Two forms of silicon dioxide exist in nature: amorphous and crystalline. The crystalline form of silicon dioxide is an abundant natural mineral, commonly found in substances such as sandstone, quartz, and granite. While inhalation of the amorphous form does not appear to cause clinically significant complications, inhalation of the crystalline compound can lead to pulmonary disease.
As silica deposits in the airways, contact with the alveolar and endobronchial surfaces generates reactive oxygen species. Smaller particles are taken up through phagocytosis into macrophages, which generate additional free radicals. Oxidative damage by activated macrophages and silica particles result in the release of inflammatory cytokines, increase in cell signaling, and apoptosis of parenchymal cells and macrophages. Fibroblast infiltration occurs in a nodular pattern as the disease progresses.
Silicosis is occupational pneumoconiosis caused by inhalation of crystalline silicon dioxide. This disease is one of several well-described pulmonary complications associated with toxic exposures in the workplace, along with asbestosis, berylliosis, coal miner's lung, hard metal pneumoconiosis, among others.