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Prenatal and early-life exposure to micro- and nanoplastics and autism-relevant neurodevelopment: An integrated review of human, experimental, and mechanistic evidence
Summary
Tiny plastic particles called micro- and nanoplastics have been found in the placenta, breastmilk, and other tissues linked to pregnancy and infancy, meaning babies may be exposed before they're even born. This review pulls together animal studies and lab research suggesting these particles could affect brain development in ways connected to autism—like changes in social behavior—likely by triggering inflammation, oxidative stress, and disruptions to gut-brain communication. The evidence is still early and mostly from animal studies rather than direct proof in humans, but it highlights an important area for future research given how common plastic exposure is in daily life.
Autism is a neurodevelopmental condition with increasing global prevalence. Human brain development is particularly vulnerable to environmental perturbations during prenatal and early life, when exposures can alter cellular organization, tissue development, and neural function. Micro- and nanoplastics (MNPs) are emerging environmental contaminants that are ubiquitous in air, water, and food, raising concern due to their potential for chronic, low-level exposure. Their small size may enable MNPs to cross physiological barriers, including the placenta and, potentially, the developing blood-brain barrier. Despite this biological plausibility, evidence linking early-life MNP exposure to autism-related neurodevelopment remains fragmented. This review synthesizes evidence from human biomonitoring studies, experimental neurobehavioral findings, and mechanistic investigations within an autism-focused framework. MNPs have been detected in the placenta, amniotic fluid, meconium, umbilical cord blood, and breastmilk, indicating prenatal and early-life exposure. Detected particles were predominantly polyethylene and polypropylene and were primarily in the micrometer to submicron size range. In rodent models, early-life exposure to MNPs has been associated with autism-relevant behavioral alterations, including deficits in social interaction, often accompanied by increased repetitive behaviors. Fish models showed alterations in early-life locomotor activity but have limited capacity to assess complex social behaviors. Mechanistic evidence implicates convergent pathways, including immune and inflammatory responses, oxidative stress, altered neurotransmitter signaling, and gut-brain axis processes. By organizing exposure characteristics, behavioral phenotypes, and biological pathways in relation to autism-relevant neurodevelopment, this review moves beyond general neurotoxicity paradigms and offers a framework to inform autism-focused epidemiologic research and assessment of MNP-related neurodevelopmental effects.