SILICOSIS - pediagenosis
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Monday, November 2, 2020



Silicosis is a chronic diffuse fibronodular interstitial lung disease caused by the inhalation of crystalline particles of silica (silicon dioxide [SiO2]). The particles must be of respirable size (0.2-10 m aerodynamic diameter) to reach the distal airspaces of the lung. The biologic activity of silica is attributable to silanol groups and other chemically reactive species on the crystal surface, not to its physical shape or sharp edges. The mineral must be in crystalline form because glass (amorphous noncrystalline silica) is essentially nontoxic in crushed, powdered, or fibrous form. The mineral silica is abundant in nature as either pure quartz or mixed in igneous rock with other minerals; whereas beach sand is pure quartz, granite contains 10% to 15% crystalline free silica. Exposure to respirable silica must be substantial and prolonged to cause clinically significant lung disease.

Silicosis usually presents as a chronic diffuse lung disease with numerous small nodules with an upper lung zone predominance, and it evolves slowly over years or decades. This form is labeled chronic simple silicosis. It may progress to more extensive disease with coalescence of the nodules into conglomerate masses with surrounding fibrosis and traction emphysema. The more advanced stage may be referred to as progressive massive fibrosis (PMF). Extremely high levels of expo- sure can cause an acute and usually fatal form of silicosis accompanied by an outpouring of alveolar surfactant lipids and proteinaceous debris, a rare condition known as acute silicosis or silicoproteinosis. An intermediate form termed accelerated silicosis may develop in 2 to 5 years if exposure is intense.



The pathology of silicosis features a characteristic lesion, the silicotic nodule, found in lung tissue and draining lymph modes. This lesion begins as a small collection of macrophages (many containing phagocytosed dust particles), lymphocytes, and fibroblasts; this early lesion is usually located near respiratory bronchioles. Whorls of type I collagen and other matrix proteins accumulate in the center as the nodules enlarge, with an outer rim of mononuclear cells and proliferating fibroblasts. Neutrophils and eosinophils are not abundant. The nodules coalesce gradually, and the fibrotic process extends to infiltrate the surrounding tissue.  Finally, dystrophic calcification may be found within the larger conglomerate masses and in the hilar and mediastinal lymph nodes. The silica mineral particles are usually abundant within these lesions and can be visualized by polarized light microscopy or by elemental analysis with scanning electron microscopy and energy dispersive spectrometry.



Patients with silicosis experience gradually progressive shortness of breath with exertion and cough, sometimes with clear or white sputum. Physical examination may be normal, or high-pitched end-inspiratory crackles (rales) may be heard over the mid-lung areas. Digital

clubbing is very uncommon in silicosis. Signs of cor pulmonale (accentuated second heart sound, peripheral edema) may be late manifestations of advanced disease. The chest radiograph early in silicosis shows small, rounded opacities with a mid- and upper-zone pre-dominance (International Labour Organization classification p/q opacities, profusion 1/1-2/1). More advanced silicosis includes more widespread opacities with some coalescence, enlarged hilar and mediastinal lymph nodes, and peripheral “egg-shell” calcification of these nodes. Extensive pleural thickening or pleural calcifications are not seen, although some of the nodules may originate at subpleural sites. High-resolution (thin section) computed tomography (CT) is helpful in revealing this pattern and may show more extensive disease than would be suspected from the plain frontal chest radiograph. The radiographic features of silicosis may be much more striking than either the patient’s complaints or the pulmonary function abnormalities. Pulmonary function tests show a pattern of mixed restrictive and obstructive physiology, commonly with oxygen desaturation with exertion. There is no effective treatment for silicosis; it must be prevented by industrial hygiene measures. Chronic silicosis must be managed with supportive care, such as oxygen therapy and treatment of intercurrent infections.



Workers may be exposed to respirable silica dust in a variety of industrial settings where the use of power machinery generates numerous fine particles. A common theme involves drilling where the work takes place in a confined space that may be poorly ventilated, such as through silica-containing rock to extract minerals (mining) or stone (quarrying) or drilling to create passageways (tunneling). Crafting stone for monuments, tombstones, or sculpture can generate substantial airborne dust. Silica sand is used to create abrasives, sandpaper, and grinding and polishing materials. Abrasive blasting using sand for grit or nonsiliceous abrasive blasted against silica-bearing stone also can cause silicosis. Sharpening tools (scissors grinding) or cleaning sand-cast foundry parts with silica-containing abrasives can produce substantial exposures.

Silicosis caused by mining, quarrying, tool grinding, and similar activities can usually be reduced to safe levels by vigilant industrial hygiene measures (air extraction, spraying water on cutting surfaces, abrasive blasting in isolation booths, respiratory protective devices, independent clean air sources). Workers involved in the production of abrasives, glass sand, and particularly silica flour (finely divided silica powder) may experience significant exposure and develop silicosis. Silica flour is used widely as an additive, absorbent, bulking agent or an abrasive in many products such as paints, plastics, toothpastes, and detergents. Control measures and regulation and surveillance of exposures to silica are the major reason for the decline in the number of cases and deaths caused by silicosis in the United States and other industrialized nations over the past 70 years. Silicosis is still common in developing nations where extractive industries are growing and power equipment is being used more widely, but worker protection and industrial hygiene remain limited. The United States Occupational Safety & Health Administration (OSHA) and the Mine Safety Administration (MSA) have established a Permissible Exposure Limit (PEL) for an 8-hour time-weighted average (TWA) for crystalline quartz of less than 0.10 mg/m3; levels between 0.05 mg/m3 and 0.10 mg/m3 are specified by most nations.



Patients with silicosis appear to be particularly susceptible to a chronic indolent form of pulmonary tuberculosis. Diagnosis may be difficult because of the silicotic radiographic changes. Complete eradication of tubercle bacilli is thought to be very difficult, and lifelong antituberculous drug therapy is usually recommended.



When silicosis or coal workers pneumoconiosis occurs in a patient who also has rheumatoid arthritis, necrobiotic nodules (rheumatoid nodules) may develop in the lung, a condition known as Caplan syndrome. The lesions are typically large (1.0 cm), round, and well-defined. These “Caplan nodules” often grow much more quickly than typical silicotic nodules and may undergo central necrosis or cavitation; they may also disappear spontaneously. The Caplan nodules are of little clinical consequence in their own right but may raise great concern about the possibility of tuberculosis caused by the cavitation or lung cancer resulting from their rapid growth.

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