Environment & Health最新文献

{"title":"Chemical-Specific Metabolic Disruption during Early Zebrafish Development is Modulated by the Microbiome","authors":"Nanna Fyhrquist,&nbsp;Lydia Gugescu,&nbsp;Emma Wincent,&nbsp;Harri Alenius","doi":"10.1021/envhealth.6c00215","DOIUrl":"https://doi.org/10.1021/envhealth.6c00215","url":null,"abstract":"<p>Environmentalcontaminants such as per- and polyfluoroalkyl substances,bisphenols, and agricultural fungicides are increasingly recognizedas metabolic disruptors, yet how individual chemicals perturb metabolicpathways during early development remains incompletely understood.Here, we used targeted and untargeted metabolomics and pathway analysisin zebrafish embryos to characterize metabolic disruption inducedby perfluorooctanesulfonic acid (PFOS), boscalid (BOS), and bisphenolF (BPF). Each compound elicited a distinct metabolic fingerprint,indicating chemical-specific patterns of metabolic stress rather thana uniform response across toxicants. Comparative analysis demonstrateddivergence in central metabolic pathways, including mitochondrialmetabolism, amino acid and nucleotide turnover, redox balance, andtryptophan metabolism. PFOS induced the most extensive metabolic perturbation,whereas BOS and BPF produced more restricted but distinct metabolicprofiles. Comparison of germ-free and conventionally colonized embryosshowed that host microbial status modulated the magnitude, but notthe direction, of chemical-induced metabolic changes. These metabolicalterations align with exposure-specific transcriptional network modules,supporting distinct chemical modes of action. Together, these findingsdemonstrate that early life exposure to PFOS, BOS, and BPF resultsin chemically distinct metabolic stress phenotypes during developmentand illustrate how integrated metabolomic profiling can resolve compound-specificmetabolic effects while accounting for contextual modifiers such ashost microbial status.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2401–2415"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188029","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":"Associations between Antimicrobial-Resistant Gram-Negative Infections and Climate-Related Exposure in a Tertiary Medical Center in Central Luzon, Philippines","authors":"Paul L. C. Chua,&nbsp;Emerald J. O’Brien,&nbsp;Shuhei Nomura,&nbsp;Sophearen Ith,&nbsp;Chris Fook Sheng Ng,&nbsp;Azenith May H. Rafanan,&nbsp;Julie Anne B. Cabantog,&nbsp;Masahiro Hashizume,&nbsp;Miguel Antonio Salazar","doi":"10.1021/envhealth.5c00842","DOIUrl":"https://doi.org/10.1021/envhealth.5c00842","url":null,"abstract":"<p>Antimicrobialresistance (AMR) can worsen due to climate change.Several studies from China, Europe, and the USA have reported linearassociations between weather and AMR. To provide additional evidence,this epidemiological study explored the nonlinear associations ofshort-term (28-day prior) and long-term (annual anomaly) temperatureand rainfall exposure with AMR cases and multidrug resistance (MDR)at a single hospital in Pampanga, Philippines, a province with a tropicalclimate and high flood risk. Robust Poisson regression was used toestimate the associations between temperature and rainfall with AMRcases and the number of resistant antibiotics across subgroups ofbacteria, priority pathogens, specimens, age, sex, and season. Severalnonlinear associations exhibited an inverted U-shape, suggesting thatthe AMR risk peaks at specific temperatures or rainfall levels beforedeclining at extreme values. Another recurring nonlinear associationwas U- or J-shaped, suggesting increased MDR severity or a greaternumber of resistant antibiotics with low or high rainfall. These findingsunderscore the possibility of a more complex link between climateand AMR, warranting further investigation across more locations andsettings, whenever individual records are available. Future researchshould integrate ecological data to elucidate the mechanisms underlyingthese associations.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2333–2342"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188032","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":"Global Analysis of Metabolic Fluxes of Glucose and Glutamine in INS-1 Cells Exposed to Arsenite Using 13C-Isotopic Tracers","authors":"Ruijia Zhang,&nbsp;Liangyu Chen,&nbsp;Yingshi Lin,&nbsp;Wenhua Lu,&nbsp;Yizheng Li,&nbsp;Yangyang An,&nbsp;Qihong Yan,&nbsp;Xubin Yang,&nbsp;Tiangang Luan,&nbsp;Baowei Chen","doi":"10.1021/envhealth.5c00614","DOIUrl":"https://doi.org/10.1021/envhealth.5c00614","url":null,"abstract":"<p>Human exposure to arsenic has been reported to inducemetabolicdisorders in pancreatic β-cells. However, metabolic fluxes ofessential carbon sources in pancreatic β-cells under arsenicexposure were not quantitatively characterized. In this study, ¹³C-labeled glucose and glutamine were used as the tracersto examine their fates in INS-1 832/13 cells treated with arsenite(iAs^III). INS-1 832/13 cells exposed to three concentrationsof iAs^III (0.05, 0.5, and 1.0 μg/mL) maintained atleast 80.0% of cell viability in comparison to the controls. Glucoseuptake of INS-1 832/13 cells exposed to 1.0 μg/mL iAs^III was approximately 2 times higher than that of the controls. Accordingly,glucose was also accumulated in the iAs^III-treated INS-1832/13 cells. The activities of glucose-derived pathways in INS-1832/13 cells, including glycolysis, tricarboxylic acid (TCA) cycle,and pentose phosphate pathway (PPP), were consistently enhanced byiAs^III. However, mitochondrial respiratory indexes of INS-1832/13 cells, including oxygen consumption rate (OCR), ATP-linkedOCR, basal OCR, maximal respiration, and spare respiratory capacity,were considerably suppressed by iAs^III. Inhibitive effectsof iAs^III on metabolic pathway activities of glutaminewere observed. Collectively, our results suggest that iAs^III exposure can induce metabolic reprogramming involved with glucoseand glutamine in INS-1 832/13 cells.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 10","pages":"2199–2207"},"PeriodicalIF":8.8,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149188082","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":"The Human Microbiome in Airborne Particulate Matter–Associated Aging-Related Chronic Diseases: An Evidence-Stratified Review","authors":"Yiting Yang,&nbsp;Xuting Liu,&nbsp;Mingyue Wang,&nbsp;Xiangyu Zhu,&nbsp;Bingwei Yang,&nbsp;Jianzhong Cao,&nbsp;Yang Song,&nbsp;Guibin Jiang","doi":"10.1021/envhealth.5c00852","DOIUrl":"https://doi.org/10.1021/envhealth.5c00852","url":null,"abstract":"<p>Airborneparticulate matter (PM) exposure is increasingly recognizedfor its profound impact on human health. Emerging evidence highlightsthe human microbiome as a plausible intermediary between environmentalexposures and host physiological responses. While current researchlargely focuses on PM’s direct toxicological effects, the roleof microbiome disruption in mediating aging-related chronic diseasesremains underexplored. This review integrates epidemiological data,animal models, and multiomics approaches to examine the impact ofPM exposure on microbial communities across the respiratory, gut,and skin microbiomes, with a particular focus on the gut microbiome’srole in aging phenotypes. We propose an evidence-stratified PM Exposure–Microbiome–Agingframework, in which the microbiome is considered a plausible exposure-sensitiveinterface linking environmental exposure to health outcomes, withthe gut microbiota representing the most mechanistically developedinterface in the current literature. By synthesizing current evidenceon microbiome-linked pathways relevant to PM-associated chronic diseaserisk, this review provides a structured framework to guide futuremechanistic and translational research.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1856–1876"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148980790","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":"Molecular Mechanisms of Indoor Environmental Pollution tt-DDE-Induced Blood Pressure Elevation and the Protective Role of Human-Specific Gene CHRFAM7A","authors":"Siwen Li,&nbsp;Ying Su,&nbsp;Peng Fang,&nbsp;Shuzi Ye,&nbsp;Yu Yuan,&nbsp;Lemei Liu,&nbsp;Junchang Wang,&nbsp;Fang Xiao","doi":"10.1021/envhealth.5c00703","DOIUrl":"https://doi.org/10.1021/envhealth.5c00703","url":null,"abstract":"<p>Cooking oil fumes (COFs), a major source of indoor airpollutants,are responsible for approximately 90% of indoor particulate matteremissions. Trans,trans-2,4-decadienal (tt-DDE), the predominant aldehydein COFs, exhibits established mutagenic and carcinogenic potential.Although CHRFAM7A remains to be validated as a cardiovascular therapeutictarget, accumulating evidence positions it as a novel modulator ofthe cardiovascular pathophysiology. This study explored the protectivemechanisms of CHRFAM7A against the tt-DDE-induced vascular injury.First, inhalation of tt-DDE was observed to elevate blood pressure,an effect attributed to associated endothelial cell damage. Additionally,we found that CHRFAM7A-transgenic mice exhibit significant resistanceto tt-DDE-induced systolic hypertension and endothelial dysfunction.Mechanistically, the observed protection was attributed to the STAT3/HO-1pathway activation. Moreover, <em>in vitro</em> revealed thattt-DDE promotes KLF5-driven inflammatory responses through METTL3-dependentm6A modification, effects that were mitigated by CHRFAM7A overexpression.Notably, inhibition of HO-1 could abolish CHRFAM7A-mediated regulationof METTL3-dependent KLF5 translation. Collectively, these resultsidentify CHRFAM7A as a molecular safeguard against tt-DDE-inducedvascular pathology, functioning through coordinated regulation ofthe STAT3/HO-1/METTL3 signaling. This work thus provides new therapeuticinsights for cardiovascular disorders associated with COF exposure.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2055–2068"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148980792","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":"Transport of Perfluoroalkyl Substances (PFAS) by Three Renal Transporters: Implications for PFAS Bioaccumulation Mechanisms","authors":"Shan Niu,&nbsp;Yifei Ma,&nbsp;Arundhati Tewari,&nbsp;Carla Ng","doi":"10.1021/envhealth.6c00088","DOIUrl":"https://doi.org/10.1021/envhealth.6c00088","url":null,"abstract":"<p>The long biological half-lives of per- and polyfluoroalkylsubstances(PFAS) in humans have been linked to interactions with renal transportproteins and polypeptides. However, only a limited number of kidneytransporters have been studied for their ability to transport specificPFAS. Moreover, few studies have investigated whether PFAS alternativesserve as substrates for these transporters. In this study, we focusedon one renal influx transporter, organic anion transporter 1 (OAT1)and two efflux transporters (P-glycoprotein (P-g) and breast cancerresistance protein (BCRP)) involved in PFAS excretion. We evaluatedtwo well-studied PFAS, perfluorooctanoic acid (PFOA) and perfluorooctanesulfonate(PFOS), along with two current substitutes. Hexafluoropropylene oxidedimer acid (HFPO-DA), the major component of the PFOA alternativeGenX, was not transported by any of the studied renal transporters.In contrast, hexafluoropropylene oxide trimer acid (HFPO-TA), a minorcomponent of GenX, as well as PFOA itself, were taken up by all studiedtransporters. Both PFOS and its tested alternative (F53B), includingboth major and minor components, were substrates of all tested renaltransporters, with PFOS and F53B showing relatively higher transportactivity. BCRP- and P-gp-mediated transport of five PFAS underwenta saturable process with Michaelis constant (<em>K</em>_m) ranging from 1.29 to 7.92 μmol/L and 1.41 to 2.78μmol/L, respectively. The highest <em>V</em>_max/<em>K</em>_m ratio was observed for PFOA transportby P-gp (279 pmol/mg protein/min/(μmol/L)). To the best of ourknowledge, this is the first study reporting interactions betweenrenal transporters and these legacy PFAS replacements. These findingsenhance our understanding of PFAS bioaccumulation at the cellularand molecular levels, offering key parameters for PFAS toxicokineticmodeling.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2150–2157"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985262","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 Pollution Exposure Induces Vascular Endothelial Cell Dysfunction via Elevated Circulating F2: Multiomics Insights from an Ex Vivo Biosensor Assay","authors":"Jianzhong Zhang,&nbsp;Wenting Cheng,&nbsp;Yanting Li,&nbsp;Wanjun Zhang,&nbsp;Jiayin Sun,&nbsp;Jiahui Zhao,&nbsp;Yuxin Ma,&nbsp;Rong Zhang,&nbsp;Yuxin Zheng,&nbsp;Wei Han,&nbsp;Jinglong Tang","doi":"10.1021/envhealth.5c00833","DOIUrl":"https://doi.org/10.1021/envhealth.5c00833","url":null,"abstract":"<p>Air pollution-induced cardiovascular disease is a leadingcontributorto the increasing global disease burden. Disruption of vascular endothelialfunction is a central driver of disease onset; however, the systemicmechanisms linking pollution exposure to endothelial dysfunction remainpoorly defined. Here, we investigated early molecular responses toshort-term exposure via integrated proteomic, metabolomic, and transcriptomicanalyses. In a panel study of eight college students traveling fromQingdao to Shijiazhuang, China, where PM_2.5, PM₁₀, SO₂, NO₂, and CO levels were substantiallyhigher, we collected serum samples at multiple time points and assessedendothelial responses via <em>ex vivo</em> biosensors. Proteomicprofiling revealed the activation of hemostasis-related processeswith interaction network analysis identifying F2 (prothrombin) asa central node strongly correlated with pollutant exposure. Metabolomicanalysis revealed significant perturbations in bile acid biosynthesisand arginine–proline metabolism, with PM_2.5-associatedmetabolites predominantly enriched in energy metabolism-related pathways.Transcriptomic profiling of endothelial cells provided further corroboratingevidence that acute exposure to ambient air pollutants is capableof triggering endothelial cell activation. Subsequent weighted genecoexpression network analysis identified F2 as a pivotal molecularmediator underlying air pollutant-induced endothelial dysfunction.Together, these findings delineate the molecular architecture of acutepollution-induced endothelial cell dysfunction and identify F2-centeredpathways as potential early targets for mitigating cardiovasculartoxicity.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1896–1909"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985181","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":"Heterogeneous Risks of Chemical Components and Sources in Size-Resolved Particulate Matter on Ischemic and Hemorrhagic Stroke","authors":"Kun Hua,&nbsp;Miaomiao Wei,&nbsp;Mengyu Wang,&nbsp;Fuyin Wang,&nbsp;Qiyan Ding,&nbsp;Xinyao Feng,&nbsp;Lin Wang,&nbsp;Yingze Tian,&nbsp;Xin Li,&nbsp;Yinchang Feng","doi":"10.1021/envhealth.6c00019","DOIUrl":"https://doi.org/10.1021/envhealth.6c00019","url":null,"abstract":"<p>Atmosphericparticulate matter (PM) from different emission sourcesexhibits distinct size distributions and chemical compositions, whichmay differentially influence stroke risk. However, how particle size,chemical composition, and emission source jointly shape subtype-specificstroke risks remains unclear. In this study, 58,763 ischemic stroke(IS) and 2,588 hemorrhagic stroke (HS) hospitalizations were analyzedalongside 41 PM chemical components and 6 major emission sources identifiedacross 9 aerodynamic size fractions below 10 μm. Associationsbetween PM physicochemical properties and stroke were assessed ina time-series framework. Stroke risks exhibited pronounced heterogeneityacross particle size, chemical composition, emission source, strokesubtype, and demographic groups. IS was associated with a broad rangeof components below 1.1 μm and above 3.3 μm, whereas HSshowed stronger links to specific metals (As, Cu, Fe, Mn, Ni, Pb)and polycyclic aromatic hydrocarbons. Coal combustion (RR per IQR= 1.05; 95% CI: 1.01–1.10) and industrial emissions (RR perIQR = 1.18; 95% CI: 1.00–1.41) were the principal contributorsto IS and HS, respectively. Individuals younger than 60 years showedincreased HS risks related to most components in size &lt;0.43 μmand industrial emissions. Females showed stronger susceptibility toCu, traffic-related sources, and resuspended dust. Overall, our findingsshow that stroke risk varies according to particle size, chemicalcomposition, and emission sources, with distinct patterns across strokesubtypes and population groups. This integrative understanding helpsclarify the priority drivers of stroke risk and supports more strategicallytargeted air quality interventions.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1941–1953"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985229","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":"Occurrence of Waterborne Protozoa in a Full-Scale Drinking Water Treatment Plant in China by High-Throughput Screening and Genotyping","authors":"Huican Zhang,&nbsp;Ziming Han,&nbsp;Fuming Duan,&nbsp;Shumin Xiao,&nbsp;Min Yang,&nbsp;Yu Zhang","doi":"10.1021/envhealth.5c00863","DOIUrl":"https://doi.org/10.1021/envhealth.5c00863","url":null,"abstract":"<p>Thisstudy investigates potential risk points for waterborne protozoain a full-scale drinking water treatment plant using high-throughputscreening and genotyping. Among 19 protozoan targets of high-throughputquantitative PCR (HT-qPCR), 11 were positive, with <em>Cryptosporidium</em> (22.2%) and <em>Enterocytozoon bieneusi</em> (22.2%) exhibiting the highest detectionrates. Three and two protozoan species were detectable in the sourcewater of the reservoir and plant influents, respectively; while noprotozoa were detected above the detection limit in plant effluents,as confirmed by both HT-qPCR and an immunofluorescence assay targeting<em>Cryptosporidium</em> oocysts and <em>Giardia</em> cysts. Notably, backwash water (from the sand filter and activatedcarbon filter) and sediment (from the sedimentation tank) samplesexhibited higher prevalence and abundance of protozoa. Particularly,backwash water from the sand filter contained eight protozoan targets,with a total abundance of 1.5 × 10⁵ copies/g. Furthernested PCR-based genotyping revealed that detected <em>Cryptosporidium parvum</em> belonged to <em>gp60</em> subtype IIdA19G1 and <em>E. bieneusi</em> wasidentified as genotype AAE1, suggesting that <em>C. parvum</em> may pose a threat to human health. Overall, the current drinkingwater treatment process ensures effective protozoan removal in theeffluent, but the backwash water and sediment pose potential risk.This study suggested enhancing monitoring and implementing additionalmeasures for key risk points to optimize the prevention and controlof waterborne protozoa.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"1977–1986"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985233","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 Legacy of Exposure: Lactational PFAS Transfer and Early-Life Accumulation in Northern Elephant Seals","authors":"Kara M. Joseph,&nbsp;Sarah J. Rehm,&nbsp;Jessie R. Chappel,&nbsp;Daniel E. Crocker,&nbsp;Rachel R. Holser,&nbsp;Daniel P. Costa,&nbsp;Jane I. Khudyakov,&nbsp;Erin S. Baker","doi":"10.1021/envhealth.5c00782","DOIUrl":"https://doi.org/10.1021/envhealth.5c00782","url":null,"abstract":"<p>Although PFAS are widely acknowledged as ubiquitous andpersistentorganic pollutants, critical gaps remain in mapping environmentaldistribution and clarifying health-relevant exposure pathways, especiallyin early life. Marine mammal milk provides a unique window into bothenvironmental occurrence and intergenerational transfer, especiallyin capital-breeding species in which lactation occurs during prolongedfasting with rapid lipid mobilization. Here, we investigated PFASburdens and maternal transfer in the northern elephant seal (<em>Mirounga angustirostris</em>). Elephant seals, with highlycharacterized nursing behavior and foraging patterns, serve as a valuablesentinel for modeling both patterns of lactational transfer and assessingPFAS concentrations in deep-ocean ecosystems. This study assessedplasma from 14 mother-pup pairs and milk from 9 mothers using a non-targeteddata acquisition platform coupling liquid chromatography, ion mobilityspectrometry, and high-resolution mass spectrometry (LC-IMS-HRMS).Twenty-seven PFAS were identified across all matrices and age groups,and quantitative analyses revealed concentrations in milk and plasmathat exceeded relevant human-based exposure and dietary intake thresholds.Across all pairs, pup plasma PFAS concentrations were consistentlyhigher than maternal concentrations. Specifically, the highest PFASconcentrations were observed in weaned pups (average ∑16 PFAS= 89.08 ng/mL), indicating pronounced early-life accumulation and/orredistribution during the postweaning fast. Concentrations of PFASin the milk also correlated with maternal and pup plasma levels, demonstratingpair-specific contaminant profiles. Suspect screening further illustratedmatrix- and lineage-specific exposure patterns within matched mother-puppairs, consistent with shared foraging grounds and lactational transfermechanisms. Together, these findings indicate that neonatal marinemammals in extreme capital-breeding systems experience elevated PFASbody burdens during sensitive developmental windows.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 9","pages":"2093–2105"},"PeriodicalIF":8.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148985259","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}