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Black lung disease, also known as coal workers' pneumoconiosis (CWP), 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.

Coal workers' pneumoconiosis, in its most severe state, develops after the initial, milder form of the disease known as anthracosis (anthrac - coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of carbon dust can result in more serious forms of the disease, simple coal workers' pneumoconiosis and complicated coal workers' pneumoconiosis.

History and prevention efforts

There are currently about 42,000 underground coal miners actively working in the United States. The mining and production of coal is a major part of the economy in several developed countries. In the past ten years, over 10,000 American miners have died from CWP. Although this disease is preventable, many miners are still developing advanced and severe cases.

In the 40 years since the Federal Coal Mine Health and Safety Act of 1969 became law, the proportion of miners with black lung disease has gone down by about 90%. But the downward trend of this disease in coal miners has stopped. Rates of black lung are on the rise, and have almost doubled in the last 10 years. From 1994 to 2004, over 14,000 miners died from black lung disease in the United States.

The National Institute for Occupational Safety and Health (NIOSH), with support of the Mine Safety and Health Administration (MSHA), has started a Mobile Health Screening Program. This Mobile Unit travels to mining regions around the United States. Miners who participate in the Program receive health evaluations once every five years, at no cost to themselves. Chest x-rays can detect the early signs of and changes in CWP, often before the miner is aware of any lung problems. The screening program is only available to current miners.


Pioneering work to investigate the relationship between respirable dust exposure and coal worker's pneumoconiosis was carried out in Britain by the Institute of Occupational Medicine. This research was known as the Pneumoconiosis Field Research (PFR). The research underpinned the recommendations for more stringent airborne dust standards in British coalmines and the PFR was ultimately used as the basis for many national dust standards around the world.

Following observations on industry workers in Lucknowmarker (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against the harmful effects of coal 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. Aggregations of carbon-laden macrophages can be visualised 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 centres of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung.


Simple CWP is marked by the presence of 1-2mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1-2mm in diameter are known as coal macules, with larger aggregations known as coal nodules. These structures occur most frequently around the initial site of coal dust accumulation - the upper regions of the lungs around respiratory bronchioles.

Continued exposure to coal dust following the development of simple CWP may result in its progression to complicated CWP, which generally requires a number of years to develop. Large, black, fibrotic scars 2-10 cm in diameter are present, with accompanying decreased lung function. The lung itself appears blackened. A minority of these cases progresses to progressive massive fibrosis (PMF), the most serious form of CWP.


Both CWP and mild complicated CWP are often asymptomatic or only affect lung function slightly. Shortness of breath and pain may be felt. However, progression to PMF is marked by lung dysfunction, pulmonary hypertension, and cor pulmonale.

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