Does Mother's Smoking Influence Girls’ Smoking More Than Boys’ Smoking? A 20-Year Review of the Literature Using a Sex- and Gender-Based Analysis
Faculty of Health and Social Development, University of British Columbia Okanagan, Kelowna, British Columbia, Canada. Substance Use & Misuse
(Impact Factor: 1.23).
11/2010; 46(5):656-68. DOI: 10.3109/10826084.2010.528122
A systematic literature review was conducted to examine whether mother's smoking influences girls' smoking more than boys' smoking. Fifty-seven studies, published between 1989 and 2009, were analyzed using a sex and gender lens. Results indicate that mother's prenatal and postnatal smoking influences girls' smoking more than boys' smoking. Despite evidence that sex and gender are important determinants of smoking among adolescents when examined in relation to mother's smoking, the theoretical understanding of why girls are more likely to smoke if prenatally and postnatally exposed to mother's smoking remains unclear. Implications for future research are discussed.
Available from: Louise C Abbott
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ABSTRACT: Numerous epidemiological studies in the human population clearly indicate that smoking while pregnant has deleterious effects on fetal development as well as long-term adverse consequences on postnatal development and maturation of several organ systems. Low birth weight, sudden infant death syndrome (SIDS), behavioral disorders including attention deficit hyperactivity disorder (ADHD), externalizing and internalizing behavioral problems and conduct disorders in children have all been linked to prenatal exposure to tobacco smoke. The major pharmacologically active chemical found in tobacco smoke is nicotine, and prenatal exposure to nicotine has been shown to have significant effect on the development of multiple organ systems, including the nervous, respiratory, and cardiovascular systems. In this review, we define mainstream and sidestream smoke, summarize the major classes of compounds found in cigarette smoke, and describe how use of laboratory animal models can be used to assess mechanisms of toxicity and risk in the human population in general. We then discuss the association with smoking during pregnancy and the occurrence of reduced lung function, low birth weight, the incidence of congenital structural malformations, SIDS, ADHD, cognitive impairment, and mood disorders in children, and review pertinent experimental studies using a variety of animal models of developmental nicotine exposure, including, rats, mice, monkeys, lambs, and pigs that have increased our understanding of the pathophysiology of these disorders.
Available from: pediatrics.aappublications.org
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Using longitudinal data from the multigenerational Youth Development Study (YDS), this article documents how parents' long-term smoking trajectories are associated with adolescent children's likelihood of smoking. Prospective data from the parents (from age 14-38 years) enable unique comparisons of the parents' and children's smoking behavior, as well as that of siblings.
Smoking trajectories are constructed using latent class analysis for the original YDS cohort (n = 1010). Multigenerational longitudinal data from 214 parents and 314 offspring ages 11 years and older are then analyzed by using logistic regression with cluster-corrected SEs.
Four latent smoking trajectories emerged among the original cohort: stable nonsmokers (54%), early-onset light smokers who quit/reduce (16%), late-onset persistent smokers (14%), and early-onset persistent heavy smokers (16%). Although 8% of children of stable nonsmokers smoked in the last year, the other groups' children had much higher percentages, ranging from 23% to 29%. Multivariate logistic regression models confirm that these significant differences were robust to the inclusion of myriad child- and parent-level measures (for which child age and grade point average [GPA] are significant predictors). Older sibling smoking, however, mediated the link between parental heavy smoking and child smoking.
Even in an era of declining rates of teenage cigarette use in the United States, children of current and former smokers face an elevated risk of smoking. Prevention efforts to weaken intergenerational associations should consider parents' long-term cigarette use, as well as the smoking behavior of older siblings in the household.
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ABSTRACT: Maternal smoking during pregnancy (MSDP) is an independent risk factor for offspring nicotine dependence (ND), but mechanisms remain unknown. We investigated prenatal glucocorticoid (cortisol) and androgen (testosterone) associations with offspring ND over 40 years and the possibility that prenatal glucocorticoids and androgens would mediate links between MSDP and offspring ND.
Participants were 1086 mother-adult offspring pairs (59% female) from the New England Family Study, a 40-year longitudinal follow-up of the Collaborative Perinatal Project. MSDP was assessed prospectively at each prenatal visit. Maternal cortisol, testosterone, and cotinine (nicotine metabolite) were assayed from third trimester maternal sera. Offspring lifetime ND was assessed via structured interview.
Significant bivariate associations emerged for: 1) MSDP/cotinine and lifetime ND; and 2) maternal cortisol and lifetime ND, for daughters only. In multivariate models, maternal cortisol and MSDP/cotinine remained significantly and independently associated with increased odds of lifetime ND of daughters. However, cortisol did not mediate the MSDP-lifetime ND relation. No associations emerged between maternal testosterone and offspring ND.
Results provide the first evidence in support of prenatal glucocorticoid programming of adult ND over 40 years in daughters only. Our study highlights two independent prenatal pathways leading to increased risk for ND in daughters: elevated prenatal glucocorticoids and MSDP/nicotine exposure. Daughter-specific effects of glucocorticoid and MSDP programming over 40 years highlight the breadth and persistence of sexually dimorphic programming effects in humans. Results do not support androgen programming of offspring ND.
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