Fibre distribution in the lungs and pleura of subjects with asbestos related diffuse pleural fibrosis

Our plain-English summary of Fibre distribution in the lungs and pleura of subjects with asbestos related diffuse pleural fibrosis, by A.R. Gibbs, M. Stephens, D.M. Griffiths, et al (British Journal of Industrial Medicine, 1991).

The study

• Authors: A.R. Gibbs, M. Stephens, D.M. Griffiths, B.J. Blight, F.D. Pooley
• Journal: British Journal of Industrial Medicine
• Published: 1991;48(11):762-70
• Cited by: 33 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 004158).

Abstract

The lungs from 13 cases of diffuse pleural fibrosis associated with a history of exposure to asbestos were examined. Samples were taken from the visceral pleura and central and subpleural zones of the lungs for histopathological and mineralogical studies. The fibre type, size, and number were estimated for each of these regions by transmission electron microscopy and energy dispersive x ray analysis. Amphibole fibre counts were raised when compared with a non-occupationally exposed group and matched those seen in cases of pleural plaques, mild asbestosis, and mesothelioma. A wide case to case variation of distribution was seen. No significant difference was apparent between central and subpleural zones, whereas low asbestos counts were found in the pleura; these were mainly short chrysotile fibres. Within the lungs more (45%) of the longer (greater than 4 microns) and thinner (less than 0.25 micron) amphibole fibres were retained in keeping with other studies implicating such fibre profiles in the pathogenesis of asbestos related disease.

In plain English

This study examined lungs removed at 13 postmortem examinations performed between 1979 and 1988. All were men, aged 47 to 80 at death, with diffuse pleural fibrosis (widespread thickening of the lung lining) and documented occupational asbestos exposure lasting one to 35 years. Using electron microscopy, the authors counted, identified and measured crocidolite, amosite and chrysotile fibres in the central lung, the lung just under the lining, and the thickened pleura. In their opinion, asbestos was likely the cause in only 11 cases. In those cases, total asbestos counts were generally higher than in people without occupational exposure, and this applied to amphibole rather than chrysotile fibres. Counts varied widely from case to case. The pleura held little fibre, mostly chrysotile, and its fibres were shorter than those in lung tissue. In the lungs, 45% of amphibole fibres were longer than 4 micrometres, compared with 9% of chrysotile fibres. The authors concluded that amphiboles rather than chrysotile are retained in the lung, and that a high percentage of them are long and thin.

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: Postmortem (necropsy) case series with tissue examination and mineral fibre analysis by transmission electron microscopy and energy dispersive x ray analysis
• Who was studied: 13 men with bilateral diffuse pleural fibrosis and documented asbestos exposure, aged 47 to 80 at death, from routine hospital necropsies or cases referred by the Medical Boarding Centre (UK), 1979 to 1988; seven had been reported in the authors' earlier study
• Exposure: Occupational asbestos exposure of one to 35 years in jobs including pipe fitter, boiler maker, asbestos sprayer, boiler lagger, mixing and moulding blue asbestos, and ship and shipyard work; fibres analysed in tissue were crocidolite, amosite and chrysotile
• Main results:
  • In the authors' opinion, the findings were likely caused by asbestos in only 11 of the 13 cases. Subject 13 had tuberculosis, and subject 11 had a vague exposure history; both had asbestos counts within the range of the authors' non-occupationally exposed controls.
  • In the 11 cases, total asbestos counts were generally higher than in the non-occupationally exposed population. The authors noted this applied to amphibole rather than chrysotile concentrations.
  • Fibre counts varied considerably from case to case. Case 6 had extreme values and was treated as an outlier and left out of the pooled figures.
  • Total asbestos concentrations in the subpleural lung (just under the lining) were not significantly higher than in the central lung.
  • The pleural tissue contained little fibre, most of it chrysotile, with only occasional amphibole fibres.
  • Amosite fibres were longer (p less than 0.025) and wider (p less than 0.0001) than crocidolite fibres. Crocidolite fibres were in turn longer and wider (p less than 0.0001) than chrysotile fibres.
  • Fibre dimensions did not differ between central and subpleural lung, but pleural fibres were generally shorter than those in lung tissue (p less than 0.05).
  • Of retained amphibole fibres, 9% were longer than 10 micrometres and 45% were longer than 4 micrometres. For chrysotile fibres the figures were 2% and 9%.
  • Among thin fibres (less than 0.25 micrometres in diameter), 37% of amphiboles were longer than 4 micrometres, compared with 9% of chrysotile fibres.
• The authors' conclusion: The authors concluded that amphiboles rather than chrysotile fibres are retained in the lung and that a high percentage of these are long and thin. They also concluded that asbestos fibres are unevenly distributed in the lung, with low fibre content in the pleura, mostly chrysotile. They stated that the asbestos concentrations implicate asbestos in diffuse pleural fibrosis but do not show why this particular reaction occurs rather than another.
• Limitations the authors state:
  • The clinical data were not detailed enough to assess any biological factor that might increase susceptibility to this pleural reaction.
  • The fibre findings do not indicate why asbestos produced diffuse pleural fibrosis rather than another disease.
  • Fibre content measured at necropsy reflects fibres retained in the lung, not total lifetime exposure.
  • The statistical assumption that fibre sizes follow a log-normal pattern was supported for length but less so for width.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Amosite, Chrysotile, Crocidolite.

Medical terms in this study, explained in our Lexicon: Pleura, Fibrosis, Visceral Pleura, Transmission Electron Microscopy (TEM), Amphibole Group, Pleural Plaques, Mesothelioma, Chrysotile.

Related studies

• Asbestos induced diffuse pleural fibrosis: pathology and mineralogy — M. Stephens, A.R. Gibbs, et al. (1987)
• Evaluation of the exposure, dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to TiO2, chrysotile, crocidolite or amosite asbestos in a 90-day quantitative inhalation toxicology study - Interim results Part 1: Experimental design, aerosol exposure, lung burdens and BAL — D.M. Bernstein, B. Toth, et al. (2020)
• Evaluation of the dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to TiO2, chrysotile, crocidolite or amosite asbestos in a 90-day quantitative inhalation toxicology study - Interim results Part 2: Histopathological examination, Confocal microscopy and collagen quantification of the lung and pleural cavity — D.M. Bernstein, B. Toth, et al. (2020)
• Focused X-Ray Histological Analyses to Reveal Asbestos Fibers and Bodies in Lungs and Pleura of Asbestos-Exposed Subjects — L. Pascolo, A. Gianoncelli, et al. (2016)
• Quantification of the pathological response and fate in the lung and pleura of chrysotile in combination with fine particles compared to amosite-asbestos following short-term inhalation exposure — D.M. Bernstein, R.A. Rogers, et al. (2011)
• Evaluation of the fate and pathological response in the lung and pleura of brake dust alone and in combination with added chrysotile compared to crocidolite asbestos following short-term inhalation exposure — D.M. Bernstein, R.A. Rogers, et al. (2015)

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