AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Mustard gas is one of several types of blister agents. Mustard gas is an agent used in war and is unlikely to be seen in typical civilian medical establishments. It has 2 basic forms: sulfur mustard (HD) and nitrogen mustard. Sulfur mustard, bis-(2-chloroethyl) sulfide, may be distilled or mixed with the sulfur impurities of the manufacturing process, also referred to as Levinstein mustard. HD may be combined with other vesicants, such as agent T or lewisite, to form the mixtures HT or HL, respectively.

Nitrogen mustard has been produced in 3 forms: (1) HN1, bis-(2-chloroethyl), ethylamine; (2) HN2, bis-(2-chloroethyl), methylamine; and (3) HN3, tris-(2-chloroethyl), amine.

Nitrogen mustards are similar to HD in their vesicant qualities, but they have slightly more severe systemic effects, particularly in the CNS. Unlike other vesicants such as lewisite or phosgene oxime, which cause immediate pain upon initial contact, mustards have a characteristic latent period of 1-24 hours between exposure and the onset of clinical signs and symptoms.

Gas warfare during the early years of World War I expanded rapidly as the combatants developed the ability to manufacture and deliver various toxic substances. These early agents were primarily inhalation hazards and were nonpersistent; therefore, early masking was a fully effective defense. Chemical agents such as chlorine and phosgene could not compete with conventional explosives because of the logistical complications involved in delivering a momentarily lethal quantity of chemical agents, which were affected by the weather and defensive measures.

Pathophysiology

Liquid mustard is somewhat heavier than water, although droplets may remain on the water surface. Its oiliness is reminiscent of motor oil, with brown coloration likely resulting from some impurities. A faint odor of mustard, similar to garlic or horseradish, may be noted.

Mustard is a fairly persistent chemical agent because of its low volatility (610 mg/m³ at 200°C). In cool weather, little vapor is present; however, evaporation of mustard increases as the temperature increases. For example, the persistency of mustard in sand decreases from 100 hours to 7 hours as the temperature rises from 100°C to 380°C (500°F to 1000°F). It may remain in an area for several months, particularly during periods of cool damp weather. Although heat increases the vapor hazard, rapid evaporation decreases the task of decontamination. Mustard is relatively insoluble in water; however, the high solubility of mustard in fats contributes to its rapid skin penetration.

Mustard vapor has a density 5.4-fold greater than that of air, causing it to hug the ground and sink into trenches and gullies. The freezing temperature for mustard is 57°F. This high freezing point makes mustard unsuitable for delivery by aircraft spraying or for winter dispersal. To lower the freezing point, mustard must be mixed with another substance.

Mechanism of action

HD is a vesicant, producing damage primarily to the skin, respiratory tract, and eyes. After a significant amount of mustard has been absorbed through the skin or has been inhaled, the hemopoietic system, gastrointestinal tract, and CNS may be affected.

The principal cause of injury is the alkylating effect of mustard. In the presence of a polar solvent (eg, water), the 2 side chains of HD cyclize and become biologically active. These 2 chains can attach to 2 other molecules and specifically bind to the guanine nitrogen in DNA strands, causing cross-linking and, eventually, cellular death. As expected, with the effect on DNA, cell lines with rapid turnover (eg, those in the bone marrow and gastrointestinal tract) are affected most by systemic uptake of mustard. Skin sensitization may occur; therefore, individuals with a previous mustard exposure may be affected to a greater degree on a second exposure. Mustard detoxifies in the human body at a slow rate; therefore, repeated small exposures may have a cumulative effect. This can be worsened further by a developing sensitivity.

The mustards, both sulfur and nitrogen, are alkylating agents that act through cyclization of an ethylene group to form a highly reactive sulfonium or ammonium electrophilic center. This reactive electrophile is capable of combining with any of the numerous nucleophilic sites present in the macromolecules of cells. The products of these reactions are stable adducts that can modify the normal function of the target macromolecule.

Because nucleophilic areas exist in peptides, proteins, RNA, DNA, and membrane components, researchers have tried to identify the critical biomolecular reactions leading to mustard injury, whether the initiating event is alkylation of DNA or modification of other cellular macromolecules. However, these steps would disrupt the epidermal-dermal junction. Once the site of tissue injury is established, the pathogenic process leading to formation of fully developed blisters must involve an active inflammatory response and altered fluid dynamics in the affected tissue. Mustard also has cholinergic action, stimulating both muscarinic and nicotinic receptors.

Frequency

United States

HD is stored extensively in projectiles, mortars, and ton containers at 7 sites. In addition, scattered, buried, or recovered chemical warfare materials with HD exist in mortars, projectiles, and 100- to 125-lb bombs. In the continental United States, both sulfur and nitrogen mustard may be found in small quantities within chemical agent identification sets. Potential exposures to mustard may occur during workplace operations involving the storage, recovery, or disposal of mustard materials or with accidental discoveries of materials.

International

The Germans first used mustard gas at Ypres, Belgium, on July 12, 1917. Mustard was particularly dangerous to troops because several hours must elapse before the individual detects a disabling or lethal dose. After the introduction of mustard gas, the warfare environment changed drastically. Since World War I, a number of isolated incidents have occurred in which mustard agent reportedly was used. In 1935, Italy probably used mustard against Ethiopia. Japan allegedly used mustard against the Chinese from 1937-1944. Egypt apparently used mustard in the 1960s against Yemen. More recently, the Iraqis used it against the Iranians and the Kurdish population in northern Iraq.¹ Mustard agent remains an important chemical warfare agent today.

Mortality/Morbidity

During World War I, mustard attacks frequently were conducted at night, and the liquid agent did not evaporate readily in the cool night air. However, several hours after daybreak, the sun-warmed air would cause the mustard to vaporize. By this time, thinking the danger from the attack was over, the soldiers removed their masks and fell victim to the evaporating mustard. This combination of events produced a significant number of casualties among the soldiers. Because of these nighttime shellings, it soon became standard policy to not unmask for many hours after daybreak.

• Historically, although the soldiers' hands were exposed readily, they were not affected as often as other areas of the body. In World War I, 75% of all eye and skin lesions were mild, commonly seen in areas of tight constrictive clothing or in moist body areas. The low rate of acute battlefield respiratory failure during World War I was attributable to the relatively low volatility of mustard in the colder European climate. Sudden death from inhalation exposure occurred when troops made indoor cooking fires with mustard-contaminated wood.
• Today, the maximum safe dose for mustard vapor is 5 mg/min/m³ for skin exposure and 2 mg/min/m³ for eye exposure. The threshold for olfactory detection of HD appears to be in the concentration range of 2-10 mg/m³. Despite a distinctive garliclike or horseradish smell, the odor threshold varies among exposed persons; therefore, odor cannot be used as an adequate warning measure. The workplace airborne exposure limit established by the US Surgeon General for HD is 0.003 mg/m³ as an 8-hour, time-weighted average.
• For skin exposure to liquid mustard, the lethal dose to 50% of the exposed population (LD₅₀) is approximately 100 mg/kg, or approximately 7 g for a person weighing 70 kg. This is approximately 1-1.5 teaspoons of liquid, an amount that will cover approximately 25% of the body surface area. An area of erythema, with or without blisters, caused by liquid mustard covering 25% or more of the skin suggests that the exposed recipient has received a lethal amount of mustard agent. For vesication to be observed, a 10-mg droplet is necessary.

CLINICAL

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History

Clinical Effects of Exposure to Mustard Agents

• Toxicity for liquid exposure
• • Conjunctival injection may occur following brief exposures (10-30 min) to low concentrations of vapor. This translates to a dose of 1-3 mg/min/m³.
  • With higher doses (50-100 mg/min/m³), conjunctivitis with grittiness under the eyelids, tearing, and photophobia may occur. Doses in excess of 200 mg/min/m³ may cause corneal edema, keratitis, and blepharospasm, leading to temporary blindness.
• The LD₅₀ for ingestion of mustard is estimated as 0.7 mg/kg.
• Mild skin erythema may be observed with doses of 50 mg/min/m³.
• Irritation of the nasal mucous membranes and hoarseness may be observed first at doses as low as 12 mg/min/m³.
• Lower airway effects, such as tracheobronchitis, tachypnea, cough, and bronchopneumonia, begin to occur with doses exceeding 200 mg/min/m³.
• Severe erythema followed by blistering may begin at concentration profiles exceeding 300 mg/min/m³.
• A warm humid environment may allow the development of erythema and vesication at lower doses with more rapid onset.

Physical

• General clinical effects
• • Mustard as a vapor or liquid fixes to the skin rapidly (within the first 2 min). Initially, no symptoms of pain, burning, or itching are present. This initial period may last up to 24 hours.
  • Depending on dose, the initial period is followed by erythema, burning, and itching. Nausea may occur during the latent period if a very high dose has been absorbed. Vesicles appear 2-12 hours after onset of erythema; this is dose-dependent and occurs much faster in warm environments.
• Clinical eye effects
• • With mild vapor exposures, conjunctivitis appears at 4-12 hours, with itching, burning, and photophobia. Edema of the eyelids with blepharospasm may render the patient functionally blind.
  • Moderate vapor exposures produce symptoms earlier (3-6 h). Severe conjunctivitis, blepharospasm, and lid edema occur. Iritis and corneal roughening (edema) also may be observed. Following moderately severe exposures, miosis may occur because of cholinergic effects.
  • Severe vapor exposures may produce symptoms within 1-3 hours. A severe inflammatory response with corneal damage, occasionally leading to corneal ulcer or anterior chamber perforation, is present. Liquid mustard exposures produce intense pain and severe progressive necrotic damage.
  • Recovery times following eye exposure depend on the degree of damage and any secondary infection that may occur. Blepharospasm begins to subside within 10 days. Photophobia typically persists for 2-6 weeks. Severe conjunctivitis or keratitis may take many weeks or months to resolve completely.
• Clinical respiratory effects
• • Respiratory effects of mustard result from vapor exposure, with onset time and intensity related to degree of exposure. Initial symptoms are inflammatory, with complaints referable to the areas of direct exposure. The primary airway lesion from mustard involves damage to respiratory mucosal lining, bronchi, and larger bronchioles. This damage begins in the upper airways and descends to the lower airways in a dose-dependent manner. Usually, the terminal airways and alveoli are affected only as a terminal event.
  • Mild exposures may manifest 24-36 hours after exposure, with sneezing, sinus discomfort, hoarseness, and mild cough. A chemical pneumonia may ensue, with an increase in WBC count, mild fever, and pulmonary infiltrates. Bronchospasm may be induced in up to 15% of an exposed population; wheezing respiration should be considered an asthma equivalent. Moderate exposures have a more rapid onset, with tense cough and dyspnea. Epistaxis may be noted. These symptoms become evident within 12-24 hours.
• Other respiratory effects
• • One other particular concern is signs and symptoms of laryngeal involvement. Approximately 2-4 days later, signs of bacterial infection may occur, including a higher WBC count and a shift in the differential with new infiltrates and a change in sputum production. If an exposure is in the moderate-to-severe range, then the symptoms may appear within 2-12 hours. Affected individuals with a severe exposure usually die within the first 3-4 hours if no additional supportive care is taken, such as respiratory support.
  • Severe dyspnea with hemoptysis and subsequent pseudomembrane formation may be present. Those individuals who do not die immediately are likely to develop secondary infections. Secondary bacterial infections occur in up to 50% of mustard-related respiratory injuries. Typically, these infections occur at 48-96 hours. They are more likely to occur in individuals who have been severely exposed.
• Systemic poisoning
• • Occasionally, CNS effects such as fatigue, depression, anxiety, and agitation are observed.
  • Distinguishing between CNS effects caused by mustard exposure and posttraumatic stress syndrome is difficult.
• Gastrointestinal system
• • Gastrointestinal effects of intense mustard exposures include nausea and vomiting. Further effects may occur from mustard ingested in contaminated water or tracheal secretions.
  • Nausea and vomiting are common within the first few hours after mustard exposure, beginning at approximately the same time the initial lesions become apparent. Early nausea and vomiting, which generally are transient and not severe, may be caused by the cholinergic activity of mustard, by a general reaction to injury, or by the unpleasant odor.
  • Nausea and vomiting occurring days later probably are caused by the generalized cytotoxic activity of mustard and damage to the mucosa of the gastrointestinal tract.
• Hematopoietic effects
• • As an alkylating agent, HD may have potent bone marrow effects. Initial leukocytosis is followed by progressive effects on rapidly proliferating cells of the hematologic system. Leukopenia begins to appear at 3-5 days postexposure, with the WBC count approaching zero in 7-10 days.
  • For individuals who have been severely exposed, systemic absorption of mustard may be sufficient to create a profound leukopenia with associated sepsis, pneumonitis, and death. A leukopenia of less than 200 WBCs/mm³ is a bad prognostic sign. Death from pneumonia can occur at 8-10 days.
• Chronic health effects
• • The International Agency for Research on Cancer considers epidemiological evidence sufficient to establish HD as a human carcinogen. HD has been shown to inhibit DNA synthesis and induce mutations and chromosome aberrations in a number of in vitro systems.
  • Human epidemiological evidence also indicates a causal relationship between exposure to high concentrations of mustard and the development of ocular diseases (eg, delayed recurrent keratitis) and chronic nonreversible respiratory disorders (eg, chronic bronchitis, asthma).

DIFFERENTIALS

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Other Problems to be Considered

Delayed hypersensitivity (type IV) contact dermatitis
Contact irritation
Contact urticaria syndrome

WORKUP

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Lab Studies

• Diagnosis
• • The differential diagnosis of mustard agent is not difficult. The history of a chemical exposure is useful, particularly if the chemical agent is known.
  • Questioning the patient about when the pain started and whether it started immediately after the exposure or hours later is very helpful. Immediate pain is not consistent with mustard exposure unless the mucus membrane is involved.
  • For mild skin reactions, ruling out other disorders in the differential diagnosis, such as delayed hypersensitivity (type IV) contact dermatitis, contact irritation, and contact urticaria syndrome, is important.
• Confirmatory tests
• • Tests such as the urinary thiodiglycol assay for HD may be helpful if results are positive. This assay may be nondiagnostic for very mild exposures.
  • Mustard is hydrolyzed and metabolized to thiodiglycol in the body and excreted in the urine. The collection of 24-hour urine samples for 1 day following exposure allows the clinician to quantify the amount of thiodiglycol and excretion kinetics. Generally, urinary thiodiglycol excretion peaks 48-72 hours after exposure, with a first-order half-life of elimination of 1-15 days. This assay is very specific for HD.

Histologic Findings

Skin sloughing (Nikolsky sign) may occur. Coagulation necrosis of the dermis with a complete absence of epidermis may occur. The epidermis surrounding the hair follicle frequently is involved. Regeneration of the epidermis typically begins at the hair follicle.

TREATMENT

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Medical Care

• Decontamination
• • Decontamination of a mustard exposure should be completed within the first 2 minutes. Bleach is an excellent detoxifying compound for several agents, including mustard (common household bleach is 5%). The recommended strength for decontamination is 0.5% for skin wounds. To decontaminate equipment and clothing, 5% bleach may be used. This is followed by a thorough water rinse or irrigation with soap and water.
  • Mustard is not detoxified by water alone and will remain in the effluent as an active contaminant.
  • Scrubbing exposed skin with a scrub brush can worsen skin damage.
  • If any mustard remains on the skin, late decontamination may prevent its spread to other areas of the skin, and it will prevent mustard from spreading to personnel who have contact with patients.
  • By the time a skin lesion has developed, most of the mustard already will have been absorbed, and, unless the site was occluded, the remaining unabsorbed agent will have evaporated.
  • Mustard droplets disappear from the surface of the eye very quickly; therefore, late flushing of the eye is of no major benefit.
• Treatment of skin lesions
• • Skin lesion recovery is slow. The promotion of skin healing is accomplished primarily through debridement and good aseptic technique.
  • Treatment for itching and pain is symptomatic and generally involves the use of analgesics and antihistamines.
• Treatment of blisters
• • If the blister is about to rupture, use good aseptic technique to drain the blister and cover it lightly. Small blisters in noncritical areas should be left intact.
  • The blister fluid is not a vesicant.
• Volume replacement: Unlike thermal burns, chemical burns do not require massive fluid replacement. Do not overhydrate.
• Treatment of erythema
• • Erythema may appear as early as 2 minutes or as late as 24-48 hours after exposure, depending on the intensity of exposure.
  • Decontamination, if not already completed, should be initiated. This removes the risk of exposure to other individuals and precludes secondary contamination.
  • For mild erythema, usually no treatment is needed. Erythema is much like sunburn, and the recovery time is approximately the same. The objective is to prevent secondary infection.
• Eye lesion treatment
• • Mustard fixes within the first 2 minutes after exposure. Irrigation with saline during this time is very important. Aggressive attempts to pry apart severely painful blepharospastic eyelids to accomplish irrigation are of questionable value and may create unnecessary physical and emotional trauma.
  • Eye treatment consists of at least 1 daily irrigation, preferably more. Administration of a topical antibiotic 3-4 times daily is recommended to assist in removal of inflammatory debris. Administer a topical mydriatic (eg, atropine, homatropine) as needed to keep the pupil dilated to prevent synechiae formation. Vaseline or a similar material should be applied to the eyelid edges to prevent them from adhering to each other; this reduces later scarring and keeps a path open for possible infection to drain.
  • Control pain with systemic analgesics. Topical analgesics may be used for the initial examination; however, they should not be used routinely because they might cause corneal damage.
  • The benefit of topical steroids is unknown; however, some ophthalmologists feel that topical steroids may be helpful if used within the first 48 hours after the exposure (but not afterward). Consult an ophthalmologist as early as possible regarding this and other questions of eye care.
  • Usually, transient loss of vision is the result of edema of the lids and other structures and is not caused by corneal damage.
  • Keeping the patient in a dim room or providing sunglasses reduces the discomfort from photophobia.
  • Recovery may occur within days for milder injuries, while those with severe damage will take approximately a month or longer to recover.
• Treatment of respiratory tract injury
• • The first priority is to ensure and establish a patent airway and to manage the airway appropriately.
  • Laryngospasm and vocal cord edema should be suspected whenever respiratory stridor or hoarseness is present. Under these circumstances, examination of the vocal cords may be appropriate, followed potentially by endotracheal intubation.
  • Oxygen supplementation may be necessary for prolonged periods. This primarily depends on the intensity of mustard exposure and the presence of any underlying pulmonary disorder.
  • Hypercarbia may result from a previously unrecognized hyperreactive airway state or from abnormal central sensitivity to carbon dioxide complicated by increased work of respiration. This state may result from bronchospasm.
  • The therapeutic goal for patients with mild airway effects, such as irritation of the throat or nonproductive cough, is to keep them comfortable. For patients with severe effects, the goal is to maintain adequate oxygenation.
  • Antitussives are helpful for persistent, severe, nonproductive cough. Steam inhalation also may be useful for symptomatic relief. Consider steroids if a prior history of asthma or hyperreactive airways disease is determined. Initially, bronchitis resulting from mustard exposure is nonbacterial.
  • Take care when hydrating patients with significant body surface area skin burns. Overhydration of these patients may result in third spacing of fluids within damaged lungs and may worsen a ventilation-perfusion mismatch. Ventilatory support may be necessary to assist adequate carbon dioxide clearance. The use of certain antibiotic skin creams (eg, mafenide acetate) to treat skin lesions may complicate the acid-base status of the individual by inducing a metabolic acidosis.
  • Hypoxia is generally secondary to abnormalities in the ventilation-perfusion ratio caused by toxic bronchitis. Mucosal sloughing further complicates this abnormality.
  • Underlying irritable airways disease (hyperreactive airways) is triggered easily; consequently, therapy with bronchodilators may be necessary. Individuals with hyperreactive airways may benefit from steroid treatment with careful attention to the added risk of superinfection. WBC count elevation, fever, pulmonary infiltrates observed on a chest radiograph, and colored sputum may be present. Careful assessment of sputum through Gram stain and culture demonstrates that bacterial superinfection typically is not present during the first 3-4 days. Antibiotic therapy should be withheld until the identity of a specific organism becomes available.
  • Of particular importance is the patient's immune status, which may be compromised by a progressive leukopenia beginning approximately on day 4-5. Development of leukopenia signals severe immune system dysfunction; massive medical support may be necessary for these patients. In these instances, sepsis typically supervenes, and despite combination antibiotic therapy, death can occur.
  • Intubate patients with severe pulmonary signs early, before laryngeal spasm makes intubation difficult or impossible. Intubation assists in ventilation and allows suction of necrotic and inflammatory debris. Bronchoscopy may be necessary to remove intact pseudomembranes or fragments of pseudomembranes. Early use of positive end-expiratory pressure or continuous positive airway pressure may be beneficial. The need for continuous ventilatory support suggests a bad prognosis.
  • Patients with severe airway lesions may later have postrecovery scarring and stenosis, which predisposes the individual to bronchiectasis and recurrent pneumonia.

Surgical Care

Consultation to plastic surgery or dermatology may be necessary for some skin lesions.

Consultations

Consultation to critical care internist is necessary with respiratory exposure.

MEDICATION

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Treatment is supportive, and the patient may require supplemental oxygen or, potentially, ventilatory support. Use of analgesics for pain may be recommended, as necessary. Various anti-inflammatory and sulfhydryl-scavenging agents (eg, vitamin E, promethazine, sodium thiosulfate) have been suggested as possible therapeutic drugs. Some animal studies suggest the value of these agents for prophylactic therapy or as adjunct therapy immediately after a mustard exposure; however, no data support their use after lesions develop. Activated charcoal, administered orally, has been administered with unknown results, although it may provide some benefit if given immediately after mustard is ingested.

FOLLOW-UP

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Further Inpatient Care

If a terrorist action occurs and a mustard agent is involved in a civilian area, further follow-up with occupational medicine or pulmonary medicine is necessary.

Further Outpatient Care

No traditional outpatient care exists because exposure to HD tends to be a battlefield problem and any severe exposure may be lethal.

Transfer

If respiratory symptoms worsen or progress, transfer the patient to an ICU, if available.

Prognosis

• Long-term effects
• • Individuals who survive an acute single mustard exposure with few or no systemic or infectious complications appear to recover fully.
  • Mustard burns may leave areas of hypopigmentation or hyperpigmentation, sometimes with scarring.
  • Diseases such as previous cardiopulmonary disorders, severe or inadequately treated bronchitis or pneumonitis, a history of smoking, and advanced age all appear to contribute to development of long-term chronic bronchitis.
• Death
• • Patients who die from exposure die of massive pulmonary damage complicated by infection and sepsis resulting from loss of the immune mechanism.
  • If mustard exposure is not by inhalation, the mechanism of death is less clear. In studies with animals in which mustard was administered via routes other than inhalation, the animals died 3-7 days after the exposure. Those tested had no signs of pulmonary damage and often had no signs of sepsis. The mechanism of death was not clear, but autopsy findings resembled those observed after radiation exposure.
  • Mustard is considered a radiomimetic because it causes tissue damage similar to that observed after radiation exposure.

Patient Education

• For excellent patient education resources, visit eMedicine's Bioterrorism and Warfare Center. Also, see eMedicine's patient education articles Chemical Warfare and Personal Protective Equipment.

MISCELLANEOUS

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Medical/Legal Pitfalls

Failure to make the diagnosis is one medicolegal pitfall.

MULTIMEDIA

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Media file 1:  Chemical terrorism agents and syndromes, signs and symptoms. Chart courtesy of North Carolina Statewide Program for Infection Control and Epidemiology (SPICE), copyright University of North Carolina at Chapel Hill, www.unc.edu/depts/spice/chemical.html.
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REFERENCES

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1. Benschop HP, van der Schans GP, Noort D, Fidder A, Mars-Groenendijk RH, de Jong LP. Verification of exposure to sulfur mustard in two casualties of the Iran-Iraq conflict. J Anal Toxicol. Jul-Aug 1997;21(4):249-51. [Medline].
2. Dacre JC, Goldman M. Toxicology and pharmacology of the chemical warfare agent sulfur mustard. Pharmacol Rev. Jun 1996;48(2):289-326. [Medline].
3. Momeni AZ, Aminjavaheri M. Skin manifestations of mustard gas in a group of 14 children and teenagers: a clinical study. Int J Dermatol. Mar 1994;33(3):184-7. [Medline].
4. Ruhl CM, Park SJ, Danisa O, Morgan RF, Papirmeister B, Sidell FR, et al. A serious skin sulfur mustard burn from an artillery shell. J Emerg Med. Mar-Apr 1994;12(2):159-66. [Medline].
5. Sidell FR, Takafuji ET, Franz DR. Textbook of Military Medicine, Medical Aspects of Chemical and Biologic Warfare Part 1. Office of the Surgeon General; Washington, DC:. TMM Publications; Borden Institute Walter Reed;1997. [Full Text].
6. Smith KJ, Casillas R, Graham J, Skelton HG, Stemler F, Hackley BE Jr. Histopathologic features seen with different animal models following cutaneous sulfur mustard exposure. J Dermatol Sci. Feb 1997;14(2):126-35. [Medline].
7. Solberg Y, Alcalay M, Belkin M. Ocular injury by mustard gas. Surv Ophthalmol. May-Jun 1997;41(6):461-6. [Medline].
8. US Army. Toxic Chemical Training Course Manual for Medical Support Personnel. SAIC. 1999.
9. Vena GA, Foti C, Grandolfo M, Angelini G. Contact irritation associated with airborne contact irritation from mustard gas. Contact Dermatitis. Aug 1994;31(2):130-1. [Medline].

Article Last Updated: Mar 23, 2008