Despite this, there is reluctance to regulate cigarette smoking in certain areas such as private homes selleck EPZ-5676 and cars (Mills, White, Pierce, & Messer, 2011; Semple et al., 2012). For children, parental smoking remains the major determinant of ETS exposure, with maternal smoking having been reported to play a more important role than paternal smoking (Jarvis et al., 1985). Understanding the strength of association between parental smoking and child ETS exposure will inform the development of future tobacco control policies. The majority of studies of the association between parental smoking and ETS exposure in children have focused on children at an age when active smoking is a possibility (i.e., early adolescence onwards; Heron, Hickman, Macleod, & Munafo, 2011; Sims et al., 2010).

This raises the potential problem of misclassification in such studies, where child reports of active smoking may be particularly inaccurate (Dolcini, Adler, Lee, & Bauman, 2003). Unfortunately, using cotinine levels to validate smoking status in children and young adolescents can be imprecise, when light, irregular smoking is common (Benowitz, 1996). Therefore, in order to more accurately assess the association between parental smoking and child ETS exposure, data on children collected at an age before active smoking is common are required. By comparing estimates at two ages, where active smoking is and is not likely, respectively, we can make indirect comparisons to assess the extent to which we have adequately adjusted for potential biases in measurement.

The use of cotinine as an assessment for ETS exposure, which is the primary metabolite of nicotine, can further improve the precision of these comparisons. Earlier studies may have underestimated the health consequences of ETS exposure through the use of self-report measures of exposure given that adults are likely to underreport their active smoking in the presence of children (Jefferis et al., 2010; Whincup et al., 2004). In this study, we sought to explore the association between maternal smoking behavior and child cotinine levels within nonsmokers, adjusting for other potential confounders. We also investigated the association child smoking has on cotinine levels of all participants. We used data from a birth cohort study based in the United Kingdom, where cotinine levels in the child were assessed when the child was aged 7 and 15 years.

This allowed a comparison of the impact of maternal smoking behavior on child cotinine levels at an age when child smoking was unlikely (7 years) and at an age where it was more likely (15 years). METHODS Avon Longitudinal Study of Parents and Children The sample for this study was drawn from the Avon Longitudinal Study of Parents and Children Anacetrapib (ALSPAC) (Boyd et al., 2012), an on-going population-based cohort study in the South-West of England. Recruitment to ALSPAC began in 1990�C1992.