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Sarin
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Sarin, also known by its NATO designation of GB, 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.
Chemical characteristics
Sarin is a fluorinated phosphonate and is similar in structure and has a similar mechanism of action as some commonly used insecticides, such as malathion.
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Sarin, also known by its NATO designation of GB, 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.
Chemical characteristics
Sarin is a fluorinated phosphonate and is similar in structure and has a similar mechanism of action as some commonly used insecticides, such as malathion. It is similar in biological activity to carbamates used as insecticides such as sevin, and medicines such as pyridostigmine, neostigmine, and physostigmine.
At room temperature, sarin is a colorless, odorless liquid. Its low vapor pressure (2.9 mmHg at 25 °C) 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 isopropylamine. The isopropylamine neutralizes the hydrogen fluoride generated during the chemical reaction.
Production of sarin is extremely dangerous given its inherent toxicity, as well as the fact that the fluoride ion is also extremely corrosive to the manufacturing equipment itself. Therefore in early synthesis and production, injurious leaks and accidents were commonplace.
Shelf life
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 Iraqi Government 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:
- The shelf life of unitary (pure) sarin may be lengthened by increasing the purity of the precursor and intermediate chemicals and refining the production process.
- Incorporating a stabilizer chemical called tributylamine. Later this was replaced by diisopropylcarbodiimide (DIC), which allowed for sarin to be stored in aluminum casings.
- Developing binary chemical weapons, where the two precursor chemicals 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 making the issue of shelf life irrelevant and greatly increasing the safety of sarin munitions. Experts, however, do not put the shelf life of this type of weapon past 5 years.
Biological effects
Like other nerve agents, sarin attacks the nervous system of a living organism. It is an extremely potent irreversible cholinesterase inhibitor.
When a functioning pre-synaptic motor neuron or parasympathetic neuron is stimulated, it releases the neurotransmitter acetylcholine to transmit an action potential across the synaptic cleft to an effector muscle or organ. Once the action potential has been sent, the enzyme acetylcholinesterase breaks down the acetylcholine in the synaptic cleft in order to allow the effector muscle or organ to relax.
Sarin 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, 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 convulsive spasms.
Sarin has a high volatility relative to similar nerve agents. Inhalation and absorption through the skin pose a great threat. Even vapor 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 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.
It is estimated that sarin is more than 500 times more toxic than cyanide.
The short- and long-term symptoms experienced by those affected included:
Although bleeding from the nose and mouth were symptoms seen in the 1995 sarin gas attacks in Tokyo, this had been attributed to impurities within the sarin used as it is not usually seen.
History
Students at the United States Army and Marine Corps' Nuclear, Biological and Chemical Defense Schools at Fort Leonard Wood in Missouri conduct a Mission Oriented Protective Posture (MOPP) chemical protective gear confidence exercise in an environment containing live Sarin (GB) gas, as well as VX nerve agent. This exercise is carried out inside of the heavily guarded Chemical Defense Training Facility (CDTF).
Origin
Sarin was discovered in 1939 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
* 1950s (early): NATO adopted sarin as a standard chemical weapon, and both the U.S.S.R 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.
- 1960s (developing): The US unsuccessfully sought Australian permission to test Sarin and VX gas on 200 "mainly Australian" troops, probably in the Iron Range rainforest near Lockhart River, Queensland.
- 1978: Michael Townley in a sworn declaration indicated that sarin was produced by the secret police of Chile's Pinochet regime DINA, by Eugenio Berríos, it indicated that it was used to assassinate the state archives custodian Renato León Zenteno and the Army Corporal Manuel Leyton.
- 1980–1988: Iraq used sarin against Iran during the 1980–88 war. During the 1990–91 Gulf War, Iraq still had large stockpiles available which were found as coalition forces advanced north.
- 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.
- 1991: UN Resolution 687 established the term "weapon of mass destruction" and called for the immediate destruction of chemical weapons in Iraq, and eventual destruction of all chemical weapons globally.
- 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 Subway. Twelve people died. (see Sarin gas attack on the Tokyo subway)
- 1998: 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. After investigations both internally and by the Pentagon, CNN and Time Magazine retracted the stories and fired the producers responsible.
- 1999: The 3D crystal structure of sarin complexed with acetylcholinesterase was determined by Millard et al. (1999), and can be seen at .
- 2004: On May 14 Iraqi insurgency fighters in Iraq detonated a 155 mm shell containing several litres of binary precursors for sarin. 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 significantly with age. Two United States soldiers were treated for exposure after displaying the early symptoms of exposure to sarin.
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