Black lung disease

Last updated
Black lung disease
Other namesCoal workers' pneumoconiosis, anthracosis, black lung, coal mine dust lung disease
BIRMINGHAM COAL MINER'S LUNG SHOWING EFFECT OF BLACK LUNG DISEASE. (FROM THE SITES EXHIBITION. FOR OTHER IMAGES IN... - NARA - 553848.jpg
Lung affected by black lung disease
Specialty Pulmonology
Complications Chronic obstructive pulmonary disease
Types
  • Anthracosis
  • Simple coal workers’ pneumoconiosis
  • Progressive massive fibrosis
CausesProlonged exposure to coal dust
Deaths25,000 per year (2013)

Black lung disease (BLD), also known as coal workers' pneumoconiosis, [1] or simply black lung, is an occupational type of pneumoconiosis caused by long-term inhalation and deposition of coal dust in the lungs and the consequent lung tissue's reaction to its presence. [2] It is common in coal miners and others who work with coal. It is similar to both silicosis from inhaling silica dust and asbestosis from inhaling asbestos dust. [3] Inhaled coal dust progressively builds up in the lungs and leads to inflammation, fibrosis, and in worse cases, necrosis.

Contents

Black lung disease develops after the initial, milder form of the disease known as anthracosis (from the Greek ἄνθραξ, or ánthrax – coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers [4] 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, PMF). [5] [6] More commonly, workers exposed to coal dust develop industrial bronchitis, [7] clinically defined as chronic bronchitis (i.e. a productive cough for three months per year for at least two years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In non-smokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16% [8] to 17% [9] incidence of industrial bronchitis.

In 2013, BLD resulted in 25,000 deaths globally—down from 29,000 deaths in 1990. [10] In the US, a 2018 study by the National Institute of Occupational Safety and Health shows a resurgence among veteran coalminers, recording the highest rate of BLD in roughly two decades. [11]

Pathogenesis

Coal dust is not as fibrogenic as silica dust. [12] Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar macrophages 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, [13] which are important in the development of inflammation and fibrosis in BLD. 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.

Appearance

Simple BLD is marked by the presence of 1–2 mm (0.039–0.079 in) nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1–2 mm 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. [4] The coal macule is the basic pathological feature of BLD and has a surrounding area of enlargement of the airspace, known as focal emphysema. [14] [15] Focal emphysema extends into progressive centrilobular emphysema. Less commonly a variant of panacinar emphysema develops. [16]

Continued exposure to coal dust following the development of simple BLD may progress to complicated BLD with progressive massive fibrosis (PMF), wherein large masses of dense fibrosis develop, usually in the upper lung zones, measuring greater than 1 cm (0.39 in) 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, BLD can appear strikingly similar to silicosis. In simple BLD, small rounded nodules predominate, tending to first appear in the upper lung zones. The nodules may coalesce and form large opacities (>1 cm), characterizing complicated BLD, or PMF.

Diagnosis

Micrograph of anthracosis, with interstitial pigment deposition (black arrow) and an anthracotic macrophage (white arrow) Histopathology of anthracotic macrophage in lung, annotated.jpg
Micrograph of anthracosis, with interstitial pigment deposition (black arrow) and an anthracotic macrophage (white arrow)

There are three basic criteria for the diagnosis of BLD:

  1. Chest radiography consistent with BLD
  2. An exposure history to coal dust (typically underground coal mining) of sufficient amount and latency
  3. Exclusion of alternative diagnoses (mimics of BLD)

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 BLD 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.

Treatment

There is no cure or discovered treatments for pneumoconiosis. The treatments that are available only relieve the symptoms but do not reverse or stop the illness. Some patients are given supplemental oxygen to help with their breathing and are advised to stop smoking to prevent further decline in lung function. In the most extreme cases, a lung transplant could be done to help prolong the patient's life expectancy. [17]

Prevention of pneumoconiosis

The main way to avoid contracting coal worker's pneumoconiosis is to avoid the inhalation of coal dust. Some of the ways to prevent this disease include: wearing ventilated masks, such as NIOSH-certified respirators, when coming in contact with potentially dangerous airborne particles; regular pulmonary exams; and becoming educated about the risks of lung diseases in your work environment. [18] Pneumoconiosis can also be caused by inhaling other dusts including aluminum, antimony, barium, graphite, iron, kaolin, mica, and talc. [19]

Epidemiology

A video from 2008 on the history of black lung disease

In 2013, BLD resulted in 25,000 deaths down from 29,000 deaths in 1990. [10] Between 1970 and 1974, prevalence of BLD among US coal miners who had worked over 25 years was 32%; the same group saw a prevalence of 9% in 2005–2006. [20] In Australia, BLD was considered to be eliminated in the 1970s due to strict hazard control measures. However, there has been a resurgence of BLD in Australia, with the first new cases being detected in May 2015. [21] From 1999 to 2016, the average years of life lost due to BLD increased from 8.1 to 12.6 years, most likely due to the increased severity and progression of BLD. [22]

History

A miner at the Black Lung Laboratory in the Appalachian Regional Hospital in Beckley, West Virginia in 1970 Black Lung Laboratory-556568.jpg
A miner at the Black Lung Laboratory in the Appalachian Regional Hospital in Beckley, West Virginia in 1970

Black lung is actually a set of conditions and until the 1950s its dangers were not well understood. Over time this disease has taken a large toll on the mining industry and the workers involved. [23] 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, which would be sustained by 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 Federal Coal Mine Health and Safety Act of 1969, the US 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 has spent 25 years in underground coal mines has a 5–10% risk of contracting the disease. [24]

21st century

After the Federal Coal Mine Health and Safety Act of 1969 became law in the United States, the percentage of American miners with black lung disease decreased by about 90 percent. [25] More recently, however, rates of the disease have been on the rise. The 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. [26] [27]

New findings have shown that BLD can be a risk for surface coal miners, who are 48% of the workforce. Data from the Coal Workers' Health Surveillance Program of NIOSH, which examined chest X-rays from more than 2,000 miners in 16 US states from 2010 to 2011, showed that 2% of miners with greater than one year of surface mining experience developed BLD. [28] 0.5% of these miners had PMF. Most of these workers had never worked in an underground mine prior to surface mining. A high proportion of the X-rays suggested that these miners had developed silicosis.

NIOSH, with support from the Mine Safety and Health Administration (MSHA), operates a Mobile Health Screening Program, which 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 BLD, often before the miner is aware of any lung problems. [29]

A 2016–17 investigation by National Public Radio found that NIOSH had under-reported cases of PMF (a complication of black lung) by at least a factor of 20. NPR identified over 2,000 cases at certain clinics in Kentucky, Virginia, West Virginia, Pennsylvania, and Ohio, compared to 99 that NIOSH reported. [30] [31] NIOSH confirmed in 2018 the largest cluster of PMF ever scientifically documented, despite near-elimination of the disease in the 1990s. The causes of the spike are believed to include longer working shifts, mining of thinner coal seams (which causes mining machines to put more non-coal silica dust in the air), and retirements and layoffs that have prompted more former employees to visit health clinics. [32]

New U.S. MSHA rules took effect in August 2016 that lowered maximum allowed dust concentrations for surface and underground mines, and exposure by miners who have been found to be developing pneumoconiosis. [33]

Research

Work to investigate the relationship between respirable dust exposure and coal worker's pneumoconiosis was carried out in the United Kingdom 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.

In October of 2023 Summit Consulting LLC did research for the US Department of Labor about incidents of black lung disease. The point of their research was to answer some key questions that would shed some light on the prevalence and danger of black lung disease in specific subpopulations. The sub populations researched included miners, mining communities, the Navajo Nation, and Appalachia residents. [34] The data sets that Summit used were compiled from the US Census Bureau American Community Survey, US Energy Information Administration, US Census Bureau County Business Patters, the CDC, online data for Epidemiologic Research, Coal Workers Health and Surveillance programs, and the MSHA Mines Data Set. These statistics were used to determine if the increasing number of cases can be abated, and to design predictions for future numbers of the disease.

The report's first finding was the rate of black lung disease across the United States, with an average of 4.34 cases and 3.44 deaths per county. In certain areas of the country, these numbers go up dramatically. In Appalachia it was discovered that there were 28.79 cases and 10.88 deaths per county [34] due to the larger mining populations in the Appalachia region. There were 103 counties in America that reported the disease during the entire data acquisition process which lasted from 1970 to 2014. However, 333 counties reported deaths from black lung disease during this time, indicating that where people worked and developed the disease may not match where people seek treatment or die afterwards. The research also led to the discovery that since 1990s CWP (Coal Workers Pneumoconiosis) has been increasing. [34] The numbers collected may even be undercounted as the Coal Workers Health Surveillance Programs had a low output of screenings, and compensation approval rates were very slow. Despite these issues, the numbers still show an increase in cases which is concerning. [35] A study released in May of 2018 showed that 4,600 coal miners developed the worst kind of the disease with over half of these cases happening since 2000. [36]

The report's second finding involved a comparison of black lung disease rates in mining communities, former mining communities, and non-mining communities. The results indicate black lung disease rates are highest in current mining communities and significantly lower in former mining communities. [34] Non-mining communities reported low rates of black lung disease cases or deaths.

A third finding of the study compared rates of black lung disease in the Navajo nation to the residents of Appalachia and the rest of the country. While the residents of Appalachia suffered much higher rates of the disease and deaths from the disease compared to other areas of the country, the Navajo nation didn't report major differences compared to the rest of the country with just ten deaths being reported over the course of the collection period from 1970-2020. [34] This may be due to underreporting in the Navajo nation.

The last finding of the study was to determine the correlation of residential coal burning and instances of black lung disease. In comparison to the rest of the US outside Appalachia, an increase of cases and deaths was found in residential areas where coal is burned. [34] Residential coal burning may be a contributing factor and not the main cause though, as these areas also have more mines and miners that could develop the disease from their occupation.

There is ongoing research and data is being collected in states all over the country. [37]

See also

Related Research Articles

Coal dust is a fine-powdered form of coal which is created by the crushing, grinding, or pulverization of coal rock. Because of the brittle nature of coal, coal dust can be created by mining, transporting, or mechanically handling it.

<span class="mw-page-title-main">Pneumoconiosis</span> Class of interstitial lung diseases

Pneumoconiosis is the general term for a class of interstitial lung disease where inhalation of dust has caused interstitial fibrosis. The three most common types are asbestosis, silicosis, and coal miner's lung. Pneumoconiosis often causes restrictive impairment, although diagnosable pneumoconiosis can occur without measurable impairment of lung function. Depending on extent and severity, it may cause death within months or years, or it may never produce symptoms. It is usually an occupational lung disease, typically from years of dust exposure during work in mining; textile milling; shipbuilding, ship repairing, and/or shipbreaking; sandblasting; industrial tasks; rock drilling ; or agriculture. It is one of the most common occupational diseases in the world.

<span class="mw-page-title-main">Asbestosis</span> Pneumoconiosis caused by inhalation and retention of asbestos fibers

Asbestosis is long-term inflammation and scarring of the lungs due to asbestos fibers. Symptoms may include shortness of breath, cough, wheezing, and chest tightness. Complications may include lung cancer, mesothelioma, and pulmonary heart disease.

<span class="mw-page-title-main">National Institute for Occupational Safety and Health</span> US federal government agency

The National Institute for Occupational Safety and Health is the United States federal agency responsible for conducting research and making recommendations for the prevention of work-related injury and illness. NIOSH is part of the Centers for Disease Control and Prevention (CDC) within the U.S. Department of Health and Human Services. Despite its name, it is not part of either the National Institutes of Health nor OSHA. Its current director is John Howard.

<span class="mw-page-title-main">Silicosis</span> Pneumoconiosis caused by inhalation of silica, quartz or slate particles

Silicosis is a form of occupational lung disease caused by inhalation of crystalline silica dust. It is marked by inflammation and scarring in the form of nodular lesions in the upper lobes of the lungs. It is a type of pneumoconiosis. Silicosis, particularly the acute form, is characterized by shortness of breath, cough, fever, and cyanosis. It may often be misdiagnosed as pulmonary edema, pneumonia, or tuberculosis. Using workplace controls, silicosis is almost always a preventable disease.

<span class="mw-page-title-main">Mine Safety and Health Administration</span>

The Mine Safety and Health Administration (MSHA) is a large agency of the United States Department of Labor which administers the provisions of the Federal Mine Safety and Health Act of 1977 to enforce compliance with mandatory safety and health standards as a means to eliminate fatal accidents, to reduce the frequency and severity of nonfatal accidents, to minimize health hazards, and to promote improved safety and health conditions in the nation's mines. MSHA carries out the mandates of the Mine Act at all mining and mineral processing operations in the United States, regardless of size, number of employees, commodity mined, or method of extraction. David Zatezalo was sworn in as Assistant Secretary of Labor for Mine Safety and Health, and head of MSHA, on November 30, 2017. He served until January 20, 2021. Jeannette Galanais served as Acting Assistant Secretary by President Joe Biden on February 1, 2021 until Christopher Williamson took office on April 11, 2022.

<span class="mw-page-title-main">Federal Coal Mine Health and Safety Act of 1969</span> US law

The Federal Coal Mine Health and Safety Act of 1969, U.S. Public Law 91-173, generally referred to as the Coal Act, was passed by the 91st United States Congressional session and enacted into law by the 37th President of the United States Richard Nixon on December 30, 1969.

The Safety and Health in Mines Convention, 1995 is an International Labor Organization Convention adopted at the 82nd International Labor Conference (ILC). The convention (C176) was developed and adopted to better recognize the inherent hazards of the mining workplace and the necessity of addressing these hazards on a global scale.

Progressive massive fibrosis (PMF), characterized by the development of large conglomerate masses of dense fibrosis, can complicate silicosis and coal worker's pneumoconiosis. Conglomerate masses may also occur in other pneumoconioses, such as talcosis, berylliosis (CBD), kaolin pneumoconiosis, and pneumoconiosis from carbon compounds, such as carbon black, graphite, and oil shale. Conglomerate masses can also develop in sarcoidosis, but usually near the hilae and with surrounding paracicatricial emphysema.

Occupational lung diseases comprise a broad group of diseases, including occupational asthma, industrial bronchitis, chronic obstructive pulmonary disease (COPD), bronchiolitis obliterans, inhalation injury, interstitial lung diseases, infections, lung cancer and mesothelioma. These can be caused directly or due to immunological response to an exposure to a variety of dusts, chemicals, proteins or organisms. Occupational cases of interstitial lung disease may be misdiagnosed as COPD, idiopathic pulmonary fibrosis, or a myriad of other diseases; leading to a delay in identification of the causative agent.

Caplan's syndrome is a combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogeneous and well-defined on chest X-ray.

The ILO International Classification of Radiographs of Pneumoconioses is a system of classifying chest radiographs (X-rays) for persons with a form of pneumoconiosis. The intent is to provide a standardized, uniform method of interpreting and describing abnormalities in chest x-rays that are thought to be caused by prolonged dust inhalation. In use, it provides a system for both epidemiological comparisons of many individuals exposed to dust and evaluation of an individual's potential disease relative to established standards.

A "B" reader is a physician certified by the National Institute for Occupational Safety and Health (NIOSH) as demonstrating proficiency in classifying radiographs of the pneumoconioses.

Mineral dust airway disease is a general term used to describe complications due to inhaled mineral dust causing fibrosis and narrowing of primarily the respiratory bronchioles. It is a part of a group of disorders known as pneumoconioses which is characterized by inhaled mineral dust and the effects on the lungs.

Stannosis is an occupational, non-fibrotic pneumoconiosis caused by chronic exposure and inhalation of tin. Pneumoconiosis is essentially when inorganic dust is found on the lung tissue; in this case, caused by tin oxide minerals. Dust particles and fumes from tin industries, stannous oxide (SnO) and stannic oxide (SnO2), are specific to stannosis diagnoses. Hazardous occupations such as, tinning, tin-working, and smelting are where most cases of stannosis are documented. When melted tin ions are inhaled as a fume, the tin oxides deposit onto the lung nodules and immune response cells. If a worker is exposed to tin oxides over multiple events for an extended time, they are at risk of developing stannosis.

<span class="mw-page-title-main">Mine safety</span> Practice of controlling mining hazards

Mine safety is a broad term referring to the practice of controlling and managing a wide range of hazards associated with the life cycle of mining-related activities. Mine safety practice involves the implementation of recognised hazard controls and/or reduction of risks associated with mining activities to legally, socially and morally acceptable levels. While the fundamental principle of mine safety is to remove health and safety risks to mine workers, mining safety practice may also focus on the reduction of risks to plant (machinery) together with the structure and orebody of the mine.

<span class="mw-page-title-main">Occupational dust exposure</span> Occupational hazard in agriculture, construction, forestry, and mining

Occupational dust exposure occurs when small particles are generated at the workplace through the disturbance/agitation of rock/mineral, dry grain, timber, fiber, or other material. When these small particles become suspended in the air, they can pose a risk to the health of those who breath in the contaminated air.

<span class="mw-page-title-main">Environmental justice and coal mining in Appalachia</span>

Environmental justice and coal mining in Appalachia is the study of environmental justice – the interdisciplinary body of social science literature studying theories of the environment and justice; environmental laws, policies, and their implementations and enforcement; development and sustainability; and political ecology – in relation to coal mining in Appalachia.

A tapered element oscillating microbalance (TEOM) is an instrument used for real-time detection of aerosol particles by measuring their mass concentration. It makes use of a small vibrating glass tube whose oscillation frequency changes when aerosol particles are deposited on it increasing its inertia. TEOM-based devices have been approved by the U.S. Environmental Protection Agency for environmental air quality monitoring, and by the U.S. Mine Safety and Health Administration for monitoring coal dust exposure for miners to prevent several respiratory diseases.

J. Davitt McAteer is an American lawyer, author, and activist from Fairmont, West Virginia. McAteer was appointed to the position of assistant secretary for the Mine Safety and Health Administration from 1993 to 2000 under President Bill Clinton. Throughout his career, McAteer has been an advocate for safe working conditions for miners, particularly in the coal industry. After the Upper Big Branch Mine disaster of 2010, where an explosion caused by negligence led to the death of 29 miners, McAteer Served on Governor Earl Ray Tomblin's independent investigation panel to determine the cause of the explosion. McAteer is the author of "Monongah: The Tragic Story of the 1907 Monongah Mine Disaster".

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