Environment International最新文献

{"title":"Risk of sand and dust storms on cardiometabolic diseases: a cohort study of over 2.2 million participants","authors":"Weidong Ji ,&nbsp;Kuiying Gu ,&nbsp;Limei Ke ,&nbsp;Weiling Shao ,&nbsp;Lin Li ,&nbsp;Yushan Zhang ,&nbsp;Kai Wang ,&nbsp;Yining Yang ,&nbsp;Yinlin Cheng","doi":"10.1016/j.envint.2025.109821","DOIUrl":"10.1016/j.envint.2025.109821","url":null,"abstract":"<div><div>Climate change has intensified the occurrence of sand and dust storms (SDS), contributing to an increasing public health burden. However, limited evidence exists on the long-term impact of SDS exposure on the incidence of cardiometabolic diseases (CMDs). In this study, we analyzed data from a population-based cohort of 2,260,855 individuals in Northwestern China (2019–2023). Individual-level SDS exposure over a three-year period was estimated using three machine learning models, with extreme gradient boosting demonstrating the best predictive performance. An Accelerated Failure Time (AFT) model was employed to explore the association between SDS exposure and CMD risk, including dyslipidemia, diabetes mellitus, hypertension, and cardiovascular disease. Restricted cubic spline (RCS) analysis revealed a non-linear association between SDS exposure and the time to onset of CMDs. Compared to participants exposed to SDS in the first tertile, those exposed in the highest tertile experienced earlier onset of dyslipidemia (Time Ratio [TR]: 0.854, 95 % CI: 0.848–0.860), diabetes mellitus (TR: 0.784, 95 % CI: 0.776–0.793), hypertension (TR: 0.914, 95 % CI: 0.906–0.922), and cardiovascular disease (TR: 0.732, 95 % CI: 0.714–0.752). Subgroup analysis indicated that individuals aged &lt;50 years, those with obesity (BMI &gt; 25 kg/m²), smokers, drinkers, and individuals with a family history of CMDs were more susceptible to the adverse effects of SDS, leading to a significantly earlier onset of CMDs. These findings suggest that chronic exposure to SDS significantly elevates CMD risk, underscoring the need for public health strategies and air quality standards that address SDS-related health impacts, especially for vulnerable populations.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109821"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153820","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":"Integrating air pollution-health feedback into climate projections: towards endogenous environmental-social links in the integrated models","authors":"Kedi Liu ,&nbsp;Ranran Wang ,&nbsp;Samir K.C. ,&nbsp;Anne Goujon ,&nbsp;Gregor Kiesewetter ,&nbsp;Rutger Hoekstra","doi":"10.1016/j.envint.2025.109817","DOIUrl":"10.1016/j.envint.2025.109817","url":null,"abstract":"<div><div>Integrated assessment models (IAMs), often coupling Shared Socioeconomic Pathways (SSPs) and Representative Concentration Pathways (RCPs), simulate how socioeconomic drivers, technology, policy, and environmental processes interact over time. However, these models typically treat socioeconomic drivers as exogenous input, overlooking how environmental outcomes, like air pollution, can in turn affect health and demographics. This limits our understanding of health co-benefits and weakens the basis for climate-health policy integration. Here, we tackle this gap by linking ambient PM_2.5 concentrations from four SSP-RCP scenarios to the cause-specific risk functions and use the resulting risk impacts to adjust the age- and sex-specific demographic projections from the SSPs. This allows for more coherent estimation of how air quality trajectories influence health outcomes across 186 countries and territories through 2050. Our results reveal notable deviations from conventional SSP-based projections. In low-emission scenario (SSP1-1.9), PM_2.5-related deaths over 2020–2050 are overestimated by 8 % (10 million) due to improved air quality. In contrast, deaths are underestimated by 6 % (15 million) in high-emission scenario (SSP3-7.0), where pollution worsens. These differences translate into life expectancy at birth changes of +0.23 and −0.16 years, respectively. The feedback effects are pronounced in Southeast Asian countries with elevated pollution exposure and population vulnerability, exacerbating the Global North-South mortality gaps under SSP3-7.0 while narrowing them in SSP1-1.9/2.6. Our findings underscore the need and potential of incorporating air pollution-health feedback into the integrated modeling frameworks, which would enhance the realism of long-term demographic projections, especially in pollution-prone regions, and support better-aligned climate and public health strategies.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109817"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153829","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":"Guidance to undertaking systematic evidence maps","authors":"H. Khalil ,&nbsp;V. Welsh ,&nbsp;M. Grainger ,&nbsp;F. Campbell","doi":"10.1016/j.envint.2025.109827","DOIUrl":"10.1016/j.envint.2025.109827","url":null,"abstract":"<div><div>Systematic Evidence Maps (SEMs) are a form of evidence synthesis offering structured approaches to categorizing and organizing scientific evidence by identifying trends and gaps. SEMs support researchers and policymakers in navigating complex evidence landscapes. By synthesizing evidence, they lay the foundation for targeted systematic reviews and primary research, supporting evidence-informed decision-making. These outputs can be hosted on websites, providing an interactive tool. In environmental health, SEMs are systematically used to categorize evidence on topics such as pollution control measures, climate change impacts, and health disparities. The methodological framework for conducting SEMs involves defining the research scope, employing a systematic search strategy, screening studies systematically, optionally conducting critical appraisal (risk of bias assessment) when studies are categorized by effect direction or intended to inform subsequent syntheses, and coding data for synthesis and visualization. Narrative synthesis, heatmaps and network diagrams enhance SEMs usability. However, challenges remain, including methodological inconsistencies and the need for standardization. Advances in automation, machine learning, and stakeholder engagement can further refine SEMs methodologies. This commentary situates SEMs within the broader family of evidence synthesis, emphasizing their role in environmental health science. By enhancing methodological clarity and leveraging innovative tools, SEMs can support researchers and decision-makers in navigating complex evidence ecosystems and implementing evidence-based solutions for environmental scientists.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109827"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183086","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 A impairs developmental potential of mouse blastoids through oxidative stress","authors":"Yookyung Kang ,&nbsp;Yeji Lee ,&nbsp;Seung Yeon Oh,&nbsp;Kwonho Hong,&nbsp;Jeong Tae Do","doi":"10.1016/j.envint.2025.109820","DOIUrl":"10.1016/j.envint.2025.109820","url":null,"abstract":"<div><div>Bisphenol A (BPA) is a widely encountered environmental endocrine disruptor with detrimental effects on embryonic development and implantation. Conventional reproductive toxicity tests often rely on animal-derived gametes or embryos. However, these approaches are invasive and limited in their ability to assess early germline development. To address these limitations, we used a synthetic embryo model derived from pluripotent stem cells (PSCs) to evaluate BPA-induced embryotoxicity without using actual oocytes or embryos. Mouse PSCs were converted into chemically induced totipotent-like stem cells (ciTotiSCs) using a defined small-molecule combination. These ciTotiSCs generated blastoids (ciToti-blastoids) through three-dimensional aggregation in inverted pyramid-shaped microwell plates (AggreWell system) and cultured for 5 d. To investigate the impact of environmental toxicants on early embryogenesis, blastoids were exposed to 5  μM BPA during formation. Blastoid formation efficiency was reduced to approximately 14 % following treatment with 5 μM BPA, compared with approximately 73 % in the control. To assess implantation potential, established blastoids were further cultured on the Matrigel-coated dish. BPA-treated blastoids exhibited a reduction in inner cell mass (ICM) area and in trophectoderm (TE) area, approximately 96 % and 72 %, respectively, indicating impaired implantation potential. These detrimental effects of BPA were accompanied by elevated reactive oxygen species (ROS) levels during ciToti-blastoid formation. Co-treatment with the antioxidant glutathione (GSH; 0.5 mM), a ROS scavenger, restored blastoid formation efficiency (approximately 54 %) and resulted in a similar normalized ICM and TE areas comparable to control. Transcriptomic analysis revealed that BPA induced endoplasmic reticulum stress, DNA damage, and apoptosis, all of which were mitigated by GSH treatment. These results highlight the role of oxidative stress in BPA-induced embryotoxicity and support the utility of stem cell-derived blastoid models as egg-free platforms for assessing the reproductive toxicity of environmental chemicals.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109820"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183091","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":"Particulate air pollution from different emission sources, cognitive performance, and cognitive declines in India","authors":"Boya Zhang ,&nbsp;Sara D. Adar ,&nbsp;Emma Nichols ,&nbsp;Alden L. Gross ,&nbsp;Gavin Shaddick ,&nbsp;Matthew L. Thomas ,&nbsp;Jennifer D’Souza ,&nbsp;Sarah Petrosyan ,&nbsp;Sandy Chien ,&nbsp;Albert Weerman ,&nbsp;Kenneth M. Langa ,&nbsp;Aparajit B. Dey ,&nbsp;Sharmistha Dey ,&nbsp;Jinkook Lee","doi":"10.1016/j.envint.2025.109826","DOIUrl":"10.1016/j.envint.2025.109826","url":null,"abstract":"<div><h3>Background</h3><div>Low- and middle-income countries experience some of the highest fine particulate matter (PM_2.5) exposures globally, with emissions from sources like residential combustion, industry, and transportation continuing to increase in many locations. While total PM_2.5 has been linked to cognitive decline, little is known about the relative importance of PM_2.5 from different emission sources, especially in low and middle-income settings.</div></div><div><h3>Methods</h3><div>We used cognitive performance data from the 2017–2019 and 2022–2024 waves of the Harmonized Diagnostic Assessment of Dementia for the Longitudinal Aging Study in India (LASI-DAD) and 5-year average PM_2.5 concentrations of total mass and mass from 9 emission sources estimated at each participant’s residential location using spatiotemporal models. We then quantified associations of these exposures with cognitive performance and decline using generalized estimating equation models accounting for survey weights and clustering, as well as adjusted for age, gender, individual and community-level socioeconomic status, urbanicity, place-related covariates, fuel type use, and co-pollutants.</div></div><div><h3>Results</h3><div>Among 5,699 participants (mean age: 70±8 years), we observed total PM_2.5 concentrations ranging from 16 to 206 μg/m³. Higher concentrations of total PM_2.5 were not associated with cognitive performance at baseline but were associated with faster declines over time (−0.012/year per SD, 95 % CI: −0.021, −0.004). Among PM_2.5 from different sources, PM_2.5 from energy production, industry, and residential combustion were associated with steeper cognitive declines over time, whereas PM_2.5 from agriculture, transportation, wildfires, and windblown dust were associated with slower cognitive declines.</div></div><div><h3>Conclusion</h3><div>Higher long-term total ambient PM_2.5 concentrations and those from residential combustion sources were associated with accelerated cognitive declines. This suggests that intervention in residential sources might reduce or delay the onset of dementia and promote healthier aging in low and middle-income settings.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109826"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183131","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":"Ecotoxicological assessment of p-benzoquinone oxidation byproducts in water treatment systems: oxidative stress responses and mechanisms","authors":"Zirui Liu ,&nbsp;Dehua Ma ,&nbsp;Qiang Cheng ,&nbsp;Aroob Abid ,&nbsp;Shuaijie Zhao ,&nbsp;Chenyi Li ,&nbsp;Qingzhuo Niu ,&nbsp;Min Zheng","doi":"10.1016/j.envint.2025.109833","DOIUrl":"10.1016/j.envint.2025.109833","url":null,"abstract":"<div><div><em>p-</em>Benzoquinone analogues, a class of ubiquitous oxidation byproducts, are increasingly detected in effluents from various oxidative treatment systems. While halogenated derivatives have received substantial research attention, the ecotoxicological impacts of non-halogenated analogues—particularly <em>in vivo</em>—remain poorly characterized. This study systematically compared the toxicity of 2,6-dichloro-<em>p</em>-benzoquinone (2,6-DCBQ) and 2,6-dimethyl-<em>p</em>-benzoquinone (2,6-DMBQ) using zebrafish embryos. 2,6-DMBQ exhibited comparable lethality to 2,6-DCBQ (48 h EC₅₀ = 221.72 vs. 169.17 μg/L), with developmental malformations of cardiac edema and notochord malformation mainly emerging in juvenile fish at 250 μg/L. Exposure to 2,6-DCBQ of 2.5 μg/L and 2,6-DMBQ of 25 μg/L induced significant oxidative stress, elevating reactive oxygen species (ROS) levels and upregulating antioxidant enzymes of total superoxide dismutase, catalase, and glutathione peroxidase. PCR gene chip analysis showed that 23 oxidative stress-related genes were coordinately upregulated in both treatment groups. Co-exposure with N-acetylcysteine (20 μM) or Na₂SO₃ (Na₂SO₃:<em>p</em>-BQs = 10:1) synergistically mitigated toxicity of 2,6-DCBQ and 2,6-DMBQ at 250 μg/L, restoring morphological and biochemical endpoints to control levels. Electron paramagnetic resonance confirmed semiquinone radicals and hydroxyl radicals as key drivers of ROS amplification. These findings establish radical-mediated mechanisms as critical toxicological pathways and inform risk management strategies for quinoid byproducts in water treatment systems.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109833"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145195451","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":"Hallmarks of EDCs among children in Southern China in Relation with obstructive sleep apnea","authors":"Lixin Zhou ,&nbsp;Suhan Wang ,&nbsp;Dongcai Li ,&nbsp;Jiehao Li ,&nbsp;Xia-Yuhui Wang ,&nbsp;Siyi Zhong ,&nbsp;Xiaojie Li ,&nbsp;Songyi Huang ,&nbsp;Chenyan Zeng ,&nbsp;Tiantian Duan ,&nbsp;Yu Wu ,&nbsp;Guolong Qi ,&nbsp;Fengrui Jing ,&nbsp;Yajie Gong ,&nbsp;Pan Yang ,&nbsp;Hanrong Cheng","doi":"10.1016/j.envint.2025.109829","DOIUrl":"10.1016/j.envint.2025.109829","url":null,"abstract":"<div><div>Childhood obstructive sleep apnea (OSA) is a common pediatric sleep disorder characterized by recurrent sleep-related upper airway dysfunction. China has the highest number of OSA sufferers (176 million) globally. Environmental endocrine-disrupting chemicals (EDCs) posed unrecognized threats to pediatric OSA are not clear. We examined the associations of 34 kinds of EDCs with childhood OSA in Southern China. We recruited 334 children aged ≤ 15 years (July-September 2022) from a tertiary sleep clinic in Shenzhen. Using HPLC-MS/MS, we quantified 7 organophosphate flame retardants (OPFRs), 3 parabens, 10 phthalate metabolites (PAEs), 4 benzophenones (BPs), 7 synthetic phenolic antioxidants (SPAs), and 3 bisphenols. Multivariable linear regression evaluated single-chemical associations with polysomnography-derived indices: apnea-hypopnea index (AHI), obstructive AHI (OAHI), oxygen desaturation index (ODI), and blood oxygen saturation (SpO₂) levels. Mixture effects were assessed through quantile-based g-computation (Qgcomp). Multiple EDCs demonstrated significant dose–response relationships with AHI, OAHI, and ODI (p &lt; 0.05), while inversely associated with SpO₂. Qgcomp revealed each tertile increase in EDC mixture concentration corresponded to elevated AHI [18.53 % (95 % CI: 6.18 to 32.31)], OAHI [23.27 % (13.88 to 34.99)], and ODI [15.03 % (5.13 to 24.61)], along with decreased baseline SpO₂ [-0.25 (−0.49 to −0.01)], lowest SpO₂ [-1.09 (−2.17 to −0.01)], and mean SpO₂ [-0.39 (−0.70 to −0.07)], with DBP exhibiting the strongest negative effects on AHI, OAHI, and ODI, and BCIPP showing the greatest positive effects on baseline and mean SpO₂. This first biomonitoring study implicates EDC mixtures, particularly phthalates and OPFRs, in pediatric OSA pathogenesis. Our findings underscore the need for chemical policy reforms and longitudinal investigations elucidating biological mechanisms linking environmental exposures to sleep-disordered breathing.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109829"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145216189","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":"Incorporating maternal metabolome and genome to understand the effects of prenatal phenol exposure on the first 1000-day growth in an exposome-based study","authors":"Wen Jiang ,&nbsp;Xiaoqing He ,&nbsp;Azhu Han ,&nbsp;Shengju Yin ,&nbsp;Weifeng Tang ,&nbsp;Hong Jin ,&nbsp;Xiaojing Zeng ,&nbsp;Yuexin Gan ,&nbsp;Xuanfang Wang ,&nbsp;Yun Huang ,&nbsp;Fengxiu Ouyang ,&nbsp;Fei Li ,&nbsp;Qianlong Zhang ,&nbsp;Ying Tian ,&nbsp;Jun Zhang ,&nbsp;for the Shanghai Birth Cohort","doi":"10.1016/j.envint.2025.109816","DOIUrl":"10.1016/j.envint.2025.109816","url":null,"abstract":"<div><div>Previous studies on prenatal environmental factors and early-life growth generally applied the single-exposure strategy, mostly relying on cross-sectional growth indicators. No attempt has been made to explore the environmental effects on longitudinal growth at the exposome level. Further, the underlying bio-mechanisms and gene-environment interactions are poorly understood. Within 1,944 mother–child pairs from the Shanghai Birth Cohort, neonatal sex-specific z-scores of weight-for-age (WAZ), length-for-age (LAZ), and weight-for-length (WLZ) were used as the fetal growth outcomes. The growth trajectories of WAZ, LAZ, and WLZ before 2 years old were used as the child growth outcomes. We combined multiple exposome analysis strategies to screen for prenatal environmental factors that continuously affect the first 1000-day growth, based on which maternal metabolome and genome were incorporated to explore the underlying bio-mechanisms and effect modification by genetic predisposition. We found that phenols were the environmental factors that had a lasting growth impact, showing negative associations with neonatal WAZ, LAZ, and WLZ and positive associations with the risks of slow WAZ and LAZ growth trajectories and rapid WLZ growth trajectory in children. Metabolomic and gene-environment interaction analyses suggested the chemicals may exert such lasting effects by upregulating maternal glucose and lipid metabolism during pregnancy, and the effects were specifically more pronounced in mothers with high glucose and low lipid genetic predispositions. Our study suggests that prenatal exposure to phenols has lasting effects on offspring’s first-1000-day growth by disturbing maternal glucose and lipid metabolism. The effects may be aggravated by maternal high glucose and low lipid genetic predispositions.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109816"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145134351","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 mortality burden attributed to regional indoor temperatures in China","authors":"Zhongguo Huang ,&nbsp;Jianxiong Hu ,&nbsp;Jinghua Gao ,&nbsp;Min Yu ,&nbsp;Mengen Guo ,&nbsp;Ruilin Meng ,&nbsp;Chunliang Zhou ,&nbsp;Yize Xiao ,&nbsp;Biao Huang ,&nbsp;Jiangmei Liu ,&nbsp;Maigeng Zhou ,&nbsp;Ryan J. Gainor ,&nbsp;Ramune Reliene ,&nbsp;Guanhao He ,&nbsp;Tao Liu ,&nbsp;Wenjun Ma","doi":"10.1016/j.envint.2025.109822","DOIUrl":"10.1016/j.envint.2025.109822","url":null,"abstract":"<div><h3>Background</h3><div>Despite predominant indoor occupancy patterns, mortality risks and burdens associated with regional (county/district level) indoor temperature remain underexplored in epidemiological research.</div></div><div><h3>Objective</h3><div>To construct a reliable regional indoor temperature prediction model and estimate the disease burden attributed to non-optimal regional indoor temperature.</div></div><div><h3>Design</h3><div>The outdoor meteorological parameters were from the Fifth Generation European Reanalysis dataset, while regional determinants were from national statistical yearbooks. Indoor temperature and building characteristics were collected from 99 buildings across 33 cities. Employing a random forest (RF) algorithm, we developed a prediction model of regional indoor temperatures based on outdoor meteorological parameters, regional determinants and building characteristics. Subsequently, we estimated the regional temperature-mortality associations for both indoor and outdoor temperatures using a distributed lag non-linear model (DLNM) based on cause-specific mortality data collected from 364 counties/districts in China during 2006–2017. Finally, we compared the temperature-related mortality burdens associated with both indoor and outdoor temperature.</div></div><div><h3>Results</h3><div>The RF algorithm identified outdoor meteorological parameters (temperature, relative humidity, wind speed, and precipitation) and regional determinants (green space, latitude, longitude, education attainment, penetration rate of air conditioner, and seasonal variation) as primary determinants of regional average indoor temperature, whereas building characteristics exhibited limited influence. The developed prediction model demonstrated superior predictive accuracy with performance metrics including a root mean square error (RMSE) of 1.473 °C, mean absolute error (MAE) of 1.034 °C, and R² value of 0.938. Analysis of 6.5 million non-accidental death records revealed consistent inverse J-shaped associations for both regional indoor and outdoor temperature-mortality relationships, with indoor temperature demonstrating greater mortality risks. Comparative assessment showed higher temperature-attributable fractions for indoor exposure (18.09 %, 95 %CI:17.87–18.31 %) versus outdoor exposure (14.46 %, 95 %CI:14.41–14.52 %), particularly notable for heat-related mortality burden (indoor:8.38 % vs outdoor:3.66 %).</div></div><div><h3>Conclusions</h3><div>Meteorological parameters and regional determinants emerged as primary predictors of indoor temperature. Regional indoor temperature exposure exhibited greater mortality risks and burden compared to regional outdoor temperature, particularly during heat condition.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109822"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153828","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":"Chemical structure drives developmental toxicity of alkyl-substituted naphthalenes in zebrafish","authors":"Mackenzie L. Morshead,&nbsp;Lisa Truong,&nbsp;Steven J. Carrell,&nbsp;Richard Scott,&nbsp;Kim A. Anderson,&nbsp;Robyn L. Tanguay","doi":"10.1016/j.envint.2025.109837","DOIUrl":"10.1016/j.envint.2025.109837","url":null,"abstract":"<div><div>Naphthalene and its alkyl-substituted derivatives are among the most abundant polycyclic aromatic hydrocarbons (PAHs) in environmental and human exposure studies, yet their developmental toxicity and mode of action remain poorly understood due to challenges in testing semi-volatile compounds. This study developed a vial based, high throughput method to effectively assess the activity of naphthalenes and a set of 24 alkyl-substituted naphthalenes. Early life stage zebrafish were exposed to a concentration series of each chemical (0–50 µM) in rotating sealed glass vials to minimize volatilization. Benchmark concentration (BMC₅₀) values were calculated for morphological endpoints and lowest effect levels were determined for behavioral effects. The data were assessed for evidence of a narcotic mode of action using body burden measurements for select chemicals and logK_ow modeling. Targeted transcriptomics at a single concentration and timepoint as well as <em>in silico</em> molecular docking were conducted to generate mode of action hypotheses. The vial method enabled detection of highly variable developmental toxicity not previously observed using standard 96-well plate exposures. LogK_ow and body burden were poor predictors of toxicity, suggesting a non-narcotic mode of action. Transcriptomic analysis revealed evidence for the disruption of glucocorticoid signaling pathways. Molecular docking identified potential protein targets (e.g., CYP1A2, NT5E, FOLR1) that may mediate observed effects. This study demonstrates the importance of appropriate exposure methods for semi-volatile compounds, reveals structure-dependent toxicity among alkyl-substituted naphthalenes, and provides a foundation for further mechanistic studies and improved risk assessment of alkyl-substituted PAHs.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"204 ","pages":"Article 109837"},"PeriodicalIF":9.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203348","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}