Idiopathic pulmonary fibrosis in asbestos-exposed workers

Our plain-English summary of Idiopathic pulmonary fibrosis in asbestos-exposed workers, by E.A. Gaensler, P.J. Jederlinic, A. Churg (The American Review of Respiratory Disease, 1991).

The study

• Authors: E.A. Gaensler, P.J. Jederlinic, A. Churg
• Journal: The American Review of Respiratory Disease
• Published: 1991;144(3 Pt 1):689-96
• Type of article: Case report
• Cited by: 39 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 004740).

Abstract

Diffuse interstitial lung disease in asbestos-exposed workers is presumed to represent asbestosis. Among 176 asbestos-exposed persons for whom lung tissue was available, we found nine with clinical features consistent with asbestosis, but histologic sections failed to demonstrate asbestos bodies, the usual requirement for pathologic diagnosis of asbestosis (Group I). These nine were compared by analytic electron microscopy with nine persons with idiopathic pulmonary fibrosis (Group II), and with nine persons with all the criteria of asbestosis (Group III). The three groups did not differ significantly with respect to lung burden of chrysotile or tremolite and actinolite, but Group III had a lung burden of amosite and crocidolite that was three orders of magnitude greater than in Groups I and II, with no overlap. We conclude that (1) the American Thoracic Society criterion of "a reliable history of exposure" is sometimes difficult to define; (2) asbestos bodies are seen in tissue sections only when exposure has been reasonably high, and given the proper clinical setting, the presence of diffuse fibrosis and asbestos bodies in tissue sections are sensitive and specific criteria for a diagnosis of asbestosis; and (3) the prevalence here of 5.1% nonasbestos-induced interstitial lung disease among asbestos-exposed persons is artefactually high because of atypical case selection. However, because asbestosis is a disappearing disease, such cases will become more frequent. The identification of these other diseases is important because therapy and prognosis may differ from that of asbestosis.

In plain English

This study looked at asbestos-exposed workers who had scarring of the lung tissue (interstitial lung disease) but whose lung samples showed no asbestos bodies. The authors drew on patients studied from 1952 to 1986 and found 176 asbestos-exposed persons with available lung tissue. In 9 of them (5.1%), no asbestos bodies were found (Group I). The authors used electron microscopy to measure fibers in lung tissue. They compared Group I with 9 people with idiopathic pulmonary fibrosis and no known asbestos exposure (Group II), and with 9 asbestos-exposed people with classic asbestosis (Group III). The three groups did not differ significantly in chrysotile or tremolite-actinolite fibers. Amosite plus crocidolite averaged 0.18 and 0.03 million fibers per gram of dry lung in Groups I and II, against 96.9 million in Group III, with no overlap. The tissue diagnoses in Group I included idiopathic pulmonary fibrosis in five cases. The authors concluded that asbestos bodies are seen in tissue only when exposure has been reasonably high. They also concluded that the 5.1% figure is artificially high because of atypical case selection. They noted two limitations: the paraffin tissue samples were small, and the analysis could miss chrysotile exposure.

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: Case series with two comparison groups. Lung tissue was analyzed by electron microscopy for asbestos fiber content. Two individual case reports are included.
• Who was studied: 176 asbestos-exposed persons with lung tissue from open-lung biopsy, resection or autopsy. They were drawn from 750 patients with interstitial or diffuse infiltrative lung disease studied from 1952 to 1986. The 9 without asbestos bodies (Group I) were compared with two groups selected at random and matched for age (within 5 years) and smoking history: 9 patients with interstitial fibrosis and no history of asbestos exposure (Group II), and 9 asbestos-exposed patients with classic asbestosis (Group III).
• Exposure: Group I: 7 of the 9 had worked in shipyards for 4 to 38 years, mostly as bystanders (shipfitters, riggers, sweepers, foundry work). None had worked directly with asbestos as pipe coverers. The other two were a steamfitter and a sheet metal worker. Mean latent period was 28 years. Group III: eight had worked directly with asbestos in factories or as insulators, and one was a shipfitter. Their exposure was mostly mixed-fiber, except one patient who worked with crocidolite only. Lung fibers were classified as chrysotile, tremolite plus actinolite, or amosite plus crocidolite.
• Main results:
  • Mean chrysotile content in lung tissue was not significantly different among the three groups.
  • Mean tremolite (plus actinolite) concentrations were 0.26, 0.36 and 0.53 x 10^6 fibers per gram in Groups I, II and III. These were not significantly different.
  • Mean amosite plus crocidolite counts were 0.18 x 10^6 fibers per gram in Group I and 0.03 x 10^6 in Group II, which did not differ significantly from each other. Group III's mean was 96.9 x 10^6, three orders of magnitude greater.
  • Group III's amosite plus crocidolite content was statistically different from both other groups (p less than 0.0001). There was no overlap: every individual Group III value was greater than 2.4 x 10^6 fibers per gram.
  • All Group I patients met the clinical criteria for asbestosis.
  • Tissue diagnoses in Group I included idiopathic pulmonary fibrosis in five cases. Other diagnoses were a probable burned-out eosinophilic granuloma, fibrosis related to past sarcoidosis, and bronchiolitis obliterans organizing pneumonia.
  • Pleural plaques were obvious in six of nine Group III patients. Only one Group I patient had a small plaque.
• The authors' conclusion: The authors concluded that asbestos bodies are seen in tissue sections only when exposure has been reasonably high. They also concluded that the 5.1% rate of non-asbestos interstitial lung disease among asbestos-exposed persons in this series is artificially high because of atypical case selection.
• Limitations the authors state:
  • Paraffin blocks provide only a small amount of tissue. Fiber content varies from site to site within the lung, so results could be unrepresentative.
  • Chrysotile does not accumulate in the lung to the extent amphiboles do, so this type of analysis could miss significant chrysotile exposure.
  • The 176 patients who had lung tissue taken were not representative of a random asbestosis population.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Idiopathic, Pulmonary Fibrosis, Interstitial Lung Disease, Asbestos Bodies, Chrysotile, Tremolite, Actinolite, Amosite.

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• Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis — J.N. Kline, D.A. Schwartz, et al. (1993)
• Pulmonary fibrosis in asbestos insulation workers with lung cancer: a radiological and histopathological evaluation — H.M. Kipen, R. Lilis, et al. (1987)

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