The asbestos fibre burden in human lungs: new insights into the chrysotile debate

Our plain-English summary of The asbestos fibre burden in human lungs: new insights into the chrysotile debate, by I.S. Feder, I. Tischoff, A. Theile, et al (The European Respiratory Journal, 2017).

The study

• Authors: I.S. Feder, I. Tischoff, A. Theile, I. Schmitz, R. Merget, A. Tannapfel
• Journal: The European Respiratory Journal
• Published: 2017;49(6)
• Cited by: 32 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The traceability of asbestos fibres in human lungs is a matter of discussion especially for chrysotile. This issue is of high significance for differential diagnosis, risk assessment and occupational compensation. At present no intra-individual longitudinal information is available. This study addresses the question whether the asbestos fibre burden in human lungs decreases with time after exposure cessation.The database of the German Mesothelioma Register was screened for patients with asbestos body counts of at least 500 fibres per gram of wet lung, which had been analysed twice from different tissue excisions at minimum intervals of 4 years.Twelve datasets with individual longitudinal information were discovered with a median interval of about 8 years (range 4-21 years). Both examinations were performed after exposure cessation (median: surgery, 9.5 years; autopsy, 22 years). Pulmonary asbestos fibre burden was stable between both examinations (median 1623/4269 asbestos bodies per gram wet lung). Electron microscopy demonstrated a preponderance of chrysotile (median 80%).This study is the first to present longitudinal intra-individual data about the asbestos fibre burden in living human lungs. The high biopersistence of amphiboles, but also of chrysotile, offers mechanistic explanations for fibre toxicity, especially the long latency period of asbestos-related diseases.

Copyright ©ERS 2017.

In plain English

Using the German Mesothelioma Register, the authors asked whether asbestos in human lungs decreases after exposure ends. They found 12 men with past occupational asbestos exposure whose lungs had been analysed twice, at least 4 years apart: first in surgical tissue or lung-wash (BAL) fluid, later at autopsy. The interval was 4 to 21 years (median 8 years). In the 10 patients with lung tissue both times, the median highest count was 1623 asbestos bodies per gram of wet lung at the first analysis and 4269 at autopsy. The authors found no relevant decrease (p=0.9863). Electron microscopy of autopsy tissue from 6 patients found chrysotile as the main fibre in 4 and mainly amphibole in 2. The authors concluded that both amphibole and chrysotile are highly biopersistent in the lung, and that the chrysotile loss reported elsewhere must happen early after exposure. They noted that light microscopy only shows fibres thicker than 0.2 µm and that surgical samples were limited in size.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Retrospective analysis of register records: a longitudinal comparison within the same patients of asbestos counts from an earlier surgical tissue or bronchoalveolar lavage (BAL) sample and a later autopsy sample
• Who was studied: 12 patients, all male, selected from 23955 datasets in the German Mesothelioma Register (1987–2015). Each had an asbestos body count above 500 per gram of wet lung and two analyses from different tissue excisions at least 4 years apart. First analyses were done 1987–2011 and autopsies 1996–2015. Age at death was 62 to 82 years (median 76.5). All died of asbestos-related disease, and all had pleural plaques at autopsy.
• Exposure: Past occupational asbestos exposure in jobs such as ship's carpenter, insulation lagger in shipbuilding, welder, metalworker, papermaker, plumber and power-plant insulator, for a median of about 30 years. At the first analysis, last exposure had ended 3 to 29 years earlier (median 9.5 years). Fibre types identified were chrysotile and amphibole; no specific amphibole type was named.
• Main results:
  • The time between the first and second analyses ranged from 4 to 21 years (median 8 years).
  • Using each patient's highest count, the median was 1623 (range 431–9750) asbestos bodies per gram of wet lung tissue at the first analysis and 4269 (range 714–53663) at the second. The two patients whose first sample was BAL fluid were not included in these medians.
  • For the whole group, the authors found no relevant decrease in asbestos fibre burden over time (p=0.9863, one-sided Wilcoxon signed rank test).
  • In 8% of patients (one patient), the autopsy count was lower than the surgical count. In that patient, amphibole was the dominant fibre type at autopsy.
  • Electron microscopy was done on 6 available samples, all of them autopsy tissue. Chrysotile was the dominant fibre in 66.7% of these samples (80% to 95% chrysotile). Mainly amphibole was found in 33.3%. Fibre type was not determined at the first analysis.
  • The proportion of chrysotile fibres did not correlate with the duration of asbestos exposure (p=0.65) or with the time since last exposure (p=0.74).
• The authors' conclusion: The authors concluded that the study demonstrates high biopersistence of both amphibole and chrysotile asbestos in the human lung, which they said gives mechanistic explanations for fibre toxicity and the long latency of asbestos-related diseases. They also concluded that the reduction of chrysotile reported elsewhere must have occurred early after exposure.
• Limitations the authors state:
  • Light microscopy with phase contrast detects only fibres thicker than 0.2 µm.
  • Surgical tissue was limited in size or came from the tumour side, while autopsies allowed several samples. The authors used this to explain why some autopsy counts were higher.
  • Where exact data were missing, the end of exposure was assumed to be retirement age or the 1993 European asbestos ban, and the actual end might have been earlier.
  • Electron microscopy was qualitative only, used to identify fibre type.
  • One patient's first tissue had active tuberculosis, so that fibre count may be underestimated.
  • A prospective study of lung asbestos burden in living people is not possible for ethical reasons.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile, Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Chrysotile, Differential Diagnosis, Mesothelioma, Asbestos Bodies, Autopsy, biopersistence, Amphibole Group, Latency.

Related studies

• Correspondence regarding the article "The asbestos fibre burden in human lungs: new insights into the chrysotile debate" — I.S. Feder, I. Tischoff, et al. (2017)
• Correspondence regarding the article "The asbestos fibre burden in human lungs: new insights into the chrysotile debate" — L.C. Oliver, F. Belpoggi, et al. (2017)
• Correspondence regarding the article "The asbestos fibre burden in human lungs: new insights into the chrysotile debate" — P. Sartorelli (2017)
• Misleading "New Insights into the Chrysotile Debate" — H.J. Woitowitz, X. Baur (2018)
• Effects of Chrysotile Exposure in Human Bronchial Epithelial Cells: Insights into the Pathogenic Mechanisms of Asbestos-Related Diseases — G.R. Gulino, M. Polimeni, et al. (2016)
• New insights into the toxicity of mineral fibres: A combined in situ synchrotron μ-XRD and HR-TEM study of chrysotile, crocidolite, and erionite fibres found in the tissues of Sprague-Dawley rats — A.F. Gualtieri, N. Bursi Gandolfi, et al. (2017)

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