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Characterizing adaptive capacity for the future heat-related cardiovascular morbidity burden in U.S. Metropolitan areas 表征适应能力的未来热相关心血管疾病负担在美国大都市地区
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110022
Wei-Lun Tsai , E.Melissa Mcinroe , Anna M. Jalowska , Corinna Y. Keeler , Stephanie E. Cleland , Cassandra R. O’Lenick , Tanya L. Spero , Alexandra Schneider , Ana G. Rappold
Exposure to excess heat is linked to increased risks of cardiovascular diseases (CVD). As temperatures increase globally, it is crucial to examine the potential increase in excess heat-related CVD (xHEAT-CVD) burden to inform strategies for adaptation. This study aimed to identify the contextual factors associated with future xHEAT-CVD burden among older adults across eighty U.S. metropolitan statistical areas (MSAs).
The MSA-specific xHEAT-CVD risk for adults ≥ 65 years was estimated using hospitalization and temperature data from 2000 to 2017, with excess heat defined as temperatures above the minimum hospitalization percentile (TMHP). Future xHEAT-CVD hospitalizations were estimated using temperature projections for 2025–2054, 2045–2074, and 2070–2099 under three climate scenarios. Area-level variables were used to identify demographic and economic status, health, environment, and infrastructure contexts and derive Urban Heat Health Risk (UHHR) scores using confirmatory factor analysis. The associations between adaptive capacity (the UHHR scores) and future xHEAT-CVD burden were examined.
In 2070–2099 under the mildest scenario, 36 more days annually were projected to be ≥ TMHP, and xHEAT-CVD burden was projected to increase by at least 20.4-fold. Lower adaptive capacity was associated with greater increases in future xHEAT-CVD burden, over 9-fold increase per 1-unit increase in UHHR score (9.1, 95 % Confidence Intervals: 2.8–15.4). The historical xHEAT-CVD burden (2000–2017) was largely driven by the health context, whereas environment played a more important role in the future.
Our findings suggest that drivers of the xHEAT-CVD burden may vary across time. Targeting the areas with the highest xHEAT-CVD burden at varying timeframes can help mitigate xHEAT-CVD burden more effectively.
暴露在过热环境中会增加患心血管疾病(CVD)的风险。随着全球气温的升高,研究与过量热相关的CVD (xHEAT-CVD)负担的潜在增加,为适应战略提供信息至关重要。本研究旨在确定美国80个大都市统计区(msa)老年人未来xHEAT-CVD负担的相关背景因素。使用2000年至2017年的住院和温度数据估计成人 ≥ 65 岁的msa特异性xHEAT-CVD风险,其中过热定义为高于最低住院百分位数(TMHP)的温度。在三种气候情景下,使用2025-2054、2045-2074和2070-2099的温度预测来估计未来xHEAT-CVD住院人数。区域水平变量用于确定人口和经济状况、健康、环境和基础设施背景,并使用验证性因子分析得出城市热健康风险(UHHR)评分。研究了适应能力(UHHR评分)与未来xHEAT-CVD负担之间的关系。在2070-2099年,在最温和的情况下,预计每年 ≥ TMHP的天数将增加36天,预计xHEAT-CVD负担将增加至少20.4倍。较低的适应能力与未来xHEAT-CVD负担的增加有关,UHHR评分每增加1个单位增加9倍以上(9.1,95 %置信区间:2.8-15.4)。历史上的xHEAT-CVD负担(2000-2017)主要由健康背景驱动,而未来环境将发挥更重要的作用。我们的研究结果表明,xHEAT-CVD负担的驱动因素可能随时间而变化。针对不同时间范围内xHEAT-CVD负荷最高的区域,可以帮助更有效地减轻xHEAT-CVD负荷。
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引用次数: 0
Ecological filtering enhanced by smaller PBS biodegradable microplastics constrains ARG dynamics in the soil plastisphere 由较小的PBS可生物降解微塑料增强的生态过滤限制了土壤塑性圈中的ARG动态
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110030
Congxun Huang , Pan Huang , Yi Zhang , Mark Bartlam , Yingying Wang
Microplastics (MPs) are increasingly recognized as hotspots for antibiotic resistance genes (ARGs), yet the combined effects of polymer type and particle size on ARG dynamics in the soil plastisphere remain unclear. Here, we employed metagenomic assembly and binning to explore how MP polymer type and particle size jointly modulate ARG carrying frequencies (ACFs), mobility, and microbial hosts with polyethylene (PE), polystyrene (PS), and biodegradable polybutylene succinate (PBS) MPs across a size gradient (1000, 500, and 106 μm). PBS, PS, and PE plastispheres exhibited different size-related trends in ARG association, with PBS showing the strongest and most consistent decline in ACFs. Only PBS showed a corresponding reduction in ARG–MGE co-localization, suggesting size-dependent constraints on horizontal gene transfer. Distinct ARG combinations in ARG-Carrying Contigs (ACCs) also showed plastic-type selectivity, with complex resistance clusters absent in 106 μm PBS samples, potentially due to environmental constraints that limit the assembly or persistence of multigene resistance structures. Potential pathogens Enterobacter bugandensis and Stutzerimonas urumqiensis were markedly reduced in 106 μm PBS samples, a pattern not observed in PS or PE. Bacterial community analysis revealed that smaller PBS particles were associated with reduced richness, increased evenness, and more competitive interactions within co-occurrence networks. These features, together with the decline in ARG abundance and mobility, suggest that enhanced ecological filtering may occur in smaller biodegradable plastispheres, jointly limiting the persistence of resistance genes and their bacterial hosts. Together, our findings highlight the importance of considering both MP type and particle size in assessing plastisphere-associated ARG risks.
微塑料(MPs)越来越被认为是抗生素耐药基因(ARGs)的热点,但聚合物类型和粒径对土壤塑料圈中ARG动态的综合影响尚不清楚。在这里,我们采用宏基因组组装和分组来探索MP聚合物类型和粒径如何在尺寸梯度(1000、500和106 μm)上共同调节聚乙烯(PE)、聚苯乙烯(PS)和可生物降解的聚丁二酸丁二酯(PBS) MPs的ARG携带频率(ACFs)、迁移率和微生物宿主。PBS、PS和PE塑料球在ARG关联中表现出不同的尺寸相关趋势,其中PBS表现出最强和最一致的ACFs下降。只有PBS显示出ARG-MGE共定位的相应减少,表明大小依赖于水平基因转移的限制。携带ARG的Contigs (ACCs)中不同的ARG组合也表现出可塑性选择性,106 μm PBS样品中没有复杂的抗性簇,这可能是由于环境限制了多基因抗性结构的组装或持久性。106 μm PBS样品中潜在致病菌布甘肠杆菌和乌鲁木齐Stutzerimonas显著减少,而PS和PE样品中未观察到这一现象。细菌群落分析表明,较小的PBS颗粒与共生网络中丰富度降低、均匀度增加和竞争性相互作用有关。这些特征,连同ARG丰度和流动性的下降,表明在较小的可生物降解塑料球中可能发生增强的生态过滤,共同限制了抗性基因及其细菌宿主的持久性。总之,我们的研究结果强调了在评估与塑料球相关的ARG风险时考虑MP类型和颗粒大小的重要性。
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引用次数: 0
Priority control strategies derived from updated measurement of VOCs source profiles for plastic product industry 根据塑料制品工业VOCs源概况的最新测量得出的优先控制策略
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110019
Xiuying Zhao , Wutao Zeng , Chenghao Liao , Hao Han , Minhui Li , Zhiyang Liu , Yongbo Zhang
To address the lack of localized volatile organic compounds (VOCs) source profiles in the plastic products industry, this study measured VOCs emissions from 17 representative manufacturers in Guangdong Province, the leading plastic producer in China. A total of 114 VOCs species were identified, and source profiles for 10 production processes were established. Oxygenated volatile organic compounds (OVOCs), aromatics, and alkanes were the predominant species across various manufacturing stages. Molding and post-processing were identified as the main emission processes: OVOCs, aromatics and alkanes were dominant in molding, whereas OVOCs and aromatics were more prevalent in post-processing. The Ozone formation potential (OFP) was calculated to identify priority control species. OFP values ranged from 0.39 to 17.03 mg/m3, identifying isopropanol, toluene, and hexanal as key control species. Furthermore, emission factors were updated based on product type. This study established the first comprehensive VOC source profiles and process-specific emission factors for the plastic industry in Guangdong, providing a scientific basis for targeted emission management and pollution control strategies.
为了解决塑料制品行业缺乏局部挥发性有机化合物(VOCs)来源概况的问题,本研究测量了广东省17家具有代表性的制造商的挥发性有机化合物(VOCs)排放量。共鉴定出114种挥发性有机化合物,建立了10种生产工艺的来源概况。含氧挥发性有机化合物(OVOCs)、芳烃和烷烃是各制造阶段的优势物质。成型和后处理是主要的排放过程:成型过程中OVOCs、芳烃和烷烃占主导地位,后处理过程中OVOCs和芳烃占主导地位。通过计算臭氧形成势(OFP)来确定优先控制物种。OFP值在0.39 ~ 17.03 mg/m3之间,确定异丙醇、甲苯和己醛为主要控制物质。此外,根据产品类型更新了排放因子。本研究首次建立了广东省塑料工业VOC源分布图和工艺特定排放因子,为制定针对性排放管理和污染控制策略提供科学依据。
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引用次数: 0
Insights from an invited expert panel using a World Café: Developing a national policy for a human biomonitoring programme 使用世界咖啡馆的特邀专家小组的见解:为人类生物监测规划制定国家政策
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110025
Richa Singh , Sewon Lee , Darragh Doherty , Conor Buggy , Holger Martin Koch , Marike Kolossa-Gehring , Alison Connolly
Human biomonitoring (HBM) is a powerful tool for quantifying internal chemical levels via biological samples such as blood and urine. Between 2000 and 2017, global synthetic chemical production doubled from approximately 1.15 billion tonnes to 2.3 billion tonnes, with this trend continuing to increase. There has been an extensive expansion of national HBM programmes to evaluate actual chemical exposures and safeguard their citizens.
A key factor in the development of HBM is to include policymakers and to utilise HBM data for policy impact. This study, part of the HBM4IRE (Human Biomonitoring for Ireland) feasibility study, employed a World Café approach for engaging 25 stakeholders from government agencies, industry, and academia to co-create a national HBM roadmap. Using a critical realist approach and thematic analysis of qualitative data, four key themes emerged from the discussion: (1) targeted HBM for exposure hotspots, (2) mapping HBM to EU and National policy frameworks, (3) monitoring chemical exposures as an early warning system, and (4) aligning HBM with national legislative needs.
Results highlight HBM’s critical role in identifying at-risk groups (such as workers in high-exposure industries, children exposed to recycled materials like playground tyres) and validating policy effectiveness (e.g., lead restriction impacts). It also highlighted challenges such as data gaps, high costs, and limited baseline information. Study participants expressed a need for a governance framework, including a national HBM Steering Committee and inter-institutional collaboration, to bridge science-to-policy gaps, offering a scalable model for other nations to enhance chemical risk management, ensure regulatory compliance, and strengthen public health protection.
Overall, stakeholders expressed a high interest and strong willingness in establishing a national HBM programme in Ireland, viewing this as an opportune time for Ireland to implement such a system. The approach adopted for this study could be utilised to engage different stakeholders across an array of relevant topics. Given its valuable outcomes, the HBM4IRE World Café approach has demonstrated that it can serve as a model for other countries to build consensus, identify gaps, and foster stakeholder ownership in establishing long-term and sustainable national HBM programmes.
人体生物监测(HBM)是通过血液和尿液等生物样本定量体内化学物质水平的有力工具。2000年至2017年间,全球合成化学品产量翻了一番,从约11.5亿吨增至23亿吨,而且这一趋势还在继续增加。已经广泛扩大了国家HBM规划,以评估实际的化学品接触并保护其公民。发展HBM的一个关键因素是纳入政策制定者并利用HBM数据产生政策影响。这项研究是HBM4IRE项目的一部分,采用世界咖啡的方法,让来自政府机构、行业和学术界的25个利益相关者共同制定国家HBM路线图。采用批判现实主义方法和对定性数据的专题分析,讨论中出现了四个关键主题:(1)针对暴露热点的HBM,(2)将HBM映射到欧盟和国家政策框架,(3)作为预警系统监测化学品暴露,以及(4)与国家立法需求保持一致。结果强调HBM在识别风险群体(例如,高暴露行业的工人,暴露于游乐场轮胎等回收材料的儿童)和验证政策有效性(例如,铅限制影响)方面的关键作用。它还强调了数据差距、高成本和有限的基线信息等挑战。研究参与者表示,需要一个治理框架,包括一个国家HBM指导委员会和机构间合作,以弥合科学与政策之间的差距,为其他国家提供一个可扩展的模式,以加强化学品风险管理,确保遵守法规,并加强公共卫生保护。总体而言,利益相关者表达了在爱尔兰建立国家HBM计划的高度兴趣和强烈意愿,认为这是爱尔兰实施这样一个系统的时机。本研究采用的方法可用于涉及一系列相关主题的不同利益相关者。鉴于其宝贵的成果,HBM4IRE世界咖啡模式表明,它可以作为其他国家在建立长期和可持续的国家HBM规划方面建立共识、确定差距和促进利益攸关方所有权的典范。
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引用次数: 0
Integrated network toxicology and molecular docking are used to elucidate the mechanism by which chlorpyrifos induces hepatotoxicity (Cyprinus carpio) 采用综合网络毒理学和分子对接的方法,阐明毒死蜱诱导鲤肝毒性的机制。
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110032
Xiaojing Li , Huanqi Zhang , Peizhong Yu , Xiaozhe Chen , Yuhong Yang , Shiwen Xu
Chlorpyrifos (CPF), a typical organophosphorus pesticide, is frequently applied for pest control in households and agriculture worldwide. Liver, being the primary site for xenobiotic metabolism, is extremely vulnerable to drug threats. To elucidate the hepatotoxic mechanism of CPF and identify targets for its relief, the overlapping data between CPF-associated targets and liver injury-related genes were analyzed. It was found that CPF hepatotoxicity targets were mainly involved in oxidoreductase activity, fatty acid metabolism, glutathione metabolic process, response to biotic stimulus, ferroptosis, and mitochondrion disorders. TP53 molecular exhibited the strong binding stability with CPF, and TP53-mediated SLC7A11/GPX4 signaling suppression contributed to CPF-induced hepatotoxicity in Cyprinus carpio. CPF disrupted iron homeostasis by downregulating FTH, NCOA4, and FPN expressions, while simultaneously increasing ACSL4 expression to promote the accumulation of lipid peroxides MDA and LPO. Meanwhile, CPF reduced intracellular GPX4 levels, thereby diminishing lipid ROS scavenging capacity and triggering ferroptosis. Selenium (Se) could reverse CPF- and Erastin-induced ferroptosis and mitochondrial dysfunction. GSH depletion and GPX4 silencing reversed the alleviating effect of Se on CPF-induced lipid peroxidation, but they had little effect on iron contents. Meanwhile, Se addition also increased GSH contents and GPX4 protein expressions. The results revealed some targets of CPF-induced hepatotoxicity. These studies provided the theoretical basis for the future development of environmental monitoring and pollutant control strategies.
毒死蜱(Chlorpyrifos, CPF)是一种典型的有机磷农药,在世界范围内经常用于家庭和农业害虫防治。肝脏作为外源代谢的主要部位,极易受到药物的威胁。为了阐明CPF的肝毒性机制并确定其缓解靶点,我们分析了CPF相关靶点与肝损伤相关基因之间的重叠数据。发现CPF的肝毒性靶点主要涉及氧化还原酶活性、脂肪酸代谢、谷胱甘肽代谢过程、对生物刺激的反应、铁死亡和线粒体紊乱。TP53分子与CPF具有较强的结合稳定性,TP53介导的SLC7A11/GPX4信号通路抑制是CPF诱导鲤鱼肝毒性的重要机制之一。CPF通过下调FTH、NCOA4和FPN的表达来破坏铁稳态,同时增加ACSL4的表达,促进脂质过氧化物MDA和LPO的积累。同时,CPF降低细胞内GPX4水平,从而降低脂质ROS清除能力,引发铁凋亡。硒(Se)可以逆转CPF-和erastin诱导的铁下垂和线粒体功能障碍。GSH耗竭和GPX4沉默逆转了硒对cpf诱导的脂质过氧化的缓解作用,但对铁含量的影响不大。硒的添加也增加了GSH含量和GPX4蛋白的表达。结果揭示了cpf诱导的一些肝毒性靶点。这些研究为今后环境监测和污染物控制策略的发展提供了理论依据。
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引用次数: 0
Compounding hazards posed by wildfires, flooding, and resource extraction: Assessing multimedia metal(loid) exposures and risk in rural, southwestern U.S. Populations 野火、洪水和资源开采造成的复合危害:评估美国西南部农村人口的多媒体金属(loid)暴露和风险。
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110034
Zain Alabdain Alqattan , God’sgift N. Chukwuonye , Camille Tinerella , Miriam Jones , Mónica D. Ramírez-Andreotta
Understanding the extent of contamination due to climatic events in rural areas is necessary to protect environmental health, especially when these spaces disproportionately bear the burden of resource extraction. Using a Monte Carlo-based probabilistic assessment, this study investigates how wildfire and subsequent flooding influences As, Cd, Cu, Cr, Pb, Mn, Ni, and Zn exposure from non-residential sediment and residential soil and indoor/outdoor dust. Carcinogenic/cumulative target cancer risk (TCR) and noncarcinogenic/cumulative hazard index (HI) were evaluated across multiple exposure pathways and scenarios (residential, nonresidential) for children and adults in rural, Arizona communities. In residential settings, flooding significantly increased (p ≤ 0.05) Pb and Cu surface soil concentrations. In both populations, HIflooded > 1, while TCRflooded falls within the tolerable U.S.EPA risk threshold. The mean HIt-Child > 1 was driven by As, Cu, and Mn in outdoor dust followed by Pb and Zn in soil. Arsenic incidental ingestion and to a lesser degree Pb from residential outdoor dust was the prominent exposure pathway, leading to 1.6 cancer cases for every 10,000 children, whereas an adult’s exposure/associated risk was dominated by soil. Outdoor dust led to an unacceptable carcinogenic risk for children and cleanup efforts are imperative. Children growing up in rural, southwestern resource extraction communities experiencing climate extremes are bearing the burden, facing increased health risks. When navigating climatic challenges in rural, resource extraction regions, community-centered environmental research translation and nature-based solutions are critical to mitigating environmental exposures and associated health risks.
了解农村地区气候事件造成的污染程度对于保护环境健康是必要的,特别是当这些地区不成比例地承担着资源开采的负担时。利用蒙特卡罗概率评估,本研究调查了野火和随后的洪水如何影响从非住宅沉积物和住宅土壤以及室内/室外灰尘中暴露的As, Cd, Cu, Cr, Pb, Mn, Ni和Zn。对亚利桑那州农村社区儿童和成人的多种暴露途径和场景(住宅和非住宅)进行了致癌/累积靶癌风险(TCR)和非致癌/累积危害指数(HI)评估。在居住环境中,洪水显著提高了(p≤0.05)表层土壤中Pb和Cu的浓度。在这两个人群中,hip淹水的风险值都在110,而tcr淹水的风险值都在美国环保局可容忍的风险阈值之内。室外粉尘中As、Cu、Mn对HIt-Child的影响最大,其次是土壤中的Pb、Zn。偶然摄入的砷和较小程度的住宅室外粉尘中的铅是主要的暴露途径,导致每10,000名儿童中有1.6例癌症病例,而成人的暴露/相关风险主要是土壤。室外粉尘对儿童的致癌风险是不可接受的,因此清理工作势在必行。在经历极端气候的农村和西南部资源开采社区长大的儿童承受着负担,面临着越来越大的健康风险。在应对农村和资源开采地区的气候挑战时,以社区为中心的环境研究转化和基于自然的解决方案对于减轻环境暴露和相关的健康风险至关重要。
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引用次数: 0
Evaluation of a mother–child dyad toxicokinetic model paired with environmental doses for estimation of serum per- and polyfluoroalkyl substances in early life 评估母婴双毒性动力学模型与环境剂量配对,用于估计生命早期血清中全氟烷基和多氟烷基物质
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2026.110046
Yerin Jung , Marc-André Verner , Scott M. Bartell
Contact-based exposure estimation paired with empirically evaluated toxicokinetic (TK) modeling can complement direct measurements of serum concentrations for characterizing individual exposures and provide a proxy for risk assessment. This study examined whether a mother–child dyad TK model paired with PFAS exposure estimates provide reasonable predictions of serum PFAS concentrations for children. A previously published mother–child dyad TK model was used to estimate the child serum concentrations. We modified the model by updating with recent TK parameter estimates. Background intake rates via food, indoor dust, and indoor air were from published studies. Estimation of child serum PFOA concentrations in PFOA-contaminated regions additionally considered exposure to contaminated drinking water and outdoor air. TK-modeled serum concentrations were then compared with measured serum concentrations from child cohorts for four PFAS (PFOA, PFOS, PFHxS, and PFNA) from other published studies. Individual serum PFOA measurements from the C8 Health Study were compared with modeled serum concentrations using the modified and other published TK models. Modeled child PFAS serum concentrations using the modified dyad TK model were in good accordance with measured serum concentrations. The median model predictions of serum PFOA were highly correlated with the median of measured values and the percentage of TK-modeled serum PFOA within 2-fold and 10-fold of measured values was 34% and 94%, respectively, which was similar or higher than the estimates from the other TK models. The modified dyad TK model can provide reasonable estimates of dynamic serum PFAS concentrations for children when only environmental doses are available.
基于接触的暴露估计与经验评估的毒性动力学(TK)模型相结合,可以补充血清浓度的直接测量,以表征个体暴露,并为风险评估提供代理。本研究考察了母子双TK模型与PFAS暴露估计是否能提供儿童血清PFAS浓度的合理预测。使用先前发表的母子二元TK模型来估计儿童血清浓度。我们通过更新最近的TK参数估计来修正模型。通过食物、室内灰尘和室内空气摄入的本底率来自已发表的研究。对全氟辛酸污染地区儿童血清全氟辛酸浓度的估计还考虑了受污染的饮用水和室外空气的暴露。然后将tk模型的血清浓度与来自其他已发表研究的四种PFAS (PFOA, PFOS, PFHxS和PFNA)的儿童队列测量的血清浓度进行比较。将C8健康研究的个体血清PFOA测量值与使用改进的和其他已发表的TK模型建模的血清浓度进行比较。采用改进的双TK模型建模的儿童PFAS血清浓度与测定的血清浓度吻合良好。血清PFOA的中位数模型预测值与实测值的中位数高度相关,TK模型的血清PFOA在实测值2倍和10倍范围内的百分比分别为34%和94%,与其他TK模型的估计值相似或更高。当只有环境剂量时,改进的二元TK模型可以提供儿童动态血清PFAS浓度的合理估计。
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引用次数: 0
Integrating nontargeted metabolomics and machine learning to assess PFAS exposure associations with liver cancer risk 整合非靶向代谢组学和机器学习来评估PFAS暴露与肝癌风险的关系
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110014
Tong Wu , Jiamian Fang , Jiawei Hong , Yifan Jiang , Keyi Du , Weichen Zhang , Siqi Zhang , Tingting Pan , Liyun Fu , Weili Mao , Hangbiao Jin , Wendi Hu , Shusen Zheng , Linping Cao
Per- and polyfluoroalkyl substances (PFASs) are persistent synthetic chemicals, showing global presence in environment and human populations. Despite accumulating evidence implicating PFASs in liver toxicity, epidemiological data linking PFAS exposure to liver cancer risk remain limited, particularly regarding the underlying molecular mechanisms in humans. In this case-control study, we quantified concentrations of nine PFASs and performed nontargeted metabolomics in serum samples from 116 newly diagnosed liver cancer cases and 400 matched controls. Advanced supervised machine learning models were employed to identify PFAS exposure-associated metabolic features, followed by pathway enrichment and mediation analyses to elucidate biological mechanisms. Higher human serum levels of perfluorooctanoic acid (PFOA), perfluorononanoate, perfluorodecanoate, perfluorohexane sulfonate, perfluorooctanesulfonic acid, and 6:2 chlorinated polyfluoroether sulfonic acid were significantly correlated with the increased liver cancer risk. Weighted quantile sum index for the PFAS mixture was significantly correlated with an elevated liver cancer risk, with PFOA identified as the dominant contributor to this association. Least absolute shrinkage and selection operator (LASSO) approach based on metabolomic variables achieved the greatest predictive accuracy. Disruptions in methionine metabolism and phospholipid biosynthesis were identified as significant mediators in the association between serum PFAS levels and liver cancer risk, as revealed by LASSO modeling and mediation analyses. To our awareness, this study first demonstrates that multiple PFAS exposure may promote liver carcinogenesis through perturbations in amino acid and membrane lipid metabolism in humans.
全氟烷基和多氟烷基物质(PFASs)是持久性合成化学品,在全球环境和人群中普遍存在。尽管越来越多的证据表明PFAS与肝毒性有关,但将PFAS暴露与肝癌风险联系起来的流行病学数据仍然有限,特别是关于人类潜在的分子机制。在这项病例对照研究中,我们量化了116例新诊断的肝癌患者和400例匹配对照的血清样本中9种PFASs的浓度,并进行了非靶向代谢组学分析。采用先进的监督机器学习模型来识别PFAS暴露相关的代谢特征,然后通过途径富集和中介分析来阐明生物学机制。人血清中全氟辛酸(PFOA)、全氟壬酸盐、全氟癸酸盐、全氟己烷磺酸、全氟辛烷磺酸和6:2氯化多氟醚磺酸水平升高与肝癌风险增加显著相关。PFAS混合物的加权分位数和指数与肝癌风险升高显著相关,PFOA被确定为这种关联的主要贡献者。基于代谢组学变量的最小绝对收缩和选择算子(LASSO)方法达到了最高的预测精度。LASSO模型和中介分析显示,蛋氨酸代谢和磷脂生物合成的中断被确定为血清PFAS水平与肝癌风险之间关联的重要介质。据我们所知,本研究首次证明了多重PFAS暴露可能通过扰乱人体氨基酸和膜脂代谢而促进肝癌的发生。
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引用次数: 0
Gut-lung axis: a novel mechanism involving microbiota dysbiosis-coordinated PLA2-TRPV1 neuroimmune crosstalk in nanoplastic-induced asthma exacerbation 肠-肺轴:一种涉及微生物群失调与PLA2-TRPV1神经免疫串扰在纳米塑料诱导的哮喘加重中的新机制
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2026.110047
Xin Zeng , Chuhao He , Jitong Li , Qing Feng , Zhenjie Lu , Long Li , Yongkang Qiao , Wei Han , Faming Wang , Mingqing Chen , Chan Lu , Rong She , Yang Wu , Yanling Sun , Xu Yang , Ping Ma , Surui Lu
This study, based on an OVA-sensitized mouse model, systematically elucidates the molecular mechanisms through which 20 nm polystyrene nanoplastics (PS-NPs) exacerbate asthma. A series of assessments were conducted, including measurements of airway hyperresponsiveness (AHR), histopathological analysis of lung tissue using HE, PAS and Masson staining, immunohistochemical detection of phospholipase A2 (PLA2) and TRPV1 expression, quantification of serum immunoglobulins and tissue cytokines, as well as lung metabolomics and gut microbiota profiling. Exposure to PS-NPs activated PLA2 in lung tissue, leading to the accumulation of arachidonic acid metabolites such as prostaglandin E2 and leukotriene B4. This process increased TRPV1 channel expression and promoted the release of neuropeptides including substance P and calcitonin gene-related peptide. The resulting cascade activated the NF-κB signaling pathway, thereby enhancing Th2-type inflammatory responses characterized by elevated IL-4, IL-5 and IL-13, reduced IFN-γ, and increased oxidative stress markers such as 8-OHdG. PS-NPs also significantly altered the gut microbiota, increasing the abundance of Pseudomonadota, Actinomycetota and Verrucomicrobiota. Gram-negative bacteria released substantial amounts of hexa-acylated LPS, which activated the intestinal TLR4/NF-κB pathway and promoted pulmonary inflammation through the gut–lung axis. Furthermore, dysbiosis-induced reductions in short-chain fatty acid production and abnormalities in glycerophospholipid and amino acid metabolism further enhanced pulmonary PLA2 activity, forming a PLA2–TRPV1–neuroimmune positive feedback loop that aggravated airway hyperresponsiveness and lung tissue damage. Overall, this study suggests the central role of a metabolism–immune–neuroinflammatory network mediated by the gut–lung axis in asthma aggravated by PS-NPs, providing new insights into the respiratory toxicity of environmental nanoplastics.
本研究基于ova致敏小鼠模型,系统阐明了20 nm聚苯乙烯纳米塑料(PS-NPs)加重哮喘的分子机制。进行了一系列的评估,包括气道高反应性(AHR)的测量,肺组织的组织病理学分析(HE, PAS和Masson染色),磷脂酶A2 (PLA2)和TRPV1表达的免疫组织化学检测,血清免疫球蛋白和组织细胞因子的量化,以及肺代谢组学和肠道微生物群谱。暴露于PS-NPs会激活肺组织中的PLA2,导致花生四烯酸代谢物如前列腺素E2和白三烯B4的积累。这一过程增加了TRPV1通道的表达,促进了P物质和降钙素基因相关肽等神经肽的释放。由此产生的级联激活了NF-κB信号通路,从而增强了th2型炎症反应,其特征是IL-4、IL-5和IL-13升高,IFN-γ降低,8-OHdG等氧化应激标志物升高。PS-NPs还显著改变了肠道微生物群,增加了假单胞菌群、放线菌群和疣菌群的丰度。革兰氏阴性菌释放大量六酰化LPS,激活肠道TLR4/NF-κB通路,通过肠-肺轴促进肺部炎症。此外,生态失调引起的短链脂肪酸生成减少以及甘油磷脂和氨基酸代谢异常进一步增强了肺PLA2活性,形成PLA2 - trpv1 -神经免疫正反馈回路,加重了气道高反应性和肺组织损伤。总体而言,本研究提示了由肠-肺轴介导的代谢-免疫-神经炎症网络在PS-NPs加重哮喘中的核心作用,为环境纳米塑料的呼吸毒性提供了新的见解。
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引用次数: 0
Evaluating the effects of heat strain and air pollution on kidney health 评价热应变和空气污染对肾脏健康的影响
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.envint.2025.110042
Jaime Butler-Dawson , Diana Jaramillo , Lyndsay Krisher , Karely Villarreal Hernandez , Laura Calvimontes , Grant Erlandson , James Seidel , Colton Castro , Stephen Brindley , Yaqiang Li , Miranda Dally , Katherine A. James , Richard J. Johnson , Daniel Pilloni , Alex Cruz , Nicholas Smith , Evan Johnson , Joshua W. Schaeffer , John L. Adgate , Lee S. Newman

Background

Rising global temperatures raise concerns about climate change’s health impacts. Agricultural workers are particularly vulnerable due to prolonged exposure to heat and environmental pollutants, including airborne particulate matter (PM), which may increase their risk for kidney injury. This study explores the relationships between core body temperature (CBT), markers of hydration, PM exposure, and kidney injury, offering insights into public health risks related to climate change.

Methods

We conducted a longitudinal study of 148 sugarcane workers in Guatemala, monitoring them over 378 person-workdays. CBT and personal PM exposure were recorded throughout the workday, while markers of hydration and kidney function were assessed pre- and post-shift. Linear mixed-effects models were used to assess the relationships between these exposure factors, dehydration markers, and serum creatinine changes, an indicator of kidney injury.

Findings

CBT exceeded 38.0 °C on 53 % of workdays, with 15 % surpassing 38.5 °C. Higher urinary specific gravity (β: 3.82, 95 % CI: 0.84, 6.80), serum uric acid (β: 2.46, 95 % CI: 0.70, 2.14), average heat index (β: 1.33, 95 % CI: 0.53, 2.14), and CBT exceeding 38.5 °C (β: 8.95, 95 % CI: 2.89, 15.02) were significantly associated with cross-shift increases in serum creatinine. Despite substantial PM5 exposure, no significant association with creatinine changes was found.

Conclusions

Heat strain and dehydration are significant contributors to kidney injury in agricultural workers, highlighting critical public health risks. These findings emphasize the urgent need for interventions to mitigate heat-related health hazards, including workplace protections, hydration strategies, and climate adaptation policies to safeguard vulnerable populations worldwide.
全球气温上升引发了人们对气候变化对健康影响的担忧。由于长期暴露于高温和环境污染物,包括空气中的颗粒物(PM),农业工人特别容易受到伤害,这可能会增加他们肾脏损伤的风险。本研究探讨了核心体温(CBT)、水合标志物、PM暴露和肾损伤之间的关系,为气候变化相关的公共卫生风险提供了见解。方法对危地马拉148名甘蔗工人进行了纵向研究,对他们进行了378个工作日的监测。在整个工作日记录CBT和个人PM暴露,同时在轮班前和下班后评估水合作用和肾功能指标。使用线性混合效应模型来评估这些暴露因素、脱水标志物和血清肌酐变化(肾损伤指标)之间的关系。53%的工作日scbt超过38.0°C, 15%的工作日超过38.5°C。较高的尿比重(β: 3.82, 95% CI: 0.84, 6.80),血清尿酸(β: 2.46, 95% CI: 0.70, 2.14),平均热指数(β: 1.33, 95% CI: 0.53, 2.14)和CBT超过38.5°C (β: 8.95, 95% CI: 2.89, 15.02)与血清肌酐的交叉移位升高显著相关。尽管大量接触PM5,但未发现与肌酐变化有显著关联。结论干旱和脱水是造成农业工人肾损伤的重要因素,具有重大的公共卫生风险。这些研究结果强调,迫切需要采取干预措施来减轻与热相关的健康危害,包括工作场所保护、补水策略和气候适应政策,以保护全世界的弱势群体。
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引用次数: 0
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Environment International
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