http://www.pbs.org/newshour/rundown/2013/09/how-to-survive-a-chemical-weapons-attack.html
Sarin, a clear, odorless, tasteless nerve gas, was developed in Nazi Germany in 1938, originally for use as a pesticide, though it was produced and stockpiled as a weapon by American operatives after the war. Also known as GB, it's thought to have been deployed during the Iran-Iraq War in the 1980s, and it was released by the Aum Shinrikyo religious cult on five Tokyo subway trains in 1995. Its chemical structure is similar to that of organophosphates, a common class of insecticides, which contain carbon-based groups coupled to a phosphorous atom. And it is believed to work on the body in the same way that the pesticides act on the bugs - or on agricultural workers who are exposed to too much of the stuff.
Except Sarin is immensely more powerful. A dab the size of a pea is enough to cause death, according to Pete Estacio, a physician and chemist who works with Lawrence Livermore National Laboratory's Forensics Science Center.
Sarin and other nerve gases work to disrupt bodily functions by blocking the brain's ability to control muscle movement. For a muscle to contract, the brain must send that muscle a message in the form of electrical pulses across a system of nerves. Passing from one nerve to the next requires a neurotransmitter called acetylcholine, which is naturally produced by the body. But as soon as this chemical does its job, it must immediately get broken down, or the muscles will contract uncontrollably.
Enter acetylcholinesterase, the enzyme that breaks down the chemical. Normally, the chemical acetylcholine is released, sends its message, and then the enzyme binds to the acetylcholine molecule to essentially shut it off.
"The bigger the dose you're exposed to, the more quickly you need early intervention," Estacio said. "You've got 15 minutes to be treated, and if exposed to a large dose, you're done for."
But here's where the nerve agents come in. Sarin gums up that process by binding to the exact same dock as the acetylcholinesterase, blocking the enzyme from doing its job.
"It that's messed up, that messes everything up," said Carlos Fraga, a chemist with the Pacific Northwest National Laboratory. "If you're not able to destroy acetylcholine, it just builds up and causes the nerves to keep firing."
Delivery of the chemical message without interruption by the enzyme leads to overstimulation, Estacio added.
"For example, if it's a secretion in the mouth, it will make the person foam at the mouth," he said. If it's tear ducts, it will make you cry. if its muscles in the leg, it will make the muscles twitch."
The result is the terrible symptoms seen in the recent attack in Syria. Pupils narrow to the size of pinpoints. People experience sudden nausea, diarrhea, vomiting, seizures, muscle spasms, excessive runny nose and most dangerously, difficulty breathing - ultimately the main cause of death, Fraga said.
The good news is that there's a suite of antidotes that can counter these effects. A drug called atropine blocks the acetylcholine receptor, reversing the immediate effects of the nerve agent. Another drug called 2-PAM breaks the chemical bond between the acetylcholine molecule and the nerve agent, preventing the poison gas molecules from binding irreversibly to the nerve cells -- a process known as "aging."
But here's the problem: to work, these drugs must be administered immediately - within minutes.
"The bigger the dose you're exposed to, the more quickly you need early intervention," Estacio said. "You've got 15 minutes to be treated, and if exposed to a large dose, you're done for."
Bottom line: you have to be prepared for a chemical attack in order for the treatment to work.
"You have to have it on you," Fraga said. "When you start seeing symptoms, you've got minutes. You have to know that you're in that situation."
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