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Early-life exposure to polypropylene microplastics and DEHP induces ASD-relevant neurodevelopmental alterations involving mTOR-regulated autophagy impairment
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Young mice exposed to two common plastic-related chemicals, tiny polypropylene microplastic particles (found in food packaging) and DEHP (a plastic softener), developed autism-like behaviors, including less social interaction and more anxiety, along with brain changes affecting genes linked to autism. Scientists traced this to a cellular pathway that disrupts the brain's "cleanup system," and were able to reverse the effects using a drug that restores this process, suggesting a possible target for future prevention or treatment. While this study was done in mice, not humans, it raises real concerns given that infants and young children are estimated to ing
The health risks of polypropylene plastic, a major food-grade polymer, are often underestimated. Current evidence indicates that infants and young children may ingest millions of polypropylene microplastic particles (PP-MPs) daily, accompanied by co-exposure to di(2-ethylhexyl) phthalate (DEHP). However, the neurotoxic effects of such co-exposure, particularly the underlying molecular mechanisms, remain poorly understood. Here, we established an early-life exposure model by orally administering PP-MPs and/or DEHP to 3-week-old male ICR mice for 28 consecutive days. Based on assessments of neurobehavior, histopathology and representative biomarkers, we found that PP-MPs and/or DEHP exposure caused autism spectrum disorder (ASD)-relevant neurodevelopmental alterations in immature mice, including deficits in spontaneous exploration and social interaction, increased anxiety-like behaviors, neuronal and synaptic damage in the prefrontal cortex, and downregulated expression of the ASD-risk genes Shank3 and Nlgn1. Proteomic analyses of the brain identified the mTOR signaling pathway as a key mechanism involved in the ASD-relevant neurodevelopmental alterations resulting from PP-MPs and/or DEHP exposure. Further quantitative analyses demonstrated activation of the mTOR signaling pathway, coupled with autophagic impairment and dysregulated expression of genes linked to synaptic plasticity following exposure. Notably, inhibiting the mTOR signaling pathway with rapamycin restored autophagic activity and ameliorated the ASD-relevant neurodevelopmental alterations induced by PP-MPs and/or DEHP. Collectively, these findings suggest that mTOR-regulated autophagic impairment may underlie the neurodevelopmental toxicity caused by early-life exposure to PP-MPs and DEHP, providing a theoretical basis for risk assessment and health protection strategies against neurodevelopmental hazards posed by plastic consumer products during early life.
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Early-life exposure to polystyrene nanoplastics at ambient doses induces neurotoxicity via mTOR-mediated autophagy-lysosomal dysfunction and proteostasis imbalance
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Researchers exposed young mice to environmentally relevant doses of polystyrene nanoplastics and found that the particles penetrated their brains and caused behavioral and emotional disorders. The study identified a specific molecular mechanism in which nanoplastics disrupted the mTOR signaling pathway, leading to lysosomal dysfunction and a buildup of misfolded proteins that ultimately caused neurotoxicity. Treatments targeting these pathways were able to alleviate the harmful effects, suggesting potential avenues for intervention.
Prenatal and early-life exposure to micro- and nanoplastics and autism-relevant neurodevelopment: An integrated review of human, experimental, and mechanistic evidence
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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.
Pre/post-natal exposure to microplastic as a potential risk factor for autism spectrum disorder
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Researchers investigated whether microplastic exposure could be a risk factor for autism spectrum disorder by testing the effects of polyethylene particles on mice at different life stages. They found that microplastics accumulated in the brain and that prenatal exposure in particular led to behavioral changes in offspring resembling autistic traits. The study suggests a possible link between early microplastic exposure and neurodevelopmental effects, though more research is needed to understand the relevance to humans.
Early clues and molecular mechanism involved in neurodegenerative diseases induced in immature mice by combined exposure to polypropylene microplastics and DEHP
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Researchers exposed young mice to polypropylene microplastics combined with DEHP, a chemical commonly found in plastics, and observed significant brain damage including memory problems and damage to the hippocampus. The combined exposure was worse than either substance alone, showing additive or synergistic toxic effects on the developing brain. This is particularly concerning for young children, who are most commonly exposed to polypropylene products and may be more vulnerable to these neurotoxic effects.
Single-cell and metabolomic profiling reveals brain cellular and metabolic disruptions in pregnant mice exposed to micro- and nanoplastics.
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In pregnant mice, tiny plastic particles crossed into the developing brain, damaging blood vessel protection, triggering inflammation, and disrupting important brain chemistry, patterns similar to those seen in Alzheimer's disease. While this is animal research, it raises real concerns about whether plastic exposure during pregnancy could affect a baby's brain development in humans too.
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