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Microplastics (MPs), plastic particles with a diameter of < 5 mm, are intentionally produced or formed by the breakdown of a variety of larger plastics. Polyethylene terephthalate (PET) is a common source of MPs and PET-MPs are prevalent in the environment. Owing to their persistence, PET-MPs can enter ecosystems, air, and food sources, posing significant health risks. This study aimed to investigate the toxicological effects and in vivo accumulation of PET-MPs smaller than 10 µm. To track their biodistribution, fluorescently labeled PET-MPs were prepared. Particle size and morphology were confirmed using physical and chemical characterization. Following the oral administration of PET-MPs in ICR (CD-1®) outbred mice, accumulation occurred predominantly in lungs, as confirmed by IVIS spectrum CT analysis and in vivo and ex vivo imaging. Toxicity assays revealed the development of granulomatous inflammation in the lungs at medium and high doses, indicating a concentration-dependent response. The recorded no-observed-adverse-effect levels were 1.75 mg/kg for males and 7 mg/kg for females. This study highlights the potential of PET-MPs to induce persistent inflammation in respiratory tissues and reveals the need for further research to support the regulatory standards and long-term health effects of MP exposure.

A great deal of attention has been paid lately to release of phthalate esters (PAEs) from polyethylene terephthalate (PET) bottles into PET bottled drinking water due to their potential endocrine-disrupting effects. Three kinds of PAEs, including diethyl phthalate (DEP), dimethyl phthalate (DMP) and dibutyl phthalate (DBP), were detected in 10 popular brands of PET bottles in Beijing, ranging from 101.97 μg/kg to 709.87 μg/kg. Meanwhile, six kinds of PAEs, including DEP, DMP, DBP, n-butyl benzyl phthalate (BBP), di-n-octyl phthalate (DOP) and di(2-ethylhexyl) phthalate (DEHP), were detected in PET bottled water, ranging from 0.19 μg/L to 0.98 μg/L, under an outdoor storage condition, while their concentrations ranged from 0.18 μg/L to 0.71 μg/L under an indoor storage condition. Furthermore, the concentrations of PAEs in brand D and E bottles were slightly increased when the storage time was prolonged. In addition, the concentrations of PAEs in commercial water contained in brand B and H bottles and pure water contained in brand E and G bottles were also slightly increased with the increase of storage temperature. Interestingly, DBP mainly contributed to the increased PAEs levels in simulation water. These results suggest that a part of the PAEs in PET bottled water originated from plastic bottles, which was related to the storage time and temperature. However, the PAEs in PET bottled water only pose a negligible risk to consumers if they follow the recommendations, such as storage at a common place (24 °C), away from sun and in a short period of time.

Micro- and nanoplastics are widespread throughout the world. In particular, polyethylene (PE) and polyethylene terephthalate or polyester (PET) are two of the most common polymers, used as plastic bags and textiles. To analyze the toxicity of these two polymers, oligomers with different numbers of units were used as models. The use of oligomers as polymeric templates has been used previously with success. We started with the monomer and continued with different oligomers until the chain length was greater than two nm. According to the results of quantum chemistry, PET is a better oxidant than PE, since it is a better electron acceptor. Additionally, PET has negatively charged oxygen atoms and can promote stronger interactions than PE with other molecules. We found that PET forms stable complexes and can dissociate the guanine-cytosine nucleobase pair. This could affect DNA replication. These preliminary theoretical results may help elucidate the potential harm of micro- and nanoplastics.

Despite the extensive use of polyethylene terephthalate (PET), the public health implications of its micro- and nanoparticles (MNPs) remain poorly understood, raising credible concerns about human exposure and health risks. We conducted a comprehensive literature search to synthesise evidence on human exposure to PET MNPs, their detection in human tissues and biological fluids, and the human-relevant toxicity of PET particles in vitro and in vivo. Studies consistently identify PET MNPs across consumer and environmental sources, and several investigations have detected PET in human matrices, supporting the plausibility of systemic translocation across biological barriers. Toxicological findings consistently indicate size- and shape-dependent uptake and effects: smaller particles exhibit greater cellular internalisation, reactivity, and biodistribution, with predominant oxidative, inflammatory, metabolic, and genotoxic responses, whereas larger microplastics more often provoke mechanical irritation. Key gaps include limited protocol harmonisation, unrealistic exposure levels, scarce long-term/kinetic data, and insufficiently standardised, well-characterised PET MNPs preparations. While evidence for exposure, detection in human matrices, and biological activity is growing, these deficits still hinder robust cross-study comparisons and clinically meaningful quantitative risk assessment.

Polyethylene terephthalate microplastics (PET-MPs) are emerging environmental pollutants, but the molecular mechanisms underlying their hepatotoxicity remain poorly understood. Here, we combined network toxicology with experimental validation to investigate how PET-MPs induce liver injury. In silico, we investigated the PET-repeating unit as the molecular basis for target interactions. We identified 59 overlapping genes between 157 putative PET-MPs targets and 1693 liver injury-associated genes. Protein–protein interaction analysis revealed six hub genes (AKT1, PIK3CA, PIK3CB, PIK3CD, PIK3R1, and SRC), all components of the PI3K/AKT signaling pathway. Gene ontology analysis showed that PET-MPs affect cellular stress responses and kinase activities, while pathway enrichment analysis identified PI3K-Akt, Ras, and reactive oxygen species pathways as primary targets. Molecular docking demonstrated strong binding affinity between PET-MPs and these core targets (binding free energies <−5 kcal/mol). In vitro, PET-MPs induced mitochondrial depolarization, oxidative stress, upregulation of TNF-α and IL-6, and decreased p-AKT/AKT ratio, accompanied by increased apoptosis; the apoptotic effect was reversed by the AKT agonist SC79. In vivo experiments confirmed that AKT activation reduced PET-MP-induced liver injury, evidenced by decreased inflammation, lower serum transaminases, and restored oxidative balance. These protective effects were abolished by PI3K/AKT pathway inhibitors. Our study identifies potential therapeutic targets and strategies for PET-MP-induced liver injury.

Medicines, food packaging, personal care products, and cosmetics extensively use polyethylene terephthalate nanoplastics (PET-NaPs). However, they also have harmful impacts on several organs. Betaine demonstrates potent antioxidant and anti-inflammatory characteristics. Our goal was to investigate the detrimental impact of PET-NaPs on the mouse brain and evaluate the neuroprotective properties of betaine. We allocated 40 completely mature male Swiss albino mice into four distinct groups: control group, betaine group, PET-NaPs group, and betaine-co-treated group. Following a 30-day duration, euthanasia was performed on the mice, and analyzed tissue samples were obtained from the cerebrum, cerebellum, and hippocampus. PET-NaPs resulted in an elevated level of malondialdehyde and upregulated cyclooxygenase-2 and interleukin-1 beta (IL-1β) expression while significantly reducing the levels of glutathione and downregulating acetylcholinesterase. The PET-NPs also caused significant changes in the histopathology of the brain tissue, and there was a demonstrable rise in the immunostaining of IL-1β and glial fibrillary acidic proteins. Consequently, betaine effectively alleviated the negative consequences of PET-NaPs. Therefore, betaine possesses the capacity to mitigate the neurotoxic consequences induced by PET-NaPs.

The rise of microplastic (MPs) pollution presents a pressing environmental issue, raising concerns about its potential health impacts on human populations. Given the critical role of the liver in detoxification and metabolism, understanding the effects of MPs on the human hepatoma cell line HepG2 cells is essential for comprehensively assessing the dangers associated with MPs pollution to human health. Until now, the assessment of the harmful impact of polyethylene (PE) and polyethylene terephthalate (PET) on HepG2 has been incomplete and lacks certain essential data points. In this particular setting, we examined parameters such as cell viability, oxidative stress, mtDNA integrity, mitochondrial membrane potential, and autophagy in HepG2 cells exposed for 72 h to PET and PE at a concentration of 10 µg/mL. Our data revealed that exposure of HepG2 to MPs causes an increase in cell viability accompanied by a heightened ROS and altered mitochondrial function, as revealed by decreased mtDNA integrity and membrane potential. In addition, results demonstrated that exposure to PET and PE activated autophagic events, as suggested by the increased levels of the specific markers LC3 and p62. This last point was further confirmed using bafilomycin, a specific blocker that hinders the merging of autophagosomes and lysosomes, thereby blocking autophagic degradation processes. Given the increasing evidence of food chain MPs contamination and its possible harmful effects, our data should be carefully considered.

The escalating prevalence of diabetic nephropathy (DN) has raised concerns about environmental pollutants, particularly polyethylene terephthalate microplastics (PET-MP), as potential contributors to metabolic diseases. However, the molecular mechanisms linking PET-MP exposure to DN remain unclear. This study integrates network toxicology and bioinformatics to explore PET-MP-induced nephrotoxicity in DN. PET-MP-related toxicity targets were identified using SwissTargetPrediction and SuperPred. DN-associated differentially expressed genes (DEGs) were derived from the GSE96804 dataset. Overlapping genes were analyzed via enrichment analyses (GO, KEGG), Gene Set Variation Analysis (GSVA), and protein-protein interaction (PPI) networks. Immune cell infiltration was assessed with CIBERSORT. Key genes were identified using machine learning models (LASSO, RF, SVM-RFE) and validated by a nomogram and molecular docking. Among 10,124 DN-related DEGs, 64 overlapped with PET-MP targets. These genes were enriched in pathways like VEGF signaling, PI3K activity, and oxidative stress responses. GSVA revealed significant dysregulation in 2,258 pathways, including inflammation, immune response, and ROS metabolism. Immune infiltration analysis showed reduced CD8 + T cells, monocytes, and neutrophils in DN, alongside increased Tregs and M2 macrophages. Machine learning models identified CASP3 and GRB2 as key feature genes, validated by robust cross-validation and two independent DN datasets. Molecular docking indicated favorable binding affinities of PET to CASP3 (Vina score: -5.3) and GRB2 (Vina score: -5.2), suggesting disruptions in apoptosis and signal transduction pathways. PET-MP may exacerbate DN by disrupting critical molecular and cellular pathways, compromising the regulation of apoptosis, immune responses, and cellular homeostasis. CASP3 and GRB2 emerge as central mediators, providing mechanistic insights into PET-MP-driven nephrotoxicity. This study underscores the role of environmental microplastics in metabolic disorders and highlights potential therapeutic targets for DN.

Background During inhalation, airborne particles such as particulate matter ≤ 2.5 μm (PM 2.5 ), can deposit and accumulate on the alveolar epithelial tissue. In vivo studies have shown that fractions of PM 2.5 can cross the alveolar epithelium to blood circulation, reaching secondary organs beyond the lungs. However, approaches to quantify the translocation of particles across the alveolar epithelium in vivo and in vitro are still not well established. In this study, methods to assess the translocation of standard diesel exhaust particles (DEPs) across permeable polyethylene terephthalate (PET) inserts at 0.4, 1, and 3 μm pore sizes were first optimized with transmission electron microscopy (TEM), ultraviolet-visible spectroscopy (UV-VIS), and lock-in thermography (LIT), which were then applied to study the translocation of DEPs across human alveolar epithelial type II (A549) cells. A549 cells that grew on the membrane (pore size: 3 μm) in inserts were exposed to DEPs at different concentrations from 0 to 80 µg.mL − 1 ( 0 to 44 µg.cm − 2 ) for 24 h. After exposure, the basal fraction was collected and then analyzed by combining qualitative (TEM) and quantitative (UV-VIS and LIT) techniques to assess the translocated fraction of the DEPs across the alveolar epithelium in vitro. Results We could detect the translocated fraction of DEPs across the PET membranes with 3 μm pore sizes and without cells by TEM analysis, and determine the percentage of translocation at approximatively 37% by UV-VIS (LOD: 1.92 µg.mL − 1 ) and 75% by LIT (LOD: 0.20 µg.cm − 2 ). In the presence of cells, the percentage of DEPs translocation across the alveolar tissue was determined around 1% at 20 and 40 µg.mL − 1 (11 and 22 µg.cm − 2 ), and no particles were detected at higher and lower concentrations. Interestingly, simultaneous exposure of A549 cells to DEPs and EDTA can increase the translocation of DEPs in the basal fraction. Conclusion We propose a combination of analytical techniques to assess the translocation of DEPs across lung tissues. Our results reveal a low percentage of translocation of DEPs across alveolar epithelial tissue in vitro and they correspond to in vivo findings. The combination approach can be applied to any traffic-generated particles, thus enabling us to understand their involvement in public health.

Polyethylene terephthalate microplastics (PET-MPs) have emerged as a significant environmental issue, primarily due to their durability and associated health hazards. Nevertheless, their contribution to the pathogenesis of atherosclerosis (AS) is not well elucidated, highlighting the necessity for a comprehensive assessment of their molecular toxicology. In the present investigation, we utilized network toxicology and molecular docking methodologies to explore the toxic mechanisms by which PET-MPs may induce AS. Evaluations of datasets from GEO, ChEMBL, and SwissTargetPrediction led to the identification of 28 potential targets linked to PET-MPs exposure, which were narrowed down to seven key targets through machine learning techniques. Enrichment analyses involving Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways indicated that PET-MPs affect significant pathways related to inflammation and metabolism. Further, molecular docking validated robust binding affinities between PET-MPs and the identified core targets, implying their capacity to interfere with essential cellular functions. These results suggest that PET-MPs may facilitate the progression of AS by altering inflammatory responses and metabolic processes. This research offers new insights into the molecular mechanisms driving PET-MPs-related AS. It illustrates the effectiveness of network toxicology in evaluating the toxicity of novel environmental contaminants, thereby providing a theoretical framework for understanding the health implications of PET-MPs and informing strategies to alleviate their effects on cardiovascular health.