Jianzhao Bi1, Rohan R D'Souza2, David Q Rich3, Philip K Hopke4, Armistead G Russell5, Yang Liu6, Howard H Chang2, Stefanie Ebelt6. 1. Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA. Electronic address: jianzhao.bi@outlook.com. 2. Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA, USA. 3. Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA; Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA; Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA. 4. Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA; Center for Air Resources Engineering and Science, Clarkson University, Potsdam, NY, USA. 5. School of Civil and Environmental Engineering, Georgia Institute of Technology, Atlanta, GA, USA. 6. Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Abstract
BACKGROUND: Emissions control programs targeting certain air pollution sources may alter PM2.5 composition, as well as the risk of adverse health outcomes associated with PM2.5. OBJECTIVES: We examined temporal changes in the risk of emergency department (ED) visits for cardiovascular diseases (CVDs) and asthma associated with short-term increases in ambient PM2.5 concentrations in Los Angeles, California. METHODS: Poisson log-linear models with unconstrained distributed exposure lags were used to estimate the risk of CVD and asthma ED visits associated with short-term increases in daily PM2.5 concentrations, controlling for temporal and meteorological confounders. The models were run separately for three predefined time periods, which were selected based on the implementation of multiple emissions control programs (EARLY: 2005-2008; MIDDLE: 2009-2012; LATE: 2013-2016). Two-pollutant models with individual PM2.5 components and the remaining PM2.5 mass were also considered to assess the influence of changes in PM2.5 composition on changes in the risk of CVD and asthma ED visits associated with PM2.5 over time. RESULTS: The relative risk of CVD ED visits associated with a 10 μg/m3 increase in 4-day PM2.5 concentration (lag 0-3) was higher in the LATE period (rate ratio = 1.020, 95% confidence interval = [1.010, 1.030]) compared to the EARLY period (1.003, [0.996, 1.010]). In contrast, for asthma, relative risk estimates were largest in the EARLY period (1.018, [1.006, 1.029]), but smaller in the following periods. Similar temporal differences in relative risk estimates for CVD and asthma were observed among different age and season groups. No single component was identified as an obvious contributor to the changing risk estimates over time, and some components exhibited different temporal patterns in risk estimates from PM2.5 total mass, such as a decreased risk of CVD ED visits associated with sulfate over time. CONCLUSIONS: Temporal changes in the risk of CVD and asthma ED visits associated with short-term increases in ambient PM2.5 concentrations were observed. These changes could be related to changes in PM2.5 composition (e.g., an increasing fraction of organic carbon and a decreasing fraction of sulfate in PM2.5). Other factors such as improvements in healthcare and differential exposure misclassification might also contribute to the changes.
BACKGROUND: Emissions control programs targeting certain air pollution sources may alter PM2.5 composition, as well as the risk of adverse health outcomes associated with PM2.5. OBJECTIVES: We examined temporal changes in the risk of emergency department (ED) visits for cardiovascular diseases (CVDs) and asthma associated with short-term increases in ambient PM2.5 concentrations in Los Angeles, California. METHODS: Poisson log-linear models with unconstrained distributed exposure lags were used to estimate the risk of CVD and asthma ED visits associated with short-term increases in daily PM2.5 concentrations, controlling for temporal and meteorological confounders. The models were run separately for three predefined time periods, which were selected based on the implementation of multiple emissions control programs (EARLY: 2005-2008; MIDDLE: 2009-2012; LATE: 2013-2016). Two-pollutant models with individual PM2.5 components and the remaining PM2.5 mass were also considered to assess the influence of changes in PM2.5 composition on changes in the risk of CVD and asthma ED visits associated with PM2.5 over time. RESULTS: The relative risk of CVD ED visits associated with a 10 μg/m3 increase in 4-day PM2.5 concentration (lag 0-3) was higher in the LATE period (rate ratio = 1.020, 95% confidence interval = [1.010, 1.030]) compared to the EARLY period (1.003, [0.996, 1.010]). In contrast, for asthma, relative risk estimates were largest in the EARLY period (1.018, [1.006, 1.029]), but smaller in the following periods. Similar temporal differences in relative risk estimates for CVD and asthma were observed among different age and season groups. No single component was identified as an obvious contributor to the changing risk estimates over time, and some components exhibited different temporal patterns in risk estimates from PM2.5 total mass, such as a decreased risk of CVD ED visits associated with sulfate over time. CONCLUSIONS: Temporal changes in the risk of CVD and asthma ED visits associated with short-term increases in ambient PM2.5 concentrations were observed. These changes could be related to changes in PM2.5 composition (e.g., an increasing fraction of organic carbon and a decreasing fraction of sulfate in PM2.5). Other factors such as improvements in healthcare and differential exposure misclassification might also contribute to the changes.
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