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.
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.
Numerous occupations may place workers at risk for exposure to silica dust across a wide variety of industries.  High-risk occupations include road repair, concrete manufacturing, coal mining, brick working, and rock excavation. Also at risk are workers employed in stone cutting, petroleum extraction, steel working, sandblasting, and others. According to the Occupational Safety and Health Administration, there are over two million workers exposed to some form of respirable silicon dioxide on a regular basis. Improved awareness and safety measures in the workplace have led to a substantial decrease in this disease over the last several decades; however, safeguards remain imperfect and there continue to be new cases of silicosis that arise.
Inhalation of crystalline silicon dioxide causes mineral deposits to form at the level of terminal bronchioles and alveoli. The presence of foreign material results in the activation of alveolar macrophages and also exerts direct toxic effects on the surrounding lung parenchyma. Cellular damage results in the release of inflammatory cytokines (such as IL-1 and TNF-alpha), the generation of free radicals, and augmentation of cell-signaling pathways. The different cytokines result in the promotion of fibrosis. A role of tissue mast cells has also been reported. There is also evidence that silica interferes with the ability of macrophages to inhibit the growth of mycobacteria and this effect explains the common association silicosis/tuberculosis. In the acute form of silicosis, a direct toxic effect of alveolar type 2 cells, as well as on macrophages may occur. A role of immunologic factors has long been postulated but not proven in silicosis.
Nodular silicosis is characterized by the presence of silicotic nodules. Grossly, silicotic nodules are firm, discrete, rounded lesions that contain a variable amount of black pigment. The nodules tend to occur around respiratory bronchioles and small pulmonary arteries and in the subpleural and paraseptal areas. Progressive expansion causes obliteration of small airways and pulmonary vessels. The latter are characterized by concentrically arranged hyalinized collagen bundles surrounded by variable numbers of dust-filled histiocytes. In early nodules, fibroblasts and histiocytes are prominent with acellular collagen lamellae. Small, polarizable, doubly refractile, round or oval particles are often found within nodules. Their presence helps to confirm the diagnosis but they may be absent in some cases and they are not specific of silicosis. Granulomatous reaction may be observed in the capsule of silicotic nodules. Its presence raises the possibility of the coexistence of mycobacterial infection. Central necrosis is unusual. The surrounding lung may be unremarkable although dust macules and pigment-laden macrophages are usually seen around small airways. A non specific type of interstitial fibrosis has been reported occasionally in patients with chronic silicosis.
In acute silicosis, microscopic findings mimic pulmonary alveolar proteinosis. Unlike ordinary alveolar proteinosis, there are usually also interstitial inflammation and fibrosis or irregular hyaline scars as well as a variable amount of pigment. Silicotic nodules are poorly formed or absent in most cases.
Microscopic exam may be helpful in revealing some complications including progressive massive fibrosis or tuberculosis and non tuberculous infections. Progressive massive fibrosis is characterized by the presence of a nodular fibrosis that is greater than 1 cm in dimension. Usually, there is a large amorphous mass of fibrous tissue that is composed of conglomerated nodules causing obliteration and contracture of lung parenchyma. this lesion also occurs in other pneumoconioses including asbestosis, coal workers' pneumoconiosis or mixed dust fibrosis. Tuberculosis and non tuberculous mycobacteriosis can be suspected when facing a granulomatous infection with necrosis.
Three clinical entities exist along the spectrum of disease including chronic forms, accelerated forms, and acute silicosis. Nodular or pure silicosis can occur after 20 or more years of exposure in occupations. An accelerated form of the disease occurs after a heavier exposure for 5 to 10 years.  Acute silicosis is an unusual reaction caused by heavy exposure over a short period to high levels of silica of small particle size.
Radiologic findings depend on the form of silicosis. In simple silicosis, chest X-ray shows variable features consisting mainly in well-defined opacities ranging from 1 to 10 mm in diameter, located in the upper lobe and posterior portion of the lung. CT-scan findings consist of multiple small nodules with hilar and mediastinal lymphadenopathy. Some nodules may be calcified.
In acute silicosis, chest X-ray shows bilateral consolidation associated with ground-glass opacities. CT-scan findings consist of numerous centrilobular ground-glass opacities with consolidation.
There are no specific therapeutic modalities. The primary treatment procedure consists of removing the source of exposure.
The principal differential diagnosis is rheumatoid arthritis. The silicotic nodules may show features mimicking a rheumatoid nodule. These nodules are characterized by central, acellular areas of necrosis surrounded by palisading histiocytes and a peripheral rim of lymphocytes and plasma cells.
Complications of silicosis are represented by:
There are reports of an increased incidence of scleroderma in patients who suffer chronic exposure to silica but this phenomenon remains unexplained. Reports of acute glomerulonephritis are also in the literature.
Silicosis is mainly a professional disease necessitating an eviction of the source of exposure.
The clinical symptoms and radiologic findings are nonspecific.
The microscopic exam is necessary to assess the diagnosis and to rule out the major diagnostic pitfalls consisting of progressive massive fibrosis and tuberculosis and nontuberculous mycobacteriosis.
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