Inhalation Toxicology最新文献

{"title":"Inhaled aerosol dosimetry update.","authors":"Robert F Phalen, Chantal Darquenne, Jessica Oakes, Laleh Golshahi, Flemming R Cassee","doi":"10.1080/08958378.2026.2691193","DOIUrl":"https://doi.org/10.1080/08958378.2026.2691193","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate recent advances and current challenges in inhaled aerosol dosimetry research, with a focus on understanding how particles affect human health through deposited doses, and to identify key research needs for improving exposure assessment and risk evaluation.</p><p><strong>Methods: </strong>The findings were based on discussions and presentations from the Fourth International Aerosol Dosimetry Conference held in 2024 in Irvine, California. The conference used plenary sessions to promote cross-disciplinary communication and collaboration. Topics included computational models and simulations, in vitro and in vivo aerosol exposure systems, and variability in inhaled aerosol deposition. State-of-the-art research was presented, followed by open discussions to identify knowledge gaps and future priorities.</p><p><strong>Results: </strong>Significant advances were reported in computational modeling, particularly in integrating different model types to better represent all major regions of the respiratory tract. Improvements in in vitro exposure systems enhanced particle delivery, dose measurement, and applicability to human health studies. Research also highlighted the importance of the upper airways as entry routes for inhaled medications. Dose variability emerged as a critical issue across aerosol dosimetry studies. New findings showed that inhaled ultrafine particles may acquire surface coatings after deposition and can penetrate tissues, including fetal tissues. Standardization and validation of in vitro approaches were identified as essential steps for reducing reliance on animal testing and improving human risk assessment.</p><p><strong>Conclusion: </strong>Internal aerosol dosimetry research continues to advance through improved models, exposure systems, and mechanistic understanding of deposited particle behavior. However, addressing dose variability, standardizing alternative testing methods, and improving data sharing remain essential for advancing risk assessment and supporting more accurate evaluations of inhaled particle effects on human health.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-11"},"PeriodicalIF":2.1,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673646","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":"Oleanic acid inhibits LPS-induced inflammation and pyroptosis in pulmonary epithelial cells via mediation of TNFAIP3/NF-κB axis.","authors":"Xianghui Li","doi":"10.1080/08958378.2026.2670655","DOIUrl":"10.1080/08958378.2026.2670655","url":null,"abstract":"<p><strong>Background: </strong>The progression of sepsis seriously threatens people's life. In addition, acute lung injury can contribute to the injury of epithelial cells. Meanwhile, oleanic acid can inhibit the inflammatory responses in ALI, while the mechanism underlying the function of oleanic acid remains unclear.</p><p><strong>Methods: </strong>For investigating the impact of oleanic acid in ALI, pulmonary epithelial cells were treated with LPS. Then, CCK8 assay was employeed to detect the cell viability. RT-qPCR and western blot were applied for testing the mRNA and protein levels, respectively. Furthermore, ELISA was used to test the inflammatory factors in pulmonary epithelial cells.</p><p><strong>Results: </strong>Oleanic acid could significantly inhibit LPS-caused inflammation in pulmonary epithelial cells. LPS significantly induced pyroptosis in pulmonary epithelial cells <i>via</i> upregulation of NLRP3, ASC, cleaved caspase-1 and cleaved GSDMD, which was reversed by oleanic acid. In addition, oleanic acid notably reversed LPS-activated NF-κB signaling in cells. LPS obviously inhibited the level of TNFAIP3 in pulmonary epithelial cells, which was significantly reversed by oleanic acid. Knockdown of TNFAIP3 aggravated LPS-caused inflammation in pulmonary epithelial cells through activation of NF-κB signaling.</p><p><strong>Conclusion: </strong>Oleanic acid inhibits LPS-caused inflammation and pyroptosis in pulmonary epithelial cells <i>via</i> mediation of TNFAIP3/NF-κB axis, which may serve as a new agent against ALI.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"370-380"},"PeriodicalIF":2.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972198","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":"Regional and size-dependent effects of ambient agricultural particulate matter on Ah-receptor activity and inflammatory responses in human U937 macrophages.","authors":"Xiyuan Li, Jiang Chengcheng, Chuanzhen Zhang, Qianqian Lin, Savannah M D'Evelyn, Toby Clark, Keith J Bein, Qi Zhang, Alyssa Lundberg, Sarah Kado, Jack C Connolly, Thomas Haarmann-Stemmann, Christopher R Niedek, Yi He, Wei Li, Kent E Pinkerton, Christoph F A Vogel","doi":"10.1080/08958378.2026.2676722","DOIUrl":"10.1080/08958378.2026.2676722","url":null,"abstract":"<p><strong>Aims: </strong>Size-fractionated ambient particulate matter (PM) was collected from two of the most highly PM-polluted agricultural regions in California the Imperial Valley (PMIV), and San Joaquin Valley (Parlier, PMPA), to compare the effects of particle source, size, and duration of exposure on inflammatory gene expression, cell viability, and aryl hydrocarbon receptor (AhR) activation.</p><p><strong>Methods: </strong>Here we tested that the chemical composition of the PM would provoke different effects unique to the PM size fraction and with an association between exposure time, activation of AhR, and the expression of inflammatory genes. Human U937-derived macrophages were used to measure inflammatory biomarkers, cell viability and engulfment of PM. Particles across three size fractions - ultrafine (≥ 0.1 µm), fine (0.1-2.5 µm), and coarse (2.5-10 µm) were tested.</p><p><strong>Results: </strong>Gene expression varied by PM source, size, and duration of exposure. PMIV typically induced a greater level of gene expression than PMPA of the same size fraction. For the 12-h experiments, ultrafine and coarse particle fractions were the most potent stimulators of gene expression compared to the control, irrespective of PM source. The results show that ultrafine/fine PMIV and fine PMPA typically produced the greatest increase in mRNA levels compared to the control in an AhR-dependent manner.</p><p><strong>Conclusions: </strong>Ultrafine and fine PM from both sites (PMIV and PMPA) preferentially engaged AhR-dependent signaling, whereas coarse PM activated NF-κB-mediated inflammatory pathways. Overall, this study demonstrates PM size- and time-dependent effects on inflammatory gene expression and highlights a distinction between AhR- and NF-κB-driven responses across PM fractions.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"394-415"},"PeriodicalIF":2.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224682","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":"Acute ozone exposure results in airway epithelial and immune cell disturbances in mice.","authors":"Kshitiz Paudel, Sivapriya Ramamoorthy, Sonika Patial, Yogesh Saini","doi":"10.1080/08958378.2026.2673405","DOIUrl":"10.1080/08958378.2026.2673405","url":null,"abstract":"<p><strong>Objective: </strong>Elevated levels of ambient ozone (O₃), a criteria air pollutant produced by industries and automobiles, are significantly correlated with increased respiratory morbidity. Acute O₃ exposure disrupts airway epithelial integrity, compromising lung function and aggravating existing lung diseases. Despite prior work, the detailed kinetics of O₃-induced acute lung injury and resolution remain unclear.</p><p><strong>Methods: </strong>To delineate the temporal progression and resolution of O₃-induced acute lung injury in mice, we exposed eight-week-old female mice to filtered air or 1.5 ppm O3 for 4h and assessed lung injury markers at 12h, 36h, 60h, 108h, and 204h post-exposure.</p><p><strong>Results: </strong>Analysis of bronchoalveolar lavage fluid (BALF) revealed that neutrophil counts peaked at 12h and protein concentration at 36h, followed by a progressive decrease from 60h to baseline levels at 204h. The acute O₃ exposure also induced time-dependent alterations in multiple cytokines, including eotaxin, G-CSF, KC, MIP-1α, MIP-1β, IL-5, IL-6, IL-12, and MCP-1. At 12h post-exposure, severe denudation of airway epithelial cells was observed. Basal cell proliferation peaked between 36h and 60h, while ciliated cell restoration began at 60h, with normal epithelial composition achieved by 204h.</p><p><strong>Conclusion: </strong>This study elucidates the temporal sequence of events in O₃-induced acute lung injury, demonstrating a progression from initial epithelial damage and inflammatory cell infiltration to subsequent epithelial regeneration and inflammation resolution over 204h. These findings provide important insights into the kinetics of O₃-induced acute lung injury and repair mechanisms.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"381-393"},"PeriodicalIF":2.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13576332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148137891","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":"A Monte Carlo simulation for evaluating hypothetical mesothelioma risk in a person exposed to talcum powder.","authors":"Andrey A Korchevskiy, Ann G Wylie","doi":"10.1080/08958378.2026.2689661","DOIUrl":"10.1080/08958378.2026.2689661","url":null,"abstract":"<p><strong>Objective: </strong>Some of the varieties of talc were reported to contain a small fraction of elongate particles, including tremolite. The biological effects of tremolite were demonstrated in literature as dependent on the habit of particles (asbestiform vs. non-asbestiform). The objective of this paper is to utilize advanced methodologies of risk evaluation to determine if risk of mesothelioma could be elevated in persons utilizing talcum powder.</p><p><strong>Methods: </strong>Monte Carlo simulation was used to calculate potency factors, cumulative exposure, and mesothelioma risk for a hypothetical scenario.</p><p><strong>Results: </strong>Excess risk of mesothelioma for the person would be estimated as 0.22 cases per 1,000,000 per lifetime, with 5th percentile of 0.003 and 95th percentile of 0.873. Upper bound of excess mesothelioma risk is lower than the U.S. EPA benchmark for the general population and also comprises only about 1.4% of the mesothelioma baseline level in unexposed people. The morphological habit of tremolite particles reported in talc was typical for non-asbestiform variety.</p><p><strong>Conclusions: </strong>Quantitative risk assessment can be used to evaluate possible health outcomes of airborne exposure to talcum powder.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"355-369"},"PeriodicalIF":2.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338556","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":"Sex-specific associations between ambient air pollution exposure thresholds and lung function in middle-aged and older Canadians: an analysis of CLSA data.","authors":"Ugochukwu Odimba, Jamie Farrell, Mohsen Sadatsafavi, Xianta Jiang, Zhiwei Gao","doi":"10.1080/08958378.2026.2700549","DOIUrl":"https://doi.org/10.1080/08958378.2026.2700549","url":null,"abstract":"<p><strong>Background: </strong>Ambient air pollution is associated with reduced lung function, but whether sex modifies the association with threshold-based exposures remains unclear. This cross-sectional study examined sex-specific associations between threshold-based exposures to fine particulate matter (PM_2.5), nitrogen dioxide (NO₂), ozone (O₃), and lung function.</p><p><strong>Methods: </strong>Data from 21,339 adults aged 45-85 years in the Canadian Longitudinal Study on Aging were analyzed. Annual average air pollutant concentrations representing multi-year exposure estimates (2012-2015) were assigned to participants based on their residential postal codes. Decision tree regression was used to derive exposure cut points and classify participants into low, intermediate, and high exposure thresholds for each pollutant with respect to lung function (FEV₁, FVC, and FEV₁/FVC ratio). Survey-weighted multivariable linear regression models were used to estimate sex-specific associations with percent-predicted lung function, including interaction terms between sex and exposure thresholds.</p><p><strong>Results: </strong>Significant sex interactions were observed for PM_2.5 and NO₂ with percent-predicted FEV₁ and FVC, and for O₃ with percent-predicted FVC and the FEV₁/FVC ratio. Among males, high vs. low PM_2.5 exposure was associated with lower FEV₁ (-3.11%; 95% CI: -4.47, -1.74) and FVC (-2.72%; 95% CI: -3.76, -1.69). Among females, a significant but smaller FVC reduction was observed (-1.53%; 95% CI: -2.59, -0.47) but not for FEV₁. High vs. low NO₂ exposure was associated with greater reductions in FEV₁ among males (-5.00%; 95% CI: -7.16, -2.84) than among females (-1.99%; 95% CI: -2.79, -1.19), and significantly reduced FVC among males(-3.58%; 95% CI: -5.15, -2.00) but not among females (-1.64%; 95% CI: -3.39, 0.11). High vs. low O₃ exposure was associated with reduced FVC in both sexes, with a stronger association among males (-3.34%; 95% CI: -4.37, -2.31) than among females (-2.60%; 95% CI: -3.56, -1.65).</p><p><strong>Conclusions: </strong>Sex significantly modified the inverse associations between ambient air pollution exposure thresholds and lung function, with greater reductions observed in males. These associations occurred at exposure thresholds at or below current regulatory standards, underscoring the need for continuous reassessment of air quality guidelines to better protect respiratory health.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-17"},"PeriodicalIF":2.1,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455798","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":"Establishing an air-liquid interface system for exposure of mouse laryngeal epithelial cells to cigarette smoke.","authors":"Akari Kimura, Amirbahador Golchin, Meena Easwaran, Patrick Timothy Kiessling, Mohammed Imran Khan, Joshua D Martinez, Elizabeth Erickson-DiRenzo","doi":"10.1080/08958378.2026.2657360","DOIUrl":"10.1080/08958378.2026.2657360","url":null,"abstract":"<p><strong>Objective: </strong>The laryngeal epithelium is one of the first lines of defense against inhaled insults, including cigarette smoke (CS). However, a lack of suitable <i>in vitro</i> models has limited mechanistic studies of laryngeal epithelial injury and disease pathogenesis in response to CS. The purpose of this investigation was to establish an air-liquid interface (ALI) system for modeling airborne CS exposure in laryngeal epithelial cells.</p><p><strong>Methods: </strong>Primary mouse laryngeal epithelial cells were harvested, cultured, and transitioned from submerged to ALI conditions to induce epithelial differentiation. ALI cultures were characterized by electrophysiological evaluation of transepithelial resistance (TEER), histology, and immunofluorescent staining and quantification for epithelial markers and compared with native laryngeal tissue. ALI cultures were exposed to increasing doses of CS during differentiation, and epithelial barrier integrity was assessed by evaluating cytotoxicity, TEER, and structure.</p><p><strong>Results: </strong>Submerged laryngeal epithelial cultures were primarily proliferating basal cells. Differentiated ALI cultures demonstrated progressive epithelial maturation, with formation of a multilayered structure and high TEER, indicative of robust barrier integrity. Epithelial marker localization in ALI cultures closely resembled that of native mouse vocal fold epithelium. CS exposure disrupted epithelial barrier integrity in a dose-dependent manner, including increased cytotoxicity and reductions in TEER. Moderate exposure permitted some recovery of function and structure, underscoring the intrinsic resilience of laryngeal epithelial cells.</p><p><strong>Conclusion: </strong>This investigation establishes a physiologically relevant <i>in vitro</i> model system that recapitulates key features of native laryngeal epithelium and provides a robust platform for investigating the cellular and molecular pathways governing CS-induced epithelial injury and repair.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"321-338"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770338","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":"Exposure to electronic cigarette aerosols triggers alterations in genomic DNA methylation that impacts cancer pathways in mice.","authors":"Christina Awada, Catherine B Klein, Terry Gordon, Amna Raja, Kent E Pinkerton, Morgan Poindexter, Emma Karey, Arul Veerappan, Judith T Zelikoff","doi":"10.1080/08958378.2026.2649516","DOIUrl":"10.1080/08958378.2026.2649516","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this laboratory study was to characterize the effects of sub-chronic electronic cigarette (E-cig) aerosol exposures on genome-wide DNA methylation in mice to begin to elucidate the pathophysiology of E-cig-related pulmonary diseases and cancer.</p><p><strong>Materials and methods: </strong>Male C57BL/6 and FVBN mice were randomly assigned to one of two treatment groups (n = 6 per group) and exposed daily to either filtered air or a 50:50 mixture of propylene glycol and vegetable glycerol containing 24 mg/mL nicotine (+Nic). Whole-body inhalation exposures were conducted for 3 h/d, 5 d/week, for a total of 1-month. Sequences for ∼285 000 CpG probes were aligned to the mouse genome, and mixed linear models were used to model DNA methylation levels (β values). These evaluations were followed by ingenuity pathway analysis (IPA), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Ontology (GO) analysis.</p><p><strong>Results and discussion: </strong>E-cig inhalation exposure induced significant DNA methylation changes in adult male mice, with a notable impact on cancer-related pathways. A total of 2300 genes in C57BL/6 mice and 6732 genes in FVBN mice were hypomethylated, while 1673 and 5529 genes were hypermethylated, respectively. KEGG and GO analyses highlighted key pathways such as Wnt/β-catenin signaling and proteoglycans in cancer, suggesting that E-cig aerosol exposure could disrupt critical genomic regulation and potentially promote carcinogenesis. These in vivo findings underscore the potential cancer-promoting effects of E-cig aerosols through epigenetic modifications.</p><p><strong>Conclusions: </strong>Findings from this study provide compelling evidence that sub-chronic E-cig exposure induces genomic DNA methylation changes linked to cancer pathways in two strains of adult male mice, highlighting the serious adverse consequences of E-cig use and strain-specific response differences.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"297-320"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13629434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770317","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":"Mapping six decades of air pollution and cardiovascular health research: global trends, collaborations, and emerging themes.","authors":"Saanu Sidharthan, Gurleen Kaur Anand","doi":"10.1080/08958378.2026.2673442","DOIUrl":"10.1080/08958378.2026.2673442","url":null,"abstract":"<p><strong>Background: </strong>Air pollution is a major global health concern and a well-established risk factor for cardiovascular disease (CVD). While earlier bibliometric efforts provided useful insights into early research patterns using MeSH term clustering, they were limited in scope and time frame. A more comprehensive synthesis is needed to reflect the expanding and evolving nature of this field.</p><p><strong>Objectives: </strong>To map the global research landscape on air pollution and cardiovascular health, identifying trends, key contributors, and thematic developments through bibliometric analysis.</p><p><strong>Methods: </strong>A bibliometric study was conducted using the Scopus database, including 6,663 publications from 1963 to 2025. Data was analyzed using Bibliometrix (R), VOSviewer, and CiteSpace. Analytical approaches included performance analysis, coauthorship networks, co-citation mapping, keyword co-occurrence, and thematic evolution analysis.</p><p><strong>Results: </strong>The dataset showed an annual growth rate of 6.83%, with contributions from 22,322 authors across 1,658 sources<i>. Environmental Health Perspectives</i> was the most prolific journal. Keyword analysis revealed dominant themes such as PM_2.5, cardiovascular outcomes (e.g. hypertension, myocardial infarction), and biological mechanisms (e.g. inflammation, oxidative stress). Thematic evolution reflected a shift from acute exposure studies to broader interdisciplinary concerns like climate change, urban planning, and environmental justice. Collaboration networks highlighted strong interregional partnerships, particularly among North American, European, and Asian researchers. However, contributions from low-income regions remain limited.</p><p><strong>Conclusion: </strong>This study provides an expanded and updated overview of research linking air pollution to cardiovascular health. By building on earlier bibliometric work, it highlights emerging interdisciplinary priorities and underscores the need for equitable, evidence-based policy responses to environmental health risks.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"283-296"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940900","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 impact of increased living temperature on the cardiopulmonary response of male and female mice to benzene toluene ethylbenzene and xylene (BTEX).","authors":"Sydnie Toler, Michelle F Fyle, Logan Klein, Molly Vaziri, Brendan Yoo, Ashley Lewis, Chloe Davis, Wendy Oshiro, Mette Schladweiler, Wanda Williams, Thomas Jackson, Paul Evansky, M Ian Gilmour, Aimen K Farraj, Mehdi S Hazari","doi":"10.1080/08958378.2026.2670650","DOIUrl":"10.1080/08958378.2026.2670650","url":null,"abstract":"<p><strong>Objective: </strong>Benzene, toluene, ethylbenzene, and xylene (BTEX) are ubiquitous pollutants, and leakage of underground storage tanks has increased the risk of inhalation exposure and health effects that are likely impacted by ambient temperature.</p><p><strong>Methods: </strong>In this study, male and female C57BL6J mice were housed at either normal (NT - 70 °F/22 °C) or high temperature (HT - 90 °F/32 °C) for five weeks, followed by nose-only exposure to either filtered air (FA) or BTEX (316 ppm) for four hours on two consecutive days. Whole-body plethysmography was performed after the first exposure and high-frequency echocardiography after the second.</p><p><strong>Results: </strong>HT significantly increased tidal volume (TV), and inspiratory/expiratory times (Ti/Te) and flows (PIF/PEF) and decreased enhanced pause (Penh) in female and male mice. At NT, BTEX increased frequency (f) and decreased Ti and Te in female mice but not male. At HT, BTEX decreased f and Penh and increased TV, Te, Ti, and relaxation time (RT) in female mice, and only increased TV, PEF, PIF in males. HT caused a significant decrease in heart rate in female mice, while BTEX reversed that effect. Dobutamine increased HR in all HT females and cardiac output (CO) in males. BTEX decreased HR and CO in the latter.</p><p><strong>Discussion: </strong>Thus, BTEX altered breathing and cardiovascular function in a sex-dependent manner, causing rapid ventilation in females, irrespective of temperature, whereas BTEX caused cardiovascular decrements in only HT males challenged with exercise-like stress. These results indicate that sex and ambient temperature play a role in BTEX cardiopulmonary effects, which underscores their importance for air pollution risk.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"339-353"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948288","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}