title: Endocrine disruptors and childhood social impairment.
abstract: Prenatal exposure to endocrine disruptors has the potential to impact early brain development. Neurodevelopmental toxicity in utero may manifest as psychosocial deficits later in childhood. This study investigates prenatal exposure to two ubiquitous endocrine disruptors, the phthalate esters and bisphenol A (BPA), and social behavior in a sample of adolescent inner-city children. Third trimester urines of women enrolled in the Mount Sinai Children's Environmental Health Study between 1998 and 2002 (n=404) were analyzed for phthalate metabolites and BPA. Mother-child pairs were asked to return for a follow-up assessment when the child was between the ages of 7 and 9 years. At this visit, mothers completed the Social Responsiveness Scale (SRS) (n=137), a quantitative scale for measuring the severity of social impairment related to Autistic Spectrum Disorders (ASD) in the general population. In adjusted general linear models increasing log-transformed low molecular weight (LMW) phthalate metabolite concentrations were associated with greater social deficits (β=1.53, 95% CI 0.25-2.8). Among the subscales, LMWP were also associated with poorer Social Cognition (β=1.40, 95% CI 0.1-2.7); Social Communication (β=1.86, 95% CI 0.5-3.2); and Social Awareness (β=1.25, 95% CI 0.1-2.4), but not for Autistic Mannerisms or Social Motivation. No significant association with BPA was found (β=1.18, 95% CI -0.75, 3.11). Prenatal phthalate exposure was associated with childhood social impairment in a multiethnic urban population. Even mild degrees of impaired social functioning in otherwise healthy individuals can have very important adverse effects over a child's lifetime. These results extend our previous finding of atypical neonatal and early childhood behaviors in relation to prenatal phthalate exposure.
authors.affiliation: Department of Preventive Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. amir.miodovnik@mssm.edu
authors.forename: Amir
authors.initials: A
authors.lastname: Miodovnik
authors.forename: Stephanie M
authors.initials: SM
authors.lastname: Engel
authors.forename: Chenbo
authors.initials: C
authors.lastname: Zhu
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Ye
authors.forename: Latha V
authors.initials: LV
authors.lastname: Soorya
authors.forename: Manori J
authors.initials: MJ
authors.lastname: Silva
authors.forename: Antonia M
authors.initials: AM
authors.lastname: Calafat
authors.forename: Mary S
authors.initials: MS
authors.lastname: Wolff
mesh_terms: D000328:Adult; D002648:Child; D002653:Child Behavior Disorders / Q000139:chemically induced* / Q000175:diagnosis / Q000523:psychology*; D002675:Child, Preschool; D015331:Cohort Studies; D052244:Endocrine Disruptors / Q000008:administration & dosage / Q000633:toxicity*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced* / Q000175:diagnosis / Q000523:psychology*; D011446:Prospective Studies; D055815:Young Adult
chemical_list: D052244:Endocrine Disruptors