TY - JOUR

T1 - Prenatal and postnatal bisphenol A exposure and social impairment in 4-year-old children

AU - Lim, Youn-Hee

AU - Bae, Sanghyuk

AU - Kim, Bung-Nyun

AU - Shin, Choong Ho

AU - Lee, Young Ah

AU - Kim, Johanna Inhyang

AU - Hong, Yun-Chul

PY - 2017

Y1 - 2017

N2 - BACKGROUND: Prenatal and postnatal exposure to bisphenol A (BPA) may affect early brain development. Rodent studies suggest that prenatal and postnatal neurodevelopmental toxicity from BPA exposure may manifest as social deficits in offspring. We investigated the association between prenatal and postnatal exposure to BPA and social impairments in a sample of 4-year-old children.METHODS: We recruited second-trimester pregnant women between 2008 and 2011, and measured their creatinine-adjusted prenatal urine BPA levels. In 2014-2015, a subset of 4-year-old children born to these women underwent neurobehavioral assessment and physical examination. We collected urine and blood from the children and assessed social impairments, including deficits in social interaction, social communication, and other behavior patterns using the Korean version of the Social Communication Questionnaire (K-SCQ) (n = 304). We examined social impairments associated with prenatal exposure at mid-term pregnancy and postnatal exposure to BPA at 4 years of age, using linear and piecewise linear regression models.RESULTS: The relationship between prenatal BPA exposure and social communication was non-linear and statistically significant at or above the flexion point for BPA levels of 3.0 μg/g creatinine in girls (58.4%, 95% confidence interval [CI], 6.5% to 135.8%). Each 2-fold increase in postnatal BPA exposure was significantly associated with an 11.8% (95% CI, 0.6% to 24.3%) increase in impairment in social communication in 4-year old girls, as indicated by the linear regression model.CONCLUSION: Prenatal and postnatal BPA exposure is associated with social impairment at 4 years of age, particularly in girls.

AB - BACKGROUND: Prenatal and postnatal exposure to bisphenol A (BPA) may affect early brain development. Rodent studies suggest that prenatal and postnatal neurodevelopmental toxicity from BPA exposure may manifest as social deficits in offspring. We investigated the association between prenatal and postnatal exposure to BPA and social impairments in a sample of 4-year-old children.METHODS: We recruited second-trimester pregnant women between 2008 and 2011, and measured their creatinine-adjusted prenatal urine BPA levels. In 2014-2015, a subset of 4-year-old children born to these women underwent neurobehavioral assessment and physical examination. We collected urine and blood from the children and assessed social impairments, including deficits in social interaction, social communication, and other behavior patterns using the Korean version of the Social Communication Questionnaire (K-SCQ) (n = 304). We examined social impairments associated with prenatal exposure at mid-term pregnancy and postnatal exposure to BPA at 4 years of age, using linear and piecewise linear regression models.RESULTS: The relationship between prenatal BPA exposure and social communication was non-linear and statistically significant at or above the flexion point for BPA levels of 3.0 μg/g creatinine in girls (58.4%, 95% confidence interval [CI], 6.5% to 135.8%). Each 2-fold increase in postnatal BPA exposure was significantly associated with an 11.8% (95% CI, 0.6% to 24.3%) increase in impairment in social communication in 4-year old girls, as indicated by the linear regression model.CONCLUSION: Prenatal and postnatal BPA exposure is associated with social impairment at 4 years of age, particularly in girls.

KW - Benzhydryl Compounds/blood

KW - Child, Preschool

KW - Endocrine Disruptors/blood

KW - Environmental Exposure

KW - Environmental Pollutants/blood

KW - Female

KW - Humans

KW - Male

KW - Phenols/blood

KW - Pregnancy

KW - Prenatal Exposure Delayed Effects/chemically induced

KW - Prospective Studies

KW - Republic of Korea/epidemiology

KW - Social Behavior Disorders/chemically induced

U2 - 10.1186/s12940-017-0289-2

DO - 10.1186/s12940-017-0289-2

M3 - Journal article

C2 - 28747197

VL - 16

JO - Environmental Health

JF - Environmental Health

SN - 1476-069X

IS - 1

M1 - 79

ER -