Contrary to expectations, we did not find racial differences in this association, sellckchem indicating that late timing may be protective for both White and Black girls. Our study shows that a racial disparity may not exist when assessing the effect of pubertal timing on smoking behavior for White and Black adolescents. However, possible differences should be examined for other racial minority groups. Additionally, this result provides evidence for the importance of assessing puberty in studies of substance use. While there are clearly multiple factors that contribute to the etiology and maintenance of substance use, we show that omitting puberty is overlooking a substantial influence on early substance use.

Future models should aim to incorporate these numerous influences, including a reliable measure of puberty so that we can better understand these complex relationships and work toward the prevention of prolonged substance use. Funding This work was supported by the National Institute of Drug Abuse (grant number R01 DA 16402) to LDD, Principal Investigator; the National Center for Research Resources at the National Institutes of Health (USPHS grant UL1RR026314); and National Research Service Award Training grant 1T32PE10027 from the National Institutes of Health. Declaration of Interests None declared.
Nearly 40 million children in the United States are exposed to secondhand cigarette smoke (Department of Health and Human Services, 2006), and the majority of this exposure takes place in the home. In 2002, 59.6% of nonsmoking children aged 3�C11 years had serum cotinine levels greater than 0.

05 ng/ml (Pirkle, Bernert, Caudill, Sosnoff, & Pechacek, 2006), which indicates recent exposure to smoke. Chronic exposure to secondhand smoke (SHS) in children is associated with a range of adverse health consequences, including increased rates of sudden infant death syndrome, asthma, pneumonia, and impaired lung growth. The Surgeon General Report of 2006 stated that even brief exposure to SHS can be harmful and, based on a synthesis of evidence, stated conclusively that there are no safe levels of exposure to SHS. Much of the data pertaining to harms of SHS exposure have been extrapolated from analyses of direct smoking effects. The acute physiologic effects of standardized smoking have been well described in adults (Winniford, 1990).

Specifically, Entinostat cigarette smoking is associated with an acute increase in heart rate (HR) and systolic blood pressure (SBP), and a dose�Cresponse relationship exists between nicotine level and the degree of rise in these hemodynamic factors (Spohr et al., 1979). While these effects have been confirmed by other studies (Benowitz, Hansson, & Jacob, 2002; Perkins, Epstein, Jennings, & Stiller, 1986), few studies have looked at acute physiologic changes related to SHS exposure (Corwin, McCoy, Whetzel, Ceballos, & Klein, 2006; Mahmud & Feely, 2004; McMurray, Hicks, & Thompson, 1985; Otsuka et al.