Shaowei Wu1, Di Yang1, Lu Pan1, Jiao Shan1, Hongyu Li1, Hongying Wei1, Bin Wang2, Jing Huang1, Andrea A Baccarelli3, Masayuki Shima4, Furong Deng5, Xinbiao Guo6. 1. Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China. 2. Institute of Reproductive & Child Health, Peking University School of Public Health, Beijing, China. 3. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 4. Department of Public Health, Hyogo College of Medicine, Hyogo, Japan. 5. Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China. Electronic address: lotus321321@126.com. 6. Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China. Electronic address: guoxb@bjmu.edu.cn.
Abstract
BACKGROUND: Exposure to ambient air pollution has been associated with endothelial dysfunction as reflected by short-term alterations in circulating biomarkers, but the chemical constituents and pollution sources behind the association has been unclear. METHODS: We investigated the associations between various ambient air pollutants including gases and 31 chemical constituents and seven sources of fine particles (PM2.5) and biomarkers of endothelial function, including endothelin-1 (ET-1), E-selectin, soluble intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), based on 462 repeated measurements in a panel of 40 college students who were followed for three study periods before and after relocating from a suburban area to an urban area in Beijing, China in 2010-2011. Air pollution data were obtained from central air-monitoring stations. Linear mixed-effects models were used to estimate the changes in biomarkers associated with exposures. RESULTS: Total PM2.5 mass showed few appreciable associations with examined biomarkers. However, several PM2.5 constituents and related sources showed significant associations with examined biomarkers. PM2.5 from dust/soil and several crustal and transition metals, including strontium, iron, titanium, cobalt and magnesium, were significantly associated with increases in ET-1 at 1-day average; manganese and potassium were significantly associated with increases in ICAM-1 at 2-day average; and PM2.5 from industry and metal cadmium were significantly associated with decreases in VCAM-1 at 1-day average. In addition, carbon monoxide was significantly associated with increasing ICAM-1 at 1-day and 2-day averages, whereas nitric oxide was significantly associated with decreasing ICAM-1 at 1-day and 3-day averages. CONCLUSIONS: Our results suggest that certain PM2.5 metal constituents were more closely associated with circulating biomarkers of endothelial function than PM2.5, and therefore highlight the research necessity to examine pollution chemical constituents in future studies.
BACKGROUND: Exposure to ambient air pollution has been associated with endothelial dysfunction as reflected by short-term alterations in circulating biomarkers, but the chemical constituents and pollution sources behind the association has been unclear. METHODS: We investigated the associations between various ambient air pollutants including gases and 31 chemical constituents and seven sources of fine particles (PM2.5) and biomarkers of endothelial function, including endothelin-1 (ET-1), E-selectin, soluble intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), based on 462 repeated measurements in a panel of 40 college students who were followed for three study periods before and after relocating from a suburban area to an urban area in Beijing, China in 2010-2011. Air pollution data were obtained from central air-monitoring stations. Linear mixed-effects models were used to estimate the changes in biomarkers associated with exposures. RESULTS: Total PM2.5 mass showed few appreciable associations with examined biomarkers. However, several PM2.5 constituents and related sources showed significant associations with examined biomarkers. PM2.5 from dust/soil and several crustal and transition metals, including strontium, iron, titanium, cobalt and magnesium, were significantly associated with increases in ET-1 at 1-day average; manganese and potassium were significantly associated with increases in ICAM-1 at 2-day average; and PM2.5 from industry and metalcadmium were significantly associated with decreases in VCAM-1 at 1-day average. In addition, carbon monoxide was significantly associated with increasing ICAM-1 at 1-day and 2-day averages, whereas nitric oxide was significantly associated with decreasing ICAM-1 at 1-day and 3-day averages. CONCLUSIONS: Our results suggest that certain PM2.5 metal constituents were more closely associated with circulating biomarkers of endothelial function than PM2.5, and therefore highlight the research necessity to examine pollution chemical constituents in future studies.
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