Excerpt from CBRNE - Nerve Agents, G-series: Tabun, Sarin, Soman

G-series nerve agents share a number of common physical and chemical properties. At room temperature, the G-series nerve agents are volatile liquids, making them a serious risk for 2 types of exposure: dermal contact with liquid nerve agent or inhalation of nerve agent vapor. GB is the most volatile of these agents and evaporates at the same rate as water; GD is the next most volatile. Dispersal devices or an explosive blast also can aerosolize nerve agents. Nerve agent vapors are denser than air, making them particularly hazardous for persons in low areas or underground shelters. GB and GD are colorless, while GA ranges from colorless to brown. GB is odorless, while GA and GD smell fruity.

Because nerve agents are soluble in fat and water, they are absorbed readily through the eyes, respiratory tract, and skin. Vapor agents penetrate the eyes first, producing localized effects, then pass into the respiratory tract, with more generalized effects when the exposure is greater. Liquid agents penetrate the skin at the point of contact, producing localized effects followed by deeper penetration and generalized effects if the dose is large enough. Accordingly, the lethality of these agents varies with the route of exposure. For inhalational exposures to GB, the lethal concentration time product in 50% of the exposed population is 75-100 mg·min/m³. For dermal exposures, the lethal dose in 50% of the exposed population is 1700 mg.

Pathophysiology: Nerve agents act by first binding and then irreversibly inactivating acetylcholinesterase (AChE), producing a toxic accumulation of acetylcholine (ACh) at muscarinic, nicotinic, and CNS synapses. Excessive ACh at these cholinergic receptors may account for the spectrum of clinical effects observed in nerve agent exposure. At muscarinic receptors, nerve agents cause miosis, glandular hypersecretion (salivary, bronchial, lacrimal, bronchoconstriction, vomiting, diarrhea, urinary and fecal incontinence, bradycardia). At nicotinic receptors in skin, nerve agents cause sweating, and on skeletal muscle, they cause initial defasciculation followed by weakness and flaccid paralysis. At CNS cholinergic receptors, nerve agents produce irritability, giddiness, fatigue, lethargy, amnesia, ataxia, seizures, coma, and respiratory depression.

Nerve agents also cause tachycardia and hypertension via stimulation of the adrenal medulla. They also appear to bind nicotinic, cardiac muscarinic, and glutamate N-methyl-d-aspartate (NMDA) receptors directly, suggesting that they may have additional mechanisms of action yet to be defined. Nerve agents also antagonize gamma-aminobutyric acid (GABA) neurotransmission, which in part may mediate seizures and CNS neuropathology.

Clinical effects of nerve agents depend on the route and amount of exposure. The effect of inhalational exposure to nerve agent vapor in turn depends on the vapor concentration and the time of exposure. Exposure to low concentrations of nerve agent vapor produces immediate ocular symptoms, rhinorrhea, and in some patients, dyspnea. These ocular effects are secondary to the localized absorption of GB vapor across the outermost layers of the eye, causing lacrimal gland .....