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Coal Workers’ Pneumoconiosis
(Anthracosis; Black Lung Disease; Coal Miner’s Pneumoconiosis)
Coal workers’ pneumoconiosis (CWP) is caused by inhalation of coal dust. Deposition of dust produces dust-laden macrophages around bronchioles (coal macules), occasionally causing focal bronchiolar emphysema. CWP usually causes no symptoms but can progress to progressive massive fibrosis (PMF) with impaired lung function. Diagnosis is based on history and chest x-ray findings. Treatment is generally supportive.
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 CWP are described:
Patients with simple CWP develop PMF at a rate of about 1 to 2% /yr. Recently, rapid progression of CWP to PMF has been recognized in young miners, especially in the eastern US.
In PMF, nodules coalesce to form black, rubbery parenchymal masses usually in the upper posterior fields. The masses may encroach on and destroy vascular supply and airways or may cavitate. PMF can develop and progress even after exposure to coal dust has ceased. Despite the similarity of coal-induced PMF and conglomerate silicosis, the development of PMF in coal workers is unrelated to the silica content of the coal.
An association between CWP and features of rheumatoid arthritis (RA) is well-described. It is unclear whether CWP predisposes miners to developing RA, whether RA takes on a unique form in patients with CWP, or whether RA 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. Patients with CWP are at a slightly increased risk of developing active TB and non-TB mycobacterial infections. Weak associations have been reported between CWP and progressive systemic sclerosis and stomach cancer.
CWP 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.
PMF causes progressive dyspnea. Occasionally, patients cough up black sputum (melanoptysis), which occurs when PMF lesions rupture into the airways. PMF often progresses to pulmonary hypertension with right ventricular and respiratory failure.
Diagnosis is based on a history of exposure and chest x-ray or chest CT appearance. In patients with CWP, x-ray or CT reveals diffuse, small, rounded opacities or nodules. The finding of at least one opacity > 10 mm suggests PMF. The specificity of the chest x-ray for PMF is low because up to one third of the lesions identified as being PMF 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 PMF, and cavitation.
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 CWP and in those with complicated CWP, baseline and periodic measures of diffusing capacity for carbon monoxide (DL co ) and ABG at rest and during exercise are recommended.
Because patients with CWP often have had exposure to both silica dust and coal dust, surveillance for TB is usually done. Patients with CWP 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 CWP, although smoking cessation and TB surveillance are recommended. Patients with pulmonary hypertension, hypoxemia, or both are given supplemental O 2 therapy. Pulmonary rehabilitation can help more severely affected workers carry out activities of daily living. Workers with CWP, especially those with PMF, should be restricted from further exposure, especially to high concentrations of dust. TB is treated in accordance with current recommendations (see Tuberculosis (TB) : Treatment).
Preventive measures include eliminating exposure, stopping smoking, and giving pneumococcal and influenza vaccinations. CWP 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 (CWP) is caused by chronic inhalation of dust from high-carbon coal (anthracite and bituminous) and rarely graphite, typically over ≥ 20 yr.
Most patients have simple CWP, with small, asymptomatic nodules seen on imaging.
Some patients with CWP 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.
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