Environmental Health Perspectives最新文献

{"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":"Long-term exposure to nitrate and trihalomethanes in drinking-water and gastric cancer: A Multicase-Control Study in Spain (MCC-Spain).","authors":"Carolina Donat-Vargas, Manolis Kogevinas, Gemma Castaño-Vinyals, Beatriz Pérez-Gómez, Nuria Aragonés, Marcela Guevara, Inés Gómez-Acebo, Antonio Molina, Guillermo Fernandez-Tardon, Mercedes Vanaclocha-Espí, Ana Molina-Barceló, Victor Moreno, Marina Pollan, Cristina M Villanueva","doi":"10.1289/EHP15039","DOIUrl":"https://doi.org/10.1289/EHP15039","url":null,"abstract":"<p><strong>Background: </strong>Disinfection byproducts and N-nitroso compounds (NOC) formed endogenously after nitrate ingestion have been shown to be carcinogenic in animal studies, but epidemiological evidence is limited, especially in relation to gastric cancer.</p><p><strong>Objective: </strong>We evaluated the association between drinking-water exposure to nitrate and trihalomethanes (THMs) and gastric cancer in the Multicase-Control Study conducted in Spain (MCC-Spain).</p><p><strong>Methods: </strong>In 2008-2013, 254 hospital-based incident gastric cancer cases and 2,365 population-based controls were recruited, providing information on residential histories and type of water consumed. Adult lifetime average nitrate and THM levels in residences from age 18 until 2 years before the interview were estimated and linked with water consumption information to calculate waterborne ingested nitrate, brominated (Br)-THMs and chloroform. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression, with adjustment for potential confounders. We assessed the effect modification by factors influencing endogenous NOC formation.</p><p><strong>Results: </strong>Median (P25-P75) lifetime waterborne ingested nitrate (mg/day), Br-THMs (μg/day) and chloroform (μg/day) were 2.7 (1.4-5.6), 3.8 (1.5-8.1), and 12.2 (4.0-23.7), respectively, in cases; and 3.8 (1.8-8.5), 5.7 (2.6-19.2) and 12.9 (4.6-24.5) in controls. Adjusted OR (95%CI) for gastric cancer comparing nitrate intake > vs. ≤ 9.7 mg/day (80th percentile) was 1.42 (0.88-2.29). This association was more pronounced among participants with low consumption of vegetables (2.24 (1.02-4.91)), vitamin C (2.10 (0.94-4.71)), and vitamin E (2.81 (1.16-6.78)), and among those with high consumption of alcohol (2.78 (0.98-7.93) or processed meat (1.91 (0.97-3.75). When stratified by age, the association only remained in the >65 years group (median 73 years). OR for gastric cancer comparing Br-THM ingestion ≥ vs. < 80th percentile was 0.65 (0.33-1.28) and for chloroform was 1.36 (0.87-2.14). Comparable ORs were found for residential concentrations.</p><p><strong>Conclusions: </strong>Long-term waterborne nitrate exposure below regulatory limits may increase gastric cancer risk among older adults and in those with poor dietary patterns. These findings need to be confirmed by cohort studies with larger sample sizes.. https://doi.org/10.1289/EHP15039.</p>","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":""},"PeriodicalIF":10.1,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963127","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":"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":"Invited Perspective: Toward Making Environmental Epidemiology Research More Impactful in Policy-Relevant Risk Assessments.","authors":"Anneclaire J De Roos","doi":"10.1289/EHP16725","DOIUrl":"10.1289/EHP16725","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":"41301"},"PeriodicalIF":10.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11980914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575563","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":"Invited Perspective: Should You Scrap Your Plastic Cutting Board?","authors":"Eliseo F Castillo, Katrina Smith Korfmacher, Anna Christina Tyler","doi":"10.1289/EHP17049","DOIUrl":"10.1289/EHP17049","url":null,"abstract":"","PeriodicalId":11862,"journal":{"name":"Environmental Health Perspectives","volume":" ","pages":"41302"},"PeriodicalIF":10.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11980917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585155","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}