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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 脂质失调作为苯、甲苯和二甲苯共暴露遗传毒性的中介:来自石化工人和网络毒理学分析的纵向研究的见解
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 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.
苯、甲苯和二甲苯(BTX)在工业环境中普遍存在。然而,它们共同的亲脂性和脂质失调如何在低剂量暴露下协同促进遗传毒性仍不清楚,这限制了有针对性预防措施的发展。在736名石化工人的纵向队列中(523人随访5年),累积暴露剂量来自工作场所监测。测定血脂[总胆固醇(TC)、甘油三酯(TG)、低/高密度脂蛋白胆固醇(LDL-C/HDL-C)]和遗传毒性标志物[橄榄尾力矩(OTM)、尾DNA%、尾力矩、8-羟基-2′-脱氧鸟苷(8-OHdG)]。广义线性和对数二项回归模型评估基线和纵向关联,而广义加权分位数和(gWQS)回归捕获混合效应。中介模型评估了脂质驱动的遗传毒性。BTX共暴露与基线时TC、LDL-C和HDL-C升高以及随访期间高胆固醇血症(RR = 1.64, 95% CI: 1.05, 2.58)和高LDL-C (RR = 1.32, 95% CI: 1.01, 1.71)的风险升高相关。基线高脂血症的工人在暴露下表现出更强的脂质反应和更大的DNA损伤(p -相互作用<; 0.05)。纵向分析显示,苯和甲苯暴露会使高胆固醇血症工人的8-OHdG水平升高(p相互作用<; 0.05),支持氧化损伤是一种下游机制。总胆固醇介导8.22%的btx相关遗传毒性(P < 0.05)。网络毒理学一致强调脂质代谢是连接BTX暴露与DNA损伤的关键途径。这些发现表明,BTX共同暴露会破坏脂质稳态,而甲苯和二甲苯对这种失调起着重要作用,从而加剧了苯引发的遗传毒性。该研究强调了脂质代谢是BTX混合物毒性的关键中介和放大器,强调了将代谢途径和混合物效应纳入职业风险评估的必要性。
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引用次数: 0
Impacts of urban runoff pollutants on biofilm communities 城市径流污染物对生物膜群落的影响
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2025.12.018
Neus Besolí-Mestres , Anna Freixa , Lorena Cojoc , M. Isabel Cadena-Aizaga , Mira Petrovic , Sergi Sabater

Background

Urban runoff transports a wide array of inorganic and organic materials, such as organic matter, salt, dust, plastics and a high diversity of pollutants, which may harm freshwater ecosystems, especially during the initial runoff inputs. The aim of this study is to assess the structural and functional impacts on freshwater biofilms subjected to urban runoff pollutants.

Methods

We provide a first assessment exposing natural freshwater biofilms to progressive dilution of pure first-flush urban runoff under controlled laboratory conditions. In parallel, we examined the effects of selected pollutants found in urban runoff on biofilms, testing them individually and in combination.

Findings

Urban runoff contained 47 compounds from 9 different families. The most abundant were 1,3-diphenylguanidine (a tire-related additive), caffeine (a stimulant), and zinc (a metal), each reaching concentrations close to 30 μg L- 1. Dissolved organic carbon was also high (25 mg L−1). Impacts of urban runoff on biofilms were strongest at 25 % dilution, and overall impacts were moderate, reflecting a balance inhibitory influence of pollutants and stimulatory effects of dissolved organic carbon and nutrients. The selected pollutants experiment revealed that biofilms were most sensitive to the mixture of pollutants and to diuron, followed by the 16PAHs and BBP.

Conclusions

Overall, our results highlight the complex and non-linear responses of stream biofilms to urban runoff inputs, emphasizing the need to control the types and quantities of pollutants released, with particular attention to emerging contaminants.
城市径流输送了大量的无机和有机物质,如有机质、盐、粉尘、塑料和多种污染物,这些物质可能会损害淡水生态系统,特别是在最初的径流输入期间。本研究的目的是评估城市径流污染物对淡水生物膜结构和功能的影响。方法我们提供了第一个评估,在受控的实验室条件下,将天然淡水生物膜暴露于纯首次冲洗的城市径流的逐步稀释中。同时,我们研究了城市径流中选定的污染物对生物膜的影响,分别对它们进行了测试和组合测试。发现城市径流含有来自9个不同科的47种化合物。其中含量最高的是1,3-二苯基胍(一种与轮胎有关的添加剂)、咖啡因(一种兴奋剂)和锌(一种金属),它们的浓度都接近30 μg L- 1。溶解有机碳也很高(25 mg L−1)。在稀释度为25%时,城市径流对生物膜的影响最大,总体影响中等,反映了污染物的抑制作用与溶解有机碳和营养物质的刺激作用的平衡。选择污染物实验表明,生物膜对污染物混合物最敏感,对diuron最敏感,其次是16PAHs和BBP。总体而言,我们的研究结果强调了河流生物膜对城市径流输入的复杂和非线性响应,强调需要控制污染物释放的类型和数量,特别是对新出现的污染物。
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引用次数: 0
Complex co-contaminant responses of Chlorella sp. and its phycosphere microbiota under co-exposure to PET microfibers and oxytetracycline PET微纤维和土霉素对小球藻及其藻球微生物群的复合共污染响应
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2025.12.025
Jiaye Deng , Wenyan Lu , Jiamei Wang , Shuyuan Zhong , Xinrui Xu , Liufu Wang , Hui Yang , Yingying Zhang
Microplastics (MPs) and antibiotics co-occur in aquatic environments, yet their joint ecological effects remain poorly understood. We examined polyethylene terephthalate microplastic fibers (PET-MFs) and oxytetracycline (OTC, 2 mg/L), alone and in combination, on Chlorella sp. and its phycosphere microbiome over 28 days. Microscopy revealed extensive algal adhesion to fibers and aggregated clusters. PET-MFs dose-dependently inhibited algal growth by lowering photosynthetic efficiency, disrupting pigment synthesis, and inducing oxidative stress, and shifted the phycosphere microbiome by reducing Rhodobacter and Brevundimonas and enriching Paucibacter. Transcriptomics showed a strong dose response: LMF (5000 particles/L MFs) induced 216 DEGs, versus 2920 DEGs in HMF (50,000 particles/L MFs); OTC alone caused 2443 DEGs and suppressed glycolysis/pyruvate metabolism and photosynthesis related gene expression despite limited biomass effects. Co-exposure amplified disturbance to 7126 DEGs in LMO (LMF and OTC) and 12,880 DEGs in HMO (HMF and OTC), exceeding either single treatment. Although total bacterial abundance changed little, ARGs/MGEs increased, with intI2 elevated in all MF-containing groups and tet genes promoted by OTC. Correlation analyses support an algae–microbiome–resistome linkage: algal traits (OD680, Chl-a, Fv/fm) tracked shifts in dominant genera, which co-varied with int and tet modules, while soluble protein/EPS aligned with higher int/tet signals. Together, these results indicate complex, non-linear PET-MF–OTC interactions, with algal physiology likely mediating microbiome structure and ARG dynamics. This study advances mechanistic understanding of pollutant–microalgae–microbiome crosstalk and highlights ecological risks from co-occurring MPs and antibiotics.
微塑料(MPs)和抗生素在水生环境中共同存在,但它们的联合生态效应仍然知之甚少。我们检测了聚对苯二甲酸乙二醇酯微塑料纤维(PET-MFs)和土霉素(OTC, 2mg /L)单独或联合使用对小球藻及其藻球微生物群28天的影响。显微镜检查显示广泛的藻类附着在纤维和聚集的簇上。PET-MFs通过降低光合效率、破坏色素合成和诱导氧化应激来剂量依赖地抑制藻类生长,并通过减少红杆菌和短单胞菌和丰富贫杆菌来改变藻圈微生物组。转录组学显示出强烈的剂量反应:LMF(5000颗粒/L MFs)诱导216个deg,而HMF(50,000颗粒/L MFs)诱导2920个deg;OTC单独产生2443个deg,抑制糖酵解/丙酮酸代谢和光合作用相关基因表达,尽管生物量影响有限。共暴露将干扰放大到LMO (LMF和OTC)的7126 deg, HMO (HMF和OTC)的12,880 deg,超过任何单一处理。虽然细菌总丰度变化不大,但ARGs/MGEs增加,所有含mf组的intI2升高,OTC促进了tet基因。相关分析支持藻类-微生物组-抵抗组的联系:藻类性状(OD680, Chl-a, Fv/fm)跟踪优势属的变化,这些变化与int和tet模块共同变化,而可溶性蛋白/EPS与较高的int/tet信号一致。总之,这些结果表明复杂的,非线性PET-MF-OTC相互作用,藻类生理可能介导微生物组结构和ARG动力学。这项研究促进了对污染物-微藻-微生物群串扰的机制理解,并强调了MPs和抗生素共同发生的生态风险。
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引用次数: 0
An integrated approach unveils novel mechanisms of nicotine-induced neurotoxicity in zebrafish larvae 一种综合的方法揭示了尼古丁诱导斑马鱼幼虫神经毒性的新机制
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2025.12.014
Yu Kou , Changsheng Guo , Yan Zhang, Yanghui Deng, Xingxing Yin, Jian Xu
Nicotine is a ubiquitous environmental pollutant which may exert neurotoxicity to aquatic organisms. However, the mechanisms at environmentally relevant concentrations remain inadequately understood. This study employed an integrated approach combining in silico predictions, in vivo zebrafish assays, transcriptomics and targeted metabolomics to decipher the mechanistic framework of nicotine-driven developmental neurotoxicity to zebrafish. Network toxicology and molecular docking identified six core targets (CXCR4, CHRNB1, CHRNA1, CHRNA3, STAT3, HIF1A) and predicted key pathways, including neuroactive ligand-receptor interaction and calcium signaling. Experimental validation in zebrafish larvae revealed that nicotine exposure, even at low environmental levels (0.03–3 μg/L), significantly induced developmental delays, heart rate imbalances, and neurobehavioral deficits. Targeted metabolomics demonstrated that nicotine caused a pronounced neurotransmitter imbalance, characterized by a sharp increase in acetylcholine and disrupted levels of dopamine, norepinephrine, and serotonin. Transcriptomics further confirmed the dysregulation of key pathways, including calcium signaling, MAPK inflammation cascade, and neuroactive ligand-receptor interaction. An integrated multi-omics analysis delineated a cohesive adverse outcome pathway: nicotine initially disrupts neuroactive ligand-receptor interactions, leading to intracellular calcium overload, which subsequently triggers MAPK-mediated inflammatory apoptosis and FoxO/p53-related oxidative stress, ultimately resulting in neuronal damage and behavioral dysfunction. Our findings provide novel and comprehensive insights into the mechanistic basis of nicotine-induced neurotoxicity, highlighting significant ecological risks at environmental concentrations and offering a robust framework for assessing the neurotoxic potential of environmental contaminants.
尼古丁是一种普遍存在的环境污染物,对水生生物具有神经毒性。然而,在与环境有关的浓度下的机制仍然没有得到充分了解。本研究采用集成的方法,结合计算机预测、斑马鱼体内实验、转录组学和靶向代谢组学,来破译尼古丁驱动斑马鱼发育神经毒性的机制框架。网络毒理学和分子对接确定了6个核心靶点(CXCR4、CHRNB1、CHRNA1、CHRNA3、STAT3、HIF1A),并预测了关键通路,包括神经活性配体-受体相互作用和钙信号转导。斑马鱼幼鱼的实验验证表明,即使在低环境水平(0.03-3 μg/L)下,尼古丁暴露也会显著诱导发育迟缓、心率失衡和神经行为缺陷。目标代谢组学表明,尼古丁引起明显的神经递质失衡,其特征是乙酰胆碱急剧增加,多巴胺、去甲肾上腺素和血清素水平被破坏。转录组学进一步证实了关键通路的失调,包括钙信号、MAPK炎症级联和神经活性配体-受体相互作用。一项综合多组学分析描绘了一个紧密相关的不良后果途径:尼古丁最初破坏神经活性配体与受体的相互作用,导致细胞内钙超载,随后触发mapk介导的炎症细胞凋亡和FoxO/p53相关的氧化应激,最终导致神经元损伤和行为功能障碍。我们的研究结果为尼古丁诱导神经毒性的机制基础提供了新颖而全面的见解,突出了环境浓度下的重大生态风险,并为评估环境污染物的神经毒性潜力提供了一个强有力的框架。
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引用次数: 0
Male-biased sensitivity to wastewater effluent exposure in Harpagifer antarcticus from Fildes Bay, King George Island 乔治国王岛菲尔德斯湾南极Harpagifer对废水暴露的男性偏敏感性
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2025.12.023
Karen Fabres , Elvira Vergara , Ivan Sola , María José Díaz , Fabio Blanco-Murillo , Fernando Valenzuela , Diana M. Cárdenas , Mark R. Servos , Mario Sanhueza , Gustavo Chiang , Paulina Bahamonde
Antarctica has experienced a growing human presence in recent decades, with year-round scientific and military stations concentrated along the coast. Wastewater effluents from these settlements represent a growing concern, as they contain pharmaceuticals and personal care products (PPCPs) capable of disrupt endocrine functions in aquatic organisms at environmentally relevant concentrations. This study evaluated the impact of wastewater exposure on the gonadal transcriptome of the Antarctic fish Harpagifer antarcticus, collected nearby human settlements and research stations in Fildes Bay, King George Island. Chemical analysis revealed bioaccumulation of diclofenac, carbamazepine, and fluoxetine in fish muscle. Morphological endpoints indicate significant decreases in male gonadosomatic index (GSI) at impacted sites. Molecular analysis suggested disruption of genes related to reproduction. Females displayed significant overexpression of zp at impacted sites, while males from contaminated areas showed increased expression of both zp and esr1.Transcriptomic analysis revealed a male-biased response, with enriched GO terms associated to sperm motility, nervous system function, and immune and inflammatory regulation, as well as chemical homeostasis and lipid metabolism. Females were less impacted, exhibiting transcriptomic alterations mainly linked to metabolic homeostasis. Together, these findings suggest that male H. antarcticus are particularly sensitive to wastewater-derived contaminants, with transcriptional shifts serving as early warning signals of impaired reproduction, physiology, and population resilience. This study highlights the vulnerability of Antarctic coastal ecosystems to anthropogenic pressures and underscores the urgent need for improved wastewater management in this fragile environment.
近几十年来,人类在南极洲的活动越来越多,全年的科学和军事站都集中在沿海地区。这些定居点的废水日益引起人们的关注,因为它们含有能够以环境相关浓度破坏水生生物内分泌功能的药品和个人护理产品(PPCPs)。本研究评估了污水暴露对南极Harpagifer antarcticus鱼性腺转录组的影响,该鱼收集于乔治国王岛菲尔德斯湾附近的人类住区和研究站。化学分析显示双氯芬酸、卡马西平和氟西汀在鱼类肌肉中的生物蓄积。形态学终点显示受影响部位的男性性腺指数(GSI)显著降低。分子分析表明与繁殖有关的基因被破坏。雌性在受影响部位表现出明显的zp过表达,而来自污染区域的雄性则表现出zp和esr1的高表达。转录组学分析揭示了一种男性偏向的反应,与精子活力、神经系统功能、免疫和炎症调节、化学稳态和脂质代谢相关的氧化石墨烯富集。雌性受影响较小,表现出主要与代谢稳态相关的转录组改变。在一起,这些发现表明,男性h . antarcticus strain wastewater-derived污染物尤为敏感,与转录变化作为预警信号受损生殖,生理学以及人口弹性。这项研究强调了南极沿海生态系统对人为压力的脆弱性,并强调了在这一脆弱环境中改善废水管理的迫切需要。
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引用次数: 0
Periphytic biofilm at saline soil-water interface captured more cadmium than at non-saline ones: process, mechanism, and implication 含盐土壤-水界面的周围植物生物膜比非含盐土壤捕获更多的镉:过程、机制和启示
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2026.01.015
Lingyuan Chen , Wanying Li , Shuai Pan , Yanyun Han , Dongmei Zhou , Yinlong Zhang , Junzhuo Liu , Yonghong Wu , Jiangang Han , Imran Ali , Haiying Lu
Soil salinity inhibits rice growth and enhances cadmium (Cd) mobility, threatening rice production and human health. Periphytic biofilm (PB), widely distributed at the soil-water interface of paddy filed, exhibits strong Cd capture capability. However, PB at saline soil-water interface (SPB) and its capability for Cd capture remain unclear. Herein, SPB from coastal mudflat-reclaimed paddy filed was sampled to evaluate its Cd captured process and mechanism by advanced technologies. Results showed that the process of Cd capture by SPB was a spontaneous physical adsorption process driven mainly by extracellular polymeric substances (EPS), which contributed over 90%. Among different EPS layer of SPB, the soluble EPS (S-EPS) accounting more than 50% for Cd adsorption. The maximum Cd adsorption capability of SPB was 619.7 mg/kg, which was 69% higher than PB grown on non-saline soil (NPB). The enhanced Cd adsorption capability of SPB was mainly attributed to the higher amount of EPS, which contained more CHON and CHONS compounds. Furthermore, non-invasive micro-test technique (NMT) analysis indicated ion exchange process occurring in SPB was 3 times higher than that in NPB. Finally, microbial metagenomic sequencing analysis showed that SPB possessed higher abundances of metal-tolerant taxa (e.g., Coleofasciculus chthonoplastes) and enhanced expression of Cd-related (e.g., cmtR) and EPS-related genes (e.g., lptG, mleP). These findings expand the understanding of Cd biogeochemistry in saline wetland with PB, but highlight the potential of SPB for Cd pollution remediation in paddy fields.
土壤盐碱化抑制水稻生长,提高镉(Cd)的流动性,威胁水稻生产和人类健康。周围植物生物膜(PB)广泛分布于稻田土壤-水界面,具有较强的镉捕获能力。然而,盐碱地-水界面(SPB)上的铅及其对镉的捕获能力尚不清楚。本文以滨海滩涂水田SPB为研究对象,对其采用先进技术捕获Cd的过程和机理进行了评价。结果表明,SPB吸附Cd的过程是一个自发的物理吸附过程,主要由胞外聚合物(EPS)驱动,贡献超过90%。在SPB的不同EPS层中,可溶性EPS (S-EPS)对Cd的吸附作用大于50%。SPB对Cd的最大吸附能力为619.7 mg/kg,比在非盐碱地(NPB)上生长的PB高69%。SPB对Cd的吸附能力增强主要是由于EPS含量较高,EPS中含有较多的CHON和CHONS化合物。此外,非侵入性微测试技术(NMT)分析表明,SPB发生的离子交换过程比NPB高3倍。最后,微生物宏基因组测序分析表明,SPB具有较高的耐金属类群(如Coleofasciculus chthonoplastes)丰度,cd相关基因(如cmtR)和eps相关基因(如lptG、mleP)表达增强。这些发现扩大了对含铅盐渍湿地Cd生物地球化学的认识,同时也突出了SPB在稻田Cd污染修复中的潜力。
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引用次数: 0
Long-term carbon disulfide exposure impairs pulmonary function in urban adults: Prevention insights from genetic susceptibility and lifestyle improvement in a repeated-measured cohort 长期二硫化碳暴露损害城市成年人肺功能:重复测量队列中遗传易感性和生活方式改善的预防见解
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2026.01.020
Jiahao Song , Yongfang Zhang , Shuhui Wan , Xiaojie You , Wei Liu , Linling Yu , Yueru Yang , Ruyi Liang , Le Hong , Zhiying Huo , Qing Liu , Bin Wang , Weihong Chen

Background

Efforts on interactions of carbon disulfide (CS2) exposure, genetic susceptibility, and lifestyle on pulmonary function that are critical to prevention are lacking.

Methods

Urinary CS2 metabolite (2-thiothiazolidine-4-carboxylic acid, TTCA) and pulmonary function parameters for 4409 observations from 2025 individuals were measured at baseline and two follow-ups in the Wuhan-Zhuhai cohort. The polygenic risk score (PRS) was derived from 1020 pulmonary function-associated genetic variants, and the healthy lifestyle score (HLS) was comprehensively constructed using life habits including smoking, drinking, physical exercise, and diet status. Linear mixed-effects models with interaction plots were employed to estimate the independent and interaction effects of TTCA, PRS, and HLS on pulmonary function.

Findings

Elevated urinary TTCA, elevated PRS, and decreased HLS were significantly associated with reduced ratio of forced expiratory volume in the first second to forced vital capacity (FEV1/FVC) and peak expiratory flow (PEF) (all P < 0.05). Notably, the estimated adverse effect of urinary TTCA on PEF interactively became more pronounced with increasing PRS or/and decreasing HLS (P interaction < 0.05). Particularly, the most substantial effects of urinary TTCA on PEF were observed in participants with high PRS and low HLS in both cross-sectional and longitudinal analyses, with the estimated effects of −90.56 mL/s (95% confidence interval: −146.66, −34.71) for continuous TTCA cross-sectionally and −406.31 mL/s (−746.61, −64.63) for persistently high TTCA longitudinally.

Conclusion

Our findings highlight that reducing CS2 exposure and improving lifestyle, particularly in individuals with higher genetic susceptibility to pulmonary function decline, may help in the early prevention of pulmonary injury from CS2 exposure.
背景二硫化碳(CS2)暴露、遗传易感性和生活方式对肺功能的相互作用对预防至关重要,但缺乏相关研究。方法对武汉-珠海队列中2025例患者的4409例血清CS2代谢物(2-硫代噻唑烷-4-羧酸,TTCA)和肺功能参数进行基线和两次随访。多基因风险评分(PRS)来源于1020个肺功能相关的遗传变异,健康生活方式评分(HLS)由吸烟、饮酒、体育锻炼和饮食状况等生活习惯综合构建。采用带交互作用图的线性混合效应模型来估计TTCA、PRS和HLS对肺功能的独立和交互作用。结果尿TTCA升高、PRS升高、HLS降低与第一秒用力呼气量与用力肺活量之比(FEV1/FVC)及呼气峰流量(PEF)降低显著相关(P < 0.05)。值得注意的是,随着PRS的增加或/和HLS的降低,尿TTCA对PEF的相互作用的不良影响变得更加明显(P相互作用<; 0.05)。特别是,在横断面和纵向分析中,尿TTCA对PEF的影响最显著的是高PRS和低HLS的参与者,连续TTCA横断面的估计影响为- 90.56 mL/s(95%置信区间:- 146.66,- 34.71),而持续高TTCA纵向的估计影响为- 406.31 mL/s(- 746.61, - 64.63)。结论减少CS2暴露和改善生活方式,特别是对肺功能下降遗传易感性较高的个体,可能有助于早期预防CS2暴露引起的肺损伤。
{"title":"Long-term carbon disulfide exposure impairs pulmonary function in urban adults: Prevention insights from genetic susceptibility and lifestyle improvement in a repeated-measured cohort","authors":"Jiahao Song ,&nbsp;Yongfang Zhang ,&nbsp;Shuhui Wan ,&nbsp;Xiaojie You ,&nbsp;Wei Liu ,&nbsp;Linling Yu ,&nbsp;Yueru Yang ,&nbsp;Ruyi Liang ,&nbsp;Le Hong ,&nbsp;Zhiying Huo ,&nbsp;Qing Liu ,&nbsp;Bin Wang ,&nbsp;Weihong Chen","doi":"10.1016/j.enceco.2026.01.020","DOIUrl":"10.1016/j.enceco.2026.01.020","url":null,"abstract":"<div><h3>Background</h3><div>Efforts on interactions of carbon disulfide (CS<sub>2</sub>) exposure, genetic susceptibility, and lifestyle on pulmonary function that are critical to prevention are lacking.</div></div><div><h3>Methods</h3><div>Urinary CS<sub>2</sub> metabolite (2-thiothiazolidine-4-carboxylic acid, TTCA) and pulmonary function parameters for 4409 observations from 2025 individuals were measured at baseline and two follow-ups in the Wuhan-Zhuhai cohort. The polygenic risk score (PRS) was derived from 1020 pulmonary function-associated genetic variants, and the healthy lifestyle score (HLS) was comprehensively constructed using life habits including smoking, drinking, physical exercise, and diet status. Linear mixed-effects models with interaction plots were employed to estimate the independent and interaction effects of TTCA, PRS, and HLS on pulmonary function.</div></div><div><h3>Findings</h3><div>Elevated urinary TTCA, elevated PRS, and decreased HLS were significantly associated with reduced ratio of forced expiratory volume in the first second to forced vital capacity (FEV<sub>1</sub>/FVC) and peak expiratory flow (PEF) (all <em>P</em> &lt; 0.05). Notably, the estimated adverse effect of urinary TTCA on PEF interactively became more pronounced with increasing PRS or/and decreasing HLS (<em>P</em> <sub>interaction</sub> &lt; 0.05). Particularly, the most substantial effects of urinary TTCA on PEF were observed in participants with high PRS and low HLS in both cross-sectional and longitudinal analyses, with the estimated effects of −90.56 mL/s (95% confidence interval: −146.66, −34.71) for continuous TTCA cross-sectionally and −406.31 mL/s (−746.61, −64.63) for persistently high TTCA longitudinally.</div></div><div><h3>Conclusion</h3><div>Our findings highlight that reducing CS<sub>2</sub> exposure and improving lifestyle, particularly in individuals with higher genetic susceptibility to pulmonary function decline, may help in the early prevention of pulmonary injury from CS<sub>2</sub> exposure.</div></div>","PeriodicalId":100480,"journal":{"name":"Environmental Chemistry and Ecotoxicology","volume":"8 ","pages":"Pages 1091-1101"},"PeriodicalIF":8.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077235","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}
引用次数: 0
PFAS bioaccumulation in food crops: Structure-informed machine learning and mechanistic evidence for priority control PFAS在粮食作物中的生物积累:结构信息机器学习和优先控制的机制证据
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2025.12.029
Yuhan Cui , Wenyu Xiao , Yisu Fang , Beicheng Li , Maosheng Zheng , Yu Li
Per- and polyfluoroalkyl substances (PFASs), as globally emerging persistent organic pollutants, pose severe threats to agroecosystems due to their ubiquity and bioaccumulation potential. In this study, 108 environmentally detected PFASs were systematically evaluated using molecular docking to characterize their accumulation in wheat, tomato, and strawberry root-stem tissues. A hierarchical evaluation framework was established to generate prioritized control lists, identifying 15, 16, and 8 high-risk PFASs in wheat, tomato, and strawberry, respectively, with 16 compounds consistently detected across crops. Source apportionment revealed food packaging, wastewater, landfill leachate, personal care products, and paints as key entry pathways into agricultural environments. Building on this foundation, a machine learning prediction model was constructed to extend the evaluation to 6203 PFASs. The results highlighted that emerging structural features, including cyclic, heterocyclic, quaternary ammonium, and amphoteric groups, substantially enhance crop bioaccumulation effects. Furthermore, for the first time, crop-specific adverse outcome pathway (AOP) frameworks were established, providing mechanistic insights into PFAS bioaccumulation in crops. Protein-ligand docking further demonstrated that highly bioaccumulative PFASs engage in stronger hydrogen bonding, hydrophobic, and electrostatic interactions with key receptors, thereby validating structure-activity relationships underlying their enhanced accumulation. This study provides robust mechanistic evidence and predictive insight into the environmental fate and bioaccumulation behavior of PFASs in agroecosystems, offering a scientific basis for exposure assessment and ecological risk management.
全氟烷基和多氟烷基物质作为全球新出现的持久性有机污染物,由于其普遍存在和生物积累潜力,对农业生态系统构成严重威胁。本研究利用分子对接技术对108种环境检测到的全氟磺酸进行了系统评价,以表征它们在小麦、番茄和草莓根茎组织中的积累特征。建立了分级评价框架,生成了优先控制列表,分别确定了小麦、番茄和草莓中的15、16和8种高风险PFASs,其中16种化合物在作物中一致检测到。来源分析显示,食品包装、废水、垃圾填埋场渗滤液、个人护理产品和油漆是进入农业环境的主要途径。在此基础上,构建了机器学习预测模型,将评估扩展到6203个PFASs。结果表明,新出现的结构特征,包括环、杂环、季铵和两性基团,大大增强了作物的生物积累效应。此外,首次建立了作物特异性不良后果途径(AOP)框架,为PFAS在作物中的生物积累提供了机制见解。蛋白质-配体对接进一步表明,高生物蓄积性PFASs与关键受体进行更强的氢键、疏水和静电相互作用,从而验证了其增强蓄积性背后的结构-活性关系。本研究为全氟辛烷在农业生态系统中的环境命运和生物积累行为提供了强有力的机制证据和预测性见解,为全氟辛烷的暴露评估和生态风险管理提供了科学依据。
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引用次数: 0
Insight into catalytic performance of chlorobenzene over phosphate-modified MnCeOx catalysts and suppression mechanism of polychlorinated byproducts 氯苯在磷酸盐改性MnCeOx催化剂上的催化性能及多氯副产物抑制机理研究
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2025.12.020
Runtong Dong , Yunfeng Ma , Yi Liu , Fanxiang Meng , Jiabao Lv , Angjian Wu , Zhongkang Han , Yujue Yang , Bingcheng Lin , Rong Jin , Minghui Zheng , Guorui Liu
Efficient catalytic oxidation of chlorinated volatile organic compounds (CVOCs) with minimal polychlorinated byproducts remains challenging, and the positive effect of water vapor could facilitate it. Based on MnCeOx catalyst, the formation characteristics of polychlorinated benzenes, highly toxic polychlorinated byproducts (PCDD/Fs, PCBs, and PCNs), and PAHs during catalytic oxidation of chlorobenzene (CBCO) were systemically revealed. A phosphate-modified strategy (trimethyl phosphate, CePO4, and H3PO4) was developed for promoting chlorine desorption and desirable inhibition on the polychlorinated byproducts. The trimethyl phosphate TMP-modified catalyst demonstrated highest CB conversion (T90 = 205 °C), stability, and water resistance. A series of experiments involving D2O-TPD-MS, radical trapping, and DFT calculation provided complete insights into promotion effect of phosphate-modification strategy on the formation of Brønsted acid sites and the hydrolysis effect on H2O molecule. H2O performed an essential proton-rich environment and highly reactive water-source oxygen species (·OH), thereby improving dechlorination and deep oxidation properties. The generation pathways of polychlorinated byproducts mainly include reaction steps such as free radical coupling, dechlorination, and condensation. TMP-modified MnCeOx catalyst exhibited the strongest suppression effect on the formation of chlorinated and non-chlorinated byproducts, and their concentrations were decreased by 87.7 % (Polychlorinated benzenes), 82.2 %(PCDD/Fs), 8.5 %(PCBs), and 92.0 %(PAHs), respectively. This work demonstrates a valuable phosphate-modified strategy to suppress the generation of polychlorinated byproducts during CVOCs elimination process and improved the application potential of Mn-based catalysts under practical application conditions (containing water vapor).
有效的催化氧化氯化挥发性有机化合物(CVOCs)并减少多氯副产物仍然是一个挑战,而水蒸气的积极作用可以促进它。基于MnCeOx催化剂,系统揭示了氯苯(CBCO)催化氧化过程中多氯联苯、高毒性多氯联苯副产物(PCDD/Fs、PCBs和PCNs)和多环芳烃的生成特征。采用磷酸三甲基磷酸、CePO4和H3PO4三种磷酸盐改性策略促进了氯的脱附,并对多氯副产物有良好的抑制作用。三甲基磷酸tmp改性催化剂表现出最高的CB转化率(T90 = 205℃)、稳定性和耐水性。通过D2O-TPD-MS、自由基捕获和DFT计算等一系列实验,全面了解了磷酸盐修饰策略对Brønsted酸位形成的促进作用以及对H2O分子的水解作用。H2O是必需的富质子环境和高活性的水源氧(·OH),从而改善了脱氯和深度氧化性能。多氯副产物的生成途径主要包括自由基偶联、脱氯、缩合等反应步骤。tmp修饰的MnCeOx催化剂对氯化副产物和非氯化副产物的生成抑制作用最强,其浓度分别降低87.7%(多氯苯)、82.2% (PCDD/Fs)、8.5% (PCBs)和92.0% (PAHs)。本研究展示了一种有价值的磷酸盐改性策略,可以抑制CVOCs消除过程中多氯副产物的产生,并提高了锰基催化剂在实际应用条件下(含水蒸气)的应用潜力。
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引用次数: 0
The differential cardiotoxicity effects and molecular mechanisms induced by two emerging organophosphorus flame retardants (EHDPP and DPHP) with similar parent structures in zebrafish 两种新型亲本结构相似的有机磷阻燃剂EHDPP和DPHP对斑马鱼的不同心脏毒性作用及其分子机制
IF 8.2 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-01-01 DOI: 10.1016/j.enceco.2025.12.017
Miaocui Xi, Xue Bai, Lu Fang, Xuedong Wang, Jin Yan, Qiuhui Qian, Zejun Wang, Huili Wang
Herein, we systematically compared the cardiotoxicity effects of two structurally similar organophosphate flame retardants (OPFRs; EHDPP and its major metabolite DPHP) using zebrafishi as a model organism. Predictive toxicity data from two aquatic species, together with empirical LC₅₀ values obtained in zebrafish larvae, consistently demonstrated that 2-ethylhexyl diphenyl phosphate (EHDPP) is substantially more toxic than diphenyl phosphate (DPHP). At LC₅₀-scaled concentrations, both contaminants induced the reduced heart rate, pericardial edema, and cardiac malformations, in concomitant with enhanced activities of creatine kinase (CK) and lactate dehydrogenase (LDH) and downregulated cardiac transcription factors (gata4 and Nkx2.5) and upregulated structural gene cmlc2. Even at low concentrations, EHDPP triggered apoptosis and elevated reactive oxygen species (ROS) levels in cardiac and pericardial tisues, along with prominent lipid accumulation in the heart, vasculature, and intersegmental arteries. It activated multiple pathways including MAPK, calcium signaling, and excitation-contraction coupling, while DPHP primarily affected cardiac function via calcium pump regulation and neuro-signaling pathways. Disease ontology (DO) enrichment analysis revealed that both EHDPP and DPHP associated target genes were most significantly enriched in cardiovascular-related diseases. Pharmacological rescue experiments using pathway-specific agents (Y-27632 and isoproterenol) further validated the functional roles of key signaling pathways in mediating the observed cardiotoxicity. Albeit differing in only one alkyl chain, EHDPP and DPHP displayed significantly differential cardiotoxicity and molecular mechanisms in zebrafish. These observations are conducive to illustrating OPFRs' structure-activity relationship and their health risk.
本文以斑马鱼为模型生物,系统比较了两种结构相似的有机磷阻燃剂(OPFRs、EHDPP及其主要代谢物DPHP)的心脏毒性作用。来自两种水生物种的预测毒性数据,以及在斑马鱼幼虫中获得的经验LC₅0值,一致表明2-乙基己基磷酸二苯酯(EHDPP)的毒性比磷酸二苯酯(DPHP)大得多。在LC₅0标度浓度下,两种污染物均诱导心率降低、心包水肿和心脏畸形,同时肌酸激酶(CK)和乳酸脱氢酶(LDH)活性增强,心脏转录因子(gata4和Nkx2.5)下调,结构基因cmlc2上调。即使在低浓度下,EHDPP也会引发心脏和心包组织的细胞凋亡和活性氧(ROS)水平升高,并在心脏、脉管系统和节段间动脉中产生显著的脂质积累。它激活了包括MAPK、钙信号和兴奋-收缩耦合在内的多种通路,而DPHP主要通过钙泵调节和神经信号通路影响心功能。疾病本体(DO)富集分析显示,EHDPP和DPHP相关靶基因在心血管相关疾病中富集最为显著。利用途径特异性药物(Y-27632和异丙肾上腺素)进行的药理学救援实验进一步验证了关键信号通路在介导所观察到的心脏毒性中的功能作用。尽管EHDPP和DPHP仅在一个烷基链上存在差异,但在斑马鱼中表现出明显不同的心脏毒性和分子机制。这些结果有助于阐明OPFRs的构效关系及其健康风险。
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引用次数: 0
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Environmental Chemistry and Ecotoxicology
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