Environment & HealthPub Date : 2026-07-17Epub Date: 2026-03-02DOI: 10.1021/envhealth.5c00566
Jiexia Cheng, Gang Tang, Ziniu Wang, Yun Ding, Jing Zhao, Yinjie Zhang, Haijiang Tian, Guangxuan Wang, Chunzhen Shi, Jie Gao, Guangbo Qu, Nan Sang, Guibin Jiang
{"title":"Nitrogen Dioxide Inhalation Disrupts Bone Marrow Hematopoiesis by Inducing Stage-Specific Developmental Blockage in Erythroid and Granulocytic Lineages in Mice","authors":"Jiexia Cheng, Gang Tang, Ziniu Wang, Yun Ding, Jing Zhao, Yinjie Zhang, Haijiang Tian, Guangxuan Wang, Chunzhen Shi, Jie Gao, Guangbo Qu, Nan Sang, Guibin Jiang","doi":"10.1021/envhealth.5c00566","DOIUrl":"10.1021/envhealth.5c00566","url":null,"abstract":"<p>Nitrogen dioxide (NO<sub>2</sub>) exposure is a knownrisk factorfor respiratory, cardiovascular, and neurological diseases and hasalso been linked to systemic hematological alterations, includingan increased risk of anemia. However, the effects of NO<sub>2</sub> exposure on the immune and hematopoietic function, which play acrucial role in the pathogenesis of these disorders, remain unclear.In this study, mice were exposed to environmentally relevant concentrationsof NO<sub>2</sub> (2.5 ppm, 5 h/day) for 28 days to investigate systemicimmune and hematopoietic effects across the lung, spleen, and bonemarrow (BM). NO<sub>2</sub> exposure triggered experimental anemia,with approximately 10% decreases in red blood cell (RBC) count andhemoglobin (HGB) concentration. Further investigation revealed a heightenedsensitivity of the BM to NO<sub>2</sub> exposure. Notably, NO<sub>2</sub>-induced hematopoietic and immune dysregulation was specificto the BM, with minimal effects observed in the peripheral lung orspleen. Flow cytometry analysis indicated disrupted erythropoiesis,characterized by an expansion of precolony-forming unit-erythroid(preCFU-E) precursors and a differentiation block at the orthochromaticerythroblast (ortho-EB) stage. Granulopoiesis in the BM was also altered,with a 31% decrease in mature neutrophils (NEs), potentially due todevelopmental defects at the metamyelocyte (MM) stage. In addition,upstream hematopoietic progenitors, including common myeloid progenitors(CMPs) and common lymphoid progenitors (CLPs), were significantlyexpanded, potentially reflecting myeloid-lineage compensation forRBC and NE deficits and broader hematopoietic stress. This study revealsthat NO<sub>2</sub> exposure can lead to both erythroid and granulocytichematopoietic abnormalities in the BM, providing novel mechanisticinsights into the potential health risks associated with NO<sub>2</sub>.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 7","pages":"1502–1514"},"PeriodicalIF":8.8,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148550857","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":"Circular RNA circDNAJC5 Regulates Ultrafine Particle–Disrupted Microglial Lipid Metabolism via the Sphingolipid Signaling Pathway","authors":"Hui-Xian Zeng, Guoliang Li, Qing-Guo Zeng, Qiong Zhang, Lili Liu, Xiao-Wen Zeng","doi":"10.1021/envhealth.5c00701","DOIUrl":"10.1021/envhealth.5c00701","url":null,"abstract":"<p>Ultrafine particles(PM<sub>0.1</sub>) can penetrate the brainand disrupt microglial function. Dysregulated lipid metabolism inactivated microglia contributes to the development of Alzheimer’sdisease (AD), yet the epigenetic mechanisms underlying PM<sub>0.1</sub>-induced lipid metabolic disruption remain poorly understood. CircularRNAs (circRNAs) are emerging regulators of lipid metabolism, promptingus to investigate their role in PM<sub>0.1</sub>-exposed microglia. <em>In vitro</em> models of PM<sub>0.1</sub>-treated microglia (HMC3and BV2) were established. We identified <em>circDNAJC5</em>, a lipid metabolism–associated circRNA, as significantlydownregulated during PM<sub>0.1</sub>-induced lipid metabolic disruption. <em>circDNAJC5</em> silencing aggravated lipid dysregulation, whereasits overexpression mitigated PM<sub>0.1</sub>-induced metabolic alterations. <em>circDNAJC5</em> functioned as a molecular sponge for <em>miR-98–5p</em>, thereby regulating sphingomyelin synthase1 (SMS1), a key enzyme in the sphingolipid signaling pathway. <em>circDNAJC5</em> downregulation and lipid metabolic abnormalitieswere further validated in the brains of PM-exposed mice and AD mousemodels, as well as in the blood of elderly individuals with cognitiveimpairment and hyperlipidemia. These findings highlight an epigeneticmechanism linking environmental exposure to microglial lipid metabolismand suggest <em>circDNAJC5</em> as a potential biomarker forneurodegenerative and metabolic disorders.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 7","pages":"1454–1468"},"PeriodicalIF":8.8,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148550593","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}
Environment & HealthPub Date : 2026-07-17Epub Date: 2026-03-13DOI: 10.1021/envhealth.5c00615
Peng Du, Jing Yang, Chunjie Li, Kailai Lu, Jie Ban, Can Zhang, Chen Wang, Jingwei Zhang, Qinghua Sun, Yi Zhang, Lin Cai, Shuiyin Ding, Feng Liu, Shengli Li, Rongshan Li, Yanping Lyu, Jianlin Hu, Ting Liu, Chuanyu Gao, Yong Huo, Tiantian Li
{"title":"Quantifying the Health Benefits Linked to Reduced Traffic-Related PM2.5 Exposure on Acute Coronary Syndrome Incidence in China","authors":"Peng Du, Jing Yang, Chunjie Li, Kailai Lu, Jie Ban, Can Zhang, Chen Wang, Jingwei Zhang, Qinghua Sun, Yi Zhang, Lin Cai, Shuiyin Ding, Feng Liu, Shengli Li, Rongshan Li, Yanping Lyu, Jianlin Hu, Ting Liu, Chuanyu Gao, Yong Huo, Tiantian Li","doi":"10.1021/envhealth.5c00615","DOIUrl":"10.1021/envhealth.5c00615","url":null,"abstract":"<p>The transportation sector powered by fossil fuels isa significantcontributor to PM<sub>2.5</sub> pollution. Systematic evaluation oftraffic-related PM<sub>2.5</sub> on acute coronary syndrome (ACS)onset is not yet characterized, and the health benefits of reducedtraffic-related PM<sub>2.5</sub> and evidence-based mitigation strategiesare currently absent. We investigated the association of ACS onsetwith short-term traffic-related PM<sub>2.5</sub> exposure in a nationwidetime-stratified case-crossover study, using 627,828 ACS cases extractedfrom the China Cardiovascular Association. We evaluated the risksof ACS onset associated with traffic-related PM<sub>2.5</sub>, calculatedthe attributable onsets, and then conducted cluster analysis usingthe K-means algorithm to identify priority cities for emission reduction.We found a robust association between traffic-related PM<sub>2.5</sub> and ACS onset, i.e., an increased risk of 2.39% (95% CI: 1.79–3.00%)for same-day (lag 0) PM<sub>2.5</sub> per 10 μg/m<sup>3</sup> increase. The greatest health benefits due to a 1 μg/m<sup>3</sup> PM<sub>2.5</sub> reduction were achieved by traffic-relatedPM<sub>2.5</sub>, reaching 10,267 (95%CI: 4503–16,063) onsetsper year. In addition, three obvious categories were clustered, andtraffic-polluted cities were highlighted (cluster 2, not belongingto megacities), with high emissions and concentrations of traffic-relatedPM<sub>2.5</sub>. Therefore, intensified efforts to mitigate traffic-relatedPM<sub>2.5</sub> emissions should be promoted, and the prioritizationof emission reduction strategies in these traffic-polluted citiesis imperative for safeguarding public health.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 7","pages":"1545–1555"},"PeriodicalIF":8.8,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148550868","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}
Environment & HealthPub Date : 2026-07-17Epub Date: 2026-04-20DOI: 10.1021/envhealth.5c00679
Kristína Raticová, Julia Howanski, Beate Fink, Stefan Röder, Mario Bauer, Anne Schumacher, Ana C. Zenclussen, Tobias Kretschmer
{"title":"Combined Exposure to Endocrine Disruptors, BPA and BP-3, during Pregnancy and Lactation Alters Postnatal Body Mass, Growth, White Adipose Tissue Morphology, and Adipogenic Gene Expression in a Sex-Specific Manner","authors":"Kristína Raticová, Julia Howanski, Beate Fink, Stefan Röder, Mario Bauer, Anne Schumacher, Ana C. Zenclussen, Tobias Kretschmer","doi":"10.1021/envhealth.5c00679","DOIUrl":"10.1021/envhealth.5c00679","url":null,"abstract":"<p>Endocrine-disrupting chemicals (EDCs) like bisphenolA (BPA) andbenzophenone-3 (BP-3) are omnipresent and previously linked to variousmetabolic disorders. As EDC exposure already begins during prenataldevelopment, we investigated the effects of BPA and BP-3 exposureduring gestation and lactation using a murine model on adipogenesisand metabolic pathways in white adipose tissue (WAT) in the offspring.We monitored postnatal body mass and analyzed the morphology and geneexpression of WAT in adult male and female offspring. BPA- and BPA+BP-3-exposedmales showed an increase in body mass in early adulthood, whereasBP-3-exposed females presented a decreased growth rate later in life.We identified altered adipocyte area and distribution, suggestinghyperplasia in the WAT of BPA and BPA+BP-3-exposed males. Gene expressionanalysis showed Pparg upregulation in BPA+BP-3-exposed males and Fabp4and Adipoq downregulation in BP-3-exposed females. Sex-specific associationsbetween gene expression, adipocyte area, and body mass in controlswere disrupted by EDC exposure. Our findings suggest increased postnatalbody mass and Pparg-mediated WAT hyperplasia in BPA+BP-3-exposed malemice. Fabp4 and Adipoq downregulation may be responsible for counteractingthe BP-3-induced metabolic dysregulation in females. This calls forconsideration of sex-specific differences of endocrine disruptionin the future development of preventive and therapeutic targets formetabolic disorders.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 7","pages":"1373–1387"},"PeriodicalIF":8.8,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148550674","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}
Environment & HealthPub Date : 2026-06-19Epub Date: 2026-02-02DOI: 10.1021/envhealth.5c00450
Pin Wang, Xinyin Liu, Yankai Xia, Hang Chang, Bo Hang, Jian-Hua Mao
{"title":"A Critical Perspective on the Role of Thirdhand Smoke in Tumorigenesis: Initiator or Promoter","authors":"Pin Wang, Xinyin Liu, Yankai Xia, Hang Chang, Bo Hang, Jian-Hua Mao","doi":"10.1021/envhealth.5c00450","DOIUrl":"10.1021/envhealth.5c00450","url":null,"abstract":"<p>Thirdhandsmoke (THS), lingering tobacco residues onsurfaces andin dust after smoking, has emerged as a growing public health concern.While the carcinogenic risks of first- and secondhand smoke are wellestablished, the tumorigenic potential of THS remains inadequatelyunderstood. In this perspective, we systematically review the knownTHS-related compounds together with the existing biological findingsto provide evidence on the carcinogenic potential of THS. We assessthe role of THS in the context of the classic multistage model oftumorigenesis to address whether THS acts primarily as a tumor initiator,or as a promoter, or both. We also discuss methodological challengesin isolating the effects of THS on human health and the importanceof animal models and outline emerging strategies for risk assessment,biomarker discovery, and precision prevention. This Perspective isthe first to integrate chemical, toxicological, and mechanistic evidenceto evaluate the carcinogenic potential of THS within the frameworkof the multistage model of tumorigenesis, offering a new conceptualfoundation for understanding the role of THS in human cancer etiology,which is crucial for informing public health policies aimed at mitigatingits impact.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 6","pages":"1054–1060"},"PeriodicalIF":8.8,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148319529","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}
Environment & HealthPub Date : 2026-06-19Epub Date: 2026-02-10DOI: 10.1021/envhealth.5c00268
Nicolò Baranzini, Antonio Calisi, Gaia Marcolli, Camilla Bon, Davide Rotondo, Davide Gualandris, Laura Pulze, Annalisa Grimaldi, Francesco Dondero
{"title":"Incomplete versus Sustained Innate-Immune Responses in the Medicinal Leech following Chronic, Environmentally Relevant Per- and Polyfluoroalkyl Substance Exposure","authors":"Nicolò Baranzini, Antonio Calisi, Gaia Marcolli, Camilla Bon, Davide Rotondo, Davide Gualandris, Laura Pulze, Annalisa Grimaldi, Francesco Dondero","doi":"10.1021/envhealth.5c00268","DOIUrl":"10.1021/envhealth.5c00268","url":null,"abstract":"<p>Per- and polyfluoroalkyl substances (PFAS) persist inaquatic systems,yet hazard evaluations still rely largely on short-term tests. Wechronically exposed the medicinal leech <em>Hirudo verbana</em> for two months to four PFAS congeners at 1 nmol L<sup>–1</sup> aligned with the EU Drinking Water Directive thresholds (PFAS total= 0.50 μg L<sup>–1</sup>): a legacy long-chain acid (PFOA),two short-chain ether replacements (HFPO-DA and PFMoBa), and an intermediatemethoxy analogue (PFMOPrA). Histology, enzymatic histochemical staining,immunofluorescence, and quantitative polymerase chain reaction trackedthe canonical inflammatory sequence, represented by CD11b<sup>+</sup> granulocyte influx, CD31<sup>+</sup> neovessel formation, and recruitmentof CD45<sup>+</sup>/ACP<sup>+</sup> macrophage-like cells, togetherwith transcriptional responses of oxidative stress genes (<em>SOD</em> and <em>GST</em>) and two immune mediators (<em>Hv</em>RNASET2 and <em>Hm</em>AIF-1), chosen for theirknown role in leech innate immunity. PFOA and PFMOPrA sustained thefull CD11b/CD45/CD31 cascade, maintained high ACP activity, and stronglyupregulated <em>Hv</em>RNASET2, <em>Hm</em>AIF-1, <em>SOD</em> and <em>GST</em>, signaling stability, and tissue-remodelinginflammation. By contrast, HFPO-DA and PFMoBa induced a granulocyteinflux but failed to promote macrophage recruitment or neovascularization; <em>Hv</em>RNASET2 transcripts rose, whereas <em>Hm</em>AIF-1expression, ACP activity, and CD31 signal remained at the baseline.These outcomes suggest that while all PFAS trigger the same innate-immuneprogram, only PFOA and PFMOPrA sustained its full development. Takentogether, these observations suggest that multiple structural andbioactivity determinants, potentially including but not limited tothe chain length, shape the sustained response at the chronic levelin leeches. This supports the need for multitemporal, policy-relevantPFAS hazard assessment.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 6","pages":"1125–1138"},"PeriodicalIF":8.8,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148319269","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}
Environment & HealthPub Date : 2026-06-19Epub Date: 2026-01-23DOI: 10.1021/envhealth.5c00439
Lu Chen, Yuxuan Zhao, Jun Lv, Dianjianyi Sun, Pei Pei, Ling Yang, Yiping Chen, Huaidong Du, Shichun Yan, Dan Schmidt, Junshi Chen, Zhengming Chen, Liming Li, Canqing Yu
{"title":"Ambient Air Pollution and Hospital Admissions of AECOPD in 10 Regions of China: A Self-Controlled Study Based on a Cohort","authors":"Lu Chen, Yuxuan Zhao, Jun Lv, Dianjianyi Sun, Pei Pei, Ling Yang, Yiping Chen, Huaidong Du, Shichun Yan, Dan Schmidt, Junshi Chen, Zhengming Chen, Liming Li, Canqing Yu","doi":"10.1021/envhealth.5c00439","DOIUrl":"10.1021/envhealth.5c00439","url":null,"abstract":"<p>Gapsexist concerning the associations of PM<sub>2.5–10</sub>, gaseouspollutants, and composite pollutants with the acute exacerbationof chronic obstructive pulmonary disease (AECOPD). The interactioneffects of lifestyle factors, indoor air pollution, and meteorologicalconditions with air pollutants have been underexplored. This time-stratifiedcase-crossover study was nested within the China Kadoorie Biobankcohort study of middle-aged and elderly participants from five urbanand five rural areas in China spanning from 2004 to 2018. 10,712 participantswere included, each with a mean of 2.3 episodes of AECOPD hospitalizationsduring the observation period. A composite air pollution score wasderived through principal component analysis. <strong>S</strong>hort-termexposure to particulate matter and NO<sub>2</sub> was positively associatedwith hospital admissions for AECOPD, with the largest temperature-and humidity-adjusted odds ratio (95% confidence interval) of 1.101(1.073, 1.129) at a lag of 1 day for per 1 standard deviation increasein air pollution score. The effect of O<sub>3</sub> appeared to beconflicting. The associations were further corroborated by the self-controlledcase-series design. Unfavorable body shapes, cold season, and lowhumidity could exacerbate the influence of air pollution. These findingsreinforce the evidence of links between air pollution and AECOPD andimplicate the management of body weight and cold and dry circumstances.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 6","pages":"1176–1184"},"PeriodicalIF":8.8,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148319536","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":"Black Phosphorus Nanosheets Penetrate the Blood–Testis Barrier and Induce Reproductive Toxicity in Male Mice","authors":"Suhua Jiang, Fengkai Ruan, Fucong Zhang, Zewei Long, Xiaoyan Ding, Sihao Zhu, Zhineng Fu, Zhenghong Zuo, Xiaoming Jiang, Chengyong He","doi":"10.1021/envhealth.5c00379","DOIUrl":"10.1021/envhealth.5c00379","url":null,"abstract":"<p>Black phosphorus nanosheets (BPNSs), as an emerging subclassoftwo-dimensional (2D) nanomaterials, have exhibited extensive applicabilityin electronics, optoelectronics, and medical sciences. However, itsexpanding application in diverse fields has raised concerns aboutinadvertent environmental release, which might lead to potential ecologicaland health risks. Herein, mice were continuously exposed at dosesof 0.1 mg/kg/day (possible acceptable daily intake dose, ADI) and1 mg/kg/day (possible occupational exposure dose) to BPNSs for 28days. Using hyperspectral imaging and Evans blue fluorescence chromogenicassay, we confirmed that partial BPNSs penetrated the blood–testisbarrier (BTB) and distributed throughout the spermatogenic microenvironmentof testes. Mice exposed to BPNSs exhibited significant reproductivetoxicity, evidenced by abnormal sperm parameters, disordered spermatogeniccell layers, sloughed germ cells, and disrupted sex hormone levels.Further, BPNSs promoted the steroid synthesis pathway and inhibitedtestosterone aromatization, leading to testicular endocrine homeostasisdisorders. BPNSs also damaged germ cells in the testes via the apoptosispathway. In conclusion, our study not only highlights the male reproductivetoxicity of BPNSs but also demonstrates that BPNSs can penetrate theBTB and have bioaccumulation potential in the male reproductive system,which provides new insights into the toxicological implications of2D nanomaterials for mammalian fertility.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 6","pages":"1083–1095"},"PeriodicalIF":8.8,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147884419","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}
Environment & HealthPub Date : 2026-06-19Epub Date: 2026-01-29DOI: 10.1021/envhealth.5c00623
Shuo Zhang, Jun Guo, Yunkun Qian, Mengjun Mao, Dong An
{"title":"AI-Enabled Mapping of Structure-Hazard Relationships for Emerging Contaminants","authors":"Shuo Zhang, Jun Guo, Yunkun Qian, Mengjun Mao, Dong An","doi":"10.1021/envhealth.5c00623","DOIUrl":"10.1021/envhealth.5c00623","url":null,"abstract":"<p>Emerging contaminant hazards are widespread, yet evidenceis fragmentedacross the literature, registries, inventories, and bioassays. Thisstudy presents an integrated, reproducible framework that aligns literature-derivedsignals with molecular structure and regulatory hazard dimensionswithin a persistence, bioaccumulation, mobility, and toxicity (PBMT)lens. A task-tuned large language model extracted 21,277 mentionsfrom 9,557 publications; harmonization across CompTox, PubChem, andWikipedia yielded 1,081 unique candidates with 94.6% name consistencyagainst 17 inventories. The landscape shows abundant toxicity informationbut limited mobility data. Structure profiling identified a recurringmotif─an aromatic core with branched alkyl substituents andoxygenated groups─and directional associations with compositehazard (positive for halogenation and negative for several oxygenatedgroups). To extend pathway inference to list-naïve chemicals,AutoGluon models trained on Tox21/ToxCast were applied to 49 additionalcandidates. This produced end-point-level predictions concentratedat the protein-function level (receptors, enzymes, transcription factors),which is operationally useful for prioritization. Combining modelscores with PBMT evidence density yielded an auditable prioritization,highlighting where mobility measurements and focused assays wouldmost increase confidence. The framework links textual, structural,regulatory, and predictive streams to enable rapid screening, targeteddata acquisition, safer substitution, and adaptive regulatory updating.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 6","pages":"1251–1262"},"PeriodicalIF":8.8,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148319551","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}
Environment & HealthPub Date : 2026-06-19Epub Date: 2026-03-03DOI: 10.1021/envhealth.5c00684
Haoduo Zhao, Yun-Chung Hsiao, Chih-Wei Liu, Emily Werder, Jake Thistle, Yifei Yang, Jiahao Feng, Xueying Wang, Jingya Peng, Taylor Teitelbaum, Stephanie M. Engel, Kun Lu
{"title":"High-Throughput Suspect Screening Reveals Widespread Pesticide Exposure in Early Childhood","authors":"Haoduo Zhao, Yun-Chung Hsiao, Chih-Wei Liu, Emily Werder, Jake Thistle, Yifei Yang, Jiahao Feng, Xueying Wang, Jingya Peng, Taylor Teitelbaum, Stephanie M. Engel, Kun Lu","doi":"10.1021/envhealth.5c00684","DOIUrl":"10.1021/envhealth.5c00684","url":null,"abstract":"<p>Characterization of the human exposome, the totalityof exposure,provides unprecedented insights into the role of broad environmentalfactors in human diseases. Environmental exposures during developmentperiods are increasingly recognized as key determinants of long-termhealth outcomes, yet full-scale characterization of early life exposureremains largely underexplored. In the present study, we establisheda nontarget data acquisition for target analysis-based suspect screeningworkflow capable of screening over 1000 pesticides in a 14 min run.It was next applied to the analysis of 438 urine samples collectedfrom 187 children to comprehensively assess their pesticide exposurelandscapes. A total of 215 pesticide residues were identified, with51 detected in at least 20% of the samples. On average, 31 pesticideswere identified per child, with individual exposures ranging from21 to 50 compounds. Significant associations were observed for detectionfrequencies between child age, sex, and gestational age at birth andsubstantial pesticide co-occurrence patterns, suggesting potentialcoexposure risks. In total, this study constructs a high-throughputsuspect screening pipeline and reveals widespread pesticide exposurein a vulnerable subpopulation, representing significant advancementstoward characterizing, deciphering, and prioritizing the human exposome.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 6","pages":"1162–1175"},"PeriodicalIF":8.8,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148319277","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}