Discussion 7
Biological, Radiological, and Nuclear Agents
A. Categories of Bioterrorism Agents
Biological warfare has been known, and applied to great effect, for millennia. In
recent years, however, with enhanced knowledge of microbiology, culturing techniques,
and means of dissemination, the threat has become acute. Bioweapons have been used by
terrorists, and several nations are known to be manufacturing tactical biological weapons.
Therefore, awareness of this potential threat by first responders, medical care providers,
public health agencies, elected officials, and ultimately the general public, including how
to identify such weapons and to respond appropriately, is essential. Given the events of
the past two decades, it is essential that the U.S. public health system and primary
healthcare providers be prepared to address a wide range of biological agents, including
pathogens that rarely occur in the United States. Even before the bioterror attacks of 2001
in which anthrax spores were deliberately released in the U.S. postal system, public
health officials expressed concerned regarding the potential for such an event. In 1999,
the U.S. Centers for Disease Control and Prevention (CDC), one of the key units of the
Department of Health and Human Services, devised a classification scheme for major
biological agents that terrorists could use to harm civilians (please see the lists of
categories of CDC biological agents and examples of CDC category A, B, and C agents).
The use of biological weapons has been detected as far back as the proto-
Neolithic (late Stone Age, approximately 10,000 b.c.e.) hunter–gatherer societies in
Southern Africa. Hunters used poisoned arrows, tipping stone points with venom
obtained from scorpions or snakes. Extracts from poisonous plants were also used. The
arrow was fired into the target, and the hunter tracked the animal until the poison caused
its death. Documented usage of biological weapons on the battlefield is abundant. In
ancient times, many varieties of biological warfare were used, often with startling
success; for example, Scythian archers used arrows dipped in decomposing corpses (and
also blood and manure) as far back as 400 b.c.e. The Assyrians poisoned enemy wells
with rye ergot, which contains a psychoactive agent. The fungus that causes ergot
produces ergotamine, a hallucinogen that causes delusions, paranoia, seizures, and
cardiovascular problems that can lead to death. Those affected seemed to go insane,
which intensified the terror aspect and demoralized fellow soldiers.
One of the best-documented historic incidents of biological warfare occurred in
1346 during the siege of Kaffa (now Feodossia, Ukraine), a port city located on the
Crimean Peninsula of the Black Sea. The attacking Tatar forces of Kipchak khan Janibeg,
backed by Venetian forces, catapulted plague-infected corpses into the city. The ensuing
epidemic within the already weakened city forced the defenders to surrender. Some
infected citizens who fled Kaffa by ship may have started the Black Death pandemic,
which spread throughout Europe. This same stratagem of hurling infected corpses was
repeated in 1710 by the Russians besieging Swedish forces at Reval in Estonia. The
Spanish deliberately contaminated wine with the blood of leprosy patients for use against
the French near Naples in 1495. Another innovative attempt at biological warfare
occurred in 1650 by Kazimierz Siemienowicz, a Polish artillery general, who placed
saliva from rabid dogs into hollow projectiles for firing against his enemies.
The use of biological weapons during World War I was not nearly as widespread
as that of chemical warfare (see Chapter 2). However, it is believed that by 1915 the
Germans infected the Allies’ horses and cattle with various microbes on both the western
and eastern fronts. Also in 1915, the Germans allegedly inoculated pathogenic bacteria
into horses and cattle leaving U.S. ports for shipment to the Allies in Europe (Figure 4.1)
(Smart, 1996, 1997; Stockholm, 1971). Erich von Steinmetz, a captain in the German
navy, entered the United States with cultures of glanders to inoculate horses intended for
the western front. His efforts were not successful, however. Dr. Anton Dilger, a German-
American physician, developed a microbiology facility in Maryland, where he produced
large quantities of anthrax and glanders bacteria, using starter cultures provided by the
German government. German agents inoculated horses in Baltimore that were awaiting
shipment to the Allied forces in Europe; they inoculated 3000 horses, mules, and cattle.
Several hundred military personnel were reported to have received secondary infections.
In 1928, Shiro Ishii (Figure 4.2), a Japanese military officer, toured foreign
research laboratories and came to the conclusion that several of the world powers were
secretly researching biological warfare (his conclusion was at least accurate for the Soviet
Union). In 1929, the Soviets were reported to have established a biological warfare
facility north of the Caspian Sea (Robertson and Robertson, 1995; Smart, 1997;
Stockholm, 1971; Williams and Wallace, 1989). In 1933, Germany began military
training in offensive biological warfare and was reported to have secretly tested Serratia
marcescens, considered a biological simulant, in the Paris Metro ventilation shafts and
near several French forts (Smart, 1997). Soon afterward, the Germans conducted
experiments on livestock infections with foot and mouth disease (FMD). The German
Military Bacteriological Institute in Berlin began developing anthrax as a biological
weapon, while the Agricultural Hochschule in Bonn examined spraying of crops with
bacteria.
By 1936, France had established a large-scale biological warfare research
program that investigated microbial viability while in storage and during detonation of
explosives. Canada also initiated biological warfare research, studying anthrax,
botulinum toxin, plague, and psittacosis. By 1940, Britain instituted a biological warfare
laboratory at Porton Down. In 1933, Japan—under the direction of General Ishii—set up
an offensive biological warfare laboratory near Harbin in occupied Manchuria. The
laboratory complex, codenamed Unit 731, was used for research on the effects of
biological agents on numerous organisms and also prisoners of war (Figure 4.3). About
1000 human autopsies were carried out at Unit 731, mostly on victims exposed to
anthrax. Many more prisoners and Chinese nationals may have died in this facility,
however. Unit 731 developed and tested a biological bomb within 3 years. Additional
biological warfare facilities were established in 1939.
By 1940, Japan had developed and tested several different biological devices in
the field; more than 1600 bombs were constructed. Some are known to have been filled
with a mixture of shrapnel and anthrax spores. By 1945, Ishii’s program had stockpiled
400 kg of anthrax to be carried in specially designed fragmentation bombs (Smart, 1997).
The Japanese had apparently used cholera, dysentery, typhoid, plague, anthrax, and
paratyphoid on Chinese troops. Hundreds of Chinese citizens are known to have died
from plague epidemics. By the start of World War II, Japanese laboratories devoted
significant attention to the use of vectors such as the common flea to carry biological
agents.
During the 1950s, the biological warfare programs of many nations were geared
toward standardizing selected biological agents and weaponizing them. Highest priority
was placed on antipersonnel agents. In the United States, Major General Bullene, Chief
Chemical Officer, continued to give utmost priority to the development of anthrax
(Smart, 1997). Biological agents were produced at several sites in the United States until
1969, when President Nixon halted all offensive biological weapon research and
production by Executive Order. Between 1971 and 1972, all stockpiles of biological
agents from the U.S. program were destroyed. The agents eliminated included Bacillus
anthracis, Francisella tularensis, Coxiella burnetii, Venezuelan equine encephalitis virus,
Brucella suis, Staphylococcal enterotoxin B, and botulinum toxin. The United States
created a medical defensive program in 1953 that continues today at the U.S. Army
Medical Research Institute for Infectious Diseases (USAMRIID) at Fort Detrick,
Maryland.
In April 1979, public attention became focused on an incident that occurred in
Sverdlovsk (now Yekaterinburg) in the former Soviet Union. Spores of B. anthracis were
accidentally released from the Soviet Military’s Compound 19, a microbiology
laboratory. Workers at a ceramic plant across the street fell ill during next few days, and
almost all died within a week. Some residents living downwind from the facility also
became ill and died within days of the event. All cases occurred within a narrow zone
extending 4 km downwind in a southerly direction from the facility (Figure 4.4). The
Soviet Ministry of Health claimed that the deaths were the result of consumption of
contaminated meat; however, controversy as to the actual cause continued for years. The
death toll from the incident totaled at least 105, but the exact number is unknown as all
hospital records and other evidence were destroyed by the Komitet Gosudarstvennoy
Bezopasnosti (KGB), according to former Biopreparat deputy director Ken Alibek
(Alibek and Handelman, 1999). Livestock downwind from the site also succumbed to the
disease.
In 1991, the Minnesota Patriots Council extracted ricin from castor beans
obtained through a mail order. They planned to disseminate the agent as an aerosol but
were arrested after the FBI infiltrated the group and learned of their plan. Two members
of the group, Doug Baker and Charles Wheeler, were the first individuals to be indicted
and convicted under the Biological Weapons Anti-Terrorism Act of 1989. In October
1992, Shoko Asahara, leader of the Aum Shinrikyo cult, with 40 followers, traveled to
Zaire reportedly to assist victims of an outbreak of Ebola hemorrhagic fever. According
to a report by the U.S. Senate’s Permanent Subcommittee on Investigations, however, the
cult’s true motive was to obtain virus samples to be used for biological attacks. By 1995,
it was reported that on at least 10 occasions Aum Shinrikyo attempted to disperse
anthrax, botulinum toxin, Q fever, and Ebola against civilian populations and government
figures in Japan.
In 1995, a group called The Covenant and the Sword smuggled ricin into the
United States from Canada. The ricin was baked into cakes that were to be given to the
local Internal Revenue Service office at Christmas. The perpetrator hanged himself
shortly after his arrest. Also in 1995, a Kansas City oncologist, Deborah Green, attempted
to murder her husband by contaminating his food with ricin. In May 1995, a laboratory
technician from Ohio (Larry Wayne Harris) ordered plague bacterium (Yersinia pestis)
from a Maryland biomedical supply firm using a credit card and a false letterhead. He
received three vials of Y. pestis. As a result of his suspicious behavior, the supplier
contacted federal authorities. An investigation revealed that he was a member of a white
supremacist organization. Harris was arrested after he threatened to release anthrax in Las
Vegas. The strain in his possession, however, was a harmless veterinary vaccine strain. In
China in 2001, 120 people became ill after food products were laced with rat poison by
manufacturers of competing products. In 2002, a similar rat poisoning incident killed at
least 38 people and made more than 300 seriously ill (BBC, 2002; CNN, 2002). In 2003,
it was discovered that 200 lb of ground beef was contaminated with an insecticide
containing nicotine by a disgruntled supermarket employee in Michigan. This episode
resulted in 111 people becoming ill, including 40 children.
B. Bacterial and Viral Diseases
Bacteria are one-celled organisms that can survive in a wide variety of
environments. The majority of bacteria are either beneficial or do no particular harm to
other organisms. Only a minority are pathogenic, that is, disease-causing, in animals and
humans. As a consequence of the differences in physiology between bacteria and their
hosts, it is possible to treat most bacterial diseases by using antibiotics. Two pathogenic
bacterial agents—B. anthracis and Coxiella burnetii—have the capability of converting to
a highly resistant form, that is, a spore, when the environment becomes hostile to the
organism’s survival (too dry, too cold, extremes of pH, etc.). The spore is capable of
remaining viable for extended periods and will subsequently revert to the vegetative,
disease-producing form when favorable environmental conditions return. The following
section will describe a spore-forming bacterial species with a long history of adverse
public health impacts.
Anthrax is an acute infectious disease caused by the bacterium B. anthracis. The
CDC has classified B. anthracis as a Category A bioterrorism agent. Anthrax is thought to
be the fifth plague of Egypt as chronicled in the book of Exodus. The disease is probably
best known for its role in the 2001 bioterrorist attacks in the United States in which lethal
anthrax spores were sent via U.S. mail to offices in the U.S. Senate and several news
media companies (Box 4.2). Twenty-two people became ill and five died as a result of
the attacks. The perpetrator is believed to have been Dr. Bruce Ivins, a biodefense
scientist who was working on a vaccine for anthrax at the U.S. Army Biodefense
Laboratories at Fort Detrick, Maryland. In 2009, he committed suicide during the FBI
investigation of his possible role in the attacks.
The causative agent of anthrax, B. anthracis, is a relatively large (approximately 1
by 6 μm) Gram-positive, spore-forming, rod-shaped bacterium. Anthrax was the first
bacterium ever to be documented to cause disease, by Robert Koch in 1877. B. anthracis
lives in soil, and the vegetative form has evolved a survival tactic (i.e., spore formation)
that allows it to withstand harsh conditions for decades. The spore, which measures
approximately 1 by 0.5 μm, serves as a resilient resting phase that can tolerate extreme
heat, cold, and desiccation. When environmental conditions eventually become favorable,
the spores germinate into active bacteria.
Although the spore stage will allow the bacteria to survive in unfavorable
environments, the potency of anthrax as a killer is the ability of the vegetative form to
produce toxins. The resilience of the spore and the production of toxins combine to make
B. anthracis a formidable bioterrorism agent. B. anthracis possesses several virulence
factors: a capsule surrounding the vegetative cell, a protective antigen, and two protein
exotoxins, termed lethal factor and edema factor. The capsule prevents the bacterial cell
from being engulfed and killed by phagocytes (i.e., specialized white blood cells). The
protective antigen binds to the cell of the infected organism, creates a pore, and channels
the edema factor and lethal factor into the cell. Once inside, the edema factor causes fluid
to accumulate at the site of infection. The edema factor can contribute to a fatal buildup
of fluid in the cavity surrounding the lungs; it can also inhibit some of the body’s immune
functions. The lethal factor also works inside the cell, disrupting a key molecular process
that regulates cell function. The lethal factor can kill infected cells or prevent them from
functioning properly.
Cutaneous anthrax is the most common manifestation of natural B. anthracis
infection. Individuals with cuts or open sores can succumb to cutaneous anthrax if they
come in direct contact with the bacteria or its spores through broken skin, usually on the
hands, arms, or face. Handling contaminated animal products is a common source of
infection. The spores germinate within hours after infection and the vegetative cells
multiply and produce toxins. The first obvious sign of cutaneous anthrax is typically is a
small reddish macule that develops within a few days after infection. The macule
progresses to a papular and eventually a pustular stage (a fluid-filled vesicle), and the
surrounding tissue becomes swollen. Secondary vesicles may surround the initial infected
site. The final stage involves the formation of an ulcer with a blackened necrotic eschar
surrounded by a zone of edema (Figure 4.5). The term anthrax arises from the Greek
word meaning coal, because of the development of the black lesions in cutaneous
victims. The fully developed lesion is painless.
Humans can become infected with GI anthrax from eating undercooked meat
contaminated with anthrax bacteria or their spores. GI anthrax is most likely to occur in
warm, tropical regions of Asia, Africa, and the Middle East. There have been no
confirmed cases of GI anthrax in the United States, although a Minnesota farm family
experienced symptoms of the disease in 2000 after eating meat from an anthrax-infected
steer (NIH, 2007). The infections were discovered early and treated successfully. GI
anthrax is characterized by an acute inflammation of the intestinal tract. Clinical
symptoms begin within days after ingesting spores. If the spores germinate in the upper
intestinal tract, ulcers may develop in the mouth or esophagus and cause swelling in the
lymph nodes of the neck and surrounding tissues. Septicemia may follow. Spores that
germinate in the lower intestinal tract will create lesions and may be severe enough to
cause intestinal hemorrhage. Early symptoms include loss of appetite, nausea, vomiting,
and fever. These symptoms are followed by abdominal pain, vomiting of blood, and
severe diarrhea. If left untreated, GI anthrax results in death in 25–60% of cases (U.S.
CDC, 2008). Antibiotic treatment can cure the GI form of anthrax.
The inhalation form of the disease, also known as Woolsorters disease, is highly
lethal, causing a hemorrhagic inflammation of the mediastinum (generally speaking, the
space in the chest between the pleural sacs of the left and right lungs) and often,
hemorrhagic mediastinitis (Figure 4.6). Fatality rates are very high in untreated cases and
may occur in as many as 95% of treated cases if therapy is delayed after the appearance
of symptoms. Spores of B. anthracis occurring as airborne particles measure less than 5
μm in diameter and can be deposited directly into the alveoli of the lungs. After spores
are inhaled, phagocytes (white blood cells) engulf them. The spores are carried by the
phagocytes to the mediastinal nodes where they germinate and release toxins soon
afterward. Symptoms usually appear from 1 to 7 days after exposure, but may take as
long as 60 days. The time difference is apparently a function of dose received.
Anthrax is not contagious; therefore, communicability is not a concern in
managing patients with inhalation anthrax (U.S. CDC, 2008). DNA identification
techniques combined with microbial culture of body fluids can provide an accurate
diagnosis of the disease. To date, there are several successful rapid diagnostic tests for B.
anthracis. Untreated inhalation anthrax has an extremely high fatality rate. In the event of
inhalation exposure, the immediate administration of antibiotics is critical. Antibiotics are
effective if provided early during the course of the disease; antibiotic treatment is not
effective if begun more than 24 h after symptoms appear. Large doses of intravenous and
oral antibiotics, such as ciproflaxin (Cipro®), penicillin, doxycycline, tetracycline, and
erythromycin, are effective. Antibiotic treatment should ideally begin before the onset of
symptoms. It should be noted that some antibiotic-resistant strains of anthrax have been
identified. Laboratory studies have shown that B. anthracis can develop resistance to
ciprofloxacin, doxycycline, and β-lactam antibiotics.
Anthrax toxins are being studied to learn how to block their production and
ultimately their action. Researchers have discovered the three-dimensional molecular
structure of the anthrax protective antigen protein that is used to enter host cells; they
have subsequently been able to block the attachment of protective antigen in laboratory
experiments, thereby inhibiting anthrax toxin activity (NIH, 2007). In other studies, the
National Institute of Allergy and Infectious Diseases has synthesized a molecule that
interferes with anthrax toxin in cell culture and in rodents. The molecule blocks the pore
formed by anthrax protective antigen, which prevents lethal factor and edema factor
toxins from entering cells (NIH, 2007). In 2015, The U.S. FDA approved Anthrasil,
Anthrax Immune Globulin Intravenous, to treat patients with inhalation anthrax in
combination with appropriate antibacterial drugs. Anthrasil is manufactured from the
plasma of individuals vaccinated against anthrax. The plasma contains antibodies that
neutralize toxins produced by the anthrax bacteria. Anthrax spores were weaponized by
the U.S. military in the 1950s and 1960s before the U.S. offensive program was
terminated. Other countries have been or are currently suspected of weaponizing this
agent. The anthrax bacterium is relatively easy to cultivate. The formation of spores
facilitates both storage and weaponization of the organism. Anthrax spores are highly
resistant to sunlight, heat, and disinfectants—properties that are advantageous when
choosing a bacterial weapon.
A virus (from the Latin poison) consists of small units of DNA or RNA; a virus
does not constitute a complete cell. Virus particles (virions) are much smaller than
bacteria—they cannot be seen using conventional light microscopy. Each viral particle is
enclosed within a protective protein coat termed a capsid. The capsid shape varies from
simple helical and icosahedral forms to more complex structures. Viruses act by
parasitizing selected host cells; they are unable to grow or reproduce outside those cells.
Viruses are classified into animal, plant, and bacterial types, depending on the type of
host infected. Viral infections in human and animal hosts typically result in disease and
an immune response. In many cases, an invading virus is completely destroyed and
removed by the immune system. A key practical difference between viruses and bacteria
is that viruses cannot be treated using antibiotics. However, vaccines are effective in
preventing some viral infections or in limiting their effects. In some cases, antiviral drugs
have been developed to treat life-threatening infections.
The name smallpox is derived from the Latin word for spotted and refers to the
raised bumps that appear on the face and body of an infected victim. Two clinical forms
of smallpox exist; variola major is the most severe and most common form of smallpox,
characterized by an extensive rash and high fever. Variola minor is less common and a
less severe disease, with death rates historically of 1% or less. Variola is a member of the
Orthopoxvirus genus of poxviruses, which includes many species isolated from
mammals. Humans are the only natural hosts of variola; smallpox is not known to be
transmitted by insects or animals. Smallpox is highly contagious, and outbreaks have
been recorded for thousands of years. The last case of smallpox in the United States was
in 1949. The last known endemic case was recorded in October 1977 in Somalia. After a
successful worldwide vaccination program, the disease was declared eradicated from the
planet in 1980. After this historic event, routine vaccination against smallpox ended. The
United States discontinued vaccinations for civilians in 1972, and by 1985 the military no
longer vaccinated its recruits. The smallpox virus still exists, however—both the United
States and Russia retain stocks of the virus. It is fairly certain that some clandestine
stocks of smallpox virus exist in other nations as well.
Following entry into the body the virus travels to nearby lymph nodes where it
multiplies and causes viremia (contamination of the bloodstream with the virus). The
virus later spreads to the spleen, liver, and lungs. An incubation period of about 12–14
days follows, during which no symptoms are apparent and the victim may feel well.
During this time, infected individuals are not contagious. The first obvious symptoms of
the disease include fever, malaise, head and body aches, and sometimes vomiting (the
prodrome phase). The fever is usually high, in the range of 101–104°F. At this time,
victims become incapacitated. This phase may last for 2–4 days (U.S. CDC, 2007a).
After the prodrome phase, the first visible lesions occur in the mouth as red spots on the
tongue and on the oral and pharyngeal mucosa. These lesions enlarge and ulcerate
quickly, releasing large amounts of virus into the saliva. It is during this phase that the
victim is most contagious. As the sores in the mouth disappear, a rash appears on the
skin, starting on the face and spreading to the arms and legs and then to the hands and
feet (Figure 4.7). Usually, the rash spreads to all parts of the body within 24N h. During
this time, the lesions progress from macules to papules, then to pustular vesicles (a small
round raised area of inflamed skin filled with pus). As the rash appears, the fever usually
falls and the victim may start to feel better. However, fever often will rise again and
remain high until scabs form over the bumps (U.S. CDC, 2007a). The scabs begin to fall
off, leaving marks on the skin that eventually become pitted scars. Most scabs fall off
within 3 weeks after the rash appears. The victim is contagious until all scabs have fallen
off. Fatalities are usually caused by systemic toxicity and occur more frequently during
the second week of illness.
At the time of the last endemic cases in Somalia, supportive care was the only
possible treatment. As is the case with all viral diseases, antibiotics have no effect on the
progress of the disease. Smallpox vaccine, a live virus preparation derived from vaccinia
virus (another member of the Orthopoxvirus genus), is highly effective in inducing
immunity against the disease before exposure. Dryvax® is the vaccinia-based
formulation currently licensed in the United States. Vaccinia preparations do not contain
smallpox (variola) virus. The vaccine had previously been prepared using calf lymph
tissue; however, a reformulated vaccine, produced using cell culture techniques, was
subsequently developed. If administered within 3 days after exposure to smallpox virus,
the vaccine may prevent the disease or decrease the severity of disease and the risk of
death.
Smallpox virus was researched as a weapon by the Soviet Union during their
offensive biological program, and the status of former stockpiles is uncertain. Dr. Ken
Alibek, a former official of the Soviet bioweapons program, asserts that Russia continues
to research and manufacture biological weapons (Alibek and Handelman, 1999). The
Soviet government in 1980 is reported to have begun an ambitious program to produce
large volumes of smallpox virus and adapt it for payloads in intercontinental ballistic
missiles. The program was known to have an industrial capacity capable of producing
tons of smallpox virus annually. It is also reported that the Russian research program
continues working to produce more virulent and contagious recombinant strains
(Henderson et al., 1999). Many scientists in the Soviet bioweapons industry were put out
of work when Russia officially discontinued its offensive biological weapons program in
the 1990s, and there are concerns that some may be assisting rogue states working to
develop their own biological weapons programs.
Ebola hemorrhagic fever is a disease of humans and other primates caused by
ebolaviruses. The virus is a member of the family Filoviridae and the genus Ebolavirus
with five strains including Ebola (Zaire ebolavirus), Sudan virus (Sudan ebolavirus), Tai
Forest virus (Tai Forest ebolavirus), Bundibugyo virus (Bundibugyo ebolavirus), and
Reston virus (Reston ebolavirus) (U.S. CDC, 2014b). Ebola is one of the most virulent
viral diseases known, resulting in death in 20–90% of all clinically ill cases (WHO,
2015). Ebola was first identified in 1976 in two simultaneous outbreaks, one in Nzara,
Sudan, and the other in Yambuku, in modern-day Democratic Republic of the Congo, in
a village near the Ebola River where the disease takes its name (WHO, 2015). Ebola
viruses are currently found in several African countries. Since the 1976 occurrence,
outbreaks have occurred sporadically in Africa.
No specific treatment for the disease is available, although many potential
treatments are under investigation. Treatment is primarily supportive. Early supportive
care includes either oral rehydration therapy or administering intravenous fluids as well
as treating symptoms (management of pain, nausea, fever, and anxiety). Blood products
such as packed red blood cells, platelets, or fresh plasma may also be used. Other
regulators of coagulation have also been attempted including heparin, and clotting factors
to decrease bleeding. These efforts have been found to improve survival. Many Ebola
vaccine candidates had been developed and investigated over the past decade. The WHO
announced in mid-2015 that a vaccine has shown great promise in halting the spread of
the virus during clinical trials in Guinea (Phillip et al., 2015). The vaccine, VSVEBOV,
contains no live Ebola virus. Instead, it deploys a different virus, one that is alive and
replicating, and has been modified to replace one of its genes with a single Ebola virus
gene. The result is that the body’s immune system has an Ebola-specific response and is
better able to fight off an Ebola infection. The vaccine was found to be 100% effective in
treated individuals (Phillip et al., 2015). More than 4000 have been vaccinated with
VSVEBOV, and none developed Ebola after 6 to 10 days, the amount of time needed for
people to develop immunity.
C. Biological Toxins
Ricin is a highly toxic glycoprotein that occurs naturally in castor beans (Ricinis
communis). The ricin molecule consists of two polypeptide chains, the A chain and the B
chain, linked by a disulfide bond. Ricin can be produced easily and inexpensively; it is
highly toxic, stable in aerosolized form, and has no approved vaccine. Ricin can be
disseminated as an aerosol, by injection, or as a contaminant in food or water. The toxin
is not communicable from person to person, however. One of the more notorious
incidents involving ricin intoxication in recent years is the case of Georgi Markov, a
Bulgarian dissident. Markov was assassinated in 1978 at a London bus stop. Agents of
the Soviet KGB are believed to have used a modified umbrella equipped with a
compressed gas cylinder to fire a tiny ricin pellet into Markov’s leg (FigureN4.9). After
the injection, he developed severe gastroenteritis and high fever, and died in a hospital a
few days later. His body was autopsied and the ricin pellet was discovered. The initial
suspects were the Bulgarian secret police; Markov had defected from Bulgaria and
written books that were highly critical of the Bulgarian communist regime. Later,
however, some high-profile KGB defectors confirmed the involvement of the Soviet
KGB in the assassination.
Treatment of ricin poisoning depends on the route of exposure. Treatment is
supportive; no antidote is currently available for ricin. In the case of aerosol exposure,
treatment should be directed toward acute lung injury and pulmonary edema. It is critical
to ensure adequate oxygenation and ventilation for the patient. For GI exposure, the GI
tract should be decontaminated (i.e., lavaged) with superactivated charcoal. For exposure
via puncture, the injection site should be excised, if possible, within the shortest amount
of time. Antibiotics may help prevent infection. For dermal exposure, a dilute sodium
hypochlorite solution or soap and water will serve to decontaminate the skin.
Investigations are underway with potential vaccines and ricin inhibitors as antidotes.
Ricin can be disseminated as an aerosol, by injection, or as a food and water
contaminant. A large quantity of ricin is necessary to produce the effects of a weapon of
mass destruction, however. For example, the amount of ricin necessary to cover a 100-
km2 area and cause 50% lethality, assuming an aerosol toxicity of 3 μg/kg and optimum
dispersal conditions, is approximately 4 metric tons, whereas only 1 kg of B. anthracis
will cause the same damage (Kortepeter and Parker, 1999; Mirarchi, 2008). Ricin would,
however, be effective as a disabling agent. If used as a food and water contaminant, ricin
could easily incapacitate many and overwhelm local healthcare resources.
The U.S. military investigated the potential of ricin as a weapon during World
WarNI. At that time, it was being considered for use either as a toxic dust or as a coating
for bullets. The dust cloud method could not be perfected by war’s end, and the coated
bullet method would have violated The Hague Convention of 1899. During World War
II, the U.S. military studied the use of ricin in cluster bombs. Although there were plans
for mass production and several field trials with different bomb concepts, it was
eventually concluded that ricin was no more economical than using phosgene. Ricin was
given the military symbol W and later WA. Interest in ricin continued for a short period
after World War II but diminished when the U.S. Army Chemical Corps began a program
to weaponize sarin. Ricin was never used in battle.
lthough ricin is easy to produce, it is neither as practical nor likely to cause as
many casualties as other agents. Ricin becomes inactivated (i.e., its polypeptide chains
become denatured, thus becoming less dangerous) much more readily than anthrax
spores, which may remain lethal for decades. It is known that al-Qaeda experimented
with ricin, which has been interpreted as an inability by their weapons makers to produce
and/or weaponize botulin or anthrax.
D. Agroterrorism
Agricultural diseases have evolved to remain viable in soil for months to years in
spite of exposure to ultraviolet light, heat, lack of moisture, and other stressful conditions.
Thus, they are highly resilient in the natural environment and are expected to persist in
storage as well. In addition, the supplies and equipment necessary to carry out an
agroterror attack are relatively easy to obtain (Kohnen, 2000). Small quantities may be
needed, for example, of a specific livestock pathogen that would be relatively simple to
transport to the site of intended use. Infection of a small number of animals may be
sufficient to cause a disease outbreak. An epidemic could be caused by placing bird
droppings contaminated with Newcastle disease into a feeding trough, or by placing oral
scrapings from an FMDinfected animal onto the floor of a cattle barn.
Over many decades, a wide range of diseases were weaponized by the United
States, the former Soviet Union, China, Iraq, and other countries. The scientific expertise
and technology for developing such weapons on a large scale have been available for
more than a century. There are approximately 150 diseases of concern within the
livestock disease category alone. he most successful agriculture biological warfare
program was developed by the former Soviet Union, where a wide range of animal
pathogens were studied. The Soviets successfully used ticks to transmit FMD and avian
ticks to transmit ornithosis to chickens. Plant pathogens typically occur as fungi and, to a
lesser extent, as viruses and bacteria. Plant pathogens usually kill or injure a particular
crop species; however, in some unusual cases, the disease may produce toxins that can be
harmful to humans.
Rice and wheat are two cereal crops that supply the majority of the world’s daily
intake of calories. A disease event involving either of these crops, whether by natural
outbreak or from terrorist activity, would have significant social, political, and economic
consequences. Rice blast is a destructive disease of rice as well as a number of other
agriculturally important cereals including wheat, rye, barley, and pearl millet
(Knowledgebank, 2005). The disease is particularly damaging to upland rice crops
(Figure 4.11). A fungus, Magnaporthe grisea, is responsible for the disease, which is
known to occur in 85 countries worldwide. Rice blast is widespread and causes severe
economic losses—each year, it is estimated to destroy enough rice to feed more than 50
million people.
Karnal bunt, a fungal disease of wheat, was first discovered in wheat-growing
areas of India in 1931. It has subsequently been located in all major wheat-growing areas
in India, Pakistan, Iraq, Afghanistan, and South Africa. The disease was introduced to
Mexico in 1960, and by 1996 Karnal bunt was found in the United States in Arizona. The
disease does not severely impact crop production; however, because of international
regulations, an outbreak of Karnal bunt would significantly restrict export of wheat
overseas. The U.S. Department of Agriculture conducts an annual national survey to
certify the U.S. wheat crop is free from Karnal bunt.
Zoonotic diseases are those transferred from animals to man or from man to
animals. Approximately 150 such diseases are known to exist (University of Minnesota,
2005). Zoonotic diseases are of significant concern to U.S. public and animal health
sectors. The recent emergence of avian influenza and West Nile virus demonstrates the
vulnerability of industrialized nations to the spread of zoonotic diseases, and the general
inability to contain such diseases once they become established in wild animal
populations. Response to agroterror events is different from responses to human disease
events in a number of ways. The primary intent of response to an agricultural disease
event is to contain and destroy the disease by isolating the infected crops or animals. This
usually includes destruction of the crops and euthanasia of the animals involved.
Emergency responders may be involved in the containment, eradication, and/or
quarantine enforcement to limit the spread of agricultural diseases.
E. Nuclear Weapons
Nuclear weapons are by far the most powerful of all weapons of mass destruction
(WMDs). The detonation of a nuclear device by a terrorist group would result in
catastrophic physical effects, including blast overpressure, thermal effects, and radiation
contamination, and also cause tremendous psychological impacts worldwide. During the
Cold War between the United States and the Soviet Union (late 1940s to early 1990s), the
nations of the world lived with the constant threat of nuclear war. With the end of the
Cold War came the hope that the nuclear arsenals stockpiled by these and other countries
would eventually be dismantled. Unfortunately, however, international terrorist
organizations have been attempting to gain access to WMDs, including nuclear weapons,
by trying to recruit nuclear weapon scientists. In addition, several nuclear nations still
pose a military threat to others.
Nuclear weapons are designed and constructed based on two unstable materials,
uranium and plutonium. The uranium-based weapons are not manufactured directly from
this metal; the naturally occurring mineral must be enriched before it is usable in a
weapon. Enrichment processes are costly and extremely complex; therefore, only large
national institutes or industries possess the resources needed to carry out enrichment and
weapon fabrication. In other words, a terrorist group is unlikely to engage in such
activities without being detected. Plutonium does not exist in nature and is only produced
within a nuclear reactor, which is another complex technology limited solely to large-
scale enterprises.
Early in the twentieth century, the science of physics achieved remarkable
advances; much was discovered regarding the nature of atoms and their behavior. In the
late 1800s at the University of Wurzburg (Germany), Wilhelm Konrad Roentgen
conducted experiments involving high voltage currents in vacuum tubes and in 1895
discovered x-rays. In 1898, Pierre and Marie Skladowska Curie discovered a new
substance occurring within pitchblende (an ore of uranium) that emitted massive amounts
of energy (this energy was later to be termed radioactivity). The work of the Curies led to
the discovery of polonium in 1896 and radium in 1897. Different types of radioactive
emissions were soon identified; in 1899, Henri Becquerel found that some radiation
emissions were electrically charged. British chemist and physicist Ernest Rutherford went
on to distinguish two types of charged emissions— alpha and beta. He demonstrated that
alpha particles were actually helium atoms minus their planetary electrons. In 1900, Paul
Villard, a French physicist, identified gamma rays, which were determined to be
uncharged waves of electromagnetic radiation.
Also in 1932, John Cockcroft and Ernest Walton (English and Irish physicists,
respectively) were the first scientists known to have split the atom, and by late 1933
Hungarian physicist Leo Szilard conceived the idea of using a chain reaction of neutron
collisions with omic nuclei to release energy. He also realized the potential of using this
chain reaction to make bombs. In 1934, Szilard received a patent for the atomic bomb,
although he had no intentions of pursuing such a weapon; rather, his intent was to protect
the concept of the bomb to prevent its destructive use. He offered his theory to the British
government so that it could be made classified and protected under British secrecy laws.
The British War Office rejected Szilard’s offer; however, a few months later in February
1936, he succeeded in getting the British Admiralty to safeguard the new discovery
(Atomicarchive, 2008a). Nuclear fission (splitting) was documented in December 1938,
when German chemists Otto Hahn and Fritz Strassmann reported that they had detected
the element barium after bombarding uranium with neutrons (Hahn and Strassmann,
1939). On January 25, 1939, a research team at Columbia University conducted the first
nuclear fission experiment in the United States.
With the start of World War II, many of Europe’s most distinguished physicists
fled the continent. Scientists now understood that nuclear fission could be used in a
weapon; however, no one had yet determined how this could be accomplished. There was
a sense of alarm among scientists of the Allied nations that Nazi Germany might develop
its own project to create fission-based weapons. Urgent research began in the United
States and Britain with the intention of beating Hitler in the race to construct the bomb.
By 1942, the U.S. nuclear program was placed under the supervision of a military team
led by General Leslie Groves and became known as the Manhattan Project. Led by the
American physicist Robert Oppenheimer (Figure 5.1), the project brought together top
scientific minds including many European exiles. The United States and Britain agreed to
combine their resources for the project; however, the Soviet Union, the other major
Allied power, was not informed of plans for the bomb. In the early years of the war,
physicists halted all publishing on the topic of nuclear fission to prevent Nazi Germany
(and the Soviets, whom the United States and Britain did not trust) from gaining any
advantage in nuclear weapons development.
After considering arguments from scientists and military officers regarding the
possible use of atomic weapons against Japan, President Truman ordered dropping them
on Japanese cities with the hope that these weapons would stun the Japanese government
to the point of their country’s capitulation. Initial proposed targets of the first atomic
bomb included Tokyo, but this suggestion was dropped. The Target Committee
recommended Kyoto, Hiroshima, Yokohama, and a weapons depot at Kokura as possible
targets. On August 6, 1945 a uranium-based weapon, Little Boy, was dropped on
Hiroshima (FigureN5.2). Three days later, a plutonium-based device, Fat Man, was
dropped onto Nagasaki. The two bombs, specifically the blast wave, heat, and radiation
that were generated, killed at least 100,000 Japanese immediately, most of them civilians.
Tens of thousands died later of radiation sickness and cancer. Truman threatened to
destroy Japanese cities one by one until Japan accepted unconditional surrender. Japan
surrendered on August 15. Truman’s threat was actually a bluff, because the United
States had no more atomic bombs in its arsenal at the time.
The Soviet Union was not privy to intelligence about the U.S. atomic bomb
program; however, a substantial unit of Soviet spies was directly involved with the
Manhattan Project and regularly forwarded detailed plans about Allied weapons
development to their home country. One of the most notorious moles was Klaus Fuchs, a
German émigré physicist who had participated in the early British nuclear program
(Figure 5.3). During the war, Fuchs went on to work with the U.K. division at Los
Alamos. Fuchs was closely involved with the development of the plutonium weapon and
passed on detailed cross sections of the device to his Soviet contacts. The diverted
information, in combination with the Soviet’s own nuclear program led by physicist Yuli
Khariton, provided that country with the necessary resources for developing a tactical
nuclear weapon.
The first fusion device, code-named Mike, was tested by the United States during
Operation Ivy on November 1, 1952, at Eniwetok Atoll of the Marshall Islands (Figure
5.4). The device was very large, standing more than 20 ft tall and weighing more than 60
tons. The detonation yielded 10.4 megatons (Mt) of energy, almost 500 times the power
of the bomb dropped onto Nagasaki—obliterating the atoll and leaving an underwater
crater 6200 ft wide and 160 ft deep. On January 7, 1953, President Truman announced
the development of the hydrogen bomb to the world. The Soviet Union detonated its first
thermonuclear device, designed by physicist Andrei Sakharov, on August 12, 1953. The
Soviet weapon was cause of great concern within U.S. government and military agencies
because unlike Mike, the Soviet device was a deliverable weapon, which the United
States did not yet have. Although its yield was not in the megaton range, it was
nonetheless a powerful propaganda tool for the Soviets. On February 28, 1954, the
United States detonated its first deliverable thermonuclear weapon during the Castle
Bravo test at Bikini Atoll in the Marshall Islands. The yield of the device was 15 Mt,
more than twice its expected energy. This detonation also became the worst radiological
disaster in U.S. history. The exceptionally large blast combined with poor weather
conditions caused a cloud of radioactive nuclear fallout to contaminate more than 7000
mi2, including Marshall Island natives, and the crew of a Japanese fishing boat.
Early during U.S. and Soviet nuclear programs, most tests were conducted either
above ground (atmospheric tests) or under water. Concerns began to be raised about the
safety of the tests, which were now known to release nuclear fallout to the atmosphere.
Several prominent scientists and leaders called for an outright ban on nuclear testing. In
1958, the United States, USSR, and the United Kingdom (which had recently become a
nuclear state) declared a temporary testing moratorium for both political and public
health reasons. In 1961, the Soviet Union renounced the moratorium, and both the USSR
and the United States began testing their latest devices with greater urgency and
frequency. The Soviets tested the massive Tsar Bomba, the largest-ever nuclear weapon,
in October 1961. The device was detonated in a reduced state with a yield of about 50
Mt. The weapon was impractical for actual military use; however, it was hot enough to
induce third-degree burns at a distance of 62 mi (100 km).
By the 1950s and 1960s, other nations became members of the nuclear club. In
1952, British Prime Minister Winston Churchill announced that the United Kingdom had
an atomic bomb; a successful test took place in October of that year. Early U.K. weapons
were freefall bombs, soon followed by missiles, for example, Blue Steel, and later by
submarinebased ballistic missiles. In the 1950s, a French civil nuclear research program
began, which eventually generated plutonium as a by-product but also as a potential
nuclear fuel. A successful nuclear test, called Gerboise bleue (blue jerboa) took place on
February 13, 1960 in the French Sahara. On October 16, 1964, China’s first atomic bomb
was successfully tested at Lop Nur. A hydrogen bomb became operational less than 3
years later, in June 1967. It is believed that Chinese warheads had been improved and
miniaturized using designs obtained by espionage from the United States. The current
number of Chinese nuclear weapons is unknown; however, it is thought that up to 2000
warheads may have been produced.
F. Properties of the Atom and Radioactivity
The tremendous power of nuclear weapons originates from reactions occurring
within atomic nuclei. In nuclear reactions, matter is converted to energy. The amount of
energy generated is many orders of magnitude greater than that available from any
chemical reaction. A total of 92 elements are known to occur naturally; hydrogen (H) is
the lightest (having 1 proton) and uranium (U) the heaviest, with 92. There are also at
least 25 artificially created elements, termed transuranic (i.e., beyond uranium) elements,
used in research and industry. These elements comprise all matter on earth. The atom is
the simplest structural unit of any element that can exist, while still retaining the unique
chemical and physical characteristics of the element. An atom is composed of a central
nucleus containing most of its mass, with electrons orbiting in shells around the nucleus.
The nucleus consists of two fundamental particles, protons and neutrons (FigureN5.10).
The proton is a particle that possesses a positive charge. The neutron is an uncharged
particle with mass similar to that of the proton. Electrons are negatively charged particles
of extremely low mass.
Atoms of different elements possess unique numbers of protons in their nuclei.
The term atomic number describes the number of protons in a nucleus. An element may
contain varying numbers of neutrons, however. The total number of protons plus neutrons
in a nucleus is termed the atomic mass. When atoms have the same number of protons
but different numbers of neutrons, they remain the same element, but are termed isotopes
(Table 5.1). Some isotopes are known to be quite unstable. This instability is termed
radioactivity, which is truly the cornerstone of our discussion of nuclear science (and
nuclear weapons).
The nuclei of certain naturally occurring isotopes, and of others produced
artificially, contain excess energy, that is, they are unstable. To attain stability, those
energetic nuclei emit their excess energy in the form of nuclear radiation. Isotopes that
emit ionizing radiation from their nuclei to achieve stability are termed radioactive.
Radioactive isotopes are also referred to as radioisotopes or radionuclides. Each
radioisotope has its own unique radioactive decay scheme. A decay scheme identifies the
types of ionizing radiation emitted, the range of energies of the radiation emitted, and the
half-life of the decaying radioisotope.
The half-life of a radioisotope is the time required for half of the atoms of a
sample to decay to nonradioactive forms. Half-life values range from fractions of a
second to thousands of years, depending on the isotope. The concept of half-life is
extremely important in discussions of soil, structures, and debris contaminated by
radiation, and radioactive fallout. Radioactive decay can be plotted in linear or
semilogarithmic form (Figure 5.12). These line forms are used to determine, by simple
inspection, an isotope’s activity at a specific time.
G. Ionization and Forms of Radiation
Why is radiation such a significant hazard to the human body and to all biota? It is
well established that ionizing radiation significantly increases the risk of certain forms of
ancer. There are conflicting reports regarding the potential for radiation to increase the
risk of birth defects, however. Let us look at the root cause of the concern to emergency
responders, healthcare officials, and the public as regards radiation. Ionizing radiation
results in the deposition of energy in living tissue. Radioactive particles or waves (alpha,
beta, gamma radiation, and neutrons, discussed later) all possess significant energy. The
transfer of energy to the atoms of a recipient material (in this discussion, human tissue)
may occur via several mechanisms.
Excitation process involves the addition of energy to an atom, thereby elevating it
from its stable state (ground state) to an excited state. Excitation occurs when relatively
small amounts of energy are transferred. Depending on the type of interaction, either the
nucleus of the atom or one of its electrons will absorb the excitation energy. The excited
nucleus or electron will not retain this higher energy but tends to return to its original
energy level either by transferring the excess energy to other atoms or by emitting it as
electromagnetic radiation, often in the form of light or of x-rays. The ionization process is
especially significant in DNA, the genetic repository that codes for structure, physiology,
and behavior of an organism. It is accepted that random mutation of DNA is a natural
process (and is, in fact, the basis for natural selection and evolution); however, when
living tissue is bombarded with radioactive particles or waves, the incidence of DNA
mutation is considerably increased. DNA chains will therefore have a significantly
greater chance of fragmenting and recombining, resulting in the coding of new,
undesirable, and possibly detrimental changes in the affected organism (e.g.,
development of carcinomas).
There are four types of ionizing radiation that can be emitted from radioactive
elements. When large, unstable nuclides such as uranium or radium decay, they may emit
several forms of radiation. One common form is a particle composed of two protons and
two neutrons, essentially the nucleus of a helium atom minus its planetary electrons
(Figure 5.14). This form is termed alpha radiation. Alpha radiation is relatively heavy, of
low energy, and carries a net positive charge. Alpha travels only a few centimeters in air
and has little penetrating power. Most alpha radiation is stopped by 1–2 in of air or a
sheet of paper or cloth. Alpha cannot even penetrate the outer layer of dead skin on the
body. For this reason, alpha is considered an internal hazard only, that is, it must enter the
body to cause biological damage. For example, if radon gas (an alpha emitter) is inhaled,
the alpha particles can reach cells deep in the lungs and deposit large quantities of energy
in a small volume of unprotected tissue. Radon gas is therefore known to increase the risk
of lung cancer.
Beta radiation is essentially an electron minus an electrical charge, ejected from
the nucleus at high energy (Figure 5.15). Given its small size, beta particles have
extremely low mass. Externally, beta radiation is potentially hazardous to the skin and
eyes. Beta particles cannot penetrate through all skin layers to damage internal organs,
however. Beta radiation becomes an internal hazard if the beta emitter is ingested or
inhaled; in such cases, the source of the beta radiation is in proximity to living cells and
deposits energy over a small area. The range of beta radiation in air is about 10 ft. Most
beta radiation can be shielded by about ¼ in of plastic sheeting, aluminum foil, thick
clothing, or safety glasses.
Gamma rays and x-radiation have no mass and no charge; they are composed of
electromagnetic energy, not matter. Gamma radiation is illustrated in Figure 5.16. As
gamma and x-ray radiation have no charge and no mass, they have very high penetrating
power. Gamma rays travel great distances in air (thousands of yards to miles) at the speed
of light. They are considered a whole body hazard, that is, internal and external. Gamma
radiation can be extremely destructive to living tissue via ionization. A single gamma ray
may ionize many thousands of atoms along its path of travel. The more electrons it
removes (ionizes), the less energy remains. Eventually, the gamma radiation gives up the
last of its energy and disappears. Gamma radiation and x-rays must be shielded by very
dense materials such as concrete (6 in or more), lead (1 in or more), water (1 ft or more),
soil (1 ft or more), or thick steel (several inches).
As mentioned earlier, neutrons are one of the key subatomic particles occurring
within an atom’s nucleus. A neutron has mass, but no electrical charge. Emission of a
neutron particle is illustrated in Figure 5.17. Ionization of matter occurs as the result of
collisions between neutrons and target atoms. The neutrons continue on, smashing into
other atoms until they dissipate all their energy. Neutron radiation has a high penetrating
ability—they are difficult to shield and stop. The range for neutrons in air is up to several
miles. It follows that neutron radiation is a whole body hazard (internal and external)—it
easily penetrates body tissues and is quite destructive to cells. Neutron radiation is best
shielded by materials with high hydrogen content such as water or thick plastic (6–10 in
or more). In addition, thick concrete (1 ft or more), water (several feet), and soil (several
feet) are very effective for neutron shielding.
H. Nuclear Reactions
When nuclear materials are tightly packed such as in nuclear reactors and nuclear
weapons, such a process will cascade, resulting in a virtual avalanche of neutrons being
released that go on to split more and more nuclei. Each generation of neutrons released
can generate a tremendous number of fissions. This phenomenon is the so-called nuclear
chain reaction, or self-sustaining reaction. Ultimately, the energy recovered from such a
process may be extremely large. In theory, a single neutron could initiate a chain reaction
of nuclear fissions that could result in the splitting of each fissionable atom in a fuel
mass. In reality, however, not all the neutrons produce more fission reactions. Many
escape from the fissionable mass; others are removed by nonfission reactions. Both of
these effects were significant practical problems affecting the development of the first
atomic weapons.
The first requirement for generating a fission detonation is that sufficient material
be present and in the proper configuration so that successive generations of neutrons can
cause greater numbers of fission reactions. The quantity of fuel capable of sustaining a
chain reaction is termed a critical mass. A tremendous number of fissions is required for
the release of such immense amounts of energy as occurs in a nuclear detonation. One of
three types of chain reactions may occur for a given mass of fissionable fuel. Under
extreme heat and pressure, the nuclei of two isotopes of hydrogen (deuterium and tritium)
can fuse together to form a single atom of helium. This process is known as nuclear
fusion. For the fusion process to occur, the two nuclei must be forced together by enough
energy so that the strong, attractive, short-range nuclear forces overcome the electrostatic
forces of repulsion (U.S. Army, Navy, Air Force, 1996). Nuclear fusion occurs in the Sun
and is responsible for producing light, heat, and other energy forms. The two conditions
required for fusion to occur are: (1) extremely high temperatures (to accelerate the nuclei)
and (2) high pressure density (to increase the probability of interaction). For the
development of a weapon, the only practical means to attain the required temperatures
and pressures is by means of a fission detonation. Consequently, fusion weapons must
contain a fission component. The energy released in the detonation of a fission–fusion
weapon originates from approximately equal contributions of fission and fusion
processes.
Nuclear weapons are explosive devices that rapidly release the energy generated
from the fission or fusion of atomic nuclei. Nuclear devices are thousands of times more
powerful than any known chemical explosive. The explosive power, or yield, of a nuclear
weapon is typically expressed in terms of the quantity of TNT that would release an
equivalent amount of energy, often measured in thousands of tons of TNT (kilotons). For
the most powerful weapons, however, yield is measured in millions of tons of TNT
(megatons). The first of the fission bombs (July and August, 1945) had yields in the
range of 10–20 kt. Substantially greater yields have since been designed for fission
weapons. Fission weapons are designed to rapidly assemble a supercritical mass of fissile
material to create an uncontrolled fission chain reaction. The energy of this reaction is
released within a fraction of a second, resulting in a powerful detonation. Fission
weapons are the only type of nuclear weapon ever used in wartime. The United States
used a fission weapon against the Japanese city of Hiroshima and a second against the
city of Nagasaki near the end of World War II, in August, 1945. Since then, no nuclear
weapon of any type has been used in combat.
An implosion fission weapon is a significantly more sophisticated device
compared with the gun-type design. In the implosion assembly method (Figure 5.21), a
subcritical mass of U-235 or Pu-239 is compressed to produce a supercritical mass.
Compression is achieved by the detonation of many specially positioned high explosives
around a subcritical sphere of fissionable material. When the high explosive is detonated,
implosion occurs. The imploding blast wave compresses the sphere of fissionable
material, thus making the mass supercritical. Once compressed, the mass will undergo a
rapid chain reaction. The first nuclear weapon ever detonated, at the Trinity test near
Alamogordo, New Mexico, on July 16, 1945 was an implosion-type weapon. The Fat
Man bomb used against Nagasaki in World War II was an implosion-type weapon with
an explosive yield of about 21 kt.
Thermonuclear weapons derive their explosive yield from the combined power of
nuclear fission and fusion. An initial fission reaction with plutonium fuel generates the
extreme temperatures needed to trigger a secondary fusion reaction. The fission
component relies on implosion of plutonium fuel. Radiation from the fission detonation
heats and compresses a separate core of deuterium and tritium, which undergoes fusion.
In thermonuclear weapons, the key fusion reaction is known as the D–T reaction. Using
the heat and pressure of fission, deuterium (2H), fuses with tritium (3H) (Box 5.3), to
form helium-4 (4He) plus one neutron (η) and energy.
The fusion reaction generates additional explosive energy, but more importantly,
releases more neutrons within the core. These neutrons will bombard more of the fissile
plutonium, causing it to undergo fission rather than being dispersed by the detonation.
This boosting process significantly reduces the quantity of fissile material that might have
been wasted. Thermonuclear weapons are significantly more difficult to design, build,
and maintain than fission weapons (Figure 5.23). Thermonuclear weapons can be
extremely powerful, with yields measured in megatons. The largest nuclear weapon ever
produced was the Tsar Bomba tested by the Soviet Union on October 31, 1961. The
USSR claimed that the designed yield of the Tsar Bomba was 100 Mt; however, the yield
was reduced to 50NMt for safety reasons. There was, nevertheless, concern by the
weapon’s designers that the nuclear reaction might run away and cause damage on an
even greater scale. U.S. nuclear scientists concluded that the total yield of the weapon
was about 57 Mt.
An IND is essentially a home-made weapon designed to produce a nuclear
detonation. These devices may be fabricated in a completely improvised manner or may
be a modification to a weapon already present in a national nuclear stockpile. The
destructive capability of an IND depends on the explosive yield of the weapon and
location of the detonation. The possibility exists that an IND could generate a substantial
yield, as might be expected for a tactical nuclear weapon; however, the more likely
scenario would be a low-yield device of 5 kt or less that could be easily concealed and
transported. In the case of detonation of a low-yield weapon, damage would be much
greater than that of the largest high explosive devices deployed in truck bombs. Radiation
released from the blast may injure large numbers of people, who may exhibit no
symptoms for hours. The spread of radioactive fallout will create panic among the
general public.
I. Effects of Nuclear Detonations
The energy released by a nuclear detonation results in extensive damage to
buildings, infrastructure, and humans and other biota. As noted earlier, nuclear
detonations can potentially release millions of times more destructive force than the
largest conventional explosions (e.g., using TNT or RDX). Both nuclear weapons and
conventional explosives rely on the destructive force of the blast, or shock wave.
However, the temperatures attained in a nuclear detonation are markedly higher than are
those in a conventional explosion, and a large proportion of the energy is released in the
form of heat. Nuclear detonations are also accompanied by radiation, fallout, and
electromagnetic pulse (EMP). Blast, thermal radiation, and prompt ionizing radiation
occur within seconds or minutes of the detonation. Delayed effects, including radioactive
fallout, inflict damage over hours to years. The relative distribution of these effects
depends on the yield of the weapon, the location of the detonation, and the characteristics
of the blast environment.
The major proportion (approximately 50%) of energy from a nuclear weapon
detonated either on the Earth’s surface or within the atmosphere is released in the form of
blast and shock waves. At the instant of a nuclear detonation, the heat from the fireball
produces a high-pressure wave that moves outward. The front of the blast wave (the
shock front, shock wave, or incident shock wave) is a moving wall of highly compressed
air that travels rapidly away from the fireball, sharply increasing air pressure. The
pressure can crush structures and create hurricane-force winds at hundreds of miles per
hour (Figure 5.24). These winds, in turn, create pressure against objects facing the blast.
When this shock wave comes into contact with a solid object, it will either move the
object in the direction of the wave propagation or shatter it, depending on the strength of
the shock wave and the characteristics of the recipient object. The overpressure reaches
its maximum value upon the arrival of the shock wave (see Box 5.4). It then decays over
a period ranging from a few tenths of a second to several seconds, depending on the blast
strength and the weapon’s yield.
If the nuclear detonation occurs aboveground, the expanding blast wave will
quickly strike the surface of the Earth. This wave is immediately reflected from the
surface to form a second shock wave traveling behind the first. This reflected wave
travels faster than the first, or incident, shock wave because it is traveling through air
already moving at high speed owing to the passage of the incident wave. The reflected
blast wave merges with the incident shock wave to form a single wave, known as the
Mach stem. The overpressure at the front of the Mach wave is generally about twice as
great as that of the direct blast wave front (Figure 5.26). At first the height of the Mach
Stem wave is small, but as the wave front continues to move outward, the height
increases steadily.
Upon contact with human populations, the nuclear shock wave will push the
person in the direction of propagation and compress the body as the wave passes,
resulting in damage ranging from burst eardrums to destruction and liquefaction of
internal organs, depending on the amount of overpressure. Approximately 35% of the
energy of a nuclear weapon is released as heat, reaching temperatures at the moment of
detonation of 180,000,000°F (100 million °C). In contrast, the temperature due to
explosion of a conventional chemical explosive (e.g., TNT or RDX) is a few thousand
degrees.
About 15% of the energy released from a nuclear detonation occurs as various
types of radiation. The initial nuclear radiation comprises about one-third of this total.
Initial nuclear radiation, also termed prompt radiation, is defined as that produced within
about 1 min from detonation. Prompt radiation is quite destructive and is composed
mainly of neutrons, gamma rays, x-rays, and alpha and beta particles. Although prompt
radiation lasts for only about 1 min, it is lethal to all life forms within a few thousand
yards. At these distances, blast and thermal effects are also lethal. The electromagnetic
radiation (chiefly gamma rays) interacts with the molecules in the air (including debris)
so that its intensity is eventually reduced. The intensity and effects of such radiation
follow the inverse square law.
Radiation adversely affects the structure and function of cells. Two general
mechanisms of radiation damage are known in biological systems: direct action and
indirect action mechanisms. The direct action mechanism occurs from the direct attack on
a molecule by ionizing radiation and the consequent destruction of the molecule. Thus,
radiation damages cells by changing the structure of organic molecules such as DNA,
ribonucleic acid (RNA), and enzymes. For example, the molecular structure of a specific
enzyme that is essential to substrate metabolism in a cell is altered by radiation. As a
consequence, cell metabolism is disrupted and energy can no longer be generated. This
disruption causes the cell to die. The indirect action mechanism occurs when water in the
cell is irradiated. The water molecule is split and the resulting free radicals subsequently
damage the cell.
Many atoms can be converted into radioactive isotopes by neutron activation. In
the process, a nonradioactive atom absorbs a slow neutron (i.e., one whose kinetic energy
is below about 1 keV) and becomes a radioactive isotope having one additional mass
unit. The new atom can emit radiation as alpha, beta, or neutron particles, or x-rays or
gamma rays. Building materials, water, and soil can undergo neutron activation and thus
become radioactive. Most isotopes created by neutron activation have short half-lives and
quickly decay. Thus, the intensity of induced radioactivity decreases rapidly. About 10%
of the total energy from a nuclear blast occurs in fallout, that is, fine particles of
radioactive dust that settle back to earth over a period of minutes to years. This radiation
is largely attributable to the radioactivity of the fission products present in weapon debris,
plus irradiated soil and moisture thrust into the atmosphere from the detonation. It is
estimated that the radioactivity from detonation of a fission-type nuclear weapon results
from about 300 different radionuclides representing about 40 elements. As an example,
uranium-235 can split via many reactions to form numerous products. Equation 5.4
shows one possible fission reaction, where U-235 is converted to strontium-95, xenon-
139, and two neutrons (η), plus energy.
