Silica dust and tobacco smoking: association in lung damage [Sílica e tabagismo: associação na produção de dano pulmonar]
Fecha
2018
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Associacao Nacional de Medicina do Trabalho
Resumen
Background: The relationship between silica dust and tobacco smoking as enhancers of pulmonary fibrosis development has not yet been well established. Some pathophysiological mechanisms which might support this relationship were postulated. The role of different cells involved in the inflammatory response, and of different biological pathways needs to be recognized. These facts encouraged us to perform the present descriptive review. Results: Growing evidence suggests that local inflammation induced by exposure to silica dust and tobacco smoking might be modulated by genetic factors, epigenetic mechanisms, autoimmune reactions and local hypoxia, giving rise to the epithelial-mesenchymal transition. These phenomena lead to accumulation of necrotic material in the lungs, which contributes to inflammation's perpetuation and to an exaggerated innate immunological response among workers with silicosis who smoke. Conclusion: Direct comparisons of different measurement studies of inflammatory biomarkers associated with silicosis and tobacco smoking should be performed cautiously due to several possible confounding factors, such as compartmentalization or interaction among the various biological pathways and cell types involved. Ventilation systems should be improved and exposure reduced to prevent lung damage in workers exposed to silica. In regard to smoking cessation, psychotherapy approaches are needed for early prevention of lung damage. © 2018 Associacao Nacional de Medicina do Trabalho. All rights reserved.