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).

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).

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).

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).

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 dataset includes data for the manuscript in progress, Intracerebroventricular kynurenic acid modulation differentially regulates the immune and neuroendocrine stress response to acute ozone exposure. This study employed the use of kynurenic acid or the kynurenic acid synthesis inhibitor, PF-04859989 infused into the dorsal third ventricle of the brain in male WKY rats, prior to acute ozone exposure at 0.8 ppm, to evaluate the role of kynurenic acid in modulating the neuroendocrine stress response to ozone. Our results indicate that kynurenic acid may have a protective role in the brain, in attenuating the pulmonary and systemic effects of ozone exposure, perhaps through multiple mechanisms. This dataset is associated with the following publication: Rentschler, K., M.C. Schladweiler, R. Grindstaff, W. Williams, P.R. Kodavanti, D. Freeborn, L. Klein, G. Jung, D. Herr, P. Evansky, J. McKee, S. Gavett, and U. Kodavanti. Differential Effects of Intracerebroventricular Kynurenic Acid Regulation on the Inflammatory and Neuroendocrine Response to Acute Ozone Exposure. Presented at Society of Toxicology, Orlando, FL, USA, 03/16/2025 - 03/20/2025.

This dataset includes the results of a long term adult female rat oral exposure to triclosan and includes hormone, estrous cyclicity, thyroid histology and liver gene expression data. This dataset is associated with the following publication: Louis, G., D. Hallinger, J. Braxton, A. Kamel, and T. Stoker. Effects of Chronic Exposure to Triclosan on Reproductive and Thyroid Endpoints in the Adult Wistar Female Rat. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH. Taylor & Francis, Inc., Philadelphia, PA, USA, 236-249, (2017).

To link health benefits derived from advanced CS usage to increasing combustion efficiencies of the cookstove, a wide variety of general health and respiratory system parameters that are often altered acutely following exposure to air pollutants were assessed. The figures and tables reflect the health outcomes. This dataset is associated with the following publication: Gibbs-Flournoy, E., I. Gilmour, M. Higuchi, J. Jetter, I. George, L. Copeland, R. Harrison, V. Moser, and J. Dye. Differential exposure and acute health impacts of inhaled solid-fuel emissions from rudimentary and advanced cookstoves in female CD-1 mice.. ENVIRONMENTAL RESEARCH. Academic Press Incorporated, Orlando, FL, USA, 161: 35-48, (2018).

To link health benefits derived from advanced CS usage to increasing combustion efficiencies of the cookstove, a wide variety of general health and respiratory system parameters that are often altered acutely following exposure to air pollutants were assessed. The figures and tables reflect the health outcomes. This dataset is associated with the following publication: Gibbs-Flournoy, E., I. Gilmour, M. Higuchi, J. Jetter, I. George, L. Copeland, R. Harrison, V. Moser, and J. Dye. Differential exposure and acute health impacts of inhaled solid-fuel emissions from rudimentary and advanced cookstoves in female CD-1 mice.. ENVIRONMENTAL RESEARCH. Academic Press Incorporated, Orlando, FL, USA, 161: 35-48, (2018).

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).