Pub Date : 2026-01-01DOI: 10.1016/j.enceco.2026.01.013
Siyuan Li , Caiqing Li , Zhixiang Xu , Guangzhou He , Yitao Ma , Hao Lu , Keying Chen , Longlong Miao , Xianyao Zheng , Xuejun Pan
The synergistic effects between antibiotic resistance genes (ARGs) and horizontal gene transfer involving non-antibiotic pollutants such as microplastics represent an emerging frontier in ecological and public health research. Diisobutyl phthalate (DIBP), a prevalent phthalate (PAE) plasticizer, volatilizes into aquatic environments, posing significant risks to aquatic ecosystems. This study systematically investigated the regulatory mechanisms by which DIBP promotes conjugative transfer of ARGs at environmentally relevant concentrations (0.01–100 μg/L), showing increases of 1.02–1.67-fold and 1.02–1.36-fold compared to controls. By establishing both intra- and inter-genus systems, we elucidated the synergistic interactions among oxidative stress, membrane permeability, and energy metabolism that collectively drive ARG dissemination. Moving beyond previous studies, the present work establishes a more comprehensive mechanistic evaluation framework through with DIBP induced ARG conjugation, namely “oxidative stress-membrane permeability-energy metabolism” coupling model. Related results extend the specificity of PAEs in facilitating ARG transfer from straight-chain to branched-chain isomers, representing a deep attempt to move from observational phenomena to systematic mechanistic analysis within this field. These findings reveal potential aquatic ecological and public health risks, ultimately providing novel theoretical support for mitigating PAE-induced antibiotic resistance transmission.
{"title":"Diisobutyl phthalate at environmental concentration promotes the conjugative transfer of antibiotic resistance genes: Mechanistic insights and ecological implications","authors":"Siyuan Li , Caiqing Li , Zhixiang Xu , Guangzhou He , Yitao Ma , Hao Lu , Keying Chen , Longlong Miao , Xianyao Zheng , Xuejun Pan","doi":"10.1016/j.enceco.2026.01.013","DOIUrl":"10.1016/j.enceco.2026.01.013","url":null,"abstract":"<div><div>The synergistic effects between antibiotic resistance genes (ARGs) and horizontal gene transfer involving non-antibiotic pollutants such as microplastics represent an emerging frontier in ecological and public health research. Diisobutyl phthalate (DIBP), a prevalent phthalate (PAE) plasticizer, volatilizes into aquatic environments, posing significant risks to aquatic ecosystems. This study systematically investigated the regulatory mechanisms by which DIBP promotes conjugative transfer of ARGs at environmentally relevant concentrations (0.01–100 μg/L), showing increases of 1.02–1.67-fold and 1.02–1.36-fold compared to controls. By establishing both intra- and inter-genus systems, we elucidated the synergistic interactions among oxidative stress, membrane permeability, and energy metabolism that collectively drive ARG dissemination. Moving beyond previous studies, the present work establishes a more comprehensive mechanistic evaluation framework through with DIBP induced ARG conjugation, namely “oxidative stress-membrane permeability-energy metabolism” coupling model. Related results extend the specificity of PAEs in facilitating ARG transfer from straight-chain to branched-chain isomers, representing a deep attempt to move from observational phenomena to systematic mechanistic analysis within this field. These findings reveal potential aquatic ecological and public health risks, ultimately providing novel theoretical support for mitigating PAE-induced antibiotic resistance transmission.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 1079-1090"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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.enceco.2025.12.013
Pan Yi , Jianqiu Chen , Hanxiao Han , Yuqing Liu , Shuo Yang , Guodong Kang , Ruixin Guo , Yanhua Liu
Persistent organic pollutants (POPs) are a class of long-lasting, high-risk contaminants in aquatic environments, and their toxicity is modulated by fluctuations in environmental factors. Dispersed black carbon (DBC) is a prevalent particulate matter in water bodies that exhibits a strong adsorption capacity, which can alter the bioavailability and toxicity of pollutants. This study investigated the intergenerational toxicity mechanisms of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47), a representative POPs, through a 60-day exposure experiment. BDE-47 was administered at concentrations of 0, 2, 20, and 200 μg/L, with DBC at 0.5 mg/L, to assess its interference. The results demonstrate that DBC can adsorb BDE-47 efficiently, with an adsorption capacity of 34.6 mg/g, thereby modifying its bioavailability. Through a 60-day exposure experiment on adult zebrafish, we established that BDE-47 induces sex-specific toxicity. Females showed higher survival rates than males, but surviving females displayed more severe tissue damage and behavioral impairments. DBC-mediated adsorption mitigated the BDE-47-induced toxic effects in adult zebrafish via the modulation of steroidogenic pathways. Specifically, DBC increased gonad weight by 27.6 %, reduced the occurrence of atretic follicles, and elevated sperm count. At the molecular level, DBC alleviated the transcriptional dysregulation of key steroidogenic genes, notably upregulating the expression of Cyp17a1 and Star by approximately two-fold and three-fold, respectively. Conversely, in a 7-day assessment of offspring (F1), DBC enhanced the toxicity of BDE-47 in offspring, exacerbating tachycardia and behavioral disturbances in offspring fish. Based on evidence from gonadal histopathology, steroid synthesis gene dysregulation, and the behavioral phenotypes of the offspring, this study discovered the intergenerational paradox of particle-mediated POPs toxicity, namely that DBC reduces the bioavailability of BDE-47 in adult zebrafish but exacerbates intergenerational health risks. The research results emphasize that under the mediation of DBC, the persistent impact of POPs on aquatic ecosystems has intensified.
{"title":"Dispersed black carbon mediates intergenerational BDE-47 toxicity in zebrafish by regulating steroidogenesis: Attenuated parental toxicity with exacerbated offspring impairment","authors":"Pan Yi , Jianqiu Chen , Hanxiao Han , Yuqing Liu , Shuo Yang , Guodong Kang , Ruixin Guo , Yanhua Liu","doi":"10.1016/j.enceco.2025.12.013","DOIUrl":"10.1016/j.enceco.2025.12.013","url":null,"abstract":"<div><div>Persistent organic pollutants (POPs) are a class of long-lasting, high-risk contaminants in aquatic environments, and their toxicity is modulated by fluctuations in environmental factors. Dispersed black carbon (DBC) is a prevalent particulate matter in water bodies that exhibits a strong adsorption capacity, which can alter the bioavailability and toxicity of pollutants. This study investigated the intergenerational toxicity mechanisms of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47), a representative POPs, through a 60-day exposure experiment. BDE-47 was administered at concentrations of 0, 2, 20, and 200 μg/L, with DBC at 0.5 mg/L, to assess its interference. The results demonstrate that DBC can adsorb BDE-47 efficiently, with an adsorption capacity of 34.6 mg/g, thereby modifying its bioavailability. Through a 60-day exposure experiment on adult zebrafish, we established that BDE-47 induces sex-specific toxicity. Females showed higher survival rates than males, but surviving females displayed more severe tissue damage and behavioral impairments. DBC-mediated adsorption mitigated the BDE-47-induced toxic effects in adult zebrafish via the modulation of steroidogenic pathways. Specifically, DBC increased gonad weight by 27.6 %, reduced the occurrence of atretic follicles, and elevated sperm count. At the molecular level, DBC alleviated the transcriptional dysregulation of key steroidogenic genes, notably upregulating the expression of <em>Cyp17a1</em> and <em>Star</em> by approximately two-fold and three-fold, respectively. Conversely, in a 7-day assessment of offspring (F1), DBC enhanced the toxicity of BDE-47 in offspring, exacerbating tachycardia and behavioral disturbances in offspring fish. Based on evidence from gonadal histopathology, steroid synthesis gene dysregulation, and the behavioral phenotypes of the offspring, this study discovered the intergenerational paradox of particle-mediated POPs toxicity, namely that DBC reduces the bioavailability of BDE-47 in adult zebrafish but exacerbates intergenerational health risks. The research results emphasize that under the mediation of DBC, the persistent impact of POPs on aquatic ecosystems has intensified.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 688-707"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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.enceco.2026.01.004
Yuanqin Gao , Bingcai Xiong , Xiaoyu Huang , Xingyue Sun , Hongxia Du , Ming Ma , Feng Luo
Gaseous elemental mercury (Hg0) poses significant risks to ecosystems due to its high volatility and bioavailability. However, it remains largely unknown how the endophytes of Tillandsia usneoides (Spanish moss), a biological indicator responds to Hg0. In this study, after 14 days of exposure to the vapor from 0.22 mL of liquid Hg0, T. usneoides accumulated a markedly elevated Hg content of 164, 900 ± 28, 900 μg kg−1. High-throughput sequencing of 16S rRNA and ITS genes revealed that Hg0 exposure significantly reduced the α-diversity of endophytic bacteria and altered the β-diversity of both bacterial and fungal communities. Under Hg0 stress, taxonomic shifts included increased relative abundances of Pseudomonas, Enterobacter, and Acidiella. Functional predictions further indicated upregulated expression of key enzymes involved in Hg detoxification and antioxidant defense, such as mercuric reductase (MerA), glutathione S-transferase (GST), catalase (CAT), and superoxide dismutase (SOD). From Hg0-exposed T. usneoides, we isolated five endophytic bacteria (Staphylococcus sp. L3, Pseudomonas sp. L9, Enterobacter L19, Enterobacter L6, Bacillus LE) and two fungi (Aspergillus G1, G2), all of which demonstrated strong Hg2+ transformation and tolerance. Scanning electron microscopy (SEM) and energy-dispersive spectroscopy (EDS) confirmed morphological adaptations and Hg enrichment on microbial surfaces. Foliar inoculation with strains L6, LE, and G2 significantly alleviated Hg0-induced growth inhibition in Arabidopsis thaliana, enhancing biomass, leaf/root length, and root surface area, while mitigating auxin suppression. Overall, this study clarifies how T. usneoides endophytes respond to Hg0 and highlights their promising role in microbial-assisted phytoremediation of Hg0 pollution.
{"title":"Endophytic bacteria and fungi from atmospheric mercury bioindicator Tillandsia usneoides (Spanish moss) alleviate mercury stress and promote plant growth","authors":"Yuanqin Gao , Bingcai Xiong , Xiaoyu Huang , Xingyue Sun , Hongxia Du , Ming Ma , Feng Luo","doi":"10.1016/j.enceco.2026.01.004","DOIUrl":"10.1016/j.enceco.2026.01.004","url":null,"abstract":"<div><div>Gaseous elemental mercury (Hg<sup>0</sup>) poses significant risks to ecosystems due to its high volatility and bioavailability. However, it remains largely unknown how the endophytes of <em>Tillandsia usneoides</em> (Spanish moss), a biological indicator responds to Hg<sup>0</sup>. In this study, after 14 days of exposure to the vapor from 0.22 mL of liquid Hg<sup>0</sup>, <em>T. usneoides</em> accumulated a markedly elevated Hg content of 164, 900 ± 28, 900 μg kg<sup>−1</sup>. High-throughput sequencing of 16S rRNA and ITS genes revealed that Hg<sup>0</sup> exposure significantly reduced the α-diversity of endophytic bacteria and altered the β-diversity of both bacterial and fungal communities. Under Hg<sup>0</sup> stress, taxonomic shifts included increased relative abundances of <em>Pseudomonas</em>, <em>Enterobacter</em>, and <em>Acidiella</em>. Functional predictions further indicated upregulated expression of key enzymes involved in Hg detoxification and antioxidant defense, such as mercuric reductase (MerA), glutathione S-transferase (GST), catalase (CAT), and superoxide dismutase (SOD). From Hg<sup>0</sup>-exposed <em>T. usneoides</em>, we isolated five endophytic bacteria (<em>Staphylococcus</em> sp. L3, <em>Pseudomonas</em> sp. L9, <em>Enterobacter</em> L19, <em>Enterobacter</em> L6, <em>Bacillus</em> LE) and two fungi (<em>Aspergillus</em> G1, G2), all of which demonstrated strong Hg<sup>2+</sup> transformation and tolerance. Scanning electron microscopy (SEM) and energy-dispersive spectroscopy (EDS) confirmed morphological adaptations and Hg enrichment on microbial surfaces. Foliar inoculation with strains L6, LE, and G2 significantly alleviated Hg<sup>0</sup>-induced growth inhibition in <em>Arabidopsis thaliana</em>, enhancing biomass, leaf/root length, and root surface area, while mitigating auxin suppression. Overall, this study clarifies how <em>T. usneoides</em> endophytes respond to Hg<sup>0</sup> and highlights their promising role in microbial-assisted phytoremediation of Hg<sup>0</sup> pollution.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 881-893"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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.enceco.2025.12.028
Sisi Wang , Lan Chen , Xiaopan Wu , Yatao Wu , Lei Zhang , Xin Liu , Yu Wang , Jingguang Li , Shen Wen , Jing Huang , Yongning Wu
Persistent Organic Pollutants (POPs) are globally distributed, bioaccumulative chemicals that are increasingly implicated as environmental contributors to metabolic toxicity; however, the mechanistic pathways underlying their effects during early pregnancy remain poorly characterized. In this maternal cohort study, high-resolution mass spectrometry revealed that women with early metabolic abnormalities carried higher serum burdens of several POP congeners, with polybrominated diphenyl ethers (PBDEs; e.g., BDE-153, BDE-154) and polychlorinated biphenyl-52 (PCB-52) showing the most consistent elevations. Targeted metabolomics further identified marked alterations in bile acid profiles: putatively protective bile acids such as glycoursodeoxycholic acid (GUDCA) (2.32 vs. 2.79 ng/mL, P < 0.05) and glycochenodeoxycholic acid (GCDCA) (2.32 vs. 4.77 ng/mL, P < 0.05) were depleted in women with early metabolic abnormalities compared with those without, whereas taurine-conjugated species, including tauroursodeoxycholic acid (TUDCA), were elevated. Correlation analyses revealed inverse associations between brominated congeners and conjugated bile acids (e.g., BDE-154 with TUDCA, r = −0.29, P < 0.001), whereas PCB-52 was positively associated with serum cholesterol levels. In mediation analyses, GUDCA and TUDCA jointly mediated up to 24 % of the association between PBDEs and dysregulated glucose metabolism, sulfated bile acids mediated 21–25 % of PBDE–triglyceride associations and norcholic acid (NorCA) accounted for 19 % of the PCB-52–cholesterol relationship. These findings provide human evidence that maternal POP exposure is associated with perturbations in bile acid metabolism that may contribute to impaired glucose–lipid homeostasis during early pregnancy, and highlight bile acids as mechanistic mediators and potential early biomarkers of pollutant-induced metabolic toxicity.
持久性有机污染物（POPs）是全球分布的、具有生物蓄积性的化学品，越来越多地被认为是代谢性毒性的环境因素；然而，其在妊娠早期影响的机制途径仍不清楚。在这项母体队列研究中，高分辨率质谱分析显示，早期代谢异常的女性血清中几种POP同系物的负荷较高，其中多溴联苯醚（PBDEs，如BDE-153、BDE-154）和多氯联苯-52 （PCB-52）的升高最为一致。靶向代谢组学进一步确定了胆汁酸谱的显著变化：与没有早期代谢异常的女性相比，早期代谢异常的女性中，被认为具有保护作用的胆汁酸，如糖醛酸去氧胆酸（GUDCA） （2.32 vs. 2.79 ng/mL, P < 0.05）和糖醛酸去氧胆酸（GCDCA） （2.32 vs. 4.77 ng/mL, P < 0.05）减少，而牛磺酸结合的物种，包括牛磺酸去氧胆酸（TUDCA），则升高。相关分析显示溴化同源物与共轭胆汁酸呈负相关（例如，BDE-154与TUDCA， r = - 0.29, P < 0.001），而PCB-52与血清胆固醇水平呈正相关。在中介分析中，GUDCA和TUDCA共同介导了高达24%的多溴二苯酯和糖代谢失调之间的关联，硫酸胆汁酸介导了21 - 25%的多溴二苯酯甘油三酯关联，去胆酸（NorCA）介导了19%的多溴二苯酯-52 -胆固醇关系。这些发现提供了人类证据，证明母体POP暴露与胆汁酸代谢紊乱有关，胆汁酸代谢紊乱可能导致妊娠早期糖脂稳态受损，并强调胆汁酸是污染物诱导代谢毒性的机制介质和潜在的早期生物标志物。
{"title":"Early-pregnancy exposure to persistent organic pollutants and bile acid alterations in relation to gestational glucose–lipid homeostasis","authors":"Sisi Wang , Lan Chen , Xiaopan Wu , Yatao Wu , Lei Zhang , Xin Liu , Yu Wang , Jingguang Li , Shen Wen , Jing Huang , Yongning Wu","doi":"10.1016/j.enceco.2025.12.028","DOIUrl":"10.1016/j.enceco.2025.12.028","url":null,"abstract":"<div><div>Persistent Organic Pollutants (POPs) are globally distributed, bioaccumulative chemicals that are increasingly implicated as environmental contributors to metabolic toxicity; however, the mechanistic pathways underlying their effects during early pregnancy remain poorly characterized. In this maternal cohort study, high-resolution mass spectrometry revealed that women with early metabolic abnormalities carried higher serum burdens of several POP congeners, with polybrominated diphenyl ethers (PBDEs; e.g., BDE-153, BDE-154) and polychlorinated biphenyl-52 (PCB-52) showing the most consistent elevations. Targeted metabolomics further identified marked alterations in bile acid profiles: putatively protective bile acids such as glycoursodeoxycholic acid (GUDCA) (2.32 vs. 2.79 ng/mL, <em>P</em> < 0.05) and glycochenodeoxycholic acid (GCDCA) (2.32 vs. 4.77 ng/mL, <em>P</em> < 0.05) were depleted in women with early metabolic abnormalities compared with those without, whereas taurine-conjugated species, including tauroursodeoxycholic acid (TUDCA), were elevated. Correlation analyses revealed inverse associations between brominated congeners and conjugated bile acids (e.g., BDE-154 with TUDCA, <em>r</em> = −0.29, <em>P</em> < 0.001), whereas PCB-52 was positively associated with serum cholesterol levels. In mediation analyses, GUDCA and TUDCA jointly mediated up to 24 % of the association between PBDEs and dysregulated glucose metabolism, sulfated bile acids mediated 21–25 % of PBDE–triglyceride associations and norcholic acid (NorCA) accounted for 19 % of the PCB-52–cholesterol relationship. These findings provide human evidence that maternal POP exposure is associated with perturbations in bile acid metabolism that may contribute to impaired glucose–lipid homeostasis during early pregnancy, and highlight bile acids as mechanistic mediators and potential early biomarkers of pollutant-induced metabolic toxicity.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 924-933"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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.enceco.2026.01.003
M. Elisabetta Michelangeli , Steven Brooks , Sebastian Kuehr , Emelie Forsman , Elisabeth S. Rødland , Sicco H. Brandsma , Maria Margalef , Manuel Heinzelmann , Davide Spanu , Jan Thomas Rundberget , Tânia Gomes
Tyre particles contain complex chemical additives that can leach out into the aquatic environment, posing potential risks to marine organisms. Despite growing evidence of adverse effects, the relative importance of particle-driven versus chemically mediated toxicity remains poorly explored, especially under environmentally relevant exposure scenarios. This study used the blue mussel (Mytilus edulis) as a model to differentiate these effects by exposing individuals to cryomilled tyre particles (TP), their leachates (L) and pre-leached particles (TPL) over 36 days at the environmentally relevant concentration of 0.1 g/L. Chemical analysis confirmed uptake of key organic additives such as poly(1,2-dihydro-2,2,4-trimethylquinoline) (TMQ), N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD), and 6PPD-quinone (6PPDQ), with certain compounds persisting after depuration. Particle-exposed mussels accumulated higher additive concentrations than those exposed to only leachates, indicating enhanced chemical release from particles. Biomarker responses revealed signs of oxidative stress and neurotoxicity in exposed mussels across all treatments, with earlier responses in leachate exposure and delayed responses during particle exposures. These results demonstrate that chemical additives are key toxicity drivers alongside physical particles, highlighting the importance of considering both pathways in environmental risk assessments. To our knowledge, this study is among the first to experimentally separate particle and leachate specific effects in mussels by using tyre particles before and after leaching to create contrasting chemical loads, thereby providing novel insights into their distinct and combined impacts on marine biota.
{"title":"Tyre-derived ecotoxicity: Differentiating the effects from particles and chemical leachates on the blue mussel Mytilus edulis","authors":"M. Elisabetta Michelangeli , Steven Brooks , Sebastian Kuehr , Emelie Forsman , Elisabeth S. Rødland , Sicco H. Brandsma , Maria Margalef , Manuel Heinzelmann , Davide Spanu , Jan Thomas Rundberget , Tânia Gomes","doi":"10.1016/j.enceco.2026.01.003","DOIUrl":"10.1016/j.enceco.2026.01.003","url":null,"abstract":"<div><div>Tyre particles contain complex chemical additives that can leach out into the aquatic environment, posing potential risks to marine organisms. Despite growing evidence of adverse effects, the relative importance of particle-driven versus chemically mediated toxicity remains poorly explored, especially under environmentally relevant exposure scenarios. This study used the blue mussel (<em>Mytilus edulis</em>) as a model to differentiate these effects by exposing individuals to cryomilled tyre particles (TP), their leachates (L) and pre-leached particles (TPL) over 36 days at the environmentally relevant concentration of 0.1 g/L. Chemical analysis confirmed uptake of key organic additives such as poly(1,2-dihydro-2,2,4-trimethylquinoline) (TMQ), N-(1,3-dimethylbutyl)-<em>N</em>′-phenyl-<em>p</em>-phenylenediamine (6PPD), and 6PPD-quinone (6PPDQ), with certain compounds persisting after depuration. Particle-exposed mussels accumulated higher additive concentrations than those exposed to only leachates, indicating enhanced chemical release from particles. Biomarker responses revealed signs of oxidative stress and neurotoxicity in exposed mussels across all treatments, with earlier responses in leachate exposure and delayed responses during particle exposures. These results demonstrate that chemical additives are key toxicity drivers alongside physical particles, highlighting the importance of considering both pathways in environmental risk assessments. To our knowledge, this study is among the first to experimentally separate particle and leachate specific effects in mussels by using tyre particles before and after leaching to create contrasting chemical loads, thereby providing novel insights into their distinct and combined impacts on marine biota.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 934-951"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Thyroid hormone (TH), coordinating with its receptor (TRβ), plays a conserved role in regulating retinal cone differentiation. Environmental thyroid disrupting chemicals (TDCs) exposure has been proved as an emerging cause of retinal photosensitive dysfunction; however, the molecular target and underlying mechanisms of action have not been well explored. Here, a TH- and TDCs-sensitive transgenic zebrafish, of which the TRE:TRβ promoter-driven mCherry expressed in red cones, was constructed. By using this model, it was revealed that bisphenol S (BPS), a widely-used plastic additive with similar structure to TH, exhibited an agonist effect on TRβ and specialized retinal progenitor cells (RPCs) into red cones in larval zebrafish retina. Then, the essential role of TRβ in both BPS- and TH- stimulated red cone differentiation was convinced by a loss-of-function study. Single cone cell transcriptomic data showed both BPS and TH diminished the phototransduction cascade in red cone cells by interfering with different aspects of the transduction process, finally causing color vision defects in larval fish. Overall, it was demonstrated that BPS exposure, mimicking TH, disturbed RPCs specifying into red (not UV) cones via activating TRβ signaling, which further induced photosensitive dysfunction in cone cells. Our work highlights a new way of TRβ-mediated modulation of cone differentiation fate upon TDCs exposure.
{"title":"New insight into the adverse effect and molecular mechanism of thyroid disrupting chemicals on retinal cone differentiation: A case study of bisphenol S.","authors":"Liguo Qiu , Shuhui Wei , Meiping Guo , Yunsheng Wang , Liping Hao , Xuefu Li , Shaoguo Ru , Xiaona Zhang","doi":"10.1016/j.enceco.2026.01.014","DOIUrl":"10.1016/j.enceco.2026.01.014","url":null,"abstract":"<div><div>Thyroid hormone (TH), coordinating with its receptor (TRβ), plays a conserved role in regulating retinal cone differentiation. Environmental thyroid disrupting chemicals (TDCs) exposure has been proved as an emerging cause of retinal photosensitive dysfunction; however, the molecular target and underlying mechanisms of action have not been well explored. Here, a TH- and TDCs-sensitive transgenic zebrafish, of which the TRE:<em>TRβ</em> promoter-driven mCherry expressed in red cones, was constructed. By using this model, it was revealed that bisphenol S (BPS), a widely-used plastic additive with similar structure to TH, exhibited an agonist effect on TRβ and specialized retinal progenitor cells (RPCs) into red cones in larval zebrafish retina. Then, the essential role of TRβ in both BPS- and TH- stimulated red cone differentiation was convinced by a loss-of-function study. Single cone cell transcriptomic data showed both BPS and TH diminished the phototransduction cascade in red cone cells by interfering with different aspects of the transduction process, finally causing color vision defects in larval fish. Overall, it was demonstrated that BPS exposure, mimicking TH, disturbed RPCs specifying into red (not UV) cones <em>via</em> activating TRβ signaling, which further induced photosensitive dysfunction in cone cells. Our work highlights a new way of TRβ-mediated modulation of cone differentiation fate upon TDCs exposure.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 973-985"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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.enceco.2026.01.008
Zhipeng Qi , Peng Li , Xiang Gao , Qiuchen Wu , Keying Li , Zhuoyi Xie , Xilan Xia , Tianchen Wang , Xiangrong Zhou , Jianan Li , Xinying Zhao , Hui Yuan , Weiyi Song
Environmental exposure to benzophenones (BPs) has emerged as a potential risk factor for the comorbidity of anxiety and depression. Among them, BP1 has attracted increasing attention due to its potential neurotoxic effects. However, whether and how long-term exposure to BP1 induces anxiety- and depression-like behaviors remains unclear. To investigate the adverse effects of BP1 on mental health, zebrafish were exposed to environmentally relevant concentrations of BP1 (0 to 1 μM) from 0 to 180 days post-fertilization (dpf). Chemical analysis confirmed significant accumulation of BP1 in zebrafish brain tissue, indicating effective internal exposure of the nervous system. We then showed that exposure to BP1 increased scototaxis and bottom-dwelling behaviors while reducing exploratory activity in adult zebrafish, suggesting that BP1 exposure can cause anxiety- and depression-like behaviors. Moreover, histopathological analysis revealed that BP1 exposure induced morphological damage in the zebrafish midbrain, characterized by neuronal degeneration, interstitial vacuolation, and loss of Nissl bodies. Transcriptomic analysis revealed that life cycle BP1 exposure activated endoplasmic reticulum (ER) stress signaling and downregulated dopamine receptor drd4a. Furthermore, BP1 exposure suppressed the proliferation of dopaminergic neurons and decreased dopamine levels in the zebrafish brain. At the translational level, BP1 exposure significantly increased GRP78 and ATF4B protein levels and decreased EIF2α phosphorylation level, indicating activation of chronic ER stress. Concomitantly, the protein levels of TH and DRD4 were reduced. To further validate these findings, parallel experiments in PC12 cells demonstrated that BP1 exposure similarly dysregulated GRP78, ATF4B, p-EIF2α, TH, and DRD4. Importantly, pharmacological inhibition of ER stress with 4-phenylbutyric acid (4-PBA) effectively rescued the BP1-induced downregulation of TH and DRD4 in vitro. Taken together, these findings provide crucial evidence elucidating the underlying mechanism by which BP1 exposure induces anxiety- and depression-like behaviors in aquatic organisms, offering novel insights into its neurotoxic effects.
{"title":"Life cycle benzophenone 1 exposure induces anxiety- and depression-like behaviors in zebrafish via endoplasmic reticulum stress-mediated dopaminergic system dysfunction","authors":"Zhipeng Qi , Peng Li , Xiang Gao , Qiuchen Wu , Keying Li , Zhuoyi Xie , Xilan Xia , Tianchen Wang , Xiangrong Zhou , Jianan Li , Xinying Zhao , Hui Yuan , Weiyi Song","doi":"10.1016/j.enceco.2026.01.008","DOIUrl":"10.1016/j.enceco.2026.01.008","url":null,"abstract":"<div><div>Environmental exposure to benzophenones (BPs) has emerged as a potential risk factor for the comorbidity of anxiety and depression. Among them, BP1 has attracted increasing attention due to its potential neurotoxic effects. However, whether and how long-term exposure to BP1 induces anxiety- and depression-like behaviors remains unclear. To investigate the adverse effects of BP1 on mental health, zebrafish were exposed to environmentally relevant concentrations of BP1 (0 to 1 μM) from 0 to 180 days post-fertilization (dpf). Chemical analysis confirmed significant accumulation of BP1 in zebrafish brain tissue, indicating effective internal exposure of the nervous system. We then showed that exposure to BP1 increased scototaxis and bottom-dwelling behaviors while reducing exploratory activity in adult zebrafish, suggesting that BP1 exposure can cause anxiety- and depression-like behaviors. Moreover, histopathological analysis revealed that BP1 exposure induced morphological damage in the zebrafish midbrain, characterized by neuronal degeneration, interstitial vacuolation, and loss of Nissl bodies. Transcriptomic analysis revealed that life cycle BP1 exposure activated endoplasmic reticulum (ER) stress signaling and downregulated dopamine receptor <em>drd4a</em>. Furthermore, BP1 exposure suppressed the proliferation of dopaminergic neurons and decreased dopamine levels in the zebrafish brain. At the translational level, BP1 exposure significantly increased GRP78 and ATF4B protein levels and decreased EIF2α phosphorylation level, indicating activation of chronic ER stress. Concomitantly, the protein levels of TH and DRD4 were reduced. To further validate these findings, parallel experiments in PC12 cells demonstrated that BP1 exposure similarly dysregulated GRP78, ATF4B, p-EIF2α, TH, and DRD4. Importantly, pharmacological inhibition of ER stress with 4-phenylbutyric acid (4-PBA) effectively rescued the BP1-induced downregulation of TH and DRD4 <em>in vitro</em>. Taken together, these findings provide crucial evidence elucidating the underlying mechanism by which BP1 exposure induces anxiety- and depression-like behaviors in aquatic organisms, offering novel insights into its neurotoxic effects.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 961-972"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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.enceco.2026.01.016
Haode He , Mei Wang , Wanru Zhang , Yuhui Sun , Hongyan Tian , Chao Wei , Haoyu Liu , Yuxia Yang
Accelerated global climate change has profoundly altered ecosystems and pollutant dynamics, severely hindering the accurate assessment of ecological risks associated with organophosphate esters (OPEs) due to the limitations of conventional monitoring approaches. To address these challenges, we developed an integrative “environment-biota-pollutant” framework, combining spatial statistics, machine learning, and structural equation modeling to elucidate OPE bioaccumulation in dragonfly larvae using a dataset comprising 6099 samples. The study reveals that dragonfly larvae exhibit pronounced spatial aggregation (Moran's I = 0.899–0.933) and exceptional bioconcentration capacity (mean log BAF = 3.63), surpassing traditional media. Through random forest modeling, nutrient salts (total phosphorus, total nitrogen, nitrate nitrogen) were identified as the primary drivers of OPE bioaccumulation in larvae, accounting for 25.22% of the variance, over three times greater than the contribution from direct aqueous OPE exposure (7.67%). Further analysis using partial least squares structural equation modeling demonstrated that warming enhances nitrate bioavailability (β = 0.742), which subsequently promotes OPE accumulation in larvae (β = 0.409). This finding indicates that climate-driven nutrient cycling is a more significant driver than aqueous OPEs concentration. As climate change continues to influence nutrient cycling and bioavailability, this integrative approach offers a robust framework for understanding and addressing the ecological risks associated with OPEs in an evolving environment.
{"title":"Nutrient–warming synergy governs organophosphate esters bioavailability to dragonfly larvae","authors":"Haode He , Mei Wang , Wanru Zhang , Yuhui Sun , Hongyan Tian , Chao Wei , Haoyu Liu , Yuxia Yang","doi":"10.1016/j.enceco.2026.01.016","DOIUrl":"10.1016/j.enceco.2026.01.016","url":null,"abstract":"<div><div>Accelerated global climate change has profoundly altered ecosystems and pollutant dynamics, severely hindering the accurate assessment of ecological risks associated with organophosphate esters (OPEs) due to the limitations of conventional monitoring approaches. To address these challenges, we developed an integrative “environment-biota-pollutant” framework, combining spatial statistics, machine learning, and structural equation modeling to elucidate OPE bioaccumulation in dragonfly larvae using a dataset comprising 6099 samples. The study reveals that dragonfly larvae exhibit pronounced spatial aggregation (Moran's <em>I</em> = 0.899–0.933) and exceptional bioconcentration capacity (mean log BAF = 3.63), surpassing traditional media. Through random forest modeling, nutrient salts (total phosphorus, total nitrogen, nitrate nitrogen) were identified as the primary drivers of OPE bioaccumulation in larvae, accounting for 25.22% of the variance, over three times greater than the contribution from direct aqueous OPE exposure (7.67%). Further analysis using partial least squares structural equation modeling demonstrated that warming enhances nitrate bioavailability (β = 0.742), which subsequently promotes OPE accumulation in larvae (β = 0.409). This finding indicates that climate-driven nutrient cycling is a more significant driver than aqueous OPEs concentration. As climate change continues to influence nutrient cycling and bioavailability, this integrative approach offers a robust framework for understanding and addressing the ecological risks associated with OPEs in an evolving environment.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 1111-1121"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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.enceco.2026.01.024
Xiaoyong Wang , Zhan Jin , Shunfeng Jiang , Ke Bei , Min Zhao , Zuxiang Li , Xiangyong Zheng
Source-separated urine is increasingly recognized as a promising resource for nutrient recovery; however, compared with conventional wastewater systems, the occurrence, behavior, and removal of emerging contaminants (ECs) in urine remain insufficiently characterized. Most existing urine-focused reviews primarily address nitrogen and phosphorus recovery or sanitation performance, while ECs are often only briefly discussed, resulting in fragmented evidence across contaminant classes and regions and limiting a coherent urine-centered understanding of exposure patterns and treatment needs.
This review synthesizes current knowledge on the occurrence and removal of ECs in source-separated urine, focusing on antibiotics, endocrine-disrupting chemicals, microplastics, and related persistent pollutants. By integrating bibliometric analysis with mechanistic evaluation of representative treatment technologies, we provide a structured overview of research trends, dominant contaminant groups, and key methodological limitations. Critical gaps are identified, including the scarcity of urine-specific datasets, inconsistencies in reported concentration metrics, and insufficient consideration of contaminant fate during urine treatment and resource recovery. The implications of these gaps for safe urine reuse are discussed, highlighting the need for targeted treatment strategies and standardized monitoring frameworks. Overall, this review offers a urine-centered perspective on ECs and provides guidance for advancing safe and sustainable urine resource recovery.
{"title":"A review on occurrence characteristics and removal technologies of emerging contaminants in source-separated urine","authors":"Xiaoyong Wang , Zhan Jin , Shunfeng Jiang , Ke Bei , Min Zhao , Zuxiang Li , Xiangyong Zheng","doi":"10.1016/j.enceco.2026.01.024","DOIUrl":"10.1016/j.enceco.2026.01.024","url":null,"abstract":"<div><div>Source-separated urine is increasingly recognized as a promising resource for nutrient recovery; however, compared with conventional wastewater systems, the occurrence, behavior, and removal of emerging contaminants (ECs) in urine remain insufficiently characterized. Most existing urine-focused reviews primarily address nitrogen and phosphorus recovery or sanitation performance, while ECs are often only briefly discussed, resulting in fragmented evidence across contaminant classes and regions and limiting a coherent urine-centered understanding of exposure patterns and treatment needs.</div><div>This review synthesizes current knowledge on the occurrence and removal of ECs in source-separated urine, focusing on antibiotics, endocrine-disrupting chemicals, microplastics, and related persistent pollutants. By integrating bibliometric analysis with mechanistic evaluation of representative treatment technologies, we provide a structured overview of research trends, dominant contaminant groups, and key methodological limitations. Critical gaps are identified, including the scarcity of urine-specific datasets, inconsistencies in reported concentration metrics, and insufficient consideration of contaminant fate during urine treatment and resource recovery. The implications of these gaps for safe urine reuse are discussed, highlighting the need for targeted treatment strategies and standardized monitoring frameworks. Overall, this review offers a urine-centered perspective on ECs and provides guidance for advancing safe and sustainable urine resource recovery.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 1122-1137"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tire wear particles (TWPs) are pervasive microplastic pollutants whose hazard varies with environmental weathering and emission source. Here, we investigated how water leaching modifies the physicochemical properties of TWPs from heavy-duty (HTWPs) and light-duty (LTWPs) tires and assessed both particle-associated effects in adult zebrafish and leachate-mediated developmental toxicity in embryos (Danio rerio). Simulated leaching increased surface roughness and oxygenated functional groups and mobilized Zn, with stronger release from HTWPs. Under a phase-separation design in which leachates were removed, pristine particles induced more pronounced systemic toxicity in adult fish, including impaired growth and organ function, oxidative stress, gut dysbiosis, and activation of immune, apoptotic, and xenobiotic metabolism pathways, whereas leached particles showed attenuated particle-associated effects. Embryonic exposure to graded leachates caused concentration-dependent cardiotoxicity, delayed hatching, and developmental defects, with HTWP leachates more strongly disrupting mitochondrial function and phototransduction than LTWP leachates. Multi-omics analyses consistently indicated lower systemic stress in leached-particle groups yet persistent developmental hazards in the dissolved phase. Accordingly, environmental risk reflects the combined and context-dependent contributions of aged particles and their coexisting leachates, and remains strongly source-dependent (HTWPs > LTWPs). These findings clarify how weathering redistributes, rather than simply reduces, TWP toxicity and should inform ecological risk assessment and management of non-exhaust vehicular emissions.
{"title":"Weathering-modulated gut-liver toxicity of tire wear particles in zebrafish: Source-specific effects and multi-omics insights","authors":"Xinrui Meng, Fan Wang, Qi Liang, Qingxuan Meng, Qianqian Song, Jing Cong","doi":"10.1016/j.enceco.2026.01.021","DOIUrl":"10.1016/j.enceco.2026.01.021","url":null,"abstract":"<div><div>Tire wear particles (TWPs) are pervasive microplastic pollutants whose hazard varies with environmental weathering and emission source. Here, we investigated how water leaching modifies the physicochemical properties of TWPs from heavy-duty (HTWPs) and light-duty (LTWPs) tires and assessed both particle-associated effects in adult zebrafish and leachate-mediated developmental toxicity in embryos (<em>Danio rerio</em>). Simulated leaching increased surface roughness and oxygenated functional groups and mobilized Zn, with stronger release from HTWPs. Under a phase-separation design in which leachates were removed, pristine particles induced more pronounced systemic toxicity in adult fish, including impaired growth and organ function, oxidative stress, gut dysbiosis, and activation of immune, apoptotic, and xenobiotic metabolism pathways, whereas leached particles showed attenuated particle-associated effects. Embryonic exposure to graded leachates caused concentration-dependent cardiotoxicity, delayed hatching, and developmental defects, with HTWP leachates more strongly disrupting mitochondrial function and phototransduction than LTWP leachates. Multi-omics analyses consistently indicated lower systemic stress in leached-particle groups yet persistent developmental hazards in the dissolved phase. Accordingly, environmental risk reflects the combined and context-dependent contributions of aged particles and their coexisting leachates, and remains strongly source-dependent (HTWPs > LTWPs). These findings clarify how weathering redistributes, rather than simply reduces, TWP toxicity and should inform ecological risk assessment and management of non-exhaust vehicular emissions.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 1057-1068"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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