Tabun (NATO designation GA) is an extremely toxic compound and nerve agent chemical weapon of the organophosphate family. 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, with the vapor having a slight fruity or almond-like odor. As the compound has a much higher molecular mass (162 g/mol) compared to air, tabun gas tends to accumulate in low-lying areas. It is a potent inhibitor of acetylcholinesterase, a key enzyme within the human body as well as in other animals. 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, 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. Tabun was the first nerve agent discovered, in 1936 by Gerhard Schrader in Nazi Germany, and named after the German word Tabu (taboo) for its extreme toxicity. The country stockpiled over 12,000 tons of the weapon, but it was not used for fear of Allied retaliation. After the war, the Western Allies and Soviet Union both discovered the agent, and nerve agent production became central to the Soviet and United States chemical weapons programs in the Cold War. Tabun was impractical, with the countries focusing on sarin, soman, and VX nerve agents instead. Tabun was only known to have been used in the extensive Iraqi chemical attacks of the Iran–Iraq War. Production and storage of tabun has been strictly regulated under the Chemical Weapons Convention and its implementing agency OPCW since 1997. As a Schedule 1 Toxic Chemical, 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. Modern usage of Tabun is limited to research purposes in minute amounts.
Chemistry and synthesis
Reactions Tabun can be deactivated chemically using common oxidizing agents such as sodium hypochlorite.
Historic synthesis 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, the second a product later in the war).
Effects of exposure The symptoms of exposure include: 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. 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. A person's clothing can release the toxic chemical for up to 30 minutes after exposure. 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. The median lethal dose (LD50) for tabun is about 400 mg-min/m3. 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. Treatment for suspected tabun poisoning is often three injections of a nerve agent antidote, such as atropine. 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.
History
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