Pub Date : 2026-01-01DOI: 10.1016/j.enceco.2025.12.032
Ying-Jie Zhang , Ting-Ting Xu , Jing-Feng Yi , Yu-Ling Luan , Eddy Y. Zeng , Ying Guo
Atmospheric particulate matter-driven oxidative stress is a crucial benchmark in evaluating health risk, yet the direct evidence linking environmental oxidability to human internal oxidative damage remains elusive. Here, we systematically quantified oxidative potential (OP) in respirable size-segregated PM10 collected longitudinally from waste recycling plants in Southern China, and monitored oxidative damage to DNA, lipids and proteins in workers using biomarker techniques. By self-developed high-throughput microplate dithiothreitol (DTT) assay, we found that maximum OP values (both mass and volume normalized) were primarily derived from fine particles (0.43–0.65 μm), with 62 %–82 % of oxidability in pulmonary alveoli attributed to <2.1 μm fractions. Each unit increase (1 × 1016 spins/g) of environmentally persistent free radicals (EPFRs) was associated with 1.316 pmol/μg/min rise in OPDTT_m. Critically, we introduced “respirable particle-bound oxidability (RPO)” metric, integrating OP with individualized respiratory rates to capture bioavailable exposure. Mixed-effect modeling revealed a robust association between that RPO and lipid peroxidation, with each 1 % increase correlating with a 2.92 % (95 % CI: 1.66 %, 4.17 %) increase in urinary malondialdehyde (MDA), particularly in pulmonary alveoli. While no significant effect is observed for DNA or protein oxidation. These findings successfully established the quantitative linkage between ambient PM oxidizing capacity and internal oxidative injury, highlighting RPO as an advanced metric for environmental risk assessment and offering new insight into the mechanistic evaluation of air pollution toxicity.
{"title":"Personalized oxidative toxicity exposure assessment: Unveiling feasibility of linking respiratory PM10 oxidative potential to human oxidative damage","authors":"Ying-Jie Zhang , Ting-Ting Xu , Jing-Feng Yi , Yu-Ling Luan , Eddy Y. Zeng , Ying Guo","doi":"10.1016/j.enceco.2025.12.032","DOIUrl":"10.1016/j.enceco.2025.12.032","url":null,"abstract":"<div><div>Atmospheric particulate matter-driven oxidative stress is a crucial benchmark in evaluating health risk, yet the direct evidence linking environmental oxidability to human internal oxidative damage remains elusive. Here, we systematically quantified oxidative potential (OP) in respirable size-segregated PM<sub>10</sub> collected longitudinally from waste recycling plants in Southern China, and monitored oxidative damage to DNA, lipids and proteins in workers using biomarker techniques. By self-developed high-throughput microplate dithiothreitol (DTT) assay, we found that maximum OP values (both mass and volume normalized) were primarily derived from fine particles (0.43–0.65 μm), with 62 %–82 % of oxidability in pulmonary alveoli attributed to <2.1 μm fractions. Each unit increase (1 × 10<sup>16</sup> spins/g) of environmentally persistent free radicals (EPFRs) was associated with 1.316 pmol/μg/min rise in OP<sup>DTT_m</sup>. Critically, we introduced “respirable particle-bound oxidability (RPO)” metric, integrating OP with individualized respiratory rates to capture bioavailable exposure. Mixed-effect modeling revealed a robust association between that RPO and lipid peroxidation, with each 1 % increase correlating with a 2.92 % (95 % CI: 1.66 %, 4.17 %) increase in urinary malondialdehyde (MDA), particularly in pulmonary alveoli. While no significant effect is observed for DNA or protein oxidation. These findings successfully established the quantitative linkage between ambient PM oxidizing capacity and internal oxidative injury, highlighting RPO as an advanced metric for environmental risk assessment and offering new insight into the mechanistic evaluation of air pollution toxicity.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 846-856"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-01DOI: 10.1016/j.enceco.2025.12.019
Shuangqi Li , Yanrong Lv , Zhaoqing Tan , Qing Liu , Chunlan Zhu , Zihao Long , Qing Wang , Liping Chen , Haohan Chen , Hongyun Chen , Xiumei Xing , Qiansheng Hu , Yongmei Xiao
Benzene, toluene, and xylene (BTX) are pervasive in industrial settings. However, how their shared lipophilicity and lipid dysregulation synergistically contribute to genotoxicity at low dose exposures remain unclear, limiting the development of targeted preventive measures. In a longitudinal cohort of 736 petrochemical workers (523 followed for 5 years), with cumulative exposure doses derived from workplace monitoring. Blood lipids [total cholesterol (TC), triglycerides (TG), low−/high-density lipoprotein cholesterol (LDL-C/HDL-C)] and genotoxicity markers [olive tail moment (OTM), Tail DNA%, Tail moment, 8-hydroxy-2′- deoxyguanosine (8-OHdG)] were measured. Generalized linear and log-binomial regression models evaluated baseline and longitudinal associations, while generalized weighted quantile sum (gWQS) regression captured mixture effects. Mediation models assessed lipid-driven genotoxicity. BTX co-exposure was associated with increased TC, LDL-C, and HDL-C at baseline, and elevated risks of hypercholesterolemia (RR = 1.64, 95 % CI: 1.05, 2.58) and high LDL-C (RR = 1.32, 95 % CI: 1.01, 1.71) during follow-up. Workers with baseline hyperlipidemia showed stronger lipid responses and greater DNA damage under exposure (P-interaction < 0.05). Longitudinal analyses showed that benzene and toluene exposure elevated higher follow-up 8-OHdG levels among hypercholesterolemic workers (Pinteraction < 0.05) supporting oxidative damage as a downstream mechanism.Total cholesterol mediated 8.22 % of BTX-related genotoxicity (P < 0.05). Consistently, network toxicology highlighted lipid metabolism as key pathway linking BTX exposure to DNA damage. These findings demonstrate that BTX co-exposure disrupts lipid homeostasis and that toluene and xylene contribute significantly to this dysregulation, which in turn exacerbates benzene-initiated genotoxicity. The study highlights lipid metabolism as a critical mediator and amplifier of BTX mixture toxicity, underscoring the necessity of incorporating metabolic pathways and mixture effects into occupational risk assessments.
{"title":"Lipid dysregulation as a mediator of genotoxicity from benzene, toluene, and xylene co-exposure: Insights from a longitudinal study of petrochemical workers and network toxicology analysis","authors":"Shuangqi Li , Yanrong Lv , Zhaoqing Tan , Qing Liu , Chunlan Zhu , Zihao Long , Qing Wang , Liping Chen , Haohan Chen , Hongyun Chen , Xiumei Xing , Qiansheng Hu , Yongmei Xiao","doi":"10.1016/j.enceco.2025.12.019","DOIUrl":"10.1016/j.enceco.2025.12.019","url":null,"abstract":"<div><div>Benzene, toluene, and xylene (BTX) are pervasive in industrial settings. However, how their shared lipophilicity and lipid dysregulation synergistically contribute to genotoxicity at low dose exposures remain unclear, limiting the development of targeted preventive measures. In a longitudinal cohort of 736 petrochemical workers (523 followed for 5 years), with cumulative exposure doses derived from workplace monitoring. Blood lipids [total cholesterol (TC), triglycerides (TG), low−/high-density lipoprotein cholesterol (LDL-C/HDL-C)] and genotoxicity markers [olive tail moment (OTM), Tail DNA%, Tail moment, 8-hydroxy-2′- deoxyguanosine (8-OHdG)] were measured. Generalized linear and log-binomial regression models evaluated baseline and longitudinal associations, while generalized weighted quantile sum (gWQS) regression captured mixture effects. Mediation models assessed lipid-driven genotoxicity. BTX co-exposure was associated with increased TC, LDL-C, and HDL-C at baseline, and elevated risks of hypercholesterolemia (<em>RR</em> = 1.64, 95 % <em>CI</em>: 1.05, 2.58) and high LDL-C (<em>RR</em> = 1.32, 95 % <em>CI</em>: 1.01, 1.71) during follow-up. Workers with baseline hyperlipidemia showed stronger lipid responses and greater DNA damage under exposure (<em>P</em>-<sub>interaction</sub> < 0.05). Longitudinal analyses showed that benzene and toluene exposure elevated higher follow-up 8-OHdG levels among hypercholesterolemic workers (<em>P</em><sub>interaction</sub> < 0.05) supporting oxidative damage as a downstream mechanism.Total cholesterol mediated 8.22 % of BTX-related genotoxicity (<em>P</em> < 0.05). Consistently, network toxicology highlighted lipid metabolism as key pathway linking BTX exposure to DNA damage. These findings demonstrate that BTX co-exposure disrupts lipid homeostasis and that toluene and xylene contribute significantly to this dysregulation, which in turn exacerbates benzene-initiated genotoxicity. The study highlights lipid metabolism as a critical mediator and amplifier of BTX mixture toxicity, underscoring the necessity of incorporating metabolic pathways and mixture effects into occupational risk assessments.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 708-719"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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