Complicated Coal Workers' Pneumoconiosis Research Articles

Emphysema and Airflow Obstruction in Non-Smoking Coal Miners with Pneumoconiosis.

BackgroundAccumulating evidence shows that functional impairment in subjects with coal workers’ pneumoconiosis (CWP) is principally due to emphysema and airflow obstruction, rather than underlying restrictive mechanisms. However, cigarette smoking has remained a major confounder. The aim of this study was to assess whether coal dust exposure was associated with emphysema and/or airflow obstruction in the absence of smoking history.Material/MethodThe subjects evaluated for possible pneumoconiosis between 2013 and 2015 were retrospectively enrolled into this study. After excluding those with history of smoking, tuberculosis, or lung cancer, the study population was a total of 57 subjects. The emphysema severity and airflow obstruction were quantified by computed tomographic densitometry analysis and spirometry, respectively. For comparability regarding emphysema, 9 age- and sex-matched nonsmoker (n=9) control subjects without known lung disease were randomly selected from a radiology database.ResultsEmphysema severity was significantly higher in the CWP group compared with the control group (15% vs. 4%, p<0.001). The median percent emphysema and percentage of those with FEV1/FVC <0.7 was 13% and 37% in subjects with simple CWP and 18% and 67% in subjects with complicated CWP, respectively. Percent emphysema and Perc15 (15th percentile of the attenuation curve) was correlated with FEV1/FVC (r=−0.45, r=−0.47) and FEF25–75 (r=−0.36, r=−0.56), respectively, but not with perfusion score. A linear regression analysis showed that factors associated with emphysema were FEV1/FVC (β=−0.24, p=0.009) and large opacity (β=−3.97, p=0.079), and factors associated with FEV1/FVC were percent emphysema (β=−0.51, p=0.018) and tenure (β=−0.63, p=0.044).ConclusionsOur results support the observation that coal dust exposure is associated with emphysema and airflow obstruction, independent of smoking status.

The clinical pathological analysis of 14 autopsy cases of pneumoconiosis

To investigate the histopathological features, complications, diagnosis, and differential diagnosis of coal workers' pneumoconiosis (CWP). The lung tissue sections from 14 autopsy cases of CWP were subjected to HE staining and observed under a light microscope, and a retrospective analysis was performed considering the occupational history and clinical features. The 14 cases were 46-71 years of age (mean, 57.7 years). Two cases were diagnosed as dust reaction, 1 case as simple CWP (stage I anthracosilicosis), and 11 cases as complicated CWP (9 cases of stage II anthracosilicosis, 1 case of stage III anthracosilicosis, and 1 case of stage III silicosis). Twelve cases were complicated by chronic bronchitis and emphysema, 8 cases by pulmonary heart disease, 4 cases by pulmonary tuberculosis, 3 cases by liver cirrhosis and liver cancer with pulmonary metastases, and 2 cases by cerebral hemorrhage. Among patients with CWP, the pathological changes of lung tissue become more complex with increasing years of dust exposure. Coal macule is the common pathological feature of CWP, and dust nodules and massive fibrosis are the necessary indices of pathological diagnosis.

Mycobacterial infections in coal workers’ pneumoconiosis patients in South Korea

Coal workers' pneumoconiosis (CWP) is the most common occupational disease in South Korea and is an important factor in the development of infections with Mycobacterium tuberculosis (MTB) and non-tuberculous mycobacteria (NTM). In the current study, we identified mycobacterial species that cause pulmonary infections in CWP patients, using rpoB DNA-PCR-restriction analysis. Among the 129 CWP patients studied, 35 (27.1%) were diagnosed as having mycobacterial infections. Among these, the proportion of NTM infections (21/35, 60.0%) was higher than that for MTB infections (14/35, 40.0%). Of the 21 NTM strains, the most common was M. intracellulare (6/21, 28.6%), followed by M. avium (5/21, 23.8%). We also compared the characteristics of CWP patients between the MTB and NTM infection groups. A higher proportion of CWP patients with NTM infections compared with those with MTB infections had a history of having been involved in rock work (38.1% vs 21.4%), and had complicated CWP (85.7% vs 35.7%) and a past history of TB treatment (61.9% vs 50.0%). We also discovered 3 MTB mutants that are resistant to first-line anti-TB drugs, in CWP patients. These results demonstrate the features of pulmonary mycobacterial infections with a predominance of NTM in CWP patients in South Korea.

An Unusual Case of Large Opacity in Pneumoconiosis

Coal dust inhalation can result in industrial bronchitis and coal workers’ pneumoconiosis (CWP) presenting as either simple pneumoconiosis or complicated CWP. With prolonged excessive exposure, small opacities in simple pneumoconiosis may coalesce and form larger opacities, recognized as progressive massive fibrosis (PMF) greater than 1 cm in diameter on a chest X-ray. Even though the degree of respiratory impairment or the presence of symptoms does not always correlate well with the extent of PMF, most workers frequently describe dyspnea, a cough and sputum production. It may be caused by deviation of the prominent area of coalescence, loss of upper zone lung volume, elevation of the hila, and basilar emphysema. We present a case of large opacity in pneumoconiosis which included a finding of ischemic necrosis. Rapid change in the solitary mass caused a diagnostic dilemma in attempting to distinguish a primary or metastatic neoplasm from an unusual presentation of PMF.

Silicosis and coal workers' pneumoconiosis.

Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; d) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.

FROM COAL MINE DUST TO QUARTZ: Mechanisms of Pulmonary Pathogenicity

Exposure to coal mine dust or crystalline silica can result in the initiation and progression of interstitial lung disease. Pathogenesis is the consequence of damage to lung cells and resulting lung scarring associated with activation of fibrotic processes. This review presents the radiologic and histologic characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathological indices of acute and chronic silicosis. This presentation also reviews the results of in vitro, animal, and human investigations that elucidate mechanisms involved in the development of these pneumoconioses. Results support the involvement of four basic mechanisms in the etiology of CWP and silicosis: 1. Direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring. 2. Activation of oxidant production by pulmonary phagocytes, such as alveolar macrophages. When oxidant production exceeds antioxidant defenses, lipid peroxidation and protein nitrosation occur, resulting in tissue injury and consequent scarring. 3. Activation of mediator release from alveolar macrophages and alveolar epithelial cells. Chemokines recruit polymorphonuclear leukocytes and macrophages from the pulmonary capillaries into the air spaces. Once within the air spaces, these leukocytes are activated by proinflammatory cytokines to produce reactive species, which increase oxidant injury and lung scarring. 4. Secretion of growth factors from alveolar macrophages and alveolar epithelial cells. Release of such mediators stimulates fibroblast proliferation and induces fibrosis. In conclusion, results of in vitro and animal studies have provided the basis for proposing mechanisms that may lead to the initiation and progression of CWP and silicosis. Data obtained from exposed workers has lent support to these proposals. The mechanistic understanding obtained for the development of CWP and silicosis should be useful in elucidating the possible pathogenicity of other inhaled particles.

From Coal Mine Dust To Quartz: Mechanisms of Pulmonary Pathogenicity

Exposure to coal mine dust or crystalline silica can result in the initiation and progression of interstitial lung disease. Pathogenesis is the consequence of damage to lung cells and resulting lung scarring associated with activation of fibrotic processes. This review presents the radiologic and histologic characteristics of simple and complicated coal workers’ pneumoconiosis (CWP) as well as pathological indices of acute and chronic silicosis. This presentation also reviews the results of in vitro, animal, and human investigations that elucidate mechanisms involved in the development of these pneumoconioses. Results support the involvement of four basic mechanisms in the etiology of CWP and silicosis:1. Direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring.2. Activation of oxidant production by pulmonary phagocytes, such as alveolar macrophages. When oxidant production exceeds antioxidant defenses, lipid peroxidation and protein nitrosation occur, resulting in tissue injury and consequent scarring.3. Activation of mediator release from alveolar macrophages and alveolar epithelial cells. Chemokines recruit polymorphonuclear leukocytes and macrophages from the pulmonary capillaries into the air spaces. Once within the air spaces, these leukocytes are activated by proinflammatory cytokines to produce reactive species, which increase oxidant injury and lung scarring.4. Secretion of growth factors from alveolar macrophages and alveolar epithelial cells. Release of such mediators stimulates fibroblast proliferation and induces fibrosis.In conclusion, results of in vitro and animal studies have provided the basis for proposing mechanisms that may lead to the initiation and progression of CWP and silicosis. Data obtained from exposed workers has lent support to these proposals. The mechanistic understanding obtained for the development of CWP and silicosis should be useful in elucidating the possible pathogenicity of other inhaled particles.

An Unusual Form of Progressive Massive Fibrosis In Pneumoconiosis

Pneumoconiosis, very popular to coal miners who are exposed to coal dusts dominantly, was introduced in the 19th century to describe diseases consequent to the inhalation of mineral dusts. Coal workers' pneumoconiosis(CWP) colloquially called black lung in the United States, is a distinct pathologic entity resulting from the tissue reaction to deposits of dust include the coal macule, which associated with focal emphysema constitutes the characteristic lesion of simple CWP and complicated CWP or progressive massive fibrosis(PMF). Coal mining are also associated with chronic bronchitis, chronic airflow limitation, and/or generalized emphysema. Progressive massive fibrosis lesions may imprint on and obliterate airways and vessels, and cavitation is not uncommon, being the consequence of ischemic necrosis or mycobacterial infections. We report a case which is unusual form of progressive massive fibrosis to be differentiated from carcinoma. It is a rapid growing PMF with ischemic necrosis. By the studies which are about risk of having progressive massive fibroois, it is predicted to be 1.4%. And the other study shows that simple pneumoconiosis clearly predisposed to PMF, with five year attack rates of 13.9%, 12.5%, 4.4% and 0.2% among men with categories 3, 2, 1, and 0 respectively at the start of the risk periods.

Airways obstruction, coal mining, and disability.

It has recently been suggested that the inhalation of coal in the absence of complicated coal workers' pneumoconiosis (CWP) or smoking can lead to disabling airways obstruction. The cause of such obstruction has been variously attributed to emphysema or bronchitis. The frequency of significant airways obstruction in a group of United States coal miners seeking compensation for occupationally induced pulmonary impairment was therefore determined. In a sample of 611 "Black Lung" claimants there was only one subject who was a non-smoker and who in the absence of other non-occupationally related diseases,--for example, asthma and bronchiectasis--had sufficient airways obstruction to render it difficult for him to carry out hard labour. An alternative explanation for his reduced ventilatory capacity other than coal dust or smoking may be available. If the inhalation of coal dust in the absence of smoking and complicated CWP ever induces sufficient ventilatory impairment to preclude a miner from working, it is indeed rare.

Life expectancy of Pennsylvania coal miners compensated for disability as affected by pneumoconiosis and ventilatory impairment.

From December 1965 through December 1967, 13,000 Pennsylvania coal miners were awarded compensation for complete disability due to coal workers’ pneumoconiosis (CWP). Standardized mortality ratios compare all deaths occurring in a sample of 4,004 of these men with deaths expected (1959 to 1961) of white men in Pennsylvania; similar ratios are shown for anthracite and bituminous miners by category and stage of CWP and, in some cases, according to whether the ratio of forced expiratory volume during the first second of a forced exhalation after maximum inhalation to vital capacity (FEV1/FVC) was greater or less than 55%. Excess deaths were found primarily in subjects with a reduced ventilatory capacity, and secondarily with complicated CWP of stage C or, for anthracite miners, stage B. No excess deaths were found for simple CWP or stage A complicated with FEV1/FVC more than 55%.