Research

Role of pyrite in formation of hydroxyl radicals in coal: possible implications for human health

Corey A Cohn^1,4 , Richard Laffers¹ , Sanford R Simon² , Thomas O'Riordan³ and Martin AA Schoonen¹

¹  Department of Geosciences and Center for Environmental Molecular Science, Stony Brook University, Stony Brook, NY 11794-2100, USA

²  Department of Pathology, Stony Brook University Hospital, Stony Brook, NY 11794, USA

³  Department of Medicine, Stony Brook University Hospital, Stony Brook, NY 11794, USA

⁴  National Institute of Occupational Health, Lerso Parkalle 105, 2100 Copenhagen, Denmark

author email corresponding author email

Particle and Fibre Toxicology 2006, 3:16doi:10.1186/1743-8977-3-16

Published:	19 December 2006

Abstract

Background

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. 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.

Results

Coals 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.

Conclusion

The 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.