The science of the Syrian chemical attack
Sarah Cate Baker | Tuesday, April 11, 2017
In 1938, a lab in Germany developed the chemical sarin for use as a pesticide. In 1939 the Nazis began producing it as a potential chemical weapon; they never used it. In the 1970s the Chilean secret police assassinated Pinochet’s enemies with it. In 1988 Saddam Hussein’s regime used it to massacre three to five thousand Kurdish civilians. It was used twice in the 1990s by a Japanese religious cult, killing 19. In 2013, Bashar al-Assad’s regime used it in the Syrian Ghouta attack, which killed somewhere between three hundred and two thousand people. And on April 4, 2017, the Syrian government released it on the town of Khan Sheikhoun. The death toll is hovering around 70.
Sarin is a nerve gas. In its vaporized, weaponized form it can be inhaled, or penetrate the skin directly or get into the eyes. It can persist in clothing for up to thirty minutes. It can kill someone in 10. It is colorless, odorless and tasteless. It is 50 more deadly than cyanide.
Sarin works by over-stimulating muscles. It is a small molecule — three carbons, two oxygens, a phosphorous and fluorine — and a chemist would call it an organophosphate. Sarin operates at a person’s neuromuscular junctions, the place where neurons tell muscles what to do. There’s a molecule in these junctions called acetylcholine, which acts like a molecular on-switch. When released from a neuron, acetylcholine binds receptors on a muscle cell and tells it to contract. Then, acetylcholine gets degraded by acetylcholinesterase, and the muscle relaxes. Unless there is sarin present.
Sarin binds acetycholinesterase, inhibiting it from degrading acetycholine. The on-switch stays on, and muscles contract again. And again. And again.
Victims of the attack last Tuesday went into convulsions as their muscles could not stop spasming. Some of them went into respiratory failure because their lungs could not exchange gasses fast enough to keep up. Some of them lost consciousness as their bodies were exhausted. These are the people who died on Tuesday. Reports estimate there were between seventy and one hundred of them; around thirty were probably children.
But sarin is not always fatal. If a patient exhibits the above symptoms, they will likely die within an hour. But if a patient is exposed to a smaller dose and they have different symptoms, they may survive. Sarin attacks almost always leave more injured than dead; for example, the 1988 attack by Hussein killed five thousand, but injured seven to 10,000 more. The Matsumoto attack of 1994 killed eight people, and injured 200. In Khan Sheikhoun right now, there at least 70 are dead, and 300-500 injured.
The non-fatal symptoms of sarin poisoning include severe headaches, exhaustion, blurred or teary vision, rapid breathing, excessive sweating, nausea, vomiting and diarrhea. Aid workers reported that victims bled from the nose and mouth when oxygen was administered. Severe muscle twitching is common.
There has been limited research on the long-term effects of sarin exposure. Studies of the Japanese victims of the 90s noted abnormal brain activity for up to five years after the attacks. In most cases there was eventually complete physical recovery, although there may have been lingering psychological problems. The survivors in Syria may have fewer problems from the physical effects of sarin than from the mental weight of watching their friends, family and neighbors writhing and gasping for breath as bombs fell from the sky.
That is the science of sarin. It is an organophosphate; it inhibits acetylcholinesterase and causes constant muscle contraction; its symptoms range from respiratory failure to nosebleeds, and the long-term neurological effects are unclear. It killed at least 70 people last Tuesday. Now you know.
So what are you going to do about it?
The views expressed in this column are those of the author and not necessarily those of The Observer.