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).

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).

This data set is an excel file pertaining to the study that examined ozone-induced systemic and pulmonary effects in rats that underwent SHAM surgery (control), adrenal demedullation or total bilateral adrenalectomy. Different pages of the spreadsheet shows individual animal data for markers of lung injury and inflammation, body weights, whole body plethysmography measurements, levels of circulating hormones and lipids, and circulating white blood cell count as well as platelet count. This dataset is associated with the following publication: Miller, D., S. Snow, M. Schladweiler , J. Richards , A. Ghio , A. Ledbetter , and U. Kodavanti. Acute Ozone-Induced Pulmonary and Systemic Metabolic Effects are Diminished in Adrenalectomized Rats#. TOXICOLOGICAL SCIENCES. Society of Toxicology, 150(2): 312-22, (2016).

This data set is an excel file pertaining to the study that examined ozone-induced systemic and pulmonary effects in rats that underwent SHAM surgery (control), adrenal demedullation or total bilateral adrenalectomy. Different pages of the spreadsheet shows individual animal data for markers of lung injury and inflammation, body weights, whole body plethysmography measurements, levels of circulating hormones and lipids, and circulating white blood cell count as well as platelet count. This dataset is associated with the following publication: Miller, D., S. Snow, M. Schladweiler , J. Richards , A. Ghio , A. Ledbetter , and U. Kodavanti. Acute Ozone-Induced Pulmonary and Systemic Metabolic Effects are Diminished in Adrenalectomized Rats#. TOXICOLOGICAL SCIENCES. Society of Toxicology, 150(2): 312-22, (2016).

This data set contains one Excel file. In this file are all the data pertaining to the effects of propranolol and mifepristone on ozone induced lung injury and inflammation . The different tabs of the spreadsheet pertain to each figure found in the manuscript. This dataset is associated with the following publication: Henriquez, A., S. Snow, M. Schladweiler, C. Miller, J. Dye, A. Ledbetter, J. Richards, K. Mauge-Lewis, M. McGee, and U. Kodavanti. Adrenergic and glucocorticoid receptor antagonists reduce ozone-induced lung injury and inflammation. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 339: 161-171, (2018).

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).

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).

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).

Data include: trans-epithelial electrical resistance, FITC-dextran permeability, cell viability and gene expression (RNA and protein). This dataset is associated with the following publication: Faber, S., N. McNabb, P. Ariel, E. Aungst, and S. McCullough. Exposure Effects Beyond the Epithelial Barrier: Trans-Epithelial Induction of Oxidative Stress by Diesel Exhaust Particulates in Lung Fibroblasts in an Organotypic Human Airway Model. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 177(1): 140-155, (2020).