Environment & Health最新文献

{"title":"Cotinine Promotes Cancer Cell Proliferation and m1A RNA Methylation in Smoking-Associated Lung Cancer by Targeting PLK1/β-Catenin/TRMT6 Axis","authors":"Panlong Li,&nbsp;Xuyun Peng,&nbsp;Sihuang Wu,&nbsp;Jiani Wang,&nbsp;Yiju Huang,&nbsp;Zexiao Lin,&nbsp;Yang Yang,&nbsp;Weicheng Liang","doi":"10.1021/envhealth.6c00013","DOIUrl":"https://doi.org/10.1021/envhealth.6c00013","url":null,"abstract":"<p>Nicotineis the most abundant alkaloid in tobacco, and 70%–80%of its metabolites are cotinine. In terms of that, numerous cigarettesare consumed worldwide, resulting in a large amount of cotinine beingreleased into the environment and posing potential hazards. However,the biological effects of cotinine are poorly understood. In the currentstudy, we identified that the oncogene Polo-like kinase 1 (PLK1) isa direct target of cotinine, and cotinine could upregulate the proteinlevel of PLK1. Public epidemiological data indicated a positive correlationbetween PLK1 expression and smoking. Subsequent studies validatedthat PLK1 directly interacted with β-catenin, leading to transcriptionalactivation of tRNA methyltransferase 6 (TRMT6), a canonical methyltransferaseinvolved in m¹A methylation modification of RNA. Dot blotshowed that cotinine enhanced m¹A RNA methylation in lungcancer cells. Public epidemiological data also demonstrated a positivecorrelation between the expression of TRMT6 and smoking. Knockdownof TRMT6 impaired cell proliferation and sensitized lung cancer cellsto common chemotherapeutic agents. Taken together, our current studyindicated a previously unknown role of cotinine in promoting cancercell proliferation by targeting the PLK1/β-catenin/TRMT6 axis,which may shed light on the connection between smoking and RNA modifications.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1741–1753"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810270","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}

{"title":"Long-Term Ambient Ozone Exposure and Nonaccidental Mortality among Chinese Adults: A Nationwide Cohort Study","authors":"Jialing Zou,&nbsp;Yuchang Zhou,&nbsp;Renjie Chen,&nbsp;Peng Yin,&nbsp;Su Shi,&nbsp;Xia Meng,&nbsp;Jing Cai,&nbsp;Haidong Kan,&nbsp;Yue Niu,&nbsp;Maigeng Zhou","doi":"10.1021/envhealth.5c00617","DOIUrl":"https://doi.org/10.1021/envhealth.5c00617","url":null,"abstract":"<p>Existing evidence on long-term ozone exposure and totalmortalitywas mainly from Europe and the United States, with inconsistent findings.In China, there is a critical lack of localized cohort-based evidenceon this association to inform air quality standard revisions. In thisnationwide cohort study of 96,955 adults across 31 Chinese provinces,peak-season and warm-season ozone exposure were estimated using apreviously developed random forest model. Stratified Cox proportionalhazards models were employed to examine the associations between long-termozone exposure and nonaccidental mortality and to characterize theirexposure–response relationships. In the fully adjusted model,each 10 μg/m³ increase in peak-season and warm-seasonaverage ozone concentrations was associated with increased nonaccidentalmortality risks of 3.0% (hazard ratio [HR] = 1.030; 95% CI: 1.010,1.050) and 2.9% (HR = 1.029; 1.010, 1.048), respectively. The exposure–responsecurves provided weak evidence for a threshold effect of long-termozone exposure. We estimated that 487,207 (95% UI: 168,705, 786,351)deaths could be attributed to long-term ozone exposure in China in2019. These findings underscore an urgent need to establish standardsfor semiannual average ozone concentrations and to strengthen ozoneair pollution control.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1688–1696"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810380","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}

{"title":"A NANOG-EGFP iPSC-Based Reporter Platform for High-Throughput Screening of Environmental Pollutant Effects on Pluripotency","authors":"Yanyi Zhao,&nbsp;Hanyue Li,&nbsp;Renjun Yang,&nbsp;Nuoya Yin,&nbsp;Francesco Faiola","doi":"10.1021/envhealth.5c00797","DOIUrl":"https://doi.org/10.1021/envhealth.5c00797","url":null,"abstract":"<p>Humansare frequently exposed to diverse environmental pollutantsthat may pose potential risks during early embryonic development.Advances in stem cell toxicology have introduced new opportunitiesfor environmental toxicity assessment, enabling the development ofphysiologically relevant models based on human induced pluripotentstem cells (iPSCs). However, current systems remain limited by lowthroughput and the inability to achieve real-time monitoring. In thisstudy, we established a <em>NANOG</em>-<em>EGFP</em> iPSC reporter line by precisely inserting a T2A-<em>EGFP</em> cassette into the endogenous <em>NANOG</em> locus usingCRISPR/Cas9, enabling dynamic and quantitative visualization of pluripotencystatus. Using this reporter system, we systematically evaluated theeffects of 38 representative environmental pollutants spanning sixmajor chemical categories, including bisphenols, per- and polyfluoroalkylsubstances (PFAS), halogenated flame retardants, organophosphate esters,neonicotinoids, and phenolic compounds. Most pollutants induced varyingdegrees of reduction in <em>NANOG</em>-<em>EGFP</em> expression, suggesting perturbation of core transcriptional networksinvolved in pluripotency maintenance rather than nonspecific cytotoxiceffects. Notably, bisphenol B (BPB), bisphenol Z (BPZ), perfluorobutanesulfonicacid (PFBS), tributyl phosphate (TnBP), tris(2-chloroethyl) phosphate(TCEP), and 3,5-di<em>-tert</em>-butyl-4-hydroxybenzoic acid(BHT-COOH) exhibited pronounced low-dose activity, causing significantsuppression of <em>NANOG-EGFP</em> signals even at 10 nmol/L.Furthermore, during neuroectoderm differentiation, several bisphenolsand PFAS delayed the normal downregulation of <em>NANOG</em>, indicating disruption of the tightly regulated timing of pluripotencyexit and lineage transition during early developmental progression.Overall, the <em>NANOG</em>-<em>EGFP</em> iPSC reportermodel provides a sensitive, stable, and practical platform for high-throughputscreening of environmental toxicants and offers mechanistically informedinsight into how pollutant exposure may interfere with early humandevelopmental regulatory programs.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1732–1740"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810269","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}

{"title":"Live Airway Prevotella Attenuated Diesel Exhaust-Induced Lung Injury and Neutrophil Activation via Bacterial Extracellular Vesicles","authors":"Bojia Wang,&nbsp;Lihua Yang,&nbsp;Jiahua Cai,&nbsp;Qixiao Jiang,&nbsp;Hongna Zhang,&nbsp;Jinmei Piao,&nbsp;Wei Han,&nbsp;Yuxin Zheng,&nbsp;Menghui Jiang","doi":"10.1021/envhealth.5c00648","DOIUrl":"https://doi.org/10.1021/envhealth.5c00648","url":null,"abstract":"<p>Diesel exhaust (DE), as a principal contributor to traffic-relatedair pollution, poses significant public and occupational health risks.The lung microbiome could be shaped by inhaled pollutants, which playa crucial role in sustaining pulmonary health. Our prior study founda lower abundance of airway <em>Prevotella nanceiensis</em> (<em>P.nan.</em>) in DE-exposed individuals. Here, in thisstudy, live <em>P.nan.</em> and its bacterial extracellularvesicles (BEVs) alleviated lung damage under inhaled DE exposure,accompanied by reduced neutrophil infiltration and activation. Notably,DE triggered lipid droplet accumulation in the lung, mitigated bythe live <em>P.nan.</em>/BEVs intervention. Additionally,inhibitors targeting lipid oxidation, synthesis, and transport attenuatedneutrophil activation in response to diesel exhaust particle (DEP)stimulation. Moreover, the intervention of BEVs resulted in decreasedlevels of inflammatory mediators, neutrophil recruitment-associatedchemokines, and lipid-related genes. This study highlights live <em>P.nan.</em>/BEVs’ protective role against DE-induced lunginjury, implicating neutrophil recruitment and lipid metabolism askey mechanisms and offering potential therapeutic avenues.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1790–1803"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810280","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}

{"title":"Engineered Protein Coronas Reveal That Apolipoprotein E Enhances Transport of Particulate Pollutants across the Blood-Brain Barrier","authors":"Hua Qin,&nbsp;Zhaojia Deng,&nbsp;Wenjing Xie,&nbsp;Guorui Liu,&nbsp;Guangbo Qu,&nbsp;Hanyong Peng,&nbsp;Guibin Jiang","doi":"10.1021/envhealth.5c00803","DOIUrl":"https://doi.org/10.1021/envhealth.5c00803","url":null,"abstract":"<p>Ultrafine and nanoscale particulate matter (PM) is increasinglyimplicated in adverse neurological outcomes, yet the molecular mechanismsgoverning its interaction with blood proteins and transport acrossthe blood–brain barrier (BBB) remain unclear. Here, we establishan engineered protein–corona model to dissect how blood-borneparticles acquire BBB-relevant transport properties. Gold nanoparticleswere used as a controlled surrogate for PM and functionalized withthiolated DNA aptamers to enable reproducible assembly of definedcoronas composed of three physiologically relevant proteins─humanserum albumin (HSA), apolipoprotein E (ApoE), and complement componentC3b. In a bEnd.3 Transwell BBB model, corona identity dictated enhancedcolloidal stability and transcytosis efficiency, with ApoE-enrichedcoronas nearly doubling apparent permeability and increasing 24 htransport by 1.6-fold relative to bare particles. Mechanistic studiesrevealed an energy-dependent, predominantly clathrin-mediated uptakepathway. Importantly, ApoE precoronation also enhanced endothelialpenetration of polystyrene particles and increased the endothelialcytotoxicity of diverse industrial-source PM samples. This work providesa mechanistic framework linking protein corona composition to BBBpenetration, advancing molecular risk assessment of environmentallyrelevant particulate matter.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1754–1765"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810271","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}

{"title":"Health Benefits of Air Purification: A Systematic Review","authors":"Xiaowei Xue,&nbsp;Yixuan Jiang,&nbsp;Weijie Qian,&nbsp;Renjie Chen,&nbsp;Haidong Kan","doi":"10.1021/envhealth.5c00836","DOIUrl":"https://doi.org/10.1021/envhealth.5c00836","url":null,"abstract":"<p>Air pollution is a critical global public health challengethatposes a wide range of health threats. As people spend most of theirtime indoors, household air pollution is a significant yet often overlookedsource of exposure. Existing evidence suggests that air purificationis a promising intervention to mitigate these risks. This systematicreview synthesized evidence from studies published between January1990 and August 2025 on the effectiveness of air purifiers for improvingthe indoor air quality and mitigating health impacts. We also assessthe cost-effectiveness and identify major limitations in current research.The findings demonstrate that air purifiers significantly reduce indoorpollution levels, leading to substantial respiratory and cardiovascularbenefits, particularly in high-risk populations. However, evidenceof neurocognitive outcomes remains limited. Despite heterogeneityin study designs, air purifiers represent a potentially cost-effectivestrategy for mitigating the adverse effects from air pollution. Standardizeddevice certification, supportive policies to improve access, and continuedresearch to optimize intervention strategies are warranted for thefuture.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1587–1608"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810343","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}

{"title":"Identification of Key Indicators in the Adverse Outcome Pathway for Genetic Damage Induced by Chromate Exposure: A Machine Learning-Based Cross-Sectional Study","authors":"Zhiqiang Ji,&nbsp;Zekang Su,&nbsp;Yali Zhang,&nbsp;Shiyi Hong,&nbsp;Xiaoli Wang,&nbsp;Guiping Hu,&nbsp;Guang Jia","doi":"10.1021/envhealth.5c00681","DOIUrl":"https://doi.org/10.1021/envhealth.5c00681","url":null,"abstract":"<p>How chronic inflammation and immune dysregulation drivegeneticdamage upon environmental exposure is a pivotal question in toxicology.Focusing on hexavalent chromium [Cr(VI)], a human carcinogen, we dissectedthis link using a machine-learning approach in an occupational population.We discovered that specific immune checkpoint molecules (PD-L1, PD-1,LAG-3) and regulatory patterns mediated the effect of blood Cr onkey immune populations, including PD-1(+) B cells and CD8(+) T cells.Furthermore, we defined a core set of four inflammatory-immune indicators(NLRP3, positive/negative immune patterns, CD8(+) T cells) that robustlyexplain genotoxicity. From this, we conjectured a coherent cascadeinvolving the NLRP3 inflammasome, immune regulatory patterns, andeffector cell subsets, culminating in genetic damage. This study establishesa novel paradigm for understanding the immunoinflammatory mechanismsof environmental carcinogens by employing, for the first time, machinelearning within an adverse outcome pathway (AOP) framework to systematicallyidentify and validate NLRP3, positive/negative immune regulatory patterns,and CD8(+) T cells as central players in Cr(VI)-induced genetic damage.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1766–1777"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810273","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}

{"title":"Apigenin Mitigates PFOA-Induced Activation of the NLRP3-Pyroptosis Axis and Associated Neurological Damage","authors":"Vikrant Rahi,&nbsp;Priyanka Pandey,&nbsp;Dipan Maity,&nbsp;Ravinder K. Kaundal","doi":"10.1021/envhealth.5c00763","DOIUrl":"https://doi.org/10.1021/envhealth.5c00763","url":null,"abstract":"<p>Perfluorooctanoic acid (PFOA), a persistent per- andpolyfluoroalkylsubstance (PFAS), is an environmental contaminant increasingly associatedwith neurotoxicity, although its precise molecular mechanisms remainpoorly understood. Here, we investigated the role of the NF-κB/NLRP3-GSDMDpyroptotic pathway in PFOA-induced neurotoxicity and evaluated theprotective potential of apigenin. In in-vitro, N2a neuronal cellswere exposed to PFOA, with or without apigenin, and assessed for cellviability, oxidative stress, and inflammasome activation. In in-vivo,mice were administered PFOA with or without apigenin, followed bybehavioral, biochemical, and histopathological analyses. PFOA exposureinduced significant oxidative stress, reduced neuronal viability,and activated NF-κB signaling, leading to NLRP3 inflammasomeactivation and GSDMD-mediated pyroptosis. These molecular alterationswere associated with neuroinflammation, neuronal injury, demyelination,and cognitive and behavioral deficits in mice. Apigenin treatmentmarkedly attenuated oxidative stress, suppressed NF-κB/NLRP3signaling, inhibited caspase-1 and GSDMD activation, and improvedneurobehavioral outcomes. Collectively, these findings demonstratethat PFOA induces neurotoxicity via activation of the NF-κB/NLRP3-GSDMDpyroptotic axis and identify apigenin as a potential therapeutic agentfor mitigating PFAS-associated neurological damage.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1674–1687"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810318","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}

{"title":"Prospective Metabolomic Cohort of 123,037 Men Reveals Lipid Mediators Linking Air Pollution to Benign Prostatic Hyperplasia","authors":"Chuzhong Wei,&nbsp;Yuwei Wu,&nbsp;Zhufeng Peng,&nbsp;Qingli Yu,&nbsp;Bolai Qing,&nbsp;Zehan Li,&nbsp;Jindong Xie,&nbsp;Lu Yang,&nbsp;Shi Qiu","doi":"10.1021/envhealth.5c00806","DOIUrl":"https://doi.org/10.1021/envhealth.5c00806","url":null,"abstract":"<p>Benignprostatic hyperplasia (BPH) is increasingly prevalent amongaging male populations and is often accompanied by a lower urinarytract symptoms (LUTS). This study aimed to comprehensively analyzethe impact of air pollution and lifestyle on the incidence of BPHand LUTS. In a prospective study-based U.K. Biobank (UKB) cohort,every 1 μg/m³ increase of PM_2.5 was associatedwith a 2.18% increased risk of BPH (<em>P</em> = 0.0029).Furthermore, PM_2.5–10, PM₁₀, NO₂, and NO<em>_X</em> also showed similar risk effects.As for mixed exposures, the weighted quantile sum (WQS) and quantileg-computation (qgcomp) method indicated that for each additional unit,the risk of BPH increased by 3.53% (<em>P</em> = 0.0265) and2.20% (<em>P</em> &lt; 0.0001). Analyses of LUTS in malesshowed that for each additional unit of mixed exposure, the risk ofLUTS increased by 6.78% (<em>P</em> &lt; 0.0001) and 9.17%(<em>P</em> &lt; 0.0001). A cross-country cohort in westernChina was also replicated. As for single air pollutant exposure, therisk of BPH increased by 2.77% (<em>P</em> &lt; 0.0001) forevery 1 μg/m³ increase of PM_2.5. The othersingle and mixed pollutants also remained dangerous. Further analysisrevealed that each additional 1 μg/m³ of PM_2.5 increased 2.34% risk of LUTS (<em>P</em> = 0.0014). Theother pollutants also remained dangerous. The same applies to othersingle and mixed pollutants. The restricted cubic spline (RCS) curvefound that there was a dose–response relationship between PM_2.5 concentration and BPH risk (<em>P</em> = 0.0169)and determined that 9.83 μg/m³ was the risk thresholdfor BPH. Compared with participants’ exposure to low PM_2.5 and low-fat diet, participants with high PM_2.5 exposure and high-fat diet had 16% increased risk of BPH (<em>P</em> &lt; 0.0001). Mediation analysis identified 34 lipid-relatedmetabolites as potential mediators. This study emphasizes the significanceof environmental and lifestyle factors in the prevention and managementof BPH.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1832–1842"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810444","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}

{"title":"Washable Face Masks: An Emerging Source of Metal and Nanoparticle Contamination in Aquatic Environments","authors":"Danyang Li,&nbsp;Linlin Yao,&nbsp;Xingchen Zhao,&nbsp;Runzeng Liu,&nbsp;Jianbo Shi,&nbsp;Guangbo Qu,&nbsp;Guibin Jiang","doi":"10.1021/envhealth.5c00834","DOIUrl":"https://doi.org/10.1021/envhealth.5c00834","url":null,"abstract":"<p>Metal nanoparticle (MNP)-added face masks are increasinglymarketedas washable antimicrobial products, yet their potential to releasemetals and MNPs during use and disposal remains poorly understood.In this study, three types of commercially available masks incorporatingMNPs (Ag-, Cu-, and Pt-masks) were obtained to characterize theirmetal composition and to evaluate the release of metals and MNPs undersimulated leaching conditions using ultrapure water and a simulateddetergent solution. Apart from Pt, As, and Cd, all masks containedmeasurable Ag, Cu, Cr, Ni, Pb, and Sb, indicating the widespread incorporationof multiple metals during fabrication. These metals and their correspondingMNPs were subsequently detected in the leachates. Although highermetal contents in the masks often resulted in greater leachate concentrations,the proportion of released metals did not consistently correspondto their initial in-mask abundance. The significant correlation observedbetween Cu NPs and Pb NPs in Cu-mask leachates suggests shared releasepathways or coupled mobilization processes. Prolonged immersion furthercontributed to increased particle size and broader size distributionof Ag NPs and Cu NPs. Single-particle analysis showed that, comparedwith ultrapure water, the detergent promoted a more pronounced releaseof most metals and facilitated the initial desorption of relativelylarger nanoparticles. These findings demonstrate that improperly discardedmasks can serve as a non-negligible source of metal and MNP contamination,underscoring the need for strengthened environmental risk assessmentand supporting the development of improved regulatory oversight andend-of-life management strategies.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 8","pages":"1720–1731"},"PeriodicalIF":8.8,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148810440","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}