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Early-Life Environmental Pollutants and Neurodevelopmental Risks: Unraveling Exposure Pathways, Mechanisms, and Preventive Strategies
Summary
This review synthesizes evidence from 112 studies on how early-life exposure to pollutants such as lead, fine particulate matter, and phthalates disrupts neurodevelopment in children by impairing the blood-brain barrier, altering dopamine and thyroid signaling, and inducing epigenetic changes linked to ASD and ADHD, while calling for multi-omics longitudinal research and stronger regulatory action.
Exposure to environmental pollutants in early life represents a main modifiable risk factor for neurodevelopmental disorders of infants and children including ASD/ADHD. In this review, we integrate evidence from 112 studies (2015-2025) on pathways involving maternal-fetal transfer, inhalation of airborne pollutants, household contact and neuro-disrupting mechanisms underlying childhood neurodevelopment. Early-life exposure to lead, fine particulate matter, and phthalates disrupts the blood-brain barrier, triggering neuroinflammatory responses and oxidative damage by disrupting thyroxine action, dopamine regulation and epigenetics; potentiated each other's effects, further amplifying the hazards of cognizance or behavioral deficits. Despite progress made, conflicts regarding low dose results and socio-economic status are ubiquitous. Decreasing plastic use, upholding pollution-control acts, promoting labeling-endocrine disruptor free products could attenuate such risks. Further works should combine multiple omics approaches and adopt longitudinal methods to uncover sensitive pathways through which pollutants act via geno-epigenetic actions, thereby tailoring evidentiary-based policies to foster early-life neural development.