Inhalation Toxicology最新文献

{"title":"Meta-analysis of the association between low concentration PM_2.5 and cardiovascular mortality in the United States and Canada.","authors":"Chloe S Chung, Giffe T Johnson, Annette C Rohr","doi":"10.1080/08958378.2025.2457639","DOIUrl":"https://doi.org/10.1080/08958378.2025.2457639","url":null,"abstract":"<p><strong>Objectives: </strong>The adverse effects of fine particulate matter (PM_2.5), including cardiovascular outcomes, are well established. This review and meta-analysis investigates the association between long-term exposure to low concentration PM_2.5 (<12 µg/m³) and CVD mortality in U.S. and Canadian populations.</p><p><strong>Methods: </strong>We conducted a literature search and completed random effect meta-analyses.</p><p><strong>Results: </strong>Twenty-four studies were reviewed, with 12 from each of the U.S. and Canada. Fifteen of eighteen studies that reported hazard ratios (HRs) for total CVD mortality reported statistically significant positive associations with low concentration PM_2.5. For cause-specific CVD mortality, more consistent results were shown for ischemic heart disease (IHD) mortality, with all eleven studies reporting statistically significant associations (HR = 1.09 to 2.48). Only three of 12 studies evaluating cerebrovascular mortality reported statistically significant associations (HR = 1.10 to 1.27). Studies that restricted analyses to participants with mean exposures <12 µg/m³ found statistically significant associations between PM_2.5 and at least some of the CVD mortality outcomes of interest. However, the shape of the concentration-response functions varied widely. Only six studies controlled for at least one additional air pollutant, and multi-pollutant models generally showed an attenuated impact of PM_2.5. Despite existing gaps in understanding the association between low concentrations of PM_2.5 and cardiovascular mortality, this review highlights the critical importance of ongoing efforts to improve air quality for public health benefits.</p><p><strong>Conclusions: </strong>Continued focus on understanding the shape of the concentration-response function for PM_2.5, the impact of co-pollutants on observed effects, and how particle composition may impact effect estimates, is recommended.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-17"},"PeriodicalIF":2.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364637","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":"Mouse pulmonary response following solid surface composite dust inhalation.","authors":"W Kyle Mandler, Walter G McKinney, Mark Jackson, Alycia K Knepp, Sarah L Keeley, Sherri A Friend, Lori A Battelli, Yong Qian","doi":"10.1080/08958378.2024.2447699","DOIUrl":"https://doi.org/10.1080/08958378.2024.2447699","url":null,"abstract":"<p><p><b>Purpose</b>: Pulmonary exposure to emissions from manipulating solid surface composite (SSC) materials has been associated with adverse health effects in humans and laboratory animals. Previous <i>in vitro</i> and <i>in vivo</i> investigations of SSC toxicity have been limited by particle delivery methods that do not fully recapitulate the workplace environment. This study sought to determine the acute SSC-induced pulmonary responses <i>via</i> whole-body inhalation exposure. <b>Materials and Methods</b>: A chamber for dust particle generation and an exposure system for characterization and animal exposures was constructed. The system successfully generated SSC at a concentration of 19.9 ± 1.5 mg/m³. The aerosol count median aerodynamic diameter was 820 nm. First, C57BL/6 mice were exposed to SSC particles for 4 h (<i>n</i> = 6) or filtered air control followed by euthanasia either immediately or 24 h post-exposure. Lungs were analyzed for aluminum (Al) content using inductively coupled plasma atomic emission spectroscopy (ICP-AES) which measured a lung deposition of 19.13 ± 5.03 µg/g elemental Al, or approximately 64 µg/g SSC dust. Second, a group of mice (<i>n</i> = 9) was exposed to SSC particles at 20 mg/m³ for 4 days, 4 h/day to assess the acute and sub-chronic pulmonary effects of SSC inhalation. Animals were euthanized at 1- and 56-days post-exposure. <b>Results</b>: Total estimated pulmonary deposition for these animals was 49.2 µg SSC dust/animal. No histopathologic changes were observed at any post-exposure time point; however, BALF total protein was increased at 1-day post-exposure. <b>Conclusions</b>: We conclude that exposure to dust from cutting SSC at this dose and post-exposure durations induces mild, transient inflammation.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-13"},"PeriodicalIF":2.0,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004757","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":"Urinary oxidative stress biomarkers in nephrotoxicity induced by PM_2.5 in a rat model.","authors":"Jessica Baldriche-Acosta, Marisela Uribe-Ramírez, Juana Narváez-Morales, Andrea De Vizcaya-Ruiz, Olivier Christophe Barbier, Octavio Gamaliel Aztatzi-Aguilar","doi":"10.1080/08958378.2025.2450393","DOIUrl":"10.1080/08958378.2025.2450393","url":null,"abstract":"<p><strong>Objective: </strong>The present study evaluated urinary oxidative stress (OxS) biomarkers to explain the extrapulmonary effect of renal function decline due to subchronic inhalation exposure to particles smaller than 2.5 μm, as well as the correlation of the biomarkers with the particles' endotoxin content.</p><p><strong>Materials and methods: </strong>Adult male Sprague-Dawley rats were exposed to subchronic inhalation of particles smaller than 2.5 μm (8 weeks, 4 days/week, 5 h/day). The control group was exposed to filtered air. MiniVol and HiVol samplers were used to estimate the concentration and collected particles, respectively. Biomarkers were assessed in weekly urine samples harvested by the metabolic cage. The OxS biomarkers assessed were methylglyoxal, non-esterified fatty acids, malondialdehyde, advanced oxidative protein products, arginase, myeloperoxidase, glutathione S-transferase, and gamma-glutamyl transferase, all of which were evaluated by colorimetric assays. Creatinine was evaluated by the Jaffe reaction, and cystatin-C (Cys-C) and neutrophil gelatinase-associated lipocalin-2 were quantified using Luminex technology. Endotoxin content was analyzed with the Limulus Amebocyte Lysate Pyrochrome Chromogenic Test Kit.</p><p><strong>Results and discussion: </strong>Subchronic exposure to PM_2.5 increased OxS biomarkers in urine. Endotoxin content showed a positive correlation with the urinary OxS biomarkers evaluated. Additionally, urinary OxS biomarkers correlated with creatinine and the early kidney damage biomarkers Cys-C and neutrophil gelatinase-associated lipocalin-2, where the strongest and positive correlations were observed with the latter two biomarkers.</p><p><strong>Conclusions: </strong>Inhalation of environmental airborne particles smaller than 2.5 μm increased urinary OxS biomarkers, correlated with endotoxin content and early kidney damage biomarkers. This finding corroborates the extrapulmonary nephrotoxic effect of inhaled particles.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-10"},"PeriodicalIF":2.0,"publicationDate":"2025-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970536","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":"GRP78 mediates mitochondrial fusion and fission in cigarette smoke-induced inflammatory responses in airway epithelial cells.","authors":"Yong Wang, Ya-Jing Li, Chen-Chen Li, Li Pu, Wan-Li Geng, Fei Gao, Qing Zhang","doi":"10.1080/08958378.2024.2428163","DOIUrl":"10.1080/08958378.2024.2428163","url":null,"abstract":"<p><strong>Objective: </strong>Chronic obstructive pulmonary disease (COPD) is characterized by persistent airway inflammation, with cigarette smoke being a major contributor to epithelial injury. Recent studies have shown that abnormal mitochondrial function is closely linked to the onset and progression of airway inflammation. This study aims to explore the role and underlying molecular mechanisms of mitochondrial dynamics in cigarette smoke-induced airway inflammation.</p><p><strong>Materials and methods: </strong>Human bronchial epithelial (HBE) cells were exposed to cigarette smoke extract (CSE) to assess the expression of mitochondrial fusion markers MFN2 and OPA1, the fission marker DRP1, and the glucose-regulated protein GRP78. The siRNA and pharmaceutics targeting DRP1, MFN2, and GRP78 were employed. Both cells and supernatants were analyzed for inflammatory factor levels and the related signaling pathways.</p><p><strong>Results: </strong>In this study, HBE cells exposed to CSE showed a significant decrease in the proteins MFN2 and OPA1 and an increase in DRP1. The inhibition of DRP1 expression mitigated inflammation while silencing MFN2 exacerbated it. This was similarly corroborated by the use of the DRP1 inhibitor mdivi-1 and the MFN2 activator leflunomide. Additionally, we proved that GRP78 played an important regulatory role as an essential endoplasmic reticulum protein, regulating the mitochondrial fusion/fission process and subsequently activating the NF-κB pathway to regulate airway inflammation.</p><p><strong>Discussion and conclusion: </strong>Taken together, these results suggested that the GRP78-mediated mitochondrial fusion and fission process played a vital role in cigarette smoke-induced airway inflammation and might be a potential therapeutic target in this regard.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"511-520"},"PeriodicalIF":2.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675753","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":"<i>MiR-421</i> mediates PM_2.5-induced endothelial dysfunction via crosstalk between bronchial epithelial and endothelial cells.","authors":"Yiqing Chen, Mengting Zeng, Jinxin Xie, Zhihao Xiong, Yuxin Jin, Zihan Pan, Michail Spanos, Tianhui Wang, Hongyun Wang","doi":"10.1080/08958378.2024.2356839","DOIUrl":"10.1080/08958378.2024.2356839","url":null,"abstract":"<p><strong>Objective: </strong>PM_2.5 is closely linked to vascular endothelial injury and has emerged as a major threat to human health. Our previous research indicated that exposure to PM_2.5 induced an increased release of <i>miR-421</i> from the bronchial epithelium. However, the role of <i>miR-421</i> in PM_2.5-induced endothelial injury remains elusive.</p><p><strong>Materials and methods: </strong>We utilized a subacute PM_2.5-exposure model in mice <i>in vivo</i> and an acute injury cell model <i>in vitro</i> to simulate PM_2.5-associated endothelial injury. We also used quantitative real-time polymerase chain reaction, western blot, enzyme-linked immunosorbent assay, and immunohistochemistry to investigate the role of <i>miR-421</i> in PM_2.5-induced endothelial injury.</p><p><strong>Results: </strong>Our findings reveal that inhibition of <i>miR-421</i> attenuated PM_2.5-induced endothelial injury and hypertension. Mechanistically, <i>miR-421</i> inhibited the expression of <i>angiotensin-converting enzyme 2 (ACE2</i>) in human umbilical vein endothelial cells and upregulated the expression of the downstream molecule inducible <i>nitric oxide synthase (iNOS)</i>, thereby exacerbating PM_2.5-induced endothelial injury.</p><p><strong>Conclusions: </strong>Our results indicate that PM_2.5 exposure facilitates crosstalk between bronchial epithelial and endothelial cells <i>via miR-421</i>/<i>ACE2</i>/<i>iNOS</i> signaling pathway, mediating endothelial damage and hypertension. <i>MiR-421</i> inhibition may offer a new strategy for the prevention and treatment of PM_2.5-induced vascular endothelial injury.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"501-510"},"PeriodicalIF":2.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141079939","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":"Temporal evaluation of lung injury following chlorine Inhalation in a ventilated pig model.","authors":"Matthew Neal, Jill Harvilchuck, David Pressburger, William Coley, Tom C-C Hu","doi":"10.1080/08958378.2024.2433762","DOIUrl":"10.1080/08958378.2024.2433762","url":null,"abstract":"<p><strong>Objective: </strong>Chlorine (Cl₂) is a widely used industrial chemical and toxic human exposures have occurred from Cl₂ releases. No approved medical countermeasures (MCMs) exist for Cl₂-induced lung injuries. The objective of this study was to develop and characterize swine Cl₂ inhalation injuries to understand lung injury and histopathological sequalae.</p><p><strong>Materials and methods: </strong>Male swine (approximately 14 weeks old) were anesthetized, paralyzed, intubated, and exposed to clean air or Cl₂ while connected to a ventilator. The exposed LD_50/24 hr of 1.8 mg/kg was delivered within a 15-20-minute timeframe. Scheduled terminal timepoints were 6 h, 7- and 30-days post-exposure.</p><p><strong>Results: </strong>Following Cl₂ exposure, 46% of the animals succumbed with an average time to death of 1.42 h. Dynamic lung compliance at 6 h post-exposure was reduced 45%. Clinical observations demonstrated respiratory abnormalities similar to Cl₂ exposed humans. Compared to air shams, Cl₂-exposed animals had decreased SpO₂, arterial blood pH, pO₂, sO₂, increased blood lactate levels and deoxyhemoglobin levels at early timepoints. Increased neutrophils 6 h post- exposure occurred concurrent with increased inflammatory cytokines, bronchiolar epithelial necrosis with alveolar edema, cellular infiltrates, and lobular atelectasis.</p><p><strong>Discussion/conclusions: </strong>Potentially relevant biomarkers involved in the progression and recovery from acute Cl₂ lung injury in this model include lung compliance, select cytokines/chemokines, arterial blood gas parameters, and histopathological evaluation. Normal lung histopathological observations beyond 7- days indicates that histopathological evaluations should occur earlier. This animal model delivers accurate and consistent Cl₂ exposures resulting in a human-relevant lung injury for evaluating MCM efficacy against Cl₂-mediated acute lung injury.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"521-537"},"PeriodicalIF":2.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768649","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":"Administration of airborne pathogens in non-human primates.","authors":"Justina R Creppy, Benoit Delache, Julien Lemaitre, Branka Horvat, Laurent Vecellio, Frédéric Ducancel","doi":"10.1080/08958378.2024.2412685","DOIUrl":"10.1080/08958378.2024.2412685","url":null,"abstract":"<p><strong>Purpose: </strong>Airborne pathogen scan penetrate in human respiratory tract and can cause illness. The use of animal models to predict aerosol deposition and study respiratory disease pathophysiology is therefore important for research and a prerequisite to test and study the mechanism of action of treatment. NHPs are relevant animal species for inhalation studies because of their similarities with humans in terms of anatomical structure, respiratory parameters and immune system.</p><p><strong>Materials and methods: </strong>The aim of this review is to provide an overview of the state of the art of pathogen aerosol studies performed in non-human primates (NHPs). Herein, we present and discuss the deposition of aerosolized bacteria and viruses. In this review, we present important advantages of using NHPs as model for inhalation studies.</p><p><strong>Results: </strong>We demonstrate that deposition in the respiratory tract is not only a function of aerosol size but also the technique of administration influences the biological activity and site of aerosol deposition. Finally, we observe an influence of a region of pathogen deposition in the respiratory tract on the development of the pathophysiological effect in NHPs.</p><p><strong>Conclusion: </strong>The wide range of methods used for the delivery of pathogento NHP respiratory airways is associated with varying doses and deposition profiles in the airways.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"475-500"},"PeriodicalIF":2.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464301","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":"Impact of soluble epoxide hydrolase inhibition on silica-induced pulmonary fibrosis, ectopic lymphoid neogenesis, and autoantibody production in lupus-prone mice.","authors":"Olivia F McDonald, James G Wagner, Ryan P Lewandowski, Lauren K Heine, Vanessa Estrada, Elham Pourmand, Megha Singhal, Jack R Harkema, Kin Sing Stephen Lee, James J Pestka","doi":"10.1080/08958378.2024.2413373","DOIUrl":"10.1080/08958378.2024.2413373","url":null,"abstract":"<p><strong>Objective: </strong>Acute intranasal (IN) instillation of lupus-prone NZBWF1 mice with crystalline silica (cSiO₂) triggers robust lung inflammation that drives autoimmunity. Prior studies in other preclinical models show that soluble epoxide hydrolase (sEH) inhibition upregulates pro-resolving lipid metabolites that are protective against pulmonary inflammation. Herein, we assessed in NZBWF1 mice how acute IN cSiO₂ exposure with or without the selective sEH inhibitor TPPU influences lipidomic, transcriptomic, proteomic, and histopathological biomarkers of inflammation, fibrosis, and autoimmunity.</p><p><strong>Methods: </strong>Female 6-week-old NZBWF1 mice were fed control or TPPU-supplemented diets for 2 weeks then IN instilled with 2.5 mg cSiO₂ or saline vehicle. Cohorts were terminated at 7 or 28 days post-cSiO₂ instillation (PI) and lungs analyzed for prostaglandins, cytokines/chemokines, gene expression, differential cell counts, histopathology, and autoantibodies.</p><p><strong>Results: </strong>cSiO₂-treatment induced prostaglandins, cytokines/chemokine, proinflammatory gene expression, CD206⁺ monocytes, Ly6B.2⁺ neutrophils, CD3⁺ T cells, CD45R⁺ B cells, centriacinar inflammation, collagen deposition, ectopic lymphoid structure neogenesis, and autoantibodies. While TPPU effectively inhibited sEH as reflected by skewed lipidomic profile in lung and decreased cSiO₂-induced monocytes, neutrophils, and lymphocytes in lung lavage fluid, it did not significantly impact other biomarkers.</p><p><strong>Discussion: </strong>cSiO₂ evoked robust pulmonary inflammation and fibrosis in NZBWF1 mice that was evident at 7 days PI and progressed to ELS development and autoimmunity by 28 days PI. sEH inhibition by TPPU modestly suppressed cSiO₂-induced cellularity changes and pulmonary fibrosis. However, TPPU did not affect ELS formation or autoantibody responses, suggesting sEH minimally impacts cSiO₂-triggered lung inflammation, fibrosis, and early autoimmunity in our model.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"442-460"},"PeriodicalIF":2.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11606782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464304","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":"Bergapten attenuates sepsis-induced acute lung injury in mice by regulating Th17/Treg balance.","authors":"Shanqiu Shi, Rui Deng, Renchun Huang, Shitai Zhou","doi":"10.1080/08958378.2024.2400479","DOIUrl":"10.1080/08958378.2024.2400479","url":null,"abstract":"<p><strong>Background: </strong>The abnormality of the immune system caused by infection is a contributor to the organ dysfunctions associated with sepsis. The balance between Th17/Treg cells is essential for maintaining immune homeostasis. Bergapten is a natural furocoumarin and has been reported to alleviate the Th17/Treg imbalance. Here, we explored the effects of bergapten on the inflammation and immune state in mouse models of sepsis.</p><p><strong>Methods: </strong>The model was established using the cecal ligation and puncture method. Mice were administered 30 mg/kg bergapten. Histological examination, RT-qPCR, enzyme-linked immunosorbent assay, immunoblotting, immunofluorescence, immunohistochemistry, and flow cytometry were used to evaluate the effects of bergapten <i>in vivo</i>.</p><p><strong>Results: </strong>Bergapten ameliorated lung damage, reduced lung wet/dry weight ratio, inhibited myeloperoxidase activity, and reduced inflammatory cell infiltration. Bergapten also restrained sepsis-induced inflammation via inhibition of inflammatory cytokines and NF-κB signaling. These effects were accompanied by the restored Th17/Treg balance induced by bergapten. Bergapten decreased the number of Th17 cells and elevated the number of Tregs, and this effect was mediated by the signal transducer and activator of transcription 5 (STAT5)/Forkhead box P3 (Foxp3) and STAT3/retinoid-related orphan receptor-γt (RORγt) pathways.</p><p><strong>Conclusions: </strong>Bergapten exerted anti-inflammatory effects in acute lung injury by improving the Th17/Treg balance, which suggested a potential of bergapten as an immunomodulatory drug treating sepsis-associated diseases.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"421-430"},"PeriodicalIF":2.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464302","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":"Co-existing ambient fine particulate matter exacerbated electronic cigarette toxicity on human respiratory cells.","authors":"Guanghe Wang, Wenjing Liu, Yujie Cao, Wanqi Chen, Nuo Chen","doi":"10.1080/08958378.2024.2416428","DOIUrl":"10.1080/08958378.2024.2416428","url":null,"abstract":"<p><p>Respiratory co-exposure to ambient PM_2.5 and electronic cigarettes (e-cigarettes) frequently occurs in public. However, the combined effects on human respiratory health have not been well documented. To discuss potential co-effects and possible biological mechanisms, A549/THP-1 co-cultures and BEAS-2B cells were exposed to unvapedtobacco or mint-flavored e-liquids (0-7.2% v/v), e-cigarette aerosol extract (ECE, 0-50% v/v), PM_2.5 (60 μg/mL), or PM_2.5 + ECE for 24 h. Cell viability assessments on e-liquids, ECE, PM_2.5 + ECE showed that the mint flavor exhibited higher cytotoxicity compared to the tobacco flavor in both A549/THP-1 and BEAS-2B. However, the influence of flavors on ROS levels and mRNA expression of inflammatory markers (IL-6, TNF-α, IL-8, IL-1β) after ECE exposure demonstrated inconsistency in the two cell models. PM_2.5 + ECE treatment notably elevated ROS production and inflammation responses compared to ECE alone exposure. Only co-exposure induced a significant increase in nuclear transcription factor-κB p65 (NF-κB p65) and NOD-like receptor 3 (NLRP3) protein expression regardless of flavors. Our results indicate that PM_2.5-treated cells exacerbate the adverse effects induced by ECE in both A549/THP-1 and BEAS-2B cells. Flavors in unvaped e-liquids affect cytotoxicity, oxidative stress and inflammation response, but these effects vary depending on the vaping process and the specific cell line.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"461-473"},"PeriodicalIF":2.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464303","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}