Environment International最新文献

{"title":"Corrigendum to ‘Effects of radiofrequency electromagnetic field exposure on cancer in laboratory animal studies, a systematic review’ [Environ. Int. 199 (2025) 109482]","authors":"Meike Mevissen, Angélique Ducray, Jerrold M. Ward, Annette Kopp-Schneider, James P. McNamee, Andrew W. Wood, Tania M. Rivero, Kurt Straif","doi":"10.1016/j.envint.2026.110369","DOIUrl":"10.1016/j.envint.2026.110369","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"214 ","pages":"Article 110369"},"PeriodicalIF":10.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148384050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “An AI-based integrative framework with multi-omics and experimental validation reveals mechanisms of DABP-induced neurotoxicity” [Environ. Int. 211 (2026) 110269]","authors":"Jinchao Zhu, Linglong Chen, Wenjing Li, Yanqing Liu, Nayab Ibrahim, Jinrui Dong, Haojun Fan","doi":"10.1016/j.envint.2026.110376","DOIUrl":"10.1016/j.envint.2026.110376","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"214 ","pages":"Article 110376"},"PeriodicalIF":10.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational cadmium exposure triggers POI-Like ovarian dysfunction and accelerated ovarian aging through epigenetic repression of Kl in mice","authors":"Junyu Jiang,&nbsp;Muran He,&nbsp;Haotian Shi,&nbsp;Yanyan Xiong,&nbsp;Bo Li,&nbsp;Chenxi Yuan,&nbsp;Hua Wang,&nbsp;Zhibing Liu,&nbsp;Dexiang Xu,&nbsp;Jun Zhang","doi":"10.1016/j.envint.2026.110431","DOIUrl":"10.1016/j.envint.2026.110431","url":null,"abstract":"<div><div>Cadmium (Cd), a bioaccumulative toxic heavy metal, poses a growing concern for offspring reproductive health following gestational exposure. Premature ovarian insufficiency (POI), a major cause of female infertility, remained poorly understood in terms of environmental etiology. This study investigated whether gestational Cd exposure induced ovarian functional decline via epigenetic mechanisms in mice. Using a mouse model of maternal Cd exposure via drinking water, we found that gestational Cd exposure led to POI-like ovarian dysfunction in adult offspring, characterized by diminished ovarian reserve, disrupted estrous cycles, altered serum hormone profiles, and accelerated ovarian aging with fibrosis and DNA damage. Mechanistically, Cd exposure upregulated DNMT1 and DNMT3A expression in offspring ovaries, promoting hypermethylation of the <em>Klotho</em> (<em>Kl</em>) promoter and suppressing its expression. <em>Kl</em> downregulation subsequently attenuated its inhibition of the p53/p21 pathway, triggering granulosa cell senescence and premature follicular depletion. Importantly, administration of the DNA methylation inhibitor 5-aza-2′-deoxycytidine (5-Aza) during gestation partially reversed these Cd-induced epigenetic modifications and ameliorated the ovarian phenotypes in offspring. Our findings revealed a complete pathway through which gestational Cd exposure promoted ovarian aging via DNMT-mediated <em>Kl</em> silencing and p53/p21 activation. This work provided novel mechanistic insights into environmental reproductive toxicity and identified potential targets for intervention.</div></div><div><h3>Environmental implication</h3><div>Cd is a pervasive environmental toxicant threatening female reproductive health, yet its long-term developmental impacts on offspring ovarian aging remain unclear. This study reveals that gestational Cd exposure epigenetically silences the anti-aging gene <em>Kl</em> via promoter hypermethylation, activating the p53/p21/p16-Rb senescence pathway and triggering POI-like ovarian dysfunction in offspring. Importantly, this epigenetic damage is partially reversible with 5-Aza, offering a potential intervention strategy. These findings provide mechanistic insights into how Cd pollution contributes to rising POI incidence, informing developmental origins of reproductive dysfunction and guiding preventive policies for hazardous material regulation.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"214 ","pages":"Article 110431"},"PeriodicalIF":10.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148589864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A moment of heat, a lifetime exposure? Integrating effects of temperature and heatwaves into toxicokinetic modelling of a neonicotinoid in aquatic invertebrates","authors":"Johannes Raths,&nbsp;Markus Hermann,&nbsp;Clarissa von Au,&nbsp;Juliane Hollender","doi":"10.1016/j.envint.2026.110424","DOIUrl":"10.1016/j.envint.2026.110424","url":null,"abstract":"<div><div>Chemical pollution and climate change are major threats towards aquatic communities. Yet, their interactions remain poorly understood. Recent studies described the temperature-dependent toxicokinetics of contaminants in aquatic invertebrates but showed limitations for elimination resistant contaminants such as the receptor-binding neonicotinoids. The present study examined temperature effects on toxicokinetics of the neonicotinoid thiacloprid in aquatic invertebrates to improve predictions of bioaccumulation from laboratory to field conditions.</div><div>A recently developed two-compartment model including irreversible receptor binding was applied to analyze the toxicokinetics of thiacloprid in <em>Gammarus pulex</em> and <em>Hyalella azteca</em> (50 µg L⁻¹ at 6–21 °C). The Arrhenius equation was used to describe the temperature dependency of the toxicokinetic rate constants. Model parametrization was supported by receptor-binding assays. To test the predictivity of the model under dynamic exposure conditions, additional experiments were carried out in experimental stream mesocosms spiked with thiacloprid (10 <!--> <!-->µg L⁻¹) under natural ambient and simulated heatwave (+8 °C) conditions (10–34 °C).</div><div>The two-compartment model improved fits (R² = 0.78–0.98) compared to previously applied one-compartment models. The temperature dependency of toxicokinetic rate constants (Arrhenius temperature T_A = 7200–8300 K⁻¹) matched with physiological endpoints from previous experiments (8000 K⁻¹). Implementing temperature effects provided good estimates of tissue concentrations in the mesocosm experiment, thereby validating the model. Tissue concentrations have doubled under heatwave conditions compared to ambient conditions (46 vs. 23 µg kg⁻¹) and remained constant after the event of exposure.</div><div>The present study advances the mechanistic understanding of chemical exposure and bioaccumulation under changing climatic conditions and highlights how extreme heat events can intensify risks caused by neonicotinoids. These findings emphasize the need for regulatory strategies, such as dynamic models, to address the interactions of contaminants and a warming climate.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"214 ","pages":"Article 110424"},"PeriodicalIF":10.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148460719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Exposure to nanoplastics exacerbates light pollution hazards to mammalian” [Environ. Int. 197 (2025) 109338]","authors":"Haipeng Huang,&nbsp;Jiaqi Hou,&nbsp;Yilie Liao,&nbsp;Jing Yu,&nbsp;Beidou Xi","doi":"10.1016/j.envint.2026.110406","DOIUrl":"10.1016/j.envint.2026.110406","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"214 ","pages":"Article 110406"},"PeriodicalIF":10.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148434419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parental ochratoxin A exposure induces multigenerational and transgenerational neurotoxicity and visual impairment in zebrafish","authors":"Meng Li,&nbsp;Yingqiu Mi,&nbsp;Zhenfeng Liao,&nbsp;Xijiao Song,&nbsp;Hongtao Zheng,&nbsp;Chenxi Li,&nbsp;Mengai He,&nbsp;Jiayin Hou,&nbsp;Xueli Yu,&nbsp;Liezhong Chen,&nbsp;Hua Fang","doi":"10.1016/j.envint.2026.110428","DOIUrl":"10.1016/j.envint.2026.110428","url":null,"abstract":"<div><div>Ochratoxin A (OTA), a ubiquitous mycotoxin detected in humans and animals, has attracted increasing concern owing to its potential health risks. However, its multigenerational and transgenerational neurotoxicity, visual impairment, and the underlying mechanisms remain largely unclear. In the present study, parental exposure to OTA (0, 10, and 100 ng/L) for 3 months induced developmental impairment in unexposed F1 larvae and provided evidence of parental OTA transfer. Whole-genome DNA methylation sequencing revealed that parental OTA exposure altered DNA methylation patterns in F1 larvae, characterized by disruptions in retinol metabolism, neurotransmitter homeostasis, and xenobiotic detoxification. Consistently, decreased dopamine, serotonin, and norepinephrine concentrations were observed in F1 larvae. Moreover, neurodevelopmental abnormalities, altered behaviors (increased swimming speed, anxiety-like behavior, social behavior deficits), and reduced lens size in F1 larvae indicated the multigenerational neurotoxicity and visual impairments of OTA. In F1 adults, 8-OHdG levels showed an upward trend, suggesting persistent multigenerational toxicity. Meanwhile, sex-dependent effects on thigmotaxis and social interaction were observed. Although the adverse effects on locomotor behavior and neurotransmitter levels were alleviated in F2 larvae, social behavior deficits and visual impairment were intensified, indicating the transgenerational toxicity of OTA. Overall, this study demonstrates, for the first time, the transgenerational neurotoxicity and visual impairment of OTA, and highlights the need for rigorous risk assessment of OTA exposure in unexposed offspring.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"214 ","pages":"Article 110428"},"PeriodicalIF":10.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148576349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A framework for risk assessment of plastic additives – Part 1: fundamental elements","authors":"Claire Doskey,&nbsp;Daniel E. Arrieta,&nbsp;Craig Warren Davis,&nbsp;Björn Hidding,&nbsp;Trent A. Key,&nbsp;Taryn Kirsch,&nbsp;Sander Koster,&nbsp;Erik Rushton,&nbsp;Satinder S. Sarang,&nbsp;Ursula G. Sauer,&nbsp;Thomas Stroheker,&nbsp;Antony J. Williams,&nbsp;Susanne N. Kolle,&nbsp;Heli Miriam Hollnagel","doi":"10.1016/j.envint.2026.110403","DOIUrl":"10.1016/j.envint.2026.110403","url":null,"abstract":"<div><div>There is a growing worldwide focus on evaluating the risk potential of substances associated with the manufacture and use of plastic, including the intentionally added constituents (additives) that impart specific technical functions as well as their transformation products. To enhance the consistent and effective evaluation of plastic additive uses, the European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC) is proposing a framework for risk assessment of plastic additives in complex scenarios. Here, the fundamental elements of the framework are presented, including an overview of available databases, tools and methodologies that enable the safety assessment of individual additives in plastic. The framework is comprised of five modules to identify and efficiently gather pertinent information. Data needs are tailored to the specific plastic additive and/or its major known transformation product(s) and to the scope of the risk assessment. As a risk-based approach, the five modules are pursued in an iterative, ‘circular’ manner. The risk assessment is terminated as soon as it is possible to either exclude risk potential or to characterise and manage any identified risks. While the framework for plastic additive risk assessment, as presented here, is applicable to individual plastic additives and/or their major known transformation products, it can be supplemented by further considerations for the assessment of aggregate or cumulative exposures and complex material cycles. Building thereupon, the second article by ECETOC shall present such further elements to consider when applying the framework for risk assessment of plastic additives at diverse recycling stages.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"214 ","pages":"Article 110403"},"PeriodicalIF":10.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148547307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Chemical structure drives developmental toxicity of alkyl-substituted naphthalenes in zebrafish” [Environ. Int. 204 (2025) 109837]","authors":"Mackenzie L. Morshead,&nbsp;Lisa Truong,&nbsp;Yijie Geng,&nbsp;Steven J. Carrell,&nbsp;Richard Scott,&nbsp;Kim A. Anderson,&nbsp;Robyn L. Tanguay","doi":"10.1016/j.envint.2026.110354","DOIUrl":"10.1016/j.envint.2026.110354","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"213 ","pages":"Article 110354"},"PeriodicalIF":10.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148238493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental exposure to perfluorooctanoic acid promotes early gastric carcinogenesis via PPAR-γ-mediated ferroptosis","authors":"Zhen Qi,&nbsp;Xuefei Yang,&nbsp;Ziqing Huang,&nbsp;Shi Chongwen,&nbsp;Fang Zhang","doi":"10.1016/j.envint.2026.110363","DOIUrl":"10.1016/j.envint.2026.110363","url":null,"abstract":"<div><div>Perfluorooctanoic Acid (PFOA) has gained our attention for it is resistant to natural degradation and can migrate over long distances. We have already found that PFASs were related to gastric cancer in previous work. However, the systematic evidence on the gastric toxicity of PFOA and its mechanisms remains scarce. In this study, network toxicology pinpointed the peroxisome proliferator-activated receptor (PPAR) pathway as the pivotal driver between PFOA exposure and gastric cancer progression. In the cell experiments, PPAR inhibitor (10 μM) and ferroptosis inhibitor (2 μM) protect gastric cells from ferroptosis induced by PFOA (200 ng L⁻¹). In the animal experiments, we set 3 PFOA concentrations (34.85 ng kg⁻¹ day⁻¹,1mg kg⁻¹ day⁻¹, 2.5 mg kg⁻¹ day⁻¹). Based on differential metabolic rate, the environmental dosage of PFOA in human was transferred to the lowest mice dosage. The RNA-seq analysis identified PPAR-γ as a differentially expressed gene. Compared with the normal group, the PFOA-L group of PPAR-γ decreased by 31.6%, the PFOA-M group of PPAR-γ decreased by 14.4%, and the PFOA-H group decreased by 46.8%. By organoid experiments, 5 days PFOA induced PPAR-γ downregulation and the increase of cancer marker P53. We elucidate that PFOA disrupts the PPAR-γ axis to induce gastric cancer progression, highlighting an overlooked gastric liability in PFOA health risk assessments.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"213 ","pages":"Article 110363"},"PeriodicalIF":10.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148256569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “High-throughput screening of ancient forest plant extracts shows cytotoxicity towards triple-negative breast cancer” [Environ. Int. 181 (2023) 108279]","authors":"Yiyang Li,&nbsp;Nyuk Ling Ma,&nbsp;Huiling Chen,&nbsp;Jiateng Zhong,&nbsp;Dangquan Zhang,&nbsp;Wanxi Peng,&nbsp;Su Shiung Lam,&nbsp;Yafeng Yang,&nbsp;Xiaochen Yue,&nbsp;Lijun Yan,&nbsp;Ting Wang,&nbsp;Bjarne Styrishave,&nbsp;Tomasz Maciej Ciesielski,&nbsp;Christian Sonne","doi":"10.1016/j.envint.2026.110362","DOIUrl":"10.1016/j.envint.2026.110362","url":null,"abstract":"","PeriodicalId":308,"journal":{"name":"Environment International","volume":"213 ","pages":"Article 110362"},"PeriodicalIF":10.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148269617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}