Participants in the CHARGE study were children born in 2000-2007 of mothers who lived in the agricultural area of the California Central Valley or the urban and suburban areas of Sacramento and the San Francisco Bay Area during pregnancy.
Data on exposures were obtained through telephone interviews during the period 3 months before conception until the children were 2-5 years old.
Children who were diagnosed with ASD between the ages of 2-5 were age-matched with normal-developing children as controls.
The CHARGE study is based on the paradigm that the etiology of ASD is multifactorial, and previous reports have relied on its data to evaluate numerous different exposures.
In a report published by Schmidt et al. in Environmental Health Perspectives (2017), researchers analysed data from the CHARGE study to explore whether associations between prenatal pesticide exposures and ASD in children are modified by maternal folic acid intake.
Participants with information available on both folic acid intake and at least one of the pesticide exposure variables were included in the analysis (296 with ASD and 220 controls).
Total folic acid intake (from food and supplements) during the first month of pregnancy was dichotomised as high (above 800 µg/d) or low (below 800 µg/d).
Household indoor pesticide use, household outdoor pesticide use, agricultural pesticide exposure, and occupational pesticide exposure were also dichotomised as any versus no exposure.
Overall, adjusted odds ratios (ORs) for ASD were highest in mothers exposed to pesticides and taking low folic acid in the first month of pregnancy.
Compared with women taking >800 µg of folic acid and with no indoor pesticide exposure, women taking <800 µg of folic acid with regular indoor pesticide exposure were more than twice as likely to have a child with ASD (OR=2.6; 95% CI, 1.3-5.2).
These odds were higher than for women with independent exposure to either low folic acid intake (OR=1.3) or indoor pesticides (OR=1.9).
Similar statistics were observed for indoor pesticide exposure, outdoor pesticide exposure, and agricultural pesticide exposure. In all of these situations, the ORs for those with double exposure (low folic acid + pesticide exposure) were greater than expected by additive or multiplicative models of each exposure alone.
The authors of this study suggest that folic acid might protect against the neurotoxic effects of pesticides by acting as an antioxidant and by supporting methylation.
Although the results of this study cannot establish any causal relationships, they do show that adequate folic acid intake during the first month of pregnancy might reduce, but not eliminate, the effects of pesticides on neurodevelopment.
The authors conclude that these findings support a recommendation to avoid pesticide exposure and to supplement folic acid during early pregnancy.
