For continuous www.selleckchem.com/products/U0126.html variables, Student��s t tests or the Wilcoxon��s rank sum tests were used; for categorical variables, Fisher��s exact test of proportions was used. The primary analysis consisted of comparing mean acute changes in physiological measures (HR, SBP, DBP, and CO) following parent intervention (i.e., smoking one cigarette vs. no parental smoking). Analysis of covariance (ANCOVA) was used for each physiological outcome adjusting for child age, gender, and body mass index. In addition, in secondary analyses aimed more at evaluating effects of chronic exposure, alternate definitions of parent exposure status were assessed based on questionnaire information and physiological measures at baseline.

This included (a) self-reported smoking frequency (never, some days, and every day), (b) hours child was in a room with a smoker (never, <3 hr/week, ��3 hr/week but <1 hr/day, ��1 hr/day but <3 hr/day, and >3 hr/day), (c) household rules about smoking (no one permitted, smoking permitted in some rooms/times, and smoking permitted anywhere), (d) urine cotinine (0 or 1, 2�C5, and 6), and (e) eCO (<4.3, 4.3 to <13, and ��13). For these analyses, ANCOVA was used with a linear test of trend for each outcome across exposure levels. By study design, we sought a target sample size of 20 children exposed and 20 children not exposed to SHS to compare acute physiological changes. Assuming two-sided Type I error rate of 0.05 and no correction for multiple comparisons, this corresponded to 80% power to detect a large effect size of 0.91 or higher.

Results Sample description Forty-one parent�Cchild dyads were enrolled and completed all study measures. First, to verify accurate chronic exposure classification via biochemical analyses, distributions of parent and children urine cotinine levels prior to intervention were examined. ��Exposed�� parents had a median urine cotinine level of 6.0 ng/ml compared with 1.0 ng/ml in ��unexposed�� parents (p < .0001). Importantly, the distributions between the two groups did not overlap, indicating accurate biochemical classification of parent smokers and nonsmokers. Similarly, levels of urine cotinine were much lower, on average (p = .003), in unexposed compared with exposed children, albeit less pronounced than the differences observed in parents. These observations indicate that children of parents who smoked cigarettes were indeed recently exposed to smoke.

Prior to intervention, mean eCO levels (ppm) were 23.0 �� 14.0 in exposed parents compared with 4.1 �� 2.8 in unexposed parents (p < .0001), again validating accurate classification of smoking status in parents. In contrast to urine cotinine levels in child subjects, mean eCO levels Entinostat (ppm) at baseline were similar in exposed (3.2 �� 3.1) and unexposed children (3.6 �� 3.5, p = .87). This suggests similar smoke exposure to both groups of children immediately prior to (e.g.