Etiology of lung cancer: Evidence from epidemiologic studies

Our plain-English summary of Etiology of lung cancer: Evidence from epidemiologic studies, by K. Zou, P. Sun, H. Huang, et al (Journal of the National Cancer Center, 2022).

The study

• Authors: K. Zou, P. Sun, H. Huang, H. Zhuo, R. Qie, Y. Xie, J. Luo, N. Li, J. Li, J. He, B. Aschebrook-Kilfoy, Y. Zhang
• Journal: Journal of the National Cancer Center
• Published: 2022;2(4):216-225
• Type of article: Review
• Cited by: 45 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Lung cancer is one of the leading causes of cancer incidence and mortality worldwide. While smoking, radon, air pollution, as well as occupational exposure to asbestos, diesel fumes, arsenic, beryllium, cadmium, chromium, nickel, and silica are well-established risk factors, many lung cancer cases cannot be explained by these known risk factors. Over the last two decades the incidence of adenocarcinoma has risen, and it now surpasses squamous cell carcinoma as the most common histologic subtype. This increase warrants new efforts to identify additional risk factors for specific lung cancer subtypes as well as a comprehensive review of current evidence from epidemiologic studies to inform future studies. Given the myriad exposures individuals experience in real-world settings, it is essential to investigate mixture effects from complex exposures and gene-environment interactions in relation to lung cancer and its subtypes.

© 2022 Chinese National Cancer Center. Published by Elsevier B.V.

In plain English

This article was a narrative review, not a new study. The authors summarized published epidemiologic research on causes of lung cancer, including smoking, alcohol, occupational exposures, radon, air pollution, diet, physical activity, psychological factors, family history and genetics. They did not describe how studies were chosen or how many were reviewed. Asbestos appeared briefly. It was listed with diesel fumes, arsenic, beryllium, cadmium, chromium, nickel and silica as established occupational lung carcinogens, which a cited study estimated together accounted for roughly 10% of lung cancer cases, with large regional variations. The review also noted that genetic studies had reported gene regions on 22q13.31, 11q13, 7q32.1 and 2q34 that interact with asbestos. The authors said gene-environment research was still at an exploratory stage. They did not name asbestos fiber types or discuss mesothelioma. The authors concluded that smoking, radon, air pollution and these occupational exposures are well-established risk factors. They called for studies of combined exposures and gene-environment interactions, and named residual confounding by smoking as a major challenge.

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: Narrative review of published epidemiologic studies on the causes of lung cancer; no new data were collected and no search method is described
• Who was studied: Published epidemiologic studies on lung cancer risk factors from many countries. The review does not report how studies were selected or how many were included.
• Exposure: Many suspected and established lung cancer risk factors. Asbestos is mentioned only as one of several established occupational lung carcinogens, along with diesel fumes, arsenic, beryllium, cadmium, chromium, nickel and silica. No fiber types are named.
• Main results:
  • Citing an earlier study, the review stated that established occupational lung carcinogens, asbestos among them, together accounted for roughly 10% of lung cancer cases, with large regional variations
  • Citing an earlier study, an estimated 9.5% of lung cancer deaths in China in 2005 were attributed to occupational exposure (all occupational exposures, not asbestos alone)
  • Citing two genetic studies, the review reported gene regions on 22q13.31, 11q13, 7q32.1 and 2q34 that interact with asbestos exposure in lung cancer risk
  • Citing earlier studies, the review stated that the strength of the link between cigarette smoking and lung cancer varies by histologic subtype
  • Citing earlier data, the review stated that in the United States adenocarcinoma overtook squamous cell carcinoma in 1985 as the most commonly diagnosed lung cancer subtype
• The authors' conclusion: The authors concluded that smoking, radon, air pollution and occupational exposure to asbestos, diesel fumes, arsenic, beryllium, cadmium, chromium, nickel and silica are well-established lung cancer risk factors. They said the roles of other suggested factors remain inconclusive, and called for research on mixtures of exposures and gene-environment interactions.
• Limitations the authors state:
  • The authors stated that residual confounding from smoking, and overlap between correlated exposures, has been a major challenge in studying lung cancer risk factors (a limitation of the studies reviewed)
  • The authors noted that studies classifying occupational exposure by job or industry title were prone to exposure misclassification
  • The authors noted that the healthy worker effect means that comparisons of workers with the general population are likely to underestimate true associations
  • The authors stated that gene-environment interaction studies are limited by the lack of study populations with sufficient statistical power and exposure data

Topics

Medical terms in this study, explained in our Lexicon: Etiology, Lung Cancer, Occupational Exposure, Adenocarcinoma, Squamous Cell Carcinoma, Histological Subtype.

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