VX Agent

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VX Agent

VX poisoning

Treatment of VX poisoning

Resources

VX nerve agent (O-ethyl S-[2-diisoproylaminoethyl] methyl phsophonothioate) is one of the most toxic substances ever developed. Like other nerve agents, it is an organophosphate. Although it is often called a nerve gas, VX is usually a clear, odorless, tasteless liquid. A tiny amount of VX, about 10 mg, absorbed through the skin, eyes, or ingested is fatal, and death usually occurs within an hour of exposure. VX poisons by binding to the enzyme cholinesterase, inactivating it. As a result, the chemical signals passed between nerve cells are transmitted uncontrollably. Symptoms of VX poisoning include constriction of the pupils, headache, runny nose, and nasal congestion, chest tightness, giddiness, anxiety and nausea, eventually progressing to convulsions and respiratory failure. VX poisoning can be treated immediately with two antidotes: atropine and pralidoxome chloride. Because of its extreme toxicity, VX is considered a weapon of mass destruction.

VX poisoning

Chemical signals are transmitted between nerve cells by means of small molecules called neurotransmitters. One of the most common neurotransmitters in the central and peripheral nervous system is acetylcholine. Under normal conditions, acetylcholine is released from the terminal axon of one nerve cell, crosses the synaptic cleft between nerve cells and binds with a receptor on the membrane of the post-synaptic nerve cell. Then, the enzyme cholinesterase binds to acetylcholine and inactivates it. This completes the chemical signaling between nerve cells.

When the VX nerve agent is present in the nervous system, it inactivates the enzyme cholinesterase. As a result, the receptor on the post-synaptic nerve cell is indefinitely stimulated by acetylcholine. In addition, the pre-synaptic nerve cell continues to release acetylcholine. Nervous signals are never completed and the nervous system is eventually destroyed.

VX poisoning can occur by exposure to the eyes or skin, inhalation, or ingestion. Symptoms occur within minutes. Autonomic nervous system symptoms include constricted pupils, reduced vision and other visual effects, drooling, sweating, diarrhea, nausea, vomiting, and abdominal pain. Neuromuscular symptoms include twitching, weakness, paralysis, and eventually respiratory failure. Symptoms affecting the central nervous system are headache, confusion, depression, convulsions, coma, respiratory depression, and respiratory arrest.

Treatment of VX poisoning

Two antidotes for VX poisoning exist: atropine and pralidoxime chloride, also called 2-PAM. Atropine blocks one type of acetylcholine receptor on the post-synaptic nerve cell membrane. This prevents acetylcholine that is in the synaptic cleft from binding to the receptor. Pralidoxime chloride prevents VX from binding to cholinesterase. These two drugs are combined in an antidote kit called Mark I.

VX is an extremely toxic material with low volatility and therefore, it dissipates very slowly. VX also has adhesive properties, which make it difficult to remove from surfaces. These characteristics make a powerful strategic contaminant. For example, military bases contaminated with VX could result in casualties for several weeks if the base continued to be used. In order to counter such tactics by terrorist groups, scientists at the Department of Energy’s Idaho National Engineering and Environmental Laboratory have recently developed technology to detect VX and to predict its degradation rate on concrete surfaces.

See also Bioterrorism.

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Resources

BOOKS

Haugen, David M., ed. Biological and Chemical Weapons. San Diego: Greenhaven Press, Inc., 2001.

Sifton, David W., ed. PDR Guide to Biological and Chemical Warfare Response. Montvale, NJ: Thompson/Physician’s Desk Reference, 2002.

OTHER

Centers for Disease Control and Prevention, U.S. Government. “Facts about VX.” February 22, 2006.

<http://www.bt.cdc.gov/agent/vx/basics/facts.asp> (accessed November 27, 2006). Safety Emporium. “Material Safety Data Sheet: Lethal

Nerve Agent VX.” September 29, 1999. <http://www.ilpi.com/msds/vx.html> (accessed November 27, 2006).

University of Washington. “Chemical Weapons: Nerve Agents.” <http://faculty.washington.edu/chudler/weap.html> (accessed November 27, 2006).

Juli Berwald

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