Sarin

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**Sarin**
Discovery
Image:Sarin-skeletal.png
Discovered by	Gerhard Schrader Ambrose Rüdiger van der Linde
Discovered in	1938
Chemical Characteristics
Chemical Name	2-(fluoro-methyl-phosphoryl)oxypropane
Chemical Family	Fluorinated organophosphorus compound
Chemical Formula	C₄H₁₀FO₂P
NFPA Rating	Health - 4 Flammability - 1 Reactivity - 1 </small>
Airborne exposure limit	0.0001 mg/m³
Boiling point	158 °C
Freezing/melting point	-56 °C
Vapor pressure	2.9 at 25 °C
Vapor relative density (Air=1)	4.86
Liquid density	1.0887 g/cm³ at 25 °C 1.102 g/cm³ at 20 °C
Solubility in Water	Complete
Appearance and color	Colorless liquid. Odorless in pure form.
Precursors
Key precursors	methylphosphonyl difluoride methylphosphonyl dichloride diisopropyl methylphosphonochloridate
Precursors	Dimethyl methylphosphonate isopropyl methylphosphonate
Other chemicals	Trimethylphosphite phosphorus trichloride triisopropyl phosphite

This article is about the chemical. For the finch, see Serin; for the star Delta Herculis, see Sarin (star); for diamond technologies corporation, see Sarin Technologies

Sarin or GB (O-Isopropyl methylphosphonofluoridate) is an extremely toxic substance. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations according to UN Resolution 687, and its production and stockpiling was outlawed by the Chemical Weapons Convention of 1993.

1 Chemical characteristics
- 1.1 Shelf life
  - 1.1.1 Efforts to lengthen shelf life
2 Biological Effects
3 History
4 External links
5 References

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Chemical characteristics

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 colourless, odourless liquid. Its relatively high vapor pressure means that it evaporates quickly (about 36 times faster than tabun, another common chemical nerve agent). 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.

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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 [1], 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.

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Efforts to lengthen shelf life

According to the CIA, nations such as Iraq have tried to overcome the problem of sarin's short shelf life in two ways:

The shelf life of unitary (i.e., pure) sarin may be lengthened by increasing the purity of the precursor and intermediate chemicals and refining the production process.

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

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Biological Effects

Like other nerve agents, sarin attacks the nervous system of a living organism.

When a functioning motor nerve 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 site of the enzyme where acetylcholine normally undergoes hydrolysis. This allows acetylcholine to build up and continue to act so that any nerve impulses are, in effect, continually transmitted.

Initial symptoms following exposure to sarin (and other nerve agents) are a runny nose, tightness in the chest and contraction 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 is a highly volatile liquid. 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 acetylcholine inhibitor, is given to treat the physiological symptoms of poisoning. Pralidoxime can regenerate cholinesterases if administered within approximately five hours.

It is estimated that sarin is more than 500 times as toxic as cyanide.

The short- and long-term symptoms experienced by those affected included:

bleeding from the nose and mouth
coma
convulsions
difficulty breathing
disturbed sleep and nightmares
extreme sensitivity to light
foaming at the mouth
high fevers
influenza-like symptoms
loss of consciousness
loss of memory
nausea and vomiting
paralysis
post-traumatic stress disorder
respiratory problems
seizures
uncontrollable trembling
vision problems, both temporary and permanent
death

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History

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 .

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Origin

Sarin was discovered in 1938 in Wuppertal-Elberfeld in the Ruhr valley of Germany by two German scientists while 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.

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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, and they were concerned that the Allies' ability to reach German targets would prove devastating in a chemical war.

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Sarin after World War II

1950s (early): NATO adopts sarin as a standard chemical warfare agent, and both Russia and the United States produce 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.

1980-1988: Iraq employed 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 twenty chemical and cluster bombs, which included sarin. An estimated 5,000 people died. (see Halabja poison gas attack)

1991: UN Resolution 687 establishes the term "weapon of mass destruction" and calls for the immediate destruction of chemical weapons in Iraq, and eventual destruction of all chemical weapons globally. [2]

1993: The United Nations Chemical Weapons Convention is signed by 162 member countries, banning the production and stockpiling of many chemical agents, including sarin. It goes into effect on 29 April 1997, and calls for the complete destruction of all specified stockpiles of chemical agents by April 2007. [3]

1994: The Japanese religious sect Aum Shinrikyo releases an impure form of sarin in Matsumoto, Nagano Prefecture. (see Matsumoto incident)

1995: Aum Shinrikyo sect releases an impure form of sarin in the Tokyo subway. (see Sarin gas attack on the Tokyo subway)

1998: In its June 15 issue Time Magazine runs a story entitled "Did The U.S. Drop Nerve Gas?". The story is broadcast June 7 on the CNN program NewsStand. The Time article alleges that U.S. Air Force A-1E Skyraiders engaged in a covert operation called Operation Tailwind, in which they deliberately dropped CBU-15 Cluster Bomb Units containing submunitions that were filled with sarin on defected U.S. troops in Laos. The report causes a scandal, and The Pentagon launches a study that finds that no nerve gas use took place. After an internal investigation, both CNN and Time magazine (both owned by the media conglomerate Time Warner) retracted the story and fired the reporters responsible for it. [4]

2004: May 14 Iraqi insurgency fighters in Iraq detonate a 155 mm shell containing several litres of binary precursors for sarin. The shell is designed to mix the chemicals as it spins during flight. The detonated shell releases 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 are treated for exposure after displaying the early symptoms. [5]

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