| Coalworker's pneumoconiosis | |
|---|---|
| Classification and external resources | |
Coal |
|
| ICD-10 | J60 |
| ICD-9 | 500 |
| DiseasesDB | 10145 |
| MedlinePlus | 000130 |
| eMedicine | med/398 |
| MeSH | D011009 |
Coal workers' pneumoconiosis (CWP), colloquially referred to as 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 worse cases, necrosis.
Coal workers' pneumoconiosis, 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[1] due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, simple coal workers' pneumoconiosis and complicated coal workers' pneumoconiosis (or Progressive massive fibrosis, or PMF). More commonly, workers exposed to coal dust develop industrial bronchitis,[2] clinically defined as chronic bronchitis (i.e. productive cough for 3 months per year for at least 2 years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In nonsmokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16%[3] to 17%[4] incidence of industrial bronchitis.
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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 United Mine Workers of America, 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. In the Coal Mine Health and Safety Act of 1969, the U.S. Congress set up standards to reduce dust and created the Black Lung Disability Trust. The mining companies agreed to a clause, by which a ten-year history of mine work, coupled with X-ray or autopsy evidence of severe lung damage, guaranteed compensation. Equally important was a "rate retention" clause that allowed workers with progressive lung disease to transfer to jobs with lower exposure without loss of pay, seniority, or benefits. Financed by a federal tax on coal, the Trust by 2009 had distributed over $44 billion in benefits to miners disabled by the disease and their widows. A miner who spent 25 years in underground coal mines has a 5–10% risk of contracting the disease.[5]
There are currently about 130,000 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 1966 Doctors I.E. Buff, Hawey Wells, and Donald Rasmussen started studies on effects of working in coal mines. They soon had the first miner who would allow experimental tests to find out how his lungs were affected, Earl Stafford, then a 48 year old miner who had been forced to leave the mines due to his lung condition.
In the following years, Doctors Buff, Wells, and Rasmussen, and Mr. Stafford, continued to lobby for action to provide help and develop preventive measures to eliminate this disease. Mr. Stafford along with a group of disabled miners lobbied congress. Mr. Stafford later testified before the U.S. congress about the conditions to which miners were subjected. He later lead this band of miners to conduct local strikes and work stoppages to bring attention to miners suffering from Black Lung, its effects and possible preventative measures. In addition he lectured at several universities, including Berea College in 1974.
By January 1986, Mr. Stafford was considered a lay expert on the cause and effect of the disease. Less than 20 years after being forced to leave the industry he loved, at the age of 68, Earl Stafford passed away quietly as a result of black lung.
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 not continued. Rates of black lung are on the rise, and have almost doubled in the last 10 years. The US National Institute for Occupational Safety and Health (NIOSH) reported that close to 9 percent of miners with 25 years or more experience tested positive for black lung in 2005–2006, compared with 4 percent in the late 1990s.[6][7]
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.[8]
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 Lucknow (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against the harmful effects of coal dust.[9]
Coal dust is not as fibrogenic as is silica dust.[10] 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,[11] which are important in the inflammation and fibrosis of CWP. 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[1]. The coal macule is the basic pathological feature of CWP, and has a surrounding area of enlargement of the airspace, known as focal emphysema.[12]
Continued exposure to coal dust following the development of simple CWP may progress to complicated CWP with progressive massive fibrosis (PMF), wherein large masses of dense fibrosis develop, usually in the upper lung zones, measuring greater than 1 cm in diameter, with accompanying decreased lung function. These cases generally require a number of years to develop. Grossly, the lung itself appears blackened. Pathologically, these consist of fibrosis with haphazardly-arranged collagen and many pigment-laden macrophages and abundant free pigment. Radiographically, CWP can appear strikingly similar to silicosis. In simple CWP, small rounded nodules (see ILO Classification) predominate, tending to first appear in the upper lung zones. The nodules may coalesce and form large opacities (>1 cm), characterizing complicated CWP, or PMF.
There are three basic criteria for the diagnosis of CWP:
Symptoms and pulmonary function testing relate to the degree of respiratory impairment, but are not part of the diagnostic criteria. As noted above, the chest X-ray appearance for CWP can be virtually indistinguishable from silicosis. Chest CT, particularly high-resolution scanning (HRCT), are more sensitive than plain X-ray for detecting the small round opacities.
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