Jia Zhong1, Akin Cayir1, Letizia Trevisi1, Marco Sanchez-Guerra1, Xinyi Lin1, Cheng Peng1, Marie-Abèle Bind1, Diddier Prada1, Hannah Laue1, Kasey J M Brennan1, Alexandra Dereix1, David Sparrow1, Pantel Vokonas1, Joel Schwartz1, Andrea A Baccarelli2. 1. From Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA (J.Z., A.C., L.T., M.S.-G., C.P., M.-A.B., D.P., H.L., K.J.M.B., A.D., J.S., A.A.B.); Vocational Health College, Canakkale Onsekiz Mart University, Çanakkale, Turkey (A.C.); Singapore Institute for Clinical Sciences, Singapore (X.L.); Department of Statistics, Harvard University, Cambridge, MA (M.-A.B.); Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología, Mexico City, Mexico (D.P.); and VA Normative Aging Study, Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, MA (D.S., P.V.). 2. From Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA (J.Z., A.C., L.T., M.S.-G., C.P., M.-A.B., D.P., H.L., K.J.M.B., A.D., J.S., A.A.B.); Vocational Health College, Canakkale Onsekiz Mart University, Çanakkale, Turkey (A.C.); Singapore Institute for Clinical Sciences, Singapore (X.L.); Department of Statistics, Harvard University, Cambridge, MA (M.-A.B.); Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología, Mexico City, Mexico (D.P.); and VA Normative Aging Study, Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, MA (D.S., P.V.). abaccare@hsph.harvard.edu.
Abstract
BACKGROUND: Exposure to black carbon (BC), a tracer of vehicular-traffic pollution, is associated with increased blood pressure (BP). Identifying biological factors that attenuate BC effects on BP can inform prevention. We evaluated the role of mitochondrial abundance, an adaptive mechanism compensating for cellular-redox imbalance, in the BC-BP relationship. METHODS AND RESULTS: At ≥ 1 visits among 675 older men from the Normative Aging Study (observations=1252), we assessed daily BP and ambient BC levels from a stationary monitor. To determine blood mitochondrial abundance, we used whole blood to analyze mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA) using quantitative polymerase chain reaction. Every standard deviation increase in the 28-day BC moving average was associated with 1.97 mm Hg (95% confidence interval [CI], 1.23-2.72; P<0.0001) and 3.46 mm Hg (95% CI, 2.06-4.87; P<0.0001) higher diastolic and systolic BP, respectively. Positive BC-BP associations existed throughout all time windows. BC moving averages (5-day to 28-day) were associated with increased mtDNA/nDNA; every standard deviation increase in 28-day BC moving average was associated with 0.12 standard deviation (95% CI, 0.03-0.20; P=0.007) higher mtDNA/nDNA. High mtDNA/nDNA significantly attenuated the BC-systolic BP association throughout all time windows. The estimated effect of 28-day BC moving average on systolic BP was 1.95-fold larger for individuals at the lowest mtDNA/nDNA quartile midpoint (4.68 mm Hg; 95% CI, 3.03-6.33; P<0.0001), in comparison with the top quartile midpoint (2.40 mm Hg; 95% CI, 0.81-3.99; P=0.003). CONCLUSIONS: In older adults, short-term to moderate-term ambient BC levels were associated with increased BP and blood mitochondrial abundance. Our findings indicate that increased blood mitochondrial abundance is a compensatory response and attenuates the cardiac effects of BC.
BACKGROUND: Exposure to black carbon (BC), a tracer of vehicular-traffic pollution, is associated with increased blood pressure (BP). Identifying biological factors that attenuate BC effects on BP can inform prevention. We evaluated the role of mitochondrial abundance, an adaptive mechanism compensating for cellular-redox imbalance, in the BC-BP relationship. METHODS AND RESULTS: At ≥ 1 visits among 675 older men from the Normative Aging Study (observations=1252), we assessed daily BP and ambient BC levels from a stationary monitor. To determine blood mitochondrial abundance, we used whole blood to analyze mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA) using quantitative polymerase chain reaction. Every standard deviation increase in the 28-day BC moving average was associated with 1.97 mm Hg (95% confidence interval [CI], 1.23-2.72; P<0.0001) and 3.46 mm Hg (95% CI, 2.06-4.87; P<0.0001) higher diastolic and systolic BP, respectively. Positive BC-BP associations existed throughout all time windows. BC moving averages (5-day to 28-day) were associated with increased mtDNA/nDNA; every standard deviation increase in 28-day BC moving average was associated with 0.12 standard deviation (95% CI, 0.03-0.20; P=0.007) higher mtDNA/nDNA. High mtDNA/nDNA significantly attenuated the BC-systolic BP association throughout all time windows. The estimated effect of 28-day BC moving average on systolic BP was 1.95-fold larger for individuals at the lowest mtDNA/nDNA quartile midpoint (4.68 mm Hg; 95% CI, 3.03-6.33; P<0.0001), in comparison with the top quartile midpoint (2.40 mm Hg; 95% CI, 0.81-3.99; P=0.003). CONCLUSIONS: In older adults, short-term to moderate-term ambient BC levels were associated with increased BP and blood mitochondrial abundance. Our findings indicate that increased blood mitochondrial abundance is a compensatory response and attenuates the cardiac effects of BC.
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