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Occurrence and toxicity of haloketones: emerging class of disinfection byproducts in drinking water of Nanning City, Southwest China 卤素酮的存在和毒性:南宁市饮用水中新兴的一类消毒副产物
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-01-22 DOI: 10.1016/j.envint.2026.110097
Yuwen Huang , Zan Sheng , Qiuyan Wei , Mingliang Wu , Jingyi Xiao , Qing Zhong , Zhanmou Liu , Mengting Yang , Xiao Wei
Haloketones (HKs) are an emerging class of unregulated drinking water disinfection byproducts (DBPs) that are primarily responsible for drinking water cytotoxicity and also exhibit genotoxicity and carcinogenicity. We determined the concentrations of 11 HKs in drinking water and conducted quantitative and comparative analyses of their toxicity. Nine HKs were detected in drinking water from Nanning City in Southwest China, with median concentrations ranging from 0.03 to 3.32 μg/L. 1,1,3-Tribromopropanone and 1-bromo-1,1-dichloropropanone were identified in drinking water for the first time in China. The descending rank order of HK cytotoxicity was 1,3-dichloropropanone > bromopropanone > 1,1,3-tribromopropanone > 1,1,3-trichloropropanone ≈ chloropropanone > 1,1-dichloropropanone > 1,1,3,3-tetrachloropropanone > 1-bromo-1,1-dichloropropanone ≈ 1,1,3,3-tetrabromopropanone > 1,1,1-trichloropropanone ≈ 1,1-dibromopropanone (F10,208 = 4672.689, P < 0.001). The rank order for HK genotoxicity was 1,3-dichloropropanone > bromopropanone > chloropropanone > 1,1-dibromopropanone > 1,1,3-trichloropropanone ≈ 1,1,3-tribromopropanone > 1-bromo-1,1-dichloropropanone ≈ 1,1,3,3-tetrachloropropanone > 1,1,3,3-tetrabromopropanone > 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (F10,66 = 7028.528, P < 0.001). The rank order for HK thiol reactivity was 1,1-dibromopropanone ≈ 1,3-dichloropropanone ≈ chloropropanone ≈ bromopropanone ≈ 1-bromo-1,1-dichloropropanone ≈ 1,1,3-tribromopropanone > 1,1,3,3-tetrabromopropanone > 1,1,3-trichloropropanone ≈ 1,1,3,3-tetrachloropropanone ≈ 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (F10,154 = 473.640, P < 0.001). Quantitative structure activity relationship models indicated that HK toxicity was closely correlated with hydrophobicity, boiling point, and topological properties. HKs exhibited higher cytotoxicity and genotoxicity than regulated haloacetic acids and trihalomethanes. In particular, 1,3-dichloropropanone showed higher toxicity than nitrogenous DBPs. Further studies are required to expand the investigation of HK pollution, elucidate their formation and toxic mechanisms, and evaluate the potential human health risks.
卤酮(hk)是一类新兴的不受管制的饮用水消毒副产物(DBPs),主要负责饮用水的细胞毒性,也表现出遗传毒性和致癌性。我们测定了饮用水中11种hk的浓度,并对其毒性进行了定量和比较分析。南宁市饮用水中检出9种hk,中位浓度范围为0.03 ~ 3.32 μg/L。1,1,3-三溴丙烷和1-溴-1,1-二氯丙烷为国内首次在饮用水中检出。细胞毒性是1港元的降序排序,3-dichloropropanone 祝辞 bromopropanone 祝辞 1,1,3-tribromopropanone 祝辞 1,1,3-trichloropropanone≈chloropropanone 祝辞 1,1-dichloropropanone 祝辞 1,1,3,3-tetrachloropropanone 祝辞 1-bromo-1, 1-dichloropropanone≈1,1,3,3-tetrabromopropanone 祝辞 1,1,1-trichloropropanone≈1,1-dibromopropanone (F10,208 = 4672.689,P & lt; 0.001)。香港基因毒性的等级次序为1,3-dichloropropanone 祝辞 bromopropanone 祝辞 chloropropanone 祝辞 1,1-dibromopropanone 祝辞 1,1,3-trichloropropanone≈1,1,3-tribromopropanone 祝辞 1-bromo-1, 1-dichloropropanone≈1,1,3,3-tetrachloropropanone 祝辞 1,1,3,3-tetrabromopropanone 祝辞 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (F10 66 = 7028.528,P & lt; 0.001)。香港硫醇反应的等级次序为1,1-dibromopropanone ≈ 1,3-dichloropropanone ≈ chloropropanone ≈ bromopropanone ≈ 1-bromo-1, 1-dichloropropanone ≈ 1,1,3-tribromopropanone 祝辞 1,1,3,3-tetrabromopropanone 祝辞 1,1,3-trichloropropanone ≈ 1,1,3,3-tetrachloropropanone ≈ 1,1-dichloropropanone ≈ 1,1,1-trichloropropanone (F10,154 = 473.640,P & lt; 0.001)。定量构效关系模型表明,HK毒性与疏水性、沸点和拓扑性质密切相关。与受调控的卤乙酸和三卤甲烷相比,HKs具有更高的细胞毒性和遗传毒性。特别是1,3-二氯丙烷的毒性高于含氮dbp。需要进一步的研究,以扩大对香港污染的调查,阐明其形成和毒性机制,并评估潜在的人类健康风险。
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引用次数: 0
The role of coronary artery calcification in metal-related cardiovascular disease 冠状动脉钙化在金属相关心血管疾病中的作用
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-01-21 DOI: 10.1016/j.envint.2026.110095
Arce Domingo-Relloso , Katlyn E. McGraw , Irene Martinez-Morata , Yuchen Zhang , Kathrin Schilling , Ronald A. Glabonjat , Ziqing Wang , Kiros Berhane , Brent A. Coull , Marta Galvez-Fernandez , Miranda R. Jones , Wendy S. Post , Joel Kaufman , Tiffany R. Sanchez , Maria Tellez-Plaza , Graham R. Barr , Steven Shea , Ana Navas-Acien , Linda Valeri
Metals are associated with cardiovascular disease (CVD), but the underlying pathways remain largely unclear. We evaluated the potential intermediate role of coronary artery calcification (CAC) trajectory on the association between urinary metals and incident CVD, accounting for competing risks by death from other causes. We used data from 6,459 participants of the Multi-Ethnic Study of Atherosclerosis (MESA). CAC was measured longitudinally using the spatially weighted calcium score in five exams, starting in 2000. Participants were followed for CVD events through 2019. Cadmium, cobalt, copper, uranium, tungsten, and zinc were measured in urine at the baseline visit (2000–2002). We used a causal inference algorithm with a path-specific effects approach for longitudinal mediation analysis to evaluate the intermediate role of CAC on the association between metals and incident CVD. The association with incident CVD mediated through the CAC trajectory was statistically significant for cadmium, cobalt, copper, tungsten, and zinc. The number of CVD cases (95% CI) per 100,000 person-years attributable to an interquartile range (IQR) increase in metal levels through the longitudinal trajectory of CAC was 44 (20, 72) for cadmium, 21 (6, 39) for cobalt, 19 (2, 36) for copper, 18 (2, 38) for tungsten, and 43 (26, 62) for zinc. This study supports that part of the association between urinary metals and CVD is attributable to changes in CAC over time. In particular, half of the association between urinary cadmium and CVD might be mediated by longitudinal changes in CAC. This study could inform strategies for early detection and prevention of CVD based on urinary metal levels.
金属与心血管疾病(CVD)有关,但潜在的途径在很大程度上仍不清楚。我们评估了冠状动脉钙化(CAC)轨迹在尿金属与CVD事件之间的关联中的潜在中间作用,并考虑了其他原因死亡的竞争风险。我们使用了来自多种族动脉粥样硬化研究(MESA)的6459名参与者的数据。从2000年开始,CAC在五次考试中使用空间加权钙分数进行纵向测量。参与者的心血管疾病事件被跟踪到2019年。在基线访问时(2000-2002年)测量尿液中的镉、钴、铜、铀、钨和锌。我们使用因果推理算法和路径特异性效应方法进行纵向中介分析,以评估CAC在金属与事件CVD之间的关联中的中间作用。对于镉、钴、铜、钨和锌,通过CAC轨迹介导的CVD与事件的关联具有统计学意义。通过CAC的纵向轨迹,由于金属水平四分位数范围(IQR)增加而导致的CVD病例数(95% CI)每100,000人年为镉44例(20,72),钴21例(6,39),铜19例(2,36),钨18例(2,38),锌43例(26,62)。该研究支持尿金属与CVD之间的部分关联可归因于CAC随时间的变化。特别是,尿镉和心血管疾病之间的一半关联可能是由CAC的纵向变化介导的。这项研究可以为基于尿金属水平的CVD早期检测和预防策略提供信息。
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引用次数: 0
Long-term pet ownership promotes resistome similarity between cats and their owners 长期养宠物会促进猫和主人之间的抵抗力相似
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-01-14 DOI: 10.1016/j.envint.2026.110074
Zhenlong Wang , Ji Lu , Xiumin Wang , Wei An , Ya Zhao , Bing Han , Hui Tao , Jie Liu , Jianhua Guo , Jinquan Wang
Pet ownership offers physical and mental health benefits, but the risks of antibiotic resistance genes (ARGs) transmission between pets and humans remain underexplored. In this study, we used metagenomics analysis of fecal samples to compare resistome profiles among four groups: owned cats and their owners, and caged cats and non-cat owners. Our findings show significant similarities in gut microbial composition, ARGs, and mobile genetic elements (MGEs) between owned cats and their owners, identifying 73 shared core ARGs and 80 shared MGEs. In contrast, caged cats and non-cat owners shared only 30 ARGs and 73 MGEs. Long-term contact was positively correlated with a higher number of shared ARGs (from 20 + to 60 + ) and MGEs (from 10 + to 40 + ), as well as increased resistome risk (2.47- to 4.92-fold) between pet cats and owners. The gut microbiota played a key role in shaping the ARGs and MGEs profiles, with Escherichia coli and Klebsiella pneumoniae identified as primary carriers, each genome harboring 20 to 62 ARGs and 6 to 29 MGEs. ARGs transfer events were more frequent between pet cats and their owners than in other groups. These findings underscore a potential risk of shared antimicrobial resistance between companion animals and humans within the studied population in China.
养宠物对身心健康都有好处,但抗生素抗性基因(ARGs)在宠物和人类之间传播的风险仍未得到充分研究。在这项研究中,我们对粪便样本进行宏基因组学分析,比较了四组人群(养猫和养猫的人、关在笼子里的猫和不养猫的人)的抗性组谱。我们的研究结果显示,被养猫和主人之间的肠道微生物组成、ARGs和移动遗传元件(MGEs)存在显著的相似性,确定了73个共享核心ARGs和80个共享MGEs。相比之下,关在笼子里的猫和不养猫的猫只分享了30个arg和73个mge。长期接触与共享arg数量(从20个 + 到60个 + )和MGEs(从10个 + 到40个 + )呈正相关,以及宠物猫和主人之间抵抗组风险增加(2.47- 4.92倍)。肠道微生物群在形成ARGs和MGEs谱方面发挥了关键作用,大肠杆菌和肺炎克雷伯菌被确定为主要携带者,每个基因组含有20至62个ARGs和6至29个MGEs。与其他组相比,宠物猫和主人之间的arg转移事件更为频繁。这些发现强调了在中国研究人群中伴侣动物和人类之间存在共同抗微生物药物耐药性的潜在风险。
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引用次数: 0
Co-exposure to PFOA, PFBA and nanoplastics synergistically exacerbates neurotoxicity by impairing PINK1/Parkin-mediated mitophagy 共暴露于PFOA、PFBA和纳米塑料中,通过损害PINK1/帕金森介导的线粒体自噬,协同加剧神经毒性
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-01-24 DOI: 10.1016/j.envint.2026.110102
Helei Cai , Shihao Luo , Zhengrong Zhou , Feixia Chen , Jiawei Ying , Qiufang Wu , Yize Wu , Shihua Chen , Xinxin Yao , Feiqin Xie , Wenhui Xu , Ke Xu , Renyi Peng
Perfluorooctanoic acid (PFOA) and perfluorobutyric acid (PFBA), as representative long-chain and short-chain per- and polyfluoroalkyl substances (PFAS), are widely distributed in the environment. These compounds can interact with nanoplastics (NPs) to form complex mixed pollutants, posing potential threats to aquatic organisms and human health. The nervous system, characterized by high sensitivity and energy dependence, is particularly vulnerable to such pollutants. However, the mechanisms underlying neurological toxicity induced by co-exposure to PFOA, PFBA, and NPs remain largely unclear. In this study, zebrafish larvae and human neuroblastoma SH-SY5Y cells were employed as model systems to systematically evaluate the effects of PFOA and PFBA, alone or in combination with NPs, on neural development, behavior, cell viability, mitochondrial function, and autophagy. The results demonstrated that NPs exhibited a significantly higher adsorption capacity for PFOA than for PFBA, and that co-exposure exacerbated neurodevelopmental impairments, behavioral abnormalities, and reductions in cell viability. At the molecular level, co-exposure markedly inhibited the PINK1/Parkin-mediated mitophagy pathway, resulting in mitochondrial damage accumulation, disruption of energy metabolism, and blockade of autophagic flux. Through PINK1 overexpression and pharmacological activation experiments, the pivotal role of the PINK1/Parkin-mediated mitophagy pathway in mitigating neurotoxicity was functionally validated. Collectively, this study elucidates the molecular mechanism by which co-exposure to PFOA, PFBA, and NPs induces neurotoxicity via suppression of mitophagy. These findings identify a potential molecular target for the prevention and treatment of PFAS- and NPs-induced neurological injury and provide valuable theoretical and experimental evidence for evaluating the neurotoxic risks of mixed environmental pollutants.
全氟辛酸(PFOA)和全氟丁酸(PFBA)作为长链和短链全氟烷基和多氟烷基物质(PFAS)的代表,广泛分布于环境中。这些化合物可与纳米塑料相互作用形成复杂的混合污染物,对水生生物和人类健康构成潜在威胁。神经系统的特点是高度敏感和能量依赖,特别容易受到这些污染物的影响。然而,共同暴露于PFOA、PFBA和NPs诱导的神经毒性机制仍不清楚。本研究以斑马鱼幼鱼和人神经母细胞瘤SH-SY5Y细胞为模型系统,系统评价PFOA和PFBA单独或联合NPs对神经发育、行为、细胞活力、线粒体功能和自噬的影响。结果表明,NPs对PFOA的吸附能力明显高于PFBA,并且共同暴露加剧了神经发育障碍、行为异常和细胞活力降低。在分子水平上,共暴露显著抑制了PINK1/ parkin介导的线粒体自噬途径,导致线粒体损伤积累,能量代谢中断,自噬通量阻断。通过PINK1过表达和药理激活实验,从功能上验证了PINK1/ parkinson介导的线粒体自噬通路在减轻神经毒性中的关键作用。总的来说,本研究阐明了PFOA、PFBA和NPs共同暴露通过抑制线粒体自噬诱导神经毒性的分子机制。这些发现确定了预防和治疗PFAS和nps诱导的神经损伤的潜在分子靶点,并为评估混合环境污染物的神经毒性风险提供了有价值的理论和实验证据。
{"title":"Co-exposure to PFOA, PFBA and nanoplastics synergistically exacerbates neurotoxicity by impairing PINK1/Parkin-mediated mitophagy","authors":"Helei Cai ,&nbsp;Shihao Luo ,&nbsp;Zhengrong Zhou ,&nbsp;Feixia Chen ,&nbsp;Jiawei Ying ,&nbsp;Qiufang Wu ,&nbsp;Yize Wu ,&nbsp;Shihua Chen ,&nbsp;Xinxin Yao ,&nbsp;Feiqin Xie ,&nbsp;Wenhui Xu ,&nbsp;Ke Xu ,&nbsp;Renyi Peng","doi":"10.1016/j.envint.2026.110102","DOIUrl":"10.1016/j.envint.2026.110102","url":null,"abstract":"<div><div>Perfluorooctanoic acid (PFOA) and perfluorobutyric acid (PFBA), as representative long-chain and short-chain per- and polyfluoroalkyl substances (PFAS), are widely distributed in the environment. These compounds can interact with nanoplastics (NPs) to form complex mixed pollutants, posing potential threats to aquatic organisms and human health. The nervous system, characterized by high sensitivity and energy dependence, is particularly vulnerable to such pollutants. However, the mechanisms underlying neurological toxicity induced by co-exposure to PFOA, PFBA, and NPs remain largely unclear. In this study, zebrafish larvae and human neuroblastoma SH-SY5Y cells were employed as model systems to systematically evaluate the effects of PFOA and PFBA, alone or in combination with NPs, on neural development, behavior, cell viability, mitochondrial function, and autophagy. The results demonstrated that NPs exhibited a significantly higher adsorption capacity for PFOA than for PFBA, and that co-exposure exacerbated neurodevelopmental impairments, behavioral abnormalities, and reductions in cell viability. At the molecular level, co-exposure markedly inhibited the PINK1/Parkin-mediated mitophagy pathway, resulting in mitochondrial damage accumulation, disruption of energy metabolism, and blockade of autophagic flux. Through PINK1 overexpression and pharmacological activation experiments, the pivotal role of the PINK1/Parkin-mediated mitophagy pathway in mitigating neurotoxicity was functionally validated. Collectively, this study elucidates the molecular mechanism by which co-exposure to PFOA, PFBA, and NPs induces neurotoxicity via suppression of mitophagy. These findings identify a potential molecular target for the prevention and treatment of PFAS- and NPs-induced neurological injury and provide valuable theoretical and experimental evidence for evaluating the neurotoxic risks of mixed environmental pollutants.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110102"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146048275","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}
引用次数: 0
Development of a physiologically based pharmacokinetic (PBPK) model for cobalt in the Chinese population based on population exposure data 基于人群暴露数据建立中国人群中钴的生理药代动力学(PBPK)模型
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-02-04 DOI: 10.1016/j.envint.2026.110132
Xingyu Zhan , Wen Gu , Miaoying Shi , Chenglei Qi , Fuchang Deng , Xu Zhang , Guoqing Xiong , Jing Yang , Yican Wang , Mengyao Wang , Jiajun Xiao , Song Tang , Yufei Dai
Cobalt is a critical raw material for consumer electronic products such as electric vehicles and mobile communication devices. Currently, its recovery rate remains relatively low, resulting in a large amount of waste cobalt entering soil and groundwater environments, which poses a potential threat to human health. Previous studies have mostly focused on the effects of acute cobalt exposure. However, the in vivo metabolic mechanism of long-term low-dose cobalt exposure remains unclear, and the long-term toxic effects of cobalt on the heart await further investigation. Based on the existing model framework, this study constructed a cobalt Physiologically based pharmacokinetic (PBPK) model incorporating a heart compartment, filling the research gap in this field. Meanwhile, the study calibrated the parameters of the PBPK model by integrating the specific exposure scenarios and dietary exposure characteristics of the Chinese population, and conducted model evaluation and evaluation using epidemiological data of the Chinese population. With the help of Monte Carlo simulation (MCS) technology, this study conducted an in-depth analysis of the inter-individual exposure and metabolic characteristics. The results showed that the deviation between the cobalt concentrations in blood, urine, liver, kidneys, and heart of the Chinese population predicted by the model and the measured values was basically controlled within a 2-fold range. The cobalt PBPK model constructed in this study provides a key tool for the accurate risk assessment and practical application of cobalt exposure in the Chinese population, and also offers a referable research paradigm for accurate risk assessment under the specific characteristics of different ethnic groups.
钴是电动汽车和移动通信设备等消费电子产品的关键原材料。目前,其回收率仍然较低,导致大量废钴进入土壤和地下水环境,对人类健康构成潜在威胁。以前的研究主要集中在急性钴暴露的影响上。然而,长期低剂量钴暴露的体内代谢机制尚不清楚,钴对心脏的长期毒性作用有待进一步研究。本研究在现有模型框架的基础上,构建了含心脏隔室的钴生理药代动力学(PBPK)模型,填补了该领域的研究空白。同时,结合中国人群的具体暴露情景和饮食暴露特征,对PBPK模型参数进行校准,并利用中国人群的流行病学数据进行模型评价和评价。本研究借助蒙特卡罗模拟(Monte Carlo simulation, MCS)技术,对个体间暴露和代谢特征进行了深入分析。结果表明,模型预测的中国人群血、尿、肝、肾、心钴浓度与实测值的偏差基本控制在2倍范围内。本研究构建的钴PBPK模型为中国人群钴暴露的准确风险评估和实际应用提供了关键工具,也为不同族群具体特征下的准确风险评估提供了可借鉴的研究范式。
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引用次数: 0
Prenatal exposure to wildfire-related PM2.5 and autism spectrum disorder in children born in California between 2001–2019 2001年至2019年期间在加州出生的儿童产前暴露于野火相关的PM2.5和自闭症谱系障碍
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-02-06 DOI: 10.1016/j.envint.2026.110131
Karl O’Sharkey , Sanjali Mitra , Ting Chow , Amanda J. Goodrich , Kathryn C. Conlon , Miriam Nuño , Deborah H. Bennett , Sean Raffuse , Mohammad Astaneh , Yusheng Zhao , Michael Kleeman , Beate Ritz , Rebecca J. Schmidt

Background

Wildfire smoke is an increasingly prevalent source of air pollution and contains a complex mixture of neurotoxic constituents that could affect neurodevelopment, yet its potential role in autism spectrum disorder (ASD) etiology remains unexplored. We examined associations between wildfire-specific PM2.5 exposures and ASD risk in California births, considering exposure timing, intensity, and background air pollution.

Methods

We analyzed 8.6 million births in California from 2001 to 2019, linking records to ASD diagnoses in California Department of Developmental Services records through 2022. Wildfire-related PM2.5 exposures, including biomass burning and wildland-urban-interface (WUI) source tracers, were estimated for preconception, pregnancy, and post-pregnancy periods. Exposure metrics included continuous, percentile-based, and episode-based indicators. Logistic regression was used to estimate odds ratios, adjusting for sociodemographic covariates. Stratified analyses were conducted by background PM2.5, urbanicity, diagnostic era, and sex.

Results

Continuous wildfire-specific exposures during the pregnancy-period were weakly associated with ASD, but stronger effects emerged at high exposure percentiles and during intense wildfire episodes (≥ 35 µg/m3). Associations were most pronounced among children in the lowest quartile of prenatal background PM2.5, with odds of ASD increasing by 50% for those in the > 90th percentile of wildfire PM2.5 during pregnancy. WUI-related PM2.5 was associated with ASD in metro areas, suggesting unique toxicity. Effects were stronger in non-metro regions, with the exception of WUI-related PM2.5, for births occurring after the implementation of DSM-5, and in White children. Sex differences were minimal, but showed stronger effect estimates for WUI-related PM2.5 and high exposure episodes for males.

Conclusion

Wildfire smoke exposure during pregnancy may increase ASD risk, particularly in low background air pollution and rural settings. High-intensity wildfire events were most strongly associated with ASD, underscoring the need for targeted policies, such as vegetation management, land use planning, and indoor filtration upgrades in the context of increasing wildfire frequency and severity.
野火烟雾是一种日益普遍的空气污染源,它含有可能影响神经发育的神经毒性成分的复杂混合物,但其在自闭症谱系障碍(ASD)病因学中的潜在作用仍未被探索。考虑到暴露时间、强度和背景空气污染,我们研究了加州出生的野火特定PM2.5暴露与ASD风险之间的关系。方法:我们分析了2001年至2019年加州860万名新生儿,将记录与加州发展服务部截至2022年的ASD诊断记录联系起来。估算了与野火相关的PM2.5暴露,包括生物质燃烧和荒地-城市界面(WUI)源示踪剂,用于孕前、怀孕和怀孕后。暴露指标包括连续的、基于百分位数的和基于事件的指标。使用逻辑回归来估计优势比,调整社会人口统计学协变量。按背景PM2.5、城市化程度、诊断时代和性别进行分层分析。结果怀孕期间持续暴露于野火与ASD的相关性较弱,但高暴露百分位数和强烈野火发作期间(≥35 µg/m3)的影响更强。这种关联在产前PM2.5最低四分位数的儿童中最为明显,在怀孕期间野火PM2.5的 >; 第90百分位数的儿童中,ASD的几率增加了50%。在大都市地区,wui相关的PM2.5与ASD相关,表明其独特的毒性。对于实施DSM-5之后出生的婴儿,以及白人儿童,除与wui相关的PM2.5外,非大都市地区的影响更强。性别差异很小,但对wui相关的PM2.5和男性高暴露事件的影响估计更强。结论孕期接触野火烟雾可能增加ASD风险,特别是在低本底空气污染和农村地区。高强度野火事件与ASD的关系最为密切,这强调了在野火频率和严重程度不断增加的背景下,需要有针对性的政策,如植被管理、土地利用规划和室内过滤升级。
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引用次数: 0
Key role of nitrogen-containing organic species in haze formation and health implications: an ion mobility-analysis based study 含氮有机物种在雾霾形成和健康影响中的关键作用:一项基于离子迁移分析的研究
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-02-07 DOI: 10.1016/j.envint.2026.110136
Mi Tian , Xinquan Zhao , Wei Zhang , Jinyitao Wang , Arthur W.H. Chan , Fumo Yang , Yang Chen , Shunyao Wang
Despite the ubiquitous impacts on ecosystem and human health, the formation mechanisms of nitrogen-containing organic compounds (NOCs) remain poorly understood in the atmosphere. In this study, wintertime PM2.5 samples were collected in Chongqing with molecular-level composition characterized by an ion mobility spectrometry (IMS) − time of flight mass spectrometry to elucidate key formation/evolution factors and health implications of NOCs in ambient particles. Generally, nitrogen-containing organic species (CHNOs) were found to be critical PM2.5 components for haze formation and health impacts during polluted episodes. Evidence from IMS-derived collision cross sections calculation further illustrated organic nitrates/nitrites (ONs) as the main contributors to CHNOs observed in this study. Secondary transformation process was identified as the major formation pathway for CHNOs. Significant levels of NH4+ and NO2 accompanied by high relative humidity (RH) resulted in enhanced production of particulate CHNOs during wintertime haze episodes, which was also remediated by aerosol liquid water content and aerosol acidity. In addition, CHNOs (e.g., C8H13NO8-9, C9H13NO8, and C9H15NO8-9) were found to be associated with acellular and cellular oxidative potential metrics (OPAA, OPGSH, and in vitro ROS). Further in vitro results from human bronchial epithelial (BEAS-2B) cells confirmed that both authentic PM2.5 sampels and atmospherically relevant nitrogen containing species, including organonitrate/nitrite, nitrosamine, nitrophenol, amide, and amines, can significantly induce intracellular ROS and the expression of proinflammatory biomarkers (e.g., IL-8, NQO1, and Nrf2). By illustrating this very initial evidence between molecular-level CHNOs and oxidative stress effects characterized for wintertime PM2.5, our study sheds light on future regional air quality mitigation strategies based on source, composition, and health implications under complex pollution conditions.
尽管含氮有机化合物对生态系统和人类健康的影响无处不在,但对大气中含氮有机化合物(NOCs)的形成机制仍知之甚少。本研究以重庆市冬季PM2.5为研究对象,采用离子迁移谱法(IMS) -飞行时间质谱法对其分子水平组成进行了表征,以阐明环境颗粒物中NOCs的形成/演化关键因素及其对健康的影响。总体而言,含氮有机物种(CHNOs)是污染期霾形成和健康影响的关键PM2.5组分。来自ims碰撞截面计算的证据进一步表明,有机硝酸盐/亚硝酸盐(ONs)是本研究中观察到的CHNOs的主要贡献者。二级转化过程被确定为CHNOs的主要形成途径。高相对湿度(RH)下NH4+和NO2的显著水平导致冬季雾霾期间颗粒CHNOs的产生增加,气溶胶液态水含量和气溶胶酸度也能弥补这一现象。此外,CHNOs(如C8H13NO8-9、C9H13NO8和C9H15NO8-9)被发现与非细胞和细胞氧化电位指标(OPAA、OPGSH和体外ROS)相关。此外,来自人支气管上皮细胞(BEAS-2B)的体外实验结果证实,真实的PM2.5样本和大气中相关的含氮物质,包括有机硝酸盐/亚硝酸盐、亚硝胺、硝基酚、酰胺和胺,都能显著诱导细胞内ROS和促炎生物标志物(如IL-8、NQO1和Nrf2)的表达。通过阐明分子水平的CHNOs与冬季PM2.5特征的氧化应激效应之间的初步证据,我们的研究揭示了在复杂污染条件下基于来源、成分和健康影响的未来区域空气质量缓解策略。
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引用次数: 0
Unveiling the contextual nonstationary effects of the built environment on individual air pollution exposure: a mobile sensor big data driven research design 揭示建筑环境对个体空气污染暴露的上下文非平稳影响:移动传感器大数据驱动的研究设计
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-01-10 DOI: 10.1016/j.envint.2026.110054
Daming Lu , Mei-Po Kwan
While existing studies have extensively examined the relationship between the built environment and air pollution using monitoring station data, few have considered individual-level exposure. This study addresses that gap by adopting a real-time exposure tracking research design that integrates mobile air quality sensing and GPS tracking. Using 1.40 million mobile sensor observations, we developed an interpretable multiple XGBoost machine learning framework with SHapley Additive exPlanations (SHAP) analysis to investigate the nonstationary effects of built environment factors on individual-level air pollution exposure across indoor, outdoor, and in-vehicle contexts. The key findings are as follows. In indoor contexts, transport land use and bus stop density emerge as the most influential factors. In outdoor contexts, bus stop density, building coverage, and population density have the strongest effects. In in-vehicle contexts, population density and building coverage are the primary contributors. Besides, commercial and transport land use exhibit diminishing marginal effects. Open space, intersection density, and bus stop density exhibit threshold effects on individual exposure, with threshold values observed at 15%, 20 to 40 intersections per square kilometer, and 50 bus stops per square kilometer, respectively. Methodologically, this study introduces a transferable framework for analyzing individual-level environmental exposure in relation to the built environment. Practically, it provides a foundation for context-specific planning strategies and offers actionable guidance for prioritizing key planning indicators and selecting appropriate threshold ranges for local environmental planning.
虽然现有的研究利用监测站的数据广泛地研究了建筑环境和空气污染之间的关系,但很少有人考虑到个人水平的暴露。本研究通过采用集成移动空气质量传感和GPS跟踪的实时暴露跟踪研究设计来解决这一差距。利用140万个移动传感器观测数据,我们开发了一个可解释的多XGBoost机器学习框架,并使用SHapley加性解释(SHAP)分析来研究建筑环境因素对室内、室外和车内个人水平空气污染暴露的非平稳影响。主要发现如下。在室内环境中,交通用地和公交站点密度是最重要的影响因素。在室外环境中,公交车站密度、建筑覆盖率和人口密度的影响最大。在车内环境中,人口密度和建筑物覆盖率是主要因素。此外,商业和交通用地的边际效应呈递减趋势。开放空间、十字路口密度和公交车站密度对个体暴露表现出阈值效应,阈值分别为15%、每平方公里20 ~ 40个十字路口和每平方公里50个公交车站。在方法上,本研究引入了一个可转移的框架,用于分析与建筑环境相关的个人层面的环境暴露。实际上,它为因地制宜的规划策略提供了基础,并为确定关键规划指标的优先顺序和选择适当的地方环境规划阈值范围提供了可操作的指导。
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引用次数: 0
The joint impact of temperature, humidity, and air pollution on COVID-19 incidence: a multi-country time-series study in 439 cities 温度、湿度和空气污染对COVID-19发病率的共同影响:在439个城市进行的多国时间序列研究
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-01-24 DOI: 10.1016/j.envint.2026.110090
Keita Wagatsuma , Denise Feurer , Wenhua Yu , Rongbin Xu , Tim Riffe , Maxi Stella Kniffka , Enrique Acosta , Ben Armstrong , Malcolm Mistry , Rachel Lowe , Dominic Royé , Masahiro Hashizume , Aurelio Tobias , Ana Maria Vicedo-Cabrera , Lina Madaniyazi , Chris Fook Sheng Ng , Carmen Íñiguez , Martina S. Ragettli , Eric Lavigne , Patricia Matus Correa , Francesco Sera
Several studies have explored the short-term effects of environmental stressors on coronavirus disease 2019 (COVID-19) transmission and severity. However, evidence on the interactive effects of meteorological conditions and air pollution remains limited and geographically variable. We therefore aimed to quantify the independent and interactive effects of short-term exposure to humidex, a composite index of temperature and relative humidity, and fine particulate matter ≤ 2.5 μm (PM2.5) on daily COVID-19 incidence across multiple cities and in multiple countries. Daily time-series data on confirmed COVID-19 cases, meteorological factors, and PM2.5 concentrations were collected from 439 cities in 22 countries during January 2020–August 2022 as part of the Multi-Country Multi-City Collaborative Research Network. A two-stage design was applied: first, city-specific quasi-Poisson models with distributed lag non-linear models estimated exposure–response associations; second, multilevel random-effects meta-analyses pooled city-specific estimates. Effect modification by PM2.5 was assessed using a product term between non-linear humidex function and linear PM2.5 function. Approximately 95.1 million confirmed COVID-19 cases were analyzed. Lower humidex values (0.1 °C versus 15.1 °C) were associated with increased daily cases (relative risk [RR]: 1.1192, 95% confidence interval [CI]: 1.0214–1.2262). A 10 μg/m3 increase in PM2.5 over the current and preceding 2 days was associated with a modest increase in daily cases (RR: 1.0079, 95% CI: 1.0001–1.0161). No statistically significant interaction between humidex and PM2.5 was observed. Short-term exposure to cold–dry conditions and elevated PM2.5 independently increased COVID-19 incidence, highlighting the need to consider both thermal environment and air quality when designing climate-resilient public health responses. These findings enhance understanding of how climate-related environmental stressors influence COVID-19 transmission.
一些研究探讨了环境压力源对2019冠状病毒病(COVID-19)传播和严重程度的短期影响。然而,关于气象条件和空气污染相互影响的证据仍然有限,而且在地理上存在变数。因此,我们旨在量化短期暴露于humidex(温度和相对湿度的复合指数)和细颗粒物 ≤ 2.5 μm (PM2.5)对多个城市和多个国家的每日COVID-19发病率的独立和交互影响。作为多国家多城市合作研究网络的一部分,在2020年1月至2022年8月期间,从22个国家的439个城市收集了关于COVID-19确诊病例、气象因素和PM2.5浓度的每日时间序列数据。采用两阶段设计:首先,使用具有分布滞后非线性模型的城市准泊松模型估计暴露-反应关联;其次,多层次随机效应荟萃分析汇集了特定城市的估计。采用非线性humidex函数与线性PM2.5函数之间的乘积项评价PM2.5对效果的影响。分析了约9510万例新冠肺炎确诊病例。较低的湿度值(0.1 °C vs 15.1 °C)与每日病例增加相关(相对危险度[RR]: 1.1192, 95%可信区间[CI]: 1.0214-1.2262)。PM2.5在当前和之前2 天增加10 μg/m3与每日病例的适度增加相关(RR: 1.0079, 95% CI: 1.0001-1.0161)。湿度与PM2.5之间无统计学意义的交互作用。短期暴露于干冷条件和PM2.5升高分别增加了COVID-19的发病率,这突出表明,在设计气候适应型公共卫生应对措施时,需要同时考虑热环境和空气质量。这些发现加强了对气候相关环境压力因素如何影响COVID-19传播的理解。
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引用次数: 0
Confronting pesticide exposure predictions from different models to observations from a monitoring study in small freshwater streams in Germany 面对来自不同模型的农药暴露预测和来自德国小型淡水溪流监测研究的观察结果
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-02-01 Epub Date: 2026-01-09 DOI: 10.1016/j.envint.2026.110057
Paula Scharlach , Gustaf Boström , Jörg Klasmeier , Amelie Leonardi , Andreas Focks
Plant protection products are integral to European agriculture but can cause unwanted environmental impacts. Before authorisation, predicted concentrations in environmental compartments are compared with effect thresholds in a regulatory risk assessment. This study evaluates the agreement between predicted and measured concentrations for the established FOCUS surface water models (Steps 1–3) and the recently published PEC-CKB model. Model results were compared with monitoring data from lowland streams in Germany, and particular attention was paid to the models’ conservatism. The conservative character of FOCUS Step 1 can be confirmed, but underestimations were observed for FOCUS Step 2 and 3 models. PEC-CKB results are similar to those of the higher-tier FOCUS models, while having lower model complexity and requiring less input data. Using real application rates and landscape information generally improved model predictions by nearly halving the bias, but led to increased underestimations of measured concentrations. Linking prospective and retrospective environmental risk assessment (ERA) by incorporating real data can make prospective ERA more realistic and identify opportunities for simplification. Finally, we discuss the challenges in evaluating prediction models for pesticide concentrations in surface waters, particularly with regard to the environmental variability of measured concentrations.
植物保护产品是欧洲农业不可或缺的一部分,但可能会造成不必要的环境影响。在批准之前,将环境隔间中的预测浓度与监管风险评估中的影响阈值进行比较。本研究评估了建立的FOCUS地表水模型(步骤1-3)和最近发表的PEC-CKB模型的预测浓度和测量浓度之间的一致性。将模型结果与德国低地河流的监测数据进行了比较,并特别注意了模型的保守性。FOCUS Step 1的保守性可以得到证实,但FOCUS Step 2和3的模型被低估。PEC-CKB结果与高层FOCUS模型相似,但模型复杂度较低,需要的输入数据较少。使用实际应用速率和景观信息通常使模型预测的偏差减少了近一半,但导致测量浓度的低估增加。通过纳入真实数据将前瞻性和回顾性环境风险评估联系起来,可以使前瞻性环境风险评估更加现实,并确定简化的机会。最后,我们讨论了评估地表水中农药浓度预测模型的挑战,特别是关于测量浓度的环境变异性。
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引用次数: 0
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Environment International
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