Tabun (nerve agent)

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Tabun
Tabun
Discovery
Discovered by Gerhard Schrader
Discovered in 1936
Chemical characteristics
Chemical name Ethyl N,N-dimethylphosphoramidocyanidate
Chemical family Organophosphorus compound
Chemical formula C5H11N2O2P
NFPA 704 Rating
2
4
1
 
Boiling point 247.5 °C (477.5 °F) / 907.17°R
Freezing/melting point −50 °C (−58 °F) / 401.67°R
Vapor pressure 0.07 mmHg (9 Pa) at 25 °C
Vapor density (Air=1) 5.6
Liquid density 1.0887 g/cm³ at 25 °C
1.102 g/cm³ at 20 °C
Solubility in water 9.8 g/100 g at 25 °C
7.2 g/100 g at 20 °C
Specific gravity Not available
Appearance and color Colorless to brown liquid.
Faintly fruity odor (none when pure)
Fire and Explosion Data
Flashpoint 78 °C (172 °F) / 631.67°R
Unusual hazards Fires involving this chemical may result
in the formation of hydrogen cyanide

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Overview

Tabun or GA (Ethyl N,N-dimethylphosphoramidocyanidate) is an extremely toxic substance that has the potential to be one of the world's most dangerous military weapons. It is a clear, colorless, tasteless liquid with a faint fruity odor. Because it fatally interferes with normal functioning of the mammalian nervous system, it is classified as a nerve agent. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations according to UN Resolution 687, and its production is strictly controlled and stockpiling outlawed by the Chemical Weapons Convention of 1993. Tabun is the first of the so-called G-series nerve agents (along with GB (sarin), GD (soman) and GF (cyclosarin)).

Tabun is a colorless to brown liquid (depending on purity). It is volatile (evaporating readily at normal temperatures), although less volatile than either sarin or soman. Tabun may also be used to contaminate water as it mixes easily with water.

Tabun can be destroyed with bleaching powder, though the poisonous gas cyanogen chloride is produced.

Effects of overexposure

The exact symptoms of overexposure are similar to those created by all nerve agents. Tabun, like all nerve agents, is toxic even in minute doses. The number and severity of symptoms which appear vary according to the amount of the agent absorbed and rate of entry into the body. Very small skin dosages sometimes cause local sweating and tremors accompanied with characteristically constricted pupils with few other effects. Tabun is about half as toxic as sarin by inhalation, but tabun in very low concentrations is more irritating to the eyes than sarin. Also tabun breaks down slowly in the body, which after repeated exposure to tabun can lead to build up in the body.

The effects of exposure appear much more slowly when tabun is absorbed through the skin rather than inhaled: although a victim may absorb a lethal dose quickly, death may be delayed for 1 to 2 hours. Inhaled lethal dosages kill in 1 to 10 minutes, and liquid in the eye kills almost as fast. However, most people who experience mild to moderate exposure to tabun can recover completely if treated almost as soon as exposure occurred. Most of what is known about lethal dosages are known from animal studies on monkeys.

Alternative names

Tabun is occasionally referred to names other than tabun or GA:

  • Ethyl dimethylphosphoramidocyanidate
  • Dimethylaminoethoxy-cyanophosphine oxide
  • Dimethylamidoethoxyphosphoryl cyanide
  • Ethyl dimethylaminocyanophosphonate
  • Ethyl ester of dimethylphosphoroamidocyanidic acid
  • Ethyl phosphorodimethylamidocyanidate
  • Cyanodimethylaminoethoxyphosphine oxide
  • EA1205


History

For an in-depth discussion, see main article on nerve agent history

Tabun, the first known nerve agent, was discovered accidentally in 1936 by the German researcher Dr. Gerhard Schrader. Dr. Schrader was experimenting with a class of compounds called organophosphates, which kill insects by interrupting their nervous systems, in order to create a more effective insecticide for the IG Farben pharmaceutical conglomerate at Elberfield. Instead of a new insecticide, however, he discovered tabun, a chemical which is enormously toxic to humans as well as to insects.

During World War II as part of the Grün 3 program, a plant for the manufacture of tabun was established in Dyhernfurth (now Brzeg Dolny, Poland), producing the nerve agent under the codename Trilon-83. Run by Anorgana GmbH, the plant began production in 1942. Large scale manufacturing of the agent resulted in problems with the product's degradation over time and only around 12,500 tons of material were manufactured before the plant was over-run by the advancing Soviet forces. The plant initially produced shells and aerial bombs using a 95:5 mix of tabun and chlorobenzene, designated "Variant A" before switching in the latter half of the war to "Variant B," an 80:20 mix of tabun and chlorobenzene designed to make the mixture disperse more easily. The Soviet government had the plant dismantled and taken back to Russia.

Like the other Allied governments, the Soviets soon abandoned GA for GB and GD. Large quantities of the German-manufactured agent were dumped into the sea.

Since GA is much easier to produce than the other G-series weapons and the process is comparatively widely understood, countries which are developing a nerve agent capability but which lack advanced industrial facilities often start by producing GA.

During the Iran-Iraq War, Iraq employed large quantities of chemical weapons against ground forces of Iran. Although the most commonly used agents were mustard gas and sarin, tabun and cyclosarin were also used.

See also

References

[2]

  • Tabun-Encyclopedia.com [3]

External links

de:Tabunfr:Tabun

hu:Tabun nl:Tabun ja:タブンsl:Tabun sv:Tabun

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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