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).

Cardiac and ventilatory physiological data for mice exposed to acrolein. This dataset is associated with the following publication: Kurhanewicz, N., A. Ledbetter, A. Farraj, and M. Hazari. TRPA1 mediates the cardiac effects of acrolein through parasympathetic dominance but also sympathetic modulation in mice. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 347: 104-114, (2018).

We have examined the potential for interactive cardiovascular effects of repeated, intermittent co-exposure to concentrated ambient particulate matter (CAPs) and acrolein, and the potential role of transient receptor potential cation channel A1 (TRPA1), which we previously linked to air pollution-induced cardiac arrhythmogenesis. Chemical and source characteristics of collected particles was evaluated, as well as wind and weather patterns during exposure. Female B6129 mice and Trpa1-/- mice (n=6) were exposed to filtered air (FA), CAPs (46 µg/m3 of PM2.5 approximately 160 nm diameter), Acrolein (0.42 ppm) or CAPs+Acrolein for 3hrs/day, 2days/week, for 4 weeks. Cardiac strain data, heart function and dimensions, and transmitral blood flow were investigated with echocardiography (40 MHz) before exposures, 1 day after the first exposure, and 1 day after the final exposure. Several other biological endpoints were evaluated but the key findings from ultrasound echocardiography assessments were: elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased by ~5-fold in B6129 mice after the final exposure to CAPs+Acrolein when compared to strain delay in B6129 mice exposed to FA, CAPs, or Acrolein alone, and when compared to strain delay in Trpa1-/- mice exposed to CAPs+Acrolein. There were no changes after the first exposure in any group. This dataset is associated with the following publication: Thompson, L., L. Walsh, B. Martin, J. Mcgee, C. Wood, K. Kovalcik, P. Pancras, N. Coates, A. Ledbetter, D. Davies, W. Cascio, M. Higuchi, M. Hazari, and A. Farraj. Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice: Evidence for TRPA1 Involvement. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 167(2): 559-572, (2019).

This data shows the heart rate, heart rate variability and cardiac mechanical function of mice exposed to acrolein or ozone. This dataset is associated with the following publication: Kurhanewicz, N., R. McIntosh-Kastrinsky, H. Tong, A. Ledbetter, L. Walsh, A. Farraj, and M. Hazari. TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein. TOXICOLOGICAL AND APPLIED PHARMICOLOGY. Elsevier Science BV, Amsterdam, NETHERLANDS, 324: 51-60, (2017).

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).

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).

cardiovascular responses of exposure to simulated smog atmospheres in animals. This dataset is associated with the following publication: Tong, H., J. Krug, T. Krantz, C. King, M. Hargrove, I. Gilmour, and S. Gavett. Inhalation of Simulated Smog Atmospheres Affects Cardiac Function in Mice#. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 18(6): 569-578, (2019).

cardiovascular responses of exposure to simulated smog atmospheres in animals. This dataset is associated with the following publication: Tong, H., J. Krug, T. Krantz, C. King, M. Hargrove, I. Gilmour, and S. Gavett. Inhalation of Simulated Smog Atmospheres Affects Cardiac Function in Mice#. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 18(6): 569-578, (2019).