Environment & Health最新文献

{"title":"Comparing In Vivo Methylmercury Detoxification in Hunted Duck: Implications for Wildlife and Human Health","authors":"Samuel F. Lopez,&nbsp;Sarah E. Janssen,&nbsp;Brett A. Poulin,&nbsp;William P. Johnson,&nbsp;Michael T. Tate,&nbsp;Pieter Glatzel,&nbsp;Tylor J. Rosera,&nbsp;Grace J. Armstrong,&nbsp;Alain Manceau","doi":"10.1021/envhealth.6c00108","DOIUrl":"https://doi.org/10.1021/envhealth.6c00108","url":null,"abstract":"<p>Great Salt Lake (GSL) waterfowl have elevated mercury(Hg) concentrations,and <em>in vivo</em> detoxification of neurotoxic and bioaccumulativemethylmercury (MeHg) can occur through Hg-selenium (Se) complexation,influencing the suitability of Hg consumption advisories. Here, wepresent Hg chemical speciation and Hg stable isotope measurementsof brain, breast muscle, liver, and kidney samples from two GSL duckspecies─northern shoveler (<em>Spatula clypeata</em>) and cinnamon teal (Spatula cyanoptera). Chemical and stable isotopemeasurements, along with high energy resolution fluorescence detectedX-ray absorption near-edge structure (HERFD-XANES) spectroscopy, indicatethe occurrence of <em>in vivo</em> MeHg demethylation in bothbird species. The percentage of total Hg (THg) as MeHg (% MeHg) variedwith tissue type (brain &gt; breast muscle &gt; kidney &gt; liver),and differencesbetween δ²⁰² THg and δ²⁰² MeHg werelinearly correlated with % MeHg. Demethylated inorganic Hg was a mixtureof Hg-dithiolate (Hg(SR)₂) and Hg-tetraselenolate (Hg(Sec)₄) in both bird species. Notably, liver THg concentrationswere elevated in northern shoveler liver tissues relative to thoseof cinnamon teal (7.54 ± 4.69 mg/kg versus 2.19 ± 1.27 mg/kg,dry weight, respectively) and % MeHg liver values were significantlylower (40% ± 19% versus 68% ± 14%), indicating taxonomicdifferences in Hg detoxification and depuration. THg concentrationsin waterfowl species from this study were comparable to previouslyreported levels, indicating that elevated Hg concentrations in northernshoveler and cinnamon teal at GSL have persisted over the past twodecades. Due to <em>in vivo</em> demethylation, we show thatTHg is not an effective proxy for MeHg within duck species, carryingimplications for current GSL waterfowl consumption advisories andassessments exposure risk. This study highlights important differencesin MeHg detoxification between waterbird taxa and provides furtherinsights into Hg toxicity risk to GSL waterbirds.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2137–2149"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148980769","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":"Air Conditioning Use and Ambulance Transports for Heat-Related Illness Across Summer Months in the Tokyo Metropolitan Area","authors":"Lisa Yamasaki,&nbsp;Chris Fook Sheng Ng,&nbsp;Aurelio Tobias,&nbsp;Yuya Takane,&nbsp;Kazuki Yamaguchi,&nbsp;Masahiro Hashizume","doi":"10.1021/envhealth.5c00808","DOIUrl":"https://doi.org/10.1021/envhealth.5c00808","url":null,"abstract":"<p>Heatis a growing public health threat, yet seasonalvariationsin adaptation including air conditioning (AC) use remain poorly understood.We examined the modifying role of electricity consumption (EC), aproxy for air conditioning (AC) use, in the association between maximumtemperature and ambulance transports for heat-related illness in theTokyo Metropolitan Area. Daily ambulance transport data (June-September,2015–2019), alongside maximum temperature and EC data, wereanalyzed across seven prefectures. Using a two-stage approach, wefitted quasi-Poisson regression models to estimate relative risks(RRs) per 1 °C increase in maximum temperature under high andlow EC conditions, and pooled prefecture-month-specific estimatesthrough multivariate meta-analysis. Attributable fractions (AFs) andattributable numbers (ANs) were also calculated. A total of 88,893transports were analyzed. In June, higher risks were observed underhigh EC (RR = 1.37, 95%CI: 1.32–1.42) compared with low EC(RR = 1.28, 95%CI: 1.25–1.32). In July, the pattern reversed,with lower risks under high EC (RR = 1.33, 95%CI: 1.30–1.36)than low EC (RR = 1.39, 95%CI: 1.35–1.44). EC modified theassociation between heat and ambulance transport in both early summermonths (<em>p</em> = 0.01 and 0.03, respectively), but notin August or September. Across months and EC strata, heat-attributablefractions ranged from 22.1% to 34.0%. The higher risks under highEC in June may have reflected delayed or insufficient air conditioninguse, whereas the lower risks in July are consistent with a possibleprotective role of AC emerging as the season progresses. These findingsunderscore the need for early season adaptation measures.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2119–2125"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985260","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":"Neuronal and Astrocytic Lipid Metabolic Coupling Mediates Ozone-Induced Learning and Memory Impairment","authors":"Ben Li,&nbsp;Xiaomin Liang,&nbsp;Xue Cui,&nbsp;Wenxu Zhao,&nbsp;Jinjin Xue,&nbsp;Su Wang,&nbsp;Ting Liu,&nbsp;Liangpo Liu,&nbsp;Jianquan Guo,&nbsp;Wenping Zhang,&nbsp;Yulan Qiu,&nbsp;Huifang Zhang,&nbsp;Jinzhu Yin,&nbsp;Xin Li,&nbsp;Xiaopeng Ji,&nbsp;Meiqiong Wu,&nbsp;Tingting Ku,&nbsp;Tong Wang","doi":"10.1021/envhealth.5c00851","DOIUrl":"https://doi.org/10.1021/envhealth.5c00851","url":null,"abstract":"<p>Surface ozone (O₃) induces chronic oxidativestressand lipid peroxidation in the brain, increasing the risk of neurodegenerativedisease. Lipid metabolic coupling between neurons and astrocytes isvital for brain health. However, its response to O₃-inducedoxidative stress remains largely unexplored. In this study, subacuteO₃ exposure (0.5 or 1.5 ppm, 4 h/day, for 28 days) resultedin learning and memory impairments, accompanied by neuronal loss,glial cell activation, neuroinflammation, and lipid peroxidation inmice. An important outcome of exposure to reactive oxygen species(ROS) generated by O₃ is the buildup of lipid dropletsin the astrocytes. Interestingly, in neurons, O₃ exposureactivates c-Jun N-terminal kinase and sterol regulatory element-bindingprotein, promoting lipogenesis. As cells attempt to cope with thisstress, O₃ interferes with the liver X receptor/apolipoproteinE/ATP-binding cassette transporter A1 pathway in astrocytes, reducingthe efficiency of lipid transport from neurons to astrocytes. Thisimbalance─where the astrocytic transport machinery fails tocompensate for accelerated neuronal lipid synthesis─leads toa breakdown of lipid detoxification processes. Meanwhile, impairedexpression of genes related to lipid degradation exacerbates O₃-induced lipotoxicity and neuronal damage. Supplementationwith <em>N</em>-acetylcysteine or citicoline sodium mitigatedthe O₃-induced disordered lipid metabolism and learningand memory impairments. This study highlights the role of neuron-astrocytelipid metabolic coupling in mediating O₃-induced neurotoxicityand offers a potential approach for addressing O₃ pollution-inducedneurodegenerative diseases.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2069–2083"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985295","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":"BPM Exposure Induces Pulmonary Dysfunction in Adult Mice and Adverse Intergenerational Pulmonary Effects in Offspring","authors":"Jie Zhao,&nbsp;Zehong Wu,&nbsp;Kelei Pan,&nbsp;Chenming Yi,&nbsp;Liuyan Fu,&nbsp;Wenjuan Zhang,&nbsp;Jie Zhang,&nbsp;Yong Liang","doi":"10.1021/envhealth.5c00825","DOIUrl":"https://doi.org/10.1021/envhealth.5c00825","url":null,"abstract":"<p>Bisphenol M (BPM), a structural analogue of bisphenolA, has becomeincreasingly prevalent in the environment, raising concerns aboutits potential health impacts. However, the pulmonary toxicity of BPM,particularly with regard to direct exposure in adults and potentialintergenerational respiratory effects, is not well understood. Thisstudy systematically investigates the mechanisms of BPM-induced pulmonarydysfunction in adult mice using integrated transcriptomic and proteomicanalyses while also evaluating intergenerational respiratory effectsin the offspring of a pregnant mouse. In adult mice, BPM exposureimpaired pulmonary function and induced histopathological alterationsincluding inflammatory infiltration and early-stage fibrotic changes.At the molecular level, BPM disrupted pulmonary immune-inflammatoryhomeostasis by synergistically activating the NF-κB and MAPKpathways, while suppressing T-cell receptor─and Fc receptor─mediatedimmunoregulatory signals. Notably, maternal BPM exposure resultedin pulmonary impairment in female offspring, as evidenced by alteredlung function parameters and the corresponding histopathological abnormalities.In summary, these findings demonstrate that BPM induces pulmonarydysfunction in adult mice by disrupting immune-inflammatory homeostasiswhile also conferring sex-specific intergenerational respiratory healthrisks.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1954–1964"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985231","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":"Gestational Low-Dose Bisphenol A Exposure Enhances Susceptibility to Metabolic Disorders in Adult Offspring Mice: Role of the Gut Microbiota-SCFAs-GPRs Axis","authors":"Yun Hong,&nbsp;Yujie Qiu,&nbsp;Qingqing Yang,&nbsp;Bingbing Sun,&nbsp;Yuheng Zhang,&nbsp;Zhiyuan Zhu,&nbsp;Zuo Li,&nbsp;Tong Shen","doi":"10.1021/envhealth.6c00171","DOIUrl":"https://doi.org/10.1021/envhealth.6c00171","url":null,"abstract":"<p>Bisphenol A (BPA), frequently detected at low levelsin pregnantwomen, has been linked to long-term metabolic disturbances in offspring.Emerging evidence indicates that maternal gut microbiota criticallyinfluence offspring susceptibility to metabolic diseases through theirmetabolites. This study aimed to investigate how maternal gut microbiotaand short-chain fatty acids (SCFAs) mediate the increased susceptibilityto high-fat-diet (HFD)-induced metabolic disorders in adult offspringfollowing gestational low-dose BPA exposure. Pregnant mice were exposedto 0, 10, 100, and 1000 nmol/L BPA via drinking water throughout gestation,after which pups were cross-fostered by unexposed dams and fed normalchow or HFD until adulthood. Adult offspring from BPA-exposed damsexhibited aggravated HFD-induced dyslipidemia and insulin resistance.Maternal BPA exposure decreased the abundance of f_<em>Prevotellaceae</em> and g_<em>Bacteroides</em>, accompanied by reduced circulatingSCFAs in both dams and offspring. Reduced SCFAs impaired embryonicpancreas and intestinal development by downregulating GPR41 and GPR43,which may predispose offspring to metabolic disorders at adulthood.Importantly, maternal high-fiber diet restored gut microbiota compositionalong with SCFA production, normalized embryonic GPRs expression,and subsequently alleviated offspring metabolic impairments. Thesefindings provide key insights into BPA-induced developmental programmingof metabolic disorders and offer promising strategies against metabolicdysfunction induced by endocrine-disrupting chemicals.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2041–2054"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985294","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":"Role of Cellular-Ferroptosis-Mediated HMGB1 Nuclear Translocation in Indium-Tin-Oxide-Nanoparticle-Induced Inflammatory Lung Injury","authors":"Yueyue Mu,&nbsp;Jiawei Wu,&nbsp;Xiaomeng Ding,&nbsp;Yanting Pang,&nbsp;Yuna Cao,&nbsp;Jing Qu,&nbsp;Haopeng Zhang,&nbsp;Qing Liu,&nbsp;Ting Zhang","doi":"10.1021/envhealth.5c00667","DOIUrl":"https://doi.org/10.1021/envhealth.5c00667","url":null,"abstract":"<p>Indium tin oxide (ITO) particles, widely utilized inelectronicsand energy technologies, pose significant pulmonary risks due to occupationalexposure during manufacturing. While emerging evidence links ITO tosevere lung pathologies, critical gaps persist in understanding size-dependenteffects and molecular mechanisms. This study systematically investigatesthe size-dependent effects of nanoscale ITO (N-ITO) and submicron-scaleITO (U-ITO) on pulmonary toxicity, focusing on ferroptosis as a keymechanism. <em>In vivo</em>, repeated oropharyngeal exposureof mice to ITO (3.6 and 36 mg/kg) induced dose-dependent lung inflammationand ferroptosis, marked by lipid peroxidation, Fe²⁺ accumulation,and dysregulation of Gpx4 and Scl7a11 proteins, with pulmonary macrophagesidentified as primary targets. <em>In vitro</em>, THP-1 macrophagesexposed to 6.25–25 μg/mL ITO exhibited size-dependentcytotoxicity, inflammation, and ferroptotic hallmarks. Mechanistically,ITO-triggered ferroptosis promoted HMGB1 secretion and nuclear translocation,which activated the RAGE/p38MAPK pathway, amplifying inflammatoryresponses. Notably, N-ITO induced stronger ferroptosis and inflammationthan U-ITO, correlating with enhanced macrophage uptake due to itsnanoscale dimensions. Integrating these findings, we propose an AdverseOutcome Pathway (AOP) framework for ITO-induced lung injury, whichcellular uptake may serve as the molecular initiating event and linkferroptosis-driven high mobility group protein B1 (HMGB1) release,RAGE/p38MAPK activation, and chronic inflammation to adverse pulmonaryoutcomes. This study underscores the necessity of size-specific occupationalexposure limits for ITO nanoparticles and provides a mechanistic foundationfor risk assessment and management strategies in occupational settings.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1910–1929"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148980736","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":"Unveiling the Mechanisms of Ozone-Induced Male Reproductive Toxicity: Insights from Testicular Proteomics and CTD Database","authors":"Ruijian Zhuge,&nbsp;Jiaze Ren,&nbsp;Yurou Zhu,&nbsp;Shurui Wang,&nbsp;Ruohui Chen,&nbsp;Bo Lai,&nbsp;Zhen Yan,&nbsp;Yanbo Li,&nbsp;Caixia Guo","doi":"10.1021/envhealth.5c00826","DOIUrl":"https://doi.org/10.1021/envhealth.5c00826","url":null,"abstract":"<p>Ambient ozone (O₃) is a major air pollutant,yet itsmechanistic impact on male reproduction remains poorly understood,despite links to reduced sperm quality. We developed a short-termO₃ exposure mouse model and utilized testicular proteomics,Comparative Toxicology Database (CTD) mining, and <em>in vitro</em> investigations to identify mediators. Results showed that O₃ exposure dose-dependently impaired sperm quality, disruptedhistology, and altered testosterone and luteinizing hormone levels.Proteomics revealed disturbances in cholesterol, steroid hormone,and retinol metabolism in mice testicular tissue in response to O₃ exposure, alongside impaired spermatogenesis. More importantly,HIF-1α/mTOR signaling was suggested as a crucial mediator toO₃-elicited testicular toxicity based on proteomic andCTD analysis. Further mechanistic validation using an <em>in vitro</em> air–liquid interface (ALI) coculture of MLE-12 alveolar epithelialand TM3 Leydig cells demonstrated that O₃ exposure triggeredreactive oxygen species (ROS)-mediated oxidative stress, subsequentlyinactivated HIF-1 signaling, and impaired Leydig cell steroidogenesis,thereby contributing to testicular injury and declined sperm quality.Overall, our findings identify HIF-1 signaling as a pivotal regulatorlinking the exposure of O₃ to steroidogenic dysfunctionand spermatogenic disruption in male reproduction, offering novelmechanistic insights for male reproductive toxicology.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2024–2040"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148980791","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":"Updated Knowledge on Radon Exposure: Quantification Methods, Health Effects, and Molecular Mechanisms","authors":"Jianfang Han,&nbsp;Weihai Zhuo,&nbsp;Bo Chen,&nbsp;Jarosław Wieczorek,&nbsp;Yupan Zhang,&nbsp;Yining He,&nbsp;Bin Feng","doi":"10.1021/envhealth.5c00835","DOIUrl":"https://doi.org/10.1021/envhealth.5c00835","url":null,"abstract":"<p>Radon, the primary source of natural ionizing radiationand oneof the leading causes of lung cancer, is a critical yet often neglectedcomponent of exposomics. Integrating radon into the exposome frameworkrequires accurate exposure quantification and a clear understandingof dose–response relationships, while relevant knowledge remainsfragmented across disciplines. This review synthesizes three decadesof multidisciplinary research across three key areas: exposure quantification,health effects, and molecular mechanisms. Our key findings highlight:(1) Despite Internet of Things and artificial intelligence have improvedthe estimation of radon exposure at the population level, challengesin terms of model scalability, interpretability, universality, andindividual exposure uncertainty still need to be addressed. (2) Thecausal link to lung cancer has been established, yet evidence fornonlung cancer outcomes (e.g., cardiovascular disease, leukemia) remainsuncertain, necessitating the need for large-scale prospective studies.(3) Molecular pathways like oxidative stress and DNA damage are implicated,but requiring high-throughput multiomics approaches to define preciseinteraction networks and identify robust biomarkers. Therefore, wepropose a roadmap prioritizing refined exposure assessment techniques,systematic evaluation of nonlung cancer health effects, and multiomics-drivenbiomarker discovery. This review emphasizes the necessity of incorporatingradon into exposomics and offers a foundation for developing moreeffective, evidence-based public health interventions.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1877–1895"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985238","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":"Socioeconomic Disparities in PFAS Exposure and Susceptibility to Diabetes in Chinese Adults: A Nationwide Cross-Sectional Study","authors":"Saisai Ji,&nbsp;Jinghua Wang,&nbsp;Yingli Qu,&nbsp;Zheng Li,&nbsp;Yitao Pan,&nbsp;Yawei Li,&nbsp;Haocan Song,&nbsp;Linna Xie,&nbsp;Wenli Zhang,&nbsp;Jiayi Cai,&nbsp;Feng Zhao,&nbsp;Ying Zhu,&nbsp;Zhaojin Cao,&nbsp;Shilu Tong,&nbsp;Yuebin Lv,&nbsp;Jiayin Dai,&nbsp;Guang Jia,&nbsp;Xiaoming Shi","doi":"10.1021/envhealth.6c00036","DOIUrl":"https://doi.org/10.1021/envhealth.6c00036","url":null,"abstract":"<p>Emergingevidence indicates that socioeconomic status (SES) shapesnot only patterns of environmental exposure but also the susceptibilityto environmental hazards. Per- and polyfluoroalkyl substances (PFAS)represent a distinctive case in which socioeconomically disadvantagedpopulations often exhibit lower exposure levels, raising criticalquestions about how such exposure patterns translate into health inequalities,particularly for diabetes. Using cross-sectional data from 10 302adults participating in the China National Human Biomonitoring (CNHBM)program, we examined socioeconomic disparities in serum PFAS concentrationsand assessed whether lower SES is associated with stronger PFAS-diabetesassociations among Chinese adults. We found that individuals withhigher SES exhibited 4–10% higher serum concentrations of PFOA,PFUnDA, PFHxS, PFHpS, PFOS, and 6:2 Cl-PFESA (all <em>p</em> values &lt;0.05). In contrast, associations between PFAS exposureand diabetes were generally stronger among low-SES participants. Acrossmultiple PFAS, odds ratios for diabetes in the low-SES group were0–17% greater relative to the high-SES group, with statisticallysignificant effect modification observed for PFUnDA, PFOS, and 6:2Cl-PFESA. These findings indicate that socioeconomic disadvantagemay be associated with greater susceptibility, even at lower exposurelevels, underscoring the importance of considering differential susceptibilitywhen assessing environmental health risks and advancing health equity.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2126–2136"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985261","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":"Protecting High-Vulnerability Elderly in Climate Emergencies: Lessons from Beijing’s 2025 Floods","authors":"Guanhao He,&nbsp;Jianxiong Hu,&nbsp;Wenjun Ma","doi":"10.1021/envhealth.6c00292","DOIUrl":"https://doi.org/10.1021/envhealth.6c00292","url":null,"abstract":"","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1853–1855"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985263","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}