Inhalation Toxicology最新文献

Puffing topography: a tool to evaluate vaping behavior and exposure risks. 雾化地形：评估电子烟行为和暴露风险的工具。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-07-11 DOI: 10.1080/08958378.2025.2524728

Shaligram Sharma, Maureen Meister, Xiaojia He, Mark Wilson, Qian Zhang, Jin-Ah Park, Travis Goldsmith, Cristi Bell-Huff, Marilyn Black, Jonathan Shannahan, Christa Wright

{"title":"Puffing topography: a tool to evaluate vaping behavior and exposure risks.","authors":"Shaligram Sharma, Maureen Meister, Xiaojia He, Mark Wilson, Qian Zhang, Jin-Ah Park, Travis Goldsmith, Cristi Bell-Huff, Marilyn Black, Jonathan Shannahan, Christa Wright","doi":"10.1080/08958378.2025.2524728","DOIUrl":"https://doi.org/10.1080/08958378.2025.2524728","url":null,"abstract":"The ever-changing popularity of electronic nicotine delivery systems (ENDS) among both youth and adults in the United States has been influential in shaping users' perceptions and behaviors. This behavior driven ENDS usage is described as puffing topography (PT) which includes user's puff duration, flow rate, intra puff interval, the volume of e-liquid used and total number of puffs per session. These metrics are not only useful for characterizing individual vaping behaviors but are also critical for assessing the extent of exposure to potentially harmful substances such as nicotine, volatile organic compounds (VOCs), and particulate matter emitted during use. Previous studies have indicated that puff volume and flow rate are distinct but related parameters that determine exposure to hazardous emissions among users and bystanders. However, current evidence suggests that vaping behavior is also influenced by the age at which users first encounter ENDS, the strength of the nicotine present, and whether users develop circadian patterns of ENDS usage. This review article, which is a part of the Special Issue Science Education and Research on Vaping and Interventions for Community Engagement summarizes the critical aspects of PT and explores how various factors including lifestyle, gender, e-liquid composition (such as flavor and nicotine concentration), and device parameters can influence exposure risks. The standardization of puffing topography as a tool to evaluate vaping behavior and exposure risks to toxic emissions could be instrumental in developing consensus standards for ENDS and protecting public health.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-12"},"PeriodicalIF":2.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144612093","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}

引用次数: 0

CREBBP stabilizes GNG3 protein through acetylation, thereby activating the NF-κB pathway and exacerbating airway inflammation in allergic rhinitis. CREBBP通过乙酰化稳定GNG3蛋白，从而激活NF-κB通路，加重变应性鼻炎气道炎症。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-07-05 DOI: 10.1080/08958378.2025.2528747

Meng Chen, Zhihui Yuan

{"title":"CREBBP stabilizes GNG3 protein through acetylation, thereby activating the NF-κB pathway and exacerbating airway inflammation in allergic rhinitis.","authors":"Meng Chen, Zhihui Yuan","doi":"10.1080/08958378.2025.2528747","DOIUrl":"https://doi.org/10.1080/08958378.2025.2528747","url":null,"abstract":"Objective: Allergic rhinitis (AR), an allergen-driven chronic inflammatory disorder of nasal mucosa, is characterized by airway inflammation as its cardinal pathological manifestation. While acetylation is known to regulate airway inflammation, its mechanistic involvement in AR-related inflammation remains elusive. This study aims to investigate the acetylation-dependent mechanisms governing airway inflammation in AR.Materials and methods: RNA-seq analysis identified differentially expressed genes in peripheral blood of AR patients and healthy controls. Ovalbumin-sensitized BALB/c mice were performed as the AR mouse model. Airway inflammation was assessed by measuring inflammatory cytokine levels, inflammatory cell numbers, macrophage counts in whole lung lavage fluid (WLLF), and specific IgE levels in plasma using ELISA and Diff-Quick staining. The underlying mechanism was investigated through Western blotting, immunoprecipitation (IP), and Co-IP.Results: GNG3 expression was significantly increased in AR patients and the AR mouse model. Knockdown of GNG3 significantly reduced airway inflammation and inhibited NF-κB pathway activation in the AR mouse model. CREBBP overexpression enhanced GNG3 protein stability, and CREBBP mRNA expression was significantly increased in patients with AR and positively correlated with GNG3 expression. Furthermore, GNG3 overexpression restored airway inflammation that was suppressed by CREBBP knockdown in the AR mouse model.Conclusion: These results demonstrate that CREBBP aggravated airway inflammation in AR by activating the NF-κB pathway via GNG3 upregulation mediated by GNG3 acetylation.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-11"},"PeriodicalIF":2.0,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567393","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}

引用次数: 0

An economical in vitro model of wood smoke exposure. 木材烟雾暴露的经济体外模型。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-07-01 DOI: 10.1080/08958378.2025.2523297

Jennifer Krznarich, Tessa Schumann, James Bjork, Matthew Slattery, Sarah E Lacher

{"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":"https://doi.org/10.1080/08958378.2025.2523297","url":null,"abstract":"Objective: 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. In vitro exposure systems are necessary to dissect the effects of wood smoke on various cell types, but current in vitro 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.Materials and methods: 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.Results: 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.Conclusion: 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.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-8"},"PeriodicalIF":2.0,"publicationDate":"2025-07-01","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}

引用次数: 0

Saikosaponin D ameliorates sepsis-induced acute lung injury by maintaining alveolar epithelial barrier integrity and inhibiting ferroptosis via Nrf2/HO-1 pathway. Saikosaponin D通过Nrf2/HO-1途径维持肺泡上皮屏障完整性和抑制铁上塌，改善脓毒症诱导的急性肺损伤。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-06-26 DOI: 10.1080/08958378.2025.2519006

Lijie Song, Yanyan Tao, Guoyu Lu, Chenchen Wu

{"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":"https://doi.org/10.1080/08958378.2025.2519006","url":null,"abstract":"Background: Saikosaponin D (SSD), a triterpenoid saponin extracted from Bupleurum chinensis, has many pharmacological properties. The goal of our study is to assess the roles and mechanisms of SSD in septic acute lung injury (ALI).Methods: 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 in vitro model of septic lung injury was established in MLE-12 cells via LPS stimulation. Cytotoxicity, TEER values, and FITC-dextran flux were detected. Intracellular ROS content was evaluated by DCFH-DA staining.Results: 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 in vitro.Conclusion: SSD ameliorates septic ALI by maintaining alveolar epithelial barrier integrity and suppressing ferroptosis via the activation of Nrf2 signaling.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-13"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","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}

引用次数: 0

The Fli1 transcription factor aggravates lipopolysaccharide-induced human pulmonary microvascular endothelial cell dysfunction by regulating CXCL2 promoter. Fli1转录因子通过调节CXCL2启动子加重脂多糖诱导的人肺微血管内皮细胞功能障碍。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-06-17 DOI: 10.1080/08958378.2025.2510311

Zhou Zheng, Lei Liu, Hao Zhang, Siming Chen

{"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":"https://doi.org/10.1080/08958378.2025.2510311","url":null,"abstract":"Objective: 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.Materials and methods: Human PMECs (HPMECs) were treated with lipopolysaccharide (LPS) for the establishment of in vitro 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.Results: 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.Conclusions: The Fli1 transcription factor aggravates LPS-induced HPMEC dysfunction via binding to CXCL2 promoter in septic ALI.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-12"},"PeriodicalIF":2.0,"publicationDate":"2025-06-17","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}

引用次数: 0

Correction. 修正。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-06-15 DOI: 10.1080/08958378.2025.2514900

引用次数: 0

TMEM175 activity in BK-deficient macrophages maintains lysosomal function and mediates silica-induced inflammatory response in macrophages. TMEM175在bk缺陷巨噬细胞中的活性维持溶酶体功能并介导巨噬细胞中硅诱导的炎症反应。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-05-22 DOI: 10.1080/08958378.2025.2507251

Rebekah L Kendall, Britten Postma, Andrij Holian

{"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":"https://doi.org/10.1080/08958378.2025.2507251","url":null,"abstract":"Objective: 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 via 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. Methods: Bone marrow derived macrophages (BMdM) from C57BL/6 wildtype (WT) and BK-/- mice were exposed in vitro to silica and IL-1β release and cell death assessed. The effect of BK-/- on lysosomal pH, proteolytic activity, and cholesterol accumulation was evaluated. Results: 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. Conclusion: 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.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-10"},"PeriodicalIF":2.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beyond the puff: health consequences of vaping. 吸烟之外：电子烟对健康的影响。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-05-14 DOI: 10.1080/08958378.2025.2500646

Maureen Meister, Xiaojia He, Alexandra Noël, Jin-Ah Park, Laura Crotty Alexander, Judith Zelikoff, David Christiani, Joseph Hess, Jonathan Shannahan, Christa Wright

{"title":"Beyond the puff: health consequences of vaping.","authors":"Maureen Meister, Xiaojia He, Alexandra Noël, Jin-Ah Park, Laura Crotty Alexander, Judith Zelikoff, David Christiani, Joseph Hess, Jonathan Shannahan, Christa Wright","doi":"10.1080/08958378.2025.2500646","DOIUrl":"https://doi.org/10.1080/08958378.2025.2500646","url":null,"abstract":"Electronic nicotine delivery systems (ENDS) arrived on the U.S. market in 2007 and rapidly grew in popularity as a harm reduction tool for traditional cigarette users. While initially marketed as a healthier alternative to combustible cigarettes, the unique mixture of chemical constituents in ENDS products and their emissions have led to rising concern about their safety and the long-term health implications. Given the lack of long-term, epidemiological research on the health effects of these products, recent research has sought to understand the impacts on cellular components and gain understanding of acute effects to inform potential chronic health implications. Studies have demonstrated the deleterious effects the use of ENDS has on the oral cavity, respiratory, and cardiovascular systems. ENDS use has been linked to gingival inflammation and alterations in the oral microbiome contributing to periodontal disease. Further, the presence of heavy metals and other constituents in ENDS emissions contribute to aberrant oxidative stress and inflammation within the lung, contributing to alterations in functional lung capacity and respiratory symptoms in ENDS users. In addition, harmful components of ENDS emissions make their way to the circulatory system, leading to detrimental impacts in cardiovascular functioning such as a rise in blood pressure, impaired vascular functioning, and increased heart rate, all of which are known to underscore long-term cardiovascular ailments. This review will provide an in-depth discussion of the current literature available on the consequences of ENDS use on the oral cavity, respiratory, and cardiovascular systems as well as provide insight into long-term implications that may result.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-14"},"PeriodicalIF":2.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077758","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}

引用次数: 0

Deconstructing ENDS aerosols: generation and characterization methods. 解构ENDS气溶胶：生成和表征方法。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-03-27 DOI: 10.1080/08958378.2025.2481434

Shaligram Sharma, Maureen Meister, David Christiani, Qian Zhang, Mark Wilson, Travis Goldsmith, I Mark Olfert, Anand Ranpara, Cristi Bell-Huff, Marilyn Black, Jonathan Shannahan, Christa Wright

{"title":"Deconstructing ENDS aerosols: generation and characterization methods.","authors":"Shaligram Sharma, Maureen Meister, David Christiani, Qian Zhang, Mark Wilson, Travis Goldsmith, I Mark Olfert, Anand Ranpara, Cristi Bell-Huff, Marilyn Black, Jonathan Shannahan, Christa Wright","doi":"10.1080/08958378.2025.2481434","DOIUrl":"https://doi.org/10.1080/08958378.2025.2481434","url":null,"abstract":"While electronic nicotine delivery systems or ENDS are often marketed as a safer alternative to traditional cigarettes, emissions generated during the operation of these devices contain a complex mixture of toxic substances. ENDS emissions are primarily composed of fine particulate matter (PM2.5, smaller than 2.5 µm in size) and ultrafine particles/nanoparticles (PM0.1, smaller than 100 nm in size), metals (nickel, copper, zinc, tin, lead, and their oxides), carbonyls (formaldehyde, acetaldehyde (a carcinogen), and acrolein), volatile organic compounds (VOCs) (benzene, toluene, and over 70 other VOCs), nicotine, and many unknown chemicals. The levels and composition of these toxic emissions can vary based on factors like device design, e-liquid formulation, device power and temperature levels, and vaping behavior of the user. Within this section of the Special Issue 'Science Education and Research on Vaping and Interventions for Community Engagement', important parameters in defining and characterizing ENDS aerosols will be discussed. Hazardous components of ENDS aerosols including particulate matter, heavy metals, and volatile organic compounds will be delineated and appropriate analytical methods to accurately determine physicochemical properties will be highlighted. Definitions and comparisons of first-hand, second-hand, and third-hand emissions will also be explored alongside pertinent device parameters that influence each type of ENDS emission.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-13"},"PeriodicalIF":2.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730090","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}

引用次数: 0

The beginning of ENDS (electronic nicotine delivery systems): origins, trends, and regulatory considerations. 电子尼古丁输送系统的开始：起源、趋势和监管考虑。

IF 2 4区医学

Inhalation Toxicology Pub Date : 2025-03-27 DOI: 10.1080/08958378.2025.2479518

Shaligram Sharma, Maureen Meister, Scott Weaver, Judith Zelikoff, Cristi Bell-Huff, Marilyn Black, Jonathan Shannahan, Christa Wright

{"title":"The beginning of ENDS (electronic nicotine delivery systems): origins, trends, and regulatory considerations.","authors":"Shaligram Sharma, Maureen Meister, Scott Weaver, Judith Zelikoff, Cristi Bell-Huff, Marilyn Black, Jonathan Shannahan, Christa Wright","doi":"10.1080/08958378.2025.2479518","DOIUrl":"https://doi.org/10.1080/08958378.2025.2479518","url":null,"abstract":"Electronic nicotine delivery systems (ENDS), commonly known as e-cigarettes, are battery-operated devices that produce aerosols by vaporizing e-liquids, which typically contain propylene glycol and/or vegetable glycerin, nicotine, and flavorings. Since their launch in the U.S. in 2007, ENDS have evolved significantly to meet consumer demands, prompting federal regulation in 2016 under the Family Smoking Prevention and Tobacco Control Act. The first ENDS resembled conventional tobacco cigarettes and were initially marketed as smoking cessation tools. While their smoking cessation efficacy under advantageous conditions has been supported by randomized clinical trials, observational cohort studies have raised doubt about their utility for smoking cessation under more typical real-world use conditions. In 2018, the U.S. Surgeon General declared youth vaping a national epidemic as prevalence of current ENDS use rose to 27.5% among high school. The youth vaping trend alongside injury reports and deaths related to e-cigarette or vaping product use-associated lung injury (EVALI) raised public health alarms in 2019. Although youth vaping has since declined, over 1.6 million high school students and 410, 000 middle school students reported ENDS usage in 2024. Thus, the ongoing challenges surrounding vaping including adolescent usage and smoking cessation efficacy continue to attract public health concern and debate. Within this section of the Special Issue \"Science Education and Research on Vaping and Interventions for Community Engagement\", an overview of the history of the vaping epidemic, current formats and ENDS generations, usage statistics across various demographics along with market trends and regulatory guidelines will be discussed.","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-9"},"PeriodicalIF":2.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718660","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}

引用次数: 0