Prenatal bisphenol A exposure, fetal thyroid hormones and neurobehavioral development in children at 2 and 4 years: A
Fen Li1, Fen Yang2, De-Kun Li3
1NHC Key Lab of Reproduction Regulation (Shanghai Institute of Planned Parenthood Research), Fudan University, Shanghai, China; Department of Chronic Infectious Disease Control and Prevention, Putuo District Center for Disease Control and Prevention, Shanghai, China.
Insights
Prenatal exposure to Bisphenol A (BPA) is linked to increased behavioral problems in children, particularly boys. While BPA may affect fetal thyroid hormones, this pathway does not explain the observed neurobehavioral effects.
Area of Science:
- Environmental Health
- Developmental Psychology
- Endocrinology
Background:
- Prenatal exposure to Bisphenol A (BPA) has been inconsistently linked to child neurobehavioral development.
- The potential mediating role of fetal thyroid hormones (THs) in this association remains unclear.
Purpose of the Study:
- To investigate the association between prenatal BPA exposure and behavioral problems in children at 2 and 4 years of age.
- To determine if fetal THs mediate the relationship between prenatal BPA and neurobehavioral outcomes.
Main Methods:
- Utilized data from the Shanghai-Minhang Birth Cohort Study (S-MBCS).
- Measured BPA in maternal urine and THs in cord plasma.
- Assessed child neurobehavioral development using the Child Behavior Checklist (CBCL) at 2 and 4 years.
- Employed generalized estimating equation (GEE) and multiple linear regression models, including mediation analysis.
Main Results:
- Higher prenatal BPA levels were associated with increased risks of various behavioral problems (Emotionally Reactive, Anxious/Depressed, Somatic Complaints, Aggressive Behavior, Internalizing/Externalizing Problems), especially in boys.
- An inverse association was observed between prenatal BPA and fetal TH levels.
- Mediation analysis did not support THs as a mediator for the observed BPA-induced neurobehavioral effects.
Conclusions:
- Prenatal BPA exposure may disrupt fetal TH levels and lead to persistent behavioral alterations in children, with a stronger effect observed in boys.
- Thyroid hormones do not appear to mediate the neurotoxic effects of BPA on child behavior in this cohort.
Abstract:
Findings about the association between prenatal Bisphenol A (BPA) exposure and neurobehavioral development in children are still inconsistent. In addition, whether fetal thyroid hormones (THs) mediate the reported association remains unclear. The present study aimed to examine the association between prenatal BPA exposure and risks of child behavioral problems at 2 and 4 years of age and whether the association could be explained by alteration of fetal THs as measured in cord plasma. Using the Shanghai-Minhang Birth Cohort Study (S-MBCS), BPA concentration was measured in maternal urine samples collected at 12-16 weeks of gestation. Children's neurobehavioral development was assessed using the Child Behavior Checklist/1.5-5 (CBCL), at 2 and 4 years of age. Using generalized estimating equation (GEE) models, 745 mother-pairs were included to examine associations of BPA with CBCL scores, Using multiple linear regression models, 348 mother-pairs were included to evaluate the association between maternal BPA and THs in cord plasma. A mediation analysis was conducted to explore the potential mediating role of THs. After adjusting for potential confounders, prenatal BPA level was associated with increased risks of Emotionally Reactive problem, Anxious/Depressed problem, having Somatic Complaints, exhibiting Aggressive Behavior, and Internalizing and Externalizing Problems: compared to the lowest tertile, the risks in the highest tertile and middle tertile, ranged between 1.55-fold (95% CI: 1.09, 2.21) and 2.59-fold (95% CI: 1.52, 4.42). The association was more pronounced among boys. None of the associations reached statistical significance among girls. An inverse association between prenatal BPA and fetal TH level was also observed. However, the observed neurotoxic effects of prenatal BPA exposure did not appear to be mediated by THs levels. The current findings suggest that prenatal exposure to BPA may disrupt fetal THs levels and may induce long-lasting behavioral alterations, especially in boys.
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