43, CI = 1 11–1 85) (Thun et al 2006) Given that DNA

43, CI = 1.11–1.85) (Thun et al. 2006). Given that DNA adducts are associated with the development of lung tumors, it is plausible

that African Americans would have higher adduct levels (Tang et al. 2001; Peluso et al. 2005). However, our data do not support this hypothesis. There are some possible explanations for our findings. First, we measured adducts in a surrogate tissue (WBCs) rather than the target tissue (lung). Thus, the WBC DNA adducts may not represent the aggregate amount of tobacco-induced damage occurring in the lungs. Moreover, WBCs may represent a surrogate for PARP inhibitor other exposures in adults that are not experienced by children, to the same see more extent. Thus, these exposures could be associated with a smoking lifestyle. In addition, our cohort consisted solely of non-smoking children; studies of racial differences in lung cancer have focused primarily on smoking adults, and may be racial differences in DNA adducts occur only among active smokers. Lastly, the absence of racial differences in 1-Hydroxypyrene could

indicate that there may have been unmeasured sources of PACs in our study. Our results are subject to some limitations. First, our study was cross-sectional in design. At best, we could only identify an association between adducts and tobacco smoke exposure. Second, air nicotine levels were only measured in the main activity room C-X-C chemokine receptor type 7 (CXCR-7) of the home. Thus, there may have been unmeasured exposures in other parts of the home or outside of the home that contributed to adduct formation. Thus, parents may have smoked around their child in other parts of the home that would not have been captured by the

nicotine dosimeter. In addition, we were unable to determine the impact of the air cleaners on PACs—compounds likely leading to adduct formation—as airborne levels of these compounds were not directly measured. Unfortunately, urine 1-HP levels cannot differentiate inhaled versus ingested exposure to PACs, and 1-HP levels reflect only recent exposure to PAC materials. While we did MCC950 measure serum and hair cotinine levels that would capture ETS exposures outside of the home, it is well known that these biomarkers differ significantly by race. Still, we did not find any association of WBC DNA adducts with serum cotinine or hair cotinine—which operate as aggregate biomarkers of exposure. Third, we only measured PAC-DNA adducts, which may represent only a fraction of DNA damage induced by tobacco smoke. Aromatic amines are another family of compounds found in ETS that can form adducts with DNA (Talaska et al. 1991a, b; Hecht 2001, 2004). Fourth, there may have been sources of PACs other than ETS—such as exhaust from automobiles or dietary intake—that were not measured by the air nicotine dosimeters.

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