333

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I ฀฀฀฀฀ ฀฀฀฀฀฀ &W\U1U', Ll1K-1 I CHAPTER SEVEN

t Gender Transformed: Endocrine

f Disruptors in the Environment

I Nancy Langston

I I

I I In the late 1970s, anglers in England began reporting that they were

catching bizarre fish-rainbow trout that seemed to be partly male and

partly female. Perplexed, a biologist from Brunei University named John, Sumpter went out to investigate these reports of what the media called

"sexually confused fish."l He discovered that the trout were males that

had indeed developed female characters, and he found that the best I places to find these gender-bending fish were near sewage plants, in the

I lagoons and pools just below the discharge outlets for treated waste. The

obvious question occurred to him: could anything in the sewage effluent

I be affecting the masculinity of the fish?

Sumpter, with the help of fellow Brunei University biologist Charles

I R. Tyler and researchers from the Ministry of Agriculture, Fisheries, and

Food, found male fish that were producing elevated levels of vitel-

I logenin, a protein responsible for making egg yolks in female fish. Male

fish possess a gene that can produce vitellogenin when triggered by es- \

trogen, but ordinarily males lack enough estrogen-a female sex hor-

mone--to trigger this gene. To test whether sewage treatment plants had I anything to do with the elevated levels of vitellogenin in the male fish

blood, the scientists took healthy male trout raised in captivity, put themI in cages, and placed them for three weeks near the discharge points of

I thirty different sewage treatment plants. Soon those males began pro-

ducing vitellogenin, just like females. 2

Some of the scientists suspected that industrial chemicals such as I nonylphenols-breakdown products of detergents, pesticides, and cos-

I metics-might be responsible for feminizing the males. But initial studies

failed to support this hypothesis. They wondered next if the problem

I might stem from birth control pills. Estrogens from contraceptives, they

reasoned, might not be completely breaking down in the women's bod-I I ies or in the sewer treatment process, so those estrogens might be ending

up in the effluent and somehow stimulating males to become females.

129

l.. I

130 BODIES

Lab experiments showed that ethynylestradiol, the main estrogenic com-

pound in birth control pills, could indeed stimulate male fish to produce

female proteins, even when concentrations were as low as one nanogram

per liter of water. But the scientists could not initially find ethynylestra_

diol in the rivers at levels their instruments could detect.3 Other re-

searchers suspected that the male fishes' problems might stem from

something even stranger: during certain times of their menstrual cycles,

women's urine is brimming with estrogen. Perhaps this urine was pow-

erful enough so that, even after being diluted and treated, it could alter

the natural world. Could hormones in women's urine-whether of natu-

ralor synthetic origin-be feminizing male fish?

Sumpter's results suggested several disturbing things. First, we

might be poisoning wildlife with chemicals that alter their hormonal sys-

tems, sometimes even transforming them from one gender to another-

transformations that could harm their ability to successfully reproduce

and thus threaten their survival. Second, some researchers suspected that

what was happening to the fish might also happen to humans. And third,

the results suggested that industrial chemicals were not the only poten-

tial problem: our private bodily functions might also be altering gender

in the environment.4

On the most basic level, we tend to assume that what happens inside

our bodies is a personal matter. When we take those pills, those cups of

coffee, those birth control hormones, we assume that they're disappear-

ing into the black box of our innermost bodies. Yet those chemicals, both

natural and unnatural, don't end with us; they come out, get flushed

down the toilet, and make it through our septic tanks or sewer systems

into the waters we share with other creatures. In many places now, water

carrying our bodily effluents may form more than half the flow in a sum-

mer stream. And remnants from our bodily wastes may be changing the

nature of gender, turning male fish into female fish and female fish into

male fish-and potentially affecting human development as well.

In this chapter, I will examine some transformations in the biological

constructions of gender since the 1930s.5 To do this, I will look at two sets

of changes. First, I will examine changes in the levels of natural sex hor-

mones in women's bodies, changes stimulated in part by larger societal

transformations. Second, I will examine what are called endocrine dis-

ruptors, the industrial pollutants that mimic female sex hormones and

disrupt the endocrine systems that control the biological expression of

gender in wildlife as well as people.

Endocrine disruptors connect environmental histories of the body

with environmental histories of wild places and wild animals.6 What we

eat, what we drink, what we excrete, how we procreate: these are at the

core of our animal selves. Our bodies are how we're most natural, but

1 I NANCY LANGSTON 131

l- now they're also how we're most industrialized, since our bodies areI :e where our industrial chemicals are coming back to haunt us. As strange

as it may seem, even our pee has become hazardous waste, capable ofn I }- turning male fish into quasi-females. In this chapter I will explore what ,- I endocrine disruptors might mean for the nature of gender and for our re-

lationships with the environment.

s, I f- The more researchers looked, the more they found that the waters of

n

I Britain, Europe, and America were laden with chemicals excreted in peo-

I- ple's urine and that these chemicals could be causing Widespread repro- I ductive impairment in males from many different species. For example,

re scientists in Minnesota found male carp and walleyes in the effluent of

s- sewage plants that weren't making sperm but were producing high

quantities of vitellogenin instead.! Other studies in the Great Lakes re-

:e gion found male white perch that had become intersex-part male, part

at female, and completely uninterested in sex.s Urine, researchers found,

฀฀

I i, could contain over sixty different synthetic chemicals, not to mention

:1- plenty of natural hormones as well.9 It turns out that our pee is dousedI er with poisons-metabolites from the breakdown of birth control pills, caf-

\ feine from all the coffee and Mountain Dew we're quaffing, remnants

ie from the aspirin and Tylenol and anticholesterol drugs we use to stanch

of I the pain of our modern ailments. These chemicals in sewage effluent

r- seemed to be altering the action of hormones during development, with

th I potentially profound effects on the fetus. 10

฀฀฀ Industrial chemicals as well as sewage effluents were also implicated

1S I in gender switches. Students on a biology field trip in Florida noticed that

er every single mosquitofish they found seemed to be a male, for each had

n- I a gonopodium-an anal fin that males use for copulation. But many of

1e these "males" turned out to be pregnant, and the students found that all

to I the females in this stretch of the creek had been masculinized. The prob-

lem, biologist W. Mike Howell learned, was that wastes from pulp and

al paper mills were contaminated with chemicals that acted like androgens,

·ts male sex hormones that trigger the production of testosterone. ll Females lr- from other fish species also became masculinized when exposed to pulp al mill wastes; killifish and sailfin mollys developed fins resembling

I lS- gonopodia, becoming extremely aggressive as well. In one researcher's ld words, female killifish stopped acting like normal, well-behaved femalesI of and instead became "like little sharks."12 Bluegill sunfish, American eels,

I Swedish eelpouts-all these fish became masculinized in the presence of iy pulp mill waste in streams across the world. ve I Gender confusion wasn't limited to fish. Male alligators exposed to he DDT in Florida's Lake Apopka had abnormally small penises. They were ut I just one-half to one-third the normal size, too small to function, and these

\

.....I

฀฀

,

132 BODIES

males also seemed to have ovaries, \vhile the females produced abnormal

eggs.13 Two-thirds of male Florida panthers-an endangered species

whose total population only numbered thirty to fifty individuals in

1994-were found to have cryptorchidism, a condition in which the testes

doesn't descend, much less produce normal sperm. These male panthers

are producing twice as much estrogen as testosterone, while normal male

panthers do the reverse. In some western rivers, male Chinook salmon

have undergone sex-reversal; many of the fish that look like females are

actually males that have suffered a hormonal emasculation. Prothonotary

warblers in Alabama, sea turtles in Georgia, mink and otters around the

Great Lakes-all show reproductive malformations.14

The list of recent gender transformations in wildlife can go on and on:

female Great Lakes gulls and terns that try to mate with other females in-

stead of with males. "Gulls in these colonies show excessive chick mortal-

ity, birth defects, and skewed sex ratios, with an excess of females."15 Male

Atlantic cod and winter flounder that show reduced testosterone levels,

hampering reproduction. Female Atlantic croakers (a kind of fish) that

aren't growing normal ovaries. Male porpoises that don't have enough

testosterone to reproduce. Polar bears on the Arctic island of Svarlbard

that are hermaphrodites, which is not something one normally sees in a

polar bear.16 In perhaps the most disturbing example of gender switches,

Gerald A. LeBlanc of North Carolina State University in Raleigh found

that over one hundred species of marine snails were experiencing some-

thing known as imposex, a pollution-induced masculinization. Females

developed a huge malformed penis that blocked their release of eggs.

They swelled up with eggs that couldn't get out and then they died.J7

By the 1990s, researchers noticed that it wasn't only wildlife that

were showing difficulties with their reproductive health. Increasing num-

bers of people were as well. As with panthers, the incidence of cryp-

torchidism (undescended testicles) in British men doubled in two

decades. In the three decades since 1970, American boys appear to have

become increasingly likely to develop severe hypospadias, a birth defect

of the penis.18 Testicular cancer has increased in many industrialized

countries. For example, in Denmark, the incidence of testicular cancer has

more than tripled since Wbrld War II, while in the United States, the inci-

dence increased by 51 percent between 1973 and 1995. Similar increases

are occurring in other Scandinavian countries and in Scotland.19

Since the 1950s, sperm counts in some (but not all) regions across the

world have declined significantly.20 Men in many industrial nations are

showing increases in prostate cancer; for example, a 1999 review found that

men in the United States in 1994 had "about a three- to four-fold risk of be-

ing diagnosed with prostate cancer compared with their fathers."21 Much

of this increase in the number of diagnosed cases was probably due to bet-

ter screenir

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NANCY LANGSTON 133

ter screening tests, but researchers were nonetheless concerned that actual

incidence was also increasing for unexplained reasons. Studies suggest

that, across the United States and Puerto Rico, many girls are developing

breasts at younger ages.22 Other research on women's reproductive health

shows an increase in the incidence of misshapen wombs, infertility, en-

dometriosis, fibroids, breast cancer, and ovarian cancer since the 1950s.23

What, if anything, connects all these bizarre problems with gender

and reproductive health? Are there any links between human and

wildlife problems? Possibly; many researchers now believe these changes

may stem from the consequences of fetal events-namely, imbalances in

sex hormones during fetal development. Since the 1950s, we may have

been changing the biological basis of gender by filling the world's waters

with synthetic chemicals that alter the balance of sex hormones control-

ling the biological development of gender. Hundreds of the synthetic

chemicals we started dumping into the environment since World War

TI-PCBs, DDT and other pesticides, dioxins, many compounds in plas-

tics-disrupt the action of natural sex hormones, particularly on the fe-

tus. Endocrine disruptors don't just shut down the endocrine system:

they can actually fool it into "accepting new instructions that distort the

natural development of the organism."24

These estrogen-disrupting chemicals are not rare; some of them are

among the most common synthetic chemicals in production. We now live

submerged in a sea of estrogens, some natural and some synthetic. These

estrogens affect men as well as women, wildlife as well as humans. Trac-

ing the pathways of that estrogen-its naturalness and its unnatural-

ness-can illuminate an environmental history of gender.

The Greeks called the main female sex hormone "estrogen" because

it produced the state of "estrus," when a female goes into heat. Estrus, in

tum, derives from the Greek word oistros, which means "frenzy" or a

woman driven wild.25 Estrogen, like other hormones, is a chemical pro-

duced by the body that regulates the body's growth and development.

Hormones are messengers that create a complex signaling system (called

the endocrine system) that tells the body what to produce, where, and

when. Sex hormones tell the developing fetus to develop a penis or not,

as the case may be. Sex hormones tell a boy's testicles to descend, a girl's

breasts to develop, a woman's ovaries to grow eggs. They control what

makes us female and what makes us male.

Postrnodernists like to imagine that gender is culturally constructed,

and clearly cultural forces do shape the expression of gender differences in

our SOCiety. But gender is also profoundly biological. Hormones control the

biological construction of gender, and now hormone mimics may control

the biological deconstruction of gender as well. To complicate matters, cul-

tural constructions influence the biological constructions of gender because

....".,

!

134 BOD1ES

behavior, social interactions, and expectations can all change the ways OUr bly tiny bodies produce sex hormones. On a more direct level as well, culture alters enormo the biological control of gender differences because many of the chemicals FOI

our culture produces have powerful effects on hormonal functions. several, Sex hormones link wildlife and humans, wild places and human androgl

places, because we share our hormonal systems with animals. Surpris- lesteroL ingly, the same chemical can act like a hormone in an alligator, a fish, a even 01

panther, and a woman. For 300 million years of evolutionary history, the site for

hormonal system has been remarkably conserved, the reproductive en- tell a gi

docrinologist Frederick vom Saal argues, because "it's so critical to life. breasts

So if a chemical can disrupt the endocrine system by acting as an estro- increas{

gen in a fish, for instance, the likelihood is that it will do that in humans. manye

Endocrine disruption in fish has to be a concern with regard to human late the

health. Not just mice, not just birds or reptiles, it's all of them. They're all grow, a:

sentinels for our health because these chemicals are in all likelihood op- Aft

erating on systems that we all share."26 The fact that we share our hor- the bloc

monal systems with other vertebrates means that what happens out in of orgal

wild places also happens within our bodies. For example, the PCBs to a reCl

dumped in the Hudson River decades ago may well be stimulating tu- of that·

mors in women's wombs and breasts to swell. It is within our bodies that nucleus

we are most vulnerable to the pollutants we think we've disposed of. pressiOl

to start

Wi

HOW HORMONES WORK: CREATING GENDER breasts

duction

Normal development of a creature, from egg to adult, is controlled by the mones

balance between hormones. Tiny changes in this balance signal growth, Certain

sexual differentiation, and other critical functions from the control of the blo<

blood sugar and metabolism to brain development to the growth and from ac

function of reproductive systems. The endocrine system, like the nervous it ฀฀฀฀฀

system, is a communication network that regulates all functions of the or malE

body. Glands within the body secrete chemical messengers-hormones- quantiti

which travel through the bloodstream until they encounter cells with spe- it's not

cific target receptors. Each hormone has a unique shape that fits the shape tio betv

of the receptor protein at the target cell; imagine the hormone as your key trogen,

and the receptor protein as the lock in your door. But hormones are also Est

flexible: a given receptor protein may exist on different cells in different too): in

organs, so that the body can use the same hormone to perform radically selS,livl

different functions in different tissues. Hormones act slowly (compared, hormor

say, to the nervous system, the other communication network in the are ver)

body), and their effects persist in the body for long periods of time (again, Other n

compared to the nervous system, whose effects are very rapid and very ily gen<

short). Most important, the endocrine system is designed so that incredi- cause tl

1

I

NANCY LANGSTON 135 I

bly tiny amounts of a chemical (on the order of molecules) can produce IYS our I

enormous changes in the bodyP฀ alters For example, consider estrogen (which isn't just one chemical, but฀฀฀฀฀฀฀ \

several, including estradiol, estrone, and estriol). Estrogen, like the male

androgens, is a steroid, meaning a fat soluble hormone derived from cho-human \

lesterol. Several locations within the female body can make estrogen-urpris- I even our fat cells do as we age--but the ovaries are the most important. fish, a ,

site for estrogen production. Estrogens help develop gender in the fetus,Jry, the I tell a girl's body to begin developing breasts and hairy armpits, tell the:ive en-

breasts to prepare for lactation, regulate changes during menstruation,to life. I increase libido, protect the heart, and help bones to grow denser. Too n estro-

lumans. many estrogens at the wrong time, however, are a problem: they stimu- \

late the replication of cancer cells, tell tumors in women's uteruses tohuman

ey're all \

grow, and derail normal male development.

ood op- After the ovaries release a molecule of estrogen, it travels through

mr hor- the blood until it encounters receptors at the breast (or any of a numberI s out in of organs). The estrogen molecule passes within the breast cell and binds

Ie PCBs I to a receptor protein inside that cell, which triggers a change in the shape

lting tu- of that receptor protein. This receptor-estrogen complex enters the cell's

iies that \ nucleus and binds to the DNA, which causes a change in the gene's ex-

฀฀ of. pression and changes in the cell's activity-for example, telling the breast

I to start growing.28

What keeps estrogen from going wild in the body, from growing I breasts the size of houses, for example? First, the body controls the pro-

duction of hormones by having the pituitary gland produce other hor-

·d by the I mones that signal the ovaries to regulate their secretion of estrogen.

growth, Certain proteins, such as sex hormone binding globulin, circulate within

mtrol of \ the bloodstream, binding to loose estrogen in the blood and keeping it

wth and from acting on target cells. For estrogen to function correctly in the body,

nervous \ it needs to be in a certain ratio with other sex hormones: the androgens

1S of the or male sex hormones (which are also present in females but in lowerI mones- quantities, just as estrogens are present in males, at low quantities). Often

Nith spe- I it's not the absolute quantity of estrogen that matters, but instead the ra-

he shape tio between estrogen and androgen, or the change in the amount of es-

your key \ trogen, that signals genes to get to work.29

; are also Estrogen receptors are everywhere in a woman's body (and a man's

different I too): in breast cells, the uterus, the ovaries, bone cells, hair cells, blood ves-

radically sels, liver, kidneys, eyes, and even a man's prostrate. To complicate matters,

)mpared, I hormone receptors don't come in just one shape. Some hormone receptors

-k in the are very specific, allowing only a single configuration of a molecule to fit.

le (again, \ Other receptors are much less choosy. Using language that is extraordinar-

and very ily gendered, cellular biologists call estrogen receptors "womb-like" be-

t incredi- \ cause they have "wobble"-they are t1exible and accommodating. Or, as

I

1

฀฀

I 136 BODIES

some male biologists put it, estrogen receptors have a "promiscuous"

pouch that welcomes lots of different chemicals.3D Cells. don't need to

hear from real estrogens; anything that binds to their estrogen receptors

can have estrogenic effects, switching on cellular processes just as if a nor-

mal estrogen molecule had bound. And this method is how many syn-

thetic chemicals seem to disrupt the endocrine system: they bind to

estrogen receptors, fooling the body into thinking ,it has received a mes-

sage from a real estrogen molecule.

Estrogen and other sex hormones control gender in fundamental

ways, beginning with telling certain fetal tissues to turn into structures

that are either male or female. 31 About six weeks into a pregnancy, sex de-

termination begins. The developing fetus is extremely sensitive at this

point to confused signals from synthetic chemicals. For example, in the

male fetus, Sertoli cells direct the development and descent of the testes,

control the development of germ cells, and control the cells that secrete

the hormones responsible for masculinization. Turning on too many es-

trogen receptors in the developing fetus could reduce the multiplication

of Sertoli cells and fix their numbers at very low levels. This result could

also affect descent of the testes and the development of urethra, setting

into motion events that might lead to birth defects and testicular cancer.32

The obvious question, however, is this: since natural estrogen occurs in

very high levels in a pregnant woman, why isn't her own estrogen con-

fusing the development of her sons? The answer seems to be that most of

a pregnant woman's natural estrogen is tied up by something called "sex

hormone binding globulin" (SHGB), a protein that protects the fetus from

the mother's high hormone levels. Synthetic estrogen-mimicking chemi-

cals are not tied up by SHGB, making them potentially more powerful at

lower doses than a woman's own estrogen.33

Normal sexual development depends upon getting the right hor-

monal signals at the right time in the fetus. If there is a tiny shift in the

balance between hormones, a fetus might end up with the wrong num-

ber of digits, seriously confused genitalia, a uterus that's shaped wrong,

a reproductive tract that cannot function, an immune system that later in

life will turn against itself, and testicles or breasts that are programmed

to develop cancer years down the road.34 Yet those effects might not be

detected for many decades because problems that start in the womb's en-

vironment may not emerge until puberty or adulthood.

CHANGES IN SEX HORMONES

In the last fifty years, American women have been exposed to increas-

ing levels of estrogen, not just from synthetic sources but also from our

body's 0,

reproduc1

greater p(

case. We

start our]

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brains.37

NANCY LANGSTON 137

5CUOUS" body's own natural estrogen. Throughout much of history, women ofI need to reproductive age were likely to have been pregnant or lactating for a

฀฀฀฀฀฀฀฀ I greater percentage of their reproductive years than is now typically the

if a nor- case. We put off pregnancies, or else we don't ever get pregnant; we

lny syn- I start our periods earlier, and we go into menopause later than our an-

bind to cestors, which means that many women now have from 355 to 450 men-

i a mes- I strual cycles during their lives. In earlier generations, many women

may have averaged far fewer. As we get exposed to more menstrual cy- amental I cles, we get exposed to more estrogen.35 Hormone replacement therapy

ructures can also bring more estrogen into women's bodies, as do most birth con- I(, sex de- trol pills.

e at this Obesity rates in America have increased over the past fifty years, I le, in the which increases estrogen levels, since fat cells produce estrogen from cir- 1e testes, culating adrenal hormones. Our diets contain more estrogen than theyI It secrete did half a century ago, especially through meat and dairy products.

lnanyes- Changes in dairy production mean that cows are now often pregnantI plication while they're being milked. This determinant leads to higher levels of bIt could natural bovine estrogen in that milk, since pregnant cows have more es- I .

I :1, settmg trogen. Changes in diet during the last half century have also altered the

32Icancer.. I ways women metabolize their own estrogen: the more fat and protein in occurs ill a woman's diet, the more she recycles her own estrogens in her gut, in ef- I. gen con- I fect eating them twice. Drinking alcohol leads to higher levels of estro- lit most of gens as well, because the liver is important in breaking down and ltlled "sex I excreting estrogen. When a woman drinks more than about fourteen ฀฀฀฀฀ from drinks a week, the liver can no longer break down estrogen effectively, Ilg chemi- I leading to higher estrogen levels in the body.36 I,werful at Not only do women have their own estrogens to contend with; sinceI World War II, women have had to deal with ever-increasing sources of 'ight hor- synthetic estrogens and estrogen mimics. Although women's bodies pro-

I]lift in the duce natural estrogens and women also eat phytoestrogens (estrogens Img num- from plant sources) in their food, synthetic estrogen mimics differ fromI฀฀฀ wrong, both. Synthetic estrogen mimics tend to be flexible molecules that can lat later in I bend into many shapes and fit into many different cellular receptors, Igrammed which means they can play havoc with the body's endocrine system. Un- I'ht not be I like natural estrogen, estrogen mimics rarely bind with sex hormone)

bmb's en- binding globulin, so while they may at first be present in much lower

I levels than our own estrogen, their effective concentration can soon be

much higher. Unlike natural estrogens, many synthetic estrogen mimics I Such as PCBs cannot be easily broken down by the body. During preg-

nancy and breast-feeding, these synthetic chemicals can be released, I only to enter the fetus or the child. At other times, synthetic estrogen

a increas- mimics accumulate in a woman's fatty tissues: breasts, ovaries, and ,from our I brains.37

I

I ฀

138 BO IES

ES

he first signs that synthetic hormones might disrupt development came

with ES daughters. In a huge, uncontrolled experiment, over five mil-

lion women during the 1 0s and 1 60s -vere given ES, a potent syn-

thetic estrogen, to prevent miscarriages. After years of increasing

problems with the children of ES mothers, researchers in the 1 70s fi- .

nally starting connecting their problems with the hormones given to their

mothers. Ironically, the 1 30s researchers had known that ES caused

cancer in l.ab animals, yet these studies were ignored when the A ap-

proved ES for pregnant women in 1 47. Why? And why were people so

slow to consider that treating millions of women with a synthetic,

untested hormone might be a bad idea? Examining these questions will il-

luminate how our problems with endocrine disruptors have developed.38

ES is notable because it is the only large experiment done on estro-

genic chemicals with human subjects. ES was not a perfect experiment,

of course, because it was not designed as one: few follow-up studies were

done on the children of ES mothers, and many women had no idea they

were even being given ES during their pregnancies. Most of the doctors

who prescribed ES had retired by the time its effects were being recog-

nized, so those patients have never been followed. Nevertheless, it has

become a model for the "long-term effects possible from in-utero expo-

sure to an endocrine disruptor."3 What happened with ES illustrates

both the effects that synthetic hormones can have on people and the dan-

gers of our culture's assumptions that people are so different from ani-

mals that animal experiments need not apply to humans.

In 1 38, an English biochemist named Edward Charles odds first

synthesized estrogen, creating diethylstilbestrol, or ES. odds's work

showed that hormonal function in people and animals could be induced

by synthetic substances-something no one had been certain was possi-

ble, even though now it seems obvious to those of us who have grown up

in the age of the contraceptive pill. After odds's discovery (which he

never patented), ES was manufactured quite cheaply from coal tar de-

rivatives, soon becoming available under more than four hundred differ-

ent trade names. (Since the drug was prescribed under so many trade

names, most women never knew they had been given ES. oday, at least

64 percent of ES-exposed daughters do not know that their mothers had

ever taken the drug.)40

When ES was first produced, people knew two things about it: it

was extremely estrogenic, even more so than a woman's own estrogen,

and it was highly carcinogenic in lab animals. Studies in the late 1 30s

showed that mice exposed in utero to ES developed breast cancer, while

in and 1 40, studies showed that mice exposed in utero to ES

sometimes de

ductive organ

proved the dr

or centu

riages. Suspec

synthetic hon:

low estrogen ]

lished in 1 47

riages, and I

Only two earl

riages, and lat

1 8, two revi

creased the risl

creasing misca

ES was Soon

pregnancy mo

ogy recommen

Meanwhi

their diet. Beg]

growth promc

were soon beir

one hundred t

mice. When e

tence, and brei

1 , while all

be promoted a

Given the

cause problerr

and doctors hi

fected by the (

provided a bal

flected availal

1 70s, the fetu

the developmE

ment was sepe

In 1 6 ,

with profound

not cross the F raised about I

fects, while no

tors or resean

pregnancy mi

when the child

nent came

r five mil-

otent syn-

lncreasing

e 1970s fi-

en to their

ES caused

e FDAap-

฀ people so

synthetic,

ons will il-

฀฀฀฀฀฀฀฀฀฀฀

Le on estro-

xperiment,

udies were

o idea they

the doctors

eing recog-

-less, it has

Itero expo-

; illustrates

l.d the dan-

t from ani-

Dodds first

dds's work

be induced

was possi-

e grown up

r (which he

coal tar de-

dred differ-

many trade

,day, at least

nothershad

, about it: it

In estrogen,

,e late 1930s

ancer, while

tero to DES

I

I

\

I

NANCY LANGSTON 139

sometimes developed liver cancer and were born with deformed repro-

ductive organs.41 Yet these experiments were ignored when the FDA ap-

proved the drug.

For centuries, doctors had tried to figure out how to prevent miscar-

riages. Suspecting that low levels of estrogen might be the problem, the

synthetic hormone DES was at first given only to pregnant women with

low estrogen levels and a history of miscarriage. A Harvard study pub-

lished in 1947 suggested that the drug might reduce the risk of miscar-

riages, and FDA approval was given that year for use during pregnancy.

Only two early studies suggested that DES reduced the rates of miscar-

riages, and later, more careful studies showed the opposite. In 1953 and

1958, two reviews of the available research showed that DES slightly in-

creased the risk of miscarriages, even though it was supposed to be de-

creasing miscarriages. Nevertheless, the drug continued to be prescribed.

DES was soon prescribed even for "normal" women "to make a normal

pregnancy more normal."42 By 1957, the Tournai of Obstetrics and Gynecol-

ogy recommended it for all women to produce bigger and stronger babies.

Meanwhile, millions of people were being exposed to DES through

their diet. Beginning in the 1940s, DES was used in the United States as a

growth promoter in poultry, hogs, and cattle. Very high levels of DES

were soon being detected in poultry sold for human consumption-up to

one hundred times the concentrations necessary to cause breast cancer in

mice. When exposed male agricultural workers suffered sterility, impo-

tence, and breast growth, the FDA banned its use in chicken and lambs in

1959, while allowing its use in cattle feed to continue and allowing itto

be promoted as a wonder drug for pregnancy.43

Given these findings, why didn't scientists ask whether DES might

cause problems for the developing fetus? Until very recently, scientists

and doctors had assumed the womb was inviolate and could not be af-

fected by the outside world. People believed that the mother's placenta

provided a barrier, protecting the fetus from harm. This belief partly re-

flected available technology: until the invention of ultrasound in the

1970s, the fetus was hidden off in the womb. People could not visualize

the development of the fetus, so it was easy to assume the fetal environ-

ment was separate.44

In 1962, when thalidomide was found to cross the placental barrier

with profound effects on limb development, this belief that drugs could

not cross the placenta was finally disrupted. Yet concerns were still not

raised about DES. Thalidomide produced immediate, massive birth de-

fects, while no birth defects were initially apparent with DES. Few doc-

tors or researchers could comprehend that a hormone given during

pregnancy might have effects that would only emerge decades later

When the children of DES mothers reached adulthood.

..I

140 BODIES

By the late 1960s, some of the children born to mothers who had

taken DES were becoming sexually mature. Problems began to appear in

these children, but it wasn't until 1971, after Arthur Herbst at Harvard

Medical School showed a relationship between DES use and rare vaginal

cancers in daughters (clear cell adenocarcinoma), that researchers sus-

pected DES might be a problem. By November 1971, twenty-one cases of

a formerly extremely rare clear cell vaginal cancer were linked to DES

use, and the FDA issued an alert advising against the use of DES during

pregnancy.45

Ensuing research revealed that only about 1 percent of the daughters

developed vaginal cancers linked to DES, but nearly 90 percent of DES

daughters have experienced reproductive tract problems, including men-

strual irregularities and infertility.46 For example, half of DES daughters

have fertility problems, well above the rate of the general population.

Sons of DES mothers have higher rates of undescended testicles, cysts of

the reproductive tract, low sperm counts, and testicular cancer, while

both sons and daughters showed depressed immune systems, higher

rates of depression, and lowered libido. As these findings emerged, the

FDA began trying to withdraw the chemical from use, but this action

proved extremely difficult. In 1972, the FDA withdrew all approval for

animal uses, but it took five years of litigation before the courts upheld

this ban on the use of DES in animals.

At the peak of its use in the 1960s, DES was given to five million

pregnant women and to nearly thirty million cattle, which means mil-

lions of people consumed meat tainted with artificial estrogen.47 The

press usually depicts DES as simply an individual woman's concern (like

so many other things that affect women's health). The message is: ask

your mother if she used DES, and if the answer is yes, then worry. DES is

rarely portrayed as a larger environmental concern. But DES is an envi-

ronmental exposure issue as well, since through food and waste from

feedlots, and possibly through women's urine, the chemical entered the

environment at large, exposing wildlife as well as women.

In the early 1970s, the toxicologist John McLachlan became con-

cerned about the effects of DES in the food supply. He began studying its

effects on development in mice, trying to find out if animal models could

replicate the effects seen in daughters of DES mothers. Much to every-

one's surprise, he showed just that: DES-exposed female mice had in-

creased rates of vaginal cancer, and exposed male mice exhibited reduced

fertility, undescended or stunted testicles, and genital tumors.48 Work on

the effects of DES on mice also showed that the artificial estrogen was

feminizing male mice at the molecular level: male mice exposed prena-

tally to DES would express female proteins in the reproductive systems

later in life, a result that at the time seemed astonishing. These findings,

and ฀฀฀฀฀฀฀฀฀฀฀

concern that estr

people. He first c

in 1979, long bef<

ogists, he was ne

tive disorders. ฀

isolated him wit!

One clear m,

that research on

unWillingness to

one of the biggesi

disruptors. Man}

compound's han

As one of the lea,

vom Saal, said, "]

it was clear from

But we have this i

the rest of life on

that's an animal. 1

the endocrine dis

fect model for hm

testing probably

humans. Most co

and vigor, and thE

of estrogen.51

Although DES wa

ologists were fine

DES. In 1950, H

American biologi

Male chicks inject.

cent of normal siz

acteristies compar

were chemically c

ter the formation <

mation and regu

affecting reproduc

further investigatE

were not followed

Meanwhile, si

posed to DDT and

tal chemicals migl

1950s that DDT, a]

10 had

pear in

arvard

{aginal

'rs sus-

:ases of

to DES

during

ughters

of DES

19 men-

ughters

ulation,

cysts of

r, while

higher

฀฀฀฀ the

5 action

oval for

upheld

million

ms mil-

n.47 The

ern (like

e is: ask

'I. DES is

an enV1-

ste from

ered the

me con-

:iying its

฀฀฀ could

o every-

had in-

reduced

Work on

gen was

d prena-

systems

'indings,

[

I

I NANCY LANGSTON 141

I and McLachlan's concern about DES in animals, stimulated his growing

concern that estrogenic substances in the environment might be affecting

I people. He first organized a symposium on estrogens in the environment

in 1979, long before most people were concerned.49 Yet, like most toxicol-

ogists, he was not fully aware of the wildlife research showing reprOduc-I tive disorders. Moreover, his growing interest in endocrine disrupters

I isolated him within his own field.

One clear message from the DES story is that we should not assume

I that research on animals has no meaning for people. Yet our culture's

unwillingness to believe that we are similar to animals may have been I one of the biggest difficulties in creating a coherent response to endocrine

disruptors. Many doctors and lawmakers are unwilling to believe that a I compound's harmful effects on animals can be extrapolated to humans.

As one of the leading researchers on endocrine disruptors, Dr. Frederick I

vom Saal, said, "Before DES was used on five million women in the U.S.,

it was clear from animal studies that DES would be damaging to fetuses. I But we have this absolutely bizarre notion that humans are separate from

the rest of life on Earth. You will hear physician after physician say, 'But I that's an animal. What relevance does that have to humans?'''50 Critics of

the endocrine disrupter hypothesis argue that animal testing is not a per-I fect model for human effects, which is correct. Yet the irony is that animal

testing probably underestimates the effects of estrogenic compounds onI humans. Most common lab animals have been bred for large litter size

and vigor, and these two qualities make them more resistant to the effects

of estrogen.51 .

Although DES was still being prescribed to pregnant women, wildlife bi-

\ ologists were finding events in nature that resembled those induced by

DES. In 1950, Howard Burlington and Verlus Frank Lindeman, two I American biologists, showed that DDT could have estrogenic effects.

Male chicks injected with a form of DDT had smaller testes (only 18 per- I cent of normal size) and arrested development of secondary sexual char-

acteristics compared to controls.52 They looked like hens-in effect, theyI were chemically castrated. Other researchers showed that DDT could al-

ter the formation of enzymes in the liver, which would then alter the for-

mation and regulation of estrogen, progesterone, and testosterone,

affecting reproduction.53 Burlington and Lindeman urged researchers to I further investigate these estrogenic effects of DDT, but their connections

were not followed through by others.I Meanwhile, signs of reproductive trouble in wildlife populations ex-

I posed to DDT and PCBs were emerging. An early sign that environmen-

tal chemicals might impair endocrine function was the discovery in the

I 1950s that DDT, a persistent organochlorine pesticide, caused bald eagles

I

I •

I

142 BODIES

to lay eggs with thin shells. Reproduction in gull colonies heavily ex-

posed to DDT began to decline in the late 1960s. Wildlife biologists ob-

served that often two females, instead of a male and female, were sharing

nests, and the young in the colonies had "grossly feminized reproductive

organs."54In the 1960s, as Rachel Carson warned of the ecological effects

of pesticides and the links between humans and wildlife, scientists began

wondering why eagles, peregrine falcons, and similar birds were not re-

producing. Carson singled out DDT as the likely culprit in eagle eradica-

tion and noted that "the insecticidal poison affects a generation once

removed from initial contact with it.''55 Few people, including Carson,

imagined that the problems might be hormonal in origin, yet in her in-

sistence that wildlife effects had implications for humans, Carson's work

was central to the core of the endocrine disruption hypothesis.56 But not

for three more decades, until a wildlife biologist named Theo Colborn

was studying problems with the Great Lakes, did anyone connect repro-

ductive problems in wildlife to hormonal problems in people.

After finishing her Ph.D. in 1985, Theo Colborn took a position with

the Conservation Foundation examining wildlife responses to pollutants

in the Great Lakes. The Great Lakes have long been a trash can for in-

dustrial pollutants; DDT, PCBs, pesticides, and dioxins have all accumu-

lated in their waters. About one-fifth of American industry and one-half

of Canadian industry are located along the Great Lakes or tributary

streams, making them a microcosm for problems with pollutants in in-

dustrial society.

Colborn found no shortage of wildlife problems in the Great Lakes

region, but few consistent patterns. Some studies suggested elevated

rates of cancer in certain species; other studies showed impaired fetal de-

velopment, while others revealed changes in behavior. Little seemed to

tie these results together.

Research by Frederick vom Saal had shown that developing fetuses

could be extraordinarily sensitive to tiny differences in the amount of

hormones in the fetal environment. Vom Saal noticed that female mice

from the same litter-mice that were genetically identical to each other-

showed dramatic differences in size and aggression. He discovered that

womb position had a powerful influence on a female mouse's adult be-

havior. Certain positions within the womb were more exposed to andro-

gens, bathing the mouse fetus in a few more molecules of sex hormones

at certain critical stages of growth. In maturity, those mice were much

more aggressive, slower to mature, and more "masculine"-all because

of parts-per-trillion differences in hormones within the womb.57

Vom Saal's work made Colborn wonder if the disparate effects she

was seeing in Great Lakes species might be linked by problems with fe-

tal development. If vom Saal had shown that tiny amounts of hormones

could lead to

same be true f

docrine syster

Peterson desc

posed prenat;

Saal describe(

knew that enl

tion."5B Colbc

problems she

certain synthE

thus disruptil

leading to prc

Althougr

Colborn's hYI

turns out that

port for this i(

thesis of estre

had been ove]

Dodd's labor,

trogenic respe

ied the chemi

synthetic com

likely that a " will be found

The next

proliferation \

iniscent of thE

relation betw4

carcinogenic I

estrogenic act

no scientific n

ferent types 0

the compounl

were ones tha

day, this class

of the most I

many PCBs.

Other w

emerged as ea

the rush to Sy

French chemi:

eer in male n

removed and

l

I

NANCY LANGSTON 143 I

'ily ex- could lead to great effects later in life for laboratory animals, might the I

lsts ob- same be true for wildlife? Might synthetic chemicals be disrupting the en-

;haring docrine system in developing fetuses? In 1989, when Colborn heard DickI :luctive Peterson describe "the changes in the development of male rat pups ex-

effects I posed prenatally to very low doses of dioxin-the same changes vom

, began Saal described in male mice that developed between two females-she

not re- I knew that endocrine disruption was not just a product of her imagina-

'radica- I

tion."S8 Colborn proposed a unified explanation to explain the myriad IIn once problems she observed in Great Lakes wildlife. She hypothesized that

::::arson, certain synthetic chemicals in the Great Lakes were mimicking estrogen, Iher in- thus disrupting the action of sex hormones on fetal development and

's work leading to problems in reproduction and behavior later in life.s9

I But not Although many in the scientific community were initially critical of

:::olborn Colborn's hypothesis that synthetic chemicals could mimic estrogen, itI t repro- turns out that Charles Dodd, the inventor of DES, had found some sup-

port for this idea in the 1930s. Yet in the excitement that greeted his syn-I on with thesis of estrogen, his work on the estrogenic effects of other chemicals

,llutants I had been overlooked. From 1933 to 1938, a series of journal articles from 1 for in- Dodd's laboratory reported that certain chemicals seemed to induce es-

lccumu- I trogenic responses in animal tests. As early as January 1933, having stud- Jne-half ied the chemical properties of ovarian hormones, he had foreseen that ributary I synthetic compounds could indeed act like estrogens, writing, "It seems ts in in- likely that a whole group of substances of related chemical constitution

I will be found to have estrus-exciting properties." it Lakes The next month, Dodd wrote to the journal Nature that "because cell ?levated I proliferation which characterizes the estrus state is in some respects rem- fetal de- iniscent of the early stages of a malignant growth, we have sought a cor- emed to I relation between substances having estrogenic action and those having

carcinogenic properties." He had found that two potent carcinogens had ; fetuses I

estrogenic activity as well, a result that he believed was "striking" since lOunt of no scientific model explained how one compound could create such dif-I ale mice ferent types of biological activity-estrogenic and carcinogenic.60 Among lother-

I the compounds that showed estrogenic activity in Dodd's early studies

฀฀฀฀ that were ones that had two phenol groups, what he called the diphenyls. To- ldult be- I day, this class of compounds is called the biphenyls and includes many o andro- of the most problematic endocrine disruptors: DES, bisphenol-A, and ormones I many PCBs. re much Other warnings that estrogens could cause serious problems because I emerged as early as the 1930s, but these warnings were largely ignored in

the rush to synthesize new chemicals. For example, during the 1930s, a fects she I French chemist showed that estrogen exposure could induce breast can- , with fe- cer in male mice. Doctors recognized that if women had their ovaries ormones I removed and thus weren't exposed to estrogen, they rarely developed

I

I.....

144 BODIES

breast cancer-in retrospect, a clear suggestion that estrogen could lead

to cancer, so synthetic estrogens might be problematic.61

Half a century later, in 1987, Professors Ana Soto and Carlos Son-

nenschein at Tufts University discovered the first hints that extremely

common synthetic substances-plastics-might be leaching chemicals

that could cause estrogen-like responses. Soto and Sonnenschein were ex-

amining how estrogens can make breast cancer cells multiply. They used

a special line of breast cancer cells, isolated and grown in a lab, for their

research; these cells will only grow in the presence of estrogens. Suddenly

something went wrong with their work. Breast cancer cell cultur;s

started growing and dividing on their own, even before the experiments

had started, when nobody had added anything to them. Soto assumed

someone in the lab had been careless and had contaminated the clean

cells; then she thought someone in the lab had simply made a mistake

and added estrogen to the wrong cell lines.

Eventually, she realized no one in the lab had made a mistake. The

problem was in the new plastic tubes: something from these tubes was

leaching into their cultures and stimulating the growth of breast cancer

cells. The manufacturer had changed the formulation of the tubes with-

out telling anyone, and those sterile tubes were leaching something that

acted like an estrogen. This development astonished Soto and Sonnen-

schein because they knew of no one who had reported estrogens leaching

out of plastics. Everyone, including the manufacturers, assumed plastics

were inert.

The problem turned out to be something called nonylphenoL a

chemical widely used in industry and domestic products such as paints,

detergents, oils, toiletries, and agrochemicals (ironically, this was one of

the chemicals that Dodd in the 1930s had reported to possess estrogenic

properties). Nonylphenols are just one in a larger class of related chemi-

cal compounds called alkylphenols, many of which turn out to be weakly

estrogenic, making breast cancer cells multiply in lab cultures. I Britain

alone, twenty thousand tons of these chemicals are used a year, and a

third of these end up in our rivers and lakes at concentrations of fifty

micrograms per liter-levels higher than those that induce cancer cell re-

sponses in the lab.62

Similar problems with other plastics emerged in the early 1990s.

During the effort to create artificial estrogens in the 1930s, researchers

had first synthesized bisphenol-A (one of the chemicals Dodd noted "ex-

cited estrus" in his lab animals.)63 Not as powerful as DES, bisphenol-A

was ignored until researchers realized that, when polymerized, it formed

a useful plastic known as polycarbonate. Polycarbonate is now used for

numerous common items: plastic baby bottles, water bottles, dental

sealants, coatings for the inside of food cans. Unfortunately, bisphenol-A

T

I

I leaches out of the

I wildlife at concen

sponses in lab al r

showed that, f<

in amounts high I

cent of cans shovv In the past dE

with cavity-retaY<

taining high con<

procedure, levels

even six months

saliva. The sealan

are getting chew<

these levels high

ductive systems a

are safe, either. [

compounds at cor

the FDA has neVE

children.66 The A

finding was that il

ommendation tha

ological implicati<

The ADA cannot

[study's] observat

The ADA is r

say the estrogenic

harm them. But d

the absence of ev

the FDA requires 1

do not cause hal

Chemicals are ass

the problem is the

unethical to test p

Animal expe

causes mice to en

normal (how ironi

cause we exercise

prenatal exposurE

cently demonstrat

nol-A. In only twe

maximum -coneen,

Vom Saal's ea

ulated Theo Colbe

"'r

I

I NANCY ANGS ON 145

leaches out of those products, ending up in food, children's teeth, and incould lead I wildlife at concentrations higher than the levels that induce estrogenic re-

I sponses in lab animals. or example, in one study in Spain, scientists :arlos Son- showed that, in fourteen out of twenty cans, food contained bisphenol-Aextremely in amounts high enough to make breast cancer cells divide. Seventy per-chemicals I cent of cans showed estrogenicity.64in were ex-

hey used I In the past decade, most children's teeth in America have been sealed

with cavity-retarding dental sealants, which consist of a solution con-b, for their

. Suddenly I taining high concentrations of bisphenol-A. uring and right after the

procedure, levels of the chemical in the saliva were found to be very high11 cultures

cperiments I even six months after treatment, bisphenol-A was still leaching into

saliva. he sealants wear down after about five years, which means they) assumed are getting chewed and some, presumably, are being swallowed.65 Arel the clean these levels high enough to cause problems for children as their repro-a mistake ductive systems are developing? No one knows. But no one knows if they

are safe, either. entists have filled children's mouths with estrogenicstake. he I compounds at concentrations high enough to induce cancer in the lab, yettubes was the A has never required tests to see if these compounds are safe for

฀฀฀฀ cancer I children.66 he American ental Association's written response to thisubes with- finding was that it was "interesting." But they refused to change their rec-฀฀฀฀฀฀ that I

ommendation that all children get their teeth sealed, writing that "the bi-d Sonnen- ological implication of this observation needs to be further elucidated....lS leaching I

he A A cannot at this time draw definitive conclusions from thised plastics

I study's] observation."67

he A A is right that more research needs to be done before we canlphenol, a say the estrogenic substances leaching into children from dental sealantsas paints, I harm them. But does that mean it's fine to continue business as usual, invas one of

I the absence of evidence that shows the compounds are safe? Althoughestrogenic

:ed chemi- the A requires pharmaceutical manufacturers to show that their drugs

be weakly I do not cause harm, no such requirement exists for other chemicals.

Chemicals are assumed safe until proven to cause harm in humans-butIn Britain I the problem is that is nearly impossible to do this, since it is consideredear, and a

ns of fifty unethical to test potentially toxic compounds on human fetuses. I Animal experiments show that prenatal exposure to bisphenol-Acer cell re-

causes mice to enter puberty earlier and to weigh 0 percent more than I

rly 1 0s. normal (how ironic if Americans turn out to be getting fatter not just be-

cause we exercise less and eat more fast food, but also because we had฀฀฀฀฀฀฀฀฀฀ I loted "ex- prenatal exposure to endocrine disrupters).68 Japanese researchers re-

phenol-A cently demonstrated that the placenta does not act as a barrier to bisphe- t

it formed nol-A. In only twenty minutes, maternally ingested bisphenol-A reached

v used for maximum concentration in the fetuses of lab rats. 6I ฀฀฀ dental om Saal's early work on the low-level effects of hormones had stim-

phenol-A I ulated heo Colborn to develop the endocrine disruptor hypothesis. Re-

I

I

"T'

I 146 BODIES

cently, vom Saal showed that extremely low levels of bisphenol-A-the

levels found in our background, our levels of "normal" exposure--could

induce potent responses. These are levels thought completely trivial by

traditional toxicology. These are the background levels experienced by

most of us living our normal lives in the normal world, not the levels of

those living near a toxic waste dump. As OUf Stolen Future's Web site

states, "Vom Saal's work shows that every day levels matter."70

A third group of chemicals used in making plastics that leach estro-

genic compounds are phthalates. These are incredibly common sub-

stances, perhaps the most abundant synthetic compounds in the

environment. Phthalates are oily solvents that make plastics flexible but

strong. Since phthalates need to be flexible, that means the molecules

can't be too rigidly locked together, for flexibility requires molecules that

slide over each other. But that lack of molecular rigidity also means they

leach out easily.71 Phthalates keep your car dashboard from cracking and

your nail polish from splintering; they allow plastic wrap to be shaped

around food. They help cosmetics absorb quickly into your skin, so they

are added to shampoos, skin creams, sunscreens-all the stuff we smear

on our skin to stay pretty. In fact, as ABC News reported, loopholes in

federal laws allow cosmetics manufacturers to put unlimited amounts of

industrial chemicals such as phthalates into personal care products with-

out any testing for adverse health effects.72

Phthalates are in all of us. In March 2001, the U.s. Centers for Disease

Control recently released the results of its first study of the levels of

twenty-seven chemicals found within American bodies. Researchers

found phthalates in nearly every person they examined (out of 3,800 peo-

ple drawn from healthy individuals around the country with no special

exposure to toxic substances),73 The highest concentrations came from

certain phthalates (such as di-ethyl phthalate) used in toiletries like bar

soaps, perfumes, and shampoos, perhaps because direct skin contact in-

creases body burden. Some of the highest concentrations were in women

of childbearing age-not the results anyone wanted to find, since fetal ex-

posure is likely to be the riskiest?4 These levels were much higher than

scientific models and a government panel had predicted just six months

earlier.

In mice, phthalates "undermine the masculinity of mice exposed

during lactation and weaning, creating individuals with both male and

female sexual (intersex) characteristics."75 They do this by blocking the

action of male sex hormones as they program sexual development. A

team of Environmental Protection Agency researchers led by L. Earl Gray

Jr. gave phthalates to female rats from weaning through lactation at doses

of two hundred to one thousand milligrams per kilogram of body weight

(levels similar to those that people are exposed to). The sons of these rats

produced f

ticle,76 Anc

Chemicall

in male roc

grams of F

testosteron

when the c

What

necting hu

tion, not c

study indic

velopment

girls,?8 Pm

opment ev

high ฀฀฀฀฀฀

ganic polh

normal se:

widely USE

indicated'

breasts at i

Yet ar

higher the

curred in t

PCBs and ,

migrant g

metabolite

gen mimic

not proof I

man healtl

when girl:

even with

tion with (

Recer

American

younger t]

exposure

Marcia HE

girls were

year earliE

the best q

by those t

girls were

percent of

I'

I NANCY LANGST N 1 7

I

1e I produced far less testosterone than normal, and some males lacked a tes-

Id ticle.76 Another team of researchers from an industry group known as the

)y Chemical Industry Institute of Toxicology found developmental defects I

)y in male rodents whose mothers were given as little as one hundred milli-

of grams of phthalate per kilogram of body weight. The chemical halvedI ete testosterone production in the fetus while leading to testicular tumors

I when the animals became adults.77

'0- hat do these results mean for people Nobody knows yet; con-

b- I necting human problems to phlatate exposure is an exercise in correla-

he tion, not causation. For example, consider early puberty. ne recent ,ut I study indicates that in Puerto ico, girls who show premature breast de-

les velopment have significantly elevated phthalate levels compared to other Itat girls.78 Puerto ico has the highest incidence of premature breast devel-

ey opment ever reported, and 70 percent of girls studied have significantly Ind high levels of phthalates. As the authors of this study wrote, "Some or-

ed ganic pollutants, including pesticides and some plasticizers, can disrupt I

ey normal sexual development in wildlife, and many of these have been

฀฀฀ widely used in Puerto ic ."79 Another study on these Puerto ican girls I in indicated that those who had consumed DES in meat developed large of I breasts at an early age and had other signs of precocious puberty.8o

th- Yet another study (this time in North Carolina) showed that the

higher the level of prenatal exposure to PCBs, the earlier puberty oc-I lse curred in the girls, while a study in ichigan found a correlation between of PCBs and early onset of menstruation.81 A Belgian study showed that im-

ers migrant girls with precocious puberty had higher levels of D E (a eo- metabolite of DDT) in their blood.82 Such correlations suggest that estro- :ial gen mimics might contribute to premature puberty, but correlations are m not proof of a causal relationship. Proving that an observed trend in hu-

oar man health is real turns out to be very difficult, for we lack good data on in- when girls entered puberty in the early twentieth century. oreoever, len even with good historical records, it is nearly impossible to prove causa- ex- tion with correlations. Ian ecent research has found that some girls-particularly African- ths American and Latina girls-are developing breasts and pubic hair much

younger than in past generations, a trend that may be linked to estrogen sed exposure (although the source of those estrogens is not clear). In 1997, md arcia erman-Giddens's data on 17,707 American girls suggested that the

I

girls were developing breasts and pubic hair' on average as much as a .A year earlier than expected based on historical data (data that were not of ray

I

the best quality). Not only did the average age of puberty (as measured lses I by those two indices) appear to be decreasing, but significant numbers of ght girls were maturing sexually long before the average. By age eight, 8 rats I percent of black girls and almost 15 percent of white girls were showing

I

I ........

148 BODIES

signs of sexual development.; 3 percent of African-American girls had be-

gun to develop breasts by the age of three.83

Why would some girls be entering puberty earlier? Some of the

changes may be due to changes in diet, which as mentioned earlier have

led to increased estrogen exposure. Some of the changes may be due to in-

creases in obesity, which is correlated with increased estrogen in the body

(as well as with increased leptin, a hormone that is also linked with the

onset of puberty).84 Some of the changes may be due to synthetic estrogen

mimics in the environment, while others may be due to social factors such

as increased exposure to sexual stimuli in the culture, which might trig-

ger a girl's body to begin puberty early. Although the science on people is

uncertain, animal experiments do show that exposure to estrogen mimics

reduces the age of puberty, suggesting the same might be true in girls. For

example, a recent experiment reported in Nature showed that pregnant

mice exposed to bisphenol-A at "a dose equivalent to that typically found

in the environment" had daughters who entered puberty early.85

What do we do with this research? How do we think about women's

health from a historical perspective in a world where chemical contami-

nation may be changing fundamentally the biological nature of what

makes us female? Women's bodies are biologically different from men's

bodies; sexual differentiation is not just a cultural construction. Yet the

biological differences between men and women are also shaped by cul-

ture and by cultural expectation.86 For example, consider sexual size di-

morphism, which is a measure of the size differences between men and

women. Male humans are, on average, larger than female humans. Yet

these differences, while partly biological, are also shaped by culture. The

degree of difference in size predicted by biological factors is much

smaller than the actual difference you observe in many segments of

American culture. Why? Largely because societal pressures on women to

diet increase the amount of sexual size dimorphism in white American

culture. Expectations for women to be thin (or, in different cultures, to be

fat) are clearly cultural constructions that can magnify the effects of ge-

netic differences between men and women.87

Because women's bodies are biologically and culturally different

from men's bodies, women react to endocrine disruptors differently than

men do, and "women may be disproportionately affected by environ-

mental pollution."88 Or, as one government scientist put it, "Men's and

women's bodies don't just look different-they also react differently to

environmental agents."89 Women manufacture more estrogen than men

do, so they are exposed to more estrogen to start with. Women tend to

carry more fat, and fat is where most endocrine disruptors are stored and

can accumulate. Our ovaries and breasts have very high fat concentra-

tions, making them especially vulnerable to endocrine disruptors. Be-

T

I

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during [dietiJI a significant j

factors. "90 We I

than men do,

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tied to culture

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menstrual cycJ

eat more fish.

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Barbara J. Da\

"the effects of

Two incre

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sure to estrogc

gens).96 And 1:

1950s. EndOffil

King novel, oe

lines the ฀฀฀฀฀฀

and implants

vagina. Endorr

Sons it is incre

percent of prer

the world's hig

an girls had be-

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led earlier have

tay be due to in-

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estrogen mimics

true in girls. For

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t typically found T ฀฀฀฀฀฀฀฀

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lemical contami-

nature of what

-rent from men's

truction. Yet the

) shaped by cul-

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etween men and

tale humans. Yet

:i by culture. The

factors is much

my segments of

res on women to

white American

nt cultures, to be

the effects of ge-

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s differently than

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)rs are stored and

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1

I NANCY LANGSTON 149

I

cause of pressures on white American women to diet, their weight tendsI to yo-yo more than men. "If toxicants stored in fat tissue are mobilized

during [dieting], as some researchers have suggested, then this could beI a significant factor in gender differences in responding to environmental

factors."9o Women retain higher levels of certain pollutants such as dioxinI than men do, for reasons that aren't yet dear.91 Women have smaller liv-

I ers with less capacity for getting rid of toxic chemicals, and their livers

are more susceptible to damage from alcohol, which in turn exposes them

I to more problems from endocrine disruptors.

Women's production of babies illustrates the tangled relationships I between cultural and biological constructions of gender.92 The timing and

numbers of pregnancies are partly constrained by biology-two-year-old I girls and ninety-year-old women don't get pregnant. But within those bi-

ological constraints, cultural forces shape whether a woman spends all I

her reproductive years pregnant or whether she spaces her pregnancies

by choice, American women have fewer children than women at the turnI of the century for reasons that are largely social and political, but biolog-

ical factors related to chemical influences on fertility may also playa role.I Infertility appears to be increasing in American women (and in

American men, but that is a different story). Part of this trend is probablyI tied to cultural changes: many women are delaying their first pregnan-

cies, and older women are biologically less fertile. But infertility is also I linked to chemical con!aminants-causes that are environmental and po-

[ litical, not just personal. For example, women who eat fish from Lake On-

tario (contaminated with PCBs) are less likely to conceive during a given

I menstrual cycle than those who eat less contaminated fish.93 Women who

eat more fish from Lake Michigan (again, contaminated with PCBs) are \ much more likely to have problems with their pregnancies, if they can

even get pregnant.94 Some phthalates clearly harm the ovaries in rodents; I Barbara J. Davis, the leading researcher on ovarian toxicity, argues that

"the effects of DEHP [a phthalate] could lead to infertility."95 I Two increasingly important causes of female infertility in America

are endometriosis and uterine fibroid tumors. Both are affected by expo-I sure to estrogens (the body's own estrogens as well as synthetic estro-

gens).96 And both problems have become far more common since theI 1950s. Endometriosis, which sounds like something out of a Stephen

King novel, occurs when endometrial tissue-the tissue that normally \

lines the uterus and gets shed during a period-grows outside the uterus

I and implants itself on the ovaries, fallopian tubes, bladder, bowel, or

vagina. Endometriosis can often lead to infertility, and for unknown rea-

I sons it is increasing in industrialized nations. Anywhere from 10 to 15

percent of premenopausal women suffer from the disease. Belgium has I the world's highest incidence; 60 to 80 percent of Belgian women who are

I

1

150 BO IES

infertile or have pelvic pain have endometriosis. Although the exact

cause is unknown, we do know that many of the risk factors are related

to estrogen exposure and so environmental estrogens may contribute. 7

or example, dioxin is a known estrogen mimic, and monkeys given

dioxin have been shown to develop endometriosis. Belgian breast milk

has some of the highest dioxin levels in the world, and some small stud-

ies have shown that dioxin levels are highest in women with en-

dometriosis. Other studies, however, have not found that infertile women

who had the disease had higher levels of dioxin in their blood than in-

fertile women who didn't have it. 8

ibroids are another example of a condition often leading to infertil-

ity that may be related to endocrine disruptors. he most common tu-

mors in women are nonmalignant ones in the uterus called fibroids (or,

more technically, uterine leiomyomas), which are clearly linked to estro-

gen exposure. ibroids are the leading cause for hysterectomies-at least

550,000 American women a year have hysterectomies because of problems

with them. Clinical studies show that these tumors are increasingly com-

mon. In one large study, 77 percent of women had fibroids growing in

their uteruses (most of these tumors were subclinical-too small to cause

problems), with the highest rates in African-American women.1 0o Another

study found that 73 percent of black women had uterine fibroids com-

pared to 48 percent of white women.lOl Animal studies show that en-

docrine disruptors increase fibroid growth in rodents and monkeys, yet no

human studies have been published that examine this potential link.10

he womb is an environment of its own, yet one that is linked to the

outside world. he chemicals that a woman has been exposed to through-

out her life-not just what she consumes while she's pregnant-reach her

fetus, connecting one generation to the other. regnant women hope that

if they don't take weird drugs like thalidomide or ES, their children will

be fine. But chemical contamination is inside most women: 30 percent of

pregnant women in one study had detectable levels of CBs, , and

lindane and estrogenic compounds in their amniotic fluid, many at con-

centrations high enough to cause problems in lab animals.l03 And these

background levels of chemicals could have effects on developing fetuses.

or example, in Missouri, the state health department showed that chil-

dren exposed to pesticides in the womb developed 600 percent more

brain cancer than other children (which sounds terrible, but the levels

were still extremely low). sing roach control chemicals during preg-

nancy led to a doubled risk of cancer in the child using termite pesticides

led to a 300 percent increase in brain cancer in the children. Yet the mes-

sage that pregnant women shouldn't be using toxic chemicals is not get-

ting out: the Missouri State Health epartment found that 80 percent of

pregnant women used pesticides while pregnan 04

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in breast milk I

ronmental Heal

nated with eI

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claims of the en

scientists, even t

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chemicals can bi

expression. he)

centrations of ce

most people are

lems. hey agre

cells multiply iJ

build up in hull'

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are related

mtribute.97

(eys given

reast milk

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with en-

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d than in-

; to infertil-

ammon tu-

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growing in

all to cause ,100 Another

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\

A CY LA GSTO 151

l Once a baby is born, problems don't stop there. ust about the only

way for a woman to reduce her own body's burden of toxic chemicals is

[ to breast-feed, since many of those toxic chemicals end up in breasts and

only leave the woman's body within her breast milk. But there's an obvi-

I ous problem here, since she's giving those toxic chemicals to her child.

Breast milk is the food with the highest levels of PCBs and DDT and its

I metabolites such as DOEs (all endocrine disruptors ,105 In 1976, 99 per-

cent of women's breast milk in America contained PCBs; a uarter had I concentrations exceeding the legal limit (these concentrations have been

declining since regulations reduced PCB use . The PCBs in breast milk I can get into the children's blood; a 1998 study from the etherlands

showed that the blood of children who were breast-fed as infants had I three times the levels of PCBs than children who weren't breast-fed.106

What do these levels mean for children obody knows for sure. A I

long-term study of children in the etherlands finds that background

levels of prenatal PCB exposure experienced in the womb led to higher I

risk for childhood diseases, while "the latest study of the cohort of boys

exposed in the womb to PCBs because of cooking oil contamination inI Taiwan finds significant degradation in sperm uality in exposed indi-

viduals compared to their unexposed counterparts."107 PCBs are labeledI as a probable human carcinogen by the u.s. Environmental Protection

Agency, while other studies show that they affect learning in both ani-

mals and humans. But could the levels found in breast milk harm chil-

dren The answer is unclear, since studies on postnatal exposure to PCBs

in breast milk have been inconclusive. The ational Institute for Envi-

I ronmental Health Sciences argues that breast milk, even when contami-

nated with PCBs and pesticides and other endocrine disruptors, is still I better for the child than formula (especially given that both soy- and

dairy-based formulas have their own sources of estrogens and estrogen \ mimics .108

II

Are endocrine disruptors a serious problem or not Some of the central

claims of the endocrine disruption hypothesis are now agreed upon by all \

scientists, even those from industry. Everyone agrees that wildlife exposed

to certain synthetic chemicals demonstrate responses similar to those in-I duced by sex hormones. They agree that lab studies show that synthetic

I chemicals can bind with and activate hormone receptors, resulting in gene

expression. They agree that exposing pregnant mice to extremely low con-

I centrations of certain synthetic chemicals-concentrations similar to those

most people are exposed to-results in offspring with reproductive prob- I lems. They agree that some synthetic chemicals can make breast cancer

cells multiply in culture. They agree that persistent organic chemicals \ b ild up in human tissue and are passed to the developing fetus and to

I

1

152 BODIES

the breast-feeding infant. They agree that many male fish and alligators

exposed to industrial effluent show signs of feminization, a result also

found in the lab when eggs are exposed to some synthetic chemicals.l09

But people still disagree on a fundamental issue: what do these ani-

mal and lab studies mean for people? Do average people-those who

don't work at toxic waste sites, for example-have anything to worry

about? Can endocrine disruptors explain any of the apparent increases in

infertility, reproductive cancers, birth defects, reduced sperm counts, or

lowered ages of puberty? Or are endocrine disruptors present at such low

levels that they are a trivial concern?

Circumstantial evidence is accumulating that supports the hypothe-

sis that endocrine disruptors may be harming male reproductive health,

while experimental studies have shown similar effects in laboratory ani-

mals. But you cannot ethically do these experiments on human fetuses to

test whether the correlations between endocrine disruptors and repro-

ductive disorders are real. Instead, we have to rely on epidemiology,

which cannot always untangle confounding variables. Since we can't eth-

ically do experiments on fetal exposure in humans, we need to rely on the

weight of the evidence, rather than experimental proof, to form policy.1l0

And this assumption is where reasonable people disagree.

In August 1999, the National Research Council (of the National Acad-

emy of Sciences) released its consensus report on endocrine disruption, a

report commissioned in 1995 by the EPA and Congress. The team of au-

thors included independent scientists who are proponents of the hypothe-

sis as well as those with strong ties to industry who are critics of it. After

four years of review and debate, the team finally managed to agree that en-

docrine disruptors at high concentrations do affect human and wildlife

health, yet they could not agree on the extent of harm caused by levels

common in the environment. Moreover, they argued that their disagree-

ments were not only due to gaps in scientific knowledge but also to major

epistemologic differences on how one interprets data and draws conclu-

sions. The consensus report stated: "Much of the division among commit-

tee members appears to stem from different views of how we come to

know what we know. How we understand the natural world and how we

decide among conflicting hypotheses about the natural world is the

province of epistemology. Committee members seemed to differ on some

basic epistemologic issues, which led to different interpretations and con-

clusions on the issues of hormonally active agents in the environment."m

The chemical industry's response to this report was to focus on the

conclusion that no scientific certainty on human health effects had been

established. Without certainty, the industry argued, endocrine disruption

was not an issue for public health concern. As Myers argues, "This is a

classic argument from industry spokespeople: that the absence of data

'T

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proves safety.

firm proof, "'-

should do not

response is UT

ity stated, "Wt

spread exposl

to multiple m.

quirements fo

quirement for

which fail to e

As indivi,

write this, I pa

there might p

cals in which '

ican womenn

presence of es

drink my weI

ruptor), when

when I padd

nearby wildlif

der what strar

When I \\

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lands. For sou1

cry overhead,

coons and wo,

out in the sun

rated with ฀฀฀฀

water runs

der if I really \"

and hawks ar

residues end u

low backwater

soup. Can any

ally knows.

What we (

gets sprayed 0

in the fish, the

also ends up iT

wildlife and w

studies of wile

connect enviroJ

of wild places.

and alligators

, a result also

chemicals.l 9

: do these ani-

e-those who

1ing to worry

nt increases in

฀฀฀ counts, or

฀฀฀ at such low

s the hypothe-

luctive health,

aboratoryani-

man fetuses to

)rs and repro-

epidemiology,

e we can't eth- Id to rely on the

Iform policy.no

' ational Acad-

e disruption, a l Ibe team of au-

of the hypothe-

litics of it. After

bagree that en-

n and wildlife

used by levels

their disagree-

lt also to major

draws conelu-

mong commit-

IW we come to

Id and how we

l฀ world is the

Idiffer on some ations and con-

iwironment." 112

Ito focus on the 1- bi:fects had een

rine disruption ,"ues "This is a i' , .

bsence ot data

'I

\

NAr--;CY LANGST N 153

I proves safety. In reality, all it proves is ignorance. "ll3 So, in the absence of

\ firm proof, what should society do Many in industry argue that we

should do nothing until we have absolute proof. thers argue that such a I

response is unethical, for as the Boston Physicians for Social Responsibil-

I ity stated, "We are engaged in a large global experiment. It involves wide-

spread exposure of all species of plants and animals in diverse ecosystems

to multiple manmade chemicals.... The limits of science and rigorous re-I quirements for establishing causal proof often conspire with a perverse re-

I quirement for proving harm, rather than safety, to shape public policies

which fail to ensure protection of public health and the environment."114

I As individuals, what do we do with this uncertain information? As I

write this, I pat my own fibroid-filled belly and wonder what connections \ there might possibly be between my own tumors and the sea of chemi-

cals in which we've immersed ourselves. Like the vast majority of Amer- I ican women now, inside my uterus I have cells gone wild, cells that in the

presence of estrogen mushroom into tumors beyond my control. When I I drink my well water (tainted with atrazine, yet another endocrine dis-

ruptor), when I eat my plastic-wrapped cheese soaked in phthalates,

when I paddle my kayak through the pesticide-laden waters of the

nearby wildlife preserve, when I walk through my ordinary days, I won-

der what strange world we've created for ourselves.

When I was writing this chapter, I spent a lot of time on the Sugar

River, a little muddy river that runs through wildlife refuges and farm-

lands. For southern Wisconsin, this is a wild place. Herons rise up, hawks

cry overhead, geese and cranes and mallards and wood ducks fly, rac-

coons and woodchucks and chipmunks and squirrels and coyotes hang

out in the surrounding forest. Yet for all its wildness, the water is satu-

rated with poisons. When I dip the paddle blade too deeply into the river,

water runs over the shaft and down my wrists, and I can't help but won- I der if I really want that water anywhere near my skin. I watch the herons

and hawks and cranes around me and wonder how many pesticide I residues end up in their body fat. Hunters motor their boats into the shal-

low backwaters, and solvents from their fuel tanks add to the chemicalI soup. Can any of this hurt us? Can any of it hurt the birds? Nobody re-

ally knows. I

What we do know is that we're all in this together: the atrazine that ,

gets sprayed on my neighbor's cornfield ends up in the river water, then

in the fish, then in the herons and the raccoons that eat the fish-and it

also ends up in my breasts, my belly, and my blood. What's out there in I Wildlife and wild places is also in our bodies. Just as Colborn connected

studies of wildlife with studies of human bodies, endocrine disruptorsI connect environmental histories of the body withenvironmental histories

\ of wild places and wild animals.

1 \

T 154 BODIES

I One of our culture's fondest illusions is that we can control our sep-

aration from nature: we can visit nature when we feel like it and live in a

human world the rest of the time. According to a commentator on Na-

tional Public Radio, most Americans spend only fifteen minutes outside

each day. The rest of the time we drive in our cars, stare into our com-

puter screens, watch our TVs, sit in our offices or schools, eat our phtha-

late-saturated suppers, and think the rest of the world is outside, staying

where it belongs. But that's not true. What is outside has come inside,

making itself at home in our testes, in our wombs, in our most private re-

productive dysfunctions. The environment includes wild places and wild

things, but it also includes hair dye, golf courses, and ice cream-all full

of endocrine disruptors. Our most intimate reproductive environments,

the places that make us most female or most male, the places we are most

vulnerable and most natural, may have been hijacked by the residues of

our industrial world. This is a disturbing thought.

NOTES

1. For an example of the media response, see Elizabeth Smith, "Fibrocystic

Breast Diseases Provoked by Xenoestrogens Are Found in Everyday Synthetic

Materials," n.d., http://wwwjibrocystic.com/xeno.htm. For the research, see S.

Jobling and J. Sumpter, "Detergent Components in Sewage Effluent Are Weakly

Oestrogenic to Fish: An In Vitro Study Using Rainbow Trout (Onchorhynchus

mykiss) Hepatocytes," Aquatic Toxicology 27 (1994): 361-72; S. Jobling, C. Tyler,

M. Nolan, and J. P. Sumpter, The Identification of Oestrogenic Effects in Wild Fish

(1998), Technical Report W119, BruneI University Environmental Agency Na-

tional Fish Health Laboratory; C. E. Purdom, P. A. Hardiman, . J. Bye, N. C. Eno,

C. . Tyler, and J. P. Sumpter, "Estrogenic Effects of Effluents from Sewage-Treat-

ment Works," Chemistry and Ecology 8 (1994): 275-85; and T. P. Rodgers-Gray,

S. Jobling, S. Morris, C. Kelly, S. Kirby, A. Janbakhsh, J. E. Harries, M. J. Waldock,

J. P. Sumpter, and C. . Tyler," Long-Term Temporal Changes in the Estrogenic

Composition of Treated Sewage Effluent and Its Biological Effects on Fish," Envi-

ronmental Science and Technology 34 (2000): 1521-28. For a useful overview of re-

search on sexual disruption in fish, see S. Jobling, M. Nolan, C. . Tyler,

G. Brighty, and J. P. Sumpter, "Widespread Sexual Disruption in Wild Fish," En-

vironmental Science and Technology 32 (1998): 2498-2506.

2. J. P. Sumpter and S. Jobling, "Vitellogenesis as a Biomarker for Estrogenic

Contamination of the Aquatic Environment," Environmental Health Perspectives

103, Supp!. 7 (1995): 173-77; and J. E. Harries, D. A. Sheahan, S. Jobling,

P. Matthiessen, P. Neall, J. P. Sumpter, T. Tylor, and N. Zaman, "Estrogenic Activ-

ity in Five United Kingdom Rivers Detected by Measurement of Vitellogenesis in

Caged Male Trout," Environmental Science and Toxicology 16 (1997): 534-42.

3. J. Raloff, "The Gender Benders: Are Environmental 'Hormones' Emascu-

lating Wildlife?" Science News 145 ( January 8, 1994): 24; online at http://www.

sciencenews.org/s.

ethynylestradiolI instruments wer

, Environm,I http://ehpnet1.nie!

I 4. Both the.

tors have exploc

general attentior

Peterson Myers,

and Survival? (Nt

the hypothesis is

gins of the EnvirOi

sity Press, 2000,

endocrine disrup

tal Effects of End,

menta] Health ฀฀฀฀

journalism on en.

eluding "Excretec

"Macho Waters: ฀

(January 6, 2001)

(April 3, 1999): 21

26,1997): 254; "SF

1997): 142; "Are 1

monal' ฀฀฀฀฀฀฀฀฀฀

5. For a discL

Landa Schiebinge

Beacon Press, 199.

to Freud (Cambrid

The Body Project: A 1997).

6. For a disc

mental history, sec

mental History," I

7. L. C. Folm

Marcino, and L.

Testosterone Conc

Major Metropolita

104 (1996): 1096-1

see S. L. Goodbrec

R. Schoeb, Reconnc

nad Histopathology

nant-Induced Endo

96-627.

8. Chris Mete.

ment" (abstract, (

gsa. confex. coI11/gsa/L

"Excreted Drugs."

control our sep-

e it and live in a

1entator on Na-

minutes outside

'C into our com-

" eat our phtha-

outside, staying

las come inside,

most private re-

l places and wild

e cream-all full

'e environments,

aces we are most

y the residucs of

:3mith, "Fibrocystic I h . I:veryday Synt ehc

฀฀ research, see S.

!ffluent Are Weakly

I'JUt (OnchorhynchuS

I;. Jobling, C. Tyler,

IEffects in Wild Fish

Ilental Agency Na-

IV. J. Bye,]\i. C. Eno,

I'rum Sewage-Treat- I

r. P. Rodgers-Gray,

des, :vI. J. Waldock,

's in the Estrogenic

'ects on Fish," Envi-

'ful overview of re-

฀฀฀฀฀฀ C. R. Tyler,

1 in Wild Fish," En-

lrker for Estrogenic

Health Perspectives

,eahan, S. Jobling,

, "Estrogenic Activ-

of Vitellogenesis 1Il

997): 534-42.

10rmones' EmasCu-

nline at http://Wzvw,

NANCY LANGSTON 155

sciencenews.org/sn_edpikllsj.htm. This finding didn't rule out the possibility that

ethynylestradiol was in the river at biologically active concentrations since their

instruments weren't powerful enough to detect the chemicals. See C. Potera, "Fo-

rum," Environmental Health Perspectives 108 (October 2000): 108--10; online at

http://ehpnet1.niehs. nih.gov/docs/2000/1 08-1 Olforum.html#wa ter.

4. Both the scientific research and the popular writing on endocrine disrup-

tors have exploded in recent years. The important popular work that brought

general attention to the issue was Theo Colborn, Dianne Dumanoski, and John

Peterson Myers, Our Stolen Future: Are We Threatening Our Fertility, Intelligence,

and Survival? (New York: Plume, 1997). A scholarly examination of the origins of

the hypothesis is Sheldon Krimsky, Hormonal Chaos: The Scientific and Social Ori-

gins of the Environmental Endocrine Hypothesis (Baltimore: Johns Hopkins Univer-

sity Press, 2000). An early scientific review article summarizing effects of

endocrine disruptors is T. Colborn, F. S. vom Saal, and A. M. Soto, "Developmen-

tal Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans," Environ-

mental Health Perspectives 101 (1993): 378-84. For an overview of popular scientific

journalism on endocrine disruptors, see Janet Raloff's series for Science News, in-

duding "Excreted Drugs: Something Looks Fishy," vol. 157 (January 22, 2000): 66;

"Macho Waters: Some River Pollution Spawns Body-Altering Steroids," vol. 159

(January 6, 2001): 8-10; "Common Pollutants Undermine Masculinity," vol. 155

(April 3,1999): 213; "Hormone Mimics Get Harder to Pigeonhole," vol. 151 (April

26,1997): 254; "Sperm Changes Linked to Drinking Water," vol. 145 (February 26,

1997): 142; "Are Men Suffering from Prenatal or Childhood Exposures to 'Hor-

monal' Toxicants?" vol. 145 (Jan. 22, 1994): 56.

5. For a discussion of historical constructions of gender in earlier periods, see

Landa Schiebinger, Nature's Body: Gender in the Making of Modern Science (Boston:

Beacon Press, 1993); Thomas Laquer, Making Sex: Body and Gender from the Greeks

to Freud (Cambridge, Mass.: Harvard University Press, 1990); and Joan Brumberg,

The Body Project: An Intimate Histury ufAmerican Girls (New York: Random House,

1997).

6. For a discussion of the importance of considering the body in environ-

mental history, see C. Sellers, "Thoreau's Body: Towards an Embodied Environ- I mental History," Envirunmental History 4 (October 1999): 486-514.

7. L. C. Folmar, N. D. Denslow, V. Rao, M. Chow, A. D. Crain, J. Enblom, J. I Marcino, and L. J. Guillette Jr., "Vitellogenin Induction and Reduced Serum

Testosterone Concentrations in Feral Male Carp (Cyprinus carpio) Captured near a I Major Metropolitan Sewage Treatment Plant," Environmental Health Perspectives

104 (1996): 1096-1101. For a comparison across five regions of the United States, I See S. L. Goodbred, R. J. Gilliom, T. S. Gross, N. P. Denslow, W. L. Bryant, and T.

R. Schoeb, Reconnaissance uf 17jJ-Estradiol, ll-Ketotestosterone, Vitellogenin. and Go- I nad Histopathology in Common Carp of United States Streams: Potential for Contami-

nant-Irlduced Endocrine Disruption, U.s. Geological Survey Open-File Report

I 96-627.

8. Chris Metcalfe, "Sex and Sewage: Estrogenic Compounds in the Environ- I ment" (abstract, Geological Society of America annual meeting, 2001), http://

฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀ reviewed in Raloff,

I Excreted Drugs."

I

1

"."

156 BODIES

9. C. G. Daughton and T. A. Ternes, "Pharmaceuticals and Personal Care

Products in the Environment: Agents of Subtle Change?" Environmental Health

Perspectives 107, Suppl. 6 (December 1999): 907-38.

10. Raloff, "Common Pollutants Undermine Masculinity."

11. For the story on the students, see Raloff, "Macho Waters." For the re-

search, see R. A. Angus, H. McNatt, W. M. Howell, and S. D. Peoples,

"Gonopodium Development in Normal and 11-Ketotesfosterone-Treated Mos-

quitofish (Gambusia affinis): A Quantitative Study Using Computer Image Analy-

sis," General and Comparative Endocrinology 123 (2001): 222-34; R. Jenkins, R. A.

Angus, H. McNatt, W. M. Howell, J. A. Kemppainen, M. Kirk, and E. M. Wilson

"Identification of Androstenedione in a River Containing Paper Mill ฀฀฀฀฀฀

ent,"Environmental Toxicology and Chemistry 20 (2001): 1325-31; and K. R. Munkit-

trick, M. E. McMaster, L. H. McCarthy, M. R. Servos, and G. J. Van Der Kraak, "An

Overview of Recent Studies on the Potential of Pulp Mill Effluents to Alter Re-

productive Parameters in Fish," Journal of Toxicology and Environmental Health,

Part B 1 (1998): 347-71 .

12. William P. Davis of the EPA, cited in Raloff, "Macho Waters."

13. L. H. Guillette Jr., T. S. Gross, G. R. Masson, J. M. Matter, H. F. Percival,

and A. R. Woodward, "Developmental Abnormalities of the Gonad and Abnor-

mal Sex Hormone Concentrations in Juvenile Alligators from Contaminated and

Control Lakes in Florida," Environmental Health Perspectipes 102 (1994): 680-88.

14. C. F. Facemire, T. S. Gross, and L. J. Guillette Jr., "Reproductive Impair-

ment in the Florida Panther: Nature or Nurture?" Environmental Health Perspec-

tives 103, Suppl. 4 (1995): 79-86. For work on salmon, see J. J. Nagler, J. Bouma,

G. H. Thorgaard, and D. D. Dauble, "High Incidence of a Male-Specific Genetic

Marker in Phenotypic Female Chinook Salmon from the Columbia River," Envi-

ronmental Health Perspectives 109 (2001): 67-69. For a review, see J. Raloff, "Salmon

Puzzle: Why Did Males Turn Female?" Science News 158 (December 23, 2000):

404-5, online at http://www.sciencenews.org/20001223;Job2.asp. and Raloff, "The

Gender Benders."

15. T. Schettler, "Endocrine Disruptors: The State of the Science," Greater

Boston Physicians for Social Responsibility (1997), online at http://www.psr.

org/tedfs.htm.

16. This particular report was from the BBC, September 2000; cited at Our

Stolen Future's Web site, written and maintained by John Peterson Myers. The

Web site maintains abstracts on recent research and links to scientific journals; see

http://www.ourstolenfuture.org.

17. Raloff, "Macho Waters." See also J. Oehlmann, U. Schulte-Oehlmann,

M. Tillmann, and B. Markert, "Effects of Endocrine Disruptors on Prosobranch

Snails (Mollusca: Gastropoda) in the Laboratory. Part I: Bisphenol-A and

Octylphenol as Xenoestrogens," Ecotoxicology 9 (2001): 383-97; P. E. Gibbs, P. L.

Pascoe, and G. W. Bryan, "Tributyltin-Induced Imposex in Stenoglossan Gas-

tropods: Pathological Effects on the Female Reproductive System," Comparative

Biochemistry and Physiology 100C (1991): 231-35; and G. A. LeBlanc, "Are Envi-

ronmental Sentinels Signaling?" Environmental Health Perspectives 103 (1995), and

"Steroid Hormone-Regulated Processes in Invertebrates and Their Susceptibility

to Environmental Endocrine Disruption," in Environmental Endocrine Disrupters:

I I

An Evolutionary F I and Francis, 2000

18. For the C

I pospadias, see L

Trends in Two U I analysis of intern,

eling off in many

I Rates of Hypospa

(1999): 297-302. FI

I pospadias and E

Health Perspectives

I 19. Raloff, "p R. Garcfa-Rodrigu

I Castillo, M. Espig

cides and Crypto

I Environmental Hei

Hensle, and H. H

Cohort in the UI R. Bergstrom, H.-

S. Tretli, L. Teppo,I dence in Six EuroF

I 727-33; and J. Top]

L. J. Guillette Jr., E

McLachlan, O. Mf I Sumpter, and N. E

I Xenoestrogens," E;

20. The literal

findings supporti

E. Carlsen, A. GilA

creasing Quality a

(1992): 609-13; S. H

clined? A Reanalys

(1997): 1228-32; an

clining Sperm Df

1934-1996," Envirol

For findings s

declining (at least

C. Wang, "Data fro

men Quality: Furth

graphicallY Uniforr

Goluboff, A. H. Ols

ses in 1,283 Men fl

Quality," Fertility ar

21. G. E. Dinse

explained Increases

Annual Review of Pu

22. For a revie\

1d Personal Care

'ironmental Health

ters." For the re-

I S. D. Peoples,

me-Treated Mos-

tter Image Analy-

R. Jenkins, R. A.

md E. M. Wilson,

"aper Mill Efflu-

md K. R. Munkit-

In Der Kraak, "An

lents to Alter Re-

iron mental Health,

raters."

ler, H. F. Percival,

;onad and Abnor-

:ontaminated and

. (1994): 680-88.

roductive Impair-

tal Health Perspec-

Nagler, J. Bouma,

e-Specific Genetic

nbia River: Envi-

J. Raloff, "Salmon

cember 23, 2000):

and Raloff, "The

Science," Greater

at http://www.psr.

2000; cited at Our

erson Myers. The

ntific journals; see

chulte-Oehlmann,

rs on prosobranch

Bisphenol-A and

; P. E. Gibbs, P. L.

3tenoglossan Gas-

;tem: Comparative

-Blanc, "Are Envi-

ues 103 (1995), and

heir Susceptibility

Idocrine Disrupters:

I

I

l I

I I

I

I

I I

I

I

\

I

I

I

\

I

I

\

I

I ,.....

NANCY LANGSTON 157

An Evolutionary Perspective, ed. L. H. Guillette Jr. and D. A. Crain (London: Taylor

and Francis, 2000), 126-54.

18. For the CDC data that showed a doubling in the incidence of severe hy-

pospadias, see L. J. Paulozzi, J. D. Erickson, and R. J. Jackson, "Hypospadias

Trends in Two U.s. Surveillance Systems: Pediatrics 100 (1997): 831-34. For an

analysis of international data that suggests that the increases may have been lev-

eling off in many countries since 1985, see L. J. Paulozzi, "International Trends in

Rates of Hypospadias and Cryptorchidism: Environmental Health Perspectives 107

(1999): 297-302. For an overview, see L. S. Baskin, K. Himes, and T. Colborn, "Hy-

pospadias and Endocrine Disruption: Is There a Connection?" Environmental

Health Perspectives 109 (2001): 1175-83.

19. Raloff, "Are Men Suffering from Prenatal or Childhood Exposures?" See

R. Garda-Rodriguez, M. Garda-Martin, M. Nogueras-Ocana, J. de Dios Luna-del-

Castillo, M. Espigares Garda, N. Olea, and P. Lardelli-Claret, "Exposure to Pesti-

cides and Cryptorchidism: Geographical Evidence of a Possible Association:

Environmental Health Perspectives 104 (1996): 1090-95; J. M. McKiernan, T. W.

Hensle, and H. Fisch, "Increasing Risk of Developing Testicular Cancer by Birth

Cohort in the United States: Dialogues in Pediatric Urology 23 (2000): 7-8;

R. Bergstrom, H.-O. Adami, M. Mohner, W. atonski, H. Storm, A. Ekhom,

S. TretH, L. Teppo, O. Akre, and T. Hakulinen, "Increase in Testicular Cancer Inci-

dence in Six European Countries: Journal of the National Cancer Institute 88 (1996):

727-33; and J. Toppari, J. C. Larsen, P. Christiansen, A. Giwercman, P. Grandjean,

L. J. Guillette Jr., B. Jegou, T. K. Jensen, P. Jouannet, N. Keiding, H. Leffers, J. A.

McLachlan, O. Meyer, J. Muller, E. Rajpert-De Meyts, T. Scheike, R. Sharpe, J.

Sumpter, and N. E. Skakkebaek, "Male Reproductive Health and Environmental

Xenoestrogens: Environmental Health Perspectives 104, Supp . 4 (1996): 741-806.

20. The literature on declines in sperm counts is large and contentious. For

findings supporting the hypothesis that sperm counts are declining, see

E. Carlsen, A. Giwercman, N. Keiding, and N. Skakkebaek, "Evidence for De-

creasing Quality of Semen during the Past 50 Years: British Medical Journal 305

(1992): 609-13; S. H. Swan, E. P. Elkin, and L. Fenster, "Have Sperm Densities De-

clined? A Reanalysis of Global Trend Data: Environmental Health Perspectives 105

(1997): 1228-32; and S. H. Swan, E. P. Elkin, and L. Fenster: The Question of De-

clining Sperm Density Revisited: An Analysis of 101 Studies Published

1934-1996:' Environmental Health Perspectives 108 (2000): 961-66.

For findings supporting the alternate hypothesis that sperm counts are not

declining (at least in some locations), see C. A. Paulsen, N. G. Berman, and

C. Wang, "Data from Men in Greater Seattle Reveals No Downward Trend in Se-

men Quality: Further Evidence That Deterioration of Semen Quality Is Not Geo-

graphically Uniform: Fertility and Sterility 65 (1996): 1015-20; and H. Fisch, E. T.

Goluboff, A. H. Olson, J. Feldshuh, S. J. Broder, and D. H. Barad, "Semen Analy-

Ses in 1,283 Men from the United States over a 25-year Period: No Decline in

Quality," Fertility and Sterility 65 (1996): 1009-14.

21. G. E. Dinse, D. M. Umbach, A. T. Sasco, D. G. Hoel, and D. L. Davis, "Un- .

explained Increases in Cancer ฀฀฀฀฀฀฀฀฀ in the United States from 1975 to 1994:

Annual Review of Public Health 20 (1996): 173-209.

22. For a review of conflicting evidence on changes in the timing of puberty,

158 BODIES

see D. Zuckerman, "When Little Girls Become Women: Early Onset of Puberty in

Girls," The Ribbon 6 (2001); this is the newsletter for the Cornell University Pro-

gram on Breast Cancer and Environmental Risk Factors in New York State; online

at http://www.cfe.comell.edulbcerf/Newsletter/generallv6ill1ittle.girls.cftn.

23. M. E. Herman-Giddens, E. J. Slora, and R. C. Wasserman, "Secondary

Sexual Characteristics and Menses in Young Girls Seen in Office Practice: A Study

from the Pediatric Research in Office Settings Network," Pediatrics 99 (1997):

505-12; P. B. Kaplowitz, E. J. Slora, R. C. Wasserman, S. E. Pedlow, and M. E. Her-

man-Giddens, "Earlier Onset of Puberty in Girls: Relation to Increased Body

Mass Index and Race," Pediatrics 108 (2001): 347-53. For a study showing that an

endocrine disrupter advanced the age of puberty in laboratory mice, see K. L.

Howdeshell, A. K. Hotchkiss, K. A. Thayer, J. G. Vandenbergh, and F. S. vom Saal,

"Exposure to Bisphenol-A Advances Puberty," Nature 401 (1999): 763-64.

24. Krimsky, Hormonal Chaos, 2. For a list of currently known endocrine dis-

rupters, see http://www.ourstolenfuture.org/Basicslchemlist.htm. For studies from the

mid-1990s that review the data suggesting a common cause for reproductive

problems, see R. Sharpe and N. E. Skakkebaek, "Are Oestrogens Involved in

Falling Sperm Counts and Disorders of the Male Reproductive Tract?" Lancet 341

(1993): 1392-95; A. Giwercman, E. Carlsen, N. Keiding, and N. E. Skakkebaek,

"Evidence for Increasing Incidence of Abnormalities of the Human Testis: A Re-

view," Environmental Health Perspectives 101, Supp!. 2 (1993): 65-71; and E. Carl-

sen, A. Giwercman, N. Keiding, and N. E. Skakkebaek, "Declining Semen Quality

and Increasing Incidence of Testicular Cancer: Is There a Common Cause?" Envi-

ronmental Health Perspectives 103, Supp!. 7 (1995): 137-39.

25. D. Lindsey Berkson, Hormone Deception: How Everyday Foods and Products

Are Disrupting Your Hormones----and How to Protect Yourself and Your Family

(Chicago: Contemporary Books, 2000), xxii; Deborah Cadbury, Altering Eden: The

Feminization of Nature (New York: St. Martin's Press, 1999),41. For an exploration

of the meanings of estrogen, both biological and cultural, see Natalie Angier,

Woman: An Intimate Geography (New York: Houghton Mifflin, 1999).

26. Berkson, Hormone Deception, 16.

27. Mary W. Eubanks, "Focus," Environmental Health Perspectives 105 (May

1997): 5; online at http://chpnetl.niehs.nih.gov/docs/1997/105-5,1(ocus.html.

28. Ibid.

29. Berkson, Hormone Deception, 51.

30. Ibid., 48.

31. Raloff writes: "Gender-both its physical expression and its character-

istic behavior-traces more to the relative concentrations of various sex hor-

mones circulating in the body than to the mere existence of certain dominant

ones. For example,. women produce some androgens, or male hormones. In-

deed, a woman's body synthesizes estrogens from androgens such as testos-

terone. Similarly, though estradiol is the animal kingdom's primary estrogen, or

feminizing hormone, it plays important roles in both men and women. At no

time does an imbalance of sex hormones produce more obvious results than

during fetal development. Too much estrogen at the wrong moment can turn an

organism with male genes into what to all outward appearances is a female.

Similarly, an overabundance of androgens can produce the sex organs of a male

in a fetus with the ge

Childhood Exposures

32. Cadbury, Alte

33. Cadbury, Alte

34. Myers, "Cont

ample, see R. M. Shar

Adverse Effects of E

221-32.

35. Although it i:

evolutionary history, ,

current hunter-gathen

have found that AmE

many menstrual perio(

hunter-gatherer societi<

birth, nurse for 3 to 4 .

menopause of 47 years:

trast, American womer

birth, nurse for an aver

years old at menopause

their lifetime; data fron

R. A. Hatcher, J. W. We

K. R. Hill, R. Bailey, anc

lutionary Context," Q

B. Strassmann, "Menstr

tive," Journal of Women':

III, "Breast Cancer in E

Trevathan, E. O. Smith,

1999), 429--42. For a rev

Impact of Increased Me

Cancers," (2001); onlil

RcsearchPapers/RachelBm

36. Cadbury, Alter;

37. Berkson, Hormc

38. For a review of

K. Iwamoto, and E. E. H

Term Health Effects," AJ

39. Berkson, Hormo

40. Krimsky, Hormc

41. Krimsky, Hormo

42. Berkson, HomiD.

43. Berkson, Honno:

44. Cadbury, Alterir.

45. A. L. Herbst, an

lescence: A Report of 7

Mesonephromas)," Cane.

46. Editorial staff, "j

Perspectives 107 (Septem

\set of Puberty in

I University Pro-

'iork State; online

.cfm· man, "Secondary

Practice: A Study

iiatrics 99 (1997):

w, and M. E. Her-

) Increased Body

y showing that an

'y mice, see

md S. vom Saal,

J): 763-64.

wn endocrine dis-

Ir studies from the

. for reproductive

1gens Involved in

Tract?" Lancet 341

\1. Skakkebaek,

Iman Testis: A Re-

5-71; and E. Carl-

ing Semen Quality

non Cause?" Envi-

Foods and Products

, and Your Family

Altering Eden: The

For an exploration

ee Natalie Angier,

1999).

'spectives 105 (May :us.html.

\ and its character-

'f various sex hor-

f certain dominant

lale hormones. I -

฀฀฀ such as testos-

rimary estrogen, or

lOd women. At nO

lvious results than

loment can turn an

rances is a female.

ex organs of a male

I

I

I

I

I

\

I

I

I

I I I

I I

J..

NANCY LANGSTON 159

in a fetus with the genes to be female" ("Are Men Suffering from Prenatal or

Childhood Exposures?").

32. Cadbury, Altering Eden, 36; Berkson, Hormone Deception, 43.

33. Cadbury, Altering Eden, 38.

34. Myers, "Contamination Threatens a Basic Reproductive Right." For ex-

ample, see R. M. Sharpe, "Hormones and Testis Development and the Possible

Adverse Effects of Environmental Chemicals," Toxicology Letters 120 (2001):

221-32.

35. Although it is impossible to know reproductive patterns from human

evolutionary history, we can compare average numbers of menstrual cycles in

current hunter-gatherer societies with current industrial societies. Researchers

have found that American women experience approxiamably three times as

many menstrual periods as women in foraging societies. For example, women in

hunter-gatherer societies are about 16 years old at menarche, 19.5 years old at first

birth, nurse for 3 to 4 years, average 5.9 live births, and have an average age at

menopause of 47 years, with an average of 160 ovulations in their lifetime. In con-

trast, American women average 12.5 years old at menarche, 24 years old at first

birth, nurse for an average of 3 months, average 1.8 live births, and average 50.5

years old at menopause, with an average of approximately 450 ovulations within

their lifetime; data from S. B. Eaton, M. C. Pike, R. V. Short, N. C. Lee, J. Trussell,

R. A. Hatcher, J. W. Wood, C. M. Worthman, N. G. Blurton Jones, M. J. Konner,

K. R. Hill, R. Bailey, and A. M. Hurtado, "Women's Reproductive Cancers in Evo-

lutionary Context," Quarterly Review of Biology 69 (1994): 353-67. See also

B. Strassmann, "Menstrual Cycling and Breast Cancer: An Evolutionary Perspec-

tive," Journal of Women's Health 8 (1999): 193-202; and S. B. Eaton and S. B. Eaton

lII, "Breast Cancer in Evolutionary Context," in Evolutionary Medicine, ed. W. R.

Trevathan, E. O. Smith, and J. J. McKenna (New York: Oxford University Press,

1999), 429--42. For a review of this controversial subject, see Rachel Bayer, "The

Impact of Increased Menstruation Rates on Women's Health and Reproductive

Cancers," (2001); online at http://webpub.alleg.edu/employee/r/rmummeIFS101/

ResearchPapers/RacheIBayer.html.

36. Cadbury, Altering Eden, 82-83; Berkson, Hormone Deception, 55. 37. Berkson, Hormone Deception, 29-30.

38. For a review of the scientific literature on DES effects, see R. M. Giusti,

K. Iwamoto, and E. E. Hatch, "Diethylstilbestrol Revisited: A Review of the Long-

Term Health Effects," Annals of Internal Medicine 122 (1995): 778-88.

39. Berkson, Hormone Deception, 63

40. Krimsky, Hormonal Chaos,S, 9; Berkson, Hormone Deception, 65. 41. Krimsky, Hormonal Chaos, 9; Berkson, Hormone Deception, 63.

42. Berkson, Hormoyze Deception, 62-63.

43. Berkson, Hormone Deception, 67; Krimsky, Hormonal Chaos, 9-10.

44. Cadbury, Altering Eden, 48.

45. A. L. Herbst, and R. E. Scully, "Adenocarcinoma of the Vagina in Ado-

lescence: A Report of 7 Cases Including 6 Clear-Cell Carcinomas (So-Called

Mesonephromas)," Cancer 25 (1970): 745--47.

46. Editorial staff, "An Environment for Development," Environmental Health Perspect'Ives 107 (September 1999). For recent research on second- and third-

T 160 BODIES

generation DES effects, see R. H. Kaufman, E. Adam, E. E. Hatch, K. NOller

A. Herbst, J.R. Palmer, and R. N. Hoover, "Continued Follow-up of Pregnane;

Outcomes in Diethylstilbestrol-Exposed Offspring," Obstetrics and Gynecology 96

(2000): 483-89; R. Newbold, "Cellular and Molecular Effects of Developmental

Exposure to Diethylstilbestrol: Implications for Other Environmental Estrogens,"

Envirollmental Health Perspectives 103, Supp!. 7 (1995). R. R. Newbold, R. B. Han-

son, W. N. Jefferson, B. C. Bullock, J. Haseman, and J. A. McLachlan, " Prolifera_

tive Lesions and Reproductive Tract Tumors in Male Descendants of Mice

Exposed Developmentally to Diethylstilbestrol," Carcinogenesis 21 (2000):

1355-63; and R. R. Newbold, R. B. Hanson, W. N. Jefferson, B. C. Bullock, J. Hase-

man, and J. A. McLachlan, "Increased Tumors but Uncompromised Fertility in the

Female Descendants of Mice Exposed Developmentally to Diethylstilbestrol,"

Carcinogenesis 19 (1998): 1655-63.

47. Krimsky, Hormonal Chaos, 10.

48. Eubanks, "Focus." For some of the early laboratory research on DES ef-

fects in mice, see J. A. McLachlan, R. Newbold, and B. Bullock, "Reproductive

Tract Lesions in Male Mice Exposed Prenatally to Diethylstilbestrol," Science 190 (1975): 991-92; H. C. Shah and J. A. McLachlan, "The Fate of Diethylstilbestrol in

the Pregnant Mouse," Journal of Pharmacology and Experimental Therapeutics 197 (1976): 687-96; J. A. McLachlan, "Prenatal Exposure of Dethylstilbestrol in Mice:

Toxicological Studies," Journal of Toxicology and Environmental Health 2 (1977):

527-37; J. A. McLachlan, R. R. Newbold, and B. C. Bullock, "Long-term Effects on

the Female Mouse Genital Tract Associated with Prenatal Exposure to Diethyl-

stilbestrol," Cancer Research 40 (1980): 3988-99; J. C. Lamb IV, R. R. Newbold, and

J. A. McLachlan, "Visualization by Light and Scanning Electron Microscopy of Re-

productive Tract Lesions in Female Mice Treated In Utero with Diethylstilbestrol,"

Cancer Research 41 (1981): 4057-62; J. A. McLachlan, R. R. Newbold, H. C. Shah, M.

Hogan, and R. L. Dixon, "Reduced Fertility in Female Mice Exposed Transplacen-

tally to Diethylstilbestrol," Fertility and Sterility 38 (1982): 364-71; R. R. Newbold

and J. A. McLachlan, "Vaginal Adenosis and Adenocarcinoma in Mice Transpla-

centally Exposed to Diethylstilbestrol," Cancer Research 42 (1982): 2003-11.

49. Editorial staff, "Extra Ingredients: Hormones in Food," Environmental

Health Perspectives 102 (August 1994); Krimsky, Hormonal Chaos, 11, 13.

50 Berkson, Hormone Deception, 16.

51. Ibid., 15.

52. H. Burlington and V. F. Lindeman, "Effect of DOT on Testes and Sec-

ondary Sex Characteristics of White Leghorn Cockerels," Society for Expcrimmtal

Biology and Medicine Proceedings 74 (1950).

53. R. M. Welch, W. Levin, K. Kuntzman, M. N. Jacobson, and A. H. Conney,

"Effect of Halogenated Hydrocarbon Insecticides on the Metabolism and

Uterotropic Action of Estrogens in Rats and Mice," Toxicology and Applied PIJarma-

coloty 19 (1971): 234-46; A. H. Conney, R. M. Welch, R. Kuntzman, and J. J. Burns,

"Effects of Pesticides on Drug and Steroid Metabolism," Pharmacological Therapy

8 (1966): 2-8.

54. Editorial staff, "Extra Ingredients: Hormones in Food"; Raloff, "The

Gender Benders."

55. Rachel Carson, Silent Spring (New York: Houghton Mifflin, 1962).

I [

I

I

I

I

I I (

r

I

I

I

I I

I

I

I

I I

I

I

I

I

I

I

56. Krim

57. F. VOl

Are CorrelatE

ment," Scienc

enon: Effects

House Mice,'

chard, and D,

(1984): 135-7'

Influence of ฀

1824-40,

58. Pers(

59. Krirr

60. Cadl

"Synthetic ฀฀

(1936): 996, a

pounds with

(1938): 222-3:

61. Cadl

62. Ibid.

essay in "in-

The research

schein, "P-N

Polystyrene:

63. Dod,

Structure in I

64. J. A.

"XenoestrogE

Health Perspe,

and R. S. Ly(

Epoxy Can'

bisphenol-A

The chemica

groups belie'

spective, see

For conflictir

tion at http://

http://WWW.OI

tional Toxica

report (whic

http://ntp-sen

65.N,C

V. Pedraza, J

pasites and

(1996): 298-3

'Estrogenicit

rom1lCntai Hi;

N. Olea, "Ce

NANCY LANGSTON 161

56. Krimsky, Hormonal Chaos, 6.

57. F. vom Saal and F. Bronson, "Sexual Characteristics of Adult Female Mice

Are Correlated with Their Blood Testosterone Levels during Prenatal Develop-

ment," Science 20 (1980): 597-99; F. vom Saal, "The Iritrauterine Position Phenom-

enon: Effects on Physiology, Aggressive Behavior, and Population Dynamics in

House Mice," in Biological Perspectives on Aggression, ed. K. Flannelly, R. Blan-

chard, and D. Blanchard, a special issue of Progress in Clinical Biology Research 169

(1984): 135-79; F. vom Saal, "Sexual Differentiation in Litter-Bearing Mammals:

Influence of Sex of Ad acent Fetuses In tero," Journal ofAnimal Science 67 (1989):

1824-40.

58. Personal communication, anonymous reviewer.

59. Krimsky, Hormonal Chaos, 4.

60. Cadbury, Altering Eden, postscript. See E. C. Dodds and W. Lawson,

"Synthetic Estrogenic Agents without the Phenanthrene Nucleus," Nature 137

(1936): 996, and "Molecular Structure in Relation to Oestrogenic Activity: Com-

pounds without a Phenanthrene Nucleus," Proceedings of the Royal Society B 125

(1938): 222-32.

61. Cadbury, Altering Eden, 43.

62. Ibid., 136. Soto describes this discovery in her untitled autobiographical

essay in "in-cites," October 2001; http://www.in-cites.com/papers/dr-ana-soto.html.

The research is reported in A. M. Soto, H. Justicia, J. W. Wray, and C. Sonnen-

schein, "P-Nonyl-Phenol: An Estrogenic enobiotic Released from 'Modified'

Polystyrene," Environmental Health Perspectives 92 (1991): 167-73.

63. Dodds and Lawson, "Synthetic Estrogenic Agents," 996, and "Molecular

Structure in Relation to Oestrogenic Activity," 222-32.

64. J. A. Brotons, M. F. Olea-Serrano, M. Villalobos, V. Pedraza, and N. Olea,

" enoestrogens Released from Lac uer Coatings in Food Cans," Environmental

Health Perspecti'ves 103 (1995): 608-12. Another study (S. R. Howe, L. Borodinsky,

and R. S. Lyon, "Potential Exposure to Bisphenol-A from Food-Contact ses of

Epoxy Can Coatings," Journal of Coatings Technology 70 1997 : 69-74) found

bisphenol-A migration from food cans into food at thirty-seven parts per billion.

The chemical industry believes this level to be safe, while many environmental

groups believe it to be unsafe, or at least not proven safe. For an industry per-

spective, see "Bisphenol-A Global Industry Group" at http://www.bisphenol-a.org.

For conflicting claims about the low-dose health effects, see the industry's posi-

tion at http://www.bisphenol-a.org/new/051601.html; Our Stolen Future's position at

http://www.ourstolenfuture.org/NewScience/lowdose/lowdoseresults.htm; and the Na-

tional TO icology Program's endocrine disrupters low-dose peer review interim

report (which fails to find sufficient evidence in support of either position) at

http://ntp-server.niehs.nih.gov/htdocs/liason/LowDosePeerFinalRpt.pdf

65. N. Olea, R. Pulgar, P. Perez, F. Olea-Serrano, A. Rivas, A. Novillo-Fertrell,

V. Pedraza, A. Soto, and C. Sonnenschein, "Estrogenicity of Resin-Based Com-

Posites and Sealants sed in Dentistry," Environmental Health Perspectives 104

฀฀฀฀฀฀฀ 298-305. A response to this article can be found in Y. Imai, "Comments on

Estrogenicity of Resin-Based Composites and Sealants sed in Dentistry:" Envi-

ronmental Health Perspectives 107 (1999): A290. The response to this response is

N. Olea, "Comments on 'Estrogenicity of Resin-Based Composites and Sealants

162 BODIES

sed in Dentistry': .Res.ponse," ฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀ Health Perspectives 107 (1999):

A290-92. See also Edrtonal staff, Forum, Envzromnental Health Perspectives 104

(1996); online at http://ehpnetl.niehs.nih.gov/docs/1996/104-4/{orum.html#dental. A

study showing low-dose effects of bisphenol-A on mice is S. C. Nagel, F. S. vom

Saal, K. A. Thayer, M. G. Dhar, M. Boechler, and W. V. Welshon, "Relative Bind-

ing Affinity-Serum Modified Access (RBA-SMA) Assay Predicts In Vivo Bioac-

tivity of the enoestrogens Bisphenol-A and Octylphenol," Environmental Health

Perspectives 105 (1997): 70-76.

66. Myers, "Contamination threatens a basic reproductive right."

67. Editorial staff, "Forum."

68. K. Howdeshell, A. K. Hotchkiss, K. A. Thayer, J. G. Vandenbergh, and

F. S. vom Saal, "Plastic Bisphenol-A Speeds Growth and Puberty," Nature 401

(1999): 762-64.

69. H. Miyakoda, M. Tabata, S. Onodera, and K. Takeda, "Passage of Bisphe-

nol-A into the Fetus of the Pregnant Rat," Journal of Health Science 45 (1999):

318-23; O. Takahashi and S Oishi, "Disposition of Orally Administered 2,2-

Bis(4-hydroxyphenyl) propane (Bisphenol-A) in Pregnant Rats and the Placental

Transfer to Fetuses," Environmental Health Perspectives 108 (2000): 931-35;

J. Josephson, "Breaching the Placenta," Environmental Health Perspectives 108 (2000); online at http://ehpnetl.niehs.nih.gov/docs/2000/108-10/ss.html#breaching.

70. Myers, http://ourstolenfuture.org. Frederick vom Saal recently found that

bisphenol-A had measurable effects in laboratory experiments at levels thou-

sands of times lower than previously thought. These low-dose effects challenge

the ade uacy of countless toxicity tests undertaken to establish standards. For

years, the acceptable daily dose for bisphenol-A had been set at a no-effect level

of fifty milligrams kg, or fifty parts per million, based on data reported by the So-

ciety of Plastics Industry. Vom Saal, however, found effects at lower levels: at two

parts per billion, twenty-five thousand times lower. When he fed pregnant mice

bisphenol-A at two parts per billion (two micrograms per kg day), their male

sons had enlarged and hypersensitized prostates when they reached adulthood.

An overview of this work can be found at http://ourstolenfuture.org/NewScience.

The original research is S. C. Nagel et aI., "Relative Binding Affinity-Serum Mod-

ified Access (RBA-SMA) Assay Predicts the Relative In Vivo Bioactivitv," 70-76.

See also C. Gupta, "Reproductive Malformation of the Male Offspring Following

Maternal Exposure to Estrogenic Chemicals," Proceedings of the Society for Experi-

mental Biologtj and Medicine 224 (2000): 61-68. See also C. M. Markey, E. H. Lu ue,

M. Munoz de Toro, C. Sonnenschein, and A. M. Soto, "In tero Exposure to

Bisphenol-A Alters the Development and Tissue Organization of the Mouse

Mammary Gland," Biology of Reproduction 65 (2001): 1215-23.

71. Cadbury, Altering Eden, 144, 155.

72. http://abcnews.go.com/sections/living/DailyNews/toxicpolish_dbp001128.htnzl.

73. Centers for Disease Control and Prevention, National Report on Human

Exposure to Environmental Chemicals, March 2001, Atlanta. The report can be found

online at htlp://www.cdc.gov/nceh/dls/report/Highlights.htm.

74. Bob Weinhold "Forum," Environmental Health Perspectives 109 (May

2001); online at http://ehpnetl.niehs.nih.gov/docs/2001/109-5/forum.html#baby Forum:

Washmgton Post, March 21, 2001; online at htlp://washingtonpost.com/ac2/wp-dyn.

''?

I

I 75. Myers, ht,

76. Gray's tei'I et aL "Administr

Linuron, lprodionI stances (Dibutyl- ,

I Sulphonate) durir

ductive Malforma'

94, "Environment< I

ter Sexual Differen

tiandrogenic Pesti. I

without Affecting

ibid., 37; cited in R 77. This wor:

culinity," who rep,

the Society of Toxi

Foster, "Dose-ResI

tion Induced by 0

Foster, "Di(n-buty

Receptor Levels in

78. 1. Colon, I

thalate Esters in tl

Development," En

79. Ibid.

80. Editorials

81. H. M. Blal

Hertzberg, R. H.

Girls Exposed In T-

ogy 11 (2000): 641-

82. M. ฀฀฀฀฀฀฀

richs, C. de Beaufo

Immigration from

sure to Organochlc

83. M. Helma

Bhapkar, G. G. Koc

Menses in Young'

search in Office SI

ourstolellfuture.org/l

84. P. B. Kapl

Herman-Giddens,

Mass Index and Ri'

85. K. L. How

vom Saal, "EnvirOl

Nature 401 (1999): :

86. For fuller

The Biological Diffel

Anne Fausto-Sterli

(New York: Basic E

107 (1999):

rspectives 104

'ml#dental. A

฀฀฀฀ F. S. vom

฀฀฀฀฀฀฀฀ Bind-

1 Vivo Bioac-

mental Health

t."

enbergh, and

," Nature 401

Ige of Bisphe-

ce 45 (1999):

inistered 2,2-

the Placental

000): 931-35;

rspectives 108

·breaching.

:ly found that

t levels thou-

ects challenge

tandards. For

no-effect level

-ted by the So-

. levels: at two

xegnant mice

y), their male

ed adulthood.

rg/NI?WScience.

'-Serum Mod-

:tivity," 70-76.

'ing Following

'iety for Experi-

'I, E. H. Luque,

:J Exposure to

of the Mouse

bp001128.html.

rort on Human

-t can be found

Iives 109 (May

nl#baby Fonlm;

I \1/ac2/wp-dyn..

฀

NANCY LANGSTON 163

75. Myers, http://www.ourstolenfuture.org/New/newstuffhtm.

76. Gray's team reported the research in the following reports: E. L. Gray Jr.

et al., "Administration of Potentially Antiandrogenic Pesticides (Procymidone,

Linuron, Iprodione, Chlozolinate, p, p'-DDE, and Ketoconazole) and Toxic Sub-

stances (Dibutyl- and Diethylhexyl Phthalate, PCB 169, and Ethane Dimethane

Sulphonate) during Sexual Differentiation Produces Diverse Profiles of Repro-

ductive Malformations in the Male Rat:' Toxicology and IIldustrial Health 15 (1999):

94, "Environmental Antian;irogens: Low Doses of the Fungicide Vinclozolin Al-

ter Sexual Differentiation of the Male Rat," ibid., 48, and "The Estrogenic and An-

tiandrogenic Pesticide Methoxychlor Alters the Reproductive Tract and Behavior

without Affecting Pituitary Size or LH and Prolactin Secretion in Male Rats,"

ibid., 37; cited in Raloff, "Common Pollutants Undermine Masculinity."

77. This work was cited in Raloff, "Common pollutants undermine mas-

culinity:' who reported on a series of papers given at the March 1999 meeting of

the Society of Toxicology in New Orleans, including E. Mylchreest, and P. M. D.

Foster, "Dose-Response for Altered Male Reproductive Development and Func-

tion Induced by Di(n-butyl) Phthalate:' and M. Sar, E. Mylchreest, and P. M. D.

Foster, "Di(n-butyl) Phthalate Induces Changes in Morphology and Androgen

Receptor Levels in the Fetal Testis."

78. I. Colon, D. Caro, C. J . Bourdony, and O. Rosario, "Identification of Ph-

thalate Esters in the Serum of Young Puerto Rican Girls with Premature Breast

Development:' Environmental Health Perspectives 108 (2000): 895-900.

79. Ibid.

80. Editorial staff, "Extra Ingredients: Hormones in Food.

81. H. M. Blanck, M. Marcus, P. E. Tolbert, C. Rubin, A. K. Henderson, V. S.

Hertzberg, R. H. Zhang, and L Cameron, "Age at Menarche and Tanner Stage in

Girls Exposed In Utero and Postnatally to Polybrominated Biphenyl," Epidemiol-

ogy 11 (2000): 641-47; Berkson, Hormone Deception, 109.

82. M. Krstevska-Konstantinova, C. Charlier, M. Craen, M. Du Caju, C. Hein-

richs, C. de Beaufort, G. Plomteux, and J. P. Bourguignon, "Sexual Precocity after

Immigration from Developing Countries to Belgium: Evidence of Previous Expo-

sure to Organochlorine Pesticides," Human Reproduction 16 (2001): 1020-26.

83. M. Herman-Giddens, E. J. Slora, . C. Wasserman, C. J. Bourdony, M. V.

Bhapkar, G. G. Koch, and C. H. Hasemeier, "Secondary Sexual Characteristics and

Menses in Young Girls Seen in Office Practice: A Shldy from the Pediatric Re-

search in Office Settings Network:' Pediatrics 99 (1999): 505-12. See also www.

Ourstolenfuture.org/NewSciencelreproductionIPubertylpubertydebate.htm.

84. P. B. Kaplowitz, E. J. Slora, R. C. Wasserman, S. E. Pedlow, and M. E.

Herman-Giddens, "Earlier Onset of Puberty in Girls: Relation to Increased Body

Mass Index and Race," Pediatrics 108 (2001): 347-53.

85. K. L. Howdeshell, A. K. Hotchkiss, K. A. Thayer, J. G. Vandenbergh, F. S.

Vom Saal, "Environmental Toxins: Exposure to Bisphenol-A Advances Puberty:'

Nature 401 (1999): 763-64.

86. For fuller discussions of this point, see Deborah Blum, Sex on the Brain:

The Biological Differences between Men and Women (New York: Viking, 1998), and

Anne Fausto-Sterling, Myths of Gender: Biological Theories about Women and Men

(New York: Basic Books, 1985).

฀฀

164 BODIES

87. Brumberg, The Body Project; see also Laura Fraser, Losing It: America's Ob-

session with Weight and the Industry That Feeds on It (New York: Viking, 1996),32-44

88. Brandy E. Fisher, "Gender Matters," Environmental Health Perspectives.

106 (1998); online at http://ehpnetl.niehs.nih.gov/docs/1998/106-6/niehsnews.html.

89. Editorial staff, "Working for Women's Health," Enl'ironmental Health

PerspectIVes 108 (January 2000); online at http://ehpnetl.niehs.nih.gov/docs/2000/108_

l/niehsnews.html, citing Barbara J. Davis, head of the Female Reproductive Pathol-

ogy Group and now acting chief of the newly created Laboratory of Women's

Health at the National Institute of Environmental Health Sciences (NIEHS).

90. Fisher, "Gender Matters."

91. Berkson, Hormone Deception, 146.

92. For a review that discusses the many difficulties researchers face when

they try to test for relationships between human reproductve problems and envi-

ronmental toxicants, see F. 1. Sharara, D. B. Seifer, and J. A. Flaws, "Environmen_

tal Toxicants and Female Reproduction," Fertility and Sterility 70 (1998): 613-22,

and a response from W. H. James, "Environmental Toxicants and Sex Ratios-

Effects?" Fertility and Sterility 71 (1999): 775.

93. G. M. Buck, J. E. Vena, E. . Schisterman, J. Dmochowski, P. Mendola

. . Sever, E. Fitzgerald, P. Kostyniak, H. Greizerstein, and J. Olson, "Parental

Consumption of Contaminated Sport Fish from Lake Ontario and Predicted Fe-

cundability," Epidemiology 11 (2000): 388-93; cited at Myers, www.ourstolenfuture.

org!NewScience!

94. Editorial staff, "Extra Ingredients: Hormones in Food."

95. Cited in Editorial staff, "Working for Women's Health."

96. Berkson, Hormone Deception, 148.

97. National Institute for Environmental Health Sciences, "Women's

Health," Fact Sheet no. 10 (August 1997); online at http://www.niehs.nih.gov/oc/

factsheets/womens.htm.

98. The studies that showed effects were P. . Koninckx, P. Braet, S. H.

Kennedy, and D. H. Barlow, "Dioxin Pollution and Endometriosis in Belgium,"

Human Reproduction 9 (1994): 1001-02; . S. Birnbaum, "Developmental Effects of

Dioxin," Environmental Health Perspectives 103, Supp!. 7 (1995): 89-94; and . Gib-

bons, "Dioxin Tied to Endometriosis," Science 262 (1993): 1373. The studies that

failed to find correlations were . Pauwels, P. J. . Schepens, T. D'Hooghe, . Del-

beke, M. Dhont, . Brouwer, and J. Weyler, "The Risk of Endometriosis and Ex-

posure to Dioxins and Polychlorinated Biphenyls: A Lase-Control Study of

Infertile Women," Human Reproduction 16 (2001): 2050-55, and G. Lebel et a!',

"Organochlorine Exposure and the Risk of Endometriosis," Fertility and Sterility

69 (1998): 221-28.

99. . . Hodges, D. S. Hunter, J. S. Bergerson, . Fuchs-Young, and . .

Walker, "An In Vivo/In Vitro Model to Assess Endocrine Disrupting Activity of

Xenoestrogens in Uterine Leiomyoma," Annals of the New York Academy of Sciences.

Environmental Hormones: The Scientific Basis of Endocrine Disruption 948 (2001):

100-111.

100. . . Newbold, . P. DiAugustine, J. I. Risinger, J. I. Everitt, D. K.

Walmer, E. . Parrott, and D. Dixon, "Advances in Uterine Leiomyoma Re-

search," Environmental Health Perspectives 108, Supp!. 5 (October 2000): 769-73.

I I

I 101. Nationa

Environmental H

I thome.htm. 102. D. S. Ht

J. S. Bergerson, an

I

I ands on Uterine I

for Uterine Fibrc

829-34. For the re

gard, U. P. Thorg

I ministration of

Clinical Oncology 1

r cinogenicity of DI

ical Oncology 126

l I 103. For exan

of Endocrine-Disr

niotic Fluid," Jour

104. J. R. Da'

I pected of ฀฀฀฀฀฀฀

cology 24 (1993): E

between exposureI T. Nurminen, "TI

demiology 12 (2001 I 105. Berkson,

I of PCBs were ove]

250 ppb; see Cad\:

I contamination, se

Environmental Cl

grams," Environn

T. Chuvakova, G.

K. Benedict, Y. Y. (

posure to ChloriJ

chlorodibenzo-p-c

Kazakhstan," Eln "Breast Milk Mon

for Polyhalogenab

Health," Environn

M. X. Petreas, T. C

D. Hayward, J. 51-

and R. D. Stepher

Contaminants in

(TCDD) in Agricl

Perspectives 106 (I'

106. Myers,

011 ฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀฀

through breast-fel

P. C. Dagnelie, P.

Kuperus, and P. J.

, It: America's Ob-

lng, 1996), 32--44.

reaWl Perspectives

iehsnews.html. ironmental Health

'ov/docs/2000/108-

฀฀฀฀฀฀฀฀฀ Pathol-

tory of Women's

:es (NIEHS).

lrchers face when

roblems and envi-

NS, "Environmen-

70 (1998): 613--22,

and Sex Ratios-

,wski, P. Mendola,

. Olson, "Parental

and Predicted Fe-

ww.ourstolenfuture.

d."

th."

iences, "Women's

:uw.niehs.nih.gov!oc!

:kx, P. Braet, S. H.

riosis in Belgium,"

)pmental Effects of

89-94; and A. Gib-

'3. The studies that

. D'Hooghe, L. Del-

lometriosis and Ex- ฀฀฀฀฀฀฀฀฀ Study of

lnd G. Lebel et a1.,

฀฀฀฀฀฀฀฀฀ and Sterility

1s-Young, and C. L. ..ty of

;;rupting ActiVl Academy of Sciences.

sruption 948 (2001):

'tt D K J I Even,' . L' . rna Re-

ne elOmyO.. , 2000)' 769-73.

฀฀฀ !

NANCY LANGSTON 165

101. National Institute for Environmental Health Sciences, "Disparities in

Environmental Health," online at http://www.niehs.nih.gov/oclfactsheets/disparity/

thome.htm.

102. D. S. Hunter, L. C. Hodges, P. K. Eagon, P. M. Vonier, R. Fuchs-Young,

J. S. Bergerson, and C. L. Walker, "Influence of Exogenous Estrogen Receptor Lig-

ands on Uterine Leiomyoma: Evidence from an In Vitro/In Vivo Animal Model

for Uterine Fibroids," Environmental Health Perspectives 108, Suppl. 5 (2000):

829-34. For the research on monkeys, see S. Takayama, S. M. Sieber, D. W. Dal-

gard, U. P. Thorgeirsson, and R. H. Adamson, "Effects of Long-Term Oral Ad-

ministration of DDT on Nonhuman Primates," Journal of Cancer Research and

Clinical Oncology 125 (1999): 219-25, and L. Tomatis and J. Huff, "Evidence of Car-

cinogenicity of DDT in Nonhuman Primates," Journal of Cancer Research and Clin-

ical Oncology 126 (2000): 246.

103. For example, see W. Foster, S. Chan, L. Platt, and C. Hughes, "Detection

of Endocrine-Disrupting Chemicals in Samples of Second Trimester Human Am-

niotic Fluid," Joumal of Clinical Endocrinology and Metabolism 85 (2000): 1.

104. J. R. Davis, R. C. Brownson, and R. Garcia, "Family Pesticide Use Sus-

pected of Causing Child Cancers," Archives of Environmental Contamination Toxi-

cology 24 (1993): 87-92. For an overview of the difficulties in establishing links

between exposure to pesticides (or other synthetic chemicals) and fetal effects, see

T. Nurminen, "The Epidemiologic Study of Birth Defects and Pesticides," Epi-

demiology 12 (2001): 145--46.

105. Berkson, Hormone Deception, 91. In Germany, studies showed that levels

of PCBs were over 100 parts per billion; in Denmark, over 140 ppb; in Spain, over

250 ppb; see Cadbury, Altering Edell, 72. For some of the research on breast milk

contamination, see K. Hooper and T. A. McDonald, "The PBDEs: An Emerging

Environmental Challenge and Another Reason for Breast-Milk ฀฀฀฀฀฀฀฀฀฀ Pro-

grams," Ellvirollmelltal Health Perspectives 108 (2000): 387-92; Kim Hooper,

T. Chuvakova, G. Kazbekova, D. Hayward, A. Tulenova, M. X. Petreas, T. J. Wade,

K. Benedict, Y. y. Cheng, and J. Grassman, "Analysis of Breast Milk to Assess Ex-

posure to Chlorinated Contaminants in Kazakhstan: Sources of 2,3,7,8-tetra-

chlorodibenzo-p-dioxin (TCDD) Exposures in an Agricultural Region of Southern

Kazakhstan," Environmental Health Perspectives 107 (1999): 447-57; K. Hooper,

"Breast Milk Monitoring Programs (BMMPs): World-wide Early Warning System

for Polyhalogenated POPs and for Targeting Studies in Children's Environmental

Health," Ellvironmental Health Perspectivl's 107 (1999): 429-30; and K. Hooper,

M. X. Petreas, T. Chuvakova, G. Kazbekova, N. Druz, G. Seminova, T. Sharmanov,

D. Hayward, J. She, P. Visita, J. Winkler, M. McKinney, T. J. Wade, J. Grassman,

and R. D. Stephens, "Analysis of Breast Milk to Assess Exposure to Chlorinated

Contaminants in Kazakstan: High Levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin

(TCDD) in Agricultural Villages of Southern Kazakstan," Environmental Health Perspectives 106 (1998): 797-806.

106. Myers, Our Stolen Future; new research online at hftp://www.

ourstolenfutllre.or'{(New/newstllffhtm#. For a comparison between exposure thr c

pough breast-feeding and long-term exposure through food, see S. Patandin, . C. Da . .

I< gnehe, P. G. H. Mulder, E. Op de Coul, J. E. van der Veen, N. Welsglas-

up'n", and P. J. J. SaUe<, "Diet"y Expo,",e to Polyehlminated Biphenyl, ,md

T'

I 166 BODIES

I

Dioxins from Infancy until Adulthood: A Comparison between Breast-feeding,

Toddler, and Long-term Exposure," Environmental Health Perspectives 107 (1999).

107. Myers, Our Stolen Future; new research online at http://www.

ourstolenfuture.org/New/newstu!f.htm#. 108. J. S. LaKind, C. M. Berlin, and D. Q. Naiman, "Infant Exposure to Chem-

icals in Breast Milk in the United States: What We Need to Learn from a Breast

Milk Monitoring Program," Environmental Health Perspectives 109 (2001).

109. Krimsky, Hormonal Chaos, 231.

110. Ibid., 232. 111. National Research Council, Hormonally Active Agents in the Environment

(Washington, nc.: National Academy of Sciences Press, 1999).

112. Ibid., 15. This section of the NRC report is a fascinating exploration of

how different groups and individuals construct knowledge.

113. Myers, Our Stolen Future; online at http://ourstolel1future.org/Consensus/

nrc.htm. 114. Schettler, "Endocrine Disruptors."