VX Agent

VX Agent


VX nerve agent (O-ethyl S-[2-diisoproylaminoethyl] methylphsophonothioate) 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 or eyes is fatal—and death usually occurs within an hour of exposure. VX poisons by binding to the enzyme cholinesterase and 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, 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 are 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 exist for VX poisoning: 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. Together, these drugs have been combined in an antidote kit called Mark I. Mark I is issued to United States troops, in particular those serving in the Persian Gulf region. Diazepam can also be used to treat the seizures and convulsions that may occur as a result of VX poisoning.

If VX is exposed to the eyes, they should be flushed with water for 10 to 15 minutes. Skin contact should be treated with washing in soap and water, 10% sodium carbonate solution or 5% bleach solution. If sweating and muscular twitching occur, then Mark I should be administered. If VX is ingested, Mark I should be injected immediately.

The history of VX. VX nerve agent was developed in 1952 by British chemists who were researching different types of insecticides. The United Kingdom traded information about VX with the United States government in exchange for information about thermonuclear weapons in 1953. A program to thoroughly study VX was subsequently begun at the Department of the Army's Edgewood Arsenal in Maryland. In 1957, scientists at Edgewood developed a binary system for delivery of VX in weapons. During the 1960s or 1970s, the Soviet Union's intelligence agencies learned the formula for VX and soviet scientists developed a program for the mass production of VX.

Although VX has not yet been used as a weapon, in 1968, the U.S. Army experimented with open-air tests of weapons containing VX at Dugway Proving Ground near Salt Lake City in Utah. During a test on March 14, a valve failed on an aircraft carrying the nerve gas and 320 gallons of VX were inadvertently sprayed over fields. Subsequently, 6,400 sheep that were grazing in the area died. The Army eventually took responsibility for the mishap and reimbursed ranchers for their loss.

The Iraqi government has admitted to manufacturing VX during the 1990s. It is possible that the formula for producing VX could have passed to Iraq via Russia, however the U.S. government has found no solid evidence of such a transfer of information. Further, reports surfaced in 2002 that the al-Qaeda terrorist network has obtained VX, but they had not been substantiated as of early 2003.

The use of VX as a weapon. VX is an extremely toxic material with low volatility and therefore, it dissipates very slowly. VX also has adhesive properties, which makes 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. Because of its potent toxicity, if VX were used on a missile, it could be an extremely deadly weapon. The LD50, or lethal dose for at least 50% of those exposed to VX is 10 ml. Therefore, VX is considered a weapon of mass destruction.



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Chemical Weapons: Nerve Agents. < http://faculty.washington.edu/chudler/weap.html > (February 11, 2003).

Material Safety Data Sheet: Lethal Nerve Agent VX. < http://www.ilpi.com/msds/vx.html > (February 11, 2003).

United States Army. Chemical Agent Fact Sheet: VX. < http://www.sbccom.army.mil/services/edu/vx.htm > (February 11, 2003).


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