Pub Date : 2024-10-10DOI: 10.1080/08958378.2024.2410736
Jong-Uk Lee, Jisu Hong, Eunji Park, Junyeong Baek, Ye Min Choi, Su Sie Chin, Ki-Joon Jeon, Woo-Jin Kim, Sung Woo Park, Sung Hwan Jeong
Introduction: Particulate matter (PM) air pollution is associated with an increased incidence of lung diseases, but the underlying mechanisms have not been fully elucidated. In this study, a mouse model of subacute lung inflammation was employed to investigate the cellular responses and gene expression changes induced by exposure to natural ambient air pollution.
Methods: C57BL/6J mice were exposed to road dust (primarily PM10) at 150 µg/m³ for 21 days (8 h/day) through a nose-only inhalation exposure system. Lung tissues were analyzed for the expression of proinflammatory signaling, oxidative stress, and fibrosis markers. RNA-sequencing analysis was conducted to identify differentially expressed genes (DEGs). A gene ontology over-representation analysis was performed to identify the altered genetic pathways.
Results: Elevated levels of proinflammatory cytokines, including IL-1β, IL-6, and TNF-α, and an increase in phosphorylated MAPK were determined in the road dust exposure group compared to the control group. Histopathological examinations revealed more severe lung inflammation and damage in the exposed mice, including fibrosis and bronchiolar hyperplasia. Gene expression profiling identified 108 DEGs, with decreases in most except genes such as Krt15 and Reg3g. The protein-protein interaction network analysis together with text-mining identified 18 key hub genes, associated with fatty acid oxidation, lipid metabolism, and peroxisomes.
Conclusion: This study identified key genes, signaling pathways, and cellular responses in mouse lung affected by road dust exposure. These findings contribute to a deeper understanding of the transcriptional and cellular responses induced by subacute exposure to the PM in road dust.
{"title":"Gene expression changes in mouse lung induced by subacute inhalation of PM<sub>10</sub>-rich particulate matter.","authors":"Jong-Uk Lee, Jisu Hong, Eunji Park, Junyeong Baek, Ye Min Choi, Su Sie Chin, Ki-Joon Jeon, Woo-Jin Kim, Sung Woo Park, Sung Hwan Jeong","doi":"10.1080/08958378.2024.2410736","DOIUrl":"https://doi.org/10.1080/08958378.2024.2410736","url":null,"abstract":"<p><strong>Introduction: </strong>Particulate matter (PM) air pollution is associated with an increased incidence of lung diseases, but the underlying mechanisms have not been fully elucidated. In this study, a mouse model of subacute lung inflammation was employed to investigate the cellular responses and gene expression changes induced by exposure to natural ambient air pollution.</p><p><strong>Methods: </strong>C57BL/6J mice were exposed to road dust (primarily PM10) at 150 µg/m³ for 21 days (8 h/day) through a nose-only inhalation exposure system. Lung tissues were analyzed for the expression of proinflammatory signaling, oxidative stress, and fibrosis markers. RNA-sequencing analysis was conducted to identify differentially expressed genes (DEGs). A gene ontology over-representation analysis was performed to identify the altered genetic pathways.</p><p><strong>Results: </strong>Elevated levels of proinflammatory cytokines, including IL-1β, IL-6, and TNF-α, and an increase in phosphorylated MAPK were determined in the road dust exposure group compared to the control group. Histopathological examinations revealed more severe lung inflammation and damage in the exposed mice, including fibrosis and bronchiolar hyperplasia. Gene expression profiling identified 108 DEGs, with decreases in most except genes such as Krt15 and Reg3g. The protein-protein interaction network analysis together with text-mining identified 18 key hub genes, associated with fatty acid oxidation, lipid metabolism, and peroxisomes.</p><p><strong>Conclusion: </strong>This study identified key genes, signaling pathways, and cellular responses in mouse lung affected by road dust exposure. These findings contribute to a deeper understanding of the transcriptional and cellular responses induced by subacute exposure to the PM in road dust.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400165","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 : 2024-07-01Epub Date: 2024-06-23DOI: 10.1080/08958378.2024.2367419
Bahman Asgharian, Owen Price, Scott Wasdo, Cissy Li, Kamau O Peters, Ryan M Haskins, Susan Chemerynski, Jeffry Schroeter
Objective: Cigarette smoking can lead to a host of adverse health effects such as lung and heart disease. Increased lung cancer risk is associated with inhalation of carcinogens present in a puff of smoke. These carcinogenic compounds deposit in the lung at different sites and trigger a cascade of events leading to adverse outcomes. Understanding the site-specific deposition of various smoke constituents will inform the study of respiratory diseases from cigarette smoking. We previously developed a deposition model for inhalation of aerosol from electronic nicotine delivery systems. In this study, the model was modified to simulate inhalation of cigarette smoke consisting of soluble and insoluble tar, nicotine, and cigarette-specific constituents that are known or possible human carcinogens.
Materials and methods: The deposition model was further modified to account for nicotine protonation and other cigarette-specific physics-based mechanisms that affect smoke deposition. Model predictions showed a total respiratory tract uptake in the lung for formaldehyde (99%), nicotine (80%), and benzo[a]pyrene (60%).
Results: The site of deposition and uptake depended primarily on the constituent's saturation vapor pressure. High vapor pressure constituents such as formaldehyde were preferentially absorbed in the oral cavity and proximal lung regions, while low vapor pressure constituents such as benzo[a]pyrene were deposited in the deep lung regions. Model predictions of exhaled droplet size, droplet retention, nicotine retention, and uptake of aldehydes compared favorably with experimental data.
Conclusion: The deposition model can be integrated into exposure assessments and other studies that evaluate potential adverse health effects from cigarette smoking.
{"title":"The fate of an inhaled cigarette puff in the human respiratory tract.","authors":"Bahman Asgharian, Owen Price, Scott Wasdo, Cissy Li, Kamau O Peters, Ryan M Haskins, Susan Chemerynski, Jeffry Schroeter","doi":"10.1080/08958378.2024.2367419","DOIUrl":"10.1080/08958378.2024.2367419","url":null,"abstract":"<p><strong>Objective: </strong>Cigarette smoking can lead to a host of adverse health effects such as lung and heart disease. Increased lung cancer risk is associated with inhalation of carcinogens present in a puff of smoke. These carcinogenic compounds deposit in the lung at different sites and trigger a cascade of events leading to adverse outcomes. Understanding the site-specific deposition of various smoke constituents will inform the study of respiratory diseases from cigarette smoking. We previously developed a deposition model for inhalation of aerosol from electronic nicotine delivery systems. In this study, the model was modified to simulate inhalation of cigarette smoke consisting of soluble and insoluble tar, nicotine, and cigarette-specific constituents that are known or possible human carcinogens.</p><p><strong>Materials and methods: </strong>The deposition model was further modified to account for nicotine protonation and other cigarette-specific physics-based mechanisms that affect smoke deposition. Model predictions showed a total respiratory tract uptake in the lung for formaldehyde (99%), nicotine (80%), and benzo[a]pyrene (60%).</p><p><strong>Results: </strong>The site of deposition and uptake depended primarily on the constituent's saturation vapor pressure. High vapor pressure constituents such as formaldehyde were preferentially absorbed in the oral cavity and proximal lung regions, while low vapor pressure constituents such as benzo[a]pyrene were deposited in the deep lung regions. Model predictions of exhaled droplet size, droplet retention, nicotine retention, and uptake of aldehydes compared favorably with experimental data.</p><p><strong>Conclusion: </strong>The deposition model can be integrated into exposure assessments and other studies that evaluate potential adverse health effects from cigarette smoking.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141440452","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 : 2024-07-01Epub Date: 2024-05-22DOI: 10.1080/08958378.2024.2352748
Molly E Harmon, Michelle Fiamingo, Sydnie Toler, Kaleb Lee, Yongho Kim, Brandi Martin, Ian Gilmour, Aimen K Farraj, Mehdi S Hazari
Objectives: Living conditions play a major role in health and well-being, particularly for the cardiovascular and pulmonary systems. Depleted housing contributes to impairment and development of disease, but how it impacts body resiliency during exposure to environmental stressors is unknown. This study examined the effect of depleted (DH) versus enriched housing (EH) on cardiopulmonary function and subsequent responses to wildfire smoke. Materials and Methods: Two cohorts of healthy female mice, one of them surgically implanted with radiotelemeters for the measurement of electrocardiogram, body temperature (Tco) and activity, were housed in either DH or EH for 7 weeks. Telemetered mice were exposed for 1 h to filtered air (FA) and then flaming eucalyptus wildfire smoke (WS) while untelemetered mice, which were used for ventilatory assessment and tissue collection, were exposed to either FA or WS. Animals were continuously monitored for 5-7 days after exposure. Results: EH prevented a decrease in Tco after radiotelemetry surgery. EH mice also had significantly higher activity levels and lower heart rate during and after FA and WS. Moreover, EH caused a decreased number of cardiac arrhythmias during WS. WS caused ventilatory depression in DH mice but not EH mice. Housing enrichment also upregulated the expression of cardioprotective genes in the heart. Conclusions: The results of this study indicate that housing conditions impact overall health and cardiopulmonary function. More importantly, depleted housing appears to worsen the response to air pollution. Thus, non-chemical factors should be considered when assessing the susceptibility of populations, especially when it comes to extreme environmental events.
{"title":"The effect of enriched versus depleted housing on eucalyptus smoke-induced cardiovascular dysfunction in mice.","authors":"Molly E Harmon, Michelle Fiamingo, Sydnie Toler, Kaleb Lee, Yongho Kim, Brandi Martin, Ian Gilmour, Aimen K Farraj, Mehdi S Hazari","doi":"10.1080/08958378.2024.2352748","DOIUrl":"10.1080/08958378.2024.2352748","url":null,"abstract":"<p><p><b>Objectives:</b> Living conditions play a major role in health and well-being, particularly for the cardiovascular and pulmonary systems. Depleted housing contributes to impairment and development of disease, but how it impacts body resiliency during exposure to environmental stressors is unknown. This study examined the effect of depleted (DH) versus enriched housing (EH) on cardiopulmonary function and subsequent responses to wildfire smoke. <b>Materials and Methods:</b> Two cohorts of healthy female mice, one of them surgically implanted with radiotelemeters for the measurement of electrocardiogram, body temperature (Tco) and activity, were housed in either DH or EH for 7 weeks. Telemetered mice were exposed for 1 h to filtered air (FA) and then flaming eucalyptus wildfire smoke (WS) while untelemetered mice, which were used for ventilatory assessment and tissue collection, were exposed to either FA or WS. Animals were continuously monitored for 5-7 days after exposure. <b>Results:</b> EH prevented a decrease in Tco after radiotelemetry surgery. EH mice also had significantly higher activity levels and lower heart rate during and after FA and WS. Moreover, EH caused a decreased number of cardiac arrhythmias during WS. WS caused ventilatory depression in DH mice but not EH mice. Housing enrichment also upregulated the expression of cardioprotective genes in the heart. <b>Conclusions:</b> The results of this study indicate that housing conditions impact overall health and cardiopulmonary function. More importantly, depleted housing appears to worsen the response to air pollution. Thus, non-chemical factors should be considered when assessing the susceptibility of populations, especially when it comes to extreme environmental events.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141079941","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 : 2024-07-01Epub Date: 2024-07-10DOI: 10.1080/08958378.2024.2374394
Ghada N El-Sarnagawy, Fatma M Elgazzar, Mona M Ghonem
Objectives: Delayed neuropsychiatric sequelae (DNS) are critical complications following acute carbon monoxide (CO) poisoning that can substantially affect the patient's life. Identifying high-risk patients for developing DNS may improve the quality of follow-up care. To date, the predictive DNS determinants are still controversial. Consequently, this study aimed to construct a practical nomogram for predicting DNS in acute CO-poisoned patients.
Methods: This retrospective study was conducted on patients with acute CO poisoning admitted to the Tanta University Poison Control Center (TUPCC) from December 2018 to December 2022. Demographic, toxicological, and initial clinical characteristics data, as well as laboratory investigation results, were recorded for the included patients. After acute recovery, patients were followed up for six months and categorized into patients with and without DNS.
Results: Out of 174 enrolled patients, 38 (21.8%) developed DNS. The initial Glasgow Coma Scale (GCS), carboxyhemoglobin (COHb) level, CO exposure duration, oxygen saturation, PaCO2, and pulse rate were significantly associated with DNS development by univariate analysis. However, the constructed nomogram based on the multivariable regression analysis included three parameters: duration of CO exposure, COHb level, and GCS with adjusted odd ratios of 1.453 (95% CI: 1.116-1.892), 1.262 (95% CI: 1.126-1.415), and 0.619 (95% CI: 0.486-0.787), respectively. The internal validation of the nomogram exhibited excellent discrimination (area under the curve [AUC] = 0.962), good calibration, and satisfactory decision curve analysis for predicting the DNS probability.
Conclusions: The proposed nomogram could be considered a simple, precise, and applicable tool to predict DNS development in acute CO-poisoned patients.
目的:迟发性神经精神后遗症(DNS)是急性一氧化碳(CO)中毒后的重要并发症,会严重影响患者的生活。识别发生 DNS 的高危患者可提高后续护理的质量。迄今为止,预测 DNS 的决定因素仍存在争议。因此,本研究旨在构建一个实用的提名图,用于预测急性 CO 中毒患者的 DNS:这项回顾性研究针对 2018 年 12 月至 2022 年 12 月期间坦塔大学中毒控制中心(TUPCC)收治的急性 CO 中毒患者。研究记录了纳入患者的人口统计学、毒理学、初始临床特征数据以及实验室检查结果。急性康复后,对患者进行为期六个月的随访,并将其分为有 DNS 和无 DNS 患者:在 174 名登记患者中,38 人(21.8%)出现 DNS。通过单变量分析,最初的格拉斯哥昏迷量表(GCS)、碳氧血红蛋白(COHb)水平、CO 暴露持续时间、血氧饱和度、PaCO2 和脉搏与 DNS 的发生显著相关。然而,基于多变量回归分析构建的提名图包括三个参数:一氧化碳暴露持续时间、一氧化碳血红蛋白水平和 GCS,调整后的奇异比分别为 1.453(95% CI:1.116-1.892)、1.262(95% CI:1.126-1.415)和 0.619(95% CI:0.486-0.787)。提名图的内部验证显示了极好的区分度(曲线下面积 [AUC] = 0.962)、良好的校准性以及令人满意的预测 DNS 概率的决策曲线分析:结论:所提出的提名图可被视为预测急性 CO 中毒患者 DNS 发展的简单、精确和适用的工具。
{"title":"Development of a risk prediction nomogram for delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning.","authors":"Ghada N El-Sarnagawy, Fatma M Elgazzar, Mona M Ghonem","doi":"10.1080/08958378.2024.2374394","DOIUrl":"10.1080/08958378.2024.2374394","url":null,"abstract":"<p><strong>Objectives: </strong>Delayed neuropsychiatric sequelae (DNS) are critical complications following acute carbon monoxide (CO) poisoning that can substantially affect the patient's life. Identifying high-risk patients for developing DNS may improve the quality of follow-up care. To date, the predictive DNS determinants are still controversial. Consequently, this study aimed to construct a practical nomogram for predicting DNS in acute CO-poisoned patients.</p><p><strong>Methods: </strong>This retrospective study was conducted on patients with acute CO poisoning admitted to the Tanta University Poison Control Center (TUPCC) from December 2018 to December 2022. Demographic, toxicological, and initial clinical characteristics data, as well as laboratory investigation results, were recorded for the included patients. After acute recovery, patients were followed up for six months and categorized into patients with and without DNS.</p><p><strong>Results: </strong>Out of 174 enrolled patients, 38 (21.8%) developed DNS. The initial Glasgow Coma Scale (GCS), carboxyhemoglobin (COHb) level, CO exposure duration, oxygen saturation, PaCO<sub>2</sub>, and pulse rate were significantly associated with DNS development by univariate analysis. However, the constructed nomogram based on the multivariable regression analysis included three parameters: duration of CO exposure, COHb level, and GCS with adjusted odd ratios of 1.453 (95% CI: 1.116-1.892), 1.262 (95% CI: 1.126-1.415), and 0.619 (95% CI: 0.486-0.787), respectively. The internal validation of the nomogram exhibited excellent discrimination (area under the curve [AUC] = 0.962), good calibration, and satisfactory decision curve analysis for predicting the DNS probability.</p><p><strong>Conclusions: </strong>The proposed nomogram could be considered a simple, precise, and applicable tool to predict DNS development in acute CO-poisoned patients.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563331","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 : 2024-07-01Epub Date: 2024-07-02DOI: 10.1080/08958378.2024.2367422
Tyler Ferracini, Sarah Brown, Brooke Simmons, Heather Avens, Shannon Gaffney, Scott Dotson, Jennifer Sahmel
Objectives: To evaluate potential airborne asbestos exposures during brake maintenance and repair activities on a P&H overhead crane, and during subsequent handling of the mechanic's clothing.
Methods: Personal (n = 27) and area (n = 61) airborne fiber concentrations were measured during brake tests, removal, hand sanding, compressed air use, removal and reattachment of chrysotile-containing brake linings, and reinstallation of the brake linings. The mechanic's clothing was used to measure potential exposure during clothes handling.
Results: All brake linings contained between 19.9% to 52.4% chrysotile asbestos. No amphibole fibers were detected in any bulk or airborne samples. The average full-shift airborne chrysotile concentration was 0.035 f/cc (PCM-equivalent asbestos-specific fibers, or PCME). Average task-based personal air samples collected during brake maintenance, sanding, compressed air use, and brake lining removal tasks ranged from 0 to 0.48 f/cc (PCME). The calculated 30-minute time-weighted average (TWA) airborne chrysotile concentration associated with 5-15 minutes of clothes handling was 0-0.035 f/cc PCME.
Conclusion: The results indicated that personal and area TWA fiber concentrations measured during all crane brake maintenance and clothes handling tasks were below the current OSHA 8-h TWA Permissible Exposure Limit for asbestos of 0.1 f/cc. Further, no airborne asbestos fibers were measured during routine brake maintenance tasks following the manufacturer's maintenance manual procedures. All short-term airborne chrysotile concentrations measured during non-routine tasks were below the current 30-minute OSHA excursion limit for asbestos of 1 f/cc. This study adds to the available data regarding chrysotile exposure potential during maintenance on overhead cranes.
{"title":"Evaluation of airborne asbestos concentrations associated with the maintenance of brakes on an industrial overhead crane.","authors":"Tyler Ferracini, Sarah Brown, Brooke Simmons, Heather Avens, Shannon Gaffney, Scott Dotson, Jennifer Sahmel","doi":"10.1080/08958378.2024.2367422","DOIUrl":"10.1080/08958378.2024.2367422","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate potential airborne asbestos exposures during brake maintenance and repair activities on a P&H overhead crane, and during subsequent handling of the mechanic's clothing.</p><p><strong>Methods: </strong>Personal (<i>n</i> = 27) and area (<i>n</i> = 61) airborne fiber concentrations were measured during brake tests, removal, hand sanding, compressed air use, removal and reattachment of chrysotile-containing brake linings, and reinstallation of the brake linings. The mechanic's clothing was used to measure potential exposure during clothes handling.</p><p><strong>Results: </strong>All brake linings contained between 19.9% to 52.4% chrysotile asbestos. No amphibole fibers were detected in any bulk or airborne samples. The average full-shift airborne chrysotile concentration was 0.035 f/cc (PCM-equivalent asbestos-specific fibers, or PCME). Average task-based personal air samples collected during brake maintenance, sanding, compressed air use, and brake lining removal tasks ranged from 0 to 0.48 f/cc (PCME). The calculated 30-minute time-weighted average (TWA) airborne chrysotile concentration associated with 5-15 minutes of clothes handling was 0-0.035 f/cc PCME.</p><p><strong>Conclusion: </strong>The results indicated that personal and area TWA fiber concentrations measured during all crane brake maintenance and clothes handling tasks were below the current OSHA 8-h TWA Permissible Exposure Limit for asbestos of 0.1 f/cc. Further, no airborne asbestos fibers were measured during routine brake maintenance tasks following the manufacturer's maintenance manual procedures. All short-term airborne chrysotile concentrations measured during non-routine tasks were below the current 30-minute OSHA excursion limit for asbestos of 1 f/cc. This study adds to the available data regarding chrysotile exposure potential during maintenance on overhead cranes.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476549","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 : 2024-07-01Epub Date: 2024-05-20DOI: 10.1080/08958378.2024.2354398
Mary Buford, Sarah Lacher, Matthew Slattery, Daniel C Levings, Britten Postma, Andrij Holian, Chris Migliaccio
Due to climate change, wildfires have increased in intensity and duration. While wildfires threaten lives directly, the smoke has more far-reaching adverse health impacts. During an extreme 2017 wildfire event, residents of Seeley Lake, Montana were exposed to unusually high levels of wood smoke (WS) causing sustained effects on lung function (decreased FEV1/FVC). Objective: The present study utilized an animal model of WS exposure to research cellular and molecular mechanisms of the resulting health effects. Methods: Mice were exposed to inhaled WS utilizing locally harvested wood to recapitulate community exposures. WS was generated at a rate resulting in a 5 mg/m3 PM2.5 exposure for five days. Results: This exposure resulted in a similar 0.28 mg/m2 particle deposition (lung surface area) in mice that was calculated for human exposure. As with the community observations, there was a significant effect on lung function, increased resistance, and decreased compliance, that was more pronounced in males at an extended (2 months) timepoint and males were more affected than females: ex vivo assays illustrated changes to alveolar macrophage functions (increased TNFα secretion and decreased efferocytosis). Female mice had significantly elevated IL-33 levels in lungs, however, pretreatment of male mice with IL-33 resulted in an abrogation of the observed WS effects, suggesting a dose-dependent role of IL-33. Additionally, there were greater immunotoxic effects in male mice. Discussion: These findings replicated the outcomes in humans and suggest that IL-33 is involved in a mechanism of the adverse effects of WS exposures that inform on potential sex differences.
{"title":"A mouse model of wildfire smoke-induced health effects: sex differences in acute and sustained effects of inhalation exposures.","authors":"Mary Buford, Sarah Lacher, Matthew Slattery, Daniel C Levings, Britten Postma, Andrij Holian, Chris Migliaccio","doi":"10.1080/08958378.2024.2354398","DOIUrl":"10.1080/08958378.2024.2354398","url":null,"abstract":"<p><p>Due to climate change, wildfires have increased in intensity and duration. While wildfires threaten lives directly, the smoke has more far-reaching adverse health impacts. During an extreme 2017 wildfire event, residents of Seeley Lake, Montana were exposed to unusually high levels of wood smoke (WS) causing sustained effects on lung function (decreased FEV<sub>1</sub>/FVC). <b><i>Objective</i>:</b> The present study utilized an animal model of WS exposure to research cellular and molecular mechanisms of the resulting health effects. <b><i>Methods</i>:</b> Mice were exposed to inhaled WS utilizing locally harvested wood to recapitulate community exposures. WS was generated at a rate resulting in a 5 mg/m<sup>3</sup> PM<sub>2.5</sub> exposure for five days. <b><i>Results</i>:</b> This exposure resulted in a similar 0.28 mg/m<sup>2</sup> particle deposition (lung surface area) in mice that was calculated for human exposure. As with the community observations, there was a significant effect on lung function, increased resistance, and decreased compliance, that was more pronounced in males at an extended (2 months) timepoint and males were more affected than females: <i>ex vivo</i> assays illustrated changes to alveolar macrophage functions (increased TNFα secretion and decreased efferocytosis). Female mice had significantly elevated IL-33 levels in lungs, however, pretreatment of male mice with IL-33 resulted in an abrogation of the observed WS effects, suggesting a dose-dependent role of IL-33. Additionally, there were greater immunotoxic effects in male mice. <b><i>Discussion</i>:</b> These findings replicated the outcomes in humans and suggest that IL-33 is involved in a mechanism of the adverse effects of WS exposures that inform on potential sex differences.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11298299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070893","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}
Objective: PM2.5 is closely linked to vascular endothelial injury and has emerged as a major threat to human health. Our previous research indicated that exposure to PM2.5 induced an increased release of miR-421 from the bronchial epithelium. However, the role of miR-421 in PM2.5-induced endothelial injury remains elusive.
Materials and methods: We utilized a subacute PM2.5-exposure model in mice in vivo and an acute injury cell model in vitro to simulate PM2.5-associated endothelial injury. We also used quantitative real-time polymerase chain reaction, western blot, enzyme-linked immunosorbent assay, and immunohistochemistry to investigate the role of miR-421 in PM2.5-induced endothelial injury.
Results: Our findings reveal that inhibition of miR-421 attenuated PM2.5-induced endothelial injury and hypertension. Mechanistically, miR-421 inhibited the expression of angiotensin-converting enzyme 2 (ACE2) in human umbilical vein endothelial cells and upregulated the expression of the downstream molecule inducible nitric oxide synthase (iNOS), thereby exacerbating PM2.5-induced endothelial injury.
Conclusions: Our results indicate that PM2.5 exposure facilitates crosstalk between bronchial epithelial and endothelial cells via miR-421/ACE2/iNOS signaling pathway, mediating endothelial damage and hypertension. MiR-421 inhibition may offer a new strategy for the prevention and treatment of PM2.5-induced vascular endothelial injury.
{"title":"<i>MiR-421</i> mediates PM<sub>2.5</sub>-induced endothelial dysfunction via crosstalk between bronchial epithelial and endothelial cells.","authors":"Yiqing Chen, Mengting Zeng, Jinxin Xie, Zhihao Xiong, Yuxin Jin, Zihan Pan, Michail Spanos, Tianhui Wang, Hongyun Wang","doi":"10.1080/08958378.2024.2356839","DOIUrl":"https://doi.org/10.1080/08958378.2024.2356839","url":null,"abstract":"<p><strong>Objective: </strong>PM<sub>2.5</sub> is closely linked to vascular endothelial injury and has emerged as a major threat to human health. Our previous research indicated that exposure to PM<sub>2.5</sub> induced an increased release of <i>miR-421</i> from the bronchial epithelium. However, the role of <i>miR-421</i> in PM<sub>2.5</sub>-induced endothelial injury remains elusive.</p><p><strong>Materials and methods: </strong>We utilized a subacute PM<sub>2.5</sub>-exposure model in mice <i>in vivo</i> and an acute injury cell model <i>in vitro</i> to simulate PM<sub>2.5</sub>-associated endothelial injury. We also used quantitative real-time polymerase chain reaction, western blot, enzyme-linked immunosorbent assay, and immunohistochemistry to investigate the role of <i>miR-421</i> in PM<sub>2.5</sub>-induced endothelial injury.</p><p><strong>Results: </strong>Our findings reveal that inhibition of <i>miR-421</i> attenuated PM<sub>2.5</sub>-induced endothelial injury and hypertension. Mechanistically, <i>miR-421</i> inhibited the expression of <i>angiotensin-converting enzyme 2 (ACE2</i>) in human umbilical vein endothelial cells and upregulated the expression of the downstream molecule inducible <i>nitric oxide synthase (iNOS)</i>, thereby exacerbating PM<sub>2.5</sub>-induced endothelial injury.</p><p><strong>Conclusions: </strong>Our results indicate that PM<sub>2.5</sub> exposure facilitates crosstalk between bronchial epithelial and endothelial cells <i>via miR-421</i>/<i>ACE2</i>/<i>iNOS</i> signaling pathway, mediating endothelial damage and hypertension. <i>MiR-421</i> inhibition may offer a new strategy for the prevention and treatment of PM<sub>2.5</sub>-induced vascular endothelial injury.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141079939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01Epub Date: 2023-12-25DOI: 10.1080/08958378.2023.2297698
Osazuwa Clinton Ekhator, Fortune Chiemelie Orish, Ernest O Nnadi, Daprim Samuel Ogaji, Success Isuman, Orish Ebere Orisakwe
Rivers State, Niger Delta, Nigeria often referred to as the 'treasure bed of the nation' is the seat of crude oil production activities with the accompanying environmental degradation. The severity of the environmental pollution and contaminated air quality took a new turn for the worse in November 2016, when the residents of Port Harcourt city, Rivers State, a major oil producing State experienced for the first time, aerosol deposition of plumes of black soot. This systematic review paper is aimed at quantifying the severity of this public health challenge. Using appropriate search words, the following databases SCOPUS, PUBMED, Google Scholar, and AJOL were searched from 1990 to 2022 to enable comparative analyses of data before and after the emergence of black soot deposition. Air-related morbidities and mortalities such as cerebrospinal meningitis (CSM), chronic bronchitis, measles, pertussis, hemoptysis, cough, pulmonary tuberculosis, pneumonia, and upper respiratory tract infection (URTI), pneumonia, eye irritation, conjunctivitis, traumatic skin outgrowth, cancers, cardiovascular diseases, and child deformities were compared with levels of air pollutants and particulate matter. The results showed that Port Harcourt city's ambient air quality data were above the standard National Ambient Air Quality data and that of other regulatory agencies having higher levels of both inorganic and organic pollutants. There were significant relationships between air pollutants concentration with morbidities. These correlations were significant in the period covering 2016-2022. Consequently, it is concluded that the black soot emissions in Port Harcourt city, Nigeria has worsened the public health situation in the city.
{"title":"Impact of black soot emissions on public health in Niger Delta, Nigeria: understanding the severity of the problem.","authors":"Osazuwa Clinton Ekhator, Fortune Chiemelie Orish, Ernest O Nnadi, Daprim Samuel Ogaji, Success Isuman, Orish Ebere Orisakwe","doi":"10.1080/08958378.2023.2297698","DOIUrl":"10.1080/08958378.2023.2297698","url":null,"abstract":"<p><p>Rivers State, Niger Delta, Nigeria often referred to as the 'treasure bed of the nation' is the seat of crude oil production activities with the accompanying environmental degradation. The severity of the environmental pollution and contaminated air quality took a new turn for the worse in November 2016, when the residents of Port Harcourt city, Rivers State, a major oil producing State experienced for the first time, aerosol deposition of plumes of black soot. This systematic review paper is aimed at quantifying the severity of this public health challenge. Using appropriate search words, the following databases SCOPUS, PUBMED, Google Scholar, and AJOL were searched from 1990 to 2022 to enable comparative analyses of data before and after the emergence of black soot deposition. Air-related morbidities and mortalities such as cerebrospinal meningitis (CSM), chronic bronchitis, measles, pertussis, hemoptysis, cough, pulmonary tuberculosis, pneumonia, and upper respiratory tract infection (URTI), pneumonia, eye irritation, conjunctivitis, traumatic skin outgrowth, cancers, cardiovascular diseases, and child deformities were compared with levels of air pollutants and particulate matter. The results showed that Port Harcourt city's ambient air quality data were above the standard National Ambient Air Quality data and that of other regulatory agencies having higher levels of both inorganic and organic pollutants. There were significant relationships between air pollutants concentration with morbidities. These correlations were significant in the period covering 2016-2022. Consequently, it is concluded that the black soot emissions in Port Harcourt city, Nigeria has worsened the public health situation in the city.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139037564","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 : 2024-05-01Epub Date: 2024-07-21DOI: 10.1080/08958378.2024.2373094
Antonio F Saporito, Judith T Zelikoff
{"title":"An introduction to the adverse health impacts of inhaled toxicants in global marginalized communities.","authors":"Antonio F Saporito, Judith T Zelikoff","doi":"10.1080/08958378.2024.2373094","DOIUrl":"https://doi.org/10.1080/08958378.2024.2373094","url":null,"abstract":"","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141734021","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 : 2024-05-01Epub Date: 2023-04-19DOI: 10.1080/08958378.2023.2197941
Ramsés Santacruz-Márquez, Alison M Neff, Vasiliki E Mourikes, Endia J Fletcher, Jodi A Flaws
Important differences in health that are closely linked with social disadvantage exist within and between countries. According to the World Health Organization, life expectancy and good health continue to increase in many parts of the world, but fail to improve in other parts of the world, indicating that differences in life expectancy and health arise due to the circumstances in which people grow, live, work, and age, and the systems put in place to deal with illness. Marginalized communities experience higher rates of certain diseases and more deaths compared to the general population, indicating a profound disparity in health status. Although several factors place marginalized communities at high risk for poor health outcomes, one important factor is exposure to air pollutants. Marginalized communities and minorities are exposed to higher levels of air pollutants than the majority population. Interestingly, a link exists between air pollutant exposure and adverse reproductive outcomes, suggesting that marginalized communities may have increased reproductive disorders due to increased exposure to air pollutants compared to the general population. This review summarizes different studies showing that marginalized communities have higher exposure to air pollutants, the types of air pollutants present in our environment, and the associations between air pollution and adverse reproductive outcomes, focusing on marginalized communities.
{"title":"The effects of inhaled pollutants on reproduction in marginalized communities: a contemporary review.","authors":"Ramsés Santacruz-Márquez, Alison M Neff, Vasiliki E Mourikes, Endia J Fletcher, Jodi A Flaws","doi":"10.1080/08958378.2023.2197941","DOIUrl":"10.1080/08958378.2023.2197941","url":null,"abstract":"<p><p>Important differences in health that are closely linked with social disadvantage exist within and between countries. According to the World Health Organization, life expectancy and good health continue to increase in many parts of the world, but fail to improve in other parts of the world, indicating that differences in life expectancy and health arise due to the circumstances in which people grow, live, work, and age, and the systems put in place to deal with illness. Marginalized communities experience higher rates of certain diseases and more deaths compared to the general population, indicating a profound disparity in health status. Although several factors place marginalized communities at high risk for poor health outcomes, one important factor is exposure to air pollutants. Marginalized communities and minorities are exposed to higher levels of air pollutants than the majority population. Interestingly, a link exists between air pollutant exposure and adverse reproductive outcomes, suggesting that marginalized communities may have increased reproductive disorders due to increased exposure to air pollutants compared to the general population. This review summarizes different studies showing that marginalized communities have higher exposure to air pollutants, the types of air pollutants present in our environment, and the associations between air pollution and adverse reproductive outcomes, focusing on marginalized communities.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10584991/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9773240","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}