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Coal Workers Pneumoconiosis

Coal worker's pneumoconiosis (CWP), a progressive nodular pulmonary disease, occurs in two forms. This disease goes by several names, including black lung disease, coal miner's disease, miner's asthma, and anthracosis.

Simple CWP is characterized by small lung opacities. In complicated CWP, also known as progressive massive fibrosis, masses of fibrous tissue occasionally develop in the lungs of patients with simple CWP.

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 severe ventilatory failure and right-sided heart failure secondary to pulmonary hypertension.

Causes

Simple CWP may progress to the more complicated form if the disease involves one or both lungs. If this happens, fibrous tissue masses enlarge and coalesce, causing gross distortion of pulmonary structures (destruction of vasculature, alveoli, and airways).

Signs and symptoms

Simple CWP is asymptomatic, especially in nonsmokers. Symptoms appear if complicated CWP develops; they include exertional dyspnea and a cough that occasionally produces inky-black sputum when fibrotic changes undergo avascular necrosis and their centers cavitate.

Other clinical features of CWP include increasing dyspnea and a cough that produces milky, gray, clear, or coalflecked sputum. Recurrent bronchial and pulmonary infections produce thick yellow or green sputum.

Complications include pulmonary hypertension, right ventricular hypertrophy and cor pulmonale, and pulmonary tuberculosis. In cigarette smokers, chronic bronchitis and emphysema may also complicate the disease.

Diagnosis

The patient history reveals exposure to coal dust. Physical examination shows a barrel chest, hyperresonant lungs with areas of dullness, diminished breath sounds, crackles, rhonchi, and wheezes.

In simple CWP, chest X-rays show small opacities (< 10 mm in diameter), which may be present in all lung zones but are more prominent in the upper lung zones. In complicated CWP one or more large opacities (1 to 5 cm in diameter), possibly exhibiting cavitation, are seen.

Treatment

The goal of treatment is to relieve respiratory symptoms, to manage hypoxia and cor pulmonale, and to avoid respiratory tract irritants and infection. If tuberculosis develops, the patient will need antitubercular therapy.

Respiratory symptoms may be relieved through bronchodilator therapy with theophylline or aminophylline (if bronchospasm is reversible), oral or inhaled sympathomimetic amines (metaproterenol), corticosteroids (oral prednisone or an aerosol form of a corticosteroid), or cromolyn sodium aerosol. Chest physiotherapy techniques, such as controlled coughing and segmental bronchial drainage, combined with chest percussion and vibration help remove secretions.

Other measures include increased fluid intake (at least 3 qt [3 L] daily) and respiratory therapy techniques, such as aerosol therapy, inhaled mucolytics, and intermittent positive-pressure breathing. Diuretics, digitalis glycosides, and salt restriction may be indicated in cor pulmonale.

In severe cases, oxygen may be administered by cannula or mask (1 to 2 Llminute) if the patient has chronic hypoxia or by mechanical ventilation if arterial oxygen can't be maintained above 40 mm Hg. Respiratory infections require prompt administration of antibiotics.

Prevention

To minimize workers' exposure to coal dust, maximum permitted dust levels should be enforced and workers should wear protective masks.