Discussion:The low enrollment rate suggests that the program was not feasible or acceptable. Alternative approaches are needed to improve the reach and efficacy of cessation interventions for Alaska Native women. IntroductionTobacco use during pregnancy is a major public health problem in the United States. Estimates of smoking prevalence during pregnancy among U.S. women range from 11% to 22% (Goodwin, Keyes, & Simuro, 2007;L. T. Martin, McNamara, et al., 2008). Among U.S. women who gave birth in 2005, the smoking rates during pregnancy were American Indian and Alaska Native (AI/ AN) women (18%), non-Hispanic White (14%), non-Hispanic Black (9%), Hispanic (3%), and Asian women (2%; Substance Abuse and Mental Services Administration [SAMHSA], 2007). Smoking during pregnancy is the leading preventable cause of low infant birth weight and is associated with other maternal and infant adverse perinatal events (Cnattingius, 2004). Less than 1% of U.S. women report smokeless tobacco (ST) use during pregnancy (SAMHSA, 2007). A number of studies report potential adverse health risks of ST use during pregnancy for both the mother and infant including increased risk for preterm birth, stillbirth, and low birth weight (England et al., 2003;Gupta & Subramoney, 2006;Steyn, de Wet, Saloojee, Nel, & Yach, 2006). AbstractBackground: Among Alaska Native women residing in the Yukon-Kuskokwim (Y-K) Delta region of Western Alaska, about 79% smoke cigarettes or use smokeless tobacco during pregnancy. Treatment methods developed and evaluated among Alaska Native pregnant tobacco users do not exist. This pilot study used a randomized two-group design to assess the feasibility and acceptability of a targeted cessation intervention for Alaska Native pregnant women. Methods:Recruitment occurred over an 8-month period. Enrolled participants were randomly assigned to the control group (n = 18; brief face-to-face counseling at the first visit and written materials) or to the intervention group (n = 17) consisting of faceto-face counseling at the first visit, four telephone calls, a video highlighting personal stories, and a cessation guide. Interviewbased assessments were conducted at baseline and follow-up during pregnancy (≥60 days postrandomization). Feasibility was determined by the recruitment and retention rates. Results:The participation rate was very low with only 12% of eligible women (35/293) enrolled. Among enrolled participants, the study retention rates were high in both the intervention (71%) and control (94%) groups. The biochemically confirmed abstinence rates at follow-up were 0% and 6% for the intervention and control groups, respectively.

Background Cotinine, a nicotine metabolite, is a biomarker of tobacco, nicotine and carcinogen exposure. However a given cotinine level may not represent the same tobacco exposure; for example, African Americans have higher cotinine levels than Caucasians after controlling for exposure. Methods Cotinine levels are determined by the amount of cotinine formation and the rate of cotinine removal which are both mediated by the enzyme CYP2A6. Since CYP2A6 activity differs by sex (estrogen induces CYP2A6) and genotype, their effect on cotinine formation and removal were measured in non-smoking Caucasians (Study 1, n=181) infused with labeled nicotine and cotinine. The findings were then extended to ad libitum smokers (Study 2, n=163). Results Study 1: Reduced CYP2A6 activity altered cotinine formation less than cotinine removal resulting in ratios of formation to removal of 1.31 and 1.12 in CYP2A6 reduced and normal metabolizers (P=0.01), or 1.39 and 1.12 in males and females (P=0.001), suggesting an overestimation of tobacco exposure in slower metabolizers. Study 2: Cotinine again overestimated tobacco and carcinogen exposure by ≥25% in CYP2A6 reduced metabolizers (≈2 fold between some genotypes) and in males. Conclusions In people with slower, relative to faster, CYP2A6 activity cotinine accumulates resulting in substantial differences in cotinine levels for a given tobacco exposure. Impact Cotinine levels may be misleading when comparing those with differing CYP2A6 genotypes within a race, between races with differing frequencies of CYP2A6 gene variants (i.e. African Americans have higher frequencies of reduced function variants contributing to their higher cotinine levels) or between the sexes.