Tabun (nerve agent)

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Tabun (military designation GA) is an extremely toxic compound of the organophosphate family.<ref>Template:Cite journal</ref><ref name=":0">Template:Cite journal</ref> 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 into a yellow or brown liquid. Exposed to environs, it slowly volatizes into the atmosphere,<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> with the vapor having a slight fruity or almond-like odor.<ref name=":1">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> As the compound has a much higher molecular mass (162 g/mol) compared to air, Tabun gas tends to accumulate in low-lying areas.<ref name=":1" />

It is a potent inhibitor of acetylcholinesterase, a key enzyme within the human body as well as in other animals.<ref name="PubChem 6500 Tabun">Template:PubChem</ref> Acetylcholinesterase is responsible for breaking down acetylcholine, a neurotransmitter released into the synaptic cleft by motor neurons. The presence of acetylcholine within the cleft signals the post-synaptic (downstream) motor neuron to contract the neuron's associated muscle fibers, and vice versa. By irreversibly phosphorylating the enzyme,<ref name=":0" /> 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 the diaphragm and intercostals, become exhausted and paralyzed from constant contraction, leading to loss of respiratory functions.<ref name=":0" />

The production and storage of Tabun has been strictly regulated under the Chemical Weapons Convention and its implementing agency OPCW since 1997.<ref>Template:Cite book</ref><ref>Template:Cite book</ref> As a Schedule 1 Toxic Chemical,<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> the synthesis of more than 100 grams of the substance per year must be declared to the organization, and no signing nation can possess more than 1 ton of the chemical.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Modern usage of Tabun is limited to research purposes in minute amounts.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Chemistry and SynthesisEdit

ReactionsEdit

Tabun can be deactivated chemically using common oxidizing agents such as sodium hypochlorite.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Historic synthesisEdit

Tabun was made on an industrial scale by Germany during World War II, based on a process developed by Gerhard Schrader. In the chemical agent factory in Dyhernfurth 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,Template:Inconsistent the second a product later in the war).<ref name=Lohs1967>Template:Cite book Template:Better source The translations of chapter and book title here were editor-generated.</ref>Template:Verification needed Template:Better source

File:TabunSynthesis.png

Effects of exposureEdit

The symptoms of exposure include:<ref name="cbw">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name=military>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref name=ency>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> 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) and lung blisters. The symptoms of exposure 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. Tabun also breaks down slowly, which after repeated exposure can lead to build up in the body.<ref name="nta">Facts About Tabun, National Terror Alert Response System</ref>

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.<ref name=military/> A person's clothing can release the toxic chemical for up to 30 minutes after exposure.<ref name="nta"/> Inhaled lethal dosages kill in one to ten minutes, and liquid absorbed through the eyes 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.<ref name="nta"/> The median lethal dose (LD₅₀) for tabun is about 400 mg-min/m³.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

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 2 hours.<ref name="PubChem 6500 Tabun"/>

Treatment for suspected tabun poisoning is often three injections of a nerve agent antidote, such as atropine.<ref name="ency"/> 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.<ref>Emergency Response Safety and Health Database. TABUN (GA): Nerve Agent. National Institute for Occupational Safety and Health. Accessed April 30, 2009.</ref>

HistoryEdit

Template:Details Research into ethyl dialkylaminocyanophosphonate began in the late 19th century, In 1898, Adolph Schall, a graduate student at the University of Rostock under professor August Michaelis, synthesised the diethylamino analog of tabun, as part of his PhD thesis Über die Einwirkung von Phosphoroxybromid auf secundäre aliphatische Amine.<ref>Template:Cite journal</ref> However, Schall incorrectly identified the structure of the substance as an imidoether, and Michaelis corrected him in a 1903 article in Liebigs 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 and dimethylamidophosphoric dichloride) wasn't noted at the time,<ref>Template:Cite book</ref> most likely due to the low yield of the synthetic reactions used.Template:Speculation inline

Tabun became the first nerve agent known after a property of this chemical was discovered by pure accident in late December 1936<ref name="nta"/><ref name=cbw/><ref>Chemical Warfare Weapons Fact Sheets Template:Webarchive, about.com</ref><ref>Chemical Weapons: Nerve Agents, University of Washington</ref><ref name=shorthistory>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> by German researcher Gerhard Schrader.<ref name=shorthistory/> Schrader was experimenting with a class of compounds called organophosphates, which kill insects by interrupting their nervous systems, to create a more effective insecticide for IG Farben, a German chemical and pharmaceutical industry conglomerate, at Elberfeld.<ref>Template:Cite book</ref> The substance he discovered, as well as being a potent insecticide, was enormously toxic to humans; hence, it was named tabun, to indicate that the substance was 'taboo' (German: tabu) for its intended purpose.<ref>Template:Cite news</ref>

During World War II, as part of the Grün 3 program, a plant for the manufacture of tabun was established at Dyhernfurth (now Brzeg Dolny, Poland), in 1939.<ref name=shorthistory/> Run by Anorgana GmbH, the plant began production of the substance in 1942.<ref name=shorthistory/> The reason for the delay was the extreme precautions used by the plant.<ref name=shorthistory/> 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.<ref name=shorthistory/> 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 the Soviet Army.<ref>Template:Cite book</ref> The plant initially produced shells and aerial bombs using a 95:5 mix of tabun and chlorobenzene, designated "Variant A".Template:Inconsistent In the latter half of the war, the plant switched to "Variant B",Template:Inconsistent an 80:20 mix of tabun and chlorobenzene designed for easier dispersion.<ref name=Lohs1967/>Template:Verification needed Template:Better source The Soviets dismantled the plant and shipped it to Russia.<ref>Template:Cite book</ref> 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.<ref name=Hogg187>Template:Cite book</ref>

During the Nuremberg Trials, Albert Speer, Minister of Armaments and War Production for the Third Reich, testified that he had planned to kill Adolf Hitler in early 1945 by introducing tabun into the Führerbunker ventilation shaft.Template:Sfn He said his efforts were frustrated by the impracticality of tabun and his lack of ready access to a replacement nerve agent,Template:Sfn and also by the unexpected construction of a tall chimney that put the air intake out of reach.Template:Verification needed

The US once considered repurposing captured German stocks of tabun (GA) prior to production of Sarin (GB).<ref>Template:Cite journal</ref> Like the other Allied governments, the Soviets soon abandoned tabun (GA) for Sarin (GB) and Soman (GD).<ref>Template:Cite book</ref> The German magazine Spiegel 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.<ref>Template:Cite news</ref>

Since GA is much easier to produce than the other G-series weapons<ref>Template:Cite book</ref> and the process is comparatively widely understood, countries that develop a nerve agent capability but lack advanced industrial facilities often start by producing GA.<ref>Template:Cite book</ref>

During the Iran–Iraq War of 1980 to 1988, Iraq employed quantities of chemical weapons against Iranian ground forces. Although the most commonly used agents were mustard gas and sarin, tabun and cyclosarin were also used.<ref name=ency/><ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>Template:Better source

Tabun was also used in the 1988 Halabja chemical attack.<ref>Template:Cite news</ref>

Producing or stockpiling tabun was banned by the 1993 Chemical Weapons Convention. The worldwide stockpiles declared under the convention were 2 tonnes, and as of December 2015 these stockpiles had been destroyed.<ref>Template:Cite report</ref>

ReferencesEdit

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BibliographyEdit

Template:Citation. Republished in paperback in 1997 by Simon & Schuster, Template:ISBN
(Original German edition: Template:Citation)