Tabun_(nerve

Tabun

IUPAC name	Ethyl N,N-Dimethylphosphoramidocyanidate
Other names	GA; Ethyl dimethylphosphoramidocyanidate; Dimethylaminoethoxy-cyanophosphine oxide; Dimethylamidoethoxyphosphoryl cyanide; Ethyl dimethylaminocyanophosphonate; Ethyl ester of dimethylphosphoroamidocyanidic acid; Ethyl phosphorodimethylamidocyanidate; Cyanodimethylaminoethoxyphosphine oxide; Dimethylaminoethodycyanophosphine oxide; EA1205
Properties
Molecular formula	C₅H₁₁N₂O₂P
Molar mass	162.13 g mol⁻¹
Appearance	Colorless to brown liquid
Density	1.0887 g/cm³ at 25 °C 1.102 g/cm³ at 20 °C
Melting point	-50 °C, 223 K, -58 °F
Boiling point	247.5 °C, 521 K, 478 °F
Solubility in water	9.8 g/100 g at 25 °C 7.2 g/100 g at 20 °C
Vapor pressure	0.07 mmHg (9 Pa)
Hazards
Main hazards	Toxic. Fires involving this chemical may result in the formation of hydrogen cyanide
NFPA 704	2 4 1
Flash point	78 °C
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) Infobox references

Tabun or GA is an extremely toxic chemical substance. It is a clear, colorless, and tasteless liquid with a faint fruity odor.¹ It is classified as a nerve agent because it fatally interferes with normal functioning of the mammalian nervous system. 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 ranges in color from clear to a brown color depending on purity of the substance. It is a volatile chemical, although less so than either sarin or soman, because of this Tabun can be used to contaminate water.¹

Effects of overexposure

The symptoms of exposure include:²³⁴ nervousness/restlessness, miosis (contraction of the pupil), rhinorrhea (runny nose), excessive salivation, dyspnea (difficulty in breathing due to bronchoconstriction/secretions), sweating, bradycardia (slow heartbeat), loss of consciousness, convulsions, flaccid paralysis, loss of bladder and bowel control, apnea (breathing stopped). The exact symptoms of overexposure are similar to those created by all nerve agents. Tabun 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 of it 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 in very low concentrations it is more irritating to the eyes than sarin. Also, tabun breaks down slowly, which after repeated exposure can lead to build up in the body.¹

The effects of tabun appear slowly when tabun is absorbed through the skin rather than inhaled. A victim may absorb a lethal dose quickly, although death may be delayed for one to two hours.³ It should be noted that a person's clothing can release the toxic chemical for up to 30 minutes after exposure.¹ Inhaled lethal dosages kill in one to ten minutes, and liquid absorbed through the eyes kills almost as fast. However, people who experience mild to moderate exposure to tabun can recover completely, if treated almost as soon as exposure occurred.¹ The LCt50 for tabun is about 400 mg-min/m₃⁵ Treatment for suspected tabun poisoning is often three injections of a nerve agent antidote, such as atropine. ⁶

History

Tabun was the first nerve agent to be discovered by accident in January 1936¹⁷²⁸⁹ by the German researcher Gerhard Schrader.⁹ 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 IG Farben, a famous pharmaceutical conglomerate, at Elberfield. Instead of a new insecticide, he discovered tabun, a chemical enormously toxic to humans as well as insects.

During World War II, as part of the Grün 3 program, a plant for the manufacture of tabun was established at Dyhernfurth⁹ (now Brzeg Dolny, Poland), in 1939. Run by Anorgana, GmbH, the plant finally began production of the substance in 1942.⁹ The reason that the plant took so long to get started was the extreme precautions used by the plant.⁹ Intermediate products of tabun were corrosive, and had to be contained in quartz or silver-lined vessels. Tabun, itself, was highly toxic and that final reactions had to be conducted in double glass walls.⁹ Large scale manufacturing of the agent resulted in problems with the tabun's degradation over time and only around 12,500 tons of material were manufactured before the plant was over-run by the advancing Soviet Army. 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," a 80:20 mix of tabun and chlorobenzene designed to make the mixture disperse easier. The Soviet government had the plant dismantled and taken back to Russia.

The United States once had an active tabun production program,⁴ however it was ended many decades ago. 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 to neutralize the substance.

Since GA is much easier to produce than the other G-series weapons and the process is comparatively widely understood, countries that develop a nerve agent capability but 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.⁴¹⁰

Contents

Effects of overexposure

History

See also

References

Additional reading