A major study reveals that prenatal exposure to chlorpyrifos, formerly widely used in houses and farms, can have lasting effects on the brain of children, from metabolism disturbed to lower motor skills.
Study: Brain anomalies in children exposed prenattlely in pesticide chlorpyrifos. Image credit: Hedgehog94 / Shutterstock.com
And Jama neurologies The study used a sample of school -aged children to examine associations between prenatal exposure to ChlorPyrifos (CPF) and brain anomalies. Exposure to the CPF during prenatal development was associated with changes in the differentiation of neuronal tissue, increased myelinization of the internal capsule, a fine motor speed and motor programming skills and a motor programming program and considerably disrupted regional blood flow and neural metabolism located throughout the brain.
Exhibition in chlorpyrifos and brain development
The CPF is a very common insecticide used worldwide, so it is generally everywhere, including in grains, vegetables and non -biological fruits, as well as in air and dust. In the New York cohort of this study, prenatal exposure is largely from interior residential spraying before its 2001 American residential ban. In pregnant women, it was found to cross the placenta and reach the fetal brain. In rodent models, prenatal and neonatal exposure on the CPF had a negative impact on the brain, hinders the generation of neurons and Glia and interfere with neuronal differentiation. Early exposure to CPF is more toxic to glial cells than neurons.
The undesirable effects of exposure to the CPF could be mediated at the molecular level, including neuroinflammation, oxidative stress, altered neurotrophins and altered mitochondrial function. Research using rodent models has shown that these molecular effects lead to motor hyperactivity, learning and memory of behaviors and behaviors in adulthood resembling anxiety and depression.
Prenatal exposure to CPF in humans has been linked to lower fetal growth, lower birth weight, smaller head size, abnormal newborns and other disorders. The preclinical and clinical research carried out so far has highlighted the neurotoxicity of prenatal exposure on the CPF, but its effects on the human brain are unknown.
About the study
This prospective study of a longitudinal pregnancy cohort examined the impact of the prenatal exposure of the CPF on the metabolism, the structure and the function of the brain of offspring in the midst of childhood. The study was carried out between January 1998 and July 2015 in pregnant women (n = 727) of African-American or Dominican origin aged 18 to 35.
During pregnancy, women filled questionnaires and self-identified their race and ethnicity. These data were collected to assess the representativeness of the sample. In a postpartum day, the maternal blood was taken and the blood of the umbilical cord was also obtained at childbirth; The plasma levels of the CPF of one or the other source have been measured. Of the 727 original women, 512 had measured CPF levels and MRI analyzes were carried out on 270 children aged 6 to 14.
The cortical thickness and the local volumes of the white substance on the brain surface were evaluated using anatomical MRI measurements. The management and the water diffusion rate have been evaluated by imaging of the diffusion tensor (DTI). Fractionary anisotropy (FA) in DTI has represented the directional preference for diffusion, and the average diffusion rate on three space directions was represented using the average diffusion coefficient (ADC).
In addition, the regional brain blood flow (RCBF) was measured using the marking of arterial spin (ASL), and cerebral metabolite concentrations were measured using spectroscopic imaging by magnetic resonance (MRSI).
Study results
A positive association was observed between the prenatal exposure of the CPF and the cortical thickness in the frontal, temporal and posteroid regions. An inverse association was noted between exposure to the CPF and the cortical thickness in the dorsal parietal region. With regard to the local volumes of the white substance in the front, temporal and displayed regions, an inverse association was noted with exposure to the CPF.
Exposure to the CPF is inversely associated with the ADC and associated positively with FA values in the internal capsule (CI). This was particularly true for previous members of the IC and goig for FA, and for the previous member, the gent and the posterior limb for the ADC. The long axis of IC fiber bundles has shown reduced diffusion in the radial and axial directions, contributing to lower ADC values. In most brain regions, there was a reverse association between the prenatal exposure of the CPF and the RCBF values.
The concentration of N-ACYLL-ASPARTATE (NAA), an index of density of healthy neurons, was measured using Mrsi. In the leaflets of the deep white substance and the gray matter of the island cortex, the NAA was inversely associated with exposure to the CPF. The results of other metabolites were rare. A positive association was found between the concentrations of CPF and glutamate / glutamine (GLX) in the anterior cingular cortex, after having normalized the concentrations of metabolites in creatine. The association between CPF and MRI measures in any modality has not been significantly moderated by age or gender.
Regarding behavioral results, a significant inverse association was noted between CPF values and the speed of the fine engine and the engine programming between both hands. The effects were disproportionate in the non -dominant hand for motor programming.
Conclusions
Prenatal exposure on the CPF was associated with higher myelinization of the internal capsule, a modified differentiation of the neuronal fabric in white and cortical gray matters and with engine programming and lower fine engine. Generalized reductions in brain blood flow and dispersed and localized reductions in neuronal density (NAA) suggest a metabolic disturbance. Some of the associations observed are taken into account by the molecular and cellular effects of the CPF, including oxidative stress, inflammation, altered mitochondrial functioning and the deregulation of oligodendrocytes.
A key limitation of this study is the lack of generalization of the results, because the sample was made up of Dominican and Urban African American women. There could have been selection bias concerning cohorts could be contacted and who agreed to participate in an MRI. In addition, the postnatal exposure of the CPF and exposure to other insecticides were not taken into account and could have influenced the results.
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