Pathology of carcinoma of the lung associated with asbestos exposure

Our plain-English summary of Pathology of carcinoma of the lung associated with asbestos exposure, by M. Kannerstein, J. Churg (Cancer, 1972).

The study

• Authors: M. Kannerstein, J. Churg
• Journal: Cancer
• Published: 1972;30(1):14-21
• Cited by: 96 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. 001335).

In plain English

This retrospective pathology study compared lung carcinomas from 50 men occupationally exposed to asbestos with lung carcinomas from 50 men who had no history of asbestos exposure and no asbestos bodies in lung sections. The two groups were matched by type of specimen (autopsy, surgical removal or biopsy). The groups differed significantly only in which lobes the tumors were in. In the exposed group, 19 tumors were in a lower lobe and 13 in an upper lobe. In the control group, 29 were in an upper lobe and 12 in a lower lobe. Extensive spread of tumor over the pleura was seen in five exposed cases and one control, a difference the authors called statistically less striking. Position within the lobe, cell type and metastases showed no significant difference. Lung fibrosis was more frequent and more severe in the exposed group. The authors concluded that the similarity fits the view that asbestos is a co-carcinogen, weak in itself, that markedly augments another carcinogen, probably cigarette smoke. Smoking histories were available for only some cases.

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 comparative pathology study: asbestos-associated lung carcinomas compared with matched control lung carcinomas, using the same gross and microscopic criteria
• Who was studied: 50 cases of lung carcinoma in men occupationally exposed to asbestos, drawn from different institutions over a considerable time span (most obtained through Dr. Irving J. Selikoff). These were compared with 50 male control cases of lung carcinoma from the authors' own material that had no history of asbestos exposure or asbestos bodies in lung sections. Specimen types were matched: 33 autopsies, 11 lobectomies or pneumonectomies and 6 biopsies in each group. Average age was 60.3 years (range 43 to 77) in the exposed group and 61.1 (range 38 to 81) in controls. About a dozen cases with incomplete information were excluded.
• Exposure: Occupational exposure to asbestos. The article does not specify fiber types, products, jobs or doses for the cases studied.
• Main results:
  • Tumor distribution by lobe differed significantly between the two series. Exposed group: upper lobe 13, lower lobe 19, middle lobe 4, two lobes 3, no data 11. Controls: upper 29, lower 12, middle 1, two lobes 1, no data 7.
  • Extensive pleural spread of tumor was found in 5 cases in the asbestos-associated group and 1 in the control group. The authors said this may be a significant difference and described it as statistically less striking than the lobe difference.
  • Position within a lobe, cell types and metastatic incidence and pattern showed no significant difference between the series. Peripheral tumors predominated in both groups: 22 peripheral and 16 central in exposed cases, 28 peripheral and 17 central in controls.
  • Cell types in the exposed group: squamous 11, anaplastic small cell 11, adenocarcinoma 11, anaplastic large cell 6, combined 8, unclassified 3. In controls: 12, 14, 9, 8, 7 and 0. The proportion of adenocarcinomas was very similar in both series.
  • Fibrosis of the lung tissue was much more frequent and of higher grade in the asbestos-associated cases.
  • In the 44 cases with enough lung tissue to compare, there was no apparent correlation between the number of asbestos bodies and the degree of fibrosis.
• The authors' conclusion: The authors concluded that the essential similarity between the two series appeared consistent with asbestos acting as a co-carcinogen: weak in itself, but markedly augmenting the effect of another potent carcinogen, probably cigarette smoke in the human population. They said they could not accept fibrosis as an essential intermediate causal step. They suggested, as speculation, that the lower lobe location and increased pleural involvement may result from structural changes in the lungs that come before the cancer.
• Limitations the authors state:
  • Cigarette smoking history was available for only some cases in both series. The authors assumed smoking frequencies matched those of the broader groups.
  • The material was retrospective, of diverse origin and varying quality, and the number of cases was limited, so subtle differences may have gone undetected.
  • The cell-type classification could not be a truly blind study by both authors, because one author had already studied the exposed cases. Initial disagreement occurred in about 10% of cases.
  • Fibrosis grading was relatively subjective.
  • For the asbestos body comparison, the number of sections varied from case to case and the site in the lung of the tissue blocks was generally unknown.

Topics

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

Medical terms in this study, explained in our Lexicon: Pathology, Carcinoma, Asbestos Exposure.

Related studies

• Surgical pathology of lung cancer — M.K. Rezaei, N.J. Nolan, et al. (2013)
• Unsuspected exposure to asbestos and bronchogenic carcinoma — K.M. Martischnig, D.J. Newell, et al. (1977)
• Whole exome sequencing of independent lung adenocarcinoma, lung squamous cell carcinoma, and malignant peritoneal mesothelioma: A case report — I. Vanni, S. Coco, et al. (2016)
• Keratin proteins and carcinoembryonic antigen in lung carcinoma: an immunoperoxidase study of fifty-four cases, with ultrastructural correlations — J.W. Said, G. Nash, et al. (1983)
• Use of antibodies to carcinoembryonic antigen and human milk fat globule to distinguish carcinoma, mesothelioma, and reactive mesothelium — R.J. Marshall, A. Herbert, et al. (1984)
• Thrombomodulin expression in transitional cell carcinoma — N.G. Ordóñez (1998)

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