Tobacco Smoke Carcinogens and Lung Cancer
Abstract
The complexity of tobacco smoke leads to some confusion about the mechanisms by which it causes lung cancer. Among the multiple components of tobacco smoke, 20 carcinogens convincingly cause lung tumors in laboratory animals or humans and are, therefore, likely to be involved in lung cancer induction. Of these, polycyclic aromatic hydrocarbons and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone are likely to play major roles. This review focuses on carcinogens in tobacco smoke as a means of simplifying and clarifying the relevant information that provides a mechanistic framework linking nicotine addiction with lung cancer through exposure to such compounds. Included is a discussion of the mechanisms by which tobacco smoke carcinogens interact with DNA and cause genetic changes--mechanisms that are reasonably well understood--and the less well defined relationship between exposure to specific tobacco smoke carcinogens and mutations in oncogenes and tumor suppressor genes. Molecular epidemiologic studies of gene-carcinogen interactions and lung cancer--an approach that has not yet reached its full potential--are also discussed, as are inhalation studies of tobacco smoke in laboratory animals and the potential role of free radicals and oxidative damage in tobacco-associated carcinogenesis. By focusing in this review on several important carcinogens in tobacco smoke, the complexities in understanding tobacco-induced cancer can be reduced, and new approaches for lung cancer prevention can be envisioned.
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We may never be able to map each detail of the complex process by which cigarette smoking causes lung cancer.
“we may never be able to map each detail of the complex process by which cigarette smoking causes lung cancer”
From The Role of Common Factors in Psychotherapy Outcomes (2019) · cites this paper as Hecht 1999
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- Authors
- Hecht, S. S.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Hecht, S. S.
- ORCID
- Hecht, S. S.
- Venue
- JNCI Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 1999-07-21
- Volume
- 91
- Issue
- 14
- Pages
- 1194-1210
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2101324933
- Cited by
- 1,976
- References
- 3
- Citations by year
- 2026: 24 · 2025: 35 · 2024: 47 · 2023: 60 · 2022: 73 · 2021: 65 · 2020: 51 · 2019: 63 · 2018: 71 · 2017: 68 · 2016: 82 · 2015: 92 · 2014: 97 · 2013: 94 · 2012: 84
- FWCI
- 4.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- JNCI Journal of the National Cancer Institute (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r35ca044377-13)
- National Cancer Institute (CA46535, CA81301, CA44377)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
- Keywords
- tobacco smoke carcinogens, lung cancer, polycyclic aromatic hydrocarbons, NNK, tobacco-specific nitrosamines, DNA adducts, oncogenic mutations, tumor suppressor, oxidative DNA damage, free radicals, nicotine dependence, carcinogenesis mechanisms, lung cancer prevention
- MeSH terms
- Animals, Carcinogens, DNA, Free Radicals, Humans, Lung Neoplasms, Mutation, Nitrosamines, Oncogenes, Polycyclic Aromatic Hydrocarbons, Smoking, Tobacco Smoke Pollution, Genes, Tumor Suppressor
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