Nerve agents were synthesized in the 1930s by both German and Allied (U.K.) scientists during World War II, although only Germany produced actual wartime stocks of these very toxic substances. In the later stages of the war (1944–1945), German military scientists produced large quantities of Tabun nerve agent (apparently code-named after a nonsensical word). More commonly known nerve agents developed for use in CW are Sarin and VX. All nerve agents share the same toxic principle: Disruption of the biochemistry vital for normal function of the nervous system. These compounds have been used in the Iran-Iraq War (1980–1988) and in two major terrorist attacks in Japan during the mid- 1990s.
Nerve agents were first created from investigative research into new insecticides based on organophosphorus molecules (those possessing carbon and phosphorus in their structures). In 1937, the German chemist Gerhard Schräder and his team synthesized a potential organophosphorus insecticide but found that it was highly toxic to mammals. A drop of the substance, later called Tabun, fell on the laboratory table. Schräder and an assistant soon began to show signs of poisoning, including the classic symptom of pinpoint pupils (miosis). This compound was given to the German wartime government as a possible chemical weapon. During the 1940s, British scientists, notably Bernard Saunders, also experimented with nerve agent compounds, as well as with cyanide and other compounds with fluorine.
Nerve agents like Tabun share in common a so-called leaving group, a chemical constituent of the molecule that leaves to reveal a reactive site. This site can react (phosphorylate) with susceptible groups in enzymes. The primary enzyme targeted by the nerve agent molecule is acetylcholinesterase (AChE). Normally, AChE performs the life-sustaining function of taking the nerve signal transmitter (neurotransmitter) acetylcholine and splitting it into acetic acid and choline, both of which are recycled by yet another enzyme to form acetylcholine again later when needed. AChE splits acetylcholine at a rate of hundreds of molecules per second. This enzyme not only provides for muscle fiber flexing, but also for fluid excretion and normal breathing, among many other bodily functions. If this enzyme is blocked or inhibited, levels of acetylcholine will continue to rise. This sets off a series of events that leads to death by respiratory arrest, either due to exhaustion or, more likely, asphyxiation by accumulating mucous and saliva in the airways. Thus, despite their very different mechanisms, nerve agents can also produce “dry land drowning” as does chlorine in the classic sense of “gas warfare.”
Nerve agents are extremely toxic even when compared to other CW agents. All nerve agents are liquid at room temperature, but different types of nerve agents vary in their volatility. As with mustard, high concentrations of nerve agent are best delivered through the use of aerosols. VX nerve agent does not evaporate very quickly, much less so than mustard, but sarin, a nerve agent used on the Tokyo subway by terrorists in 1995, volatilizes at about the same rate as water. Therefore, although militaries would use nerve agents as aerosols to maximize their effectiveness in the field, terrorists may employ simpler, even crude methods of delivery.
Sarin
Sarin (NATO code GB from the first generation “German” nerve agents) was the second deadly G-series nerve agent discovered by the German chemist Gerhard Schräder and his colleagues in 1938. The name sarin is attributed to its discoverers— Schräder, Ambrose, Rudriger, and van der Linde. Germany tried to produce the agent on a large scale, but several technical and logistical hurdles prevented it from doing so. Only small quantities were produced by Germany in 1944. The sarin production process is more complicated than the one for tabun, partly due to the use of corrosive agents in sarin’s manufacture. Techniques for mass production of sarin were later perfected by the major powers in the years following World War II.
Following inspections by the UN Special Commission in Iraq (UNSCOM) during the 1990s, Iraq claimed to have produced 790 tons of sarin, 30 tons of which were destroyed by UNSCOM, the remainder reportedly having been destroyed by the Iraqis. Sarin was also employed by the Japanese cult Aum Shinrikyo in 1994 at Matsumoto, where 7 people were killed, and during the 1995 Tokyo subway attack, which killed 12 people and injured about 1,000.
Sarin is an odorless, colorless liquid and is highly lethal. Its primary precursors include isopropyl alcohol, hydrogen fluoride, hydrochloric acid, and phosphorus trichloride. Sarin is not a very persistent agent (evaporating very quickly) and it is miscible (soluble) in water as well as organic solvents.
Like other nerve agents, sarin inhibits the action of the acetylcholinesterase enzyme, resulting in the production of excessive secretions, including mucous in the upper airways, and loss of muscular functions. Death may occur either due to respiratory paralysis or asphyxiation from fluid in the upper respiratory tract.
