Combined Exposures to Prenatal Pesticides and Folic Acid Intake in Relation to Autism Spectrum Disorders

Friday, May 13, 2016: 5:30 PM-7:00 PM
Hall A (Baltimore Convention Center)
R. J. Schmidt1, V. Kogan2, J. Shelton3, L. Delwiche4, R. Hansen5, S. Ozonoff6, D. J. Tancredi7, I. Hertz-Picciotto8 and H. E. Volk9, (1)Public Health Sciences and the MIND Institute, University of California at Davis, Davis, CA, (2)3Departments of Preventive Medicine and Pediatrics, Zilkha Neurogenetic Institute, Keck School of Medicine, Children’s Hospital Los Angeles, University of Southern California, Los Angeles, CA, (3)Public Health Sciences, University of California Davis, Davis, CA, (4)Public Health Sciences, University of California, Davis, Davis, CA, (5)Pediatrics and the MIND Institute, University of California Davis, Davis, CA, (6)UC Davis MIND Institute, Sacramento, CA, (7)Pediatrics, UC Davis School of Medicine, Sacramento, CA, (8)Dept of Public Health Sciences, School of Medicine, UC Davis MIND Institute, Davis, CA, (9)Wendy Klag Center for Autism and Developmental Disabilities, JHBSPH, Baltimore, MD

Many pesticides are neurotoxic by design and some have been linked to autism spectrum disorder (ASD). Periconceptional folic acid (FA) is associated with reduced ASD risk. In animal studies, maternal FA provides protection from environmental chemicals with developmental toxicity.


We examined combined exposures to maternal FA and selected pesticides, both in-home and agricultural, in relation to ASD risk.


California children aged 24-60 months enrolled in the CHARGE case-control study from 2003-2011 were clinically confirmed to have ASD (n=505) or typical development (n= 346). Maternal supplemental FA intake before and during pregnancy and indoor use of products containing pesticides were retrospectively collected by telephone interview. Agricultural pesticide exposure was determined by linking mothers‘ addresses shortly before, during, and after pregnancy to California’s commercial Pesticide Use Reports using 1250 m buffers.


For all comparisons, the reference group was women with above-median FA intake (800+ µg) during the first pregnancy month and no pesticide exposure. ORs were adjusted for home ownership.  Women with <800 µg FA intake and regular exposure (for 6+ pregnancy months) to indoor pesticides had children with elevated ASD risk (OR=5.1, 95% CI: 2.3-11.4). This was over twice that of those with 800+ µg FA and regular pesticide exposure (OR=2.3, 1.3-4.1).  ORs for combined low maternal FA intake and any exposure to agricultural pesticides 3 months before or after conception  were: 1.6 (0.6-4.4) for chlorpyrifos, 2.1 (1.0-4.4) for organophosphates, 1.9 (0.9-4.1) for pyrethroids, and  2.1 (0.7-5.9)  for carbamates. Except for carbamates, these ORs were larger than those for combinations of pesticide exposure with higher FA intake. All results were consistent with joint multiplicative or additive effects.


Supplemental FA could potentially reduce the risk of ASD associated with pesticide exposure.  Larger studies and research on potential mechanisms are warranted.

See more of: Epidemiology
See more of: Epidemiology