Inhalation Toxicology最新文献

{"title":"Sputum and nasal lavage lung-specific biomarkers in occupational exposure to nanomaterials; a mixed methods systematic review with meta-synthesis and meta-analysis.","authors":"Nafiseh Nasirzadeh, Jamal Biganeh, Erfan Khalatbari, Saman Mohammadpour, Soqrat Omari Shekaftik","doi":"10.1080/08958378.2025.2544713","DOIUrl":"10.1080/08958378.2025.2544713","url":null,"abstract":"<p><p>The main route of occupational exposure to nanomaterials is inhalation. Sputum and nasal lavage are the most important biological samples to analyze lung-specific biomarkers in occupational exposure. So, the aim of this study is to conduct a mixed-method systematic review with meta-synthesis and meta-analysis for assessment of sputum and nasal lavage lung-specific biomarkers in occupational exposure to nanomaterials. This systematic review was conducted through the end of June 2025. Search was done using 'Biomarkers', 'Occupational exposure', 'Sputum', 'Nanomaterials' and 'Nasal Lavage' keywords on PubMed, Scopus and WOS. After the data extraction, qualitative data was used to draw a qualitative model. Comprehensive Meta-Analysis Software (CMA) was used for meta-analysis and the pooled mean concentration of the biomarkers were calculated by the random effect model (REM). Thirty-three studies were primarily achieved, and six studies were finally analyzed. Pro-inflammatory, inflammatory, oxidative stress, cancer/fibrosis and cardiovascular biomarkers were the most important biomarkers investigated. Inflammatory biomarkers including IL-6, IL-8, IL-1β and TNF-α were involved better than other inflammatory biomarkers in nasal, in occupational exposure to nanomaterials. The pooled mean concentration of sputum inflammatory biomarkers interleukin including IL-1β, IL-2, IL-4, IL5, IL-6, IL-8 was estimated 404.76, 196.9, 156.47, 219.26, 33.98 and 2344.42 pg/mL, respectively. Moreover, concentration of Nasal lavage inflammatory biomarkers interleukin including IL-1β, IL-6, and IL-8 were 1.438, 0.911 and 17.847 pg/mL, respectively. Due to a lack of information about OEL for nanomaterials, evaluating the occupational exposure to them through measuring the level of specific biomarkers, especially in the upper respiratory system, requires more studies.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"241-255"},"PeriodicalIF":2.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144872971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The immunological impact of traffic-related air pollution in an Iraqi population; a prospective cross-sectional study.","authors":"Salih A Hama, Dunya H Bapir, Hawbash M Rahim, Gasha S Ahmed","doi":"10.1080/08958378.2025.2549544","DOIUrl":"10.1080/08958378.2025.2549544","url":null,"abstract":"<p><strong>Objective: </strong>Iraqi automobiles use some of the poorest quality fuel in the world, characterized by extremely high sulfur content. In this study, we aim to investigate the immunological impact of traffic-related air pollution (TRAP) on individuals residing in the Kurdistan Region of Iraq.</p><p><strong>Materials and methods: </strong>This prospective cross-sectional study (June 2021 and January 2022) assessed the immunological profile of 77 male participants in Sulaymaniyah Governorate who were grouped based on predefined exposure zones; High TRAP Group (<i>n</i> = 46) from urban areas with high exposure to TRAP and Low TRAP Group (<i>n</i> = 31) from rural areas with low exposure. An Aeroqual Series 500 monitor was used to estimate 24-hour arithmetic mean concentrations of PM1.0, PM2.5, and PM10 in the two exposure zones.</p><p><strong>Results and discussion: </strong>Age distribution was comparable between the groups. Participants of High TRAP Group had significantly lower total lymphocyte counts (1.09 ± 0.36 vs. 1.90 ± 0.41, <i>p <</i> 0.001), T-cell (601.41 ± 60.02 vs. 799.80 ± 56.04; <i>p <</i> 0.001), B-cell levels (113.05 ± 48.23 vs. 230.68 ± 57.90; <i>p <</i> 0.001), IgG (11.94 ± 2.52 vs. 13.35 ± 2.77; <i>p =</i> 0.024), and IgM levels (0.96 ± 0.40 vs. 1.4 ± 0.66, <i>p <</i> 0.001) compared to Low TRAP Group. No significant differences were found in total WBC, granulocytes, or IgA levels <i>(p</i> > 0.05<i>)</i>. The presence of inflammatory diseases (mostly thyroiditis) was significantly more common among the individuals of High TRAP Group (13, 28.26% vs. 3, 9.68%; <i>p =</i> 0.048).</p><p><strong>Conclusion: </strong>Individuals with high exposure to TRAP are associated with significant reductions in lymphocyte count, IgM and IgG levels.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"284-292"},"PeriodicalIF":2.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling environmental inhalant exposure in rheumatoid arthritis.","authors":"Caroline de Ocampo, K Michael Pollard, Lisa M F Janssen","doi":"10.1080/08958378.2025.2542555","DOIUrl":"10.1080/08958378.2025.2542555","url":null,"abstract":"<p><p>The mucosal origins hypothesis posits that environmental inhalant exposures, including cigarette smoke (CS) and crystalline silica (c-silica), trigger immune responses in the lung mucosa, an extra-articular site, which precede initiating events of rheumatoid arthritis (RA) pathogenesis in distant joints. Epidemiological data strongly associates these exposures with RA risk, especially in genetically susceptible individuals carrying HLA-DRB1 alleles, and with the production of autoantibodies such as anti-citrullinated peptide antibodies (ACPA) and rheumatoid factor (RF). However, establishing causality remains challenging due to unsynchronized exposure and disease onset and the lack of suitable animal models to study early disease events. This review synthesizes evidence linking inhalant exposures to RA, focusing on CS and c-silica, and evaluates experimental animal models used to investigate disease initiation and progression in the context of inhalant exposures. While models like collagen-induced arthritis (CIA) replicate joint pathology, they often fail to capture the lung-joint axis and gene-environment interactions critical for RA onset. We highlight the need for refined models with genetic susceptibility to subclinical autoimmunity to better mimic human RA, emphasizing the importance of standardized exposure protocols to address variability in outcomes. These advancements are crucial for elucidating mechanisms of inhalant exposure-induced RA and developing preventive strategies.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"217-240"},"PeriodicalIF":2.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12453084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TMEM175 activity in BK-deficient macrophages maintains lysosomal function and mediates silica-induced inflammatory response in macrophages.","authors":"Rebekah L Kendall, Britten Postma, Andrij Holian","doi":"10.1080/08958378.2025.2507251","DOIUrl":"10.1080/08958378.2025.2507251","url":null,"abstract":"<p><p><b>Objective:</b> Lysosomal ion channel function in macrophages contributes to the development of silica-induced inflammation. Recent studies have shown that blocking K⁺ entry into the lysosome <i>via</i> the BK channel reduces silica-induced damage and inflammation in macrophages. This study aims to explore the mechanisms of particle-induced inflammation in BK^-/- macrophages. <b>Methods:</b> Bone marrow derived macrophages (BMdM) from C57BL/6 wildtype (WT) and BK^-/- mice were exposed <i>in vitro</i> to silica and IL-1β release and cell death assessed. The effect of BK^-/- on lysosomal pH, proteolytic activity, and cholesterol accumulation was evaluated. <b>Results:</b> BK^-/- BMdM failed to demonstrate a reduction in IL-1β or cell death following silica exposure. BK^-/- BMdM had comparable lysosome function to WT suggesting a compensatory mechanism was maintaining lysosome function. BK^-/- macrophages demonstrated an upregulation of a second lysosomal potassium channel, TMEM175. Inhibition of TMEM175 activity caused an increase in lysosomal pH and reduced silica-induced cell death and IL-1β release in both BK^-/- and WT BMdM. <b>Conclusion:</b> BK^-/- BMdM did not exhibit the same phenotype seen with pharmaceutical abrogation of BK channel activity and showed no differences from WT in response to silica exposure. Upregulation of TMEM175 in BK^-/- macrophages appears to prevent changes in lysosomal pH and cholesterol accumulation. Inhibiting TMEM175 activity in both BK^-/- and WT BMdM resulted in an increase in lysosomal pH and reduced silica-induced inflammation, suggesting that reduced particle-induced cell damage and inflammation is not dependent on the activity of a single lysosomal ion channel but rather on mechanisms that elevate lysosomal pH.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"173-182"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12303735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Fli1 transcription factor aggravates lipopolysaccharide-induced human pulmonary microvascular endothelial cell dysfunction by regulating CXCL2 promoter.","authors":"Zhou Zheng, Lei Liu, Hao Zhang, Siming Chen","doi":"10.1080/08958378.2025.2510311","DOIUrl":"10.1080/08958378.2025.2510311","url":null,"abstract":"<p><strong>Objective: </strong>Pulmonary microvascular endothelial cell (PMEC) injury is a hallmark of septic acute lung injury (ALI). Elevation of chemokine C-X-C motif ligand 2 (CXCL2) is associated with inflammatory response in various diseases. Recent studies have demonstrated the involvement of CXCL2 in septic ALI. Herein, the role and mechanism of CXCL2 in regulating PMEC inflammation and apoptosis in septic ALI were explored.</p><p><strong>Materials and methods: </strong>Human PMECs (HPMECs) were treated with lipopolysaccharide (LPS) for the establishment of <i>in vitro</i> septic ALI models. HPMEC viability was validated using CCK-8 assay. HPMEC apoptosis was evaluated by flow cytometry analysis. Measurement of proinflammatory cytokine concentration was conducted using enzyme-linked immunosorbent assay kits. RT-qPCR were required for determining gene levels. Western blotting was prepared for testing friend leukemia integration 1 (Fli1) and CXCL2 protein levels. The binding of Fli-1 to CXCL2 promoter was confirmed by chromatin immunoprecipitation and luciferase reporter assays.</p><p><strong>Results: </strong>LPS upregulated CXCL2 expression in HPMECs. Moreover, LPS administration suppressed HPMEC viability and accelerated HPMEC inflammation and apoptosis, which was antagonized by CXCL2 depletion. Mechanistically, Fli1 served as a transcription factor and bound to CXCL2 promoter. In rescue assays, CXCL2 overexpression counteracted the restrictive impact of Fli1 deficiency on LPS-induced HPMEC apoptotic behaviors and inflammatory response.</p><p><strong>Conclusions: </strong>The Fli1 transcription factor aggravates LPS-induced HPMEC dysfunction <i>via</i> binding to CXCL2 promoter in septic ALI.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"183-194"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An economical in vitro model of wood smoke exposure.","authors":"Jennifer Krznarich, Tessa Schumann, James Bjork, Matthew Slattery, Sarah E Lacher","doi":"10.1080/08958378.2025.2523297","DOIUrl":"10.1080/08958378.2025.2523297","url":null,"abstract":"<p><strong>Objective: </strong>The increasing frequency and intensity of wildfires pose significant environmental and public health risks. While existing research has highlighted the effects of wildfire smoke exposure on chronic diseases, the cellular and molecular mechanisms underlying these effects remain unclear. <i>In vitro</i> exposure systems are necessary to dissect the effects of wood smoke on various cell types, but current <i>in vitro</i> exposure systems are often expensive and technically complex. This study introduces the GunSmoke Exposure Chamber (GSEC), a cost-effective, user-friendly system for modeling wildfire smoke exposure.</p><p><strong>Materials and methods: </strong>The GSEC consists of readily available components, including a 25 L egg incubator, a food service smoke infuser gun, and an at-home air quality monitor. The BEAS-2B human bronchial epithelial cell line was used to assess its effectiveness in activating wood smoke-responsive and xenobiotic signaling pathways.</p><p><strong>Results: </strong>Gene expression analysis confirmed activation of the NRF2 and AhR xenobiotic response pathways after wood smoke exposure. The GSEC will allow researchers to model a variety of exposure conditions. The GSEC can also be adapted for more complex protocols, specialized culture systems and a variety of cell types.</p><p><strong>Conclusion: </strong>The GSEC provides an affordable and practical approach for studying wildfire smoke exposure. Its adaptability and accessibility make it a valuable tool for investigating the public health impact of wildfire smoke under different experimental conditions.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"208-215"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Saikosaponin D ameliorates sepsis-induced acute lung injury by maintaining alveolar epithelial barrier integrity and inhibiting ferroptosis via Nrf2/HO-1 pathway.","authors":"Lijie Song, Yanyan Tao, Guoyu Lu, Chenchen Wu","doi":"10.1080/08958378.2025.2519006","DOIUrl":"10.1080/08958378.2025.2519006","url":null,"abstract":"<p><strong>Background: </strong>Saikosaponin D (SSD), a triterpenoid saponin extracted from <i>Bupleurum chinensis</i>, has many pharmacological properties. The goal of our study is to assess the roles and mechanisms of SSD in septic acute lung injury (ALI).</p><p><strong>Methods: </strong>ALI in mice was induced by cecal ligation and puncture (CLP). After CLP surgery, mice were intragastrically administered with SSD (4 mg/kg) or vehicle for five consecutive days. Alveolar epithelial barrier function was detected by measuring total protein in BALF and tight junction proteins in lung tissues. Morphological changes of lung tissues were examined by hematoxylin-eosin staining. ROS content in lung tissues was measured by DHE staining. GSH and MDA levels were estimated to evaluate oxidative stress. Western blotting was used to evaluate protein levels. An <i>in vitro</i> model of septic lung injury was established in MLE-12 cells <i>via</i> LPS stimulation. Cytotoxicity, TEER values, and FITC-dextran flux were detected. Intracellular ROS content was evaluated by DCFH-DA staining.</p><p><strong>Results: </strong>SSD improved alveolar epithelial barrier function and suppressed ferroptosis in CLP-induced septic mice. SSD activated Nrf2/HO-1 signaling in CLP mice and LPS-exposed MLE-12 cells. ML385 (an Nrf2 inhibitor) attenuated SSD-mediated protective effects against ferroptosis and alveolar epithelial cell barrier dysfunction <i>in vitro</i>.</p><p><strong>Conclusion: </strong>SSD ameliorates septic ALI by maintaining alveolar epithelial barrier integrity and suppressing ferroptosis <i>via</i> the activation of Nrf2 signaling.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"195-207"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/08958378.2025.2514900","DOIUrl":"10.1080/08958378.2025.2514900","url":null,"abstract":"","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"216"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The empirical metric of mesothelial carcinogenicity for carbon nanotubes and elongate mineral particles.","authors":"Andrey A Korchevskiy, Ann G Wylie","doi":"10.1080/08958378.2025.2486087","DOIUrl":"10.1080/08958378.2025.2486087","url":null,"abstract":"<p><strong>Introduction: </strong>Carcinogenic potential of elongate particles depends on many characteristics, with dimensional parameters playing an important role at all stages of disease origination and progression. It is important to develop quantitative metrics of mesothelial carcinogenicity for particles in order to predict their behavior within biological systems. It would be especially valuable if such metrics could be developed for both carbon nanotubes (CNTs) and elongate mineral particles (EMPs) to demonstrate similarities and differences in the estimations of mesothelioma risk.</p><p><strong>Methods: </strong>The database is organized with dimensional characteristics of EMPs, containing 570,950 records for 246 asbestiform, non-asbestiform, and mixed datasets. A database on carbon nanotubes (CNTs) with various toxicological outcomes of animal experiments, including mesothelioma, was also created. Mathematical modeling was used to determine the best metric of mesotheliomagenicity that would work for CNTs and EMPs.</p><p><strong>Results: </strong>The dimensional coefficient of carcinogenicity (DCC) was introduced with the formula DCC = 1-exp(-AxSA/(BxWidth³+C)), where SA - surface area of the elongate particle, Width - particle width, A, B, C - coefficients. It was demonstrated that DCC can efficiently determine mesotheliomagenic varieties of CNTs and EMPs, with a threshold for carcinogenic potential of 0.05 with <i>A</i> = 0.11, <i>B</i> = 1000, <i>C</i> = 1.</p><p><strong>Discussion: </strong>The new quantitative metric of carcinogenicity can be used for the purposes of mineralogical evaluation and toxicological analysis. It was confirmed that DCC-based models predict negligible mesothelioma potency for non-asbestiform amphiboles.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"107-132"},"PeriodicalIF":2.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of functional roles and therapeutic targets of the STAT pathway in PM_2.5-induced allergic rhinitis.","authors":"ChiHang Zhang, JianShu Guo, Lei Lei, Lu Yu, DongXia Fan, Biao Wu, Ge Wang, WenQing Zhang, Lin Lin, XinLei Xu, XiHao Du, JinZhuo Zhao","doi":"10.1080/08958378.2025.2502791","DOIUrl":"10.1080/08958378.2025.2502791","url":null,"abstract":"<p><strong>Background: </strong>Increasing evidence suggests that exposure to fine particulate matter (PM_2.5) is associated with an elevated risk of respiratory diseases. However, the precise mechanisms by which PM_2.5 influences inflammatory processes in allergic rhinitis (AR) remain insufficiently understood. The STAT pathway has been identified as a critical mediator of immune and inflammatory responses, but its specific role in modulating PM_2.5-induced effects in the nasal mucosa of AR remains unclear. This study aims to investigate the impact of PM_2.5 on the STAT pathway in the inflammatory response of the nasal mucosa during AR.</p><p><strong>Methods: </strong>We analyzed mRNA expression profiles (GSE215411) from the Gene Expression Omnibus (GEO) database to investigate the effects of PM_2.5 on human nasal mucosa-derived fibroblasts. Differential expression analysis identified differential expression genes (DEGs), which were visualized through hierarchical clustering and radar plots. GO/KEGG enrichment and Gene Set Enrichment Analysis (GSEA) identified key pathways, focusing on STAT pathway enrichment. Protein-protein interactions (PPIs) within the STAT pathway were analyzed using STRING and Cytoscapedatabase, revealing immune response and cytokine signaling as predominant functional pathways. An AR model, induced by ovalbumin sensitization and whole-body ambient PM_2.5 exposure, was utilized to assess the activation of the STAT pathway in nasal mucosal tissue.</p><p><strong>Results: </strong>A total of 426 DEGs were identified in human nasal mucosa-derived fibroblasts following PM_2.5 exposure, emphasizing STAT pathway involvement. Validation in an AR mouse model confirmed that allergens and PM_2.5 activate the STAT pathway, modulating Th2 and inflammatory cytokines.</p><p><strong>Conclusion: </strong>PM_2.5 exposure significantly activates the STAT pathway in the nasal mucosa of AR, amplifying Th2-related inflammatory cytokine response.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"156-171"},"PeriodicalIF":2.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}