Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2025.119662
Xia Ning, Yan Zhi, Shuo Wang, Zhaoli Li, Zhihua Ren, Tingting Ku, Guangke Li, Nan Sang
Flufenoxuron has been widely applied in agriculture for decades because of high insecticidal efficiency. However, its environmental persistence and potential phytotoxicity raise alarming ecological concerns, with mechanisms that remain unclear. This study investigated the physiological role of flufenoxuron in regulating auxin and carbohydrate metabolism in barley. Flufenoxuron exposure significantly inhibited barley growth and reduced biomass accumulation in both roots and leaves. Endogenous indole-3-acetic acid (IAA) levels were notably decreased, indicating a disruption of auxin homeostasis. Molecular docking analysis showed that flufenoxuron had a higher binding affinity to transport inhibitor response 1 (TIR1) than IAA, thereby interfering with auxin perception and signal transduction. Enzyme assays demonstrated that flufenoxuron exposure altered sucrose-cleaving and glycolytic enzyme activities, with tissue-specific metabolic adaptations in roots and leaves. Correlation analysis revealed a negative association between IAA levels and cytInv activity in leaves, underscoring the interplay between hormonal regulation and carbohydrate metabolism. Overall, these findings provide mechanistic insights into flufenoxuron-induced phytotoxicity, highlighting the organ-specific association between auxin signaling and carbon metabolism and offering a new perspective into the assessment of ecological risks involving persistent insecticides.
{"title":"Phytotoxicity of flufenoxuron in barley: Disrupted crosstalk between auxin signaling and carbon metabolism","authors":"Xia Ning, Yan Zhi, Shuo Wang, Zhaoli Li, Zhihua Ren, Tingting Ku, Guangke Li, Nan Sang","doi":"10.1016/j.ecoenv.2025.119662","DOIUrl":"10.1016/j.ecoenv.2025.119662","url":null,"abstract":"<div><div>Flufenoxuron has been widely applied in agriculture for decades because of high insecticidal efficiency. However, its environmental persistence and potential phytotoxicity raise alarming ecological concerns, with mechanisms that remain unclear. This study investigated the physiological role of flufenoxuron in regulating auxin and carbohydrate metabolism in barley. Flufenoxuron exposure significantly inhibited barley growth and reduced biomass accumulation in both roots and leaves. Endogenous indole-3-acetic acid (IAA) levels were notably decreased, indicating a disruption of auxin homeostasis. Molecular docking analysis showed that flufenoxuron had a higher binding affinity to transport inhibitor response 1 (TIR1) than IAA, thereby interfering with auxin perception and signal transduction. Enzyme assays demonstrated that flufenoxuron exposure altered sucrose-cleaving and glycolytic enzyme activities, with tissue-specific metabolic adaptations in roots and leaves. Correlation analysis revealed a negative association between IAA levels and cytInv activity in leaves, underscoring the interplay between hormonal regulation and carbohydrate metabolism. Overall, these findings provide mechanistic insights into flufenoxuron-induced phytotoxicity, highlighting the organ-specific association between auxin signaling and carbon metabolism and offering a new perspective into the assessment of ecological risks involving persistent insecticides.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119662"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2025.119658
Dandan Wang , Peng Li
Depression is a prevalent mental disorder in modern society, with a complex and incompletely understood etiology. Accumulating evidence indicates that pesticide exposure is a potential risk factor for mental health disorders. Atrazine (ATR), a widely used herbicide with the highest global application rates and frequently detected in environmental media, has been confirmed to possess neurotoxicity. However, there are currently no reports examining its effects on depression. Therefore, this study aimed to investigate the effects of subchronic ATR exposure on depression-like phenotypes in mice through behavioral tests, pathological examinations, and molecular analyses. The results demonstrated that ATR exposure induced significant depressive-like behaviors and led to neuronal reductions in key brain regions associated with depression, such as the hippocampus and prefrontal cortex. These effects were mechanistically linked to oxidative damage and decreased expression levels of 5-hydroxytryptamine (5-HT) and brain-derived neurotrophic factor (BDNF). Collectively, this study not only reveals the potential role and mechanism of ATR as an environmental risk factor for depression, but also provides a theoretical basis for the prevention and treatment of its new neurotoxicological effects and future related research.
{"title":"The effect and mechanism of atrazine induced depression-like in mice","authors":"Dandan Wang , Peng Li","doi":"10.1016/j.ecoenv.2025.119658","DOIUrl":"10.1016/j.ecoenv.2025.119658","url":null,"abstract":"<div><div>Depression is a prevalent mental disorder in modern society, with a complex and incompletely understood etiology. Accumulating evidence indicates that pesticide exposure is a potential risk factor for mental health disorders. Atrazine (ATR), a widely used herbicide with the highest global application rates and frequently detected in environmental media, has been confirmed to possess neurotoxicity. However, there are currently no reports examining its effects on depression. Therefore, this study aimed to investigate the effects of subchronic ATR exposure on depression-like phenotypes in mice through behavioral tests, pathological examinations, and molecular analyses. The results demonstrated that ATR exposure induced significant depressive-like behaviors and led to neuronal reductions in key brain regions associated with depression, such as the hippocampus and prefrontal cortex. These effects were mechanistically linked to oxidative damage and decreased expression levels of 5-hydroxytryptamine (5-HT) and brain-derived neurotrophic factor (BDNF). Collectively, this study not only reveals the potential role and mechanism of ATR as an environmental risk factor for depression, but also provides a theoretical basis for the prevention and treatment of its new neurotoxicological effects and future related research.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119658"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145973133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2026.119710
Liu Ji , Guiting Yang , Maoyao Ling , YanLin Xiao , Huajin Ou , YaLan Jiang , Xiaoting Liao , Jinyuan Lin , Linghui Pan
Breast cancer is the most common malignancy among women worldwide, with environmental chemical exposure increasingly implicated in its development. Parabens (PBs) are widely used preservatives with endocrine-disrupting properties, but their role in breast carcinogenesis remains unclear. This study integrated epidemiological analyses of the National Health and Nutrition Examination Survey (NHANES), network toxicology, machine learning, transcriptomic profiling, molecular docking, and in vitro assays to investigate associations between PBs exposure and breast cancer risk and to explore potential mechanisms. NHANES analysis (2005–2016, n = 9615) revealed significant associations between higher urinary concentrations of ethyl paraben (EPB), methyl paraben (MPB), and propyl paraben (PPB) and breast cancer prevalence. Network toxicology identified 14 candidate molecular targets, with estrogen receptor 1 (ESR1), enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2), and platelet-derived growth factor receptor alpha (PDGFRA) prioritized through machine learning and SHapley Additive exPlanations (SHAP), highlighting EZH2 as the most influential predictor. Transcriptomic analyses indicated these hub targets influence immune cell infiltration and exhibit distinct expression patterns within the tumor microenvironment. Molecular docking simulations suggested strong interactions between PBs and these hub proteins. In vitro assays demonstrated that PBs upregulated ESR1 and EZH2, induced DNA damage in normal breast epithelial cells, and enhanced proliferation and migration in breast cancer cells—effects reversed by ESR1 and EZH2 inhibitors. Together, these findings suggest that PBs may affect pathways relevant to breast cancer progression and act as potential environmental contributors.
{"title":"Article title: Associations between paraben exposure and breast cancer risk: An integrative epidemiologic, network toxicology, multi-omics and experimental analysis","authors":"Liu Ji , Guiting Yang , Maoyao Ling , YanLin Xiao , Huajin Ou , YaLan Jiang , Xiaoting Liao , Jinyuan Lin , Linghui Pan","doi":"10.1016/j.ecoenv.2026.119710","DOIUrl":"10.1016/j.ecoenv.2026.119710","url":null,"abstract":"<div><div>Breast cancer is the most common malignancy among women worldwide, with environmental chemical exposure increasingly implicated in its development. Parabens (PBs) are widely used preservatives with endocrine-disrupting properties, but their role in breast carcinogenesis remains unclear. This study integrated epidemiological analyses of the National Health and Nutrition Examination Survey (NHANES), network toxicology, machine learning, transcriptomic profiling, molecular docking, and in vitro assays to investigate associations between PBs exposure and breast cancer risk and to explore potential mechanisms. NHANES analysis (2005–2016, n = 9615) revealed significant associations between higher urinary concentrations of ethyl paraben (EPB), methyl paraben (MPB), and propyl paraben (PPB) and breast cancer prevalence. Network toxicology identified 14 candidate molecular targets, with estrogen receptor 1 (ESR1), enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2), and platelet-derived growth factor receptor alpha (PDGFRA) prioritized through machine learning and SHapley Additive exPlanations (SHAP), highlighting EZH2 as the most influential predictor. Transcriptomic analyses indicated these hub targets influence immune cell infiltration and exhibit distinct expression patterns within the tumor microenvironment. Molecular docking simulations suggested strong interactions between PBs and these hub proteins. In vitro assays demonstrated that PBs upregulated ESR1 and EZH2, induced DNA damage in normal breast epithelial cells, and enhanced proliferation and migration in breast cancer cells—effects reversed by ESR1 and EZH2 inhibitors. Together, these findings suggest that PBs may affect pathways relevant to breast cancer progression and act as potential environmental contributors.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119710"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study developed and validated a simplified QuEChERS-based isotope dilution ultra-performance liquid chromatography–tandem mass spectrometry (ID-UPLC–MS/MS) method for the simultaneous quantification of neonicotinoids (NEOs), parabens (PBs), and bisphenols (BPs) in meat products. Twenty-seven fresh and thirty processed meat samples collected in Taiwan were analyzed by the validated ID-UPLC-MS/MS method with isotope dilution to determine seven NEOs, nine PBs, and five BPs, achieving low limits of detection (0.00015–0.194 ng/g ww) and acceptable recoveries (83–105 %). Because of high sensitivity of the method, acetamiprid and imidacloprid were quantitated in most samples with quantitation rate (QR) ≥ 94.7 % at trace concentrations of 0.027 – 0.099 ng/g ww and 0.057 – 0.228 ng/g ww, respectively. Methylparaben (0.005 – 6.221 ng/g ww) was quantified with QR of 64.9 %, while bisphenol A (BPA, 0.081 – 1.728 ng/g ww), bisphenol S (0.015 – 2.374 ng/g ww), and bisphenol AF (0.004 – 0.269 ng/g ww) was determined with QR of 45.6 %, 29.8 % and 33.3 %, respectively. Estimated dietary intakes for most analytes were well below their reference doses; however, BPA (up to 0.54 ng/kg-BW/day) exceeded the revised tolerable daily intake (0.2 ng/kg-BW/day) set by the European Food Safety Authority, suggesting a potential noncancer health concern. The findings reveal the presence of multiple emerging contaminants in meat products and demonstrate the utility of a simplified, high-throughput QuEChERS UPLC–MS/MS method for multi-class chemical monitoring in food.
{"title":"Simplified QuEChERS-based UPLC–MS/MS for determination of neonicotinoids, bisphenols, and parabens in fresh and processed meat","authors":"Po-Chin Huang , Yi-Hsi Chen , Jung-Wei Chang , Yu-Hsin Lin , Hsin-Chang Chen","doi":"10.1016/j.ecoenv.2025.119606","DOIUrl":"10.1016/j.ecoenv.2025.119606","url":null,"abstract":"<div><div>This study developed and validated a simplified QuEChERS-based isotope dilution ultra-performance liquid chromatography–tandem mass spectrometry (ID-UPLC–MS/MS) method for the simultaneous quantification of neonicotinoids (NEOs), parabens (PBs), and bisphenols (BPs) in meat products. Twenty-seven fresh and thirty processed meat samples collected in Taiwan were analyzed by the validated ID-UPLC-MS/MS method with isotope dilution to determine seven NEOs, nine PBs, and five BPs, achieving low limits of detection (0.00015–0.194 ng/g ww) and acceptable recoveries (83–105 %). Because of high sensitivity of the method, acetamiprid and imidacloprid were quantitated in most samples with quantitation rate (QR) ≥ 94.7 % at trace concentrations of 0.027 – 0.099 ng/g ww and 0.057 – 0.228 ng/g ww, respectively. Methylparaben (0.005 – 6.221 ng/g ww) was quantified with QR of 64.9 %, while bisphenol A (BPA, 0.081 – 1.728 ng/g ww), bisphenol S (0.015 – 2.374 ng/g ww), and bisphenol AF (0.004 – 0.269 ng/g ww) was determined with QR of 45.6 %, 29.8 % and 33.3 %, respectively. Estimated dietary intakes for most analytes were well below their reference doses; however, BPA (up to 0.54 ng/kg-BW/day) exceeded the revised tolerable daily intake (0.2 ng/kg-BW/day) set by the European Food Safety Authority, suggesting a potential noncancer health concern. The findings reveal the presence of multiple emerging contaminants in meat products and demonstrate the utility of a simplified, high-throughput QuEChERS UPLC–MS/MS method for multi-class chemical monitoring in food.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119606"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2026.119724
Liusen Fang , Litang Qin , Weihao Yao , Jinfang Nie , Huazhou Wei , Yanpeng Liang , Honghu Zeng , Lingyun Mo
Di(2-ethylhexyl) phthalate (DEHP) is a typical endocrine disrupter. Plastic films containing DEHP, widely used in agriculture, have caused severe soil pollution and pose potential risks to human health through the food chain. This study investigated the effects of DEHP stress on the rhizosphere microenvironment of Brassica chinensis L. (Shanghai Qing) using a multi-omics approach. The results showed that soil dehydrogenase (S-DHA), soil urease (S-UE), and soil polyphenol oxidase (S-PPO) activities reached their maximum values at DEHP concentrations of 50, 20 and 20 mg/kg, respectively. S-DHA activity increased a dose-dependent manner, whereas S-UE index demonstrated a decreasing trend and S-PPO showed an increasing trend with increasing DEHP levels. The addition of DEHP significantly downregulated the contents of soil metabolites Trifolirhizin, Glycitin, Ganoderic acid D2, and Ceratodictyol, while Toddalolactone, Methylguanidine, Guanine, Calycanthine, Urea, and Hydrocortisone were significantly upregulated. As DEHP concentrations increased, both the Chao1 index and Shannon index decreased under stress treatment (2 mg/kg, 20 mg/kg, 50 mg/kg) compared with the control (0 mg/kg). DEHP altered soil bacteria community structure, reducing both diversity and abundance. Overall, this study provides insights into the complex interactions among DEHP, soil bacterial communities and soil metabolism, highlighting the need for targeted remediation strategies to mitigate DEHP-induced soil contamination.
{"title":"Soil metabolism and bacterial response to Di(2-ethylhexyl) phthalate (DEHP) stress in Brassica chinensis L. (Shanghai Qing)","authors":"Liusen Fang , Litang Qin , Weihao Yao , Jinfang Nie , Huazhou Wei , Yanpeng Liang , Honghu Zeng , Lingyun Mo","doi":"10.1016/j.ecoenv.2026.119724","DOIUrl":"10.1016/j.ecoenv.2026.119724","url":null,"abstract":"<div><div>Di(2-ethylhexyl) phthalate (DEHP) is a <u>t</u>ypical endocrine disrupter. Plastic films containing DEHP, widely used in agriculture, have caused severe soil pollution and pose potential risks to human health through the food chain. This study investigated the effects of DEHP stress on the rhizosphere microenvironment of <em>Brassica chinensis</em> L. (Shanghai Qing) using a multi-omics approach. The results showed that soil dehydrogenase (S-DHA), soil urease (S-UE), and soil polyphenol oxidase (S-PPO) activities reached their maximum values at DEHP concentrations of 50, 20 and 20 mg/kg, respectively. S-DHA activity increased a dose-dependent manner, whereas S-UE index demonstrated a decreasing trend and S-PPO showed an increasing trend with increasing DEHP levels. The addition of DEHP significantly downregulated the contents of soil metabolites Trifolirhizin, Glycitin, Ganoderic acid D2, and Ceratodictyol, while Toddalolactone, Methylguanidine, Guanine, Calycanthine, Urea, and Hydrocortisone were significantly upregulated. As DEHP concentrations increased, both the Chao1 index and Shannon index decreased under stress treatment (2 mg/kg, 20 mg/kg, 50 mg/kg) compared with the control (0 mg/kg). DEHP altered soil bacteria community structure, reducing both diversity and abundance. Overall, this study provides insights into the complex interactions among DEHP, soil bacterial communities and soil metabolism, highlighting the need for targeted remediation strategies to mitigate DEHP-induced soil contamination.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119724"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145964779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2026.119726
Xinliang Zhu , Xumin He , Xuanfang Long , Peijing Li , Fengfeng Lei
Trichloroethylene (TCE), a persistent environmental pollutant, poses potential health risks through multiple exposure routes, such as inhalation of vapor-phase TCE or ingestion of contaminated water and food. While recognized as a carcinogen, its neurobehavioral effects remain poorly characterized. This study investigated the mechanisms of TCE neurotoxicity in adult zebrafish following chronic exposure to environmentally relevant concentrations (20, 60, and 180 μg/L). Behavioral assessments revealed concentration-dependent anxiety-like behavior, reduced exploration, and memory impairment. Transcriptomic analysis identified progressive disruption of visual perception, synaptic signaling, and ion channel activity pathways. Building on this, we validated the expression of key genes by qPCR: gabrr3a (a GABA receptor subunit) was significantly upregulated in the 60 μg/L group, which was highly correlated with anxiety-like behaviors; cryba1b (a crystallin protein) showed a non-monotonic expression pattern, while lim2.1 (a lens membrane protein) exhibited a highly significant dose-dependent upregulation with increasing concentrations, indicating that the visual system is a sensitive target of TCE toxicity. Metabolomic profiling showed altered amino acid metabolism at low concentrations and severe energy metabolism suppression with inflammatory activation at high concentrations. The integrated multi-omics approach demonstrates that TCE induces neurobehavioral deficits through coordinated disruption of neural function and metabolic homeostasis, highlighting visual system impairment as a novel sensitive endpoint. These findings provide new insights into TCE's ecological risk and mechanistic toxicity.
{"title":"Integrated behavioral, transcriptomic and metabolomic analysis reveals the neurotoxicity of trichloroethylene in adult zebrafish (Danio rerio)","authors":"Xinliang Zhu , Xumin He , Xuanfang Long , Peijing Li , Fengfeng Lei","doi":"10.1016/j.ecoenv.2026.119726","DOIUrl":"10.1016/j.ecoenv.2026.119726","url":null,"abstract":"<div><div>Trichloroethylene (TCE), a persistent environmental pollutant, poses potential health risks through multiple exposure routes, such as inhalation of vapor-phase TCE or ingestion of contaminated water and food. While recognized as a carcinogen, its neurobehavioral effects remain poorly characterized. This study investigated the mechanisms of TCE neurotoxicity in adult zebrafish following chronic exposure to environmentally relevant concentrations (20, 60, and 180 μg/L). Behavioral assessments revealed concentration-dependent anxiety-like behavior, reduced exploration, and memory impairment. Transcriptomic analysis identified progressive disruption of visual perception, synaptic signaling, and ion channel activity pathways. Building on this, we validated the expression of key genes by qPCR: <em>gabrr3a</em> (a GABA receptor subunit) was significantly upregulated in the 60 μg/L group, which was highly correlated with anxiety-like behaviors; <em>cryba1b</em> (a crystallin protein) showed a non-monotonic expression pattern, while <em>lim2.1</em> (a lens membrane protein) exhibited a highly significant dose-dependent upregulation with increasing concentrations, indicating that the visual system is a sensitive target of TCE toxicity. Metabolomic profiling showed altered amino acid metabolism at low concentrations and severe energy metabolism suppression with inflammatory activation at high concentrations. The integrated multi-omics approach demonstrates that TCE induces neurobehavioral deficits through coordinated disruption of neural function and metabolic homeostasis, highlighting visual system impairment as a novel sensitive endpoint. These findings provide new insights into TCE's ecological risk and mechanistic toxicity.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119726"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2025.119605
Yanhui Hao , Wen Yu , Yingyu Yue , Siyue Chen , Han Liu , Yanting Wu , Hefeng Huang
Parabens (PBs) are associated with altered fetal growth parameters, but the underlying mechanisms—particularly those involving placental function—remain unclear. To elucidate the mechanisms through PB exposure impairs placental steroidogenic function, thereby contributing to the pathogenesis of fetal growth restriction (FGR). Metabolic profiles in maternal serum samples from FGR cases (n = 20) and the matched controls (n = 20) within a Maternal-Child Health Cohort (Obstetrics & Gynecology Hospital of Fudan University), which were prospectively collected in the first-trimester, were analyzed using UPLC-MS/MS. Trophoblast-derived JEG-3 cells were exposed to butylparaben (BuPB; 1–100 μM, 6–24 h) to assess steroidogenic pathway disruption. Pregnant C57BL/6 mice received subcutaneous BuPB (0, 100 and 400 mg/kg/day, GD 0–13.5) for longitudinal evaluation of exposure effects on placental and fetal development. Pregnancies complicated by FGR exhibited elevated PBs burdens in first-trimester, along with steroidogenic metabolomes significantly disrupted. In vitro exposure of JEG-3 cells to BuPB further confirmed that the estrogen biosynthesis pathway was preferential impaired, as demonstrated by dose-dependent upregulation of HSD3B1 and HSD17B1 expression (1.40–1.42-fold; p < 0.05), while suppression of CYP19A1 expression (35 %–68 % reduction; p < 0.01). In vivo, gestational BuP exposure (GD 0.5-G13.5) induced FGR phenotypes in mice, characterized by reduced fetal weight (28 % decrease; p < 0.01), placental damage. At GD13.5, placental Hsd17b1 was upregulated, while Cyp19a1 was suppressed (p < 0.05) with concomitant estrogen deficiency. Our findings indicate that early gestational BuPB exposure may disrupt placental steroidogenesis, specifically through placental steroidogenesis homeostasis, resulting in placental estrogen deficiency and impaired placenta and fetal development. Our study provided integrated evidences of developmental toxicity of PBs in the pathogenesis of FGR.
{"title":"Exposure to paraben in early gestational period: Impact on placental estrogen biosynthesis and fetal growth restriction","authors":"Yanhui Hao , Wen Yu , Yingyu Yue , Siyue Chen , Han Liu , Yanting Wu , Hefeng Huang","doi":"10.1016/j.ecoenv.2025.119605","DOIUrl":"10.1016/j.ecoenv.2025.119605","url":null,"abstract":"<div><div>Parabens (PBs) are associated with altered fetal growth parameters, but the underlying mechanisms—particularly those involving placental function—remain unclear. To elucidate the mechanisms through PB exposure impairs placental steroidogenic function, thereby contributing to the pathogenesis of fetal growth restriction (FGR). Metabolic profiles in maternal serum samples from FGR cases (n = 20) and the matched controls (n = 20) within a Maternal-Child Health Cohort (Obstetrics & Gynecology Hospital of Fudan University), which were prospectively collected in the first-trimester, were analyzed using UPLC-MS/MS. Trophoblast-derived JEG-3 cells were exposed to butylparaben (BuPB; 1–100 μM, 6–24 h) to assess steroidogenic pathway disruption. Pregnant C57BL/6 mice received subcutaneous BuPB (0, 100 and 400 mg/kg/day, GD 0–13.5) for longitudinal evaluation of exposure effects on placental and fetal development. Pregnancies complicated by FGR exhibited elevated PBs burdens in first-trimester, along with steroidogenic metabolomes significantly disrupted. <em>In vitro</em> exposure of JEG-3 cells to BuPB further confirmed that the estrogen biosynthesis pathway was preferential impaired, as demonstrated by dose-dependent upregulation of <em>HSD3B1</em> and <em>HSD17B1</em> expression (1.40–1.42-fold; <em>p</em> < 0.05), while suppression of <em>CYP19A1</em> expression (35 %–68 % reduction; <em>p</em> < 0.01). <em>In vivo</em>, gestational BuP exposure (GD 0.5-G13.5) induced FGR phenotypes in mice, characterized by reduced fetal weight (28 % decrease; <em>p</em> < 0.01), placental damage. At GD13.5, placental <em>Hsd17b1</em> was upregulated, while <em>Cyp19a1</em> was suppressed (<em>p</em> < 0.05) with concomitant estrogen deficiency. Our findings indicate that early gestational BuPB exposure may disrupt placental steroidogenesis, specifically through placental steroidogenesis homeostasis, resulting in placental estrogen deficiency and impaired placenta and fetal development. Our study provided integrated evidences of developmental toxicity of PBs in the pathogenesis of FGR.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119605"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2025.119578
Yukai Yang , Huajiang Dong , Nan Wang , Jiaxing Zhang , Zhen Zhang , Quan Sun , Weiran Zhang , Junchi Wang , Jing Liu , Yeming Liu , Dongbin Wang , Guangbo Qu , Guibin Jiang , Liqun Chen , Dong Ming
Global warming is expected to alter indoor thermal environments and indoor air composition, yet the specific effects of these changes on learning and cognition remain insufficiently understood. In this climate chamber study, we examined the combined effects of experimentally elevated indoor CO₂ concentrations (500 and 5000 ppm, added from a gas cylinder under constant ventilation) and temperatures (22 °C and 28 °C) on cognitive-related outcomes. Twenty-four participants completed a within-subject protocol involving two neuropsychological tasks (Stroop and delayed-matching-to-sample), subjective evaluations, physiological measurements, and electroencephalography (EEG). EEG features were further used to construct a deep learning-based Cognitive Comfort Model (CCM). Significant interactions between CO₂ level and temperature were observed for noise acceptability, thermal comfort, and EEG power in the alpha, theta, and delta bands, whereas behavioral task performance showed only limited changes across conditions. These results suggest that combined thermal–CO₂ stress can modulate subjective comfort and neural indicators of cognitive load even when overt performance is largely preserved. Our findings help to clarify the specific effects of elevated CO₂ and temperature, independent of general poor ventilation, and support the refinement of indoor environmental control strategies aimed at protecting cognitive well-being in warming climates.
{"title":"Impact of experimentally elevated CO₂ concentrations and temperature on cognitive function: An EEG-based study under constant ventilation","authors":"Yukai Yang , Huajiang Dong , Nan Wang , Jiaxing Zhang , Zhen Zhang , Quan Sun , Weiran Zhang , Junchi Wang , Jing Liu , Yeming Liu , Dongbin Wang , Guangbo Qu , Guibin Jiang , Liqun Chen , Dong Ming","doi":"10.1016/j.ecoenv.2025.119578","DOIUrl":"10.1016/j.ecoenv.2025.119578","url":null,"abstract":"<div><div>Global warming is expected to alter indoor thermal environments and indoor air composition, yet the specific effects of these changes on learning and cognition remain insufficiently understood. In this climate chamber study, we examined the combined effects of experimentally elevated indoor CO₂ concentrations (500 and 5000 ppm, added from a gas cylinder under constant ventilation) and temperatures (22 °C and 28 °C) on cognitive-related outcomes. Twenty-four participants completed a within-subject protocol involving two neuropsychological tasks (Stroop and delayed-matching-to-sample), subjective evaluations, physiological measurements, and electroencephalography (EEG). EEG features were further used to construct a deep learning-based Cognitive Comfort Model (CCM). Significant interactions between CO₂ level and temperature were observed for noise acceptability, thermal comfort, and EEG power in the alpha, theta, and delta bands, whereas behavioral task performance showed only limited changes across conditions. These results suggest that combined thermal–CO₂ stress can modulate subjective comfort and neural indicators of cognitive load even when overt performance is largely preserved. Our findings help to clarify the specific effects of elevated CO₂ and temperature, independent of general poor ventilation, and support the refinement of indoor environmental control strategies aimed at protecting cognitive well-being in warming climates.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119578"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2025.119614
Tingting Wang , Zhiheng Yi , Yuhan Tan , Yangshen Huang , Tengli Li , Weikun Lu , Weiduan Zhuang , Shaowei Guo
The exponential growth in global plastic production has resulted in pervasive environmental contamination of micro- and nanoplastics (MNPs). Although MNPs have been detected in various human specimens, their presence in the central nervous system and potential neurological impacts remain poorly understood. This study investigated MNP concentrations in paired cerebrospinal fluid (CSF) and blood samples from patients with neurological disorders, and assessed potential associations with cerebral metabolic changes. We analyzed paired CSF (n = 20) and blood (n = 20) samples from individuals with neuroimmune diseases, neuroinfectious diseases, and controls using pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS) to quantify 11 types of MNPs. Untargeted metabolomic profiling of CSF was performed to identify associated metabolic disturbances. Five types of MNP polymers, namely PVC, PA66, PE, PP, and PS, were detected in both biofluids. Total MNP concentrations were significantly higher in blood (121.43–151.52 µg/mL) than in CSF (7.59–16.07 µg/mL). Strong correlations between CSF and blood MNP concentrations were observed in the neuroimmune (r = 0.56, p < 0.001) and neuroinfection (r = 0.52, p < 0.01) groups, but not in controls (r = 0.01, p > 0.05). Metabolomic analysis revealed 23 disrupted pathways in the high MNP group, including FcγR-mediated phagocytosis and glycerophospholipid metabolism, with specific metabolites like N2-Acetylornithine showing strong correlations with MNP levels (r = 0.75, p < 0.01). This pilot study indicates potential associations of MNPs with metabolic changes in the brain, underscoring the need for further investigation into their roles in neurological diseases.
{"title":"Detection of micro- and nanoplastics in cerebrospinal fluid and blood: Implications for brain diseases","authors":"Tingting Wang , Zhiheng Yi , Yuhan Tan , Yangshen Huang , Tengli Li , Weikun Lu , Weiduan Zhuang , Shaowei Guo","doi":"10.1016/j.ecoenv.2025.119614","DOIUrl":"10.1016/j.ecoenv.2025.119614","url":null,"abstract":"<div><div>The exponential growth in global plastic production has resulted in pervasive environmental contamination of micro- and nanoplastics (MNPs). Although MNPs have been detected in various human specimens, their presence in the central nervous system and potential neurological impacts remain poorly understood. This study investigated MNP concentrations in paired cerebrospinal fluid (CSF) and blood samples from patients with neurological disorders, and assessed potential associations with cerebral metabolic changes. We analyzed paired CSF (n = 20) and blood (n = 20) samples from individuals with neuroimmune diseases, neuroinfectious diseases, and controls using pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS) to quantify 11 types of MNPs. Untargeted metabolomic profiling of CSF was performed to identify associated metabolic disturbances. Five types of MNP polymers, namely PVC, PA66, PE, PP, and PS, were detected in both biofluids. Total MNP concentrations were significantly higher in blood (121.43–151.52 µg/mL) than in CSF (7.59–16.07 µg/mL). Strong correlations between CSF and blood MNP concentrations were observed in the neuroimmune (r = 0.56, p < 0.001) and neuroinfection (r = 0.52, p < 0.01) groups, but not in controls (r = 0.01, p > 0.05). Metabolomic analysis revealed 23 disrupted pathways in the high MNP group, including FcγR-mediated phagocytosis and glycerophospholipid metabolism, with specific metabolites like N2-Acetylornithine showing strong correlations with MNP levels (r = 0.75, p < 0.01). This pilot study indicates potential associations of MNPs with metabolic changes in the brain, underscoring the need for further investigation into their roles in neurological diseases.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119614"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145938809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.ecoenv.2025.119572
Ying Shen , Yifan Ning , Fangyuan Chen , Xiaoyan Wang , Dongming Zheng , Yanli Sun , Xiaowen Zhang , Xue Zhang
Despite growing concern about microplastic contamination in human tissues, the relationship between placental microplastic exposure and fetal anthropometric outcomes remains unexplored. This study investigated associations between placental microplastic content and birth weight (BW), birth length (BL), and head circumference (HC), in a large prospective cohort in China. We recruited 1750 mother–infant pairs between 2022–2024. Placental tissues were collected immediately after delivery from maternal and fetal sides using strict contamination-prevention protocols. Microplastics were identified and quantified via laser direct infrared (LD-IR) chemical imaging. Associations between polymer-specific microplastics (PVC, PP, PBS, PET) and fetal growth were assessed using multivariable linear regression, sex-stratified analyses, and mixture models, including g-computation (g-comp), generalized weighted quantile sum regression (gWQS), and Bayesian kernel machine regression (BKMR). Median placental microplastic concentrations were 7.0, 5.0, 4.0, and 3.0 particles/10 g tissue for PVC, PP, PBS, and PET, respectively. Higher microplastic exposure was consistently associated with reduced BW, BL, and HC. Total MPs were linked to a 107.7 g decrease in BW (95 % CI: –138.87, –76.49; p < 0.001). Sex-stratified analyses showed stronger effects in male infants, particularly for BW (p-interaction = 0.04). Mixture analyses indicated cumulative negative effects across polymers. The g-comp approach estimated a BW reduction of –117.7 g (95 % CI: –155.3, –80.1) and a BL decrease of –0.89 cm (95 % CI: –1.20, –0.58). The gWQS model produced comparable estimates for BW (–100.9 g, 95 % CI: –146.2, –55.5) and BL (–0.96 cm, 95 % CI: –1.34, –0.58), while BKMR confirmed monotonic negative associations for BW, BL, and HC, with PBS and PP contributing most to the mixture effect. Placental microplastic exposure is associated with impaired fetal growth, with boys appearing more vulnerable. Future studies should investigate biological mechanisms and long-term outcomes.
尽管人们越来越关注人体组织中的微塑料污染，但胎盘微塑料暴露与胎儿人体测量结果之间的关系仍未得到探讨。本研究在中国进行了一项大型前瞻性队列研究，探讨了胎盘微塑料含量与出生体重（BW）、出生长度（BL）和头围（HC）之间的关系。我们在2022-2024年间招募了1750对母婴。采用严格的污染预防方案，在分娩后立即从母胎两侧收集胎盘组织。采用激光直接红外（LD-IR）化学成像技术对微塑料进行了鉴定和定量。使用多变量线性回归、性别分层分析和混合模型（包括g计算（g-comp）、广义加权分位数和回归（gWQS）和贝叶斯核机回归（BKMR））评估聚合物特异性微塑料（PVC、PP、PBS、PET）与胎儿生长之间的关系。PVC、PP、PBS和PET的中位胎盘微塑料浓度分别为7.0、5.0、4.0和3.0颗粒/10 g组织。较高的微塑料暴露始终与体重、BL和HC降低相关。总MPs与体重下降107.7 g相关(95 % CI: -138.87, -76.49; p
{"title":"Impact of placental microplastics on birth anthropometrics: A cross-sectional study","authors":"Ying Shen , Yifan Ning , Fangyuan Chen , Xiaoyan Wang , Dongming Zheng , Yanli Sun , Xiaowen Zhang , Xue Zhang","doi":"10.1016/j.ecoenv.2025.119572","DOIUrl":"10.1016/j.ecoenv.2025.119572","url":null,"abstract":"<div><div>Despite growing concern about microplastic contamination in human tissues, the relationship between placental microplastic exposure and fetal anthropometric outcomes remains unexplored. This study investigated associations between placental microplastic content and birth weight (BW), birth length (BL), and head circumference (HC), in a large prospective cohort in China. We recruited 1750 mother–infant pairs between 2022–2024. Placental tissues were collected immediately after delivery from maternal and fetal sides using strict contamination-prevention protocols. Microplastics were identified and quantified via laser direct infrared (LD-IR) chemical imaging. Associations between polymer-specific microplastics (PVC, PP, PBS, PET) and fetal growth were assessed using multivariable linear regression, sex-stratified analyses, and mixture models, including g-computation (g-comp), generalized weighted quantile sum regression (gWQS), and Bayesian kernel machine regression (BKMR). Median placental microplastic concentrations were 7.0, 5.0, 4.0, and 3.0 particles/10 g tissue for PVC, PP, PBS, and PET, respectively. Higher microplastic exposure was consistently associated with reduced BW, BL, and HC. Total MPs were linked to a 107.7 g decrease in BW (95 % CI: –138.87, –76.49; p < 0.001). Sex-stratified analyses showed stronger effects in male infants, particularly for BW (p-interaction = 0.04). Mixture analyses indicated cumulative negative effects across polymers. The g-comp approach estimated a BW reduction of –117.7 g (95 % CI: –155.3, –80.1) and a BL decrease of –0.89 cm (95 % CI: –1.20, –0.58). The gWQS model produced comparable estimates for BW (–100.9 g, 95 % CI: –146.2, –55.5) and BL (–0.96 cm, 95 % CI: –1.34, –0.58), while BKMR confirmed monotonic negative associations for BW, BL, and HC, with PBS and PP contributing most to the mixture effect. Placental microplastic exposure is associated with impaired fetal growth, with boys appearing more vulnerable. Future studies should investigate biological mechanisms and long-term outcomes.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"309 ","pages":"Article 119572"},"PeriodicalIF":6.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145916422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号