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).

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 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).

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).

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 data consists of a series of tables containing individual identifiers; countrywide high-resolution (1 km × 1 km) modeled PM2.5 from a model built by Harvard collaborators; daily concentrations of relative humidity (RH) and temperature; and troponin I measurements. 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: Data can be accessed with an approved IRB. Format: The data consists of a series of tables containing individual identifiers; countrywide high-resolution (1 km × 1 km) modeled PM2.5 from a model built by Harvard collaborators; daily concentrations of relative humidity (RH) and temperature; and troponin I measurements. This dataset is associated with the following publication: Wyatt, L., G. Kamat, J. Moyer, A. Weaver, D. Diazsanchez, R. Devlin, Q. Di, J. Schwartz, W. Cascio, and C. Ward-Caviness. Associations between short-term exposure to PM2.5 and cardiomyocyte injury in myocardial infarction survivors in North Carolina. Open Heart. BMJ Publishing Group Ltd, London, UK, 9: e001891, (2022).

This dataset contains deidentified subject level data from the study titled: Responses to Exposure to Low Levels of Concentrated Ambient Particles in Healthy Young Adults (RECAP). Subject, exposure, and health endpoint data are included in the dataset. Health endpoint data includes inflammatory, heart rate variability and cardiac repolarization, lung function, blood chemistry, and lipids measures. This dataset is associated with the following publication: Wyatt, L., R. Devlin, A. Rappold, and M. Case. Low levels of fine particulate matter increase vascular damage and reduce pulmonary function in young healthy adults. Particle and Fibre Toxicology. BioMed Central Ltd, London, UK, 17(1): 58, (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).

The dataset contains data of air pollution, blood lipids, vascular injury markers, coagulation markers, and heart rate variability and repolarization markers. This dataset is associated with the following publication: Chen, H., S. Zhang, W. Shen, C. Salazar, A. Schneider, A. Rappold, D. Diazsanchez, R. Devlin, J. Samet, and H. Tong. Omega-3 Fatty Acids Attenuate Cardiovascular Effects of Short-term Exposure to Ambient Air Pollution. Particle and Fibre Toxicology. BioMed Central Ltd, London, UK, 19(12): 1, (2022).

Studies have linked exposure to ultrafine particulate matter (PM) and adverse cardiovascular events. Particulate matter-induced oxidative stress is believed to be a key mechanism underlying observed adverse vascular effects. Advanced age is one factor known to decrease anti-oxidant defenses and confer susceptibility to the detrimental vascular effects seen following PM exposure. The present study was designed to investigate the vasomotor responses following ultrafine PM exposure in wild type (WT) and superoxide dismutase 2 deficient (SOD2+/-) mice which possess decreased anti-oxidant defense. Thoracic aortic rings isolated from young and aged WT and SOD2+/- mice were exposed to ultrafine PM in a tissue bath system. Aortic rings were then constricted with increasing concentrations of phenylephrine, followed by relaxation with rising amounts of nitroglycerin (NTG). Data demonstrated that ultrafine PM decreased the relaxation response in both young WT and young SOD2+/- mouse aortas, and relaxation was significantly reduced in young SOD2+/- compared to WT mice. Ultrafine PM significantly diminished the NTG-induced relaxation response in aged compared to young mouse aortas. After ultrafine PM exposure, the relaxation response did not differ markedly between aged WT and aged SOD2+/- mice. Data demonstrate that the greater vascular effect in aortic rings in aged mice ex vivo after ultrafine PM exposure may be attributed to ultrafine PM-induced oxidative stress and loss of anti-oxidant defenses in aged vascular tissue. Consistent with this conclusion is the attenuation of NTG-induced relaxation response in young SOD2+/- mice. This dataset is associated with the following publication: Carter, J., N. Madamanchi , G. Stouffer, M. Runge, W. Cascio, and H. Tong. Ultrafine Particulate Matter Exposure Impairs Vasorelaxant Response in Superoxide Dismutase 2 Deficient Murine Aortic Rings. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 81(5): 106-115, (2018).