Abstract
Microplastics (MPs) pollution represents an increasing worldwide problem and a real global challenge for human health, which also affects unborn children. Specifically, during their degradation, they can release a broad range of toxic and hormonally active agents, such as plasticizers. Thus, microplastics alone are pernicious, but they often also carry other harmful chemicals and even problematic bacteria on their surface and within their structure (heavy metals, pesticides, parabens, etc.), which amplifies their toxic potential. Due to their induction of oxidative damage, inflammation, mitochondrial apoptosis, and microbiota dysbiosis, and more, microplastics act as neurotoxic agents. Periods particularly sensitive to this neurotoxicity include fetal development and childhood, during which microplastics can negatively affect proper neuronal development. When expecting mothers are exposed, microplastics can cross the placenta barrier, reach the developing embryo, and accumulate in its organs. During fetal development, even minor interferences in neuronal migration can result in deficient neuronal innervation in the gut, potentially leading to congenital enteric neuropathy. Although an accurate estimation of human exposure is still pending, this may produce serious intestinal motility disorders and compromise the long-term quality of life of newborns. In this review, we analyze how microplastic neurotoxicity could be an aggravating factor in the development of congenital enteric aganglionosis and, consequently, postnatal motility disorders. Finally, we propose reducing pregnant women’s exposure to microplastics as an important preventive measure to protect the fetus from neurotoxicity.
1 Introduction
1.1 Microplastic exposure: an emerging health problem
During the last decades, global plastic production has grown exponentially (Geyer et al., 2017), resulting in plastic waste reaching all ecosystems (Geyer et al., 2017; Senathirajah et al., 2021). As these plastics reach the end of their life cycle, they degrade under the effects of mechanical erosion, sunlight, air, or water (Julienne et al., 2019) into smaller pieces, classified by size into microplastics (MPs, ranging from 5 mm to 0.1 μm) or nanoplastics (NPs, <0.1 μm). Among these degraded fragments, the most abundant polymer types are polypropylene (PP), polyethylene (PE), polyethylene terephthalate (PET), polystyrene (PS), polycarbonate (PC), poly-(methyl methacrylate) (PMMA), and polyvinyl chloride (PVC) (; Nair et al., 2025). Furthermore, additional plasticizers, such as diethylhexyl-phthalate (DEHP), which are released during the degradation of PVC, have also demonstrated their considerable toxic potential, particularly for the liver (Loff et al., 2000).
Consequently, MPs have, over the years, reached and polluted most ecosystems worldwide () and have already been detected ubiquitously in water, soil, and air (Lu et al., 2025; Nair et al., 2025). Furthermore, MPs have emerged as a significant and pervasive health and environmental problem globally () as they are persistent, toxic, and possess bioaccumulative potential (Weis and Alava, 2023).
Industry, paints, and tire wear, and sewage sludge (Kwiatkowska and Ormaniec, 2024; Thompson et al., 2024) contribute significantly to MPs emissions into the environment (Kole et al., 2017; Paruta et al., 2022). However, MPs can also be found in a wide array of products, including plastic packaging, synthetic textiles (Rovira and Domingo, 2019), seafood (; Vega-Herrera et al., 2024), fruits and vegetables (Oliveri Conti et al., 2020), salt, sugar, tap and bottled water (Panneerselvam et al., 2025), and even cosmetics and personal care products (Guerranti et al., 2019; Sun et al., 2020; ). They also enter the food chain almost inevitably, originating from food packaging, cooking pots, and plastic bottles (; van Raamsdonk et al., 2020). Hence, MPs abundance in the food chain has already been proven by several studies (; Senathirajah et al., 2021; ). Due to their accumulation in the food chain, MPs disrupt the delicate balance of ecosystems and may impair cognitive function and behavioral patterns in living organisms (Lu et al., 2025). As a result, humans are continuously exposed to microplastic-induced toxicity from the environment on a daily basis (Nair et al., 2025).
MPs can enter the human body through various ways, including ingestion, inhalation, and dermal contact with personal care products (; Lu et al., 2025; Panneerselvam et al., 2025). Truly, we are breathing (), eating, and drinking them every day, so they later accumulate in our intestines (Zhu et al., 2024), tissues, and organs (; ; van Raamsdonk et al., 2020; Nihart et al., 2025).
Once they enter the body, MPs show a systematic distribution (), being detected in all human samples, except for kidneys and cerebrospinal fluid (). They have also been isolated in the human respiratory system () and in human stool (Schwabl et al., 2019). MPs can penetrate physiological barriers in humans, such as the placental, blood–brain, and blood–testis barriers (; ; Lu et al., 2025). This barrier transfer depends on MPs characteristics, exposure dose, route, time, co-exposure to other pollutants, and genetic predisposition.
Chronic exposure to MPs has been associated with several organ-specific toxicities, including gastrointestinal toxicity, hepatotoxicity, neurotoxicity, reproductive and developmental toxicities (; ), and, more recently, with carcinogenesis (Gutiérrez-García et al., 2025).
Finally, maternal exposure to MPs has been reported to cause adverse effects on pregnancy outcomes in pregnant mice (Hu et al., 2021) and is related to reproductive toxicity and low growth offspring, also in humans (Luo et al., 2019).
However, an accurate estimation of human exposure is still pending due to the lack of standardized methods for processing and analyzing MPs in human samples (). For instance, most of the research was conducted using mainly polystyrene (PS), but this polymer represents only 7% of total plastic production. In addition, differently sized particles, concentrations, incubation times, and models have been analyzed, complicating the later comparison of results ().
Recently, further controversy has arisen regarding the accuracy of MPs quantification methods, calling into question previous MPs studies on both the environment () and human tissues (Monikh et al., 2025) and consequently sparking a renewed debate on the challenges of achieving precise methodologies (; Thompson et al., 2024; Monikh et al., 2025; ). Nevertheless, efforts are underway to unify protocols and improve methodology in the future (; ; Nardella et al., 2025).
1.2 Microplastics induce neurotoxicity
Although the neurotoxic effects of MPs vary according to individual particle types, shapes, sizes, exposure concentrations, and durations, it is clear that exposure to MPs implicates a neurotoxic risk (see Table 1) (Prüst et al., 2020).
TABLE 1
| Mechanism | References | Associated with | References |
|---|---|---|---|
| ↑Oxidative stress | and Ullah et al. (2023) | Neurodegeneration | Lu et al. (2025) |
| Endocrine disruption | and Panneerselvam et al. (2025) | Neurodevelopmental issues | , , and Singh et al. (2022) |
| Microbiota dysbiosis | , Lee et al. (2024), and Saraluck et al. (2024) | Behavioral | Prüst et al. (2020) |
| Inflammation | Dementia | and Lu et al. (2025) | |
| Inhibition of acetylcholinesterase | Prüst et al. (2020) | ||
| Neurotransmitter disruption | Prüst et al. (2020) | Cognitive | ; Jin et al. (2018), (2019); and Zheng et al. (2024) |
| ↑Autophagia | Lu et al. (2025) | ||
| Mitochondrial disruption | Prüst et al. (2020) | Behavioral | Zheng et al. (2024) |
Overview of MPs neurotoxicity mechanisms.
Ingested MPs can disrupt gut microbiota, breach intestinal and blood–brain barriers, and accumulate in neural tissues through systemic distribution (). Specifically, the disruption of the mucous barrier might present a gateway for bacterial metabolites and toxins, thus adding to the direct effect of the toxic microplastic components a secondary by-stander effect, which severely aggravates their impact.
Mechanistic studies have revealed that MPs induce oxidative stress, leading to cellular damage, neuroinflammation, protein aggregation, alterations in neurotransmitter levels, and inhibition of acetylcholinesterase activity (Prüst et al., 2020). MPs exposure has also been related to mitochondrial injury, inflammatory signaling, and impaired protein homeostasis (Prüst et al., 2020; ). Given this evidence, MPs have been shown to induce neurotoxicity, brain damage, and impaired neuronal development in different animal models (Pahwa and Kalra, 1993; Qu and Wang, 2020; Sökmen et al., 2020; Zheng et al., 2024).
Moreover, ingested MPs appear to increase neurological risk and contribute to the development of cognitive dysfunction and pathways leading to neurodegenerative diseases. Not surprisingly, high MPs burdens in brain tissue have been associated with dementia, neuronal disorders (; Nihart et al., 2025), behavioral alterations, and increasing rates of neurodegenerative diseases (Lu et al., 2025).
On top of that, MPs contain other toxic chemicals within their structure but also adsorb additional toxicants from the environment on their surfaces (), including polychlorinated biphenyls (PCBs), pesticides, heavy metals (Al, Cd, Co, Cr, Cu, Hg, Mn, and Pb), polycyclic aromatic hydrocarbons (PAHs), persistent organic pollutants (POPs), and antibiotics (; Weis and Alava, 2023; Rafa et al., 2024). Some of these contaminants are commonly used as additives in plastic production. As they are not covalently bonded to plastics, they can easily leach into milk, water, and other liquids (Ullah et al., 2023). MPs particles act as solid substrates for various microorganisms, promoting the formation of microbial biofilms with different metabolic activities (Kwiatkowska and Ormaniec, 2024).
As concerning evidence, MPs particles have been detected to leach from medical parenteral nutrition bags used in neonatal intensive care into the administered nutritional solution, from where they may reach the digestive system of the premature parenterally fed neonates but may also cause obstruction and pulmonary inflammation since they exceeded the diameter of lung and tissue capillaries (Vercauteren et al., 2024). Previous studies associated parenteral nutrition in premature neonates with serious hepatobiliary dysfunction (Loff et al., 1998; 1999). Previously, parenteral nutrition was assumed to be responsible for liver damage. Now, MPs leaching into parenteral nutrition circuits have emerged as a plausible cause.
The physicochemical properties of microplastics, such as size, structure, and functional groups, and properties of environmental compartments, such as pH, temperature, and salinity, influence the sorption of pollutants by microplastics (Rafa et al., 2024). Toxicity induced by MPs and NPs is size-dependent as smaller particles have better absorption capacity and larger surface area, releasing more toxic chemicals and endocrine disruptors, leading to oxidative stress, reproductive toxicity, neurotoxicity, cytotoxicity, developmental abnormalities, decreased sperm quality, and immunotoxicity (Ullah et al., 2023).
All these toxic pollutants transported by MPs can bioaccumulate and induce oxidative stress and cellular toxicity (). For instance, phthalates have been linked to various neurotoxic mechanisms, such as endocrine disruption, oxidative stress, and cellular apoptosis (Tseng et al., 2013; Wójtowicz et al., 2017).
Human exposure to metals has also been shown to induce neurotoxicity through various mechanisms such as autophagy (Zhang et al., 2013), synaptic transmission (), oxidative stress (), and alterations in neurotransmitter metabolism (Pohanka, 2014). Regarding metals, even low concentrations of As, Pb, Cd, and Hg during gestation must be considered due to their severe effects on the fetus. In particular, Cd is harmful because when Cd accumulates in the placental tissue, other metals such as As, Cr, Cu, Pb, Mn, Ni, Se, and Zn are, as a consequence, transferred from maternal tissue to the placenta and from there to the fetus, putting the newborn’s life at risk (Serafim et al., 2012) and particularly affecting neurodevelopment (Meyrueix et al., 2019).
Other common additives in MPs, including phthalates, bisphenol A, and parabens (Iribarne-Durán et al., 2022; Mejías et al., 2023), are particularly concerning due to their interference with the neuroendocrine system, which plays a crucial role in regulating physiological functions. Furthermore, studies indicate that when MPs are present alongside these harmful additives, they may exhibit synergistic toxicity, which intensifies the detrimental effects (; Lu et al., 2025).
Thus, MPs can not only trigger neurotoxicity and inflammation but also enhance endocrine disruption (; Kim et al., 2025). Regarding this, we should not forget that pregnancy is a particularly vulnerable period for the potential risks of endocrine disruptors (Leppert et al., 2020).
1.3 Microplastics can cross the placental barrier and accumulate in fetal tissues
MPs have been detected in a variety of human tissues, including ovarian follicular fluid (Montano et al., 2025), maternal blood and urine (Sun et al., 2024), the placenta (; Nair et al., 2025), and even the umbilical cord (see Table 2).
TABLE 2
| Sample | Pollutant | References |
|---|---|---|
| Ovarian follicular fluid | Microplastics | Montano et al. (2025) |
| Placenta | Microplastics | , , , Ragusa et al. (2021), , Kim et al. (2025), and Nair et al. (2025) |
| Metals | ||
| Parabens | Vela-Soria et al. (2017) | |
| Benzophenones | Vela-Soria et al. (2017) | |
| Ammniotic fluid | Microplastics | Sun et al. (2024) |
| Umbilical cord | Microplastics | Sun et al. (2024) |
| Benzophenones | ||
| Maternal urine/blood | Microplastics | and Sun et al. (2024) |
| Benzophenones | Huo et al. (2016) and | |
| Parabens | Leppert et al. (2020) | |
| Breast milk | Microplastics | Liu et al. (2023) and Saraluck et al. (2024) |
| Bisphenol | Iribarne-Durán et al. (2022) | |
| Parabens | Iribarne-Durán et al. (2022) and Zhang et al. (2023) | |
| Benzophenones | Iribarne-Durán et al. (2022) | |
| Meconium | Microplastics | and Liu et al. (2023) |
| Infant feces | Microplastics | Liu et al. (2023) |
Detection of microplastics and their co-adsorbed pollutants in maternal and fetal samples.
MPs have been found in maternal and infant paired samples (), indicating that MPs can cross the placenta and blood–brain barrier, reaching fetal tissues, where they accumulate (; Kim et al., 2025). In addition, other pollutants adsorbed to MPs, such as metals (), parabens, and ultraviolet filters (Vela-Soria et al., 2017), can cross the placental barrier. The detection of MPs in the first neonate feces, known as meconium, provides further evidence that MPs can reach the fetus (; Liu et al., 2023).
In animal experiments, when MPs derived from disposable paper cups (DPCs) were administered to pregnant mice, the particles were later detected in multiple tissues, with preferential accumulation in the fetus, placenta, kidney, spleen, lung, and heart, contributing to impaired phenotypes. A dose-responsive harmful effect on fetal development and maternal physiology was observed ().
Exposure of mated mice to polystyrene nanoplastics (PS-MPs) showed an elevated embryo resorption rate during the peri-implantation period that led to a reduction in the number and diameter of uterine arterioles, which might reduce the uterine blood supply and increase miscarriage risk. In addition, disturbances in immune cell and cytokine secretion were observed (Hu et al., 2021).
Prenatal exposure to toxins may be especially harmful, given that the developing brain is a more susceptible target to toxicity as neurons proliferate, migrate, and forge important synaptic connections to create an optimum adult brain structure (Rodier, 1995).
Animal experiments have demonstrated that exposure to PS-NPs influences the development of the offspring’s hippocampus and induces neurotoxicity, which contributes to a reduction in learning and memory function (Tian et al., 2025). Another study linked maternal exposure to MPs, such as polystyrene, to the development of metabolic disorders in the offspring (Luo et al., 2019).
Recent research has found a higher number of MPs (mainly PET and PPC) in the feces of infants than in adults, indicating that infants are exposed to higher levels of MPs than adults and to a probable microplastic accumulation during the gestation period (Zhang et al., 2021).
Worryingly, exposure to these pollutants continues after pregnancy: evidence shows the presence and concentrations of MPs (Liu et al., 2023; Saraluck et al., 2024), bisphenols, parabens (PBs), and benzophenones (BPs) in human breast milk (Iribarne-Durán et al., 2022) as well as in infant formula (Liu et al., 2023) and processed infant food products, such as milk-based infant formula and cereal-based complementary foods (Zhang et al., 2023). This evidence indicates that babies are exposed even after the gestational period, as also demonstrated by later MPs identification in infant feces (Liu et al., 2023).
In addition, MPs have been observed to change the bacterial composition of human milk (Saraluck et al., 2024), which may have implications for the establishment of the newborn’s intestinal microbiota. As another piece of evidence, a study using in vitro infant gut models has already found that MPs ingestion induces perturbations in the intestinal microbiome ().
In short, MPs found in blood, breast milk, and placenta raise concerns about fetal development and long-term health, compromising endocrine function and neurological development issues in offspring (Panneerselvam et al., 2025). Currently, a European project (AURORA) is underway to assess the effects of MPs exposure during pregnancy and early life ().
2 Microplastic neurotoxicity may disrupt enteric neuronal migration
The pregnancy period is highly sensitive, such that disturbances at any sequential steps can alter the normal embryonic development, during which a single-celled zygote undergoes multiple divisions and differentiations to give rise to a fully formed multicellular organism.
Exposure to MPs and NPs during early developmental stages may trigger neurotoxicity and inflammatory responses, which could cause abnormal embryonic development (Lu et al., 2025; Nair et al., 2025).
This is especially true for congenital enteric neuropathies, such as Hirschsprung disease (HSCR, incidence 1/5,000), which is characterized by a deficient gastrointestinal innervation of the colon due to a failure of enteric neural crest cell migration during early embryogenesis (from 5 to 12 weeks) (Heuckeroth, 2018). The regulation of this process is critical, with numerous genes and proteins involved in both migratory and colonization events (Lake and Heuckeroth, 2013). Although some mutations have been identified in HSCR, the condition is not fully explained by the genetic load (Tang et al., 2018; Luzón-Toro et al., 2020), and many non-genetic factors could also impair the development of the enteric nervous system (ENS) and contribute to the risk (Heuckeroth, 2018). Therefore, identifying an environmental trigger may help prevent HSCR in some cases (Heuckeroth, 2015).
The main treatment for HSCR involves the surgical removal of the deficiently innervated (aganglionic) segment of the intestine. Later on, many patients undergo complications such as recalcitrant constipation, toxic megacolon, and enterocolitis, leading to compromised quality of life (Menezes and Puri, 2006). On the other hand, minor impacts on ENS development may not be sufficient to cause HSCR but may still produce mild clinical symptoms, such as continuous constipation. As a result, the maternal exposure during early pregnancy might be critical for developing congenital aganglionosis or, in milder cases, for the development of less severe motility disorders in children.
One of the main routes of MPs into the body is ingestion. When MPs enter the gastrointestinal tract, they may exert harmful effects through various mechanisms, including microbiota disturbances, mutagenicity, cytotoxicity, reproductive toxicity, neurotoxicity, and increased oxidative stress (; ).
Exposure to MPs induces gut microbiota dysbiosis, intestinal barrier dysfunction, metabolic perturbations, and neurotoxicity in different rodents and disturbs metabolic dysfunction in the mouse brain and intestine. The results showed that MPs altered microbiota composition, accompanied by metabolic perturbations in the mouse gut and brain. Specifically, Firmicutes and Bacteroidetes were suggested to be important phyla for MPs exposure, partially dominating further metabolite alterations (Lee et al., 2024). Thus, MPs have been pointed out as disruptors of the gut microbiota, namely, to gastrointestinal dysbiosis (Lu et al., 2019; Li et al., 2020; Lee et al., 2024), which can later cause neurotoxicity and neurodegeneration (Niesler et al., 2021; Singh et al., 2022).
Additional mechanisms by which MPs affect the nervous system are as include inhibition of AChE activity, inflammatory responses, oxidative stress, mitochondrial dysfunction, autophagy–lysosomal injury, and dysbiosis of the intestinal microbiota (Lu et al., 2025).
Regarding specific MPs neurotoxic mechanisms that may negatively affect enteric neuronal growth and migration and thus result in deficient intestinal innervation, we found the following possible explanations: disturbing neuronal generation and synapse formation (Gupta et al., 2024), inhibiting expression of neurodevelopment-related genes, such as brain-derived neurotrophic factor (BDNF) (Lu et al., 2025), reducing neuronal number, inducing abnormal morphology, and affecting neuronal proliferation, differentiation, and migration (Tian et al., 2025).
Confirming our hypothesis, a recent study on pigs demonstrated that oral PET-MPs administration produces histological changes (injury of the apical parts of the villi, accumulations of cellular debris and mucus, eosinophil infiltration, and hyperemia) and also changes in the enteric nervous system of the porcine jejunum ().
Further animal experiments showed that when MPs extracted from disposable paper cups were administered to pregnant mice, a moderate exposure equivalent to 3.3 cups daily was sufficient to alter the cecal microbiome, disrupt global metabolic functions, and impair immune health, thereby increasing the risk of neurodegeneration and miscarriage ().
In addition, even low concentrations of PS-NPs in Caenorhabditis elegans were sufficient to accumulate in the digestive system, compromise the intestinal barrier and induce a “leaky gut,” and penetrate into extraintestinal tissues. Moreover, NP exposure in C. elegans and human cells induced Parkinson’s disease-like symptoms, such as dopaminergic neuronal degeneration, locomotor dysfunction, and accumulation of α-synuclein aggregates (Jeong et al., 2024).
Finally, pregnant rats exposed to polystyrene nanoplastics during gestation and lactation exhibited abnormalities in cortical thickness and neuronal migration, characterized by increased proliferation of cortical cells and a decreased number of deep-layer neurons (Tian et al., 2025).
In summary, exposure to MPs and NPs during early developmental stages may trigger neurotoxicity and inflammatory responses, which could, among other effects, cause abnormal neuronal migration in the gut and impaired intestinal innervation.
3 Reducing exposure to microplastics during pregnancy as a preventive measure
Although MPs have reached all ecosystems and we are in a scenario where chronic and daily exposure seems unavoidable, there are ways to reduce it. The timing and duration of exposure during pregnancy play a critical role in the associated risk and harm (Panneerselvam et al., 2025).
We know that there are many compounds, drugs, and hormones that affect the gene-environment during development. The ENS is highly sensitive to these (Heuckeroth and Schäfer, 2016), making it likely that compounds from degrading MPs exert similar effects.
Although it is currently challenging to determine the precise risk without accurate quantification of human exposure, existing evidence from nutritional studies and animal experiments indicates a substantial risk to the fetus. Therefore, we recommend minimizing overall exposure to MPs.
The main sources of MPs exposure during pregnancy are identified as indoor dust (Zhang et al., 2020), tooth paste, food packaging, plastic bottles and cups, biomedical material, and cosmetics (Nair et al., 2025). Of concern here, the use of cosmetics by pregnant women is quite frequent (Li et al., 2019; ), maybe due to a lack of risk perception by consumers (Marie et al., 2016). However, we could recently describe the hazard neurotoxic potential of cosmetics for the future born (Jones et al., 2024).
Another important MPs source is dermal exposure through clothing microfibers, which have a non-negligible presence in some textiles, increasing the potential systemic risks. Here, it should be taken into account that common final consumers of textiles with printed PVC are small children, who are the most vulnerable group due to their developmental status (Rovira and Domingo, 2019).
The water intake should also be noted: more than 105 particles have been quantified per liter of bottled water, the majority of which are nanoplastics (Qian et al., 2024). Although both tap and bottled water contain MPs, the concentration is higher in bottled water than in tap water. Taking this evidence into account, pregnant women should be encouraged to drink tap water instead of bottled water to limit the fetal exposure to MPs ().
The DPCs release millions of MPs when used for hot beverages. Even a moderate consumption of 3.3 cups daily in pregnant mice was sufficient to induce tissue-specific accumulation and metabolic and reproductive toxicities (). The use of tea bags has also been reported to release high quantities of MPs into beverages (; Yaroslavov et al., 2025; Jayasekara et al., 2026).
Other recommendations for pregnant women (see Table 3) include avoiding single-use plastics and choosing MPs-free personal care products (Panneerselvam et al., 2025), keeping off seafood (; Vega-Herrera et al., 2024), reducing the use of cosmetics (Guerranti et al., 2019), and dressing in natural fibers.
TABLE 3
| Reduce consumption of | Increase consumption of |
|---|---|
| Synthetic textiles | Natural fiber textiles (i.e.: cotton, wool, and linen) |
| Plastic bottled water/drinks | Tap water |
| Cosmetics | MPs-free personal care products |
| Disposable plastic/paper cups | MPs-free toothpaste |
| Packaged food | Prebiotics |
| Single use plastics | Glass or ceramic pots/recipients |
| Muscles and fish | Daily home ventilation to remove indoor dust |
Safeguarding recommendations for pregnant women.
Finally, the use of feeding bottles, pacifiers, and plastic toys may serve as sources of MPs exposure for infants (Liu et al., 2023) and should therefore be avoided.
As a ray of hope, probiotics consumption seems to play a protective role against PS-MPs. Probiotics can re-balance gut dysbiosis and intestinal leakage induced by MPs, reducing inflammatory biomarkers and avoiding unnecessary activation of the immune system. Thus, probiotics may overcome the toxicity of PS-MPs in humans (), and its consumption may be recommendable during pregnancy.
4 Concluding remarks
Altogether, microplastics may act as neurotoxicants, affect the nervous system, cross the placenta, and reach the fetus, making them likely disruptors of enteric nervous system development and proper intestinal innervation during fetal growth.
Overall, microplastic neurotoxicity appears as an aggravating factor for developing congenital enteric aganglionosis and, therefore, for postnatal motility disorders.
Therefore, although human exposure to microplastics has not yet been adequately measured and the precise risk remains uncertain, we recommend minimizing the exposure of future mothers to microplastics to protect the developing fetus from potential neurotoxic effects.
Statements
Author contributions
RK: Investigation, Writing – review and editing. MB: Funding acquisition, Resources, Writing – review and editing. LW: Funding acquisition, Resources, Writing – review and editing. K-HS: Funding acquisition, Resources, Writing – review and editing. MT-L: Conceptualization, Supervision, Validation, Visualization, Writing – original draft, Writing – review and editing.
Funding
The author(s) declared that financial support was received for this work and/or its publication. The authors acknowledge financial support by Heidelberg University for the publication fee.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
The author LW declared that they were an editorial board member of Frontiers at the time of submission. This had no impact on the peer review process and the final decision.
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References
1
AbassD.AlarabyM.ElkadyE. F.Morataya-ReyesM.BanaeiG.Martín-PérezJ.et al (2025). Polytetrafluoroethylene (PTFE, Teflon) microplastics and nanoplastics induce oxidative stress, mitochondrial damage, and genotoxicity in human intestinal cells. J. Hazard. Mat.499, 140255. 10.1016/j.jhazmat.2025.140255
2
AengenheisterL.KeevendK.MuothC.SchönenbergerR.DienerL.WickP.et al (2018). An advanced human in vitro co-culture model for translocation studies across the placental barrier. Sci. Rep.8, 5388. 10.1038/s41598-018-23410-6
3
AltmannK.WimmerL.Alcolea-RodriguezV.WaniekT.WachtendorfV.MatzdorfK.et al (2025). Quality-by-design and current good practices for the production of test and reference materials for micro- and nano-plastic research. J. Hazard. Mat.497, 139595. 10.1016/j.jhazmat.2025.139595
4
Baeza-MartínezC.OlmosS.González-PleiterM.López-CastellanosJ.García-PachónE.Masiá-CanutoM.et al (2022). First evidence of microplastics isolated in European citizens’ lower airway. J. Hazard. Mat.438, 129439. 10.1016/j.jhazmat.2022.129439
5
BaiC.-L.WangD.LuanY.-L.HuangS.-N.LiuL.-Y.GuoY. (2024). A review on micro- and nanoplastics in humans: implication for their translocation of barriers and potential health effects. Chemosphere361, 142424. 10.1016/j.chemosphere.2024.142424
6
BanaeiG.AbassD.TavakolpournegariA.Martín-PérezJ.GutiérrezJ.PengG.et al (2024). Teabag-derived micro/nanoplastics (true-to-life MNPLs) as a surrogate for real-life exposure scenarios. Chemosphere368, 143736. 10.1016/j.chemosphere.2024.143736
7
BazeliJ.BanikazemiZ.HamblinM. R.Sharafati ChaleshtoriR. (2023). Could probiotics protect against human toxicity caused by polystyrene nanoplastics and microplastics?Front. Nutr.10, 1186724. 10.3389/fnut.2023.1186724
8
BhattacharyyaS.GreerM. L.SalehiM. (2025). Impact of micro- and nanoplastics exposure on human health: focus on neurological effects from ingestion. Front. Public Health13, 1681776. 10.3389/fpubh.2025.1681776
9
BissonnetteJ. R.HarveyN. E.RowsellM. L.KiefteS.HouthuijsK. J.BéenF. M.et al (2025). Identification of micro-/nanoplastics in human placental blood using comprehensive multidimensional pyrolysis - gas chromatography x ion mobility mass spectrometry. Anal. Chim. Acta1376, 344606. 10.1016/j.aca.2025.344606
10
BrachnerA.FragouliD.DuarteI. F.FariasP. M. A.DembskiS.GhoshM.et al (2020). Assessment of human health risks posed by nano-and microplastics is currently not feasible. Int. J. Environ. Res. Public Health17, 8832. 10.3390/ijerph17238832
11
BragaM. F. M.PereiraE. F. R.MarchioroM.AlbuquerqueE. X. (1999). Lead increases tetrodotoxin-insensitive spontaneous release of glutamate and GABA from hippocampal neurons. Brain Res.826, 10–21. 10.1016/S0006-8993(99)01193-2
12
BraunT.EhrlichL.HenrichW.KoeppelS.LomakoI.SchwablP.et al (2021). Detection of microplastic in human placenta and meconium in a clinical setting. Pharmaceutics13, 921. 10.3390/pharmaceutics13070921
13
CampanaleM.MassarelliC.SavinoI.LocaputoV.UricchioV. F. (2020). A detailed review study on potential effects of microplastics and additives of concern on human health. Int. J. Environ. Res. Public Health17 (4), 1212. 10.3390/ijerph17041212
14
CampenM. J.WestA. B.GarciaM.GullapalliR.El HayekE. (2025). Reply to: challenges in studying microplastics in human brain. Nat. Med.31, 4036–4037. 10.1038/s41591-025-04046-2
15
CatalánJ.AfanouA. K.ArranzJ. A.RiazaA. B.BanićI.DirvenH.et al (2025). An integrated approach to assess exposure and early health effects in human populations exposed to micro- and nanoplastics. NanoImpact40, 100600. 10.1016/j.impact.2025.100600
16
ChanM.PrestonE. V.FruhV.QuinnM. R.HackerM. R.WylieB. J.et al (2023). Use of personal care products during pregnancy and birth outcomes – a pilot study. Environ. Res.225, 115583. 10.1016/j.envres.2023.115583
17
ChenQ.PengC.XieR.XuH.SuZ.YilihanG.et al (2024). Placental and fetal enrichment of microplastics from disposable paper cups: implications for metabolic and reproductive health during pregnancy. J. Hazard. Mat.478, 135527. 10.1016/j.jhazmat.2024.135527
18
ChewK. C. M.AngE.-T.TaiY. K.TsangF.LoS. Q.OngE.et al (2011). Enhanced autophagy from chronic toxicity of iron and mutant A53T α-Synuclein. J. Biol. Chem.286, 33380–33389. 10.1074/jbc.M111.268409
19
CoxK. D.CoverntonG. A.DaviesH. L.DowerJ. F.JuanesF.DudasS. E. (2019). Human consumption of microplastics. Environ. Sci. Technol.53, 7068–7074. 10.1021/acs.est.9b01517
20
CubasA. L. V.BianchetR. T.ReisI. M. A. S. dosGouveiaI. C. (2022). Plastics and microplastic in the cosmetic industry: aggregating sustainable actions aimed at alignment and interaction with UN sustainable development goals. Polym. (Basel)14, 4576. 10.3390/polym14214576
21
DengY.ZhangY.LemosB.RenH. (2017). Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure. Sci. Rep.7, 46687. 10.1038/srep46687
22
DiNardoJ. C.DownsC. A. (2019). Can oxybenzone cause Hirschsprung’s disease?Reprod. Toxicol.86, 98–100. 10.1016/j.reprotox.2019.02.014
23
DubeyI.KhanS.KushwahaS. (2022). Developmental and reproductive toxic effects of exposure to microplastics: a review of associated signaling pathways. Front. Toxicol.4, 901798. 10.3389/ftox.2022.901798
24
DurkinA. M.ZouR.BoucherJ. M.BoylesM. S.van BoxelJ.BustamanteM.et al (2024). Investigating exposure and hazards of Micro- and nanoplastics during pregnancy and early life (AURORA project): protocol for an interdisciplinary study. JMIR Res. Protoc.13, e63176. 10.2196/63176
25
EvangelouI.BucciS.StohlA. (2026). Atmospheric microplastic emissions from land and ocean. Nature649, 1186–1189. 10.1038/s41586-025-09998-6
26
FerranteM.PietroZ.AlleguiC.MariaF.AntonioC.PulvirentiE.et al (2022). Microplastics in fillets of Mediterranean seafood. A risk assessment study. Environ. Res.204, 112247. 10.1016/j.envres.2021.112247
27
FournierE.RatelJ.DenisS.LevequeM.RuizP.MazalC.et al (2023). Exposure to polyethylene microplastics alters immature gut microbiome in an infant in vitro gut model. J. Hazard. Mat.443, 130383. 10.1016/j.jhazmat.2022.130383
28
FreireC.AmayaE.GilF.FernándezM. F.MurciaM.LlopS.et al (2018). Prenatal co-exposure to neurotoxic metals and neurodevelopment in preschool children: the environment and childhood (INMA) project. Sci. Total Environ.621, 340–351. 10.1016/j.scitotenv.2017.11.273
29
FreireC.AmayaE.GilF.MurciaM.LLopS.CasasM.et al (2019). Placental metal concentrations and birth outcomes: the environment and childhood (INMA) project. Int. J. Hyg. Environ. Health222, 468–478. 10.1016/j.ijheh.2018.12.014
30
GałęckaI.CałkaJ. (2024). Oral exposure to microplastics affects the neurochemical plasticity of reactive neurons in the Porcine Jejunum. Nutrients16, 2268. 10.3390/nu16142268
31
GambinoI.BagordoF.GrassiT.PanicoA.De DonnoA. (2022). Occurrence of microplastics in tap and bottled water: current knowledge. Int. J. Environ. Res. Public Health19, 5283. 10.3390/ijerph19095283
32
GelbkeH.-P.BantonM.BlockC.DawkinsG.EisertR.LeiboldE.et al (2019). Risk assessment for migration of styrene oligomers into food from polystyrene food containers. Food Chem. Toxicol.124, 151–167. 10.1016/j.fct.2018.11.017
33
GeyerR.JambeckJ. R.LawK. L. (2017). Production, use, and fate of all plastics ever made. Sci. Adv.3, e1700782. 10.1126/sciadv.1700782
34
GuerrantiC.MartelliniT.PerraG.ScopetaniC.CincinelliA. (2019). Microplastics in cosmetics: environmental issues and needs for global bans. Environ. Toxicol. Pharmacol.68, 75–79. 10.1016/j.etap.2019.03.007
35
GuptaP.MahapatraA.MannaB.SumanA.RayS. S.SinghalN.et al (2024). Sorption of PFOS onto polystyrene microplastics potentiates synergistic toxic effects during zebrafish embryogenesis and neurodevelopment. Chemosphere366, 143462. 10.1016/j.chemosphere.2024.143462
36
Gutiérrez-GarcíaJ.EgeaR.BarguillaI.NymarkP.García-RodríguezA.GuyotB.et al (2025). Long-term exposure to real-life polyethylene terephthalate nanoplastics induces carcinogenesis in vitro. Environ. Sci. Technol.59, 10891–10904. 10.1021/acs.est.5c01628
37
HeuckerothR. O. (2015). Hirschsprung’s disease, down syndrome, and missing heritability: too much collagen slows migration. J. Clin. Investigation125, 4323–4326. 10.1172/JCI85003
38
HeuckerothR. O. (2018). Hirschsprung disease—integrating basic science and clinical medicine to improve outcomes. Nat. Rev. Gastroenterol. Hepatol.15, 152–167. 10.1038/nrgastro.2017.149
39
HeuckerothR. O.SchäferK.-H. (2016). Gene-environment interactions and the enteric nervous system: neural plasticity and Hirschsprung disease prevention. Dev. Biol.417, 188–197. 10.1016/j.ydbio.2016.03.017
40
HuJ.QinX.ZhangJ.ZhuY.ZengW.LinY.et al (2021). Polystyrene microplastics disturb maternal-fetal immune balance and cause reproductive toxicity in pregnant mice. Reprod. Toxicol.106, 42–50. 10.1016/j.reprotox.2021.10.002
41
HuoW.CaiP.ChenM.LiH.TangJ.XuC.et al (2016). The relationship between prenatal exposure to BP-3 and Hirschsprung’s disease. Chemosphere144, 1091–1097. 10.1016/j.chemosphere.2015.09.019
42
Iribarne-DuránL. M.PeinadoF. M.FreireC.Castillero-RosalesI.Artacho-CordónF.OleaN. (2022). Concentrations of bisphenols, parabens, and benzophenones in human breast milk: a systematic review and meta-analysis. Sci. Total Environ.806, 150437. 10.1016/j.scitotenv.2021.150437
43
JayasekaraP. M.AbhishekP.KahandawalaB. S.DamithN.WeerasingheM.KahatapitiyaN. S.et al (2026). Brewing plastics: OCT reveals microplastic release from nylon tea bags in simulated brewed tea infusions. Environ. Sci. Process. Impacts.28, 392–404. 10.1039/D5EM00644A
44
JeongA.ParkS. J.LeeE. J.KimK. W. (2024). Nanoplastics exacerbate Parkinson’s disease symptoms in C. elegans and human cells. J. Hazard. Mat.465, 133289. 10.1016/j.jhazmat.2023.133289
45
JinY.XiaJ.PanZ.YangJ.WangW.FuZ. (2018). Polystyrene microplastics induce microbiota dysbiosis and inflammation in the gut of adult zebrafish. Environ. Pollut.235, 322–329. 10.1016/j.envpol.2017.12.088
46
JinY.LuL.TuW.LuoT.FuZ. (2019). Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice. Sci. Total Environ.649, 308–317. 10.1016/j.scitotenv.2018.08.353
47
JonesK.WesselL. M.SchäferK.-H.Tapia-LalienaM. Á. (2024). Use of cosmetics in pregnancy and neurotoxicity: can it increase the risk of congenital enteric neuropathies?Biomolecules14, 984. 10.3390/biom14080984
48
JulienneF.DelormeN.LagardeF. (2019). From macroplastics to microplastics: role of water in the fragmentation of polyethylene. Chemosphere236, 124409. 10.1016/j.chemosphere.2019.124409
49
KimJ.ChenM.WhiteR. S. (2025). Microplastics and the placenta: a call to action for perinatal research. Am. J. Perinatol.43, 433–436. 10.1055/a-2657-6249
50
KoleP. J.LöhrA. J.Van BelleghemF.RagasA. (2017). Wear and tear of tyres: a stealthy source of microplastics in the environment. Int. J. Environ. Res. Public Health14, 1265. 10.3390/ijerph14101265
51
KwiatkowskaK.OrmaniecP. (2024). Microbial succession on microplastics in wastewater treatment plants: exploring the complexities of microplastic-microbiome interactions. Microb. Ecol.87, 105. 10.1007/s00248-024-02422-y
52
LakeJ. I.HeuckerothR. O. (2013). Enteric nervous system development: migration, differentiation, and disease. Am. J. Physiol.-Gastroint. Liver Physiol.305, G1–G24. 10.1152/ajpgi.00452.2012
53
LeeS.-H.LinW.-Y.ChengT.-J. (2024). Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure. Chemosphere350, 141026. 10.1016/j.chemosphere.2023.141026
54
LeppertB.StrunzS.SeiwertB.SchlittenbauerL.SchlichtingR.PfeifferC.et al (2020). Maternal paraben exposure triggers childhood overweight development. Nat. Commun.11, 561. 10.1038/s41467-019-14202-1
55
LiH.ZhengJ.WangH.HuangG.HuangQ.FengN.et al (2019). Maternal cosmetics use during pregnancy and risks of adverse outcomes: a prospective cohort study. Sci. Rep.9, 8030. 10.1038/s41598-019-44546-z
56
LiB.DingY.ChengX.ShengD.XuZ.RongQ.et al (2020). Polyethylene microplastics affect the distribution of gut microbiota and inflammation development in mice. Chemosphere244, 125492. 10.1016/j.chemosphere.2019.125492
57
LiuS.GuoJ.LiuX.YangR.WangH.SunY.et al (2023). Detection of various microplastics in placentas, meconium, infant feces, breastmilk and infant formula: a pilot prospective study. Sci. Total Environ.854, 158699. 10.1016/j.scitotenv.2022.158699
58
LoffS.WaagK.-L.KränzlinB.ZovkoD.DzakovicA.JesterI.et al (1998). Long-term total parenteral nutrition-induced hepatobiliary dysfunction in a rabbit model. J. Pediatr. Surg.33, 694–699. 10.1016/S0022-3468(98)90189-0
59
LoffS.KränzlinB.MoghadamM.DzakovicA.WesselL.BackW.et al (1999). Parenteral nutrition-induced hepatobiliary dysfunction in infants and prepubertal rabbits. Pediatr. Surg. Int.15, 479–482. 10.1007/s003830050643
60
LoffS.KabsF.WittK.SartorisJ.MandlB.NiessenK. H.et al (2000). Polyvinylchloride infusion lines expose infants to large amounts of toxic plasticizers. J. Pediatr. Surg.35, 1775–1781. 10.1053/jpsu.2000.19249
61
LuL.LuoT.ZhaoY.CaiC.FuZ.JinY. (2019). Interaction between microplastics and microorganism as well as gut microbiota: a consideration on environmental animal and human health. Sci. Total Environ.667, 94–100. 10.1016/j.scitotenv.2019.02.380
62
LuK.QueY.WangL.WangY.QiuJ.JiaY.et al (2025). Environmental exposure pathways of microplastics and their toxic effects on ecosystems and the nervous system. Front. Toxicol.7, 1649282. 10.3389/ftox.2025.1649282
63
LuoT.ZhangY.WangC.WangX.ZhouJ.ShenM.et al (2019). Maternal exposure to different sizes of polystyrene microplastics during gestation causes metabolic disorders in their offspring. Environ. Pollut.255, 113122. 10.1016/j.envpol.2019.113122
64
Luzón‐ToroB.Villalba‐BenitoL.TorroglosaA.FernándezR. M.AntiñoloG.BorregoS. (2020). What is new about the genetic background of Hirschsprung disease?Clin. Genet.97, 114–124. 10.1111/cge.13615
65
MarieC.CabutS.VendittelliF.Sauvant-RochatM.-P. (2016). Changes in cosmetics use during pregnancy and risk perception by women. Int. J. Environ. Res. Public Health13, 383. 10.3390/ijerph13040383
66
MejíasC.MartínJ.SantosJ. L.AparicioI.AlonsoE. (2023). Role of polyamide microplastics as vector of parabens in the environment: an adsorption study. Environ. Technol. Innov.32, 103276. 10.1016/j.eti.2023.103276
67
MenezesM.PuriP. (2006). Long-term outcome of patients with enterocolitis complicating Hirschsprung’s disease. Pediatr. Surg. Int.22, 316–318. 10.1007/s00383-006-1639-2
68
MeyrueixL.AdairL.NorrisS. A.IderaabdullahF. (2019). Assessment of placental metal levels in a South African cohort. Environ. Monit. Assess.191, 500. 10.1007/s10661-019-7638-2
69
MonikhA.MaterićD.Valsami-JonesE.GrossartH.-P.AltmannK.HolzingerR.et al (2025). Challenges in studying microplastics in human brain. Nat. Med.31, 4034–4035. 10.1038/s41591-025-04045-3
70
MontanoL.RaimondoS.PiscopoM.RicciardiM.GuglielminoA.ChamayouS.et al (2025). First evidence of microplastics in human ovarian follicular fluid: an emerging threat to female fertility. Ecotoxicol. Environ. Saf.291, 117868. 10.1016/j.ecoenv.2025.117868
71
NairS. R.NihadM.Shenoy PS.GuptaS.BoseB. (2025). Unveiling the effects of micro and nano plastics in embryonic development. Toxicol. Rep.14, 101954. 10.1016/j.toxrep.2025.101954
72
NardellaF.BritsM.van VelzenM. J. M.ScibettaL.DurkinA.VermeulenR.et al (2025). Advancing pyrolysis-gas chromatography-mass spectrometry for the accurate quantification of micro- and nanoplastics in human blood. Micropl. Nanoplast.5, 48. 10.1186/s43591-025-00152-7
73
NieslerB.KuertenS.DemirI. E.SchäferK.-H. (2021). Disorders of the enteric nervous system — a holistic view. Nat. Rev. Gastroenterol. Hepatol.18, 393–410. 10.1038/s41575-020-00385-2
74
NihartA. J.GarciaM. A.El HayekE.LiuR.OlewineM.KingstonJ. D.et al (2025). Bioaccumulation of microplastics in decedent human brains. Nat. Med.31, 1114–1119. 10.1038/s41591-024-03453-1
75
Oliveri ContiG.FerranteM.BanniM.FavaraC.NicolosiI.CristaldiA.et al (2020). Micro- and nano-plastics in edible fruit and vegetables. The first diet risks assessment for the general population. Environ. Res.187, 109677. 10.1016/j.envres.2020.109677
76
PahwaR.KalraJ. (1993). A critical review of the neurotoxicity of styrene in humans. Vet. Hum. Toxicol.35 (6), 516–520.
77
PanneerselvamD.MurugesanA.RaveendranS. K.KumarJ. S.VenkataramanP. (2025). Examining the hidden dangers: understanding how microplastics affect pregnancy. Eur. J. Obstet. and Gynecol. Reprod. Biol.304, 53–62. 10.1016/j.ejogrb.2024.11.024
78
ParutaP.PucinoM.BoucherJ. (2022). Plastic paints the environment. Lausanne, Switzerland: EA – Environmental Action.
79
PohankaM. (2014). Copper, aluminum, iron and calcium inhibit human acetylcholinesterase in vitro. Environ. Toxicol. Pharmacol.37, 455–459. 10.1016/j.etap.2014.01.001
80
PrüstM.MeijerJ.WesterinkR. H. S. (2020). The plastic brain: neurotoxicity of micro- and nanoplastics. Part. Fibre Toxicol.17, 24. 10.1186/s12989-020-00358-y
81
QianN.GaoX.LangX.DengH.BratuT. M.ChenQ.et al (2024). Rapid single-particle chemical imaging of nanoplastics by SRS microscopy. Proc. Natl. Acad. Sci.121, e2300582121. 10.1073/pnas.2300582121
82
QuM.WangD. (2020). Toxicity comparison between pristine and sulfonate modified nanopolystyrene particles in affecting locomotion behavior, sensory perception, and neuronal development in Caenorhabditis elegans. Sci. Total Environ.703, 134817. 10.1016/j.scitotenv.2019.134817
83
RafaN.AhmedB.ZohoraF.BakyaJ.AhmedS.AhmedS. F.et al (2024). Microplastics as carriers of toxic pollutants: source, transport, and toxicological effects. Environ. Pollut.343, 123190. 10.1016/j.envpol.2023.123190
84
RagusaA.SvelatoA.SantacroceC.CatalanoP.NotarstefanoV.CarnevaliO.et al (2021). Plasticenta: first evidence of microplastics in human placenta. Environ. Int.146, 106274. 10.1016/j.envint.2020.106274
85
RodierP. M. (1995). Developing brain as a target of toxicity. Environ. Health Perspect.103, 73–76. 10.1289/ehp.95103s673
86
RoviraJ.DomingoJ. L. (2019). Human health risks due to exposure to inorganic and organic chemicals from textiles: a review. Environ. Res.168, 62–69. 10.1016/j.envres.2018.09.027
87
SaraluckA.TecharangT.BunyapipatP.BoonchuwongK.PullaputY.MordmuangA. (2024). Detection of microplastics in human breast milk and its association with changes in human milk bacterial microbiota. J. Clin. Med.13, 4029. 10.3390/jcm13144029
88
SchwablP.KöppelS.KönigshoferP.BucsicsT.TraunerM.ReibergerT.et al (2019). Detection of various microplastics in human stool. Ann. Intern. Med.171, 453–457. 10.7326/M19-0618
89
SenathirajahK.AttwoodS.BhagwatG.CarberyM.WilsonS.PalanisamiT. (2021). Estimation of the mass of microplastics ingested – a pivotal first step towards human health risk assessment. J. Hazard. Mat.404, 124004. 10.1016/j.jhazmat.2020.124004
90
SerafimA.CompanyR.LopesB.RosaJ.CavacoA.CastelaG.et al (2012). Assessment of essential and nonessential metals and different metal exposure biomarkers in the human placenta in a population from the south of Portugal. J. Toxicol. Environ. Health A75, 867–877. 10.1080/15287394.2012.690704
91
SinghS.SharmaP.PalN.KumawatM.ShubhamS.SarmaD. K.et al (2022). Impact of environmental pollutants on gut microbiome and mental health via the gut–brain axis. Microorganisms10, 1457. 10.3390/microorganisms10071457
92
SökmenT. Ö.SulukanE.TürkoğluM.BaranA.ÖzkaracaM.CeyhunS. B. (2020). Polystyrene nanoplastics (20 nm) are able to bioaccumulate and cause oxidative DNA damages in the brain tissue of zebrafish embryo (Danio rerio). Neurotoxicology77, 51–59. 10.1016/j.neuro.2019.12.010
93
SunQ.RenS.-Y.NiH.-G. (2020). Incidence of microplastics in personal care products: an appreciable part of plastic pollution. Sci. Total Environ.742, 140218. 10.1016/j.scitotenv.2020.140218
94
SunH.SuX.MaoJ.LiuY.LiG.DuQ. (2024). Microplastics in maternal blood, fetal appendages, and umbilical vein blood. Ecotoxicol. Environ. Saf.287, 117300. 10.1016/j.ecoenv.2024.117300
95
TangC. S.LiP.LaiF. P.-L.FuA. X.LauS.-T.SoM. T.et al (2018). Identification of genes associated with Hirschsprung disease, based on whole-genome sequence analysis, and potential effects on enteric nervous system development. Gastroenterology155, 1908–1922.e5. 10.1053/j.gastro.2018.09.012
96
ThompsonR. C.Courtene-JonesW.BoucherJ.PahlS.RaubenheimerK.KoelmansA. A. (2024). Twenty years of microplastic pollution research—what have we learned?Science386 (1979), 386. 10.1126/science.adl2746
97
TianL.ChenJ.LiuX.WeiY.ZhaoY.ShiY.et al (2025). Prenatal exposure on nanoplastics: a study of spatial transcriptomics in hippocampal offspring. Environ. Pollut.366, 125480. 10.1016/j.envpol.2024.125480
98
TsengI.-L.YangY.-F.YuC.-W.LiW.-H.LiaoV. H.-C. (2013). Phthalates induce neurotoxicity affecting locomotor and thermotactic behaviors and AFD neurons through oxidative stress in Caenorhabditis elegans. PLoS One8, e82657. 10.1371/journal.pone.0082657
99
UllahS.AhmadS.GuoX.UllahS.UllahS.NabiG.et al (2023). A review of the endocrine disrupting effects of micro and nano plastic and their associated chemicals in mammals. Front. Endocrinol. (Lausanne)13, 1084236. 10.3389/fendo.2022.1084236
100
van RaamsdonkL. W. D.van der ZandeM.KoelmansA. A.HoogenboomR. L. A. P.PetersR. J. B.GrootM. J.et al (2020). Current insights into monitoring, bioaccumulation, and potential health effects of microplastics present in the food chain. Foods9, 72. 10.3390/foods9010072
101
Vega-HerreraA.SavvaK.LacomaP.SantosL. H. M. L. M.HernándezA.MarmeloI.et al (2024). Bioaccumulation and dietary bioaccessibility of microplastics composition and cocontaminants in Mediterranean mussels. Chemosphere363, 142934. 10.1016/j.chemosphere.2024.142934
102
Vela-SoriaF.Gallardo-TorresM. E.BallesterosO.DíazC.PérezJ.NavalónA.et al (2017). Assessment of parabens and ultraviolet filters in human placenta tissue by ultrasound-assisted extraction and ultra-high performance liquid chromatography-tandem mass spectrometry. J. Chromatogr. A1487, 153–161. 10.1016/j.chroma.2017.01.041
103
VercauterenM.PanneelL.JorensP. G.CovaciA.CleysP.MulderA.et al (2024). An ex vivo study examining migration of microplastics from an infused neonatal parenteral nutrition circuit. Environ. Health Perspect.132, 37703. 10.1289/EHP13491
104
WeisJ. S.AlavaJ. J. (2023). (Micro)Plastics are toxic pollutants. Toxics11, 935. 10.3390/toxics11110935
105
WójtowiczA. K.SzychowskiK. A.WnukA.KajtaM. (2017). Dibutyl phthalate (DBP)-induced apoptosis and neurotoxicity are mediated via the aryl hydrocarbon receptor (AhR) but not by estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), or peroxisome proliferator-activated receptor gamma (PPARγ) in mouse cortical neurons. Neurotox. Res.31, 77–89. 10.1007/s12640-016-9665-x
106
YaroslavovA. A.EfimovaA. A.GrokhovskayaT. E.BadikovaA. G.SpiridonovV. V.PozdyshevD. V.et al (2025). Evolution of microplastics released from tea bags into water. Polym. (Basel)17, 2700. 10.3390/polym17192700
107
ZhangJ.CaoR.CaiT.AschnerM.ZhaoF.YaoT.et al (2013). The role of autophagy dysregulation in manganese-induced dopaminergic neurodegeneration. Neurotox. Res.24, 478–490. 10.1007/s12640-013-9392-5
108
ZhangJ.WangL.KannanK. (2020). Microplastics in house dust from 12 countries and associated human exposure. Environ. Int.134, 105314. 10.1016/j.envint.2019.105314
109
ZhangJ.WangL.TrasandeL.KannanK. (2021). Occurrence of polyethylene terephthalate and polycarbonate microplastics in infant and adult feces. Environ. Sci. Technol. Lett.8, 989–994. 10.1021/acs.estlett.1c00559
110
ZhangD.XiaoJ.XiaoQ.ChenY.LiX.ZhengQ.et al (2023). Infant exposure to parabens, triclosan, and triclocarban via breastfeeding and formula supplementing in southern China. Sci. Total Environ.858, 159820. 10.1016/j.scitotenv.2022.159820
111
ZhengY.XuS.LiuJ.LiuZ. (2024). The effects of micro- and nanoplastics on the central nervous system: a new threat to humanity?Toxicology504, 153799. 10.1016/j.tox.2024.153799
112
ZhuL.KangY.MaM.WuZ.ZhangL.HuR.et al (2024). Tissue accumulation of microplastics and potential health risks in human. Sci. Total Environ.915, 170004. 10.1016/j.scitotenv.2024.170004
Summary
Keywords
congenital enteric neuropathies, enteric nervous system (ENS), Hirschsprung’s disease (HSCR), microplastics, neurotoxicity, pregnancy
Citation
Khasanov R, Boettcher M, Wessel LM, Schäfer K-H and Tapia-Laliena MÁ (2026) Microplastics and neurotoxicity: could prenatal exposure to microplastics boost congenital enteric neuropathies?. Front. Toxicol. 8:1756622. doi: 10.3389/ftox.2026.1756622
Received
28 November 2025
Revised
12 February 2026
Accepted
24 February 2026
Published
24 March 2026
Volume
8 - 2026
Edited by
Alicia Ruiz, University of Granada, Spain
Reviewed by
Claude Lambre, Institut National de la Santé et de la Recherche Médicale (INSERM), France
Updates
Copyright
© 2026 Khasanov, Boettcher, Wessel, Schäfer and Tapia-Laliena.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: María Ángeles Tapia-Laliena, mariaangeles.tapia-laliena@medma.uni-heidelberg.de; Karl-Herbert Schäfer, karlherbert.schaefer@hs-kl.de
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