Mustard gas (HD) was a widely used chemical warfare agent during World War I and more recently in the Iraq-Iran war (1980-1988). To date, dramatically, 45,000 Iranians are suffering from late respiratory complications due to MG exposure. This review covers two decades of researches on latent pulmonary effects of MG. Findings from clinical manifestations, pathologic examinations, laboratory data, lung function tests, and radiological evaluations are reviewed. From this review we are able to provide a suitable practical plan for workup and management of patients in this setting.

We conclude that about half of patients had diagnostic constrictive bronchiolitis, or bronchiolectasis and mucus stasis consistent with more proximal luminal compromise. The fact that there were no differences between the low- and high-dose groups suggests that effects of SM are not solely dependent on the severity of exposure. The results also indicate that the diagnosis of chronic lung disease due to SM may be difficult. Surgical lung biopsy may be helpful in difficult cases, as constrictive (obliterative) bronchiolitis can be present in symptomatic patients with normal PFTs and chest HRCT.

The marked difference in biopersistence and pathological response between chrysotile and amphibole asbestos has been well documented. This study is unique in that it has examined a commercial chrysotile product that was used as a joint compound. The pathological response was quantified in the lung and translocation of fibers to and pathological response in the pleural cavity determined. This paper presents the final results from the study. Rats were exposed by inhalation 6 h/day for 5 days to a well-defined fiber aerosol. Subgroups were examined through 1 year. The translocation to and pathological response in the pleura was examined by scanning electron microscopy and confocal microscopy (CM) using noninvasive methods.The number and size of fibers was quantified using transmission electron microscopy and CM. This is the first study to use such techniques to characterize fiber translocation to and the response of the pleural cavity. Amosite fibers were found to remain partly or fully imbedded in the interstitial space through 1 year and quickly produced granulomas (0 days) and interstitial fibrosis (28 days). Amosite fibers were observed penetrating the visceral pleural wall and were found on the parietal pleural within 7 days postexposure with a concomitant inflammatory response seen by 14 days. Pleural fibrin deposition, fibrosis, and adhesions were observed, similar to that reported in humans in response to amphibole asbestos. No cellular or inflammatory response was observed in the lung or the pleural cavity in response to the chrysotile and sanded particles (CSP) exposure. These results provide confirmation of the important differences between CSP and amphibole asbestos.

Sulfur mustard (2,2-dichlorodiethyl sulfide, SM) is one of the vesicant classes of chemical warfare agents that causes blistering in the skin and mucous membranes, where it can have lingering long-term effects for up to ten years (1). SM was employed extensively by the Iraqi army against not only Iranian soldiers but also civilians between 1983 and 1988, resulting in over 100,000 chemical casualties. Approximately 45,000 victims are still suffering from long-term effects of exposure (2,3). More than 90% of the patients exposed to SM exhibit various cutaneous lesions in the affected area. The human skin can absorb approximately 20% of the SM through exposure. Up to 70% of the chemical is concentrated in the epidermis and the remainder in the basement membrane and in the dermis (4).Sulfur mustard exists in different physical states. The liquid form of SM evaporates slowly in cold weather and can penetrate through the clothing, thereby increasing exposure. However, the gas form readily diffuses in the air and it can be inhaled, leading to systemic absorption. In addition, warm temperatures are ideal conditions that liquid SM present in the clothing of the exposed individual could be converted to gas form. SM-induced clinical cutaneous symptoms include itching and burning. Other clinical findings include erythema or painless sunburn, bulla, hypo- and hyper pigmentation in both exposed and unexposed areas (5,6) The mechanism and biochemical cascade of SM-induced cutaneous manifestations are not completely understood but several published pathways support many of the know facts. Our current understanding fails to explain the time interval between the acute chemical exposure and the late-onset and delayed tissue damage (7,8). The aim of this article is to review the acute and long-term cutaneous findings resulting from SM exposure. Also, cellular and molecular mechanism involved in SM-induced skin pathology have been discussed.

It would be very useful to have a more effective and more rapid method available for the treatment of cutaneous leishmaniasis (CL). The main aim of the present, Iranian study, was to see if the combination of cryotherapy and intralesional injections with meglumine antimoniate (C + MA) would be more effective than the injections given alone (MA) or the combination of cryotherapy plus intralesional sodium stibogluconate (C + SS). Forty patients (with 67 lesions) were treated with C + MA, another 40 (with 65 lesions) were treated with C + SS and 100 patients (with 180 lesions) were treated with MA. Follow-up for 6 months after the final treatment indicated that 89.5% of the lesions treated with C + MA, 92.3% of those treated with C + SS but only 50% of the lesions treated with MA only were completely cured. The frequencies of cure in the two cryotherapy groups were similar, both being significantly higher than that in the MA group (P < 0.05). The combination of cryotherapy with intralesional injections of meglumine antimoniate or sodium stibogluconate, which is much more effective than the use of intralesional meglumine antimoniate alone, should be promoted.