Pneumoconioses of coal industry workers

Coal workers' pneumoconiosis (anthracosis; black lung disease; miners' pneumoconiosis) is caused by inhalation of coal dust. Dust deposition results in accumulation of dust-laden macrophages around the bronchioles (coal macules), sometimes causing central bronchiolar emphysema.

Pneumoconiosis usually causes no symptoms, but may progress to progressive massive fibrosis with decreased lung function. Diagnosis is based on history and chest x-ray. Treatment of pneumoconiosis is generally effective.

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What causes pneumoconiosis?

Pneumoconiosis is caused by chronic inhalation of high-carbon coal dust (anthracite and bituminous coal), typically for more than 20 years. Inhalation of silica contained in the coal may also contribute to the clinical manifestations of the disease. Alveolar macrophages ingest the dust, release cytokines that stimulate inflammation, and accumulate in the lung interstitium around the bronchioles and alveoli (coal macules). Coal nodules develop due to collagen accumulation, and central emphysema develops due to weakening and dilation of the bronchiolar walls. Fibrosis may occur but is usually limited to areas adjacent to the coal macules. Changes in lung architecture, bronchial obstruction, and functional impairment are usually mild but may be severe in some patients.

Two forms of the disease have been described: simple, with isolated coal macules, and complicated, with coalescing macules and progressive massive fibrosis (PMF). In patients with simple pneumoconiosis, PMF develops with an incidence of approximately 1% to 2%. In this condition, nodules coalesce to form black, rubbery parenchymatous masses, usually in the upper posterior lung regions. The masses may become invasive and impair blood supply and airways or develop into cavities. PMF may develop and progress even after coal dust exposure has ceased. Despite the similarities between coal-induced PMF and silicotic conglomerate, the development of coal workers' pneumoconiosis is not related to the quartz content of the coal.

The relationship between pneumoconiosis and the characteristic symptoms of rheumatoid arthritis is well described. It is unclear whether miners' pneumoconiosis predisposes patients to rheumatoid arthritis, whether patients with pneumoconiosis develop a special form of rheumatoid arthritis, or whether rheumatoid arthritis increases miners' sensitivity to coal dust. Multiple rounded pulmonary nodules appearing in a relatively short time (Caplan syndrome) represent an immunopathological reaction associated with rheumatoid diathesis. Histologically, they resemble rheumatoid nodules but have a peripheral zone of more acute inflammation. Patients with pneumoconiosis are at moderately increased risk of developing active tuberculosis and nontuberculous mycobacterial infection. The same principles of observation and treatment of tuberculosis as those for silicosis apply to pneumoconiosis. A weak association has been found between pneumoconiosis and progressive systemic sclerosis and gastric cancer.

Symptoms of pneumoconiosis

Pneumoconiosis is usually asymptomatic. Most chronic pulmonary symptoms in miners are caused by other conditions, such as industrial bronchitis caused by coal dust or associated emphysema from smoking. Cough may be chronic and may persist even after workers have changed jobs, even in nonsmokers.

PMF causes progressive dyspnea. Black sputum (melanophthisis) is rare and is caused by rupture of PMF areas into the airways. PMF often progresses to pulmonary hypertension with right ventricular failure.

Diagnosis of pneumoconiosis

The diagnosis depends on the history of exposure to the insult and the demonstration on chest radiography or chest CT of scattered, small rounded infiltrates or nodules (SRIs) or at least one infiltrate greater than 10 mm in the presence of pneumoconiosis (PMF). The specificity of chest radiography for PMF is low because up to one-third of lesions identified as PMF turn out to be malignancies, scars, or other lesions. Chest CT is more sensitive than chest radiography for detecting confluent nodules, early PMF, and cavitation. Pulmonary function tests are not diagnostic but are useful for assessing pulmonary function in patients who may develop obstructive, restrictive, or mixed lung disorders. Because disturbances of gas exchange occur in a number of patients with extensive simple pneumoconiosis and with complicated pneumoconiosis, it is recommended that studies of the diffusion capacity of carbon monoxide (DLC0) and arterial blood gases be performed early in the course of pulmonary disease and periodically at rest and during exercise.

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Treatment of pneumoconiosis

Treatment of pneumoconiosis is rarely necessary in simple pneumoconiosis, although smoking cessation and tuberculosis surveillance are recommended. Supplemental oxygen therapy is given to patients with pulmonary hypertension and/or hypoxemia. Pulmonary rehabilitation may help more severely affected workers tolerate everyday physical activities.

How to prevent pneumoconiosis?

Preventive measures include eliminating dust exposure, stopping smoking, and getting vaccinated against pneumococcus and influenza. Workers with pneumoconiosis, especially PMF, should be protected from further exposure to dust, especially at high concentrations. Tuberculosis is treated according to current recommendations.

Pneumoconiosis can be prevented by suppressing coal dust formation in coal seams. Despite numerous regulations, dust exposure continues to occur in the mining industry. Respiratory masks provide only limited protection.