Reduced granulocyte and other marrow-derived cells in the peripheral blood cause a diminished protective effect from polymorphonuclear leukocytes, macrophages, monocytes, and other cell types that are active in the destruction and scavenging of organisms that invade and impede healing of wounds.
Residual cutaneous lesions most often take the form of scars that result from uncontrolled fibroblastic activity and overgrowth of connective tissue during the process of wound repair. Even well cared for wounds over body sites and parts that are not easily immobilized, such as shoulders, knees, elbows, and male genitalia, often heal with severe residual scar formation. Pigmentation is often altered (either increased or decreased) at these sites, although the degree of alteration does not differ from that observed in injuries caused by burns and other forms of physical and chemical insult. In the absence of melanocyte destruction, hyperpigmentation will predominate. If melanocytes are locally destroyed, and inward migration from destroyed adnexal structures does not occur, depigmentation will predominate. Some previously injured sites have been described as "sensitive" to subsequent mechanical injury. These sites may show recurrent blisters after mild injury.
Skin tumors (basal cell, squamous cell, and Bowen's intraepidermal squamous cell cancer) and rapidly spreading skin ulcers that are resistant to therapy have been reported (Inada et al., 1978; Jackson and Adams, 1973; Klehr, 1984; Wada et al., 1963). To date, the number of cutaneous cancers reported subsequent to acute and chronic sulfur mustard exposure is low, and it is unclear whether some of these cutaneous cancers are related to the carcinogenic effects of sulfur mustard or are related to the presence of chronic skin ulcers (Jackson and Adams, 1973). The occurrence of skin cancers at the site of old scar formation is an acknowledged biological phenomenon (Novick et al., 1977; Treves and Pack, 1930). It appears that cutaneous cancers following acute sulfur mustard exposure usually localize in cutaneous scars, whereas those following chronic exposure can occur on any exposed site (Inada et al., 1978). Many questions remain unanswered in sulfur mustard human carcinogenicity. Some subjects who develop cutaneous cancers after chronic sulfur mustard exposure, particularly Bowen's disease, have had exposure to multiple potential cancer-causing agents, including Lewisite (Inada et al., 1978; Wada et al., 1963). Yet, Kravitz and McDonald (1978) have reported cutaneous cancer induction following chronic topical application of nitrogen mustard in the treatment of cutaneous T-cell lymphoma.
Long-term effects of sulfur mustard exposure have been most frequently described in people previously employed in the manufacture of