Coal Worker’s Pneumoconiosis
Also known as black lung, coal miner’s disease, miner’s asthma, anthracosis, and anthracosilicosis, coal worker’s pneumoconiosis is a progressive nodular pulmonary disease resulting from occupational or environmental injury. The disease occurs in two forms: simple and complicated. With the simple form, the patient has characteristically limited lung capacity that may lead to complicated coal worker’s pneumoconiosis (also known as progressive massive fibrosis). In the complicated form, fibrous tissue masses form in the lungs.
A person’s risk of coal worker’s pneumoconiosis depends on various factors, including how long he has been exposed to coal dust (usually 15 or more years), the intensity of his exposure (dust count and size of inhaled particles), his proximity to the mine site, the silica content of the coal (anthracite has the highest silica content), and his susceptibility. The highest incidence of this disease is among anthracite miners in the eastern United States. The number of deaths in 1998 was 1,498.
Causes
Inhalation and prolonged retention of respirable coal dust particles (less than 5 microns wide) cause coal worker’s pneumoconiosis. In the simple form, macules
(coal dust-laden macrophages) form around terminal and respiratory bronchioles and are surrounded by a halo of dilated alveoli. At the same time, supporting tissues atrophy and harden, causing permanent small-airway dilation (focal emphysema). Simple coal worker’s pneumoconiosis may progress to the complicated form—most likely if the disease begins after a relatively short exposure.
(coal dust-laden macrophages) form around terminal and respiratory bronchioles and are surrounded by a halo of dilated alveoli. At the same time, supporting tissues atrophy and harden, causing permanent small-airway dilation (focal emphysema). Simple coal worker’s pneumoconiosis may progress to the complicated form—most likely if the disease begins after a relatively short exposure.
Complicated coal worker’s pneumoconiosis may involve one or both lungs. Fibrous tissue masses enlarge and coalesce, grossly distorting pulmonary structures as the disease progressively destroys vessels, alveoli, and airways.
Metal, inorganic, and silicate dusts cause pneumoconiosis as well. Occupations that involve manufacturing of tin, glass, insecticides, rock, pottery, cement, and insulation create inert dusts.
Complications
Pulmonary hypertension, cor pulmonale, and pulmonary tuberculosis can complicate coal worker’s pneumoconiosis. In cigarette smokers, chronic bronchitis and emphysema can also complicate the disease.
Assessment
Whether the patient has simple or complicated coal worker’s pneumoconiosis, the history will disclose exposure to coal dust. In the simple form, the patient is typically asymptomatic, especially if he’s a nonsmoker.
In complicated coal worker’s pneumoconiosis, the patient history may reveal exertional dyspnea and a cough. This patient may state that he occasionally coughs up inky-black sputum (from avascular necrosis and cavitation).
Additionally, the patient may report a productive cough with milky, gray, clear, or coal-flecked sputum or yellow, green, or thick sputum with recurrent bronchial and pulmonary infections.
Inspection may reveal a barrel chest. Percussion may uncover hyperresonant lungs with areas of dullness. On auscultation, you’ll hear diminished breath sounds, crackles, rhonchi, and wheezes.
Diagnostic tests
