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0.10 percent (Miyaji, 1963). Comparable figures have been reported by other Japanese authors (Kitamura, 1954), although a study in Hiroshima, the site of a Japanese pre-WWII war gas factory, reported an incidence of 0.16 percent (Hosokawa, 1961). When the geographical distribution of skin cancers in Japan was examined, there was a greater incidence in southern and western Japan (including the prefecturate of Hiroshima), areas where the largest amount of annual sunlight is seen (Miyaji, 1963).

In a report on the British occupational experience, Easton and colleagues (1988) looked at mortality data from a World War II mustard gas manufacturing site in Cheshire, England. The observed number of deaths from skin cancer was zero, versus the expected number of two. The implication from this study is that there is a low or nonexistent death rate from skin cancer in this cohort of individuals, and certainly the death rate is lower than generally expected in a group of exposed workers. Indeed, the incidence of all expected diseases and deaths has been less in the British workers than in workers from other nations, a difference attributed to better worker protection measures in British war gas factories.

Battlefield Exposure

To date, there has been only a single report describing delayed toxic effects of sulfur mustard exposure during battlefield operations. Balali (1986), in a prospective study of delayed toxic effects, has followed a cohort of Iranian solders exposed to mustard gas during the Iran-Iraq war. After two years of observation, 41 percent of the exposed victims are experiencing pigmentary disorders. No other abnormalities have as yet surfaced.

Medical Therapeutic Exposure

For a number of years, Russian and Eastern European physicians have studied the effects of a topical preparation containing sulfur mustard 0.005 percent in petrolatum (psoriasin) on a hyperproliferative disease of the skin, psoriasis. The delivery of therapeutic dosages requires about 0.01 µg psoriasin/cm2 of skin. This amount results in inhibition of DNA synthesis sufficient to reduce basal cell replication, causing a return of the bulk of cells back to a state comparable to normal, yet the cells' ability to repair DNA cross-linking is not impaired. This dosage level is 10-100 times lower than that required to cause erythema in normal skin (Renshaw, 1946). Short-term (15 days) observation of patients treated with psoriasin reveals cutaneous hyperpigmentation like that seen after the application of nitrogen mustard to the skin,

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