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Sarin, also known by its NATO designation of GB, (O-Isopropyl methylphosphonofluoridate) is an extremely toxic substance whose sole application is as a nerve agent. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations in UN Resolution 687. Production and stockpiling of Sarin was outlawed by the Chemical Weapons Convention of 1993.
Sarin is similar in structure and biological activity to some commonly used insecticides, such as Malathion, and is similar in biological activity to carbamates used as insecticides such as Sevin, and medicines such as Mestinon, Neostigmine, and Antilirium.
At room temperature, sarin is a colorless, odorless liquid. Its low vapor pressure (2.9 mmHg at 20 degrees Celsius) makes it relatively ineffective as a terrorist inhalation weapon. Its vapor is also colorless and odorless. It can be made more persistent through the addition of certain oils or petroleum products.
Sarin can be used as a binary chemical weapon; its two precursors are methylphosphonyl difluoride and a mixture of isopropyl alcohol and isopropyl amine. The isopropyl amine binds the hydrogen fluoride generated during the chemical reaction.
Sarin has a relatively short shelf life, and will degrade after a period of several weeks to several months. The shelf life may be greatly shortened by impurities in precursor materials. According to the CIA, in 1989 the Iraqis destroyed 40 or more tons of sarin that had decomposed, and that some Iraqi sarin had a shelf life of only a few weeks owing mostly to impure precursors.
Like other nerve agents, Sarin can be chemically deactivated with a strong alkali. Sodium hydroxide can be used in a hydrolysis reaction to destroy sarin converting it to effectively harmless sodium salts..
Efforts to lengthen shelf life
Nations stockpiling sarin have tried to overcome the problem of its short shelf life in three ways:
When a functioning motor neuron or parasympathetic neuron is stimulated it releases the neurotransmitter acetylcholine to transmit the impulse to a muscle or organ. Once the impulse has been sent, the enzyme acetylcholinesterase breaks down the acetylcholine in order to allow the muscle or organ to relax.
Sarin is an extremely potent organophosphate compound that disrupts the nervous system by inhibiting the cholinesterase enzyme by forming a covalent bond with the particular serine residue in the enzyme which forms the site where acetylcholine normally undergoes hydrolysis; the fluorine of the phosphonyl fluoride group reacts with the hydroxyl group on the serine side-chain, forming a phosphoester and releasing HF. With the enzyme inhibited, acetylcholine builds up in the synapse and continues to act so that any nerve impulses are, in effect, continually transmitted.
Initial symptoms following exposure to sarin are a runny nose, tightness in the chest and constriction of the pupils. Soon after, the victim has difficulty breathing and experiences nausea and drooling. As the victim continues to lose control of bodily functions, he vomits, defecates and urinates. This phase is followed by twitching and jerking. Ultimately, the victim becomes comatose and suffocates in a series of convulsive spasms.
Sarin has a high volatility relative to similar nerve agents. Inhalation and absorption through the skin pose a great threat. Even vapour concentrations immediately penetrate the skin. People who absorb a nonlethal dose but do not receive immediate appropriate medical treatment may suffer permanent neurological damage.
Even at very low concentrations, sarin can be fatal. Death may follow in one minute after direct ingestion of about 0.01 milligram per kilogram of body weight if antidotes, typically atropine and pralidoxime, are not quickly administered. Atropine, an antagonist to acetylcholine receptors of muscarinic type, is given to treat the physiological symptoms of poisoning (since muscular response to acetylcholine is mediated through nicotinic acetylcholine receptors, atropine does not counteract muscular symptoms). Pralidoxime can regenerate cholinesterases if administered within approximately five hours.
The short- and long-term symptoms experienced by those affected included:
The following is the specific history of sarin, which is closely linked to the history of similar nerve agents also discovered in Germany during or soon after World War II. That broader history is detailed in Nerve Agent: History .
Sarin was discovered in 1938 in Wuppertal-Elberfeld in Germany by two German scientists attempting to create stronger pesticides; it is the most toxic of the four G-agents made by Germany. The compound, which followed the discovery of the nerve agent tabun, was named in honor of its discoverers: Gerhard Schrader, Ambros, Rüdiger and Van der LINde.
Sarin in Nazi Germany during World War II
In mid-1939, the formula for the agent was passed to the chemical warfare section of the German Army Weapons Office, which ordered that it be brought into mass production for wartime use. A number of pilot plants were built, and a high-production facility was under construction (but was not finished) by the end of World War II. Estimates for total sarin production by Nazi Germany range from 500 kg to 10 tons.
Though sarin, tabun and soman were incorporated into artillery shells, Germany ultimately decided not to use nerve agents against Allied targets. German intelligence was unaware that the Allies had not developed similar compounds, but they understood that unleashing these compounds would lead the Allies to develop and use chemical weapons of their own, and they were concerned that the Allies' ability to reach German targets would prove devastating in a chemical war.
Sarin after World War II
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Sarin". A list of authors is available in Wikipedia.|