Sarin is an organophosphorus compound that was created as one of the “G” (German) agents during WWII. Sarin was synthesized in 1938 and named for its developers: Schrader, Ambrose, Rudringer, and Van der Linde. The mechanism of action is the same as insecticide organophosphorus compounds: inhibition of acetylcholinesterase. An accumulation of acetylcholine (Ach) occurs in the synapse resulting in a cholinergic toxidrome with muscarinic and nicotinic effects.
Unlike the insecticide versions, the “G” agents (sarin, tabun, soman) are volatile and can be vaporized from their liquid form. Sarin is the most volatile and does not have an odor to provide warning properties to the intended victims. Exposure to vapors results in rapid onset (seconds to minutes) of cholinergic effects since there is pulmonary absorption. The upper respiratory tract and eyes are affected early after exposure with resulting rhinorrhea, lacrimation, salivation, miosis, and vision changes. Depending on the concentration of vapor, only a few breaths may result in rapid onset of systemic and central nervous system effects in the victims. One of the other important characteristics of an organophosphorus compound is the time to “aging”. “Aging” is an irreversible reaction after which the organophosphorous compound can no longer be removed from the acetylcholinesterase enzyme. The “aging” time of the bond between sarin and acetylcholinesterase is only a few hours (3-5 hours). After “aging” is complete, oximes such as pralidoxime are unable to reactivate the acetylcholinesterase. The victims will then require supportive care, antimuscarinic agents, etc. for weeks to months.
Thus, the victims are rapidly affected and remaining population is effectively terrorized.
This question prepared by: Saralyn Williams, MD Medical Toxicologist
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Donna Seger, MD
Medical Director
Tennessee Poison Center
Poison Help Hotline: 1-800-222-1222