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Cancer Epidemiology Biomarkers & Prevention Vol. 11, 677-685, August 2002
© 2002 American Association for Cancer Research

Environmental Toxins and Breast Cancer on Long Island. I. Polycyclic Aromatic Hydrocarbon DNA Adducts1

Marilie D. Gammon2, Regina M. Santella, Alfred I. Neugut, Sybil M. Eng, Susan L. Teitelbaum, Andrea Paykin, Bruce Levin, Mary Beth Terry, Tie Lan Young, Lian Wen Wang, Qiao Wang, Julie A. Britton, Mary S. Wolff, Steven D. Stellman, Maureen Hatch, Geoffrey C. Kabat, Ruby Senie, Gail Garbowski, Carla Maffeo, Pat Montalvan, Gertrud Berkowitz, Margaret Kemeny, Marc Citron, Freya Schnabel, Allan Schuss, Steven Hajdu and Vincent Vinceguerra

Department of Epidemiology, University of North Carolina, School of Public Health, Chapel Hill, North Carolina 27599 [M. D. G.]; Divisions of Environmental Health Sciences [R. M. S., T. L. Y., L. W. W., Q. W., G. G.], Epidemiology [A. I. N., S. M. E., M. B. T. S. D. S., R. S., G. G.], Biostatistics [A. P., B. L.], and Sociomedical Sciences [R. S.], Columbia University, Mailman School of Public Health, New York, New York 10032; Departments of Medicine [A. I. N.] and Surgery [F. S.]; Columbia University, College of Physicians and Surgeons, New York, New York 10032; Department of Community and Preventive Medicine, Mt. Sinai School of Medicine, New York, New York 10029 [S. L. T., J. A. B., M. S. W., M. H., G. B.]; American Health Foundation, Valhalla, New York 10595 [S. D. S.]; Departments of Preventive Medicine [G. C. K.] and Surgery [M. K.], State University of New York, Stony Brook, New York 11794; Westat, Inc., Rockville, Maryland 20850 [C. M., P. M.]; ProHealth Care Associates, LLP, Lake Success, New York 11042 [M. C.]; Department of Pathology, Winthrop University Hospital, Mineola, New York 11042 [A. S.]; and Departments of Pathology [S. H.] and Medicine [V. V.], North Shore University Hospital, Manhasset, New York 11030

Polycyclic aromatic hydrocarbons (PAH) are potent mammarycarcinogens in rodents, but their effect on breast cancer development in women is not clear. To examine whether currently measurable PAH damage to DNA increases breast cancer risk, a population-based case-control study was undertaken on Long Island, NY. Cases were women newly diagnosed with in situ and invasive breast cancer; controls were randomly selected women frequency matched to the age distribution of cases. Blood samples were donated by 1102 (73.0%) and 1141 (73.3%) of case and control respondents, respectively. Samples from 576 cases and 427 controls were assayed for PAH-DNA adducts using an ELISA. The geometric mean (and geometric SD) of the log-transformed levels of PAH-DNA adducts on a natural scale was slightly, but nonsignificantly, higher among cases [7.36 (7.29)] than among controls [6.21 (4.17); P = 0.51]. The age-adjusted odds ratio (OR) for breast cancer in relation to the highest quintile of adduct levels compared with the lowest was 1.51 [95% confidence interval (CI), 1.04–2.20], with little or no evidence of substantial confounding (corresponding multivariate-adjusted OR, 1.49; 95% CI, 1.00–2.21). There was no consistent elevation in risk with increasing adduct levels, nor was there a consistent association between adduct levels and two of the main sources of PAH, active or passive cigarette smoking or consumption of grilled and smoked foods. These data indicate that PAH-DNA adduct formation may influence breast cancer development, although the association does not appear to be dose dependent and may have a threshold effect.




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