Nerve agents acute exposure

Acute Exposure If recovery from nerve agent poisoning occurs, it will be complete unless anoxia or convulsions have gone unchecked so long that irreversible central nervous system changes due to anoxemia have occurred. 

Rapid response (seconds) (e.g. severe pain relief, acute exposure nerve agents)... 

OPs have been in use for several decades as important chemicals for the control of crop pests. With their chemical and biochemical reactions, OPs have been well established as extremely poisonous chemicals. This classification is due to the inhibition of the marker enzyme ChE, which is produced in the liver. Blood enzymes provide an estimate of tissue enzyme activity. After acute exposure to OPs or a nerve agent, the erythrocyte enzyme activity most closely reflects the activity of the tissue enzyme. Once the OPs inhibit the tissue enzyme, it cannot hydrolyze ACh, and the accumulation stimulates the affected organ. Based on the manner of exposure (dose and duration) to different OPs, a series of toxicity signs and symptoms set in the organism, leading to death. These are important aspects to be closely monitored among pest control operators and occupational workers exposed to OPs. 

Relative potency of nerve agents can also be expressed in terms of the in vivo dose necessary to produce the same level of cholinesterase inhibition by a specific exposure route. As would be expected, the effectiveness of the agents in inhibiting cholinesterase is closely correlated with their acute toxicity (see Appendix A). 

As noted in section 3.1, the neurotoxic effects following acute exposures to nerve agents such as GD can range from minor symptoms such as fatigue, headache, mild vertigo, weakness, and loss of concentration to convulsions, respiratory arrest and death. 

Exposure to acutely toxic concentrations of nerve agents can result in excessive bronchial, salivary, ocular and intestinal secretions, sweating, miosis, bronchospasm, intestinal hypermotility, bradycardia, muscle fasciculations, twitching, weakness, paralysis, loss of consciousness, convulsions, depression of the central respiratory drive, and death (Grob and Harvey, 1953 Grob, 1956 Marrs, 2007 Sidell, 1997 Yanagisawa et al, 2006 many others). Minimal effects observed at low vapor concentrations... 

Cannard, K. (2006). The acute treatment of nerve agent exposure. J. Neurol. Sci. 249 86-94. 

Nambiar, M., Gordon, N.K., Rezk, P.E., Katos, A.M., Wajda, N.A., Moran, T.S., Steele, K.E., Doctor, B.P., Sciuto, A.M. (2007). Medical countermeasures against respiratory toxicity and acute lung injury following inhalation exposure to chemical warfare nerve agent VX. Toxicol. Appl. Pharmacol. 219 142-50. 

Watson, A., Opresko, D., Young, R., Hauschild, V. (2006a). Development and application of acute exposure guideline levels (AEGLs) for chemical warfare nerve and sulfur mustard agents. J. Toxicol. Environ. Health, Part B. 9 173-263. 

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