Coal Workers' Pneumoconiosis

Coal Workers' Pneumoconiosis (CWP), widely known as black lung disease, is an incurable occupational lung disease caused by the inhalation and accumulation of coal mine dust in the lungs. Despite decades of regulatory effort, CWP has resurged in the United States: after a low point in the late 1990s, its prevalence among working underground miners with 25 or more years of tenure exceeded 10% nationally and reached 20.6% in central Appalachia, and the prevalence of its most severe form — progressive massive fibrosis — among long-tenured central Appalachian miners reached its highest level since the early 1970s. Pathology and dust-sampling studies link the resurgence to excess exposure to respirable crystalline silica, with thinner coal seams and smaller mines associated with higher silica exposure. CWP is preventable, no curative treatment exists, and dust control, surveillance, and federal compensation programs are the main public-health responses.

Table of Contents

  1. Overview & Epidemiology
  2. Coal Dust Composition & Pathogenicity
  3. Pathogenesis
  4. Types of CWP: Simple vs. Complicated
  5. Progressive Massive Fibrosis (PMF)
  6. Caplan Syndrome
  7. Diagnosis
  8. Associated Conditions
  9. Treatment & Federal Benefits
  10. Prevention & Regulation
  11. Key Research Papers
  12. Connections
  13. Featured Videos

Overview & Epidemiology

Coal Workers' Pneumoconiosis is classified among the pneumoconioses — a group of occupational lung diseases caused by inhalation of inorganic mineral dusts. CWP results specifically from the accumulation of respirable coal mine dust in the lungs, triggering a macrophage-driven inflammatory and fibrotic response that can progress from asymptomatic nodular disease to devastating respiratory failure. The disease is entirely preventable through dust control but is irreversible once established.

Historically, CWP was a defining occupational hazard of the coal industry. The Federal Coal Mine Health and Safety Act of 1969 established mandatory dust standards and created the NIOSH-administered Coal Workers' Health Surveillance Program. CWP prevalence among long-tenured working miners then fell to a low point in the late 1990s (Blackley 2018, AJPH), and PMF reached historic lows, with 31 cases identified by the surveillance program during 1990–1999 (Blackley 2016). That decline made the subsequent reversal all the more alarming.

NIOSH surveillance data document a dramatic resurgence beginning in the early 2000s. Key findings include:

The geographic concentration in central Appalachia — eastern Kentucky, southwestern Virginia, and southern West Virginia — coincides with thinner coal seams and smaller mines, both associated with higher respirable quartz concentrations (Shao 2024). Among working miners examined during 2014–2022, central Appalachian miners were 4.1 times as likely as all others to have radiographic pneumoconiosis and 1.4 times as likely to have abnormal spirometry (Hall 2024).

Back to Table of Contents

Coal Dust Composition & Pathogenicity

Coal mine dust is not a single substance but a complex mixture whose composition varies by geology, mining method, and the specific tasks performed underground. Understanding this composition is essential for understanding why some mines and some miners develop severe disease while others do not.

Carbonaceous Particles

The primary component is carbonaceous (coal) dust itself — particles of partially metamorphosed organic carbon. Coal rank describes the degree of metamorphic change from plant material to pure carbon: anthracite (highest rank, hardest, found primarily in northeastern Pennsylvania) contains roughly 86–97% carbon; bituminous coal (most common mining coal, Appalachian states) contains 45–86% carbon; lignite (lowest rank, softer, mostly western US strip mines) contains 25–35% carbon. Higher-rank coals are more fibrogenic, and a dose-response relationship exists between cumulative coal dust exposure and CWP severity.

Crystalline Silica Content — The Critical Variable

Crystalline silica (quartz, SiO2) in the dust is a major driver of severe disease. Coal itself has relatively low inherent silica content, but the surrounding rock — roof, ribs, and floor strata — includes sandstone, shale, and other quartz-bearing formations, and cutting it adds silica to the respirable dust. In lung tissue from 13 US coal miners with severe disease, 12 had PMF, 11 had silicosis and only four had the classic lesions of simple CWP; mineral particles consistent with silica and silicates were abundant and carbonaceous coal dust was less prominent (Cohen 2016). Among 85 miners with PMF, silica-type PMF was found in 57% of contemporary miners (born in or after 1930) versus 18% of historical miners (born 1910–1930) (Cohen 2022). Compliance sampling from 1982 to 2021 (322,919 respirable quartz samples from 5,064 underground mines) showed that mean quartz mass concentrations fell over time but were consistently higher in Central Appalachian mines, and that smaller mines, thinner coal seams and the lack of a mine safety committee predicted higher concentrations; the authors conclude the data support an association between silica overexposure and the resurgence (Shao 2024).

Particle Size

Only respirable particles — those with aerodynamic diameters less than approximately 7 µm (50th percentile cut-point at 3.5 µm) — deposit in the gas-exchange regions of the lung where CWP develops. Larger particles are cleared by mucociliary action in the upper airways. Modern continuous mining machines and roof bolting equipment generate high proportions of very fine respirable dust that penetrates deeply into the alveolar zone.

Regulatory Exposure Limits

NIOSH recommends an exposure limit (REL) of 1 mg/m³ for total respirable coal mine dust. The Mine Safety and Health Administration (MSHA) mandatory standard has historically been 2 mg/m³, with a stricter limit in seams where coal dust contains more than 5% quartz. Since 1999, miners from underground mines with fewer than 50 workers have been five times as likely as miners from larger mines to show PMF on radiographs (1.0% vs 0.2%) (Laney 2010).

Back to Table of Contents

Pathogenesis

The pathological hallmark of CWP arises from the interaction between inhaled coal mine dust and the lung's innate immune macrophage system. The sequence from dust inhalation to coal macule to nodule to PMF involves progressive cellular and structural changes.

Coal Macule — The Characteristic Early Lesion

When respirable coal dust particles deposit in respiratory bronchioles and alveoli, they are engulfed by alveolar macrophages. Unlike crystalline silica, coal particles resist complete lysosomal digestion, but they trigger persistent macrophage activation and cytokine release. Dust-laden macrophages accumulate around respiratory bronchioles, forming the coal macule — the pathognomonic early lesion of CWP. Coal macules are typically 1–5 mm in diameter, composed of aggregates of carbon-filled macrophages within a minimal fibrous stroma, clustered around respiratory bronchioles with dilation of the immediately surrounding alveolar spaces. This focal dilation is termed focal emphysema (centriacinar emphysema), and it is specific to coal miners — it occurs around the dust deposits rather than throughout the acinus as in smoking-related emphysema.

Cytokine Cascade

Macrophage activation by coal dust triggers release of pro-inflammatory and pro-fibrotic mediators including TNF-α, IL-1β, and TGF-β. Macrophage apoptosis and necrosis release these mediators into the interstitium, recruiting additional macrophages and neutrophils, sustaining the inflammatory cycle. TGF-β in particular drives fibroblast activation and collagen deposition, progressively transforming the cellular coal macule into a more fibrous coal nodule.

Coal Nodule

With ongoing exposure and inflammation, coal macules may evolve into coal nodules — larger lesions (up to 1 cm) with a more defined fibrous component. Unlike the concentric whorled hyaline collagen of the classic silicotic nodule, coal nodules have a less organized architecture with more abundant carbon pigment and less cellular fibrous tissue. When the coal dust also contains significant crystalline silica, a mixed-dust fibrotic nodule may form with features of both silicotic and coal nodules.

Progressive Fibrosis

In some miners, coal macules and nodules undergo progressive enlargement and coalescence, driven by ongoing inflammation, additional dust exposure, and potentially genetic susceptibility factors. This progression leads ultimately to Progressive Massive Fibrosis (PMF) when lesions exceed 1 cm in diameter. This progression can continue after dust exposure ends: among 130 former eastern Kentucky miners with repeat post-employment radiographs, 41 (31.5%) showed radiographic progression after leaving the workforce, over a median of 3.6 years (Hall 2022).

Back to Table of Contents

Types of CWP: Simple vs. Complicated

Simple CWP

Simple CWP is defined by the presence of small rounded opacities on chest radiograph, classified using the ILO International Classification of Radiographs of Pneumoconioses. Opacities are typed by shape and size: p opacities (<1.5 mm), q opacities (1.5–3 mm), and r opacities (3–10 mm). The profusion (density per zone) is graded 0 to 3. Coal macules and nodules producing these opacities are characteristically distributed in the upper lung zones, reflecting the preferential deposition of dust in upper-lobe respiratory bronchioles due to greater ventilation distribution and airflow patterns. Many miners with simple CWP have no respiratory symptoms; cough and mild exertional dyspnea may develop over time. Pulmonary function tests are often normal or show only mild changes in simple CWP.

Complicated CWP (Progressive Massive Fibrosis)

Complicated CWP is defined by the presence of opacities greater than 1 cm in diameter on chest radiograph — the threshold that defines entry into the PMF category (ILO Category A: one or more large opacities with a combined longest diameter of up to 5 cm; Category B: larger than A but not exceeding the area of the right upper zone; Category C: exceeding the area of the right upper zone). Complicated CWP produces significant respiratory symptoms, progressive dyspnea, and ultimately cor pulmonale and respiratory failure. This distinction between simple and complicated CWP is clinically important because it marks the transition from largely asymptomatic radiographic disease to progressive, disabling, and life-threatening illness.

Back to Table of Contents

Progressive Massive Fibrosis (PMF)

Progressive Massive Fibrosis represents the most severe complication of CWP and can progress even after mining stops (Hall 2022). PMF is defined by conglomerate fibrous masses exceeding 1 cm in diameter, typically in the upper lobes. These masses form by the coalescence and progressive enlargement of multiple coal nodules driven by ongoing macrophage-mediated fibrosis.

Radiographic and Clinical Features

On chest radiograph, PMF masses appear as dense, irregular opacities in the upper lobes, often bilateral but asymmetric. The classic description is "angel wings" or a "butterfly" pattern when large bilateral upper-lobe masses sweep inward toward the hila. As masses grow, they migrate centrally toward the hilum while the peripheral lung tissue contracts, creating characteristic peripheral emphysema. HRCT reveals the masses with greater clarity than plain radiograph and can demonstrate internal architecture, including areas of central necrosis or cavitation. PMF masses may cavitate, particularly when complicated by tuberculosis — an important diagnostic consideration, because tuberculosis is part of the differential diagnosis of an upper-lobe cavity in a coal miner.

Progression and Prognosis

PMF masses can continue to enlarge after coal dust exposure ends (Hall 2022). Respiratory function declines progressively: spirometry typically shows a restrictive pattern (reduced FVC, reduced TLC) with or without superimposed airflow obstruction from coexisting COPD. Hypoxemia develops as gas exchange is progressively impaired. Cor pulmonale — right heart failure secondary to pulmonary hypertension — is the terminal complication in many patients. Median survival from diagnosis of PMF depends heavily on mass size and rate of progression, but Category C disease carries a substantially shortened life expectancy. The resurgence has included rapidly progressive pneumoconiosis in younger miners, mainly in the eastern United States (Petsonk 2013; Antao 2005).

Back to Table of Contents

Caplan Syndrome

Caplan syndrome is a distinctive condition in which coal miners (or workers with other pneumoconioses) who also have rheumatoid arthritis (RA) develop multiple well-defined rounded pulmonary nodules that are histologically distinguishable from silicotic nodules and PMF (Schreiber 2010). The pattern was described by Anthony Caplan in 1953 in Welsh coal miners with rheumatoid arthritis (Caplan 1953). The Belgian rheumatologist Émile Colinet had described a similar case in a silica-exposed worker in 1950, and the condition was at first called Colinet-Caplan syndrome in the French-language literature (Ronsmans 2023).

Features

Broader Occurrence

Caplan syndrome is not exclusive to coal miners. Similar nodules with rheumatoid arthritis have been described in silica-exposed workers in other industries — the earliest cases were in workers packing a silica-based scouring powder in Belgium, and later reports described rheumatoid arthritis and other autoimmune diseases among scouring-powder workers across Europe (Ronsmans 2023). The pathogenetic link between silica exposure, pneumoconiosis and rheumatoid arthritis has not been conclusively clarified, and individual susceptibility is thought to play a role (Schreiber 2010).

Back to Table of Contents

Diagnosis

The diagnosis of CWP rests on three pillars: appropriate occupational history, characteristic radiographic findings, and exclusion of conditions that may mimic CWP radiographically.

Occupational History

A diagnosis of CWP requires a compatible occupational exposure history — typically years of underground coal mining, though surface workers at coal preparation facilities, coal handling operations, or mining-adjacent dusty trades may also develop the disease. The type of mining work (continuous miner operator, roof bolter, shuttle car operator, face worker vs. belt worker), years of tenure, and whether engineering controls (water sprays, ventilation, enclosed cabs) were in place all inform exposure estimation. Miners who worked in thin-seam mines or in mines requiring extensive rock cutting may have substantially higher silica co-exposure than their coal dust exposures alone suggest.

Chest Radiograph and ILO Classification

The ILO International Classification of Radiographs of Pneumoconioses is the standard radiographic classification system for CWP. NIOSH-certified B-readers — physicians with special training and examination certification in pneumoconiosis radiograph interpretation — read chest radiographs using ILO standard reference films. The classification records: opacity profusion (0/0 through 3/+), opacity shape and size (p/q/r for rounded, s/t/u for irregular), distribution by lung zone, and large opacity category (A/B/C for PMF). The B-reader certification program exists because CWP radiographs are notoriously difficult to read consistently without specialized training, and the classification has important legal and benefits implications.

High-Resolution CT (HRCT)

HRCT is more sensitive than plain chest radiograph for detecting early coal macules, emphysema, early PMF, and mediastinal lymphadenopathy. HRCT can identify focal centriacinar emphysema around coal macules — a finding specific to CWP that is poorly visible on plain radiograph. For evaluating PMF masses, HRCT characterizes internal architecture (solid vs. cavitating vs. mixed density), identifies satellite nodules, and helps guide decisions about lung biopsy when the diagnosis is uncertain.

Spirometry

Pulmonary function testing typically shows a restrictive pattern (reduced FVC with preserved or elevated FEV1/FVC ratio) in miners with significant PMF. However, coal mine dust also causes chronic airway disease (Petsonk 2013), and many coal miners have mixed obstructive-restrictive patterns reflecting coexisting COPD. Simple CWP often produces only subtle spirometric changes disproportionate to the radiographic findings.

Exclusion of Tuberculosis

Tuberculosis is part of the evaluation of a coal miner with upper-lobe disease, particularly when PMF masses show cavitation, because the clinical presentations of cavitating PMF and post-primary TB can overlap. IGRA (interferon-gamma release assay) or tuberculin skin test, sputum mycobacterial cultures, and BAL culture are the tests used to exclude TB before cavitation is attributed solely to PMF.

Back to Table of Contents

Associated Conditions

Tuberculosis

The link between mineral dust and tuberculosis is best documented for silica: a 2021 systematic review and meta-analysis found a pooled relative risk of tuberculosis of 4.01 with radiological silicosis (high confidence) and 1.92 for silica exposure without silicosis (low confidence) (Ehrlich 2021). The review did not estimate a separate risk for coal workers' pneumoconiosis; its relevance to coal miners rests on the silica content of coal mine dust and the silica-type lesions found in many contemporary miners with severe disease (Cohen 2022).

Lung Cancer

The International Agency for Research on Cancer (IARC) evaluated coal dust in 1997 and placed it in Group 3 (not classifiable as to its carcinogenicity to humans); the same volume placed crystalline silica inhaled from occupational sources in Group 1 (carcinogenic to humans) (IARC 1997). In a 23-year follow-up of 8,899 US underground coal miners first examined in 1969–1971, lung cancer mortality was not elevated, whereas mortality from nonmalignant respiratory disease was, and it was related to cumulative coal mine dust exposure even among never-smokers (Attfield 2008).

COPD

Besides the classic nodular disease, coal mine dust causes chronic airway diseases, including emphysema and chronic bronchitis (Petsonk 2013). In the 23-year US cohort, dust-exposure relative risks for mortality were similar for pneumoconiosis, nonmalignant respiratory disease and chronic airways obstruction, and dust-related mortality was found in never-smokers as well (Attfield 2008). The combination of coal-dust COPD and CWP-associated restriction produces complex mixed spirometric patterns that complicate both disability assessment and clinical management.

Autoimmune Associations

Beyond Caplan syndrome (rheumatoid arthritis), a historical review notes that autoimmune disorders linked to occupational exposure to silica and coal dust have not disappeared and are re-emerging among people who work with silica-based artificial stone and in other dusty trades (Ronsmans 2023). Evidence for specific autoimmune diseases such as systemic sclerosis or lupus comes mainly from silica-exposed workers; rates specific to coal miners are not reported in the sources cited on this page.

Back to Table of Contents

Treatment & Federal Benefits

Medical Management

No pharmacological treatment reverses or halts the fibrotic progression of established CWP. Management is supportive:

Federal Black Lung Benefits Program (BLBA)

The Black Lung Benefits Act (Title IV of the Federal Coal Mine Health and Safety Act of 1969, as amended) provides federal workers' compensation to coal miners totally disabled by CWP and to survivors of miners who died from the disease. The program is administered by the Department of Labor and funded partly by an excise tax on coal production. Two program parts exist: Part B covers the earliest claims (filed in 1973 or earlier) and was originally administered by the Social Security Administration; Part C covers all subsequent claims under the Department of Labor's Office of Workers' Compensation Programs (OWCP).

The claims process is adversarial: a claim can be contested by the responsible mine operator, which may submit its own medical evidence, and the burden of proving total disability due to pneumoconiosis rests with the miner. Benefits records also document the resurgence: among federal black lung claimants, PMF cases fell from 404 (0.5% of claimants) in 1978 to a low of 18 (0.6%) in 1988 and rose to 353 (8.3%) in 2014, and in 2009 more than 17% of claimants who last mined in Virginia received a PMF determination (Almberg 2018).

Back to Table of Contents

Prevention & Regulation

Mine Safety and Health Administration (MSHA)

MSHA is the primary federal agency responsible for mandatory coal mine dust standards under the Federal Mine Safety and Health Act. MSHA enforces the permissible exposure limit (PEL) for respirable coal mine dust, conducts mine inspections, and issues citations for dust standard violations. The 2014 MSHA rule lowered the dust standard from 2.0 mg/m³ to 1.5 mg/m³ respirable coal mine dust (with full implementation by 2016), and mandated continuous personal dust monitors for miners in the highest-exposure jobs.

NIOSH Coal Workers' Health Surveillance Program (CWHSP)

The Coal Workers' Health Surveillance Program, administered by NIOSH, provides free chest X-rays at five-year intervals to working coal miners. Under a NIOSH rule of August 2014 the program was extended from underground to surface coal miners and expanded to include respiratory symptom assessment and spirometry (Blackley 2014). The program uses NIOSH-certified B-readers for radiograph interpretation and has been the primary source of surveillance data documenting the CWP resurgence. Early detection through CWHSP allows miners to make informed decisions about continued exposure and to file for benefits before severe disease develops. Participation is voluntary; NIOSH recommends that all working miners take part at 5-year intervals, and participation patterns limit what surveillance can show about how fast disease progresses (Laney 2017).

Engineering Controls

Dust suppression in underground coal mines relies on a hierarchy of engineering controls: ventilation (dilution and removal of airborne dust from work areas), water sprays on mining machines at the point of dust generation, enclosed and pressurized operator cabs on continuous miners and shuttle cars, wet drilling for roof bolt holes, and scrubber systems (dust collectors mounted on continuous mining machines). Water infusion of the coal seam before cutting can reduce respirable dust generation. The effectiveness of these controls depends on proper installation, maintenance, and operation; smaller mines have been associated with higher PMF prevalence (Laney 2010) and higher respirable quartz concentrations (Shao 2024).

Silica Awareness

Pathology and dust-sampling studies implicating respirable crystalline silica in the resurgence (Cohen 2016; Cohen 2022; Shao 2024) have led researchers to stress the control of workplace silica exposure itself, not only total coal mine dust (Cohen 2022). Continuous personal dust monitors are widely used in US coal mines, but their samples cannot be analysed directly for silica; methods for more frequent silica monitoring of these samples are under development (Greth 2025).

Back to Table of Contents

Key Research Papers

  1. Blackley DJ, Crum JB, Halldin CN, Storey E, Laney AS. Resurgence of progressive massive fibrosis in coal miners — eastern Kentucky, 2016. MMWR Morb Mortal Wkly Rep. 2016;65(49):1385–1389. — PubMed PMID: 27977638
  2. Blackley DJ, Halldin CN, Laney AS. Resurgence of a debilitating and entirely preventable respiratory disease among working coal miners [letter]. Am J Respir Crit Care Med. 2014;190(6):708–709. — PubMed PMID: 25221884
  3. Go LHT, Cohen RA. Coal workers' pneumoconiosis and other mining-related lung disease: new manifestations of illness in an age-old occupation. Clin Chest Med. 2020;41(4):687–696. — PubMed PMID: 33153687
  4. Laney AS, Blackley DJ, Halldin CN. Radiographic disease progression in contemporary US coal miners with progressive massive fibrosis. Occup Environ Med. 2017;74(7):517–520. — PubMed PMID: 28408654
  5. Caplan A. Certain unusual radiological appearances in the chest of coal-miners suffering from rheumatoid arthritis. Thorax. 1953;8(1):29–37. — PubMed PMID: 13038735
  6. Cohen RA, Patel A, Green FH. Lung disease caused by exposure to coal mine and silica dust. Semin Respir Crit Care Med. 2008;29(6):651–661. — PubMed PMID: 19221963
  7. Kreiss K, Zhen B. Risk of silicosis in a Colorado mining community. Am J Ind Med. 1996;30(5):529–539. — PubMed PMID: 8909602
  8. CDC/NIOSH. Work-related lung disease surveillance report. NIOSH Publication No. 2007-105. 2007. — Search PubMed
  9. Blackley DJ, Halldin CN, Laney AS. Continued increase in prevalence of coal workers' pneumoconiosis in the United States, 1970–2017. Am J Public Health. 2018;108(9):1220–1222. — PubMed PMID: 30024799
  10. Centers for Disease Control and Prevention (CDC). Advanced cases of coal workers' pneumoconiosis — two counties, Virginia, 2006. MMWR Morb Mortal Wkly Rep. 2006;55(33):909–913. — PubMed PMID: 16929235
  11. Attfield MD, Kuempel ED. Mortality among U.S. underground coal miners: a 23-year follow-up. Am J Ind Med. 2008;51(4):231–245. — PubMed PMID: 18247381
  12. Blackley DJ, Reynolds LE, Short C, Carson R, Storey E, Halldin CN, Laney AS. Progressive massive fibrosis in coal miners from 3 clinics in Virginia. JAMA. 2018;319(5):500–501. — PubMed PMID: 29411024
  13. Cohen RA, Petsonk EL, Rose C, et al. Lung pathology in U.S. coal workers with rapidly progressive pneumoconiosis implicates silica and silicates. Am J Respir Crit Care Med. 2016;193(6):673–680. — PubMed PMID: 26513613
  14. Cohen RA, Rose CS, Go LHT, et al. Pathology and mineralogy demonstrate respirable crystalline silica is a major cause of severe pneumoconiosis in U.S. coal miners. Ann Am Thorac Soc. 2022;19(9):1469–1478. — PubMed PMID: 35353671
  15. Shao Y, Almberg KS, Friedman LS, Cohen RA, Go LHT. Thin seams and small mines are associated with higher exposures to respirable crystalline silica in US underground coal miners. Occup Environ Med. 2024;81(6):308–312. — PubMed PMID: 38937079
  16. Laney AS, Attfield MD. Coal workers' pneumoconiosis and progressive massive fibrosis are increasingly more prevalent among workers in small underground coal mines in the United States. Occup Environ Med. 2010;67(6):428–431. — PubMed PMID: 20522823
  17. Antao VC, Petsonk EL, Sokolow LZ, et al. Rapidly progressive coal workers' pneumoconiosis in the United States: geographic clustering and other factors. Occup Environ Med. 2005;62(10):670–674. — PubMed PMID: 16169911
  18. Hall NB, Blackley DJ, Markle T, Crum JB, Halldin CN, Laney AS. Postexposure progression of pneumoconiosis among former Appalachian coal miners. Am J Ind Med. 2022;65(12):953–958. — PubMed PMID: 36161659
  19. Hall NB, Reynolds L, Blackley DJ, Laney AS. Assessment of the respiratory health of working US coal miners since 2014 — radiography, spirometry, and symptom assessments. J Occup Environ Med. 2024;66(2):123–127. — PubMed PMID: 37907411
  20. Petsonk EL, Rose C, Cohen R. Coal mine dust lung disease. New lessons from old exposure. Am J Respir Crit Care Med. 2013;187(11):1178–1185. — PubMed PMID: 23590267
  21. Schreiber J, Koschel D, Kekow J, Waldburg N, Goette A, Merget R. Rheumatoid pneumoconiosis (Caplan's syndrome). Eur J Intern Med. 2010;21(3):168–172. — PubMed PMID: 20493416
  22. Ronsmans S, Blanc PD. Colinet-Caplan syndrome: history of an outbreak of autoimmune disease in scouring powder workers. Ann Intern Med. 2023;176(2):260–265. — PubMed PMID: 36623284
  23. Ehrlich R, Akugizibwe P, Siegfried N, Rees D. The association between silica exposure, silicosis and tuberculosis: a systematic review and meta-analysis. BMC Public Health. 2021;21(1):953. — PubMed PMID: 34016067
  24. International Agency for Research on Cancer. Coal dust. In: Silica, some silicates, coal dust and para-aramid fibrils. IARC Monogr Eval Carcinog Risks Hum. 1997;68:337–406. — PubMed PMID: 9268740
  25. Almberg KS, Halldin CN, Blackley DJ, et al. Progressive massive fibrosis resurgence identified in U.S. coal miners filing for black lung benefits, 1970–2016. Ann Am Thorac Soc. 2018;15(12):1420–1426. — PubMed PMID: 30114941
  26. Greth A, Elie G, Sarver E. Toward rapid silica analysis of CPDM samples: a study of dust recovery and quartz estimation using lab and field samples. J Occup Environ Hyg. 2025;22(6):460–473. — PubMed PMID: 40063955

Back to Table of Contents

Connections

Back to Table of Contents