Inhalation Toxicology最新文献

{"title":"Crystalline silica-induced pulmonary inflammation and autoimmunity in mature adult NZBW/f1 mice: age-related sensitivity and impact of omega-3 fatty acid intervention.","authors":"Lauren K Heine, Tasha Scarlett, James G Wagner, Ryan P Lewandowski, Abby D Benninghoff, Ashleigh N Tindle, Anna E Skedel, Jack R Harkema, James J Pestka","doi":"10.1080/08958378.2024.2318378","DOIUrl":"10.1080/08958378.2024.2318378","url":null,"abstract":"<p><strong>Objective: </strong>Occupational exposure to respirable crystalline silica (cSiO₂) has been linked to lupus development. Previous studies in young lupus-prone mice revealed that intranasal cSiO₂ exposure triggered autoimmunity, preventable with docosahexaenoic acid (DHA). This study explores cSiO₂ and DHA effects in mature lupus-prone adult mice, more representative of cSiO₂-exposed worker age.</p><p><strong>Methods: </strong>Female NZBWF1 mice (14-week old) were fed control (CON) or DHA-supplemented diets. After two weeks, mice were intranasally instilled saline (VEH) or 1 mg cSiO₂ weekly for four weeks. Cohorts were then analyzed 1- and 5-weeks postinstillation for lung inflammation, cell counts, chemokines, histopathology, B- and T-cell infiltration, autoantibodies, and gene signatures, with results correlated to autoimmune glomerulonephritis onset.</p><p><strong>Results: </strong>VEH/CON mice showed no pathology. cSiO₂/CON mice displayed significant ectopic lymphoid tissue formation in lungs at 1 week, increasing by 5 weeks. cSiO₂/CON lungs exhibited elevated cellularity, chemokines, CD3⁺ T-cells, CD45R ⁺ B-cells, IgG ⁺ plasma cells, gene expression, IgG autoantibodies, and glomerular hypertrophy. DHA supplementation mitigated all these effects.</p><p><strong>Discussion: </strong>The mature adult NZBWF1 mouse used here represents a life-stage coincident with immunological tolerance breach and one that more appropriately represents the age (20-30 yr) of cSiO2-exposed workers. cSiO₂-induced robust pulmonary inflammation, autoantibody responses, and glomerulonephritis in mature adult mice, surpassing effects observed previously in young adults. DHA at a human-equivalent dosage effectively countered cSiO₂-induced inflammation/autoimmunity in mature mice, mirroring protective effects in young mice.</p><p><strong>Conclusion: </strong>These results highlight life-stage significance in this preclinical lupus model and underscore omega-3 fatty acids' therapeutic potential against toxicant-triggered autoimmune responses.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"106-123"},"PeriodicalIF":2.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140109974","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":"Lipid mediators of inhalation exposure-induced pulmonary toxicity and inflammation.","authors":"Arjun Pitchai, Kimberly Buhman, Jonathan H Shannahan","doi":"10.1080/08958378.2024.2318389","DOIUrl":"10.1080/08958378.2024.2318389","url":null,"abstract":"<p><p>Many inhalation exposures induce pulmonary inflammation contributing to disease progression. Inflammatory processes are actively regulated <i>via</i> mediators including bioactive lipids. Bioactive lipids are potent signaling molecules involved in both pro-inflammatory and resolution processes through receptor interactions. The formation and clearance of lipid signaling mediators are controlled by multiple metabolic enzymes. An imbalance of these lipids can result in exacerbated and sustained inflammatory processes which may result in pulmonary damage and disease. Dysregulation of pulmonary bioactive lipids contribute to inflammation and pulmonary toxicity following exposures. For example, inhalation of cigarette smoke induces activation of pro-inflammatory bioactive lipids such as sphingolipids, and ceramides contributing to chronic obstructive pulmonary disease. Additionally, exposure to silver nanoparticles causes dysregulation of inflammatory resolution lipids. As inflammation is a common consequence resulting from inhaled exposures and a component of numerous diseases it represents a broadly applicable target for therapeutic intervention. With new appreciation for bioactive lipids, technological advances to reliably identify and quantify lipids have occurred. In this review, we will summarize, integrate, and discuss findings from recent studies investigating the impact of inhaled exposures on pro-inflammatory and resolution lipids within the lung and their contribution to disease. Throughout the review current knowledge gaps in our understanding of bioactive lipids and their contribution to pulmonary effects of inhaled exposures will be presented. New methods being employed to detect and quantify disruption of pulmonary lipid levels following inhalation exposures will be highlighted. Lastly, we will describe how lipid dysregulation could potentially be addressed by therapeutic strategies to address inflammation.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"57-74"},"PeriodicalIF":2.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11022128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139996189","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":"Inhaled endotoxin induces a systemic neutrophil response without affecting cardiovascular measures in a randomized cross-over exposure study.","authors":"Stephen A Schworer, Alan L Hinderliter, Melissa C Caughey, Carole Robinette, Kelly D Chason, Haolin Li, Haibo Zhou, Amika K Sood, Allison J Burbank, David B Peden, Michelle L Hernandez","doi":"10.1080/08958378.2024.2316241","DOIUrl":"10.1080/08958378.2024.2316241","url":null,"abstract":"<p><strong>Objective: </strong>The gram-negative bacterial cell wall component endotoxin (lipopolysaccharide, LPS) is a key component of particulate matter (PM). PM exposure is associated with cardiovascular morbidity and mortality. However, the contribution of individual components of PM to acute and chronic cardiovascular measures is not clear. This study examines whether systemic inflammation induced by LPS inhalation causes acute changes in cardiovascular physiology measures.</p><p><strong>Materials and methods: </strong>In this double blinded, placebo-controlled crossover study, fifteen adult volunteers underwent inhalation exposure to 20,000 EU Clinical Center Reference Endotoxin (CCRE). Peripheral blood and induced sputum neutrophils were obtained at baseline and six hours post-exposure. Blood pressure, measures of left ventricular function (ejection fraction (LVEF) and global longitudinal strain (LVGLS)), and indices of endothelial function (flow mediated dilation (FMD) and velocity time integral during hyperemia (VTIhyp)) were measured before and after treatment. Wilcoxon sign-rank tests and linear mixed models were used for statistical analysis.</p><p><strong>Results: </strong>In comparison with normal saline, LPS inhalation resulted in significant increases in peripheral blood and sputum neutrophils but was not associated with significant alterations in blood pressure, LVGLS, LVEF, FMD, or VTIhyp.</p><p><strong>Discussion and conclusions: </strong>In healthy adults, systemic inflammation after LPS inhalation was not associated with acute changes in cardiovascular physiology. Larger studies are needed to investigate the effects of other PM components on inflammation induced cardiovascular dysfunction.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"100-105"},"PeriodicalIF":2.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11151184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139897971","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":"Comparison of the effects of active and passive smoking of tobacco cigarettes, electronic nicotine delivery systems and tobacco heating products on the expression and secretion of oxidative stress and inflammatory response markers. A systematic review.","authors":"Paulina Natalia Kopa-Stojak, Rafal Pawliczak","doi":"10.1080/08958378.2024.2319315","DOIUrl":"10.1080/08958378.2024.2319315","url":null,"abstract":"<p><strong>Objectives: </strong>This work attempts to summarize current knowledge on the effects of active and passive smoking of cigarettes, electronic nicotine delivery systems and tobacco heating products on the expression and secretion of oxidative stress and inflammatory response mediators, and on their possible impact on chronic obstructive pulmonary disease development.</p><p><strong>Materials and methods: </strong>The literature was searched by the terms: 'smoking', 'active smoking', 'passive smoking', 'main-stream smoke', 'side-stream smoke', 'secondhand smoke', 'cigarette' 'THP', 'tobacco heating product', 'ENDS', 'electronic nicotine delivery system', 'e-cigarette', 'electronic cigarette', oxidative stress', inflammatory response' and 'gene expression'.</p><p><strong>Results: </strong>Cigarette smoking (active and passive) induces oxidative stress and inflammatory response in the airways. We present the effect of active smoking of e-cigarettes (EC) and heat-not-burn (HnB) products on the increased expression and secretion of oxidative stress and inflammatory response markers. However, there is only a limited number of studies on the effect of their second-hand smoking, and those available mainly describe aerosol composition.</p><p><strong>Discussion: </strong>The literature provides data which confirm that active and passive cigarette smoking induces oxidative stress and inflammatory response in the airways and is a key risk factor of COPD development. Currently, there is a limited number of data about ENDS and THP active and passive smoking effects on the health of smokers and never-smokers. It is particularly important to assess the effect of such products during long-term use by never-smokers who choose them as the first type of cigarettes, and for never-smokers who are passively exposed to their aerosol.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"75-89"},"PeriodicalIF":2.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139939959","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":"Lysosomal BK channels facilitate silica-induced inflammation in macrophages.","authors":"Rebekah L Kendall, Andrij Holian","doi":"10.1080/08958378.2024.2305112","DOIUrl":"10.1080/08958378.2024.2305112","url":null,"abstract":"<p><strong>Background: </strong>Lysosomal ion channels are proposed therapeutic targets for a number of diseases, including those driven by NLRP3 inflammasome-mediated inflammation. Here, the specific role of the lysosomal big conductance Ca²⁺-activated K⁺ (BK) channel was evaluated in a silica model of inflammation in murine macrophages. A specific-inhibitor of BK channel function, paxilline (PAX), and activators NS11021 and NS1619 were utilized to evaluate the role of lysosomal BK channel activity in silica-induced lysosomal membrane permeabilization (LMP) and NLRP3 inflammasome activation resulting in IL-1β release.</p><p><strong>Methods: </strong>Murine macrophages were exposed <i>in vitro</i> to crystalline silica following pretreatment with BK channel inhibitors or activators and LMP, cell death, and IL-1β release were assessed. In addition, the effect of PAX treatment on silica-induced cytosolic K⁺ decrease was measured. Finally, the effects of BK channel modifiers on lysosomal pH, proteolytic activity, and cholesterol transport were also evaluated.</p><p><strong>Results: </strong>PAX pretreatment significantly attenuated silica-induced cell death and IL-1β release. PAX caused an increase in lysosomal pH and decrease in lysosomal proteolytic activity. PAX also caused a significant accumulation of lysosomal cholesterol. BK channel activators NS11021 and NS1619 increased silica-induced cell death and IL-1β release. BK channel activation also caused a decrease in lysosomal pH and increase in lysosomal proteolytic function as well as a decrease in cholesterol accumulation.</p><p><strong>Conclusion: </strong>Taken together, these results demonstrate that inhibiting lysosomal BK channel activity with PAX effectively reduced silica-induced cell death and IL-1β release. Blocking cytosolic K⁺ entry into the lysosome prevented LMP through the decrease of lysosomal acidification and proteolytic function and increase in lysosomal cholesterol.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"31-43"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11080613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139541630","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":"Comparison of microparticle transport and deposition in nasal cavity of three different age groups.","authors":"John Valerian Corda, B Satish Shenoy, Kamarul Arifin Ahmad, Leslie Lewis, Prakashini K, Anoop Rao, Mohammad Zuber","doi":"10.1080/08958378.2024.2312801","DOIUrl":"10.1080/08958378.2024.2312801","url":null,"abstract":"<p><p><b>Objective:</b> The nasal cavity effectively captures the particles present in inhaled air, thereby preventing harmful and toxic pollutants from reaching the lungs. This filtering ability of the nasal cavity can be effectively utilized for targeted nasal drug delivery applications. This study aims to understand the particle deposition patterns in three age groups: neonate, infant, and adult.<b>Materials and methods:</b> The CT scans are built using MIMICS 21.0, followed by CATIA V6 to generate a patient-specific airway model. Fluid flow is simulated using ANSYS FLUENT 2021 R2. Spherical monodisperse microparticles ranging from 2 to 60 µm and a density of 1100 kg/m³ are simulated at steady-state and sedentary inspiration conditions.<b>Results:</b> The highest nasal valve depositions for the neonate are 25% for 20 µm, for infants, 10% for 50 µm, 15% for adults, and 15% for 15 µm. At mid nasal region, deposition of 15% for 20 µm is observed for infant and 8% for neonate and adult nasal cavities at a particle size of 10 and 20 µm, respectively. The highest particle deposition at the olfactory region is about 2.7% for the adult nasal cavity for 20 µm, and it is <1% for neonate and infant nasal cavities.<b>Discussion and conclusions:</b> The study of preferred nasal depositions during natural sedentary breathing conditions is utilized to determine the size that allows medication particles to be targeted to specific nose regions.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"44-56"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722367","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":"Long-term health complications of chemical weapon exposure: a study on Halabja chemical attack survivors (Iraqi Kurds).","authors":"Belal A Muhammad, Salih A Hama, Karzan A M Hawrami, Salar H Karim, Gasha S Ahmed, Hawbash M Rahim","doi":"10.1080/08958378.2024.2301985","DOIUrl":"10.1080/08958378.2024.2301985","url":null,"abstract":"<p><strong>Objective: </strong>In 1988, the Iraqi government used a range of chemical weapons (CWs) against the Iraqi Kurds of Halabja. Here, we aim to investigate the long-term health consequences in exposed survivors as they are not sufficiently studied.</p><p><strong>Materials and methods: </strong>This was a retrospective study conducted from November 2019 to May 2020 assessing the health status of all exposed Halabja chemical attack survivors compared to non-exposed people from the same area.</p><p><strong>Results and discussion: </strong>Two hundred thirty survivors and 240 non-exposed participants were enrolled in this study, with control participants matched to age, gender, and occupation. Among the survivors, females were more prevalent. The respiratory system was the most common single exposure route (83, 36.1%), with 138 (60%) of the survivors being exposed by multiple routes. The vast majority (88.7%) of survivors had activities of daily living (ADL) impairment. There was female predominance in mild and moderate cases, with more males in severe cases (<i>p < 0.01</i>). Respiratory and cardiac diseases were significantly more common in the survivors compared to the controls (<i>p < 0.001</i>). Survivors with multiple CW exposure routes had significantly higher rates of ADL impairment (<i>p</i> < 0.001) and cardiac disease, respiratory diseases, and miscarriage (<i>p</i> < 0.01), than those with a single exposure route.</p><p><strong>Conclusion: </strong>In this study comparing CW survivors with a local control population, a single, high-dose exposure to CWs was associated with significant increases in chronic respiratory and cardiac conditions, in addition to high rates of ADL impairment. Similar studies are needed in other, more recent CW survivor cohorts.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"26-30"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139402660","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 short-term occupational exposure limits (STELs) for sensory irritants using predictive and <i>in silico</i> respiratory rate depression (RD₅₀) models.","authors":"Anthony J Russell, Melissa Vincent, Amanda N Buerger, Scott Dotson, Jason Lotter, Andrew Maier","doi":"10.1080/08958378.2023.2299867","DOIUrl":"10.1080/08958378.2023.2299867","url":null,"abstract":"<p><p>Sensory irritation is a health endpoint that serves as the critical effect basis for many occupational exposure limits (OELs). Schaper 1993 described a significant relationship with high correlation between the measured exposure concentration producing a 50% respiratory rate decrease (RD₅₀) in a standard rodent assay and the American Conference of Governmental Industrial Hygienists (ACGIH®) Threshold Limit Values (TLVs®) as time-weighted averages (TWAs) for airborne chemical irritants. The results demonstrated the potential use of the RD₅₀ values for deriving full-shift TWA OELs protective of irritant responses. However, there remains a need to develop a similar predictive model for deriving workplace short-term exposure limits (STELs) for sensory irritants. The aim of our study was to establish a model capable of correlating the relationship between RD₅₀ values and published STELs to prospectively derive short-term exposure OELs for sensory irritants. A National Toxicology Program (NTP) database that included chemicals with both an RD₅₀ and established STELs was used to fit several linear regression models. A strong correlation between RD₅₀s and STELs was identified, with a predictive equation of ln (STEL) (ppm) = 0.86 * ln (RD₅₀) (ppm) - 2.42 and an R² value of 0.75. This model supports the use of RD₅₀s to derive STELs for chemicals without existing exposure recommendations. Further, for data-poor sensory irritants, predicted RD₅₀ values from <i>in silico</i> quantitative structure activity relationship (QSAR) models can be used to derive STELs. Hence, <i>in silico</i> methods and statistical modeling can present a path forward for establishing reliable OELs and improving worker safety and health.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"13-25"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139520575","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":"Analysis of abnormal expression of signaling pathways in PQ-induced acute lung injury in SD rats based on RNA-seq technology.","authors":"Nan Li, Yue Huang, Yang Yi, Jin Qian, Qi Li, Shuang-Qin Xu, Hang-Fei Wang, Xin-Xin Wu, Ji-Chao Peng, Li-Hua Li, Jin-Jian Yao, Xiao-Ran Liu","doi":"10.1080/08958378.2023.2300373","DOIUrl":"10.1080/08958378.2023.2300373","url":null,"abstract":"<p><p><b>Background</b>: Paraquat (PQ) plays an important role in agricultural production due to its highly effective herbicidal effect. However, it has led to multiple organ failure in those who have been poisoned, with damage most notable in the lungs and ultimately leading to death. Because of little research has been performed at the genetic level, and therefore, the specific genetic changes caused by PQ exposure are unclear.<b>Methods</b>: Paraquat poisoning model was constructed in Sprague Dawley (SD) rats, and SD rats were randomly divided into Control group, paraquat (PQ) poisoning group and Anthrahydroquinone-2,6-disulfonate (AH₂QDS) treatment group. Then, the data was screened and quality controlled, compared with reference genes, optimized gene structure, enriched at the gene expression level, and finally, signal pathways with significantly different gene enrichment were screened.<b>Results</b>: This review reports on lung tissues from paraquat-intoxicated Sprague Dawley (SD) rats that were subjected to RNA-seq, the differentially expressed genes were mainly enriched in PI3K-AKT, cGMP-PKG, MAPK, Focal adhesion and other signaling pathways.<b>Conclusion</b>: The signaling pathways enriched with these differentially expressed genes are summarized, and the important mechanisms mediated through these pathways in acute lung injury during paraquat poisoning are outlined to identify important targets for AH₂QDS treatment of acute lung injury due to paraquat exposure, information that will be used to support a subsequent in-depth study on the mechanism of PQ action.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"1-12"},"PeriodicalIF":2.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086714","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":"Adjuvant effect of inhaled particulate matter containing free radicals following house-dust mite induction of asthma in mice","authors":"Alexandra Noël, Ashlyn C. Harmon, Balamurugan Subramanian, Zakia Perveen, Ankit Aryal, Kelsey Legendre, Hasan Zaman, Daniel B. Paulsen, Kurt J. Varner, Tammy R. Dugas, Arthur L. Penn","doi":"10.1080/08958378.2023.2289024","DOIUrl":"https://doi.org/10.1080/08958378.2023.2289024","url":null,"abstract":"Introduction: Exposures to particulate matter (PM) from combustion sources can exacerbate preexisting asthma. However, the cellular and molecular mechanisms by which PM promotes the exacerbation of...","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"2 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138567830","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}