Coal worker’s pneumoconiosis
Coal worker’s pneumoconiosis (CWP) goes by several names, including black lung disease, coal miner’s disease, miner’s asthma, and anthracosis. It’s a progressive nodular pulmonary disease and occurs in two forms: Simple CWP is characterized by small lung opacities; and complicated CWP, also known as progressive massive fibrosis, is characterized by masses of fibrous tissue that develop in the lungs.
The risk of developing CWP depends on the duration of exposure to coal dust (usually 15 years or longer), intensity of exposure (dust count, particle size), location of the mine, silica content of the coal (anthracite coal has the highest silica content), and the worker’s susceptibility. Incidence of CWP is highest among anthracite coal miners in the eastern United States.
The prognosis varies. Simple asymptomatic disease is self-limiting, although progression to complicated CWP is more likely if CWP begins after a relatively short period of exposure. Complicated CWP may be disabling, resulting in severe ventilatory
failure and right-sided heart failure secondary to pulmonary hypertension.
failure and right-sided heart failure secondary to pulmonary hypertension.
Causes
CWP is caused by the inhalation and prolonged retention of respirable coal dust particles (less than 5 microns in diameter). Simple CWP results in the formation of macules (accumulations of macrophages laden with coal dust) around the terminal and respiratory bronchioles, surrounded by a halo of dilated alveoli. Macule formation leads to atrophy of supporting tissue, causing permanent dilation of small airways (focal emphysema).
Simple CWP may progress to the more complicated form if the disease involves a lung. If this happens, fibrous tissue masses enlarge and coalesce, causing gross distortion of pulmonary structures (destruction of vasculature, alveoli, and airways).
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