Clinical Overview, Appendix A: Emphysema and Chronic Bronchitis
Emphysema and Chronic Bronchitis
Chronic obstructive pulmonary disease (COPD) is the most common chronic lung disease in developed countries, affecting 5-10% of the population. Lung function testing typically shows airflow limitation (reduced ratio of FEV1 to FVC) that is not fully reversible, often accompanied by air trapping based on an elevated residual volume, and decreased diffusion capacity for carbon monoxide. Though cigarette smoking is the most common cause of COPD, it is now recognized that COPD occurs in non-smokers and that cigarette smoking accounts for only 50-70% of the variation in COPD prevalence found in epidemiological studies. Multiple studies from over 30 countries show a population attributable fraction for COPD of 15-20% for workplace exposures [Balmes et al. 2003; Eisner et al. 2010]. COPD caused by occupational exposures has no clinical or pathophysiological features that distinguish it from non-occupational COPD. COPD from any cause is characterized histologically by destruction of alveolar walls (emphysema) with epithelial thickening and peri-bronchiolar fibrosis and reduction in the number of small airways.
A number of specific industries and exposures have been linked to increased COPD risk. Cross sectional and longitudinal studies show that cumulative exposure to coal mine dust is associated with an accelerated decline in FEV1, and the effect of coal mine dust exposure is similar to that of cigarette smoking [Rogan et al. 1973]. Autopsy studies of coal miners show relationships between lifetime coal mine dust, post mortem lung dust content, and the presence and severity of emphysema [Kuempel et al 2009]. Elevated standardized mortality ratios for COPD have been reported in silica-exposed workers, with some studies showing exposure-response relationships [Kreuzer et al. 2013; Hnizdo et al. 1991; Hnizdo et al. 2000]. Other reported causes of occupational COPD and/or emphysema include metals (cadmium, aluminum, beryllium, and cobalt); other inorganic dusts (carbon black, potash); specific fume and gas exposures (welding fumes, diesel exhaust, coke oven emissions, and chlorine and sulfur dioxide exposures in paper and pulp mill workers); organic dusts (in animal farming, cotton processing, silk and hemp workers, and those exposed to wood dusts); and hypersensitivity pneumonitis [Erkinjuntti-Pekkanen et al. 1998] . (Fig. 2). Studies examining more general occupational exposures to vapor, gas, dust and fume (VGDF) have shown that such exposures are associated with risk for COPD, and indicate the public health importance of these workplace exposures on COPD disease burden [Harber et al. 2007].
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