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Late pulmonary pathology following sulfur mustard inhalation in the guinea pig model

TitleLate pulmonary pathology following sulfur mustard inhalation in the guinea pig model
Publication TypeConference Proceedings
Year of Conference2008
AuthorsDachir S., Kadar T., Rabinovitz Y., Cohen M., Cohen L., Sahar R., Amir A., Allon N.
Conference NameProceedings of the U.S. Army Medical Defense Bioscience Review
Volume1, A143
Conference LocationHunt Valley, MD

The impact of sulfur mustard (SM) inhalation on the respiratory system is one of the most complicated clinical problems that result from SM vapor inhalation. Reports from the Iran-Iraq war indicate that about 90% of casualties exposed to SM vapor developed pulmonary injury and suffered long-term respiratory complications such as chronic bronchitis, bronchiectasis, asthma, and interstitial fibrosis. These data are based on 16-20 years of clinical followup of Iranian casualties exposed to SM vapor. The purpose of the present study was to characterize the acute and late effects of SM inhalation on the respiratory system and to evaluate the association between those two phases. Guinea pigs were exposed, head only, to 5%-10% of the lethal concentration (LCt5-10) of SM vapor for 10 minutes. Respiratory, clinical, and histopathological changes were monitored for up to 4 months after exposure. SM inhalation resulted in decreased minute volume and respiratory rate, followed by severe pulmonary edema and inflammation, reduction in O2 diffusion, rhinorrhea, dyspnea, and death. Peak clinical effects were observed at approximately 6 hours postexposure, as expressed by lung edema and shortness of breath. At 48 hours, a significant increase in neutrophil and red blood cell counts and in protein concentration was detected in bronchoalveolar lavage. At the same time, typical histological damage was observed in lungs and trachea, characterized by obstruction of alveoli, infiltration of inflammatory cells into the alveoli, and damage of the tracheal epithelium as expressed by reduction in the number of goblet cells and cilia. Within 2 weeks postexposure, animals seemed to recover spontaneously. However, despite the apparent clinical healing, at 3 months after exposure about 20% of the guinea pigs developed respiratory complications that, in some cases, resulted in delayed death. Similarly severe histological damage was observed in the lungs and trachea. Furthermore, a positive relationship was found between the severity of early and late clinical scores. Thus, finding a treatment that will ameliorate the acute injury and eventually prevent the delayed pathology associated with SM poisoning is of great importance.

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