Pub Date : 2026-03-15Epub Date: 2026-03-12DOI: 10.1016/j.ecoenv.2026.119990
Joelithon de Lima Costa , Jose Manuel Martínez , Nuria Rodríguez , Fabrício Motteran , Lourdinha Florêncio , Mario Takayuki Kato , Ricardo Amils , José Luis Sanz
Nitrogen and iron are central to Earth’s biogeochemical cycles. The Iberian Pyrite Belt (IPB), a vast iron reservoir, hosts extremophilic microorganisms adapted to high metal and sulfur concentrations. This study investigates two isolates from the deep IPB subsurface, Citrobacter telavivensis T1.2D-1 and Stutzerimonas stutzeri T2.31D-1, evaluating their nitrate-reducing capacity and the role of iron in denitrification, with emphasis on nitrate-dependent ferrous iron oxidation (NDFO). Both species could reduce nitrate in sucrose-, lactate-, or acetate-fed medium, while their consortium enhanced nitrate consumption and biomass production. Genome analysis revealed no genes for iron (II) oxidation, yet NDFO likely occurs, as proposed, via a heterotrophic-lithotrophic mechanism: enzymatic nitrate reduction to nitrite, followed by abiotic iron (II) oxidation that converts nitrite to nitric oxide and then to nitrous oxide. This is particularly relevant for C. telavivensis, which can perform only of the first reduction step. Experimentally, iron sometimes inhibited nitrate consumption, likely because it accumulated in crusts on bacterial cells. However, extracellular polymeric substances (EPS) production could reduce iron toxicity and allow iron to act beneficially by supporting microbial activity, as observed with sucrose supplementation. Ecologically, nitrate reducers may significantly influence IPB subsurface cycles. Even lacking iron (II) oxidation genes, these bacteria could contribute to pyrite bioleaching through: (i) chemical attack by NDFO-generated iron (III), (ii) organic acids produced by metabolism, or (iii) yet undescribed mechanisms. Overall, these findings highlight the adaptive strategies and potential environmental roles of these nitrate-reducing microorganisms in the IPB subsurface.
{"title":"Nitrate reduction and iron (II) oxidation by subsurface bacteria from the Iberian Pyritic Belt: Insights into the biogeochemical cycles in this environment","authors":"Joelithon de Lima Costa , Jose Manuel Martínez , Nuria Rodríguez , Fabrício Motteran , Lourdinha Florêncio , Mario Takayuki Kato , Ricardo Amils , José Luis Sanz","doi":"10.1016/j.ecoenv.2026.119990","DOIUrl":"10.1016/j.ecoenv.2026.119990","url":null,"abstract":"<div><div>Nitrogen and iron are central to Earth’s biogeochemical cycles. The Iberian Pyrite Belt (IPB), a vast iron reservoir, hosts extremophilic microorganisms adapted to high metal and sulfur concentrations. This study investigates two isolates from the deep IPB subsurface, <em>Citrobacter telavivensis</em> T1.2D-1 and <em>Stutzerimonas stutzeri</em> T2.31D-1, evaluating their nitrate-reducing capacity and the role of iron in denitrification, with emphasis on nitrate-dependent ferrous iron oxidation (NDFO). Both species could reduce nitrate in sucrose-, lactate-, or acetate-fed medium, while their consortium enhanced nitrate consumption and biomass production. Genome analysis revealed no genes for iron (II) oxidation, yet NDFO likely occurs, as proposed, via a heterotrophic-lithotrophic mechanism: enzymatic nitrate reduction to nitrite, followed by abiotic iron (II) oxidation that converts nitrite to nitric oxide and then to nitrous oxide. This is particularly relevant for <em>C. telavivensis</em>, which can perform only of the first reduction step. Experimentally, iron sometimes inhibited nitrate consumption, likely because it accumulated in crusts on bacterial cells. However, extracellular polymeric substances (EPS) production could reduce iron toxicity and allow iron to act beneficially by supporting microbial activity, as observed with sucrose supplementation. Ecologically, nitrate reducers may significantly influence IPB subsurface cycles. Even lacking iron (II) oxidation genes, these bacteria could contribute to pyrite bioleaching through: (i) chemical attack by NDFO-generated iron (III), (ii) organic acids produced by metabolism, or (iii) yet undescribed mechanisms. Overall, these findings highlight the adaptive strategies and potential environmental roles of these nitrate-reducing microorganisms in the IPB subsurface.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 119990"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147451929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-15Epub Date: 2026-03-14DOI: 10.1016/j.ecoenv.2026.120027
Lu Liu , Yongchang Chen , Wenying Lin , Mian Zheng , Tianqi Yu , Ruyan Chen , Yanru Yang , Lingling Jiao , Qinli Ruan , Jia Sun
Phthalate esters (PAEs), the most prevalent class of plasticizers, are widely acknowledged as environmental endocrine disruptors (EDCs) and have been linked to the pathogenesis of various diseases. However, their specific role and intrinsic mechanism in inducing cartilage damage in bone-related diseases remain unclear. This study aimed to clarify the correlation between PAEs and cartilage damage, and to explore their potential molecular mechanisms. The core pathological change of knee osteoarthritis (KOA) is the progressive degeneration of articular cartilage. Based on this, this study first systematically explored the association between PAEs and KOA using network toxicology combined with molecular docking technology, and screened out core regulatory molecules including MMP9, EGFR, IL-10, BCL2, and CASP3. Subsequently, verification experiments on core molecules showed that PAEs exposure could activate the CASP3 pathway to induce apoptosis of human chondrocytes and significantly promote the formation of the inflammatory phenotype of chondrocytes.
To further reveal the underlying mechanism, we conducted proteomic analysis and cell experiments in human articular chondrocytes (HCs). The results showed that exposure to PAEs triggered reprogramming of glycolysis metabolism, inhibited oxidative phosphorylation, and damaged mitochondrial homeostasis. Collectively, this study provides a robust theoretical basis for understanding the inflammatory phenotypes and underlying mechanisms of chondrocyte damage driven by PAEs exposure, and further lays a foundation for the design of novel therapeutic interventions and the optimization of environmental toxicity assessment protocols targeting PAEs.
{"title":"Glycolytic metabolic reprogramming and mitochondrial dysfunction: A novel mechanism underlying PAEs-promoted cartilage inflammatory phenotype","authors":"Lu Liu , Yongchang Chen , Wenying Lin , Mian Zheng , Tianqi Yu , Ruyan Chen , Yanru Yang , Lingling Jiao , Qinli Ruan , Jia Sun","doi":"10.1016/j.ecoenv.2026.120027","DOIUrl":"10.1016/j.ecoenv.2026.120027","url":null,"abstract":"<div><div>Phthalate esters (PAEs), the most prevalent class of plasticizers, are widely acknowledged as environmental endocrine disruptors (EDCs) and have been linked to the pathogenesis of various diseases. However, their specific role and intrinsic mechanism in inducing cartilage damage in bone-related diseases remain unclear. This study aimed to clarify the correlation between PAEs and cartilage damage, and to explore their potential molecular mechanisms. The core pathological change of knee osteoarthritis (KOA) is the progressive degeneration of articular cartilage. Based on this, this study first systematically explored the association between PAEs and KOA using network toxicology combined with molecular docking technology, and screened out core regulatory molecules including MMP9, EGFR, IL-10, BCL2, and CASP3. Subsequently, verification experiments on core molecules showed that PAEs exposure could activate the CASP3 pathway to induce apoptosis of human chondrocytes and significantly promote the formation of the inflammatory phenotype of chondrocytes.</div><div>To further reveal the underlying mechanism, we conducted proteomic analysis and cell experiments in human articular chondrocytes (HCs). The results showed that exposure to PAEs triggered reprogramming of glycolysis metabolism, inhibited oxidative phosphorylation, and damaged mitochondrial homeostasis. Collectively, this study provides a robust theoretical basis for understanding the inflammatory phenotypes and underlying mechanisms of chondrocyte damage driven by PAEs exposure, and further lays a foundation for the design of novel therapeutic interventions and the optimization of environmental toxicity assessment protocols targeting PAEs.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 120027"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-15Epub Date: 2026-03-13DOI: 10.1016/j.ecoenv.2026.120023
João Alves Barbosa , James De Backer , Marijke Neyts , Koen Parmentier , Frédéric Laduron , Kris Geukens , Philippe François , Colin R. Janssen , Jana Asselman
Vast amounts of munitions dumped in the marine environment, have been reported to leak chemicals due to munition corrosion. The subsequent increased levels of explosives and related chemicals (E&RC), as well as chemical warfare agents and related chemicals (CWA&RC), raise risks for environmental and human health Yet, ecotoxicity data on primary producers is currently scarce. Therefore, this study investigated the acute effects of three CWA&RC (1,4-oxathiane, 1,4-dithiane, and thiodiglycol) and four E&RC (2,4,6-trinitrotoluene (TNT), tetryl, 1,3-dinitrobenzene (1,3-DNB), and picric acid) on Phaeodactylum tricornutum, a key marine diatom at the basis of the aquatic food web. Results showed that none of the three CWA&RC significantly inhibited the growth rate of Phaeodactylum tricornutum at the tested concentrations. Interestingly, picric acid stimulated growth up under the experimental conditions, suggesting a hormetic effect. TNT, tetryl, and 1,3-DNB strongly inhibited growth, with experimentally derived EC10 and EC50 values approaching environmentally relevant concentrations near dumpsites. Consequently, diatom biomass may be significantly affected by TNT, tetryl, and 1,3-DNB, potentially disturbing primary production and ocean chemistry. Future research should examine potential synergies between munition compounds and other marine pollutants, which may aggravate toxic effects, as well as consider long-term toxicity tests.
{"title":"Contrasting toxicity between explosives– and chemical warfare agents–related compounds to the marine primary producer Phaeodactylum tricornutum","authors":"João Alves Barbosa , James De Backer , Marijke Neyts , Koen Parmentier , Frédéric Laduron , Kris Geukens , Philippe François , Colin R. Janssen , Jana Asselman","doi":"10.1016/j.ecoenv.2026.120023","DOIUrl":"10.1016/j.ecoenv.2026.120023","url":null,"abstract":"<div><div>Vast amounts of munitions dumped in the marine environment, have been reported to leak chemicals due to munition corrosion. The subsequent increased levels of explosives and related chemicals (E&RC), as well as chemical warfare agents and related chemicals (CWA&RC), raise risks for environmental and human health Yet, ecotoxicity data on primary producers is currently scarce. Therefore, this study investigated the acute effects of three CWA&RC (1,4-oxathiane, 1,4-dithiane, and thiodiglycol) and four E&RC (2,4,6-trinitrotoluene (TNT), tetryl, 1,3-dinitrobenzene (1,3-DNB), and picric acid) on <em>Phaeodactylum tricornutum</em>, a key marine diatom at the basis of the aquatic food web. Results showed that none of the three CWA&RC significantly inhibited the growth rate of <em>Phaeodactylum tricornutum</em> at the tested concentrations. Interestingly, picric acid stimulated growth up under the experimental conditions, suggesting a hormetic effect. TNT, tetryl, and 1,3-DNB strongly inhibited growth, with experimentally derived EC10 and EC50 values approaching environmentally relevant concentrations near dumpsites. Consequently, diatom biomass may be significantly affected by TNT, tetryl, and 1,3-DNB, potentially disturbing primary production and ocean chemistry. Future research should examine potential synergies between munition compounds and other marine pollutants, which may aggravate toxic effects, as well as consider long-term toxicity tests.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 120023"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147451411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-15Epub Date: 2026-03-14DOI: 10.1016/j.ecoenv.2026.119901
Xiaoxi Yang , Xuemei Li , Xingqiang Li , Hongyan Zhang , Ce Wang , Xinyue Chen
Per- and polyfluoroalkyl substances (PFAS) are globally persistent pollutants increasingly implicated in adverse cardiovascular outcomes. Although research on PFAS toxicity has expanded rapidly, existing literature remains fragmented, with limited integration across exposure science, epidemiological evidence, molecular mechanisms, and mitigation strategies. Current reviews typically provide broad summaries of PFAS toxicity but seldom focus specifically on cardiovascular disease (CVD) or the mechanistic pathways underlying PFAS-induced cardiovascular injury. Moreover, the rapid emergence of short-chain and replacement PFAS introduces additional uncertainty regarding their cardiovascular relevance. To address these gaps, this review provides a comprehensive and mechanistically focused synthesis of PFAS exposure and CVD. A literature search through November 2025 identified eligible epidemiological, clinical, and experimental studies evaluating PFAS, including legacy compounds (Perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane sulfonate (PFHxS), and perfluorononanoic acid (PFNA)) and emerging PFAS, and their associations with hypertension, blood pressure variation, vascular dysfunction, atherosclerosis, arrhythmias, cardiac injury, and cardiovascular mortality. Studies using serum or plasma biomarkers, drinking-water contamination records, cord blood measurements, and advanced mixture-modeling approaches were included. Extracted evidence encompassed exposure assessment, cardiovascular endpoints, mechanistic pathways, and potential therapeutic or risk-mitigating strategies. Across studies, PFAS exposure was consistently associated with modest but meaningful increases in systolic and diastolic blood pressure, higher risks of hypertension and gestational hypertensive disorders, impaired endothelial function, greater carotid intima-media thickness, and increased CVD incidence and mortality. Mechanistic evidence converges on several key pathways, including endothelial dysfunction, oxidative stress, inflammation, renin–angiotensin system activation, epithelial sodium channel upregulation, dyslipidemia, and placental vascular impairment linked to developmental programming. Vulnerable populations, including women, individuals with metabolic disorders, and those with impaired kidney function, exhibit heightened susceptibility. By integrating evidence across exposure science, epidemiology, mechanistic toxicology, and emerging intervention research, this review advances current understanding of PFAS-related cardiovascular toxicity and supports informed public health policy, clinical risk assessment, and regulatory decision-making.
{"title":"Per- and polyfluoroalkyl substances and cardiovascular disease: A mechanistic and epidemiological synthesis","authors":"Xiaoxi Yang , Xuemei Li , Xingqiang Li , Hongyan Zhang , Ce Wang , Xinyue Chen","doi":"10.1016/j.ecoenv.2026.119901","DOIUrl":"10.1016/j.ecoenv.2026.119901","url":null,"abstract":"<div><div>Per- and polyfluoroalkyl substances (PFAS) are globally persistent pollutants increasingly implicated in adverse cardiovascular outcomes. Although research on PFAS toxicity has expanded rapidly, existing literature remains fragmented, with limited integration across exposure science, epidemiological evidence, molecular mechanisms, and mitigation strategies. Current reviews typically provide broad summaries of PFAS toxicity but seldom focus specifically on cardiovascular disease (CVD) or the mechanistic pathways underlying PFAS-induced cardiovascular injury. Moreover, the rapid emergence of short-chain and replacement PFAS introduces additional uncertainty regarding their cardiovascular relevance. To address these gaps, this review provides a comprehensive and mechanistically focused synthesis of PFAS exposure and CVD. A literature search through November 2025 identified eligible epidemiological, clinical, and experimental studies evaluating PFAS, including legacy compounds (Perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane sulfonate (PFHxS), and perfluorononanoic acid (PFNA)) and emerging PFAS, and their associations with hypertension, blood pressure variation, vascular dysfunction, atherosclerosis, arrhythmias, cardiac injury, and cardiovascular mortality. Studies using serum or plasma biomarkers, drinking-water contamination records, cord blood measurements, and advanced mixture-modeling approaches were included. Extracted evidence encompassed exposure assessment, cardiovascular endpoints, mechanistic pathways, and potential therapeutic or risk-mitigating strategies. Across studies, PFAS exposure was consistently associated with modest but meaningful increases in systolic and diastolic blood pressure, higher risks of hypertension and gestational hypertensive disorders, impaired endothelial function, greater carotid intima-media thickness, and increased CVD incidence and mortality. Mechanistic evidence converges on several key pathways, including endothelial dysfunction, oxidative stress, inflammation, renin–angiotensin system activation, epithelial sodium channel upregulation, dyslipidemia, and placental vascular impairment linked to developmental programming. Vulnerable populations, including women, individuals with metabolic disorders, and those with impaired kidney function, exhibit heightened susceptibility. By integrating evidence across exposure science, epidemiology, mechanistic toxicology, and emerging intervention research, this review advances current understanding of PFAS-related cardiovascular toxicity and supports informed public health policy, clinical risk assessment, and regulatory decision-making.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 119901"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147451930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Freshwater ecosystems face mixture-dominated pressures that often elude conventional monitoring. We assessed eight rivers in Latium (Central Italy) to jointly evaluate ecological status and teratogenic risk within a One Health perspective. We combined in-situ physico-chemical measurements and elemental profiling by inductively coupled plasma mass spectrometry (ICP-MS; including the rare-earth tracer gadolinium) with two biological lines of evidence: benthic diatom assemblages to derive the Intercalibration Common Metric Index (ICMi) and screen teratological valves, and the Hydra vulgaris regeneration assay summarized as the Teratogenic Risk Index (TRI), with behavioural endpoints. Environmental conditions were heterogeneous, with eutrophication and high organic load at some sites. ICMi classified Almone and Arrone as Poor, Marta and Sacco as Good, and Mignone, Aniene, Tevere and Ninfa as High. TRI indicated Very High teratogenic risk at Almone; High at Marta, Sacco and Tevere; Low at Arrone, Mignone and Aniene; and No risk at Ninfa. Diatom teratologies were detected at all sites and peaked at Tevere. ICMi showed a negative association with gadolinium (r = -0.76, p < 0.05), whereas TRI and ICMi were not correlated. These results demonstrate that ecological status and teratogenic hazard need not converge. TRI captured organism-level developmental and neuro-functional impairment at low doses and in complex mixtures, even where ICMi was Good/High. Integrating organism- and community-level indicators with targeted chemistry offers a sensitive, cost-effective framework to flag hotspots, prioritize monitoring of emerging contaminants, and support risk management under the Water Framework Directive.
淡水生态系统面临着以混合物为主的压力,而传统的监测方法往往无法做到这一点。我们评估了拉蒂姆(意大利中部)的八条河流,以“同一个健康”视角共同评估生态状况和致畸风险。我们通过电感耦合等离子体质谱(ICP-MS,包括稀土示踪剂钆)将现场物理化学测量和元素谱分析与两个生物证据线结合起来:底栖硅藻组合,得出了Intercalibration Common Metric Index (ICMi)和筛选致畸风险,以及水螅再生试验,总结为致畸风险指数(TRI),具有行为终点。环境条件不均匀,部分站点富营养化,有机负荷高。ICMi将Almone和arone分类为“差”,Marta和Sacco分类为“好”,Mignone, Aniene, Tevere和Ninfa分类为“高”。TRI提示Almone有极高致畸风险;在玛尔塔、萨科和提维尔高中;洛在阿罗内、米尼奥内和阿涅内;在尼法没有风险。在所有地点均检测到硅藻致畸,并在Tevere达到峰值。ICMi与钆呈负相关(r = -0.76,p <; 0.05),而TRI与ICMi不相关。这些结果表明,生态状况和致畸危害不需要趋同。在低剂量和复杂混合物中,即使在ICMi为好/高的情况下,TRI也捕获了生物体水平的发育和神经功能损伤。将生物和社区层面的指标与目标化学结合起来,提供了一个敏感的、具有成本效益的框架,可以标记热点,优先监测新出现的污染物,并支持水框架指令下的风险管理。
{"title":"A One Health framework integrating teratogenic risk and ecological assessment in freshwaters","authors":"Giulia Cesarini , Massimiliano Scalici , Marco Colasanti , Federica Spani","doi":"10.1016/j.ecoenv.2026.120015","DOIUrl":"10.1016/j.ecoenv.2026.120015","url":null,"abstract":"<div><div>Freshwater ecosystems face mixture-dominated pressures that often elude conventional monitoring. We assessed eight rivers in Latium (Central Italy) to jointly evaluate ecological status and teratogenic risk within a One Health perspective. We combined in-situ physico-chemical measurements and elemental profiling by inductively coupled plasma mass spectrometry (ICP-MS; including the rare-earth tracer gadolinium) with two biological lines of evidence: benthic diatom assemblages to derive the Intercalibration Common Metric Index (ICMi) and screen teratological valves, and the <em>Hydra vulgaris</em> regeneration assay summarized as the Teratogenic Risk Index (TRI), with behavioural endpoints. Environmental conditions were heterogeneous, with eutrophication and high organic load at some sites. ICMi classified Almone and Arrone as Poor, Marta and Sacco as Good, and Mignone, Aniene, Tevere and Ninfa as High. TRI indicated Very High teratogenic risk at Almone; High at Marta, Sacco and Tevere; Low at Arrone, Mignone and Aniene; and No risk at Ninfa. Diatom teratologies were detected at all sites and peaked at Tevere. ICMi showed a negative association with gadolinium (r = -0.76, p < 0.05), whereas TRI and ICMi were not correlated. These results demonstrate that ecological status and teratogenic hazard need not converge. TRI captured organism-level developmental and neuro-functional impairment at low doses and in complex mixtures, even where ICMi was Good/High. Integrating organism- and community-level indicators with targeted chemistry offers a sensitive, cost-effective framework to flag hotspots, prioritize monitoring of emerging contaminants, and support risk management under the Water Framework Directive.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 120015"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147451931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-15Epub Date: 2026-03-12DOI: 10.1016/j.ecoenv.2026.120007
Zhiyang Han , Luan Wang , Xiang Li , Yumeng Dai , Xinyu Guan , Zhencheng Su , Xu Li , Xiujuan Wang , Tiegang Li , Mingkai Xu
Atmospheric nanoplastics represent an emerging environmental health concern, as their small size and physicochemical properties facilitate unintentional inhalation. However, their pulmonary toxicity under repeated exposure and following exposure cessation remains poorly understood. Here, polystyrene nanoplastics (PS-NPs) with different particle sizes (25, 100, and 500 nm) were intratracheally instilled into C57BL/6 mice at doses of 1 and 5 mg/kg body weight, three times per week for four weeks (exposure period, EXP), followed by a two-week post-exposure period (PEP). A ddH₂O-treated group was included as the control. PS-NPs accumulated extensively in the lungs and translocated to the heart, liver, spleen, and kidneys. Notably, inhaled nanoplastics sustained in lung tissue after PEP. Exposure to PS-NPs disrupted the alveolar epithelial barrier, induced inflammation, and oxidative stress in lung tissue, altered lung function, led to pulmonary fibrosis, and reduced peripheral white blood cell counts. These toxic effects were particle size-dependent, with smaller particles inducing greater toxicity. Moreover, adverse effects sustained during PEP, indicating that PS-NPs–induced injury was not readily reversible in the short term. Furthermore, our results suggest that macrophage polarization is involved in the progression of PS-NPs–induced pulmonary fibrosis. These findings demonstrate that repeated inhalation exposure to PS-NPs can induce sustained pulmonary injury, with incomplete recovery observed during PEP, highlighting potential respiratory health concerns associated with airborne nanoplastics.
{"title":"Repeated inhalation exposure to polystyrene nanoplastics induced sustained pulmonary injury and fibrosis in mice","authors":"Zhiyang Han , Luan Wang , Xiang Li , Yumeng Dai , Xinyu Guan , Zhencheng Su , Xu Li , Xiujuan Wang , Tiegang Li , Mingkai Xu","doi":"10.1016/j.ecoenv.2026.120007","DOIUrl":"10.1016/j.ecoenv.2026.120007","url":null,"abstract":"<div><div>Atmospheric nanoplastics represent an emerging environmental health concern, as their small size and physicochemical properties facilitate unintentional inhalation. However, their pulmonary toxicity under repeated exposure and following exposure cessation remains poorly understood. Here, polystyrene nanoplastics (PS-NPs) with different particle sizes (25, 100, and 500 nm) were intratracheally instilled into C57BL/6 mice at doses of 1 and 5 mg/kg body weight, three times per week for four weeks (exposure period, EXP), followed by a two-week post-exposure period (PEP). A ddH₂O-treated group was included as the control. PS-NPs accumulated extensively in the lungs and translocated to the heart, liver, spleen, and kidneys. Notably, inhaled nanoplastics sustained in lung tissue after PEP. Exposure to PS-NPs disrupted the alveolar epithelial barrier, induced inflammation, and oxidative stress in lung tissue, altered lung function, led to pulmonary fibrosis, and reduced peripheral white blood cell counts. These toxic effects were particle size-dependent, with smaller particles inducing greater toxicity. Moreover, adverse effects sustained during PEP, indicating that PS-NPs–induced injury was not readily reversible in the short term. Furthermore, our results suggest that macrophage polarization is involved in the progression of PS-NPs–induced pulmonary fibrosis. These findings demonstrate that repeated inhalation exposure to PS-NPs can induce sustained pulmonary injury, with incomplete recovery observed during PEP, highlighting potential respiratory health concerns associated with airborne nanoplastics.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 120007"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147451932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-15Epub Date: 2026-03-13DOI: 10.1016/j.ecoenv.2026.120026
Wenxin Chen , Ziqiang Han , Qingxiang Xu , Yikun He , Sang Van Vu , Tong Li , Huayong Que
Acquired thermotolerance (heat priming) enables organisms to withstand lethal heat stress after prior sublethal exposure. While documented in bivalves through survival analyses, histological mechanisms in gills—their primary environmental interface—remain unclear. This study investigated heat priming effects on Crassostrea angulata gills using four experimental groups: control, sublethal, priming (sublethal + lethal), and lethal. Histopathology (HE staining and SEM) and apoptosis (TUNEL) were analyzed under varying thermal regimes. Lethal stress induced more than 20% gill shrinkage (vs. control) with elevated mucus cell counts, while SEM revealed exacerbated filament breakage and ciliary loss. Priming pretreatment significantly reduced filament contraction and mitigated structural damage. TUNEL-positive cell density peaked in the lethal group, showing an eightfold increase over priming at 48 h, whereas priming and sublethal groups exhibited comparable level. These findings indicate that heat priming synergistically alleviates both mechanical damage (gill shrinkage/filament disruption) and TUNEL-detected cell-death signals during subsequent lethal stress. The study establishes a tissue-level foundation for understanding acquired thermotolerance in oysters.
{"title":"Heat priming protects oyster gills from subsequent lethal heat stress: Histopathology and apoptosis evidence in Crassostrea angulata","authors":"Wenxin Chen , Ziqiang Han , Qingxiang Xu , Yikun He , Sang Van Vu , Tong Li , Huayong Que","doi":"10.1016/j.ecoenv.2026.120026","DOIUrl":"10.1016/j.ecoenv.2026.120026","url":null,"abstract":"<div><div>Acquired thermotolerance (heat priming) enables organisms to withstand lethal heat stress after prior sublethal exposure. While documented in bivalves through survival analyses, histological mechanisms in gills—their primary environmental interface—remain unclear. This study investigated heat priming effects on <em>Crassostrea angulata</em> gills using four experimental groups: control, sublethal, priming (sublethal + lethal), and lethal. Histopathology (HE staining and SEM) and apoptosis (TUNEL) were analyzed under varying thermal regimes. Lethal stress induced more than 20% gill shrinkage (vs. control) with elevated mucus cell counts, while SEM revealed exacerbated filament breakage and ciliary loss. Priming pretreatment significantly reduced filament contraction and mitigated structural damage. TUNEL-positive cell density peaked in the lethal group, showing an eightfold increase over priming at 48 h, whereas priming and sublethal groups exhibited comparable level. These findings indicate that heat priming synergistically alleviates both mechanical damage (gill shrinkage/filament disruption) and TUNEL-detected cell-death signals during subsequent lethal stress. The study establishes a tissue-level foundation for understanding acquired thermotolerance in oysters.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 120026"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147451336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The bursa of Fabricius (BF), a regressive lymphoid organ unique to avian species, plays a pivotal role in early immune defense post-hatching: it not only mediates innate immune responses but also provides a microenvironment necessary for B-cell maturation, thereby playing an indispensable role in the development and functional maturation of the avian adaptive immune system. Life history theory predicts energy allocation trade-offs in response to environmental challenges, which often suppresses costly processes like immunity to prioritize survival. This study investigated effects of long-term environmental heavy metal pollution on these trade-offs and BF development in the tree sparrow (Passer montanus). Contrary to the paradigm of stress-induced immunosuppression, we found that despite significant impairments in body condition and growth rate, nestlings from a polluted site exhibited enhanced BF development. This was demonstrated through three key phenotypic adaptations: (1) an increased BF coefficient, (2) accelerated follicular development and histological maturation, and (3) increased B-lymphocyte density and migration to the spleen. Nestlings from a polluted site also displayed enhanced innate immunity and antioxidant defenses. An Integrated Biological Response (IBR) model suggested a strategic energy reallocation where investment in growth was suppressed to prioritize immune organ development and function. These findings provide a novel perspective on adaptive life-history strategies, demonstrating that birds can prioritize immune resilience to persist in contaminated environments at a cost to somatic development.
法氏囊(bursa of Fabricius, BF)是鸟类特有的退行性淋巴器官,在孵化后的早期免疫防御中起着关键作用:它不仅介导先天免疫应答,还提供b细胞成熟所需的微环境,因此在鸟类适应性免疫系统的发育和功能成熟中起着不可或缺的作用。生命史理论预测了能量分配的权衡,以应对环境挑战,这通常会抑制昂贵的过程,如优先考虑生存的免疫力。本研究探讨了长期环境重金属污染对树雀(Passer montanus)这些权衡和BF发育的影响。与应激诱导免疫抑制的范式相反,我们发现,尽管受到污染的雏鸟身体状况和生长速度明显受损,但来自污染地点的雏鸟表现出增强的BF发育。这通过三个关键的表型适应来证明:(1)BF系数增加,(2)卵泡发育和组织学成熟加速,(3)b淋巴细胞密度增加和向脾脏迁移。来自污染地区的雏鸟也表现出增强的先天免疫和抗氧化防御能力。综合生物反应(IBR)模型表明,在抑制生长投资以优先考虑免疫器官发育和功能的战略能量重新分配中。这些发现为适应性生活史策略提供了一个新的视角,表明鸟类可以优先考虑免疫弹性,以维持在污染环境中,以牺牲体细胞发育为代价。
{"title":"Survival over growth: Accelerated bursa of Fabricius development enhances immune resilience in heavy metal-exposed tree sparrows","authors":"Yue Shen, Zhaocun Lin, Yuquan Miao, Ming Zhang, Wenya Zhang, Yingmei Zhang","doi":"10.1016/j.ecoenv.2026.120004","DOIUrl":"10.1016/j.ecoenv.2026.120004","url":null,"abstract":"<div><div>The bursa of Fabricius (BF), a regressive lymphoid organ unique to avian species, plays a pivotal role in early immune defense post-hatching: it not only mediates innate immune responses but also provides a microenvironment necessary for B-cell maturation, thereby playing an indispensable role in the development and functional maturation of the avian adaptive immune system. Life history theory predicts energy allocation trade-offs in response to environmental challenges, which often suppresses costly processes like immunity to prioritize survival. This study investigated effects of long-term environmental heavy metal pollution on these trade-offs and BF development in the tree sparrow (<em>Passer montanus</em>). Contrary to the paradigm of stress-induced immunosuppression, we found that despite significant impairments in body condition and growth rate, nestlings from a polluted site exhibited enhanced BF development. This was demonstrated through three key phenotypic adaptations: (1) an increased BF coefficient, (2) accelerated follicular development and histological maturation, and (3) increased B-lymphocyte density and migration to the spleen. Nestlings from a polluted site also displayed enhanced innate immunity and antioxidant defenses. An Integrated Biological Response (IBR) model suggested a strategic energy reallocation where investment in growth was suppressed to prioritize immune organ development and function. These findings provide a novel perspective on adaptive life-history strategies, demonstrating that birds can prioritize immune resilience to persist in contaminated environments at a cost to somatic development.</div></div>","PeriodicalId":303,"journal":{"name":"Ecotoxicology and Environmental Safety","volume":"313 ","pages":"Article 120004"},"PeriodicalIF":6.1,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147451338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}