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Prenatal Exposure to Endocrine-disrupting Chemicals in Relation to Autism Spectrum Disorder and Intellectual Disability

Hamra, Ghassan B.a; Lyall, Kristenb; Windham, Gayle C.c; Calafat, Antonia M.d; Sjödin, Andreasd; Volk, Heathere; Croen, Lisa A.f

doi: 10.1097/EDE.0000000000000983
Perinatal Epidemiology

Background: Exposure to endocrine disruptors is unavoidable. Many such compounds are suspected to impact neurologic development of children, but most studies conducted have considered effects of individual chemicals in isolation. Because exposures co-occur, it is important to consider their health impacts in a single regression framework.

Methods: We applied Bayesian statistical tools (including shared mean and mixture priors for 25 unique chemicals) to study independent associations of endocrine disruptor biomarkers with autism spectrum disorder (ASD) (n = 491) and intellectual disability (n = 155), compared with 373 general population controls, in the Early Markers for Autism study. We measured biomarkers in maternal serum collected and stored from midpregnancy and considered them individually or as a class (i.e., summed polychlorinated biphenyls). We adjusted all models for original matching factors (child sex and month and year of birth), maternal age, maternal race/ethnicity, parity, and maternal education at the time samples were collected. We estimated the change in the odds of ASD or intellectual disability per 1 SD increase in the z-score of measured biomarker concentration for each chemical.

Results: Odds of ASD and intellectual disability did not change with increasing concentration for any specific endocrine disruptor. The effect estimates for each chemical were centered on or near an odds ratio of 1.00 in both models where we applied a shared mean or a mixture prior.

Conclusion: Our mixtures analyses do not suggest an independent relationship with ASD or intellectual disability with any of the 25 chemicals examined together in this mixtures analysis.

From the aDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD

bAJ Drexel Autism Institute, Drexel University, Philadelphia, PA

cDivision of Environmental and Occupational Disease Control, California Department of Public Health, Richmond, CA

dNational Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA

eDepartment of Mental Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD

fDivision of Research, Kaiser Permanente, Oakland, CA.

Submitted May 30, 2018; accepted January 28, 2019.

L.A.C. was partially funded by National Institutes of Health grant R01-ES016669.

The authors report no conflicts of interests.

The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention (CDC) or the California Department of Public Health. Use of trade names is for identification only and does not imply endorsement by the CDC, the Public Health Service, or the US Department of Health and Human Services.

Availability of data/code: Data are available on approval from the project principal investigator (Lisa Croen). Analytic code is available from the corresponding author’s personal web page and as an eSupplement.

Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (

Correspondence: Ghassan B. Hamra, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore, MD 21205. E-mail:

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