Lewisite Levels

Real-time, low-level monitors (with alarm) are required for Lewisite operations. In their absence, an Immediately Dangerous to Life and Health (IDLH) atmosphere must be presumed. Laboratory operations conducted in appropriately maintained and alarmed engineering controls require only periodic low-level monitoring. 

A special derivatization reaction is required for lewisite 1, which is so reactive that it cannot be determined by GC/MS in low quantities (e.g. below 10 ng per injection). It has been known for a long time that lewisite 1 reacts with compounds having an a, P-dithiol structure, such as 2,3-dimercaptopropanol-l (British-Anti-Lewisite (BAL) also used for medical treatment). The derivatization reaction can be performed at an analytical level and several examples have been described (29). The reaction product of lewisite 1 with 3,4-dimercaptotoluene, 2-(2-chlorovinyl)-5-methyl-l,3,2-benzodithiarsole (see (1)), is a useful derivative for GC/MS analysis. Its mass spectrum is simple with molecular ion peaks at m/z 290/292 and the base peak at m/z 229 due to the loss of the 2-chlorovinyl group (30). 

Table 2. Summary of Effect Levels for Lewisite Toxicity Studies 9...

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. ... 

In high concentrations, lewisite produees irritation and blistering of the skin and injury to the eyes and lungs promptly after exposure while, at lower levels, the effeets resemble exposure to tear gas, with irritation of skin, eyes, and respiratory traet. Chronie exposure may lead to development of chronie bronchitis and predispose to Bowen s squamous eell intraepithelial eaneer of the skin. 

Although the use of lewisite was suspected at times during the Iran-Iraq War, it was never proved present in the munitions studied (DIA, 1997 Dunn et al., 1997 UN, 1984) and no elevated levels of arsenic were found in the blood and tissues of Iranian casualties treated in Europe (Heyndrickx, 1984). There is some human exposure experience from accidental exposure to lewisite (Pechura and Rail, 1993). The levels of exposure that resulted from accidents in occupational workers are not known. 

Lewisite is reported to possess a characteristic (geraniumlike) odor in the range of 0.8 mg/m to more commonly cited 14-23 mg/m median detection (Pechura and Rail, 1993). US forces have detectors for lewisite-paper and kits (M7 and M9A). Other forensic techniques for soil and material analysis already exists (e.g. gas chromatography). In biological tissues, increased arsenic levels are a surrogate for lewisite (Haddad and Wincester, 1983). 

Immediate eye pain and blepharospasm result from lewisite exposure, followed by conjunctival and lid edema. Severe exposures can produce necrotic injuries of the iris with depigmentation, hypopion, and synechia development. In contrast, very low levels may only involve the conjunctivae (McManus and Huebner, 2005). The eye lesions produced by lewisite are particularly serious blindness will follow contamination of the eye with liquid lewisite unless decontamination is prompt. 

In acute exposure prompt medical attention is critical. The victim should be immediately removed to fresh air and away from the source of exposure. Oxygen should be provided if there is a respiratory distress. Initial therapy should be directed at stopping the ongoing hemolysis by performing exchange transfusion. Currently there is no other treatment to decrease arsine hemolysis however, studies in vitro have shown that some dithiol chelators (meso-2,3-dimercaptosuccinic acid, DMSA 2,3-dimercapto-l-propanesulfonic acid, DMPS and 2,3-butanedithiol) are effective (see Further Reading). This should be followed by aims to restore renal function or compensate for lost renal function (hemodialysis). This process does not remove any formed arsenic from the exposed body. Administration of dimercaprol (British Anti-Lewisite, BAL) has no effect on arsine hemolysis, but it lowers blood arsenic levels resulting from arsine exposure. The use of chelators must be... 

Lewisite is the only vesicant with a proven antidote—British anti-lewisite (2,3-dimercaptopropa-nol). Increasing antioxidant levels have been found to be protective against the mustards analog, NAC. NAC, which we have used in our studies with CEES, is immediately clinically available. It is most commonly used for acetaminophen overdose. NAC has a long history of several gram quantities administered in several doses and has minimal adverse reactions. In the case of acetaminophen overdose, it is administered via the oral-gastric route, which increases hepatic GSH levels, and in turn, suppresses inflammatory cytokines (Dambach et al., 2006). Liposome encapsulation of both water- and fat-soluble antioxidants was proven to be more effective in the suppression of OS than the free molecule of NAC. 

Lewisite will rapidly react with water to form chlorovinylarsonous acid (CVAA). CVAA will slowly convert to the arsinoxide form and polymerization reactions can also occur. Earlier studies indicated that animals (species not specified) exposed to lewisite either topically or via injection were found to have measurable levels of CVAA in the urine and throughout the digestive system (Waters and Williams, 1950). 

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