Pneumoconiosis in Coal Workers: Cellular Concepts of Dust-Induced Lung Injury, Radiographic Diagnosis, and Pulmonary Infections With Mycobacteria


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Abstract

Coal workers’ pneumoconiosis (CWP) and silicosis contribute substantially to the mortality rate in developed countries. Both diseases evolve after dust inhalation. Macrophage activation with an excessive inflammatory response triggers consecutive tissue fibrosis. Tumor necrosis factor-α has been identified as one key mediator within the cytokine network. Genetic polymorphism of the promoter gene or a specific apoptosis pattern may contribute to susceptibility of the individual to develop disease. The diagnosis is based on nodules and opacities in the posteroanterior chest radiograph, which are scored according to the International Labour Office classification. The sensitivity of the chest radiograph to detect either lower-grade CWP or silicosis in subjects who have been exposed is poor, when compared with postmortem examinations. Computed tomography of the chest may be a complementary method for further clarification or detection of other parenchymal abnormalities in some individuals. The susceptibility to pulmonary infections with Mycobacterium tuberculosis is not limited to patients with radiographic evidence of advanced pneumoconiosis but also includes subjects with early disease and those without radiographic evidence but with dust exposure. It is widely assumed that toxic dust inhalation induces defects in macrophage-mediated defense mechanisms, but very little convincing evidence exists to explain why dust exposure or pneumoconiosis is associated with mycobacterial infections.

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