Plastics Reach the Placenta and the Developing Brain, Review Warns

Micro- and nanoplastics have become one of the most pervasive contaminants of the modern world, and a new narrative review published in Pediatric Research argues that the youngest members of the human population may be carrying them from before birth. The review, authored by Saheli Chatterjee Misra of PKG Medical College and Hospital in Kolkata and Kaushik Mukhopadhyay of AIIMS Kalyani, synthesizes evidence from animal models, human biomonitoring studies, and mechanistic laboratory work to build a picture of how these particles travel through the body during pregnancy and early childhood, and what they might be doing to the developing brain. The authors conclude that children are exposed to micro- and nanoplastics during critical developmental windows and that biologically plausible mechanisms exist linking such exposure to adverse neurodevelopmental outcomes, while stressing that causality in humans has not yet been established.

The scale of the exposure problem is striking. Human studies have now detected microplastics in the placenta, in amniotic fluid, in umbilical cord blood, in infant feces, and in breast milk. The landmark 2021 study that first identified microplastic fragments in human placentas, dubbed by its authors with the memorable term Plasticenta, has been followed by work showing that the particles can reside within the intracellular compartment of placental tissue. Researchers have also reported microplastics and plastic additives in the amniotic fluid of pregnancies, including cases of preterm birth, and in maternal blood and umbilical vein blood, findings that together support the idea of transplacental transfer as a genuine exposure route rather than a laboratory curiosity. Ex vivo perfusion experiments using human placental tissue have demonstrated bidirectional transfer of polystyrene nanoparticles across the placental barrier, and advanced three-dimensional in vitro models of the placental barrier have shown that nanoparticles can cross this interface and alter trophoblast function.

Once born, infants face a distinct and arguably heavier set of exposures. Polypropylene feeding bottles release microplastic particles during formula preparation, steam disinfection liberates micro- and nanoplastics from silicone-rubber baby teats, and breastmilk storage bags shed particles into expressed milk. Infant formula itself has been found to contain microplastics, as have toy building bricks, personal care products, and wet wipes. Indoor environments add another layer: house dust carries synthetic fibers, atmospheric fallout deposits microplastics on surfaces, and studies of particle resuspension dynamics show that infants crawling and playing near the floor inhabit a microenvironment with elevated exposure to resuspended particles. Frequent hand-to-mouth behavior, a hallmark of early childhood, amplifies nondietary ingestion of everything that settles on small hands. The review emphasizes that this combination of high relative exposure and developmental susceptibility is what makes fetuses, infants, and young children a uniquely vulnerable population.

The mechanistic case rests on what these particles do once they cross biological barriers. Experimental evidence indicates that nanoplastics, in particular, can penetrate epithelial and endothelial linings and accumulate in tissues. Studies in mice have documented tissue accumulation of polystyrene microplastics, and research on deceased humans has found bioaccumulation of microplastics in brain tissue and in blood, demonstrating that these particles are not merely passing through the body. At the cellular level, the review identifies several converging mechanisms of harm: oxidative stress driven by reactive oxygen species, chronic inflammation, endocrine disruption from plastic additives such as bisphenols and phthalates, and altered neurotransmitter signaling. Cell culture work with human cerebral and epithelial cells has shown cytotoxic effects from commonly used micro- and nanoplastics, and human pluripotent stem cell-derived cortical spheroids, a laboratory model of the developing human cortex, show disturbed neural development when exposed to microplastics.

Animal studies provide the most consistent evidence of neurodevelopmental effects. In rodents, maternal exposure to polystyrene nanoplastics has been associated with structural brain abnormalities in offspring, altered developmental milestones, and impaired hippocampus-dependent learning and memory. One study reported selective bioaccumulation of polystyrene nanoplastics in the fetal rat brain with damage to myelin development, while another found that co-exposure to polystyrene micro- and nanoparticles injured the fetal thalamus by inducing reactive oxygen species-mediated apoptosis. Maternal nanopolystyrene exposure has been shown to trigger neurotoxicity in the rat hippocampus through P53-mediated ferritinophagy and ferroptosis, a form of iron-dependent cell death. Neonatal exposure to polystyrene nanoplastics in mice impaired microglia-mediated synaptic pruning, the essential developmental process by which excess synapses are eliminated, and produced social behavioral defects that persisted into adulthood. Lifelong exposure studies have even induced ADHD-like phenotypes and accelerated brain aging in mice, and long-term polystyrene exposure has been linked to exacerbation of seizure symptoms.

Aquatic models add breadth to this picture. Zebrafish larvae exposed to polypropylene microplastics show behavioral impairments and disrupted mitochondrial energy metabolism, while photoaged polystyrene microplastics, particles degraded by ultraviolet light, produce neurotoxicity associated with altered neurotransmission in zebrafish. Work in the nematode Caenorhabditis elegans has shown that photoaged microplastics damage serotonergic, glutamatergic, dopaminergic, and GABAergic neuronal systems, the four major chemical signaling systems of the nervous system. Microplastics have also been shown to alter neurogenesis and DNA methyltransferase activity in early-life zebrafish, suggesting that these particles may interfere with both the generation of new neurons and the epigenetic programs that regulate brain development. The consistency of structural and behavioral findings across species, exposure routes, and polymer types is what lends the animal literature its weight, even as the authors caution that doses in laboratory studies often exceed measured human exposures.

The endocrine dimension deserves particular attention because plastic is never chemically inert. Plastic polymers carry additives, including bisphenols and phthalates, that are recognized endocrine-disrupting compounds capable of interfering with hormone signaling during development. Studies in children have reported altered bisphenol A and phthalate metabolism in those with neurodevelopmental disorders, and elevated serum phthalate and bisphenol A concentrations have been documented in children with autism spectrum disorder, though such associations do not prove causation. Animal work supports the plausibility of these links: perinatal bisphenol A exposure produces anxiety-like behavior in mice associated with a decreased ratio of excitatory to inhibitory synaptic density in the male brain, and gestational and lactational phthalate exposure increases neurobehavioral perturbations across multiple generations of rats. Because the first thousand days of life represent a period of exquisite hormonal sensitivity for brain wiring, the review argues that endocrine disruption provides a coherent pathway by which plastic particles and their chemical passengers could shape neurodevelopment.

Human epidemiological data are only beginning to emerge, but the first signals are noteworthy. Recent studies of primary school children have measured urinary microplastic markers and examined their relationship to behavioral and cognitive outcomes. One study found associations between urinary microplastic contaminants and behavioral development measures in children, and a companion study reported associations with cognitive function. The review treats these findings as preliminary and explicitly states that causality remains unestablished, noting that urinary biomarkers capture only a fraction of the total body burden and that confounding factors in observational pediatric studies are difficult to fully control. Nevertheless, the existence of measurable exposure biomarkers in children, combined with consistent animal evidence and plausible mechanisms, creates what the authors describe as a pressing rationale for rigorous longitudinal research.

Advances in analytical chemistry underpin much of this progress and much of the remaining uncertainty. Micro-Fourier-transform infrared spectroscopy and Raman spectroscopy allow researchers to identify and characterize microplastic particles in biological samples, while pyrolysis-gas chromatography-mass spectrometry enables simultaneous trace identification and quantification of common polymer types. Newer techniques include flow cytometry-based separation and analysis of micro- and nanoplastics, mass spectrometry imaging of particles in living organisms, and fluorescent staining methods such as Nile Red for detecting small microplastics in the one micrometer to twenty micrometer range. The review highlights the urgent need for standardized detection methods, because differences in sampling, digestion, and analytical protocols currently make it difficult to compare results across laboratories and to build the child-specific dose-response data that formal risk assessment requires.

The authors frame their conclusions as a call to action rather than an alarm. Current evidence, they write, indicates that children are exposed to micro- and nanoplastics during critical developmental windows, with biologically plausible mechanisms linking exposure to adverse neurodevelopmental outcomes, but longitudinal human studies and child-specific dose-response data are urgently needed before firm causal claims or regulatory thresholds can be established. Early research into interventions, including studies suggesting that ingesting chitosan can promote excretion of microplastics and that probiotic bacteria can degrade bisphenol A, hints at possible mitigation strategies, but these remain far from clinical application. What the review makes clear is that the exposure begins earlier than most people assume, in the placenta itself, and continues through the bottles, teats, dust, and air of infancy. Protecting children from micro- and nanoplastic toxicity, the authors conclude, represents a public health priority for future generations, one that will require standardized measurement, long-term cohort studies, and a willingness to act on precaution while the science matures.

Subject of Research: Micro- and nanoplastic exposure in children from placental transfer to neurodevelopmental outcomes

Article Title: Micro- and nanoplastics in pediatric health: from placental transfer to neurodevelopmental outcomes

Article References: Misra, S. C., & Mukhopadhyay, K. (2026). Micro- and nanoplastics in pediatric health: from placental transfer to neurodevelopmental outcomes. Pediatric Research. https://doi.org/10.1038/s41390-026-05419-0

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05419-0

Keywords: microplastics, nanoplastics, pediatric health, placental transfer, neurodevelopment, endocrine disruption, oxidative stress, children's exposure, biomonitoring, public health, plastic additives, risk assessment