ABSTRACT
BACKGROUND: Early life exposure to organophosphate (OP) pesticides is linked with adverse neurodevelopment and brain function in children. However, we have limited knowledge of how these exposures affect functional connectivity, a measure of interaction between brain regions. To address this gap, we examined the association between early life OP pesticide exposure and functional connectivity in adolescents. METHODS: We administered functional near-infrared spectroscopy (fNIRS) to 291 young adults with measured prenatal or childhood dialkylphosphates (DAPs) in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) study, a longitudinal study of women recruited during pregnancy and their offspring. We measured DAPs in urinary samples collected from mothers during pregnancy (13 and 26 weeks) and children in early life (ages 6 months, 1, 2, 3, and 5 years). Youth underwent fNIRS while they performed executive function and semantic language tasks during their 18-year-old visit. We used covariate-adjusted regression models to estimate the associations of prenatal and childhood DAPs with functional connectivity between the frontal, temporal, and parietal regions, and a mediation model to examine the role of functional connectivity in the relationship between DAPs and task performance. RESULTS: We observed null associations of prenatal and childhood DAP concentrations and functional connectivity for the entire sample. However, when we looked for sex differences, we observed an association between childhood DAPs and functional connectivity for the right interior frontal and premotor cortex after correcting for the false discovery rate, among males, but not females. In addition, functional connectivity appeared to mediate an inverse association between DAPs and working memory accuracy among males. CONCLUSION: In CHAMACOS, a secondary analysis showed that adolescent males with elevated childhood OP pesticide exposure may have altered brain regional connectivity. This altered neurofunctional pattern in males may partially mediate working memory impairment associated with childhood DAP exposure.
Subject(s)
Memory, Short-Term , Pesticides , Prenatal Exposure Delayed Effects , Humans , Female , Adolescent , Male , Memory, Short-Term/drug effects , Pesticides/toxicity , Pesticides/adverse effects , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , Longitudinal Studies , Brain/drug effects , Brain/diagnostic imaging , Spectroscopy, Near-Infrared , Child, Preschool , Infant , Young Adult , Organophosphorus Compounds/urine , Organophosphorus Compounds/toxicity , Organophosphorus Compounds/adverse effects , Organophosphates/toxicity , Organophosphates/adverse effects , Organophosphates/urine , Environmental Exposure/adverse effectsABSTRACT
BACKGROUND: Prenatal and early-life exposure to polybrominated diphenyl ethers (PBDEs) is associated with detrimental and irreversible neurodevelopmental health outcomes during childhood. Breastfeeding may be a child's largest sustained exposure to PBDE- potentially exacerbating their risk for adverse neurodevelopment outcomes. However, breastfeeding has also been associated with positive neurodevelopment. Our study investigates if breastfeeding mitigates or exacerbates the known adverse effects of prenatal exposure to PBDEs and child neurodevelopment. METHODS: Participants included 321 mother-infant dyads from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a longitudinal birth cohort in California. PBDE concentrations were measured in maternal serum blood samples collected during pregnancy or at delivery. Using generalized estimated equations (GEE), we estimated associations of PBDE concentrations with children's attention, executive function, and cognitive scores assessed longitudinally between 7 and 12 years of age, stratified by duration of exclusive and complementary breastfeeding. RESULTS: We observed that higher maternal prenatal PBDE concentrations were associated with poorer executive function among children who were complementary breastfed for a shorter duration compared to children breastfed for a longer duration; preservative errors (ß for 10-fold increase in complementary breastfeeding <7 months = -6.6; 95 % Confidence Interval (CI): -11.4, -1.8; ß ≥ 7 months = -5.1; 95 % CI: -10.2, 0.1) and global executive composition (ß for 10-fold increase <7 months = 4.3; 95 % CI: 0.4, 8.2; ß for 10-fold increase ≥7 months = 0.6; 95 % CI: -2.8, 3.9). CONCLUSIONS: Prolonged breastfeeding does not exacerbate but may mitigate some previously observed negative associations of prenatal PBDE exposure and child neurodevelopment.