Nerve agents vapor exposure

In the approximately 70 years since the discovery of the toxic G agents and 50 years since the subsequent development of the V agents, humans have only occassionally served as test subjects in laboratory studies designed to determine threshold toxic effects associated with low-level (nonlethal) sarin and VX vapor exposures (2-10 min) (Johns, 1952 Sim, 1956 Bramwell et al., 1963). In addition, although the toxic effects of accidental exposures and nonexperimental exposures from terrorist or military attacks are documented, critical information related to the exposure conditions can only be estimated at best. Thus, estimates of human dose-responses to nerve agent vapor exposures from such sources are often associated with significant uncertainty and are of limited utility in predicting health hazard risks. 

The choice of appropriate treatment for nerve agent intoxication depends on the agent as well as extent and route(s) of exposure. Very mild exposure to nerve agent vapor may necessitate only decontamination and observation severe exposure to vapor or liquid requires immediate decontamination, antidote administration, artificial respiration, monitoring, and supportive therapy over hours to multiple days (ATSDR, 2007 Sidell, 1997 Vale et al, 2007 Pulley and Jones, 2008). Convenient triage classifications have been developed by ATSDR (2007) in collaboration with the US Army Medical Research Institute of Chemical Defense. 

Sekowski, J.W., Orehek, M. A., Bucher, J. et al. (2004). Low-level inhalation exposure to chemical nerve agent vapor induces expression of neuronal apoptosis and regeneration genes. Proceedings of the 24th Annual Army Science Conference, November 29-December 2, 2004, Orlando, FL. 

Rhinorrhea may precede miosis as the first indication of exposure to even small amounts of nerve agent vapor. After exposure to high concentrations/ doses by any route, rhinorrhea occurs as part of the generalized increase in secretions. Direct ocular contact to nerve agents may cause miosis, conjunctival injection, pain in or around the eyes, and dim or blurred vision. 

The initial effects of nerve agents depend on the dose and route of exposure. A small inhalation exposure from nerve agent vapor causes a response in the eyes, nose and airway, such as miosis, conjunctival injection, eye pain, rhinorrhea, bron-choconstriction, excessive bronchial secretions, and mild to moderate dyspnea (9,13,18). Larger exposures cause central nervous system effects within seconds to minutes, including loss of consciousness, seizures, and central apnea. Death can occur within 5-lOmin of a lethal dose, usually due to respiratory failure from the combined effects of respiratory muscle paralysis, loss of airway control and profuse bronchorrhea (13,14). 

A tight chest or shortness of breath is another typical complaint following exposure to small amounts of nerve agent vapor. Dyspnea (difficult or labored breath-... 

Small Areas Ventilation. In heavily contaminated areas, decontamination with copious amounts of aqueous sodium hydroxide solution (a nunimum of 10 percent by weight) may be required. If sodium hydroxide solution is not available, then sodium carbonate may be used. Removal of porous material, including painted surfaces, that may have absorbed Nerve Agent vapor may be required as these materials could continue to re-release vapor after exposure has ceased. 

Miosis (pinpointing of pupils) and rhinorrhea (runny nose) may be the first indications of exposure to nerve agent vapor. Miosis is indicative of vapor exposure unless liquid has been in contact with the eyes. Difficulty breathing (shortness of breath or tightness of the chest) may also be present. Lethal amounts of vapor cause loss of consciousness and convulsions within 30 seconds to 2 minutes of exposure, followed by cessation of breathing and flaccid paralysis after several more minutes. 

III. Ocular Effects of Nerve Agent Vapor/Aerosol Exposure.236... 

III. OCULAR EFFECTS OF NERVE AGENT VAPOR/AEROSOL EXPOSURE... 

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