Chemical weapons organophosphorus effects

Exposure to nerve agents is not restricted to the battlefield. Possible terrorist use of these weapons and the destruction of the chemical weapon depots certainly will increase the risk of exposure. Since treatment for intoxication with at least some of these organophosphorus (OP) acetylcholinesterase (AChE) inhibitors is still far from ideal, research efforts are devoted towards finding an effective treatment. 

The toxicity of the P-halidc anhydrides, like that of phosphoroxychloride (POCl3) and of other organophosphorus compounds discussed earlier in this section, is due to their high efficiency as irreversible inactivators of acetylcholinesterase [157]. The main target organs for the lethal effects of these chemical weapons are the brain and diaphragm. As for the detoxification of the P-halide anhydrides, it can occur by a number of biochemical mechanisms, namely chemical hydrolysis, enzymatic hydrolysis, and binding to hydrolases such as carboxylesterases, cholinesterases, and albumin [68][158][159]. 

In addition to battlefield trauma, there is also the risk of exposure to chemical weapons such as the nerve agents, notably the organophosphorus gases (soman, sarin, VX, tabun) [6]. Organophosphorus toxicity arises largely from their ability to irreversibly inhibit acetyl-cholinesterases, leading to effects associated with peripheral acetyl-choline accumulation (muscarinic syndrome) such as meiosis, profuse sweating, bradychardia, bronchioconstriction, hypotension, and diarrhoea. Central nervous system effects include anxiety, restlessness, confusion, ataxia, tremors. 

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