The toxicity of sarin inhaled (vapor) is estimated (median lethal dose, or LD50) to be 100mg-min/m3, or 1.7 grams through the skin. Production of sarin can be performed using a variety of schemes, the more modern of which is the synthesis of difluor (difluoro methylphosphonate) and then reacting this with isopropyl alcohol and a organic base. This scheme is also employed in binary munitions, consisting of one part difluor (DF), isopropyl alcohol, and a promoter to facilitate the reaction to produce sarin.

Sarin was used by the terrorist-cult Aum Shinrikyo in Japan, relying upon its high volatility to spray its vapors in a Matsumoto neighborhood (June 1994), killing seven and injuring some 500, and in a crude attack on the Tokyo subway in March 1995 that killed 12 and injured hundreds of people.

The toxic principle of sarin is its ability to inhibit acetylcholinesterase (AChE), the body’s enzyme required for proper nerve transmission at the molecular level. Increased levels of acetylcholine produce exaggerated levels of bodily secretions and muscular twitching, as well as pronounced effects on the cardiovascular and central nervous systems. While death from respiratory paralysis can occur as a consequence, victims are also prone to asphyxiate due to mucous and salivary excretions from the upper respiratory tree. Without timely medical intervention and follow-up treatment, those who do survive exposure to large doses of nerve agents can suffer permanent neurological damage.