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Nerve Gas

Nerve Gas

JUDYTH SASSOON

Nerve gases, or nerve agents, are mostly odorless compounds belonging to the organophosphate family of chemicals. Nerve gasses are either colorless or yellow-brown liquids under standard conditions. Two examples of nerve gases that have gained some notoriety through their powerful physiological effects are Sarin and VX. Even in small quantities, nerve gases inhibit the enzyme acetylcholinesterase and disrupt the transmission of nerve impulses in the body. Acetylcholinesterase is a serine hydrolase belonging to the esterase enzyme family, which acts on different types of carboxylic esters in higher eukaryotes. Its role in biology is to terminate nerve impulse transmissions at cholinergic synapses. It does this by rapidly hydrolysing the neurotransmitter, acetylcholine, which is released at the nerve synapses. Inhibition of the acetylcholinesterase results in the excessive buildup of acetylcholine in, for example, the parasympathetic nerves leading to a number of important locations in the body: the smooth muscle of the iris, ciliary body, the bronchial tree, gastrointestinal tract, bladder and blood vessels; also the salivary glands and secretory glands of the gastrointestinal tract and respiratory tract; and the cardiac muscle and endings of sympathetic nerves to the sweat glands. An accumulation of acetylcholine at parasympathetic sites gives rise to characteristic muscarinic signs, such as emptying of bowels and bladder, blurring of vision, excessive sweating, profuse salivation and stimulation of smooth muscles. The accumulation of acetylcholine at the endings of motor nerves leading to voluntary muscles ultimately results in paralysis.

Nerve gases are highly toxic, stable, and easily dispersed. They produce rapid physiological effects both when absorbed through the skin or through the respiratory tract. They are also fairly easy to synthesize and the raw materials required for their manufacture are inexpensive and readily available. This means that anyone with a basic laboratory can produce them. Nerve gases are, therefore, a significant concern for authorities as they are an easily available weapon for terrorist groups.

In 1936, the German chemist Gerhard Schrader of the I. G. Farbenindustrie laboratory in Leverkusen first prepared the agent Tabun (ethyl-dimethylphosphoramidocyanidate). At the time, Schrader was leading a program to develop new types of insecticides, working first with fluorine-containing compounds such as acyl fluorides, sulfonyl fluorides, fluoroethanol derivatives and fluoroacetic acid derivatives. Schrader's research eventually led to the synthesis of Tabun as an extremely powerful

agent against insects. Schrader found that as little as 5 parts per million (ppm) of Tabun killed all the leaf lice used in his experiments. Soon after Schrader's experiments, the potential use of this substance as an agent of war was realized.

In 1939, a pilot plant for Tabun production was set up at Munster-Lager, near the German Army training grounds at Raubkammer. In January 1940, Germany began the construction of a full-scale plant, code named Hochwerk, at Dyernfurth-am-Oder (now Brzeg Dolny in Poland). A total of 12,000 tons of Tabun was produced during the ensuing three years (19421945) and at the end of WWII, large quantities were seized by the Allied Forces. In addition to Tabun, Schrader and his colleagues produced some 2000 new organophosphates, including Sarin in 1938 and the third of the "classic" nerve agents, Soman, in 1944. These three nerve agents, Tabun, Sarin and Soban, are known as G-agents. The manufacture of Sarin was never fully developed in Germany and only about 0.5 tons were produced in a pilot plant before the end of WWII in 1945.

After 1945, a great deal of research began to focus on understanding the physiological mechanisms of nerve gas action, so that more effective means of protection could be devised against them. However, these efforts also allowed for the development of new and more powerful agents, closely related to the earlier ones. The first official publications on these compounds appeared in 1955. The authors, British chemists Ranajit Ghosh and J. F. Newman, described Amiton, one of the newly developed nerve agents, as being particularly effective against mites. At this time, researchers were devoting a great deal of energy to studying organophosphate insecticides both in Europe and in the United States. At least three chemical firms independently studied and quantified the intense toxic properties of these compounds during the years 195253 and some of them became available on the market as pesticides. By the mid-1950s, following in the wake of the intensive research activity, a new group of highly stable nerve agents had been developed. These were known as the V-agents and were approximately ten-fold more poisonous than Sarin. The V-agents can be numbered among the most toxic substances ever synthesized. VX, a persistent nerve gas, was discovered by Ghosh and was touted as being more toxic than any previously synthesized compound. Since the discovery of VX, there have been only minor advancements in the development of new nerve agents.

A contemporary use of nerve gas occurred during the Iran-Iraq war of 19841988. In this conflict, the United Nations confirmed that Iraq used Tabun and other nerve gases against Iran. This incident is a prime example of how the technology of chemical weapons was shared during the Cold War. The Soviets would arm their allies while the U.S. did the same for its allies. Iraq was a benefactor and implemented its chemical stockpiles during this period. Another contemporary incident of nerve gas use occurred in Japan in 1995. Members of the Aum Shinrikyo cult introduced Sarin gas into Tokyo's subway system. This incident gives an example of the possible new roles that nerve gases may play in the future, as tools of terrorism rather than the weapons of powerful nations.

FURTHER READING:

BOOKS:

Paxman, J., and R. Harris. A Higher Form of Killing: The Secret Story of Chemical and Biological Warfare. New York: Hill and Wang, 1982.

Poolos, J. Nerve Gas Attack on the Tokyo Subway. Rosen Publishing Group Inc., 2002.

Stockholm International Peace Research Institute. The Problem of Chemical and Biological Warfare. A Study of the Historical Technical, Military, Legal, and Political Aspects of CBW and Possible Disarmament Measures. Vol. 1. The Rise of CB Weapons. New York: Humanities Press, 1971.

PERIODICALS:

Evison D, D. Hinsley, and P. Rice. "Chemical Weapons." BMJ 324 (2002): 332335.

Yergler, M. "Nerve Gas Attack." Am. J. Nurs. 1 (2002): 5760.

ELECTRONIC:

Lenthall, Joe. University of Oxford. "Molecule of the month, VX gas." <http://www.chem.ox.ac.uk/mom/vx/VX.htm> (February 20, 2003).

SEE ALSO

Chemical and Biological Defense Information Analysis Center (CBIAC)
Chemical and Biological Detection Technologies
Chemical Biological Incident Response Force, United States
Chemical Warfare
Chemistry: Applications in Espionage, Intelligence, and Security Issues
Terrorist Threat Integration Center

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Nerve Gas

Nerve Gas

Noxious gases can injure or kill people, and so can be of significance in a forensic investigation. One example is nerve gas. Its offensive military use makes nerve gas of particular relevance for military forensic scientists. As well, the specter of the use of agents like sarin gas by rogue organizations and extremists has made the forensic detection of nerve gas a national security issue.

Nerve gases, or nerve agents, are mostly odorless compounds belonging to the organophosphate family of chemicals. Nerve gasses are either colorless or yellow-brown liquids under standard conditions. Two examples of nerve gases that have gained some notoriety through their powerful physiological effects are sarin and VX.

Even in small quantities, nerve gases inhibit the enzyme acetylcholinesterase and disrupt the transmission of nerve impulses in the body. Acetylcholinesterase is a serine hydrolase belonging to the esterase enzyme family, which acts on different types of carboxylic esters in higher eukaryotes. Its role in biology is to terminate nerve impulse transmissions at cholinergic synapses. It does this by rapidly hydrolyzing the neurotransmitter, acetylcholine, which is released at the nerve synapses. Inhibition of the acetylcholinesterase results in the excessive build up of acetylcholine in, for example, the parasympathetic nerves leading to a number of important locations in the body, such as the smooth muscle of the iris, ciliary body, the bronchial tree, gastrointestinal tract, bladder and blood vessels; also the salivary glands and secretory glands of the gastrointestinal tract and respiratory tract; and the cardiac muscle and endings of sympathetic nerves to the sweat glands. An accumulation of acetylcholine at parasympathetic sites gives rise to characteristic muscarinic signs, such as emptying of bowels and bladder, blurring of vision, excessive sweating, profuse salivation, and stimulation of smooth muscles. The accumulation of acetylcholine at the endings of motor nerves leading to voluntary muscles ultimately results in paralysis.

Nerve gases are highly toxic, stable, and easily dispersed. They produce rapid physiological effects both when absorbed through the skin or through the respiratory tract. They are also fairly easy to synthesize and the raw materials required for their manufacture are inexpensive and readily available. This means that anyone with a basic laboratory can produce them. Nerve gases are, therefore, a significant concern for authorities as they are an easily available weapon for terrorist groups.

In 1936 the German chemist Gerhard Schrader of the I. G. Farbenindustrie Laboratory in Leverkusen first prepared the agent tabun (ethyl-dimethylphosphoramidocyanidate). At the time, Schrader was leading a program to develop new types of insecticides, working first with fluorine-containing compounds such as acyl fluorides, sulfonyl fluorides, fluoroethanol derivatives, and fluoroacetic acid derivatives. Schrader's research eventually led to the synthesis of tabun as an extremely powerful agent against insects. Schrader found that as little as 5 parts per million (ppm) of tabun killed all the leaf lice used in his experiments. Soon after Schrader's experiments, the potential use of this substance as an agent of war was realized.

In 1939, a pilot plant for tabun production was set up at Munster-Lager, on Luneberg heath near the German Army training grounds at Raubkammer. In January 1940, Germany began the construction of a full-scale plant, code named Hochwerk, at Dyernfurth-am-Oder (now Brzeg Dolny in Poland). A total of 12,000 tons of tabun was produced during the ensuing three years (19421945) and at the end of WWII, large quantities were seized by the Allied Forces. In addition to tabun, Schrader and his colleagues produced some 2,000 new organophosphates, including sarin in 1938 and the third of the "classic" nerve agents, soman, in 1944. These three nerve agents, tabun, sarin, and soban, are known as G agents. The manufacture of sarin was never fully developed in Germany and only about 0.5 tons were produced in a pilot plant before the end of WWII in 1945.

After 1945, a great deal of research began to focus on understanding the physiological mechanisms of nerve gas action, so that more effective means of protection could be devised against them. However, these efforts also allowed for the development of new and more powerful agents, closely related to the earlier ones. The first official publications on these compounds appeared in 1955. The authors, British chemists Ranajit Ghosh and J. F. Newman, described amiton, one of the newly developed nerve agents, as being particularly effective against mites. At this time, researchers were devoting a great deal of energy to studying organophosphate insecticides both in Europe and in the United States. At least three chemical firms independently studied and quantified the intense toxic properties of these compounds during the years 195253 and some of them became available on the market as pesticides. By the mid-1950's, following in the wake of the intensive research activity, a new group of highly stable nerve agents had been developed. These were known as the V-agents and were approximately ten-fold more poisonous than sarin. The V-agents can be numbered among the most toxic substances ever synthesized. VX, a persistent nerve gas, was discovered by Ghosh and was touted as being more toxic than any previously synthesized compound. Since the discovery of VX, there have been only minor advancements in the development of new nerve agents.

A contemporary use of nerve gas occurred during the Iran-Iraq war of 19841988. In this conflict, the United Nations confirmed that Iraq used tabun and other nerve gases against Iran. This incident is a prime example of how the technology of chemical weapons was shared during the Cold War. The Soviets armed their allies while the U.S. did the same for its allies. Iraq was a benefactor and implemented its chemical stockpiles during this period.

Another contemporary incident of nerve gas use occurred in Japan in 1995. Members of the Aum Shinrikyo cult introduced sarin gas into Tokyo's subway system. This incident gives an example of the possible new roles that nerve gases may play in the future, as tools of insurrection rather than the weapons of powerful nations.

see also Chemical warfare; Chemical Biological Incident Response Force, United States; Mustard gas; Sarin gas; Tabun.

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nerve gas

nerve gas The term ‘nerve gas’ implies substances manufactured with the intent of killing populations or decimating armies in time of war. They have never been used as such in a major world war. The idea that an enemy could stealthily pollute the air with a gas that when breathed would cause death, without affecting property, is horrific and the use of poisonous gases in this way is rightly banned by international treaty. Nevertheless the whole population of Britain, including children and babies, were issued with respirators (‘gas masks’) in World War II. Chlorine gas shells were used by the German Army in World War I, but it proved a hazardous business as wind changes often blew the gas back across the lines from where it came. Chlorine is not a nerve gas, and many soldiers survived the attacks, but were left with lifelong bronchitic type conditions because of the damage to the lungs.

The nerve gases are not really gases, and were designed to be sprayed as aerosols over enemy territory, the fine droplets being absorbed through the skin following contact, either directly from the air or by touching surfaces on which the droplets rested. Thus ‘gas masks’ were of no use, as the fine droplets of poison could easily be distributed without detection and persisted for some time after the air raid. The principle upon which the nerve gases worked was to inhibit a particular enzyme in the body, namely acetylcholinesterase, which rapidly breaks down the neurotransmitter, acetylcholine. Acetylcholinesterase is associated with many nerve endings, both in the brain and in the periphery. Acetylcholine is the neuromuscular transmitter at motor nerve endings in skeletal muscle, in ganglia (the relay stations of the autonomic nervous system), and at all parasympathetic nerve endings on the tissues they affect. The parasympathetic nervous system controls many vegetative functions of involuntary organs and is active under normal sedentary conditions, promoting secretions for example of saliva, and the digestive enzymes in the gut, and also, through the vagus nerve, serving to slow the heart rate and lower the blood pressure. If the enzyme which destroys the transmitter is itself inhibited then the transmitter will persist for much longer, so that overactivity at all situations where acetycholine is involved will be apparent. The consequences therefore are increased salivation, tears, and gastrointestinal and bronchial secretions; bronchoconstriction; slowing of the heart and a fall in blood pressure; constriction of the pupil; and a fall in pressure in the eyeball. Effects caused within the brain lead eventually to convulsions, loss of consciousness, and respiratory failure. It is of course possible to treat some of these symptoms and it is particularly important to give an atropine-like drug (which counteracts the effects of acetylcholine) to prevent the heart stopping altogether.

The nerve gases, and there are many of them, are pentavalent phosphorus compounds (known as organophosphorus compounds), such as dyflos (di-isopropyl fluorophosphonate) and parathion, which react irreversibly with acetylcholinesterase, so the effects are long-lasting, requiring the body to synthesize new enzyme, which takes several weeks. The reason is that the organophosphorus compounds transfer a phoshate group to the enzyme, making it inactive. A little later there is a ageing process when the phosphorylated enzyme changes its structure. It is only before the ageing process occurs that it is possible to remove the phosphate group with nucleophilic drugs, such as pralidoxime. Clearly, treatment of any kind would be unlikely during a nerve gas attack with thousands of people affected.

Nerve gases have proved to have important peacetime uses. They are widely used as insecticides. The compounds can penetrate the insect cuticle as they can human skin. Occasionally farmers contaminate themselves when diluting the concentrate for spraying and need to be treated as described above. Dyflos is used in eyedrops to treat glaucoma (raised intraocular pressure); applied locally in the eyes it produces no effects elsewhere in the body.

Alan W. Cuthbert


See also chemical warfare; poisons.

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nerve gas

nerve gas, any of several poison gases intended for military use, e.g., tabun, sarin, soman, and VX. Nerve gases were first developed by Germany during World War II but were not used at that time. These gases generally cause death by asphyxiation, often preceded by such symptoms as blurred vision, excessive salivation, and convulsions. Physiologically, the toxic effect of nerve gases arises because they inactivate the enzyme cholinesterase, which normally controls the transmission of nerve impulses; the impulses continue without control, causing breakdown of respiration and other body functions. Atropine is an effective antidote against most nerve gases. See also chemical warfare.

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nerve gas

nerve gas • n. a poisonous vapor that rapidly disables or kills by disrupting the transmission of nerve impulses.

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nerve gas

nerve gas n. any gas that disrupts the normal functioning of nerves and thus of the muscles they supply.

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