Krumbhaar (1919a,b) observed that among the first changes in the circulating blood of patients exposed to sulfur mustard was an exhaustion of leukocyte-forming centers. This downward trend in leukocyte count ultimately leads to severe leukopenia. Thus the leukocyte counts in four fatal cases were observed to fall steadily from (1) 10,200 to 2,900; (2) 17,800 to 3,200; (3) 20,400 to 7,600; and (4) 36,000 to 14,000/mm3. Postmortem examination of the femoral bone marrow revealed only a slight mottling, shown histologically to be due to primordial cells and megablasts with a greater or lesser disappearance of normoblast, myelocytes, and adult forms. This was interpreted as an inadequate attempt at blood regeneration, and the resulting lack of leukocytes in the bloodstream suggested a weakening of the immune system. Even in bronchopneumonia that frequently supervenes in heavily gassed patients, little or no reactive rise in leukocyte count was observed.
In another study, the femoral bone marrow in 55 of 75 autopsies of mustard gas-exposed patients was examined (Krumbhaar and Krumbhaar, 1919). The results: 14 marrows were classified as showing almost no regenerative potential; 8 showed only slight reaction; and only 13 showed moderate reaction. In no case was the marrow as hyperplastic as in ordinary lobar pneumonia or acute infections accompanied by leukopenia. The authors concluded that
the blood and bone marrow changes are due to direct action of the poison and not the secondary infections (1) because they have been found well marked in cases where infection was slight or absent; (2) because influenza, typhoid, malaria, and such leucopenia infections played no part in these cases; and (3) because the kind of infection found to be present (pyogenic) does not lead to leucopenia or impaired bone marrow function.
In 1946, Anslow and Houck reviewed classified literature concerning the pharmacological action of sulfur and nitrogen mustard. They reported that evidence from soldiers gassed or burned in World War I was essentially the same as seen in experimental animals. Marked leukopenia and loss of reactivity of the bone marrow were observed in severe cases of mustard intoxication. In mask volunteers, sublethally exposed to sulfur mustard under temperate or tropical climate conditions, there was a moderate to marked leukocytosis appearing as early as four hours after exposure. This was followed by a moderate reduction in the number of leukocytes in the blood.
Another set of clinical observations comes from reports on over 600 sulfur mustard casualties following the release of sulfur mustard in Bari harbor, Italy, in December 1943 (Alexander, 1947). The effects upon the leukocytes in the circulating blood were most severe: white