Coal Workers’ Pneumoconiosis

William G. Hughson

Coal workers’ pneumoconiosis, formerly called anthracosis or anthracosilicosis, exists in two forms: simple and complicated. Simple coal workers’ pneumoconiosis is diagnosed by a history of exposure to coal dust and chest radiographs showing an increased profusion of small, round parenchymal densities (categories 0, 1, 2, and 3 as rated by the International Labor Office system for grading radiographs for pneumoconiosis). Complicated coal workers’ pneumoconiosis is known as progressive massive fibrosis. The diagnosis of progressive massive fibrosis requires densities larger than 1 cm in diameter; some authorities require lesions larger than 2 cm.

Bronchial stenosis associated with black pigmentation of the overlying mucosa was thought to be complication of tuberculosis. However, this condition has now been reported where tuberculosis was excluded, and the term anthracofibrosis is used to describe it. The stenosis and associated postobstructive atelectasis can mimic lung cancer.

PATHOPHYSIOLOGY

The basic pathologic lesion in simple coal workers’ pneumoconiosis is the coal macule. This is a collection of coal dust-laden macrophages, reticulin, and collagen located within the walls of respiratory bronchioles and adjacent alveoli. Macules range in size from 1 to 5 mm in diameter and are located predominantly in the upper lobes. As the number of macrophages grows, fibrosis increases, creating micronodules (<7 mm) and macronodules (7–20 mm). A zone of focal emphysema is usually seen around macules and nodules, possibly caused by mechanical traction on adjacent parenchyma or digestion of alveolar walls by proteolytic enzymes released from macrophages. A tendency is seen for nodules to cluster and eventually to coalesce to produce progressive massive fibrosis lesions. There is some evidence that coal workers may be at risk for chronic interstitial pneumonia, even when coal workers’ pneumoconiosis is not present.

PATHOGENESIS

The pathogenesis of coal workers’ pneumoconiosis is unclear. Silica in coal dust was thought to be the cause; it is now recognized that coal workers’ pneumoconiosis is a pathologic entity distinct from silicosis, although the two conditions can coexist. Coal is composed predominantly of elemental carbon and varying amounts of minerals, metals, and organic compounds. Electrically charged surface radicals on coal dust damage biologic membranes. Regional differences in the frequency and severity of coal workers’ pneumoconiosis may be caused by the content of Fe²⁺ and the buffering capacity of the dust. Higher (hardness)-rank coals are associated with increased risk of simple coal workers’ pneumoconiosis and progressive massive fibrosis. Anthracite is the highest rank, followed by bituminous and lignite. Experimentally, high-rank coals are cleared more slowly from the lungs and are more cytotoxic. The attack rate for progressive massive fibrosis rises with increasing total lung dust; progressive massive fibrosis usually occurs in the setting of advanced simple coal workers’ pneumoconiosis (categories 2 and 3). Increased silica content of inhaled dust also increases the incidence of progressive massive fibrosis. Historically, tuberculosis has been considered as a risk factor for progressive massive fibrosis; its role has diminished in recent decades, although this organism should always be sought in a patient with expanding upper-lobe lesions. Cavitation of progressive massive fibrosis lesions usually results from tissue necrosis, not tuberculosis. Coal miners do not have a greater incidence of tuberculosis compared with the general population.

The pulmonary macrophage plays a central role in the pathogenesis of coal workers’ pneumoconiosis by releasing inflammatory factors, recruiting polymorphonuclear leukocytes into the lung, and stimulating fibroblast production of collagen. A number of immunologic abnormalities have been found in miners with coal workers’ pneumoconiosis. Their causative role, if any, is unknown and their prevalence has varied in different studies. Miners with coal workers’ pneumoconiosis have elevated serum levels of IgA, IgG, C3, antinuclear antibodies, rheumatoid factor, and α₁-proteinase inhibitor; similar findings are seen in other forms of pneumoconiosis.

No clear correlation is found between serologic factors and the risk or severity of coal workers’ pneumoconiosis except for rheumatoid pneumoconiosis (Caplan syndrome), which describes coal miners with rheumatoid arthritis. The characteristic radiographic features of rheumatoid pneumoconiosis are rapidly enlarging, evenly distributed nodules ranging in size from 0.3 to 5.0 cm in diameter, occurring in lungs that otherwise show little evidence of pneumoconiosis. Microscopically, the active lesions are similar to subcutaneous rheumatoid nodules; vasculitis is a common feature. Coal mining does not predispose to rheumatoid arthritis.

REGULATIONS AND RISK OF COAL WORKERS’ PNEUMOCONIOSIS

The risk of development and progression of coal workers’ pneumoconiosis increases with cumulative dust exposure. Most affected miners worked before 1969, when the Federal Coal Mine Health and Safety Act (known as the Coal Act) was passed. It required that a coal worker’s exposure to respirable dust be maintained at or below 2 mg/m³. The Federal Mine Safety and Health Act of 1977 (known as the Mine Act

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