Kim Hartley1, Melinda C MacDougall2, Brandon Terrizzi3, Yingying Xu4, Kim M Cecil5, Aimin Chen6, Joseph M Braun7, Bruce P Lanphear8, Nicholas C Newman9, Ann M Vuong10, Andreas Sjödin11, Kimberly Yolton12. 1. Cincinnati Children's Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati, OH, USA. Electronic address: Kim.Hartley@cchmc.org. 2. Cincinnati Children's Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati, OH, USA. Electronic address: Melinda.MacDougall@cchmc.org. 3. Cincinnati Children's Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati, OH, USA. 4. Cincinnati Children's Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati, OH, USA. Electronic address: Yingying.Xu@cchmc.org. 5. Cincinnati Children's Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati, OH, USA; University of Cincinnati, College of Medicine, Cincinnati, OH, USA. Electronic address: Kim.Cecil@cchmc.org. 6. University of Pennsylvania, Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, Philadelphia, PA, USA. Electronic address: Aimin.Chen@pennmedicine.penn.edu. 7. Brown University, Department of Epidemiology, Providence, RI, USA. Electronic address: Joseph_Braun_1@brown.edu. 8. Simon Fraser University, Faculty of Health Sciences, Burnaby, British Columbia, Canada. Electronic address: Bruce_Lanphear@sfu.ca. 9. Cincinnati Children's Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati, OH, USA. Electronic address: Nicholas.Newman@cchmc.org. 10. University of Nevada, Las Vegas School of Public Health, Las Vegas, NV, USA. Electronic address: Ann.Vuong@unlv.edu. 11. Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Mail Stop F-20, 4770 Buford Highway NE, Atlanta, GA, USA. Electronic address: zrq4@cdc.gov. 12. Cincinnati Children's Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati, OH, USA; University of Cincinnati, College of Medicine, Cincinnati, OH, USA. Electronic address: Kimberly.Yolton@cchmc.org.
Abstract
BACKGROUND: Polybrominated diphenyl ethers (PBDEs) are persistent environmental pollutants used as flame retardants. Gestational PBDE exposure has been associated with a variety of behavior problems in children, but little is known about its impact into adolescence, particularly on social skills, which are important for achieving social competence, establishing identity, and forming lasting relationships. OBJECTIVE: We investigated associations between gestational exposure to PBDEs and social skills and problem behaviors in early adolescence in a longitudinal pregnancy and birth cohort in Cincinnati, Ohio (recruited 2003-2006). METHODS: We measured maternal serum concentrations of five PBDE congeners during gestation. At age 12, we measured social skills and problem behaviors scores for 243 adolescents using self- and caregiver-report on the Social Skills Improvement System (SSiS). We used multivariable linear regression models to estimate associations between maternal PBDE concentrations and SSiS scores, controlling for potential covariates. We report associations for the five congeners and a summary exposure variable (∑5BDE: the sum of BDE- 28, 47, 99, 100, and 153, n = 197). RESULTS: We found sex-specific associations of ∑5BDE concentrations with adolescent-reported Problem Behaviors (∑5BDE × sex pint = 0.02) and caregiver-reported Social Skills (∑5BDE × sex pint = 0.02). In sex-stratified models, log10 transformed data revealed increased maternal ∑5BDE concentration among males was associated with decreased caregiver-reported Social Skills composite score (β = -10.2, 95% CI: -19.5, -1.0), increased adolescent-reported Problem Behaviors composite score (β = 12.1, 95% CI: 5.4, 18.8), and increased caregiver-reported Problem Behaviors composite score (β = 6.2, 95% CI: 0.7, 11.7). Further analysis on SSiS subscales revealed similar patterns in significant associations among males. There were no statistically significant associations in stratified models among females despite higher ∑5BDE exposure (Female GM=40.15 ng/g lipid, GSE=1.10; Male GM=35.30 ng/g lipid, GSE=1.09). DISCUSSION: We found gestational PBDE exposure in males was associated with poorer behavioral outcomes, extending previous findings among this cohort into early adolescence.
BACKGROUND: Polybrominated diphenyl ethers (PBDEs) are persistent environmental pollutants used as flame retardants. Gestational PBDE exposure has been associated with a variety of behavior problems in children, but little is known about its impact into adolescence, particularly on social skills, which are important for achieving social competence, establishing identity, and forming lasting relationships. OBJECTIVE: We investigated associations between gestational exposure to PBDEs and social skills and problem behaviors in early adolescence in a longitudinal pregnancy and birth cohort in Cincinnati, Ohio (recruited 2003-2006). METHODS: We measured maternal serum concentrations of five PBDE congeners during gestation. At age 12, we measured social skills and problem behaviors scores for 243 adolescents using self- and caregiver-report on the Social Skills Improvement System (SSiS). We used multivariable linear regression models to estimate associations between maternal PBDE concentrations and SSiS scores, controlling for potential covariates. We report associations for the five congeners and a summary exposure variable (∑5BDE: the sum of BDE- 28, 47, 99, 100, and 153, n = 197). RESULTS: We found sex-specific associations of ∑5BDE concentrations with adolescent-reported Problem Behaviors (∑5BDE × sex pint = 0.02) and caregiver-reported Social Skills (∑5BDE × sex pint = 0.02). In sex-stratified models, log10 transformed data revealed increased maternal ∑5BDE concentration among males was associated with decreased caregiver-reported Social Skills composite score (β = -10.2, 95% CI: -19.5, -1.0), increased adolescent-reported Problem Behaviors composite score (β = 12.1, 95% CI: 5.4, 18.8), and increased caregiver-reported Problem Behaviors composite score (β = 6.2, 95% CI: 0.7, 11.7). Further analysis on SSiS subscales revealed similar patterns in significant associations among males. There were no statistically significant associations in stratified models among females despite higher ∑5BDE exposure (Female GM=40.15 ng/g lipid, GSE=1.10; Male GM=35.30 ng/g lipid, GSE=1.09). DISCUSSION: We found gestational PBDE exposure in males was associated with poorer behavioral outcomes, extending previous findings among this cohort into early adolescence.
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