1993; Perera et al. 2005). Lastly, all of the subjects in this study had asthma. It is unknown whether these results

are generalizable to children without asthma. Despite the results, our study did employ some unique strategies. We assembled a bi-racial cohort of tobacco-exposed children with OSI-906 asthma, which allowed us to explore factors that might contribute to DNA damage. While other studies have used ELISA tests, we used 32P-postlabeling with nuclease P1 enhancement to measure DNA adducts in our study sample. This process allowed for the detection of very low levels of PAC-DNA adducts (0.01 adducts per 109 nucleotides) without prior knowledge of the identity of the compounds (Reddy et al. 1981; Reddy and Randerath 1986). AMN-107 concentration We assessed ETS exposure in the home using a validated air nicotine dosimeter. The dosimeters provided

an objective measurement of the child’s in-home exposure to ETS for 6 months check details prior to the measurement of the DNA adducts. To our knowledge, this is the first study to attempt to correlate air nicotine levels with DNA adducts in a cohort of ETS-exposed children with asthma. Also, we demonstrated a non-significant trend toward an inverse relationship between air cleaner use and DNA adduct levels. Even though there were no differences in adduct levels between subjects with active and control filters, it is notable that increased use of the Cyclic nucleotide phosphodiesterase air cleaner trended toward lower DNA adduct levels. Potentially, improved room ventilation may reduce DNA adduct levels. Further studies are required to confirm and extend these findings. Acknowledgments We would like to thank Dr. Nancy Hopf for her assistance with the 1-hydroxypyrene

analyses. Funding for this study was provided by NCI—1K01CA123355-01A1 (SEW, GT, ACL, BS), The American Academy of Pediatrics Julius P. Richmond Center and Flight Attendant Medical Research Institute, and NHLBI-HL65731 (BPL). Conflict of interest statement The authors of this manuscript declare no competing interest. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. References Ahijevych K, Garrett BE (2004) Menthol pharmacology and its potential impact on cigarette smoking behavior. Nicotine Tob Res 6(Suppl 1):S17–S28CrossRef Ahijevych K, Tyndale RF et al (2002) Factors influencing cotinine half-life during smoking abstinence in African American and Caucasian women. Nicotine Tob Res 4:423–431CrossRef Benowitz NL, Perez-Stable EJ et al (1999) Ethnic differences in N-glucuronidation of nicotine and cotinine. J Pharmacol Exp Ther 291:1196–1203 Benowitz NL, Herrera B et al (2004) Mentholated cigarette smoking inhibits nicotine metabolism.