Author:
Mourino Nerea,Zhang Zhuoya,Pérez-Ríos Mónica,Yolton Kimberly,Lanphear Bruce P.,Chen Aimin,Buckley Jessie P.,Kalkwarf Heidi J.,Cecil Kim M.,Braun Joseph M.
Abstract
Abstract
Background
Prenatal or early childhood secondhand tobacco smoke (SHS) exposure increases obesity risk. However, the potential mechanisms underlying this association are unclear, but obesogenic eating behaviors are one pathway that components of SHS could perturb. Our aim was to assess associations of prenatal and early childhood SHS exposure with adolescent eating behaviors.
Methods
Data came from a prospective pregnancy and birth cohort (N = 207, Cincinnati, OH). With multiple informant models, we estimated associations of prenatal (mean of 16 and 26 weeks of gestation maternal serum cotinine concentrations) and early childhood cotinine (average concentration across ages 12, 24, 36, and 48 months) with eating behaviors at age 12 years (Child Eating Behaviors Questionnaire). We tested whether associations differed by exposure periods and adolescent’s sex. Models adjusted for maternal and child covariates.
Results
We found no statistically significant associations between cotinine measures and adolescent’s eating behaviors. Yet, in females, prenatal cotinine was associated with greater food responsiveness (β: 0.23; 95% CI: 0.08, 0.38) and lower satiety responsiveness (β: -0.14; 95% CI: -0.26, -0.02); in males, prenatal and postnatal cotinine was related to lower food responsiveness (prenatal: β: -0.25; 95% CI: -0.04, -0.06; postnatal: β: -0.36; 95% CI: -0.06, -0.11). No significant effect modification by sex or exposure window was found for other eating behaviors.
Conclusion
Prenatal and early childhood SHS exposures were not related to adolescent’s eating behavior in this cohort; however, biological sex may modify these associations.
Funder
National Institutes of Environmental Health Sciences
Publisher
Springer Science and Business Media LLC
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