Environment & Health最新文献

{"title":"Polystyrene Nanoplastics at an Environmentally Relevant Concentration Promote Ovarian Cancer Progression via CDK4/6-Dependent Signaling.","authors":"Xiaoyu Yuan, Zhenyan Cui, Sinan Xu, Kelie Chen, Yuwei Wang, Fang Zheng, Han-Ming Shen, Shurong Sun, Yihua Wu, Dajing Xia","doi":"10.1021/envhealth.5c00329","DOIUrl":"10.1021/envhealth.5c00329","url":null,"abstract":"<p><p>Nanoplastics (NPs) are emerging global contaminants, which are known to harm respiratory, digestive, neural, and cardiovascular systems; their tumorigenic risks at environmentally relevant levels remain unclear. Here, we sought to clarify the potential promoting effects of PS-NPs on ovarian cancer. Our results first showed that ovarian cancer cells could internalize 50 nm PS-NPs, with significant internalization observed at concentrations starting from 20 μg/mL, which aligns with environmental exposure levels. RNA-seq and subsequent experiments indicated that treatment with 20 μg/mL PS-NPs significantly promoted ovarian cancer cell proliferation, and this phenotype was closely associated with CDK4/6-dependent cell cycle regulation. The CDK4/6 inhibitor Palbociclib effectively reverses the cell proliferation induced by PS-NPs. An oral exposure model in mice found tissue deposition of PS-NPs in the ovaries, kidneys, heart, and lungs. In vivo models further confirmed that mice exposed to PS-NPs had larger subcutaneous tumor weights and volumes compared to the control group, while Palbociclib could successfully block these effects. In conclusion, our research revealed that low-dose PS-NPs could stimulate ovarian tumor progression both in vivo and in vitro in a CDK4/6-dependent manner. Taken together, our study provides potential evidence for risk management of exposure to nanoplastics related to cancer development.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"488-501"},"PeriodicalIF":6.3,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FTO-ACKR3 Axis Regulates Polycyclic Aromatic Hydrocarbons-Induced Asthma Attacks via AhR-Mediated m⁶A RNA Methylation.","authors":"Shengbin Liu, Jiangzhou Chu, Jinxiu Xin, Xiaolin Yin, Zhongshan He, Shugang Qin, Xiangrong Song","doi":"10.1021/envhealth.5c00261","DOIUrl":"10.1021/envhealth.5c00261","url":null,"abstract":"<p><p>Airborne polycyclic aromatic hydrocarbons (PAHs) are increasingly linked to asthma onset and exacerbation, yet their molecular mechanisms remain unclear. Building on our previous finding that PM2.5 alters m6A RNA methylation, we hypothesized that PAHs drive asthma progression through epitranscriptomic regulation. Here, we show that PAH exposure aggravated lung injury, airway remodeling, and fibrosis while reducing global m6A levelsan effect reversed by AhR inhibition. Mechanistically, PAH-activated AhR suppressed transcription of the m6A demethylase FTO, leading to widespread hypomethylation. Reduced m6A deposition on ACKR3 mRNA enhanced its stability through IGF2BP1/2/3 binding, thereby increasing ACKR3 expression. Elevated ACKR3 promoted autophagy and inflammatory signaling in bronchial epithelial cells. Consistently, FTO-deficient mice displayed exacerbated airway inflammation, fibrosis, and ACKR3-driven autophagy. Moreover, PAHs activated the TNFα/NF-κB pathway, further amplifying autophagy and inflammation. Together, these findings define a previously unrecognized AhR-FTO-ACKR3 epitranscriptomic axis through which PAHs potentiate NF-κB signaling, autophagy, and airway injury, providing new mechanistic insight and potential therapeutic targets for pollution-driven asthma.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"473-487"},"PeriodicalIF":6.3,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantifying Depuration of Methylmercury from Fish Consumption by Travelers.","authors":"Ryan F Lepak, Jean Hervé Mve Beh, Clotaire Moukegni-Sika, Jean Noël Bibang Binguema, Sarah E Janssen, Jacob M Ogorek, Michael T Tate, Peter B McIntyre","doi":"10.1021/envhealth.5c00389","DOIUrl":"https://doi.org/10.1021/envhealth.5c00389","url":null,"abstract":"<p><p>During a two-week field sampling expedition in Gabon, two American scientists consumed fish daily from the Ogooué River watershed. We sampled their scalp and facial hair periodically to evaluate hair as a biomarker to track shifts in methylmercury (MeHg) exposure from diet. Each individual differed in the onset and extent of MeHg accumulation but showed similar depuration rates. Pretrip baseline Hg isotope values between participants were distinct from Gabonese fishes allowing us to detect shifts in MeHg sources in the hair of both individuals. δ²⁰²Hg values tracked the mass-dependent fractionation of MeHg depuration stemming from <i>in vivo</i> metabolism, leading to δ²⁰²Hg increases of 0.014 ± 0.001 per mille and total Hg losses of 8.3 ± 1.1 ng g^-1 daily. While limited in scope due to minimal participants, our findings reveal a complex interaction between prior MeHg burdens, contemporary MeHg intakes, and sources of consumed fishes (locally caught versus market-sourced) in determining the dynamics of MeHg concentrations and δ²⁰²Hg in human hair. We also suggest that the offset in δ²⁰²Hg values used in literature between fish and human hair (1.75 ± 0.25‰) may overlook a time domain that increases starting fish-hair δ²⁰²Hg offsets (0.94‰), through time.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 2","pages":"324-330"},"PeriodicalIF":6.3,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12930318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral Intake of Plasticizer Di-(2-ethylhexyl) Phthalate Disrupts Cerebellar Myelination via Thyroid Signaling in Aging Mice.","authors":"Qu-Nan Wang, Fengjie Yang, Xianyan Wang, Xiaoquan Ma, Xiaohan Yang, Lingyu Li, Shenglong Cao, Yán Wa̅ng","doi":"10.1021/envhealth.5c00167","DOIUrl":"10.1021/envhealth.5c00167","url":null,"abstract":"<p><p>Aging is a significant global health challenge, with neurodegenerative diseases severely affecting the quality of life in the elderly. Di-(2-ethylhexyl) phthalate (DEHP), a commonly used plasticizer in food packaging, has been identified as an environmental contaminant with thyroid hormone (TH) disruption and neurotoxic effects. Myelination in the central nervous system is crucial for neurological function, and oligodendrocytes play a central role in this process by forming myelin around axons. THs regulate oligodendrocyte differentiation and the expression of myelin-related genes. This study investigates whether environmental exposure to DEHP in aging mice disrupts thyroid hormone signaling and contributes to myelin damage. 22-month-old male C57BL/6J mice were orally administered DEHP at doses of 0, 0.2, 20, and 200 mg/kg·bw/day (mg/kg·bw/d) for 30 days (d). Nissl staining revealed significant neuronal loss in the cerebellum at higher DEHP doses. Luxol Fast Blue staining showed notable hypomyelination in DEHP-treated mice. Immunofluorescence results demonstrated an increase in oligodendrocyte progenitor cells (NG2⁺), while mature (CC1⁺) and myelinating oligodendrocytes (MBP⁺) were significantly reduced, indicating impaired oligodendrocyte differentiation and myelination. Furthermore, KLF9, a transcriptional regulator critical for oligodendrocyte differentiation, was downregulated. TH levels (T3, T4), transporters (MCT8, OATP1C1), and receptors (TRα, TRβ) were decreased locally, while deiodinases (DIO2, DIO3) were upregulated, reflecting disruption in thyroid signaling. Environmental exposure to DEHP disrupts thyroid hormone signaling in aged mice, impairing oligodendrocyte differentiation and myelin formation. This process is accompanied by microglial activation and neuroinflammation, which may serve as a pathological basis for neuronal loss and further neurodegeneration. Daily oral intake of plasticizer DEHP may induce cerebellar demyelination, contributing to neurodegeneration in the elderly. These results highlight that inappropriate exposure to environmental pollutants, such as DEHP, could increase the risk of cerebellar dysfunction and neurodegeneration in elderly individuals.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 12","pages":"1475-1489"},"PeriodicalIF":6.3,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12723533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145828636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Human-Derived Pathogen Signatures Captured by SERS and Deep Learning for Environmental Exposure Risk Assessment.","authors":"Zhonghua Shen, Linguo Xie, Yuwei Hou, Zeying He, Junjie Liang, Yuchi Jia, Haipeng Zhang, Jingjing Du, Wenjing Liu, Chunyu Liu","doi":"10.1021/envhealth.5c00365","DOIUrl":"10.1021/envhealth.5c00365","url":null,"abstract":"<p><p>Microbial contamination and antibiotic-resistant bacteria (ARB) pose significant threats to environmental ecosystems, particularly in regions lacking adequate sanitation. Urinary pathogens of human origin, frequently detected in contaminated water and surfaces, represent early indicators of ARB-related exposure. However, current exposure assessment approaches rely heavily on standard strains, limiting their effectiveness in real-world scenarios. In this study, a label-free platform was developed by integrating surface-enhanced Raman spectroscopy (SERS) with a convolutional neural network (CNN) for the ARB exposure assessment. A comprehensive spectral database consisting of 368 clinical urinary isolates was established. The CNN achieved the highest classification accuracy (97.6%), surpassing random forest (93.1%) and PCA-SVM (91.2%). Robust performance was further confirmed in wastewater samples (92.2%) and independent urine specimens (90.3%). Importantly, SHAP-based interpretation revealed key discriminatory features in the 724-738 cm^-1 region, associated with adenine and tryptophan, thereby enhancing model interpretability. Together, these findings establish a practical and transparent framework for microbial surveillance and ARB exposure assessment. This approach supports real-time monitoring and provides a practical tool for environmental health management.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"462-472"},"PeriodicalIF":6.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of Air Pollution Exposure on the microRNA Content of Neuronal Extracellular Vesicles in Subjects Affected by Major Depressive Disorder.","authors":"Paola Monti, Elisa Borroni, Rachele Matsagani, Eva Dariol, Laura Dioni, Davide Biganzoli, Simona Iodice, Guido Nosari, Francesca Legnani, Valentina Bollati, Luca Ferrari, Massimiliano Buoli, Michele Carugno","doi":"10.1021/envhealth.5c00336","DOIUrl":"10.1021/envhealth.5c00336","url":null,"abstract":"<p><p>Major depressive disorder (MDD) has been recently linked to air pollution exposure; nevertheless, the biological mechanisms underlying this association remain underinvestigated. Air pollution might modulate the microRNA (miRNA) content of neuron-derived extracellular vesicles (NdEVs), potentially mirroring brain epigenetic alterations. In the present study, we investigated the relationship between air pollution, NdEV miRNAs, and MDD severity in a population of 200 patients with depression. After signing informed consent, participants compiled questionnaires about demographics, lifestyle and clinical history, and donated a blood sample. MDD severity was assessed by five scales. Particulate matter ≤2.5 μm (PM_2.5) and nitrogen dioxide (NO₂) exposure was assigned based on participants' residential address. Plasma NdEVs were obtained by L1CAM immunocapture. NdEV miRNAs were queried by RT-qPCR (microarray) following a two-stage approach. Associations between air pollutants, NdEV miRNAs, and MDD severity were assessed by multivariable regression models. The regulatory function of NdEV miRNAs was investigated by gene target and pathway analysis. As a result, exposure to NO₂ was associated with decreased levels of miR-191 and miR-24, while PM_2.5 was negatively associated with miR-191, miR-223, miR-24, miR-320, miR-451, miR-572, and miR-638. Decreased miR-126, miR-19b, miR-320, miR-451, miR-572, and miR-638 were associated with higher MDD severity scores. Target genes at the interface between air pollution exposure and MDD severity were mainly involved in inflammation and cell cycle regulation. These findings suggest that air pollutants might modulate MDD severity by triggering NdEV miRNA alterations. Longitudinal studies are needed to evaluate whether NdEV miRNAs might serve as novel biomarkers for MDD prognosis.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 1","pages":"154-166"},"PeriodicalIF":6.3,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12813701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Landscape Remodeling Unravels the Cross-Links of Microplastics-Induced Lipidomic Fluctuations, Nutrient Disorders and Energy Disarrangements.","authors":"Miao Wang, Jing Wang, Xinglin Sun, Kena Zhang, Jing Gao, Xiaoying Xu, Jiarui Wu, Fangfang Tao, Dayi Zhang, Mingying Liu","doi":"10.1021/envhealth.5c00132","DOIUrl":"10.1021/envhealth.5c00132","url":null,"abstract":"<p><p>Microplastics are emerging contaminants that pose health risks. They can cause hepatic lipid interventions, but the underlying mechanisms require investigation. This study assessed the retention of polypropylene microplastics in mouse liver and determined the intercorrelations between hepatic lipid fluctuations and transcriptomic changes. Microplastic-induced liver dysfunction was confirmed by the variations of transamination, cholesterol metabolism, biotransformation, and redox state. Chronic high-dose treatment induced distinct pathological changes, including regional fibrotic remodeling and ultrastructural mitochondrial abnormalities. Raman biospectra of liver slice proposed vital peaks of 1060, 1132, 1168, 1340, 1446, 1618, and 1670 cm^-1, representing the liver biomolecule landscapes. Transcriptomic changes were mainly involved in mRNA transcription, multicellular organism development, various stimuli response, cell differentiation, and lipid metabolic process. Microplastic exposure dosage exerted more profound effects than exposure duration on gene expressions of oxidation-reduction process, signal transduction, and lipid metabolism. WGCNA analysis proposed 47 hub genes involved gene expression orchestration, cell fate monitor, and mitochondria translation modulation. Nine differentially expressed genes associated with lipid biomarkers were related to mitochondria transcription (<i>Mrps12</i> and <i>Mrpl53</i>), cell differentiation <i>(Bbc3</i>, <i>Lrrc15</i> and <i>Gdf15</i>), lipid catabolism (<i>Etnppl</i> and <i>lipg</i>) and tRNA methyltransferase (<i>Trmt112</i>), and Raman peak at 1670 cm^-1 intimately connected with aggregated forms of protein. Our findings suggested that polypropylene microplastics could change the liver molecular landscape and induce lipid metabolism disorders and transcriptomic changes in mitochondrial protein translation and expression regulation, highlighting their significant consequences in nutrient and energy imbalance.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"448-461"},"PeriodicalIF":6.3,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Concentration-Specific Neurotoxic Pathways of Tetrabromobisphenol A and Tetrabromobisphenol A Bis(2-Hydroxyethyl Ether) in Zebrafish Larvae.","authors":"Hai Xu, Xing Dong, Wenhui Qiu, Xuchun Qiu, Zhen Zhang","doi":"10.1021/envhealth.5c00341","DOIUrl":"10.1021/envhealth.5c00341","url":null,"abstract":"<p><p>Tetrabromobisphenol A (TBBPA) and its derivative, TBBPA bis-(2-hydroxyethyl ether) (TBBPA-BHEE), are widely used brominated flame retardants commonly detected in environmental media and biota. While regulatory bodies deem these chemicals unlikely to pose significant risks, emerging evidence highlights their potential neurotoxic effects. In this study, we evaluated the neurodevelopmental toxicity of TBBPA and TBBPA-BHEE in zebrafish embryos exposed to nonlethal (94-470 μg/L for TBBPA, 610-2030 μg/L for TBBPA-BHEE) and environmentally relevant concentrations (0.094-0.47 μg/L for TBBPA, 0.061-0.203 μg/L for TBBPA-BHEE) for up to 120 h postfertilization (hpf). Our findings show that at nonlethal concentrations, both TBBPA and TBBPA-BHEE impaired craniofacial development, induced apoptosis, reduced γ-aminobutyric acid (GABA) levels, and disrupted motor behavior, with significant alterations in the expression of genes involved in GABAergic signaling and synaptic plasticity. Transcriptomic and miRNA profiling revealed that downregulation of GABA receptor genes and miRNAs (e.g., let-7i, miR-192,) contributed to neurodevelopmental defects through disruption of CREB signaling and synaptogenesis. In contrast, exposure to environmentally relevant concentrations induced similar phenotypes (craniofacial malformations and apoptosis) without major changes in neurotransmitter levels, suggesting that low-dose neurotoxicity might be mediated by alternative, less understood mechanisms, possibly involving epigenetic modifications or compensatory neuronal adaptations. These findings underscore the complexity of low-dose toxicity and the need for further research into the molecular pathways underlying the neurotoxic effects of TBBPA and its derivatives, particularly at environmentally relevant concentrations.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"434-447"},"PeriodicalIF":6.3,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistance Gene Dynamics, Biogeochemical Coupling, and Ecological Risks in Sediments of Anthropogenically Impacted Lake Wetlands in China.","authors":"Chengzhi Mao, Yunfeng Wang, Xinghao Li, Qiaoyi Kong, Saleh A Al-Farraj, Elvis Genbo Xu, Hans-Peter Grossart, Jie Huang, Weibo Song","doi":"10.1021/envhealth.5c00278","DOIUrl":"10.1021/envhealth.5c00278","url":null,"abstract":"<p><p>Antibiotic resistance is a growing global threat to both public health and ecosystem stability. While the \"One Health\" framework emphasizes the need to monitor antibiotic resistance genes (ARGs) across diverse environments worldwide, the risks posed by ARGs in lakes affected by human activities, particularly in lake sediments that serve as natural reservoirs of ARGs, remain poorly understood. Metagenomics enables culture-independent analysis of microbial communities and resistance genes, providing essential insights into ARG dynamics. This study investigates microbial communities, ARGs, metal resistance genes (MRGs), and mobile genetic elements (MGEs) in sediments from Lake Donghu and Lake Weishan in China, two contrasting lake ecosystems subject to urbanization and agricultural activities for over four decades, using high-throughput metagenomic sequencing and assembly. ARGs and MRGs were more strongly influenced by deterministic environmental factors, particularly heavy metals (Cd, Pb, Cu), whereas microbial community structures were predominantly shaped by stochastic processes. Metagenomic binning yielded 293 metagenome-assembled genomes (MAGs), 125 of which were identified as potential ARG hosts, with Proteobacteria and Desulfobacterota being the most common. These hosts frequently cocarried MGEs, virulence factor genes (VFGs), and MRGs and exhibited metabolic pathways linked to carbon, nitrogen, and greenhouse gas (CO₂ and N₂O) cycling. Dissolved organic carbon (DOC) was determined as a key factor influencing microbial metabolism and promoting resistance gene dissemination. Our findings highlight a tight coupling between ARG dissemination, microbial ecological functions, and biogeochemical processes, underscoring ecosystem-level risks associated with resistance proliferation in human-impacted wetlands of China and elsewhere.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"420-433"},"PeriodicalIF":6.3,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microplastics and Nanoplastics Cause Thyroid Dysfunction in Adolescent Mice through the Intestinal Microbiota-Mediated Hypothalamus-Pituitary-Thyroid Axis.","authors":"Jinpeng Zhang, Jiaoyang Ji, Xiaowei Dai, Bo Li, Tianyu Liu, Shaoxuan Zhang, Yong Yu","doi":"10.1021/envhealth.5c00170","DOIUrl":"https://doi.org/10.1021/envhealth.5c00170","url":null,"abstract":"<p><p>Polypropylene (PP) and poly-(ethylene terephthalate) (PET) plastic products are widely used in diet packaging and may generate microplastics (MPs) and nanoplastics (NPs) during use. However, their effects and mechanisms on causing endocrine system diseases remain unclear. Here, we established a dietary exposure mouse model using micro and nanoplastics (MNPs) and found that MNPs caused a decrease in thyroid function in adolescent mice. Fecal microbiota transplantation (FMT) was used to reconstruct the intestinal microbiota of mice to reveal the mechanisms of thyroid dysfunction. The abundance of <i>Bacteroides</i> in the intestinal tract significantly changed after FMT. PP-MPs and NPs affected the levels of lysophosphatidylethanolamine and fatty acid esters of hydroxy fatty acids, respectively, which competitively bound to thyrotropin receptor (TSHR) on the thyroid gland, thus affecting the thyroid function. PET-MNPs affected the level of 4-hydroxy-3-methoxyphenylglycol sulfate, which regulated the activity of sympathetic nervous system by acting on the thyrotropin-releasing hormone receptor and TSHR in mice, thereby interfering with the regulatory function of the hypothalamus-pituitary-thyroid (HPT) axis on the synthesis and secretion of thyroid hormones. This study emphasizes the key role of intestinal microbiota-mediated HPT axis in thyroid dysfunction caused by MNP exposure and provides theoretical basis for the prevention of endocrine-related diseases during adolescence caused by MNPs.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 2","pages":"313-323"},"PeriodicalIF":6.3,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12930315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147290626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}