Traffic-Related Air Pollution, Blood Pressure, and Adaptive Response of Mitochondrial Abundance

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dc.authoridSanchez-Guerra, Marco/0000-0002-8354-1157
dc.authoridCAYIR, AKIN/0000-0002-2014-6635
dc.authoridLaue, Hannah/0000-0002-2578-103X
dc.authoridLin, Xinyi Cindy/0000-0002-7209-6588
dc.contributor.authorZhong, Jia
dc.contributor.authorCayir, Akin
dc.contributor.authorTrevisi, Letizia
dc.contributor.authorSanchez-Guerra, Marco
dc.contributor.authorLin, Xinyi
dc.contributor.authorPeng, Cheng
dc.contributor.authorBind, Marie-Abele
dc.date.accessioned2025-01-27T20:25:11Z
dc.date.available2025-01-27T20:25:11Z
dc.date.issued2016
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractBackground 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.
dc.description.sponsorshipNational Institutes of Health [R01ES015172, R21ES021895, R01ES021733, R01ES020836, R01ES021357, P30ES000002]; US Environmental Protection Agency [RD-83479801]; Cooperative Studies Program/Epidemiology Research and Information Center of the US Department of Veterans Affairs (VA); VA Research Career Scientist award
dc.description.sponsorshipThis study was supported by National Institutes of Health grants R01ES015172, R21ES021895, R01ES021733, R01ES020836, R01ES021357, and P30ES000002; and US Environmental Protection Agency funding (RD-83479801). The Normative Aging Study is supported by the Cooperative Studies Program/Epidemiology Research and Information Center of the US Department of Veterans Affairs (VA) and is a component of the Massachusetts Veterans Epidemiology Research and Information Center, Boston, Massachusetts. Dr Sparrow was supported by a VA Research Career Scientist award.
dc.identifier.doi10.1161/CIRCULATIONAHA.115.018802
dc.identifier.endpage387
dc.identifier.issn0009-7322
dc.identifier.issn1524-4539
dc.identifier.issue4
dc.identifier.pmid26660284
dc.identifier.scopus2-s2.0-84950140675
dc.identifier.scopusqualityQ1
dc.identifier.startpage378
dc.identifier.urihttps://doi.org/10.1161/CIRCULATIONAHA.115.018802
dc.identifier.urihttps://hdl.handle.net/20.500.12428/22452
dc.identifier.volume133
dc.identifier.wosWOS:000369259100006
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofCirculation
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20250125
dc.subjectair pollution
dc.subjectblood pressure
dc.subjectmitochondria
dc.subjectoxidative stress
dc.titleTraffic-Related Air Pollution, Blood Pressure, and Adaptive Response of Mitochondrial Abundance
dc.typeArticle

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