Ecotoxicology and Environmental Safety最新文献_第6页

A comprehensive review on environmental dynamics of chlorpyrifos: Fate, toxicity, remediation, and regulatory aspects 毒死蜱的环境动态：命运、毒性、修复和监管方面的综合综述。

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119484

Saad Ahmed Sami , Bakul Akter , Md. Nipatul Hasan Nirob , Ishrat Jahan , Md. Lokman , Mst. Hajera Khatun , Mohammed Kamrul Hossain , Jaytirmoy Barmon

Chlorpyrifos is a broad-spectrum organophosphate insecticide which has raised environmental concerns due to its persistence, toxicity and global distribution. This review aims to elucidate the environmental nature of chlorpyrifos by discussing its environmental fate, toxicity, remediation options, and regulatory advancements from published articles within 1991–2025. Ecologically, chlorpyrifos is highly adsorptive to soil with moderate persistence, depending on temperature, microbial action, and photolytic degradation. Its major breakdown product 3,5,6-trichloro-2-pyridinol (TCP) is more water soluble than the parent compound and prone to groundwater contamination. Being an acetylcholinesterase inhibitor, it initiates neurological damage in both humans and animals. At acute exposures, it causes cholinergic symptoms and at low levels, it causes cognitive deficits, developmental delays, and behaviour problems over sustained periods of time. To alleviate the environmental effects, remediation strategies namely microbial bioremediation of chlorpyrifos using bacteria has been most promising globally. Controlled-release technology, biopesticides and advanced oxidation processes are also greatly considered for remediation in soil and water. Regulatory actions have escalated with mounting scientific evidence. This insecticide has been banned or restricted in many countries, including the United States and the European Union. Nevertheless, it is still used in a number of low- and middle-income countries, raising global health and environmental equity issues. In contrast to existing review, this article highlights the importance of more effective remediation strategies, rigorous international regulations and the implementation of safer alternatives and integrated pest management (IPM) approaches to mitigate both ecological and human health risks.

毒死蜱是一种广谱有机磷杀虫剂，由于其持久性、毒性和全球分布而引起了环境问题。本综述旨在通过讨论毒死蜱的环境命运、毒性、补救方案和1991-2025年间发表的法规进展来阐明毒死蜱的环境性质。在生态学上，毒死蜱对土壤具有高度的吸附性，并具有中等持久性，这取决于温度、微生物作用和光解降解。其主要分解产物3,5,6-三氯-2-吡啶醇（TCP）比母体化合物更易溶于水，容易受到地下水污染。作为一种乙酰胆碱酯酶抑制剂，它会对人类和动物造成神经损伤。在急性暴露时，它会引起胆碱能症状，在低水平暴露时，它会在持续的一段时间内引起认知缺陷、发育迟缓和行为问题。为了减轻毒死蜱对环境的影响，利用细菌对毒死蜱进行微生物修复是目前全球范围内最具发展前景的修复策略。控释技术、生物农药和高级氧化工艺也被广泛用于土壤和水的修复。随着越来越多的科学证据，监管行动已经升级。这种杀虫剂在包括美国和欧盟在内的许多国家已被禁止或限制使用。然而，它仍然在一些低收入和中等收入国家使用，引发了全球健康和环境公平问题。与现有的综述相反，本文强调了更有效的补救策略、严格的国际法规以及实施更安全的替代品和有害生物综合治理（IPM）方法的重要性，以减轻生态和人类健康风险。

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引用次数: 0

F-53B-induced placental vascular endothelial dysfunction leads to intrauterine growth retardation of fetal mice f - 53b诱导的胎盘血管内皮功能障碍导致胎鼠宫内生长迟缓。

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119467

Ping Guo , Xianjie Li , Shuai Wang , Jianqiang Gan , Jing Zhang , Jinfeng Gao , Yirui Yang , Dan Cai , Caixia Wu

Chlorinated polyfluoroalkyl ether sulfonic acid (Cl-PFESAs, trade name F-53B) is a perfluorinated compound substitute whose concentration in the placenta is negatively correlated with neonatal weight, yet its toxic mechanism remains unclear. In this study, pregnant C57BL/6 mice were orally administered with 5, 50, and 500 μg/kg of F-53B from gestational days 0.5 to 17.5. By integrating in vivo imaging and laser scattering imaging, we found that F-53B exposure resulted in increased placental barrier permeability and reduced maternal-fetal blood perfusion, which may underline the observed fetal growth retardation. Pathological and immunofluorescence examination revealed that F-53B may trigger the endothelial-to-mesenchymal transition (EndMT) in the placental labyrinth vasculature. Combining RNA sequencing and trophoblast-endothelial cell co-culture experiments, we identified EndMT induced placental vascular injury as a key mechanism in F-53B induced fetal growth retardation, potentially initiated by interfered pro-angiogenic function of trophoblasts. Our results indicate that EndMT driven placental vascular injury is a key event in F-53B-induced fetal growth restriction, providing a new perspective on the developmental toxicity mechanism of F-53B.

氯化多氟烷基醚磺酸（Cl-PFESAs，商品名F-53B）是一种全氟化合物替代品，其在胎盘中的浓度与新生儿体重呈负相关，但其毒性机制尚不清楚。在本研究中，怀孕的C57BL/6小鼠在妊娠0.5 ~ 17.5天分别口服5、50和500 μg/kg的F-53B。结合体内成像和激光散射成像，我们发现F-53B暴露导致胎盘屏障通透性增加，母胎血液灌注减少，这可能强调了所观察到的胎儿生长迟缓。病理和免疫荧光检查显示，F-53B可能触发胎盘迷宫室血管内皮向间质转化（EndMT）。结合RNA测序和滋养层内皮细胞共培养实验，我们发现EndMT诱导的胎盘血管损伤是F-53B诱导胎儿生长迟缓的关键机制，可能是由滋养层细胞的促血管生成功能受到干扰引起的。我们的研究结果表明，EndMT驱动的胎盘血管损伤是F-53B诱导的胎儿生长限制的关键事件，为F-53B的发育毒性机制提供了新的视角。

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引用次数: 0

Cadmium exposure upregulates TXNIP and aggravates calcium oxalate kidney stone formation by promoting cell-crystal adhesion, apoptosis and macrophage M1 polarization 镉暴露通过促进细胞晶体粘附、细胞凋亡和巨噬细胞M1极化，上调TXNIP，加重草酸钙肾结石形成。

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119481

Heng Xiang , Yijun Yang , Liang Chen , Ziqi He , Qixuan Zhou , Caitao Dong , Qinhong Jiang , Qingfeng Chen , Xiaozhe Su , Sixing Yang

We systematically evaluated how cadmium (Cd) exposure synergizes with calcium oxalate (CaOx) to promote kidney stone formation and renal injury, focusing on the central role of thioredoxin-interacting protein (TXNIP). Clinical kidney stones, in vitro assays, and mouse models were analyzed. X-ray diffraction and inductively coupled plasma analysis confirmed cadmium accumulation in stones. In vitro, cadmium chloride altered CaOx crystal morphology, surface energy, and zeta potential, enhancing crystal adhesion, deposition, and aggregation on renal epithelial cells. Transcriptomic sequencing and bioinformatic enrichment identified pathways activated by combined Cd and CaOx exposure. In a murine kidney stone model, co-exposure increased renal crystal deposition, fibrosis, inflammation, and functional impairment. Tubular epithelial cells exhibited elevated CXCL5 secretion, promoting macrophage chemotaxis and polarization toward a pro-inflammatory M1 phenotype, thereby establishing a fibrogenic microenvironment. TXNIP was markedly upregulated; its knockdown reduced crystal adhesion, M1 polarization, activation of the ASK1–JNK–Caspase-3 apoptotic pathway, interstitial fibrosis, and tubular apoptosis, preserving renal function. These findings reveal that cadmium accelerates CaOx stone formation and kidney injury by driving a TXNIP-mediated oxidative stress–inflammation–apoptosis axis. Targeting TXNIP may offer a novel therapeutic strategy to disrupt this pathogenic feedback loop and prevent toxin-associated kidney stones and renal damage.

我们系统地评估了镉（Cd）暴露如何与草酸钙（CaOx）协同促进肾结石形成和肾损伤，重点研究了硫氧还蛋白相互作用蛋白（TXNIP）的核心作用。对临床肾结石、体外实验和小鼠模型进行分析。x射线衍射和电感耦合等离子体分析证实了镉在石头中的积累。在体外，氯化镉改变CaOx晶体形态、表面能和zeta电位，增强晶体在肾上皮细胞上的粘附、沉积和聚集。转录组测序和生物信息学富集鉴定了Cd和CaOx联合暴露激活的途径。在小鼠肾结石模型中，共暴露增加了肾脏晶体沉积、纤维化、炎症和功能损害。小管上皮细胞表现出CXCL5分泌升高，促进巨噬细胞趋化和向促炎M1表型极化，从而建立成纤维微环境。TXNIP明显上调；其敲除可减少晶体粘附、M1极化、ASK1-JNK-Caspase-3凋亡通路的激活、间质纤维化和小管凋亡，从而保护肾功能。这些发现表明，镉通过驱动txnip介导的氧化应激-炎症-凋亡轴加速CaOx结石形成和肾损伤。靶向TXNIP可能提供一种新的治疗策略来破坏这种致病反馈回路，预防毒素相关性肾结石和肾损害。

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引用次数: 0

Human cardiac organoids highlight cardiotoxicity of the tire rubber antioxidant 6PPD 人类心脏类器官突出了轮胎橡胶抗氧化剂6PPD的心脏毒性。

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119496

Sung-Ae Hyun , Ji-Hye Park , Moon Yi Ko , Euijun Min , Minjeong Kim , Sun-Woong Kang , Minhan Ka

N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD), a tire rubber antioxidant and environmental contaminant, poses potential human cardiovascular health risks. However, these remain poorly understood. In this study, we established human induced pluripotent stem-cell–derived cardiac organoids (hiPSC-COs) to evaluate 6PPD cardiotoxicity. The organoids exhibited mature cardiac characteristics, containing multiple cell types, including cardiomyocytes, smooth muscle cells, and cardiac fibroblasts. There was also robust expression of cardiac structural and electrophysiological markers. 6PPD exposure induced concentration-dependent cytotoxicity and apoptosis, with increased cleaved caspase-3 and Bax expression with concurrent BCL2 suppression. Sub-cytotoxic concentrations disrupted cardiac electrophysiology within 60 min, causing tachycardia and shortened field potential duration that persisted at 24 h. Transcriptomic profiling showed dose-dependent molecular responses. 10 μM 6PPD activated DNA damage responses while suppressing cardiac contractile genes. Meanwhile, 100 μM triggered endoplasmic reticulum stress, autophagy, and apoptosis alongside disrupted calcium homeostasis and cardiac development programs. 6PPD induces multifaceted cardiotoxicity with functional impairment occurring below cytotoxic thresholds, highlighting the potential cardiovascular risks from environmental exposure and establishing hiPSC-COs as a valuable platform for environmental cardiotoxicant assessment.

N-（1,3-二甲基丁基）-N'-苯基-对苯二胺（6PPD）是一种轮胎橡胶抗氧化剂和环境污染物，具有潜在的心血管健康风险。然而，人们对这些仍然知之甚少。在这项研究中，我们建立了人类诱导多能干细胞衍生的心脏类器官（hiPSC-COs）来评估6PPD的心脏毒性。类器官表现出成熟的心脏特征，包含多种细胞类型，包括心肌细胞、平滑肌细胞和心脏成纤维细胞。心脏结构和电生理标志物也有很强的表达。6PPD暴露诱导浓度依赖性细胞毒性和细胞凋亡，cleaved caspase-3和Bax表达增加，同时BCL2抑制。亚细胞毒性浓度在60 min内破坏心脏电生理，导致心动过速和持续24 h的缩短场电位持续时间。转录组学分析显示剂量依赖性分子反应。10 μM 6PPD激活DNA损伤反应，同时抑制心脏收缩基因。同时，100 μM触发内质网应激、自噬和凋亡，同时破坏钙稳态和心脏发育程序。6PPD诱导多方面的心脏毒性，并发生低于细胞毒性阈值的功能损害，突出了环境暴露的潜在心血管风险，并将hiPSC-COs建立为环境心脏毒性评估的有价值平台。

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引用次数: 0

Perinatal BPS exposure induces offspring neurotoxicity via ferroptosis mediated by the SLC7A11/GPX4 pathway 围产期BPS暴露通过SLC7A11/GPX4途径介导的铁下垂诱导子代神经毒性

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119489

Xinxin Guo , Meilin Qin , Kaixing Lin , Mengfen Pan , Nuo Xu , Yan Su , Zhensong Ma , Haozhe Zhou , Huaicai Zeng

Bisphenol S (BPS), a common substitute for bisphenol A, has raised considerable concern due to its potential neurotoxicity. However, the understanding of generational effect of BPS on neurotoxic effect is still unclear. Herein, parental pregnant mice and HT22 cells were exposed to varying BPS concentrations to investigate its neurotoxicity on offspring mice and explore the role of ferroptosis in this process. These results revealed a spatial memory and synaptic impairment in offspring mice after early BPS exposure, characterized by hippocampal pathological damage and decreased expression of PSD95, SYP, and BDNF. as evidenced by increased lipid peroxidation, iron accumulation, disrupted mitochondrial ultrastructure, and altered expression of ferroptosis-related proteins (SLC7A11, GPX4, FTH1, and ACSL4). Furthermore, Fer-1 pre-treatment mitigated lipid peroxidation and iron overload while restoring the expression of SLC7A11, GPX4, PSD95, and SYP in HT22 cells. Collectively, our results demonstrate that perinatal BPS exposure causes neurotoxicity in offspring, which is mediated by ferroptosis through the SLC7A11/GPX4 pathway. This report lays the foundation investigating the correlation between BPS neurotoxicity and ferroptosis, and offers novel insights for assessing the multigenerational toxicity of BPS.

双酚S （BPS）是一种常见的双酚a替代品，由于其潜在的神经毒性而引起了相当大的关注。然而，对BPS对神经毒性作用的代际效应的理解仍不清楚。本研究将不同浓度的BPS暴露于亲代妊娠小鼠和HT22细胞，研究其对子代小鼠的神经毒性，并探讨铁凋亡在这一过程中的作用。这些结果表明，早期BPS暴露后，后代小鼠的空间记忆和突触功能受损，其特征是海马病理损伤，PSD95、SYP和BDNF的表达降低。这可以通过脂质过氧化、铁积累、线粒体超微结构破坏和铁中毒相关蛋白（SLC7A11、GPX4、FTH1和ACSL4）表达改变来证明。此外，fe -1预处理减轻了脂质过氧化和铁超载，同时恢复了HT22细胞中SLC7A11、GPX4、PSD95和SYP的表达。总的来说，我们的研究结果表明围产期BPS暴露会导致后代神经毒性，这是通过SLC7A11/GPX4途径由铁中毒介导的。本报告为研究BPS神经毒性与铁下垂之间的相关性奠定了基础，并为评估BPS的多代毒性提供了新的见解。

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引用次数: 0

Associations of per- and polyfluoroalkyl substances and alternatives with thyroid hormones in pregnant women: A cross-sectional study in China 全氟烷基和多氟烷基物质及其替代品与孕妇甲状腺激素的关系：中国的一项横断面研究。

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119498

Chenyang Liu , Simeng Gu , Fanjia Guo , Guangming Mao , Yuanyang Wang , Peiwei Xu , Xueqing Li , Yahui Li , Zhijian Chen , Xiaofeng Wang , Xiaoming Lou , Zhe Mo

Per- and polyfluoroalkyl substances (PFAS) have been recognized as potential disruptors of thyroid function, but the health implications of their increasingly used emerging alternatives, particularly during pregnancy, remain poorly understood. To address this, we conducted a cross-sectional study involving 492 pregnant women in Zhejiang, China, quantifying thirty PFAS and three thyroid hormones and employing advanced statistical models to assess their associations. The study findings revealed that exposure to perfluorododecanoic acid (PFDoDA) was associated with a 6.37 % decrease in free 3,5,3’,5’-tetraiodothyronine (FT4), exposure to perfluoro-2-methoxyacetic acid (PFMOAA) resulted in a 32.52 % increase in thyroid stimulating hormone (TSH) and a 2.33 % decrease in FT4, and exposure to 8:2 Chlorinated polyfluorinated ether sulfonic acid (8:2 Cl-PFESA) led to a 28.46 % increase in TSH. Quantile g-computation (Qgcomp) models demonstrated a significant 21.04 % increase in TSH (95 % CI: 3.11 %, 42.09 %) association with PFAS mixtures, with 8:2 Cl-PFESA (0.25) and PFMOAA (0.23) showing the highest positive weights. These findings were further corroborated by the adaptive elastic net (AENET) models, which confirmed the positive correlation between PFAS mixtures and TSH. Bayesian statistics-based benchmark dose (BBMD) analyses indicated that 8:2 Cl-PFESA (0.01 ng/mL), PFMOAA (0.02 ng/mL), and PFDoDA (0.42 ng/mL) might possess lower safety margin levels for thyroid disruption, warranting more stringent regulatory standards. These findings highlight the necessity of conducting routine biomonitoring and further exploration into the toxicological mechanisms of the emerging PFAS alternatives to address the potential health risks.

全氟烷基和多氟烷基物质（PFAS）已被认为是甲状腺功能的潜在干扰物，但越来越多地使用它们的新兴替代品对健康的影响，特别是在怀孕期间，仍然知之甚少。为了解决这个问题，我们对中国浙江的492名孕妇进行了一项横断面研究，量化了30种PFAS和3种甲状腺激素，并采用先进的统计模型来评估它们之间的关联。研究结果显示，暴露于全氟十二烷酸（PFDoDA）与游离3,5,3',5'-四碘甲状腺原氨酸（FT4）减少6.37% %有关，暴露于全氟2-甲氧基乙酸（PFMOAA）导致促甲状腺激素（TSH）增加32.52% %，FT4减少2.33% %，暴露于8:2氯化多氟醚磺酸（8:2 Cl-PFESA）导致TSH增加28.46% %。分位数g计算（Qgcomp）模型显示，与PFAS混合物相关的TSH显著增加21.04 %(95 % CI: 3.11 %,42.09 %)，其中8:2 Cl-PFESA（0.25）和PFMOAA（0.23）的阳性权重最高。自适应弹性网（AENET）模型进一步证实了PFAS混合物与TSH之间的正相关。基于贝叶斯统计的基准剂量（BBMD）分析表明，8:2 Cl-PFESA（0.01 ng/mL）、PFMOAA（0.02 ng/mL）和PFDoDA（0.42 ng/mL）可能具有较低的甲状腺功能障碍安全裕度水平，需要更严格的监管标准。这些发现强调了进行常规生物监测和进一步探索新兴PFAS替代品的毒理学机制以解决潜在健康风险的必要性。

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引用次数: 0

Metabolic modulation by antibiotic levofloxacin alters Cis-bifenthrin-induced neurotoxicity in amphibian tadpoles 抗生素左氧氟沙星代谢调节改变顺式联苯菊酯诱导的两栖动物蝌蚪神经毒性。

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119480

Yuqing Ma , Tingting Liu , Lei Huang , Xiyu Zhang , Wenjing Wang , Mengcen Wang , Qiangwei Wang

Synthetic pyrethroids (SPs) and fluoroquinolones (FQs) are widely detected in aquatic environments and food chains, raising growing concern over their combined toxicity. However, the interaction between antibiotics and pesticides, particularly through host metabolism and microbiota, remains poorly understood. In this study, we investigated how the antibiotic levofloxacin (LEV) modulates cis-bifenthrin (cis-BF)-induced neurotoxicity in Xenopus laevis tadpoles. A 21-day co-exposure significantly impaired growth and locomotor behavior. Brain metabolomics revealed depletion of neuroprotective lipids (FAHFAs, PUFAs) and accumulation of potentially harmful organic acids and heterocycles. Transcriptomic analysis showed dysregulation of lipid metabolism, inflammation, and amino acid pathways. Given that LEV is a broad-spectrum antibiotic known to perturb gut microbiota composition, we speculated that its protective effects against cis-BF-induced neurotoxicity might involve modulation of the microbiota–gut–brain axis. Based on biochemical assays of intestinal tissues, LEV was found to mitigate cis-BF-induced oxidative stress and intestinal inflammation. However, 16S rRNA sequencing demonstrated microbiota alterations affecting SCFA- and amino acid- producing genera. Functional microbial shifts paralleled changes in brain metabolites, suggesting a microbiota-metabolism-neurotoxicity axis. This study demonstrates that although antibiotics can alleviate pesticide-induced intestinal inflammation, they concurrently exacerbate neurotoxicity, as evidenced by significant alterations in brain metabolites, transcriptomic profiles, and neurotransmitter levels. These findings highlight the complexity of microbial-metabolic interactions in environmental toxicology and the need for further investigation into their causal roles.

合成拟除虫菊酯（SPs）和氟喹诺酮类（FQs）广泛存在于水生环境和食物链中，引起了人们对其综合毒性的日益关注。然而，抗生素和农药之间的相互作用，特别是通过宿主代谢和微生物群，仍然知之甚少。在这项研究中，我们研究了抗生素左氧氟沙星（LEV）如何调节顺式联苯菊酯（cis-BF）诱导的非洲爪蟾蝌蚪神经毒性。21天的共暴露显著损害了生长和运动行为。脑代谢组学显示神经保护脂质（FAHFAs, PUFAs）的消耗和潜在有害有机酸和杂环化合物的积累。转录组学分析显示脂质代谢、炎症和氨基酸途径失调。鉴于LEV是一种已知会扰乱肠道微生物群组成的广谱抗生素，我们推测其对顺式bf诱导的神经毒性的保护作用可能涉及调节微生物-肠-脑轴。通过对肠道组织的生化分析发现，LEV可减轻顺式bf诱导的氧化应激和肠道炎症。然而，16S rRNA测序显示，微生物群的改变影响了产生SCFA和氨基酸的属。功能性微生物的变化与脑代谢物的变化是平行的，表明存在微生物-代谢-神经毒性轴。这项研究表明，尽管抗生素可以减轻农药引起的肠道炎症，但它们同时加剧了神经毒性，这一点可以通过脑代谢物、转录组谱和神经递质水平的显著改变来证明。这些发现强调了环境毒理学中微生物-代谢相互作用的复杂性，以及进一步研究其因果作用的必要性。

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引用次数: 0

Hydrogeochemical impacts of coal mining on multi-aquifer systems: A case study in the Linhuan Mining District, China 煤矿开采对多含水层系统的水文地球化学影响——以临环矿区为例

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119492

Qiding Ju, Youbiao Hu, Qimeng Liu

Coal mining activities present significant threats to groundwater quality in multi-aquifer systems. This study examines the hydrogeochemical processes and evolutionary pathways induced by mining operations in the Linhuan mining district, located in the Huaibei coalfield, China. Through a combination of mineralogical analysis, hydrogeochemical data, and inverse geochemical modelling, carbonate minerals, gypsum, and clay minerals were identified as the primary reactants, with dissolution/precipitation of minerals, sulfate reduction, and cation exchange as the predominant processes. The modelling results revealed three distinct runoff patterns: (1) fault-controlled recharge from shallow-to-intermediate aquifers to mine water, (2) anticline-guided recharge from shallow-to-deep aquifers to limestone water, and (3) mining-induced recharge to shallow unconsolidated aquifers. These processes facilitate interactions between loose pore water, coal-bearing sandstone water, and limestone water. Therefore, rising water levels in abandoned mines could exacerbate flooding risks and foster cross-aquifer contamination, thereby posing a significant threat to the pristine Carboniferous limestone aquifer. This study provides invaluable insights for predicting the evolution of water quality and for informing water resource management in this and other mining regions characterised by complex hydrogeological conditions.

煤矿开采活动对多含水层系统的地下水质量构成重大威胁。本文研究了淮北煤田临环矿区开采过程中水文地球化学过程及其演化路径。通过矿物学分析、水文地球化学数据和逆地球化学模拟相结合，确定碳酸盐矿物、石膏和粘土矿物为主要反应物，矿物的溶解/沉淀、硫酸盐还原和阳离子交换是主要过程。模拟结果揭示了三种不同的径流模式：(1)断层控制的浅层到中层含水层向矿井水补给，(2)背斜引导的浅层到深层含水层向石灰岩水补给，以及(3)开采诱导的浅层松散含水层补给。这些过程促进了松散孔隙水、含煤砂岩水和石灰岩水之间的相互作用。因此，废弃矿井水位上升可能加剧洪水风险，并造成跨含水层污染，从而对原始石炭系石灰岩含水层构成重大威胁。这项研究为预测水质的演变提供了宝贵的见解，并为该地区和其他具有复杂水文地质条件的矿区的水资源管理提供了信息。

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引用次数: 0

Cadmium sub-lethal effects on Daphnia magna – A new take on an old subject 镉对大水蚤的亚致死效应——一个老课题的新进展

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119487

Albano Pinto , Inês P.E. Macário , Guilherme Jeremias , Sérgio M. Marques , Joana Lourenço , Ana Rita Guimarães , Sofia L. Marques , Gabriela Moura , Jana Asselman , Patrícia Pereira , Joana L. Pereira

Rising production and use of electronic products leads to higher cadmium usage, increasing the risk of exposure to this dangerous metal. Despite being a classic environmental contaminant, cadmium’s full toxicity spectrum and mechanisms of action towards aquatic biota are still in need of further clarification. This work contributes to such clarification by comprehensively characterizing cadmium mechanisms of toxic action resulting from a seven-day exposure to a sub-lethal concentration (EC20; 4.5 µg L^-1) on the freshwater species Daphnia magna. A holistic approach starting at molecular level responses with epigenetic endpoints (total DNA methylation and DNA methyltransferases activity) and transcriptomic analysis (RNA-Seq), then working up to phenotypic effects at the sub-cellular and individual level was applied. Cadmium exposure caused global genome hypomethylation and altered DNA methyltransferases activity. These methylome changes were accompanied by significant changes in gene expression, that correlate with the observed phenotypic effects. A significant increase in the activity of the main antioxidant enzymes, lipid peroxidation levels and DNA damage was recorded, along with a reduction in heart rate and somatic growth in exposed organisms. These findings provide new insights into cadmium lesser-known effects spanning multiple levels of biological organization in D. magna even at a low environmentally relevant concentration.

电子产品生产和使用的增加导致镉的使用量增加，增加了接触这种危险金属的风险。尽管镉是一种典型的环境污染物，但其全毒性谱及其对水生生物的作用机制仍有待进一步阐明。这项工作通过全面表征镉对淡水物种大水蚤（Daphnia magna）暴露于亚致死浓度（EC20; 4.5 μ g L-1） 7天的毒性作用机制，有助于澄清这一问题。采用整体方法，从表观遗传端点（总DNA甲基化和DNA甲基转移酶活性）和转录组分析（RNA-Seq）的分子水平反应开始，然后在亚细胞和个体水平上研究表型效应。镉暴露导致全球基因组低甲基化和DNA甲基转移酶活性改变。这些甲基组变化伴随着基因表达的显著变化，这与观察到的表型效应相关。主要抗氧化酶的活性、脂质过氧化水平和DNA损伤显著增加，同时暴露的生物体的心率和躯体生长也有所下降。这些发现为即使在低环境相关浓度下，镉在D. magna中跨越多个生物组织水平的鲜为人知的影响提供了新的见解。

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引用次数: 0

High-temperature exposure impairs cognitive function by disrupting the gut-brain axis: Evidence from human and rat studies 高温暴露通过破坏肠-脑轴损害认知功能：来自人类和大鼠研究的证据。

IF 6.1 2区环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES

Ecotoxicology and Environmental Safety

Pub Date : 2025-12-01 DOI: 10.1016/j.ecoenv.2025.119500

Lai-Bao Zhuo , Jie Zhao , Weidong Wu , Yu-ming Chen , Zhen Yan

Background

To investigate the impact of high temperature (HT) exposure on cognitive function in humans and rats, focusing on the gut-brain axis as a potential mediating pathway.

Methods

The study population was derived from the Guangzhou Nutrition and Health Study, with cognitive function assessed using the Addenbrooke's Cognitive Examination Revised (ACE-R) scale. HT exposure was defined as exposure for more than one year during the career. In animal experiments, 36 male Sprague Dawley rats were exposed to controlled temperatures (25°C, 30°C, 35°C, and 40°C) for four hours daily over 15 days. Cognitive function was evaluated using the Morris Water Maze (MWM) test. Neurodegeneration, glial activation, neuroinflammation, intestinal barrier function and inflammation were evaluated by Western blot, Elisa, immunohistochemistry and immunofluorescence staining. 16S rRNA sequencing was employed to profile the gut microbiota. Targeted metabolomics analysis was conducted using gas chromatography-mass spectrometry to quantify short-chain fatty acids (SCFAs) in fecal samples.

Results

Human participants in the HT group exhibited significantly lower ACE-R and memory scores compared to controls. Similarly, HT exposure in rats led to a notable decline in spatial learning and memory, accompanied by damage to hippocampal neurons. Further examinations revealed that HT exposure disrupted intestinal homeostasis, characterized by a reduced abundance of SCFA-producing bacteria and decreased SCFA levels in the intestines. This disruption was accompanied by intestinal inflammation, compromised intestinal barrier integrity, and neuroinflammation.

Conclusion

This study suggests that HT exposure may negatively impact cognitive function through mechanisms potentially involving the gut-brain axis, offering insights into possible underlying biological pathways.

背景：研究高温暴露对人类和大鼠认知功能的影响，重点研究肠-脑轴作为一种潜在的介导途径。方法：研究人群来自广州营养与健康研究，使用阿登布鲁克认知检查（ACE-R）量表评估认知功能。高温辐射暴露定义为在职业生涯中暴露超过一年。在动物实验中，将36只雄性Sprague Dawley大鼠置于控制温度（25°C、30°C、35°C和40°C）下，每天4小时，持续15天。采用Morris水迷宫（MWM）测验评估认知功能。采用Western blot、Elisa、免疫组化、免疫荧光染色评价神经变性、神经胶质活化、神经炎症、肠屏障功能和炎症。采用16S rRNA测序分析肠道微生物群。采用气相色谱-质谱联用技术对粪便样品中的短链脂肪酸（SCFAs）进行靶向代谢组学分析。结果：与对照组相比，HT组的人类参与者表现出明显较低的ACE-R和记忆评分。同样，暴露在高温下的大鼠空间学习和记忆能力显著下降，并伴有海马神经元损伤。进一步的检查显示，高温暴露破坏了肠道内的稳态，其特征是产生SCFA的细菌丰度减少，肠道内SCFA水平降低。这种破坏伴随着肠道炎症、肠屏障完整性受损和神经炎症。结论：本研究表明，HT暴露可能通过可能涉及肠-脑轴的机制对认知功能产生负面影响，为可能的潜在生物学途径提供了见解。

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引用次数: 0