructure received less than 2% of federal highway spending that year (FHWA, 2015). Pedestrian and bicycle advocacy groups can influence transportation design choices and the inclusion of pedestrian and bicycle facilities in design decisions made by local transportation planners.
Healthy Food Healthy eating is a central strategy in reducing obesity and chronic diseases. Chapter 19 offers a detailed discussion of the food system and its impact on public health; here, we focus on one aspect, the food environment in communities. This includes the location of food stores and the availability of healthy, affordable foods at those locations (Glanz, Sallis, Saelens, & Frank, 2005) (Figure 15.7). Low- income communities often have a disproportionate number of unhealthy, fast food outlets and limited access to grocery stores that sell high-quality fruits and vegetables, a phenomenon known as a food desert (Lovasi, Hutson, Guerra, & Neckerman, 2009; Walker, Keane, & Burke, 2010). While there is debate about how food deserts affect nutritional choices and health—for instance, food prices, cultural preferences, and transportation to markets may be as important as the nearby presence of markets—the bulk of the evidence suggests that readily available fresh food options improve nutritional health (Larson, Story, & Nelson, 2009; Whitacre, Tsai, & Mulligan, 2009).
835
Figure 15.7 Access to Healthy Food Options Source: Jorchr, 2006. Permission granted under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation.
Zoning, transportation decisions, public infrastructure development, and other land-use decisions may encourage or discourage development of a healthy food environment. Strategies to improve the food environment include providing incentives for grocery store and supermarket development, restricting fast food retail store density (Mair, Pierce, & Teret, 2005), and encouraging community-supported agricultural programs, farmers' markets, street carts with fruit and vegetables, and community gardens. Land-use policy and environmental changes are emerging as important loci for public health interventions to improve the food environment (Story, Kaphingst, Robinson-O'Brien, & Glanz, 2008).
Noise City dwellers routinely endure unwanted noise from neighbors, industrial and commercial activities, motor vehicles, and aircraft. Noise exposure contributes to a range of health problems: hearing loss, stress, anxiety, increased blood pressure, heart disease,
836
changes in hormonal levels, sleep disturbances, and performance difficulties at work and school (Passchier-Vermeer & Passchier, 2000; Zaharna & Guilleminault, 2010). Noise-induced hearing loss begins to occur with prolonged exposure to noise levels over 70 decibels (dB).
Two leading sources of noise in cities are traffic and aircraft. There are several ways to reduce community exposure to transportation noise: reduce the amount of noise produced per vehicle, reduce the number or speed of vehicles driving past communities, construct sound barriers around highways and other noise sources, use road surface materials that produce less noise, and route new or expanded highways through less densely populated areas (FHWA, 2006). Aircraft noise exposure can be reduced by compatible land- use zoning, installing sound insulation in buildings, and making changes in runway use, flight path location, and hours of operation.
Social Capital Social capital refers to the social networks and resources within a community and the norms of reciprocity and social benefit that arise from them (see Chapter 9). The strength of these resources and networks reflects the level of involvement in such local organizations as community centers, churches, and locally focused philanthropic organizations, and also the existence of support systems that ensure disadvantaged community members have access to food, shelter, and health care. Social capital is associated with a wide range of health benefits. Indicators of low social capital, such as social isolation and income inequality, are associated with higher mortality (Kawachi, Subramanian, & Kim, 2008). Social capital also contributes to resilience in the face of disaster, as described in Chapter 24. After hurricanes, floods, and earthquakes, in communities with high levels of social capital, friends, families, and neighbors help each other in the immediate response and disaster recovery phases.
Community design may affect social capital in several ways. Long commute times reduce social capital, perhaps by reducing the time or the will to become involved in social activities (Besser, Marcus, & Frumkin, 2008). According to Robert Putnam (2000, p. 213), “each 10 additional minutes in daily commuting time cuts involvement in community affairs by 10 percent.” Another feature of community
837
design relevant to social capital is the presence of “great good places”—the “cafés, coffee shops, bookstores, bars, hair salons, and other hangouts at the heart of a community” where people gather to socialize (Oldenburg, 1989). Communities that have an ample stock of such places and are designed to encourage walking may provide more opportunities for social interchange (Leyden, 2003). A third feature of community design that may affect social capital is the mix of housing types. Neighborhoods suitable for young families often have little housing suitable for “empty nesters” or for elders who can no longer drive. Zoning codes that permit accessory dwelling units, also known as granny flats, can help to address this problem. Without such options, people are obliged to move from their communities as they age, which deprives them of the opportunity for aging in place and disrupts community networks formed over many years (Alley, Liebig, Pynoos, Banerjee, & Choi, 2007). Social capital contributes to mental well-being in elders (Nyqvist, Forsman, Giuntoli, & Cattan, 2013). This realization has given rise to a field called environmental gerontology, reflecting the recognition that community design has a great impact on the well- being of elders.
Mental Health Mental health can be affected by a variety of factors in the social, natural, and built environments, some of them related to community design (Evans, 2003) (also see Chapter 9). Two have already been mentioned: the effects of noise (as from traffic) and of automobile commuting in heavy traffic. Third, commuting may also trigger anger, aggression, and loss of impulse control, a phenomenon known as road rage (Asbridge, Smart, & Mann, 2006). Fourth, and on a more positive note, parks and green space can provide opportunities for relaxation, attention restoration, reduced stress, and social interactions, as discussed in Chapter 25. Finally, since physical activity is an effective antidepressant (Mammen & Faulkner, 2013), places that facilitate and encourage physical activity, such as parks, trails, and sidewalks, can help to improve mental health.
Social Equity and Environmental Justice Vulnerable populations, including children, the elderly, persons
838
with disabilities, members of racial and ethnic minorities, and people with low incomes, are at particular risk of adverse health impacts from poorly designed communities (see Chapter 11). Such people may have less access to parks and open space for physical activity and to convenient grocery stores for healthy food choices. They may live near busy roads that make walking difficult and contribute to high noise levels and poor air quality. They may not have an automobile and may be poorly served by public transit, thus limiting their access to many of the goods and services available to other members of society. For children, for whom outdoor play is a vital part of growing up, the absence of nearby parks and green spaces is a special burden (American Academy of Pediatrics, Committee on Environmental Health, 2009). In general, strategies to promote healthy community design for vulnerable populations yield benefits for all members of society (U.S. EPA, 2013). One particularly promising approach to improving community design for vulnerable populations is the health impact assessment, which is described in Text Box 15.5.
839
Text Box 15.5 Health Impact Assessment: A Tool for Land-Use and Transportation Decision Making Health impact assessment (HIA) is a tool that focuses on the health consequences of decisions in nonhealth sectors, including community design. An HIA can be used to evaluate the potential health effects of a project before it is built or a policy before it is implemented. It can provide recommendations to increase positive and minimize adverse health outcomes. A major benefit of the HIA process is that it brings public health issues to the attention of decision makers in areas outside traditional public health concerns, such as transportation and land use. HIA is defined as “a systematic process that uses an array of data sources and analytic methods and considers input from stakeholders to determine the potential effects of a proposed policy, plan, program, or project on the health of a population and the distribution of those effects within the population. HIA provides recommendations on monitoring and managing those effects” (National Research Council, 2011). For example, an HIA of the multibillion-dollar Atlanta Beltline, a parks, trails, and transit and land, redevelopment project, led to the incorporation of health issues into the decision support tool used to guide BeltLine planning, early construction of parks and trails, and inclusion of public health professionals on decision-making boards and project advisory committees (Ross et al., 2012). In San Francisco an HIA of a project to build expensive condominiums while displacing the current low-income tenants led to an agreement with the developer to provide one-for-one replacement housing for the people being displaced (Bhatia, 2007).
The major steps in conducting an HIA are
Screening to identify a proposed project or policy for which an HIA would be useful.
840
Scoping to identify which health effects to consider.
Conducting an assessment to identify the people who may be affected and how they may be affected.
Developing recommendations for changes to the proposal to promote positive or mitigate adverse health effects.
Reporting to present the results to decision makers.
Evaluating and monitoring to determine the effect of the HIA on the decision process.
HIAs are similar in some ways to environmental impact assessments (EIAs), which are mandated analyses of the potential impacts of policies or projects on environmental outcomes such as air and water quality. Under existing laws, EIAs can incorporate health impacts but seldom do (Bhatia & Wernham, 2008). Unlike EIAs, HIAs can be either voluntary or regulatory processes that focus on health outcomes such as obesity, physical inactivity, asthma, injuries, mental health, social capital, and social equity. An HIA encompasses a wide array of qualitative and quantitative methods and tools. HIAs can be completed in a few days or may take many months, depending on availability of time and resources.
Numerous HIAs have been performed in Europe, Australia, Canada, and elsewhere. In the United States, over 350 HIAs have been conducted by public health departments, universities, community-based organizations, and private firms. Many HIAs have been funded by foundations such as the Robert Wood Johnson Foundation and Pew Charitable Trusts (see, e.g., www.healthimpactproject.org) and by the Centers for Disease Control and Prevention. Some health departments have conducted HIAs without external funding. Training to conduct HIAs is available in a free online course from the American Planning Association and in some universities and health departments.
841
Cities as Healthy Human Habitats With a majority of the global population now living in cities, it is essential to envision and create cities that are healthy human habitats, places in which people can thrive. As described earlier, the built environment—from the scale of neighborhoods to the scale of metropolitan areas—has wide-ranging impacts on human health and well-being. This recognition, in turn, permits us to design places that support human thriving.
Linking Healthy Cities with Other Goals The goal of healthy cities is closely linked to other goals. Cities must also be sustainable, resilient, and ecologically functional—three frameworks that imply physical and social arrangements that overlap in many ways with those of healthy cities (Figure 15.8).
Figure 15.8 Overlapping Frameworks for Healthy Community Design
Sustainable cities implement many of the sustainability principles described in Chapter 3. They emphasize the use of renewable energy; transportation systems that balance motor vehicle use with walking, cycling, and transit; water conservation; waste minimization and recycling; environmentally friendly
842
buildings; and protection of natural areas. Many have implemented innovations such as urban agriculture, the use of information technology to optimize the function of such systems as transportation, the sharing economy, and green roofs (Portney, 2003; Newman & Jennings, 2008). Importantly, sustainable cities also emphasize social equity and good governance. A key feature of sustainable cities is the use of metrics (or indicators) so that city governments and civil society can track progress toward goals (Reed, Fraser, & Dougill, 2006; Sustainable Cities International, 2012). These indicators usually include direct metrics of health and also many health-relevant metrics (such as air quality). Cities that routinely score high on indices of sustainability include Frankfurt, London, Amsterdam, Copenhagen, Oslo, Vancouver, San Francisco, New York, Curitiba, Bogotá, Mexico City, Melbourne, and Singapore.
Eco-cities are closely related to sustainable cities, but with a strong emphasis on the ecological function of the city (Yang, 2012). Eco- cities aim to reduce energy use, to shift to renewable energy sources such as solar and wind, to capture and reuse rainwater, and to plant local vegetation—in many ways mimicking the function of the land before it was a city. This framework emphasizes ecosystem services (introduced in Chapter 2) at the urban level (Douglas, 2012; Gómez- Baggethun & Barton, 2013), and the development of a self-sufficient local economy, one that uses local resources. As a corollary to this framework, eco-city advocates promote voluntary simplicity in lifestyle choices and reduced material consumption.
Resilient cities are cities with “the capacity…to survive, adapt, and grow no matter what kinds of chronic stresses and acute shocks they experience.” This capacity is distributed across “individuals, communities, institutions, businesses, and systems within a city” (100 Resilient Cities, 2015). The City Resilience Framework, introduced in 2014 by the private firm Arup and the Rockefeller Foundation (Arup and Rockefeller Foundation, 2014), includes many of the elements also present in the sustainable city and eco- city frameworks, but two—fostering long-term and integrated planning and ensuring continuity of critical services—underlie a special orientation toward resiliency. As long-term challenges to cities—climate change, population growth, and resource scarcity— grow, and as shocks become more likely, this orientation is highly
843
relevant (Coyle, 2011).
Healthy Communities and Cities It is within this context that public health aims to promote healthy communities and cities. This undertaking has a long history. In a landmark 1926 decision (Village of Euclid v. Ambler Realty), the U.S. Supreme Court upheld a local government's authority to regulate land use through zoning, citing the protection of public health as part of its justification. In recent years urban planners, transportation engineers, and related professionals have rediscovered their professional links to public health, and public health professionals have rediscovered the importance of community design in promoting health(Malizia, 2005; Dannenberg et al., 2011). These efforts have yielded many insights into the unintended health consequences of contemporary land-use and transportation decisions, and also many strategies for promoting health through people-centered community design (Capon & Blakely, 2007; Gehl, 2010).
On the global scale the Healthy Cities program, begun in 1986 by the World Health Organization (WHO), was the first widespread, community-level application of an ecological health promotion model to highlight the links between people's behavior and their environment (www.who.int/healthy_settings/types/cities/en). The 11 initial European cities now anchor a global movement that numbers over 4,000 cities. Healthy Cities has also inspired the creation of WHO's Healthy Settings program, which brings health promotion not only to cities but also to villages, workplaces, universities, marketplaces, and prisons. Healthy Cities uses a set of guiding principles focused on the creation of healthy communities and individuals (Barton & Grant, 2013).
Cities are complex systems and urban health is dependent on many interactions (Rydin et al., 2012). Systems thinking, as introduced in Chapter 2, is essential, and a growing field of research is approaching healthy urban design through this lens (Bai, Nath, Capon, Hasan, & Jaron, 2012; Douglas, 2012). Systems approaches can help decision makers identify potential intervention points, understand policy resistance, and be alert for unintended consequences. Accordingly, in 2011, the International Council for Science (www.icsu.org) launched Health and Well-Being in the
844
Changing Urban Environment: A Systems Analysis Approach, a ten- year, global, interdisciplinary science program that aims to build knowledge and capacity for decision making in cities and thereby protect and promote human health in sustainable ways.
Many strategies that promote human health, as well as sustainability, resiliency, and ecological function, are found in an approach known as smart growth (Geller, 2003). The smart growth principles (Text Box 15.6) were established primarily for their economic, environmental, and aesthetic benefits. They are designed to work with market forces, not by dictating where or how Poeple must live, but by producing attractive and affordable options. Many people prefer to live in walkable communities and near multiuse trails—assets that predict more walking (Berry et al., 2010). Smart growth principles also mitigate climate change (Younger, 2008), which in turn promotes health—examples of co- benefits.
845
Text Box 15.6 Smart Growth Principles to Promote Equitable, Healthy, and Sustainable Communities 1. Mix land uses to reduce distances among destinations.
2. Take advantage of compact building design.
3. Create a range of housing opportunities and choices.
4. Create walkable neighborhoods connected to multiple destinations.
5. Foster distinctive, attractive communities with a strong sense of place.
6. Create parks and preserve open space, farmland, natural beauty, and critical environmental areas.
7. Strengthen and direct development toward existing communities.
8. Provide a variety of transportation choices, including walking, cycling, public transit, and automobiles.
9. Make development decisions predictable, fair, and cost- effective.
10. Encourage community and stakeholder collaboration in development decisions.
Source: Adapted from U.S. EPA, 2015.
Smart growth typically incorporates strategies familiar to public health. For example, it emphasizes community and stakeholder involvement in planning. To better serve vulnerable populations, it can incorporate universal design principles (Text Box 15.7) to ensure access to community facilities regardless of ability. Smart growth principles are implemented through a combination of market forces, social marketing, and deliberate policymaking, often with the active participation of public health professionals (De Ville & Sparrow, 2008).
846
Text Box 15.7 Principles of Universal Design Universal design is the designing of products and environments so they are usable by all people, to the greatest extent possible, without the need for adaptation or specialized design.
1. Equitable use: the design is useful and marketable to people with diverse abilities.
2. Flexibility in use: the design accommodates a wide range of individual preferences and abilities.
3. Simple and intuitive use: use of the design is easy to understand, regardless of the user's experience, knowledge, language skills, or current concentration level.
4. Perceptible information: the design communicates necessary information effectively to the user, regardless of ambient conditions or the user's sensory abilities.
5. Tolerance for error: the design minimizes hazards and the adverse consequences of accidental or unintended actions.
6. Low physical effort: the design can be used efficiently and comfortably and with a minimum of fatigue.
7. Size and space for approach and use: appropriate size and space are provided for approach, reach, manipulation, and use regardless of user's body size, posture, or mobility.
Source: Center for Universal Design, 1997.
Other frameworks overlap with smart growth. New Urbanism is an architectural and planning movement whose principles similarly include walkable neighborhoods, a range of housing choices, mixed land uses, participatory planning, and revitalization of urban neighborhoods (www.cnu.org). A traditional neighborhood
847
development (TND) is a compact, mixed-use, transit-oriented, pedestrian-friendly community of a type that was common before World War II. A transit-oriented development (TOD) follows similar principles with a focus on easy access to public transit. A brownfield redevelopment often incorporates a mixed-use, walkable community while focusing on cleaning up and reusing a contaminated urban area (www.epa.gov/brownfields). New York City's Active Design Guidelines (www.nyc.gov/adg) highlight the design of outdoor and indoor spaces to promote physically active lifestyles.
The elements of smart growth are mutually reinforcing. For example, land-use strategies that support compact development and mixed use create the density needed to make mass transit economically feasible. Choices such as selecting sites for schools near children's homes and providing safe walking routes to such schools encourage children's physical activity, reduce automobile trips, and offer benefits for the larger community. Infrastructure investments in sidewalks and bicycle paths, combined with policy initiatives such as bicycle parking and showers at workplaces and more costly automobile parking, can lead to changes in travel behavior. For example, Portland, Oregon, experienced a dramatic increase in bicycle usage after expanding its bicycle infrastructure (Figure 15.9). Other solutions that reduce traffic congestion are collectively known as transportation demand management (TDM). These measures include transit, employer, and ride-sharing incentives; dedicated highway lanes for high-occupancy vehicles; car insurance rates based on number of miles driven per year; increased charges for or reduced availability of parking spaces; and promotion of telecommuting.
848
Figure 15.9 Relationship Between Growth of Bicycle Infrastructure and Amount of Cycling in Portland, Oregon
Source: City of Portland Office of Transportation, 2012, p. 9.
Between 1991 and 2012, the City of Portland increased its established bikeways from 79 to 328 miles, and otherwise improved bicycle-related infrastructure, while the number of daily bicycle trips across Portland's four main bridges increased from 2850 in 1991 to 18,794 in 2012 (number of trips extrapolated from peak period counts). Portland has the highest percentage of workers commuting by bicycle (6.1%) among the fifty-two largest U.S. cities (Alliance for Biking and Walking, 2014).
A number of tools are available to facilitate community designs that incorporate smart growth principles and health-promoting attributes. LEED for Neighborhood Development (LEED- ND) is a set of prerequisites and credits used to assess and acknowledge energy efficiency, sustainability, and health promotion characteristics (Text Box 15.8). Health impact assessment, described earlier in Text Box 15.5, is a tool that can be used by public health professionals and others to examine the health consequences of a proposed project or policy prospectively and then formulate recommendations that promote the positive health impacts and mitigate the adverse health consequences of the proposal. A number of organizations, such as the American Public Health Association, National Association of County and City Health Officials, and American Planning Association, provide guidance to
849
their members on incorporating health into community planning (see the For Further Information section at the end of this chapter).
850
Text Box 15.8 LEED for Neighborhood Development Certification Program LEED (Leadership in Energy and Environmental Design) is a third-party certification program managed by the U.S. Green Building Council (USGBC). Under the LEED system, building designers, builders, owners, and operators can benchmark their performance through a series of measurable indicators in areas including location and transportation, materials and resources, water efficiency, energy, sustainable sites, indoor environmental quality, and innovation (www.usgbc.org/leed). In 2008, the USGBC introduced LEED for Neighborhood Development (LEED-ND) (www.usgbc.org/guide/nd). LEED-ND includes twelve prerequisites such as smart location, compact development, and a minimum building energy performance. LEED-ND offers up to 110 possible credits; the number of credits successfully documented by the project builder or developer determines the level of LEED-ND certification achieved (certified, silver, gold, or platinum). Among the design features that receive credits and that also promote health are the following:
Neighborhood schools that promote community interactions and encourage daily physical activity associated with walking and biking.
Bicycle networks that encourage use of bicycles for transportation, thereby encouraging regular physical activity.
Mixed-income diverse communities that promote equitable and socially engaging communities by enabling citizens of a wide range of ages and from varied economic levels, and household sizes to live within a community.
Access to public spaces that provide open spaces close to home and work to encourage physical activity and time spent outdoors.
851
Source: U.S. Green Building Council, 2012.
Other Healthy Community Design Policies Other policies compatible with smart growth principles also promote healthy community design, especially by encouraging physical activity and reducing automobile dependence. For example:
Joint use policies allow community members to share school playgrounds and open space during evenings and weekends (changelabsolutions.org/publications/model-JUAs-national).
Unbundled parking separates the cost of a house or apartment from the cost of the parking space; an expensive parking space may discourage car ownership (the parking space may cost more than the car parked in it) and thereby reduce vehicle miles traveled (www.mapc.org/resources/parking- toolkit/strategies-topic/unbundled-parking).
Rail-to-trail conversion takes advantage of abandoned railroad rights-of-way and in the United States has created over 20,000 miles of multiuse trails for both transportation and recreation (www.railstotrails.org).
Walk Score® calculates the walkability of a location based on proximity to local destinations, and is used in some real estate listings to encourage home purchasers and renters to select walkable neighborhoods (www.walkscore.com).
Bike share programs in hundreds of cities in dozens of countries encourage bicycling for short trips (Shaheen, Guzman, & Zhang, 2012).
Walk-friendly and bicycle-friendly community certification programs encourage communities to improve their walking and cycling infrastructure, sometimes in competition with neighboring communities (www.walkfriendly.org and bikeleague.org/community).
The Future of Global Cities While many of the principles described here may seem most relevant to wealthy nations, there is a robust movement to create
852
healthy cities in the global south. For example, in Bogotá, Colombia, the high-capacity Transmilenio bus rapid transit system moves large numbers of local residents daily and has led to a substantial reduction in air pollution and in motor vehicle–related fatalities. In Windhoek, Namibia, where water is scarce, reclaimed wastewater is used for irrigation, treated surface water is used to recharge municipal boreholes, and water conservation laws are strictly enforced during droughts. Mexico City once had some of the world's worst urban air pollution from industrial and vehicular sources, but a series of policies and programs has now substantially improved the city's air quality (C40 Cities, 2015). These examples give cause for optimism that the typical human habitat—the city—can be a setting that promotes health while advancing sustainability, equity, and prosperity.
853
Summary Land-use patterns and transportation systems in neighborhoods, towns, and cities directly and indirectly affect the health of the people living in those communities. The choices made by decision makers, typically public officials and private developers, about the design of their communities may either promote or undermine physical activity, air quality, safety, social interaction, mental well- being, social equity, and other determinants of health. Communities that follow smart growth design principles receive co-benefits for human health, environmental sustainability, and resiliency. Health impact assessment is a tool that can assist decision makers in considering the potential impacts of proposed plans, projects, and policies on the health of populations. Emerging research and trends in both community development and public health are conducive to increasing collaboration between land-use planners and public health professionals.
854
Key Terms Active Design Guidelines
A manual of strategies developed for New York City to help architects and urban designers create healthier buildings, streets, and urban spaces, based on research and best practices in the field.
active transportation A means of travel that entails physical activity, such as walking or cycling.
bike share program A service in which bicycles are made available to individuals on a short-term, shared basis, usually to travel between two points in an hour or less within a city.
body mass index A measure used to define obesity, calculated as weight in kilograms divided by height in meters squared: kg/m2.
brownfield redevelopment The incorporation of a mixed-use, walkable community into the redevelopment of an abandoned, idled, or underused industrial site where expansion or redevelopment is complicated by real or perceived environmental contamination.
building codes Regulations that prescribe the bulk, scale, massing, and style of structures, and features within those structures, typically to promote safety, habitability, and appearance.
built environment Settings designed, created, modified, and maintained by human efforts, such as homes, schools, workplaces, shops, neighborhoods, parks, roadways, and transit systems.
co-benefits Additional benefits, often favorable to health or sustainability, obtained when a design choice is selected for an unrelated primary purpose.
complete streets Streets designed and operated so that all users, including
855
pedestrians, bicyclists, motorists, and transit riders of all ages and abilities, can safely move along and across the streets.
comprehensive plan An official document adopted by a local government that serves as a guide for making land-use changes, preparing capital improvement programs, and determining the rate, timing, and location of future growth (also known as a master plan or general plan).
connectivity The degree of directness or ease of travel on sidewalks, paths, and streets between two points: high connectivity is an essential component of walkability.
density The number of people, jobs, or dwellings per unit area.
eco-city An environmentally sustainable city, one that minimizes its use of energy, water, and other resources, and promotes the development of a self-sufficient local economy.
food desert An area that has little or no access to the foods needed to maintain a healthy diet and that is typically served by numerous fast food restaurants and/or convenience stores.
food environment All aspects of our surroundings that may influence our diets, including physical locations of stores, marketing, media, and online exposures.
health impact assessment A “systematic process that uses an array of data sources and analytic methods and considers input from stakeholders to determine the potential effects of a proposed policy, plan, program, or project on the health of a population and the distribution of those effects within the population. HIA provides recommendations on monitoring and managing those effects” (National Research Council, 2011).
Healthy Cities program A movement originating in the 1980s, and now led by the World Health Organization, that advocates a health-promoting approach to urban governance, environmental design, and
856
service delivery. historic preservation
The conservation and protection of buildings, objects, landscapes, and other artifacts of historical significance.
joint use policy An arrangement that allows community members to share school playgrounds and open space during evenings and weekends.
land use The manner in which portions of land and/or the structures on them are used, such as commercial, residential, industrial, or recreational uses.
land-use mix The different uses for physical space, including residential, office, retail/commercial, and public spaces including whether district uses are segregated or near each other.
LEED for Neighborhood Development (LEED-ND) A certification system that integrates the principles of smart growth, New Urbanism, and green building with a focus on neighborhood design.
metropolitan planning organization (MPO) A federally required organization of local officials and other interested parties that provides oversight to transportation planning on the regional rather than the single-city level in areas with a population of more than 50,000 persons.
mode share The distribution of different modes of travel such as walking, bicycling, using public transit, and driving a motor vehicle.
New Urbanism An urban design movement that promotes walkable neighborhoods, mixed land use, connectivity, and vibrant public spaces and activity centers.
parks Areas in urban, suburban, and rural settings established for recreational use including physical activity, contact with nature, and mental health restoration, as well as for land preservation.
pollution hot spots
857
Areas with high levels of air pollution, often near heavily used highways.
rail to trail conversion The conversion of abandoned railroad rights-of-way to multimodal trails that can be used for both transportation and recreation.
resilient city A city whose residents and systems have the capacity to survive, adapt, and grow even in the face of short- or long-term disturbances or disasters.
road rage An act of aggression on the part of one driver directed toward another driver, passenger, or pedestrian.
sanitary movement The improvement of housing, water supply, sewage disposal, and solid waste management in the late 1800s and early 1900s that led to major declines in infectious disease rates and other public health improvements.
smart growth An urban planning approach that aims to manage the growth and land use of a community so as to minimize damage to the environment, reduce sprawl, and build livable, walkable, mixed- use communities.
social capital The processes between people that establish networks, norms, and social trust and facilitate coordination and cooperation for mutual benefit.
spatial scale A concept of geographic extent, ranging from small (such as a room or building) to intermediate (such as a neighborhood or city) to large (such as a region, nation, or planet).
subdivision regulations Local ordinances that outline specific requirements for the conversion of undivided land into building lots for residential or other purposes.
sustainable cities Cities developed to meet “the needs of the present without compromising the ability of future generations to meet their own
858
needs” (World Commission on Environment and Development, 1987).
traditional neighborhood development An approach to planning neighborhoods that features human scale, diversity of land uses, walkability, connectivity, and public spaces, drawing inspiration from historical approaches to city planning.
transit-oriented development A pedestrian-oriented, walkable, high-density, high-quality, mixed-use development near a rail or bus station with limited parking, thereby integrating mass transit into land-use planning.
transportation The movement of people and goods from one location to another using various modes, such as walking, bicycling, public transit, cars, trucks, railroads, ships, pipelines, and airplanes.
transportation demand management Policies, programs, and infrastructure to provide efficient transportation of people and goods.
transportation planning A field of planning that focuses on transportation infrastructure, including roads, transit, freight, airports, and bicycle and pedestrian infrastructure.
travel demand A transportation planning concept referring to an individual's or population's need for travel; travel demand is directly related to distances among and between destinations such as homes, schools, workplaces, stores, and recreation facilities.
unbundled parking A policy under which the cost of a parking space is separate from the cost of the associated house or apartment in order to discourage car ownership.
universal design The designing of products and environments so they are usable by all people without the need for adaptation or specialized design.
urban health The health of a population whose members live close together in a city and have common needs for resources, such as food,
859
water, transportation, energy, and waste management. urban planning
The design approach that envisions, designs, and monitors the development and redevelopment of towns, cities, and entire regions, especially in terms of land use, transportation, and environmental decisions.
urban sprawl The unplanned and often haphazard growth of an urban area throughout a larger geographic area, characterized by low- density land use and dependence on the automobile for transportation.
urbanism The characteristics of cities at particular points in time, and their impacts on the people who live there (also called urbanicity).
urbanization A dynamic process of change in cities, often featuring population growth, expanding urban boundaries, changes in density, and demographic changes such as greater heterogeneity.
vehicle miles traveled (VMT) The total number of miles traveled by motor vehicles in a given geographic area and specific time period.
walk-friendly and bike-friendly community certification programs
Programs designed to assess and then encourage communities to improve their walking and bicycling infrastructure and policies.
Walk Score® An index based on Google Maps (www.walkscore.com) that measures distances from a specific location to stores, parks, schools, and other destinations and provides a walkability score ranging from 0 (car-dependent) to 100 (“walker's paradise”).
zoning codes The implementing legislation for policies described in a municipality's master plan, specifying the allowable land uses.
860
Discussion Questions 1. Assume you are moving to a new city. What are the priorities
you might consider as you make your decision about where in that city to live? What are the potential direct health impacts of your decision? What are the indirect health impacts?
2. You have been asked by local officials to increase the number of children who walk to school in your community. How would you undertake this project?
3. Given limited resources, what changes to the built environment could you recommend in a disadvantaged, low-income community to promote physical activity? What outcome would you expect from such changes?
4. You have been asked to perform a health impact assessment for a highway expansion project. What information about the community and about the project would you request? What kinds of recommendations are you likely to be making to mitigate the adverse impacts and promote the healthy aspects of this proposed project?
5. Name three vulnerable populations in your city or town. For each one, answer these questions: Why is this population vulnerable? What specific health challenges does this populations face as a result of community design choices?
6. What are the reasons that some land-use and transportation planners might offer if they are reluctant to incorporate health considerations into their decisions?
7. What is the metropolitan planning organization for your city? Study its Web site and answer these questions: What are the organization's urban and regional planning initiatives that promote health? What are its urban and regional planning initiatives that inadequately address health?
8. Given resources from a major international foundation, what three interventions would you propose to improve the health of urban populations in a low-income country?
861
References 100 Resilient Cities. (2015). [Web site.] Retrieved from http://www.100resilientcities.org
Air monitoring centre of India freezes off the WHO report. (2014). Newzfeed.org, May 15. Retrieved from http://www.newzfeed.org/general/13563-air-monitoring-centre-of- india-freezes-off-the-who-report.html
Alley, D., Liebig, P., Pynoos, J., Banerjee, T., & Choi, I. H. (2007). Creating elder-friendly communities: Preparations for an aging society. Journal of Gerontological Social Work, 49(1–2), 1–18.
Alliance for Biking and Walking. (2014). Bicycling and walking in the United States 2014: Benchmarking report. Retrieved from http://www.bikewalkalliance.org/resources/benchmarking
American Academy of Pediatrics, Committee on Environmental Health. (2009). The built environment: Designing communities to promote physical activity in children. Pediatrics, 123(6), 1591–1598.
American Planning Association. (2006). Smart growth codes. Retrieved from http://www.planning.org/research/smartgrowth
Arup and Rockefeller Foundation. (2014). City Resilience Framework. Retrieved from https://www.rockefellerfoundation.org/report/city-resilience- framework
Asbridge, M., Smart, R. G., & Mann, R. E. (2006). Can we prevent road rage? Trauma, Violence, & Abuse, 7(2), 109–121.
Bai, X., & Imura, H. A. (2000). Comparative study of urban environment in East Asia: Stage model of urban environmental evolution. International Review for Environmental Strategies, 1, 135–158.
Bai, X., Nath, I., Capon, A., Hasan, N., & Jaron, D. (2012). Health and wellbeing in the changing urban environment: Complex challenges, scientific responses, and the way forward. Current Opinion in Environmental Sustainability, 4, 465–472.
862
Barton, H., & Grant, M. (2013). Urban planning for healthy cities: A review of the progress of the European Healthy Cities Programme. Journal of Urban Health, 90(Suppl. 1), 129–141.
Berry, T. R., Spence, J. C., Blanchard, C. M., Cutumisu, N., Edwards, J., & Selfridge, G. (2010). A longitudinal and cross- sectional examination of the relationship between reasons for choosing a neighbourhood, physical activity and body mass index. International Journal of Behavioral Nutrition and Physical Activity, 7, 57.
Besser, L. M., Marcus, M., & Frumkin, H. (2008). Commute time and social capital in the U.S. American Journal of Public Health, 34(3), 207–211.
Bhatia, R. (2007). Protecting health using an environmental impact assessment: A case study of San Francisco land use decision- making. American Journal of Public Health, 97, 406–413.
Bhatia, R., & Wernham, A. (2008). Integrating human health into environmental impact assessment: An unrealized opportunity for environmental health and justice. Environmental Health Perspectives, 116(8), 991–1000.
Booth, G., Leonard, B., & Pawlukiewicz, M. (2002). Ten principles for reinventing America's suburban business districts. Washington, DC: Urban Land Institute. Retrieved from http://www.smartgrowth.org/pdf/uli_Ten_Principles.pdf
Bunn, F., Collier, T., Frost, C., Ker, K., Roberts, I., & Wentz, R. (2003). Traffic calming for the prevention of road traffic injuries: Systematic review and meta-analysis. Injury Prevention, 9, 200– 204.
Bygbjerg, I. C. (2012). Double burden of noncommunicable and infectious diseases in developing countries. Science, 337(6101), 1499–1501.
C40 Cities. (2015). Mexico City: ProAire. Retrieved from http://www.c40.org/profiles/2013-mexicocity
Capon, A. G., & Blakely, E. J. (2007). Checklist for healthy and sustainable communities. New South Wales Public Health Bulletin,
863
18(3–4), 51–54.
Center for Universal Design. (1997). The principles of universal design, Version 2.0. Raleigh: North Carolina State University, Center for Universal Design. Retrieved from http://www.ncsu.edu/ncsu/design/cud/about_ud/udprinciplestext.htm
Centers for Disease Control and Prevention. (2014). Facts about physical activity. Retrieved from http://www.cdc.gov/physicalactivity/data/facts.html
Centers for Disease Control and Prevention. (2015a). Obesity prevalence maps. Retrieved from http://www.cdc.gov/obesity/data/prevalence-maps.html
Centers for Disease Control and Prevention. (2015b). Ten leading causes of death and injury. Retrieved from http://www.cdc.gov/injury/wisqars/leadingcauses.html
City of Portland Office of Transportation. (2012). Portland bicycle count report 2012. Retrieved from https://www.portlandoregon.gov/transportation/article/448401
Clark, D. E., & Cushing, B. M. (2004). Rural and urban traffic fatalities, vehicle miles, and population density. Accident Analysis and Prevention, 36, 967–972.
Cohen, B. (2006). Urbanization in developing countries: Current trends, future projections, and key challenges for sustainability. Technology in Society, 28, 63–80.
Coyle, S. J. (2011). Sustainable and resilient communities: A comprehensive action plan for towns, cities, and regions. Hoboken, NJ: Wiley.
Dannenberg, A. L., Burton, D. C., & Jackson, R. J. (2004). Economic and environmental costs of obesity: The impact on airlines. American Journal of Preventive Medicine, 27, 264.
Dannenberg, A. L., Frumkin, H., & Jackson, R. J. (2011). Making healthy places: Design and building for health, well-being, and sustainability. Washington, DC: Island Press.
De Ville, K. A., & Sparrow, S. E. (2008). Zoning, urban planning,
864
and the public health practitioner. Journal of Public Health Management and Practice, 14, 313–316.
Douglas, I. (2012). Urban ecology and urban ecosystems: Understanding the links to human health and well-being. Current Opinion in Environmental Sustainability, 4(4), 385–392.
Duffy, J. (1990). The sanitarians: A history of American public health. Urbana: University of Illinois Press.
Durand, C. P., Andalib, M., Dunton, G. F., Wolch, J., & Pentz, M. A. (2011). A systematic review of built environment factors related to physical activity and obesity risk: Implications for smart growth urban planning. Obesity Reviews, 12(5), e173–182.
Eckert, S., & Kohler, S. (2014). Urbanization and health in developing countries: A systematic review. World Health & Population, 15(1), 7–20.
Evans, G. W. (2003). The built environment and mental health. Journal of Urban Health, 80, 536–555.
Ewing, R., Schieber, R.A., & Zegeer, C.V. (2003). Urban sprawl as a risk factor in motor vehicle occupant and pedestrian fatalities. American Journal of Public Health, 93(9), 1541–1549.
Federal Highway Administration. (2006). Highway traffic noise in the United States: Problem and response (FHWA-HEP-06-020). Washington, DC: U.S. Department of Transportation. Retrieved from http://www.fhwa.dot.gov/environment/probresp.htm
Federal Highway Administration. (2012). Metropolitan area transportation planning for healthy communities. Retrieved from http://www.planning.dot.gov/documents/Volpe_FHWA_MPOHealth_12122012.pdf
Federal Highway Administration. (2015). Federal-Aid Highway Program funding for pedestrian and bicycle facilities and programs: FY 1992 to 2014 Obligations. Retrieved from http://www.fhwa.dot.gov/environment/bicycle_pedestrian/funding/bipedfund.cfm
Fink, G., Gunther, I., & Hill, K. (2014). Slum residence and child health in developing countries. Demography, 51(4), 1175–1197.
Frank, L., & Engelke, P. (2000). How land use and transportation
865
systems impact public health. Centers for Disease Control and Prevention. Retrieved from http://www.cdc.gov/nccdphp/dnpa/pdf/aces-workingpaper1.pdf
Freeland, A. L., Banerjee, S. N., Dannenberg, A. L., & Wendel, A. M. (2013). Walking associated with public transit: Moving toward increased physical activity in the United States. American Journal of Public Health, 103(3), 536–542.
Frumkin, H., Frank, L., & Jackson, R. (2004). Urban sprawl and public health: Designing, planning, and building for healthy communities. Washington, DC: Island Press.
Fuller, D., & Morency, P. (2013). A population approach to transportation planning: Reducing exposure to motor-vehicles. Journal of the Environment and Public Health. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694553/pdf/JEPH2013- 916460.pdf
García-Palomares, J. C. (2010). Urban sprawl and travel to work: The case of the metropolitan area of Madrid. Journal of Transport Geography, 18(2), 197–213.
Gehl, J. (2010). Cities for people. Washington, DC: Island Press.
Geller, A. L. (2003). Smart growth: A prescription for livable cities. American Journal of Public Health, 93(9), 1410–1415.
Glanz, K., Sallis, J. F., Saelens, B. E., & Frank, L. D. (2005). Healthy nutrition environments: Concepts and measures. American Journal of Health Promotion, 19(5), 330–333, ii.
Global Road Safety Facility at the World Bank and Institute for Health Metrics and Evaluation. (2014). Transport for health: The global burden of disease from motorized road transport. Retrieved from http://www.healthdata.org/sites/default/files/files/policy_report/2014/Transport4Health/IHME_Transport4Health_Full_Report.pdf
Gómez-Baggethun, E., & Barton, D. N. (2013). Classifying and valuing ecosystem services for urban planning. Ecological Economics, 86, 235–245.
Halliday, S. (2007). The great filth: The war against disease in
866
Victorian England. Stroud, Gloucestershire: Sutton.
Jackson, K. T. (1985). Crabgrass frontier: The suburbanization of the United States. New York: Oxford University Press.
Jacobsen, P. L. (2003). Safety in numbers: More walkers and bicyclists, safer walking and bicycling. Injury Prevention, 9, 205– 209.
Jones, C., & Kammen, D. M. (2014). Spatial distribution of U.S. household carbon footprints reveals suburbanization undermines greenhouse gas benefits of urban population density. Environmental Science & Technology, 48(2), 895–902.
Jorchr. (2006, September 23). [Photo of vegetable stand at Möllevångstorget, Malmö, Sweden]. Retrieved from Wikimedia Commons at Wikimedia Commons, http://commons.wikimedia.org/wiki/File:Gr%C3%B6nsaksf%C3%B6rs%C3%A4ljning,_M%C3%B6llev%C3%A5ngstorget,_Malm%C3%B6.jpg
Kawachi, I., Subramanian, S., & Kim, D. (2008). Social capital and health. New York: Springer.
Larson, N. I., Story, M. T., & Nelson, M. C. (2009). Neighborhood environments: Disparities in access to healthy foods in the U.S. American Journal of Preventive Medicine, 36(1), 74–81.
Lee, I. M., Shiroma, E. J., Lobelo, F., Puska, P., Blair, S. N., & Katzmarzyk, P. T. (2012). Effect of physical inactivity on major non- communicable diseases worldwide: An analysis of burden of disease and life expectancy. Lancet, 380(9838), 219–229.
Lemanne, D., Cassileth, B., & Gubili, J. (2013). The role of physical activity in cancer prevention, treatment, recovery, and survivorship. Oncology, 27(6), 580–585.
Leyden, K. (2003). Social capital and the built environment: The importance of walkable neighborhoods. American Journal of Public Health, 93(9), 1546–1551.
Lovasi, G. S., Hutson, M. A., Guerra, M., & Neckerman, K. M. (2009). Built environments and obesity in disadvantaged populations. Epidemiologic Reviews, 31(1), 7–20.
Lozano, R., Naghavi, M., Foreman, K., Lim, S., Shibuya, K.,
867
Aboyans, V.,…Memish, Z. A. (2012). Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380(9859), 2095–2128.
Mair, J. S., Pierce, M. W., & Teret, S. P. (2005). The use of zoning to restrict fast food outlets: A potential strategy to combat obesity. Baltimore, MD: Center for Law and the Public's Health at Johns Hopkins and Georgetown Universities. Retrieved from http://www.publichealthlaw.net/Zoning%20Fast%20Food%20Outlets.pdf
Malizia, E. E. (2005). City and regional planning: A primer for public health officials. American Journal of Health Promotion, 19(5, Suppl.) 1–13.
Mammen, G., & Faulkner, G. (2013). Physical activity and the prevention of depression: A systematic review of prospective studies. American Journal of Preventive Medicine, 45(5), 649–657.
McCahill, C. (2014). Per capita VMT drops for ninth straight year; DOTs taking notice (State Smart Transportation Initiative, News from 2014). Retrieved from http://www.ssti.us/2014/02/vmt- drops-ninth-year-dots-taking-notice
McCann, B. (2013). Completing our streets: The transition to safe and inclusive transportation networks. Washington, DC: Island Press.
McCormack, G. R., Rock, M., Toohey, A. M., & Hignell, D. (2010). Characteristics of urban parks associated with park use and physical activity: A review of qualitative research. Health & Place, 16(4), 712–726.
McCormack, G. R., & Shiell, A. (2011). In search of causality: A systematic review of the relationship between the built environment and physical activity among adults. International Journal of Behavioral Nutrition and Physical Activity, 8, 125.
McDonald, B. C., Gentner, D. R., Goldstein, A. H., & Harley, R. A. (2013). Long-term trends in motor vehicle emissions in U.S. urban areas. Environmental Science & Technology, 47, 10022−10031.
Melosi, M. V. (2000). The sanitary city: Urban infrastructure in
868
America from colonial times to the present. Baltimore: MD Johns Hopkins University Press.
Montgomery, M. (2008). The urban transformation of the developing world. Science, 319, 761–764.
Nadesan-Reddy, N., & Knight, S. (2013). The effect of traffic calming on pedestrian injuries and motor vehicle collisions in two areas of the eThekwini Municipality: A before-and-after study. South African Medical Journal, 103(9), 621–625.
National Highway Traffic Safety Administration. (2014). Traffic safety facts 2012: A compilation of motor vehicle crash data from the Fatality Analysis Reporting System and the General Estimates System. Retrieved from http://www- nrd.nhtsa.dot.gov/Pubs/812032.pdf
National Research Council. (2011). Improving health in the United States: The role of health impact assessment. Washington, DC: National Academies Press. Retrieved from http://www.nap.edu/catalog.php?record_id=13229
Newman, P., & Jennings, I. (2008). Cities as sustainable ecosystems: Principles and practices. Washington, DC: Island Press.
Nyqvist, F., Forsman, A. K., Giuntoli, G., & Cattan, M. (2013). Social capital as a resource for mental well-being in older people: A systematic review. Aging & Mental Health, 17(4), 394–410.
Ogden, C. L., Carroll, M. D., Kit, B. K., & Flegal, K. M. (2014). Prevalence of childhood and adult obesity in the United States, 2011–2012. JAMA, 311(8), 806–814.
Oldenburg, R. (1989). The great good place: Cafés, coffee shops, community centers, beauty parlors, general stores, bars, hangouts, and how they get you through the day. New York: Paragon House.
Passchier-Vermeer, W., & Passchier, W. F. (2000). Noise exposure and public health. Environmental Health Perspectives, 108(Suppl. l), 123–131.
Pedestrian and Bicycle Information Center, Image Center. (2009).
869
[Photo.] https://www.pedbikeimages.org/pubdetail.cfm?picid=15
Portney, K. E. (2003). Taking sustainable cities seriously: Economic development, the environment, and quality of life in American cities. Cambridge, MA: MIT Press.
Pucher, J., & Dijkstra, L. (2003). Promoting safe walking and cycling to improve public health: Lessons from the Netherlands and Germany. American Journal of Public Health, 93(9), 1509–1516.
Putnam, R. D. (2000). Bowling alone: The collapse and revival of American community. New York: Simon & Schuster.
Reed, M. S., Fraser, E.D.G., & Dougill, A. J. (2006). An adaptive learning process for developing and applying sustainability indicators with local communities. Ecological Economics, 59, 406– 418.
Ricklin, A., & Kushner, N. (n.d.). Healthy plan making: Integrating health into the comprehensive planning process: An analysis of seven case studies and recommendations for change. Chicago: American Planning Association. Retrieved from https://www.planning.org/research/publichealth/pdf/healthyplanningreport.pdf
Ross, C. L., Leone de Nie, K., Dannenberg, A. L., Beck, L. F., Marcus, M. J., & Barringer, J. (2012). Health impact assessment of the Atlanta BeltLine. American Journal of Preventive Medicine, 42(3), 203–213.
Rundle, R. L. (2002). U.S.'s obesity woes put a strain on hospitals in unexpected ways. Wall Street Journal, May 1. Retrieved from http://www.wsj.com/articles/SB1020194636122710680
Rydin, Y., Bleahu, A., Davies, M., Dávila, J. D., Friel, S., De Grandis, G.,…Wilson, J. (2012). Shaping cities for health: Complexity and the planning of urban environments in the 21st century. Lancet, 379(9831), 2079–2108.
Schilling, J., & Linton, L. (2005). The public health roots of zoning: In search of active living's legal genealogy. American Journal of Preventive Medicine, 28(2, Suppl. 2), 96–104.
Shaheen, S. A., Guzman, S., & Zhang, H. (2012). Bikesharing across
870
the globe. J. Pucher & R. Buehler (Eds.), City cycling (chap. 9). Cambridge MA: MIT Press.
Stimpson, J. P., Wilson, F. A., Araz, O. M., & Pagan, J. A. (2014). Share of mass transit miles traveled and reduced motor vehicle fatalities in major cities of the United States. Journal of Urban Health, 91(6), 1136–1143.
Story, M., Kaphingst, K. M., Robinson-O'Brien, R., & Glanz, K. (2008). Creating healthy food and eating environments: Policy and environmental approaches. Annual Review of Public Health, 29, 253–272.
Stroppa, G. (2012). Kibera slum, Nairobi, Kenya [Photo]. Retrieved from http://www.panoramio.com/photo/78567558
Sustainable Cities International. (2012). Indicators for sustainability: How cities are monitoring and evaluating their success. Retrieved from http://sustainablecities.net/our- resources/document-library/doc_download/232-indicators-for- sustainability
Sverdlik, A. (2011). Ill-health and poverty: A literature review on health in informal settlements. Environment and Urbanization, 23, 123–155.
Tammelin, T. (2005). A review of longitudinal studies on youth predictors of adulthood physical activity. International Journal of Adolescent Medicine and Health, 17(1), 3–12.
Transportation Research Board and Institute of Medicine. (2005). Does the built environment influence physical activity? Examining the evidence (TRB Special Report 282). Washington DC: National Academy of Sciences.
Tsai, A. G., Williamson, D. F., & Glick, H. A. (2011). Direct medical cost of overweight and obesity in the USA: A quantitative systematic review. Obesity Reviews, 12(1), 50–61.
United Nations. (2014). World urbanization prospects: The 2014 revision: Highlights. Retrieved from http://esa.un.org/unpd/wup/Highlights/WUP2014-Highlights.pdf
871
UN-Habitat. (2013). State of the world's cities 2012/2013: Prosperity of cities. Nairobi: UN-Habitat. Retrieved from http://mirror.unhabitat.org/pmss/listItemDetails.aspx? publicationID=3387
U.S. Environmental Protection Agency. (2013). Creating equitable, healthy, and sustainable communities: Strategies for advancing smart growth, environmental justice, and equitable development. Retrieved from http://www.epa.gov/smartgrowth/pdf/equitable- dev/equitable-development-report-508-011713b.pdf
U.S. Environmental Protection Agency. (2015). What is smart growth? Retrieved from http://www2.epa.gov/smartgrowth/about- smart-growth
U.S. Green Building Council. (2012–2015). LEED v4 for Neighborhood Development. Retrieved from http://www.usgbc.org/DisplayPage.aspx?CMSPageID=148
Vlahov, D., & Galea, S. (2002). Urbanization, urbanicity, and health. Journal of Urban Health, 79(4, Suppl. 1), S1–12.
Walker, R. E., Keane, C. R., & Burke, J. G. (2010). Disparities and access to healthy food in the United States: A review of food deserts literature. Health & Place, 16(5), 876–884.
Whitacre, P. T., Tsai, P., & Mulligan, J. (2009). The public health effects of food deserts: Workshop summary. Washington DC: National Academies Press.
Wilson, W. J. (1987). The truly disadvantaged: The inner city, the underclass, and public policy. Chicago: University of Chicago Press.
Wilson, W. J. (1997). When work disappears: The world of the new urban poor. New York: Vintage.
Woodyard, C. (2007). Car weight limits are a big, fat problem. USA Today, September 14.
World Commission on Environment and Development. (1987). Report of the World Commission on Environment and Development: Our common future. New York: United Nations.
World Health Organization and UN-HABITAT. (2010). Hidden
872
cities: Unmasking and overcoming health inequities in urban settings. Kobe: WHO Centre for Health Development.
Yang, Z. (2012) Eco-cities: A planning guide. Boca Raton, FL: CRC Press.
Younger, M., Morrow-Almeida, H. R., Vindigni, S., & Dannenberg, A. L. (2008). The built environment, climate change, and health: Opportunities for co-benefits. American Journal of Preventive Medicine, 35(5), 517–526.
Zaharna, M., & Guilleminault, C. (2010). Sleep, noise and health: Review. Noise and Health, 12(47), 64–69.
Zhao, P. (2010). Sustainable urban expansion and transportation in a growing megacity: Consequences of urban sprawl for mobility on the urban fringe of Beijing. Habitat International, 34(2), 236–243.
Zhao, P. (2011). Managing urban growth in a transforming China: Evidence from Beijing. Land Use Policy, 28(1), 96–109.
873
For Further Information Books and Articles
Healthy Community Design
Bullard, R. D., & Johnson, G. S. (Eds.). (1997). Just transportation: Dismantling race and class barriers to mobility. Gabriola Island, BC: New Society.
Corburn, J. (2009). Toward the healthy city: People, places and the politics of urban planning. Cambridge, MA: MIT Press.
Jacobs, J. (1961). The death and life of great American cities. New York: Random House.
Urban Health
Freudenberg, N., Klitzman, S., & Saegert, S. (Eds.). (2009). Urban health and society: Interdisciplinary approaches to research and practice. San Francisco: Jossey-Bass/Wiley.
Galea, S., & Vlahov, D. (2005). Handbook of urban health: Populations, methods, and practice. New York: Springer.
Global Cities and Health
Davis, M. (2006). Planet of slums. New York: Verso.
Vlahov, D., Boufford, J. I., Pearson, C., & Norris, L. (2011). Urban health: Global perspectives. San Francisco: Jossey-Bass/Wiley.
Health Impact Assessment
Dannenberg, A. L., Bhatia, R., Cole, B. L., Heaton, S. K., Feldman, J. D., & Rutt, C. D. (2008). Use of health impact assessment in the U.S.: 27 Case studies, 1999–2007. American Journal of Preventive Medicine, 34(3), 241–256.
Kemm, J. R. (Ed.). (2012). Health impact assessment: Past achievement, current understanding, and future progress. Oxford, U.K.: Oxford University Press.
874
Ross, C. L., Orenstein, M., & Botchwey, N. (2014). Health impact assessment in the United States. New York: Springer.
WHO Regional Office for Europe and European Centre for Health Policy. (1999). Health impact assessment: Main concepts and suggested approach (Gothenburg Consensus Paper). Brussels: European Centre for Health Policy. Available at http://www.euro.who.int/document/PAE/Gothenburgpaper.pdf
World Health Organization. (2015). Health impact assessment guidelines. Available at http://www.who.int/hia/en
Agencies and Organizations AARP Livable Communities: http://www.aarp.org/livable- communities
American Planning Association. Planning and Community Health Center: https://www.planning.org/nationalcenters/health
Association of Public Health Observatories, Health Impact Assessment Gateway: http://www.apho.org.uk/default.aspx? QN=P_HIA
Centers for Disease Control and Prevention, Healthy Community Design Initiative: http://www.cdc.gov/healthyplaces
Congress for the New Urbanism: http://www.cnu.org
ICLEI–Local Governments for Sustainability: http://www.iclei.org and http://www.icleiusa.org
Local Government Commission, Center for Livable Communities: http://www.lgc.org/center
National Association of County and City Health Officials. Community Design/Land Use Planning: http://www.naccho.org/topics/environmental/landuseplanning/index.cfm
Robert Wood Johnson Foundation, Active Living Research program: http://www.activelivingresearch.org
Safe Routes to Schools National Partnership: http://www.saferoutespartnership.org
Smart Growth Network: http://www.smartgrowth.org
875
Urban Land Institute: http://www.uli.org
U.S. Department of Transportation, Federal Highway Administration, Health in Transportation: http://www.fhwa.dot.gov/planning/health_in_transportation
U.S. Department of Transportation, Federal Highway Administration, National Center for Safe Routes to School: http://www.saferoutesinfo.org
U.S. Environmental Protection Agency, Smart Growth program: http://www.epa.gov/smartgrowth
World Health Organization, Healthy Cities project: http://www.euro.who.int/en/health-topics/environment-and- health/urban-health/activities/healthy-cities
876
Chapter 16 Water and Health
Timothy Ford
Dr. Ford reports no conflicts of interest related to the authorship of this chapter. Megan Cartwright reports no conflicts of interest related to the authorship of the tox boxes.
877
Key Concepts Water is critical to all forms of life on this planet.
There are many ways in which we directly threaten both the quality and quantity of this resource and thus our health and the planet's health.
To protect our health and our environment we must conserve water, reduce water pollution and wastewater production, and begin to recycle water.
A regulatory framework exists in the United States to ensure the provision of safe drinking water to the public.
We need to begin to think about future risks to our water resources and potential mitigation activities, both in the developed and the developing worlds.
878
The Role of Water in Life The existence of life, from the largest mammals to the smallest microbes, depends on water (Text Box 16.1). The search for life (as we understand it) on other planets is always predicated on the search for evidence of water. We humans are approximately 60% water, and we cannot survive for more than a few days without it. It is therefore not surprising that human culture has been defined by water over the centuries. One has only to look at the concentration of development along the coasts and major river systems of the world to realize how the water environment has dominated, and continues to dominate, human cultures.
879
Text Box 16.1 Water as a Nutrient We're not used to thinking about water as a nutrient, but in fact it is the most important nutrient! All biochemical reactions depend on water, and numerous human health risks can be linked to a deficit in water intake: including risks for different types of cancers, childhood and adolescent obesity, and the overall health of the elderly (Kleiner, 1999). Severe dehydration is in itself life threatening, as we see with the infectious diseases that cause acute diarrhea: the killer is dehydration, not the bacterial toxins that cause the diarrhea in the first place. For infants and young children this is an acute problem worldwide; their proportion of water may be close to 75%, much higher than in adults, and their less developed organs are less capable of regulating water balance and temperature (Ford & Hamner, 2014). There may also be long-term health effects of chronic mild dehydration, such as cognitive impairment (e.g., Edmonds & Burford, 2009). Water intake needs to be at the forefront of nutrition programs and dietary practice.
The Hydrological Cycle Our planet would appear to have a surfeit of water, but most of this water is unavailable for human use. Over 97% of the world's water is salty, found in the oceans and (to a much lower extent) in inland seas and saltwater lakes. What remains is freshwater, but over two thirds of this is locked in the Antarctic and Arctic ice caps. The freshwater that remains, in rivers and lakes, in the atmosphere, and in the ground, makes up less than 1% of the world's water. This is the supply potentially available for drinking, irrigating crops, and other uses.
Water is in continuous motion between these various compartments, in a so-called hydrological cycle that dominates the health of the planet. Without continuous evaporation from the oceans, precipitation on land, and runoff back to the oceans, no surface or groundwater recharge can take place, and we would
880
eventually exhaust our available freshwater supplies. Figure 16.1 provides a diagrammatic overview of the hydrological cycle; the dominant flows, or fluxes; and the critical reservoirs, or pools.
Figure 16.1 The Hydrological Cycle Source: Redrawn from Winter, Harvey, Franke, & Alley, 1998. Originally modified from W. H. Schlesinger, Biogeochemistry—An Analysis of Global Change (San Diego, CA: Academic Press, 1991), with permission from Elsevier.
Note: Pools (oceans, atmosphere, groundwater, ice) are in cubic miles; fluxes are in cubic miles per year.
The hydrological cycle teaches us to view water and health with a holistic perspective. The compartments of the hydrological cycle are either directly or indirectly connected, and perturbation in one compartment is likely to affect all other compartments and therefore both human and ecological health. These interconnections are diagrammatically illustrated in Figure 16.2. This chapter explores these interconnections. It describes several processes that are crucially important to humans, including water consumption, waste production, waste treatment and discharge, and treatment for water reuse, and outlines the multitude of health concerns at each step.
881
Figure 16.2 Schematic of the Interconnections Between Water and Health
Surface Water and Groundwater Available freshwater supplies are often conceptually divided into surface water and groundwater. Surface water includes all water naturally open to the atmosphere (rivers, lakes, reservoirs, ponds, streams, impoundments, seas, estuaries, etc.). Groundwater is the supply of freshwater found beneath the Earth's surface, usually in aquifers (U.S. Environmental Protection Agency [U.S. EPA], 2014d). Groundwater supplies wells and springs.
Because surface water and groundwater are not independent of each other, an overlap category is also recognized: groundwater under the direct influence of surface water (GWUDI). This is defined as any water beneath the surface of the ground with (1) significant occurrence of insects or other microorganisms, algae, or large-diameter pathogens; or with (2) significant and relatively rapid shifts in water characteristics such as turbidity, temperature, conductivity, or pH that closely correlate to climatological or surface water conditions (U.S. EPA, 2014d).
These distinctions are important because they directly affect how we
882
view the quality of a water resource and how we manage that resource. Ideally, water used as a drinking-water source (often called source water) should be of the highest quality, reducing the cost of water treatment and the risk of contamination. Groundwater has traditionally been considered a high-quality resource, because as rainfall and other surface waters percolate through soil into groundwater, they are cleaned by physical, chemical, and microbiological processes in the soil. However, the traditional confidence in groundwater may not always be well placed, because human activities such as land management practices can influence even relatively deep aquifers. Surface water and GWUDI have traditionally been less favored as sources for drinking water. However, groundwater is not always available, and municipalities may have no choice but to use surface water, requiring extensive and costly water treatment. At present just over half of Americans get their drinking water from surface sources.
Surface water and GWUDI may be considered suitable for agricultural, industrial, or recreational uses with no or limited treatment. Different criteria are therefore developed and applied to source waters depending on their ultimate use. Surface waters that are used as drinking-water sources are regulated by far stricter criteria, for example, than waters used to irrigate crops. (A fuller discussion of water regulations appears later in this chapter.)
Water Use and Water Scarcity Water scarcity may be one of the most critical health threats to human society today. In the long term, as discussed in Chapter 3, societies must be able to survive on renewable resources. When a resource is extracted faster than it can be renewed, then eventually supplies will not meet demand. This pattern of use is nonsustainable. The most familiar examples of finite resources are fossil fuels. As explained in Chapter 14, fossil fuel use is nonsustainable in the long term, leading to considerable pressure to develop alternative energy sources. Just as fossil fuels are mined, so is water. Technology has allowed us to extract more and more of the water trapped within the Earth's crust. This has allowed human habitation, and its ensuing agricultural and industrial development, to spread to arid areas of the planet that are poorly suited to sustain human life. In arid regions aquifer recharge rates are low, and
883
the deep aquifers laid down by countless ice ages are gradually being depleted. (Several authors provide informative discussions of water use and water scarcity; see, e.g., Clarke, 2013; Postel, 2013; Gleick, 2014.)
Population and Water Scarcity Whether or not a water supply is adequate depends on the balance that exists among water availability, population, and the ways in which people use water. In many parts of the world, population pressure places a severe strain on water resources. Each year, projections on future water scarcity look increasingly dire. The United Nations “Water for Life” water scarcity Web page reports that approximately 700 million people in forty-three countries currently suffer from water scarcity, and projects that by 2025, 1.8 billion people will live in countries or regions with absolute water scarcity. In addition, two thirds of the world's population could be living under water-stressed conditions (United Nations, 2014). Water stress is defined as a water supply at or below 1700 cubic meters (m3) per person per year; water scarcity as at or below 1000 m3 per person per year; and absolute water scarcity as at or below 500 m3 per person per year.
Although some countries have enormous supplies of water, others are arid and are entirely dependent on other countries for their water supply (see, e.g., Text Box 16.2). The UN Water for Life Web page provides links to more detailed information on water stress and scarcity.
884
Text Box 16.2 A Gross Inequity Water use varies not only with population but with the level of development and affluence. At one extreme, people in wealthy countries with ample water supplies are relatively profligate users of water. In the United States, for example, where the supply of renewable freshwater is estimated to be 9,666 m3 per person per year, the estimated annual per capita withdrawal is 1,575 m3. Of this, 14% is used in homes, 46% in industry, and 40% in agriculture (Food and Agriculture Organization of the United Nations [FAO], 2014). The roughly 14% used in homes represents 590 liters per person per day, of which less than 0.2% is required for drinking (based on the U.S. Environmental Protection Agency's estimated daily ingestion of community water of 926 milliliters (mL) per person per day; U.S. EPA, 2004). Advanced sanitation (including flush toilets) is the norm in the United States and requires large amounts of domestic water use.
In contrast, Somalia's supply of renewable freshwater is far lower, an estimated 1,442 m3 per person per year. The per capita withdrawal is also far lower than that in the United States, an estimated 370 m3 per year, of which <0.5% is used in homes, a negligible amount is used in industry, and 99.5% is used for agriculture (FAO, 2014). In this case, domestic water use represents 4.6 liters per person per day, of which >20% is required for consumption. There is little margin of safety in this situation, and a temporary disruption of the water supply, such as a drought, can be devastating.
Agriculture and Water Scarcity An enormous amount of water is needed to grow food. In fact, on the global scale, agriculture accounts for 70% of water withdrawal (FAO, 2014). An oft-quoted figure is that 1,000 tons of water are required to produce 1 ton of wheat (Postel, 1999). As a result, it is not surprising that agricultural uses of water are the greatest global
885
contributors to water scarcity and aquifer depletion. Considerable efforts have been made over the past decade to replace conventional irrigation with methods that minimize water wastage, such as drip or other micro-irrigation techniques.
Political Implications The dependence of food production on irrigation links freshwater use with food security and therefore with human nutrition and well- being. Accordingly, the political implications of water scarcity are enormous. Most of the major rivers and aquifers of the world cross international or at least state borders. Any use of water by one nation or state affects all downstream users. Impoundments (dams) are particularly damaging to downstream users, as they dramatically reduce water flow for these communities, particularly during dry seasons. There are numerous examples of national and international crises emerging from shared water resources, as shown in Table 16.1. In extreme instances these crises may erupt into what have been called resource wars (Klare, 2001).
Table 16.1 Hot Spots of Current and/or Potential Water Conflicts
River basin Length (km)
Countries Sources of conflict
Nile 6,693 Tanzania, Kenya, Zaire, Burundi, Rwanda, Ethiopia, Uganda, Sudan, and Egypt
Irrigation
Tigris/Euphrates 1,840/2,700 Turkey, Syria, Iraq, and Iran
Hydroelectric projects, irrigation
Indus/Beas/Sutlej/Ravi 2,896 (Indus)
India, Pakistan, and Tibet
Diversions, Sikh vs. Hindu
Ganges/Brahmaputra 2,414/2,896 India, Bangladesh,
Deforestation and siltation,
886
Nepal, and Bhutan
diversions
Jordan 93 Israel, Jordan, Lebanon, and Syria
Diversions— arguably an underlying cause of Arab-Israeli conflicts
Paraná/Paraguay 3,998 (Paraná)
Brazil, Paraguay, Bolivia, Argentina, and Uruguay
Dams— hydroelectric
Rio Grande 3,057 United States and Mexico
Development, irrigation
Colorado 2,336 United States and Mexico
Development, irrigation
Climate Change and Water Global climate change is discussed in detail in Chapter 12. Here, we consider the effects of climate change on water. Warming global temperatures result in increased evaporation from the oceans, an increase in water vapor in the atmosphere, and increasing precipitation, including more severe weather events. Weather changes are expected to be complex, with precipitation increasing in some regions and decreasing in others. The burden of water scarcity may therefore shift, with some arid regions benefiting from increased rainfall, while mountainous regions will experience shortages if warmer temperatures prevent snow accumulation. Although climate models include uncertainties and predictions must be viewed with caution, it appears likely that the hydrological cycle as we now know it will change in coming decades and that in some regions water scarcity may substantially worsen.
Human Impacts on Aquatic Systems Not only do water quantity and quality affect human health, but human activities also affect every aspect of aquatic ecosystems. Hydrodynamics—the way water moves—is dramatically altered
887
by such construction projects as dams, levees, and canals and by such activities as channelization, concretization, and extraction.
Waste generation from industrial, municipal, and agricultural activities has resulted in the discharge of vast quantities of nutrients, such as nitrogen and phosphorus, to aquatic systems. The resulting changes in fundamental nutrient cycles can completely change the biology and chemistry of a system. In extreme cases this can lead to eutrophication (when high nutrient loads stimulate blooms of algae in the water, in turn stimulating microbial activity). The algae themselves may produce highly toxic chemicals and oxygen can be depleted resulting in massive fish kills. As shown in Table 16.2, changes such as these can directly affect health, completing a cycle of humans to water to humans.
Table 16.2 Examples of Large-Scale Human Impacts on Aquatic Systems
Engineering schemes
Examples Some Environmental consequences
Health effects
Dams, hydroelectric and irrigation projects
Hoover Dam, U.S. Aswan High Dam, Egypt; Sennar Dam, Sudan Akosombo Dam, West Africa Three Gorges Dam, China James Bay, Canada
Population displacement; lowering of water tables; significant hydrological changes downstream; interruption of migratory patterns; climatological effects; depletion of downstream sediments, gravels, and nutrients, reducing aquatic habitat and floodplain productivity;
Downstream droughts; dramatic increases in schistosomiasis; levels of mercury in Inuit that exceed World Health Organization health guidelines.
888
creation of habitat for snails that carry the schistosome parasite; creation of conditions for methylation of mercury in sediments and subsequent accumulation through the food chain.
Channelization Mississippi River
Exacerbated extreme Midwest flooding events.
Huge economic consequences; loss of property and livestock; mental depression.
Channelization; intensive draining, diking, and developing
Florida's Kissimmee River, Lake Okeechobee, and the Everglades
Destroyed habitat for wildfowl and fish nurseries; caused lake eutrophication, algal blooms, and fish kills; reduced groundwater recharge; and dramatically changed the Everglades ecosystem.
Primarily ecological and economic effects. Long-term effects on human health of changes in Florida's hydrological cycle as yet unknown.
Eutrophication Lake Erie Created conditions for toxic algal blooms.
Cyanobacteria- derived toxins in drinking water, which can be particularly deadly, have resulted in
889
drinking-water bans and advisories, and also present the potential for livestock, wildlife, and pet fatalities.
Water contaminants fall into two general categories, chemical and biological. Chemical contaminants, such as arsenic, may occur naturally or may be discharged into water through industrial, agricultural, municipal, or recreational activity. Biological contaminants include bacteria, viruses, protozoa, fungi, parasites and their vectors; these contaminants originate from many sources, including human and animal wastes.
Routes of Exposure Exposure to both chemicals and waterborne pathogens can occur through multiple transmission routes. Some are obvious, such as ingestion of contaminated water or exposure to it through recreational use, either through unintended ingestion or through skin abrasions or alternative portals of entry (eye, ear, anal, urogenital). Other, perhaps less obvious, routes of exposure include breathing contaminated aerosols arising from showers, toilet flushing, dishwashing, garden hoses, fountains, waterfalls, and cooling towers and from air conditioner, humidifier, and refrigerator drip pans. The following two sections present information on both chemical and biological contaminants.
Chemical Contaminants A wide variety of chemicals can contaminate water, as shown in Table 16.3. A contaminant may originate from either a point source or a nonpoint source. These are defined (U.S. EPA, 2014d) as follows. A point source is a stationary location or fixed facility from which pollutants are discharged, such as a pipe, ditch, or ship. Examples of point source chemical releases include discharges of mercury, solvents, or polychlorinated biphenyls (PCBs) from industrial drainpipes and leakages of MTBE and petrochemicals
890
from corroding underground gasoline tanks. Nonpoint sources are diffuse pollution sources without a single point of origin. Common nonpoint sources include agricultural runoff containing pesticides and nutrients, and urban surfaces such as city streets and parking lots; the latter can massively contaminate surface and groundwaters, as the impermeable surfaces accumulate high concentrations of contaminants such as oils and household wastes that run off during heavy rainfall. Some contaminants, such as toxic metals and acidic drainage from mines, can arise from both point and nonpoint sources.
Table 16.3 Classes of Chemical Contaminants in Water
Classes Examples Petroleum and coal hydrocarbons
Crude oil Alkanes, heterocyclics, and aromatics
Refined oil Gasoline, diesel, and heating fuels
Combustion/conversion products
PAHs, synfuels, and by- products
Synthetic organics
Halogenated hydrocarbons
PCBs, CFCs, pesticides, and solvents
Plasticizers, phthalic acid esters
PVC, DEHP
Others Surfactants, organophosphate pesticides, synthetic pyrethroids, and fuel additives (MBTE)
Metals Cd, Hg, Pb, Ag, Zn, Cu, Cr, Ni, As
Radionuclides Transuranics Pt, Am, Cm
Fission products 137Cs, 90Sr
Activation products 60Co, 54Mn, 65Zn, 51Cr Natural U-Th decay series
Disinfection Chlorination, Chloroform,
891
by-products chloramination, and ozonation by-products
trichloroacetic acids, chlorinated furanones, and bromate
Industrial wastes
Process by-products, including mining, dredging, and other resource extraction processes
Many of the above chemicals plus acids, ash, desalination brines, heat (from cooling water), anticorrosion chemicals, cyanide, etc.
Municipal and agricultural wastes (not including pathogens)
Nutrients, range of household and agricultural chemicals, including those suspected to cause endocrine disruption
Phosphorus, nitrogen, carbon, silicon, antibiotics, disinfectants, pesticides, fluoride, nonylphenol ethoxylates, etc.
Naturally occurring chemical contaminants
Chemicals that naturally occur in the Earth's soils and rocks, or are toxins produced by algae, etc.
Nitrate, fluoride, arsenic, and cyanobacteria-derived toxins. Even salt can be considered a contaminant when it renders water undrinkable, through, e.g., saltwater intrusion.
Source: Adapted in part from Capone & Bauer, 1992.
Other sources of anthropogenic contaminants include deep injection of wastes into groundwater, lead leaching from old drinking-water distribution pipes, and the vast quantities of pharmaceuticals (see Text Box 16.3) and personal care products (PPCPs) that are released into water from human sewage and from agricultural and aquacultural activities. It is also important to recognize that certain naturally occurring chemicals such as arsenic (Tox Box 16.1) are toxic and can also contaminate our water sources (see Table 16.3).
892
Text Box 16.3 Antibiotic Resistance Few scientists today would argue that widespread contamination of the environment with pharmaceuticals is a good idea, yet we continue to discharge these chemicals to receiving waters in vast quantities, through wastewater discharge and agricultural and aquacultural practices. One likely consequence of these discharges is increased antibiotic resistance among naturally occurring microbes, with the potential for transfer of resistance factors to human pathogens. It is highly likely that these environmental reservoirs of antibiotics (and genes for antibiotic resistance) have contributed to our current epidemic (and pandemic) of antibiotic-resistant infections (Finley et al., 2013). The more recent revelations that antibiotics are associated with the epidemic of childhood obesity make an even more compelling argument to keep these pharmaceuticals out of our drinking water (Cox et al., 2014).
Anthropogenic Chemical Contaminants It is sobering to think about the number of chemicals that are dispersed into the environment. The U.S. Environmental Protection Agency (EPA) (Grube, Donaldson, Kiely, & Wu, 2011) estimates that more than 1.1 billion pounds of traditional pesticides are used in the United States every year. If wood preservatives, specialty biocides, and chlorine and hypochlorites are included in this estimate, the total jumps to more than 5 billion pounds. Very few of the pesticides discharged to the environment have been rigorously tested for aquatic toxicity. However, many are persistent organic pollutants (POPs; see Tox Box 2.1) that remain in sediments and soils for many years, decades, or even centuries.
893
Tox Box 16.1 Arsenic
What Is It? Arsenic is a semimetallic element naturally present in the environment. It can take the form of inorganic compounds when combined with elements such as oxygen, chlorine, and sulfur; organic compounds when combined with carbon and hydrogen; and highly flammable arsine gas when combined with hydrogen. While all these forms are dangerous to human health, inorganic arsenic and arsine gas are especially toxic, and they are the reason the World Health Organization (WHO) classifies arsenic as one of the ten chemicals of major public concern.
How Is It Used? Arsenic compounds are mostly used as wood preservatives and in copper and lead smelting, while arsine gas is used in the manufacture of semiconductors. Organic arsenic is also incorporated into several pesticides. To a much lesser extent, arsenic is used medically for certain leukemia chemotherapies and in traditional Asian medicines.
Historically, inorganic arsenic was used as a poison for thousands of years because it is odorless and tasteless. In 82 bc, its popularity as a poison led to the Roman Republic
894
issuing the Lex Cornelia—the first known law against poisoning. However, arsenic continued to be widely used as a poison until the nineteenth century, when the English chemist James Marsh developed forensic tests for detecting arsenic in body fluids.
More recently, arsenic has been used militarily. In the 1920s, it was developed into lewisite, a component of chemical weaponry. While lewisite was phased out in the 1950s, the United States used arsenic-based Agent Blue as a defoliant during the Vietnam War in the 1960s.
How Are People Exposed? The major route of arsenic exposure is by ingestion of inorganic or organic arsenic compounds, although some workers may be exposed through inhalation of arsenic and arsine gas.
In the general population the major route of exposure is through drinking groundwater naturally contaminated with inorganic arsenic. The largest at-risk population is in Bangladesh, but inorganic arsenic also contaminates groundwater in parts of India, China, Argentina, Chile, Mexico, and the western United States. Other important routes of exposure include consuming rice or smoking tobacco grown with arsenic-contaminated water and soil and consuming seafood that naturally contains organic arsenic. People may also be exposed by consuming arsenic- contaminated naturopathic remedies.
Among workers, the major route of exposure is inhalation. People involved in carpentry and the preservative treatment of wood may inhale arsenic-contaminated sawdust, while people involved in semiconductor manufacturing may inhale arsine gas. Pesticide applicators may inhale arsenical pesticides. Although dermal absorption is a lesser route of exposure, workers and the general population can be exposed by this route when handling preservative-treated wood.
What Are the Toxic Effects? As with many chemicals, arsenic's acute, high-dose effects
895
differ from its chronic, low-dose effects. Chronic exposure is much more common. Arsenic toxicity also varies depending on its form: arsine gas is the most toxic, followed by inorganic arsenic, and then organic arsenic.
An acute dose of inorganic arsenic or arsine gas is often lethal. An acute exposure to inorganic arsenic is followed, in hours to days, by nausea and diarrhea, then by numbness, delirium, and possibly death. Inhaling a high concentration of arsine gas can lead to headaches, vomiting, and hemolytic anemia, which can lead to kidney failure and death.
In contrast, the effects of chronic, low-dose exposure to arsenic can take years to develop. The major effect is skin cancer following chronic ingestion of inorganic arsenic. The International Agency for Research on Cancer (IARC) therefore classifies inorganic arsenic as a known human carcinogen. In addition to causing cancer, chronic ingestion of inorganic arsenic can also cause skin discolorations, lesions, and hard patches on the palms and soles of the feet. Furthermore, people may develop peripheral neuropathy and an increased risk of diabetes and cardiovascular disease.
There is less information about the effects of chronic arsine and organic arsenic exposure in humans. Animal studies suggest that chronic arsine exposure may cause hemolysis, and chronic organic arsenic exposure may cause diarrhea and damage the kidneys.
How Are People Protected? The general population is mainly protected by laws and technical approaches that provide a safe water supply. In the United States, the EPA has set a maximum contaminant level of 10 ppb for arsenic in drinking water, and has also restricted and canceled uses of inorganic arsenic in pesticides. Worldwide, the WHO recommends testing groundwater for arsenic, and either filtering out the arsenic or substituting rain and surface water for groundwater.
In the United States, workers are protected through regulations, engineering controls, and personal protective equipment. Regulations vary depending on the regulating
896
agency and the arsenical compound. For inorganic arsenic compounds and arsine gas, the Occupational Safety and Health Administration (OSHA) sets permissible exposure limits five to one hundred times higher, respectively, than the stricter recommended exposure limits set by the National Institute for Occupational Safety and Health (NIOSH). In contrast, OSHA sets a limit for airborne organic arsenic, whereas NIOSH sets no exposure limit. For workers exposed to airborne inorganic arsenic and arsine gas, NIOSH recommends they protect themselves with self-contained respirators and avoid skin and eye contact with the arsenicals.
Want to Learn More? A historical account of arsenic poisoning and forensic science is Sandra Hempel's The Inheritor's Powder: A Tale of Arsenic, Murder, and the New Forensic Science (New York: Norton, 2014).
The ATSDR Toxicological Profile for Arsenic is available at www.atsdr.cdc.gov/toxprofiles/TP.asp?id=22&tid=3, and a recent review is U. Schuhmacher-Wolz, H. H. Dieter, D. Klein, & K. Schneider, “Oral Exposure to Inorganic Arsenic: Evaluation of Its Carcinogenic and Non-Carcinogenic Effects,” Critical Reviews in Toxicology, 2009, 39(4), 271– 298.
Contributed by Megan Cartwright
It was long thought that chemicals discharged into receiving waters would simply be diluted to the point where they could be ignored. In recent years it has become abundantly clear that dilution is no solution. Chapter 6 describes how chemicals move through the body in predictable ways, a keystone of toxicology; the same is true for chemicals in ecosystems, including hydrological cycles, as demonstrated in Figure 16.3. The fate of a given chemical in receiving waters is a function of both its physical and its chemical nature. The degree to which a chemical may partition into sediments or into the biota depends to some degree on its partition coefficient, a measure of its relative affinity for an
897
organic solvent (octanol) and for water. This, in turn, depends to some degree on measures of solubility and hydrophobicity. In turn, each of these parameters affects the bioavailability and subsequent toxicity of a given chemical.
898
Figure 16.3 Pesticide Movement in the Hydrological Cycle,
899
Including Movement to and from Sediment and Aquatic Biota in a Stream
Source: U.S. Geological Survey, 2014, as modified from Majewski & Capel, 1995.
Health Effects Evidence suggests multiple health effects from exposure to toxic chemicals discharged into water, ranging from birth defects to cancer (Table 16.4). However, the links between waterborne chemical exposures and health outcomes have been difficult to prove conclusively. Epidemiological studies face several challenges: exposures that are relatively low and difficult to measure, exposures to the chemicals of concern through routes other than water, the synergistic and antagonistic effects of mixtures of chemicals, and confounding by competing causes of diseases of interest. (These challenges are explored in Chapter 4.)
Table 16.4 Examples of Studies of Possible Links Between Exposure to Chemicals in Drinking Water and Increased Health Risk
Place Contaminant Source Health effect
Cape Cod, Massachusetts
Tetrachlorethylene (PCE)
Leachate from vinyl lining of water pipes
Breast cancer
Churchill County, Nevada
Tungsten and arsenic
Unknown Leukemia
Woburn, Massachusetts
Solvents, including trichloroethylene (TCE)
Chemical manufacturing wastes
Childhood leukemia
Bergen, Essex, Morris, and Passaic Counties, New Jersey
TCE and PCE Not specified Leukemia and non- Hodgkin's lymphoma
Gassim Petroleum oils Refineries? Carcinoma of the
900
Region, Saudi Arabia
esophagus
Northwestern Illinois
TCE, PCE, and other solvents
Landfill? Bladder cancer
Rural America Nitrate Well water Methemoglobinemia (blue baby syndrome)
Several states in India
Fluoride Groundwater Fluorosis (dental and skeletal)
Bangladesh and West Bengal
Arsenic Groundwater Arsenical keratosis; cancers
Microbiological Contaminants Since ancient times, people have recognized that human and animal wastes can contaminate water and threaten health. A great many pathogenic organisms can be found in water. Many of these are shown in Table 16.5, together with the diseases they cause and approaches to prevention and treatment. (This table may seem overwhelming, but it is far from exhaustive. There are other pathogens in every class, including fungal pathogens, that may have a relationship with water.) Like chemicals, biological contaminants can come from point sources, such as leaking septic systems, or nonpoint sources, such as runoff from city streets. There may also be environmental pathogens in our water—pathogens that persist, grow and even proliferate in the environment. Legionella pneumophila is one of the better known examples. Examples of pathogens with life cycles related to water, such as the Plasmodium
901
species (spp.) that cause malaria, are also included in Table 16.5.
Table 16.5 Pathogens in or Related to Water, Diseases They Cause, and Approaches to Prevention and Treatment
Pathogen Disease Methods of prevention and treatment
Bacterial Vibrio cholerae Cholera Public sanitation,
vaccination; oral or IV rehydration, antibiotics
Salmonella typhi Typhoid Public sanitation, vaccination; antibiotics
Salmonella spp. Salmonellosis Food-related hygiene; rehydration, antibiotics
Toxigenic/diarrheagenic E. coli
Diarrheal diseases Public sanitation, hygiene; rehydration, antibiotics
E.g., E. coli O157:H7 Diarrhea, hemorrhagic colitis, hemolytic-uremic syndrome (HUS)
Food-related hygiene; rehydration (antibiotics are contraindicated)
Shigella spp. Shigellosis Sanitation, hygiene; rehydration, antibiotics
Campylobacter spp. Campylobacteriosis; Guillain-Barré syndrome
Food hygiene; rehydration
Leptospira spp. Leptospirosis Sanitation, vaccination; rehydration, antibiotics
Francisella tularensis Tularemia Hygiene, sanitation, insect repellents,
902
vaccination; antibiotics
Yersinia enterocolitica Yersiniosis Food-related hygiene; rehydration, antibiotics for bacteremia
Aeromonas spp. Skin and respiratory infections
Avoid exposure, boil water if immunocompromised; antibiotics
Helicobacter pylori Gastric ulcers and cancer
Personal hygiene, reduce crowding; antibiotics
Legionella pneumophila Legionellosis, Pontiac fever
Maintenance of water systems; antibiotics
Mycobacterium avium Disseminated infections, pulmonary disease
Avoid exposure, boil water if immunocompromised; antibiotics
Burkholderia pseudomallei
Melioidosis Vaccination (experimental); high- intensity IV antibiotics followed by maintenance dosage of oral antibiotics
Protozoal Giardia lamblia Giardiasis Sanitation, hygiene;
metronidazole Cryptosporidium spp. Cryptosporidiosis Sanitation, hygiene;
nitazoxanide, rehydration
Naegleria fowleri Primary amoebic meningoencephalitis
Avoid exposure in surface waters; amphotericin B
Acanthamoeba spp. Granulomatous amebic encephalitis, keratitis, and others
Avoid exposure, boil water if immunocompromised;
903
not well established Entamoeba histolytica Amoebiasis,
including amoebic dysentery
Food-related hygiene, sanitation; metronidazole, tinidazole
Cyclospora cayetanensis
Cyclosporidiosis (cyclosporiasis)
Sanitation; rehydration, trimethoprim- sulfamethoxazole
Isospora belli Isosporiasis Sanitation; rehydration, trimethoprim- sulfamethoxazole
The Microsporidia Microsporidiosis Counseling for immunosuppressed patients; rehydration, albendazole
Balantidium coli Balantidiasis Avoiding contact with pigs (primary reservoir); rehydration, tetracycline, metronidazole
Toxoplasma gondii Toxoplasmosis Hygiene, vaccine may be close; pyrimethamine
Viral*
Norovirus Viral gastroenteritis Vaccine may be close; rehydration
Hepatitis A virus Fever, malaise, nausea, anorexia, and abdominal discomfort, jaundice
Hygiene, vaccination; immune globulin, symptom relief
Hepatitis E virus Fever, malaise, nausea, anorexia, hepatomegaly, abdominal pain and
Vaccine may be close; rest
904
tenderness, jaundice Rotavirus Acute gastroenteritis Vaccination;
rehydration Major parasitic diseases related to water Plasmodium spp. Malaria Behavior modification,
insecticides, impregnated bed nets; artemisinin- combination therapy
Dracunculus medinensis
Dracunculiasis Behavior modification, insecticides; careful removal of worms
Schistosoma spp. Schistosomiasis Interrupt transmission though annual mass drug administration (MDA), behavior modification; praziquantel
Wuchereria spp. and Brugia spp.
Lymphatic filariasis MDA, insecticides (larvicides); diethylcarbamazine citrate (DEC) plus albendazole
Onchocerca volvulus Onchocerciasis MDA, insecticides (larvicides); ivermectin
* Also poliovirus, coxsachievirus, echovirus, reovirus, adenovirus, astrovirus, coronavirus, and others yet to be identified.
Source: Adapted from Ford & Hamner, 2010.
Sources of Outbreaks The etiology of waterborne disease is strongly affected by the sources of the infectious agents. For example, Shigella species are primarily human pathogens, and outbreaks of shigellosis are usually associated with contamination from human sewage. Escherichia coli (E. coli), Campylobacter, Salmonella, and many of the
905
protozoan and viral pathogens are zoonotic (associated with livestock and wildlife). In recent years, waterborne disease outbreaks in North America have been linked to exceptionally heavy rainfall and resultant flooding. This is not surprising, given the increased emphasis on high-density farming practices and their proximity to water supplies. Two outbreaks are illustrative: the massive outbreak of cryptosporidiosis in Milwaukee in 1993 and the outbreak of E. coli O157 in Walkerton, Ontario, in 2000 (The Walkerton outbreak is summarized in Text Box 16.4). These and other outbreaks are discussed in detail by Hrudey and Hrudey (2004).
906
Text Box 16.4 Chronology of Events During the Walkerton, Ontario, E. coli O157 Outbreak in 2000 An outbreak of waterborne disease in Walkerton, Ontario, in May of 2000 was one of the most severe such outbreaks in North America in recent years. The town relied for part of its source water on a well adjacent to a local farming operation. The problems began after a period of heavy rain.
May 12: Heavy rain falls over several days. The rain is thought to have caused pathogens in cattle manure either to infiltrate the wellhead or to contaminate the aquifer through seepage.
May 17: Tests of drinking-water samples taken on May 15 indicate the presence of coliforms and E. coli. However, the general manager of the Public Utilities Commission fails to notify appropriate health officials.
May 18: Walkerton residents begin to report symptoms of gastrointestinal illness; two children with bloody diarrhea are hospitalized.
May 19: Health officials contact the Public Utilities Commission and are assured that the water is safe.
May 20–21: The number of illnesses continues to rise. The government health officer orders a “boil water” advisory, despite continued assurances from utility personnel.
May 22: First person dies.
May 23: Independent tests show that E. coli O157:H7 is present in the drinking water. Hundreds of people complain of symptoms, more than 150 people seek hospital treatment, and a two-year-old girl dies.
May 24: Two more deaths.
May 25: Fifth death, and four children listed as critical.
907
May 29: Sixth death.
May 30: Seventh death.
May 31: Public inquiry ordered.
Investigation revealed that the utility had been falsifying records for some time, and that the chlorination system had not been functioning properly. The utility operator “did not like the taste of chlorine.” Class action lawsuits and criminal investigations followed. The tragedy also resulted in implementation of far stricter regulations for Ontario's drinking water, and the realization that proper operator training is critical.
Source: Adapted from Ford, Rupp, Butterfield, & Camper, 2005.
Over recent decades, the calicivirus group, and particularly the noroviruses, have been implicated in outbreaks of gastroenteritis, and have been estimated to account for more than 85% of all nonbacterial outbreaks (Lopman et al., 2003). A recent meta- analysis suggests that noroviruses account for almost a fifth of all cases of acute gastroenteritis worldwide (Ahmed et al., 2014).
Wastewater Treatment Because most (but not all) biological contaminants result from human or animal wastes, waste treatment practices play a major role in water contamination and consequent outbreaks. Sewage is managed in many ways, from the primitive to the highly technical, as illustrated in Figure 16.4. Human waste can be discharged directly to receiving waters through surface water runoff from open defecation sites, a common occurrence in many developing countries, or processed in ways ranging from a simple shallow pit to a larger community sewage system. These latter systems require large volumes of water for efficient operation, so large amounts of wastewater are generated, requiring subsequent treatment before release to receiving waters. Wastewater treatment and discharge can place a heavy burden on receiving waters in terms of pathogens, nutrients, and toxic chemicals. For some river systems, wastewater makes up the primary flow during dry seasons. Groundwater can also be contaminated with human pathogens from leaking septic systems, contaminated runoff infiltrating wellheads, and seepage
908
from animal feedlots.
Figure 16.4 Sanitation Options Source: Diagrams reproduced from Franceys, Pickford, & Reed, 1992. © World Health Organization.
An idealized wastewater treatment process, loosely based on Boston's Deer Island treatment plant (see Massachusetts Water Resources Authority, 2009), is shown in Figure 16.5. Systems such as this are expensive to build and maintain, and in general only the wealthiest municipalities can afford such extensive systems. Table 16.6 displays some of the challenges facing the global population, particularly in the low- and middle-income countries.
909
Figure 16.5 An Idealized Wastewater Treatment System, Based on Boston's Deer Island System
Most municipal wastewater can be treated using this or a similar treatment train. However, if industrial or other sources of toxic chemicals are present, wastes may need to undergo far more sophisticated and expensive tertiary treatment. Further discussion of wastewater treatment is beyond the scope of this chapter, and many excellent texts are available to the reader (e.g., Bitton, 2011).
aManholes give access from the street to the main sewer for maintenance. However, there may also be direct connections to street drains in the case of a combined sewer system. This may dramatically increase the volume of wastewater that the treatment plant has to process, often overwhelming the system and allowing untreated wastewater to be released to receiving waters.
bBiological oxygen demand, or BOD, is a measure of the readily assimilable organic carbon present in wastewater. BOD is defined as the amount of oxygen used by microorganisms in the aerobic degradation of organic wastes over a set time period and at a constant temperature (usually five days at 20°C).
cSecondary treatment can range from an energy-intensive, activated sludge system, where oxygen is added to accelerate microbial activity, to simple aeration ponds, which rely on the action of wind, algae, and macrophytes to facilitate oxygen transfer.
dLand application of sewage sludge is facing increasingly stringent regulations due to concerns about pathogens and toxic chemicals in the food chain and about potential contamination of ground and surface waters.
910
Table 16.6 Global Challenges in Water and Sanitation, Particularly in Low- and Middle-Income Countries
About 748 million people lack access to improved water supplies.
173 million use untreated surface water.
>90% rural.
About 2.5 billion people do not use an improved sanitation facility.
1 billion people still practice open defecation.
70% rural.
About 81% of the global population do not wash their hands with soap after contact with excreta.
Sources: WHO and UNICEF, 2014; Freeman et al., 2014.
The Indicator Concept Monitoring the microbiological quality of water requires measurable indicators. Although many microbial species could be chosen for this purpose (see Table 16.7), the traditional indicator has been the coliform group. The premise has been that the concentration of coliform organisms reflects the overall microbial quality of water. Methods to detect and quantify coliform counts have become increasingly sophisticated. In the early 1900s, growth of bacteria on a nutrient agar plate at 37°C was thought to be indicative of possible contamination by enteric organisms. Later, coliform bacteria were enumerated in selective liquid culture media, using a technique known as the most probable number method. More recently the membrane filtration technique gained in popularity, and today, enzyme specific, colorimetric assays, which are accurate and can be easily conducted by water utility personnel, are frequently employed.
Table 16.7 The Indicator Approach to Monitoring Water Quality
Indicator What does it indicate Limitations Coliforms Presence of the coliform Certain coliforms
911
group of bacteria, many of which are present in human or animal fecal material.
grow naturally in drinking-water biofilms, particularly at warmer temperatures. Not indicative of protozoa or viruses.
E. coli Presence of E. coli; strong indication of fecal contamination.
Inactivated more rapidly than other pathogens. Not indicative of protozoa or viruses.
Coliphages Indicative of the presence of viruses specific to E. coli.
May or may not be indicative of viral pathogens. Not indicative of protozoa or bacteria.
Enterococci May be indicative of presence of animal wastes as well as human waste.
Not indicative of protozoa or viruses.
Clostridium Spore-forming bacteria; anaerobes; protozoa.
Not indicative of viruses.
Pseudomonas Survives in drinking-water biofilms; may indicate presence of bacterial pathogens that are more persistent than coliforms.
Not indicative of protozoa or viruses.
Aeromonads Survive in drinking-water biofilms; may indicate presence of bacterial pathogens that are more persistent than the coliforms.
Not indicative of protozoa or viruses.
Human- specific Bacteroides fragilis bacteriophages
Indicative of the presence of viruses specific to B. fragilis; may be present when coliphages are absent.
May or may not be indicative of viral pathogens. Not indicative of protozoa or bacteria.
912
Turbidity May indicate that the water exceeds turbidity regulations. Some studies show increased risk for waterborne disease at high turbidity (pathogens adhere to particles).
Measures only turbidity; cannot be directly correlated to pathogen loading.
Residual chlorine
Measures the disinfectant residual at the tap. Absence of residual chlorine has been shown in some studies to be consistent with waterborne disease.
Measures only residual chlorine; cannot be directly correlated to pathogen loading.
However, the indicator concept, with its reliance on total coliform counts, has been challenged. Once human pathogens have contaminated groundwater and surface water, their fate is very much organism specific. In fact the coliform group is inactivated relatively rapidly, whereas other human pathogens can survive for extended periods. This is particularly true for the pathogenic protozoa that form highly resistant cysts or oocysts and the viruses that appear to survive adsorbed to particulate material. As a result, a reassuringly low coliform count could belie the true (and perhaps dangerous) levels of other organisms. (The advantages and shortcomings of the indicator approach have been discussed extensively in the literature; see, e.g., Rose & Grimes, 2001; Lin & Ganesh, 2013; Gruber, Ercumen, & Colford, 2014.)
Global Burden of Waterborne Disease The primary sources of information on the global burden of disease are the World Health Organization (WHO, 2014a) and the Institute of Health Metrics and Evaluation (IHME) (Lim et al., 2012). The burden is quantified in terms of both mortality and morbidity (reported as disability-adjusted life years, or DALYs), to express the years lost through both premature death and severity of disease. Although waterborne disease is not specifically identified, the category of diarrheal disease is included, as are malaria and a number of other tropical diseases related to water. Risk factors include both unimproved water sources and unimproved sanitation. WHO estimates that diarrheal disease amounts to 3.6% of the total
913
DALYs in the global burden of disease (99.7 million DALYs per year), and is responsible for the deaths of 1.5 million people every year. This burden is comparable to the annual mortality and morbidity figures for other leading infectious diseases: 1.53 million deaths and 91.9 million DALYs for HIV/AIDS, 0.94 million deaths and 44 million DALYs for tuberculosis, and 0.62 million deaths and 55 million DALYs for malaria.
It is important to remember that these numbers are likely to underestimate significantly the actual burden of waterborne disease, due to a number of factors (discussed in detail in Ford & Hamner, 2014). The most common outcome from exposure to waterborne pathogens is acute gastrointestinal infection (AGI). Symptoms similar to AGI may also be caused by chemical contaminants. AGI is frequently undiagnosed and seldom officially reported, even in cases where death is the final outcome (see Hamner et al., 2006).
In addition to the multiple ways we are exposed to waterborne contaminants, as discussed earlier, the situation is further complicated by the fact that many infectious (and chemical) causes of disease can be transmitted through water or food and also person to person. It is virtually impossible to distinguish these routes clearly, as the spread of diarrheal disease within a population can be dominated by secondary transmission. An initial infection may be caused by consumption of contaminated drinking water but may then rapidly spread through person-to-person transmission or through food contaminated by the water itself or by the infected individual (Text Box 16.5).
914
Text Box 16.5 Risk Factors and the Changing Burden of Disease A recent analysis of inadequate water, sanitation, and hygiene suggests that this cluster of risk factors is responsible for 56% of diarrheal disease deaths, or a total of 842,000 deaths annually (Prüss-Ustün et al., 2014). This number (and analysis from Lim et al., 2012) suggests a significant decrease in mortality from inadequate water, sanitation, and hygiene since the previous edition of this book was prepared. This is in part due to continuing improvements in risk assessment methodologies, but also to considerable successes in reducing the global burden of waterborne disease through access to improved water supplies and sanitation since 1990. The greatest success is that we reached the Millennium Development Goal of 88.5% global population with access to improved water by 2015. But there is still much to be achieved, as this burden of disease remains largely preventable. (A related health concern is addressed in Figure 16.6.)
915
Figure 16.6 Carrying Water Source: Timothy Ford.
Our tendency is to associate contaminated water with human disease, but it is important not to overlook some of the other global health concerns associated with accessing safe drinking water. One example is the skeletal damage that can result from carrying drinking water—particularly among young children, who are often assigned this task.
Waterborne diseases may be controlled, and in some cases eliminated, through changes in water sources, water quality, and human behavior, offering enormous prospects for public health advances.
Safe Drinking Water For most developing countries, hygiene and sanitation remain the cornerstones of public health. The simplest interventions, such as educating people to avoid defecation near drinking-water sources, providing simple treatment options (Table 16.8; also see Text Box 16.6), and providing bed nets (to reduce exposure to mosquitoes), can dramatically reduce the burden of disease. In
916
wealthier nations, a multibarrier approach is more economically feasible, so that the process of making drinking water safe extends from the source to the faucet, with protection of water sources from contamination, water treatment to remove contamination, and protection of water from recontamination during distribution.
Table 16.8 Simple, Low-Cost Water Treatment Options
Treatment option Mode of pathogen removal
Information sources
Safe Water System: bleach, storage vessel, and behavior change
Sodium hypochlorite CDC, 2014
Flocculant/disinfectant: P&G Purifier of Water™
Calcium hypochlorite P&G Heath Sciences Institute, 2014
Ceramic water filters Variety of types, colloidal silver and also copper
Potters for Peace, 2014
Biosand filter Adsorption/competition Center for Affordable Water and Sanitation Technology, 2014
Boiling Temperature Many sources: e.g., Sodha et al., 2011
Solar water disinfection UV and temperature SODIS, 2014 Llaveoz UV Gutierrez-
Jimenez et al., 2014
LifeStraw® Iodine and silver Vestergaard, 2013
Sari cloth Prefilter for particles and pathogen hosts: e.g., copepods
Huq et al., 2010
917
The Drinkable Book Filtration (each page is a readable filter)
WATERisLIFE, 2014
Source: Adapted from Ford & Hamner, 2010.
918
Text Box 16.6 Water Treatment More Than a Century Ago (1881) Drinking-water treatment is not a new idea. The chapter author's great-great-grandfather, Reginald Craufuird Sterndale, described (and drew) the basic process in 1881 (Figure 16.7).
Figure 16.7 Basic Drinking-Water Treatment Process Source: Sterndale, 1881, pp. 168–169, reproduced in Ford & Hamner, 2015.
“There can be no doubt,” Sterndale wrote,
that, if the people could be induced to boil and filter the water used by them, that many dangerous waters might be thus used with comparative safety; but this cannot be expected, the very cost of fuel would prevent the poorer classes from taking this precaution; nor is it probable that they could, to any extent be brought to filter their drinking water, although materials for constructing a
919
most efficient filter is to their hand, and at an outlay of but a few pice [a former monetary unit]—a rough wooden stand, three ordinary porous earthenware culshis or jars, a small quantity of charcoal or sand being all that is necessary [Sterndale, 1881, pp. 168–169, reproduced in Ford & Hamner, 2015].
Today, simple interventions can be surprisingly effective at reducing waterborne disease. A great example is the use of sari cloth in Bangladesh to remove cholera bacteria (see Table 16.8).
Source Protection Probably the most important consideration for the protection of human health in relation to potable water supplies is provision of high-quality source water. Watershed protection is critical to this process but often comes into direct conflict with development and with recreational uses of watersheds. In many metropolitan areas development has dramatically outstripped the availability of high-quality source water. Inevitably, many municipalities now depend on surface waters that receive wastewater, both treated and untreated. Protection of source water involves maintaining generous buffers, limiting access for recreational purposes, and preventing agricultural and industrial uses. Many would argue that all wildlife and wildfowl should be prevented from accessing source water, however impractical this may be.
Water Treatment Given that many source waters are of poor quality and that even high-quality source water can become contaminated, some level of water treatment is considered essential. Arguably, the water treatment process begins with conveyance of water from the source to the plant. Prevention of contamination during conveyance, which in certain cases could involve hundreds of miles of pipeline, aqueduct, or even open ditches, is clearly important.
Water treatment consists of several steps, as shown in Figure 16.8. The process can be summarized as sequentially removing material from the source water, from large solids down to microorganisms and even chemical contaminants. Actual filtration methods range
920
from simple, time-honored techniques such as slow sand filtration to sophisticated technologies such as nanofiltration, depending on the resources available and the size of population served.
Figure 16.8 A Multibarrier Approach to Maximize Microbiological Water Quality
Note: This presumes a treatment system that has sufficient capacity to maintain adequate pressure throughout the distribution system for twenty-four hours per day and that minimizes opportunities for microbial colonization of the pipelines.
aDisinfection by-products, including aldehydes and brominated by-products, are formed by ozonation of source waters (discussed in Krasner, 2009; see also Tox Box 16.2). UV disinfection, used extensively in wastewater treatment, is rapidly gaining acceptance as an alternative to ozonation.
bAOC = Assimilable organic carbon, carbon that can be readily utilized by microorganisms and therefore stimulates their growth.
cResidual disinfection requires a chemical that will not be rapidly broken down in the distribution system so that it retains some disinfecting activity at point of use (the tap). To date the only practical chemicals appear to be chlorine or chloramines. Chloramination may be preferable to chlorination, as chloramines may penetrate biofilms more effectively than chlorine alone. They also reduce formation of disinfection by-products and are more effective at a high pH (a high pH is often necessary for corrosion control). Where chloramination is used, intermittent
921
chlorination and system flushing is recommended, as chlorine is the more powerful oxidizing agent.
dA rigorous program is necessary to upgrade distribution system networks and to prevent interconnections through leakage, backflushing, improper hydrant use, and so forth.
The final step is postfiltration disinfection. Since the early twentieth century, chlorination has been the most widely used form of disinfection. Chlorine and chlorine compounds are thought to act as disinfectants by denaturing enzymes. Chlorine has the advantage of forming a residual in water as it flows from the treatment plant through the pipes of the distribution system to faucets. This helps to prevent regrowth of microorganisms in the distribution system (although biofilms impede this goal). More recently, with concerns about potential toxicity of chlorination by-products, alternative forms of disinfection such as ozonation and pulsed UV have been gaining popularity. Table 16.9 compares alternative forms of disinfection and chlorination.
Table 16.9 Approaches to Disinfection
Disinfectant Benefits Concerns Cost Chlorine Retains a residual;
strong disinfectant. Taste and odor; toxicity of by- products; some microbes are resistant; not effective at a high pH.
Moderate.
Chloramine Retains a residual; used for a wider range of pHs; may penetrate biofilms more effectively than free chlorine.
Weaker disinfectant; some by-products formed but fewer than from free chlorine.
Moderate.
Chlorine dioxide
Powerful disinfectant; no by- products formed.
Toxic; chemically unstable and cannot be stored; no residual.
Expensive.
Ozone Powerful disinfectant; can be
Must be generated on site;
Expensive, but can be
922
effective against chlorine-resistant microbes.
can increase assimilable organic carbon; forms bromates.
economical with a large operation.
UV (pulsed) Short contact time; no toxic by- products; not influenced by pH or temperature.
No residual; not effective with high turbidity water.
Increasingly competitive and gaining in popularity.
Solar Inexpensive; simple; uses readily available supplies.
Small scale; slow; potential chemical leaching from polyethylene terephalate (PET) plastic bottles.
Low.
Disinfection Resistance and By-Product Toxicity One reason for exploring alternatives to chlorination is the growing realization that a number of microbes are apparently capable of surviving at the “safe” chlorination levels typically maintained in drinking water (Ford, 1999). However, at this date, there appears to be no alternative to chlorination (or chloramination) for maintaining a residual.
Given the necessity for residual disinfection in distributed water, a quantity of chlorine (or chloramines) must be added posttreatment. However, chlorine compounds react with naturally occurring organic matter to form disinfection by-products (DBPs). The best recognized DBPs are trihalomethanes such as chloroform and trichloroacetic acid, although the potential range of disinfection by- products is enormous, given the vast number of chemical precursors that can occur in source water. DBPs are explored in Tox Box 16.2.
923
Tox Box 16.2 Disinfection By-Products
What Are They? Disinfection by-products are chemicals formed when water disinfectants such as chlorine, ozone, and bleach react with inorganic or organic matter in water. The most common types of disinfection by-products are trihalomethanes and haloacetic acids, which are both a consequence of chlorination. The less common by-products are bromate, a consequence of ozonation, and chlorite, a consequence of disinfection with chlorine dioxide gas. Disinfection by- products illustrate a common risk versus benefit conundrum in public health: even though their by-products are undesirable, disinfectants play a major role in reducing the burden of waterborne diseases, particularly in the developing world.
How Are People Exposed? People are exposed to low concentrations of disinfection by- products when they drink disinfected water. People bathing or showering in disinfected water may also inhale low concentrations of volatile disinfection by-products or may absorb them dermally. When people bathe in hot water, the higher temperature further volatilizes the by-products and increases dermal absorption. Accordingly, inhalation and dermal absorption may account for more exposure to trihalomethanes than ingestion.
924
What Are the Toxic Effects? Most information about the toxic effects of chronic exposure to very low concentrations of disinfection by-products is extrapolated from animal studies. In these studies animals were exposed over shorter periods of time to higher concentrations than humans confront. Therefore there is uncertainty and controversy about how well these animal data apply to humans.
For trihalomethanes and bromate there is enough animal evidence that the International Agency for Research on Cancer (IARC) classifies these by-products as possible human carcinogens. Furthermore, inhalation or ingestion of trihalomethanes can cause liver necrosis in animals, and at higher doses can cause nephrosis.
In contrast, IARC, citing a lack of data, has not reached a finding on haloacetic acids. The EPA disagrees, and classifies various haloacetic acids as either possible or probable human carcinogens, based on observations of liver cancer in exposed rodents. Very high doses of haloacetic acids can also damage the testes and disrupt sperm formation in male animals.
Similarly, IARC considers chlorite to be currently unclassifiable. In animals that ingested acute doses of chlorite, the chlorite irritated their digestive tracts and caused developmental delays in offspring born to exposed mothers.
How Are People Protected? People are protected from exposure to high concentrations of disinfection by-products through a combination of regulation, public disclosure, and technical alternatives. While these methods aim to keep by-product concentrations very low, the WHO cautions that adequate disinfection is more important to public health than further reducing the generally low levels of disinfection by-products, given that diarrheal disease kills many children and infants in the developing world.
In the United States, people are mostly protected by
925
regulation and disclosure. Under the 1974 Safe Drinking Water Act—which established that levels for drinking-water contaminants must be set where no adverse health effects are likely to occur—the EPA sets enforceable maximum contaminant levels (MCLs) for trihalomethanes, haloacetic acids, bromate, and chlorite. Furthermore, water suppliers must routinely monitor disinfection by-product levels; when these levels exceed the MCLs, the suppliers must take steps to lower the by-product levels, and must notify consumers within thirty days of becoming aware of the violation.
Technical alternatives exist for disinfection methods, but they usually involve trade-offs. For example, replacing chlorination with ozonation reduces exposure to trihalomethanes but may increase exposure to bromate. Furthermore, chlorination can better prevent recontamination of drinking water after it leaves the treatment plant, whereas ozonation is effective only while the water is in the plant.
Want to Learn More? The toxicity of specific types of disinfection by-products is reviewed in the ATSDR Toxicological Profile for Chloroform (www.atsdr.cdc.gov/ToxProfiles/TP.asp?id=53&tid=16) and the Toxicological Profile for Bromoform & Dibromochloromethane (www.atsdr.cdc.gov/toxprofiles/tp.asp? id=713&tid=128#bookmark05). A useful review of how water disinfection forms by-products is Shah, A. D., & Mitch, W. A. (2012). Halonitroalkanes, halonitriles, haloamides, and N- nitrosamines: a critical review of nitrogenous disinfection byproduct formation pathways. Environ Sci Technol, 46(1), 119–131.
Contributed by Megan Cartwright
Water Distribution Water distribution is a critical step, and its failure has been implicated in many cases of drinking-water contamination and
926
waterborne disease outbreaks. Water, generally containing a disinfectant residual, may be distributed through hundreds of miles of pipeline throughout a major city. In addition to passing through the major distribution lines, the water also flows through building pipelines. All of these pipes are potential sites for cross- contamination through a variety of processes. Metal pipes are susceptible to corrosion and over time can develop holes that may allow external sources of water to enter during periods of low pressure. This happens, for example, when hydrants are extensively used during firefighting. Low pressure in the drinking-water system can also cause back siphonage from pipes or tubing left hanging in sinks or other water or waste storage. This is a particular issue in high-rise buildings, where distribution system pressure may be insufficient to maintain supply to top floors throughout a twenty- four-hour period. Where this is the case, there is a tendency for residents to fill bathtubs and other vessels to provide a reserve. Even when there is no external contamination, regrowth of microorganisms in distribution lines remains a very real problem. This is particularly true at dead-end sites such as fire hydrants. Water remains essentially stagnant at these sites, and any residual chlorine in the system rapidly combines with organic matter, allowing microbes to grow and proliferate (Ercumen, Gruber, & Colford, 2014).
Point-of-Use Treatment and Bottled Water Alternatives to tap water that consumers increasingly consider for the potable water that they consume directly are point-of-use treatment and bottled water. Point-of-use treatment refers to the simple techniques used in homes to disinfect water, such as filtering the water or adding bleach to plastic water storage vessels. These are certainly viable options, but it is necessary to maintain a point-of-use device properly to avoid exacerbating water quality problems by providing, in effect, a “biofilm reactor” that encourages microbial growth. Biofilms are the microbial slimes that grow on the walls of drinking-water pipes, in faucets, showerheads, and in fact on any surface in contact with water. They can harbor pathogens and are very difficult to effectively disinfect (Wingender & Flemming, 2011).
Bottled water places the consumer at the mercy of the
927
manufacturer, as bottled water is not currently as rigorously regulated as municipal water. There is some evidence that, in developing nations, bottled water from small manufacturers has a high probability of microbiological contamination (Igbeneghu & Lamikanra, 2014). In addition, there is a compelling argument that if the money people are willing to pay for point-of-use filters or bottled water were invested in municipal treatment and distribution, many current health risks (real and perceived) could be mitigated.
928
Regulatory Framework Water quality monitoring regulations are well developed for a vast suite of chemicals, driven primarily by the increasingly sensitive technologies that can be used for measuring trace levels of contaminants. Unfortunately, the same is not true for microbial contaminants. The indicator approach (Table 16.7) remains the primary method for assessing microbiological quality of drinking water, despite the fact that many pathogens survive for extended periods in drinking water in the absence of these indicators. Indeed, a number of environmental pathogens may be present in drinking water in the complete absence of any contamination source.
The Clean Water Act The Clean Water Act (CWA), enacted in 1972, was built on the Federal Water Pollution Control Act of 1948 and was put in place to regulate pollutant discharge to U.S. waters. Pollution control programs included setting wastewater discharge and surface water standards, and establishing strict requirements for permits that allowed pollutants to be legally discharged into water. The U.S. EPA is the federal agency charged with enforcing the requirements of the CWA, and more information about the Act and the enforcement policies can be can be found on its Web site (U.S. EPA, 2014a).
The Safe Drinking Water Act In the Safe Drinking Water Act (SDWA) (U.S. EPA, 2014c), passed in 1974 and amended in 1986 and 1996, the U.S. Congress mandated the EPA to regulate contaminants in drinking water that might pose a risk to human health. This complex piece of legislation has a number of important provisions.
A central strategy of the SDWA is to set permissible levels of contaminants in drinking water provided by public drinking-water utilities. (Private wells and systems with fewer than fifteen connections or serving fewer than twenty-five people are not regulated by the SDWA.) The EPA establishes two sets of benchmarks, one based on ideal health goals and the other based on feasibility. In the first set, which contains maximum contaminant
929
level goals (MCLGs), a goal is defined as the “level of a contaminant in drinking water below which there is no known or expected risk to health” for a person after drinking two liters of water each day for seventy years. These goals are set to include a margin of safety. For many contaminants, such as carcinogens, lead, and some pathogens, MCLGs are set at zero. MCLGs are public health goals, not enforceable standards. In contrast, the second set of goals contains the maximum contaminant levels (MCLs) discussed earlier in Tox Boxes 16.1 and 16.2. These goals are legal limits. They are set as close to MCLGs as possible, taking into account both technological feasibility and cost.
The National Primary Drinking Water Regulations (NPDWR) promulgated by the EPA are based on these benchmarks. These regulations extend to fifty-three organic compounds, sixteen inorganic compounds, four classes of radionuclides, four types of disinfection by-products, and three disinfectants. In terms of microbial contaminants, Cryptosporidium, Giardia lamblia, Legionella, and viruses are regulated, but only in terms of percentage of removal or inactivation by treatment. Heterotrophic plate counts (a measure of microbial load), turbidity, and total coliform levels (including fecal coliform and E. coli) are also regulated. The EPA also publishes the National Secondary Drinking Water Regulations (NSDWR), which are nonenforceable guidelines for contaminants that cause cosmetic or aesthetic problems in drinking water.
The SDWA also sets additional regulatory requirements. To meet these requirements, the EPA has, for example, established monitoring schedules, monitoring methods, and acceptable treatment technologies, and it maintains the Contaminant Candidate List (CCL) (Text Box 16.7). The EPA has also established the Surface Water Treatment Rule, which governs filtration of public water supply systems.
930
Text Box 16.7 The Contaminant Candidate List Under the 1996 Amendment to the SDWA, the EPA is required to publish, every five years, a list of contaminants that are not subject to regulation at the time of publication but that are anticipated to occur in drinking water and that may require future regulation. Known as the Contaminant Candidate List (CCL), the 2009 iteration, CCL 3, named 93 chemical and 11 microbial contaminants. In 2015, the EPA released a draft of CCL4, which listed 100 chemicals or chemical groups and 12 microbial contaminants. The CCL provides an important indication of contaminants that will receive growing public health attention and helps to guide the EPA's research agenda. Chemicals on the list undergo extensive toxicity assessments, and risks of exposure through drinking water are characterized to the degree current methodologies allow.
Total Coliform Rule In 1989, the EPA finalized the Total Coliform Rule. This rule is currently the driving force behind drinking-water safety and the testing it requires frequently serves as the first indication (other than turbidity) of potential contamination. The rule requires a water system to establish a regular coliform sampling plan, with sample sites that accurately represent water quality throughout the distribution system. Any sample that is positive for total coliforms requires repeat samples and must be tested for fecal coliforms or E. coli. Specific requirements vary somewhat depending on the size of the population served (U.S. EPA, 2013b).
A component of the Total Coliform Rule that is designed to protect smaller public water systems is the sanitary survey. Every system collecting fewer than five samples per month is required to have regular sanitary surveys, usually every five years. This survey is designed to evaluate the entire water system, its operations, and its maintenance in order to ensure public health (U.S. EPA, 2012).
931
Consumer Confidence Reports An important outcome from the 1996 Amendment to the SDWA was the requirement that utilities provide annual Consumer Confidence Reports (CCRs) (U.S. EPA, 2013a). These reports inform consumers about the sources of their drinking water, any detected contaminants, and related information. The CCRs are designed to allow consumers to make informed choices about their drinking water.
Recreational Water Standards The EPA and state agencies also regulate recreational waters. For example, swimming advisories are posted where indicator organisms exceed recommended levels. For freshwater, current standards are 126 E. coli per 100 mL or 33 enterococci per 100 mL. Regulations state that only one of these two indicator organisms should be used. For seawater, the standard is set at 35 enterococci per 100 mL. (For further information on recreational water safety and on the rationale for standards, see Bartram & Rees, 2000; U.S. EPA, 2014b; WHO, 2014b.)
932
Risk Characterization for Water Contaminants Risk assessment is the process used to prioritize interventions and to reduce human exposure to environmental sources of chemicals and pathogens, as described in Chapter 27. However, microbiological risk assessment raises some additional considerations.
To identify microbial hazards, spot samples are generally taken from finished water at the treatment plant and occasionally at conveniently accessible sites in the distribution system. However, distribution of pathogens is extremely heterogeneous in drinking water. Most consumers will not ingest an infectious dose of a pathogen, and measurements of water samples will frequently be zero. However, a few individuals may consume a large number of infectious microbes. Moreover, as previously discussed, routinely monitored coliform bacterial counts do not reliably signal the presence of most pathogens. Utilities expect that major contamination events in a watershed will be recognized from turbidity spikes; however, this is not always the case. Turbidity spikes were not excessive for the contamination event in Milwaukee in 1993 (MacKenzie et al., 1994). An event of far smaller magnitude may not result in elevated turbidity, or minor spikes may be missed. A rare event, a plug of infectious oocysts, cysts, or viruses, could enter the distribution system and very easily be missed by a spot sampling program, yet contain sufficient numbers to virtually ensure that ingestion will result in infection (Gale, 2001). Exposure assessment therefore remains a challenge in microbial risk assessment. (The heterogeneity of pathogen distribution and the many other factors that contribute to the challenge of microbial risk assessment are discussed in detail in Haas, Rose, and Gerba, 2014.)
933
Emerging Issues Public health issues related to water are highly dynamic. Emerging issues include new and shifting diseases, new techniques for assessing water quality, and new approaches to managing water quality.
The Phenomenon of a New Disease Many factors can promote the real or apparent emergence of a new disease. New ecological niches, such as the hot-water systems that support growth of Legionella, may contribute. Factors such as population density and increasing numbers of susceptible individuals (the very young, the elderly, pregnant women, and the immunocompromised) could provide an extensive human reservoir for opportunistic pathogens and promote changes in virulence patterns, even in developed countries. Increased adaptation to the human host might be responsible for increased infection rates (of mycobacterial diseases, for example) in populations with no underlying susceptibility.
Legionella pneumophila, E. coli O157, Vibrio cholerae O139, Helicobacter pylori, Cryptosporidium parvum, and Hepatitis E virus, are all examples of microorganisms categorized as new or newly recognized pathogens. Well-established pathogens should arguably be added to this list as they develop antibiotic resistance and change virulence patterns (Ford, 1999). Research is clearly needed to better understand the ecology of the water environment that may promote new disease emergence.
Online Monitoring The dream of online monitoring for pathogens in drinking-water systems remains frustratingly elusive. A 2001 American Academy of Microbiology report began with a scenario of gene chips (tiny devices whose surfaces contain arrays of DNA or RNA fragments) being placed in a flow of water, detecting the presence of specific pathogens, and sending signals directly to operators to alert them of the imminent risk (Rose & Grimes, 2001). We are still not close to this point although research continues (e.g., Brinkman et al., 2013;
934
Besmer et al., 2014). Beyond molecular detection of specific pathogens, research has also focused for several years on use of physical and chemical techniques for online biofilm monitoring. Biofilms not only present pathogen risk but also affect distribution system operation and integrity by contribution to corrosion and flow restrictions. A good review of some of these techniques is provided by Janknecht and Melo (2003).
Wastewater Reuse This discussion cannot be complete without returning to the topic of wastewater. A vital step in providing adequate, safe drinking water is to understand that wastewater is a valuable resource. Today, wastewater reuse programs are increasingly encouraged in the more arid states in the United States, primarily for nonpotable uses. This involves separate collection of blackwater (primarily toilet wastes, although it may also include other wastewater rich in organics, such as the effluent from a garbage disposal system) and graywater (other sources of wastewater such as bath and shower water). The graywater can then be used to irrigate nonedible plants and in some cases can also be used for toilet flushing.
The use of recycled wastewater to augment diminishing supplies of drinking water is just beginning. The barriers to wastewater recycling are as much related to public perception as they are to cost. Many of the more affluent nations are increasingly having to rely on desalination to supply drinking water for their more arid regions. Treatment technologies are equally capable of recycling wastewater to a potable quality. The predicted increase in the number of water-scarce countries during the twenty-first century makes education in this area critical. However, water recycling alone will not be sufficient; we will also need a concerted effort to conserve the available remaining resources.
935
Summary Water is critical to all forms of life on this planet, yet we would appear to have been systematically threatening this precious resource through agricultural, municipal, and industrial development. This development has happened with little regard for the amount of water we squander, the wastes we produce, or the engineering schemes that degrade this resource. The key messages to be learned from a careful evaluation of the critical role that water plays in human and ecological health are that we must conserve the resource, we must reduce our waste production, and we must recycle what we use. We must also educate communities on how to reduce their burden of waterborne disease. Finally, we must improve our abilities to predict future waterborne disease outbreaks, and be ready to provide public health intervention on a global scale to prevent future pandemic disease.
936
Key Terms absolute water scarcity
A shortage of water relative to demand, defined as at or below 500 m3 per person per year.
acute gastrointestinal infection (AGI) A general term for infection of the gastrointestinal tract, usually resulting from an infectious cause, and featuring nausea, diarrhea, pain, and other symptoms.
aquifer recharge The return of water to groundwater supplies, usually involving percolation through soil and consequent improvement of water quality.
biofilm An agglomeration of microorganisms and extracellular slime that forms on a surface, such as on the interior surfaces of pipes in water distribution systems.
biological oxygen demand (BOD) A measured parameter of wastewater, referring to the amount of readily assimilable organic carbon present, and defined as the amount of oxygen used by microorganisms in aerobically degrading organic wastes under specific conditions.
blackwater Waste water from sources such as toilets.
bottled water Water commercially bottled and sold to consumers. Bottled water often bypasses the regulatory oversight applied to municipal water systems. It is an important form of water provision in low-resource settings.
Clean Water Act A U.S. law, initially enacted in 1972, regulating pollution discharge into rivers and streams, and the quality of these bodies of water.
Consumer Confidence Reports Annual reports issued to consumers by public drinking-water systems, providing information on water quality, contaminants,
937
and other factors. Contaminant Candidate List
A list, published by the EPA, of contaminants that are not subject to regulation at the time of publication but that are anticipated to occur in drinking water and may require future regulation.
cross-contamination The entry of a nonpotable liquid, solid, or gas, or of water of poor microbial or chemical quality, into a potable water system.
cyanobacteria A phylum of photosynthetic bacteria (long called blue-green algae) that may produce toxins.
DALYs Disability-adjusted life years, a measure of morbidity and mortality. One DALY can be thought of as one lost year of “healthy” life, either through premature mortality or through living with a disability.
disinfection by-products Chemical species formed inadvertently when disinfecting agents such as chlorine or ozone react with organic matter in water.
E. coli A bacterium, Escherichia coli, traditionally used as an indicator of water contaminated with animal or human feces.
eutrophication An ecosystem impairment that follows the excessive deposition of nutrients, such as fertilizers, into lakes and rivers. The nutrients promote the growth of algae and other aquatic plants, which deplete the water of oxygen and distort the balance of aquatic life.
global burden of disease The quantification of health loss from hundreds of diseases, injuries, and risk factors, with the aim of improving health systems and eliminating disparities. The Global Burden of Disease Study originated with the World Bank in the early 1990s, was later housed at the World Health Organization, and is now coordinated by the Institute for Health Metrics and Evaluation. This research quantifies both the prevalence of a given disease or risk factor and the relative harm it causes.
938
graywater Wastewater from sources such as sinks and showers.
groundwater The supply of fresh water found beneath the Earth's surface, usually in aquifers.
groundwater under the direct influence of surface water (GWUDI)
Subsurface water with organisms or physical characteristics such as turbidity or pH that closely correlate to climatological or surface water conditions.
hydrodynamics The patterns of water movement through the environment.
hydrological cycle The continuous movement of water on, above, and below the surface of the Earth, including changes in phase (liquid, vapor, and ice) and processes such as precipitation and evaporation.
hydrophobic A feature of a molecule, referring to low solubility in water due to nonpolarity.
hygiene Practices designed to achieve microbial cleanliness and to reduce the risk of infection.
indicator In the context of this chapter, a parameter of water quality. Coliform counts are the principal traditional indicator of the microbial status of water.
irrigation The provision of water to land by artificial means, such as diverting streams or spraying, usually for agricultural purposes.
maximum contaminant level (MCL) A legal limit, under the Safe Drinking Water Act, on the levels of certain specific contaminants in drinking water.
microbiological risk assessment Risk assessment related to microbial contamination of water (or food), depending upon assessment of the concentration, exposure and pathogenicity of pathogens.
multibarrier approach
939
A series of integrated, sequential barriers from source water to tap, designed to prevent or reduce the entry of microbial and chemical contaminants into the water supply system.
National Primary Drinking Water Regulations Regulations promulgated by the EPA under the Safe Drinking Water Act, governing the quality of drinking water.
nonpoint source A diffuse pollution source without a single point of origin, such as farmland or the road and parking lot network of a city.
partition coefficient A ratio referring to a chemical's relative affinity for an organic solvent (octanol) and for water. It helps to determine the degree to which a chemical may settle into sediments or into the biota.
point source A stationary location or fixed facility from which pollutants are discharged, such as a pipe, ditch, or ship.
point-of-use treatment Simple, inexpensive treatment of water in the home to improve its microbial quality. Useful in low-resource settings where water treatment infrastructure is not available.
precipitation The falling of water in some form, as rain, snow, hail, or sleet, from the atmosphere to the Earth's surface.
resource wars Armed conflicts triggered or fueled by scarcity of key resources, such as water.
Safe Drinking Water Act A U.S. law, initially enacted in 1974, regulating the quality of drinking water.
sanitation Public health practices centered on provision of potable water, management of sewage, and provision of safe food.
secondary transmission Transmission of an infectious disease not from an initial reservoir of the pathogen, such as the aquatic environment, but through a human-to-human pathway mediated by the ingestion of contaminated water or food.
940
source water Water used as a source of drinking water.
surface water Water naturally open to the atmosphere (rivers, lakes, reservoirs, ponds, streams, impoundments, seas, estuaries, etc.).
swimming advisories Advisories issued by public agencies to warn the public of the danger of recreational swimming when indicator organisms exceed recommended levels.
Total Coliform Rule An EPA rule, finalized in 1989, that requires water systems to sample regularly for coliform organisms and to conduct periodic sanitary surveys.
wastewater reuse The recycling or reclamation of treated wastewater for beneficial purposes such as agricultural and landscape irrigation, industrial processes, domestic use, and ground water recharge.
wastewater treatment A set of processes designed to reduce the microbial and/or chemical load of wastewater, to prepare it for return to surface water bodies or to a system for human use.
water distribution The conveyance of water from water treatment plants to consumers, usually via systems of pipes.
water scarcity A shortage of water relative to demand, defined as at or below 1,000 m3 per person per year (cf. absolute water scarcity and water stress).
water stress A shortage of water relative to demand, defined as a water supply at or below 1,700 m3 per person per year (cf. water scarcity and absolute water scarcity).
water treatment Processes intended to improve the quality of water, preparing it for discharge into surface water bodies or for human consumption.
waterborne disease outbreaks
941
Infectious disease outbreaks in which the infectious agent is ingested with water.
watershed protection Procedures on a large spatial scale—say, across an entire river system—to maintain the cleanliness of source water and facilitate the delivery of high-quality drinking water.
942
Discussion Questions 1. Global warming may bring increasing temperatures over the
next twenty years. What might be the potential consequences for waterborne and water-related diseases? Choose a specific disease, and discuss how it may be affected.
2. Almost every city has a deteriorating water distribution system. As a result, municipalities lose between 30% and 50% of distributed water. Imagine yourself to be the manager of a municipal water facility, and discuss options for reducing water loss. What are the alternatives, if any, to distributed water, and what would be the health risks associated with each alternative?
3. Given the number of options for water treatment available today, what would your recommendations need to take into account if you were involved in installing a new water treatment plant in a developing country with high rates of enteric diseases?
4. The coliform group has been used for most of the past century as an indicator of fecal pollution. However, directly monitoring for pathogens such as Vibrio cholerae would be far more protective of public health. Do you agree or disagree with this statement? Explain the reasons for your choice.
5. Research and describe the Aral Sea disaster. What are the health consequences for the local communities? What is likely to be the long-term fate of this ecosystem?
6. The answer to a waterborne disease outbreak is to “shock” chlorinate. Explore this statement. What are the health risks that would be mitigated by the treatment it advocates? What new health risks might emerge from the application of large doses of chlorine?
7. What health concerns arise from reuse of wastewater? What pathogen exposure pathways might occur from land application of sewage sludge and from reuse of wastewater for irrigation of garden plants and toilet flushing?
8. Relative to the situation in developing countries, waterborne disease in the United States is a nonissue. The CDC reports very few deaths from waterborne disease outbreaks, and we
943
therefore have no reason to worry. What are the potential fallacies in this statement? How would you explain the hazards of this type of thinking to someone not involved in public health?
944
References Ahmed, S. M., Hall, A. J., Robinson, A. E., Verhoef, L., Premkumar, P., Parashar, U. D.,…Lopman, B. A. (2014). Global prevalence of norovirus in cases of gastroenteritis: A systematic review and meta- analysis. Lancet: Infectious Diseases, 14, 725–730.
Amer, M. H., El-Yazigi, A., Hannan, M. A., & Mohamed, M. E. (1990). Water contamination and esophageal cancer at Gassim Region, Saudi Arabia. Gastroenterology, 98, 1141–1147.
Arlappa, N., Aatif Qureshi, I., & Srinivas, R. (2013). Fluorosis in India: An overview. International Journal of Research & Development of Health, 1, 97–102.
Aschengrau, A., Rogers, S., & Ozonoff, D. (2003). Perchloroethylene-contaminated drinking water and the risk of breast cancer: Additional results from Cape Cod, Massachusetts, USA. Environmental Health Perspectives, 111, 167–173.
Bartram, J., & Rees, G. (Eds.). (2000). Monitoring bathing waters: A practical guide to the design and implementation of assessments and monitoring programmes. World Health Organization. Retrieved from http://www.who.int/water_sanitation_health/bathing/bathing3/en
Besmer, M. D., Weissbrodt, D. G., Kratochvil, B. E., Sigrist, J. A., Weyland, M. S., & Hammes, F. (2014). The feasibility of automated online flow cytometry for in-situ monitoring of microbial dynamics in aquatic ecosystems. Frontiers in Microbiology, 5, 265.
Bitton, G. (2011). Wastewater microbiology (4th ed.). Hoboken, NJ: Wiley-Blackwell.
Brinkman, N. E., Francisco, R., Nichols, T. L., Robinson, D., Schaefer, F. W., 3rd, Schaudies, R. P., & Villegas, E. N. (2013). Detection of multiple waterborne pathogens using microsequencing arrays. Journal of Applied Microbiology, 114, 564–573.
Capone, D. G., & Bauer, J. E. (1992). Microbial processes in coastal pollution. In R. Mitchell (Ed.), Environmental microbiology (pp.
945
191–237). Hoboken, NJ: Wiley.
Center for Affordable Water and Sanitation Technology. (2014). Biosand filter. Retrieved from http://www.cawst.org/en/resources/biosand-filter
Centers for Disease Control and Prevention. (2003). Cross-sectional exposure assessment of environmental contaminants in Churchill County, Nevada. Retrieved from http://www.cdc.gov/nceh/clusters/Fallon/study.htm
Centers for Disease Control and Prevention. (2014). The Safe Water System. Retrieved from http://www.cdc.gov/safewater
Chowdhury, U. K., Biswas, B. K., Chowdhury, T. R., Samanta, G., Mandal, B. K., Basu, G. C.,…Chakraborti, D. (2000). Groundwater arsenic contamination in Bangladesh and West Bengal, India. Environmental Health Perspectives, 108, 393–397.
Clarke, R. (2013). Water: The international crisis. New York: Routledge.
Cohn, P., Klotz, J., Bove, F., Berkowitz, M., & Fagliano, J. (1994). “Drinking water contamination and the incidence of leukemia and non-Hodgkin's lymphoma.” Environmental Health Perspectives, 102, 556–561.
Costas, K., Knorr, R. S., & Condon, S. K. (2002). A case-control study of childhood leukemia in Woburn, Massachusetts: The relationship between leukemia incidence and exposure to public drinking water. Science of the Total Environment, 300, 23–35.
Cox, L. M., Yamanishi, S., Sohn, J., Alekseyenko, A. V., Leung, J. M., Cho, I.,…Blaser, M. J. (2014). Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences. Cell, 158, 705–721.
Del Porto, D., & Steinfeld, C. (2000). The composting toilet system book. Concord, MA: Center for Ecological Pollution Prevention.
Edmonds, C. J., & Burford, D. (2009). Should children drink more water? The effects of drinking water on cognition in children. Appetite, 52, 776–779.
946
Ercumen, A., Gruber, J. S., & Colford, J. M., Jr. (2014). Water distribution system deficiencies and gastrointestinal illness: A systematic review and meta-analysis. Environmental Health Perspectives, 122(7), 651–660.
Finley, R. L., Collignon, P., Larsson, D. G., McEwen, S. A., Li, X. Z., Gaze, W. H.,…Topp, E. (2013). The scourge of antibiotic resistance: The important role of the environment. Clinical Infectious Diseases, 57, 704–710.
Food and Agriculture Organization of the United Nations. (2014). AQUASTAT. Retrieved from http://www.fao.org/nr/water/aquastat/main/index.stm
Ford, T. E. (1999). Microbiological safety of drinking water: United States and global perspectives. Environmental Health Perspectives, 107, 191–206.
Ford, T. E., & Hamner, S. (2010). Control of water-borne pathogens in developing countries. In R. Mitchell & J.-D. Gu (Eds.), Environmental microbiology (2nd ed., pp. 33–56). Hoboken, NJ: Wiley.
Ford, T. E., & Hamner, S. (2014). Water pollution. In P. J. Landrigan & R. Etzel (Eds.), Textbook of children's environmental health (pp. 232–242). New York: Oxford University Press.
Ford, T. E., & Hamner, S. (2015). A perspective on the global pandemic of waterborne disease. Microbial Ecology. doi:10.1007/s00248-015-0629-0
Ford, T. E., Rupp, G., Butterfield, P., & Camper, A. (2005). Protecting public health in small water systems: Report of an international colloquium. Montana Water Center. Retrieved from http://water.montana.edu/colloquium
Franceys, R., Pickford, J., & Reed, R. (1992). Guide to the development of on-site sanitation. World Health Organization. Retrieved from http://www.who.int/water_sanitation_health/hygiene/envsan/onsitesan/en
Freeman, M. C., Stocks, M. E., Cumming, O., Jeandron, A., Higgins, J. P., Wolf, J.,…Curtis, V. (2014). Hygiene and health: Systematic
947
review of handwashing practices worldwide and update of health effects. Tropical Medicine & International Health, 19, 906–916.
Gale, P. (2001). Developments in microbiological risk assessment for drinking water. Journal of Applied Microbiology, 91, 191–205.
Gleick, P. H. (Ed.). (2014). The world's water: The biennial report on freshwater resources (Vol. 8). Washington, DC: Island Press.
Greer, F. R., Shannon, M., American Academy of Pediatrics Committee on Nutrition and Committee on Environmental Health. (2005). Infant methemoglobinemia: The role of dietary nitrate in food and water. Pediatrics, 116, 784–786.
Grube, A., Donaldson, D., Kiely, T., & Wu, L. (2011). Pesticides industry sales and usage, 2006 and 2007 market estimates. Retrieved from http://www.epa.gov/opp00001/pestsales/07pestsales/market_estimates2007.pdf
Gruber, J. S., Ercumen, A., & Colford, J. M., Jr. (2014). Coliform bacteria as indicators of diarrheal risk in household drinking water: Systematic review and meta-analysis. PLoS One, 9(9), e107429.
Gutierrez-Jimenez, J., Cassassuce, F., Martinez-de la Cruz, L., De Aquino-Lopez, J. A., Hernandez-Shilon, J. A., Schlie-Guzman, M. A., & Vidal, J. E. (2014). Evaluation of a point-of-use water purification system (Llaveoz) in a rural setting of Chiapas, Mexico. Journal of Microbiology & Experimentation, 1, 00015.
Haas, C. N., Rose, J. B., & Gerba, C. P. (2014). Quantitative microbial risk assessment (2nd ed.). Hoboken, NJ: Wiley.
Hamner, S., Tripathi, A., Mishra, R. K., Bouskill, N., Broadaway, S. C., Pyle, B. H., & Ford, T. E. (2006). The role of water use patterns and sewage pollution in incidence of water-borne/enteric diseases along the Ganges river in Varanasi, India. International Journal of Environmental Health Research, 16, 113–132.
Hrudey, S. E., & Hrudey, E. J. (2004). Safe drinking water: Lessons from recent outbreaks in affluent nations. London: IWA.
Huq, A., Yunus, M., Sohel, S. S., Bhuiya, A., Emch, M., Luby, S. P., & Colwell, R. R. (2010). Simple sari cloth filtration of water is
948
sustainable and continues to protect villagers from cholera in Matlab, Bangladesh. mBio, 1.
Igbeneghu, O. A., & Lamikanra, A. (2014). The bacteriological quality of different brands of bottled water available to consumers in Ile-Ife, south-western Nigeria. BMC Research Notes, 7, 859.
Janknecht, P., & Melo, L. F. (2003). Online biofilm monitoring. Reviews in Environmental Science and Bio/Technology, 2, 269– 283.
Klare, M. T. (2001). Resource wars: The new landscape of global conflict. New York: Holt.
Kleiner, S. M. (1999). Water: An essential but overlooked nutrient. Journal of the American Dietetic Association, 99, 200–206.
Krasner, S. W. (2009). The formation and control of emerging disinfection by-products of health concern. Philosophical Transactions. Series A: Mathematical, Physical, and Engineering Sciences, 367(1904), 4077–4095.
Lim, S. S., Vos, T., Flaxman, A. D., Danaei, G., Shibuya, K., Adair- Rohani, H.,…Memish, Z. A. (2012). A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380, 2224– 2260.
Lin, J., & Ganesh, A. (2013). Water quality indicators: Bacteria, coliphages, enteric viruses. International Journal of Environmental Health Research, 23(6), 484–506.
Lopman, B. A., Reacher, M. H., Van Duijnhoven, Y., Hanon, F. X., Brown, D., & Koopmans, M. (2003). Viral gastroenteritis outbreaks in Europe, 1995–2000. Emerging Infectious Diseases, 9, 90–96.
MacKenzie, W. R., Hoxie, N. J., Proctor, M. E., Gradus, M. S., Blair, K. A., Peterson, D. E., & Davis, J. P. (1994). A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. New England Journal of Medicine, 331, 161– 167.
949
Majewski, M. S., & Capel, P. D. (1995). Pesticides in the atmosphere: Distribution, trends, and governing factors. Chelsea, MI: Ann Arbor Press.
Mallin, K. (1990). Investigation of a bladder cancer cluster in northwestern Illinois. American Journal of Epidemiology, 132, 96– 106.
Massachusetts Water Resources Authority. (2009). The Deer Island Sewage Treatment Plant. Retrieved from http://www.mwra.state.ma.us/03sewer/html/sewditp.htm
P&G Heath Sciences Institute. (2014). Safe drinking water. Retrieved from http://www.pghsi.com/pghsi/safewater
Postel, S. (1999). Pillar of sand: Can the irrigation miracle last? New York: Norton.
Postel, S. (2013). Last oasis: Facing water scarcity. London: Earthscan.
Potters for Peace. (2014). Ceramic Water Filters Project. Retrieved from http://pottersforpeace.com/ceramic-water-filter-project
Prüss-Ustün, A., Bartram, J., Clasen, T., Colford, J. M., Jr., Cumming, O., Curtis, V.,…Cairncross, S. (2014). Burden of disease from inadequate water, sanitation and hygiene in low- and middle- income settings: A retrospective analysis of data from 145 countries. Tropical Medicine & International Health, 19, 894–905.
Rose, J. B., & Grimes, D. J. (2001). Reevaluation of microbial water quality: Powerful new tools for detection and risk assessment. Washington, DC: American Academy of Microbiology. Retrieved from http://academy.asm.org/index.php/water/455- reevaluation-of-microbial-water-quality-powerful-new-tools-for- detection-and-risk-assessment
Sodha, S. V., Menon, M., Trivedi, K., Ati, A., Figueroa, M. E., Ainslie, R.,…Quick, R. (2011). Microbiologic effectiveness of boiling and safe water storage in South Sulawesi, Indonesia. Journal of Water and Health, 9, 577–585.
SODIS. (2014). Safe drinking water for all. Retrieved from
950
http://www.sodis.ch/index_EN
Sterndale, R. C. (1881). Municipal work in India. Calcutta: Thacker, Spink.
United Nations. (2014). International Decade for Action: “Water for Life” 2005–2015: Water scarcity. Retrieved from http://www.un.org/waterforlifedecade/scarcity.shtml
U.S. Environmental Protection Agency. (2004). Estimated per capita water ingestion and body weight in the United States—an update (EPA-822-R-00-001). Retrieved from http://water.epa.gov/action/advisories/drinking/upload/2005_05_06_criteria_drinking_percapita_2004.pdf
U.S. Environmental Protection Agency. (2012). Sanitary survey. Retrieved from http://water.epa.gov/learn/training/dwatraining/sanitarysurvey
U.S. Environmental Protection Agency. (2013a). Consumer Confidence Reports (CCR). Retrieved from http://water.epa.gov/lawsregs/rulesregs/sdwa/ccr/index.cfm
US. Environmental Protection Agency. (2013b). Total Coliform Rule. Retrieved from http://water.epa.gov/lawsregs/rulesregs/sdwa/tcr/index.cfm
U.S. Environmental Protection Agency. (2014a). Clean Water Act. Retrieved from http://www2.epa.gov/laws-regulations/summary- clean-water-act
U.S. Environmental Protection Agency. (2014b). Recreational water quality criteria. Retrieved from http://water.epa.gov/scitech/swguidance/standards/criteria/health/recreation
U.S. Environmental Protection Agency. (2014c). Safe Drinking Water Act. Retrieved from http://water.epa.gov/lawsregs/rulesregs/sdwa/index.cfm
U.S. Environmental Protection Agency. (2014d). Terminology services. Retrieved from http://ofmpub.epa.gov/sor_internet/registry/termreg/home/overview/home.do
U.S. Geological Survey. (2014). National Water-Quality Assessment (NAWQA) program. Retrieved from http://water.usgs.gov/nawqa
951
Vestergaard. (2013). LifeStraw® Community. Retrieved from http://www.vestergaard.com/lifestraw-community
WATERisLIFE. (2014). The Drinkable Book. Retrieved from http://www.waterislife.com/index.php
Wingender, J., & Flemming, H. C. (2011). Biofilms in drinking water and their role as reservoir for pathogens. International Journal of Hygiene and Environmental Health, 214(6), 417–423.
Winter, T. C., Harvey, J. W., Franke, O. L., & Alley, W. M. (1998). Ground water and surface water—a single resource (U.S. Geological Survey Circular 1139). Retrieved from http://pubs.usgs.gov/circ/circ1139
World Health Organization. (2014a). Global health estimates. Retrieved from http://www.who.int/healthinfo/global_burden_disease/en
World Health Organization. (2014b). Recreational, or bathing, waters. Retrieved from http://www.who.int/water_sanitation_health/bathing/en
World Health Organization and UNICEF. (2014). Progress on drinking water and sanitation: 2014 update. Retrieved from http://www.who.int/water_sanitation_health/publications/2014/jmp- report/en
952
For Further Information American Water Works Association (AWWA): http://www.awwa.org. This association of water professionals provides consumer information on drinking water and many other water-related topics, and its home page contains many useful links.
British Geological Survey, “Arsenic Contamination of Groundwater”: http://www.bgs.ac.uk/arsenic. This organization's Web site provides information on the greatest mass poisoning from contaminated water ever recorded, the arsenic crisis in Bangladesh.
Centers for Disease Control and Prevention (CDC), Morbidity and Mortality Weekly Report: http://www.cdc.gov/mmwr. MMWR is the authoritative source on outbreaks of infectious disease in the United States. However, at least for waterborne disease, reports likely underestimate by orders of magnitude the actual incidence.
Pacific Institute: http://www.pacinst.org. This organization produces “research that advances a sustainable environment, healthy economy, and social equity with science-based solutions that lead to social and political change.” Its Web site has links to a selection of publications that form a considerable database on a wide range of critical water issues.
United Nations: http://www.un.org. UN agencies offer a number of water-related Web sites, see, for example:
United Nations Children's Fund (UNICEF), “Water, Sanitation and Hygiene”: http://www.unicef.org/wash
United Nations Development Programme (UNDP), “Water and Ocean Governance”: http://www.undp.org/content/undp/en/home/ourwork/environmentandenergy/focus_areas/water_and_ocean_governance.html
United Nations Educational, Scientific and Cultural Organization (UNESCO), “Water”: http://www.unesco.org/new/en/natural- sciences/environment/water. Also see the UNESCO water portal with worldwide water links:
953
http://www.unesco.org/water/water_links
United Nations Environmental Programme (UNEP), “Freshwater”: http://www.unep.org/themes/Freshwater/index.asp
U.S. Environmental Protection Agency (U.S. EPA): http://www.epa.gov. The EPA's Web site offers numerous useful resources related to water and health. In addition to the EPA Web sites in the References, see, for example, “Ground Water and Drinking Water” (http://water.epa.gov/drink); “Drinking Water Contaminants” (http://water.epa.gov/drink/contaminants); and “Superfund” (http://www.epa.gov/superfund). The publications of the EPA's National Risk Management Research Laboratory (NRMRL) are also of interest (http://www.epa.gov/nrmrl/publications.html).
U.S. Geological Survey (USGS), National Water-Quality Assessment (NAWQA) Program: http://water.usgs.gov/nawqa. The USGS maintains an extremely useful online resource with current assessments of ground and surface water quality in many U.S. river basins and aquifers. As part of its NAWQA program, the USGS is conducting the Pesticide National Synthesis Project to obtain an assessment of pesticides in the streams, rivers, and groundwater of the United States.
Water and Sanitation Program (WSP): http://www.wsp.org. The WSP describes itself as “a multi-donor partnership administered by the World Bank to support poor people in obtaining affordable, safe and sustainable access to water and sanitation services.”
Water Environment Federation (WEF): http://www.wef.org. The WEF describes itself as a “not-for-profit technical and educational organization” with members from varied disciplines around the world who “proudly work to achieve our mission to provide bold leadership, champion innovation, connect water professionals, and leverage knowledge to support clean and safe water worldwide.”
Water Environment Research Foundation: http://www.werf.org. This foundation is “America's leading independent scientific research organization dedicated to wastewater and stormwater
954
issues”; information on its reports and research is available on its Web site.
World Bank: http://www.worldbank.org. The World Bank Web site provides links to major World Bank–funded projects. Under “Topics,” for example (http://www.worldbank.org/en/topic), are links to “Climate Change,” “Sanitation,” “Water,” “Water Resources Management,” “Water Supply,” and more.
Woods Hole Oceanographic Institution (WHOI), “Harmful Algae”: http://www.whoi.edu/redtide. This WHOI Web site offers a comprehensive source of online information on toxic algal blooms.
World Health Organization (WHO): http://www.who.int/en. WHO publishes the Weekly Epidemiological Record (http://www.who.int/wer/en) and the annual World Health Report (http://www.who.int/whr/en) and is arguably the leading source of information for internationally accepted statistics on human health, including water and health; see, for example, “Health Topics” (http://www.who.int/topics/en), a Web site with links to pages on water, drinking water, sanitation, diarrheal disease, cholera, dracunculiasis, malaria, and so forth. The drinking-water page, for instance, takes you to technical information (including guidelines) that addresses small community water supply management, household water treatment and safe storage, and drinking-water quality, among other topics. Also of note is the WHO's “Water, Sanitation and Health” Web site (http://www.who.int/water_sanitation_health/en).
World Water Council: http://www.worldwatercouncil.org. The mission of the World Water Council is to “promote awareness, build political commitment and trigger action on critical water issues at all levels.” The council's Web site offers many articles on water policies and the barriers to and solutions for effective management of the world's water resources.
955
Part 4 Environmental Health on the Local Scale
956
Chapter 17 Solid and Hazardous Waste
Sven E. Rodenbeck and Henry Falk
Dr. Rodenbeck and Dr. Falk report no conflicts of interest related to the authorship of this chapter.
957
Key Concepts Waste is an important by-product of human activities. It can be divided into several categories, including solid waste, hazardous waste, and specialized waste, such as medical waste.
The amount and type of waste and the management methods used vary with social and economic situations.
Each kind of waste may have potential effects on human health.
Various laws and policies govern the management of waste.
The preferred approach to waste is to minimize waste generation.
Waste can be managed in a variety of ways, such as incineration and landfilling. Each has potential health consequences, and each must be carried out in ways that maximally protect health and environment.
Humans, like all animal species, are producers of wastes. It is significant, however, that as humankind has evolved, the character of the waste produced has changed markedly. No other species in the animal kingdom shares this trait. Like animals' waste, the waste of early humans was highly organic. It consisted of such materials as excreta, bedding materials, crude clothing, and implements. As humans evolved, however, refined materials such as paper and cloth and also inorganic materials such as ceramics and metals were added to their wastes.
For many centuries human waste products reflected a fundamentally agrarian lifestyle. As human endeavors evolved to include more technology and industry, the mix of wastes produced by society changed radically and irrevocably. Mining spoils, ashes and slag from metal processing, and other industrial wastes became commonplace. As industry grew in complexity throughout the nineteenth and twentieth centuries, the waste mix became more varied and complex to manage. Waste management has emerged as a significant challenge because of the growing variety of wastes and
958
the trend throughout the twentieth century toward more packaging and disposability features.
Finally, along with the industrialization and modernization of society, the steady trend toward urbanization of much of the population has challenged waste management. As cities became more crowded, a shortage of space to accommodate all the waste developed. In developed countries, open dumping and backyard burn barrels are generally frowned upon as means of waste disposal. This chapter describes the types of wastes produced by modern society, the significance of these wastes with respect to human health and the environment, and some of the ways in which these wastes are managed.
959
Solid Waste Determining whether something is solid waste is not a trivial matter. People have debated for years about what solid waste is and how it should be managed. In fact some material that is managed as solid waste is not a solid at room temperature but rather a liquid or gas (e.g., gases in cylinders). A fundamental premise is that a material is waste if it no longer has value—a judgment that may be subjective and may vary over time. On occasion, material designated as waste was later found to have value. For example, using new technology former mining wastes have been reextracted to recover residual metals. Cultural norms also influence waste value judgments. Western industrial societies often throw away material with little thought of reuse or repair alternatives. However, as a starting point, the fundamental premise that it lacks value is probably adequate to characterize solid waste.
In the United States and in most developed industrial countries, waste material is typically divided into three broad categories:
1. Municipal solid waste
2. Special waste
3. Hazardous waste
Complex laws and regulations govern how these materials are identified, stored, collected, transported, treated, and finally disposed of (Text Box 17.1).
960
Text Box 17.1 U.S. Solid and Hazardous Waste Laws and Policy Prior to 1965, there were no federal laws to govern the management and disposal of solid and hazardous waste. Each state and territory had its own set of laws and regulations, and these rules were not always consistent. The Solid Waste Disposal Act of 1965 brought about, for the first time, a national focus on the management of these wastes. That Act granted limited authority to the U.S. Public Health Service to provide money to assist in the development of statewide solid waste management plans, provide technical assistance to state and local waste management authorities, and conduct applied and basic research.
In 1976, Congress enacted the Resource Conservation and Recovery Act of 1976 (RCRA), granting the U.S. Environmental Protection Agency (U.S. EPA) regulatory and enforcement authority over the management of solid and hazardous waste. RCRA provided, for the first time, a national regulatory framework for solid and hazardous waste management. The most significant innovation was the requirement that hazardous waste be tracked from its point of generation to its final disposal or treatment. The regulations also required that all future solid waste landfills be designed and constructed to meet minimum standards, including having liners to prevent the movement of water through the waste into the underlying aquifer.
The RCRA is not the only legal framework for regulating hazardous waste management. During the 1970s, a series of hazardous waste sites came to light around the country— Love Canal, in upstate New York (Figure 17.1); Times Beach, on the Meramec River in eastern Missouri; and Valley of the Drums, in Louisville, Kentucky. These shocked the public, and led Congress to enact the Comprehensive Environmental Response Compensation and Liability Act—also known as CERCLA, or Superfund—in 1980.
961
Figure 17.1 Chemical Drums at Love Canal Source: Hill, 2012.
CERCLA authorized the EPA (working closely with the states) to address the nation's hazardous waste sites. Several provisions of the law, together, define the national approach to hazardous waste sites:
1. Systematically identify such sites, and prioritize those that pose the greatest potential risk to human health or the environment. The EPA estimates that there are over 300,000 wastes sites in the nation; of these, nearly 2,000 reached high enough scores on the EPA's Hazard Ranking System, or were otherwise of sufficient concern, to be placed on the National Priorities List (NPL). A new public health agency, the Agency for Toxic Substances and Disease Registry (ATSDR), was created to assist with this process.
962
2. Provide for remedial cleanup, both in the short term, when releases or threatened releases call for prompt action, and in the long term, when definitive remediation is appropriate. The lengthy cleanup process got under way at most of the nearly 2,000 sites on the NPL, and by 2015, several hundred of these cleanup operations had been completed and the sites delisted.
3. Implement a “polluter pays” principle, both by taxing the chemical and petroleum industries to establish a trust fund for cleaning up waste sites and by identifying responsible polluters in individual cases, when possible, and assigning them liability for cleanup costs.
4. Incorporate community input into the process of identifying and remediating sites.
Further information is available on the EPA's Web site at www.epa.gov/superfund
Municipal Solid Waste Municipal solid waste consists of everyday items that are commonly generated from homes. Over half of the U.S. municipal solid waste generated in 2012 consisted of containers, packaging, and nondurable goods such as newspapers and magazines (Figure 17.2). Other major components of municipal solid waste include yard trimmings, food wastes, and durable goods such as appliances, tires, and batteries. Local laws and regulations may prohibit the disposal of some of these materials (such as tires) as municipal solid waste. More and more frequently, municipal and county governments are also prohibiting the disposal of yard clippings with municipal solid waste, requiring that the clippings be composted or disposed of in some other, more environmentally friendly manner.
963
Figure 17.2 Composition of the 251 Million Tons of Municipal Solid Waste Produced in the United States (Before Recycling), 2012
Source: Adapted from U.S. EPA, 2012a.
In the United States the per capita generation of municipal solid waste has steadily increased over recent decades. In 2012, the average American generated approximately 4.38 pounds of waste each day, a 70% increase from the 1960 average of 2.7 pounds per person per day (Figure 17.3).
964
Figure 17.3 Total Amount and Per Capita Generation Rate of Municipal Solid Waste Produced in the United States (Before Recycling), 1960–2012
Source: Adapted from U.S. EPA, 2012a.
According to the World Bank, approximately 1.3 billion tons of municipal solid waste is generated each year, and that number is expected to increase to 2.2 billion tons by 2025 (Hoornweg & Bhada-Tata, 2012). The amount of waste generated per person varies by economic status, with low- and high-income individuals generating about 1.3 and 4.7 pounds per person per day, respectively. Waste generated by lower income individuals tends to have more organic material (65% for low-income versus 28% for high-income) and less paper (5% for low-income versus 31% for high-income).
Special Waste Special waste is a catchall category. However, if a waste is neither municipal solid waste nor a designated hazardous waste, it likely has a special designation and associated laws or regulations. Some commonly identified special wastes are
Medical waste
Construction debris
Asbestos
965
Mining waste
Agricultural waste
Radioactive waste
Sewage sludge
Electronic waste
Medical Waste Medical waste includes items that are generated from health care treatment or research facilities (human and nonhuman) and that have come into contact with bodily fluids (e.g., blood) or other materials that may contain infectious agents and may cause disease. Some examples of medical waste are
Soiled or blood-soaked bandages
Culture dishes and other associated glassware
Items such as gloves, gowns, and scalpels used during surgery
Needles used to give injections or draw blood
Bodily fluids and tissues
One of the reasons medical waste is handled separately from municipal solid waste is to protect sanitation workers from infectious agents in the waste materials. The challenge of medical waste is further explored in Text Box 17.2.
966
Text Box 17.2 The Challenge of Medical Waste The proper management and disposal of waste material generated during health care activities is a perennial concern, and it intensifies during incidents such as the “syringe tides” of 1987 and 1988, when medical waste washed up on ocean shorelines in New Jersey and New York, and the 2014 to 2015 Ebola outbreak (Wines, 2014; Morin, 2014). In addition to aesthetic concerns, fear of diseases that are perceived to have high risk, such as AIDS (acquired immunodeficiency syndrome), Ebola, and other infectious diseases, contributes to the public's anxiety regarding medical waste.
The predominant health risk associated with medical waste is the presence of infectious organisms (parasites, bacteria, and viruses). It is important to remember that infectious disease can occur only when all of the following are present: an infectious agent, a sufficient quantity of this agent to cause infection, a susceptible host, and an appropriate portal of entry into that susceptible host. If any one of these factors is missing, then disease will not occur. Many infectious agents do not remain viable for an extended period of time outside a host. For example, the Ebola virus is thought to remain viable for less than twenty-four hours in the open environment (Centers for Disease Control and Prevention [CDC], 2015b). Therefore the potential for transmitting disease is greatest at the point where the waste is generated, usually in a hospital, clinic, or medical office. People who provide medical care at home may also be exposed to infectious wastes. The greatest risk of disease transmission from medical waste is associated with accidental skin punctures from hypodermic needles and other sharps. This is particularly true for sharps contaminated with blood-borne pathogens (specifically, Ebola, the hepatitis B or C viruses, and to a much lesser extent, HIV).
Owing to both aesthetic concerns and studies demonstrating that health care workers have a higher risk than the general
967
public of being infected with Ebola, hepatitis B or C, or HIV, medical waste is separated at the source from municipal solid waste. Separate containers are located in or near medical treatment areas of health care facilities. Medical care of patients with hemorrhagic fevers (e.g., Ebola) and other highly contagious diseases dramatically increases waste generation—eight 55-gallon barrels of medical waste per day per Ebola patient, by one estimate (Morin, 2014)—because health care workers must repeatedly don and dispose of multiple layers of personal protective equipment (PPE) (CDC, 2015a), and because patients with profuse diarrhea and blood loss generate thirty to forty times more contaminated waste material than other types of patients do (Institute of Medicine, 2014). To avoid accidental puncture wounds, sharps are placed in penetration-resistant containers. Medical waste containers are then sealed and, usually, shipped to specifically designed and managed medical waste incinerators. In some situations the waste material is treated in large autoclaves. After incineration or autoclaving, the waste can be safely disposed of in a municipal landfill (Chartier et al., 2014).
Studies in developing nations have revealed widespread breaches in safe handling of medical wastes, attributed to inadequate staff training, inadequate staffing, and inadequate resources (Hossain, Santhanam, Nik Norulaini, & Omar, 2011; Caniato, Tudor, & Vaccari, 2015). The extent of the resulting health risk has not been well documented.
Construction Debris Unless a construction material is regulated separately (as asbestos is, for example), the construction debris waste stream consists of material generated from the construction and demolition of buildings and other facilities. Typically this rubble is disposed of in specific construction debris landfills or in municipal solid waste landfills. Recent research has found that construction debris is not as innocuous as previously thought. If water is allowed to infiltrate through the waste drywall (gypsum wallboard) in a landfill, hydrogen sulfide can be formed, and the surrounding population could be exposed to hydrogen sulfide levels that are a health
968
concern (Agency for Toxic Substances and Disease Registry [ATSDR], 2006).
Asbestos In the United States asbestos is designated as a special waste, with its own rules and regulations. In the past this class of fibrous minerals was used extensively in such consumer products as car brake linings and construction materials (see Tox Box 20.3, in Chapter 20). Most uses of asbestos have been banned in the United States because of its demonstrated capacity to cause disease in workers and other exposed people. To prevent the airborne release of asbestos fibers, federal regulations provide detailed guidance on the removal, packaging, and disposal of materials containing asbestos.
Mining Waste The extraction of metals, coal, and oil from the Earth's crust generates huge quantities of mining waste materials. The volume of wastes from mining operations exceeds the volume of wastes from all other categories combined (U.S. EPA, 1985). The disposal of this leftover rubble and liquid material is regulated both by solid waste laws and regulations and by water pollution control and land- use and reuse laws and regulations.
Recent technical advances in oil and natural gas extraction from shale formations, using hydraulic fracturing, or fracking, have resulted in the generation of a new mining waste stream. Fracking generates large quantities of liquid waste that can contain high levels of total dissolved solids (TDS), fracturing fluid additives, metals, and naturally occurring radioactive materials. The U.S. government and state governments have taken different approaches to regulating this new waste stream. For example, New York State has banned any use of fracking within state boundaries, Pennsylvania has declined to regulate fracking activities, and the U.S. government has issued regulations that require specific waste management practice for wells being developed on federal or tribal lands (New York State Department of Health, 2014; A Rule by the Land Management Bureau, 2015).
Agricultural Waste
969
In technologically advanced countries the production of food has become highly industrialized. A common arrangement for raising animals on a large scale is the concentrated animal feed operation (CAFO). As described in Chapter 19, CAFOs can bring thousands of poultry, swine, or cattle together in confined spaces. These facilities can become large-scale sources of agricultural waste in the form of air emissions (such as ammonia, hydrogen sulfide, odors, and particles contaminated with a wide range of microorganisms) (Heederik et al., 2007) and animal waste. The animal waste in turn contains nutrients, microbes, and veterinary chemicals. For example, where antibiotics have been used in raising animals, they can be discharged through waste into the environment, where they may contribute to the development of antibiotic-resistant pathogens (Gilchrist et al., 2007; Silbergeld, Graham, & Price, 2008). Recent U.S. Food and Drug Administration guidance issued in December 2013 should reduce the amount of antibiotics used in this manner (A Notice by the Food and Drug Administration, 2013). The waste stream may also contain other veterinary chemicals, such as arsenic (Silbergeld & Nachman, 2008). The EPA's clean water protection program regulates the management of the liquid waste and the sludge, or manure, coming from animal feed lots and CAFOs. Those waste materials not regulated by federal laws are managed either by local authorities or in accordance with best practices developed by the industry. There is concern, however, that these protective strategies may not suffice to protect the public's health (Burkholder et al., 2007).
Radioactive Waste Radioactive waste contains radioactive chemical elements. Generally, it is divided into two subcategories: low-level waste and high-level waste. Low-level waste consists of used protective clothing and other items that contain low levels of radioactivity per mass or volume. This waste is typically disposed of in specifically designated landfills. High-level radioactive waste consists of spent nuclear fuel and waste materials left after spent fuel is reprocessed. The disposal of this nuclear waste is very controversial. The United States has been trying for years to establish a permanent, high-level radioactive waste repository inside Yucca Mountain, Nevada. Currently, most of the high-level radioactive waste in the United States is stored temporarily in spent fuel pools and in dry cask
970
storage facilities.
Sewage Sludge Before waste water is discharged back into the environment, it undergoes a series of treatments (mostly biological and chemical) to remove or break down any hazardous biological or chemical constituents. One of the main by-products of this treatment processes is sewage sludge, which is made up primarily of concentrated solid materials. The disposal of sewage sludge is regulated, and the methods allowed are based on whether any hazardous materials are present. Some sewage sludge is safe enough after it has been disinfected to be applied to cropland.
Electronic Waste More commonly called e-waste, electronic waste includes unwanted, obsolete, or unusable electronic equipment such as computers, computer display monitors, televisions, VCRs, DVD players, cell phones, and electronic games. This waste stream is described in Text Box 17.3.
971
Text Box 17.3 e-Waste The volume of e-waste is growing rapidly as technology advances (Schmidt, 2002). The EPA has estimated that in 2010, e-waste totaled 2.4 million tons, or about 1% of the municipal waste steam. About 71% of that e-waste was discarded, primarily in landfills, and the rest was recycled (U.S. EPA, 2011).
Improper disposal of e-waste is of concern because electronic components contain hazardous metals, such as lead, cadmium, and mercury, and the plastic housings and cables contain brominated flame retardants, such as polybrominated diphenyl ethers (PBDEs) and polybrominated biphenyls (PBBs). Cathode ray tubes (CRTs), or picture tubes, are of particular concern because they contain, on average, about 4 pounds of lead. If disposed of in an unlined landfill, this lead could leach into groundwater. Under RCRA regulations, households and small-volume generators can dispose of CRTs in municipal trash. However, large-volume generators (more than 100 kilograms of hazardous wastes per month) must dispose of the e-waste in a hazardous waste landfill. Some states, such as California and Massachusetts, regulate all CRTs as hazardous waste and ban their disposal in municipal landfills (Schmidt, 2006; Osibanjo & Nnorom, 2007).
As with other waste materials, the preferred strategies for e- waste management are (in order of preference) to
1. Reuse the equipment
2. Recycle the materials
3. Properly dispose of the equipment in an approved landfill
In the United States the EPA is working with stakeholders in the private and public sectors to promote greater electronic products stewardship. Efforts are being made to reduce the amounts of toxic substances in electronic equipment and to increase the reuse and recycling of used electronics. To
972
encourage recycling, some states have imposed fees on new computers and televisions, which will be used to establish a statewide electronics recycling system, and several electronics manufactures have implemented take-back programs. In the United States the high costs of labor and equipment and strict environmental regulations are obstacles to economically viable recycling of e-waste. Consequently, the United States and other industrialized nations ship large quantities of e-waste to Asia and more recently to Africa for recycling (Ramesh Babu, Parande, & Ahmed Basha, 2007; Duan, Miller, Gregory, & Kirchain, 2013). This practice has been characterized as international trafficking in hazardous wastes, as discussed later in Text Box 17.5.
Hazardous Waste Hazardous waste can be defined simply as waste with properties that make it capable of harming human health or the environment. However, for regulatory purposes this simple definition is not sufficient. In the United States the EPA, in order to carry out the RCRA provisions, has developed specific criteria for defining hazardous waste. Two different mechanisms are applied. The first is to include the materials from approximately 500 specific industrial waste streams. These listed wastes include spent solvents, electroplating wastes, and wood-preserving wastes. The second mechanism relates to the waste's characteristics. The EPA has developed standardized test criteria to determine a waste's ignitability, corrosiveness, reactivity, and toxicity. If a waste possesses defined levels of any of these characteristics, it is classified as hazardous. At the same time, under the terms of the Act many waste materials (such as petroleum) are specifically excluded from the hazardous waste definition and regulations.
In 2011, approximately 34 million tons of hazardous waste was generated in the United States (U.S. EPA, 2012b). The states that generated the most hazardous waste tended to be those with a large petrochemical industry.
In general, other industrialized countries designate hazardous waste much as the United States does, although they may use different coding or terminology.
973
Solid Waste Management Strategies Because solid and hazardous wastes may affect human health and the environment, waste management is a fundamental part of environmental public health. Waste management is best accomplished through a multitier approach. The first tier is primary waste stream avoidance and reduction. Materials recycling, substitution of materials, and changes in consumer habits, among other methods, can help industries, communities, and other groups achieve waste stream reduction. All sectors of a modern society, when approached with effective informational campaigns and incentives, can practice waste avoidance and reduction.
The second tier of solid waste management involves proper handling and disposal of waste, that is, in a manner that protects the public health and the environment. Although complete avoidance of solid waste generation is the ideal, it is likely that there will always be some residual of mankind's activities requiring disposal.
In the United States, landfilling is the means of disposal for approximately 54% of municipal waste (U.S. EPA, 2012a). Hazardous waste is disposed of in landfills and surface impoundments (approximately 15%), energy recovery units (approximately 13%), metals recovery operations (approximately 13%), deep well or underground injection (approximately 10%), and other methods (U.S. EPA, 2012b). All of these approaches have public health implications.
974
Primary Prevention of Waste The ideal waste management strategy is not to produce the waste in the first place. This goal can be approached in several ways: that is, through efforts to reduce, reuse, and recycle. In an industrial setting this goal might be achieved by altering production processes to avoid or reduce the use of a hazardous chemical. For example, in some electroplating operations, less toxic alternatives can replace highly toxic cyanide salts. In office settings, converting to electronic commerce and records management can reduce waste paper production. Industry is also using life cycle analysis to design and produce things that can readily reclaimed at the end of their expected life.
Waste reduction also applies to municipal wastes. The quantity of raw materials in food and beverage containers is being reduced because of economic pressures. In the past few decades, manufacturers have reduced the amount of steel and aluminum in cans and the amount of plastic in milk jugs and plastic bags. These efforts have reduced the cost of these containers and decreased the amount of waste to be disposed. Further reductions in packaging could be achieved if consumers routinely carried reusable canvas shopping bags instead of expecting plastic or paper bags with each purchase.
If the generation of waste cannot be avoided or reduced, then the next best alternative is to recycle the waste. Recycling can refer to using waste material to produce more of the original product or to using waste material in something else. Examples of the first kind of recycling include making glass or paper from used glass or paper and making new lead batteries from old lead batteries. An example of the second kind of recycling is using mining wastes as aggregate for asphalt and concrete production. In recent years, increased efforts to reduce the amount of trash dumped into landfills have led municipalities to encourage recycling of paper, plastic, aluminum, and glass. In some communities homeowners are also encouraged to compost yard waste to recycle it into a useful soil amendment. Recycling of municipal solid waste has steadily increased in the United States; today about 34.5% of municipal solid waste is recycled (Figure 17.4). Other industrialized nations tend to have a
975
higher rate of recycling (Figure 17.5).
Figure 17.4 Total Amount and Percentage of Municipal Solid Waste Recycled in the United States, 1960–2012
Source: Adapted from U.S. EPA, 2012a.
Figure 17.5 Glass and Paper Recycling in Industrial Nations Source: Zeller, 2008.
The importance of waste minimization has led to the emerging field of industrial ecology. Industrial ecology is the study of the
976
physical, chemical, and biological interactions and interrelationships both within and between industrial systems and ecological systems (Garner & Keoleian, 1995). A primary goal of industrial ecology is to change the nature of our industrial systems from linear systems, in which raw materials are used and products and wastes are discarded, to cyclical systems that use the wastes as raw materials or energy for another product.
A famous example of an eco-industrial park is the Kalundborg industrial park in Denmark (Ehrenfeld & Gertler, 1997). In this park the companies reuse each other's wastes in the production of their own products. For example, Asnæsværket, a coal-fired power plant, captures sulfur dioxide from its flue stack gas and converts it to calcium sulfate (gypsum), which is sold to a drywall board plant. Another example is Novo Nordisk, a biotechnology company that produces insulin and industrial enzymes and then supplies biosludge waste to a nearby farm that uses it for fertilizer. These examples illustrate an industrial symbiosis in which energy and wastes are recycled and reused by another process within the system.
977
Waste Treatment and Disposal As discussed earlier, it would be ideal if all solid and hazardous or special waste could be recycled, reused, or avoided. Unfortunately, this ideal goal may not be attained. As a result, society should strive to dispose of all such wastes in a manner that minimizes harm to human health and the environment (see the discussions in Text Boxes 17.4 and 17.5). Both budgetary limitations and the need to comply with applicable regulations influence selection of the most practical option.
In years past it was common to burn wastes in backyard barrels, open dumps, and crude incinerators. All these methods had undesirable environmental and health impacts. During the second half of the twentieth century, public demand and government regulations led to improved waste treatment and disposal methods in upper-middle- and high-income countries. Controlled or sanitary landfills replaced dumps. More sophisticated and controlled combustion systems replaced crude incinerators. Newer incinerators are specifically designed for the type of wastes burned, such as medical waste, industrial waste, or municipal solid waste. Some industrial wastes, such as liquid brines, are discharged far beneath the Earth's surface, through deep well injection. Potentially harmful industrial wastes that had been previously discarded haphazardly in dumps or burial pits are now treated with remedial technologies designed to reduce or limit harmful impacts.
Unfortunately, burning and dumping of wastes is still a common practice in low-income and lower-middle-income countries. For example, it is estimated that more than 40% of the world's waste is burned in an uncontrolled manner (Wiedinmyer, Yokelson, & Gullett, 2014). China and India are believed to have the most waste burned by residents, while China, Brazil, and Mexico burn the most waste at open dumps. The air emissions from these practices have been estimated to account for 29% of the global particulate matter, 10% of airborne mercury emissions, and 5% of the world's anthropogenic carbon dioxide (a potent greenhouse gas—see Chapter 12).
978
Text Box 17.4 Tire Reuse and Recycling Some types of wastes have evolved to pose unique challenges and opportunities. Just over 100 years ago, waste from transportation operations consisted mainly of horse manure and also ash and clinker produced from burning coal in steam engines. One century later these transportation wastes have been replaced with, among other things, an estimated yearly production of 0.8 billion waste rubber tires in the United States alone.
Waste tires are problematic for both storage and disposal (Figure 17.6). They are hard to bury in landfills. Landfill operators report that tires tend to work their way up to the surface of the fill and disrupt the integrity of the cover. Tires also collect water and serve as mosquito-breeding sites when stored outdoors. And when stored in large piles, tires are vulnerable to fire. Tire fires are very difficult to extinguish and can cause substantial pollution of both the air and underlying soil and water environment.
Figure 17.6 Waste Tires Source: Agency for Toxic Substances and Disease Registry, via the author.
In the United States the number of stockpiled scrap tires has been reduced from a total of 1 billion in 1990 to 76 million in 2011(Rubber Manufacturers Association, 2014). Although
979
great strides have been made to recycle the stockpile of scrap tires, more needs to be done.
After being broken into chunks of rubber, used tires are being used in truck bed liners, antifatigue mats, soaker hoses, shoe soles, swings, and civil engineering material (for leachate drainage material and for an alternative daily cover at solid waste landfills). Ground, or crumb, rubber has been added to asphalt for paving, and research has been done on adding crumb rubber to concrete. When crumb rubber is blended with plastic, the resultant material can be processed like plastic but retains some of the elasticity of rubber. Pallets and railroad ties have been made from plastic and rubber blends.
As with any material recycling, economic factors enter into the ultimate fate of a particular waste stream, such as used tires. One potential use of waste tires is as tire-derived fuel (TDF), which is blended with coal and used as a fuel supplement. Cement kilns have been considered good candidates for such fuel blends because the resultant ash can be incorporated directly into the final product and the air pollution impacts from the blended fuel are less than from burning coal alone. As energy costs continue to escalate, the prospects for using more TDF seem favorable.
Sanitary Landfill Open-burning municipal waste dumps, which were once prevalent throughout the United States, were the source of many environmental and public health problems. These problems included air pollution; groundwater pollution; and rats, flies, and other disease-carrying vectors, as well as nuisance odors and unsightly conditions. The creation of the EPA in 1970 prompted a major move in the United States to eliminate open dumps and replace them with the improved sanitary landfill. Careful site selection and preparation, the application of a daily covering of earth for each day's accumulation of waste, and other procedural provisions (e.g., not permitting the disposal of liquids) eliminated most of the problems with open dumping. Between 1996 and 2006, the number of operating municipal sanitary landfills in the United
980
States decreased from about 3,100 to 1,754 (U.S. EPA, 2012a), as old small landfills were replaced by larger sanitary landfills. Current landfill capacity appears to be sufficient for total national needs, but some areas of the country lack adequate landfill capacity.
Sanitary landfills vary in design, depending on local site considerations. However, by definition, all sanitary landfills share certain design features and operating principles. These include selecting a location that has adequate space to provide waste disposal capacity for a reasonable time period, sufficient separation to protect regional surface and groundwaters, and an adequate buffer between the landfill and surrounding populations.
Once a landfill site has been selected and appropriate community concurrence and regulatory approval obtained, site preparation can begin. In addition to grading and installing sediment and erosion controls to protect local surface waters, provisions must also be made to protect groundwater from leachate. Leachate, a liquid, organic waste decomposition product, sometimes contaminated with chemicals, can migrate down and into the local aquifer. In the absence of a natural barrier, installing an underlying man-made impervious barrier can provide protection. Where significant amounts of leachate are anticipated, some landfills have systems to collect and treat the leachate. Similarly, provisions are often made for collecting and controlling the gaseous products of waste decomposition, consisting mainly of methane. In some cases the methane is cleaned and used as fuel for local energy production. Figure 17.7 provides a generalized depiction of a modern sanitary landfill.
981
Figure 17.7 Generalized Depiction of a State-of-the-Art Sanitary Landfill
Sanitary landfills are operated in a manner intended to contain and control waste. Each day's accumulation of waste is placed in its cell, compacted, and covered with earth. Usually waste is spread and compacted by heavy equipment on a sloped working face within the cell. This compaction reduces the waste volume, thereby extending the life of the landfill, and it also reduces the potential for fires, while the sloped working face diverts water from infiltrating into the waste. At the end of the day the working face and entire cell are covered with approximately six inches of compacted soil. This minimizes litter problems, helps control odors, and largely eliminates problems from animal and insect vectors. Some municipalities use precompacted, baled solid waste so landfill
982
operators can stack the waste like building blocks each day and thereby maximize site life.
Industrial and hazardous waste landfills share many of the containment and control features of sanitary landfills; however, they are much more stringently regulated. The type of waste allowed in a given landfill is strictly defined in the operating permit. In some cases certain hazardous wastes must be specially treated, packaged, or stabilized before being placed in the landfill. Periodic analysis of the wastes may be required to ensure that adequate characterization of the fill is maintained. The ultimate use of the land after the landfill is closed must also be determined.
Incineration Broadly defined, incineration is the controlled combustion of a waste. Incineration has been used for all types of wastes, including municipal solid wastes, sewage sludge, industrial and hazardous waste, and medical wastes. Some large municipal and industrial incinerators are designed to capture energy for reuse. The goal of incineration is to reduce the volume of the waste being processed or to reduce the hazardous characteristics of a particular waste stream, or both. All incineration attempts to control several variables in an effort to maximize the completeness of combustion. The classic 3 T's of combustion are:
1. Time: the length of time that solids and combustion gases are in the ignition and burn zones of the incinerator
2. Temperature: an indication of the amount of heat energy in the combustion chambers available to break molecular bonds and facilitate oxidation toward the desired end products of combustion (carbon dioxide, water vapor, inorganic ash)
3. Turbulence: the agitation of both solids and the combustible by- products, needed to provide opportunity for complete oxidation to take place.
The other major factor in fundamental combustion control is the provision of adequate oxygen, usually in the form of combustion air, to complete all oxidation reactions. The theoretically required amount of air for complete combustion of a given waste stream is known as the stoichiometric air requirement. In actual incineration
983
systems, air in excess of this requirement is provided to force the reaction toward complete oxidation of the organic wastes. This excess air is usually reported as a percentage of stoichiometric air.
Specific incineration designs vary widely in the ways that wastes are introduced into the units and in the ways that air control and mixing are achieved (Figure 17.8). Some incinerators have multiple chambers for combustion. Ignition and preliminary combustion take place in a primary chamber. The volatile products from the primary chamber are oxidized to completion in a secondary chamber, or afterburner.
Figure 17.8 Generalized Diagram of Incineration Material and Process Flow
Early incinerators were noted for smoke, odors, and sometimes even live embers coming out of the exhaust stacks. Because of these unacceptable conditions, regulations now require strict air pollution control technology. Now, devices such as wet or caustic scrubbers control acid gas. Electrostatic precipitators, venturi scrubbers, and baghouses capture fine particulates. Some of the newest hazardous
984
waste incinerators have a final activated-carbon filtration system. This polishing device minimizes emission of low-level products of incomplete combustion (PICs), such as dioxins and polycyclic aromatic hydrocarbons (PAHs). Inorganic waste contaminants, such as heavy metals (mercury, lead, and chromium, for example) can be difficult to control and can require special pollution control systems or elimination from the waste being fed to the incinerator. Because of increased traffic from trucks hauling in wastes and also because of odors and aesthetic objections, communities rarely welcome incinerators or waste landfills.
Deep Well Injection Deep well injection is a liquid waste disposal technology that uses deep injection wells to force treated or untreated liquid waste into geological formations that do not allow migration of contaminants into potential potable water aquifers. These wells, typically several thousand feet deep, extend into permeable injection zones containing highly saline brines that render the water nonpotable. Impermeable rock or soil layers confine the injection zone vertically. The wastes injected can be radioactive wastes, hydrocarbon wastes, oil and gas drilling brines, hazardous wastes, and other wastes not suitable for landfill. In the United States injection wells are regulated and classified under an EPA definition that addresses uses and characteristics of such wells.
Injection wells can be located only in areas free of faults and other geological features that could allow wastes to migrate into potable water aquifers. Liquid wastes high in suspended solids, iron content, or organic substrates that could serve as food for microbial growth should not be disposed of in such wells because of their potential to foul or clog the well. Injection wells are double sleeved to allow monitoring for system integrity and to provide dual boundaries for protecting intervening geological layers.
Other Technologies The previous discussion touches on some of the most prevalent methods for treatment and disposal of wastes, but many other waste treatment techniques are in practice or evolving. Treatment methods such as supercritical water oxidation, molten metals and molten salt oxidation, glass melt and vitrification processes, and
985
waste-specific biological treatment systems and composting are a few such technologies. Dedicated treatment technologies, such as thermal desorption, have been developed for in situ and extractive remediation of old industrial waste disposal sites. Waste disposal technology has undergone tremendous technological evolution to keep pace with the changing character of society's waste products.
986
Health Concerns Exposure to solid and hazardous wastes can adversely affect human health in several ways. The aesthetic impact of poor waste management—trash piling up in streets and vacant lots—can undermine the livability and even the safety of a community. At least five kinds of health hazards are well recognized:
1. Infectious disease risks from poorly managed solid waste
2. Contamination of drinking water and soil by biological, chemical, and mining wastes
3. Gas migration and leachate discharges from landfills
4. Emissions of air pollutants from incinerators
5. Contamination of food by waste chemicals that escape into the environment
Poorly operated landfills can be havens for flies, mosquitoes, rats, and mice. Uncovered garbage and trash provide them with food, shelter, and a breeding ground. These insects and animals can be vectors for disease by carrying pathogenic microbes into the surrounding community. As described in chapter 18, rats and mice can spread a range of diseases to humans, including leptospirosis, hantavirus pulmonary syndrome, and lymphocytic choriomeningitis virus (CDC, 2008). Furthermore, rats can carry many kinds of mites, lice, fleas, and ticks that act as disease vectors. Modern landfills, which require wastes to be covered daily with clean soil, have greatly reduced the spread of disease by these vectors.
Improper disposal of solid and hazardous wastes can contaminate drinking water. Both groundwater and surface water can be affected. Most old landfills or dumps lack liners, which allows chemicals buried in the landfill to leach down into the underlying aquifer. Volatile organic compounds (VOCs), such as trichloroethylene, tetrachloroethylene, and petroleum distillates are common contaminants in municipal and industrial landfills. These organic solvents are widely used as degreasers, dry cleaning fluids, and components of paints, varnishes, and adhesives. Because these chemicals are highly mobile, they readily migrate through unlined landfills into the underlying groundwater. Heavy metals in landfills,
987
such as lead, cadmium, mercury, and chromium, can also be a source of groundwater contamination. Moreover, microbial degradation of garbage and vegetative wastes in a landfill can produce organic acids that lower the pH of the milieu, making buried metals more soluble. Old industrial sites where waste chemicals were sometimes dumped into open pits or onto the ground have also been known to contaminate nearby groundwater. If the contaminated groundwater migrates off site, it can affect people who drink from down-gradient private and public water wells. In Hardeman County, Tennessee, for example, leachate from a hazardous waste landfill contaminated private drinking-water wells with carbon tetrachloride and other VOCs (Clark et al., 1982). People who drank from these wells experienced headaches, nausea, and visual disturbances. Physicians who examined the victims reported that several of them had enlarged livers. In addition, clinical laboratory tests documented the presence of elevated levels of liver enzymes and altered serum chemistries, evidence of liver toxicity. Fortunately, these abnormalities resolved several months after the people stopped drinking the contaminated water.
Municipal landfills can also be a source of air pollutants such as methane, hydrogen sulfide, and VOCs. Anaerobic microbial digestion of organic matter buried in landfills generates large quantities of methane gas. In 1969, in Winston-Salem, North Carolina, methane gas from a landfill migrated underground through the soil into the basement of an armory building adjacent to the landfill. The methane built up to an explosive level in the basement, and a lit cigarette triggered an explosion that killed three men and injured five others. Methane and carbon dioxide released to the atmosphere from landfills can also have ecological effects, given that these gases may contribute to global warming (see Chapter 12). It has been estimated that landfills accounted for about 23% of total U.S. methane emissions to the atmosphere from anthropogenic sources in 2006 (U.S. EPA, 2008).
As mentioned, wastes from mining and petroleum production form the largest category of solid wastes produced in the United States. Huge piles of mine tailings, left behind after the extraction of metals, are a potential source of environmental contamination (Figure 17.9). Smelters are often located near the mining areas and release additional metal-contaminated particulates to the ambient
988
air and soil. At several mining and smelting sites, it has been demonstrated that children's exposure to lead-contaminated soil has contributed to increased blood lead concentrations (Gulson et al., 1994; Murgueytio et al., 1998). Such exposures are of health concern because there is no clear threshold for lead-induced neurotoxicity in children (Advisory Committee on Childhood Lead Poisoning Prevention, 2012) (see Tox Box 11.1).
Figure 17.9 Mine Tailings Pile: The Legacy of Sixty Years of Lead and Zinc Mining in Ottawa County, Oklahoma
Source: Photo supplied by Ken Orloff.
Municipal and hazardous waste incinerators and open burning of waste releases particulates, vapors, and gases to the ambient air that are also of potential health concern. Burning even nontoxic materials, such as wood and paper, produces particulate matter, carbon monoxide, aldehydes, and polycyclic aromatic hydrocarbons. In addition, burning commonplace materials, such as paints, solvents, insecticides, and plastics, can produce chlorinated dibenzodioxins and chlorinated dibenzofurans, collectively known as dioxins (see Tox Box 19.1 in Chapter 19). Small amounts of dioxins are released from hazardous waste incinerators, which operate under strict environmental regulations. Backyard burning of household trash in open barrels can also be a significant source of atmospheric dioxin emissions. It has been estimated that backyard
989
trash burning by only two to forty households can generate as much dioxin as a municipal waste incinerator (Lemieux, Lutes, Abbott, & Aldous, 2000).
Although inhalation of dioxins in ambient air is a potential source of exposure, the major source of exposure to dioxins is through food consumption. Once dioxins are released to the environment, they resist chemical, physical, and biological degradation, and they can bioaccumulate in aquatic and terrestrial animals. More than 90% of the dioxin exposure in the general population is derived from background, low-level dioxin contamination in dairy products, meats, fish, eggs, and other foodstuffs (ATSDR, 1998).
Public health practice emphasizes prevention over treatment (see Chapter 26). This principle is especially relevant in the field of environmental health because preventing environmental contamination is easier and less costly than cleaning it up after it has occurred. Therefore both industrialized and developing countries should learn from the mistakes of the past and strive to manage and treat wastes in a manner that protects public health.
990
Text Box 17.5 International Trafficking in Hazardous Wastes As industrialized countries' environmental laws for disposing of hazardous wastes became more stringent and expensive to comply with, some generators began shipping wastes to other countries for disposal (Orloff & Falk, 2003). The United Nations Environmental Programme estimates that about 10% of hazardous waste produced worldwide is shipped across international borders. In some cases the recipient country is ill prepared to safely handle the hazardous wastes. Hazardous waste workers often lack adequate personal protective equipment and training, which puts their health and safety at risk. Furthermore, if the wastes are not adequately treated and disposed of, they can create a potentially dangerous environmental legacy for the recipient country.
Concern over the international shipping of hazardous wastes led to the establishment in 1989 of a treaty known as the Basel Convention. The convention's goal is to regulate the international movement of hazardous materials and to ensure that these wastes are managed and disposed of in an environmentally sound manner. One of the key provisions of the convention is that transboundary movement of hazardous wastes can take place only upon prior written notification by the state of export to competent authorities of the state of import.
As of early 2016, 182 countries and the European Union were parties to the Basel Convention (www.basel.int/Countries/StatusofRatifications/PartiesSignatories/tabid/4499/Default.aspx The United States signed the convention in 1992 but has not ratified it, which would require Congressional action. One factor preventing the United States from ratifying the convention is that its acceptance would require changes in Resource Conservation and Recovery Act regulations that specify how hazardous wastes are defined and how those wastes are managed.
991
One of the challenges facing the convention is how to deal with trafficking in recyclable materials, such as spent lead- acid batteries and other nonferrous scrap metal. These wastes are valuable commodities on the world market, and recycling these materials provides jobs and generates income in countries with struggling economies. Under a proposed amendment to the Basel Convention, the transfer of such materials from industrialized to developing countries would be banned.
In recent years the practice of ship breaking has attracted the attention of the environmental community. Some environmental groups have characterized this practice as being a covert form of international trafficking in hazardous wastes. The term ship breaking refers to sending decommissioned ships to other countries where they are dismantled to recover steel and other recyclables. Concerns have been raised because workers may not be protected from exposure to lead, asbestos, polychlorinated biphenyls, mercury, and other hazardous materials during ship dismantling operations. Nearly all of the world's ship breaking occurs in five nations: India, Pakistan, Bangladesh, China, and Turkey (Sarraf et al., 2010).
992
Summary Human activities produce a huge volume and variety of waste materials that are regulated by federal, tribal, state, and local laws and regulations. Waste management strategies emphasize the importance of reducing, reusing, and recycling waste materials. When this is not possible, proper disposal and treatment of wastes is important. Selection of the best means for waste disposal or treatment requires consideration of factors such as technological feasibility, compliance with regulatory requirements, long-term effectiveness, community acceptance, and cost. Proper handling and disposal of wastes is necessary to prevent environmental contamination and potential adverse impacts on public health and ecological systems.
993
Key Terms agricultural waste
Discarded material generated from the production of food and other products.
animal waste Feces, urine, and spilled food from animals.
construction debris Discarded material generated from construction and demolition of buildings and other facilities.
deep well injection A disposal technology that forces treated or untreated liquid waste into geological formations that do not allow migration of contaminants into potential potable water aquifers.
electronic waste (e-waste) Discarded electronic equipment such as computers, computer display monitors, televisions, DVD players, cell phones, and electronic games.
hazardous waste Discarded material that is capable of harming human health or the environment.
incineration The controlled combustion of discarded materials.
industrial ecology The study of the physical, chemical, and biological interactions and interrelationships both within and between industrial systems and ecological systems.
industrial waste Discarded material from industrial processes such as manufacturing, cleaning, recycling, and others.
leachate A liquid generated by organic waste decomposition within a landfill or dump.
life cycle analysis A technique for assessing the environmental and social (including health) impacts associated with all the stages of a
994
product's life, from cradle to grave, and for designing and producing products that minimize waste and pollution at the end of their useful life.
medical waste Discarded items that are generated from health care treatment and research and that have come into contact with body fluids or contain infectious agents.
mining waste Discarded items generated as a result of the extraction of metal, coal, and oil from the Earth's crust.
municipal solid waste Discarded everyday items generated from homes and businesses.
radioactive waste Discarded materials that contain radioactive chemical elements.
reduce, reuse, and recycle Primary goals of an ideal waste management strategy.
sanitary landfill Land disposal areas specifically planned, constructed, and managed to prevent impact on human health and the environment.
sewage sludge Concentrated solid material remaining after the treatment of waste water or sewage.
solid waste Material (solid, liquid, or gas) that lacks value and is discarded.
special waste A subcategory of solid waste that is designated by laws and regulations.
waste management A multitier approach to prevent the generation of or to manage discarded materials so that human health and the environment are not impacted.
995
Discussion Questions 1. What are the different approaches to solid waste management?
What are the advantages and disadvantages of each approach?
2. What are the different types of solid wastes, and how are they identified?
3. How does the composition and management of solid waste vary around the world?
4. How can you reduce the amount of waste you produce? Name each way and discuss it.
5. Select one of the waste treatment or disposal technologies discussed in this chapter. How could this technology be effectively used in a solid waste management program? Specify the type of solid waste, and discuss how using the technology would protect the health of people and the environment.
6. What are the ways in which people can be exposed to toxic substances in solid waste and hazardous waste?
7. Research and summarize the management of municipal waste in your community. Where does the trash go? How much is produced per person? What steps is your community taking to reduce waste generation?
996
References Advisory Committee on Childhood Lead Poisoning Prevention. (2012). Low level lead exposure harms children: A renewed call for primary prevention. Atlanta: Centers for Disease Control and Prevention.
Agency for Toxic Substances and Disease Registry. (1998). Toxicological profile for dibenzo-p-dioxins (Update). Atlanta: Public Health Service, Agency for Toxic Substances and Disease Registry.
Agency for Toxic Substances and Disease Registry. (2006). Health consultation: Exposure investigation report, air sampling for sulfur gases, Warren Township, Trumball County, Ohio. Atlanta: Public Health Service, Agency for Toxic Substances and Disease Registry.
Burkholder, J., Libra, B., Weyer, P., Heathcote, S., Kolpin, D., Thorne, P. S., & Wichman, M. (2007). Impacts of waste from concentrated animal feeding operations on water quality. Environmental Health Perspectives, 115, 308–312.
Caniato, M., Tudor, T., & Vaccari, M. (2015). International governance structures for health-care waste management: A systematic review of scientific literature. Journal of Environmental Management, 153, 93–107.
Centers for Disease Control and Prevention. (2008). Got mice? Seal, trap, and clean up to control rodents. Retrieved from http://www.cdc.gov/Features/Rodents
Centers for Disease Control and Prevention. (2015a). Infection prevention and control recommendations for hospitalized patients under investigation (PUIs) for Ebola virus disease (EVD) in U.S. hospitals. Retrieved from http://www.cdc.gov/vhf/ebola/hcp/infection-prevention-and- control-recommendations.html
Centers for Disease Control and Prevention. (2015b). Interim guidance for environmental infection control in hospitals for Ebola
997
virus. Retrieved from http://www.cdc.gov/vhf/ebola/hcp/environmental-infection- control-in-hospitals.html
Chartier, Y., Emmanuel, J., Pieper, U., Prüss, A., Rushbrook, P., Stringer, R.,…Zghondi, R. (2014). Safe management of wastes from health care activities (2nd ed.). Geneva: World Health Organization.
Clark, C. S., Meyer, C. R., Balistreri, W. F., Gartside, P. S., Elia, V. J., Majeti, V. A., & Specker, B. (1982). An environmental health survey of drinking water contamination by leachate from a pesticide waste dump in Hardeman County, Tennessee. Archives of Environmental Health, 37(1), 9–18.
Duan H., Miller T.R., Gregory J., & Kirchain R. (2013). Quantitative characterization of domestic and transboundary flows of used electronics: Analysis of generation, collection, and export in the United States. Cambridge, MA: Massachusetts Institute of Technology, Materials Systems Laboratory. Retrieved from http://www.step-initiative.org/files/step/_documents/MIT- NCER%20US%20Used%20Electronics%20Flows%20Report%20- %20December%202013.pdf
Ehrenfeld, J., & Gertler, N. (1997). Industrial ecology in practice: The evolution of interdependence at Kalundborg. Journal of Industrial Ecology, 1, 67–79.
Garner, A., & Keoleian, G. A. (1995). Industrial ecology: An introduction. Ann Arbor: University of Michigan, National Pollution Prevention Center for Higher Education. Retrieved from http://www.umich.edu/ ∼nppcpub/resources/compendia/INDEpdfs/INDEintro.pdf
Gilchrist, M. J., Greko, C., Wallinga, D. B., Beran, G. W., Riley, D. G., & Thorne, P. S. (2007). The potential role of concentrated animal feeding operations in infectious disease epidemics and antibiotic resistance. Environmental Health Perspectives, 115, 313– 316.
Gulson, B. L., Davis J. J., Mizon K. J., Korsch M. J., Law A. J., & Howarth, D. (1994). Lead bioavailability in the environment of
998
children: Blood lead levels in children can be elevated in a mining community. Archives of Environmental Health, 49(5), 326–331.
Heederik, D., Sigsgaard, T., Thorne, P. S., Kline, J. N., Avery, R., Bønløkke, J. H.,…Merchant, J. A. (2007). Health effects of airborne exposures from concentrated animal feeding operations. Environmental Health Perspectives, 115, 298–302.
Hill, S. (2012). Bad reaction: The toxicity of chemical-free claims. Retrieved from http://www.csicop.org/specialarticles/show/bad_reaction_the_toxicity_of_chemical- free_claims
Hoornweg, D., & Bhada-Tata, P. (2012). What a waste: A global review of solid waste management (Urban Development Series Knowledge Papers). Washington, DC: World Bank.
Hossain, M. S., Santhanam, A., Nik Norulaini, N. A., & Omar, A. K. (2011). Clinical solid waste management practices and its impact on human health and environment—A review. Waste Management, 31(4), 754–766.
Institute of Medicine. (2014). Research priorities to inform public health and medical practice for Ebola virus disease: Workshop in brief. Washington, DC: National Academy of Sciences. Retrieved from http://www.iom.edu/Reports/2014/Research-Priorities-to- Inform-Public-Health-and-Medical-Practice-for-Ebola-Virus- Disease-WIB.aspx
Lemieux, P. M., Lutes, C. C., Abbott, J. A., & Aldous, K. M. (2000). Emissions of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans from the open burning of household waste in barrels. Environmental Science & Technology, 34, 377– 384.
Morin, M. (2014). Another Ebola challenge: Disposing of medical waste. Los Angeles Times, October 20. Retrieved from http://www.latimes.com/science/la-sci-ebola-waste-disposal- 20141020-story.html
Murgueytio, A. M., Evans, R. G., Sterling, D. A., Clardy, S. A., Shadel, B. N., & Clements, B. W. (1998). Relationship between lead mining and blood lead levels in children. Archives of
999
Environmental Health, 53(6), 414–423.
New York State Department of Health. (2014). High volume hydraulic fracturing for shale gas development. Albany: Author.
A Notice by the Food and Drug Administration (Guidance for industry on new animal drugs and new animal drug combination products administered in or on medicated feed or drinking water of food-producing animals: Recommendations for drug sponsors for voluntarily aligning product use conditions with guidance for industry #209; Availability), 78 FR 75570 (2013).
Orloff, K., & Falk, H. (2003). An international perspective on hazardous waste practices. International Journal of Hygiene and Environmental Health, 206, 291–302.
Osibanjo, O., & Nnorom, I. C. (2007). The challenge of electronic waste (e-waste) management in developing countries. Waste Management & Research, 25(6), 489–501.
Ramesh Babu, B., Parande, A. K., & Ahmed Basha, C. (2007). Electrical and electronic waste: A global environmental problem. Waste Management & Research, 25(4), 307–318.
Rubber Manufacturers Association. (2014). 2013 U.S. scrap tire management summary. Washington, DC: Author.
A Rule by the Land Management Bureau (Oil and gas; Hydraulic fracturing on federal and Indian lands), 80 FR 16577 (2015).
Sarraf, M., Stuer-Lauridsen, F., Dyoulgerov, M., Bloch, R., Wingfield, S., & Watkinson, R. (2010). The ship breaking and recycling industry in Bangladesh and Pakistan (Report No. 58275). Washington, DC: World Bank. Retrieved from http://siteresources.worldbank.org/INTPOPS/Publications/22816687/ShipBreakingReportDec2010.pdf
Schmidt, C. W. (2002). e-Junk explosion. Environmental Health Perspectives, 110(4), A188–194.
Schmidt, C. W. (2006). Unfair trade: e-Waste in Africa. Environmental Health Perspectives, 114(4), A232–235.
Silbergeld, E. K., Graham, J., & Price, L. B. (2008). Industrial food animal production, antimicrobial resistance, and human health.
1000
Annual Review of Public Health, 29, 151–169.
Silbergeld E. K., & Nachman, K. (2008). The environmental and public health risks associated with arsenical use in animal feeds. Annals of the New York Academy of Sciences, 1140, 346–357.
U.S. Environmental Protection Agency. (1985). Report to Congress: Wastes from the extraction and beneficiation of metallic ores, phosphate rock, asbestos, overburden from uranium mining, and oil shale. Washington, DC: Author.
U.S. Environmental Protection Agency. (2008). Inventory of U.S. greenhouse gas emissions and sinks: 1990–2006. Retrieved from http://epa.gov/climatechange/emissions/downloads/08_ES.pdf
U.S. Environmental Protection Agency. (2011). Electronics waste management in the United States through 2009. Washington, DC: Author.
U.S. Environmental Protection Agency. (2012a). Municipal solid waste generation, recycling, and disposal in the United States: Facts and figures for 2012. Washington, DC: Author.
U.S. Environmental Protection Agency. (2012b). The national biennial RCRA hazardous waste report (based on 2011 data). Washington, DC: Author.
Wiedinmyer, C., Yokelson, R. J., & Gullett, B. K. (2014). Global emissions of trace gases, particulate matter, and hazardous air pollutants from open burning of domestic waste. Environmental Science and Technology, 48, 9523–9530.
Wines, M. (2014). Waste from Ebola poses challenge to hospitals. New York Times, October 17.
Zeller, T. (2008). Recycling: The big picture. National Geographic, January, pp. 82–87.
1001
For Further Information Books and Articles Carroll, C. (2008) High-tech trash: Will your discarded TV or computer end up in a ditch in Ghana? National Geographic, January, pp. 64–87.
Chang, H. O. (2000). Hazardous and radioactive waste treatment technologies handbook. Boca Raton, FL: CRC Press.
Gorner, I. K. (2003). Waste incineration: European state of the art and new developments. IFRF Combustion Journal, art. 200303.
Gwin, P. (2014). The ship-breakers. National Geographic, May, pp. 80–88. Available at http://ngm.nationalgeographic.com/2014/05/shipbreakers/gwin- text where an extensive gallery of photos from Bangladesh is also available.
Hickman, H. L. (1999). Principles of integrated solid waste management. Annapolis: American Academy of Environmental Engineers.
Johnson, B. L. (1999). Impact of hazardous waste on human health: Hazard, health effects, equity, and communications issues. New York: Lewis.
Lichtveld, M. Y., Rodenbeck S. E., & Lybarger J. A. (1992). The findings of the Agency for Toxic Substances and Disease Registry Medical Waste Tracking Act report. Environmental Health Perspectives, 98, 243–250.
Manuel, J. S. (2003). Unbuilding for the environment. Environmental Health Perspectives, 111(16), A881–887.
National Research Council. (1991). Environmental epidemiology: Public health and hazardous wastes. Washington, DC: National Academies Press.
Rathje, W. L., & Murphy, C. (2001). Rubbish! The archaeology of garbage. Tucson: University of Arizona Press.
1002
Schneider, A., & McCumber, D. (2004). An air that kills. New York: Putnam.
Taylor, D. (1999). Talking trash: The economic and environmental issues of landfills. Environmental Health Perspectives, 108(7), A404–409.
Tchobanoglous, G., & Kreith, F. (2002). Handbook of solid waste management (2nd ed.). New York: McGraw-Hill.
Willis, B. C., Howie, M. M., & Williams, R. C. (2002). Public health reviews of hazardous waste thermal treatment technologies: A guidance manual for public health assessors. Atlanta: Agency for Toxic Substances and Disease Registry, Division of Health Assessment and Consultation.
Nongovernmental Organizations Basel Action Network (BAN): www.ban.org. The BAN is an NGO based in Seattle that addresses global hazardous waste, with a focus on two waste streams: electronic waste (e-waste), and end- of-life ships.
NGO Shipbreaking Platform: www.shipbreakingplatform.org. This is a Brussels-based coalition of environmental, human rights, and labor rights organizations working to prevent the dangerous pollution and unsafe working conditions caused when end-of-life ships containing toxic materials in their structures are freely traded in the global marketplace.
StEP (solving the e-waste problem): www.step-initiative.org. Based in Bonn, Germany, and hosted by the United Nations University Institute for the Advanced Study of Sustainability (UNU-IAS), StEP focuses on reducing e-waste.
Agencies Because federal government agencies frequently revise and update the information and data posted on their Web sites, specific Web pages are not provided. However, each of these home page Web sites has a search engine that will assist you in locating appropriate information.
Agency for Toxic Substances and Disease Registry:
1003
http://www.atsdr.cdc.gov
Centers for Disease Control and Prevention: http://www.cdc.gov
U.S. Environmental Protection Agency: http://www.epa.gov
1004
Chapter 18 Pest Control and Pesticides
Mark Gregory Robson, George C. Hamilton, Wattasit Siriwong, and Héctor Luis Maldonado Pérez
Dr. Robson, Dr. Hamilton, Dr. Siriwong, and Mr. Maldonado report no conflicts of interest related to the authorship of this chapter. Megan Cartwright and Anna Engstrom report no conflicts of interest related to the authorship of the tox boxes.
1005
Key Concepts Pests are plants, animals, or microorganisms that threaten human health.
Each pest has specific biological and ecological characteristics.
Pest control relies heavily on chemical agents.
There are many different classes of pesticides.
People are exposed to pesticides in many ways.
Pesticide regulation is complex and relies on federal and state laws.
Integrated pest management (IPM) is a strategy combining chemical and nonchemical methods.
Pests have plagued humankind since the beginning of time, as recorded in the ancient writings of the Chinese, Egyptian, and Hebrew peoples. The Book of Exodus (10:14–15) memorably recounts that “the locusts came up over all the land of Egypt and settled on the whole country of Egypt… [T]hey covered the face of the whole land so that the land was darkened and they ate all the plants in the land and all the fruit of the trees;…not a green thing remained, neither tree nor plant of the field, through all the land of Egypt.” Diseases such as plague and malaria—both propagated by pests—have changed the course of human history (McNeill, 1976; Zinsser, 2007).
Efforts to control pests are also as old as history. Some control measures used chalk, plant extracts, mercury, arsenic, lead, and other compounds—not to mention sacrifices, prayers, rituals, and dancing!
Recently chemicals have dominated pest control. As with medications, the ideal pesticide is both safe in terms of human and ecosystem health and effective at controlling the target species. Paris green (copper acetoarsenite) was among the first compounds to be used on a large scale in agricultural production. In the 1860s, it was shown to have insecticidal properties. Paris green was also an
1006
effective fungicide. Later in the nineteenth century lead arsenate became a popular pesticide and was widely used. Chemical pest control changed dramatically in 1939 when Paul Müller found that DDT, or dichlorodiphenyltrichloroethane, could be used as an insecticide. DDT was widely used during World War II and is still used in many parts of the world for vector control, particularly for malaria and other mosquito-borne diseases.
After the war DDT and similar chlorinated pesticides made their way into agriculture (Figures 18.1 and 18.2 display modes of applying agricultural pesticides; Figure 18.3 is an example of a serious agricultural pest, the corn borer). The introduction of these compounds into agriculture changed pest control and food production worldwide. Public health and ecological research has increasingly revealed problems with pesticides, ranging from human toxicity to wildlife toxicity to ecosystem disruption. Rachel Carson's Silent Spring, published in 1962, alerted the public and policymakers to the risks associated with pesticide use. Pimentel (2009) estimated that the environmental and societal impacts of pesticide use in the United States cost $12 billion. Areas impacted include public health, livestock and livestock product losses; increased control expenses resulting from pesticide-related destruction of natural pest predators and from the development of pesticide resistance in pests; crop pollination problems and honeybee losses; crop and crop product losses; bird, fish, and other wildlife losses; and government expenditures to reduce the environmental and social costs of the recommended application of pesticides. Today we are moving beyond exclusive reliance on pesticides, using combinations of chemical and nonchemical methods.
1007
Figure 18.1 Application of Lead Arsenate in the Early 1900s Source: Photo supplied by E. G. Christ.
Figure 18.2 Modern Pesticide Application Equipment Source: Photo supplied by M. G. Robson.
1008
Figure 18.3 A Corn Borer, an Example of an Insect Pest, Causing Damage in the Stalk of a Corn Plant
Source: Photo supplied by M. G. Robson
The borers cause the stalks to lodge (fall over), making the corn difficult to harvest. One fourth to one third of the global corn harvest is lost to pests.
A pest can be any species of plant, animal, or microorganism that threatens human health and well-being. Most pests fill specific ecological niches and have functions that are important to ecosystem integrity. For example bees sting but pollinate plants and make honey; ants interrupt picnics and may sting but play an essential role in nutrient cycles.
The U.S. Environmental Protection Agency (U.S. EPA) defines seven categories of public health pests:
1. Cockroaches. Cockroaches are controlled to reduce asthma, allergies, and food contamination.
2. Body, head, and crab lice. These lice are controlled to prevent the spread of skin irritations and rashes and to prevent the occurrence of louse-borne diseases, such as epidemic typhus, trench fever, and epidemic relapsing fever.
3. Mosquitoes. Mosquitoes are controlled to prevent the spread of mosquito-borne diseases such as malaria, yellow fever, dengue fever, and certain encephalitides (e.g., St. Louis, Eastern, Western, West Nile, and LaCrosse).
4. Rats and mice. Rats and mice are controlled to prevent the
1009
spread of rodent-borne diseases and the contamination of food for human consumption.
5. Microorganisms, including bacteria, viruses, and protozoa. Microorganisms listed as public health pests are controlled by public health agencies and hospitals for the purpose of preventing the spread of diseases.
6. Reptiles and birds. Certain reptiles and birds are controlled to prevent the spread of disease and to prevent physical injury.
7. Various mammals. Certain mammals have the potential to inflict physical human injury and can act as reservoirs of disease (e.g., rabies).
1010
Insect Pests Insects belong to the class Insecta or Hexapoda and have three body regions (head, thorax, and abdomen), six legs that are connected to the thorax, and in the adults of most species, thoracic wings (Triplehorn & Johnson, 2005).
All insects go through one of two types of development, or metamorphosis: gradual (egg, nymph, and adult) or complete (egg, larva, pupa, and adult). Eight examples of common insect pests are discussed below (also see Text Box 18.1).
Bedbugs Bedbugs are human ectoparasites, that is, they live on external surfaces. Bedbugs must feed on blood in order to survive. Humans are the preferred host of bedbugs. Bedbugs feed at night and hide in areas such as cracks and crevices, the folds of mattresses, the upholstery of chairs and sofas, and bedsprings.
1011
Text Box 18.1 Insect Repellants Insect repellents come in many forms, including aerosols, sprays, liquids, creams, and sticks. Some are made from chemicals and some have natural ingredients.
Insect repellents prevent bites from biting insects but not stinging insects. Biting insects include mosquitoes, ticks, fleas, chiggers, and biting flies. Stinging insects include bees, hornets, and wasps (American Academy of Pediatrics, 2014).
Insect repellants are designed not to kill insects but to deter them from settling on skin and clothes. The public health benefit of reducing insect bites is considerable; for instance, mosquitoes alone transmit disease to more than 700 million people annually. Malaria remains a common disease in poor and middle-income countries (as discussed in Text Box 18.4), and in the United States, mosquitoes transmit chikungunya, dengue and hemorrhagic dengue, eastern equine encephalitis, western equine encephalitis, St. Louis encephalitis, La Crosse encephalitis, and West Nile virus.
DEET is a chemical used in insect repellents. The amount of DEET in insect repellents varies from product to product, so it's important to read the label of any product you use. The amount of DEET may range from less than 10% to more than 30%.
Studies show that products with higher amounts of DEET protect people longer. For example, products with amounts around 10% may repel pests for about two hours, while products with amounts of about 24% last an average of five hours. But studies also show that products with amounts of DEET greater than 30% don't offer any extra protection (American Academy of Pediatrics, 2014).
The American Academy of Pediatrics (AAP) recommends that repellents should contain no more than 30% DEET when used on children. Insect repellents also are not recommended for children younger than two months.
1012
The Centers for Disease Control and Prevention (CDC) has also recommended other repellents that may work as well as DEET, repellents with picaridin and repellents with oil of lemon eucalyptus or 2% soybean oil. Currently these products have a duration of action that is comparable to that of about 10% DEET (CDC, 2013a).
Is DEET safe? Once applied to the skin it is absorbed, in quantities that have ranged between 5% and 15% in different studies (Antwi, Shama, & Peterson, 2008; Osimitz, Murphy, Fell, & Page, 2010). Acute toxicity is extremely rare; fewer than fifty cases of serious toxic effects have been documented in the medical literature (Fradin & Day, 2002). Animal testing has suggested that high-dose DEET may cause neurological effects (Antwi et al., 2008).
Permethrin- and DEET-impregnated clothing is often issued to military personnel for the control of insect pests. Efficacy studies on these pesticides have shown a significant reduction of pest bites when the impregnated clothing has been used. There have been reports of serious health problems associated with military personnel exposed to these compounds (Punareewattana et al., 2000). While no pesticide is without some risk, it is widely held that, in areas of vector-borne disease transmission, the pesticide-treated clothing and the use of repellents pose a far lower risk than the risk of being bitten by an insect that carries a disease.
Cockroaches Most cockroaches are tropical, and they are very common in the southern areas of the United States. In northern areas, those most commonly encountered are the ones that live indoors. Cockroaches are not known to transmit any serious diseases; however, they contaminate food, produce an unpleasant odor, and can become a serious nuisance. Exposure to cockroach antigen is an important risk factor for developing asthma. Most cockroaches are nocturnal but may be seen during the day when their population numbers are high.
The four most common problem species in the United States are the German, American, Oriental, and brown-banded cockroaches. The
1013
German cockroach, Blattella germanica, is the most common cockroach in homes in the United States. The American cockroach, Periplaneta americana—or water bug, Bombay canary, or flying water bug—is the largest of the house-dwelling cockroaches. The Oriental cockroach, Blatta orientalis—or water bug, black beetle, or shad roach—is a cosmopolitan pest, found throughout the world. The brown-banded cockroach, Supella longipalpa, is a small cockroach, with two lighter transverse bands across the base of the wings and abdomen.
Fleas Fleas are small ectoparasites. As juveniles they have chewing mouthparts, and as adults they have piercing-sucking mouthparts, which are used to feed on blood. Eggs are laid on the host animal but fall off into carpets, upholstery, and pet bedding material. Fleas are important because they carry diseases such as plague and murine typhus.
There are several species of fleas, including those that feed on humans and pets. The cat flea, Ctenocephalides felis, and the dog flea, C. canis, are common throughout the United States and prefer to feed on dogs, cats, and humans and sometimes rats.
Lice Lice that attack humans are flightless, ectoparasitic insects. They are small insects that exhibit gradual metamorphosis. Sucking lice insert their mouthparts into their host in order to feed on blood.
There are approximately 500 species of sucking lice that feed on mammals. Only two species attack humans: Pediculus humanus— which includes the body louse, P. humanus and the head louse, P. humanus capitis—and the crab or pubic louse, Phthirus pubis.
Mosquitoes Mosquitoes are a large (169 species in North America), well-known, and important group of biting flies that spend their larval life living in water and their adult life above the water's surface. Mosquitoes are the vector for numerous human diseases, including malaria, dengue fever, yellow fever, and several encephalitis viruses. Only the species that feed on humans are directly associated with the
1014
transmission of disease.
Several species of mosquitoes are responsible for transmitting the most serious diseases. Malaria is transmitted by Anopheles species. Aedes aegypti transmits both yellow fever and dengue fever. The Asian tiger mosquito, Aedes albopictus, is a vector of dengue fever, eastern equine encephalitis, West Nile virus, and chikungunya virus (Gratz, 2004). Filariasis, which is caused by a filarial worm, is transmitted by Culex species. West Nile virus is spread by a variety of species, primarily in the genus Culex, that have fed on birds. Eastern equine encephalitis is known to be circulated by Culiseta melanura in birds, but Aedes sollicitans, Aedes vexans, and Coquillettidia perturbans are suspected as major vectors of the disease in humans (Murray, Mertens, & Despres, 2010). Culex pipiens, the common house mosquito, transmits St. Louis encephalitis. Because C. pipiens is an urban mosquito, St. Louis encephalitis is prevalent in urban centers.
Sand Flies Sand flies are bloodsucking as adults and occur in the southern United States and tropical areas. From a public health perspective there are ninety-eight species proven or suspected to be vectors of human leishmaniases, a group of diseases that usually present as sores, which erupt weeks or months after a human or animals is bitten (Maroli, Feliciangeli, Bichaud, Charrel, & Gradoni, 2013). Some patients with leishmaniasis develop enlarged spleens, which can affect blood cell counts and function. Globally, insecticide- sprayed bed nets are widely used to prevent sand fly bites.
Termites Termites are insects that are responsible for millions of dollars of damage to wood and wooden structures throughout the world. Worldwide there are about 1,900 species of termites. Termites live in highly organized societies with three distinct castes: reproductive females and males, workers, and soldiers.
Termites are important for several reasons. First, because of their affinity for wood, they are very destructive to the wooden portions of buildings, furniture, books, utility poles, fence posts, and other wooden structures. Worldwide they also produce large amounts of
1015
atmospheric methane. However, termites are also important because they convert dead trees and other plant substances into decayed matter that can be used by other organisms.
Ticks Ticks are relatives of insects. Ticks have piercing-sucking mouthparts and undergo a development cycle similar to that of insects with gradual metamorphosis. As vectors of a wide range of disease, ticks are a major public health concern.
Lyme disease is one of the most serious tick-borne diseases. First recognized in 1975, it is caused by the bacterium Borrelia burgdorferi and is transmitted to humans through the bite of infected blacklegged ticks.
Ticks are also vectors for Rocky Mountain spotted fever, ehrlichiosis, and tularemia. Rocky Mountain spotted fever, a cause of potentially fatal human illness in North and South America, is caused by the bacterium Rickettsia rickettsii. In the United States the species that transmit it include the American dog tick, Rocky Mountain wood tick, and brown dog tick. Ehrlichiosis is the general term for several bacterial diseases that affect animals and humans; the Lone Star Tick is the primary vector. Tularemia has many names including rabbit fever and deer fly fever. Tularemia is a serious infectious disease caused by the bacterium Francisella tularensis, which is transmitted by ticks as well as the deer fly.
1016
Vertebrate Pests Vertebrate pests include rats, mice, and birds. Rodents are the most abundant and diversified order of living mammals in the world. We have known since the Middle Ages that they can contribute to human disease, as black rats were associated with the transmission of plague. In modern times rodents continue to pose a threat to public health (Meerburg, Singleton, & Leirs, 2009).
Rats are relatively large rodents that are important pests. They contaminate grain, destroy food in processing and storage plants, and can bite sleeping children and adults. Rats have caused more human death, misery, and economic hardship than any other vertebrate pest. Rats are known carriers of insects (lice, fleas, and mites) that transit plague and murine typhus and they helped to cause the outbreaks of plague in the fourteenth century that killed an estimated 25 million people (Cantor, 2001).
Several species of mice, including field mice and house mice, can invade homes and other structures. The house mouse, Mus musculus, is the species most often encountered. House mice can enter structures using holes the size of dimes. Mice can transmit diseases to humans and can be a vector for rat-bite fever and Weil's disease. In addition, their droppings can carry organisms that cause food poisoning. House mice can also carry fleas that transmit murine typhus, and they harbor mites that transmit rickettsialpox.
Hantavirus pulmonary syndrome (HPS) is another disease transmitted by infected rodents, through urine, droppings, or saliva (CDC, 2005).
Many birds are common inhabitants of urban areas. Species such as pigeons, European starlings, and English house sparrows are common sights in parks, along sidewalks, and at feeders in our residential yards. One of the best-recognized bird diseases is ornithosis in pigeons. This disease is similar to viral pneumonia and is transmitted to people though infected droppings or respiratory droplets. It may infect 30% to 75% of the pigeons in a given area without being noticed. Several species of birds, including pigeons, have been shown to be reservoirs for encephalitides.
1017
Pesticides Pesticides, materials that are used to kill, repel, or change the behavior of an unwanted organism, are a mainstay of pest control. They are sprayed on crops and alongside residential streets, poured on gardens, squirted along baseboards and in basements, and impregnated into clothing and bed nets. The worldwide consumption of pesticides is about 2 million metric tons per year. Of this amount, 45% is used in Europe, 25% in the United States, and 25% in the rest of the world. India accounts for just 3.75% of global pesticide use. On an applied rate basis, the usage of pesticides in Korea and Japan is 6.6 and 12.0 kilograms per hectare (kg/ha), respectively, whereas in India, it is only 0.5 kg/ha (De, Bose, Kumar, & Mozumdar, 2014).
In the United States, pesticide sales were approximately $12.5 billion in 2007, and about 80% of all U.S. pesticide use was in agriculture. The pattern of use has not been stable; total pesticide use in the United States decreased by approximately 8% from 2000 to 2007, and organophosphate use decreased by 63% during that same period (De et al., 2014).
Pesticides are often classified according to the type of pest they control, as shown in Table 18.1. Pesticides may also be classified according to chemical structure. Although many categories of chemicals have some action against insects or other pests, four categories account for most pesticides in use: organophosphates (Tox Box 18.1), carbamates, organochlorines (Tox Box 18.2), and pyrethroids. A fifth category, defined not so much by chemical structure as by origin, consists of the biopesticides.
Table 18.1 Pesticides Classified by Target or Mode of Action
Algicides Substances that control algae in lakes, canals, swimming pools, water tanks, and other sites
Antifouling agents
Substances that kill or repel organisms that attach to underwater surfaces, such as boat bottoms
Antimicrobials Substances that kill microorganisms (such as bacteria and viruses)
Attractants Substances that attract pests (e.g., to lure an insect
1018
or rodent to a trap; food, however, is not considered a pesticide when used as an attractant)
Biocides Substances that kill microorganisms Biopesticides Pesticides that are derived from such natural
materials as animals, plants, bacteria, and certain minerals
Disinfectants and sanitizers
Substances that kill or inactivate disease-producing microorganisms on inanimate objects
Fumigants Substances that produce gas or vapor intended to destroy pests in buildings or soil
Fungicides Substances that kill fungi (including blights, mildews, molds, and rusts)
Herbicides Substances that kill weeds and other plants that grow where they are not wanted
Insecticides Substances that kill insects and other arthropods Microbial pesticides
Microorganisms that kill, inhibit, or outcompete pests, including insects and other microorganisms
Miticides (also called acaricides)
Substances that kill mites that feed on plants and animals
Molluscicides Substances that kill snails and slugs Nematicides Substances that kill nematodes (microscopic,
wormlike organisms that feed on plant roots) Ovicides Substances that kill the eggs of insects and mites Repellents Substances that repel pests, including insects (such
as mosquitoes) and birds Rodenticides Substances that control mice and other rodents Additional Agricultural Chemicals Referred to as Pesticides Defoliants Substances that cause leaves or other foliage to
drop from a plant, usually to facilitate harvest Desiccants Substances that promote drying of living tissues,
such as unwanted plant tops Insect growth Substances that disrupt the molting, maturing from
1019
regulators pupal to adult stage, or other life processes of insects
Pheromones Biochemicals that disrupt the mating behaviors of insects
Plant growth regulators
Substances (excluding fertilizers and other plant nutrients) that alter the expected growth, flowering, or reproduction rate of plants
Organophosphates (OPs) were developed in the nineteenth century, but their utility was not discovered until 1932. Organophosphate pesticides are neurotoxins, as described in Tox Box 18.1. They function by inactivating acetylcholinesterase, the enzyme that regulates the neurotransmitter acetylcholine. Some of the more toxic organophosphates have been used as nerve gases. Sarin, for example, was used in the Tokyo subway attacks in 1995 (Olson, 1999). Examples of organophosphates in common use are chlorpyrifos, diazinon, malathion, and azinphos-methyl.
1020
Tox Box 18.1 Organophosphates
WHAT ARE THEY? Organophosphates (OPs) are synthetic chemicals used as insecticides and as nerve agents in chemical warfare. Their general structure consists of an organic compound with a phosphorous atom attached to either an oxygen or a sulfur atom. Common organophosphate insecticides include chlorpyrifos, methyl parathion, diazinon, and malathion; organophosphate nerve agents include sarin gas and VX.
HOW ARE THEY USED?
1021
OP insecticides are used to reduce pest damage to crops and livestock, and to control insects such as mosquitoes which can spread disease. They are also used in buildings to control cockroaches and termites, and as the active ingredient in some pet flea collars. OPs are used widely because they are highly effective pesticides and, unlike persistent insecticides such as DDT, degrade naturally in the environment after several days. Unlike OP insecticides, OP nerve agents have no civilian applications: they are used only to kill people.
HOW ARE PEOPLE EXPOSED? The general population can be exposed unintentionally or intentionally to OP pesticides, with ingestion and inhalation
1022
representing the major routes of exposure. However, biomonitoring in the general population of the United States indicates that while unintentional exposure to OP pesticides is widespread, people are exposed to very low concentrations. This pervasive but low-level exposure can occur when people eat freshly picked foods contaminated with trace pesticide residues, and through ingestion or inhalation of household dust contaminated with pesticide residue. People who live near fields sprayed with OPs may be exposed to higher levels of OPs through inhalation and ingestion.
While intentional exposure occurs to fewer people overall, it represents a significant public health threat: in developing countries, approximately 200,000 people die annually from intentional ingestion of OP pesticides (Eddleston, Buckley, Eyer, & Dawson, 2008), representing about two thirds of the global burden of pesticide suicides. Less commonly, OP nerve agents are intentionally used to kill people, as in the 1995 terrorist attack on the Tokyo subway system using Sarin gas.
Farmworkers and pesticide applicators are more likely to be exposed to high concentrations of OP pesticides than members of the general population are, and this exposure can occur through inhalation, dermal absorption, or ingestion. Workers can inhale the spray during or soon after application, and can also accidentally spill the pesticide on skin and clothing. Ingestion can occur when workers lack facilities to wash before eating, or smoke while handling sprayed materials.
Like asbestos, OP pesticides are a “take-home toxin,” because workers may unintentionally transport OPs home on contaminated clothing and skin. Their families may then be exposed to higher concentrations of OPs than the general population.
WHAT ARE THE TOXIC EFFECTS? The main toxic effect of OPs is poisoning of the nervous system, with the extent of this poisoning dependent on dose and the length of time since exposure. The effects of an acute
1023
dose are well known, while the effect of chronic exposure to low doses is still being investigated.
Soon after exposure to an acute dose, OPs can trigger a potentially lethal cholinergic crisis. This happens when OPs inhibit acetylcholinesterase, the enzyme necessary to break down the essential neurotransmitter acetylcholine. When acetylcholine builds up in the junctions between nerves, it triggers a cholinergic crisis, the victim sweats, salivates, suffers from tremors and nausea, and can die when the respiratory muscles become paralyzed. Several days after the cholinergic crisis, approximately half of survivors develop an intermediate syndrome—a potentially lethal weakness in respiratory and other muscles. This may be followed later by the development of OP-induced polyneuropathy—a loss of sensation and progressive weakness in the limbs. Unlike the other syndromes, however, this polyneuropathy is related to OPs inhibiting another enzyme, neuropathy target esterase, and damaging the long nerves in the victim's arms and legs.
The toxic effects of chronic, low-dose OP exposure are less well understood than the effects of acute exposure. Some epidemiological studies in chronically exposed farmers suggest that low doses of OPs can have subtle effects on neurological function. Similarly, some animal studies suggest that neurotransmission and behavior can be altered by chronic low doses.
HOW ARE PEOPLE PROTECTED? The general population is protected through regulation aimed at reducing pesticides on food and in water, registering pesticides, washing food to remove pesticide residue, and wearing protective clothing when applying pesticides around the home. Pesticide regulation is described in later in this chapter.
OP nerve agents are banned in warfare by international agreement. The history of this agreement dates back more than a century; key milestones include the Geneva Protocol for the Prohibition of the Use in War of Asphyxiating, Poisonous or Other Gases, and Bacteriological Methods of
1024
Warfare, promulgated after the horrors of World War I, and the Chemical Weapons Convention, which entered into force in 1997. The Organisation for the Prohibition of Chemical Weapons (www.opcw.org) now has 190 member states worldwide.
Workers are protected through regulations, biomonitoring, technical alternatives, and personal protective equipment such as respirators and skin protection. The Occupational Safety and Health Administration and the National Institute for Occupational Safety and Health both set exposure limits for specific OP pesticides, such as malathion and methyl parathion, with NIOSH's limits generally being stricter. To ensure that workers are not being poisoned by acute doses of OP pesticides, many states operate agricultural worker biomonitoring programs, which monitor blood enzymes that are sensitive to inhibition by OPs. Workers can also be protected through the use of less-toxic alternatives to OP pesticides, such as the integrated pest management system.
After an acute exposure to OP pesticides or nerve agents, victims can be treated with atropine, which reduces the effects of the excess acetylcholine, and with oximes, which help to reverse the enzyme inhibition causing acetylcholine buildup.
WANT TO LEARN MORE? The National Pesticide Information Center has information available about OP pesticides on its website (npic.orst.edu/index.html). ATSDR's Toxic Substance Portal for Organophosphates and Carbamates is at www.atsdr.cdc.gov/substances/toxchemicallisting.asp? sysid=39.
A standard source is the EPA's Recognition and Management of Pesticide Poisoning; the sixth edition was released in 2013. It is available at www2.epa.gov/pesticide- worker-safety/recognition-and-management-pesticide- poisonings.
A recent review of biomarkers of exposure to organophosphates is R. M. Black and R. W. Read, “Biological
1025
Markers of Exposure to Organophosphorus Nerve Agents,” Archives of Toxicology, 2013, 87(3), 421–437.
Contributed by Megan Cartwright
Many uses of OPs have been eliminated in the United States because of their toxicity, but worldwide OP use is still widespread, posing a risk to farmers and farmworkers, especially in developing countries. The OPs are very quick acting so the insecticidal results are seen immediately—but serious injury or death to humans can occur also. However, OPs offer an environmental benefit, as compared to organochlorines: OPs do not persist in the environment.
Carbamates function through a mechanism similar to organophosphates, binding to and inactivating acetylcholinesterase. Carbamates have lower affinity for acetylcholinesterase than do organophosphates, which reduces their toxicity to humans. Examples of carbamates include carbaryl and methomyl. Carbamates are also nonpersistent in the environment.
Organochlorine insecticides (OCs) were commonly used in the past. Most OCs are less acutely toxic than the OPs mentioned above. As explored in Tox Box 18.2, organochlorines are leading examples of persistent organic pollutants; they are persistent in the environment and can bioaccumulate, with potential for harm to both ecosystems and human health.
1026
Tox Box 18.2 Organochlorine Pesticides
WHAT IS IT? Organochlorine pesticides are a group of synthetic chlorinated hydrocarbons. Organochlorine (OC) pesticides are considered persistent organic pollutants (POPs) because they are highly lipophilic (soluble in oils and fats), stable, mobile, and resistant to breakdown in the environment.
HOW ARE THEY USED? During the first half of the twentieth century, OC pesticides were widely and intensively used as pesticides to control agricultural pests and vectors of diseases such as malaria and typhus. Several classes of OC pesticides were used, including the aromatic, DDT-type (dichlorodiphenyltrichloroethane) pesticides and the chlorinated alicyclic (aldrin, dieldrin, heptachlor, chlordane, and endosulfan) pesticides. DDT and the other broad-spectrum OC insecticides were very popular because they were highly effective, inexpensive, and persistent (required fewer applications), and had low acute mammalian toxicity. DDT production peaked at 82,000 metric tons per year in 1963, and approximately 2 million metric tons of DDT have been produced worldwide.
HOW ARE PEOPLE EXPOSED? Inhalation or dermal absorption of OC pesticides can occur
1027
during the production, handling, and application of these products. However, most people are exposed to DDT and other OCs through the ingestion of food contaminated with small amounts of these pesticides. Like other POPs, OCs persist in the environment and can bioconcentrate (accumulate in animal and human fatty tissues) and biomagnify (increase in concentration at higher levels of the food chain). OC levels are highest in foods with a relatively high fat content, such as meat, dairy products, and certain fish, as well as breast milk.
WHAT ARE THE TOXIC EFFECTS? OCs, like other insecticides, are effective because they target the nervous systems of insects. However, many insecticides are not highly selective and can cause toxic effects, particularly nervous system toxicity, in nontarget species. In humans, acute exposure to OC pesticides may lead to headaches, dizziness, convulsions, disorientation, nausea, tremors and muscle weakness, salivation, and sweating. Chronic OC exposure is associated with liver, kidney, thyroid, bladder, and central nervous system damage. DDT is classified as a possible human carcinogen by the IARC. Importantly, DDT and the other DDT-type OCs and their metabolites are endocrine disrupters, and they can adversely affect development and reproduction in both humans and wildlife. For example, the widespread use of DDT in the 1950s and 1960s caused significant reproductive failure in many bird species (particularly birds of prey) due to the thinning and cracking of eggshells before hatching. Rachel
1028
Carson described the detrimental ecological effects of DDT and other pesticides in her book Silent Spring, whose publication in 1962 helped propel the modern environmental movement.
HOW ARE PEOPLE PROTECTED? The Stockholm Convention on Persistent Organic Pollutants, dating from 2004 (chm.pops.int), seeks the elimination of almost two dozen chemicals or classesof chemicals. Several of these are OC insecticides. Today, most of the OC pesticides, including DDT, dieldrin, aldrin, heptachlor, and chlordane, have been banned in the United States and many other countries except for use in a public health emergency. These bans have contributed to a slow decline in environmental OC levels, the human OC pesticide body burden, and OC residue levels in food. Importantly, in adherence with the Stockholm Convention, DDT use is still used for vector control to combat malaria in certain countries (Text Box 18.4 explores the trade-offs that arise with continued DDT use).
WANT TO LEARN MORE? See the ATSDR Toxicological Profile for DDT, DDE, and DDD at www.atsdr.cdc.gov/toxprofiles/tp.asp?id=81&tid=20
Also see the following helpful article and books: D. Rosner and G. Markowitz, “Persistent Pollutants: A Brief History of the Discovery of the Widespread Toxicity of Chlorinated Hydrocarbons,” Environmental Research, 2013, 120, 126– 133; R. Carson, Silent Spring (New York: Houghton Mifflin, 1962); and T. Colborn, J. P. Myers, and D. Dumanoski, Our Stolen Future (New York: Dutton, 1996).
Contributed by Anna Engstrom
Pyrethroid pesticides were developed as a synthetic version of naturally occurring pyrethrin, which is found in certain chrysanthemum flowers. These pyrethroids have been modified to increase their stability in the environment. Examples include allethrin, permethrin, fenvalerate, and resmethrin. All synthetic pyrethroids are toxic to the nervous system; however, they are less
1029
toxic than organophosphates. For this reason pyrethroids are used for household pest control more often than organophosphates.
Biopesticides are derived from such natural materials as animals, plants, bacteria, and certain minerals. For example, canola oil and baking soda have pesticidal activity and are considered biopesticides. Biopesticides fall into four major classes:
Microbial pesticides have a microorganism (e.g., a bacterium, fungus, virus, or protozoan) as the active ingredient. The most widely used microbial pesticides are strains of Bacillus thuringiensis, or Bt.
Plant-incorporated protectants (PIPs) are pesticidal substances that plants produce from genetic material that has been added to the plant. For example, scientists can introduce the gene for the Bt pesticidal protein into a plant's own genetic material, enabling the plant to manufacture the substance that destroys the pest that preys on that plant.
Biochemical pesticides are naturally occurring substances that control pests by nontoxic mechanisms. Among the biochemical pesticides are insect sex pheromones, which interfere with mating.
Botanical pesticides are those derived from plants. Botanicals are popular pest control compounds because they are safe for nontarget organisms and natural enemies. Botanicals have low mammalian toxicity and are often less expensive than their synthetic counterparts.
Herbicides are the most widely used type of pesticide in the agricultural sector. Among the top ten pesticides used, by weight, were the herbicides glyphosate (known commercially as Roundup), atrazine, metolachlor, acetochlor, 2,4-D, and pendimethalin, and the fumigants metam sodium, dichloropropene, methyl bromide, and chloropicrin. Herbicides are also the most widely used type of pesticide in the home and garden and the industrial, commercial, and government market sectors, and the herbicides 2,4-D and glyphosate were the most widely used active ingredients (U.S. EPA, 2011a). Herbicide use may be facilitated by genetic modification of crops to be resistant to herbicide action. This widespread and controversial practice is discussed in Chapter 19.
1030
Patterns of Pesticide Use and Human Exposure People encounter pesticides by inhalation of sprayed pesticides near farms or in offices, by ingestion of pesticides on foods, and by skin contact.
Residential exposure is common. While current data are not available, data from the 1990s suggest that 80% of U.S. households used pesticides more than once a year in and around their homes (Davis, Brownson, & Garcia, 1992; Whitmore et al., 1994; Damalas & Eleftherohorinos, 2011). Many of the pesticides applied indoors are semivolatile. Semivolatile pesticides can vaporize from treated surfaces and can be distributed in and on targeted and nontargeted surfaces (Hore et al., 2005). This raises concern about children's exposures because they may spend much of their time indoors in or around pesticide-treated areas.
Occupational exposure is also common among farmworkers and other high-risk occupations. Workers who directly handle pesticides are at highest risk (Figure 18.4), followed by those who apply pesticides. Finally, farmworkers who enter fields where pesticides have been applied, in order to harvest a crop or perform other work, are also at risk (see Text Box 18.2).
1031
Figure 18.4 Farmers Applying Organophosphate Insecticides in Thailand
Source: Photo supplied by M. Robson and W. Siriwong.
1032
Text Box 18.2 Who Is Responsible for Applying Pesticides? Humans and insects prefer many of the same ecosystems, so they encounter each other in many settings—on agricultural fields, in gardens, in homes, and elsewhere. As a result, efforts at pest control, including pesticide use, take many forms. Who actually applies pesticides?
For regulatory purposes, the U.S. EPA divides pesticides into two categories: general use and restricted use. The difference between them is analogous to the difference between over-the-counter medications and prescription medications. The regulation aims to ensure that pesticides in the more toxic category (restricted use) be applied only by or under the direct supervision of trained and certified applicators.
Homeowners can buy a variety of general use pesticides at garden centers, hardware stores, and grocery stores to combat day-to-day pests. These pesticides are usually less toxic and less concentrated than restricted use pesticides. Many are in ready-to-use formulations, such as household sprays and garden sprays.
Commercial pesticide use is more tightly regulated. It is generally carried out by private firms, which may be small local businesses or large national franchises. These firms must be registered as pest control businesses with the appropriate state agency. They must have certified applicators, and they must show proof of liability insurance, in case a misapplication should occur. Most specialize in a particular type of pest control.
Farmers are among the largest users of pesticide products. Although some hire commercial applicators, some seek training and certification to qualify as private applicators in order to apply pesticides to their own land. Pesticides registered for agricultural use may not be used for residential or interior needs.
1033
Pesticides and Public Health Pesticides are toxic, accounting for their ability to kill unwanted species. Pesticide toxicity may also affect humans, making this a public health issue (Text Box 18.3).
1034
Text Box 18.3 Pesticide Toxicity Categories and Labeling Requirements The World Health Organization (WHO) and the U.S. EPA have similar classification systems to alert people to the relative danger of different pesticide products. (The For Further Information section at the end of this chapter provides Web sites for both sources.)
The EPA's four categories alert the user as to the relative toxicity of the product and the required precautions, including personal protective equipment.
Toxicity Category I: Pesticide products meeting this criteria shall bear on the front panel the signal word “Danger.” In addition if assigned on the basis of its oral, inhalation or dermal toxicity (as distinct from skin and eye local effects) the word “Poison” shall appear in red on a background of distinctly contrasting color and the skull and crossbones shall appear in immediate proximity to the word “Poison.”
Toxicity Category II: Pesticide products shall bear on the front panel the signal word “Warning.”
Toxicity Category III: Pesticide products shall bear on the front panel the signal word “Caution.”
Toxicity Category IV: Pesticide products shall bear on the front panel the signal word “Caution.”
Child hazard warning: Every pesticide product label shall bear on the front panel the statement “keep out of reach of children” [U.S. EPA, 2011b].
Few data are available on intentional and unintentional pesticide poisoning in the United States and globally. The major occupational risk is to farmers and farmworkers; the CDC estimates that 10,000 to 20,000 physician-diagnosed pesticide poisonings occur each year among the approximately 2 million U.S. agricultural workers. In addition to agricultural workers, groundskeepers, pet groomers,
1035
fumigators, and people in a variety of other occupations are at risk for exposure to pesticides including fungicides, herbicides, insecticides, rodenticides, and sanitizers (Blondell, 1997, 2007; CDC, 2013b).
Pesticide self-poisoning is a major contributor to population patterns of morbidity and mortality in developing nations. While reliable statistics are elusive, pesticides account for roughly one third of the nearly million suicides globally each year, and are principal means of suicide in China, India, Bangladesh, and other developing nations (Gunnell, Eddleston, Phillips, & Konradsen, 2007; Wu, Chen, & Yip, 2012). In 2010, in India alone, an estimated 88,000 people committed suicide by ingesting pesticides (Patel et al., 2012). The ready availability of pesticides, especially in rural areas, likely contributes to their use in suicide.
The standard reference for pesticide toxicity is the U.S. EPA's Recognition and Management of Pesticide Poisonings (6th edition). It is updated regularly and can be downloaded from www2.epa.gov/pesticide-worker-safety/recognition-and- management-pesticide-poisonings.
Pesticide Regulation Pesticide policy and law make up a complicated patchwork, with different legal structures addressing different aspects of health, safety, and the environment across the pesticide life cycle. Different regulations affect the production, distribution, and use of pesticides; the safety of those who apply them; and the levels of pesticides permitted on end products such as food.
In the United States the principal pesticide law is the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) (www.epa.gov/agriculture/lfra.html). FIFRA stipulates several major policy approaches:
It requires product “registration,” or licensure, prior to manufacture, sales, or use.
It requires toxicity data from manufacturers.
It requires specific labeling (see Text Box 18.3).
It requires training of applicators (see Text Box 18.2).
1036
It restricts the handling and uses of pesticides.
Another important law is the Federal Food, Drug, and Cosmetic Act (FFDCA) (www.fda.gov/regulatoryinformation/legislation/federalfooddrugandcosmeticactFDCAct/default.htm As its name implies, this is a very broad Act, governing medications, medical devices, food additives, and much more. One section of the Act, titled “Tolerances and exemptions for pesticide chemical residues,” authorizes the EPA to set tolerances, or permissible levels, of pesticide residues in food. The tolerances are health based —requiring a “reasonable certainty of no harm”—and must explicitly consider infants and children. Under this Act, as discussed in Chapter 19, the EPA monitors pesticide residue levels in fruits, vegetables, and seafood, while the Department of Agriculture performs this monitoring for meat, poultry, dairy products, and eggs.
The Food Quality and Protection Act (FQPA) of 1996 (www2.epa.gov/laws-regulations/summary-food-quality- protection-act) updated both FIFRA and the FFDCA by mandating a single, health-based standard for all pesticides in all foods, based on a relatively strong criterion: “reasonable certainty of no harm.” The FQPA mandates explicit consideration of infants and children, and requires that safety factors be incorporated in setting tolerances to reflect their vulnerability. The FQPA requires consideration of cumulative exposures, reflecting the science of how exposures typically occur (see Chapter 8), and requires data collection, both on dietary patterns and on residue levels in foods.
The impacts of pesticides on workers and on wildlife are addressed by still other laws and regulations. Under its Worker Protection Standard (WPS) (www2.epa.gov/pesticide-worker- safety/revisions-worker-protection-standard), the EPA regulates occupational health of pesticide applicators and agricultural workers (a function usually handled by OSHA, as described in Chapter 21). The WPS uses a number of strategies: mandated pesticide safety training, notification of pesticide applications and restricted intervals before reentry, use of personal protective equipment, and decontamination and medical assistance in the event of overexposure. Finally, the Endangered Species Act (ESA) of 1973 requires the EPA to ensure that the pesticides it registers will not harm endangered species.
1037
Global approaches to pesticide policy vary widely (Hough, 2003; Verger & Boobis, 2013). Wealthy nations generally incorporate many of the same elements described in U.S. policy, including licensing of pesticides, regulation of who may apply them and how they may be used, regulation of pesticide levels in foods, monitoring of food and other environmental media, reporting and information sharing, and training. The Codex Alimentarius Commission (CAC) of the UN's Food and Agricultural Organization (FAO) and the World Health Organization establishes maximum residue limits (MRLs), the maximum levels of pesticide residue that foods can contain and still be expected not to harm human health; countries can use these MRLs to develop national regulations, but do not always do so. A recent study (Matthews et al., 2011) showed that one in four countries lacked protective legislation, and laws that did exist often lacked basic provisions on aspects such as pesticide registration, labeling, storage, transport, and disposal. Moreover, enforcement capacity was low in many countries, owing to a lack of technical expertise, laboratories, and data collection. A patchwork of regulations governs the import and export of pesticides across national borders. International organizations such as the WHO, FAO, and Organisation for Economic Co-operation and Development have initiatives to achieve more consistent policy and practice in pesticide protection.
Global Pesticide Use Agriculture forms a central part of the economy in many developing nations. Small farms, with relatively little mechanization and with farmers and their families living in close proximity to their fields, are more typical there than in wealthy nations. Developing countries use only 20% of the world's agrochemicals, yet they suffer 99% of deaths from pesticide poisoning. There are several contributing reasons (Ecobichon, 2001; Williamson, Ball, & Pretty, 2008; Schreinemachers & Tipraqsa, 2012).
First, dangerous pesticides are used. Pesticides classified as being extremely or highly hazardous by the FAO and WHO, including those banned by wealthy countries, remain available on the world market and continue to be used in developing countries. In some countries, farmers still use the “older,” nonpatented, less expensive, more acutely toxic, and more environmentally persistent agents that
1038
can be manufactured in-country or formulated from active ingredients imported from other countries. Informal distribution networks, and “black market” venders, make such products readily available.
Second, unsafe storage and handling practices are common. One contributor is the scarcity of resources such as safe transfer facilities and adequate personal protective equipment. Many farmers store pesticides in or near their homes. These problems are compounded by illiteracy and lack of training; even when labels and warning signs are designed for nonreaders, farmers may pay them little attention and/or have little comprehension of their messages (Waichman, Eve, & da Silva Nina, 2007).
Third, in areas where farmers choose to grow cash crops for distant markets, they may find these crops highly susceptible to pests, driving high levels of pesticide use.
Fourth, pesticide regulations in many countries have not kept pace with increasing use of pesticides, and regulations that are on the books are often only weakly enforced (Phung, Connell, Miller, Rutherford, & Chu, 2012; Stadlinger, Mmochi, & Kumblad, 2013). Finally, medical care for cases of pesticide toxicity is often unavailable.
Despite these challenges, progress is occurring in some low-income countries. Encouraging signs include the use of safer pesticides, stricter regulations, and better training of farmers (Galt, 2008). Rising consumer demand in importing countries for pesticide-free products may accelerate this trend.
1039
Integrated Pest Management Integrated pest management (IPM) is defined as “a comprehensive approach to pest control that uses combined means to reduce the status of pests to tolerable levels while maintaining a quality environment” (Pedigo, 2002, p. 294). The IPM concept was first developed for use in agriculture in the 1960s in response to concerns about health threats, environmental damage, and pesticide resistance associated with heavy reliance on pesticides. Several elements are central to IPM.
Management and Cultural Practices to Control Pests Farmers and public health officials use various management and cultural practices to reduce pest populations or to make conditions less favorable for their establishment and buildup. For farmers this can include planting a crop at a time when the pest population is lower, such as later in the season; using a cultivar that has been shown to have more resistance to a particular pest problem; or using plastic mulch to reduce weeds, conserve moisture, and make the growing area less favorable for pathogens. Public health officials can take steps to avoid standing water to reduce mosquito populations, to control garbage buildup to manage flies, and to recommend meticulous cleaning and waste management to reduce other nuisance pests. Such approaches modify the environment to make it less hospitable to pests.
Structural Maintenance Structural maintenance such as placing screens over attic vents and fixing water leaks can keep pests from entering structures and thriving in buildings.
Monitoring In IPM, routine application of pesticides is replaced by regular monitoring of pest populations. Most crops and residential settings can tolerate a few pests; the problems arise when the pest population increases to a level that causes economic damage, reduced crop yield, or risk of human disease. Hence control
1040
measures are reserved for situations of demonstrated need and are targeted and data based.
Control Measures When monitoring indicates a pest problem despite sanitation and cultural management, the use of a control measure is considered. The optimal control measure is the one that is least harmful to the environment and human health while still providing effective control. Options include physical and mechanical interventions, biological control agents (used in agriculture), and chemical pesticide applications. The use of chemical pesticides should be seen as a last resort, and when they are used, those that are comparatively less harmful to health and the environment should be chosen.
1041
Text Box 18.4 DDT in Antimalaria Campaigns: An Example of Public Health Trade-Offs Malaria remains a common and deadly disease in much of the developing world. The World Health Organization estimates that roughly 200 million new cases occur each year, with nearly 600,000 people, most of them children in Africa, dying. The Institute for Health Metrics and Evaluation estimates the number of deaths to be 1.2 million— twice the WHO estimate and including many adults as well. All agree that the majority of cases, and deaths, occur in the setting of poverty, with six African nations—Nigeria, Democratic Republic of the Congo, Tanzania, Uganda, Mozambique, and Côte d'Ivoire—accounting for much of the global burden. Malaria is estimated to impose US$12 billion per year in direct costs on Africa—most of these borne by poor rural families—and to reduce GDP growth by 1.3% annually (Roll Back Malaria, 2015). Fortunately, the global burden of malaria is declining; between 2000 and 2013, malaria incidence fell by 30% globally and 34% in Africa, and malaria mortality fell by 47% worldwide and 54% in Africa (WHO, 2014).
The four species of Plasmodium parasite that cause malaria —falciparum, vivax, malariae, and ovale—are spread by dozens of species of Anopheles mosquitoes. Transmission varies with factors related to the parasite, the vector, the human host, and the environment.
Through the first part of the twentieth century, malaria control relied on environmental approaches such as drainage and landfills to eliminate the larval mosquito habitat, on biological controls such as larvivorous fish in ponds, and on larvicidal applications of oil and Paris green (Nájera, 2001). These methods were effective, especially in Europe and North America, but malaria continued to afflict many poor nations.
1042
DDT was introduced as an agricultural pesticide during the 1930s, and during World War II, military forces used it for typhus control. During the 1950s and 1960s, as part of malaria control campaigns worldwide, DDT played an important role in reducing mosquito populations and reducing the burden of disease.
However, concerns about DDT soon arose, and were given eloquent voice with Rachel Carson's Silent Spring in 1962. As discussed earlier, DDT belongs to a category of chemicals known as persistent organic pollutants; it persists for years in the environment, it bioconcentrates as it moves up the food chain (as described in Chapter 2), and it can be toxic to wildlife and even humans. Although DDT has low acute toxicity in humans, it is disrupts reproductive and endocrine functions. In birds, DDT inhibits enzymes essential for deposition of calcium carbonate in eggshells, resulting in soft, easily broken eggs, and dramatically reduced birth rates —hence the loss of songbirds, causing Rachel Carson's “silent spring.” Because of these concerns, Sweden banned the use of DDT in 1970, the United States did so in 1972, and many other countries followed. The Stockholm Convention on Persistent Organic Pollutants, an international treaty that requires the elimination of DDT and other POPs, took effect in 2004.
In the negotiations that led to the treaty, there was concern that a sudden ban on DDT use could undermine malaria control efforts. Thus DDT production and use were permitted for the purpose of disease control (Kapp, 2004). In 2006, the World Health Organization announced increased support for the use of DDT in combating malaria. Limited application, such as impregnating mosquito netting or spraying on interior walls, was felt to be less dangerous than widespread fumigation. Ironically, DDT use in Africa has increased since the Stockholm Convention came into effect (van den Berg et al., 2011)
This is a classic example of a trade-off in public health, a dilemma in which one public health goal—the elimination of a persistent chemical pollutant—collides with another public health goal—the control of a killer disease. Strong arguments
1043
have been advanced both for and against continued DDT use.
Arguments Against Continued DDT Use DDT accumulates in ecosystems, persists for years or even decades, bioconcentrates, and has been shown to cause reproductive failure and other adverse outcomes in fish, birds, and other species beyond the target insect species (Turusov, Rakitsky, & Tomatis, 2002).
DDT accumulates in the adipose tissue of humans and other organisms (WHO, 1989).
Although the acute toxicity of DDT is low, there is evidence that DDT may disrupt reproductive and endocrine functions and neurological development (Longnecker, Rogan, & Lucier, 1997; Longnecker, Klebanoff, Zhou, & Brock, 2001). There is also laboratory evidence of carcinogenicity, leading the National Toxicology Program (2005) to classify DDT as reasonably anticipated to be a human carcinogen, and the International Agency for Research on Cancer (1991) to classify it as possibly carcinogenic to humans. A precautionary approach would dictate avoiding the use of such a chemical.
Continued use of DDT will result in increasing insect resistance, so in the long run this will not be a useful strategy.
Alternatives to DDT, including nonchemical approaches and synthetic pyrethroids, are readily available.
Arguments in Favor of Continued DDT Use DDT has very low acute toxicity for humans (Smith, 2000), and the evidence for human carcinogenicity and other adverse effects is weak (Curtis & Lines, 2000; Smith, 2000). In contrast, the burden of mortality and morbidity from malaria is enormous. Therefore a cost- benefit analysis clearly favors the use of DDT.
DDT is relatively inexpensive compared to alternatives and therefore more accessible to poor countries. The cost of alternatives such as malathion and pyrethroid
1044
insecticides can be two times to twenty times that of DDT, and bed nets are also prohibitively expensive (Tren, 1999).
DDT is easy to mix and apply, thereby reducing the need for training and supervision (Tren, 1999). This makes it practical for widespread use in developing nations.
Malaria surged in many areas following the phase out of DDT, underlining the importance of DDT in malaria control (Roberts, Manguin, & Mouchet, 2000).
DDT is now used for house spraying, a selective approach that requires much less volume than the previous agricultural and area spraying. This results in a much lower environmental load than resulted from applications in the past.
What do you think? Should the continued use of DDT be permitted for malaria control? (For further information see Roberts et al., 2004; Rogan & Chen, 2005; Eskenazi et al., 2009; Bouwman, van den Berg, & Kylin, 2011.)
Consumer Education The general public and potential users of IPM must be aware of IPM principles and understand IPM's different components and how these components fit into a complete management program, one that reduces hazards to themselves and the environment.
1045
Summary Pests are plants, animals, or microorganisms that threaten human health or well-being. They include insect pests such as cockroaches, fleas, lice, mosquitoes, and ticks, and vertebrate pests such as rats, mice, and birds. Humans have contended with pests since ancient times.
Modern pest control has come to rely heavily on pesticides. Pesticides have varying levels of toxicity, both in acute intoxication and in chronic effects such as cancer and neurological disease. People can sustain pesticide exposures in a wide range of settings and through a wide range of pathways.
Pesticide regulation is complex, relying on several federal laws. The control of pesticide exposure relies not only on laws but also on techniques such as integrated pest management. IPM combines chemical and nonchemical approaches to pest control, reducing the need to use pesticides.
1046
Key Terms biochemical pesticides
Naturally occurring substances that control pests by nontoxic mechanisms.
biopesticides Pesticides that are derived from such natural materials as animals, plants, bacteria, and certain minerals.
Federal Food, Drug, and Cosmetic Act (FFDCA) U.S. federal legislation, originally promulgated in 1938 and updated many times since then, that governs medications, medical devices, food additives, and much more. One section of the Act authorizes the EPA to set tolerances, or permissible levels, of pesticide residues in food.
Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA)
U.S. federal legislation that establishes the framework for pesticide regulation to protect applicators, members of the public, and the environment.
Food Quality Protection Act (FQPA) U.S. federal legislation passed in 1996, updating both FIFRA and the FFDCA by mandating a single, health-based standard for all pesticides in all foods, mandating explicit consideration of infants and children, and requiring regulatory safety factors to reflect their vulnerability.
general use A category of pesticides, generally of low toxicity, available for retail purchase by members of the public, analogous to over-the- counter medications (cf. restricted use pesticides).
integrated pest management (IPM) A comprehensive approach to pest control that uses a range of procedures and strategies to control pest populations rather than exclusive reliance on pesticides.
maximum residue limits (MRLs) The maximum levels of pesticide residue that foods can contain and still be expected not to harm human health, as established by the Codex Alimentarius Commission of the UN's Food and
1047
Agricultural Organization and the World Health Organization. microbial pesticides
Microorganisms that kill, inhibit, or outcompete pests, including insects and other microorganisms.
organochlorine pesticides A class of pesticides characterized by generally low acute toxicity but also able to persist in the environment, bioaccumulate, and cause chronic toxicity such as endocrine disruption. Examples include DDT, aldrin, dieldrin, and chlordane.
organophosphate pesticides A class of pesticides that function by interfering with normal neural transmission. Some are acutely toxic; organophosphates have also been used as nerve gases. Examples include chlorpyrifos and malathion.
persistent organic pollutants (POPs) Organic compounds that resist degradation and therefore persist in the environment, bioaccumulate through the food chain, and pose a risk of adverse effects on human and animal health and the environment. Examples include organochlorine pesticides, polychlorinated biphenyls (PCBs), and dioxins.
pest An unwanted insect or other animal that threatens human health or well-being in some way, such as by destroying crops or spreading disease. More broadly, any unwanted animal or plant species (such as a weed).
pesticide A substance used to destroy or mitigate a pest, including insecticides, fungicides, rodenticides, and pediculicides.
restricted use A category of pesticides, generally with some toxicity, whose use is regulated (e.g., that must be applied by certified applicators) (cf. general use pesticides).
tolerances In the context of pesticides, permissible levels of pesticide residues in food.
Worker Protection Standard (WPS) A U.S. EPA regulation, originally promulgated in 1992, designed to protect the occupational health of pesticide applicators and
1048
agricultural workers.
1049
Discussion Questions 1. Pesticides are economic poisons, meaning that they are used to
control plants or animals that have economic significance as pests. Unlike other toxins or contaminants with which people come into contact, pesticides are intentionally applied to food, living spaces, and people. What are some of the risk-benefit issues in the application of pesticides? Is it worth the risk to apply pesticides?
2. Integrated pest management (IPM) is a logical approach for many pest problems, but it is not widely used. What are some of the societal trade-offs when using IPM?
3. Pesticide use continues to be a major part of agricultural production; after fifty years of intense chemical use, we still see a quarter to a third of the global harvest being lost to pests. Is this progress? What else can we do to improve the world food supply?
4. Are current pesticide regulations protective of public health, especially for susceptible populations?
5. WHO and other agencies still apply DDT and similar compounds to control many vector-borne diseases, such as malaria. The risks associated with DDT have been known for many decades. Please read Text Box 18.4 and then answer these questions. Is it appropriate that these compounds are still used for vector control? What is the reasoning behind your answer?
1050
References American Academy of Pediatrics. (2014). Insect repellents. Retrieved from https://www.aap.org/en-us/about-the-aap/aap- press-room/aap-press-room-media-center/Pages/Insect- Repellents.aspx
Antwi, F. B., Shama, L. M., & Peterson, R.K.D. (2008). Risk assessments for the insect repellents DEET and picaridin. Regulatory Toxicology and Pharmacology, 51(1), 31–36.
Blondell, J. (1997). Epidemiology of pesticide poisonings in the United States, with special reference to occupational cases. Occupational Medicine, 12, 209–220.
Blondell, J. (2007). Decline in pesticide poisonings in the United States from 1995 to 2004. Clinical Toxicology, 45(5), 589–592.
Bouwman, H., van den Berg, H., & Kylin, H. (2011). DDT and malaria prevention: Addressing the paradox. Environmental Health Perspectives, 119(6), 744–747.
Cantor, N. (2001). In the wake of the plague: The Black Death and the world it made. New York: Free Press.
Carson, R. (1962). Silent spring. Boston: Houghton Mifflin.
Centers for Disease Control and Prevention. (2005). Hantavirus pulmonary syndrome (HPS). Retrieved from http://www.cdc.gov/ncidod/diseases/hanta/hps
Centers for Disease Control and Prevention. (2013a). Biomonitoring summary: DEET. Retrieved from http://www.cdc.gov/biomonitoring/DEET_BiomonitoringSummary.html
Centers for Disease Control and Prevention. (2013b). Pesticide illness and injury surveillance. Retrieved from http://www.cdc.gov/niosh/topics/pesticides
Curtis, C. F., & Lines, J. D. (2000). Should DDT be banned by international treaty? Parasitology Today, 16(3), 119–121.
Damalas, C. A., & Eleftherohorinos, I. G. (2011). Pesticide exposure,
1051
safety issues, and risk assessment indicators. International Journal of Environmental Research and Public Health, 8(5), 1402–1419.
Davis, J. R., Brownson, R. C., & Garcia, R. (1992). Family pesticide use in the home, garden, orchard, and yard. Archives of Environmental Contamination and Toxicology, 22, 260–266.
De, A., Bose, R., & Kumar, A., & Mozumdar, S. (2014). Worldwide pesticide use. In Targeted delivery of pesticides using biodegradable polymeric nanoparticles. New York: Springer.
Ecobichon, D. J. (2001). Pesticide use in developing countries. Toxicology, 160(1–3), 27–33.
Eddleston, M., Buckley, N. A., Eyer, P., & Dawson, A. H. (2008). Management of acute organophosphorus pesticide poisoning. Lancet, 371(9612), 597–607.
Eskenazi, B., Chevrier, J., Rosas, L. G., Anderson, H. A., Bornman, M. S., Bouwman, H.,…Stapleton, D. (2009). The Pine River statement: Human health consequences of DDT use. Environmental Health Perspectives, 117(9), 1359–1367.
Fradin, M. S., & Day, J. F. (2002). Comparative efficacy of insect repellants against mosquito bites. New England Journal of Medicine, 347, 13–18.
Galt, R. E. (2008). Beyond the circle of poison: Significant shifts in the global pesticide complex, 1976–2008. Global Environmental Change, 18(4), 786–799.
Gratz, N. G. (2004). Critical review of the vector status of Aedes albopictus. Medical and Veterinary Entomology, 18, 215–227.
Gunnell, D., Eddleston, M., Phillips, M. R., & Konradsen, F. (2007). The global distribution of fatal pesticide self-poisoning: Systematic review. BMC Public Health, 7, 357.
Hore, P., Robson, M., Freeman, N., Zhang, J., Wartenberg, D., Ozkaynak, H.,…Lioy, P. J. (2005). Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Environmental Health Perspectives, 113, 211–219.
1052
Hough, P. (2003). Poisons in the system: The global regulation of hazardous pesticides. Global Environmental Politics, 3(2), 11–24.
International Agency for Research on Cancer. (1991). IARC monographs on the evaluation of carcinogenic risks to humans: Vol. 53. Occupational exposures in insecticide application, and some pesticides. Lyon: Author.
Kapp, C. (2004). New international convention allows use of DDT for malaria control. Bulletin of the World Health Organization, 82, 472–473.
Longnecker, M. P., Klebanoff, M. A., Zhou, H., & Brock, J. W. (2001). Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Lancet, 358, 110–114.
Longnecker, M. P., Rogan, W. J., & Lucier, G. (1997). The human health effects of DDT (dichlorodiphenyltrichloroethane) and PCBs (polychlorinated biphenyls) and an overview of organochlorines in public health. Annual Review of Public Health, 18, 211–244.
Maroli, M., Feliciangeli, M. D., Bichaud, L., Charrel, R. N., & Gradoni, L. (2013). Phlebotomine sandflies and the spreading of leishmaniases and other diseases of public health concern. Medical and Veterinary Entomology, 27(2), 123–147.
Matthews, G., Zaim, M., Yadav, R. S., Soares, A., Hii, J., Ameneshewa, B.,…van den Berg, H. (2011). Status of legislation and regulatory control of public health pesticides in countries endemic with or at risk of major vector-borne diseases. Environmental Health Perspectives, 119(11), 1517–1522.
McNeill, W. (1976). Plagues and peoples. New York: Anchor Books.
Meerburg, B. G., Singleton, G. R., & Leirs, H. (2009). The Year of the Rat ends—time to fight hunger. Pest Management Science, 65(4), 351–352.
Murray, K., Mertens, E., & Despres, P. (2010). West Nile virus and its emergence in the United States of America. Veterinary Research, 41(6), 67.
1053
Nájera, J. A. (2001). Malaria control: Achievements, problems and strategies. Parassitologia, 43, 1–89.
National Toxicology Program. (2005). Report on carcinogens (11th ed.). Washington, DC: Public Health Service, National Toxicology Program.
Olson, K. B. (1999). Aum Shinrikyo: Once and future threat? Emerging Infectious Diseases, 5(4). Retrieved from http://wwwnc.cdc.gov/eid/article/5/4/99-0409
Osimitz, T. G., Murphy, J. V., Fell, L. A., & Page, B. (2010). Adverse events associated with the use of insect repellents containing N,N diethyl-m-toluamide (DEET). Regulatory Toxicology and Pharmacology, 56(1), 93–99.
Patel, V., Ramasundarahettige, C., Vijayakumar, L., Thakur, J. S., Gajalakshmi, V., Gururaj, G.,…Jha, P. (2012). Suicide mortality in India: A nationally representative survey. Lancet, 379(9834), s2343–s2351.
Pedigo, L. P. (2002). Agricultural entomology and pest management (4th ed.). Upper Saddle River, NJ: Prentice Hall.
Phung, D. T., Connell, D., Miller, G., Rutherford, S., & Chu, C. (2012). Pesticide regulations and farm worker safety: The need to improve pesticide regulations in Viet Nam. Bulletin of the World Health Organization, 90(6), 468–473.
Pimentel, D. (2009). Environmental and economic costs of the application of pesticides primarily in the United States. In R. Peshin & A. K. Dhawan (Eds.), Integrated pest management: Innovation- development process (pp. 89–111). New York: Springer.
Punareewattana, K., Smith, B. J., Blaylock, B. K., Robertson, J. L., Gogal, R. M., Jr., Prater, M. R.,…Holladay, S. D. (2000). Topical permethrin exposure causes thymic atrophy and persistent inhibition of the contact hypersensitivity response in C57BI/6 mice. International Journal of Toxicology, 19, 383–389.
Roberts, D., Curtis, C., Tren, R., Sharp, B., Shiff C., & Bate, R. (2004). Malaria control and public health. Emerging Infectious Diseases, 10, 1170–1171.
1054
Roberts, D. R., Manguin, S., & Mouchet, J. (2000). DDT house spraying and re-emerging malaria. Lancet, 356, 330–332.
Rogan, W. J., & Chen, A. (2005). Health risks and benefits of bis(4- chlorophenyl)-1,1,1-trichloroethane (DDT). Lancet, 366, 763–773.
Roll Back Malaria. (2015). About malaria. Retrieved from www.rollbackmalaria.org/about/about-malaria/key-facts
Schreinemachers, P., & Tipraqsa, P. (2012). Agricultural pesticides and land use intensification in high, middle and low income countries. Food Policy, 37(6), 616–626.
Smith, A. G. (2000). How toxic Is DDT? Lancet, 356, 267–268.
Stadlinger, N., Mmochi, A. J., & Kumblad, L. (2013). Weak governmental institutions impair the management of pesticide import and sales in Zanzibar. Ambio, 42, 72–82.
Tren, R. (1999). The economic cost of malaria in South Africa: Malaria control and the DDT issue. London: Institute of Economic Affairs.
Triplehorn, C. A., & Johnson, N. F. (2005). Borror and DeLong's introduction to the study of insects (7th ed.). Pacific Grove, CA: Brooks/Cole.
Turusov, V., Rakitsky, V., & Tomatis, L. (2002). Dichlorodiphenyltrichloroethane (DDT): Ubiquity, persistence, and risks. Environmental Health Perspectives, 110, 125–128.
U.S. Environmental Protection Agency. (2011a). 2006–2007 Pesticide market estimates: Usage. Retrieved from http://www.epa.gov/opp00001/pestsales/07pestsales/table_of_contents2007.htm
U.S. Environmental Protection Agency. (2011b). Label review manual. http://www2.epa.gov/pesticide-registration/label-review- manual
van den Berg, H., Hii, J., Soares, A., Mnzava, A., Ameneshewa, B., Dash, A. P.,…Zaim, M. (2011). Status of pesticide management in the practice of vector control: A global survey in countries at risk of malaria or other major vector-borne diseases. Malaria Journal, 10, 125.
1055
Verger, P.J.P., & Boobis, A.R. (2013). Reevaluate pesticides for food security and safety. Science, 341(6147), 717–718.
Waichman, A.V., Eve, E., & da Silva Nina, N. C. (2007). Do farmers understand the information displayed on pesticide product labels? A key question to reduce pesticides exposure and risk of poisoning in the Brazilian Amazon. Crop Protection, 26(4), 576–583.
Whitmore, R. W., Immerman, F. W., Camann, D. E., Bond, A. E., Lewis, R. G., & Schaum, J. L. (1994). Non-occupational exposures to pesticides for residents of two U.S. cities. Archives of Environmental Contamination and Toxicology, 26, 47–59.
Williamson, S., Ball, A., & Pretty, J. (2008). Trends in pesticide use and drivers for safer pest management in four African countries. Crop Protection, 27(10), 1327–1334.
World Health Organization. (1989). DDT and its derivatives: Environmental aspects (Environmental Health Criteria 83). Geneva: Author.
World Health Organization. (2014). World malaria report 2014. Geneva: Author. Retrieved from http://www.who.int/entity/malaria/publications/world_malaria_report_2014/en/index.html
Wu, K.-C., Chen, Y.-Y., & Yip, P.S.F. (2012). Suicide methods in Asia: Implications in suicide prevention. International Journal of Environmental Research and Public Health, 9, 1135–1158.
Zinsser, H. (2007). Rats, lice, and history. Boston: Little, Brown.
1056
For Further Information Books Reigart, R., & Roberts, J. (Eds.). (2013). Recognition and management of pesticide poisonings (6th ed.). Washington, DC: U.S. Environmental Protection Agency, Office of Pesticide Programs. Published in both English and Spanish, this work covers about 1,500 pesticide products, in an easy-to-use format. Toxicology, signs and symptoms of poisoning, and treatment are covered in nineteen chapters on major types of pesticides. Can be downloaded as a PDF: http://www2.epa.gov/pesticide-worker- safety/recognition-and-management-pesticide-poisonings
Shadick, N., Maher, N., & Hoak, D. (2014). Tickborne diseases of the United States: A reference manual for health care providers (2nd ed.). Atlanta, GA: Centers for Disease Control and Prevention. A thoughtful and well-illustrated guide to tick-borne disease with information on symptoms, geographic distribution, and treatment. Can be downloaded as a PDF: http://www.cdc.gov/lyme/resources/TickborneDiseases.pdf
World Health Organization. (2009). The WHO recommended classification of pesticides by hazard. Available at http://www.who.int/ipcs/publications/pesticides_hazard_2009.pdf? ua=1
U.S. Environmental Protection Agency Web Sites About Pesticides (2014): http://www.epa.gov/pesticides/about/types.htm
Pesticides (2014): http://www.epa.gov/pesticides
Precautionary Statements (2014; chap. 7 in Label Review Manual): http://www2.epa.gov/sites/production/files/2014- 07/documents/chapter7_revised_final_0714.pdf
Poison Control Centers The United States has a national network of poison control centers (the American Association of Poison Control Centers). The national
1057
hotline number for help after exposure to a poison is 1-800-222- 1222.
1058
Chapter 19 Food Systems, the Environment, and Public Health
Pamela Rhubart Berg, Leo Horrigan, and Roni Neff
Ms. Berg, Mr. Horrigan, and Dr. Neff report no conflicts of interest related to the authorship of this chapter. Dr. Nachman and Dr. Love report no conflicts of interest related to the authorship of their text boxes. Anna Engstrom reports no conflicts of interest related to the authorship of the tox box.
1059
Key Concepts The food system, from initial inputs to production to distribution to consumer choices, is a complex system, best understood using a systems approach.
The Green Revolution, including the use of fertilizers, pesticides, machinery, and innovative crops, greatly altered traditional methods of food production, and increased output, but with some adverse environmental and health consequences.
In the United States, most food is produced and distributed using large-scale industrial methods. This system is efficient and productive by some measures, but also raises environmental and health concerns.
A healthy food system has been defined as “health- promoting, sustainable, resilient, diverse, fair, economically balanced, and transparent.”
Food safety is a traditional core function of environmental health, and practicing food safety is important for controlling both bacteriological and chemical contamination and spoilage.
If the history of Homo sapiens were compressed into a single year, we would not have started farming until the evening of December 13. If the history of food production were compressed into a single year, we would not have introduced industrial agriculture, the mainstream food production system serving the United States today, until the morning of December 29. That's how new and different our modern food system is.
The modern food system is extremely large and permeates many aspects of our lives. In the United States, food production accounts for over half of our land, 16% of our energy, and 80% of consumptive water use (water lost to the environment by evaporation, crop transpiration, or incorporation into products). One in five private sector workers focuses on producing, processing, distributing, or selling our food, and food represents 13% of the U.S.
1060
gross domestic product (Neff, 2014). All that effort and expense produces a food supply that is more plentiful and costs less for consumers than it ever has.
In addition to these benefits, the way modern nations produce, process and distribute food has also created a wealth of challenges. In this chapter, we provide an overview of today's industrialized food system, focusing on threats to environmental public health, including contamination of soil, water, air and food, resource overuse, and food environments that promote unhealthy food choices. We then present a systems approach to the issue of food safety, both because of its importance to environmental health, and to illustrate the additional insight and problem-solving ability that this approach offers. Lastly, we briefly discuss some of the important policies that shape our food system's environmental health impacts. Rather than trying to be comprehensive (the system is too multifaceted for that), we give examples illustrating key concepts along the supply chain and in the policies shaping the system.
1061
What Is the Food System? Food travels through the landscape via food supply chains of varying lengths, but all involve some form of production, distribution, consumption, and waste disposal; most also involve processing and sales (see Figure 19.1). Food supply chains are embedded within broader food systems, encompassing all the activities, resources, and inputs involved in the supply chain, as well as the outputs and outcomes of those processes; all the involved people, businesses, and organizations; and the related politics, policy, culture, marketing, and economics. What makes it a system rather than a collection of food-related components is its connective web of interacting relationships.
Figure 19.1 Selected Components of the Food System Source: Brent Kim and Michael Milli, Johns Hopkins Center for a Livable Future, 2015.
This figure shows examples of the flow of inputs and resources in food supply chains, influences that shape them, and resulting outputs and outcomes—many of which have direct and/or indirect impacts on public health. The arrows shown here represent only the prevailing directions of flow; in reality, relationships among food system components are often bidirectional or cyclical (e.g., manure and food waste may be composted and directed back into production), while many food system outcomes in turn influence supply chain activities and the use of inputs and resources. The dashed lines reflect the open nature of the system; each component operates not in isolation,
1062
but in relation to the others, and within the context of the social and biophysical environment.
The food system interacts with other systems. It brings in inputs such as fertilizers, pesticides, energy, water, knowledge, and labor, and produces outputs, both positive and negative, including food, contamination, greenhouse gases (GHGs), and waste, with varying impacts on health, food security, and environmental health. The food system is shaped by environmental influences from outside as well, including climate change and land use, and social influences, such as population, policy, economics, culture, and marketing.
One important feature of a system is its dynamism; systems change constantly. This chapter describes many problems in today's food system, but there is also positive change afoot. Millions of consumers are seeking ways to make the food system—and the food they eat—healthier and more sustainable, while many businesses are recognizing that making changes can be profitable and can strengthen their businesses.
1063
Food Production: Industrial Agriculture Food production is the first stage in the food chain, and it has the greatest impact on environmental health. Food production includes producing crops, food animals (for meat, eggs, and dairy products), and both farmed and wild-caught seafood.
Most of our food is produced using industrial methods, which rely heavily on off-farm inputs such as fossil fuels, pesticides, chemical fertilizers, and large-scale machinery and which aim to produce the greatest possible yield with the lowest possible input cost. Agriculture was the last major sector of our economy to be industrialized, as some inherent difficulties in farming (e.g., unpredictable weather, crop failures, regional variations in climate) made it less amenable to industrialization.
Industrial agriculture requires much less labor than traditional methods that use human and animal power for seeding, plowing, and harvesting. Mechanization enabled each farmer to manage more land, so industrial agriculture made it possible to feed more people with fewer farmers and fewer farms. The United States had 7 million farms in 1935—when it had 127 million people. Today it has 316 million people but only 2 million farms (U.S. Environmental Protection Agency [U.S. EPA], 2013).
Industrial Agriculture and Natural Resources Agriculture relies on natural resources, such as soil, water, and biodiversity, and natural functions, such as pollination, decomposition, and predators that control pests (i.e., the ecosystem services described in Chapter 2). Unfortunately, some agricultural practices can damage natural resources and functions, as described in the next sections. We mention some specific implications for public health, but the overarching health threat here is that damaging and depleting these resources threatens our future food security.
Soil Healthy soils contain thriving ecosystems—up to a billion bacteria in each teaspoon—and are resilient to drought. Once soil is eroded it
1064
can take a century or more to form an inch of new topsoil. Plowing, overgrazing, excessive fertilization (e.g., with manure from concentrated animal agriculture), and other agricultural practices degrade topsoil much faster than it can be replenished. The Food and Agriculture Organization of the United Nations (FAO) says 25% of the world's land is severely degraded (Montgomery, 2007; FAO, 2011b).
Water Agriculture is by far the world's biggest freshwater user globally, at 70% of all usage, with livestock products using far more water than most other agricultural products. Much water for agriculture is drawn from underground aquifers—some of which are nonrechargeable fossil aquifers. One of these, the Ogallala Aquifer, provides water for about one fourth of the irrigated acres in the United States, or more than 15 million acres. It has been estimated that as much as one third of the underground water extracted for agriculture is nonrenewable (Wada et al., 2010). Besides depleting water as a resource, agriculture is a leading source of pollution in U.S. water bodies. Pesticides and fertilizers can impair water quality, especially following high-intensity application, as can excessive plowing, overgrazing, or poor management of animal wastes.
Biodiversity Biodiversity, or the existence of a variety of different species and organisms in an ecosystem, is important for agriculture. Today's agriculture has dramatically narrowed the range of plant and animal species produced in the United States and globally. Industrial agriculture threatens biodiversity in multiple additional ways. Most important is the use of monocultures, or large expanses of the same crop (Figure 19.2). About half of U.S. cropland is used to grow monocultures of genetically uniform corn and soybeans (U.S. EPA, 2009). While monocultures can create economies of scale, they are also vulnerable to pest invasions and plant diseases, because any pest or disease that prefers the monocultured crop as a food source will have an easier time becoming established.
1065
Figure 19.2 Applying Herbicide to a North Carolina Cornfield Source: North Carolina State Soil Science photostream, n.d.
This photograph demonstrates an agricultural monoculture, mechanization, and chemical inputs—three features of industrial agriculture.
Energy Our industrialized food system is the first in human history to use more energy than it produces, requiring, by some estimates, about 7 to 10 calories of input energy for each calorie of food energy produced (Pimentel & Pimentel, 1996). Much labor in agriculture has been replaced by machinery that runs on fossil fuels, and the pesticides and fertilizers used in conventional agriculture are also made with fossil fuel inputs. There has been an increasing movement to incorporate energy efficiency and renewable energy into farming, including wind, solar, and biomass power produced on- and off-farm. Much long-distance transportation of food occurs on energy-efficient trains and boats, though substantial quantities travel on trucks as well.
Our dependence on fossil fuels to produce food raises public policy concerns and public health concerns, for at least four reasons (Neff, Parker, Kirschenmann, Tinch, & Lawrence, 2011): (1) Fossil fuels are limited resources. Some may be nearing their peak of supply, after which available supplies will decline. For some energy types,
1066
such as liquid gasoline and diesel, there are not yet cost-effective, environmentally sound replacements. (2) As stocks decline the price of energy will rise and become more volatile, leading to food price spikes, with profound food security and public health effects. (3) Burning more fossil fuels to grow our food means exacerbating climate change, which in turn severely threatens future food security (see Chapter 12). (4) Reliance on fossil fuels additionally contributes to air pollution, including ozone and particulate matter, which in turn can aggravate health problems such as cardiovascular and respiratory diseases (see Chapter 13).
Climate Stable climate is also a “resource” for agriculture, but it is becoming less and less a reality as climate change unfolds. As explored in Chapter 12, climate change is expected increasingly to stress both crops and livestock, leading to declines in productivity in many parts of the world. Extreme weather events such as severe drought, floods, and strong storms are all expected to become more common and add to the difficulties of producing food. Many weed species benefit more than crop species when temperature, rainfall, and carbon dioxide concentrations increase. Warmer temperatures will also help pest insects shift or expand their ranges. Some agricultural pests will likely have more rapid life cycles that will make them harder for farmers to control. Rising sea levels are a concern for coastal agriculture because of saltwater intrusion into soils, groundwater, and river deltas that farmers depend on for irrigation. All of these phenomena, along with increasingly uncertain rainfall and temperature patterns, will lead to increased crop failures, undermining food security (Porter et al., 2014).
Besides being impacted by climate change, agriculture and food systems contribute to it. Food systems have been estimated to emit between 19% and 29% of global GHGs, and 80% to 86% of those emissions are attributed to agriculture (Vermeulen, Campbell, & Ingram, 2012).
Manufactured Agricultural Inputs In addition to the resources described above, industrial farms use a variety of manufactured inputs to produce crops, many of which have potential environmental health impacts. Here we focus on
1067
three: pesticides, fertilizers, and genetically engineered seeds. In the next section we discuss additional inputs of concern used in food animal production.
Pesticides Pests, such as insects and weeds, are often crop-specific, and thrive when a single crop is planted in a large area and/or over multiple years. Manufactured pesticides, however, have enabled farmers to plant monocultures without worrying about pest reproduction cycles. Applying the chemical takes care of the problem, at least in the short term. Unfortunately, though, pesticides have also created new problems, as explored in detail in Chapter 18. One problem is that heavy pesticide use has increasingly led to pesticide resistance (similar to drug resistance), in which the pesticide loses effectiveness against a pest. More than 500 pest species are now resistant to one or more pesticides (Whalon, Mota-Sanchez, & Hollingworth, 2008).
Pesticides create public health risks for farmers, farmworkers, and farm neighbors, primarily at the time when they are being applied. Pesticide residues on food also create public health risks for consumers. Exposure to pesticides can put farmers and farmworkers, in particular, at risk for acute effects, such as poisonings by organophosphates or carbamates, which can cause neurological and gastrointestinal problems (see Tox Boxes 18.1 and 18.2, in Chapter 18). Chronic health risks associated with pesticide exposure can include hormonal disruptions, reproductive and fetal development problems, asthma, and allergies. Some cancers have been linked to pesticides in animal studies and epidemiological studies (see Chapter 18).
Fertilizers Traditionally, farms had a mix of animals and crops, with the animals' manure serving as fertilizer for the crops. Once science discovered a way to fix atmospheric nitrogen to produce synthetic fertilizers (the Haber-Bosch process), animal manure was no longer an essential fertilizer on the farm. Globally, the use of synthetic fertilizers took off, increasing by about 800% between 1960 and 2000 (Canfield, Glazer, & Falkowski, 2010).
Synthetic fertilizers helped spur the dramatic increases in crop
1068
yields known as the Green Revolution during the twentieth century (although high yields are possible with organic fertilizers as well). But there are downsides. Under current agricultural practices, crops take up only 30% to 50% of fertilizer nitrogen and about 45% of applied phosphorus (Tilman, Cassman, Matson, Naylor, & Polasky, 2002). Some of the excess runs off the land and becomes nutrient pollution in marine ecosystems, river deltas, and estuaries, a phenomenon known as eutrophication. This nutrient load stimulates the growth of algae. As the algae sink and decompose, the decomposition consumes oxygen in the water that is essential to healthy aquatic life. This has resulted in dead zones in hundreds of coastal locations worldwide (Diaz & Rosenberg, 2008). In addition to their ecological effects, some algae give rise to harmful algal blooms (HABs). Toxins from these blooms can cause acute neurotoxic disorders or chronic disease in humans. Many farmers today reduce fertilizer overuse and save money by using precision application systems that calibrate the quantities of fertilizer used based on soil needs.
Genetically Engineered Seeds One of the most controversial technologies to be introduced to the industrial agriculture toolkit is genetic engineering, resulting in genetically modified organisms (GMOs), including food crops. GM corn and soybean seeds only came on the market in 1996, but they already account for the vast majority of U.S. plantings of those crops, and now cover almost half of U.S. cropland (U.S. Department of Agriculture [USDA], 2014). These crops have genes for herbicide tolerance or genes that allow the plants to produce their own insecticide, or both. While the seeds can be costly, they have increased yields in some cases and saved U.S. farmers time and money, though as described below, this may change. Many consumers have focused on concerns about safety, and have demanded labeling to identify products with GM ingredients. Assessments in the United States (American Association for the Advancement of Science, 2102) and Europe (European Commission, Directorate-General for Research and Innovation, 2010) and by the United Nations (World Health Organization, 2005) have not found significant evidence that these crops pose risk, though monitoring and research are ongoing, and some have called for more precautionary approaches in the short term (Hilbeck
1069
et al., 2015). Social concerns are also significant, as GMO technology is controlled by private firms that obligate farmers to purchase their seeds each year. Moreover, given the size of their investment, some of these companies aggressively defend their intellectual property rights in ways that impede independent research (Scientific American Editors, 2009).
From an environmental health standpoint, the impacts of the insecticides and herbicides used with GM crops are more pressing concerns. Herbicide-tolerant crops led to use of an additional 527 million pounds of the herbicide glyphosate in the United States between 1996 and 2011 (Benbrook, 2012). The World Health Organization (WHO) has designated glyphosate, the active ingredient in Roundup (the most common glyphosate product), a probable human carcinogen (Guyton et al., 2015), and glyphosate has also been linked to birth defects in some studies (Paganelli, Gnazzo, Acosta, López, & Carrasco, 2010; Antoniou et al., 2012).
Extensive use of glyphosate has led to the evolution of weeds that are resistant to the chemical. This cycle may continue, requiring increasingly toxic products. On the insecticide front, use decreased by a combined 123 million pounds from 1996 to 2011, although target insects are showing increasing resistance to the pesticide known as Bt (a natural toxin produced by the bacterium Bacillus thuringiensis and exuded by “Bt crops”) (Benbrook, 2012).
1070
Industrial Food Animal Production The more than 9 billion food animals slaughtered in the United States each year exert an outsized impact on the environment and environmental health. Nearly all of the meat, milk, and eggs consumed in the United States are produced in a system known as industrial food animal production (IFAP), which raises animals in concentrated animal feeding operations (CAFOs), a legally defined term referring to facilities that confine animals, above certain numbers, without grass or other vegetation in the confinement area. The animals are raised under protocols created by integrators, companies that sign contracts with the CAFO operators. The contracts specify production methods but assign CAFO operators responsibility for managing the animals' waste. IFAP animals eat manufactured feeds containing a substantial portion of the corn and soybeans raised in the United States. CAFO animals' feed also routinely includes antimicrobials (in chicken and hog operations, although some major companies report plans to phase them out) and can also include rendered animal products and animal waste (Sapkota, Lefferts, McKenzie, & Walker, 2007). Despite the many limitations described below, the IFAP model has been exported, in particular to China, India, and Brazil.
Public Health Concerns One of the major concerns about CAFOs is their routine use of antibiotics, which are fed to food animals in low doses that do not kill all of the target bacteria and so foster the development of antibiotic-resistant bacterial strains. These low doses are used to promote faster growth and compensate for the immune- compromising conditions in which they live. IFAP accounts for about 80% of the antibiotics used in the United States, and uses many of the same types of antibiotics that are used in human medicine (Collignon, Powers, Chiller, Aidara-Kane, & Aarestrup, 2009). This practice contributes to the unfolding crisis of antibiotic resistance, whereby human diseases once cured easily with antibiotics have become more difficult—and sometimes impossible —to treat. Text Box 19.1 describes policy approaches to addressing
1071
agricultural antibiotic use.
Animal waste can contain disease-causing organisms such as certain Salmonella, Listeria, and E. coli species. As a result, if it has not been composted for a sufficient period of time, CAFO manure used to fertilize food crops can contaminate fresh produce and lead to outbreaks of foodborne illness, as discussed below (Graham & Nachman, 2010). Manure can also contain antimicrobials, 25% to 75% of which are estimated to be excreted unaltered (Kummerer, 2004), and heavy metals. Cattle are routinely fed large amounts of grain—which is not part of their natural diet—and this alters their digestive tracts in a way that promotes a disease-causing strain of E. coli.
Pathogens from animal waste, including antibiotic-resistant bacteria, spread from the farm into the community primarily through occupational exposures, environmental contamination, and contact with contaminated food products (You & Silbergeld, 2014) (also see Figure 19.3).
Figure 19.3 Potential Pathways for the Spread of Antibiotic- Resistant Bacteria from Animals to Humans
Note: This figure is not intended to represent the full complexity of resistance transmission. For example, antibiotic-resistant bacteria can also be transferred from humans to animals.
1072
Source: U.S. Government Accountability Office [U.S. GAO], 2011, p. 6.
Numerous noncommunicable ailments have also been documented among people who live near industrial swine facilities and who are exposed to these facilities' air and water emissions. These conditions include elevated rates of depression, stress, fatigue, headaches, sore throats, nausea, and respiratory problems (Donham, 2010). Because poor communities and communities and communities of color are disproportionately located near CAFOs, these risks are environmental justice concerns (Nicole, 2013).
1073
Text Box 19.1 Policy Approaches to Antibiotic Use in Animal Agriculture
Keeve Nachman
Antibiotic-resistant infections are responsible for a significant disease burden in the United States. According to the Centers for Disease Control and Prevention (CDC), these infections claim at least 23,000 lives and sicken more than 2 million people each year (CDC, 2013a). While the data needed to determine the fraction of these illnesses and deaths attributable to antibiotic use in animal agriculture are not being collected, the nature and magnitude of agricultural antibiotic use strongly suggest that it accounts for a considerable portion of this burden (Kim et al., 2013). In the United States, legislative attempts to limit (or even track) antibiotic use in the agricultural industry have been largely unsuccessful (Lawrence, Nachman, & Smith, 2013). As a result, the only regulatory intervention that has been pursued is a U.S. Food and Drug Administration voluntary initiative for drug manufacturers; this has been criticized as being unlikely to motivate changes in the animal production industry (Nachman, Smith, & Martin, 2014).
Other countries have been more proactive in controlling antibiotic use in agriculture. Denmark was the first country to implement a series of significant changes aimed at addressing the problem (Wielinga, Jensen, Aarestrup, & Schlundt, 2014). In 1995, that country restricted the revenue veterinarians could receive from antibiotic sales, eliminating a key conflict of interest. As of 1999, Denmark had banned all nontherapeutic use of antibiotics in food animals, resulting in significant declines in the quantity of antibiotics used by the industry. The Danish government also implemented a rigorous surveillance system to monitor antibiotic use and resistance among recovered pathogens. The results were impressive; reductions were seen in recoverable antibiotic- resistant bacteria from meat and from humans, suggesting reductions in infection risks faced by the Danish public.
1074
Further, these changes were implemented in tandem with improvements in animal husbandry procedures, resulting in the industry becoming more efficient. The Danish success was a factor in prompting the European Union to ban the use of antibiotics for growth promotion in 2006 (Levy, 2014).
Waste Management Swine, poultry, and cattle raised in U.S. CAFOs produce more than 300 million tons of dry waste each year (U.S. Department of Agriculture, Agricultural Research Service, 2005), or more than forty times the amount of human solid waste processed by U.S. wastewater treatment plants (Graham & Nachman, 2010). In stark contrast to human biosolids, for which treatment must meet regulatory requirements for removing pathogens and chemical contaminants, there is no requirement to treat animal manure before releasing it into the environment (by spraying it on crop fields, for example) (Graham & Nachman, 2010). Separating food animals from the land has turned an agricultural asset—animal manure deposited directly on pastureland or used on a farm's nearby cropland as fertilizer—into a waste management problem. There are typically many CAFOs clustered in relatively small areas, intensifying the waste management challenge. For example, North Carolina's Duplin County, with a human population of 60,000, is raising 2.3 million hogs at any one time, or 38 hogs per resident (Agriculture and Community Development Services, n.d.). IFAP animal waste is commonly stored in large manure cesspits, as shown in Figure 19.4.
1075
Figure 19.4 Manure Cesspit Outside Hog CAFO in Duplin County, North Carolina
Source: Horrigan & Moore, 2010.
When manure is applied at a greater rate than can be absorbed by the land, rainfall carries off the excess, which can then contaminate surface waters and create dead zones, or contaminate the air and also the shallow aquifers on which most rural residents depend for drinking water.
1076
Sustainable Agriculture This is a time of enormous interest in the food system and enormous efforts to bring about food system change. Consumers increasingly want to learn about their food, know where it came from, and trust its quality. According to a recent poll, 66% of Americans have thought about the sustainability of their food and beverages in the past year, 39% have shopped at farmers' markets, 26% have bought organic products (Text Box 19.2), and 22% have grown their own food (International Food Information Center Foundation, 2012). College students around the country have successfully called for changes to campus food, through participation in the Real Food Challenge (www.realfoodchallenge.org).
What are the features of a healthy, sustainable, and resilient food system? In short:
A sustainable food system has the capacity to keep producing food into the future.
A resilient food system has the capacity to bounce back after disturbances.
A healthy food system supports the short- and long-term health of the population. It is, as defined by four major professional associations, “health-promoting, sustainable, resilient, diverse, fair, economically balanced, and transparent” (Academy of Nutrition and Dietetics, American Nurses Association, American Planning Association, and American Public Health Association, 2012).
Changes in food production may be categorized into two types. First, most conventional farms have now adopted at least some practices that make their operations more sustainable (and generally save money). Second, many farms have adopted agroecological practices, meaning they try to mimic natural systems as they design and manage their agricultural systems. As an example of the first, conservation tillage, to reduce soil loss and save gasoline, has become the norm rather than the exception in U.S. agriculture. It involves leaving residue from the previous crop on the ground rather than tilling the soil between crops. Other
1077
increasingly common methods are high-efficiency irrigation systems to conserve water; use of precision technology in fertilizer application, and use of cover crops for weed suppression, soil conservation, and soil enhancement, among other benefits. Another increasingly widespread method is integrated pest management (IPM) (described in Chapter 18), which emphasizes using biological controls for pests (e.g., introducing natural predators or creating habitat for them) and other nontoxic controls before applying least-toxic chemical pesticides only as a last resort (National Research Council, 2010).
All these changes in industrial agriculture represent incremental progress. But creating a more sustainable agriculture goes beyond substituting one farming practice for another; it focuses on mimicking natural systems. A 2013 United Nations report on the state of agriculture called for a “rapid and significant shift from conventional, monoculture-based and high external-input- dependent industrial production towards mosaics of sustainable, regenerative production systems” (United Nations Conference on Trade and Development, 2013).
Good soil is seen by many as the foundation of healthy agricultural systems. One of the central goals of sustainable agriculture is to maintain and build soil health by adding organic matter and using cover crops, among other techniques. Biologically healthy soil improves retention of moisture and nutrients, provides substantial drought resistance, and sequesters more carbon than other soils. Soil holds about 80% of all the carbon found in terrestrial ecosystems (Ontl & Schulte, 2012).
Japanese farmer Takao Furuno (2001) created a well-known example of a farming system that mimics natural systems. His approach incorporates ducks into rice paddies to eat weeds and insects while also adding fertility to the water with their waste (see Figure 19.5). This reduces input costs for pesticides and fertilizers while creating additional revenue streams from duck meat and duck eggs. Furuno then added fish into his paddies to provide even more revenue—a practice that rice farmers had abandoned because the insecticides used in industrial rice farming would kill their fish. His system was shown to yield 20% more rice than a traditional rice production system (Hossain, Sugimoto, Ahmed, & Islam, 2005). Through Furuno's promotional efforts and those of his institutional
1078
partners, his method has spread to more than 75,000 farmers across eleven Asian countries and also to Cuba (Schwab Foundation for Social Entrepreneurship and the World Economic Forum, 2001).
Figure 19.5 Ducks in One of Takao Furuno's Rice Paddies in Japan Source: Mamemachi, n.d.
1079
Text Box 19.2 Organic Agriculture: What Does It Mean?
Leo Horrigan
Early advocates of organic agriculture, such as Sir Albert Howard and Lady Eve Balfour, envisioned an agriculture system in which farmers would think ecologically and develop whole-farm approaches to farm management, rather than seeing each farming problem in isolation from the rest of the farm and its neighboring wild ecosystems (Balfour, 1977). Howard said: “The maintenance of the fertility of the soil is the first condition of any permanent system of agriculture” (Howard, 1943, p. 1).
Yet the USDA Organic label, launched in 2002, does not set any requirements related to soil fertility or certain other environmental concerns. Instead, it establishes a set of production standards that are mostly an assurance of what has not been used in producing the labeled food—no synthetic fertilizers, pesticides, or GMOs, and no antibiotics or artificial growth hormones in meat, eggs, or dairy products. These are positives for consumers; studies have shown—not surprisingly—that consuming organic foods reduces exposures to pesticides when compared to consuming conventionally grown foods (Lu, Barr, Pearson, & Waller, 2008).
The USDA Organic label, however, is not synonymous with sustainable. Growing demand for organic food has fueled the rise of industrial organic farming, large-scale agriculture that meets the requirements of the USDA Organic label but mimics the conventional agriculture system in its scale, input inefficiencies, and level of specialization. Some critics argue that the concept of organic has in some ways been reduced to an input substitution model—substituting natural inputs for synthetic ones.
Organic farmer and sustainable agriculture advocate Fred Kirschenmann effectively sums up the paradox of
1080
industrialized organic farming: “Certainly, providing an incentive for large farmers to move away from toxic inputs and substitute them with more environmentally benign ones has the potential to benefit both the environment and human health. But we are losing something vital in the process. We lose the ecological wisdom of the farmers who live close to the land, listen to the land, and consider themselves a member of the land community” (Kirschenmann, 2000).
1081
Food Consumption and Food Environments The penultimate stage of the food chain is food consumption. It may not seem intuitive that food consumption is an environmental health issue, but daily choices about what we will eat and not eat are strongly affected by our food environment. This term refers to all aspects of our surroundings that may influence our diets, including both the built environment in and around our homes, workplaces, and schools (as discussed in Chapter 15) and the marketing and social environments that surround us less tangibly but with no less impact. Food environments are shaped by numerous factors, including government policy, advertising, cultural norms, and what food outlets are available to consumers (supermarkets, corner stores, restaurants, etc.) (Truant & Neff, 2014).
Communities with poor access to affordable, healthy food are sometimes termed food deserts (or, to the extent they are awash in less healthy food, food swamps). These characterizations have been effective in policy advocacy, although some dislike them, particularly because of their emphasis on a community's limitations.
Evidence is mixed regarding the extent to which healthy food access affects food choices and health (although there is no question that the inconvenience of low access to healthy food makes it an environmental justice issue as it disproportionately affects low- income communities). As discussed in Chapters 9 and 15, physical proximity to markets is only one factor affecting food choices, and its impact is balanced against other factors such as perceived proximity, available transportation options, variations in food prices, and the many factors that shape food demand. While research results are mixed, some studies suggest that increased access to supermarkets is associated with healthier diet quality, lower prevalence of overweight and obesity, and greater consumption of fruits and vegetables, whereas increased access to convenience stores is associated with increased risk of obesity (Beaulac, Kristjansson, & Cummins, 2009; Lucan, 2015). At the very small scale—say, the experience of a child moving down a cafeteria line—there is evidence that the presentation and positioning of food can affect food choices—a phenomenon that is explored in Chapter 9.
1082
The final step in the food chain is the disposal of waste. As described in Chapter 17, waste is managed in many ways, from landfilling to incineration, and in some cases through conversion to biofuels. Waste occurs at every stage of the food chain, and has important environmental implications. These are explored in Text Box 19.3.
1083
Text Box 19.3 The Environmental Impacts of Wasted Food
Feed people, not landfills.
—U.S. Environmental Protection Agency
Each year, up to 40% of the U.S. postharvest food supply—an estimated 1,249 calories per person per day—ends up uneaten, including irregularly shaped carrots discarded because stores can't sell them, remains of restaurant entrees that were too big to finish, and neglected lettuce that has turned to mush in home refrigerators (Hall, Guo, Dore, & Chow, 2009; Buzby, Wells, & Hyman, 2014). Food is a major contributor to municipal solid waste (U.S. EPA, 2014a), becoming a significant source of methane—a potent greenhouse gas with twenty-one times the global warming potential of carbon dioxide.
In addition, wasting food is also wasting the water, energy, soil, pesticides, fertilizers, seeds, and labor used to produce, process, and distribute that food. In North America and Oceania we essentially “discard” about 35% of all freshwater that is used, 31% of cropland use, and 30% of fertilizers in the form of wasted food. The global environmental impacts from losing over 1.3 billion tons of food are even more staggering; indeed, the FAO (2013) has noted that if wasted food were a country, it would be the No. 3 greenhouse gas emitter in the world, after China and the United States.
Food waste and food loss occur across the food supply chain from production to consumption. In low-income countries food loss is concentrated at the production and distribution levels; this is related to economic and technical constraints in infrastructure, harvesting techniques, refrigeration, and storage. In wealthy countries, waste tends to occur further along the supply chain, during retail and consumption (FAO, 2011a).
In addressing waste of food it is important to take a public
1084
health approach (see Figure 19.6), prioritizing the primary prevention of waste over approaches such as composting or generating energy from food that took so many resources to produce. Indeed, by the time waste reaches the consumer level, it contains three times its original embodied energy, due to the effort to pick, transport, process, package, store, and prepare it (Thompson, 2011).
Figure 19.6 The EPA Food Recovery Hierarchy Prioritizes Actions to Prevent and Divert Wasted Food
Source: U.S. EPA, 2014a.
As expanding populations increase pressure on land, water, energy, and food supplies, reducing waste of food is a key part of a comprehensive strategy for improving the short- and long-term sustainability of our food system.
1085
Food Safety and Environmental Health: A Systems Perspective Disease-causing bacteria, viruses, chemicals, and other threats to health can enter the food supply at many points along the supply chain. Although the major focus of food safety has been the reduction of health risks associated with foodborne pathogens (bacteria, parasites, and viruses), food safety can also be compromised by pesticides and other chemicals, as well as physical hazards such as glass.
Contaminated food can pose serious risks to those who are exposed, causing acute nausea, diarrhea, fever, chronic illness, and in some cases, death. Vulnerable populations—the very young or elderly, those with weakened immune systems, and workers who grow, process and distribute food—are at increased risk. The CDC estimates that one in six Americans suffers a foodborne illness each year, leading to approximately 128,000 hospitalizations and 3,000 deaths (CDC, 2011).
Poor surveillance in many countries makes it difficult to estimate the global burden, but the World Health Organization estimates there are over 580 million cases of illness and 351,000 associated deaths annually from contaminated food and water (WHO, 2015). Foodborne illness is likely greater where sanitation is substandard and malnutrition increases susceptibility to the health effects of consuming unsafe food, particularly among children, who bear the brunt of foodborne illness and death. Many low-income countries lack infrastructure, such as refrigeration along the supply chain, and have limited capacity for basic environmental and public health services, such as water treatment. Food safety, however, remains a public health challenge even in industrialized countries, despite advances in risk identification, assessment, and management.
As the scale of the food chain grows, so does the number of people at risk from a single outbreak. Rapid changes in agricultural practices and food processing, new biotechnology, and a growing reliance on a globalized food system introduce new hazards and challenges for risk identification and traceability (see Text Box 19.4). Processed food items can include dozens of ingredients from
1086
multiple countries. A typical fast food cheeseburger can contain more than fifty ingredients that come from virtually every continent (Hueston & McLeoad, 2012).
The following sections of this chapter briefly describe the major categories of contaminants, discuss regulatory and other approaches to reduce the public health burden of foodborne illness, and highlight several challenges to food safety efforts in our increasingly complex supply chain.
1087
Text Box 19.4 Globalization, Seafood, and Food Safety
Dave Love
Seafood (fish, crustaceans, mollusks, aquatic plants) is one of the most widely traded food products globally. Roughly 90% of the seafood consumed in the United States is imported, from over sixty countries around the world. The most striking seafood safety issues are related to the globalized seafood industry and the mislabeling of seafood sold to consumers. From 2005 to 2010, the CDC found that fish were the products most commonly implicated in foodborne disease outbreaks from imported foods (seventeen of thirty- nine outbreaks).
As much as one third of seafood sold in the United States is willfully or accidentally mislabeled (Buck, 2010; Warner, Timme, Lowell, & Hirschfield, 2013). An important example is fish that carry health advisories due to contamination with heavy metals such as mercury. Avoiding these fish is especially critical for vulnerable populations such as pregnant women and young children. Yet U.S. grocery stores and restaurants have been found to be selling fish subject to health advisories mislabeled as fish with no such advisories (e.g., tilefish sold as red snapper and halibut, and king mackerel sold as grouper) (Warner et al., 2013).
The first line of defense for seafood safety is the U.S. Food and Drug Administration (FDA), which uses a strategic rubric to select about 2% of imported seafood for inspection at the port of entry, using (1) a check for proper labeling and documentation; (2) a sniff test for food spoilage and visual inspection; and (3) laboratory screening for heavy metals, PCBs, toxins, microbial pathogens, and veterinary drugs. Contamination can occur at any point along the supply chain from harvesting and production to processing, transportation, and point of sale.
One common food safety issue is inadequate refrigeration at
1088
some point along the supply chain, allowing food spoilage and dangerous growth of pathogenic bacteria. Among aquacultured (farm-raised) seafood, additional concerns arise when exporting countries have weaker farming, labor, or food safety standards than the importing countries do.
Biological Pathogens in the Supply Chain Estimates suggest that in the United States, only fourteen pathogens account for 95% of illnesses and hospitalizations and 98% of deaths from foodborne pathogens (Scallan et al., 2011), and that these illnesses cost an estimated $14 billion each year (Batz, Hoffmann, & Morris, 2012). The public health threat of foodborne illness is growing as pathogens are linked to new food sources and new pathogens are discovered, and the rise of antibiotic resistance can make foodborne illnesses increasingly difficult to treat. Salmonella, Toxoplasma gondii, Listeria monocytogenes, and Campylobacter pathogens and noroviruses are the most dangerous of the pathogens responsible for serious illnesses and hospitalizations and for deaths (Batz et al., 2012). In a CDC analysis of foodborne illness data, produce accounted for nearly half of illnesses, most often caused by noroviruses, while meat and poultry were the primary sources of fatal infections, with most due to salmonella and listeria (Painter et al., 2013) (see Figure 19.7). Although chronic illness or death is possible, foodborne pathogens most often result in severe gastrointestinal symptoms that run their course and abate.
1089
Figure 19.7 Contribution of Different Food Categories to Estimated Domestically Acquired Illness and Death, United States, 1998–2008
Note: Chart does not show 5% of illnesses and 2% of deaths attributable to other commodities. In addition, 1% of illnesses and 25% of deaths were not attributed to commodities; these were caused by pathogens not included in the outbreak database, mainly Toxoplasma and Vibrio vulnificus.
Source: CDC, 2013b.
One of the primary pathways of exposure to pathogens such as salmonella and E. coli is handling or eating food contaminated by animal waste. This can occur in several ways. First, livestock and pests such as insects and rodents carry disease-causing microbes. The pathogens from the waste can contaminate food via irrigation water, tainted equipment, and worker handling. Pathogens can also be introduced when food handlers have illnesses. Sometimes the meat itself may carry the microbes, while in many more cases small
1090
nicks to the digestive tract during meat processing can introduce fecal matter onto meat surfaces. A small amount of fecal matter or tainted meat can contaminate a large batch of processed meat, such as ground beef or turkey. In 2014, 18.7 million pounds of meat and poultry were recalled, including 13.2 million pounds of beef and beef products (Center for Science in the Public Interest, 2014; U.S. Department of Agriculture, Food Safety and Inspection Service, 2015).
Once a pathogen enters the food system, it is possible to prevent its growth through proper handling techniques and avoidance of cross-contamination. Time and temperature controls are particularly important for potentially hazardous food (PHF), including meat, seafood, dairy, eggs, cooked starches, melons, and sprouts (see Figure 19.8). Many of the pathogens that cause foodborne illness thrive at temperatures between 40° and 140°F and can double in number every twenty minutes (U.S. Department of Agriculture, Food Safety and Inspection Service [USDA, FSIS], 2013a). Of course, not all food is contaminated; when it is, refrigeration and freezing can slow or stop reproduction, but will not necessarily destroy bacteria, leaving proper cooking as the primary strategy for consumers to use to prevent foodborne illnesses.
1091
Figure 19.8 A Health Inspector Tests the Temperature of Refrigerated Meat at a Restaurant
1092
Source: Photo by Christopher Berg, REHS.
Inspections of food service establishments continue to be an important function of local health departments.
In a CDC analysis of foodborne outbreaks that occurred between 1998 and 2008, a majority of cases (60%) were associated with food prepared in a restaurant or deli (Gould et al., 2013) (Figure 19.9). Lack of paid sick days and employer-provided safety equipment, pressures to cut corners, inadequate training, and high turnover in the low-wage jobs typical across the food supply chain, particularly in the food service industry, compromise safety for workers and, ultimately, consumers.
Figure 19.9 A 1993 Outbreak Caused by E. Coli 0157 in Undercooked Beef at Jack in the Box Restaurants Sickened 732 People and Killed 4 Children
Source: Hathorn, 2012.
This outbreak prompted the creation of the CDC's PulseNet Pathogen Detection and Tracking System.
Chemicals in the Food Supply While the reduction of exposure to foodborne pathogens tends to be the focus of food safety initiatives, food can also contain harmful
1093
chemicals. Synthetic and naturally occurring chemicals can contaminate foods intentionally or unintentionally during production (pesticides, dioxins [Tox Box 19.1], PCBs, arsenic), processing (monosodium glutamate, aspartame, dyes), packaging (phthalates, bisphenols, including BPA), and preparation (acrylamide, furans) (Jackson, 2009).
1094
Tox Box 19.1 Dioxins
WHAT IS IT? Polychlorinated dibenzo-p-dioxins, or simply dioxins, are a class of seventy-five chemical congeners that are classified according to the number of chlorine substitutions in each compound. The most toxic dioxin congener is 2,3,7,8- tetrachloro-p-dibenzo-dioxin (tetra-chlorinated dioxin, or TCDD), and it is the dioxin of greatest public health importance. TCDD is a colorless to white solid, and it is lipophilic and persists in the environment. For these reasons, dioxins are also classified as persistent organic pollutants (POPs).
HOW IS IT USED? TCDD and other dioxins are not manufactured for any commercial use. Instead, these compounds are by-products that form as a result of incomplete combustion of carbon- based molecules, as in fossil fuel combustion. TCDD and other dioxins are also released when materials containing chlorine, such as plastics, treated wood, or bleached paper, are burned. For example, a large amount of TCDD is generated and emitted when materials such as plastics are burned at municipal, medical, solid, and hazardous waste incinerators. TCDD and other dioxins are also produced during the chlorine bleaching process utilized in pulp and paper mills and in the production of chlorinated organic chemicals (such as pesticides and wood preservatives).
1095
HOW ARE PEOPLE EXPOSED?
© Pangfolio | Dreamstime.com.
TCDD is emitted into the air from incinerators and vehicle exhaust, and it is released into the water from pulp and paper mills. In addition, chlorinated pesticides (such as the organochlorine pesticides) and herbicides are often contaminated with TCDD (a by-product from the pesticide production process), so TCDD may be released into the environment when these products are applied. Dioxins are found at low levels in all environmental media (air, soil, and water), and people are exposed through the air, food and milk, or dermal contact with contaminated soil or other materials. Importantly, the herbicide known as Agent Orange, used in the Vietnam War, was contaminated with TCDD, and its use was associated with significant TCDD exposure.
WHAT ARE THE TOXIC EFFECTS? Depending on the level and duration of exposure, TCDD can cause chloracne, cancer, and reproductive (miscarriage) and developmental (birth defects, immunosuppression) toxicity. Liver and heart toxicity, immunosuppression, and chloracne (acne associated with high exposure to halogenated aromatic
1096
compounds) are associated with high levels of TCDD exposure. High TCDD levels can also lead to endocrine disruption, including altered hormone synthesis and transport. Across many species, including humans, the developing nervous, immune, and reproductive systems appear to be the most sensitive to TCDD toxicity. Some of these effects can occur at low (background) TCDD levels. Importantly, TCDD and some of the other dioxins are also classified as human carcinogens (there is sufficient evidence for carcinogenicity).
HOW ARE PEOPLE PROTECTED? In the United States, the Food and Drug Administration has developed recommendations for TCDD levels in certain foods, such as shellfish and fish. In addition, the EPA has set a maximum contaminant level (MCL) for TCDD in drinking water and regulates TCDD emissions from municipal and hazardous waste incinerators. In incinerators, TCDD formation can be reduced by reducing the amount of chlorinated organic matter (like PCBs) in the waste and also by strictly controlling the temperature and oxygen levels in the incinerator to make the combustion process more efficient. In addition, scrubbers and other air pollution control systems can be implemented to reduce the amount of TCDD emitted into the air. The EPA's emission regulations, along with industry efforts, have resulted in a significant (over 90%) reduction in industrial dioxin emissions since 1987.
WANT TO LEARN MORE? The ATSDR Toxicological Profile for Chlorinated Dibenzo-p- dioxins was released in 1998, and a partial update was issued in 2008 (www.atsdr.cdc.gov/toxprofiles/tp.asp? id=366&tid=63).
A useful review is R. A. Hites, “Dioxins: An Overview and History,” Environmental Science & Technology, 2011, 45, 16–20.
Contributed by Anna Engstrom
1097
In some cases chemicals are used improperly or added unintentionally. In 2008, over 300,000 babies in China fell ill, 54,000 were hospitalized, and at least 6 died after a Chinese manufacturer added melamine, an industrial chemical used to make flame-retardant resin and plastics, to baby formula and milk powder to increase its apparent protein content (Gossner et al., 2009). In 2013, at least 23 children in the Indian state of Bihar died within hours of consuming a free lunch prepared using cooking oil stored in containers that had once held a dangerous and widely banned pesticide (United Nations News Centre, 2013).
Many of the most commonly used pesticides in the past, and some still in use in lower income countries, are now classified as persistent organic pollutants (POPs). POPs have been associated with reproductive, developmental, behavioral, neurological, immunological, and endocrine effects, including type 2 diabetes. Despite international bans decades ago, POPs such as DDT, dioxin, and PCBs continue to bioaccumulate and remain virtually unavoidable in the global food chain today. (Another group of toxic contaminants, mycotoxins, is addressed in Text Box 19.5 and Figure 19.10.)
Figure 19.10 An Example of Improper Grain Storage Source: A. Qadri; Associated Press, 2012.
Properly drying and storing grains to control moisture is one of the most effective methods of preventing dangerous molds and mycotoxins.
1098
Text Box 19.5 Mycotoxins Mycotoxins are one of the most important foodborne contaminants in terms of global impacts on human health, economics, and food security. Mycotoxins are potent, natural substances produced by molds that can easily infest grains, seeds, and other foods during production and storage and that pose serious risks to human and animal health. Exposure to mycotoxins is associated with a wide range of acute and chronic illnesses, including cancers and immune deficiencies. Aflatoxin, a well-known mycotoxin produced primarily from aspergillus, increases the risk for liver cancer and also for childhood stunting and its associated immunological and cognitive impacts (Kensler, Roebuck, Wogan, & Groopman, 2011). A primary source is peanuts, including peanut butter.
Not only do mycotoxins pose a greater health risk to people living in lower income countries who rely on grains and cereals as the foundation of their diet, they also cause significant food waste where agricultural commodities make up a sizable portion of exports, imposing a significant economic burden. Data on the economic burden of mycotoxins are lacking, but over the last ten years, mycotoxin contamination has accounted for 30% to 60% of the commodities rejected by the European Union (Lelieveld, 2015). Market demands and stringent standards in wealthier countries mean that low-income countries export their highest quality food. This leaves substandard, often contaminated food to be fed to livestock or sold in local markets, further increasing the risk of exposure and illness. Mold growth can be prevented through on-farm strategies and postharvest interventions, primarily proper sorting, drying, and storage of food crops.
Addressing Food Safety Threats The food safety system is a moving target, complicated by emerging
1099
and newly identified threats and an increasingly globalized food supply chain. Even though a completely safe food supply is an unrealistic goal, most foodborne illnesses are preventable. Food safety illustrates the benefits of a systems perspective that goes beyond a simple “wash your countertops” approach. In many cases, preventive actions early in the supply chain to protect human, animal, and ecosystem health yield the co-benefits of safer food. Reducing density in livestock operations, reducing line speeds in processing plants, and providing proper safety equipment to workers are examples of steps that can yield downstream effects for food safety and public health.
Just as the risk factors for foodborne illness are diverse and multilevel, so too are the interventions to address it, which include the following:
Regulations and standards at the international, federal, state, and local levels
Inspections of food products, processing plants, restaurants, and retailers (see Figure 19.8)
Training of food system workers, technical assistance in achieving compliance with regulations, and policy and workplace interventions to provide workers with paid sick days and other needed supports
Tracking illnesses through physician reporting and other epidemiologic surveillance strategies
Investigations following outbreaks to identify sources and contact those who may have been exposed
Food recalls, both voluntary and mandated
Public education to increase use of routine safety measures
Threats of negative publicity and legal action
Research to improve all of these strategies
The trend in food safety efforts is toward risk assessment and management tools, guidelines, and programs to reduce contamination risk during production, processing, and retail. Prerequisite programs (PRPs) generally serve as a foundation for overall quality and hygiene. These include good agricultural
1100
practices (GAPs), good manufacturing processes (GMPs), good hygienic practices (GHPs), and good storage practices (GSPs). When PRPs are in place and working effectively, Hazard Analysis and Critical Control Point (HACCP) systems can further enhance risk reduction. HACCP was developed by NASA and Pillsbury to produce food guaranteed to be safe for consumption by astronauts during the early days of the U.S. space program (Hulebak & Schlosser, 2002). This stepwise approach to primary prevention (Table 19.1) aims to identify and address potential risks to food safety before they can occur and has become a standard in modern food safety approaches. HACCP systems are now required for manufacturers of meat, poultry, seafood, and juice products and are also employed in some segments of the food service industry.
Table 19.1 HACCP Principles
1. Conduct a hazard analysis. 2. Identify critical control points (CCPs) in the process. 3. Establish critical limits for each CCP. 4. Establish CCP monitoring procedures. 5. Establish corrective actions for instances when CCP monitoring
reveals deviations. 6. Keep records. 7. Establish procedures to verify that HACCP is functioning
properly.
Food Safety Regulations The first attempts at food safety regulation in the United States date back to the early decades of the twentieth century in response to the public's outcry over Upton Sinclair's book The Jungle (Burkett, 2012). In 1906, the Pure Food and Drug Act established what is now the FDA, while the Meat Inspection Act established the USDA's Food Safety and Inspection Service. On this foundation, today's food safety framework developed as a patchwork of laws and regulations that were put in place largely in reaction to deadly foodborne disease outbreaks (Table 19.2). Laws were enacted over the latter part of the twentieth century increasing the USDA's power to regulate and inspect meat products. The FDA's authority over the
1101
remaining 80% of the food supply was recently strengthened under the 2010 Food Safety Modernization Act (FSMA). The FSMA gave the FDA expanded recall capabilities, authority to mandate HACCP systems more broadly across the food manufacturing sector, and enhanced oversight of food processing and imported food (Taylor, 2011).
Table 19.2 Jurisdiction over Food Safety in the United States
FDA Oversees the safety of approximately 80% of domestic and imported food, including seafood, dairy, produce, eggs in the shell, and bottled water. Monitors for the safety of animal feed. Supports state and local efforts through the Model Food Code, guidance, training and technical assistance, and evaluation services.
USDA Oversees the safety of meat, poultry, and some egg products, in settings including processing plants, retail outlets, and restaurants. Inspects meat processing plants, which can be carried out in conjunction with state programs and certification of imported meat products. Establishes quality and marketing grades for many foods and oversees the national organic labeling standards (see Text Box 19.2).
CDC Monitors and investigates foodborne illness outbreaks, often in coordination with state and local health departments. Coordinates FoodNet surveillance (www.cdc.gov/foodnet) and data analysis of 9 foodborne pathogens. Oversees DNA tracing of pathogens through PulseNet, a network of laboratories in each state.
EPA Monitors drinking water and regulates toxic chemicals, such as pesticides, through the Food Quality Protection Act.
State and local Inspect restaurants, grocery stores, day-care
1102
agencies and health departments
facilities, hospitals, schools, and some food manufacturing plants, and investigate complaints. Train food service workers. Conduct outreach to food service establishments and consumers during recalls and foodborne outbreaks. Coordinate surveillance and responses to outbreaks with the CDC.
One of the criticisms of the U.S. food safety regulatory framework is the almost comical fragmentation of authority across different agencies. Although the FDA and USDA continue to have primary jurisdiction (Figure 19.11), authority over the food safety measures listed earlier is dispersed across a total of fifteen agencies and hundreds of state and local health departments, involving twenty- eight House and Senate committees and three dozen food safety– related statutes. For example, the USDA regulates egg-laying facilities and processed egg products, but the FDA has authority over the grain fed to laying hens and the eggs themselves while still in the shell. Responsibility for frozen pizza depends on the pizza topping: the FDA for cheese, the USDA for pepperoni (Sheingate, 2014). The USDA inspects sausage meat, but the casings that enclose the meat are the FDA's jurisdiction because they have no nutritional value (Goetz, 2010); or that sausage may be covered under state or local authority if it is made and sold in the same location (USDA, FSIS, 2013b). This overlapping of jurisdiction can complicate and hinder efforts to protect the food supply.
1103
Figure 19.11 A U.S. Department of Agriculture Food Safety Inspection Service Inspector at a Poultry Processing Facility in Accomac, Virginia, Testing for Cleanliness and the Avian Influenza (AI) Virus
Source: USDA, 2006.
The Codex Alimentarius is a set of internationally recognized standards and procedures for food safety and fair trading practices in the increasingly global food trade. Codex member countries cover 99% of the global population and the standards are managed by a commission operating within the Food and Agricultural Organization of the United Nations and the World Health
1104
Organization (Codex Alimentarius, 2015). The Codex has far- reaching implications, often serving as the basis for national food safety legislation in countries without national food safety programs. World Trade Organization members may cite the Codex in challenging food safety and quality measures that are stricter than Codex standards.
Gaps and Challenges in Food Safety Protection The U.S. Government Accountability Office is highly critical of the fragmentation and inefficiency of government oversight over food safety, although it acknowledges that improvements have been made under the FSMA (U.S. GAO, 2004, 2014). Its recommendations include a broad overhaul of the food safety framework to create more centralized leadership and establish an institutionalized collaboration among agencies with a government- wide food safety plan. Such a broad approach to prevention is highly consistent with public health principles (see Chapter 26). Importantly, to be effective, new food safety programs must be based on a clear understanding of actual conditions contributing to risk and on data-driven priority setting. For example, food safety policy affecting workers commonly focuses on training, but many food service workers say they know what to do but are stymied by social and structural barriers to using hygienic practices, including a lack of paid sick days and intense pressures to perform quickly in often-insecure, low-paying jobs (Clayton, Smith, Neff, Pollack, & Ensminger, 2015).
With an increasing push for harmonization of food safety regulations and practices in the United States and worldwide, there is debate about the extent to which policies should be tailored according to risk, based on such factors as food type, farm size or a company's performance record. Broadly applying stringent food safety policies, such as HACCP requirements, would likely simplify global trade for the largest food manufacturers and result in more universal use of certain practices. It could, however, pose a significant burden for small-scale farmers, processors, or retailers who do not benefit from the same economies of scale, and who operate largely outside the lengthy industrial food chain (such as the farmers' market in Figure 15.7, in Chapter 15).The new FSMA rules will likely include some exemptions and considerations for
1105
small-scale farmers who sell direct to customers.
1106
Making Change: Food System Policy It is clear that the way we grow, process, distribute, and choose food can have substantial effects on our health, the health of the environment, and long-term food security. There are many ways to shift toward a healthier food system, including encouraging entrepreneurial activities, creating demand for alternative products, building infrastructure, supporting research and development on improved agricultural methods, incentivizing production and consumption of healthier foods and other desirable activities, and restricting or disincentivizing unwanted activities. Additionally, consumers impact the food system with every purchase they make, every bite they eat, and every vote they cast.
Consumer demand has had major impacts on the food system, particularly in recent years with people's increasing awareness and concern about how food gets from farm to plate. It has been argued, however, that far greater potential for improving public health outcomes would come from addressing socioeconomic factors, such as poverty, and improving food environments so that individuals' “default” food choices are healthier (Story, Kaphingst, Robinson- O'Brien, & Glanz, 2008). Well-crafted policies can address the negative impacts of food production practices, increase the availability of healthy foods, shift demand, and more. In this section we explore the roles specific policies have played in shaping our current food system and the importance—and challenge—of using policy as a tool to create food system change.
In the United States, food system policy is dispersed among thousands of laws, regulations, and agreements across many different agencies at the local, state, federal, and international levels (Table 19.3). While food policies originally focused on correct labeling and the safety of products for consumers, farm policies have historically been based on the economic needs of farmers, the need for a steady supply of food, and maintaining the soil and water resources for food production (Muller, Tagtow, Roberts, & Macdougall, 2009).
Table 19.3 Some of the Many Policies Shaping the U.S. Food System
1107
Federal levels State and local levels Farm Bill Trade policy (domestic, international) Food assistance (domestic, international) Child Nutrition Act Food safety policies (including the Food Safety Modernization Act) Regulations on food labeling and marketing Dietary guidelines Procurement policies Tax policy Regulation of feed additives Regulation of biotechnology Labor standards Clean Water Act Clean Air Act Occupational safety and health standards and regulations
Food safety policies, such as restaurant inspections and training Zoning and licensing requirements Land-use policies and planning Economic development policies and planning Infrastructure investments Nuisance laws Tax policy and incentives Limits on industry access to schools Food procurement Food policy councils Limits on specific additives
Note: These categorizations are not absolute; for example, some states do engage in policymaking in areas listed in the federal category.
Some agencies juggle competing interests as they make policy. The USDA, for example, has a leading role in developing the national nutrition guidelines that recommend eating more fruits and vegetables, but at the same time it supports the corn-based agricultural system that contributes to the ubiquity and relatively low retail price of meat and high-sugar, processed foods.
One of the largest policies that influences the operation of our food system is the federal Farm Bill, multiyear “omnibus” legislation with provisions for farm commodity supports, land conservation, nutrition assistance programs, and many other large and small government programs affecting agriculture and food. The 2014 Farm Bill is projected to cost approximately $490 billion in mandatory spending over five years, with programs and initiatives under the nutrition title, which includes funding for the
1108
Supplemental Nutrition Assistance Program (SNAP), receiving about 80% of those funds (Monke, 2014). Approximately $65 billion is designated to support commodity crops such as corn and soybeans, enabling purchasers to buy them at prices below the cost of production for uses including animal feed, biofuels, and processed food. Relatively little funding goes to support so-called specialty crops, including the fruits and vegetables that are supposed to make up the majority of a healthy diet, although the portion is growing. Funds to encourage farm use of conservation and sustainable practices are also relatively small but growing.
Given its size and impact, the Farm Bill would seem a logical platform for promoting public health, and indeed, public health professionals have advocated changes in recent Farm Bills. But gridlock in Congress has caused many advocates to grow frustrated with federal policy and to turn their focus to opportunities at the state and local levels. Often more workable, state and local policy arenas can also serve as laboratories for piloting new programs that can be scaled up if appropriate. Certain policy approaches may also make sense on a state or local scale yet not be suitable for a national program. Food policy councils bring together stakeholders, including engaged consumers, to address many of the food system– related policy decisions that largely take place at a local level, such as decisions on land use and zoning, on food safety regulations for such sources as food trucks and mobile vendors, and on rules governing school food sourcing. Between 2000 and 2014, the number of food policy councils in North America grew from 16 to 263 (Scherb, Palmer, Frattaroli, & Pollack, 2012).
The nature of agriculture and the infrastructure involved in the industrialized food system make reform slow, particularly at the national and international levels. Crafting effective food system policy is difficult because of the complexity of the interactions among the various parts, stakeholder interests, and the potential for far-ranging consequences. Too often, potential solutions to complex problems challenge conventional wisdom, assumptions, and beliefs. For example, despite shorter transport distances, locally produced food may have higher levels of embedded transportation-related energy than food from the conventional food supply chain does, due to the different vehicle types used. Similarly, in terms of food- related greenhouse gas emissions, forgoing dairy and meat one day
1109
per week would reduce food-related greenhouse gas emissions more than buying only locally grown foods (Weber & Matthews, 2008). Despite these realities, local food systems have many social, economic, and community benefits.
1110
Summary The food system nourishes us and provides livelihoods for a significant portion of the global population. But the modern industrialized food system wastes or undermines many of the resources on which it depends—water, energy, soil, a stable climate, and biodiversity. Population growth, urbanization, and growing volumes of travel and trade have contributed to new threats to food safety, global food security, and long-term food system sustainability.
Although important environmental public health hazards emerge from every sector of the food system, food waste, the increasing demand for meat, and the industrial food animal production system that meets that demand have been recognized as having particularly significant impacts on the environment and human health. Reducing both meat consumption and waste of food and also shifting toward more sustainable food production practices could help us meet our future food needs with fewer resources.
1111
Key Terms agroecological practices
Practices that apply ecological principles to agriculture in ways that mimic natural processes and conserve ecological integrity. Related terms include ecological agriculture, agricultural ecology, sustainable agriculture, and permaculture.
Bacillus thuringiensis (Bt) A soil-dwelling bacterium often used as a biological pesticide. Food crops have had Bt genes inserted; these crops are a major example of genetically modified organisms.
biodiversity The variety, and degree of variation, of different types of organisms found within an area or ecosystem or on the planet.
biomass Biological material derived from living or recently living organisms.
Codex Alimentarius A collection of internationally recognized standards, codes of practice, guidelines, and other recommendations relating to foods, food production, and food safety.
commodities Agricultural crops produced and marketed on a large scale, including corn, soybeans, cotton, rice, and wheat.
concentrated animal feeding operation (CAFO) Agricultural operations that keep and raise animals in confined situations. The EPA defines a CAFO (pronounced kayfo) as a facility that confines animals for at least forty-five days per year, without grass or other vegetation, in the confinement area during the normal growing season.
conservation tillage Any method of soil cultivation that leaves the previous year's crop residue (e.g., corn stalks or wheat stubble) on fields between harvesting one crop and planting the next crop, to reduce soil erosion and runoff.
critical control point (CCP) In the HACCP system, a step in the food production process at
1112
which a potential food safety hazard exists but can be controlled by an intervention.
cross-contamination The spread of pathogens between foods via, for example, unwashed hands, equipment, or cooking utensils.
dead zone An area of water in which excess nutrients have caused excessive algal blooms that, as they die off and decompose, deplete the oxygen in the water and make it uninhabitable for aquatic life.
ecosystem services Benefits that humans derive from ecosystems.
embodied energy The sum of all the energy required to produce a good or a service.
eutrophication The enrichment of a body of water with nutrients, typically phosphates or nitrates, leading to excessive algal growth, depletion of oxygen in the water, and possibly the death of other organisms such as fish. Eutrophication may occur naturally, but human activity such as fertilizer application on nearby land or poor sewage management can greatly accelerate it.
Farm Bill A multiyear, highly complex piece of U.S. federal legislation that governs an array of agricultural and food programs.
Food Code A model, published by the FDA, that provides state, local, and tribal food control authorities with a technical and legal basis for regulating the retail and food service industries, including restaurants, grocery stores, and institutions such as nursing homes (also called Model Food Code).
food desert An area with low access to healthy foods, commonly a low- income urban or rural area without nearby supermarkets.
food environment All aspects of our surroundings that may influence our diets, including physical locations of stores, marketing, media, and online exposures.
1113
food loss The decrease in edible food mass at the production, postharvest, and processing stages of the food chain.
Food Quality Protection Act A 1996 U.S. federal law amending the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) and the Federal Food, Drug, and Cosmetic Act (FFDCA). Major provisions altered the EPA's approach to pesticide regulation, requiring stricter safety standards, especially for infants and children, a complete reassessment of all existing pesticide tolerances, and the establishment of a standard of “reasonable certainty of no harm.”
food recalls Voluntary actions by manufacturers or distributors to protect the public from products that may cause health problems or possibly death.
Food Safety Modernization Act (FSMA) U.S. federal legislation passed in 2011 that reformed federal regulation of food safety.
food security A condition in which all people, at all times, have physical and economic access to sufficient, safe, and nutritious food to meet their dietary needs and food preferences for an active and healthy life.
food waste Discarded edible foods, either at any point along the food chain or, in some definitions, only at the retail and consumer levels. Examples include cooking loss; natural shrinkage (such as with moisture loss); loss from mold, pests, or inadequate climate control; food discarded by retailers due to color or appearance; and plate waste and other food discarded by consumers.
FoodNet Foodborne Diseases Active Surveillance Network, a collaborative effort of the CDC, USDA, FDA, and local health departments to conduct surveillance for common foodborne pathogens.
fossil aquifer An underground body of water, in a bed or layer of earth, gravel, or porous stone, established thousands or millions of years ago
1114
under past climatic and geological conditions, that cannot be replenished on a human time scale.
genetically modified organism (GMO) An organism whose genome has been altered through the techniques of genetic engineering so that its DNA contains one or more genes not normally found there.
glyphosate A broad-spectrum, systemic herbicide used to kill weeds that compete with commercial crops and grow in lawns and gardens. The most common glyphosate product is Roundup. A gene for glyphosate resistance, inserted into corn and other food crops, is a major example of genetic modification of food.
harmful algal bloom (HAB) An accumulation of algae in a body of water that can damage other organisms.
Hazard Analysis and Critical Control Point (HACCP) HACCP (pronounced hassip) is a food safety system in which each step in the manufacture, storage, and distribution of food is analyzed and measures are implemented to reduce and/or eliminate identified potential risks before they occur.
herbicide tolerance The ability of a plant species to survive and reproduce after being exposed to an herbicide.
industrial food animal production (IFAP) IFAP (pronounced eye-fap) is an approach to meat, dairy, and egg production characterized by specialized operations designed for a high rate of production, large numbers of animals confined at high density, large quantities of localized animal waste, and substantial inputs of capital, fossil fuel, feed, pharmaceuticals, and indirect inputs (e.g., fuel and water) embodied in feed.
inputs Resources and materials entering a production system: for example, the feed, drugs, energy, water, and labor that go into the food system.
integrated pest management (IPM) A system of controlling pests that applies the least toxic pesticides possible and only as a last resort after trying other control measures.
1115
integrators Companies that coordinate multiple successive stages of the supply chain in the hog and poultry industries.
manure cesspits Open-air, earthen storage basins for liquid cattle or swine waste from concentrated animal feeding operations (CAFOs).
monocultures Extensive plantings of a single variety of a single crop.
organic food Food produced without the use of synthetic pesticides and fertilizers, and animal products produced without hormones or antibiotics.
persistent organic pollutants Toxic chemicals that persist and accumulate in the environment and are passed from one species to the next through the food chain.
potentially hazardous food Food that contains moisture and protein, is pH neutral or slightly acidic, and is capable of supporting the rapid and accelerating growth of infectious or toxigenic microorganisms.
prerequisite programs Practices and conditions considered essential for food safety, implemented prior to and during the implementation of HACCP.
PulseNet A network of federal, state, and local laboratories that conduct DNA “fingerprinting” of bacteria to analyze and detect foodborne outbreaks.
specialty crops Noncommodity crops, including fruits, vegetables, tree nuts, and horticulture and nursery plants.
time and temperature controls Procedures that aim to avoid the growth of pathogens, including avoiding keeping food in the “danger zone” (between 40° and 140°F).
traceability In food safety, the ability to track any food, feed, substance, or livestock through all stages of production, processing, and
1116
distribution.
1117
Discussion Questions 1. Please review Text Box 19.1, regarding policy approaches to
agricultural antibiotic use.
Do you think the United States can accomplish changes in how antibiotics are used animal agriculture like those seen in Denmark? Why or why not?
What are the main barriers to minimizing or ending antibiotic misuse in animal agriculture in the United States? How could these barriers be addressed?
2. Go to the Web site of your local health department. Look up the food inspection results from the last three restaurants at which you ate. Describe any violations you see. Do you have any concerns? Are you confident that the inspectors were able to detect all significant problems?
3. Please review Text Box 19.2. What does the USDA Organic label mean to you? What are the pros and cons of large multinational food companies dominating the organic food sector?
4. What are the benefits of taking a systems approach to studying the environmental public health implications of our food?
5. Which comes first in changing the food system: supply or demand?
1118
References Academy of Nutrition and Dietetics, American Nurses Association, American Planning Association, and American Public Health Association. (2012). Principles of a healthy, sustainable food system. Retrieved from https://www.apha.org/ ∼/media/files/pdf/topics/healthy_sustainable_food_systems_principles_2012may.ashx
Agriculture and Community Development Services. (n.d.). Agricultural trends profile for Duplin County, NC. Retrieved from http://www.duplincountync.com/pdfs/Agricultural%20Trends%20Profile%20for%20Duplin%20County.pdf
American Association for the Advancement of Science. (2102). Statement by the AAAS board of directors on labeling of genetically modified foods. http://www.aaas.org/sites/default/files/AAAS_GM_statement.pdf.
Antoniou, M., Habib, M.E.M., Howard, C. V., Jennings, R. C., Leifert, C., Nodari, R. O.,…Fagan, J. (2012). Teratogenic effects of glyphosate-based herbicides: Divergence of regulatory decisions from scientific evidence. Journal of Environmental and Analytical Toxicology, S4-006.
Balfour, Lady Eve. (1977). Towards a sustainable agriculture—the living soil. Presentation at the IFOAM Conference, Sissach, Switzerland. Retrieved from http://www.soilandhealth.org/01aglibrary/010116balfourspeech.html
Batz, M. B., Hoffmann, S., & Morris, J. G. (2012). Ranking the disease burden of 14 pathogens in food sources in the United States using attribution data from outbreak investigations and expert elicitation. Journal of Food Protection, 75(7), 1278–1291.
Beaulac, J., Kristjansson, E., & Cummins, S. (2009). A systematic review of food deserts, 1966–2007. Preventing Chronic Disease, 6(3), A105.
Benbrook, C. M. (2012). Impacts of genetically engineered crops on pesticide use in the U.S.—the first sixteen years. Environmental Sciences Europe, 24, 24.
1119
Buck E. H. (2010). Seafood marketing: Combating fraud and deception. Congressional Research Service. Retrieved from http://nationalaglawcenter.org/wp- content/uploads/assets/crs/RL34124.pdf
Burkett, A. (2012). Food safety in the United States: Is the Food Safety Modernization Act enough to lead us out of the jungle? Alabama Law Review, 63(4), 919–940.
Buzby, J. C., Wells, H. F., & Hyman, J. (2014). The estimated amount, value, and calories of postharvest food losses at the retail and consumer levels in the United States (U.S. Department of Agriculture Economic Information Bulletin No. EIB-121). Retrieved from http://www.ers.usda.gov/publications/eib-economic- information-bulletin/eib121.aspx#.VEp2mRYnmHs
Canfield, D. E., Glazer, A. N., & Falkowski, P. G. (2010) The evolution and future of Earth's nitrogen cycle. Science, 330(6001), 192–196.
Center for Science in the Public Interest. (2014). Risky meat: A CSPI field guide to meat & poultry safety. Retrieved from http://cspinet.org/foodsafety/riskymeat.html
Centers for Disease Control and Prevention. (2011). CDC estimates of foodborne illnesses in the United States. Retrieved from http://www.cdc.gov/foodborneburden/2011-foodborne- estimates.html
Centers for Disease Control and Prevention. (2012, March 14). CDC research shows outbreaks linked to imported foods increasing: Fish and spices the most common sources (Press release). Retrieved from http://www.cdc.gov/media/releases/2012/p0314_foodborne.html
Centers for Disease Control and Prevention. (2013a). Antibiotic resistance threats in the United States, 2013. Retrieved from http://www.cdc.gov/drugresistance/threat-report-2013/pdf/ar- threats-2013-508.pdf
Centers for Disease Control and Prevention. (2013b). Contribution of different food commodities (categories) to estimated domestically-acquired illnesses and deaths, 1998-2008. Retrieved
1120
from http://www.cdc.gov/foodborneburden/attribution- image.html#foodborne-illnesses
Centers for Disease Control and Prevention. (2013c). PulseNet & foodborne disease outbreak detection. Retrieved from http://www.cdc.gov/features/dsPulseNetFoodborneIllness
Clayton, M. L., Smith, K. C., Neff, R. A., Pollack, K. M., & Ensminger, P. (2015). Listening to food workers: Factors that impact proper health and hygiene practice in food service. International Journal of Occupational and Environmental Health. Advance online publication.
Codex Alimentarius. (2015). About Codex. Retrieved from http://www.codexalimentarius.org/about-codex/en
Collignon, P., Powers, J. H., Chiller, T. M., Aidara-Kane, A., & Aarestrup, F. M. (2009). World Health Organization ranking of antimicrobials according to their importance in human medicine: A critical step for developing risk management strategies for the use of antimicrobials in food production animals. Clinical Infectious Diseases, 49(1), 132–141.
Diaz, R. J., & Rosenberg, R. (2008). Spreading dead zones and consequences for marine ecosystems. Science, 321(5891), 926–929.
Donham, K. J. (2010). Community and occupational health concerns in pork production: A review. Journal of Animal Science, 88(13, Suppl.), E102–111.
European Commission, Directorate-General for Research and Innovation. (2010). A decade of EU-funded GMO research (2001– 2010). Luxembourg: Publications Office of the European Union. Retrieved from http://ec.europa.eu/research/biosociety/pdf/a_decade_of_eu- funded_gmo_research.pdf
Food and Agriculture Organization of the United Nations. (2011a). Global food losses and food waste—extent, causes, and prevention. Retrieved from http://www.fao.org/docrep/014/mb060e/mb060e.pdf
Food and Agriculture Organization of the United Nations. (2011b).
1121
State of land and water resources for agriculture. Retrieved from http://www.fao.org/docrep/015/i1688e/i1688e00.pdf
Food and Agriculture Organization of the United Nations. (2013). Food wastage footprint: Impacts on natural resources. Retrieved from http://www.fao.org/docrep/018/i3347e/i3347e.pdf
Furuno, T. (2001). The power of duck: Integrated rice and duck farming. Sisters Creek, Tasmania: Tagari.
Goetz, G. (2010). Who inspects what? A food safety scramble. Food Safety News. Retrieved from http://www.foodsafetynews.com/2010/12/who-inspects-what-a- food-safety-scramble/#.VEuvPRYnmHt
Gossner, C. M.-E., Schlundt, J., Ben Embarek, P., Hird, S., Lo-Fo- Wong, D., Beltran, J. J.,…Tritscher, A. (2009). The melamine incident: Implications for international food and feed safety. Environmental Health Perspectives, 117(12), 1803–1808.
Gould, L. H., Walsh, K. A., Vieria, A. R., Herman, K., Williams, I. T., Hall, A. J., & Cole, D. (2013). Surveillance for foodborne disease outbreaks—United States, 1998–2008. Morbidity and Mortality Weekly Report, 62(SS02), 1–34.
Graham, J. P., & Nachman, K. E. (2010). Managing waste from confined animal feeding operations in the United States: The need for sanitary reform. Journal of Water and Health, 8(4), 646–670.
Guyton, K. Z., Loomis, D., Grosse, Y., El Ghissassi, F., Benbrahim- Tallaa, L., Guha, N.,…Straif, K. (2015). Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate. Lancet: Oncology, 16(5), 490–491.
Hall, K. D., Guo, J., Dore, M., & Chow, C. C. (2009). The progressive increase of food waste in America and its environmental impact. PLoS One, 4(11).
Hathorn, B. (2012). Jack in the Box in Laredo, Texas IMG 6011 [Photo]. Retrieved from http://commons.wikimedia.org/wiki/File:Jack_in_the_Box_in_Laredo,_Texas_IMG_6011.JPG#/media/File:Jack_in_the_Box_in_Laredo,_Texas_IMG_6011.JPG
Hilbeck, A., Binimelis, R., Defarge, N., Steinbrecher, R., Székács, A.,
1122
Wickson, F.,…Wynne, B. (2015). No scientific consensus on GMO safety. Environmental Sciences Europe, 27, 4.
Horrigan, L. (Producer), & Moore, A. (Director). (2010). Out to pasture: The future of farming? [Motion picture]. USA.
Hossain, S. T., Sugimoto, H., Ahmed, G.J.U., & Islam, M. R. (2005). Effect of integrated rice-duck farming on rice yield, farm productivity, and rice-provisioning ability of farmers. Asian Journal of Agriculture and Development, 2(1&2), 79–86.
Howard, Sir Albert. (1943). An agricultural testament. New York: Oxford University Press.
Hueston, W., & McLeoad, A. (2012). Improving food safety through a One Health approach: Workshop summary. Washington, DC: National Academies Press.
Hulebak, K. L., & Schlosser, W. (2002). Hazard Analysis and Critical Control Point (HACCP) history and conceptual overview. Risk Analysis, 22(3), 547–552.
International Food Information Center Foundation. (2012). Food and health survey. Retrieved from www.foodinsight.org/Content/5519/IFICF_2012_FoodHealthSurvey.pdf
Jackson, L. S. (2009). Chemical food safety issues in the United States: Past, present and future. Journal of Agriculture and Food Chemistry, 57(18), 8161–8170.
Kensler, T. W., Roebuck, B. D., Wogan, G. N., & Groopman, J. D. (2011). Aflatoxin: A 50-year odyssey of mechanistic and translational toxicology. Toxicological Sciences, 120, S28–48.
Kim, B., Laestadius, L., Lawrence, R., Martin, R., McKenzie, S., Nachman, K.,…Truant, P. (2013) Industrial food animal production in America: Examining the impact of the Pew Commission's priority recommendations. Johns Hopkins Center for a Livable Future. Retrieved from http://www.jhsph.edu/research/centers- and-institutes/johns-hopkins-center-for-a-livable- future/_pdf/research/clf_reports/CLF-PEW-for%20Web.pdf
Kirschenmann, F. (2000). The hijacking of organic agriculture…and
1123
how USDA is facilitating the theft. International Federation of Organic Agriculture Movements (IFOAM); Ecology and Farming. Retrieved from www.organicconsumers.org/old_articles/Organic/kirschenmann.php
Kummerer, K. (2004). Resistance in the environment. Journal of Antimicrobial Chemotherapy, 54, 311–320.
Kummu, M., de Moel, H., Porkka, M., Siebert, S., Varis, O., & Ward, P. J. (2012). Lost food, wasted resources: Global food supply chain losses and their impacts on freshwater, cropland, and fertiliser use. Science of the Total Environment, 438, 477–489.
Lawrence, R. S., Nachman, K. E., & Smith, T. J. (2013). Antibiotics: Collect more US data. Nature, 500(7463), 400.
Lelieveld, H. (2015). Mycotoxins: A food safety crisis. Food Safety, February 3. Retrieved from http://www.foodsafetymagazine.com/enewsletter/mycotoxins-a- food-safety-crisis
Levy, S. (2014). Reduced antibiotic use in livestock: How Denmark tackled resistance. Environmental Health Perspectives, 122, A160– 165.
Lu, C., Barr, D. B., Pearson, M. A., & Waller, L. A. (2008). Dietary intake and its contribution to longitudinal organophosphorus pesticide exposure in urban/suburban children. Environmental Health Perspectives, 116, 537–542.
Lucan, S. C. (2015). Concerning limitations of food-environment research: A narrative review and commentary framed around obesity and diet-related diseases in youth. Journal of the Academy of Nutrition and Dietetics, 115(2), 205–212.
Mamemachi, Y. (n.d.). Ducks in rice paddies under spotlights. Retrieved from http://www.detourjapan.com/furuno.html
Monke, J. (2014). Budget issues that shaped the 2014 Farm Bill (Congressional Research Service, 7-5700). Retrieved from http://nationalaglawcenter.org/wp- content/uploads/assets/crs/R42484.pdf
1124
Montgomery, D. R. (2007). Soil erosion and agricultural sustainability. Proceedings of the National Academy of Sciences of the United States of America, 104(33), 13268–13272.
Muller, M., Tagtow, A., Roberts, S. L., & Macdougall, E. (2009). Aligning food systems policies to advance public health. Journal of Hunger & Environmental Nutrition, 4(3–4), 225–240.
Nachman, K. E., Smith, T.J.S., & Martin, R. P. (2014). Antibiotics: Call for real change. Science, 343(6167), 136.
National Research Council. (2010). Toward sustainable agricultural systems in the 21st century. Washington, DC: National Academies Press.
Neff, R. A. (Ed.). (2014). Introduction to the U.S. food system: Public health, environment, and equity. San Francisco: Jossey- Bass/Wiley.
Neff, R. A., Parker, C. L., Kirschenmann, F. L., Tinch, J., & Lawrence, R .S. (2011). Peak oil, food systems, and public health. American Journal of Public Health, 101(9), 1587–1597.
Nicole, W. (2013). CAFOs and environmental justice: The case of North Carolina. Environmental Health Perspectives, 121(6), A182– 189.
North Carolina State Soil Science photostream. (n.d.). Herbicide application to corn [Photo]. Retrieved from https://www.flickr.com/photos/soilscience/5084823250
Ontl, T. A., & Schulte, L. A. (2012) Soil carbon storage. Nature Education Knowledge, 3(10), 35. Retrieved from http://www.nature.com/scitable/knowledge/library/soil-carbon- storage-84223790
Paganelli, A., Gnazzo, V., Acosta, H., López, S., L., & Carrasco, A. E. (2010). Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling. Chemical Research in Toxicology, 23(10), 1586–1595.
Painter, J. A., Hoekstra, R. M., Ayers, T., Tauxe, R. V., Braden, C. R., Angulo, F. J., & Griffin, P. M. (2013). Attribution of foodborne
1125
illnesses, hospitalizations, and deaths to food commodities by using outbreak data, United States, 1998–2008. Emerging Infectious Diseases, 19(3). Retrieved from http://wwwnc.cdc.gov/eid/article/19/3/pdfs/11-1866.pdf
Pimentel, D., & Pimentel, M. (1996). Energy use in fruit, vegetable, and forage production. In D. Pimentel & M. Pimentel (Eds.), Food, energy, and society (Rev. ed., pp. 131–147). Niwot: University Press of Colorado.
Porter, J. R., Xie, L., Challinor, A. J., Cochrane, K., Howden, M., Iqbal, M. M.,…Travasso, M. I. (2014). Food security and food production systems. In C. B. Field, V. R. Barros, D. J. Dokken, K. J. Mach, M. D. Mastrandrea, T. E. Bilir,…L. L. White (Eds.), Climate change 2014: Impacts, adaptation, and vulnerability: Part A. Global and sectoral aspects. Contribution of Working Group II to the Fifth Assessment Report of the Intergovernmental Panel on Climate Change (pp. 485–533). New York: Cambridge University Press.
Qadri, A.; Associated Press. (2012). India rotting grain [Photo]. Retrieved from http://www.apimages.com/metadata/Index/India- Rotting-Grain/b9334b69ccb8463db6d479c5f0953541/9/0
Sapkota, A. R., Lefferts, L. Y., McKenzie, S., & Walker, P. (2007). What do we feed to food-production animals? A review of animal feed ingredients and their potential impacts on human health. Environmental Health Perspectives, 115(5), 663–670.
Scallan, E., Hoekstra, R. M., Angulo, F. J., Tauxe, R. V., Widdowson, M. A., Roy, S. L.,…Griffin, P. M. (2011). Foodborne illness acquired in the United States—Major pathogens. Emerging Infectious Diseases, 17(1), 7–15.
Scherb, A., Palmer, A., Frattaroli, S., & Pollack, K. (2012). Exploring food system policy: A survey of food policy councils in the United States. Journal of Agriculture, Food Systems, and Community Development, 2(4), 3–14.
Schwab Foundation for Social Entrepreneurship and the World Economic Forum. (2001). Takao Furuno profile as Social Entrepreneur of the Year. Retrieved from
1126
http://www.schwabfound.org/content/takao-furuno
Scientific American Editors. (2009). Do seed companies control GM crop research? Scientific American, July 20. Retrieved from http://www.scientificamerican.com/article/do-seed-companies- control-gm-crop-research
Sheingate, A. (2014). Why America's food is still not safe. In R. Neff (Ed.), Introduction to the U.S. food system: Public health, environment, and equity (pp. 198–200). San Francisco: Jossey- Bass/Wiley.
Story, M., Kaphingst, K. M., Robinson-O'Brien, R., & Glanz, K. (2008). Creating healthy food and eating environments: Policy and environmental approaches. Annual Review of Public Health, 29, 253–272.
Taylor, M. R. (2011). Will the Food Safety Modernization Act help prevent outbreaks of foodborne illness? New England Journal of Medicine, 365(9), e18.
Thompson, F. (2011). Setting priorities for resource productivity. London: McKinsey Global Institute. Retrieved from https://www.mckinsey.com/assets/dotcom/HomeFeatures/Resource_Revolution/pdf/McKinsey_Resource_productivity.pdf
Tilman, D., Cassman, K. G., Matson, P. A., Naylor, R., & Polasky, S. (2002). Agricultural sustainability and intensive production practices. Nature, 418(6898), 671–677.
Truant, P. L., & Neff, R. A. (2014). Healthy food environments. In R. Neff (Ed.), Introduction to the U.S. food system: Public health, environment, and equity (chap. 17). San Francisco: Jossey- Bass/Wiley.
United Nations Conference on Trade and Development. (2013). Wake up before it is too late: Make agriculture truly sustainable now for food security in a changing climate (Trade and Environment Review 2013). Retrieved from http://unctad.org/en/pages/publicationwebflyer.aspx? publicationid=666
United Nations News Centre. (2013). India school deaths highlight need to phase out toxic pesticides. Retrieved from
1127
http://www.un.org/apps/news/story.asp? NewsID=45525#.VTabqJPzqap
U.S. Department of Agriculture. (2006). A U.S. Department of Agriculture Food Safety Inspection Service inspector at a poultry processing facility in Accomac, Virginia, testing for cleanliness and the avian influenza (AI) virus (Photo No. 20120106-OC-AMW- 0061). Retrieved from https://www.flickr.com/photos/usdagov
U.S. Department of Agriculture. (2014). Adoption of genetically engineered crops in the U.S. Retrieved from http://www.ers.usda.gov/data-products/adoption-of-genetically- engineered-crops-in-the-us/recent-trends-in-ge-adoption.aspx
U.S. Department of Agriculture, Agricultural Research Service. (2005). National Program 206: Manure and byproduct utilization; FY 2005 annual report. Retrieved from http://www.ars.usda.gov/research/programs/programs.htm? np_code=206&docid=13337
U.S. Department of Agriculture, Food Safety and Inspection Service. (2013a). Danger zone: (40°F–140°F). Retrieved from http://www.fsis.usda.gov/wps/portal/fsis/topics/food-safety- education/get-answers/food-safety-fact-sheets/safe-food- handling/danger-zone-40-f-140-f/ct_index
U.S. Department of Agriculture, Food Safety and Inspection Service. (2013b). Sausages and food safety (Fact sheet). Retrieved from http://www.fsis.usda.gov/wps/portal/fsis/topics/food-safety- education/get-answers/food-safety-fact-sheets/meat- preparation/sausages-and-food-safety/ct_index
U.S. Department of Agriculture, Food Safety and Inspection Service. (2015). Summary of recall cases in calendar year 2014. Retrieved from http://www.fsis.usda.gov/wps/portal/fsis/topics/recalls-and- public-health-alerts/recall-summaries
U.S. Environmental Protection Agency. (2009). Ag 101: Major crops grown in the United States. Retrieved from http://www.epa.gov/oecaagct/ag101/cropmajor.html
U.S. Environmental Protection Agency. (2013). Ag 101: Demographics. Retrieved from
1128
http://www.epa.gov/agriculture/ag101/demographics.html
U.S. Environmental Protection Agency. (2014a). Food recovery hierarchy. Retrieved from http://www2.epa.gov/sustainable- management-food/food-recovery-hierarchy
U.S. Environmental Protection Agency. (2014b). Sustainable management of food basics. Retrieved from http://www2.epa.gov/sustainable-management-food/sustainable- management-food-basics#what
U.S. Government Accountability Office. (2004). Federal food safety and security system: Fundamental restructuring is needed to address fragmentation and overlap (GAO-04-588T). Retrieved from http://www.gao.gov/products/GAO-04-588T
U.S. Government Accountability Office. (2011). Antibiotic resistance: Agencies have made limited progress addressing antibiotic use in animals (GAO-11-801). Washington, DC: Author.
U.S. Government Accountability Office. (2014). Federal food safety oversight: Additional actions needed to improve planning and collaboration (GAO-15-180). Retrieved from http://www.gao.gov/products/GAO-15-180
Vermeulen, S. J., Campbell, B. M., & Ingram, J.S.I. (2012). Climate change and food systems. Annual Review of Environment and Resources, 37(1), 195–222.
Wada, Y., van Beek, L.P.H., van Kempen, C. M., Reckman, J.W.T.M., Vasak, S., & Bierkens, M.F.P. (2010). Global depletion of groundwater resources. Geophysical Research Letters, 37, L20402.
Warner, K., Timme, W., Lowell, B., & Hirschfield, M. (2013). Oceana study reveals seafood fraud nationwide. Retrieved from http://oceana.org/sites/default/files/reports/National_Seafood_Fraud_Testing_Results_FINAL.pdf
Weber, C. L., & Matthews, H. S. (2008). Food-miles and the relative climate impacts of food choices in the United States. Environmental Science & Technology, 42(10), 3508–3513.
Whalon, M. E., Mota-Sanchez, D., & Hollingworth, R. M. (2008). Analysis of global pesticide resistance in arthropods. In M. E.
1129
Whalon, D. Mota-Sanchez, & R. M. Hollingworth (Eds.), Global pesticide resistance in arthropods (pp. 5–31). Cambridge, MA: CABI.
Wielinga, P. R., Jensen, V. F., Aarestrup, F. M., & Schlundt, J. (2014). Evidence-based policy for controlling antimicrobial resistance in the food chain in Denmark. Food Control, 40, 185– 192.
World Health Organization. (2005). Modern food biotechnology, human health and development: An evidence-based study. Geneva: World Health Organization, Food Safety Department. Retrieved from http://www.who.int/foodsafety/publications/biotech/biotech_en.pdf
World Health Organization. (2015). World Health Day 2015: From farm to plate, make food safe (News release). Retrieved from: http://www.who.int/mediacentre/news/releases/2015/food- safety/en
You, Y., & Silbergeld, E. K. (2014). Learning from agriculture: Understanding low-dose antimicrobials as drivers of resistome expansion. Frontiers in Microbiology, 5, 284.
1130
For Further Information Web Sites and Online Resources
The Food System
American Public Health Association, Toward a Healthy Sustainable Food System (Association policy, November 2007): http://www.apha.org/policies-and-advocacy/public-health-policy- statements/policy-database/2014/07/29/12/34/toward-a-healthy- sustainable-food-system
Nourish, Food system tools: http://www.nourishlife.org/teach/food-system-tools
Food Safety Just as food regulation is distributed among many agencies, so is food safety information. A gateway Web site is http://www.foodsafety.gov. Maintained by the Department of Health and Human Services, it aggregates information from several agencies, including the Centers for Disease and Control and Prevention, the Department of Agriculture, and the Food and Drug Administration. These agencies also maintain their own food safety Web sites:
CDC: http://www.cdc.gov/foodsafety
FDA: http://www.fda.gov/Food
USDA: http://www.usda.gov/wps/portal/usda/usdahome? navid=food-safety
Additional food safety Web sites are maintained by the Codex Alimentarius, European Commission, and World Health Organization:
Codex Alimentarius: http://www.codexalimentarius.org
EC: http://ec.europa.eu/food
WHO: http://www.who.int/foodsafety/en
1131
Books and Reports
The Food System In addition to Neff (2014) listed above in the References, see the following:
Alkon, A. & Agyeman, J. (2011) Cultivating food justice: Race, class, and sustainability. Cambridge, MA: MIT Press.
Blatt, H. (2008). America's food: What you don't know about what you eat. Cambridge, MA: MIT Press.
Brownell, K., & Horgen, K. B. (2004). Food fight: The inside story of the food industry, America's obesity epidemic, and what we can do about it. New York: McGraw-Hill.
Chen, W.-T., Clayton, M. L., & Palmer, A. (2015). Community food security in the United States. A survey of the scientific literature (Vol. 2). Baltimore: Johns Hopkins Center for a Livable Future. Available at http://www.jhsph.edu/research/centers-and- institutes/johns-hopkins-center-for-a-livable- future/_pdf/research/clf_reports/CFS-Lit-Review-II-final.pdf
DeGregori, T. R. (2002). Bountiful harvest: Technology, food safety, and the environment. Washington, DC: Cato Institute. Unlike most of the books cited here, this one, from a conservative think tank, celebrates the increased food production that technology has enabled, and argues that fears of adverse effects on health and the environment are overstated.
Friedberg S. (2009) Fresh: A perishable history. Cambridge, MA: Harvard University Press.
Genoways, T. (2014). The chain: Farm, factory, and the fate of our food. New York: Harper.
Hauter, W. (2014). Foodopoly: The battle over the future of food and farming in America. New York: New Press.
Low, S. A., Adalja, A., Beaulieu, E., Key, N., Martinez, S., Melton, A., …Jablonski, B.B.R. (2015). Trends in U.S. local and regional food systems: A report to Congress (Administrative Publication NO. AP- 068). Washington, DC: U.S. Department of Agriculture, Economic
1132
Research Service. Available at http://www.ers.usda.gov/publications/ap-administrative- publication/ap-068.aspx
Miller, D. (2013). Farmacology: What innovative family farming can teach us about health and healing. New York: HarperCollins.
National Research Council, Committee on Twenty-First Century Systems Agriculture. (2010). Toward sustainable agricultural systems in the 21st century. Washington, DC: National Academies Press.
Pollan, M. (2007). The omnivore's dilemma: A natural history of four meals. New York: Penguin.
Ronald, P., & Adamchak, R. (2010). Tomorrow's table: Organic farming, genetics and the future of food. New York: Oxford University Press.
Schlosser, E. (2001). Fast food nation: The dark side of the all- American meal. Boston: Houghton Mifflin.
Meat and Produce and the Balance Between Them
Hayes, D., & Hayes, G. B. (2015). Cowed: The hidden impact of 93 million cows on America's health, economy, politics, culture, and environment. New York: Norton.
Imhoff, D. (Ed.). (2010). The CAFO reader: The tragedy of industrial animal factories. Healdsburg, CA: Watershed Media.
Jacobson, M. F. (2006). Six arguments for a greener diet: How a more plant-based diet could save your health and the environment. Washington, DC: Center for Science in the Public Interest.
Kirby, D. (2011). Animal factory: The looming threat of industrial pig, dairy, and poultry farms to humans and the environment. New York: St. Martin's Press.
Leonard, C. (2014). The meat racket: The secret takeover of America's food business. New York: Simon & Schuster.
Lymbery, P. (2014). Farmageddon: The true cost of cheap meat. London: Bloomsbury.
1133
Niman, N. H. (2014). Defending beef: The case for sustainable meat production. White River Junction, VT: Chelsea Green.
Ogle, M. (2013). In meat we trust: An unexpected history of carnivore America. Boston: Houghton Mifflin Harcourt.
Pew Commission on Industrial Farm Animal Production. (2008). Putting meat on the table: Industrial farm animal production in America. Washington, DC, and Baltimore, MD: The Pew Charitable Trusts and Johns Hopkins Bloomberg School of Public Health. Available at http://www.ncifap.org/_images/PCIFAPFin.pdf
Sinclair, U. (1906). The jungle. New York: Doubleday, Page. Many modern reprints are available of this classic book, now over a century old, which portrayed the harsh lives of immigrants working in Chicago's meatpacking industry but also ignited public outrage over health and sanitary violations in the plants.
Food Safety
Benedict, J. (2001). Poisoned: The true story of the deadly E. coli outbreak that changed the way Americans eat. Buena Vista, VA: Inspire Books.
Institute of Medicine. (1998). Ensuring safe food: From production to consumption. Washington, DC: National Academies Press.
Knechtges, P.L. (2011). Food safety: Theory and practice. Burlington, MA: Jones & Bartlett Learning.
McSwane, D., Rue, N. R., & Linton, R. (2004). Essentials of food safety and sanitation (4th ed.). Upper Saddle River, NJ: Prentice Hall.
Shaw, I. C. (2012). Food safety: The science of keeping food safe. Hoboken, NJ: Wiley-Blackwell.
Food Policy and Politics
Alemanno, A., & Gabbi, S. (Eds.). (2014). Foundations of EU food law and policy: Ten years of the European Food Safety Authority. Burlington, VT: Ashgate.
Curtis, P.A. (Ed.). (2013). Guide to U.S. food laws and regulations.
1134
Hoboken, NJ: Wiley-Blackwell.
Fortin, N.D. (2007). Food regulation: Law, science, policy, and practice. Hoboken, NJ: Wiley.
Nestle, M. (2010). Safe food: The politics of food safety. Berkeley: University of California Press.
Nestle, M. (2013). Food politics: How the food industry influences nutrition and health (Rev. ed.). Berkeley: University of California Press.
Wilde, P. (2013). Food policy in the United States: An introduction. New York: Routledge.
1135
Chapter 20 Buildings and Health
Howard Frumkin
Dr. Frumkin's disclosures appear in the front of this book, in the section titled “Potential Conflicts of Interest in Environmental Health: From Global to Local.” Megan Cartwright, Anna Engstrom, and Marissa Smith report no conflicts of interest related to the authorship of the tox boxes.
1136
Key Concepts People spend about 90% of their time in buildings, so building conditions may have an important impact on health.
Principal building types include homes, schools, workplaces, and health care facilities.
Important health-related aspects of buildings include injury risks, exposure to pests, exposure to mold and moisture, indoor air quality, toxic exposures, and mental health effects.
Some populations are disproportionately exposed to building-related hazards and merit special public health attention.
Some people are especially vulnerable to building-related hazards; among these people are the elderly and people with disabilities.
Many techniques are available to achieve safe, healthy buildings.
Green buildings—buildings designed for environmental performance—offer a complementary approach to safe, healthy buildings.
“We give shape to our buildings, and they in turn shape us,” said Winston Churchill in a 1943 speech to the House of Commons. Indeed, we spend about 90% of our time in buildings, about two thirds of this at home. Employed people typically spend about eight hours per day at their workplaces, and students spend almost as much time in their schools. Some people (sometimes especially vulnerable people) may spend prolonged periods of time in specialized buildings, such as hospitals and prisons. Buildings are a typical human environment, and they matter greatly to our health and well-being.
This chapter explores environmental health on the scale of buildings. We take a broad view of health, extending beyond physical ailments to mental health and well-being. Buildings that are well built and maintained, welcoming, easily navigated, clean,
1137
safe, and comfortable can promote mental health (Evans, Wells, Chan, & Saltzman, 2000) and enhance comfort and well-being (Alexander, Ishikawa, & Silverstein, 1977; de Botton, 2006), and buildings that are environmentally sustainable can conserve energy and resources—important parts of health in the broadest sense.
1138
The Range of Buildings This chapter focuses on homes, schools, and health care facilities (workplaces are discussed in Chapter 21). These are the categories of buildings in which people spend most of their time, and/or are most vulnerable.
Homes Homes are where people spend more time than they do in any other building, and homes have long been recognized as a critical influence on health. In the words of Florence Nightingale, “The connection between the health and the dwelling of the population is one of the most important that exists” (quoted in Lowry, 1991).
The American Housing Survey, conducted about every four years by the U.S. Census Bureau for the Department of Housing and Urban Development, is a rich source of information. According to the 2011 survey (U.S. Census Bureau, 2013), there are approximately 132 million homes in the United States, of which 115 million are occupied year-round. Of these 132 million, approximately 76 million are owner occupied, 39 million are rental properties, 4 million are seasonal, and 13 million are vacant. About 83 million homes are detached, single-family houses, about 40 million are parts of multiple-unit structures such as duplexes and apartment houses, and about 9 million are manufactured homes or trailers (Figure 20.1 and Text Box 20.1). The median year of construction is 1974, and more than 40 million homes are over fifty years of age.
1139
Figure 20.1 Housing Can Take Many Forms and Vary Greatly in Desirability and Safety
Sources: High-rise apartment building: Marlith, 2007; hut: Tatoute, 2005; row houses:
1140
©iStockphoto.com/Frank van den Bergh; house with lawn: © Aberenyi/Dreamstime.com
1141
Text Box 20.1 Manufactured Structures In the aftermath of Hurricanes Katrina and Rita in 2005, more than 120,000 manufactured housing units (Figure 20.2) were deployed in the Gulf of Mexico region to shelter people who had been displaced from their homes. Within the first year, concerns arose about possible health problems among these residents. Many of these concerns focused on formaldehyde, but other concerns—such as moisture and mold—were raised as well.
Figure 20.2 Trailer Provided by FEMA after Hurricane Katrina
Source: Infrogmation, 2006. Permission granted under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation.
What were these units? Sometimes lumped together under the term trailers, manufactured structures in fact come in a variety of designs. Most common among the units used after Hurricanes Katrina and Rita were travel trailers—small
1142
(generally under 320 square feet), wheel-mounted trailers, originally designed to provide temporary living quarters during recreation, camping, or travel and regulated as vehicles rather than as buildings. There were also manufactured homes (formerly known as mobile homes)— larger (generally more than 320 square feet) structures built on a permanent chassis; containing plumbing, heating, air- conditioning, and electrical systems; and designed to be used as dwellings (with or without a permanent foundation) when connected to the required utilities. Still another design used was the park model, a larger version of a travel trailer, used as temporary living quarters.
These housing units deployed after the 2005 hurricanes were only a small part of a much larger universe. Millions of Americans live, go to school, and work in manufactured structures every day. With regard to housing, some units are used on a long-term basis, others for short-term recreational and travel use, and still others as temporary housing following disasters. In the 2011 American Housing Survey, of 132 million housing units in the United States, 9 million (6.8%) were manufactured homes, housing over 18 million Americans. With regard to schools, almost one in three public schools uses portable buildings (sometimes called modular classrooms) (Alexander & Lewis, 2014). Urban schools are more likely to have portable buildings than suburban or rural schools are, and the prevalence of portable buildings rises with minority enrollment, from a low of 13% in schools with less than 6% minority enrollment to a high of 45% in schools with 50% or more minority enrollment (Alexander & Lewis, 2014). No data are available on how many people work each day in manufactured structures, but construction trailers, sales offices, and other such uses are common.
Could manufactured structures raise health concerns? Indoor air quality is one such issue. Manufactured structures are built with particleboard, oriented strand board, fiberboard, and similar materials, and these can release volatile compounds, especially formaldehyde, over time. After Hurricane Katrina, a study of 519 temporary housing
1143
units in the Gulf Coast region showed elevated formaldehyde levels. The geometric mean was 77 parts per billion (ppb), two or three times the typical level in U.S. houses, and measurements ranged as high as several hundred ppb. Certain factors, such as small size (travel trailers as opposed to manufactured homes), high temperatures, and closed windows, predicted higher levels of formaldehyde. Because formaldehyde levels tend to be higher in newly constructed manufactured structures and during warmer weather, the Centers for Disease Control and Prevention (CDC) cautioned that observed levels likely underrepresented long-term exposures; many of the units studied were approximately two years old, and the study was conducted during the winter (CDC, 2008). As discussed in Tox Box 20.1, formaldehyde is irritating and may contribute to the development of respiratory and allergic symptoms in children. In addition it is considered a probable human carcinogen by several agencies.
Formaldehyde is not the only indoor air concern in manufactured structures; among the others are pesticides, environmental tobacco smoke, other volatile organic compounds, and carbon monoxide, as in any building. Nor is indoor air the only potential health issue in manufactured structures. Others exist, as may be true for any building: moisture and mold, fire safety issues, injury risks, and pests such as rats and mice, cockroaches, and dust mites. In addition, manufactured structures pose some unique challenges related to utility hookups (including water, sewage, and electricity), structural integrity, and proper tethering. The combination of light weight and lack of tethering helps to explain the devastation that tornadoes and other severe storms can wreak in trailer communities. Some of these problems may be widespread. For example, the 2011 American Housing Survey (U.S. Census Bureau, 2013) reported that of 9.0 million manufactured homes, more than 1.5 million had signs of rodents, 247,000 had sagging roofs, 231,000 had a visible holes in the roof, 779,000 had water leakage from the outside, 496,000 had broken windows, and 333,000 had foundations with visible crumbling or open cracks or holes.
1144
Manufactured structures offer important advantages. They are affordable, flexible, and rapidly installed. At a time when affordable housing is an ever more important national goal, and when school districts need affordable, flexible space options, manufactured structures will continue to play an important role. Standard public health principles apply in keeping people safe and healthy as they live, study, and work in these structures. Good design involves such features as adequate ventilation. Good construction involves using materials that do not emit dangerous levels of formaldehyde. Good installation involves secure placement and tethering. Good maintenance involves caring for the entire structure, avoiding leaks, maintaining good hygiene, and avoiding the introduction of hazards (Centers for Disease Control and Prevention and U.S. Department of Housing and Urban Development [CDC and HUD], 2011). Through these measures, the health and safety of the millions of people who use manufactured structures can be protected.
Some homes are substandard, posing obvious dangers to their inhabitants. In the 2011 American Housing Survey, safety hazards were common and included missing roofing material (3.1 million homes), broken windows (3.6 million), sagging roofs (1.7 million), broken or missing stairway railings (1.5 million) or steps (0.7 million), cracked or crumbling foundations (4.7 million), and loose steps (3.0 million). Over 14 million homes had signs of rodent infestation, and over 13 million signs of cockroaches. Water leakage was common, both from within the home (9.7 million) and from outside (12.5 million, about half of these through the roof). Six million homes lacked working smoke detectors, and 63 million homes lacked working carbon monoxide detectors.
1145
Tox Box 20.1 Volatile Organic Compounds (VOCs): The Case of Formaldehyde
What Is It? VOCs are organic compounds that, with high vapor pressures and low boiling points, evaporate quickly from solid or liquid forms. VOCs occur naturally in scents important to plant and animal communication. Manufactured products, such as paints and solvents also contain VOCs. One of the most commonly encountered, and best-studied, VOCs is formaldehyde.
Formaldehyde is the simplest aldehyde; its single carbon atom is bonded to an oxygen atom (via a double bond) and to two hydrogen atoms. The boiling point of formaldehyde is −2° Fahrenheit, so it vaporizes rapidly at room temperature.
How Is It Used? Formaldehyde is used as a chemical intermediate and in the manufacturing of many consumer products. Its chemical properties and low cost make it a useful component of adhesives, dyes, lubricants, paints, construction products such as particle board and insulation, paper, rubber, and textiles.
1146
HOW ARE PEOPLE EXPOSED? People are exposed to formaldehyde almost exclusively through inhalation. Everyone has low-level exposure to formaldehyde, but certain environments and occupations can greatly increase people's exposures. Formaldehyde can be released into indoor air from various consumer products. Cigarette smoke is the leading exposure source, followed by off-gassing from paints, glues, or solvents. Similarly, construction materials release formaldehyde, making newly constructed homes a potentially hazardous source of indoor inhalation exposure to formaldehyde. Following Hurricane Katrina, the U.S. Federal Emergency Management Agency (FEMA) deployed more than 120,000 mobile homes as temporary housing. Unfortunately, poor manufacturing and the high temperatures characteristic of the Gulf States led to substantial formaldehyde off-gassing and high exposures for people living in the so-called FEMA trailers. Outdoor air contains formaldehyde derived from vehicle exhaust, industrial manufacturing facilities, power plants, and incinerators; however, compared to indoor concentrations these amounts are relatively small. The relative concentrations of formaldehyde in outdoor air and indoor air
1147
are shown in Table 20.1. Mobile homes have significantly higher concentrations of formaldehyde than conventional homes. For reference, the concentration of formaldehyde in cigarette smoke is also shown.
Table 20.1 Average Exposure Concentrations of Formaldehyde and Contribution of Various Atmospheric Environments to Exposure to Formaldehyde
Formaldehyde in the air Concentration (mg/m3)
Outdoor air (10% of time, 2 m3/day) 0.001–0.02 Indoor air: homes (65% of time, 10 m3/day) Conventional 0.03–0.06 Mobile home 0.1 Environmental tobacco smoke: home or workplace
0.05–0.35
Smoking (20 cigarettes a day) 60–130
Source: World Health Organization, 2001.
Another way people encounter formaldehyde is on the job. Workers in the manufacturing sector are frequently exposed to formaldehyde. Recently, hair salons came under fire for exposing workers and customers to high levels of formaldehyde through a hair-straightening process called the Brazilian Blowout. The chemical interaction used in this process creates formaldehyde as a by-product at levels found to exceed the limit set by the Occupational Safety and Health Administration (OSHA). Other occupational exposures occur in laboratories where technicians use formaldehyde to preserve tissue samples.
WHAT ARE THE TOXIC EFFECTS? Like many toxicants, formaldehyde has different acute and chronic effects. Acute exposure to formaldehyde can lead to irritation of the respiratory system, eyes, skin, nose, and throat. High acute exposure can lead to more serious health
1148
impacts, including vomiting, nausea, coma, and possibly death. Formaldehyde is mutagenic, meaning it can damage DNA, which can lead to cancer. Both the U.S. Environmental Protection Agency (U.S. EPA) and the International Agency for Cancer Research (IARC) have classified formaldehyde as a probable human carcinogen, and the European Chemical Agency classifies formaldehyde as a known human carcinogen. Animal studies suggest that formaldehyde may cause birth defects following prenatal exposure. Vulnerable populations include pregnant women (fetal impacts), babies, children, and asthmatics.
HOW ARE PEOPLE PROTECTED? Primary prevention—replacing formaldehyde with other, less toxic substances, to eliminate exposure—is a key principle. Similarly, good manufacturing practices can greatly reduce off-gassing of formaldehyde. Formaldehyde standards exist at both international and national levels. The World Health Organization (WHO) recommends that indoor air concentrations not exceed 0.1 mg/m3. For many mobile home residents, this recommendation is exceeded because the average concentration of formaldehyde in mobile homes is 0.1 mg/m3. In the United States the EPA regulates formaldehyde emissions from composite wood products under the Toxic Substances Control Act. Regulation of indoor emissions from consumer products is complex because the concentration released changes over time and with environmental conditions, such as temperature and humidity. Occupationally, OSHA limits worker exposure to 0.27 parts of formaldehyde per million parts of air (ppm) over an eight-hour workday.
WANT TO LEARN MORE? A good (but dated) source is ATSDR's Toxicological Profile for Formaldehyde, published in 1999 (www.atsdr.cdc.gov/toxprofiles/tp111.pdf). A more current authoritative report is the section on formaldehyde in WHO Guidelines for Indoor Air Quality: Selected Pollutants, published in 2010
1149
(www.ncbi.nlm.nih.gov/books/NBK138711).
To learn more about formaldehyde exposure following Hurricane Katrina, see the CDC's Final Report on Formaldehyde Levels in FEMA-Supplied Travel Trailers, Park Models, and Mobile Homes, published in 2008 (www.cdc.gov/nceh/ehhe/trailerstudy/pdfs/femafinalreport.pdf).
Contributed by Marissa Smith
Substandard housing threatens well-being in a fundamental sense by undermining residents' dignity and security (Dupuis & Thorns, 1998). In addition, substandard housing can be a direct cause of injury and death. As described in Chapter 23, about 18,000 accidental deaths occur in homes each year in the United States, of which about 33% are due to falls, 26% to poisonings, 19% to burns, and the remainder to other causes. In addition to safety hazards, substandard housing may pose exposures to lead paint, cockroaches and dust mites, rats and mice, carbon monoxide, and other hazards (Krieger & Higgins, 2002; Howden-Chapman, 2004). Some of these hazards disproportionately target people with particular susceptibilities, such as the very young, the very old, and people with respiratory diseases such as asthma. People who live in substandard housing are more likely to report poor health (Adamkiewicz et al., 2013). Accordingly, improving housing for low- income communities is a key public health opportunity (Haines et al., 2013). Equally compelling is the provision of housing to those who are homeless, as discussed in Text Box 20.2.
Low-income families and members of ethnic minorities disproportionately live in substandard housing. But some housing hazards affect people across the population. For example, about one in seventeen U.S. homes has a radon level above 4 picocuries per liter (pCi/L), the Environmental Protection Agency's action level (National Research Council, Committee on Health Risks of Exposure to Radon, 1999). As discussed in Chapter 22 and in Tox Box 20.2 in this chapter, this exposure contributes substantially to lung cancer risk, especially among smokers.
1150
Text Box 20.2 Homelessness: An Environmental Health Problem? If a good home provides stability and security, and if substandard housing undermines these bedrocks of health and well-being, then housing insecurity and homelessness are especially pressing public health challenges. Housing insecurity is associated with unhealthy behaviors, with poor health outcomes, and with poor self-reported health (Liu, Njai, Greenlund, Chapman, & Croft, 2014; Stahre, VanEenwyk, Siegel, & Njai, 2015). And homelessness is associated with high rates of infectious diseases, mental disorders, substance abuse, and noncommunicable diseases, and with elevated mortality rates (Fazel, Geddes, & Kushel, 2014).
An obvious solution to homelessness is housing. In recent years experts on homelessness have advocated an approach called Housing First, which involves rapidly moving homeless people into permanent housing. Once people are housed, case management and supportive services are provided (Atherton & Nicholls, 2008). The notion is that permanent housing provides a needed foundation for addressing other issues, such as treating mental illness or locating employment.
This approach has been tested in Chicago (Sadowski, Kee, VanderWeele, & Buchanan, 2009), Seattle (Larimer et al., 2009), and other cities. Results have generally shown that rapid provision of housing leads to reduced health care utilization, improved health behaviors, and improved health outcomes (Fitzpatrick-Lewis et al., 2011). So while homelessness is a complex social problem, an important port of the solution lies in the built environment: providing housing.
Schools Schools are a second important category of building (Figure 20.3).
1151
There are 98,000 public schools in the United States, and about 50 million students attend them. An additional 5.1 million students attend 31,000 private schools. Children spend more time in their schools than in any other environment except home. And it is not only children who spend time in schools. They are joined by more than 3.5 million teachers, and over 2 million administrators, custodians, food service workers, security guards, and other staff (National Center for Education Statistics, 2013).
Figure 20.3 School Design Sources: Neighborhood school: Infrogmation, 2007; community school: Tewy, 2006. Permission granted under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation.
School design has changed dramatically over recent decades, from small, multistory schools embedded in neighborhoods to low-rise, rambling structures on large suburban or exurban parcels of land.
Like homes, schools may confront their occupants with a range of environmental hazards (Frumkin, Geller, Rubin, & Nodvin, 2006). In the mid-1990s, the U.S. General Accounting Office (GAO) issued detailed reports on the conditions of U.S. schools (GAO, 1995, 1996a, 1996b). The GAO found that at that time, one in three schools had buildings in need of extensive repair or replacement, and almost 60% reported a major building feature that needed extensive repairs, an overhaul, or replacement. In addition, about half the schools reported one or more unsatisfactory environmental conditions, such as poor ventilation, heating or lighting problems, or poor physical security.
1152
More recently, the U.S. Department of Education assessed public school conditions during the 2012–13 school year. There had not been much improvement in two decades. Essentially every building system and feature was found to be in fair or poor condition in a large proportion of schools: windows (32%); plumbing/lavatories (31%); HVAC system (30%); energy management system, security systems, and exterior lighting (29% each); the roof (25%); the electrical system (22%); interior lighting and life safety features (19% each); exterior walls/finishes (18%); and framing, floors, and foundations (14%) (Alexander & Lewis, 2014). These findings reflected conditions in permanent school buildings; in temporary structures such as trailers, which were present at nearly one third of schools, conditions were worse.
Mishaps occur in schools with disturbing regularity: in a high school on Long Island, New York, a ceiling collapsed onto a chemistry class, injuring nine students (Keane, 2003); an elementary school in Austin had to evacuate all 777 pupils and be closed for gutting and renovation when large amounts of Stachybotrys and Penicillium molds resulted from roof leaks (Mann, 2000), and another in Fairfield, Connecticut, had to be closed and razed because mold infestation had been associated with so much illness among students and staff (Wakefield, 2002); a roof collapsed at a Tennessee high school after heavy rains (at a time when, fortunately, nobody was inside) (Boehnke, 2013); and in Indiana a high school stage collapsed during a school performance, injuring sixteen students (Longnecker, 2015).
In addition to injury risks, longer term hazards are common in schools. These include inadequate ventilation and excessive levels of carbon dioxide, volatile organic compounds, bioaerosols, bacteria, dust mites, and animal allergens (Tranter, 2005; Godwin & Batterman, 2007; Annesi-Maesano et al., 2013). Conditions such as these pose both short-term and long-term threats to children's health and academic performance (Mendell & Heath, 2005; Mendell et al., 2013), as well as to teachers' health (Ervasti et al., 2012; Muscatiello et al., 2015), and may translate into higher health care costs as well. In developing nations, where ambient air pollution levels may be very high, and where many schools lack air filtration capabilities, the impacts on health can be substantial (Mi, Norbäck, Tao, Mi, & Ferm, 2006).
1153
Health Care Facilities Health care facilities are a special category of buildings. Patients with various ailments may be especially susceptible to environmental hazards and may stand to benefit greatly from healthy, restorative buildings. In addition, health care workers spend long hours in these facilities, often in high-stress jobs, so careful building design and operation protect them as well.
Health care facilities use a wide range of potentially toxic chemicals, such as mercury (in thermometers and other instruments), plastics (containing such components as phthalates), sterilizing agents (such as ethylene oxide), and cleaning materials (which are heavily used because sanitation is so important in health care facilities). Some medications, such as chemotherapeutic agents and radionuclides, can be toxic. However, safe and healthy clinical facilities do more than prevent exposure to dangerous chemicals. Growing evidence suggests that well-designed facilities can help prevent medical errors, reduce stress in both patients and staff, improve sleep, and improve clinical outcomes. These observations have given rise to the concept of evidence-based design—the idea that empirical data can guide architects and designers to achieve the best outcomes for patients and staff (Ulrich et al., 2008; Ferris, 2013). Research has documented best practices in settings ranging from operating rooms (Palmer et al., 2013) to intensive care units (Hamilton & Shepley, 2010) and from mental health facilities (Connellan et al., 2013) to hospice settings (Verderber, 2014). Some features that promote health and well-being include single rooms (as opposed to multibed rooms); noise reduction; high-quality lighting (including natural daylight); effective ventilation; and ergonomic designs (Ulrich, Zimring, Quan, & Choudhary, 2004; Marberry, 2006; Rashid & Zimring, 2008; Beale & Kittredge, 2014; Laursen, Danielsen, & Rosenberg, 2014). (Indeed, although evidence-based design originated in health care architecture, it is relevant to all types of buildings!)
Design features that promote health can also advance environmental goals. For example, avoiding the use of volatile organic chemicals protects both health and the environment. The use of natural daylight for lighting not only improves well-being and performance but also reduces energy demand. An exciting
1154
development in recent years has been the alignment of healthy health care design, with its primary focus on the health of patients and staff, and green health care, with its primary focus on environmental performance (Guenther & Vittori, 2013).
1155
Key Elements of a Healthy Building Good Lighting Good lighting is an important part of a healthy building. Whereas our ancestors used a variety of light sources—candles, fires, lanterns, and so forth—(or simply went to sleep when it got dark), modern buildings use two general sources of light: natural light and electric light. Sunlight refers to the direct, parallel rays of the sun; it is very bright, casts strong shadows, and may cause glare at close range. Daylight (or diffuse sunlight) is sunlight diffused by clouds, the Earth's atmosphere, reflection off a surface, or passage through translucent material. It is a soft, even source of light. Electric light comes from a variety of bulb types, including incandescent, fluorescent, and light-emitting diodes (LEDs).
Good lighting promotes health, well-being, and performance (Mead, 2008). In a school-based study, more daylight in classrooms was associated with 20% faster progress in acquiring math and reading skills (Heschong Mahone Group, 1999). In a hospital study, patients in intensive care units recovered faster if they were in rooms with windows (Guzowski, 2000). Office workers with windows report better health and job satisfaction (California Energy Commission, 2003). Conversely, poor lighting has negative consequences. Excessively bright lighting can cause squinting and headaches, dim lighting can cause eye strain, and flickering can cause headaches and discomfort. Adequate lighting in buildings is needed not only for comfort and performance but for safety; people need to be able to see potential trip and fall hazards and to find their way to exits in case of emergency.
Many guidelines for good lighting are available (Ander, 2003; Boubekri, 2008). Daylighting should be prioritized, not only because it promotes comfort and performance, but because it reduces energy demand. Daylight may come from windows, skylights, louvers, and clerestories. But because daylight is variable, it should be integrated with electric lighting. Areas where people need good illumination, such as at desks in schools and offices and at workstations in workplaces, should be well provided with soft, even light. Glare—as comes from direct views of a direct light source
1156
—should be minimized.
Injury Prevention Many types of injuries can occur in buildings. Some are work related, and those are discussed in Chapter 21. Others are common in homes, schools, and other buildings. Of these, the two most common are falls and burns.
Falls are a common cause of injuries in buildings, especially in homes; some statistics are presented in Chapter 23. Several risk factors are well recognized. These include stairs without banisters or handrails (a particular danger for small children and the elderly), windows on upper floors without window locks or safety guards (a danger for small children), bathtubs without mats or nonskid strips, poor lighting, slippery floors, uneven surfaces, and tripping hazards such as electrical cords (Tinetti, Speechley, & Ginter, 1988; American Academy of Pediatrics, 2001). Personal risk factors combine with environmental risk factors to play a role; among the elderly, for example, risks include having medical conditions such as orthostatic hypotension, visual or cognitive impairment, and balance and gait abnormalities, and taking certain medications (Chang et al., 2004). Although falls have been recognized as a major problem for the elderly (Rubenstein & Josephson, 2006), children are also at risk, both in the United States (Phalen, Khoury, Kalkwarf, & Lanphear, 2005) and in developing nations (Hyder, Sugerman, Ameratunga, & Callaghan, 2007). Many preventive strategies have been proposed, including banisters, railings, and stairway gates; locks and safety guards on windows; padded or carpeted floor surfaces; correction of hazards such as loose electrical cords; and attention to personal risk factors. Sometimes these approaches are combined in multifactorial risk reduction programs, in both home and institutional settings, although the evidence to support such interventions is incomplete (Gates, Fisher, Cooke, Carter, & Lamb, 2008; Young, Wynn, He, & Kendrick, 2013).
Burns are another common cause of injuries in buildings, and fire safety has long been recognized as a priority for safe buildings. In 2013, there were 487,500 structural fires in the United States, causing 2,855 deaths and 14,075 injuries (excluding those suffered by firefighters) and $9.5 billion in property damage (National Fire Protection Association, 2015). Fire extinguishers, fire escapes
1157
(especially on multistory buildings), sprinkler systems, design features such as stairways that are separated from floor spaces, nonflammable structural elements such as steel beams, and the use of fireproofing are all important safety measures (Buchanan, 2001; Purkiss, 2006). Many of these measures have been incorporated into the Fire Code and the related standards issued by the National Fire Protection Association (www.nfpa.org) and implemented at the state and local levels.
Smoke alarms are a key means of preventing injury or death due to home fires. They are associated with reductions in injuries and deaths due to residential fires in the range of 50% (Warda & Ballesteros, 2007) and possibly as much as 80% (Mallonee et al., 1996).
However, as is the case for falls, environmental measures need to be supplemented by behavioral interventions. It is a challenge to get people to install and maintain smoke alarms at home; programs that promote this behavior have had mixed results (Pearson, Garside, Moxham, & Anderson, 2011). One promising residential fire prevention program included smoke alarms, educational activities, and cooperation among local health departments, fire departments, community organizations, and the media (Ballesteros, Jackson, & Martin, 2005). In commercial buildings, schools, and other institutional settings, fire drills are an important adjunct to environmental approaches. Extensive recommendations are available at a Web site hosted jointly by the Centers for Disease Control and Prevention, the Consumer Product Safety Commission, and the U.S. Fire Administration (www.firesafety.gov).
Pest Control For as long as people have built and occupied buildings, they have shared them with pests. Chief among these pests are insects such as mites, termites, and cockroaches, and rodents such as mice and rats. These unwelcome visitors can have important consequences for health. Cockroach allergy, for instance, is a major contributor to asthma among inner-city children whose homes are infested (Matsui, 2014). Flies can spread foodborne pathogens such as salmonella. Rats can spread diseases such as rat-bite fever and plague and can infect people with hantavirus, aggravate allergies, and cause electrical damage by chewing wires. Termites can cause
1158
structural damage by destroying wooden beams. Strategies for controlling pests are described in Chapter 18.
Moisture and Mold Control Molds are those fungi that grow in the form of multicellular filaments called hyphae. Many thousands of species of mold are recognized, but only a small subset of them are described as occurring in buildings, with names such as Alternaria, Aspergillus, Cladosporium, Fusarium, Penicillium, Rhizopus, Stachybotrys, and Trichoderma. Molds share several features. First, they reproduce through spores, which can often survive for prolonged periods in inhospitable conditions. Second, they require moisture to reproduce and grow. Third, they derive their energy not through photosynthesis but from organic matter such as starch and cellulose. Molds are ubiquitous in nature, where they play essential roles in breaking down organic waste such as dead leaves. Molds have many useful applications; some are used to make cheese, soy sauce, and other foods, and others have given rise to medications such as penicillin (from Penicillium chrysogenum) and lovastatin (from Aspergillus terreus).
Mold spores are common throughout the environment, including building interiors, where they generally cause no problems. For mold to grow, three conditions are required: warmth, moisture, and nutrients. Most buildings contain plenty of nutrients, in walls, carpets, insulation, and other materials. Hence warm, moist conditions—say, in basements or showers—complete the requirements and may trigger excessive mold growth. Some buildings or parts of buildings routinely have conditions that encourage mold growth; think of a greenhouse, an indoor pool, or a laundry room. If a portion of a building becomes moist—say, if water infiltrates a roof or wall or accumulates under a carpet—then mold growth may result. Following a flood, when parts of a building have been immersed in water, mold growth is common (see Figure 20.4). Mold is not the only biological exposure that may occur in damp indoor spaces; others include bacteria such as Legionella, bacterial endotoxins, and dust mites.
1159
Figure 20.4 Mold-Damaged Building in New Orleans Following Hurricane Katrina
Source: Infrogmation, 2005. Permission granted under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation.
Mold can threaten health in several ways (Institute of Medicine, Committee on Damp Indoor Spaces and Health, 2004; World Health Organization, 2009; Meheust, Le Cann, Reboux, Millon, & Gangneux, 2014). First, some molds produce chemicals. These may be volatile organic compounds (VOCs), such as alcohols, ketones, and esters (Tox Box 20.1). These VOCs can cause the musty odors sometimes associated with mold growth, and they can cause symptoms in some people, such as irritation of the mucous membranes and headaches. Molds may also produce metabolic by- products called mycotoxins, which are toxic to humans (and other
1160
animals). The best known example, aflatoxin (from Aspergillus flavus), is not building related; it is encountered as a food contaminant. But some building-related molds, such as Stachybotrys, can also produce mycotoxins. Mycotoxins are not usually volatile; instead they settle on spores, on hyphal fragments, and on dust, become airborne, and are inhaled (Institute of Medicine, Committee on Damp Indoor Spaces and Health, 2004). Mycotoxins have been suspected of causing human disease after building exposures, but there is scientific uncertainty about the nature and extent of such mycotoxin-related disease (Institute of Medicine, Committee on Damp Indoor Spaces and Health, 2004; WHO, 2009).
A second way in which mold can affect health is by eliciting immune responses. Some immune responses, such as allergies, are familiar; symptoms include sneezing, coughing, and having a runny nose, red eyes, or a skin rash. Asthma commonly has an immune component, and exposure to damp indoor spaces and mold can aggravate this condition (Quansah, Jaakkola, Hugg, Heikkinen, & Jaakkola, 2012). More severe immune responses, such as a lung disease called hypersensitivity pneumonitis, are far less common.
Third, some molds can cause infections. The victims of these infections are typically people with compromised immune systems, such as transplant patients, people on chemotherapy, or people with infections such as HIV. Aspergillosis, caused by Aspergillus molds, is the best known example of such an infection.
A mold problem is usually initially recognized by visual inspection— people see discolored patches on walls or other surfaces, sometimes with a fuzzy texture—or by the musty smell that often accompanies mold. It is possible to measure mold growth in buildings and to identify the species that are growing, but the value of this measurement is unclear (Johnson, Thompson, Clinkenbeard, & Redus, 2008), as any significant infestation needs to be cleaned up, irrespective of species.
There are two key actions for remediating a mold problem: cleaning up the mold that has accumulated and correcting the moisture problem that allowed the mold to grow in the first place. Limited patches of mold are cleaned up with materials such as detergent or bleach, but if mold has infiltrated more broadly—say, after a major
1161
flood—then entire sections of wall or other building components may need to be replaced. Preventing the formation of mold is key, and several guidelines exist: keeping the relative humidity between 40% and 60%; promptly correcting moisture sources such as leaky roofs, windows, and pipes; promptly cleaning up after flooding; and ventilating shower, laundry, and cooking areas (Warsco & Lindsey, 2003).
High-Quality Indoor Air The quality of the air in a building can have a substantial impact on the people in that building (Samet & Spengler, 2003; Sundell, 2004). One of the largest such challenges on a global scale is the indoor burning of biomass fuel. As explored in Chapter 14, pollutants from this activity account for an important portion of global burden of disease. Here, we consider other contaminants that can undermine indoor air quality, including radon, tobacco smoke, carbon monoxide, and asbestos.
Radon is a colorless, odorless, radioactive gas that occurs naturally in the rock and soil of many parts of the world. When building foundations are sunk into the ground in such areas, radon can off- gas from the soil, enter the basement air, and go on to permeate the building air. In the 1980s, radon gained notoriety when media reports described a Pennsylvania home with such high radon levels that the resident, a nuclear power plant worker, set off alarms when he arrived at work. Radon is explored in Tox Box 20.2.
1162
Tox Box 20.2 Radon
WHAT IS IT? Radon is a radioactive gas formed naturally by the decay of uranium in soil and water.
HOW ARE PEOPLE EXPOSED? As explained in Chapter 22, most people's primary exposure to radon occurs through inhalation of radon gas inside homes or other buildings. Radon from uranium-containing soil enters buildings through cracks and holes in the foundation, and then becomes trapped inside by the walls and ceilings. In the United States, approximately one in fifteen homes has levels of radon gas that are of health concern.
To a much lesser extent, the general population can also be exposed by drinking radon-contaminated water or by inhaling the radon off-gassing from the water. This exposure pathway is most likely for people who drink well water, because radon may contaminate groundwater.
Certain workers may have far higher radon exposure than the general population does, also through inhaling radon gas. Those at highest risk are underground miners of uranium, tin, fluorspar, and iron.
1163
WHAT ARE THE TOXIC EFFECTS? Concern for radon in homes and its health risks rose in the United States following the oil price shocks of the 1970s, in part because home construction methods, materials, and barriers were sealing homes more tightly.
The main toxic effect of radon exposure is an increased risk of lung cancer. Two principal lines of human evidence implicate radon as a cause of lung cancer: occupational cohort studies of miners, especially uranium miners, and population-based case-control studies of lung cancer patients. Animal studies corroborate the epidemiological findings. Estimates are that between 8% and 15% of lung cancers are attributable to radon exposure, making it the second cause of this disease after smoking (IARC, 2012b). Radon and cigarette smoking may be synergistic in causing lung cancer; the radon-associated risk is far higher among smokers than among nonsmokers (Torres-Duran, Barros- Dios, Fernandez-Villar, & Ruano-Ravina, 2014)—higher than would be expected from adding the two risks. In the United States, approximately 21,000 people die annually of radon- associated lung cancer, making it more lethal than drunk driving (U.S. EPA, 2003). IARC classifies radon as carcinogenic to humans.
Much of our understanding of radon comes from studies performed in the 1950s by the Public Health Service, which found very high lung cancer rates among Navajo and white uranium miners. At the time, the miners were not informed of the association between radon exposure and cancer. In 1980, Congress apologized to these miners and their families, and passed the Radiation Exposure Compensation Act, which compensated eligible survivors with up to $100,000 for lung diseases associated with uranium mining.
HOW ARE PEOPLE PROTECTED?
1164
Sources: www.lung.org/healthy-air/home/resources/radon.htm
The general population is protected from radon through regulatory guidelines, widely available home testing, and engineering controls. In the United States the EPA recommends that people test their homes and implement controls to reduce radon levels below 4 pCi/L of air. Control may be as simple as improved ventilation to remove trapped radon gas, and may also rely on specific renovation and construction techniques to reduce the amount of gas entering the household from the soil. Radon detection can be passive, using such devices as charcoal canisters and alpha-track detectors, as shown here, or it can be active, using continuous radon monitors. Advice on radon testing is available at www.epa.gov/radon
Workers are protected through regulations by multiple agencies and engineering controls. Both the Mine Safety and Health Administration (MSHA) and the Occupational Safety and Health Administration (OSHA) set exposure limits for workers. While OSHA sets a permissible exposure limit of 100 pCi/L of air for one work week, MSHA's exposure limit for underground miners varies with factors such as the length of exposure and proportion of radon decay products attached to dust in the air. Like the general population, underground miners are protected by ventilation systems that vent accumulated radon gas to the outside.
WANT TO LEARN MORE? The toxicology of radon is well reviewed in the ATSDR
1165
Toxicological Profile for Radon (www.atsdr.cdc.gov/toxprofiles/tp.asp?id=407&tid=71).
A useful review of the radon–lung cancer link is M. Torres- Duran, J. M. Barros-Dios, A. Fernandez-Villar, and A. Ruano-Ravina, “Residential Radon and Lung Cancer in Never Smokers: A Systematic Review,” Cancer Letters, 2014, 345(1), 21–26.
An EPA publication, A Citizen's Guide to Radon, describes home testing for radon (www.epa.gov/radon/pubs/citguide.html); and a dated but still authoritative source is Health Effects of Exposure to Radon: BEIR VI—a report of the National Research Council's Committee on Health Risks of Exposure to Radon, published by the National Academies Press in 1999.
A good source of general background information is H. Zeeb and F. Shannoun (Eds.), WHO Handbook on Indoor Radon: A Public Health Perspective (Geneva: WHO, 2009), available at whqlibdoc.who.int/publications/2009/9789241547673_eng.pdf? ua=1.
Tobacco smoke is also a well-recognized contaminant of indoor air in buildings in which people smoke—offices, homes, restaurants, and others. By the 1980s, epidemiological research had established that this exposure increases the risk of asthma and respiratory disease (especially in children), cancer, cardiovascular disease, and other adverse outcomes (National Research Council, Committee on Passive Smoking, 1986; U.S. Public Health Service, Office of the Surgeon General, 1986). Based on this evidence, a broad movement to limit or ban smoking in public places, including workplaces, restaurants, airports, and other buildings, has spread rapidly. Evidence suggests that such limits result in substantial reductions in exposure to tobacco smoke, and in corresponding health benefits (Fichtenberg & Glantz, 2002; Wakefield et al., 2008), making this policy a major public health victory.
Carbon monoxide is a unique indoor air contaminant, as described in Tox Box 13.1 in Chapter 13. It can accumulate in buildings when combustion sources are present and the air is not adequately
1166
ventilated (Centers for Disease Control and Prevention, 2007). One source, for example, is generators that burn diesel or other fuel in or near buildings, a common practice after disasters and when electric power is otherwise interrupted. Another, less common source of carbon monoxide exposure is the ice maintenance machines (called Zambonis) found at ice skating rinks. When inhaled, carbon monoxide bonds with hemoglobin in red blood cells, preventing these cells from transporting oxygen properly. Low levels of exposure can cause headaches, fatigue, and aggravation of ischemic heart disease, and high levels of exposure can be fatal. The best approach is prevention—preventing combustion from occurring in indoor spaces and ensuring plenty of ventilation when it does occur, so that dangerous levels of carbon monoxide cannot accumulate.
Asbestos has been recognized as a hazard for many decades, as described in Tox Box 20.3. Asbestos exposure increases the risk of a fibrosing lung disease (asbestosis), of several kinds of cancer, and of other conditions. Until the 1970s asbestos was widely used to insulate commercial buildings, schools, and homes and to manufacture building materials such as floor tiles. As a result, asbestos emerged as an important indoor air contaminant. The initial approach to remediation, in the 1980s, was to remove the asbestos, a costly and sometimes dangerous job. More recently, in- place management through containment and encapsulation has gained more acceptance.
1167
Tox Box 20.3 Asbestos
Source: U.S. Department of Agriculture, Forest Service, n.d.
WHAT IS IT? Asbestos is a family of naturally occurring, fibrous minerals, consisting of silicate and various elements such as magnesium, iron, calcium, and sodium. These fibers are strong and flexible, and can resist heat, chemical, and electrical degradation. (The accompanying photo shows a scanning electron microscope image of asbestos fibers.) Six types of fibers are conventionally included in the term asbestos--actinolite, amosite, anthophyllite, chrysotile, crocidolite, and tremolite—although other minerals, such as richterite and winchite, have asbestiform properties. Asbestos is found in many parts of the world, including the Ural Mountains of Russia, the Appalachian Mountains of the United States, Turkey, and South Africa. Asbestos may contaminate deposits of minerals such as talc and vermiculite.
HOW IS IT USED? Asbestos has long been used as an insulating and fireproofing material, as a structural element of such building materials as cement and floor tiles, and in such products as vehicle brakes. While the world's production of asbestos peaked at 5 million metric tons in 1975 (IARC, 2012a), its use has declined since because of health concerns, litigation, and regulation. However, asbestos consumption remains high in China, India, and parts of Eastern Europe.
1168
HOW ARE PEOPLE EXPOSED? The most common form of exposure is inhalation. Occupational exposure is highest; approximately 125 million workers worldwide are exposed to asbestos fibers, in mining and in manufacturing or through handling asbestos- containing products (WHO, 2015). General environmental exposures may occur in areas of naturally occurring asbestos. (Libby, Montana, is a famous example, and numerous areas throughout southeastern Turkey are similarly affected.) Finally, lower level exposures may occur in several ways. Workers' families may be exposed through “fouling the nest”—that is, when workers bring home clothing contaminated with asbestos fibers or when the fibers contaminate workers' hair. People may also be exposed when asbestos-containing materials in older buildings, such as insulation or floor tiles, degrade, and friable asbestos releases airborne fibers (The accompanying photo shows how asbestos insulation can degrade over time, permitting inhalation of fibers.)
Following disasters, both the general population and workers in certain occupations can be exposed to transient high levels of asbestos. When the World Trade Center in New York City was destroyed by terrorist attacks in 2001, survivors, first responders, and construction workers who cleared the rubble were exposed to asbestos. Similarly, the 2008 earthquake in Sichuan, China, destroyed buildings made with asbestos cement and released asbestos into the air. Still more fibers became airborne during the cleanup with heavy equipment, which was largely performed by workers and volunteers
1169
without safety equipment or training.
Source: ©www.earldotter.com.
WHAT ARE THE TOXIC EFFECTS? All types of asbestos fibers are toxic. While acute exposure to airborne asbestos can irritate the eyes and lungs, its major toxic effects develop after decades of chronic exposure. Chronic inhalation of asbestos fibers can damage the lungs and surrounding membranes, eventually causing asbestosis— the development of stiff, scarlike tissue that interferes with breathing. Chronic inhalation can also cause several kinds of cancer, most notably lung cancer and mesothelioma, an otherwise rare cancer affecting the tissues that line the lungs and abdomen. Approximately 107,000 people worldwide die annually from asbestos-related cancer (WHO, 2015).
The risk of developing lung cancer from asbestos exposure is much higher when exposed individuals smoke. This higher risk represents a synergistic effect between asbestos exposure and smoking; their joint effect is greater than would be expected from adding the risk from asbestos exposure and risk from smoking together.
HOW ARE PEOPLE PROTECTED?
1170
Both workers and the general population are protected by asbestos bans. Since the early 2000s, asbestos products have been banned in many countries, including Japan, Australia, Argentina, Brazil, Chile, and the countries of the European Union. In contrast, the United States allows many asbestos products, although the EPA does ban its use in paper and spray-on materials under the Toxic Substances Control Act and Clean Air Act.
Workers are further protected through regulation by multiple agencies, the development of technical alternatives to asbestos, personal protective equipment, medical surveillance programs, and awareness raised by asbestos litigation. In the United States the OSHA 8-hour time- weighted average (TWA) exposure limit is 0.1 asbestos fiber/cm3 of air. NIOSH recommends that workers handling asbestos wear respirators and avoid skin contact with the material. Thanks to these policies, few workers in the United States continue to sustain asbestos exposure. To protect workers' families, the Workers' Family Protection Act of 1992 mandates workplace practices to help workers avoid fouling the nest, by, for example, providing workers with the ability to shower and change clothing before going home.
In the United States, workers who have handled asbestos are often enrolled in medical surveillance programs to monitor them for signs of cancer and asbestosis. The Navy maintains an extensive registry of service members and civilians who have had occupational exposure to asbestos and who receive regular medical exams and chest X-rays. Similarly, the World Trade Center Worker and Volunteer Medical Screening Program monitors 9/11 first responders for changes in respiratory function and health.
Workers and the general population have also benefited from asbestos litigation, which has increased awareness of the use of asbestos and its toxic effects. Since 1972 in the United States, thousands of workers have sued and won awards or out-of-court settlements from manufacturers for failing to warn them of toxic effects that had been suspected since the 1930s. This is an interesting example of public health policy —in this case, the reduction of asbestos use in many sectors
1171
of industry—being prompted in large part by litigation.
WANT TO LEARN MORE? There is a wealth of sources on the toxicology and epidemiology of asbestos exposure. ATSDR's Toxicological Profile for Asbestos can be found at www.atsdr.cdc.gov/toxprofiles/tp.asp?id=30&tid=4. The WHO International Programme on Chemical Safety maintains an asbestos Web page at www.who.int/ipcs/assessment/public_health/asbestos/en. The International Agency for Research on Cancer updated its asbestos findings in a 2012 monograph titled Arsenic, Metals, Fibres and Dusts, which is available at monographs.iarc.fr/ENG/Monographs/vol100C/index.php. A useful recent review is L. Stayner, L. S. Welch, & R. Lemen, “The Worldwide Pandemic of Asbestos-Related Diseases,” Annual Review of Public Health, 2013, 34, 205–216.
The ravages of asbestos exposure, and the human, legal, and policy consequences, have been the subject of several books, including P. Brodeur, Outrageous Misconduct: The Asbestos Industry on Trial (New York: Pantheon, 1985); A. Peacock, Libby, Montana: Asbestos and the Deadly Silence of an American Corporation (Boulder, CO: Johnson, 2003); A. Schneider and D. McCumber, An Air That Kills: How the Asbestos Poisoning of Libby, Montana, Uncovered a National Scandal (New York: Putnam, 2004); and R. Maines, Asbestos and Fire: Technological Tradeoffs and the Body at Risk (New Brunswick, NJ: Rutgers University Press, 2013).
Contributed by Megan Cartwright
Elimination of Toxic Chemicals Lead is a well-recognized hazard, discussed in Tox Box 11.1 in Chapter 11. Lead has historically been used in many ways—as a gasoline additive, in tin cans, consumer goods, batteries, and even in medications—resulting in many exposure pathways. One of the major uses of lead in past years was as a component of paint,
1172
because it made the paint more durable. Although lead is no longer used in paint, tens of millions of homes still contain lead-based paint; fortunately, this number is declining steadily (Jacobs et al., 2002). As lead-based paint breaks down over time, lead can be found in paint chips on window sills or other woodwork, in household dust, and in soil near the house. When older homes are renovated, large amounts of lead can be released. (Text Box 20.3 lists a number of chemicals, including lead, that pose risks when used in buildings. Also see the discussion of PBDEs in Tox Box 20.4.)
1173
Text Box 20.3 Chemical Safety in Buildings Building materials—from adhesives to paints to insulation— may contain a wide range of toxic chemicals. There are many approaches to reducing dangerous exposures. One is disclosure—the idea being that transparency and accountability about materials will help drive suppliers to offer safer products, and consumers to make safer choices. A leading example is the Health Product Declaration (www.hpd-collaborative.org), a standard format for disclosing the contents of a building product.
Another approach is to discourage, or even prohibit, the use of certain chemicals—either by voluntary systems or through regulation. One of the most ambitious voluntary building certification programs is the Living Building Challenge (living-future.org/lbc/about), which “defines the most advanced measure of sustainability in the built environment possible today and acts to diminish the gap between current limits and ideal solutions.” The Living Building Challenge is applied in seven performance categories: Place, Water, Energy, Health & Happiness, Materials, Equity and Beauty. The Materials category, in turn, defines the Red List, a set of chemicals that must not be used in building materials, including
Alkylphenols
Asbestos
Bisphenol A (BPA)
Cadmium
Chlorinated polyethylene and chlorosulfonated polyethlene
Chlorinated polyvinyl chloride (CPVC)
Chlorobenzenes
1174
Chlorofluorocarbons (CFCs)
Chloroprene (neoprene)
Chromium VI
Formaldehyde (added)
Halogenated flame retardants (HFRs)
Hydrochlorofluorocarbons (HCFCs)
Lead
Mercury
Perfluorinated compounds (PFCs)
Phthalates
Polychlorinated biphenyls (PCBs)
Polyvinyl chloride (PVC)
Polyvinylidene chloride (PVDC)
Short chain chlorinated paraffins
Volatile organic compounds (VOCs), in wet applied products
Wood treatments containing creosote, arsenic, or pentachlorophenol
Efforts such as these, and the market changes they promote, will likely reduce the use of toxic materials in buildings in coming years.
In many ways the story of lead-based paint exemplifies a public health success (Jacobs, Kelly, & Sobolewski, 2007). First, the science base was built. This included developing and validating methods for measuring lead in dust (Lanphear et al., 1995), and showing that lead-based paint and contaminated dust and soil were major pathways of childhood lead exposure (Lanphear & Roghmann, 1997; Lanphear et al., 1998). Then remediation approaches were studied, and the most and least effective ones identified (Yeoh et al., 2014). In addition, scientists and economists showed that the benefits of lead hazard control far outweighed the costs, with a return on investment as high as 221 times the cost
1175
(U.S. Department of Housing and Urban Development, 1999; Gould, 2009). These developments, in turn, spurred health- protective public policies that established standardized procedures for removing lead safely (U.S. Department of Housing and Urban Development, 1995) and health-based exposure standards for paint, dust, and soil in housing undergoing remediation, renovation, or repainting (A Final Rule by the U.S. Environmental Protection Agency, 2001). The proportion of children with elevated levels of lead in their blood has continued to decline (Wheeler & Brown, 2013).
1176
Tox Box 20.4 Polybrominated Diphenyl Ethers (PBDEs)
WHAT ARE THEY? Polybrominated diphenyl ethers (PBDEs) are a group of synthetic organic chemicals consisting of two brominated aromatic rings. There are up to 209 different PBDE congeners (only a few of which are used commercially), which vary by the number and site of bromine substitutions around the aromatic rings. PBDEs are classified as persistent organic pollutants (POPs). They are lipophilic (soluble in oils and fats), they biomagnify as they move up food chains and bioaccumulate in tissues, and they are stable (resistant to physical, chemical, or biological breakdown), making them persistent both in the environment and in biological tissues.
HOW ARE THEY USED? PBDEs are used as flame retardants. They are added to numerous consumer products, such as televisions, computers, electrical devices and equipment, textiles, and foam furniture. At their peak, over 33,000 metric tons of PBDEs were consumed each year in the United States (over half of the PBDEs consumed globally). The main PBDE congeners used commercially are the penta-, hepta-, octa-, and deca-BDEs.
HOW ARE PEOPLE EXPOSED? PBDEs readily leach from consumer products into the
1177
environment. The primary route of exposure for people is the consumption of food, particularly meat, dairy products, and fish with a high fat content. PBDEs have been detected in the blood, fat tissue, and breast milk of populations around the world; these biomonitoring results rise steeply with increasing use. For example, Figure 20.5 displays a time trend of the combined concentration of 8 PBDE congeners in pooled breast milk samples from mothers in Stockholm, from 1972 to 1997. Importantly, infants and young children have the highest PBDE body burdens, as a result of unique exposure pathways (breast milk) and frequent hand-to- mouth behavior (ingestion of household dust).
Figure 20.5 Concentrations of PBDE in Breast Milk, Stockholm, 1972–1997
Source: ©www.earldotter.com.
WHAT ARE THE TOXIC EFFECTS? The health effects of PBDEs in people are not well understood. Acute, high-level exposure to PBDEs is unlikely and rare; the health concerns center on low-level, chronic exposure. The main adverse health effects associated with PBDEs are developmental neurotoxicity and endocrine
1178
disruption. Animal studies suggest that chronic, low-level exposure to some PBDE congeners and mixtures may result in impaired learning and memory. PBDEs can also disrupt thyroid hormone homeostasis. Thyroid hormones are important for brain development; thus the effects of PBDEs on the developing brain may be mediated by thyroid effects during pregnancy. Epidemiological studies have found an association between higher PBDE body burdens and hyperthyroidism, and in utero and early life PBDE exposure is associated with neurobehavioral deficits and altered thyroid hormone levels. Little is known about the carcinogenicity of PBDEs; only one congener (deca-BDE) is currently classified as a possible human carcinogen. Importantly, the PBDE congeners used in industrial mixes can be metabolized to more toxic (hydroxylated) metabolites in humans, and these metabolites may be responsible for much of the toxicity associated with PBDE exposure.
HOW ARE PEOPLE PROTECTED? In the United States the production and the importation of the penta-, octa-, and deca-BDE congeners were phased out in 2004. In addition, the Stockholm Convention on Persistent Organic Pollutants banned the production of penta- and octa-BDE mixtures in ratifying nations. Despite these bans, exposure to PBDEs will continue for a long time because PBDEs will continue to leach from the numerous consumer products that were manufactured prior to any bans. The case of PBDEs provides a good example of the trade-offs—the risks versus the benefits—that public health officials must consider. While the addition of PBDEs to consumer products may decrease the risk of fire, this benefit has to be weighed against the harm caused by adverse health effects (which may not be fully understood) associated with PBDE exposure. In addition, decision makers must consider what chemicals will replace PBDEs and whether these replacements are actually safer. In the case of PBDEs, there is little toxicological information on the new, alternative flame retardants that will replace PBDEs.
1179
WANT TO LEARN MORE? The ATSDR Toxicological Profile for PBDEs is at www.atsdr.cdc.gov/toxprofiles/tp.asp?id=529&tid=94
A recent review is L. V. Dishaw, L. J. Macaulay, S. C. Roberts, and H. M. Stapleton, “Exposures, Mechanisms, and Impacts of Endocrine-Active Flame Retardants,” Current Opinion in Pharmacology, 2014, 19, 125–133.
For more on the study of PBDEs in human milk see D. Meironyté, K. Norén, and Å. Bergman, “Analysis of Polybrominated Diphenyl Ethers in Swedish Human Milk: A Time-Related Trend Study, 1972–1997,” Journal of Toxicology and Environmental Health: Part A, 1999, 58, 329–341; and D. Meironyté Guvenius and K. Norén, “Polybrominated Diphenyl Ethers in Swedish Human Milk: The Follow-Up Study,” in Proceedings of the Second International Workshop on Brominated Flame Retardants (Stockholm: The Swedish Chemical Society, 2001, pp. 303– 305).
Contributed by Anna Engstrom
Pesticides are commonly applied in buildings and can be a source of toxic exposures. Some classes of pesticides, such as organophosphates, are especially toxic, and others, such as pyrethroids, are less toxic, as discussed in detail in Chapter 18. Pest control solutions in buildings include choosing less toxic pesticides, applying them as sparingly as possible, and using nonchemical strategies such as physical barriers and careful food storage techniques (often as part of an integrated pest management approach).
Cleaning materials are commonly used in buildings. Three basic processes are used in cleaning: mechanical processes, such as sweeping and vacuuming; chemical processes, which employ substances such as detergents or ammonia to dissolve dirt or to create barriers (as stripping and waxing floors does); and surface- abrasion processes, such as burnishing. Some cleaning products may be dangerous. Household cleaning products are the third leading category of exposures reported to U.S. Poison Control
1180
Centers overall, and the second among young children (Mowry, Spyker, Cantilena, McMillan, & Ford, 2014). Cleaning agents have also been implicated in long-term outcomes such as asthma, in both children (Sherriff, Farrow, Golding, & Henderson, 2005) and adults (Zock, Vizcaya, & Le Moual, 2010). Examples of dangerous ingredients in cleaners are shown in Table 20.2.
Table 20.2 Hazardous Ingredients of Cleaners (Partial Listing)
Product category
Hazardous ingredients
Health effects
Glass cleaners, general purpose cleaners, carpet spot removers
2-Butoxyethanol (ethylene glycol monobutyl ether)
Blood and liver toxicity; possible carcinogenicity.
Toilet cleaners Acids (hydrochloric, phosphoric)
Acid burns.
Oven cleaners, heavy-duty degreasers
Lye (sodium hydroxide)
Lye burns.
Floor strippers Ammonium hydroxide, ethanolamine2- butoxyethanol
Skin, eye, and respiratory irritation and burns; central nervous system toxicity; blood and liver toxicity; possible carcinogenicity.
Sanitizers, laundry whiteners
Bleach (sodium hypochlorite)
Skin and eye irritation. Mixing bleach with ammonia or acids can release highly toxic gases.
Metal polishes Tetrachloroethylene, other volatile organic compounds
Central nervous system, liver, and kidney toxicity; carcinogenicity (some compounds).
Sources: Western Sustainability and Pollution Prevention Network, 2002; Ashkin & Ellis, 2006.
There are many ways to reduce the risk associated with such chemicals. Dangerous chemicals can be replaced with safer ones. Cleaning procedures can be altered. For example, instead of
1181
cleaning on a rigid schedule, cleaning can be done only when conditions warrant. Similarly, cleaning can be scheduled during hours when other people are least likely to be present. Those who do the cleaning, such as janitors, can be trained in the careful use of chemicals. And steps can be taken to reduce the soiling of buildings, through such measures as wiping feet when entering, to reduce the frequency of needed cleaning.
Sick building syndrome is a term applied to buildings in which symptoms seem to cluster—often in connection with suspected chemical exposures. This situation is described in Text Box 20.4.
Features That Promote Mental Health Buildings may play an important role in mental health, and no building is more important in this respect than housing. Although a house is simply a structure, the term home carries much more meaning. It suggests a source of permanence and continuity in a changing world; a setting for the establishment of predictable, comforting routines; a source of intergenerational support and help; and a place where people can feel in control and construct their identities—functions that together have been called ontological security (Dupuis & Thorns, 1998).
Specific features of buildings may also promote (or threaten) mental health. Crowding offers one example (Solari & Mare, 2002). Crowding is not easy to define. As an objective measurement, crowding is the number of people per unit of area or the number of people per room, but there is no widely accepted density that defines crowding. As a subjective experience, crowding is marked by a feeling of inability to control interactions with other people or by interference with activities such as reading, conversing, or studying. Two hallmarks of crowding are loss of privacy and overstimulation. As explored in Chapter 9, crowding is associated with psychological distress and dysfunction; these in turn may manifest as interpersonal conflict, aggressive behavior and social withdrawal, not only at home, but also at school, where crowding is also associated with diminished academic performance.
1182
Text Box 20.4 Sick Building Syndrome From time to time, people who share space in a building develop shared health complaints. Workers in an office building might develop irritation of the eyes, nose, and throat. Students in a school might develop headaches. Or guests in a hotel might develop respiratory disease. These and other illnesses are often called building-related illnesses. Health care providers and public health officials often need to evaluate such situations, to search for and control possible causes, and to treat the affected individuals.
In some cases, outbreaks of illness in a building can be traced to a specific cause. One example is legionellosis, an infectious disease caused by the gram-negative bacterium Legionella pneumophila. This organism was famously identified after a disease outbreak in a Philadelphia hotel during the 1976 American Legion convention (Fraser et al., 1977). Legionella can colonize cooling towers, air-conditioning systems, hot water systems, and fountains, which explains why legionellosis can be a building-associated disease. Another cause of building-related illness is toxic exposures, such as exposures to organic chemicals from roofing, cleaning, or other building activities.
But often no specific cause can be identified when illness clusters in a building. This situation is termed sick building syndrome. Sick building syndrome emerged as a problem following the energy crises of the 1970s, when efforts at energy efficiency led to “sealing” buildings and reducing outdoor air exchange. The hallmark of sick building syndrome is a clustering of acute symptoms such as headache; eye, nose, or throat irritation; cough; dry or itchy skin; dizziness and nausea; difficulty in concentrating; fatigue; and sensitivity to odors (Redlich, Sparer, & Cullen, 1997). In general it is difficult to document clinical abnormalities with laboratory testing or to identify a specific cause of the symptoms (Thörn, 1998; Brauer, Kolstad, Ørbaek, & Mikkelsen, 2006a, 2006b). Symptoms usually
1183
resolve promptly when people leave the building.
Even if standard medical diagnosis is elusive, investigation of sick buildings may reveal remediable problems. These may include air contaminants; malfunction of the heating, ventilating, and air-conditioning system; and problems in the social environment such as low job satisfaction, stress, and interpersonal conflict. Air sampling may seem an appealing approach, but it is costly and often uninformative.
Solutions generally include controlling any identified sources of air contaminants and making general improvements in building systems, including providing increased ventilation and perhaps air filtration. (Interestingly, increased ventilation seems to predict improved health and well-being, even if no particular culprit can be identified in the indoor air [Sundell et al., 2011].) Effective communication is key, because sick building syndrome is typically accompanied by a high level of concern and even panic among those affected (communication in such settings is described in Chapter 28).
Other features of buildings have been shown to affect mental health: some intuitive, such as noise (Lercher, Evans, Meis, & Kofler, 2002); and some less clear, such as high-rise design (Gifford, 2007) or high moisture levels (Hopton & Hunt, 1996). (These factors may be proxies for other building conditions.) Overall, buildings that are in poor condition—especially housing units—seem to threaten mental health (Gifford & Lacombe, 2006; Liddell & Guiney, 2015). In one study (Evans et al., 2000), investigators identified and measured these aspects of housing quality:
Cleanliness/clutter
Privacy
Presence or absence of hazards
Structural quality
Child resources, such as play areas and child care
They found that better housing quality predicted less psychological distress (as measured with the Demoralization Index of the Psychiatric Epidemiology Research Instrument). Safe, secure housing—and perhaps healthy buildings more generally—are
1184
foundations of mental health (Evans et al., 2000; Bashir, 2002; Howden-Chapman, Chandola, Stafford, & Marmot, 2011).
Universal Design Certain features of building design can pose barriers to some people. For example, people with poor vision have difficulty with dim lighting, elderly people have difficulty with stairs, and people who use wheelchairs have difficulty with narrow doorways. As described in Chapter 11, children are especially vulnerable to some exposures, and this is true in homes, schools, and other buildings (Weitzman et al., 2013). Observations such as these gave rise to the concept of universal design, which the Center for Universal Design (1997) defines as the “design of products and environments to be usable by all people, to the greatest extent possible, without the need for adaptation or specialized design.” Text Box 20.5 describes a particular instance of universal design.
1185
Text Box 20.5 Building Design for the Elderly As the population ages, more and more elderly people need buildings designed to minimize their risks and to help them thrive and function optimally. One challenge is mobility limitations. Design principles include having an outside entrance that requires neither steps nor a ramp, placing all the basics (kitchen, bathroom, bedroom, if not the entire living unit) on one floor to obviate the need to climb stairs, and widening hallways and doorways to allow easy passage of wheelchairs. Good lighting is important because many elderly people experience decreased visual acuity. Light switches should be positioned so as to avoid the need to walk through darkened areas, and these and other controls should be placed within easy reach. Fixtures too should be installed within easy reach (say, mounted on walls instead of on ceilings) for changing light bulbs. Easy-to-use handles and switches, such as lever-style door handles, are helpful. Fall prevention is also important, given the high risk of falls in the elderly; design principles include
Minimizing changes in walking surfaces
Using slip-resistant surfaces, such as rough tile and carpet with short, dense pile
Installing handrails on both sides of stairs
Installing secure grab bars in tubs and showers and near toilets
Minimizing the use of extension cords and other trip hazards
These principles can be applied not only in private homes and apartments but also in nursing homes and other facilities where the elderly reside and in hotels, libraries, and other facilities that serve elderly visitors. Many of these principles are part of universal design, so other groups of people may benefit from these design principles as well.
1186
Sources: Rollins, 2000; Mitka, 2001; Steinfeld & Maisel, 2012.
1187
Toward Safe, Healthy Buildings As is true across the environmental health field, many strategies exist for promoting health in buildings. Some are a matter of policy, others are technical or environmental solutions, and still others are behavioral.
Public policies that ensure safe, healthy buildings differ from other environmental health policies. For some challenges—say, outdoor air pollution—there are specific laws, dedicated agencies, and clear strategies to protect health (as described in Chapter 13). But for buildings this is not the case. No agencies at the federal, state, or local levels have overall responsibility for conditions in homes, schools, or health care facilities. Jacobs and others (2007) note the lack of concerted public action for indoor air quality in homes and suggest that this has come about because “there is not a perceived Shared Common for which the public feels a communal benefit and responsibility”—in contrast to, say, public concern over outdoor air pollution. Certain specific issues, such as elevator safety, are assigned to agencies. In some cases nongovernmental organizations offer guidance. For example, the American National Standards Institute (ANSI) and the American Society of Heating, Refrigerating, and Air-Conditioning Engineers (ASHRAE) publish standards for ventilation to achieve acceptable indoor air quality (ASHRAE, 2007), and many in government and industry use these standards as a benchmark. (The For Further Information section at the end of this chapter identifies other organizations that promote healthy homes, schools, and health care facilities.)
Many local public health departments have initiated healthy homes programs to promote residential health and safety. These are collaborative efforts; the public health agencies must work in concert with housing authorities, homeowners and landlords, environmental agencies, and others. A cardinal feature of these programs is their cross-cutting agendas. Community health workers who visit homes are typically equipped to assess a wide range of housing conditions, including asthma triggers, moisture and mold, lead and other chemical exposures, safety measures such as smoke detectors, and more (Krieger & Higgins, 2002; Krieger et al., 2002). Handbooks and other sources of information assist families wishing
1188
to make their homes healthy (Bower, 2000; CDC and HUD, 2006; Wentz & Wentz, 2012).
In recent years the science base that guides public health protection in buildings has expanded considerably (Thomson, Pettigrew, & Morrison, et al., 2001; Saegert, Klitzman, Freudenberg, Cooperman-Mroczek, & Nassar, et al., 2003; Sandel, Phelan, Wright, Hynes, & Lanphear, et al., 2004; Wu, Jacobs, Mitchell, Miller, & Karol, et al., 2007; Rashid & Zimring, 2008; Ulrich et al., 2008; Zimring & Bosch, 2008; Gibson et al., 2011; Morley, MIckalide, & Mack, 2011). Several conclusions emerge from this work. First, many solutions are well understood and empirically supported. Second, few solutions are as simple as they seem; even the most straightforward approach can carry hidden costs and risks. Third, many approaches can be bundled to achieve greater public health impact more efficiently. Fourth, environmental interventions are often combined with other approaches, such as education, policy change, and so on. Fifth, many interventions do more than protect health and safety; they can be economical, environmentally friendly, and aesthetically pleasing. Examples of these features are shown in Table 20.3.
Table 20.3 Approaches to Protecting Health and Safety in Buildings
Goal Strategies Comments Reducing asthma triggers in homes
Placing impermeable covers on mattresses and pillows Treating carpets and bedding with acaricides (to eliminate dust mites) Using air filtration Removing old carpets and bedding Intensive cleaning and extermination (to eliminate cockroaches) Installing central ventilation and humidity control
Many trials show little or no success. Success tends to depend on using multiple strategies. Additional benefit of education on home maintenance and asthma care.
1189
Reducing lead exposure in homes
Removing (abatement) or encapsulating of lead- containing paint Replacing windows and door frames Repainting deteriorated paint Using professional dust control
Strong evidence for reducing dust lead levels, but less evidence for reducing blood lead. Incorrect abatement techniques can increase exposure. Additional benefit of education regarding hygiene.
Controlling injuries in homes, day care facilities, and nursing homes
Installing smoke alarms Installing window guards (to prevent falls, especially among children) Reducing hot water temperature (to prevent scalds) Using radiator covers (to prevent burns) Improving lighting (to prevent falls, especially among the elderly) Putting visual cues on floors, such as tile patterns (to prevent falls, especially among the elderly)
Demonstrated benefit of home visits with counseling. Benefit of addressing multiple injury risks. Different risks for children and the elderly.
Reducing mold and moisture
Repairing leaks Replacing water- damaged materials (walls, carpets, and so forth) Maintaining optimal humidity
Reducing stress, infection, and medical errors in
Installing effective air quality control Having hand-washing
Measures are designed to benefit both patients and health
1190
health care facilities
stations at key locations Using easy-to-clean floor, wall, and furniture coverings Having single-bed, acuity-adaptable rooms Using natural lighting, with views of nature Putting noise-absorbing materials on ceilings and walls Planting hospital gardens
care workers.
Reducing pesticide exposure
Applying integrated pest management (see Chapter 17)
1191
Architecture, Environment, and Human Health Neighborhood Context This chapter discusses buildings, rather than the larger scale of neighborhoods, communities, and cities. However, there is no sharp line separating the two. Buildings exist in a context, and the impacts of buildings on health may stem both from features of the buildings themselves and from what surrounds the buildings. Imagine a decrepit building in a safe, well-maintained neighborhood or a comfortable new home in a dangerous, rundown neighborhood; clearly the experience of living in either home would be affected by the neighborhood context.
One example of applying this idea is the broken windows theory, which holds that signs of disorder in a community—broken windows, graffiti, untended yards, and so on, some evident in buildings and others in the surrounding neighborhood—predict uncivil behavior and poor health (Wilson & Kelling, 1982; Cohen et al., 2000). Another example comes from studies of people who have moved from poor housing in poor neighborhoods to better housing in neighborhoods with higher incomes (Acevedo-Garcia et al., 2004; Briggs, Goering, & Popkin, 2010; Ludwig et al., 2012). Although the evidence base is limited, it appears that such moves improve health. The features of a healthy home can be reinforced when the surrounding community provides opportunities for routine physical activity, nearby destinations such as shopping and schools, clean air, nearby parks and green space, and similar assets. (These topics are discussed in Chapter 15.)
Green Building Green building (also known as sustainable or high-performance building), according to the EPA (2009), is “the practice of creating structures and using processes that are environmentally responsible and resource-efficient throughout a building's life-cycle from siting to design, construction, operation, maintenance, renovation and deconstruction.” As this definition suggests, green building arose from the intersection of building science and environmental
1192
concerns. The principal components of green building are
Appropriate site selection
Energy efficiency and renewable energy
Water efficiency
Environmentally preferable building materials and specifications
Waste reduction
Toxics reduction
Good indoor air quality
The design and architecture fields are displaying a growing interest in green building. A prime example is LEED (Leadership in Energy and Environmental Design), an initiative of the U.S. Green Building Council. To encourage the adoption of sustainable green building practices, LEED provides specific performance criteria for such issues as site selection, water management, and energy systems. It also offers a certification process that measures building sustainability. LEED criteria are available for many categories of buildings, such as homes, commercial buildings, schools, and retail stores.
Increasingly, there is also recognition that green building yields not only environmental benefits, but also public health benefits (Fisk, 2000; Singh, Syal, Grady, & Korkmaz, 2010; Howden-Chapman, 2015; Willand, Ridley, & Maller, 2015). Some of these are direct; for example, reducing pesticide use in favor of integrated pest management reduces both environmental contamination and human exposure to potentially toxic chemicals. Careful design, construction, and building management can simultaneously optimize energy efficiency, indoor temperature, humidity, and air quality for building users (Colton et al., 2014; Hamilton et al., 2015). Other benefits are indirect; for example, a more energy efficient building draws less electricity from power plants, helping to reduce air pollution and greenhouse gas emissions (and thus reducing health threats). A growing literature offers advice on healthy green design and construction for homes (Yudelson, 2008; Baker-Laporte et al., 2008; Cook & Garrett, 2014), schools (Karliner, 2005; National Research Council, 2007; Gelfand & Freed,
1193
2010; Okcu, Ryherd, & Bayer, et al., 2011), and health care facilities (Frumkin & Coussens, 2007; Guenther & Vittori, 2013).
Biophilic Design Biophilic design is another way in which architecture intersects with human health and well-being. Biophilic design is based on the theory of biophilia—the notion that humans have an affinity with nature, as explored in Chapter 25. This leads to the concept of restorative design—the idea that if buildings embody natural design elements, they can offer people the same kind of restorative experience that occurs with nature contact. Biophilic design includes an organic (or naturalistic) dimension—shapes and forms that reflect the human affinity for nature—and a place-based (or vernacular) dimension—design that connects to the culture and ecology of a locale. Examples of such design elements include natural materials such as wood, stone, and clay; water features; natural daylight; botanical and animal motifs; and building shapes that fit into the landscape. Figure 25.7, in Chapter 25, shows a well- known example, Frank Lloyd Wright's Fallingwater in southwestern Pennsylvania. Evidence suggests that buildings with such features offer health benefits to the people who live, work, and study in them (Knowles, 2006; Kellert, Heerwagen, & Mador, 2008).
1194
Summary Much of modern life is lived indoors—in homes, schools, workplaces, and other specialized settings, such as health care facilities. The conditions in buildings therefore have great potential to affect health, well-being, and comfort. Ambient conditions such as lighting, crowding, and air quality; injury risks such as fall and burn hazards; exposure to such hazards as toxins and mold; and even the less tangible aesthetic qualities of buildings, may all play an important role.
Not everybody is equally affected by buildings. People with disabilities, the elderly, and people living in substandard housing are examples of populations with specific vulnerabilities and needs. Efforts to provide safe, healthy, and accessible buildings need to take these requirements into account.
Many techniques are available to achieve safe, healthy buildings, often based on the core tools of public health. These range from design decisions, such as installing wide doorways to permit mobility, to primary preventive strategies, such as lead paint removal, to maintenance and to such devices as carbon monoxide detectors and smoke alarms. In some cases these strategies dovetail with green strategies designed for environmental performance. Such co-benefits are welcome, as they help to achieve health and environmental goals simultaneously.
1195
Key Terms bioaerosols
An airborne suspension of living organisms or particles originating with living organisms.
biophilic design An approach in architecture, landscape architecture, and interior design that incorporates natural elements, in response to biophilic preferences. Biophilic design features shapes and forms that reflect the human affinity for nature, and elements that reflect the culture and ecology of a locale.
broken windows theory A theory, originally from the criminology field, that holds that signs of disorder in a community—broken windows, graffiti, untended yards, and so on—predict uncivil behavior and poor health.
evidence-based design Design embodying the idea that empirical data can guide architects and designers to achieve desired outcomes such as buildings that promote health.
green building “The practice of creating structures and using processes that are environmentally responsible and resource-efficient throughout a building's life-cycle from siting to design, construction, operation, maintenance, renovation and deconstruction” (U.S. EPA, 2009). (Also called sustainable or high performance building.)
green health care The application of green building and life cycle analysis to health care, combining environmental goals (such as energy conservation and waste minimization) with health goals (for patients, health care workers, and others).
Health Product Declaration An open standard format for reporting the contents and potential health hazards of building materials.
indoor air quality The quality of the air inside a building, especially in relation to
1196
the health and comfort of people within the building. LEED (Leadership in Energy and Environmental Design)
A green building certification program managed by the U.S. Green Building Council. LEED categories include building design and construction, interior design and construction, building operations and maintenance, neighborhood development, and homes.
Living Building Challenge™ A building certification program, advocacy tool, and philosophy managed by the International Living Future Institute, and oriented toward highly advanced sustainability practices. Living Building Challenge performance categories include Place, Water, Energy, Health & Happiness, Materials, Equity, and Beauty.
manufactured structures Prefabricated structures such as mobile homes, travel trailers, and modular classrooms and offices.
modular classrooms Manufactured structures used at schools as classrooms.
mold Fungi that grow in the form of multicellular filaments. Mold may proliferate in warm, moist indoor spaces.
mycotoxins Secondary metabolic products of fungi, especially molds. Important in public health as contaminants of food and of indoor air in buildings affected by mold growth.
Red List A set of chemicals, defined by the Living Building Challenge of the International Living Futures Institute, that must be avoided in building materials for environmental and human health reasons, as part of meeting the Living Building Challenge.
restorative design Design based on the idea that if buildings embody natural elements, they can offer people the same kind of restorative experience that occurs with nature contact.
sick building syndrome The clustering of symptoms in the people using a building, often in connection with suspected chemical exposures.
1197
universal design The designing of products and environments so they are usable by all people, including the elderly and people with disabilities, without the need for adaptation or specialized design.
1198
Discussion Questions 1. Why is outdoor air quality regulated more effectively than
indoor air quality?
2. Examine your own home taking a public health perspective. Can you identify at least three hazards? How would you correct them?
3. Why might children and the elderly face different injury risks in buildings?
4. People with disabilities face special challenges in buildings and may need various accommodations to ensure access, health, and safety. What is the concept of universal design, and how does it address these challenges? What are three specific accommodations that may be needed, and why would each one be necessary?
5. Promoting health, protecting the environment, and saving money can be highly compatible goals when designing and operating buildings, but sometimes these goals are in opposition. Describe a situation in which trade-offs among these goals are necessary. How you would handle the situation?
6. A good example of trade-offs in environmental health is the debate over flame retardants. In theory, flame retardants in furniture and other household items, such as draperies, could reduce the spread of flames and thus protect people during fires. However the major category of chemical flame retardants used for this purpose, the polybrominated diphenyl ethers (PBDEs), has a number of adverse health effects. With a partner, research this trade-off. One of you should make the case for using flame retardants, and the other should make the opposing case.
1199
References Acevedo-Garcia, D., Osypuk, T. L., Werbel, R. E., Meara, E. R., Cutler, D. M., & Berkman, L. F. (2004). Does housing mobility policy improve health? Housing Policy Debate, 15(1), 49–98.
Adamkiewicz, G., Spengler, J. D., Harley, A. E., Stoddard, A., Yang, M., Alvarez-Reeves, M., & Sorensen, G. (2013). Environmental conditions in low-income urban housing: Clustering and associations with self-reported health. American Journal of Public Health, 104(9), 1650–1656.
Alexander, C., Ishikawa, S., & Silverstein, M. (1977). A pattern language: Towns, buildings, construction. New York: Oxford University Press.
Alexander, D., & Lewis, L. (2014). Condition of America's public school facilities: 2012–2013 (NCES 2014-022). Washington, DC: U.S. Department of Education, National Center for Education Statistics. Retrieved from https://nces.ed.gov/pubsearch/pubsinfo.asp?pubid=2014022
American Academy of Pediatrics. (2001). Falls from heights: Windows, roofs, and balconies. Pediatrics, 107, 1188–1191.
American Society of Heating, Refrigerating, and Air-Conditioning Engineers. (2007). Ventilation for acceptable indoor air quality (ANSI/ASHRAE 62.1–2007). Washington, DC: American National Standards Institute and American Society of Heating, Refrigerating, and Air-Conditioning Engineers.
Ander, G. D. (2003). Daylighting performance and design. Hoboken, NJ: Wiley.
Annesi-Maesano, I., Baiz, N., Banerjee, S., Rudnai, P., Rive, S., & Group, S. (2013). Indoor air quality and sources in schools and related health effects. Journal of Toxicology and Environmental Health: Part B. Critical Reviews, 16(8), 491–550.
Ashkin, S., & Ellis, R. (2006). Cleaning materials and methods. In H. Frumkin, R. J. Geller, I. L., Rubin, & J. Nodvin (Eds.), Safe and
1200
healthy school environments (pp. 169–188). New York: Oxford University Press.
Atherton, I., & Nicholls, C. M. (2008). “Housing First” as a means of addressing multiple needs and homelessness. European Journal of Homelessness, 2, 289–303.
Baker-Laporte, P., Elliott, E., & Banta, J. (2008). Prescriptions for a healthy house: A practical guide for architects, builders & homeowners (3rd ed.). Gabriola Island, BC: New Society.
Ballesteros, M. F., Jackson, M. L., & Martin, M. W. (2005). Working toward the elimination of residential fire deaths: The Centers for Disease Control and Prevention's Smoke Alarm Installation and Fire Safety Education (SAIFE) program. Journal of Burn Care & Rehabilitation, 26 (5), 434–439.
Bashir, S.A. (2002). Home is where the harm is: Inadequate housing as a public health crisis. American Journal of Public Health, 92(5), 733–738.
Beale, C., & Kittredge, F. D., Jr. (2014). Current trends in health facility planning, design, and construction. Frontiers of Health Services Management, 31(1), 3–17.
Boehnke, M. (2013). Officials begin inspecting damage from Jefferson County High roof collapse. Knoxville News-Sentinel, July 8. Retrieved from http://www.knoxnews.com/news/local- news/officials-begin-inspecting-damage-from-jefferson
Boubekri, M. (2008). Daylighting, architecture and health: Building design strategies. Burlington, MA: Architectural Press/Elsevier.
Bower, L. M. (2000). Creating a healthy household. Bloomington, IN: Healthy House Institute.
Brauer, C., Kolstad, H., Ørbaek, P., & Mikkelsen, S. (2006a). No consistent risk factor pattern for symptoms related to the sick building syndrome: A prospective population based study. International Archives of Occupational and Environmental Health, 79(6), 453–464.
1201
Brauer, C., Kolstad, H., Ørbaek, P., & Mikkelsen, S. (2006b). The sick building syndrome: A chicken and egg situation? International Archives of Occupational and Environmental Health, 79(6), 465– 471.
Briggs, X., Goering, J., & Popkin, S. J. (2010). Moving to opportunity: The story of an American experiment to fight ghetto poverty. New York: Oxford University Press.
Buchanan, A. H. (2001). Structural design for fire safety. Hoboken, NJ: Wiley.
California Energy Commission. (2003). Windows and offices: A study of worker performance and the indoor environment (Technical Report P500-03-082-A-9). White Salmon, WA: New Buildings Institute.
Center for Universal Design. (1997). The principles of universal design: Version 2.0. North Carolina State University. Retrieved from http://www.ncsu.edu/ncsu/design/cud/about_ud/udprinciplestext.htm
Centers for Disease Control and Prevention. (2007). Carbon monoxide exposures—United States, 1999–2004. Morbidity and Mortality Weekly Report, 56(50), 1309–1312.
Centers for Disease Control and Prevention. (2008). Final report on formaldehyde levels in FEMA-supplied travel trailers, park models, and mobile homes. Retrieved from http://www.cdc.gov/nceh/ehhe/trailerstudy/pdfs/femafinalreport.pdf
Centers for Disease Control and Prevention and U.S. Department of Housing and Urban Development. (2006). Healthy housing reference manual. Atlanta, GA: U.S. Department of Health and Human Services.
Centers for Disease Control and Prevention and U.S. Department of Housing and Urban Development. (2011). Safety and health in manufactured structures. Atlanta, GA: U.S. Department of Health and Human Services.
Chang, J. T., Morton, S. C., Rubenstein, L. Z., Mojica, W. A., Maglione, M., Suttorp, M. J.,…Shekelle, P. G. (2004). Interventions
1202
for the prevention of falls in older adults: Systematic review and meta-analysis of randomised clinical trials. BMJ, 328(7441), 680.
Cohen, D., Spear, S., Scribner, R., Kissinger, P., Mason, K., & Wildgen, J. (2000). “Broken windows” and the risk of gonorrhea. American Journal of Public Health, 90(2), 230–236.
Colton, M. D., MacNaughton, P., Vallarino, J., Kane, J., Bennett- Fripp, M., Spengler, J. D., & Adamkiewicz, G. (2014). Indoor air quality in green vs conventional multifamily low-income housing. Environmental Science & Technology, 48(14), 7833–7841.
Connellan, K. P., Gaardboe, M.M.A., Riggs, D. P., Due, C. P., Reinschmidt, A., & Mustillo, L. (2013). Stressed spaces: Mental health and architecture. HERD, 6(4), 127–168.
Cook, M., & Garrett, D. (2014). Green home building: Money- saving strategies for an affordable, healthy, high-performance home. Gabriola Island, BC: New Society.
de Botton, A. (2006). The architecture of happiness. New York: Pantheon.
Dupuis, A., & Thorns, D. C. (1998). Home, home ownership and the search for ontological security. Sociological Review, 46, 24–47.
Ervasti, J., Kivimaki, M., Kawachi, I., Subramanian, S. V., Pentti, J., Oksanen, T.,…Virtanen, M. (2012). School environment as predictor of teacher sick leave: Data-linked prospective cohort study. BMC Public Health, 12, 770.
Evans, G. W., Wells, N. M., Chan, H.-Y. E., & Saltzman, H. (2000). Housing quality and mental health. Journal of Consulting and Clinical Psychology, 68, 526–530.
Fazel, S., Geddes, J. R., & Kushel, M. (2014). The health of homeless people in high-income countries: Descriptive epidemiology, health consequences, and clinical and policy recommendations. Lancet, 384(9953), 1529–1540.
Ferris, T.K.P. (2013). Evidence-based design and the fields of human factors and ergonomics: Complementary systems-oriented approaches to healthcare design. HERD, 6(3), 3–5.
1203
Fichtenberg, C. M., & Glantz, S. A. (2002). Effect of smoke-free workplaces on smoking behaviour: Systematic review. BMJ, 325, 188–191.
A Final Rule by the U.S. Environmental Protection Agency (Lead; Identification of dangerous levels of lead). 66 FR 1206 (2001). Retrieved from http://www.gpo.gov/fdsys/pkg/FR-2001-01- 05/pdf/01-84.pdf
Fisk, W. J. (2000). Health and productivity gains from better indoor environments and their relationship with building energy efficiency. Annual Review of Energy and the Environment, 25(1), 537–566.
Fitzpatrick-Lewis, D., Ganann, R., Krishnaratne, S., Ciliska, D., Kouyoumdjian, F., & Hwang, S. W. (2011). Effectiveness of interventions to improve the health and housing status of homeless people: A rapid systematic review. BMC Public Health, 11, 638.
Fraser, D. W., Tsai, T. R., Orenstein, W., Parkin, W. E., Beecham, H. J., Sharrar, R. G.,…Brachman, P. S. (1977). Legionnaires' disease: Description of an epidemic of pneumonia. New England Journal of Medicine, 297(22), 1189–1197.
Frumkin, H., & Coussens, C. (2007). Green healthcare institutions: Health, environment and economics. Washington, DC: National Academies Press.
Frumkin, H., Geller, R. J., Rubin, I. L., & Nodvin, J. (Eds.). (2006). Safe and healthy school environments. New York: Oxford University Press.
Gates, S., Fisher, J. D., Cooke, M. W., Carter, Y. H., & Lamb, S. E. (2008). Multifactorial assessment and targeted intervention for preventing falls and injuries among older people in community and emergency care settings: Systematic review and meta-analysis. BMJ, 336, 130–133.
Gelfand, L., & Freed, E. C. (2010). Sustainable school architecture: Design for elementary and secondary schools. San Francisco: Jossey-Bass/Wiley.
Gibson, M., Petticrew, M., Bambra, C., Sowden, A. J., Wright, K. E.,
1204
& Whitehead, M. (2011). Housing and health inequalities: A synthesis of systematic reviews of interventions aimed at different pathways linking housing and health. Health & Place, 17(1), 175– 184.
Gifford, R. (2007). The consequences of living in high-rise buildings. Architectural Science Review, 50, 2–17.
Gifford, R., & Lacombe, C. (2006). Housing quality and children's socioemotional health. Journal of Housing and the Built Environment, 21, 177–189.
Godwin, C., & Batterman, S. (2007). Indoor air quality in Michigan schools. Indoor Air, 17, 109–121.
Gould, E. (2009). Childhood lead poisoning: Conservative estimates of the social and economic benefits of lead hazard control. Environmental Health Perspectives, 117, 1162–1167.
Guenther, R., & Vittori, G. (2013). Sustainable healthcare architecture (2nd ed.). Hoboken NJ: Wiley.
Guzowski, M. (2000). Daylighting for sustainable design. New York: McGraw-Hill.
Haines, A., Bruce, N., Cairncross, S., Davies, M., Greenland, K., Hiscox, A.,…Wilkinson, P. (2013). Promoting health and advancing development through improved housing in low-income settings. Journal of Urban Health, 90(5), 810–831.
Hamilton, D. K., & Shepley, M. M. (2010). Design for critical care: An evidence-based approach. Burlington, MA: Architectural Press/Elsevier.
Hamilton, I., Milner, J., Chalabi, Z., Das, P., Jones, B., Shrubsole, C.,…Wilkinson, P. (2015). Health effects of home energy efficiency interventions in England: A modelling study. BMJ Open, 5(4), e007298.
Heschong Mahone Group. (1999). Daylighting in schools: An investigation into the relationship between daylighting and human performance (HMG Project No. 9803). San Francisco: Pacific Gas and Electric. Retrieved from http://www.h-m-
1205
g.com/downloads/Daylighting/schoolc.pdf
Hopton, J. L., & Hunt, S. M. (1996). Housing conditions and mental health in a disadvantaged area in Scotland. Journal of Epidemiology and Community Health, 50, 56–61.
Howden-Chapman, P. (2004). Housing standards: A glossary of housing and health. Journal of Epidemiology and Community Health, 58, 162–168.
Howden-Chapman, P. (2015). How real are the health effects of residential energy efficiency programmes? Social Science & Medicine, 133, 189–190.
Howden-Chapman, P. L., Chandola, T., Stafford, M., & Marmot, M. (2011). The effect of housing on the mental health of older people: The impact of lifetime housing history in Whitehall II. BMC Public Health, 11, 682–682.
Hyder, A. A., Sugerman, D., Ameratunga, S., & Callaghan, J. A. (2007). Falls among children in the developing world: A gap in child health burden estimations? Acta Paediatrica, 96 (10), 1394–1398.
Infrogmation. (2005). New Orleans after Hurricane Katrina: Mold infestations (Photo]. Retrieved from http://commons.wikimedia.org/wiki/File:DublinMold.jpg
Infrogmation. (2006). FEMA trailer [Photo]. Retrieved from http://commons.wikimedia.org/wiki/File:FEMAtrailerNapoleonFreret.jpg
Infrogmation. (2007). School entrance [Photo]. Retrieved from http://commons.wikimedia.org/wiki/File:FallRiverMADurfeeShcoolEntrance.jpg
Institute of Medicine, Committee on Damp Indoor Spaces and Health. (2004). Damp indoor spaces and health. Washington, DC: National Academies Press.
International Agency for Research on Cancer. (2012a). IARC monographs on the evaluation of carcinogenic risks to humans: Vol. 100C. Arsenic, metals, fibres and dusts. Retrieved from monographs.iarc.fr/ENG/Monographs/vol100C/index.php
International Agency for Research on Cancer. (2012b). IARC monographs on the evaluation of carcinogenic risks to humans:
1206
Vol. 100D. Radiation. Lyon: Author.
Jacobs, D. E., Clickner, R. P., Zhou, J. Y., Viet, S. M., Marker, D. A., Rogers, J. W.,…Friedman, W.. (2002). The prevalence of lead-based paint hazards in U.S. housing. Environmental Health Perspectives, 110, A599–606.
Jacobs, D. E., Kelly, T., & Sobolewski, J. (2007). Linking public health, housing, and indoor environmental policy: Successes and challenges at local and federal agencies in the United States. Environmental Health Perspectives, 115, 976–982.
Johnson, D., Thompson, D., Clinkenbeard, R., & Redus, J. (2008). Professional judgment and the interpretation of viable mold air sampling data. Journal of Occupational and Environmental Hygiene, 5(10), 656–663.
Karliner, J. (2005). The little green schoolhouse: Thinking big about ecological sustainability, children's environmental health and K–12 education in the USA. Retrieved from http://www.greenschools.net/greenschools.pdf
Keane, C. (2003). Ceiling collapses in third floor science wing: Sewanhaka High School students, staff evacuated. Floral Park Dispatch, March 7. Retrieved from http://www.antonnews.com/floralparkdispatch/2003/03/07/news
Kellert, S. R., Heerwagen, J., & Mador, M. (2008). Biophilic design: The theory, science and practice of bringing buildings to life. New York: Wiley.
Knowles, R. L. (2006). Ritual house: Drawing on nature's rhythms for architecture and urban design. Washington, DC: Island Press.
Krieger, J., & Higgins, D. L. (2002). Housing and health: Time again for public health action. American Journal of Public Health, 92, 758–768.
Krieger, J., Takaro, T. K., Allen, C., Song, L., Weaver, M., Chai, S., & Dickey, P. (2002). The Seattle-King County healthy homes project: Implementation of a comprehensive approach to improving indoor environmental quality for low-income children with asthma. Environmental Health Perspectives, 110(Suppl. 2), 311–322.
1207
Lanphear, B. P., Emond, M., Jacobs, D. E., Weitzman, M., Tanner, M., Winter, N. L.,…Eberly, S. (1995). A side-by-side comparison of dust collection methods for sampling lead-contaminated house dust. Environmental Research, 68, 114–123.
Lanphear, B. P., Matte, T. D., Rogers, J., Clickner, R. P., Dietz, B., Bornschein, R. L.,…Jacobs, D. E. (1998). The contribution of lead- contaminated house dust and residential soil to children's blood lead levels: A pooled analysis of 12 epidemiological studies. Environmental Research, 79, 51–68.
Lanphear, B. P., & Roghmann, K. J. (1997). Pathways of lead exposure in urban children. Environmental Research, 74, 67–73.
Larimer, M. E., Malone, D. K., Garner, M. D., Atkins, D. C., Burlingham, B., Lonczak, H. S.,…Marlatt, G. A. (2009). Health care and public service use and costs before and after provision of housing for chronically homeless persons with severe alcohol problems. JAMA, 301(13), 1349–1357.
Laursen, J., Danielsen, A., & Rosenberg, J. (2014). Effects of environmental design on patient outcome: A systematic review. HERD, 7(4), 108–119.
Lercher, P., Evans, G. W., Meis, M., & Kofler, W. W. (2002). Ambient neighbourhood noise and children's mental health. Occupational and Environmental Medicine, 59(6), 380–386.
Liddell, C., & Guiney, C. (2015). Living in a cold and damp home: Frameworks for understanding impacts on mental well-being. Public Health, 129(3), 191–199.
Liu, Y, Njai, R. S., Greenlund, K. J., Chapman, D. P., & Croft, J. B. (2014). Relationships between housing and food insecurity, frequent mental distress, and insufficient sleep among adults in 12 US states, 2009. Preventing Chronic Disease, 11, E37.
Longnecker, E. (2015). Sixteen injured in stage collapse at Westfield High School auditorium. WTHR. Retrieved from http://www.wthr.com/story/28886818/critical-injuries-reported- in-stage-collapse-at-westfield-high-school-auditorium
Lowry, S. (1991). Housing. BMJ, 303(6806), 838–840.
1208
Ludwig, J., Duncan, G. J., Gennetian, L. A., Katz, L. F., Kessler, R. C., Kling, J. R., & Sanbonmatsu, L. (2012). Neighborhood effects on the long-term well-being of low-income adults. Science, 337(6101), 1505–1510.
Mallonee, S., Istre, G. R., Rosenberg, M., Reddish-Douglas, M., Jordan, F., Silverstein, P., & Tunell, W. (1996). Surveillance and prevention of residential-fire injuries. New England Journal of Medicine, 335, 27–31.
Mann, A. (2000). Mold in schools: A health alert. USA Weekend, August 20. http://www.usaweekend.com/00_issues/000820/000820mold.html
Marberry, S. O. (Ed.). (2006). Improving healthcare with better building design. Chicago: Health Administration Press.
Marlith (2007). An apartment building [Photo]. Retrieved from http://commons.wikimedia.org/wiki/File:Apartment_Building.JPG
Matsui, E. C. (2014). Environmental exposures and asthma morbidity in children living in urban neighborhoods. Allergy, 69(5), 553–558.
Mead, M. N. (2008). Benefits of sunlight: A bright spot for human health. Environmental Health Perspectives, 116(4), A160–167.
Meheust, D., Le Cann, P., Reboux, G., Millon, L., & Gangneux, J. P. (2014). Indoor fungal contamination: Health risks and measurement methods in hospitals, homes and workplaces. Critical Reviews in Microbiology, 40(3), 248–260.
Meironyté, D., Norén, K., & Bergman, Å. (1999). Analysis of polybrominated diphenyl ethers in Swedish human milk: A time- related trend study, 1972–1997. Journal of Toxicology and Environmental Health: Part A, 58(6), 329–341.
Mendell, M. J., Eliseeva, E. A., Davies, M. M., Spears, M., Lobscheid, A., Fisk, W. J., & Apte, M. G. (2013). Association of classroom ventilation with reduced illness absence: A prospective study in California elementary schools. Indoor Air, 23(6), 515–528.
Mendell, M. J., & Heath, G. A. (2005). Do indoor pollutants and
1209
thermal conditions in schools influence student performance? A critical review of the literature. Indoor Air, 15, 27–52.
Mi, Y. H., Norbäck, D., Tao, J., Mi, Y. L., & Ferm, M. (2006). Current asthma and respiratory symptoms among pupils in Shanghai, China: Influence of building ventilation, nitrogen dioxide, ozone, and formaldehyde in classrooms. Indoor Air, 16(6), 454– 464.
Mitka, M. (2001). Home modifications to make older lives easier. JAMA, 286, 1699–1700.
Morley, R. L., Mickalide, A. D., & Mack, K. A. (2011). Healthy & safe homes: Research, practice, & policy. Washington DC: American Public Health Association.
Mowry, J. B., Spyker, D. A., Cantilena, L. R., Jr., McMillan, N., & Ford, M. (2014). 2013 Annual report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 31st annual report. Clinical Toxicology (Philadelphia, PA), 52(10), 1032–1283.
Muscatiello, N., McCarthy, A., Kielb, C., Hsu, W. H., Hwang, S. A., & Lin, S. (2015). Classroom conditions and CO2 concentrations and teacher health symptom reporting in 10 New York State schools. Indoor Air, 25(2), 157–167.
National Center for Education Statistics. (2013). Digest of education statistics. Washington, DC: U.S. Department of Education. Retrieved from https://nces.ed.gov/programs/digest
National Fire Protection Association. (2015). Fires in the U.S. Retrieved from http://www.nfpa.org/research/reports-and- statistics/fires-in-the-us
National Research Council. (2007). Green schools: Attributes for health and learning. Washington, DC: National Academies Press.
National Research Council, Committee on Health Risks of Exposure to Radon. (1999). Health effects of exposure to radon: BEIR VI. Washington, DC: National Academies Press.
National Research Council, Committee on Passive Smoking. (1986).
1210
Environmental tobacco smoke: Measuring exposures and assessing health risks. Washington, DC: National Academies Press.
Okcu, S., Ryherd, E., & Bayer, C. (2011). The role of physical environment on student health and education in green schools. Reviews on Environmental Health, 26(3), 169–179.
Palmer, G., 2nd, Abernathy, J. H., 3rd, Swinton, G., Allison, D., Greenstein, J., Shappell, S.,…Reeves, S. T. (2013). Realizing improved patient care through human-centered operating room design: A human factors methodology for observing flow disruptions in the cardiothoracic operating room. Anesthesiology, 119(5), 1066–1077.
Pearson, M., Garside, R., Moxham, T., & Anderson, R. (2011). Preventing unintentional injuries to children in the home: A systematic review of the effectiveness of programmes supplying and/or installing home safety equipment. Health Promotion International, 26(3), 376–392.
Phalen, K. J., Khoury, J., Kalkwarf, H., & Lanphear, B. P. (2005). Residential injuries in U.S. children and adolescents. Public Health Reports, 120, 63–70.
Purkiss, J. A. (2006). Fire safety engineering: Design of structures (2nd ed.). Boston: Butterworth-Heinemann.
Quansah, R., Jaakkola, M. S., Hugg, T. T., Heikkinen, S. A., & Jaakkola, J. J. (2012). Residential dampness and molds and the risk of developing asthma: A systematic review and meta-analysis. PLoS ONE, 7(11), e47526.
Rashid, M., & Zimring, C. (2008). A review of the empirical literature on the relationships between indoor environment and stress in health care and office settings: Problems and prospects of sharing evidence. Environment and Behavior, 40, 151–190.
Redlich, C. A., Sparer, J., & Cullen, M. R. (1997). Sick-building syndrome. Lancet, 349(9057), 1013–1016.
Rollins, G. (2000). Preventing the fall: Designs on building safe homes for the elderly. National Safety Council. Retrieved from http://www.nsc.org/resources/issues/articles/fallfalls.aspx
1211
Rubenstein, L. Z., & Josephson, K. R. (2006). Falls and their prevention in elderly people: What does the evidence show? Medical Clinics of North America, 90(5), 807–824.
Sadowski, L. S., Kee, R. A., VanderWeele, T. J., & Buchanan, D. (2009). Effect of a housing and case management program on emergency department visits and hospitalizations among chronically ill homeless adults: A randomized trial. JAMA, 301(17), 1771–1778.
Saegert, S. C., Klitzman, S., Freudenberg, N., Cooperman-Mroczek, J., & Nassar, S. (2003). Healthy housing: A structured review of published evaluations of US interventions to improve health by modifying housing in the United States, 1990–2001. American Journal of Public Health, 93, 1471–1477.
Samet, J. M., & Spengler, J. D. (2003). Indoor environments and health: Moving into the 21st century. American Journal of Public Health, 93, 1489–1493.
Sandel, M., Phelan, K., Wright, R., Hynes, H. P., & Lanphear, B. P. (2004). The effects of housing interventions on child health. Pediatric Annals, 33, 474–481.
Sherriff, A., Farrow, A., Golding, J., & Henderson, J. (2005). Frequent use of chemical household products is associated with persistent wheezing in pre-school age children. Thorax, 60(1), 45– 49.
Singh, A., Syal, M., Grady, S. C., & Korkmaz, S. (2010). Effects of green buildings on employee health and productivity. American Journal of Public Health, 100(9), 1665–1668.
Solari, C. D., & Mare, R. D. (2012). Housing crowding effects on children's wellbeing. Social Science Research, 41(2), 464–476.
Stahre, M., VanEenwyk, J., Siegel, P., & Njai, R. (2015). Housing insecurity and the association with health outcomes and unhealthy behaviors, Washington State, 2011. Preventing Chronic Disease, 12, E109.
Steinfeld, E., & Maisel, J. (2012). Universal design: Creating inclusive environments. San Francisco: Jossey-Bass/Wiley.
1212
Sundell, J. (2004). On the history of indoor air quality and health. Indoor Air, 14, 51–58.
Sundell, J., Levin, H., Nazaroff, W. W., Cain, W. S., Fisk, W. J., Grimsrud, D. T.,…Weschler, C. J. (2011). Ventilation rates and health: Multidisciplinary review of the scientific literature. Indoor Air, 21(3), 191–204.
Tatoute. (2005). African Hut at Bana, Cameroon [Photo]. Retrieved from http://commons.wikimedia.org/wiki/File:Case_%C3%A0_la_chefferie_de_Bana.jpg
Tewy. (2006). Central High School [Photo]. Retrieved from http://commons.wikimedia.org/wiki/File:Central_High_School_(Grand_Junction,_Colorado).jpg
Thomson, H., Pettigrew, M., & Morrison, D. (2001). Health effects of housing improvement: Systematic review of intervention studies. BMJ, 323, 187–190.
Thörn, Å. (1998). The sick building syndrome: A diagnostic dilemma. Social Science & Medicine, 47(9), 1307–1312.
Tinetti, M. E., Speechley, M., & Ginter, S. F. (1988). Risk factors for falls among elderly persons living in the community. New England Journal of Medicine, 319, 1701–1707.
Torres-Duran, M., Barros-Dios, J. M., Fernandez-Villar, A., & Ruano-Ravina, A. (2014). Residential radon and lung cancer in never smokers: A systematic review. Cancer Letters, 345(1), 21–26.
Tranter, D. C. (2005). Indoor allergens in settled school dust: A review of findings and significant factors. Clinical and Experimental Allergy, 35(2), 126–136.
Ulrich, R., Zimring, C., Quan, X., & Choudhary, R. (2004). The role of the physical environment in the hospital of the 21st century: A once-in-a-lifetime opportunity. Center for Health Design. Retrieved from https://www.healthdesign.org/chd/research/role-physical- environment-hospital-21st-century
Ulrich, R. S., Zimring, C., Zhu, X., DuBose, J., Seo, H. B., Choi, Y. S., …Joseph, A. (2008). A review of the research literature on evidence- based healthcare design. HERD, 1(3), 61–125.
1213
U.S. Census Bureau. (2013). American Housing Survey for the United States: 2011 (Current Housing Report, Series H150/11). Retrieved from http://www.census.gov/library/publications/2013/demo/h150- 11.html
U.S. Department of Agriculture, Forest Service. (n.d.). Asbestos exposure and health facts. Retrieved from http://www.fs.usda.gov/detail/r5/landmanagement/resourcemanagement/? cid=stelprdb5363851
U.S. Department of Housing and Urban Development. (1995). Guidelines for the evaluation and control of lead paint hazards in housing (HUD-1547-LBP). Retrieved from http://www.hud.gov/offices/lead/lbp/hudguidelines/index.cfm
U.S. Department of Housing and Urban Development. (1999). Economic analysis of the final rule on lead-based paint. Retrieved from http://www.nhl.gov/offices/lead/library/enforcement/completeRIA1012.pdf
U.S. Environmental Protection Agency. (2003). Assessment of risks from radon in homes. Retrieved from www.epa.gov/radiation/docs/assessment/402-r-03-003.pdf
U.S. Environmental Protection Agency. (2009). Green building. Retrieved from http://www.epa.gov/greenbuilding/pubs/about.htm
U.S. General Accounting Office. (1995). School facilities: Condition of America's schools (GAO/HEHS-95-61). Retrieved from http://www.gao.gov/archive/1995/he95061.pdf
U.S. General Accounting Office. (1996a). School facilities: America's schools report differing conditions (GAO/HEHS-96-103). Retrieved from http://www.gao.gov/archive/1996/he96103.pdf
U.S. General Accounting Office. (1996b). School facilities: Profiles of school conditions by state (GAO/HEHS-96-148). Retrieved from http://www.gao.gov/archive/1996/he96148.pdf
U.S. Public Health Service, Office of the Surgeon General. (1986). The health consequences of involuntary smoking: A report of the
1214
surgeon general (DHHS Publication CDC-87-8398). Rockville, MD: U.S. Department of Health and Human Services.
Verderber, S. (2014). Residential hospice environments: Evidence- based architectural and landscape design considerations. Journal of Palliative Care, 30(2), 69–82.
Wakefield, J. (2002). Learning the hard way: The poor environment of America's schools. Environmental Health Perspectives, 110(6), A298–305.
Wakefield, M. A., Durkin, S., Spittal, M. J., Siahpush, M., Scollo, M., Simpson, J. A.,…Hill, D. (2008). Impact of tobacco control policies and mass media campaigns on monthly adult smoking prevalence. American Journal of Public Health, 98(8), 1443–1450.
Warda, L. J., & Ballesteros, M. F. (2007). Interventions to prevent residential fire injury. In L. S. Doll, S. Bonzo, D. Sleet, J. Mercy, & E. N. Haas, (Eds.). Handbook of injury and violence prevention (pp. 97–116). New York: Springer.
Warsco, K., & Lindsey, P. F. (2003). Proactive approaches for mold- free interior environments. Archives of Environmental Health, 58(8), 512–522.
Weitzman, M., Baten, A., Rosenthal, D. G., Hoshino, R., Tohn, E., & Jacobs, D. E. (2013). Housing and child health. Current Problems in Pediatrics and Adolescent Health Care, 43(8), 187–224.
Wentz, D., & Wentz, M. (2012). The healthy home: Simple truths to protect your family from hidden household dangers. New York: Vanguard.
Western Sustainability and Pollution Prevention Network. (2002). Janitorial Products Pollution Prevention Project. Retrieved from http://www.westp2net.org/Janitorial/jp4.cfm
Wheeler, W., & Brown. M. J. (2013). Blood lead levels in children aged 1–5 years—United States, 1999–2010. Morbidity & Mortality Weekly Report, 62(13), 245–248.
Willand, N., Ridley, I., & Maller, C. (2015). Towards explaining the health impacts of residential energy efficiency interventions—a
1215
realist review: Part 1. Pathways. Social Science & Medicine, 133, 191–201.
Wilson, J. Q., & Kelling, G. L. (1982). Broken windows: The police and neighborhood safety. Atlantic Monthly, March. Retrieved from http://www.theatlantic.com/doc/198203/broken-windows
World Health Organization. (2001). Formaldehyde. In WHO air quality guidelines for Europe (2nd ed., chap. 5.8). Retrieved from http://www.euro.who.int/_data/assets/pdf_file/0014/123062/AQG2ndEd_5_8Formaldehyde.pdf
World Health Organization. (2009). Guidelines for indoor air quality: Dampness and mould. Geneva: Author.
World Health Organization. (2015). International Programme on Chemical Safety: Asbestos. Retrieved from http://www.who.int/ipcs/assessment/public_health/asbestos/en
Wu, F., Jacobs, D., Mitchell, C., Miller, D., & Karol, M. H. (2007). Improving indoor environmental quality for public health: Impediments and policy recommendations. Environmental Health Perspectives, 115, 953–957.
Yeoh, B., Woolfenden, S., Lanphear, B., Ridley, G. F., Livingstone, N., & Jorgensen, E. (2014). Household interventions for preventing domestic lead exposure in children. Cochrane Database of Systematic Reviews, 12, CD006047.
Young, B., Wynn, P. M., He, Z., & Kendrick, D. (2013). Preventing childhood falls within the home: Overview of systematic reviews and a systematic review of primary studies. Accident; Analysis and Prevention, 60, 158–171.
Yudelson, J. (2008). Choosing green: The homeowner's guide to good green homes. Gabriola Island, BC: New Society.
Zimring, C., & Bosch, S. (2008). Building the evidence base for evidence-based design: Editors' introduction. Environment and Behavior, 40, 147–150.
Zock, J. P., Vizcaya, D., & Le Moual, N. (2010). Update on asthma and cleaners. Current Opinion in Allergy and Clinical Immunology, 10(2). 114–120.
1216
For Further Information Organizations for Healthy Buildings
American Institute of Architects: http://www.aia.org/practicing/designhealth. The AIA is the major professional organization of the architecture profession. Its Design and Health initiative focuses on health aspects of buildings.
Delos: http://delos.com/about/well-building-standard. This private firm released its WELL Building Standard in 2013, aiming to promote market adoption of healthy building design.
Healthy Building Network: http://www.healthybuilding.net. A national network of green building professionals, environmental and health activists, and others who promote healthier building materials as a means of improving public health and preserving the global environment.
Organizations for Healthy Health Care Design Academy of Architecture for Health (AAH): http://www.aia.org/aah_default. This component of the American Institute of Architects specializes in health care architecture.
Alliance for Healthy Homes: http://www.afhh.org. A national, nonprofit, public interest organization working to prevent and eliminate hazards in homes such as lead, mold, carbon monoxide, radon, pests, and pesticides.
Center for Health Design: http://www.healthdesign.org. Through research, education, advocacy, and technical assistance, this organization supports health care and design professionals all over the world in their quest to improve the quality of health care through evidence-based building design.
Green Guide for Health Care: http://www.gghc.org. Green Guide for Health Care compiles a best practices guide for healthy and sustainable building design, construction, and operations for the health care industry.
1217
Health Care Without Harm: http://www.noharm.org/us. A coalition of organizations working to protect health by improving environmental performance in the health care sector.
Hospitals for a Healthy Environment (H2E): http://www.h2e- online.org. A national movement for environmental sustainability in health care, jointly founded by the American Hospital Association, the U.S. Environmental Protection Agency, Health Care Without Harm, and the American Nurses Association. H2E educates health care professionals about pollution prevention opportunities and provides tools and resources to facilitate the industry's movement toward environmental sustainability.
Practice Greenhealth: http://www.practicegreenhealth.org. A nonprofit membership organization formed through a merger of Hospitals for a Healthy Environment, Green Guide for Health Care, and Healthcare Clean Energy Exchange. It offers environmental solutions for the health care sector to use to achieve better, safer, and greener workplaces and communities.
Organizations for Healthy Homes National Center for Healthy Housing: http://www.centerforhealthyhousing.org. Founded as the National Center for Lead-Safe Housing to bring the public health, housing, and environmental communities together to combat childhood lead poisoning, and renamed National Center for Healthy Housing to reflect an expanded mission to help to decrease children's exposure to additional biological, physical, and chemical hazards in the home.
U.S. Department of Housing and Urban Development, Healthy Homes Initiative: http://www.hud.gov/offices/lead/hhi/index.cfm. A federal program that holistically addresses a variety of environmental health and safety concerns, including mold, lead, allergens, asthma, carbon monoxide, home safety, pesticides, and radon.
Organizations for Healthy Schools Healthy Schools Network: http://www.healthyschools.org. A national nonprofit organization that does research and
1218
education, coalition building, and advocacy to ensure that every child has a healthy learning environment that is clean and in good repair.
U.S. Environmental Protection Agency, Healthy Schools Web site: http://www.epa.gov/schools. A federal agency Web site designed to provide one-stop access to the many programs and resources available to prevent and resolve environmental issues in schools. It includes the EPA's Healthy School Environments Assessment Tool (HealthySEATv2), a customizable, user- friendly software program that helps school districts to evaluate and manage environmental, safety, and health issues.
U.S. Green Building Council, Center for Green Schools: http://www.centerforgreenschools.org. Part of USGBC, the major green building organization, this center works to drive the transformation of all schools into sustainable and healthy places to live, learn, work, and play. The Web site offers a range of practical information.
Organizations for Green Building International Living Future Institute: http://living-future.org. This organization houses the Living Building Challenge, a rigorous green building performance standard.
Southface Energy Institute: http://www.southface.org. A nonprofit organization that promotes sustainable homes, workplaces, and communities through the use of environmentally friendly technologies and techniques, and that also provides information on residential and commercial buildings.
U.S. Environmental Protection Agency, Green Building Web site: http://www.epa.gov/greenbuilding. A federal agency Web site that provides information on various aspects of green building, including energy efficiency, water efficiency, and waste reduction.
U.S. Green Building Council: http://www.usgbc.org. A nonprofit organization that promotes environmentally friendly buildings and is well known for its Leadership in Energy and Environmental Design (LEED) Green Building Rating System™,
1219
which provides tools and performance criteria for those designing, building, and operating buildings. LEED standards are available for new construction, existing buildings, specific building types such as schools and retail stores, and neighborhoods.
Organizations for Universal Design, Including Building Design for the Elderly
American Institute of Architects (AIA), Design for Aging: http://www.aia.org/practicing/groups/kc/AIAS075684? dvid=&recspec=AIAS075684. An AIA knowledge community that aims to foster design innovation and disseminate the knowledge necessary to enhance the built environment and quality of life for an aging society.
American Society of Interior Designers, Design for Aging: https://www.asid.org/content/design-aging#.Vbj-wvm6eUk. An initiative of interior designers working to meet the needs and wishes of older persons, and of the entities and providers who support them.
Cornell Medical School, Environmental Geriatrics: http://www.environmentalgeriatrics.org. Defining environmental geriatrics as the study and application of design principles to interiors and products to optimize the health, function, and well-being of older adults, this Web site offers information about and links to elder-friendly building design.
1220
Chapter 21 Work, Health, and Well-Being
David Michaels and Gregory R. Wagner
Dr. Michaels and Dr. Wagner report no conflicts of interest related to the authorship of this chapter.
1221
Key Concepts Work, health, and well-being are closely and inextricably linked.
The health of workers in any type of workplace, from the assembly line to the white-collar office, can be affected by exposure to health or safety hazards, by workplace policies, and by the organization of work itself.
As a result of exposure to workplace hazards, millions of workers are injured on the job every year, hundreds of thousands become sick, and tens of thousands die from occupational causes.
The costs of these injuries, illnesses, and deaths are borne primarily by workers and their families and by taxpayer- supported social safety net programs. Employers bear only a small fraction of these costs.
Employers in the United States are required under the law to provide safe workplaces to their employees. Government agencies attempt to ensure that employers meet this legal responsibility. Successful interventions to prevent and reduce occupational injury and illness require particular attention to those modifiable environmental risk factors resulting from hazardous exposures as well as to work policies and practices. The most effective way to prevent workplace injuries, illnesses, and fatalities is for employers to adopt comprehensive safety and health management systems.
Worker safety and health is more than a labor issue or a factor in an economics discussion; it is an issue with broad implications for public health and global human rights.
People work in a wide range of environments—indoors or outdoors, from underground or under water to in the air, and from large factories to small retail shops and restaurants. And many work in their own homes or cars. What they have in common is the important role their work environment—including physical,
1222
chemical, and psychosocial exposures and the way their work is organized—plays in their health and well-being.
This chapter explores the interactions of work and health and how we learn about them. We will consider a few specific exposures that are commonly faced and the results of these exposures. Many of these exposures are similar to but frequently more intense than those faced by people in the general environment. Workers are often exposed “first and worst.” Health risk from work is unevenly distributed throughout the working population, and we focus on some of the most vulnerable workers and the reasons for their vulnerability. Finally, we look at some of the legal protections that are supposed to prevent or mitigate risk to workers and respond to those who are injured or sickened by their work.
1223
The Interaction of Work and Health Work and health are closely and inextricably linked. Income from employment provides the material means to obtain basic life necessities such as shelter and food and enables acquisition of desired goods and services.
For many people, work is an important if not the dominant activity in their lives, with work and work travel time consuming as much as half of their waking hours in most weeks. Work and the skills used at work are central to self-identity for many individuals. From childhood onward we talk about careers and what we hope to do “when we grow up.” Your occupation—what you “do”—is commonly an important component of introductory conversations, defining you to others.
Work is also closely associated with health status. People who are able to work are generally healthier than those who cannot. Workers with higher incomes have better physical and mental health status and live longer on average than lower wage workers. There are several mechanisms through which this occurs. Lower income individuals and families tend to have poorer nutrition and reduced educational opportunity, and are more likely to live in polluted or high crime neighborhoods or to be employed in a job that damages their health. The risk of heart disease, cancer, mental illness, and numerous other diseases and conditions is influenced greatly by income level.
The connection of work to health is a two-way street: unemployment is associated with higher incidence of many diseases, poorer physical and mental health in general, increased hospital admissions and use of medical care, and premature mortality. People who become sick or injured at work are more likely to leave employment and end up sicker.
In addition to income, work arrangements and policies have a powerful effect on the ability of families to address health and non- health-related challenges and crises, and therefore they impact the health of all family members. A large percentage of Americans obtain their health insurance through their employment, and the quality and extent of that coverage is influenced by their income and
1224
the policies offered by their employer. Many people work more than one job to obtain adequate income. This may result in less time for family interaction and child raising. Many jobs offer little or no flexibility in work hours or in the use of leave time, making it difficult for workers who are also caregivers to be there when their child, parent, or other family member needs help.
Although some jobs may sustain or improve health, others may cause or contribute to injury, illness, or death through exposure to physical, chemical, biological, or psychological hazards. And many jobs have elements that can improve health and well-being but also expose workers to hazards.
Work Injuries and Illnesses Impose Heavy Costs on Workers, Families, and the Economy Globally, someone dies every fifteen seconds from an occupational disease or fatal work-related injury. The International Labour Organization (ILO) estimates that more than 2.3 million deaths occur annually from work-related causes. Another 313 million incidents occur each year that result in serious and disabling injuries and an economic burden of 4% on global gross domestic product (ILO, n.d.).
According to the U.S. Bureau of Labor Statistics (BLS), approximately 4,700 American workers suffer fatal traumatic injuries on the job each year, and employers record more than 3 million serious occupational injuries annually on the injury and illness logs they are required by law to maintain (BLS, 2014a–2015). Recordable workplace injuries range in severity from those requiring care beyond first aid to fatal injuries. Nearly half of recorded injuries require at least a day away from work, a job transfer, or work restriction for recovery (BLS, 2014b). The economic costs of occupational injuries are enormous. The National Safety Council, for example, estimates that fatal and nonfatal work injuries in the United States cost more than $200 billion in 2013 (National Safety Council, 2015). To put this in perspective, these estimates are in the same range as the estimated costs of dementia or of diabetes (American Diabetes Association, 2013; Hurd, Martorell, Delavande, Mullen, & Langa, 2013).
Following a series of studies showing that employer logs did not
1225
contain a substantial portion of workplace injuries reported elsewhere (among, for example, workers' compensation claims or records of emergency department visits), it is now widely recognized that the government's estimates of work-related injuries substantially understate the incidence of workplace injuries, probably by between 40% and 70% (Spieler & Wagner, 2014). This suggests that the actual costs of workplace injuries are also likely to be far higher than current estimates.
Even less is known about the extent of work-related illnesses, since for most occupational illnesses there is usually a time lag (known as a latent period) between hazardous exposures and the development of symptoms. In part because of this latency, most illnesses with an occupational cause or contribution are not recognized as work related. However, several studies have estimated that approximately 50,000 annual U.S. deaths are attributable to past workplace exposure to hazardous agents such as asbestos, silica, and benzene, with another 400,000 workers suffering nonfatal illnesses from such exposures (Shulte, 2005; Steenland, Burnett, Lalich, Ward, & Hurrell, 2003). In comparison, about 33,000 people died in traffic crashes in the United States in 2013 (National Highway Traffic Safety Administration, 2014).
The workplace hazards that cause or contribute to injuries and illnesses differ depending on the industry and nature of the work. Garment and textile industry workers, for example, may be exposed to cotton dust, which can cause lung disease, and repetitive motion hazards, which can lead to carpal tunnel syndrome and other musculoskeletal disorders (MSDs). They may work in close quarters, with fire hazards or poor ventilation. The 2013 Rana Plaza factory collapse in Bangladesh, which killed more than 1,100 mostly women workers, was a harsh reminder that many people work in dangerous structures with building code violations. Factories where electronics are assembled, in contrast, must be clean and temperatures well controlled. The global electronics industry employs vast numbers of workers. For example, one company, Foxconn, employs nearly 2 million workers in China alone to make cell phones, computers, and other electronic products. Workers in electronics manufacturing may be exposed to a variety of chemical solvents that are associated with neurological symptoms and cancer, as well as to hazards associated with excessive work hours and
1226
production quotas.
While this is especially true for workers in developing countries, harsh working conditions continue for many U.S. workers as well. About 250,000 workers in the United States are employed in poultry processing plants, facing production line speeds up to 140 birds per minute. They frequently suffer disabling musculoskeletal injuries from forceful, repetitive movements; respiratory symptoms from disinfecting agents and organic dusts; and also lacerations and skin infections.
More than 500,000 workers employed in health care and social assistance jobs are injured each year, the largest number in any industry. The likelihood of a hospital worker being injured on the job is higher than that for a worker in construction or manufacturing. According to the BLS, almost one in every seven employees of state-run nursing or residential care facilities is injured each year. Other high-hazard industries include agriculture, forestry, fishing, and hunting; arts entertainment and recreation; and transportation and warehousing (BLS, 2014a–2015).
Perhaps the most common workplace hazards come from ways a worker's body must act to perform the requirements of a job that is designed without adequate consideration of that worker's health and safety. These hazards are called ergonomic hazards; they are characterized by physical activities that require combining repetitive and/or forceful motions with awkward postures and positions. Musculoskeletal disorders, caused primarily by ergonomic hazards, account for one third of all employer-recorded, work-related injuries that result in days away from work; these conditions are prevalent across many industries and occupations (BLS, 2014b).
There is much evidence that the prevalence of these conditions is greatly underestimated, especially in industries in which African American and Latino workers are disproportionately employed. When scientists from the National Institute for Occupational Safety and Health (NIOSH) surveyed workers employed in a large poultry processing plant in South Carolina, they found that more than 40% of workers had evidence of carpal tunnel syndrome, an MSD associated with repetitive, forceful hand activities (such as cutting up chicken). Few if any of those cases had made it onto the
1227
employer's log of injuries and illnesses. (Text Box 21.1 examines the consequences of work injuries.)
Low and stagnant wages have forced some wage earners, especially those supporting a family, to hold two or more jobs. Beyond its detrimental impact on family life, working long hours leads to worker fatigue and increases the risk of work-related and non-work- related injuries, as well as motor vehicle crashes (Dembe, Erickson, Delbos, & Banks, 2005).
1228
Text Box 21.1 “Statistics Are People with the Tears Wiped Away” Reports and studies based primarily on statistical analyses can feel like a disservice to the people who make up the statistics, since individuals' experiences are aggregated to produce “averages.” This is certainly true of the workers and their families who suffer the consequences of work injuries and illnesses. The challenges faced by workers trying to support their families after suffering a disabling injury are daunting, and statistics alone cannot convey their reality. Here is one example.
Robert worked for a Virginia foam insulation manufacturer. One day, he climbed up on a foam grinder to clean out some material, and the manager, not realizing he was there, turned on the machine. Robert's right foot was mangled by the machine. Since then he has had multiple surgeries and must wear a special boot to walk. After his injury Robert and his wife, Jessica, could no longer save money toward a new home. The family lived in a homeless shelter until they found a new apartment—one that was mold-ridden and infested with fleas. Jessica wrote to then President Obama:
My husband lives with constant chronic pain every day of the week and he tosses and turns throughout the night. Before being injured my husband played basketball or football every single day and he ran and played outside with our two toddler sons. He was a weight lifter and a fisherman and a hunter, these are all things he can no longer partake in due to his injuries from work.
His life the way he lived it was robbed from him and he will never be the same. We have three children, Evan who is 3, Tristan who is 2, and their new sister Halley who is 3 months old. We are struggling financially so badly because of this “accident” and the negative effect it has had on his pay.
1229
Vulnerable Workers While all workers exposed to hazardous conditions at work may be injured or sickened, some workers are more likely than others to have such exposures and are less likely to report hazardous conditions, be appropriately trained or supplied with protective equipment to deal with the conditions, or receive compensation and medical benefits if they are injured. These vulnerable workers are likely to work in high-hazard occupations, have a higher probability of being first-generation immigrants, and are unlikely to be represented by a union.
Historically, many of the most dangerous jobs in the United States have been held by immigrants or by African Americans. For example, studies have shown that throughout the twentieth century, African American workers employed on coke ovens and in tire manufacturing plants were assigned to the jobs with the highest levels of exposure to toxic substances and, as a result, were at greatly increased risk of developing cancer (Michaels, 1983).
Today, many of the most hazardous jobs in the United States are held by immigrant workers (Steege, Baron, Marsh, & Menendez, 2014). According to BLS data, the overall fatality rate in 2013 for U.S. construction workers was 8.6 deaths per 100,000 workers, but for Latino construction workers the rate was 9.8 (Byler, 2013). Workers who do not have legal documentation to work in the United States are at particularly increased risk of injury and illness. Although they are concentrated in hazardous jobs, their legal status (and fear of deportation) makes it less likely they will raise safety concerns with either their employer or with government agencies who might assist them.
As in other maturing economies, employment patterns in the United States have changed substantially over the last half century. In the 1960s, half of the jobs were in manufacturing and goods- producing industries. Today, 70% of jobs are in the service sector, from hospitality and retail to delivery drivers and home care aides. People may work for dozens of different companies throughout their lives, with a larger share than ever involved in nontraditional work, such as independent contracting or temporary work.
Many workers in temporary jobs work for multiple employers or are hired either through staffing agencies or from day-labor pools.
1230
Temporary workers are generally the first hired and first fired; their numbers grow in times of economic recovery but fall quickly when a downturn occurs. Working in different settings with frequent changes makes it difficult to recognize and respond to worksite-specific hazards. Warning signs and work instructions may not be provided in a language spoken by the worker. These workers may also be unaware of the protections that are supposed to be provided on the job, and be worried that identifying problems may result in job loss. These most vulnerable workers disproportionately bear the burden of occupational injuries and illnesses. Many lower wage jobs (defined as jobs whose median wages do not raise a family of four above the poverty line) are also high-hazard jobs, and low-wage workers are injured on the job at a disproportionate rate (Steege, Baron, Marsh, & Menendez, 2014).
The health of workers in any type of workplace, from the assembly line to the white-collar office, can be affected by workplace policies and the organization of work itself. Workplace policies cover such diverse health-relevant areas as availability of paid sick leave; the amount of advance notice a worker gets when a working shift is cancelled, extended, or otherwise changed; whether the employer can mandate overtime shifts; the availability of protective clothing, a place to change, and toilet facilities; how workers are disciplined for rule infractions; and so forth. All of these policies can have a profound impact on a worker's sleep patterns, availability to deal with family responsibilities and emergencies, and overall health and well-being. While any type of work can be the source of stress, studies have shown that high-stress jobs may not have a deleterious impact on individual workers if they can adequately control their environments and the demands put on them. In other words, the assembly-line job in which the worker cannot control the speed of the environment will have a more consequential effect on the worker than the stress faced by the chief executive, who may feel great pressure but who has a greater ability to control how he or she responds to the stress.
Health Care Facilities: Occupational Safety and Health Challenges and Opportunities Preventable medical errors cause tens of thousands of deaths every year, and one in every twenty patients develops a health care–
1231
associated infection while hospitalized. With good reason, patient safety and improving the quality of care received by hospital patients have become well-known national priorities for the American health care system.
Less well known but also startling are the rates of work-related injuries and illnesses among health care workers—even higher than for construction and manufacturing, and for some occupations, more than double the average for all private industry. Across the country, nursing aides, orderlies, and attendants have an incidence rate of musculoskeletal injuries more than seven times the average for all industries, and it is increasing. Ultimately, the toll of such injuries and illnesses echoes not only through the lives of workers and their families but also through health care institutions and the care of patients.
There is a clear link between patient safety and worker safety in hospitals. If nursing aides are unable to lift patients without endangering their backs and if emergency room personnel are fearful of being assaulted, the quality of their patient care suffers.
The consequences of the health care industry's failure to improve the work environment are substantial not only for the workers affected but also for society. Along with chronic pain and loss of function, absenteeism, and turnover among workers, health care worker injuries also result in higher employer costs due to medical expenses, disability compensation, and litigation. As many as 20% of nurses leave direct patient care positions because of risks associated with their work.
1232
Protecting Safety and Health on the Job In the late nineteenth and early twentieth centuries, immigrant workers built the railroads and produced the steel needed for America's rapid industrial development. It is no exaggeration to say that the nation's evolution as an industrial power was marked by carnage in the workplace. An early survey of workplace fatalities in the United States took place in Allegheny County, Pennsylvania, from July 1906 through June 1907. The results are represented on a gruesome “Death Calendar” (see Figure 21.1). In that county alone, 526 workers died in “work accidents” during that twelve-month period, and 195 of them were steelworkers—a steelworker death on the job roughly every two days (Eastman, 1910). While there were no national surveys of work-related fatalities in that era, in 1913 the Bureau of Labor Statistics estimated 23,000 industrial deaths in a workforce of 38 million, equivalent to a rate of 61 deaths per 100,000 workers, almost twenty times the current rate. (Centers for Disease Control and Prevention, 1999).
1233
Figure 21.1 From July 1906 Through June 1907, 526 Workers Were Killed on the Job in Allegheny County, Pennsylvania
Adapted from: Eastman, 1910.
Social activists in the progressive era focused considerable energy on workplace safety, attempting to reduce the high injury and fatality rates among these workers. In The Jungle, Upton Sinclair alerted the country to dangerous working conditions facing immigrant packinghouse workers in Chicago, who slaughtered countless cows and pigs to feed the nation. (Sinclair was disappointed that his book was seen as a call for improved food safety rather than worker protection, lamenting “I aimed at the public's heart, and by accident I hit it in the stomach.”) Dr. Alice Hamilton, who later was the first woman appointed to the faculty of the Harvard Medical School, lived in working-class, immigrant neighborhoods and investigated the impact of the residents' harsh
1234
working conditions on their health. Her survey in 1910 of occupational illness in the State of Illinois led to one of the first laws requiring employers to implement certain safety practices.
On March 25, 1911, fire broke out on the top floors of the factory building near Greenwich Village, in lower Manhattan. The mostly young women employed in the sweatshop operated by the Triangle Shirtwaist Company saw the smoke and heard the cries from floors below and tried to flee the building, but the exit doors had been locked by their employer to prevent theft. Sprinklers and other fire prevention devices had never been installed in this ten-year-old building; they were available at the time, but there was no law requiring them in private workplaces.
Hundreds gathered outside the building to watch the tragedy unfold. The onlookers saw that the firefighters' ladders were too short and water from the hoses could not reach the top floors. And they watched as dozens of women and girls jumped to their deaths, more than 100 feet to the street below, to avoid the flames. A total of 146 workers, mostly Italian and Jewish immigrants and their children, were killed.
The social and political impact of this tragedy was enormous. Clothing workers' unions led the protests, and their membership grew enormously following the fire. Over the next several decades these unions were able to achieve significant economic gains for previously low-paid garment workers, and bring stability to a ferociously competitive industry.
The response to the Triangle fire marks the beginning of concerted government intervention in workplace safety. In New York State and elsewhere, there was for the first time widespread recognition that government intervention was needed to protect workers from hazardous conditions. Over the objections of business groups, New York adopted laws that limited the number of hours women and children could work, improved eating and toilet facilities for workers, and implemented fire codes that required, among other things, access to fire exits and the installations of sprinklers in commercial buildings.
One of the witnesses to the fire was a young social worker named Francis Perkins, who was having tea with a friend in nearby Greenwich Village when the fire broke out. Perkins described what
1235
she saw: “One by one, the people would fall off… There began to be panic jumping. There was no place to go. The fire was between them and any means of exit. It's that awful choice people talk of—what kind of choice to make?” (Downey, 2010). Witnessing the tragedy propelled Perkins to a life of advocacy for worker rights. In 1933, President Franklin Roosevelt appointed her to the position of Secretary of Labor, the nation's first female cabinet member. She was the longest serving secretary in the history of the Labor Department, and she was instrumental in the enactment of many of the nation's most important worker protections, including pensions for older Americans, unemployment benefits, and minimum wage and overtime laws.
In the years after the Triangle Shirtwaist fire, some states, particularly northern industrial states, implemented factory inspections programs. These programs focused primarily on safety, although many also attempted to limit acute exposures to highly toxic chemicals. In general, though, these programs were small and not well resourced.
During the Great Depression, much of the United States was riveted by Congressional hearings into an occupational health disaster of a different sort: silicosis. Several thousand workers, mainly African Americans, were hired to dig a tunnel for a hydroelectric project in Gauley Bridge, West Virginia. When it was discovered that the mountain through which they dug was more than 90% pure silica, the excavation was expanded to extract more of this industrial- grade material. Men started dying of silicosis within months after exposure began. Hundreds if not thousands died and many of the survivors were disabled for life. There is no exact count of the dead, since the bodies of many workers were simply buried in unmarked graves, with no death certificate or autopsy (Cherniack, 1986).
The Government's Role in Protecting Workers The social upheavals of the 1960s brought a new focus on the need for federal programs to protect the public's health, safety, and environment. Just as civil rights and antiwar demonstrations compelled changes in federal policies, environmentalists and labor unions forced public attention on unsafe air, water, and workplaces. Coal miners picketed on Capitol Hill to demand protections from black lung disease. Labor union members who worked in chemical
1236
plants, automobile factories, and steel mills insisted that lawmakers address high rates of cancer and other ailments in their ranks. Efforts at the state level were inadequate to address these national problems. Congress responded to several coal mine disasters, as well as massive protests over the failure of the workers' compensation systems in West Virginia, Kentucky, and other coal mining states, by passing the Federal Coal Mine Health and Safety Act of 1969, generally referred to as the Coal Act (also see Text Box 21.2). The following year, Congress passed the Occupational Safety and Health Act (OSH Act) of 1970, creating the Occupational Safety and Health Administration (OSHA) and the National Institute for Occupational Safety and Health (NIOSH), and, for the first time, establishing as national policy the right of workers to a safe workplace. In its early years OSHA issued regulations to address many of the most serious hazards faced by workers, including rules addressing scaffolds and machine guarding and also exposure to asbestos, lead, benzene, and cotton dust.
By law, employers are required to provide safe workplaces, free of recognized serious hazards. Under the OSH Act, OSHA, located in the U.S. Department of Labor, is the primary government agency charged with ensuring that employers meet the requirements of the law. One notable aspect of the law is that it provides states with the option of implementing their own OSHA programs, as long as they are “at least as effective” as the federal OSHA regulations. In all, twenty-one states have chosen to operate state OSHA programs covering both private and public sector workers, leaving the federal OSHA with responsibility in twenty-nine states and the District of Columbia. Of these twenty-nine states, only five have OSHA programs that cover public sector workers; the 8 million state and county workers in the remaining twenty-four states have no OSHA coverage and do not have the legal right to a safe workplace.
1237
Text Box 21.2 Mine Disasters, Miner Protections Some commentators have noted that occupational safety and health legislation has been written with the blood of workers. This is nowhere more true than in the laws protecting miners. Each of the modern laws has resulted at least in part from disasters, enacted while the consequences of mining hazards were fresh in the minds of the public and legislators.
The U.S. Bureau of Mines was created in 1910 following the 1907 explosion at the Monongah Mine in West Virginia that killed at least 362 miners and the 1909 fire at the Cherry Mine in Illinois that killed 259 men.
The Coal Mine Health and Safety Act of 1969 was passed soon after a 1968 fire and explosion killed 78 miners in a mine near Farmington, West Virginia.
The Federal Mine Safety and Health Act of 1977 (known as the Mine Act), extending and improving protections for both coal and non-coal (mineral and rock) miners, was passed following a 1976 disaster at the Scocia Mine in Kentucky that resulted in 28 deaths.
The Mine Improvement and New Emergency Response Act (MINER Act), amending the Mine Act, was passed in 2006 following disasters at the Sago, Darby, and Crandall Canyon mines that resulted in 23 deaths.
Mine workers are covered by the Mine Safety and Health Administration (MSHA), also part of the U.S. Department of Labor. The U.S. Department of the Interior's Bureau of Safety and Environmental Enforcement provides safety and health coverage for workers drilling for oil or gas three or more miles beyond the shore, and various agencies in the U.S. Department of Transportation cover safety and health for truck drivers and some workers involved with railroads, air transportation, and pipelines.
In theory, each of these agencies has a similar set of tools at its
1238
disposal to help protect the safety and health of workers. Each agency issues regulations that require employers to take certain steps to ensure workers are protected from hazards. The agencies produce and disseminate materials to help employers comply with agency regulations and make their workplaces safer. And each agency employs inspectors to determine whether employers are meeting the requirements of the regulations.
However, these tools are, for the most part, quite limited, and none of the agencies has adequate resources to fulfill its mission successfully. Together, federal and state OSHA programs employ approximately 2200 inspectors, to safeguard roughly 130 million workers employed in between 7 million and 8 million workplaces— nearly 60,000 workers, and 3,600 workplaces, per inspector. In all, OSHA inspectors visit fewer than 100,000 workplaces a year. The relative size of the safety and health inspectorate has changed dramatically over time. In the late 1970s, there were about fifteen federal compliance officers for every million covered workers. Currently, there are roughly seven inspectors for every million covered workers (AFL-CIO, 2015).
Many employers need little encouragement from government agencies to provide safe workplaces. These employers recognize the importance of safety, not only for the sake of their workforce but because they understand that “safety pays”—firms that are managed for safety are more profitable (see the section on sustainability, below). Other employers, however, allow workplace hazards to exist, perhaps out of ignorance or through thinking the hazards are unlikely to result in an injury to any of their employees. OSHA, MSHA, and other worker protection agencies focus their attention on these employers.
When OSHA was established in 1971, 28% of private sector workers were members of labor unions. Organized labor was a key player not only in the passage of the OSH Act but in pushing the agency to fully use its authority. Many of OSHA's health and safety standards were issued following petitions filed by labor unions urging OSHA to act. Today, less than 8% of workers belong to a union, making it more difficult for organized labor to influence occupational health and safety policy.
NIOSH, located within the U.S. Department of Health and Human
1239
Services, is the third federal agency with a primary focus on occupational health and safety. NIOSH is responsible for conducting research and applying research results—its own and those of other investigators—in order to make science-based recommendations for reducing occupational disease, injury, and deaths. Through its Health Hazard Evaluation program, NIOSH also responds to some requests from workers, employers, and other government agencies to investigate workplaces experiencing unusual outbreaks of disease or injury. In addition, NIOSH supports the training of health and safety professionals and scientific research, as well as the dissemination of information to those in a position to improve worker health, safety, and well-being.
Researchers, occupational medicine physicians, nurses, epidemiologists, ergonomists, industrial hygienists, safety engineers, and worker advocates are also key players in the public health community's efforts to improve health and safety protections for workers. Joining them are new coalitions of social justice, interfaith, and civil rights groups representing some of the most vulnerable workers in the United States. Groups such as the National Day Laborer Organizing Network, the National Domestic Workers Alliance, the Restaurant Opportunities Center, and worker centers affiliated with Interfaith Worker Justice provide resources for workers to learn about their rights to a safe workplace. Although worker centers are not labor unions, their members learn to engage collectively to raise safety and health concerns with government officials and speak up for their rights with less fear of retaliation from their employer. While public health professionals, unions, and other workers' rights organizations continue to advocate for stronger worker protections, trade associations and employer groups often hold that employers should be allowed to determine the level of safety in their workplaces with minimal government interference.
Safety and Health Management Systems (or Injury and Illness Prevention Programs) In order to protect the health and safety of their employees effectively, employers must go beyond simply complying with legal standards to embracing a comprehensive approach to prevention. The most effective way employers can accomplish this is by
1240
implementing a safety and health management system (also known as an injury and illness prevention program), a process in which employers and workers identify and fix workplace hazards in order to prevent workers from getting injured, sick, or killed on the job (Text Box 21.3). Many nations around the world, along with more than thirty U.S. states, require or encourage certain employers to implement such programs. Not only do employers with injury and illness prevention programs experience dramatic decreases in workplace injuries but they often report a transformed workplace culture that results in higher productivity and quality, reduced turnover, reduced costs, and greater employee satisfaction (OSHA, 2012).
1241
Text Box 21.3 Core Elements of All Safety and Health Management Systems
Management leadership. Managers at all levels of the organization demonstrate their commitment to improved safety and health, communicate their commitment, and document performance. Managers make safety and health a top priority, establish goals and objectives, provide adequate resources and support, and set a positive example.
Employee participation. Workers are actively involved in all aspects of the program, including setting goals, identifying hazards, investigating incidents, and tracking progress. Barriers to worker participation are eliminated, and workers are encouraged to communicate openly about safety and health concerns without fear of retaliation.
Hazard identification and assessment. Managers put processes and procedures in place to continually identify workplace hazards, evaluate risks, and monitor the effectiveness of prevention and control measures.
Hazard prevention and control. Managers ensure that processes, procedures, and programs are implemented to eliminate or control workplace hazards, and to track progress implementing them.
Education and training. All managers and workers receive education or training to carry out their responsibilities under the program.
Program evaluation and improvement. Managers and workers assess periodically the effectiveness of control measures, including identifying deficiencies and opportunities for improvement and taking the necessary actions to improve overall safety and health performance.
Safety and Health Standards
1242
OSHA, like other regulatory agencies, issues rules that employers must follow in certain situations (Table 21.1). One of the reasons these safety standards are effective is that most employers want to protect the health and safety of their employees and have no desire to break the law. Most employers thus instruct their managers to take the steps are necessary to comply with OSHA standards.
Table 21.1 The Public Health Impact of OSHA Regulations
OSHA standard (year) Public health impact Cotton Dust Standard (1978) Virtually eliminated brown
lung disease. Grain Handling Standard (1987) Grain bin explosions reduced
by >40%. Excavation & Trenching Standard (1989)
Trench fatalities reduced by 35%.
Bloodborne Pathogens (1991) and Needlestick Safety & Prevention Act (2001)
HIV and hepatitis B infections in health care workers reduced by >90%.
The hierarchy of controls (described more fully in Chapter 8, and corresponding to the prevention hierarchy discussed in Chapter 26) embodies the principle that the most effective way to control a hazard is to address it at its source. U.S. occupational health and safety regulations implement this principle by requiring or encouraging employers to use the most effective way to address the hazard, such as reducing exposure to toxic substances through substitution, putting barriers between workers and electrical hazards, using sound-dampening enclosures to reduce noise exposures, creating closed systems to avoid toxic exposures, or installing ventilation systems. Lowest priority is given to personal protective equipment, such as respirators, which are dependent on human behavior, often uncomfortable to wear, and inherently less reliable.
Control of Chemical Hazards With few exceptions, workers are the group with the highest exposures to chemical substances. In those workplaces where chemicals are produced or used, exposure levels are often many
1243
times higher than are found in the general environment. For example, children living near lead smelters have been found to be overexposed to that metal, although their exposures were only a fraction of the worker exposure levels in the smelter itself. Similarly, the cancer-causing chemical benzene is emitted by oil refineries, where worker exposure levels are several times higher than the exposure of the general public.
The U.S. legal structure allows workplace exposures to be far higher than exposures to the general public. In theory, EPA chemical regulations attempt to reduce the lifetime risk of illness from exposure to less than one in a million (see Chapter 6). The EPA also has specific mandates and authority to protect the most vulnerable —the very young and chronically ill—from airborne toxics. OSHA and MSHA standards are intended to protect people who are healthy enough to work, even if they are exposed throughout their working lifetime. While the goals of both the EPA and the worker protection agencies are often unmet, the EPA's standards are far stricter than those of OSHA and MSHA for the same substance.
These regulatory differences have implications for scientific research. Because workers sustain higher exposures than members of the general public, they are the proverbial “canaries in the coal mine.” It is for this reason that much of the epidemiological research on toxic chemicals is performed on workers; measuring the effects on less exposed nonworkers is more difficult. For example, chemical workers in China who were exposed to bisphenol A (BPA), a chemical used to make plastic products such as water bottles, were found to have low sperm counts (Li et al., 2011). These kinds of findings provide some of the strongest evidence supporting concerns about exposure to BPA in consumer products and in the general environment, (see Tox Box 6.1).
OSHA has been successful in limiting exposure to some of the best- known and most dangerous workplace chemicals, chemicals that were virtually unregulated before OSHA. For example, asbestos was widely present in commercial construction, shipyards, and the manufacture of certain friction products like brakes. OSHA tightly regulates current use, and few workers remain exposed to the substance (see Tox Box 20.3). However, OSHA's standards regulating workplace exposure to chemicals are for the most part out of date and inadequately protective. When Congress passed the
1244
OSH Act, it gave OSHA two years to adopt any then-existing national consensus or established federal standards. During that two year period, the agency adopted about 500 legally enforceable permissible exposure limits (PELs). Since then, OSHA has updated or issued new standards for only thirty or so chemicals— the remaining PELs are based on evidence from the late 1960s or earlier. For most workplace chemicals, OSHA has no standard at all.
OSHA does not have standards for many of the other hazards encountered by inspectors in the course of their work. In situations in which no standard exists, OSHA may issue citations under the General Duty Clause of the OSH Act, which states that the employer is required to provide a workplace “free from recognized hazards.”
OSHA Inspections and Penalties With its limited number of inspectors, OSHA will generally visit a worksite for one of the following reasons: because of a worker complaint, a fatality, or a serious injury or because the site is in a high-hazard industry and therefore subject to random visits. In theory, the threat of a monetary penalty encourages employers to comply with OSHA's requirements. OSHA penalties, however, have only been increased once in the agency's forty-five-year history. As of December 2015, the maximum penalties were $7,000 for a serious violation and $70,000 for a repeat or willful violation. At that time, the median OSHA penalty was issued at around $4,400 per inspection, and the median penalty issued resulting from an inspection following a worker fatality was just $9,800.
Even with these significant limitations, progress has been made in preventing work-related injury. In 1970, an estimated 14,000 workers were killed on the job, an annual rate of 18 per 100,000, or about 38 workers killed on the job every day. Today, with a far larger workforce, that rate has fallen to 3.3 per 100,000, or about 13 every day (BLS, 2015).
Fix the Workplace, Not the Worker Just as the obligation to control workplace hazards has generated controversy, our understanding of the root causes of workplace injuries and illnesses, and the means to prevent them from occurring, is contested terrain. For decades, many safety
1245
professionals were influenced by the work done in the 1930s by a safety expert named Herbert Heinrich. Heinrich claimed, based on his review of thousands of reports of injuries compiled by the insurance industry and employers, that 88% of work “accidents” were caused by “unsafe acts.” Although his assertion that the actions of workers were responsible for most workplace injuries was widely accepted, Heinrich was badly misguided on several levels. His most basic mistake was attributing the incident in which the worker was injured to a single cause, the act of a generally careless worker. By doing so, he gave license to employers to blame the victims (the workers) rather than look for the root causes. A more accurate and useful understanding of workplace incident causation involves recognition that there are many factors that contribute to the occurrence of an event and that the work environment—both physical and organizational—is critically important. Successful interventions to prevent and reduce occupational injury and illness require particular attention to modifiable risk factors such as hazardous exposures and also factors embedded in work policies and practices.
1246
Workers' Compensation In the first two decades of the twentieth century, most U.S. states established social insurance systems—workers' compensation plans—intended to provide medical care and partial wage replacement for injured workers until they had recovered sufficiently from their injuries to return to work. Over time, these systems evolved to cover (and exclude) various injuries and began to cover some illnesses as well. Each state system has its own rules and regulations as well as different benefit levels and durations for injured workers. There is no national (federal) system that applies to all workers with occupational diseases and injuries, although certain specific working groups, such as railroad workers and federal employees, are covered by national plans.
System Limitations The workers' compensation system was originally designed so that employer-provided insurance would reimburse workers for lost wages while providing medical coverage and rehabilitation associated with work-related injuries. Under this “no-fault” system, workers no longer have the right to sue their employer for an injury they suffered at work but, in theory, have relatively certain access to medical care and wages lost while they recuperate.
Injured workers, however, face numerous barriers to filing and receiving compensation for their injuries (Azaroff, Levenstein, & Wegman, 2002), and only a fraction of injured workers receive any benefits through the state workers' compensation programs (Shannon & Loew, 2012). For example, in an enumeration of all recordable work-related amputations in Massachusetts, less than 50% of the cases received any workers' compensation benefits (Davis et al., 2014). A similar study in California found that one third of employer-recorded amputation and carpal tunnel syndrome cases had not received workers' compensation benefits (Joe et al., 2014).
The workers' compensation system performs even more poorly for low-wage workers. Many injured low-wage workers face additional barriers to filing, including greater job insecurity, lack of knowledge
1247
about their rights, or a limited command of English. In particular, immigrant workers may fear wrongful termination or retaliation for filing or even reporting an injury. These barriers are documented in numerous surveys of low-wage and immigrant workers who report being injured on the job and not filing a workers' compensation claim (Smith, 2012).
The challenges facing individuals with occupational illnesses are even greater, and it is the rare worker with an occupational illness who receives any benefits from the compensation system. Most cases of work-related chronic disease are rarely diagnosed as work related. When that linkage is made, the diagnosis generally comes long after employment ends. Even when the proper diagnosis is made, a worker who is eligible for benefits under Medicare, Medicaid, the Veterans Health Administration, or a private insurer is more likely to take that route, and avoid the challenges of obtaining benefits through the workers' compensation system (Leigh, 2011; Leigh & Robbins, 2004).
Who Pays for Work-Related Injuries and Illnesses? The workers' compensation system was originally designed so that employers would bear the costs of workplace injury and illness. In theory, bearing these costs provides an incentive to employers to eliminate hazards and therefore prevent injuries and illnesses from occurring. However, in the United States currently, the costs of workplace injury and illness are borne primarily by injured workers, their families, and taxpayer-supported safety net programs. Workers' compensation payments cover only about 21% of lost wages and medical costs due to work injuries and illnesses, and private health insurance handles only 13%. Workers and their families pay for 50% of these costs, with taxpayers shouldering the remaining 16% (Leigh & Marcin, 2012) (also see Figure 21.2).
1248
Figure 21.2 Who Bears the Cost of Worker Injuries? Source: Leigh & Marcin, 2012.
For working families struggling to meet basic necessities and set aside some savings, a work injury to a breadwinner can be especially devastating. A recent study of the impact on earnings, for instance, found that workers in New Mexico who receive workers' compensation benefits for wage loss caused by workplace injuries lose an average of 15% of predicted earnings over the ten years following the injury. Even with workers' compensation benefits, an injured worker's income is, on average, almost $36,000 less over ten years than if the injury had not occurred (Scherer, Seabury, O'Leary, & Ozonoff, 2014).
Workplace injuries can also cause loss of self-esteem and self- confidence, stress in relationships between spouses and with children, and strained relations with colleagues and supervisors. These indirect costs can translate into tangible economic costs, including lower wages (Keogh, Nuwayhid, Gordon, & Gucer, 2000; Strunin & Boden, 2004).
It is likely that the proportion of the costs of work injuries and illnesses covered by working families and taxpayers has risen in recent years, as many state legislatures have enacted changes in their workers' compensation systems that have made it more difficult for injured workers to obtain benefits. Indeed, during the first decade of this century, reductions in workers' compensation benefits have correlated with expansions in the Social Security
1249
Disability Insurance program, the federal program that provides benefits to disabled workers below the age of 66.
1250
Sustainability The health and safety of the workforce is an important but often neglected component in sustainable economic development. In the fossil fuel industries—coal mining and oil and gas drilling and refining—workers suffer high levels of injuries, illnesses, and fatalities (in addition to the better-known environmental issues linked with the use of these fuels, as discussed in Chapters 12 and 14). The transition from carbon dependence to sustainable energy provides hope for improving overall worker health and safety. More generally, according to the ILO, “Economic growth is not sustainable when it is based on poor and unsafe working conditions, suppressed wages and rising working poverty and inequalities.” Developing and emerging economies that invest in quality jobs experience greater improvement in living standards than nations that do not make quality jobs a priority (ILO, 2014).
However, a shift to sustainability—for example, to renewable energy and recycled or “green” products—does not necessarily guarantee improved workplace health and safety. For example, workers involved with wind turbines are at high risk of injury from falls and welding arc flashes. New techniques developed to construct green buildings, such as skylights and wastewater recovery, have resulted in worker fatalities. Workers at recycling facilities are exposed to arsenic, cadmium, other heavy metals, and organic dusts, as well as fire hazards and the risk of injury from repetitive motion. Insulating homes to be more energy efficient can expose the applicators to foams containing isocyanates, which can lead to adult-onset asthma. Thus even though emerging technologies are creating new green jobs and products, old safety hazards still exist in these workplaces.
A key aspect of sustainability is life cycle analysis—a reckoning of the health and environmental costs of products, from raw material harvesting, to manufacturing, to use, to disposal. Understanding the connections between workers' exposures during production and community and consumer exposures during use and disposal provides an important opportunity for cross-cutting public health interventions. Life cycle analysis also entails understanding the global supply chains that convey goods from place to place and
1251
expose workers, their families, and communities along the way. Worker safety and health is more than a labor issue or a factor in an economics discussion; it is an issue with broad implications for public health and global human rights.
Worker safety is also becoming a component of various measures of sustainability, especially as investors are looking to invest in sustainable firms. This investor interest in worker safety stems from the growing recognition that well-managed firms are safe firms, and that high injury rates are signs of a poorly managed firms. Public reporting of a firm's worker safety performance is therefore useful to investors who want to invest in well-managed firms. To support this interest, worker injury and illness rates are being incorporated into voluntary corporate reporting efforts, efforts supported by such organizations as the Global Reporting Initiative and, in the United States, the Sustainability Accounting Standards Board.
The close relationship between safety and sustainable management can be seen in the transformation of the aluminum producer Alcoa under the leadership of CEO Paul O'Neil. When O'Neil (who was later appointed Secretary of the Treasury by President George W. Bush) became CEO of Alcoa, he focused the entire corporation on the goal of zero injuries. As the company took tight control of production processes to drive down injury rates, Alcoa workers were able to produce higher quality products in a more efficient manner. Under O'Neil's leadership, Alcoa's net annual income increased fivefold, and its market capitalization grew by $27 billion. At the same time, the injury rate among Alcoa workers dropped dramatically, and it continues to be one of the safest manufacturing firms in the world (Duhigg, 2012).
1252
Globalization As a result of our drive toward globalization, work and its hazards no longer respect national boundaries. Many goods are assembled in one country from parts manufactured in multiple other places, and then the finished goods are distributed both nationally and internationally. Occasionally a large multinational employer takes responsibility for ensuring the health and safety of workers all along these complex supply chains, but more often hazards are confronted and addressed (or ignored) at the local level. In all countries the hazards confronting workers and the means of addressing them reflect evolving economic and political priorities and realities, social norms, legal structures, labor availability, and experience with prior approaches. Many low- and middle-income countries have limited means to ensure workforce protections. Many countries rely in whole or in part on standards or conventions developed by international organizations such as the International Labour Organization, a United Nations agency, to identify and describe the goals of their health and safety efforts. The ILO does not have enforcement powers, so the implementation of any conventions or standards that are adopted depends on local resources, legal powers, and commitment. The ILO aggregates and makes available extensive data relevant to work and working conditions, including occupational injuries (www.ilo.org/global/statistics-and- databases/lang-en/index.htm).
The ILO and the World Health Organization (WHO) have also provided leadership for international efforts to reduce or eliminate certain work hazards through technical assistance, training, and education. For example, the ILO has developed the Global Programme for Elimination of Silicosis, and has assisted a number of countries in developing national programs tailored to local conditions. The ILO and WHO have worked together to provide the technical support and training that enables countries to develop and implement these programs. Both organizations have focused on reducing or eliminating the use of asbestos as well, because of the risk it poses to both workers and others who inhale asbestos fibers in the general environment. They have also highlighted the plight of the most vulnerable workers, particularly children.
1253
National and international nongovernmental organizations, including labor unions and human rights organizations, actively promote worker protections. Some investigate, monitor, and report on working conditions and advocate for improved protections. Others are active in promoting specific legislation or control of particularly hazardous work. All have important roles to play in the recognition and mitigation of workplace risk and the prevention of injury and disease from workplace exposures.
In some instances, international pressure has led to improvements in working conditions in developing countries. For example, a series of catastrophic events in Bangladesh, culminating with the death of more than 1,100 workers in the 2013 Rana Plaza factory collapse, triggered international outrage at some of the well-known U.S. and European clothing brands that had contracted for the work being performed in those unsafe factories. In response, some Western clothing brands have formed organizations whose aim is to help identify and eliminate the most significant hazards in Bangladesh clothing factories. While it appears that these programs have had some impact on conditions in this one country's clothing factories, the success of any program that aims at a single country will be limited. This limitation stems from the propensity of industries will move to locations where costs, including worker wages and safety requirements, are lower.
This raises important questions for citizens of all countries, but especially the developed ones: What is our responsibility to the worker in a developing country or an emerging industrial power, laboring in unsafe conditions to produce consumer products for Europe or the United States? As consumers of the products of her labor, do we share an obligation to ensure that she is able to work without putting her health and safety at risk?
If we believe that all workers should be able to come home safely to their families at the end of their shifts, then worker safety and health is more than a labor issue or a factor in an economics discussion; it is an issue of global human rights.
1254
Summary Work is a primary human activity and a key determinant of health. Accordingly, understanding the workplace—both physical circumstances, such as chemical exposures and injury risks, and social constructs, such as work organization—is essential to a full understanding of environmental health. Occupational injuries and illnesses occur in predictable patterns, related to particular industries, work practices, and levels of economic development; are often undercounted; and can impose a substantial burden on workers and their families. Among vulnerable populations such as low-wage workers, immigrants, and members of minority groups, this burden is especially high. Workers have the right to safe workplaces, and employers are responsible for providing workplaces free from serious hazards. Application of the hierarchy of controls and the systematic implementation of safety and health management systems by employers can greatly reduce risk of injury and illness; these practices are reinforced by government regulation. Compensation systems exist to pay for medical care and lost wages of workers who are injured or sickened on the job, and to assist them in rehabilitation and a return to functioning and employment, but these systems have serious limitations and often fail to provide the benefits to which these workers are entitled. Both globalization and the transition to sustainable economic activity will continue to shape occupational safety and health risks, and public health strategies, in coming years.
1255
Key Terms employment
Paid work. ergonomic hazards
Hazards that stem from work activities that are poorly designed, so that accomplishing them is associated with increased risk of injury or illness.
globalization The international integration of economic systems, featuring the increased movement of goods, people, and capital across the globe.
hazards Substances or situations that pose a risk to health, safety, or well-being.
hierarchy of controls An ordered set of priorities for the implementation of strategies (from most effective to least effective) to protect health and safety. Controls that protect all workers from the hazard without their active involvement (such as elimination of the hazard altogether or substitution of less hazardous materials and processes) are at the top of the hierarchy. Engineering controls (such as enclosing and ventilation) are the next level. Administrative controls (such as setting limits on the duration of work in high heat and humidity) are next. Finally, personal protective equipment (such as protective clothing or properly fitted and cleaned respirators) can be used in an emergency and to supplement higher levels of protection.
injury and illness prevention programs See safety and health management systems.
International Labour Organization (ILO) A specialized agency of the United Nations with a self-described mission “to promote rights at work, encourage decent employment opportunities, enhance social protection and strengthen dialogue on work-related issues.”
life cycle analysis A technique for assessing the environmental and social
1256
(including health) impacts associated with all the stages of a product's life, from cradle to grave, and for designing and producing products that minimize waste and pollution at the end of their useful life.
Mine Safety and Health Administration (MSHA) The U.S. government agency, located in the Department of Labor, focused on prevention of death, disease, and injury from mining and promotion of safe and healthful workplaces for U.S. miners. MSHA inspects all working mines at least annually in order to ensure compliance with existing regulations and identify new problems. MSHA develops and promulgates regulations, disseminates information, and supports and oversees training of miners.
musculoskeletal disorders (MSDs) Disorders of the muscles, joints, tendons, ligaments, bones, and nerves, often caused by work and commonly because of exposure to ergonomic hazards.
National Institute for Occupational Safety and Health (NIOSH)
The U.S. federal government agency that conducts research, supports research, and makes recommendations to prevent worker injury and illness. NIOSH also supports health professional training, investigates unusual outbreaks of disease or injury in workplaces, and disseminates information to assist those in a position to prevent or reduce safety and health risks for people who work.
Occupational Safety and Health Administration (OSHA) Created by the Occupational Safety and Health Act of 1970, OSHA is located in the Department of Labor. Employers in the US are required by the OSH Act to provide safe and healthful workplaces, and OSHA is the U.S. government agency charged with making that happen. To accomplish this, the agency sets and enforces standards and provides training, outreach, education, and assistance. OSHA's jurisdiction includes most private sector workplaces in the United States other than mines, which are within the jurisdiction of MSHA.
permissible exposure limits (PELs) Legally enforceable limits to exposure to workplace hazards issued by OSHA.
1257
safety and health management system A systematic approach taken by employers to managing safety and health activities by integrating occupational safety and health programs, policies, and objectives into organizational policies and procedures. It is a set of safety and health program components that interact in an organized way.
sustainability The ability of a system to continue functioning without depleting or damaging the things it needs to function, thereby fulfilling the social, economic, and other requirements of present and future generations.
temporary worker A worker who is hired for a limited period of time, with no employer commitment for future employment. Many temporary workers are hired by labor staffing agencies and assigned to work at places of employment not owned or controlled by the staffing agency.
unemployment A state of not having paid work but desiring or seeking it.
vulnerable workers Workers at increased risk of injury or illness because of their language, lack of ability to read, legal status, or other characteristics.
workers' compensation Social insurance programs intended to provide partial or complete wage replacement and resources for health care and rehabilitation for workers who have been injured or made sick by exposure to hazards at work. The specific requirements and structures of the programs (e.g., what is and is not covered and how much is paid for what duration of disability) vary substantially by state and by country.
1258
Discussion Questions 1. What are some of the ways that work and health interact? How
do these differ for workers in different industries?
2. What are the characteristics of workers who are at greatest risk for workplace injury?
3. What are some of the reasons employers have when they choose to invest in workplace safety? What are the reasons why they may choose not to invest?
4. What factors play a role in the underreporting of workplace injuries and illnesses?
5. In the United States the Occupational Safety and Health Administration (OSHA) and the Mine Safety and Health Administration (MSHA) have the job of encouraging employers to follow the law and provide safe workplaces. What tools do these agencies have? In what situations are these tools more or less effective?
6. Even though it been disproved conclusively, why do some safety professionals still believe that worker carelessness is the primary cause of work injuries? What are the potential consequences of the widespread prevalence of this mistaken belief?
7. Please look at each item of clothing you are now wearing. In what countries were your clothes manufactured? If you wanted to assess the working conditions of the people who made your clothes, how would you collect that information?
1259
References AFL-CIO. (2015). Death on the job, the toll of neglect: A national and state-by-state profile of worker safety and health in the United States (24th ed.). Retrieved from http://www.aflcio.org/content/download/154671/3868441/DOTJ2015Finalnobug.pdf
American Diabetes Association. (2013). Economic costs of diabetes in the U.S. in 2012. Diabetes Care, 36, 1033–1046.
Azaroff, L. S., Levenstein, C., & Wegman, D. H. (2002). Occupational injury and illness surveillance: Conceptual filters explain underreporting. American Journal of Public Health, 92, 1421–1429.
Bureau of Labor Statistics. (2014a). Employer-reported workplace injuries and illnesses 2013 (News release). Retrieved from http://www.bls.gov/news.release/osh2.nr0.htm
Bureau of Labor Statistics. (2014b). Nonfatal occupational injuries and illnesses requiring days away from work, 2013 (News release). Retrieved from http://www.bls.gov/news.release/osh2.nr0.htm
Bureau of Labor Statistics. (2015). Census of Fatal Occupational Injuries Summary, 2014. Retrieved from http://www.bls.gov/news.release/cfoi.nr0.htm
Byler, C. G. (2013). Hispanic/Latino fatal occupational injury rates. Monthly Labor Review, 136(2), 14–23.
Centers for Disease Control and Prevention. (1999). Improvements in workplace safety—United States, 1900–1999. Morbidity and Mortality Weekly Report, 48, 461–469.
Cherniack, M. (1986). The Hawk's Nest incident: America's worst industrial disaster. New Haven, CT: Yale University Press.
Davis, L. K., Grattan, K. M., Tak, S., Bullock, L. F., Ozonoff, A., & Boden, L. I. (2014). Use of multiple data sources for surveillance of work-related amputations in Massachusetts, comparison with official estimates and implications for national surveillance. American Journal of Industrial Medicine, 57, 1120–1132.
1260
Dembe, A. E., Erickson, J. B., Delbos, R. G., & Banks, S. M. (2005). The impact of overtime and long work hours on occupational injuries and illnesses: New evidence from the United States. Journal of Occupational and Environmental Medicine, 62, 588– 597.
Downey, K. (2010). The woman behind the New Deal: The life and legacy of Frances Perkins—social security, unemployment insurance and the minimum wage. New York: Anchor Books.
Duhigg, C. (2012). The power of habit: Why we do what we do in life and business. New York: Random House.
Eastman, C. (1910). Work-accidents and the law. New York: Russell Sage Foundation, Charities Publications Committee.
Hurd, M. D., Martorell, P., Delavande, A., Mullen, K. J., & Langa, K. M. (2013). Monetary costs of dementia in the United States. New England Journal of Medicine, 368, 1326–1334.
International Labour Organization. (2014). World of work report 2014: Developing with jobs (Executive summary). Retrieved from http://www.ilo.org/wcmsp5/groups/public/-dgreports/- dcomm/documents/publication/wcms_243962.pdf
International Labour Organization. (n.d.). Safety and health at work. Retrieved from http://www.ilo.org/global/topics/safety-and- health-at-work/lang--en/index.htm
Joe, L., Roisman, R., Beckman, S., Jones, M., Beckman, J., Frederick, M., & Harrison, R. (2014). Using multiple data sets for public health tracking of work-related injuries and illnesses in California. American Journal of Industrial Medicine, 57, 1110–1119.
Keogh, J. P., Nuwayhid, I., Gordon, J. L., & Gucer, P. W. (2000). The impact of occupational injury on injured worker and family: Outcomes of upper extremity cumulative trauma disorders in Maryland workers. American Journal of Industrial Medicine, 38(5), 498–506.
Leigh, J. P. (2011). Economic burden of occupational injury and illness in the United States. Milbank Quarterly, 89, 728–772.
1261
Leigh, J. P., & Marcin, J. (2012). Workers' compensation benefits and shifting costs for occupational injury and illness. Journal of Occupational and Environmental Medicine, 54, 445–450.
Leigh, J. P., & Robbins, J. A. (2004). Occupational disease and workers' compensation: Coverage, costs, and consequences. Milbank Quarterly, 2, 689–721.
Li, D. K., Zhou, Z., Miao, M., He, Y., Wang, J., Ferber, J.,…Yuan, W. (2011). Urine bisphenol-A (BPA) level in relation to semen quality. Fertility and Sterility, 95(2), 625–630.
Michaels, D. (1983). Occupational cancer in the black population: The health effects of job discrimination. Journal of the National Medical Association, 75(10), 1014–1018.
National Highway Traffic Safety Administration. (2014). 2013 Motor vehicle crashes: Overview Retrieved from http://www- nrd.nhtsa.dot.gov/Pubs/812101.pdf
National Safety Council. (2015). Injury facts: 2015 Edition. Itasca, IL: National Safety Council.
Occupational Safety and Health Administration. (2012). Injury and illness prevention programs (White paper). Retrieved from https://www.osha.gov/dsg/InjuryIllnessPreventionProgramsWhitePaper.html
Scherer, E., Seabury, S. A., O'Leary, P., Ozonoff, A., & Boden, L. (2014). Using linked federal and state data to study the adequacy of workers' compensation benefits. American Journal of Industrial Medicine, 57, 1165–1173.
Schulte, P. (2005). Characterizing the burden of occupational injury and disease. Journal of Occupational and Environmental Medicine, 47, 607–622.
Shannon, H. S., & Lowe, G. S. (2002). How many injured workers do not file claims for workers' compensation benefits? American Journal of Industrial Medicine, 42, 467–473.
Smith, J.D.R. (2012). Immigrant workers and workers' compensation: The need for reform. American Journal of Industrial Medicine, 55, 537–544.
1262
Spieler, E. A., & Wagner, G. R. (2014). Counting matters: Implications of undercounting in the BLS Survey of Occupational Injuries and Illnesses. American Journal of Industrial Medicine, 57, 1077–1084.
Steege, A. L., Baron, S. L., Marsh, S. M., & Menendez, C. C. (2014). Examining occupational health and safety disparities using national data: A cause for continuing concern. American Journal of Industrial Medicine, 57, 527–538.
Steenland, K., Burnett, C., Lalich, N., Ward, E., & Hurrell, J. (2003). Dying for work: The magnitude of U.S. mortality from selected causes of death associated with occupation. American Journal of Industrial Medicine, 43, 461–482.
Strunin, L., & Boden, L. I. (2004). Family consequences of chronic back pain. Social Science & Medicine, 58, 1385–1393.
1263
For Further Information Useful Web Sites
Bureau of Labor Statistics; Injuries, Illnesses, and Fatalities program: http://www.bls.gov/iif
Center for Construction Research and Training: http://www.cpwr.com
National Council for Occupational Safety and Health: http://www.coshnetwork.org
National Institute for Occupational Safety and Health: http://www.cdc.gov/NIOSH
Occupational Safety and Health Administration: http://www.osha.gov
OSHWiki of the European Agency for Safety and Health at Work: http://oshwiki.eu/wiki/Main_Page
Books The following three books, written across a forty-year period, explore general trends in U.S. workplaces, focusing on the social dimensions of work and how these affect workers.
Ehrenreich, B. (2001). Nickel and dimed: On (not) getting by in America. New York: Metropolitan Books.
Terkel, S. (1974). Working: People talk about what they do all day and how they feel about what they do. New York: Pantheon Books.
Weil, D. (2014). The fissured workplace: Why work became so bad for so many and what can be done to improve it. Cambridge, MA: Harvard University Press.
The next book is a standard text of occupational health, with detailed information on a variety of industries and health conditions.
Levy, B. S., Wegman, D. H., Baron, S. L., & Sokas, R. K. (2011). Occupational and environmental health: Recognizing and
1264
preventing disease and injury (6th ed.). New York: Oxford University Press.
The following five books provide historical accounts of occupational health and safety disasters, beginning with the 1911 Triangle Shirtwaist Factory fire and continuing with accounts of occupational cancer and lung diseases during the twentieth century. Great reads for those interested in history.
Brodeur, P. (1985). Outrageous misconduct: The asbestos industry on trial. New York: Pantheon Books.
Cherniack, M. (1986). The Hawk's Nest incident: America's worst industrial disaster. New Haven, CT: Yale University Press.
Levenstein, C., & Delaurier, G. F. (2002). The cotton dust papers: Science, politics, and power in the “discovery” of byssinosis in the U.S. Amityville, NY: Baywood.
Randall, W. S., & Solomon, S. D. (1977). Building 6: The tragedy at Bridesburg. Boston: Little, Brown.
von Drehle, D. (2004). Triangle: The fire that changed America. New York: Atlantic Monthly Press.
This final book explores how science has been used, and abused, in occupational and environmental health policy.
Michaels, D. (2008). Doubt is their product: How industry's war on science threatens your health. New York: Oxford University Press.
1265
Chapter 22 Radiation
Matthew P. Moeller
This chapter is an update to the chapter on radiation in the second edition prepared by Arthur C. Upton. The author also acknowledges the contributions to this chapter by Steven E. Merwin, CHP, who, as a founder of Dade Moeller & Associates, has always advanced science, demanded thoughtful reasoning, and supported this colleague as both peer and friend. This revision is dedicated to my father, Dade W. Moeller, PhD, CHP, who was an extraordinary health physicist, environmentalist, scientist, and educator. Matthew P. Moeller, CHP, is CEO of Dade Moeller & Associates, a consulting company with roots in radiation protection that specializes in the occupational and environmental sciences by providing professional and technical services to federal, state, and commercial clients in support of nuclear, radiological, and environmental operations. Major company projects include those for the U.S. Department of Energy, National Institute for Occupational Safety and Health, and National Oceanic and Atmospheric Administration.
1266
Key Concepts There are several forms of radiation, with both common features and important differences. Each may interact with living cells, and each presents potential public health concerns.
The risk of each type of radiation-induced injury varies with the dose of radiation.
Exposure to each form of radiation occurs from specific sources and via specific pathways, and there are public health policies designed to limit undue exposures. These policies balance benefits (e.g., from diagnostic procedures) with risks.
Radiation is all around us. It comes from a fundamental event: an atom that has excess energy in an excited state rids itself of energy to move to a more stable state.
Radiation is energy in an electromagnetic form. In all its forms, radiation is one of the most common environmental exposures, from both naturally occurring sources, radioactive materials, and radiation-generating devices. We are exposed to radiation during airline flights, in our homes, during medical procedures, and on the beach. Radiation is integral in numerous industrial and professional settings, including medicine, dentistry, scientific research, nuclear electric power generation, and oil and gas exploration. When radiation interacts with matter, energy is deposited—and when that matter happens to be living tissue, adverse changes at the cellular level may result. Radiation is therefore a core topic in environmental health.
Modern knowledge of radiation is just over a century old. The discovery of radiation and radioactive materials correlates directly with experiments designed to understand the atomic structure. While the ancient Greek philosopher Democritus, in the fifth century b.c., postulated that all matter is made up of a set of particles called atoms, it was not until 1895 that X-rays were discovered (by Roentgen), followed in short order by Becquerel's discovery of radioactivity in 1896 (although the term radioactivity was coined by Marie Curie two years later), and the electron by J. J.
1267
Thomson in 1897. A veritable Golden Age of theoretical and empirical advances followed. In 1911, Rutherford deduced the atom was composed of a tiny central core, or nucleus, containing all the positive charge and almost all the mass of the atom, and a nearly empty surrounding cloud region containing the light, negatively charged electrons in sufficient number to balance the inner positive charge. In 1932, Chadwick proved the existence of neutrons, establishing that all nuclei are composed of closely packed protons and neutrons. This insight was critical to understanding the atom and radioactivity: certain combinations of protons and neutrons are stable and remain intact unless disrupted by nuclear collisions, while other combinations are unstable. These unstable nuclei undergo transformations—spontaneous disintegration processes— that alter the proton to neutron ratio to achieve a stable state.
Further developments in nuclear research came in rapid succession. In 1939, researchers discovered uranium fission in the laboratory. On December 2, 1942, at the University of Chicago, the first self- sustaining nuclear fission chain reaction was started, making atomic energy a practical possibility—one that was realized in 1951, when a nuclear reactor first produced electricity. On July 16, 1945, the Trinity test in Alamogordo, New Mexico, marked the detonation of the first atomic weapon; the use of atomic weapons in Hiroshima and Nagasaki followed within months.
Radiation is propagated through space in energy packets called photons. Each photon has an associated wavelength and frequency. A wave motion consists of a series of crests and troughs; the distance between successive crests, or successive troughs, is wavelength. Given that all photons travel at the speed of light (3 × 1010 cm/s), the number of individual waves, or cycles, passing through a certain point of a medium over the course of a second is frequency. The energy of a photon is inversely proportional to its wavelength and directly proportional to its frequency; it is expressed in terms of electron volts (eV). The energy ranges for the various types of radiation have not been precisely defined and overlaps in these energy ranges are common.
All electromagnetic radiations are fundamentally the same—all traveling at the same velocity (speed of light), and differing only in wavelength, frequency, and energy. Figure 22.1 shows the electromagnetic spectrum, arrayed along these factors. These
1268
factors are key in determining the characteristics of the radiation and the amount of harm it may cause. As the wavelength shortens and frequency increases, more energy is released at close range, potentially harming living things.
Figure 22.1 The Electromagnetic Spectrum
One characteristic essential to understanding the mechanism of harm is ionization potential; that is, whether the radiation contains sufficient energy to ionize atoms. When sufficient energy is present, the radiation interacts with one or more orbiting electrons of an atom and strips them away. The removed electron exhibits a unit negative charge while the residual atom exhibits a unit positive charge; these are known as an ion pair. The accompanying transfer of energy can result in chemical and biological changes that are harmful to health.
This chapter begins by describing nonionizing radiation types with
1269
longer wavelengths and lower frequencies—the lower part of Figure 22.1—and progresses up the spectrum, toward shorter wavelengths and greater frequencies, to ionizing radiations. Following this progression, the health effects of exposure to radiation increase in hazard.
1270
Nonionizing Radiations Extremely Low Frequency Electromagnetic Fields Electric and magnetic fields are usually coupled, hence the term electromagnetic fields (EMFs), but at extremely low frequencies they may exist separately. An electric field can be produced by transferring electrons from one object to another, creating an imbalance of charged particles. A familiar example is the attraction between a comb and a person's hair. A magnetic field can be produced by sending electrical charges (electricity) through a wire. Any home appliance that has a motor can be a source of a magnetic field; examples are a refrigerator, a blender, and a vacuum cleaner. These EMFs do not carry enough energy to ionize matter, and are therefore called nonionizing radiation.
Extremely low frequency (ELF) EMFs, time-varying magnetic fields with wavelengths greater than 108 cm and frequencies less than 300 Hz (Figure 22.1), are widely present throughout the environment. They arise with solar activity and thunderstorms, generally intermittently, and with low intensity. Stronger ELF EMFs are the localized 50 to 60 Hz fields generated by electric power lines, transformers, motors, household appliances, video display tubes (VDTs), and various medical devices, notably magnetic resonance imaging (MRI) systems. Some occupations, such as power line workers, welders, railway engine drivers, and sewing machine operators, have especially high exposures.
Types and Mechanisms of Injury The induction of electric fields and currents results in energy being absorbed in the human body. The most common effects of ELF field exposure are awareness and annoyance, as with the “shock” of discharging an electrical charge. Some people report a sensitivity to EMFs, but scientific studies have not substantiated this condition. ELF EMFs may interfere with pacemakers. Some epidemiological data suggest an association between ELF magnetic field exposure and childhood leukemia, leading the International Agency for Research on Cancer (IARC) to classify ELF magnetic fields as “possibly carcinogenic to humans” (IARC, 2012); however, this
1271
claim is controversial as no experimental and mechanistic data exist to support this association. In fact no accepted mechanism has been identified to link ELF EMFs and significant adverse human health effects (World Health Organization, 2007; Foster & Moulder, 2013).
Radiation Protection and Prevention Areas containing EMFs stronger than 0.5 mT (such as exist around transformers, accelerators, MRI systems, and other electrical devices) should be posted with warning signs and should be avoided by persons wearing pacemakers. Organizations such as the American Conference of Governmental Industrial Hygienists and the International Commission on Non-Ionizing Radiation Protection recommend exposure limits for workers, members of the general public, and people wearing medical devices such as pacemakers.
Radio and Microwave Radiations Microwave and radiofrequency radiation (MW/RFR), the second category of nonionizing radiation, has wavelengths from 107
cm to 0.1 cm with frequencies from about 3 × 103 Hz to 3 × 1011 Hz (Figure 22.1). MW/RFR sources are common and include radars, televisions, radios, cellular phones (Text Box 22.1), cell phone towers, and other telecommunications systems; industrial operations such as metalworking; household appliances such as microwave ovens; and medical applications such as diathermy and hyperthermia (Sliney & Colville, 2000).
The human body is largely transparent to the longer wavelength radiations of microwaves. As the wavelength shortens and the frequency increases, energy is increasingly absorbed, peaking at the ultra high frequency (UHF) television range (about 3 × 108 Hz). At frequencies above 109 Hz, less energy is absorbed and above 1010 Hz, the energy is reflected by the skin. For this reason, microwaves in the range between 109 Hz and 1010 Hz are potentially the most hazardous, as there is heating of the skin without thermal receptors being stimulated; in effect, a person does not recognize energy is being absorbed.
1272
Text Box 22.1 Is Cell Phone Use Linked to Cancer? As cellular telephones have become commonplace across the world, concern about potential health risks has grown (Figure 22.2). Fears of increased risks of cancer from radiofrequency radiation have prompted public objections to the siting of television, radio, and cell phone transmission towers. As cell phone use expands, it will become the leading source of RFR exposure globally.
Figure 22.2 Cell phones Are Virtually Ubiquitous, and Entail Exposure to Radiofrequency Radiation
Source: Wood, 2013.
Evidence to date is not definitive. Early epidemiological studies were generally negative. However, they were conducted when cell phones produced higher field strength than modern phones, when cell phone use was lower, and when long-term follow-up was not yet possible, limiting the conclusions that could be drawn. The largest study to date, the INTERPHONE study, enrolled over 5,000 glioma and
1273
meningioma cases, along with matched controls, and found suggestive results: an increased risk of gliomas in the very highest category of phone users, and a possible increased risk on the side of the head where the phone was used (INTERPHONE Study Group, 2010). However, subsequent studies have not consistently replicated these results (e.g., Hardell, Carlberg, & Hansson Mild, 2011), and other findings that would be corroborative, such as a dose-response relationship, increasing risk with increasing latency and/or lower age at first exposure, and increased risk in the temporal lobe (the part of the brain nearest the phone), have not consistently emerged. Almost all (but not all) animal studies have been negative. It is perhaps no surprise that reviewers and official bodies have reached inconsistent conclusions, with the International Agency for Research on Cancer (IARC) designating radiofrequency EMFs as “possibly carcinogenic to humans” (Group 2B) (Baan et al., 2011), while the German Commission on Radiological Protection (SSK), found “lack of, or insufficient evidence of, causality” (Leitgeb, 2012).
The major health impacts of cell phones may not relate to EMFs at all, but rather to the (likely far higher) risks of distraction while using cell phones (Collet, Guillot, & Petit, 2010; Klauer et al., 2014). Cell phones also offer health benefits, such as their utility in calling for help in emergencies and in delivering health care. No comprehensive assessment, weighing risks and benefits, has yet been performed.
Types and Mechanisms of Injury The biological effects of MW/RFR appear to be primarily thermal. MW/RFR can penetrate deeply enough to burn dermal and subcutaneous tissues, burns that are slow to heal. Cataracts of the lens of the eye also can result from high-intensity exposures (1.5 kW/m2) (Lipman, Tripathi, & Tripathi, 1988), and death from hyperthermia has occurred in the industrial use of MW/RFR sources (Roberts & Michaelson, 1985). MW/RFR can also interfere with cardiac pacemakers and other medical devices. Although the biological effects of MW/RFR are attributed primarily to thermal
1274
mechanisms, some evidence suggests that nonthermal mechanisms may operate as well. These may include damage to DNA (Blank, 2008; Mazor et al., 2008), impairment of fertility, developmental disturbances, neurobehavioral abnormalities, depression of immunity, stimulation of cell proliferation, and carcinogenic effects (Tenforde, 1998; International Commission on Non-Ionizing Radiation Protection [ICNIRP], 2004: Hardell et al., 2007; Sadetski et al., 2008). Concern about cancer risk from radiofrequency radiation has gained significant attention due to the widespread use of cell phones.
Radiation Protection and Prevention Prevention of injury from MW/RFR requires proper design and shielding of MW/RFR sources, along with appropriate training and supervision of potentially exposed people (especially those wearing pacemakers or other sensitive devices). To prevent detectable heating of tissue, exposures to MW/RFR of different frequencies should be kept below the relevant threshold limit values, which are based on the amount of radiofrequency energy absorbed in tissue, or the specific absorption rate (SAR) (ICNIRP, 1998; Sliney & Colville, 2000). The current SAR limit for cell phones, set by the Federal Communications Commission (FCC), is 1.6 watts per kilogram (FCC, 2015).
Infrared Radiation Infrared radiation (IR), electromagnetic waves with frequencies from about 3 × 1011 Hz to 4.3 × 1014 Hz (Figure 22.1), is commonly experienced as heat. Examples are the heat from the sun, a burning log fire, hot blacktop on a sunny day, and such industrial sources as furnaces, welding arcs, and heating lamps. The hazard from IR is excessive heat.
Types and Mechanisms of Injury The injuries caused by IR are mainly burns of the skin and cataracts of the lens of the eye. Human skin contains heat sensors, which usually prompt aversion in time or distance to prevent injuries from a significant heat source. In contrast, the lens of the eye lacks heat sensors and the ability to dissipate heat received. For this reason it is particularly vulnerable. Consequently, glassblowers, blacksmiths,
1275
oven operators, and those working around heating and drying lamps are at risk of IR-induced cataracts (Lydahl, 1984).
Radiation Protection and Prevention Control of IR hazards and avoidance of IR-related injuries requires limiting the duration of exposures and shielding sources, as may be achieved with proper training, adequate supervision of potentially exposed people, and the use of physical barriers and other engineered controls as well as personal protective devices such as specialized clothing and goggles. It is recommended that people not be exposed to intensities of IR exceeding 10 mW/cm2.
Visible Light Visible light consists of electromagnetic waves ranging in wavelength from approximately 7.6 × 10−5 cm (red) to 3.8 × 10−5 cm (violet), which corresponds to 760 and 380 nm, with frequencies from 3.9 × 1014 Hz to 7.9 × 1014 Hz (Figure 22.1). Sources of visible light in the environment vary widely in the intensity of their emissions. Common high-intensity sources other than the sun include lasers, electric welding or carbon arcs, and tungsten filament lamps.
Types and Mechanisms of Injury A light that is too bright can injure the eye through photochemical reactions in the retina. Sustained exposure to intensities exceeding 0.1 mW/cm2, such as can result from gazing at a bright source of light, can produce photochemical blue-light injury, and brief exposure of the retina to intensities exceeding 10 mW/cm2, depending on image size, may cause a retinal burn, resulting in a scotoma (blind spot), which can be permanent. The lens, iris, cornea, and skin are also vulnerable to injury from the thermal effects of laser radiation. Conversely, too little illumination can also be harmful, causing eyestrain and aggravating seasonal affective disorder (SAD).
Radiation Protection and Prevention Industrial applications involving potential exposure are carbon arcs, lasers, or other high-intensity sources. Protection against injuries
1276
requires avoiding exposures. Strategies include engineering controls such as shielding materials, proper training, effective procedures, adequate supervision of potentially exposed people, and personal protective devices such as protective eye shields.
Ultraviolet Radiation Ultraviolet radiation (UVR) consists of electromagnetic waves, subdivided for convenience into three bands of the spectrum (Figure 22.1): UVA, 315 to 440 nm (or black light); UVB, 280 to 315 nm; and UVC, 100 to 280 nm (which is germicidal). UVR is nonionizing at lower frequencies and ionizing at higher frequencies. The chief source of population exposure to UVR is sunlight, which varies in intensity with latitude, elevation, and season. Important man-made sources of high-intensity exposure include sunlamps and tanning lamps, welding arcs, plasma torches, germicidal and black light lamps, electric arc furnaces, hot-metal operations, mercury- vapor lamps, and lasers. Common low-intensity sources include fluorescent lamps and certain laboratory equipment. While UVR may damage health, it is also essential in vitamin D synthesis.
Types and Mechanisms of Injury Because UVR does not penetrate deeply into human tissues, the injuries it causes are confined chiefly to the skin and eyes. Dermal reactions to UVR, common among fair-skinned people, include sunburn, pigmentation, skin cancers (basal cell and squamous cell carcinomas and possibly, to a lesser extent, melanomas), aging of the skin, telangiectasia, solar elastoses, and solar keratoses (Figure 22.3). Injuries of the eye include photokeratitis and photoconjunctivitis, which may result from brief exposure to a high- intensity UVR source (welder's flash) or from more prolonged exposure to intense sunlight (snow blindness); prolonged exposure may also cause cataracts, macular degeneration (evidence is equivocal), and other conditions (Yam & Kwok, 2014).
1277
Figure 22.3 A Basal Cell Carcinoma of the Skin of Twenty Years, Duration in a Fifty-Eight-Year-Old Man
Source: Warren, 1953. Reprinted with permission from Elsevier.
Such tumors are the commonest of cancers and occur primarily in sun-exposed areas of the skin.
The effects of UVR result both from its immunosuppressive effects and from its absorption by DNA, leading to pyrimidine dimer formation and mutational changes in exposed cells (Halliday, Byrne, & Damian, 2011; Pfeifer & Besaratinia, 2012). Sensitivity to UVR can therefore be increased by DNA repair defects (e.g., xeroderma pigmentosum), by agents (such as caffeine) that inhibit the repair enzymes, and by photosensitizing agents (such as tetracyclines and some other medications) that produce UVR- absorbing DNA photoproducts. UVB, although far less intense than UVA in sunlight, plays a more important role in sunburn and skin carcinogenesis. UVA contributes to these outcomes, as well as to tanning, some photosensitivity reactions, aging of the skin, photokeratitis, and cortical lens opacities.
Radiation Protection and Prevention Exposure to sunlight or other sources of UVR should be limited in
1278
exposure in intensity and duration, especially for fair-skinned people. Even at higher frequencies, UVR is shielded by an ordinary window. Protection afforded by clothing depends on its color and composition; for example, cream-colored and bright pink cotton cloth provide sun protection factors (SPFs) of 10 and >30, respectively (Gies, 2007). Most topical sunscreens protect against UVB, and broad-spectrum sunscreens also protect against UVA. UVR-blocking sunglasses are useful for eye protection. In the workplace, methods of protection may include engineering and administrative controls.
The Earth's protective layer of stratospheric ozone has been depleted by chlorofluorocarbons and other air pollutants, increasing the UVR reaching the Earth, and raising the risk of nonmelanotic skin cancer, especially at high latitudes. The Montreal Protocol is expected to avert further thinning of the ozone layer, and to allow it to be restored over coming decades. This success is credited with avoiding as many as 2 million cases of skin cancer globally each year by the year 2030 (van Dijk et al., 2013).
1279
Ionizing Radiation: The Basics The X-ray, gamma ray, and cosmic ray radiations comprise the remainder of the electromagnetic spectrum. They are of progressively shorter wavelengths and greater frequencies (see Figure 22.1). All are ionizing radiations, which means they can deposit enough localized energy in a living cell to break chemical bonds and give rise to ion pairs and free radicals. Radiation may cause ionization either directly or indirectly. Electrically charged particles with sufficient kinetic energy to produce ionization by collision are called directly ionizing particles; these include protons, alpha particles, and beta particles. Electrons may also be directly ionizing. In contrast, uncharged neutrons, gamma rays, and neutral mesons may impart only enough energy to liberate directly ionizing particles; these are called indirectly ionizing radiations.
Radioactivity may be defined as spontaneous nuclear transformations that result in the formation of new elements (Cember & Johnson, 2008). A starting point for understanding this process is understanding the various transformation mechanisms; these are shown in Figure 22.4.
1280
Figure 22.4 Nuclear Transformation Mechanisms That Release Radioactivity
Through these transformation mechanisms, unstable nuclei assume more stable forms. Which mechanism occurs depends upon the nature of the instability, and the mass- energy relationship among the parent nucleus, resulting progeny nucleus, and emitted
1281
particle.
In several of the transformation mechanisms shown in Figure 22.4, gamma ray emission and X-ray emission serve to dissipate excess energy. Gamma rays are photons originating in the nucleus while X-rays are photons originating from the inner orbits of the atom. The two kinds of radiation are indistinguishable, although gamma radiation usually carries more energy. Gamma rays lose energy through chance encounters that result in the ejection of electrons from atoms. Both X-rays and gamma rays are sparsely ionizing in comparison with charged particles; that is, their energy deposition is less concentrated as their energy is deposited over a greater distance.
A radionuclide (see Text Box 22.2) can be quantified by its transformation kinetics, including its half-life and activity. Each radionuclide is transformed at a different, unique rate. These transformation rates range from nanoseconds to billions of years. Half-life is the time required for any given radionuclide to decrease to one-half of its original quantity by nuclear transformations. Radionuclides with very long half-lives, such as some components of nuclear waste, pose challenges to safe storage, as discussed in Chapter 14. Activity, the rate of transformations per unit time, is a measure of radioactivity. The becquerel (Bq), a unit of activity, is defined as that quantity of material in which one atom is transformed per second. Of historical importance, the original unit of activity was named for Marie and Pierre Curie; this measure is still used in some settings, such as in assessing home to radon exposure. (The U.S. Environmental Protection Agency [U.S. EPA] recommends abatement of a home if the measured air concentration exceeds 4 picocuries per liter of air, or pCi/L.) The concentration of radioactivity, or the relationship between the mass of radioactive material and the activity, is called specific activity. The specific activity is the number of becquerels per unit mass or volume.
1282
Text Box 22.2 What Are Isotopes? For any particular element, the number of neutrons within the nucleus may vary. The element oxygen, which always contains eight protons, consists of three naturally occurring and stable (nonradioactive) nuclear species: ones with a nucleus containing eight, nine, and ten neutrons, resulting in atomic mass numbers of 16, 17, and 18. These three nuclear species of the same element are called isotopes of oxygen. Isotopes cannot be distinguished chemically as they have the same extranuclear electronic structure and therefore undergo the same chemical reactions. Nuclear species of different elements are called nuclides and radioactive species of different elements are called radionuclides.
One of the challenges to understanding the measurement and effect of radiation is an abundance of terms for units of exposure and dose. The units presented in Table 22.1 are those of the International System, introduced in the 1970s to standardize usage throughout the world. They have largely supplanted earlier units, such as the curie.
Table 22.1 Units of Radiation Exposure and Dose
Parameter Units Description Absorbed dose
Gray (Gy), in units of joule/kg
Energy imparted to tissue.
Equivalent dose
Sievert (Sv), in units of joule/kg
Absorbed dose corrected for the LET (linear energy transfer) deposition density.
Effective dose
Sievert (Sv), in units of joule/kg
Equivalent dose corrected for the sensitivity of the exposed tissue (or organ).
Committed effective dose
Sievert (Sv), in units of joule/kg
Cumulative effective dose to be received over time from an intake of radioactivity.
1283
effective dose
(person-Sv), in units of joule/kg
population.
Radiation exposures are divided into external and internal doses. An external dose is received from sources outside the body; the energy is imparted immediately upon exposure. An internal dose occurs when radioactive material enters the body through inhalation, ingestion, absorption through the skin or via a wound. An internal dose may be received over an extended period of time because the radioactive material inside the body continues to deposit energy within the body as it decays, unless it is removed by some other biological, therapeutic, or physical mechanism.
1284
Sources of Ionizing Radiation Exposure People are exposed to radiation from a wide variety of natural and anthropogenic sources. Natural sources include cosmic rays from outer space and gamma-emitting photons emitted from naturally occurring radioactive minerals in the Earth, especially radon. The major anthropogenic exposures occur in medical diagnosis and treatment, although other exposures, ranging from consumer products to industrial uses to nuclear waste, may be important. Table 22.2 shows the average radiation doses received by a U.S. resident. Importantly, these are only averages; a person who frequently flies across the country or who needs frequent diagnostic X-rays may have a substantially different exposure profile.
Table 22.2 Average Amounts of Ionizing Radiation Received Annually by a U.S. Resident
Source Dose (mSv)a Percentage of total Natural Cosmic 0.27 4 Terrestrial 0.28 4
Radonb 1.9 31 Internal 0.39 7 Total natural 2.84 46 Human made X-ray diagnosis 2.4 39 Nuclear medicine 0.8 13 Total medical 3.2 52 Consumer products 0.10 2 Occupational <0.01 <0.03 Nuclear fuel cycle <0.01 <0.03 Nuclear fallout <0.01 <0.03
Miscellaneousc <0.03 <0.03
1285
Total human made 3.35 54 Total all sources 6.2 100
Note: The values tabulated represent average values for the entire population; doses to specific individuals and subgroups may be substantially lower or higher.
a Average effective dose to soft tissue.
b Average effective dose to respiratory epithelium.
c Includes U.S. Department of Energy facilities, smelters, transportation, and other sources.
Sources: Adapted from National Research Council, 2006; Mettler & Upton, 2008.
Cosmic Radiation Every second, about 2 × 1018 primary cosmic rays of energy greater than 1 billion electron volts are incident on the atmosphere (Shapiro, 2002). They interact with atoms such as nitrogen and oxygen in the atmosphere and produce a large variety of secondary particles. At sea level, essentially all the cosmic rays have disappeared, and the radiation dose is produced by the secondary particles. Two factors affect the dose to the human population: latitude and elevation. Because the Van Allen belt provides protection along the equator, cosmic dose rate increases closer to the poles. As with ultraviolet radiation, because the Earth's atmosphere provides protection, cosmic dose rate increases with increasing altitude above sea level. The annual dose from cosmic radiation at sea level is 0.3 mSv/year; at 12,000 feet of altitude, it is 1.0 mSv/y (Moeller, 2011). At the altitudes of typical commercial aircraft travel, the dose rate is 45–70 mSv/y (although, of course, no one flies for an entire year!). Space travel poses even higher exposures; for a crew member on the Mir space station, the dose during a 90-day mission was about 70 mSv—an annualized rate of about 280 mSv/y.
Terrestrial Radiation Some minerals that comprise the Earth's crust are radioactive. Because the mineral composition varies significantly depending upon location, the dose rates to human populations vary significantly. The major sources of exposure are potassium, thorium, and uranium. The regions of the United States with the highest terrestrial doses, up to 1 mSv/y, are those associated with
1286
highest terrestrial doses, up to 1 mSv/y, are those associated with uranium deposits in the Colorado plateau, granite deposits in New England, and phosphate deposits in Florida. The estimated average dose rate in the United States from terrestrial sources is 0.28 mSv/y (National Council on Radiation Protection and Measurements [NCRP], 2009). Far higher levels of terrestrial radiation exposure have been reported from areas of India, China, Brazil, Iran, and elsewhere. Epidemiological studies in these areas have shown conflicting results, without consistent findings of excess cancer, possibly due to a true absence of effect or possibly due to ecological study designs and poor exposure assessment (Hendry et al., 2009). Some studies have even suggested an inverse relationship between exposure and cancer incidence, which some observers have interpreted as evidence of beneficial effects (or hormesis) of low-level irradiation (Jolly & Meyer, 2009).
Radon Radon is a naturally occurring gas. It originates from radium, a naturally radioactive element found in trace amounts in nearly all rocks, soils, and groundwater as well as in building materials, plants, animals, and the human body. Radium decays to radon, a colorless, odorless, radioactive gas. Radon, in turn, decays to solid particles called radon decay products, which are also radioactive. When radium in soil decays, radon and its radioactive decay products can accumulate in basements and other parts of buildings in relatively high concentrations. The less exchange with outside fresh air, typically the greater the concentrations.
Radon levels vary across the world. In the United States, levels are highest across a broad swath of the Northern tier, from eastern Washington State to Wisconsin and down to the Great Plains, east across Ohio and Pennsylvania, and up into New England. On average, inhaled radon decay products account for more than two thirds of the natural background radiation dose to the population. (Further information on radon exposure, and its health effects, appears in Tox Box 20.2 in Chapter 20.)
Internal Some exposure to radiation comes from radionuclides in our own bodies, called internal emitters. Approximately half of the annual
1287
internal dose is attributable to potassium. Potassium is a naturally radioactive element, with approximately 99.99% being stable atoms and 0.01% existing as radioisotope 40K with a half-life of slightly over 1 billion years. A typical adult contains about 160 grams of potassium, of which about 0.02 grams is 40K. This results in about 5,000 Bq within the human body and an annual dose of about 0.2 mSv (Watson & Strom, 2011). Because potassium is an essential element in the human body, this dose is unavoidable. It is abundant in most vegetables, notably spinach, broccoli, lima beans, and sweet potatoes, and some fruits, notably bananas.
Most of the remaining internal dose is attributable to naturally occurring radionuclides from the uranium and thorium decay series (Watson & Strom, 2011). Both elements are abundant in the Earth's crust. On average, only a very small amount (<1%) of our internal dose is attributable to radionuclides associated with nuclear weapons fallout or other man-made sources; exceptions include people with a history of unusual exposures, such as certain diagnostic and therapeutic procedures, certain occupational exposures, and proximity to nuclear weapons testing or nuclear accidents (Simon & Bouville, 2002).
Radioactivity in Consumer Products and Food Sources Some consumer products and consumer uses of natural radioactive materials may pose exposure to ionizing radiation. In the past, radiation was used in ways that likely produced high exposures and minimal benefit, such as in fitting shoes (Duffin & Hayter, 2000) (Figure 22.5). Current uses include some compact fluorescent light bulbs, luminous timepieces, ceramics, fertilizers, lantern mantles, and granite countertops. Some smoke detectors contain 241Am. Certain building materials may contain radionuclides; the annual dose to a person living in a brick or concrete house is estimated to be 0.7 mSv. In general these doses are very small; the average person's radiation dose from consumer products in the United States is equivalent to 2% of that contributed by natural background sources. In some cases, such as smoke detectors, the substantial benefits outweigh the very small risk.
1288
Figure 22.5 Using X-Rays for Fitting Shoes Sources: Becker, 2012; photo by Rex/Alamy; Oak Ridge Associated Universities.
From the 1930s to the 1950s, shoe-fitting fluoroscopes were marketed as the modern way to assure healthy feet. Doses were substantial. The Pedoscope allowed both customer and salesperson to view the bones of the feet. Certificates gave customers the results of the X-ray fitting test.
Many ingested foods and inhaled products contain naturally occurring radioactive materials. Perhaps the best example is 40K in bananas. Brazil nuts contain relatively high quantities of 226Ra. A particular health concern is the presence of naturally occurring 210Po and 210Pb in cigarette tobacco. The annual radiation dose to the critical lung tissues of a smoker is as high as 160 mSv (Little, Radford, McCombs, & Hunt, 1965)—an example of synergy, as the presence of both the chemical carcinogens in tobacco and the radiation confers a risk substantially higher than the sum of each hazard alone (Moeller & Sun, 2010).
Radiation in Medicine Radiation doses are commonplace in hospitals and clinics, during diagnostic imaging exams and procedures such as heart valve replacement, making medical applications the leading source of radiation exposure of human origin (NCRP, 2009). Radiation doses for diagnostic X-rays and interventional and nuclear medicine procedures are presented in Table 22.3; these vary with differences in X-ray machines and their settings, the amount of radioactive material given in a nuclear medicine procedure, and the individual's metabolism.
Table 22.3 Representative Radiation Doses in Select Medical Procedures Performed in the United States
1289
Examination or procedure
Location Dose (Sv)
Diagnostic X-raya Dental bitewing 0.005
Diagnostic X-raya Dental (panoramic) 0.01
Diagnostic X-raya Chest 0.1
Diagnostic X-raya Mammogram (2 views) 0.36
Diagnostic X-raya Pelvis 0.7
Diagnostic X-raya Lumbar spine 1.5
Computed tomographyb CT head 2.0
Computed tomographyb CT chest 7.0
Computed tomographyb CT abdomen and pelvis 10.0
Computed tomographyb CT whole-body screening 10.0
Multipleb Peripheral vascular angioplasties
5.0
Multipleb Upper GI 6.0
Multipleb Barium enema 7.0
Multipleb Coronary angiography 20.0
Multipleb Cardiac 30.0
Multipleb Noncardiac embolization 55.0
Positron emission tomography
Various PET studies using 18F- FDG
14.0
Nuclear medicine Hepatobiliary (liver flow) using 99mTc
2.1
Nuclear medicine Kidney (tubular function) using 99mTc
2.2
Nuclear medicine Bone using 99mTc 6.3
Nuclear medicine Brain (perfusion) using 99mTc 6.9
Nuclear medicine Heart (stress-rest) using 99mTc 11.0
Nuclear medicine Heart (stress-rest) using 201Tl chloride
41.0
1290
a Single X-ray exposure.
b Entire or multiple procedures that may be diagnostic or interventional; for example, a lumbar spine series usually consists of five X-ray exams.
Sources: NCRP, 2009; Mettler, Huda, Yoshizumi, & Mahesh, 2008.
On average, medical procedures involving radiation contribute 3.1 mSv to each person in the United States, about half the amount contributed by natural background. Like background radiation, these doses are not evenly distributed across the population. Annually in the United States, 2 billion diagnostic medical X-ray examinations are performed, including more than 500 million dental X-ray examinations. In recent years, doses from medical examinations have increased sharply—by a factor of 3.6 from 1982 to 2006 (Mettler et al., 2008)—largely as a result of the use of advanced diagnostic and therapeutic equipment such as computed tomography (CT). Such scans are the largest medical source of radiation and account for more than half of all medical doses today. While CT offers significant benefits through avoiding traditional surgical exploration and invasive testing, there have been numerous incidents of patients receiving relatively high doses and acute skin burns (NCRP, 2009). These procedures exemplify two general principles of radiation and health. First, proper procedure involves using the lowest practical dose and proper protections for both medical personnel and patients. Second, the benefits of diagnostic procedures must outweigh the risks of the radiation exposure. Mammography, for example, has proven to be highly beneficial in saving lives through the early detection of breast cancer, while the radiation doses associated with the procedure pose very little risk (Nelson et al., 2009).
Radiation-Related Accidents Between 1945 and 2014, some 287 nuclear reactor accidents were reported in various countries. Three accidents are particularly noteworthy: at Three Mile Island Nuclear Generating Station near Harrisburg, Pennsylvania (1979), at Chernobyl Nuclear Power Plant near Kiev, Ukraine (1986), and at Fukushima Daiichi Nuclear Power Plant in Okuma, Japan (2011). The Chernobyl accident resulted in the highest radiation exposures by a wide margin (Figure 22.6). Some 400 emergency workers received whole-body doses up to 10 Gy (NEA Committee on Radiation Protection and Public Health
1291
[NEA], 1995). Several dozen deaths occurred acutely, and according to one estimate based on no-threshold assumptions (a controversial approach), several thousand deaths from cancer among exposed populations may have followed (representing about 0.01% of incident cancers in the years after the accident) (Cardis et al., 2006). Heavy radioactive contamination near the plant necessitated the evacuation of about 116,000 inhabitants. Evacuees received whole-body doses (estimated to be 15 mSv) and internal thyroid doses from radioisotopes of iodine (ranging from 1 Sv in young children to 70 mSv in adults) (NEA, 1995). Ongoing whole-body external doses in the worst affected areas, attributable primarily to radioisotopes of cesium deposited on the ground, have been estimated to average about 15 mSv annually, peaking at about six times that level (calculated from NEA, 1995). Most of the population of the northern hemisphere was exposed, to varying degrees, to radioactive material from the release. Exposures following the Three Mile Island and Fukushima accidents were substantially lower. (See Text Box 22.3.)
Figure 22.6 The Chernobyl Disaster Source: The Chernobyl Disaster: What caused the disaster? (n.d.).
The 1986 Chernobyl Nuclear Power plant disaster, in Ukraine, was the world's worst
1292
nuclear power plant accident. It released large amounts of radioactive materials into the environment, affecting large areas in Ukraine, Belarus, Russia, and elsewhere in Europe.
1293
Text Box 22.3 What Happens During Most Nuclear Power Plant Accidents? Simply stated, the sustained fission reaction occurring in the core of a nuclear reactor needs to be cooled during operations. Water is typically the coolant. Despite numerous safety systems, the accidents at Three Mile Island and at Fukushima Daiichi were caused when the flow of water to the cores was interrupted. The ensuing buildup of heat caused the reactor fuel to begin melting and control of the fission reaction to be lost. At Three Mile Island the containment dome kept the great majority of the radioactive materials within the structure. At Fukushima Daiichi, the containment structure was damaged catastrophically due to a hydrogen explosion, resulting in widely dispersed radioactive materials.
1294
Cellular and Biological Effects of Ionizing Radiation Ionizing radiation has biological effects because it interacts with matter—specifically, with living tissues. Understanding how radiation interacts with matter enables radiation protection professionals to design and deploy shielding to attenuate the effects of radiation. It also enables them to understand the effects of different types of radiation on living cells.
The way radiation deposits energy depends on the energy, mass, and charge of the radiation, and the energy absorbing characteristics of the medium. Energy deposition can be described by its rate (per unit distance) or density (energy per mass or volume). The spatial distance of ionizing events along the path of a radiation is known as linear energy transfer (LET). Relative mass stopping power is used to compare quantitatively the energy absorption of different media; this is critical to selecting optimal shielding materials. LET is also critical in assessing the impact on living cells. Because different types of radiation deposit energy at different rates (or densities) in cells, it takes a different amount of radiation for each type to deliver the same radiation dose and therefore the same effect—a concept known as relative biological effectiveness (RBE). X- and gamma radiation give up energy in chance encounters and therefore travel farther in a given mass or volume of a media as compared to massive, slow, and highly charged alpha radiation, which typically gives up all its energy in traversing a short distance. For this reason, the RBE of densely ionizing radiations exceeds that of sparsely ionizing radiations for most forms of injury.
Two main categories of radiation effects on cells are of concern. Genetic effects causing DNA damage are related to heritable defects. Somatic effects, at higher doses, are related to cell death.
Genetic Effects Radiation exposures may cause genetic damage and mutagenic effects. Cells may repair this damage. The mutation rate is a measure of damage to DNA that remains unrepaired or that is
1295
misrepaired; it is approximately 10−5 to 10−6 per locus per Sv (National Research Council [NRC], 2006). The mutation rate is affected by both the total dose received and the rate at which the dose is delivered. It appears to increase as a linear nonthreshold function of the dose, implying that a single ionizing particle traversing the DNA may suffice to cause a mutation (NCRP, 2001a; NRC, 2006). With low-LET (sparsely ionizing) radiation, the yield of mutations per unit dose as a function of dose rate is not linear. It typically decreases with decreasing dose rate, passing through a minimum in the range of 0.1 to 1.0 cGy (centigray) per minute, below which it rises again with further reduction of the dose rate (Vilenchik & Knudson, 2000). This pattern suggests that there is an optimal range for effort-free DNA repair (0.1 to 1.0 cGy per minute), and that repair becomes less effective at lower dose rates (Vilenchik & Knudson, 2000). Of note, the ability to repair DNA is not static; exposure to an appropriate conditioning dose of radiation can elicit a DNA repair-enhancing, adaptive response in some cells (Wojcik, 2000; NRC, 2006). However, the mechanisms that normally facilitate DNA repair or eliminate cells with unrepaired damage may not operate effectively in cells in which one or more of the responsible homeostatic genes has been mutated or lost.
In addition to its mutagenic effects, radiation may also cause changes in chromosome number and structure. The type and the frequency of this damage vary with the stage of the cell cycle in which it occurs. The dose-response relationships for such chromosome aberrations are typically linear-quadratic at high doses and dose rates, and more nearly linear, with shallower slopes, at lower doses and dose rates of low-LET radiation (NCRP, 2001a). Chromosome aberrations in blood lymphocytes serve as a useful biological dosimeter; they are elevated in radiation workers and in people who live in areas of high natural background radiation levels (Bender et al., 1988; Mettler & Upton, 2008).
Irradiation can also cause chromosome aberrations to arise in the progeny of exposed cells, many cell generations later. This transgenerational genome instability may be an epigenetic phenomenon (Merrifield & Kovalchuk, 2013; Zielske, 2015). In some types of cells irradiated in vitro, preexposure to a conditioning dose can reduce the frequency of chromosome aberrations produced by a subsequent test dose. However, it is questionable
1296
whether such an adaptive response protects against the effects of chronic low-level irradiation in humans, for three reasons: a dose of at least 5 mGy (milligrays) delivered at a rate of at least 50 mGy per minute appears to be required to elicit the response; the protective effect of the response lasts for only a few hours; and, the response varies markedly from person to person, with some individuals appearing to be entirely nonresponsive (Wojcik, 2000; NRC, 2006).
Heritable genetic effects from irradiation have not been demonstrated conclusively in humans, although they have been well documented in other organisms. Studies of more than 76,000 children of Japanese atomic bomb survivors have not detected any elevations in untoward pregnancy outcomes, neonatal deaths, malignancies, balanced chromosomal rearrangements, sex chromosome aneuploids, alterations of serum or erythrocyte protein phenotypes, changes in sex ratio, or disturbances in growth and development (NRC, 1990, 2006; Mettler & Upton, 2008). Likewise, although a case-control study has suggested an excess of leukemia and non-Hodgkin's lymphoma in young people in the village of Seascale, England, related to the occupational irradiation of their fathers (Gardner et al., 1990), this finding is controversial, and there are strong reasons for rejecting it (Doll, Evans, & Darby, 1994; Wakeford et al., 1994a, 1994b).
In the absence of definitive evidence of heritable effects of radiation in humans, estimates of the risks of such effects must rely heavily on extrapolation from findings in laboratory animals. Available data suggest that human germ cells are probably no more radiosensitive than those of the mouse and that a dose of at least 1.0 Sv would be required to double the rate of heritable mutations in humans (NRC, 2006). On this basis it is estimated that less than 1% of inherited disease in the human population is attributable to natural background irradiation (NRC, 2006; Mettler & Upton, 2008).
Somatic Effects Somatic effects are those affecting cell survival within the tissues and organs of the body. This section considers the early, acute somatic effects. Radiation damage to genes, chromosomes, and other vital organelles can be lethal to affected cells, especially dividing cells, which are highly radiosensitive as a class. Although a dose below 0.5 Sv kills too few cells to cause clinically detectable
1297
injury in most organs other than those of the embryo, a larger dose may kill enough of the progenitor cells in a tissue to interfere with the orderly replacement of its senescent cells, thereby causing tissue atrophy. This atrophy develops more slowly in organs characterized by slow cell turnover, such as the liver and vascular endothelium, and faster in organs characterized by rapid cell turnover, such as the bone marrow, epidermis, and intestinal mucosa. Also, if only a small volume of tissue is irradiated, or if the dose is accumulated gradually over an extended period of time, the severity of the injury tends to be reduced by the compensatory proliferation of surviving cells.
The acute effects of radiation are diverse and vary markedly in their dose-response relationships, clinical manifestations, timing, and prognosis. Such acute reactions generally result from the severe depletion of progenitor cells in the exposed tissues and occur only at doses above the thresholds high enough to kill many such cells. These reactions are therefore classified as nonstochastic effects (or deterministic effects). In contrast, stochastic effects—those that are mutagenic and carcinogenic—manifest as increased probabilities of occurrence at greater doses. These effects are thought to result from random molecular alterations in individual cells that increase in frequency as linear nonthreshold functions of the dose.
1298
Human Health Effects of Ionizing Radiation Acute Effects The acute human health effects of ionizing radiation increase dramatically with a high-dose-rate whole-body dose. Major forms and features of acute radiation syndrome are presented in Table 22.4. A dose of 3.5 to 4.5 Sv, without subsequent medical care, will be fatal to about half of exposed people. The lifetime risk is about 10% per Gy to persons exposed acutely to whole-body radiation; exposure to greater than 10 Gy will be fatal to virtually 100% of those exposed, whether treatment is provided or not (Merck, 2013).
Table 22.4 Major Forms and Features of Acute Radiation Syndromes
Dose >6 Sv to lungs
2–10 Sv 10–20 Sv >50 Sv
Form Pulmonary Hemopoietic Gastrointestinal Cerebral Initial effects
Nausea Vomiting
Nausea Vomiting Diarrhea
Nausea Vomiting Diarrhea
Nausea Vomiting Diarrhea Headache Disorientation Ataxia Coma Convulsions
Onset Second to eighth months
Third to sixth weeks
Second week First day
Progressive effects
Cough Dyspnea Fever Chest pain Respiratory failure (?)
Weakness Fatigue Anorexia Fever Hemorrhage Epilation Recovery (?) Death (?)
Nausea Vomiting Diarrhea Fever Erythema Prostration Death
Death
1299
Source: Adapted from Mettler & Upton, 2008.
Prominent features of the acute effects of ionizing radiation on the more radiosensitive tissues of the body are as described below (International Commission on Radiological Protection [ICRP], 1984; Mettler & Upton, 2008).
Skin. Brief exposure of the skin to a dose of 6 Sv or more produces a sunburn-like rash and loss of hair in the exposed area. If the dose exceeds 10 to 20 Sv, blistering and ulceration may ensue, followed by scarring of the underlying tissue, and a second wave of atrophy and ulceration months or years later.
Bone marrow and lymphoid tissue. A dose of 2 to 3 Sv delivered rapidly to the whole body leads to a marked depression of the lymphocyte count and immune response within hours and a comparable depression of the leukocyte and platelet counts within three to five weeks. After a larger dose, the latter changes may be severe enough to result in fatal infection or hemorrhage, or both. In Hiroshima and Nagasaki, for example, the majority of the many thousands of fatally injured victims within 1 km of ground zero who did not die from blast injuries or burns succumbed to bone marrow damage (Okita, 1975).
Intestine. An acute dose of 10 Sv causes the lining of the small intestine to become denuded within days, and if a large enough area of the lining is affected, a fulminating, rapidly fatal, dysentery-like syndrome results.
Gonads. A dose of 0.15 Sv delivered rapidly to both testes can kill enough immature sperm-forming cells to lower the sperm count, and a dose of 2 to 4 Sv is likely to cause permanent sterility. Likewise, a dose of 1.5 to 2.0 Sv delivered rapidly to both ovaries kills enough oocytes to cause temporary sterility, and a larger dose permanent sterility, depending on the age of the woman at the time of exposure.
Respiratory tract. Although the lung is not highly radiosensitive, a dose of 6 to 10 Sv may cause the exposed area to become severely inflamed within one to three months. If a large enough volume of the lung is affected, respiratory failure may follow within weeks, or other complications may occur months or years later.
1300
Lens of the eye. Acute exposure of the lens to more than 1 Sv can be followed within months by the formation of a microscopic lens opacity, and 2 to 3 Sv received in a single brief exposure (or 5.5 to 14 Sv accumulated over a period of months) may cause a vision-impairing cataract.
Other tissues. The other tissues of the body have thresholds for acute injury that are substantially higher than those for the reactions described above. All tissues in a rapidly growing state tend to be more radiosensitive.
Whole-body radiation injury. Rapid exposure of a major part of the body to more than 1 Sv may cause acute radiation syndrome (radiation sickness). This syndrome is characterized by (1) an initial prodromal stage with malaise, anorexia, nausea, and vomiting; (2) an ensuing asymptomatic, latent period; (3) a second (main) phase of illness; and (4) finally, either recovery or death. The main phase of illness typically takes one of the following four forms, depending on the predominant locus of radiation injury: hematological, gastrointestinal, cerebral, or pulmonary (Table 22.4). Another syndrome, termed chronic radiation sickness, has been reported in chronically exposed workers at the Mayak nuclear facility in Russia, and in people residing downriver from the facility who were exposed to radioactive effluents from the plant. These workers received protracted exposures to external gamma radiation at high cumulative doses, with average and maximum doses to the whole body of 0.8 Gy and >10 Gy, respectively (Shilnikova et al., 2003). These workers also received significant internal doses from depositions of plutonium. The clinical findings in these groups, though not observed in other irradiated populations, include varying and persistent leukopenia, thrombocytopenia, arthralgia, asthenia, and various other ill-defined neurological complaints (Shilnikova et al., 1996).
Localized radiation injury. In contrast to the clinical manifestations of acute whole-body radiation injury, which are often dramatic and prompt, the reaction to sharply localized irradiation, whether from an external radiation source or from an internally deposited radionuclide, tends to evolve more slowly and to produce few symptoms unless the volume of tissue irradiated or the dose is relatively large. Of note, some
1301
radionuclides (such as 3H, 14C, and 137Cs) tend to be distributed systemically and to irradiate the whole body to varying degrees, whereas others are characteristically concentrated in specific organs. Radioisotopes of radium and 90Sr, for example, are deposited predominantly in bone, causing skeletal injuries primarily, whereas radioisotopes of iodine concentrate in the thyroid gland, which is the primary site of any resulting injury.
Carcinogenic Effects The carcinogenic effects of ionizing radiation, first manifested early in the twentieth century by skin cancers and leukemia in pioneer radiation workers, have since been documented extensively by the occurrence of dose-dependent excesses of osteosarcomas and cranial sinus carcinomas in radium dial painters, carcinomas of the respiratory tract in underground hard rock miners, and cancers of many organs in atomic bomb survivors, radiotherapy patients, and experimentally irradiated laboratory animals. The tumors caused by irradiation characteristically take years or decades to appear and exhibit no features distinguishing them from other tumors. The estimated lifetime risk of fatal cancer attributable to 0.1 Sv low- dose-rate whole-body radiation is presented in Table 22.5.
Table 22.5 Estimated Lifetime Risks of Fatal Cancer Attributable to 0.1 Sv Low-Dose-Rate Whole-Body Irradiation
Type or site of cancer
Excess cancer deaths per 100,000
Percentage excess above baselinea
Lung 200 7 Bone marrow (leukemia)
65 13
Colon 61 3 Breast 40 2 Urinary bladder
25 4
Gonads 24 5 Stomach 22 4 Esophagus 20 6
1302
Liver 16 9 Thyroid 8 8 Bone 5 5 Skin 2 2 Remainder 87 2 Total 575 2
a Percentage increase in the baseline risk expected for a nonirradiated population.
Source: Adapted from NRC, 2006.
With few exceptions, cancer has been detectable only after relatively large doses (0.5 Sv) and has varied in frequency with the type of neoplasm as well as the age and gender of the exposed individuals. The neoplasms typically evolve through a succession of stages, and in experimental animals the carcinogenic effects of radiation have included initiating effects, promoting effects, and effects on the progression of neoplasia, depending on the experimental conditions (NRC, 2006). Although the molecular mechanisms of these effects remain to be fully elucidated, the activation of oncogenes or the inactivation or loss of tumor suppressor genes, or both, appear to be involved in many if not all instances (NRC, 2006). Furthermore, the carcinogenic effects of radiation resemble those of chemical carcinogens in being modifiable by hormones, nutritional variables, and other factors; and in combination with chemical carcinogens, the effects of radiation may be additive, synergistic, or mutually antagonistic, depending on the specific chemicals and exposure conditions (Mettler & Upton, 2008).
When we turn to occupational risks, carcinogenic effects of occupational irradiation are no longer readily demonstrable in most U.S. radiation workers, thanks to modern radiation protection practices. Underground hard rock miners may represent an exception, possibly remaining at elevated risk of lung cancer mortality (Wakeford, 2009). Some (but not all) analyses of data for several large cohorts of nuclear workers suggest a dose-dependent excess of leukemia and other cancers in this population (Cardis et al., 2007) that is comparable in magnitude with the estimate displayed in Table 22.5. Excesses of multiple myeloma and other forms of cancer have also been reported in some cohorts of occupationally exposed workers, with some variability in findings
1303
(Mettler & Upton, 2008).
Among populations exposed to radioactive fallout, carcinogenic effects on the thyroid gland have been well documented. One example is Marshall Islanders who received large doses to the thyroid in childhood and infancy (possibly up to 20 Gy) from radioactive iodine, tellurium, and external gamma ray emitters in fallout released by a thermonuclear weapons test at Bikini atoll in 1954 (Robbins & Adams, 1989). Other examples are children who lived downwind of the Nevada nuclear weapons test site (Kerber et al., 1993; Simon, Bouville, & Land, 2006) and children in Belarus and Ukraine affected by the Chernobyl accident (Heidenreich et al., 1999). (Cancer risks near nuclear power plants are discussed in Chapter 14.)
Effects on the Developing Embryo Radiosensitivity is relatively high throughout prenatal life. The effects of a given dose can vary markedly depending on the developmental stage of the embryo or fetus at the time of exposure (Mettler & Upton, 2008). During the preimplantation period, the embryo is maximally susceptible to killing by irradiation. During critical stages in organogenesis, the fetus is susceptible to the induction of malformations and other disturbances of development. A dramatic example is the dose-dependent increase in the frequency of mental retardation and the dose-dependent decrease in IQ test scores observed in atomic bomb survivors who were irradiated between the eighth and fifteenth weeks (and seen to a lesser extent in those irradiated between the sixteenth and twenty-fifth weeks) after conception (United Nations Scientific Committee on the Effects of Atomic Radiation [UNSCEAR], 1986; NRC, 1990; Mettler & Upton, 2008). Susceptibility to the carcinogenic effects of radiation also appears to be comparatively high throughout the prenatal period; that is, the available data suggest that irradiation in utero may increase a child's risk of leukemia and other cancers by as much as 40% per Sv (Doll & Wakeford, 1997; Mettler & Upton, 2008).
1304
Radiation Protection Radiation protection measures are selected to prevent either internal or external exposures, or both, depending on the conditions and radionuclides involved. Radioactive materials can enter the body through four basic means: inhalation, ingestion, absorption through the skin, or via a wound. Each internal pathway has associated engineering controls and protective measures to avoid exposures. Internal radiation protection methods include confinement of contaminated air and, if that proves impractical, removal of radioactive materials from contaminated breathing air; avoiding potential for ingestion; and preventing direct contact that could result in contamination or absorption. Personal protective equipment, including specialized clothing and respiratory protection, is used when engineering controls are not feasible. The basics of external radiation protection methods are to eliminate the source of the exposure. When the source cannot be removed, engineering controls are preferred. In addition, exposures can be controlled by applying the following techniques: minimizing exposure time; maximizing distance from the source; and shielding the radiation source.
Several principles guide efforts to minimize risks of radiation injury, consistent with general preventive approaches in environmental health (see Chapter 26). First, no activity involving ionizing radiation should be considered justifiable unless it produces a sufficient benefit to those who are exposed, or to society at large, to offset any harm it may cause. Second, in any such activity the dose or likelihood of exposure should be kept as low as reasonably achievable (ALARA), taking all relevant economic and social factors into account. Third, the radiation exposure should be subject to dose limits low enough to prevent nonstochastic effects altogether and also low enough to prevent the risks of any stochastic effects (which may have no thresholds) from exceeding socially acceptable levels. For members of the public, therefore, it is generally recommended that the effective dose not exceed 5 mSv in any given year (infrequent) or 1 mSv per year on average over any three years (frequent) (NCRP, 1993; International Atomic Energy Agency [IAEA], 1996; Mettler & Upton, 2008). Dose limits for the
1305
public are lower than those for workers, which is typical for most types of hazards. While all limits for routine exposures are intended to prevent adverse health effects, those for the public account for individuals who may be less healthy or more sensitive or otherwise vulnerable physically.
To comply with these precautionary guidelines, any workplace dealing with ionizing radiation must (1) have proper design and engineering controls; (2) have licenses and operating parameters consistent with its design; (3) have a robust radiation protection program; (4) have workers who are adequately trained and supervised; (5) conduct operations with sufficient planning, procedures, and oversight to effectively integrate safety management; (6) have independent oversight affording root cause analyses, lessons learned, corrective actions, and continuous improvement; and (7) have a well-developed and maintained emergency preparedness plan, in order to be able to respond promptly and effectively in the event of a malfunction, spill, or other type of radiation accident (Gusev, Guskova, & Mettler, 2001; Shapiro, 2002). These guidelines apply to both developed countries and developing countries (UNSCEAR, 1988; IAEA, 1996).
1306
Assessing Radiation Risks Although nonstochastic effects of radiation are produced only by relatively large doses, genetic and carcinogenic effects appear to increase in frequency as nonthreshold functions of the dose (NCRP, 2001a; Mettler & Upton, 2008; Pawel & Puskin, 2012). The existing data are not sufficient to describe the dose-incidence relationship unambiguously for any type of neoplasm in the low-dose domain or to define how long after irradiation the risk may remain elevated in an exposed population. Therefore, any risks attributable to low-level irradiation can be estimated only by extrapolation, based on models (NCRP, 2001a). Numerous dose-effect models have been used to estimate the risks of low-level irradiation. Most of these models involve the assumption that the overall risk of cancer increases in proportion with the dose at low-dose levels. Some research data conflict with this assumption. For example, the carcinogenic potency of X rays and gamma rays in laboratory animals has been found to be reduced by as much as an order of magnitude when the exposure is prolonged, and the risk to humans is generally estimated to increase less steeply at low doses and dose rates than it does at high doses and dose rates. Furthermore, available data suggest that a threshold may exist in the mSv (low) dose range (NCRP, 2001a; NRC, 2006; Ulsh, 2010), so existing estimates may overstate the true risks of cancer from small doses or doses accumulated over weeks, months, or years (NRC, 2006; Mettler & Upton, 2008). Estimated risks are nevertheless useful in establishing dose limits for workers and members of the public because they are likely to ensure adequate protection relative to other risks encountered (Moghissi, Gerraa, McBride, & Swetnam, 2014).
These uncertainties notwithstanding, models have been applied to epidemiological data from the atomic bomb survivors and other irradiated populations and have yielded estimates of the lifetime risks of different forms of cancer that may be attributable to ionizing irradiation (see the examples in Table 22.5). These are based on population averages and hence cannot be assumed to apply equally to all individuals. Susceptibility to certain types of cancer (notably cancers of the thyroid and breast) is substantially
1307
higher in children than in adults, and susceptibility also increases in association with certain hereditary disorders, such as retinoblastoma and nevoid basal cell carcinoma syndrome (Sankaranarayanan & Chakraborty, 1995; ICRP, 1998; Little, 2000; Mettler & Upton, 2008).
Because diagnostic radiography and indoor radon constitute the most important controllable sources of ionizing radiation exposure for the general public, prudent measures to limit exposure from these sources are clearly warranted (NCRP, 1993; IAEA, 1996; U.S. EPA, 2007). Other potential risks to human health and the environment that call for increased attention are the millions of cubic feet of radioactive and mixed wastes (mine and mill tailings, spent nuclear fuel, waste from the decommissioning of nuclear power plants, dismantled industrial and medical radiation sources, radioactive pharmaceuticals and reagents, heavy metals, polycyclic aromatic hydrocarbons, and other contaminants) that are present in ever-growing quantities and that severely tax existing storage capacities at numerous sites (see, e.g., NRC, 1989; U.S. Department of Energy, 1993; Crowley & Ahearne, 2002). There is also a need to prevent terrorist attacks that use radioactive materials (NCRP, 2001b).
1308
Summary There is a wide gap between public understanding of radiation and scientific understanding. The association of radiation with nuclear weapons evokes images of suffering and annihilation. Early in its discovery, radiation was thought to be the cure for certain health problems. The development and use of X-ray machines opened new frontiers of noninvasive diagnostics. The envisioned peaceful use for the atom in the form of nuclear power generation was believed to make metering electricity unnecessary. With such a high bar, practices involving radiation have not met expectations. Faulty designs, poor practices, and human errors have led to accidents, overexposures, and even deaths. Radiation is best accepted in medicine because of the understood benefit. It is either avoided or accepted with reservations in most other uses.
This chapter began with the perspective that humans have always been surrounded by a sea of radiation. Today, most radiation doses received by members of the public are low. Exceptions are doses to the bronchial airways and lungs from smoking cigarettes and inhaling high indoor concentrations of radon decay products, and whole-body or localized doses incurred during specialized therapeutic or diagnostic medical procedures. Radiation is easily detectable and quantified. Occupational radiation doses are controlled better today than at any time since the discovery of radiation. Although some degree of radiation injury may be inevitable given the significant doses associated with radiotherapy, few patients treated with modern methods experience severe or disabling radiation injuries. Modern facilities and safety practices have essentially eliminated the radiation injuries due to excessive occupational exposure that were prevalent among pioneer radiation workers.
The human health effects from higher dose and higher dose-rate exposures are very well understood. The effects from low-dose and lower dose-rate exposures remain a source of controversies and fears because experimental data generated to date are insufficient to fully characterize adverse health effects. It is understandable that the public wants to know whether or not low doses of radiation do indeed cause cancer and whether all exposures should be avoided. A
1309
new study of over 1 million radiation workers in the United States (Bouville et al., 2015) seeks to help answer those questions, however, even that study might prove insufficient due to the many confounding factors and the complexity of possible relationships between radiation dose and cancer causation. Most radiation protection professionals believe that all radiation exposures should result in a net benefit, that infants and children are the most sensitive to adverse effects, and that for healthy adults low doses are safe compared to the multitude of risks we face in everyday life.
Two areas will continue to dominate the use of radioactive materials. These areas are medicine and energy production. Ever- advancing equipment for diagnostic and therapeutic medical applications continues to use radioactive materials or to rely on the generation of radiation. Considering that radiation was only first discovered in 1895, medical equipment has advanced with exceptional purpose and speed. As discussed in Chapter 14, nuclear power may continue to play an important role in the overall energy supply both in the United States and internationally, especially with continued efforts to reduce the use of fossil fuels. Within the next 100 years, smaller more modular reactors will likely produce local power both in developed and developing nations potentially transforming the current extensive and overwhelming needs for infrastructure. Future perspectives on radiation will likely change dramatically.
1310
Key Terms absorbed dose
Energy imparted to tissue by radiation. activity
The rate of transformations of a radionuclide per unit time, a measure of radioactivity. Units of activity are the curie (Ci) and the becquerel (Bq).
ALARA (as low as reasonably achievable) An approach to controlling radiation exposure that makes every reasonable effort consistent with the limits of technology, cost, and feasibility.
alpha particle A positively charged particle made up of two neutrons and two protons emitted by certain radioactive nuclei.
beta particle An electron or positron emitted by certain radioactive nuclei.
cosmic radiation Radiation arriving at the Earth's surface from space.
deterministic effects See nonstochastic effects.
directly ionizing particles Electrically charged particles with sufficient kinetic energy to produce ionization by collision.
effective dose The equivalent dose, corrected for tissue sensitivity.
electromagnetic fields (EMFs) Fields that feature coupled electric and magnetic fields, characterized by long wavelength and low frequency.
electromagnetic spectrum The sequence of radiation forms, from long wavelength, low frequency forms, such as electromagnetic fields, to short wavelength, high frequency forms, such as cosmic rays.
equivalent dose (or dose equivalent) The absorbed dose, corrected for the linear energy transfer.
1311
external dose A dose of radiation received from outside the body, such as with exposure to an X-ray.
external radiation protection Protection designed to reduce the amount of external radiation reaching a person's body.
extremely low frequency (ELF) EMFs Time-varying magnetic fields with wavelengths greater than 108 cm and frequencies less than 300 Hz.
fallout The atmospheric presence, and deposition, of particles of radioactive debris following a nuclear explosion.
frequency In radiation, the number of individual waves, or cycles, passing through a certain point of a medium over the course of a second.
gamma rays A form of electromagnetic radiation with high energy, high frequency, and a short wavelength, emitted by certain radionuclides when their nuclei transition from a higher to a lower energy state.
half-life In radiation, the time it takes for half of a given quantity of a radionuclide to decay.
indirectly ionizing radiations Uncharged neutrons, gamma rays, and neutral mesons without sufficient kinetic energy to produce ionization by collision, but capable of imparting sufficient energy to liberate directly ionizing particles.
infrared radiation (IR) A form of nonionizing radiation with frequencies between about 3 × 1011 Hz and 4.3 × 1014 Hz, and wavelengths between about 800 nm and 1mm.
internal dose A dose of radiation received from inside the body, as from radioactive iodine that has been absorbed.
internal radiation protection Protection from internal radiation emitters: for example,
1312
measures to prevent inhalation of radionuclides. ionization potential
Whether radiation contains sufficient energy to ionize atoms. ionizing radiation
Radiation capable of displacing electrons from atoms or molecules, thereby producing ions, including alpha, beta, gamma, and X rays.
isotopes Forms of an element with the same number of protons but a different number of neutrons.
light Electromagnetic waves ranging in wavelength from approximately 760 nm (red) to 380 nm (violet), with frequencies from 3.9 × 1014 Hz to 7.9 × 1014 Hz.
linear energy transfer (LET) A parameter of radiation, referring to rate of energy deposited per unit of distance a particle penetrates matter (e.g., tissue). Higher energy ionizing radiation has a higher LET.
linear nonthreshold function In radiation, a type of dose-response relationship in which each incremental unit of dose is associated with a unit of response (say, increased cancer risk) and in which there is no detectable level of exposure below which this relationship does not operate.
microwave and radiofrequency radiation (MW/RFR) Forms of electromagnetic radiation with intermediate energy, frequencies between 3 Hz and 300 GHz, and wavelengths between 1 mm and 100,000 km.
neutron A small particle with no electrical charge typically found within an atom's nucleus.
nonionizing radiation Radiation with lower energy levels, lower frequencies, and longer wavelengths than ionizing radiation. It lacks sufficient energy to change the atomic structure of material it encounters, although it can heat tissue and can cause harmful biological effects.
nonstochastic effects
1313
Associations characterized by a clear relationship between the exposure and the effect, and often by a threshold dose below which the effect does not occur (cf. stochastic effects). Also referred to as deterministic effects.
nuclear transformation The defining event of radioactivity, occurring when an unstable nucleus decays, emitting radiation and achieving a more stable state.
photon An energy packet through which radiation and other electromagnetic energy is propagated.
proton A small positively charged particle, typically found within an atom's nucleus.
radioactivity Spontaneous nuclear transformations that result in the formation of new elements.
radionuclides Variant forms of a radioactive element with differing numbers of neutrons in their nuclei.
radon A naturally occurring radioactive gas, the decay product of uranium and radium, found in soils, rock, and water. The largest naturally occurring source of radiation exposure.
relative biological effectiveness (RBE) A characteristic of a particular form of radiation, referring to its ability to deposit energy in tissue.
somatic effects Radiation effects such as cell death that are limited to an exposed cell, tissue, or organism, as distinguished from genetic effects, which may affect subsequent generations.
specific absorption rate (SAR) A measure of the absorption of energy by the human body when exposed to radiation, measured in watts per kilogram.
specific activity The concentration of radioactivity, or the relationship between the mass of radioactive material and the activity
1314
stochastic effects Associations in which the exposure and the effect are linked in probabilistic ways, with a sense of random occurrence (cf. nonstochastic effects).
terrestrial radiation Radiation emitted by naturally occurring radioactive materials in the Earth's crust, such as uranium, thorium, and radon.
transformation kinetics The processes that characterize a radionuclide's decay, including half-life and activity.
ultraviolet radiation (UVR) Forms of electromagnetic radiation with intermediate energy, frequencies between 8 × 1014 and 3 × 1016 Hz, and wavelengths between 100 nm and 440 nm.
wavelength In radiation, the distance between successive crests, or successive troughs, of the wave motion that conveys energy.
X-ray A form of electromagnetic radiation with high energy, high frequency, and a short wavelength, emitted by atoms when electrons fall from a higher energy shell to a lower energy shell.
1315
Discussion Questions 1. What is the spectrum of electromagnetic radiation in terms of
the relationship among wavelength, frequency, and energy? Identify the various forms of radiation occurring along the spectrum.
2. What types of injury of public health concern are associated with exposure to each of the different forms of radiation, and how does the risk of each such injury vary with the dose of the radiation in question?
3. What is the fundamental purpose of a nuclear transformation occurring within a radionuclide, and how do specific mechanisms increase or decrease the proton to neutron ratio, or release excess energy?
4. What are the mechanisms through which the different forms of radiation interact with living cells at the molecular level, and how may they lead to adverse effects on human health?
5. Choose a routinely performed radiological exam, such as the CT scan for trauma victims, preemployment chest X-ray, or screening mammogram. What are the risks and the benefits of the exam? Be sure to consider different age groups, as the risk may differ across the lifespan.
1316
References Baan, R., Grosse, Y., Lauby-Secretan, B., El Ghissassi, F., Bouvard, V., Benbrahim-Tallaa, L.,…Straif, K. (2011). Carcinogenicity of radiofrequency electromagnetic fields. Lancet: Oncology, 12(7), 624–626.
Becker, B. (2012). My close encounter with the fabulous shoe-fitting machine. Telegraph, July 16. Retrieved from http://www.telegraph.co.uk/news/health/9366921/My-close- encounter-with-the-fabulous-shoe-fitting-machine.html
Bender, M. A., Awa, A. A., Brooks, A. L., Evans, H. J., Groer, P. G., Littlefield, L. G.,…Wachholz, B. W. (1988). Current status of cytogenetic procedures to detect and quantify previous exposures to radiation. Mutation Research, 196, 103–159.
Blank, M. (2008). Protein and DNA reactions stimulated by electromagnetic fields. Electromagnetic Biology and Medicine, 27, 3–23.
Bouville, A., Toohey, R. E., Boice, J. D., Jr., Beck, H. L., Dauer, L. T., Eckerman, K. F.,…Zeitlin, C. (2015). Dose reconstruction for the Million Worker Study: Status and guidelines. Health Physics, 108, 206–220.
Cardis, E., Krewski, D., Boniol, M., Drozdovitch, V., Darby, S. C., Gilbert, E. S.,…Boyle, P. (2006). Estimates of the cancer burden in Europe from radioactive fallout from the Chernobyl accident. International Journal of Cancer, 119(6), 1224–1235.
Cardis, E., Vrijheid, M., Blettner, M., Gilbert, E., Hakama, M., Hill, C.,…Veress, K. (2007). The 15-Country Collaborative Study of Cancer Risk Among Radiation Workers in the Nuclear Industry: Estimates of radiation-related cancer risks. Journal of Radiation Research, 167, 396–416.
Cember, H., & Johnson, T. E. (2009). Introduction to health physics (4th ed.). New York: McGraw-Hill Medical.
The Chernobyl Disaster: What caused the disaster? (n.d.). Retrieved
1317
from http://disasteratchernobyl.weebly.com
Collet, C., Guillot, A., & Petit, C. (2010). Phoning while driving I: A review of epidemiological, psychological, behavioural and physiological studies. Ergonomics, 53(5), 589–601.
Crowley, K. D., & Ahearne, J. F. (2002). Managing the environmental legacy of U.S. nuclear-weapons production. American Scientist, 90, 514–523.
Doll, R., Evans, N. J., & Darby, S. C. (1994). Paternal exposure not to blame. Nature, 367, 678–680.
Doll, R., & Wakeford, R. (1997). Risk of childhood cancer from fetal irradiation. British Journal of Radiology, 70, 130–139.
Duffin, J., & Hayter, C. R. (2000). Baring the sole: The rise and fall of the shoe-fitting fluoroscope. Isis, 91(2), 260–282.
Federal Communications Commission. (2015). Specific absorption rate (SAR) for cellular telephones. Retrieved from https://www.fcc.gov/encyclopedia/specific-absorption-rate-sar- cellular-telephones
Foster, K. R., & Moulder, J. E. (2013). Wi-fi and health: Review of current status of research. Health Physics, 105, 561–575.
Gardner, M. J., Snee, M. P., Hall, A. J., Powell, C. A., Downes, S., & Terrell, J. D. (1990). Results of case-control study of leukaemia and lymphoma among young people near Sellafield nuclear plant in West Cumbria. BMJ, 300, 423–429.
Gies, P. (2007). Photoprotection by clothing. Photodermatology, Photoimmunology, & Photomedicine, 23, 264–274.
Gusev, I. A., Guskova, A. K., & Mettler, F. A. (Eds.). (2001). Medical management of radiation accidents (2nd ed.). Boca Raton, FL: CRC Press.
Halliday, G. M., Byrne, S. N., & Damian, D. L. (2011). Ultraviolet A radiation: Its role in immunosuppression and carcinogenesis. Seminars in Cutaneous Medicine and Surgery, 30(4), 214–221.
Hardell, L., Carlberg, M., & Hansson Mild, K. (2011). Pooled
1318
analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects. International Journal of Oncology, 38(5), 1465–1474.
Hardell, L., Carlberg, M., Söderqvist, F., Mild, K. H., & Morgan, L. L. (2007). Long-term use of cellular phones and brain tumours: Increased risk associated with use for >10 years. Journal of Occupational and Environmental Medicine, 64, 626–632.
Heidenreich, W. F., Kenigsberg, J., Jacob, P., Buglova, E., Goulko, G., Paretzke, H. G.,…Golovneva, A. (1999). Time trends of thyroid cancer incidence in Belarus after the Chernobyl accident. Radiation Research, 181, 617–625.
Hendry, J. H., Simon, S. L., Wojcik, A., Sohrabi, M., Burkart, W., Cardis, E.,…Hayata, I. (2009). Human exposure to high natural background radiation: What can it teach us about radiation risks? Journal of Radiological Protection, 29(2A), A29–42.
International Agency for Research on Cancer. (2012). IARC monographs on the evaluation of carcinogenic risks to humans: Vol. 100D. Radiation. Lyon: IARC.
International Atomic Energy Agency. (1996). International basic safety standards for protection against ionizing radiation and for the safety of radiation sources. Vienna: Author.
International Commission on Non-Ionizing Radiation Protection. (1998). Guidelines for limiting exposure to time-varying electric, magnetic, and electromagnetic fields (up to 300 GHz). Health Physics, 74, 494–522.
International Commission on Non-Ionizing Radiation Protection. (2004). Epidemiology of health effects of radiofrequency exposure. Environmental Health Perspectives, 112, 1741–1754.
International Commission on Radiological Protection. (1984). Nonstochastic effects of ionizing radiation. Annals of the ICRP, 14(3), 1–33.
International Commission on Radiological Protection. (1998). Genetic susceptibility to cancer. Annals of the ICRP, 28(1–2), 1–157.
1319
INTERPHONE Study Group. (2010). Brain tumour risk in relation to mobile telephone use: Results of the INTERPHONE international case-control study. International Journal of Epidemiology, 39, 675–694.
Jolly, D., & Meyer, J. (2009). A brief review of radiation hormesis. Australasian Physical & Engineering Sciences in Medicine, 32(4), 180–187.
Kerber, R. A., Till, J. E., Simon, S. L., Lyon, J. L., Thomas, D. C., Preston-Martin, S., Rallison, M. L.,…Stevens, W. (1993). A cohort study of thyroid disease in relation to fallout from nuclear weapons testing. JAMA, 270, 2076–2082.
Klauer, S. G., Guo, F., Simons-Morton, B. G., Ouimet, M. C., Lee, S. E., & Dingus, T. A. (2014). Distracted driving and risk of road crashes among novice and experienced drivers. New England Journal of Medicine, 370(1), 54–59.
Leitgeb, N. (2012). Improved classification of evidence for EMF health risks. Health Physics, 103, 195–199.
Lipman, R. M., Tripathi, B. J., & Tripathi, R. C. (1988). Cataracts induced by microwave and ionizing radiation. Survey of Ophthalmology, 33, 200–210.
Little, J. B. (2000). Radiation carcinogenesis. Carcinogenesis, 21, 397–404.
Little, J. B., Radford, E. P., Jr., McCombs, H. L., & Hunt, V. R. (1965). Distribution of polonium-210 in pulmonary tissues of cigarette smokers. New England Journal of Medicine, 273(25), 1343–1351.
Lydahl, E. (1984). Infrared radiation and cataract. Acta Ophthalmologica, 166(Suppl.), 1–63.
Mazor, R., Korenstein-Ilan, A., Barbul, A., Eshet, Y., Shahadi, A., Jerby, E., & Korenstein, R. (2008). Increased levels of numerical chromosome aberrations after in vitro exposure of human peripheral blood lymphocytes to radiofrequency electromagnetic fields for 72 hours. Radiation Research, 169, 28–37.
1320
Merck Sharp & Dohme. (2013). Radiation exposure and contamination. Whitehouse Station, NJ: Merck Manuals, Merck Sharp & Dohme Corp.
Merrifield, M., & Kovalchuk, O. (2013). Epigenetics in radiation biology: A new research frontier. Frontiers in Genetics, 4, 40.
Mettler, F. A., Jr., Huda, W., Yoshizumi, T. T., & Mahesh, M. (2008). Effective doses in radiology and diagnostic nuclear medicine: A catalog. Radiology, 248(1), 254–263.
Mettler, F. A., Jr., & Upton, A. C. (2008). Medical effects of ionizing radiation (3rd ed.). Philadelphia: Saunders.
Moeller, D. W. (2011). Environmental health (4th ed.). Cambridge, MA: Harvard University Press.
Moeller, D. W., & Sun, L. S. (2010). Chemical and radioactive carcinogens in cigarettes: Associated health impacts and responses of the tobacco industry, U.S. Congress, and federal regulatory agencies. Health Physics, 99(5), 674–679.
Moghissi, A. A., Gerraa, V. K., McBride, D. K., & Swetnam, M. (2014). Scientific foundation of regulating ionizing radiation: Application of metrics for evaluation of regulatory science information. Health Physics, 107, 388–394.
National Council on Radiation Protection and Measurements. (1993). Limitation of exposure to ionizing radiation (NCRP Report No. 116). Bethesda, MD: Author.
National Council on Radiation Protection and Measurements. (2001a). Evaluation of the linear-nonthreshold dose-response model for ionizing radiation (NCRP Report No. 136). Bethesda, MD: Author.
National Council on Radiation Protection and Measurements. (2001b). Management of terrorist events involving radioactive materials (NCRP Report No. 138). Bethesda, MD: Author.
National Council on Radiation Protection and Measurements. (2009). Ionizing radiation exposure of the population of the United States (NCRP Report No. 160). Bethesda, MD: Author.
1321
National Research Council. (1989). The nuclear weapons complex. Washington, DC: National Academies Press.
National Research Council. (1990). Health effects of exposure to low levels of ionizing radiation: BEIR V. Washington, DC: National Academies Press.
National Research Council. (2006). Health risks from exposure to low levels of ionizing radiation: BEIR VII Phase 2. Washington, DC: National Academies Press.
NEA Committee on Radiation Protection and Public Health. (1995). Chernobyl ten years on: Radiological and health impact. Paris: Organisation for Economic Co-Operation and Development, Nuclear Energy Agency.
Nelson, H. D., Tyne, K., Naik, A., Bougatsos, C., Chan, B., Nygren, P., & Humphrey, L. (2009). Screening for breast cancer: Systematic evidence review update for the US Preventive Services Task Force (Evidence Syntheses, No. 74). Rockville, MD: Agency for Healthcare Research and Quality.
Oak Ridge Associated Universities. (n.d.). Shoe-fitting fluoroscope (ca. 1930–1940). Retrieved from https://www.orau.org/ptp/collection/shoefittingfluor/shoe.htm
Okita, T. (1975). A review of thirty years study of Hiroshima and Nagasaki atomic bomb survivors: II. Biological effects: A. Acute effects. Journal of Radiation Research, 16(Suppl.), 49–66.
Pawel, D. J., & Puskin, J. S. (2012). U.S. Environmental Protection Agency radiogenic risk models and projections for the U.S. population. Health Physics, 102, 646–656.
Pfeifer, G. P., & Besaratinia, A. (2012). UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer. Photochemical & Photobiological Sciences, 11(1), 90–97.
Robbins, J., & Adams, W. (1989). Radiation effects in the Marshall Islands. In S. Nagataki (Ed.), Radiation and the thyroid (pp. 11– 24). Amsterdam: Excerpta Medica.
Roberts, N. J., Jr., & Michaelson, S. M. (1985). Epidemiological
1322
studies of human exposures to microwave radiation: A critical review. International Archives of Occupational and Environmental Health, 56, 169–178.
Sadetski, S., Chetrit, A., Jarus-Hakak, A., Cardis, E., Deutch, Y., Duvdevani, S.,…Wolf, M. (2008). Cellular phone use and risk of benign and malignant parotid gland tumors—a nationwide case- control study. American Journal of Epidemiology, 167, 457–467.
Sankaranarayanan, K., & Chakraborty, R. (1995). Cancer predisposition, radiosensitivity and the risk of radiation-induced cancers, I: Background. Radiation Research, 143, 121–143.
Shapiro, J. (2002). Radiation protection: A guide for scientists and physicians (4th ed.). Cambridge, MA: Harvard University Press.
Shilnikova, N. S., Koshurnikova, N. A., Bolotnikova, M. G., Kabirova, N. R., Kreslov, V. V., Lyzlov, A. F., & Okatenko, P. V. (1996). Mortality among workers with chronic radiation sickness. Health Physics, 71(1), 86–89.
Shilnikova, N. S., Preston, D. L., Ron, E., Gilbert, E. S., Vassilenko, E. K., Romanov, S. A.,…Koshurnikova, N. A. (2003). Cancer mortality risk among workers at the Mayak nuclear complex. Radiation Research, 159(6), 787–798.
Simon, S. L., & Bouville. A. (2002). Radiation doses to local populations near nuclear weapons test sites worldwide. Health Physics, 82(5), 706–725.
Simon, S. L., Bouville, A., & Land, C. E. (2006). Fallout from nuclear weapons tests and cancer risks. American Scientist, 94, 48– 57.
Sliney, D. H., & Colville, F. (2000). Microwaves and electromagnetic fields. In M. Lippmann (Ed.), Environmental toxicants (2nd ed., pp. 577–593). Hoboken, NJ: Wiley-Interscience.
Tenforde, T. S. (1998). Electromagnetic fields and carcinogenesis— an analysis of biological mechanisms. In G. L. Carlo (Ed.), Wireless phones and health: Scientific progress (pp. 183–196). Boston: Kluwer Academic.
1323
Ulsh, B. A. (2010). Checking the foundation: Recent radiobiology and the linear no-threshold theory. Health Physics, 99, 747–758.
United Nations Scientific Committee on the Effects of Atomic Radiation. (1986). Genetic and somatic effects of ionizing radiation: Report to the General Assembly, with annexes. New York: United Nations.
United Nations Scientific Committee on the Effects of Atomic Radiation. (1988). Sources, effects, and risks of ionizing radiation: 1988 Report to the General Assembly, with annexes. New York: United Nations.
U.S. Department of Energy. (1993). Interim mixed waste inventory report: Waste streams, treatment capacities and technologies (DOE/NBM-1100). Springfield, VA: National Technical Information Services.
U.S. Environmental Protection Agency. (2007). A citizen's guide to radon: The guide to protecting yourself and your family from radon (EPA-402-K-07-009). Washington, DC: Author.
van Dijk, A., Slaper, H., den Outer, P. N., Morgenstern, O., Braesicke, P., Pyle, J. A.,…Bais, A. F. (2013). Skin cancer risks avoided by the Montreal Protocol—worldwide modeling integrating coupled climate-chemistry models with a risk model for UV. Photochemistry and Photobiology, 89(1), 234–246.
Vilenchik, M. M., & Knudson, A. G., Jr. (2000). Inverse radiation dose-rate effects on somatic and germ-line mutations and DNA damage rates. Proceedings of the National Academy of Sciences of the United States of America, 97, 5381–5386.
Wakeford, R. (2009). Radiation in the workplace—a review of studies of the risks of occupational exposure to ionising radiation. Journal of Radiological Protection, 29(2A), A61–79.
Wakeford, R., Tawn, E. J., McElvenny, D. M., Binks, K., Scott, L. E., & Parker, L. (1994a). The Seascale childhood leukaemia cases—the mutation rates implied by paternal preconceptional radiation doses. Journal of Radiological Protection, 14, 17–24.
Wakeford, R., Tawn, E. J., McElvenny, D. M., Scott, L. E., Binks, K.,
1324
Parker, L.,…Smith, J. (1994b). The descriptive statistics and health implications of occupational radiation doses received by men at the Sellafield nuclear installation before the conception of their children. Journal of Radiological Protection, 14, 3–16.
Warren, S. (1953). Neoplasms. In W.A.D. Anderson (Ed.), Anderson's pathology. St. Louis: Mosby.
Watson, D. J., & Strom, D. J. (2011). Radiation doses to members of the U.S. population from ubiquitous radionuclides in the body: Part 3. Results, variability, and uncertainty. Health Physics, 100, 402– 416.
Wojcik, A. (2000). The current status of the adaptive response to ionizing radiation in mammalian cells. Human and Ecological Risk Assessment, 6, 281–300.
Wood, J. (2013). Students' frequent cell phone use tied to lower grades, higher anxiety. Retrieved from http://collegiatecoachingservices.com/2013/12/college-students- frequent-cell-phone-use-tied-to-lower-grades-higher-anxiety
World Health Organization. (2007). Extremely low frequency (ELF) fields (Environmental Health Criteria 238). Geneva: Author.
Yam, J. C., & Kwok, A. K. (2014). Ultraviolet light and ocular diseases. International Ophthalmology, 34(2), 383–400.
Zielske, S. P. (2015). Epigenetic DNA methylation in radiation biology: On the field or on the sidelines? Journal of Cellular Biochemistry, 116(2), 212–217.
1325
For Further Information Organizations Several government or quasi-governmental organizations provide authoritative information on radiation and its public health implications. These organizations include the following:
Health Physics Society: http://www.hps.org
International Atomic Energy Agency: https://www.iaea.org
International Commission on Radiological Protection: www.icrp.org
International Radiation Protection Association: www.irpa.net
National Council on Radiation Protection & Measurements: http://www.ncrponline.org
Union of Concerned Scientists: www.ucsusa.org. A nongovernmental organization with a focus on nuclear power and nuclear weapons, among other issues.
United Nations Scientific Committee on the Effects of Atomic Radiation: www.unscear.org
World Nuclear Association: http://www.world-nuclear.org. A group representing the nuclear energy industry.
Agency Web Sites Several government agencies maintain Web sites on radiation safety:
U.K. Department of Health: https://www.gov.uk/topic/health- protection/radiation
U.S. Centers for Disease Control and Prevention: http://www.bt.cdc.gov/radiation
U.S. Environmental Protection Agency: http://www.epa.gov/radiation
Books
1326
The BEIR (Committee on the Biological Effects of Ionizing Radiation) reports, from the National Academy of Sciences, are authoritative compilations of information on various aspects of radiation and health. While somewhat dated, they provide a useful framework. The most recent report, BEIR VII Phase 2 (2006), is titled Health Risks from Exposure to Low Levels of Ionizing Radiation. Also see Cember and Johnson (2008) and Mettler and Upton (2008), listed in the References, and the following books:
Hall, E., & Giaccia, A. (2006). Radiobiology for the radiologist. Philadelphia: Lippincott Williams & Wilkins.
Health Physics Society. (2013). Radiation and risk: Expert perspectives. McLean, VA: Author.
Stabin, M. G. (2008). Radiation protection and dosimetry: An introduction to health physics. New York: Springer.
1327
Chapter 23 Injuries
Jeremy J. Hess, Anna Q. Yaffee, Jason R. Holmes, and Junaid A. Razzak
Dr. Hess, Dr. Yaffee, Dr. Holmes, and Dr. Razzak report no conflicts of interest related to the authorship of this chapter.
1328
Key Concepts Injuries result when humans are exposed to intolerable levels of energy or deprived of elements essential to life and function.
Injuries, both intentional and unintentional, are preventable.
Injuries constitute a major public health burden, particularly in low- and middle-income countries, and are the ninth leading cause of mortality worldwide.
Injuries affect the poor, the marginalized, and women and children disproportionately.
The injury pyramid illustrates that for every injury resulting in death, there are often thousands of injuries resulting in short- or long-term disability.
The Haddon matrix is a staple of injury prevention and control; it guides conceptualization of the factors facilitating injury and the management of these factors.
Injury prevention and control is context-specific and includes educating people at risk, enforcing relevant laws and regulations, and engineering passive controls.
The word injury originates from the Latin in jur (from jus), which literally means “not right.” In cellular terms, injury is physical damage caused by the excessive transfer of energy to human tissues (whether mechanical, electrical, chemical, thermal, radiant, or nuclear) or by the lack of essential factors for energy production (such as a lack of oxygen, from suffocation or drowning, for example) or for maintenance of homeostasis (resulting in frostbite, for example).
Historically, public health officials ignored injuries, assuming they were random, unavoidable “accidents,” with no clear causal pathways. We now know, however, that many injuries, like diseases, affect identifiable high-risk groups via a predictable chain of events and are therefore preventable. When prevention fails, the severity of an injury may still be reducible through prompt provision of acute
1329
care and, subsequently, of rehabilitation. The combination of these three strategies—prevention, acute care, and rehabilitation—is termed injury prevention and control.
Injury prevention and control is important in environmental health because it demonstrates both the necessity of environmental approaches and their limits. On the one hand, injuries are context- specific and the environments in which they occur can facilitate, amplify, dampen, and otherwise modify injury exposures and outcomes. Environmental modification is a major injury prevention and control strategy. On the other hand, because environmental modification is not always sufficient, modifications of behavior through education and through policy development are also key injury prevention and control strategies. Reliance on some strategies outside the environmental health sphere distinguishes injury prevention and control from many of the other topics you will encounter in this book.
The learning objectives of this chapter consist of
To know what is meant by key terms such as injury and injury prevention and control.
To understand how injuries are conceptualized as a public health problem and how this leads to prevention and control strategies.
To become familiar with the global burden of disease associated with injury morbidity and mortality.
To become conversant with important injury prevention and control tools and frameworks such as the Haddon matrix and the three E's.
To learn how injury prevention and control strategies are developed, implemented, and evaluated.
To gain exposure to specific injury prevention and control activities in context and in particular settings.
To achieve these objectives we provide a general outline of injuries from a public health perspective with a focus on environmental factors. We begin with definitions, provide some epidemiological data to frame the problem, and then describe injury outcomes as well as risk and preventive factors. Next, we discuss general injury prevention and control principles. Finally, we examine certain
1330
injuries and environments in greater detail to illustrate key points about injury causes and present creative strategies to reduce the significant burdens that injuries impose.
1331
Injury Prevention and Control Injury prevention and control draws on the expertise of many disciplines within and outside environmental health, including epidemiology, disease prevention, health promotion, biomechanics, environmental and community design, acute care, rehabilitation, law, and public administration. It follows the four generic steps of the public health approach (National Center for Injury Prevention and Control, 2006):
1. Define the health problem.
2. Identify causes, risk factors, and protective factors associated with the problem.
3. Develop and test interventions to reduce the problem's impact.
4. Implement successful interventions, evaluate their impact, and ensure widespread acceptance and implementation of prevention principles and strategies of control.
Defining the Problem Injury epidemiology involves characterizing the distribution of injuries in given populations, quantifying the problem's scope, monitoring patterns and trends, and evaluating the impact of countermeasures. Several information sources may be used for this purpose. Vital records can be used to determine morality rates and causes, but do not provide information about nonfatal injuries. Hospital records, trauma registries, emergency department (ED) data, emergency medical services (EMS) reports, and police reports, alone or in combination, can provide essential information about cases of major trauma, depending on local resources and the nature of the information being sought.
In the United States the National Hospital Discharge Survey (Centers for Disease Control and Prevention [CDC], 2014b) and the National Hospital Ambulatory Medical Care Survey: Emergency Department Summary (CDC 2014a) are important injury data sources, as is the National Electronic Injury Surveillance System (U.S. Consumer Product Safety Commission, 2014). Other high- income countries (HICs) have similar systems for monitoring
1332
morbidity and mortality data associated with injuries.
Although middle-income and low-income countries (MICs and LICs, respectively) often do not have similar extensive surveillance systems in place, some of the other data sources listed above may be available. The World Health Organization (WHO) has published guidelines for injury surveillance applicable across a range of settings (Holder, Peden, Krug, Lund, & Gururaj, 2001), and injury registries in these low- and middle-income countries are proliferating (Schuurman et al., 2010) and experience in developing injury surveillance activities in low-resource settings is accumulating (Mehmood, Razzak, Kabir, MacKenzie, & Hyder, 2013).
Types of Injuries Relying on these data sources, investigators have identified a wide range of injuries and classified them according to several schemes. The most widely used approach divides injuries by intent. Purposefully inflicted injuries, or intentional injuries, are subdivided into those caused by self-directed harm, such as suicide, attempted suicide, or a suicidal gesture (sometimes called parasuicide), and those due to interpersonal violence. Violence- related injuries are further subdivided into individual violence (e.g., assault or homicide), group violence (e.g., gang violence), and collective violence (e.g., religious or ethnic violence or state- sanctioned warfare). Unintentional injuries are often subdivided by mechanism—road traffic injuries, falls, burns, poisonings, drownings, and so forth. Injuries may also be classified in other ways: according to the environment or circumstances in which they occur (e.g., home, workplace, or roadway), by the body parts or systems most affected (e.g., spinal cord injury), or by a particular pattern or context that results in injuries (e.g., intimate partner violence).
Global Burden of Injury Injuries are a significant cause of both morbidity and mortality globally. They are responsible for 11% of the world's disability- adjusted life years (DALYs) annually, meaning they take approximately 300 million years of healthy life from the global population each year (Murray et al., 2012). Injuries were among the
1333
top ten causes of death worldwide (Murray et al., 2012) and killed an estimated 5 million people in 2012, accounting for 9% of the global total (WHO, 2014b). A wide range of injuries is responsible, but road traffic injuries (RTIs) predominate, accounting for 27% of the total injury burden in 2010 (Murray et al., 2012) and taking almost 3,500 lives a day in 2012 (WHO, 2014a). There is substantial regional variation in injury rates. For instance, deaths from RTIs rank third among all causes in Central and South America and nineteenth in Oceania (Lozano et al., 2012).
In the United States, for instance, injuries are the number one cause of death between the ages of 1 and 44 (Hoyert & Xu, 2012). Unintentional injuries ranked as the sixth leading cause of death in 2011 and intentional injuries ranked tenth (Hoyert & Xu, 2012). RTIs rank in the top five causes of years of life lost (U.S. Burden of Disease Collaborators, 2013), and injuries account for just over 35% of ED visits (Pitts, Niska, Xu, & Burt, 2008).
Globally, injury mortality has a multimodal age distribution, most heavily affecting children, adolescents, young adults, and parents of young children. Young people between the ages of 15 and 44 years account for nearly half of the world's fatal injuries. Because of their vulnerability and often close proximity to water and fire, children under 5 years of age account for approximately 18% of drowning deaths and just over 23% of fire-related deaths worldwide (WHO, 2013b).
Injury rates are higher in males than in females. For example, global injury mortality is twice as high among males as among females, and for some types of injuries—RTIs and interpersonal violence— the disparity approaches threefold. However, this pattern varies by injury type; in some regions female mortality rates from suicide and burns are as high as or even higher than male rates.
The global injury burden is expected to increase further in coming years. One study projected a 40% increase in injury deaths from 2002 to 2030, largely from increasing RTIs (Mathers & Loncar, 2006). This study estimated that RTI deaths would grow to 2.1 million a year by 2030, primarily from increased exposure (secondary to rising incomes) in LICs and MICs, and that RTIs would be the fourth leading cause of death by 2030. A later estimate from the WHO projected RTIs to be the seventh leading cause of
1334
death by 2030 (WHO, 2013a). These projections also include reductions in injury mortality rates—for instance, injury death rates actually declined by 16.3% from 1990 to 2010 (Lozano et al., 2012)— though others have pointed out that death rates could decline more substantially if proven strategies are implemented more widely (Shakur et al., 2012).
It is important to note that the impact of injury deaths is felt far beyond the individuals who die. As injuries tend to affect males and younger individuals disproportionately, often in their most productive years, their dependents are affected disproportionately as well. Studies have found that acute care costs and loss of income after RTI deaths commonly force households into debt and decrease their food security (Aeron-Thomas, Jacobs, Sexton, Gururaj, & Rahman, 2004), demonstrating the ripple effects of injury mortality.
The Injury Pyramid Injury mortality represents a fraction of the total injury burden. For every injured victim who dies, typically many more sustain serious but nonfatal injuries and suffer long-lasting or even permanent disabilities. Because, in general, nonfatal events greatly outnumber fatalities, the relationship among injury deaths, hospitalizations, and ED or office visits can be viewed as an injury pyramid (Figure 23.1).
1335
Figure 23.1 The Injury Pyramid
For example, a study of injuries in Missouri and Nebraska identified 13,052 deaths, 131,210 hospital admissions, and 1.9 million ED visits—each level differing from the next by an order of magnitude. RTIs and firearm-related injuries were the leading causes of fatal injury in both states, but falls were a far more common cause of hospital admissions and ED visits than firearms, ranking second only to RTIs (Wadman, Muelleman, Coto, & Kellermann, 2003).
A more recent study outlined the injury pyramid in the United Kingdom, using DALYs instead of injury counts. This metric changed the slope of the pyramid's walls considerably, with injury deaths accounting for 29.5% of DALYs; injuries requiring hospital admission accounting for 33.3%, and minor injuries accounting for 37.3% (Polinder, Haagsma, Toet, & van Beeck, 2012). Looking at disease burden expressed as DALYs instead of counts provides another perspective and highlights the significant disease burden from injury mortality even while confirming the relatively larger burden of nonfatal injuries.
It is likely that similar patterns prevail in LICs and MICs. For
1336
instance, a study in Iran demonstrated a similar relationship among injury fatalities, injuries requiring hospitalization, and injuries requiring little or no medical care (Saadat, Mafi, & Sharif-Alhoseini, 2011). However, many countries lack the data systems necessary to tabulate these counts routinely and reliably. As a result, mortality data are often the only information available to quantify the public health impact of injuries. This means that conclusions are based on only the tip of a very large pyramid.
Identifying Risk and Protective Factors The second step of the public health approach calls for characterizing risk and protective factors. In practice this is done through descriptive epidemiological studies. These studies characterize who is injured; what injuries are involved; and where, when, and, why particular injuries occur. These data can also generate hypotheses for further investigation with analytical studies. In some cases the link between a risk factor and injury is so strong that no additional research is needed. For example, early studies of RTIs in the United States revealed that half of all fatal crashes and 60% of fatal single-vehicle crashes involved alcohol (Polen & Friedman, 1988). In other cases, in order to quantify the impact of particular risk factors, it is necessary to compare the injury rate among those with those risk factors to the rate among similar individuals without these risk factors. Conversely, protective factors can prevent an injury or diminish its effects. The protective effect of bicycle helmets against closed head injuries is an excellent example of a strong protective factor that mitigates the effect of a potentially devastating injury.
Developing and Testing Interventions Once risk and protective factors have been investigated, interventions can be conceived, developed, and tested. As with any intervention, the target population's characteristics, candidate countermeasure feasibility and acceptability, and cost are all important considerations. Pilot programs are often helpful to test various strategies, and the most promising can be selected for widespread implementation. The Haddon matrix is particularly useful for conceptualizing prevention opportunities.
William Haddon, a physician, established the field of injury control
1337
by applying the core principles of public health to the prevention and mitigation of injuries. Using the time-tested concept of the epidemiological triangle—the idea that many diseases result from harmful interactions among the host, the disease vector, and the environment—Haddon showed how these factors interact to cause many injuries. He assigned factors to three temporal phases: the pre-event phase, the event itself, and the post-event phase. This yielded a phase-factor matrix of nine cells, as shown in Table 23.1 (Haddon, 1972). Examining each cell can suggest various strategies to prevent or control injuries. Since its introduction, the Haddon matrix has proven an invaluable injury prevention and control tool. Below we recount Haddon's application of his matrix to RTIs, and in Text Box 23.1 we outline the application to an unintentional fatal shooting.
Table 23.1 The Haddon Matrix Applied to Motor Vehicle Crashes
Phases Host Agent Environment Pre- event
Alcohol; speed Tires, brakes Signs; signals; road surface
Event Belt use; helmet use
Seat belt; air bags
Side slope; guardrails
Post- event
Health, age Fuel system; materials
EMS response; road shoulders
Source: Haddon, 1972.
Haddon (1973) later outlined ten generic injury-control strategies that can be used to break the chain of injury causation (Table 23.2). Examining this list to identify the most promising approaches is known as options analysis. The best strategy is not always the one that is most obvious or the most proximate to the injury, and a combination of strategies is often superior to any single one.
Table 23.2 Options Analysis in Injury Control
Options Examples 1. Prevent creation of hazard. Ban production and civilian sale
of assault weapons. 2. Reduce the amount of
hazard. Limit water heater temperature to 125°F (47.25°C).
1338
3. Prevent the release of a hazard that already exists.
Put dangerous medications in childproof containers.
4. Modify the rate of distribution of release of the hazard from its source.
Require fire-safe cigarettes that cannot easily ignite furniture or bedding.
5. Separate, by time or space, the hazard from the host.
Construct overpasses or underpasses to eliminate crossing streams of traffic.
6. Physically separate, by barriers, the hazard from the host.
Equip taxicabs with bulletproof and knifeproof partitions.
7. Modify surfaces and basic structures to minimize injury.
Equip all new cars with driver- side and passenger-side air bags.
8. Make that which is to be protected more resistant to damage.
Issue bulletproof vests to law enforcement officers and security guards.
9. Mitigate damage already done.
Promote citizen training in first aid and cardiopulmonary resuscitation (CPR).
10. Stabilize, repair, and rehabilitate the injured person.
Implement trauma care.
Source: Haddon, 1973.
Haddon's ideas were first applied to RTI prevention and control and yielded dramatic results. According to the Centers for Disease Control and Prevention (CDC), between 1925 and 1999 the number of drivers increased sixfold, the number of motor vehicles increased elevenfold, and the number of vehicle miles traveled (VMT) increased tenfold. Despite this dramatic increase in automobile use, the death rate per 100 million VMT plummeted from 18 in 1925 to only 1.7 in 1997, a 90% decrease (CDC, 1999).
On the strength of this accomplishment, the CDC acclaimed the reduction in RTI fatalities as one of the top ten public health achievements of the twentieth century. Other countries, such as Sweden and United Kingdom, have achieved equal if not more
1339
impressive improvements in road traffic safety (Evans, 2004). Assuredly, this reduction in mortality began before Haddon applied his theories to injury control, and there were significant advances in road safety and automobile engineering that resulted in substantial safety gains. Nevertheless, Haddon's approach to traffic safety was revolutionary and facilitated a great public health accomplishment. In recent years, as RTIs have come to dominate the injury disease burden globally, there have been studies highlighting the burden of disease that could be avoided if the affordable solutions were implemented more widely (Chisholm, Naci, Hyder, Tran, & Peden, 2012).
1340
Text Box 23.1 Fatal Occupational Injury at a Gun Range On Monday, August 25, 2015, firearms instructor Charles Vacca sustained an unintentional, fatal gunshot to the head at the shooting range in Las Vegas, Nevada, where he worked. Vacca was shot while teaching a 9-year-old girl how to fire an Uzi submachine gun at the firing range. While gun ranges are generally safe environments for firearms training and target practice, applying the Haddon matrix to this tragic incident can help to identify possible countermeasures that may prevent similar incidents in the future.
The shooting occurred while Vacca was standing behind the girl during her first attempt at shooting the gun. The Uzi is an automatic weapon, meaning that its trigger does not need to be repeatedly pulled in order to fire multiple shots. According to witness accounts, the girl was not strong enough to control the weapon's recoil, and the gun's muzzle rose uncontrollably and was inadvertently directed at Vacca's head. Scene reports suggest there was confusion immediately after the event and a brief delay in recognizing that Vacca had been injured. Despite aggressive resuscitative efforts Vacca succumbed to his wounds.
In Haddon's terms, the host of the fatal injury in this case was the instructor, a 39-year-old Army veteran who had worked as an instructor at the shooting range for eighteen months. The agent was a submachine gun. The environment was a shooting range in Arizona.
There were several significant pre-event factors in this fatal injury. There are several host factors, including the lack of protective equipment (though it is not clear that protective equipment could have prevented the fatal injury in this case) and the host's positioning in relation to the agent. Experts have noted that Vacca's position behind and to the left of his pupil, who was right-handed, with his hand under her left arm, was less protective than a position behind her and to
1341
her right with his hand on her right shoulder. Other significant factors relate to the agent and the operator. An Uzi can fire up to fourteen rounds per second and is known to have significant recoil. There was a mismatch between the physical strength of the girl who was learning to shoot and the kinetic energy released in the gun's recoil. The fully automatic gun was also loaded with a full clip of bullets, maximizing the potential for harm in the event that the inexperienced operator lost control. Significant pre-event environmental factors include the shooting range's minimum age limit of 8 (with parental supervision), no state age limits on firing weapons, and legal sanction for buying and selling automatic weapons manufactured before 1986.
Event factors were closely related to the pre-event concerns. Specifically, when the operator was not able to contain the gun's recoil there was positive feedback from its automatic firing—enabled by a full clip—that led to muzzle rise and endangered the host. The host's position made it difficult for him to intervene effectively and control the muzzle rise and evade injury.
Post-event factors include delayed recognition of significant injury (albeit brief), as the 9-year-old girl's shoulder was strained by the gun and her family was focused on her injury until they realized Vacca had been shot. Another post-event factor was the remote location of the firing range relative to an urban center and major health care providers, which lengthened EMS response time. Reports from EMS calls suggest that Vacca did not die immediately after he was hit with the bullet, though it is not clear that the injury was survivable regardless of when help arrived.
This brief analysis illustrates a host of injury prevention and control principles and opportunities for reducing the likelihood of similar incidents in the future. Pre-event interventions could include raising institutional and state age limits for firing guns, requiring minimal levels of training and strength before introducing operators to automatic weapons, and limiting the number of bullets loaded into a clip until technical proficiency is achieved. Firing range personnel could wear personal protective equipment and
1342
ranges could be designed to remind instructors to position themselves so they can exert maximum safe control over their pupils. Post-event factors could include training in advanced trauma life support for firing range staff and potentially pre-positioning of EMS assets. While firing ranges generally operate quite successfully, such minimally restrictive interventions have the potential to further reduce the potential for future fatal occupational injuries.
Sources: Information and data from Blackstone, 2014; Cohen, 2014; McGee & Fernanda, 2014; Peralta, 2014.
Implementing Interventions and Ensuring Acceptance of Control Strategies The fourth component of the public health approach, implementing interventions and pursuing widespread adoption of the most effective strategies, is best considered jointly with the third component, developing and testing interventions. In this section we outline some of the basic concepts of injury prevention strategies and illustrate that developing such strategies and ensuring their widespread adoption form something of a continuum. (Another part of the fourth component is evaluation, and we discuss that separately later.)
Active Versus Passive Interventions Most injury prevention strategies can be classified as either active or passive. Active countermeasures require people to consciously cooperate to be effective; examples include manual safety belts, motorcycle helmets, child safety seats, and protective eyewear in the workplace. Passive countermeasures require little or no cooperation by the person being protected and are thus more reliably protective. Passive countermeasures include air bags in cars, sprinkler systems in buildings, flotation hulls on watercraft, and shields that prevent workers from becoming ensnared in hazardous equipment.
The Three E's of Injury Control Most injury control countermeasures employ one of three generic strategies: education, enforcement of regulations, or engineering of physical structures (including environmental changes). These are
1343
known as the three E's of injury control, and each approach offers advantages and disadvantages.
Education is often the first approach taken to promote safe behavior. Educational interventions encourage the public to adopt safe behaviors and practices voluntarily. Implicit in this approach is the belief that once people know what to do to reduce their risk of injury, they will change their behavior. Examples of such interventions are driver's education, child pedestrian training (Stevenson, Sleet, & Ferguson, 2015), education of parents and caregivers to reduce playground injuries among children (Morrongiello, 2012), education promoting safe behavior in the workplace (Palmer et al., 2012), and various training materials that promote burn prevention (Lehna, Ramos, Myers, Coffey, & Kirk, 2011; Heard, Latenser, & Liao, 2013).
Public education campaigns are popular because they are voluntary and can be less expensive than other alternatives. However, even though educational programs do lead to an increase in knowledge, they may have little impact on behavior and on injury rates, especially if carried out in isolation. For example, a systematic review of randomized, controlled trials on improving pedestrian safety showed improvements in some road safety behaviors among trained pedestrians but no consistent, overall behavioral change (Duperrex, Bunn, & Roberts, 2002). Considerable effort is now being devoted to educating drivers about the danger of texting while driving, but regulation is also likely to be necessary to achieve changes in this behavior (see Text Box 23.2).
1344
Text Box 23.2 Texting and Driving Distracted driving is highly dangerous for the driver, passengers, and those nearby—people in other vehicles, pedestrians, and cyclists. Few activities are as distracting and dangerous as texting while driving. Text messaging is associated with drivers taking their eyes off the road for an average of twenty-three seconds, and texting has been shown to take the driver's attention away from driving more frequently and for longer periods than other distractions. Yet it is common practice: a 2011 CDC study based on data from the national Youth Risk Behavior Surveillance System showed that nearly half of all U.S. high school students aged 16 or older text or email while driving (Olsen, Shults, & Eaton, 2013).
This inattention can be fatal. According to the National Highway Traffic Safety Administration (NHTSA), in 2013, 10% of fatal crashes (in which 3,154 people were killed) and 18% of injury crashes (in which 424,000 people were injured) involved driver distraction (NHTSA, 2015). Text messaging while driving has been estimated to increase the crash risk by two (Fitch et al., 2013) to four (Klauer et al., 2014) times.
A raft of education and enforcement initiatives may be turning the tide. In September 2009, President Obama issued an executive order prohibiting federal employees from texting while driving on government business or with government equipment. In September 2010, the Federal Railroad Administration banned cell phone and other electronic device use by employees on the job. In October 2010, the Federal Motor Carrier Safety Administration enacted a ban that prohibits commercial vehicle drivers from texting while driving, and in 2011, the Federal Motor Carrier Safety Administration and the Pipeline and Hazardous Materials Safety Administration banned all handheld cell phone use by commercial drivers and drivers carrying hazardous materials. Perhaps most important from a
1345
population health perspective, many states are enacting laws to ban texting while driving. A recent study found a 7% reduction in crash-related hospitalizations among all age groups in states with bans, strong evidence in support of more widespread bans (Ferdinand et al., 2015).
The impact of educational interventions is also often blunted by effect attenuation, wherein the impact is decreased at each step in the process. No matter how powerful, pervasive, and repetitive a safety message may be, some people never encounter it. Among those who do, some will actively reject the message. Some who accept the message will be insufficiently motivated to change their behavior. Among those who do change their behavior, some will relapse over time, and some will fail to follow the message consistently. Finally, not everyone who adopts a protective strategy escapes injury.
Enforcement of laws and regulations may increase compliance when voluntary acceptance of an effective countermeasure is poor. Motorcycle helmets provide a telling example. Wearing a motorcycle helmet reduces the risk of death or severe traumatic brain injury in a crash by approximately 55%. In states where helmet use is voluntary, only about half of motorcyclists wear one, whereas in states where helmet use is mandated and the law is aggressively enforced, helmet usage exceeds 98% (NHTSA, 2003). Evaluations have conclusively shown that states with mandatory helmet laws have lower motorcycle crash fatality rates than do states that lack these laws (Ulmer & Preusser, 2003), and a recent review concluded that national adoption of universal helmet laws would save 500 to 1,000 lives a year (Byrnes & Gerberich, 2012). A review of the effect of helmet laws in the fifty U.S. states from 1975 to 2004 supports these findings: after controlling for other factors, states with universal helmet laws have motorcyclist mortality rates 22% to 33% lower than the rates in states without such laws (Houston & Richardson, 2008). It follows that states that repeal mandatory motorcycle helmet laws see a rise in injury rates and deaths: in Pennsylvania, after that state's 2003 repeal of a mandatory helmet law, helmet use among riders involved in crashes decreased from 82% to 58%, and head injury deaths increased by 66% (Mertz & Weiss, 2008).
1346
Bicycle helmet use is protective against head injuries, particularly serious ones (Amoros, Chiron, Martin, & Laumon, 2011), and rates of this type of helmet use are also lower in the absence of enforcement (Page, Macpherson, Middaugh-Bonney, & Tator, 2012). As with motorcycle helmets, bicycle helmet use can be increased with legislation (Karkhaneh, Rowe, Saunders, Voaklander, & Hagel, 2011). The health impact seems to be beneficial, but the evidence is not consistent. On the one hand, a study evaluated the effect of a 1995 law mandating helmet use for riders under age 18 in Montreal and found a 55% decrease in the mortality rate for riders aged 15 and under but little change in the rate for adults, supporting the efficacy of the law and suggesting that it should be extended to adults as well (Wesson et al., 2008). Some studies in other settings have confirmed a protective effect that is durable over time (Olivier, Walter, & Grzebieta, 2013). On the other hand, a large study across Canada found that mandatory helmet laws did not substantially contribute to reductions in serious head injuries (Dennis, Ramsay, Turgeon, & Zarychanski, 2013).
The importance of this question has unfolded in the context of bike sharing programs, which have become increasingly common in recent years. Bike share riders use helmets relatively rarely (Fischer et al., 2012). One recent study found an increase in the proportion of bicycle-related head injuries after implementation of ride share programs and recommended that provisions for promoting helmet use be made when programs are instituted (Graves et al., 2014). This has prompted several questions regarding how to promote and encourage helmet use, potentially through the use of social marketing (Ethan & Basch, 2013), without limiting program use, as mandatory helmet use has been seen as discouraging participation (Fishman, Washington, & Haworth, 2012). (Please see Discussion Question 8.)
The related question of whether mandatory helmet laws reduce overall health—essentially owing to the trade-off between the cardiovascular health benefits that are lost when cycling is discouraged through mandatory helmet laws and the protective effect of helmet use—has also been posed. The overall impact on health across a spectrum of safe to risky cycling environments has been modeled, and while mandatory helmet laws are of net benefit in very risky environments, in relatively safe ones such laws may
1347
have an overall adverse public health impact (de Jong, 2012). This, along with a recent finding that helmet use is not protective against overall rates of serious injury (Rivara et al., 2015), highlights the important environmental health point that engineering safe environments for cyclists in which they are physically separated from road and other hazards is ultimately likely to have the greatest impact on public health.
In general, strategies combining education and enforcement work better than relying on one strategy alone. For instance, in Elmira, New York, a publicity campaign combined with highly visible enforcement of the state's seat belt law boosted rates of use from 49% to 77%. Four months after the effort ceased, seat belt use declined to 66%, but it rebounded to 80% during a reminder campaign (Williams, Preusser, Blomberg, & Lund, 1987). In Hawaii, a combination of targeted education and enforcement has maintained high seat belt use for decades and even increased seat belt use rates in some instances (Kim, Yamashita, Pant, & Ghimire, 2014). In Colombia, which reduced the legal blood alcohol concentration for drivers in 2008, a significant reduction in injuries and fatalities was seen, particularly in high-enforcement regions (Andreuccetti et al., 2011).
Although mandatory-use laws are often effective, they may be difficult to enact. Opponents of such argue that such laws infringe on personal freedom and that individuals have the right to choose hazardous behavior if the risk is acceptable to them (see Text Box 1.2). Moreover, enforcement of regulations can be difficult in many LICs due to limited resources. A study in Thailand, for example, found that the current mix of public education campaigns and sobriety checkpoints was a cost-effective strategy for reducing drunk driving, but that it could be considerably more effective if more sobriety checkpoints were funded (Ditsuwan, Lennert Veerman, Bertram, & Vos, 2013). Laws are generally of little benefit without enforcement. In the early twenty-first century, there was almost no traffic law enforcement in northern Kosovo, and drivers there were found to have significantly higher rates of risky behaviors—from speeding to drunk driving to not using seat belts— compared with drivers in the higher-enforcement environment of Serbia (Stanojević, Jovanović, & Lajunen, 2013). A study of helmet use among motorcyclists in an area of southern China with
1348
mandatory helmet laws that are not routinely enforced showed high awareness of the benefits of helmet use but little adoption (Li, Li, & Cai, 2008).
In workplace settings, as described in Chapter 21, rules to promote safe behavior by employees may be easily introduced, but they are unlikely to be effective unless they are visibly and consistently enforced. Examples include requiring the use of hard hats in construction zones, safety goggles near ocular hazards, and safety straps when working in high places, and enforcing a strict no- smoking policy around flammable materials.
Engineering solutions are the injury control strategy that draws most directly on the preventive paradigm of environmental health (see Chapter 26). Many injuries can be prevented by designing and building safety into products or environments. The up-front cost of engineering may exceed the cost of education or enforcement campaigns, but the downstream benefits are often greater as well. Engineering is usually more effective than behavioral change because it does not require the cooperation of users to exert its protective effects.
Consider the following examples. In contrast to unsuccessful efforts to “fix the nut behind the wheel,” adoption of federal standards for passenger restraint systems (seat belts), safety glass, fuel system integrity, and nonflammable interior fabric saved an estimated 37,000 lives between 1975 and 1978 alone. The subsequent introduction of air bags cut the annual toll of crash-related deaths and injuries still further (Kahane, 1998).
Seat belts in cars are a good example of successful engineering for injury prevention. When properly used, they reduce motor vehicle fatalities by about 50% and serious injuries by about 55%. They are affordable and feasible in countries where automobile use is prevalent or rapidly increasing, but it is difficult to encourage widespread use of seat belts without high-visibility enforcement (Forjuoh, 2012).
LICs differ from HICs in their patterns of road traffic deaths. Whereas in HICs motor vehicle occupants make up the majority of fatal road traffic injury victims, in LICs the majority of victims are vulnerable road users—pedestrians, passengers riding in large vehicles such as trucks and buses, and riders of two-wheelers
1349
(bicycles and motorcycles) (Peden et al., 2004; Razzak, Laflamme, Luby, & Chotani, 2004). Because it is difficult if not impossible to get pedestrians to change their behavior consistently, engineering interventions are often the most effective strategy for protecting them. Some options include installation of sidewalks, imposition of roadway barriers between pedestrians and traffic, placement of flexible “pedestrian crossing” signs in the center of a roadway, creation of one-way-street networks in urban areas, school zone signage, and installation of adequate lighting so that pedestrians crossing roadways are visible at night (Retting, Ferguson, & McCartt, 2003). Other effective strategies include red-light cameras, traffic-calming measures, and provision of bicycling and pedestrian facilities (Mohan, 2004). Many of these interventions can be adopted by LICs, particularly in locations where pedestrian injuries occur with great frequency (Forjuoh, 2012). In the near future, as explored in Text Box 23.3, driverless vehicles have the potential to revolutionize RTI prevention and control by engineering the operator out of the equation altogether.
1350
Text Box 23.3 Engineering the Driver Out of the Equation Autonomous vehicles, also known as driverless vehicles, were first prototyped in the 1920s, but only recently have they become a realistic, mainstream possibility. A fully autonomous vehicle is capable of sensing and navigating its environment without any additional input from a human operator, and vehicles with varying levels of automaticity have also been designed. An official classification system of automaticity put forth by the National Highway Traffic Safety Administration denotes degree of automaticity, ranging from Level 0 (driver completely controls vehicle) to Level 3 (driver can fully cede control in certain conditions) to Level 4 (driver is not expected to control the vehicle at any time). While autonomous vehicles are primarily an engineering advance, it has been proposed that these vehicles could lead to increased highway safety through various enforcement, engineering, and environmental effects, providing an interesting example of injury prevention and control.
In 2011 alone, there were more than 32,000 roadway deaths in the United States, 14,000 of which involved a single vehicle. Assuming that many of these single vehicle collisions involve some element of driver error, Level 3 and 4 autonomous vehicles have the potential to reduce these deaths by reducing driver error through the engineering solutions inherent in the vehicle's automaticity. Alcohol was involved in 39% of motorist fatalities, so allowing impaired drivers to give up control in Level 3 and 4 vehicles would reduce impaired driving and would provide additional support to enforcement efforts aimed at reducing impaired driving, preventing the potential driver error before it happens (rather than relying on the mainly consequence- driven system currently in place for driving while impaired).
In addition, autonomous vehicles provide an environmental solution to traffic fluctuation by increasing the overall number of vehicles able to travel the roads safely at one time.
1351
Their ability to monitor overall traffic conditions and react with finely tuned adjustments in speed would reduce traffic fluctuations while also reducing the amount of space necessary between vehicles to accommodate safe adjustments. A decrease in traffic fluctuations could lead to a decrease in driver error in unpredictable situations and thus a safer driving environment.
Although these vehicles are currently in prototype form and need more study to determine true causal relationships between autonomous vehicles and road safety trends, such engineering innovations are an excellent example of how proactive countermeasures may be used to prevent RTIs in the near future.
Sources: Information and data from Frey, 2012; Anderson et al., 2014.
In South Asia, high death rates from burns among females result from using portable stoves on uneven surfaces (where they can overturn and explode) or on the floor (where long skirts can catch fire and where refueling and maintenance are difficult) (Fauveau & Blancet, 1989; Marsh et al., 1996). Women also confront the risk of assault when gathering solid fuel for household use (Gaye, 2007). Simple changes in stove design to keep heat and flames away from clothing and out of reach of children could prevent many burns, and increasing efficiency has the potential to decrease assault risk as a result of lower fuel needs. Changes to stove design combined with educational activities show even greater promise than engineering changes alone according to a recent review (Parbhoo, Louw, & Grimmer-Somers, 2010). Loose, flammable clothing is another important risk factor for burns among children and women in some LICs. Proven interventions from HICs (Baker, O'Neill, Ginsburg, & Li, 1992), such as use of fabrics that are less flammable, fire- resistance standards for children's sleepwear, and a change from loose, frilly dresses to more close-fitting clothes, can be applied in LIC settings with significant advantage. Peck and others (2008) applied the Haddon matrix to this issue and identified a host of potential strategies, including alternative energy sources, better kerosene containment, modifications to appliance engineering, improved ventilation in cooking areas, consumer education, and training for caregivers and emergency responders. Several of these interventions also have the advantage of decreasing indoor air
1352
pollution, a major source of respiratory morbidity and mortality in the developing world (Wilkinson, Smith, Joffe, & Haines, 2007), highlighting the opportunity for multiple public health benefits when injury prevention and control is wedded to other public health priorities.
Engineering strategies can be applied to equipment and devices, or they can be applied, on a larger scale, to environments. Seat belts are an example of an engineering change within an automobile; banked curves, guardrails, and separation of opposing lanes of traffic are examples of larger scale environmental changes. Both of these types of change are usually considered engineering strategies, but in the examples later in this chapter, we distinguish engineering change and environmental change, in part to emphasize the role of environmental health approaches in injury control. Certain interventions, including early warning systems for severe weather events such as floods, storms, and heat waves, apply engineering methods to larger scale environmental concerns. They employ solutions such as remote-sensing technology and computer modeling to project hazards and provide targeted prevention messaging before the hazardous exposure arrives. Because engineering solutions can increase the cost of a product, they are often unpopular with manufacturers. For this reason many advocates of injury prevention support consumer product safety laws to compel manufacturers to act. Manufacturers often oppose such legislation because they fear it will raise the prices of their products, discourage sales, and reduce their ability to compete with less regulated manufacturers in other countries. When efforts to regulate a hazardous product fail, product liability lawsuits may be the only way to force a needed change in product design. That can elicit another form of legislative backlash, as manufacturers seek protection from product liability lawsuits under the guise of “tort reform” (Vernick, Mair, Teret, & Sapsin, 2003).
Evaluating and Refining Interventions Program evaluation is an important part of the public health approach. Without well-designed modes of program evaluation, it is difficult to assess intervention impacts and make ongoing management decisions. Program evaluation uses established methods to reach valid conclusions about the effects of a given
1353
intervention. This large field is beyond the scope of this chapter, but in general, prevention programs are evaluated by determining their impact on factors in the causal chain of an injury or on morbidity or mortality in the target population. When good surveillance systems are in place, this approach is worthwhile and can produce valid results. However, large-scale surveillance is not always possible, or it might fail to detect the effects of smaller scale projects. In some instances, surrogate measures may be used to assess program impact. For example, rates of smoke detector use in a target neighborhood before and after a promotional program might be used because quantifying fire-related injuries—which are rare events—might take too long. Also, as surveillance is time consuming and expensive, sampling techniques can establish patterns in population subsets that can then be extrapolated to the population as a whole. This can be useful for MICs and LICs, where resource constraints can limit sample size. Regardless of the form the evaluation takes, it must be tailored to the intervention and the outcome of interest. Once a good program evaluation has been performed, intervention priorities can be reorganized, the Haddon matrix can be revisited, and new prevention goals can be pursued.
1354
Policy for Injury Prevention and Control In the United States, injury prevention and control policy and regulation emanate without central coordination from a wide variety of sources. Multiple government agencies regulate various aspects of safety—roadway, workplace, and consumer—in addition to the numerous independent agencies that assist with safety testing and safety standards. These agencies conduct policy-related activities that encompass all of the three E's mentioned earlier. A few examples are discussed next.
Highway Safety Policy At the federal level, highway safety is regulated by the National Highway Traffic Safety Administration (www.nhtsa.gov), which was created as part of the Highway Safety Act of 1970. As the number of cars manufactured continued to grow and cars became more affordable in the post–WWII era and improvement of roadways led to faster speeds and easier access, highway safety became an important policy issue. With the Highway Safety Act, Congress passed legislation making seat belts mandatory in all vehicles and created NHTSA to continue these regulatory efforts.
Today, NHTSA continues to administer laws and regulations designed to hold all aspects of vehicles—from air bags and tires to child and disabled passenger safety—to a high standard of safety. This organization also publishes standards of driver safety and conducts research into improving various aspects of vehicular safety on the roads (see Text Box 23.2). It is involved in investigation of high-profile recalls and defects as well.
One such high-profile event was the Firestone tire recall in 2000. It was noted by NHTSA that certain Firestone tires manufactured at a Firestone plant in Decatur, Illinois, and installed mainly on Ford Explorers had higher failure rates than should be expected. NHTSA was instrumental in this recall and the ensuing investigation, determining that Ford Explorers themselves were no more likely to experience rollovers in motor vehicle crashes than any other sports utility vehicle in the setting of tire failure. This led to the second largest tire recall in U.S. history, and a temporary severing of the
1355
business relationship between Firestone and Ford.
Consumer Safety Policy In the United States, consumer safety is regulated by the Consumer Product Safety Commission (CPSC) (www.cpsc.gov), an independent government agency whose commissioners are nominated by the president of the United States. This organization is responsible for developing standards for consumer products and also banning products when required. Its work includes investigating and researching the safety of products, initiating recalls of consumer products (with the exception of firearms and vehicles), and providing public consumer safety education. (Firearms are regulated by the Bureau of Alcohol, Tobacco, Firearms and Explosives [www.atf.gov].)
For example, the safety of infants in cribs is a cause championed by the CPSC. In addition to carrying out several large-scale crib recalls involving millions of cribs, CPSC has partnered with the National Institutes of Health to promote the Safe to Sleep public education campaign (see www.cpsc.gov/en/Safety-Education/Safety- Education-Centers/cribs). This campaign involves the distribution of multimedia educational materials to parents to promote infants' safe sleep.
Voluntary Industry Standards While industries may be subject to external regulation, many have also developed and now conform to basic sets of safety standards. These “voluntary” standards are collected by the CPSC and made available to the public as baseline standards to uphold (see www.cpsc.gov/en/Regulations-Laws--Standards/Voluntary- Standards). There are many organizations that charge themselves with creating these standards for each industry. For example, UL (www.ul.co), formerly called Underwriters Laboratories, is an independent company that has developed standards for the electrical industry, while the American National Standards Institute (ANSI) (www.ansi.org) has become known for creating far-reaching standards across industry lines, both nationally and internationally.
Both ANSI and UL have begun campaigns for environment and public health safety and sustainability. ANSI established the Energy
1356
Efficiency Standardization Coordination Collaborative (EESCC) (http://www.ansi.org/standards_activities/standards_boards_panels/eescc/overview.aspx? menuid=3) to put forth a framework for standards in energy and water efficiency for future building and systems planning. Similarly, in addition to providing standards and codes for food and water safety, UL also guides building planners to consider environmental sustainability in their projects (ul.com/code- authorities/environmental-and-public-health). CPSC provides technical support for developing some voluntary standards, especially for products where these standards are lacking. These standards are not regulatory, and cannot be enforced. However, at times, CPSC and other organizations can incorporate these standards into regulations, which then can be enforced.
Other Stakeholders There are numerous other government and nongovernmental organizations that regulate various aspects of safety and injury prevention. The Occupational Safety and Health Administration (OSHA) (www.osha.gov) sets forth regulations for workplace safety (see Chapter 21).. The National Fire Protection Association (NFPA) (www.nfpa.org) outlines codes and standards for fire safety, and also conducts fire safety–related public education campaigns.
In addition the Centers for Disease Control and Prevention's National Center for Injury Prevention and Control (NCIPC) (www.cdc.gov/injury) conducts epidemiological research on violence and injury prevention, and then applies this research toward prevention activities (also see Text Box 23.4). The NCIPC has no regulatory or enforcement jurisdiction and so relies on disseminating research findings and supporting collaborative injury control and prevention efforts.
Unfortunately, the fact that there are so many different stakeholders involved in standards and regulation can lead to disjointed policies, with some regulatory efforts overlapping and others incomplete. When there is no specific standard or regulation in place for a safety risk, for better or worse, tort law can be used as a way to set a legal precedent on safety.
1357
Text Box 23.4 Firearm Policy Firearm use and gun control is a major public safety issue and a polarizing political concern that has long engendered strong opinions and bruising political fights. In 1993, a small CDC-funded study assessed the risk of owning a firearm in relation to firearm-related injuries. Published in the New England Journal of Medicine, its findings were that “[r]ather than confer protection, guns kept in the home are associated with an increase in the risk of homicide by a family member or intimate acquaintance” (Kellermann et al., 1993). The CDC was accused by the National Rifle Association (NRA) (www.nra.org) of promoting gun control, and Congress threatened to cut off the agency's funding. Exercising the power of the purse, Congress stipulated in a subsequent appropriation for the CDC: “None of the funds made available for injury prevention and control at the Centers for Disease Control and Prevention may be used to advocate or promote gun control.” The CDC imposed an internal ban on further research into firearm injuries.
In 2013, after the shooting deaths of twenty children and six adult staff at Sandy Hook Elementary School in Newtown, Connecticut, President Obama issued an Executive Order directing the CDC to resume research into the public health causes and effects of gun violence. However, as of 2015, CDC had undertaken no new research in this area (Frankel, 2015). This is an ongoing debate with no clear end in sight.
1358
Injury Prevention in Practice Now that you have learned about the public health approach to injury prevention and control, we can turn to several specific injury types to illustrate its application.
Intentional Injuries (Violence) In the WHO's World Report on Violence and Health, Krug, Dahlberg, Mercy, Zwi, and Lozano (2002, p. 5) defined violence as “the intentional use of physical force or power, threatened or actual, against oneself, another person, or against a group or community that either results in or has a high likelihood of resulting in injury, death, psychological harm, mal-development or deprivation.” This report divides violence into three broad categories: self-directed violence, interpersonal violence, and collective violence. These terms describe, respectively, attempted and completed suicides (as well as parasuicides); violence inflicted by another individual or by small groups of individuals; and violence inflicted by larger groups such as states, organized political groups, militia groups, and terrorist organizations. These three broad categories may each be divided further to reflect specific subsets of violence, including physical, sexual, and psychological violence and violence involving deprivation or neglect. This typology is graphically presented in Figure 23.2.
Figure 23.2 Typology of Violence
Epidemiology and Risk Factors
1359
Violence caused 57,786 deaths and 2,238,615 nonfatal injuries in 2013 in the United States; among these deaths were approximately 11,000 homicides involving guns (NCIPC, 2015). The economic impact of fatal gunshot wounds in the United States alone is estimated at $41 billion annually (NCIPC, 2015). Overall, the economic burden of interpersonal violence is estimated to account for 3.3% of the U.S. gross domestic product (Waters, Hyder, Rajkotia, Basu, & Butchart, 2005). In recent years the United States has suffered several spasms of mass murders and spree killings involving firearms, a total of sixty-one separate incidents from 1982 to 2012 (Follman, Aronsen, & Pan, 2012), though suicide and episodes of gun violence affecting smaller numbers of individuals claim a much larger number of lives in total. In 2012, an estimated 1.4 million people worldwide died as a result of violence and intentional injuries (WHO, 2013b). Violence is a leading cause of death for people aged 15 to 44 worldwide, accounting for about 16% of deaths among males and 7% of deaths among females in this age group, mostly in LICs and MICs. Over half of violence-related deaths in any given year are suicides, one third are homicides, and about one tenth are war related. Mortality figures represent the tip of the iceberg. For every person who dies as a result of violence, many more sustain nonfatal injuries. Many survivors of violence suffer a range of continuing physical, sexual, reproductive, and mental health problems.
Countermeasures There are several countermeasures for intentional injuries. Many countries attempt to reduce the degree of harm caused by violence by controlling access to or use of firearms, the most common means of interpersonal violence (Kellermann, Lee, Mercy, & Banton, 1991); Krug et al., 2002. Legislative restrictions on gun access in Australia had dramatic impacts on the incidence of both suicide gun deaths and mass shootings (Chapman, Alpers, Agho, & Jones, 2006). Other strategies are also effective: Using local agencies to perform background checks was found to reduce gun-related suicide by 27% and homicide by 22% (Sumner, Layde, & Guse, 2008). Lessons learned from the fight against tobacco have yielded a wide variety of effective strategies that can be deployed against gun violence in particular (Mozaffarian, Hemenway, & Ludwig, 2013). Although some of the best-known violence countermeasures rely on education
1360
and enforcement, a surprising number relate to environmental change. These measures are sometimes known as crime prevention through environmental design, or CPTED (Sherman et al., 1998). The measures are broadly applicable and have been shown to reduce robberies and violent crime in certain contexts (Carter, Carter, & Dannenberg, 2003; Casteel, Peek-Asa, Howard, & Kraus, 2004), though the evidence base is still developing (Lorenc et al., 2012), as are strategies for developing and studying CPTED interventions and their impacts on violent crime (Johnson, Gibson, & McCabe, 2014). Some general examples of violence countermeasures are shown in Table 23.3.
Table 23.3 Countermeasures for Intentional Injuries
Education Anger management interventions Enforcement Community policing
Targeted patrols, to discourage the carrying of concealed weapons Earlier closing hours for bars
Engineering Safety locks on guns Environmental change
Improved street lighting Safe pedestrian routes Bulletproof booths at all-night gas stations and selected retail outlets Drop safes, to limit cash on hand Protective shields between the front seats and backseats in taxicabs
Burns A burn occurs when some or all of the layers of the skin are destroyed by a hot liquid (scald), a hot solid (contact burn), or a flame (flame burn). Burns can also be produced by exposure to ultraviolet radiation, radioactivity, electricity, and certain chemicals.
Epidemiology and Risk Factors In the United States, in 2013, there were 450,000 burns requiring medical treatment, 40,000 burn hospitalizations, and 3,400 deaths from fires, burns, and smoke inhalation (American Burn
1361
Association, 2014). Globally, fire-related burns accounted for an estimated 267,889 deaths in 2012 (WHO, 2013b). At least 80% of these deaths occurred in homes. More than 91% of fatal fire-related burns worldwide occur in LICs and MICs. Almost half of fire-related mortality is in sub-Saharan Africa, where males have the highest fire-related burn mortality rates in the world, followed by females in Africa. Children under 5 years of age and the elderly (those over 70 years old) have the highest burn mortality rates. In India alone there are approximately 100,000 deaths due to burns each year; 600,000 burn victims require hospital admission and treatment in a burn unit.
Countermeasures Countermeasures for burns include a wide range of strategies, as shown in Table 23.4.
Table 23.4 Countermeasures for Burns
Education Burn prevention campaigns Enforcement Building codes
Smoking rules around flammable material Engineering Tap water temperature reduction
Temperature regulating valves Modified tap handles Smoke detectors Automatic sprinklers Control of ignition sources (cigarettes, matches, and lighters) Reduction of clothing flammability
Environmental Elevated hearths for cooking and heating fires
Poisoning A poison exposure is the ingestion of or contact with a substance that can produce toxic effects. Poisonings can be acute or chronic, as discussed in Chapter 6. Acute poisonings are classified as injuries.
Epidemiology and Risk Factors In 2008, poisoning became the leading cause of fatal injury in the
1362
United States with over 41,000 deaths (Warner, Chen, Makuc, Anderson, & Miniño, 2011). In 2012, poison centers in the United States fielded over 2,275,000 calls related to human poison exposures (Mowry, Spyker, Cantilena, Bailey, & Ford, 2013). More than 90% of poison exposures occur at home, and just over half of these exposures involve children younger than age 6. The most common poison exposures for children are ingestion of household products, such as cosmetics and personal care products, cleaning substances, pain relievers, foreign bodies, and plants. For adults, the most common poison exposures are pain relievers, sedatives, cleaning substances, antidepressants, and bites or stings. Carbon monoxide (CO) results in more fatal non-drug related unintentional poisonings in the United States than any other agent, with the highest number occurring during the winter months.
Medical spending for poisoning totaled $26 billion in 2000, the most recent year for which estimates are available (Finkelstein, Corso, & Miller, 2006). Spending would be considerably higher in the United States without the established network of poison control centers that aid in the triage and treatment of acute poisonings (Miller & Lestina, 1997; Darwin, 2003).
Worldwide, poisonings rank fifth as a cause of unintentional injury, and in 2012 there were an estimated 193,460 poisoning deaths (WHO, 2013b). Data on poisonings in developing countries are scarce (though in recent years there has been increasing discussion of the role of poison centers in the developing world; Laborde, 2004) but suggest that pesticides, kerosene, and other chemicals are most often implicated; pesticides have the largest role in fatal exposures (Konradsen et al., 2003). This has led to calls for regulation of the most harmful pesticides and removal of certain pesticides from distribution entirely (Konradsen et al., 2003).
Countermeasures Countermeasures for poisoning rely more heavily on education, enforcement, and engineering than on environmental changes, as shown in Table 23.5.
Table 23.5 Countermeasures for Poisoning
Education Warning labels Physician-based education programs
1363
Community-based education programs Poison control centers
Enforcement Carbon monoxide alarms Engineering Child-resistant packaging
Carbon monoxide alarms Distinctive shapes and sizes for tablets of medicine
Environmental Locked storage for pesticide stocks on farms
Falls A fall is an event that results in a person coming inadvertently to rest on the ground or floor or other lower level.
Epidemiology and Risk Factors More than one in three U.S. adults aged 65 and older falls each year, making falls a leading cause of fatal injuries and the most common cause of nonfatal injuries and hospital admissions for trauma among that age group in the United States. Globally, an estimated 693,131 people died due to falls in 2012 (WHO, 2013b) and falls are a significantly increasing cause of injury mortality (Lozano et al., 2012). Seventeen percent of all fatal falls occurred in the HICs. LICs and MICs in South and East Asia and the Pacific combined account for just over 60% of the total number of fall-related deaths worldwide.
There are two distinct at-risk populations for falls: children and the elderly. In all regions of the world, adults over the age of 70 years, particularly females, have significantly higher fall-related mortality rates than younger people do. In lowland areas of tropical countries where tree agriculture is widespread, occupational falls from trees and other tree-related injuries are a leading cause of death, hospitalization, or permanent disability from spinal cord injury. In some countries, building-related falls from unprotected rooftops, windows, and stairs are a common source of injury for children. The home environment has been identified as a potential contributor to as many as 50% of falls occurring among the elderly. Falls among children, in contrast, are related to their age. Young children most frequently fall in and around the home: for example, from chairs, from beds, and downstairs. Older children fall from playground equipment, during other play and recreational activities, and during
1364
sports.
Countermeasures Countermeasures for falls rely heavily on environmental interventions, as shown in Table 23.6.
Table 23.6 Countermeasures for Falls
Education Physical activity and balancing exercises Enforcement Legislation for roof, window, and stairway barriers
in high-rise buildings Engineering Barriers in high-rise buildings Environmental Removal of obstructed pathways and loose throw
rugs Well-maintained stairways Improved lighting and visibility Modification of hard surfaces on which people might fall Safety devices, such as grab bars Barriers in high-rise buildings
Drowning Drowning is fatal respiratory impairment from submersion or immersion in liquid.
Epidemiology and Risk Factors In the United States more than 3,000 people died in unintentional drownings in 2007, averaging 9 people per day (NCIPC, 2014). About three times that number receive care in EDs for near- drownings. In 2012, 372,442 people drowned worldwide, making drowning the third leading cause of unintentional injury death after road traffic injuries and falls (WHO, 2013b). These figures underestimate drowning deaths because they exclude drowning due to floods, boating, and water transport. Over 90% of all drowning deaths occur in LICs and MICs. LICs and MICs in the Pacific and Southeast Asia regions account for almost 60% of the drowning mortality. Males in Africa have the highest drowning mortality rates worldwide. Among the various age groups, children under 5 years of
1365
age have the highest drowning mortality rates. Over one third of the global mortality due to drowning and 50% of the total number of DALYs due to drowning occur among children younger than 15 years of age.
Countermeasures Drowning countermeasures are summarized in Table 23.7.
Table 23.7 Countermeasures for Drowning
Education Swimming instruction Training in resuscitation techniques
Enforcement Supervision; lifeguards Engineering Pool alarms; pool covers
Personal flotation devices Environmental Fencing that completely encloses pools
1366
Injury Control in Special Settings Certain settings have special importance for injury control, either because they pose a particular risk or because specific control strategies are available. One example, the workplace, is discussed in Chapter 21. This section discusses three such settings: roadways, playgrounds, and the home.
Roadways Transportation injuries, especially those that occur on and near roadways, represent one of the leading categories of injuries worldwide. A road traffic injury is defined as any injury due to a crash involving one or more vehicles and originating or terminating on a public roadway.
Epidemiology The worldwide epidemic of road traffic injuries is only just beginning. At present over a million people die each year and some 10 million people sustain permanent disabilities in road traffic crashes. For people under 44 years of age, road traffic crashes are a leading cause of death and disability, second only to HIV/AIDS. Many developing countries are still at comparatively low levels of motorization, and the incidence of road traffic injuries in these countries is likely to increase as motor vehicle use proliferates. In 2012, road traffic crashes were ranked eighth among the conditions constituting the world disease burden, measured in DALYs, up from tenth in 2000.
Several categories of risk factors for road injuries can be identified. These relate to road users, the road itself, and vehicles. These factors, in turn, suggest a variety of injury control strategies (Peden et al., 2004).
All road users are at risk of being injured or killed in a road traffic crash, although especially vulnerable road users, such as pedestrians and people using two-wheelers, usually bear the greatest burden. This is particularly true in LMICs, where exposure of such vulnerable road users is increasing (Zegeer & Bushell. 2012). Multicountry studies have shown that individuals from less
1367
privileged socioeconomic groups or living in poorer areas are at greatest risk of being killed or injured. Seat belt use among drivers and vehicle occupants has been found to decrease death and nonfatal injuries by 50%. Similarly, a child who is properly restrained in a safety seat is 71% less likely to die in a crash than is a child who is not properly restrained. Another major risk factor for road traffic injuries is use of alcohol. Alcohol consumption increases the probability both that a crash will occur and that death or serious injury will follow. A survey of studies in LICs and MICs found that an elevated blood alcohol level was noted in 8% to 29% of drivers involved in crashes who were not fatally injured and in 33% to 69% of fatally injured drivers.
Roadway factors are also extremely important. Roads built to facilitate transport without consideration of safety can dramatically increase the incidence of serious and fatal traffic injuries. In many countries roads have multiple users, ranging from pedestrians to two-wheelers to automobiles and large vehicles. From the perspective of pedestrians and cyclists, proximity to motor vehicles capable of traveling at high speeds is the most important road safety problem. A road network planned for safety includes a hierarchy of roads, each intended to serve a certain function. This network should also include infrastructure that protects pedestrians and bicyclists from automobiles and large transport vehicles. Each road should be designed according to its particular function in the network. A key characteristic of a well-designed road is that it protects vulnerable road users from large vehicles and makes compliance with the intended speed limit a natural choice for drivers. Such design can not only prevent injuries but also achieve other public health goals, such as promoting walking and bicycling (see Chapter 15).
Vehicle design can have considerable influence on crash injuries. The risk of injury can be increased by many factors, such as poor design of the crush zone so it fails to absorb energy, failure of the structural cage around the passenger compartment to provide a protective shell, absence of features that protect occupants from side impacts or stop them from being ejected from the vehicle, and lack of high-mounted brake lights in the rear. Similarly, vehicles that are not clearly visible are at high risk of involvement in crashes, especially at night, and slow-moving vehicles on fast-moving
1368
roadways are at risk for rear end crashes. Daytime running lights for cars, though not required in many countries, reduce the incidence of daytime crashes by 10% to 15% (Elvik, 1996). Bus and truck fronts designed to reduce injuries to pedestrians and cyclists could also lower the injury burden, as could minimizing differences in vehicle design in ways that would reduce injuries when a higher riding vehicle and a lower riding vehicle collide.
Countermeasures Countermeasures to reduce road injuries draw on a broad spectrum of strategies, from driver and pedestrian education to environmental modifications. Examples appear in Table 23.8 and Text Box 23.3, on autonomous vehicles.
Table 23.8 Countermeasures for Road Injuries
Education Pedestrian safety education Bicyclist training schemes Motorist education Helmet and seat belt promotion
Enforcement Speed limits Graduated driver's licenses Strategies for reducing alcohol-impaired driving Helmet and seat belt use laws
Engineering Puncture-resistant gas tanks Energy-absorbing interiors Crush zones and reinforced cages around occupants Air bags
Environmental Area-wide traffic calming Bicycle paths and lanes Energy-absorbing materials in front of bridge columns and other fixed objects Breakaway light poles Roadway lighting at high-frequency pedestrian crossings
Playgrounds In terms of Haddon's approach, children are the host of playground
1369
injuries; the vector is often potential energy, in the form of gravity, as many playground injuries result from falls (from swings, slides, or other equipment, for example). As children may not be supervised and cannot be relied on to generate active injury control themselves, the playground environment must be engineered with passive injury control in mind.
Epidemiology More than 200,000 children are treated for playground equipment–related injuries in U.S. hospital emergency rooms each year. Two thirds of these injuries occur on public playgrounds. Four out of five injuries involve falls, primarily to the surface below playground equipment. The leading type of injury in this patient population was fracture (Tinsworth & McDonald, 2001; Vollman, Witsaman, Comstock, & Smith, 2009).
Countermeasures Countermeasures for playground injuries rely heavily on engineering and environmental changes, as shown in Table 23.9.
Table 23.9 Countermeasures for Playground Injuries
Education Education of children, parents, and teachers Enforcement Adult playground supervision to prevent bullying
and hazardous behavior Engineering Average inclines of no more 30 degrees on slides
Handrails on stairways and stepladders Playground surfaces that are covered with wood chips, double-shredded bark mulch, or pea gravel
Environmental Organization of equipment to prevent injuries from conflicting activities and from children running between activities Separation of equipment by user age
Home Injuries Injuries that occur in the home are conceptually grouped according to the environment in which they occur, rather than by the particular mechanism of injury or by intent. The most common
1370
home injuries are falls, being struck or hit by an object (including intentional acts of violence), cuts, and overexertion injuries (such as back strain). Other home injuries are burns and scalds, poisoning, animal bites, and a host of less common injury types.
Epidemiology Given the wide range of injuries in the home environment, it is difficult to present a unifying epidemiological picture, but recent studies have provided significant insight into this constellation of injuries. In total, there are more than 30,000 fatalities from unintentional home injuries annually in the United States (Mack, Rudd, Mickalide, & Ballesteros, 2013), and in 1999 (the last year for which data are available) nearly 13 million nonfatal home injuries required medical attention (Runyan et al., 2005). Epidemiological data on some of the most common home injuries—notably falls, a particularly important home injury—have been presented in other sections of this chapter. Unintentional injuries in the home are quite costly: $217 billion in 1998, by one estimate (Zaloshnja, Miller, Lawrence, & Romano, 2005).
Countermeasures A wide range of interventions has been shown to be effective at reducing home injuries. Some of the more notable interventions that have not been presented in other parts of this chapter are displayed in Table 23.10.
Table 23.10 Countermeasures for Home Injuries
Education Fire hazard and escape route education for children and families Poison control education for children Babysitter training Choking response training Gun safety education (store guns safely or do not keep them at home)
Enforcement Building code enforcement Sprinkler and fire alarm system code enforcement
Engineering Hot water heater temperature controls Gun trigger locks; trigger fingerprint recognition
1371
devices Childproof cigarette lighters Fire-resistant fabrics for sleepwear and furnishings Fire escapes and escape routes Child safety caps on medications
Environmental Cupboard locks Electrical outlet covers Fire hazard reduction Fire alarms Stair gates
1372
Summary Injury, whether caused by unintentional or intentional events, is a significant public health problem. The burden of injury is greatest in LICs and among individuals of lower socioeconomic status in HICs. Most of these injuries are preventable. Public health professionals can play an important role in reducing the global burden of injuries by identifying, implementing, and evaluating population-based countermeasures to prevent and control injuries. Which strategy is employed in a particular setting will depend in large part on the nature of the local problem, the concerns of the population, the availability of resources, and competing demands. Nonetheless, there is ample reason to believe that even simple countermeasures may make a big impact on reducing the substantial global burden of death and disability due to injury.
1373
Key Terms crime prevention through environmental design (CPTED)
A multi-disciplinary approach to deterring criminal behavior through environmental design, using such techniques as increased visibility and lighting.
disability-adjusted life years (DALYs) Units used to express disease burden, including both years of life lost as a result of premature death from a particular disease and years lived in a suboptimal state of health as a result of disease morbidity.
Haddon matrix A tool for conceptualizing the risk factors for an injury. It separates out host, agent, and environmental factors and stratifies these factors according to phases reflecting their relationship with the injury event: that is, whether they are pre- event, event, or post-event factors.
injury Physical damage caused by the excessive transfer of energy to human tissues (whether that energy is mechanical, electrical, chemical, thermal, radiant, or nuclear), by the lack of essential factors for energy production (such as oxygen), or by the loss of homeostasis (as in hypothermia).
injury prevention and control The application of a public health approach to reducing injury disease burden by preventing injuries from occurring.
injury pyramid A tool for depicting injury disease burden stratified by severity. Typically, the top of the pyramid represents deaths from injury and the bottom represents minor associated morbidity.
intentional injuries Injuries resulting from violence.
poison control centers Quasi-governmental organizations whose mission is to prevent and control injuries associated with poisoning, frequently on an emergency basis.
transportation injuries
1374
Injuries resulting from transportation activities. May be classified by the injury host (e.g., pedestrians, cyclists, single- occupancy vehicles, mass transit riders), the mechanism (e.g., motor vehicle crash, airplane crash), the setting (e.g., road traffic injuries, railroad crossing injuries), and contributing factors (e.g., distraction-associated driving or driving while intoxicated).
unintentional injuries Injuries in which violence was not a driving factor. Like other types of injury, unintentional injuries are classified according to host (e.g., pedestrian injury), mechanism (e.g., smoke inhalation), context (e.g., recreational drowning), affected system (e.g., occupational hearing loss), or other schemes.
1375
Discussion Questions 1. What is the difference between an injury and an accident? Why
is it important to make the distinction? Discuss some strategies for highlighting the differences between accidents and injuries, using examples from your home, school, or community.
2. How do injury prevention and control and environmental health overlap? How do they differ?
3. Describe an injury sustained by you or a member of your family. How well does it meet the injury definition laid out in this chapter? Create a Haddon matrix for the injury. What are several solutions that could minimize the incidence or impact of this injury among other people? Make sure you identify at least one educational, one environmental, and one engineering solution.
4. Scan the headlines of the last week, and identify an injury mentioned there. What would a public health approach for reducing morbidity and mortality from that injury look like? Your response should (a) create a precise definition of the injury; (b) outline strategies for clarifying its distribution, risk factors, and protective factors; (c) suggest intervention strategies for reducing the injury's morbidity and mortality; and (d) describe how you would evaluate the effectiveness of your proposed intervention(s).
5. Assume that you are a consultant to the Minister of Health of a modernizing poor country with a significant burden of illness and death from road traffic injuries. The Minister asks you to set up a surveillance system for injury morbidity and mortality. How would you do it? Would you recommend expressing injury burden in terms of counts or DALYs? How might an injury pyramid using counts differ from one using DALYs?
6. Gun violence imposes a significant burden on citizens of the United States. Create a Haddon matrix for interpersonal violence involving firearms in the United States (identify a subset of gun violence, such as shootings in the home or hunting injuries, if you wish). What are at least three interventions that are not listed in this chapter and that could be used for reducing
1376
morbidity and mortality from gun-related injuries? Conduct an options analysis of these interventions, and identify those that you believe would have the highest yield.
7. For one hour of your day, catalogue all the injury prevention mechanisms that you encounter (directly or indirectly). For instance, what are the major injury prevention and control measures in your car? Attempt to include educational, environmental, and engineering solutions in your list.
8. Sometimes, a measure to control injuries may collide with another public health priority. For example, laws requiring bike helmet use in order to reduce injuries can limit participation in bike share programs intended to produce other benefits. Some advocates suggest that environmental approaches such as changes in community design can be used to minimize conflicts between competing public health priorities. What are the issues and public health priorities involved in bike share programs?
1377
References Aeron-Thomas, A., Jacobs, G., Sexton, B., Gururaj, G., & Rahman, F. (2004). The involvement and impact of road crashes on the poor: Bangladesh and India case studies. Wokingham, U.K.: Transport Research Laboratory.
American Burn Association. (2014). Burn incidence and treatment in the United States: 2013 fact sheet. Retrieved from http://www.ameriburn.org/resources_factsheet.php
Amoros, E., Chiron, M., Martin, J.-L., & Laumon, B. (2011). Bicycle helmet wearing and the risk of head, face, and neck injury: A French case–control study based on a road trauma registry. Injury Prevention, 18(1), 27–32.
Anderson, M., Kalra, N., Stanley, K. D., Sorensen, P., Samaras, C., & Oluwatola, O. A. (2014). Autonomous vehicle technology: A guide for policy makers. RAND Corporation. Retrieved from http://www.rand.org/pubs/research_reports/RR443-1.html
Andreuccetti, G., Carvalho, H. B., Cherpitel, C. J., Ye, Y., Ponce, J. C., Kahn, T., & Leyton, V. (2011). Reducing the legal blood alcohol concentration limit for driving in developing countries: A time for change? Results and implications derived from a time–series analysis (2001–10) conducted in Brazil. Addiction, 106(12), 2124– 2131.
Baker, S. P., O'Neill, B., Ginsburg, M. J., & Li, G. (1992). The injury fact book (2nd ed.). New York: Oxford University Press.
Blackstone, J. (2014). Was proper safety protocol followed in gun range death? CBS News, August 27. Retrieved from http://www.cbsnews.com
Byrnes, M., & Gerberich, S. (2012). Motorcycle helmet use and legislation: A systematic review of the literature. Minnesota Medicine, 95(1), 60.
Carter, S. P., Carter, S. L., & Dannenberg, A. L. (2003). Zoning out crime and improving community health in Sarasota, Florida: Crime
1378
prevention through environmental design. American Journal of Public Health, 93, 1442–1445.
Casteel, C., Peek-Asa, C., Howard, J., & Kraus, J. F. (2004). Effectiveness of crime prevention through environmental design in reducing criminal activity in liquor stores: A pilot study. Journal of Occupational and Environmental Medicine, 46, 450–458.
Centers for Disease Control and Prevention. (1999). Achievements in public health: 1900–1999 motor-vehicle safety: A 20th century public health achievement. Morbidity and Mortality Weekly Report, 48(18), 369–374.
Centers for Disease Control and Prevention. (2014a). Ambulatory health care data. Retrieved from http://www.cdc.gov/nchs/ahcd.htm
Centers for Disease Control and Prevention. (2014b). National Hospital Discharge Survey. Retrieved from http://www.cdc.gov/nchs/nhds.htm
Chapman, S., Alpers, P., Agho, K., & Jones, M. (2006). Australia's 1996 gun law reforms: Faster falls in firearm deaths, firearm suicides, and a decade without mass shootings. Injury Prevention, 12(6), 365–372.
Chisholm, D., Naci, H., Hyder, A. A., Tran, N. T., & Peden, M. (2012). Cost effectiveness of strategies to combat road traffic injuries in sub-Saharan Africa and South East Asia: Mathematical modelling study. BMJ, 344.
Cohen, R. (2014). How does a 9-year-old come to shoot a fully automatic weapon? Mother Jones, August 28. Retrieved from http://www.motherjones.com/politics/2014/08/uzi-arizona-9- year-old-girl
Darwin, J. (2003). Reaffirmed cost-effectiveness of poison centers. Annals of Emergency Medicine, 41, 159–160.
de Jong, P. (2012). The health impact of mandatory bicycle helmet laws. Risk Analysis, 32(5), 782–790.
Dennis, J., Ramsay, T., Turgeon, A. F., & Zarychanski, R. (2013).
1379
Helmet legislation and admissions to hospital for cycling related head injuries in Canadian provinces and territories: Interrupted time series analysis. BMJ, 346.
Ditsuwan, V., Lennert Veerman, J., Bertram, M., & Vos, T. (2013). Cost-effectiveness of interventions for reducing road traffic injuries related to driving under the influence of alcohol. Value in Health, 16(1), 23–30.
Duperrex, O., Bunn, F., & Roberts, I. (2002). Safety education of pedestrians for injury prevention: A systematic review of randomised controlled trials. BMJ, 324, 1129.
Elvik, R. (1996). A meta-analysis of studies concerning the safety effects of daytime running lights on cars. Accident Analysis & Prevention, 28, 685–694.
Ethan, D., & Basch, C. H. (2013). Using social marketing as a tool to increase helmet use among bicycle-share riders in urban settings. Journal of Mass Communication & Journalism, 3, e7.
Evans, L. (2004). Evans responds to letters on “Roles of Litigation and Safety Belts.” American Journal of Public Health, 94, 171–172.
Fauveau, U., & Blancet, T. (1989). Deaths from injuries and induced abortion among rural Bangladesh women. Social Science & Medicine, 29, 1121–1127.
Ferdinand, A. O., Menachemi, N., Blackburn, J. L., Sen, B., Nelson, L., & Morrisey, M. (2015).The impact of texting bans on motor vehicle crash–related hospitalizations. American Journal of Public Health, 105, e1–7.
Finkelstein, E., Corso, P., & Miller, T. (2006). The incidence and economic costs of injury in the United States. New York: Oxford University Press.
Fischer, C. M., Sanchez, C. E., Pittman, M., Milzman, D., Volz, K. A., Huang, H.,…Sanchez, L. D. (2012). Prevalence of bicycle helmet use by users of public bikeshare programs. Annals of Emergency Medicine, 60(2), 228–231.
Fishman, E., Washington, S., & Haworth, N. (2012). Barriers and
1380
facilitators to public bicycle scheme use: A qualitative approach. Transportation Research: Part F. Traffic Psychology and Behaviour, 15(6), 686–698.
Fitch, G. A., Soccolich, S. A., Guo, F., McClafferty, J., Fang, Y., Olson, R. L.,…Dingus, T. A. (2013). The impact of hand-held and hands-free cell phone use on driving performance and safety- critical event risk (DOT Report No. HS-811-757). Washington, DC: National Highway Traffic Safety Administration. Retrieved from http://www.distraction.gov/downloads/pdfs/the-impact-of-hand- held-and-hands-free-cell-phone-use-on-driving-performance-and- safety-critical-event-risk.pdf
Follman, M., Aronsen, G., & Pan, D. (2012). A guide to mass shootings in America. Mother Jones, July 20, p. 119.
Forjuoh, S. (2012). Intervention in low-income countries. In G. Li & S. P. Baker (Eds.), Injury research (pp. 599–618). New York: Springer.
Frankel, T. (2015). Why the CDC still isn't researching gun violence, despite the ban being lifted two years ago. Washington Post, January 14. Retrieved from http://www.washingtonpost.com/news/storyline/wp/2015/01/14/why- the-cdc-still-isnt-researching-gun-violence-despite-the-ban-being- lifted-two-years-ago
Frey, T. (2012). Driverless highway: Creating cars that talk to the roads. Journal of Environmental Health, 75(5), 38–40.
Gaye, A. (2007). Access to energy and human development (Human development report: Occasional paper). New York: United Nations Development Programme.
Graves, J. M., Pless, B., Moore, L., Nathens, A. B., Hunte, G., & Rivara, F. P. (2014). Public bicycle share programs and head injuries. American Journal of Public Health, 104(8), e106–111.
Haddon, W. A. (1972). Logical framework for categorizing highway safety phenomena and activity. Journal of Trauma, 12, 193–207.
Haddon, W. (1973). Energy damage and the ten countermeasure strategies. Journal of Trauma, 13, 321–331.
1381
Heard, J. P., Latenser, B. A., & Liao, J. (2013). Burn prevention in Zambia: A targeted epidemiological approach. Journal of Burn Care & Research, 34(1), 65–73.
Holder, Y., Peden, M., Krug, E., Lund, J., & Gururaj, G. (Eds.). (2001). Injury surveillance guidelines. Geneva: World Health Organization.
Houston, D. J., & Richardson, L. E. (2008). Motorcyclist fatality rates and mandatory helmet-use laws. Accident Analysis & Prevention, 40, 200–208.
Hoyert, D., & Xu, J. (2012). Deaths: Preliminary data for 2011. National Vital Statistics Reports, 61(6), 1–52.
Johnson, D., Gibson, V., & McCabe, M. (2014). Designing in crime prevention, designing out ambiguity: Practice issues with the CPTED knowledge framework available to professionals in the field and its potentially ambiguous nature. Crime Prevention & Community Safety, 16(3), 147–168.
Kahane, C. J. (1998). Fatality reduction by air bags: Analysis of accident data through early 1996 (DOT Report No. HS-808–470). Washington, DC: National Highway Traffic Safety Administration.
Karkhaneh, M., Rowe, B., Saunders, L. D., Voaklander, D., & Hagel, B. E. (2011). Bicycle helmet use four years after the introduction of helmet legislation in Alberta, Canada. Accident Analysis & Prevention, 43(3), 788–796.
Kellermann, A. L., Lee, R. K., Mercy, J. A., & Banton, J. (1991). The epidemiologic basis for the prevention of firearm injuries. Annual Review of Public Health, 12(1), 17–40.
Kellermann, A. L., Rivara, F. P., Rushforth, N. B., Banton, J. G., Reay, D. T., Francisco, J. T.,…Somes, G. (1993). Gun ownership as a risk factor for homicide in the home. New England Journal of Medicine, 329, 1084–1091.
Kim, K., Yamashita, E., Pant, P., & Ghimire, J. (2014). Sustaining seat belt use in a high-use state. Transportation Research Record, 2425(1), 32–40.
1382
Klauer, S. G., Guo, F., Simons-Morton, B. G., Ouimet, M. C., Lee, S. E., & Dingus, T. A. (2014). Distracted driving and risk of road crashes among novice and experienced drivers. New England Journal of Medicine, 370(1), 54–59.
Konradsen, F., van der Hoek, W., Cole, D. C., Hutchinson, G., Daisley, H., Singh, S., & Eddleston, M. (2003). Reducing acute poisoning in developing countries—options for restricting the availability of pesticides. Toxicology, 192, 249–261.
Krug, E. G., Dahlberg, L. L., Mercy, J. A., Zwi, A. B., & Lozano, R. (Eds.). (2002). World report on violence and health. Geneva: World Health Organization.
Laborde, A. (2004). New roles for poison control centres in the developing countries. Toxicology, 198, 273–277.
Lehna, C., Ramos, P., Myers, J., Coffey, R., & Kirk, E. (2011). A web- based educational module increases burn prevention knowledge over time. Burns, 37(7), 1255–1258.
Li, G. L., Li, L. P., & Cai, Q. E. (2008). Motorcycle helmet use in southern China: An observational study. Traffic Injury Prevention, 9, 125–128.
Lorenc, T., Clayton, S., Neary, D., Whitehead, M., Petticrew, M., Thomson, H.,…& Renton A. (2012). Crime, fear of crime, environment, and mental health and wellbeing: Mapping review of theories and causal pathways. Health & Place, 18(4), 757–765.
Lozano, R., Naghavi, M., Foreman, K., Lim, S., Shibuya, K., Aboyans, V.,…Memish, Z. A. (2012). Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380(9859), 2095–2128.
Mack, K. A., Rudd, R. A., Mickalide, A. D., & Ballesteros, M. F. (2013). Fatal unintentional injuries in the home in the U.S., 2000– 2008. American Journal of Preventive Medicine, 44(3), 239–246.
Marsh, D., Sheikh, A., Khalil, A., Kamil, S., Jaffer-uz-Zaman, Qureshi, I.,…Effendi, S. (1996). Epidemiology of adults hospitalized with burns in Karachi, Pakistan. Burns, 22, 225–229.
1383
Mathers, C. D., & Loncar, D. (2006). Projections of global mortality and burden of disease from 2002 to 2030. PLoS Medicine, 3(11), e442.
McGee, K., & Fernanda, S. (2014). A 9-year-old at a shooting range, a spraying Uzi and outrage. New York Times, August 27. Retrieved from http://www.nytimes.com
Mehmood, A., Razzak, J. A., Kabir, S., MacKenzie, E. J., & Hyder, A. A. (2013). Development and pilot implementation of a locally developed trauma registry: Lessons learnt in a low-income country. BMC Emergency Medicine, 13(1), 4.
Mertz, K. J., & Weiss, H. B. (2008). Changes in motorcycle-related head injury deaths, hospitalizations, and hospital charges following repeal of Pennsylvania's mandatory motorcycle helmet law. American Journal of Public Health, 98(8), 1464–1467.
Miller, T. R., & Lestina, D. C. (1997). Costs of poisoning in the United States and savings from poison control centers: A benefit- cost analysis. Annals of Emergency Medicine, 49(2), 239–245.
Mohan, D. (2004). Evidence-based interventions for road traffic injuries in South Asia. Journal of the College of Physicians & Surgeons—Pakistan, 14, 746–747.
Morrongiello, B. (2012). Innovations in child injury prevention: Evidence-based strategies that address fire safety for young children and playground safety for older children. Injury Prevention, 18(Suppl. 1), A62.
Mowry, J. B., Spyker, D. A., Cantilena, L. A., Jr., Bailey, J. E., & Ford, M. (2013). 2012 Annual report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 30th Annual report. Clinical Toxicology, 51(10), 949–1229.
Mozaffarian, D., Hemenway, D., & Ludwig, D. S. (2013). Curbing gun violence: Lessons from public health successes. JAMA, 309(6), 551–552.
Murray, C.J.L., Vos, T., Lozano, R., Naghavi, M., Flaxman, A. D., Michaud, C.,…Memish, Z. A. (2012). Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990–2010: A
1384
systematic analysis for the Global Burden of Disease Study 2010. Lancet, 380(9859), 2197–2223.
National Center for Injury Prevention and Control. (2006). CDC injury factbook. Atlanta: Centers for Disease Control and Prevention. Retrieved from http://www.cdc.gov/injury/publications/factbook/injurybook2006.pdf
National Center for Injury Prevention and Control. (2014). Web- based Injury Statistics Query and Reporting System (WISQARS). Retrieved from http://www.cdc.gov/ncipc/wisqars
National Center for Injury Prevention and Control. (2015). Web- based Injury Statistics Query and Reporting System (WISQARS). Retrieved from http://www.cdc.gov/injury/wisqars
National Highway Traffic Safety Administration. (2015). Distracted Driving 2013 (DOT HS 812 132). Retrieved from http://www.distraction.gov/downloads/pdfs/Distracted_Driving_2013_Research_note.pdf
Olivier, J., Walter, S. R., & Grzebieta, R. H. (2013). Long term bicycle related head injury trends for New South Wales, Australia following mandatory helmet legislation. Accident Analysis & Prevention, 50, 1128–1134.
Olsen, E.O.M., Shults, R. A., & Eaton, D. K. (2013). Texting while driving and other risky motor vehicle behaviors among US high school students. Pediatrics, 131(6), e1708–1715.
Page, J. L., Macpherson, A. K., Middaugh-Bonney, T., & Tator, C. H. (2012). Prevalence of helmet use by users of bicycles, push scooters, inline skates and skateboards in Toronto and the surrounding area in the absence of comprehensive legislation: An observational study. Injury Prevention, 18(2), 94–97.
Palmer, K. T., Harris, E. C., Linaker, C., Barker, M., Lawrence, W., Cooper, C., & Coggon, D. (2012). Effectiveness of community- and workplace-based interventions to manage musculoskeletal-related sickness absence and job loss: A systematic review. Rheumatology, 51(2), 230–242.
Parbhoo, A., Louw, Q. A., & Grimmer-Somers, K. (2010). Burn prevention programs for children in developing countries require
1385
urgent attention: A targeted literature review. Burns, 36(2), 164– 175.
Peck, M. D., Kruger, G. E., van der Merwe, A. E., Godakumbura, W., Oen, I. M., Swart, D., & Ahuja, R. B. (2008). Burns and injuries from non-electric-appliance fires in low- and middle-income countries: Part II. A strategy for intervention using the Haddon matrix. Burns, 34, 312–319.
Peden, M., Scurfield, R., Sleet, D., Mohan, D., Hyder, A., Jarawan, E., & Mathers, C. (Eds.). (2004). World report on road traffic injury prevention. Geneva: World Health Organization.
Peralta, E. (2014). Fatal shooting at firing range sparks debate about safety. National Public Radio, August 28. Retrieved from http://www.npr.com
Pitts, S. R., Niska, R. W., Xu, J., & Burt, C. W. (2008). National Hospital Ambulatory Medical Care Survey: 2006 Emergency department summary (National Health Statistics Report No. 7). Hyattsville, MD: National Center for Health Statistics.
Polen, M. R., & Friedman, G. D.; U.S. Preventive Services Task Force. (1988). Automobile injury: Selected risk factors and prevention in the health care setting. JAMA, 259, 76–80.
Polinder, S., Haagsma, J. A., Toet, H., & van Beeck, E. F. (2012). Epidemiological burden of minor, major and fatal trauma in a national injury pyramid. British Journal of Surgery, 99(Suppl. 1), 114–120.
Razzak, J. A., Laflamme, L., Luby, S. P., & Chotani, H. (2004). Childhood injuries in Pakistan: When, where and how? Public Health, 118(2), 114–120.
Retting, R. A., Ferguson, S. A., & McCartt, A. T. (2003). A review of evidence-based traffic engineering measures designed to reduce pedestrian-motor vehicle crashes. American Journal of Public Health, 93, 1456–1462.
Rivara, F. P., Thompson, D. C., & Thompson, R. S. (2015). Epidemiology of bicycle injuries and risk factors for serious injury. Injury Prevention, 21(1), 47–51.
1386
Runyan, C. W., Perkis, D., Marshall, S. W., Johnson, R. M., Coyne- Beasley, T., Waller, A. E.,…Baccaglini, L. (2005). Unintentional injuries in the home environment in the United States: Part II. Morbidity. American Journal of Preventive Medicine, 28, 80–87.
Saadat, S., Mafi, M., & Sharif-Alhoseini, M. (2011). Population based estimates of non-fatal injuries in the capital of Iran. BMC Public Health, 11(1), 608.
Schuurman, N., Cinnamon, J., Matzopoulos, R., Fawcett, V., Nicol, A., & Hameed, S. M. (2010). Collecting injury surveillance data in low- and middle-income countries: The Cape Town Trauma Registry pilot. Global Public Health, 6(8), 874–889.
Shakur, H., Roberts, I., Piot, P., Horton, R., Krug, E., & Mersch, J. (2012). A promise to save 100000 trauma patients. Lancet, 380(9859), 2062–2063.
Sherman, L. W., Gottfredson, D. C., MacKenzie, D. L., Eck, J., Reuter, R., & Bushway, S. D. (1998). Preventing crime: What works, what doesn't, what's promising. Washington, DC: National Institute of Justice.
Stanojević, P., Jovanović, D., & Lajunen, T. (2013). Influence of traffic enforcement on the attitudes and behavior of drivers. Accident Analysis & Prevention, 52, 29–38.
Stevenson, M., Sleet, D., & Ferguson, R. (2015). Preventing child pedestrian injury: A guide for practitioners. American Journal of Lifestyle Medicine. doi:10.1177/1559827615569699
Sumner, S. A., Layde, P. M., & Guse, C. E. (2008). Firearm death rates and association with level of firearm purchase background check. American Journal of Preventive Medicine, 35, 1–6.
Tinsworth, D. K., & McDonald, J. E. (2001). Special study: Injuries and deaths associated with children's playground equipment. Washington, DC: U.S. Consumer Product Safety Commission.
Ulmer, R. G., & Preusser, D. F. (2003). Evaluation of the repeal of motorcycle helmet laws in Kentucky and Louisiana (DOT Report No. HS-809–530). Washington, DC: National Highway Traffic Safety Administration.
1387
U.S. Burden of Disease Collaborators. (2013). The state of US health, 1990–2010: Burden of diseases, injuries, and risk factors. JAMA, 310(6), 591–608.
U.S. Consumer Product Safety Commission. (2014). National Electronic Injury Surveillance System (NEISS). Retrieved from http://www.cpsc.gov/en/Research--Statistics/NEISS-Injury-Data
Vernick, J. S., Mair, J. S., Teret, S. P., & Sapsin, J. W. (2003). Role of litigation in preventing product-related injuries. Epidemiologic Reviews, 25, 90–98.
Vollman, D., Witsaman, R., Comstock, R. D., & Smith, G. A. (2009). Epidemiology of playground equipment-related injuries to children in the United States, 1996–2005. Clinical Pediatrics, 48(1), 66–71.
Wadman, M. C., Muelleman, R. L., Coto, J. A., & Kellermann, A. L. (2003). The pyramid of injury: Using e-codes to accurately describe the burden of injury. Annals of Emergency Medicine, 42, 468–478.
Warner, M., Chen, L. H. Makuc, D. M. Anderson, R. N., & Miniño, A. M. (2011). Drug poisoning deaths in the United States, 1980– 2008 (NCHS Data Brief No. 81). Retrieved from http://www.cdc.gov/nchs/data/databriefs/db81.htm
Waters, H. R., Hyder, A. A., Rajkotia, Y., Basu, S., & Butchart, A. (2005). The costs of interpersonal violence—an international review. Health Policy, 73(3), 303–315.
Wesson, D. E., Stephens, D., Lam, K., Parsons, D., Spence, L., & Parkin, P. C. (2008). Trends in pediatric and adult bicycling deaths before and after passage of a bicycle helmet law. Pediatrics, 122, 605–610.
Wilkinson, P., Smith, K. R., Joffe, M., & Haines, A. (2007). A global perspective on energy: health effects and injustices. Lancet, 370(9591), 965–978.
Williams, A. F., Preusser, D. F., Blomberg, R. D., & Lund, A. D. (1987). Seat belt use law enforcement and publicity in Elmira, New York: A reminder campaign. American Journal of Public Health, 77, 1450–1451.
1388
World Health Organization. (2013a). Global health estimates summary tables: Projection [Dataset]. Retrieved from http://www.who.int/healthinfo/global_burden_disease/projections/en
World Health Organization. (2013b). Health statistics and information systems: Estimates for 2000–2012:Cause-specific mortality. Retrieved from http://www.who.int/healthinfo/global_burden_disease/estimates/en/index1.html
World Health Organization (2014a). The top 10 causes of death (Fact sheet No. 310). Geneva: Author. Retrieved from http://www.who.int/mediacentre/factsheets/fs310/en
World Health Organization. (2014b). World health statistics 2014. Retrieved from http://apps.who.int/iris/bitstream/10665/112738/1/9789240692671_eng.pdf? ua=1
Zaloshnja, E., Miller, T. R., Lawrence, B. A., & Romano, E. (2005). The costs of unintentional home injuries. American Journal of Preventive Medicine, 28, 88–94.
Zegeer, C. V., & Bushell, M. (2012). Pedestrian crash trends and potential countermeasures from around the world. Accident Analysis & Prevention, 44(1), 3–11.
1389
For Further Information Books
Barss, P., Smith, G. S., Baker, S. P., & Mohan, D. (1998). Injury prevention: An international perspective: Epidemiology, surveillance and policy. New York: Oxford University Press.
Christoffel, T., & Gallagher, S. S. (1999). Injury prevention and public health: Practical knowledge, skills, and strategies. Gaithersburg, MD: Aspen.
Mohan, D., & Tiwari, G. (Eds.). (2000). Injury prevention and control. Boca Raton, FL: CRC Press.
Rivara, F. P., Cummings, C., Koepsell, T. D., Grossman, D. C., & Maier, R. V. (Eds.). (2000). Injury control: Research and program evaluation. New York: Cambridge University Press.
Robertson, L. S. (1999). Injury epidemiology. New York: Oxford University Press.
Journals Accident Analysis & Prevention: http://www.elsevier.com/wps/find/journaldescription.cws_home/336/description#description Published by Elsevier and affiliated with the Association for the Advancement of Automotive Medicine (AAAM).
Injury Control and Safety Promotion: http://www.tandf.co.uk/journals/titles/17457300.asp. Published by Taylor & Francis and associated with EuroSafe (European Association for Injury Prevention and Safety Promotion).
Injury Prevention: http://ip.bmjjournals.com. Published by BMJ Publishing Group, this is the official journal of the International Society for Child and Adolescent Injury Prevention (ISCAIP) and the Society for Advancement of Violence and Injury Research (SAVIR).
Journal of Safety Research: http://www.nsc.org/lrs/res/jsr.aspx and
1390
http://www.elsevier.com/wps/find/journaldescription.cws_home/679/description#description A joint publication of Elsevier and the National Safety Council (NSC).
Traffic Injury Prevention: http://www.tandf.co.uk/journals/titles/15389588.asp. Published by Taylor & Francis, this is the official journal of the Association for the Advancement of Automotive Medicine (AAAM), International Traffic Medicine Association (ITMA), International Council on Alcohol, Drugs and Traffic Safety (ICADTS), and International Research Council on the Biomechanics of Impact (IRCOBI).
Agencies and Organizations American College of Emergency Physicians (ACEP): http://www.acep.org. This professional organization of emergency physicians addresses a number of injury control issues in its policies and resources.
Centers for Disease Control and Prevention (CDC), National Center for Injury Control and Prevention (NCICP): http://www.cdc.gov/ncipc. The NCICP maintains information on injury control, including surveillance data and statistics, for the United States. The NCICP's Web site also offers program information and funding sources.
Injury Prevention Web: http://www.injuryprevention.org. The Injury Prevention Web is a meta-site that hosts the Web pages of several injury prevention organizations and serves as an excellent source for injury prevention resources.
National Safety Council: http://www.nsc.org. A nongovernmental organization that promotes safety in homes, at work, in communities, and on the roads through leadership, research, education, and advocacy.
SafetyLit: http://www.safetylit.org. SafetyLit is an online resource for recent injury prevention research.
World Health Organization, Injuries and Violence Prevention: http://www.who.int/violence_injury_prevention/en. WHO's Department of Violence and Injury Prevention and Disability maintains a clearinghouse for information about injury control,
1391
including epidemiology and prevention, the world over, with a regularly updated list of campaigns, conferences, and other injury control activities.
1392
Chapter 24 Environmental Disasters
Mark E. Keim
The author wishes to thank Braeden Benson, MPH, Hugh Green, MPH, and Casey Owens for their support provided in the literature search for this chapter. Dr. Keim reports no conflicts of interest related to the authorship of this chapter.
1393
Key Concepts Environmental disasters occur when three things come together: population exposure to an environmental hazard, conditions of vulnerability in that population and its environment, and insufficient capacity to reduce or cope with negative consequences.
Environmental hazards that lead to disasters may be natural or technological.
The hazards that cause disasters may vary greatly, but the public health consequences and the public health and medical needs of affected populations tend to be relatively consistent across disaster types.
Disaster risk is the product of the probability of disaster occurrence and the probability of a vulnerable population becoming affected minus the absorptive capacity of that population.
Disaster risk management is a comprehensive, all-hazard approach that entails developing and implementing strategies for all phases of the disaster life cycle—prevention, mitigation, preparedness, response, and recovery—in the context of sustainable development.
A disaster is “a serious disruption of the functioning of a community or a society causing widespread human, material, economic or environmental losses that exceed the ability of the affected community or society to cope using its own resources” (United Nations Office for Disaster Risk Reduction [UNISDR], 2009). A disruption that does not exceed a community's or society's capacity to cope is classified as an emergency. Emergencies and disasters are thus part of a continuum and differ only by their degree of severity.
A standard definition of disaster comes from the Emergency Events Database (EM-DAT) at the Centre for Research on the Epidemiology of Disasters, or CRED, at the Catholic University of Louvain, in Belgium. In order for an event to qualify as a disaster
1394
and be entered into EM-DAT, at least one of the following criteria must be fulfilled:
Ten (10) or more people reported killed.
One hundred (100) or more people reported affected.
Declaration of a state of emergency.
Call for international assistance.
Disaster consequences may include loss of life, injury, disease, and other negative effects on human physical, mental, and social well-being, together with damage to property, destruction of assets, loss of services, social and economic disruption, and environmental degradation. The severity of the consequences is referred to as the disaster impact.
Traditionally, disasters may be classified according to the causative agent or hazard (natural, technological, or complex). Natural disasters may be caused by either environmental hazards (including hydrometeorological and geological hazards) or biological hazards (pandemics, epidemics, and disease outbreaks). Technological (or man-made) disasters may be caused by environmental hazards (such as hazardous materials, fire, structural failure, and transportation accidents) or a complex mix of social, economic, and political hazards involving displacement (such as a forced mass migration originating in conflict or lack of food security) (see Table 24.1). Hybrid disasters are environmental disasters resulting from simultaneously occurring natural hazards and technological hazards. Examples include massive urban fires after both the 1906 San Francisco and 1995 Kobe earthquakes as well as the radiation disaster that followed the 2010 Fukushima earthquake and tsunami.
Table 24.1 A Typology of Environmental Disasters
Natural Technological Drought Chemical Wildfires
Hydrometeorological Heat waves Toxic Radiological
Stormsa
1395
Floods Earthquakes Fires Nuclear
Geophysical Landslidesb Thermal Volcanic eruptions
Explosions
Tsunamis Mechanical Transport accidents
aStorms include cyclones, tornadoes, windstorms, snow or ice storms, and dust storms.
bLandslides include debris flows, mud flows, volcanic lahars, and snow avalanches.
But few “natural” disasters are purely natural. For example, climate change—a result of human activities—is expected to increase hurricane intensity and flood frequency. Moreover, the way natural disasters unfold reflects an interplay of the physical event with human development patterns, societal adaptation (or maladaptation) to the physical environment, and vulnerability. According to this perspective, earthquakes, droughts, floods, and storms are natural hazards, but “unnatural disasters” are the deaths and damage that result from human acts of omission and commission. Every disaster is unique, but each exposes actions—by individuals and organizations at different levels—that, had they been different, would have resulted in fewer deaths and less damage (World Bank, 2010).
This complexity was recognized in 2005 with the global adoption of the Hyogo Framework for Action, an initiative led by the United Nations (UNISDR, 2007). The Hyogo Framework recognizes that all disaster risk (including natural, technological, and complex disasters) is a function of linked physical, social, economic, and environmental vulnerabilities. There is now international acknowledgment that disaster risk reduction must be systematically integrated into sustainable development, poverty reduction, and climate policy (Keim, 2008), and supported through bilateral, regional, and international cooperation, including partnerships.
Disaster risk is now recognized to occur as a result of the combination of population exposure to an environmental hazard,
1396
the conditions of human vulnerability that are present, and insufficient capacity or measures to reduce or cope with the hazard's negative consequences. Disaster risk management activities are therefore transitioning from a focus on reacting to specific categories of hazards and their associated effects (such as morbidity, mortality, and displacement) to an approach that also addresses the root causes of disaster-related losses (such as exposure, vulnerability, and capacity).
1397
Scope of the Problem During the past five decades (1964–2013), 19,555 environmental disasters (excluding epidemics, wars, and conflict-related famines) were reported to have killed 5.4 million people worldwide, affected 7 billion lives, and resulted in property damage exceeding US$2.7 billion, in time-adjusted 2014 dollars (CRED, 2015). Environmental disasters accounted for 93% (natural disasters 53% and technological disasters 40%) of the world's disasters during that time, eclipsing the 7% that were biological disasters (CRED, 2015).
Within the environmental disaster category, natural disasters accounted for 62% and technological disasters the remaining 38% (CRED, 2015). Specifically, transportation disasters represented 25% of environmental disasters, floods 15%, cyclones 9%, and earthquakes 5%. Hydrometeorological disasters accounted for the greatest burden among environmental disasters (65% of fatalities, 68% of costs, and 96% of all people affected) (CRED, 2015).
Nor was the pattern static from 1964 through 2013. The incidence of environmental disasters increased, with extreme weather disasters increasing much more rapidly than geological or biological disasters, affecting an increasing number of people, and causing increasingly large economic losses. However, there may be early indications of a downward trend for both natural and technological disasters since 2000 (Figure 24.1).
1398
Figure 24.1 Annual Incidence of Natural and Technological Environmental Disasters—Worldwide, 1964–2013
Source: CRED, 2015.
Table 24.2 shows the ten deadliest environmental disasters during the years from 1964 to 2013. Of note, all ten were natural disasters occurring in low-income settings.
Table 24.2 The Ten Deadliest Environmental Disasters— Worldwide, 1964–2013
Disaster type Year Location Estimated fatalities Drought 1965 India 1,502,000 Drought 1983 Ethiopia, Sudan 450,520 Tropical cyclone 1970 Bangladesh 304,495 Earthquake 1976 China 276,994 Earthquake 2004 Indonesia 227,290 Earthquake 2010 Haiti 226,735 Tropical cyclone 1991 Bangladesh 146,297 Tropical cyclone 2008 Myanmar 140,985 Drought 1981 Mozambique 103,000 Drought 1973 Ethiopia 100,000
Source: CRED, 2015.
1399
The Public Health Consequences of Environmental Disasters Annual disaster frequency does not correlate closely with health impacts such as mortality, injury, and displacement, illustrating that disaster-related health effects reflect not just the number of events but also the complex interplay of exposures (quality, intensity, duration, etc.), vulnerability (demographics, comorbidity, education, socioeconomic status, etc.), and adaptive capacity (quality of preparedness resources, access to health care, community resilience, etc.).
Figure 24.2 compares the health impacts of natural and technological disasters. While natural disasters represent 62% of environmental disasters, they account for far larger relative burdens of deaths, injuries, and other impacts (despite higher mortality and injury rates for technological disasters).
1400
1401
Figure 24.2 Comparison of the Public Health Impacts of Natural and Technological Disaster Events, 1964–2013
Source: CRED, 2015.
Mortality Associated with Environmental Disasters Among environmental disasters over the past fifty years, natural disasters were responsible for the overwhelming majority of deaths, for three main reasons: natural disasters were nearly twice as frequent as technological disasters, natural disasters affected far more people per event than technological disasters, and the mean number of deaths per event was far greater for natural disasters (1,282) than that for technological disasters (32).
However, the mortality rate for technological disasters (14,955/100,000 affected people) is nearly nine times that of natural disasters (1,708). In addition, the mean number of deaths per injury for technological disasters (0.78) is 35% higher than that for natural disasters (0.58).
When considering individual types of environmental disasters, tsunamis have by far the highest mean number of deaths per event (7,621), followed by drought (3,604), earthquakes (1,088), and heat waves (966) (Figure 24.3). Structural collapse has the highest mean number of reported deaths per event among technological disasters (45), closely followed by poisonings (43) and transportation disasters (41) (CRED, 2015).
1402
1403
Figure 24.3 Key Public Health Impacts for Natural and Technological Disasters, 1964–2013
Note: The dotted line indicates the mean value for each set of values.
Source: CRED, 2015.
Transportation disasters have an extremely high mortality rate (92,037/100,000 affected people), meaning that 92% of people affected by transportation disasters worldwide lose their lives. This reflects the low survival from such incidents as aircraft crashes. Tsunamis have the second highest mortality rate among environmental disasters (13,563/100,000 affected people). The third and fourth highest mortality rates are associated with technological disasters: structural collapse (5,437/100,000 affected people) and explosions (4,880/100,000 affected people) (CRED, 2015) (Figure 24.3). A tragic example of structural collapse mortality, emphasizing the vulnerability of poor nations, was the Rana Plaza disaster of 2013, which killed over 1,000 workers in Bangladesh; this is described in Chapter 21.
Tsunamis have the highest death to injury ratio of all environmental disasters. During tsunami disasters, there were 4.9 times more reported deaths than injuries. Other environmental disasters with a high number of deaths relative to injuries include landslides (3.6 deaths per injury), volcanic eruptions (2.5). transportation accidents (2), heat waves (1.7), structural collapse (1.3), and (urban) fires (1.1) (Also see Table 24.3.)
Table 24.3 Major Causes of Death During Environmental Disasters
Natural Technological
1404
Drought Malnutrition Chemical release
Poisoning, asphyxia
Wildfires Asphyxiation, burns, toxic exposures
Poisonings Poisoning
Heat waves Heat stroke, exacerbations of cardiovascular disease
Nuclear Traumatic injury, burns, radiation illness
Storms Drowning, traumatic injury
Floods Drowning Radiological Radiation illness
Earthquakes Traumatic injury, asphyxia
Fires Burns, asphyxia
Landslides Traumatic injury, asphyxia
Explosions Traumatic injury, burns
Volcanic eruptions
Traumatic injury, burns, toxic exposures
Transportation accidents
Traumatic injury, burns, drowning
Tsunamis Drowning, traumatic injury
Structural collapse
Traumatic injury, asphyxia
Cold weather
Hypothermia
Sources: Bailey & Walker, 2007; Bertazzi, 1989; Binder, 1989; Centers for Disease Control and Prevention, 1983, 1993, 1998, 2002; Chowdhury et al., 1992; Cronin & Sharp, 2002; Duclos, Sanderson, Thompson, Brackin, & Binder, 1987; Floret, Viel, Mauny, Hoen, & Piarroux, 2006; Guha-Sapir & van Panhuis, 2005; Hull, Grindlinger, Hirsch, Petrone, & Burke, 1985; International Federation of Red Cross and Red Crescent Societies, 2007; Keim, 2002, 2008; Lillibridge, 1997; Malilay, 1997; Mehta, Mehta, Mehta, & Makhijani, 1990; Sanderson, 1992, 1997; Sattler et al., 2002; Toole, 1997; World Health Organization, 2009.
Morbidity Associated with Environmental Disasters
Injury
1405
Overall, the injury rate (number of injuries/100,000 affected) for natural disasters (144/100,000) is nearly the same as that for technological disasters (137/100,000). Among specific types of disasters, technological disasters show the highest injury rates: transportation accidents (45,964/100,000), chemical releases (11,263/100,000), poisoning (7,963/100,000), explosions (6,814/100,000), and structural collapse (4,158/100,000). The highest injury rates reported for natural disasters are for cold weather (1,976/100,000), heat waves (1,883/100,000), tsunamis (1,728/100,000), and earthquakes (1,304/100,000). Most injuries associated with technological disasters occur at the time of disaster impact (when populations are in direct contact with the disaster hazard). However, in the case of natural disasters, the timing of injuries is often bimodal. In these circumstances, injuries occur not only in the impact phase but also during the postimpact recovery phase, as survivors work to clean up or rehabilitate disaster damages. For example, in a study of the 2014 China earthquake, 24% of the 2,010 injury victims studied sustained their injuries during evacuation after the impact phase, when seismic activity had receded (Zhang et al., 2014).
Communicable Disease While members of the public and the media frequently fear infectious disease outbreaks after disasters, such outbreaks are actually quite rare. The risk of an epidemic after geophysical disasters is considered negligible (Floret et al., 2006). Floods and cyclones are in rare circumstances followed by outbreaks of infectious disease, mostly in low-income nations where baseline infrastructure and recovery capabilities are inadequate. In these settings, disasters may exacerbate diseases that are normally endemic, such as acute respiratory infections, leptospirosis, dengue fever, typhoid, malaria, and cholera. The rare outbreaks of posthurricane infectious disease in high-income countries have consisted of self-limiting gastrointestinal disease, dermatological infections, and respiratory infections. Flooding may also result in episodes of near-drowning and pulmonary aspiration of floodwater resulting in pneumonia. Near-drowning is also common in tsunamis and is associated with aspiration pneumonia or tsunami lung, a necrotizing pneumonia notable for flora commonly associated with sea water aspiration (Allworth, 2005).
1406
Wound and respiratory infections are common after tsunamis and earthquakes and are often associated with a high mortality rate. In a study following the 2014 earthquake in China, lung infections were the most common infection among hospitalized patients (60 individuals, or 37.7%), followed by skin and soft tissue infections (26, 16.4%) and secondary open wound infections (25, 15.7%) (Zhang et al., 2014). Earthquake-related pneumonitis has been associated with the inhalation of debris dust, particularly concrete.
Noncommunicable Disease Environmental disasters such as earthquakes, floods, and storms may be associated with exacerbation of chronic diseases such as mental illness, cardiovascular disease, and chronic obstructive pulmonary disease. In some cases these effects are nonspecific and may relate to post-traumatic response; for instance, the 2011 earthquake in Japan was followed by increases in new onset, acute coronary syndrome and exacerbations of congestive heart failure (Nozaki et al., 2013). Chronic disease exacerbations may also reflect loss of medications or interruptions in ongoing medical care. Finally, specific effects of some disasters may be operative in cases such as exacerbations of chronic obstructive lung disease and asthma from smoke inhalation during wildfires and volcanoes and exacerbations of respiratory and cardiovascular disease during heat waves.
Behavioral health effects are among the most debilitating long-term health outcomes of environmental disasters, and in some cases represent the largest health burden (Davidson & McFarlane, 2006; Halpern & Tramontin, 2007; Neria, Galea, & Norris, 2009). Research conducted several months after Hurricane Katrina, for example, showed that 49.1% of those surveyed in New Orleans, and 26.4% in other hurricane-affected areas, suffered from anxiety- mood disorders as defined in DSM-IV, of which half or more were post-traumatic stress disorder (PTSD) (Galea et al., 2007). According to a study two years after the hurricane, the prevalence of PTSD and depression had actually increased (Kessler et al., 2008). Disaster epidemiology has documented similar outcomes—in some cases accompanied by increases in suicide, substance abuse, and domestic violence—in most cultures studied and following widely varying disasters: floods, dam collapses, heat waves, tsunamis,
1407
landslides, and wildfires. Risk factors for depression and/or PTSD vary but often include female sex, childhood, low levels of social capital or social support, physical injury, property loss, witnessing people suffering or dying during the disaster, loss of family members, relocation or displacement, history of psychiatric illness, and not having insurance. Interestingly, exposure to news coverage during and after the disaster, especially when graphic or violent images are shown, is a risk factor in some studies. Protective factors include personal resiliency, prompt provision of recovery resources, high levels of social capital, and the ability to keep communities intact. These findings suggest a variety of adaptation strategies to protect postdisaster mental health (King, Reifels et al., 2013; Silove & Steel, 2006; Ursano, Fullerton, Weisaeth, & Raphael, 2011; Burkle, Walsh, & North, 2015), including strengthening predisaster social support, providing post-disaster mental health and psychosocial services, targeting at-risk groups, paying attention to the content and framing of news coverage, and ensuring prompt implementation of recovery assistance such as insurance compensation for property loss.
Toxic Exposures There is a potential for exposure to hazardous materials during the impact and also the cleanup phase of environmental disasters. During floods, industrial and stored household chemicals may be mobilized. For example, in 1999, landslides in Venezuela destroyed parts of the port facilities used to store hazardous materials. These chemicals were inundated by the debris flow and came dangerously close to causing an explosion with the potential to affect 80,000 nearby residents, and also closed the nation's largest airport and second largest seaport (Keim, Humphrey, & Dreyfus, 2000; “Venezuela Seeks Contractors…,” 2000). Other toxic exposures include mold, a potential public health problem following major floods and hurricanes, and carbon monoxide, which becomes a hazard when disaster-affected populations lose electrical power and improperly use carbon monoxide–emitting fuel sources in poorly ventilated spaces.
Malnutrition Generalized food shortages severe enough to cause nutritional
1408
problems usually do not occur after disasters other than drought, but may arise in low-income nations in two ways. First, food stock destruction within the disaster area may reduce the absolute amount of food available, and/or second, disruption of distribution systems may curtail access to food, even when there is no absolute shortage. Throughout human history the most feared impact of drought has been a shortage of food. During the 2011 floods in Southeast Asia, food security became a major issue as it became difficult to deliver food supplies to flood-affected areas (Kim, 2006). In addition, severe damage to agricultural land and livestock affects those who rely on these forms of food production, with main food crops often being severely damaged, along with losses in livestock and poultry.
Displacement Beyond the morbidity that results directly from disaster-related environmental hazards, much of the secondary morbidity is associated with displacement. All environmental disasters can interfere with access to adequate shelter, water, sanitation, hygiene, health care, nutrition, security, public services, and/or utilities among affected populations. These factors have a significant influence on morbidity following a disaster.
Homeless populations are more vulnerable to continued environmental exposures as well as to social disruption and psychosocial stress. Displaced populations and those suffering the loss of public utilities also risk loss of safe food and water and experience inadequate hygiene and sanitation. People who engage in postdisaster cleanup activities risk injuries such as falls, electrocutions, and equipment (e.g., chainsaw) injuries.
Displacement from homes carries substantial potential for psychosocial impacts. The long-term effects of displacement on psychological health may outweigh other illness or injury related to natural disasters (Fussell & Lowe, 2014; Neria, Galea & Norris, 2009).
Natural and technological disasters have roughly similar displacement rates, at about 2% of those affected. The environmental disasters with the highest displacement rate are radiation disasters (48,250/100,000 affected), an outcome
1409
driven largely by two large-scale radiation disasters during the 1964 to 2013 period, at Chernobyl and Fukushima. Following close behind are two technological disasters—explosions (36,934/100,000) and fires (36,109/100,000)—as well as displacements due to natural disasters, most notably, tsunamis (35,222/100,000) and landslides (30,835/100,000) (CRED, 2015). After two major disasters in 2010—the flood in Pakistan and earthquake in Haiti—millions of households in each country were displaced. A year later, displacement persisted among 53% of affected households in Pakistan, and among 39% in Haiti (Weiss, Kirsch, Doocy, & Perrin, 2014).
1410
Disaster Risk and Its Determinants Risk is the probability that something will cause injury or harm. While risk can rarely be completely eliminated, it can be managed. Risk management is activity directed toward assessing, controlling, and monitoring risks. In risk management, evidence on risk factors is collected and analyzed, risks in particular contexts are assessed, and control measures are implemented, using standard strategies. The risk of disaster-related morbidity and mortality is a complex function of factors both extrinsic and intrinsic to the individual.
Extrinsic Factors Affecting Disaster Risk Extrinsic disaster risk factors relate to exposure and capacity. Exposure is defined as contact with a potentially dangerous hazard, such as wind from tornadoes, water from floods, or heat from heat waves. Capacity is the combination of all external resources that can be deployed to minimize morbidity and mortality following exposure. Capacity includes four major categories of resources: economic resources (e.g., occupation, income, savings, and health insurance); material resources (e.g., emergency equipment and supplies, food and water, medicines, health care, transportation, shelter, and quality of housing and the built environment); behavioral resources (e.g., emergency plans, mutual aid agreements, memoranda of understanding, and communication plans); and sociopolitical resources (e.g., social support and capital, political representation, and formal and informal communication networks).
Intrinsic factors Affecting Disaster Risk Intrinsic risk factors for disaster-related morbidity and mortality include attributes related to human vulnerability. Vulnerability includes four major categories of attributes: demographics (e.g., age, gender, and family position); education and personal experience (e.g., educational level and disaster training); race, language, and ethnicity (e.g., minority status in the affected population and language barriers); and health status (e.g., chronic illness, physical disability, malnutrition, mental illness, and
1411
dependence upon life-sustaining treatment).
Epidemiological studies following disasters have pinpointed some of these risk factors. One of the best-known examples is a study of the 1995 Chicago heat wave (Klinenberg, 2002). During that disaster, mortality was elevated among socially isolated, elderly, inner-city African American populations; other risk factors included low- quality housing and lack of air conditioning. In general, poverty may be the single most important risk factor for vulnerability to all environmental disasters (Thomas, Phillips, Lovekamp, Fothergill, & Toole, 2013). For example, as discussed in Chapter 11, dangerous facilities such as chemical plants, with their attendant risk of accidents, are disproportionately concentrated in poor and/or minority communities (Elliott, Wang, Lowe, & Kleindorfer, 2004). Similarly, the overwhelming majority of casualties in the Bhopal, India, disaster occurred among extremely poor day laborers (Mehta, 1990).
1412
Managing Disaster Risk Disaster risk management applies the general principles of risk management to disasters. Risk management has standard operational categories, including risk avoidance, risk reduction, risk transfer, and risk retention. Emergency managers think in terms of a different set of categories: prevention, mitigation, preparedness, response, and recovery. And public health professionals, with a prevention orientation, often think in terms of primary, secondary, and tertiary prevention. These three frameworks align well with each other, as shown in Figure 24.5.
Disaster risk management is a comprehensive approach that entails developing and implementing strategies for each phase of the disaster life cycle. The emphasis on a life cycle approach, beginning well before a disaster and continuing through the aftermath, is important in all disasters. While the depiction of disasters as cyclical may seem to imply that disasters are inevitable, this is not the case. The goals of risk avoidance and risk reduction are to avert disasters and retained risk, thus breaking the disaster cycle. The ultimate goal of disaster risk management is to break the disaster life cycle. A key aspect of meeting this goal is building resilience, as discussed in Text Box 24.1.
1413
Text Box 24.1 Disaster Resilience Resilience is a recurring concept in environmental health. In Chapter 2 (on ecology) and Chapter 3 (on sustainability), resilience is defined as the “capacity of a system to absorb disturbance; to undergo change and still retain essentially the same function, structure, and feedbacks” (Walker & Salt, 2006). This definition applies well to complex systems. In the context of disasters, resilience has a related, but more specialized meaning.
Disaster resilience is defined in the Hyogo Framework of Action (United Nations Office for Disaster Risk Reduction, 2007) as “the capacity of a system, community or society potentially exposed to hazards to adapt, by resisting or changing in order to reach and maintain an acceptable level of functioning and structure.” The U.K. Department for International Development (2011) offers a similar definition: “the ability of countries, communities and households to manage change, by maintaining or transforming living standards in the face of shocks or stresses—such as earthquakes, drought or violent conflict—without compromising their long-term prospects.” The Hyogo Framework identifies the foundation of disaster resilience: the degree to which individuals, communities, and public and private organizations can organize themselves to learn from past disasters and reduce their risks of future ones, and improve risk reduction measures.
Resilience has become a central theme of disaster preparedness and response. A schematic approach to disaster resilience is shown in Figure 24.4. When a community, city, or region is affected by a disaster—such as a tsunami, a drought, or a chemical spill—the capacity to deal with it is a function of exposure, sensitivity (or vulnerability), and adaptive capacity. Following the disturbance, a new equilibrium is reached—somewhere on the spectrum from collapse, to worsening of function (as described in the Haiti case study in this chapter), to bouncing back, to a recovery
1414
that is an improvement on predisaster conditions. The goal of disaster recovery is risk reduction—to bounce back better, ending up stronger than before the disaster.
Figure 24.4 Three Conceptual Frameworks for Disaster Risk Management
Source: U.K. Department for International Development, 2011.
1415
Figure 24.5 The Four Elements of a Resilience Framework
What determines disaster resilience? There are many components: social, institutional, human, physical, financial, and natural. Social factors are important; as described in Chapter 9, social capital includes networks of trust, reciprocity, and mutual assistance. This is critical at the local level, where much resilience is rooted. Institutional factors include the integrity and functionality of government, nongovernmental organizations, and the private sector. Low capacity and high levels of corruption, undermine resiliency. Human factors include the levels of training and technical skills in the affected population. Physical factors include such assets as roads, health care facilities, and communications infrastructure. Understanding these factors is a first step in assessing, and strengthening, disaster resilience.
Versailles, a neighborhood in east New Orleans, is a case study in disaster resiliency. This community was among the first to begin rebuilding in the months after Hurricane Katrina, in late 2005 and early 2006. Strong bonds of history, religion, and tradition among the Vietnamese American residents, and a robust church to which many belonged, drew them back to their community. They launched an inclusive process, with meetings and charrettes,
1416
to envision the rebuilt community. Within a year over 90% of the Vietnamese American homes in Versailles were reoccupied—about three times the proportion of non- Vietnamese-American homes. Within several years the residents had rebuilt homes, businesses, a school, a health clinic, and a senior center. Analysts attributed this remarkable recovery to strong social capital and community leadership within the Vietnamese community (Leong, Airriess, Li, Chen, & Keith, 2007).
Anticipation, Hazard Identification, Risk Assessment, and Planning For all of the frameworks shown in Figure 24.5, anticipation, recognition, risk assessment, and planning come first. Ideally, disaster risk management is based on a prioritization process. Once risks have been identified, they are assessed in terms of the potential severity of loss and the probability of occurrence. The risks likely to incur the greatest loss and having the greatest probability of occurrence are addressed first, and risks presenting a potentially lower loss and lower probability of occurrence are handled in descending order. In practice the prioritization process can be very difficult.
Risk Avoidance and Prevention Risk avoidance, in risk management parlance, corresponds to primary prevention in both public health and emergency management terms. Primary prevention seeks to prevent the disaster hazard exposure from ever occurring. For example, floodplain management may prevent flood disasters altogether, and logging restrictions on unstable hillsides may prevent landslides.
Much of the approach to primary prevention of technological disasters is based on regulation of industrial and commercial practices, including the manufacture, storage, transport, and utilization of hazardous materials as well as the promotion of safe practices in the construction and transportation industries.
Risk Reduction
1417
Risk reduction involves methods that reduce the likelihood of occurrence and/or the severity of the loss. This corresponds to secondary prevention, the general public health strategy that aims to detect a hazard early to control its advance and to reduce the resulting health burden—or in emergency management terms, preparedness, and mitigation. Risk reduction activities seek to prepare for and mitigate the health effects of disasters that cannot be prevented, using strategies that address the root causes of disaster-related morbidity and mortality (i.e., exposure, vulnerability, and lack of capacity).
Mitigation measures reduce population vulnerability by reducing exposure to disaster hazards. The Federal Emergency Management Agency (FEMA; 2013) identifies four types of mitigation measures: local plans and regulations, structure and infrastructure projects, natural system protection, and education and awareness programs. Local plans and regulations may include a wide range of strategies. For example, hazard source control aims to reduce the probability or magnitude of an event at the source—say, by limiting the quantity of chemicals stored on-site at a water treatment plant—and land-use practices limit hazard exposure by minimizing development in risky areas, such as by restricting building in floodplains or in landslide- prone areas. Structure and infrastructure projects might include community protection works that interrupt hazard transmission— say, by placing berms around chemical storage tanks to contain leaks—or building construction practices that limit physical vulnerability through structural means, such as seismic design (in earthquake-prone areas) or placing generators on the upper floors of hospitals (in flood-prone areas). Natural systems protection might include sediment and erosion control and stream corridor restoration or wetland restoration to help protect against flooding (while providing other kinds of ecosystem services, as described in Chapter 2). Education and awareness programs inform and educate citizens and decision makers about hazards and potential ways to mitigate them. Examples include local hurricane evacuation or heat wave preparedness training, or participation in national programs such as StormReady or Firewise Communities. For other kinds of disasters, especially those that emerge slowly, other kinds of mitigation measures are used, such as providing drought-tolerant seeds to farmers in arid areas.
1418
Preparedness is closely linked to mitigation, as part of risk reduction. Preparedness implies a behavioral approach focused on actions taken in advance of a disaster in order to reduce its impact. This reduces population vulnerability.
Populations at risk for disasters face a vast range of hazards within a nearly infinite set of scenarios. This unpredictability is poorly suited to scenario-based approaches to risk management. While the hazards that cause disasters vary greatly, the potential public health consequences and subsequent needs of those affected are far more consistent across disasters. For example, warfare, chemical releases, floods, hurricanes. and earthquakes all displace people from their homes. These hazards require the same sheltering capability with only minor adjustments based on the rapidity of onset, scale, duration, location, and intensity. Regardless of the hazard, disasters can be seen as causing fifteen public health consequences that are addressed by thirty-two categories of public health and medical capabilities (Table 24.4) (Keim, 2006). All-hazards preparedness, accordingly, is the idea that common capabilities can serve well in a variety of disaster situations, with variation based more on severity of the disaster (scale or degree of impact) than on disaster type.
Table 24.4 Public Health Consequences and Capabilities Associated with All Disasters
Public health consequences
Public health capabilities
Common to all consequences
Resource management Mental health services Reproductive health services Social services Occupational health and safety Business continuity
Deaths Mortuary care Social services Mental health services
Illness and injuries Health services Injury prevention and control Epidemiology
1419
Disease prevention and control Loss of clean water Access to safe water Loss of shelter Shelter and settlement
Social services Security
Loss of personal and household goods
Replacement of personal and household goods
Loss of sanitation and routine hygiene
Sanitation, excreta disposal, and hygiene promotion
Disruption of solid waste management
Solid waste management
Public concern for safety Risk communication Public information Security
Increased pests and vectors Pest and vector control Loss or damage of health care system
Health system and infrastructure support
Worsening of chronic illnesses
Health services
Food scarcity Food safety, security, and nutrition Standing surface water Public works and engineering Toxic exposures Risk assessment
Population protection Health services Hazmat emergency response Occupational health and safety
Source: Adapted from Keim, 2006.
The 11 E's of public health preparedness (Text Box 24.2) offer an easy way to summarize and recall those capabilities commonly involved in public health preparedness.
1420
Text Box 24.2 The 11 E's of Public Health Preparedness
Evaluation and monitoring of hazard
Early warning
Evacuation
Emergency operations planning
Education and training
Exercises and drills
Engagement of the public
Electronic media and communication
Epidemiology
Equipment and supplies
Economic and political incentive
Disaster Risk Transfer Disaster risk transfer includes such mechanisms as insurance contracts and risk retention pools. By purchasing an insurance contract, people are able to transfer and share risk across a large population. Risk retention pools are similar; but instead of assessing premiums in advance, these pools assess losses across all members of the group once they occur.
Disaster Response Disaster risk retention is a risk management term that means accepting the loss when it occurs and focusing on response and recovery. All residual risks that are not avoided or transferred are retained by default. This corresponds to the public health concept of tertiary prevention—seeking to prevent additional harm once an adverse event has occurred. This stage of prevention aims to reduce morbidity, avoid complications, and restore function. In the emergency management disaster cycle, this corresponds to the
1421
response and recovery phases (Keim, 2008).
Disaster response, sometimes called disaster relief, is predominantly focused on immediate and short-term needs. Response usually includes those actions immediately necessary to remove the affected population from ongoing exposure or risk of harm. The emergency operations plan is central to emergency management. Emergency operations plans describe who will do what—as well as when they will do it, with what resources, and by what authority—before, during, and immediately after an emergency (FEMA, 2010). In the United States the National Response Framework (NRF) establishes guiding principles to enable all levels of domestic response partners to prepare for and provide a unified national response to disasters and emergencies. Public health has a well-defined role under Emergency Support Function No. 8 (ESF-8) of the NRF, which addresses all public health and medical issues.
The Incident Command System (ICS) is a standardized, on- scene, all-hazard incident management protocol under the NRF. It is based on a flexible, scalable, common response framework designed to facilitate people's working together effectively. The National Incident Management System (NIMS), in turn, is a form of incident command system used in the United States to provide a systematic, proactive guidance to departments and agencies at all levels of government, nongovernmental organizations, and the private sector in working seamlessly together before, during, and after emergencies.
Immediately after the disaster impact, rapid needs assessments are conducted in order to identify any gap between the health needs of an affected community and the available resources. In addition to performing health surveillance, public health practitioners are often involved in decisions regarding housing and public safety, assist in delivery of health care, perform food safety and water quality inspections, and assess sanitation and hygiene in shelters. The demands for environmental health services and consultation are quite high during and after natural disasters. Public health practitioners also become involved in health risk assessments and technical assistance related to any suspected hazardous material exposures after an environmental disaster, such as chemical spills.
1422
Health and risk communication is essential before and after disaster impact (e.g., to publicize protective behaviors that can help to prevent drowning or heat illness). Injuries such as electrocutions, burns, and carbon monoxide poisonings are examples of disaster- related morbidity that can be prevented through public awareness and health education. Communication principles and strategies are discussed in Chapter 28.
Recovering from the Public Health Impact of Environmental Disasters Rehabilitation and reconstruction begin soon after the emergency phase has ended, and should be based on preexisting strategies and policies that facilitate clear institutional responsibilities for recovery action and enable public participation. The division between the response stage and the subsequent recovery stage is not clear-cut. Some response actions, such as the supply of temporary housing and water supplies, may extend well into the recovery stage.
Recovery programs, coupled with the heightened public awareness after a disaster, also afford a valuable opportunity to develop and implement disaster risk reduction measures and to apply the build back better principle.
Long-term recovery from the public health impact of major disasters can take years to achieve (as described in Text Box 24.3). Additional financial, health, and emotional costs may continue long after basic utilities and shelter have been reinstated. The disaster recovery phase may also offer a window of opportunity for improving risk reduction strategies, such as preparedness and mitigation efforts.
1423
Text Box 24.3 A Case Study of Haiti's Troubled Recovery Recovery efforts after the Haiti earthquake in January 2010 offer an informative case study for the concept of building back better (the widely described goal of Haiti's reconstruction). Following the earthquake more than fifty countries and international agencies pledged more than US$12.4 billion in humanitarian and development aid. While much of the aid was channeled toward rebuilding the infrastructure and economy and toward improving health care and law enforcement, many of the risk factors associated with disaster-related morbidity and mortality remained unchanged five years later. Continued lack of building codes and land-use regulation in areas of high seismicity allowed families to remain in unreinforced masonry houses, one of the most common causes of hazard exposure in earthquakes. Indicators of human vulnerability changed only slightly during these first five years. Life expectancy at birth increased from 61.9 to 63.1 years, a trend relatively unchanged since 2000. In 2009, the United Nations Development Programme (UNDP) had placed Haiti's ranking on the Human Development Index (a measure of long-term progress on three basic dimensions of human development: a long and healthy life, access to knowledge, and a decent standard of living) at 149th out of 187 nations (UNDP, 2009). By 2014, this ranking had dropped to 168th, placing Haiti in the bottom 10% of nations (UNDP, 2014). Finally, the capacity of the average Haitian citizen remained extremely low. Despite an infusion of the equivalent of $12,400 for every Haitian citizen, the gross national income per capita increased by only $142 during the first four years following the disaster (UNDP, 2014).
Thus, in terms of disaster risk management, the population's relatively unchanged level of hazard exposures, increasing level of human vulnerability, and dwindling capacity predict a continued high risk of disaster-related morbidity and
1424
mortality should an earthquake or similar disaster occur again.
1425
Summary Environmental disasters represent a significant health threat worldwide. The public health impacts of environmental disasters include deaths, injuries, communicable and noncommunicable diseases, toxic exposures, and a diminished ability to maintain adequate shelter, water supplies, sanitation, hygiene, public services, and utilities. In the environmental disasters of the past fifty years, natural disasters have greatly exceeded technological disasters in public health impacts, because of their greater frequency and scale. However, technological disasters result in greater morbidity and mortality among affected populations. While the hazards that cause disasters may vary greatly, the potential public health consequences and subsequent public health and medical needs of the population do not. A comprehensive approach to disaster risk management addresses not only the adverse health effects caused by disasters but also the root causes of these health effects.
1426
Key Terms affected people
People requiring immediate assistance during a period of emergency, including both the injured and the homeless.
all-hazards preparedness The idea that common capabilities can serve well in a variety of disaster situations, with variation based more on severity of the disaster (scale or degree of impact) than on disaster type.
capacity The combination of all the strengths, attributes, and resources available in a community, society, or organization that can be used to minimize morbidity and mortality following exposure to a hazard.
chemical releases Disasters caused by the uncontrolled release of a hazardous chemical.
cold weather A disaster can be caused by what is usually an abrupt onset of uncharacteristically cold weather, which may also be associated with loss of public utilities.
consequences In a disaster, adverse conditions caused by the disaster (as compared to impact, a measure of the degree of such consequences).
cyclones Weather phenomena featuring a central region of low pressure surrounded by air flowing in an inward spiral and generating maximum sustained wind speeds of 74 mph or more. Tropical cyclones—those that form over warm water—are called hurricanes in the Atlantic basin and the western Coast of Mexico, typhoons in the western Pacific, and cyclones in the Indian Ocean and Australasia.
damage Disaster-related loss of individual and societal assets or functionality, often expressed in terms of economic indicators.
disaster
1427
A “serious disruption of the functioning of a community or a society causing widespread human, material, economic or environmental losses that exceed the ability of the affected community or society to cope using its own resources” (UNISDR, 2009).
disaster risk The potential losses, in lives, health status, livelihoods, assets, and services, that c a particular community or a society could suffer during a disaster over some specified future time period.
droughts Disasters caused by a protracted period of deficient precipitation.
earthquakes Disasters caused by a sudden release of energy in the Earth's crust that creates seismic waves resulting in violent shaking of the ground.
emergency operations plan A plan, drawn up in advance, that describes who will do what, when, with what resources, and by what authority before, during, and immediately after an emergency.
environmental disasters Disasters that occur as a result of the presence of either naturally occurring or human-generated health hazards resulting in the creation of environments that are potentially harmful to human health.
explosions Disasters caused by a violent expansion of energetic materials in which the energy is transmitted outward as a shock wave. Causes may be intentional or unintentional in origin.
exposure Contact with a potentially dangerous hazard. Also, the people, property, systems, or other elements present in hazard zones that are thereby subject to potential losses.
fires Disasters caused by fires located in urban areas.
floods Disasters caused by the overflow of water into areas not normally submerged or by a stream that has broken its normal
1428
confines or by water that has accumulated due to lack of drainage.
hazard A dangerous phenomenon, substance, human activity, or condition that may cause loss of life, injury, or other negative health impacts; property damage; loss of livelihoods and services; social and economic disruption; and/or environmental damage.
heat waves Disasters caused by higher than normal ambient temperatures, of sufficient extremes to create a safety hazard for populations exposed to the heat.
hybrid disasters Disasters caused by a mixture of nearly simultaneously occurring natural and technological hazards, such as fires and hazardous material releases occurring after earthquakes.
impact The degree of severity associated with disaster consequences, often measured in terms of number of fatalities and injuries; functionality of critical facilities and community lifelines; property and environmental damage; economic, social, and political disruptions; and size of the area or number of people affected. (Impact is often erroneously used to mean consequences.)
Incident Command System (ICS) A standardized, on-scene, all-hazard incident management protocol under the NRF.
injury An adverse health condition, including the physical injuries, trauma, or illnesses requiring medical treatment as a direct result of a disaster.
landslides Disasters resulting from the sudden mass movement of ground surface material caused by gravity.
National Incident Management System (NIMS) A form of incident command system used in the United States to provide systematic, proactive guidance to departments and agencies at all levels of government, nongovernmental
1429
organizations, and the private sector. National Response Framework (NRF)
In the United States, the guiding principles of unified national response to disasters and emergencies. The NRF defines specific emergency support functions, including Emergency Support Function No. 8 (ESF-8), which addresses public health and medical issues.
natural hazards Natural processes or phenomena that may cause loss of life, injury or other health impacts, property damage, loss of livelihoods and services, social and economic disruption, or environmental damage.
poisoning Ingestion or inhalation of toxic substances. Poisoning can constitute a disaster when it occurs on a large scale, generally due to contamination of food products or exposure to commercial products containing hazardous materials.
radiation disasters Disasters caused by population exposure to high-energy radioactive materials.
recovery In the disaster context, the restoration, and improvement where appropriate, of facilities, livelihoods, and living conditions of disaster-affected communities, including efforts to reduce disaster risk factors.
resilience, disaster In the disaster context, the ability of nations, localities, institutions, communities, families, and individuals to absorb and recover from shocks such as earthquakes and heat waves, and to maintain living standards while adapting and transforming to long-term changes and uncertainty. Greater reslience connotes reduced vulnerability.
risk The probability that something will cause injury or harm.
risk acceptance A risk management technique based upon the notion of “acceptable risk”—the level of potential losses that a society or community considers acceptable given existing social, economic,
1430
political, cultural, technical, and environmental conditions. risk avoidance
A risk management technique aimed at the elimination of hazards, activities, and exposures that can cause potential losses
risk management Systematic activity directed toward assessing, controlling, and monitoring risks to minimize potential harm and loss.
risk reduction Risk management technique aimed at reducing the likelihood that a risk will occur.
risk retention Risk management technique aimed at accepting the loss when it occurs (e.g., acceptable risk) and focusing on response and recovery.
risk transfer Risk management technique aimed at shifting particular risks from one party to another, so that one party will obtain resources from the other after a disaster occurs, in exchange for social or financial benefits.
storm Any disturbed state of Earth's atmosphere, strongly implying severe weather. It may be marked by strong wind, thunder and lightning, heavy precipitation, and/or wind transporting some substance through the atmosphere (such as dust, snow, rain, or hail).
structural collapse A disaster resulting from the collapse or failure of man-made structures, such as buildings, large storage facilities, dams, and levees.
technological hazard A hazard originating from technological or industrial conditions, including accidents, dangerous procedures, infrastructure failures, or specific human activities, that may cause loss of life, injury, illness or other health impacts, property damage, loss of livelihoods and services, social and economic disruption, or environmental damage.
tornado A violently rotating column of air extending between, and in
1431
contact with, a cloud and the surface of the earth. Tornadoes are smaller and briefer in duration than cyclones but have higher wind speeds.
transportation disasters Disasters associated with means of air, ground, or water mass transportation, usually associated with malicious intent, human error, mechanical failure, or hazardous environmental conditions.
vulnerability Having characteristics and circumstances that make a community or individual, or a system or asset, susceptible to the damaging effects of a hazard.
wildfires Disasters caused by an uncontrolled fire in a rural or wilderness area of combustible vegetation.
Sources: A number of these definitions are based on UNISDR, 2009, or CRED, 2014.
1432
Discussion Questions 1. What are three major natural and technological hazards that
currently place your community at risk for disaster? What are the health risks presented, and how would you describe the community's preparedness?
2. Which groups of people and which facilities in your community are most vulnerable to the potential disasters you identified in Question 1? What characteristics make them vulnerable?
3. While the scale and the frequency of natural disasters are greater than those of technological disasters, technological disasters are far more hazardous when considering risk of morbidity and mortality among those populations affected. Why might this be?
4. The relationship between disasters and communicable diseases is frequently misconstrued. What are some of the reasons why this might be the case?
5. Who in your community is responsible for disaster planning and response? What plans and arrangements do they have in place, and how would you assess these plans and arrangements? Would you make any recommendations for improvement?
6. Disaster preparedness and response are fundamentally based in communities, and the most prepared, resilient communities enjoy many co-benefits. What, in some detail, are the various implications of this statement for your community?
7. Disaster epidemiology is essential to understanding the health aspects of disasters, but this field of epidemiology confronts some unique methodological challenges. What are some of these challenges? What suggestions do you have for ways to overcome them?
1433
References Allworth, A. (2005). Tsunami lung: A necrotizing pneumonia in survivors of the Asian tsunami. Medical Journal of Australia, 182(7), 364.
Bailey, G., & Walker, J. (2007). Heat-related disasters. In D. E. Hogan & J. L. Burstein (Eds.), Disaster Medicine (2nd ed., pp. 256– 265). Philadelphia: Lippincott Williams & Wilkins.
Bertazzi, P. (1989). Industrial disasters and epidemiology. Scandinavian Journal of Work, Environment & Health, 15, 85– 100.
Binder, S. (1989). Deaths, injuries and evacuations from acute hazardous materials releases. American Journal of Public Health, 79, 1042–1044.
Centers for Disease Control and Prevention. (1983). Outbreak of diarrheal illness associated with a natural disaster—Utah. Morbidity and Mortality Weekly Report, 32(50), 662–664.
Centers for Disease Control and Prevention. (1993). Injuries and illnesses related to Hurricane Andrew—Louisiana, 1992. Morbidity and Mortality Weekly Report, 42, 242–243, 249–251.
Centers for Disease Control and Prevention. (1998). Needs assessment following Hurricane Georges—Dominican Republic. Morbidity and Mortality Weekly Report, 48, 93–95.
Centers for Disease Control and Prevention. (2002). Tropical Storm Allison rapid needs assessment—Houston, Texas, June 2001. Morbidity and Mortality Weekly Report, 51(17), 365–369.
Centre for Research on the Epidemiology of Disasters. (2015). EM- DAT: The international disaster database. Brussels: Ecole de santé publique, Université catholique de Louvain. Retrieved from http://www.emdat.be
Chowdhury, M., Choudhury, Y., Bhuiya, A., Islam, K., Hussain, Z., Rahman, O.,…Bennish, M. (1992). Cyclone aftermath: Research and directions for the future. In H. Hossain, C. P. Dodge, & F. H. Abed
1434
(Eds.), From crisis to development: Coping with disasters in Bangladesh (pp. 101–133). Dhaka: University Press.
Cronin, S., & Sharp, D. (2002). Environmental impacts on health from continuous volcanic activity at Yasur (Tanna) and Ambrym, Vanuatu. International Journal of Environmental Health Research, 12, 109–123.
Davidson, J. R., & McFarlane, A. C. (2006). The extent and impact of mental health problems after disaster. Journal of Clinical Psychiatry, 67(Suppl. 2), 9–14.
Duclos, P., Sanderson, L., Thompson, F., Brackin, B., & Binder, S. (1987). Community evacuation following a chlorine release, Mississippi. Disasters, 11(4), 286–289.
Elliott, M., Wang, Y., Lowe, R., & Kleindorfer, P. R. (2004). Environmental justice: Frequency and severity of US chemical industry accidents and the socio-economic status of surrounding communities. Journal of Epidemiology and Community Health, 58, 24–30.
Federal Emergency Management Agency. (2010). CPG 101, developing and maintaining emergency operations plans, version 2. Retrieved from http://www.fema.gov/media- library/assets/documents/25975
Federal Emergency Management Agency. (2013). Local mitigation planning handbook. Retrieved from http://www.fema.gov/media- library-data/20130726-1910-25045- 9160/fema_local_mitigation_handbook.pdf
Floret, N., Viel, J., Mauny, F., Hoen, B., & Piarroux, R. (2006). Negligible risk for epidemics after geophysical disasters. Emerging Infectious Diseases, 12(4), 543–548.
Fussell, E., & Lowe, S. R. (2014). The impact of housing displacement on the mental health of low-income parents after Hurricane Katrina. Social Science & Medicine, 113, 137–144.
Galea, S., Brewin, C. R., Gruber, M., Jones, R. T., King, D. W., King, L. A., & Kessler, R. C. (2007). Exposure to hurricane-related stressors and mental illness after Hurricane Katrina. Archives of
1435
General Psychiatry, 64(12), 1427–1434.
Guha-Sapir, D., & van Panhuis, W. (2005). The Andaman Nicobar earthquake and tsunami 2004: Impact on diseases in Indonesia. Brussels: Centre for Research on the Epidemiology of Disasters.
Halpern, J., & Tramontin, M. (2007). Disaster mental health: Theory and practice. Belmont, CA: Thomson.
Hull, D., Grindlinger, G., Hirsch, E., Petrone, S., & Burke, J. (1985). The clinical consequences of an industrial aerosol plant explosion. Journal of Trauma, 25(4), 303–308.
International Federation of Red Cross and Red Crescent Societies. (2007). Disaster data. In World Disasters Report 2007 (pp. 172– 181). Geneva: Author. Retrieved from http://www.ifrc.org/en/publications-and-reports/world-disasters- report/wdr2007
Keim, M. (2002). Intentional chemical disasters. In D. E. Hogan & J. L. Burstein (Eds.), Disaster medicine (pp. 340–348). Philadelphia: Lippincott Williams & Wilkins.
Keim, M. (2006). Disaster preparedness. In G. R. Ciottone (Ed.), Disaster medicine (pp. 164–173). Philadelphia: Mosby Elsevier.
Keim, M. (2008). Building human resilience: The role of public health preparedness and response as an adaptation to climate change. American Journal of Preventive Medicine, 35(5), 508–516.
Keim, M., Humphrey, A., & Dreyfus, A. (2000). Situation assessment report involving the hazardous material disaster site at La Guaira Port, Venezuela. In CDC Report to Office of Foreign Disaster Assistance, US Agency for International Development.
Kessler, R. C., Galea, S., Gruber, M. J., Sampson, N. A., Ursano, R. J., & Wessely, S. (2008). Trends in mental illness and suicidality after Hurricane Katrina. Molecular Psychiatry, 13(4), 374–384.
Kim, S. (2006). Flood. In G. R. Ciottone (Ed.), Disaster medicine (pp. 489–491). Philadelphia: Mosby Elsevier.
King, R. V., Burkle, F. M., Jr., Walsh, L. E., & North, C. S. (2015). Competencies for disaster mental health. Current Psychiatry
1436
Reports, 17(3), 548.
Klinenberg, E. (2002). Heat wave: A social autopsy of disaster in Chicago. Chicago: University of Chicago Press.
Leong, K. J., Airriess, C. A., Li, W., Chen, A. C., & Keith, V. M. (2007). Resilient history and the rebuilding of a community: The Vietnamese American community in New Orleans East. Journal of American History, 94, 770–779.
Lillibridge, S. (1997). Industrial disasters. In E. K. Noji (Ed.), The public health consequences of disasters (pp. 354–372). New York: Oxford University Press.
Malilay, J. (1997). Floods. In E. K. Noji (Ed.), The public health consequences of disasters (pp. 287–300). New York: Oxford University Press.
Mehta, P. S., Mehta, A. S., Mehta, S. J., & Makhijani, A. B. (1990). Bhopal tragedy's health effects. JAMA, 264(21), 2781–2787.
Neria, Y., Galea, S., & Norris, F. H. (2009). Mental health and disasters. New York: Cambridge University Press.
Nozaki, E., Nakamura, A., Abe, A., Kagaya, Y., Kohzu, K., Sato, K., & Mochizuki, I. (2013). Occurrence of cardiovascular events after the 2011 Great East Japan Earthquake and tsunami disaster. International Heart Journal, 54(5), 247–253.
Reifels, L., Pietrantoni, L., Prati, G., Kim, Y., Kilpatrick, D. G., Dyb, G.,…O'Donnell, M. (2013). Lessons learned about psychosocial responses to disaster and mass trauma: An international perspective. European Journal of Psychotraumatology, 4(10), 3402.
Sanderson, L. (1992). Toxicologic disasters: Natural and technologic. In J. Sullivan & G. Krieger (Eds.), Hazardous materials toxicology: Clinical principles of environmental health (pp. 326– 331). Baltimore: Williams & Wilkins.
Sanderson, L. (1997). Fires. In E. K. Noji (Ed.), The public health consequences of disasters (pp. 373–396). New York: Oxford University Press.
1437
Sattler, D. N., Preston, A. J., Kaiser, C. F., Olivera, V. E., Valdez, J., & Schlueter, S. (2002). Hurricane Georges: A cross-national study examining preparedness, resource loss, and psychological distress in the U.S. Virgin Islands, Puerto Rico, Dominican Republic, and the United States. Journal of Traumatic Stress, 15, 339–350.
Silove, D., & Steel, Z. (2006). Understanding community psychosocial needs after disasters: Implications for mental health services. Journal of Postgraduate Medicine, 52(2), 121–125.
Thomas, D.S.K., Phillips, B. D., Lovekamp, W. E., Fothergill, A., & Toole, M. J. (Eds.). (2013). Social vulnerability to disasters (2nd ed.). Boca Raton, FL: CRC Press.
Toole, M. J. (1997). Communicable disease and disease control. In E. K. Noji (Ed.), The public health consequences of disasters (pp. 79–100). New York: Oxford University Press.
United Nations Development Programme. (2009). Human development report 2009. Retrieved from http://hdr.undp.org/en/content/human-development-report-2009
United Nations Development Programme. (2014). Human development report 2014. Retrieved from http://hdr.undp.org/sites/default/files/hdr14-report-en-1.pdf
United Nations Office for Disaster Risk Reduction. (2007). Hyogo Framework for Action 2005–2015: Building the resilience of nations and communities to disasters. Geneva: Author. Retrieved from http://www.unisdr.org/files/1037_hyogoframeworkforactionenglish.pdf
United Nations Office for Disaster Risk Reduction. (2009). Terminology on disaster risk reduction. Retrieved from http://www.unisdr.org/we/inform/terminology
U.K. Department for International Development. (2011). Defining disaster resilience: A DFID approach paper. London: Author. Retrieved from https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/186874/defining- disaster-resilience-approach-paper.pdf
Ursano, R. J., Fullerton, C. S., Weisaeth, L., & Raphael, B. (2011).
1438
Textbook of disaster psychiatry. New York: Cambridge University Press.
Venezuela seeks contractors for hazardous cleanup. (2000). Hazardous Substances Spill Report, 3(2).
Walker, B., & Salt, D. (2006). Resilience thinking: Sustaining ecosystems and people in a changing world. Washington, DC: Island Press.
Weiss, W., Kirsch, T., Doocy, S., & Perrin, P. (2014). A comparison of the medium-term impact and recovery of the Pakistan floods and the Haiti earthquake: Objective and subjective measures. Prehospital and Disaster Medicine, 29(3), 237–244.
World Bank. (2010). Natural hazards, unnatural disasters. Washington, DC: Author. Retrieved from http://www.gfdrr.org/sites/gfdrr.org/files/nhud/files/NHUD- Report_Full.pdf
World Health Organization. (2009) Vegetation fires (Fact sheet). Retrieved from http://www.who.int/hac/techguidance/ems/vegetation_fires/en
Zhang, L., Zhao, M., Fu, W., Gao, X., Shen, J., Zhang, Z.,…Chen, X. (2014). Epidemiological analysis of trauma patients following the Lushan earthquake. PLoS ONE, 9(5), e97416.
1439
For Further Information Frameworks and Programs
Grand Challenges for Disaster Reduction: http://sdr.gov/SDRGrandChallengesforDisasterReduction.pdf. The Subcommittee on Disaster Reduction, an element of the President's National Science and Technology Council, has developed a ten-year strategy called Grand Challenges for Disaster Reduction. It describes six grand challenges for disaster reduction and provides a framework for prioritizing the federal investments in science and technology.
Hyogo Framework for Action 2005–2015: Building the Resilience of Nations and Communities to Disasters: http://www.unisdr.org/we/inform/publications/1037. The Hyogo Framework for Action (HFA) is the key instrument for implementing disaster reduction that has been adopted by the member states of the United Nations. Its overarching goal is to build the resilience of nations and communities to disasters by achieving substantial reductions of disaster losses by 2015.
International Strategy for Disaster Reduction (ISDR): http://www.unisdr.org/eng/about_isdr/isdr-mission- objectives-eng.htm. The ISDR, which is implemented by the United Nations Office for Disaster Risk Reduction (UNISDR), aims at building disaster resilient communities by promoting increased awareness of the importance of disaster reduction as an integral component of sustainable development, with the goal of reducing human, social, economic, and environmental losses due to natural hazards and related technological and environmental disasters.
National Incident Management System of the Federal Emergency Management Agency: http://www.fema.gov/pdf/emergency/nims/NIMS_core.pdf. The National Incident Management System (NIMS) provides a systematic, proactive approach to guide departments and agencies at all levels of government, nongovernmental organizations, and the private sector to work seamlessly together before, during, and after emergencies.
1440
National Response Framework of the Federal Emergency Management Agency: http://www.fema.gov/pdf/emergency/nrf/nrf-core.pdf. The national response framework is a guide for conducting all responses to hazards in the United States. It is built on a scalable, flexible, and adaptable coordinating structure that aligns key roles and responsibilities across the nation, linking all levels of government, nongovernmental organizations, and the private sector.
National Voluntary Organizations Active in Disaster (National VOAD): http://www.nvoad.org. National VOAD is a forum where organizations can share knowledge and resources throughout the disaster cycle—preparation, response, and recovery—to help disaster survivors and their communities. Members of National VOAD come together as a coalition of nonprofit organizations that respond to disasters as part of their overall missions.
Preparedness and Emergency Response Learning Centers (PERLCs): http://www.cdc.gov/phpr/perlc.htm. A program of the Centers for Disease Control and Prevention that provides funding for fourteen PERLCs across the United States. PERLCs provide training to state, local, and tribal public health authorities in the area of public health preparedness and response.
Reducing Disaster Risk: A Challenge for Development: http://www.undp.org/cpr/disred/documents/publications/rdr/english/rdr_english.pdf The aim of this report from the United Nations Development Programme is to map out an agenda for change in the way disaster risk is perceived within the development community. It presents a range of opportunities for moving development pathways toward meeting the UN Millennium Development Goals by integrating disaster risk reduction into development planning.
Yokohama Strategy and Plan of Action for a Safer World: Guidelines for Natural Disaster Prevention, Preparedness and Mitigation: http://www.unisdr.org/we/inform/publications/8241. This document provides guidelines for natural disaster prevention,
1441
preparedness, and mitigation. It is divided into three sections: Part I describes the principles on which a disaster reduction strategy should be based, Part II is a plan of action agreed upon by all member states of the United Nations, and Part III gives some guidelines concerning the follow-up of action.
Guides and Handbooks Two general and comprehensive guides to disaster response are the following:
Ciottone, G. R. (Ed.). (2006). Disaster medicine. Philadelphia: Mosby Elsevier. This book is designed to serve as both a comprehensive text and a quick resource. Part 1 introduces the many topics of disaster medicine and management, with an emphasis on the multiple disciplines. Part 2 introduces the reader to every conceivable disaster scenario and the management issues surrounding each of them.
Landesman, L. (2005). Public health management of disasters: The practice guide. Washington, DC: American Public Health Association. Among the useful features of Dr. Landesman's guide is a recognition of the public health component of disasters—a neglected area. Frequently, emergency response focuses on environmental degradation or terrorism concerns but not on the basic health concerns of each disaster, which are at least as likely to pose challenges. In support of this idea, the author delineates various types of disasters and the public health implications of each.
Following is a listing of guidebooks commonly used during responses to environmental disasters.
Centers for Disease Control and Prevention. (2011). Public health emergency response guide for state, local, and tribal public health directors (Version 2.0). Available at http://www.bt.cdc.gov/planning/responseguide.asp
The Sphere Project. (2004). Humanitarian charter and minimum standards in disaster response. Available at www.sphereproject.org
UNICEF. (2005). Emergency field handbook: A guide for UNICEF staff. New York: Author.
1442
United Nations High Commissioner for Refugees. (2000). Handbook for emergencies (2nd ed.). Geneva: Author.
U.S. Department of Agriculture and U.S. Agency for International Development. (n.d.). Field operations guide for disaster assessment and response. Available for purchase at https://bookstore.gpo.gov/products/sku/001-300-00003-2? ctid=688
World Health Organization. (2003). Emergency response manual: Guidelines for WHO representatives in country offices in the Western Pacific region. Manila: Author.
World Health Organization. (2013). A systematic review of public health emergency operations centres (EOC) (WHO/HSE/GCR/2014.1). Geneva: Author. Available at www.who.int/ihr/publications/WHO_HSE_GCR_2014.1/en
World Health Organization, Regional Office for Africa. (2014). Standard operating procedures for coordinating public health event preparedness and response in the WHO African Region. Brazzaville: Author. Available at www.who.int/hac/techguidance/tools/standard_operating_procedures_african_region_en_2014.pdf? ua=1
World Health Organization and Pan American Health Organization. (2003). WHO-PAHO guidelines for the use of foreign field hospitals in the aftermath of sudden-impact disasters. San Salvador: PAHO, 2003.
1443
Chapter 25 Nature Contact
Howard Frumkin
Dr. Frumkin's disclosures appear in the front of this book, in the section titled “Potential Conflicts of Interest in Environmental Health: From Global to Local.”
1444
Key Concepts Humans have a deep-seated connection with the natural world—a connection that may have an evolutionary basis.
Benefits of nature contact may occur through a variety of mechanisms, such as stress reduction and attention restoration.
Nature also offers indirect benefits for health, such as providing settings that encourage healthy behaviors.
Nature contact may occur many ways, including contact with plants, views of landscapes, activities in natural settings, and contact with animals.
Evidence supports the idea that nature contact is a sound public health strategy.
There remain important gaps in knowledge, such as what constitutes an optimal “dose” of nature, that further research will need to address.
Much of this book is about hazards. We learn that contaminated water can cause diarrheal diseases (Chapter 16), that air pollution can cause respiratory disease (Chapter 13), that poorly designed roadways can result in injuries (Chapters 15 and 23), that degraded urban environments may encourage violence (Chapter 9). Clearly, environmental exposures can threaten health—and this is a central focus of the environmental health field.
But the environment, and in particular the natural world, may also enhance health. One example, the concept of ecosystem services, is explored in Chapter 2 (Kareiva, Tallis, Ricketts, Daily, & Polasky, 2011); many pharmaceuticals derive from plants (a compelling argument for preserving biodiversity). Another example is even more intuitive: contact with the natural world may directly benefit health. That idea is the starting point for this chapter.
1445
The Links Between Nature and Human Health Many people appreciate a walk in the park, the sound of a bird's song, or the sight of ocean waves lapping at the seashore. In the words of University of Michigan psychologist Rachel Kaplan (1983, p. 155): “Nature matters to people. Big trees and small trees, glistening water, chirping birds, budding bushes, colorful flowers— these are important ingredients in a good life.” Cross-cultural studies suggest that these preferences are so widely held as to be nearly universal. In recent years researchers have asked whether these are more than simply aesthetic preferences. If people find tranquility in certain natural environments—a sense of comfort, restoration, even healing—then contact with nature might be an important component of health and well-being.
From an evolutionary perspective, a deep-seated connection with the natural world would be no surprise. Primate evolution began at least 65 million years ago, and the first hominids appeared as much as 5 million years ago. Two million years ago australopithecines were fashioning primitive stone tools and hunting in bands on the grassy savannas of Africa. Homo habilis probably appeared 2 or 3 million years ago, and our immediate predecessor, Homo erectus, appeared about 1.5 million years ago. Human history as we now know it began during the Neolithic period, just 10,000 to 15,000 years ago, when the last great ice age ended and climate and ecology came to resemble those of our current world. Our ancestors—true Homo sapiens—began to form settlements, cultivate crops, domesticate animals, dig mines, and even make art. If the last 2 million years of our species' history were scaled to a single human lifetime of seventy years, then the first humans would not have begun settling into villages until eight months after their 69th birthday. Some people—indigenous groups in Australia, South America, the Pacific Islands, and elsewhere—would remain hunter- gatherers until a day or two before turning 70. We have broken with long-established patterns of living rather late in our life as a species.
For the great majority of human existence, human lives have been embedded in the natural environment. Those who could navigate it
1446
well—who could smell the water, find the plants, follow the animals, recognize the safe haven—must have enjoyed survival advantages. According to biologist E. O. Wilson (1993, p. 32), “It would…be quite extraordinary to find that all learning rules related to that world have been erased in a few thousand years, even in the tiny minority of peoples who have existed for more than one or two generations in wholly urban environments.” Wilson hypothesized the existence of biophilia, “the innately emotional affiliation of human beings to other living organisms” (Wilson, 1984, p. 31). Building on this theory, others have postulated an affinity for nature that goes beyond living things to include streams, ocean waves, and wind (Heerwagen & Orians, 1993).
The human connection to nature and the idea that this connection might be a component of good health have a long history in philosophy, art, and popular culture (see, e.g., Nash, 1982; McLuhan, 1994). The New England transcendentalists, almost two centuries ago, argued that the human spirit was rooted in nature, and a leading exponent, Henry David Thoreau, wrote of the “tonic of wildness.” A century later the conservationist John Muir (Figure 25.1) observed, “Thousands of tired, nerve-shaken, over-civilized people are beginning to find out that going to the mountains is going home; that wilderness is a necessity; and that mountain parks and reservations are useful not only as fountains of timber and irrigating rivers, but as fountains of life” (Fox, 1981, p. 116).
1447
Figure 25.1 John Muir ({–1914) Was a Naturalist and Conservationist Whose Writings Had a Profound Influence on American Attitudes Toward Nature
Source: Library of Congress, Prints and Photographs, n.d.
But the history of human culture has also in many ways been the history of separation from nature. David Abram (1996) argues that this separation began with the very development of language, which replaced nature images with abstract symbols as central elements of human cognition and communication. Although our ancestors lived in close proximity to nature, their struggle to survive was in many ways a struggle to vanquish nature, or at least to shape it to their ends and to control its most drastic exigencies. The book of Genesis,
1448
which dates from about 3,000 years ago, included the often- repeated divine mandate, “Be fruitful, and multiply, and replenish the earth, and subdue it: and have dominion over the fish of the sea, and over the fowl of the air, and over every living thing that moveth upon the earth.” (Contemporary environmental thinkers have imputed a gentler meaning to this passage, emphasizing stewardship rather than conquest.) The ancient Greeks abstracted human learning from nature. In the Platonic dialogue Phaedrus, Socrates finds himself outside the city walls, and grumbles to his companion, “I'm a lover of learning, and trees and open country won't teach me anything, whereas men in town do” (Hamilton & Cairns, 1961, p. 479). For Socrates, wisdom and comfort were to be found in human society, apart from, and above, the world of nature. Subsequent developments have led most people, at least in wealthy nations, to live lives that are effectively insulated from the natural world. In the words of environmental historian Roderick Nash (1982, p. 267), “For thousands of years after our race opted for a civilized existence, we dreamed of and labored toward an escape from the anxieties of a wilderness condition only to find, when we reached the promised land of supermarkets and air conditioners, that we had forfeited something of great value.”
Through what mechanisms might nature contact benefit health? Some of the answer may lie in psychological explanations. In addition, nature contact may facilitate healthy behaviors such as physical activity and socializing. Finally, the natural environment provides services, such as improving air quality, that promote health.
Environmental Psychology and Nature Contact Environmental psychology offers three perspectives that shed light on the benefits of nature contact: attention restoration, stress reduction, and child development.
Attention Restoration Kaplan and Kaplan (1989) emphasized the importance of directed attention, the ability to focus and block competing stimuli during purposeful activity. They proposed that people can develop attentional fatigue from excessive concentration, resulting in memory loss, diminished ability to focus, and greater impatience
1449
and frustration in interpersonal interactions. Moreover, they suggested that contact with nature could be restorative—renewing attention and improving cognitive abilities. This construct is called attention restoration (S. Kaplan, 1995; Kaplan & Berman, 2010). Kaplan and Kaplan (1989) noted four aspects of restorative environments: fascination (effortless interest or curiosity); a sense of being away from one's usual setting, extent, or scope (being part of a larger whole); and compatibility with one's preferences.
Research has supported the link between nature contact and attention restoration. For example, one study (Tennessen & Cimprich, 1995) showed that college students with more natural views from their dormitory windows had higher levels of attention and cognitive function than those without. A study of apartment dwellers (S. Kaplan, 2001) showed that those with window views of landscaped lawns and gardens, trees, farms, and fields scored higher on measures of effective functioning (including “focused,” “ effective,” and “attentive”) and lower on measures of distraction (including “forgetful,” “disorganized,” and “difficult to finish things you have started”) than those without such views. Other research shows that people with illnesses that may impair their attention or cognitive performance, from breast cancer to depression, benefit from contact with nature in this way. Such results have been demonstrated in children as well. For example, children who had moved from substandard housing to “greener” homes (with more views of nearby nature) were found to have higher levels of cognitive functioning after the move than before (Wells, 2000), girls in a low-income housing project were found to have greater self- discipline if they had nature views from home than did girls in the same project who lacked such views (Faber Taylor, Kuo, & Sullivan, 2002), and children with attention deficit/hyperactivity disorder were rated by their parents as having reduced symptoms after playing in relatively natural settings, compared to their behavior after playing in built outdoor and indoor settings (Kuo & Taylor, 2004). Nature contact may be beneficial, at least in part, through attention restoration.
Stress Reduction Nature contact may also function through stress reduction. This is an intuitive notion; many people choose vacations in beautiful
1450
natural locations, probably expecting their stress to diminish. Again, research supports this notion. For example, Ulrich et al. (1991) exposed undergraduate students to a stressful film, followed by a variety of videotapes of natural and urban settings. The students' stress recovery, as measured by self-report and cardiovascular measurements, was significantly faster when they viewed the nature scenes. In recent studies using functional magnetic resonance imaging, people who were brought up in cities and/or currently lived in cities showed enhanced brain activity in regions related to stress response, such as the anterior cingulate cortex, compared to rural counterparts (Lederbogen et al., 2011). Among both children (Wells & Evans, 2003) and adults (van den Berg, Maas, Verheij, & Groenewegen, 2010a), individuals who live in greener areas react to stressful life events with significantly less psychological distress than those in less green areas. Green schoolyards function as “havens from stress” for children (Chawla, Keena, Pevec, & Stanley, 2014). Results such as these suggest that nature contact may function, at least acutely, to mitigate stress. In turn, stress reduction, perhaps together with attention restoration and/or direct antidepressant effects (Berman et al., 2012; Cohen- Cline, Turkheimer, & Duncan, 2015), may yield cognitive and emotional benefits (Bratman, Hamilton, & Daily, 2012).
Child Development Nature contact might be healthy in a third way: by playing a role in wholesome child development. Psychologists and others (Nabhan & Trimble, 1994; Kahn & Kellert, 2002; Louv, 2005) have argued that children's ability to develop perceptual and expressive skills, imagination, moral judgments, and other attributes is greatly enhanced by contact with nature. For example, studies of Barcelona schoolchildren found that playtime in green settings, living near green space, and visiting “bluespace” (lakes and beaches) were associated with fewer emotional symptoms, fewer conduct problems, less hyperactivity/inattention, and fewer peer relationship problems (Amoly et al., 2014), and that green space near schools was associated with improved cognitive development (Dadvand et al., 2015). Chapter 11 introduces the concept that children have windows of vulnerability to toxic exposures; children may also have developmental windows during which nature contact fills important needs (Text Box 25.1).
1451
Text Box 25.1 Getting Kids Outside: A Public Health Strategy? Do children have a special need to connect with nature? Child development theory suggests that this may be the case. As children mature, they have a growing need to explore and manipulate their environments (Heerwagen & Orians, 2002). Children's affinity for “secret spaces”—hidden spots under low tree canopies or within clumps of shrubbery—may exemplify this process (Kirkby, 1989). Contact with nature offers children benefits as diverse as stress reduction (Wells & Evans, 2003) and improved cognitive function (Wells, 2000).
In an influential 2005 book, Last Child in the Woods, author Richard Louv called attention to a problem he dubbed nature deficit disorder—not a formal diagnosis but the notion that contemporary children suffer from a lack of unstructured play and exploration in natural settings. This idea resonated widely and helped spur federal, state, and local initiatives to reconnect children with nature. In many states and cities, community and environmental groups launched Leave No Child Inside initiatives designed to reconnect children with nature. Nationally, the Children and Nature Network (www.childrenandnature.org) was formed to coordinate and support these efforts. Several state legislative initiatives emerged, including a series of bills in Washington State, from 2006 to 2015, that mandated a study of the effects of outdoor education, with a priority on underserved children, and followed it with funding for environmental education programs; the Outdoor Bill of Rights in California in 2007; and the No Child Left Inside Act in New Mexico in 2008 (funded by a tax on televisions and video games). A federal No Child Left Inside Act has been proposed several times since the mid-2000s (although not promulgated); it would amend federal education law to provide for training teachers in environmental and outdoor education, funding environmental education programs in schools, and
1452
promoting environmental literacy.
The rapid spread of these initiatives suggests that nature contact for children may become a mainstream strategy in environmental health.
Nature as a Setting for Healthy Behaviors
Physical Activity Physical activity is a powerful predictor of good health, so settings that encourage physical activity are likely to promote health. As described in Chapter 15, a range of environmental factors predict how active people are, both in the ways they travel (active transportation) and in their leisure time activities; these factors include pedestrian and bicycle infrastructure, proximity of destinations, perceived safety, and more. Green space is another such factor; it may encourage physical activity by providing attractive settings. Much research suggests that natural features such as street trees, nature views, and proximity to parks promote physical activity. However, not all studies support this association, perhaps because plentiful green space is sometimes associated with low-density communities, meaning that residents have longer distances to destinations and more automobile dependence (Hartig, Mitchell, de Vries, & Frumkin, 2014; Bancroft et al., 2015). Among children, being outside predicts higher levels of physical activity (e.g., Cleland et al., 2008; Schaefer et al., 2014); contact with nature may be an important part of this effect.
Social Connectedness Parks and similar natural settings may encourage the development of social ties. This may be mediated through one of the mechanisms noted above; for example, being with other people in a low-stress setting may facilitate social bonding. Evidence suggests that parks promote social capital in neighborhoods (Kaźmierczak, 2013; Holtan, Dieterlen, & Sullivan, 2014; Kemperman & Timmermans, 2014) and that people who live in green neighborhoods feel less lonely than people who live in less green neighborhoods (Maas et al., 2009). A study in Zurich found that children who regularly played outside in natural areas had more than twice as many
1453
playmates as children restricted to indoor play because of heavy nearby traffic (Hüttenmoser, 1995)—a benefit that extended to their parents as well. Interestingly, the social connectedness provided by nature may not relate only to other people. There is a social quality to pet ownership, both in the relationship between pet owners and their pets (pets are called companion animals for a reason) and in the way that pet owners interact with other people through their pets (McConnell, Brown, Shoda, Stayton, & Martin, 2011; Stanley, Conwell, Bowen, & Van Orden, 2014). Some of the health benefits of pet ownership may relate to these social ties.
Ecosystem Services and Health
Air Quality Trees, shrubs, and other vegetation may affect ambient air quality, which in turn affects human health and well-being. Interestingly, the effects are not all positive. Trees and other vegetation effectively reduce levels of some pollutants, including gases and particulate matter (Escobedo, Kroeger, & Wagner, 2011). However, these are generally not large effects (Nowak, Hirabayashi, Bodine, & Greenfield, 2014). Indoors, plants can be effective at removing contaminants from the air, especially if the right species are chosen (Yoo, Kwon, Son, & Kays, 2006). On the negative side, trees may contribute to air pollution by releasing hydrocarbons such as pinenes and terpenes, precursors of ozone and secondary organic aerosols (Sartelet, Couvidat, Seigneur, & Roustan, 2012). Some trees and plants release pollen, aggravating allergies (Cariñanos & Casares-Porcel, 2011). Finally, trees can improve air quality indirectly. During warm weather, trees help cool places down by offering shade and through the cooling effects of evapotranspiration. This in turn reduces both ozone formation and energy demand, which, in areas served by coal-fired power plants, reduces air pollution derived from coal combustion.
Other Services Nature provides a range of other ecosystem services that benefit people. For example, in cities, trees help counteract the urban heat island effect and provide cooling during heat waves, provide stormwater management that helps prevent flooding, and provide
1454
noise reduction. In addition, nearby trees, parks, and open space increase residential property values, enabling communities to collect the tax revenues needed to maintain such amenities (Crompton, 2005).
These direct and indirect mechanisms suggest a range of ways in which nature may benefit health and well-being. Where and how does nature contact occur, and what are the implications for public health policy?
1455
Domains of Nature Contact Evidence that our contacts with nature can be beneficial to health is available from at least four aspects of the natural world—animals, plants, landscapes, and wilderness experiences.
Animals Animals have played a prominent part in human life since prehistoric times (Clutton-Brock, 1981; Caras, 1996). According to the Association of Zoos and Aquariums (www.aza.org), over 175 million people visit zoos and aquariums in the United States each year—more than attend professional football, baseball, hockey, and basketball games combined. About two thirds of U.S. households have a pet: about 44% of households have one or more dogs and about 35% have one or more cats, corresponding to national populations of about 78 million dogs and 86 million cats (American Pet Products Association, 2015) (Figure 25.2). More than 90% of the characters used in preschool books to teach children language and counting are animals (Kellert, 1993, p. 52). Numerous studies have established that household animals are considered family members; people talk to their pets as if they were human, carry their photographs, buy them birthday presents, and share their bedrooms with them (Beck & Katcher, 1983; Fleishman-Hillard Research, 2007). Half of pet owners report that if faced with financial hardship, they would cut back on groceries, entertainment, and household goods before they would cut back on pet care (Fleishman-Hillard Research, 2007). Among pet owners, 50% of adults and 70% of adolescents confide in their pets (Beck & Meyers, 1996). During disasters, many pet owners refuse to evacuate without their pets (as was seen during Hurricane Katrina, for example), and those who lose their pets suffer considerable mental distress (Hunt, Al-Awadi, & Johnson, 2008).
1456
Figure 25.2 The Human-Animal Bond Source: Addicks, 2008. Photo © 2008 Trisha Addicks.
A wide body of evidence links animals with human health (Friedman & Son, 2009; Natterson-Horowitz & Bowers, 2013; Cherniack & Cherniack, 2014; Matchock, 2015). Some of the evidence relates to pet ownership, and some relates to the use of animals in therapy, for conditions as diverse as autism spectrum disorders, loneliness, dementia, and having been the victim of sexual abuse. Results generally suggest benefits, although many reviewers comment that the available research lacks sufficient rigor and leaves important questions unanswered. Human-animal interaction (HAI) seems to be health promoting for child development (Endenburg & van Lith, 2011), cardiovascular health (Levine et al., 2013), healthy aging (Cherniack & Cherniack, 2014), and in other ways. And human-animal interaction seems to improve outcomes in a variety of conditions, such as autism spectrum disorder (Muñoz Lasa, Ferriero, Brigatti, Valero, & Franchignoni, 2011; O'Haire, 2013), stress (Beetz, Uvnäs-Moberg, Julius, & Kotrschal, 2012), and even HIV infection (Saberi, Neilands, & Johnson, 2014).
Several examples are instructive. In a study in a Melbourne cardiovascular disease risk clinic, nearly 6,000 patients were divided into those who owned pets and those who did not. The pet
1457
owners had lower systolic blood pressure, cholesterol, and triglycerides than the non–pet owners, an effect that reached statistical significance among men but not women. These findings could not be explained by differences in exercise levels (say, from dog walking), in diet, in social class, or in other confounders (Anderson, Reid, & Jennings, 1992). In a study at clinical sites across the United States and Canada, 369 survivors of myocardial infarction were followed for one year. Of these, 112 owned pets and 257 did not. The dog owners had a one-year survival rate six times higher than that of the non–dog owners, and this benefit was not due to physiological differences. (Cat owners showed no such advantage, perhaps reflecting the adage “dogs have owners and cats have staff.”) (Friedmann & Thomas, 1995). In a study of 240 married couples, half with pets and half without, participants were exposed to two stressors (a mathematical task and immersing a hand in cold water) under one of four conditions: alone, with a companion (the pet for pet owners and a friend for non–pet owners), with the spouse, or with both companion and spouse. Pet owners had lower baseline heart rate and blood pressure, lower cardiovascular reactivity to the stressors, and faster recovery, and the advantage was most marked when the pet was present during the testing (Allen, Blascovich, Wendy, & Mendes, 2002).
Investigators in Cambridge, England, followed seventy-one adults who had just acquired pets and compared them with twenty-six petless controls over a ten-month period. Within a month of acquiring the pet the pet owners showed a statistically significant decrease in minor health problems. In the dog owners (but not the cat owners) this improvement was sustained for the entire ten months of observation (Serpell, 1991). In another study, this one in the United States, 938 Medicare enrollees were divided into pet owners and non–pet owners. The pet owners, especially the dog owners, had fewer physician visits than non–pet owners. Moreover, stressful life events triggered more doctor visits among those without pets but not among pet owners, suggesting that owning a pet helped mediate stress (Siegel, 1990). (Some of the results in these examples were not replicated by other studies, emphasizing that there is more to learn about these effects [McNicholas et al., 2005].)
Animal-assisted therapy has been utilized in treating a range of
1458
conditions, including pervasive developmental disorders, cardiovascular disease, psychiatric disorders, chronic pain, Alzheimer's disease, and cancer (Muñoz Lasa et al., 2011; D. A. Marcus, 2013). For example, in a Virginia psychiatric hospital, 230 patients with mood disorders, schizophrenia, substance abuse disorders, and other diagnoses were treated with both a session of animal-assisted therapy (featuring interaction with a dog) and a session of conventional recreational therapy, using a crossover design. Both therapies reduced the patients' anxiety levels as measured by the State-Trait Anxiety Inventory, but in all diagnostic groups except the group with mood disorders, the animal-assisted therapy achieved substantially greater reductions (Barker & Dawson, 1998).
The mechanisms of benefit from animal contact are unclear. They may relate to the link to nature (through stress reduction and/or attention restoration), to companionship (with other pet owners or with the animals themselves), or to other factors (Beck & Katcher, 1983; Wood, Giles-Corti, & Bulsara, 2005; Wood, Giles-Corti, Bulsara, & Bosch, 2007). The relationship with a pet may even involve mirror neuron activity (Toohey, McCormack, Doyle-Baker, Adams, & Rock, 2013). Whatever the mechanism, the bulk of the evidence supports the conclusion of animal researchers Alan Beck and N. Marshall Meyers (1996, p. 249): “Preserving the bond between people and their animals, like encouraging good nutrition and exercise, appears to be in the best interests of those concerned with public health.”
Plants People feel good around plants. Survey research (and subjective experience) confirms that people like access to plants at home, at work, at school, in their gardens, and in their neighborhoods (Lohr, 2010). Access to plants has been credited with a range of benefits, such as stress reduction, improved performance, and feelings of contentment and happiness. Four kinds of encounters with plants are instructive: while indoors, gardening, in neighborhoods, and in therapeutic settings.
Indoor exposure to plants may occur at work, at home, and in classrooms. At work employees report that plants make them feel calmer and more relaxed, and that an office with plants is a more
1459
desirable place to work (although work performance does not necessarily improve) (Larsen, Adams, Deal, Kweon, & Tyler, 1998; Pearson-Mims & Lohr, 2000). Research in schools yields similar findings. In a study of a junior high school (Han, 2009), students with plants in their classrooms reported stronger feelings of preference, comfort, and friendliness; had less sick leave; and had less misbehavior than students in a control classroom, and in a study of university students (Doxey, Waliczek, & Zajicek, 2009), those with plants in their classrooms rated their learning and their instructor's performance significantly higher than did students in control classrooms. In neither case did academic performance improve with the presence of plants.
Gardening, which involves intimate contact with plants, also seems to offer benefits. For example, in the Dubbo Study, a longitudinal cohort study of 2,805 elderly people in New South Wales, 56% of men and 41% of women gardened daily. Compared with those not gardening, daily gardeners enjoyed a 40% lower risk of admission for dementia, and those gardening weekly or less often had an 11% reduction (Simons, Simons, McCallum, & Friedlander, 2006). While some of the benefit likely comes from physical activity (Nicklett, Anderson, & Yen, 2014) and the social aspects of gardening, additional benefit may come directly from contact with plants. Community gardening has been studied as a public health strategy, as explored in Text Box 25.2.
1460
Text Box 25.2 Community Gardens Community gardens are an increasingly common initiative in many communities, especially in urban neighborhoods where people otherwise have little or no access to land for cultivation (Figure 25.3). Community gardens are parcels of land that are typically community managed, and individuals or families are allocated patches within the garden for their own use. Participants grow vegetables, herbs, flowers, and other edible or ornamental plants. Among the benefits claimed for community gardens are that they help to
Figure 25.3 A Community Garden Community gardens offer participants, including urban residents, the opportunity to connect with nature, learn valuable skills, and raise some of their own food.
Source: Courtesy of Council on the Environment of New York City.
Build a sense of community among participants (including socialization for new immigrants).
Restore blighted neighborhoods.
1461
Provide improved access to fresh, nutritious, affordable food.
Build skills among participants.
Improve mental health and well-being.
Promote physical activity.
Reduce stress.
Few public health interventions offer such a range of benefits at such low cost and with so few downsides.
Sources: Armstrong, 2000; Blair, Giesecke, & Sherman, 1991; Schukoske, 2000; van den Berg, van Winsum-Westra, de Vries, & van Dillen, 2010b; Harris, Minniss, & Somerset, 2014.
At the neighborhood scale, contact with plants comes from nearby parks and green spaces and from tree canopies over streets— features comprising what are sometimes called green neighborhoods. Trees hold a special place in many people's hearts. Psychologist Michael Perlman (1994) has written of the psychological power of trees, as evidenced by mythology, dreams, and self-reported emotional responses, and the poet Joyce Kilmer, in 1913, famously (and humbly) wrote, “I think that I shall never see / A poem lovely as a tree.” Green neighborhoods, generally measured by the extent of tree canopy, have been associated with positive health outcomes across the lifespan: improved birth outcomes (Dadvand et al., 2012), lower body mass index and slower weight gain in children (Bell, Wilson, & Liu, 2008), improved social ties (Holtan et al., 2014), more resilience to stressful life events (van den Berg et al., 2010a), better self-reported health (Carter & Horwitz, 2014), and longer life expectancy among elders (Takano, Nakamura, & Watanabe, 2002). In a study in Toronto (Kardan et al., 2015), investigators found that after controlling for relevant risk factors, greener neighborhoods were associated with better self- reported health and lower rates of cardiovascular risk factors, cardiovascular disease, and diabetes. In that study an increment of ten trees per city block improved self-reported health to the same extent as a $10,000 increase in income or being seven years younger!
The long-standing view that plant contact is good for health has led to therapeutic approaches such as healing gardens and
1462
horticultural therapy. The great neurologist Oliver Sacks highlighted this approach in a memorable passage in his 1984 account of recovery from a serious leg injury, A Leg to Stand On. After more than two weeks in a small hospital room with no outside view, and a third week on a dreary surgical ward, he was finally taken out to the hospital garden:
This was a great joy—to be out in the air—for I had not been outside in almost a month. A pure and intense joy, a blessing, to feel the sun on my face and the wind in my hair, to hear birds, to see, touch, and fondle the living plants. Some essential connection and communion with nature was re-established after the horrible isolation and alienation I had known. Some part of me came alive, when I was taken to the garden, which had been starved, and died, perhaps without my knowing it [pp. 133–134].
Sacks credited his garden contact with an important role in his recovery and mused that perhaps more hospitals should have gardens or even be set in the countryside or near woods. In fact, gardens have been a feature of hospitals and other health care settings since ancient times, and interest has resurged in recent years (C. C. Marcus, 2007; Marcus & Sachs, 2013).
The therapeutic potential of plants is also harnessed in a treatment approach called horticultural therapy (Simson & Straus, 2003; Haller & Kramer, 2006). Horticultural therapy is used not only in hospitals but also in community-based programs, geriatrics programs, prisons, developmental disabilities programs, and special education (Mattson, 1992). In prisons, one observer noted that gardening has a “strangely soothing effect,” making “pacifists of potential battlers” (Neese, 1959) and seemingly decreasing the numbers of assaults among prisoners (Hunter, 1970, reported in Lewis, 1990). Horticultural therapy has been used to treat dementia, severe mental illness such as schizophrenia, bipolar disorder, and major depression, and in cardiac and stroke rehabilitation. Although rigorous evidence is scarce, some studies support the efficacy of horticultural therapy (Annerstedt & Währborg, 2011; Kamioka et al., 2014). For example, researchers at New York's Rusk Institute of Rehabilitation Medicine compared horticultural therapy with routine patient education in cardiac rehabilitation patients. Horticultural therapy significantly reduced
1463
both the heart rate and the total mood disturbance as measured by the Profile of Mood States (POMS) inventory, whereas patient education classes did not (Wichrowski, Whiteson, Haas, Mola, & Rey, 2005). Such evidence offers support for the hypothesis that proximity to plants, like proximity to animals, may in some circumstances enhance health.
Landscapes Natural landscapes may also offer health benefits. Returning to an evolutionary perspective, human history probably began on the African savanna, a region of open grasslands punctuated by scattered copses of trees and denser woods near rivers and lakes. If this sounds like the choicest real estate in most cities and towns, that may not be a coincidence. As E. O. Wilson (1984, pp. 109–110) wrote, “certain key features of the ancient physical habitat match the choices made by modern human beings when they have a say in the matter”—a pattern that repeats in parks, cemeteries, golf courses, and lawns. “It seems that whenever people are given a free choice,” Wilson observed, “they move to open tree-studded land on prominences overlooking water.”
Could evolution have selected for certain landscape preferences? Perhaps. A crucial step in the lives of most organisms, including humans, is selection of a habitat. If a creature gets into the right place, everything is likely to be easier. “Habitat selection depends on the recognition of objects, sounds, and odors to which the organism responds as if it understood their significance for future behavior and success” (Heerwagen & Orians, 1993, p. 140). For example, many birds use patterns of tree density and vertical arrangement of branches as primary settling cues; presumably these cues correlate with crucial information about such benefits as food availability and concealment from predators. For early humans a place with an open view would have offered opportunities to spot food and shelter and to avoid predators. But not too open a view: clumps of trees would offer hiding places in a pinch and, like streams and lakes, might also signal the presence of prey for the hunter (Ulrich, 1993). Going further, perhaps the ability to identify relaxing, restorative settings, which could also improve the capacity to recover from fatigue and stress, could also have been adaptive (Kaplan & Kaplan, 1989; Ulrich, 1993). If you can run away from a saber-toothed tiger, your
1464
survival is enhanced. But if, having run away, you can then get to a peaceful place, relax, and gather your strength, that may further enhance your survival. Perhaps individuals who chose such settings gained a survival advantage (Ulrich, 1993).
There is considerable evidence that people's aesthetic preferences conform to this prediction (Ward Thompson, 2011). As suggested above, when offered a variety of landscapes, people react most positively to savanna-like settings, with moderate to high depth or openness, relatively smooth or uniform-length grassy vegetation or ground surfaces, scattered trees or small groupings of trees, and water (Schroeder & Green, 1985; Kaplan, Kaplan, & Ryan, 1998). Notably, these findings emerge cross-culturally, in studies of North Americans, Europeans, Asians, and Africans (see, e.g., Hull & Revell, 1989; Purcell, Lamb, Mainardi Peron, & Falchero, 1994; Korpela & Hartig, 1996).
There is a great deal of research on people's reactions to landscapes. People viewing savanna–like settings report feelings of peacefulness, tranquility, or relaxation (Ulrich, 1993), decreased fear and anger, and enhanced positive affect (Honeyman, 1992). Moreover, viewing nature scenes is associated with enhanced mental alertness, attention, and cognitive performance, as measured by tasks such as proofreading and by formal psychological testing (Tennessen & Cimprich, 1995; Cimprich & Ronis, 2003). (Also see Text Box 25.3.)
1465
Text Box 25.3 Nature Contact in the Inner City A landmark series of studies at the University of Illinois Landscape and Human Health Laboratory focused on nature contact in a rarely studied setting: inner-city housing projects. Investigators took advantage of a natural experiment at Chicago's Robert Taylor Homes. This complex, which no longer stands, consisted of twenty-eight identical high-rise buildings arrayed along a three-mile urban tract bounded by busy roadways and railway lines. Some of the buildings were surrounded by pleasant stands of trees, whereas others opened onto barren stretches of ground (Figure 25.4). Residents were in essence randomly assigned to a building with one landscape type or the other, because assignment depended on where a vacancy existed when their names came up on the housing authority list. The research compared residents of the buildings with and without trees, and was limited to those who lived on the lower floors (to ensure that participants in buildings surrounded by trees did have tree views from their windows).
1466
1467
Figure 25.4 Robert Taylor Homes, Chicago: An Aerial View, the Buildings Without Nearby Trees, and the Buildings with Nearby Trees
In use from 1962 to 1997, this project was home to as many as 27,000 people. It provided a setting for studying the effects of nearby nature on residents' health and well-being.
Source: William Sullivan, University of Illinois. Used with permission.
This research yielded surprising and important findings. Compared to living in a building with barren surroundings, living in a building with trees was associated with
Higher levels of attention and greater effectiveness in managing major life issues (Kuo, 2001)
Substantially lower levels of aggression and violence (both as victims and as perpetrators) among women (Kuo & Sullivan, 2001a)
Lower levels of reported crime (Kuo & Sullivan, 2001b)
Higher levels of self-discipline (as measured by tests of concentration, impulse inhibition, and delay of gratification) among girls (but not among boys) (Taylor, Kuo, & Sullivan, 2002)
These findings suggest that nature contact in otherwise deprived urban environments—even relatively simple forms of contact such as having trees outside an apartment building —can offer powerful benefits to the people who live there.
These reactions seem to transfer to health outcomes as well. For example, consider four different vantage points for viewing landscapes: from a workplace, a prison, or a hospital room or during a medical procedure.
In a workplace study, 615 office workers were surveyed regarding their work satisfaction, levels of frustration, enthusiasm for work, patience, and life satisfaction. Each of these outcomes was significantly better among those with views of nature through their windows (Kaplan, 1993).
In 1981, Ernest Moore, a University of Michigan architect, took advantage of a natural experiment at the State Prison of
1468
Southern Michigan, a massive depression-era structure. Half the prisoners occupied cells along the outside wall, with a window view of rolling farmland and trees, and the other half occupied cells that faced the prison courtyard. Assignment to one or the other kind of cell was random. Compared to the prisoners in the exterior cells, the prisoners in the inside cells had a 24% higher frequency of sick call visits. Moore could not identify any design feature to explain this difference and concluded that the outside view “may provide some stress reduction” (Moore, 1981–1982).
A short 1984 article in Science bore the provocative title “View Through a Window May Influence Recovery from Surgery.” Like the Michigan prison study, this study also took advantage of an inadvertent architectural experiment. On the surgical floors of a 200-bed, suburban Pennsylvania hospital, some rooms faced a stand of deciduous trees and others faced a brown brick wall. Postoperative patients were assigned essentially randomly to one or the other kind of room. The investigator reviewed the records of all cholecystectomy patients over a ten-year interval, restricted to the summer months when the trees were in foliage. Compared to patients with brick wall views, patients with tree views had significantly shorter hospitalizations (7.96 days compared to 8.70 days), less need for pain medications, and fewer negative comments in the nurses' notes (Ulrich, 1984).
In a randomized clinical trial of patients undergoing bronchoscopy (insertion of a flexible fiber-optic tube through the trachea into the lungs), patients who viewed a nature scene (a mountain stream in a spring meadow) and heard recorded nature sounds (water in a stream or chirping birds) experienced better pain control than did patients who received only conventional sedation (although anxiety levels did not differ between the two groups) (Diette, Lechtzin, Haponik, Devrots, & Rubin, 2003).
Viewing landscapes and related nature scenes, whether in actuality or in pictures, seems to have a salutary effect. Certain landscape types, such as broadleaf woodland, improved grassland, and seascapes, may have especially positive effects (Wheeler et al., 2015) (Text Box 25.4).
1469
Text Box 25.4 Parks and Public Health Parks have long been prized as features of towns and cities. Pioneering urban planners such as Frederick Law Olmsted and municipal officials of the nineteenth and early twentieth centuries considered parks essential oases in cities, allowing urban dwellers to connect with nature, enjoy each other's company, breathe fresh air, and pursue recreational activities (Olmsted, 1870/1999; Cranz, 1982) (Figure 25.5).
Figure 25.5 A Sunday Afternoon on the Island of LaGrande Jatte, 1884–1886, by Georges Seurat
This is not only a famous example of pointillist painting, it also illustrates the long-standing appreciation of parks as venues for nature contact, relaxation, social interaction, and physical activity.
Parks may range from small pockets of green space within deep urban canyons to vast reserves of natural land in rural areas. Parks offer a range of health benefits (Sherer, 2006). One of the best studied is physical activity; some (but not all) research shows that living near a park promotes physical activity (Bancroft et al., 2015), and certain park features, such as safety, greenery, good maintenance, recreational
1470
facilities, and restrooms, are known to predict greater use (Bedimo-Rung, Mowen, & Cohen, 2005; Cohen et al., 2007; Han et al., 2014; Stark et al., 2014). Parks also offer mental health benefits, perhaps through stress reduction (Orsega- Smith, Mowen, Payne, & Godbey, 2004)—benefits that result not only from visiting parks but from living near them. Indirect health benefits arise from the role of parks in protecting watersheds, reducing air pollution, and cooling urban heat islands.
The ways in which these benefits operate may vary across the population. Ethnic and racial groups differ in their preferences and in the ways they use parks (Virden & Walker, 1999; Gobster, 2002; Ho et al., 2005). Children benefit from specific features of parks, as do older adults (Payne, Orsega- Smith, Godbey, & Roy, 1998). Parks and recreation professionals, like public health professionals, need to take these differences into account in order to address the needs of a diverse population and assure equitable service delivery.
Many park systems recognize parks' links with public health, and some have even adopted health themes in promoting park use. The slogan of the parks department of the state of Victoria, Australia, for example, is “Healthy Parks, Healthy People” (www.parkweb.vic.gov.au). Public health initiatives have been launched by such groups as the National Parks and Recreation Association (www.nrpa.org) and the City Parks Alliance (www.cityparksalliance.org). These groups emphasize not only the health benefits but also the synergistic environmental and economic benefits of parks.
Parks exemplify the role of nature contact in promoting public health.
Wilderness Experiences Wilderness experiences—entering the landscape rather than only viewing it—may also be therapeutic. John Muir (1901, p. 56) wrote lyrically of his emotional and physical response to being in the wilderness: “Climb the mountains and get their good tidings. Nature's peace will flow into you as sunshine flows into trees. The winds will blow their own freshness into you, and the storms their
1471
energy, while cares will drop off like autumn leaves.” David Cumes (1998a, 1998b) described a phenomenon he called wilderness rapture, involving self-awareness; feelings of awe, wonder, and humility; a sense of comfort in and connection to nature; increased appreciation of others; and a feeling of renewal and vigor. Others have described the spiritual inspiration that comes from wilderness experiences (Fredrickson & Anderson, 1999). Green exercise (Text Box 25.5) may represent a less intense version of this same phenomenon.
1472
Text Box 25.5 Green Exercise Exercise is clearly good for health; the benefits include weight loss, blood pressure and cholesterol reduction, and decreased risk of heart attacks, stroke, diabetes, and some cancers. Exercise is also good for mental health; it improves attention, lifts mood, and relieves depression. Could it matter where you exercise?
Research suggests that exercise in natural settings may be more beneficial than exercise in barren or heavily built settings (Thompson Coon et al., 2011). For example, Swedish investigators asked twelve regular runners to take two hour- long runs, one through a nature reserve of pine and birch forest, open fields, and a lakeshore and the other on an urban route past apartment houses, commercial development, and heavy traffic. The runners preferred the green route and rated it more psychologically restorative than the urban route. In addition, self-rated anxiety or depression and anger decreased more and self-rated revitalization and tranquility improved more with the park than with the urban route (although these differences did not reach statistical significance) (Bodin & Hartig, 2003). Larger observational studies—of participants in Walking for Health programs in England (Marselle, Irvine, & Warber, 2013), and of respondents to the Scottish Health Survey (Mitchell, 2013)— found similar results. Such evidence suggests that the well- known health benefits of exercise may be further enhanced by exercising in pleasing natural settings—something that golfers, hikers, and resort owners (among others) may already believe (Figure 25.6).
1473
Figure 25.6 Green Exercise Evidence suggests that an outdoor setting might enhance the benefits of exercise.
Clinicians have worked to transfer these benefits to therapeutic interventions, using wilderness therapy (also called adventure therapy) for emotionally disturbed or delinquent children and adolescents, bereaved people, rape and incest survivors, and patients with cancer, psychiatric illness, end-stage renal disease,
1474
post-traumatic stress disorder (PTSD), and addiction disorders, among other ailments (Russell, 2001). The literature on wilderness therapy includes both before-and-after comparisons and controlled studies; mental health end points are the most commonly studied. In one such study, a group of 5.5- to 11.5-year-olds, emotionally disturbed boys attending an outdoor day camp, was compared to a group of similar boys not attending the camp. The campers' self- ratings of their emotional adjustment and also their teachers' ratings were significantly better than those of the controls, although neither parents' ratings nor scores on formal psychological testing showed an improvement (Shniderman, 1974). In a convenience sample of more than 700 people who had participated in wilderness excursions lasting two to four weeks, 90% described “an increased sense of aliveness, well-being, and energy,” and 90% reported that the experience had helped them break an addiction (defined broadly and ranging from nicotine to chocolate) (Greenway, 1995). In a group of Australian wilderness adventure camps serving adults with mental illness, participants reported improved self-esteem, mastery, and social connectedness at the end of the camp, but had returned to baseline by four weeks later (Cotton & Butselaar, 2013).
The literature on wilderness adventures is extensive, but several features make it difficult to interpret (Wilson & Lipsey, 2000; Russell & Phillips-Miller, 2002; Ray & Jakubec, 2014). Much of the published research comes from “true believers” or proponents, such as adventure companies, with a personal or commercial interest in wilderness experiences. Much of the research refers to structured trips or summer camp programs rather than to the more general phenomenon of contact with wilderness. Beneficial outcomes may be due to the vacation quality of the experience, to the psychological value of setting and achieving difficult goals, or to the group bonding that occurs on some such trips (or to some combination of these), rather than (or in addition to) the wilderness contact itself. Few studies have been randomized, and selection bias can rarely be excluded. Blinding of subjects is impossible, and blinding of investigators has not been attempted. Despite these limitations, many published accounts do suggest some benefit from wilderness experiences, especially short-term benefit for behavioral health problems.
Risks of Nature Contact
1475
While nature contact offers a range of health benefits, it also entails some risks. As with other public health interventions, optimizing the benefits means recognizing and controlling risks.
Chief among the risks of animal contact are bites and scratches, allergic reactions, and zoonotic diseases. With regard to allergy, the role of pets is complex. Exposure to animals early in life may protect against later allergy, while for people who are already sensitized, exposure may trigger symptoms (Dharmage, Lodge, Matheson, Campbell, & Lowe, 2012; Lodge et al., 2012; Smallwood & Ownby, 2012). Zoonotic diseases, from the unusual (e.g., psittacosis, brucellosis, leishmaniasis, echinococcosis, and dermatophytosis) to the common (e.g., infections with giardia, salmonella, or methicillin-resistant Staphylococcus aureus), may spread from companion animals to humans. While dogs and cats may transmit some of these diseases, exotic pets such as snakes, turtles, and birds pose some unique risks (Boseret, Losson, Mainil, Thiry, & Saegerman, 2013). As backyard chickens become more popular, public health officials have had to warn the public not to nuzzle the chickens, to reduce the risk of infection with salmonella or Newcastle or Marek's disease. Most at risk of zoonotic infections are young children, the elderly, pregnant women, and immunocompromised hosts (Mani & Maguire, 2009; Elad, 2013; Stull & Stevenson, 2015). For each of these hazards, preventive strategies, such as home hygiene, are available (Morris, 2010).
Contact with plants and engaging in outdoor activities also pose risks. These include allergic reactions to plants such as poison ivy, exposure to weather extremes, encounters with animals ranging from mosquitoes to snakes to large predators, and injuries such as falls and drowning. A full discussion of these risks, and how to control them, is beyond the scope of this chapter, but is available elsewhere (Auerbach, 2012). Public health principles very much apply: prevention, preparedness, and training are key to reducing risk.
There is evidence, then, that contact with the natural world—with animals, plants, landscapes, and wilderness—may offer health benefits. Perhaps this reflects ancient learning habits, preferences, and tastes, echoes of human origins as creatures of the wild. Satisfying these preferences by promoting contact with the natural world may be an effective way to enhance health (not to mention
1476
cheaper and freer of side effects than medications). If so, this implies a broad vision of environmental health, one that stretches from landscape architecture to horticulture, from interior design to forestry, from botany to veterinary medicine.
1477
The Greening of Environmental Health With accumulating evidence that nature contact provides health benefits, the public health response might take three forms: research, collaboration, and public health intervention.
Research Clinical and epidemiological research in environmental health addresses many variants of the same questions: Is there an association between exposure and outcome? And what interventions are effective in improving health outcomes? A focus on nature contact suggests a research agenda directed not only at potentially hazardous exposures but also at potentially healthy ones, and at outcomes that reflect not only impaired health but also enhanced health (Frumkin, 2003, 2013). If people have regular contact with flowers or trees, do they report greater well-being, better sleep, fewer headaches, reduced joint pain? Do inner-city children who attend a rural summer camp have better health during the next semester of school than their friends who spent the summer in the city? Do patients with cancer or AIDS survive longer, or have fewer infections or less pain or higher T cell counts, if they have pets? Do gardens in hospitals speed postoperative recovery? Does psychotherapy that employs contact with nature—known as ecopsychology (Roszak, Gomes, & Kanner, 1995; Buzzell & Chalquis, 2009; Kahn & Hasbach, 2012)—have an empirical basis? If these or related therapeutic approaches show promise, which patients will benefit and what kinds of contact with nature will have the greatest efficacy and cost effectiveness? (Also see Text Box 25.6.)
1478
Text Box 25.6 Nature Contact, Poverty, and Health: A Connection? Poverty is one of the strongest predictors of poor health. People who are poor have worse self-reported health, higher rates of many diseases, higher rates of disability, and lower life expectancy.
Nature contact may help to blunt the toxic effects of poverty. One line of evidence comes from studies of the effects of green space in deprived neighborhoods. Text Box 25.3 describes the positive effects of trees in a public housing complex in Chicago. In Philadelphia, when blighted vacant lots were improved through cleaning them up and planting grass and trees to create a parklike setting, nearby residents reported less stress and more physical activity (Branas et al., 2011). Unemployed people in deprived neighborhoods in Dundee, Scotland, had lower levels of stress, as measured by salivary cortisol levels, if they lived in greener neighborhoods (Ward Thompson et al., 2012).
But perhaps the most suggestive evidence comes from studies by Scottish scientists who examined the joint impacts of nature contact and income (or social class) (Mitchell & Popham, 2008; Mitchell, Richardson, Shortt, & Pearce, 2015). They found the expected health disparities in relation to social class: the lower the social class, the higher the all- cause mortality, cardiovascular mortality, and mental distress. But there was another trend: within each social class, the greener the neighborhood, the better these health measures. And the greener the neighborhood, the smaller the health disparities between the best-off and the worst-off people.
This effect of nature contact—reducing the health disparities associated with socioeconomic inequality—has been described as equigenic. If further studies confirm this effect, the public health policy response might well be to work toward better access to and maintenance of parks and green
1479
space in deprived communities—a consequential conclusion, since poor communities and communities of color generally have disproportionately less access to high-quality parks and green space (Bruton & Floyd, 2014; Wolch, Byrne, & Newell, 2014).
Answering these questions requires an orientation toward empirical research among professions, from landscape architecture to horticulture, that have traditionally not emphasized such research. It also requires an ability to define and operationalize variables currently unfamiliar to health researchers. What is exposure to nature, what does the concept of a dose mean in this context, and how do we measure it? Similarly, the outcome variables that reflect health instead of disease are less researched and need to be developed and validated. These challenges offer broad opportunities for methods development and hypothesis testing.
Collaboration Environmental health specialists, from researchers to clinicians, have long recognized the need to collaborate with other professionals. They work with mechanical engineers to build exposure chambers, with chemists to measure exposures, and with software engineers to apply geographic information systems to health data. A focus on natural environments suggests collaborations with other kinds of professionals: landscape architects, who can help with identifying the salient features of outdoor exposures; interior designers, who can do the same for microenvironments; veterinarians, who can help with understanding human relationships with animals; and urban and regional planners, who can help with linking environmental health principles with large-scale environmental design.
Public Health Intervention Finally, evidence of the health benefits of particular environments needs to be translated into action. On the clinical level this may have implications for patient care. Perhaps physicians and nurses will advise patients to take a few days in the country, to spend time gardening, or to adopt a pet if clinical evidence offers support for such measures. Perhaps hospitals will be built in scenic locations,
1480
and rehabilitation centers will routinely include gardens. Health promotion professionals may include nature contact among the healthy behaviors they encourage (St. Leger, 2003). Perhaps health care payers will come to fund such interventions, especially if they prove to rival pharmaceuticals in cost and efficacy. Urban planners, developers, and landscape architects may increasingly work to provide nature contact in neighborhoods, such as readily available parks, and architects may increasingly incorporate biophilic elements into building design (Text Box 25.7). In all these actions, steps to reduce any risks must also be part of implementation.
1481
Text Box 25.7 Biophilic Design If nature contact offers health benefits, then the obvious public health strategy would be to get people into nature. But a complementary strategy is also available: bringing nature to people. Because people spend most of their time indoors, this means designing buildings that build on people's affinity with nature. Biophilic design is “an approach that fosters beneficial contact between people and nature in modern buildings and landscapes” (Kellert, 2008, p. 5). Biophilic design is characterized by two basic design elements. One is an organic or naturalistic approach, with shapes and forms that reflect people's affinity for nature; examples include such features as water, sunlight, plants, and natural materials. The second is place-based, or vernacular, design that connects to the culture and ecology of a locality; this might involve geography, history, and/or landscape orientation, and a host of other features. Biophilic design can be seen on the small scale in a window planter or an artfully designed walkway in a home (Figure 25.7) and on the large scale in such iconic buildings as the Sydney Opera House, with its bird- and sail-like forms soaring over Sydney Harbour.
1482
Figure 25.7 Frank Lloyd Wright's Fallingwater This house illustrates some of the principles of biophilia: the use of natural materials and motifs and close contact with nature.
Source: Photo Courtesy of Philip Sites, WeekendRoady.com.
1483
Summary There is evidence that nature contact promotes health and well- being. This effect may have an evolutionary basis, and one or more of several mechanisms may operate. Nature contact occurs in a variety of ways and in many settings: through contact with animals and plants, through views of natural scenes such as landscapes, and through activities in green neighborhoods, parks, or wilderness areas. Programs and policies have begun to implement nature contact as a health promotion strategy. While important questions remain to be answered through research, this approach is highly promising, offering effective health promotion at low cost, with few adverse effects, and with many co-benefits.
1484
Key Terms attention restoration
Directed attention, a voluntary effort, is a finite cognitive resource, which can be depleted. Attention restoration is the replenishment of this resource; according to attention restoration theory, contact with nature is a key method of restoring attention.
biophilia “The innately emotional affiliation of human beings to other living organisms” (Wilson, 1984, p. 31).
biophilic design An “approach that fosters beneficial contact between people and nature in modern buildings and landscapes” (Kellert, 2008, p. 5).
ecopsychology A field of psychology and a therapeutic approach rooted in the relationship between humans and nature.
green exercise Exercise that takes place in natural settings such as parks and woodlands.
nature deficit disorder A term coined by Richard Louv in his 2005 book, Last Child in the Woods, referring to the deprivation of nature contact that results from a lack of play and exploration in natural settings.
wilderness therapy The use of wilderness activities, such as camping, for therapeutic purposes, for such conditions as mental illness, post-traumatic stress, and substance abuse (also known as adventure therapy).
1485
Discussion Questions 1. Describe your last contact with a natural setting—on a vacation,
a weekend outing, or even a recent visit to a park. How did it make you feel? How would you design research to demonstrate these effects across a broad population?
2. Consider the availability of parks and green space in your city or town. Are they available near the places where people live and work? Do some sections of your city or town have better access to them than others? What about poor and minority communities? Is this an environmental justice issue?
3. Suppose your community is considering a land conservation initiative that would set aside tracts of green space and prohibit future development on them. Environmental advocates are leading this effort, and they ask you to support it with an argument based on public health considerations. How would you make the case?
4. As described in Chapter 8, exposure assessment is a key part of any environmental epidemiology research. How would you measure exposure to nature? What is a “dose” of nature?
1486
References Abram, D. (1996). The spell of the sensuous: Perception and language in a more-than-human world. New York: Vintage Books.
Addicks, P. (2008). [Photo.] Retrieved from http://www.trishaaddicksphotography.com
Allen, K., Blascovich, J., Wendy, B., & Mendes, W. B. (2002). Cardiovascular reactivity and the presence of pets, friends, and spouses: The truth about cats and dogs. Psychosomatic Medicine, 64, 727–739.
American Pet Products Association. (2015). 2015–2016 APPA National Pet Owners Survey. Retrieved from http://www.americanpetproducts.org/pubs_survey.asp
Amoly, E., Dadvand, P., Forns, J., Lopez-Vicente, M., Basagana, X., Julvez, J.,…Sunyer, J. (2014). Green and blue spaces and behavioral development in Barcelona schoolchildren: The BREATHE project. Environmental Health Perspectives, 122, 1351–1358.
Anderson, W. P., Reid, C., & Jennings, G. (1992). Pet ownership and risk factors for cardiovascular disease. Medical Journal of Australia, 157, 298–301.
Annerstedt, M., & Währborg, P. (2011). Nature-assisted therapy: Systematic review of controlled and observational studies. Scandinavian Journal of Public Health, 39, 371–388.
Armstrong, D. A. (2000). Survey of community gardens in upstate New York: Implications for health promotion and community development. Health & Place, 6, 319–327.
Auerbach, P. S. (2012). Wilderness medicine (6th ed.). Philadelphia: Elsevier/Mosby.
Bancroft, C., Joshi, S., Rundle, A., Hutson, M., Chong, C., Weiss, C. C.,…Lovasi, G. (2015). Association of proximity and density of parks and objectively measured physical activity in the United States: A systematic review. Social Science & Medicine, 138, 22–30.
1487
Barker, S. B., & Dawson, K. S. (1998). The effects of animal-assisted therapy on anxiety ratings of hospitalized psychiatric patients. Psychiatric Services, 49(6), 797–801.
Beck, A. M., & Katcher, A. H. (1983). Between pets and people: The importance of animal companionship. New York: Perigree Books.
Beck, A. M., & Meyers, N. M. (1996). Health enhancement and companion animal ownership. Annual Review of Public Health, 17, 247–257.
Bedimo-Rung, A. L., Mowen, A. J., & Cohen, D. A. (2005). The significance of parks to physical activity and public health: A conceptual model. American Journal of Preventive Medicine, 28, 159–168.
Beetz, A., Uvnäs-Moberg, K., Julius, H., & Kotrschal, K. (2012). Psychosocial and psychophysiological effects of human-animal interactions: The possible role of oxytocin. Frontiers in Psychology, 3, 234.
Bell, J. F., Wilson, J. S., & Liu, G. C. (2008). Neighborhood greenness and 2-year changes in body mass index of children and youth. American Journal of Preventive Medicine, 35(6), 547–553.
Berman, M. G., Kross, E., Krpan, K. M., Askren, M. K., Burson, A., Deldin, P. J.,…Jonides, J. (2012). Interacting with nature improves cognition and affect for individuals with depression. Journal of Affective Disorders, 140(3), 300–305.
Blair, D., Giesecke, C. C., & Sherman, S. A. (1991). Dietary, social and economic evaluation of the Philadelphia Urban Gardening Project. Journal of Nutrition Education and Behavior, 23, 161–167.
Bodin, M., & Hartig, T. (2003). Does the outdoor environment matter for psychological restoration gained through running? Psychology of Sport and Exercise, 4, 141–153.
Boseret, G., Losson, B., Mainil, J. G., Thiry, E., & Saegerman, C. (2013). Zoonoses in pet birds: Review and perspectives. Veterinary Research, 44, 36.
Branas, C. C., Cheney, R. A., MacDonald, J. M., Tam, V. W.,
1488
Jackson, T. D., & Ten Have, T. R. 2011. A difference-in-differences analysis of health, safety, and greening vacant urban space. American Journal of Epidemiology, 174, 1296–1306.
Bratman, G. N., Hamilton, J. P., & Daily, G. C. (2012). The impacts of nature experience on human cognitive function and mental health. Annals of the New York Academy of Sciences, 1249, 118– 136.
Bruton, C. M., & Floyd, M. F. (2014). Disparities in built and natural features of urban parks: Comparisons by neighborhood level race/ethnicity and income. Journal of Urban Health, 91(5), 894– 907.
Buzzell, L., & Chalquis, C., (Eds.). (2009). Ecotherapy: Healing with nature in mind. Berkeley, CA: Counterpoint Press.
Caras, R. A. (1996). A perfect harmony: The intertwining lives of animals and humans throughout history. New York: Fireside.
Cariñanos, P., & Casares-Porcel, M. (2011). Urban green zones and related pollen allergy: A review; Some guidelines for designing spaces with low allergy impact. Landscape and Urban Planning, 101, 205–214.
Carter, M., & Horwitz, P. (2014). Beyond proximity: The importance of green space useability to self-reported health. EcoHealth, 11(3), 322–332.
Chawla, L., Keena, K., Pevec, I., & Stanley, E. (2014). Green schoolyards as havens from stress and resources for resilience in childhood and adolescence. Health & Place, 28, 1–13.
Cherniack, E. P., & Cherniack, A. R. (2014). The benefit of pets and animal-assisted therapy to the health of older individuals. Current Gerontology and Geriatrics Research, 2014, 623203.
Cimprich, B., & Ronis, D. L. (2003). An environmental intervention to restore attention in women with newly diagnosed breast cancer. Cancer Nursing, 26, 284–292.
Cleland, V., Crawford, D., Baur, L. A., Hume, C., Timperio, A., & Salmon, J. (2008). A prospective examination of children's time
1489
spent outdoors, objectively measured physical activity and overweight. International Journal of Obesity, 32(11), 1685–1693.
Clutton-Brock, J. (1981). Domesticated animals from early times. Austin: University of Texas Press.
Cohen, D. A., McKenzie, T. L., Sehgal, A., Williamson, S., Golinelli, D., & Lurie, N. (2007). Contribution of public parks to physical activity. American Journal of Public Health, 97(3), 509–514.
Cohen-Cline, H., Turkheimer, E., & Duncan, G. E. (2015). Access to green space, physical activity and mental health: A twin study. Journal of Epidemiology and Community Health, 69(6), 523–529.
Cotton, S., & Butselaar, F. (2013). Outdoor adventure camps for people with mental illness. Australasian Psychiatry, 21(4), 352– 358.
Cranz, G. (1982). The politics of park design: A history of urban parks in America. Cambridge, MA: MIT Press.
Crompton, J. L. (2005). The impact of parks on property values: Empirical evidence from the past two decades in the United States. Managing Leisure, 10(4), 203–218.
Cumes, D. (1998a). Inner passages outer journeys: Wilderness, healing, and the discovery of self. Minneapolis: Llewellyn.
Cumes, D. (1998b). Nature as medicine: The healing power of the wilderness. Alternative Therapies in Health and Medicine, 4, 79– 86.
Dadvand, P., Nieuwenhuijsen, M. J., Esnaola, M., Forns, J., Basagaña, X., Alvarez-Pedrerol, M.,…Sunyer, J. (2015). Green spaces and cognitive development in primary schoolchildren. Proceedings of the National Academy of Sciences of the United States, 112, 7937–7942.
Dadvand, P., Sunyer, J., Basagana, X., Ballester, F., Lertxundi, A., Fernandez-Somoano, A.,…Nieuwenhuijsen, M. J. (2012). Surrounding greenness and pregnancy outcomes in four Spanish birth cohorts. Environmental Health Perspectives, 120(10), 1481– 1487.
1490
Dharmage, S. C., Lodge, C. L., Matheson, M. C., Campbell, B., & Lowe, A. J. (2012). Exposure to cats: Update on risks for sensitization and allergic diseases. Current Allergy and Asthma Reports, 12(5), 413–423.
Diette, G. B., Lechtzin, N., Haponik, E., Devrots, A., & Rubin, H. R. (2003). Distraction therapy with nature sights and sounds reduces pain during flexible bronchoscopy. Chest, 123, 941–948.
Doxey, J. S., Waliczek, T. M., & Zajicek, J. M. (2009). The impact of interior plants in university classrooms on student course performance and on student perceptions of the course and instructor. HortScience, 44(2), 384–391.
Elad, D. (2013). Immunocompromised patients and their pets: Still best friends? Veterinary Journal, 197(3), 662–669.
Endenburg, N., & van Lith, H. A. (2011). The influence of animals on the development of children. Veterinary Journal, 190(2), 208– 214.
Escobedo, F. J., Kroeger, T., & Wagner, J. E. (2011). Urban forests and pollution mitigation: Analyzing ecosystem services and disservices. Environmental Pollution, 159(8–9), 2078–2087.
Faber Taylor, A., Kuo, F. E., & Sullivan, W. C. (2002). Views of nature and self-discipline: Evidence from inner city children. Journal of Environmental Psychology, 22, 49–63.
Fleishman-Hillard Research. (2007). Pet spending survey. Retrieved from http://cdn.fleishmanhillard.com/wp- content/uploads/2008/01/Fleishman-Hillard-Pet-Spending- Survey.pdf
Fox, S. (1981). John Muir and his legacy. Boston: Little, Brown.
Fredrickson, L. M., & Anderson, D. H. (1999). A qualitative exploration of the wilderness experience as a source of spiritual inspiration. Journal of Environmental Psychology, 19, 21–39.
Friedmann, E., & Son, H. (2009). The human-companion animal bond: How humans benefit. Veterinary Clinics of North America— Small Animal Practice, 39(2), 293–326.
1491
Friedmann, E., & Thomas, S. A. (1995). Pet ownership, social support, and one-year survival after acute myocardial infarction in the Cardiac Arrhythmia Suppression Trial (CAST). American Journal of Cardiology, 76, 1213–1217.
Frumkin, H. (2003). Healthy places: Exploring the evidence. American Journal of Public Health, 93, 1451–1456.
Frumkin, H. (2013). The evidence of nature and the nature of evidence. American Journal of Preventive Medicine, 44, 196–197.
Greenway, R. (1995). The wilderness effect and ecopsychology. In T. Roszak, M. E. Gomes, & A. D. Kanner (Eds.), Ecopsychology: Restoring the earth, healing the mind (pp. 122–135). San Francisco: Sierra Club Books.
Gobster, P. (2002). Managing urban parks for a racially and ethnically diverse clientele. Leisure Sciences, 24, 143–159.
Haller, R. L., & Kramer, C. L. Horticultural therapy methods: Making connections in health care, human service, and community programs. Philadelphia: Haworth Press, 2006.
Hamilton, E., & Cairns, H. (Eds.). (1961). Plato: The collected dialogues. Princeton, NJ: Princeton University Press, 1961.
Han, B., Cohen, D. A., Derose, K. P., Marsh, T., Williamson, S., & Raaen, L. (2014). How much neighborhood parks contribute to local residents' physical activity in the City of Los Angeles: A meta- analysis. Preventive Medicine, 69(Suppl. 1), S106–110.
Han, K.-T. (2009). Influence of limitedly visible leafy indoor plants on the psychology, behavior, and health of students at a junior high school in Taiwan. Environment and Behavior, 41(5), 658–692.
Harris, N., Minniss, F. R., & Somerset, S. (2014). Refugees connecting with a new country through community food gardening. International Journal of Environmental Research and Public Health, 11(9), 9202–9216.
Hartig, T., Mitchell, R., de Vries, S., & Frumkin, H. (2014). Nature and health. Annual Review of Public Health, 35, 207–228.
Heerwagen, J. H., & Orians, G. H. (1993). Humans, habitats, and
1492
aesthetics. In S. R. Kellert & E. O. Wilson (Eds.), The biophilia hypothesis (pp. 138–172). Washington, DC: Island Press.
Heerwagen, J. H., & Orians, G. H. (2002). The ecological world of children. In P. H. Kahn Jr. & S. R. Kellert (Eds.), Children and nature: Psychological, sociocultural, and evolutionary investigations (pp. 29–63). Cambridge, MA: MIT Press.
Ho, C.-H., Sasidharan, V., Elmendorf, W., Willits, F. K., Graefe, A., & Godbey, G. (2005). Gender and ethnic variations in urban park preferences, visitation, and perceived benefits. Journal of Leisure Research, 37, 281–306.
Holtan, M. T., Dieterlen, S. L., & Sullivan, W. C. (2014). Social life under cover: Tree canopy and social capital in Baltimore, Maryland. Environment and Behavior, 47(5), 502–525.
Honeyman, M. K. (1992). Vegetation and stress: A comparison study of varying amounts of vegetation in countryside and urban scenes. In D. Relf (Ed.), The role of horticulture in human well– being and social development (pp. 143–145). Portland, OR: Timber Press.
Hull, R. B., & Revell, G.R.B. (1989). Cross-cultural comparison on landscape scenic beauty evaluations: A case study in Bali. Journal of Environmental Psychology, 9, 177–191.
Hunt, M., Al-Awadi, H., & Johnson, M. (2008). Psychological sequelae of pet loss following Hurricane Katrina. Anthrozoös, 21(2), 109–121.
Hunter, N. L. (1970). Horticulture programs in prisons. San Luis Obispo: California State Polytechnic College, Horticulture Department.
Hüttenmoser, M. (1995). Children and their living surroundings: Empirical investigations into the significance of living surroundings for the everyday life and development of children. Children's Environments, 12, 403–413.
Kahn, P. H., Jr., & Hasbach, P. H. (Eds.). (2012). Ecopsychology: Science, totems, and the technological species. Cambridge, MA: MIT Press.
1493
Kahn, P. H., Jr., & Kellert, S. R. (Eds.). (2002). Children and nature: Psychological, sociocultural, and evolutionary investigations. Cambridge, MA: MIT Press.
Kamioka, H., Tsutani, K., Yamada, M., Park, H., Okuizumi, H., Honda, T.,…Mutoh, Y. (2014). Effectiveness of horticultural therapy: A systematic review of randomized controlled trials. Complementary Therapies in Medicine, 22(5), 930–943.
Kaplan, R. (1983). The role of nature in the urban context. In I. Altman & J. F. Wohlwill (Eds.), Human behavior and environment: Vol. 6. Behavior and the natural environment (pp. 127–161). New York: Plenum.
Kaplan, R. (1993). The role of nature in the context of the workplace. Landscape and Urban Planning, 26, 193–201.
Kaplan, R., & Kaplan, S. (1989). The experience of nature: A psychological perspective. New York: Cambridge University Press.
Kaplan, R., Kaplan, S., & Ryan, R. L. (1998). With people in mind: Design and management of everyday nature. Washington, DC: Island Press.
Kaplan, S. (1995). The restorative benefits of nature: Toward an integrative framework. Journal of Environmental Psychology, 15, 169–182.
Kaplan, S. (2001). Meditation, restoration, and the management of mental fatigue. Environment and Behavior, 33, 480–506.
Kaplan, S., & Berman, M. G. (2010). Directed attention as a common resource for executive functioning and self-regulation. Perspectives on Psychological Science, 5(1), 43–57.
Kardan, O., Gozdyra, P., Misic, B., Moola, F., Palmer, L. J., Paus, T., & Berman, M. G. (2015). Neighborhood greenspace and health in a large urban center. Scientific Reports, 5. doi:10.1038/srep11610
Kareiva, P., Tallis, H., Ricketts, T. H., Daily, G. C., & Polasky, S. (2011). Natural capital: Theory and practice of mapping ecosystem services. New York: Oxford University Press.
Kaźmierczak, A. (2013). The contribution of local parks to
1494
neighbourhood social ties. Landscape and Urban Planning, 109(1), 31–44.
Kellert, S. R. (1993). The biological basis for human values of nature. In S. R. Kellert & E. O. Wilson (Eds.), The biophilia hypothesis (pp. 42–69). Washington, DC: Island Press.
Kellert, S. R. (2008). Dimensions, elements, and attributes of biophilic design. In S. R. Kellert, J. Heerwagen, & M. Mador (Eds.), Biophilic design: The theory, science and practice of bringing buildings to life (pp. 3–19). Hoboken, NJ: Wiley.
Kemperman, A., & Timmermans, H. (2014). Green spaces in the direct living environment and social contacts of the aging population. Landscape and Urban Planning, 129, 44–54.
Kirkby, M. (1989). Nature as refuge in children's environments. Children's Environments Quarterly, 6, 7–12.
Korpela, K., & Hartig, T. 1996. Restorative qualities of favorite places. Journal of Environmental Psychology, 16, 221–233.
Kuo, F. E. (2001). Coping with poverty: Impacts of environment and attention in the inner city. Environment and Behavior, 33(1), 5–34.
Kuo, F. E., & Sullivan, W. C. (2001a). Aggression and violence in the inner city: Effects of environment via mental fatigue. Environment and Behavior, 33(4), 543–571.
Kuo, F. E., & Sullivan, W. C. (2001b). Environment and crime in the inner city: Does vegetation reduce crime? Environment and Behavior, 33(3), 343–367.
Kuo, F. E., & Taylor, A. F. (2004). A potential natural treatment for attention-deficit/hyperactivity disorder: Evidence from a national study. American Journal of Public Health, 94, 1580–1586.
Larsen, L., Adams, J., Deal, B., Kweon, B. S., & Tyler, E. (1998). Plants in the workplace: The effects of plant density on productivity, attitudes, and perceptions. Environment and Behavior, 30(3), 261– 281.
Lederbogen, F., Kirsch, P., Haddad, L., Streit, F., Tost, H., Schuch, P.,…Meyer-Lindenberg, A. (2011). City living and urban upbringing
1495
affect neural social stress processing in humans. Nature, 474(7352), 498–501.
Levine, G. N., Allen, K., Braun, L. T., Christian, H. E., Friedmann, E., Taubert, K. A.,…Lange, R. A. (2013). Pet ownership and cardiovascular risk: A scientific statement from the American Heart Association. Circulation, 127, 2353–2363.
Lewis, C. A. (1990). Gardening as healing process. In M. Francis & R. T. Hester (Eds.), The meaning of gardens (pp. 244–251). Cambridge, MA: MIT Press.
Library of Congress, Prints and Photographs. (n.d.). American conservationist John Muir (1838–1914) [Photo]. Retrieved from https://commons.wikimedia.org/wiki/File:John_Muir.jpg
Lodge, C. J., Allen, K. J., Lowe, A. J., Hill, D. J., Hosking, C. S., Abramson, M. J., & Dharmage, S. C. (2012). Perinatal cat and dog exposure and the risk of asthma and allergy in the urban environment: A systematic review of longitudinal studies. Clinical and Developmental Immunology, 2012, 176484.
Lohr, V. I. (2010). What are the benefits of plants indoors and why do we respond positively to them? Acta Horticulturae, 881(2), 675– 682.
Louv, R. (2005). Last child in the woods: Saving our children from nature-deficit disorder. Chapel Hill, NC: Algonquin Press.
Maas, J., Verheij, R. A., de Vries, S., Spreeuwenberg, P., Schellevis, F. G., & Groenewegen, P. P. (2009). Morbidity is related to a green living environment. Journal of Epidemiology and Community Health, 63, 967–973.
Mani, I., & Maguire, J. H. (2009). Small animal zoonoses and immunocompromised pet owners. Topics in Companion Animal Medicine, 24, 164–174.
Marcus, C. C. (2007). Healing gardens in hospitals. Interdisciplinary Design and Research e-Journal, 1(1).
Marcus, C. C., & Sachs, N. A. (2013). Therapeutic landscapes: An evidence-based approach to designing healing gardens and
1496
restorative outdoor spaces. San Francisco: Jossey-Bass/Wiley.
Marcus, D. A. (2013). The science behind animal-assisted therapy. Current Pain and Headache Reports, 17(4), 322.
Marselle, M. R., Irvine, K. N., & Warber, S. L. (2013). Walking for well-being: Are group walks in certain types of natural environments better for well-being than group walks in urban environments? International Journal of Environmental Research and Public Health, 10(11), 5603–5628.
Matchock, R. L. (2015). Pet ownership and physical health. Current Opinion in Psychiatry, 28, 386–92
Mattson, R. H. (1992). Prescribing health benefits through horticultural activities. In D. Relf (Ed.), The role of horticulture in human well-being and social development (pp. 161–168). Portland, OR: Timber Press.
McConnell, A. R., Brown, C. M., Shoda, T. M., Stayton, L. E., & Martin, C. E. (2011). Friends with benefits: On the positive consequences of pet ownership. Journal of Personality and Social Psychology, 101(6), 1239–1252.
McLuhan, T. C. (1994). The way of the earth: Encounters with nature in ancient and contemporary thought. New York: Simon & Schuster.
McNicholas, J., Gilbey, A., Rennie, A., Ahmedzai, S, Dono, J. A., & Ormerod, E. (2005). Pet ownership and human health: A brief review of evidence and issues. BMJ, 331(7527), 1252–1254.
Mitchell, R. (2013). Is physical activity in natural environments better for mental health than physical activity in other environments? Social Science & Medicine, 91, 130–34
Mitchell, R., & Popham, F. (2008). Effect of exposure to natural environment on health inequalities: An observational population study. Lancet, 372, 1655–1660.
Mitchell, R. J., Richardson, E. A., Shortt, N. K., & Pearce, J. R. (2015). Neighborhood environments and socioeconomic inequalities in mental well-being. American Journal of Preventive
1497
Medicine, 49(1), 80–84.
Moore, E. O. (1981–1982). A prison environment's effect on health care service demands. Journal of Environmental Systems, 11, 17– 34.
Morris, D. O. (2010). Human allergy to environmental pet danders: A public health perspective. Veterinary Dermatology, 21(5), 441– 449.
Muir, J. (1901). Our national parks. Boston: Houghton Mifflin.
Muñoz Lasa, S., Ferriero, G., Brigatti, E., Valero, R., & Franchignoni, F. (2011). Animal-assisted interventions in internal and rehabilitation medicine: A review of the recent literature. Panminerva Medica, 53(2), 129–136.
Nabhan, G. P., & Trimble, S. (1994). The geography of childhood: Why children need wild places. Boston: Beacon Press.
Nash, R. (1982). Wilderness and the American mind (3rd ed.). New Haven, CT: Yale University Press.
Natterson-Horowitz, B., & Bowers, K. (2013). Zoobiquity: The astonishing connection between human and animal health. New York: Vintage.
Neese, R. (1959). Prisoners escape. Flower Grower, 46, 39–40.
Nicklett, E. J., Anderson, L. A., & Yen, I. H. (2014). Gardening activities and physical health among older adults: A review of the evidence. Journal of Applied Gerontology. doi:10.1177/0733464814563608
Nowak, D. J., Hirabayashi, S., Bodine, A., & Greenfield, E. (2014). Tree and forest effects on air quality and human health in the United States. Environmental Pollution, 193, 119–129.
O'Haire, M. E. (2013). Animal-assisted intervention for autism spectrum disorder: A systematic literature review. Journal of Autism and Developmental Disorders, 43(7), 1606–1622.
Olmsted, F. L. (1999). Public parks and the enlargement of towns. In R. T. LeGates & F. Stout (Eds.), The city reader (2nd ed., pp.
1498
314–320). London: Routledge. (Originally published 1870)
Orsega-Smith, E., Mowen, A., Payne, L., & Godbey, G. (2004). The interaction of stress and park use on psycho-physiological health in older adults. Journal of Leisure Research, 36, 232–257.
Payne, L., Orsega-Smith, E., Godbey, G., & Roy, M. (1998). Local parks and the health of older adults: Results from an exploratory study. Parks & Recreation, 33(10), 64–70.
Pearson-Mims, C. H., & Lohr, V. I. (2000). Reported impacts of interior plantscaping in office environments in the United States. HortTechnology, 10(1), 82–86.
Perlman, M. (1994). The power of trees: The reforesting of the soul. Woodstock, CT: Spring.
Purcell, A. T., Lamb, R. J., Mainardi Peron, E., & Falchero, S. (1994). Preference or preferences for landscape? Journal of Environmental Psychology, 14, 195–209.
Ray, H., & Jakubec, S. L. (2014). Nature-based experiences and health of cancer survivors. Complementary Therapies in Clinical Practice, 20(4), 188–192.
Roszak, T., Gomes, M. E., & Kanner, A. D. (Eds.). (1995). Ecopsychology: Restoring the earth, healing the mind. San Francisco: Sierra Club Books.
Russell, K. C. (2001). What is wilderness therapy? Journal of Experiential Education, 24(2), 70–79.
Russell, K. C., & Phillips-Miller, D. (2002). Perspectives on the wilderness therapy process and its relation to outcome. Child & Youth Care Forum, 31(6), 415–437.
Saberi, P., Neilands, T. B., & Johnson, M. O. (2014). Association between dog guardianship and HIV clinical outcomes. Journal of the International Association of Providers of AIDS Care, 13(4), 300–304.
Sacks, O. (1984). A leg to stand on. New York: HarperCollins.
St. Leger, L. (2003). Health and nature—new challenges for health
1499
promotion [Editorial]. Health Promotion International, 18, 173– 175.
Sartelet, K. N., Couvidat, F., Seigneur, C., & Roustan, Y. (2012). Impact of biogenic emissions on air quality over Europe and North America. Atmospheric Environment, 53, 131–141.
Schaefer, L., Plotnikoff, R. C., Majumdar, S. R., Mollard, R., Woo, M., Sadman, R.,…McGavock, J. (2014). Outdoor time is associated with physical activity, sedentary time, and cardiorespiratory fitness in youth. Journal of Pediatrics, 165(3), 516–521.
Schroeder, H. W., & Green, T. L. (1985). Public preference for tree density in municipal parks. Journal of Arboriculture, 11, 272–277.
Schukoske, J. E. (2000). Community development through gardening: State and local policies transforming urban open space. Legislation and Public Policy, 3, 351–393.
Serpell, J. (1991). Beneficial effects of pet ownership on some aspects of human health and behaviour. Journal of the Royal Society of Medicine, 84, 717–720.
Sherer, P. M. (2006). The benefits of parks: Why America needs more city parks and open space. Trust for Public Land. Retrieved from https://www.tpl.org/benefits-parks-white-paper
Shniderman, C. M. (1974). Impact of therapeutic camping. Social Work, 19, 354–357.
Siegel, J. (1990). Stressful life events and use of physician services among the elderly: The moderating role of pet ownership. Journal of Personality and Social Psychology, 58, 1081–1086.
Simons, L. A., Simons, J., McCallum, J., & Friedlander, Y. (2006). Lifestyle factors and risk of dementia: Dubbo Study of the elderly. Medical Journal of Australia, 184, 68–70.
Simson, S., & Straus M. C. (2003). Horticulture as therapy: Principles and practice. Philadelphia: Haworth Press.
Smallwood, J., & Ownby, D. (2012). Exposure to dog allergens and subsequent allergic sensitization: An updated review. Current Allergy and Asthma Reports, 12(5), 424–428.
1500
Stanley, I. H., Conwell, Y., Bowen, C., & Van Orden, K. A. (2014). Pet ownership may attenuate loneliness among older adult primary care patients who live alone. Aging & Mental Health, 18(3), 394– 399.
Stark, J. H., Neckerman, K., Lovasi, G. S., Quinn, J., Weiss, C. C., Bader, M.D.M.,…Rundle, A. (2014). The impact of neighborhood park access and quality on body mass index among adults in New York City. Preventive Medicine, 64, 63–68.
Stull, J. W., & Stevenson, K. B. (2015). Zoonotic disease risks for immunocompromised and other high-risk clients and staff: Promoting safe pet ownership and contact. Veterinary Clinics of North America—Small Animal Practice, 45(2), 377–392.
Takano, T., Nakamura, K., & Watanabe, M. 2002. Urban residential environments and senior citizens' longevity in megacity areas: The importance of walkable green spaces. Journal of Epidemiology and Community Health, 56, 913–918.
Taylor, A. F., Kuo, F. E., & Sullivan, W. C. (2002). Views of nature and self-discipline: Evidence from inner city children. Journal of Environmental Psychology, 22, 49–63.
Tennessen, C. M., & Cimprich, B. (1995). Views to nature: Effects on attention. Journal of Environmental Psychology, 15, 77–85.
Thompson Coon, J., Boddy, K., Stein, K., Whear, R., Barton, J., & Depledge, M. H. (2011). Does participating in physical activity in outdoor natural environments have a greater effect on physical and mental wellbeing than physical activity indoors? A systematic review. Environmental Science & Technology, 45, 1761–1772.
Toohey, A. M., McCormack, G. R., Doyle-Baker, P. K., Adams, C. L., & Rock, M. J. (2013). Dog-walking and sense of community in neighborhoods: Implications for promoting regular physical activity in adults 50 years and older. Health & Place, 22, 75–81.
Ulrich, R. S. (1984). View through a window may influence recovery from surgery. Science, 224, 420–421.
Ulrich, R. S. (1993). Biophilia, biophobia, and natural landscapes. In S. R. Kellert & E. O. Wilson (Eds.), The biophilia hypothesis (pp.
1501
73–137). Washington, DC: Island Press.
Ulrich, R. S., Simons, R. F., Losito, B. D., Fiorito, E., Miles, M. A., & Zelson, M. (1991). Stress recovery during exposure to natural and urban environments. Journal of Environmental Psychology, 11, 201–230.
Van den Berg, A. E., Maas, J., Verheij, R. A., & Groenewegen, P. P. (2010a). Green space as a buffer between stressful life events and health. Social Science & Medicine, 70, 1203–1210.
Van den Berg, A. E., van Winsum-Westra, M., de Vries, S., & van Dillen, S. (2010b). Allotment gardening and health: A comparative survey among allotment gardeners and their neighbors without an allotment. Environmental Health, 9, 74.
Virden, R. J., & Walker, G. J. (1999). Ethnic/racial and gender variations among meanings given to, and preferences for, the natural environment. Leisure Sciences, 21, 219–239.
Ward Thompson, C. (2011). Linking landscape and health: The recurring theme. Landscape and Urban Planning, 99(3–4), 187– 195.
Ward Thompson, C., Roe, J., Aspinall, P., Mitchell, R., Clow, A., & Miller, D. (2012). More green space is linked to less stress in deprived communities: Evidence from salivary cortisol patterns. Landscape and Urban Planning, 105, 221–229.
Wells, N. M. (2000). At home with nature: Effects of “greenness” on children's cognitive functioning. Environment and Behavior, 32, 775–795.
Wells, N. M., & Evans, G. W. (2003). Nearby nature—a buffer of life stress among rural children. Environmental Behavior, 35, 311–330.
Wheeler, B. W., Lovell, R., Higgins, S. L., White, M. P., Alcock, I., Osborne, N. J.,…Depledge, M. H. (2015). Beyond greenspace: An ecological study of population general health and indicators of natural environment type and quality. International Journal of Health Geographics, 14, 17.
Wichrowski, M., Whiteson, J., Haas, F., Mola, A., & Rey, M. J.
1502
(2005). Effects of horticultural therapy on mood and heart rate in patients participating in an inpatient cardiopulmonary rehabilitation program. Journal of Cardiopulmonary Rehabilitation, 25, 270–274.
Wilson, E. O. (1984). Biophilia: The human bond with other species. Cambridge, MA: Harvard University Press.
Wilson, E. O. (1993). Biophilia and the conservation ethic. In S. R. Kellert & E. O. Wilson (Eds.), The biophilia hypothesis (pp. 31–41). Washington, DC: Island Press.
Wilson, S. J., & Lipsey, M. W. (2000). Wilderness challenge programs for delinquent youth: A meta-analysis of outcome evaluations. Evaluation and Program Planning, 23, 1–12.
Wolch, J. R., Byrne, J., & Newell, J. P. (2014). Urban green space, public health, and environmental justice: The challenge of making cities “just green enough.” Landscape and Urban Planning, 125, 234–244.
Wood, L., Giles-Corti, B., & Bulsara, M. (2005). The pet connection: Pets as a conduit for social capital. Social Science & Medicine, 61, 1159–1173.
Wood, L. J., Giles-Corti, B., Bulsara, M. K., & Bosch, D. A. (2007). More than a furry companion: The ripple effect of companion animals on neighborhood interactions and sense of community. Society and Animals, 15, 43–56.
Yoo, M. H., Kwon, Y. J., Son, K. C., & Kays, S. J. (2006). Efficacy of indoor plants for the removal of single and mixed volatile organic pollutants and physiological effects of the volatiles on the plants. Journal of the American Society for Horticultural Science, 131, 452–458.
1503
For Further Information Books In addition to Kahn and Kellert (2002), Kellert and Wilson (1993), and Natterson-Horowitz and Bowers (2013) listed in the References, see the following:
Altman, I., & Wohlwill, J. F. (Eds.). (1983). Human behavior and environment: Vol. 6. Behavior and the natural environment. New York: Plenum.
Arluke, A., & Sanders, C. R. (Eds.). (2008). Between the species: A reader in human-animal relationships. New York: Routledge.
DeMello, M. (2012). Animals and society: An introduction to human-animal studies. New York: Columbia University Press.
Fine, A. (Ed.). (2000). Handbook on animal-assisted therapy: Theoretical foundations and guidelines for practice. San Diego: Academic Press.
Flagler, J., & Poincelot, R. P. (1994). People-plant relationships: Setting research priorities. Binghamton, NY: Food Products Press.
Francis, M., Lindsey, P., & Rice, J. S. (Eds.). (1994). The healing dimensions of people-plant relations: Proceedings of a research symposium. Davis: University of California Davis, Center for Design Research.
Gerlach-Spriggs, N., Kaufman, R., & Warner, S. B., Jr. (1998). Restorative gardens: The healing landscape. New Haven, CT: Yale University Press.
Louv, R. (2012). The nature principle: Reconnecting with life in a virtual age. Chapel Hill, NC: Algonquin.
Marcus, C. C., & Barnes, M. (1999). Healing gardens: Therapeutic benefits and design recommendations. Hoboken, NJ: Wiley.
Relf, D. (Ed.). (1992). The role of horticulture in human well-being and social development: A national symposium, 19–21 April 1990,
1504
Arlington, Virginia. Portland, OR: Timber Press.
Serpell, J. (1996). In the company of animals: A study of human- animal relationship. New York: Cambridge University Press.
Tyson, M. M. (1998). The healing landscape: Therapeutic outdoor environments. New York: McGraw-Hill.
University-Based Web Sites Edinburgh College of Art, OPENspace: http://openspace.eca.ac.uk. OPENspace is a research center for inclusive access to outdoor environments. Its Web site includes reviews on the health benefits of access to open space and nature (with titles such as Health, Well-Being, and OpenSpace focusing on such groups as ethnic minorities and teenagers).
European Centre for Environment and Human Health at the University of Exeter Medical School: https://beyondgreenspace.wordpress.com. The Beyond Greenspace blog reports the use of ecological, socioeconomic, and health data to understand relationships between nature, health, and well-being.
Purdue University, Center for the Human-Animal Bond: http://www.vet.purdue.edu/chab. This research and education center investigates the health effects of animal contact. Its Web site provides research results and links to a number of related sites.
Tufts University, Center for Animals and Public Policy: http://vet.tufts.edu/center-for-animals-and-public-policy. This group conducts and promotes evaluation and understanding of the changing role and impact of animals in society. Its Web site includes sections on animals in the community, research, the environment, and society.
University of Denver, Institute for Human-Animal Connection: http://www.du.edu/humananimalconnection. This center studies the interrelationship and health of people, animals, and the environment.
University of Illinois, Landscape and Human Health Laboratory: http://www.lhhl.uiuc.edu. This laboratory is a leader in research
1505
on the benefits of nature contact. Its Web site contains information in a variety of interesting categories, such as green landscaping and “ADHD Symptoms in Kids Across the U.S.,” “Inner City Girls & Self-discipline,” “Coping in the Inner City,” “Inner City Crime,” “Domestic Violence in the Inner City,” and “Building Strong Inner City Communities.”
Professional Organizations American Horticultural Therapy Association: http://www.ahta.org
Delta Society (the human-animal health connection): http://www.deltasociety.org
Healthy Parks Healthy People Central: http://www.hphpcentral.com
People-Plant Council: http://www.hort.vt.edu/HUMAN/PPC.htm
Nongovernmental Organizations Children & Nature Network (C&NN): http://www.childrenandnature.org. C&NN is dedicated to reconnecting children with nature. Its Web site includes news, reviews of current research, and links to key resources.
Outdoors Alliance for Kids (OAK): http://outdoorsallianceforkids.org. OAK is a national strategic partnership of organizations from diverse sectors with a common interest in connecting children, youth, and families with the outdoors.
1506
Part 5 The Practice of Environmental Health
1507
Chapter 26 Environmental Public Health: From Theory to Practice
Lynn R. Goldman
Dr. Goldman reports no conflicts of interest related to the authorship of this chapter.
1508
Key Concepts Prevention lies at the core of environmental public health. It includes not only the control of hazards but also health promotion through environmental strategies.
Environmental public health efforts have deep historical roots in human efforts to ensure clean food and safe water and living conditions.
Prevention in environmental health extends upstream to the root causes of environmental change and to the resulting environmental pressures that eventually have an impact on human health and well-being.
Prevention efforts can be divided into primary, secondary, and tertiary prevention. All are relevant in environmental health.
The prevention hierarchy ranges from definitive approaches such as completely removing a hazard (more preferable) to administrative, behavioral, and end-of-pipe approaches (less preferable).
The precautionary principle proposes that cost-effective preventive measures should proceed, even in the face of scientific uncertainty.
In environmental public health practice, all the core functions of public health—in the categories of assessment, policy development, and assurance—are used to pursue prevention.
Modern environmental public health includes a wide range of activities and responsibilities, such as food protection, water sanitation, air quality protection, safe and healthy housing, occupational health, injury prevention, and healthy community design.
The mission of environmental public health extends well beyond remediating, cleaning up, or otherwise making up for past mistakes. It is to ensure conditions that enhance the health of humans and
1509
other species. This chapter examines the concept of prevention and its application in environmental public health. It explores the principles and frameworks that underlie prevention in environmental public health, and how prevention strategies in environmental public health fit within the general practice of public health.
The environment has a major impact on the risk of chronic diseases such as cancers, chronic lung disease, and birth defects and on the risk of acute illnesses such as viral gastroenteritis, respiratory infections, and such vector-borne diseases as malaria. Accordingly, environmental public health is concerned with the prevention of these conditions.
But the environment has far broader impacts on health. Some environmental conditions confer resilience to even the most harmful natural disasters, while others put people directly in harm's way (e.g., through building on flood plains and earthquake-prone faults.) Some environments promote health by providing nutritious food, adequate supplies of drinking water, opportunities for outdoor recreation, and the aesthetic and mental health benefits of nature contact. The state of knowledge about causation of communicable diseases is more advanced than that for chronic diseases and natural disasters, which are in turn better understood than environmental aspects of health promotion. However, prevention efforts in environmental health need to address all of these concerns.
From the outset it is important to emphasize that certain environmental health problems are much more serious in developing countries than in wealthy countries. In developing nations, for example, drinking water contaminated by microorganisms and toxic substances causes considerable morbidity and mortality (see Chapter 16), and burning coal, wood, and other biomass fuel sources for cooking and heating contributes to indoor and outdoor air pollution (see Chapter 13). Chemical releases are more common, and there are fewer means to protect workers, nearby communities, and passersby. Worldwide there are large numbers of deaths and injuries due to earthquakes, storms, and floods; many of these deaths are preventable with appropriate environmental measures such as construction standards for homes and buildings, which are less likely to be implemented in developing
1510
nations.
René Dubos, in 1965, noted that indices of environmental health are “expressions of the success or failure experienced by the (human) organism in its efforts to respond adaptively to environmental challenges.” Prevention in environmental health is at its core a continuous effort to adapt to environmental challenges, most of which are created by human activities. With rapid population growth, development, and technological change on a global scale, prevention efforts have become more and more complex.
Despite these challenges there is evidence of remarkable success in environmental health protection over the last two centuries. The sanitary movement of the 1800s resulted in enormous reductions in mortality from infectious diseases. This accounted for remarkable increases in life expectancy in much of the world—in the United States, from 47 years in 1900 to 80 in 2012. In the last forty-five years in the industrialized nations, stronger environmental laws have resulted in cleaner air, safer drinking water, and recovery of some rivers and lakes that in 1970 had unacceptable levels of pollution for fishing and recreation. In many parts of the world, to a great extent, the easiest problems have been addressed, leaving environmental threats that are much more difficult to control and require more participation from a broader range of society. Environmental health problems today often involve multiple small sources of pollutants rather than a few large and visible ones. Many of these small sources are from sectors such as agriculture and small business, where individual farmers and owners may be less familiar with environmental regulations and often resistant to change. Further, as countries confront climate change by reducing carbon emissions, new technologies will emerge and, with them, new challenges for prevention of health threats.
Global trends in environmental health are disturbing. Worldwide, cities are overcrowded, polluted, and provide too little open space and too few safe walking and cycling routes. Economic development and the rapid pace of urbanization have resulted in alarming increases in air and water pollution and in waste generation. Emissions of greenhouse gases, particulate air pollutants, and nitrous and sulfur dioxides from burning fuels are a major cause of morbidity and mortality globally. Drinking water is under pressure both from pollution and from overconsumption and aging drinking-
1511
water infrastructure. In many parts of the world there are serious shortages of potable water. Weather extremes associated with global warming are associated with increased risk of heat-related mortality, increased severity of weather events and the resultant impacts on human health and well-being, changes in the ranges of vector-borne diseases, altered agricultural productivity, and uncertain water supplies. Pollution and overfishing are threatening fish harvests. At the same time, efforts to produce more fish via fish farming have too often had other undesirable environmental consequences, such as water pollution. Globally, there is little control of chemicals and pesticides (Chapter 18) in commerce and in consumer goods and in how they are disposed of. Prevention of noncommunicable diseases is especially challenging for developing countries because these diseases are multifactorial, and because the scarcity of local data makes prevention efforts highly dependent on international practices instead of being rooted in local culture, lifestyles, and climate (McMichael, Woodruff, & Hales, 2006).
1512
Concepts of Environmental Health Prevention The DPSEEA (driving forces-pressures-state-exposure-effects- actions) model, presented in Chapter 1 (see Figure 1.4), is useful in understanding environmental health prevention efforts. Driving forces are factors such as population growth and technology development that motivate environmental processes. These result in the generation of environmental pressures, for example, increases in vehicle miles driven or in the number of coal-fired power plants. The state of the environment, such as the concentration of pollutants in air (and whether such concentrations are potentially hazardous), is modified by such pressures. Exposure occurs when people are present both at the place and at the time the hazard occurs, and when there is an intact pathway for exposure. Depending on the amount of exposure (dose) and timing of exposure, as well as other factors such as life stage and co- exposures, exposure may lead to health effects.
Actions to reduce or control the hazards (or to promote environmental health) can be taken at all points in this chain of events. In 1958, Leavell and Clark defined a model for prevention that remains relevant. In this three-level model, primary prevention involves interventions prior to the development of any signs of ill health. In the case of environmental health, strategies directed toward modifying driving forces, pressures, and state of the environment are primary prevention efforts. Such efforts are divided into two categories:
Health promotion: interventions that are directed not toward the prevention of a specific disease but rather toward further general health and well-being. Education about safe household pest management strategies is an example of such an intervention (see Chapter 18).
Specific protection: interventions taken to intercept known causes of diseases. The phaseout of lead (a known developmental neurotoxicant) in gasoline is an example of such an intervention (see Tox Box 11.1, in Chapter 11).
Secondary prevention is early detection of a health problem,
1513
prior to the onset of disease, for the purpose of intervening at an early stage to prevent the development of the disease. In environmental health this is usually a preventive effort targeting the phase when exposure has begun to occur but prior to the development of any health impacts. An example of such a prevention strategy is occupational lead screening, to identify workers at an early stage of exposure and to take steps to prevent further exposure. Tertiary prevention involves early identification and treatment of people with a disease, to prevent or forestall disability and/or death. An example of tertiary prevention is the effort to ensure that patients with asthma follow recommended guidelines for medical treatment and environmental remediation in order to reduce the frequency and severity of asthma attacks.
The case of childhood lead poisoning is a good illustration of the value of primary prevention. In the United States, early efforts to control childhood lead poisoning were focused on massive efforts to assess children's blood lead levels, via blood lead screening campaigns. This was tertiary prevention: these programs identified children with clinically elevated blood lead levels (initially, 60 μg/dL and above) so that they could be treated to avert the most severe consequences of lead poisoning. As a result of discoveries about lead toxicity the CDC's reference level for lead was lowered, in several steps, from 60 to (by 2012) 5 μg/dL. At the same time, government began to fund efforts to remediate lead contamination in households where there were children with elevated blood lead levels. This was secondary prevention, and it stopped lead-poisoned children from being reexposed when they returned home. By the 1990s in the United States, most children identified with elevated blood lead levels did not require specific medical therapy. The emphasis shifted to primary prevention efforts: control of lead in paint, pipe solder, and other plumbing materials and in numerous other consumer products and the phaseout of lead in gasoline in the 1980s. These measures lowered lead exposures across the entire population. Most recently, efforts to abate lead-based paint have focused on all housing that is likely to expose children to lead, not just homes with lead-poisoned children—often as part of broader “healthy housing” initiatives. This is a transition from an illness- based model, one predicated on identifying and treating clinically ill children, to a model of wellness promotion, one that seeks to
1514
prevent lead toxicity and to promote healthy residential settings. While physicians and other medical professionals continue to have a role to play, there is a much stronger role for environmental and housing experts and for community efforts to enforce housing codes (American Academy of Pediatrics, Committee on Environmental Health, 2005).
The practice of industrial hygiene is an approach to prevention in occupational health that hews to a prevention hierarchy that is similar in concept to primary and secondary prevention (see Chapter 8). From preferable to less preferable prevention approaches, the hierarchy is
Substitution. Use safer chemicals, products, processes, or activities to eliminate the hazard from the workplace.
Engineering controls. Use equipment that reduces or controls exposure in and around work areas (part of a strategy called isolation). This includes ventilation methods, such as introducing fresh air.
Administrative controls. Change the way that workers do their job in order to reduce or eliminate exposures to hazards.
Personal protective equipment (PPE). Enforce the use of such equipment as respirators, hard hats, face and eye protection, hearing protection, gloves, and protective clothing and/or footwear that reduces or eliminates exposure to the hazard.
Pollution prevention is an approach to environmental health prevention akin to the concept of primary prevention. It extends approaches used in industrial hygiene to the general environment. The principles of pollution prevention as defined by the 1990 Pollution Prevention Act are that
“Pollution should be prevented or reduced at the source whenever feasible”;
“Pollution that cannot be prevented should be recycled in an environmentally safe manner whenever feasible”;
“Pollution that cannot be prevented or recycled should be treated in an environmentally safe manner whenever feasible”; and
1515
“Disposal or other release into the environment should be employed only as a last resort and should be conducted in an environmentally safe manner.”
Pollution prevention aims for increased efficiency in the use of raw materials, energy, water, or other resources, or for protection of natural resources by conservation. Pollution prevention can be envisioned as a ladder of potential environmental health strategies, in order of most to least preferable:
Source reduction
Waste minimization
Reuse of materials
Recycling of materials
Emissions controls
Proper waste disposal
Cleanup of wastes and spills
Source reduction practices are varied and include equipment or technology modifications; process modifications; reformulation of materials; redesign of products; substitution of raw materials; and improvements in housekeeping, maintenance, training, or inventory control. When all costs are taken into account, reduction of pollution at the source is generally less expensive than end-of-pipe controls on emissions and/or environmental cleanup. Pollution prevention strategies can also be more effective than efforts to address pollution in one medium at a time. Multimedia approaches look at all impacts of decisions “from cradle to grave”; such an analysis, called a life cycle analysis, can result in the adoption of more effective preventive strategies (life cycle analysis is described in detail in Chapter 3).
1516
Principles of Prevention in Environmental Public Health In 1992, more than one hundred nations represented at the United Nations Conference on Environment and Development (UNCED) in Rio de Janeiro signed the Rio Declaration on Environment and Development, a document that formally adopted the goal of sustainable development and twenty-seven principles of sustainable development, many of which have a direct bearing on prevention. Chief among these is Principle 1, which states: “Human beings are at the center of concerns for sustainable development. They are entitled to a healthy and productive life in harmony with nature” (UNCED, 1992). Additional principles for sustainable development that are key to public health prevention are the precautionary principle and the principles of intergenerational equity, of access to information and the decision-making process, of integrated decision making, and of polluter pays.
The precautionary principle, as formally stated in 1992, says: “In order to protect the environment, the precautionary approach shall be widely applied by States according to their capabilities. Where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be used as a reason for postponing cost-effective measures to prevent environmental degradation”(UNCED, 1992). For example, the pesticide dichlorodiphenyltrichloroethane (DDT) was banned in the United States long before its precise mechanisms of action had been described by scientists (see Chapter 18). Another example concerns the introduction of tens of thousands of chemicals into commerce without requiring premarket testing or regulation of those chemicals, as described in Chapter 6. Adoption of the precautionary principle in this case would imply a duty to take “cost-effective” measures to reduce environmental degradation without the demand for “full scientific certainty” about the harm of toxic chemicals, greenhouse gases, and so forth prior to taking action to prevent damage to health and the environment from such hazards.
The principle of intergenerational equity states: “The right to development must be fulfilled so as to equitably meet
1517
developmental and environmental needs of present and future generations.” This principle emphasizes the responsibility of the present generation to take steps to prevent adverse circumstances for generations that follow. For example, persistent organic pollutants (POPs), such as DDT (discussed in Chapter 18), PCBs (see Tox Box 2.1, in Chapter 2), methylmercury (see Tox Box 13.2, in Chapter 13), and dioxins (see Tox Box 19.1, in Chapter 19), have left a legacy of pollution for future generations. Emissions of greenhouse gases have set into motion processes that will alter the earth's climate for generations to come. This principle can come into conflict with economic models that assume that actions need to be judged only against the expected economic return from other similar investments, an approach that can zero out benefits to future generations. In practice, decision makers need to include both economic analyses and consideration of the principle of intergenerational equity, particularly for outcomes such as climate change, for which the consequences (and therefore the economic costs) are very difficult to predict but likely to be large and irreversible (see Chapter 10).
The principle of access to information and the decision-making process states: “At the national level, each individual shall have appropriate access to information concerning the environment that is held by public authorities, including information on hazardous materials and activities in their communities, and the opportunity to participate in decision-making processes. States shall facilitate and encourage public awareness and participation by making information widely available.” This principle, often referred to as the right to know, can be found in U.S. law, including OSHA's right-to-know standard for workers, and the Emergency Planning and Community Right-to-Know Act (EPCRA) of 1986, a mainstay of preparedness for chemical and other disasters. Many different actors—environmental experts, farmers, industries, utilities, developers, government agencies at all levels, and individual consumers—are involved in environmental decision making and need environmental information to manage risk. Having shared information and input into decision-making processes is also a key element of any democratic process.
According to the principle of integrated decision making, “In order to achieve sustainable development, environmental protection
1518
shall constitute an integral part of the development process and cannot be considered in isolation from it.” This means that environmental considerations need to be incorporated into decision-making processes at all levels. This principle has been incorporated into the health in all policies movement in public health in the United States and globally. In the United States, the National Environmental Policy Act (NEPA) requires the preparation of environmental impact reports for all federally funded projects, and many states have such requirements as well. A related tool, the health impact assessment, focuses specifically on health consequences of decisions “upstream” from health. (HIAs are explored in detail in Text Box 15.5, in Chapter 15.) For example, a health impact assessment might assemble data comparing the health consequences of a highway expansion, a transit investment, and improved pedestrian infrastructure to help planners reach the most health-promoting decision on the use of transportation funds (Dannenberg et al., 2006).
The polluter pays principle embodies the notion that those who cause and profit from pollution should bear the burden of cleaning it up. In economic terms this is an effort to internalize the costs of externalities. More recently, this principle has also evolved into the concept of economic instruments such as pollutant trading systems that seek to shift the societal cost of pollution to the polluter, in order to reduce the overall levels of pollution. The ability to assign the cost of emissions and cleanups to polluters serves as a powerful incentive for pollution prevention.
1519
Core Functions of Environmental Public Health In 1988, the U.S. Institute of Medicine published The Future of Public Health, a report that defined three core public health functions: assessment, policy development, and assurance (Institute of Medicine, 1988).
Exposure assessment—the science behind environmental public health assessment—is discussed extensively in Chapter 8; this chapter focuses only on aspects of public health assessment having to do with prevention. The DPSEEA framework (described earlier) helps to identify a number of potential targets for monitoring environmental conditions and associated health outcomes (also see Text Box 26.1). As a tool for prevention, monitoring can provide the data needed to
Forecast the likely impacts of new technologies and population growth.
Assess trends in drivers of environmental health.
Track trends in the state of the environment and human exposure levels.
Track health trends.
1520
Text Box 26.1 Keeping Track in Environmental Health Given that assessment is one of the core public health functions, public health surveillance—“the systematic, ongoing collection, management, analysis, and interpretation of data followed by the dissemination of these data to public health programs to stimulate public health action” (Lee, Teutsch, Thacker, & St. Louis, 2010) p. viii—has long been considered a pillar of public health. As shown in Table 26.1, environmental public health surveillance involves monitoring environmental and health status to identify and solve community environmental health problems. Given the vast variety of environmental and health data, that is a tall order!
Table 26.1 Essential Services of Environmental Public Health
Ten Essential Services of Public Health
Ten Essential Services of Environmental Health
1. Monitor health status to identify and solve community health problems.
1. Monitor environmental and health status to identify and solve community environmental health problems.
2. Diagnose and investigate health problems and health hazards in the community.
2. Diagnose and investigate environmental health problems and health hazards in the community.
3. Inform, educate, and empower people about health issues.
3. Inform, educate, and empower people about environmental health issues.
4. Mobilize community partnerships and action to identify and solve health
4. Mobilize community partnerships and actions to identify and solve
1521
problems.
5. Develop policies and plans that support individual and community health efforts.
5. Develop policies and plans that support individual and community environmental health efforts.
6. Enforce laws and regulations that protect health and ensure safety.
6. Enforce laws and regulations that protect environmental health and ensure safety.
7. Link people to needed personal health services and assure the provision of health care when otherwise unavailable.
7. Link people to needed environmental health services and assure the provision of health care when otherwise unavailable.
8. Assure a competent public and personal health care workforce.
8. Assure a competent public health and personal health care workforce.
9. Evaluate effectiveness, accessibility, and quality of personal and population- based health services.
9. Evaluate effectiveness, accessibility, and quality of personal and population- based environmental health services.
10. Research for new insights and innovative solutions to health problems.
10. Research for new insights and innovative solutions to environmental health problems.
Sources: CDC, 2008, 2011.
Health data include the results of such national surveys as, in the United States, the National Health and Nutrition Examination Survey (NHANES) and the National Health Interview Survey (NHIS), vital statistics reports, and records from the health care system. This latter source is increasingly informative under the Patient Protection and Affordable Care Act of 2010, with the growth of accountable care organizations, but stringent patient privacy safeguards limit data access. Emerging innovative sources of health data, such as smartphone apps that record physical activity, food
1522
purchasing records on consumer databases, social media mentions of symptoms, and search engine records of health- related searches, offer intriguing possibilities, albeit ones whose utility and limitations are not fully understood and that raise considerable privacy concerns.
Environmental data are even more extensive. They include traditional data sources on toxic exposures, such as biomonitoring results carried out during health surveys, results of air and water monitoring, results of food sample testing, and data on the location of hazardous waste sites. But environmental data also include ecosystem data—for example, temperatures, hydrology, insect species prevalence, vegetation—and built environment data such as walkability, density, fresh food availability, park proximity, and transit access.
Given this complexity, environmental public health surveillance is challenging. Moreover, all these data are being collected at different temporal and spatial scales and organized using different database architectures. Often access is controlled by a variety of agencies and organizations. The data volumes are enormous, requiring the complex techniques of big data management and analysis. Metadata—which are critical to valid analyses and interpretations of data—can be difficult to access and to understand. Correlations alone do not prove causation; when numerous variables are collected and analyzed, many statistically significant associations will emerge by chance alone; many of these will be of little or no public health significance. This in turn creates a communication challenge; how should complex, sometimes ambiguous data best be shared with stakeholders and the public?
A national effort to tackle these challenges is the National Environmental Public Health Tracking Program of the Centers for Disease Control and Prevention (CDC) (www.cdc.gov/nceh/tracking), started in 2002. This program grew out of a recognition, by advocates and public health professionals, that diverse streams of information needed to be brought together to help clarify environmental health trends, set priorities, and assess the effectiveness of
1523
interventions. State and local health departments were funded to identify data sources, build data linkages, and perform data analyses and reporting. Examples of the approaches used include the tracking of air pollution and asthma, of cancer and water contamination, and of extreme heat and heat-related illness.
Research is also an important component of the assessment process. Information about mechanisms of environmental health risks, including gene-environment interactions, will assist researchers in developing more informed and targeted strategies for disease prevention. Additionally, we have considerable uncertainty about the value of ecosystem services to human health and welfare. There have been serious disruptions in fundamental planetary processes, as described in Chapters 2 and 3, most famously the carbon cycle with a multitude of potential health effects (see Chapter 12) but also the nitrogen and phosphorus cycles, which have implications for pollution of sensitive water bodies. Species extinctions, overfishing, overfarming, and overirrigation have been documented in dramatic terms, but we do not fully understand the impacts on health.
From the standpoint of prevention it is important to learn not only about the proximate causes of a problem but also the root causes. As an example, scientists have identified in utero exposure to methylmercury as a risk factor for neurodevelopmental delays in children (see Tox Box 13.2, in Chapter 13). This is an issue of intergenerational equity, and effort has been directed toward protection of the fetus by advising women who are or who may become pregnant to reduce their consumption of mercury- contaminated fish. Going upstream from the problem of mercury- laden fish, however, one can also identify major sources of mercury emissions, such as coal-fired power plants and require the installation of pollution control equipment to remove the mercury from these emissions. Examination of root causes might suggest a very different set of policy approaches than fish consumption advisories. In fact, because mercury releases have global impacts, the recently adopted Minamata Convention on Mercury has identified a range of causes of mercury pollution to be addressed, including phasing out nonmedical uses of mercury batteries, mercury switches and relays, some compact fluorescent lamps,
1524
mercury in soaps and cosmetics, and certain mercury-containing medical devices such as thermometers and blood pressure devices. Governments have also identified the need to reduce mercury emissions from small-scale gold mining and from coal-fired power plants as well as from large-scale industrial plants (United Nations Environment Programme, 2015).
Environmental health policy has undergone major transformations over the years. There are numerous examples of environmental health policy failures, most reflecting an inability to predict, prepare for, and prevent adverse effects of new technologies. This includes the massive food safety and consumer products problems in the early 1900s (well documented by author Upton Sinclair); the decision in the early part of the twentieth century to permit the use of lead in gasoline; the killer smog episodes in London in the mid- twentieth century caused by soot from coal burning; a very long term problem resulting from “playing catch-up” with the risks of industrial chemicals and pesticides (see Chapter 18), leading, for example, to epidemics of cancers from asbestos (see Tox Box 20.3, in Chapter 20) and the industrial chemical vinyl chloride; and today, the continued construction of polluting industrial and energy plants that burn fossil fuels even while the evidence of global warming is incontrovertible. In addition, nanotechnology-based industries in the United States and elsewhere have expanded at a much more rapid pace than the development of a policy framework to anticipate and mitigate the possible adverse consequences of this new technology.
At the same time, there are many examples of successful prevention strategies. The National Environmental Protection Act (NEPA) and similar laws in the United States and internationally have required environmental impact studies that have been effective tools for pollution prevention. The Toxics Release Inventory in the United States (known as a pollutant release and transfer registry elsewhere) is an example of a right-to-know approach to policy development that has promoted pollution prevention through informing industry and communities of toxic releases and driving pollution reduction and pollution prevention efforts; such efforts have been particularly effective in states such as Massachusetts that have toxic use reduction laws. In the United States the Clean Air Act for new sources and the Food Quality Protection Act have been
1525
effective in preventing risks. An ethic of pollution prevention has caught hold in a number of sectors. The American Chemical Society, chemists, and many in the chemical industry have advanced the science of green chemistry and green engineering to develop new materials and processes that are inherently safe from cradle to grave. Builders and architects are increasingly embracing the green building movement (discussed in Chapter 20) with voluntary certification programs, stimulating customer demand for buildings that are more sustainable. Movements such the initiative begun by the Health Care Without Harm coalition have captured the imagination of the medical community, which is in turn evolving more environmentally benign ways to build and operate hospitals and other medical facilities. Many companies, as well as governments at many levels, have undertaken environmental purchasing policies. All of these voluntary approaches have been driven by the availability of information about the potential hazards associated with various alternatives.
A fundamental issue in environmental health policy development is that there are often great uncertainties in every aspect of policy development. Risk characterizations often include large ranges of potential risks, but there can be large uncertainties in risk management decisions as well. It is when decisions must be made in the face of uncertainty that principles such as precaution may be invoked. Technology-based approaches, such as the Maximum Available Control Technology (MACT) standards developed for hazardous air pollutants under the Clean Air Act, can be a useful strategy for preventing risks (of magnitude unknown) in the face of uncertainty by applying available technologies. The hazardous air pollutant standards promulgated by the U.S. Environmental Protection Agency (U.S. EPA) have been extolled for resulting in a 90% reduction of hazardous air emissions during the decade after the passage of the 1990 Clean Air Act Amendments. While such approaches do achieve prevention goals to an extent, failure to analyze and understand risk across the life cycle can have adverse consequences. For example, in the case of the hazardous air pollutant standards, control of ambient air emissions could come at the cost of greater exposures within the workplace, in discharges to water or waste, or even in a final product (Goldstein, 2004). Without an effort to reduce uncertainties about the risk of a substance, such exposures could go unnoticed and uncontrolled, but
1526
the Clean Air Act does not drive the generation of such data. Conversely, excessive analysis can also have adverse and even paralyzing consequences; for example, the U.S. EPA's dioxin assessment took more than twenty years (see Tox Box 19.1, in Chapter 19).
A second limitation to our ability to prevent environmental health risks is that all too often there are trade-offs among risks. An example of a risk-risk trade-off is the disinfection of drinking water with chlorine. Chlorine not only kills most pathogens in source waters but also leaves a residual level that protects against pathogens that may be introduced within the water distribution system. Yet as described in Chapter 16, chlorination can form disinfection by-products, some of which have chronic, low-level toxicity. It is almost axiomatic that, as in the case of medicine, every environmental intervention that prevents one adverse effect is likely to have adverse side effects as well. A prevention strategy takes a careful look at all implications of alternative interventions.
Environmental public health assurance is complex because of the myriad parties who have a stake in environmental health issues and/or must take action in order to implement policies. Few of those parties are environmental health experts. In many cases, policymakers in the executive, legislative, and judicial branches of government must be persuaded that a particular policy can be implemented. Thus it is critical that the public be engaged at every stage of the process and that there be broad agreement with the assessment of the problem, as well as trust in the policymaking process. In other words, there needs to be a shared sense that there is a problem that needs to be addressed, a shared view of the magnitude of the problem and the uncertainties, and assurance that a reasonable effort was made to develop fair, effective policies and to engage all involved parties. Vested interests may opt to oppose implementation of a new policy, in which case it is particularly important to secure the agreement of other parties. Increasingly, in the case of pollutants with global transport, such as mercury, there are efforts to craft global agreements, such as the Minamata Convention on Mercury, adopted in 2013 and mentioned earlier. These international agreements are complex and difficult to negotiate, involving the entire cast of affected parties from multiple countries.
1527
One particularly challenging aspect of implementing preventive policies is the difficulty of proving what would have happened in the absence of a given policy. As has recently been observed in the case of climate change, some parties disbelieve the results of models and predictions of future scenarios, and they may be reluctant to invest in preventive strategies on that basis. Furthermore, for those who think primarily in economic terms, preventive interventions may appear to be bad investments. As already noted above, because economists use a discount rate to calculate the future value of money that is invested in the present, economic analyses tend to downplay the value of measures that provide benefits in the remote future. Finally, the urgent may be the enemy of the important; more pressing and immediate issues may eclipse longer range concerns. Accordingly, it is crucial that preventive actions be accompanied by efforts to monitor the consequences of those actions, to link that information to policies that have been implemented, to modify actions based on this review, and to provide accurate and timely feedback to the public and policymakers about the successes and failures of such actions.
In the United States, public health organizations have defined a set of ten essential services of public health, all of which are necessary to support the three core functions of assessment, assurance, and policy development. More recently the CDC's National Center for Environmental Health (NCEH) has defined the ten essential services of environmental health, services relevant to the environmental health practice community. Both sets of services are shown in Table 26.1.
Each of these services is an important component of the overall public health infrastructure. For instance, the first essential service requires the creation of an environmental health surveillance system, which supports detection of environmental hazards and related illnesses and assessments of the need for additional services. Using data from this system, public health professionals can advocate for the necessary legal support and resources for programs to address community needs. In recent years the development of spatial data technology and its use in geographic information systems has allowed public health officials to map the occurrence of hazards and illnesses in their communities and then to use these maps in dialogues with citizens and elected officials to create
1528
awareness and the political will to address these concerns (see Chapter 5).
To reinforce, support, and standardize public health systems, the CDC developed a set of performance standards tools that can be used to assess the capacity of state and local agencies and local boards of health to provide the ten essential services of public health. These tools have been utilized by the NCEH to develop the Environmental Public Health Performance Standards (www.cdc.gov/NCEH/ehs/EnvPHPS/default.htm), a set of standards for environmental health agencies and other practitioners, based on the ten essential services of environmental health. Through voluntary use of these standards at the federal, tribal, state, and local levels, the NCEH aims to enhance the capacity, consistency, and accountability of the nation's environmental health services. A number of local and state agencies have used these standards to improve their environmental health services.
There also has been a need for assessments of the quality of local governments' environmental health services. In the United States an assessment protocol has been developed: Protocol for Assessing Community Excellence in Environmental Health: A Guidebook for Local Health Officials (PACE-EH) (National Association of County and City Health Officials [NACCHO], 2004). This multistep protocol (see Table 26.2) evaluates progress and supports planning for the future. (www.naccho.org/topics/environmental/PACE-EH/index.cfm). The NCEH strongly supports the use of community environmental health assessments as a means to improve community health, and makes a variety of resources and case studies available for this purpose (see, e.g., www.cdc.gov/nceh/ehs/ceha/default.htm). A number of other agencies, such as the U.S. Environmental Protection Agency, have developed tools for community involvement, centering around the core value of community empowerment and voice in the design of environmental health services and healthier communities. The EPA's CARE program (Community Action for a Renewed Environment) is one such example (www.epa.gov/care).
Table 26.2 The Protocol for Assessing Community Excellence in Environmental Health (PACE-EH) Process
1529
Task 1 Determine community capacity. Task 2
Define and characterize the community.
Task 3
Assemble a community-based environmental health assessment team.
Task 4
Define the goals, objectives, and scope of the assessment.
Task 5
Generate a list of community-specific environmental health issues.
Task 6
Analyze the issues with a systems framework.
Task 7 Develop locally appropriate indicators. Task 8
Select standards against which local status can be compared.
Task 9
Create issue profiles.
Task 10
Rank the issues.
Task 11
Set priorities for action.
Task 12
Develop an action plan.
Task 13
Evaluate progress and plan for the future.
Note: Detailed instructions for each of the thirteen tasks in the PACE EH process are outlined in Protocol for Assessing Community Excellence in Environmental Health: A Guidebook for Local Health Officials (NACCHO, 2004).
1530
Environmental Public Health Systems The need for environmental health practices has been recognized since ancient times. The biblical book Leviticus mentions food protection, housing quality, and quarantine. Engineers and public officials in ancient Rome planned for the water supply and waste disposal, and medieval England used quarantine to limit the spread of disease. Later, as recounted in Chapter 1, social reformers in England advocated for improved housing conditions and clean drinking water (as Edwin Chadwick did in his 1842 Sanitary Report, for example), and documented important environmental health protections (as in the 1871 Report of the Royal Sanitary Commission). Their counterparts in the United States published a similar report in Massachusetts and campaigned effectively for the establishment of a Massachusetts state board of health in 1869. By the end of the nineteenth century, forty of the forty-five states in the United States could claim health departments. The late years of the nineteenth century and the first six decades of the twentieth century saw the first of the modern eras of environmental health practice. During the first fifty years of the twentieth century, the United States and many industrialized nations passed public health laws that regulated water and sewage treatment and addressed protection of food, provision of safe housing and human and solid waste disposal, and reduction of insect- and rodent-borne diseases, resulting in a corresponding decrease in human morbidity and mortality and an increase in life expectancy (Duffy, 1990).
The rapid industrialization that had begun during the late nineteenth century continued with the economic expansion that followed World War II. Additional widespread pollution of land, water, and air and the creation of new pollutants such as synthetic organic compounds helped to usher in the second modern era of environmental health protection. That era saw the creation of increasingly complex national and local laws to regulate the production and certain uses of chemicals and pesticides and to control air and water pollution, as well as disposal of hazardous substances.
In the United States at the state level, legislatures created environmental agencies, adding responsibility for the enforcement
1531
of new environmental laws and regulations for air, water, and hazardous waste. In some cases, traditional environmental public health activities such as food protection and sanitary sewage disposal were also transferred to these new agencies. Although the increased visibility and funding were important in supporting necessary environmental health programs, the separation of these programs from health agencies over the last fifty years has resulted in the creation of separate data systems, uncoordinated planning, and the loss of a comprehensive picture of the community's health and environment. In addition, many environmental health specialists, and indeed their agencies, became increasingly isolated from their public health counterparts in the state and local departments of health, losing valuable affiliations that would later take years to reestablish.
Along with the new environmental laws and agencies came a new generation of environmental health specialists who devoted their careers to one specific area of the environment, such as solid waste, hazardous waste, air quality, or drinking water. Their training often did not include training in general public health concepts or in the use of public health tools such as epidemiology and effective public health campaigns. More recently, environmental health agencies have needed to learn how to address the environmental justice and equity concerns of their multicultural communities more effectively (Chapter 11) and to enhance community participation and communicate risk (Chapter 28). In the United States many laws have been written or amended to require public involvement in the development of policies, permits, and hazardous waste site remediation plans. Agencies have needed to expand their workforces, not only to include experts in environmental science, engineering, management, and law but also to bring in experts in communication who can support community engagement efforts (see Text Box 26.2).
1532
Text Box 26.2 Careers in Environmental Health Environmental health offers a rich variety of career options— not all of which are named or even recognized as environmental health occupations!
Federal, state, and local health departments employ environmental health professionals to perform a wide range of essential duties. In many local health departments, environmental health professionals represent a major part of the workforce, given the importance of such functions as restaurant inspections and water and sewage inspections. In addition to general public health training, these professionals often earn additional credentials, whose names give an indication of the corresponding expertise:
Certified in Comprehensive Food Safety (CCFS) and Certified Professional–Food Safety (CP-FS)
Registered Environmental Health Specialist/Registered Sanitarian (REHS/RS)
Certified Environmental Health Technician (CEHT) and Registered Environmental Technician (RET)
Certified Installer of Onsite Wastewater Treatment Systems (CIOWTS)
Registered Hazardous Substances Professional (RHSP) and Registered Hazardous Substances Specialist (RHSS)
Healthy Homes Specialist (HHS)
Environmental health professionals work extensively in the private sector, managing health, safety, and environmental programs for companies or working for consulting firms that provide such services. In nongovernmental organizations (NGOs), environmental health professionals work in a range of positions—focusing on general environmental health issues for environmental organizations, on workplace safety and health issues for labor unions, and on disaster
1533
preparedness and response for relief organizations.
Clinicians, including physicians, nurses, and others, deliver clinical services, such as diagnosing and treating chemical toxicity, managing worksite health promotion programs, and working in related fields such as travel medicine. Both physicians and nurses can receive special training and certification in occupational and environmental medicine (for physicians) and occupational health nursing (for nurses).
Environmental health specialists employed by the military and other government agencies are engaged in the full range of all the activities that occur in state and local government, private sector, and health care agencies.
Finally, many professionals “do” environmental health without identifying themselves as environmental health professionals—the transportation planner who works to provide more options for walking and cycling, the park superintendent who works to get kids outside, the environmental official who works to reduce chemical emissions, the architect who designs environmentally friendly buildings without toxic materials, and the manufacturer who reduces adverse health and environmental impacts throughout the life cycle of products, protecting both workers and communities.
Professional organizations that support environmental health professionals are listed in the For Further Information section at the end of this chapter.
In the United States, environmental health services are provided at federal, tribal, state, and local levels and in the medical, academic, nonprofit, and private sectors. The federal laws governing various aspects of the environment are enforced by numerous federal agencies, including the U.S. Environmental Protection Agency (EPA), the U.S. Department of Agriculture (USDA), the U.S. Food and Drug Administration (FDA), and others. Many federal laws contain provisions that supersede state laws in order to provide equal environmental health protection to all citizens. Some of the federal Acts, such as the Clean Air Act, permit delegation of authority to states and, under certain circumstances of local home
1534
rule, to local jurisdictions. State governments have the authority to enact further environmental legislation, as long as it does not conflict with federal law. Many of these state laws provide additional protections or address areas not covered by federal law. Within states, municipalities and counties usually have the authority, given by their state legislature, to enact local laws to protect health and environment for their citizens.
Who decides what agencies should provide environmental health services, how they should be organized, and what services should be included? Historically, environmental health agencies (or parts of agencies) have been created through a combination of public health leadership, citizen advocacy, and political will. Their creation begins with the perception of a need to protect the public from environmental hazards and with the desire for a government unit charged with the provision of those services that will be responsive to elected officials and the public. The specific services provided are built around a core set of environmental health services, such as food protection, water sanitation, and air quality protection, with further services added as determined by public health data and public interest. Ideally, the community-specific tailoring of these agencies becomes a method of ensuring that the highest priority services for that community are provided. Yet this necessary and desirable local political process has also resulted in a patchwork of services that are not coordinated and that leave large gaps in the core public health functions of assessment, assurance, and policy development.
Because the authority for these services has developed over many decades and in multiple locations, the organization and delivery of environmental health services is now complex and is not easily understood by professionals themselves, much less the general public. While federal environmental laws have driven the design and authority of state regulatory agencies in the United States, there has been no organizational standardization for enforcement of these laws. Many state regulatory agencies have become oriented toward specific media and often lack the public health support, such as capacity in epidemiology, public health evaluation, or applied research, that would allow a larger perspective on the environment and health (Burke, Shalauta, & Tran, 1995a). As a consequence, state regulatory enforcement efforts have often taken precedence
1535
over disease prevention and health promotion, as reflected by levels of funding and activities (Burke, Shalauta, & Tran, 1995b). However, over the last two decades in the United States a multitude of efforts have been undertaken to reconnect the practice of environmental health to prevention. These efforts have emphasized use of public health data to guide and assess environmental health policies and practices, the engagement of communities with disparate environmental and public health impacts, and an increased emphasis on measurement of indices of health whether via measurement of human exposures (e.g., biomonitoring) or tracking of health outcomes (e.g., asthma morbidity).
1536
Summary Prevention of illness, injury, premature death, and disability is a central mission of public health, and this is nowhere truer than in environmental public health. Prevention includes both the control of hazards—cleaning up a hazardous waste site or reducing air pollutants coming from a smokestack or tailpipe—and also health promotion through environmental strategies—providing parks, sidewalks, and bicycle paths. Prevention in environmental health extends upstream to such domains as energy, transportation, housing, and agriculture, whose practices have an impact on human health and well-being. Primary prevention, such as the replacement of a hazardous chemical by a safe one, is a trademark environmental health approach, but secondary prevention (such as blood lead screening) and tertiary prevention (such as maintenance treatment of childhood asthma) are also relevant in environmental health. The prevention hierarchy ranges from definitive approaches, such as completely removing a hazard, which are preferred, to administrative, behavioral, and end-of-pipe approaches, which are less preferred. The precautionary principle proposes that cost- effective preventive measures should proceed even in the face of scientific uncertainty. In environmental public health practice, all the core functions of public health—in the categories of assessment, policy development, and assurance—are used to pursue prevention.
1537
Key Terms administrative controls
Methods that modify or control exposures based on changing work practices or procedures, with the goal of reducing the duration, frequency, and severity of exposure to hazardous chemicals or situations.
discount rate An annual percentage rate used in cost-benefit analysis to determine the future value of money invested in health and social programs in the present, as well as the future value of the benefits expected to accrue from those investments (also referred to as the social discount rate).
1538
DPSEEAs Driving forces
Macro-scale factors that ultimately drive human health processes (see Chapter 3).
Pressures Responses to driving forces, as manifested by changes to the physical, built, and social environment, occurring in a number of sectors: e.g., transport, energy, agriculture, industry, tourism.
State Alterations in the conditions of the physical, built, and social environment, as found by monitoring, for example, pollutant levels, weather patterns, social determinants, and pathogen loads.
Exposure For chemical and biological agents, a continuum of contact with disease risk factors from skin contact, ingestion, inhalation, and injection to metabolism and to delivery to vulnerable organs and cells. Exposure also occurs in the form of physical forces that are associated with injuries, such as motor vehicle crashes and falls, and in the form of both beneficial and harmful social influences, such as stress, discrimination, and mass media messages, which in turn may modify exposure to other agents (see Chapters 6 and 8).
Effects Biological changes that are indicative of response to exposure, predisease states, onset of disease, injury, and/or disease progression (see Chapter 6).
Actions The steps taken at every level of the DPSEEA framework, from the individual to the policy level, in order to enhance health and well-being and prevent ill health and premature death.
end-of-pipe controls Means of controlling pollution by cleaning contaminated flows of water or air at the point where the effluent enters the environment.
engineering controls
1539
Use of machinery or equipment engineered to eliminate or reduce exposure to a chemical or physical hazard.
environmental impact reports and statements Analyses required under U.S. federal law (statements) or state laws (reports) that describe the positive and negative environmental effects of a proposed action, and alternative actions, as an aid to decision making and to promote cooperation and communications among various actors involved in environmental decision making. Also, and more generally, “environmental impact assessment” is Principle 17 in the Rio Declaration.
environmental justice (1) A social movement promoting a fair distribution of environmental hazards such as waste sites and highways, and benefits such as clean air, safe drinking water, green space, public transit, and economic opportunity; and (2) laws and policies that promote the fair treatment and meaningful involvement of all people regardless of race, ethnicity, national origin, or income, with regard to environmental laws, regulations, and policies.
Environmental Public Health Performance Standards A framework for assessing the capacity and performance of a local environmental health system, to help identify areas for system improvement, strengthen partnerships, and ensure that a strong system is in place for addressing environmental health issues.
essential services of environmental health Services that have been identified by the National Center for Environmental Health at the CDC as essential for environmental public health practitioners to provide. They are listed in Table 26.1.
green chemistry The designing of chemical products and processes that reduce or eliminate the generation of hazardous substances (see Chapter 6).
health impact assessment (HIA) An evaluation that combines quantitative and qualitative methods to assess the health impacts of proposed policies, plans,
1540
and projects and to explicitly address impacts on socially excluded or vulnerable populations and, more generally, to increase positive health outcomes and minimize adverse health outcomes (see Text Box 15.5).
health in all policies A strategy that aims to include health considerations in policymaking across the many sectors that influence health, such as transportation, agriculture, land use, housing, public safety, and education.
health promotion Strategies that enable people to increase control over their health and its determinants, and thereby improve their health and well-being.
integrated decision making Decision-making processes that ensure that socioeconomic and environmental issues are fully integrated into the process and that a broad range of public participation is assured, particularly when economic development is being considered.
intergenerational equity The concept that there should be fairness or justice in the balance between benefits accruing to and costs borne by adults and seniors and those accruing to and borne by children, youth, and future generations in consequence of environmental decisions.
isolation The containing of or limiting of access to hazardous materials: for example, by placing a physical barrier such as a container between a hazardous agent and a worker.
life cycle analysis A technique for assessing the environmental and social (including health) impacts associated with all the stages of a product's life, from cradle to grave, and for designing and producing products that minimize waste and pollution at the end of their useful life.
personal protective equipment (PPE) Clothing and other work accessories designed to create a barrier against workplace hazards (see Chapter 21).
polluter pays principle
1541
The principle that the polluter should bear the cost of pollution. Equivalent to internalization of environmental costs, which is Principle 16 of the Rio Declaration.
pollution prevention Reducing or eliminating hazardous waste and emissions at the source by modifying production processes, promoting the use of nontoxic or less toxic substances, and reducing the use of materials and/or reusing materials.
precautionary principle The concept articulated in Principle 15 of the Rio Declaration, “Where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be used as a reason for postponing cost-effective measures to prevent environmental degradation.” prevention
primary prevention A practice designed to prevent the onset of a disease or health problem.
secondary prevention A practice designed to identify asymptomatic persons who have preclinical disease, in order to intervene and prevent disease development.
tertiary prevention A practice designed to diagnose a disease in its early clinical stages in order to restore highest function, minimize the worst disease outcomes, and prevent disease-related complications.
prevention hierarchy The prevention hierarchy aims to focus efforts on primary prevention and source reduction approaches rather than on tertiary prevention and end-of-pipe measures that are less effective. The pollution prevention hierarchy, for example, establishes the following priority scale, from more to less preferable ways of managing chemical wastes: source reduction, reuse, recycling, recovery, and disposal. Protocol for Assessing Community Excellence in Environmental Health (PACE- EH) A methodology that guides communities and local health officials in conducting community-based environmental health assessments. public health functions Sometimes referred to as core public health functions: assessment Surveillance of diseases
1542
and injuries—monitoring trends, analyzing causes, conducting research, and identifying needs. policy development Identification and evaluation of policy alternatives including, with the aid of community involvement, analysis of evidence supporting various strategies, and development and testing of comprehensive public health policies. assurance Delivery of public health services via a number of approaches, legislative, regulatory, informational, direct provision of clinical preventive services, and linking populations to health care. public health surveillance The “systematic, ongoing collection, management, analysis, and interpretation of data followed by the dissemination of these data to public health programs to stimulate public health action” (Lee, Teutsch, Thacker, & St. Louis, 2010) right to know A principle, sometimes written into law, that individuals have the right to know the chemicals to which they may be exposed at work, in the general environment, and in consumer goods, and how to protect themselves from exposure and harm. risk-risk trade-off An analytical approach that considers whether countervailing risks may partially or completely offset the reduction in the targeted risk that results from an environmental health action, either proposed or ongoing. source reduction Any practice that reduces the amount of a hazardous substance, pollutant, or contaminant that is entering waste streams or otherwise being released into the environment. Source reduction precedes recycling, treatment, or disposal. substitution Replacing a hazardous agent, such as a chemical or pesticide, with a less hazardous or environmentally benign alternative. sustainable development Economic development that “meets the needs of the present without compromising the ability of future generations to meet their own needs” (World Commission on Environment and Development, 1987) (also see Chapter 3).
1543
Discussion Questions 1. An old adage is that “an ounce of prevention is worth a pound of
cure.” What is an environmental health example of this adage? In your example, what is the “ounce of prevention” that would prevent having to apply a “pound of cure”?
2. Sometimes, preventive goals seem to collide with each other. Examples include fish consumption advisories, breast feeding advisories, and the use of DDT to control malaria. Please pick one of these or another suitable example, and then answer these questions. What are the trade-offs between the different preventive strategies involved? How could the competing goals be balanced?
3. The precautionary principle has been the subject of considerable debate. Please do some research on this principle, and then answer these questions. What are the supporting arguments? What are the opposing arguments? What are your conclusions about this principle?
4. How would you explain the prevention hierarchy to another person as it applies to occupational health? As it applies to environmental health? Why are some kinds of prevention strategies preferred over other kinds?
5. Why is prevention more effective upstream than downstream? Be sure to explain your reasoning.
6. Opponents of environmental health regulation sometimes raise the specter of the “nanny state”—an overweening government that controls behavior, narrows people's options, and threatens liberty. Please select an environmental health policy, and then answer these questions. What is the “nanny state” argument against this policy? How could you defend this policy against this argument?
7. Discuss the links among democracy, environment, economic development, and equity. Within these linkages, what barriers exist to creating healthy people in healthy communities? What are some steps that still need to be taken to reduce these barriers in order to achieve healthy environments for all?
1544
References American Academy of Pediatrics, Committee on Environmental Health. (2005). “Lead exposure in children: Prevention, detection, and management.” Pediatrics, 116(4), 1036–1046.
Burke, T. A., Shalauta, N. M., & Tran, N. L. (1995a). The environmental web: Impact of federal statutes on state environmental health & protection, services, structure and funding. Rockville, MD: U.S. Department of Health and Human Services.
Burke, T. A., Shalauta, N. M., & Tran, N. L. (1995b). Who's in charge? 50-State profile of environmental health and protection services, organization, programs, functions/activities and state budgets. Rockville, MD: U.S. Department of Health and Human Services.
Centers for Disease Control and Prevention. (2008). 10 Essential public health services. Retrieved from http://www.cdc.gov/od/ocphp/nphpsp/essentialphservices.htm
Centers for Disease Control and Prevention. (2011). 10 Essential environmental public health services. Retrieved from http://www.cdc.gov/nceh/ehs/Home/HealthService.htm
Dannenberg, A. L., Bhatia, R., Cole, B. L., Dora, C., Fielding, J. E., Kraft, K.,…Tilson, H. H. (2006). Growing the field of health impact assessment in the United States: An agenda for research and practice. American Journal of Public Health, 96, 262–270.
Dubos, R. (1965). Man adapting. New Haven, CT: Yale University Press.
Duffy, J. (1990). The sanitarians: A history of American public health. Urbana: University of Illinois Press.
Goldstein, B. D. (2004). The precautionary principle, toxicological science, and European-U.S. scientific cooperation. Drug Metabolism Reviews, 36(3–4), 487–495.
Institute of Medicine. (1988). The future of public health.
1545
Washington, DC: National Academies Press.
Leavell, H. R., & Clark, E. G. (1958). Preventive medicine for the doctor in his community. New York: McGraw-Hill.
Lee, L. M., Teutsch, S. M., Thacker, S. B., & St. Louis, M. E. (2010). Principles and practice of public health surveillance (3rd ed.). New York: Oxford University Press, vii.
McMichael, A. J., Woodruff, R. E., & Hales, S. (2006). Climate change and human health: Present and future risks. Lancet, 367(9513), 859–869.
National Association of County and City Health Officials. (2004). Protocol for assessing community excellence in environmental health: A guidebook for local health officials [PACE-EH]. Retrieved from http://pace.naccho.org
Pollution Prevention Act of 1990. 42 U.S.C. §§ 13101–13102 et seq.
United Nations Conference on Environment and Development. Rio Declaration on Environment and Development. United Nations: Rio de Janeiro, 1992.
United Nations Environment Programme. (2015). Minamata Convention on Mercury. Retrieved from http://mercuryconvention.org
World Commission on Environment and Development. (1987). Report of the World Commission on Environment and Development: Our common future. New York: United Nations.
1546
For Further Information Books and Articles
Prevention in General
Cohen, L., Chavez, V., & Chehimi, S. (2010). Prevention is primary: Strategies for community well being (2nd ed.). San Francisco: Jossey-Bass/Wiley.
Institute of Medicine, Committee on Assuring the Health of the Public in the 21st Century. (2003). The future of the public's health in the 21st century. Washington, DC: National Academies Press.
O'Brien, M. (2000). Making better environmental decisions: An alternative to risk assessment. Cambridge, MA: MIT Press.
Prevention as Applied to Chemicals
Allen, D. T., & Shonnard, D. R. (2000). Green engineering: Environmentally conscious design of chemical processes. Upper Saddle River, NJ: Prentice Hall.
Anastas, P. T., & Warner, J. C. (2000). Green chemistry: Theory and practice. New York: Oxford University Press.
Geiser, K. (2001). Materials matter: Toward a sustainable materials policy. Cambridge, MA: MIT Press.
Organizations
Environmental Health Training Association of Environmental Health Academic Programs (AEHAP): http://www.aehap.org. An association that promotes environmental health education at the undergraduate level and administratively supports the National Environmental Health Science & Protection Accreditation Council (EHAC).
Association of Schools and Programs of Public Health (ASPPH): http://www.aspph.org. An organization of accredited public health schools and programs; these schools and programs offer
1547
graduate training in environmental health.
Environmental Health Practice American College of Preventive Medicine: http://www.acpm.org
American Public Health Association (APHA): http://www.apha.org. The largest U.S. organization of public health professionals, APHA has an active environmental health staff and membership section and related sections in such areas as occupational health.
Association for Prevention Teaching and Research: http://www.aptrweb.org
Association of State and Territorial Health Officials (ASTHO): http://www.astho.org. A national organization representing state and territorial public health agencies across the United States, ASTHO has an active environmental health program that supports states in a wide range of efforts.
Centers for Disease Control and Prevention: National Center for Environmental Health (NCEH), http://www.cdc.gov/nceh, and Agency for Toxic Substances and Disease Registry (ATSDR), http://www.atsdr.cdc.gov. Federal agencies that share environmental public health responsibility, with ATSDR focusing on hazardous chemical exposures and NCEH having a broader portfolio.
National Association of County and City Health Officials (NACCHO): http://www.naccho.org. A national organization representing local public health agencies across the United States, NACCHO has an active environmental health program that supports county and city health departments in a wide range of efforts.
National Environmental Health Association (NEHA): http://www.neha.org. A national professional society for environmental health practitioners, NEHA emphasizes training and education, credentialing, advocacy, and organizational capacity building.
National Pollution Prevention Roundtable: http://www.p2.org
Partnership for Prevention: http://www.prevent.org
1548
Chemical Safety American Chemical Society, Green Chemistry Institute: www.acs.org/greenchemistry
Beyond Benign Foundation: http://www.beyondbenign.org
International Council of Chemical Associations (ICCA), Responsible Care Project: http://www.responsiblecare.org/page.asp?p=6341&l=1
United Nations Environment Programme (UNEP), Cleaner Production Project: http://www.unep.fr/scp/cp/understanding/concept.htm
University of Massachusetts, Lowell; Lowell Center for Sustainable Production: http://sustainableproduction.org/publ.shtml
Clinical Practice American Association of Occupational Health Nurses (AAOHN): http://www.aaohn.org. The professional association for occupational health nurses.
American College of Occupational and Environmental Medicine (ACOEM): http://www.acoem.org. A professional organization of more than 5,000 physicians and other health care professionals specializing in the field of occupational and environmental medicine.
Association of Occupational and Environmental Clinics (AOEC): http://www.aoec.org. A network of more than sixty clinics, many in academic medical centers, and more than 250 individuals committed to improving the practice of occupational and environmental medicine.
1549
Chapter 27 Risk Assessment in Environmental Health
Mary C. Sheehan, Juleen Lam, and Thomas A. Burke
Drs. Sheehan, Lam, and Burke report no conflicts of interest related to the authorship of this chapter.
1550
Key Concepts Risk is the probability of an adverse effect occurring.
Risk assessment is a tool for decision making in environmental health and protection.
Risk assessment uses a stepwise process of organizing scientific information about a hazard in order to understand population exposure and vulnerability and to characterize the probability of adverse health effects.
The U.S. National Academy of Sciences (NAS) 1983 Red Book codified a four-step risk assessment paradigm that forms the basis for most risk assessment methods used worldwide.
In 2009, the NAS Silver Book modernized this risk assessment paradigm. The process now has five steps: (1) problem formulation, (2) hazard identification, (3) dose- response assessment, (4) exposure assessment, and (5) risk characterization.
Risk management is the separate but related process of deciding on policy options to reduce risk. This process involves economic, political, and institutional factors and consultation with stakeholders in addition to the scientific results of risk assessment.
The practice of environmental health is based on the application of scientific evidence to inform difficult decisions about risks. From the earliest efforts to prevent illness from polluted air or to protect communities from unidentified pathogens in drinking water supplies, public health professionals have applied the fundamental steps of risk assessment: identify hazards, determine who is exposed, and take steps to communicate and reduce community risks. Today, virtually every aspect of environmental health involves decisions about risk, and risk assessment has evolved as a valuable tool for practitioners and policymakers. This chapter presents an overview of the history, methods, and application of risk science in environmental health, including the recent recommendations of the
1551
U.S. National Academy of Sciences (NAS) to “strengthen the scientific basis, credibility, and effectiveness of future risk- management decisions” (National Research Council [NRC], 2009).
Risk is the probability that some adverse event will occur (Rodricks, 2006). In environmental health, measures of risk directly or indirectly guide many public services and private activities. For example, avoiding adverse health impacts, or risks, from pathogens and chemical contaminants in water is the rationale for regulation and monitoring of drinking water supplies. Similarly, health-based standards for air pollutants, food contaminants and residues, and hazardous cleanups are all based on assessments of risk. Risk assessments are also used to guide decisions in emergencies, such as whether to evacuate or shelter in place.
Risk assessment (RA) is a stepwise process of organizing information about a hazard or agent of concern. It involves identifying potential adverse effects and the dose levels at which they occur, measuring or estimating exposure levels, and characterizing the probability of those adverse effects in the population of concern. The ultimate goal of most environmental health RA is to inform decisions about the management or reduction of risk. The RA itself does not define “acceptable risk,” which is a policy decision. However, RA results may be compared to exposure standards or guidelines—themselves set based on definitions of acceptable risk—to provide critical public health information and risk management guidance. Environmental health RA may be focused on the protection of vulnerable groups or communities, a large citizenry in the case of national standards, or the global population in the case of environmental treaties.
There are many factors that contribute to population risk, from socioeconomic factors to individual environmental exposures (Figure 27.1). These factors combine to determine the background or baseline risk of a population. For example, the baseline lifetime risk of cancer in the U.S. population is about one in three (American Cancer Society, 2014). Globally, one in eight deaths annually is due to air pollution exposure (WHO, 2014). In environmental health, most RAs are focused on specific chemical agents or hazards, with the goal of measuring and preventing incremental risk to the population.
1552
Figure 27.1 The Multitude of Factors Affecting Risk of Disease Source: Adapted from an unpublished 2008 conference presentation slide and provided by H. Zenick, 2015.
International bodies such as the World Health Organization (WHO) use RA to evaluate regional or global risks. The tools of RA can also form inputs to broader approaches used to evaluate environmental health challenges, such as health impact assessment (HIA), which uses multisectoral and multifaceted analyses to assess health and well-being effects of projects, programs, or policies (NRC, 2011) (also see Text Box 15.5), or environmental impact assessment (EIA), which examines effects from a similarly broad perspective on ecological systems. The RA of a chemical contaminant's potential effects on health within an HIA or EIA for a transnational pipeline would be an example. A global environmental challenge of growing relevance is climate change (see Chapter 12). The evolving methodology for understanding potential hazards to human health and well-being from climate change rests on risk and opportunity- based analysis employing RA, HIA, and EIA and other analyses.
1553
History There is evidence that as far back as ancient times, that humans carefully evaluated risk, whether for the purposes of anticipating poor agricultural harvests, inauspicious weather patterns, or other adversities. Following World War II, formal methods for assessing risk from human exposure to radiation and other related hazards emerged in the nuclear and aerospace fields (Wilson, 2012). Around this time the public in many countries also became increasingly aware of the presence of harmful chemicals in the environment and their potential impacts on health. The period from 1950 to 1970 was one of heightened awareness of environmental impacts on health, which catalyzed the development of what we now see as environmental and risk assessment milestones (Figure 27.2). Rachel Carson's 1962 book, Silent Spring, widely popularized concern about long-term, low-dose chemical exposures, in particular to DDT, noting that “for the first time…every human being is now subjected to contact with dangerous chemicals, from the moment of conception to death” (Carson, 2002). In the United States, public and media pressure from such awareness raising as well as from high-profile chemical accidents stimulated government action and led to Congressional passage of new laws regulating air and water and the creation of the U.S. Environmental Protection Agency (U.S. EPA). The EPA determined that an organized approach was needed to assess information in order to inform the determination of whether, and at what levels, an environmental hazard could cause harm to exposed persons.
1554
Figure 27.2 Timeline of Milestones in the History of Risk Assessment
Source: Author's content in a format based on Harris-Roxas & Harris, 2011.
Meanwhile, this need for formal risk assessment procedures had been reinforced over the same period by the experience of the U.S. Food and Drug Administration (FDA) with thalidomide, a drug linked with incidence of severe birth defects in children born to women who had used the drug during pregnancy, and with the artificial sweetener saccharin, shown to lead to bladder cancers in high-dose animal experiments (Rodricks, 2006). Evaluation and proposed regulation of these chemicals raised controversy in the scientific community and helped form the basis for calls to standardize the process for organizing and evaluating scientific information and making decisions about hazards to health and the environment.
1555
In 1983, the NAS published Risk Assessment in the Federal Government: Managing the Process (commonly referred to as the Red Book), a landmark report by the National Research Council (NRC) of the National Academy of Sciences that brought the principles of evaluating environmental chemical risks to human health together for the first time, presenting them in a framework that formalized the risk assessment process and outlined its four key steps (NRC, 1983). These steps were (1) hazard identification to understand the extent of harm caused by a specific environmental stressor; (2) dose-response assessment to quantify how much risk, or potential harm, may be caused at any given level of exposure or dose;(3) exposure assessment to diagnose actual or likely exposure or dose in a given population; and(4) risk characterization to synthesize the risk for a specific population.
The Red Book also established as a separate phase a risk management (RM) process. In risk management, decision makers choose appropriate health-protective policy options based not only on the scientific analysis of the RA but also on key nonscience criteria, such as net economic cost, institutional feasibility, and political and other factors. While RM involves a separate step after formal RA, it constitutes an integral part of the science-based decision-making process.
The codification in 1983 of environmental health RA with publication of the Red Book influenced other national and international agencies. For example, the WHO's International Programme on Chemical Safety (IPCS) employs RA to evaluate health impacts of a broad range of environmental contaminants, using a process similar to that outlined in the Red Book (World Health Organization, International Programme on Chemical Safety, 2014). The European Environment Agency (EEA) of the European Union also uses an approach with steps similar to those in the Red Book (EEA, 1998).
While the Red Book created a unifying framework for evaluating environmental risks and organizing scientific information to make public health decisions, by the turn of the new century progress in understanding chemical risks had also brought recognition of the need for updating the risk assessment process. Advanced analytical techniques had improved the understanding of biological processes, enabling researchers to address complex questions regarding
1556
chemical modes of action, effects from multiple chemical exposures, and human susceptibility, variability, and uncertainty. During the first decade of the present century, new NAS reports on cumulative risk assessment (NRC, 2008), toxicity testing methods (NRC, 2007), and risk assessment (NRC, 2009) offered strategies to strengthen the scientific basis, credibility, and effectiveness of RA practice and RM decisions. In particular the latter report, Science and Decisions: Advancing Risk Assessment (commonly referred to as the Silver Book), integrated recent findings in order to modernize the recommended design and methods of risk assessment (NRC, 2009).
1557
Risk Assessment The RA process described above is used today by public health agencies, environmental regulators, private firms, scientists, and nongovernmental organizations around the world to further the understanding of environmental chemical hazards and their risks to public health. RA is also a public policy tool for informing regulatory and technology decisions, setting priorities among research needs, and developing approaches for considering the costs and benefits of public health policies (NRC, 2009).
The Silver Book lays out an updated paradigm for RA, noting particularly that—due to the complexity of both environmental health challenges and RA itself—the analytical process and regulatory and policy decisions reliant upon it needed to become more relevant to policymakers. The Silver Book makes a number of technical refinements in each of the four Red Book analytical steps. In addition, in a key modification, it includes an up-front problem formulation step, which places the specific risk analysis being undertaken within the context of available policy options for managing risk. In this way the problem formulation step explicitly links the RA process to the subsequent decision-making and policymaking process covered in RM. With this change, the recommended risk assessment process now has five steps: (1) problem formulation, (2) hazard identification, (3) dose-response assessment, (4) exposure assessment, and (5) risk characterization. This RA process is then followed by a separate RM phase (Figure 27.3). Each of these is discussed in turn in greater detail next.
1558
Figure 27.3 The Process of Using Environmental Health Risk Assessment to Protect Public Health
Source: NRC, 2009.
Step 1. Problem Formulation Problem formulation is a systematic planning step linked to the regulatory and policy context. It identifies the major factors to be considered in RA, and results in a conceptual model identifying sources, environmental stressors, and exposed populations; the relationships among these elements; and a detailed plan for the RA.
Introduction The first step in any RA is designing its goals, scope, and technical requirements. In this step, policymakers and decision makers interact with stakeholders and technical risk assessors. The problem formulation step defines the environmental health problem within the policy context and decides on the specific technical and analytical approach needed to carry out the RA.
Goal Problem formulation aims to identify the issues to be assessed and the goals, breadth, depth, and focus of the risk assessment, and it also aims to establish the roles of the decision maker, stakeholders
1559
and risk assessor (NRC, 2009). It takes into account exposure pathways, exposed populations, likely health outcomes, data requirements, and the time frame of the analysis.
Methods and Tools Used The main products of problem formulation are a conceptual model and an analysis plan for the RA, along with the technical details of how the analysis will be carried out. The conceptual model identifies the detailed environmental stressors, pathways, sources, populations at risk, and potential adverse health effects. The analysis plan defines the analytical approach for the RA, identifying how data on pollution sources will be located, which chemicals are of concern, how their exposure pathways will be assessed, how exposure concentrations will be estimated or measured, and what risk metrics will be used. The analytical approach also maps out technical requirements, including what epidemiological and toxicological data are available, what specific tools and methods (e.g., exposure and dose-response models) should be used, and what level of uncertainty analysis is needed (Text Box 27.1).
1560
Text Box 27.1 Example of Problem Formulation: Assessing a New Incinerator A community is concerned about the possible health impacts of air pollution from a solid waste incinerator being built nearby. In some countries such a project would by law require an ex-ante EIA and/or HIA that would include a risk assessment. In other countries, residents may need to voice their concern in order for the relevant authority to undertake an RA. The RA problem formulation step would determine which chemicals were of interest (e.g., heavy metals and persistent organic pollutants), the likely human health risks associated (e.g., neurological, immune, cardiovascular, and cancer outcomes), possible exposure routes (e.g. air, water, and soil contamination), and the population at risk (e.g., those living or working within a certain distance of the incinerator), including the most sensitive (e.g., reproductive- age women). Problem formulation would also identify potential policy options (e.g., installing pollution emissions reductions technology and providing risk communication related to hazards for local residents). The policy choices of no change in plans, as well as no incinerator construction, would also be included.
Issues and Importance While commonly performed in an EIA and present in numerous EPA guidance documents, the problem formulation step had not been formally part of RA until it was introduced with the Silver Book. Therefore it may take time for this step to be fully integrated. However, problem formulation is likely to emerge as one of the most critical RA steps in that it can help to ensure greater commitment from both stakeholders and decision makers by fully involving them from the start of the process. This leads to a greater probability that an acceptable policy solution will be found. When carefully done, RA problem formulation can also save time and
1561
resources. A challenge is the trade-off between extensive dialogue and practical efficiency: “The process requires a balance among the competing values of deliberative input…timeliness…and the resource burden” (NRC, 2009).
Summing Up The RA problem formulation step identifies the environmental health problem, the risk context and stressors, the population concerned and the potential adverse effect, and sets out the RA goal and plan. The next step is to more fully identify the nature of the stressor, through hazard identification.
Step 2. Hazard Identification
Introduction The second step in risk assessment is hazard identification, the process of examining the evidence for adverse health effects due to human exposures to an environmental contaminant. Traditionally, the principal sources of evidence have been observational human studies (epidemiology; see Chapter 4) and experimental animal evidence (toxicology; see Chapter 6). However, recent advances in technology have brought novel sources of evidence such as in vitro (cell-based) studies and in silico (computer modeling) methods to contribute useful toxicity information. The hazard identification step produces a list of potential toxic effects, and a characterization of the nature and strength of established causal associations with adverse effects in humans.
Goal Hazard identification seeks to determine adverse health effects related to exposure to an environmental contaminant, and to evaluate the quality, nature, and strength of the scientific evidence supporting causation. This requires a process of gathering, organizing, evaluating, and integrating scientific studies of various types.
Methods and Tools Used Hazard identification uses the available toxicological, epidemiological, and other sources of evidence to assess the
1562
contaminant, its degradation products, and metabolites. This process also considers the determinants of toxicity, including the level, frequency, and duration of dose or exposure; what human (or nonhuman) populations are exposed; the exposure routes; the manner in which the contaminant is absorbed and metabolized; the physical form of the contaminant, and the presence of other contaminants that may have synergistic or additive effects. The definition of adverse health effects is typically broad, and is likely to include overt diseases (e.g., cancer or birth defects), but may also include more subtle biological effects (e.g., alterations in gene expression) that can play an early role leading to disease, called upstream effects. Evaluation of the combined scientific evidence involves a characterization based on effects, target organs, and mode of action (or how the chemical affects a target cell or organ), and concludes with a judgment on the quality of the evidence (e.g., strengths or weaknesses of particularly studies) and the likelihood of health effects in humans via the given exposure route. This is typically done using a weight of evidence analysis, a judgment regarding the adequacy of the entire body of available evidence to support a conclusion that the substance poses a hazard to humans (Text Box 27.2)
1563
Text Box 27.2 Example of Hazard Identification: Evaluating Methylmercury Methylmercury (MeHg) is a neurotoxin described in Tox Box 13.2, in Chapter 13. The following example is an excerpt from the weight of evidence evaluation of methylmercury performed by the EPA's Integrated Risk Information System (IRIS). After evaluating the available toxicological and epidemiological evidence, IRIS researchers identified “developmental neurospsychological impairment” (specifically delays in motor and verbal function) as the critical adverse health effect for MeHg in humans:
Methylmercury is a highly toxic substance; a number of adverse health effects associated with exposure to it have been identified in humans and in animal studies. Most extensive are the data on neurotoxicity, particularly in developing organisms. The nervous system is considered to be the most sensitive target organ… There are three epidemiological studies for which quantitative analyses have become available… These longitudinal, developmental studies were conducted in the Seychelles Islands, the Faroe Islands, and New Zealand. The Seychelles study yielded scant evidence of impairment related to in utero methylmercury exposure, whereas the other two studies found dose-related effects on a number of neuropsychological end points. In [this] assessment, emphasis is placed on the results of the Faroe Islands study, the larger of the two studies that identified methylmercury-related developmental neurotoxicity. Supporting evidence from the New Zealand study provides assurance that choosing this focus is the appropriate strategy for protecting public health [U.S. EPA, 2001].
Issues and Importance High-quality scientific studies, such as those that have been peer
1564
reviewed by qualified experts in the field and/or whose findings have been corroborated by other studies, provide the best evidence for hazard identification. However, such studies are not always available, and existing studies may suffer from design or methodological limitations. For instance, human data are considered the gold standard for assessing hazards. However, many of these scientific studies examine occupational populations— groups consisting of healthy workers who are not representative of the general population (which includes children, the elderly, and people with preexisting medical conditions). The utility of observational studies in the general population may be limited by uncertainties about the amount and duration of exposure in the population or the presence of potential confounders, such as smoking or alcohol use. Animal studies offer the advantage of being performed under controlled laboratory conditions that reduce some of the uncertainties associated with human studies. However, they also present the challenge of determining whether an effect seen in animals is relevant to humans. These issues must be carefully weighed when interpreting studies.
Summing Up Hazard identification produces a characterization of the nature of the hazard associated with the contaminant of concern. It considers all the available scientific evidence and assesses it collectively to come to a judgment concerning the causal links between exposure and adverse outcome. The next RA step is dose-response assessment, in which potential adverse effects from the contaminant of concern are determined.
Step 3. Dose-Response Assessment
Introduction A dose-response assessment characterizes the relationship between the dose of a chemical administered or received and the resulting incidence or severity of an adverse effect. Paracelsus's maxim “the dose makes the poison” is a good rule of thumb (with some exceptions, as noted in Chapter 6). In other words, a substance may have no adverse effect at low levels, but increasing effects may be seen as the dose increases. This relationship is characterized
1565
through a mathematical model called the dose-response relationship.
Goal The goal of dose-response assessment is to employ the information obtained in the hazard identification step to characterize the likelihood and severity of adverse health effects at different levels of exposures to a chemical. Mathematical models expressing this dose- response relationship are then developed. The ultimate goal of dose- response assessment is to estimate toxicity values that can then be used to characterize the incidence of risk in human populations.
Methods and Tools Used Traditionally, dose-response assessment has been performed differently for chemicals that cause cancer (carcinogens) and those that cause other health effects (noncarcinogens). The reason for this is that the mode of action of carcinogens has been assumed not to have a threshold; that is, for carcinogens it has been assumed that no level of exposure is without some risk of cancer. In contrast, agents causing noncancer effects, such as asthma, nervous system disorders, birth defects, or cardiovascular disease, are typically assumed to act in relation to a threshold. This means that exposure at low levels of the chemical may occur without causing any adverse health effects; however, once a biological threshold has been passed, exposure to the chemical increases the prevalence or severity of the effect. The difference between the threshold and nonthreshold dose- response can be seen when the two cases are presented graphically, as in Figure 27.4.
1566
Figure 27.4 Threshold Compared to Nonthreshold Dose-Response Models
Source: NRC, 2009.
This underlying threshold versus nonthreshold assumption in risk assessment has led to different dose-response model determination processes for carcinogenic chemicals on one hand and for noncarcinogenic chemicals on the other (Figure 27.5). In simple terms, for carcinogens a dose-response model is fit to the available data to derive the slope of the dose-response curve. Based on this slope, a cancer slope factor (CSF), also called a unit cancer risk (UCR), is derived. (Combined with exposure data, the CSF is used to characterize risk in the final step of the RA.)
1567
Figure 27.5 Approach to Carcinogen and Noncarcinogen Dose- Response Assessment
Source: NRC, 2009, p. 130.
For noncarcinogens, a threshold dose is typically based on the no observed adverse effect level (NOAEL), or if that level is not identified, is based instead on the lowest observed adverse effect level (LOAEL). These threshold estimates are used as the point of departure (POD) for extrapolating to a human dose that is without risk of substantial adverse effects if the chemical exposure occurs over a lifetime; this dose is called a reference dose (RfD), or a reference concentration (RfC). An RfD is set by dividing the NOAEL by one or more uncertainty factors. These are typically a value of 10 for interspecies extrapolation (if the NOAEL
1568
was derived from an animal study) and 10 for intraspecies extrapolation (to account for natural variability in response within the human population). Additional uncertainty factors may be used: for instance in the case of sensitive populations such as children or if few relevant studies were available. (For noncarcinogens, the RfD is used with exposure data to characterize risk in the final step of the RA.)
Issues and Importance In recent years the underlying assumption of the threshold and nonthreshold dichotomy in dose-response assessment has been brought into question. Scientific evidence suggests that noncarcinogens do not always exhibit a threshold and, similarly, that carcinogens may potentially demonstrate a threshold, given that the mode of action for carcinogenicity has been determined to vary widely. The Silver Book therefore recommends harmonizing the cancer and noncancer approaches, and it is expected that this is the general direction RA will take with time. For noncarcinogens, this will mean replacing the NOAEL/LOAEL with a calculation of a benchmark dose (BMD), an estimate of the dose at which a specified increase in adverse effects (called the benchmark response, or BMR) is apparent. Because of the uncertainty that may exist when fitting a dose-response curve to the data, typically the lower 95% confidence bound of the BMD (BMDL) will be used as the POD for estimating population risk.
Summing Up Dose-response assessment produces a characterization of the relationship between the dose of a chemical and the prevalence or severity of an adverse effect. The next step in RA is to characterize exposure in the population, through exposure assessment.
1569
Text Box 27.3: Technical Terminology in Risk Assessment
Benchmark dose (BMD): a dose that produces a change in the response rate (BMR) of an effect compared to the control or background exposure group.
Benchmark dose–lower bound (BMDL): a lower confidence limit on the dose at the BMD.
Benchmark response (BMR): a selected percentage increase in response from effects measured in the background exposure group, used as a point of departure from the observed data.
Hazard index (HI): a measure of the ratio between the measured population exposure and the calculated RfD. A smaller number (i.e., <1) typically indicates that the population exposure is lower than the level of concern.
Lowest observed adverse effect level (LOAEL): the lowest dose, among doses tested in a study, that demonstrates a statistically or biologically significant difference from effects measured in control animals.
Margin of exposure (MOE): a measure of the ratio between the calculated NOAEL or BMD and the measured population exposure. A larger number (i.e., >100) typically indicates that the population exposure is lower than the level of concern.
No observed adverse effect level (NOAEL): the highest dose, among doses tested in a study, that demonstrates no significant difference from effects measured in control animals.
Point of departure (POD): the starting point for extrapolating to lower doses; it can be the lower bound on the dose for an estimated incidence or change in response level from a dose-response model (BMD), or a NOAEL or LOAEL.
1570
Population cancer risk: the lifetime average daily dose (LADD) multiplied by the cancer slope factor.
Reference dose (RfD) (or reference concentration [RfC]): an estimate of the daily oral (or inhaled) exposure (with uncertainty spanning perhaps an order of magnitude) to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime.
Unit cancer risk (UCR) (or cancer slope factor [CSF]): an upper bound, approximating a 95% confidence limit, on the increased cancer risk from lifetime exposure.
Step 4. Exposure Assessment
Introduction The next step in RA is exposure assessment, in which potential exposures in the population are calculated or estimated. Individuals can be exposed to chemicals in many ways—through the air they breathe, food they eat, or water they drink or through exposures in their workplace. Furthermore, they can be exposed continuously or intermittently, at varying levels, and during different stages of their lives. All these factors must be considered in order to estimate chemical exposure. Exposures can be acute (occurring for a relatively short period of time) or chronic (occurring over long periods of time, even a lifetime). Environmental health RA typically involves evaluation of chronic exposures to low levels of chemicals in the environment.
Goal The goal of exposure assessment is to determine the concentration of the chemical of interest in time and space at the location where the target population is exposed. Exposure assessment describes the magnitude, duration, timing, and route of exposure to the chemical, along with the size, nature, and categories of the human population exposed.
Methods and Tools Used Exposure assessment seeks to determine the who (population
1571
characteristics), how (exposure routes), time period (duration), when (particular life stages), how often (frequency), and how much (magnitude) of chemical contaminant exposure in a population (Figure 27.6). These questions can be thought of as falling into four categories guiding identification of information: (1) characterizing the exposure setting; (2) identifying exposure pathways; (3) quantifying exposure with in regard to magnitude, frequency, and duration; and (4) quantifying potential human intakes (i.e., the mass or concentration of chemical in contact with the human body normalized to the unit body weight (BW) per unit time, typically expressed as mg/kg-BW/day). Here we recall the distinction, introduced in Chapters 6 and 8, between exposure and dose: exposure occurs once a chemical contacts the outer boundary of a person, for instance at the nostrils, mouth, or skin, while dose (sometimes called the internal dose) is the amount of chemical taken into the body.
Figure 27.6 Some Common Exposure Pathways Source: Based on Agency for Toxic Substances and Disease Registry, 2005.
1572
Several exposure characterization methods are used, as described in Chapter 8, including (1) direct or indirect measurements of actual frequency, intensity, and/or duration of exposure or dose through sampling air, water, soil, or food products; (2) surveying people about their actual or hypothetical habits involving a particular exposure pathway; and (3) taking biological samples (biomonitoring) from those exposed (e.g., urine, blood, or hair) and identifying the concentrations of chemicals or chemical metabolites present in them. Another approach is modeling, which uses mathematical equations to estimate hypothetical exposures resulting from the release of a chemical into the environment.
Exposure assessment requires standard approaches to expressing dose. Two important examples are average daily dose and lifetime average daily dose. Average daily dose (ADD) is an estimate of the average daily dose level, used to characterize acute, subchronic, and chronic exposures for noncancer end points. Lifetime average daily dose (LADD) is an estimate of the average daily dose level over a person's lifetime, used to characterize lifetime exposures for noncancer or cancer end points. These values, when used in dose- response calculations (see below), support estimates of risk.
Issues and Importance Without exposure, there is no risk. Thus measurement or estimation of exposure is essential. However, variability across the population means that exposures will differ across individuals, geographic regions, and time. Further, chemicals often move across the environment, making it difficult to accurately characterize the resulting human exposures. As a result, uncertainty and measurement error are common challenges in exposure assessment. It is for these reasons that assumptions about common exposure patterns must often be made. One important category of assumptions is called exposure defaults. For example, two commonly used exposure defaults are that an average adult drinks 2 liters of water per day (and an average child 1 liter) and breathes 22 cubic meters per day of air (U.S. EPA, 2011). Calculating a range of exposures based on assumptions, and employing a final exposure estimate near the high end (e.g., the 95th percentile) of this range to avoid underestimation, is a common approach to ensuring a health- protective exposure estimate for a population.
1573
Summing Up Exposure assessment produces a description of a population's exposure—how much, over what time period, by what pathways—to the contaminant of concern. This leads to the final step in RA, in which the results of hazard identification, dose-response assessment and exposure assessment are used to characterize risk.
Step 5. Risk Characterization
Introduction Once the risk assessment design, hazard identification, dose- response assessment and exposure assessment are completed, risk characterization provides a synthesis of the risk level for the particular health effect of a particular chemical contaminant in a particular population. Risk characterization should respond to the original RA problem formulation statement by addressing the specific chemicals, pathways, adverse health effects, and populations identified at the outset.
Goal The purpose of risk characterization is to make a judgment on the risk to the population evaluated, including characterizing uncertainty where it exists. Risk characterization in this sense is a synthesis of each previous step in risk assessment, a summary that restates the scope and assumptions of the analysis, expresses results and interprets them, separating possible policy judgments from actual science findings.
Methods and Tools Used For carcinogens, the population cancer risk is calculated by multiplying the cancer slope factor (CSF) determined in the dose- response assessment by the lifetime average daily dose (LADD) determined in the exposure assessment step. While a resulting risk lower than 1 in 1,000,000 (1 × 10−6) is ideal, a population lifetime cancer risk in the range of 1 in 10,000 to 1 in 100,000 (1 × 10−4 to 1 × 10−5) may typically be considered acceptable. For noncarcinogens, the RfD calculated in dose-response assessment is commonly used as a “bright line” to guide environment risk management in public
1574
health. Thus population exposures below the RfD are often considered acceptable risks in environmental health decisions. Specifically, this is calculated using a hazard index (HI), which is the relationship between an actual population exposure and an established RfD. An HI lower than 1 (i.e., signifying exposure level below the RfD) suggests low risk whereas an HI greater than 1 is indicative of concern. Another approach for characterizing noncarcinogen risk is the margin of exposure (MOE). The MOE compares actual exposure to a NOAEL or to another POD such as a BMDL. An MOE greater than 100 suggests relatively low risk, whereas an MOE of 1 suggests the risk level is of concern (Text Box 27.4). Typically, risk is characterized both for the average population (e.g., the mean or median of the exposure distribution) and for individuals at the highest end of the exposure distribution (e.g., the 90th, 95th, or 99th percentiles), in order to understand the greater risk of the most highly exposed.
1575
Text Box 27.4 Risk Characterization for a Methylmercury Risk Assessment A local government agency contracted with a risk assessor to undertake an RA among local reproductive-age women for exposure to methylmercury (MeHg), a chemical typically taken in through seafood consumption. Because MeHg damages the fetal neurological system, reproductive-age women were considered the target sensitive population for this risk assessment. The risk assessor conducted a biomonitoring study of MeHg levels in the hair of a sample of reproductive-age women and found the median concentration of hair MeHg to be 0.24 ppm and the concentration at the 95th percentile to be 12 ppm. The benchmark dose–lower bound (BMDL) at the national level had been determined to be 12 ppm. Calculating the MOE (actual exposure divided by the BMDL), the risk assessor found that the MOE at the median of women's exposure was 50 (12 ppm/0.24 ppm), a level indicative of fairly low risk. However, the MOE at the 95th percentile of the women's exposure was just 1 (12 ppm/12 ppm), suggesting a risk level of concern.
Summing Up Risk characterization is the final step in formal risk assessment, however it is by no means an end point; it leads directly to risk management and risk communication. The synthesized quantitative results of risk characterization—often in the form of a hazard index, margin of exposure, or population cancer risk comparing actual population exposures to a risk level considered acceptable—are used to evaluate appropriate policy options through risk management and to develop a plan to communicate these options.
1576
Risk Management and Communication Once the quantitative, scientific RA has been completed, risk characterization summarizing the process is used as an input to defining a risk management strategy, including an approach to communicating findings. Risk management is the process of identifying, evaluating, prioritizing, and choosing among policy options. It is a decision-making step. RA and RM were already firmly divided into two separate processes at the time of the Red Book, and in 1997, the Presidential/Congressional Commission on Risk Assessment and Risk Management issued specific guidance on risk management. This guidance focused on identifying options, decisions, and actions based on the scientific findings of RA but also incorporating nonscience factors, such as economic costs and benefits, legal requirements and restrictions, administrative ease and implementability, the concerns of stakeholders, and political factors (Presidential/Congressional Commission, 1997). While risk assessors have an important role in providing technical input to the RM process, choices among policy options are made by decision makers in the light of multiple factors and in the context of consultation with stakeholders (Text Box 27.5).
The evaluation of policy options in RM should flow from defining the policy options identified in the problem formulation stage of RA. For each policy option the RM evaluation process will examine several factors, which may include
Acceptable level of risk, that is, the level of risk a society is willing to accept. While this may be based largely on science findings, different interpretations of those findings are possible (e.g., reference doses for a particular chemical may differ across countries).
Existing legislation, and whether the proposed policy fits within it or requires a new legal framework, which may involve constraints and political challenges.
Economic costs and benefits. Some policy options will be more costly than others, and some will address health risks more fully (have higher benefits) than others. Economic cost-benefit analysis and cost-effectiveness analysis are tools used to evaluate
1577
different policy options.
Administrative considerations, which may suggest that some policies are more complicated (and therefore more costly) to implement and administer, whereas others may be much easier.
Stakeholder perceptions. A stakeholder is any person or group with an interest (or a “stake”) in a risk management situation; typically stakeholders are those affected or potentially affected by the risk, the risk managers, and groups that will be affected by any efforts to manage the source of the risk. It is essential to incorporate the views of those affected by the policy, and this should be done from the start of the RA process. If a policy is likely to be challenged or disregarded by the populations it seeks to protect from health harms, it is not likely to succeed. Therefore stakeholder consultation at every step of RA and RM is essential.
1578
Text Box 27.5 Risk Management for Methylmercury in Seafood In the risk characterization example described in Text Box 27.4, local government agencies had, at the start of the RA process, outlined several policy measures, including engaging in risk communication through a seafood advisory, reducing mercury content from local power plant emissions through technology changes, screening for MeHg among reproductive-age women, and regulating seafood sales. Equipped with the findings of the risk characterization, the agencies evaluated these options based on parameters of acceptability of risk, legal factors, economic costs and benefits, administrative ease, and stakeholder concerns. The risk characterization finding suggested the average risk for most women was modest and deemed acceptable (MOE of 50); however, the risk for the most highly exposed was not (MOE of 1). Nevertheless, in discussions with stakeholders it was clear that there was a strong concern that exposure to MeHg should be minimized among reproductive-age women, even those without elevated risk. Thus the solution of “no action” was determined to be unacceptable; however, reducing MeHg emissions through the most advanced technology (the ideal solution) was too costly, based on the small share of women actually at high risk. The government agencies ultimately identified the most appropriate choice to be definition of a clearly stated advisory for seafood- consuming, reproductive-age women indicating that fish lower in MeHg were to be prioritized and fish higher in MeHg to be avoided.
Risk Communication Once risk management decisions have been taken, a subsequent step is communicating these decisions to the public. Risk communication, as explained in detail in Chapter 28, is an interactive process of exchange of information and opinion among
1579
individuals, groups, and institutions, involving multiple messages about the nature of risk. Systematic stakeholder involvement throughout the RA and RM processes greatly facilitates effective risk communication; risk communication should, ideally, start at the beginning of RA. Populations are affected by many factors in their perception of risk, and these may color their understanding of risk communication. For example, research has found that risks seen as uncontrollable, that induce dread, are globally catastrophic, have fatal consequences, are inequitable, present high risks to future generations, or are involuntary all enhance perception of risk (Slovic, 2007). The worst outcome from a risk communication perspective is conflicting messages from those in authority, or messages that do not seem trustworthy (Centers for Disease Control and Prevention, 2011).
“Good risk communication may not always improve a situation. However, poor risk communication will almost always make it worse” (NRC, 1989). Best-practice risk communication guidance recommends messages that raise the level of information and satisfy those involved that they are informed within the limits of available knowledge. Being honest, accurate, focused on the available information, and avoiding jargon or hypothetical situations are key elements of good risk communication. With the development of social media there are many more avenues today for reaching the target audience of a risk message. In addition to public meetings, newspapers, and radio and television, communication channels such as dedicated smartphone applications, Facebook, YouTube, Twitter, and others now offer innovative, efficient, and effective way for public health authorities to reach target audiences.
The Future of Risk Assessment RA has evolved considerably since the introduction of the Red Book framework in 1983. Continual improvement in the recognition and measurement of environmental hazards as well as advances in methodologies to detect subtle biological changes have brought expanded applications, and also greater challenges, to the task of addressing many of the inherent uncertainties. The addition of a problem formulation step—to ensure RA asks the right questions— provides an improved problem-solving approach. Previous assumptions about thresholds for noncancer health effects are now
1580
being challenged and are impacting traditional methods for the determination of “acceptable risk.” There is also greater recognition of the wide range of susceptibility in the human population and the importance of considering the effects of cumulative exposures, baseline health status, and social impacts on the vulnerability of communities.
Given the high stakes of environmental regulation, risk assessment used in the regulatory process will continue to face increasing scrutiny from elected officials and the regulated community. The EPA, NAS, and other agencies continue to refine the methods and applications of the risk sciences. The EPA's Framework for Human Health Risk Assessment to Inform Decision Making (U.S. EPA, 2014) provides a roadmap for the continual refinement of RAs. The NAS report Review of the EPA's Integrated Risk Information System (IRIS) Process (NRC, 2014) calls for greater transparency in the presentation of evidence and the use of systematic review to identify and assess scientific studies that provide the basis for hazard identification and determining risk.
As the field of environmental health evolves to address ever-broader issues of sustainability and global climate change, risk assessment will also evolve. In the future there is likely to be less emphasis on single pollutants and a greater need for understanding the cumulative impacts of multiple pollutants, the natural and built environment, and the social and behavioral aspects of population health.
1581
Summary This chapter presents an overview of the history, methods, and applications of the risk sciences in environmental health, including the risk assessment framework and recommendations of the Silver Book, which are intended to “strengthen the scientific basis, credibility, and effectiveness of future risk-management decisions” (NRC, 2009). RA has evolved as an essential tool for the practice of environmental health and provides a scientific foundation for policies that protect our health and the environment. From drinking water to air quality, food contaminants to emergency response, RAs inform decision making throughout the world.
Risk is the probability that some adverse event will occur. RA is a stepwise process of organizing information about a hazard or agent of concern. It involves identifying the potential adverse effects and the dose levels at which they occur, measuring or estimating exposure levels, and characterizing the probability of those adverse effects in the population of concern. In 1983, the Red Book codified the four steps of risk assessment: (1) hazard identification, which seeks to understand the type and extent of harm caused by a specific agent; (2) dose-response assessment, which quantifies how much harm may be caused at any given level of exposure; (3) exposure assessment, which diagnoses the population exposure to, or dose from, a particular stressor; and(4) risk characterization, which brings the previous steps together to synthesize the view on overall population risk. In 2009, the Silver Book presented a new decision- driven paradigm for RA, noting that the analytical process needed to become more relevant to policymakers. The Silver Book added an up-front problem formulation step, which explicitly links RA to the subsequent decision-making and policymaking process covered in RM. This step ensures that the RA asks the right questions to address the needs of decision makers. With this change, the RA process now has five steps, anchored by problem formulation. This chapter presents a description of each of these steps.
RA continues to evolve to incorporate new methods in toxicology, epidemiology, and exposure science. The field must also adapt to address ever-broader issues of sustainability and global climate change, the cumulative health impacts of multiple pollutants, and
1582
the social and behavioral determinants of population health. Other tools, such as life cycle assessment and health impact assessment will have expanded applications and are likely to combine with RA to define the toolbox of future environmental health professionals. The practice of environmental health will continue to require tough decisions about risks, informed by the imperfect but essential methods of RA.
1583
Key Terms benchmark dose (BMD)
An estimate of the dose at which a specified increase in adverse effects, called the benchmark response, is apparent.
benchmark dose–lower bound (BMDL) A lower confidence limit on the dose at the benchmark dose.
benchmark response (BMR) A selected percentage increase in response from effects measured in the background exposure group, used as a point of departure from the observed data.
exposure defaults In risk assessment, values recommended by regulators as representative of average population exposure levels for defined environmental pathways.
hazard index (HI) The ratio between measured population exposure and the calculated reference dose. A smaller number (i.e., <1) typically indicates that the population exposure is sufficiently below the level of concern.
lowest observed adverse effect level (LOAEL) The lowest dose, among doses tested in a study, that demonstrates a statistically or biologically significant difference from effects measured in control animals.
margin of exposure (MOE) The ratio between the calculated NOAEL or BMD and the measured population exposure. A larger number (i.e., >100) typically indicates that the population exposure is sufficiently less than the level of concern.
no observed adverse effect level (NOAEL) The highest dose, among doses tested in a study, that demonstrates no significant difference from effects measured in control animals.
point of departure (POD) The starting point for extrapolating to lower doses; it can be the lower bound of a BMD or it can be a NOAEL or LOAEL.
1584
Red Book The informal name for Risk Assessment in the Federal Government: Managing the Process, the 1983 National Academy of Sciences report that established a framework for risk assessment.
reference dose (RfD) A dose of a chemical that is without risk of substantial adverse effects when the chemical exposure occurs over a lifetime.
risk The probability that some adverse event will occur.
risk assessment A stepwise process of organizing information about a hazard or agent of concern. The steps are problem formulation, hazard identification, exposure assessment, dose-response assessment, and risk characterization.
risk communication An interactive process of exchange of information and opinion among individuals, groups, and institutions, involving multiple messages about the nature of risk.
risk management A process that builds on the results of risk assessment to decide on policy options to reduce risk. Risk management involves economic, political, and institutional considerations and consultation with stakeholders.
Silver Book The informal name for Science and Decisions: Advancing Risk Assessment, a 2009 National Academy of Sciences report that updated the 1983 NAS framework for risk assessment.
unit cancer risk (UCR) An upper bound, approximating a 95% confidence limit, on the increased cancer risk from lifetime exposure (also called cancer slope factor).
weight of evidence analysis In the hazard identification step of risk assessment, a judgment regarding the adequacy of the entire body of available evidence to support a conclusion that the substance poses a hazard to humans.
1585
Discussion Questions 1. Formulating the problem. An abandoned underground storage
tank from an old gasoline station has been detected in a community. Chemical compounds have been found to be leaking from this tank, which is near the water table providing the community its well water. Concerned about health effects of several of the chemicals in their water, the community has contracted you to do a risk assessment. In one sentence, how would you define the problem? At the outset, you are charged with convening stakeholders to guide the process. Who might the key stakeholders be, and how might they contribute to your strategy for planning and carrying out the risk assessment? What types of policy alternatives might be considered?
2. Identifying the hazard. The well water of the community has been tested in residences near the leaking gasoline tank, and several compounds with potential human health effects have been found. What kinds of sources of information would you examine to carry out hazard identification for your risk assessment and to address community health concerns? One compound in particular is detected for which there is incomplete toxicological and epidemiological information about health effects at low-level chronic exposures. What might you recommend in this case where data are unavailable?
3. Assessing dose-response relationships. The major concern of community members about the gasoline tank leak is the increase in long-term cancer risk due to one compound present in the well water that has been linked to blood and lung cancers. This compound is thought to lead to respiratory effects as well. What would likely be the differences in your approach to dose- response assessment for the carcinogenic effect of this compound on the one hand and its noncarcinogenic (respiratory) effect on the other?
4. Assessing exposure. Residential well water in the community is used for everything from drinking to cooking, and from bathing to crop irrigation. What are five major exposure pathways about which you as a risk assessor, as well as local health officials and
1586
community leaders, should be concerned? What are the defaults that you might use in estimating population exposures by air and drinking water? What are some of the drawbacks and what are some of the advantages of using each of these defaults?
5. Characterizing the risk. You are nearing the completion of your risk assessment, and have found that for the compound of highest concern, the margin of exposure for respiratory effects is 5, based on a relatively limited literature (a few occupational worker studies, some of which have study design weaknesses). Meanwhile, the community lifetime cancer risk has also been calculated for the chemical, in this case based on a large literature of animal toxicology studies, and found to be 5.3 × 10−5 (or 5.3 in 100,000). What would be your overall recommendation to the community leaders who hired you for the risk assessment? Would you recommend closing the wells? How would you describe the uncertainty related to the data? How would you explain these risks to the community?
6. Managing and communicating the policy options. List three potential strategies for managing the risks faced by this community from their well water due to the gasoline tank leak. How would you identify the most vulnerable members of the population, and how would you protect them? What do you think would be the most challenging aspects of communicating the policy options to the community? How might the problem formulation process have helped you in this task?
1587
References Agency for Toxic Substances and Disease Registry. (2005). Public health assessment guidance manual (2005 Update). Retrieved from http://www.atsdr.cdc.gov/hac/PHAManual/ch6.html
American Cancer Society. (2014). Lifetime risk of developing or dying from cancer. Retrieved from http://www.cancer.org/cancer/cancerbasics/lifetime-probability- of-developing-or-dying-from-cancer
Carson, R. (2002). Silent spring (Anniversary ed.). Boston: Houghton Mifflin.
Centers for Disease Control and Prevention. (2011). Risk communication. Retrieved from www.cdc.gov/healthcommunication/risks/index.html
European Environment Agency. (1998). Environmental risk assessment—Approaches, experiences and information sources. Retrieved from http://www.eea.europa.eu/publications/GH-07-97- 595-EN-C2
Harris-Roxas, B., & Harris, E. (2011). Differing forms, differing purposes: A typology of health impact assessment. Environmental Impact Assessment Review, 31, 396–403.
National Research Council. (1983). Risk assessment in the federal government: Managing the process. Washington, DC: National Academies Press.
National Research Council. (1989). Improving risk communication. Washington, DC: National Academies Press.
National Research Council. (2007). Toxicity testing in the 21st century: A vision and a strategy. Washington, DC: National Academies Press.
National Research Council. (2008). Phthalates and cumulative risk assessment: The task ahead. Washington, DC: National Academies Press.
1588
National Research Council. (2009). Science and decisions: Advancing risk assessment. Washington, DC: National Academies Press.
National Research Council. (2011). Improving health in the United States: The role of health impact assessment. Washington, DC: National Academies Press.
National Research Council. (2014). Review of EPA's integrated risk information system (IRIS) process. Washington, DC: National Academies Press.
Presidential/Congressional Commission on Risk Assessment and Risk Management. (1997). Risk assessment and risk management in regulatory decision making (Vol. 2). Washington, DC: Author.
Rodricks, J. (2006). Calculated risks: The toxicity and human health risks of chemicals in our environment. New York: Cambridge University Press.
Slovic, P. (1987). Perception of risk. Science, 236, 280–285.
U.S. Environmental Protection Agency. (2001). Methylmercury (MeHg) (CASRN 22967-92-6). IRIS Assessments. Retrieved from http://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm? substance_nmbr=73
U.S. Environmental Protection Agency. (2011). Exposure factors handbook. Retrieved from http://ofmpub.epa.gov/eims/eimscomm.getfile? p_download_id=522996
U.S. Environmental Protection Agency. (2014). Framework for human health risk assessment to inform decision making (EPA/100/R-14/001). Retrieved from http://www2.epa.gov/sites/production/files/2014- 12/documents/hhra-framework-final-2014.pdf
Wilson, R. (2012). The development of risk analysis: A personal perspective. Risk Analysis, 32(12), 2010–19.
World Health Organization. (2014). Public health, environment and social determinants of health—Burden of disease from ambient and
1589
household air pollution. Retrieved from http://www.who.int/phe/health_topics/outdoorair/databases/en
World Health Organization, International Programme on Chemical Safety. (2014). Methods for chemicals assessment. Retrieved from http://www.who.int/ipcs/methods/en
1590
For Further Information Risk Assessment Abt, E., Rodricks, J. V., Levy, J. I., Zeise, L., & Burke, T. A. (2010). Science and decisions: Advancing risk assessment (Perspective). Risk Analysis, 30(7), 1028–1036.
Brewer, G. D. (2009). Five “easy” questions. Science, 325, 1075– 1076.
Burke, T. A. (2003). The Red Book and the practice of environmental public health: Promise, pitfalls, and progress. Human and Ecological Risk Assessment, 9, 1203–1211.
Burke, T. A., Shalauta, N. M., & Tran, N. L. (1995). Strengthening the role of public health in environmental policy. Policy Studies Journal, 23(1), 76–84.
Burke, T. A., Tran, N. L., Roemer, J. S., & Henry, C. J. (Eds.). (1993). Regulating risk: The science and politics of risk. Washington, DC: International Life Sciences Institute.
Fan, A., & Chang, L. (Eds.). (1996). Toxicology and risk assessment: Principles, methods, and applications. New York: Marcel Dekker.
Klaassen, C. (Ed.). (1996). Casarett & Doull's toxicology: The basic science of poisons. New York: McGraw-Hill.
Rodricks, J. V. (2014). In pursuit of safety: 100 Years of toxicological risk assessment. Human and Ecological Risk Assessment, 20(1). (Originally published 2012)
Stern, P. C., & Fineberg, H. V. (Eds.); Committee on Risk Characterization, National Research Council. (1996). Understanding risk: Informing decisions in a democratic society. Washington, DC: National Academies Press. Available at http://books.nap.edu/catalog.php?record_id=5138
Risk Management, Perception, and Communication
1591
Centers for Disease Control and Prevention. (2011). Risk communication. Available at http://www.cdc.gov/healthcommunication/risks/index.html
Centers for Disease Control and Prevention. (2014). Crisis & emergency risk communication (CERC). Available at http://www.bt.cdc.gov/CERC
Centers for Disease Control and Prevention, Agency for Toxic Substances and Disease Registry. (1994). A primer on health risk communication. Available at http://www.atsdr.cdc.gov/risk/riskprimer/vision.html#factors
1592
Chapter 28 Communicating Environmental Health
Edward Maibach and Vincent T. Covello
Dr. Maibach and Dr. Covello report no conflicts of interest related to the authorship of this chapter.
1593
Key Concepts Communication is a central part of public health, and environmental health is no exception. Key forms of communication include social marketing and risk communication.
To guide their communication efforts environmental health professionals can use the following heuristic: simple clear messages, repeated often, by a variety of trusted sources.
To guide their behavior change efforts, environmental health professionals can use a different heuristic: make the behavior you are promoting easy, fun, and popular.
The primary objectives of environmental risk communication are (1) to inform and educate people about risks; (2) to build, strengthen, or repair trust; (3) to encourage people to take appropriate actions.
In the setting of perceived or documented environmental hazards, effective risk communication can help to achieve positive outcomes, and ineffective risk communication can create or aggravate problems.
Risk communication must address risk perception—a complex process based on many personal, social, cultural, and other factors.
Risk communication is an interactive process that involves active listening and authentic dialogue.
Communication is a central part of public health, and environmental health is no exception. People gather information, form attitudes, and base their behaviors in large part on what they discuss with their family, friends, and coworkers; read in newspapers, social media, and Web sites; hear on the radio and at meetings; and watch on television.
In environmental health, communication can serve many purposes. People may need to be alerted to a hazard and encouraged to take steps to protect themselves; examples include preparing for a
1594
natural disaster (Chapter 24), changing behavior in response to climate change (Chapter 12), or following workplace safety procedures (Chapter 21). Sometimes people are well aware of a hazard, and need to learn more about it so they can gauge the risk they face and decide how they want to respond (Chapter 27). People may need product information to help them decide what to purchase, or information on communities to help them decide where to live, or information on water quality to help them hold their water supplier accountable.
In each of these situations, information is essential. In environmental health, as in many fields, the trend in recent years has been toward making information available—toward enabling the right to know. In the workplace, under OSHA's Hazard Communication Standard (29 CFR Parts 1910, 1915, and 1926), workers are entitled to know the hazards to which they are exposed, and employers must inform and train workers accordingly. In communities, under the Emergency Planning and Community Right-to-Know Act (EPCRA) (40 CFR Parts 350–372), companies with hazardous chemicals on their premises above a threshold amount must inform state and local authorities of this fact, and manufacturing firms above a certain size must submit a toxic chemical release report to the U.S. Environmental Protection Agency (U.S. EPA) each year. All of this information (except some trade secrets) is publicly available. Under the Safe Drinking Water Act (40 CFR Part 141), community drinking-water systems must issue Consumer Confidence Reports (CCRs) each year, quantifying the levels of contaminants in the water they provide, and disclosing violations of drinking-water regulations. Air quality information is widely available in cities, and homebuyers can learn about lead paint in homes. Similar programs exist in both developed and developing nations, some required and some voluntary. So considerable environmental health information is available, and by all accounts this openness helps to protect the public's health. (Of course, much environmental health information, such as contaminant levels in food and consumer goods, remains difficult to access.)
But providing information is not the same as communicating (Tversky & Kahneman, 1974; Ariely, 2008; Lehrer, 2009; Kahneman, 2011). People may lack the “bandwidth” or literacy
1595
needed to handle new information. They may filter information through various biases, preferences, and mental shortcuts, or heuristics; they may reject information that is inconvenient, frightening, or ideologically unacceptable. They may need dialogue and/or personal engagement if they are to assimilate information.
In environmental health, communication efforts build on a foundation of health communication, including social marketing. In addition, environmental health draws on the science and practice of risk communication.
1596
Communication, Social Marketing, and Environmental Health Public health professionals—like many groups of science-based professionals—often need to communicate key science-based ideas effectively to the public and other groups of decision makers. Sometimes, environmental health professionals also aim to influence people's actions, when behavior change by individuals or policymakers can reduce health risks or in other ways prevent harm. These two aims—spreading important ideas and influencing people's behavior—are important elements of environmental health practice, but are often not primary components of environmental health training. This chapter provides two heuristics intended to help public health professionals become more effective at using communication and social marketing to achieve these two aims.
Spreading Important Ideas Public and environmental health professionals can improve their communication effectiveness by attending to a simple formula—or heuristic—in their public communication efforts: simple clear messages, repeated often, by a variety of trusted sources. Each of the three elements of this formula offers important communication guidance based on extensive empirical evidence and shown to be practical for a broad range of health and environmental issues and for a broad range of professionals.
The Importance of Simple Clear Messages By its very nature, scientific and technical information is often complex. The inherent complexity of such information is exacerbated by the fact that most scientific and technical professionals are trained and positively reinforced for giving explanations that are precise, thorough, and appropriately nuanced. This approach is often efficient and effective when communicating with peers (internal communication), but is often ineffective when communicating with audiences who don't share the same professional training and background knowledge (external communication).
1597
Effective external communication—with journalists, policymakers, and members of the public—requires identifying and sharing the most important information first (and as discussed below, sharing it often). The most important information is that which will help members of the audience answer three key questions: What is the risk (or the issue)? (i.e., How serious is it? Who is affected by it?); What is causing the risk? and, What are the options for managing the risk?
To be effective, external communication intended to help people answer these questions must be based in the reality of how people process information. Two facets of this reality are particularly important. First, “People simplify.” Our job (as risk communicators) is to help people simplify appropriately (Fischhoff, 1989, p. 299). Second, the less we say, the more we're heard. Or stated more bluntly, “If you've said three things, you've said nothing” (Heath & Heath, 2007).
Effective external communication therefore begins with simple clear messages that have been developed specifically to help people understand and appropriately simplify the issue at hand. When the situation allows it—that is, when time and budgets allow it—such messages can be pretested to ensure that they are clear and helpful to audience members. Even in situations that do not allow it—that is, when there is a lack of time and/or money—environmental health professionals can use their best professional judgment in crafting simple messages aimed at providing clear, proactive answers to the questions that people are most likely to have.
The Importance of Message Repetition “Repetition is the mother of all learning,” an insight that originally comes to us from an ancient Latin proverb (repetitio est mater studiorum), is one of the most robust findings ever to have emerged from modern mass communication research (Lang, 2013). Repetition increases message persuasiveness both cognitively, by increasing the salience and availability of the information, and affectively, by increasing positive feelings about the message (Pechman & Stewart, 1988; Chong & Druckman, 2013).
Typically, messages must be repeated often before most members of the intended audience will hear them, consider them, and
1598
potentially accept them. The more cluttered the communication environment, the more important message repetition becomes. Moreover, the veracity of the message is often secondary to repetition, as prominent political consultant Alex Castellanos likes to remind people with this trenchant thought: “You take the truth, and I'll take repetition; I'll beat you every time” (Alex Castellanos, personal communication, 2010). He is not recommending conveyance of false information; rather he is recommending creating all possible opportunities to convey true information repeatedly.
Aristotle offered his students advice about message repetition—and message organization—that is as true today as it was in his day: “Tell them what you are going to tell them, tell them, then tell them what you told them.” While this approach is an important start, today's highly saturated information environment requires creating multiple opportunities for the communicator to convey the message through multiple channels, for example, through news media, talk radio, social media, community forums, and if possible, through entertainment programming. Each of these creates an opportunity to repeat—and thereby reinforce—the simple clear messages that were developed to help members of the target audience understand and appropriately simplify the issue at hand.
Moreover, encouraging and enabling other communicators to convey the same simple clear messages is an important way to extend communication effectiveness. Simple clear messages are easy for other communicators to embrace, and use, whereas long complicated messages are not. Ideally, our messages should be simple and clear enough that members of the target audience begin to communicate them for us.
The Importance of Trusted Messengers Trust is the most important factor in effective public communication; where there is no trust, there can be no learning. Fortunately, health professionals as a group are highly trusted, even though trust in “leaders” of the medical profession has declined (Blendon, Benson, & Hero, 2014). While public trust in other professional groups tends to wax and wane, trust in health professionals has remained relatively high over the decades in which these data have been collected.
1599
That said, when members of the target audience do not know the communicator—personally or by reputation—their trust is likely to be superficial, provisional, and vulnerable. Common communication mistakes—including unclear messages, seemingly evasive answers, and lack of empathy—can rapidly undermine public trust in a specific health professional or health organization.
This is why, in addition to their own efforts to communicate, effective communicators find other trusted people, individuals who are known personally or by reputation to members of the target audience, to repeat and validate their simple clear messages. As implied above, the ultimate aim is to have members of the target audience convey our message to one another, because people typically trust most the people they know the best—family members, friends, and coworkers (Leiserowitz, Maibach, & Roser-Renouf, 2009).
Build a Team to Implement This Heuristic Risk communication expert Baruch Fischhoff (2007) offers a highly practical piece of advice for “content” experts who need to communicate with external audiences: build a team—on an ad hoc basis if necessary—by partnering with a social scientist and a communication professional. Environmental health professionals can partner with a social scientist to design—and ideally test— simple clear messages, and they can partner with a communication professional to find ways of conveying their messages repeatedly and activating other trusted voices.
Influencing Behavior with Social Marketing While effective communication is usually necessary, it is often not sufficient to change people's behavior (Hornik, 2002; McKenzie- Mohr, 2011). Even when people understand that a recommended behavior is likely in their best interest, many still won't adopt it. Social marketing—the use of marketing methods to promote behavior change for the benefit of people and society—is a methodology that can help to solve this problem (Maibach, Rothschild, & Novelli, 2002).
There is a vast research literature on why people's knowledge and supportive attitudes often fail to translate into recommended health
1600
behaviors (Maibach, Abroms, & Marosits, 2007). One of social marketing's leading practitioners—Bill Smith (2011; also see Smith & Strand, 2008)—points to three particularly important reasons. Smith's diagnosis is that, often, the behaviors recommended by health professionals (1) are difficult for people to adopt; (2) require up-front expenditures of time—and possibly money—while the benefits of adopting the behavior accrue primarily in the future; and (3) have unclear social implications. His prescription for closing the gap between attitudes and behaviors is that health professionals should do everything possible to make the recommended behavior easy, fun, and popular. Each of the three elements of this social marketing heuristic offers important, practical guidance that is based on extensive evidence.
Make the Behavior Easy The most effective means of reducing the gap between people's positive attitudes and their (lack of) behavior is to make the recommended behavior easier to perform. Doug McKenzie-Mohr (2011) recommends taking an engineering-like approach to this task: first, identify the barriers that impede people's performance of the recommended behavior, and then find ways to eliminate—or reduce—those barriers.
Having members of the target audience demonstrate (i.e., model) the recommended behavior—live or on video—to other members of the target audience is another way of making the behavior easier. Both of these approaches—reducing barriers and modeling the behavior—will increase people's sense of self-efficacy to perform the recommended action, which in itself makes the behavior easier for them (Bandura, 2004).
Over the past several decades, STD/HIV prevention programs have become quite good at making the recommended behaviors easier. For example, condom distribution programs that make condoms freely available when and where they are most likely to be needed— for example, in baskets at the bar in popular night spots—have played an important role in promoting condom use and reducing population-wide infection rates (Cohen et al., 1999).
Make the Behavior Fun Health professionals recommend behaviors not because they are
1601
fun, but because they offer health benefits. This is perfectly reasonable, but health professionals should never lose sight of two important facts. Nearly everyone prefers behaviors that are fun to behaviors that aren't. And while people are typically willing to incur costs to secure valued benefits, the most attractive transactions are those that deliver benefits at the same time as (or even before) the costs, even if the benefits are modest, and the least attractive transactions are those that require costs up front and deliver benefits only much later (Rothschild, 1999).
Therefore, to enhance the odds that people will adopt the behaviors that they recommend, health professionals should consider two important questions. One of these questions considers fun in a literal sense, and the other considers fun in a figurative sense. What can I do to make the behavior I am recommending more fun? And what can I do to help members of my target audience get immediate benefits from the behavior I am recommending, especially benefits that they care most about?
Rothschild (n.d.) provides an excellent example of making the recommended behavior more fun. Efforts to prevent intoxicated driving among young men in rural Wisconsin had been largely unsuccessful; these men felt that drinking at a bar with friends after work was the best part of their day, and saw no viable options for getting home afterward except driving themselves. Program designers created a branded limo service—The Road Crew—to pick people up at home, drive them to the bar, and take them home at the end of the evening. The program was well received; in its first eight years of operation, it gave nearly 100,000 rides, averted an estimated 140 crashes and six deaths, and saved an estimated $31 million in public expenditures and health care costs.
Make the Behavior Popular People are highly sensitive to norms. Specifically, people are more likely to embrace behaviors that they see as descriptively normative (i.e., most people like me perform this behavior) and injunctively normative (i.e., people important to me approve of this behavior).
When health professionals seek to promote a behavior that is currently uncommon among members of a target audience, they can draw attention to specific notable people who are already
1602
performing the behavior. Shining a light on these behavioral models will not only make the behavior appear more descriptively normative than it might otherwise seem, but can also increase audience members' sense of self-efficacy and make the behavior easier for them to adopt (Bandura, 2004). Uncommon behaviors can also become popular relatively quickly when opinion leaders within a population embrace and endorse the behavior, thereby exerting their powerful influence through injunctive norms. Health professionals can seek out and recruit opinion leaders within their target population as a strategy for accelerating uptake of the behavior they are recommending (Valente, 2012). As the recommended behavior becomes more descriptively normative— that is, as it becomes more common in the population—health professionals can take steps to highlight its growing popularity, thereby reinforcing the growing norm.
Smith (2011) offers a wonderful example of a highly successful opinion leader strategy used in a campaign to promote car safety seats for infants and toddlers among Latina mothers along the U.S.- Mexico border. These young mothers saw no benefit in using a car seat because they felt the fate of their child was in God's hands. Large numbers of mothers began using the seats, however, when health professionals recruited Catholic priests to bless car seats and distribute them at church.
1603
Environmental Risk Communication Risk communication, as its name implies, is communication about something that threatens (or is perceived as threatening) people's health or well-being. There are many kinds of risks, from economic (e.g., a dangerous investment) to behavioral (unprotected sex) and from political (a terrorist attack) to social (being mugged). In the field of environmental health the main focus is on environmental risks, such as asbestos, lead, or hazardous wastes.
Three main “actors” carry out most environmental risk communication: government, the private sector, and civil society. In 2009, for example, over one billion gallons of coal ash slurry were released when a waste containment lagoon was breached at the TVA Kingston Fossil Plant in Tennessee. State and federal agencies, the power plant operator, and environmental groups all moved to communicate with the public—sometimes with very different messages!
While many risks unfold slowly, much of environmental risk communication emerges in response to crisis situations—either an acute risk such as a chemical plant explosion, or a long-standing risk that is suddenly uncovered, such as a nearby hazardous waste site. As a result, a common theme in the risk communication literature is understanding the effects of panic, stress, and mistrust on the communication process.
Objectives of Risk Communication The primary objectives of environmental risk communication are (1) to inform and education people about risks; (2) to build, strengthen, or repair trust; and (3) to encourage people to take appropriate actions.
Additional objectives consist of
Informing people of environmental policies and response plans
Providing people with timely information and instructions to reduce potential injuries, illnesses (physical and mental), economic losses, and societal disruption
Preventing stigmatization
1604
Gaining the assistance of people in identifying issues of concern
Enhancing social cohesion, social resilience, and confidence in risk management authorities
Effective environmental risk communication can directly influence how events unfold. Poor environmental risk communication can fan emotions, undermine public trust, and intensify stress. Good risk communication can promote resilience, rally support, calm a nervous public, build trust, and encourage cooperative behaviors. An environmental spokesperson who communicates badly may be perceived as incompetent, uncaring, or dishonest. A spokesperson who communicates well will be able to reach large numbers of people with clear and credible messages. Well-constructed, practiced, and delivered environmental risk communication messages will inform the public, reduce misinformation, and provide a valuable foundation for informed decision making.
Risk Perception People perceive risk in ways that are not always “objective” or data- based. Considerable research has revealed some of the factors that influence people's perception of risk. Key factors include who controls the risk and whether people assume it voluntarily, how familiar and routine the risk is, the kind of injury that might result, and who is at risk (Slovic, 1987, 2000). These and other predictors of risk perception are shown in Table 28.1.
Table 28.1 Factors Important in Risk Perception
Factor Conditions associated with increased fear and concern and perceptions of high risk
Conditions associated with decreased fear and concern and perceptions of low risk
Catastrophic potential
Fatalities and injuries grouped in time and space
Fatalities and injuries scattered and random
Familiarity Unfamiliar Familiar Understanding Mechanisms or process Mechanisms or process
1605
not understood understood Uncertainty Risks scientifically
unknown or uncertain Risks known to science
Personal controllability
Uncontrollable Controllable
Voluntariness of exposure
Involuntary Voluntary
Effects on children
Children specifically at risk
Children not specifically at risk
Timing of effects
Delayed Immediate
Effects on future generations
Risk to future generations
No risk to future generations
Victim identity Identifiable victims Statistical victims Dread Effects dreaded Effects not dreaded Trust in institutions
Low trust in responsible institutions
High trust in responsible institutions
Media attention
Much media attention Little media attention
Accident history
Major and sometimes minor accidents
No major or minor accidents
Equity Inequitable distribution of risks and benefits
Equitable distribution of risks and benefits
Benefits of the risk activity
Unclear benefits Clear benefits
Reversibility Effects irreversible Effects reversible Origin Caused by human
actions or failures Caused by acts of nature or God
The factors shown in Table 28.1 may combine either to intensify or to diminish people's perception of risk—processes that are called social amplification of risk and social attenuation of risk, respectively (Kasperson et al., 1987; Pidgeon, Kasperson, & Slovic 2003). A schematic diagram of the social amplification of risk framework is shown in Figure 28.1. Note the importance of informal
1606
social networks in mediating incoming information, and of heuristics in processing information.
Figure 28.1 Social Amplification of Risk Framework Source: Pidgeon, Kasperson, & Slovic, 2003, p. 14.
Public health professionals are concerned about both possibilities in the social amplification and attenuation of risk (Bennett, Calman, Curtis, & Fischbacher-Smith, 1999). On the one hand, for instance, when people are indifferent to a risk, they may decline to take protective action, such as preparing for a disaster, or they may oppose public health policies, such as bans on smoking in public places. On the other hand, when people overestimate a risk, they may take unwise actions, such as refusing vaccination, or they may support counterproductive policies, such as opposing the reuse of treated wastewater. While experts generally agree that the public is insufficiently concerned about some risks (such as climate change) and excessively concerned about others (such as food irradiation), there is considerable debate about the “right” level of concern about many risks (see Chapter 27).
Models of Risk Communication Effective environmental risk communication is based on several models that describe how risk information is processed, how risk perceptions are formed, and how risk decisions are made. Together these models provide the intellectual and theoretical foundation for
1607
effective environmental risk communication.
Risk Perception Model One of the most important paradoxes identified in the risk perception literature is that the risks that harm people are often very different from the risks that concern, worry, or upset people (e.g., Slovic, 1987, 2000; Covello & Sandman, 2001). For example, there is virtually no correlation between hazard ranking according to mortality statistics and ranking of the same hazards by how upsetting they are to people. There are many risks that make people worried and upset but cause little harm. At the same time, there are many risks that harm large numbers of people but arouse little concern.
This paradox is explained in part by the factors that affect how risks are perceived, shown in Table 28.1. These factors, together with actual risk numbers, determine a person's emotional response to risk information. They affect levels of public fear, worry, anxiety, anger, and outrage.
Risk perception theory contradicts the conventional notion that “facts speak for themselves.” People routinely accept some high risks and, at the same time, become outraged over much less likely risks (Covello & Sandman, 2001). For example, a person might worry about getting sick from exposure to extremely low levels of a chemical, yet not wear a seat belt, thinking that “I'll never be in an accident.”
Mental Noise Model When people are stressed and upset, their ability to process information can become severely impaired, owing to a phenomenon called mental noise (Covello, 2006, 2011b). For example, people under stress typically
Have difficulty hearing, understanding, and remembering information.
Focus most on the first and last things they hear.
Focus more on negative information than on positive information.
Process information at several levels below their educational
1608
level.
Can attend to no more than three to five messages at a time.
Respond best to information provided in chunks, buckets, or bites.
Focus intensely on issues of trust, benefits, fairness, and control (they “want to know that you care before they care what you know”).
Interpret nonverbal cues negatively.
Use nonverbal cues as a primary means of determining trust.
Use a large variety of mental shortcuts to make complex decisions.
Negative Dominance Model The negative dominance model describes the processing of negative and positive information in high-concern and emotionally charged situations (Kahneman & Tversky, 1979; Kahneman, Slovic, & Tversky, 1982; Covello, Peters, Wojtecki, & Hyde, 2001; Kahneman, 2011). In general, the relationship between negative and positive information is asymmetrical, with negative information receiving significantly greater weight.
The negative dominance model is consistent with the concept of loss aversion, a central theorem of modern psychology. This concept holds that people put greater value on losses (negative outcomes) than on gains (positive outcomes). When people face uncertainty, they do not typically evaluate information carefully or compute the risks. Instead, they base their risk decisions and judgments on a brief list of emotions, instincts, and mental shortcuts. A standard shortcut is assigning a much higher weight to the pain of loss than to the pleasure of gain. Negatives loom larger than positives.
One practical implication of the negative dominance model is that in high-concern or emotionally charged situations, it typically takes several positive or solution-oriented messages to counterbalance one negative message. Another practical implication of negative dominance theory is that communications that contain negatives— words such as no, not, never, nothing, or none and words with
1609
strong negative connotations—tend to receive closer attention, be remembered longer, and have a greater impact than messages with positive words. The use of unnecessary negatives in high-concern or emotionally charged situations can have the unintended effect of drowning out positive or solution-oriented information. Environmental risk communication is typically more effective when it focuses on what is being done rather than on what is not being done.
Trust Determination Model A central theme in the risk communication literature is the importance of trust (Peters, McCallum, & Covello, 1997; Covello, Clayton, & Minamyer, 2007; Covello, 2011b; Greenberg, 2014). Trust is generally recognized as the single most important factor determining perceptions of risk. Only when trust has been established can other risk communication goals, such as consensus building, resilience, and dialogue, be achieved.
Trust is typically built over long periods of time. Trust is easily lost. Once lost, it is difficult to regain.
Because of the importance of trust in effective risk communication, a significant part of the risk communication literature focuses on trust determination. Research indicates that among the most important trust determination factors are (1) listening, caring, empathy, and compassion; (2) competence, expertise, and knowledge; and (3) honesty, openness, and transparency. Other factors in trust determination include accountability, perseverance, dedication, commitment, responsiveness, objectivity, fairness, and consistency. When listening to a risk communicator, people often make their trust determinations in less than thirty seconds. Initial trust impressions are long-lasting.
Trust is created in part by a proven track record. It can be substantially enhanced by endorsements from trustworthy sources. Highly trusted sources in health, safety, and environmental risk controversies include (in no priority) informed citizen advisory panels, educators, firefighters, safety professionals, doctors, pharmacists, meteorologists, nurses, and clergy.
Effective Risk Communication
1610
These models help to guide effective risk communication. One important principle is that risk communication is interactive, as discussed in Text Box 28.1.
1611
Text Box 28.1 Risk Communication: A Two-Way Process In 1989, the National Academy of Sciences of the United States defined risk communication as “an interactive process of exchange of information and opinion among individuals, groups, and institutions” (National Research Council, 1989). By emphasizing “interaction” and the “exchange of information” in its definition of risk communication, the academy was recommending a major shift in thinking about risk communication (Covello, 2011b; Lundgren & McMakin, 2013). The shift was from a one-way model of communication based on the DAD (decide, announce, defend) principle to a two-way, interactive model of communication, based on active listening, dialogue, and interest-based bargaining.
In 1988, the U.S. Environmental Protection Agency published seven cardinal rules for effective environmental risk communication (Covello & Allen, 1988). These cardinal rules are widely accepted as the foundation for effective risk communication. We offer an expanded version of them here to provide more detail.
1. People have the right to have a voice and participate in decisions that affect their lives.
2. Plan and tailor risk communication strategies. Different goals, audiences, and communication channels require different risk communication strategies.
3. Listen to your audience. People's perceptions of risk are influenced by factors other than numerical data. People are usually more concerned about psychological factors, such as trust, credibility, control, voluntariness, dread, familiarity, uncertainty, ethics, responsiveness, fairness, caring, and compassion, than about the technical details of a risk. To identify public concerns about risk, organizations must be willing to listen carefully to and understand the audience.
4. Be honest and transparent. Honesty and transparency are
1612
critical for establishing trust and credibility. Trust and credibility are among the most valuable assets of a risk communicator. Once lost, they are extremely difficult to regain.
5. Coordinate and collaborate with credible sources of information and trusted voices. Communications about risks are enhanced when validated by sources of information perceived to be credible, neutral, and independent. Few things hurt credibility more than conflicts and disagreements among information sources.
6. Plan for media influence. The media play a major role in transmitting risk information. It is critical to know what messages the media are delivering and how to deliver risk messages effectively through the media.
7. Speak clearly and with compassion. Technical language and jargon are major barriers to effective risk communication. Abstract and unfeeling language often offends and confuses people. Acknowledging emotions, such as fear, anger, and helplessness, is typically far more effective.
Challenges to Effective Risk Communication While the rules listed above seem straightforward, applying them in the real world is more complicated. Two factors, in particular, pose challenges to effective risk communication: selective and/or biased media reporting, and a complex of psychological, sociological, and cultural factors that lead to misperceptions and misunderstandings about risk.
Media coverage can play a major role in delivering risk information and in shaping risk perceptions. Journalists often focus their attention on, and frame their stories around, controversy, conflict, personal drama, negligence or malfeasance, or scandal; they also present them as stories about villains, victims, and heroes— narratives that may result in selective or biased risk perception (Bomlitz & Brezis, 2008). At the same time, empirical studies in recent decades have suggested that media coverage is often more balanced than is commonly thought, and that the media's role in shaping public opinion is circumscribed (Freudenberg, Coleman, Gonzales, & Helgeland, 1996; Kitzinger, 1999; Wahlberg & Sjöberg, 2000). The availability heuristic (Tversky & Kahneman, 1974)
1613
may operate here. When using this mental shortcut, people turn to readily recalled information, such as a memorable personal experience or recent dramatic news coverage, and give it undue weight in forming their views. This might explain how an alarmist story in the media can lead people to overestimate risk—but it might also lead people to overestimate the extent of media sensationalism.
The role of the media in shaping people's views of risk is likely changing with the rapid evolution of the media. For instance, reality television is becoming more popular; how are risks and disasters depicted on these programs, and how does that influence risk perception? (Campbell, 2014). As the Internet and social media— offering blogs and microblogs, social networking sites, image sharing, and more—become more pervasive, how do those affect risk communication? (Wendling, Radisch, & Jacobzone, 2013). These tools offer important opportunities but can also lead to rapid, uncontrolled risk amplification (Krimsky, 2007; Chung, 2011; Raymond & Flood, 2014).
Risk communicators use a variety of approaches to help achieve accurate, balanced media coverage. A skilled lead spokesperson with sufficient seniority, expertise, experience, and communication skills helps to establish credibility with the media and the public. (This person is not always the most senior leader of an organization!) The agency or organization works to establish a positive, ongoing relationship with the media. Finally, a comprehensive risk and crisis communication plan is invaluable (Centers for Disease Control and Prevention [CDC], 2002; Covello, 2011a). (Also see Text Box 28.2.)
1614
Text Box 28.2 Elements of a Comprehensive Risk and Crisis Communication Plan
Identify all anticipated environmental scenarios for which risk, crisis, and emergency communication plans are needed, including worst cases and low-probability, high- consequence events.
Describe and designate staff roles and responsibilities for the different risk, crisis, or emergency scenarios.
Designate who in the organization is responsible and accountable for leading the crisis or emergency response.
Designate who is responsible and accountable for implementing various crisis and emergency actions.
Designate who needs to be consulted during the process.
Designate who needs to be informed about what is taking place.
Designate who will be the lead communication spokesperson and backup for different scenarios.
Identify procedures for information verification, clearance, and approval.
Identify procedures for coordinating with important stakeholders and partners (e.g., with other organizations, emergency responders, law enforcement, elected officials, and state or provincial and federal government agencies).
Identify procedures to secure the required human, financial, logistical, and physical support and resources (such as people, space, equipment, and food) for communication operations during a short, a medium, and a prolonged event.
Identify agreements on releasing information and on who releases what, when, and how; set policies and procedures regarding employee contacts from the media.
1615
Maintain regularly checked and updated media contact lists (including after-hours news desks).
Maintain regularly checked and updated partner contact lists (day and night).
Identify a schedule for exercises and drills in order to test the communication plan, as part of the larger preparedness and response training.
Identify subject-matter experts (e.g., university professors) willing to collaborate during an emergency, and develop and test contact lists (day and night); ensure that the experts' perspectives are known in advance.
Identify target audiences.
Identify preferred communication channels (e.g., telephone hotlines, radio announcements, news conferences, Web site updates, tweets) for communicating with the public, key stakeholders, and partners.
Have messages for core, informational, and challenge questions.
Have messages with answers to frequently asked and anticipated questions from key stakeholders, including key internal and external audiences.
Have holding statements for the different anticipated stages of the crisis.
Have fact sheets, question-and-answer sheets, talking points, maps, charts, graphics, and other supplementary communication materials.
Have a signed endorsement of the communication plan from the organization's director.
Have procedures for posting and updating information on the organization's Web site.
Prepare communication task checklists.
Set procedures for evaluating, revising, and updating the risk and crisis communication plan on a regular basis.
1616
Risk communicators need to understand the psychological, cultural, and sociological factors involved in people's response to risk communications. People typically use only a small amount of available information to make risk decisions. Using the availability heuristic, mentioned above, is one example of this. Another common bias is overconfidence, especially salient when people believe they exercise personal control. A majority of people, for example, consider themselves less likely than the average person to have a car crash, get cancer, get fired from their job, or get mugged. Similarly, many teenagers engage in high-risk behaviors (e.g., drinking and driving, smoking, unprotected sex) because of perceptions of invincibility. Confirmatory bias is the tendency to seek and accept information that is consistent with one's beliefs or preconceptions, ignore or discount information that is not consistent with those beliefs or preconceptions, and interpret information in ways that confirm those beliefs or preconceptions. Strongly held beliefs about risks, once formed, change very slowly, and can be extraordinarily persistent in the face of contrary evidence. Conformity is people's tendency to hold a belief or to behave in a particular way because everyone else is doing it.
Much risk communication is designed to address these factors. Some key strategies appear in Text Box 28.3.
1617
Text Box 28.3 Overcoming Psychological, Cultural, and Sociological Barriers to Risk Communication
Anticipate questions commonly asked, and prepare answers in advance—an especially important approach in the setting of an emergency or crisis. Some such questions are shown in Text Box 28.4.
Develop a limited number of key messages (ideally, three key messages or one key message with three parts) that address the concerns of key stakeholders. It is useful to create a message map—a succinct but detailed, hierarchically organized “package” of information that addresses key stakeholder needs (see, e.g., Covello, 2006; Covello et al., 2007).
Develop messages that can be easily understood by the target audience, typically at or below their average reading level (see, e.g., the CDC's Plain English Thesaurus for Health Communications (Centers for Disease Control and Prevention, National Center for Health Marketing, 2007).
Adhere to the primacy/recency, or first/last, principle by putting the most important messages in the first and the last position in lists.
Cite credible third parties that support or can corroborate key messages.
Provide information that indicates genuine empathy, listening, caring, and compassion.
Use graphics, visual aids, analogies, and narratives (such as personal stories).
Balance negative information with positive, constructive, or solution-oriented messages.
1618
Text Box 28.4 Questions Frequently Asked During an Emergency or Crisis Journalists (and members of the public) are likely to ask six questions in a crisis (who, what, where, when, why, and how), and these question are likely to relate to three broad topics: (1) what happened, (2) what caused it to happen, and (3) what does it mean. Here are some specific questions that are often asked.
What is your name and title?
What are your job responsibilities?
What are your qualifications?
Can you tell us what happened?
When did it happen?
Where did it happen?
Who was harmed?
How many people were harmed [or injured, or killed]?
Are those who were harmed getting help?
How are people who were harmed getting help?
What can others do to help?
Is the situation under control?
Is there anything good that you can tell us?
Is there any immediate danger?
What is being done in response to what happened?
Who is in charge?
What can we expect next?
What are you advising people to do?
How long will it be before the situation returns to normal?
1619
What help has been requested or offered from others?
What responses have you received?
Can you be specific about the types of harm that occurred?
What are the names of those who were harmed?
Can we talk to them?
How much damage occurred?
What other damage may have occurred?
How certain are you about the damage?
How much damage do you expect?
What are you doing now?
Who else is involved in the response?
Why did this happen?
What was the cause?
Did you have any forewarning that this might happen?
Why wasn't this prevented from happening?
What else can go wrong?
If you are not sure of the cause, what is your best guess?
Who caused this to happen?
Who is to blame?
Could this have been avoided?
Do you think those involved handled the situation well enough?
When did your response to this begin?
When were you notified that something had happened?
Who is conducting the investigation?
What are you going to do after the investigation?
What have you found out so far?
Why was more not done to prevent this from happening?
1620
What is your personal opinion?
What are you telling your own family?
Are all those involved in agreement?
Are people overreacting?
Which laws are applicable?
Has anyone broken the law?
What challenges are you facing?
Has anyone made mistakes?
What mistakes have been made?
Have you told us everything you know?
What are you not telling us?
What effects will this have on the people involved?
What precautionary measures were taken?
Do you accept responsibility for what happened?
Has this ever happened before?
Can this happen elsewhere?
What is the worst-case scenario?
What lessons were learned?
Were those lessons implemented?
What can be done to prevent this from happening again?
What would you like to say to those who have been harmed and to their families?
Is there any continuing danger?
Are people out of danger? Are people safe?
Will there be inconvenience to employees or to the public?
How much will all this cost?
Are you able and willing to pay the costs?
Who else will pay the costs?
1621
When will we find out more?
What steps need to be taken to avoid a similar event?
Have these steps already been taken? If not, why not?
What does this all mean? Is there anything else you want to tell us?
Communicating During and After a Major Environmental Disaster Risk communication following a major environmental disaster, such as the BP oil spill in the Gulf of Mexico in 2010 or the Fukushima nuclear power plant meltdown in 2011, is especially challenging. Many people experiencing a major environmental disaster will have strong emotional responses. Concerns focus on possible short-, medium-, and long-term negative effects, including harm to the environment, health, quality of life, infrastructure, resources, and institutions. The feelings people have about these effects can severely impact their desire and ability to process information.
Likely emotions following a major environmental disaster include the following:
Anxiety and distress (Where can we turn for help? Will there be anything left for me? What awful and horrible things are ahead? What do we do now?)
Anger (How could such a horrible thing have happened to us? Why is no one helping? Doesn't anybody care about us anymore? Where are government authorities when we need them? Why are we getting so little information? Why are we being treated so badly? Why are some people getting more than we are?)
Misery, depression, and empathy (Will things ever be the same? What can you possibly say to those who have lost everything?)
Disappointment and betrayal (Why do the authorities keep ignoring our wishes and demands? What have we done to justify this horror?)
Research has identified effective risk communication approaches in disasters (Tinker, Vanderford, & Covello, 2012). People prefer messages with clear, specific, prioritized instructions and action
1622
items that convey a sense of self-efficacy and concrete things to do (e.g., information on how to detect, measure, and assess environmental risks). They appreciate messages containing clear, jargon-free, and authoritative language (but without false certainties), from trusted sources, and delivered in real time, with clear, regular updates. People want to know that children and other vulnerable populations are safe. Comparisons may be useful. For example, the disaster risk may be benchmarked to a regulatory standard, to background exposure levels, and/or to the same risk as experienced by others at different times or places.
1623
Summary Two paradigms are highly relevant in environmental health communication: social marketing and risk communication. Social marketing aims to spread important ideas and to influence behavior, while risk communication aims to inform people and to help them feel safe, calm, connected, hopeful, resilient, cooperative, capable of solving problems, and self-sufficient—instead of unsafe, anxious, isolated, pessimistic, inflexible, uncooperative, helpless, dependent, fatalistic, and victimized. The two paradigms share important attributes. Both are grounded in theoretical and empirical understanding of how people acquire information, form conclusions, and decide to take action. Both recognize that these processes are highly social, that participation and engagement are critical, and that trusted sources—whether professionals or family and friends—are key. In both social marketing and risk communication, public health professionals rely heavily on collaboration with social scientists, communications professionals, and other partners.
Public health professionals can use two organizing heuristics in social marketing to effectively guide their communication and behavior change efforts: deliver simple clear messages, repeated often, by a variety of trusted sources; and make the behavior you are promoting easy, fun, and popular. Risk communication is also based on core principles: build strong partnerships, be meticulous about stakeholder engagement, take an inclusive approach to communication, provide strong, dedicated leadership, earn trust, and be transparent. These principles are central to the successful practice of environmental public health.
1624
Key Terms availability heuristic
A mental shortcut people use to make decisions that relies on the immediate examples that come to mind when evaluating a specific topic, concept, method, or decision. Events that can be more easily brought to mind or imagined are judged to be more likely than events that are less easily imagined.
confirmatory bias The tendency to seek, interpret, or recall information that confirms one's existing beliefs. Confirmatory bias is typically displayed when people gather or remember information selectively. The effect is stronger for emotionally charged issues and for deeply entrenched beliefs. (It is also called confirmation bias.)
conformity Holding attitudes, beliefs, or behaviors similar to those of most other people in one's society or group.
Consumer Confidence Reports (CCRs) Annual reports issued by community water systems pursuant to the EPA's National Primary Drinking Water Regulations; these reports provide information to consumers about drinking-water quality.
Emergency Planning and Community Right-to-Know Act (EPCRA)
A statute administered by the EPA and designed to facilitate the development of chemical emergency response plans by state, tribal, and local governments, and to improve community access to information about chemical hazards. Under ECPRA, companies with hazardous chemicals on their premises above a threshold amount must inform state and local authorities of this fact, and manufacturing firms above a certain size must submit a toxic chemical release report to EPA. (This Act is Title III of the Superfund Amendments and Reauthorization Act [SARA], and is thus also known as SARA Title III.)
Hazard Communication Standard An OSHA Standard (29 CFR Parts 1910, 1915, and 1926) that
1625
entitles workers to know the hazards to which they are exposed. The standard requires employers to inform and train workers accordingly.
heuristics Mental shortcuts that allow people to solve problems and make judgments quickly and efficiently. Even though heuristics can be helpful in solving complex problems or making difficult judgments, they can also lead to biases.
loss aversion The tendency for people to strongly prefer avoiding losses over acquiring gains. Most studies suggest that losses are two to three times as powerful, psychologically, as gains.
message map A visual display of an organization's messages regarding high- concern or controversial issues. Typically a one-page roadmap for displaying detailed, hierarchically organized responses to anticipated questions or concerns.
negative dominance A risk communication theory describing people's tendency to focus far more on negative information than on positive information when they are concerned, stressed, or upset.
right to know In the context of workplace and environmental law, the legal principle that people have the right to know the risks to which they may be exposed in their workplace and general environment. It is embodied in U.S and other national laws as well as in local laws in several states.
risk communication The exchange of information about risks. According to the National Academy of Sciences, risk communication is an interactive process for the exchange of information that involves multiple messages about the nature of risk and also messages not strictly about risks.
risk perception The subjective judgment that people make about the characteristics and severity of a risk.
social amplification and attenuation of risk A risk communication theory that describes how hazards
1626
interact with psychological, social, institutional, and cultural processes in ways that either increase (amplify) or decrease (attenuate) public responses to the risk or risk event. These public responses then generate secondary social or economic impacts.
social marketing The use of marketing concepts, including product (or service) development, price and distribution channel management, and promotion, to influence behaviors that benefit individuals and communities and contribute to the greater social good.
1627
Discussion Questions 1. Please select an environmental health topic, such as climate
change, healthy housing, or a dangerous chemical exposure. (Don't feel limited to one of these topics!) What would a communication strategy that includes simple clear messages, repeated often, by a variety of trusted sources, look like for your selected topic?
2. Please identify a behavior change that promotes environmental health, such as reducing energy use, bicycling, or changing dietary habits. (Don't feel limited to one of these topics!) What would social marketing strategy that makes the behavior you are promoting easy, fun, and popular look like for your selected topic?
3. Please identify somebody in your life—a friend, family member, or colleague—who engages in a behavior that is unhealthy or environmentally destructive. Interview that person, asking (a) if he or she is aware of the negative outcomes of the behavior, (b) if so, what is preventing him or her from changing the behavior, and (c) what messages or incentives he or she thinks might be effective in triggering behavior change.
4. A key goal of crisis communication is avoiding panic. Do you agree or disagree with this statement? Explain your reasoning.
5. Please select a current controversy that revolves around risk perception, such as vaccinations, genetically modified foods, or climate change. Do some research on the controversy. What factors seem to be most important in influencing risk perception on this topic—both among those who believe there is a risk, and among those who don't?
6. For the controversial topic you selected in Question 5, please identify the most trusted sources of information for the public. How would you incorporate these sources in a health communication strategy?
7. Please identify a recent disaster, such as a train crash, a ship sinking, a shooting, an earthquake, or a flood. Search for news articles from the first three days, and study the public
1628
statements of communicators such as police officials and politicians. What aspects of their crisis communication were most effective? Which were least effective? What was the impact of their communication?
1629
References Ariely, D. (2008). Predictably irrational: The hidden forces that shape our decisions. New York: HarperCollins.
Bandura, A. (2004). Health promotion by social cognitive means. Health Education & Behavior, 31, 143–164.
Bennett, P., Coles, D., & McDonald, A. (1999). Risk communication as a decision process. In P. Bennett & K. Calman (Eds.), Risk communication and public health. New York: Oxford University Press.
Blendon, R., Benson, J., & Hero, J. (2014). Public trust in physicians —U.S. medicine in international perspective. New England Journal of Medicine, 371, 1570–1572.
Bomlitz, L. J., & Brezis, M. (2008). Misrepresentation of health risks by mass media. Journal of Public Health, 30(2), 202–204.
Campbell, V. (2014). Framing environmental risks and natural disasters in factual entertainment television. Environmental Communication, 8(1), 58–74.
Centers for Disease Control and Prevention. (2002). Emergency and risk communication. Atlanta: Author.
Centers for Disease Control and Prevention, National Center for Health Marketing. (2007). Plain English thesaurus for health communications. Atlanta: Author. Retrieved from www.nphic.org/files/editor/file/thesaurus_1007.pdf
Chong, D., & Druckman, J. (2013). Counterframing effects. Journal of Politics, 75, 1–16.
Chung, I. J. (2011). Social amplification of risk in the Internet environment. Risk Analysis, 31(12), 1883–1896.
Cohen, D. A., Farley, T., Bedimo-Etame, J. R., Scribner, R., Ward, W., Kendall, C., & Rice, J. (1999). Implementation of condom social marketing in Louisiana, 1993 to 1996. American Journal of Public Health, 89, 204–208.
1630
Covello, V. T. (2006). Risk communication and message mapping: A new tool for communicating effectively in public health emergencies and disasters. Journal of Emergency Management, 4(3), 25–40.
Covello, V. T. (2011a). Guidance on developing effective radiological risk communication messages: Effective message mapping and risk communication with the public in nuclear plant emergency planning zones (NUREG/CR-7033). Washington, DC: Nuclear Regulatory Commission.
Covello, V. T. (2011b). Risk communication, radiation, and radiological emergencies: Strategies, tools, and techniques. Health Physics, 101(5), 511–530.
Covello, V. T., & Allen, F. (1988). Seven cardinal rules of risk communication. Washington, DC: U.S. Environmental Protection Agency.
Covello, V. T., Clayton, K., & Minamyer, S. (2007). Effective risk and crisis communication during water security emergencies: Summary report of EPA sponsored message mapping workshops (EPA Report No. EPA600/R-07/027). Cincinnati, OH: National Homeland Security Research Center, Environmental Protection Agency.
Covello, V. T., Peters, R., Wojtecki, J., & Hyde, R. (2001). Risk communication, the West Nile virus epidemic, and bio-terrorism: Responding to the communication challenges posed by the intentional or unintentional release of a pathogen in an urban setting. Journal of Urban Health, 78(2), 382–391.
Covello, V. T., & Sandman, P. (2001). Risk communication: Evolution and revolution. In A. Wolbarst (Ed.), Solutions to an environment in peril (pp. 164–178). Baltimore: Johns Hopkins University Press.
Fischhoff, B. (1989). Risk: A guide to controversy. In National Research Council, Committee on Risk Perception and Communication, Improving risk communication (Appendix C, pp. 211–319). Washington, DC: National Academies Press.
Fischhoff, B. (2007). Non-persuasive communication about matters of the greatest urgency: Climate change. Environmental Science &
1631
Technology, 41, 7204–7208.
Freudenburg, W. R., Coleman, C.-L., Gonzales, J., & Helgeland, C. (1996). Media coverage of hazard events: Analyzing the assumptions. Risk Analysis, 16(1), 31–42.
Greenberg, M. R. (2014). Energy policy and research: The underappreciation of trust. Energy Research and Social Science, 1, 152–160.
Heath, C., & Heath, D. (2007). Made to stick: Why some ideas survive and others die. New York: Random House.
Hornik, R. (2002). Public health communication: Evidence for behavior change. Mahwah, NJ: Erlbaum.
Kahneman, D. (2011). Thinking, fast and slow. New York: Farrar, Straus and Giroux.
Kahneman, D., Slovic, P., & Tversky, A. (Eds.). (1982). Judgment under uncertainty: Heuristics and biases. New York: Cambridge University Press.
Kahneman, D., & Tversky, A. (1979). Prospect theory: An analysis of decision under risk. Econometrica, 47(2), 263–291.
Kasperson, R. E., Renn, O., Slovic, P., Brown, H. S., Emel, J., Goble, R.,…Ratick, S. (1987). The social amplification of risk: A conceptual framework. Risk Analysis, 8, 177–187.
Kitzinger, J. (1999). Researching risk and the media. Health, Risk & Society, 1(1), 55–69.
Krimsky, S. (2007). Risk communication in the Internet age: The rise of disorganized skepticism. Environmental Hazards, 7(2), 157– 164.
Lang, A. (2013). Discipline in crisis? The shifting paradigm of mass communication research. Communication Theory, 23, 10–24.
Lehrer, J. (2009). How we decide. Boston: Houghton Mifflin Harcourt.
Leiserowitz, A., Maibach, E., & Roser-Renouf, C. (2009). Climate change in the American mind: American's climate change beliefs,
1632
attitudes, policy preferences, and actions. New Haven, CT: Yale Project on Climate Change Communication.
Lundgren, R., & McMakin, A. (2013). Risk communication: A handbook for communicating environmental, safety, and health risks (5th ed.). Hoboken, NJ: IEEE Press.
Maibach, E., Abroms, L., & Marosits, M. (2007). Communication and marketing as tools to cultivate the public's health: A proposed “people and places” framework. BMC Public Health, 7, 88.
Maibach, E., Rothschild, M., & Novelli, W. (2002). Social marketing. In K. Glanz, B. Rimer, & F. M. Lewis (Eds.), Health behavior and health education (3rd ed.). San Francisco: Jossey- Bass.
McKenzie-Mohr, D. (2011). Fostering sustainable behavior (3rd ed.). Gabriola Island, BC: New Society.
National Research Council. (1989). Improving risk communication. Washington, DC: National Academies Press.
Pechman, C., & Stewart, D. (1988). Advertising repetition: A critical review of wear-in and wear-out. Critical Issues and Research in Advertising, 11, 285–329.
Peters, R., McCallum, D., & Covello, V. T. (1997). The determinants of trust and credibility in environmental risk communication: An empirical study. Risk Analysis, 17(1), 43–54.
Pidgeon, N. F., Kasperson, R. K., & Slovic, P. (2003). The social amplification of risk. Cambridge, U.K.: Cambridge University Press.
Raymond, M., & Flood, A. (2014). The tweeters of doom: How social media impacts food safety and risk communication. Food Safety Magazine, February/March. Retrieved from http://www.foodsafetymagazine.com/magazine- archive1/februarymarch-2014/the-tweeters-of-doom-how-social- media-impacts-food-safety-and-risk-communication
Rothschild, M. (1999). Carrots, sticks and promises: A conceptual framework for the management of public health and social issue behaviors. Journal of Marketing, 63, 24–37.
1633
Rothschild, M. (n.d.) Road crew: A case study. Retrieved from http://www.consumerfocus.org.uk/files/2012/09/Road-Crew- FULL-case-study.pdf
Slovic, P. (1987). Perception of risk. Science, 236, 280–285.
Slovic, P. (Ed.). (2000). The perception of risk. London: Earthscan.
Smith, B. (2011). Reinventing social marketing. TEDxPenn Quarter. Retrieved from https://www.youtube.com/watch? v=IECY9LJvTf4
Smith, W., & Strand, J. (2008). Social marketing behavior: A practical resource for social change professionals. Washington, DC: Academy for Educational Development. Retrieved from http://omec.uab.cat/Documentos/com_desenvolupament/0155.pdf
Tinker, T., Vanderford, M., & Covello, V. (2012). Disaster risk communication. In S. David (Ed.), Textbook in emergency medicine (chap. 141). Gurgaon: Wolters Kluwer Health (India).
Tversky, A., & Kahneman, D. (1974). Judgment under uncertainty: Heuristics and biases. Science, 185(4157), 1124–1131.
Valente, T. (2012). Network interventions. Science, 337, 49–53.
Wahlberg, A.A.F., & Sjöberg, L. (2000). Risk perception and the media. Journal of Risk Research, 3(1), 31–50.
Wendling, C., Radisch, J., & Jacobzone, S. (2013). The use of social media in risk and crisis communication (OECD Working Papers on Public Governance, No. 24). Paris: OECD Publishing.
1634
For Further Information Communication and Social Marketing See Heath and Health (2007), McKenzie-Mohr (2011), and Rothschild (1999) listed in the References, and also the following:
Abroms, L., & Maibach, E. (2008). The effectiveness of mass communication to change public behavior. Annual Review of Public Health, 29, 16.1–16.16.
Heath, C., & Heath, D. (2010). Switch: How to change things when change is hard. New York: Random House.
Risk Communication In addition to Lundgren and McMakin (2013) listed in the References, see the following:
Allan, S., Adam, B., & Carter, C. (2013). Environmental risks and the media. New York: Taylor & Francis.
Arval, J., & Rivers, L., III. (2013). Effective risk communication. London: Earthscan.
Bennett, P., Calman, K., Curtis, S., & Fischbacher-Smith, D. (2010). Understanding public responses to risk: policy and practice. In p. Bennett, K. Calman, S. Curtis, & D. Fischbacher-Smith (eds.), Risk communication and public health, 2nd edition (pp. 3–22).
Chess, C., Hance, B. J., & Sandman P. M. (1986). Planning dialogue with communities: A risk communication workbook. New Brunswick, NJ: Rutgers University, Cook College, Environmental Media Communication Research Program.
Cho, H., Reimer, T., & McComas, K. A. (2014). The Sage handbook of risk communication. Los Angeles: Sage.
Covello, V. T. (2003). Best practice in public health risk and crisis communication. Journal of Health Communication, 8(Suppl. 1), 5– 8.
1635
Covello, V. T., McCallum, D. B., & Pavlova, M. T. (Eds.). (1989). Effective risk communication: The role and responsibility of government and nongovernment organizations. New York: Plenum.
Fischhoff, B. (1995). Risk perception and communication unplugged: Twenty years of progress. Risk Analysis, 15(2), 137–145.
Heath, R. L., & O'Hair, H. D. (2009). Handbook of risk and crisis communication. New York: Routledge.
Hyer, R., & Covello, V.T. (2007). Effective media communication during public health emergencies: A World Health Organization handbook. Geneva: World Health Organization.
Morgan, M.G., Fischhoff, B., Bostrom, A., & Atman, C. J. (2001). Risk communication: A mental models approach. New York: Cambridge University Press.
Sadar, A. J., & Shull, M. D. (2000). Environmental risk communication: Principles and practices for industry. Boca Raton, FL: Lewis.
Sandman, P. (1993). Responding to community outrage: Strategies for effective risk communication. Fairfax, VA: American Industrial Hygiene Association. Available at http://www.psandman.com/book.htm
Ulmer, R. R., Seeger, M. W., & Sellnow, T. L. (2014). Effective risk communication: Moving from crisis to opportunity (3rd ed.). Thousand Oaks, CA: Sage.
1636
Index
1637
A Aarestrup, F. M.
Aatif Qureshi, I.
Abbott, J. A.
Abe, A.
Aberman, N.
Abernathy, J. H.
Abiotic components
Abonist
Aboyans, V.
Abraham, J. L.
Abram, D.
Abramson, M. J.
Abroms, L.
Absolute water scarcity
Absorbed dose
Absorption
Absorption factor
Abundance
Academy of Nutrition and Dietetics
Accessibility (food)
Acenaphthene (PAH)
Acevedo-Garcia, D.
Acosta, H.
Active: living; sampling; transport; transportation
Active Design Guidelines
Activism
1638
Activity
Acute exposure
Acute gastrointestinal infection (AG)
Acute water scarcity
Adair, H.
Adair-Rohani, H.
Adak, G. K.
Adamkiewicz, G.
Adams, C. L.
Adams, J.
Adams, O.
Adams, W. N.
Adaptation
Adaptive management
Addicks, P.
Adelman, Z.
Adenine (A)
Adil, M. M.
Administrative controls
Advisory Committee on Childhood Lead Poisoning Prevention
Advocacy
Aerodynamic diameter
Aeron-Thomas, A.
Affect
Affected people
Affluence
Affordances
Aflatoxin BI (AFBI)
1639
AFL-CIO
Agency for Toxic Substances and Disease Registry (ATSDR)
Agenda 21 (Rio de Janeiro)
Aggregate exposure
Agho, K.
Aging in place
Agonist
Agouti gene
Agricultural waste
Agriculture, and water scarcity
Agriculture and Community Development Services
Agroecological practices
Aguilera, F.
Aguirre, A. A.
Agusto, F.
Ahearne, J. F.
Ahern, M. M.
Ahmed, G.J.U.
Ahmed, S. M.
Ahmed Basha, C.
Ahmedzai, S.
Ahuja, R. B.
Ahumada, J. A.
Aichinger, E.
Aidara-Kane, A.
Ainsley, C. G.
Ainslie, R.
Air pollutants: and air toxics; and carbon monoxide; definition
1640
of; major ambient; and mercury (HG); and nitrogen oxide; and particulate matter (PM); sources and effects of outdoor; and sulfur dioxide; and tropospheric ozone; and volatile organic compounds
Air pollution: and aeroallergens; history of; key concepts in; larger effects of regional; and ozone; prevention and control; studies of, and health; types of ambient; in world's dirtiest cities
Air quality
Airriess, C. A.
Akerlof, K.
Alameddine, I.
Alamogordo, New Mexico
Álamo-HernÁndez, U.
ALARA (as low as reasonably achievable)
Al-Awadi, H.
Albedo
Alberti, M.
Alcamo, J.
Alcoa Corporation
Alcock, I.
Alcohol: dehydrogenase (ADH); primary biotransformation pathway for
Aldous, K. M.
Aldy, J. E.
Alekseyenko, A. V.
Alexander, C.
Alexander, D.
Allcott, H.
Allele; variant
Allen, C.
1641
Allen, F.
Allen, K.
Allen, K. J.
Allen, K. M.
Allen, M. R.
Allergy USA
Alley, D.
Alley, W. M.
All-hazards preparedness
Alliance for Biking and Walking
Allison, C. G.
Allison, D.
Allworth, A.
Alonso, A.
Alpers, P.
Alpha particle
Alsema, E.
Alston, L. J.
Alvarez-Pedrerol, M.
Alvarez-Reeves, M.
Ambler Realty, Village of Euclid v.
Ameneshewa, B.
Amer, M. H.
Ameratunga, S.
American Academy of Microbiology
American Academy of Pediatrics; Committee on Environmental Health
American Burn Association
1642
American Cancer Society
American Chemical Society
American Cold Ash Association
American College of Epidemiology
American Conference of Governmental Industrial Hygienists
American Diabetes Association
American Housing Survey
American Lung Association in California
American National Standards Institutes (ANSI)
American Nurses Association
American Planning Association
American Public Health Association
American Society of Heating, Refrigerating, and Air Conditioning Engineers (ASHRAE)
Amino acids
Amoly, E.
Amoros, E.
Amphipathic
Analytical studies; and "Carcinogenicity of Polychlorinated Biphenys and Polybrominated Biphenyls" (Lancet Oncology)
Andalib, M.
Ander, G. D.
Anderson, B.
Anderson, D.
Anderson, D. H.
Anderson, D. M.
Anderson, G. B.
Anderson, H. A.
Anderson, H. R.
1643
Anderson, J. F.
Anderson, L. A.
Anderson, M.
Anderson, R.
Anderson, R. N.
Anderson, W. P.
Andreuccetti, G.
Andrews, K. G.
Angulo, F. J.
Animal Pet Products Association
Animal testing
Animal waste
Animal-assisted therapy
Annerstedt, M.
Annesi-Maesano, I.
Annual Review of Public Health
Antabuse
Antagonist
Anthracen (PAH)
Anthropocene era
Antibiotic resistance
Anticipation; role of, in assessing electronics manufacturing facility
Antoniou, H.
Antwi, F. B.
Anyamba, A.
Applegate, J. S.
Apte, M. G.
1644
Aquatic systems, large scale human impacts on
Aquifer recharge
Aramini, J. J.
Araz, O. M.
Archer, D.
Archibald, A. T.
Area sampling
Ariely, D.
Arimoto, A.
Arkema, K. K.
Arlappa, N.
Armitage, D.
Armstrong, B. G.
Armstrong, D. A.
Arnold, B. F.
Aroh, K. N.
Aron, J. L.
Aronsen, G.
Arrow, K.
Arsenic
Arsenic, Metals, Fibres and Dusts (IARC)
Artioli, Y.
Arup and Rockerfeller Foundation
Asbestos
Asbridge, M.
Aschengrau, A.
Ash, M.
Ashdown, S. P.
1645
Ashkin, S.
Askren, M. K.
Aspinall, P.
Assessment, policy development and assurance (Institute of Medicine)
Assis, A. M.
Association ethics codes
Association of American Railroads
Association of Zoos and Aquariums
Aston, L. M.
Athanasiou, T.
Athanosos, P.
Athersuch, T. J.
Atherton, I.
Ati, A.
Atkins, D. C.
Atkinson, R. W.
Atmosphere, geosphere, hydrosphere and
ATSDR Toxicological Profile on PAHs
Attention, directed
Attention restoration
Attfield, M. D.
Attributable fraction
Attribute
Auckland University of Technology
Auerbach, P. S.
Ausubel, K.
Autonomy
1646
Autosomes
Autotrophs (primary producers)
Availability (food)
Availability heuristic
Average daily dose (ADD)
Avery, R.
Awa, A. A.
Ayers, T.
Ayres, R. U.
Azaroff, L. S.
1647
B Baan, R.
Babcock, B. A.
Baccaglini, L.
Bachran, M.
Bacillus thuringiensis (Bt)
Bader, D. A.
Bader, M.D.M.
Bahri, T.
Bai, X.
Bailey, G.
Bailey, R.
Bailey, W. J.
Bais, A. F.
Baiz, N.
Baker, D. B.
Baker, P. J.
Baker, S. P.
Baker-Laporte, P.
Balakrishnan, K.
Balazs, C.
Balbus, J. M.
Baldwin, P.
Balfour, E.
Balistreri, W. F.
Ball, A.
Ballester, F.
1648
Ballesteros, M. F.
Baltran, J. J.
Bambace, L.
Bambra, C.
Bammler, T. K.
Bancroft, C.
Bandura, A.
Banerjee, S. N.
Banerjee, T.
Banister, D.
Banks, S. M.
Banta, J.
Banton, J.
Baptized in PCBs (Griffith Spears)
Barbul, A.
Barker, D. J.
Barker, I. K.
Barker, M.
Barker, S. B.
Barnard, L. T.
Barnard, S.
Baron, S. L.
Barr, D. B.
Barreto, M. L.
Barrett, M.
Barrett, S.
Barringer, J.
Barriopedro, D.
1649
Barros-Dios, J. M.
Barsh, G. S.
Barton, D. M.
Barton, H.
Barton, J.
Bartram, J.
Basagaña, X.
Basch, C. H.
Base map
Base population
Basel Convention
Bases (genes)
Bashir, S. A.
Basu, G. C.
Basu, R.
Basu, S.
Bate, R.
Baten, A.
Bateson, W.
Batllori, E.
Batterman, S.
Batz, M. B.
Bauer, J. E.
Bauman, A.
Baur, L. A.
Baxter, A. J.
Baxter, L. K.
Bayer, C.
1650
Bazyka, D. A.
Beaglehole, R.
Beale, C.
Beauchamp, D. E.
Beaulac, J.
Bebeshko, V.
Beck, A. M.
Beck, H. L.
Beck, L. F.
Becker, B.
Becker, F. D.
Beckerman, W.
Beckman, J.
Beckman, S.
Bedimo-Etame, J. R.
Bedimo-Rung, A. L.
Beecham, H. J.
Beelen, R.
Beetz, A.
Beevers, S.
Begon, M.
Behavior settings
Behrens, W. W.
Belflower, A.
Bell, J. F.
Bell, M. L.
Ben Embarek, P.
Ben-Ari, T.
1651
Benbrahim-Tallaa, L.
Benbrook, C. M.
Benchmark dose (BMD)
Benchmark dose-lower bound (BMDL)
Benchmark response (BMR)
Bender, M. A.
Bennett, F. M.
Bennett, P.
Bennett-Fripp, M.
Bennish, M.
Benson, J.
Bentham, G.
Bentham, J.
Benz(a)anthracene (PAH)
Benzene; protection from; toxic effects of
Benzo(a)pyrene; metabolic transformations of
Benzo(b)fluoranthene (PAH)
Benzo(e)pyrene (PAH)
Benzo(ghi)perylene (PAH)
Benzo(j)fluoranthene (PAH)
Benzo(k)fluoranthene (PAH)
Beran, G. W.
Berg, P. R.
Bergman, A.
Berkes, F.
Berkman, L.
Berkman, L. F.
Berkowitz, M.
1652
Berman, M. G.
Berman, M. L.
Bernard, S. M.
Bernardo, M. F.
Berner, J.
Bernhardt, E. S.
Bernstein, A. S.
Berry, C. L.
Berry, H. L.
Berry, P.
Berry, T. R.
Bertazzi, P.
Bertok, I.
Bertollini, R.
Bertram, M.
Berylliosis
Besaratinia, A.
Besmer, M. D.
Besser, L. M.
Beta particle
Beusen, A.
Bhada-Tata, P.
Bhatia, R.
Bhatnagar, A.
Bhopal, India, Union Carbide plant in
Bhuiya, A.
Bi, X.
Bias
1653
Bible, Revised Standard Version
Bichaud, L.
Bielory, I.
Bierkens, M.F.P.
Bierwagen, B. G.
Big data
Big data revolution
Bigelow, F. S.
Bigras-Poulin, M.
Bihar, India
Bike share program
Bilotta, E.
Binder, S.
Binding site
Binimelis, R.
Binks, K.
Bioaccumulation
Bioactivation
Bioaerosols
Bioavailability
Biochemical pesticides
Biodeisel
Biodiversity
Bioethics
Biofilm
Biofuels
Bioinformatics
Biological: amplification; hazards; invasions; oxygen demand
1654
(BOD); plausibility; sampling; system
Biological markers. See Biomarkers
Biomagnification
Biomarkers; of exposure; reviews of exposure
Biomass
Biomonitoring
Biopesticides
Biophic design
Biophilia
Biophilic design
Biotic components
Biotransformation
Birnbach, D.
Bisesi, M.
Bisphenol A (BPA)
Biswas, B. K.
Bitton, G.
Bivand, R. S.
Blachford, T.
Black, M. M.
Black, R. E.
Black Death
Blackburn, J. L.
Blackstone, J. L.
Blackwater
Blair, D.
Blair, K. A.
Blair, S. N.
1655
Blakely, E. J.
Blancato, J.
Blanchard, C. M.
Blank, M.
Blanke, D.
Blascovich, J.
Blaser, M. J.
Blashki, G. A.
Blaylock, B. K.
Bleahu, A.
Blees, T.
Blendon, R.
Blettner, M.
Bloch, R. W.
Blomberg, R. D.
Blondell, J.
Bloom, A. J.
Board of Sustainable Development (U.S. National Academy of Sciences)
Boardman, B.
Boddy, K.
Boden, L. I.
Bodin, M.
Bodine, A.
Body mass index (BMI)
Boehnke, M.
Bogdanova, T.
Böhm, G.
1656
Bohme, S. R.
Boice, J. D., Jr.
Boisson, S.
Bojilova, D.
Bok, S.
Bolotnikova, M. G.
Bomlitz, L. J.
Bond, A. E.
Bondeau, A.
Boniol, M.
Bonita, R.
Bønløkke, J. H.
Bonta, D.
Boobis, A. R.
Booth, G.
Bopp, C. A.
Borchardt, M. A.
Borja-Aburto, V. H.
Bornman, M. S.
Bornschein, R. L.
Borucke, M.
Bos, R.
Bosch, D. A.
Bosch, S.
Bose, R.
Boseret, G.
Bossé, Y.
Bostrom, A.
1657
Bottled water
Boubekri, M.
Bouchama, A.
Bouchard, M.
Bougatosos, C.
Bouma, M. J.
Boundaries, in systems thinking
Bouskill, N.
Bouvard, V.
Bouville, A.
Bouwman, H.
Bouwman, L.
Bove, F.
Bowen, C.
Bowen, K.
Bower, L. M.
Bowers, K.
Boyce, J. K.
Boykoff, M.
Boyle, P.
BPA. See Bisphenol A (BPA)
Brachman, P. S.
Brackin, B.
Bracsicke, P.
Braden, C. R.
Bradley, R.
Brady, S. S.
Branas, C. C.
1658
Brandt, A. R.
Bratman, G. N.
Braubach, M.
Brauer, C.
Brauer, M.
Braun, J.
Braun, L. T.
Braungart, M.
Brazel, A. J.
Brazilian Blowout
Brenner, A.
Brewer, D.
Brewin, C. R.
Breysse, P. N.
Brezis, M.
Briceño, B.
Brigatti, E.
Briggs, D.
Briggs, X.
Brimblecombe, P.
Brinkman, N. E.
Britt, E. B.
Broadaway, S. C.
Brock, J. W.
Brody, H.
Brody, J. G.
Broken windows hypothesis
Bromet, E. J.
1659
Bronfenbrenner, U.
Brook, B. W.
Brook, J. R.
Brook, R. D.
Brooks, A. L.
Broome, J.
Browdy, B. L.
Brown, B. B.
Brown, C. M.
Brown, D.
Brown, D. A.
Brown, D. E.
Brown, H. S.
Brown, L. R.
Brown, M. J.
Brown, P.
Brown, R.J.C.
Brown, V. A.
Brown, W. T.
Brownfield redevelopment
Brownson, R. C.
Brubaker, M.
Bruce, N.
Brulle, R. J.
Brundtland, Gro Harlem
Brundtland Report
Bruneau, S.
Brunekreef, B.
1660
Brunner, J. L.
Bruton, C. M.
Bruvoll, A.
Bryan, R.
Buchanan, A. H.
Buchanan, D.
Buchman, T. G.
Buck, E. H.
Buckley, N. A.
Buffering; examples of
Buglova, E.
Bui, A.
Building codes
Building Resilience against Climate Effects (BRACE)
Buildings: approaches to protecting health and safety in; and asbestos; and biophilic design; and building design for elderly; chemical safety in; and elimination of toxic chemicals; and features that promote mental health; and formaldehyde; and good lighting; and green building; and hazardous ingredients of cleaners; and health care facilities; and high-quality indoor air; and homelessness; and homes; and injury prevention; key concepts in; key elements of healthy; and manufactured structures; and moisture and mold control; and neighborhood context; and pest control; and polybrominated diphenyl ethers (PBDEs); and radon; range of; and schools; and sick building syndrome; towards safe, healthy; and universal design
Built environment
Bulbena, A.
Bullard, R. D.
Bullock, L. F.
Bulsara, M. K.
1661
Bunn, F.
Buonocore, J. J.
Bureau of Alcohol, Tobacco, Firearms, and Explosives
Burford, D.
Burkart, W.
Burke, J.
Burke, J. G.
Burke, M.
Burke, S.
Burke, T. A.
Burkett, A.
Burkholder, J.
Burkle, F. M.
Burlingham, B.
Burnett, R. T.
Burson, A.
Burt, C. W.
Burton, D. C.
Burton, I.
Burwell, D.
Bush, G. W.
Bush, K. R.
Bushell, M.
Bushway, S. D.
Butchart, A.
Butler, C.
Butselaar, F.
Butterfield, P.
1662
Buzby, J. C.
Buzzell, L.
Bygbjerg, I. C.
Byler, C. G.
Byrne, J.
Byrne, S. N.
Byrnes, M.
1663
C C8 Science Panel
C40 Cities
Cai, H.
Cai, Q. E.
Cai, T.
Cairncross, S.
Cairns, H.
Caldeira, K.
Caldwell, G.
Caldwell, J. C.
California: Assembly Bill; Assembly Bill; Energy Commission; Environmental Protection Agency; Senate Bill
Callaghan, J. A.
Calle, E. E.
Calman, K.
Cama, R. I.
Camacho, F.
Camann, D. E.
Caminade, C.
Campbell, B.
Campbell, B. M.
Campbell, C. J.
Campbell, J. E.
Campbell, L. P.
Campbell, V.
Campbell-Landrum, D.
1664
Camper, A.
Campleman, S.
Canada Land Survey
Cancer Prevention Study II (CPSII; American Cancer Society)
Cancer slope factor (CSF)
Candidate gene
Caney, S.
Canfield, D. E.
Caniato, M.
Cann, K.
Cantilena, L. A.
Cantilena, L. R., Jr.
Cantor, N.
Canziani, O. F.
Cao, J.
Cao, L.
Cao, Y.
Cap and trade
Capacity
Capel, P. D.
Capon, A. G.
Capone, D. G.
Caras, R. A.
Carbamates
Carbon cycle
Carbon Dioxide Information Analysis Center
Carbon monoxide
Carbon tax
1665
Carcinogenesis; stages of
Carcinogens
Cardarelli, K. M.
Cardis, E.
Care ethics
Cariñanos, P.
Caríno Olivera, M.
Carlberg, M.
Carlson, C.
Carmichael, J.
Carpenter, S. R.
Carrasco, A. E.
Carrier, G.
Carroll, M. D.
Carrying capacity, concept of
Carson, Rachel
Carter, M.
Carter, S. L.
Carter, S. P.
Carter, Y. H.
Cartwright, M.
Carvalho, H. B.
Casares-Porcel, M.
Case, J. L.
Case, S. C.
Case-control studies
Casey, P. H.
Caspi, C. E.
1666
Cassel, C. K.
Cassileth, B.
Cassman, K. G.
Cassussuce, F.
Casteel, C.
Catchment area
Categorical variables
Cathode ray tubes (CRTs)
Catholic University of Louvain
Cattan, M.
Causal inference
Causal relationship (in measuring exposure)
Cayan, D. R.
Ceccato, P.
Cembella, A. D.
Cember, H.
Center for Affordable Water and Sanitation Technology
Center for Alternatives to Animal Testing
Center for Land Use Interpretation
Center for Naval Analysis Military Advisory Board
Center for Science in the Public Interest
Center for Universal Design
Centers for Disease Control and Prevention; Building Resilience against Climate Effects (BRACE) framework; National Center for Environmental Health (NCEH); National Center for Health Marketing; National Center for Injury Prevention (NCIPC); National Environmental Public Health Tracking Program; National Hospital Ambulatory Medical Care Survey: Emergency Department Summary; National Hospital Discharge Survey; Plain English Thesaurus for Health Communications; PulseNet
1667
Pathogen Detection and Tracking System
Central Board of Health (Great Britain)
Centre for Research on the Epidemiology of Disasters (CRED)
Cerin, E.
Chadeau-Hyam, A.
Chadwick, Edwin
Chafe, Z.
Chai, S.
Chakaborti, D.
Chakraborty, S.
Chalabi, Z.
Challinor, A. J.
Chalquis, C.
Chan, B.
Chan, C. K.
Chan, G.
Chan, H.-Y.E.
Chan, K. S.
Chandola, T.
Chang, D.
Chang, G.
Chang, H.
Chang, J. T.
Chapin, F. S.
Chapman, D. P.
Chapman, R. G.
Chapman, S.
Chari, R.
1668
Charrel, R. N.
Charron, D. F.
Chartier, Y.
Chavan, R.
Chaves, L. F.
Chawla, L.
Checkley, W.
Cheek, J. E.
Cheek, K. A.
Chekin, S. Y.
Chemical: carcinogenesis; hazards; releases
Chemical contaminants: anthropogenic; classes of, in water
Chen, A.
Chen, A. C.
Chen, L. E.
Chen, L. H.
Chen, M.-J.
Chen, W.
Chen, X.
Chen, Y.
Chen, Y.-Y.
Cheney, R. A.
Cheng, J. J.
Cherniack, A. R.
Cherniack, E. P.
Cherniack, M.
Chernobyl Nuclear Power Plant (1986)
Cherpitel, C. J.
1669
Chetrit, A.
Cheung, S. L.
Chevalier, V.
Chevrier, J.
Chicago heat wave (1995)
Child development
Children and Nature Network
Children Safe Products Act (Washington State)
Childs, B.
Chiller, T. M.
Chilton, M.
China earthquake 2014
Chiron, M.
Chisholm, D.
Chisso Corporation
Chivian, E.
Cho, I.
Choi, I. H.
Choi, Y. S.
Chokshi, D. A.
Cholinergic crises
Chong, C.
Chong, D.
Choropleth
Chotani, H.
Choudhury, R.
Choudhury, Y.
Chow, C. C.
1670
Chowdhury, M.
Chowdhury, T. R.
Chowdhury, U. K.
Christian, H. E.
Christian, P. J.
Christodouleas, J. P.
Christophides, G. K.
Chromosomes
Chronic exposure
Chrysene
Chu, E.
Chumak, V. V.
Chung, I. J.
Chung, J. W.
Churchill, Winston
Cialdini, R. B.
Cifuentes, L. A.
Ciliska, D.
Cimprich, B.
City Parks Alliance
City Resilience Framework
Clancy, L.
Clardy, S. A.
Clark, C. M.
Clark, C. S.
Clark, D. E.
Clark, E. G.
Clark, J. S.
1671
Clark, M.
Clarke, K. L.
Clarke, L.
Clarke, R.
Clasen, T.
Clayton, G. D.
Clayton, K.
Clayton, M. L.
Clayton, S.
Clean Air Act (EPA); Amendments (1990)
Clean Up Green Up (Los Angeles, California)
Clean Water Act
Cleaning materials
Cleland, V.
Clements, B. W.
Cleveland, C. J.
Clickner, R. P.
Climate: gap; justice; variability
Climate change; and air pollution; and earth system changes; ethical considerations in; and food and malnutrition; and greenhouse gases; and infectious diseases; key concepts in; mental health effects of; and migration and adaptation; policy; processes and pathways through which, influence human health Fig. 12.3; public belief in; and public health action; and warming earth; and water; and weather extremes and disasters
Climate-related disasters: anxiety and despair related to; and heat and mental illness; mental health effects of; mental health impacts of displacement from; refugees and population displacement from, and war
Climax communities
Clinical ecology
1672
Clinical trials
Clinkenbeard, R.
Clinton, Bill
Clow, A.
Club of Rome
Clusters; and measuring exposure; understanding
Clutton-Brock, J.
CNA Military Advisory Board
Coal; gasification; and health impacts of Dublin Coal Ban
Coal Act (1969)
Coal Ash Association
Coal Mine Health and Safety Act (1969)
Coarse PM (PM 2.5)
Cobb, C. W.
Co-benefits
Cochran, R. C.
Cochrane, K.
Codex Alimentarius Commission (CAC)
Codons
Cofala, J.
Coffey, R.
Coggon, D.
Cognitive map
Cohen, B.
Cohen, D.
Cohen, D. A.
Cohen, M. J.
Cohen, R.
1673
Cohen, R. A.
Cohen, S.
Cohen Hubal, E. A.
Cohn, P.
Cohn, S. K.
Cohort studies; example of community
Colborn, T.
Colby, W. D.
Cold weather
Colding, J.
Cole, B. L.
Cole, D.
Cole, D. C.
Cole, L. W.
Cole, T. B.
Cole, Thomas
Coleman, C.-L.
Coles, D.
Colford, J. M., Jr.
Collapse; human societal
Collapse (Diamond)
Collectivism, individualism versus
Collet, C.
Collier, T.
Collignon, P.
Collins, F. S.
Collins, L. B.
Collins, W. D.
1674
Colon-Gonzalez, F. J.
Colton, M. D.
Colville, F.
Colwell, R. R.
Commensalism
Commodities
Common good
Commoner, B.
Community; ecology; gardens
Community-based participatory research (CBPR)
Competition
Complementary strands
Complete streets
Complex systems
Complexity
Comprehensive Environmental Response Compensation and Liability Act (CERCLA)
Comprehensive plan
Computed tomography (CT)
Comrie, A. C.
Comstock, R. D.
Concentrated animal feeding operation (CAFO)
Concentration; understanding
Condon, S. K.
Confalonieri, U.
Conference of Parties (COP)
Conference of State and Territorial Epidemiologists
Confidence interval
1675
Confirmatory bias
Conformity
Confounders
Confounding
Congressional Budget Office
Conjugation
Connectivity
Connellan, K. P.
Conroy, L. M.
Conservation biology
Conservation tillage
Conserved (genes)
Consistency
Constable, John
Construction debris
Consumer Candidate List
Consumer Confidence Reports
Consumer Product Safety Commission
Consumerism; population growth versus
Consumption
Contaminant Candidate List (CCL)
Context (environmental psychology)
Continuous variables
Contraction and convergence
Control. See under Industrial hygiene
Convention on Biological Diversity
Conversation medicine
Conway, E. M.
1676
Conwell, Y.
Cook, J. T.
Cook, M.
Cooke, M. W.
Cooney, G.
Cooper, C.
Copy number variation (CNV)
Corburn, J.
Cornell, S. E.
Correlational studies
Corso, P.
Cory, D. C.
Cosco, N. G.
Cosmic radiation
Costa, L. G.
Costanza, R.
Costas, K.
Coto, J. A.
Cotton, S.
Council on the Environment of New York City
Coupled human-natural systems
Coussens, C.
Couture, C.
Couvidat, F.
Covello, V. T.
Cowett, F. D.
Cox, L. M.
Cox, N.
1677
Cox, S.
Coyle, S. J.
Coyne-Beasley, T.
Crabb, D. W.
Crabb, S.
Craig, S. B.
Cranz, G.
Crawford, D.
Creech, J. L.
Crews, D.
Crick, F.
Crime prevention, through environmental design (CPTED)
Criteria pollutants
Critical control point (CCP)
Croft, J. B.
Cromley, E. K.
Crompton, J. L.
Croner, C.
Cronin, S.
Cross-contamination
Cross-examination
Cross-sectional studies
Crowding
Crowley, K. D.
Crutzen, P.
CSD. See U.N. Commission on Sustainable Development
Cullen, M. R.
Cumberland, W. G.
1678
Cumes, D.
Cumming, O.
Cummins, S.
Cumulative: exposure; impacts; incidence; risk
Cunillera, J.
Cura, J. J.
Curie, Marie
Curriero, F.
Curtis, C. F.
Curtis, V.
Cusack, L.
Cushing, B. M.
Cushing, L.
Cutler, D.
Cutler, D. M.
Cutts, D. B.
Cutumisu, N.
Cyanobacteria
Cycles
Cyclones
Cystic fibrosis mutation
Cytochrome P450
Cytosine (C)
1679
D da Silva Nina, N. C.
Dadvand, P.
Dahlberg, L. L.
Daily, G. C.
Daisley, H.
Dalan, D.
Dale, V. H.
DALYs. See Disability-adjusted life years
Damage
Damalas, C. A.
Damian, D. L.
Danaei, G.
Danese, A.
Dangerous interference
Dangour, A. D.
Danielsen, A.
Danis-Lozano, R.
Dannemiller, K. C.
Dannenberg, A. L.
Danninger, T.
Darby, S. C.
Darwin, J.
Das, P.
Dash, A. P.
Dauer, L. T.
Davidson, J. R.
1680
Davies, E.H.S.
Davies, M.
DÁvila, J. D.
Davis, D. L.
Davis, J. J.
Davis, J. P.
Davis, J. R.
Davis, L. K.
Davis, S.
Davis, S. J.
Dawson, A. H.
Dawson, K. S.
Day, J. F.
DDE (dichlorodiphenyldichloroethylene)
DDT; in antimalaria campaigns
De, A.
De Aquino-Lopez, J. A.
de Botton, A.
De Bourdeaudhuij, I.
De Castro, M. C.
de Crespigny, C.
De Grandis, G.
De Jong, P.
De Man, H.
de Roda Husman, A. M.
De Sarro, G.
de Sherbinin, A.
De Simone, L.
1681
De Ville, K. A.
de Vries, S.
de Wet, N.
De Young, C.
De Young, R.
Dead zone
Deal, B.
Dear, K.B.G.
Death Calendar
Debono, R.
Decomposers (detritivores)
Deddens, J.
Deep well injection
Deepwater Horizon oil spill (2010)
Deer Island System (Boston, Massachusetts)
DEET
Defarge, N.
Defensible space
Deffeyes, K. S.
Defries, R. S.
Degenhardt, L.
Dehbi, M.
DeKalb County, Georgia
Del Porto, D.
Delavande, A.
Delbos, R. G.
Deldin, P. J.
DeMaria, A., Jr.
1682
Dembe, A. E.
Demirbas, A.
Democritus
Demography
Demoralization Index of the Psychiatric Epidemiology Research Instrument
den Outer, P. N.
Denison, R. A.
Dennis, J.
Density
Deontology
Deoxyribose
DePaola, A.
Department of Housing and Urban Development
Depledge, M. H.
Derevyanko, A.
Dermal: exposure
ingestion; inhalation
Derose, K. P.
Descriptive studies
Despres, P.
Deterministic effects
Detroit News
Deutch, Y.
Devenport, L.
Devrots, A.
Dew, M. A.
Dewailly, E.
1683
Dhara, R.
Dhara, V. R.
Dharmage, S. C.
Dhillon, G. P.
Dhiman, R. C.
Diamond, J.
Diao, G.
Diaz, J. H.
Diaz, R. J.
Dibenz(ah)anthracene (PAH)
Dichotomous variable
Dickerson, S. M.
Dickey, P.
Dieterlen, S. L.
Diette, G. B.
Dietz, B.
Dietz, T.
Diez Roux, A.
Dijkstra, L.
Dills, R.
Dingus, T. A.
Dioxins
Diploid
Direct reading instruments
Directly ionizing particles
Dirks, K. N.
Disability-adjusted life years (DALYs)
Disaster: consequences, Debono; hazard; resilience; response
1684
Disaster risk; extrinsic factors affecting; intrinsic factors affecting; and its determinants; managing; and risk avoidance and prevention; and risk reduction; three conceptual frameworks for; transfer
Disasters; public health consequences and capabilities associated with all
Discount (expectations)
Discount rate
Disease, changing burden of
Disease gene
Disease Registry Toxicological Profile for PCBs
Disinfection; approaches to; by-products; resistance
Distribution
Ditsuwan, V.
DNA (deoxyribonucleic acid)
Dobie, R.
Dockery, D. W.
Doering, O. C.
Doherty, T. J.
Dokken, D. J.
Dolinoy, D. C.
Doll, R.
Domenech, J.
Dominici, F.
Donaldson, D.
Donato, F.
Dong, F.
Donham, K. J.
Dono, J. A.
1685
Donora, Pennsylvania
Doocy, S.
Dora, C.
Dose; absorbed; rate; target organ; understanding
Dose-response; assessment; curve; relationship
Dot maps
Double helix
Dougill, A. J.
Douglas, I.
Dow Chemical Company
Dowie, M.
Downes, S.
Downey, K.
Downs, M. A.
Doxey, J. S.
Doyle, T. J.
Doyle-Baker, P. K.
DPSEEA (driving forces-pressures-state-exposure-effects- actions) model
Drahos, P.
Drewski, D.
Dreyfus, A.
Driver, J. H.
Driving forces
Drociuk, D.
Drought
Drozdovitch, V.
Druckman, J.
1686
Drug responses
DSM-IV (Diagnostic and Statistical Manual of Mental Disordersth Edition)
Duan, H.
Dubbo Study (New South Wales)
Dublin coal ban, Ireland
Dubos, R.
DuBose, J.
Duclos, P.
Due, C. P.
Duffin, J.
Duffy, J.
Duhigg, C.
Duhl, D.M.J.
Duncan, G. J.
Dunne, J. P.
Dunton, G. F.
Duperrex, O.
Duplicate diet study
Dupont
Dupuis, A.
Durand, C. P.
Duration of exposure
Durkin, S.
Duvdevani, S.
Dwight, R. H.
Dwyer, J.
Dyb, G.
1687
Dyer, C. A.
Dyoulgerov, M.
Dyson, M. E.
Dziura, J. D.
1688
E Eagle, N.
Earle, D. P.
Earley, J.
Earth Day
Earth in the Balance (Gore)
Earth Summit. See Earth Summit); United Nations Conference on Environment and Development (UNCED)
Earth system changes; ocean temperatures, hurricanes and; and particularly vulnerable regions; and sea level rise
Earthquakes
Easterling, D. R.
Eastman, C.
Eaton, D. K.
Eaton, D. L.
Eberly, S.
Ebi, K. L.
Ebisu, K.
Ebola
Echeverria, D.
Eck, J.
Eckerle, K.
Eckerman, K. R.
Eckert, S.
Ecobichon, D. J.
Eco-cities
Ecohealth
1689
EcoHealth
E.coli
Ecological: footprint; integrity; literacy; processes; studies
Ecological communities; richness of
Ecology; ecosystem; population; scale in, and some disciplines that contribute to each level
Ecopsychology
Ecosystem; ecology; functions; services
Ecotoxicology
Eddleston, M.
Edelstein, M. R.
Eden, North Carolina
Edmond, M.
Edmonds, C. J.
Edmonds, J. A.
Edwards, P.
Edwards, S. J.
Edwards, S. W.
Edwards, T.
Effect modification
Effect size
Effective dose
Effects, health
Effects of Principal Arts (Thackrah)
Effendi, S.
Egilman, D.
Ehrenfeld, J.
Ehrlich, P. R.
1690
EIA. See Energy Information Administration (EIA)
Eisentraut, A.
El Ghissassi, F.
El Majidi, N.
El Niño-Southern Oscillation (ENSO)
Elad, D.
Elder, M. A.
Electric Power Research Institute
Electromagnetic fields (EMFs)
Electromagnetic spectrum
Electronic waste (e-waste)
Eleftherohorinos, I. G.
El-Fadel, M.
Elgowainy, A.
Elia, V. J.
Eliseeva, E. A.
Elkin, E. P.
Elliot, A. J.
Elliott, E.
Elliott, M.
Ellis, A. G.
Ellis, R.
Ellner, S. P.
Elmendorf, W.
Elobeid, A.
Elvik, R.
Elvin-Lewis, M.P.F.
El-Yazigi, A.
1691
Embodied energy
Emch, M.
Emel, J.
Emergence
Emergency Events Database (EM-DAT)
Emergency operations plan
Emergency Planning and Community Right-to-Know Act (EPCRA)
Emergent properties
Emerson, Ralph W.
Emmanuel, J.
Employment
Enanoria, W.
Endangered Species Act (ESA)
Endangerment finding
Endemic disease
Endenburg, N.
Endocrine disruptors; structures of some suspected
End-of-pipe controls
Endogenous estrogen
Energy; association between use of, and health; and biofuels; conservation; efficiency; efficiency and conservation; and fossil fuels; and health co-benefits of conservation and efficiency; household; and hydroelectric power; key concepts in; nuclear; pathways linking, and health; poverty; renewable sources of; security; solar; use within certain countries; wind; and world energy consumption
Energy Information Administration (EIA)
Engelke, P.
Engineering controls
1692
Englander, J. G.
English, P.
Engstrom, A.
Enright, P. L.
Ensmininger, P.
Environment: primacy of
Environment
Environmental: estrogens; ethics; factors; gerontology; hazards; impact assessment; impact reports and statements; indexing; response gene; responsibility; stress
Environmental Defense Fund
Environmental disasters; annual incidence of natural and technological environmental, worldwide; and case study of Haiti's troubled recovery; and communicable disease; and comparison of public health impacts of natural and technological disaster events; key concepts regarding; key public health impacts for natural and technological disasters; major causes of death during; and malnutrition; morbidity associated with; mortality associated with; and noncommunicable disease; public health consequences of; recovering from public health impact of; scope of problem of; ten deadliest, worldwide; and toxic exposures; typology of
Environmental Equality: Reducing Risk for All Communities (U.S. EPA)
Environmental health; essential services of e; further information on children's; genes, genomics, and; greening of; policy
Environmental health communication: and environmental risk communication; key concepts in; social marketing and
Environmental health ethics: and climate change; and defining ethics and morals; and discounting; expanding horizons and challenges in; holism and interconnection in; and implications for professional ethics; and justice; key concepts in; key principles of; and moral standing of nature; and next
1693
generations; and philosophical ethics principles and consensus; and scientific integrity; and sustainability and resilience; technological prospects for; typical elements in professional code of; and welfare
Environmental Health Perspectives
Environmental justice; and climate gap; and cumulative impacts; and distribution of major industrial facilities by proportion of census tract residents living below federal poverty line in Southern California; and distribution of major industrial facilities by racial composition of census tracts in Southern California; elements of; further information on; and generational equity; key concepts in; meets urban forestry; movement; from research to action on; roots of; roots of, in Warren County, North Carolina; and vulnerable populations
Environmental psychology; contrasting toxicology and; and direct/indirect effects; and ecological perspective; exposure in; and health promotion; and humans as dynamic organisms; key concepts in; and outcomes of interest; and reduction of crime; and reduction of infections in hospitals; and saving energy; and toxicology
Environmental psychology process: and aesthetic preference; and child care outdoor learning environments; and commuting environment and physical activity; and crowding; diet and physical activity in; and effects of noise exposure on reading acquisition, mediated by poor auditory discrimination; health, behavior and; and housing and neighborhood conditions; and neighborhood food environment; and physical layout; and pro- environment behavior; and school cafeterias as food environments; and stress and coping
Environmental public health: and actions to reduce health hazards; assessment in; assurance in; careers in; and concepts of environmental health prevention; core functions of; essential services of; keeping track in; key concepts in; principles of prevention in; systems; from theory to practice; toxicology and
Environmental Public Health Performance Standards
Environmental quality: explanation for effects of social inequality on environment; social inequality and
1694
Enzyme induction
EPA. See U.S. Environmental Protection Agency
EPA, Massachusetts v.
Epidemics
Epidemiology; and bias; and clinical trials; and correlational (ecological) studies; and data analysis; and descriptive studies; and drawing epidemiologic conclusions; environmental; and etiologic (analytical) studies; and kinds of epidemiological studies; and observational studies; occupational; primer on; and risk assessment
Epigenetic modification; chromatin dynamic in response to
Epigenetics
Epigenome
Epigonomics
Epstein, L. D.
Epstein, P. R.
Epstein, S.
Equilibrate
Equivalent dose
Ercumen, A.
Ergonomic hazards
Erickson, J. B.
Eriksson, M.
Erlich, P. R.
Ernst, K.
Erskine, H. E.
Ervasti, J.
Escobido, F. J.
Eshet, Y.
Eshleman, K. N.
1695
Eskenazi, B.
Esnaola, M.
Esrey, S. A.
Essay on the Principle of Population (Malthus)
Esty, D. C.
Ethan, D.
Ethics; art of; care; codes, environmental responsibility in; environmental; feminist; modern; religious
Etiological studies
Etzel, R. A.
Etzioni, A.
Euclid v. Ambler
European Chemical Agency
European Commission
European Environment Agency (EEA)
European Union; REACH (Registration, Evaluation, Authorization and Restriction of Chemicals) initiative
Eutrophication
Evaluation (industrial hygiene)
"Evaluation of Polycyclic Aromatic Hydrocarbons Using Analytical Methods, Toxicology, and Risk Assessment Research" (Environmental Health Perspectives)
Evans, G. W.
Evans, H. J.
Evans, J. S.
Evans, K. J.
Evans, L.
Evans, N. J.
Evans, R. G.
1696
Eve, E.
Evidence-based design
Evidence-based medicine
E-waste
Ewing, R.
Excretion
Executive Order No. 12898 Fed. Reg. 34
Executive Order No. 13045 Fed. Reg. 78
Exodus, Book of
Exogenous synthetic estrogen
Exon Valdez spill
Exons
Expected value
Experimental studies
Explosions
Exponential growth
Exposome; reviews of
Exposure; acute; aggregate; assessment; chronic; cumulative; dermal; determinants; duration of; in environmental psychology; frequency of; imputing; ingestion; inhalation; intensity of; mapping and spatial analysis of; modeling; pathway; profile; scenarios; science; subchronic; understanding
Exposure assessment: and air pollution monitoring station for ozone and particulate matter in Atlanta for; to carbon monoxide; exposure science, industrial hygiene and; information on (organizations); in occupational setting; population sampling for; published overviews of; use of direct reading instruments in; use of sample collections instruments in
Exposure defaults
Exposure science; and aggregate and cumulative exposure assessment; and exposure assessment methods; and frequency,
1697
intensity, and duration of exposure; and imputing or modeling exposures; and ingestion and skin absorption; and measuring biomarkers; and measuring environmental exposures; and measuring personal exposures; and routes and pathways of exposure
External dose
External radiation protection
Extinction
Extremely low frequency (ELF) EMFs
Eyer, P.
Eyles, J.
Eze, C. L.
1698
F Faber Taylor, A.
Fabiani, D.
Fabiosa, J.
Factory Act (U.K.; 1833)
Fagan, J.
Fagin, D.
Fagliano, J.
Fahs, M. C.
Fairlie, I.
Falchero, S.
Falconer, R.
Falk, H.
Fallout
False discovery rate
Falter, K. H.
Fang, Y.
FAO. See Food and Agriculture Organizations of the United Nations
Farber, A.
Fardin, M. S.
Fargione, J.
Farin, F. M.
Farley, H. M.
Farley, T.
Farm Bill
Farr, William
1699
Farrow, A.
Faruque, A. S.
Faulkner, G.
Fauveau, U.
Fay, M. E.
Fazel, S.
Fedan, K.
Federal Coal Mine Health and Safety Act (1969)
Federal Emergency Management Agency (FEMA)
Federal Food, Drug, and Cosmetic Act (FFDCA; 1938); Delaney clause (1958)
Federal Highway Administration
Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA)
Federal Mine Safety and Health Act (Mine Act; 1977)
Federal Motor Carrier Safety Administration
Federal Railroad Administration
Federal Water Pollution Control Act (1948)
Feedback loops
Feinberg, G.
Feinberg, M.
Feitshans, I. L.
Feliciangeli, M. D.
Fell, L. A.
Feminist ethics
Fenster, L.
Ferber, J.
Ferguson, R.
Ferguson, S. A.
1700
Fernanda, S.
Fernandez-Somoano, A.
Fernandez-Villar, A.
Ferrari, A. J.
Ferriero, G.
Ferris, T.K.P.
Fetal origins, of adult disease
Fetzer, I.
Fewtrell, L.
Fichtenberg, C. M.
Fick's law of diffusion
Field, C. B.
Fielding, J. E.
Figueroa, D.
Figueroa, M. E.
Figueroa, W. G.
Filisetti, B.
Finch, S. C.
Fine PM (PM2.5)
Fink, G.
Finkel, M. L.
Finkelstein, E.
Finkelstein, N.
Finland
Finley, R. L.
Fiore, A. M.
Fiorito, E.
Firearm policy
1701
Fires
Firestone tire recall
Firewise Communities
Firket, J.
Fischer, C. M.
Fischer, E. M.
Fischhoff, B.
Fisher, G. T.
Fisher, J. D.
Fishman, E.
Fisk, W. J.
Fitch, G. A.
Fitzpatrick, M.
Fitzpatrick-Lewis, D.
Five Oaks neighborhood (Dayton, Ohio)
Flanders, W. D.
Flaxman, A. D.
Flegal, K. M.
Fleishman-Hillard Research
Flemming, H. C.
Fletcher, T.
Flint, Michigan
Flood, A.
Floods
Floret, N.
Flows, and systems
Floyd, M. F.
Fluoranthene (PAH)
1702
Fluorene (PAH)
Focal points
Foley, J.
Foley, J. A.
Folke, C.
Follman, M.
Food: desert; environment; loss; recalls; security
Food and Agriculture Organization of the United Nations (FAO)
Food Code
Food Quality Protection Act (FQPA)
Food Quality Protection Act (FQPA; 1996)
Food Safety Modernization Act (FSMA)
Food system: and addressing food safety threats; and biological pathogens in supply chain; and chemicals in food supply; and contributions of different food categories to domestically acquired illness and death; defining; and environmental impacts of wasted food; and food consumption and food environments; and food production, industrial agriculture in; and food safety regulations; and food system policy; and gaps and challenges in food safety protection; and globalization, seafood, and food safety; and industrial food animal production; and jurisdiction over food safety in U.S.; key concepts regarding; and meaning of organic agriculture; and mycotoxins; and public health; selected components of; and sustainable agriculture; and systems perspective on food safety and environmental health; and U.S. food system policies
Food waste
Food web; in North American food ecosystem
FoodNet
Ford, M.
Ford, T.
Ford, T. E.
1703
Foreman, K. J.
Foresight Land Use Futures Project
Forjuoh, S.
Formaldehyde
Forns, J.
Forrest, R. D.
Forsberg, B.
Forsman, A. K.
Foruno, T.
Fossil aquifer
Fossil fuels; and coal; and gas; and peak petroleum and public health; and petroleum
Foster, K. R.
Foster, S. R.
Fothergill, A.
Foufoula-Georgiou, E.
Fox, S.
Fracking
Fradin, M. S.
Fragar, L.
Framework for Human Health Risk Assessment to Inform Decision Making (U.S. EPA)
Francesco, J. T.
Franceys, R.
Francis, Pope
Francisco, R.
Frank, D. A.
Frank, L.
Frank, R. H.
1704
Franke, O. L.
Frankel, T.
Franklin, C.
Fraser, A. E.
Fraser, D. W.
Fraser, E.D.G.
Frattaroli, S.
Frederick, M.
Fredrickson, L. M.
Freed, E. C.
Freed, J.
Freeland, A. L.
Freeman, M. C.
Freeman, N.
Frenz, D.
Frequency
Freudenberg, N.
Freudenberg, W. R.
Friedlander, Y.
Friedman, G. D.
Friedman, T.
Friedman, W.
Friedmann, E.
Friedrich, Caspar David
Friel, S.
Frieler, K.
Fritze, J. G.
Fröling, M.
1705
Frost, C.
Frumkin, H.
Fthenakis, V. M.
Fu, F. X.
Fu, Q.
Fu, W.
Fu, X.
Fuchs, G.
Fuel ladder
Fukushima disaster (2011)
Fuller, D.
Fullerton, C. S.
Fullerton, D.
Fundamental cause; role of
Furlong, C. E.
Fussell, E.
Future Earth (website)
Future of Public Health (Institute of Health)
1706
G Gaardboe, M.M.A.
Gafafer, W. M.
Gaffikin, L.
Gaffney, J. S.
Gage, K. L.
Gajalakshmi, V.
Gale, P.
Galea, S.
Galkowski, P. G.
Gallagher, J.
Galli, A.
Galliani, S.
Galt, R. E.
Gamma rays
Ganesh, A.
Gannan, R.
Ganz, D. J.
Gao, X.
Garcia, R.
García-Herrera, R.
García-Palomares, J. C.
Gardiner, S. M.
Gardner, K.
Gardner, M. J.
Garner, A.
Garner, M. D.
1707
Garner, S. T.
Garnett, T.
Garrett, D.
Garrod, A.
Garside, R.
Gartside, P. S.
Garvey, J.
Gates, I.
Gates, S.
Gaudreault, N.
Gauley Bridge, West Virginia
Gaze, W. H.
Geddes, J. R.
Gehl, J.
Gelfland, L.
Geller, A. L.
Geller, R. J.
Gene; basic structural elements of; expression, epigenic regulation of; expression, regulation of
Gene-environment interactions; and alcohol; approaches for identifying; and benzene; and chronic beryllium disease; and dietary, occupational, and environmental exposures; and drug responses; examples of, in real world; and genetic susceptibility for environmental mercury; and pesticides
General use
Generalizability (external validity)
Generational equity
Genesis, Book of
Genetic: association studies; carcinogens; code; mutagens; toxicants
1708
Genetically modified organism (GMO)
Genetics
Genetics and Genomics: and basic components of gene or genome; and types of genetic variability
Geneva Protocol for the Prohibition of the Use in War of Asphyxiating, Poisonous or Other Gases, Na Bacteriological Methods of Warfare
Gennetian, L. A.
Genome human
Genome-wide association study (GWAS)
Genomics
Genotype
Genser, B.
Gentner, D. R.
Geographical information system (GIS); and analysis of environmental justice; basic, operations; and characterizing built environment; limitations of; and study of physical activity among park users
Georefrenced data; components of
George, K.
Georgescu, M.
Georgopoulos, P.
Geosphere, hydrosphere, atmosphere and
Gerba, C. P.
Gerberich, S.
German Commission on Radiological Protection (SSK)
Gertler, N.
Gertler, P. J.
Ghanimeh, S.
Ghimire, J.
1709
Ghosh, S.
Gibbs, H. K.
Gibbs, L. M.
Gibson, J. J.
Gibson, M.
Gibson, V.
Gies, P.
Giesecke, C. C.
Gifford, R.
Gignac, G. E.
Gilani, S. I.
Gilani, W. I.
Gilbert, E.
Gilbert, E. S.
Gilbert, P. M.
Gilbey, A.
Gilchrist, M. J.
Giles-Corti, B.
Gillespie, I. A.
Gillette, R.
Gilman, R. H.
Gingold, D. B.
Gingras, S.
Ginsburg, M. J.
Ginter, S. F.
Giovis, C.
GIS. See Geographic information system
Githeko, A. K.
1710
Giudice, L. C.
Giuntoli, G.
Glantz, S. A.
Glanz, K.
Glass, D. C.
Glass, G. E.
Glatstein, E.
Glazer, A. N.
Gleeson, D.
Gleick, P. H.
Glick, H. A.
Global: change; ecosystem; justice; warming
Global Burden of Disease Study (Lim)
Global Energy Assessment
Global Mercury Partnership
Global Reporting Initiative
Global Road Safety Facility (World Bank)
Global Warming Solutions Act (2006)
Globalization
Glouberman, S.
Glynn, M. W.
Glyphosate
Gnazzo, V.
Goble, R.
Gobo, A. E.
Gobster, P.
Godakumbura, W.
Godbey, G.
1711
Godgey, C.
Godwin, C.
Goering, J.
Goetz, G.
Gogal, R. M., Jr.
Gohlke, J. M.
Golden, C. D.
Goldenberg, D.
Golding, J.
Goldman, L. R.
Goldmann, E.
Goldstein, A. H.
Goldstein, B. D.
Gollinelli, D.
Golovneva, A.
Gomaa, A.
Gomes, M. E.
Gømez-Baggethun, E.
Gømez-Rubio, V.
Gonzales, J.
Goodchild, M. F.
Goodess, C. M.
Goodman, P.
Goodman, R. A.
Google Earth
Gordon, I. B.
Gordon, J. L.
Gordon, L. U.
1712
Gordon, T.
Gore, A.
Gorman, N.
Gosselin, P.
Gossner, C.M.-E.
Gottfredson, D. C.
Gottlieb, R.
Gotway, C. A.
Gould, E.
Gould, L. H.
Goulder, I. H.
Goulko, G.
Gouveia, N.
Goyal, N.
Gozdyra, P.
Graber, J. M.
Grabow, M. L.
Gradoni, L.
Gradus, M. S.
Grady, S. C.
Graefe, A.
Graham, J.
Graham, J. P.
Grambsch, A.
Granchignoni, F.
Grant, M.
Grattan, K. M.
Grattan, L. M.
1713
Gratz, N. G.
Graunt, John
Graves, J. M.
Gray, K.
Graywater
Great Acceleration
Green: building; chemistry; exercise; health care; neighborhoods
Green, T. L.
Greenberg, M. R.
Greenblatt, J. B.
Greene, K.
Greene, S.
Greenfield, E.
Greenhouse gases; main tab. 12.1
Greenland, K.
Greenland, S.
Greenlund, K. J.
Greenstein, J.
Greenstone, M.
Greenway, R.
Greer, F. R.
Gregory, J.
Greko, C.
Griffin, P. M.
Griffith Spears, Ellen
Griffiths, C.
Griffiths, J. K.
Griffiths, P. T.
1714
Grimes, D. J.
Grimmer-Somers, K.
Grindlinger, G.
Grinevald, J.
Groenewegen, P. P.
Groer, P.
Gronlund, C. J.
Groombridge, B.
Groopman, J. D.
Grootjans, J.
Gross, T. S.
Grosse, Y.
Ground-level ozone
Groundwater
Groundwater under the direct influence of surface water (GWUDI)
Group, S.
Growth, limits to
Grube, A.
Gruber, J. S.
Gruber, M.
Gruber, M. J.
Grübler, A.
Grzebieta, R. H.
GSTM Polymorphism
Guanine (G)
Guannel, G.
Guano
1715
Gubili, J.
Gubler, D. J.
Gucer, P. W.
Guenther, R.
Guerra, M.
Guerry, A.
Guey, L. T.
Guha, N.
Guha-Sapir, D.
Guignard, J. C.
Guilleminault, C.
Guillette, L. J., Jr.
Guillot, A.
Guiney, C.
Gullett, B. K.
Gulson, B. L.
Gunderson, L.
Gunkel, G.
Gunnell, D.
Gunther, I.
Guo, F.
Guo, J.
Gururaj, G.
Guse, C. E.
Gusev, I. A.
Guskova, A. K.
Gutierrez-Jimenez, J.
Guyton, K. Z.
1716
Guzman, M. A.
Guzman, S.
1717
H Haagsma, J. A.
Haas, C. N.
Haas, F.
Habeeb, D.
Habib, M.E. M.
Habitat
Haddad, L.
Haddon, W. A.
Haddon, W. J.
Haddon matrix; applied to motor vehicle crashes
Haeckel, Ernst
Hagel, B. E.
Hahn, M. B.
Hahn, S. M.
Hahn, T.
Haigler, E.
Haines, A.
Haiti earthquake
Hajat, S.
Hakama, M.
Hakian, J.
Hales, S.
Half-life
Hall, A. J.
Hall, C.
Hall, C.A.S.
1718
Hall, E. T.
Hall, K. D.
Hallegraeff, G. M.
Haller, L.
Haller, R. L.
Halliday, G. M.
Halliday, S.
Hallock, J.
Halpern, J.
Halstead, J.
Halstead, T.
Hambling, T.
Hamburg, S. P.
Hamilton, Alice
Hamilton, D. K.
Hamilton, E.
Hamilton, G. C.
Hamilton, I.
Hamilton, J. P.
Hamlin, C.
Hammes, F.
Hammond, R. A.
Hamner, S.
Han, B.
Han, J.
Han, K.-T.
Han, Y. Y.
Hanan, F. X.
1719
Hancock, T.
Hankey, S.
Hanks, A. S.
Hanley, N.
Hannan, M. A.
Hannon, J. C.
Hansen, J. E.
Hansson Mild, K.
Haponik, E.
Haq, G.
Hardell, L.
Hardeman County, Tennessee
Hardin, G.
Hare, W.
Haring, D.
Harlan, S. L.
Harle, J.
Harley, A. E.
Harley, R. A.
Harmful algal blooms (HAB)
Harpignies, J. P.
Harr, A.
Harrell, A.
Harris, E.
Harris, E. C.
Harris, N.
Harrison, J. L.
Harrison, J. P.
1720
Harrison, R.
Harris-Roxas, B.
Harry, I. M.
Hart, C.
Hartig, T.
Harvey, J. W.
Harvey, M.
Hasan, N.
Hasbach, P. H.
Hatch, E. E.
Hatch, M.
Hatheway, A. W.
Hathorn, B.
Havenaar, J. M.
Hawken, P.
Haworth, N.
Hawthorne, P.
Hawthorne, V.
Hayata, I.
Hayden, M.
Hayes, R. B.
Hayhoe, K.
Hays, M. D.
Hayter, C. R.
Hazard; index (HI)
Hazard Analysis and Critical Control Point (HACCP); principles
Hazard Communication Standard
Hazardous: air pollutants (HAPs); waste
1721
Hazen, S. L.
HCC (hepatocellular carcinoma)
He, Y.
He, Z.
Healing gardens
Health
Health, human: climate change and human; ecological approaches to, and home; ecological characteristics as foundation for; ecosystems as settings for, and well-being; energy and
Health and Well-Being in the Changing Urban Environment
Health care, sustainability in
Health Care without Harm (noharm.org)
Health Effects Institute
Health hazards
Health impact assessment (HIA)
Health in all policies (HiAP)
Health Product Declaration
Health promotion
Healthy Cities program
Healthy communities: and air quality; and community design and health; and consumption and urban sprawl of modern metropolis; and design for physical activity; and history of cities; and impacts of community design on health; and injury risk; key concepts in; and parks and green spaces; and physical activity and obesity; and poverty and industrialization in cities; and urbanization versus urbanism
Healthy homes projects
Healthy policies, concept of
Healthy worker effect
Heard, J. P.
1722
Hearne, V.
Heat islands
Heat wave
Heath, C.
Heath, C. W., Jr.
Heath, D.
Heath, G. A.
Heathcote, S.
Heederik, D.
Heerwagen, J.
Hegg, L. A.
Heibeck, T.
Heidenreich, W. F.
Heikkinen, S. A.
Heimann, H.
Heimlich, R.
Heinberg, R.
Heinrich, Herbert
Held, I. M.
Helgeland, C.
Hellberg, R. S.
Hemehway, D.
Hemming, D.
Henderson, J.
Henderson, S. B.
Hendry, J. H.
Hendryx, M.
Hepatitis B virus (HBV)
1723
Hepatocellular carcinoma (HCC)
Hepatoxic chemicals
Hepburn, C.
Herbicide tolerance
Herbicides
Herbivores
Herbivory
Herlihy, D.
Herman, K.
Hernandez-Shilon, J. A.
Hero, J.
Herrman, D.
Herrmann, F. R.
Heschong Mahone Group
Hess, J. J.
Heterotrophs (consumers)
Heuristics
Heyer, N. J.
Hibbard, K. A.
Hidalgo, H. G.
Hierarchy
Hierarchy of controls
Higgins, D. L.
Higgins, J. P.
Higgins, S. L.
High production volume chemical
Highway Safety Act (1970)
Hignell, D.
1724
Hii, J.
Hilbeck, A.
Hill, A. B.
Hill, C.
Hill, D. J.
Hill, E. M.
Hill, J.
Hill, K.
Hill, S.
Hill criteria
Hinterthuer, A.
Hipp, J.
Hippocrates
Hirabayashi, S.
Hird, S.
Hirohashi, N.
Hirsch, E.
Hirschfield, M.
Hiscox, A.
Histones; and histone deacetylases (HDACs)
Historic preservation
HLPE
Ho, C.-H.
Hodur, N. M.
Hoek, G.
Hoekstra, R. M.
Hoel, D. G.
Hoen, B.
1725
Hoener, B.
Hoet, P.H.M.
Hoffert, M. I.
Hoffmann, S.
Hoffmann, W.
Hogan, A.
Hohenheim, Philippus Aureolus Theophrastus von. See Paracelsus
Holder, Y.
Holdren, J. P.
Hole, D.
Holford, T. R.
Holism
Holladay, S.
Hollingworth, R. M.
Holloway, T.
Holmer, I.
Holmes, J. R.
Holt, J.
Holtan, M. T.
Holtzman, D. C.
Homer-Dixon, T. F.
Homo erectus
Homo habilis
Homo sapiens
Homozygous
Homozygous null
Honda, T.
1726
Honeyman, M. K.
Hoornweg, D.
Hopkin, S. P.
Hopton, J. L.
Hornik, R.
Horrigan, L.
Horticultural therapy
Horton, R.
Horton, R. M.
Horwitz, P.
Hoshino, R.
Hosier, R. H.
Hosking, C. S.
Hosoi, Y.
Hossain, M. S.
Hossain, S. T.
Hough, P.
Houghton, R. A.
House, C.
Household energy: and exposure to household fuel combustion products; and health effects of household fuel combustion; and interventions to protect health; patterns of use of
Housing First
Houston, D. J.
Howard, A.
Howard, C. V.
Howard, J.
Howarth, D.
Howarth, M.
1727
Howarth, R. W.
Howden, M.
Howden-Chapman, P. L.
Howe, G. R.
Howe, H. L.
Howe, P. G.
Hoxie, N. J.
Hoyert, D.
Hricko, A.
Hrudey, E. J.
Hrudey, S. E.
Hsiang, S. M.
Hsu, W. H.
Hu, H.
Huang, D.
Huang, H.
Huang, T.T.K.
Huang, W.
Hubbard, A. E.
Hubbard, K.
Hubbert, M. K.
Huda, W.
Hudson Alpha Institute for Biotechnology
Hueston, W.
Hugg, T. T.
Hughes, E.
Hulebak, K. L.
Hull, D.
1728
Hull, R. B.
Human ecology
Human-animal bond
Humanity, safe operating space for
Hume, C.
Humphrey, A.
Humphrey, L.
Hunt, A.
Hunt, M.
Hunt, S. M.
Hunt, V. R.
Hunte, G.
Hunter, N. L.
Huo, H.
Huq, A.
Hurd, M. D.
Hurley, W.
Hurrell, J.
Hurricane Katrina
Hurricane Mitch
Hurricane Rita
Hussain, Z.
Hussein, S.
Hutchinson, G.
Hutson, M.
Hutson, M. A.
Hüttenmoser, M.
Huybers, P.
1729
Hvistindahl, M.
Hwang, S. S.
Hwang, S. W.
Hybrid disasters
Hyde, R.
Hyder, A. A.
Hydroelectric power
Hydrodynamics
Hydrological cycle
Hydrolysis
Hydrophilic
Hydrophobic
Hygiene
Hyman, J.
Hynes, H. P.
Hyogo Framework of Action
Hypermethylation
Hypomethylation
Hypothesis-generating studies
1730
I IARC. See International Agency for Research on Cancer (IARC)
Icarus Allen, J.
Ichihara, G.
IEA. See International Energy Agency (IEA)
Igbeneghu, O. A.
Iha, K.
Illinois
Immerman, F. W.
Impact
Imura, H. A.
Incidence rate
Incident Command System (ICS)
Incineration; and diagram of incineration material and process flow
Incivilities
Indels
Indeno (1,2,3-cd)pyrene
Indicator concept
Indirect exposure assessment
Indirectly ionizing radiations
Individualism, versus collectivism
Indoor air Quality
Industrial ecology
Industrial food animal production (IFAP)
Industrial hygiene; anticipation in; concept of; control in; and evaluation; information on (organizations); standard references in
1731
Industrial organic farming
Industrial Poisons in the United States (Hamilton)
Industrial Toxicology (Hamilton)
Industrial waste
Infectious disease: as ecological and social process; and effects of weather and climate on vector- and rodent-borne diseases; foodborne; and freshwater ecosystems; and marine ecosystems; mosquito-borne; rodent-borne; tick-borne; vector-borne; waterborne
Information bias
Infrared radiation (IR)
Infrogmation
Ingestion
Ingestion exposure
Ingraffea, A.
Ingram, J.S.I.
Inhalation
Incident Command System (ICS)
Initiation
Injury
Injury and illness prevention programs
Injury control in special settings: and countermeasures for home injuries; and countermeasures for playground injuries; and countermeasures for road injuries; and home injuries; on playgrounds; on roadways
Injury prevention and control; and active versus passive interventions; and defining problem; and developing and testing interventions; and engineering driver out of equation; and evaluating and refining interventions; and global burden of injury; and identifying risk and protective factors; and implementing interventions and ensuring acceptance of control strategies; and injury pyramid; key concepts regarding; options
1732
analysis in; texting and driving and; and three E's of injury control; and types of injuries
Injury prevention and control policy: and consumer safety policy; and firearm policy; and highway safety policy; other stakeholders in; and voluntary industry standards
Injury prevention in practice: and burns; and countermeasures; and countermeasures for burns; and countermeasures for drowning; and countermeasures for falls; and countermeasures for intentional injuries; and countermeasures for poisoning; and epidemiology and risk factors for burns; and epidemiology and risk factors for drowning; and epidemiology and risk factors for falls; and epidemiology and risk factors for poisoning; and epidemiology and risk factors for violence; and falls; and intentional injuries (violence); and typologies of violence
Injury pyramid
Injury rate numbers
Inputs
Insect repellants
Institute of Health Metrics and Evaluation (IHME)
Institute of Medicine: Committee on Damp Indoor Spaces and Health
Integrated decision making
Integrated pest management (IPM)
Integrators
Intentional injuries
Intergenerational equity
Intergenetic regions
Intergovernmental Panel on Climate Change
Internal dose
Internal radiation protection
International Agency for Research on Cancer (IARC)
International Association for Ecology & Health
1733
International Atomic Energy Agency (IAEA)
International Commission on Large Dams
International Commission on Non-Ionizing Radiation Protection
International Commission on Radiological Protection (ICRP)
International Council for Science
International Energy Agency (IEA)
International Federation of Red Cross and Red Crescent Societies (IFRC)
International Food Information Center Foundation
International Institute for Environment and Development (IIED)
International Institute for Sustainable Development (IISD)
International Labour Organization (ILO)
International Occupational Hygiene Association
International Physical Activity and Environment Network (IPEN)
International Society for Environmental Epidemiology
International Union for Conservation of Nature (IUCN)
INTERPHONE study
Interpolation
Intragenic region
Intron
Ionization potential
Ionizing radiation
Iowa Public Health Association, r1
I$=$PAT equation
Iqbal, M. M.
Irrigation
Irvine, K. N.
1734
Ishikawa, S.
Islam, K.
Islam, M. R.
Isolation
Isotopes
Israel, B. A.
Istre, G. R.
Ito, K.
IUCN. See International Union for Conservation of Nature
Ivanov, V. K.
Iwasaka, Y.
1735
J Jaakkola, J. J.
Jaakkola, M. S.
Jack, D. W.
Jack in the Box Restaurant E. Coli outbreak
Jackson, K. T.
Jackson, L. S.
Jackson, M. L.
Jackson, R. B.
Jackson, R. J.
Jackson, T. D.
Jacob, B.
Jacob, P.
Jacobs, D. E.
Jacobs, G.
Jacobsen, P. L.
Jacobson v. Massachusetts
Jacobzone, S.
Jaffer-uz-Zaman
Jagai, J. S.
Jäger, J.
Jahan, S. A.
Jakubec, S. L.
Jameton, A.
Jamieson, M.
Janknecht, P.
Janssen, S.
1736
Jantzen, C. M.
Jarawan, E.
Jaron, D.
Jarus-Hakak, A.
Jeandron, A.
Jeffeson, M.
Jemelkova, B.
Jenerette, G. D.
Jenkins, J. C.
Jenkins, J. D.
Jenkins, M.
Jenkins, M. F.
Jennings, G.
Jennings, I.
Jennings, R. C.
Jenny, A.
Jensen, V. F.
Jerby, E.
Jerrett, M.
Jesdale, B. M.
Jess, J. J.
Jetter, J.
Jha, P.
Jia, Y.
Jimenez, F. E.
Jinping
Jirtle, R. L.
Job-exposure matrix (JEM); reviews of
1737
Jobin, W. R.
Joe, L.
Joffe, M.
John, J. G.
Johns Hopkins Center for a Livable Future
Johnson, D.
Johnson, E. J.
Johnson, M.
Johnson, M. N.
Johnson, M. O.
Johnson, N. F.
Johnson, R. M.
Johnson, S.
Johnson, T. E.
Johnston, F. H.
Johnstone, R. W.
Joint use policy
Jolly, D.
Jones, B.
Jones, C.
Jones, J.
Jones, M.
Jones, N. S.
Jones, R. T.
Jones-Rounds, M. L.
Jonides, J.
Jorchr
Jordan, F.
1738
Jorgensen, E.
Joseph, A.
Josephson, K. R.
Joshi, S.
Journal of Environmental Science and Health
Jovanović, D.
Judson, B.
Julius, H.
Julvez, J.
Jungle, The (Sinclair)
Just, D. R.
Justice. See also Environmental health ethics
1739
K Kaatch, P.
Kabir, E.
Kabir, S.
Kabir, Z.
Kabirova, N. R.
Kagawa, J.
Kagaya, Y.
Kahane, C. J.
Kahn, P. H., Jr.
Kahn, T.
Kahneman, D.
Kaiser, C. F.
Kalkstein, L. S.
Kalkwarf, H.
Kalra, N.
Kalundborg industrial park (Denmark)
Kamil, S.
Kamioka, H.
Kamiya, K.
Kammen, D. M.
Kanaroglou, P.
Kane, C. A.
Kane, J.
Kang, E.
Kang, S.
Kanner, A. D.
1740
Kaphingst, K. M.
Kaplan, Rachel
Kaplan, S.
Kaplan, Stephen
Kapos, V.
Kapp, C.
Kardan, O.
Kareiva, P. M.
Karkhanch, M.
Karliner, J.
Karol, M. H.
Kartha, S.
Kashcheev, V. V.
Kasperson, R. F.
Kasperson, R. K.
Katcher, A. H.
Katz, B. G.
Katz, E.
Katz, L. F.
Katzmarzyk, P. T.
Kaufman, J. D.
Kaufmann, R.
Kaufmann, R. B.
Kausrud, K. I.
Kavlock, R.
Kawachi, I.
Kay, D.
Kays, S. J.
1741
Kaźmierczak, A.
Keane, C. R.
Kee, R. A.
Keena, K.
Keenan, E. A.
Keim, M. E.
Keiser, J.
Keith, V. M.
Kellermann, A. L.
Kellermann, M.
Kellert, S. R.
Kelling, G. I.
Kelly, J.
Kelly, T.
Kemp-Benedict, E.
Kemperman, A.
Kendall, C.
Kendrick, D.
Kenigsberg, J.
Kensler, T. W.
Keogh, J. P.
Keoleian, G. A.
Ker, K.
Kerber, R. A.
Kerr, J.
Kersten, E.
Kerwin, J.
Kessler, R. C.
1742
Khait, S. E.
Khalil, A.
Khan, A. S.
Khan, B.
Khanna, M.
Kharecha, P. A.
Khoury, J.
Kielb, C.
Kiely, T.
Kilbourne, E. M.
Kilmer, Joyce
Kilpatrick, D. G.
Kim, B.
Kim, C. H.
Kim, D.
Kim, H. C.
Kim, K.
Kim, K.-H.
Kim, S.
Kim, Y.
King, D. W.
King, L. A.
King, R. V.
Kingston, Tennessee
Kinney, P. L.
Kinzig, A. P.
Kirch, W.
Kirchain, R.
1743
Kirk, E.
Kirkby, M.
Kirsch, P.
Kirsch, T.
Kirschenmann, F. L.
Kirshnan, R. M.
Kissinger, P.
Kit, B. K.
Kittredge, F. D., Jr.
Kitzinger, J.
Kivimaki, M.
Kjellstrom, T.
Klaasen, C. D.
Klare, M. T.
Klauer, S. G.
Klebanoff, M. A.
Kleindorfer, P. R.
Kleiner, S. M.
Kline, J. N.
Klinenberg, E.
Kling, J. R.
Kloog, I.
Klotz, J.
Knight, S.
Knopper, L. D.
Knorr, R. S.
Knowles, R. L.
Knowlton, K.
1744
Knudson, A. G., Jr.
Knutson, T. R.
Knutti, R.
Ko, C.-Y.
Kobe earthquake (1995)
Koch, J.
Koch, T.
Koelking, C.
Koenig, J. Q.
Koeth, R. A.
Kofler, W. W.
Koger, S.
Kohler, M.
Kohler, S.
Kohzu, K.
Kol, L.
Kolbert, E.
Kolpin, D.
Kolstad, C.
Kolstad, H.
Kominski, G.
Kondo, N.
Konradsen, F.
Koo, J.
Koopmans, M.
Kopecky, K. J.
Koren, H.
Korenstein, R.
1745
Korenstein-Ilan, A.
Korkmaz, S.
Korpela, K.
Korsch, M. J.
Koshurnikova, N. A.
Kosnik, L.
Kotrschal, K.
Kouyoumdjian, F.
Kovalchuk, O.
Kovats, R. S.
Kovats, S.
Kraft, K.
Kramer, C. L.
Krasner, S. W.
Kratochvil, B. E.
Kraus, J. F.
Krawchuk, M. A.
Kreiss, K.
Kreppel, K.
Kreslake, J.
Kreslov, V. V.
Krewski, D.
Krieger, J.
Kriging
Krimsky, S.
Krishnaratne, S.
Kristjansson, E.
Kroeger, T.
1746
Kross, E.
Krpan, K. M.
Krug, E.
Krug, E. G.
Kruger, G. E.
K-selected species
Kullman, G.
Kumagai, S.
Kumar, A.
Kumblad, L.
Kummerer, K.
Kundiyev, Y. I.
Kunkel, K. E.
Künzli, N.
Kuo, F. E.
Kuptsova, J.
Kurumatani, N.
Kushel, M.
Kushner, N.
Kverndokk, S.
Kweon, B. S.
Kwiatkowski, C.
Kwok, A. K.
Kwon, Y. J.
Kyle, A. D.
Kylin, H.
Kyoto Protocol
Kyrtopoulos, S. A.
1747
L Labonté, R.
Laborde, A.
Lackney, J. A.
Lacombe, C.
Laestadius, L.
Laffon, B.
Laflamme, L.
Laherrèrre, J. H.
Lajunen, T.
Lake, I. R.
Lake Apopka, Florida
Laliberté, C.
Lally, C.
Lam, J.
Lam, K.
Lamarque, J.-F.
Lamb, R. J.
Lamb, S. E.
Lambin, E.
Lamers, V.
Lamikanra, A.
Lamontagne, M.
Lancet
Lancet Oncology
Land, C. E.
Land use
1748
Landrigan, P. J.
Landslides
Land-use mix
Lane, C.
Laney, A. S.
Lang, A.
Lang, T.
Langa, K. M.
Lange, L.
Lange, R. A.
Lang-Yona, N.
Lankford, M. G.
Lanphear, B. P.
Lapierre, D.
Lapola, D. M.
Larimer, M. E.
Larouche, R.
Larsen, L.
Larson, N. I.
Larsson, D. G.
Lasch, C.
Last Child in the Woods (Louv)
Latency period
Latenser, B. A.
Lau, C. L.
Lauby-Secretan, B.
Laudisoit, A.
Laumon, B.
1749
Laursen, J.
Lavolette, M.
Law, A.
Law, A. J.
Lawrence, B. A.
Lawrence, R. J.
Lawrence, R. S.
Lawrence, W.
Lawson, A. B.
Layde, P. M.
Layering; hypothetical example of operation of
Layouts
Lazarus, E.
Lazer, D.
LD50, for various compounds
Le Moual, N.
Le Roy, S.
Leach, S. A.
Lead (Pb); exposure to; protection from; toxic effects of; use of
League of Conservative Voters
Leakey, A. D.
Learned helplessness
Learning for Sustainability
Leary, N. A.
Leavell, H. R.
Leavitt, J. W.
Lechtzin, N.
Lederbogen, F.
1750
LeDuc, S. D.
Lee, C.
Lee, D. R.
Lee, I. M.
Lee, K. S.
Lee, L. M.
Lee, R. K.
Lee, S. E.
Lee, T. M.
Lee, W. E.
LEED (Leadership in Energy and Environmental Design)
LEED for Neighborhood Development (LEED-ND)
Leeds, England
Leenen, E.
Lefferts, L. Y.
Leg to Stand on (Sacks)
Legibility
Legionella
Legionnaires' disease
Lehna, C.
Lehrer, J.
Leibensperger, E. M.
Leifert, C.
Leirs, H.
Leiserowitz, A. A.
Leistritz, R. L.
Leith, J. P.
Lele, S.
1751
Leliveld, H.
Lemanne, D.
Lemieux, P. M.
Lemke, B.
Lempert, L. B.
Lennert Veerman, J.
Leonard, B.
Leone de Nie, K.
Leong, K. J.
Lepore, S. J.
Leptospirosis; and life cycle and transmission of leptospira bacteria
Lercher, P.
Lerner, S.
Lertxundi, A.
Lestina, D. C.
Leung, C. C.
Leung, J. M.
Levenstein, C.
Leventhall, G.
Levin, R. J.
Levin, Y.
Levine, A.
Levine, G. N.
Levison, B. S.
Leviticus
Levy, B. S.
Levy, J. I.
1752
Levy, M.
Levy, S.
Lewandowsky, S.
Lewis, C. A.
Lewis, J. J.
Lewis, L.
Lewis, R. G.
Lewis, W. H.
Leyden, K.
Leyton, V.
Li, D.
Li, D. K.
Li, G. L.
Li, L. P.
Li, S.
Li, W.
Li, X. Z.
Liao, J.
Libra, B.
Lichtenberg, J.
Liddell, C.
Liebig, P.
Life cycle analysis
Lifetime average daily dose (LADD)
Ligand-activated nuclear transcription factors
Light
Light, A.
Lighting
1753
Likhtarev, I.
Lillibridge, S.
Lim, E.
Lim, S.
Lim, S. S.
Lima, I.
Limits to Growth (Club of Rome)
Lin, B. B.
Lin, C.-Y.
Lin, J.
Lin, S.
Linaker, C.
Lindgren, E.
Lindhjem, C.
Lindsay, L. R.
Lindsey, P. F.
Linear energy transfer (LET)
Linear nonthreshold function
Linear regression
Lines, J. D.
Link, B. G.
Linthurst, R. A.
Linton, L.
Linton, L. S.
Lioy, P.
Lipman, R. M.
Lipophilic
Lippmann, M.
1754
Lipscomb, D. M.
Lipsett, M.
Lipton, J. M.
Lisa, D.
Lissi, E. A.
Little, J. B.
Littlefield, J.
Littlefield, L. G.
Liu, G. C.
Liu, J.
Liu, Y.
Live cycle analysis
Living Building Challenge
Livingstone, N.
Lloyd, B.
Lloyd, S. J.
Lobell, D. B.
Lobelo, F.
Lobscheid, A.
Location
Lock, K.
Lockout tag-out
Locus
Lodge, C. J.
Lodge, C. L.
Lodito, B. D.
Lo-Fo-Wong, D.
Logistic regression
1755
Loh, J.
Lohr, V. I.
Lombard, J.
Loncar, D.
Lonczak, H. S.
London, England (London Fog 1952)
London Epidemiological Society
London School of Hygiene and Tropical Medicine
Long, P. V.
Longley, P. A.
Longnecker, E.
Longnecker, M. P.
Loomis, D.
Lopez, A.
Lopez, R.
López, S. L.
Lopez-Vicente, M.
Lopman, B. A.
Lorenc, T.
Lorenzoni, L.
Loss aversion
Losson, B.
Loughry, M.
Louv, R.
Louw, Q. A.
Lovasi, G. S.
Love Canal, New York
Lovekamp, W. E.
1756
Lovell, R.
Lovins, A.
Lovins, L. H.
Low as reasonably achievable (ALARA)
Lowe, A. J.
Lowe, D.
Lowe, R.
Lowe, S. R.
Lowell, B.
Lowest observed adverse effect level (LOAEL)
Lowry, S.
Lozano, R.
Lu, C.
Luber, G.
Lubin, J. H.
Lubroth, J.
Luby, S. P.
Lucan, S. C.
Lucier, G.
Luckow, P.
Ludwig, D.
Ludwig, J.
Ludwig, L.
Luke, D. A.
Lund, A. D.
Lund, J.
Lundgren, R.
Lung, S.-C.
1757
Lurie, N.
Luterbacher, J.
Lutes, C. C.
Luther, C.
Lydahl, E.
Lyon, J. L.
Lyzlov, A. F.
1758
M Ma, R.
Maarouf, A.
Maas, J.
Maccarone, E. M.
Maccougall, E.
MacDonald, J. M.
MacDonald, R.
MacGillvray, A.
Mack, K. A.
MacKenzie, D. L.
MacKenzie, E. J.
MacKenzie, W. R.
MacNaughton, P.
MacNeill, I. B.
Macpherson, A. K.
Mador, M.
Madsen, A. M.
Mafi, M.
Maglione, M.
Magnani, E.
Maguire, D. J.
Maguire, J. H.
Mahalov, A.
Mahan, W. T., Jr.
Mahesh, M.
Maibach, E. W.
1759
Maier, M. A.
Mailbach, E.
Mainardi Peron, E.
Mainil, J. G.
Mair, J. S.
Maisel, J.
Majeti, V. A.
Majewski, M. S.
Majorin, F.
Majumdar, S. R.
Makhijani, A. B.
Maksioutov, M. A.
Makuc, D. M.
Maldonado Pérez, H. L.
Malecki, K.
Malilay, J. N.
Malina, C.
Malins, Joseph
Malizia, E. E.
Maller, C.
Mallin, K.
Mallonee, S.
Malone, D. K.
Maltese, M. F.
Malthus, T.
Mamemachi, Y.
Mammen, G.
Mandal, B. K.
1760
Mangano, J.
Manguin, S.
Mani, I.
Manikkam, M.
Mann, A.
Mann, R. E.
Manning, M. R.
Mansell, G. E.
Manuel, J.
Manufactured structures
Manure cesspits
Map of Genesee County, Michigan, block groups (1990 census)
Marberry, S. O.
Marcelino, L. A.
Marcin, J.
Marcus, C. C.
Marcus, D. A.
Marcus, M.
Mare, R. D.
Margetts, B.
Margin of exposure (MOE)
Marinucci, G. D.
Markell, D.
Marker, D. A.
Market justice
Markowitz, E. M.
Markowitz, S.
Marlatt, G. A.
1761
Marley, N. A.
Marlier, M.
Marlith (building)
Marmot, M.
Maroli, M.
Marosits, M.
Maroun, R.
Marriott, J.
Marselle, M. R.
Marsh, D.
Marsh, J.
Marsh, S. M.
Marsh, T.
Marshall, B. J.
Marshall, J. D.
Marshall, S. C.
Marshall, S. W.
Marsillach, J.
Martin, C. E.
Martin, J.-L.
Martin, M. D.
Martin, M. W.
Martin, R.
Martin, R. P.
Martin, V.
Martin, W. J.
Martinek, K. A.
Martinez, A.
1762
Martinez, J.
Martinez, M.
Martinez-d la Cruz, L.
Martorell, P.
Masera, O. R.
Mason, K.
Massachusetts, Jacobson v.
Massachusetts v. EPA
Massachusetts Water Resources Authority
Masson, G. R.
Massy-Westropp, N.
Masyakin, V. B.
Matchock, R. L.
Material safety data sheets
Mathers, C.
Mathers, C. D.
Matheson, M. C.
Matson, P. A.
Matsueda, M.
Matsui, E. C.
Matsumoto, M.
Matte, T. D.
Matter, J. M.
Matthews, G.
Matthews, H. S.
Matthews, K. A.
Matthies, F.
Mattison, D. R.
1763
Mattoon, S.
Mattson, R. H.
Matyas, B.
Mauny, F.
Mawson, A. R.
Maximum Available Control Technology (MACT)
Maximum contaminant level (MCL)
Maximum residue limits (MRLs)
Maxwell, L. E.
Mayer, L. P.
Mazor, R.
McBride, D.
McCabe, M.
McCahill, C.
McCallum, D.
McCallum, J.
McCally, M.
McCann, B.
McCarthy, A.
McCarthy, J.
McCartt, A. T.
McCarty, J. P.
McClafferty, J.
McCombs, H. L.
McConnell, A. R.
McConnell, L. L.
McCormack, G. R.
McCoy, J. M.
1764
McCracken, J. P.
McCully, P.
McCunney, R. J.
McDermott, A.
McDonald, A.
McDonald, B. C.
McDonald, J. E.
McDonald-Wilmsen, B.
McDonough, W.
McElvenny, D. M.
McEwan, B. S.
McEwan, S. A.
McFarlane, A. C.
McGavock, J.
McGee, K.
McGeehin, M.
McGrath, J. J.
McHugh-Pemu, K. P.
McKee, M.
McKenzie, S.
McKenzie, T. L.
McKenzie-Mohr, D.
McKeown, A.
McKeown, R. E.
McKeown, T.
McKinnon, C.
McKone, T. E.
McLafferty, S. L.
1765
McLaughlin, J. B.
McLaughlin, P. K.
McLellan, S. L.
McLeoad, A.
McLuhan, T. C.
McMakin, A.
McMichael, A. J.
McMichael, C.
McMichael, T.
McMillan, J.
McNeill, J.
McNeill, W.
McNicholas, J.
MEA. See Millennium Ecosystem Assessment
Mead, M. N.
Meadows, D. H.
Meadows, D. L.
Meara, E. R.
Measure of effect
Meat Inspection Act
Medeiros, D. T.
Media coverage
Medicaid
Medical waste
Medicare
Medlock, J. M.
Mednick, A. C.
Medvedovsky, C.
1766
Meeker, J. D.
Meerburg, B. G.
Meerman, J.
Meheust, D.
Mehl, A.
Mehmood, A.
Mehta, A. S.
Mehta, P. S.
Mehta, S. J.
Meinhausen, M.
Meinhausen, N.
Meironyté, D.
Meis, M.
Melillo, J. M.
Melo, L. F.
Melosi, M. V.
Meltzer, D. O.
Memish, Z. A.
Menachemi, N.
Mendell, M. J.
Mendes, W. B.
Méndez, J.
Mendola, P.
Meneley, D. A.
Menne, B.
Menon, M.
Mental health
Merchant, J. A.
1767
Merck Sharp & Dohme
Mercury (HG); genetic susceptibility to environmental
Mercury Export Ban Act (2008)
Mercy, J. A.
Mergler, D.
Merletti, F.
Merriam-Webster's Collegiate Dictionary
Merrifield, M.
Mersch, J.
Mertens, E.
Mertz, K. J.
Message map
Messenger RNA (mRNA)
Meta-analysis
Metabolism; of acetaminophen
Metabolome
Metabolomics
Metastasis
Methylation
Methylmercury
Methylome
Metropolitan planning organization (MPO)
Mettler, F. A., Jr.
Metts, T. A.
Meuse Valley, Belgium
Meyer, C. R.
Meyer, J.
Meyer-Lindenberg, A.
1768
Meyers, N. M.
Mi, Y. H.
Mi, Y. L.
Mi, Z.
Miao, M.
Michael, E.
Michael, J. P.
Michaels, D.
Michaelson, S. M.
Michaud, C.
Mickalide, A. D.
Microbial pesticides
Microbiological contaminants; sources of outbreaks of
Microbiological risk assessment
Microbiome
MicroRNA (miRNA)
Microwave and radiofrequency radiation (MW/RFR)
Middaugh, J. P.
Middaugh-Bonney, T.
Migration and adaptation
Miguel, E.
Mikkelsen, S.
Milanovic, B.
Mild, K. H.
Miles, M. A.
Millennium Developmental Goals (United Nations)
Millennium Ecosystem Assessment (MEA); conceptual framework
1769
Miller, D.
Miller, G. W.
Miller, K. A.
Miller, T.
Miller, T. R.
Miller, Z.
Milli, M.
Mills, D. M.
Mills, I. C.
Mills, J. N.
Millstein, D.
Milner, J.
Milzman, D.
Minamata Bay (Japan)
Minamata Convention on Mercury
Minamata disease
Minamyer, S.
Mine disasters, miner protections
Mine Improvement and New Emergency Response Act (MINER Act)
Mine Safety and Health Administration (MSHA)
Mines Act (U.K.; 1842)
Mini-neighborhoods
Mining waste
Miniño, A. M.
Minkler, M.
Minniss, F. R.
Misak, J.
1770
Misclassification
Mishra, F. K.
Misic, B.
Mismeasurement
MitÁs, J.
Mitchell, C.
Mitchell, R.
Mitigation
Mitka, M.
Mizon, K. J.
Mmochi, A. J.
Mnzava, A.
Moch, A.
Mochizuki, I.
Mode share
Modeling exposures
Modern ethics
Modular classrooms
Moe, C. L.
Moeller, M. P.
Moghissi, A. A.
Mohai, P.
Mohamed, G.
Mohamed, M. E.
Mohan, D.
Mohan, J. E.
Mojica, W. A.
Mola, A.
1771
Mold
Molds
Mollard, R.
Monke, J.
Monmonier, M.
Monocultures
Montgomery, D. R.
Montgomery, M.
Montgomery D.
Montreal Protocol
Moola, F.
Moo-Llanes, D.
Moore, A.
Moore, B.
Moore, E. O.
Moore, L.
Moore, R. C.
Morales, J. C.
Morality
Moran, E.
Morello-Frosch, R.
Morency, P.
Morgan, L. L.
Morgenstern, H.
Morgenstern, O.
Morin, C. W.
Morin, M.
Morland, K.
1772
Morley, R. L.
Moro, J.
Morris, D. O.
Morris, J. G., Jr.
Morris, R. E.
Morrisey, M.
Morrison, D.
Morrongiello, B.
Morrow-Almeida, H. R.
Morse, A. P.
Morshed, M. G.
Mortality rate
Mortiz, M. A.
Morton, S. C.
Moser, S. C.
Moss, R. H.
Mota-Sanchez, D.
Motulsky, A. G.
Mouchet, J.
Moulder, J. E.
Mount Sinai School of Medicine
Mountford, H.
Moustaoui, M.
Mowen, A. J.
Mowry, J. B.
Moxham, T.
Mozaffarian, D.
Mozumdar, S.
1773
Muelleman, R. L.
Mueller, S. A.
Muir, J.
Mujahid, M.
Mukherjee, B.
Mullen, K. J.
Muller, M.
Mulligan, J.
Multibarrier approach
Multiple comparisons problem
Multivariate analysis
Municipal solid waste
Muñoz Lasa, S.
Munro, M
Murgueytio, A. M.
Murphy, J. V.
Murray, C.J.L.
Murray, K.
Muscatiello, N.
Musculoskeletal disorders (MSDs)
Mustillo, L.
Mutagens
Mutations
Mutoh, Y.
Muturalism
Mycotoxins
Myers, J.
Myers, S. S.
1774
Myers, T. A.
Mytoxins
1775
N Nabhan, G. P.
Nachman, K.
Nachman, K. E.
Naci, H.
Nadesan-Reddy, N.
Naeher, L. P.
Naeth, M. A.
Nagataki, S.
Naghavi, M.
Naik, A.
Naik, V.
NÁjera, J. A.
Nakajima, Hiroshi
Nakamura, A.
Nakamura, K.
Namboodiri, M. M.
Nanny state
Napolilli, N. P.
Narayan, K. V.
Nasci, R.
Nash, Roderick
Nath, I.
Nathens, A. B.
National Academy of Sciences
National Ambient Air Quality Standards (NAAQS)
National Association of County and City Health Officials
1776
(NACCHO)
National Center for Education Statistics
National Center for Injury Prevention and Control (NCIPC)
National Climatic Data Center
National Council on Radiation Protection and Measurements (NCRP)
National Death Index
National Environmental Justice Advisory Council
National Environmental Policy Act (NEPA)
National Fire Protection Association
National Health and Nutrition Examination Survey (NHANES)
National Health Interview Survey (NHIS)
National Highway Traffic Safety Administration (NHTSA)
National Incident Management System (NIMS)
National Institute for Occupational Safety and Health (NIOSH)
National Institute of Child Health and Human Development
National Institute of Environmental Health Sciences
National Institutes of Health
National Oceanic and Atmospheric Administration
National Parks and Recreation Association
National Primary Drinking Water Regulations (NPDWR)
National Research Council (NRC); Committee on Health Risks of Exposure to Radon; Committee on Passive Smoking
National Response Framework (NRF)
National Rifle Association
National Safety Council
National Snow & Ice Data Center
National Toxicology Program (NYP)
Natterson-Horowitz, B.
1777
Natural and Political Observations upon the Bills of Mortality (Graunt)
Natural disasters
Natural experiments
Natural gas
Natural hazards
Natural Resources Defense Council
Natural systems protection
Nature (Emerson)
Nature contact: and air quality; and animal domain; and attention restoration; and biophilic design; and child development; and collaboration; domains of; and ecosystem services and health; environmental psychology and; and green exercise; in inner city; key concepts regarding; and landscape domain; and links between nature and human health; and nature as setting for healthy behaviors; and parks and public health; and physical activity; and plant domain; and poverty; and public health intervention; risks of; and social connectedness; and stress reduction; and wilderness experiences
Nature deficit disorder
Naumova, E. N.
Naylor, R.
Nduagu, E.
NEA Committee on Radiation Protection and Public Health
Neary, D.
Neckerman, K. M.
Needham, L. L.
Needleman, H.
Neerinckx, S.
Neese, R.
Neff, R. A.
1778
Negative dominance
Neighborhood School Information
Neilands, T. B.
Nelson, E.
Nelson, G. C.
Nelson, H. D.
Nelson, J. W.
Nelson, K.
Nelson, L.
Nelson, M. C.
Nelson, M. P.
Nemery, B.
Nemmar, A.
Neo-sustainability
Nephrotoxic chemicals
Neria, Y.
Nerr, R.
Nesting
Neurotoxic chemicals
Neutrons
Nevin, R.
Nevo, I.
New England Journal of Medicine
New England Transcendentalists
New Kanawha Power Company
New Urbanism
New York State Department of Health
New York Times
1779
Newell, J. P.
Newman, O.
Newman, P.
Newmann, C.
Newton, A. C.
Newton, K. L.
Niche
Nicholls, C. M.
Nichols, G. L.
Nichols, T. L.
Nicklett, E. J.
Nicole, W.
Nieuwenhuijsen, M. J.
Nightengale, Florence
Nik Norulaini, N. A.
Nilekani, J.
Nisbet, M.
Niska, R. W.
Niskar, A. S.
Nitrogen cycle
Nitrogen oxides (NOx)
Njai, R. S.
Nnorom, I. C.
No Child Left Inside Act (New Mexico; 2008)
No observed adverse effect level (NOAEL)
NOAEL (no-observed-adverse-effect level)
Nodari, R. O.
Nodvin, J.
1780
Nondifferential error
Nonionizing radiation
Nonpoint source
Nonpolar chemicals
Nonstachastic effects
Nonsustainability, drivers of
Non-synonymous cSNP
No-observed-adverse-effect level (NOAEL)
Noone, K.
Norberg, J.
Norén, K.
Normative
Norris, F. H.
North, C. S.
Noskin, G. A.
Novelli, W.
Novo Nordisk
Nowak, D. J.
Nozaki, E.
Nuclear energy
Nuclear Energy Institute
Nuclear transformation
Nucleotide
Null hypothesis
Nussbaum, R.
Nuwayhid, I.
Nye, D. E.
Nygren, P.
1781
Nyqvist, F.
1782
O Oakland, California
Obama, Barack
Oberdörster, E.
Oberdörster, G.
Oberdörster, J.
Objectivity
Observational studies
Occupational Disease Commission (Illinois)
Occupational exposure
Occupational hygiene. See Industrial hygiene
Occupational Safety and Health Administration (OSHA); inspections and penalties; public health impact of, regulations
Ocean acidification
O'Connor, D.
Odds ratio
O'Donnell, M.
Oen, I. M.
Office of Environmental Equity
Office of Environmental Health Hazard Assessment
Office of Population Censuses and Surveys (U.K.)
Ogden, C. L.
Ogden, N. H.
O'Haire, M. E.
Oikos
Oimet, M. C.
Ojovan, M. I.
1783
Okatenko, P. V.
Okcu, S.
Okita, T.
Oksanen, T.
Okuizumi, H.
Oldenburg, R.
Oldham, R. L.
O'Leary, P.
Oliver, M. A.
Olivera, V. E.
Olivier, J.
Ollson, C. A.
Olmstead, Fredrick Law
Olmstead, J.
Olmsted, F. L.
Olsen, E.O.M.
Olson, B. H.
Olson, K. B.
Olson, R. L.
Olsson, P.
Oluwatola, O. A.
Omar, A. K.
Omenn, G. S.
Omics technologies
One Common Future (World Commission on Environment and Development)
One Health (Wilcox)
100 Resilient Cities
1784
O'Neal, T.
O'Neil, Paul
O'Neill, B.
O'Neill, M. S.
O'Neill, S.
Ontl, T. A.
Ontological security
Onuoha, F. C.
OPOWER (software firm)
ørbaeck, P.
Orenstein, W.
Oreskes, N.
Oreszczyn, T.
Organic food
Organisation for Economic Co-operation and Development
Organisation for the Prohibition of Chemical Weapons
Organochloride
Organochlorine pesticides
Organochlorine pesticides (OC pesticides)
Organophosphate pesticides (OPs)
Orians, G. H.
Orloff, K.
Orlov, M. Y.
Ormandy, D.
Ormerod, E.
Orr, D. W.
Orsega-Smith, E.
Osbaldiston, R.
1785
Osborn, S. G.
Osborne, N. J.
OSHA. See Occupational Safety and Health Administration (OSHA)
Osibanjo, O.
Osimitz, T. G.
Osofsky, S. A.
Ostfeld, R. S.
Ostro, B.
Ostrom, E.
O'Sullivan, K.
Osypuk, T. L.
Ottawa Charter for Health Promotion (WHO)
Otwell, W. S.
Ouimet, M. C.
Out Common Future (Brundtland Report)
Outdoor Bill of Rights in California
Overshoot, state of
Owen, D.
Owen, J.
Owen, N.
Ownby, D.
Oxidation
Ozkaynak, H.
Ozone (O3)
Ozone layer
Ozonoff, A.
Ozonoff, D.
1786
P Pacala, S.
Pachauri, S.
Packer, C.
Padilla, E.
Pagan, J. A.
Page, B.
Page, E. A.
Page, J. L.
Page, L. A.
Page, M. J.
Pagnelli, A.
PAHs. See Polycyclic aromatic hydrocarbons
Pahwa, S.
Painter, J. A.
Palinkas, L. A.
Palmer, A.
Palmer, G.
Palmer, K. T.
Palmer, L. J.
Palmer, M. A.
Palmer, Samuel
Pan, D.
Panasyuk, G. D.
Pande, R.
Paneth, N.
Panko, J.
1787
Pant, P.
Paracelsus
Parande, A. K.
Parashar, U. D.
Parasitism
Parbhoo, A.
Parent compound
Paretzke, H. C.
Parham, P. E.
Parisien, M.-A.
Park, H.
Parker, C. L.
Parker, J. D.
Parker, L.
Parkes, M. W.
Parkin, P. C.
Parkin, W. E.
Parkinson, A. J.
Parkinson's disease
Parks
Parks, C.
Parmet, W. E.
Parsons, D.
Particulate matter (PM)
Partition coefficient
PÁsaro, E.
Pascual, M.
Passchier, W. F.
1788
Passchier-Vermeer, W.
Passive sampling
Pastor, M.
Patel, V.
Patient Protection and Affordable Care Act (2010)
Pattanayak, S. K.
Patterns
Patterson, J. T.
Patz, J. A.
Paus, T
Paustenbach, D. J.
Pawel, D. J.
Pawlukiewicz, M.
Payne, L.
Payton, M.
Paz, S.
PCBs. See Polychlorinated Biphenyls (PCBs)
Peak concentration
Peak petroleum
Peakall, D. B.
Pearce, J. R.
Pearce, N.
Pearl, M. C.
Pearson, M. A.
Pearson-Mims, C. H.
Pebesma, E.
Peccia, J.
Pechman, C.
1789
Peck, M. D.
Peden, M.
Peek-Asa, C.
Peletz, R.
Pellow, D. N.
Penning, T. M.
Pentland, A.
Pentti, J.
Pentz, M. A.
Peralta, E.
Percival, H. F.
Pérez, C.
Perez, I.
Perfluorooctanoic acid (PFOA)
Perkins, Francis
Perkins, D.
Perlman, M.
Permissible exposure limits (PELs)
Perrin, P.
Persistent organic pollutants (POPs)
Personal protective equipment (PPE)
Personal sampling
Personal space
Persson, A.
Pest
Pest control; and bedbugs; and consumer education; and control measures; and fleas; and insect pests; and insect repellants; and integrated pest management (IPM); key concepts in; and lice; and management and cultural practices to control pests; and
1790
monitoring; and mosquitos; and pesticides; and sand flies; and structural maintenance; and termites; and ticks; and use of DDT in antimalaria campaigns; and vertebrate pests
Pesticides; biochemical; botanical; classified by target or mode of action; global; microbial; and organochlorine pesticides (OC pesticides); and organophosphates; patterns of use of, and human exposure; and pesticide toxicity categories and labeling requirements; and plant-incorporated protectants (PIPs); and public health; regulation of; who is responsible for applying
Pesticides in the Diets of Infants and Children (National Academies)
Peters, A.
Peters, R.
Peterson, A. T.
Peterson, D. E.
Peterson, R.K.D.
Petit, C.
Petkova, E. P.
Petroleum
Petrone, S.
Pett, J.
Petterson, J. S.
Petticrew, M.
Pettigrew, M.
Petting, R. A.
Pevec, I.
Pew Research
Pfefferbaum, B.
Pfeifer, G. P.
PFOA. See Perfluorooctanoic acid
1791
P&G Health Sciences Institute
Phaedrus (Socrates)
Phalen, K. J.
Pharmacogenetics
Pharmacokinetics
Phase I reactions
Phase II reaction
Phelan, J. C.
Phelan, K.
Phenanthrene (PAH)
Phenotype
Phillips, B. D.
Phillips-Miller, D.
Phosphorus cycle
Photon
Photons
Phthalates
"Phthalates and Diet" (Environmental Health)
"Phthalates: European Regulation, Chemistry, Pharmacokinetic and Related Toxicity" (Environmental Toxicology and Pharmacology)
Physical activity
Physical Activity Guideline (CDA; 380)
Physical hazards
Piacitelli, L.
Piarroux, R.
Pickett, K. E.
Pickford, J.
Pickle, L. W.
1792
Pidgeon, N.
Pieper, U.
Pierce, M. W.
Pietrantoni, L.
Piketty, T.
Pilgrim, S.
Pillai, P. B.
Pillsbury Corporation
Pimentel, D.
Pimentel, M.
Piot, P.
Pipeline and Hazardous Materials Safety Administration
Pirkle, J. L.
Pittman, M.
Pitts, S. R.
Plain English Thesaurus for Health Communications (Centers for Disease Control and Prevention, National Center for Health Marketing)
Planetary health
Plant-incorporated protectants (PIPs)
Pless, B.
Plotikoff, R. C.
Plourde, A.
Plummer, R.
PM2.5, 322 PM10, 322 Point of departure (POD)
Point source
1793
Point-of-use treatment
Poison control centers
Poisoning
Polar chemicals
Polasky, S.
Polen, M. R.
Policy development (public health)
Polinder, S.
Pollack, A. K.
Pollack, K.
Pollan, M.
Polluter pays principle
Pollution hot spots
Pollution prevention
Polybrominated Diphenyl Ethers (PBDEs)
Polychlorinated Biphenyls (PCBs)
"Polychlorinated Biphenyls and Cancer" (Journal of Environmental Science and Health)
Polymorphisms
Polz, M. F.
Ponce, J. C.
Poole, C.
Poor Laws (Great Britain)
Pope, C. A.
Popham, F.
Popkin, S. J.
Popper, Karl
Population; sampling, for exposure assessment
1794
Population cancer risk
Population decline
Population ecology
Population growth; versus consumerism; regulating
Porter, J. R.
Portier, C. J.
Portland, Oregon, city of, Office of Transportation
Portmann, R. W.
Portney, K. E.
Postel, S.
Postma, D. S.
Potash, J. B.
Potential Human Reproductive and Developmental Effects of Bisphenol A (National Toxicology Program)
Potentially hazardous food
Potters for Peace
Powell, C. A.
Power
Powers, J. H.
Powles, J. W.
Prashad, L.
Prater, M. R.
Prati, G.
Pratt, M.
Precautionary principle
Precipitation
Precision
Predation
1795
Predators
Premkumar, P.
Prentice, A. M.
Preparedness
Prerequisite programs (PRPs)
Presidential/Congressional Commission on Risk Assessment and Risk Management (1997)
Pressures
Preston, A. J.
Preston, D. L.
Preston-Martin, S.
Pretty, J.
Preusser, D. F.
Prevalence studies. See also Cross-sectional studies
Prevention; primary; secondary; tertiary
Prevention hierarchy
Price, L. B.
Priess, J. A.
Primary energy sources
Primary pollutant
Primary prevention
Priming, of immune system
Princeton Environmental Institute, Carbon Migration Initiative
Principles of Environmental Justice (ejnet.org)
Pringle, C. M.
Proctor, M. E.
Pro-environment
Professionalism; characteristics of ethical (text box 10.3); and common resources; and environmental justice; and global
1796
ecosystem; and global health ethics; and nondisclosure versus right to know; people and cultures in; and public regulation of behavior versus individual freedom; and scientific research and public health advocacy; and time frame of environmental health; and typical elements in professional code of ethics (10.4)
Profile of Mood States (POMS) inventory
Progression stage
Promoter (5'-flanking region)
Promotion stage
Prospective studies
Protective devices
Proteome
Proteomics
Protocol for Assessing Community Excellence in Environmental Health (PACE-EH)
Protons
Proxemics
Proximity, geographic
Pruitt Igoe public housing complex (St. Louis, Missouri)
Prüss, A.
Prüss-Ustün, A.
Pruzzo, C.
Phthalates
Public health: essential services of; functions; policy, from regulatory toxiology to; preparedness E's of; surveillance
Public Health Act of 1848 (U.K.)
Public Health Leadership Society
Public Health Service
Pucher, J.
Pugliese, A.
1797
Pulido, L.
PulseNet
Punareewattana, K.
Population Bomb (Ehrlich)
Purcell, A. T.
Pure Energies
Pure Food and Drug Act
Purkiss, J. A.
Puska, P.
Puskin, J. S.
Putnam, R. D.
$p$-value
Pyle, B. H.
Pyle, J. A.
Pynoos, J.
Pyrene (PAH)
Pyrethroid
1798
Q Qadri, A.
Quan, X.
Quansah, R.
Quick, R.
Quimio, W.
Quinn, J.
Qureshi, A. I.
Qureshi, I.
1799
R R Core Team
Raabe, G. K.
Raaen, L.
Rabinowitz, P. M.
Rachman, S.
Radford, E. P., Jr.
Radiation: acute effects of; and assessing radiation risks; carcinogenic effects of; cellular and biological effects of ionizing; cosmic; disasters; effects on developing embryo; genetic effects of; infrared; internal; ionizing; key concepts regarding; from medical procedures performed in U.S.; in medicine; and nonionizing radiation; protection and prevention; protection from; and radiation-related accidents; radio and microwave; and radioactivity in consumer products and food sources; and radon; somatic effects of; and sources of ionizing radiation exposure; terrestrial; types and mechanisms of injury from; ultraviolet; and visible light
Radiative forcing
Radioactive waste
Radioactivity; nuclear transformation mechanisms that release
Radionuclides
Radisch, J.
Radon
Radon Exposure Compensation Act
Raeburn, J.
Rafaj, P.
Rahim, B.
Rahman, F.
Rahman, O.
1800
Rahman, T.
Rail to trail conversion
Rajagopalan, S.
Rajktia, Y.
Rakitsky, V.
Rallison, M. L.
Ram, P. K.
Ramasundarahettige, C.
Ramaswamy, V.
Ramesh Babu, B.
Ramos, F.
Ramos, M.
Ramos, P.
Ramsay, T.
Ramsey, J. M.
Rana Plaza factory collapse (Bangladesh)
Randa, M. A.
Randall, W.
Randers, J.
Randerson, J. T.
Randomized clinical trials
Raper, S.C.B.
Raphael, B.
Rapp, R.r
Rashid, M.
Raskowski, R.
Rate
Rate ratio
1801
Ratick, S.
Raw utility
Ray, H.
Ray, I.
Ray, J.
Raymond, M.
Raymond-Whish, S.
Rayner, G.
Razzak, J. A.
Rea, W. J.
REACH (Registration, Evaluation, Authorization and Restrictions of Chemicals)
Reacher, M. H.
Reagan, Ronald
Real Food Challenge
Reality mining
Reay, D. T.
Recall bias
Receptor
Rechman, J.W.T.M.
Reciprocity
Recognition. See under Industrial hygiene
Recognition and Management of Pesticide Poisonings (U.S. EPA)
Recovery
Recreational activity
Red Book
Red List
Red List scheme (IUCN)
1802
Red tide. See Harmful algal blooms (HAB)
Reddish-Douglas, M.
Redford, K. H.
Redlich, C. A.
Redmond, K.
Reduce, reuse, and recycle
Reduction
Redus, J.
Reed, M. S.
Reed, R.
Rees, G.
Rees, W.
Rees, W. E.
Reeves, S. T.
Reference dose (RfD)
Registration (pesticides)
Rego, R. F.
Regression analysis
Regulatory toxicology
Rehm, J.
Reid, C.
Reifels, L.
Reinschmidt, A.
Reisen, W. K.
Reiter, P.
Relative biological effectiveness (RBE)
Relative risk
Religious ethics
1803
REN21 (Renewable Energy Policy Network for the 21st Century)
Renewable energy sources
Renn, O.
Rennie, A.
Renton, A.
Report of the Royal Sanitary Commission (1871)
Residential exposure
Residual risks
Resilience Alliance
Resilience; and four elements of, framework; sustainability and
Resilient city
Resource Conservation and Recovery Act (RCRA; 1976)
Resource wars
Respiratory system
Responsibility
Restoration ecology
Restorative design
Restricted use
Retrospective studies
Reuter, R.
Revell, G.R.B.
"Review of Airborne Polycyclic Aromatic Hydrocarbons (PAHs) and Their Human Health Effects" (Environmental International)
Review of the EPA's Integrated Risk Information System (IRIS) Process (NRC)
Rey, M. J.
Rhind, D. W.
Rhodes, J. D.
1804
Ribonucleic acid (RNA)
Rice, J.
Richard, A. M.
Richardson, D. B.
Richardson, E. A.
Richardson, K.
Richardson, L. E.
Richardson, M. J.
Ricketts, T. H.
Ricklin, A.
Rickwood, D.
Ridley, C. E.
Ridley, G. F.
Ridley, I.
Ries, N.
Riggs, D. P.
Right to know
Riley, D. G.
Ringquist, E. J.
Rio Declaration on Environment and Development (United Nations Conference on Environment and Development
Riojas-Rodríguez, H.
Rip, M. R.
Risk; acceptance; avoidance; management (RM); perception; factors important in; reduction; retention; transfer
Risk assessment (RA): definition of; and dose-response assessment; in environmental health; epidemiology and; and exposure assessment; future of; and hazard identification; history of; key concepts in; and multitude of factors affecting risk of disease; problem formulation in; process of using, to
1805
protect public health; and risk characterization; and risk management and communication; technical terminology in; timeline of milestones in history of
Risk Assessment in the Federal Government (National Academy of Sciences)
Risk communication; challenges to; and communicating during and after major environmental disaster; effective; and elements of comprehensive risk and crisis communication plan; mental noise model of; models of; objectives of; overcoming psychological, cultural, and sociological barriers to; and questions frequently asked during an emergency or crisis; and risk perception; and social amplification of risk framework; trust determination model of; as two-way process
Risk-risk trade-off
Ritchie, J.
Rittel, H.W.J.
Rivara, F. P.
Rive, S.
RNA (ribonucleic acid)
Road rage
Robbins, J.
Robbins, J. A.
Robert Taylor Homes (Chicago)
Roberts, D. R.
Roberts, I.
Roberts, J. A.
Roberts, L.
Roberts, N. J., Jr.
Roberts, S.
Roberts, S. L.
Robertson, G. P.
1806
Robertson, J. L.
Robertson, R. D.
Robertson, W. J.
Robine, J.-M.
Robinson, A. E.
Robinson, D.
Robinson-O'Brien, R.
Robock, A.
Robson, M. G.
Rock, M.
Rockefeller Foundation-Lancet Commission on Planetary Health
Rocklov, J.
Rockström, J.
Rodenbeck, S. E.
Rodó, X.
Rodricks, J.
Roe, J.
Roebroeks, W.
Roebuck, B. D.
Rogalsky, D. K.
Rogan, W. J.
Rogers, C.
Rogers, J. V.
Rogers, J. W.
Rogers, S.
Roghmann, K. J.
Roisman, R.
Roll Back Malaria
1807
Rollings, K. A.
Rollings, L.
Rollins, G.
Rom, W.
Romanenko, A. Y.
Romano, E.
Romanov, S. A.
Romieu, I.
Ron, E.
Ronis, D. L.
Rooney, D. M.
Roosevelt, F. D.
Root, G. P.
Rosa, R.
Rosas, L. G.
Rose, J.
Rose, J. B.
Rose, S. K.
Rosegrant, M. W.
Rose-Jacobs, B.
Rosen, G.
Rosenberg, C.
Rosenberg, D. M.
Rosenberg, J.
Rosenberg, M.
Rosenberg, R.
Rosenfeld, L. C.
Rosenthal, D. G.
1808
Rosenthal, E.
Rosenthal, S.
Roser-Renouf, C.
Ross, A. Y.
Ross, C. I.
Ross, D.
Roszak, T.
Rothman, K.
Rothman, N.
Rothschild, M.
Rousseau, J. -J.
Roustan, Y.
Routray, P.
Rowe, B.
Rowe, J.
Roy, M.
Roy, S. L.
Royal Commission of Enquiry on the Poor Laws (U.K.)
Royal Society of Canada
R-selected species
Ruano-Ravina, A.
Rubber Manufacturers Association
Rubenstein, L. Z.
Rubin, C. H.
Rubin, H. R.
Rubin, I. L.
Rubin, J.
Rubio, M. A.
1809
Ruckelshaus, M.
Rudd, R. A.
Rudel, R. A.
Rudich, Y.
Rudnai, P.
Rudolph, L.
Ruiz-Mercado, I.
Rule by the Land Management Bureau
Rundle, A.
Rundle, R. L.
Runge, C. F.
Runnels, V.
Running, S. W.
Runyan, C. W.
Rupp, G.
Rushbrook, P.
Rushforth, N. B.
Rusk Institute of Rehabilitation Medicine
Russell, J.
Russell, K. C.
Russo, E.
Russo, J. E.
Ryan, J. J.
Ryan, N.
Ryan, P. B.
Ryan, R. L.
Rydin, Y.
Ryherd, E.
1810
S Saadat, S.
Saari, D.
Saatkamp, B. D.
Sabaté, J.
Saberi, P.
Sachs, N. A.
Sacks, O.
Sadd, J.
Sadetski, S.
Sadman, R.
Sadowski, L. S.
Saegerman, C.
Saegert, S. C.
Saelens, B. E.
Safe Drinking Water Act (SDWA; EPA)
Safe to Sleep campaign
Safety and health management system
Safety engineering
Safety hazards
Saha, R.
Saha, S.
Sahn, J.
Saint-Charles, J.
Salamanca, F.
Sallis, J. F.
Salmon, J.
1811
Salmon, R.
Salt, D.
Saltzman, H.
Salutogenesis
Samanta, G.
Samaras, C.
Samenow, J.
Samet, J. M.
Samia, N. I.
Sample collection instruments
Sample size
Sampling: active; passive; stratified
Sampson, N. A.
San Francisco earthquake (1906)
Sanbonmatsu, L.
Sanchez, C. E.
Sanchez, L. D.
Sandel, M.
Sanderson, L.
Sanderson, R. A.
Sandifer, P. A.
Sandman, P.
Sandstrom, T.
Sandy Hook Elementary School (Newtown, Connecticut)
Sanitary: issues; landfill; movement
Sanitary Conditions of the Labouring Population (Chadwick)
Sanitary Report (1842; England)
Sanitation; global challenges in; options; water
1812
Sankaranarayanan, K.
Santhanam, A.
Santoro, R.
Sapkota, A. R.
Sapsin, J. W.
Sari Kovats, R.
Sarraf, M.
Sartelet, K. N.
Sasser, H.
Sassidharan, V.
Sathyanarayana, S.
Satin, K. P.
Sato, K.
Sattler, D. N.
Sauby-Secretan, B.
Saunders, L. D.
Saussy, J.
Savenkova, M. I.
Savitz, D. A.
Scale; importance of
Scallan, E.
Scammell, M. K.
Scarpino, S. V.
Schaefer, F. W.rd
Schaefer, L.
Schaldach, R.
Schamberg, M. A.
Scharber, H.
1813
Schaudies, R. P.
Schaum, J. L.
Schaupp, C. M.
Schechter, C. B.
Schein, A.
Scheinman, S.
Schellevis, F. G.
Schelling, E.
Scherb, A.
Scherer, E.
Schets, F. M.
Schieber, R. A.
Schiff, C.
Schijven, J. F.
Schilling, J.
Schindler, D. W.
Schipper, E. L.
Schivelbusch, W.
Schivley, G.
Schlesinger, W. H.
Schlosberg, D.
Schlosser, W.
Schlueter, S.
Schlundt, J.
Schlünssen, V.
Schmidt, C. W.
Schmiedel, S.
Schneider, M.
1814
Schoendorf, K. C.
School cafeteria: examples of convenience, attractiveness, and normativeness applied to; as food environment; illustrations of convenience, attractiveness, and normativeness applied to
Schöpp, W.
Schott, J. P.
Schrecker, T.
Schreinemachers, P.
Schrenk, H. H.
Schroeder, H. W.
Schuch, P
Schukoske, J. E.
Schulte, L. A.
Schults, R. A
Schultz, A. J.
Schultz, D.
Schultz, K.
Schulze-Rath, R.
Schurr, S. H.
Schuster, C. J.
Schuurman, N.
Schwab Foundation for Social Entrepreneurship
Schwartz, B. S.
Schwartz, J., r14
Schwartz, J. D.
Schwartz, J. M.
Schwarzkopf, M. D.
Science (journal)
Science and Decisions: Advancing Risk Assessment (Silver
1815
Book)
Scientific American Editors
Scientific integrity
Scoggins, J.
Scollo, M.
Scott, L.
Scott, L. E.
Scottish Health Survey
Scovronick, N.
Scribner, R.
Scudder, T.
Scurfield, R.
Seabury, S. A.
Searchinger, T.
Seasonal affective disorder (SAD)
Secondary energy forms
Secondary pollutant
Secondary prevention
Secondary transmission
Sehgal, A.
Seigneur, C.
Seilo, M. T.
Selanikio, J. D.
Selection bias
Self-organizing (in systems)
Selfridge, G.
Selikoff, Irving
Sellers, M. A.
1816
Sembajwe, G.
Semenza, J. C.
Sen, B.
Senauer, B.
Sensitivity (to chemicals)
Seo, H. B.
Sergiyenko, N. M.
Serpell, J.
Serrano, E.
Seurat, Georges
Sewage, sludge
Sexton, B.
Sexton, K.
Shabedoff, P.
Shadel, B. N.
Shah, I.
Shah, P.
Shahadi, A.
Shaheen, S. A.
Shakhtarin, V. V.
Shakur, H.
Shalauta, N. M.
Shama, L. M.
Shamasunder, B.
Shang, Y.
Shannon, H. S.
Shannon, M.
Shapiro, J.
1817
Shappell, S.
Sharif-Alhoseini, M.
Sharing economy
Sharp, B.
Sharp, D.
Sharp, R. R.
Sharrar, R. G.
Sheehan, J. J.
Sheehan, M. C.
Sheikh, A.
Sheingate, A.
Shekelle, P. G.
Shekhter, I.
Shen, J.
Shepherd, D.
Shepley, M. M.
Sherer, P. M.
Sherman, L. W.
Sherman, S. A.
Sherriff, A.
Shi, Y.
Shibata, Y.
Shibuya, K.
Shields, T. M.
Shiell, A.
Shiff, C.
Shilnikova, N. S.
Shilton, T.
1818
Shin, H. M.
Shiroma, E. J.
Shniderman, C. M.
Shoda, T. M.
Shonkoff, S. B.
Shore, R. E.
Shortt, N. K.
Shoukri, M.
Shrubsole, C.
Shue, H.
Siahpush, M.
Sibly, R. M.
Sicher, R. C.
Sichuan, China, earthquake
Sick building syndrome
Sidel, V. W.
Siegel, J.
Siegel, P.
Sigrist, J. A.
Sigsgaard, T.
Silbergeld, E. K.
Silent Spring (Carson)
Silicon Valley Toxics Coalition
Silva, R. A.
Silver, J. M.
Silver, K.
Silver Book
Silverstein, M.
1819
Silverstein, P.
Silvone, D.
Simmons, R. F.
Simoes, E. J.
Simon, J.
Simon, S. L.
Simons, J.
Simons, L. A.
Simons-Morton, B. G.
Simple
Simpson, C. D.
Simpson, J. A.
Simson, S.
Sin, D. D.
Sinclair, H.
Sinclair, U.
Singer, B. H.
Singer, J.
Singer, J. E.
Singh, A.
Singh, S.
Single nucleotide polymorphism (SNP)
Singleton, G. R.
Sinha, A.
Siriwong, A.
Sirutis, J. J.
Sjöberg, L.
Skinner, M. K.
1820
Skone, T. J.
Skov, S.
Slaney, D.
Slaper, H.
Sleet, D.
Sliney, D. H.
Slizovskiy, I. B.
Slovic, P.
"Slum surgery in St. Louis"
Slusser, W. M.
Smallwood, J.
Smart, R. G.
Smart growth
Smil, V.
Smith, A. G.
Smith, A. M.
Smith, B.
Smith, D.
Smith, G. A.
Smith, G. D.
Smith, J.
Smith, J. N.
Smith, J.D.R.
Smith, K. C.
Smith, K. R.
Smith, L. M.
Smith, M. T.
Smith, Marissa
1821
Smith, R. D.
Smith, S. J.
Smith, T.J.S.
Smith, W. E.
Smith, W. Eugene
Smith, W. R.
Smith, Z. A.
Smog
Smythe, I. D.
Snee, M. P.
Snilstveir, B.
Snmith, B. J.
Snow, J.
Snow, John
SNPs (single nucleotide polymorphisms)
Soares, A.
Sobolewski, J.K
Soccolich, S. A.
Social: amplification and attenuation of risk; capital; comparison; connectedness; determinants of health; justice; marketing
Social Security Disability Insurance program
Social-ecological systems; and social ecological model
Society for Epidemiological Research
Socioeconomic status (SES)
Sociopetal
Socolow, R.
Socrates
Söderqvist, F.
1822
Sodha, S. V.
Sodiofugal
SODIS
Sohel, S. S.
Sohrabi, M.
Solari, C. D.
Solid fuels
Solid waste
Solid Waste Disposal Act (1965)
Solomon, G. M.
Somatic effects
Somerset, S.
Somes, G.
Son, H.
Son, K. C.
Søndergaard, B.
Song, J.
Song, L.
Sorahan, T.
Sorensen, G.
Sorensen, P.
Soret, S.
Sörlin, S.
Soto, D.
Source reduction
Source water
South Pacific Applied Geoscience Commission
Sowden, A. J.
1823
Spak, S. N.
Sparer, J.
Sparrow, S. E.
Spatial: queries; scale; statistics
Spatial analysis; mapping and, of disease risk; mapping and, of exposure; and what makes good maps of good data
Spatial scale
Spear, S.
Spears, E.
Spears, M.
Special waste
Specialty crops
Species; assemblage of; introduced; invasive, and their impact; types of relationships between different
Specific absorption rate (SAR)
Specific activity
Specific prevention
Specker, B.
Speechley, M.
Speewenberg, P.
Speiler, E. A.
Speizer, F. E.
Spence, J. C.
Spence, L.
Spengler, J. D.
Sperry, L.
Spiegel, J.
Spittal, M. J.
Spix, C.
1824
Splice junctions
Splicing
Spot samples
Spreng, D.
Spyker, C. A.
Spyker, D. A.
Squire, O. J.
Srebotnjak, T.
Srinivas, R.
St. Francis Prayer Center (Flint, Michigan)
St. Leger, L.
St. Louis, M. E.
Stabilization wedges
Stadlinger, N.
Stafford, M.
Stahre, M.
Stamatakis, K. A.
Stanley, E.
Stanley, I. H.
Stanley, K. D.
Stanojević, P
Stapleton, D.
Stark, J. H.
State Prison of Southern Michigan
State-Trait Anxiety Inventory
Statistical power
Statistical significance
Statistics
1825
Stavins, R. N.
Stayner, L. T.
Stayton, L. E.
Steege, A. L.
Steele, F.
Steele, Z.
Steenland, K.
Stefanow, W. L.
Steffen, W.
Stein, K.
Steinbrecher, R.
Steinfeld, C.
Steinfeld, E.
Steinmann, P.
Steinsapir, C.
Stemdale, R. C.
Stenseth, N. C.
Stepanenko, V. F.
Stephens, C.
Stephens, D.
Sterling, D. A.
Stern, N.
Stern, N. H.
Stern, P. C.
Sterndale, R. C.
Stevens, W.
Stevenson, K. B.
Stevenson, M.
1826
Stewart, D.
Stillerman, K. P.
Stimpson, J. P.
Stine, N. W.
Stochastic effects
Stockholm Convention on Persistent Organic Pollutants
Stockholm Environment Institute
Stockholm Resilience Centre
Stocks, M. E.
Stoddard, A.
Stoichiometric air requirement
Stone, B.
StormReady program
Storms
Story, M. T.
Stott, R.
Stouffer, R.
Stout, B. M.
Stowe, M. H.
Stowe, R.
Straif, K.
Strand, J.
Stratification
Stratified sampling
Straus, M. C.
Streit, F.
Stress reduction
Strickland, M. J.
1827
Strina, A.
Stringer, R.
Strom, D. J.
Stroppa, G.
Structural collapse
Strunin, L.
Stuer-Lauridsen, F.
Stull, J. W.
Su, H.-J.
Subchronic exposure
Subdivision regulations
Subpopulation
Subramanian, S.
Substitution
Succession, ecological; classical model of, in North American forest ecosystem
Sudarshan, A.
Sugathan, A.
Sugerman, D.
Sugimoto, H.
Sugiyama, T.
Suk, J. E.
Sulfur dioxide (SO2)
Sullivan, R.
Sullivan, W.
Sullivan, W. C.
Sulser, T.
Summers, J. K.
1828
Sumner, S. A.
Sun, L. S.
Sun, Y.
Sun, Z.
Sunday Afternoon on the Island of La Grande Jette (Seurat)
Sundell, J.
Sung, T.-I.
Sunyer, J.
Superfund. See Comprehensive Environmental Response Compensation and Liability Act (CERCLA)
Supplemental Nutrition Assistance Program (SNAP)
Support
Surface water
Surface Water Treatment Rule
Suri, M.
Surprise, in ecological system
Susceptible groups, focus on
Sustainability; development; in health care; historical considerations of; measuring progress toward; metrics; nested model of; new definition of; possibility of achieving; and resilience; and sustainable development; and sustainable human well-being and three-legged stool
Sustainability Accounting Standards Board
Sustainability in all policies (SiAP)
Sustainable cities
Sustainable Cities International
Sustainable Communities Online
Sustainable development
Sustainable Development Goals
Suttorp, M. J.
1829
Sveiby, K.
Sverdlik, A.
Swan, S. H.
Swart, D.
Sweeney, R.
Swetnam, T. W.
Swimming advisories
Swimming water
Swinton, G.
Syal, M.
Sydney Opera House
Symbiosis
Synchronymous cSNP
Synergism
Synonymous cSNP
"Syringe tides"
Systems: boundaries in
Systems map, of U.K. land use and domains that influence it
Systems thinking; linear thinking versus; links between ecology and, as basis for health; and restoration ecology
SzékÁcs, A.
1830
T Tabor, G. M.
Tagtow, A.
Tail risk
Tak, S.
Takano, T.
Takaro, T. K.
Talbott, E. O.
Tallis, H.
Tam, V. W.
Tammelin, T.
Tan, M.
Tang, W. H.
Tanigawa, K.
Tanner, M.
Target organ
Target organ dose
Tarr, J. A.
Tator, C. H.
Tatoute
Tatters, A. O.
Taubert, K. A.
Tauxe, R. V.
Tawn, E. J.
Taylor, A. F.
Taylor, D. A.
Taylor, M. R.
1831
Taylor, R. B.
Taylor, W. W.
Technological hazard
Tehranifar, P.
Teixeira, M. G.
Tempalski, B.
Temporal relationship
Temporary worker
Ten Have, T. R.
Tenenbaum, D. J.
Tenforde, T. S.
Tennessen, C. M.
Teret, S. P.
Terrell, J. D.
Terrestrial radiation
Terret, S. P.
Territoriality
Terschuren, C.
Tertiary prevention
Teutsch, S. M.
Tewy (Central High School)
Texcalac-Sangrador, J. L.
Texting, and driving
Thacker, S. B.
Thackrah, C. T.
Thakur, J. S.
Tharakan, P.
Thatcher, Margaret
1832
The Fiber School
Therrien, R.
Thiry, E.
Thomas, D. R.
Thomas, D.S.K.
Thomas, L.
Thomas, R.
Thomas, R. B.
Thomas, S. A.
Thompson, B.
Thompson, D.
Thompson, D. C.
Thompson, F.
Thompson, H.
Thompson, J. J.
Thompson, J. R.
Thompson, L. M.
Thompson, R. S.
Thompson, W.
Thompson Coon, J.
Thomson, J.
Thoreau, Henry David
Thörn, Å
Thorne, P. S.
Thorns, D. C.
Thoroughman, D. A.
Three Mile Island (1979)
Threlfall, E. J.
1833
Thun, M. J.
Thurston, G. D.
Thymine (T)
Tierney, N.
Tiffany, D.
Till, J. E.
Tilman, D.
Tilman, F.
Tilson, H. H.
Time and temperature controls
Timme, W.
Timmermans, H.
Timperio, A.
Tinch, J.
Tinetti, M. E.
Tinker, T.
Tinsworth, D. K.
Tipping point
Tipraqsa, P.
Tirado, M. C.
Tire reuse and recycling
Tobacco smoke
Tobias, D. A.
Tochner, Z.
Toet, H.
Tohn, E.
Tokyo subway attacks
Tolerances (pesticides)
1834
Toman, M. A.
Tomatis, L.
Tomita-Mitchell, A.
Tompkins, A. M.
Toninelli, G.
Tonn, B.
Tonne, C.
Toohey, A. M.
Toohey, R. E.
Toole, M. J.
Topp, E.
Tornado
Torres-Duran, M.
Tost, H.
Total Coliform Rule
Total exposure
Total suspended particles (TSP)
Tours China
Townsend, M.
Toxic Chemicals in Children's Products Act (Maine)
Toxic Release Inventory (TRI; U.S. EPA)
Toxic Substances Control Act (TSCA)
Toxic Wastes and Race in the United States (United Church of Christ)
Toxicant classifications: and absorption; and chemical carcinogenesis; and distribution; and endocrine disruptors; and excretion; IARC results of, as of March 2015; and metabolism; and phthalates; and polycyclic aromatic hydrocarbons (PAHs); and toxicokinetics
Toxicants
1835
Toxicokinetics; key steps in
Toxicological data
Toxicology; environmental psychology and; and environmental public health; laboratory animals in; microbiome and; from populations to molecules; from regulatory, to public health policy; and testing compounds for toxicity; and toxicant classifications
Toxicology in the 21st Century (Tox21)
Toxics Release Inventory in the United States
Toxins
Traceability
Tracy, M.
Traditional neighborhood development
Tragedy of the Commons (Hardin)
Trailers
Tramontin, M.
Tran, N. L.
Tran, N. T.
Transcription; factors
Transcriptomics
Transformation kinetics
Transgenerational epigenetic inheritance
Transition Network
Transit-oriented development
Translation
Transportation; demand management; disasters; injuries; planning
Transportation Research Board
Transuranic elements
Tranter, D. C.
1836
Trasande, L.
Travasso, M. I.
Travel demand
Traver, R. D.
Tren, R.
Triangle Shirtwaist Company
Trigo, R. M.
Trimble, S.
Tripathi, A.
Tripathi, R. C.
Triplehorn, C. A.
Triploid
Trivedi, K.
Tronko, M.
Trophic levels
Tropospheric ozone
Truant, P.
Trufan, S. J.
Tsai, A. G.
Tsai, P.
Tsai, S. P.
Tsai, T. R.
TSCA. See Toxic Substances Control Act (TSCA)
Tsunami lung
Tsunamis
Tsutani, K.
Tsyb, A. F.
Tudor, T.
1837
Tuleya, R. E.
Tuller, D.
Tumanov, K. A.
Tunnell, W.
Turgeon, A. F.
Turusov, V.
TVA Kingston Fossil Plant (Tennessee)
Tversky, A.
Tyler, E.
Tyne, K.
Tyson, P. D.
1838
U Ubong, I. U.
Uejio, C. K.
U.K. Ministry of Health
Ulmer, R. G.
Ulrich, R.
Ulrich, R. S.
Ulsh, B. A.
Ultrafine PM
Ultraviolet radiation (UVR)
UmeÅ University
Umo-Otong, J. C.
Unbundled parking
Underwriters Laboratories (UL)
Unemployment
UN-HABITAT
Unintentional injuries
Union Carbide Corporation
Unit cancer risk (UCR)
United Farm Workers
United Kingdom Department for International Development
United Nations; Commission on Sustainable Development (CSD); Conference on Environment and Development (UNCED; Earth Summit); Conference on Trade and Development; Department of Economic and Social Affairs (Population Division); Department of Health and Human Services; Development Programme (UNDP); Environment Programme (UNEP); Food and Agriculture Organization (FAO); Framework Convention on Climate Change (UNFCCC); Framework on
1839
Climate Change (UNFCC); High Commissioner for Refugees; Intergovernmental Panel on Climate Change (IPCC); Millennial Summit (2000); Office for Disaster Risk Reduction; Scientific Committee on the Effects of Atomic Radiation (UNSCEAR); Summit on Sustainable Development (Johannesburg); Universal Declaration of Human Rights; Water for Life Web page; World Commission on Environment and Development
Universal design
University of Auckland
University of Chicago
University of Illinois Landscape and Human Health Laboratory
University of Louvain
UNU-IHDP
Updated Review of Literature and Data on Bisphenol A (Food and Drug Administration)
Upstream effects
Upton, A. C.
Uracil
Urama, K.
Urban evolution, and characteristic environmental conditions and health issues
Urban health
Urban heat island
Urban planning
Urban Relief
Urban sprawl; and automobile-oriented transportation system; comparison of, and smart growth; consumption and; and disinvestment in central cities; and dispersion of activity centers; and low-density development; and policies that regulate land use; and separation of land uses through zoning
Urbanism
Urbanization; versus urbanism
1840
Ursano, R. J.
U.S. Affordable Care Act
U.S. Agency for Toxic Substances and Disease Registry
U.S. Burden of Disease Collaborators
U.S. Bureau of Labor Statistics (BLS)
U.S. Bureau of Mines
U.S. Census Bureau
U.S. Civil Rights Act (1964), Title VI
U.S. Consumer Product Safety Commission, National Electronic Injury Surveillance System
U.S. Department of Agriculture (USDA)
U.S. Department of Defense
U.S. Department of Education
U.S. Department of Energy
U.S. Department of Health, Education, and Welfare
U.S. Department of Health and Human Services
U.S. Department of Housing and Urban Development
U.S. Department of Labor
U.S. Department of the Interior, Bureau of Safety and Environmental Enforcement
U.S Environmental Policy
U.S. Environmental Protection Agency (EPA); Air Quality Index; CARE (Community Action for a Renewed Environment) program
U.S. Federal Emergency Management Agency (FEMA)
U.S. Fire Administration
U.S. Food and Drug Administration (FDA)
U.S. General Accounting Office (GAO)
U.S. Geological Survey (USGS)
1841
U.S. Government Accountability Office (GAO)
U.S. Green Building Council
U.S. Institute of Medicine (IOM)
U.S. National Academy of Sciences (NAS); Red Book (1983); Silver Book
U.S. National Climate Assessment
U.S. National Research Council, Policy Division, Board on Sustainable Development
U.S. Occupational Safety and Health Administration (OSHA)
U.S. Poison Control Centers
U.S. Public Health Service
U.S.-China Joint Announcement on Climate Change and Clean Energy Cooperation
USGS. See U.S. Geological Survey
Usui, Y.
Utilitarian activity
Utilitarianism
Utzinger, J.
Uvnäs-Moberg, K.
1842
V Vacca, Charles
Vaccari, M.
Valdez, J.
Valente, T.
Valero, R.
Validity (internal)
Vallarino, J.
van Beek, L.P.H.
van Dam, R. M.
van den Berg, H.
van der Hoek, W.
Van Der Kraak, G.
van der Merwe, A. E.
van der Vliet, J. C.
van Dijk, A.
van Dillen, S.
Van Dorn, J.
Van Duijnhoven, Y.
van Erp, J. B.
van Kempen, C. M.
van Lith, H. A.
Van Orden, K. A.
Van Oyen, H.
van Panhuis, W.
Van Sickle, D., r6
van Veldhoven, K.
1843
van Vuuren, D. P.
van Winsum-Westra, M.
Van Wyk, B.-E.
Vanderford, M.
VanderWeele, T. J.
VanEenwyk, J.
Vanwey, I.
Vargo, J.
Vassilenko, E. K.
Vaughan, S.
Vavrus, S. J.
Vecchi, G. A.
Vehicle miles traveled (VMT)
Veitch, J.
Vengosh, A.
Venkatesh, A. K.
Ventilation
Ventrice, D.
Ventrice, P.
Verderber, S.
Veress, K.
Verger, P.J.P
Verheij, R. A.
Verhoef, L.
Vermeulen, S. J.
Vernick, J. S.
Verutes, G.
Vestergaard
1844
Veterans Benefits Administration
Vezzulli, I.
Vidal, J. E.
Video exposure monitoring (VEM)
Viel, J.
Viera, A. R.
Viet, S. M.
Viggers, H.
Vijayakumar, I.
Vilenchik, M. M.
Viljugrein, H.
Villa, P.
Village of Euclid v. Ambler Realty
Villegas, E. N.
Vimont, D. J.
Vinck, P.
Vinclozolin
Vindigni, S.
Vindigni, S. M.
Vineis, P.
Vinten-Johansen, P.
Violence, typology of
Virden, R. J.
Virtanen, M.
Vitalone, A.
Vitte, P. M.
Vittori, G.
Vizcaya, D.
1845
Vlahov, D.
Voaklander, D.
Vogel, S. A.
Volatile organic compounds (VOCs)
Vollman, D.
Volz, K. A.
von Braun, J.
Vos, T.
Voss, T.
Vrieling, H.
Vrijheid, M.
Vucetich, J. A.
Vulnerability; windows of
Vulnerability assessment
Vulnerable populations
Vulnerable workers
1846
W Wachholz, B. W.
Wackernagel, M.
Wada, Y.
Waddington, H.
Wadman, M. C.
Wagner, G. R.
Wagner, J. E.
Wagner, R. W.
Wahlberg, A.A.F.
Währborg, P.
Waichman, A. V.
Wakefield, J.
Wakefield, M. A.
Wakefield, R.
Wakeford, R.
Waldock, J.
Waliczek, T. M.
Walk Score (Website)
Walker, B.
Walker, C. H.
Walker, G. J.
Walker, J.
Walker, P.
Walker, R. E.
Walkerton, Ontario, outbreak of E. coli
Walk-friendly and bike-friendly community certification
1847
programs
Walking for Health programs (England)
Walk-through
Wall, S.
Waller, A. E.
Waller, L. A.
Wallinga, D. B.
Wallington, T. J.
Walls, H. L.
Walsh, K. A.
Walsh, L. E.
Walter, S. R.
Waltner-Toews, D.
Walton, H. A.
Wander, M.
Wander, M. M.
Wang, J.
Wang, M.
Wang, M. Q.
Wang, X.
Wang, Y.
Wang, Z.
Wansink, B.
Warber, S. I.
Ward, D. S.
Ward, W.
Ward Thompson, C.
Warda, L. J.
1848
Ware, J. H.
Warm, D.
Warner, K.
Warner, M.
Warner, N. R.
Warr, B. S.
Warren, J.
Warren, S.
Warren County, North Carolina
Warsco, K.
Wartenberg, D.
Wasak, S.
Washington, S.
Wasson, R. J.
Waste: and asbestos; challenge of medical; and construction debris; and deep well injection; electronic (e-Waste); and glass and paper recycling in industrial nations; hazardous; health concerns regarding; and incineration; international trafficking in hazardous; key concepts in; medical; mining; municipal solid; primary prevention of; and sanitary landfill; solid; solid and hazardous; special; treatment and disposal; U.S. solid and hazardous waste laws and policy
Waste management
Wastewater reuse
Wastewater treatment
Watanabe, M.
Water; agriculture and scarcity of; and anthropogenic chemical contaminants; and antibiotic resistance; and chemical contaminants; classes of chemical contaminants in; climate change and; emerging issue; and examples of large-scale human impacts on aquatic systems; and health; and hot spots of current and/or potential water conflicts; and human impacts on aquatic
1849
systems; and hydrological cycle; key concepts in; as nutrient; pathogens in or related to water; political implications of; population and scarcity of; and risk characterization for water contaminants; role of; and routes of exposure; safe drinking; and source protection; and surface and groundwater; use and scarcity
Water conflicts, hot spots
Water distribution
Water scarcity; population and
Water stress
Water treatment
Waterborne disease: global burden of; outbreaks
WATERisLIFE
Watershed protection
Watkinson, R.
Watson, D. J.
Watson, J.
Watt, G.
Watts, C. M.
Wavelength
Wayfinding
Wayland, M. S.
Weather extremes: and climate-related disasters; and heat waves
Weathers, M.
Weaver, M.
Weaver, S. C.
Webb, J.
Webber, M. M.
Weber, C. L.
1850
Weber, E. U.
Weber, J.-P.
Weber, M. W.
Webster, R.
Webster, T. F.
Weed, D. L.
Wegman, D. H.
Weight of evidence analysis
Weinhold, B.
Weinstein, P.
Weisaeth, L.
Weiss, C. C.
Weiss, H. B.
Weiss, W.
Weissbrodt, D. G.
Weissman, D. N.
Weitzman, M.
Welch, D.
Welfare
Wells, H. F.
Wells, N. M.
Wells,N. M.
Wenck, M. A.
Wendel, A. M.
Wendling, C.
Wendt, J. K.
Wendy, B.
Wener, R. E.
1851
Wentz, D.
Wentz, M.
Wentz, R.
Werbel, R. E.
Werner, C. M.
Wernham, A.
Wertelecki, W.
Wesoloski, J.
Wessely, S.
Wesson, D. E.
West, J. J.
Westerling, A.
Western Case Reserve University
Western Sustainability and Pollution Prevention Network
Weston, B. H.
Wexler, H.
Weyer, P.
Whalon, M. E.
Whear, R.
Wheeler, B. W.
Wheeler, T.
Wheeler, W.
Whipple, S. S.
Whisnant, M. D.
Whitacre, P. T.
White, A.
White, K. S.
White, M. P.
1852
Whiteford, H. A.
Whitehead, M.
Whitelegg, J.
Whiteson, J.
Whitmarsh, I.
Whitmore, R. W.
WHO. See World Health Organization
Wichman, M.
Wichrowski, M.
Wickerson, F.
Wickliffe, J.
Widdowson, M. A.
Wiedinmyer, C.
Wielinga, P. R
WikiMedia Commons
Wilbanks, T. J.
Wilcox, B. A.
Wild, C. P.
Wilderness rapture
Wilderness therapy
Wildfires
Wildgen, J.
Wiley, L. F.
Wilhelm, J. L.
Wilhelm, M.
Wilhelm, W. W.
Wilkinson, P.
Wilkinson, R. G.
1853
Willand, N.
Willer, R.
Williams, A. F.
Williams, D. R.
Williams, E. S.
Williams, F. L.
Williams, I. T.
Williams, P. L.
Williamson, D. F.
Williamson, S.
Willits, F. K.
Wilson, E. O.
Wilson, F. A.
Wilson, G.
Wilson, J.
Wilson, J. Q.
Wilson, J. S.
Wilson, N.
Wilson, R.
Wilson, S.
Wilson, S. J.
Wilson, W. J.
Wines, M.
Wing, S.
Wingender, J.
Wingfield, S.
Wink, M.
Winquist, A.
1854
Winter, D.
Winter, N. L.
Winter, T. C.
Wiseman, J.
Wisman, J. D.
Witsaman, R.
Wogan, G. N.
Wojcik, A.
Wojtecki, J.
Wolch, J.
Wolch, J. R.
Wolf, J.
Wolf, M.
Wolff, G. L.
Wollard, R. F.
Wolterstorff, C.
Wong, O.
Wong, T.
Woo, M.
Wood, J.
Wood, L.
Wood, S. A.
Woodcock, J.
Woodruff, R. E.
Woodruff, T. J.
Woods, J. S.
Woodward, A.
Woodward, A. R.
1855
Woodyard, C.
Woolfenden, S.
Worgul, B. V.
Work health: and control of chemical hazards; and core elements of all safety and health management; and cost of work injuries; and fixing the work place; and globalization; and government role in protecting workers; and health care facilities; and interaction of work and health; key concepts in; and protecting safety and health on job; and safety and health management systems; and safety and health standards; and sustainability; and vulnerable workers
Worker Protection Standard (WPS)
Workers' Compensation; and system limitations; and who pays for work-related injuries and illnesses?
Workers' Family Protection Act (1992)
World Bank
World Commission on Dams
World Commission on Environment and Development
World Commission on Health and the Environment (WHO)
World Disasters Report (IFRC)
World Economic Forum
World Health Organization (WHO); International Programme on Chemical Safety (IPCS)
World Meteoroligical Organization (WMO)
World population, urban and rural
World Report on Violence and Health (Krug, Dahlberg, Mercy, Zwi, and Lozano)
World Trade Center; Worker and Volunteer Medical Screening Program
World War II
Worldwatch Institute
1856
"Worldwide Pandemic of Asbestos-Related Diseases" (Annual Review of Public Health)
Wrangham, R.
Wright, B.
Wright, K. E.
Wright, R.
Wrigley, N.
Wu, F.
Wu, K.-C.
Wu, L.
Wu, X. H.
Wyn-Jones, A.
Wynn, P. M.
Wynne, B.
1857
X X ray
Xcel Energy
Xenobiotic
Xenoestrogens
Xi, J.
Xi Jinping, Chinese President
Xia, T.
Xiang, S.
Xie, L.
Xinhua News Agency
Xu, J.
Xu, S.
Xu, Z.
1858
Y Yadav, R. S.
Yaffee, A. Q.
Yale, S. H.
Yam, J. C.
Yamada, M.
Yamagata, Z.
Yamanishi, S.
Yamashita, E.
Yamashita, S.
Yan, B.
Yang, M.
Yang, Y.
Yang, Z.
Yao, X.
Yap, W.
Yarden, O.
Ye, Y.
Yeh, S.
Yelverton, T.
Yen, I. H.
Yip, P.S.F.
Yokelson, R. J.
Yoo, M. H.
Yoshizumi, T. T.
Yost, M. G.
You, M.
1859
You, Y.
Youk, A. O.
Young, B.
Youngblood, C.
Younger, M.
Yu, I. T.
Yu, T.-H.
Yuan, W.
Yudelson, J.
Yuen, B.
Yunus, M.
1860
Z Zablotska, L. B.
Zaharna, M.
Zaim, M.
Zajicek, J. M.
Zaloshnja, E.
Zamora, H.
Zani, C.
Zanobetti, A.
Zarychanski, R.
Zaval, I.
Zborowski, J. V.
Zegeer, C. V.
Zeger, S. L.
Zeitlin, C.
Zelikoff, J. T.
Zeller, T.
Zelson, M.
Zghondi, R.
Zhang, H.
Zhang, J.
Zhang, L
Zhang, Y.
Zhang, Z.
Zhao, L.
Zhao, M.
Zhao, P.
1861
Zhao, Y.
Zhong, L.
Zhong, W. Y.
Zhou, H.
Zhou, J. Y.
Zhou, X. N.
Zhou, Y.
Zhou, Z.
Zhu, H. M.
Zhu, T.
Zhu, X.
Zielske, S. P.
Zimmerman, B.
Zimring, C.
Zinsser, H.
Zinstag, J.
Ziska, L. H.
Zock, J. P.
Zoning codes
Zota, A. R.
Zubrod, C. G.
Zuk, M.
Zvonova, I.
Zwi, A. B.
1862
WILEY END USER LICENSE AGREEMENT Go to www.wiley.com/go/eula to access Wiley's ebook EULA.
1863
Table of Contents
Title Page 27 Copyright 28 Dedication 30 Tables, Figures, Text Boxes, and Tox Boxes 31 The Editor 47 The Contributors 49 Acknowledgments 60 Potential Conflicts of Interest in Environmental Health: From Global to Local 63
References 67 Part 1: Methods and Paradigms 71
Chapter 1: Introduction to Environmental Health 72 What Is Environmental Health? 76 The Evolution of Environmental Health 78 Spatial Scales, from Global to Local 98 The Forces that Drive Environmental Health 100 Key Terms 108 Discussion Questions 110 References 111 For Further Information 118
Chapter 2: Ecology and Ecosystems as Foundational for Health 120 Environment as Ecology: Ecology as the Study of Our Home 123
Population Ecology 128 Community Ecology 139 Ecosystem Ecology 142 Systems Thinking: From Ecology to Human Health 148 Features of Our Home: Ecological Characteristics as Foundational for Health 154
Toward Ecological Approaches to Health and Home 160
1864
Summary 163 Key Terms 164 Discussion Questions 172 References 176 For Further Information 179
Chapter 3: Sustainability and Health 182 Historical Considerations of Sustainability 187 Sustainable Human Well-Being and the Three-Legged Stool 192 Drivers of Nonsustainability, Limits to Growth, and Collapse 195
What Should Concern Us More: Population Growth Or Consumerism? 197
Limits to Growth 199 Human Societal Collapse? Prevention Through Systems Thinking and Early Action 203
The Importance of Scale 206 The Way Forward 207 Summary 215 Key Terms 216 Discussion Questions 220 References 221 For Further Information 228
Chapter 4: Environmental and Occupational Epidemiology 230 A Primer on Epidemiology 232 Environmental and Occupational Epidemiology 248 Epidemiology and Risk Assessment 260 Future Directions 263 Summary 266 Key Terms 267 Discussion Questions 275 References 277 For Further Information 280
Chapter 5: Geospatial Data for Environmental Health 282 Components of Georeferenced Data 286 Basic GIS Operations 287
1865
Mapping and Spatial Analysis of Exposure 291 Mapping and Spatial Analysis of Disease Risk 293 What Makes Good Maps of Good Data? 295 What Can We Do with GIS? 297 Are There Any Limitations? 302 Summary 304 Key Terms 305 Discussion Questions 307 References 308 For Further Information 310
Chapter 6: Toxicology 311 Introduction to Toxicology 313 Toxicology and Environmental Public Health 324 Toxicant Classifications 327 Testing Compounds for Toxicity 352 From Regulatory Toxicology to Public Health Policy 356 Summary 360 Key Terms 361 Discussion Questions 366 References 367 For Further Information 369
Chapter 7: Genes, Genomics, and Environmental Health 370 Fundamental Concepts of Genetics and Genomics 373 Approaches for Identifying Gene-Environment Interactions 389 Examples of Gene-Environment Interactions in the Real World 392
Summary 405 Key Terms 406 Discussion Questions 415 References 416 For Further Information 418
Chapter 8: Exposure Science, Industrial Hygiene, and Exposure Assessment 419
Anticipation, Recognition, Evaluation, and Control 422
1866
Exposure Science 433 Summary 448 Key Terms 449 Discussion Questions 456 References 457 For Further Information 459
Chapter 9: Environmental Psychology 462 Environmental Psychology and Toxicology 465 Environmental Psychology Processes 471 So What? Interventions That Work 494 Summary 499 Key Terms 500 Discussion Questions 503 References 504 For Further Information 511
Chapter 10: Environmental Health Ethics 513 Defining Ethics and Morals 515 The Modern Philosophical Background 517 Professionalism 524 Expanding Horizons and Challenges 529 Implications for Professional Ethics 536 Concluding Discussion 541 Summary 542 Key Terms 543 Discussion Questions 546 References 549 For Further Information 553
Chapter 11: Environmental Justice and Vulnerable Populations 554 The Roots of Environmental Justice 558 Elements of Environmental Justice 561 From Research to Action on Environmental Justice 567 Social Inequality and Environmental Quality 581 Summary 584 Key Terms 586
1867
Discussion Questions 588 References 589 For Further Information 598
Part 2: Environmental Health on the Global Scale 600 Chapter 12: Climate Change and Human Health 601
Greenhouse Gases 604 A Warming Earth: From Past to Future 607 Earth System Changes 608 Food and Malnutrition 613 Weather Extremes and Disasters 615 Air Pollution 621 Infectious Diseases 624 Mental Health Effects 635 The Public Health Response to Climate Change 638 Climate Change as a Public Issue 647 Summary 654 Key Terms 655 Discussion Questions 659 References 660 For Further Information 681
Part 3: Environmental Health on the Regional Scale 684 Chapter 13: Air Pollution 685
History of Air Pollution 688 Types of Ambient Air Pollution 693 Studies of Air Pollution and Health 701 Sources and Effects of Outdoor Pollutants 703 Air Pollution Prevention and Control 721 Larger Effects of Regional Air Pollution 724 Summary 725 Key Terms 726 Discussion Questions 729 References 730 For Further Information 735
Chapter 14: Energy and Human Health 736
1868
Household Energy 746 Fossil Fuels 750 Nuclear Energy 761 Renewable Sources of Energy 766 Energy Conservation and Efficiency 774 Summary 778 Key Terms 780 Discussion Questions 783 References 784 For Further Information 806
Chapter 15: Healthy Communities 807 The History of Cities 810 Poverty and Industrialization in Cities 815 The Modern Metropolis: Consumption and Urban Sprawl 818 Community Design and Health 825 Cities as Healthy Human Habitats 842 Summary 854 Key Terms 855 Discussion Questions 861 References 862 For Further Information 874
Chapter 16: Water and Health 877 The Role of Water in Life 879 Regulatory Framework 929 Risk Characterization for Water Contaminants 933 Emerging Issues 934 Summary 936 Key Terms 937 Discussion Questions 943 References 945 For Further Information 953
Part 4: Environmental Health on the Local Scale 956 Chapter 17: Solid and Hazardous Waste 957
Solid Waste 960
1869
Solid Waste Management Strategies 974 Primary Prevention of Waste 975 Waste Treatment and Disposal 978 Health Concerns 987 Summary 993 Key Terms 994 Discussion Questions 996 References 997 For Further Information 1002
Chapter 18: Pest Control and Pesticides 1005 Insect Pests 1011 Vertebrate Pests 1017 Pesticides 1018 Integrated Pest Management 1040 Summary 1046 Key Terms 1047 Discussion Questions 1050 References 1051 For Further Information 1057
Chapter 19: Food Systems, the Environment, and Public Health 1059 What Is the Food System? 1062 Food Production: Industrial Agriculture 1064 Industrial Food Animal Production 1071 Sustainable Agriculture 1077 Food Consumption and Food Environments 1082 Food Safety and Environmental Health: A Systems Perspective 1086
Making Change: Food System Policy 1107 Summary 1111 Key Terms 1112 Discussion Questions 1118 References 1119 For Further Information 1131
Chapter 20: Buildings and Health 1136
1870
The Range of Buildings 1139 Key Elements of a Healthy Building 1156 Toward Safe, Healthy Buildings 1188 Architecture, Environment, and Human Health 1192 Summary 1195 Key Terms 1196 Discussion Questions 1199 References 1200 For Further Information 1217
Chapter 21: Work, Health, and Well-Being 1221 The Interaction of Work and Health 1224 Protecting Safety and Health on the Job 1233 Workers' Compensation 1247 Sustainability 1251 Globalization 1253 Summary 1255 Key Terms 1256 Discussion Questions 1259 References 1260 For Further Information 1264
Chapter 22: Radiation 1266 Nonionizing Radiations 1271 Ionizing Radiation: The Basics 1280 Sources of Ionizing Radiation Exposure 1285 Cellular and Biological Effects of Ionizing Radiation 1295 Human Health Effects of Ionizing Radiation 1299 Radiation Protection 1305 Assessing Radiation Risks 1307 Summary 1309 Key Terms 1311 Discussion Questions 1316 References 1317 For Further Information 1326
Chapter 23: Injuries 1328
1871
Injury Prevention and Control 1332 Policy for Injury Prevention and Control 1355 Injury Prevention in Practice 1359 Injury Control in Special Settings 1367 Summary 1373 Key Terms 1374 Discussion Questions 1376 References 1378 For Further Information 1390
Chapter 24: Environmental Disasters 1393 Scope of the Problem 1398 The Public Health Consequences of Environmental Disasters 1400
Disaster Risk and Its Determinants 1411 Managing Disaster Risk 1413 Summary 1426 Key Terms 1427 Discussion Questions 1433 References 1434 For Further Information 1440
Chapter 25: Nature Contact 1444 The Links Between Nature and Human Health 1446 Domains of Nature Contact 1456 The Greening of Environmental Health 1478 Summary 1484 Key Terms 1485 Discussion Questions 1486 References 1487 For Further Information 1504
PART 5: The Practice of Environmental Health 1507 Chapter 26: Environmental Public Health: From Theory to Practice 1508
Concepts of Environmental Health Prevention 1513 Principles of Prevention in Environmental Public Health 1517
1872
Core Functions of Environmental Public Health 1520 Environmental Public Health Systems 1531 Summary 1537 Key Terms 1538 Discussion Questions 1544 References 1545 For Further Information 1547
Chapter 27: Risk Assessment in Environmental Health 1550 History 1554 Risk Assessment 1558 Risk Management and Communication 1577 Summary 1582 Key Terms 1584 Discussion Questions 1586 References 1588 For Further Information 1591
Chapter 28: Communicating Environmental Health 1593 Communication, Social Marketing, and Environmental Health 1597
Environmental Risk Communication 1604 Summary 1624 Key Terms 1625 Discussion Questions 1628 References 1630 For Further Information 1635
Index 1637 End User License Agreement 1863
1873
- Title Page
- Copyright
- Dedication
- Tables, Figures, Text Boxes, and Tox Boxes
- The Editor
- The Contributors
- Acknowledgments
- Potential Conflicts of Interest in Environmental Health: From Global to Local
- References
- Part 1: Methods and Paradigms
- Chapter 1: Introduction to Environmental Health
- What Is Environmental Health?
- The Evolution of Environmental Health
- Spatial Scales, from Global to Local
- The Forces that Drive Environmental Health
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 2: Ecology and Ecosystems as Foundational for Health
- Environment as Ecology: Ecology as the Study of Our Home
- Population Ecology
- Community Ecology
- Ecosystem Ecology
- Systems Thinking: From Ecology to Human Health
- Features of Our Home: Ecological Characteristics as Foundational for Health
- Toward Ecological Approaches to Health and Home
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 3: Sustainability and Health
- Historical Considerations of Sustainability
- Sustainable Human Well-Being and the Three-Legged Stool
- Drivers of Nonsustainability, Limits to Growth, and Collapse
- What Should Concern Us More: Population Growth Or Consumerism?
- Limits to Growth
- Human Societal Collapse? Prevention Through Systems Thinking and Early Action
- The Importance of Scale
- The Way Forward
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 4: Environmental and Occupational Epidemiology
- A Primer on Epidemiology
- Environmental and Occupational Epidemiology
- Epidemiology and Risk Assessment
- Future Directions
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 5: Geospatial Data for Environmental Health
- Components of Georeferenced Data
- Basic GIS Operations
- Mapping and Spatial Analysis of Exposure
- Mapping and Spatial Analysis of Disease Risk
- What Makes Good Maps of Good Data?
- What Can We Do with GIS?
- Are There Any Limitations?
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 6: Toxicology
- Introduction to Toxicology
- Toxicology and Environmental Public Health
- Toxicant Classifications
- Testing Compounds for Toxicity
- From Regulatory Toxicology to Public Health Policy
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 7: Genes, Genomics, and Environmental Health
- Fundamental Concepts of Genetics and Genomics
- Approaches for Identifying Gene-Environment Interactions
- Examples of Gene-Environment Interactions in the Real World
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 8: Exposure Science, Industrial Hygiene, and Exposure Assessment
- Anticipation, Recognition, Evaluation, and Control
- Exposure Science
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 9: Environmental Psychology
- Environmental Psychology and Toxicology
- Environmental Psychology Processes
- So What? Interventions That Work
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 10: Environmental Health Ethics
- Defining Ethics and Morals
- The Modern Philosophical Background
- Professionalism
- Expanding Horizons and Challenges
- Implications for Professional Ethics
- Concluding Discussion
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 11: Environmental Justice and Vulnerable Populations
- The Roots of Environmental Justice
- Elements of Environmental Justice
- From Research to Action on Environmental Justice
- Social Inequality and Environmental Quality
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Part 2: Environmental Health on the Global Scale
- Chapter 12: Climate Change and Human Health
- Greenhouse Gases
- A Warming Earth: From Past to Future
- Earth System Changes
- Food and Malnutrition
- Weather Extremes and Disasters
- Air Pollution
- Infectious Diseases
- Mental Health Effects
- The Public Health Response to Climate Change
- Climate Change as a Public Issue
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Part 3: Environmental Health on the Regional Scale
- Chapter 13: Air Pollution
- History of Air Pollution
- Types of Ambient Air Pollution
- Studies of Air Pollution and Health
- Sources and Effects of Outdoor Pollutants
- Air Pollution Prevention and Control
- Larger Effects of Regional Air Pollution
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 14: Energy and Human Health
- Household Energy
- Fossil Fuels
- Nuclear Energy
- Renewable Sources of Energy
- Energy Conservation and Efficiency
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 15: Healthy Communities
- The History of Cities
- Poverty and Industrialization in Cities
- The Modern Metropolis: Consumption and Urban Sprawl
- Community Design and Health
- Cities as Healthy Human Habitats
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 16: Water and Health
- The Role of Water in Life
- Regulatory Framework
- Risk Characterization for Water Contaminants
- Emerging Issues
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Part 4: Environmental Health on the Local Scale
- Chapter 17: Solid and Hazardous Waste
- Solid Waste
- Solid Waste Management Strategies
- Primary Prevention of Waste
- Waste Treatment and Disposal
- Health Concerns
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 18: Pest Control and Pesticides
- Insect Pests
- Vertebrate Pests
- Pesticides
- Integrated Pest Management
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 19: Food Systems, the Environment, and Public Health
- What Is the Food System?
- Food Production: Industrial Agriculture
- Industrial Food Animal Production
- Sustainable Agriculture
- Food Consumption and Food Environments
- Food Safety and Environmental Health: A Systems Perspective
- Making Change: Food System Policy
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 20: Buildings and Health
- The Range of Buildings
- Key Elements of a Healthy Building
- Toward Safe, Healthy Buildings
- Architecture, Environment, and Human Health
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 21: Work, Health, and Well-Being
- The Interaction of Work and Health
- Protecting Safety and Health on the Job
- Workers' Compensation
- Sustainability
- Globalization
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 22: Radiation
- Nonionizing Radiations
- Ionizing Radiation: The Basics
- Sources of Ionizing Radiation Exposure
- Cellular and Biological Effects of Ionizing Radiation
- Human Health Effects of Ionizing Radiation
- Radiation Protection
- Assessing Radiation Risks
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 23: Injuries
- Injury Prevention and Control
- Policy for Injury Prevention and Control
- Injury Prevention in Practice
- Injury Control in Special Settings
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 24: Environmental Disasters
- Scope of the Problem
- The Public Health Consequences of Environmental Disasters
- Disaster Risk and Its Determinants
- Managing Disaster Risk
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 25: Nature Contact
- The Links Between Nature and Human Health
- Domains of Nature Contact
- The Greening of Environmental Health
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- PART 5: The Practice of Environmental Health
- Chapter 26: Environmental Public Health: From Theory to Practice
- Concepts of Environmental Health Prevention
- Principles of Prevention in Environmental Public Health
- Core Functions of Environmental Public Health
- Environmental Public Health Systems
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 27: Risk Assessment in Environmental Health
- History
- Risk Assessment
- Risk Management and Communication
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Chapter 28: Communicating Environmental Health
- Communication, Social Marketing, and Environmental Health
- Environmental Risk Communication
- Summary
- Key Terms
- Discussion Questions
- References
- For Further Information
- Index
- End User License Agreement
.jpg){kind=link}
