A study by researchers at Columbia University Mailman School of Public Health, Children’s Hospital Los Angeles, and Keck School of Medicine has found evidence of a link between prenatal exposure to the widely used insecticide chlorpyrifos (CPF), structural abnormalities in the brain, and poorer motor function in New York City children and adolescents.
Findings from the prospective longitudinal birth cohort study, which analyzed imaging data from hundreds of participants aged six to 14 years, 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.
First authors Bradley S. Peterson, MD, Sahar Delavari, MD, and colleagues reported on their findings in JAMA Neurology, in a paper titled “Brain Abnormalities in Children Exposed Prenatally to the Pesticide Chlorpyrifos,” in which they stated, “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.”
Chlorpyrifos (CPF) is one of the most widely used insecticides globally, and is commonly used for agricultural purposes in the U.S. As a result, the authors commented, “CPF is nearly ubiquitous in nonorganic fruits, vegetables, and grains and in outdoor air and dust samples near agricultural areas.” Preclinical and clinical studies have suggested that prenatal CPF exposure is neurotoxic, they noted, although its effects on the human brain are unknown.
CPF can enter the bloodstream through ingestion, inhalation, or skin contact, the authors explained, and in pregnant women, it crosses the placenta to reach the fetal blood stream, from where it can cross the fetal blood-brain barrier to enter the brain. Studies in rodents have found that the molecular and cellular effects of prenatal exposure to subtoxic doses of CPF result in learning and memory problems, as well as motor hyperactivity, anxiety- and depressive-like behaviors in adulthood. “In humans, prenatal exposures to CPF and other organophosphate pesticides have been associated with fetal growth restriction and smaller head size, lower birth weight, abnormal newborn reflexes, and neurodevelopmental symptoms in toddlers that include autism spectrum disorder, inattention, and lower overall intelligence,” the investigators noted.
Their newly reported study investigated whether prenatal CPF exposure may be associated with brain structure, function, and metabolism in school-aged children. “Based on prior findings that prenatal CPF exposure affects higher-order cognitive processes (intelligence, attention, executive functioning, and socialization), our hypothesis was that prenatal CPF exposure would associate significantly with brain measures in regions that support these capacities—frontal and temporal cortices, basal ganglia, and the white matter pathways that connect them,” they wrote.
The study included 270 children and adolescents who are participants in the Columbia Center for Children’s Environmental Health birth cohort study and were born to Latino and African American mothers. The participants had measurable quantities of CPF in their umbilical cord blood and were assessed by brain imaging and behavioral tests between the ages of six and 14 years. The collective data showed that 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.
The observed link between higher CPF and greater anomalies across different neuroimaging modalities suggests that prenatal exposure produces enduring disturbances in brain structure, function, and metabolism in direct proportion to the level of exposure, the authors suggested. “Prenatal CPF exposure was associated with altered differentiation of neuronal tissue into cortical gray and white matter, increased myelination of the internal capsule, brain-wide impaired metabolism, and poor motor performance that endured into late childhood and early adolescence, likely as a result of CPF-induced oxidative stress and inflammation.”
For this cohort study the primary source of CPF exposure was residential use, and while EPA banned indoor residential use of CPF 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,” noted Virginia Rauh, ScD, senior author on the study and the Jane and Alan Batkin professor of population and family health at Columbia Mailman School. “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.”
“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,” added Peterson, vice chair for research and chief of child & adolescent psychiatry in the department of psychiatry at the Keck School of Medicine of USC.
Noting limitations of the study, in their paper the team further stated, “Because other pesticides also induce oxidative stress and inflammation, minimizing prenatal and early life exposure to these chemicals is likely important for optimal childhood brain development.”
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