Environmental Health Perspectives最新文献

{"title":"Invited Perspective: How Do Green- and Bluespaces Reduce Heat-Related Health Risks? Gaining New Insights from Street-View Imagery, Deep Learning Models, and Smartphone Data","authors":"Li Yi, Peter James","doi":"10.1021/ehp.6c00547","DOIUrl":"https://doi.org/10.1021/ehp.6c00547","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"46 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148687903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Household Fuel Use and Kidney Disease-Related Mortality: The Golestan Cohort Study.","authors":"Michele Sassano, Monireh Sadat Seyyedsalehi, Sudabeh Alatab, Hossein Poustchi, Mahdi Sheikh, Arash Etemadi, Reza Malekzadeh, Paolo Boffetta","doi":"10.1021/EHP.6c00520","DOIUrl":"10.1021/EHP.6c00520","url":null,"abstract":"<p><strong>Background: </strong>A large proportion of the global population uses solid fuels for household purposes, and limited evidence from previous studies suggests that it might be associated with reduced renal function.</p><p><strong>Objectives: </strong>To investigate the association between household use of different types of fuels and kidney disease-related mortality.</p><p><strong>Methods: </strong>We analyzed data from the Golestan Cohort Study, a population-based prospective cohort study conducted in northeastern Iran, with 50 045 individuals aged 40-75 years enrolled in the period 2004-2008 and followed through April 2023. Information about household fuel use was collected using validated questionnaires. We estimated adjusted hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) using Cox proportional hazards models. The outcome of interest was death due to any kidney disease, excluding kidney cancer (ICD-10 codes: N00-N19 and N25-N29).</p><p><strong>Results: </strong>During 724,063.62 person-years of follow-up, 262 participants died due to kidney disease. The risk of kidney disease-related mortality was higher with increasing duration of biomass use for cooking or house heating (HR for every 10-year increase: 1.20; 95% CI: 1.04-1.37), while it was not associated with increased duration of using kerosene (10-y HR: 1.09; 95% CI: 0.95-1.24) or gas (10-y HR: 1.00; 95% CI: 0.86-1.16). Estimates for lifetime duration of fuel burning for both cooking and house heating (exclusive fuel use) did not differ according to whether used heating stoves were chimney-equipped or not for kerosene, while they differed for biomass (10-y HR, chimney-equipped: 1.06 [95% CI: 0.95-1.18]; 10-y HR, not chimney-equipped: 1.19 [95% CI: 1.06-1.34]; <i>P</i> _difference = 0.025).</p><p><strong>Discussion: </strong>The findings of our study suggest that burning biomass for household purposes under poor ventilating conditions is associated with kidney disease-related mortality.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"485-493"},"PeriodicalIF":10.9,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multibehavioral Phenotyping in Early-Life-Stage Zebrafish for Identifying Disruptors of Nonassociative Learning.","authors":"David Leuthold, Nadia K Herold, Jana Nerlich, Kristina Bartmann, Ilka Scharkin, Stefan J Hallermann, Nicole Schweiger, Ellen Fritsche, Tamara Tal","doi":"10.1021/EHP.6c00394","DOIUrl":"10.1021/EHP.6c00394","url":null,"abstract":"<p><strong>Background: </strong>The vertebrate nervous system is vulnerable to chemical toxicity, and the widespread release of chemicals into the environment outstrips the capacity to assess their safety. The zebrafish (<i>Danio rerio</i>) is a powerful vertebrate model that can bridge the gap between <i>in vitro</i>- and mammalian-based <i>in vivo</i> studies. However, the behavior-rich repertoire of larval zebrafish, a 3R-compliant model amenable to higher throughput chemical screens, has yet to be fully deployed to identify and characterize chemical compounds that cause neurotoxicity.</p><p><strong>Objective: </strong>We sought to establish a multibehavioral phenotyping approach in larval zebrafish to identify and mechanistically elucidate neuroactive chemicals, with particular focus on chemical compounds that affect nonassociative habituation learning.</p><p><strong>Methods: </strong>We devised a battery of automated behavioral assays in larval zebrafish. The battery captures stereotypical visual and acoustic behaviors including habituation, a form of nonassociative learning. To elucidate mechanisms underlying exposure-induced behavioral alterations in zebrafish, <i>in silico</i> target predictions, pharmacological interventions, patch-clamp recordings in cultured mouse cortical neurons, and human multineurotransmitter (hMNR) assay in 3D BrainSpheres were used.</p><p><strong>Results: </strong>Known pharmacological modulators of habituation in zebrafish evoked distinct behavioral patterns. By screening chemicals positive for <i>ex vivo N</i>-methyl-d-aspartate receptor (NMDAR) modulation, we identified chlorophene, a biocide that caused sedation, paradoxical excitation, and reduced habituation in zebrafish. Using <i>in silico</i> target predictions and pharmacological interventions, we discovered that chlorophene acts via gamma-aminobutyric acid A receptors (GABA_ARs), a previously unknown target site. Orthogonal validation in cultured mouse cortical neurons and human stem cell-derived BrainSpheres confirmed chlorophene's interaction with GABA_ARs. Chlorophene's behavioral profile resembled that of flupirtine, a Kv7 potassium channel (M-current) activator, suggesting that habituation deficits stem from M-current rather than GABA_AR modulation.</p><p><strong>Conclusions: </strong>These studies combined a series of behavior assays in a phenotypically rich, rapid, and inexpensive nonmammalian vertebrate test system to screen chemicals for neurotoxicity. Together with <i>in silico</i> target predictions and mouse- and human-based models, our findings establish multibehavioral phenotyping in zebrafish as a powerful toolkit for neurotoxicity testing and mechanism identification, with relevance for humans.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"465-484"},"PeriodicalIF":10.9,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposures to Drinking Water Contaminants in Community Water Systems and Risk of Ovarian Cancer in the California Teachers Study Cohort.","authors":"Maya Spaur, Lauren M Hurwitz, Danielle N Medgyesi, Alexander P Keil, Laura E Beane Freeman, Jared A Fisher, Jessica M Madrigal, Samantha Ammons, Emma S Spielfogel, Komal Bangia, Paul S Albert, Tiffany R Sanchez, James V Lacey, Rena R Jones, Mary H Ward","doi":"10.1021/EHP.6c00169","DOIUrl":"10.1021/EHP.6c00169","url":null,"abstract":"<p><strong>Background: </strong>Several drinking water contaminants are known or suspected carcinogens; however, there are only a few investigations of drinking water exposure and ovarian cancer. We evaluated associations between regulated contaminants in community water systems (CWS) and ovarian cancer risk in the California Teachers Study, a prospective cohort of female California educators.</p><p><strong>Methods: </strong>Participants were cancer-free, without bilateral oophorectomy, living in California at baseline (1995-1996) with geocoded addresses linked to a CWS (<i>N</i> = 91,127, 92%), with follow-up through 2020 (mean = 19.0 years). Among participants with a residential duration at enrollment of at least 10 years, we computed 15-year (1990-2005) averages of log2-transformed arsenic, nitrate, total trihalomethanes (TTHM) (<i>N</i> = 59,881), and uranium concentrations (<i>N</i> = 56,314). We estimated hazard ratios (HRs, 95% CIs) for all epithelial ovarian cancers (<i>n</i> = 413) and the high-grade serous histotype (<i>n</i> = 199), using Cox proportional hazards regression, adjusting for age, body mass index, menopause status, oral contraceptive use, and parity. We evaluated the mixture effect (per IQR in log2 concentrations) using quantile-based g-computation.</p><p><strong>Results: </strong>Almost all women (>99%) had average exposures below regulatory limits for all contaminants. In single contaminant analyses, a doubling in average uranium concentrations was associated with all ovarian cancer (HR_perlog2 = 1.07, CI 1.00-1.15), whereas a doubling in nitrate was associated with the high-grade serous histotype (HR_perlog2 = 1.09, 95% CI 1.01, 1.17). Findings were similar in models adjusted for other contaminants. We observed positive but imprecise associations for arsenic and TTHM in single-contaminant and contaminant-adjusted analyses. HRs per increase in the mixture were 1.34 (0.95, 1.88) and 1.77 (1.09, 2.87) for all ovarian cancer and the high-grade serous histotype, respectively. Uranium was the largest contributor (56%) to the mixture effect for all ovarian cancers, and nitrate was the largest contributor (48%) for the high-grade serous histotype.</p><p><strong>Conclusions: </strong>Novel associations between drinking water contaminants and ovarian cancer risk at levels below regulatory limits warrant further investigation.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"452-464"},"PeriodicalIF":10.9,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A New Mouse Model for Ozone Health Effects Research.","authors":"Gregory J Smith, Robert M Immormino, Martin T Ferris, Sarah A Lester, Timothy P Moran, Jack R Harkema, Samir N P Kelada","doi":"10.1021/EHP.6c00312","DOIUrl":"10.1021/EHP.6c00312","url":null,"abstract":"<p><strong>Background: </strong>Exposure to the ambient air pollutant ozone (O₃) is associated with adverse respiratory health outcomes. Rodent models have been used to identify mechanisms of response to O₃, but their utility has been questioned owing to species differences in physiologic response, most notably exposure-induced hypothermia, which renders rodents relatively resistant to O₃ compared to humans.</p><p><strong>Objectives: </strong>First, to test whether a recombinant inbred mouse strain from the Collaborative Cross population, CC002/Unc, provides a sensitive model of ozone response by benchmarking it to the most commonly used inbred strain, C57BL/6J. Second, to identify the genetic basis of CC002/Unc's sensitivity.</p><p><strong>Methods: </strong>We examined the responses of CC002/Unc and C57BL/6J mice to either acute (0.4 or 0.8 ppm O₃ 4 h) or repeated (0.8 ppm O₃ × 4 h/day × 3 or 9 weekdays) O₃ exposure. Then, we mapped quantitative trait loci (QTL) for responses to 9 days of O₃ in a CC002/Unc × CC005/TauUnc (O₃-resistant) backcross population.</p><p><strong>Results: </strong>CC002/Unc was far more responsive to acute O₃ than C57BL/6J, exhibiting significant inflammation following a single 0.4 ppm O₃ exposure and greater inflammation and injury after 0.8 ppm O₃. Enhanced sensitivity of CC002/Unc mice was associated with decreased breathing frequency and diminished hypothermic responses. Following repeated exposure, C57BL/6J lungs appeared normal, while CC002/Unc lungs had eosinophilic inflammation and centriacinar fibrosis. We identified five QTL for airway eosinophilia, including a large-effect QTL on chromosome 11 that accounts for 18% of phenotypic variation and contains genes with plausible links to aberrant immune responses.</p><p><strong>Discussion: </strong>The CC002/Unc strain provides an improved model to study the effects of acute and repeated O₃ exposure due to its enhanced sensitivity vs C57BL/6J and more human-like thermoregulatory response. Further genetic analysis to pinpoint causal genes underlying CC002/Unc's susceptibility will provide new insights into mechanisms of O₃-induced lung disease.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"438-451"},"PeriodicalIF":10.9,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linking \"Big\" Geospatial and Health Data: Implications for Research in Environmental Epidemiology.","authors":"Andrea R Titus, Tarik Benmarhnia, Lorna E Thorpe","doi":"10.1021/EHP.6c00321","DOIUrl":"10.1021/EHP.6c00321","url":null,"abstract":"<p><strong>Background: </strong>Environmental epidemiology studies increasingly integrate \"big\" geospatial and health data sets to examine associations between environmental factors and health outcomes. Using such data sets ─ and linking between them ─ presents a number of complexities with regard to study design and analytic approaches. These complexities are often magnified with the integration of additional contextual data representing other neighborhood characteristics including socioeconomic factors. Guidance regarding the design of environmental health studies that leverage \"big\" geospatial and health outcome data is limited and fragmented.</p><p><strong>Objective: </strong>Drawing on methodological literature and case studies, this commentary outlines common challenges related to geospatial and health data linkages, posing a series of guiding questions and considerations for investigators conducting environmental health studies, particularly analyses with an etiological focus.</p><p><strong>Discussion: </strong>Recommendations include: 1) using a target trial approach to guide causal analysis, 2) aligning measures with hypothesized causal mechanisms, 3) exploring opportunities to \"groundtruth\" and validate data, and 4) prioritizing interdisciplinary science. The goal of the commentary is to consolidate insights from multiple disciplines ─ including exposure science, epidemiology, and sociology ─ to provide a foundation for etiologic research focused on advancing environmental health for all populations.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"375-382"},"PeriodicalIF":10.9,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to Organophosphate Ester Flame Retardants and Plasticizers during Pregnancy and Autism-Related Outcomes in the ECHO Cohort.","authors":"Jennifer L Ames, Assiamira Ferrara, Juanran Feng, Stacey Alexeeff, Lyndsay A Avalos, Emily S Barrett, Theresa M Bastain, Deborah H Bennett, Jessie P Buckley, Courtney C Carignan, Patricia Cintora, Akhgar Ghassabian, Monique M Hedderson, Ixel Hernandez-Castro, Kurunthachalam Kannan, Margaret R Karagas, Catherine J Karr, Jordan R Kuiper, Donghai Liang, Kristen Lyall, Cindy T McEvoy, Rachel Morello-Frosch, Thomas G O'Connor, Jiwon Oh, Alicia K Peterson, Lesliam Quiros-Alcala, Sheela Sathyanarayana, Susan Schantz, Rebecca J Schmidt, Anne P Starling, Tracey J Woodruff, Heather E Volk, Yeyi Zhu, Lisa A Croen","doi":"10.1021/EHP.6c00247","DOIUrl":"https://doi.org/10.1021/EHP.6c00247","url":null,"abstract":"<p><p><b>BACKGROUND</b>: Organophosphate ester flame retardants and plasticizers (OPEs) have myriad uses in industry and consumer products. Increasing human exposure to OPEs has raised concerns about their potential effects on child neurodevelopment during the pregnancy. <b>Objective:</b> We investigated whether OPE urinary concentrations during pregnancy were associated with child's autism-related outcomes. <b>METHODS:</b> We included 4159 mother-child pairs from 15 cohorts in the NIH Environmental influences on Child Health Outcomes (ECHO) Consortium, with children born from 2006-2020 (median age [interquartile range]: 6 [4,10] years). Nine OPE biomarkers were measured in urine samples collected mid- to late pregnancy. Dilution-adjusted biomarkers were modeled continuously, categorically (high [>median], moderate [≤median], nondetect), or as detect/nondetect depending on their detection frequency. We assessed child autism-related traits via a) parent report on the Social Responsiveness Scale (SRS) and b) clinical autism diagnosis. We examined associations of OPEs with child outcomes, including modification by child sex, using generalized estimating equations to account for clustering by ECHO cohort. <b>RESULTS:</b> Compared with nondetectable concentrations, high exposure to bis-(butoxyethyl) phosphate (BBOEP) was associated with higher autistic trait scores (adj-β 0.97, 95% confidence interval [CI]: 0.42, 1.52) and greater odds of autism diagnosis (adjusted odds ratio [adj-OR]: 1.27, 95% CI: 1.07, 1.50). Bis-(1-chloro-2-propyl) phosphate (BCPP) showed associations with autistic trait scores (BCPP adj-β for high exposure vs nondetect: 0.34, 95% CI: -0.46, 1.13; BCPP adj-β for moderate exposure vs nondetect: 0.72, 95% CI: 0.24, 1.20). High exposure to bis-(2-chloroethyl) phosphate (BCETP) was associated with lower odds of autism diagnosis (adj-OR: 0.76, 95% CI: 0.60, 0.95). Other OPEs showed no associations in adjusted models. Associations between BBOEP and higher autistic trait scores were stronger in males than females. <b>DISCUSSION:</b> Prenatal exposure to OPEs, specifically BCPP and BBOEP, may be associated with a higher risk of autism diagnosis and related traits in childhood.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"423-437"},"PeriodicalIF":10.9,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Utero Per- and Polyfluoroalkyl Substances (PFAS) Exposure and Changes in Infant T Helper Cell Development among UPSIDE-ECHO Cohort Participants.","authors":"Darline Castro-Melendez, Nathan Laniewski, Todd Jusko, Xing Qiu, B Paige Lawrence, Zorimar Rivera-Núñez, Brunner Jessica, Meghan Best, Allison Macomber, Alena Leger, Kurunthachalam Kannan, Richard K Miller, Emily S Barret, Thomas G O'Connor, Kristin Scheible","doi":"10.1021/EHP.6c00037","DOIUrl":"10.1021/EHP.6c00037","url":null,"abstract":"<p><p><b>BACKGROUND</b>: Environmental exposures to toxicants, such as per- and polyfluoroalkyl substances (PFAS), during gestation can disrupt immune development, causing long-term impacts on a child's ability to generate a well-regulated, protective immune response. T-cells coordinate with all immune cell types to orchestrate both cellular and antibody-mediated responses. While there is compelling evidence that PFAS alters immunity in humans, the specific effects of early life PFAS exposure on infant T-cell development are unreported. Because of their central role in immunity, altered T-cell development in infants would have implications on immune responses broadly and long-term. <b>OBJECTIVES</b>: We seek to model longitudinal changes in the frequency of functionally distinct CD4+ T-cell subpopulations from birth through 12 months and their association with in utero PFAS exposure. <b>METHODS</b>: Maternal-infant dyads were recruited as part of the UPSIDE-ECHO cohort during the first trimester between 2015 and 2019 in Rochester, New York; dyads were followed through the infant's first birthday. Maternal PFAS concentrations (PFOS, PFOA, PFNA, PFHXS and PFDA) were quantified in serum during the second trimester using high-performance liquid chromatography and tandem mass spectrometry. Infant lymphocyte frequencies were assessed at birth, 6- and 12-months using mass cytometry and high-dimensional clustering methods. Linear mixed-effects models were employed to analyze the relationship between maternal PFAS concentrations and CD4+ T-cell subpopulations (<i>n</i> = 200). All models included a PFAS and age interaction and were adjusted for parity, infant sex, and prepregnancy body mass index. <b>RESULTS</b>: In utero PFAS exposure correlated with multiple CD4+ T-cell subpopulations in infants. The greatest effect sizes were seen in T follicular helper (Tfh) and T-helper 2 (Th2) cells at 12 months. A log₂-unit increase in PFOS was associated with lower Tfh [0.17% (95% CI: -0.30, -0.40)] and greater Th2 [0.27% (95% CI: 0.18, 0.35)] cell percentages at 12 months. Similar trends were observed for PFOA, PFNA, PFHXS, and PFDA. <b>DISCUSSION</b>: Maternal PFAS exposures correlate with cell-specific changes in the infant T-cell compartment, including key CD4+ T-cell subpopulations that play central roles in coordinating well-regulated protective immunity. Future studies into the role of PFAS-associated T-cell distribution and the risk of adverse immune-related health outcomes in children are warranted.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"408-422"},"PeriodicalIF":10.9,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A New Start.","authors":"Joel D Kaufman","doi":"10.1021/EHP.6c00320","DOIUrl":"10.1021/EHP.6c00320","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 1","pages":"1-2"},"PeriodicalIF":10.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13250798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Source-Specific Air Pollution and Risk of Chronic Obstructive Pulmonary Disease: A Pooled Cohort Study.","authors":"Manuella Lech Cantuaria, Aslak Harbo Poulsen, Ole Raaschou-Nielsen, Étienne Audureau, Ralph Epaud, Sophie Lanone, Jørgen Brandt, Lise Marie Frohn, Matthias Ketzel, Anja Olsen, Lau Caspar Thygesen, Mette Sørensen","doi":"10.1021/EHP.6c00128","DOIUrl":"10.1021/EHP.6c00128","url":null,"abstract":"<p><strong>Background: </strong>The evidence linking long-term exposure to air pollution and the development of chronic obstructive pulmonary disease (COPD) is still controversial. Furthermore, most studies have investigated associations with particulate matter (PM) and nitrogen dioxide (NO₂), disregarding their emission source and other relevant air pollutants, such as ultrafine particles (UFP) and elemental carbon (EC).</p><p><strong>Objectives: </strong>This study aimed to assess associations between long-term residential exposure to PM_2.5, NO₂, UFP, and EC and the risk of COPD, distinguishing the effects of air pollution from local traffic and other sources.</p><p><strong>Methods: </strong>We pooled data from two large Danish cohorts, the Diet, Cancer, and Health cohort and the Danish National Health Survey. For all participants (<i>N</i> = 159,769), we estimated long-term air pollution exposure to total, local traffic, and other contributions, based on complete address histories. We used Cox proportional hazards models to estimate associations between 10-year time-weighted averaged air pollution and incident COPD, adjusting for demographic, socioeconomic, and lifestyle factors, including smoking. We evaluated the possible modification of these associations by sex, smoking status, and previous asthma diagnosis.</p><p><strong>Results: </strong>Long-term exposures to PM_2.5, NO₂, UFP, and EC were associated with higher risk of COPD. The highest hazard ratio (HR) per interquartile range of total contributions was observed for PM_2.5 (HR: 1.11 [95% confidence interval: 1.05, 1.17]), followed by NO₂ (1.08 [1.04, 1.13]), UFP (1.05 [0.99, 1.11]), and EC (1.02 [1.00, 1.05]), after full adjustment. PM_2.5 from other sources than local traffic was more strongly associated with COPD than PM_2.5 from local traffic, while for UFP and EC, the contributions from local traffic seemed to be the most harmful. Effect modification analyses showed stronger associations among women, never smokers, and those with an asthma diagnosis.</p><p><strong>Discussion: </strong>Our findings suggest that air pollution from local traffic and other sources contributes to COPD risk, with variations depending on the pollutant type. Further research is needed to validate these findings across different populations and geographical settings.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"134 4","pages":"386-396"},"PeriodicalIF":10.9,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}