tabun

Tabun, designated GA by NATO, is a highly toxic organophosphorus nerve agent developed in Germany in the late 1930s as part of early chemical weapons research. It is a member of the G-series of nerve agents and was among the first to be produced for potential combat use.

Tabun inhibits the enzyme acetylcholinesterase, causing an accumulation of acetylcholine at nerve junctions and neuromuscular junctions. This leads to a cholinergic crisis with effects on the muscarinic, nicotinic, and central nervous systems. Exposure can result in a range of symptoms, including pinpoint pupils, excessive secretions, sweating, bronchial constriction, diarrhea, muscle fasciculations, seizures, and potentially fatal respiratory failure if not treated promptly. Both inhalation and dermal absorption are possible routes of exposure.

History and regulation: Tabun was synthesized by chemist Gerhard Schrader at IG Farben in 1936–37. Under the Chemical Weapons Convention, Tabun is classified as a Schedule 1 substance, meaning its production, stockpiling, and transfer are heavily restricted and subject to destruction obligations, with only limited, controlled uses for research or defensive purposes under strict oversight.

Properties and safety: Tabun is typically a colorless to pale liquid with moderate volatility. It hydrolyzes in water and can be absorbed through skin or inhalation. Decontamination and medical treatment follow standard nerve agent protocols, including rapid administration of atropine to block muscarinic effects and oximes such as pralidoxime to reactivate acetylcholinesterase, along with supportive care for seizures and respiratory support as needed.