The participant then smoked ad lib the entire cigarette or the portion of the B&M that they had previously indicated was a usual amount smoked (identified by a line drawn on the product). Immediately after smoking, physiologic measures, a blood sample (i.e., for nicotine boost), and DAPT secretase GSI-IX exhaled CO levels were collected. Dependent Measures Physiologic Measures HR and BP were collected before and within 2 min after smoking using an automated BP monitor (DRE, Inc., Louisville, KY). Biochemical Measures A 7 ml sample of venous blood was drawn before and within 2 min after smoking from a forearm vein using a Vacutainer blood collection set (Becton Dickinson, Franklin Lakes, NJ). Blood samples were centrifuged, and the plasma was removed and frozen until analysis (Labstat International, Kitchener, Ontario, Canada) using flame ionic detection methods.

Exhaled CO was measured before and within 5 min after smoking using a BreathCO Monitor (Vitalograph, Lenexa, KS). Data Analysis A mixed analysis of variance with a within-subjects factor (i.e., change pre to post) and between-subjects factor (i.e., difference across conditions) was used. The within-subjects factor was used to test the primary hypothesis that smoking any product (i.e., conventional cigarette, B&M, or B&Mf) caused changes in HR, CO, and nicotine boosts. The between-subjects factor was used to test the secondary hypothesis that there were significant differences in toxin exposure among the products. Tukey��s post-hoc tests were used to determine specific sources of differences.

The data were examined for normality, and two outliers were identified for CO (outlier = 97 ppm) and nicotine (outlier = 57.1 ng/ml) boosts. Nicotine dependency (Heatherton et al., 1991) and the percent of the cigar smoked were evaluated as potential covariates in the analyses; however, neither were significantly associated with the HR, CO, or nicotine boosts (p > .05). There was a trend toward significance for CO boost and percent smoked, r (12) = .55, p < .10. Results Change in HR, Nicotine and CO Pre- to Postsmoking The primary hypothesis was partially supported in that HR, F(11, 33) = 4.36, p = .002, ��2 = .67, and CO, F(11, 33) = 3.22, p = .009, ��2 = .50, significantly increased from pre- to postsmoking for all smoking conditions. Nicotine boost only trended toward a significant increase from pre- to postsmoking, F(11, 33) = 2.

16, p = .065 (see Table 1). Table 1. Denotes the Average HR, Exhaled CO, and Plasma Nicotine Across the Three Conditions Variation in HR, Nicotine and CO Boosts Across Conditions The secondary hypothesis was partially supported AV-951 in that CO boost, F(2, 33) = 6.69, p = .005, ��2 = .19, and nicotine, F(2, 33) = 5.67, p = .011, ��2 = .02, significantly varied across the three conditions. The boost in HR did not vary across the three conditions, F(2, 33) = 0.74, p = .489.