Inhalation Toxicology最新文献

{"title":"Effect of single inhalation of hypochlorous acid on the activity of cysteine cathepsins in rat blood plasma.","authors":"Bohdan Murashevych, Olha Abraimova, Olha Netronina, Dmitry Girenko, Tetiana Herhel, Hanna Maslak","doi":"10.1080/08958378.2025.2558569","DOIUrl":"10.1080/08958378.2025.2558569","url":null,"abstract":"<p><strong>Objective: </strong>Gaseous hypochlorous acid HOCl(g) is a promising agent for continuous complex disinfection of premises, but the toxic effect of its inhalation has been practically not studied. In this study, the effect of inhalation of 0.75 and 1.79 ppm HOCl(g) on ​​the activity of cysteine ​​cathepsins B, H and L, and alpha-1 antitrypsin in the blood plasma of rats was studied to assess the extent of lysosome damage as an element of oxidative stress.</p><p><strong>Materials and methods: </strong>the inhalation exposure was carried out in the 'whole-body' mode during a single 4-hour treatment of animals of two age groups in inhalation chamber equipped with a specially designed evaporative unit. Biochemical parameters were analyzed 2 h and 24 h after the procedure.</p><p><strong>Results and discussion: </strong>it was found that the activity of cathepsin L did not change in any of the animal groups, while the activities of cathepsins B and H significantly increased. Inhalation had the greatest effect on cathepsin H, which increased by 1.6-6.4 times in different groups, and the reaction of young animals was more intense. Alpha-1 antitrypsin levels were also elevated both 2 and 24 h after exposure, but age-dependent differences were not significant. In all cases, an increase in the deviation of biochemical parameters from the norm was noted with an increase in the HOCl(g) concentration.</p><p><strong>Conclusions: </strong>HOCl(g) inhalation at the concentrations used causes pronounced oxidative stress in animals. More detailed biochemical, histological and immunohistochemical studies are needed to assess the toxic consequences of such exposure.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"293-309"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039892","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":"Fragrance inhalation toxicity assessment: a proactive testing strategy using <i>ex vivo</i> precision cut lung slices (PCLuS) for the prioritization of selected aroma ingredients candidates for <i>in vivo</i> testing.","authors":"Tizia Thoma, Olga Lemke, Lan Ma-Hock, Lars Hareng, Markus Wahl","doi":"10.1080/08958378.2025.2566446","DOIUrl":"10.1080/08958378.2025.2566446","url":null,"abstract":"<p><strong>Objective: </strong>To date, exposure thresholds for fragrance chemicals are most often extrapolated from oral administration data. Due to limited inhalation toxicity data, the potentially high exposure levels toward fragrances - especially in air care applications - are sometimes perceived as potentially critical. Herein, we assessed the potential inhalation toxicity of various commonly used fragrances with main focus on respiratory tract effects.</p><p><strong>Methods: </strong>19 high volume fragrances were screened for their cytotoxic potential by using rat precision cut lung slices (PCLuS). Based on the screening data, chemicals were categorized into low, mid, and high cytotoxicity groups. From these groups, five fragrances were selected for further <i>in vivo</i> investigation. In a 14-day inhalation study, male 7-week old Wistar rats were exposed to geraniol, geranyl acetate, citral, L-menthol, and p-tert-butyl-alpha-methylhydro-cinnamic aldehyde (BMHCA) to investigate the respiratory and sensory irritation potential.</p><p><strong>Results: </strong><i>Ex vivo</i> screening allowed for a preliminary classification of the cytotoxic potential, facilitating the selection of candidates for <i>in vivo</i> inhalation assessments. Local respiratory irritation was observed for liquid aerosol fractions of citral and geraniol, but not for other substances or vapor only exposure. Overall, no systemic effects related to treatment were observed. Sensory irritation was only observed for citral and BMHCA but not for other fragrance chemicals.</p><p><strong>Discussion: </strong>While PCLuS and further model development could not fully replace animal testing at this stage, this study's findings contribute to the reduction and refinement according to 3 R principles and might serve as a foundation for future testing strategies aiming toward a complete replacement.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"310-329"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244461","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":"Episodic ozone exposure over two weeks alters pulmonary inflammation and gene expression in Long-Evans rats.","authors":"Janice A Dye, Makala M Moore, Helen H Nguyen, Mette C Schladweiler, Victoria R Adams, Judy H Richards, Wanda C Williams, Rachel D Grindstaff, Urmila P Kodavanti, Colette N Miller","doi":"10.1080/08958378.2025.2576492","DOIUrl":"10.1080/08958378.2025.2576492","url":null,"abstract":"<p><strong>Objective: </strong>Elevated exposure to ozone (O₃) may occur episodically over short windows of time. However, laboratory investigations have consistently shown that repeated ozone exposures produce an adaptation response, reducing the effects of O₃ on ventilatory function. To better understand these responses, we developed a rodent model of episodic O₃ exposure to characterize differing exposure patterns on pulmonary toxicity.</p><p><strong>Methods: </strong>Male, Long-Evans rats were exposed for either two days or two weeks of episodic exposure to 0.4 or 0.8 ppm O₃ (4 h/day). Rats in the two-week group were exposed for a total of five nonconsecutive days, with one- to four-day periods of recovery between each exposure. Whole body plethysmography was performed following each exposure. Markers of lung injury and inflammation in the bronchoalveolar lavage fluid were measured, and lung expression of select genes were assessed using qPCR ∼24 h after the final exposure.</p><p><strong>Results: </strong>Concentration-dependent effects of O₃ on breathing parameters and lung injury were observed following two days of exposure. However, these responses were less evident in rats exposed episodically over two weeks. Comparable increases in bronchoalveolar lavage fluid inflammatory cells and cytokine concentrations were observed irrespective of exposure duration. Furthermore, reduced expression of genes involved in neuroendocrine signaling was detected only following two weeks of episodic exposure (<i>Adrb2</i>, <i>Nr3c1</i>, <i>Dusp1</i>, <i>Glccl1</i>).</p><p><strong>Conclusions: </strong>Aspects of the adaptation response were still present in rats episodically exposed to O₃ over two weeks. On the other hand, O₃-mediated alterations in pulmonary immune populations show continued responsiveness in this model, suggesting that adaptation may be endpoint specific.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"343-356"},"PeriodicalIF":2.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13188205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145344957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of protective effects of tannic acid/iron complex against lung fibrosis induced by bleomycin in rat.","authors":"Amir Siahpoosh, Narges Atefipour, Paria Javam, Ali Reza Malayeri","doi":"10.1080/08958378.2025.2577242","DOIUrl":"10.1080/08958378.2025.2577242","url":null,"abstract":"<p><strong>Objective(s): </strong>Pulmonary fibrosis (PF) is a seriousand advancing respiratory condition that arises from various contributing factors. Bleomycin (BLM) is a chemotherapeutic drug known to cause different side effects, including PF. The current study aimed to assess the protective effects of the Tannic Acid/Iron complex (TAIC) against PF induced by BLM in a rat model.</p><p><strong>Materials and methods: </strong>PF was induced in Wistar rats by a single dose of BLM (7.5 U/kg) on the 7th day. The rats were then randomly assigned to six groups: control, BLM, and four treatment groups receiving BLM + different doses of TAIC or TA alone (28 days, gavage). Animals were sacrificed on the 29th day and lung samples were collected to assess histopathological alterations and biochemical parameters such as lung index, nitric oxide (NO), malondialdehyde (MDA), hydroxyproline (HP), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and tumor necrosis factor- α (TNF-α).</p><p><strong>Results: </strong>The results demonstrated that the TAIC complex significantly attenuated BLM-induced elevation in lung index as well as the levels of MDA, NO, HP, and TNF-α. Additionally, TAIC enhanced the activities of key antioxidant enzymes, including CAT, SOD, GPx, and increased GSH content. This complex also inhibited the infiltration of fibroblasts and inflammatory cells, thereby preventing alveolar thickening. Notably, the effect of TA at 400 mg/kg, while beneficial, was slightly less pronounced compared to the TAIC complex at the same dosage.</p><p><strong>Conclusion: </strong>The results revealed that TAIC hasa protective effect on BLM -induced pulmonary fibrosis.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"382-394"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145389097","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":"Efficacy of different oxygen delivery methods in carbon monoxide poisoning: a prospective observational study.","authors":"Safa Donmez, Alp Sener, Nurullah Ishak Isık, Nazlı Gormeli Kurt, Kadir Yenal, Reyhan İrem Mutlu, İlker Akbaş","doi":"10.1080/08958378.2025.2580328","DOIUrl":"10.1080/08958378.2025.2580328","url":null,"abstract":"<p><strong>Objective: </strong>Carbon monoxide (CO) poisoning impairs oxygen transport by forming carboxyhemoglobin (COHb). Normobaric oxygen (NBO) is standard therapy, but its COHb elimination rate is slow. This study compared the effectiveness of NBO, NIMV, and EzPAP in reducing COHb levels in acute CO poisoning.</p><p><strong>Materials and methods: </strong>This prospective cohort study included patients with acute CO poisoning in an emergency department. Participants received one of three treatment modalities: standard NBO therapy, NIMV with positive pressure support, or the EzPAP system. COHb levels were recorded at baseline, 30 min, and 60 min after initiation of therapy. The primary outcome was the change in COHb concentration over time.</p><p><strong>Results and discussion: </strong>A total of 66 patients were included in the study (NIMV: <i>n</i> = 29, EzPAP: <i>n</i> = 18, and NBO: <i>n</i> = 19). Significant differences were observed in symptom distribution, with headache more frequent in the EzPAP and NBO groups and dyspnea more common in NIMV and EzPAP groups (<i>p</i> < 0.001). Baseline COHb levels did not differ between groups (<i>p</i> = 0.849). At 30 and 60 min, NIMV achieved significantly greater COHb reduction compared to NBO (<i>p</i> < 0.001), while EzPAP showed superiority over NBO at 60 min (<i>p</i> = 0.031). Pairwise analyses indicated NIMV was also superior to EzPAP at 60 min (<i>p</i> = 0.003).</p><p><strong>Conclusions: </strong>While NBO remains the standard therapy, this study suggests NIMV - and to a lesser extent, EzPAP - may serve as effective adjuncts in the management of CO poisoning. These findings provide a rationale for further randomized controlled trials.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"395-404"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145458287","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":"Impact of secondhand smoke and e-cigarette aerosol on overweight or obesity in adolescents: a network pharmacology and toxicology study.","authors":"Yalan Liu, Hong Xiao, Hua Zong, Li He","doi":"10.1080/08958378.2025.2567447","DOIUrl":"10.1080/08958378.2025.2567447","url":null,"abstract":"<p><strong>Objective: </strong>Rising childhood obesity is a global concern, with environmental tobacco exposure as a potential risk factor. However, the mechanisms linking secondhand smoke and e-cigarette aerosol to adolescent obesity remain unclear.</p><p><strong>Methods: </strong>We analyzed data from 968 participants aged 3- 19 years in the NHANES 2017- 2020 cycles. Passive exposure was assessed using self-reported household exposure and objectively measured serum cotinine levels. Multivariate logistic regression was used to evaluate the associations between exposure categories and overweight/obesity status. Cotinine-related molecular targets were identified through network pharmacology and toxicology analyses, with protein-protein interaction networks, enrichment analyses, and molecular docking used to explore relevant pathways.</p><p><strong>Results: </strong>Compared with unexposed individuals, participants exposed to both secondhand smoke and e-cigarette aerosols had significantly greater odds of overweight or obesity (adjusted odds ratio [aOR] = 3.9; 95% CI: 1.4-11.0; <i>p</i> = 0.009). Serum cotinine levels were also positively associated with obesity risk in a dose-dependent manner, with those in the highest quartile (Q4) showing aOR = 3.8 (95% CI: 2.1-6.8; <i>p</i> < 0.001) compared with those in Q1. Network analyses identified CHRNA2 and CHRNB2 as key targets involved in cholinergic signaling and metabolic regulation. Cotinine demonstrated strong binding affinity to these targets in molecular docking, supporting its potential biological activity beyond being a nicotine biomarker.</p><p><strong>Conclusion: </strong>Passive nicotine exposure is significantly associated with overweight or obesity among adolescents, and cotinine may be involved in relevant biological pathways related to energy regulation. These findings may inform future research and preventive strategies.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"330-342"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286010","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":"Network toxicology reveals mechanisms of Endosulfan-induced lung injury.","authors":"Fuat Karakuş, Burak Kuzu","doi":"10.1080/08958378.2025.2577233","DOIUrl":"10.1080/08958378.2025.2577233","url":null,"abstract":"<p><strong>Objective: </strong>Endosulfan, an organochlorine pesticide, consists of two isomers (α-Endosulfan and β-Endosulfan) and a primary metabolite, Endosulfan sulfate (END-SO₄). Due to its pervasive environmental contamination and harmful effects-such as neurotoxicity, endocrine disruption, and reproductive toxicity in humans-END was included in the Stockholm Convention on Persistent Organic Pollutants (Annex A) in 2011, leading to its prohibition in many regions. The toxic effects of END have been extensively studied, but the specific mechanism of its lung injury remains unknown. This study explores how α/β-Endosulfan and END-SO₄ may induce lung injury using <i>in silico</i> approaches.</p><p><strong>Methods: </strong>Toxicity prediction was performed using STopTox, ADMETlab 3.0, and Deep-PK. Network toxicology analyses were conducted <i>via</i> the Comparative Toxicogenomic Database, DAVID, Metascape, GeneMANIA, STRING, and Cytoscape. AUTODOCK was used for molecular docking of α/β-END and END-SO₄ with key targets.</p><p><strong>Results: </strong>The study identified 4658 targets for α/β-END and 21 for END-SO4, with 126 linked to lung injury. Of these, 53 targets were common to both the compounds and lung injury, primarily associated with inflammation and fibrosis. Centrality analysis highlighted IL1B, TNF, and IL6 as key targets. Docking results showed binding affinities ranging from -4.53 to -8.32 kcal/mol between α/β-END, END-SO₄, and IL1B/TNF.</p><p><strong>Conclusion: </strong>These findings suggest that exposure to α/β-END and END-SO₄ may trigger inflammation and fibrosis, contributing to lung injury. These findings provide a basis for further experimental studies aimed at validating the role of IL1B and TNF in α/β-END-induced lung injury.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"357-368"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145370295","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":"Genetic ablation of p16 leads to pulmonary remodeling, pro-senescence response, and immune modulation in mice exposed to low-dose, Sub-chronic, environmental tobacco smoke.","authors":"Thivanka Muthumalage, Irfan Rahman","doi":"10.1080/08958378.2025.2577236","DOIUrl":"10.1080/08958378.2025.2577236","url":null,"abstract":"<p><strong>Objective: </strong>Cyclin-dependent kinase inhibitor 2 A, CDKN2A/p16INK4a (p16), is a gene involved in regulating the cell cycle, cellular senescence, and inflammatory responses. The role of p16 in pulmonary immune-inflammatory and cellular senescence responses to low-dose, sub-chronic environmental tobacco smoke (ETS) is not known. We hypothesized that p16-deficient (knockout, KO) mice would exhibit adverse lung responses compared to wild-type (WT) mice, characterized by a decline in lung function, impaired immune responses, lung remodeling, and dysregulated inflammatory responses at low-level ETS exposure.</p><p><strong>Materials and methods: </strong>C57BL/6J (WT) and p16 knockout, p16^-/-, were exposed to low dose ETS [10 mg/m³ total particulate matter (TPM)] for 3 months. Bronchoalveolar fluid (BALF) and lung tissue were used in subsequent analyses.</p><p><strong>Results: </strong>Histological analysis revealed mild alveolar simplification in p16 KO mice compared to WT mice. CDKN2A/p16 KO BALF did not have the same immune cell infiltration or cytokine response as the WT counterparts, where IL-17A, TNF-α, and GM-CSF were significantly elevated, indicating impaired immune response with p16 deficiency. Proteomic analysis revealed significantly elevated proteins related to inflammation, extracellular matrix remodeling, cellular metabolism, pro-senescence, and oxidative stress in p16 KO mice (Kynu, Col5a3, Lamtor3). NLRP3 and PTGS2 (COX-2) activation z-scores were lower in p16 KO mice, while IL33 and CCR5 activation z-scores were higher compared to WT mice.</p><p><strong>Discussion: </strong>Thus, p16 deficiency amplifies ETS-induced alveolar architecture, impaired immune responses, and altered inflammatory pathways, contributing to heightened susceptibility to emphysema-like changes compared to WT mice even at low ETS levels. This study revealed that p16 deletion alters response to low-level ETS, not necessarily by amplifying the classic 'damage response' but by modifying immune and senescence signaling in the lungs.</p><p><strong>Conclusion: </strong>Overall, p16 has a complex and nuanced protective role in lung health, and careful targeting p16-related pathways could offer therapeutic strategies for mitigating chronic lung diseases.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"369-381"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145503661","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":"CREBBP stabilizes GNG3 protein through acetylation, thereby activating the NF-κB pathway and exacerbating airway inflammation in allergic rhinitis.","authors":"Meng Chen, Zhihui Yuan","doi":"10.1080/08958378.2025.2528747","DOIUrl":"10.1080/08958378.2025.2528747","url":null,"abstract":"<p><strong>Objective: </strong>Allergic rhinitis (AR), an allergen-driven chronic inflammatory disorder of nasal mucosa, is characterized by airway inflammation as its cardinal pathological manifestation. While acetylation is known to regulate airway inflammation, its mechanistic involvement in AR-related inflammation remains elusive. This study aims to investigate the acetylation-dependent mechanisms governing airway inflammation in AR.</p><p><strong>Materials and methods: </strong>RNA-seq analysis identified differentially expressed genes in peripheral blood of AR patients and healthy controls. Ovalbumin-sensitized BALB/c mice were performed as the AR mouse model. Airway inflammation was assessed by measuring inflammatory cytokine levels, inflammatory cell numbers, macrophage counts in whole lung lavage fluid (WLLF), and specific IgE levels in plasma using ELISA and Diff-Quick staining. The underlying mechanism was investigated through Western blotting, immunoprecipitation (IP), and Co-IP.</p><p><strong>Results: </strong>GNG3 expression was significantly increased in AR patients and the AR mouse model. Knockdown of GNG3 significantly reduced airway inflammation and inhibited NF-κB pathway activation in the AR mouse model. CREBBP overexpression enhanced GNG3 protein stability, and CREBBP mRNA expression was significantly increased in patients with AR and positively correlated with GNG3 expression. Furthermore, GNG3 overexpression restored airway inflammation that was suppressed by CREBBP knockdown in the AR mouse model.</p><p><strong>Conclusion: </strong>These results demonstrate that CREBBP aggravated airway inflammation in AR by activating the NF-κB pathway <i>via</i> GNG3 upregulation mediated by GNG3 acetylation.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"256-266"},"PeriodicalIF":2.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishing a novel combustion generator system to simulate and study emissions from diverse applications.","authors":"Anand Ranpara, William T Goldsmith, Thomas P Batchelor, Jingxin Wang, Robert Burns, Gary Casuccio, Kristin Bunker, Keith Rickabaugh, Mark Wilson, Timothy R Nurkiewicz","doi":"10.1080/08958378.2025.2531115","DOIUrl":"10.1080/08958378.2025.2531115","url":null,"abstract":"<p><p>Inhalation of emissions from combustion events such as military burn pits and wildland-urban interface fires result in exposures to complex aerosols that may cause adverse health effects. A surrogate combustion generator was created to study these events. A pellet stove was modified to burn diverse fuels comprised of materials found in burn pits (plastic, rubber, and wood). Jet fuel (JF) was added during combustion. The purpose of this project was to: 1) operate the generator over diverse parameters; and 2) characterize the resultant emissions. Pellet combustion (8 g/minute; range: 1-34) ± JF (0.2 mL/minute; range: 0-1) was conducted at fixed rates. Real-time and off-line aerosol characterizations (size distributions, concentrations, morphology) and chemical measures (total and speciation of volatiles, organics, elementals) with subsequent analytic methodology were performed. Pellet combustion produced an average particle concentration of 7.0e+6±1.1e+6 #/cc, and a total volatile organic compound concentration (TVOC) of 0.97+0.41 parts per million (PPM). The addition of JF accelerated the combustion process and increased the total particle counts to 4.5e+7±8.3e+6 #/cc, but decreased the TVOC to 0.63±0.26 ppm. Ultrafine particles were predominantly generated with similar count median diameters (<100 nm) and polydisperse distributions (GSD>1.5). Chemical speciation revealed potential human carcinogens (formaldehyde, acetaldehyde) and the addition of JF resulted in a >40-fold drop in organic carbon constituents. Adding plastic and rubber into the pellet mixture resulted in emissions containing 4% methyl-methacrylate and 10% methyl-isobutyl-ketones. Future experiments will assess diverse wood varieties, synthetic building constituents, and asses the biological effects that follow these inhalation exposures.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":" ","pages":"267-283"},"PeriodicalIF":2.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12423657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952666","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}