Steven Stellman - Residential environmental exposures and other characteristics associated with detectable PAH-DNA adducts in peripheral mononuclear cells in a population-based sample of adult females

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      Shantakumar, S., Gammon, M. D., Eng, S. M., Sagiv, S. K., Gaudet,   M. M., Teitelbaum, S. L., Britton, J. A., Terry, M. B., Paykin,   A., Young, T. L., Wang, L. W., Wang, Q., Stellman, S. D., Beyea,   J., Hatch, M., Camann, D., Prokopczyk, B., Kabat, G. C., Levin,   B., Neugut, A. I., Santella, R. M. 15 (6) 482-90-

      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.

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