Pesticide Exposure and Neurodevelopmental Outcomes

Pesticides remain indispensable for crop protection yet pose a recognised threat to early brain development. Broadly categorised into organophosphates, pyrethroids and neonicotinoids, these compounds may traverse the placental barrier or reach infants through lactation and contaminated food, water or air. Mechanistically, acute organophosphate exposure inhibits acetylcholinesterase, leading to cholinergic overstimulation, whereas pyrethroids alter voltage‐gated sodium channels and neonicotinoids target nicotinic acetylcholine receptors. Chronic low‐level exposure has been linked with oxidative stress, endocrine disruption and subtle alterations in synaptic formation. Epidemiological studies increasingly document associations between prenatal or early‐life pesticide burdens and deficits in cognitive function, motor skills and attention, as well as elevated risks of autism spectrum disorders and behavioural disorders. Critical windows in the first and second trimesters appear particularly sensitive. Advances in biomonitoring and physiologically based kinetic modelling enable improved dose–response forecasting and the identification of susceptible subpopulations. The global burden of disease from neurodevelopmental impairment underscores the need for harmonised exposure limits, improved agricultural practices and translational research to inform public health policy.

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Pesticide Exposure and Neurodevelopmental Outcomes publication trend

The graph below shows the total number of articles in pesticide exposure and neurodevelopmental outcomes across all publications each year (not limited to Nature Index journals).

Technical terms

Organophosphate pesticide: Compound that inhibits acetylcholinesterase, affecting cholinergic neurotransmission.

Pyrethroid pesticide: Synthetic derivative of natural pyrethrin that modifies sodium channel gating in nerves.

Neonicotinoid pesticide: Insecticide class acting on nicotinic acetylcholine receptors, with potential off‐target effects in mammals.

Physiologically based kinetic (PBK) modelling: Computational framework that simulates absorption, distribution, metabolism and excretion of chemicals in living organisms.

Acetylcholinesterase (AChE): Enzyme that terminates cholinergic signalling by hydrolysing acetylcholine at synapses.

References

1. Acetylcholinesterase Inhibition in Rats and Humans Following Acute Fenitrothion Exposure Predicted by Physiologically Based Kinetic Modeling-Facilitated Quantitative In Vitro to In Vivo Extrapolation. Environmental Science and Technology (2023).
2. Pyrethroid pesticides: An overview on classification, toxicological assessment and monitoring. Journal of Hazardous Materials Advances (2023).
3. Association of Prenatal Exposure to Organophosphate, Pyrethroid, and Neonicotinoid Insecticides with Child Neurodevelopment at 2 Years of Age: A Prospective Cohort Study. Environmental Health Perspectives (2023).