Dermal toxicity lewisite

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). 

Acute Toxicity. Liquid lewisite applied by eye-dropper to the forearms of men caused blanching and discoloration of the skin followed by extensive erythema within 15-30 min and vesication within 12 hr (Wardell 1941 as cited in Goldman and Dacre 1989). The pain associated with these dermal exposures reportedly occurred within 2 min, and considerable discomfort persisted for about 1 wk. Other tests with human subjects and clinical reports also indicate a similar temporal sequence of events. Exposure to lewisite vapor (0.06-0.33 mg/ L) caused discoloration and blistering, with the maximum effect occurring by 36 8 hr after exposure (Wardell 1941). At a concentration of 0.01 mg/L, lewisite vapor caused inflammation of the eyes and swelling of the eyelids after 15 min of exposure, and inhalation of 0.5 mg/L for 5 min is considered to be potentially lethal. 

Blister agents or vesicants are chemicals that cause blister or vesicle formation upon dermal contact. Agents such as mustards or lewisite have been used as CWAs in the past (Yu et al., 2003). Although these agents have less toxicity than nerve agents, they cause prolonged... 

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