Abstract
BackgroundThe harmful effects from inhalation of coal dust are well-documented. The prevalence of lung disease varies by mining region and may, in part, be related to regional differences in the bioavailable iron content of the coal. Pyrite (FeS2), a common inorganic component in coal, has been shown to spontaneously form reactive oxygen species (ROS) (i.e., hydrogen peroxide and hydroxyl radicals) and degrade nucleic acids. This raises the question regarding the potential for similar reactivity from coal that contains pyrite. Experiments were performed to specifically evaluate the role of pyrite in coal dust reactivity. Coal samples containing various amounts of FeS2 were compared for differences in their generation of ROS and degradation of RNA.ResultsCoals that contain iron also show the presence of FeS2, generate ROS and degrade RNA. Coal samples that do not contain pyrite do not produce ROS nor degrade RNA. The concentration of generated ROS and degradation rate of RNA both increase with greater FeS2 content in the coals.ConclusionThe prevalence of coal workers' pneumoconiosis can be correlated to the amount of FeS2 in the coals. Considering the harmful effects of generation of ROS by inhaled particles, the results presented here show a possible mechanism whereby coal samples may contribute to CWP. This suggests that the toxicity of coal may be explained, in part, by the presence of FeS2.
Highlights
The harmful effects from inhalation of coal dust are well-documented
The prevalence of coal workers' pneumoconiosis can be correlated to the amount of FeS2 in the coals
Considering the harmful effects of generation of reactive oxygen species (ROS) by inhaled particles, the results presented here show a possible mechanism whereby coal samples may contribute to coal workers' pneumoconiosis (CWP)
Summary
The harmful effects from inhalation of coal dust are well-documented. The prevalence of lung disease varies by mining region and may, in part, be related to regional differences in the bioavailable iron content of the coal. Pyrite (FeS2), a common inorganic component in coal, has been shown to spontaneously form reactive oxygen species (ROS) (i.e., hydrogen peroxide and hydroxyl radicals) and degrade nucleic acids. The causes of coal-induced pulmonary disease are complex but several endpoints are used in studies to evaluate the mechanisms of toxicity and compare different coals for their toxicological potential. These include cytotoxicity, genotoxicity, generation of reactive oxygen species (ROS) and signs of oxidative stress, chemokine, cytokine, and growth factor release [5,6,7]. High iron concentrations in biological systems (e.g., iron released by ferritin under pathological conditions) can cause oxidation to biomolecules [12,13,14,15,16] and iron associated with asbestos [17,18], quartz [19], iron oxides [20,21], and iron sulfides [22,23,24] has been shown to be a key reactant in the mechanisms leading to lung injury
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