| Tabun (GA) was the first of the military nerve agents synthesized by German chemists Schräder and others during the late 1930s. (The name “tabun” apparently was a nonsensical word invented for this new compound in order to maintain secrecy.) Eventually, Nazi Germany produced about 12,000 tons of tabun nerve agent during 1944-45 (but none was ever used in World War II). Because it was the first of the so-called “German” series of nerve agents classified by NATO, tabun was designated “GA.” A liquid at room temperature, tabun has been described as having a brownish color and, in its more impure state, an odor of rotting fruit.
Tabun nerve agent is much less volatile than sarin or soman. Due to its persistency, tabun may survive for days, weeks, or even longer during cold weather. In terms of median lethal dose (LD50), the toxicity of tabun inhaled is 400mg-min/m3, and skin contact is estimated to be about one gram. (Although a cyanide molecule is liberated from tabun in aqueous solutions, its contribution towards its toxicity is limited to its capacity as a leaving group.) Unlike other military nerve agents (sarin, soman, VX), tabun’s chemical structure lacks a methyl-phosphorus bond. Like other nerve agents, the toxic principle of tabun 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. |
Close
Window