Lewisite

Lewisite[1]
IUPAC name 2-chloroethenylarsonous dichloride
Other names 2-chloroethenyldichloroarsine 2-chlorovinyldichloroarsine
Identifiers
CAS number	541-25-3 Y
PubChem	5372798
ChemSpider	4522971 Y
MeSH	lewisite
Jmol-3D images	{{#if:Cl[As](Cl)\C=C\Cl|Image 1
SMILES Cl[As](Cl)\C=C\Cl
InChI InChI=1S/C2H2AsCl3/c4-2-1-3(5)6/h1-2H/b2-1+ Y Key: GIKLTQKNOXNBNY-OWOJBTEDSA-N Y InChI=1/C2H2AsCl3/c4-2-1-3(5)6/h1-2H/b2-1+ Key: GIKLTQKNOXNBNY-OWOJBTEDBF
Properties
Molecular formula	C2H2AsCl3
Molar mass	207.32 g/mol
Density	1.89 g/cm3
Melting point	–18 °C
Boiling point	190 °C
Hazards
NFPA 704	1 4 1
Y (verify) (what is: Y/N?) Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
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) sodium 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]

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.

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.^[5] Generalised symptoms also include restlessness, weakness, subnormal temperature and low blood pressure.

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.^[6][7][8] His method involved reacting acetylene with arsenic trichloride in the presence of an aluminium chloride catalyst .^[7] Exposure to the resulting compound made Nieuwland so ill he was hospitalized for a number of days.^[7]

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..^[9] Lewis then attempted to purify the compound through distillation but found that the mixture exploded on heating until it was washed with HCl.^[9]

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^[10]) and given the name "G-34" (which had previously been the code for mustard gas) in order to confuse its development with mustard gas.^[11] Production began at a plant in Willoughby, Ohio on November 1, 1918.^[12] It was not used in World War I, but experimented with in the 1920s as the "Dew of Death."^[13]

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 charactistic odor and lacrymation forced troops to don masks and avoid contaminated areas.^{[citation needed]} 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,^[14] 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.^[15]

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.^[16]

References