Exposure of the airways to cigarette smoke (CS) is the primary risk factor for developing several lung diseases such as Chronic Obstructive Pulmonary Disease (COPD). CS consists of a complex mixture of over 6000 chemicals including the highly reactive α,β-unsaturated aldehyde acrolein. Acrolein is thought to be responsible for a large proportion of the non-cancer disease risk associated with smoking. Emerging evidence suggest a key role for CS-induced abnormalities in mitochondrial morphology and function in airway epithelial cells in COPD pathogenesis. Although in vitro studies suggest acrolein-induced mitochondrial dysfunction in airway epithelial cells, it is unknown if in vivo inhalation of acrolein affects mitochondrial content or the pathways controlling this. In this study, rats were acutely exposed to acrolein by inhalation (nose-only; 0-4 ppm), 4 hours/day for 1 or 2 consecutive days (n=6/group). Subsequently, the activity and abundance of key constituents of mitochondrial metabolic pathways as well as expression of critical proteins and genes controlling mitochondrial biogenesis and mitophagy were investigated in lung homogenates. A transient decreasing response in protein and transcript abundance of subunits of the electron transport chain complexes was observed following acrolein inhalation. Moreover, acrolein inhalation caused a decreased abundance of key regulators associated with mitochondrial biogenesis, respectively a differential response on day 1 versus day 2. Abundance of components of the mitophagy machinery was in general unaltered in response to acrolein exposure in rat lung. Collectively, this study demonstrates that acrolein inhalation acutely and dose-dependently disrupts the molecular regulation of mitochondrial metabolism in rat lung. Hence, understanding the effect of acrolein on mitochondrial function will provide a scientifically supported reasoning to shortlist aldehydes regulation in tobacco smoke. This dataset is not publicly accessible because: EPA does not own the data and therefore EPA does not have right to publish the data. It can be accessed through the following means: Data can be obtained from corresponding author of the paper. Format: The data in this paper are collected from lung tissue that were isolated from air or acrolein-exposed Wistar Kyoto rats. All data are derived from lung tissue assessment of many biological markers associated with mitochondrial homeostasis. For these data n=8 animals were used for each group of samples. This dataset is associated with the following publication: Tulen, C., S. Snow , P. Leermakers, U. Kodavanti, F. van Schooten, A. Opperhuizen, and A. Remels. Acrolein inhalation acutely affects the regulation of mitochondrial metabolism in rat lung. TOXICOLOGY. Elsevier Science Ltd, New York, NY, USA, 469(153129): 1, (2022).

The revised paper dataset includes data shown in the main paper and supplemental file and are derived from Excel files associated with this Science Hub entry. The Word file "Science Hub Record summary Revised.docx" lists all main paper and supplemental tables and figures, and which specific Excel files are associated with each one. Further details on navigating individual Excel files are found within each Excel file. This dataset is associated with the following publication: Jackson, T., J. Murray, C. Schacht, P. Evansky, M. Monsees, J. Harrill, I. Gilmour, A. Johnstone, W. Williams, R. Grindstaff, M. Schladweiler, S. Vance, and S. Gavett. Bridging in vitro and in vivo inhalation toxicity: Volatile organic compounds elicit similar transcriptomic points of departure in human airway cells and mouse respiratory tract. ENVIRONMENTAL POLLUTION. Elsevier Science Ltd, New York, NY, USA, 387: 127342, (2025).

This data set is an Excel file pertaining to the study that examined nasal, pulmonary, and systemic effects of acrolein in rats acutely exposed to a range of concentrations. The different tabs of the spreadsheet pertain to each figure found in the manuscript. This dataset is associated with the following publication: Snow, S., M. McGee, A. Henriquez, J. Richards, M. Schladweiler, A. Ledbetter, and U. Kodavanti. Respiratory Effects and Systemic Stress Response Following Acute Acrolein Inhalation in Rats#. TOXICOLOGICAL SCIENCES. Society of Toxicology, 158(2): 454-464, (2017).

Background Free radicals generated in biological systems by cigarette smoke (CS) inhalation can cause oxidative stress in tissues, resulting in lipid peroxidation (LPO). In view of the antioxidant properties of α-tocopherol (AT), in the present study, effects of AT on antioxidant defence system and LPO were investigated in mice inhaling CS for different time intervals. Results Male Balb/c mice were fed orally with AT (5 I.U./Kg.b.wt.) and /or exposed to CS for 2, 4, 6 or 8 weeks. No effect was observed on body growth, diet consumption, water intake and lung weight due to AT and /or CS treatment in any of the groups as compared to their control counterparts. After two weeks of treatment, no change in LPO, reduced glutathione (GSH) levels and antioxidant enzymes were observed except for glutathione reductase (GR) which increased in all the treated groups. A significant increase in pulmonary LPO levels was observed in mice exposed to CS inhalation for 4, 6 or 8 weeks. There was a gradual increase in the LPO levels as the extent of CS inhalation increased from 4 to 8 weeks. However, the extent of increase in LPO levels due to CS exposure for 4, 6 or 8 weeks in the mice treated with AT was comparatively less. A significant decrease in the GSH levels was also observed in all the animals exposed to CS for 4, 6 or 8 weeks. There was a significant increase in the activities of catalase, glutathione peroxidase (GSH-Px) and GR observed in all the groups exposed to CS for 4,6 or 8 weeks. The increase in above antioxidant enzymes seems to be insufficient to combat the oxidative stress posed by CS inhalation. There was a marked decrease observed in the LPO levels in the animals treated with AT alone for 4, 6, or 8 weeks, when compared to their control counterparts. However, the supplementation of AT for 4, 6 or 8 weeks demonstrated a significant increase in GSH levels. Conclusion It appears from our studies that AT exhibits its antioxidant role either directly by scavenging the oxidative species or indirectly by modulating the GSH levels.

This data set pertains to the manuscript "Exacerbation of ozone-induced pulmonary and systemic effects by 2-adrenergic and/or glucocorticoid agonist/s". It shows the raw data for each figure in the manuscript that is created with these data. Basically examining the influence of beta adrenergic and glucocorticoid receptor agonists on ozone-induced lung injury and inflammation. This dataset is associated with the following publication: Henriquez, A., S. Snow, M. Schladweiler, C. Miller, J. Dye, A. Ledbetter, M. Hargrove, U. Kodavanti, and J. Richards. Exacerbation of ozone-induced pulmonary and systemic effects by beta2-adrenergic and/or glucocorticoid agonist/s. Scientific Reports. Nature Publishing Group, London, UK, 9(1): 17925, (2019).

we examined the cardiovascular effects acrolein inhalation, particularly on myocardial synchrony and performance via ultrasound echocardiography. Male C57Bl/6J mice (n=6/group) were exposed to filtered air (FA), 0.3 ppm acrolein, or 3.0 ppm acrolein for 3 hours in whole body plethysmography chambers. Cardiac strain data, heart function, and transmitral blood flow were investigated with echocardiography (40 MHz) 1 day prior to exposure, 1 hour after exposure, and 1 day after exposure. During the first 30 minutes of exposure, breathing frequency decreased. tidal volume increased, and expiratory/inspiratory time ratio increased in response to 3.0 ppm acrolein. Elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased significantly in mice exposed to 3.0 ppm acrolein at 1 and 24 hours post-exposure. Mice exposed to 0.3 ppm acrolein did not demonstrate changes in myocardial synchrony but did show decreases in myocardial performance, i.e. increased Tei index, at both 1 and 24 hours post-exposure. This dataset is associated with the following publication: Thompson, L., A. Ledbetter , N. Coates , W. Cascio , M. Hazari , and A. Farraj. Acrolein inhalation alters myocardial synchrony and performance at and below exposure concentrations that cause ventilatory responses. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 17(2): 97-108, (2017).

we examined the cardiovascular effects acrolein inhalation, particularly on myocardial synchrony and performance via ultrasound echocardiography. Male C57Bl/6J mice (n=6/group) were exposed to filtered air (FA), 0.3 ppm acrolein, or 3.0 ppm acrolein for 3 hours in whole body plethysmography chambers. Cardiac strain data, heart function, and transmitral blood flow were investigated with echocardiography (40 MHz) 1 day prior to exposure, 1 hour after exposure, and 1 day after exposure. During the first 30 minutes of exposure, breathing frequency decreased. tidal volume increased, and expiratory/inspiratory time ratio increased in response to 3.0 ppm acrolein. Elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased significantly in mice exposed to 3.0 ppm acrolein at 1 and 24 hours post-exposure. Mice exposed to 0.3 ppm acrolein did not demonstrate changes in myocardial synchrony but did show decreases in myocardial performance, i.e. increased Tei index, at both 1 and 24 hours post-exposure. This dataset is associated with the following publication: Thompson, L., A. Ledbetter , N. Coates , W. Cascio , M. Hazari , and A. Farraj. Acrolein inhalation alters myocardial synchrony and performance at and below exposure concentrations that cause ventilatory responses. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 17(2): 97-108, (2017).

Pulmonary gene expression related to the regulation of DNA methylation following an exposure to ozone in rats. Epigenetic regulation of a pulmonary hypertensive gene, apelin, was also quantified. This dataset is associated with the following publication: Miller, C., J. Dye, M. Schladweiler, J. Richards, A. Ledbetter, E. Stewart, and U. Kodavanti. Acute inhalation of ozone induces DNA methylation of apelin in lungs of Long-Evans rats.. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 30(4): 178-186, (2018).

Employing acrolein, a potent airway irritant, and TCE, with low irritancy, authors hypothesized that airway injury and inflammation would be involved in eliciting neuroendocrine-mediated systemic alterations. Male and female Wistar-Kyoto rats were exposed nose-only to air, acrolein or trichloroethylene (TCE) in incremental concentrations over 30 min, followed by 3.5-hr exposure to the highest concentration (acrolein - 0.0, 0.1, 0.316, 1, 3.16 ppm; TCE - 0.0, 3.16, 10, 31.6, 100 ppm) while performing head-out plethysmography (HOP), and animals were necropsied immediately post-exposure to assess nasal and lung injury/inflammation, systemic neurohormones, circulating stress hormones and also metabolic hormones. This dataset is associated with the following publication: Alewel, D., T. Jackson, S. Vance, M. Schladweiler, P. Evansky, A. Henriquez, R. Grindstaff, S. Gavett, and U. Kodavanti. Sex-specific respiratory and systemic endocrine effects of acute acrolein and trichloroethylene inhalation. TOXICOLOGY LETTERS. Elsevier Science Ltd, New York, NY, USA, 382: 22-32, (2023).