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Agents and Ammo in Depth
Nerve Agents

VX Structure

In the early 1930s, a German company called I. G. Farbenindustrie began investigating chemical compounds called organophosphates for potential use as insecticides. In December 1936, Dr. Gerhard Schrader, who headed this research effort for the company, synthesized a highly toxic organophosphate that would later be given the name Tabun. Over a year later, he synthesized a second organophosphorous compound that he called Sarin. At that time, the German Ministry of Defense required any substance passing certain toxicity tests, which both compounds did, be submitted to the government for further investigation. When Tabun and Sarin were submitted, the German government quickly realized their potential as military weapons. Shortly thereafter, a large production facility was constructed in Dyhernfurth (then in Germany, now called Brzeg Dolny in Poland) and production of Tabun weapons commenced in 1942. Production of Sarin followed. Late in World War II, Soviet troops captured the Dyhernfurth facility, dismantled it, and moved it, along with several key personnel, to the Soviet Union where the production of nerve agent weapons began in 1946.

During WWII, Germany produced and put between 10,000 and 30,000 tons of Tabun into munitions. These weapons were never used, and toward the end of the War, U.S. and British troops seized large quantities of Tabun weapons stored at the German testing facility at Raubkammer. The munitions were taken to the United States and to the United Kingdom to be studied. The agent was unknown to these countries at the time. However, in a single weekend a small group of scientists at the U.K. Chemical Defence Establishment deciphered the toxicity of Tabun and identified a potential antidote.

Following WWII, organophosphate research mainly focused on the agents’ mechanism of action, in order to discover effective forms of protection against them. These studies resulted not only in better forms of protection, but also in the development of new, closely related chemical agents. By the mid-1950s, a group of more stable agents had been developed, which became known as V agents. The agent known as VX was first synthesized in the United Kingdom in the early 1950s, and was given to the United States for military development.

The United States began producing Sarin in the early 1950s and VX in the early 1960s for potential military use. Production continued for about a decade. In accordance with the Chemical Weapons Convention (CWC) of 1997, the United States is currently in the process of destroying its nerve agent stockpile.

Nerve agents have been used in terrorist attacks. In June 1994, members of a Japanese cult called Aum Shinrikyo released Sarin in an apartment complex in Matsumoto, Japan, killing seven and injuring over 300. On 20 March 1995, cult members released Sarin in the Tokyo subway system. In this incident, more than 5,500 people sought medical care and 12 died. The large majority of those seeking medical care suffered no ill effects from the agent.

Although no conclusive evidence exists, it is widely believed that Iraq under Saddam Hussein used VX against Iranian forces during the 1980-88 Iran-Iraq War, and then again in a 1988 chemical attack on Iraqi Kurds in the town of Halabja. That massacre reportedly killed 5,000 people and created serious health problems for thousands more. Iraq admitted to UNSCOM that it had researched VX, but claimed it had failed to weaponize the agent due of production problems.

Nerve agents consist of the highly toxic organophosphates Tabun (GA), Sarin (GB), Soman (GD), cyclosarin (GF), VX, VE, VG, and VM. Nerve agents are so-called because of their toxic effects on the nervous system. They are the most toxic and most rapidly acting of the known chemical warfare agents. Nerve agents are stable and easily dispersed, and have rapid effects both when absorbed through the skin or via respiration. G agents produce more toxic vapor than V agents, but V agents persist longer on clothing and surfaces after release. V agents are also about ten times more toxic than G agents and are less volatile.

VX is the most potent of all nerve agents. Exposure to no more than a pin-head-sized drop of VX is lethal to humans. Having the consistency of motor oil, it is also the least volatile of the nerve agents. This means that it is the slowest to evaporate and the most persistent in the environment. Under average weather conditions, VX can persist on surfaces for days. Under very cold conditions, it can last for months. Sarin is the most volatile nerve agent. It persists on surfaces for about 30 minutes.

The toxic effects of nerve agents are caused by the inactivation of the enzyme acetylcholinesterase (AChE). AChE is responsible for breaking down acetylcholine (ACh), an important neurotransmitter. In humans with normally functioning nervous systems, a signal from the brain is transmitted through nerves to the target muscle by the release of ACh into the neuromuscular junction. ACh triggers the muscle to contract. AChE then breaks down the ACh, which causes the muscle contraction to release. In the absence of active AChE, ACh accumulates at nerve endings, causing muscles to convulse continuously.

The extent of poisoning caused by nerve agents depends on the route of exposure, the amounts to which the person was exposed, and the length of time of the exposure. The latent period, or time between exposure and onset of symptoms, ranges from seconds to minutes when exposure is via inhalation. It ranges from minutes to hours when exposure is via absorption through the skin. Depending on the dose and length of exposure, symptoms can range from blurred vision and eye pain, watery eyes, runny nose, and chest tightness, to convulsions, paralysis, sudden loss of consciousness, and death. Fatigue, irritability, nervousness, and memory defects may persist for as long as six weeks after recovery from an exposure episode. Mildly or moderately exposed people usually recover completely, but severely exposed people are not likely to survive.

In the event of exposure to a nerve agent, the emergency response should consist of decontamination, ventilation, administration of antidotes, and supportive therapy. Although an antidote treatment exists, it must be administered immediately in order to be effective due to the rapid action of nerve agents. Small, lightweight, easy-to-use auto-injectors are available to military personnel for administering an antidote to themselves or to cohorts in the event of an exposure to nerve agents.