Cellular and molecular mechanisms, as well as associated gene expressions, in silicosis and asbestosis are widely investigated, and compound mechanisms involved in initiating inflammation and progression to fibrosis are comprehensively studied, though not yet totally understood. Recent advances in this field, especially concerning pathophysiology of these pneumoconioses, are reviewed in this article. Silicosis and asbestosis are two major types of pneumoconiosis. Although the clinico-pathologic features presented are apparently different, silicosis and asbestosis are both interstitial lung diseases caused by chronic exposure to airborne inorganic dusts, and the pathology of these two diseases is essentially a fibrosis.