Lewisite exposure, inhalational

Lewisite is a vesicant and toxic lung-irritant that is absorbed into tissues. If inhaled in high concentrations, it can be fatal in as little as 10 minutes the body is unable to detoxify itself from lewisite exposure. Routes of entry into the body include the eyes, skin absorption, and inhalation. Eye contact results in pain, inflammation, and blepharospasm (spasms of the muscles of the eyelid), which leads to closure of the eyelids, comeal scarring, and iritis (inflammation of the iris). If decontamination of the eyes occurs quickly after exposure, damage may be reversible however, permanent injury or blindness can occur within one minute of exposure. 

Inhalation death occurs within 10 minutes, primarily a result of dry land drowning in which the lungs and throat fill with mucus, blood, and dead tissue, causing asphyxiation. Two milliliters of pure liquid lewisite absorbed by a 150-pound adult by any means would likely be fatal. Those who survive exposure may continue to show symptoms including pulmonary edema, neural disorders, subnormal body temperature, low blood pressure, and permanent damage to the endocrine system for an indefinite period.1... 

Liquid lewisite applied by eye-dropper to the forearms of men caused blanching and discoloration of the skin followed by extensive erythema within 15 to 30 minutes and vesication within 12 hours or less (Wardell, 1941, as cited in Goldman and Dacre, 1989). The pain associated with these dermal exposures reportedly occurred within two minutes and considerable discomfort persisted for about one week. Other tests with human subjects and clinical reports also indicate a similar temporal sequence of events. Exposure to lewisite vapor (0.06 to 0.33 mg/L) caused discoloration and blistering with the maximum effect occurring by 36 to 48 hours 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 minutes of exposure, and inhalation of 0.5 mg/L for five minutes is considered to be potentially lethal. 

The US Army has developed HBESLs for lewisite (USACHPPM, 1999). Additionally, a chronic oral reference dose (RfD) is available (NRC, 1999 USACHPPM, 1999), as are inhalation and dermal RfDs (USACHPPM, 1999). Interim Acute Exposure Guidelines values (AEGLs) have been developed for lewisite. 

Signs can be seen when lewisite is contacted dermally, orally, ocularly, inhaled, or ingested. Dermal and respiratory exposures are seen most frequently. Lewisite causes dermal, ocular, and respiratory lesions similar to mustard gas. Lewisite is about ten times more volatile than mustard gas (Budavari, 2000). 

BAL reduced the mortality in dogs when it was given within 100 min after they had inhaled a lethal amount of Lewisite (Harrison et al., 1946). Burns of the eyes from Lewisite can be prevented if BAL is applied within 2-5 min of exposure when it was apphed within 1 h after exposure, BAL prevented vesication in humans (Peters et al., 1945 Goldman and Dacre, 1989). BAL has some unpleasant side effects, including hypertension and tachycardia the user should read the package insert. 

The inhalation toxicity of neutralents from the RRS red process treatment of HD, HN, and lewisite was tested in rats by 14-day exposures. The neutralent contained 53 percent chloroform, 30 percent t-butyl alcohol, trace amounts of DCDMH, and less than 1 ppm HN or HD, or 37 ppm lewisite. The toxicity of the waste stream was compared with that of an aerosol containing 58.3 percent chloroform, 39.1 percent tert-butanol, and 2.6 percent water (the vehicle control). Concentrations of 24,000 ppm of the vehicle control or neutralent killed all of the test animals. Lower doses caused excessive salivation, ocular and nasal discharge, lack of coordination, listlessness, difficult breathing, and corneal opacity. The inhalation effects of the nentralent on test animals were consistent with those of the t-butanol and chloroform components of the O/SS (Morgan et al., 1997). 

Immediate pain occurs upon inhalation, dermal, or ocular contact with lewisite. Skin penetration occurs within 3-5 min, especially following liquid exposures (Sidell et al, 1997). The skin becomes red, then gray, within 15-30 min after exposure (EPA, 1985a Goldman and Dacre, 1989 Sidell et al, 1997 Pohanish, 2002). Severe blisters develop within 12 h. The blisters rupture... 

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