Micro(nano)plastics (M/NPs) are pervasive in marine environments. Benzo[a]pyrene (B[a]P), a typical polycyclic aromatic hydrocarbon (PAH), possesses teratogenic, mutagenic, and carcinogenic properties. B[a]P can accumulate on M/NPs, altering their toxicity. This study investigated individual and combined effects of M/NPs and B[a]P on the intestinal regeneration of the benthic invertebrate Apostichopus japonicus. Eviscerated sea cucumbers were exposed to 0.1 mg L-1 M/NPs (80 nm [NP80] or 20 μm [MP20]) and/or 0.03 μg L-1 B[a]P for 28 days. Cell proliferation, antioxidant and immunoenzyme activity, gene expression, and microbial community in the regenerated intestine were assessed. It demonstrated that combined exposure prolonged regeneration process, leading to increased oxidative stress and intestinal damage. Differential gene expression analysis revealed that co-exposure and single NP80 exposure both significantly changed translation-related processes, while single MP20 exposure primarily affected lipid metabolism. All treatments significantly altered the intestinal microbiota. Under the MP20+B[a]P treatment, Ralstonia abundance significantly increased, while Cobetia and Paracoccus abundances decreased. In general, co-exposure exerted more detrimental effects on intestinal regeneration than any single exposure, with MP20+B[a]P demonstrating more severe impacts. This study provides novel insights into the biotoxicity of M/NPs and B[a]P, contributing to better understanding of the detriments of microplastics and PAHs on marine benthic invertebrates.

The gut-liver axis is vital for organism health. Nanoplastics (NPs) and bisphenol A (BPA) can harm zebrafish intestines and livers, yet their combined impact on the gut-liver axis and transgenerational effects are unknown. In this study, F0 zebrafish were exposed to NPs and/or BPA for 28 days. Lipid indices of F0, F1, and F2 zebrafish, as well as the developmental indices of offspring, were detected. 16S rRNA sequencing and metabolomics were used to analyze F0 zebrafish gut microbiota and liver metabolites, exploring underlying mechanisms. The mTOR inhibitor Rapa was injected into F0 zebrafish to examine the mTOR pathway's role in lipid disorders caused by NPs and BPA exposure. The results showed that the exposure of F0 generation zebrafish to NPs and BPA led to lipid metabolism disorders in all generations of zebrafish and abnormal development in F1 and F2 zebrafish. Omics analysis revealed that the combined exposure to NPs and BPA significantly exacerbated the gut microbiota disorder in F0 zebrafish. The differential metabolites identified by untargeted metabolomics were enriched in the mTOR signaling pathway. After Rapa intervention, the lipid disorders in each group of F0 zebrafish were improved. In summary, the combined exposure to NPs and BPA may lead to lipid disorders in all generations of zebrafish and abnormal development of offspring by exacerbating the dysregulation of the gut microbiota-liver axis in F0 zebrafish. The results of this study provide mechanistic insights into the transgenerational effects induced by the combined exposure to NPs and BPA.

Microplastics are emerging pollutants with a wide range of ecological and biological effects, including the ability to accumulate in organisms and induce toxicity. Although numerous studies have investigated the distribution and toxicity of microplastics in murine models and cell lines, the conclusions are inconsistent owing to variations in experimental designs, particle sizes, exposure methods, and dose quantifications. To address these gaps, we systematically evaluated the size-dependent internalization and toxicity of polystyrene microplastics (PS-MPs) using in vitro and in vivo models. Fluorescently labeled PS-MPs were used to confirm the negligible toxicity of fluorophores on macrophages, demonstrating their suitability for tracking particle accumulation. In vitro experiments using RAW 264.7 cell lines and primary peritoneal macrophages revealed size-dependent phagocytosis and cytotoxicity, with smaller particles (0.5 µm) demonstrating higher internalization and causing greater mitochondrial depolarization, reactive oxygen species generation, and apoptosis compared to that with larger particles (5 µm). Acute in vivo experiments comparing oral administration and tail-vein injection revealed that the absorbed dose and toxicity were significantly influenced by particle size, with smaller PS-MPs showing higher organ retention and alterations in hematological and metabolic parameters. Additionally, a 28-day subacute oral exposure study highlighted systemic toxicity, including weight loss, disrupted food intake, elevated oxidative stress markers, and reduced antioxidant enzyme activity. By integrating multiple exposure routes, macrophage models, and fluorescence toxicity evaluations, this study provided a comprehensive and realistic assessment of microplastic toxicity, offering valuable insights for advancing toxicological evaluations and regulatory frameworks. However, this study did not address the influence of other plastic types, shapes, or environmental factors on toxicity. Future studies are thus needed to explore these variables and the long-term implications of real-world microplastic exposure.

Microplastics (MPs) and nanoplastics (NPs) are pervasive pollutants widely distributed across aquatic ecosystems. They have gained significant attention due to their potential adverse effects on marine organisms. Many marine species, particularly sea cucumbers, inadvertently ingest these plastic particles due to their non-selective feeding behavior. In this study we carried out a 14-day exposure experiment and investigated the effects of polyethylene MPs and NPs on gene expression, oxidative stress, immune condition and histology of a tropical sea cucumber, Holothuria leucospilota, a most abundant sea cucumbers species in the world. The results showed that MPs and NPs dramatically altered gene expression in discrepant profiles. NPs caused down-regulation of the majority of genes related to metabolic processes. In contrast to the enrichment of GO terms which related to regulation, differentiation and development after being exposed to MPs, metabolome-related GO terms were significantly enriched in NPs exposure. The toxicity mechanism associated with the NPs and MPs exposure involves the activation of the antioxidant defense system and the disruption of immune balance. Furthermore, histological destruction of the respiratory tree in NP and MP groups provided robust evidence for the unstable physiological condition. Our study deepens the comprehension of size-dependent plastic toxicity on marine benthic invertebrates, thereby posing a potential hazard to marine ecosystems.

Enrofloxacin (ENR) and atrazine (ATZ) are common co-contaminants in marine environments. Although the immunosuppressive effects of ENR and the endocrine-disrupting properties of ATZ are well established, the combined effects of these pollutants on hepatotoxicity, particularly concerning the regulation of the hypothalamic-pituitary-thyroid (HPT) and gut-liver axes, remain poorly understood. In this study, Larimichthys crocea was exposed to ENR and ATZ at environmentally relevant concentrations, individually and in combination, to investigate the hepatotoxicity. Liver cell swelling, necrosis, oxidative stress, and elevated liver injury markers were observed, indicating hepatic damage, with co-exposure exacerbating liver injury. Decreased levels of thyrotropin-releasing hormone and thyroid-stimulating hormone, increased triiodothyronine and thyroxine, and altered expression of HPT axis-related genes demonstrated enhanced disruption of the HPT axis under co-exposure, which was strongly associated with oxidative stress and liver dysfunction. Molecular docking confirmed that ENR and ATZ inhibited thyroid hormone binding to target proteins, likely provoking the enhanced hepatotoxicity. Additionally, ATZ significantly intensified the intestinal bacterial disturbances induced by ENR, further aggravating hepatotoxicity through the gut-liver axis. This study is the first to reveal the increased risk associated with ENR and ATZ co-exposure, highlighting the need for attention to such co-contaminants.

Micro and nanoplastics (MNPs) contamination constitute a pressing global issue with considerable ramifications for human health. Particles originating from the decomposition of plastic waste permeate ecosystems and disturb biological systems, especially the gastrointestinal (GI) tract. MNPs compromise the intestinal barrier, provoke oxidative stress, inflammation, and immunological dysfunction, and modify gut microbiota, which is associated with metabolic problems, inflammatory bowel disease (IBD), and colorectal cancer. MNPs traverse biological barriers beyond the gastrointestinal system, including the blood-brain barrier, colonic mucus layer, and placental barrier, resulting in accumulation in essential organs such as the liver, kidneys, and brain. This results in inflammatory damage, metabolic abnormalities, and oxidative stress, specifically affecting liver disease due to microbiota metabolite alteration and nephrotoxicity in the kidneys. Airborne MNPs pose an additional risk to respiratory health, aggravating ailments such as asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis. At-risk groups, such as pregnant women, newborns, and the elderly, encounter increased dangers, as MNPs traverse the placental barrier and may induce neurological and intergenerational health consequences. These particles function as vectors for environmental pollutants, exacerbating their cardiovascular and neurological effects. Addressing the long-term consequences of MNP exposure necessitates interdisciplinary collaboration to enhance comprehension and alleviate their growing risk to human health.

Environmental pollutants such as microplastics (MPs) and pesticides are becoming prevalent in aquatic ecosystems, posing risks to wildlife and human health. This study investigated the toxicological effects of polystyrene microplastics (PS-MPs) and cypermethrin (CYP) on adult female zebrafish (Danio rerio), focusing on intestinal microenvironment. Adsorption kinetics experimental results showed that PS-MPs can adsorb a certain amount of CYP on its surface, thereby forming a new type of composite pollutant. After exposure to red fluorescent PS-MPs for 4 days, it was found that the PS-MPs could enter the zebrafish and accumulate in the intestines. Five-month-old female zebrafish were exposed to PS-MPs, CYP, and a mixture of both for 21 days. After exposure, feces were collected and analyzed using metagenomic sequencing to determine microbial composition and functional changes. Metagenomic sequencing of naturally excreted feces showed that co-exposure synergistically reduced α-diversity and shifted community structure, with marked losses of beneficial Fusobacteriota, Firmicutes and Cetobacterium somerae and enrichment of pathogenic Preplasmiviricota. Functional annotation indicated that PS-MPs alone up-regulated glycoside hydrolases and glycosyl-transferases, whereas CYP and the co-exposure group suppressed a great number of the top 50 carbohydrate-active enzymes and decreased secondary metabolic pathways linked to amino-acid, lipid and carbohydrate metabolism pathways. Antibiotic-resistance gene (ARGs) profiling identified 57 ARG types (such as sul1, adeF, lnuC and mphA) after co-exposure. Finally, key genes related to amino acid metabolism, carbohydrate metabolism, and lipid metabolism in intestinal tissue were significantly altered. Collectively, our data demonstrated that PS-MPs and CYP exposure amplified gut dysbiosis, metabolic dysfunction and ARG complexity in zebrafish. Overall, the study highlighted the potential risks of combined environmental pollutants on intestinal microbiota, with implications for ecosystem health.

Human health depends on planetary health, and yet healthcare provision can have unintended consequences for the health of the planet. Emissions from the healthcare sector include greenhouse gases, air pollution and plastic pollution, alongside chemical contamination. Chemical pollution resulting in endocrine disruption has been associated with plastics, which are a source of concerning additives such as phthalates, bisphenols, perfluoroalkyl and polyfluoroalkyl substances, and flame retardants (all routinely found in healthcare products). Many endocrine-disrupting chemicals are persistent and ubiquitous in the environment (including water and food sources), with potential secondary harms for human health, including disrupting reproductive, metabolic and thyroid function. Here we review evidence-based strategies for mitigating environmental effects of healthcare delivery. We focus on what endocrinologists can do, including reducing demand for healthcare services through better preventative health, focusing on high-value care and improving sustainability of medical equipment and pharmaceuticals through adopting circular economy principles (including reduce, reuse and, as a last resort, recycle). The specific issue of endocrine-disrupting chemicals might be mitigated through responsible disposal and processing, alongside advocating for the use of alternative materials and replacing additive chemicals with those that have lower toxicity profiles, as well as tighter regulations. We must work to urgently transition to sustainable models of care provision, minimizing negative effects on human and planetary health.

The improper disposal and degradation of plastics causes the formation and spread of micro and nano-sized plastic particles in the ecosystem. The widespread presence of these micro and nanoplastics leads to their accumulation in the biotic and abiotic components of the environment, thereby affecting the cellular and metabolic functions of organisms. Despite being classified as xenobiotic agents, information about their sources and exposure related to reproductive health is limited. Micro and nano plastic exposure during early developmental stages can cause abnormal embryonic development. It can trigger neurotoxicity and inflammatory responses as well in the developing embryo. In embryonic development, a comprehensive study of their role in pluripotency, gastrulation, and multi-differentiation potential is scarce. Due to ethical concerns associated with the direct use of human embryos, pluripotent cells and its 3D in vitro models (with cell lines) are an alternative source for effective research. Thus, the 3D Embryoid body (EB) model provides a platform for conducting embryotoxicity and multi-differentiation potential research. Pluripotent stem cells such as embryonic and induced pluripotent stem cells derived embryoid bodies (EBs) serve as a robust 3D in vitro model that mimics characteristics similar to that of human embryos. Thus, the 3D EB model provides a platform for conducting embryotoxicity and multi-differentiation potential research. Accordingly, this review discusses the significance of 3D in vitro models in conducting effective embryotoxicity research. Further, we also evaluated the possible sources/routes of microplastic generation and analyzed their surface chemistry and cytotoxic effects reported till date.

The widespread use of plastic agricultural films necessitates a thorough evaluation of environmental risks posed by soil microplastics (MPs). While the intestinal tract is a critical site for MP interactions in soil organisms, current research predominantly focuses on overall physiological responses, overlooking organ-specific toxic mechanisms. To address this gap, we exposed earthworms (Eisenia fetida) to polyethylene (PE) and biodegradable polylactic acid (PLA) MPs sourced from agricultural films at an environmentally realistic concentration of 1.0 g/kg. Incorporating natural earthworm mobility, we designed two exposure scenarios: migration from clean to contaminated soil (scenario A) and vice versa (scenario B). Machine learning-driven image analysis and phenotypic profiling revealed that PE induced more severe intestinal lesions than PLA, adversely affecting intestinal immune functions. Furthermore, PE resulted in greater oxidative damage and significantly activated immune proteins such as melanin and antimicrobial peptides through reprograming immune-related gene and protein pathways. Conversely, PLA predominantly disrupted intestinal digestive and absorptive functions, though the gut microbial community partially mitigated damage through structural and compositional adaptation. Compared with scenario A, earthworms in scenario B exhibited reduced tissue damage, enhanced digestive enzyme activity, and upregulated energy-related metabolites and cell proliferation genes, indicating partial recovery from MP-induced intestinal dysfunction. These findings elucidate the distinct toxicity mechanisms of conventional and biodegradable agricultural MPs on soil organisms, while the scenario-based approach advances risk assessment by aligning experimental design with real-world ecological behaviors.

The widespread distribution of microplastics in the environment has raised concerns about their potential implications for human health. Microplastics accumulate in animals and humans, but the risks associated with these pollutants are not fully understood. This study aimed to investigate the effects of polystyrene microplastics on the male reproductive system. The 0.1 μm polystyrene (PS) could accumulate in the testicular tissue and spermatogonia GC-1, while 1 μm PS was not easy to enter and accumulate in the testicular tissue and cells. Mice continuously exposed for 3-months to 0.1 μm PS demonstrated lower fertility and inhibited spermatogonium differentiation compared to control mice. The 0.1 μm PS were dispersed throughout the seminiferous tubule of the testis. Metabolic reprogramming was found to be involved in these processes. Histone methylation and autophagy-related pathways showed significant differences following PS treatment in testis tissue and GC-1 cells. Our findings suggest that chronic exposure to 0.1 μm PS inhibited spermatogenic cell differentiation and impaired fertility in male mice. We propose that abnormal epigenetic modifications in 0.1 μm PS exposed mice contributed to the dysregulation of glycolytic enzymes, and that the impaired autophagic pathway exacerbated the accumulation of glycolytic enzymes further. Glycolysis plays a critical role in the regulation of spermatogenic cell differentiation, and its regulation partially alleviated the impairments associated with PS exposure. In conclusion, our findings suggest that chronic exposure to nanoplastics PS inhibited spermatogenic cell differentiation and impaired fertility in male mice via disrupted epigenetic modification and metabolic dysregulation.

Microplastics (MPs) are emerging as a novel pollutant, raising significant concerns regarding their adverse effects on human health. Furthermore, MPs are susceptible to light-induced aging in the environment, which alters their physical characteristics and potentially alters their toxic effects. While previous studies have documented the retention of MPs in the placenta, the specific impacts of MPs, particularly aged MPs, on placental function remain poorly understood. In the current study, we utilized 1 µm polystyrene microplastics (PS-MPs), a widely used model for MPs, to evaluate the effects of photoaged MPs on the placenta. Following oral administration of PS-MPs beginning on embryonic day 3.5 (E3.5), we observed impaired fetal growth and damage to the placental labyrinth chorionic layer in the treated pregnant mice by embryonic day 13.5 (E13.5). The photoaged PS-MPs were generated by exposure to simulated lighting for 7 or 14 days, resulting in alterations to their physical properties. Notably, enhanced cytotoxicity in trophoblast cells was observed for photoaged PS-MPs compared to pristine PS-MPs. Mechanistically, the altered physical properties of PS-MPs, along with elevated lipid peroxidation, may contribute to the increased cytotoxicity of the photoaged MPs. Our findings provide new insights into the detrimental effects and underlying mechanisms of both MPs and, in particular, aged MPs on the placenta and embryonic development. These insights are crucial for assessing the risks posed by MPs to human pregnancy.

Microplastics (MPs) and nanoplastics (NPs) are pervasive pollutants and their analyses by traditional mass spectrometric methods require time-intensive sample preparation (e.g., extraction, digestion, and separation). This study presents a rapid and novel method for detecting MPs and NPs using flame ionization mass spectrometry (FI-MS) in which a dried sample (e.g., powder, soil and tissue) is directly burnt or heated with a flame in front of the MS inlet. FI-MS enables decomposition and ionization of various plastics such as polyethylene terephthalate (PET) and polystyrene (PS), allowing for analysis to be completed as fast as 10 seconds per sample. As a demonstration of application of this technique, PET contaminants in 1 L of bottled water or in 0.65 L of apple juice contained in plastic bottles were quickly detected from a filter paper after sample filtration and brief drying. A 0.89 mg soil sample spiked with 6000 ppm PET microplastics was measured to contain 4.98 µg of PET (5595 ppm, quantitation error: 6.8 %). Strikingly, PS nanoplastics (200 nm size) in mouse placentas were successfully identified and quantified, highlighting the method's ability to analyze biological tissue without tedious sample preparation. Overall, this study demonstrates the high potential of FI-MS for real-world sample analysis of MPs and NPs in environmental, biological, or consumer product samples.

Nanoplastics have recently emerged as persistent pollutants of global concern that pose substantial risks to human health. However, the long-term adverse effects of nanoplastics on the female reproductive system remain unclear. Polystyrene nanoplastics (PS-NPs; 50 nm diameter) were selected as representative nanosized plastic particles to investigate the potential effects of subchronic prenatal and gestational exposure via drinking water on placental development in ICR (CD-1) mice. Maternal exposure to 10 mg/L PS-NPs induced an increase in fetal resorption rate and significantly increased fetal weight. Further observation of the placental morphology showed that PS-NPs exposure led to an aberrant placental structure and damaged the trophoblast cells. At the cellular level, PS-NPs exposure promoted the proliferation, migration, and invasion of HTR-8/SVneo cells. Mechanistically, transcriptomic and proteomic analyses revealed that PS-NPs triggered placental calcium disturbances and upregulated the Stam2 expression in mice. STAM2 induced by PS-NPs mediates the disruption of trophoblastic calcium homeostasis and regulates cell functions by disturbing the lysosomal degradation of the calcium channel protein IP3R3 and promoting intracellular calcium inflow by increasing the level of TRPV6 in HTR-8/SVneo cells. Therefore, our results indicated that trophoblastic calcium dyshomeostasis is the main mechanism by which subchronic PS-NPs exposure induces abnormal placental development. These findings reveal a link between subchronic PS-NPs exposure and placental damage and elucidate the underlying molecular mechanism, providing evidence for environmental triggers of adverse pregnancy and highlighting the risk of plastic products to pregnant women.

As an emerging environmental pollutant, microplastics have attracted increasing attention to their potential health hazards. However, the current understanding about the toxicity and health implications, especially about developmental toxicity with exposure to microplastics is quite limited. In the current study, we aimed to scrutinize the deleterious effects of polystyrene microplastics (PSMPs) with different sizes (0.1 and 5 μm) on the placenta that plays crucial role in fetal development, following oral exposure during gestational stages. The results showed that two sizes of PSMPs could distribute in mouse placental tissues, and nanosized PSMPs (0.1 μm) exhibited greater capability to penetrate the placenta and deposit in the liver and brain of fetuses than microsized PSMPs (5 μm). Importantly, only 0.1 μm PSMPs induced a decrease in the junctional area, a reduction in the labyrinthine vascularization and an increase in cell apoptosis in the placenta, accompanied by fetal developmental impairments. The results of metabolome and transcriptome uncovered that 0.1 μm PSMP exposure caused changes in metabolic and gene profiles of placental tissues, across multiple pathways such as vascular supply, nutrient absorption and transportation and amino acid metabolism. Overall, our results confirmed that maternal PSMP exposure led to placental damages associated with metabolic and gene expression disorders. This study would provide new insights into the developmental impacts of microplastic consumption during gestation.

With the high production and use of plastic products, a large amount of microplastics (MPs) is generated by degradation, which causes environmental pollution. MPs are particles with a diameter <5 mm; further degradation of MPs produces nano‑plastics (NPs), which could further increase the damage to cells when entering the human body. Therefore, the present review summarizes the effect of MP and NP deposition on the human gastrointestinal tract and the underlying injury mechanism of oxidative stress, inflammation and apoptosis, as well as the potential mechanism of glucose and liver lipid metabolism disorder. The present review provides a theoretical basis for research on the mechanisms of MPs in gastrointestinal injury and liver metabolism disorder. Further studies are needed for prevention and treatment of gastrointestinal diseases caused by MPs and NPs.

Micro(nano)plastics (MNPs) pose a significant threat to both ecological environments and human health. This review systematically examines the developmental toxicity of MNPs in mammals, with a particular focus on the impact of maternal and paternal exposure on offspring. Evidence indicates that MNPs can cross placental barriers, inducing abnormal development of embryos, fetuses, and placentas. This disruption leads to a range of adverse outcomes, including neurodevelopmental abnormalities, behavioral disorders, reproductive system damage, etc., in offspring. Through a comprehensive analysis of the existing literature, this review aims to provide a foundation for future research on the developmental toxicity of MNPs and highlight the urgent need for action to mitigate the detrimental effects of MNPs on human health and ecosystem integrity.

Polystyrene (PS) microplastics are pervasive environmental pollutants that are harmful to aquatic organisms upon degradation. The synthetic androgen 17α-methyltestosterone (MT) is an environmental endocrine-disrupting chemical. This study aimed to systematically evaluate the combined histological and molecular effects of MT and PS exposure on the liver and brain tissues of Danio rerio with focus on lipid metabolism and neural function disruption. Female D. rerio were exposed to 50 ng/L MT and 0.5 mg/L PS (5 μm in diameter) for 21 d. Histological observations, real-time quantitative PCR (qPCR), and RNA-sequencing (RNA-seq) analysis were employed to assess the effects of PS and MT. These results indicated that MT and PS co-exposure caused fatty degeneration of liver cells and a significant upregulation of lipid synthesis-related genes (ACSS1, CEL, FASN, and GK5). In brain tissue, the observed effects included reduced marginal layer neuron counts, cytoplasmic loosening of central layer neurons, disordered gray matter layer cells, and vascular congestion. RNA-seq analysis further revealed significant enrichment of differentially expressed genes in the "glycine, serine, and threonine metabolism" and "neuroactive ligand-receptor interaction" signaling pathways. Thus, MT and PS co-exposure induced lipid metabolism disorders in D. rerio and influence neural signaling by altering the "neuroactive ligand-receptor interaction" pathway. These findings highlight the complex risks posed by environmental pollutants to aquatic life and provide critical insights for environmental protection and aquatic health research.

Polystyrene nanoplastics (PSNPs) have been recognized as emerging environmental pollutants with potential health impacts, particularly on metabolic disorders. However, the mechanism by which gestational exposure to PSNPs induces obesity in offspring remains unclear. This study, focused on the whitening of brown adipose tissue (BAT), aims to elucidate the fundamental mechanisms by which prenatal exposure to PSNPs promotes obesity development in mouse offspring.

Pregnant dams were subjected to various doses of PSNPs (0 µg/µL, 0.5 µg/µL, and 1 µg/µL), and their offspring were analyzed for alterations in body weight, adipose tissue morphology, thermogenesis, adipogenesis, and lipophagy. The findings revealed a notable reduction in birth weight and an increase in white adipocyte size in adult offspring mice. Notably, adult male mice exhibited BAT whitening, correlated with a negative dose-dependent downregulation of UCP1 expression, indicating thermogenesis dysfunction. Further investigation revealed augmented lipogenesis evidenced by the upregulation of FASN, SREBP-1c, CD36, and DGAT2 expression, coupled with the inhibition of lipophagy, indicated by elevated levels of mTOR, AKT, and p62 proteins and reduced levels of LC3II/LCI and Lamp2 proteins in male offspring.

These findings indicate that gestational PSNP exposure plays a role in the development of obesity in offspring through the whitening of brown adipose tissue, which is triggered by lipogenesis and lipophagy inhibition, providing a novel insight into the metabolic risks associated with gestational PSNPs exposure.

To explore the intergenerational cardiotoxicity of nanoplastics, maternal mice were exposed to 60 nm polystyrene nanoplastics (PS-NP) during pregnancy and lactation. The results showed that PS-NP can enter the hearts of offspring and induce myocardial fiber arrangement disorder, acidophilic degeneration of cardiomyocytes, and elevated creatine kinase isoenzymes (CK-MB) and lactate dehydrogenase (LDH) levels after maternal exposure to PS-NP at 100 mg/kg during pregnancy and lactation. Mechanistically, KEGG analysis of RNA sequencing showed the participation of hypoxia-inducible factor-1 (HIF-1) and ferroptosis in PS-NP-induced cardiotoxicity. Key features of ferroptosis, including Fe2+ accumulation, mitochondrial injury, oxidative stress, GPX4 downregulation, and FTH1, ACSL4, and SLC7A11 upregulation, were detected. Furthermore, PS-NP treatment upregulated the expressions of HIF-1α and HO-1, and PS-NP-induced ferroptosis can be alleviated by inhibition of HIF-1α using si-HIF-1α. This study provided an insightful reference for the intergenerational cardiotoxicity assessment of PS-NP.

With the rise in global plastic production and the presence of plastic waste in the environment, microplastics are considered an emerging environmental contaminant. Human exposure and the impact of microplastics on human health are not well studied. Recent studies have observed the presence of microplastics in human tissues and several studies have noted toxicity in in vitro and in vivo mammalian models. We examined the impact of polystyrene nano- and microplastics in increasingly complex intestinal cell models. Using an undifferentiated Caco-2 mono-culture model, we assessed particle association, cytotoxicity, and particle clearance/retention, whereas in differentiated mono- and tri-culture transwell models, we assessed membrane integrity and particle translocation. Only 50 nm and 500 nm particles were internalized in the undifferentiated cells; however, no signs of cellular toxicity were observed at any concentrations tested. Additionally, polystyrene particles had no impact on barrier integrity, but the 50 nm particles were able to cross to the basolateral side, albeit attenuated in the tri-culture model that had a mucus layer. This study reduced some of the variability common to MNPL testing across various in vitro models, but further testing is needed to fully understand the potential effects of human MNPL exposure.

Recent analytical advancements have uncovered increasing micro- and nanoplastics (MNPs) in environmental, dietary, and biological domains, raising concerns about their health impacts. Preterm birth (PTB), a leading cause of maternal and neonatal morbidity and mortality, may be influenced by MNP exposure, yet this relationship remains unexplored. This study quantified 12 MNP polymers in placentae from term (n=87) and preterm (n=71) deliveries using pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS). Cumulative MNP concentrations were 28% higher in PTB placentae (mean ±SD: 224.7 ± 180.7 μg/g vs. 175.5 ± 137.9 μg/g; p=0.038). Polyvinyl chloride (PVC), polyethylene terephthalate (PET), polyurethane (PU), and polycarbonate (PC) were significantly elevated in PTB, and PET, PU, and PC inversely correlated with gestational age and birth weight. Logistic regression identified PVC and PC as independent predictors of PTB. These findings suggest total and specific MNPs are associated with PTB, providing actionable insights and emphasizing the importance of minimizing exposure during pregnancy.

Global production and widespread use of plastics are increasing dramatically. With current limited recycling and recovery options, microplastics and nanoplastics (MNPs) persist in the natural environment. Due to their ubiquity, human exposure to MNPs is inevitable. In addition to their inherent toxic effects, MNPs can adsorb harmful contaminants and act as vectors for microorganisms, compounding toxicological effects. After entering the body, bioaccumulation occurs in several tissues and organs, including the liver and the gastrointestinal (GI) tract. Proposed clinical effects of MNP absorption include endocrine disruption, alteration of the GI microbiome, and promotion of chronic inflammatory conditions. MNPs can also influence energy metabolism, activate inflammatory pathways, and increase oxidative stress leading to apoptosis. The GI tract is a major site of bioaccumulation for the MNPs in animals and humans. In this editorial, the current understanding of how MNPs are processed is discussed. Discussion on MNP effects on internal microflora, and their proposed role in developing inflammatory bowel diseases, MNP toxicokinetics, and their significance in health and disease are also reviewed. There is a need to understand the impact of MNP exposure on gut health and gut microbiota and identify current research gaps.

The presence of microplastics (MPs) in aquatic ecosystem has become a pressing global concern. MPs pose a significant threat to aquatic ecosystems, with devastating consequences for both aquatic life and human health. Notably, freshwater ecosystems are particularly vulnerable to MPs pollution. MPs, characterized by their small size (< 5 mm), have emerged as a ubiquitous environmental pollutant. They exhibit diverse characteristics, including varying sizes, forms, polymer types, and colors. Two distinct categories of MPs exist: primary and secondary. Primary MPs are incorporated into industrial hard materials, cosmetics, and hand cleaners, whereas secondary MPs result from the breakdown of larger plastic products in both terrestrial and marine environments. They enter the environment through various sources, such as household products, clothing, industrial activities, sewage waste and plastic degradation. Aquatic organisms ingest these contaminants, facilitating the transfer of MPs into the food chain and potentially causing severe health problems. This review delves into the bioaccumulation of MPs in fish, highlighting the eco-toxicological, neurological and immunological effects. This review provides an in-depth analysis of innovative solutions for MPs removal and reduction. Finally, we delineate evidence-based strategies to mitigate impacts of MPs, offering valuable insights to inform policy formulations and accelerate the development of sustainable plastic technologies.

Human health is being threatened by environmental microplastic (MP) pollution. MPs were detected in the bloodstream and multiple tissues of humans, disrupting the regular physiological processes of organs. Nanoscale plastics can breach the blood-brain barrier, leading to neurotoxic effects. How MPs cause brain functional irregularities remains unclear. This work uses high-depth imaging techniques to investigate the MPs within the brain in vivo. We show that circulating MPs are phagocytosed and lead these cells to obstruction in the capillaries of the brain cortex. These blockages as thrombus formation cause reduced blood flow and neurological abnormalities in mice. Our data reveal a mechanism by which MPs disrupt tissue function indirectly through regulation of cell obstruction and interference with local blood circulation, rather than direct tissue penetration. This revelation offers a lens through which to comprehend the toxicological implications of MPs that invade the bloodstream.

Since the widespread usage of plastic materials and inadequate handling of plastic debris, nanoplastics (NPs) and microplastics (MPs) have become global hazards. Recent studies prove that NPs/MPs can induce various toxicities in organisms, with these adverse effects closely related to gut microbiota changes. This review thoroughly summarized the interactions between NPs/MPs and gut microbiota in various hosts, speculated on the potential factors affecting these interactions, and outlined the impacts on hosts' health caused by NPs/MPs exposure and gut microbiota dysbiosis. Firstly, different characteristics and conditions of NPs/MPs often led to complicated hazardous effects on gut microbiota. Alterations of gut microbiota composition at the phylum level were complex, while changes at the genus level exhibited a pattern of increased pathogens and decreased probiotics. Generally, the smaller size, the rougher surface, the longer shape, the higher concentration, and the longer exposure of NPs/MPs induced more severe damage to gut microbiota. Then, different adaptation and tolerance degrees of gut microbiota to NPs/MPs exposure might contribute to gut microbiota dysbiosis. Furthermore, NPs/MPs could be carriers of other hazards to generally exert more severe damage on gut microbiota. In summary, both pristine and contaminated NPs/MPs posed severe threats to hosts through inducing gut microbiota dysbiosis.

Microplastics are ubiquitous in freshwater and can be absorbed into fish skin and gills, accumulate in the gut, and be transported to other tissues, thus posing a risk to fish health. Further studies are needed, however, to investigate effects such as endocrine disruption and multi-tissue toxicity. In this study, zebrafish were exposed to polystyrene (PS) microplastics and health-related indicators were measured, including skin mucus, gut damage, oxidative stress, stable isotope composition and reproduction as well as an assessment of changes to metabolites using a metabolomics approach. Results showed that concentrations of PS microplastics were higher in gills than those in the gut. Minimal impact to immunoglobulin M level and lysozyme activity in mucus indicated, however, that microplastic toxicity primarily stemmed from ingestion rather than disruption of skin mucus immunity. Female zebrafish were more affected by PS microplastics. Gut microbiota dysbiosis was induced, especially in females. Significant alterations in pathways associated with lipid and energy metabolism were observed in the liver of female fish. PS microplastics also induced sex steroid hormone disorder and reduced female egg production, possibly linked to the alteration of gut microbiota and hepatic metabolism. Combined, these results highlight the gender-specific toxicity of PS microplastics to zebrafish health, potentially harming their population.

Cadmium (Cd) and polystyrene microplastics (PS-MPs), two ubiquitous environmental contaminants, produce unique synergistic toxicity when co-existing. Key unanswered questions include specific effects on liver function and potential mechanisms.

In this study, C57BL/6 mice and AML12 cells were used to establish in vivo and in vitro models to elucidate the effects of combined exposure to PS-MPs and Cd on the liver and their mechanisms.

The results showed that the combined effects of PS-MPs and Cd caused significantly more liver damage than exposure alone. As observed by transmission electron microscopy (TEM), the number of autophagosomes was significantly increased in the PS-MPs and Cd co-treated group. In addition, autophagic flux was assayed by RFP-GFP-LC3, a reporter system expressing dual fluorescent proteins, which showed an overwhelming enhancement of autophagic flux damage by co-exposure to PS-MPs and Cd compared to exposure alone. To further investigate the involvement of carnitine palmitoyltransferase1(CPT1) in liver injury induced by co-exposure to Cd and PS-MPs, we co-exposed Baicalin, an activator of CPT1, with PS-MPs and Cd, and showed that activation of CPT1 alleviated the impairment of autophagic fluxes induced by co-exposure of Cd and PS-MPs and further alleviated the changes in lipid accumulation and associated protein levels.

In conclusion, the concurrent exposure of PS-MPs and Cd resulted in the blockage of hepatic lipid accumulation and autophagic pathway and further aggravated the toxic damage to the liver. Activation of CPT1 could alleviate the PS-MPs and Cd-induced lipid accumulation and autophagy pathway blockage thus reducing liver injury.

The increasing use of plastic food containers, particularly for pre-cooked meals and takeout services, has raised concerns regarding the potential health risks associated with plastic leachates. This study investigated the impact of leachates from heat-treated polypropylene (PP) plastic food containers on glucose and lipid metabolism using both in vitro and in vivo models. AML12 hepatocytes exposed to leachates from three different PP plastic containers exhibited significant disruptions in the homeostasis of lipid and glucose metabolism, evidenced by increased intracellular lipid content and altered gene expression related to lipogenesis, lipid uptake, lipolysis, and fatty acid β-oxidation. C57BL/6J mice were fed with the mouse diet that had been heated in two distinct types of PP plastic food containers for 8 weeks and these mice exhibited accelerated body weight gain, altered fasting blood glucose levels, and changes in serum lipid profiles. Histological analysis revealed increased adipocyte size, liver steatosis, and glycogen accumulation. Transcriptome sequencing of liver tissues highlighted significant alterations in the expression of genes involved in metabolic pathways, further corroborated by real-time qPCR validation. These findings underscore the potential metabolic health risks posed by the use of heated plastic food containers.

Long-term effects of microplastics (MPs) exposure have been demonstrated to impair reproductive function. However, in real world, the exposure level of MP is not constant and it may vary in different individuals. This study aims to evaluate the impact of short-term exposure to MPs on ovarian and endometrial function in rat models. Serum steroid hormone concentrations and the expression of ovarian steroid hormone receptor were disturbed. We found that as MPs exposure concentration increased, thickness of the endometrial glandular epithelial layer and the number of endometrial glands decreased; the number of primordial follicles decreased, while the numbers of primary and secondary oocytes significantly increased, indicating a potential oocyte overactivation. Although short-term MP exposure appears to not influence embryo implantation and hormone functions, the results of this study highlight the potential of MPs to disrupt reproductive health in women.

The pervasive presence of microplastics (MPs) in infant formula and care products has emerged as a significant and underappreciated risk to public health. Notably, infants are at an elevated risk due to their underdeveloped intestinal defenses and liver detoxification capabilities, factors that could heighten their vulnerability to MPs. This study presents a comprehensive evaluation of the health implications linked to polystyrene microplastics (PSMPs) exposure during early life, examining both environmentally plausible and elevated levels. Based on histological analysis, in vivo imaging analysis, biochemical analysis and 16S rRNA sequencing results, our study found that oral PSMPs exposure in infant mice led to profound toxicological consequences, such as intestinal barrier impairment and hepatic injury, in a dose-dependent manner. Strikingly, even low ambient concentration of PSMPs (20 ppb) was sufficient to inflict considerable harm, disrupting the intestinal barrier, manifested that lessened mucus secretion, elevated iFABP level (276.50±10.73 pg/mL), decreased sIgA levels (0.60±0.03 mg/g), and pathological damage of intestinal tissues, allowing PSMPs accumulation and leakage into blood, inducing hepatotoxicity, such as increased TG levels (0.99±0.05 mmol/gprot) and lipid droplet accumulation. Furthermore, PSMPs exposure gives rise to aberrant bacterial colonization, dropping the abundance of probiotics as well as altering the abundance of pathogenic bacteria, which may contribute to the toxicity outcomes. The study underscores the critical need for vigilance regarding the insidious effects of PSMPs at environmental-relevant concentrations, especially in the context of infant exposure.

Microplastic particles (MPs) have been detected in a variety of environmental samples, including soil, water, food, and air. Cellular studies and animal exposures reported that exposure to MPs composed of different polymers might result in adverse effects at the portal of entry (local) or throughout the body (systemic). The most relevant routes of particle uptake into the body are oral and respiratory exposure. This review describes the various processes that may contribute to the adverse effects of MPs. Only MPs up to 5 µm were found to cross epithelial barriers to a significant extent. However, MPs may also exert a detrimental impact on human health by acting at the epithelial barrier and within the lumen of the orogastrointestinal and respiratory tract. The potential for adverse effects on human health resulting from the leaching, sorption, and desorption of chemicals, as well as the impact of MPs on nutritional status and dysbiosis, are reviewed. In vitro models are suggested as a means of (1) assessing permeation, (2) determining adverse effects on cells of the epithelial barrier, (3) examining influence of digestive fluids on leaching, desorption, and particle properties, and (4) role of microbiota-epithelial cell interactions. The contribution of these mechanisms to human health depends upon exposure levels, which unfortunately have been estimated very differently.

The widespread use of microplastics and their harmful effects on the environment have emerged as serious concerns. However, the effect of microplastics on the immune system of mammals, particularly their offspring, has received little attention. In this study, polystyrene microplastics (PS-MPs) were orally administered to male mice during lactation. Flow cytometry was used to assess the immune cells in the spleens of both adult male mice and their offspring. The results showed that mice exposed to PS-MPs exhibited an increase in spleen weight and an elevated number of B and regulatory T cells (Tregs), irrespective of dosage. Furthermore, the F1 male offspring of the PS-MPs-exposed group had enlarged spleens; an increased number of B cells, T helper cells (Th cells), and Tregs; and an elevated ratio of T helper cells 17 (Th17 cells) to Tregs and T helper cells 1 (Th1 cells) to T helper cells 2 (Th2 cells). These results suggested a pro-inflammatory state in the spleen. In contrast, in the F1 female offspring exposed to PS-MPs, the changes in splenic immune cells were less pronounced. In the F2 generation of mice with exposed to PS-MPs, minimal alterations were observed in spleen immune cells and morphology. In conclusion, our study demonstrated that exposure to real human doses of PS-MPs during lactation in male mice altered the immune status, which can be passed on to F1 offspring but is not inherited across generations.

Micro- and nanoplastics (MNPs), emerging environmental pollutants, infiltrate marine, terrestrial, and freshwater systems via diverse pathways, culminating in their accumulation in the human body through food chain transmission, posing potential health risks. Researches have demonstrated that MNPs disrupt gut microbiota equilibrium and compromise intestinal barrier integrity, as well as traverse the blood-brain barrier, leading to brain damage. Moreover, the complex interaction between the gut and the nervous system, facilitated by the "gut-brain axis," indicates an additional pathway for MNPs-induced brain damage. This has intensified scientific interest in the intercommunication between MNPs and the gut-brain axis. While existing studies have documented microbial imbalances and metabolic disruptions subsequent to MNPs exposure, the precise mechanisms by which the microbiota-gut-brain axis contributes to MNPs-induced central nervous system damage remain unclear. This review synthesizes current knowledge on the microbiota-gut-brain axis, elucidating the pathogenesis of MNPs-induced gut microbiota dysbiosis and its consequent brain injury. It emphasizes the complex interrelation between MNPs and the microbiota-gut-brain axis, advocating for the gut microbiota as a novel therapeutic target to alleviate MNP-induced brain harm.

The widespread use of plastics has increased environmental pollution by micro- and nanoplastics (MNPs), especially polystyrene micro- and nanoplastics (PS-MNPs). These particles are persistent, bioaccumulative, and linked to endocrine-disrupting toxicity, posing risks to reproductive health. This review examines the effects of PS-MNPs on mammalian reproductive systems, focusing on oxidative stress, inflammation, and hormonal imbalances. A comprehensive search in the Web of Science Core Collection, following PRISMA 2020 guidelines, identified studies on the impact of PS-MNPs on mammalian fertility, including oogenesis, spermatogenesis, and folliculogenesis. An analysis of 194 publications revealed significant reproductive harm, such as reduced ovarian size, depleted follicular reserves, increased apoptosis in somatic cells, and disrupted estrous cycles in females, along with impaired sperm quality and hormonal imbalances in males. These effects were linked to endocrine disruption, oxidative stress, and inflammation, leading to cellular and molecular damage. Further research is urgently needed to understand PS-MNPs toxicity mechanisms, develop interventions, and assess long-term reproductive health impacts across generations, highlighting the need to address these challenges given the growing environmental exposure.

The female reproductive system can face serious disorders and show reproductive abnormalities under the influence of environmental pollutants. Microplastics (MPs) and nanoplastics (NPs) as emerging pollutants, by affecting different components of this system, may make female fertility a serious challenge. Animal studies have demonstrated that exposure to these substances weakens the function of ovaries and causes a decrease in ovarian reserve capacity. Also, continuous exposure to micro/nano plastics (MNPs) leads to increased levels of reactive oxygen species, induction of oxidative stress, inflammatory responses, apoptosis of granulosa cells, and reduction of the number of ovarian follicles. Furthermore, by interfering with the hypothalamic-pituitary-ovarian axis, these particles disturb the normal levels of ovarian androgens and endocrine balance and delay the growth of gonads. Exposure to MNPs can accelerate carcinogenesis in the female reproductive system in humans and animal models. Animal studies have determined that these particles can accumulate in the placenta, causing metabolic changes, disrupting the development of the fetus, and endangering the health of future generations. In humans, the presence of micro/nanoplastics in placenta tissue, infant feces, and breast milk has been reported. These particles can directly affect the health of the mother and fetus, increasing the risk of premature birth and other pregnancy complications. This review aims to outline the hazardous effects of micro/nano plastics on female reproductive health and fetal growth and discuss the results of animal experiments and human research focusing on cellular and molecular pathways.

Micro- and nano-plastics (MNPs) and per- and polyfluoroalkyl substances (PFAS) are prevalent in ecosystems due to their exceptional properties and widespread use, profoundly affecting both human health and ecosystem. Upon entering the environment, MNPs and PFAS undergo various transformations, such as weathering, transport, and accumulation, potentially altering their characteristics and structural dynamics. Their interactions, governed by factors like hydrogen bonding, hydrophobic interactions, Van der Waals forces, electrostatic attractions, and environmental conditions, can amplify or mitigate their toxicity toward human health within ecological conditions. Several studies demonstrate the in vivo effects of PFAS and MNPs, encompassing growth and reproductive impairments, oxidative stress, neurotoxicity, apoptosis, DNA damage, genotoxicity, immunological responses, behavioral changes, modifications in gut microbiota, and histopathological alterations. Moreover, in vitro investigations highlight impacts on cellular uptake, affecting survival, proliferation, membrane integrity, reactive oxygen species (ROS) generation, and antioxidant responses. This review combines knowledge on the co-existence and adsorption of PFAS and MNPs in the environment, defining their combined in vivo and in vitro impacts. It provides evidence of potential human health implications. While significant research originates from China, Europe, and the USA, studies from other regions are limited. Only freshwater and marine organisms and their impacts are extensively studied in comparison to terrestrial organisms and humans. Nonetheless, detailed investigations are lacking regarding their fate, combined environmental exposure, mode of action, and implications in human health studies. Ongoing research is imperative to comprehensively understand environmental exposures and interaction mechanisms, addressing the need to elucidate these aspects thoroughly.

Background: Humans cannot avoid plastic exposure due to its ubiquitous presence in the natural environment. The waste generated is poorly biodegradable and exists in the form of MPs, which can enter the human body primarily through the digestive tract, respiratory tract, or damaged skin and accumulate in various tissues by crossing biological membrane barriers. There is an increasing amount of research on the health effects of MPs. Most literature reports focus on the impact of plastics on the respiratory, digestive, reproductive, hormonal, nervous, and immune systems, as well as the metabolic effects of MPs accumulation leading to epidemics of obesity, diabetes, hypertension, and non-alcoholic fatty liver disease. MPs, as xenobiotics, undergo ADMET processes in the body, i.e., absorption, distribution, metabolism, and excretion, which are not fully understood. Of particular concern are the carcinogenic chemicals added to plastics during manufacturing or adsorbed from the environment, such as chlorinated paraffins, phthalates, phenols, and bisphenols, which can be released when absorbed by the body. The continuous increase in NMP exposure has accelerated during the SARS-CoV-2 pandemic when there was a need to use single-use plastic products in daily life. Therefore, there is an urgent need to diagnose problems related to the health effects of MP exposure and detection. Methods: We collected eligible publications mainly from PubMed published between 2017 and 2024. Results: In this review, we summarize the current knowledge on potential sources and routes of exposure, translocation pathways, identification methods, and carcinogenic potential confirmed by in vitro and in vivo studies. Additionally, we discuss the limitations of studies such as contamination during sample preparation and instrumental limitations constraints affecting imaging quality and MPs detection sensitivity. Conclusions: The assessment of MP content in samples should be performed according to the appropriate procedure and analytical technique to ensure Quality and Control (QA/QC). It was confirmed that MPs can be absorbed and accumulated in distant tissues, leading to an inflammatory response and initiation of signaling pathways responsible for malignant transformation.

The disposable paper cups (DPCs) release millions of microplastics (MPs) when used for hot beverages. However, the tissue-specific deposition and toxic effects of MPs and associated toxins remain largely unexplored, especially at daily consumption levels. We administered MPs and associated toxins extracted from leading brand DPCs to pregnant mice, revealing dose-responsive harmful effects on fetal development and maternal physiology. MPs were detected in all 13 examined tissues, with preferred depositions in the fetus, placenta, kidney, spleen, lung, and heart, contributing to impaired phenotypes. Brain tissues had the smallest MPs (90.35 % < 10 µm). A dose-responsive shift in the cecal microbiome from Firmicutes to Bacteroidetes was observed, coupled with enhanced biosynthesis of microbial fatty acids. A moderate consumption of 3.3 cups daily was sufficient to alter the cecal microbiome, global metabolic functions, and immune health, as reflected by tissue-specific transcriptomic analyses in maternal blood, placenta, and mammary glands, leading to neurodegenerative and miscarriage risks. Gene-based benchmark dose framework analysis suggested a safe exposure limit of 2 to 4 cups/day in pregnant mice. Our results highlight tissue-specific accumulation and metabolic and reproductive toxicities in mice at DPC consumption levels presumed non-hazardous, with potential health implications for pregnant women and fetuses.

Nanoplastics (NPs) are ubiquitous in daily life, posing potential risks to the environment and human. While their negative effects on parental organisms have been extensively studied, intergenerational effects are still in the early stages of investigation. Here, we aimed to investigate the impact of maternal exposure to an environmentally relevant level of polystyrene NPs (PSNPs, 100 nm) during gestation and lactation (∼32 days, 50 μg/mouse/day) on neurotoxicity mediated by the microbe-gut-brain axis in offspring mice. Maternal PSNPs exposure significantly increased brain TNF-α level and microglia by 1.43 and 1.48 folds respectively, compared to control, accompanied by nuclear pyknosis and cell vacuolization in cortex and hippocampus. Targeted neurotransmitter metabolomics analysis revealed dysregulation in dopamine and serotonin metabolism. Specifically, dopamine levels increased significantly from 0.007 ng/L to 0.015 ng/L, while N-acetylseroton and 3,4-dihydroxyphenylacetic acid decreased significantly from 0.002 and 0.929 ng/L to 0.001 and 0.680 ng/L, respectively. Through a combination of 16S rRNA sequencing and biochemical analysis, we discovered that maternal PSNPs exposure led to a depletion of anti-inflammatory bacteria and an enrichment of pro-inflammatory bacteria resulting in intestinal barrier damage, elevated levels of lipopolysaccharide in blood, and subsequent activation of neuroinflammation. Meanwhile, gut bacteria dysbiosis interfered with communication between gut and brain by dysregulating neurotransmitter synthesis, as evidenced by significant associations between neurotransmitter-related bacteria (Akkermansia, Family_XIII_AD3011_group, Lachnoclostridium) and dopamine/serotonin related metabolites. Furthermore, transcriptional alterations in dopamine and serotonin related pathways were observed in the enteric nervous system, suggesting abnormal signal transduction from gut to brain contributes to neurotoxicity. This study provides new insights into NPs-induced neurotoxicity within the context of microbe-gut-brain axis and highlights the risk of cerebral dysfunction in offspring with maternal NPs exposure.

The ecological threats of microplastics (MPs) have sparked research worldwide. However, changes in the topics of MP research over time and space have not been evaluated quantitatively, making it difficult to identify the next frontiers. Here, we apply topic modeling to assess global spatiotemporal dynamics of MP research. We identified nine leading topics in current MP research. Over time, MP research topics have switched from aquatic to terrestrial ecosystems, from distribution to fate, from ingestion to toxicology, and from physiological toxicity to cytotoxicity and genotoxicity. In most of the nine leading topics, a disproportionate amount of independent and collaborative research activity was conducted in and between a few developed countries which is detrimental to understanding the environmental fates of MPs in a global context. This review recognizes the urgent need for more attention to emerging topics in MP research, particularly in regions that are heavily impacted but currently overlooked.