Lewisite absorption

Inhalation and dermal absorption mustards no antidote. For lewisite and ewisite/ mustard lmixtures British Anti-Lewisite (BAL or Dimercaprol) IM (rarely available). Thermal burn therapy supportive care (respiratory support and eye care). 

Arsenic Toxicosis. Urine arsenic is the best indicator of current or recent exposure. Atomic absorption spectrophotometry is preferred as the detection method. Hair or fingernail sampling may also be helpful. Use of blood is useful if analyzed soon after exposure or in cases of continuous chronic exposure. After acute exposure, chelation therapy is instituted utilizing either (1) Dimercaprol BAL (British Anti-Lewisite) and analogues ... 

The most generally applied method for determination of an arsenical is by atomic absorption spectrometry (AAS) after reduction of the compound to AsH3. However, this only provides an indication of the presence of the element as against a natural background. Lewisite rapidly hydrolyzes to 2-chlorovinylarsonous acid (CVAA see Figure 7) in an aqueous environment such as blood plasma, and analytical methods have focused mainly on the determination of CVAA (see Chapter 16). 

Atomic Absorption Spectrometry Acetylcholinesterase British Anti-Lewisite Carboxylesterase Central Nervous System Chemical Warfare Agent 2-chlorovinylarsonous Acid Enzyme-linked Immunosorbent Assay Environmental Protection Agency... 

Althongh no data on its fate in the atmosphere are available, UV absorption spectrum of lewisite at 200 to 350 nm indicates that some photodegradation may take place. Rapid hydrolysis may occur in the gas phase (MacNanghton and Brewer, 1994). 

Little information is available regarding the toxieokineties of lewisite. Lewisite is readily absorbed by mueous membranes and, beeause of its lipophilicity, dermal absorption is signitieant (HSDB, 2004). Dermal absorption is reportedly more rapid than for sulfur mustard (Hurst and Smith, 2008). Axehod and Hamilton (1947) reported that radiolabeled ( " As) lewisite applied to a 0.4S em area of human skin was primarily fixed on the epidermis and that very little was found in the dermis most was detected in hair and hair follicles. In experiments with guinea pigs, histological examination revealed that lewisite applied to skin entered epidermis within 2 min and penetrated into the dermis within 10 min (Ferguson and Silver, 1947). Only trace amounts were detectable in the dermis at 24 h post-application. 

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). 

Precise data, i.e. a diffusion coefficient expressing the p.c. absorption of lewisite (amount absorbed per area and time), are not available. However, Inns and Rice (1993) conducted p.c. toxicity studies in rabbits and determined the LD50 at 5.3mg/kg (3.5-8.5 mg/kg, 95% confidence interval). The exposed area was 2 cm and exposure lasted for 6 h. 

Lewisite, a vesicant with HD-Uke properties, causes a similar constellation of signs and symptoms involving the skin, eyes, and airways as well as systemic effects (e.g. increased capillary permeability) after absorption. However, it does not produce immunological suppression like mustard. Another difference is that the management of lewisite toxicity includes an antidote, British Anti-Lewisite (BAL) (Yue/u/.,2003). 

Lewisite is readily absorbed from the skin, eyes, and respiratory tract, as well as after ingestion and through wounds. It causes blistering on the skin and mucous membranes on contact. After absorption, it causes an increase in capillary permeability, which produces hypovolemia, shock, and organ damage. Unlike the mustard agents, lewisite vapor or liquid causes immediate pain or irritation although lesions require up to 12 h to become full-blown cases. 

Lewisite damages skin, eyes, and airways by direct contact and has systemic effects after absorption. Unlike mustard, it does not produce immunosuppression. Data on human exposure are few. Lewisite was applied to human skin in a few studies however, most information on its clinical effects is based on animal studies (Rovida and Lewisite 1929 Wardell, 1940 Dailey et al., 1941 Buscher and Conway, 1944). 

Table 1. The main absorption bands (v, cm1) in IR spectra of mustard gas and lewisite carbon tetrachloride was used as a solvent... 

IR spectrum of triple mixture containing 1,2-dichloroethane as an additive apart from mustard gas and lewisite is presented on Fig.5. Judging from the fact that the bands at 1378 and 1010 cm 1 have relatively low intensity the sample contains lower quantity of mixed type of mustard gas in a comparison with usual one (absorption in the range of 1440-1400 cm"1 and at the band of about 1200 cm1). a-Lewisite shows up the strong bands at 933 and 1554 cm1. The last one has undoubtedly asymmetric form as it was for mustard gas-lewisite mixture what indicates the presence of P-lewisite in the sample. 

With a vapor pressure of 0.58 mmHg at 25°C, lewisite is considered non-volatile. However, it is more volatile than HD and may be used as a moderate irritant vapor over greater distances than HD (Watson and Griffin, 1992). Based on its UV absorption band (Rewick et al., 1986), some photodegradation may take place in the atmosphere. Hydrolysis may also occur in the gas phase (MacNaughton and Brewer, 1994). 

It has been said that absorption of lewisite in food would be expected to give rise to the... 

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. 

Lewisite damages skin, eyes, and airways by direct contact and has systemic effects after absorption. Unlike mustard, it does not produce immuno-... 

The Merck Index, an annual encyclopedia of chemicals and drugs, states for Lewisite Caution Extremely toxic Produces severe vesication, even through rubber. If left on skin, as little as 0.5 ml may give rise to sufficient absorption to produce severe systemic effects 2 ml may cause death. (Similar warnings do not accompany the other war gases.)... 

HL Mustard-lewisite mixture -14 2 730 200 (eye injury) 1500-2000 (skin absorption)... 

Although Lewisite has been sporadically used in the past, very little data from human exposure exist at this time. Consequently, much of what we know in the West about Lewisite s effects mostly comes from animal experimentation. Older data from the 1930s includes observing the effects of Lewisite on a human volunteer In this case. Lewisite was completely absorbed in 5 minutes with a slight burning sensation, while mustard required from 20 to 30 minutes for absorption and produced no noticeable sensation. With Lewisite, the skin commences to redden at the end of 30 minutes then the erythema increases and spreads rapidly. It occupies a surface of 12 by 15 centimeters toward the end of the third hour.22... 

---