Summary: A new study provides the strongest evidence yet that prenatal exposure to the insecticide chlorpyrifos (CPF) disrupts brain development, leaving children with structural abnormalities and impaired motor control well into adolescence. Using brain imaging and behavioral assessments of over 270 New York City children, researchers found that higher CPF exposure levels were directly linked to widespread changes in brain structure, function, and metabolism.
The findings are especially concerning because CPF remains widely used in agriculture, meaning farmworkers, pregnant women, and their infants remain at risk. Scientists warn that other organophosphate pesticides may have similar long-lasting effects on developing brains.
Key Facts
- Prenatal Risks: Exposure to CPF in the womb caused widespread brain abnormalities and poorer fine motor function in children.
- Persistent Exposure: Although banned indoors since 2001, CPF is still used on non-organic produce, keeping agricultural workers and families at risk.
- Public Health Warning: Researchers stress monitoring exposure in pregnant women and caution against organophosphate pesticide use during early brain development.
Source: Columbia University
A new study reports evidence of a link between prenatal exposure to the widely used insecticide chlorpyrifos (CPF) and structural abnormalities in the brain and poorer motor function in New York City children and adolescents.
The findings are the first to demonstrate enduring and widespread molecular, cellular, and metabolic effects in the brain, as well as poorer fine motor control among youth with prenatal exposure to the insecticide.
The study by researchers at Columbia University Mailman School of Public Health, Children’s Hospital Los Angeles, and Keck School of Medicine of USC is published in the journal JAMA Neurology.
The 270 children and adolescents are participants in the Columbia Center for Children’s Environmental Health birth cohort study and were born to Latino and African-American mothers. They had measurable quantities of CPF in their umbilical cord blood and were assessed by brain imaging and behavioral tests between the ages of 6 and 14 years.
Progressively higher insecticide exposure levels were significantly associated with progressively greater alterations in brain structure, function, and metabolism, as well as poorer measures of motor speed and motor programming.
Links between higher CPF and greater anomalies across different neuroimaging measures suggest that prenatal exposure produces enduring disturbances in brain structure, function, and metabolism in direct proportion to the level of exposure.
Residential use was the primary source of CPF exposure in this cohort. Although the EPA banned indoor residential use in 2001, agricultural use continues for non-organic fruits, vegetables, and grains, contributing to toxic exposures carried by outdoor air and dust near agricultural areas.
“Current widespread exposures, at levels comparable to those experienced in this sample, continue to place farm workers, pregnant women, and unborn children in harm’s way.
“It is vitally important that we continue to monitor the levels of exposure in potentially vulnerable populations, especially in pregnant women in agricultural communities, as their infants continue to be at risk,” said Virginia Rauh, ScD, senior author on the study and the Jane and Alan Batkin Professor of Population and Family Health at Columbia Mailman School.
“The disturbances in brain tissue and metabolism that we observed with prenatal exposure to this one pesticide were remarkably widespread throughout the brain.
“Other organophosphate pesticides likely produce similar effects, warranting caution to minimize exposures in pregnancy, infancy, and early childhood, when brain development is rapid and especially vulnerable to these toxic chemicals,” says first author Bradley Peterson, MD, Vice Chair for Research and Chief of Child & Adolescent Psychiatry in the Department of Psychiatry at at the Keck School of Medicine of USC.
Additional co-authors include Howard Andrews, Wanda Garcia, and Frederica Perera at Columbia Mailman; Sahar Delavari, Ravi Bansal, Siddhant Sawardekar, and Chaitanya Gupte at the Institute for the Developing Mind, Children’s Hospital Los Angeles; and Lori A. Hoepner at SUNY Downstate School of Public Health, Brooklyn, New York.
Funding: This study was supported by National Institute of Environmental Health Sciences (grants ES09600, ES015905, ES015579, DA027100, ES08977, ES009089); U.S. Environmental Protection Agency STAR (grants RD834509, RD832141, R827027); National Institute of Mental Health (grants MH068318, K02-74677); and the John and Wendy Neu Family Foundation.
The study was also supported by an anonymous donor, Patrice and Mike Harmon, the Inspirit Fund, and the Robert Coury family.
Peterson is President of Evolve Psychiatry Professional Corporation and an advisor to Evolve Adolescent Behavioral Health, for which he receives stock options, and he provides expert testimony.
Peterson and Bansal have a U.S. Patent (Number 61/424,172), and Peterson holds two additional U.S. Patents (61/601,772 and 8,143,890B2). All other authors have declared that they have no competing or potential conflicts of interest.
About this neurodevelopment research news
Author: Timothy Paul
Source: Columbia University
Contact: Timothy Paul – Columbia University
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Brain Abnormalities in Children Exposed Prenatally to the Pesticide Chlorpyrifos” by Virginia Rauh et al. JAMA Neurology
Abstract
Brain Abnormalities in Children Exposed Prenatally to the Pesticide Chlorpyrifos
Importance
Chlorpyrifos (CPF) is one of the most widely used insecticides throughout the world. Preclinical and clinical studies have suggested that prenatal CPF exposure is neurotoxic, but its effects on the human brain are unknown.
Objective
To identify the associations of prenatal CPF exposure with brain structure, function, and metabolism in school-aged children.
Design, Setting, and Participants
This prospective, longitudinal pregnancy cohort study was conducted from January 1998 to July 2015, with data analysis from February 2018 to November 2024 in a community in northern Manhattan and South Bronx, New York. Of 727 pregnant women of African American or Dominican descent in the original community cohort, 512 had CPF levels measured at delivery. Offspring 6 years and older were approached for magnetic resonance imaging (MRI) scanning.
Exposure
Prenatal CPF exposure.
Main Outcomes and Measures
Anatomical MRI measures of cortical thickness and local white matter volumes, diffusion tensor imaging indices of tissue microstructure, MR spectroscopy indices of neuronal density, arterial spin labeling measures of regional cerebral blood flow, and cognitive performance measures.
Prespecified hypotheses before data collection included CPF-related structural abnormalities in frontotemporal cortices, basal ganglia, and white matter pathways interconnecting them, and reduced neuronal density.
Results
Participants included 270 youths (123 boys and 147 girls) aged 6.0 to 14.7 years (mean [SD] age, 10.38 [1.12] years) with self-identified Dominican or African American mothers.
Progressively higher prenatal CPF exposure levels associated significantly in childhood with progressively thicker frontal, temporal, and posteroinferior cortices; reduced white matter volumes in the same regions; higher fractional anisotropy and lower diffusivity in internal capsule white matter; lower regional blood flow throughout the brain; lower indices of neuronal density in deep white matter tracts; and poorer performance on fine motor (β, −0.30; t261 = −5.0; P < .001) and motor programming (β, −0.27; t261 = −4.36; P < .001) tasks.
Conclusions and Relevance
Prenatal CPF exposure was associated with altered differentiation of neuronal tissue into cortical gray and white matter, increased myelination of the internal capsule, poorer motor performance, and profoundly impaired neuronal metabolism throughout the brain.
CPF is known to increase oxidative stress and inflammation and in turn impair mitochondrial functioning, neuronal development, and maturation of the oligodendrocyte precursor cells responsible for axonal myelination. These molecular and cellular effects of CPF likely account at least in part for the observed associations of CPF with poorer long-term brain and motor outcomes.
