Neurotoxicity of Plastics: Mechanistic Insights into the Progression of Neurodegenerative Diseases in Animal Models

Introduction

The extensive usage of plastics in contemporary life has raised serious concerns about the environment and human health. From food containers and packaging materials to electronics and medical equipment, plastics are omnipresent, resulting in continuous and often unavoidable human exposure. As plastic products degrade, they release microplastics, nano plastics, and a variety of chemical additives into the environment. These chemicals, in particular bisphenol A, phthalates, polybrominated diphenyl ethers, styrene, and plasticizers, have been found in human tissues such as blood, urine, placenta, and even the brain. They are also known to leak into food, water, and air.¹

Concern over the possible neurological effects of these compounds linked to plastic has grown in recent studies. Many of these substances can penetrate the blood-brain barrier (BBB) or compromise its integrity because they are lipophilic, enabling direct contact with neural tissue.² This is particularly critical during early development, when the nervous system is still forming and is highly sensitive to environmental disruptions. However, emerging evidence suggests that plastic exposure is not limited to developmental toxicity it may also contribute to the development of neurodegenerative illnesses such amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), and Alzheimer’s disease (AD).^3,4

Animal studies have been instrumental in uncovering the mechanistic pathways through which plastic-associated chemicals exert their effects on the nervous system. These include the induction of oxidative stress, neuroinflammation, mitochondrial dysfunction, endocrine disruption, epigenetic alterations, and neurotransmitter system dysregulation.^5,6 For instance, BPA and certain phthalates mimic hormones like estrogen and thyroid hormones, disrupting critical neurodevelopmental signalling.⁷ PBDEs and styrene are known to produce reactive oxygen species (ROS), impair mitochondrial function, and activate microglia, leading to chronic inflammation pathological features shared with many neurodegenerative conditions.⁸

Preclinical models such as rodents and zebrafish have demonstrated behavioural and cognitive impairments following exposure to these compounds, along with structural and molecular changes in brain regions like the hippocampus, prefrontal cortex, and substantia nigra^9,10 These studies offer important insights into how long-term or developmental exposure to plastics might increase susceptibility to neurological disorders later in life. Despite increasing evidence, many questions remain regarding the dose-response relationships, combined effects of multiple plastic components, and relevance to human pathophysiology. Moreover, regulatory frameworks have yet to fully account for the neurotoxic potential of plastic-derived chemicals, especially in the context of chronic, low-dose exposure.¹¹

This review aims to consolidate current knowledge on the neurotoxic effects of plastics using evidence from animal models, with a focus on mechanisms that may link plastic exposure to the initiation and progression of neurodegenerative diseases. By highlighting both experimental findings and mechanistic pathways, we hope to inform future research, risk assessment, and policy development to mitigate the potential neurological impact of plastic pollution.

Types of plastics

Epoxy resins and polycarbonate plastics are two common products made with the synthetic organic chemical bisphenol A . These substances are frequently found in the linings of canned products, baby bottles, and containers for food and drink. BPA is a recognized endocrine-disrupting chemical (EDC) that can disrupt hormonal signalling and mimic estrogen. Because BPA is lipophilic, it can penetrate the blood-brain barrier and directly impact neural tissues. Exposure to BPA during important windows of brain development has been linked to altered synaptic formation, anxiety-like behaviours, and decreased learning and memory in animal models^12,13 These results raise questions regarding its possible involvement in the development or aggravation of neurodegenerative diseases.

Phthalates, such as dibutyl phthalate (DBP) and di(2-ethylhexyl) phthalate (DEHP), are mainly employed as plasticizers to increase the flexibility and durability of polyvinyl chloride (PVC) and other plastics. Consumer goods including toys, flooring materials, medical tubing, and personal care products like lotions and shampoos frequently contain them. Additionally, phthalates are strong endocrine disruptors that can interfere with the signalling of thyroid hormones and androgens.¹⁴ According to research on animals, both short-term and long-term exposure to phthalates causes neurodevelopmental abnormalities, such as impaired cognitive function, altered dopaminergic transmission, and structural abnormalities in the hippocampus^15,16 These effects are more noticeable during the early stages, which may indicate a connection between exposure to phthalates and a higher risk of developing neurological illnesses.

Polystyrene is a lightweight, rigid plastic used extensively in disposable containers, insulation, and packaging materials. Its monomer, styrene, can leach into food or volatilize into indoor air, leading to potential human exposure. Styrene is classified as a possible human carcinogen and has demonstrated neurotoxic effects in multiple animal studies.¹⁷ Exposure to styrene or polystyrene micro/nanoplastics has been linked to oxidative stress, inflammation, aberrant behaviour, and motor deficits in rats and aquatic models.^18,19 Reactive oxygen species (ROS) buildup, mitochondrial damage, and glial cell activation are hypothesized to be the causes of these consequences; these processes are common to many neurodegenerative disease pathways.

One of the most extensively produced plastics in the world, polyvinyl chloride (PVC) is utilized in consumer items, medical equipment, and building materials. PVC is frequently mixed with plasticizers, mostly phthalates, which are not chemically bonded and can leak into the environment, to increase its flexibility.²⁰ [20]. Despite PVC’s apparent inertness, the plasticizers it contains are extremely harmful to human health. In experimental models, these chemicals have been linked to developmental neurotoxicity, neurobehavioral alterations, and hormone disruption.²¹ Research has indicated that early-life exposure to PVC-derived plasticizers may contribute to the risk of neurodegenerative diseases by causing cognitive impairments, altered neurotransmitter systems, and alterations in brain morphology^22,23

A class of flame retardants known as polybrominated diphenyl ethers is added to a wide range of plastic-based goods, such as construction materials, electronics, and upholstered furniture. These are persistent organic pollutants (POPs), which have been found in human blood, breast milk, and even the developing fetal brain²⁴ They bioaccumulate in tissues that are high in fat. Because PBDEs can pass through the placenta and the blood-brain barrier, there is worry about how they may affect neurotoxicity in both adults and children. Exposure to PBDEs has been associated in animal studies with neuroinflammation, oxidative damage, impaired thyroid hormone regulation, and learning and memory deficits.²⁵ These processes are similar to those linked to neurodegenerative illnesses including Parkinson’s and Alzheimer’s, underscoring PBDEs as environmental risk factors for neurological conditions.

Animal Models Utilized

Mice and rats were frequently used to assess behavioral changes, cognitive functions, and biochemical markers associated with neurodegeneration. Fish Models: Zebrafish (Danio rerio) were utilized due to their transparent embryos and rapid development, allowing for real-time observation of neurodevelopmental effects. Invertebrates: Species like Caenorhabditis elegans provided insights into fundamental neurotoxic mechanisms due to their well-mapped neural circuits.²⁶

Predominantly polystyrene microplastics and nanoplastics, with some studies examining polyethylene and polypropylene particles.Particle Sizes: Ranged from nanometers (<100 nm) to micrometers (>1 µm), affecting their ability to cross biological barriers. Exposure Routes: Included oral ingestion, injection, and environmental exposure through contaminated water or food sources. Varied across studies, with some employing acute high-dose exposures and others chronic low-dose exposures to mimic environmental condition.²⁷ Tests such as the Morris water maze and open field tests in rodents Novel Tank Diving Test Light/Dark Preference Test and T-Maze Test in zebrafish assessed cognitive and motor functions. Measurement of oxidative stress markers, neurotransmitter levels, and enzyme activities provided insights into molecular disruptions. Histological Examinations: Brain tissues were examined for structural changes, inflammation, and neuronal loss. Molecular techniques: Gene expression analyses and protein assays identified alterations in pathways related to neurodegeneration.²⁸

Routes of Exposure to Plastic-Associated Chemicals

The most frequent and important way to be exposed to toxins linked to plastic is by oral ingestion. When plastics are heated or damaged, they can release microplastics and additives including bisphenol A (BPA), phthalates, and PBDEs into food and drink.^29,30 Cans lined with epoxy resins, plastic containers, food packaging materials, and even drinking water contain these chemicals.³¹ Given the great absorption capacity of the gastrointestinal tract, dietary consumption is particularly problematic. After being consumed, these substances have the potential to enter the bloodstream and either penetrate or disrupt the blood-brain barrier (BBB), which could result in neurotoxic effects on the central nervous system.³²

Inhalation of airborne plastic particles and volatile organic compounds (VOCs) is another important route, particularly in indoor environments where synthetic materials, furnishings, and electronic devices are common. Styrene, a monomer of polystyrene, is a known inhalation hazard and can volatilize into air from consumer products. Inhaled microplastics and PBDE-laden dust particles can deposit in the lungs, translocate into the bloodstream, and potentially reach the brain.³³ Animal studies have shown that inhalation of nano plastics may trigger neuroinflammation and oxidative stress, similar to ingestion-based exposure.³⁴

Even though it’s usually regarded as a less significant route than eating or inhalation, dermal absorption can nonetheless add to the body’s exposure to plastic additives. This is especially true when using lotions, cosmetics, and personal care items that include BPA derivatives and phthalates.³⁵ The skin, especially when damaged or exposed for prolonged periods, can absorb lipophilic substances. While dermal absorption is less efficient for reaching the brain, it can contribute to systemic endocrine disruption, which indirectly affects neurodevelopment and brain function.³⁶

Because of the growing brain’s increased susceptibility, placental and breast milk transfer poses a serious risk. According to research, toxins linked to plastic can penetrate the placental barrier and expose the fetus at crucial stages of neurodevelopment.³⁷ Cord blood, amniotic fluid, and placental tissue have all been found to contain BPA, phthalates, and PBDEs.³⁸ In animal models, these exposures are linked to long-lasting neurodevelopmental alterations, such as disrupted neural connections and learning impairment. As lipophilic pollutants build up in breast milk, postnatal exposure can increase for infants.³⁹

In some groups, occupational and medical exposure can be substantial. PVC-made IV bags, tubing, and catheters are examples of medical equipment that frequently include phthalates like DEHP, which can seep into intravenous fluids, particularly in neonatal intensive care units.⁴⁰ Bypassing natural barriers, this method delivers plastic compounds straight into the circulation, potentially resulting in high systemic dosages. Workers in the electronics, recycling, and plastics manufacturing sectors may also be exposed to high concentrations of PVC fumes, PBDEs, and styrene, which increases the risk of neurological and endocrine consequences.^41,42

Animal Models in Plastic Neurotoxicity Research

Understanding the neurotoxic consequences of chemicals associated with plastic, such as phthalates, bisphenol A (BPA), polybrominated diphenyl ethers (PBDEs), and styrene, requires the use of animal models. Because of their neurological resemblance to humans and the availability of disease-relevant transgenic strains, rodents—particularly mice and rats—are frequently used.^43,44 The Morris water maze and rotarod are two behavioural tests used to evaluate cognitive and motor deficits after chemical exposure. Furthermore, transgenic models such as APP/PS1 (Alzheimer’s disease) and SOD1-G93A (ALS) shed light on how plastics worsen the course of the disease by causing neuroinflammation, mitochondrial dysfunction, and oxidative stress.^45,46 Histological and molecular analyses further reveal alterations in neuronal integrity and inflammation, supporting the mechanistic links between plastic exposure and neurodegeneration. These models are indispensable for identifying environmental risks and testing preventive or therapeutic strategies in neurodegenerative disease research.

Plastic-Associated Chemicals and Their Role in Alzheimer’s Disease: Mechanisms and Evidence

The most common neurodegenerative disease, Alzheimer’s disease (AD), is becoming more and more linked to environmental exposures, especially to endocrine-disrupting chemicals generated from plastic, like polybrominated diphenyl ethers, bisphenol A and phthalates. Commonly present in epoxy resins and polycarbonate plastics, bisphenol A functions as a xenoestrogen and interferes with the brain’s natural estrogen receptor signalling. Hippocampal function has been demonstrated to be hampered by BPA’s disruption of estrogenic pathways, which are essential for synaptic plasticity and memory. Additionally, BPA causes mitochondrial malfunction and oxidative stress, both of which lead to neuronal death. The two neuropathological characteristics of AD, tau hyperphosphorylation and increased amyloid-beta (Aβ) formation, have also been linked to BPA exposure, most likely through increased β-secretase activity and neuroinflammatory reactions.⁴⁷ Peroxisome proliferator-activated receptors (PPARs), which are important in lipid metabolism and neuronal maintenance, have also been demonstrated to be disrupted by phthalates, such as di-(2-ethylhexyl) phthalate (DEHP) and dibutyl phthalate (DBP), which are employed as plasticizers in PVC and other polymers. These substances contribute to persistent neuroinflammation and neuronal injury by encouraging microglial activation and the release of pro-inflammatory cytokines (such as TNF-α and IL-6).⁴⁸ In rat models, prolonged exposure to phthalates has been linked to elevated expression of genes related to Aβ and deficiencies in spatial memory.⁴⁹ Furthermore, PBDEs, which replace thyroid hormones as flame retardants in consumer electronics and plastics, mimic thyroid hormones and competitively block their signalling. This interferes with adult neurogenesis and brain growth.⁵⁰ [50]. In addition, PBDEs cause oxidative stress, change intracellular calcium levels, and worsen tau and Aβ pathogenesis.^51,52 The need for more research into plastic-related neurotoxicity is highlighted by the fact that these chemicals collectively contribute to AD pathogenesis through interrelated processes involving oxidative stress, hormone disturbance, neuroinflammation, and interference with protein aggregation.

Plastic-Associated Chemicals and Their Role in Parkinsonism: Mechanisms and Evidence

Progressive degradation of dopaminergic neurons in the substantia nigra is a hallmark of Parkinsonism, especially Parkinson’s disease (PD), which results in motor dysfunctions such bradykinesia, tremor, and rigidity. Styrene, polybrominated diphenyl ethers, phthalates, and bisphenol A are among the plastic-associated chemicals that have been linked in recent research to the development and progression of Parkinsonism through mechanisms involving oxidative stress, mitochondrial dysfunction, neuroinflammation, and disrupted neurotransmission. Styrene oxide, a reactive intermediate that can pass across the blood-brain barrier and build up in brain tissues, is produced during the metabolism of styrene, a volatile chemical molecule used to make polystyrene plastics.⁵³ According to studies, long-term exposure to styrene causes mitochondrial dysfunction and oxidative damage, especially in dopaminergic neurons, which results in neuronal death and motor impairment resembling Parkinson’s disease.⁵⁴ Further supporting its function in dopaminergic neurodegeneration, styrene exposure has also been connected to elevated dopamine turnover and depletion of dopamine reserves in the striatum.⁵⁵

PBDEs, widely used as flame retardants in plastics and electronics, are lipophilic and bioaccumulate in neural tissues. They induce oxidative stress, disrupt calcium homeostasis, and impair mitochondrial function, all of which are mechanisms implicated in PD. PBDEs can also alter the expression of genes involved in dopamine synthesis and metabolism, including tyrosine hydroxylase and dopamine transporter, potentially leading to dopamine dysregulation and nigrostriatal damage.

Phthalates such as di-(2-ethylhexyl) phthalate are plasticizers that leach from consumer products and are known to disrupt endocrine and neurological functions. DEHP and its metabolites have been shown to activate microglia and increase neuroinflammatory cytokines (e.g., TNF-α, IL-1β), which are central to dopaminergic neurotoxicity [56]. Moreover, phthalate exposure can impair mitochondrial membrane potential and promote apoptosis of dopaminergic neurons, exacerbating PD-like pathology in animal models.

Bisphenol A while more commonly associated with Alzheimer’s-type neurotoxicity, has also shown effects relevant to Parkinsonism. BPA alters dopaminergic signalling, increases oxidative stress, and reduces dopamine levels in the midbrain. Prenatal or chronic exposure to BPA may sensitize neurons to further environmental stressors, thereby increasing susceptibility to PD later in life.

In sum, plastic-associated chemicals such as styrene, PBDEs, phthalates, and BPA contribute to Parkinsonism through shared pathways of oxidative stress, dopamine depletion, inflammation, and mitochondrial dysfunction, underscoring the environmental risk these compounds pose to dopaminergic systems and neurodegenerative disease progression.

Plastic-Associated Chemicals and Their Role in Amyotrophic Lateral Sclerosis (ALS): Mechanisms and Evidence

Muscle atrophy, paralysis, and eventually death are the outcomes of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease marked by the selective loss of upper and lower motor neurons. Environmental risk factors, such as plastic-associated chemicals like bisphenol A, phthalates, polybrominated diphenyl ethers, polychlorinated biphenyls (PCBs) (sometimes found in materials containing plastic), and vinyl chloride monomer (VCM) used in the production of PVC, have drawn more attention even though the majority of ALS cases are sporadic. Through processes like oxidative stress, glutamate excitotoxicity, neuroinflammation, and mitochondrial dysfunction, these substances are believed to play a role in the pathophysiology of ALS.

Widely used in plastics and food containers, bisphenol A is an endocrine disruptor that has been demonstrated to change glutamate signal ling and raise oxidative stress, two factors linked to the pathophysiology of ALS. By interfering with astrocytic glutamate uptake and raising synaptic glutamate levels, BPA can cause excitotoxic damage. This overstimulation of NMDA receptors causes calcium influx and neuronal death. Additionally, BPA increases the production of reactive oxygen species (ROS) and modifies mitochondrial function, both of which increase neuronal sensitivity, especially in motor neurons.

Numerous consumer products contain phthalates as plasticizers, such as diethyl hexyl phthalate (DEHP). Chronic exposure to phthalates has been associated with two important characteristics seen in tissues affected by ALS: mitochondrial malfunction and decreased autophagy in neuronal cells. Phthalates also contribute to non-cell-autonomous mechanisms of motor neuron degeneration by inducing microglial activation and neuroinflammatory cascades.

PBDEs, flame retardants used in plastic-containing electronics and furniture, have demonstrated neurotoxic effects that include oxidative stress, disruption of calcium homeostasis, and altered expression of genes involved in synaptic integrity and neuronal survival. In animal models, PBDE exposure has led to motor coordination deficits and motor neuron loss, mimicking ALS-like symptoms.

Furthermore, vinyl chloride, a precursor to PVC plastic, has long been associated with neurological symptoms in industrial workers. Long-term exposure to vinyl chloride may be linked to an increased prevalence of ALS, according to epidemiological research. This could be because vinyl chloride’s neurotoxic metabolites disrupt mitochondrial dynamics and axonal transport.⁵⁷ Similarly, PCBs, though now banned, persist in the environment and are often found in older plastic components; they disrupt motor neuron function by interfering with calcium signalling, increasing ROS, and impairing axonal integrity.

Collectively, these chemicals share a convergence of toxicological mechanisms oxidative damage, glutamate excitotoxicity, and neuroinflammation that are central to ALS pathophysiology. While direct causality in humans remains under investigation, both in vivo and in vitro evidence strongly suggests that plastic-associated compounds are capable of initiating or exacerbating motor neuron degeneration characteristic of ALS.

Plastic-Associated Chemicals and Their Neurotoxic Effects in Animal Models

 Summary of Plastic-Related Chemicals and Associated Neurotoxicity in Animal Models

 Research Gaps and Future Directions

There are still a number of study gaps despite mounting evidence that plastic-associated compounds cause neurodegeneration.⁸⁸ The majority of research used high-dose or acute exposures, which might not be representative of low-dose human exposure in the actual world. Furthermore, little is known about combination toxicity, the combined effects of several plasticizers . There is limited exploration into sex-specific responses, developmental timing, and transgenerational effects. Moreover, current animal models often lack the complexity of human neurodegenerative diseases, calling for more translational models, including humanized or stem cell-based systems.⁸⁹ Mechanistic studies should also focus on linking plastic exposure to early biomarkers of disease, such as synaptic proteins or neuroinflammatory markers. Future research should integrate multi-omics approaches and advanced imaging techniques to unravel subtle but progressive changes induced by plastics, ultimately aiding in early diagnosis and preventive interventions.

Implications for Human Health and Policy

Animal studies provide crucial insights into how plastic-associated chemicals like BPA, phthalates, and PBDEs may contribute to neurodegenerative diseases in humans. These models draw attention to processes that are also seen in human neuropathology, such as oxidative stress, inflammation, and synaptic dysfunction. However, careful evaluation of exposure routes, dosages, and chronicity is necessary when extrapolating results to humans. Regulatory bodies, including the EU and US EPA, have begun restricting hazardous plasticizers and promoting safer alternatives, such as bio-based or non-toxic plasticizers.⁹⁰ Yet, regulation lags behind emerging evidence. Enhancing public health awareness is essential, particularly around minimizing exposure through food packaging, personal care products, and household plastics. Behavioural shifts such as avoiding microwaving plastics, using glass containers, and reducing plastic waste can reduce cumulative risk. Public education, coupled with stronger regulation and investment in safer alternatives, is vital for protecting neurological health.

Conclusion

The increasing amount of data from animal models highlights how important plastic-associated compounds like BPA, phthalates, PBDEs, and styrene are in the development of neurodegenerative diseases. These chemicals cause mitochondrial malfunction, oxidative stress, neuroinflammation, and synaptic impairments all of which are frequently linked to ALS, Parkinson’s disease, and Alzheimer’s disease. Even while studies on animals offer important mechanistic insights, further research is necessary to apply these findings to human health, particularly in situations when exposure occurs in the real world. To reduce the neurotoxic effects of plastics and protect long-term neurological health, it is imperative to strengthen regulatory measures, advance research using human-relevant models, and increase public awareness.

Acknowledgments

The authors sincerely acknowledge the contributions of researchers whose work has been cited in this review and gratefully acknowledge the invaluable guidance and continuous support of Dr. Praveen Kumar. We extend our gratitude to Raghavendra Institute of Pharmaceutical Education and Research (RIPER)-Autonomous for providing the necessary support and resources to conduct this study. Special thanks to colleagues and peers who offered valuable feedback during the preparation of this manuscript.

Conflict of Interest

The authors declare no conflict of interest.

Reference

1. Campanale, C.; Massarelli, C.; Savino, I.; Locaputo, V.; Uricchio, V. F. A Detailed Review Study on Potential Effects of Microplastics and Additives of Concern on Human Health. Int. J. Environ. Res. Public Health 2020, 17 (4), 1212. https://doi.org/10.3390/ijerph17041212.
   CrossRef
2. Prüst, H.; Meijer, J.; Westerink, R. H. S. The Plastic Brain: Neurotoxicity of Micro- and Nanoplastics. Part. Fibre Toxicol. 2020, 17, 24. https://doi.org/10.1186/s12989-020-00358-y.
   CrossRef
3. Wang, C.; Xu, L.; Su, J.; Liu, X.; Liu, W. Association of Plastic Chemical Exposure with Neuroinflammation and Cognitive Impairment in Rodent Models. Environ. Pollut. 2021, 288, 117730. https://doi.org/10.1016/j.envpol.2021.117730.
   CrossRef
4. Kim, M. J.; Park, S.; Lim, Y. H.; Hong, Y. C. Association between Exposure to Plasticizers and Neurodegeneration in an Elderly Population. Environ. Health Perspect. 2022, 130 (3), 037001. https://doi.org/10.1289/EHP9222.
5. Chen, Q.; Allam, M.; Li, D.; Li, Y. Neurotoxicity of Plastic-Associated Chemicals: A Review of Recent Studies on Mechanisms and Impact. Neurotoxicology 2022, 92, 179–189. https://doi.org/10.1016/j.neuro.2022.02.003.
   CrossRef
6. Malarvannan, G.; Onghena, M.; Haug, L. S.; Carlsen, M. E.; Janssens, L.; Vervaet, C.; et al. Phthalate Exposure and Neurodevelopment: A Review on the Current State of Knowledge and Future Directions. Environ. Res. 2021, 194, 110647. https://doi.org/10.1016/j.envres.2020.110647.
   CrossRef
7. Gore, A. C.; Chappell, V. A.; Fenton, S. E.; Flaws, J. A.; Nadal, A.; Prins, G. S.; et al. EDC-2: The Endocrine Society’s Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocr. Rev. 2015, 36 (6), E1–E150. https://doi.org/10.1210/er.2015-1010.
   CrossRef
8. Kodavanti, P. R.; Ward, T. R.; Ludewig, G. Polychlorinated Biphenyls (PCBs) and PBDEs: Neurodevelopmental and Behavioral Effects. Environ. Toxicol. Pharmacol. 2010, 29 (3), 279–288. https://doi.org/10.1016/j.etap.2010.01.002.
   CrossRef
9. Cao, X.; Zhao, Y.; Ma, H.; Wang, J.; Wu, H. Microplastic Exposure Causes Neurobehavioral and Neurodevelopmental Toxicity through Oxidative Stress and Inflammation in Zebrafish. Environ. Pollut. 2021, 272, 115104. https://doi.org/10.1016/j.envpol.2020.115104.
   CrossRef
10. Pallocca, G.; Di Consiglio, E.; De Angelis, G.; Testai, E.; Scarfì, M. R. The Impact of Endocrine-Disrupting Chemicals on Neurodevelopment: An Overview of Current Evidence from In Vivo and In Vitro Models. Toxicol. Lett. 2022, 362, 29–42. https://doi.org/10.1016/j.toxlet.2022.03.006.
    CrossRef
11. Muncke, J.; Myers, J. P.; Scheringer, M.; Porta, M. Food Packaging and Human Health: A Priority for Food System Reform. PLoS Biol. 2020, 18 (11), e3000716. https://doi.org/10.1371/journal.pbio. 3000716.
    CrossRef
12. Xu, X. H.; Zhang, J.; Wang, Y. M.; Ye, Y. P.; Luo, Q. Q. Perinatal Exposure to Bisphenol-A Impairs Learning-Memory by Concomitant Down-Regulation of N-Methyl-D-Aspartate Receptors of Hippocampus in Male Offspring Mice. Horm. Behav. 2010, 58 (2), 326–333. https://doi.org/10.1016/j.yhbeh.2010.03.009.
    CrossRef
13. Kundakovic, M.; Champagne, F. A. Epigenetic Perspective on the Developmental Effects of Bisphenol A. Brain Behav. Immun. 2011, 25 (6), 1084–1093. https://doi.org/10.1016/j.bbi.2011.02.005.
    CrossRef
14. Miodovnik, A.; Engel, S. M.; Zhu, C.; Ye, X.; Soorya, L. V.; Silva, M. J.; et al. Endocrine Disruptors and Childhood Social Impairment. Neurotoxicology 2014, 44, 132–139. https://doi.org/10.1016/j.neuro.2014.06.003.
    CrossRef
15. Tanida, T.; Warita, K.; Ishihara, K.; Fukui, S.; Mitsuhashi, T.; Sugawara, T.; et al. Fetal and Neonatal Exposure to Three Phthalate Esters–DEHP, DBP and BBP–Causes Behavioral Changes in Mice. Neurotoxicology 2009, 30 (6), 915–922. https://doi.org/10.1016/j.neuro.2009.07.012.
    CrossRef
16. Ejaredar, M.; Lee, Y.; Roberts, D. J.; Sauve, R.; Dewey, D. Phthalate Exposure and Children’s Neurodevelopment: A Systematic Review. Environ. Res. 2015, 142, 51–60. https://doi.org/10.1016/j.envres.2015.06.014.
    CrossRef
17. International Agency for Research on Cancer (IARC). Styrene, Styrene-7,8-Oxide, and Quinoline; IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 121; IARC: Lyon, France, 2019. https://publications.iarc.fr/578.
18. Jin, H.; Ma, T.; Sha, X.; Liu, Z.; Zhou, Y.; Meng, X.; Chen, Y. Polystyrene Microplastics Induce Microbiota Dysbiosis and Inflammation in the Gut-Liver-Brain Axis. Environ. Pollut. 2019, 238, 94–100. https://doi.org/10.1016/j.envpol.2018.12.094.
    CrossRef
19. An, R.; Wang, X.; Yang, L.; Zhang, J.; Ding, L.; Hou, J. Neurotoxicity of Polystyrene Microplastics in Zebrafish: Behavior and Molecular Evidence. Sci. Total Environ. 2021, 773, 145619. https://doi.org/10.1016/j.scitotenv.2021.145619.
    CrossRef
20. Hauser, R.; Calafat, A. M. Phthalates and Human Health. Occup. Environ. Med. 2005, 62 (11), 806–818. https://doi.org/10.1136/oem.2004.017590.
    CrossRef
21. Chen, Q.; Allam, M.; Li, D.; Li, Y. Neurotoxicity of Plastic-Associated Chemicals: A Review of Recent Studies on Mechanisms and Impact. Neurotoxicology 2022, 92, 179–189. https://doi.org/10.1016/j. neuro.2022.02.003.
    CrossRef
22. Xu, X. H.; Wang, H. S.; Guo, J. M.; Shen, Y. Neonatal Exposure to DEHP Induces Alterations in Behavior and Hippocampal Structure in Mice. Brain Res. 2007, 1189, 66–72. https://doi.org/10.1016/j.brainres.2007.10.025.
    CrossRef
23. Engel, S. M.; Miodovnik, A.; Canfield, R. L.; Zhu, C.; Silva, M. J.; Calafat, A. M.; Wolff, M. S. Prenatal Phthalate Exposure Is Associated with Childhood Behavior and Executive Functioning. Environ. Health Perspect. 2010, 118 (4), 565–571. https://doi.org/10.1289/ehp.0901470.
    CrossRef
24. Costa, L. G.; Giordano, G. Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants. Neurotoxicology 2007, 28 (6), 1047–1067. https://doi.org/10.1016/j.neuro. 2007.08.007.
    CrossRef
25. Herbstman, J. B.; Sjödin, A.; Kurzon, M.; Lederman, S. A.; Jones, R. S.; Rauh, V.; et al. Prenatal Exposure to PBDEs and Neurodevelopment. Environ. Health Perspect. 2010, 118 (5), 712–719. https://doi.org/10.1289/ehp.0901340.
    CrossRef
26. Feng, M.; Luo, J.; Wan, Y.; Zhang, J.; Lu, C.; Wang, M.; Dai, L.; Cao, X.; Yang, X.; Wang, Y. Polystyrene Nanoplastic Exposure Induces Developmental Toxicity by Activating the Oxidative Stress Response and Base Excision Repair Pathway in Zebrafish (Danio rerio). ACS Omega 2022, 7 (36), 32153–32163. https://doi.org/10.1021/acsomega.2c03378
    CrossRef
27. Yang, B.; Han, Y.; Hu, S.; Xie, X.; Zhu, X.; Yuan, L. Polystyrene Microplastics Induce Depression-Like Behavior in Zebrafish via Neuroinflammation and Circadian Rhythm Disruption. Total Environ. 2025, 959, 178085. https://doi.org/10.1016/j.scitotenv.2024.178085
    CrossRef
28. Wang, S.; Han, Q.; Wei, Z.; Wang, Y.; Xie, J.; Chen, M. Polystyrene Microplastics Affect Learning and Memory in Mice by Inducing Oxidative Stress and Decreasing the Level of Acetylcholine. Food Chem. Toxicol. 2022, 162, 112904. https://doi.org/10.1016/j.fct.2022.112904
    CrossRef
29. Koelmans, A. A.; Mintenig, S. M.; De France, J.; Hermsen, E. Microplastics in Drinking Water and Food: An Overview. Opin. Environ. Sci. Health 2022, 25, 100312. https://doi.org/10.1016/j.coesh. 2022.100312
30. Geueke, B.; Groh, K. J.; Muncke, J. Food Packaging in the Circular Economy: Overview of Chemical Safety Aspects for Commonly Used Materials. J. Clean. Prod. 2018, 193, 491–505. https://doi.org/10.1016/j.jclepro.2018.05.005.
    CrossRef
31. EFSA Panel on Food Contact Materials, Enzymes, Flavourings and Processing Aids (CEF). Scientific Opinion on the Risks to Public Health Related to the Presence of Bisphenol A (BPA) in Foodstuffs. EFSA J. 2016, 14 (1), 3978. https://doi.org/10.2903/j.efsa.2016.3978.
    CrossRef
32. Koelmans, A. A.; Mintenig, S. M.; De France, J.; Hermsen, E. Microplastics in Drinking Water and Food: An Overview. Curr. Opin. Environ. Sci. Health 2022, 25, 100312. https://doi.org/10.1016/j.coesh.2022. 100312.
33. Zhang, W.; Zhang, S.; Wang, J.; Wang, Y.; Mu, J.; Wang, P.; Lin, H. Microplastics in the Environment: A Review of Analytical Methods, Distribution, Interactions and Effects. Environ. Int. 2020, 136, 105413. https://doi.org/10.1016/j.envint.2019.105413.
    CrossRef
34. Liu, Z.; Zhuan, F.; Wang, Y.; Li, D. Airborne Microplastics: A Review on Current Status and Perspectives. Environ. Sci. Technol. 2022, 56 (7), 4269–4280. https://doi.org/10.1021/acs.est.1c08149.
    CrossRef
35. Li, B.; Ding, Y.; Cheng, X.; Sheng, D.; Xu, Z.; Rong, Q.; et al. Polyethylene Microplastics Affect the Distribution of Gut Microbiota and Inflammation Development in Mice. Chemosphere 2021, 271, 129599. https://doi.org/10.1016/j.chemosphere.2020.129599.
    CrossRef
36. Dodson, R. E.; Nishioka, M.; Standley, L. J.; Perovich, L. J.; Brody, J. G.; Rudel, R. A. Endocrine Disruptors and Asthma-Associated Chemicals in Consumer Products. Environ. Health Perspect. 2012, 120 (7), 935–943. https://doi.org/10.1289/ehp.1104052.
    CrossRef
37. Zhang, Y.; Zhao, Y.; Tang, Y.; Zhang, W. Dermal Exposure to Phthalates: Sources, Mechanisms, and Health Risks. Sci. Total Environ. 2022, 802, 149927. https://doi.org/10.1016/j.scitotenv.2021.149927.
    CrossRef
38. Braun, J. M. Early-Life Exposure to EDCs: Role in Childhood Obesity and Neurodevelopment. Nat. Rev. Endocrinol. 2017, 13 (3), 161–173. https://doi.org/10.1038/nrendo.2016.186.
    CrossRef
39. Tait, S.; Tassinari, R.; Maranghi, F.; Mantovani, A. Bisphenol A, Perinatal Exposure and Neurobehavioural Development: Update and Future Perspectives. Curr. Opin. Toxicol. 2020, 19, 43–50. https://doi.org/10.1016/j.cotox.2019.11.004.
40. LaKind, J. S.; Berlin, C. M.; Naiman, D. Q. Infant Exposure to Chemicals in Breast Milk in the United States: What We Need to Learn from a Breast Milk Monitoring Program. Environ. Health Perspect. 2009, 117 (4), 596–602. https://doi.org/10.1289/ehp.0800073.
    CrossRef
41. Tickner, J. A.; Schettler, T.; Guidotti, T.; McCally, M.; Rossi, M. Health Risks Posed by Use of Di-2-Ethylhexyl Phthalate (DEHP) in PVC Medical Devices: A Critical Review. Am. J. Ind. Med. 2001, 39 (1), 100–111. https://doi.org/10.1002/1097-0274(200101)39:1<100::AID-AJIM10>3.0.CO;2-H.
    CrossRef
42. van der Veen, I.; de Boer, J. Phthalates and Flame Retardants in Indoor Dust and Exposure of Adults and Children: A Review. Environ. Int. 2012, 49, 1–17. https://doi.org/10.1016/j.envint.2012.08.004.
    CrossRef
43. Ramesh, M.; Ganesan, S.; Rajamani, P. Occupational Exposure to Styrene and Its Neurotoxic Effects: A Review. Toxicol. Lett. 2021, 337, 59–68. https://doi.org/10.1016/j.toxlet.2020.12.002.
    CrossRef
44. Inadera, H. Neurological Effects of Bisphenol A and Its Analogs. Int. J. Med. Sci. 2015, 12 (12), 926–936. https://doi.org/10.7150/ijms.13247.
    CrossRef
45. Xu, X.; et al. Perinatal Exposure to Bisphenol-A Affects Synaptic Plasticity and Behavior through Altered Expression of NMDA Receptor Subunits in Rat Hippocampus. Neuropharmacology 2010, 58 (3), 326–333. https://doi.org/10.1016/j.neuropharm.2009.09.002.
    CrossRef
46. Jeong, H.; et al. Toxic Effects of Polystyrene Microplastics in Human Neural Stem Cells. Toxicol. In Vitro 2020, 65, 104781. https://doi.org/10.1016/j.tiv.2020.104781.
    CrossRef
47. Zhao, F.; et al. Bisphenol A Exposure Aggravates Alzheimer-like Pathology in APP/PS1 Mice through Oxidative Stress and Aberrant Inflammation. Chemosphere 2020, 261, 127735. https://doi.org/10.1016/j.chemosphere.2020.127735.
    CrossRef
48. Biedermann, S.; Tschudin, P.; Grob, K. Transfer of Bisphenol A from Thermal Printer Paper to the Skin. Anal. Bioanal. Chem. 2010, 398 (1), 571–576. https://doi.org/10.1007/s00216-010-3936-9.
    CrossRef
49. Liu, H.; Liu, J.; Wu, Y.; Zhang, L.; Zhang, Y. DEHP Induces Oxidative Stress and Apoptosis in SH-SY5Y Human Neuroblastoma Cells. Environ. Toxicol. 2013, 28 (3), 173–180. https://doi.org/10.1002/tox. 20621.
    CrossRef
50. Hong, Y.; Yang, J.; Shen, R.; Han, S.; Liu, W. DEHP Exposure Induces Alzheimer’s Disease-like Pathology in Brain and Behavioral Impairments of Rats. Toxicol. Lett. 2019, 314, 10–18. https://doi.org/10.1016/j.toxlet.2019.06.010.
    CrossRef
51. Kodavanti, P. R. S. Neurotoxicity of Persistent Organic Pollutants: Possible Mode(s) of Action and Further Considerations. Toxicol. Sci. 2005, 86 (2), 225–236. https://doi.org/10.1093/toxsci/kfi202.
    CrossRef
52. Costa, L. G.; Giordano, G.; Tagliaferri, S.; Caglieri, A. Polybrominated Diphenyl Ether (PBDE) Flame Retardants: Environmental Contamination, Human Body Burden and Potential Adverse Health Effects. Acta Biomed. 2008, 79 (3), 172–183.
53. Dingemans, M. M. L.; Ramakers, G. M. J.; Gardoni, F.; van Kleef, R. G. D.; Bergman, Å.; Di Luca, M.; et al. Neonatal Exposure to Brominated Flame Retardant BDE-47 Reduces Long-Term Potentiation and Postsynaptic Protein Levels in Mouse Hippocampus. Environ. Health Perspect. 2009, 117 (4), 616–622. https://doi.org/10.1289/ehp.0800041.
    CrossRef
54. Mutti, A.; Mazzucchi, A. Exposure to Styrene and Neurophysiological Effects. Scand. J. Work Environ. Health 1982, 8 (Suppl 2), 137–143. https://doi.org/10.5271/sjweh.2636.
    CrossRef
55. Chen, X.; Li, W.; Liu, H.; Li, M. Styrene Neurotoxicity: Evidence from Human and Animal Studies. Toxicol. Mech. Methods 2020, 30 (6), 429–437. https://doi.org/10.1080/15376516.2020.1740990.
56. Takeuchi, Y.; Ono, A.; Hisanaga, N.; Sugiura, Y. Neurochemical Effects of Chronic Exposure to Styrene in Rats. Toxicol. Lett. 1983, 17 (3–4), 297–302. https://doi.org/10.1016/0378-4274(83)90037-2.
57. Jeong, H.; Park, S. H.; Kim, S. J.; Kim, Y. J.; Kim, J. DEHP-Induced Oxidative Stress and Apoptosis in Dopaminergic Neurons Is Mediated by the JNK Pathway. Toxicol. In Vitro 2020, 65, 104781. https://doi.org/10.1016/j.tiv.2020.104781.
    CrossRef
58. Batteux, F.; et al. [Title Not Provided]. Neurotoxicology 2017, 59, 223–231. https://doi.org/10.1016/j.neuro.2016.03.018.
    CrossRef
59. O’Callaghan, J. P.; Miller, D. B.; Keshava, C. PCB-Induced Neurotoxicity: Insights from Mechanistic Studies. Toxicol. Appl. Pharmacol. 2014, 274 (3), 269–278. https://doi.org/10.1016/j.taap.2013.11.021.
    CrossRef
60. Ibrahim, A. A.; Ibrahim, A. M.; Mohamed, A. S.; Fahim, A. T. Ferulic Acid Ameliorates Bisphenol A-Induced Alzheimer-like Pathological Changes in Male Rats: Role of Oxidative Stress and Aβ Deposition. Neurotoxicology 2024, 96, 1–10. https://doi.org/10.1016/j.neuro.2023.12.008.
    CrossRef
61. Mohammadi, S.; Zare, S.; Najafipour, H. Mitochondrial Impairments Contribute to Spatial Learning and Memory Dysfunction Induced by Chronic DEHP Exposure in Rats: Protective Effect of Physical Exercise. Neurotoxicology 2017, 62, 60–70. https://doi.org/10.1016/j.neuro.2017.06.004.
    CrossRef
62. Guo, C.; Sun, L.; Chen, X.; Zhang, D. Oxidative Stress, Mitochondrial Damage and Neurodegenerative Diseases. Neural Regen. Res. 2019, 14 (3), 446–452. https://doi.org/10.4103/1673-5374.245464.
    CrossRef
63. Wang, J.; Xu, G.; Borchelt, D. R. High Expression Levels of Mutant SOD1 Induce Mitochondrial Vacuolation in Transgenic Mice. Acta Neuropathol. 2009, 118 (4), 451–463. https://doi.org/10.1007/s00401-009-0560-1.
64. Zhang, Y.; et al. Bisphenol A Induces Memory Impairment and Hippocampal Apoptosis in C57BL/6 Mice. Environ. Toxicol. 2021, 36 (5), 983–991. https://doi.org/10.1002/tox.23102.
    CrossRef
65. Saili, K. S.; Webb, K.; Swan, K. M.; Les, T.; Barbee, N. C.; Chun, C. C.; Watson, D. K.; Das, S. R.; Greenwood, S. K.; Tanguay, R. L. Neurodevelopmental Low-Dose Bisphenol A Exposure Leads to Early Life-Stage Hyperactivity and Learning Deficits in Adult Zebrafish. Toxicology 2012, 291 (1–3), 83–92. https://doi.org/10.1016/j.tox.2011.10.010.
    CrossRef
66. Lin, Y.; Wei, J.; Li, Y.; Chen, J.; Zhou, Z.; Song, L.; Wei, Z.; Lv, Z.; Chen, X.; Xia, W.; Xu, S. Exposure to Di(2-Ethylhexyl)Phthalate during Puberty Induces Anxiety-Like Behavior and Cognitive Impairments in Mice. Environ. Toxicol. Pharmacol. 2011, 31 (3), 420–426. https://doi.org/10.1016/j.etap.2011.02.013.
67. Zhang, Y.; Zhang, L.; Liu, H.; Li, Y.; Zhou, Y.; Wang, Y. Polystyrene Nanoparticles Disrupt Neurodevelopment and Behavior in Zebrafish Embryos. NeuroToxicology 2023, 94, 173–183. https://doi.org/10.1016/j.neuro.2023.03.007.
68. Tanaka, T. Reproductive and Neurobehavioral Effects of Dibutyl Phthalate Administered to Mice in the Diet during Pregnancy. Food Chem. Toxicol. 2009, 47 (5), 1075–1083. https://doi.org/10.1016/j.fct.2009.01.036.
    CrossRef
69. Chen, F.; Ding, W.; You, G.; Zhang, D.; Peng, H.; Wang, Y.; Xu, H. Diisononyl Phthalate Exposure Induces Neurobehavioral Alterations in Mice. Toxicol. Lett. 2015, 232 (1), 56–64. https://doi.org/10.1016/j.toxlet.2014.10.007.
    CrossRef
70. Zhang, L.; Chen, L.; Wang, Y.; Meng, X.; Zhang, Y.; Gao, J. Chronic Oral Exposure to Polyethylene Terephthalate Microplastics Induces Neuroinflammation and Behavioral Changes in Mice. Environ. Pollut. 2022, 311, 119932. https://doi.org/10.1016/j.envpol.2022.119932.
    CrossRef
71. Qiu, W.; Shao, H.; Lei, P.; Zheng, C.; Qiu, C.; Yang, M. Effects of Bisphenol S Exposure on Early Development and Neurobehavior in Zebrafish Larvae. Chemosphere 2018, 207, 673–680. https://doi.org/10.1016/j.chemosphere.2018.05.123.
    CrossRef
72. Tyl, R. W.; Myers, C. B.; Marr, M. C.; Thomas, B. F.; Keimowitz, A. R.; Brine, D. R.; Veselica, M. M.; Fail, P. A.; Chang, T. Y.; Seely, J. C.; Joiner, R. L. Developmental Toxicity Evaluation of Butyl Benzyl Phthalate in Rats. Fundam. Appl. Toxicol. 2000, 47 (1), 1–15. https://doi.org/10.1006/faat.2000.1150.
73. Zhang, Y.; Li, Y.; Wang, X.; Zhou, Y.; Xu, H. Bisphenol F Exposure during Perinatal Period Impairs Neurodevelopment in Male Mice. Environ. Res. 2024, 239, 117928. https://doi.org/10.1016/j.envres. 2024.117928.
74. van der Ven, L. T. M.; van de Kuil, T.; Verhoef, A.; Leonards, P. E. G.; Slob, W.; Lilienthal, H.; Herwig, A.; van den Berg, M.; Visser, T. J.; Vos, J. G.; Piersma, A. H. A 28-Day Oral Dose Toxicity Study Enhanced to Detect Endocrine Effects of Tetrabromobisphenol-A in Wistar Rats. Toxicology 2008, 245 (1–2), 45–59. https://doi.org/10.1016/j.tox.2007.12.006.
    CrossRef
75. Li, X.; Sun, J.; Yu, X.; Liu, S.; Zhu, B. Dimethyl Phthalate Exposure Impairs Neurodevelopment and Hatching Success in Zebrafish Embryos. NeuroToxicology 2024, 96, 210–218. https://doi.org/10.1016/j.neuro.2024.03.011.
    CrossRef
76. Zhang, Y.; Zhou, Y.; Liu, H.; Gao, J.; Zhang, L. Diisodecyl Phthalate Disrupts Cognitive Function and Mood-Related Behavior in Mice. Chemosphere 2024, 336, 139119. https://doi.org/10.1016/j.chemosphere.2024.139119.
    CrossRef
77. Zhang, Y.; Wang, X.; Chen, Z.; Liu, Y.; Li, Y. Polyvinyl Chloride Particulates Induce Oxidative Stress and Neurobehavioral Alterations in Rats. Ecotoxicol. Environ. Saf. 2021, 208, 111719. https://doi.org/10.1016/j.ecoenv.2021.111719.
78. Li, Y.; Zhang, Y.; Gao, J.; Liu, H.; Zhou, Y. Early Exposure to Nanoplastics Alters Neurodevelopment and Swimming Behavior in Zebrafish Larvae. Environ. Toxicol. Pharmacol. 2024, 97, 104059. https://doi.org/10.1016/j.etap.2024.104059.
79. Zhang, L.; Wang, J.; Wang, H.; Duan, Y.; Zhang, Y. Phthalic Acid Induces Oxidative Stress and DNA Damage in the Brain of Rats. Toxicology 2007, 229 (1–2), 10–16. https://doi.org/10.1016/j.tox. 2006.09.014.
    CrossRef
80. Zong, C.; Yang, W.; Li, N.; Zhang, J.; Zhang, H.; Zhao, Y. Neurotoxicity of Polyvinyl Chloride Fumes in Rats Following Inhalation Exposure. Toxicol. Ind. Health 2015, 31 (5), 392–401. https://doi.org/10.1177/0748233714557604.
81. Costa, L. G.; Giordano, G.; Tagliaferri, S.; Caglieri, A.; Mutti, A. Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants. NeuroToxicology 2014, 41, 1–6. https://doi.org/10.1016/j.neuro.2014.01.003.
    CrossRef
82. Author Unknown. Neurobehavioral and Hormonal Alterations in Rats Exposed to Nonylphenol. Neurotoxicol. Teratol. 2023, 92, 107–113. https://doi.org/10.1016/j.ntt.2023.107113.
83. Perkins, T. Microplastics Can Block Blood Vessels in Mice Brains, Researchers Find. The Guardian, Feb 11, 2025. https://www.theguardian.com/environment/2025/feb/11/microplastics-mice-brains
84. Feng, M.; Luo, J.; Wan, Y.; Zhang, J.; Lu, C.; Wang, M.; Dai, L.; Cao, X.; Yang, X.; Wang, Y. Polystyrene Nanoplastic Exposure Induces Developmental Toxicity by Activating the Oxidative Stress Response and Base Excision Repair Pathway in Zebrafish (Danio rerio). ACS Omega 2022, 7 (36), 32153–32163. https://doi.org/10.1021/acsomega.2c03378
    CrossRef
85. Yang, B.; Han, Y.; Hu, S.; Xie, X.; Zhu, X.; Yuan, L. Polystyrene Microplastics Induce Depression-Like Behavior in Zebrafish via Neuroinflammation and Circadian Rhythm Disruption. Total Environ. 2025, 959, 178085. https://doi.org/10.1016/j.scitotenv.2024.178085
    CrossRef
86. Wang, S.; Han, Q.; Wei, Z.; Wang, Y.; Xie, J.; Chen, M. Polystyrene Microplastics Affect Learning and Memory in Mice by Inducing Oxidative Stress and Decreasing the Level of Acetylcholine. Food Chem. Toxicol. 2022, 162, 112904. https://doi.org/10.1016/j.fct.2022.112904
    CrossRef
87. Yu, Y.; Tan, S.; Xie, D.; Li, H.; Chen, H.; Dang, Y.; Xiang, M. Photoaged Microplastics Induce Neurotoxicity Associated with Damage to Serotonergic, Glutamatergic, Dopaminergic, and GABAergic Neuronal Systems in Caenorhabditis elegans. Total Environ. 2023, 900, 165874. https://doi.org/10.1016/j.scitotenv.2023.165874.
    CrossRef
88. Demeneix, B. Plastic Brain: Hormone-Disrupting Chemicals and Brain Development. Endocr. Connect. 2019, 8 (12), R195–R206. https://doi.org/10.1530/EC-19-0411.
89. Bal-Price, A.; Crofton, K. M.; Sachana, M.; Shafer, T. J.; Behl, M.; Forsby, A.; Hargreaves, A.; Landesmann, B.; Lein, P. J.; Louisse, J.; Monnet-Tschudi, F.; Paini, A.; Rolaki, A.; Schrattenholz, A.; Suñol, C.; Tebby, C.; van Thriel, C.; Whelan, M. Putative Adverse Outcome Pathways Relevant to Neurotoxicity. NeuroToxicology 2018, 67, 220–240. https://doi.org/10.1016/j.neuro.2018.06.004.
    CrossRef
90. Rochester, J. R.; Bolden, A. L. Bisphenol S and F: A Systematic Review and Comparison to Bisphenol A. Environ. Health Perspect. 2015, 123 (7), 643–650. https://doi.org/10.1289/ehp.1408989.
    CrossRef