Asbestos-related mesothelioma: epidemiological evidence for asbestos as a promoter

Our plain-English summary of Asbestos-related mesothelioma: epidemiological evidence for asbestos as a promoter, by K. Browne (Archives of Environmental Health, 1983).

The study

• Author: K. Browne
• Journal: Archives of Environmental Health
• Published: 1983;38(5):261-6
• Cited by: 35 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. 000597).

Abstract

A series of 144 cases of mesothelioma among asbestos workers indicated important divergences from the epidemiological pattern shown to exist for asbestos-related lung cancer. Consideration of exposure duration and intensity and the latent period between first exposure and death suggests that asbestos does not act as a complete carcinogen, but as a promoter. A threshold seems probable for both duration and intensity of exposure in the induction of mesothelioma. This threshold may, in part, be related to the passage of fibers from the lungs to the pleura or peritoneum, and would, in any case, be masked in lung cancer by the retention of asbestos in the lungs. Reported cases of mesothelioma in immediate family members indicate the existence of an additional factor in mesothelioma induction, acting earlier in life than the first asbestos exposure.

In plain English

The author analysed 102 mesothelioma deaths among workers at an asbestos insulation factory in Barking, England, which used crocidolite throughout and amosite and chrysotile from 1930, plus 42 cases from related companies. Factory cases had two matched controls each. Times from first exposure to death had a very flat distribution; the author suggested cases may occur at random between 19 and 46 years. Workers employed over two years did not have longer average latent periods. Cases had a higher average exposure rank than controls (5.1 versus 3.9 on a 1 to 6 scale). 6% of cases were exposed 3 months or less, the shortest being 3 weeks of spinning in 1929. Two pairs of brothers were among the 102 cases and one among the 42; no sibling or parent-child pairs appeared among controls. The author concluded that asbestos appears to act as a promoter, not a complete carcinogen, with probable thresholds for duration and intensity, and that family cases suggest an additional factor acting early in life. Cases exposed under one month may have been missed, the author noted.

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 of mesothelioma deaths with a matched control series drawn from personnel records, examined together with other published series and reports of family clusters
• Who was studied: 102 mesothelioma deaths among employees of an asbestos products factory in Barking, England (open 1913 to 1967), who died before 1981 with diagnosis confirmed by post-mortem and histology. Also 42 cases from related companies meeting the same criteria. Two controls per factory case, matched for sex, date of first exposure (within 1 year) and age (within 3 years).
• Exposure: Work in a factory making asbestos insulation products. Crocidolite was used throughout, and amosite and chrysotile were also used from 1930. Exposure was measured as duration of employment and an intensity rank from 1 to 6 on Newhouse's rating scale. No dust counts were available.
• Main results:
  • The distribution of latent periods (first exposure to death) was extremely flat. The author suggested that for latent periods of 19 to 46 years cases may be distributed at random. On that hypothesis a Poisson distribution closely matched the observed counts: 135 total deaths, mean annual rate 4.8. The hypothesis rests on an assumption the author said cannot be quantified.
  • For both sexes, workers employed more than 2 years did not have a longer mean latent period. Females: 1 to 24 months (18 cases) 37.3 years; 25 or more months (20 cases) 36.5 years. Males: 1 to 24 months (23 cases) 34.0 years; 25 or more months (41 cases) 30.3 years.
  • Average exposure rank was 5.1 for cases compared with 3.9 for controls.
  • Only 4 cases (4%) worked in the two lowest exposure ranks, compared with 24% of controls. Those 4 had occasionally held jobs with potentially very high exposure.
  • No mesothelioma was recorded among employees, such as office or canteen staff, who did not work in the production areas. This also applied to the 42 cases at related companies.
  • 6% of the series were exposed for not more than 3 months, and 15% for not more than 6 months.
  • The minimum recorded exposure resulting in mesothelioma was 3 weeks up to 1934, 6 weeks in 1935 to 1945, and 12 weeks after 1946.
  • The shortest known exposure was a woman employed for 3 weeks on spinning in 1929.
  • Among pleural cases compared with controls employed more than 1 month, the distribution of exposure duration looked bimodal. The first mode closely followed the controls.
  • All 10 pleural cases with exposures over 16 years had asbestosis: 4 diagnosed in life and 6 at post-mortem.
  • Two pairs of brothers were found among the 102 factory cases and another pair of brothers among the 42 related-company cases. In addition, the brother of a man in the series died of mesothelioma with no occupational exposure established.
  • No sibling or parent-child pairs were identified among the original control series.
  • Across nine families with two or more mesothelioma cases (from this series and other published reports), none was a husband-wife pair (P < .03).
• The authors' conclusion: The author concluded the following. Asbestos appears to act as a promoter rather than a complete carcinogen. A threshold seems probable for both duration and intensity of exposure. Family cases suggest an additional factor, either inherited or, more probably, an environmental agent such as a virus acting at an early age.
• Limitations the authors state:
  • Mesothelioma could rarely be diagnosed before 1960, and long-latency cases had not yet occurred among recent workers. The latency distribution is therefore deficient at both ends.
  • The random-latency interpretation assumes that the number of workers with enough exposure to be at risk did not vary widely over the years. The author states this cannot be quantified.
  • No dust counts were available. The exposure ranking is only a rough index of severity.
  • Newhouse's study excluded those employed under 30 days, and other sources missed about 25% of cases. Cases with less than 1 month's exposure may therefore not have been identified.

Topics

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

Medical terms in this study, explained in our Lexicon: Mesothelioma, Lung Cancer, Pleura, Peritoneum, Asbestos Exposure.

Related studies

• Asbestos, asbestosis, and lung cancer: a critical assessment of the epidemiological evidence — P.A. Hessel, J.F. Gamble, et al. (2005)
• Mesothelioma continues to increase even 40 years after exposure - Evidence from long-term epidemiological observation — B. Świątkowska, N. Szeszenia-Dąbrowska (2017)
• The biomedical and epidemiological characteristics of asbestos-related diseases: a review — M. Huncharek (1986)
• Development of radiological and clinical evidence of parenchymal fibrosis in men with non-malignant asbestos-related pleural lesions — G.H. McMillan, C.E. Rossiter (1982)
• Asbestos and lung cancer: an analysis of the epidemiological evidence on the asbestos-smoking interaction — R. Saracci (1977)
• Human cancer from environmental pollutants: the epidemiological evidence — P. Boffetta (2006)

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