Pub Date : 2026-03-01Epub Date: 2026-02-27DOI: 10.1016/j.ecoenv.2026.119947
Xing Huang , Xuefeng Wu
Constructing scientific and effective prediction methods for the vulnerability of urban ecological environment is of great significance for effectively managing and controlling the risks of urban ecological environment vulnerability. Existing prediction methods often overlook the self-similar characteristics of the evolution trends in complex nonlinear systems, resulting in low accuracy of the prediction results. A prediction method for urban ecological environment vulnerability based on the Fractal Interpolation (FII) - Long Short-Term Memory (LSTM) model was proposed. Using the FII model, constructed an affine transformation matrix as the Iterated Function System (IFS). By estimating the scaling factor of the FII model and using equidistant sampling measures, interpolation points were generated within the interpolation interval according to certain rules. These generated interpolation points were incorporated into the FII model to calculate the corresponding interpolation results, describe the fractal interpolation curve, and reveal the distribution state of the data. Constructed the LSTM neural network structure, selecting MSE and Adam as the loss function and optimizer, respectively. Used the holdout method to train the LSTM model, establishing a method for predicting urban ecological environment vulnerability. Based on multidimensional data from 35 cities in China, the model's prediction accuracy and stability were validated. The comparison results indicated that the constructed FII-LSTM model had high prediction accuracy and stability, making it suitable for decision-making management in urban ecological environment vulnerability prediction. The FII-LSTM model was used to predict the ecological vulnerability of the sample cities in 2021–2025 and to make policy recommendations.
{"title":"Research on urban ecological environment vulnerability prediction method based on FII-LSTM","authors":"Xing Huang , Xuefeng Wu","doi":"10.1016/j.ecoenv.2026.119947","DOIUrl":"10.1016/j.ecoenv.2026.119947","url":null,"abstract":"<div><div>Constructing scientific and effective prediction methods for the vulnerability of urban ecological environment is of great significance for effectively managing and controlling the risks of urban ecological environment vulnerability. Existing prediction methods often overlook the self-similar characteristics of the evolution trends in complex nonlinear systems, resulting in low accuracy of the prediction results. A prediction method for urban ecological environment vulnerability based on the Fractal Interpolation (FII) - Long Short-Term Memory (LSTM) model was proposed. Using the FII model, constructed an affine transformation matrix as the Iterated Function System (IFS). By estimating the scaling factor of the FII model and using equidistant sampling measures, interpolation points were generated within the interpolation interval according to certain rules. These generated interpolation points were incorporated into the FII model to calculate the corresponding interpolation results, describe the fractal interpolation curve, and reveal the distribution state of the data. Constructed the LSTM neural network structure, selecting MSE and Adam as the loss function and optimizer, respectively. Used the holdout method to train the LSTM model, establishing a method for predicting urban ecological environment vulnerability. Based on multidimensional data from 35 cities in China, the model's prediction accuracy and stability were validated. The comparison results indicated that the constructed FII-LSTM model had high prediction accuracy and stability, making it suitable for decision-making management in urban ecological environment vulnerability prediction. The FII-LSTM model was used to predict the ecological vulnerability of the sample cities in 2021–2025 and to make policy recommendations.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119947"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147315863","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 : 2026-03-01Epub Date: 2026-02-20DOI: 10.1016/j.ecoenv.2026.119908
Weixia Li , Shuhao Shi , Yuanyuan Yu , Bin Chen , Lei Zhao , Zi Lin , Jiayan Ni , Xiaoqing Li , Shanjun Song , Penghui Li , Shike Hou , Liqiong Guo
Exposure to environmental pollutants has been found to be associated with epigenetic modifications of platelet mitochondria, which may influence the risk of type 2 diabetes mellitus (T2DM). However, research on the relationship between exposure to environmental endocrine disrupting chemicals (EDCs) and T2DM remains very limited at the molecular level of mitochondrial epigenetic alterations. This study aims to investigate the impact of mixed exposure to bisphenols (BPs), phthalates (PAEs), and parabens (PBs) on T2DM and platelet mitochondrial DNA (mtDNA) methylation, using a nested case-control study design. Levels of BPs, PAEs, and PBs metabolites were quantified using high-performance liquid chromatography-mass spectrometry (HPLC-MS). We used weighted quantile sum (WQS) and bayesian kernel machine regression (BKMR) models to assess the association between individual and mixed exposure to multiple EDCs and T2DM. Methylation levels of mitochondrial coding genes were measured by bisulfite pyrosequencing. In logistic regression models, MT-COX1 methylation levels were significantly negatively associated with T2DM risk, whereas MT-COX3 methylation levels were significantly positively associated. Both WQS and BKMR models indicated that mixed exposure to BPs, PAEs, and PBs was positively linked to T2DM, with DnPrP and DEHP identified as the primary contributors. Mediation analysis demonstrated that MT-COX3 methylation significantly mediated the associations of DEP, DMP, DEHP, DnPrP, DAlP, and MP with T2DM. Our findings indicate that both individual and mixed exposure to PAEs and PBs are positively associated with T2DM risk. Platelet mtDNA methylation mediates the association between EDCs exposure and T2DM risk, suggesting its potential utility as a biomarker.
{"title":"Platelet mitochondrial DNA methylation mediates the association of bisphenol, phthalate, and paraben exposures with type 2 diabetes mellitus: An exploratory nested case-control study","authors":"Weixia Li , Shuhao Shi , Yuanyuan Yu , Bin Chen , Lei Zhao , Zi Lin , Jiayan Ni , Xiaoqing Li , Shanjun Song , Penghui Li , Shike Hou , Liqiong Guo","doi":"10.1016/j.ecoenv.2026.119908","DOIUrl":"10.1016/j.ecoenv.2026.119908","url":null,"abstract":"<div><div>Exposure to environmental pollutants has been found to be associated with epigenetic modifications of platelet mitochondria, which may influence the risk of type 2 diabetes mellitus (T2DM). However, research on the relationship between exposure to environmental endocrine disrupting chemicals (EDCs) and T2DM remains very limited at the molecular level of mitochondrial epigenetic alterations. This study aims to investigate the impact of mixed exposure to bisphenols (BPs), phthalates (PAEs), and parabens (PBs) on T2DM and platelet mitochondrial DNA (mtDNA) methylation, using a nested case-control study design. Levels of BPs, PAEs, and PBs metabolites were quantified using high-performance liquid chromatography-mass spectrometry (HPLC-MS). We used weighted quantile sum (WQS) and bayesian kernel machine regression (BKMR) models to assess the association between individual and mixed exposure to multiple EDCs and T2DM. Methylation levels of mitochondrial coding genes were measured by bisulfite pyrosequencing. In logistic regression models, <em>MT-COX1</em> methylation levels were significantly negatively associated with T2DM risk, whereas <em>MT-COX3</em> methylation levels were significantly positively associated. Both WQS and BKMR models indicated that mixed exposure to BPs, PAEs, and PBs was positively linked to T2DM, with DnPrP and DEHP identified as the primary contributors. Mediation analysis demonstrated that <em>MT-COX3</em> methylation significantly mediated the associations of DEP, DMP, DEHP, DnPrP, DAlP, and MP with T2DM. Our findings indicate that both individual and mixed exposure to PAEs and PBs are positively associated with T2DM risk. Platelet mtDNA methylation mediates the association between EDCs exposure and T2DM risk, suggesting its potential utility as a biomarker.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119908"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146775812","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}
Substitute for perfluorooctanoic acid (PFOA), like hexafluoropropylene oxide trimer acid (HFPO-TA), are sparking growing environmental and health worries because of their persistence and capacity for bioaccumulation. Here, we employed an integrated multi-omics approach to systematically investigate HFPO-TA-induced hepatic lipid metabolic dysregulation in zebrafish. Exposed to a series of concentrations (0, 5, 50, 500 μg/L) of HFPO-TA induced hepatic lipid accumulation and significantly elevated serum levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C). Integrated transcriptomic and epigenome analyses revealed that HFPO-TA reprogrammed the hepatic epigenome by selectively activating lipid synthesis-associated enhancers while suppressing lipid oxidation pathways, predisposing to metabolic dysfunction-associated steatotic liver disease (MASLD). Moreover, HFPO-TA preferentially remodeled chromatin accessibility and distal enhancers, driving lipogenic gene activation through nuclear receptors, such as peroxisome proliferator-activated receptor alpha (PPARα) and farnesoid X receptor (FXR). Finally, functions of PPARα and FXR in HFPO‑TA‑induced lipid imbalance were validated by pharmacological modulators. Overall, our study delivers comprehensive evidence connecting PFOA alternatives to epigenetically driven hepatic steatosis, providing mechanistic understanding to support environmental risk evaluations of emerging perfluoroalkyl and polyfluoroalkyl substances (PFAS) compounds.
{"title":"Hexafluoropropylene oxide trimer acid (HFPO-TA) exposure predisposes to MASLD through reprogramming hepatic epigenome and transcriptome","authors":"Jiao Yu , Mengan Guo , Qiaoli Zhou , Lina Xue , Wenhua Wang , Xiao Wu , Yufeng Qin , Wei Gu , Guizhen Du","doi":"10.1016/j.ecoenv.2026.119940","DOIUrl":"10.1016/j.ecoenv.2026.119940","url":null,"abstract":"<div><div>Substitute for perfluorooctanoic acid (PFOA), like hexafluoropropylene oxide trimer acid (HFPO-TA), are sparking growing environmental and health worries because of their persistence and capacity for bioaccumulation. Here, we employed an integrated multi-omics approach to systematically investigate HFPO-TA-induced hepatic lipid metabolic dysregulation in zebrafish. Exposed to a series of concentrations (0, 5, 50, 500 μg/L) of HFPO-TA induced hepatic lipid accumulation and significantly elevated serum levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C). Integrated transcriptomic and epigenome analyses revealed that HFPO-TA reprogrammed the hepatic epigenome by selectively activating lipid synthesis-associated enhancers while suppressing lipid oxidation pathways, predisposing to metabolic dysfunction-associated steatotic liver disease (MASLD). Moreover, HFPO-TA preferentially remodeled chromatin accessibility and distal enhancers, driving lipogenic gene activation through nuclear receptors, such as peroxisome proliferator-activated receptor alpha (PPARα) and farnesoid X receptor (FXR). Finally, functions of PPARα and FXR in HFPO‑TA‑induced lipid imbalance were validated by pharmacological modulators. Overall, our study delivers comprehensive evidence connecting PFOA alternatives to epigenetically driven hepatic steatosis, providing mechanistic understanding to support environmental risk evaluations of emerging perfluoroalkyl and polyfluoroalkyl substances (PFAS) compounds.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119940"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147300571","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 : 2026-03-01Epub Date: 2026-02-24DOI: 10.1016/j.ecoenv.2026.119946
Mengjie Zhou , Xiaofei Huang , Luhao Wang , Yinling Zhou , Zhichao Chen , Lusheng Wang
Diabetic retinopathy (DR), a leading cause of vision loss in diabetes, arises from intricate metabolic and environmental interactions. This study investigates how polychlorinated biphenyls (PCBs) contribute to DR pathogenesis. Network toxicology was employed to identify overlapping gene targets between PCBs and DR. Machine learning analyses subsequently refined these targets to four core genes: TP53, ESR1, EGR1, and HSPA5. Diagnostic modeling validated using human retinal transcriptomes demonstrated TP53’s robust diagnostic accuracy, yielding area under the curve (AUC) values of 0.740 for non-proliferative DR (NPDR) and 0.920 for proliferative DR (PDR), with expression levels positively correlated with DR severity and ETDRS scores. Molecular docking confirmed strong binding affinities of toxic PCB congeners to TP53 and ESR1. Single-cell RNA sequencing in a DR mouse model revealed enriched Trp53 expression in microglia, alongside microglial depletion and a pro-inflammatory shift. In vitro PCB138 exposure upregulated TP53 in high-glucose-cultured human microglial cells, promoting M1 polarization and cytokine secretion, effects that were attenuated upon pharmacological inhibition of p53 protein activity. These findings suggest that PCBs exacerbate DR through a TP53-driven pathway that promotes pro-inflammatory microglial activation, disrupting retinal homeostasis. TP53 emerges as a key biomarker and therapeutic target, highlighting the importance of reducing PCB exposure to mitigate DR progression.
{"title":"Integrative network toxicology and single-cell transcriptomics reveal TP53 as a key mediator of PCBs-induced microglial dysfunction in diabetic retinopathy","authors":"Mengjie Zhou , Xiaofei Huang , Luhao Wang , Yinling Zhou , Zhichao Chen , Lusheng Wang","doi":"10.1016/j.ecoenv.2026.119946","DOIUrl":"10.1016/j.ecoenv.2026.119946","url":null,"abstract":"<div><div>Diabetic retinopathy (DR), a leading cause of vision loss in diabetes, arises from intricate metabolic and environmental interactions. This study investigates how polychlorinated biphenyls (PCBs) contribute to DR pathogenesis. Network toxicology was employed to identify overlapping gene targets between PCBs and DR. Machine learning analyses subsequently refined these targets to four core genes: TP53, ESR1, EGR1, and HSPA5. Diagnostic modeling validated using human retinal transcriptomes demonstrated <em>TP53</em>’s robust diagnostic accuracy, yielding area under the curve (AUC) values of 0.740 for non-proliferative DR (NPDR) and 0.920 for proliferative DR (PDR), with expression levels positively correlated with DR severity and ETDRS scores. Molecular docking confirmed strong binding affinities of toxic PCB congeners to TP53 and ESR1. Single-cell RNA sequencing in a DR mouse model revealed enriched <em>Trp53</em> expression in microglia, alongside microglial depletion and a pro-inflammatory shift. <em>In vitro</em> PCB138 exposure upregulated TP53 in high-glucose-cultured human microglial cells, promoting M1 polarization and cytokine secretion, effects that were attenuated upon pharmacological inhibition of p53 protein activity. These findings suggest that PCBs exacerbate DR through a TP53-driven pathway that promotes pro-inflammatory microglial activation, disrupting retinal homeostasis. TP53 emerges as a key biomarker and therapeutic target, highlighting the importance of reducing PCB exposure to mitigate DR progression.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119946"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147300538","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 : 2026-03-01Epub Date: 2026-02-23DOI: 10.1016/j.ecoenv.2026.119927
Ziyuan Xu , Jing Fang , Chenhui Yang , Aizhen Wang , Shunqing Xu , Zongwei Cai , Yuanyuan Li , Hongxiu Liu , Qinfen Li , Beibei Liu , Zhongqiang Cao , Wei Xia
Organochlorine pesticides (OCPs), banned decades ago due to their environmental persistence and toxicity, countinue to be detected as residual DDTs and HCHs in human populations. Previous studies suggest that prenatal exposure to OCPs may impair neurodevelopment in offspring, but the evidence remains inconsistent, especially regarding specific isomers, such as α-HCH and γ-HCH, which have rarely assessed in humans. This study investigated the association between prenatal OCP exposure and early childhood neurodevelopment, and explored the potential sex-specific effects. We measured HCH isomers (α-HCH, β-HCH, γ-HCH), DDT isomers (p,p′-DDT, o,p′-DDT), and DDT metabolites (o,p′-DDD, o,p′-DDE, p,p′-DDD, p,p′-DDE) in cord serum from 447 mother-child pairs in a birth cohort study in Wuhan, China (2014–2015). Neurodevelopment was assessed at age 2 with the Bayley Scales of Infant Development, which generated mental development index (MDI) and psychomotor development index (PDI) scores. Associations were evaluated using linear regression and weighted quantile sum (WQS) regression, with analyses stratified by sex. Most OCPs were detectable in over 50 % of samples, with median concentrations of 39.5 ng/g lipid for ∑DDTs and 10.8 ng/g lipid for ∑HCHs. Higher cord serum OCP concentrations were associated with lower MDI scores. An interquartile range (IQR) increase in γ-HCH was linked to a 2.45-point decrease in MDI (95 % CI: −4.76, −0.14) in all children, although this association did not remain significant after FDR correction. In girls, inverse associations were observed for α-HCH (−4.54 points; 95 % CI: −7.55, −1.53), γ-HCH (−5.20 points; 95 % CI: −8.04, −2.36), and p,p′-DDD (−5.25 points; 95 % CI: −9.97, −0.53). In mixture analyses, each quartile increase in OCP mixture was associated with a 6.10-point decrease in MDI and a 6.46-point decrease in PDI in girls, with γ-HCH (51.2 %) and p,p′-DDT (35.6 %) identified as the largest contributors. The results indicate that prenatal exposure to certain OCPs, particularly γ-HCH and p,p′-DDT, is associated with poorer neurodevelopment in early childhood, especially in girls. The findings highlight the need to address persistent OCP exposure and its developmental impacts.
{"title":"Prenatal exposure to organochlorine pesticides and early childhood neurodevelopment: A prospective birth cohort study","authors":"Ziyuan Xu , Jing Fang , Chenhui Yang , Aizhen Wang , Shunqing Xu , Zongwei Cai , Yuanyuan Li , Hongxiu Liu , Qinfen Li , Beibei Liu , Zhongqiang Cao , Wei Xia","doi":"10.1016/j.ecoenv.2026.119927","DOIUrl":"10.1016/j.ecoenv.2026.119927","url":null,"abstract":"<div><div>Organochlorine pesticides (OCPs), banned decades ago due to their environmental persistence and toxicity, countinue to be detected as residual DDTs and HCHs in human populations. Previous studies suggest that prenatal exposure to OCPs may impair neurodevelopment in offspring, but the evidence remains inconsistent, especially regarding specific isomers, such as α-HCH and γ-HCH, which have rarely assessed in humans. This study investigated the association between prenatal OCP exposure and early childhood neurodevelopment, and explored the potential sex-specific effects. We measured HCH isomers (α-HCH, β-HCH, γ-HCH), DDT isomers (p,p′-DDT, o,p′-DDT), and DDT metabolites (o,p′-DDD, o,p′-DDE, p,p′-DDD, p,p′-DDE) in cord serum from 447 mother-child pairs in a birth cohort study in Wuhan, China (2014–2015). Neurodevelopment was assessed at age 2 with the Bayley Scales of Infant Development, which generated mental development index (MDI) and psychomotor development index (PDI) scores. Associations were evaluated using linear regression and weighted quantile sum (WQS) regression, with analyses stratified by sex. Most OCPs were detectable in over 50 % of samples, with median concentrations of 39.5 ng/g lipid for ∑DDTs and 10.8 ng/g lipid for ∑HCHs. Higher cord serum OCP concentrations were associated with lower MDI scores. An interquartile range (IQR) increase in γ-HCH was linked to a 2.45-point decrease in MDI (95 % CI: −4.76, −0.14) in all children, although this association did not remain significant after FDR correction. In girls, inverse associations were observed for α-HCH (−4.54 points; 95 % CI: −7.55, −1.53), γ-HCH (−5.20 points; 95 % CI: −8.04, −2.36), and p,p′-DDD (−5.25 points; 95 % CI: −9.97, −0.53). In mixture analyses, each quartile increase in OCP mixture was associated with a 6.10-point decrease in MDI and a 6.46-point decrease in PDI in girls, with γ-HCH (51.2 %) and p,p′-DDT (35.6 %) identified as the largest contributors. The results indicate that prenatal exposure to certain OCPs, particularly γ-HCH and p,p′-DDT, is associated with poorer neurodevelopment in early childhood, especially in girls. The findings highlight the need to address persistent OCP exposure and its developmental impacts.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119927"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147281406","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 : 2026-03-01Epub Date: 2026-02-23DOI: 10.1016/j.ecoenv.2026.119924
Ran Ding , TingQiu Quan , Jiangxue Wu , Rong Huang , LuDan Liang , Qi Quan , ZhiQing Long
We investigated the carcinogenic effects of four endocrine-disrupting chemicals—bisphenol A (BPA), diethyl phthalate (DEP), dimethyl phthalate (DMP), and dioctyl phthalate (DOP)—in nasopharyngeal carcinoma (NPC) and thyroid carcinoma (THCA) using an integrated toxicogenomic–machine learning–docking–experimental pipeline. Intersection analysis identified 31 NPC-related overlapping genes and 39 THCA-related overlapping genes, with 19 shared core targets across both malignancies. These shared targets were enriched in oncogenic signaling pathways including Mitogen-activated protein kinase （MAPK）, Phosphoinositide 3-Kinase-Protein Kinase B (PI3K–AKT), and Janus kinase/signal transducers and activators of transcription (JAK/STAT). A multi-algorithm machine learning framework constructed 113 predictive models and prioritized six diagnostic genes (CCNA2, CDK2, MET, F2, TYMS, PPARG). High expression of CCNA2 (HR=1.43, p = 0.016), CDK2 (HR=1.66, p = 0.002), MET (HR=1.58, p = 0.002), and PPARG (HR=1.45, p = 0.0072) was associated with worse overall survival, whereas TYMS and F2 were not significant. Molecular docking showed stable ligand–protein binding with energies from –5.2 to –8.1 kcal·mol⁻¹ , with the strongest affinities observed for BPA–CDK2 (–8.1) and BPA–PPARG (–8.1); DEP also showed strong binding to CDK2 (–7.0). In vitro, BPA and DEP (but not DMP/DOP) increased colony formation (p < 0.01), accelerated wound closure, upregulated oncogenic genes (e.g., CDK2/MET/CCNA2; p < 0.05), and elevated p-MEK without changing total MEK in 5–8 F and TPC-1 cells. Collectively, BPA and DEP promote head and neck tumor progression through MEK pathway activation and cell-cycle dysregulation.
我们使用综合毒物基因组学-机器学习-对接实验管道研究了四种内分泌干扰化学物质-双酚A (BPA)，邻苯二甲酸二乙酯（DEP），邻苯二甲酸二甲酯（DMP）和邻苯二甲酸二辛酯（DOP）在鼻咽癌（NPC）和甲状腺癌（THCA）中的致癌作用。交叉分析确定了31个npc相关的重叠基因和39个thca相关的重叠基因，在这两种恶性肿瘤中有19个共享的核心靶点。这些共同靶点在致癌信号通路中富集，包括丝裂原活化蛋白激酶（MAPK）、磷酸肌苷3-激酶-蛋白激酶B （PI3K-AKT）和Janus激酶/信号转导和转录激活因子（JAK/STAT）。多算法机器学习框架构建了113个预测模型，并优先排序了6个诊断基因（CCNA2、CDK2、MET、F2、TYMS、PPARG）。高表达的CCNA2 （HR=1.43, p = 0.016）、CDK2 （HR=1.66, p = 0.002）、MET （HR=1.58, p = 0.002）和PPARG （HR=1.45, p = 0.0072）与较差的总生存率相关，而TYMS和F2不显著。分子对接显示配体-蛋白结合稳定，能量为-5.2 ~ -8.1 kcal·mol⁻¹ ，其中BPA-CDK2（-8.1）和bpa - ppar（-8.1）亲和力最强；DEP还显示出与CDK2的强结合（-7.0）。在体外，BPA和DEP（而不是DMP/DOP）增加了菌落形成(p
{"title":"Integrative computational and experimental analysis identifies MEK-mediated carcinogenic effects of bisphenol A and diethyl phthalate in head and neck cancer","authors":"Ran Ding , TingQiu Quan , Jiangxue Wu , Rong Huang , LuDan Liang , Qi Quan , ZhiQing Long","doi":"10.1016/j.ecoenv.2026.119924","DOIUrl":"10.1016/j.ecoenv.2026.119924","url":null,"abstract":"<div><div>We investigated the carcinogenic effects of four endocrine-disrupting chemicals—bisphenol A (BPA), diethyl phthalate (DEP), dimethyl phthalate (DMP), and dioctyl phthalate (DOP)—in nasopharyngeal carcinoma (NPC) and thyroid carcinoma (THCA) using an integrated toxicogenomic–machine learning–docking–experimental pipeline. Intersection analysis identified 31 NPC-related overlapping genes and 39 THCA-related overlapping genes, with 19 shared core targets across both malignancies. These shared targets were enriched in oncogenic signaling pathways including Mitogen-activated protein kinase （MAPK）, Phosphoinositide 3-Kinase-Protein Kinase B (PI3K–AKT), and Janus kinase/signal transducers and activators of transcription (JAK/STAT). A multi-algorithm machine learning framework constructed 113 predictive models and prioritized six diagnostic genes (CCNA2, CDK2, MET, F2, TYMS, PPARG). High expression of CCNA2 (HR=1.43, p = 0.016), CDK2 (HR=1.66, p = 0.002), MET (HR=1.58, p = 0.002), and PPARG (HR=1.45, p = 0.0072) was associated with worse overall survival, whereas TYMS and F2 were not significant. Molecular docking showed stable ligand–protein binding with energies from –5.2 to –8.1 kcal·mol⁻¹ , with the strongest affinities observed for BPA–CDK2 (–8.1) and BPA–PPARG (–8.1); DEP also showed strong binding to CDK2 (–7.0). In vitro, BPA and DEP (but not DMP/DOP) increased colony formation (p < 0.01), accelerated wound closure, upregulated oncogenic genes (e.g., CDK2/MET/CCNA2; p < 0.05), and elevated p-MEK without changing total MEK in 5–8 F and TPC-1 cells. Collectively, BPA and DEP promote head and neck tumor progression through MEK pathway activation and cell-cycle dysregulation.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119924"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147281381","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 : 2026-03-01Epub Date: 2026-02-26DOI: 10.1016/j.ecoenv.2026.119959
Yuan Meng , Andreas Schiwy , Yanling Qiu , Feifei Xue , Jiuyong Yang , Xiaojuan Xu , Zhiliang Zhu , Daqiang Yin , Stephan Küppers , Henner Hollert
Organophosphate esters (OPEs) can be biodegraded through phase Ⅰ process in liver by cytochrome P450 enzymes and cause adverse effects to target organs. This study examined the transformation of three OPEs using electrochemistry (EC) and rat liver S9 system to compare the distinctions between the two systems concerning their transformation products (TPs) formed. The toxic effects of OPEs and the primary TPs include endocrine disruption, genotoxicity and dioxin-like potential were further investigated across a range of exposure concentrations that do not induce significant cytotoxicity. OPEs were transformed in both EC and S9 with the degradation degree followed as tris(4-isopropylphenyl) phosphate (T4IPPP)> tris(2-butoxyethyl) phosphate (TBOEP)> tris(1,3-dichloro-2-propyl) phosphate (TDCIPP). Compared with S9 system, the transformation of OPEs in EC method was relatively slower. Bis(butoxyethyl) phosphate (BBOEP), hydroxyethyl phosphate triester (BBOEHEP) and bis(2-butoxyethyl) 2-(3-hydroxybutoxy) ethyl phosphate triester (3-OH-TBOEP) were the most abundant TPs of TBOEP, while bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) was the only TPs of TDCIPP detected in EC and S9 system. Concerning the toxic effects, OPEs declined the cell viability significantly in H4ⅡE, A549 and U2OS cells in time- and concentration- specific relationship. However, no significant cytotoxic effect occurred after exposure to the TPs up to 1000 μM. TDCIPP showed significant antagonistic activities against ERα and AR with IC10 value of 42.4 and 0.301 μM, respectively. BBOEHEP and BDCIPP also exhibited ERα agonistic activity and antagonistic AR activity, which was lower than that of their respective parent compounds. Furthermore, OPEs and their TPs caused significant micronucleus formation in the absence or presence of S9 fraction compared to the solvent control. Taken together, TDCIPP pose considerable risks to humans and the environment considering the limited transform capability and strong toxic effects.
{"title":"In vitro transformation assessment of organophosphate esters (OPEs) via electrochemistry and rat liver S9 and their toxicological evaluation","authors":"Yuan Meng , Andreas Schiwy , Yanling Qiu , Feifei Xue , Jiuyong Yang , Xiaojuan Xu , Zhiliang Zhu , Daqiang Yin , Stephan Küppers , Henner Hollert","doi":"10.1016/j.ecoenv.2026.119959","DOIUrl":"10.1016/j.ecoenv.2026.119959","url":null,"abstract":"<div><div>Organophosphate esters (OPEs) can be biodegraded through phase Ⅰ process in liver by cytochrome P450 enzymes and cause adverse effects to target organs. This study examined the transformation of three OPEs using electrochemistry (EC) and rat liver S9 system to compare the distinctions between the two systems concerning their transformation products (TPs) formed. The toxic effects of OPEs and the primary TPs include endocrine disruption, genotoxicity and dioxin-like potential were further investigated across a range of exposure concentrations that do not induce significant cytotoxicity. OPEs were transformed in both EC and S9 with the degradation degree followed as tris(4-isopropylphenyl) phosphate (T4IPPP)> tris(2-butoxyethyl) phosphate (TBOEP)> tris(1,3-dichloro-2-propyl) phosphate (TDCIPP). Compared with S9 system, the transformation of OPEs in EC method was relatively slower. Bis(butoxyethyl) phosphate (BBOEP), hydroxyethyl phosphate triester (BBOEHEP) and bis(2-butoxyethyl) 2-(3-hydroxybutoxy) ethyl phosphate triester (3-OH-TBOEP) were the most abundant TPs of TBOEP, while bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) was the only TPs of TDCIPP detected in EC and S9 system. Concerning the toxic effects, OPEs declined the cell viability significantly in H4ⅡE, A549 and U2OS cells in time- and concentration- specific relationship. However, no significant cytotoxic effect occurred after exposure to the TPs up to 1000 μM. TDCIPP showed significant antagonistic activities against ERα and AR with IC10 value of 42.4 and 0.301 μM, respectively. BBOEHEP and BDCIPP also exhibited ERα agonistic activity and antagonistic AR activity, which was lower than that of their respective parent compounds. Furthermore, OPEs and their TPs caused significant micronucleus formation in the absence or presence of S9 fraction compared to the solvent control. Taken together, TDCIPP pose considerable risks to humans and the environment considering the limited transform capability and strong toxic effects.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119959"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147315882","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 : 2026-03-01Epub Date: 2026-02-25DOI: 10.1016/j.ecoenv.2026.119951
Ran Yan , Siyuan Liu , Jie Liu , Lingyan Zhen , Yiqin Gu , Shengjie Ying , Haidong Kan
Background
Low temperatures and cold spells have recently been associated with various diseases. However, the effects of these conditions on arrhythmia onset remain insufficiently explored.
Objective
We investigated the association between low temperatures, cold spells, and the risk of arrhythmia.
Methods
A time-stratified case-crossover design was employed using outpatient records from 25,957 arrhythmia cases in Minhang District, Shanghai, China, between January 2017 and December 2019. Cold spells were defined using multiple temperature thresholds (P10, P7.5, P5, P2.5) and durations (≥2, ≥3, and ≥4 consecutive days). Conditional logistic regression models incorporating distributed lag non-linear model (DLNM) estimated the association between low temperatures, cold spells, and arrhythmia onset, considering lag periods up to 14 days.
Results
The cumulative relative risk over lags of 0–14 days for low ambient temperatures was 1.837 (95 % CI: 1.357–2.486), whereas for cold spells, it was 1.198 (95 % CI: 1.020–1.407). Stratified analyses revealed that cold spells were associated with a higher risk of other cardiac arrhythmias compared to atrial fibrillation and flutter, while low temperatures raised the risk of atrial fibrillation and flutter more than other cardiac arrhythmias. Both males and younger patients were more susceptible to cold spells and low temperatures, although the difference was not statistically significant.
Conclusions
This study offers robust evidence that low temperatures and cold spells increase the risk of arrhythmia onset.
{"title":"Low temperature and cold spells on arrhythmia onset: An individual-level case-crossover study in Minhang District, Shanghai, China","authors":"Ran Yan , Siyuan Liu , Jie Liu , Lingyan Zhen , Yiqin Gu , Shengjie Ying , Haidong Kan","doi":"10.1016/j.ecoenv.2026.119951","DOIUrl":"10.1016/j.ecoenv.2026.119951","url":null,"abstract":"<div><h3>Background</h3><div>Low temperatures and cold spells have recently been associated with various diseases. However, the effects of these conditions on arrhythmia onset remain insufficiently explored.</div></div><div><h3>Objective</h3><div>We investigated the association between low temperatures, cold spells, and the risk of arrhythmia.</div></div><div><h3>Methods</h3><div>A time-stratified case-crossover design was employed using outpatient records from 25,957 arrhythmia cases in Minhang District, Shanghai, China, between January 2017 and December 2019. Cold spells were defined using multiple temperature thresholds (P10, P7.5, P5, P2.5) and durations (≥2, ≥3, and ≥4 consecutive days). Conditional logistic regression models incorporating distributed lag non-linear model (DLNM) estimated the association between low temperatures, cold spells, and arrhythmia onset, considering lag periods up to 14 days.</div></div><div><h3>Results</h3><div>The cumulative relative risk over lags of 0–14 days for low ambient temperatures was 1.837 (95 % CI: 1.357–2.486), whereas for cold spells, it was 1.198 (95 % CI: 1.020–1.407). Stratified analyses revealed that cold spells were associated with a higher risk of other cardiac arrhythmias compared to atrial fibrillation and flutter, while low temperatures raised the risk of atrial fibrillation and flutter more than other cardiac arrhythmias. Both males and younger patients were more susceptible to cold spells and low temperatures, although the difference was not statistically significant.</div></div><div><h3>Conclusions</h3><div>This study offers robust evidence that low temperatures and cold spells increase the risk of arrhythmia onset.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119951"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147300500","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 : 2026-03-01Epub Date: 2026-02-27DOI: 10.1016/j.ecoenv.2026.119926
Ji Hye Oh , Won-Kyung Yang , Chae-Eun Shin , Ji-Hyun Yun , Gyu Min Lee , Chang Won Ahn , Seock-Yeon Hwang , Seung-Hyung Kim
Background
Given the global burden of air pollutants, as represented by particulate matter (PM) and diesel exhaust particles (DEP) exposure, and a lack of preventive strategies, identifying safe and accessible interventions is of high public health relevance. This study investigated the protective effect of four KABP strains and their combination on airway inflammation in a PM plus DEP (PM10D)-induced respiratory inflammatory process model.
Methods
To induce airway inflammation, BALB/c mice were intranasally exposed to PM10D and then orally administered for 12 days with L. plantarum KABP-033(A), −022(B), −023(C) and Pediococcus acidilactici KABP-021(D) strains alone or in various combinations. Immune cell composition, proinflammatory cytokine expression, and histopathology were evaluated in bronchoalveolar lavage fluid (BALF) and lungs. IgA and short-chain fatty acid (SCFA) levels were determined in small intestine lavage fluid. Expectorant activity was determined using phenol-red secretion.
Results
Both individual strains and various combinations protected against PM10D-induced lung damage, with KABP–AB-cx 13, a combination of strain A and B at a 1:3 ratio, exhibiting the most potent protective effect. KABP–AB-cx 13 inhibited the infiltration of neutrophils, the quantity of various inflammatory cells, such as CD62L−CD44high+, CD21/35+B220+, and Gr-1+CD11b+ cells, and the expression of cytokines and chemokines, including chemokine (C-X-C motif) ligand (CXCL)-1, macrophage inflammatory protein-2, tumor necrosis factor-α, interleukin (IL)-17A, IL-6, and IL-1β, in the BALF and lungs of mice with PM10D-triggered airway inflammation. It also decreased IL-1α and IRAK expression in alveolar macrophages along with inhibition of nuclear factor-κB (NF- κB) and JNK phosphorylation in the lungs of these mice. Furthermore, KABP–AB-cx 13 increased CD206+F4/80+ cell numbers in mesenteric lymph nodes and IgA and SCFA levels in small intestine lavage fluid. It also exhibited better expectorant activity based on increased phenol-red secretion.
Conclusion
KABP–AB-cx 13 suppressed the PM10D-induced airway inflammation and protected lung tissue from damage by inhibiting immune and inflammatory reactions in airways, activating the immune system, and increasing SCFA levels in the gut. KABP–AB-cx 13 also exhibited an expectorant effect, suggesting protective and therapeutic effects against respiratory inflammation. Overall, these findings contribute to global understanding of how probiotic interventions may help prevent or alleviate respiratory disorders induced by air pollution.
背景：鉴于以颗粒物（PM）和柴油废气颗粒（DEP）暴露为代表的全球空气污染物负担，以及缺乏预防战略，确定安全和可获得的干预措施具有高度的公共卫生相关性。本研究在PM + DEP （PM10D）诱导的呼吸道炎症过程模型中，研究了4种KABP菌株及其组合对气道炎症的保护作用。方法：将PM10D分别与植物乳杆菌KABP-033(A)、-022(B)、-023(c)和酸碱性Pediococcus KABP-021(D)单独或联合给药12 D，诱导BALB/c小鼠气道炎症。在支气管肺泡灌洗液（BALF）和肺中评估免疫细胞组成、促炎细胞因子表达和组织病理学。测定小肠灌洗液中IgA和短链脂肪酸（SCFA）水平。用酚红分泌物法测定其祛痰活性。结果：单个菌株和各种组合对pm10d诱导的肺损伤均有保护作用，其中菌株a和菌株B以1:3的比例组合的kabp - ab - cx13的保护作用最强。kabp - ab - cx13可抑制pm10d引发气道炎症小鼠BALF和肺中中性粒细胞的浸润、CD62L-CD44high+、CD21/35+B220+、Gr-1+CD11b+等多种炎症细胞的数量，以及趋化因子（C-X-C基元）配体(CXCL)-1、巨噬细胞炎症蛋白-2、肿瘤坏死因子-α、白细胞介素(IL)-17A、IL-6、IL-1β等细胞因子和趋化因子的表达。降低肺泡巨噬细胞IL-1α和IRAK的表达，抑制肺核因子-κB （NF- κB）和JNK磷酸化。此外，kabp - ab - cx13增加了肠系膜淋巴结CD206+F4/80+细胞数量和小肠灌洗液中IgA和SCFA水平。它还表现出更好的祛痰活性，基于增加酚红分泌。结论：kabp - ab - cx13通过抑制气道免疫和炎症反应，激活免疫系统，增加肠道SCFA水平，抑制pm10d诱导的气道炎症，保护肺组织免受损伤。kaba - ab - cx13还具有祛痰作用，提示其对呼吸道炎症具有保护和治疗作用。总的来说，这些发现有助于全球理解益生菌干预如何帮助预防或减轻空气污染引起的呼吸系统疾病。
{"title":"KABP–AB-cx13 for the alleviation of airway inflammation in a mouse model triggered by particulate matter 10(PM10) and diesel exhaust particles","authors":"Ji Hye Oh , Won-Kyung Yang , Chae-Eun Shin , Ji-Hyun Yun , Gyu Min Lee , Chang Won Ahn , Seock-Yeon Hwang , Seung-Hyung Kim","doi":"10.1016/j.ecoenv.2026.119926","DOIUrl":"10.1016/j.ecoenv.2026.119926","url":null,"abstract":"<div><h3>Background</h3><div>Given the global burden of air pollutants, as represented by particulate matter (PM) and diesel exhaust particles (DEP) exposure, and a lack of preventive strategies, identifying safe and accessible interventions is of high public health relevance. This study investigated the protective effect of four KABP strains and their combination on airway inflammation in a PM plus DEP (PM<sub>10</sub>D)-induced respiratory inflammatory process model.</div></div><div><h3>Methods</h3><div>To induce airway inflammation, BALB/c mice were intranasally exposed to PM<sub>10</sub>D and then orally administered for 12 days with <em>L. plantarum</em> KABP-033(A), −022(B), −023(C) and <em>Pediococcus acidilactici</em> KABP-021(D) strains alone or in various combinations. Immune cell composition, proinflammatory cytokine expression, and histopathology were evaluated in bronchoalveolar lavage fluid (BALF) and lungs. IgA and short-chain fatty acid (SCFA) levels were determined in small intestine lavage fluid. Expectorant activity was determined using phenol-red secretion.</div></div><div><h3>Results</h3><div>Both individual strains and various combinations protected against PM<sub>10</sub><span>D</span>-induced lung damage, with KABP–AB-cx 13, a combination of strain A and B at a 1:3 ratio, exhibiting the most potent protective effect. KABP–AB-cx 13 inhibited the infiltration of neutrophils, the quantity of various inflammatory cells, such as CD62L<sup>−</sup>CD44<sup>high+</sup>, CD21/35<sup>+</sup>B220<sup>+</sup>, and Gr-1<sup>+</sup>CD11b<sup>+</sup> cells, and the expression of cytokines and chemokines, including chemokine (C-X-C motif) ligand (CXCL)-1, macrophage inflammatory protein-2, tumor necrosis factor-α, interleukin (IL)-17A, IL-6, and IL-1β, in the BALF and lungs of mice with PM<sub>10</sub><span>D</span>-triggered airway inflammation. It also decreased IL-1α and IRAK expression in alveolar macrophages along with inhibition of nuclear factor-κB (NF- κB) and JNK phosphorylation in the lungs of these mice. Furthermore, KABP–AB-cx 13 increased CD206<sup>+</sup>F4/80<sup>+</sup> cell numbers in mesenteric lymph nodes and IgA and SCFA levels in small intestine lavage fluid. It also exhibited better expectorant activity based on increased phenol-red secretion.</div></div><div><h3>Conclusion</h3><div>KABP–AB-cx 13 suppressed the PM<sub>10</sub><span>D</span>-induced airway inflammation and protected lung tissue from damage by inhibiting immune and inflammatory reactions in airways, activating the immune system, and increasing SCFA levels in the gut. KABP–AB-cx 13 also exhibited an expectorant effect, suggesting protective and therapeutic effects against respiratory inflammation. Overall, these findings contribute to global understanding of how probiotic interventions may help prevent or alleviate respiratory disorders induced by air pollution.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119926"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147320982","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}
Dietary intake is a major pathway of human exposure to polycyclic aromatic hydrocarbons (PAHs), linking environmental contamination to food-chain transfer and health risks. However, conventional dietary exposure assessments often neglect bioaccessibility and the complexity of real dietary patterns, potentially biasing risk estimation and source attribution. In this study, an in vitro gastrointestinal digestion model was applied to quantify contamination levels and bioaccessibility of 15 PAHs in 43 commonly consumed foods across five categories, representative of typical urban diets. Compared with historical data, intensified contamination by certain highly toxic H-PAHs resulted in 1.15–18.5-fold increases in BaPeq levels in fruits, meats, and cereals, underscoring the importance of integrated dietary assessment. PAHs bioaccessibility varied substantially (7.87–89.6 %), with the highest levels in meat (73.5 ± 23.4 %), revealing distinct matrix effects characterized by lipid facilitation and dietary fiber inhibition. Incorporating bioaccessibility into exposure modeling shifted the dominant dietary exposure source from cereals to meat, revealing that neglecting bioaccessibility may distort source attribution in exposure assessments. The bioaccessible dietary exposure dose (70.0 ng kg−1 day−1) of PAHs accounted for only 43.9 % of the total external exposure (160 ng kg−1 day−1), reducing the estimated proportion of the population at potential carcinogenic risk from 99.8 % to 45.4 %. These findings highlight the mechanistic importance of bioaccessibility in accurately evaluating internal exposure and identifying true dietary exposure sources. The systematic PAHs bioaccessibility dataset and integrated exposure model developed here provide a scientific basis for optimizing exposure assessment frameworks and guiding precision-oriented food safety management and risk control strategies.
饮食摄入是人类接触多环芳烃（PAHs）的主要途径，将环境污染与食物链转移和健康风险联系起来。然而，传统的饮食暴露评估往往忽略了生物可及性和真实饮食模式的复杂性，这可能会使风险估计和来源归因产生偏差。本研究采用体外胃肠消化模型，量化了5类43种常见食物中15种多环芳烃的污染水平和生物可及性，这些食物代表了典型的城市饮食。与历史数据相比，某些高毒性H-PAHs污染加剧导致水果、肉类和谷物中BaPeq水平增加1.15-18.5倍，强调了综合膳食评估的重要性。多环芳烃的生物可及性差异较大（7.87 ~ 89.6 %），其中肉类的可及性最高（73.5 ± 23.4 %），显示出明显的基质效应，以脂质促进和膳食纤维抑制为特征。将生物可及性纳入暴露模型将主要的饮食暴露源从谷物转移到肉类，这表明忽视生物可及性可能会扭曲暴露评估中的来源归因。多环芳烃的生物可及膳食暴露剂量（70.0 ng kg-1 day-1）仅占总外部暴露剂量（160 ng kg-1 day-1）的43.9 %，将潜在致癌风险人群的估计比例从99.8% %降低到45.4% %。这些发现强调了生物可及性在准确评估内部暴露和确定真正的饮食暴露源方面的机制重要性。建立了系统的多环芳烃生物可及性数据集和综合暴露模型，为优化暴露评估框架、指导精准食品安全管理和风险控制策略提供了科学依据。
{"title":"Optimizing dietary exposure and health risk assessment of polycyclic aromatic hydrocarbon based on bioaccessibility: A case study of Beijing, China","authors":"Yixi Tan, Zhangwei Wu, Siqi Xing, Zhengjiang Lin, Xuepeng Wang, Yunhe Guo, Yanxin Yu","doi":"10.1016/j.ecoenv.2026.119952","DOIUrl":"10.1016/j.ecoenv.2026.119952","url":null,"abstract":"<div><div>Dietary intake is a major pathway of human exposure to polycyclic aromatic hydrocarbons (PAHs), linking environmental contamination to food-chain transfer and health risks. However, conventional dietary exposure assessments often neglect bioaccessibility and the complexity of real dietary patterns, potentially biasing risk estimation and source attribution. In this study, an <em>in vitro</em> gastrointestinal digestion model was applied to quantify contamination levels and bioaccessibility of 15 PAHs in 43 commonly consumed foods across five categories, representative of typical urban diets. Compared with historical data, intensified contamination by certain highly toxic H-PAHs resulted in 1.15–18.5-fold increases in BaP<sub>eq</sub> levels in fruits, meats, and cereals, underscoring the importance of integrated dietary assessment. PAHs bioaccessibility varied substantially (7.87–89.6 %), with the highest levels in meat (73.5 ± 23.4 %), revealing distinct matrix effects characterized by lipid facilitation and dietary fiber inhibition. Incorporating bioaccessibility into exposure modeling shifted the dominant dietary exposure source from cereals to meat, revealing that neglecting bioaccessibility may distort source attribution in exposure assessments. The bioaccessible dietary exposure dose (70.0 ng kg<sup>−1</sup> day<sup>−1</sup>) of PAHs accounted for only 43.9 % of the total external exposure (160 ng kg<sup>−1</sup> day<sup>−1</sup>), reducing the estimated proportion of the population at potential carcinogenic risk from 99.8 % to 45.4 %. These findings highlight the mechanistic importance of bioaccessibility in accurately evaluating internal exposure and identifying true dietary exposure sources. The systematic PAHs bioaccessibility dataset and integrated exposure model developed here provide a scientific basis for optimizing exposure assessment frameworks and guiding precision-oriented food safety management and risk control strategies.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"312 ","pages":"Article 119952"},"PeriodicalIF":6.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147346925","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