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Corrigendum to "You shall not pass! (unless you're stress resistant): Selection-driven restructuring and transient invasion in freshwater mussel microbiomes under antimicrobial exposure" [Environ. Int. 208 (2026) 110138]. “你不能通过!”(除非你有抗压力能力):在抗菌素暴露下淡水贻贝微生物群的选择驱动重组和短暂入侵。Int. 208(2026) 110138]。
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-26 DOI: 10.1016/j.envint.2026.110156
Lisa-Marie Streb, Michelle Kligman, Juergen Geist, Gabriela Freitas Pereira de Souza, Susanne Rath, Susanne Walch, Michael Schloter
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引用次数: 0
A modernized human physiologically based toxicokinetic model of cadmium 基于现代人体生理的镉中毒动力学模型
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-18 DOI: 10.1016/j.envint.2026.110150
Yue Cui , Jingbo Pi , Qiang Zhang , Shengnan Liu
Exposure to cadmium (Cd), an environmental heavy metal pollutant, can cause significant toxicities and is a critical public health concern. Physiologically based toxicokinetic (PBTK) modeling has been used to understand and predict Cd body burdens. Although many human PBTK models of Cd were published in the last few decades – nearly all based on the original framework developed by Kjellström and Nordberg (K&N) in 1978 – caveats still remain across these models, limiting their effective and extended use as a modern in silico tool for Cd risk assessment. Main issues include lack of physiological blood flows, systemic rather than portal blood entry of gastrointestinal (GI) tract-absorbed Cd, part of urinary and fecal Cd being excreted directly from blood, and empirical adjustment to substantially lower overpredicted plasma Cd fractions. These issues compromise the model accuracy and make it less straightforward to incorporate physiological variabilities for populational models. Here, we aimed to address these limitations. We updated the model by incorporating blood flow to tissues, splitting each tissue into tissue blood and tissue proper sub-compartments, and making liver blood as the entry point of GI tract-absorbed Cd. We also added a filtrate sub-compartment to kidney to better describe urinary Cd excretion. The updated model was rigorously calibrated by using the dietary and cigarette-smoking Cd intakes, body growth, and blood, urinary, liver, and kidney Cd dosimetry data, all from the US population. Compared with the existing models, our model performs better in various aspects across sex, age, and smoking status, especially for blood, liver, and kidney Cd concentrations, as well as different blood Cd fractions. In summary, by addressing prior model limitations, our model enables more accurate quantitative predictions of internal Cd burdens for lifetime exposure and provides a much-improved framework for future extension into populational PBTK models and precision risk assessments of Cd exposure.
镉(Cd)是一种环境重金属污染物,暴露于镉(Cd)可引起重大毒性,是一个严重的公共卫生问题。基于生理的毒物动力学(PBTK)模型已被用于了解和预测镉的身体负荷。尽管在过去几十年中发表了许多人类Cd的PBTK模型——几乎都是基于Kjellström和Nordberg (K&;N)在1978年开发的原始框架——但这些模型中仍然存在一些警告,限制了它们作为Cd风险评估的现代计算机工具的有效和扩展使用。主要问题包括缺乏生理血流,胃肠道吸收的Cd进入全身而不是门静脉,部分尿和粪便中的Cd直接从血液中排出,以及经验调整以大幅降低高估的血浆Cd含量。这些问题损害了模型的准确性,并使其不太直接纳入人口模型的生理变异。在这里,我们的目标是解决这些限制。我们更新了模型,将血流纳入组织,将每个组织分为组织血液和组织适当亚室,并使肝脏血液作为胃肠道吸收Cd的切入点。我们还在肾脏中添加了滤液亚室,以更好地描述尿Cd排泄。更新后的模型通过使用饮食和吸烟Cd摄入量、身体生长、血液、尿液、肝脏和肾脏Cd剂量学数据进行了严格校准,这些数据都来自美国人口。与现有模型相比,我们的模型在性别、年龄、吸烟状况等各方面都有更好的表现,特别是在血、肝、肾Cd浓度以及不同血Cd分数方面。总之,通过解决先前模型的局限性,我们的模型能够更准确地定量预测终生暴露的内部Cd负担,并为未来扩展到人群PBTK模型和精确的Cd暴露风险评估提供了一个改进的框架。
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引用次数: 0
A human next generation PBK model for PFOA PFOA人类下一代PBK模型
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-27 DOI: 10.1016/j.envint.2026.110161
Chrysanthi Pachoulide , Carolina Vogs , Aude Ratier , Jack Koster , Trine Husøy , Martine Vrijheid , Yiyi Xu , Antonios Georgelis , Karl Forsell , Joost Westerhout , Nynke I. Kramer
The human toxicological risk assessment of per- and polyfluoroalkyl substances (PFAS) is challenging, due to their sheer number and structural diversity, but also the paucity of the toxicity data required to characterize them. The development of Next Generation Physiologically Based Kinetic (NG-PBK) models may assist in overcoming this challenge. The mechanistic nature of NG-PBK models allows for their extrapolation from data-rich PFAS, such as perfluorooctanoic acid (PFOA), to data-poor ones, facilitating their application in Next Generation Risk Assessment (NGRA). The present study proposes a NG-PBK model for PFOA in humans, parametrized exclusively using in vitro-, and in silico-derived data. The model describes the toxicokinetic processes of 1) partitioning to plasma and tissue proteins, 2) partitioning to cell membrane lipids, 3a) transporter-mediated entero-hepatic circulation and 3b) renal elimination and reabsorption, and 4) elimination via menstruation. Global sensitivity analysis indicated that the model was most sensitive to the fraction unbound in plasma, active-transport parameters, and tissue-plasma partition coefficients. The model was equivalent to already available validated human PFOA-PBK models, while compared to those, it is not calibrated to observed animal, nor human data, illustrating its strength in being mechanistic. The serum concentrations and half-lives predicted by the NG-PBK model were within the ranges of those reported in human volunteer and biomonitoring (HBM) studies, demonstrating the model’s capacity to accurately predict PFOA toxicokinetics on exposure estimates. Extrapolation of the NG-PBK model to other PFAS, in conjunction with its integration with HBM data, will facilitate the NGRA of PFAS. This is particularly relevant given the paucity of in vivo data for most PFAS, ensuring compliance with the 3R principles.
单氟烷基和多氟烷基物质(PFAS)的人体毒理学风险评估具有挑战性,因为它们数量众多,结构多样,但也缺乏表征它们的毒性数据。下一代基于生理的动力学(NG-PBK)模型的发展可能有助于克服这一挑战。NG-PBK模型的机制性质允许它们从数据丰富的全氟辛酸(PFOA)等全氟辛酸外推到数据贫乏的全氟辛酸,从而促进了它们在下一代风险评估(NGRA)中的应用。本研究提出了人类PFOA的NG-PBK模型,仅使用体外和计算机数据进行参数化。该模型描述了1)分配到血浆和组织蛋白,2)分配到细胞膜脂质,3a)转运体介导的肠肝循环和3b)肾脏消除和重吸收,以及4)通过月经消除的毒性动力学过程。全局敏感性分析表明,该模型对等离子体中未结合分数、主动输运参数和组织-等离子体分配系数最为敏感。该模型与现有的经过验证的人类PFOA-PBK模型相当,但与这些模型相比,它没有根据观察到的动物数据或人类数据进行校准,这说明了它的机制优势。NG-PBK模型预测的血清浓度和半衰期在人类志愿者和生物监测(HBM)研究报告的范围内,表明该模型能够准确预测暴露估计的PFOA毒性动力学。将NG-PBK模型外推到其他PFAS,并将其与HBM数据相结合,将有助于PFAS的NGRA。考虑到大多数PFAS缺乏体内数据,确保符合3R原则,这一点尤为重要。
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引用次数: 0
Tree canopy configuration and Swiss adult mortality at the municipal level: A nationwide ecological study 树冠结构与瑞士市级成人死亡率:一项全国性的生态学研究
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-03-09 DOI: 10.1016/j.envint.2026.110188
Dengkai Chi , Gabriele Manoli , Jun Yang , Daniel Richards , Amy Hahs , Brenda Lin , Mark J. McDonnell , Ye Zhang , Yue Zhu , Yeshan Qiu , Jing Wang , Xing Zheng , Paolo Burlando , Simone Fatichi , Puay Yok Tan

Background

The spatial distribution of tree canopies influences ecological functions and residents’ exposure to green spaces. Although several studies have examined green space configuration at neighborhood scales, evidence on tree canopy configuration at the municipal scale, an operational unit for urban planning, remains limited.

Methods

We conducted a nationwide ecological study of 2,136 Swiss municipalities. Tree canopy coverage (PLAND), aggregation (AI, reflecting how tightly green patches are grouped together), patch density (PD, a measure of fragmentation), and area-weighted mean shape index (SHAPE_AM, a measure of shape complexity) were derived from 1-m canopy maps within municipality-specific populated areas. Natural-cause, cardiovascular, and cancer mortality (2017–2019) were obtained from the Swiss National Cohort. Fully adjusted negative binomial regression models estimated associations between canopy metric and mortality for each IQR increase in the metrics.

Results

Holding configuration constant, each IQR increase in canopy coverage (∼18%) was associated with a 3.6% [B: −0.036; 95% CI: −0.078 – 0.005] reduction in cardiovascular mortality. Higher aggregation corresponded to a 4.3% [B: 0.043; 95% CI: 0.026–0.061], an 8.9% [B: 0.089; 95% CI: 0.059–0.119], and a 2.1% [B: 0.021; 95% CI: 0–0.042] higher number of natural-cause, cardiovascular, and cancer deaths respectively. Higher fragmentation was associated with a 3.3% [B: 0.033; 95% CI: 0.016–0.050], a 4.9% [B: 0.049; 95% CI: 0.020–0.078], and a 2.2% [B: 0.022; 95% CI: 0.001–0.043] increase in these causes respectively. No meaningful associations were observed between shape complexity and any mortality outcomes. Associations for aggregation and fragmentation were generally stronger in highly urbanized municipalities.

Conclusions

At the municipal scale, mortality was lower where tree canopy was distributed across several moderately sized, spatially balanced patches rather than highly aggregated or highly fragmented structures. These findings suggest that urban greening strategies should optimize its spatial configuration to maximize health benefits.
树冠的空间分布影响着生态功能和居民对绿地的暴露。虽然有几项研究在社区尺度上考察了绿地的配置,但在城市规划的一个操作单位——市政尺度上,关于树冠配置的证据仍然有限。方法我们对瑞士2136个城市进行了全国性的生态研究。树冠覆盖度(PLAND)、聚集度(AI,反映绿色斑块组合在一起的紧密程度)、斑块密度(PD,一种碎片化的度量)和面积加权平均形状指数(SHAPE_AM,一种形状复杂性的度量)是从城市特定人口稠密地区的1米树冠图中得出的。自然原因、心血管和癌症死亡率(2017-2019)来自瑞士国家队列。完全调整的负二项回归模型估计了林冠度与死亡率之间的关系。结果在保持构型不变的情况下,林冠覆盖度每增加1 IQR(~ 18%),林冠覆盖度增加3.6% [B:−0.036;95% CI: - 0.078 - 0.005]心血管死亡率降低。较高的聚集度对应于4.3% [B: 0.043;95% CI: 0.026-0.061], 8.9% [B: 0.089;95% CI: 0.059 ~ 0.119], a = 2.1% [B: 0.021;95% CI: 0-0.042]自然原因、心血管疾病和癌症死亡人数分别较高。较高的破碎度与3.3%相关[B: 0.033;95% CI: 0.016-0.050], a 4.9% [B: 0.049;95% CI: 0.020-0.078], 2.2% [B: 0.022;95% CI: 0.001-0.043]。没有观察到形状复杂性和任何死亡结果之间有意义的关联。在高度城市化的城市,聚集性和分散性的关联通常更强。结论在城市尺度上,冠层分布在几个大小适中、空间平衡的斑块上,而不是高度聚集或高度破碎的结构,死亡率较低。这些研究结果表明,城市绿化策略应优化其空间配置,以最大限度地提高健康效益。
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引用次数: 0
Microplastics release from infusion sets during intravenous infusion induces cardiovascular toxicity 静脉输注过程中从输液器中释放的微塑料引起心血管毒性
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-03-08 DOI: 10.1016/j.envint.2026.110187
Honggui Yu , Gang Xiang , Sihan He , Zhuotong Zeng , Ang Deng , Yi Yin , Yunjia Wang
Plastic products are extensively utilized in the medical sector, with the global annual usage of single-use plastic infusion sets surpassing one million units. However, mounting evidence indicates that these infusion sets may release microplastic particles during intravenous administration, which could potentially accumulate in the cardiovascular system. In this study, by simulating specific clinical infusion conditions, including acidic, alkaline drugs and hypertonic infusions under different temperatures, we observed that irritating drugs and elevated temperatures significantly increased microplastic release. We collected the released microplastics (C-MPs) and exposed them to human umbilical vein endothelial cells (HUVECs) and transgenic zebrafish models. The results revealed that C-MPs could be internalized by cells, subsequently leads to a maximum increase in ROS production of approximately 12-fold, activating NLRP3 inflammasomes, and inhibiting angiogenesis. Transgenic zebrafish experiments further confirmed that C-MPs accumulation led to a significant decrease in survival rates, accompanied by distinct cardiovascular malformations, such as cardiac dilation, pericardial edema, abnormal angiogenesis and profound oxidative damage. In summary, our findings indicate the existence of potential health risks to the cardiovascular system from microplastics released by medical devices, thereby emphasizing the necessity to address the impact of infusion conditions.
塑料制品在医疗领域得到广泛应用,全球每年使用一次性塑料输液器超过100万套。然而,越来越多的证据表明,这些输液器在静脉给药过程中可能释放出微塑料颗粒,这可能在心血管系统中积累。在本研究中,我们通过模拟特定的临床输注条件,包括酸性、碱性药物和不同温度下的高渗输注,观察到刺激性药物和升高的温度显著增加微塑料的释放。我们收集了释放的微塑料(C-MPs),并将其暴露于人脐静脉内皮细胞(HUVECs)和转基因斑马鱼模型中。结果表明,C-MPs可以被细胞内化,随后导致ROS产生最多增加约12倍,激活NLRP3炎症小体,抑制血管生成。转基因斑马鱼实验进一步证实,C-MPs积累导致存活率显著降低,并伴有明显的心血管畸形,如心脏扩张、心包水肿、血管生成异常和深度氧化损伤。总之,我们的研究结果表明,医疗器械释放的微塑料对心血管系统存在潜在的健康风险,因此强调了解决输液条件影响的必要性。
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引用次数: 0
Integrated network toxicology, transcriptomics and metabolomics to elucidate mechanism of di(2-ethylhexyl) phthalate inducing reproductive toxicity in laying hens 综合网络毒理学、转录组学和代谢组学研究邻苯二甲酸二(2-乙基己基)诱导蛋鸡生殖毒性的机制
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-20 DOI: 10.1016/j.envint.2026.110155
Jia-Yu Du , Yi-Fei Ren , Bai-Hai Ni , Jin-Long Li , Chi-Chiu Wang , Xue-Nan Li
Di(2-ethylhexyl) phthalate (DEHP) is ubiquitous in agricultural ecosystems due to the widespread use of plastic mulch films and plasticized agrochemicals, posing a significant threat to poultry health. This study investigates DEHP’s reproductive toxicity and molecular mechanisms in laying hens. Hy-Line brown hens were divided into control and 150 mg/kg DEHP-exposed groups for 15 weeks. Production performance, egg quality and ovary oviduct histomorphology were assessed combined with transcriptomics, metabolomics, network toxicology and molecular docking. The results showed that DEHP reduced feed intake, altered yolk color, thinned eggshells and induced ovarian follicular atresia and oviduct uterine epithelial atrophy. Integrated omics showed disrupted ovarian pathways like neuroactive ligand-receptor interactions, glutathione and glycerophospholipid metabolism plus key metabolite-gene pairs such as CMPK2 and aspartic acid. Uterine transcriptomics revealed abnormal extracellular matrix, ion transport and eggshell mineralization genes. Network toxicology identified 10 core targets including Bcl2, Casp3 and PIK3CA with DEHP metabolite mono(2-ethylhexyl) phthalate (MEHP) stably binding them via docking. Integrated analysis of multi-omics and network toxicology, along with western blot results, further confirmed that the apoptosis and lysosomal pathways were activated in the ovaries and oviduct uterus of laying hens. Protein–protein interaction analysis positioned Bcl2 as a potential regulator linking these pathways. In conclusion, DEHP exposure is associated with reproductive toxicity in laying hens. Future studies should employ multi-dose designs and validate multi-omics–derived mechanisms with targeted functional experiments to strengthen causal inference.
由于塑料地膜和农药的广泛使用,邻苯二甲酸二(2-乙基己基)酯(DEHP)在农业生态系统中无处不在,对家禽健康构成重大威胁。本研究探讨了DEHP对蛋鸡的生殖毒性及其分子机制。将海兰褐鸡分为对照组和150 mg/kg dehp暴露组,连续暴露15 周。结合转录组学、代谢组学、网络毒理学和分子对接等方法,对生产性能、卵子品质和卵巢输卵管组织形态学进行评价。结果表明,DEHP降低了采食量,改变了蛋黄颜色,使蛋壳变薄,导致卵巢卵泡闭锁和输卵管子宫上皮萎缩。整合组学显示卵巢通路被破坏,如神经活性配体-受体相互作用、谷胱甘肽和甘油磷脂代谢以及关键代谢物基因对,如CMPK2和天冬氨酸。子宫转录组学显示细胞外基质、离子转运和蛋壳矿化基因异常。网络毒理学鉴定出10个核心靶点,包括Bcl2、Casp3和PIK3CA, DEHP代谢物邻苯二甲酸单(2-乙基己基)酯(MEHP)通过对接稳定结合。综合多组学和网络毒理学分析,结合western blot结果,进一步证实了蛋鸡卵巢和输卵管子宫的细胞凋亡和溶酶体通路被激活。蛋白-蛋白相互作用分析定位Bcl2作为连接这些通路的潜在调节因子。综上所述,DEHP暴露与蛋鸡生殖毒性有关。未来的研究应采用多剂量设计,并通过有针对性的功能实验验证多组学衍生的机制,以加强因果推理。
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引用次数: 0
Associations of legacy and emerging per- and polyfluoroalkyl substances (PFAS) with aquatic communities in a typical subtropical estuary 典型亚热带河口中遗留和新出现的全氟烷基和多氟烷基物质(PFAS)与水生群落的关系
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-23 DOI: 10.1016/j.envint.2026.110163
Haojie Lei , Yonglong Lu , Pei Wang , Ting Wu , Yanjun Liu , Yinyue Liu , Jialong Li , Bin Sun , Cong Wang , Xupeng An
Coastal estuarine ecosystems play a critical role in supporting biodiversity but are increasingly threatened by per- and polyfluoroalkyl substances (PFAS). This study combined in situ PFAS monitoring with environmental DNA (eDNA) metabarcoding to investigate their impacts on fish species and community structure. PFAS concentrations ranged from 7.34 to 82.04 ng L−1 in water and 1.87–4.98 ng g−1 dw in sediments. Perfluorobutanoic acid (PFBA) and perfluorobutane sulfonic acid (PFBS) replaced perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) as the predominant PFAS in water, with mean concentrations of 3.74 ± 2.67 ng L−1 and 13.84 ± 3.95 ng L−1, respectively. In organisms, PFAS concentrations ranged from 0.13 to 96.21 ng g−1 ww and were higher in benthic invertebrates. As alternatives to PFOA and PFOS, PFBA and PFBS displayed comparable or even greater bioaccumulation potential, whereas chlorinated polyfluoroalkyl ether sulfonic acids (F-53B) exhibited significant trophic magnification (p < 0.05). PFAS occurrence was closely associated with fish community diversity, and increasing PFAS concentrations were linked to a potential decline in the Shannon index (p < 0.05). From a species-community perspective, typical PFAS in estuarine environments exhibit bioaccumulation and trophic magnification, underscoring the need for further attention to their ecological impacts at both species and community levels.
沿海河口生态系统在支持生物多样性方面发挥着关键作用,但正日益受到全氟烷基和多氟烷基物质的威胁。本研究将PFAS原位监测与环境DNA元条形码技术相结合,探讨PFAS对鱼类种群和群落结构的影响。水中PFAS浓度为7.34 ~ 82.04 ng L−1,沉积物中PFAS浓度为1.87 ~ 4.98 ng g−1 dw。全氟丁酸(PFBA)和全氟丁烷磺酸(PFBS)取代全氟辛酸(PFOA)和全氟辛烷磺酸(PFOS)成为水中主要的PFAS,平均浓度分别为3.74 ± 2.67 ng L−1和13.84 ± 3.95 ng L−1。在生物中,PFAS浓度范围为0.13至96.21 ng g−1 ww,在底栖无脊椎动物中更高。作为PFOA和PFOS的替代品,PFBA和PFBS表现出相当甚至更大的生物积累潜力,而氯化多氟烷基醚磺酸(F-53B)表现出显著的营养放大(p <; 0.05)。PFAS的发生与鱼类群落多样性密切相关,PFAS浓度的增加与Shannon指数的潜在下降有关(p <; 0.05)。从物种-群落的角度来看,河口环境中典型的PFAS表现出生物积累和营养放大,强调需要进一步关注其在物种和群落水平上的生态影响。
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引用次数: 0
Air pollution and childhood asthma in Iceland – Results from a low-pollution area 冰岛的空气污染和儿童哮喘——来自低污染地区的结果
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-25 DOI: 10.1016/j.envint.2026.110170
Ane Johannessen , Throstur Thorsteinsson , Camilla Geels , Lise Marie Frohn , Michael Clausen , Jørgen Brandt , Bertil Forsberg , Thorarinn Gislason

Background

No studies have investigated associations between air pollution and childhood asthma in Iceland. We aimed to explore if air pollution during pregnancy and early life was associated with asthma hospitalisations and medication use in Icelandic children.

Methods

We included all singleton births in Iceland from 2005 to 2018 (n = 59,355). Residential air pollution exposure during pregnancy and first three years of life was analysed in relation to asthma hospitalisations (International Classification of Diseases ICD J45–J46) and medication use (Anatomical Therapeutic Chemical classification ATC R03A–R03D), using Cox regression with age as time scale and adjusting for maternal, offspring, and household factors.

Findings

Asthma hospitalisation occurred in 3.9% of children, and 18.6% had asthma medication prescriptions after age 3. Mean annual exposures to fine and course particulate matter (PM2.5 and PM10) and nitrogen dioxide (NO2) were low, but 26%, 1%, and 37%, respectively, was exposed to pollution exceeding World Health Organization (WHO) guidelines. All pollutants except ozone increased asthma hospitalisation risk (hazard ratios 1.08 to 1.59 per interquartile range (IQR) increase, lower 95% confidence intervals (95% CIs) ranging from 0.97 to 1.24 and upper 95% CIs from 1.17 to 2.04) with PM2.5 exhibiting the highest risk (HR 1.59, 95% CI 1.24–2.04). Associations during pregnancy and early life were similar. Risk estimates for asthma medication use were lower than for hospitalisations. Nevertheless, pregnancy exposures to primary organic aerosols (POA), secondary organic aerosols (SOA), sulphate (SO42-), sulphur dioxide (SO2), secondary inorganic aerosols (SIA), PM2.5 and PM10 were significantly associated with increased asthma medication use.

Interpretation

Air pollution exposure even at low levels was associated with increased risk of childhood asthma hospitalisation and medication use in Iceland. PM2.5 was the most important factor. Our findings highlight the need for continued efforts to further reduce pollution exposure.
在冰岛,没有研究调查空气污染和儿童哮喘之间的关系。我们的目的是探索冰岛儿童怀孕和生命早期的空气污染是否与哮喘住院和药物使用有关。方法纳入冰岛2005年至2018年的所有单胎分娩(n = 59,355)。使用Cox回归,以年龄为时间尺度,并对母亲、后代和家庭因素进行调整,分析孕期和生命最初三年的住宅空气污染暴露与哮喘住院(国际疾病分类ICD J45-J46)和药物使用(解剖治疗化学分类ATC r0a3 - r03d)的关系。发现哮喘住院率为3.9%,3岁以后有18.6%的哮喘药物处方。细颗粒物(PM2.5和PM10)和二氧化氮(NO2)的年平均暴露量较低,但分别有26%、1%和37%的人暴露于超过世界卫生组织(WHO)指南的污染中。除臭氧外的所有污染物都增加了哮喘住院风险(每四分位数范围(IQR)增加的风险比为1.08至1.59,95%置信区间(95% CI)的下限为0.97至1.24,95% CI的上限为1.17至2.04),其中PM2.5的风险最高(HR 1.59, 95% CI 1.24至2.04)。在怀孕和生命早期也有类似的关联。使用哮喘药物的风险估计低于住院治疗的风险估计。然而,妊娠期暴露于一次有机气溶胶(POA)、二次有机气溶胶(SOA)、硫酸盐(SO42-)、二氧化硫(SO2)、二次无机气溶胶(SIA)、PM2.5和PM10与哮喘药物使用增加显著相关。在冰岛,即使是低水平的空气污染暴露也与儿童哮喘住院和药物使用的风险增加有关。PM2.5是最重要的因素。我们的研究结果强调了继续努力进一步减少污染暴露的必要性。
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引用次数: 0
Nontargeted screening identifies mixtures of environmental pollutants that are associated with perturbations to amino acid and fatty acid metabolic pathways during early pregnancy 非靶向筛选确定与妊娠早期氨基酸和脂肪酸代谢途径扰动相关的环境污染物混合物
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-25 DOI: 10.1016/j.envint.2026.110172
Adam F. Pedersen , Lauren M. Petrick , Katherine Roth , Zhao Yang , Alexandra R. Sitarik , Amith Maroli , Georgia Dolios , Courtney Carignan , Jaclyn M. Goodrich , Jean M. Kerver , Michael Petriello
“One-chemical-at-a-time” approaches are typically used to investigate adverse health outcomes associated with exposure to environmental chemicals during pregnancy. However, nontargeted high-resolution mass spectrometry (HRMS) approaches can instead measure complex, real-world mixtures of xenobiotics and metabolic products and may better explain mechanisms of toxicity and identify biomarkers of exposure than single-chemical approaches during pregnancy, a particularly sensitive exposure window. Here, our objective was to use a nontargeted, HRMS approach that monitors endogenous and xenobiotic compounds to identify associations of pollutant mixtures with metabolic pathways in serum of 100 pregnant women from the MARCH cohort (Michigan Archive for Research on Child Health). Xenobiotic mixtures were identified based on in-house libraries as well as a discovery-based approach, FluoroMatch 3.0, to identify nonlegacy/emerging fluorinated chemicals in these same samples. Metabolic pathways of interest were determined using MetaboAnalyst software and effect estimates on metabolic profiles were estimated for both individual contaminants and mixtures of all identified chemicals. 415 endogenous metabolites and 21 individual chemical pollutants were detected with high identification confidence and included per- and poly-fluoroalkyl substances (PFAS), phthalates, bisphenols, organophosphate esters (OPEs), and parabens. An additional 105 tentative fluorinated compounds were identified via FluoroMatch. As classes of toxicants, bisphenol and PFAS mixtures showed the greatest number of associations with metabolic pathways related to arginine, proline, glycine, serine, and threonine metabolism. When the total mixture of all 21 contaminants was modeled after covariate-adjustment, biosynthesis of unsaturated fatty acids remained (FDR < 0.05). Taken together, these findings illustrate that serum concentrations of environmental contaminants may be associated with some metabolic pathways in pregnancy and that mixture modeling identified fatty acid metabolism as a possible pathway of interest for future validation. These findings further demonstrate the potential of robust nontargeted exposome-wide approaches as tools to study and identify the mechanisms of toxicity underlying human disease.
“一次使用一种化学品”的方法通常用于调查与怀孕期间接触环境化学品有关的不良健康后果。然而,非靶向高分辨率质谱(HRMS)方法可以代替测量复杂的,真实世界的异种生物制剂和代谢产物的混合物,并且可以更好地解释毒性机制并识别暴露的生物标志物,而不是怀孕期间的单一化学方法,这是一个特别敏感的暴露窗口。在这里,我们的目的是使用一种非靶向的HRMS方法来监测内源性和外源性化合物,以确定来自MARCH队列(密歇根儿童健康研究档案)的100名孕妇血清中污染物混合物与代谢途径的关联。根据内部文库以及基于发现的方法FluoroMatch 3.0确定异种生物混合物,以确定这些样品中的非遗留/新出现的氟化化学品。使用MetaboAnalyst软件确定了感兴趣的代谢途径,并估计了单个污染物和所有已鉴定化学物质混合物对代谢谱的影响。检测到415种内源性代谢物和21种单独的化学污染物,具有很高的识别置信度,包括全氟烷基和多氟烷基物质(PFAS)、邻苯二甲酸盐、双酚类、有机磷酸酯(OPEs)和对羟基苯甲酸酯。通过FluoroMatch鉴定了另外105种暂定氟化化合物。作为一类有毒物质,双酚和PFAS混合物显示出与精氨酸、脯氨酸、甘氨酸、丝氨酸和苏氨酸代谢相关的代谢途径的最大关联。当所有21种污染物的总混合物经过协变量调整后建模时,不饱和脂肪酸的生物合成仍然存在(FDR < 0.05)。综上所述,这些发现表明,环境污染物的血清浓度可能与怀孕期间的一些代谢途径有关,而混合模型确定了脂肪酸代谢作为未来验证的可能途径。这些发现进一步证明了强大的非靶向全暴露体方法作为研究和确定人类疾病潜在毒性机制的工具的潜力。
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引用次数: 0
Microplastic exposure and the role of dietary patterns in school-aged children 微塑料暴露与学龄儿童饮食模式的作用
IF 9.7 1区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2026-03-01 Epub Date: 2026-02-24 DOI: 10.1016/j.envint.2026.110164
Changmeng Liu , Hualong Zhen , Yu Hu , Ruiling Li , Juan Tong , Guopeng Gao , Xiaoyan Wu , Hong Gan , Shanshan Du , Shuangqin Yan , Fangbiao Tao , Kun Huang
Microplastics (MPs) have permeated all aspects of human life. This study aimed to assess MP exposure in schoolchildren’s urine and dietary patterns’ role in it. We followed up 10-year-olds from the Ma’anshan Birth Cohort (MABC), using a Laser Direct Infrared instrument to qualitatively/quantitatively assess MP levels in 1,308 children’s urine. The zero-inflated negative binomial (ZINB) model analyzed associations between the Mediterranean Diet Quality Index for Children and Adolescents (KIDMED) and MP exposure. A total of 19 types of MP particles were identified in urine samples. The median total MP abundance was 250 particles/mL, with an overall detection rate of 91.29%. Among all detected MP types, polytetrafluoroethylene (PTFE) exhibited the highest detection rate (50.19%). Small-sized particles (20–100 μm) accounted for 98.04% of all detected MPs. Increases in children’s KIDMED index were associated with a greater probability of zero abundance in urine for polylactic acid (PLA), ethylene–vinyl acetate copolymer (EVA), and polyvinyl alcohol (PVA) (PLA: β (95% CI) = 0.094 (0.004, 0.184); EVA: β (95% CI) = 0.113 (0.027, 0.199); PVA: β (95% CI) = 0.058 (0.001, 0.115)). Additionally, increases in the KIDMED index were associated with higher non-zero abundance levels of polyamide (PA) and lower non-zero abundance levels of PTFE (PA: β (95% CI) = 0.063 (0.020, 0.106); PTFE: β (95% CI) = -0.057 (−0.096, −0.018)). In summary, 19 MP types were detected in children’s urine, with this study identifying an association between the KIDMED index and exposure levels of several MPs.
微塑料(MPs)已经渗透到人类生活的方方面面。本研究旨在评估小学生尿液中多聚氰胺暴露及其饮食模式在其中的作用。我们对来自马鞍山出生队列(MABC)的10岁儿童进行了随访,使用激光直接红外仪器定性/定量地评估了1308名儿童尿液中的MP水平。零膨胀负二项(ZINB)模型分析了儿童和青少年地中海饮食质量指数(KIDMED)与MP暴露之间的关系。在尿样中共鉴定出19种MP颗粒。中位总MP丰度为250粒/mL,总检出率为91.29%。在所有检测到的MP类型中,聚四氟乙烯(PTFE)的检出率最高(50.19%)。20 ~ 100 μm的小颗粒占检测到的MPs的98.04%。儿童KIDMED指数的升高与尿中聚乳酸(PLA)、乙烯-醋酸乙烯共聚物(EVA)和聚乙烯醇(PVA)含量为零的可能性增大相关(PLA: β (95% CI) = 0.094 (0.004,0.184);Eva: β (95% ci) = 0.113 (0.027,0.199);Pva: β (95% ci) = 0.058(0.001,0.115))。此外,KIDMED指数的升高与聚酰胺(PA)的非零丰度水平升高和聚四氟乙烯(PTFE)的非零丰度水平降低相关(PA: β (95% CI) = 0.063 (0.020,0.106);Ptfe: β (95% ci) = -0.057(−0.096,−0.018)。总之,在儿童尿液中检测到19种MP,本研究确定了KIDMED指数与几种MP暴露水平之间的关联。
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引用次数: 0
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Environment International
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