EVIDENCE FOR THE ROLE OF PYRITE IN COAL WORKERS’ PNEUMOCONIOSIS PATHOGENESIS – ACELLULAR AND CELLULAR IN VITRO STUDIES

Despite decades of research, the etiology of coal workers’ pneumoconiosis (CWP) remains unclear. However, a recent epidemiologic study shows a correlation between the amount of bioavailable iron in the coal and the prevalence of CWP in miners. The mineral pyrite (FeS­₂), the major source of the iron in coal, is a Fenton chemistry catalyst. Pyrite dispersed in water generates reactive oxygen species (ROS) via the incomplete reduction of O₂. While ROS are vital to the normal functioning of the immune system in the human body, a foreign material entering the system can disrupt the highly regulated balance between pro- and anti-oxidants, especially if the material itself generates ROS.

In this study, the role of pyrite in CWP pathogenesis is experimentally tested using an array of complementary acellular and cellular in vitro techniques. The acellular oxidative dissolution experiments performed on pyrite demonstrate the ability of pyrite to generate ROS under biologically applicable conditions. Furthermore, pyrite’s relatively short biopersistence helps explain why no pyrite is found in the autopsied lungs of these deceased miners, despite exposure to coal with high pyritic-sulfur contents. The cellular inflammatory stress response (ISR) of A549 human lung epithelial cells, defined as the cellular upregulation of ROS (indicator of future apoptosis) normalized by cellular viability (necrosis), is a gauge of particle toxicity. Pyrites ability to generate an ISR more than a factor of 300 greater than inert glass beads demonstrates its highly oxidizing nature. Cells challenged with natural coal samples containing variable pyritic-sulfur contents demonstrate a general upwards trend in ISR values with increasing pyritic-sulfur contents. However, due to the complexity of the natural coal samples, the increase in ISR was not linear with increasing pyritic-sulfur content.