Pathology and Mineralogy Demonstrate Respirable Crystalline Silica Is a Major Cause of Severe Pneumoconiosis in U.S. Coal Miners

Abstract

Rationale The reasons for resurgent coal workers’ pneumoconiosis and its most severe forms, rapidly progressive pneumoconiosis and progressive massive fibrosis (PMF), in the United States are not yet fully understood. Objectives To compare the pathologic and mineralogic features of contemporary coal miners with severe pneumoconiosis with those of their historical counterparts. Methods Lung pathology specimens from 85 coal miners with PMF were included for evaluation and analysis. We compared the proportion of cases with pathologic and mineralogic findings in miners born between 1910 and 1930 (historical) with those in miners born in or after 1930 (contemporary). Results We found a significantly higher proportion of silica-type PMF (57% vs. 18%; P < 0.001) among contemporary miners compared with their historical counterparts. Mineral dust alveolar proteinosis was also more common in contemporary miners compared with their historical counterparts (70% vs. 37%; P < 0.01). In situ mineralogic analysis showed that the percentage (26.1% vs. 17.8%; P < 0.01) and concentration (47.3 × 10 8 vs. 25.8 × 10 8 particles/cm 3 ; P = 0.036) of silica particles were significantly greater in specimens from contemporary miners compared with their historical counterparts. The concentration of silica particles was significantly greater when silica-type PMF, mineral dust alveolar proteinosis, silicotic nodules, or immature silicotic nodules were present ( P < 0.05). Conclusions Exposure to respirable crystalline silica appears causal in the unexpected surge of severe disease in contemporary miners. Our findings underscore the importance of controlling workplace silica exposure to prevent the disabling and untreatable adverse health effects afflicting U.S. coal miners.

Pneumoconiosis in Coal Miners: Anthracosilicosis after All?

“…In spite of relatively low numbers of contemporary miners (and, hence, potentially some selection bias) and the absence of radiology, the merit of Cohen and colleagues’ study ( 1 ) is that it provides strong support for the hypothesis that the resurgence of severe pneumoconiosis is due to more intense exposure to respirable silica. The scientific conclusion and practical implication are, therefore, that even though silica is not necessary for causing CWP, high exposure to respirable silica increases the likelihood of early severe pneumoconiosis.…”

“…In this issue of AnnalsATS , Cohen and colleagues (pp. 1469–1478 ) address a question that has kept medical and nonmedical experts and stakeholders busy for more than a century: what is the role of silica in coal workers’ pneumoconiosis (CWP) ( 1 )? The question may seem futile, but it has (had) serious implications for the prevention, diagnosis, and compensation of lung disease in coal workers ( 2 ).…”

“…In a first study ( 10 ), a review of the lung pathology of 13 selected cases of coal miners with rapidly progressive pneumoconiosis indicated that silica and silicates were indeed implicated in the disease. Cohen and coworkers then smartly designed another study ( 1 ) to test formally the hypothesis that silica exposure may be implicated in the resurgence of severe pneumoconiosis in U.S. coal miners. Seven pathologists with expertise and experience in dust-related lung disease (three of whom had participated in the first study [ 10 ]) independently reviewed lung tissue slides from 85 coal miners with histologically defined progressive massive fibrosis, using a standardized scoring system (while being blinded to demographic or other individual information).…”

Becoming disenthralled with our conventional understanding of occupational lung disease

“…Ever since then, we have taken as a given that pneumoconiosis demarcates the principal pathology linked to dusty trades, even if we sometimes debate questions around its edges, such as ‘How much of coal dust lung disease is coal worker's pneumoconiosis as opposed to silicosis?’ or ‘What truly constitutes mixed‐dust pneumoconiosis?’ 5,6 As we apply state‐of‐the‐art biomedical analytic approaches to better understand the adverse health effects of the dusty trades, however, it has become increasingly clear that the ill effects of dust inhalation go well beyond the familiar borders of pneumoconiosis.…”

“…or 'What truly constitutes mixed-dust pneumoconiosis?' 5,6 As we apply state-of-the-art biomedical analytic approaches to better understand the adverse health effects of the dusty trades, however, it has become increasingly clear that the ill effects of dust inhalation go well beyond the familiar borders of pneumoconiosis.…”