Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (1,014 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A form of pneumoconiosis caused by inhalation of asbestos fibers which elicit potent inflammatory responses in the parenchyma of the lung. The disease is characterized by interstitial fibrosis of the lung, varying from scattered sites to extensive scarring of the alveolar interstitium.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Asbestoses; Pulmonary Fibrosis - from Asbestos Exposure; Idiopathic Interstitial Pneumonitis - from Asbestos Exposure.
Where it fits in the MeSH classification
- Broader topics
- Pneumoconiosis
Research landscape
PubMed indexes 4,536 records tagged with the MeSH heading “Asbestosis” (counts retrieved 2026-11-04). 163 of them (3.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,179 records.
Reviews account for 517 records (11.4%) and meta-analyses for 5. Randomized controlled trials number 7 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3,179 |
| 2000-2009 | 635 |
| 2010-2019 | 559 |
| 2020 onward | 163 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 517 | 11.4% |
| Meta-analyses | 5 | 0.1% |
| Randomized controlled trials | 7 | 0.2% |
Method: PubMed query "Asbestosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in respiratory medicine
Research on airway and lung disease mixes lung-function tests, symptom diaries, imaging and hospital records, so what was measured and in whom matters as much as the result. Many conditions here, such as asthma and COPD, vary between people and over time, and exposure studies (smoking, pollution, workplace dust) show association rather than proof of cause. Nothing on this page is advice about treatment or inhalers; anyone with breathing difficulty should seek care from a qualified clinician. Check how the condition was defined, the severity of the people studied and whether outcomes were symptoms, lung function or hospital admissions.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Global Asbestos Disaster | 2018 | Review article Design not recorded in structured metadata | 120 | cc by PMID 29772681 · DOI · PMC5982039 |
| Serum HMGB1 as a Potential Biomarker for Patients with Asbestos-Related Diseases | 2017 | Research article Design not recorded in structured metadata | 39 | cc by PMID 28348451 · DOI · PMC5350493 |
| MicroRNA Expression in Malignant Pleural Mesothelioma and Asbestosis: A Pilot Study | 2017 | Research article Design not recorded in structured metadata | 33 | cc by PMID 28757678 · DOI · PMC5512053 |
| Asbestos Disease Initiation | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41708907 · DOI · PMC12917034 |
Global Asbestos Disaster [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Introduction: Asbestos has been used for thousands of years but only at a large industrial scale for about 100⁻150 years.
- Closing excerpt
- Exposure limits do not protect properly against cancer but for asbestos removal and equivalent exposure elimination work, we propose a limit value of 1000 fibres/m³.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (539 words)
Introduction: Asbestos has been used for thousands of years but only at a large industrial scale for about 100⁻150 years. The first identified disease was asbestosis, a type of incurable pneumoconiosis caused by asbestos dust and fibres. The latest estimate of global number of asbestosis deaths from the Global Burden of Disease estimate 2016 is 3495. Asbestos-caused cancer was identified in the late 1930's but despite today's overwhelming evidence of the strong carcinogenicity of all asbestos types, including chrysotile, it is still widely used globally. Various estimates have been made over time including those of World Health Organization and International Labour Organization: 107,000⁻112,000 deaths. Present estimates are much higher. Objective: This article summarizes the special edition of this Journal related to asbestos and key aspects of the past and present of the asbestos problem globally. The objective is to collect and provide the latest evidence of the magnitude of asbestos-related diseases and to provide the present best data for revitalizing the International Labor Organization/World Health Organization Joint Program on Asbestos-related Diseases. Methods: Documentation on asbestos-related diseases, their recognition, reporting, compensation and prevention efforts were examined, in particular from the regulatory and prevention point of view. Estimated global numbers of incidence and mortality of asbestos-related diseases were examined. Results: Asbestos causes an estimated 255,000 deaths (243,223⁻260,029) annually according to latest knowledge, of which work-related exposures are responsible for 233,000 deaths (222,322⁻242,802). In the European Union, United States of America and in other high income economies (World Health Organization regional classification) the direct costs for sickness, early retirement and death, including production losses, have been estimated to be very high; in the Western European countries and European Union, and equivalent of 0.70% of the Gross Domestic Product or 114 × 10⁸ United States Dollars. Intangible costs could be much higher. When applying the Value of Statistical Life of 4 million EUR per cancer death used by the European Commission, we arrived at 410 × 10⁸ United States Dollars loss related to occupational cancer and 340 × 10⁸ related to asbestos exposure at work, while the human suffering and loss of life is impossible to quantify. The numbers and costs are increasing practically in every country and region in the world. Asbestos has been banned in 55 countries but is used widely today; some 2,030,000 tons consumed annually according to the latest available consumption data. Every 20 tons of asbestos produced and consumed kills a person somewhere in the world. Buying 1 kg of asbestos powder, e.g., in Asia, costs 0.38 United States Dollars, and 20 tons would cost in such retail market 7600 United States Dollars. Conclusions: Present efforts to eliminate this man-made problem, in fact an epidemiological disaster, and preventing exposures leading to it are insufficient in most countries in the world. Applying programs and policies, such as those for the elimination of all kind of asbestos use-that is banning of new asbestos use and tight control and management of existing structures containing asbestos-need revision and resources. The International Labor Organization/World Health Organization Joint Program for the Elimination of Asbestos-Related Diseases needs to be revitalized. Exposure limits do not protect properly against cancer but for asbestos removal and equivalent exposure elimination work, we propose a limit value of 1000 fibres/m³.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29772681 · DOI · PMC5982039
Serum HMGB1 as a Potential Biomarker for Patients with Asbestos-Related Diseases [2]
Abstract reading summary — source excerpts
- Opening excerpt
- High-mobility group box 1 (HMGB1) functions as a proinflammatory cytokine and is one of the most intriguing molecules in inflammatory disorders and cancers.
- Closing excerpt
- Thus, our study provides supporting evidence for HMGB1 as a potential biomarker either for the clinical diagnosis of high-risk AE cohorts or for evaluating ARDs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (173 words)
High-mobility group box 1 (HMGB1) functions as a proinflammatory cytokine and is one of the most intriguing molecules in inflammatory disorders and cancers. Notably, HMGB1 is a potential therapeutic target and novel biomarker in related diseases. However, the diagnostic value of HMGB1 for benign and malignant asbestos-related diseases (ARDs) remains unclear. In this work, we detected preoperative serum HMGB1 levels in Chinese asbestos-exposed (AE) and ARDs populations and further evaluated the diagnostic value of HMGB1 in patients with certain types of ARDs, including those with pleural plaques, asbestosis, or malignant mesothelioma (MM). The experimental data presented that the serum level of HMGB1 was significantly elevated in AE and ARDs subjects. Our findings indicated that serum HMGB1 is a sensitive and specific biomarker for discriminating asbestosis- and MM-affected individuals from healthy or AE individuals. In addition, serum matrix metalloproteinases 2 and 9 are not correlated with HMGB1 in ARDs. Thus, our study provides supporting evidence for HMGB1 as a potential biomarker either for the clinical diagnosis of high-risk AE cohorts or for evaluating ARDs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28348451 · DOI · PMC5350493
MicroRNA Expression in Malignant Pleural Mesothelioma and Asbestosis: A Pilot Study [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThe identification of diagnostic/prognostic biomarkers for asbestos-related diseases is relevant for early diagnosis and patient survival and may contribute to understanding the molecular mechanisms underlying the disease development and progression.
- Closing excerpt
- miRNA-16 was directly related to MPM patient prognosis, suggesting its possible use as a prognostic marker in MPM patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (189 words)
BackgroundThe identification of diagnostic/prognostic biomarkers for asbestos-related diseases is relevant for early diagnosis and patient survival and may contribute to understanding the molecular mechanisms underlying the disease development and progression.AimsTo identify a pattern of miRNAs as possible diagnostic biomarkers for patients with malignant pleural mesothelioma (MPM) and asbestosis (ASB) and as prognostic biomarkers for MPM patients.MethodsmiRNA-16, miRNA-17, miRNA-126, and miRNA-486 were quantified in plasma and formalin-fixed paraffin-embedded samples to evaluate their diagnostic and prognostic roles compared to patients with other noncancerous pulmonary diseases (controls). Results. The expression of all the miRNAs was significantly lower in patients with MPM and ASB than that in controls. miRNA-16, miRNA-17, and miRNA-486 in plasma and tissue of MPM patients were significantly correlated. Furthermore, the expression of miRNA-16 in plasma and tissue, and miRNA-486 only in tissue, was positively related with cumulative survival in MPM patients.ConclusionsAll the miRNA levels were decreased in patients with MPM or ASB, supporting the role of circulating miRNAs as a potential tool for diseases associated with exposure to asbestos fibers. miRNA-16 was directly related to MPM patient prognosis, suggesting its possible use as a prognostic marker in MPM patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28757678 · DOI · PMC5512053
Asbestos Disease Initiation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- A model is developed of disease initiation and progression for asbestos related plaque deposition and mesothelioma based on prior models of wound healing and asbestos transport.
- Closing excerpt
- Tumor development was sensitive only to a few parameters describing exposure and T-cell levels, indicating potential for immune system intervention.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (113 words)
A model is developed of disease initiation and progression for asbestos related plaque deposition and mesothelioma based on prior models of wound healing and asbestos transport. The model includes short term processes such as macrophage polarization and immune system response, extending the time frame to that of detectable disease. Model results were in a biologically reasonable range. Cancer development and plaque deposition are shown to be dependent on total exposure (intensity * duration). Plaque deposition was sensitive to many systemic parameters, suggesting that assays could be developed to identify individuals with higher risk. Tumor development was sensitive only to a few parameters describing exposure and T-cell levels, indicating potential for immune system intervention.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41708907 · DOI · PMC12917034
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Mechanisms in the pathogenesis of asbestosis and silicosis [5]
- Research article Diagnosis and initial management of nonmalignant diseases related to asbestos [6]
- Research article The role of free radicals in asbestos-induced diseases [7]
- Research article Asbestos-related diseases of the lung and other organs: their epidemiology and implications for clinical practice [8]
- Research article Asbestos, asbestosis, and cancer, the Helsinki criteria for diagnosis and attribution 2014: recommendations [9]
- Research article The worldwide pandemic of asbestos-related diseases [10]
References
- Furuya S, Chimed-Ochir O, Takahashi K, David A, Takala J. Global Asbestos Disaster. . 2018. PMID 29772681 · DOI · PMC5982039
- Ying S, Jiang Z, He X, Yu M, Chen R, Chen J, et al.. Serum HMGB1 as a Potential Biomarker for Patients with Asbestos-Related Diseases. . 2017. PMID 28348451 · DOI · PMC5350493
- Mozzoni P, Ampollini L, Goldoni M, Alinovi R, Tiseo M, Gnetti L, et al.. MicroRNA Expression in Malignant Pleural Mesothelioma and Asbestosis: A Pilot Study. . 2017. PMID 28757678 · DOI · PMC5512053
- DeStefano A, Martin C, Wallace D. Asbestos Disease Initiation. . 2026. PMID 41708907 · DOI · PMC12917034
- Mossman BT, Churg A. Mechanisms in the pathogenesis of asbestosis and silicosis. Am J Respir Crit Care Med. 1998. PMID 9603153 · DOI
- American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med. 2004. PMID 15355871 · DOI
- Kamp DW, Graceffa P, Pryor WA, Weitzman SA. The role of free radicals in asbestos-induced diseases. Free Radic Biol Med. 1992. PMID 1577332 · DOI
- Becklake MR. Asbestos-related diseases of the lung and other organs: their epidemiology and implications for clinical practice. Am Rev Respir Dis. 1976. PMID 779552 · DOI
- Wolff H, Vehmas T, Oksa P, Rantanen J, Vainio H. Asbestos, asbestosis, and cancer, the Helsinki criteria for diagnosis and attribution 2014: recommendations. Scand J Work Environ Health. 2015. PMID 25299403 · DOI
- Stayner L, Welch LS, Lemen R. The worldwide pandemic of asbestos-related diseases. Annu Rev Public Health. 2013. PMID 23297667 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.