Frederica Perera1, Emily L Roen Nolte2, Ya Wang3, Amy E Margolis4, Antonia M Calafat5, Shuang Wang3, Wanda Garcia6, Lori A Hoepner2, Bradley S Peterson7, Virginia Rauh6, Julie Herbstman2. 1. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA; Columbia Center for Children's Environmental Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA. Electronic address: fpp1@columbia.edu. 2. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA; Columbia Center for Children's Environmental Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA. 3. Columbia Center for Children's Environmental Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA; Department of Biostatistics, Mailman School of Public Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA. 4. Columbia Center for Children's Environmental Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA; Division of Child & Adolescent Psychiatry and the Center for Developmental Neuropsychiatry, Department of Psychiatry, The New York State Psychiatric Institute and the College of Physicians and Surgeons, Columbia University, 1051 Riverside Drive, New York, NY 10032, USA. 5. National Center for Environmental Health, Centers for Disease Control and Prevention, 4770 Buford Hwy, MS F17, Atlanta, GA 30341, USA. 6. Columbia Center for Children's Environmental Health, Columbia University, 722 W. 168th St., New York, NY 10032, USA; The Heilbrunn Department of Population and Family Health, Columbia University, 60 Haven Avenue, New York, NY 10032, USA. 7. Institute for the Developing Mind, Children's Hospital Los Angeles and Keck School of Medicine at the University of Southern California, USA.
Abstract
BACKGROUND: Experimental and epidemiological studies suggest that gestational exposure to Bisphenol A (BPA), an ubiquitous endocrine disrupting chemical, may lead to neurobehavioral problems in childhood; however, not all results have been consistent. We previously reported a positive association between prenatal BPA exposure and symptoms of anxiety/depression reported by the mother at child age 7-9 years in boys, but not girls. OBJECTIVES: Here, in the same birth cohort, we investigated the association of prenatal BPA exposure with symptoms of depression and anxiety self-reported by the 10-12 year olds, hypothesizing that we would observe sex-specific differences in anxiety and depressive symptoms. METHODS: African-American and Dominican women living in Northern Manhattan and their children were followed from mother's pregnancy through children's age 10-12 years. BPA was quantified in maternal urine collected during the third trimester of pregnancy and in child urine collected at ages 3 and 5 years. Children were evaluated using the Revised Children's Manifest Anxiety Scale (RCMAS) and Children's Depression Rating Scale (CDRS). We compared the children in the highest tertile of BPA concentration to those in the lower two tertiles. Associations between behavior and prenatal (maternal) BPA concentration or postnatal (child) BPA concentration were assessed in regression models stratified by sex. RESULTS: Significant positive associations between prenatal BPA and symptoms of depression and anxiety were observed among boys. Postnatal BPA exposure was not significantly associated with outcomes. There was substantial co-occurrence of anxiety and depressive symptoms in this sample. CONCLUSION: These results provide evidence that prenatal BPA exposure is associated with more symptoms of anxiety and depression in boys but not in girls at age 10-12 years.
BACKGROUND: Experimental and epidemiological studies suggest that gestational exposure to Bisphenol A (BPA), an ubiquitous endocrine disrupting chemical, may lead to neurobehavioral problems in childhood; however, not all results have been consistent. We previously reported a positive association between prenatal BPA exposure and symptoms of anxiety/depression reported by the mother at child age 7-9 years in boys, but not girls. OBJECTIVES: Here, in the same birth cohort, we investigated the association of prenatal BPA exposure with symptoms of depression and anxiety self-reported by the 10-12 year olds, hypothesizing that we would observe sex-specific differences in anxiety and depressive symptoms. METHODS: African-American and Dominican women living in Northern Manhattan and their children were followed from mother's pregnancy through children's age 10-12 years. BPA was quantified in maternal urine collected during the third trimester of pregnancy and in child urine collected at ages 3 and 5 years. Children were evaluated using the Revised Children's Manifest Anxiety Scale (RCMAS) and Children's Depression Rating Scale (CDRS). We compared the children in the highest tertile of BPA concentration to those in the lower two tertiles. Associations between behavior and prenatal (maternal) BPA concentration or postnatal (child) BPA concentration were assessed in regression models stratified by sex. RESULTS: Significant positive associations between prenatal BPA and symptoms of depression and anxiety were observed among boys. Postnatal BPA exposure was not significantly associated with outcomes. There was substantial co-occurrence of anxiety and depressive symptoms in this sample. CONCLUSION: These results provide evidence that prenatal BPA exposure is associated with more symptoms of anxiety and depression in boys but not in girls at age 10-12 years.
Authors: Frederica P Perera; Virginia Rauh; Robin M Whyatt; Wei-Yann Tsai; Deliang Tang; Diurka Diaz; Lori Hoepner; Dana Barr; Yi-Hsuan Tu; David Camann; Patrick Kinney Journal: Environ Health Perspect Date: 2006-08 Impact factor: 9.031
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