Evidence for excess colorectal cancer incidence among asbestos-exposed men in the Beta-Carotene and Retinol Efficacy Trial

Our plain-English summary of Evidence for excess colorectal cancer incidence among asbestos-exposed men in the Beta-Carotene and Retinol Efficacy Trial, by O.A. Aliyu, M.R. Cullen, M.J. Barnett, et al (American Journal of Epidemiology, 2005).

The study

• Authors: O.A. Aliyu, M.R. Cullen, M.J. Barnett, J.R. Balmes, B. Cartmel, C.A. Redlich, C.A. Brodkin, S. Barnhart, L. Rosenstock, L. Israel, G.E. Goodman, M.D. Thornquist, G.S. Omenn
• Journal: American Journal of Epidemiology
• Published: 2005;162(9):868-78
• Cited by: 27 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The relation between asbestos exposure and colorectal cancer remains controversial. The authors of this 1984-2004 US study examined the association among 3,897 occupationally exposed participants in the Beta-Carotene and Retinol Efficacy Trial (CARET) for chemoprevention of lung cancer, followed prospectively for 10-18 years. When a Cox stratified proportional hazards model was used, risks of colorectal cancer were elevated among male heavy smokers exposed to asbestos. Their relative risk was 1.36 (95% confidence interval: 0.96, 1.93) when compared with that for CARET heavy smokers not exposed to asbestos, after adjusting for age, smoking history, and intervention arm. The presence of asbestos-induced pleural plaques at baseline was associated with a relative risk of 1.54 (95% confidence interval: 0.99, 2.40); colorectal cancer risk also increased with worsening pulmonary asbestosis (p = 0.03 for trend). A dose-response trend based on years of asbestos exposure was less evident. Nonetheless, these data suggest that colorectal cancer risk is elevated among men occupationally exposed to asbestos, especially those with evidence of nonmalignant asbestos-associated radiographic changes.

In plain English

This study followed men in CARET, a US lung cancer prevention trial of beta-carotene and retinol, through December 2003. It compared 3,897 men occupationally exposed to asbestos with 7,924 male heavy smokers. Heavy smokers exposed enough to qualify for the asbestos group were excluded, though some had short exposures. Fiber types were not classified, and years in high-risk trades and chest X-ray changes served as rough measures of exposure. There were 85 colorectal cancers among the asbestos-exposed men and 123 among the heavy smokers. Asbestos-exposed men who also met heavy-smoker criteria (1,839 men, 42 cases) had a relative risk of 1.36 (95% CI 0.96 to 1.93) versus the heavy smokers, which was not statistically significant. Among them, men with pleural thickening or plaques had a relative risk of 1.54 (95% CI 0.99 to 2.40), also versus the heavy smokers. Risk rose with increasing X-ray profusion score (p = 0.03 for trend). Within the asbestos-exposed men alone, a similar pattern was not statistically significant. Cancers were self-reported and checked against medical records, without tissue review. The authors concluded the evidence was consistent with asbestos increasing colorectal cancer risk, especially with asbestos-related X-ray changes.

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: Prospective cohort analysis of men enrolled in a multicenter, randomized, double-blinded, placebo-controlled lung cancer chemoprevention trial (CARET), using internal comparisons and Cox proportional hazards models
• Who was studied: 3,897 men occupationally exposed to asbestos and 7,924 male heavy smokers from six US centers. Men enrolled in the asbestos cohort mainly during 1989 to 1993, plus an earlier Seattle pilot group. They were followed for 10 to 18 years, through December 2003. The heavy-smoker comparison group excluded 29 men whose asbestos exposure would have made them eligible for the asbestos-exposed cohort. Some remaining heavy smokers had short-duration asbestos exposures.
• Exposure: Occupational asbestos exposure. Men qualified either by at least 5 years in one of eight high-risk trades (insulation, sheet metal, plumbing, plasterboard, ship fitting, ship electrical work, boiler making, ship scaling) starting at least 15 years earlier, or by occupational exposure plus asbestos-related chest X-ray changes. Dose and fiber type were not classified. Duration of exposure and X-ray changes were used as crude surrogates.
• Main results:
  • 85 colorectal cancer cases occurred among the 3,897 asbestos-exposed men and 123 among the 7,924 heavy smokers. Crude incidence was 2.0 (95% CI 1.6, 2.5) per 1,000 person-years in the asbestos-exposed cohort and 1.6 (95% CI 1.3, 1.9) in the heavy-smoker cohort.
  • Some men in the heavy-smoker comparison cohort had short-duration asbestos exposures.
  • The asbestos-exposed smoker-eligible subcohort (1,839 men, 42 cases) had a relative risk of 1.36 (95% CI 0.96, 1.93) compared with the heavy-smoker cohort, adjusted for smoking history, age and intervention arm. This was not statistically significant.
  • Smoker-eligible asbestos-exposed men with pleural abnormalities (886 men, 24 cases) had a relative risk of 1.54 (95% CI 0.99, 2.40) compared with the heavy-smoker cohort.
  • In the comparison of the smoker-eligible subcohort with heavy smokers, colorectal cancer risk showed a significant trend with increasing radiographic profusion score (p = 0.03 for trend).
  • Within the whole asbestos-exposed cohort, compared with men with normal radiographs, risk followed a similar increasing pattern with radiographic abnormality but was not statistically significant. For pleural abnormality the relative risk was 1.40 (95% CI 0.88, 2.23).
  • In the work-history-eligible subcohort (3,067 men), the trend for years in a high-risk trade was not statistically significant. Men with 21 to 30 years had a 74 percent increased risk compared with those with less than 10 years (trade-adjusted relative risk 1.74, 95% CI 0.74, 4.10). Men with more than 40 years had lower risk. Time since first exposure had no predictive effect.
  • Survival after colorectal cancer diagnosis was similar for cases in the asbestos-exposed smoker-eligible subcohort and in the heavy-smoker cohort.
• The authors' conclusion: The authors concluded that they had provided new evidence consistent with the hypothesis that asbestos exposure increases colorectal cancer risk. An apparent dose-response relation was seen in men with radiographic changes. No clear effect was seen in men without pleural changes or asbestosis on X-ray.
• Limitations the authors state:
  • Colorectal cancer was not the trial's primary endpoint. There was no review of the tissue diagnoses, so misclassification of mesothelioma or adenocarcinoma of other origin cannot be entirely excluded.
  • More aggressive colorectal cancer screening of asbestos-exposed workers could have caused detection bias, and completeness of case finding might have differed between the cohorts.
  • The authors could not exclude effects of other unmeasured workplace exposures, such as welding fumes, diesel exhaust, silica, nickel or hexavalent chromium.
  • The authors could not exclude confounding by unmeasured risk factors such as family history, recreational activity, or use of nonsteroidal anti-inflammatory drugs.
  • Participants were volunteers. The authors said results should not be extrapolated uncritically to women, men with lower asbestos exposure, or nonsmokers.

Topics

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

Medical terms in this study, explained in our Lexicon: Colorectal Cancer, Asbestos Exposure, Lung Cancer, Relative Risk, confidence interval, Pleural Plaques, Asbestosis, Dose-response relationship.

Related studies

• Predictors of lung cancer among asbestos-exposed men in the {beta}-carotene and retinol efficacy trial — M.R. Cullen, M.J. Barnett, et al. (2005)
• The Beta-Carotene and Retinol Efficacy Trial: incidence of lung cancer and cardiovascular disease mortality during 6-year follow-up after stopping beta-carotene and retinol supplements — G.E. Goodman, M.D. Thornquist, et al. (2004)
• Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial — G.S. Omenn, G.E. Goodman, et al. (1996)
• Changes in cholesterol and triglyceride concentrations in the Vanguard population of the Carotene and Retinol Efficacy Trial (CARET) — B. Cartmel, J. Dziura, et al. (2005)
• CARET, the beta-carotene and retinol efficacy trial to prevent lung cancer in asbestos-exposed workers and in smokers — G.S. Omenn, G. Goodman, et al. (1991)
• Recruitment for the beta-carotene and retinol efficacy trial (CARET) to prevent lung cancer in smokers and asbestos-exposed workers — G.S. Omenn, G. Goodman, et al. (1992)

Browse more research in American Journal of Epidemiology, or return to medical research.