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.
{"title":"Occurrence and toxicity of haloketones: emerging class of disinfection byproducts in drinking water of Nanning City, Southwest China","authors":"Yuwen Huang , Zan Sheng , Qiuyan Wei , Mingliang Wu , Jingyi Xiao , Qing Zhong , Zhanmou Liu , Mengting Yang , Xiao Wei","doi":"10.1016/j.envint.2026.110097","DOIUrl":"10.1016/j.envint.2026.110097","url":null,"abstract":"<div><div>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 (<em>F</em><sub>10,208</sub> = 4672.689, <em>P</em> < 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 (<em>F</em><sub>10,66</sub> = 7028.528, <em>P</em> < 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 (<em>F</em><sub>10,154</sub> = 473.640, <em>P</em> < 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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110097"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014685","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}
Pub Date : 2026-02-01Epub Date: 2026-01-21DOI: 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.
{"title":"The role of coronary artery calcification in metal-related cardiovascular disease","authors":"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","doi":"10.1016/j.envint.2026.110095","DOIUrl":"10.1016/j.envint.2026.110095","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110095"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022150","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}
Pub Date : 2026-02-01Epub Date: 2026-01-14DOI: 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.
{"title":"Long-term pet ownership promotes resistome similarity between cats and their owners","authors":"Zhenlong Wang , Ji Lu , Xiumin Wang , Wei An , Ya Zhao , Bing Han , Hui Tao , Jie Liu , Jianhua Guo , Jinquan Wang","doi":"10.1016/j.envint.2026.110074","DOIUrl":"10.1016/j.envint.2026.110074","url":null,"abstract":"<div><div>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 <em>Escherichia coli</em> and <em>Klebsiella pneumoniae</em> 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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110074"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145993406","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}
Pub Date : 2026-02-01Epub Date: 2026-01-24DOI: 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.
{"title":"Co-exposure to PFOA, PFBA and nanoplastics synergistically exacerbates neurotoxicity by impairing PINK1/Parkin-mediated mitophagy","authors":"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","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}
Pub Date : 2026-02-01Epub Date: 2026-02-04DOI: 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。
{"title":"Development of a physiologically based pharmacokinetic (PBPK) model for cobalt in the Chinese population based on population exposure data","authors":"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","doi":"10.1016/j.envint.2026.110132","DOIUrl":"10.1016/j.envint.2026.110132","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110132"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146115995","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}
Pub Date : 2026-02-01Epub Date: 2026-02-06DOI: 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.
{"title":"Prenatal exposure to wildfire-related PM2.5 and autism spectrum disorder in children born in California between 2001–2019","authors":"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","doi":"10.1016/j.envint.2026.110131","DOIUrl":"10.1016/j.envint.2026.110131","url":null,"abstract":"<div><h3>Background</h3><div>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 PM<sub>2.5</sub> exposures and ASD risk in California births, considering exposure timing, intensity, and background air pollution.</div></div><div><h3>Methods</h3><div>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 PM<sub>2.5</sub> 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 PM<sub>2.5</sub>, urbanicity, diagnostic era, and sex.</div></div><div><h3>Results</h3><div>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/m<sup>3</sup>). Associations were most pronounced among children in the lowest quartile of prenatal background PM<sub>2.5</sub>, with odds of ASD increasing by 50% for those in the > 90th percentile of wildfire PM<sub>2.5</sub> during pregnancy. WUI-related PM<sub>2.5</sub> was associated with ASD in metro areas, suggesting unique toxicity. Effects were stronger in non-metro regions, with the exception of WUI-related PM<sub>2.5</sub>, 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 PM<sub>2.5</sub> and high exposure episodes for males.</div></div><div><h3>Conclusion</h3><div>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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110131"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146121996","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}
Pub Date : 2026-02-01Epub Date: 2026-02-07DOI: 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.
{"title":"Key role of nitrogen-containing organic species in haze formation and health implications: an ion mobility-analysis based study","authors":"Mi Tian , Xinquan Zhao , Wei Zhang , Jinyitao Wang , Arthur W.H. Chan , Fumo Yang , Yang Chen , Shunyao Wang","doi":"10.1016/j.envint.2026.110136","DOIUrl":"10.1016/j.envint.2026.110136","url":null,"abstract":"<div><div>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 PM<sub>2.5</sub> 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 PM<sub>2.5</sub> 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 NH<sub>4</sub><sup>+</sup> and NO<sub>2</sub> 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., C<sub>8</sub>H<sub>13</sub>NO<sub>8-9</sub>, C<sub>9</sub>H<sub>13</sub>NO<sub>8</sub>, and C<sub>9</sub>H<sub>15</sub>NO<sub>8-9</sub>) were found to be associated with acellular and cellular oxidative potential metrics (OP<sup>AA</sup>, OP<sup>GSH</sup>, and <em>in vitro</em> ROS). Further <em>in vitro</em> results from human bronchial epithelial (BEAS-2B) cells confirmed that both authentic PM<sub>2.5</sub> 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 PM<sub>2.5</sub>, our study sheds light on future regional air quality mitigation strategies based on source, composition, and health implications under complex pollution conditions.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110136"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146135235","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}
Pub Date : 2026-02-01Epub Date: 2026-01-10DOI: 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.
{"title":"Unveiling the contextual nonstationary effects of the built environment on individual air pollution exposure: a mobile sensor big data driven research design","authors":"Daming Lu , Mei-Po Kwan","doi":"10.1016/j.envint.2026.110054","DOIUrl":"10.1016/j.envint.2026.110054","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110054"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145947740","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}
Pub Date : 2026-02-01Epub Date: 2026-01-24DOI: 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。
{"title":"The joint impact of temperature, humidity, and air pollution on COVID-19 incidence: a multi-country time-series study in 439 cities","authors":"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","doi":"10.1016/j.envint.2026.110090","DOIUrl":"10.1016/j.envint.2026.110090","url":null,"abstract":"<div><div>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 (PM<sub>2.5</sub>) on daily COVID-19 incidence across multiple cities and in multiple countries. Daily time-series data on confirmed COVID-19 cases, meteorological factors, and PM<sub>2.5</sub> 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 <em>meta</em>-analyses pooled city-specific estimates. Effect modification by PM<sub>2.5</sub> was assessed using a product term between non-linear humidex function and linear PM<sub>2.5</sub> 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/m<sup>3</sup> <!-->increase in PM<sub>2.5</sub> 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 PM<sub>2.5</sub> was observed. Short-term exposure to cold–dry conditions and elevated PM<sub>2.5</sub> 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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110090"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146034181","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}
Pub Date : 2026-02-01Epub Date: 2026-01-09DOI: 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.
{"title":"Confronting pesticide exposure predictions from different models to observations from a monitoring study in small freshwater streams in Germany","authors":"Paula Scharlach , Gustaf Boström , Jörg Klasmeier , Amelie Leonardi , Andreas Focks","doi":"10.1016/j.envint.2026.110057","DOIUrl":"10.1016/j.envint.2026.110057","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":308,"journal":{"name":"Environment International","volume":"208 ","pages":"Article 110057"},"PeriodicalIF":9.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976158","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}