Environment & Health最新文献

{"title":"Seasonality in Mortality and Health: Environmental and Demographic Perspectives.","authors":"Lina Madaniyazi, Aurelio Tobias, Sergi Trias-Llimós, Júlia Almeida Calazans, Masahiro Hashizume","doi":"10.1021/envhealth.5c00121","DOIUrl":"https://doi.org/10.1021/envhealth.5c00121","url":null,"abstract":"<p><p>Seasonality is a well-documented characteristic of many health outcomes, with mortality exhibiting distinct seasonal patterns due to environmental and demographic influences. While temperature is a key driver of these variations, additional factors such as air pollution, infectious disease cycles, and socioeconomic disparities also shape seasonal health risks. This commentary discusses methodological approaches for assessing seasonality, highlighting key metrics for summarizing seasonality such as peak-to-trough ratios and attributable fractions. We further discuss how both environmental and demographic factors interact to drive seasonality in mortality as well as the potential impact of climate change on driving future seasonality patterns. Finally, we extend the discussion beyond mortality to explore seasonal variations in other health outcomes. Understanding seasonality in health through interdisciplinary research between epidemiology and demography is essential for public health preparedness.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 2","pages":"167-172"},"PeriodicalIF":6.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12930310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147310580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-Specific Biological Aging-Related Lipidomic Profiles Mediate the Impact of Urinary Polycyclic Aromatic Hydrocarbon Exposures on Cognitive Function in Healthy Older Adults.","authors":"Huimin Ren, Wanying Shi, Xiaojie Guo, Xiao Ma, Jiran Zhang, Yongjun Situ, Chenfeng Li, Chenlong Li, Peijie Sun, Yibo Xu, Kangning Cao, Jiankun Qian, Yifu Lu, Shilu Tong, Xiaoming Shi, Song Tang","doi":"10.1021/envhealth.5c00391","DOIUrl":"10.1021/envhealth.5c00391","url":null,"abstract":"<p><p>Emerging evidence suggests that exposure to polycyclic aromatic hydrocarbons (PAHs) may exacerbate cognitive deterioration and biological aging, but the biomolecular mechanisms, particularly those driving sex-specific vulnerability, remain unclear. This 5-month longitudinal panel study, conducted among 76 healthy participants aged 60-69 in Jinan, China. Urinary concentrations of six PAHs were measured, and biological age was estimated using the Klemera and Doubal method. The associations between individual and combined PAH exposures and cognitive function were examined using linear mixed-effects model, and the mediating effect of biological aging was assessed by mediation model. Additionally, lipidomic profiling including lipidome clustering and individual lipids helped identify key biomolecular mediators. The results showed that exposure to four PAHs was significantly associated with cognitive decline, with combined exposure analysis further indicated the detrimental effects of PAH mixtures. And biological aging partially mediated the association between 2-hydroxynaphthalene (2-NAP) and cognitive function. Key lipid levels, particularly phosphatidylethanolamines (PEs)-dominated clustering pattern, emerged as pivotal molecular mediator shaping this relationship. Additionally, more lipid species, notably phosphatidylcholines (PCs), mediated PAHs-induced cognitive decline in females. These findings elucidate lipid levels as a key mechanism linking biological aging and PAHs-induced cognitive decline, with specific lipid alterations partially explaining the increased vulnerability of females to cognitive decline.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"408-419"},"PeriodicalIF":6.3,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determining Location-Specific Thresholds for Heat Warning Systems to Mitigate Heatstroke Mortality in Japan.","authors":"Vera Ling Hui Phung, Yasushi Honda, Kazutaka Oka, Lina Madaniyazi, Chris Fook Sheng Ng, Aurelio Tobias, Masahiro Hashizume","doi":"10.1021/envhealth.5c00113","DOIUrl":"10.1021/envhealth.5c00113","url":null,"abstract":"<p><p>The current nationwide wet bulb globe temperature (WBGT) threshold (33 °C) of Japan's heat warning system (HWS) does not adequately account for regional variations in heat sensitivity and heatstroke mortality. In this study, we aimed to determine the critical WBGT threshold for effectively mitigating preventable heatstroke mortality across Japan. To this end, daily heatstroke mortality data (ICD-10: X30; 2010-2019) for all 47 prefectures of Japan were analyzed using a time-stratified case-crossover design based on a conditional quasi-Poisson regression combined with a distributed lag nonlinear model. Assuming that heatstroke mortality is preventable via interventions when prompted by Japan's HWS, the WBGT threshold required to reduce 50% of preventable heatstroke mortalities (\"target50\") was estimated; subgroup analyses by age, sex, and summer phase were also conducted. According to the results, 9702 heatstroke mortalities were recorded during the study period, with more cases observed in late summer and among older individuals. Further, the current HWS threshold (WBGT_max 33 °C) only accounted for 2%-3% of preventable heat-related deaths during summer months. However, a new critical threshold (WBGT_max approximately 31 °C), enabling the realization of target50 in most prefectures, was identified. Notably, northern regions required lower thresholds. Significant differences between summer phases (lower thresholds for early summer than those for late summer), as well as regional and demographic variations in heat sensitivity, were also observed. The application of the identified critical threshold, WBGT_max approximately 31 °C, aligned with the national target of reducing preventable heatstroke mortalities by half. Therefore, the findings of this study provide a scientific basis for revisiting Japan's HWS and improving mitigation measures.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 1","pages":"144-153"},"PeriodicalIF":6.3,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12813707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ambient Air Pollution, Preconceptional Thyrotropin Abnormalities, and the Risk of Preterm Birth: A Nationwide Chinese Cohort Study.","authors":"Ying Yang, Xinghou He, Hongbing Xu, Jianbin Wu, Bin Zhang, Xinyi Lv, Long Wang, Mengyao Li, Chuanyu Zhao, Xuyang Shan, Yuan He, Yan Fang, Yuanyuan Wang, Huiying Xu, Erlu Zhao, Jihong Xu, Xiaoming Song, Ya Zhang, Hongguang Zhang, Qinghong Zhang, Zifa Wang, Xu Ma, Wei Huang","doi":"10.1021/envhealth.5c00444","DOIUrl":"10.1021/envhealth.5c00444","url":null,"abstract":"<p><p>Air pollution has been associated with preterm birth (PTB); however, evidence remains limited about preconception exposure. Additionally, it remains unknown whether air pollution and thyrotropin abnormalities may synergistically contribute to incident PTB. We conducted a nationwide cohort study of 6.1 million singleton births, based on the National Free Prepregnancy Checkups Project across 29 provinces in China, 2014-2020. We observed that interquartile range increases in particulate matter with diameters ≤2.5 and ≤10 μm, nitrogen dioxide, and sulfur dioxide during 12 weeks before conception through pregnancy were associated with increased risks of PTB, with the hazard ratios of 1.25 (95% confidence intervals [CI]: 1.24, 1.25), 1.13 (95% CI: 1.13, 1.14), 1.10 (95% CI: 1.09, 1.10), and 1.24 (95% CI: 1.24, 1.25), respectively. Participants with high air pollution exposure (>75th percentile) and abnormal thyrotropin levels (<0.37 or ≥4.88 mIU/L) showed higher risks of PTB, compared to those with low air pollution exposure (<25th percentile) and normal thyrotropin levels. Additive interactions were also identified between air pollution and thyrotropin abnormalities (relative excess risk due to interaction >0, attributable proportion due to interaction >0, and synergy index >1). Our study showed that exposure to air pollution during preconception through pregnancy was associated with increased risks of PTB and that air pollution and thyrotropin abnormalities may synergistically contribute to incident PTB. These findings highlight the importance of air pollution control and thyroid management.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"392-407"},"PeriodicalIF":6.3,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147514934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibiotic Exposure and Early Reproductive Outcomes of In Vitro Fertilization (IVF) in a Chinese Couple-Based Preconception Cohort.","authors":"Yingying Chen, Shanshan Shao, Baolin Wang, Yaya Gao, Yanlan Tang, Yaning Sun, Luobin Xia, Xin Gao, Sheng Wang, Ying Tang, Shuangshuang Bao, Menglong Geng, Peng Zhu, Fangbiao Tao, Guixia Pan","doi":"10.1021/envhealth.5c00182","DOIUrl":"10.1021/envhealth.5c00182","url":null,"abstract":"<p><p>Dietary antibiotic exposure is very common, and animal studies have suggested that environmental antibiotic exposure has harmful effects on human reproduction and embryo development. However, there are no population-based cohort studies on the effects of parental antibiotic exposure on early IVF outcomes. A total of 33 antibiotics and 1 metabolite with detection rates over 10% in both female and male partners were included. Couples' early IVF reproductive outcomes included the blastocyst numbers, best-quality embryo numbers, embryo numbers, best-quality embryo rates, two pronuclei (2PN) rates, and blastocyst rates. We applied the adaptive elastic net (AENET) with 10-fold cross-validation to identify antibiotics associated with early IVF outcomes in couples. According to the antibiotics identified by AENET, quantile-based g-computation (QGC) models, group-weighted quantile sum (GWQS) regression, and partitioning around medoids (PAM) algorithms were used to evaluate the joint associations of parental antibiotic mixtures with early IVF reproductive outcomes. The independent associations between antibiotics identified by AENET, antibiotic classes, and early IVF reproductive outcomes in couples were evaluated using the multivariate generalized linear mixed model (GLMM) with random intercepts. In this couple-based prospective cohort study, 739 couples with 947 fresh cycles were included between December 2020 and August 2023. The mean age (SD) was 34.08 (5.48) years for male partners and 33.09 (5.22) years for female partners. In couple-based analyses, sulfaclozine, roxithromycin, sulfamonomethoxine, erythromycin, and penicillin V were positively related to several early IVF reproductive outcomes, while sulfamethoxazole, penicillin G, chlorotetracycline, norfloxacin, florfenicol amine (FFA), sulfadiazine, cyadox, and sulfachloropyridazine were negatively related to early IVF outcomes. Among antibiotic classes, human antibiotics (HAs), β-lactams, chloramphenicols, and quinoxalines had positive effects on early IVF outcomes, while sulfonamides, preferred as veterinary antibiotics (PVAs), and lincosamides had inverse effects on early IVF outcomes. Similar results were also observed in male partners and female partners. The association between parental antibiotic exposure and IVF outcomes requires further validation in a larger cohort of couples. Additionally, the extrapolation of our results to the general childbearing-aged couples requires caution as infertile couples may be more susceptible to antibiotics.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 3","pages":"379-391"},"PeriodicalIF":6.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13010295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147515160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ozone Exposure Induces Anemia via Immune-Inflammatory Disruption of Erythroid Homeostasis.","authors":"Yang Wang, Huifeng Yue, Nan Sang","doi":"10.1021/envhealth.5c00373","DOIUrl":"https://doi.org/10.1021/envhealth.5c00373","url":null,"abstract":"<p><p>Ground-level ozone (O₃), a major ambient air pollutant, is epidemiologically linked to anemia, but its mechanisms remain unclear. This study employed integrated phenotypic, histopathological, and transcriptomic analyses to explore the molecular mechanisms of O₃-induced anemia. Male C57BL/6J mice underwent 28-day whole-body O₃ exposure at environmentally relevant concentrations (0.25 and 0.50 ppm, 4 h/day) alongside clean air controls. Significant hematological alterations occurred only at 0.50 ppm, including reduced erythroid parameters (red blood cells, hemoglobin, hematocrit, and reticulocytes) and systemic immune-inflammatory activation (increased lymphocyte count). This exposure level induced hematopoietic damage manifested as impaired progenitor cell differentiation (CFU-GEMM colony-forming capacity decreased by 20.55%, <i>p</i> < 0.05), reduced bone marrow hematopoietic cells, and extramedullary hematopoiesis in the spleen. Transcriptomic analysis identified 30 immune-inflammatory-related differentially expressed genes (IR-DEGs). Hierarchical network analysis integrating protein-protein interaction topology and transcriptional regulation revealed a core regulatory axis of transcription factors and 7 hub genes. Quantitative real-time PCR (qRT-PCR) and protein assays demonstrated that <i>Jund</i> is one of the key nodes in the regulatory network, which regulates critical immune-inflammatory genes (Ccl5, Lck, and Ifng). These findings indicate that <i>Jund</i>, as a key transcription factor in immune-inflammatory processes, mediates O₃-induced disruption of erythrocyte homeostasis, thereby providing experimental evidence for environmental anemia prevention.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 2","pages":"301-312"},"PeriodicalIF":6.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12930314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147310531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network Toxicology and In Vivo Studies Reveal the Toxicity and Mechanisms of Tributyl Citrate Carried by Microplastics in Promoting Colitis-to-Tumorigenesis Transformation.","authors":"Haosong Chen, Yixian Cheng, Yao Zhou, Rui Fu, Jianguang Jia, Shuyuan Zhang, Junjie Chen, Haikun Cao, Peng Zhang, Qilong Geng, Jinghua Gu, Bo Chen, Wenxiu Han, Maoming Xiong, Ting Li, Guodong Cao","doi":"10.1021/envhealth.5c00214","DOIUrl":"https://doi.org/10.1021/envhealth.5c00214","url":null,"abstract":"<p><p>Tributyl citrate (TBC), a widely used substitute for phthalate plasticizers, has shown increasing environmental accumulation, raising concerns about its potential human health risks. However, its toxicological effects, particularly regarding gastrointestinal disease progression, remain largely unexplored. In this study, animal experiments first demonstrated that TBC aggravates colonic inflammation in a mouse model of microplastic-induced colitis. Computational toxicology analysis further predicted TBC to possess potential carcinogenic properties, suggesting its role in promoting colitis-associated carcinogenesis. Using integrated bioinformatics approaches, we combined network toxicology, molecular docking, and molecular dynamics simulations to identify the putative toxicological targets and molecular pathways involved in TBC-induced inflammation-to-cancer transition. A total of 299 TBC-related targets were identified from multilevel databases, and 13 core targets were highlighted through STRING and Cytoscape analyses, including AKT2, MAPK1, MAPK3, HSP90AA1, PIK3CD, BCL2, PIK3R1, PIK3CB, ESR1, CASP3, KRAS, and ERBB2. GO and KEGG enrichment analyses indicated that TBC may drive carcinogenic progression via pathways associated with oxidative stress and inflammatory responses. Molecular docking and dynamics simulations validated the stable interactions between TBC and key targets. To further confirm TBC's role in colitis-associated tumorigenesis, we employed an AOM/DSS-induced colorectal cancer mouse model and found that TBC significantly exacerbated both intestinal inflammation and tumor formation. Transcriptomic analysis further validated the enrichment of ROS-mediated chemical carcinogenesis pathways and revealed that intestinal barrier disruption may also be a critical contributor to TBC-mediated cancer progression. Collectively, this study provides a theoretical basis for understanding the molecular mechanisms by which TBC aggravates inflammation-associated colorectal cancer, and offers a framework for risk assessment and regulatory strategies addressing plasticizer exposure in digestive health.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 4","pages":"601-617"},"PeriodicalIF":6.3,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial Intelligence and Machine Learning for Environmental Health Study.","authors":"Miao Yu, Mingliang Fang, Zhenyu Tian, Bin Wang, Douglas Walker","doi":"10.1021/envhealth.5c00324","DOIUrl":"https://doi.org/10.1021/envhealth.5c00324","url":null,"abstract":"","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"3 10","pages":"1115-1116"},"PeriodicalIF":6.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12538322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145348756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental Consequences of Anthropogenic Pollution: Non-antibiotic-Drug-Driven Antibiotic Resistance Selection in a Model Aquatic Ecosystem.","authors":"Concepcion Sanchez-Cid, Stanislava Vrchovecká, Emilie Dehon, Stanisław Wacławek, Timothy M Vogel","doi":"10.1021/envhealth.5c00238","DOIUrl":"10.1021/envhealth.5c00238","url":null,"abstract":"<p><p>Non-antibiotic drugs (NADs) used in human therapy may induce antibiotic resistance selection and dissemination <i>in vitro.</i> However, the potential risks of antibiotic resistance emergence associated with environmental NAD pollution have not been addressed. Here, we conducted a multidisciplinary study on river water microcosms using growth kinetics, qPCR, metagenomics, 16S rRNA sequencing, and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to determine whether NADs alter river bacterial ecology and select for antibiotic resistance genes (ARGs). Four NADs with different mechanisms of action were included at a high (mg/L) and low (μg/L) dose to establish dose-response relationships: chlorpromazine (antipsychotic), diclofenac (anti-inflammatory), diphenhydramine (antihistamine), and fluoxetine (antidepressant). Although the community response to NAD pollution was compound-specific and dose-dependent, all NADs and doses were stable in the environment, altered the composition and activity of bacterial communities, and selected for several ARGs, mostly β-lactamases and aminoglycoside resistance genes, some of which were associated with horizontal gene transfer genes. <i>Pseudomonas</i> (including some ARG-harboring subpopulations) was identified as a key player in the response to NAD pollution. Here, we demonstrate NAD-driven antibiotic resistance selection in complex aquatic communities, raising concerns about the collateral effects on human and environmental health due to the extensive anthropocentric use of NADs.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 1","pages":"132-143"},"PeriodicalIF":6.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12813699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repeat Prolonged Chlorination at Low Dose Induces Chlorine Tolerance in <i>Legionella pneumophila</i> via Viable but Non-culturable State.","authors":"Xiaofei Yuan, Yan Zheng","doi":"10.1021/envhealth.5c00360","DOIUrl":"https://doi.org/10.1021/envhealth.5c00360","url":null,"abstract":"<p><p>Chlorine-resistant <i>Legionella pneumophila</i>, the causative agent of fatal pneumonia, poses a major global public health threat. However, the mechanistic basis for this pathogen's resistance evolution remains elusive. Our study demonstrates that a minimally dormant or the early stages of viable but non-culturable (VBNC) state of bacteria is critical to chlorine tolerance development, representing an initial stage of resistance acquisition. Prolonged low-dose chlorination (12 h exposure to 2 mg/L chloramine-T) induced VBNC transformation in <i>L. pneumophila</i>, with a resuscitation lag time ∼10-fold longer than that of parallel nonchlorinated but starved bacteria. Upon resuscitation, secondary chlorination (3 or 12 h) of stationary-phase cells maintained growth rates similar to those of untreated cells, but with significantly shortened lag times (to ∼26 and ∼41 h, vs ∼40 and ∼47 h for single-chlorinated groups, with <i>p</i> < 0.01 for the 3 h treatment). Flow cytometry showed that rechlorinated groups had a higher proportion of active cells and a lower proportion of death-analogous cells than single-chlorinated counterparts, indicating the emergence of a chlorine-tolerant subpopulation. These findings directly link the VBNC state to bacterial resistance evolution, underscoring the urgent need to investigate dormant bacteria to control antimicrobial resistance spread in water systems.</p>","PeriodicalId":29795,"journal":{"name":"Environment & Health","volume":"4 2","pages":"291-300"},"PeriodicalIF":6.3,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12930306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147291079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}