Purpose of the Review: Some physiopathological mechanisms that could support the relationship between tobacco and silicosis have been postulated but exact pathogenesis remains unknown. Recent Findings: Local inflammation in workers with silicosis is a complex process characterized by an infiltration of inflammatory cells in the respiratory alveolus, accompanied by an increase in the expression of cytokines, chemokines, enzymes, growth factors and adhesion molecules. Although in smokers without silicosis a similar pattern of inflammation can be observed, in workers with silicosis this process seems to be characterized by more pronounced increases in structural damage in the lungs. Altered balance of innate and adaptive immunity both play key roles in the pathogenesis of extensive fibrosis in a molecular level, influenced by individual susceptibilities and genetic traits. Conclusion: The identification of the molecular mechanism and a potential protective genotype for silicosis opens a window for the eradication of this occupational respiratory disease. This should encourage us to continue exploring and searching for the relation between the genetic polymorphism and the inorganic silica particle.
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