Wenyuan Li1, Marguerite M Nyhan2, Elissa H Wilker1, Carolina L Z Vieira2, Honghuang Lin3, Joel D Schwartz4, Diane R Gold5, Brent A Coull6, Abdulaziz Mansour Aba7, Emelia J Benjamin8, Ramachandran S Vasan8, Petros Koutrakis2, Murray A Mittleman9. 1. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Cardiovascular Epidemiology Research Unit, Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. 2. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States. 3. Department of Medicine, Boston University School of Medicine, Boston, MA, United States. 4. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States. 5. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States. 6. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, United States. 7. Kuwait Institute for Scientific Research, Kuwait City, Kuwait. 8. Department of Medicine, Boston University School of Medicine, Boston, MA, United States; National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA, United States; Department of Epidemiology, Boston University School of Public Health, Boston, MA, United States. 9. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Cardiovascular Epidemiology Research Unit, Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: mmittlem@hsph.harvard.edu.
Abstract
BACKGROUND: Decay products of radioactive materials may attach to ambient fine particles and form radioactive aerosol. Internal ionizing radiation source from inhaled radioactive aerosol may contribute to the fine particulate matter (PM2.5)-inflammation pathway. However, few studies in humans have examined the associations. OBJECTIVES: To examine the associations between particle radioactivity and biomarkers of oxidative stress and inflammation among participants from the Framingham Offspring and Third Generation cohorts. METHODS: We included 3996 participants who were not current smokers and lived within 50 km from our central air pollution monitoring station. We estimated regional mean gross beta radioactivity from monitors in the northeastern U.S. as a surrogate for ambient radioactive particles, and calculated the 1- to 28-day moving averages. We used linear regression models for fibrinogen, tumor necrosis factor α, interleukin-6, and myeloperoxidase which were measured once, and linear mixed effect models for 8-epi-prostaglandin F2α, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), P-selectin, and tumor necrosis factor receptor-2 that were measured up to twice, adjusting for demographics, individual- and area-level socioeconomic positions, time, meteorology, and PM2.5. We also examined whether the associations differed by median age, sex, diabetes status, PM2.5 levels, and black carbon levels. RESULTS: The mean age was 54 years and 54% were women. An interquartile range (3 × 10-3 pCi/m3) higher beta radioactivity level at the 7-day moving average was associated with 5.09% (95% CI: 0.92, 9.43), 2.65% (1.10, 4.22), and 4.71% (95% CI: 3.01, 6.44) higher levels of interleukin-6, MCP-1, and P-selectin, but with 7.01% (95% CI: -11.64, -2.15) and 2.70% (95% CI: -3.97, -1.42) lower levels of 8-epi-prostaglandin F2α and ICAM-1, respectively. CONCLUSIONS: Regional mean particle radioactivity was positively associated with interleukin-6, MCP-1, and P-selectin, but negatively with ICAM-1 and 8-epi-prostaglandin F2α among our study participants.
BACKGROUND: Decay products of radioactive materials may attach to ambient fine particles and form radioactive aerosol. Internal ionizing radiation source from inhaled radioactive aerosol may contribute to the fine particulate matter (PM2.5)-inflammation pathway. However, few studies in humans have examined the associations. OBJECTIVES: To examine the associations between particle radioactivity and biomarkers of oxidative stress and inflammation among participants from the Framingham Offspring and Third Generation cohorts. METHODS: We included 3996 participants who were not current smokers and lived within 50 km from our central air pollution monitoring station. We estimated regional mean gross beta radioactivity from monitors in the northeastern U.S. as a surrogate for ambient radioactive particles, and calculated the 1- to 28-day moving averages. We used linear regression models for fibrinogen, tumor necrosis factor α, interleukin-6, and myeloperoxidase which were measured once, and linear mixed effect models for 8-epi-prostaglandin F2α, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), P-selectin, and tumor necrosis factor receptor-2 that were measured up to twice, adjusting for demographics, individual- and area-level socioeconomic positions, time, meteorology, and PM2.5. We also examined whether the associations differed by median age, sex, diabetes status, PM2.5 levels, and black carbon levels. RESULTS: The mean age was 54 years and 54% were women. An interquartile range (3 × 10-3 pCi/m3) higher beta radioactivity level at the 7-day moving average was associated with 5.09% (95% CI: 0.92, 9.43), 2.65% (1.10, 4.22), and 4.71% (95% CI: 3.01, 6.44) higher levels of interleukin-6, MCP-1, and P-selectin, but with 7.01% (95% CI: -11.64, -2.15) and 2.70% (95% CI: -3.97, -1.42) lower levels of 8-epi-prostaglandin F2α and ICAM-1, respectively. CONCLUSIONS: Regional mean particle radioactivity was positively associated with interleukin-6, MCP-1, and P-selectin, but negatively with ICAM-1 and 8-epi-prostaglandin F2α among our study participants.
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