Neurobehavioral Consequences of Exposure to Organophosphorus Compounds

Organophosphorus compounds (OPs) were initially chemically which synthesized in the early 20th century as nerve agents; however, their high pesticide potency soon led to widespread use in agriculture and industry. Though their acute neurotoxicity via acetylcholinesterase (AChE) inhibition is well established, increasingly, evidence from epidemiological, experimental, and molecular studies suggests that chronic low-dose exposure—particularly during critical windows of neurodevelopment—can result in long-term neurobehavioral and cognitive impairment. This overview incorporates findings on the multifactorial mechanisms of OPs toxicity, including oxidative stress, mitochondrial dysfunction, inflammation, and epigenetic regulation. Particular emphasis is placed on the impact of maternal exposure to OPs during gestation on offspring neurodevelopmental trajectories. Animal models, such as rodents, zebrafish, and non-human primates, provide crucial information on OP-induced deficits in accordance with human epidemiological data, such as impairments in cognitive functions—including learning abilities, increased ADHD symptoms, and increased autism spectrum disorder rates. The results of this study highlight the need for further research to clarify the neurobehavioral effects of these compounds, with particular emphasis on evidence from experimental animal models.