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Asbestos burden and the pathology of lung cancer

Our plain-English summary of Asbestos burden and the pathology of lung cancer, by M.L. Warnock, W. Isenberg (Chest, 1986).

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The study

  • Authors: M.L. Warnock, W. Isenberg
  • Journal: Chest
  • Published: 1986;89(1):20-6
  • Cited by: 58 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. 000446).

Abstract

To determine whether we could distinguish asbestos-related lung cancers from unrelated ones, we typed and quantified by electron-optical methods the asbestos fibers in the lungs of 75 men with lung cancer. All but eight men had some history of asbestos exposure. On the basis of combined amosite and crocidolite (AC) concentrations, we divided the subjects into three groups (AC fibers per gram of dry lung): low (less than 10(5)); intermediate (10(5) to 10(6)); and high (greater than 10(6)). Age, smoking history, latent period, and type and location of tumors were similar in all three groups. Of 62 evaluated subjects, zero of 14 in the low group, seven of 29 in the intermediate group, and five of 19 in the high group had asbestosis. Epidemiologic studies suggest that persons exposed to concentrations of asbestos that can cause asbestosis are at increased risk for lung cancer. Thus, the subjects in our intermediate and high concentration groups may have been at increased risk for cancer, even when they did not have asbestosis. Because large burdens of asbestos do not always cause pulmonary fibrosis, asbestosis may be a poor marker of fiber-related lung cancer.

In plain English

The authors studied the lungs of 75 men with primary lung cancer to see whether asbestos-related cancers could be distinguished from others. All but eight had some history of asbestos exposure. Using electron-optical methods, the authors counted asbestos fibers and grouped the men by combined amosite and crocidolite concentration per gram of dry lung: under 100,000 (15 men), 100,000 to 1 million (35 men), and over 1 million (25 men). The groups did not differ significantly in age or smoking, nor in tumor type or location. Asbestosis was found in zero of 14 evaluated men in the low group, seven of 29 in the intermediate group and five of 19 in the high group. The authors concluded that asbestosis may be a poor marker of fiber-related lung cancer. They proposed that, when no amosite and crocidolite fiber count is available, an asbestos body concentration over 1,000 per gram of dry lung in a person with a history of exposure to those fibers be used in place of asbestosis as an indication that a lung cancer may be asbestos-related.

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: Pathology study of lung tissue. Asbestos bodies were counted by light microscopy, and asbestos fibers were counted and typed by electron-optical methods. Lung fibrosis was graded by eye and under the microscope. Subjects were compared across three fiber-burden groups.
  • Who was studied: 75 men with primary carcinoma of the lung, aged 35 to 82 years, from three sources. 29 lungs came from autopsies at the Solano County (California) Coroner's Office, which serves a shipyard neighborhood. 30 subjects were referred to the laboratory because of a history of asbestos exposure. 16 men had lung resection or autopsy at Moffitt Hospital or Fort Miley Veterans Hospital between Sept 1, 1980 and Dec 31, 1983. Of the specimens, 17 were surgical resections and 58 were postmortem. All but eight men had some history of asbestos exposure.
  • Exposure: Lung burden per gram of dry lung of combined amosite and crocidolite (AC) fibers, chrysotile fibers, TAAG fibers (tremolite, anthophyllite, actinolite and glaucophane), and asbestos bodies. Subjects were grouped by AC concentration: group 1, fewer than 100,000 (15 subjects); group 2, 100,000 to 1 million (35 subjects); group 3, more than 1 million (25 subjects). Occupational history was obtained by telephone interview with a relative.
  • Main results:
    • Of 62 evaluated subjects, asbestosis was present in 0 of 14 in the low group, 7 of 29 in the intermediate group, and 5 of 19 in the high group.
    • The three groups did not differ significantly in mean age or in mean pack-years smoked.
    • Over 70 percent of subjects in groups 2 and 3 were shipyard workers. In group 1, 73 percent (11 of 15) were classified as white-collar or blue-collar workers. The difference in job category between group 1 and groups 2 and 3 combined was reported as significant (p = 0.05).
    • Of all tumors, 45 percent were adenocarcinomas, 42 percent were squamous cancers and 13 percent were undifferentiated. There was no significant difference among the three groups in the frequency of any tumor type.
    • There were no differences among the groups in tumor location. Of the 67 tumors whose location could be determined, 69 percent were in the upper or middle lobes, 13 percent in the lower lobes and 18 percent in the main bronchi.
    • Combined amosite and crocidolite concentrations ranged from undetectable to 69 million per gram. Chrysotile ranged from 77,000 to 28 million per gram. Compared with group 1, group 3 had a median asbestos body concentration 260 times higher and a median amosite concentration 40 times higher, but chrysotile and TAAG concentrations were only 4 and 2.6 times higher.
    • The ratio of AC fibers to asbestos bodies varied widely between subjects, from 136,000 to 1 down to 4 to 1. The correlation coefficient between asbestos bodies and AC fibers was 0.77.
    • No fibrosis was seen with the naked eye in 13 of 14 evaluable lungs in group 1, 22 of 29 in group 2, and 14 of 19 in group 3.
    • Median microscopic fibrosis scores were 0.05 for group 1, 0.25 for group 2 and 0.28 for group 3. These scores were not significantly different.
    • Tissue sections were examined from the seven group 2 subjects with visible fibrosis. Only three of them had more than one asbestos body together with fibrosis. Conventional criteria would therefore count only some of these seven as having asbestosis; the authors proposed that all seven have asbestosis.
    • The authors found no correlation between years of exposure and AC fiber burden.
  • The authors' conclusion: The authors concluded that asbestosis may be a poor marker of fiber-related lung cancer, because large asbestos burdens do not always cause lung fibrosis. They stated that subjects in the intermediate and high groups may have been at increased risk for cancer even without asbestosis. They proposed an alternative for cases where no amosite and crocidolite fiber count is available: an asbestos body concentration over 1,000 per gram of dry lung, in a person with a history of exposure to those fibers, should be used in place of asbestosis as an indication that a lung cancer may be asbestos-related.
  • Limitations the authors state:
    • The actual fiber composition of the asbestos to which the subjects were exposed is not known. The lung asbestos burden is probably not an accurate indicator of the degree of exposure, partly because fibers are cleared over time.
    • There was not enough information about pleural plaques to analyze their significance.
    • Lung fibrosis can be difficult to judge by eye when tumor, pneumonia, bleeding or lung collapse is present.
    • The lungs, although distended, were not perfused at a constant pressure during fixation. The authors list lung distention as one of the factors that affect asbestos body counts in tissue sections.

Topics

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

Medical terms in this study, explained in our Lexicon: Pathology, Lung Cancer, Asbestos Exposure, Amosite, Crocidolite, Fibers Per Gram, Pulmonary Fibrosis.

Browse more research in Chest, or return to medical research.

Cited on this site

How to cite it

Cite the study

M.L. Warnock, W. Isenberg. Asbestos burden and the pathology of lung cancer. Chest 1986;89(1):20-6. doi:10.1378/chest.89.1.20. PMID: 3940784.

Cite our summary

“Asbestos burden and the pathology of lung cancer.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/asbestos-burden-and-the-pathology-of-lung-cancer.

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