Ocular toxicity Lewisite

British Anti-Lewisite (BAL), also known as Dimercaprol, is a chelating agent than can reduce systemic effects from Lewisite. BAL works by binding the arsenic group in Lewisite and displacing it from tissue binding sites. If applied topically within minutes, after decontamination, BAL may prevent or reduce the severity of cutaneous and ocular toxicity (8). 

Copper toxicity has been observed, althongh it is not a function of dietary overload. Abnormally low levels of ceruloplasmin associated with the genetic disorder, Wilson s disease, lead to excessive deposition of copper in the central nervous system, ocular tissue, liver, and other organs. Severe psychotic symptoms are observed. Urinary excretion of the copper can be achieved with specific chelating agents such as British anti-lewisite (BAL, 2,3-dimercaptopropanol) or penicillamine, orally administered. Symptoms of the disease are reversed as the copper levels return to normal. Reduction of dietary copper nptake by competition with relatively high levels of oral zinc is also effective. ... 

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). 

The second exception is that while an antidote is available for systemic effects of Lewisite exposure, there are no antidotes for nitrogen mustard or sulfur mustard toxicity, with one minor caveat if given within minutes after exposure, intravenous sodium thiosulfate may prevent death due to sulfur mustard exposure (25). Otherwise, the medical management for skin, ocular, and respiratory exposure is only supportive. One guideline physicians can follow is to keep skin, eye, and airway lesions free from infection. 

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). 

Despite the twentyfold to thirtyfold increase in the toxicity of lewisite compared to the mustards, the ocular injuries caused by vapor exposure to lewisite are predicted to be less significant than HD under field conditions (Gates et al., 1946). Ocular irritation is almost immediate even at low concentrations, such that exposed personnel would be alerted to the presence of an irritant and able to rapidly take protective action. Second, the rapid onset of blepharospasm, ocular pain, and edema at low concentrations causes the eyes to close involimtarily, reducing the total ocular exposure. 

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