Carbamate nerve agents exposure

Even though carbamate nerve agents are rapidly detoxified or eliminated from the body, exposures may have a cumulative effect in the short-term, placing all responders who entered the hot zone without appropriate chemical protective clothing at increased risk during the remainder of the emergency. 

Immediately dangerous to life or health (IDLH) levels are the ceiling limit for respirators other than SCBAs. However, IDLH levels have not been established for carbamate nerve agents. Therefore, any potential exposure to aerosols of these agents should be regarded with extreme caution and the use of SCBAs for respiratory protection should be considered. 

Currently, there is no information on performance testing of chemical protective clothing against carbamate nerve agents. Evaluation of fabrics used to prevent exposure to carbamate pesticides may provide guidance on selection of appropriate protective clothing. 

Miosis, pain, dim vision, and nausea can be relieved by topical atropine in the eye. Pretreatment with carbamates may protect the cholinesterase enzymes before nerve agent exposure. 

Miosis, pain, dim vision, and nausea can be relieved by topical atropine in the eye. Pretreatment with carbamates may protect the cholinesterase enzymes before nerve agent exposure. It is available in 30 mg tablets and the tablets should be administered every 8h. When used prior to exposure, it should be followed by atropine and pralidoxime chloride after exposure. 

Carbamate Nerve Agents are hazardous through inhalation, skin and eye exposure, ingestion, and abraded skin (e.g., breaks in the skin or penetration of skin by debris). 

Anderson, D.R. et al. Effects of suhacute pretreatment with carbamate together with adjunct pretreatment against nerve agent exposure. Drug Chem. Toxicol., 14, 1, 1991. 

The following factors have been suggested as alternatives to consider when presented with a potential case of exposure to nerve agents carbamate and organophosphate pesticides alkaloids such as nicotine or coniine ingestion of mushrooms containing muscarine and... 

Although bicyclophosphates do not inhibit acetylcholinesterase, they exhibit a synergistic toxic effect with materials that do. Individuals who have had previous exposure to cholinesterase inhibitors such as nerve agents and commercial organophosphate or carbamate pesticides may be at a greater risk from exposure to bicyclophosphates. 

Exposure to a toxic dose of OP results in inhibition of acetylcholinesterase and butyrylcholinesterase activities. The most common method to measure OP exposure is to assay acetylcholinesterase and butyrylcholinesterase activities in blood using a spectrophotometric method (EUman et al, 1961 Wilson et al, 2005 Worek et al, 1999). The drawbacks of activity assays are that they do not identily the OP. They show that the poison is a cholinesterase inhibitor but do not distinguish between nerve agents, OP pesticides, carbamate pesticides, and tightly bound, noncovalent inhibitors like tacrine and other anti-Alzheimer drugs. In addition, low-dose exposure, which inhibits less than 20% of the cholinesterase, carmot be determined by measuring acetylcholinesterase and butyrylcholinesterase activity because individual variability in activity levels is higher than the percent inhibition. 

Carbamates and OPs are chemicals that are often used as fungicides, insecticides, or pesticides and possess actions similar to nerve agents. These compounds are considered weapons of opportunity since their primary use is not by conventional militaries. In the USA, toxicity from these compounds is fairly rare. In 2006, there were approximately 1,200 cases of carbamate exposures and 1,500 organophosphate exposures documented for children 19 years old and younger (Bronstein et al, 2007). Although there were a few fatalities reported in 2006 from these substances, these fatalities occurred only in older individuals. 

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