|Jmol-3D images||Image 1|
|Molar mass||140.09 g mol−1|
|Appearance||Clear colorless liquid|
|Odor||Odorless in pure form|
|Density||1.0887 g/cm³ (25 °C)
1.102 g/cm³ (20 °C)
-56 °C, 217 K, -69 °F
158 °C, 431 K, 316 °F
|Solubility in water||Miscible|
|MSDS||Lethal Nerve Agent Sarin (GB)|
|EU classification||Extremely Toxic (T+)|
|Main hazards||It is a lethal anticholinergic agent.|
| (what is: / ?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Sarin, or GB, is an organophosphorus compound with the formula [(CH3)2CHO]CH3P(O)F. It is a colorless, odorless liquid, used as a chemical weapon owing to its extreme potency as a nerve agent. It has been classified as a weapon of mass destruction in UN Resolution 687. Production and stockpiling of sarin was outlawed by the Chemical Weapons Convention of 1993 where it is classified as a Schedule 1 substance.
Production and structure 
Sarin is a chiral molecule (typically racemic), with four substituents attached to the tetrahedral phosphorus center. The SP form (the RP form is shown) is the more active enantiomer due to its greater binding to acetylcholinesterase. It is prepared from methylphosphonyl difluoride and a mixture of isopropyl alcohol and isopropylamine.
- CH3P(O)F2 + (CH3)2CHOH → [(CH3)2CHO]CH3P(O)F + HF
Biological effects 
Its mechanism of action resembles that of some commonly used insecticides, such as malathion. In terms of biological activity, it resembles carbamate insecticides such as Sevin and medicines pyridostigmine, neostigmine, and physostigmine. Like other nerve agents, sarin attacks the nervous system.
Specifically, sarin is a potent inhibitor of the enzyme acetylcholinesterase, a protein that degrades the neurotransmitter acetylcholine after it is released into the synaptic cleft. In vertebrates, acetylcholine is the neurotransmitter used at the neuromuscular junction, where signals are transmitted between neurons from the central nervous systems to muscle fibres. Normally, acetylcholine is released from the neuron to stimulate the muscle, after which it is degraded by acetylcholinesterase, allowing the muscle to relax. A build-up of acetylcholine in the synaptic cleft, due to the inhibition of cholinesterase, means the neurotransmitter continues to act on the muscle fibre, so that any nerve impulses are effectively continually transmitted. Death will usually occur as a result of asphyxia due to the inability of the muscles involved in breathing to function.
Sarin acts on cholinesterase by forming a covalent bond with the particular serine residue at the active site. Fluoride is the leaving group, and the resulting phosphoester is robust and biologically inactive.
Degradation and shelf life 
The most important chemical reactions of phosphoryl halides is the hydrolysis of the bond between phosphorus and the fluoride. This P-F bond is easily broken by nucleophilic agents, such as water and hydroxide. At high pH, sarin decomposes rapidly to nontoxic phosphonic acid derivatives.
Sarin degrades after a period of several weeks to several months. The shelf life can be shortened by impurities in precursor materials. According to the CIA, some Iraqi sarin had a shelf life of only a few weeks, owing mostly to impure precursors.
Its otherwise short shelf life can be extended by increasing the purity of the precursor and intermediates and incorporating stabilizers such as tributylamine. In some formulations, tributylamine is replaced by diisopropylcarbodiimide (DIC), allowing sarin to be stored in aluminium casings. In binary chemical weapons, the two precursors are stored separately in the same shell and mixed to form the agent immediately before or when the shell is in flight. This approach has the dual benefit of solving the stability issue and increasing the safety of sarin munitions.
Effects and treatment 
Sarin has a high volatility (ease to which a liquid can turn into a gas) relative to similar nerve agents. Inhalation and absorption through the skin pose a great threat. Even vapor concentrations immediately penetrate the skin. A person’s clothing can release sarin for about 30 minutes after it has come in contact with sarin gas, which can lead to exposure of other people. People who absorb a non-lethal 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 a lethal dose unless antidotes, typically atropine and pralidoxime, are quickly administered. Atropine, an antagonist to muscarinic acetylcholine receptors, is given to treat the physiological symptoms of poisoning. Since muscular response to acetylcholine is mediated through nicotinic acetylcholine receptors, atropine does not counteract the muscular symptoms. Pralidoxime can regenerate cholinesterases if administered within approximately five hours. Biperiden, a synthetic acetylcholine antagonist, has been suggested as an alternative to atropine due to its better blood–brain barrier penetration and higher efficacy.
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, the victim vomits, defecates and urinates. This phase is followed by twitching and jerking. Ultimately, the victim becomes comatose and suffocates in a series of tolulope spasms.
Diagnostic tests 
Controlled studies in humans have shown that a minimally toxic 0.5 mg oral dose caused a 38% depression of both erythrocyte and plasma cholinesterase within several hours of exposure. The serum level of unbound isopropylmethylphosphonic acid (IMPA), a sarin hydrolysis product, ranged from 2-135 µg/L in survivors of a terrorist attack during the first 4 hours post-exposure.
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: Schrader, Ambros, Rüdiger and Van der Linde.
Use as a weapon 
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 did not use nerve agents against Allied targets.
- 1950s (early): NATO adopted sarin as a standard chemical weapon, and both the USSR and the United States produced sarin for military purposes.
- 1953: 20-year-old Ronald Maddison, a Royal Air Force engineer from Consett, County Durham, died in human testing of sarin at the Porton Down chemical warfare testing facility in Wiltshire. Maddison had been told that he was participating in a test to "cure the common cold." Ten days after his death an inquest was held in secret which returned a verdict of "misadventure". In 2004, the inquest was reopened and, after a 64-day inquest hearing, the jury ruled that Maddison had been unlawfully killed by the "application of a nerve agent in a non-therapeutic experiment."
- 1956: Regular production of sarin ceased in the United States, though existing stocks of bulk sarin were re-distilled until 1970.
- 1988: Over the span of two days in March, the ethnic Kurd city of Halabja in northern Iraq (population 70,000) was bombarded with chemical and cluster bombs, which included sarin, in the Halabja poison gas attack. An estimated 5,000 people died.
- 1993: The United Nations Chemical Weapons Convention was signed by 162 member countries, banning the production and stockpiling of many chemical weapons, including sarin. It went into effect on 29 April 1997, and called for the complete destruction of all specified stockpiles of chemical weapons by April 2007.
- 1994: The Japanese religious sect Aum Shinrikyo released an impure form of sarin in Matsumoto, Nagano. (see Matsumoto incident)
- 1995: Aum Shinrikyo sect released an impure form of sarin in the Tokyo Metro. Thirteen people died. (see Sarin gas attack on the Tokyo subway)
- 1998: In the US, Time Magazine and CNN ran news stories alleging that in 1970 U.S. Air Force A-1E Skyraiders engaged in a covert operation called Operation Tailwind, in which they deliberately dropped sarin-containing weapons on U.S. troops who had defected in Laos. CNN and Time Magazine later retracted the stories and fired the producers responsible.
- 2004: Iraqi insurgents detonated a 155 mm shell containing binary precursors for sarin near a U.S. convoy in Iraq. The shell was designed to mix the chemicals as it spins during flight. The detonated shell released only a small amount of sarin gas, either because the explosion failed to mix the binary agents properly or because the chemicals inside the shell had degraded with age. Two United States soldiers were treated after displaying the early symptoms of exposure to sarin.
- 2012: Syria was thought by the United States to have sarin gas mixed to be used as weapons.
- 2013: The United Nations has investigated reports that both sides in the Syrian civil war have used sarin, but has not yet confirmed its use by either the Syrian government or by the rebels.
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