Key result
Higher black carbon exposure is linked to ~3.5 mm Hg higher systolic BP, attenuated by mitochondrial abundance.
Why the study?
Exposure to black carbon, a marker of vehicular traffic pollution, is associated with increased blood pressure, but biological factors that attenuate this effect are not well understood.
Does increased blood mitochondrial abundance attenuate the association between black carbon exposure and increased blood pressure in older men?
Observational (n=675)
Does increased blood mitochondrial abundance attenuate the association between black carbon exposure and increased blood pressure in older men?
Mean Difference: 3.46 (95% CI 2.06–4.87)
p-value: p=<0.0001
Increased blood mitochondrial abundance acts as a compensatory response that attenuates the blood pressure-elevating effects of traffic-related air pollution in older adults.
Mitochondrial abundance may attenuate black carbon-associated BP rises in older men; extends observational links but remains hypothesis-generating.
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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Zhong et al. (2015) reported an observational. Ambient black carbon (BC) exposure vs. Lower black carbon exposure was evaluated on Systolic blood pressure (MD 3.46 mm Hg, 95% CI 2.06-4.87, p=<0.0001). Every standard deviation increase in 28-day black carbon was associated with 3.46 mm Hg higher systolic BP (P<0.0001), an effect significantly attenuated by higher blood mitochondrial abundance.