Lewisite development

The recent development and comparative application of modern separation techniques with regard to determination of alkylphosphonic acids and lewisite derivatives have been demonstrated. This report highlights advantages and shortcomings of GC equipped with mass spectrometry detector and HPLC as well as CE with UV-Vis detector. The comparison was made from the sampling point of view and separation/detection ability. The derivatization procedure for GC of main degradation products of nerve agents to determine in water samples was applied. Direct determination of lewisite derivatives by HPLC-UV was shown. Also optimization of indirect determination of alkylphosphonic acids in CE-UV was developed. Finally, the new instrumental development and future trends will be discussed. 

Toward the end of World War I, lewisite (C04-A002) was developed, produced, and weaponized but never used. Despite this, it has supplanted all other agents as the arsenic vesicant of choice and is the only one that was stockpiled in modern arsenals. 

Edgewood Research Development, and Engineering Center, Department of the Army. Material Safety Data Sheet (MSDS) for Lewisite (L). Aberdeen Proving Ground, MD Chemical Biological Defense Command, rev. March 27, 1996. 

In pure liquid form, lewisite causes blindness, immediate destruction of lung tissue, and systemic blood poisoning. It is absorbed through the skin like distilled mustard, but is much more toxic to the skin. Skin exposure results in immediate pain a rash forms within 30 minutes. Severe chemical burns are possible. Blistering of the skin takes up to 13 hours to develop. Lewisite does not dissolve in human sweat. It commingles with sweat, then flows to tender skin areas such as the inner arm, buttocks, and crotch. 

The largest of the branch laboratories was established at Catholic University in Washington, D.C. Its staff of about 75 carried out research on arsenic compounds and subsequently developed one of the new war gases produced by the United States during World War I, Lewisite C26). 

Dimercaprol (BAL, British Anti-Lewisite) was developed in World War 11 as an antidote against vesicant organic arsenicals (B). It is able to chelate various metal ions. Dimercaprol forms a liquid, rapidly decomposing substance that is given intramuscularly in an oily vehicle. A related compound, both in terms of structure and activity, is di-mercaptopropanesulfonic acid, whose sodium salt is suitable for oral administration. Shivering, fever, and skin reactions are potential adverse effects. 

Other organoarsenicals, most notably lewisite (dichloro[2-chlorovinyl]arsine), were developed in the early twentieth century as chemical warfare agents. Arsenic trioxide was reintroduced into the United States Pharmacopeia in 2000 as an orphan drug for the treatment of relapsed acute promyelocytic leukemia and is finding expanded use in experimental cancer treatment protocols (see Chapter 54). Melarsoprol, another trivalent arsenical, is used in the treatment of advanced African trypanosomiasis (see Chapter 52). 

Arsine Derivatives,Organic. Many arsine derivs were proposed as CWA s. More than 60 of such derivs are listed by Wachtel (Ref, pp 189-92). The most known of these compds is Lewisite or MI, which is f -cbloro-vinyldichloroarsine, C1-CH CH- AsC12, first isolated in 1917 by Dr W. Lee Lewis and developed as a war gas by the US Chemical Warfare Service (Ref, pp 202-6). Another important arsine CWA is Adamsite (Brit) (designated in the US as DM) or diphenylamine-chloroarsine ... 

The first chelating agent developed as an antidote to a heavy metal poison was 2,3-dimereaptopropanol (dimercaprol, British Anti-Lewisite, BAL). Originally intended for use on victims of the arsenical vesicant poison gas Lewisite52, it has since proved efficacious in the treatment of antimony, gold and mercury poisoning as well as... 

Another compound used to treat lead poisoning is British anti-Lewisite (BAL), originally developed to treat arsenic-containing poison gas Lewisite. As shown in Figure 10.6, BAL chelates lead through its sulfhydryl groups, and the chelate is excreted through the kidney and bile. 

The origins of chelation therapy can be traced back to the treatment of First World War soldiers who had suffered from gas attacks that used the arsenic-based toxin, Lewisite. A dithiol, British anti-Lewisite (BAL), was developed to remove the toxic metal. 

Procedures based on GC/MS for the determination of the lewisite 1 decomposition product 2-chlorovinylarsonous acid (CVAA, CAS number 85090-33-1) in urine and blood have also been developed. In one procedure, CVAA is converted with BAL the resulting CVAA/BAL product isolated by SPE on a C18-cartridge and further derivatized with heptafluorobutyryl imidazole (51). A later developed procedure is based on the derivatization of CVAA with 1,3-propanedithiol followed by SPME isolation and GC/MS analysis. Using SIM at the molecular ion peaks, the limit of detection was determined at 7.4 pg per ml urine (52). 

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