pulmonary disorders
Coal Worker Pneumoconiosis
Pathophysiology of Coal Worker Pneumoconiosis
Coal mining dust contains variable amounts of silica in addition to other components. In coal worker pneumoconiosis, alveolar macrophages engulf coal dust particles, which results in cell death and activation of inflammatory and fibrotic pathways. Effector cells promote inflammation and fibrosis around the coal dust particles, leading to the development of coal macules and nodules, which may be surrounded by emphysematous destruction of alveoli. Nodules can coalesce into larger lesions, which is characteristic of progressive massive fibrosis. The risk of progressive massive fibrosis increases with greater exposure to Silicosis . Progressive massive fibrosis can develop and continue to expand even after exposure to coal dust has ceased ( 1.Hall NB, Blackley DJ, Markle T, et al. Postexposure progression of pneumoconiosis among former Appalachian coal miners.Am J Ind Med2022; 65(12), 953-958. doi:10.1002/ajim.23431 