Coalworker's pneumoconiosis

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Coal workers' pneumoconiosis (CWP) colloquially referred to as black lung disease is a chronic, irreversible occupational lung disease caused by the inhalation and deposition of coal dust in the lungs. It is part of a spectrum of respiratory diseases caused by coal dust and is known more formally as coal workers’ pneumoconiosis.

With prolonged exposure, the inhaled fine dust particles overwhelm the lung’s defence mechanisms. The particles accumulate in the parts of the lung where oxygen from the air is taken up by the blood and carbon dioxide waste is released from the blood into the air (known as the “gas exchange region”).

This causes inflammation and scarring of the lung tissue. In the early stages of the disease these accumulations of coal dust and the affected lung tissue will show up as small (less than 1cm) rounded opacities (opaque masses) on x-rays.

Patients with coal workers’ pneumoconiosis may experience symptoms of shortness of breath and a chronic cough. With further exposure and time the disease may progress to a more severe form known as progressive massive fibrosis.

This occurs when the accumulations of coal dust and abnormal lung tissue lump together in larger lesions that show up as large (more than 1cm) opacities on x-ray. As these lesions lump together there is generally significant destruction of lung tissue, with debilitating severe symptoms including:

  • shortness of breath
  • chronic cough
  • coughing up black mucus
  • high blood pressure
  • heart problems
  • increased susceptibility to autoimmune conditions such as rheumatoid arthritis and scleroderma (excessive hardening of the skin).

Progressive massive fibrosis leads to premature death, with the outlook worsening with increasing severity of the disease.

What causes black lung?

The only cause of black lung is excessive inhalation of “respirable” coal dust – that is, particles that are small enough to reach the spaces in the lung where gas exchange takes place – and deposition of dust in the lungs, which causes scarring of lung tissue.

The occurrence and severity of the disease depends on the intensity and duration of exposure, and also to some extent on the type of coal being mined. Smoking does not increase the risk of developing this disease, but it may have an additional harmful effect on the lungs.

Unfortunately, once the disease process has begun it may not resolve with removal from exposure to coal dust and can progress from simple coal workers’ pneumoconiosis to progressive massive fibrosis with time.

How is it treated?

There is no specific treatment for either simple coal worker’s pneumoconiosis or progressive massive fibrosis that can slow or reverse the progressive scarring of the lung tissue.

Medical care of patients is palliative and is directed at limiting complications, such as airflow obstruction and associated lung disorders, and protecting against infectious complications.

How do you prevent it?

As black lung cannot be cured, the only way to control it is through preventing exposure to coal dust. The strict application of engineering controls such as dust suppression combined with ventilation systems in all mining operations is necessary to limit exposure to respirable coal dust to levels below recognised occupational exposure standards.

The American Conference of Governmental Industrial Hygienists has recommended threshold limit values of 0.4 mg/m³ for anthracite (a type of coal with the highest carbon content) and 0.9 mg/m³ for bituminous coal (soft coal containing bitumen) or lignite (brown coal).

Due to the extremely small size of the coal dust particles that cause this disease, overexposure will not be immediately obvious to mine workers. So it is also important to regularly monitor the actual level of worker exposures, using personal respirable dust monitoring equipment, so interventions can be made if excessive dust levels are detected.

Medical surveillance programs are also vital, aimed primarily at early detection so interventions can be made to prevent disease progression by limiting further exposure.
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