Coal Workers’ Pneumoconiosis
(Anthracosis; Black Lung Disease; Coal Miner’s Pneumoconiosis)
(See also Overview of Environmental Pulmonary Disease.)
Alveolar macrophages engulf the dust, release cytokines that stimulate inflammation, and collect in lung interstitium around bronchioles and alveoli (coal macules). Coal nodules develop as collagen accumulates, and focal emphysema develops as bronchiole walls weaken and dilate. Fibrosis can occur but is usually limited to areas adjacent to coal macules. Distortion of lung architecture, airflow obstruction, and functional impairment are usually mild but can be highly destructive in some patients.
Two forms of coal workers' pneumoconiosis are described:
Patients with simple coal workers' pneumoconiosis develop progressive massive fibrosis at a rate of about 1 to 2% /year. Recently, rapid progression of coal workers' pneumoconiosis to progressive massive fibrosis has been recognized in young miners, especially in the eastern US compared to the rest of the United States (1).
In progressive massive fibrosis, nodules coalesce to form black, rubbery parenchymal masses usually in the upper posterior lung fields. The masses may encroach on and destroy vascular supply and airways or may cavitate. Progressive massive fibrosis can develop and progress even after exposure to coal dust has ceased. Despite the similarity of coal-induced progressive massive fibrosis and conglomerate silicosis, the development of progressive massive fibrosis in coal workers is unrelated to the silica content of the coal. However, exposure to silica in coal is required for progression from coal workers' pneumoconiosis to progressive massive fibrosis, and exposure to graphite alone can cause coal workers' pneumoconiosis but not progression to progressive massive fibrosis.
A small percentage of patients with coal workers' pneumoconiosis develop diffuse pulmonary fibrosis.
An association between coal workers' pneumoconiosis and features of rheumatoid arthritis is well-described. It is unclear whether coal worker's pneumoconiosis predisposes miners to developing rheumatoid arthritis, whether rheumatoid arthritis takes on a unique form in patients with coal workers' pneumoconiosis, or whether rheumatoid arthritis alters the response of miners to coal dust. Multiple rounded nodules in the lung appearing over a relatively short time (Caplan syndrome) represent an immunopathologic response related to rheumatoid diathesis. Histologically, they resemble rheumatoid nodules but have a peripheral region of more acute inflammation.
1. Almberg KS, Halldin CN, Blackley DJ, et al: Progressive massive fibrosis resurgence identified in U.S. coal miners filing for black lung benefits, 1970-2016. Ann Am Thorac Soc 15(12):1420–1426, 2018. doi: 10.1513/AnnalsATS.201804-261OC
Coal workers' pneumoconiosis does not usually cause symptoms. Most chronic pulmonary symptoms in coal miners are caused by other conditions, such as industrial bronchitis due to coal dust or coincident emphysema due to smoking. Cough can be chronic and problematic in patients even after they leave the workplace, even in those who do not smoke.
Progressive massive fibrosis causes progressive dyspnea. Occasionally, patients cough up black sputum (melanoptysis), which occurs when progressive massive fibrosis lesions rupture into the airways. Progressive massive fibrosis often progresses to pulmonary hypertension with right ventricular failure and respiratory failure.
Diagnosis of coal workers’ pneumoconiosis is based on a history of exposure to coal dust and chest x-ray or chest CT appearance.
In patients with coal workers' pneumoconiosis, chest x-ray or CT reveals diffuse, small, rounded opacities or nodules. The finding of at least one opacity > 10 mm suggests progressive massive fibrosis. The specificity of the chest x-ray for progressive massive fibrosis is low because up to one third of the lesions identified as being progressive massive fibrosis turn out to be cancers, scars, or other disorders. Chest CT is more sensitive and specific than chest x-ray for detecting coalescing nodules, early progressive massive fibrosis, and cavitation.
Diffuse pulmonary fibrosis is characterized by lower lobe predominant reticular opacities. Honeycomb changes have also been reported.
Pulmonary function tests are nondiagnostic but are useful for characterizing lung function in patients in whom obstructive, restrictive, or mixed defects may develop. Because abnormalities of gas exchange occur in some patients with extensive simple coal workers' pneumoconiosis and in those with complicated coal worker's pneumoconiosis, baseline and periodic measures of diffusing capacity for carbon monoxide (DLCO) and arterial blood gas levels at rest and during exercise are recommended.
Because patients with coal workers' pneumoconiosis often have had exposure to both silica dust and coal dust, surveillance for tuberculosis (TB) is usually done. Patients with coal workers' pneumoconiosis should have annual tuberculin skin testing. In those with positive test results, sputum culture and cytology, CT, and bronchoscopy may be needed to confirm TB.
Treatment is rarely necessary in simple coal workers' pneumoconiosis, although smoking cessation and TB surveillance are recommended. Patients with pulmonary hypertension, hypoxemia, or both are given supplemental oxygen therapy.
Pulmonary rehabilitation can help more severely affected workers carry out activities of daily living. Workers with coal workers' pneumoconiosis, especially those with progressive massive fibrosis, should be restricted from further exposure, especially to high concentrations of dust. TB is treated in accordance with current recommendations.
Preventive measures include eliminating exposure, stopping smoking, and giving pneumococcal and influenza vaccinations. Coal workers' pneumoconiosis can be prevented by suppressing coal dust at the coal face. Despite long-standing regulations, exposures continue to occur in the mining trade, resulting in increased rates of disease, including severe forms.
Respiratory masks provide only limited protection.
Coal workers’ pneumoconiosis is caused by chronic inhalation of dust from high-carbon coal (anthracite and bituminous) and rarely graphite, typically over ≥ 20 years.
Most patients have simple coal workers' pneumoconiosis, with small, asymptomatic nodules seen on imaging.
Some patients with coal workers' pneumoconiosis develop progressive massive fibrosis, with deterioration of pulmonary function, dyspnea, and marked abnormalities on imaging studies.
Base the diagnosis on history of exposure as well as chest imaging.
Treat supportively, encourage smoking cessation, and restrict further exposure.