Black lung disease has gone by many names, including anthracosis, black lung, black spittle, coal worker's pneumoconiosis, miner's asthma, and silicosis.
There are currently about 42,000 underground coal miners actively working in the United States. In the past ten years, over 10,000 American miners have died from Black Lung Disease (Coal workers' pneumoconiosis (CWP)). Although this disease is preventable, many miners are still developing advanced and severe cases.
Black Lung Disease, is caused by long exposure to coal dust. It is a common affliction of coal miners and others who work with coal, similar to both silicosis from inhaling silica dust, and to the long-term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and is unable to be removed by the body; that leads to inflammation, fibrosis, and in the worst case, necrosis.
Black lung is actually a set of conditions and until the 1950s its dangers were not well understood. The prevailing view was that silicosis was very serious but it was solely caused by silica and not coal dust. The miners union, the UMW, realized that rapid mechanization meant drills that produced much more dust, but under John L. Lewis they decided not to raise the black lung issue because it might impede the mechanization that was producing higher productivity and higher wages. Union priorities were to maintain the viability of the long-fought-for welfare and retirement fund, and that required higher outputs of coal. After the death of Lewis, the union dropped its opposition to calling black lung a disease, and realized the financial advantages of a fund for its disabled members.
Coal dust is not as fibrogenic as is silica dust. Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial macrophages and remain in the lungs, residing in the connective tissue or pulmonary lymph nodes. Coal dust provides a sufficient stimulus for the macrophage to release various products, including enzymes, cytokines, oxygen radicals, and fibroblast growth factors, which are important in the inflammation and fibrosis of CWP. Aggregations of carbon-laden macrophages can be visualized under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs. The centers of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung.
Symptoms of Black Lung Disease:
Both CWP and mild complicated CWP are often asymptomatic or only affect lung function slightly. When symptoms do occur, shortness of breath and chronic cough are the most common. Progression to PMF is marked by lung dysfunction, pulmonary hypertension, and cor pulmonale. Unlike silicosis, patients with CWP do not appear to have a substantial increased risk for tuberculosis, but coal miners may experience significant silica dust exposure, and therefore the accompanying risks. CWP is associated with a variety of autoimmune abnormalities, including rheumatoid arthritis and scleroderma.
Some patients develop emphysema (a disease in which the tiny air sacs in the lungs become damaged, leading to shortness of breath, and respiratory and heart failure) as a complication of black lung disease. Others develop a severe type of black lung disease called progressive massive fibrosis, in which damage continues in the upper parts of the lungs even after exposure to the dust has ended.
Diagnosis of CWP:
Chest radiography consistent with CWP
An exposure history to coal dust (typically underground coal mining) of sufficient amount and latency
Exclusion of alternative diagnoses (mimics of CWP)
Treatment of Black Lung Disease:
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.
The treatment for Black Lung Disease primarily focuses on providing symptomatic relief and for improving a Black Lung patient's quality of life. Depending upon a patient's condition, some of the following treatment options may be prescribed:
Avoiding tobacco smoke,
Medication for coughing, wheezing, etc.
Combating opportunistic infections with the help of antibiotics.
Eliminating coal-dust/air-pollutants from the patient's home or workplace.
Oxygen Therapy - Improving blood oxygen levels by administering supplemental oxygen using portable oxygen tanks.
Black Lung Protection and Prevention:
Adequate Breathing Filters and Face masks
Eliminating coal dust in the work environment,
Yearly chest radiographs for early detection of Black Lung Disease.
In 1969 the US Congress ordered black lung to be eradicated from the coal industry. The Federal Coal Mine Health and Safety Act of 1969 (as amended by the Federal Mine Safety and Health Act of 1977) is intended to protect the health and safety of underground coal miners. This Act directs NIOSH to study the causes and consequences of coal-related respiratory disease and, in cooperation with the Mine Safety and Health Administration (MSHA), to carry out a program for early detection and prevention of coal workers' pneumoconiosis. Today it is estimated that 1,500 former coal miners still die of black lung each year in the US.
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