© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 7, 614-619,
April 7, 1999
© 1999 Oxford University Press
REPORTS |
Early Age at Smoking Initiation and Tobacco Carcinogen DNA Damage in the Lung
Affiliations of authors: J. K. Wiencke, A.Varkonyi, Laboratory for Molecular Epidemiology, Department of Epidemiology and Biostatistics, School of Medicine, University of California San Francisco; S. W. Thurston, Department of Biostatistics, Harvard School of Public Health, Boston, MA; K. T. Kelsey, Department of Cancer Cell Biology and Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston; J. C. Wain, Thoracic Surgery Unit, Department of Surgery, Massachusetts General Hospital, Boston; E. J. Mark, Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston; D. C. Christiani, Occupational Health Program, Department of Environmental Health, Harvard School of Public Health, Boston, and Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston.
Correspondence to: John K. Wiencke, Ph.D., Laboratory for Molecular Epidemiology, Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco, 500 Parnassus Ave., San Francisco, CA 94143-0560 (e-mail: wiencke{at}itsa.ucsf.edu).
BACKGROUND: DNA adducts formed as a consequence of exposure to tobacco smoke may be involved in carcinogenesis, and their presence may indicate a high risk of lung cancer. To determine whether DNA adducts can be used as a "dosimeter" for cancer risk, we measured the adduct levels in nontumorous lung tissue and blood mononuclear cells from patients with lung cancer, and we collected data from the patients on their history of smoking. METHODS: We used the 32P-postlabeling assay to measure aromatic hydrophobic DNA adducts in nontumorous lung tissue from 143 patients and in blood mononuclear cells from 54 of these patients. From the smoking histories, we identified exposure variables associated with increased DNA adduct levels by use of multivariate analyses with negative binomial regression models. RESULTS/CONCLUSIONS: We found statistically significant interactions for variables of current and former smoking and for other smoking variables (e.g., pack-years [number of packs smoked per day x years of smoking] or years smoked), indicating that the impact of smoking variables on DNA adduct levels may be different in current and former smokers. Consequently, our analyses indicate that models for current and former smokers should be considered separately. In current smokers, recent smoking intensity (cigarettes smoked per day) was the most important variable. In former smokers, age at smoking initiation was inversely associated with DNA adduct levels. A highly statistically significant correlation (r = .77 [Spearman's correlation]; two sided P<.001) was observed between DNA adduct levels in blood mononuclear cells and lung tissue. IMPLICATIONS: Our results in former smokers suggest that smoking during adolescence may produce physiologic changes that lead to increased DNA adduct persistence or that young smokers may be markedly susceptible to DNA adduct formation and have higher adduct burdens after they quit smoking than those who started smoking later in life.
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