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Background  Prenatal environmental conditions may influence disease risk in later life. We previously found a gene-environment interaction between the paraoxonase 1 ( PON1 ) Q192R genotype and prenatal pesticide exposure leading to an adverse cardio-metabolic risk profile at school age. However, the molecular mechanisms involved have not yet been resolved. It was hypothesized that epigenetics might be involved. The aim of the present study was therefore to investigate whether DNA methylation patterns in blood cells were related to prenatal pesticide exposure level,  PON1  Q192R genotype, and associated metabolic effects observed in the children.    Methods  Whole blood DNA methylation patterns in 48 children (6–11 years of age), whose mothers were occupationally unexposed or exposed to pesticides early in pregnancy, were determined by Illumina 450 K methylation arrays.    Results  A specific methylation profile was observed in prenatally pesticide exposed children carrying the  PON1  192R-allele. Differentially methylated genes were enriched in several neuroendocrine signaling pathways including dopamine-DARPP32 feedback (appetite, reward pathways), corticotrophin releasing hormone signaling, nNOS, neuregulin signaling, mTOR signaling, and type II diabetes mellitus signaling. Furthermore, we were able to identify possible candidate genes which mediated the associations between pesticide exposure and increased leptin level, body fat percentage, and difference in BMI  Z  score between birth and school age.    Conclusions  DNA methylation may be an underlying mechanism explaining an adverse cardio-metabolic health profile in children carrying the  PON1  192R-allele and prenatally exposed to pesticides.    Electronic supplementary material  The online version of this article (doi:10.1186/s13148-017-0336-4) contains supplementary material, which is available to authorized users.

clinical epigenetics

Interaction between prenatal pesticide exposure and a common polymorphism in the PON1 gene on DNA methylation in genes associated with cardio-metabolic disease risk—an exploratory study