Abstract
Inhalation of coal dust has been shown to produce pneumoconiosis and chronic obstructive bronchopneumopathy. The active compounds responsible for these diseases have not yet been identified. We postulate that coal dust induced lung injury could be related to exposures of coal workers to aerosols capable of producing reactive oxygen species (ROS) in the lung. In this study, we investigated whether coal dusts could produce ROS in aqueous medium and the biological significance of ROS production. We found that filtrates of coal dusts are capable of oxidizing formate anion in the presence of H2O2 or O2 and are able to suppress the elastase inhibitory activity of alpha-1-antitrypsin (α1-AT). To further confirm the role of FeSO4 in coal dust induced lung injury, we also examined the pulmonary response of guinea pigs exposed to coal dust or carbon black enriched with FeSO4. Guinea pigs (N = 6/group) were exposed to filtered air, 5 mg/m3 of pulverized Illinois #6 coal (COAL), FeSO4 enriched Illinois #6 coal (COAL+Fe, 5% FeSO4 · 7H2O by weight), Illinois #6 coal wetted in distilled deionized water (WETTED COAL), Illinois #6 coal washed twice with distilled deionized water (WASHED COAL), carbon black (CARBON), or FeSO4 enriched carbon (CARBON+Fe, 5% FeSO4 · 7H2O by weight) for 3 hours, and killed 24 hours after the end of the exposure. There was no change in lactate dehydrogenase activity in any of the exposure groups except in animals exposed to COAL. There was also no change in protein concentration of lavage fluid or the viability of lavage cells in all exposure conditions. In contrast, COAL+Fe induced a decrease in the phagocytic activities (-17.4%) of macrophages, while COAL itself had no effect. Similarly, CARBON has no effect on phagocytosis while CARBON+Fe significantly depressed phagocytosis (-22.5%). Influx of neutrophils only occurred in animals exposed to CARBON+Fe. The concentration of ROS in the macrophages of animals exposed to the COAL+Fe was significantly decreased by 30.8 percent while a significant increase of ROS (27.8%) was observed in animals exposed to CARBON+Fe. WETTED-COAL generally had similar effects as that of COAL+Fe while WASHED-COAL produced no change as compared to controls. These results clearly show that FeSO4 enrichment enhances the pulmonary response of guinea pigs to coal dust exposure.