A manuscript describing the independent roles of beta adrenergic and glucocorticoid receptors in mediating ozone-induced pulmonary and systemic effects. This dataset is associated with the following publication: Henriquez, A., S. Snow, M.C. Schladweiler, C. Miller, and U. Kodavanti. Independent roles of beta-adrenergic and glucocorticoid receptors in systemic and pulmonary effects of ozone. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 32(4): 155-169, (2020).

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).

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).

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).

We have previously shown that neuroendocrine activation leading to increased circulating stress hormones was necessary for mediating ozone-induced lung injury and inflammation since adrenalectomy rats were protected from these ozone effects. Because adrenalectomy is invasive and also eliminates circulating mineralocorticoids along with stress hormones, one cannot rule out their contribution in diminution of ozone-induced lung effects. The goal of this study was to evaluate if agonists of stress hormone receptors β2 adrenergic receptors and glucocorticoid receptors were able to restore ozone-induced lung injury, inflammation and innate immune cell trafficking in adrenalectomy rats, and exacerbate these effects in control rats with sham surgery. Here, we reconfirmed that the pulmonary and systemic effects of ozone inhalation, characterized by vascular leakage, neutrophilic inflammation, cytokine release in the lungs and peripheral vascular lymphopenia, were significantly diminished by adrenlectomy. The treatment with a combination of β2 adrenergic receptor and glucocorticoid receptor agonists (Clenbuterol and dexamethasone) was able to restore these ozone effects in AD rats, and further exacerbate ozone-induced lung protein leakage, inflammation and lymphopenia in sham surgery rats. It was also noted that clenbuterol plus dexamethasone itself caused injury and cytokine increases in the lung. Although a variety of β2 adrenergic receptor and glucocorticoid agonists have been widely used for the treatment of chronic lung diseases, β2 adrenergic receptor agonists have been shown to exacerbate lung inflammation in asthmatics and epidemiological studies have indicated exacerbation of lung inflammation in asthmatics during increased air pollution episodes. Even though high concentrations of agonists were used, our study provides a potential causal mechanistic link between activation of stress hormone receptors in mediation of air pollution health effects, and how these effects might be exacerbated in those receiving asthma therapy. This dataset is associated with the following publication: Henriquez, A., S. Snow, M. Schladweiler, C. Miller, J. Dye, A. Ledbetter, J. Richards, M. Hargrove, W. Williams, and U. Kodavanti. Beta-2 adrenergic and glucocorticoid receptor agonists modulate ozone-induced pulmonary protein leakage and inflammation in healthy and adrenalectomized rats. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 166(2): 288-305, (2018).

These are the data for the figures in the manuscript. This dataset is associated with the following publication: Corteselli, E., A. Gold, J. Surratt, T. Cui, P. Bromberg, L. Dailey, and J. Samet. Supplementation with Omega-3 Fatty Acids Potentiates Oxidative Stress in Human Airway Epithelial Cells Exposed to Ozone. ENVIRONMENTAL RESEARCH. Elsevier B.V., Amsterdam, NETHERLANDS, 187: 109627, (2020).

These are the data for the figures in the manuscript. This dataset is associated with the following publication: Corteselli, E., A. Gold, J. Surratt, T. Cui, P. Bromberg, L. Dailey, and J. Samet. Supplementation with Omega-3 Fatty Acids Potentiates Oxidative Stress in Human Airway Epithelial Cells Exposed to Ozone. ENVIRONMENTAL RESEARCH. Elsevier B.V., Amsterdam, NETHERLANDS, 187: 109627, (2020).

These data are published in a manuscript entitled Multi-tissue transcriptomic and serum metabolomic assessment reveals systemic implications of acute ozone-induced stress response in male Wistar Kyoto rats in the journal Metabolomics. This analyses explored systemic transcriptomic and circulating metabolomic effects of inhaled ozone exposure in rats. This dataset is associated with the following publication: Jackson, T., J. House, A. Henriquez, M. Schladweiler, K.M. Jackson, A. Astriab Fisher, S. Snow , D. Alewel, A. Motsinger-Reif, and U. Kodavanti. Multi-tissue transcriptomic and serum metabolomic assessment reveals systemic implications of acute ozone-induced stress response in male Wistar Kyoto rats. Metabolomics. Plenum Press, New York, NY, USA, 19: 81, (2023).

Dataset contains a list of metabolites, their fold change after ozone exposure and a p value for that change. This dataset is not publicly accessible because: EPA cannot release personally identifiable information regarding living individuals, according to the Privacy Act and the Freedom of Information Act (FOIA). This dataset contains information about human research subjects. Because there is potential to identify individual participants and disclose personal information, either alone or in combination with other datasets, individual level data are not appropriate to post for public access. Restricted access may be granted to authorized persons by contacting the party listed. It can be accessed through the following means: This dataset can be accessed by contacting Dr. Robert Devlin (devlin.rober@epa.gov). Format: The dataset was sent to us by the company (Metabolon) that did the metabolite analysis, including the statistical analysis). It is an excel spreadsheet that contains a row for each of the metabolites that were identified, fold changes in each metabolite after air and ozone exposure (and the p value of the ozone-induced change), and the pathway and superpathway to which each metabolite belongs. This dataset is associated with the following publication: Cheng, W., K. Duncan, A. Ghio, C. Ward-Caviness, E. Karoly, D. Diaz-Sanchez, R. Conolly, and R. Devlin. Changes in metabolites present in lung-lining fluid following exposure to humans to ozone. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 163(2): 430-439, (2018).