Wenyuan Li1, Kirsten S Dorans1, Elissa H Wilker1, Mary B Rice1, Petter L Ljungman1, Joel D Schwartz1, Brent A Coull1, Petros Koutrakis1, Diane R Gold1, John F Keaney1, Ramachandran S Vasan1, Emelia J Benjamin1, Murray A Mittleman2. 1. From the Departments of Epidemiology (W.L., K.S.D., E.H.W., J.D.S., M.A.M.), Environmental Health (J.D.S., P.K., D.R.G.), and Biostatistics (B.A.C.), Harvard T.H. Chan School of Public Health, Boston, MA; Cardiovascular Epidemiology Research Unit, Division of Cardiology (W.L., K.S.D., E.H.W., P.L.L., M.A.M.) and Division of Pulmonary, Critical Care and Sleep Medicine (M.B.R.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (P.L.L.); Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (D.R.G.); Division of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester (J.F.K.); National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, MA (R.S.V., E.J.B.); Preventive Medicine and Cardiology Sections, Department of Medicine, Boston University School of Medicine, MA (R.S.V., E.J.B.); and Department of Epidemiology, Boston University School of Public Health, MA (R.S.V., E.J.B.). 2. From the Departments of Epidemiology (W.L., K.S.D., E.H.W., J.D.S., M.A.M.), Environmental Health (J.D.S., P.K., D.R.G.), and Biostatistics (B.A.C.), Harvard T.H. Chan School of Public Health, Boston, MA; Cardiovascular Epidemiology Research Unit, Division of Cardiology (W.L., K.S.D., E.H.W., P.L.L., M.A.M.) and Division of Pulmonary, Critical Care and Sleep Medicine (M.B.R.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (P.L.L.); Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (D.R.G.); Division of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester (J.F.K.); National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, MA (R.S.V., E.J.B.); Preventive Medicine and Cardiology Sections, Department of Medicine, Boston University School of Medicine, MA (R.S.V., E.J.B.); and Department of Epidemiology, Boston University School of Public Health, MA (R.S.V., E.J.B.). mmittlem@hsph.harvard.edu.
Abstract
OBJECTIVE: The objective of this study is to examine associations between short-term exposure to ambient air pollution and circulating biomarkers of systemic inflammation in participants from the Framingham Offspring and Third Generation cohorts in the greater Boston area. APPROACH AND RESULTS: We included 3996 noncurrent smoking participants (mean age, 53.6 years; 54% women) who lived within 50 km from a central air pollution monitoring site in Boston, MA, and calculated the 1- to 7-day moving averages of fine particulate matter (diameter<2.5 µm), black carbon, sulfate, nitrogen oxides, and ozone before the examination visits. We used linear mixed effects models for C-reactive protein and tumor necrosis factor receptor 2, which were measured up to twice for each participant; we used linear regression models for interleukin-6, fibrinogen, and tumor necrosis factor α, which were measured once. We adjusted for demographics, socioeconomic position, lifestyle, time, and weather. The 3- to 7-day moving averages of fine particulate matter (diameter<2.5 µm) and sulfate were positively associated with C-reactive protein concentrations. A 5 µg/m3 higher 5-day moving average fine particulate matter (diameter<2.5 µm) was associated with 4.2% (95% confidence interval: 0.8, 7.6) higher circulating C-reactive protein. Positive associations were also observed for nitrogen oxides with interleukin-6 and for black carbon, sulfate, and ozone with tumor necrosis factor receptor 2. However, black carbon, sulfate, and nitrogen oxides were negatively associated with fibrinogen, and sulfate was negatively associated with tumor necrosis factor α. CONCLUSIONS: Higher short-term exposure to relatively low levels of ambient air pollution was associated with higher levels of C-reactive protein, interleukin-6, and tumor necrosis factor receptor 2 but not fibrinogen or tumor necrosis factor α in individuals residing in the greater Boston area.
OBJECTIVE: The objective of this study is to examine associations between short-term exposure to ambient air pollution and circulating biomarkers of systemic inflammation in participants from the Framingham Offspring and Third Generation cohorts in the greater Boston area. APPROACH AND RESULTS: We included 3996 noncurrent smoking participants (mean age, 53.6 years; 54% women) who lived within 50 km from a central air pollution monitoring site in Boston, MA, and calculated the 1- to 7-day moving averages of fine particulate matter (diameter<2.5 µm), black carbon, sulfate, nitrogen oxides, and ozone before the examination visits. We used linear mixed effects models for C-reactive protein and tumor necrosis factor receptor 2, which were measured up to twice for each participant; we used linear regression models for interleukin-6, fibrinogen, and tumor necrosis factor α, which were measured once. We adjusted for demographics, socioeconomic position, lifestyle, time, and weather. The 3- to 7-day moving averages of fine particulate matter (diameter<2.5 µm) and sulfate were positively associated with C-reactive protein concentrations. A 5 µg/m3 higher 5-day moving average fine particulate matter (diameter<2.5 µm) was associated with 4.2% (95% confidence interval: 0.8, 7.6) higher circulating C-reactive protein. Positive associations were also observed for nitrogen oxides with interleukin-6 and for black carbon, sulfate, and ozone with tumor necrosis factor receptor 2. However, black carbon, sulfate, and nitrogen oxides were negatively associated with fibrinogen, and sulfate was negatively associated with tumor necrosis factor α. CONCLUSIONS: Higher short-term exposure to relatively low levels of ambient air pollution was associated with higher levels of C-reactive protein, interleukin-6, and tumor necrosis factor receptor 2 but not fibrinogen or tumor necrosis factor α in individuals residing in the greater Boston area.
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