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Pathologic responses to inhaled silica.

Authors
Green-FHY; Vallyathan-V
Source
Silica and Silica-Induced Lung Diseases. Castranova V, Vallyathan V, Wallace WE, eds., Boca Raton, FL: CRC Press, 1995 Dec; :39-59
Link
NIOSHTIC No.
20037000
Abstract
Silicosis is defined as pulmonary disease resulting from the inhalation of crystalline silica. In the human, silicosis manifests as four pathologically distinct entities: acute silicosis (silicolipoproteinosis), accelerated silicosis, chronic simple silicosis, and complicated silicosis. Complicated silicosis develops to progressive massive fibrosis by the conglomeration of nodular lesions. Rheumatoid pneumoconiosis, silicotuberculosis, and scleroderma are also associated with silica exposure. The components of the silicotic response have strong temporal and exposure associations. Acute silicosis and accelerated silicosis have short latency periods (several months to several years) and are associated with intense, brief exposures. Chronic simple silicosis and complicated silicosis, by contrast, are more likely to occur a decade or more after first exposure and are associated with lower levels of exposure over long periods of time. However, overall cumulative exposure (exposure level x duration) may be similar in patients presenting with different types of disease. Although this classification and the general principles enumerated concerning latency and exposure apply to most cases of silicosis, certain qualifications apply. First, this disease classification describes a spectrum of changes that may exist in transitional forms (e.g., accelerated silicosis has features in common with both acute silicosis and chronic simple silicosis). Second, the various distinctive lesions may co-exist in the same lung (e.g., pulmonary alveolar proteinosis may be seen in patients with silicotic massive fibrosis). Third, the features of silicosis may be modified by the presence of other minerals in the dust (see Chapter 4, Section ll). The number of workers at risk for developing silicosis remains high. The National Institute for Occupational Safety and Health (NIOSH) estimated in 1986 that 2.3 million workers were exposed to quartz dust. Every year, approximately, 1,500 cases of silicosis are diagnosed in the U.S. It is likely that many more cases remain undiagnosed. However, silicosis is now rare in populations of workers exposed to quartz levels averaging less than the current permissible limit of 100 microg/m3. Most cases today occur in poorly regulated or unregulated industrial settings or in situations where the exposure was not recognized. Unusual sources of exposure resulting in silicosis include inhalation of crack cocaine, scouring powder, exposure in the electronics industry, grinding maize, farming, living in desert- like terrain, and the cutting of gemstones. Exposure to silica-containing dust can also result in cryptic pulmonary disease that is not detected radiologically. Craighead and Vallyathan described small fibrotic lesions associated with deposits of crystalline silica in post mortem specimens of 15 granite workers who lacked radiological evidence of pneumoconiosis. It is important to bear in mind that silica is not a single entity. Free silica (silicon dioxide) occurs in crystalline and amorphous forms. The major crystalline phases are quartz, cristobalite, tridymite, stishovite, and coesite. In general, the toxicity of the crystalline forms of silica is directly related to the temperature and pressure at which the minerals have formed. Thus, tridymite is more toxic than quartz, and cristobalite is more toxic than tridymite. Free silica may also exist in cryptocrystalline forms in which minute grains of quartz are cemented together with amorphous silica. Flint, chert, and chalcedony are examples of cryptocrystalline forms of silica. Diatomite and vitreous silica are examples of amorphous silica. In and of itself, amorphous silica is relatively nontoxic; however, in the industrial setting, heating and processing may convert the amorphous silicon dioxide into microcrystalline particles of tridymite and cristobalite. In a critical review, Parkes concluded that studies showing a toxic effect of amorphous silica can largely be accounted for by the presence of contaminating crystalline forms (see Chapter 1, Section II). Amorphous silica can also exist in biogenic form and may have a fibrous morphology. It occurs in many food crops and in dry plant matter. SiO2 concentrations have been measured at up to 12% by weight in rice, 3.4 to 5% in wheat and up to 16.4% in corn. A major source of release of this biogenic silica is the burning of wheat, stubble, grass, and sugarcane leaf. Airborne amorphous fibers generated during sugarcane leaf burning were found to measure between 3.5 and 65 microns in length with a mean length of 12 microns and an average diameter of 0.6 microns. The biologic significance of these fibers is uncertain; however, epidemiologic studies have associated biogenic silica with increased risk for cancers of the upper digestive tract and of the lungs and pleural cavities.
Keywords
Dust-exposure; Dust-inhalation; Respirable-dust; Silicates; Humans; Respiratory-system-disorders; Occupational-hazards; Occupational-respiratory-disease; Pulmonary-system-disorders; Pneumoconiosis; Lung-fibrosis; Lung-disease; Lung-disorders
CAS No.
14808-60-7; 14464-46-1; 15468-32-3
Publication Date
19951220
Document Type
Book or book chapter
Editors
Castranova-V; Vallyathan-V; Wallace-WE
Fiscal Year
1996
NTIS Accession No.
NTIS Price
ISBN No.
0849347092
NIOSH Division
DRDS
Source Name
Silica and Silica-Induced Lung Diseases
State
WV
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