Phenotypes of lung cancer and statistical interactions between tobacco smoking and occupational exposure to asbestos and crystalline silica from a large case-only study: The CaProMat study

Our plain-English summary of Phenotypes of lung cancer and statistical interactions between tobacco smoking and occupational exposure to asbestos and crystalline silica from a large case-only study: The CaProMat study, by M. El Zoghbi, P. Salameh, I. Stücker, et al (Lung Cancer, 2017).

The study

• Authors: M. El Zoghbi, P. Salameh, I. Stücker, C. Paris, J.C. Pairon, A. Gislard, J. Siemiatycki, V. Bonneterre, B. Clin, P. Brochard, F. Delva, A. Lacourt
• Journal: Lung Cancer
• Published: 2017;112:140-155
• Cited by: 3 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Objectives: The aim of this study was to assess the effect modification of the association between tobacco smoking and phenotypes of lung cancer (histological type, tumor location, and age at diagnosis) by occupational exposure to asbestos or to crystalline silica.

Materials And Methods: The CaProMat study is a pooled case-only study including 7256 male lung cancer cases recruited between 1996 and 2011 in France and Canada. Two job-exposure matrices (JEMs) were used to assess occupational exposure to asbestos and crystalline silica. Statistical interactions between tobacco smoking and occupational exposure to asbestos or crystalline silica were assessed using unconditional logistic regression models for histological type and tumor location and linear regression models for age at diagnosis.

Results: Tobacco smoking was associated with squamous cell carcinoma and small cell carcinomas as well as an earlier age at diagnosis. Additional exposure to either asbestos or crystalline silica did not modify the effect of tobacco smoking for either histological type or age at diagnosis. Neither tobacco smoking nor occupational exposure to asbestos or crystalline silica influenced tumor location.

Conclusions: Tobacco smoking was the main factor related to histological type and age at diagnosis. Those associations were not modified by occupational exposure to asbestos or crystalline silica.

Copyright © 2017 Elsevier B.V. All rights reserved.

In plain English

This pooled case-only study analysed 7,256 men with lung cancer recruited between 1996 and 2011 from seven French studies and one Canadian study in Montreal. The authors asked whether workplace exposure to asbestos or crystalline silica, estimated from job histories with job-exposure matrices, changed the link between smoking and three features of the cancer: cell type, upper versus lower lobe location, and age at diagnosis. Among men not exposed to asbestos, medium-high smokers were more likely than never-low smokers to have squamous cell carcinoma rather than other types (odds ratio 1.52, 95% CI 1.20–1.92). The pattern was similar in asbestos-exposed men, and the interaction test was not statistically significant (p = 0.90). Findings for crystalline silica and for small cell carcinoma were similar. Neither smoking nor either exposure was associated with tumor location. Smokers were diagnosed younger, with no statistical interaction with asbestos except for adenocarcinomas. The authors concluded that smoking was the main factor related to cell type and age at diagnosis, and that asbestos or silica exposure did not modify these associations. They noted that job-exposure matrices can misclassify exposure.

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: Pooled case-only study (lung cancer cases only, no healthy comparison group), analysed with logistic and linear regression models that tested for interaction between smoking and occupational exposure
• Who was studied: 7,256 male lung cancer cases, all histologically confirmed, out of 9,623 cases in total (the 2,367 women were not analysed). They were recruited between 1996 and 2011 from six French hospital-based studies, one French population-based case-control study (ICARE) and one Canadian (Montreal) population-based case-control study.
• Exposure: Occupational exposure to asbestos (fiber type not specified) and to crystalline silica, assigned to each job by two job-exposure matrices. Men counted as exposed if at least one job had a probability of exposure greater than 30%. On that definition 49.8% were exposed to asbestos and 32.5% to crystalline silica. Tobacco smoking was measured with a comprehensive smoking index: never-low smokers were below the 25th percentile, medium-high smokers above it.
• Main results:
  • Among men not exposed to asbestos, medium-high smokers (compared with never-low smokers) had higher odds of squamous cell carcinoma versus other histological types (OR = 1.52, 95% CI 1.20–1.92) and versus adenocarcinoma only (OR = 1.89, 95% CI 1.47–2.44).
  • For asbestos-exposed medium-high smokers (compared with the reference group of never-low smokers not exposed to asbestos), the corresponding odds ratios were 1.83 (1.45–2.32) and 2.15 (1.67–2.78). The authors described this as similar to what was expected.
  • There was no statistical interaction on a multiplicative scale between smoking and asbestos exposure for squamous cell carcinoma (p = 0.90 versus other types; p = 0.46 versus adenocarcinoma). Similar findings were seen for small cell carcinoma.
  • For crystalline silica, men not exposed showed odds ratios for squamous cell carcinoma of 1.62 (1.36–1.93) versus other types and 1.92 (1.58–2.33) versus adenocarcinoma. There was no statistical interaction between smoking and silica exposure (p = 0.17 and p = 0.12).
  • For tumor location (upper versus lower lobe, known for 4,689 cases), there was neither an association nor an interaction between smoking and asbestos exposure (beta = 0.08, p = 0.66) or crystalline silica exposure (beta = −0.02, p = 0.91).
  • Lung cancer was diagnosed earlier among smokers. Medium-high smokers exposed to asbestos were diagnosed earlier than never-low smokers who were not exposed. There was no statistical interaction, except for adenocarcinomas (interaction p less than 0.01 in Table 5).
  • In complementary analyses that used different definitions of 'exposed', the smoking–crystalline silica interaction became statistically significant for squamous cell carcinoma, and for age at diagnosis in adenocarcinomas. The authors considered these two discrepancies more likely due to chance because of multiple comparisons.
• The authors' conclusion: The authors concluded that tobacco smoking was the main factor related to histological type and age at diagnosis, and that these associations were not modified by occupational exposure to asbestos or crystalline silica.
• Limitations the authors state:
  • Job-exposure matrices can produce false-positive and false-negative exposure assignments (non-differential misclassification).
  • With misclassification, the interaction term is more likely to be underestimated.
  • The prevalence of asbestos exposure (49.8%) was higher than expected because of the sensitive cut-off used. With a cut-off of more than 70% probability it would have been 16.2%.

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, Occupational Exposure, Crystalline, Squamous Cell Carcinoma, Carcinoma.

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