mustard vapors have not been well studied, but could be involved in cases of chronic exposures to sulfur mustard (Morgenstern et al., 1947; Papirmeister et al., 1991).
Infection of the respiratory tract resulting in bronchopneumonia is a common complication of respiratory tract injury from inhaled sulfur mustard. It appears that most deaths following inhalation of sulfur mustard result, at least in part, from pulmonary infection, often complicated by septicemia (Hosseini et al., 1989; Keshmiri, 1989; Papirmeister et al., 1991; Willems, 1989). Immunosuppression from systemic absorption of sulfur mustard probably plays a major role in the pathogenesis of these infections, although its importance relative to the local pulmonary injury is not well understood. Pulmonary infection and septicemia, despite modern antibiotic therapy, were still significant causes of death in Iranians taken to Europe for treatment (Willems, 1989).
The above descriptions of the acute effects come primarily from humans who died following World War I (WWI) gas attacks and from animals that died as a result of experimentally induced lesions (Papirmeister et al., 1991). There is little contemporary information regarding the pathogenesis of the respiratory lesions or few data from people or animals exposed to nonlethal concentrations of sulfur mustard vapor. There are even fewer studies in which the histopathology of the recovery process has been studied in animals exposed to sulfur mustard. However, two studies conducted during WWI suggest that low-level exposure or survivable exposures in dogs and rabbits may produce scar tissue following small ulcerations in the trachea and larynx, causing contractions of these areas (Warthin and Weller, 1919; Winternitz, 1919). Nevertheless, the descriptions of the more severe lesions of the respiratory tract of animals exposed to sulfur mustard vapor and those in humans appear to be quite similar in type and location (Papirmeister et al., 1991). Thus, further studies in animals conducted to follow the repair of the acute respiratory tract lesions from nonlethal, inhaled sulfur mustard vapor would be of value in determining the persistence and course of such lesions in people. However, it has been difficult to induce a chronic bronchitis that persists following cessation of exposure in animals (Greene et al., 1984).
The acute effects of inhaled Lewisite vapors are similar to those discussed above for inhaled sulfur mustard vapor. A major exception is that the irritating effect of Lewisite is immediately detectable by the exposed person. Data on the histopathological lesions in the respiratory tract from inhaled Lewisite are available only from animals, but the reported lesions are generally very similar to those discussed above for sulfur mustard. However, at high concentrations, Lewisite-induced pulmonary edema appears to be more prominent than with sulfur mustard. Hemoconcentration, presumably due to this pulmonary