Iron, Oxidative Stress, and Cell Signaling in the Pathogeneses of Coal Workers' Pneumoconiosis, Silicosis, and Asbestosis

Abstract

Coal workers' pneumoconiosis (CWP), silicosis, and asbestosis were the most common occupational diseases in the 20 th Century. The passage of the Mine Health and Safety Act in 1968 resulted in reduction of occupational exposures to coal, silica, and asbestos fibers and, thus, decreased incidence of the diseases. However, the most recent data showed that, from the beginning of the 21 st Century, a significant increase in the occurrence and severity of CWP took place in the U.S. This occurrence necessitates a comprehensive review of this issue. Among many factors, cumulative dust exposure (CDE), a product of dust concentration and working tenure, is the most important cause of the disease. The molecular mechanisms mostly center on iron-mediated oxidative stress and cell signaling, leading to inflammation, possibly epithelial mesenchymal transition (EMT) to fibroblasts, and ultimately fibrotic changes. In order to combat the recent increase in CWP, reducing coal dust levels and decreasing the toxicity of the coal at the work setting are the first practical measures to take. Exposure biomarkers, which are based on iron, and early disease biomarkers in inflammation and EMT can be developed for early detection before the conventional chest x-ray diagnosis is possible. In summary, through dust reduction, delay of mining highly toxic coal, and identification of susceptible workers, CWP is preventable.