Inhalation ToxicologyPub Date : 2024-05-01Epub Date: 2024-02-13DOI: 10.1080/08958378.2024.2316875
Arthur D Stem, Matthew Gibb, Carlos A Roncal-Jimenez, Richard J Johnson, Jared M Brown
{"title":"Health burden of sugarcane burning on agricultural workers and nearby communities.","authors":"Arthur D Stem, Matthew Gibb, Carlos A Roncal-Jimenez, Richard J Johnson, Jared M Brown","doi":"10.1080/08958378.2024.2316875","DOIUrl":"10.1080/08958378.2024.2316875","url":null,"abstract":"<p><p>Sugarcane is the most widely cultivated crop in the world, with equatorial developing nations performing most of this agriculture. Burning sugarcane is a common practice to facilitate harvest, producing extremely high volumes of respirable particulate matter in the process. These emissions are known to have deleterious effects on agricultural workers and nearby communities, but the extent of this exposure and potential toxicity remain poorly characterized. As the epidemicof chronic kidney disease of an unknown etiology (CKDu) and its associated mortality continue to increase along with respiratory distress, there is an urgent need to investigate the causes, determine viable interventions to mitigate disease andimprove outcomes for groups experiencing disproportionate impact. The goal of this review is to establish the state of available literature, summarize what is known in terms of human health risk, and provide recommendations for what areas should be prioritized in research.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"327-342"},"PeriodicalIF":2.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11260540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722368","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}
S. Emma Sarles, Edward C. Hensel, Caleb Nuss, Janessa Terry, Risa Robinson
{"title":"Characterization of mass distribution in a biomimetic aerosol exposure system","authors":"S. Emma Sarles, Edward C. Hensel, Caleb Nuss, Janessa Terry, Risa Robinson","doi":"10.1080/08958378.2024.2341995","DOIUrl":"https://doi.org/10.1080/08958378.2024.2341995","url":null,"abstract":"Lack of biomimicry in geometry and flow conditions of emissions systems for analytical testing and biological exposure has led to fundamental limitations, including a poor understanding of dose del...","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"40 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140830373","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}
Rahanna N. Khan, Antonio F. Saporito, Jania Zenon, Lael Goodman, Judith T. Zelikoff
{"title":"Traffic-related air pollution in marginalized neighborhoods: a community perspective","authors":"Rahanna N. Khan, Antonio F. Saporito, Jania Zenon, Lael Goodman, Judith T. Zelikoff","doi":"10.1080/08958378.2024.2331259","DOIUrl":"https://doi.org/10.1080/08958378.2024.2331259","url":null,"abstract":"Marginalized communities are exposed to higher levels of traffic-related air pollution (TRAP) than the general population. TRAP exposure is linked to pulmonary toxicity, neurotoxicity, and cardiova...","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"1 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140584706","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}
Michael E. Stevens, Dennis J. Paustenbach, Noah J. Lockhart, Dalton E. Busboom, Blake M. Deckard, David W. Brew
{"title":"The presence of erionite in North American geologies and the estimated mesothelioma potency by region","authors":"Michael E. Stevens, Dennis J. Paustenbach, Noah J. Lockhart, Dalton E. Busboom, Blake M. Deckard, David W. Brew","doi":"10.1080/08958378.2024.2322496","DOIUrl":"https://doi.org/10.1080/08958378.2024.2322496","url":null,"abstract":"Erionite is a naturally occurring fibrous mineral found in soils in some geographical regions. Known for its potency for causing mesothelioma in the Cappadocia region of Turkey, the erionite fiber ...","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"56 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140584694","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":"Exposure to tungsten particles via inhalation triggers early toxicity marker expression in the rat brain.","authors":"Léo Macé, Chloé Brizais, Florence Bachelot, Annabelle Manoury, Sébastien Thomé, Céline Gloaguen, Imène Garali, Victor Magneron, Virginie Monceau, Amandine Sache, Frédéric Voyer, Christelle Elie, Laurence Roy, François Gensdarmes, Dmitry Klokov, Michelle L Block, Chrystelle Ibanez","doi":"10.1080/08958378.2024.2349895","DOIUrl":"https://doi.org/10.1080/08958378.2024.2349895","url":null,"abstract":"<p><strong>Objective: </strong>Our work is focused on tungsten, considered as an emerging contaminant. Its environmental dispersion is partly due to mining and military activities. Exposure scenario can also be occupational, in areas such as the hard metal industry and specific nuclear facilities. Our study investigated the cerebral effects induced by the inhalation of tungsten particles.</p><p><strong>Methods: </strong>Inhalation exposure campaigns were carried out at two different concentrations (5 and 80 mg/m<sup>3</sup>) in single and repeated modes (4 consecutive days) in adult rats within a nose-only inhalation chamber. Processes involved in brain toxicity were investigated 24 h after exposure.</p><p><strong>Results and discussion: </strong>Site-specific effects in terms of neuroanatomy and concentration-dependent changes in specific cellular actors were observed. Results obtained in the olfactory bulb suggest a potential early effect on the survival of microglial cells. Depending on the mode of exposure, these cells showed a decrease in density accompanied by an increase in an apoptotic marker. An abnormal phenotype of the nuclei of mature neurons, suggesting neuronal suffering, was also observed in the frontal cortex, and can be linked to the involvement of oxidative stress. The differential effects observed according to exposure patterns could involve two components: local (brain-specific) and/or systemic. Indeed, tungsten, in addition to being found in the lungs and kidneys, was present in the brain of animals exposed to the high concentration.</p><p><strong>Conclusion: </strong>Our data question the perceived innocuity of tungsten relative to other metals and raise hypotheses regarding possible adaptive or neurotoxic mechanisms that could ultimately alter neuronal integrity.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"36 4","pages":"261-274"},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247871","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}
Inhalation ToxicologyPub Date : 2024-04-01Epub Date: 2024-05-07DOI: 10.1080/08958378.2024.2335193
Yijue Liu, Hong Chen, Yan Wu, Fen Ai, Wei Li, Huan Peng, Feng Gui, Bo Yu, Zhen Chen
{"title":"Sinomenine attenuates bleomycin-induced pulmonary fibrosis, inflammation, and oxidative stress by inhibiting TLR4/NLRP3/TGFβ signaling.","authors":"Yijue Liu, Hong Chen, Yan Wu, Fen Ai, Wei Li, Huan Peng, Feng Gui, Bo Yu, Zhen Chen","doi":"10.1080/08958378.2024.2335193","DOIUrl":"10.1080/08958378.2024.2335193","url":null,"abstract":"<p><strong>Objective: </strong>The present work concentrated on validating whether sinomenine alleviates bleomycin (BLM)-induced pulmonary fibrosis, inflammation, and oxidative stress.</p><p><strong>Methods: </strong>A rat model of pulmonary fibrosis was constructed through intratracheal injection with 5 mg/kg BLM, and the effects of 30 mg/kg sinomenine on pulmonary inflammation, fibrosis, apoptosis, and 4-hydroxynonenal density were evaluated by hematoxylin and eosin staining, Masson's trichrome staining, TUNEL staining, and immunohistochemistry. Hydroxyproline content and concentrations of inflammatory cytokines and oxidative stress markers were detected using corresponding kits. MRC-5 cells were treated <i>with</i> 10 ng/ml PDGF, and the effects of 1 mM sinomenine on cell proliferation were assessed by EdU assays. The mRNA expression of inflammatory cytokines and the protein levels of collagens, fibrosis markers, and key markers involved in the TLR4/NLRP3/TGFβ signaling were tested with RT-qPCR and immunoblotting analysis.</p><p><strong>Results: </strong>Sinomenine attenuated pulmonary fibrosis and inflammation while reducing hydroxyproline content and the protein expression of collagens and fibrosis markers in BLM-induced pulmonary fibrosis rats. Sinomenine reduced apoptosis in lung samples of BLM-challenged rats by increasing Bcl-2 and reducing Bax and cleaved caspase-3 protein expression. In addition, sinomenine alleviated inflammatory response and oxidative stress in rats with pulmonary fibrosis induced by BLM. Moreover, sinomenine inhibited the TLR4/NLRP3/TGFβ signaling pathway in lung tissues of BLM-stimulated rats. Furthermore, TLR4 inhibitor, TAK-242, attenuated PDGF-induced fibroblast proliferation and collagen synthesis in MRC-5 cells.</p><p><strong>Conclusion: </strong>Sinomenine attenuates BLM-caused pulmonary fibrosis, inflammation, and oxidative stress by inhibiting the TLR4/NLRP3/TGFβ signaling, indicating that sinomenine might become a therapeutic candidate to treat pulmonary fibrosis.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"217-227"},"PeriodicalIF":2.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140876291","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":"Celastrol reduces lung inflammation induced by multiwalled carbon nanotubes in mice <i>via</i> NF-κb-signaling pathway.","authors":"Tao-Lin Qing, Xuan-Yao Jiang, Jin-Feng Li, Qi Shen, Xin-Yi Zhao, Li-Jun Ren, Xiao-Yu Dai, Ji-Qian-Zhu Zhang, Wen-Jing Shi, Xiao-Fang Zhang, Bin Zhang, Lang Yan, Ji-Kuai Chen, Jiang-Bo Zhu","doi":"10.1080/08958378.2024.2351098","DOIUrl":"10.1080/08958378.2024.2351098","url":null,"abstract":"<p><p>Multiwalled carbon nanotubes (MWCNTs) have numerous applications in the field of carbon nanomaterials. However, the associated toxicity concerns have increased significantly because of their widespread use. The inhalation of MWCNTs can lead to nanoparticle deposition in the lung tissue, causing inflammation and health risks. In this study, celastrol, a natural plant medicine with potent anti-inflammatory properties, effectively reduced the number of inflammatory cells, including white blood cells, neutrophils, and lymphocytes, and levels of inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, in mice lungs exposed to MWCNTs. Moreover, celastrol inhibited the activation of the NF-κB-signaling pathway. This study confirmed these findings by demonstrating comparable reductions in inflammation upon exposure to MWCNTs in mice with the deletion of NF-κB (P50<sup>-/-</sup>). These results indicate the utility of celastrol as a promising pharmacological agent for preventing MWCNT-induced lung tissue inflammation.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":"36 4","pages":"275-281"},"PeriodicalIF":2.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247870","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}
Inhalation ToxicologyPub Date : 2024-04-01Epub Date: 2024-05-13DOI: 10.1080/08958378.2024.2348165
Wisam Al Bakri, Maureen D Donovan
{"title":"The role of membrane transporters in the absorption of atrazine following nasal exposure.","authors":"Wisam Al Bakri, Maureen D Donovan","doi":"10.1080/08958378.2024.2348165","DOIUrl":"10.1080/08958378.2024.2348165","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of these studies was to investigate the uptake of atrazine across the nasal mucosa to determine whether direct transport to the brain through the olfactory epithelium is likely to occur. These studies were undertaken to provide important new information about the potential for the enhanced neurotoxicity of herbicides following nasal inhalation.</p><p><strong>Materials and methods: </strong>Transport of atrazine from aqueous solution and from commercial atrazine-containing herbicide products was assessed using excised nasal mucosal tissues. The permeation rate and the role of membrane transporters in the uptake of atrazine across the nasal mucosa were also investigated. Histological examination of the nasal tissues was conducted to assess the effects of commercial atrazine-containing products on nasal tissue morphology.</p><p><strong>Results: </strong>Atrazine showed high flux across both nasal respiratory and olfactory tissues, and efflux transporters were found to play an essential role in limiting its uptake at low exposure concentrations. Commercial atrazine-containing herbicide products showed remarkably high transfer across the nasal tissues, and histological evaluation showed significant changes in the morphology of the nasal epithelium following exposure to the herbicide products.</p><p><strong>Discussion: </strong>Lipophilic herbicides such as atrazine can freely permeate across the nasal mucosa despite the activity of efflux transporters. The adjuvant compounds in commercial herbicide products disrupt the nasal mucosa's epithelial barrier, resulting in even greater atrazine permeation across the tissues. The properties of the herbicide itself and those of the formulated products play crucial roles in the potential for the enhanced neurotoxicity of herbicides following nasal inhalation.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"250-260"},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140912148","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}
Inhalation ToxicologyPub Date : 2024-03-01Epub Date: 2024-02-27DOI: 10.1080/08958378.2024.2319708
Xiaoyong Li, Kai Chen, Xuefei Shi, Shunli Dong, Yi Chen, Bin Wang
{"title":"Notoginsenoside R1 restrains the proliferation and migration of airway smooth muscle cells isolated from rats with chronic obstructive pulmonary disease.","authors":"Xiaoyong Li, Kai Chen, Xuefei Shi, Shunli Dong, Yi Chen, Bin Wang","doi":"10.1080/08958378.2024.2319708","DOIUrl":"10.1080/08958378.2024.2319708","url":null,"abstract":"<p><strong>Objective: </strong>Chronic obstructive pulmonary disease (COPD) is a common disorder that is characterized by systemic and lung inflammation. Notoginsenoside R1 (NGR1) displays anti-inflammatory properties in numerous diseases. We aimed to explore the function and mechanism of NGR1 in COPD.</p><p><strong>Materials and methods: </strong>COPD rats were established through cigarette smoke exposure, lipopolysaccharide injection, and cold stimulation. Rat airway smooth muscle cells (ASMCs) were separated and identified. Then, ASMCs were treated with NGR1 (25 or 50 μM) and cigarette smoke extract (CSE). Thereafter, the vitality, proliferation, and migration of ASMCs were measured. Additionally, cell cycle, inflammation-related factors, α-SMA, and PI3K/AKT pathway-related marker expressions of the ASMCs were also detected. Molecular docking experiments were conducted to explore the interaction of NGR1 to PI3K, TGF-β, p65, and AKT. Moreover, 740 Y-P (a PI3K/Akt pathway agonist) were used to validate the mechanism of NGR1 on COPD.</p><p><strong>Results: </strong>NGR1 inhibited the proliferation and migration, but caused cell cycle arrest for CSE-triggered ASMCs. Furthermore, NGR1 not only decreased IL-1β, IL-6, IL-8, and TNF-α contents, but also reduced α-SMA expression in CSE-stimulated ASMCs. Moreover, NGR1restrainedTGF-β1 expression, PI3K, p65, and AKT phosphorylation in CSE-stimulated ASMCs. Molecular docking experiments showed NGR1 exhibited a strong binding ability to PI3K, TGF-β1, p65, and AKT. Notably, the effects of NGR1 on the proliferation and migration of CSE-induced ASMCs were reversed by 740 Y-P.</p><p><strong>Conclusions: </strong>NGR1 can restrain the proliferation and migration of CSE-induced ASMCs, indicating that NGR1 may be a therapeutic candidate for treating COPD.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"145-157"},"PeriodicalIF":2.1,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971733","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}
Inhalation ToxicologyPub 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
{"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":" ","pages":"174-188"},"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}