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About sarin Gas 

By: Zimbler0 in POPE IV | Recommend this post (2)
Sun, 23 Apr 17 6:09 AM | 48 view(s)
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http://www.chemeurope.com/en/encyclopedia/Sarin.html

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.

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.

>> Zim: Anyone else remember those 'harmless pesticides'
>> found in Iraq the troops test kits said was
>> nerve agent?

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.

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.

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.[2].

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 (i.e., 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 (di-c-di), which allowed for GB nerve agent to be stored in aluminium 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. However, experts still refuse to 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 irreversible cholinesterase inhibitor.

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.

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(Article does continue. Zim.)




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