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Causes and Incidence The cause is inhalation and prolonged retention of bituminous or anthracite coal dust. Susceptibility increases with length and intensity of exposure, smallness of inhaled particles, and silica content of the coal. Anthracite coal miners in the eastern United States have the highest incidence.

Disease Process The deposition of coal dust triggers a phagocytic reaction and increases the production of macrophages. As the dust overwhelms the pulmonary clearing mechanism, fibroblasts appear and lay down a network of reticulin fibers that enmesh the dust. The collections of macrophages and reticulin fibers around the bronchioles, known as coal macules, lead to dilation of the alveoli; this is known as the simple disease phase. If allowed to progress, the macules enlarge and coalesce and a massive fibrosis occurs, which destroys pulmonary structures as the vascular bed, alveoli, and airways are invaded; this is the complicated phase.

Symptoms

Simple phase

Asymptomatic

Complicated phase

Exertional dyspnea, hypoxia, black sputum

Potential Complications Pulmonary hypertension and cor pulmonale may develop in severe cases. Smoking, bronchitis, emphysema, and other respiratory diseases aggravate the disease process.

Diagnostic Tests

Clinical examination

History of exposure to coal dust, usually at least 10 years underground

Radiology

Simple phase: small, rounded opacities in both lung fields Complicated phase: large opacities (.1 cm) mixed with numerous small opacities

Pulmonary function

Simple phase: normal vital capacity Complicated phase: decreased

Arterial blood gases

Simple phase: normal; decreased PO2 Complicated phase: increased PCO2

Treatments

Surgery

None

Drugs

None

General

Simple phase: eliminate further exposure; prevent secondary infections Complicated phase: chest physiotherapy and steam inhalation to loosen and remove secretions; increased fluid intake to thin secretions; oxygen (advanced stage)