Coal remains the second largest energy source worldwide. Internationally, coal consumption has steadily increased since 2000, driven largely by the increased demand in China and India.20 The United States has the largest coal reserves globally, with the Powder River Basin of Wyoming and Montana being its largest coal producing region. The U.S. coal production decreased by about 2% year over year, amounting to about 750 million short tons in 2018.21 The U.S. coal production in 2018 was classified as follows (arranged in an increasing order of coal rank or hardness to reflect the degree of metamorphosis of the coal): lignite (8%), subbituminous (45%), bituminous (47%), and anthracite (0.3%).21 Anthracite deposits are associated with the highest rates of lung disease.22 Surface coal mining accounts for an increasing fraction of coal mined in the United States, particularly in the western states, while the underground mining workforce has been decreasing.21
In addition to carbon, coal contains silica, silicates (such as mica and kaolin), metals, and volatile compounds.23 Airborne coal mine dust also contains silica and silicate particles generated as the neighboring rock in the coal seam is cut. Coal miners may be exposed to multiple other potential respiratory hazards in the mine, such as diesel engine exhaust; microbial bioaerosols24; “rock dust” (a finely crushed powder composed of limestone and containing crystalline silica, which is applied to the mine surfaces to dilute the highly explosive finely dispersed coal dust)23; and chemicals such as isocyanates (used in roof bolt glues, and as fire retardant for ventilation systems in polyurethane foam).25 Prolonged inhalation of coal mine dust causes a spectrum of lung diseases collectively termed coal mine dust lung disease (CMDLD). “Black lung” is a generic term used legislatively and popularly to describe CMDLD.
In 2019, almost 54,000 employees worked in U.S. coal mines.21 With 28% of the world’s recoverable coal reserves, mining employment in the United States is likely to remain significant for many years despite recent mine closures.26 Significant exposure to coal mine dust may occur not only underground but also in surface mines (including strip and auger mines), in coal preparation plants, and in coal-handling operations. Workers engaged in face work and coal preparation often have the highest exposures to respirable coal dust and thus the highest rates of CMDLD. Some surface mine jobs such as drillers can involve high exposures to silica, especially if dust control measures are missing or ineffective.27 Cumulative coal mine dust exposure is the most important factor in the development of CMDLD.28
Prior to 1970, dust concentrations in face jobs in underground coal mines in the United States ranged from 6 to 10 mg/m3. Subsequent to the 1969 Federal Coal Mine Health and Safety Act,29 dust levels were reduced to 2 mg/m3. Although these regulations reduced dust exposures in coal mines,30 recent evidence suggests that the miners were not uniformly protected from developing disease.31–34 In 2011, the U.S. National Institute for Occupational Safety and Health (NIOSH) recommended that exposure to respirable coal mine dust should be limited to 1 mg/m3.27 In 2014, the U.S. Mine Safety and Health Administration (MSHA) reduced coal mine dust exposure to 1.5 mg/m3.35
Recent evidence points toward an ongoing increase in both the prevalence and severity of CMDLD since the late 1990s.26,31–34,36,37 The 2017 data from the NIOSH surveillance program showed a greater than 10% overall prevalence of radiographic pneumoconiosis for underground coal miners with over 25 years’ tenure. A 21% prevalence of radiographic pneumoconiosis was described in central Appalachian long-tenured miners.36 The rate of PMF in long-tenured underground coal miners was 1.1% in 2014, compared to 0.3% at its nadir in the late-1990s.37,38 The rate of PMF in central Appalachia reached 4.5% for the 5-year period ending 2017.36 Most of the affected coal miners worked their entire careers after the 1969 dust limits had gone into effect, calling into question the effectiveness of modern dust controls in the United States. Nationwide, disease rates are elevated among miners working in smaller mines.37
Based on experiments on rats, inhalation of coal mine dust causes an influx of inflammatory leukocytes and activated macrophages to the alveolar region.39 The activated inflammatory cells demonstrate enhanced ability to degrade fibronectin, a key for maintaining lung structure. Following cessation of exposure, rats continue to show increased proteolysis of fibronectin by bronchoalveolar leukocytes.39 Experimental lesions of emphysema were produced in rats after laryngotracheal injection of papain (a destructive biological enzyme) and coal dust.40 The lesions observed were progressive.
CMDLD is a collection of respiratory diseases resulting from the parenchymal, airway, and pleural effects of the inhalational exposure to coal mine dust. As shown in Fig. E1-1, parenchymal CMDLD may be classified as nodular lung diseases (including classic coal workers’ pneumoconiosis or CWP, and PMF), dust-related diffuse pulmonary fibrosis (or secondary UIP),41–43 other interstitial pneumonitis (including hypersensitivity pneumonitis from microbial aerosols),23,44 and alveolar proteinosis.43 Airway-dominant CMDLD may be classified as chronic bronchitis45,46 and emphysema47 phenotypes of COPD, work-related asthma,25,48–50 and small airways diseases.51 Pleural changes in CMDLD include pleural effusions,52,53 rounded atelectasis,54 circumscribed pleural thickening/pleural plaques and diffuse pleural thickening.55
Classic CWP is pathologically defined by the characteristic coal macule lesion, a 1–2 mm collection of coal dust and dust-laden macrophages in the periphery of the respiratory bronchioles. The coal macule may be surrounded by focal emphysema. Coal nodules are larger lesions containing a mixture of coal dust–laden macrophages, collagen, and reticulin. Coal nodules are responsible for the small opacities seen on the chest radiographs of miners with classic CWP. Radiologic changes described in the literature are small rounded opacities, not exceeding 1 cm in diameter, with bilateral upper lobe predominance. Recent evidence, however, indicates that the small opacities may either be equally distributed throughout all lung zones56 or be lower lung zone predominant.55 In addition, the small opacities may be irregular or linear on chest radiographs in 38–47% of coal miners.55,56 With increased profusion of small opacities in the lung comes greater functional abnormalities, but some patients with CWP may not demonstrate significant respiratory symptoms or limiting physiologic impairment.
Complicated CWP or PMF is marked by the radiological presence of one or more opacities greater than 1 cm in size and occurring on a background of classic CWP. PMF lesions are typically upper lobe predominant and tend to be bilaterally distributed as disease progresses. Significant emphysema and fibrotic scarring with hilar distortion are often present. Higher profusion of classic CWP is associated with an increased risk of developing PMF, even after cessation of exposure.57,58 Miners with PMF with large opacities of combined diameter greater than 5 cm have an increased mortality rate when compared to nonminers or miners with classic CWP.59–61
The term “rapidly progressive’” CWP refers to the radiographic progression of more than one ILO profusion category (which defines the extent of radiologic change) of small pneumoconiotic opacities within 5 years, or the development of PMF after 1985 in the United States.34 Data from 1996 to 2002 showed that 35% of newly diagnosed cases of CWP in the United States were “rapidly progressive.”34 Miners with “rapidly progressive” disease were younger and more likely to work at the mine face and in small mines.34 U.S. data suggest that respirable silica and silicate dust content from mining of thin coal seams may be a contributing factor to some “rapidly progressive” CWP.43,62
Dust-Related Diffuse Fibrosis of the Lung
Coal mine dust exposure also contributes to the dust-related diffuse fibrosis phenotype of CMDLD, or secondary UIP.41–43 The clinical, radiological, and functional characteristics of this disease mimics IPF,63 but it generally has a more benign disease course with a longer survival time.63 This phenotype of CMDLD may be misclassified as “idiopathic” in circumstances where an inadequate occupational history has been obtained,64 with important implications for both disease management and prognosis.26
Emphysema seen in CMDLD is most commonly the centriacinar type; pathologically, it is referred to as focal emphysema when a coal dust macule is also present. Bullous and panacinar emphysema have also been described and are part of the continuum of disease that may follow either smoking or coal mine dust exposure.26,47,63,65 In an autopsy study, cumulative exposures to respirable coal mine dust or coal dust retained in the lungs were significant predictors of emphysema severity and the contributions of coal mine dust exposure and cigarette smoking toward emphysema severity were similar.47
Chronic bronchitis, characterized pathologically by hypertrophy and hyperplasia of the bronchial mucous glands with an associated increase in the goblet cells of the small airways, occurs as a result of dust exposure. Clinically defined as the chronic production of phlegm, chronic bronchitis is a frequent clinical finding among coal miners, and its prevalence and incidence are related to dust exposure.45,46
The key to preventing CMDLD is prevention of prolonged inhalation of significant concentrations of coal mine dust. Secondary prevention strategies, for example, removal of miners with early evidence of CMDLD to low-dust jobs can assist in reducing the incidence of severe disease. This strategy was mandated by the U.S. Congress in the Federal Coal Mine Health and Safety Act of 196929 and has been implemented with substantial but incomplete success in underground operations of the U.S. coal industry.