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Mustard gas
Names
Preferred IUPAC name
1-Chloro-2-[(2-chloroethyl)sulfanyl]ethane
Other names
Bis(2-chloroethyl) sulfide
HD
Iprit
Schwefel-LOST
Lost
Sulfur mustard
Senfgas
Yellow cross liquid
Yperite
Distilled mustard
Mustard T- mixture
1,1'-thiobis[2-chloroethane]
Dichlorodiethyl sulfide
Identifiers
3D model (JSmol)
1733595
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.209.973 Edit this at Wikidata
EC Number
  • 684-527-7
324535
KEGG
UNII
  • InChI=1S/C4H8Cl2S/c5-1-3-7-4-2-6/h1-4H2 checkY
    Key: QKSKPIVNLNLAAV-UHFFFAOYSA-N checkY
  • InChI=1/C4H8Cl2S/c5-1-3-7-4-2-6/h1-4H2
    Key: QKSKPIVNLNLAAV-UHFFFAOYAK
  • ClCCSCCCl
Properties
C4H8Cl2S
Molar mass 159.07 g·mol−1
Appearance Colorless if pure. Normally ranges from pale yellow to dark brown. Slight garlic or horseradish type odor.[1]
Density 1.27 g/mL, liquid
Melting point 14.45 °C (58.01 °F; 287.60 K)
Boiling point 217 °C (423 °F; 490 K) begins to decompose at 217 °C (423 °F) and boils at 218 °C (424 °F)
7.6 mg/L at 20°C[2]
Solubility Alcohols, ethers, hydrocarbons, lipids, THF
Hazards
Occupational safety and health (OHS/OSH):
Main hazards
 Flammable, toxic, vesicant, carcinogenic, mutagenic
GHS labelling:[3]
GHS06: Toxic
Danger
H300, H310, H315, H319, H330, H335
P260, P261, P262, P264, P270, P271, P280, P284, P301+P310, P302+P350, P302+P352, P304+P340, P305+P351+P338, P310, P312, P320, P321, P322, P330, P332+P313, P337+P313, P361, P362, P363, P403+P233, P405, P501
NFPA 704 (fire diamond)
NFPA 704 four-colored diamondHealth 4: Very short exposure could cause death or major residual injury. E.g. VX gasFlammability 1: Must be pre-heated before ignition can occur. Flash point over 93 °C (200 °F). E.g. canola oilInstability 1: Normally stable, but can become unstable at elevated temperatures and pressures. E.g. calciumSpecial hazards (white): no code
4
1
1
Flash point 105 °C (221 °F; 378 K)
Safety data sheet (SDS) External MSDS
Related compounds
Related compounds
 Nitrogen mustard, Bis(chloroethyl) ether, Chloromethyl methyl sulfide
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Mustard gas or sulfur mustard are names commonly used for the organosulfur chemical compound bis(2-chloroethyl) sulfide, which has the chemical structure S(CH2CH2Cl)2, as well as other species. In the wider sense, compounds with the substituents −SCH2CH2X or −N(CH2CH2X)2 are known as sulfur mustards or nitrogen mustards, respectively, where X = Cl or Br. Such compounds are potent alkylating agents, making mustard gas acutely and severely toxic.[3] Mustard gas is a carcinogen.[3] There is no preventative agent against mustard gas, with protection depending entirely on skin and airways protection, and no antidote exists for mustard poisoning.[4]

Also known as mustard agents, this family of compounds comprises infamous cytotoxins and blister agents with a long history of use as chemical weapons.[4] The name mustard gas is technically incorrect; the substances, when dispersed, are often not gases but a fine mist of liquid droplets that can be readily absorbed through the skin and by inhalation.[3] The skin can be affected by contact with either the liquid or vapor. The rate of penetration into skin is proportional to dose, temperature and humidity.[3]

Sulfur mustards are viscous liquids at room temperature and have an odor resembling mustard plants, garlic, or horseradish, hence the name.[3][4] When pure, they are colorless, but when used in impure forms, such as in warfare, they are usually yellow-brown. Mustard gases form blisters on exposed skin and in the lungs, often resulting in prolonged illness ending in death.[4]

Etymology

[edit]

The name of mustard gas derived from its yellow color, smell of mustard, and burning sensation on eyes.[5] The term was first used in 1917 during World War I when Germans used the poison in combat.[5]

History as chemical weapons

[edit]

Sulfur mustard is a type of chemical warfare agent.[6] As a chemical weapon, mustard gas has been used in several armed conflicts since World War I, including the Iran–Iraq War, resulting in more than 100,000 casualties.[7][8] Sulfur-based and nitrogen-based mustard agents are regulated under Schedule 1 of the 1993 Chemical Weapons Convention, as substances with few uses other than in chemical warfare.[4][9] Mustard agents can be deployed by means of artillery shells, aerial bombs, rockets, or by spraying from aircraft.

Adverse health effects

[edit]
Soldier with moderate mustard agent burns sustained during World War I showing characteristic bullae on the neck, armpit, and hands

Mustard gases have powerful blistering effects on victims. They are also carcinogenic and mutagenic alkylating agents.[3] Their high lipophilicity accelerates their absorption into the body.[2] Because mustard agents often do not elicit immediate symptoms, contaminated areas may appear normal.[4] Within 24 hours of exposure, victims experience intense itching and skin irritation. If this irritation goes untreated, blisters filled with pus can form wherever the agent contacted the skin.[4] As chemical burns, these are severely debilitating.[3] Mustard gas can have the effect of turning a patient's skin different colors due to melanogenesis.[10][4]

If the victim's eyes were exposed, then they become sore, starting with conjunctivitis (also known as pink eye), after which the eyelids swell, resulting in temporary blindness. Extreme ocular exposure to mustard gas vapors may result in corneal ulceration, anterior chamber scarring, and neovascularization.[11][12][13][14] In these severe and infrequent cases, corneal transplantation has been used as a treatment.[15] Miosis, when the pupil constricts more than usual, may also occur, which may be the result of the cholinomimetic activity of mustard.[16] If inhaled in high concentrations, mustard agents cause bleeding and blistering within the respiratory system, damaging mucous membranes and causing pulmonary edema.[4] Depending on the level of contamination, mustard agent burns can vary between first and second degree burns. They can also be as severe, disfiguring, and dangerous as third degree burns. Some 80% of sulfur mustard in contact with the skin evaporates, while 10% stays in the skin and 10% is absorbed and circulated in the blood.[3]

The carcinogenic and mutagenic effects of exposure to mustard gas increase the risk of developing cancer later in life.[3] In a study of patients 25 years after wartime exposure to chemical weaponry, c-DNA microarray profiling indicated that 122 genes were significantly mutated in the lungs and airways of mustard gas victims. Those genes all correspond to functions commonly affected by mustard gas exposure, including apoptosis, inflammation, and stress responses.[17] The long-term ocular complications include burning, tearing, itching, photophobia, presbyopia, pain, and foreign-body sensations.[4][18][19]

Typical appearance of bullae on an arm caused by vesicant burns

Medical management

[edit]

In a rinse-wipe-rinse sequence, skin is decontaminated of mustard gas by washing with liquid soap and water, or an absorbent powder.[4] The eyes should be thoroughly rinsed using saline or clean water. A topical analgesic is used to relieve skin pain during decontamination.[4] For skin lesions, topical treatments, such as calamine lotion, steroids, and oral antihistamines are used to relieve itching.[4] Larger blisters are irrigated repeatedly with saline or soapy water, then treated with an antibiotic and petroleum gauze.[4]

Mustard agent burns do not heal quickly and (as with other types of burns) present a risk of sepsis caused by pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa. The mechanisms behind mustard gas's effect on endothelial cells are still being studied, but recent studies have shown that high levels of exposure can induce high rates of both necrosis and apoptosis. In vitro tests have shown that at low concentrations of mustard gas, where apoptosis is the predominant result of exposure, pretreatment with 50 mM N-acetyl-L-cysteine (NAC) was able to decrease the rate of apoptosis. NAC protects actin filaments from reorganization by mustard gas, demonstrating that actin filaments play a large role in the severe burns observed in victims.[20]

A British nurse treating soldiers with mustard agent burns during World War I commented:[21]

They cannot be bandaged or touched. We cover them with a tent of propped-up sheets. Gas burns must be agonizing because usually the other cases do not complain, even with the worst wounds, but gas cases are invariably beyond endurance and they cannot help crying out.

Mechanism of cellular toxicity

[edit]
Mustard gas alkylating an amino group via conversion to a sulfonium ion (2-chloroethylthiiranium)

Sulfur mustards readily eliminate chloride ions by intramolecular nucleophilic substitution to form cyclic sulfonium ions. These very reactive intermediates tend to permanently alkylate nucleotides in DNA strands, which can prevent cellular division, leading to programmed cell death.[2] Alternatively, if cell death is not immediate, the damaged DNA can lead to the development of cancer.[2] Oxidative stress is another pathology involved in mustard gas toxicity.[22]

Various compounds with the structural subgroup BC2H4X, where X is any leaving group and B is a Lewis base, have a common name of mustard. Such compounds can form cyclic "onium" ions (sulfonium, ammonium, etc.) that are good alkylating agents. These compounds include bis(2-haloethyl)ethers (oxygen mustards), the (2-haloethyl)amines (nitrogen mustards), and sesquimustard, which has two α-chloroethyl thioether groups (ClC2H4S−) connected by an ethylene bridge (−C2H4−). These compounds have a similar ability to alkylate DNA, but their physical properties vary.

Formulations

[edit]
Lewisite (top row) and mustard gas (bottom row) test with concentrations from 0.01% to 0.06%

In its history, various types and mixtures of mustard gas have been employed. These include:

  • H – Also known as HS ("Hun Stuff") or Levinstein mustard. This is named after the inventor of the "quick but dirty" Levinstein Process for manufacture,[23][24] reacting dry ethylene with disulfur dichloride under controlled conditions. Undistilled mustard gas contains 20–30% impurities, which means it does not store as well as HD. Also, as it decomposes, it increases in vapor pressure, making the munition it is contained in likely to split, especially along a seam, releasing the agent to the atmosphere.[1]
  • HD – Codenamed Pyro by the British, and Distilled Mustard by the US.[1] Distilled mustard of 95% or higher purity. The term "mustard gas" usually refers to this variety of mustard.
  • HT – Codenamed Runcol by the British, and Mustard T- mixture by the US.[1] A mixture of 60% HD mustard and 40% O-mustard, a related vesicant with lower freezing point, lower volatility and similar vesicant characteristics.
  • HL – A blend of distilled mustard (HD) and lewisite (L), originally intended for use in winter conditions due to its lower freezing point compared to the pure substances. The lewisite component of HL was used as a form of antifreeze.[25]
  • HQ – A blend of distilled mustard (HD) and sesquimustard (Q).[26]
  • Yellow Cross – any of several blends containing sulfur mustard.[27] Named for the yellow cross painted on artillery shells.[10]

Commonly-stockpiled mustard agents (class)

[edit]
Chemical Code Trivial name CAS number PubChem Structure
Bis(2-chloroethyl)sulfide H, HD Mustard 505-60-2 CID 10461 from PubChem
1,2-Bis(2-chloroethylsulfanyl) ethane Q Sesquimustard 3563-36-8 CID 19092 from PubChem
2-Chloroethyl ethyl sulfide Half mustard 693-07-2 CID 12733 from PubChem
Bis(2-(2-chloroethylsulfanyl)ethyl) ether T O-mustard 63918-89-8 CID 45452 from PubChem
2-Chloroethyl chloromethyl sulfide 2625-76-5
Bis(2-chloroethylsulfanyl) methane HK 63869-13-6
1,3-Bis(2-chloroethylsulfanyl) propane 63905-10-2
1,4-Bis(2-chloroethylsulfanyl) butane 142868-93-7
1,5-Bis(2-chloroethylsulfanyl) pentane 142868-94-8
Bis((2-chloroethylsulfanyl)methyl) ether 63918-90-1

History

[edit]

Development

[edit]

Mustard gases were possibly developed as early as 1822 by César-Mansuète Despretz (1798–1863).[28] Despretz described the reaction of sulfur dichloride and ethylene but never made mention of any irritating properties of the reaction product. In 1854, another French chemist, Alfred Riche (1829–1908), repeated this procedure, also without describing any adverse physiological properties. In 1860, the British scientist Frederick Guthrie synthesized and characterized the mustard agent compound and noted its irritating properties, especially in tasting.[29] Also in 1860, chemist Albert Niemann, known as a pioneer in cocaine chemistry, repeated the reaction, and recorded blister-forming properties. In 1886, Viktor Meyer published a paper describing a synthesis that produced good yields. He combined 2-chloroethanol with aqueous potassium sulfide, and then treated the resulting thiodiglycol with phosphorus trichloride. The purity of this compound was much higher and consequently the adverse health effects upon exposure were much more severe. These symptoms presented themselves in his assistant, and in order to rule out the possibility that his assistant was suffering from a mental illness (psychosomatic symptoms), Meyer had this compound tested on laboratory rabbits, most of which died. In 1913, the English chemist Hans Thacher Clarke (known for the Eschweiler-Clarke reaction) replaced the phosphorus trichloride with hydrochloric acid in Meyer's formulation while working with Emil Fischer in Berlin. Clarke was hospitalized for two months for burns after one of his flasks broke. According to Meyer, Fischer's report on this accident to the German Chemical Society sent the German Empire on the road to chemical weapons.[30]

The German Empire during World War I relied on the Meyer-Clarke method because 2-chloroethanol was readily available from the German dye industry of that time.[31]

Use

[edit]
Pallets of 155 mm artillery shells containing "HD" (distilled mustard gas agent) at the Pueblo Chemical Depot. The distinctive color-coding scheme on each shell is visible.

Mustard gas was first used in World War I by the German army against British and Canadian soldiers near Ypres, Belgium, on July 12, 1917,[32] and later also against the French Second Army. Yperite is "a name used by the French, because the compound was first used at Ypres."[33] The Allies used mustard gas for the first time on November 1917 at Cambrai, France, after the armies had captured a stockpile of German mustard shells. It took the British more than a year to develop their own mustard agent weapon, with production of the chemicals centred on Avonmouth Docks (the only option available to the British was the Despretz–Niemann–Guthrie process).[34][35]

Mustard gas was originally assigned the name LOST, after the scientists Wilhelm Lommel and Wilhelm Steinkopf, who developed a method of large-scale production for the Imperial German Army in 1916.[36]

Mustard gas was dispersed as an aerosol in a mixture with other chemicals, giving it a yellow-brown color. Mustard agent has also been dispersed in such munitions as aerial bombs, land mines, mortar rounds, artillery shells, and rockets.[1] Exposure to mustard agent was lethal in about 1% of cases. Its effectiveness was as an incapacitating agent. The early countermeasures against mustard agent were relatively ineffective, since a soldier wearing a gas mask was not protected against absorbing it through his skin and being blistered. A common countermeasure was using a urine-soaked mask or facecloth to prevent or reduce injury, a readily available remedy attested by soldiers in documentaries (e.g., They Shall Not Grow Old in 2018) and others (such as forward aid nurses) interviewed between 1947 and 1981 by the British Broadcasting Corporation for various World War One history programs; however, the effectiveness of this measure is unclear.

Mustard gas can remain in the ground for weeks, and it continues to cause ill effects. If mustard agent contaminates one's clothing and equipment while cold, then other people with whom they share an enclosed space could become poisoned as contaminated items warm up enough material to become an airborne toxic agent. An example of this was depicted in a British and Canadian documentary about life in the trenches, particularly once the "sousterrain" (subways and berthing areas underground) were completed in Belgium and France. Towards the end of World War I, mustard agent was used in high concentrations as an area-denial weapon that forced troops to abandon heavily contaminated areas.

US Army World War II gas identification poster, c. 1941–1945

Since World War I, mustard gas has been used in several wars and other conflicts, usually against people who cannot retaliate in kind:[37]

The use of toxic gases or other chemicals, including mustard gas, during warfare is known as chemical warfare, and this kind of warfare was prohibited by the Geneva Protocol of 1925, and also by the later Chemical Weapons Convention of 1993. The latter agreement also prohibits the development, production, stockpiling, and sale of such weapons.

In September 2012, a US official stated that the rebel militant group ISIS was manufacturing and using mustard gas in Syria and Iraq, which was allegedly confirmed by the group's head of chemical weapons development, Sleiman Daoud al-Afari, who has since been captured.[53][54]

Development of the first chemotherapy drug

[edit]

As early as 1919 it was known that mustard agent was a suppressor of hematopoiesis.[55] In addition, autopsies performed on 75 soldiers who had died of mustard agent during World War I were done by researchers from the University of Pennsylvania who reported decreased counts of white blood cells.[45] This led the American Office of Scientific Research and Development (OSRD) to finance the biology and chemistry departments at Yale University to conduct research on the use of chemical warfare during World War II.[45][56]

As a part of this effort, the group investigated nitrogen mustard as a therapy for Hodgkin's lymphoma and other types of lymphoma and leukemia, and this compound was tried out on its first human patient in December 1942. The results of this study were not published until 1946, when they were declassified.[56] In a parallel track, after the air raid on Bari in December 1943, the doctors of the U.S. Army noted that white blood cell counts were reduced in their patients. Some years after World War II was over, the incident in Bari and the work of the Yale University group with nitrogen mustard converged, and this prompted a search for other similar chemical compounds. Due to its use in previous studies, the nitrogen mustard called "HN2" became the first cancer chemotherapy drug, chlormethine (also known as mechlorethamine, mustine) to be used. Chlormethine and other mustard gas molecules are still used to this day as an chemotherapy agent albeit they have largely been replaced with more safe chemotherapy drugs like cisplatin and carboplatin.[57]

Disposal

[edit]

In the United States, storage and incineration of mustard gas and other chemical weapons were carried out by the U.S. Army Chemical Materials Agency.[58] Disposal projects at the two remaining American chemical weapons sites were carried out near Richmond, Kentucky, and Pueblo, Colorado. The last of the declared mustard weapons stockpile of the United States was destroyed on June 22, 2023 in Pueblo with other remaining chemical weapons being destroyed later in 2023.[59]

New detection techniques are being developed in order to detect the presence of mustard gas and its metabolites. The technology is portable and detects small quantities of the hazardous waste and its oxidized products, which are notorious for harming unsuspecting civilians. The immunochromatographic assay would eliminate the need for expensive, time-consuming lab tests and enable easy-to-read tests to protect civilians from sulfur-mustard dumping sites.[60]

In 1946, 10,000 drums of mustard gas (2,800 tonnes) stored at the production facility of Stormont Chemicals in Cornwall, Ontario, Canada, were loaded onto 187 boxcars for the 900 miles (1,400 km) journey to be buried at sea on board a 400 foot (120 m) long barge 40 miles (64 km) south of Sable Island, southeast of Halifax, at a depth of 600 fathoms (1,100 m). The dump location is 42 degrees, 50 minutes north by 60 degrees, 12 minutes west.[61]

A large British stockpile of old mustard agent that had been made and stored since World War I at M. S. Factory, Valley near Rhydymwyn in Flintshire, Wales, was destroyed in 1958.[62]

Most of the mustard gas found in Germany after World War II was dumped into the Baltic Sea. Between 1966 and 2002, fishermen have found about 700 chemical weapons in the region of Bornholm, most of which contain mustard gas. One of the more frequently dumped weapons was "Sprühbüchse 37" (SprüBü37, Spray Can 37, 1937 being the year of its fielding with the German Army). These weapons contain mustard gas mixed with a thickener, which gives it a tar-like viscosity. When the content of the SprüBü37 comes in contact with water, only the mustard gas in the outer layers of the lumps of viscous mustard hydrolyzes, leaving behind amber-colored residues that still contain most of the active mustard gas. On mechanically breaking these lumps (e.g., with the drag board of a fishing net or by the human hand) the enclosed mustard gas is still as active as it had been at the time the weapon was dumped. These lumps, when washed ashore, can be mistaken for amber, which can lead to severe health problems. Artillery shells containing mustard gas and other toxic ammunition from World War I (as well as conventional explosives) can still be found in France and Belgium. These were formerly disposed of by explosion undersea, but since the current environmental regulations prohibit this, the French government is building an automated factory to dispose of the accumulation of chemical shells.

In 1972, the U.S. Congress banned the practice of disposing of chemical weapons into the ocean by the United States. 29,000 tons of nerve and mustard agents had already been dumped into the ocean off the United States by the U.S. Army. According to a report created in 1998 by William Brankowitz, a deputy project manager in the U.S. Army Chemical Materials Agency, the army created at least 26 chemical weapons dumping sites in the ocean offshore from at least 11 states on both the East Coast and the West Coast (in Operation CHASE, Operation Geranium, etc.). In addition, due to poor recordkeeping, about one-half of the sites have only their rough locations known.[63]

In June 1997, India declared its stock of chemical weapons of 1,044 tonnes (1,151 short tons) of mustard gas.[64][65] By the end of 2006, India had destroyed more than 75 percent of its chemical weapons/material stockpile and was granted extension for destroying the remaining stocks by April 2009 and was expected to achieve 100 percent destruction within that time frame.[64] India informed the United Nations in May 2009 that it had destroyed its stockpile of chemical weapons in compliance with the international Chemical Weapons Convention. With this India has become the third country after South Korea and Albania to do so.[66][67] This was cross-checked by inspectors of the United Nations.

Producing or stockpiling mustard gas is prohibited by the Chemical Weapons Convention. When the convention entered force in 1997, the parties declared worldwide stockpiles of 17,440 tonnes of mustard gas. As of December 2015, 86% of these stockpiles had been destroyed.[68]

A significant portion of the United States' mustard agent stockpile was stored at the Edgewood Area of Aberdeen Proving Ground in Maryland. Approximately 1,621 tons of mustard agents were stored in one-ton containers on the base under heavy guard. A chemical neutralization plant was built on the proving ground and neutralized the last of this stockpile in February 2005. This stockpile had priority because of the potential for quick reduction of risk to the community. The nearest schools were fitted with overpressurization machinery to protect the students and faculty in the event of a catastrophic explosion and fire at the site. These projects, as well as planning, equipment, and training assistance, were provided to the surrounding community as a part of the Chemical Stockpile Emergency Preparedness Program (CSEPP), a joint program of the Army and the Federal Emergency Management Agency (FEMA).[69] Unexploded shells containing mustard gases and other chemical agents are still present in several test ranges in proximity to schools in the Edgewood area, but the smaller amounts of poison gas (4 to 14 pounds (1.8 to 6.4 kg)) present considerably lower risks. These remnants are being detected and excavated systematically for disposal. The U.S. Army Chemical Materials Agency oversaw disposal of several other chemical weapons stockpiles located across the United States in compliance with international chemical weapons treaties. These include the complete incineration of the chemical weapons stockpiled in Alabama, Arkansas, Indiana, and Oregon. Earlier, this agency had also completed destruction of the chemical weapons stockpile located on Johnston Atoll located south of Hawaii in the Pacific Ocean.[70] The largest mustard agent stockpile, at approximately 6,200 short tons, was stored at the Deseret Chemical Depot in northern Utah. The incineration of this stockpile began in 2006. In May 2011, the last of the mustard agents in the stockpile were incinerated at the Deseret Chemical Depot, and the last artillery shells containing mustard gas were incinerated in January 2012.

In 2008, many empty aerial bombs that contained mustard gas were found in an excavation at the Marrangaroo Army Base just west of Sydney, Australia.[71][72] In 2009, a mining survey near Chinchilla, Queensland, uncovered 144 105-millimeter howitzer shells, some containing "Mustard H", that had been buried by the U.S. Army during World War II.[72][73]

In 2014, a collection of 200 bombs was found near the Flemish villages of Passendale and Moorslede. The majority of the bombs were filled with mustard agents. The bombs were left over from the German army and were meant to be used in the Battle of Passchendaele in World War I. It was the largest collection of chemical weapons ever found in Belgium.[74]

A large amount of chemical weapons, including mustard gas, was found in a neighborhood of Washington, D.C. The cleanup was completed in 2021.[75]

Post-war accidental exposure

[edit]

In 2002, an archaeologist at the Presidio Trust archaeology lab in San Francisco was exposed to mustard gas, which had been dug up at the Presidio of San Francisco, a former military base.[76]

In 2010, a clamming boat pulled up some old artillery shells of World War I from the Atlantic Ocean south of Long Island, New York. Multiple fishermen suffered from blistering and respiratory irritation severe enough to require hospitalization.[77]

WWII-era tests on men

[edit]
Mustard gas test subjects enter gas chamber in Edgewood Arsenal, March 1945.

From 1943 to 1944, mustard agent experiments were performed on Australian service volunteers in tropical Queensland, Australia, by Royal Australian Engineers, British Army and American experimenters, resulting in some severe injuries. One test site, the Brook Islands National Park, was chosen to simulate Pacific islands held by the Imperial Japanese Army.[78][79] These experiments were the subject of the documentary film Keen as Mustard.[80]

The United States tested sulfur mustards and other chemical agents including nitrogen mustards and lewisite on up to 60,000 servicemen during and after WWII. The experiments were classified secret and as with Agent Orange[broken anchor], claims for medical care and compensation were routinely denied, even after the WWII-era tests were declassified in 1993. The Department of Veterans Affairs stated that it would contact 4,000 surviving test subjects but failed to do so, eventually only contacting 600. Skin cancer, severe eczema, leukemia, and chronic breathing problems plagued the test subjects, some of whom were as young as 19 at the time of the tests, until their deaths, but even those who had previously filed claims with the VA went without compensation.[81]

Arms of four test subjects after exposure to nitrogen mustard and lewisite agents

African American servicemen were tested alongside white men in separate trials to determine whether their skin color would afford them a degree of immunity to the agents, and Nisei servicemen, some of whom had joined after their release from Japanese American Internment Camps were tested to determine susceptibility of Japanese military personnel to these agents. These tests also included Puerto Rican subjects.[82]

Detection in biological fluids

[edit]

Concentrations of thiodiglycol in urine have been used to confirm a diagnosis of chemical poisoning in hospitalized victims. The presence in urine of 1,1'-sulfonylbismethylthioethane (SBMTE), a conjugation product with glutathione, is considered a more specific marker, since this metabolite is not found in specimens from unexposed persons. In one case, intact mustard gas was detected in postmortem fluids and tissues of a man who died one week post-exposure.[83]

See also

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References

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Further reading

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Mustard gas

View on Grokipedia
from Grokipedia
Mustard gas, chemically bis(2-chloroethyl) sulfide and commonly termed sulfur mustard, is a synthetic vesicant and alkylating agent deployed as a chemical warfare substance, characterized by its amber-colored oily liquid form with a garlic- or mustard-like odor that persists in the environment for days to weeks. First introduced by German forces on July 12, 1917, near Ypres, Belgium, during World War I, it inflicted widespread incapacitation through delayed-onset effects including severe skin blistering, ocular inflammation leading to temporary blindness, and pulmonary damage, rather than immediate lethality, with a fatality rate typically under 5%. Its mechanism involves alkylation of DNA guanine residues and sulfhydryl groups in proteins, disrupting cellular function and triggering inflammation and tissue necrosis hours to days post-exposure. Despite its devastating impact—contributing to over 90,000 chemical fatalities and more than one million casualties across all gases in —mustard gas's low volatility and environmental persistence made it effective for contaminating terrain and denying areas to adversaries, influencing tactics until protective measures like gas masks and timely decontamination mitigated its battlefield utility. The 1925 prohibited its use in warfare, though production and stockpiling continued, with subsequent deployments in conflicts including the Italo-Ethiopian War and the Iran-Iraq War, underscoring its enduring role as a prohibited yet sporadically employed weapon. Long-term exposure consequences, evidenced in veteran cohorts, include chronic respiratory diseases, skin cancers, and genetic damage, affirming its classification as a potent by agencies like the International Agency for Research on Cancer.

Chemical Properties and Synthesis

Molecular Structure and Formula

Sulfur mustard, commonly known as mustard gas, has the molecular formula C₄H₈Cl₂S. This corresponds to a molecular weight of 159.08 g/mol. The compound is an organosulfur molecule classified as a thioether, featuring a central sulfur atom covalently bonded to two 2-chloroethyl groups. The IUPAC name for sulfur mustard is 1-chloro-2-(2-chloroethylsulfanyl)ethane, though it is more commonly referred to by its systematic synonym bis(2-chloroethyl) sulfide. In structural terms, the molecule can be represented as Cl-CH₂-CH₂-S-CH₂-CH₂-Cl, where the sulfur atom serves as the linking bridge between the two chlorinated alkyl chains. This configuration imparts lipophilic properties, contributing to its persistence and ability to penetrate biological barriers. The highlights the tetrahedral geometry around the atom, with bond angles approximating 109 degrees due to the presence of lone pairs on . In depictions, the atoms terminate the ethyl chains, emphasizing the symmetric nature of the molecule. mustard exists primarily in its undissociated form under standard conditions, with no significant ionization due to the absence of acidic protons.

Physical and Chemical Characteristics

Sulfur mustard, with the chemical formula C₄H₈Cl₂S and systematic name bis(2-chloroethyl) sulfide, is a viscous oily liquid at ambient temperatures, exhibiting low volatility due to its vapor pressure of approximately 0.1 mmHg at 25 °C. It appears as a clear to pale yellow or amber-colored substance, though impure forms may darken to black, and possesses a molecular weight of 159.08 g/mol. The compound emits a faint odor reminiscent of garlic, mustard, or horseradish, with an air odor threshold of 0.6 mg/m³.
PropertyValueConditions/Source
Melting point13–14 °C
217.5 °C
1.2685–1.338 g/cm³13–25 °C
Water solubility0.684–0.92 g/L22–25 °C
0.082–0.106 mmHg22–25 °C
Sulfur mustard demonstrates high solubility in organic solvents such as alcohol, , acetone, , and fats, but limited in , contributing to its lipophilic nature and environmental persistence. Chemically stable at for weeks, it hydrolyzes slowly in aqueous environments to yield and , while reacting with or steam to generate toxic and fumes. It exhibits reactivity with strong oxidants, potentially leading to violent reactions, and decomposes upon heating to 149–177 °C, releasing highly toxic gases. As an alkylating agent, its chloroethyl groups enable , though this mechanism underlies its vesicant properties rather than defining basic chemical characteristics.

Methods of Synthesis

The Levinstein process, developed during World War I, represents the primary method for large-scale production of bis(2-chloroethyl) sulfide (mustard gas). In this approach, ethylene gas is passed through liquid sulfur monochloride (S₂Cl₂) at temperatures of 30–60 °C, resulting in the exothermic reaction: 2 C₂H₄ + S₂Cl₂ → (ClCH₂CH₂)₂S + SCl₂, though side reactions produce impurities such as polysulfides and thiodiglycol. The crude product requires distillation under reduced pressure to achieve purity levels of 80–96%, with yields typically around 70–80% based on sulfur monochloride consumption. This method was favored by Allied forces for its simplicity and use of readily available precursors, despite generating toxic byproducts like hydrogen chloride gas. In contrast, the Meyer process, utilized by German forces in World War I, involves a two-stage synthesis via thiodiglycol as an intermediate. Ethylene is first treated with hypochlorous acid to form 2-chloroethanol (ClCH₂CH₂OH), which reacts with aqueous sodium sulfide (Na₂S) to yield thiodiglycol ((HOCH₂CH₂)₂S); the diol is then chlorinated using hydrochloric acid or phosphorus oxychloride (POCl₃) at elevated temperatures to produce bis(2-chloroethyl) sulfide. This route allows for higher purity after fractional distillation but requires more steps and handling of aqueous intermediates, limiting throughput compared to the Levinstein method. Post-World War I refinements, including direct chlorination of with anhydrous HCl or in the presence of catalysts, enable production of distillation-grade mustard gas (>96% purity) suitable for munitions filling. These methods exploit 's stability and are monitored under chemical weapons conventions due to its role as a key precursor. Laboratory-scale syntheses, such as those originally described by Victor Meyer in 1886 involving and , are less relevant to industrial contexts but confirm the compound's reactivity with nucleophilic sulfur centers. All routes necessitate stringent safety measures owing to the agent's volatility, lachrymatory effects, and alkylating toxicity even at trace levels.

Etymology and Nomenclature

Origins of the Name

The designation "mustard gas" for sulfur mustard (bis(2-chloroethyl) sulfide) arose during World War I from its pungent odor, which Allied soldiers likened to mustard, garlic, or horseradish, particularly noticeable at concentrations above 0.0007 mg/m³. This sensory association prompted the informal naming by troops encountering the agent, first deployed by German forces on July 12, 1917, near Ypres, Belgium. Despite the moniker, sulfur mustard is not a gas but a volatile, amber-colored at ( 217°C), which vaporizes slowly to form an or vapor cloud under battlefield dispersal conditions, such as shells or projectors. The "gas" suffix reflected early 20th-century terminology for inhaled irritants, akin to or , rather than precise physical state. German forces referred to it as Lost (from the English "lost" or possibly a code), while the French called it yiprite after , but the English "mustard gas" term persisted in Allied documentation and entered widespread use post-war.

Synonyms and Classifications

Mustard gas, chemically bis(2-chloroethyl) sulfide with the molecular formula C₄H₈Cl₂S, is systematically named 1-chloro-2-(2-chloroethylsulfanyl)ethane according to IUPAC nomenclature. Common synonyms include sulfur mustard, the preferred term in scientific and toxicological contexts to distinguish it from nitrogen mustards; mustard agent; and dichloroethyl sulfide. Military designations are H for the crude, unrefined form and HD for the distilled, purified variant, reflecting differences in purity and stability. The name yperite derives from its first large-scale deployment near Ypres, Belgium, in 1917. As a chemical warfare agent, it is classified as a vesicant or blister agent due to its mechanism of inducing delayed, severe burns and blistering on skin, eyes, and mucous membranes via alkylation of cellular components, including DNA cross-linking. Chemically, it falls under organosulfur compounds, specifically thioethers, and functions as an alkylating agent capable of reacting with nucleophilic sites in biological molecules. Under the United Nations' Globally Harmonized System (GHS), it is designated for acute toxicity (categories 2-3 via inhalation, dermal, and ocular routes), skin corrosion (category 1A), serious eye damage (category 1), germ cell mutagenicity (category 1B), and carcinogenicity (category 1A), with additional hazards for specific target organ toxicity and aquatic acute toxicity. It is a Schedule 1 substance under the Chemical Weapons Convention, banning its development, production, and stockpiling except for limited research or protective purposes. The International Agency for Research on Cancer (IARC) classifies it as a Group 1 carcinogen based on sufficient evidence of lung cancer in humans from occupational exposures.

Historical Development

Pre-World War I Research

In 1822, French chemist César-Mansuète Despretz first prepared an impure form of sulfur mustard (bis(2-chloroethyl) sulfide) by reacting ethylene with sulfur dichloride, though he reported no notable irritating properties and did not isolate the pure compound. Subsequent 19th-century chemists refined synthesis techniques amid advancing understanding of organic sulfur compounds, but early efforts yielded low-purity products unsuitable for detailed study. By 1860, British chemist Frederick Guthrie achieved a more defined preparation by chlorinating ethyl disulfide, generating vapors that caused acute blistering, intense pain, and inflammation on exposed skin and eyes; he likened the effects to an exaggerated , marking the first documented recognition of its vesicant potency. Guthrie's observations, published in chemical journals, highlighted the substance's ability to penetrate and persist as an oily , but lacked quantitative data or medical analysis. In 1886, German chemist developed an efficient synthesis route using and sulfur monochloride, producing higher yields of the compound. To verify purity, Meyer inhaled its vapors, experiencing immediate eye irritation, temporary blindness, severe , and ; these personal experiments revealed its delayed-onset respiratory toxicity but exacerbated his chronic health decline, contributing to his in 1897 at age 48. Pre-1914 remained confined to academic laboratories, focusing on structural elucidation and incidental physiological effects rather than therapeutic or applications, with no evidence of scaled production or weaponization attempts.

World War I Innovation and Deployment

![German demonstration of Yperite mustard gas][float-right] The German program during , directed by chemist , sought agents that could overcome the stalemate of following the initial use of and gases. Sulfur mustard, a vesicant agent known for its blistering effects and persistence in the environment, was developed as part of this effort to deny terrain to Allied forces and cause prolonged casualties without immediate lethality. Although Haber expressed reservations about its deployment due to the lack of effective German defenses, the agent was weaponized through industrial-scale production involving reactions of with sulfur monochloride. Sulfur mustard was first deployed by the German Fourth Army on the night of July 12-13, 1917, near , , during preparations for the Third Battle of Ypres (Passchendaele). Delivered via artillery shells marked with yellow crosses for identification, approximately 50,000 rounds containing the agent were fired at British positions held by the 40th Division. The attack exploited the agent's oily liquid form, which vaporized slowly and contaminated soil and equipment for days, creating hazardous zones that hindered troop movements and required extensive . The initial deployment inflicted over 2,100 , primarily through delayed onset of symptoms including severe skin blisters, eye inflammation, and damage, which incapacitated soldiers for weeks. In the subsequent three weeks, British casualty clearing stations recorded around 14,000 gas-related admissions, the majority attributable to mustard exposure, marking a shift toward persistent agents that prioritized morbidity over mortality. By late , German production reached 1,000 tons monthly, enabling widespread use that accounted for roughly 80% of remaining chemical in the war, though overall gas fatalities remained under 5% of total deaths due to protective measures like masks. Allied forces began retaliatory use by August 1918, but German innovation maintained a tactical edge throughout.

Military Applications

World War I Usage

The German army first deployed sulfur mustard on the night of July 12–13, 1917, during the Third Battle of Ypres, targeting Allied positions near Ypres, Belgium, in an operation known as "Totentanz" or "Dance of Death." Delivered via artillery shells marked with yellow crosses, the agent contaminated ground areas with persistent liquid droplets, causing severe blistering, temporary blindness, and respiratory damage that manifested hours after exposure. This initial barrage inflicted approximately 6,400 casualties in the Armentières sector alone, exploiting the limitations of existing gas masks which primarily protected against inhalation but not skin contact. Mustard gas proved particularly effective due to its vesicant properties and low volatility, allowing it to persist in craters and trenches, denying areas to troops for days and complicating offensive operations. By late , German production scaled to thousands of tons, with shells comprising the primary delivery method, supplemented later by aerial bombs. The agent accounted for the majority of chemical casualties after its introduction, contributing to nearly 400,000 total mustard-related injuries across the war, far exceeding those from or due to its incapacitating rather than immediately lethal effects. British forces reported over 160,000 gas casualties, with mustard responsible for a significant portion after 1917. In retaliation, Allied forces, initially caught unprepared, accelerated production and first employed mustard gas in August 1918 during the , using similar shell-based tactics and Livens projectors for concentrated releases. Countermeasures evolved with the introduction of protective ointments and improved small-box respirators, though decontamination remained challenging, as mustard hydrolyzed slowly in soil and water. Overall, chemical weapons, dominated by mustard after mid-1917, caused about 1.3 million and 90,000 deaths, with mustard's role underscoring its tactical value in despite international prohibitions like the 1899 Hague Declaration.

Interwar Period and World War II Employment

In the interwar period, the 1925 Geneva Protocol, which prohibited the use of chemical weapons in warfare, failed to prevent deployments by signatory states. Italy extensively employed mustard gas during the Second Italo-Ethiopian War from October 1935 to May 1936, primarily via aerial delivery against Ethiopian troops and civilian populations lacking protective equipment; estimates indicate around 15,000 chemical casualties from mustard and other agents. This marked the first large-scale use of mustard gas since World War I, with Italian forces dropping over 300 tons of chemical munitions, including sulfur mustard, to overcome Ethiopian resistance in rugged terrain. During , all major belligerents—, the Allies, and —maintained substantial stockpiles of mustard gas, with production ramping up despite the Protocol's constraints on use (which did not extend to possession or development); for instance, the alone produced over 144,000 tons of chemical agents by 1945, including mustard variants. However, mutual deterrence prevented widespread battlefield employment in and against Western forces in the Pacific, as leaders on both sides anticipated devastating retaliation; , personally scarred by mustard exposure in , explicitly refrained from initiating chemical attacks despite Allied bombing campaigns. Japan, however, violated the Protocol by deploying mustard gas against Chinese Nationalists and Communists in multiple campaigns, such as the 1941 Zhejiang-Jiangxi offensive and the 1943 , where artillery shells containing mustard inflicted severe blistering injuries on exposed troops. In the 1944 encirclement, Japanese forces fired numerous gas shells incorporating mustard and , contributing to high non-combat incapacitation rates among Chinese defenders amid broader atrocities. These uses, totaling thousands of tons of chemical agents expended by Japan's and field armies, targeted poorly equipped adversaries but ceased against American-led forces due to anticipated reprisals.

Post-1945 Conflicts and Allegations

Egyptian forces deployed sulfur mustard during the North Yemen Civil War from 1963 to 1967, marking the first confirmed postwar use of the agent in combat. Egyptian bombed royalist positions and villages with mustard gas canisters, resulting in blisters, respiratory distress, and an estimated 1,500 casualties among Yemeni fighters and civilians. Investigations by Swedish and British medical teams in 1967 confirmed mustard gas residues in soil samples and matched victim symptoms to the agent's vesicant effects, though denied the allegations at the time. Iraq employed sulfur mustard extensively during the Iran-Iraq War (1980-1988), initiating chemical attacks as early as 1983 against Iranian troops. By 1984, Iraq had used mustard gas in over 30 documented assaults, often delivered via shells and aerial bombs, causing tens of thousands of Iranian including severe skin blistering, eye damage, and . fact-finding missions in 1984 and 1986 verified mustard agent presence through clinical examinations and environmental sampling, estimating that chemical weapons, predominantly mustard, accounted for up to 20% of Iranian battlefield deaths. Iraq's program produced over 3,500 tons of mustard agent during the conflict, with use escalating in 1988 against Kurdish civilians in alongside nerve agents, though mustard predominated in earlier phases. In the , the () used sulfur mustard in an August 2015 attack on the rebel-held town of Marea, contaminating up to 25 individuals with symptoms including skin burns and ocular irritation. The Organisation for the Prohibition of Chemical Weapons (OPCW) Fact-Finding Mission analyzed samples and victim accounts, confirming with high confidence that deployed an improvised mustard device, likely artillery rounds filled with the agent synthesized from commercially available precursors. Separate allegations of mustard use surfaced in 2015-2016, but OPCW investigations attributed confirmed incidents primarily to non-state actors like rather than regime forces, which favored and . No large-scale state uses of mustard have been verified since the , though remnant Iraqi stockpiles exposed U.S. troops to low-level mustard degradation products during the 2003 , without active deployment.

Formulations and Variants

Sulfur Mustard Types

Sulfur mustards encompass several formulations of bis(2-chloroethyl) sulfide, the prototypical vesicant agent, distinguished primarily by purity, production method, and additives for operational enhancements. The crude Levinstein mustard, designated H or HS, results from the reaction of ethylene with sulfur monochloride at 30–50°C, yielding a dark-brown liquid containing 20–30% impurities such as sesquimustard and other polysulfides that contribute to its instability and higher toxicity per unit weight compared to purified forms. This variant, developed during World War I, freezes at approximately -2°C and was widely deployed due to its rapid production despite the impurities exacerbating long-term storage degradation. Distilled mustard, coded HD, is a purified derivative obtained by vacuum distillation and washing of Levinstein mustard, achieving 95–99% purity as a colorless to amber oily liquid with a freezing point of 14–16°C and vapor pressure of 0.11 mmHg at 20°C. This form exhibits greater persistence on surfaces (lasting days under ambient conditions) and reduced impurity-related side reactions, rendering it preferable for post-World War I stockpiles and deployments. HD's alkylating reactivity remains identical to H, targeting DNA via guanine N7 sites, but its stability minimizes unintended polymerization during handling. HT represents a binary of 60% HD and 40% agent T (O-mustard, chemically bis(2-chloroethylthioethyl) ether, ClCH₂CH₂SCH₂CH₂OCH₂CH₂SCH₂CH₂Cl), engineered to depress the freezing point to 0–1°C for operations while reducing volatility ( ~0.05 mmHg at 20°C) and enhancing persistence beyond HD alone. Agent T itself is a difunctional vesicant with comparable blistering potency to HD but lower vapor hazard, and its inclusion in HT mitigates risks in munitions. Sesquimustard (Q, 1,1'-thiobis(2-chloroethane)), a common impurity in H (up to 10–20%), features the (ClCH₂CH₂S)₂CH₂ and exhibits approximately fivefold greater vesicant activity due to its solid state at ( 35–36°C) and enhanced , though it was not independently weaponized.
TypeComposition/PurityKey PropertiesHistorical Use
H (Levinstein)~70–80% bis(2-chloroethyl) sulfide + impurities (e.g., sesquimustard)Freezing point -2°C; dark liquid; less stableWorld War I production priority for volume
HD (Distilled)95–99% pure bis(2-chloroethyl) sulfideFreezing point 14–16°C; amber liquid; higher purity reduces degradationPost-1918 stockpiles; standard for later conflicts
HT60% HD + 40% O-mustard (agent T)Freezing point 0–1°C; lower volatility; increased persistenceCold-weather munitions adaptation
These variants share the core mechanism of thioether-mediated but differ in deployability; for instance, HT's formulation avoids the solidification issues of pure HD in subzero temperatures, as demonstrated in U.S. military testing during the mid-20th century. Impurities like sesquimustard in earlier batches amplified acute dermal LD50 values (e.g., ~100 mg/kg for H vs. ~450 mg/kg for HD in animal models), underscoring the trade-offs in wartime expediency versus refined .

Nitrogen Mustard Derivatives

Nitrogen mustards, also known as HN compounds, are a class of blister agents chemically distinct from sulfur mustard but sharing a similar alkylating mechanism of action. They consist of bis(2-chloroethyl)amine derivatives, such as HN-1 (bis(2-chloroethyl)methylamine), HN-2 (bis(2-chloroethyl)amine or mechlorethamine), and HN-3 (tris(2-chloroethyl)amine), which form reactive aziridinium ions that cross-link DNA and proteins, leading to cytotoxicity. Unlike sulfur mustard, which primarily causes localized vesication through skin and mucosal damage, nitrogen mustards exhibit enhanced systemic toxicity, including profound myelosuppression due to bone marrow targeting, though they are less stable and prone to polymerization over time. Development of nitrogen mustards began in the 1930s as potential agents, motivated by efforts to create more potent vesicants than sulfur mustard with improved persistence and toxicity. British and German researchers synthesized early variants, stockpiling them during , though operational deployment was limited by their volatility, short shelf life, and handling difficulties; for instance, HN-2 and HN-3 were produced in quantities exceeding 1,000 tons by Allied forces but saw no confirmed battlefield use. Post-war analyses confirmed their vesicant properties in animal models, with toxicity profiles showing delayed onset of and blistering comparable to sulfur mustard but with greater hematologic effects at lower doses. While military applications remained marginal, nitrogen mustards profoundly influenced pharmacology through their repurposing as anticancer agents. Observations of lymphoreticular suppression in WWII-exposed subjects—echoing sulfur mustard's Bari harbor incident effects—prompted Yale pharmacologist Alfred Gilman and Louis Goodman to test HN-2 on lymphomas in 1942, marking the inception of ; this led to FDA approval of mechlorethamine in 1949 for Hodgkin's disease. Derivatives like (introduced 1959), ifosfamide, , and evolved from HN-2 scaffolds, optimizing for tumor selectivity while mitigating non-specific alkylation; these agents alkylate DNA guanine residues, inducing in rapidly dividing cells, though they retain risks of secondary malignancies and infertility. Modern variants, such as bendamustine, incorporate purine analogs for dual alkylation-topoisomerase inhibition, achieving response rates up to 70% in . Under the , nitrogen mustards are Schedule 1 substances, reflecting their dual-use potential despite predominant medical applications.

Toxicological Mechanism

Vesicant and Alkylating Action

Sulfur mustard, chemically bis(2-chloroethyl) sulfide, functions as a bifunctional alkylating agent, reacting with nucleophilic sites in biological molecules through its chloroethyl groups, which cyclize to form highly reactive aziridinium ions. These electrophilic intermediates primarily target the N7 position of guanine in DNA, leading to monoadduct formation and subsequent inter- and intra-strand cross-links, such as di-(2-guanin-7-yl-ethyl)-sulfide. This alkylation disrupts DNA replication and transcription, triggering cell cycle arrest, apoptosis, and necrosis, particularly in rapidly dividing cells. As a vesicant, sulfur mustard penetrates intact skin due to its lipophilicity, diffusing through the stratum corneum to reach the basal layer of the epidermis where it alkylates DNA in keratinocytes. The resulting inhibition of mitosis and cellular detachment causes a characteristic latent period of 2–24 hours before symptoms manifest, followed by erythema, edema, and microvesicle formation due to separation at the dermal-epidermal junction. Blistering arises from the death of basal cells and release of proteases and inflammatory mediators, exacerbating tissue damage without initial pain, which delays recognition of exposure. In mucous membranes, similar alkylation leads to severe blistering and ulceration, with ocular exposure causing corneal damage and potential blindness.

Cellular and Systemic Effects

Sulfur mustard, a bifunctional alkylating agent, penetrates lipid membranes and forms a reactive sulfonium ion that primarily targets the N7 position of guanine in DNA, leading to monoadducts, intra- and interstrand cross-links, and DNA strand breaks. These modifications inhibit DNA replication and transcription, particularly in rapidly dividing cells such as basal keratinocytes and hematopoietic precursors. Alkylation also affects proteins and glutathione, depleting cellular antioxidants and exacerbating oxidative stress through reactive oxygen species generation. At the cellular level, DNA damage activates poly(ADP-ribose) polymerase (PARP), causing NAD+ and ATP depletion, metabolic failure, and release of calcium-dependent proteases that disrupt membranes and induce necrosis or apoptosis. Upregulation of p53 and downregulation of bcl-2 further promote programmed cell death, while inflammation arises from leukocytic infiltration and cytokine release. In epithelial tissues, this culminates in basal cell death, epidermal-dermal separation, and vesication, with effects delayed 2–48 hours due to the time required for alkylation and repair attempts. Systemic effects occur following absorption through skin, lungs, or eyes, distributing to , liver, kidneys, and . manifests as , , and , with leukocyte counts dropping below 100 cells/cm³ in severe cases, increasing susceptibility and risk. Respiratory systemic toxicity includes , , and chronic from epithelial and secondary s. Additional systemic impacts involve gastrointestinal hemorrhage, hepatic enzyme elevation, and neurological symptoms like and anxiety from indirect or imbalances. Immunological dysregulation features initial IgG/IgM spikes followed by depression and reduced natural killer cells, persisting years post-exposure. Haematological effects, including , stem from targeted in proliferating blood cells.

Health Impacts

Acute Exposure Symptoms

Sulfur mustard exposure elicits delayed-onset vesicant effects without immediate pain at contact, primarily targeting skin, eyes, and due to its alkylating . Symptoms typically emerge after a latent period of 1-48 hours, varying by dose, exposure route, and environmental factors; higher concentrations shorten latency and increase severity. Dermal contact induces intense pruritus followed by and within 4-8 hours, progressing to tense blisters filled with by 2-18 hours post-exposure. Blisters rupture to form shallow ulcers susceptible to bacterial , with liquid exposures causing deeper second- and third-degree burns than vapors, which produce superficial first- and second-degree lesions. Moist (e.g., axillae, ) exhibit heightened vulnerability, and histological changes include basal epidermal cell evident within 3 hours. Children display accelerated onset (4-18 hours) and amplified damage relative to adults. Ocular involvement manifests as acute , blepharospasm, lacrimation, and starting 1-12 hours after exposure, often escalating to corneal ulceration, , and temporary blindness; permanent occurs with high doses. Eyelid swelling and compound discomfort, necessitating prompt to mitigate progression. Inhalation irritates mucous membranes, yielding , epistaxis, hoarseness, and cough within hours to days, with severe cases developing , , and (ARDS) at concentrations ≥1,000 mg-min/m³, potentially culminating in or death from secondary . Upper airway may obstruct ventilation, and symptoms intensify over 24-72 hours. Gastrointestinal effects, rarer but possible via or systemic absorption, include , , and mucosal burns; acute bone marrow suppression manifests as and , heightening and risks. Overall, pediatric exposures provoke more rapid and profound responses across systems.

Chronic and Long-Term Consequences

Exposure to sulfur mustard leads to persistent respiratory disorders, including chronic bronchitis, , , and "mustard lung," characterized by obstructive and restrictive pulmonary impairments that manifest or worsen decades after initial exposure. In Iranian survivors of the Iran-Iraq War (1980-1988), approximately 45,000 individuals suffer from late-onset respiratory complications, with lung issues becoming more prominent in later years even among those without acute symptoms. These effects stem from alkylating damage to airway , resulting in , recurrent infections, and reactions, contributing to elevated morbidity and mortality rates. Studies of exposed combatants show increased risk of pulmonary complications correlating with age and lack of protective masks during exposure. Ocular sequelae include chronic , corneal opacification, and limbal deficiency, often progressing to partial or complete vision loss without timely intervention. In cohorts of severely injured veterans, persistent eye surface disorders arise from mustard's vesicant action on and , leading to neovascularization and ulceration years post-exposure. Long-term follow-up reveals that even low-dose vapor exposure can cause incapacitating injuries, with higher doses preventing full corneal recovery. Dermatological effects encompass chronic pigmentation changes, scarring, and recurrent , particularly in areas of severe acute blistering. Survivors exhibit ongoing skin vulnerability due to depleted epidermal stem cells and . Carcinogenic risks are elevated, with documented associations to from mustard's DNA-alkylating properties, as observed in veterans and Iranian exposed populations. Epidemiological data indicate higher incidence of respiratory malignancies, though confounding factors like require cautious interpretation. Additional long-term outcomes involve metabolic alterations, such as hypercholesterolemia across exposure severities, and psychological burdens including depression and . Mortality studies of over 48,000 Iranian survivors report excess deaths from respiratory causes over 39 years, underscoring mustard's role in accelerated aging of affected systems.

Clinical Management and Treatment

There is no specific for sulfur mustard exposure, and treatment relies entirely on supportive care to mitigate symptoms and prevent complications. Immediate remains the cornerstone of management, as it significantly reduces the extent of injury if performed within minutes of exposure; this involves rapid removal of contaminated clothing and thorough washing of and eyes with copious amounts of or saline, avoiding further of medical personnel. Ocular injuries, manifesting as , , and potential corneal ulceration, require prompt and prolonged irrigation with isotonic saline or water for at least 15-30 minutes initially, followed by ophthalmologic evaluation; topical mydriatics and antibiotics may be administered to prevent and reduce , though systemic corticosteroids are used judiciously due to risks of exacerbating damage. Skin lesions, characterized by progressing to bullae formation 4-24 hours post-exposure, are managed conservatively akin to second-degree burns, with unruptured blisters left intact to minimize risk, of necrotic tissue, and application of or similar antimicrobial dressings alongside systemic analgesics such as opioids for severe . Respiratory tract involvement, ranging from mild upper airway irritation to in severe cases, necessitates humidified oxygen supplementation, bronchodilators, and mucolytics like N-acetylcysteine to alleviate and secretions; with may be required for , while prophylactic antibiotics are reserved for confirmed secondary bacterial infections rather than routine use. Systemic effects, including potential from in high-dose exposures, warrant monitoring of complete blood counts and supportive transfusions if develops, with overall fluid and electrolyte balance maintained to counter insensible losses from damaged mucosa. Experimental therapies, such as methimazole for neutralizing vesicant effects or modulators for lung injury, have shown promise in preclinical models but lack established clinical efficacy and are not . Long-term follow-up focuses on scarring, chronic respiratory impairment, and surveillance, informed by historical cohorts like Iranian victims from the 1980s Iran-Iraq War.

Detection and Decontamination

Methods of Detection

Field detection of sulfur mustard primarily employs colorimetric indicators for rapid screening of liquid and vapor contamination. M8 detection paper, consisting of sheets impregnated with dyes, turns red upon contact with liquid sulfur mustard droplets in less than one minute, serving as an initial alert for vesicant agents. M9 detection tape, an adhesive-backed green strip, changes to red or pink when exposed to sulfur mustard vapors or droplets, enabling detection on surfaces or protective gear. These paper-based methods are inexpensive and portable but prone to false positives from interferents like products, necessitating confirmatory testing. For vapor detection, the M256A1 chemical agent detector kit uses enzyme-based tickets that produce a color change after approximately 15 minutes of exposure, sensitive to sulfur mustard concentrations about 500 times the acceptable exposure limit. Portable instruments such as the Chemical Agent Monitor (CAM), employing (IMS), provide graduated readouts for sulfur mustard vapors within 10-60 seconds, with a minimum detectable level roughly 50 times the exposure limit. (SAW) devices like the MiniCAD offer automated, continuous monitoring of trace sulfur mustard vapors with high specificity in field environments. Laboratory confirmation utilizes chromatographic techniques for precise quantification across matrices. Gas chromatography-mass spectrometry (GC-MS) detects sulfur mustard and metabolites like in air (via sorbent tubes, sensitivity ~0.2 ng/μL), , (5-10 ng/injection), and biological fluids (1 μg/L), often following solvent extraction or desorption. Tandem GC-MS/MS enhances selectivity for urinary β-lyase metabolites at 0.1 μg/L. Liquid chromatography-electrospray ionization-tandem (LC-ESI-MS/MS) identifies sulfur mustard in complex environmental samples, supporting forensic attribution. These methods achieve high recovery rates (48-100%) but require controlled conditions unlike field tools.

Decontamination Procedures

Decontamination of sulfur mustard exposure requires immediate action, ideally within 1-2 minutes, as this is the only reliable method to substantially reduce subsequent tissue damage from , given the agent's on surfaces and delayed onset of symptoms. Later efforts may mitigate severity but cannot fully prevent penetration into deeper tissues. For exposed individuals, the primary procedure involves rapid removal of all contaminated clothing to prevent ongoing vapor or liquid transfer, followed by thorough irrigation of skin with copious quantities of lukewarm water and mild using a rinse-wipe-rinse technique to mechanically remove residue without abrading the . In military or equipped settings, application of Reactive Skin Decontamination Lotion (RSDL), containing dekontamin, is recommended immediately on suspected areas, as it chemically neutralizes the agent via without waiting for symptoms. Eyes should be flushed continuously with water or saline for at least 15-30 minutes, avoiding neutralization agents that could exacerbate irritation. Personnel typically occurs in structured zones with entry and exit corridors to contain contamination. Environmental and equipment decontamination employs oxidizing agents such as 0.5% () solution for non-porous surfaces, applied after initial dilution to break down the agent's thioether bonds, though reactive by-products like must be considered for secondary hazards. Absorbents like or commercial granules may be used for spills to physically contain liquid pools before neutralization, but efficacy varies by agent concentration and surface type. These procedures prioritize containment to avoid , with post-decontamination monitoring essential due to mustard's oily persistence.

Scientific and Medical Derivatives

Origins of Chemotherapy from Mustard Agents

The vesicant properties of sulfur mustard, first deployed on a large scale by German forces at on July 12, 1917, were observed to cause profound through destruction of lymphoid tissues and , leading to in exposed individuals. Autopsies of victims revealed selective depletion of rapidly dividing hematopoietic cells, prompting early speculation in the about exploiting this cytocidal effect against malignancies, though sulfur mustard's volatility and toxicity precluded medical use. Nitrogen mustards, synthetic analogs like bis(2-chloroethyl)methylamine (HN2, later mechlorethamine), were developed in the 1930s as more stable agents but repurposed during for therapeutic potential due to their alkylating mechanism, which cross-links and inhibits replication in proliferating cells. Under a top-secret U.S. Office of Scientific Research and Development program initiated in 1942, Yale pharmacologists Louis S. Goodman and Alfred Gilman conducted preclinical trials, observing dramatic regression of transplanted lymphosarcoma in mice after intravenous nitrogen mustard administration. The first human application occurred on August 27, 1942, when Goodman administered HN2 to "J.D.," a 48-year-old patient with disseminated lymphosarcoma, achieving substantial tumor shrinkage and symptomatic relief within days, though relapse followed after six months. Between 1942 and 1943, controlled trials involving over 150 patients with Hodgkin's disease, lymphosarcoma, and other lymphomas demonstrated objective remissions in approximately 50% of cases, with complete responses in some advanced stages, confirming nitrogen mustard's lymphocytolytic action as a basis for antineoplastic therapy. These wartime findings, initially classified to avoid aiding Axis powers, were declassified post-1945 and published in 1946, establishing alkylating agents as the inaugural class of systemic chemotherapeutics and influencing regimens like MOPP for Hodgkin's lymphoma decades later. Mechlorethamine received U.S. Food and Drug Administration approval on May 10, 1949, as the first anticancer chemotherapy agent, validating the transition from battlefield toxin to targeted cytoreductive drug despite persistent challenges like myelosuppression and secondary malignancies. This paradigm shift prioritized empirical cytotoxicity over surgical excision, founding modern oncology's pharmacological approach.

Ongoing Research Applications

Research into nitrogen mustard derivatives, evolved from sulfur mustard's alkylating properties, continues to explore hybrid molecules for enhanced anticancer efficacy and reduced toxicity. For instance, chromone- conjugates have been synthesized and evaluated for anti-breast cancer activity, demonstrating selective against tumor cell lines via DNA cross-linking while sparing normal cells, as reported in a 2021 study. Similarly, modifications to classic agents like bendamustine, , and incorporate hypoxia-activated triggers to improve tolerability and target hypoxic tumor environments, with in vitro data from 2020 showing increased potency under low-oxygen conditions. Efforts to mitigate mustard-induced toxicities inform broader biomedical applications, including potential neuroprotective and derivatives. A 2023 investigation identified methimazole as an effective neutralizer of mustard's vesicant effects in cellular models, suggesting repurposing for topical antidotes that could extend to alkylating agent side-effect management in . Ongoing studies on long-term mustard exposure in Iranian veterans, involving over 64,000 survivors from the 1980-1988 Iran-Iraq War, link persistent and genomic instability to chronic conditions like , driving research into therapies and biomarkers for alkylating agent-related damage. Pharmacological approaches target sulfur and nitrogen mustard mechanisms, such as DNA alkylation and inflammation, with preclinical trials testing inhibitors of downstream pathways like PARP and NF-κB for lung injury reversal, as outlined in a 2022 review of potential treatments for mustard-induced pulmonary fibrosis. These efforts emphasize causal mechanisms over symptomatic relief, prioritizing empirical validation through cohort studies and animal models to develop agents with dual therapeutic roles in oncology and toxicology. Mechlorethamine remains in clinical use for cutaneous T-cell lymphoma, with 2025 updates confirming its lymphoablative role in regimens, underscoring sustained application of mustard-derived alkylators.

Controversies and Ethical Considerations

Human Experimentation Programs

During World War II, the United States military orchestrated extensive human testing programs with mustard gas to evaluate the effectiveness of protective clothing, masks, decontamination agents, and physiological responses under combat-like conditions. From 1941 to 1945, roughly 60,000 American soldiers—primarily enlisted men selected from various branches—underwent deliberate exposures at facilities such as Edgewood Arsenal in Maryland, the Naval Research Laboratory in Washington, D.C., and field sites including Camp Sibert, Alabama. Methods included skin patch or drop tests applying liquid mustard (0.15–7 mg doses), vapor chamber immersions at concentrations of 100–11,000 Ct (concentration-time units), and field traverses through agent-contaminated zones up to 10,000 Ct to simulate battlefield persistence and penetration through fabrics. These protocols aimed to quantify blister thresholds, absorption rates, and mitigation strategies amid fears of Axis chemical retaliation, though participants often received limited disclosure of risks or long-term effects. At least nine dedicated projects incorporated racial variables, disproportionately involving African American, Japanese American, and Puerto Rican troops under the hypothesis that levels altered skin permeability to mustard vapors, with exposures tailored to compare vesicant responses across groups. Approximately 2,500 subjects endured chamber tests and 1,000 field simulations, while the majority faced localized skin applications; data from these informed uniform specifications but yielded inconsistent evidence for hypothesized racial variances, later attributed more to methodological flaws than inherent biology. Allied programs paralleled U.S. efforts, with Britain conducting mustard exposures at , including on Indian troops in the to assess tropical efficacy of protectants. In , the Suffield Experimental Station near Ralston, , tested thousands of soldiers from onward, often without explicit prior consent; protocols mirrored U.S. chamber and field exposures to mustard and , evaluating gear under conditions, with some participants later qualifying for compensation due to chronic injuries like respiratory damage and skin cancers. Postwar U.S. initiatives at Edgewood Arsenal extended through 1975, incorporating mustard into broader chemical and psychochemical trials on volunteers, though with stricter protocols than wartime; an estimated additional thousands faced low-level exposures to refine antidotes and behavioral impacts. of records in 1993 exposed systemic gaps in , medical tracking, and equity, prompting veteran claims but no comprehensive restitution, as secrecy had precluded baseline health data for causation assessments. These programs, while advancing defensive capabilities, exemplified trade-offs in wartime exigency versus individual safeguards, with empirical outcomes validating agent persistence but underestimating carcinogenic sequelae.

Racial Disparities in Testing Claims

During , the military conducted extensive mustard gas experiments on approximately 60,000 American soldiers to evaluate protective equipment and physiological responses, with participant selection explicitly influenced by race to assess purported ethnic differences in susceptibility. Official records indicate that soldiers were segregated by race during testing, as military policy aimed to compare reactions across groups, including whites, , , and . In segregated units or targeted cohorts, minorities comprised a disproportionate share of subjects; for instance, in documented field tests at locations like the Edgewood Arsenal, soldiers formed a majority despite representing only about 10% of the overall U.S. Army. Claims of racial disparities stem from declassified documents revealing that experimenters prioritized non-white soldiers under the hypothesis that darker skin pigmentation conferred greater resistance to blistering agents like mustard gas, a notion rooted in contemporaneous pseudoscientific beliefs about racial physiology rather than empirical prior data. Japanese American soldiers, often from internment camp-adjacent recruitment, underwent separate exposure trials to isolate "Oriental" responses, while Puerto Rican troops were tested for tropical climate interactions. Approximately 4,000 soldiers participated in intensive full-body chamber exposures, with post-war analyses showing no significant racial differences in mustard gas effects, undermining the experiments' racial premise but confirming uniform vesicant damage across groups. Many participants experienced acute burns, respiratory distress, and later chronic conditions such as skin cancer and blindness, yet initial military classifications labeled exposures as "volunteer" without full disclosure of risks or racial targeting criteria. These practices have been critiqued as emblematic of race-based human experimentation, with historians noting that while the broader program involved diverse troops, the deliberate over-selection of minorities—evidenced in Edgewood Arsenal logs where up to 92% of some cohorts were non-white—amplified ethical concerns over consent and equity. The Department of Defense acknowledged the experiments in 1991 but withheld racial details until investigative reporting in 2015 prompted congressional demands for apologies and improved veteran benefits reviews by the . Subsequent scholarship attributes the disparities not to random sampling but to institutional biases favoring expendable demographics for hazardous research, though apologists have argued that all volunteers faced equivalent risks regardless of race. Long-term claims from affected veterans, including higher incidences of among exposed groups, continue to be adjudicated, highlighting ongoing debates over accountability.

Proliferation and Treaty Compliance Debates

The , which entered into force on April 29, 1997, prohibits the development, production, stockpiling, transfer, and use of chemical weapons, including sulfur mustard (mustard gas), under the oversight of the Organisation for the Prohibition of Chemical Weapons (OPCW). By 2025, 193 states parties had achieved approximately 99% destruction of declared stockpiles worldwide, marking a significant reduction in state-held chemical arsenals, though debates persist over verification completeness and proliferation. Proliferation concerns intensified with non-state actors, notably the (ISIL), which produced and deployed sulfur mustard in attacks in and starting in 2015, representing the first confirmed instance of a banned chemical agent weaponized by a terrorist group with rudimentary industrial capabilities. OPCW investigations confirmed ISIL's use of mustard in the Marea attack on September 1, 2015, highlighting treaty limitations against non-signatories or groups operating in ungoverned spaces, where dual-use precursors like enabled clandestine synthesis. Critics argue that CWC verification mechanisms, reliant on state declarations, inadequately address such asymmetric threats, as ISIL exploited captured Syrian stockpiles or local production without state infrastructure. In , compliance debates center on the government's 2013 declaration of over 1,300 metric tons of chemical agents, including mustard, which were largely destroyed by via OPCW-supervised neutralization aboard the U.S. vessel MV Cape Ray, more than 600 tons of priority chemicals. However, unresolved issues include allegations of undeclared sites and incomplete accounting, with OPCW reports citing Syria's insufficient cooperation on residual chemicals and potential hidden mustard precursor caches as of 2024. U.S. assessments emphasize diplomatic pressure for full transparency, noting that post-destruction incidents, such as ISIL's mustard deployments, may stem from diverted materials, underscoring causal challenges in preventing leakage from state programs to militants amid . Broader treaty debates question the CWC's nondiscriminatory , as major possessors like the U.S. and completed declared stockpile destruction by 2023 and 2017, respectively, yet face scrutiny over verification of agents and mustard remnants, with calls for enhanced challenge inspections to address dual-use trade ambiguities inherited from discussions. Non-proliferation experts highlight that while empirical destruction rates are high, causal realism demands skepticism toward self-reported compliance in politically volatile regions, where of residual risks—such as Syria's depleted but potentially retained stocks—persists despite regime changes.

Stockpiling, Disposal, and Proliferation

Historical Stockpiles

During , Germany initiated large-scale production of mustard gas following its first combat use on July 12, 1917, near , , as part of efforts to overcome stalemated ; Allied nations, including , Britain, and the , subsequently developed their own production capabilities and stockpiles in response, though exact quantities remain variably documented in declassified military records. In the and , major powers expanded mustard agent stockpiles amid fears of chemical escalation; the ramped up production at facilities like , storing sulfur mustard in munitions and bulk containers, while the maintained reserves of mustard alongside from World War I-era agents and captured German stocks post-1945. , despite treaty restrictions under the , covertly rebuilt chemical capabilities, including mustard, but refrained from battlefield deployment. Cold War-era stockpiles reached their peak, with the holding approximately 30,500 tons of total chemical agents by 1986, a significant portion comprising sulfur mustard stored at eight installations under containment policies to prevent leaks or degradation. The similarly amassed tens of thousands of tons of chemical weapons, including mustard, across multiple sites, with later declaring 39,967 metric tons of agents (encompassing mustard, mixtures, and nerve agents) upon joining the in 1997. These accumulations reflected deterrence doctrines, despite the 1925 Geneva Protocol's prohibition on use—though not possession—highlighting persistent gaps in international enforcement until the 1993 convention mandated destruction. Smaller-scale historical stockpiles included Canada's procurement of mustard quantities during for joint Allied programs, and post-war disposals such as the U.S. dumping of over 16,000 mustard-filled bombs (totaling hundreds of tons) off in the late 1940s. Non-state or rogue accumulations, like Iraq's pre-1991 mustard reserves inspected by UNSCOM, were limited compared to holdings but underscored proliferation risks outside major conflicts.

Destruction Efforts and Challenges

The (CWC), which entered into force on April 29, 1997, mandates the verifiable destruction of declared chemical weapons stockpiles, including sulfur mustard (mustard gas), by states parties, with initial deadlines requiring 45% destruction by 2007 and full elimination by 2012; these were repeatedly extended due to technical and logistical hurdles, culminating in a final global deadline of 2023. The Organisation for the Prohibition of Chemical Weapons (OPCW) oversees verification, having confirmed the destruction of over 72,304 metric tons of Category 1 agents worldwide by mid-2023, encompassing mustard gas munitions from stockpiles in the , , and other nations. Destruction methods for mustard gas primarily involve neutralization via —breaking it down into less toxic compounds like using water and catalysts—or high-temperature in specialized facilities, followed by treatment of effluents to prevent environmental release. In the United States, which declared approximately 28,600 metric tons of chemical agents including significant mustard gas holdings at sites like () and (), destruction efforts began in the under the Army's Assembled Chemical Weapons Assessment program, employing neutralization plants to process over 780,000 mustard-filled projectiles by June 2023. The final U.S. mustard agent munitions were destroyed on September 4, 2021, at Blue Grass, with overall stockpile elimination certified by the OPCW on July 7, 2023, after investing roughly $45 billion in facilities and safety protocols. Russia, declaring 39,967 metric tons of agents including mustard, , and nerve agents, initiated destruction at facilities like Shikhany and Kizner, claiming completion of its Category 1 stocks by September 2017 under OPCW verification, though earlier phases faced postponements from 2002 onward. Smaller programs, such as Libya's destruction of mustard-filled artillery shells by February 2014 amid post-conflict instability, highlighted accelerated efforts in non-superpower states. Destruction faced multifaceted challenges, including the chemical stability of mustard gas—a viscous, persistent that resists degradation and poses leakage risks during handling or transport of aging munitions, many produced decades earlier in corroded states. Technical difficulties encompassed scaling neutralization processes without incomplete reactions yielding toxic byproducts, necessitating redundant systems and on-site monitoring, while raised concerns over emissions and ash disposal. Environmental and public opposition delayed sites in both the U.S. (e.g., protests at ) and (e.g., resident fears at Chapayevsk), amplifying costs and timelines; Russia's program, for instance, encountered funding shortfalls and local resistance, contributing to missed interim targets. Logistical hurdles included securing supply chains for specialized equipment amid geopolitical tensions, with OPCW extensions granted 11 times for the U.S. and multiple for , underscoring the tension between urgency and irreversible verification. Non-stockpile legacies, such as recovered World War I-era mustard dumps in or U.S. , persist as ongoing remediation challenges beyond declared stockpiles.

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