Chemical Defense

Chemical weapons use the toxic rather than the explosive properties of chemical substances to produce physical or physiological effects on an a victim. Classic chemical weapons, such as chlorine and phosgene, were employed during World War I and consisted primarily of commercial chemicals used as choking and blood agents to induce respiratory damage and asphyxiation. The advent of blistering agents such as mustard gas and lewisite, which cause painful burns necessitating medical attention even in low doses, marked the first chemical weapons to produce a significant effect on the military. Mustard gas, because of its low cost and ability to produce resource-debilitating casualties, has been an established weapon and was used to inflict numerous casualties during the Iran-Iraq war.

Organophosphorous nerve agents, or anti-cholinesterase agents, were discovered in the 1930’s following intensive research into new insecticides. Their use in World War II represents the beginning of modern chemical warfare. These agents cause toxicity by binding to and inactivating acetylcholinesterase, an enzyme in the body that is essential for proper nervous system function. The result is an increase in acetylcholine at the junction between the nerve and its target organ which results in “cholinergic crisis”. In its most severe form, exposed individuals experience an increase in secretions, loss of muscle control, respiratory failure, paralysis, convulsions, permanent brain damage and death

Organophosphorous nerve agents are highly volatile but all are liquid at room temperature. They are lethal far more quickly and in far lower quantities than earlier chemical weapons, and they can exert their toxic effects both when inhaled and when absorbed through the skin. Organophosphorous nerve agents are classified as either G-agents (sarin, soman, tabun) or V-agents (VX), both of which are exceedingly volatile and toxic. They can be delivered through bombs, rockets, artillery shells, spray tanks, and missile warheads.