Chemical Warfare Agents

Emergency responders may be faced with hundreds and even thousands of casualties. Firefighters and EMS personnel may be unprepared to deal with chemical agents and their victims released in a terrorist attack. In the Tokyo attack, medical personnel and emergency responders didn't realize the source of the victims' medical problems until some time had passed; no decontamination was performed.

Chemical warfare agents were introduced during World War I and were used as recently as the Persian Gulf War. These agents have been stockpiled at seven sites in the mainland United States and on Johnston Island in the South Pacific since World War I.

The U.S. stockpiles of "unitary" chemical warfare agents have been slated for destruction as a result of international treaty by the year 2004. (Unitary agents are those that act on their own without having to be mixed with another chemical to be activated.) Many of the aging munitions have experienced leaks of chemical agents at some of the facilities, although to date no off-post releases of any significance have occurred.

The U.S. Army and Federal Emergency Management Agency (FEMA) are coordinating efforts to ensure public safety in the event an accident occurs involving any stockpiled chemical agents. This cooperative effort is the Chemical Stockpile Emergency Preparedness Program (CSEPP). Emergency responders in areas likely to be affected by a release are trained in chemical agent awareness, emergency medical treatment and response procedures including personal protective equipment (PPE) and decontamination. Chemical agents also have been found around the country in unexploded munitions buried on and off present and past military installations.

There are two primary types of chemical agents: mustard and nerve. Mustard agents are also referred to as vesicants or blister agents because they form blisters when they contact the skin. The two types of mustard agent are sulfur mustard and nitrogen mustard. Nitrogen mustard is similar to sulfur mustard as far as its health effects but has slightly more systemic effects (affecting the entire body).

Mustard is often incorrectly referred to as "mustard gas." Mustard agent is a viscous oily liquid, light yellow to brown in color, with an onion, garlic or mustard smell and it freezes at 57 degrees Fahrenheit. Mustard is usually non-volatile but may produce a vapor hazard in warm weather or when involved in a fire. The vapor is heavier than air, with a density of 5.4. Mustard agent is heavier than water and non-soluble in water.

There are three basic types of blister agents: sulfur mustard, lewisite and phosgene oxime. Mustard agent is designed to function through skin and tissue contact and generally is not a major inhalation hazard under normal conditions.

Vesicants are persistent agents, which means they do not readily vaporize and will remain as contaminants for long periods. Mustard agents do not cause pain on contact and do not act immediately; instead, there is a dormant period of one to 24 hours before symptoms present themselves. Symptoms of mustard exposure include: erythema (redness of the skin), blisters, conjunctivitis (eye inflammation) and upper respiratory distress; the symptoms may worsen over several hours. Once mustard has contacted tissues, the damage has already started, although there may not be any indication that contact has occurred. Mustard is highly soluble in fat, which results in rapid skin penetration.

The lethal dose of liquid mustard applied to the skin is about seven grams spread over 25 percent of the body surface area. The threshold for skin erythema and blistering is 10 micrograms (a microgram is one millionth of a gram) per square centimeter deposited on the skin. The median lethal dose (LD50, or lethal dose for 50 percent of the population) for ingestion of mustard is estimated as 0.7 mg/kg of body weight. Damage occurs primarily to the skin, eyes and respiratory tract.

Vapor threshold doses of mustard that cause effects to the eyes are 0.1 Mg/M3 over 10 to 30 minutes of continuous exposure. Doses of 200 mg-min/m3 may cause corneal edema (swelling and fluid buildup within the cornea), keratitis (inflammation of the cornea) and blepharospasm (uncontrolled winking), leading to temporary blindness.

Irritation of the nasal mucous membranes and hoarseness first occur at doses ranging from 12 to 70 mg-min/m3. Lower respiratory effects, such as tracheobronchitis (bronchitis or inflammation of the trachea), tachypnea (excessively rapid respirations), cough and bronchopneumonia (inflammation of the lungs), begin to occur with doses exceeding 200 mg-min/m3.

Mild skin erythema may be seen with doses of 50 mg-min/m3. Severe erythema, followed by blistering, may begin at concentration-time profiles exceeding 300 mg-min/m3. Warm, humid environments may cause the earlier development of erythema and blistering at lower doses. The maximum safe doses for mustard have been established as 5 mg-min/m3 for skin exposure and 2 mg-min /m3 for eye exposure. The threshold limit value-time weighted average (TLV-TWA) for mustard is 0.003 mg/m3.

The Immediately Dangerous to Life and Health (IDLH) measure for mustard is recommended at 1.67 mg/m3. There is no known antidote for mustard agent. Mustard has been established as a human carcinogen.

Unless decontamination occurs within seconds after exposure to mustard, the results will be minimal. Hypochlorite solutions or large volumes of water are used to attempt to flush the agent from affected tissues. If decontamination is begun after symptoms start, it will have no effect.

Mustard enters the body through the cells of the skin or mucous membranes and produces biochemical damage within seconds ; no known procedure can reverse the process. Treatment of mustard exposure is much the same as for thermal burns and involves managing the symptoms and lesions (blisters). Mustard is rapidly transformed when it contacts the tissues in the body but is not found to be present in the blood, blister fluid, tissue, or urine.

Mustard exposures are rarely fatal and patients recover over a period of months. In World War I, one third of all U.S. casualties were the result of chemical exposure (sulfur mustard) but the fatality rate was only 5 percent.

Lewisite is a vesicant believed to have been used by Japan against China in the 1930s. It has no other known battlefield uses. Phosgene oxime is also a vesicant which has not been used on the battlefield.

Mustard is found in artillery shells, mortar shells, land mines and ton containers, which are similar to the ton containers used to ship and store chlorine. It is not likely that mustard would be used in terrorist activity because of the time it takes for mustard to act and its low volatility; however, if it were to be used, many hours would pass before the symptoms began to surface. This time delay would make diagnosis and determination of the incident source difficult.

Nerve Agents

Nerve agents are the most toxic of all chemical agents used in weapons. Nerve agents are nothing more than close relatives of organophosphate pesticides; however, military nerve agents are much more toxic. In fact, many of the nerve agents were discovered by chemists trying to make new pesticides.

Pesticides generally work by interfering with the functions of the central nervous system, and nerve agents act by the same means. Some common organophosphate pesticides include Malathione and Parathion. Another group of pesticides called carbamates cause the same type of central nervous system damage as the nerve agents although they are not related chemically. A common carbamate is the pesticide Sevin. Nerve agents were discovered in the 1800s but their toxicity was not realized until the early 1900s.

Nerve agents under moderate temperature conditions are liquids. They are clear, colorless and tasteless and most are odorless. The primary military nerve agents of importance are GA (Tabun), GB (Sarin, used in the terrorist attacks in Japan), GD (Soman), GF and VX. GB agent is the most volatile even though the evaporation rate is less then that of water. GD has a greater evaporation rate then GA, and GA has a greater rate than GF. It is unlikely that GD would be used as a terrorist weapon because of the complexity of its manufacture. VX has a viscosity similar to light motor oil and although it produces a slight vapor it generally is not considered to be a vapor hazard unless the ambient temperature is very warm.

In addition to being inhalation hazards, all nerve agents are also absorbed through the skin and will travel through ordinary clothing. The LD50 of VX is much smaller than for GB, GD, BA and GF. However, this is because the "G-agents" will evaporate from the skin before they can penetrate.

Tabun was first made in the 1930s by a German chemist. Sarin was also discovered in Germany about two years after Tabun (see "Sarin: The Unspoken Threat," May 1996). The German government manufactured large amounts of these nerve agents and stockpiled them during World War II but never used them. The Allies were not aware of the existence of the chemical nerve agents and had no protection or antidotes against them. After World War II, Soman, GF and VX were discovered, manufactured and stockpiled by the United States and the Soviet Union. The only known battlefield use of nerve agents was during the Iraq-Iran War, when Iraq used nerve agents against Iran. The major concern presently with nerve agents is the manufacture and use by terrorist groups.

Unlike the effects of slow-acting vesicants, vapor exposure to nerve agents will cause symptoms within seconds to several minutes after contact. Large amounts of nerve agent in vapor form will cause loss of consciousness and convulsions within seconds after one or two breaths. Nerve agent exposures on the skin will not present symptoms for varying periods of time depending on the amount of the exposure. Effects may occur from several minutes to as much as 18 hours. It takes time for the agent to penetrate the skin and reach the target organ(s).

Nerve agents act by inhibiting the enzyme cholinesterase. The function of cholinesterase is to destroy the neurotransmitter acetylcholine. Neurotransmitters are chemical substances released by a nerve impulse at the nerve ending. When released, they travel to the organ that the nerve stimulates.

Once it arrives at the organ, the neurotransmitter combines with the receptor site on the organ to cause an effect on the organ. For example, to move a muscle anywhere in your body, an electrical impulse originates in the brain and travels down appropriate nerves to the nerve ending near that muscle. The electrical impulse does not go to the muscle but causes the release of a neurotransmitter, which then travels across the very tiny gap between the nerve ending and the muscle to stimulate the muscle. The muscle reacts to this stimulation by moving. The neurotransmitter is then destroyed to prevent the stimulation of the muscle again. If additional muscle movement is required, another nerve impulse causes the release of more neurotransmitter.

The neurotransmitter acetylcholine is released by nerve endings and stimulates the intended organ. It is then destroyed by the enzyme acetylcholinesterase. As long as the acetylcholinesterase is intact, the body functions normally. If the cholinesterase is inhibited, the acetylcholine builds up and overstimulates the muscles, glands and other nerves which produce the symptoms exhibited by nerve agent exposures. The cholinergic nervous system stimulates skeletal muscles (those that are voluntarily moved, such as the arms, legs, trunk and face). Additionally the exocrine glands (lacrimal glands, nasal glands, salivary glands, sweat glands, and the glands that line the airways and gastrointestinal tract) are stimulated by acetylcholine.

Smooth muscles (of primary importance are the muscles that surround the airways and the gastrointestinal tract) are also stimulated by the neurotransmitters. When the acetylcholinesterase is inhibited, the excess acetylcholine overstimulates all of these structures to cause involuntary movement in the skeletal muscles. Excess secretions develop from the lacrimal, nasal, salivary and sweat glands and continue into the airways and gastrointestinal tract with resulting constriction of muscles in the airways that cause bronchoconstriction, similar to asthma. Constriction in the gastrointestinal tract causes cramps, vomiting and diarrhea.

The effects of nerve agents can be reversed by using atropine as an antidote. Atropine blocks the effects of the excess acetylcholine and is most effective for smooth muscles and glands but does not help the skeletal muscles. A drug called pralidoxime chloride (2-PAMC1) is used in conjunction with atropine to treat the skeletal muscles. Convulsions may also occur with exposures to nerve agents and diazepam (Valium) is administered in some instances to help control the convulsions. Local protocols should be established for administration of antidotes based on advice from the local EMS medical director.

Protective Clothing

Mustard and nerve agents are chemicals and therefore require an appropriate level of chemical protective clothing. Military PPE for battlefield protection against chemical agents is composed of a charcoal suit, protective hood made of butyl rubber protected cloth, butyl rubber gloves with thin cotton inserts, vinyl boots and a powered air-purifying respirator (PAPR).

The PAPR is used instead of self-contained breathing apparatus (SCBA) because of the length of time that the respiratory protection may be needed and the difficulty in changing SCBA bottles in a hazardous atmosphere or under battlefield conditions. The PAPR will remove up to 0.5 mg/m3 of nerve agent GB for up to 16 hours based on the longest time an emergency responder has used the PAPR (tests indicate that the filters and cartridges have the shortest service life against nerve agent GB compared to other lethal chemical agents). The actual expected time of cartridge usage during an incident is up to 12 hours.

One of the major problems that occurs with any type of chemical protective clothing is heat stress (see "Hot Zone Rescue," December 1996). Because of the extended time the PAPR can be worn, the danger of heat stress is great. In reality, responders will be limited in the amount of time spent in the PPE by heat stress potential rather than the limitations of the air supply.

Most chemical agents require warm temperatures for them to pose a vapor problem; thus, if there is vapor, heat stress will be a problem.

Recommended For PPE Wearers

The PAPR should not be used in IDLH atmospheres or in atmospheres where the oxygen concentration is less than 16.5 percent. Airborne agent concentration IDLH values have been established for the following nerve agents: GA/GB 0.2 mg/m3; GD 0.06 mg/m3; and VX 0.02 mg/m3 . The PAPR uses a battery-operated blower that is designed to deliver essentially decontaminated air at a slight positive pressure into a full facepiece. The blower draws ambient air through two or three air-purifying elements (filters or chemical cartridges) which remove specific contaminants and deliver the subsequent air through a corrugated breathing tube into a facepiece assembly on the face of the respirator wearer.

There is also commercially available chemical protective clothing that has been tested against live agents and passed for use by emergency responders. The Army PPE is available for civilian use by emergency responders in CSEPP-affected communities. Many emergency responders in those areas, however, have chosen to use a commercial chemical suit with the PAPR rather than the military battle suit. The butyl rubber hood is still required even with the commercial chemical suit.

Unlike most hazardous materials incidents, decontamination for chemical agent releases will focus primarily on contaminated victims. There are likely to be hundreds and even thousands of exposed citizens who may need various levels of decontamination.

The process will be very labor intensive and unlike any other decontamination process responders have previously faced. In some cases, citizens will need to be decontaminated simply for their own peace of mind. Vapor exposures do not require as extensive a decontamination as does liquid exposures. In reality, little contamination occurs from a vapor exposure. The public, however, may perceive a need for decontamination, and it may have to be performed even if only for psychological reasons.

Decontaminating hundreds or thousands of potentially contaminated victims could create a logistical nightmare. Responders in the Chemical Stockpile Program have acquired specially designed decontamination trailers for treating large numbers of citizens. These trailers would work well for mass exposures from terrorist incidents.

When large numbers of casualties start showing up from apparently unknown sources, chemical or biological terrorism should be a consideration. These types of incidents will tax the emergency response system as never before.

Responders must plan and train for chemical as well as nuclear and biological terrorism attacks but even with planning, these will be difficult incidents. The U.S. Department of Veterans Affairs has a program available to provide chemical and biological weapons training and assistance. The agency can provide Disaster Medical Assistance Teams (DMATs) to assist local medical personnel at the scene of terrorist attacks or any other disaster.

At best, most local hospitals have only limited supplies of antidotes to chemical agent exposures. The VA's Office of Medical Preparedness (OMP) has a stockpile of antidotes for chemical agent exposures. DMATs with antidotes can be airlifted directly to a disaster scene.

Robert Burke

For additional information on chemical warfare agent training, technical information or contacts, write to the author at Firehouse.®