Silicosis

Richard D. Drucker

Silicosis is a fibrotic disease of the lungs caused by inhalation of free crystalline silica (silicon dioxide). Silica is a ubiquitous material that is a major component of the earth’s crust. The three major crystalline forms associated with lung injury are quartz, cristobalite, and tridymite. Quartz is the most common silica and is found in most rocks, including granite and sandstone. Cristobalite and tridymite are associated with high temperatures, are naturally found in lava, and can be produced from other forms of silica by exposure to high temperatures. These are termed free silica, in contrast to silicates, which are crystals of silicon dioxide complexed with inorganic cations such as calcium, iron, magnesium, or aluminum. Silicates such as asbestos, talc, and mica are also capable of inducing lung injury.

The classic occupations at risk for silicosis are mining (quarrying, tunneling), manufacturing (glass, pottery, porcelain, abrasives), and sandblasting. The development of disease is related to the duration, concentration, and structure of the free silica dust in the environment as well as each individual’s susceptibility to silica inhalation, which is incompletely characterized. Only a minority of workers at risk actually develop silicosis. The prevalence of silicosis appeared to be decreasing following introduction of improved dust control in the 1970s, but the prevalence recently has increased for unknown reasons.

The exact pathogenic mechanism of pulmonary silicosis is unclear, but there is abundant evidence that the pulmonary alveolar macrophage plays an important role in mediating lung damage. It is hypothesized that crystalline free silica interacts with water to form oxygen radicals that injure the alveolar macrophage. The macrophages release cytokines such as tumor necrosis factor, interleukin-1, and arachidonic acid metabolites. The resulting proliferation of type II pneumocytes, fibroblasts, and collagen eventually cause pulmonary fibrosis.

The classic pathologic lesion of silicosis is the hyaline nodule, consisting of concentric whorls of connective tissue and an acellular central zone containing free silica. The middle zone has fibroblasts and collagen, and the peripheral zone contains macrophages, fibroblasts, and free silica. The nodules are scattered throughout the lungs with predominance in the upper lobes. Simple nodules rarely compress airways or blood vessels, but larger coalescent masses in the advanced stage of silicosis can involve these structures. Regional lymphadenopathy and pleural adhesions are common, particularly in more severe cases of silicosis.

The three major clinical presentations of silicosis are chronic silicosis, accelerated silicosis, and acute silicosis. Chronic and accelerated silicoses present with similar symptoms and radiographs except that chronic silicosis becomes clinically apparent only decades after exposure to free silica, while accelerated silicosis becomes clinically apparent sooner and typically after exposure to heavy concentrations of silica. Radiographic abnormalities characteristically occur prior to the development of symptoms such as cough, sputum production, and dyspnea on exertion. Acute silicosis (silicoproteinosis) develops within 6 to 24 months of massive exposure to free silica. It tends to have a fulminant course consisting of cough, weight loss, rapidly progressive dyspnea, and early death. Histologically, the alveoli are filled with a PAS–positive acellular material like that seen in pulmonary alveolar proteinosis. The lungs of people exposed to free silica, whether or not silicosis is present, also may demonstrate pathologic evidence of emphysema or chronic bronchitis. Extrapulmonary involvement (kidney and liver) also has been described in acute silicosis.

Only gold members can continue reading. Log In or Register to continue