Mustard burns

It has been shown in an experimental guinea pig model that CuZnSOD and MnSOD are effective in treatment of mustard gas burns. Mustard gas, used as a warfare since World War I, causes blistering lesions that are slow to heal, and secondary inflammation. There is no antidote for burns by mustard gas. SODs were foimd to effectively reduce the burn lesion area when administered in-traperitoneally/intralesionally [260]. 

Inhalation and dermal absorption mustards no antidote. For lewisite and ewisite/ mustard lmixtures British Anti-Lewisite (BAL or Dimercaprol) IM (rarely available). Thermal burn therapy supportive care (respiratory support and eye care). 

Blister agents, which cause burns on the skin such as sulfur mustard gas, l,l -thiobis[2-chloroethane] (HD), and lewisite, (2-chloroethenyl) arsenous dichloride (L). 

Human toxicity values have not been established or have not been published. However, it can cause burns of the skin and eyes similar to those from Sulfur mustard (C03-A001), but it does not liberate chlorine or acid. 

The hazard of a mixture of mustard and Lewisite (HL) on the eyes and skin, or vapor in the eyes or respiratory tract, is immediate. Within an hour, edema of the conjunctivae and lids begin and soon results in eye closure. Any casualty experiences serious pain seconds after contact with HL liquid, but such extreme pain makes the injured person decontaminate at once. Rapid decontamination is the sole manner to avoid severe burns since after a few minutes of contact with a mixture of mustard and Lewisite, the upper layer of skin will die and appear gray, painful erythema will be apparent shortly thereafter, and... 

Dermal (skin) contact with sulfur mustard agents causes erythema and lesions (blistering), while contact with vapor may result in first and second degree burns contact with liquid typically produces second and third degree chemical burns. Any burn area covering 25 percent or more of the body surface area may be fatal. Respiratory contact is a dose-related factor in the sense that inflammatory reactions in the upper and lower airway begin to develop several hours after exposure and progress over several days. 

The only agent in this category is distilled mustard (HD). Two other mustard agents (Q and T) developed in the past were dropped from production because they were redundant or were superseded by newer agents. Mustards got their name from their unique smell that resembles burning garlic. Personnel exposed to mustards should be decontaminated immediately and given medical attention. 

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

Toxicology. Nitrogen mustards are vesicants and alkylating agents that damage the respiratory airways and cause skin and eye burns. 

Jackson and Adams studied 33 cases of extensive basal cell carcinoma, two of which involved mustard-gas burns sustained during World War I. One of those developed 35 yr after the burn, but 2 yr after irradiation with cobalt-60. In the other, basal cell carcinoma developed at the site of three separate burns, 3 yr after exposure. Some of the mustard burns did not lead to basal cell cancer. 

Eventually, Buscher experimented on human volunteers. Like Cullumbine, he found that, when a drop of H is placed on skin, the initial reaction appears in about 2 h. Vesication begins in about 24 h, but healing does not begin until after about 4 wk, and later for severe burns. Buscher wrote "There are also irreparable, permanent injuries.. . . Cicatricial contractures are very frequent sequelae.. . . Following severe wounds this scarring is very extensive so that there can be no question of complete recovery." In all cases of extensive burns from mustard gas, careful and extended treatment is required to prevent infection and other complications. 

Scholz and Woods reviewed 136 cases of mustard injuries of the eye, including the 84 described by Mann. They found no essential difference between "chronic" and "recurring" cases. Although a number of injured men retained "fair visual acuity" after the initial burn, vision degenerated later the average loss of vision (excluding five minor injuries) was about 88%. The only effective treatment for these patients was contact lenses. 

In discussing the effect of mustard on the intestinal tract, Cullumbine pointed out that severely poisoned men suffered loss of water and electrolytes because of vomiting, diarrhea, and vesication. Oligemia and irreversible circulatory failure follow, much as in thermal burns. He showed the importance of the loss of water and electrolytes by experiments in which the mortality rate of poisoned rats and rabbits was greatly reduced by the administration of physiologic saline solution either by mouth or by injection. 

Atkinson, W.S. Delayed keratitis due to mustard gas (dichloro-diethyl sulfide burns). Arch. Ophthalmol. 40 291-301, 1948. 

Hughes, W.F. Importance of mustard burns of the eye as judged by WW I statistics and recent accidents. IN National Research Council, Division of Medical Sciences, Committee on Treatment of Gas Casualties. Fasciculus on Chemical Warfare Medicine, Volume I Eye. Prepared for the Committee on Medical Research of the Office of Scientific Research and Development. 

Mustard gas A World War 1 weapon causing skin blisters and lung burns. 

In one of the final Allied chemical assaults of the First World War the British fired mustard gas into German positions at Wervick in Belgium. One of the injured was a corporal by the name of Adolf Hitler who was evacuated back to Germany burned and temporarily blinded. As a result of that experience, Hitler developed a distaste for the use of poison gas on the battlefield. The experience of this German corporal would, in turn, shape the events of another world war 20 years later. 

The first definitive studies were performed in Britain during World War II by Charlotte Auerbach.19 After the observation that injuries from war gases resembled x-ray burns, Auerbach demonstrated unequivocally that mustard gas induced sex-linked recessive lethal mutations in Drosophila. At about the same time, I. A. Rapoport361 independently reported that several other chemicals induced gene mutations and chromosomal aberrations. Their work ushered in the era of chemical studies of mutation, and within a few years a large number of chemical mutagens had been identified. 

Others were honored guests. Charlotte Auerbach suffered serious burns and rashes from the mustard compounds she used in her mutagenesis experiments in the 1940s (Beale 1993). 

The subjects tested with irritants and vesicants, including those who developed skin burns from mustard gas, reported no increased prevalence of significant skin cancer or other adverse health effects. 

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