BRIDGING THE GAP – AN INTERDISCIPLINARY APPROACH FOR DETERMINING THE CAUSE OF COAL WORKERS' PNEUMOCONIOSIS
Research into mineral-induced pathogenesis has been predominately performed by geoscientists and biomedical researchers, using different approaches. Geoscientists have focused on the role of mineral structure and composition. Most reactivity studies have been largely conducted in water, although more recent geochemical studies have started to use simulated bodily fluids (SBF). Conversely, biomedical researchers, concerned with the end result of pathogenesis, use cell lines and animal models to evaluate toxicity. Many of these studies use poorly characterized materials. Better coordination and collaboration between geological and biomedical researchers has the potential to advance our understanding of the effects of earth materials on health. In this study, we used an interdisciplinary approach to better understand what controls the toxicity of coal.
Epidemiologic studies show a correlation between the concentration of bioavailable iron (BAI) in coal and the development of Coal Workers’ Pneumoconiosis (CWP). The BAI in coal is predominately pyrite, a well-known ROS generator. Previous studies in our laboratory using NIST coal samples indicate that coal containing higher concentrations of pyrite generate more ROS in water. Another study indicates a nearly threefold initial accumulation of hydrogen peroxide in pyrite oxidation experiments performed in SBF versus water. Here we report on the inflammatory response of lung epithelial cells to exposure to coal with known pyrite content, which represents a new tool available to geochemists interested in assessing the inflammatory stress induced by the inhalation of earth materials. Preliminary results show greater cellular ROS up-regulation from coals containing pyrite than those without.