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What is black lung disease?
Black lung disease is a common name for any lung disease that develops from inhaling coal dust. This name comes from the fact that those with the disease have lungs that look black instead of pink. Medically, it is a type of pneumoconiosis called coal workers' pneumoconiosis (CWP). There are two forms: simple CWP and complicated CWP, which also involves progressive massive fibrosis (PMF).
What causes coal workers' pneumoconiosis (CWP)?
The inhalation and accumulation of coal dust causes coal workers' pneumoconiosis (CWP). This stems from working in a coal mine, coal trimming (loading and stowing coal for storage), mining or milling graphite, and manufacturing carbon electrodes (used in certain types of large furnaces) and carbon black (a compound used in many items, such as tires and other rubber goods). Because CWP is a reaction to accumulated dust in the lungs, it may appear and get worse during your exposure to the dust or after your exposure has ceased.
The severity of CWP depends on the type of coal dust, how much dust was in the air, and how long you have been exposed to it.
Is CWP the same thing as chronic obstructive pulmonary disease (COPD)?
No. Although CWP may share many of the symptoms of emphysema and/or chronic bronchitis (which are also known as COPD), CWP is not COPD and is not treated like COPD.
What is the course of CWP?
CWP starts with the inhalation and accumulation of coal dust in the lungs. For many, there are no symptoms or noticeable effect on quality of life. There may be a cough and sputum (mucus) from inhalation of coal dust, but this may be more a matter of dust-induced bronchitis. As CWP progresses and is complicated by PMF, a cough and shortness of breath develop, along with sputum and moderate to severe airway obstruction. Quality of life decreases. Complications of CWP include cor pulmonale.
Smoking does not increase the prevalence of CWP, nor does it affect the development of CWP. But it may add to lung damage and contribute to the development of COPD. Coal workers who smoke are at much greater risk of developing COPD than nonsmoking coal workers.
How does CWP affect your lungs?
When coal dust accumulates in the lungs, a coal macule may form. A coal macule is a combination of coal dust and macrophages. As the disease progresses, macules can develop into a coal nodule, an abnormality of the lung tissue. In time, a type of emphysema and fibrosis may develop.
Lung nodules wider than 1 cm (0.4 in.) have been accepted as evidence of progressive massive fibrosis (PMF), although some organizations say a minimum width of 2 cm (0.8 in.) is necessary. Nodules may grow to a large size and hinder or stop the airflow in the lungs' airways.
How is CWP diagnosed?
CWP is diagnosed through an occupational history and chest X-rays. Lung function tests may be used to determine how badly the lungs are damaged.
Occupational history is very important to the diagnosis of CWP—if a person has not been exposed to coal dust, he or she cannot have CWP. The occupational history should include not only recent and past full-time employment, but also summer jobs, student jobs, military history, and short-term jobs.
The diagnosis of CWP has legal public health implications, since some states require that all cases be reported.
Can CWP be prevented?
CWP can be prevented by controlling dust and having good ventilation in the workplace.
How is it treated?
There is no proven effective treatment for CWP, although complications can be treated.
There are several U.S. laws regarding CWP and its treatment, and the government may help pay for treatment. But to be eligible, you must be totally and permanently disabled by this disease. Most miners aren't eligible for federal black lung benefits. For information on organizations dealing with mining and black lung disease, see the Other Places to Get Help section of this topic.
Other Places To Get Help
Other Works Consulted
- Cowie RL, et al. (2010). Pneumoconioses and other mineral dust-related diseases. In RJ Mason et al., eds., Murray and Nadel's Textbook of Respiratory Medicine, 5th ed., vol. 2, pp. 1554–1586. Philadelphia: Saunders.
Primary Medical Reviewer E. Gregory Thompson, MD - Internal Medicine
Specialist Medical Reviewer Martin J. Gabica, MD - Family Medicine
Current as ofJuly 29, 2016
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