Nerve agents mild exposure

Exposure of the eyes to nerve agent vapour exposure usually causes miosis and ocular pain due to spasm of the sphincter muscles of the iris and ciliary body, and dimmed or blurred vision. The eye discomfort is characterised as a sharp or aching ocular pain and can be associated with a mild-to-severe headache. Sometimes, the pain is accompanied by nausea and vomiting. The duration of miosis is variable, ranging from several days to as long as 9 weeks. 

Meat from animals that have suffered only mild to moderate effects from exposure to nerve agents should be safe to consume. Milk should be discarded for the first 7 days postexposure and then should be safe to consume. Meat, milk, and animal products, including hides, from animals severely affected or killed by nerve agents should be destroyed. 

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. 

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. 

Nerve agents can be absorbed by any route (ocular, oral, inhalation, dermal) (RTECS, 2008 HSDB, 2008). Onset of signs and duration of effects depend on the form of nerve gas (vapor, hquid) and the route of exposure. With a vapor exposure and inhalation, local signs of nasal discharge and respiratory noise begin within one to several minutes and signs can last for a few hours (mild exposure) up to 1 to 2 days (severe exposure) (Pfaff, 1998). Inhalation of a large amount of the vapor will result in sudden loss of consciousness, apnea, flaccid paralysis, and seizures within seconds to 2 to 3 min (Sidell et al, 1997). Peak effects are seen within 20 to 30 min and death is usually due to respiratory failure (Berkenstadt et al, 1991). 

TABLE 61.3. Management of mild/moderate nerve agent exposures (Rotenberg and Newmark, 2003 Anon, 2002)... 

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). 

As for the human experience, workers exposed to small amounts of nerve agents that produced mild, nonthreatening medical signs of exposure, reported CNS effects such as headache, insomnia, excessive dreaming, restlessness, drowsiness, and weakness. Clearly, exposure to nerve CWA may produce stress reactions, organic brain syndromes, or both, McDonough and Romano provide a deeper discussion of the effects of acute or chronic exposure to nerve agents in Chapter 4 of this book. 

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