1. ^aDepartment of Epidemiology, CB#7435 McGavran-Greenberg Hall, University of North Carolina School of Public Health, Chapel Hill, North Carolina 27599-7435, USA
2. ^bGlobal Epidemiology, Safety and Risk Management, Pfizer, Inc., New York, New York, USA
3. ^cDepartment of Community Medicine, Mt. Sinai School of Medicine, New York, New York, USA
4. ^dDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA
5. ^eNew York City Department of Health and Mental Hygiene, New York, New York, USA
6. ^fDepartment of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, New York, USA
7. ^gConsulting in the Public Interest, Inc., Lambertville, New Jersy, USA
8. ^hSouthwest Research Institute, San Antonio, Texas, USA
9. ⁱDepartment of Pharmacology, Penn State College of Medicine, USA
10. ^jDepartment of Preventive Medicine, University of Stony Brook, New York, USA
11. ^kDepartment of Biostatistics, Mailman School of Public Health, Columbia University, New York, New York, USA
12. ^lDepartment of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York, USA

Correspondence: S. Shantakumar, Doctoral Candidate, Department of Epidemiology, CB#7435 McGavran-Greenberg Hall, University of North Carolina School of Public Health, Chapel Hill, NC 27599-7435, USA. E-mail: sswhite@email.unc.edu

Received 26 August 2004; Accepted 8 March 2005; Published online 27 April 2005.

Abstract

The detection of polycyclic aromatic hydrocarbon (PAH)-DNA adducts in human lymphocytes may be useful as a surrogate end point for individual cancer risk prediction. In this study, we examined the relationship between environmental sources of residential PAH, as well as other potential factors that may confound their association with cancer risk, and the detection of PAH-DNA adducts in a large population-based sample of adult women. Adult female residents of Long Island, New York, aged at least 20 years were identified from the general population between August 1996 and July 1997. Among 1556 women who completed a structured questionnaire, 941 donated sufficient blood (25+ ml) to allow use of a competitive ELISA for measurement of PAH-DNA adducts in peripheral blood mononuclear cells. Ambient PAH exposure at the current residence was estimated using geographic modeling (n=796). Environmental home samples of dust (n=356) and soil (n=360) were collected on a random subset of long-term residents (15+ years). Multivariable regression was conducted to obtain the best-fitting predictive models. Three separate models were constructed based on data from : (A) the questionnaire, including a dietary history; (B) environmental home samples; and (C) geographic modeling. Women who donated blood in summer and fall had increased odds of detectable PAH-DNA adducts (OR=2.65, 95% confidence interval (CI)=1.69, 4.17; OR=1.59, 95% CI=1.08, 2.32, respectively), as did current and past smokers (OR=1.50, 95% CI=1.00, 2.24; OR=1.46, 95% CI=1.05, 2.02, respectively). There were inconsistent associations between detectable PAH-DNA adducts and other known sources of residential PAH, such as grilled and smoked foods, or a summary measure of total dietary benzo-[a]-pyrene (BaP) intake during the year prior to the interview. Detectable PAH-DNA adducts were inversely associated with increased BaP levels in dust in the home, but positively associated with BaP levels in soil outside of the home, although CIs were wide. Ambient BaP estimates from the geographic model were not associated with detectable PAH-DNA adducts. These data suggest that PAH-DNA adducts detected in a population-based sample of adult women with ambient exposure levels reflect some key residential PAH exposure sources assessed in this study, such as cigarette smoking.