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The Impact of Black Lung and a Methodology for Controlling Respirable Dust

Affiliation.

  • 1 Pittsburgh Mining Research Division, National Institute for Occupational Safety and Health, 626 Cochrans Mill Road, Pittsburgh, PA 15236, USA.
  • PMID: 33598636
  • PMCID: PMC7885287
  • DOI: 10.1007/s42461-020-00278-7

Coal workers' pneumoconiosis (CWP), commonly known as black lung, is caused by the inhalation of respirable coal mine dust and is a disabling and potentially fatal lung disease with no cure. Historically, CWP has taken a tremendous human and financial toll in the US coal mining industry. Recent health surveillance data indicates that CWP continues to occur at elevated levels. Respirable coal dust exposure must be controlled to prevent the development of CWP. The Pittsburgh Mining Research Division of the National Institute for Occupational Safety and Health (NIOSH) conducts laboratory and mine-site research to identify control technologies that can be used to successfully reduce respirable dust levels. Various technologies, using multiple methods of control, can be applied in order to reduce dust levels. An overview of CWP's impact and a general methodology for controlling respirable dust in underground coal mines are discussed in this paper.

Keywords: Coal workers’ pneumoconiosis; Engineering controls; Respirable dust; Underground coal mining.

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Conflict of interest statement

Compliance with Ethical Standards Conflict of Interest The author declares that he has no conflict of interest.

Chest radiographs of healthy lungs…

Chest radiographs of healthy lungs (left), simple CWP Category 2 (center), and PMF…

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Efficient cutting with proper bit design (left), undercut roof rock (center), and reduced…

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Full-cone spray pattern (left), typical spray locations on a shearer drum (center) and…

Enclosed stageloader/crusher (left) and schematic…

Enclosed stageloader/crusher (left) and schematic illustrating internal spray locations (right)

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Miner removing filter from scrubber (left) and graph showing respirable dust reductions with…

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Cleaning dust from collector box (left), collector bag (center), and dust captured in…

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Canopy air curtain provides filtered air to operator (left) and commercially available unit…

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  • Pneumoconiosis and advanced occupational lung disease among surface coal miners--16 states, 2010-2011. Centers for Disease Control and Prevention (CDC). Centers for Disease Control and Prevention (CDC). MMWR Morb Mortal Wkly Rep. 2012 Jun 15;61(23):431-4. MMWR Morb Mortal Wkly Rep. 2012. PMID: 22695382
  • Coal mine dust lung disease in miners killed in the Upper Big Branch disaster: a review of lung pathology and contemporary respirable dust levels in underground US coal mines. Go LHT, Green FHY, Abraham JL, Churg A, Petsonk EL, Cohen RA. Go LHT, et al. Occup Environ Med. 2022 May;79(5):319-325. doi: 10.1136/oemed-2021-107694. Epub 2021 Dec 8. Occup Environ Med. 2022. PMID: 34880046 Review.
  • Evaluation of occupational exposures to respirable dust in underground coal mines. Onder M, Onder S. Onder M, et al. Ind Health. 2009 Jan;47(1):43-9. doi: 10.2486/indhealth.47.43. Ind Health. 2009. PMID: 19218756
  • Coal mine dust lung disease in the modern era. Perret JL, Plush B, Lachapelle P, Hinks TS, Walter C, Clarke P, Irving L, Brady P, Dharmage SC, Stewart A. Perret JL, et al. Respirology. 2017 May;22(4):662-670. doi: 10.1111/resp.13034. Epub 2017 Mar 30. Respirology. 2017. PMID: 28370783 Review.
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  • NIOSH (1995) Criteria for a recommended standard: occupational exposure to respirable coal mine dust. Cincinnati, OH: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, education and information division, DHHS (NIOSH) publication no. 95–106
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  • NIOSH (2019) Coal workers’ health surveillance program. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, https://www.cdc.gov/niosh/topics/cwhsp/default.html
  • Code of Federal Regulations (2019) Washington, DC: U.S. Government Printing Office; Office of the Federal Register, Title 30 Part 90, Coal miners who have evidence of the development of pneumoconiosis

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School of Public Health

Unearthing pathology of recent rise in black lung disease.

Coal miners walk together after a shift of work.

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Robert Cohen photo

The first new pathology standards for black lung disease in over 50 years were published based on research from the University of Illinois Chicago School of Public Health. The findings will help pathologists diagnose a new, more aggressive form of the condition and may provide public health officials with additional motivation for passing stricter mining regulations.

Rates of coal workers’ pneumoconiosis, the severe respiratory condition popularly known as black lung disease, resurged in the last two decades after a steep decline in the late 20th century. Work from UIC’s Mining Education and Research Center determined that the rise is likely caused by excessive exposure to silica dust in the coal mine atmosphere, compared with the coal dust that historically put miners at risk.

“In the past, these diseases generally took decades to develop, but we’re seeing them developing in much shorter periods of time, and that it’s much more inflammatory and rapidly progressive,” said Dr. Robert Cohen , clinical professor in the UIC School of Public Health and director of the center.

Two recent papers from the center expand upon this link, with both comparing the lungs of miners from the mid-20th century with those from more recent cases of black lung disease. The studies are the first update on the pathology of black lung disease since 1971, highlighting features in lung tissue that are unique to this newer version and making pathologists aware of its changing nature in modern miners.

“In a textbook today, the teaching would be that it would take decades and decades of exposure to develop pneumoconiosis,” said Dr. Leonard Go , research assistant professor and assistant director of center. “But we’re seeing cases of disease in people with five, six years of exposure, sometimes less. And that’s almost certainly because of a more prominent silica component of contribution to their disease.”

Silica dust is known to be highly toxic, causing lung damage, cancer and COPD. While exposure to the substance in most professions is already limited by OSHA regulations, coal miners — governed by a separate federal agency — are still legally allowed to inhale twice as much of the dust on the job. Modern changes in coal mining, such as increased use of heavy machinery and mining of thinner coal seams surrounded by silica, may also contribute to higher exposures, the researchers said.

In one paper , the center researchers conducted a statistical comparison of lung tissue from miners born between 1885 to 1950. The historical samples were gathered from an archive in West Virginia at the Respiratory Health Division of the National Institute for Occupational Safety & Health that the researchers discovered in the basement of the facility.

“It was almost like discovering archaeological evidence, because it has these ancient lungs from guys that were born in the early 20th century,” Cohen said. “It was kind of exciting for us, as pulmonary detectives, to find it.”

Researchers evaluated the specimens for the presence of progressive massive fibrosis, the most severe form of pneumoconiosis. They grouped each case into coal-type, mixed-type and silica-type based on the microscopic characteristics of the lung nodules.

When analyzed over time according to the birth year of the miner, the researchers found that the frequency of coal-type and mixed-type disease declined, likely reflecting the passage of stricter mining regulations. Conversely, rates of silica-type disease stayed constant, even increasing among miners born more recently.

“We saw the rise in disease, and now we can see under a microscope that the pattern of disease is clearly consistent with silica,” Go said. “It’s a smoking gun that something has to change to prevent this disease.”

In a second paper , an international panel of pathologists looked at 85 lung samples, but were not told whether they were from historical miners — those born before 1930 — or contemporary miners born after 1930. Once again, the researchers found that silica-type lesions were more common in contemporary miners than their earlier counterparts.

The analysis also offered detailed descriptions of additional features that are unique to the newer form of the disease, including alveolar proteinosis — a condition previously associated with heavy acute silica exposure but not previously observed in coal miners — and signs of inflammation and fibrosis. It also revealed the startling absence in contemporary miners of coal macules and nodules, once considered a hallmark of black lung disease.

The authors hope that this new information will aid diagnosis of the disease in its new form.

“We want pathologists to recognize this disease, to increase the knowledge and awareness of how this disease looks.” Cohen said. “We’re updating the literature so that pathologists are aware of the rapidly progressive nature and the new signs of disease.”

The authors also hope that the new findings will add more urgency to the debate around further limiting coal miners’ exposure to silica dust and lead to quicker passage of new regulations that further reduce miners’ exposure to dust particles. A federal rule bringing mining restrictions in line with OSHA standards is currently under consideration by the Mine Safety and Health Administration.

“We’re hoping that the studies will add more urgency to this issue and help the agency get this rule out,” Cohen said.

Black Lung in the 21st Century: Disease, Law, and Policy

120 West Virginia Law Review 797 (2018)

26 Pages Posted: 25 Apr 2018 Last revised: 22 Jul 2018

AppalReD Legal Aid

The past decade has seen many changes in the fields related to black lung. Although American coal production and employment have been declining, more coal miners are suffering from breathing problems related to coal-mine dust. 20th-century efforts to end black lung failed. The Appalachian coalfields are now the epicenter of one of the worst industrial health disasters in U.S. history. Current rates of severe black lung among career Appalachian miners are worse than when federal statistics started being kept in 1970. While the disease has worsened, the legal system has seen some important improvement. In particular, the past decade has seen four major changes to the federal law concerning black lung. First, in 2014, the U.S. Department of Labor (“DOL”) made the first changes since 1972 to the regulations limiting the dust that miners breathe while working underground. The Dust Rule reduces the permissible dust level by 25%, closes important loopholes, and provides miners with better information about their working conditions. Second, the Affordable Care Act (“ACA”) contains provisions known as the “Byrd Amendments” that automatically entitle many widows to black lung benefits and provide experienced coal miners suffering from a respiratory disability with a powerful presumption that their disabling breathing problems are due to black lung. Third, in 2000, DOL made major revisions to its regulations that went into effect in 2001 and, once ingrained, simplified black lung benefits litigation. Fourth, in 2016, DOL mandated that most medical evidence developed in black lung benefits claims be disclosed to the other parties. This Article provides an overview of the current medical reality of black lung and recent changes to federal law. It also discusses current policy issues in the black lung benefits system. This Article will argue for two changes to improve the compensation system for those miners who already have the disease. First, we must eliminate the delays plaguing the adjudication of federal black lung benefits system. Second, we must shift the responsibility of black lung medical benefits from coal operators to a federal health insurance program that covers all coal miners. This would greatly decrease the amount of litigation and provide needed health benefits for a broader group of miners. Unfortunately, black lung will continue to be a salient topic in Appalachia over the next century. This Article hopes to contribute to an inquiry into how this disease can be eliminated and how compensation can be provided to coal miners and their families consistent with the public interest.

Keywords: black lung, coal, pneumoconiosis, coal workers' pneumoconiosis, CWP, black lung benefits, workers' compensation, mine safety, public benefits, Department of Labor, DOL, Affordable Care Act, ACA, Dust Rule, Medical Disclosure, Health Insurance

JEL Classification: K39

Suggested Citation: Suggested Citation

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Black Lung Disease Resurges in Appalachian Coal Miners

Potera, Carol

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Black Lung Disease Alive and Well, After All These Years

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black lung disease research paper

“I have not hitherto met with the record of any similar affection; and partly with a view of calling the attention of those practitioners who reside in the vicinity of the great coal mines, and who may have charge of the health of the miners, to the existence of a disease, to which that numerous class of the community would appear to be peculiarly exposed.”

-  Dr. James Gregory

George Pearson, an English physician, was the first to suggest that the darkening of lungs, seen during an autopsy, might be due to the soot inhaled from the burning candles, oil, and coal of 1813 life. Nineteen years later, a Scottish physician, James Gregory, connected those blackened lungs to coal miners and the coal dust they inhaled.

In the US, coal has been an energy source since the 1700s, especially in the area of “Pennsyltucky” – West Virginia, Kentucky, Pennsylvania, and a bit of Ohio. By 1920, coal fueled 70% of America; today, that percentage is roughly 18% - including 20% of the electricity that fuels those non-polluting electric vehicles. Black lung disease, coal workers’ pneumoconiosis, has been coal production’s fellow traveler.

black lung disease research paper

Black lung was dramatically reduced by regulations governing the amount of allowable coal dust in the mines and also by technological advances in how coal was mined and worker protection. But a little over a quarter-century ago, those gains reversed and the incidence of black-lung surpassed the carnage of years earlier, something that the New York Times graph shows. What changed?

Black Lung Disease

Black lung disease is medically classified as a pneumoconiosis, a disease within the lung tissue causing inflammation followed by scarring, and fibrosis. The fibrosis slowly but surely reduces the ability of the lungs to expand and take in air as well as the lung’s ability to transfer oxygen into the bloodstream. It is the same pathological process seen in those TV ads by lawyers on the hunt for cases of asbestosis. It is also caused by silica, a mineral we will see again in our tale. Coal worker’s pneumoconiosis (CWP), another name for black lung disease, exists along a spectrum with a more virulent form, progressive massive fibrosis (PMF). There is no cure and, to be fair, no satisfactory treatment – all we can offer is oxygen or, perhaps, a lung transplant.

It takes 10 years or more for the cumulative effects of coal dust to begin to become symptomatic and apparent. CWP is a quiet thief, stealing your ability to engage in life; it can be profoundly disabling. Just imagine if your world consisted of only a portion of your home, even then, tethered to an oxygen line.

The Federal Coal Mine Health and Safety Act of 1969

“…an incurable disease caused by inhalation of coal dust…it is not caused by smoking” and “…is easy to distinguish with x-rays.”

- Dr. David Blackley , head of Respiratory Disease Studies, National Institute for Occupational Safety and Health

In addition to setting standards for dust levels, this legislation created the Black Lung Disability Trust, funded by a federal coal tax. Two clauses in that legislation are pertinent today:

  • Miners with a 10-year history of mine work and X-ray evidence of severe lung damage [1] are guaranteed compensation.
  • Miners have “rate retention,” allowing them to transfer to jobs with lesser amounts of dust exposure while maintaining their pay, seniority, and benefits

Why the increase?

“The government can claim they are doing all they can to reduce miners’ exposure to coal mine dust and operators can argue the industry isn’t at fault, but there is clearly a problem here. There is only one way miners get Black Lung disease. They are breathing air that contains excessive amounts of respirable coal dust. Having stated the obvious, it becomes clear that the law is not being properly enforced or mine operators are not following mandatory health and safety standards or both. There is no other explanation.”

 -  Cecil Roberts , President of the UMWA

black lung disease research paper

The efficiency of mining machinery also led to rapidly dwindling sources of easily mined coal despite a persistent demand for the fuel. To get at more coal, the miners simply had to dig deeper through rock that contained the seams of coal. The rock also held a great deal of silica, and silica creates far more inflammation and fibrosis than coal dust alone. In fact, it is probably the smaller amounts of silica in easily mined coal that was responsible for CWP all along.

Rising Levels of Silica

A new study in the Annals of the American Thoracic Society demonstrates the rising levels of silica in the lungs of coal miners. The researchers compared lung tissue taken from miners born between 1910 and 1930 (those working before modern mining technology) and those born after 1930 – the more contemporary miners. They looked at the characteristic nodules that form in CWP, categorizing them on silica content. The “historic” miners had a higher percentage of nodules predominantly with coal dust, 50% - threefold more than contemporary miners. The current miners had a higher percentage of nodules predominated by silica, 57%, three-fold more than historical workers. The reason for the greater amounts of silica, a known carcinogen, was all that granite they now had to dig through to get to deeper layers of coal.

“These findings provide the first direct evidence that silica is a causative agent behind the increasing incidence of progressive massive fibrosis — severe black lung disease. This is critical information that can be used to determine health-protective permissible exposure limits for coal miners,”

– Robert Cohen, MD, lead author, Respiratory Health Division, National Institute for Occupational Safety and Health

In 2019, the Mine Safety and Health Administration, the OSHA equivalent specifically for mine safety and health, requested information to change the regulations regarding silica. The Office of the Inspector General issued a report in 2020 concluding that the silica regulations were out of date, sampling was too infrequent to “be sufficiently protective,” and that no fines could be levied because silica levels were tied to coal dust exposure limits. Two years later, there has been no action on the recommendations to reduce exposure to a known carcinogen, increase sampling, and establish a separate standard for silica. The current standard is 100 micrograms/cm 3, but most of us, with no exposure to silica, need not worry; OSHA’s standard for our workplaces is 50 micrograms/cm 3 – only those miners at high-risk operate under laxer standards.

The Low Participation Rates of Screening

black lung disease research paper

  • Testing is often logistically difficult – Diagnostic centers are often placed an hour or more drive away from the mines, and there is no paid “time-off” to get tested.
  • There are disincentives – State legislation places one or two-year statutes of limitations on compensation claims. Once you are diagnosed, the clock on obtaining workers’ compensation is running; your mining job, the most lucrative job where you live, will end in 4 to 5 years. Remember the right to ask for a job with less dust exposure? It does exist but comes with some social stigma and fear, rationale or not, of economic retribution. It is a rarely exercised “right.” When exercised, it is often near the end of a mining career, long after the harmful effects of coal dust and now increasing amounts of silica have initiated your respiratory decline.
  • Work and family are entwined. Miners often go back generations, and mining, despite all of its dangers, still represents the means to successfully support your family. Miners’ self-esteem is, in part, predicated upon the difficulty and hazards of their work. Even with no economic loss, taking on a lesser role comes at a psychic price.

I had thought that Black Lung Disease was in our past. As is often the case, I was late in getting the memo. For various reasons, technology, economics, and human behavior Black Lung Disease is alive and well. Changing the regulations to protect these American citizens should be as much and as important a priority as moving away from coal as a fuel source.

[1] The pattern of changes from CWP on an X-ray of the chest is diagnostic of the condition in coal miners and does not require a tissue biopsy.

Sources: Pathology and mineralogy demonstrate respirable crystalline silica is a major cause of severe pneumoconiosis in US coal miners Annals of American Thoracic Society DOI: 10.1513/AnnalsATS.202109-1064OC

The enduring legacy of black lung: environmental health and contested illness in Appalachia Sociology of Health and Illness DOI: 10.1111/1467-9566.12777

The real story about miners, Black Lung and the life and death struggle for benefits United Mine Workers of America

The Militant Miners Who Exposed the Horrors of Black Lung JSTOR Daily

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Dr. Charles Dinerstein, M.D., MBA, FACS is Director of Medicine at the American Council on Science and Health. He has over 25 years of experience as a vascular surgeon.

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Unearthing Pathology of Recent Rise in Black Lung Disease 

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Editor’s Note: This article from UIC Today at the University of Illinois Chicago provides a timely review of recent research connecting an epidemic of complicated black lung disease to silica exposure in coal mines. This is a subject Public Health Watch has covered extensively as the Mine Safety and Health Administration proposes a new and long-delayed regulation limiting silica dust exposure. The agency just announced it will issue a final version of that regulation in April 2024. Republicans in Congress are already trying to block that regulation with a budget amendment that would prohibit spending on enforcement of the regulation.

Unearthing pathology of recent rise in black lung disease 

The first new pathology standards for black lung disease in over 50 years were published based on research from the University of Illinois Chicago School of Public Health. The findings will help pathologists diagnose a new, more aggressive form of the condition and may provide public health officials with additional motivation for passing stricter mining regulations. 

black lung disease research paper

Rates of coal workers’ pneumoconiosis, the severe respiratory condition popularly known as black lung disease, resurged in the last two decades after a steep decline in the late 20th century. Work from UIC’s Mining Education and Research Center determined that the rise is likely caused by excessive exposure to silica dust in the coal mine atmosphere, compared with the coal dust that historically put miners at risk.  

“In the past, these diseases generally took decades to develop, but we’re seeing them developing in much shorter periods of time, and that it’s much more inflammatory and rapidly progressive,” said Dr. Robert Cohen , clinical professor in the UIC School of Public Health and director of the center. 

Two recent papers from the center expand upon this link, with both comparing the lungs of miners from the mid-20th century with those from more recent cases of black lung disease. The studies are the first update on the pathology of black lung disease since 1971, highlighting features in lung tissue that are unique to this newer version and making pathologists aware of its changing nature in modern miners. 

“In a textbook today, the teaching would be that it would take decades and decades of exposure to develop pneumoconiosis,” said Dr. Leonard Go , research assistant professor and assistant director of center. “But we’re seeing cases of disease in people with five, six years of exposure, sometimes less. And that’s almost certainly because of a more prominent silica component of contribution to their disease.” 

Silica dust is known to be highly toxic, causing lung damage, cancer and COPD. While exposure to the substance in most professions is already limited by OSHA regulations, coal miners — governed by a separate federal agency — are still legally allowed to inhale twice as much of the dust on the job. Modern changes in coal mining, such as increased use of heavy machinery and mining of thinner coal seams surrounded by silica, may also contribute to higher exposures, the researchers said. 

In one paper , the center researchers conducted a statistical comparison of lung tissue from miners born between 1885 to 1950. The historical samples were gathered from an archive in West Virginia at the Respiratory Health Division of the National Institute for Occupational Safety & Health that the researchers discovered in the basement of the facility. 

“It was almost like discovering archaeological evidence, because it has these ancient lungs from guys that were born in the early 20th century,” Cohen said. “It was kind of exciting for us, as pulmonary detectives, to find it.” 

Researchers evaluated the specimens for the presence of progressive massive fibrosis, the most severe form of pneumoconiosis. They grouped each case into coal-type, mixed-type and silica-type based on the microscopic characteristics of the lung nodules.  

Dr. Robert Cohen

When analyzed over time according to the birth year of the miner, the researchers found that the frequency of coal-type and mixed-type disease declined, likely reflecting the passage of stricter mining regulations. Conversely, rates of silica-type disease stayed constant, even increasing among miners born more recently.  

“We saw the rise in disease, and now we can see under a microscope that the pattern of disease is clearly consistent with silica,” Go said. “It’s a smoking gun that something has to change to prevent this disease.” 

In a second paper , an international panel of pathologists looked at 85 lung samples, but were not told whether they were from historical miners — those born before 1930 — or contemporary miners born after 1930. Once again, the researchers found that silica-type lesions were more common in contemporary miners than their earlier counterparts. 

The analysis also offered detailed descriptions of additional features that are unique to the newer form of the disease, including alveolar proteinosis — a condition previously associated with heavy acute silica exposure but not previously observed in coal miners — and signs of inflammation and fibrosis. It also revealed the startling absence in contemporary miners of coal macules and nodules, once considered a hallmark of black lung disease. 

The authors hope that this new information will aid diagnosis of the disease in its new form. 

“We want pathologists to recognize this disease, to increase the knowledge and awareness of how this disease looks.” Cohen said. “We’re updating the literature so that pathologists are aware of the rapidly progressive nature and the new signs of disease.” 

The authors also hope that the new findings will add more urgency to the debate around further limiting coal miners’ exposure to silica dust and lead to quicker passage of new regulations that further reduce miners’ exposure to dust particles. A federal rule bringing mining restrictions in line with OSHA standards is currently under consideration by the Mine Safety and Health Administration. 

“We’re hoping that the studies will add more urgency to this issue and help the agency get this rule out,” Cohen said. 

Related Public Health Watch reporting:

Federal Fix for Silica Dust Understates What We Found: Thousands of Coal Miners Still Sick and Dying
‘This stuff is killing me’: After decades of delay, new black lung protections come too late for some West Virginia coal miners
Impact: Federal Mine Safety Agency Considers Tougher Response to Silica Dust After Public Health Watch Report
A Dozen Years of Dogged Reporting on Black Lung
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Black Lung Study Finds Biggest Cluster Ever Of Fatal Coal Miners' Disease

Howard Berkes

Howard Berkes

Adelina Lancianese

Adelina Lancianese

black lung disease research paper

In this historical image, a doctor reviews an X-ray of a patient with black lung disease. Federal researchers say they've now identified the largest cluster ever recorded of the most advanced stage of the disease. Michael Sullivan/Getty Images/Science Source hide caption

In this historical image, a doctor reviews an X-ray of a patient with black lung disease. Federal researchers say they've now identified the largest cluster ever recorded of the most advanced stage of the disease.

Updated on Feb. 6 at 3:49 p.m. ET

Epidemiologists at the National Institute for Occupational Safety and Health say they've identified the largest cluster of advanced black lung disease ever reported, a cluster that was first uncovered by NPR 14 months ago.

NPR Continues To Find Hundreds Of Cases Of Advanced Black Lung

The Two-Way

Npr continues to find hundreds of cases of advanced black lung.

Black Lung Returns To Coal Country

Black Lung Returns To Coal Country

In a research letter published Tuesday in the Journal of the American Medical Association , NIOSH confirms 416 cases of progressive massive fibrosis or complicated black lung in three clinics in central Appalachia from 2013 to 2017.

"This is the largest cluster of progressive massive fibrosis ever reported in the scientific literature," says Scott Laney, a NIOSH epidemiologist involved in the study.

"We've gone from having nearly eradicated PMF in the mid-1990s to the highest concentration of cases that anyone has ever seen," he said.

The clinics are operated by Stone Mountain Health Services and assess and treat coal miners mostly from Virginia, Kentucky and West Virginia, a region that includes what have historically been some of the most productive coalfields in the country.

"When I first implemented this clinic back in 1990, you would see ... five [to] seven ... PMF cases" a year, says Ron Carson, who directs Stone Mountain's black lung program.

The clinics now see that many cases every two weeks, he says, and have had 154 new diagnoses of PMF since the fieldwork for the NIOSH study concluded a year ago.

"That's an indication that it's not slowing down," Carson says. "We are seeing something that we haven't seen before."

black lung disease research paper

A slide from a presentation by the National Institute for Occupational Safety and Health shows the progression from a healthy lung to advanced black lung disease. NIOSH hide caption

A slide from a presentation by the National Institute for Occupational Safety and Health shows the progression from a healthy lung to advanced black lung disease.

Laney acknowledges that the full scope of what he calls an epidemic is still unknown. "Even with this number, which is substantial and unacceptable, it's still an underestimate."

"Nobody looks forward to dying"

PMF, or complicated black lung, encompasses the worst stages of the disease, which is caused by inhalation of coal and silica dust at both underground and surface coal mines. Miners gradually lose the ability to breathe, as they wheeze and gasp for air.

black lung disease research paper

Edward Brown is a 55-year-old former coal miner with progressive massive fibrosis, or complicated black lung disease. Adelina Lancianese/NPR hide caption

Edward Brown is a 55-year-old former coal miner with progressive massive fibrosis, or complicated black lung disease.

"I've seen it too many times," said Charles Wayne Stanley, a Stone Mountain client with PMF, who spoke with NPR in 2016. "My wife's grandpa ... [I] watched him take his last breath. I watched my uncle die with black lung. You literally suffocate because you can't get enough air."

Lung transplants are the only cure, and they're possible only when miners are healthy enough to qualify.

"[I] can't breathe, you know. [I] can't do nothing hardly like I used to," says Edward Brown, a 55-year-old retired miner from Harlan, Ky., who was diagnosed with PMF at both Stone Mountain and another medical clinic.

"That's all I got to look forward to is to get worser and worser," Brown says, pausing for a deep sigh and nervous chuckle. "Nobody looks forward to dying, you know, but it's a-comin' and then that worries me."

Brown's age and disease fit another finding of the NIOSH study and a trend Carson first disclosed to NPR in December 2016.

"Miners are dying at a much younger age," he says, noting that in the 1990s, the clinic's PMF diagnoses typically involved miners in their 60s, 70s and 80s. Now the disease strikes miners in their 50s, 40s and even 30s with fewer years mining coal.

"A high proportion" of the miners in the NIOSH study had severely advanced disease and "coal mining tenure of less than 20 years, which are indications of exceptionally severe and rapidly progressive disease," the study says.

black lung disease research paper

The lung of deceased West Virginia coal miner Chester Fike was taken out during a double lung transplant when he was 60. He worked in the mines for 35 years. NIOSH hide caption

The lung of deceased West Virginia coal miner Chester Fike was taken out during a double lung transplant when he was 60. He worked in the mines for 35 years.

The Stone Mountain study follows a NIOSH review of cases at a small clinic in Coal Run Village, Ky., in 2016. NIOSH researchers confirmed 60 diagnoses of PMF there in 20 months. That alarmed them because NIOSH had earlier reported only 99 cases nationwide in five years.

At the same time, an NPR survey of 11 black lung clinics in Kentucky, Virginia, Pennsylvania and Ohio identified 962 cases, 10 times the original NIOSH count. Since then, NPR's ongoing survey of clinics has counted nearly 1,000 more cases.

The NPR investigation also found that the likely cause of the epidemic is longer work shifts for miners and the mining of thinner coal seams. Massive mining machines must cut rock with coal and the resulting dust contains silica, which is far more toxic than coal dust.

The spike in PMF diagnoses is also due to layoffs and retirements brought on by the decline in coal mining. Miners who had put off getting checked for black lung earlier began streaming into clinics, especially if they needed the medical and wage replacement benefits provided by black lung compensation programs.

A public health emergency?

There is also concern for the 50,000 coal miners still working.

"They really need to declare this a public health emergency," says Joe Wolfe, an attorney in Norton, Va., who helps miners file claims for black lung compensation.

"If you had 400 cases of E. coli, [NIOSH] would flood the area with technicians and doctors and nurses checking people's health," Wolfe adds. "There are people literally working in the mines right now ... that have complicated black lung that do not have a clue."

NIOSH doesn't have that authority, according to David Weissman, who directs the agency's respiratory health program in Morgantown, W.Va. Public health emergencies are declared by the secretary of the U.S. Department of Health and Human Services.

"But I will say that this is a very important problem. We're very passionate about this problem," Weissman says. "And we're going to keep doing everything in our power to address it."

Multiple NIOSH and independent studies are underway or planned to try to pinpoint the number of miners who have the disease, as well as the causes.

A mining disaster in slow motion

black lung disease research paper

Jess Bishop, a black lung victim, takes his last breaths while his sons — also coal miners — keep vigil in Logan County, W.Va., in 1976. The disease spiked in the 1960s and '70s but then plummeted with the passage of mine safety laws. Courtesy of Earl Dotter hide caption

Jess Bishop, a black lung victim, takes his last breaths while his sons — also coal miners — keep vigil in Logan County, W.Va., in 1976. The disease spiked in the 1960s and '70s but then plummeted with the passage of mine safety laws.

Coincidentally, new federal regulations that are supposed to limit exposure to dangerous levels of coal and silica dust were fully implemented in 2016, a few months before NPR first reported the PMF epidemic. The Trump administration recently announced a "retrospective study" of the new regulations, a move that has mine safety advocates concerned, especially given the epidemic of the disease caused by mine dust.

"It would be outrageous for any undercutting of those regulations that puts miners [back] in harm's way and subjects even more of them to this terrible disease," says Joe Main, the former mine safety chief at the federal Mine Safety and Health Administration.

"When we think we know as much as we thought we should know about the disease, the next day [there's] worse information," says Main. "It shows that the depth of the disease is worse than what we knew the day before."

Main pushed for the tougher mine dust exposure limits. His successor at MSHA is David Zatezalo, a former mining company executive.

"We are not proposing to weaken this rule," Zatezalo tells NPR in a written statement. "We are planning to collect feedback on the rule from stakeholders, which was both a commitment previously made by MSHA, and a directive from President Trump, who strongly supports America's miners."

Zatezalo did not respond to requests for an interview. His agency's formal notice for the "retrospective study" labels it a "deregulatory" action, which implies less regulation.

At a congressional hearing today in Washington, Zatezalo was asked directly about his agency's "retrospective study" of the tougher mine dust limits imposed by the Obama administration.

"Do you plan to rollback any aspect of the 2014 respirable dust rule?" asked Rep. Bobby Scott, D-Va., the ranking Democrat on the House Committee on Education and the Workforce.

black lung disease research paper

David Zatezalo, the Assistant Secretary of Labor for Mine Safety and Health, was asked about the advanced black lung epidemic at a congressional hearing in Washington, D.C., on Feb. 6, 2018. Huo Jingnan/NPR hide caption

David Zatezalo, the Assistant Secretary of Labor for Mine Safety and Health, was asked about the advanced black lung epidemic at a congressional hearing in Washington, D.C., on Feb. 6, 2018.

"I do not," Zatezalo responded.

Zatezalo was also asked about his agency's own description of the "retrospective study" of the new mine dust regulations as "deregulatory."

"I can't tell you why it was listed as a deregulatory item," Zatezalo responded, unless, he added, that had something to do with the frequency of testing using new dust monitors.

"Each case of advanced black lung disease is an entirely preventable tragedy, and represents mine operators' unwillingness to adequately control mine dust exposures, and safety regulators failure to set, monitor and enforce standards necessary to protect miners," Scott said in a statement to NPR.

"MSHA should not bend to pressure from well-connected coal mine executives to roll back the regulations," Scott added. "The Mine Safety and Health Administration (MSHA) cannot keep looking the other way while the burden of this preventable disease grows."

The burden is clear on the walls of Ron Carson's office at the Stone Mountain black lung clinic in St. Charles, Va. They're lined with photographs and other mementos of clinic patients, some who died from the disease.

Carson describes a kind of mining disaster in slow motion, in which the disease takes years to develop, even though it strikes quicker now, and in which each death is solitary. He points to a half sheet of white paper tacked to his bulletin board. It shows a phrase he printed out from an article about black lung.

"Mining disasters get monuments," Carson says, his voice softening. "Black lung deaths get tombstones. And I've seen many a tombstone in [the last] 28 years from black lung. And I'm seeing more now. A lot more now."

  • black lung disease

New Research

Study Uncovers Startling Number of Black Lung Cases in Coal Miners

Miners are contracting the disease with striking frequency and at younger ages than ever before

Maris Fessenden

Former correspondent

Black lung x-ray

At the end of the 20th century, black lung, a common term for several respiratory diseases caused by coal mine dust exposure, hit an all-time low. Experts reported just 31 cases of the worst form of the disease. But reports of black lung have surged. Now, epidemiologists from the National Institute for Occupational Safety and Health (NIOSH) have found 416 cases of complicated black lung ( progressive massive fibrosis​)  in just three clinics from 2013 to 2017,  report Howard Berkes and Adelina Lancianese for  NPR .

Since 1970, the Coal Workers' Health Surveillance Program , administered by NIOSH, has monitored the health of coal miners offering free chest radiographs and examinations. In 2014, the program reported an increase in black lung disease or coal workers' pneumoconiosis. Last year, the director of the three clinics (not associated with the surveillance program) asked researchers for help in determining the scope of the problem.  The results of that request were detailed this week in a letter published in the Journal of the American Medical Association .

"This is the largest cluster of progressive massive fibrosis ever reported in the scientific literature," Scott Laney, a NIOSH epidemiologist involved in the research tells NPR .

Black lung is caused by the inhalation of coal mine dust. As the miners cut into coal seams, microscopic particles of dust are kicked into the air and can slip into miner's lungs, where they become trapped. These particles include not just coal, but also silica—a potent lung irritant, as Maya Wei-Haas reported for Smithsonian.com  last year . The particles provoke the body's immune response, but because the invaders are mineral—rather than bacterial or viral—the response spirals. Cells die, and inflammation damages tissues. Overtime, the lungs gradually degrade, depriving victims of air. Only a lung transplant can replace the dying tissue, but miners need to be healthy enough to qualify for a transplant. And even then, transplants only extend patient's lives by only a few more years.

Since the survey portion of the NIOSH study concluded a year ago, reports for black lung have continued. The three clinics, who  serve populations in Virginia, Kentucky and West Virginia,  have since diagnosed an additional 154 new miners.

These clinics are just one window into the problem. In 2016, NPR conducted its own survey of 11 black lung clinics in Virginia, West Virginia, Pennsylvania and Ohio and found 962 cases, Berkes reported in December 2016 . Since then, the ongoing investigation has counted 1,000 more, he writes.

The new study also confirms previous observations that miners are getting diagnosed with the disease earlier than in the past. Miners with black lung are now younger and have been mining for far less time than those decades before. More studies are now underway to figure out just how many miners have the disease and to better understand what may be causing it, Berkes and Lancianese write for NPR .

The NPR investigation and other experts point to longer work shifts, the mining of thinner seams that produce dust with more silica and to retirements and layoffs that may be sending miners who previously put off check-ups into the clinics.

In 2012, Rachel Nuwer wrote about the resurgence as well as the trend for younger miners to receive a diagnoses for Smithsonian.com. Recognizing this problem isn't new, but figuring out why it is happening and what to do is taking time. 

New regulations intended to protect workers from dangerous coal dust were fully implemented in 2016, but as Benny Becker reports for The Ohio Valley Resource , President Trump has ordered a review of those rules as part of his push to rollback regulations.

Meanwhile, Berkes and Lancianese report that   50,000 coal miners are still working.

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Maris Fessenden is a freelance science writer and artist who appreciates small things and wide open spaces.

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The Impact of Black Lung and a Methodology for Controlling Respirable Dust

  • Published: 30 July 2020
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Coal workers’ pneumoconiosis (CWP), commonly known as black lung, is caused by the inhalation of respirable coal mine dust and is a disabling and potentially fatal lung disease with no cure. Historically, CWP has taken a tremendous human and financial toll in the US coal mining industry. Recent health surveillance data indicates that CWP continues to occur at elevated levels. Respirable coal dust exposure must be controlled to prevent the development of CWP. The Pittsburgh Mining Research Division of the National Institute for Occupational Safety and Health (NIOSH) conducts laboratory and mine-site research to identify control technologies that can be used to successfully reduce respirable dust levels. Various technologies, using multiple methods of control, can be applied in order to reduce dust levels. An overview of CWP’s impact and a general methodology for controlling respirable dust in underground coal mines are discussed in this paper.

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Colinet, J.F. The Impact of Black Lung and a Methodology for Controlling Respirable Dust. Mining, Metallurgy & Exploration 37 , 1847–1856 (2020). https://doi.org/10.1007/s42461-020-00278-7

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Black Lung Incidence Study

About the study.

In 2022, the Chief Evaluation Office (CEO) partnered with the Mine Safety and Health Administration (MSHA) and commissioned contractor Summit Consulting, LLC (Summit) to conduct the Black Lung Incidence Study under the Administrative Data Research and Analysis portfolio of studies. This study uses secondary data to examine the rate of black lung disease across the United States, how black lung incidence compares between populations of interest (Appalachia and the Navajo Nation) and coal mining or non-coal mining communities, and how residential coal burning correlates with black lung incidence.

This Department of Labor-funded study was a result of the learning agenda process. It contributes to the labor evidence-base to inform data, methods, and tools and worker protection, labor standards, and workplace-related benefits programs and policies and addresses Departmental strategic goals and priorities.

  • Report Summary
  • What is the total number and rate per 1,000 residents of black lung cases?
  • What is the total number and rate per 1,000 residents of black lung deaths?
  • How does black lung incidence compare between current, former, and non-coal mining communities?
  • Are black lung cases and deaths more prevalent in the Navajo Nation or Appalachia than other parts of the United States? 
  • How does residential coal burning correlate with black lung cases and deaths?
  • There is a public health burden in the Navajo Nation related to residential coal use and coal mining, both of which have historically been important to the Navajo economy.
  • According to statistical models designed to estimate black lung prevalence in the Navajo Nation by considering factors associated with black lung disease, estimated black lung prevalence is higher than reported in publicly available data from Centers for Disease Control and Prevention (CDC) The National Institute for Occupational Safety and Health’s (NIOSH) Enhanced Coal Workers’ Health Surveillance Program (ECWHSP) and CDC Wide-ranging ONline Data for Epidemiologic Research.
  • Underreporting of black lung cases and deaths in the Navajo Nation may result from lack of trust in and access to healthcare and lack of trust in both researchers and the federal government.
  • The prevalence of coal workers’ pneumoconiosis (CWP) has been increasing in the United States since the 1990s.
  • The results of analyses in the Final Report show that black lung disease continues to be associated with unsafe practices in coal mining, residential coal burning, and air pollution through coal processing and transportation in the United States (based on data from the MSHA, CDC, Census, and the U.S. Energy Information Administration).
  • Black lung disease is exponentially higher in counties where coal mining activity has been more predominant, especially those counties that have maintained coal mining practices since the 1970s and 1980s.
  • The prevalence of black lung disease is highly concentrated in specific areas of the country, such as Appalachia. In the Navajo Nation where coal mining has historically been important to the economy and available studies show high levels of residential coal use, results regarding black lung disease prevalence were inconclusive, possibly due to underreporting in the Navajo Nation.

Research Brief

Summit Consulting. (2024). Black Lung Incidence Study Navajo Nation Research Brief. Chief Evaluation Office, U.S. Department of Labor.

Literature Review

Summit Consulting. (2023). Black Lung Incidence Study Literature Review . Chief Evaluation Office, U.S. Department of Labor.

Final Report

Summit Consulting. (2023). Black Lung Incidence Study Final Report . Chief Evaluation Office, U.S. Department of Labor.

The Department of Labor’s (DOL) Chief Evaluation Office (CEO) sponsors independent evaluations and research, primarily conducted by external, third-party contractors in accordance with the Department of Labor Evaluation Policy . CEO’s research development process includes extensive technical review at the design, data collection and analysis stage, including: external contractor review and OMB review and approval of data collection methods and instruments per the Paperwork Reduction Act (PRA), Institutional Review Board (IRB) review to ensure studies adhere to the highest ethical standards, review by academic peers (e.g., Technical Working Groups), and inputs from relevant DOL agency and program officials and CEO technical staff. Final reports undergo an additional independent expert technical review and a review for Section 508 compliance prior to publication. The resulting reports represent findings from this independent research and do not represent DOL positions or policies.

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  • Inflammation

Tracing the origins of lung fibrosis

  • Christopher D. Buckley   ORCID: orcid.org/0000-0001-6924-6402 1 &
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A lung-specific fibroblast that normally provides a niche for alveolar cells has been identified as the predominant source of emergent inflammatory and fibrotic fibroblast subsets. This finding has major implications for the treatment of lung diseases.

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Is there a link between chronic obstructive pulmonary disease and lung adenocarcinoma a clinico-pathological and molecular study.

black lung disease research paper

1. Introduction

2. materials and methods, 2.1. study design and population, 2.2. morphological analyses, 2.3. dna extraction, 2.4. next generation sequencing, 2.5. bioinformatics analysis.

  • Variants with variant allele frequency (VAF) < 0.05 (5%) were excluded;
  • Variants with coverage < 100X were excluded;
  • Only exonic and splicing variants were kept;
  • Synonymous SNVs were removed;
  • Polymorphisms were excluded, defined as variants having minor allele frequency (MAF) > 0.01 according to Exome Sequencing Project (ESP, https://bio.tools/esp , accessed on 14 April 2023) OR Exome Aggregation Consortium (ExAC, https://ngdc.cncb.ac.cn/databasecommons/database/id/3774 , accessed on 14 April 2023) OR 1000 Genomes Project ( http://www.internationalgenome.org , accessed on 7 August 2024) OR Genome Aggregation Database ( https://gnomad.broadinstitute.org/ , accessed on 1 June 2024);
  • We excluded possibly benign variants and variants with uncertain significance according to ClinVar (database update of 20221231, labels considered: ‘Benign’, ‘Benign/Likely benign’, ‘Likely benign’, ‘Uncertain significance’).

2.6. Statistical Analysis

3.1. study population, 3.2. distribution of mutations in copd, smokers and non smokers tumor samples, 3.3. analysis of matched pathological/healthy tissues, 4. discussion, supplementary materials, author contributions, institutional review board statement, informed consent statement, data availability statement, acknowledgments, conflicts of interest.

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Click here to enlarge figure

CharacteristicsCOPD/Smoker LUAD
N = 38
Non-COPD/Smoker LUAD
N = 54
Non-COPD/Non-Smoker LUAD
N = 18
p-Value q-Value
Sex 0.0010.015
males30 (79%)34 (63%)5 (28%)
females8 (21%)20 (37%)13 (72%)
Age72 (68, 75)69 (62, 73)65 (59, 72)0.110.3
GOLD stage >0.9>0.9
I18 (47.5%)0 (NA%)0 (NA%)
II18 (47.5%)0 (NA%)0 (NA%)
III2 (5%)0 (NA%)0 (NA%)
Smoking history (pack years)40 (27.5–50)36 (22–50)-0.2450.67
FEV1 (% of predict)76 (64, 87)93 (88, 113)117 (104, 130)<0.001<0.001
FEV1/FV (% of predict)67 (58, 70)83 (78, 85)82 (78, 86)<0.001<0.001
FVC (% of predict)92 (74, 101)92 (82, 105)119 (108, 128)<0.0010.002
DLCO/VA (%)70 (48, 89)80 (65, 91)84 (81, 99)0.0850.2
SUV6 (2, 11)6 (2, 12)2 (1, 5)0.0610.2
WBC (n × 10 /L)7.35 (5.78, 8.68)6.92 (5.45, 9.30)5.52 (4.70, 7.01)0.0120.072
RBC (n × 10 /L)4.50 (4.18, 5.00)4.42 (4.14, 4.77)4.62 (4.21, 4.96)0.70.8
HgB (g/dL)13.70 (12.35, 14.65)13.70 (12.50, 14.70)13.80 (13.03, 14.80)0.70.8
Neutrophils (n × 10 /L)4.40 (3.54, 5.74)4.02 (3.06, 6.02)2.87 (2.81, 4.52)0.0460.2
Neutrophils (%)64 (56, 69)62 (56, 69)56 (52, 66)0.30.4
Lymphocytes (n × 10 /L)1.77 (1.48, 2.12)1.75 (1.55, 2.06)1.62 (1.39, 1.93)0.70.8
Lymphocytes (%)24 (20, 32)26 (20, 32)31 (24, 33)0.30.4
Monocytes (n × 10 /L)0.60 (0.49, 0.70)0.57 (0.42, 0.70)0.49 (0.40, 0.58)0.0820.2
Monocytes (%)8.55 (7.03, 10.05)8.00 (7.10, 9.80)9.30 (6.90, 10.50)0.70.8
Eosinophils (n × 10 /L)0.16 (0.06, 0.26)0.08 (0.05, 0.16)0.12 (0.06, 0.26)0.0790.2
Eosinophils (%)2.05 (1.33, 3.63)1.30 (0.80, 2.30)2.20 (1.30, 3.80)0.0290.13
Basophils (n × 10 /L)0.030 (0.020, 0.040)0.020 (0.010, 0.030)0.020 (0.020, 0.030)0.130.3
Basophils (%)0.40 (0.30, 0.60)0.30 (0.20, 0.50)0.40 (0.30, 0.60)0.20.3
ESR (mm/h)21 (12, 32)20 (10, 28)14 (9, 20)0.0900.2
CRP (mg/L)2.0 (1.4, 6.9)2.9 (1.3, 4.7)0.8 (0.3, 2.9)0.0290.13
Clinical stage 0.20.3
IA7 (18.5%)17 (31.5%)6 (33%)
IB16 (42%)11 (20.5%)9 (50%)
IIA4 (10.5%)3 (6%)0 (0%)
IIB7 (18.5%)10 (18%)2 (11%)
IIIA4 (10.5%)10 (18%)1 (6%)
IIIB0 (0%)3 (6%)0 (0%)
CharacteristicCOPD/Smoker LUAD
N = 38
Non-COPD/Smoker LUAD
N = 54
Non-COPD/Non-Smoker LUAD
N = 18
p-Value q-Value
Tumor cells (%)70 (50, 80)65 (50, 80)70 (70, 80)0.50.7
Prevalent pattern 0.30.4
Lepidic pattern1 (2.5%)8 (15%)1 (5.6%)
Acinar pattern28 (74%)32 (59%)14 (78%)
Papillary pattern1 (2.5%)4 (7.5%)0 (0%)
Solid pattern8 (21%)10 (18.5%)3 (17%)
Lepidic pattern (%)0 (0, 5)2 (0, 24)18 (5, 30)0.0080.057
Acinar pattern (%)60 (42, 85)50 (20, 75)60 (45, 84)0.140.3
Papillary pattern (%)0 (0, 0)0 (0, 8)0 (0, 8)0.70.8
Micropapillary pattern (%)0 (0, 2)0 (0, 1)0 (0, 4)>0.9>0.9
Solid pattern (%)10 (0, 35)0 (0, 32)0 (0, 0)0.20.3
WHO Grading
11 (2%)5 (9%)1 (5%)
217 (45%)21 (39%)14 (78%)
320 (53%)28 (52%)3 (17%)
MIB1 (%)20 (10, 58)40 (20, 70)10 (9, 21)0.0010.011
Necrosis (%) 0.20.3
06 (16%)12 (22%)7 (39%)
≤10%19 (50%)25 (46%)7 (39%)
11–30%4 (10%)7 (13%)4 (22%)
>30%9 (24%)10 (19%)0 (0%)
Inflammation (%) 0.20.3
00 (0%)0 (0%)1 (6%)
≤10%13 (34%)24 (44%)4 (22%)
11–30%18 (47.5%)23 (43%)11 (61%)
>30%7 (18.5%)7 (13%)2 (11%)
Fibrosis (%) 0.20.3
03 (8%)4 (7%)0 (0%)
≤10%16 (42%)22 (41%)3 (17%)
11–30%12 (32%)18 (33%)8 (44%)
>30%7 (18%)10 (19%)7 (39%)
Vascular invasion 0.50.7
No18 (47%)23 (43%)9 (50%)
Yes20 (53%)31 (57%)9 (50%)
Pleural invasion 0.60.8
No20 (53%)27 (50%)11 (61%)
Yes18 (47%)27 (50%)7 (39%)
Type of visceral pleura invasion >0.9>0.9
PL020 (53%)27 (50%)11 (61%)
PL115 (39%)23 (43%)6 (33%)
PL23 (8%)4 (7%)1 (6%)
Perineural invasion 0.50.7
No34 (89%)50 (93%)18 (100%)
Yes4 (11%)4 (7%)0 (0%)
Lymph node invasion 0.0890.2
No30 (79%)38 (70%)17 (94%)
Yes8 (21%)16 (30%)1 (6%)
Type of lymph node invasion 0.140.3
030 (79%)38 (70%)17 (94%)
16 (16%)7 (13%)1 (6%)
22 (5%)9 (17%)0 (0%)
GeneCOPD/Smoker LUAD
N = 38
Non-COPD/Smoker LUAD
N = 54
Non-COPD/Non-Smoker LUAD
N = 18
KRAS21 (55%)27 (50%)3 (17%)
EGFR9 (24%)12 (22%)10 (56%)
NTRK38 (21%)14 (26%)5 (28%)
TP5310 (26%)15 (28%)4 (22%)
NTRK28 (21%)10 (19%)1 (6%)
PIK3CA7 (18%)9 (17%)0 (0%)
STK119 (24%)13 (24%)1 (6%)
MET5 (13%)10 (19%)0 (0%)
NOTCH16 (16%)11 (20%)2 (11%)
FBXW75 (13%)5 (9%)0 (0%)
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Lunardi, F.; Nardo, G.; Lazzarini, E.; Tzorakoleftheraki, S.-E.; Comacchio, G.M.; Fonzi, E.; Tebaldi, M.; Vedovelli, L.; Pezzuto, F.; Fortarezza, F.; et al. Is There a Link between Chronic Obstructive Pulmonary Disease and Lung Adenocarcinoma? A Clinico-Pathological and Molecular Study. J. Pers. Med. 2024 , 14 , 839. https://doi.org/10.3390/jpm14080839

Lunardi F, Nardo G, Lazzarini E, Tzorakoleftheraki S-E, Comacchio GM, Fonzi E, Tebaldi M, Vedovelli L, Pezzuto F, Fortarezza F, et al. Is There a Link between Chronic Obstructive Pulmonary Disease and Lung Adenocarcinoma? A Clinico-Pathological and Molecular Study. Journal of Personalized Medicine . 2024; 14(8):839. https://doi.org/10.3390/jpm14080839

Lunardi, Francesca, Giorgia Nardo, Elisabetta Lazzarini, Sofia-Eleni Tzorakoleftheraki, Giovanni Maria Comacchio, Eugenio Fonzi, Michela Tebaldi, Luca Vedovelli, Federica Pezzuto, Francesco Fortarezza, and et al. 2024. "Is There a Link between Chronic Obstructive Pulmonary Disease and Lung Adenocarcinoma? A Clinico-Pathological and Molecular Study" Journal of Personalized Medicine 14, no. 8: 839. https://doi.org/10.3390/jpm14080839

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We identified a Thelazia callipaeda eyeworm in an American black bear in Pennsylvania, USA, on the basis of its morphological features and molecular analysis. Our finding highlights emergence of a T. callipaeda worm sylvatic transmission cycle in the United States.

Thelaziosis is an emerging zoonotic disease caused by nematodes of the genus Thelazia (Spirurida, Thelazioidea). In the United States, 3 zoonotic species have been identified: Thelazia gulosa ( 1 ), T. californiensis ( 2 ), and most recently T. callipaeda ( 3 ). In Asia and Europe, T. callipaeda is considered the main agent of thelaziosis in humans, domestic animals, and wild animals ( 4 ). Over the past decade, the geographic distribution and prevalence of T. callipaeda infection has increased worldwide in scale and intensity ( 4 ). The first autochthonous case in the United States was reported in 2018 in a domestic dog ( Canis lupus familiaris ) from New York with a history of unilateral epiphora and blepharospasm. Since then, additional cases in domestic dogs and cats have been reported, predominately from the northeastern United States ( 3 , 5 ).

T. callipaeda eyeworms are found in the conjunctival sac and lacrimal duct of the definitive host. They are transmitted when a male zoophilic secretophagous Phortica variegata fly ingests first-stage larvae from the host’s lachrymal secretions. In the vector, the first-stage larvae develop to the infective third-stage larvae in the testes, migrate to the mouthparts, and are transferred to another host during subsequent feeding on lachrymal secretions ( 4 ).

The role of wildlife in the epidemiology and emergence of T. callipaeda eyeworms is not completely known. In Europe, cases of T. callipaeda eyeworm infection have been detected in a wide range of hosts, including wild carnivores, omnivores, and lagomorphs ( 6 , 7 ). Wild canids, particularly red foxes ( Vulpes vulpes ), seem to play a large role in maintaining the sylvatic cycle in thelaziosis-endemic areas of Europe ( 7 ). However, knowledge of the sylvatic transmission cycle of T. callipaeda eyeworms, along with their environmental and anthropogenic factors, remains limited. Considering the emergence of those zoonotic nematodes in non–thelaziosis-endemic areas and the need for more information about their ecology and epidemiology in the United States, we report a case of T. callipaeda eyeworm infection in an American black bear ( Ursus americanus ) and identify a new geographic location of transmission.

In November 2023, an adult, female American black bear was legally harvested in Coolbaugh Township, Monroe County, Pennsylvania. During processing of the bear for taxidermy preparation, multiple linear nematodes were observed behind the third eyelid. Nematodes were extracted and submitted for identification. Two additional harvested bears from Monroe and Pike Counties, Pennsylvania, were also reported to have similar ocular nematode infections, but specimens from those bears were not collected.

Morphologic features of adult female Thelazia callipaeda eyeworm isolated from an American black bear in Coolbaugh Township, Monroe County, Pennsylvania, USA, 2023. A) Anterior end showing the large, deep, cup‐shaped buccal cavity. Scale bar indicates 50 μm. B) Midbody region showing the thin transverse cuticular striations pattern and numerous coiled first-stage larvae. Scale bar indicates 100 μm. C) Anterior end showing the location of the vulvar opening anterior to the esophageal-intestinal junction. Dashed black arrow indicates esophageal-intestinal junction; solid black arrow indicates the vulval opening. Scale bar indicates 100 μm.

  • Figure 1 . Morphologic features of adult female Thelazia callipaeda eyeworm isolated from an American black bear in Coolbaugh Township, Monroe County, Pennsylvania, USA, 2023. A) Anterior end showing the large, deep,...

We identified 9 female and 4 male adult nematodes from the bear as T. callipaeda on the basis of morphologic and morphometric features ( 8 ). The nematodes were characterized by the presence of a cup-shaped buccal capsule and cuticular transverse striations, as well as the location of the vulvar opening anterior to the esophageal-intestinal junction on the female worms ( Figure 1 ). Female nematodes were 1.16–1.46 cm long and 0.36–0.42 mm wide; male worms were 0.82–1.06 cm long and 0.31–0.42 mm wide. The number of transverse cuticular striations ranged from 160 to 400/mm in the cephalic, midbody, and caudal regions.

Phylogenetic relationship of Thelazia callipaeda isolate from an American black bear in Coolbaugh Township, Monroe County, Pennsylvania, USA, 2023 (GenBank accession no. PP739308), and other species of Thelazia available in GenBank (accession numbers shown). Analysis was performed by using the maximum-likelihood method (1,000 bootstrap replicates) in MEGA X version 11 (https://www.megasoftware.net). The best-fit nucleotide substitution model for the dataset was Tamura-Nei with a discrete gamma distribution, which was used to model evolutionary rate differences among sites (5 categories [+G, parameter = 0.2578]). That analysis involved 30 nt sequences. There were 647 positions in the final dataset. Distances, defined as the number of nucleotide substitutions/site, were calculated by using that model. Branches corresponding to partitions reproduced in <50% of bootstrap replicates are collapsed.

Figure 2 . Phylogenetic relationship of Thelazia callipaeda isolate from an American black bear in Coolbaugh Township, Monroe County, Pennsylvania, USA, 2023 (GenBank accession no. PP739308), and other species of ...

We extracted genomic DNA from a midbody fragment of a female adult worm and amplified, sequenced, and analyzed the partial cytochrome oxidase c subunit I ( cox 1) gene, as previously described ( 2 ). We generated a 623-bp cox 1 sequence (GenBank accession no. PP739308), which showed 99%–100% maximum identity with T . callipaeda sequences available in GenBank. Phylogenetic analysis was performed by using the maximum-likelihood method and confirmed the taxonomic identification of T . callipaeda . The isolate clustered with all previous isolates from domestic animals in North America and with some isolates from Europe ( Figure 2 ), indicating circulation of the newly introduced pathogen in wildlife habitats and transmission from domestic animals to wildlife.

The presence of adult T. callipaeda eyeworms in an American black bear suggests the establishment of a sylvatic transmission cycle in the United States and expansion of the number of definitive host species used by the zoonotic nematode. In the past decade, wild carnivores have been identified as primary definitive hosts associated with the sylvatic cycle in thelaziosis- endemic and non–thelaziosis-endemic areas of Europe and Asia ( 7 ). American black bears are the most widely distributed species of bear in North America, inhabiting diverse regions throughout Mexico, Canada, and the United States ( 9 ). Given the bears’ extensive geographic distribution and frequent and close interaction with humans and pets ( 10 ), thelaziosis in the black bear population raises concerns about the rapidly increasing incidence and geographic range of T. callipaeda eyeworms in the United States. Although further research into the extent to which black bears play a role in the maintenance of the sylvatic cycle and transmission of T. callipaeda eyeworms is needed, the presence of the zoonotic nematode in such a wide range of hosts implicates exposure and risk for transmission to threatened and endangered species and direct or indirect risk for transmission to humans and domestic animals.

Dr. Sobotyk is an assistant professor of clinical parasitology and director of the Clinical Parasitology Laboratory at the University of Pennsylvania, Philadelphia, PA. Her research focuses on zoonotic helminth infections in domestic and wild animals and improvement and development of diagnostic techniques for detecting parasitic infections of veterinary and public health relevance.

Acknowledgment

We thank the Pennsylvania Game Commission and Dillon Gruver for their continued support. We also acknowledge Shawn Lamparter’s Wildlife Design for recognition and prompting submission of the specimens.

  • Bradbury  RS , Breen  KV , Bonura  EM , Hoyt  JW , Bishop  HS . Case report: conjunctival infestation with Thelazia gulosa : a novel agent of human thelaziasis in the United States. Am J Trop Med Hyg . 2018 ; 98 : 1171 – 4 . DOI PubMed Google Scholar
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  • Otranto  D , Dantas-Torres  F , Mallia  E , DiGeronimo  PM , Brianti  E , Testini  G , et al. Thelazia callipaeda (Spirurida, Thelaziidae) in wild animals: report of new host species and ecological implications. Vet Parasitol . 2009 ; 166 : 262 – 7 . DOI PubMed Google Scholar
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  • Figure 2 . Phylogenetic relationship of Thelazia callipaeda isolate from an American black bear in Coolbaugh Township, Monroe County, Pennsylvania, USA, 2023 (GenBank accession no. PP739308), and other species of Thelazia available...

Suggested citation for this article : Sobotyk C, Dietrich J, Verocai GG, Maxwell L, Niedringhaus K. Thelazia callipaeda eyeworms in American black bear, Pennsylvania, USA, 2023. Emerg Infect Dis. 2024 Sep [date cited]. https://doi.org/10.3201/eid3009.240679

DOI: 10.3201/eid3009.240679

Original Publication Date: August 14, 2024

Table of Contents – Volume 30, Number 9—September 2024

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Focus: Health Equity

Lung disease in central appalachia: it’s more than coal dust that drives disparities, claire l. debolt.

a Department of Medicine, University of Virginia, Charlottesville, VA, USA

Chad Brizendine

Margaret m. tomann.

b Stone Mountain Health Services, Black Lung Clinic Program, St. Charles, VA, USA

Drew A. Harris

The population living in Central Appalachia is disproportionately impacted by lung disease. This is driven, in part, by occupational hazards and environmental exposures. However, it is more than coal dust that is driving the ongoing disparity of lung disease in the region. This review describes how the decline of the coal mine industry and subsequent rise of unemployment, poverty, and educational disparities have increased risk for worse pulmonary health outcomes in the region. Additional challenges related to healthcare access, substance use, cultural characteristics, and social capital are highlighted in their relation to pulmonary health within Central Appalachia. Lastly, the review describes strategies that hold promise to reduce regional health disparities. Several healthcare and community-centered initiatives are highlighted as successful examples of collaborative efforts working towards improving pulmonary health outcomes in the region. However, significant challenges related to social, economic, and environmental factors remain. Addressing these social determinants of health must be a paramount concern for healthcare, community and political leaders seeking to impact change and improve the health and well-being of this vulnerable population.

Introduction

Central Appalachia, including Southwest Virginia, Eastern Kentucky, Southern West Virginia, Northeast Tennessee, as well as portions of Ohio and North Carolina, is a largely rural and mountainous region in the United States. The population living in Central Appalachia is disproportionately impacted by a wide range of health disparities, including lung disease. The burden of lung disease in Central Appalachia is driven, in part, by occupational exposure from underground and surface mines. At the peak of coal production and employment in the region, there were over 700,000 coal miners living and working in Central Appalachia [ 1 ]. Most of these coal miners worked in an era of inadequate workplace protections and many have developed a range of lung diseases due to their occupational exposures. The recent epidemic of progressive massive fibrosis in Central Appalachia illustrates that even with current workplace protections, ongoing exposure to respirable coal and rock dust has significant health impacts [ 2 ]. However, it is more than coal dust that is driving the ongoing disparity of lung disease in this region. The prevalence, morbidity, and mortality of lung disease in Central Appalachia far exceeds the burden of disease in other mining regions in the nation. The population in Central Appalachia faces interdependent social, economic, behavioral, and environmental challenges that contribute to the disproportionate burden of lung disease in the region. What follows is a description of the lung disease in Central Appalachia, the environmental and social determinants that impact the pulmonary health of the region, and strategies that hold promise to reduce regional disparities and improve health.

Burden of Lung Disease

In 2017, The Appalachia Regional Commission (ARC) report on Health Disparities determined that the Years of Potential Life Lost, a measure of premature mortality, is 25% higher in Appalachia than in the rest of the US [ 3 ]. Disparities in outcomes for a range of pulmonary conditions contribute to this premature mortality.

In one study of Appalachians from Eastern Kentucky, nearly 1 in 5 adults (19.6%) aged 40 years and over met the criteria for the Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition of chronic obstructive pulmonary disease (COPD) [ 4 ]. This prevalence rate is more than three times higher than national age-adjusted prevalence rates in the US (5.9%) [ 5 ]. COPD hospitalization rates are 39% higher in Appalachia than in the rest of the US. Central Appalachians’ COPD mortality rates are nearly twice as high (78 per 100,000) than rates in the US (42 per 100,000) [ 6 ].

In addition to COPD, Central Appalachians face disparities in both the prevalence and mortality from coal worker’s pneumoconiosis (CWP). Although often thought of as a disease of historical interest only, the incidence of CWP in the US has increased since the early 2000s [ 7 ]. Miners working in the coal fields of the Appalachian mountains have been shown to be particularly vulnerable to develop rapidly progressive and severe pneumoconiosis [ 8 ]. In 2014, 91% of counties in the US experienced mortality rates of < 1 death per 100,000 due to CWP; in comparison, several counties in Central Appalachia had CWP mortality rates as high as 43.5 per 100,000 [ 9 ].

Central Appalachians are additionally disproportionately burdened by lung cancer. Lung cancer rates for Appalachian men and women are nearly 25% and 8% higher than men and women living in the rest of the US, respectively [ 10 ]. In recent decades, lung cancer rates have been declining substantially among women in most of the US; however, Central Appalachia is the exception. Between 1990 and 1999, lung cancer deaths increased by 13% in Central Appalachia; while women in the rest of the US experienced a 6% decline in lung cancer deaths during the same time period [ 11 ].

Dust is Only Partially to Blame

Differences in dust exposure, including cumulative dust exposure, dust composition, and particle size, as well as host susceptibilities, can lead to a wide spectrum of coal mining-related lung disease [ 12 ]. Although CWP has historically been associated with coal dust exposure, there is increasing evidence that exposure to silica (quartz) is contributing to the disproportionate rise of lung disease in Central Appalachian coal miners [ 13 ]. In recent decades, the coal mines of Central Appalachia have thinner coal seams relative to the rest of the US. In these “low-coal” seams, mining typically involves cutting through rock above and below coal seams which leads to increased silica dust exposure [ 14 ]. A recent analysis of mean respirable coal dust concentrations collected by underground mine inspectors demonstrates a significantly higher geometric mean concentration of respirable silica in Central Appalachia (0.05mg/m 3 ) compared to the rest of the US (0.028mg/m 3 ) [ 15 ].

Both respirable coal and silica dust can have toxic effects in coal miners. COPD, including chronic bronchitis and emphysema, is independently associated with exposure to coal and silica dust [ 16 ]. Coal mine dust exposure, including both coal and silica dust, is also associated with a form of pulmonary fibrosis known as dust-related diffuse fibrosis [ 17 ]. Lung function impairment [ 18 ] and rapidly progressing lung disease [ 2 ] have been increasingly described in coal miners with relatively short mining tenures due to intense dust exposures. Coal mining-related exposures including silica dust and diesel exhaust are likely to account for recent analyses showing an association between coal mining and lung cancer [ 19 ].

Workplace protections have been enacted by the US federal government to mitigate the wide array of toxicities associated with coal mine dust exposure. The Federal Coal Mine Health and Safety Act of 1969 was enacted to “provide more effective means and measures for improving working conditions and practices in the Nation’s coal mines in order to prevent death…and occupational diseases.” Amongst the many important provisions in this act was the establishment of the federal permissible exposure limit for respirable coal mine dust. The exposure limit for respirable dust was initially set to 2.0 mg/m 3 , but a more stringent dust limit was set when quartz content exceeded 5% within dust samples [ 20 ]. Dust exposure limits, in addition to other provisions within the Federal Coal Mine Health and Safety Act, were effective at reducing the intensity of coal mine dust exposures and subsequent development of occupational lung disease over the ensuing three decades. Despite these measures, the incidence of coal mining-related lung disease in the US has increased since the turn of the century with Central Appalachians facing the highest burden of disease [ 21 ]. The worsening burden of lung disease in Central Appalachia despite workplace protections suggests that, in addition to further improvement in workplace conditions, other factors need to be considered to improve pulmonary health outcomes. The interconnected economic, social, behavioral, and environmental determinants of health that exist in Central Appalachia are critical factors contributing to the pulmonary disparity gap affecting this region.

The Decline of the Coal Industry and the Rise of Unemployment and Poverty

The coal industry has played a central role in the Central Appalachian economy for much of the past century. Due to a combination of factors, including cheap natural gas (a competing fuel source for electric power production) and a regulatory environment that increased the cost of coal production/burning, demand for coal has declined since the early 2000s [ 22 ]. While demand for coal has decreased, the process whereby coal is mined has also transformed—with increased mechanization of coal mining, fewer coal miners are needed to mine the coal. This combination of decreased demand and increased mechanization has led to a dramatic decrease in the coal mine production and employment in the US. The peak level of US coal mine employment was over 850,000; whereas current US coal mine employment is now less than 50,000 [ 23 ]. Coal mine employment in Central Appalachia has declined more rapidly than in the rest of the US. In the last decade, coal mine employment in Central Appalachia has decreased from 35,408 (2010) to 16,361 workers (2019) [ 24 ]. Six out of the nine coal companies that filed for bankruptcy in the US in 2018-2019 were located in Central Appalachia [ 25 ].

The decline of the coal mine industry in Central Appalachia has had a far-reaching economic impact. This is in part due to the lack of economic diversification in the region; in 2005, coal mining comprised more than half of total employment in many Central Appalachian counties [ 22 ]. In large part due to this decline of coal mine employment, the region now faces a high concentration of “economically distressed” counties—which is defined by the ARC as a county that ranks in the highest 10% in the nation in unemployment rates and poverty rates and in the lowest in per capita income. Across the entire Appalachian region 78 counties are classified as economically distressed. Of these, 51 are located in Central Appalachia [ 26 ]. Twenty-one counties in Central Appalachia have at least double (28%) the poverty rate compared to the national average (14%) [ 27 ].

Several recent studies highlight how the high rates of unemployment and poverty in Central Appalachia are important factors contributing to pulmonary disparities. In the US, rural residence and poverty are independent risk factors for COPD amongst both smokers and non-smokers. Environmental exposures, nutritional status, low birth weight and childhood respiratory infections and lack of access to healthcare and health education all likely contribute to this disparity [ 28 ]. In another recent multinational study of nearly 10,000 patients, poverty was associated with impaired lung function even after accounting for age, smoking, history of asthma, other exposures, and prior infections [ 29 ]. Other downstream effects of unemployment and poverty, such as educational attainment, healthcare access, and tobacco use are discussed below.

Opioid Crisis

The opioid crisis has disproportionally impacted the Appalachian Region, resulting in significantly higher overdose mortality rates in Central Appalachia compared to the rest of the US [ 30 ]. Opiate Use Disorder (OUD) is associated with a spectrum of pulmonary diseases beyond the classic association of respiratory depression. Such illnesses include increased risk of aspiration pneumonia from consciousness impairment or pulmonary edema and alveolar damage with heroin inhalation [ 31 , 32 ]. Intravenous drug users have been reported to have granulomatous pneumonias secondary to drug contaminants and more commonly can have pulmonary septic emboli secondary to endocarditis [ 31 , 32 ]. Pneumothorax is a potential complication of inhalational substance [ 32 ]. Beyond the individual morbidity and mortality is the loss of these (often working age) individuals from their families and communities.

The COVID-19 pandemic has further highlighted the opiate epidemic, in both the increased challenges of medical management of OUD and increased risk for contracting COVID-19 among persons with OUD. Many patients have had to travel further or have not been able to access treatment due to closure of substance use treatment clinics [ 33 ]. There has also been less access to acute care as hospitals have had to divert resources to acute care for COVID-19 patients and there have been less mental health resources due to overburdened healthcare centers [ 33 ]. Substance use experts have also seen a rise in relapses, potentially as people in recovery are forced into isolation and without social support systems [ 34 ]. Patients that suffer from OUD may also be at increased risk for COVID-19 due to a disproportionate reliance on informal sources for medical and COVID-19 information, an inability to maintain stable housing and meals, and an increased risk for contracting and spreading COVID-19 since drug procurement and use generally involves social contact [ 35 ]. The US Department of Health and Human Services Office of Inspector General has generated a report that suggests that measures taken to address the COVID-19 pandemic (such as relaxed rules related to telehealth and opioid prescribing, reduced access to in-person screenings for opioid misuse and treatment facilities) may have contributed to the increases in opioid overdoses and deaths in several Central Appalachian states since the beginning of the pandemic [ 36 ]. The opiate epidemic not only contributes to increased risk and worsened severity of lung disease, but also exacerbates social and economic determinants of health in Central Appalachia.

Health and education are intrinsically linked, as good health is needed for educational achievement, and education achievement is an important factor contributing to good health. Recognizing this interplay, it is a formidable regional challenge that amongst adults aged 25 and older in Central Appalachia, 21.5% have not completed a high school degree. This is nearly double the US average. Only 14.1% of Central Appalachians hold a bachelor’s degree or higher, which is less than half the US average [ 35 ]. The impact of educational disparities in Central Appalachia have wide reaching implications related to lung disease.

Low educational achievement is associated with poor health literacy: in a nationally representative sample, almost half of US adults who did not graduate from high school had low health literacy [ 37 ]. In a multivariable analysis of factors contributing to low health literacy, lower educational attainment was the strongest predictor of poor health literacy [ 38 ]. Low health literacy is a barrier to participation in lung cancer screening [ 39 ] and is associated with worse COPD outcomes [ 40 ]. Poor health literacy has also been linked to poor medication adherence, increased ED visits and increased hospital admissions [ 41 ].

Low educational attainment is also a risk factor for smoking and subsequent development of smoking related lung diseases. Low educational attainment is associated with daily smoking and nicotine dependence [ 42 ]. Individuals with less than a high school education have fewer quit attempts and are less likely to successfully quit smoking [ 43 ]. Lower education attainment is one of many factors in Central Appalachia that contributes to smoking rates, which are amongst the highest in the nation [ 6 ].

Recent data suggests some progress in reducing the educational disparity gap in Central Appalachia. The percentage of Central Appalachians aged 25 and older with less than a high school degree decreased by 3.6% in the last 12 years, compared to nationwide decrease of 1.7% overall [ 3 ]. Furthermore, the student-teacher ratio in Central Appalachia was 15, lower than the US national average of 16.5 [ 3 ].

Healthcare Access and Quality

Access to healthcare is dependent on numerous factors that range from whether an individual has health insurance coverage to less easily quantifiable factors such as the impact of family responsibilities, inability to miss work, or lack of transportation. In the last decade, the overall trend in health insurance coverage in Central Appalachia has been positive: Between the 2009-2013 and 2014-2018 periods, the rates of people without health insurance fell at least 8% in Central Appalachia [ 44 ]. The decrease in the uninsured was greater in two age groups in particular, children and those under the age of 35. The uninsured rate in Central Appalachia in the under-35 population was nearly 10% lower in 2014-2018 than in 2009-2013 [ 44 ]. This is largely due to programs designed to increase coverage including expansion of the Children’s Health Insurance Program (CHIP) and provisions of the Affordable Care Act such as the young adult coverage extension that permits children to stay on a parent’s health insurance plan until they turn 26 years old [ 44 ]. In addition, Kentucky, Virginia, and West Virginia have each implemented Medicaid expansion in the past decade. More than 500,000 Virginians have enrolled in Medicaid since the expansion was implemented in 2019 [ 45 ]. States in Central Appalachia that did not expand Medicaid (Tennessee and North Carolina) have had more limited primary care services and COVID-19 pandemic-related services. Underserved areas in these states have had less access to testing, fewer preparations, and greater financial strain on community centers and local health departments [ 46 , 47 ].

Despite these improvements, health insurance remains a challenge for many in the region. Nearly 15% of Central Appalachian residents aged 26-34 do not have health insurance coverage. As with many social determinants of health in the region, the divide is wider for those who live in rural areas where nearly 18% of residents aged 26-34 do not have health insurance coverage [ 44 ].

In addition to ongoing high rates of being under insured and not insured, Central Appalachians face additional healthcare access challenges related to geographic isolation, limited transportation options, and insufficient technology infrastructure. The physical distance required to travel from a patient’s home to a healthcare facility is a well-recognized barrier to healthcare access [ 48 ]. This is especially relevant in Central Appalachia in which the mountainous topography has led to circuitous travel routes. Traveling to reach medical care in Central Appalachia is further challenged by limited access to a personal vehicle; in Central Appalachia, more than 8% of the population do not have access to personal transportation [ 44 ]. Furthermore, only 0.5% of rural residents use public transportation because, when it is available, the systems are often limited to a single county or municipality which limit the destinations available to be reached without a car [ 49 ].

The COVID-19 pandemic led to a transformation in both healthcare regulations and practice structures that support digital accessibility to healthcare via telemedicine. This transformation has further highlighted a rural-urban “digital divide” in access to technology and internet capable of telemedicine visits. In Central Appalachia 1 in 5 households do not have a computer device, including desktop or laptop, smartphone, tablet, or other device) [ 44 ]. Only 67% of households have a broadband internet subscription that has bandwidth capable of video visits [ 33 ]. As telemedicine utilization has exponentially increased outside of Central Appalachia in 2020-2021, the impact of this digital divide on health disparities in Central Appalachia remains to be seen.

The number of healthcare providers is significantly lower in the Central Appalachian region than the nation as a whole. For example, the supply of primary care physicians in Central Appalachia is 32% lower than the national average [ 49 ]. This is compounded by a reduced supply of subspecialty physicians in the region; the supply of subspecialty physicians (110 per 100,000) is 28% lower than the national average (153 per 100,000 population) [ 50 ]. Limited access to pulmonology subspecialists in Central Appalachia necessitates that management of lung diseases is largely dependent on primary care providers [ 51 ]. There are several examples of how this reliance on primary care providers might negatively impact pulmonary health outcomes in the region. One such example is in pulmonary rehabilitation, an essential component of guideline-based therapies for many chronic lung diseases including COPD. Although recent studies have shown the feasibility and benefit of pulmonary rehabilitation in rural Appalachian communities [ 52 ], underutilization in Central Appalachia is in part because of lack of awareness of benefit by primary care providers and limited access to specialty programs in rural areas [ 53 ].

There are many examples of community organizations in Central Appalachia, including federally qualified health clinics and free medical clinics that serve vulnerable populations who lack health insurance and could not otherwise afford or access healthcare. One such example is the Health Wagon [ 54 ] in Southwest Virginia. The Health Wagon is a non-profit mobile clinic that provides free primary and subspecialty care to patients of geographically isolated regions of Central Appalachia. The clinic’s medical director is a pulmonologist and the mobile clinic is outfitted with both pulmonary function testing and x-ray testing. Another example is the Remote Area Medical (RAM) Volunteer Corps [ 55 ] which held more than 60 mobile clinic events in and around Central Appalachia each year. Volunteer dentists, physicians, nurses, and other healthcare professionals offered free on-site care through the RAM program to tens of thousands who have few other options. In 2020, RAM did not assemble to offer support, which was partially due to COVID-19 social distancing restrictions, but also due to a greater number of Virginians enrolled in Medicaid (following Virginia’s expansion in 2019) [ 56 ]. Although these community organizations can provide some safety-net care to a vulnerable population, they highlight the significant healthcare access gaps that Central Appalachians continue to face despite increased insurance availability through Medicaid expansion and the Affordable Care Act.

Social and Community Context

Social and community context can impact individual health outcomes through social capital and cohesion, neighborhood attributes, and cultural attitudes [ 57 ]. Researchers have suggested that more social cohesion and capital can improve individual health outcomes by providing opportunity to mitigate poverty, disparity, and social exclusion [ 58 ]. Qualitative studies have identified aspects of Appalachian culture that build social capital and foster social cohesion, which are generally protective for health outcomes. Men and women in focus groups interviewed by Coyne et al. (2006) vocalized a strong sense of place, deep family ties, and strong faith in God as attributes of many rural southern West Virginians; all of these might improve health outcomes [ 59 ]. There may be also Appalachian cultural beliefs that increase risk for lack of early healthcare intervention or poor health behaviors. Religious beliefs may conflict with medical care, as some patients turn exclusively towards divine help, believing that this may be enough [ 59 ]. Deep ties to the community may become exclusionary to outsiders leading to concerns about foreign-born or “outsider” physicians being untrustworthy [ 59 ]. There is also a high turnover rate of medical providers in the region, likely making it even more difficult to build trust [ 59 ]. Additionally, Coyne’s team found that there was concern that family problems would become public knowledge if help was sought from medical providers [ 59 ]. There is a risk of interpreting Appalachian beliefs as “odd” or that individuals’ religious beliefs as evidence of fatalism. However, more modern studies have found that Appalachians consider both their faith and counseling from medical professionals [ 60 ]. Ultimately, medical providers will need support to learn about Appalachian culture and build on the present social cohesion to facilitate successful medical care.

Central Appalachia lacks social capital on a political scale that impedes its ability to build healthier communities. Lee County, Virginia is an example of this, as it is closer to eight other state capitals than it is to its own capital in Richmond [ 61 ]. Distance from a state capital is associated with reduced accountability [ 62 ]. For example, newspapers give more coverage to state politics when more readers are closer to the capital; voters who live further from the capital are less knowledgeable and interested in state politics, they also have lower turnout for state elections [ 62 ]. This pattern then results in less funding from programs that might build community and healthier behaviors [ 62 ]. Tobacco use is a good example of how this impacts lung disease in Central Appalachia. Tobacco crops have been a major source of income in this region and tobacco has been normalized into the culture [ 63 ]. Higher taxes on cigarettes are recognized as a successful strategy in achieving major reductions in smoking among some high-risk populations [ 64 ] and the tobacco industry has spent significant resources to maintain low prices, particularly in low-income communities [ 65 ]. For example, tobacco taxes are significantly lower in Virginia (0.60 cents per pack) as opposed to the District of Columbia ($4.50 per pack) [ 66 , 67 ]. This low tax rate results in less funding for tobacco control programs and less access to health information about tobacco and is associated with greater use [ 64 ]. There are also higher rates of comorbid behavioral health disorders associated with higher tobacco use, likely increasing risk for smoking and tobacco use [ 63 , 68 ]. The higher prevalence of smoking in these regions contributes to the disparity in COPD and lung cancer mortality [ 63 , 68 ]. Among those who are interested in quitting, there is more social stigma in these areas, which can decrease opportunities to engage in the community and impede smoking cessation efforts [ 69 ]. Simply put, tobacco use has propagated across generations in Central Appalachia, partly because its citizens are more isolated from resources and lacking in social capital.

Future Directions

Healthcare-centered initiatives are a critical component of collaborative efforts working towards improving pulmonary health outcomes in Central Appalachia. Both West Virginia University and University of Virginia have established Project ECHO programs directed at expanding access to university pulmonary expertise for rural healthcare providers [ 70 , 71 ]. Stone Mountain Health Services is a network of 13 federally qualified health clinics in Southwest Virginia, including two respiratory care clinics. The University of Virginia has partnered with Stone Mountain Health Services to develop a pulmonary telemedicine program, a remote pulmonary rehabilitation program and a smoking cessation program [ 72 ]. Catholic Health Initiatives has developed the first mobile lung cancer screening unit (motor coach equipped with a CT scanner) in the nation to improve access to lung cancer screening [ 73 ]. These approaches hold promise to improve access and quality of healthcare directed at those at risk for poor outcomes from lung disease.

State leaders could expand access to care in the Appalachian region by increasing the size and scope of rural training programs. Physicians working in Central Appalachia are mostly graduates of medical schools in or near the region; therefore, more training programs in the region may help alleviate the area’s health professional shortages [ 74 ]. A small but growing number of health professional schools and residencies around the US have recognized this need and developed rural-specific training programs [ 75 ]. University of Kentucky, West Virginia University, and Eastern Tennessee State University Quillen College of Medicine are examples of such medical schools, with tracks that supply mentorship, clinical experience, and education designed to prepare future clinicians to provide high quality care in rural communities. Increasing funding to expand these types of programs, as well as to motivate and to facilitate trainees to serve these regions long-term will be important for their sustainability. The National Health Service Corps and Nurse Corps have successfully brought and retained physicians, nurses, nurse practitioners, and physician assistants in rural and at-need communities using support-for-service programs [ 76 ]. Loan repayment and direct financial incentive programs have demonstrated the most success [ 76 ]. However, healthcare-centered approaches are limited in their effectiveness at addressing many other social determinants of health that drive pulmonary health disparities in the region.

Community and political leaders seeking to improve the health and well-being of Central Appalachians face deep rooted social, economic, behavioral, and environmental challenges that do not have easy solutions. Developing a long-term, sustainable strategy to increase economic diversity, enhance job training, create new jobs, and attract new sources of investment is a formidable task [ 77 ]. Given Central Appalachia spans dozens of counties and multiple states, coordinating local and regional efforts is essential. In 1965, the federal government assembled the Appalachian Regional Commission (ARC), a federal-state-local economic partnership agency to strengthen communities, upgrade infrastructure, and build economic growth in the Appalachia Region. The ARC analyzes vulnerabilities and opportunities for the region, investing agency resources in projects that retrain people of struggling counties to then bring that county out of a distressed state [ 78 ]. The ARC’s recent quantitative and qualitative analysis of how best to cultivate economic resilience in Central Appalachia has led to eight recommended best practices ( Table 1 ) [ 77 ]. The ARC has been particularly focused in investing in skill development and work force training programs for citizens, with the goal of expanding job opportunities in science, technology, engineering, and healthcare [ 79 ]. The ARC’s INSPIRE Initiative has awarded $9.4 million to projects in Appalachia for the added goal of addressing the substance abuse crisis by expanding workforce entry and re-entry [ 80 ].

1. Invest in education, technology, infrastructure and broadband
2. Engage the community over the long term
3. Create communities where people want to live
4. Grow youth engagement and next-generation leadership
5. Identify and grow the assets in the community and region
6. Build networks and foster collaboration
7. Move multiple sectors forward for economic development and grow value chains
8. Cultivate entrepreneurs and develop resources for business start-ups

There are many examples of impactful collaborative programs that are working to improve the social, economic, and environmental challenges facing Central Appalachia. The United States Economic Development Administration and the ARC are collaborating with Central Appalachian Communities through the federal Partnership for Opportunity and Workforce and Economic Revitalization (POWER) initiative. The POWER initiative has thus far invested 238 million dollars to support the implementation of nearly 300 projects aimed at improving economic opportunities, promoting a ready workforce, building infrastructure and attracting new sources of investment [ 81 ]. Another example of successful community-drive initiatives is The Reclaiming Appalachia Coalition, a regional collaboration that seeks to spur mine reclamation projects throughout Central Appalachia that are responsive to community needs and accelerate the growth of new sustainable sectors. In 2019-2020, this coalition has funded over 31 million dollars into projects in Appalachia, creating an estimated 400 jobs [ 82 ].

To eliminate healthcare disparities in Central Appalachia, it is necessary to create policies that improve environmental quality and reduce occupational hazards that are unique to these communities [ 83 ]. However, it is clearly more than coal dust that is driving disparities in Central Appalachia. Rural health programs and interventions, developed through an iterative, community-based process, have demonstrated success in Central Appalachia. Addressing the social determinants of health must be a paramount concern for healthcare, community, and political leaders seeking to impact change and improve the health and well-being of this especially vulnerable population.

ARCAppalachia Regional Commission
GOLDGlobal Initiative for Chronic Obstructive Lung Disease
COPDChronic Obstructive Pulmonary Disease
CWPcoal worker’s pneumoconiosis
CHIPChildren’s Health Insurance Program
RAMRemote Area Medical Volunteer Corps
POWERPartnership for Opportunity and Workforce and Economic Revitalization
OUDOpiate Use Disorder

Author Contributions

CLB, CB, MMT, and DAH authored and edited the paper.

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    Submit your paper; Open access ... however, there is a tendency to be complacent about health risks, leading to an assumption that black lung disease is no longer a threat. This is simply not true. Deborah Yates (St Vincent's Hospital, NSW, Australia) has accumulated many years of experience in occupational lung disease research, training, and ...

  3. The enduring legacy of black lung: environmental health and contested

    Black lung attorneys interviewed in this research discussed the importance of broadening diagnoses of the disease to capture the full range of environmental health impacts on miners. An attorney described the basic clinical diagnosis of black lung, describing CWP and PMF, and then described the broader parameters of a 'legal definition' of ...

  4. The Impact of Black Lung and a Methodology for Controlling ...

    Coal workers' pneumoconiosis (CWP), commonly known as black lung, is caused by the inhalation of respirable coal mine dust and is a disabling and potentially fatal lung disease with no cure. Historically, CWP has taken a tremendous human and financial toll in the US coal mining industry. Recent health surveillance data indicates that CWP ...

  5. Unearthing pathology of recent rise in black lung disease

    The first new pathology standards for black lung disease in more than 50 years were published based on research from the UIC School of Public Health's Mining Education and Research Center. ... "It's a smoking gun that something has to change to prevent this disease." In a second paper, an international panel of pathologists looked at 85 ...

  6. Black Lung in the 21st Century: Disease, Law, and Policy

    If you need immediate assistance, call 877-SSRNHelp (877 777 6435) in the United States, or +1 212 448 2500 outside of the United States, 8:30AM to 6:00PM U.S. Eastern, Monday - Friday. The past decade has seen many changes in the fields related to black lung. Although American coal production and employment have been declining, more coal min.

  7. Current global perspectives on silicosis—Convergence of old and newly

    Dr. Leonard H. T. Go is a research assistant professor at the University of Illinois Chicago (UIC) School of Public Health and a respiratory physician at Northwestern University Feinberg School of Medicine. He is the Project Director of the Black Lung Clinic programme at UIC, and his research interests centre on mineral dust‐related lung ...

  8. Black Lung: The Social Production of Disease

    Abstract. The black lung movement that erupted in West Virginia in 1968 was not simply a struggle for recognition of an occupational disease; it grew into a bitter controversy over who would control the definition of that disease. This article examines the historical background and medical politics of that controversy, arguing that black lung ...

  9. Black Lung Disease Resurges in Appalachian Coal Miners

    The study, published in the September 2018 American Journal of Public Health, highlights that black lung is not a disease of antiquity but results from injurious exposures to coal miners today. Although PMF was rarely seen in miners who participated in the CWHSP throughout the 1990s, in 2018, according to a JAMA research letter, PMF was ...

  10. Black Lung Disease Alive and Well, After All These Years

    Black Lung Disease. Black lung disease is medically classified as a pneumoconiosis, a disease within the lung tissue causing inflammation followed by scarring, and fibrosis. The fibrosis slowly but surely reduces the ability of the lungs to expand and take in air as well as the lung's ability to transfer oxygen into the bloodstream.

  11. PDF Black Lung Literature Review

    The remainder of this paper synthesizes the available literature on black lung disease to answer the research question "What is the current state of knowledge on black lung disease, particularly as it relates to coal mining, residential coal use, Appalachian populations, and Navajo Nation residents?" Findings are organized as follows:

  12. PDF PUTTING THE TRUST BACK IN THE BLACK LUNG DISABILITY TRUST FUND

    riving the mismatch is the black lung excise tax (BLET) rates. Tax rates are currently $1.10 per short ton of coal produced from underground mines (black line) and $0.55 per short ton from surface ...

  13. PDF Black Lung Incidence Study

    2.2 Literature review on black lung disease in the Navajo Nation. Summit conducted a literature review to assess the current state of research on black lung disease.5 One area of focus within that literature review was black lung incidence due to coal mining or residential coal use within the Navajo Nation.

  14. Chronic respiratory diseases: An introduction and need for novel drug

    Abstract. Globally, chronic respiratory diseases (CRDs), both communicable and noncommunicable, are among the leading causes of mortality, morbidity, economic and societal burden, and disability-adjusted life years (DALYs). CRDs affect multiple components of respiratory system, including the airways, parenchyma, and pulmonary vasculature.

  15. PDF Black Lung Incidence Study

    and black lung disease—and a statistical analysis of publicly available data from various time periods spanning 1970-2021 to identify black lung incidence, determine whether ... research, primarily conducted by external, third-party contractors in accordance with the . Department of Labor Evaluation Policy. CEO's

  16. Unearthing Pathology of Recent Rise in Black Lung Disease

    Two recent papers from the center expand upon this link, with both comparing the lungs of miners from the mid-20th century with those from more recent cases of black lung disease. The studies are the first update on the pathology of black lung disease since 1971, highlighting features in lung tissue that are unique to this newer version and ...

  17. Black Lung Study Finds Biggest Cluster Ever Of Fatal Coal Miners ...

    In a research letter published Tuesday in the Journal of the American Medical Association, NIOSH confirms 416 cases of progressive massive fibrosis or complicated black lung in three clinics in ...

  18. Study Uncovers Startling Number of Black Lung Cases in Coal Miners

    Miners are contracting the disease with striking frequency and at younger ages than ever before. At the end of the 20th century, black lung, a common term for several respiratory diseases caused ...

  19. The Impact of Black Lung and a Methodology for Controlling ...

    Coal workers' pneumoconiosis (CWP), commonly known as black lung, is caused by the inhalation of respirable coal mine dust and is a disabling and potentially fatal lung disease with no cure. Historically, CWP has taken a tremendous human and financial toll in the US coal mining industry. Recent health surveillance data indicates that CWP continues to occur at elevated levels. Respirable coal ...

  20. Unearthing Pathology of Recent Rise in Black Lung Disease

    Two recent papers from the center expand upon this link, with both comparing the lungs of miners from the mid-20th century with those from more recent cases of black lung disease.

  21. Black Lung Incidence Study

    About the Study. In 2022, the Chief Evaluation Office (CEO) partnered with the Mine Safety and Health Administration (MSHA) and commissioned contractor Summit Consulting, LLC (Summit) to conduct the Black Lung Incidence Study under the Administrative Data Research and Analysis portfolio of studies. This study uses secondary data to examine the rate of black lung disease across the United ...

  22. Tracing the origins of lung fibrosis

    Following lung challenge with bleomycin, the alveolar fibroblast-ablated mice died of IL-17A-mediated lung disease. Next, the researchers explored the fate of these alveolar fibroblasts after lung ...

  23. Chronic Obstructive Pulmonary Disease in America's Black Population

    Chronic obstructive pulmonary disease (COPD) is a progressive, debilitating respiratory condition and currently the third leading cause of death in the United States ().Though over 11 million people have been diagnosed with COPD, many more have undiagnosed disease ().This number is projected to increase further as America's population ages.

  24. Is There a Link between Chronic Obstructive Pulmonary Disease and Lung

    Chronic Obstructive Pulmonary Disease (COPD) and lung cancer are strictly related. To date, it is unknown if COPD-associated cancers are different from the tumors of non-COPD patients. The main goal of the study was to compare the morphological/molecular profiles of lung adenocarcinoma (LUAD) samples of COPD, non-COPD/smokers and non-COPD/non-smokers, and to investigate if a genetic ...

  25. Early Release

    Thelaziosis is an emerging zoonotic disease caused by nematodes of the genus Thelazia (Spirurida, Thelazioidea). In the United States, 3 zoonotic species have been identified: Thelazia gulosa (), T. californiensis (), and most recently T. callipaeda ().In Asia and Europe, T. callipaeda is considered the main agent of thelaziosis in humans, domestic animals, and wild animals ().

  26. Lung Disease in Central Appalachia: It's More than Coal Dust that

    Burden of Lung Disease. In 2017, The Appalachia Regional Commission (ARC) report on Health Disparities determined that the Years of Potential Life Lost, a measure of premature mortality, is 25% higher in Appalachia than in the rest of the US [].Disparities in outcomes for a range of pulmonary conditions contribute to this premature mortality.