Silicosis: biomarkers and pathogenesis

The name of this disease “Pneumonoultra-microscopicsilicovolcanokoniosis”, first description by Ramazzini1 was changed due to the types of exposed dust.2 There are no reliable figures on the silica-inhalation exposed populations. Nevertheless, in 2000, the CAREX registry recorded 3.2 million silica-exposed people in the European Union.3 Silicosis is histologically characterized by hyalinized and fibrotic pulmonary nodules, accumulation of lymphocytes and alveolar macrophages, and thickening of pulmonary alveolar interstitium.4 The disease is caused by continuous inhalation of the silica dust (crystalline silica, SiO2 (Silicon dioxide)) with marked inflammation and irreversible scarring of the lungs with nodules in the upper lobes.5,6 Oxygen and silicon, together amount for 74.32% weight and 83.77% of crustal rocks are the two most occurring common elements on the surface of the earth.7 Silicon dioxide or silica is formed under the conditions of increased pressure and heat that exists in amorphous and crystalline (quartz, a typical component of rocks) form. The risk of developing silicosis is closely associated with the accumulated exposure of a person to respirable crystalline silica during his or her working lifetime. The intensity of accumulated respirable silica exposure can be calculated as the following: Accumulated silica dose = fraction of respirable dust X percentage of free silica in mg/m3 X number of years of exposure.8 Silicosis is the most frequently occurring pneumoconiosis due to wide prevalence in the atmosphere and more common than the other types of dust.1,9,10 Both in Developing and developed world, silicosis is an occupational hazard with greater risk for workers engaged in stone crushing, stone cutting, cement industries, glass manufacturing, mining, agriculture, and construction. Pathogenesis