Quartz and Pneumoconiosis in Coalminers

Seaton, Anthony; Dodgson, J S; Dick, J A; Jacobsen, Michael Hviid

doi:10.1016/s0140-6736(81)91503-8

Cited by 55 publications

(40 citation statements)

References 4 publications

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“…However, other factors, such as increased production (implying an increase in general coal mine dust exposures) and increasing hours worked, may have contributed to the observed increases in disease. However, it does seem likely that the previous reports of geographical clustering of rapidly progressing CWP in younger miners,7–9 the increasing prevalence of r-type opacities, and the greater number of cases of severe disease found in this study within the Appalachian coal fields point to excessive exposures to crystalline silica, a long recognised cause of rapid disease progression11 and severe pneumoconiosis in coal miners 10 12. Taken together, these findings stress the need for a timely, comprehensive, accurate and ongoing evaluation of crystalline silica exposures and control strategies in underground coal mines throughout the United States.…”

Section: Discussionmentioning

confidence: 54%

“…An increased proportion of crystalline silica in coal mine dust provides a plausible explanation for an increase in dust toxicity 10. Some underground coal mining jobs are known to be associated with silica exposure, and the lungs of a minority of coal miners have been demonstrated to show typical pathological lesions of silicosis 2 10 11. Additionally, rapid progression9 and progressive massive fibrosis (PMF)10 12 are more likely with silicosis than with CWP 11…”

Section: Introductionmentioning

confidence: 99%

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Pneumoconiosis among underground bituminous coal miners in the United States: is silicosis becoming more frequent?

2009

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ObjectivesEpidemiological reports since 2000 have documented increased prevalence and rapid progression of pneumoconiosis among underground coal miners in the United States. To investigate a possible role of silica exposure in the increase, we examined chest x-rays (CXRs) for specific abnormalities (r-type small opacities) known to be associated with silicosis lung pathology.MethodsUnderground coal miners are offered CXRs every 5 years. Abnormalities consistent with pneumoconiosis are recorded by National Institute for Occupational Safety and Health (NIOSH) B Readers using the International Labour Organization Classification of Radiographs of Pneumoconioses. CXRs from 1980 to 2008 of 90 973 participating miners were studied, focussing on reporting of r-type opacities (small rounded opacities 3–10 mm in diameter). Log binomial regression was used to calculate prevalence ratios adjusted for miner age and profusion category.ResultsAmong miners from Kentucky, Virginia and West Virginia, the proportion of radiographs showing r-type opacities increased during the 1990s (prevalence ratio (PR) 2.5; 95% CI 1.7 to 3.7) and after 1999 (PR 4.1; 95% CI 3.0 to 5.6), compared to the 1980s (adjusted for profusion category and miner age). The prevalence of progressive massive fibrosis in 2000–2008 was also elevated compared to the 1980s (PR 4.4; 95% CI 3.1 to 6.3) and 1990s (PR 3.8; 95% CI 2.1 to 6.8) in miners from Kentucky, Virginia and West Virginia.ConclusionsThe increasing prevalence of pneumoconiosis over the past decade and the change in the epidemiology and disease profile documented in this and other recent studies imply that US coal miners are being exposed to excessive amounts of respirable crystalline silica.

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Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Pneumoconiosis among underground bituminous coal miners in the United States: is silicosis becoming more frequent?

2009

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“…The same authors observed the same tendency for coal mining areas in Great Britain, which have a similar average quartz content (5 weight percent) when compared to the mines of the Ruhr area. Only one British study showed a clear influence of quartz in coal mines [19].…”

Section: Discussionmentioning

confidence: 99%

Immunogenetic sudies on HLA-DR in German coal miners with and without coal worker's pneumoconiosis

Lipps

May-Taube

et al. 1994

Lung

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Coal worker's pneumoconiosis is caused by the pulmonary deposition of coal dust, including silica particles. Several factors such as chemical composition and physical properties of silica-containing dust, particle size distribution, intensity, and duration of exposure influence the disease development. Genetic factors may also be involved. To define whether HLA-DRB may function as a genetic factor for predisposition to coal worker's pneumoconiosis, we determined DRB1, 3, 4, 5 alleles. For this purpose, DRB typing with sequence-specific oligonucleotide probes in 204 German miners with pneumoconiosis and in 52 German miners without pneumoconiosis was used. The miners had worked under comparable conditions. The frequency of DR8 (1*0801-0804) was increased in patients developing pneumoconiosis during the first 15 years of mining (p = 0.047). The frequency of DR1 (1*0101-0103) was elevated (p = 0.022) and that of DR52 (3*0101, 3*0201, 3*0202, and 3*0301) was reduced (p = 0.026) in miners without pneumoconiosis. Our data show that the presence of DR1 and the absence of DR52 support the resistance to coal worker's pneumoconiosis. Furthermore, DR8 may be involved in the rapid development of coal worker's pneumoconiosis.

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“…In one colliery, 3.37% of miners experienced radiological progression of simple pneumoconiosis despite low exposure to mixed coal mine dust as compared with matched controls without disease (7). The quartz content of this dust was significantly higher in cases (13%) than in controls (8%), compared to a level of about 5% in British collieries as a whole.…”

Section: Quartz Concentrationmentioning

confidence: 91%

Prevalence and pathogenesis of pneumoconiosis in coal workers.

Heppleston

1988

Environ Health Perspect

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Dust dose and composition do not appear to account wholly for changes in the prevalence of coal workers' pneumoconiosis in Europe. In certain coal pits high progression evidently occurred with relatively low dust exposure or vice versa, whereas progression in relation to dust levels might be variable. Exceptionally high quartz concentrations occur in coal mine dust when pneumoconiosis may progress with unusual rapidity. Under such circumstances lesions resembling silicotic nodules may be found, but with the customarily lower levels of quartz the pathological features assume the form characteristic of coal workers. Morphological changes in relation to dust content of human and animal lungs, as well as cellular behavior, have not accounted completely for the epidemiological findings. Considering all the pathological evidence helps explain the pathogenesis of pneumoconiosis and vagaries of progression. The origin of progressive massive fibrosis cannot be explained simply in terms of dust burden or immunological features, and the role of an infective factor cannot be dismissed. Moreover, lipid secretion by alveolar epithelium introduces a new element that could affect the development of simple and complicated pneumoconiosis. In vitro, cytotoxicity appeared to be too variable for predictive purposes, though direct assay of fibrogenicity using the macrophage fibrogenic factor suggested that dust dose was more important than dust composition. Assessing individual susceptibility presents serious obstacles.

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Quartz and Pneumoconiosis in Coalminers

Cited by 55 publications

References 4 publications

Pneumoconiosis among underground bituminous coal miners in the United States: is silicosis becoming more frequent?

Pneumoconiosis among underground bituminous coal miners in the United States: is silicosis becoming more frequent?

Immunogenetic sudies on HLA-DR in German coal miners with and without coal worker's pneumoconiosis

Prevalence and pathogenesis of pneumoconiosis in coal workers.

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