David Q Rich1, Wangjian Zhang2, Shao Lin2, Stefania Squizzato3, Sally W Thurston4, Edwin van Wijngaarden5, Daniel Croft6, Mauro Masiol3, Philip K Hopke7. 1. Department of Public Health Sciences, University of Rochester Medical Center, 265 Crittenden Boulevard, Rochester, NY 14642, USA; Department of Environmental Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box EHSC, Rochester, NY 14642, USA; Department of Medicine, Pulmonary and Critical Care, University of Rochester Medical Center, 601 Elmwood Avenue, Box 692, Rochester, NY 14642, USA. Electronic address: david_rich@urmc.rochester.edu. 2. Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, One University Place, Rensselaer, NY 12144, USA. 3. Department of Public Health Sciences, University of Rochester Medical Center, 265 Crittenden Boulevard, Rochester, NY 14642, USA. 4. Department of Biostatistics and Computational Biology, University of Rochester Medical Center, 265 Crittenden Boulevard, CU 420630, Rochester, NY 14642, USA. 5. Department of Public Health Sciences, University of Rochester Medical Center, 265 Crittenden Boulevard, Rochester, NY 14642, USA; Department of Environmental Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box EHSC, Rochester, NY 14642, USA; Department of Pediatrics, University of Rochester Medical Center, 601 Elmwood Avenue, Box 651, Rochester, NY 14642, USA. 6. Department of Medicine, Pulmonary and Critical Care, University of Rochester Medical Center, 601 Elmwood Avenue, Box 692, Rochester, NY 14642, USA. 7. Department of Public Health Sciences, University of Rochester Medical Center, 265 Crittenden Boulevard, Rochester, NY 14642, USA; Center for Air Resources Engineering and Science, Clarkson University, Box 5708, Potsdam, NY 13699, USA.
Abstract
BACKGROUND: Previous work reported increased rates of acute cardiovascular hospitalizations associated with increased PM2.5 concentrations in the previous few days across urban centers in New York State from 2005 to 2016. These relative rates were higher after air quality policies and economic changes resulted in decreased PM2.5 concentrations and changes in PM composition (e.g. increased secondary organic carbon), compared to before and during these changes. Changes in PM composition and sources may explain this difference. OBJECTIVES: To estimate the rate of acute cardiovascular hospitalizations associated with increases in source specific PM2.5 concentrations. METHODS: Using source apportioned PM2.5 concentrations at the same NYS urban sites, a time-stratified case-crossover design, and conditional logistic regression models adjusting for ambient temperature and relative humidity, we estimated the rate of these acute cardiovascular hospitalizations associated with increases in mean source specific PM2.5 concentrations in the previous 1, 4, and 7 days. RESULTS: Interquartile range (IQR) increases in spark-ignition emissions (GAS) concentrations were associated with increased excess rates of cardiac arrhythmia hospitalizations (2.3%; 95% CI = 0.4%, 4.2%; IQR = 2.56 μg/m3) and ischemic stroke hospitalizations (3.7%; 95% CI = 1.1%, 6.4%; 2. 73 μg/m3) over the next day. IQR increases in diesel (DIE) concentrations were associated with increased rates of congestive heart failure hospitalizations (0.7%; 95% CI = 0.2% 1.3%; 0.51 μg/m3) and ischemic heart disease hospitalizations (0.8%; 95% CI = 0.3%, 1.3%; 0.60 μg/m3) over the next day, as hypothesized. However, secondary sulfate PM2.5 (SS) was not. Increased acute cardiovascular hospitalization rates were also associated with IQR increases in concentrations of road dust (RD), residual oil (RO), and secondary nitrate (SN) over the previous 1, 4, and 7 days, but not other sources. CONCLUSIONS: These findings suggest a role of several sources of PM2.5 in New York State (i.e. traffic emissions, non-traffic emissions such as brake and tire wear, residual oil, and nitrate that may also reflect traffic emissions) in the triggering of acute cardiovascular events.
BACKGROUND: Previous work reported increased rates of acute cardiovascular hospitalizations associated with increased PM2.5 concentrations in the previous few days across urban centers in New York State from 2005 to 2016. These relative rates were higher after air quality policies and economic changes resulted in decreased PM2.5 concentrations and changes in PM composition (e.g. increased secondary organic carbon), compared to before and during these changes. Changes in PM composition and sources may explain this difference. OBJECTIVES: To estimate the rate of acute cardiovascular hospitalizations associated with increases in source specific PM2.5 concentrations. METHODS: Using source apportioned PM2.5 concentrations at the same NYS urban sites, a time-stratified case-crossover design, and conditional logistic regression models adjusting for ambient temperature and relative humidity, we estimated the rate of these acute cardiovascular hospitalizations associated with increases in mean source specific PM2.5 concentrations in the previous 1, 4, and 7 days. RESULTS: Interquartile range (IQR) increases in spark-ignition emissions (GAS) concentrations were associated with increased excess rates of cardiac arrhythmia hospitalizations (2.3%; 95% CI = 0.4%, 4.2%; IQR = 2.56 μg/m3) and ischemic stroke hospitalizations (3.7%; 95% CI = 1.1%, 6.4%; 2. 73 μg/m3) over the next day. IQR increases in diesel (DIE) concentrations were associated with increased rates of congestive heart failure hospitalizations (0.7%; 95% CI = 0.2% 1.3%; 0.51 μg/m3) and ischemic heart disease hospitalizations (0.8%; 95% CI = 0.3%, 1.3%; 0.60 μg/m3) over the next day, as hypothesized. However, secondary sulfatePM2.5 (SS) was not. Increased acute cardiovascular hospitalization rates were also associated with IQR increases in concentrations of road dust (RD), residual oil (RO), and secondary nitrate (SN) over the previous 1, 4, and 7 days, but not other sources. CONCLUSIONS: These findings suggest a role of several sources of PM2.5 in New York State (i.e. traffic emissions, non-traffic emissions such as brake and tire wear, residual oil, and nitrate that may also reflect traffic emissions) in the triggering of acute cardiovascular events.
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