Environmental Toxicology最新文献

{"title":"RETRACTION: Value of Hepatic Artery Digital Subtraction Angiography in the Detection of Small Hepatocellular Carcinoma Lesions","authors":"","doi":"10.1002/tox.24527","DOIUrl":"10.1002/tox.24527","url":null,"abstract":"<p>\u0000 \u0000 <b>RETRACTION</b>: <span>T. Bai</span>, <span>S. Lu</span>, <span>J. Chen</span>, <span>J. Ye</span>, <span>X. Wang</span>, <span>Z. Tang</span>, <span>H. Fu</span>, <span>L. Li</span>, and <span>F. Wu</span>, “ <span>Value of Hepatic Artery Digital Subtraction Angiography in the Detection of Small Hepatocellular Carcinoma Lesions</span>,” <i>Environmental Toxicology</i> <span>39</span>, no. <span>10</span> (<span>2024</span>): <span>4754</span>–<span>4762</span>, https://doi.org/10.1002/tox.24316.\u0000 </p><p>The above article, published online on 20 August 2024, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, April Rodd; and Wiley Periodicals LLC. Following an investigation by the publisher, the parties have concluded that this article was accepted solely on the basis of a compromised peer review process. Therefore, the article must be retracted. The authors disagree with this decision.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 7","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24527","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143862426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Hydroxysafflor Yellow A Attenuates Allergic Response of Ovalbumin Induced Allergic Rhinitis via Nrf2/HO-1 and Inflammatory Signaling Pathways”","authors":"","doi":"10.1002/tox.24518","DOIUrl":"10.1002/tox.24518","url":null,"abstract":"<p>Q. Ma, G. Li, J. He, J. Wang, and B. Ye. “Hydroxysafflor Yellow A Attenuates Allergic Response of Ovalbumin Induced Allergic Rhinitis via Nrf2/HO-1 and Inflammatory Signaling Pathways,” <i>Environmental Toxicology</i> 38, no. 7 (2023): 1520–1534, https://doi.org/10.1002/tox.23783.</p><p>This article published with corresponding author Ben Ye being linked incorrectly to two affiliations, Department of Otorhinolaryngology, Zibo Ninth People's Hospital, Zibo, China and Department of Otorhinolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.</p><p>The correct and only affiliation for Ben Ye should be Department of Otorhinolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.</p><p>This has been corrected on the article.</p><p>We apologize for this error.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 7","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24518","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of PM_2.5 Morphology, Composition and Health Risk in a Multi-Chair Dental Clinic.","authors":"Fengqin Tang, Shengcai Qi, Xiaoshan Tang, Xueyun Wen, Yiming Zhang, Guotao Peng, Jieying Huang, Guangwei Shang, Xu Zhang, Fubo Chen, Yuanzhi Xu, Jing Cai","doi":"10.1002/tox.24519","DOIUrl":"https://doi.org/10.1002/tox.24519","url":null,"abstract":"<p><p>Particulate matter with aerodynamic diameter ≤ 2.5 μm (PM_2.5) at high concentrations in dental clinics poses significant health risks to healthcare professionals. However, the morphology and chemical composition of PM_2.5 in specific environments are not yet fully elucidated. In this study, we investigated the concentration, morphology, chemical composition, and health assessment of PM_2.5 collected in a multi-chair dental clinic in Shanghai, China. Scanning electron microscopy (SEM) and energy-dispersive X-ray spectroscopy (EDS) were performed to observe the morphology and elemental composition of indoor and outdoor PM_2.5. Chemicals were measured for their concentrations using X-ray fluorescence spectrometry (XRF). In the dental clinic, the indoor PM_2.5 concentration ranged from 2.01 to 114.59 μg/m³, with a mean of 23.31 μg/m³, while the outdoor PM_2.5 concentration ranged from 2.88 to 157.4 μg/m³, with a mean of 30.98 μg/m³. Indoor particles showed more rough, irregular mineralization, which was confirmed as the dominant elements of Ca, P, Si, and zirconia (Zr) by EDS. The average concentrations of Ca, P, Cu, Sr, and Sb indoors were lower than those outdoors (p < 0.05). We also found that Cd, As, and Ni exceeded the annual limits of the Ambient Air Quality Standards of WHO. For the health assessment, the carcinogenic risks of Cd, As, and Cr were higher than the minimum acceptable level (1 × 10^-6), with values of 3.68 × 10^-5, 1.10 × 10,^-5 and 5.52 × 10^-6, respectively, and the non-carcinogenic risk of Cd was the highest, as illustrated by the Hazard Quotient of 2.04. These findings indicate that dental healthcare professionals may be exposed to PM_2.5 containing high concentrations of toxic metals and carcinogenic elements over the long term. This study highlights the importance of protective measures (e.g., the adoption of efficient air purification systems) to minimize the risk of particle inhalation for both patients and professionals.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of Cuproptosis by Dichloromethane Extract From Patrinia scabiosaefolia Fisch on K562 Cells.","authors":"Yuan Lu, Leyuan Mi, Peipei Zhang, Yang Chen, Xinyi Bai, Kejing Li, Ying Zhang, Juan Li","doi":"10.1002/tox.24516","DOIUrl":"https://doi.org/10.1002/tox.24516","url":null,"abstract":"<p><p>Cuproptosis is a newly identified form of cell death that relies on copper (Cu) ionophores to transport Cu into cancer cells. As a perennial herb, Patrinia scabiosaefolia Fisch (PS) has garnered significant attention owing to its analgesic, anti-inflammatory, antibacterial, and antitumor properties. Previous research has shown that the extract from PS (DEPS) can inhibit the growth of leukemia cell lines. However, the specific mechanism of its anti-leukemic effect has not been fully clarified. Therefore, this study was conducted to investigate the molecular mechanism of cuproptosis in the treatment of leukemia with DEPS. Our results demonstrated that DEPS up-regulated SLC31A1 and down-regulated ATP7B expression, which increased intracellular copper concentration, down-regulated FDX1, influenced the lipoylation of DLAT and DLD, and subsequently increased the expression of the stress protein HSP70 and the expression of PDHA1, inducing copper death in K562 cells. In addition, we investigated the toxicity of DEPS in vivo and demonstrated its low in vivo toxicity and adequate in vivo safety. In conclusion, our results suggest that DEPS may induce cuproptosis in cells, offering valuable insights for the future application of PS in leukemia treatment.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Glyphosate on Zebrafish (Danio rerio) Developmental Toxicity.","authors":"Ning Zhou, Ruirui Li, Jin Lu, Jiagao Cheng, Wenping Xu, Liming Tao, Yang Zhang","doi":"10.1002/tox.24503","DOIUrl":"https://doi.org/10.1002/tox.24503","url":null,"abstract":"<p><p>Glyphosate has been widely used in agricultural production as a highly effective, low-toxic, broad-spectrum organophosphorus herbicide. However, there has been controversy about whether it is toxic to the nervous system. In order to explore this issue in depth, the present study analyzed the molecular mechanism of action of glyphosate from four perspectives, namely, gene regulation, protein expression, morphological changes, and behavioral changes, and assessed the potential effects of glyphosate on the development of the nervous system of zebrafish through the establishment of a zebrafish model. The results showed that zebrafish embryos at 6 hpf after fertilization were exposed to glyphosate until 72 and 120 hpf. After exposure, it was found that the central nervous development-related gene Elavl3 was down-regulated, and GAP-43, Neurog1, and GFAP were up-regulated. The expression of HuC protein, which is used to maintain neuronal axonal homeostasis, was significantly reduced, and the expression of GFAP protein, which is used to repair neurological damage and inflammation, was significantly increased. Under the regulation of related genes and proteins, zebrafish larvae show abnormal changes during the development of a series of nervous systems such as heart rate slowing, somite shortening, spinal and brain malformations. At the same time, the zebrafish's action behavior also changed, with a significant decrease in its total time share in the low-speed shift and high-speed shift states, and a delayed response to dark-light environmental stimuli. In summary, studies have shown that glyphosate exposure may induce damage and inflammation of the zebrafish nervous system, resulting in developmental malformations, abnormal motor behavior, and potential neurotoxicity. Therefore, the possible neurotoxicity and environmental risks of glyphosate to aquatic animals should not be ignored and should be of great concern.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmentally Relevant Concentrations of Commercial Titanium Dioxide Nanoparticles Induce Ferroptosis in HUVECs.","authors":"Fangfang Huang, Yashi Feng, Zi-An Wang, Yunchang Cao, Qiong Yan, Wuxiang Wang, Shaolong Feng","doi":"10.1002/tox.24517","DOIUrl":"https://doi.org/10.1002/tox.24517","url":null,"abstract":"<p><p>Titanium dioxide nanoparticles (TiO₂-NPs) have been ever increasingly exposed to people through all possible routes, while studies focusing on their potential cardiovascular risks are relatively lacking, especially the underlying biological mechanisms that are not yet elucidated. In this study, the ferroptotic effect of TiO₂-NPs (30 nm) at environmentally relevant concentrations (0, 3, 12, and 48 μg/mL) on human umbilical vein endothelial cells (HUVECs) and the potential molecular mechanism were studied with the corresponding biochemical and molecular biology assays. The results showed that TiO₂-NPs at the tested concentrations could reduce HUVEC viability, but ferrostatin-1 might rescue this reduction in cell viability. Also, TiO₂-NPs exposure increased Fe²⁺, reactive oxygen species, and malondialdehyde, but decreased glutathione, mitochondrial membrane potential, and activities of anti-oxidative enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in HUVECs through an integrated signaling pathway. Meanwhile, enhanced p38 protein phosphorylation and keap1 protein and decreased Nrf2 protein phosphorylation with reductions in mRNA expressions of downstream anti-oxidative enzyme genes (catalase, superoxide dismutase, glutathione peroxidase, and phospholipid hydroperoxidase) were identified in the TiO₂-NPs-exposed HUVECs. These indicated that TiO₂-NPs exposure induced ferroptosis in HUVECs via the p38/keap1 inhibiting Nrf2 pathway. EC ferroptosis will be a promising biomarker for assessing the cardiovascular health risks of environmental contaminants.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chlorpyrifos Induces Apoptosis in Macrophages by Activating Both Intrinsic and Extrinsic Apoptotic Pathways.","authors":"Chen-Yu Chiang, Shin-Wu Liu, Chun-Jung Chen, Wen-Ying Chen","doi":"10.1002/tox.24515","DOIUrl":"https://doi.org/10.1002/tox.24515","url":null,"abstract":"<p><p>Although chlorpyrifos poses considerable risks to the environment and human health, it is still used in many countries. This pesticide has various toxic effects on humans, including neurotoxicity, reproductive toxicity, genotoxicity, and organ damage caused by oxidative stress and DNA damage. However, its specific toxicity to the immune system remains unclear. In this study, we explored the intrinsic and extrinsic apoptotic pathways through which chlorpyrifos induces apoptosis in macrophages. RAW 264.7 macrophages were treated with chlorpyrifos at concentrations of 0, 2, 4, 10, and 20 ppm for 3 h. Cytotoxicity was assessed using a lactate dehydrogenase assay, whereas apoptosis was evaluated through flow cytometry. The levels of cysteinyl aspartate-specific proteinase (caspase)-3, caspase-8, and caspase-9 were measured. The disruption of mitochondrial function and the expression of the death receptors Fas receptor and tumor necrosis factor-alpha receptor were assessed through JC-1 stain reagent. The release of mitochondrial cytochrome c, expression of Bcl2 family proteins, and level of cleaved caspases were analyzed through Western blotting. Chlorpyrifos induced cytotoxicity and apoptosis in a concentration-dependent manner. It activated caspase-3, caspase-8, and caspase-9, as well as disrupted mitochondrial function and Bcl2 family protein balance. Furthermore, chlorpyrifos induced the release of cytochrome c from the mitochondria and upregulated the expression of Fas receptor and tumor necrosis factor-alpha receptor. These findings suggest that chlorpyrifos induces cytotoxicity through caspase-3-dependent apoptosis via the intrinsic pathway (caspase-8 activation, mitochondrial dysfunction, Bcl2 protein imbalance, and cytochrome c release) and the extrinsic pathway (caspase-9 activation and death receptor expression).</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “METTL3-Mediated m6A Modification of Pri-miR-148a-3p Affects Prostate Cancer Progression by Regulating TXNIP”","authors":"","doi":"10.1002/tox.24513","DOIUrl":"10.1002/tox.24513","url":null,"abstract":"<p>G. Li, J. Liu, Y. Wang, et al. “METTL3-Mediated m6A Modification of Pri-miR-148a-3p Affects Prostate Cancer Progression by Regulating TXNIP,” Environmental Toxicology 38, no. 10 (2023): 2377–2390, https://doi.org/10.1002/tox.23874.</p><p>The authors regret an error in the authorship designation in the original publication of the article titled <b>“</b>METTL3-Mediated m6A Modification of pri-miR-148a-3p Affects Prostate Cancer Progression by Regulating TXNIP.<b>”</b> The author contributions were misassigned, and the correct author order is as follows:</p><p>\u0000 <b>Original authorship listing:</b>\u0000 </p><p>Guoqiang Li¹, Junwen Liu², Yinhuai Wang¹, Hanqi Liu², Jianhan Fu¹, Yuanqiao Zhao¹, Yanqing Huang^2*\u0000 </p><p>\u0000 ¹Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China</p><p>\u0000 ²Department of Histology and Embryology, Xiangya School of Medicine, Central South University, Changsha, 410000, China</p><p>*<b>Corresponding author</b>: Yanqing Huang, Department of Histology and Embryology, Xiangya School of Medicine, Central South University, 172 Tongzipo Road, Changsha, 410000, China</p><p>Email: <span>[email protected]</span>\u0000 </p><p>\u0000 <b>Corrected authorship listing:</b>\u0000 </p><p>Yanqing Huang¹, Junwen Liu¹, Yinhuai Wang², Hanqi Liu¹, Jianhan Fu², Yuanqiao Zhao², Guoqiang Li^2*\u0000 </p><p>\u0000 ¹Department of Histology and Embryology, Xiangya School of Medicine, Central South University, Changsha, 410000, China</p><p>\u0000 ²Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, 410000, China</p><p>*<b>Corresponding author</b>: Guoqiang Li, Department of Urology, The Second Xiangya Hospital, Central South University, 139 Renmin road, Changsha, 410 000, China, Changsha, 410 000, China</p><p>Email: <span>[email protected]</span>\u0000 </p><p>All authors have agreed to this correction, and we apologize for any inconvenience this may have caused.</p><p>The correction does not affect the scientific validity or conclusions of the original paper.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 6","pages":"948"},"PeriodicalIF":4.4,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Choline Alleviated Perinatal Fluoride Exposure-Induced Learning and Memory Impairment Through α4β2 nAChRs and α7nAChRs in Offspring Mice”","authors":"","doi":"10.1002/tox.24488","DOIUrl":"10.1002/tox.24488","url":null,"abstract":"<p>Y. Zhao, X. Zhao, and J. Wang, “Choline Alleviated Perinatal Fluoride Exposure-Induced Learning and Memory Impairment Through α4β2 nAChRs and α7nAChRs in Offspring Mice,” <i>Environmental Toxicology</i> 38, no. 3 (2023): 511–521.</p><p>\u0000 <b>Modification:</b>\u0000 </p><p>The immunohistochemistry results of α4β2 nAChRs in the hippocampus and cerebral cortical of the HC+NaF group were replaced with the correct images.</p><p>We apologize for this error.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"40 6","pages":"946-947"},"PeriodicalIF":4.4,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24488","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the Causal Relationship Between 731 Immunocyte Phenotypes and Asthma Risk: A Bidirectional Mendelian Randomization Analysis","authors":"Jie Lin, Zhan Zhang, Qiang Zhou, Jiayi Shi, Wanqing Li, Sen Lin, Hu Tang, Zheyu Zhang, Tianfeng Chen, Xiaojun Cai, Longhe Cao","doi":"10.1002/tox.24506","DOIUrl":"https://doi.org/10.1002/tox.24506","url":null,"abstract":"Growing evidence suggests an association between various immune cell phenotypes and the development of asthma. However, it is still not entirely clear whether specific immune cell phenotypes might causally contribute to the risk of asthma. Despite further studies required to validate this claim, our study delves deeper into explaining this relationship and paving the way toward new therapeutic approaches. Our initial aim is to reveal the causal relationship between 731 immunocyte phenotypes and asthma; a bidirectional Mendelian randomization (MR) analysis was performed. We have investigated 731 immunocyte phenotypes in asthma, using a summary of previously published GWAS. Conducting an MR analysis, we have interpreted the potential causative relationship between them. Our analytical approaches included inverse variance‐weighted average, weighted median (WM) modeling, and pattern‐based approaches. To ensure the robustness and accuracy of our findings, we conducted sensitivity analyses employing MR‐PRESSO, Cochran's <jats:italic>Q</jats:italic> test, leave‐one‐out, and MR‐Egger approaches. Additionally, we conducted a reverse MR analysis to examine potential reverse causality. Our study revealed 43 immunophenotypes with a causal connection to asthma risk. Following Bonferroni correction and sensitivity analysis, we have identified four immunophenotypes with strong causal associations and reliability, them being: HLA DR on DC (95% CI: 1.0008–1.0014, <jats:italic>p</jats:italic> = 4.26 × 10<jats:sup>−6</jats:sup>, FDR = 2.21 × 10<jats:sup>−8</jats:sup>), CD8 on CD28− CD8br (95% CI: 1.0007–1.0020, <jats:italic>p</jats:italic> = 4.01 × 10<jats:sup>−5</jats:sup>，FDR = 5.70 × 10<jats:sup>−4</jats:sup>), CD62L on monocyte (95% CI: 0.9985–0.9995，<jats:italic>p</jats:italic> = 1.06 × 10<jats:sup>−4</jats:sup>，FDR = 9.20 × 10<jats:sup>−4</jats:sup>), CD8br% leukocyte (95% CI: 1.0006–1.0019，<jats:italic>p</jats:italic> = 1.07 × 10<jats:sup>−4</jats:sup>，FDR = 1.14 × 10<jats:sup>−3</jats:sup>). We have confirmed the large co‐inheritance of all these immunophenotypes, which suggests a contribution to asthma development. In addition, reverse MR confirmed that asthma and immune cell phenotypes lack a causal association between them. Our study provides evidence of different immune phenotypes, which are either beneficial or detrimental to asthma. Given the fact that asthma is a broad disease and contains complex immune mechanisms, this research may offer improved outcomes and long‐term asthma treatment strategies.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"4 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}