Pub Date : 2024-03-01Epub Date: 2024-03-06DOI: 10.1080/08958378.2024.2322497
Leonardo Tenfen, Richard Simon Machado, Khiany Mathias, Natalia Piacentini, Larissa Joaquim, Sandra Bonfante, Lucineia Gainski Danielski, Nicole Alessandra Engel, Mariella Reinol da Silva, Gislaine Tezza Rezin, Rafaella Willig de Quadros, Fernanda Frederico Gava, Fabricia Petronilho
Background: Oxygen therapy is an alternative for many patients with hypoxemia. However, this practice can be dangerous as oxygen is closely associated with the development of oxidative stress.
Methods: Male Wistar rats were exposed to hyperoxia with a 40% fraction of inspired oxygen (FIO2) and hyperoxia (FIO2 = 60%) for 120 min. Blood and lung tissue samples were collected for gas, oxidative stress, and inflammatory analyses.
Results: Hyperoxia (FIO2 = 60%) increased PaCO2 and PaO2, decreased blood pH and caused thrombocytopenia and lymphocytosis. In lung tissue, neutrophil infiltration, nitric oxide concentration, carbonyl protein formation and the activity of complexes I and II of the mitochondrial respiratory chain increased. FIO2 = 60% decreased SOD activity and caused several histologic changes.
Conclusion: In conclusion, we have experimentally demonstrated that short-term exposure to high FIO2 can cause oxidative stress in the lung.
{"title":"Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats.","authors":"Leonardo Tenfen, Richard Simon Machado, Khiany Mathias, Natalia Piacentini, Larissa Joaquim, Sandra Bonfante, Lucineia Gainski Danielski, Nicole Alessandra Engel, Mariella Reinol da Silva, Gislaine Tezza Rezin, Rafaella Willig de Quadros, Fernanda Frederico Gava, Fabricia Petronilho","doi":"10.1080/08958378.2024.2322497","DOIUrl":"10.1080/08958378.2024.2322497","url":null,"abstract":"<p><strong>Background: </strong>Oxygen therapy is an alternative for many patients with hypoxemia. However, this practice can be dangerous as oxygen is closely associated with the development of oxidative stress.</p><p><strong>Methods: </strong>Male Wistar rats were exposed to hyperoxia with a 40% fraction of inspired oxygen (FIO<sub>2</sub>) and hyperoxia (FIO<sub>2</sub> = 60%) for 120 min. Blood and lung tissue samples were collected for gas, oxidative stress, and inflammatory analyses.</p><p><strong>Results: </strong>Hyperoxia (FIO<sub>2</sub> = 60%) increased PaCO<sub>2</sub> and PaO<sub>2</sub>, decreased blood pH and caused thrombocytopenia and lymphocytosis. In lung tissue, neutrophil infiltration, nitric oxide concentration, carbonyl protein formation and the activity of complexes I and II of the mitochondrial respiratory chain increased. FIO<sub>2</sub> = 60% decreased SOD activity and caused several histologic changes.</p><p><strong>Conclusion: </strong>In conclusion, we have experimentally demonstrated that short-term exposure to high FIO<sub>2</sub> can cause oxidative stress in the lung.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140049376","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}
Pub Date : 2024-03-01Epub Date: 2024-03-11DOI: 10.1080/08958378.2024.2327364
Kristine Krajnak, Hong Kan, Janet A Thompson, Walter McKinney, Stacey Waugh, Tim South, Dru Burns, Ryan Lebouf, Jared Cumpston, Theresa Boots, Jeffrey S Fedan
Objective: Inhalation of diesel exhaust (DE) has been shown to be an occupational hazard in the transportation, mining, and gas and oil industries. DE also contributes to air pollution, and therefore, is a health hazard to the general public. Because of its effects on human health, changes have been made to diesel engines to reduce both the amounts of particulate matter and volatile fumes they generate. The goal of the current study was to examine the effects of inhalation of diesel exhaust.
Materials and methods: The study presented here specifically examines the effects of exposure to 0.2 and 1.0 mg/m3 DE or filtered air (6h/d for 4 d) on measures of peripheral and cardio-vascular function, and biomarkers of heart and kidney dysfunction in male rats. A Tier 2 engine used in oil and gas fracking operations was used to generate the diesel exhaust.
Results: Exposure to 0.2 mg/m3 DE resulted in an increase in blood pressure 1d following the last exposure, and increases in dobutamine-induced cardiac output and stroke volume 1 and 27d after exposure. Changes in peripheral vascular responses to norepinephrine and acetylcholine were minimal as were changes in transcript expression in the heart and kidney. Exposure to 1.0 mg/m3 DE did not result in major changes in blood pressure, measures of cardiac function, peripheral vascular function or transcript expression.
Discussion and conclusions: Based on the results of this study, we suggest that exposure to DE generated by a Tier 2 compliant diesel engine generates acute effects on biomarkers indicative of cardiovascular dysfunction. Recovery occurs quickly with most measures of vascular/cardiovascular function returning to baseline levels by 7d following exposure.
目的:吸入柴油废气(DE)已被证明是运输、采矿、天然气和石油行业的一种职业危害。柴油废气也会造成空气污染,因此对普通公众的健康也有危害。由于其对人体健康的影响,人们对柴油发动机进行了改造,以减少其产生的颗粒物和挥发性烟雾。本研究的目的是检测吸入柴油机废气的影响:本研究专门探讨了雄性大鼠暴露于 0.2 和 1.0 mg/m3 DE 或过滤空气(6 小时/天,持续 4 天)对外周和心血管功能以及心脏和肾脏功能障碍生物标志物的影响。产生柴油废气的是一台用于石油和天然气压裂作业的 2 级发动机:结果:接触 0.2 mg/m3 DE 会导致血压在最后一次接触后 1d 升高,多巴酚丁胺诱导的心输出量和中风量在接触后 1d 和 27d 增加。外周血管对去甲肾上腺素和乙酰胆碱的反应变化很小,心脏和肾脏的转录表达变化也很小。暴露于 1.0 毫克/立方米 DE 不会导致血压、心脏功能测量、外周血管功能或转录物表达发生重大变化:根据这项研究的结果,我们认为,暴露于符合 2 级标准的柴油发动机产生的 DE 会对表明心血管功能障碍的生物标志物产生急性影响。大部分血管/心血管功能指标在接触后 7 天内会迅速恢复到基线水平。
{"title":"Biological effects of diesel exhaust inhalation. III cardiovascular function.","authors":"Kristine Krajnak, Hong Kan, Janet A Thompson, Walter McKinney, Stacey Waugh, Tim South, Dru Burns, Ryan Lebouf, Jared Cumpston, Theresa Boots, Jeffrey S Fedan","doi":"10.1080/08958378.2024.2327364","DOIUrl":"10.1080/08958378.2024.2327364","url":null,"abstract":"<p><strong>Objective: </strong>Inhalation of diesel exhaust (DE) has been shown to be an occupational hazard in the transportation, mining, and gas and oil industries. DE also contributes to air pollution, and therefore, is a health hazard to the general public. Because of its effects on human health, changes have been made to diesel engines to reduce both the amounts of particulate matter and volatile fumes they generate. The goal of the current study was to examine the effects of inhalation of diesel exhaust.</p><p><strong>Materials and methods: </strong>The study presented here specifically examines the effects of exposure to 0.2 and 1.0 mg/m<sup>3</sup> DE or filtered air (6h/d for 4 d) on measures of peripheral and cardio-vascular function, and biomarkers of heart and kidney dysfunction in male rats. A Tier 2 engine used in oil and gas fracking operations was used to generate the diesel exhaust.</p><p><strong>Results: </strong>Exposure to 0.2 mg/m<sup>3</sup> DE resulted in an increase in blood pressure 1d following the last exposure, and increases in dobutamine-induced cardiac output and stroke volume 1 and 27d after exposure. Changes in peripheral vascular responses to norepinephrine and acetylcholine were minimal as were changes in transcript expression in the heart and kidney. Exposure to 1.0 mg/m<sup>3</sup> DE did not result in major changes in blood pressure, measures of cardiac function, peripheral vascular function or transcript expression.</p><p><strong>Discussion and conclusions: </strong>Based on the results of this study, we suggest that exposure to DE generated by a Tier 2 compliant diesel engine generates acute effects on biomarkers indicative of cardiovascular dysfunction. Recovery occurs quickly with most measures of vascular/cardiovascular function returning to baseline levels by 7d following exposure.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11099779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140093817","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}
Pub Date : 2024-03-01Epub Date: 2024-03-15DOI: 10.1080/08958378.2024.2324033
Robyn L Prueitt, Cassandra J Meakin, Nicholas L Drury, Julie E Goodman
Objectives: Mortality from respiratory and cardiovascular health conditions contributes largely to the total mortality that has been associated with exposure to PM2.5 in epidemiology studies. A mode of action (MoA) for these underlying morbidities has not been established, but it has been proposed that some effects of PM2.5 occur through activation of neural reflexes.
Materials and methods: We critically reviewed the experimental studies of PM2.5 (including ambient PM2.5, diesel exhaust particles, concentrated ambient particles, diesel exhaust, and cigarette smoke) and neural reflex activation, and applied the principles of the International Programme on Chemical Safety (IPCS) MoA/human relevance framework to assess whether they support a biologically plausible and human-relevant MoA by which PM2.5 could contribute to cardiovascular and respiratory causes of death. We also considered whether the evidence from these studies supports a non-threshold MoA that operates at low, human-relevant PM2.5 exposure concentrations.
Results and discussion: We found that the proposed MoA of neural reflex activation is biologically plausible for PM2.5-induced respiratory effects at high exposure levels used in experimental studies, but further studies are needed to fill important data gaps regarding the relevance of this MoA to humans at lower PM2.5 exposure levels. A role for the proposed MoA in PM2.5-induced cardiovascular effects is plausible for some effects but not others.
Conclusions: Further studies are needed to determine whether neural reflex activation is the MoA by which PM2.5 could cause either respiratory or cardiovascular morbidities in humans, particularly at the ambient concentrations associated with total mortality in epidemiology studies.
{"title":"Evaluation of neural reflex activation as a potential mode of action for respiratory and cardiovascular effects of fine particulate matter.","authors":"Robyn L Prueitt, Cassandra J Meakin, Nicholas L Drury, Julie E Goodman","doi":"10.1080/08958378.2024.2324033","DOIUrl":"10.1080/08958378.2024.2324033","url":null,"abstract":"<p><strong>Objectives: </strong>Mortality from respiratory and cardiovascular health conditions contributes largely to the total mortality that has been associated with exposure to PM<sub>2.5</sub> in epidemiology studies. A mode of action (MoA) for these underlying morbidities has not been established, but it has been proposed that some effects of PM<sub>2.5</sub> occur through activation of neural reflexes.</p><p><strong>Materials and methods: </strong>We critically reviewed the experimental studies of PM<sub>2.5</sub> (including ambient PM<sub>2.5</sub>, diesel exhaust particles, concentrated ambient particles, diesel exhaust, and cigarette smoke) and neural reflex activation, and applied the principles of the International Programme on Chemical Safety (IPCS) MoA/human relevance framework to assess whether they support a biologically plausible and human-relevant MoA by which PM<sub>2.5</sub> could contribute to cardiovascular and respiratory causes of death. We also considered whether the evidence from these studies supports a non-threshold MoA that operates at low, human-relevant PM<sub>2.5</sub> exposure concentrations.</p><p><strong>Results and discussion: </strong>We found that the proposed MoA of neural reflex activation is biologically plausible for PM<sub>2.5</sub>-induced respiratory effects at high exposure levels used in experimental studies, but further studies are needed to fill important data gaps regarding the relevance of this MoA to humans at lower PM<sub>2.5</sub> exposure levels. A role for the proposed MoA in PM<sub>2.5</sub>-induced cardiovascular effects is plausible for some effects but not others.</p><p><strong>Conclusions: </strong>Further studies are needed to determine whether neural reflex activation is the MoA by which PM<sub>2.5</sub> could cause either respiratory or cardiovascular morbidities in humans, particularly at the ambient concentrations associated with total mortality in epidemiology studies.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140131359","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}
Pub Date : 2024-03-01Epub Date: 2024-03-19DOI: 10.1080/08958378.2024.2329935
Ronald F Dodson, Jacqueline Moline, Carlos D Salinas, Lee W Poye
Introduction: Tissue from a 77-year-old man diagnosed with mesothelioma was referred with a request for identification of the presence of fibrous structures in tissue samples. The individual's work history including working as a "mucker" at a specific "industrial" talc mine.
Methods: Ferruginous bodies in the tissue digests as well as asbestos fibers were found. A bulk sample of a talc containing product from that mine was also analyzed.
Discussions/conclusions: The correlation between the unique asbestos mineral/fibrous content of the talc to which he was exposed and findings of the same type of asbestos found in his lung is discussed. The type of asbestos found (tremolite) is a "non-commercial" type of asbestos that has been identified in some talc deposits. Tremolite, like all forms of asbestos is a causative agent for mesothelioma-the disease from which this individual suffered.
{"title":"Elongated particulate burden in an individual who died of mesothelioma and had an occupational history as a talc \"mucker\".","authors":"Ronald F Dodson, Jacqueline Moline, Carlos D Salinas, Lee W Poye","doi":"10.1080/08958378.2024.2329935","DOIUrl":"10.1080/08958378.2024.2329935","url":null,"abstract":"<p><strong>Introduction: </strong>Tissue from a 77-year-old man diagnosed with mesothelioma was referred with a request for identification of the presence of fibrous structures in tissue samples. The individual's work history including working as a \"mucker\" at a specific \"industrial\" talc mine.</p><p><strong>Methods: </strong>Ferruginous bodies in the tissue digests as well as asbestos fibers were found. A bulk sample of a talc containing product from that mine was also analyzed.</p><p><strong>Discussions/conclusions: </strong>The correlation between the unique asbestos mineral/fibrous content of the talc to which he was exposed and findings of the same type of asbestos found in his lung is discussed. The type of asbestos found (tremolite) is a \"non-commercial\" type of asbestos that has been identified in some talc deposits. Tremolite, like all forms of asbestos is a causative agent for mesothelioma-the disease from which this individual suffered.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140158025","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}
Pub Date : 2024-02-26DOI: 10.1080/08958378.2024.2315124
Zohreh Mohebian, Fatemeh Paridokht, Sara Karimi Zeverdegani, Farzaneh Mohammadi
Nail salons offer a developing and diverse occupation for many women, especially the new generation. Due to the increasing apprehension surrounding heavy metals in dust caused by filing nails conta...
{"title":"Inhalation exposure to toxic heavy metals in nail salon technicians and health risk assessment using Monte Carlo simulation","authors":"Zohreh Mohebian, Fatemeh Paridokht, Sara Karimi Zeverdegani, Farzaneh Mohammadi","doi":"10.1080/08958378.2024.2315124","DOIUrl":"https://doi.org/10.1080/08958378.2024.2315124","url":null,"abstract":"Nail salons offer a developing and diverse occupation for many women, especially the new generation. Due to the increasing apprehension surrounding heavy metals in dust caused by filing nails conta...","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139968178","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}
Pub Date : 2024-02-01Epub Date: 2024-03-13DOI: 10.1080/08958378.2024.2318378
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
Objective: 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.
Methods: 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.
Results: 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.
Discussion: 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.
Conclusion: These results highlight life-stage significance in this preclinical lupus model and underscore omega-3 fatty acids' therapeutic potential against toxicant-triggered autoimmune responses.
目的:职业暴露于可吸入结晶二氧化硅(cSiO2)与红斑狼疮的发病有关。以前对易患红斑狼疮的幼年小鼠进行的研究表明,鼻内接触二氧化硅会引发自身免疫,而二十二碳六烯酸(DHA)可预防这种免疫。本研究探讨了 cSiO2 和 DHA 对成熟的红斑狼疮易感成年小鼠的影响,这更能代表暴露于 cSiO2 的工人年龄:方法:雌性 NZBWF1 小鼠(14 周大)喂食对照组(CON)或添加 DHA 的饲料。两周后,每周向小鼠体内灌注生理盐水(VEH)或 1 毫克二氧化硅,连续四周。然后对灌注后1周和5周的组群进行分析,以检测肺部炎症、细胞计数、趋化因子、组织病理学、B细胞和T细胞浸润、自身抗体和基因特征,结果与自身免疫性肾小球肾炎的发病相关:cSiO2/CON小鼠的肺部表现出细胞增多、趋化因子增多、CD3+ T细胞增多、CD45R + B细胞增多、IgG + 浆细胞增多、基因表达增多、IgG自身抗体增多和肾小球肥大。补充 DHA 可减轻所有这些影响:这里使用的成熟成年 NZBWF1 小鼠代表了与免疫耐受破坏相吻合的生命阶段,也更恰当地代表了暴露于二氧化硅的工人的年龄(20-30 岁)。二氧化硅在成熟成年小鼠中诱发了强烈的肺部炎症、自身抗体反应和肾小球肾炎,超过了之前在年轻成年人中观察到的影响。在成年小鼠中,等同于人体剂量的 DHA 能有效对抗二氧化硅诱导的炎症/自身免疫反应,这反映了对幼年小鼠的保护作用:这些结果凸显了临床前狼疮模型中生命阶段的重要性,并强调了欧米伽-3 脂肪酸对毒性诱发的自身免疫反应的治疗潜力。
{"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 (cSiO<sub>2</sub>) has been linked to lupus development. Previous studies in young lupus-prone mice revealed that intranasal cSiO<sub>2</sub> exposure triggered autoimmunity, preventable with docosahexaenoic acid (DHA). This study explores cSiO<sub>2</sub> and DHA effects in mature lupus-prone adult mice, more representative of cSiO<sub>2</sub>-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 cSiO<sub>2</sub> 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. cSiO<sub>2</sub>/CON mice displayed significant ectopic lymphoid tissue formation in lungs at 1 week, increasing by 5 weeks. cSiO<sub>2</sub>/CON lungs exhibited elevated cellularity, chemokines, CD3<sup>+</sup> T-cells, CD45R <sup>+</sup> B-cells, IgG <sup>+</sup> 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. cSiO<sub>2</sub>-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 cSiO<sub>2</sub>-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":null,"pages":null},"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}
Pub Date : 2024-02-01Epub Date: 2024-02-29DOI: 10.1080/08958378.2024.2318389
Arjun Pitchai, Kimberly Buhman, Jonathan H Shannahan
Many inhalation exposures induce pulmonary inflammation contributing to disease progression. Inflammatory processes are actively regulated via 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.
{"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":null,"pages":null},"PeriodicalIF":2.1,"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}
Pub Date : 2024-02-01Epub Date: 2024-02-18DOI: 10.1080/08958378.2024.2316241
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
Objective: 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.
Materials and methods: 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.
Results: 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.
Discussion and conclusions: 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.
{"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":null,"pages":null},"PeriodicalIF":2.1,"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}
Pub Date : 2024-02-01Epub Date: 2024-02-23DOI: 10.1080/08958378.2024.2319315
Paulina Natalia Kopa-Stojak, Rafal Pawliczak
Objectives: 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.
Materials and methods: 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'.
Results: 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.
Discussion: 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.
{"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":null,"pages":null},"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}
Pub Date : 2024-01-01Epub Date: 2024-02-11DOI: 10.1080/08958378.2024.2312801
John Valerian Corda, B Satish Shenoy, Kamarul Arifin Ahmad, Leslie Lewis, Prakashini K, Anoop Rao, Mohammad Zuber
Objective: 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.Materials and methods: 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.Results: 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.Discussion and conclusions: 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.
{"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/m<sup>3</sup> 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":null,"pages":null},"PeriodicalIF":2.1,"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}