ABSTRACT

Mineral dusts can be produced naturally by wind erosion or by human activities such as mining or land use for agriculture. Some mineral dusts such as silica, coal and asbestos can lead to adverse respiratory health effects. The inhalation of these dusts can cause several different diseases like silicosis, coal workers ’ pneumoconiosis, (CWP) asbestosis and lung cancer. The pathogenesis of fibrotic lung diseases involve activation of inflammatory cells, fibroblast cell proliferation and the enhanced synthesis and/or breakdown of extracellular matrix components. Cytokines, chemokines, and growth factors play a crucial role in the onset, progression and termination of these reactions. Cytokines are playing role in inflammation and immune response, that are important mediators of the toxic effects in humans mineral dusts exposure. Existence of persistent stimulus and chronic release of cytokines may result in autoimmune and inflammatory diseases such as silicosis and CWP. Polymorphisms in cytokine genes have been reported to contribute with the inflammatory diseases. Epidemiological studies have pointed out that single nucleotide polymorphisms (SNPs) occurring in cytokine genes are associated with chronic inflammatory or immune-mediated diseases.