As I write this post, President Barack Obama and his advisers are likely in conference regarding military action against the regime of Syrian dictator Bashar al-Assad. The United States had previously declared that the use of “a whole bunch of chemical weapons” by Syrian forces would be considered a “red line,” a point at which more direct US intervention in the country’s civil war would be justified. A rocket attack conducted by Mr. Assad on Aug. 21, in which approximately 3,600 victims suffered neurotoxic symptoms and 355 were killed, is thought by many in the Obama administration to have crossed that line. Recent laboratory analysis of hair and blood samples from those killed in the attack suggests that the rockets indeed carried the chemical agent sarin, strengthening US resolve for action.
Sarin was first discovered in 1938 through an accident at the German chemical company I.G. Farben, whose scientists had been attempting to develop stronger pesticides. The compound’s toxicity arises from its similarity to acetylcholine, a molecule produced naturally in the nervous system.
Acetylcholine is a neurotransmitter, a chemical released by a neuron to trigger a response in a target cell; in this case, acetylcholine is released from a motor neuron to trigger the contraction of a muscle fiber. Normally, an enzyme called acetylcholinesterase degrades acetylcholine after the chemical has delivered its message to the muscle, allowing the muscle to relax. Sarin acts by binding to this enzyme in the place of acetylcholine, preventing it from breaking down the neurotransmitter. Without this chemical “off switch,” muscles stay contracted, straining the body and disrupting normal functions.
Symptoms of sarin poisoning can begin within seconds of exposure to the chemical. As Time’s Alexandra Sifferlin explains, initial responses include “weakness, vomiting, diarrhea and irregular heart rates,” while heavy exposure can cause “convulsions, paralysis, loss of respiratory functions and even death.” The symptoms are treatable using the antidotes pralidoxime chloride and atropine, which chemically pry sarin out of its association with acetylcholinesterase and prevent it from binding to the muscle cells themselves, respectively. However, these medicines must be administered within minutes to several hours of exposure to be effective, as sarin binds further with the enzyme in a process called “aging” if left untreated.
Due to the debilitating effects of the gas, the possession and use of sarin has been outlawed by the Chemical Weapons Convention (CWC) of 1997, to which 188 nations (including the United States) are signatories. Even before the ratification of this treaty, sarin had only been used in a handful of attacks, the most notable of which were the strikes of late Iraqi dictator Saddam Hussein against Kurdish civilians and Iranian military targets throughout the 1990s. The use of sarin by the Syrian regime is therefore extremely troubling from both scientific and historic perspectives, and it is in the interest of peace for the world at large that the use of this agent not be allowed to continue.