Lewisite

Lewisite[1]
Names
IUPAC name
2-chloroethenylarsonous dichloride
Other names
2-chloroethenyldichloroarsine
2-chlorovinyldichloroarsine
Identifiers
541-25-3 Yes
ChemSpider 4522971 Yes
Jmol-3D images Image
MeSH lewisite
PubChem 5372798
Properties
C2H2AsCl3
Molar mass 207.32 g/mol
Density 1.89 g/cm3
Melting point −18 °C (0 °F; 255 K)
Boiling point 190 °C (374 °F; 463 K)
Hazards
NFPA 704
Flammability code 1: Must be pre-heated before ignition can occur. Flash point over 93 °C (200 °F). E.g., canola oil Health code 4: Very short exposure could cause death or major residual injury. E.g., VX gas Reactivity code 1: Normally stable, but can become unstable at elevated temperatures and pressures. E.g., calcium Special hazards (white): no codeNFPA 704 four-colored diamond
1
4
1
Except where noted otherwise, data is given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
 Yes verify (what is: Yes/?)
Infobox references

Lewisite is an organoarsenic compound. It was once manufactured in the U.S., Japan, and Germany[2] for use as a chemical weapon, acting as a vesicant (blister agent) and lung irritant. Although colorless and odorless, impure samples of lewisite are a yellow or brown liquid with a distinctive odor that has been described as similar to scented geraniums.[3]

Chemical reactions

The compound is prepared by the addition of arsenic trichloride to acetylene in the presence of a suitable catalyst:

AsCl3 + C2H2 → ClCHCHAsCl2

Lewisite, like other arsenous chlorides, hydrolyses in water to form hydrochloric acid:

ClCHCHAsCl2 + 2 H2O → ClCHCHAs(OH)2 + 2 HCl

This reaction is accelerated in alkaline solutions, with poisonous (but non-volatile) alkali arsenite being the coproduct.

Mode of action as chemical weapon

Arsenite inhibits important biochemical pathways of the human body. Arsenite poisoning specifically targets the E3 component of pyruvate dehydrogenase.[4] As an efficient method to produce ATP, pyruvate dehydrogenase is involved in the conversion of pyruvate to Acetyl-CoA. The latter subsequently enters the TCA cycle. Arsenite has a high affinity for dihydrolipoamide; E3 component of the pyruvate dehydrogenase. Binding results in inhibition of the enzyme and can lead to dire consequences. Nervous pathology usually arises from arsenite poisoning as the nervous system essentially relies on glucose as its only catabolic fuel.[4] There is evidence that at high concentrations other enzymes are attacked as well, but the pyruvate oxidase system is the first point of attack by arsenicals such as lewisite.[5]

It can easily penetrate ordinary clothing and even rubber; upon skin contact it causes immediate pain and itching with a rash and swelling. Large, fluid-filled blisters (similar to those caused by mustard gas exposure) develop after approximately 12 hours.[3] These are severe chemical burns. Sufficient absorption can cause systemic poisoning leading to liver necrosis or death.

Those exposed to lewisite can develop refractory hypotension known as Lewisite shock, as well as some features of arsenic toxicity.[6]

Inhalation causes a burning pain, sneezing, coughing, vomiting, and possibly pulmonary edema.[3] Ingestion results in severe pain, nausea, vomiting, and tissue damage.[3] The results of eye exposure can range from stinging and strong irritation to blistering and scarring of the cornea.[7] Generalised symptoms also include restlessness, weakness, subnormal temperature and low blood pressure.

It is possible that Lewisite may be a carcinogen since arsenic is categorized as a respiratory carcinogen by the International Agency for Research on Cancer, though it has not been confirmed that Lewisite is a carcinogen.[8]

Chemical composition

Lewisite is usually found as a mixture, of 2-chlorovinylarsonous dichloride as well as bis(2-chloroethenyl)arsinous chloride ("lewisite 2"), and tris(2-chlorovinyl)arsine ("lewisite 3").

History

Lewisite was first synthesised in 1904 by Julius Arthur Nieuwland during studies for his PhD.[9][10][11] Within his doctoral thesis he described a reaction between acetylene and arsenic trichloride, which led to the formation of lewisite.[12] Exposure to the resulting compound made Nieuwland so ill he was hospitalized for a number of days.[10]

Lewisite is named after the US chemist and soldier Winford Lee Lewis (1878–1943). In 1918 Dr John Griffin (Julius Arthur Nieuwland's thesis advisor) drew Lewis's attention to Nieuwland's thesis at Maloney Hall, a chemical laboratory at The Catholic University of America, Washington D.C..[13] Lewis then attempted to purify the compound through distillation but found that the mixture exploded on heating until it was washed with HCl.[13]

Lewisite identification poster from WW2, likening the smell of the gas to geraniums.

Lewisite was developed into a secret weapon (at a facility located in Cleveland, Ohio (The Cleveland Plant) at East 131st Street and Taft Avenue[14]) and given the name "G-34" (which had previously been the code for mustard gas) in order to confuse its development with mustard gas.[15] Production began at a plant in Willoughby, Ohio on November 1, 1918.[16] It was not used in World War I, but experimented with in the 1920s as the "Dew of Death."[17]

After World War I, the US became interested in lewisite because it was not flammable. It had the military symbol of "M1" up into World War II, when it was changed to "L". Field trials with lewisite during World War II demonstrated that casualty concentrations were not achievable under high humidity due to its rate of hydrolysis and its characteristic odor and lacrymation forced troops to don masks and avoid contaminated areas. The United States produced about 20,000 tons of lewisite, keeping it on hand primarily as an antifreeze for mustard gas or to penetrate protective clothing in special situations.

It was replaced by the mustard gas variant HT (a 60:40 mixture of sulfur mustard and O Mustard), and declared obsolete in the 1950s. It is effectively treated with British anti-lewisite (dimercaprol). Most stockpiles of lewisite were neutralised with bleach and dumped into the Gulf of Mexico,[18] but some remained at the Deseret Chemical Depot located outside of Salt Lake City, Utah , although as of January 18, 2012 the last of the global stockpile there was destroyed.

In 2001, lewisite was found in a World War I weapons dump in Washington, D.C.[19]

Controversy over Japanese depots of lewisite in China

In mid-2006, China and Japan were negotiating disposal of stocks of lewisite in northeastern China, left by Japanese military during World War II. Residents of China have died over the past twenty years from accidental exposure to these stockpiles.[20]

References

  1. ↑ Lewisite I - Compound Summary, PubChem.
  2. ↑ A drop in the ocean: the sea-dumping of chemical weapons in Okinawa | The Japan Times
  3. ↑ 3.0 3.1 3.2 3.3 U.S. National Research Council, Committee on Review and Evaluation of the Army Non-Stockpile Chemical Materiel Disposal Program (1999). Disposal of Chemical Agent Identification Sets. National Academies Press. p. 16. ISBN 0-309-06879-7.
  4. ↑ 4.0 4.1 Berg, J.; Tymoczko, J. L.; Stryer, L. (2007). Biochemistry (6th ed.). New York: Freeman. pp. 494–495. ISBN 978-0-7167-8724-2.
  5. ↑ Peters, R. A.; Sinclair, H. M.; Thompson, R. H. S. An analysis of the inhibition of pyruvate oxidation by arsenicals in relation to the enzyme theory of vesication. Biochem. J. 1946, 40, 516-524.
  6. ↑ Chauhan, S.; Chauhan, S.; D’Cruz, R.; Faruqi, S.; Singh, K. K.; Varma, S.; Singh, M.; Karthik, V. Chemical warfare agents. Environ. Toxicol. Pharmacol. 2008, 26, 113-122
  7. ↑ "Lewisite(L): Blister Agent". Emergency Response Database. CDC / NIOSH. 2008.
  8. ↑ Doi, M.; Hattori, N.; Yokoyama, A.; Onari, Y.; Kanehara, M.; Masuda, K.; Tonda, T.; Ohtaki, M.; Kohno, N. Effect of Mustard Gas Exposure on Incidence of Lung Cancer: A Longitudinal Study. American Journal of Epidemiology 2011, 173, 659-666.
  9. ↑ Julius Arthur Nieuwland (1904) "Some Reactions of Acetylene," Ph.D. thesis, University of Notre Dame (Notre Dame, Indiana).
  10. ↑ 10.0 10.1 Vilensky, J. A. (2005). Dew of Death - The Story of Lewisite, America's World War I Weapon of Mass Destruction. Indiana University Press. p. 4. ISBN 0253346126.
  11. ↑ Vilensky, J. A.; Redman, K. (2003). "British Anti-Lewisite (Dimercaprol): An Amazing History". Annals of Emergency Medicine 41 (3): 378–383. doi:10.1067/mem.2003.72. PMID 12605205.
  12. ↑ Vilensky, J. . Father Nieuwland and the 'Dew of Death'. http://magazine.nd.edu.proxy.library.nd.edu/news/14736-father-nieuwland-and-the-dew-of-death/ (accessed 07 November, 2014)
  13. ↑ 13.0 13.1 Vilensky, J. A. (2005). Dew of Death - The Story of Lewisite, America's World War I Weapon of Mass Destruction. Indiana University Press. pp. 21–23. ISBN 0253346126.
  14. ↑ Upton native's role was the best defense; WWI masks thwarted
  15. ↑ Joel A. Vilensky, Dew of Death: The Story of Lewisite, America's World War I Weapon of Mass Destruction (Bloomington, Indiana: Indiana University Press, 2005), page 36.
  16. ↑ Vilensky, J. A. (2005). Dew of Death - The Story of Lewisite, America's World War I Weapon of Mass Destruction. Indiana University Press. p. 50. ISBN 0253346126.
  17. ↑ Tabangcura, D. Jr.; Daubert, G. P. "British anti-Lewisite Development". Molecule of the Month. University of Bristol School of Chemistry.
  18. ↑ Code Red - Weapons of Mass Destruction [Online Resource] - Blister Agents
  19. ↑ Tucker, J. B. (2001). "Chemical weapons: Buried in the backyard" (PDF). Bulletin of the Atomic Scientists 57 (5): 51–56. doi:10.2968/057005014.
  20. ↑ Abandoned Chemical Weapons (ACW) in China