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.
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