Many acute and chronic lung diseased including pneumoconiosis are characterized by the presence of increased numbers of activated macrophages. These macrophages generate several inflammatory cell chemoattractants, by which neutrophil migrate from vascular compartment to the alveolar space. Recruited neutrophils secrete toxic oxygen radicals or proteolytic enzymes and induce inflammatory response. Continuing inflammatory response results in alteration of the pulmonary structure and irreversible fibrosis. Recently, a polypeptide with specific neutrophil chemotactic activity, interleukin-8 (IL-8), has been cloned and isolated from a number of cells such as: monocytes, macrophages and fibroblasts. IL-1 and/or TNF-alpha preceded for the synthesis of IL-8, and we already observed high level of IL-1 and TNF-alpha in vivo experiments. So we hypothesized that IL-8 might play a central role in the pathogenesis of pneumoconiosis. In order to evaluate the clinical utility of IL-1, IL-8, TNF as a biomarker in the early diagnosis of pneumoconiosis, we investigated the increase of IL-1, 8, TNF in the pneumoconiotic patient and the significant (p<0.05) correlation between IL-8 level and progression of pneumoconiosis.