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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.
Photo by Robert Burke
A decontamination trailer can be used for treating mass casualties of a chemical incident.
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.