Dataset for a study examining the cardiovascular effects from acute ozone exposure in rats fed with fish oil or olive oil diets. This dataset is associated with the following publication: Tong, H., S. Snow, M.C. Schladweiler, G. Carswell, B. Chorley, and U. Kodavanti. Fish Oil and Olive Oil-Enriched Diets Alleviate Acute Ozone-induced Cardiovascular Effects in Rats. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 409: 115296, (2020).

This dataset contains data of blood miRNA, cardiovascular biomarkers (i.e. inflammation, coagulation, and blood lipids), omega-3 index levels, as well as ambient PM2.5, O3 and NO2 concentrations from the panel study "PISCES". This dataset is associated with the following publication: Chen, H., S. Zhang, B. Yu, Y. Xu, A. Rappold, D. Diaz-Sanchez, J. Samet, and H. Tong. Circulating microRNAs as putative mediators in the association between short-term exposure to ambient air pollution and cardiovascular biomarkers. ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY. Elsevier Science Ltd, New York, NY, USA, 239(113604): 1, (2022).

This study is a randomized trial to investigate whether dietary supplementation with fish oil or olive oil modulate respiratory and cardiovascular effects of acute exposure to ozone in a controlled exposure chamber in young healthy adults. The dataset contains all the data for the outcome variables. This dataset is associated with the following publication: Chen, H., H. Tong, W. Shen, T. Montilla, M. Case, M. Almond , H. Wells, N. Alexis , D. Peden , A. Rappold, D. Diazsanchez, R. Devlin, P. Bromberg , and J. Samet. Fish oil blunts lung function decrements induced by acute exposure to ozone in young healthy adults: A randomized trial. ENVIRONMENT INTERNATIONAL. Elsevier B.V., Amsterdam, NETHERLANDS, 167(107407): 1, (2022).

Background: Adverse cardiovascular events have been linked with PM2.5 exposure obtained primarily from air quality monitors, which rarely co-locate with participant residences. Modeled PM2.5 predictions at finer resolution may more accurately predict residential exposure; however few studies have compared results across different exposure assessment methods. Methods: We utilized a cohort of 5679 patients who had undergone a cardiac catheterization between 2002–2009 and resided in NC. Exposure to PM2.5 for the year prior to catheterization was estimated using data from air quality monitors (AQS), Community Multiscale Air Quality (CMAQ) fused models at the census tract and 12 km spatial resolutions, and satellite-based models at 10 km and 1 km resolutions. Case status was either a coronary artery disease (CAD) index>23 or a recent myocardial infarction (MI). Logistic regression was used to model odds of having CAD or an MI with each 1-unit (μg/m3) increase in PM2.5, adjusting for sex, race, smoking status, socioeconomic status, and urban/rural status. Results: We found that the elevated odds for CAD>23 and MI were nearly equivalent for all exposure assessment methods. One difference was that data from AQS and the census tract CMAQ showed a rural/urban difference in relative risk, which was not apparent with the satellite or 12 km-CMAQ models. Conclusions: Long-term air pollution exposure was associated with coronary artery disease for both modeled and monitored data. 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: Clinical data are located in: C:\Users\rdevlin\OneDrive - Environmental Protection Agency (EPA)\Excel Files\Cathgen Satellite data are located in : C:\Users\rdevlin\OneDrive - Environmental Protection Agency (EPA)\Excel Files\New Ikm Satellite Data C:\Users\rdevlin\OneDrive - Environmental Protection Agency (EPA)\Excel Files\Satellite Data CMAQ data are located in C:\Users\rdevlin\OneDrive - Environmental Protection Agency (EPA)\Excel Files\CMAQ Data. Format: There are two types of datasets used in this study: clinical data taken from patient records at the Duke Medical Center; and air pollution data (PM2.5) taken from a federal reference monitor located in Raleigh, CMAQ data obtained from collaborators at Georgia Tech and NERL/ORD, and satellite data obtained from collaborators at Harvard. Metadata are in the form of Excel spreadsheets that contain columns of data that specify clinical and exposure information for each individual participating in the study. This dataset is associated with the following publication: McGuinn, L., C. Ward-Caviness, A. Schneider, Q. Di, A. Chudnovsky, J. Schwartz, P. Koutrakis, A. Russell, V. Garcia, W. Krause, E. Hauser, L. Neas, W. Cascio, D. Diaz-Sanchez, and R. Devlin. Fine Particulate Matter and Cardiovascular Disease: Comparison of Assessment Methods for Long-term Exposure. ENVIRONMENTAL RESEARCH. Academic Press Incorporated, Orlando, FL, USA, 159: 16-23, (2017).

The dataset contains a list of cardiac and vascular biomarkers that were obtained on each day a participant visited the EPA Human Studies Facility. It also contains ozone concentrations on those days, which are publicly available on the EPA AirNow website. This dataset is not publicly accessible because: The dataset pertains to human research. It can be accessed through the following means: Requests to access data should be sent to Robert Devlin at devlin.robert@epa.gov. Format: The metadata are in the form of spreadsheets with health endpoints listed in columns and each human participant listed as a row. Similar spreadsheets contain exposure information in columns and participants in rows. This dataset is associated with the following publication: Mirowsky, J., M. Carraway, R. Dhingra, H. Tong, L. Neas, D. Diaz-Sanchez, W. Cascio, M. Case, J. Crooks, E. Hauser, E. Dowdy, W. Krause, and R. Devlin. Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients. ENVIRONMENTAL HEALTH. Academic Press Incorporated, Orlando, FL, USA, 16: 126, (2017).

The dataset contains a list of cardiac and vascular biomarkers that were obtained on each day a participant visited the EPA Human Studies Facility. It also contains ozone concentrations on those days, which are publicly available on the EPA AirNow website. This dataset is not publicly accessible because: The dataset pertains to human research. It can be accessed through the following means: Requests to access data should be sent to Robert Devlin at devlin.robert@epa.gov. Format: The metadata are in the form of spreadsheets with health endpoints listed in columns and each human participant listed as a row. Similar spreadsheets contain exposure information in columns and participants in rows. This dataset is associated with the following publication: Mirowsky, J., M. Carraway, R. Dhingra, H. Tong, L. Neas, D. Diaz-Sanchez, W. Cascio, M. Case, J. Crooks, E. Hauser, E. Dowdy, W. Krause, and R. Devlin. Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients. ENVIRONMENTAL HEALTH. Academic Press Incorporated, Orlando, FL, USA, 16: 126, (2017).

Oxidative stress (OS) is a contributing factor to the neuro, cardiac, and pulmonary effects caused by adverse metabolic states, such as obesity and type II diabetes, as well as inhalation of air borne toxicants, such as ozone (O3). The objective of this study is to understand diet/O3 interactions on OS parameters in young male Brown Norway rats maintained on regular (Purina 5001), high fructose (FRUC, TD.89247), or high fat (FAT, TD.06414) diet for 16 wks followed by exposure to either filtered air or 0.8 ppm O3 under an acute (1 d for 5 h) or subacute (5 h/d, 1 d/wk for four wks) paradigm. After 18 h of the last exposure, measures of ROS production (NAD(P)H:quinone oxidoreductase (NQO1) and NADH-Ubiquinone reductase (UBIQ-RD) levels), antioxidant homeostasis (total antioxidant substance (TAS) and γ-Glutamylcysteine synthetase (gGCS) activity), and oxidative damage (total aconitase activity and protein carbonyl (PC) content) were assayed in selected brain regions. Diet/O3 interaction did not have a global effect in the brain, but did show limited regional and OS parameter specific effects. HIP showed a significant interaction between FRUC diet/O3. Aconitase in CER showed a significant interaction between diet and O3. However, regional effects of either O3 or diet alone were more profound. Within the acute condition, there was a decrease in NQ01 and UBIQ-RD in STR and HIP, respectively, regardless of exposure. Also, CER and STR showed a change in TAS due to diet alone, while FC seemed to have a larger amount of TAS due to O3 alone. Diet appeared to affect gGCS negatively in all diet groups of HIP, and only in the FAT diet of STR. The CER also appear to have a decrease in PC in FRUC group and a general decrease in PC in all diets due to O3, while aconitase increased only in FRUC air exposed animals and control O3 exposed animals. Under the subacute condition, there was an increase of NQO1 activity in only the CER due to diets alone, while UBIQ-RD increased in only the FRUC group in FC and in both diet groups in HIP. TAS was decreased in FC only in the FAT group and a clear O3 effect where FAT increased the TAS and FRUC decreased in TAS. A significant interaction between diet/O3 was found in FC. The STR also showed a decrease in TAS in response to O3. Diet also increased PC formation within CER only in the FAT group, while HIP showed a decrease in PC after O3 exposure in controls. Aconitase in CER was affected both by diet in the filtered air group while O3 caused a decrease in controls and FRUC groups. O3 affected all groups within HIP and HYP. STR was most affected by FAT diet in both air and O3 groups. Diet seemed to be the driving factor in most OS measures. Overall, OS parameters measured do not suggest a consistent O3/diet interaction on oxidative damage pathways, but do give insight as to how high caloric diets could affect neuronal OS. This dataset is associated with the following publication: Valdez, J., A. Johnstone, J. Richards, J. Schmid, J. Royland, and P. Kodavanti. Interaction of Diet and Ozone Exposure on Oxidative Stress Parameters within Specific Brain Regions of Male Brown Norway Rats. International Journal of Molecular Sciences. MDPI AG, Basel, SWITZERLAND, 1-17, (2018).

This data set is broken up into 2 Excel files. In one file are all the data pertaining to the vascular and pulmonary effects of ozone exposure in rats fed either a normal diet or diet enriched with coconut oil, fish oil, or olive oil. The different tabs of the spreadsheet pertain to each figure or table found in the manuscript. This file was updated on 12/7/17 to reflect changes to Figure 3 in response to reviewers comments following submission to Toxicological Sciences. In the second file is all the data for Figure 8 pertaining to the global microRNA assessment. This dataset is associated with the following publication: Snow, S., W. Cheng, A. Henriquez, M. Hodge, V. Bass, G. Nelson, G. Carswell, J. Richards, M. Schladweiler, A. Ledbetter, B. Chorley, K. Gowdy, H. Tong, and U. Kodavanti. Ozone-Induced Vascular Contractility and Pulmonary Injury are Differentially Impacted by Diets Enriched with Coconut Oil, Fish Oil, and Olive Oil. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 163(1): 57-69, (2018).

Raw data for all figures and tables in manuscript for study analyzing the impact of living conditions on cardiovascular function in ApoE -/- mice. This dataset is associated with the following publication: Fiamingo, M., S. Toler, K. Lee, W. Oshiro, Q. Krantz, P. Evansky, D. Davies, M. Gilmour, A. Farraj, and M. Hazari. Depleted housing elicits cardiopulmonary dysfunction after a single flaming eucalyptus wildfire smoke exposure in a sex-specific manner in ApoE knockout mice.. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 24: 852-869, (2024).

Cardiovascular Physiologic and Systemic Responses to Sequential Exposure to Nitrogen Dioxide and Ozone in Rats. This dataset is associated with the following publication: Farraj , A., F. Malik, N. Coates , L. Walsh , D. Winsett , D. Terrell , L. Thompson, W. Cascio , and M. Hazari. Morning NO2 Exposure Sensitizes Hypertensive Rats to the Cardiovascular Effects of Same Day O3 Exposure in the Afternoon. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, USA, 28(4): 170-179, (2016).