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Title: Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and Silicate Disease Committee

Abstract

Silicosis, a disease of historical importance, continues to occur cryptically today. Its pathogenesis is under ongoing study as new concepts of pathobiology evolve. In this article, the gross and microscopic features of the disease in the lungs and the lesions in lymph nodes and other viscera are described. These tissue changes are then discussed in the context of clinical disease and other possible or established complications of silica exposure (ie, scleroderma and rheumatoid arthritis, glomerulonephritis, and bronchogenic carcinoma). Silicates are members of a large family of common minerals, some of which have commercial importance. Silicates are less fibrogenic than silica when inhaled into the lungs, but cause characteristic lesions after heavy prolonged exposure. The features of these disease conditions are described herein. Various aspects of the mineralogy and tissue diagnosis of silicosis and lung disease due to silicates are reviewed. An overview of contemporary regulatory considerations is provided.204 references.

Publication Date:
OSTI Identifier:
7138498
Alternate Identifier(s):
OSTI ID: 7138498
Resource Type:
Journal Article
Resource Relation:
Journal Name: Arch. Pathol. Lab. Med.; (United States); Journal Volume: 112:7
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; 59 BASIC BIOLOGICAL SCIENCES; RESPIRATORY SYSTEM DISEASES; PATHOGENESIS; SILICA; TOXICITY; MAN; MAXIMUM PERMISSIBLE EXPOSURE; REVIEWS; TALC; ALKALINE EARTH METAL COMPOUNDS; ANIMALS; CHALCOGENIDES; DISEASES; DOCUMENT TYPES; MAGNESIUM COMPOUNDS; MAGNESIUM SILICATES; MAMMALS; MINERALS; OXIDE MINERALS; OXIDES; OXYGEN COMPOUNDS; PRIMATES; SAFETY STANDARDS; SILICATE MINERALS; SILICATES; SILICON COMPOUNDS; SILICON OXIDES; STANDARDS; VERTEBRATES 560300* -- Chemicals Metabolism & Toxicology; 550900 -- Pathology

Citation Formats

Not Available. Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and Silicate Disease Committee. United States: N. p., 1988. Web.
Not Available. Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and Silicate Disease Committee. United States.
Not Available. Fri . "Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and Silicate Disease Committee". United States. doi:.
@article{osti_7138498,
title = {Diseases associated with exposure to silica and nonfibrous silicate minerals. Silicosis and Silicate Disease Committee},
author = {Not Available},
abstractNote = {Silicosis, a disease of historical importance, continues to occur cryptically today. Its pathogenesis is under ongoing study as new concepts of pathobiology evolve. In this article, the gross and microscopic features of the disease in the lungs and the lesions in lymph nodes and other viscera are described. These tissue changes are then discussed in the context of clinical disease and other possible or established complications of silica exposure (ie, scleroderma and rheumatoid arthritis, glomerulonephritis, and bronchogenic carcinoma). Silicates are members of a large family of common minerals, some of which have commercial importance. Silicates are less fibrogenic than silica when inhaled into the lungs, but cause characteristic lesions after heavy prolonged exposure. The features of these disease conditions are described herein. Various aspects of the mineralogy and tissue diagnosis of silicosis and lung disease due to silicates are reviewed. An overview of contemporary regulatory considerations is provided.204 references.},
doi = {},
journal = {Arch. Pathol. Lab. Med.; (United States)},
number = ,
volume = 112:7,
place = {United States},
year = {Fri Jul 01 00:00:00 EDT 1988},
month = {Fri Jul 01 00:00:00 EDT 1988}
}
  • Silicate substitutes for phosphate in the transitory uncoupling of rat liver mitochondria induced by hydrozine when beta-hydroxy-butyrate is the substrate. Uncoupling is blocked by rutamycin. Just as in the case when phosphate is combined with hydrazine, ATP, ADP, PPi, and Mg/sup + +/ protect against hydrazine when silicate is combined with hydrazine. A high level of ADP in the absence of added phosphate, but in the presence of silicate, induces a pseudo state three of the mitochondria. Silicate, like sulfate and arsenate which have been reported previously, is activated by the enzymes which mediate oxidative phosphorylation. These results serve tomore » explain a role for silicate in silicosis, black lung disease, and cancer. In addition, since there is suggestive evidence in the literature that lung tissue solubilizes asbestos fibers, these results not only expand the confluence between oxidative phosphorylation and chemical carcinogenesis but are correlated with the synergistic carcinogenicity of asbestos and smoking observed by epidemiologists.« less
  • A case-control study was undertaken to assess the association between lung cancer and silicosis or silica dust exposure in white South African gold miners. Cases and controls were identified from deaths reported to the Gold Miners Provident Fund for the period January, 1979-October, 1983. Two controls were matched to each case by year of birth (+/- 2 years) and by smoking (+/- 5 cigarettes or equivalents per day) assessed 10 years (+/- 2 years) prior to death. One hundred thirty-three matched triplets were identified. The results showed no overall association between lung cancer and radiological silicosis (OR = 1.08, pmore » = 0.92). Autopsy data indicated no overall associations between lung cancer and silicosis of the lung parenchyma (OR = 1.49, p = 0.11), the pleura (OR = 0.72, p = 0.30), or the hilar glands (OR = 0.85, p = 0.72). A trend toward increased severity of silicosis of the parenchyma was evident; however, this was not statistically significant (p = 0.08). Odds ratios for lung cancer and silicosis were higher at lower levels of cumulative silica dust exposure (ORs = 2.43, 1.72, 1.35 and 0.62 for lung cancer and autopsy silicosis of the parenchyma for the lowest, second, third, and highest quartiles of dust exposure, respectively; all p greater than 0.05). Cases did not differ from controls for total silica dust exposure, length of exposure, weighted average intensity of exposure, or number of shifts at high dust (all p greater than 0.20). The data do not support the hypothesis of a carcinogenic role for silica dust and no statistically sigificant associations were found between lung cancer and silicosis.« less
  • The present analysis was stimulated by previous findings on the possible influence of natural ultralow-frequency (ULF; 0.001--10 Hz) geomagnetic field variations on the cardiovascular system and indications of an effect of man-made ULF magnetic fields on the rate of myocardial infarction. In the present study, the authors considered the occupational health hazards of the strongest ULF magnetic fields in densely populated urban areas. Measurements of ULF magnetic field fluctuations produced by trains powered by DC electricity were performed by means of a computer-based, highly sensitive, three-component magnetometer. The authors found that the magnitude of magnetic field pulses inside the driver`smore » cab of electric locomotives (ELs) could be {ge} 280 {micro}T in the vertical component, and, in the driver`s compartment of electric motor unit (EMU) trains, they were approximately 50 and 35 {micro}T, respectively. The authors have investigated the relationships between the occupational exposure to ULF magnetic field fluctuations produced by electric trains and cardiovascular diseases (CVDs) among railroad workers in the former Soviet Union. They have analyzed medical statistical data for a period of 3 years for approximately 45,000 railroad workers and 4,000 engine drivers. The authors have also analyzed 3 years of morbidity data for three subgroups of engine drivers ({approximately} 4,000 in each group) operating different types of trains. They find that EL drivers have a twofold increase in risk (2.00 {+-} 0.27) of coronary heart diseases (CHDs) compared with EMU drivers. Because the analysis of major CVDs shows that the examined subpopulations of drivers can be considered to have had equal exposure to all known risk factors, the elevated CHD risk among El drivers could be attributed to the increased occupational exposure to ULF magnetic fields.« less