Impact of occupational carcinogens on lung cancer risk in a general population

Our plain-English summary of Impact of occupational carcinogens on lung cancer risk in a general population, by S. De Matteis, D. Consonni, J.H. Lubin, et al (International Journal of Epidemiology, 2012).

The study

• Authors: S. De Matteis, D. Consonni, J.H. Lubin, M. Tucker, S. Peters, R.C.H. Vermeulen, H. Kromhout, P.A. Bertazzi, N.E. Caporaso, A.C. Pesatori, S. Wacholder, M.T. Landi
• Journal: International Journal of Epidemiology
• Published: 2012;41(3):711-21
• Cited by: 80 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Background: Exposure to occupational carcinogens is an important preventable cause of lung cancer. Most of the previous studies were in highly exposed industrial cohorts. Our aim was to quantify lung cancer burden attributable to occupational carcinogens in a general population.

Methods: We applied a new job-exposure matrix (JEM) to translate lifetime work histories, collected by personal interview and coded into standard job titles, into never, low and high exposure levels for six known/suspected occupational lung carcinogens in the Environment and Genetics in Lung cancer Etiology (EAGLE) population-based case-control study, conducted in Lombardy region, Italy, in 2002-05. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated in men (1537 cases and 1617 controls), by logistic regression adjusted for potential confounders, including smoking and co-exposure to JEM carcinogens. The population attributable fraction (PAF) was estimated as impact measure.

Results: Men showed an increased lung cancer risk even at low exposure to asbestos (OR: 1.76; 95% CI: 1.42-2.18), crystalline silica (OR: 1.31; 95% CI: 1.00-1.71) and nickel-chromium (OR: 1.18; 95% CI: 0.90-1.53); risk increased with exposure level. For polycyclic aromatic hydrocarbons, an increased risk (OR: 1.64; 95% CI: 0.99-2.70) was found only for high exposures. The PAFs for any exposure to asbestos, silica and nickel-chromium were 18.1, 5.7 and 7.0%, respectively, equivalent to an overall PAF of 22.5% (95% CI: 14.1-30.0). This corresponds to about 1016 (95% CI: 637-1355) male lung cancer cases/year in Lombardy.

Conclusions: These findings support the substantial role of selected occupational carcinogens on lung cancer burden, even at low exposures, in a general population.

In plain English

The EAGLE population-based case–control study enrolled people in Lombardy, Italy, in 2002–05. Analyses were run separately for men and women, but the women's estimates were unstable, so all later analyses covered only men: 1537 with lung cancer and 1617 without. A job–exposure matrix rated interview job histories as never, low or high exposure to six agents, including asbestos, without distinguishing fiber types. After adjustment for smoking and other carcinogens, men with any asbestos exposure had an odds ratio for lung cancer of 1.78 (95% CI 1.46–2.18) versus never-exposed men. The odds ratio was 1.76 (1.42–2.18) for low exposure and 1.51 (0.94–2.44) for high exposure. Raised odds were also seen for crystalline silica and nickel–chromium, but not for diesel exhaust. The authors attributed 18.1% (95% CI 12.6–23.3) of male lung cancers to asbestos, and 22.5% (14.1–30.0) to asbestos, silica and nickel–chromium together. Applied to 2005 incidence rates, the combined figure equalled about 1016 (637–1355) cases a year in Lombardy. They concluded that asbestos still has the greatest impact on lung cancer burden. They noted that job-based exposure assignment can misclassify people, likely weakening associations.

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: population-based case–control study (EAGLE study), analysed with unconditional logistic regression
• Who was studied: Men from the EAGLE study: 1537 lung cancer cases and 1617 population controls, aged 35–79, from 216 municipalities in Lombardy, Italy, enrolled April 2002 to June 2005. Analyses were run separately by sex. Because the estimates for women (406 cases, 499 controls) were unstable, all subsequent analyses were restricted to men.
• Exposure: Occupational exposure to six known or suspected lung carcinogens: asbestos (fiber type not specified), crystalline silica, PAH, diesel motor exhaust, and chromium and nickel compounds (the last two combined as Ni–Cr). Exposure was assigned from job titles using the DOM-JEM job–exposure matrix as none, low or high. Asbestos-exposed men worked mainly in construction, for example as plumbers and electricians.
• Main results:
  • Among men, 632 cases (41.1%) and 520 controls (32.2%) had any asbestos exposure. The fully adjusted odds ratio for any asbestos exposure was 1.78 (95% CI 1.46–2.18).
  • For men with low asbestos exposure, the fully adjusted odds ratio was 1.76 (95% CI 1.42–2.18).
  • For men with high asbestos exposure, the fully adjusted odds ratio was 1.51 (95% CI 0.94–2.44).
  • Among men, asbestos showed positive but not monotonic exposure–response trends for duration, cumulative exposure and latency.
  • The population attributable fraction for any asbestos exposure in men was 18.1% (95% CI 12.6–23.3).
  • The combined population attributable fraction for asbestos, silica and Ni–Cr in men was 22.5% (95% CI 14.1–30.0).
  • The authors applied these fractions to 2005 male lung cancer incidence rates in Lombardy. They estimated 817 (95% CI 569–1052) cases attributable to asbestos and 1016 (95% CI 637–1355) attributable to the three exposures combined.
  • Among never-smoking men, any asbestos exposure (14 cases/120 controls) had an odds ratio of 2.47 (95% CI 1.15–5.31). There was no deviation from a multiplicative interaction model between asbestos and smoking (P interaction 0.19).
  • In men, any exposure to crystalline silica (OR 1.31, 95% CI 1.02–1.68) and to Ni–Cr (OR 1.28, 95% CI 1.00–1.63) was associated with increased risk. No association was found for diesel motor exhaust. PAH showed an increased odds ratio only at high exposure (1.64, 95% CI 0.99–2.70).
• The authors' conclusion: The authors concluded that past occupational exposure to asbestos, crystalline silica, nickel–chromium compounds and possibly PAH still causes a substantial proportion of lung cancer cases. They also concluded that although asbestos use in Italy dropped before the 1992 ban, asbestos continues to have the greatest impact on lung cancer burden.
• Limitations the authors state:
  • Assigning exposure from job title alone can cause non-differential exposure misclassification, likely weakening associations and exposure–response trends.
  • Recall bias was possible, though the authors expected it to be mostly non-differential.
  • Residual confounding by smoking could not be completely ruled out.
  • The lack of reliable risk estimates for women leads to an underestimate of the true occupational lung cancer burden.

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: Lung Cancer, Etiology, Case-Control Study, Odds Ratio, confidence interval, Population Attributable Fraction (PAF), Crystalline.

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