RESUMEN
Globally, organophosphate (OP) pesticide usage and exposure is widespread. Studies have found that fetuses and infants are more sensitive than adults to environmental toxicants and that prenatal exposure to low levels of OPs has been associated with Attention Deficit Hyperactivity Disorder-Like Phenotypes (ADHD-LP). Paraoxonase 1 (PON1) is an enzyme involved in detoxifying some OPs and its polymorphisms influence enzyme activity and quantity. The objective of this study was to examine whether maternal and/or child PON1 genotypes (PON1R192Q and PON1L55M) were associated with ADHD-LP in a Mexico City, Mexico birth cohort. PON1R192Q and PON1L55M genotypes in mothers (PON1R192Q: N=531; PON1L55M: N=458) and children (PON1R192Q: N=532; PON1L55M: N=478) from blood DNA were determined. We assessed ADHD-LP for children between the ages of 6 and 13 using Conners' Parent Rating Scales-Revised (CRS-R), Conners' Continuous Performance Test (CPT), and the parent scores for Behavior Assessment System for Children-2 (BASC2). Multivariable linear regression models were used to test relationships between ADHD-LP and PON1 polymorphisms. In these models, significant associations were observed with maternal genotypes but not with the child genotypes. A higher DSM IV Hyperactivity/Impulsivity score (ß=3.27 points; 95% CI (0.89, 5.65)) and a 2.17 higher score in child DSM IV Total (95% CI (0.05, 4.29)) were observed for maternal PON155MM in comparison to PON155LM+LL. The childattention problems score was 2.27 points higher (95% CI (0.002, 4.53) for maternal PON1192QQ in comparison to PON1192QR+RR. Because maternal PON1 polymorphisms were associated with child ADHD-LP, this may be a viable biomarker of susceptibility for ADHD-LP.