Lewisite pulmonary toxicity

The vesicant properties of lewisite result from direct contact with the skin. Signs of dermal toxicity (pain, inflammation) may be experienced within a minute after exposure. Acute lethality is usually the result of pulmonary injury. Ocular exposure may result in corneal necrosis. Due to its lipophilicity, percutaneous absorption of lewisite is rapid and, at a sufficient exposure, may be associated with systemic toxicity characterized by pulmonary edema, diarrhea, agitation, weakness, hypothermia, and hypotension (lOM, 1993). The threshold for severe systemic toxicity in humans following dermal exposure to lewisite has been estimated at lOmg/kg (9.1-13.4 mg/kg) (Sollman, 1957). 

Pediatric exposures to vesicants can be quite toxic however, in contrast to nerve agent exposures, HD causes significantly greater morbidity than mortality. While mustard did not cause many deaths in WWI, death from HD exposure is usually due to massive pulmonary damage complicated by infection (bronchopneumonia) and sepsis. Children often show a quicker onset and greater severity of toxicity. Skin and eye toxicity occurs in the form of blisters or irritation that can result in blindness for the most severe cases. Except for lewisite, vesicant exposures must be managed with supportive care and rapid decontamination. 

Lewisite (also known as Agent L), is no longer considered a state-of-the-art CW agent. Lewisite is a significant threat to unprotected personnel and causes prompt incapacitation from eye injuries and respiratory irritation, coupled with long-term incapacitation from skin bums, pulmonary injury, and systemic illness. Its decomposition products are toxic, making decontamination difficult. Munitions containing lewisite may contain toxic stabilizers. Lewisite is effective as vapor, aerosol, or liquid (Sidell et al., 1997). 

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