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| Names | |
|---|---|
| IUPAC name (RS)-EthylN,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; EA-1205; TL-1578 | |
| Identifiers | |
| |
3D model (JSmol) | |
| ChEMBL | |
| ChemSpider |
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| ECHA InfoCard | 100.296.240 |
| UNII | |
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| Properties | |
| C5H11N2O2P | |
| Molar mass | 162.129 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 (−58 °F; 223 K) |
| Boiling point | 247.5 °C (477.5 °F; 520.6 K) |
| 9.8 g/100 g at 25 °C 7.2 g/100 g at 20 °C | |
| Vapor pressure | 0.07 mmHg (9 Pa) |
| Hazards | |
| Occupational safety and health (OHS/OSH): | |
Main hazards | Highly toxic. Fires involving this chemical may result in the formation ofhydrogen cyanide |
| NFPA 704 (fire diamond) | |
| Flash point | 78 °C (172 °F; 351 K) |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Tabun (NATO designationGA) is an extremely toxic compound of theorganophosphate family.[1][2][verification needed] It is not present in nature. At room temperature, the pure compound is a clear and viscous liquid. However, impurities imparted during its manufacture are almost always present, turning it yellow or brown. Exposed to environs, it slowly evaporates into the atmosphere,[3] with the vapor having a slight fruity or almond-like odor.[4] As the compound has a much highermolecular mass (162 g/mol) compared to air, tabun gas tends to accumulate in low-lying areas.[4]
It is a potent inhibitor ofacetylcholinesterase, a keyenzyme within the human body as well as in other animals.[5] Acetylcholinesterase is responsible for breaking downacetylcholine, aneurotransmitter released into thesynaptic cleft by motor neurons. The presence of acetylcholine within the cleft signals the post-synaptic (downstream) motor neuron to contract the neuron's associatedmuscle fibers, and vice versa. By irreversiblyphosphorylating the enzyme,[2] tabun accomplishes a constant and involuntary contraction of the affected muscles, as the acetylcholine is not recycled and continues to build up within the cleft. Death of the organism ensues when respiratory muscles, such as thediaphragm andintercostals, become exhausted and paralyzed from constant contraction, leading to loss of respiratory functions.[2]
Production and storage of tabun has been strictly regulated under theChemical Weapons Convention and its implementing agencyOPCW since 1997.[6][7] As a Schedule 1 Toxic Chemical,[8] the synthesis of more than 100 grams of the substance per year must be declared to the organization, and no signatory nation can possess more than one ton of the chemical.[9] Modern usage of Tabun is limited to research purposes in minute amounts.[10]
Tabun can be deactivated chemically using common oxidizing agents such as sodium hypochlorite.[11]
Tabun was made on an industrial scale by Germany during World War II based on a process developed byGerhard Schrader. In the chemical agent factory inDyhernfurth an der Oder, code-named "Hochwerk", at least 12,000 metric tons of this agent were manufactured between 1942 and 1945. The manufacturing process consisted of two steps (see below); after the reactions, the mixture (consisting of ~75% solvent, ~25% desired product, plus insoluble salts and reactants) was filtered and vacuum-distilled. This yielded a technical product consisting either of 95% or 80% tabun (then known as Tabun A or B, respectively,[inconsistent] the second a product later in the war).[12][verification needed][better source needed]
The symptoms of exposure include:[13][14][15]nervousness/restlessness,miosis (contraction of the pupil),rhinorrhea (runny nose), excessive salivation,dyspnea (difficulty in breathing due tobronchoconstriction/secretions),sweating,bradycardia (slow heartbeat),loss of consciousness,convulsions,flaccid paralysis, loss of bladder and bowel control,apnea (breathing stopped) and lung blisters. The symptoms of exposure are similar to those created by allnerve 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 assarin by inhalation, but in very low concentrations it is more irritating to the eyes than sarin. Tabun also breaks down slowly, which after repeated exposure can lead tobuild up in the body.[16]
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.[14] A person's clothing can release the toxic chemical for up to 30 minutes after exposure.[16] Inhaled lethal dosages kill in one to ten minutes, and liquid absorbed through theeyes kills almost as quickly. However, people who experience mild to moderate exposure to tabun can recover completely, if treated almost as soon as exposure occurs.[16] Themedian lethal dose (LD50) for tabun is about 400 mg-min/m3.[17]
The lethal dose for a man is about .01 mg/kg. The median lethal dose for respiration is 400 mg-minute/m3 for humans. When absorbed via the skin, death may occur in 1-2 minutes, or it can take up to two hours.[5]
Treatment for suspected tabun poisoning is often three injections of a nerve agent antidote, such asatropine.[15]Pralidoxime chloride (2-PAM Cl) also works as an antidote; however, it must be administered within minutes to a few hours following exposure to be effective.[18]
Research into ethyl dialkylaminocyanophosphonate began in the late 19th century. In 1898, Adolph Schall, a graduate student at theUniversity of Rostock under professorAugust Michaelis, synthesised the diethylamino analog of tabun, as part of his PhD thesisÜber die Einwirkung von Phosphoroxybromid auf secundäre aliphatische Amine.[19] However, Schall incorrectly identified the structure of the substance as an imidoether, and Michaelis corrected him in a 1903 article inLiebigs Annalen,Über die organischen Verbindungen des Phosphors mit dem Stickstoff. The high toxicity of the substance (as well as the high toxicity of its precursors,diethylamidophosphoric dichloride anddimethylamidophosphoric dichloride) wasn't noted at the time,[20] most likely due to the low yield of the synthetic reactions used.[speculation?]
Tabun became the first nerve agent known after a property of this chemical was discovered by pure accident in late December 1936[16][13][21][22][23] by German researcherGerhard Schrader.[23] Schrader was experimenting with a class of compounds calledorganophosphates, which kill insects by interrupting their nervous systems, to create a more effectiveinsecticide forIG Farben, a German chemical and pharmaceutical industry conglomerate, at Elberfeld.[24] The substance he discovered, as well as being a potent insecticide, was enormously toxic to humans; hence, it was namedtabun, to indicate that the substance was 'taboo' (German:tabu) for its intended purpose.[25]
DuringWorld War II, a plant for the manufacture of tabun was established at Dyhernfurth (nowBrzeg Dolny,Poland), in 1939.[23][26] Run by Anorgana GmbH, the plant began production of the substance in 1942.[23] The reason for the delay was the extreme precautions used by the plant.[23] Intermediate products of tabun were corrosive, and had to be contained in quartz or silver-lined vessels. Tabun itself was also highly toxic, and final reactions were conducted behind double glass walls.[23] Large scale manufacturing of the agent resulted in problems with tabun's degradation over time, and only 12,753 metric tons were manufactured before the plant was seized by theSoviet Army.[27] The plant initially produced shells and aerial bombs using a 95:5 mix of tabun andchlorobenzene, designated "Variant A".[inconsistent] In the latter half of the war, the plant switched to "Variant B",[inconsistent] an 80:20 mix of tabun and chlorobenzene designed for easier dispersion.[12][verification needed][better source needed] The Soviets dismantled the plant and shipped it toRussia.[28] They did not inform the Western Allies of the discovery and as a result they did not become aware of tabun until it was discovered in captured German ammo dumps in April 1945.[29]
During theNuremberg Trials,Albert Speer, Minister of Armaments and War Production for the Third Reich, testified that he had planned to killAdolf Hitler in early 1945 by introducing tabun into theFührerbunker ventilation shaft. He said his efforts were frustrated by the impracticality of tabun and his lack of ready access to a replacement nerve agent, and also by the unexpected construction of a tall chimney that put the air intake out of reach.[30]
The US once considered repurposing captured German stocks of tabun (GA) prior to production ofsarin (GB).[31] Like the otherAllied governments, the Soviets soon abandoned tabun (GA) forsarin (GB) andsoman (GD).[32] The German magazineSpiegel reported in 2007 that after World War II, "the United States dumped around half a million Tabun bombs in the Skagerrak in the northern Baltic" sea.[33]
Since GA is much easier to produce than the other G-series weapons[34] and the process is comparatively widely understood, countries that develop a nerve agent capability but lack advanced industrial facilities often start by producing GA.[35]
During theIran–Iraq War of 1980 to 1988,Iraq employed quantities of chemical weapons against Iranian ground forces. Although the most commonly used agents weremustard gas andsarin, tabun andcyclosarin were also used.[15][36][better source needed]
Tabun was also used in the 1988Halabja chemical attack.[37]
Producing or stockpiling tabun was banned by the 1993Chemical Weapons Convention. The worldwide stockpiles declared under the convention were 2 tonnes, and as of December 2015 these stockpiles had been destroyed.[38]
