Environmental Health Perspectives最新文献

{"title":"Outdoor exposure to artificial light at night and breast cancer risk: A case-control study nested in the E3N-Generations Cohort.","authors":"Nirmala Prajapati,Delphine Praud,Claire Perrin,Béatrice Fervers,Thomas Coudon,Elodie Faure,Pascal Guénel","doi":"10.1289/ehp15105","DOIUrl":"https://doi.org/10.1289/ehp15105","url":null,"abstract":"BACKGROUNDExposure to light at night (LAN), particularly blue light, is suspected to disrupt circadian rhythm, inhibit melatonin production, and eventually increase the risk of breast cancer.OBJECTIVESWe assessed the association between exposure to outdoor LAN and breast cancer risk in the E3N-Générations cohort, a large population-based cohort study of French women followed-up from 1990 to 2011.METHODSWe conducted a nested case-control study in the cohort, including 5222 incident breast cancer cases and 5222 matched controls. Outdoor LAN exposure at residential addresses was assessed using radiance-calibrated satellite images from the Defense Meteorological Satellite Program (DMSP). Logistic regression models were used to obtain odds ratios (OR) and 95% confidence intervals (CI), adjusting for socio-demographic, reproductive, hormonal, and lifestyle-related factors, as well as exposure to air pollutants (NO2, PM2.5) evaluated from land use regression and chemistry transport models, and proximity to greenspaces estimated from the Normalized Difference Vegetation Index (NDVI) in a buffer of 300 m.RESULTSBefore adjustment for environmental covariates, the ORs associated for LAN exposure increased monotonically from the first to the fourth quartile. This increasing trend was less pronounced after adjustment for air pollutants (NO2 and PM2.5) and NDVI, but the fully adjusted OR per interquartile-range of LAN exposure (261 nW/cm2/sr) remained slightly elevated (ORIQR 1.11; 95% CI: 1.02, 1.20). The adjusted ORs were slightly more elevated in postmenopausal (ORIQR 1.10; 95% CI 1.02-1.18) than in pre-menopausal women, and in women living in urban areas with low greenness.CONCLUSIONThe weak positive associations observed in this study that persist after adjustment for environmental covariates, support the hypothesis that outdoor LAN may increase breast cancer risk. Our results, suggesting that urban greenness could mitigate the role of LAN exposure in breast cancer risk, should be investigated further. Future studies on cancer risk in relation to outdoor LAN should assess exposure to indoor sources, including electronic devices, and characterize the light spectrum, particularly the blue light. https://doi.org/10.1289/EHP15105.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"27 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841126","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":"The Imperative for Hazard and Place-Specific Assessment of Heat Vulnerability.","authors":"Joseph Karanja,Jennifer Vanos,Matei Georgescu,Amy E Frazier,David Hondula","doi":"10.1289/ehp14801","DOIUrl":"https://doi.org/10.1289/ehp14801","url":null,"abstract":"BACKGROUNDRepresenting vulnerability is crucial for informing targeted interventions, but existing vulnerability conceptualizations are too general for heat hazard-specific and place-specific relevance. Examining the key decision criteria centering around data choices, selection of input variables, methodological approaches, and theoretical conceptualizations are integral to progressing toward hazard-specific and place-specific vulnerability assessment. Moreover, decisions touching on Geographic Information Science (GIScience)-related issues (e.g., the implications of scale choices and accounting for contextual effects) impact how people who are at risk for adverse heat-health outcomes are represented. In turn, these representations influence how critical interventions are implemented. Given the prospects of increases in adverse heat-health outcomes associated with planetary and urban warming, it is crucial to examine how the representation of heat vulnerability can be enhanced for tailored interventions.OBJECTIVEThis commentary examines the assumptions underpinning the decision criteria for heat vulnerability analysis and identifies associated implications while recommending priority future research. Reorienting general hazard conceptualizations to reflect contextual, heat-specific nuances is crucial for attenuating heat-related health outcomes.DISCUSSIONHeat vulnerability studies lack consistent decision criteria, which undermines progress toward hazard-specific and place-specific vulnerability relevance. Some of these limitations are attributable to the persistent application of general, all-hazards conceptualizations to hazard-specific studies. Moreover, inconsistent decision criteria undermine the replicability and validity of studies and propagate uncertainty while compromising progress toward standardized, consistent, scalable approaches, and testing of existing assumptions that could strengthen heat vulnerability theory. Given GIScience technologies are central to representing spatial patterns of vulnerability, the epistemological foundation of vulnerability theory can be strengthened when GIScience concepts (e.g., the operational scale of social-environmental determinants of health and assumptions underpinning spatial relationships) are considered during vulnerability representation.CONCLUSIONExamining decision criteria for heat vulnerability assessment is crucial to identifying optimal sets of heat-specific and place-specific risk indicators, thereby enhancing the representation of vulnerability. https://doi.org/10.1289/EHP14801.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"42 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841124","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":"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":"10.1289/ehp15400","DOIUrl":"https://doi.org/10.1289/ehp15400","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"113 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836531","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":"Quantification of 16 Metals in Fluids and Aerosols from Ultrasonic Pod-Style Cigarettes and Comparison to Electronic Cigarettes.","authors":"Esther Omaiye,Prue Talbot","doi":"10.1289/ehp15648","DOIUrl":"https://doi.org/10.1289/ehp15648","url":null,"abstract":"BACKGROUNDElectronic cigarette (e-cigarette) liquids and aerosols contain metals, which can be detrimental to human health. Recently marketed ultrasonic cigarettes (u-cigarettes) claim to be less harmful than e-cigarettes that use heating coils.OBJECTIVESWe quantified chemical elements/metals in multiple flavors of SURGE u-cigarettes, JUUL e-cigarettes, and \"Other Brands\" of pod-style e-cigarettes.METHODSElements/metals were identified in atomizers of SURGE using a scanning electron microscope/energy-dispersive X-ray spectrometer. Quantitation of elements/metals in fluids and aerosols from SURGE, JUUL and Other Brands was performed using inductively coupled plasma optical emission spectroscopy.RESULTSU-cigarettes contained a sonicator, unlike e-cigarettes which had heated coils. Sixteen elements were identified in at least one fluid or aerosol sample. Generally, u-cigarette fluids and aerosols had more elements/metals at higher concentrations than aerosols from 4th generation e-cigarettes. Element concentrations generally increased in fluids after vaping. All products, including SURGE, had silicon in their fluids and aerosols. Nickel, which was present in low concentrations in all fluids except KWIT Stick (up to 66,050 μg/mL), transferred to the aerosols with low efficiency. SURGE, but not e-cigarettes, also had copper and zinc in their fluids, but little transferred to their aerosols. SURGE fluids and aerosols, unlike e-cigarettes, had relatively high concentrations of arsenic and selenium. Arsenic and selenium, which are on the FDA's Harmful and Potentially Harmful List, likely came from poor quality solvents used to produce the e-liquids in SURGE pods and possibly from the sonicator, which heats during use.DISCUSSIONSURGE u-cigarettes produce aerosols with metals equivalent to heated coil-style e-cigarettes and had high levels of arsenic and selenium, which are a health concern. Regulations limiting arsenic and selenium in these products are needed, and routine surveillance to identify rogue products, such as Kwit Stick, that have abnormally high levels of nickel or other metals could protect human health. https://doi.org/10.1289/EHP15648.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"60 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819345","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":"Perinatal Exposures to Ambient Fine Particulate Matter and Outdoor Artificial Light at Night and Risk of Pediatric Papillary Thyroid Cancer.","authors":"Nicole C Deziel,Rong Wang,Joshua L Warren,Catherine Dinauer,Jennifer Ogilvie,Cassandra J Clark,Charlie Zhong,Joseph L Wiemels,Libby Morimoto,Catherine Metayer,Xiaomei Ma","doi":"10.1289/ehp14849","DOIUrl":"https://doi.org/10.1289/ehp14849","url":null,"abstract":"BACKGROUNDPediatric thyroid cancer incidence has been increasing globally, with environmental exposures being a hypothesized risk factor.OBJECTIVEWe evaluated the association between pediatric thyroid cancer risk and perinatal exposure to ambient fine particulate matter (PM2.5) and outdoor artificial light at night (O-ALAN). Both are considered environmental carcinogens with evidence of thyroid function disruption, reported associations with thyroid cancer in adults, and concerns of distributive inequity. O-ALAN may also serve as a proxy for other outdoor air pollutants or urbanization.METHODSWe conducted a case-control study of papillary thyroid cancer nested within a California birth cohort that included 736 cases diagnosed at 0-19 years and born in 1982-2011 and 36,800 controls frequency-matched on birth year. We assigned individual-level exposures for residence at birth for ambient PM2.5 concentrations from a validated, ensemble-based prediction model and O-ALAN using the New World Atlas of Artificial Night Sky Brightness. We calculated odds ratios (OR) and 95% confidence intervals (CI) using logistic regression adjusting for potential confounders and stratified by age and race/ethnicity.RESULTSWe observed statistically significant associations between PM2.5 exposure and papillary thyroid cancer risk overall (OR per 10-µg/m3 increase in PM2.5=1.07, 95%CI: 1.01-1.14), among the 15-19 year age group (OR=1.08; 95%CI: 1.00-1.16), and among Hispanic children (OR=1.13; 95%CI: 1.02-1.24). For O-ALAN, we observed statistically significantly increased odds of papillary thyroid cancer in higher exposure tertiles compared to the reference tertile in the overall population (tertile 2: OR=1.25, 95%CI 1.04-1.50; tertile 3: OR=1.23, 95%CI: 1.02-1.50) and when modeled as a continuous variable (OR 1.07 per 1 mcd/m2). In age-stratified analyses, significant associations were observed among the 15-19-year-old age group, but not the 0-14-year-old group. No significant differences were found by race/ethnicity.DISCUSSIONThis study provides new evidence suggesting associations between early-life exposure to PM2.5 and O-ALAN and pediatric papillary thyroid cancer. Given that O-ALAN may also represent other air pollutants or broader urbanization patterns, further research and refinements to exposure metrics are needed to disentangle these factors. https://doi.org/10.1289/EHP14849.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"50 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822752","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":"Bisphenol S exposure and MASLD: a mechanistic study in mice.","authors":"Shiqi Li,Yun Fan,Min Tang,Xiaorong Wu,Shengjun Bai,Xiancheng Yang,Xueer Zhang,Chuncheng Lu,Chenbo Ji,Paul A Wade,Xu Wang,Wei Gu,Guizhen Du,Yufeng Qin","doi":"10.1289/ehp17057","DOIUrl":"https://doi.org/10.1289/ehp17057","url":null,"abstract":"BACKGROUNDBisphenol S (BPS) is a substitute for bisphenol A in various commercial products and is increasingly used globally due to restrictions on bisphenol A usage. Consequently, there are increasing public health concerns that substantial effects mediated by synthetic chemicals may impact human health. Recently, epidemiology studies reported associations between bisphenol exposure and non-alcoholic fatty liver disease (MASLD). However, the causal relationship and the molecular mechanisms affecting hepatocellular functions are still unknown.OBJECTIVESOur study aimed to understand the molecular mechanism by which BPS exposure caused hepatic lipid deposition.METHODSC57BL/6J mice were exposed to BPS for three months and its effects were assessed by histology. RNA sequencing (RNA-seq), Assay for Transposase Accessible Chromatin with high throughout sequencing (ATAC-seq) and Cleavage Under Targets and Tagmentation (CUT&Tag) were used to investigate mechanistic details. ATF3 liver-specific knock out mice and cells were used to validate its functions in BPS induced hepatotoxicity.RESULTSHere, mice that were chronically exposed to BPS showed significant lipid deposition in liver and dyslipidemia, and were predisposed to MASLD, accompanied with reprogrammed liver transcriptional network and chromatin accessibility that were enriched for Atf3 binding motif. Comparing to the control group, we identified numerous differential Atf3 binding sites associated with signaling pathways integral to lipid catabolism and synthesis in BPS exposure group, resulting in a drastic surge in lipid accumulation. Moreover, knocking out Atf3 in vitro and in vivo significantly attenuates BPS-induced hepatic lipid accumulation via the regulation of chromatin accessibility and gene expression. Besides, inhibiting the JunB also eliminates the BPS-induced Atf3 upregulation and lipid accumulation.CONCLUSIONOur study reveals a novel mechanism, through which BPS upregulates JunB and Atf3 to impair hepatic lipid metabolism and provides new insights into the hepatotoxicity of BPS.. https://doi.org/10.1289/EHP17057.","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":"35 1","pages":""},"PeriodicalIF":10.4,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819045","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":"Obtaining and evaluating information on the use, release, and health effects of two types of long-chain PFAS used as alternatives for legacy long-chain perfluoroalkyl acids: a case study.","authors":"Gloria B Post","doi":"10.1289/EHP15995","DOIUrl":"https://doi.org/10.1289/EHP15995","url":null,"abstract":"<p><strong>Background: </strong>Short-chain per- and polyfluoroalkyl substances (PFAS) that are less bioaccumulative have been introduced as replacements for long-chain perfluoroalkyl acids (PFAAs) with the intent of reducing health risks. In contrast, alternative PFAS with longer chain lengths may be at least as bioaccumulative and toxic as phased-out long-chain PFAAs. Such alternative PFAS were used and released unbeknownst to regulatory authorities or the public, causing environmental contamination of public health concern.</p><p><strong>Objective: </strong>The objective was to examine issues encountered in learning about use, release, and toxicity of alternative PFAS and to demonstrate development of human health benchmarks for alternative PFAS from previously unavailable health effects information.</p><p><strong>Discussion: </strong>Environmental contamination with chloroperfluoropolyether carboxylates (ClPFPECAs) near a New Jersey fluoropolymer manufacturing facility was revealed through a joint New Jersey Department of Environmental Protection (NJDEP)-United States Environmental Protection Agency (USEPA) Office of Research and Development study. Previously unavailable information on use, release, and toxicity of ClPFPECAs and another alternative PFAS, perfluoropolyether dicarboxylates, was obtained through a NJDEP legal directive requiring submission of information on such PFAS used in the state. It was learned that the facility discharged large amounts of these alternative PFAS to air and water for many years, both before and after use of long-chain PFAAs ended, and that they are at least as bioaccumulative and toxic in rats as long-chain PFAAs. Additionally, information from exposed workers shows that ClPFPECAs have a human half-life of several years and are associated with numerous health endpoints. Reference Doses and water concentrations protective of chronic drinking water exposure for these alternative PFAS are below those developed by NJDEP for long-chain PFAAs. The use and release of alternative PFAS described herein created concerning human health risks, unknown to regulatory authorities and the public. Such situations in other locations must be identified to allow for regulatory intervention and prevented in the future. https://doi.org/10.1289/EHP15995.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810868","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":"Exposure to long- and short-chain per- and polyfluoroalkyl substances in mice and ovarian-related outcomes: an <i>in vivo</i> and <i>in vitro</i> study.","authors":"Pawat Pattarawat, Tingjie Zhan, Yihan Fan, Jiyang Zhang, Hilly Yang, Ying Zhang, Sarahna Moyd, Nataki C Douglas, Margrit Urbanek, Brian Buckley, Joanna Burdette, Qiang Zhang, Ji-Yong Julie Kim, Shuo Xiao","doi":"10.1289/EHP14876","DOIUrl":"https://doi.org/10.1289/EHP14876","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The extensive use of per- and polyfluoroalkyl substances (PFAS) has led to environmental contamination and bioaccumulation of these substances. Previous research linked PFAS exposure to female reproductive disorders, but the mechanism remains elusive. Further, most studies focused on legacy long-chain PFOA and PFOS, yet the reproductive impacts of other long-chain PFAS and short-chain alternatives are rarely explored.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objectives: &lt;/strong&gt;We investigated the effects of long- and short-chain PFAS on the mouse ovary and further evaluated the toxic mechanisms of long-chain perfluorononanoic acid (PFNA).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A 3D &lt;i&gt;in vitro&lt;/i&gt; mouse ovarian follicle culture system and an &lt;i&gt;in vivo&lt;/i&gt; mouse model were used, together with approaches of reverse transcription-quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), RNA sequencing (RNA-seq), pharmacological treatments, &lt;i&gt;in situ&lt;/i&gt; zymography, histology, &lt;i&gt;in situ&lt;/i&gt; hybridization, analytical chemistry, and benchmark dose modeling (BMD). Using these approaches, a wide range of exposure levels (1-250 µM) of long-chain PFAS (PFOA, PFOS, PFNA) and short-chain PFAS (PFHpA, PFBS, GenX) were first tested in cultured follicles to examine their effects on follicle growth, hormone secretion, and ovulation. We identified 250 µM as the most effective concentration for further investigation into the toxic mechanisms of PFNA, followed with an &lt;i&gt;in vivo&lt;/i&gt; mouse exposure model to verify the accumulation of PFNA in the ovary and its ovarian disrupting effects.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;&lt;i&gt;In vitro&lt;/i&gt; cultured ovarian follicles exposed to long- but not short-chain PFAS showed poorer gonadotropin-dependent follicle growth, ovulation, and hormone secretion compared with control follicles. RT-qPCR and RNA-seq analyses revealed significant alterations in the expression of genes involved in follicle-stimulate hormone (FSH)-dependent follicle growth, luteinizing hormone (LH)-stimulated ovulation, and associated regulatory pathways in the PFNA-exposed group compared to the control group. The PPAR agonist experiment demonstrated that a peroxisome proliferator-activated receptor gamma (PPARγ) antagonist could reverse both the phenotypic and genotypic effects of PFNA exposure, restoring them to levels comparable to the control group. Furthermore, &lt;i&gt;in vivo&lt;/i&gt; experiments confirmed that PFNA could accumulate in ovarian tissues and validated the &lt;i&gt;in vitro&lt;/i&gt; findings. The BMD and &lt;i&gt;in vitro&lt;/i&gt; and to &lt;i&gt;in vivo&lt;/i&gt; extrapolation analyses estimated follicular rupture as the most sensitive endpoint and that observed effects occurred in the range of human exposure to long-chain PFAS.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;Our study demonstrates that long-chain PFAS, particularly PFNA, acts as a PPARγ agonist in granulosa cells to interfere with gonadotropin-dependent follicle growth, hormone secretion, and o","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802736","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":"Estimating heat-related mortality burden changes under type-specific green and blue space scenarios in China.","authors":"Kejia Hu, Shiyi Wang, Fangrong Fei, Jingqiao Fu, Yujie Shen, Feng Chen, Yunquan Zhang, Jian Cheng, Xuchao Yang, Jieming Zhong, Yuming Guo, Jiayu Wu","doi":"10.1289/EHP14014","DOIUrl":"https://doi.org/10.1289/EHP14014","url":null,"abstract":"<p><strong>Background: </strong>Green and blue spaces (GBS) are assumed to mitigate heat-induced health risks. However, few studies have explored the impact of type-specific GBS changes on heat-related mortality burden.</p><p><strong>Objectives: </strong>This study aimed to investigate the effect modifications of different GBS types on heat-related mortality risks, and to estimate the changes in mortality burden in multiple GBS scenarios.</p><p><strong>Methods: </strong>A case time-series study design was utilized based on the daily data on all-cause mortality and temperatures from 2009 to 2020 in 1,085 sub-districts in China. Mortality count data were obtained from the Zhejiang Center for Disease Control and Prevention. Meteorological data on temperature and relative humidity were acquired from the Zhejiang Meteorological Bureau. GBS exposure was assessed by integrating fine-scale population density, GBS boundary from Baidu and OpenStreetMap, and street-view image data from Baidu. Conditional Poisson regression analyses were conducted with the distributed lag non-linear model, incorporating modifiers of type-specific GBS exposure. Changes in heat-attributable mortality under different GBS scenarios were also assessed.</p><p><strong>Results: </strong>Heat-related mortality risks were lower for populations with high exposure (95%) than for those with low exposure (5%) (1) to overall green spaces, forests, parks, nature reserves, and street greenery, rather than to grasses, farms, and scrubs; and (2) to overall blue spaces, lakes, and rivers, rather than reservoirs, wetlands, or coasts. An increase of 10%, 20%, and 30% exposure to overall green spaces are expected to avoid heat-related mortality burden by 1.6% (95% empirical confidence interval [eCI]: 1.4, 1.9), 3.2% (2.5, 3.9), and 4.8% (3.5, 6.2), respectively, whereas corresponding estimates for overall blue spaces are 5.4% (4.4, 6.4), 10.8% (8.5, 13.3), and 16.2% (12.3, 20.5), respectively. Conversely, a 30% decrease in overall green and blue space exposure will increase the heat-related mortality burden by 4.8% (4.3, 5.2) and 15.9% (15.2, 16.7), respectively.</p><p><strong>Discussion: </strong>Our study revealed differences in the capacity of various GBS types to mitigate heat-related mortality risks. While the protective effects of GBS may be moderate, targeted planning strategies should prioritize their implementation for maximum benefits in mitigating heat-related health risks. The continuous shrinkage of the GBS would render other efforts futile, such as heat-health action plans. https://doi.org/10.1289/EHP14014.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794946","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":"Prenatal and childhood phthalate mixtures and adolescent sleep health in The HOME Study.","authors":"Clara G Sears, Jessie P Buckley, Kim M Cecil, Heidi J Kalkwarf, Yingying Xu, Aimin Chen, Kimberly Yolton, Joseph M Braun","doi":"10.1289/EHP15221","DOIUrl":"https://doi.org/10.1289/EHP15221","url":null,"abstract":"<p><strong>Background: </strong>The biological mechanisms linking early life phthalate exposure with adverse behaviors and cardiometabolic conditions also impact sleep health, but whether early-life exposure impacts adolescent sleep is unknown.</p><p><strong>Objectives: </strong>We evaluated whether gestational and childhood urinary phthalate metabolite mixtures were associated with sleep characteristics during adolescence. We also examined periods of heightened susceptibility to individual phthalates.</p><p><strong>Methods: </strong>In the HOME Study (Cincinnati, Ohio; 2003-2006; n=156), we quantified urinary metabolites of 8 parent phthalate diesters during pregnancy (16- and 26-weeks) and childhood (ages 1-, 2-, 3-, 4-, 5-, 8-, and 12-years). Using regression-calibration approaches, we estimated average measurement-error corrected phthalate metabolite concentrations during pregnancy and childhood. We used wrist-actigraphy to assess sleep characteristics for one-week among participants at age 12. Using quantile-based g-computation, we estimated covariate-adjusted differences in sleep efficiency (%), sleep fragmentation index scores (%), and sleep duration (minutes) per quartile increase in all phthalate metabolite concentrations (Ψ), and weights indicating the contribution of each metabolite to Ψ. Using multiple informant models, we examined whether associations between individual phthalate metabolites and sleep characteristics varied by timing of exposure.</p><p><strong>Results: </strong>Increasing all gestational phthalate metabolites by a quartile was associated with lower sleep efficiency (Ψ = -1.3%; 95%CI= -2.4, -0.3) and higher sleep fragmentation (Ψ =1.6%; 95%CI=0.3, 3.0); mono-n-butyl phthalate (MnBP) and di(2-ethylhexyl) phthalate (DEHP) metabolites contributed most to these relations. Higher childhood phthalate metabolite mixture quartiles were associated with shorter sleep duration (Ψ = -21 minutes; 95%CI= -34, -9); monoethyl phthalate (MEP) and monocarboxyoctyl phthalate (MCOP) contributed most to this association. We found that higher DEHP metabolite concentrations during pregnancy were more strongly related with higher sleep fragmentation than childhood concentrations. In contrast, higher MEP and MnBP concentrations during childhood, but not pregnancy, were consistently associated with shorter sleep duration.</p><p><strong>Discussion: </strong>Phthalate metabolite concentrations during pregnancy and childhood were associated with poorer adolescent sleep health. https://doi.org/10.1289/EHP15221.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779381","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}