| Teen Smoking, Field Cancerization, and a 'Critical Period' Hypothesis for Lung Cancer Susceptibility John K. Wiencke1 and Karl T. Kelsey2 1Department of Epidemiology and Biostatistics, University of California San Francisco, School of Medicine, San Francisco, California, USA; 2Department of Cancer Cell Biology, Harvard University School of Public Health, Boston, Massachusetts, USA Abstract
Cigarette smoking by children and adolescents continues to be prevalent, and this fact represents a major public health problem and challenge. Epidemiologic work has previously suggested that exposure of the lung to tobacco carcinogens at an early age may be an independent risk factor for lung cancer. Recent studies at the molecular and cellular levels are consistent with this, now suggesting that early exposure enhances DNA damage and is associated with the induction of DNA alterations in specific chromosomal regions. In this paper we hypothesize that adolescence, which is known to be the period of greatest development for the lung, may constitute a "critical period" in which tobacco carcinogens can induce fields of genetic alterations that make the early smoker more susceptible to the damaging effects of continued smoking. The fact that lung development differs by sex might also contribute to apparent gender differences in lung cancer susceptibility. Because this hypothesis has important implications for health policy and tobacco control, additional resources need to be devoted to its further evaluation. Targeted intervention in adolescent smoking may yield even greater reductions in lung cancer occurrence than otherwise anticipated. Key words: cigarette smoking, field cancerization, lung cancer, susceptibility, tobacco. Environ Health Perspect 110:555-558 (2002) . [Online 12 April 2002] http://ehpnet1.niehs.nih.gov/docs/2002/110p555-558wiencke/ abstract.html Address correspondence to J.K. Wiencke, Laboratory for Molecular Epidemiology, Department of Epidemiology and Biostatistics, University of California San Francisco, School of Medicine, San Francisco, CA 94143-0560 USA. Telephone: (415) 476-3059. Fax: (415) 476-6014. E-mail: wiencke@itsa.ucsf.edu We thank V. Ernster, J. Cleaver, and W.C. Willet for helpful discussions and suggestions. This work was supported by grants 06717, 08357, 00002 from the National Institute of Environmental Health Sciences and grant NCI 78609 from the National Cancer Institute. Received 12 September 2001 ; accepted 16 November 2001.
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