Induction of ferritin and lipid peroxidation by coal samples with different prevalence of coal workers' pneumoconiosis: role of iron in the coals.

Abstract

Differences in levels of bioavailable iron (BAI) in coal may be responsible for the observed regional differences in the prevalence and severity of coal workers' pneumoconiosis (CWP). Twenty-nine coal samples from three coal mine regions were tested in human lung epithelial Type II A549 cells. They were from Utah (UT), West Virginia (WV), and Pennsylvania (PA) with a prevalence of CWP of 4, 10, and 26%, respectively. Low molecular weight (LMW) chelators bound iron, a fraction of BAI in the cells released from coals, ferritin, and lipid peroxidation were significantly higher in cells treated with various coals than in control cells, with an increasing order of UT < WV < PA, in parallel to the prevalence of CWP in these coal mine regions. Deferoxamine (DFO), a specific iron chelator, was used to distinguish effects of BAI from those of other transition metals. Our results indicate that BAI in the coals of WV and UT is the main metal species in inducing ferritin and lipid peroxidation. In contrast, biological effects of PA coals are not only from BAI, but from other transition metals as well. Based on a large number of coal samples from various seams, the findings of this study provide further evidence that metals, particularly iron, play important roles in coal dust-induced cellular damage, ultimately leading to the development of CWP and contributing to the regional differences in the prevalence of the disease.