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Mechanisms of crystalline silica and coal-induced emphysema development.

Authors
Vallyathan-V; Hnizdo-E
Source
Med Lav 2002 Oct; 93(Suppl):S66
NIOSHTIC No.
20027161
Abstract
The incidence of chronic obstructive pulmonary disease (COPD) has increased dramatically in the past few decades and now ranks as a major cause of morbidity and mortality on a worldwide basis. It is estimated that approximately 14 million people in the United States have COPD. The World Health Organization predicts that by 2020 COPD will become the 3rd most common cause of death. Cigarette smoking, environmental pollution, and occupational exposure are the most important risk factors associated with the development of COPD. Although COPD encompasses chronic obstructive bronchitis and emphysema the molecular mechanisms involved in their pathogenesis and expression of symptoms are dramatically different between these two diseases. Therefore, we will be focusing only on the potential mechanisms of silica or coal-induced emphysema development. In epidemiologic and pathologic studies occupational exposure to crystalline silica and coal are two important risk factors identified to be associated with the development of emphysema. Development of focal emphysema in coal miners who have never smoked is induced by the secretion of proteolytic enzymes from coal-activated macrophages and inactivation of antitrypsin. Similarly emphysema in silica-exposed workers is thought to be induced by the enhanced generation of reactive oxygen species secreted by activated macrophages and the resultant inactivation of antitrypsin. This hypothesis is supported by epidemiological studies documenting exposure-response for air flow obstruction in silica-exposed workers even in the absence of radiological signs of silicosis. In addition, in vitro and in vivo experimental studies corroborate the oxidative inactivation of antiproteinases and the subsequent breakdown of connective tissue in a dose-response fashion due to exposure to silica or coal. These experimental studies and other clinical observations suggest that silica -and coal dust-induced: emphysema occur through similar mechanisms as that for smoking-induced emphysema.
Keywords
Silicates; Silicosis; Silica-dusts; Pulmonary-disorders; Pulmonary-function; Pulmonary-system-disorders; Lung-disease; Lung-disorders; Lung-irritants; Epidemiology; Respiratory-irritants; Respiratory-system-disorders; Health-hazards; Occupational-hazards; Occupational-exposure; Occupational-respiratory-disease; Exposure-limits
CODEN
MELAAD
Publication Date
20021025
Document Type
Conference/Symposia Proceedings; Abstract
Fiscal Year
2003
NTIS Accession No.
NTIS Price
ISSN
0025-7818
NIOSH Division
EID
Priority Area
Work Environment and Workforce: Mixed Exposures
Source Name
La Medicina del Lavoro. 3rd International Symposium on Silica, Silicosis, Cancer and Other Diseases, S. Margherita Ligure, 21-25 October 2002
State
OH
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