Chemical Warfare

Injury from chemical weapon agents, known as CWAs, may result from industrial accidents, military stockpiling, war, or a terrorist attack.

Industrial accidents are a significant potential source of exposure to chemical agents. Chemicals such as phosgene, cyanide, anhydrous ammonia, and chlorine are used widely. These chemicals are frequently transported by industry. The accidental release of a methylisocyanate cloud (composed of phosgene and isocyanate) was implicated in the Bhopal, India, disaster in 1984.

• Chemical weapons first were used in 1915, when the German military released 168 tons of chlorine gas at Ypres, Belgium, killing an estimated 5,000 Allied troops.
• Two years later, the same battlefields saw the first deployment of sulfur mustard. Sulfur mustard was the major cause of chemical casualties in World War I.
• CWAs have been used in at least 12 conflicts since, including the first Persian Gulf War (Iraq-Iran War). The Iraqi military also used chemical weapons against the Iraqi Kurds during the second Persian Gulf War.
• Civilians also have been exposed inadvertently to chemical weapons many years after weapon deployment during war. Some 50,000 tons of mustard shells were disposed of in the Baltic Sea following World War I. Since then, numerous fishermen have been burned accidentally while hauling leaking shells aboard boats. Leaking mustard shells also have injured collectors of military memorabilia and children playing on old battlefields.

Although a number of international treaties have banned the development, production, and stockpiling of chemical weapons, these agents reportedly are stillbeing produced or stockpiled in several countries.

Within the last decade, terrorists deployed chemical weapons against civilian populations for the first time in history. The release of sarin in Matsumoto, Japan, in June 1994 by the extremist Aum Shinrikyo cult left 7 dead and 280 injured. The following year, the Aum Shinrikyo cult released sarin vapor in the Tokyo subway system during morning rush hour, leaving 12 dead and sending more than 5,000 casualties to local hospitals.

Several characteristics of chemical weapon agents lend themselves to terrorist use.

• Chemicals used in CWAs are widely available, and recipes for CWA production may be found on the Internet.
• CWAs are transported easily and may be delivered by a variety of routes.
• Chemical agents often are difficult to protect against and quickly incapacitate the intended targets.
• Most civilian medical communities are inadequately prepared to deal with a chemical terrorist attack.

• Chemical weapon agents are hazardous substances. Major categories of CWAs include the following:
  • Nerve agents (such as sarin, soman, cyclohexylsarin, tabun, VX)
  • Vesicating or blistering agents (such as mustards, lewisite)
  • Choking agents or lung toxicants (such as chlorine, phosgene, diphosgene)
  • Cyanides
  • Incapacitating agents (such as anticholinergic compounds)
  • Lacrimating or riot control agents (such as pepper gas, chloroacetophenone, CS)
  • Vomiting agents (such as adamsite)
• Physical properties: CWAs generally are stored and transported as liquids and deployed as either liquid aerosols or vapors. Victims usually are exposed to agents via 1 or more of 3 routes: skin (liquid and high vapor concentrations), eyes (liquid or vapor), and respiratory tract (vapor inhalation). In general, some liquids may be harmful whether inhaled into the lungs or absorbed into the skin. Vapors can be affected by winds. Even a slight breeze can blow a nerve agent vapor away from its intended target. The effects of vapor are enhanced when used within an enclosed space.
• Clinical effects: Depending on the agent and the type and amount (concentration) of exposure, CWA effects may be immediate or delayed. Large inhalation exposures to nerve agents or mustards are likely to kill people immediately. Small exposures on the skin to nerve agents and mustards are more dangerous than they seem at first. People exposed to such agents need to be carefully observed for slowly developing or delayed effects. A chart of signs and symptoms is available from the North Carolina Statewide Program for Infection Control and Epidemiology.
• Medical management: Ideally, emergency personnel will wear personal protective equipment, decontaminate the victims immediately, provide medical support to the victims and provide specific antidotes to counteract the harmful effects.
• Personal protective equipment: First responders to a chemical attack are at serious risk themselves from the chemically contaminated environment (known as the hot zone). They can come in direct contact with the CWA or inhale the vapor. They are also at risk if they handle skin and clothing of victims if a liquid chemical agent was used. Vapors pose little added risk for anyone outside the hot zone.
• Decontamination: Decontamination is the physical process of removing the remaining chemicals from people, equipment, and the environment. Residual hazardous chemicals on those who have been exposed directly are a source of ongoing exposure to others and pose a risk of secondary exposure to first responders and emergency care personnel. Immediate decontamination is a major treatment priority for those with CWA exposure.
  • Initial decontamination involves removing all contaminated clothes and jewelry from the affected person and then washing the body thoroughly with warm water and soap.
  • Hot water and vigorous scrubbing may actually worsen the effects by increasing chemical absorption into the skin.
  • Vapor exposure alone may not require decontamination. But if it is not known whether the exposure was to a vapor or liquid, or if exposed people have symptoms, they should undergo decontamination.
  • Ideally, decontamination will take place as close as possible to the site of exposure to minimize duration of exposure and prevent further spread. Hospitals receiving contaminated people may establish an area outside the Emergency Department in which to perform initial decontamination before people and equipment are allowed entry. Portable decontamination equipment with showers and run-off water collection systems are commercially available. All hospitals should have the capacity to safely decontaminate at least 1 person.
• Supportive and specific therapy: Doctors will first make sure exposed victims are able to breathe. For many chemical warfare agents, doctors can only treat the symptoms they produce. But specific, well-established antidotes are available for nerve agent and cyanide exposures. Lab tests are not widely available in hospitals to rapidly confirm exposure to chemical agents.

The 5 nerve agents, tabun (GA), sarin (GB), soman (GD), cyclohexylsarin (GF), and VX, have chemical structures similar to the common organophosphate pesticide Malathion. These agents initially stimulate and then paralyze certain nerve transmissions throughout the body and cause other toxic effects such as seizures.

• Physical properties: Under temperate conditions, all nerve agents are volatile liquids, which means they can evaporate quickly. The most volatile agent, sarin, evaporates at about the same rate as water. The least volatile agent, VX, has the consistency of motor oil, which makes it 100-150 times more toxic than sarin when victims are exposed on their skin. A 10 mg dose applied to the skin may cause death in up to half of unprotected people. All nerve agents rapidly penetrate skin and clothing. Nerve agent vapors are heavier than air and tend to sink into low places (for example, trenches or basements).
• Signs and symptoms: Nerve agents produce various signs and symptoms depending on the agent someone might be exposed to, its concentration, and length of exposure.
  • Liquid exposure: Liquid agents easily penetrate skin and clothing. Symptoms may begin anywhere from 30 minutes to 18 hours after skin exposure. A small droplet on the skin, for example, may cause local sweating and muscle twitching, followed by nausea, vomiting, diarrhea, and generalized weakness. Even with decontamination, signs and symptoms may last for hours. In contrast, people with severe liquid exposures may show no symptoms (for 1-30 minutes) but rapidly may suffer abrupt loss of consciousness, convulsions, generalized muscular twitching, paralysis, secretions (from the nose, mouth, lungs), difficulty breathing, and death.
  • Vapor exposure: Vapor inhalation produces poisonous symptoms within seconds to several minutes. Effects may be local or throughout the body. Exposure to even a small amount of vapor usually results in at least one of the following categories of symptoms: (1) in the eyes, blurred vision, eye pain, red eyes; (2) runny nose; or (3) difficulty breathing, shortness of breath, excessive productive coughing.
  • Respiratory tract: Nerve agents act on the upper respiratory tract to produce runny nose, drooling, and weakness of the tongue and throat muscles. High-pitched, distressed breathing can occur. A great deal of phlegm production and narrowing of the airways can occur. If untreated, the combination of symptoms rapidly progresses to respiratory failure and death.
  • Cardiovascular system: Nerve agents also act on the heart and may produce abnormal heartbeats, more likely to be too fast rather than slow.
  • Central nervous system: Nerve agents produce a variety of signs and symptoms throughout the central nervous system. People may lose consciousness (sometimes within seconds of exposure) and have seizures. Symptoms such as headache, dizziness, numbness or tingling, anxiety, insomnia, depression, and emotional instability also have been reported.
  • Musculoskeletal system: Nerve agents initially stimulate and then paralyze muscles. With minimal exposure, exposed people may complain of vague weakness or difficulty walking.
  • Eyes: Nerve agent liquid or vapor readily penetrates the eye tissues and may cause the pupils to contract, blurred and dim vision, headache, redness, tears, pain, nausea, and vomiting. Although contraction of the pupils is the most consistent clinical finding after vapor exposure to nerve agents (this occurred in 99% of people exposed in the Tokyo sarin attack), it may not occur or occur later if the exposure is on the skin. In severe cases, the pupils of the eye may remain narrowed up to 45 days.
• Diagnosis: Routine testing is not reliable in identifying nerve agents in blood or urine. So doctors will make their treatment decisions based on the signs and symptoms a person shows and on information about the type of chemical exposure, if known.
• Treatment: Treatment of victims exposed to nerve gas is similar to the treatment of those poisoned by organophosphate insecticides.
  • Atropine sulfate: Victims with symptoms require immediate treatment with atropine. Atropine helps people breathe by drying secretions and opening their airways to allow them to breathe more freely. Atropine also blocks other effects of poisoning, such as nausea, vomiting, abdominal cramping, low heart rate, and sweating. Atropine, however, does not prevent or reverse paralysis. Adults and children will be given appropriate doses of atropine by IV or injection. Another medication, pralidoxime chloride, may also be given. With adequate decontamination and appropriate initial therapy, serious signs and symptoms of nerve agent toxicity rarely last more than a couple of hours.
  • Mark I kit: The Mark I kit was designed for military self-administration in the field. It consists of 2 spring-loaded devices to inject yourself, containing atropine and pralidoxime, respectively. These antidote kits are not yet available for civilian use.
• Prognosis: Peak toxic effects occur within minutes to hours and go away within 1 day. People who were exposed but show no symptoms are usually observed for at least 18 hours because some signs and symptoms can show up later.

Sulfur mustard has been used as a chemical weapon since World War I. Nitrogen mustard, a derivative of sulfur mustard, was one of the first chemotherapy agents but never has been used in warfare. These agents cause blistering of exposed surfaces. Both mustard agents rapidly penetrate cells and generate a highly toxic reaction that disrupts cell function and causes cell death. The chemical reaction is both temperature dependent and aided by the presence of water, which explains why warm, moist tissues are affected more severely. Actively reproducing cells, such as skin and blood cells, are most at risk.

Physical properties: Mustards are oily liquids with odors of mustard, onion, garlic, or horseradish. Highly soluble in oils, fats, and organic solvents, mustards quickly penetrate skin and most materials, including rubber and most textiles. Sulfur mustard is considered a persistent agent with low volatility at cool temperatures but becomes a major vapor hazard at high temperatures. Exposure to mustard vapor, not mustard liquid, is the primary medical concern. More than 80% of mustard casualties in World War I were caused by exposure to mustard vapor. Mustard vapor is 3 times more toxic than a similar concentration of cyanide gas; however, mustard liquid is also quite toxic. Skin exposure to as little as 1-1.5 teaspoons of liquid (7 g) is lethal to half of those exposed.

Mustards signs and symptoms

Mustards injure the skin, eyes, respiratory tract, GI tissues, and blood system. The pattern of toxicity depends partly on whether the person is exposed to liquid or vapor. Liquid exposure primarily damages the skin, producing an initial rash followed by blistering similar to a partial-thickness burn. Vapor exposure damages the upper respiratory tract (skin usually is not affected). Mustards penetrate cells in less than 2 minutes, yet signs and symptoms usually are delayed 4-6 hours (the range can be from 1-24 hours). The time it takes to show symptoms is shorter with high-concentration exposures, such as those occurring at increased room temperature and humidity.

• Skin: Chemical burns caused by mustard often appear deceptively superficial at first. Earliest symptoms are itching, burning, and stinging pain over exposed areas. Moist, thinner skin is affected more severely. Affected areas appear red and swollen. If contamination is more extensive, superficial blisters occur within 24 hours of exposure. Most burns are partial thickness, but full-thickness burns with deep blisters may result from exposure to higher concentrations. Blister fluid does not contain active mustard and is not toxic.
• Eyes: Eyes are especially sensitive to the effects of mustard. Symptoms begin 4-8 hours after exposure. Earliest symptoms include burning pain, a feeling that something is in the eye, sensitivity to light, tearing, and blurred vision. Permanent corneal scarring and blindness may occur with severe exposures, but is rare.
• Respiratory tract: Mustards primarily damage tissues in the upper airway through a direct inflammatory effect. Following a period of 2-24 hours after exposure, symptoms may appear. Early symptoms include sinus congestion, a sore throat, and hoarseness. Later, cough, shortness of breath, and trouble breathing may develop. People with severe and extensive contact with mustard gas may develop respiratory complications up to several days after exposure.
• Gastrointestinal tract: Rarely, mustard damages rapidly growing cells of the intestinal tract. GI involvement results in abdominal pain, nausea, vomiting, diarrhea, and weight loss.
• Blood system: Rarely, mustards cause unpredictable loss in the production of bone narrow. Certain specialized cells begin dying 3-5 days after exposure reaching its worst point in 3-14 days, depending on the severity of exposure.

Mustards Diagnosis

Diagnosis of mustard exposure is based on what the doctor observes from the person’s signs and symptoms. No laboratory tests are useful.

Personal protective equipment: Liquid mustard contamination poses a risk for emergency care personnel. Ideally, they will be wearing appropriate personal protective gear.

Mustards decontamination

Immediate decontamination within 2 minutes of exposure is the most important intervention for people who have skin exposure to mustard, because it rapidly becomes fixed to tissues, and its effects are irreversible. Even if an exposure takes place and a person shows no obvious sign and symptoms, decontamination is still urgent.

• Remove clothing immediately and wash the skin with soap and water.
• Eye exposure requires immediate washing out with a large amount of saline or water.
• Decontamination after the first few minutes of exposure does not prevent further damage later but at least prevents spread of the chemical to other parts of the body and protects emergency care personnel from further contact exposure.

Mustards Treatment

Treatment of mustard exposure is based on symptoms. Because the effects of mustards typically are delayed, people with complaints immediately after exposure may have an additional injury.

• For those with signs of upper airway obstruction, doctors may treat by using a tube in the person's throat or perform surgery to open the airway.
• Mustard-induced burns are especially painful. Doctors will use strong pain relievers. Adequate burn care is essential, because skin lesions heal slowly and are prone to infection. Severe burns may require removal of dead tissue, irrigation, and placement of antibiotics, such as silver sulfadiazine, directly on the burned area. The victim may need a tetanus shot.
• Severe eye burns may be treated with daily irrigation, topical antibiotic solutions, topical corticosteroids, and drugs that dilate the pupil. Petroleum jelly may be applied to prevent eyelids from sticking together. More severe corneal injuries may take as long as 2-3 months to heal. Permanent visual problems are rare.
• Although no antidotes currently are available to treat mustard toxicity, several agents are under investigation.
• Victims with bone marrow suppression following mustard exposure may be treated with medication to stimulate the bone marrow, such as granulocyte colony-stimulating factor.

Mustards Prognosis

Victims with significant respiratory tract burns usually require admission to the hospital’s intensive care unit. Also, victims with several skin burns will be admitted to the burn unit for burn care, pain relief, and supportive care. Blood cell counts will be monitored for 2 weeks following significant exposures. Most people recover completely. Only a small fraction have long-term eye or lung damage. About 2% of those exposed to sulfur mustard in World War I died, mostly due to burns, respiratory tract damage, and bone marrow suppression. Sulfur mustard is known to cause cancer, yet a single exposure causes only a small risk.