Abstract
Introduction: Miners are at increased risk of developing pneumoconiosis that poses a serious threat to their health. Progressive pneumosclerosis and bronchial mucosa atrophy are typical pathological changes in this disease. At the same time, there is evidence of systemic manifestations of pneumoconiosis. In this regard, a deeper understanding of how long-term exposure to coal dust affects pathophysiological processes not only in the target organ, but also in the whole body is required.
Objective: To generalize and systematize ideas about the pathogenetic foundations of systemic morphological manifestations of black lung disease.
Materials and methods: To obtain information, we have carried out a search for relevant studies published in 1995–2022 in Scopus, PubMed, and RISC databases using the following keywords: pneumoconiosis, miners, morphological changes, pathogenesis, free radical oxidation, inflammation, immune response, cytokines, growth factors, and endothelial dysfunction. We selected 59 full-text publications presenting the results of completed studies on the mechanisms of development of systemic morphological changes in coal miner’s pneumoconiosis. The systematic review was made according to PRISMA guidelines and using certain PICO(S) criteria.
Results: It has been shown that long-term exposure to coal dust causes activation of macrophage-related inflammation in the respiratory system, free radical oxidation, modulation of intracellular signaling pathways, and programmed cell death. Numerous studies have demonstrated the role of inflammation as the main pathogenetic factor of pneumoconiosis, which is closely related to oxidative stress and immune response. Inflammatory mediators ensure the immune response, regeneration and sclerosis of damaged tissues. In case of high cumulative doses of coal dust, these processes begin to have a destructive and tissue-damaging effect in both the lungs and other organs due to the systemic action of the above mediators. The key role of the endothelium in the development, course and outcome of inflammation is noted.
Publisher
Federal Center for Hygiene and Epidemiology
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