Black Carbon Exposure, Oxidative Stress Genes, and Blood Pressure in a Repeated-measures Study

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Black Carbon Exposure, Oxidative Stress Genes, and Blood Pressure in a Repeated-measures Study

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Title: Black Carbon Exposure, Oxidative Stress Genes, and Blood Pressure in a Repeated-measures Study
Author: Mordukhovich, Irina; Wilker, Elissa Hope; Suh MacIntosh, Helen H.; Wright, Robert O.; Sparrow, David; Vokonas, Pantel S; Schwartz, Joel David

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Citation: Mordukhovich, Irina, Elissa Wilker, Helen Suh, Robert Wright, David Sparrow, Pantel S. Vokonas, and Joel Schwartz. 2009. Black carbon exposure, oxidative stress genes, and blood pressure in a repeated-measures study. Environmental Health Perspectives 117(11): 1767-1772.
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Abstract: Background: Particulate matter (PM) air pollution has been associated with cardiovascular morbidity and mortality, and elevated blood pressure (BP) is a known risk factor for cardiovascular disease. A small number of studies have investigated the relationship between PM and BP and found mixed results. Evidence suggests that traffic-related air pollution contributes significantly to PM-related cardiovascular effects. Objectives: We hypothesized that black carbon (BC), a traffic-related combustion by-product, would be more strongly associated with BP than would fine PM [aerodynamic diameter ≤ 2.5 μm (PM\(_{2.5}\))], a heterogeneous PM mixture, and that these effects would be larger among participants with genetic variants associated with impaired antioxidative defense. Methods: We performed a repeated-measures analysis in elderly men to analyze associations between PM\(_{2.5}\) and BC exposure and BP using mixed-effects models with random intercepts, adjusting for potential confounders. We also examined statistical interaction between BC and genetic variants related to oxidative stress defense: GSTM1, GSTP1, GSTT1, NQO1, catalase, and HMOX-1. Results: A 1-SD increase in BC concentration was associated with a 1.5-mmHg increase in systolic BP [95% confidence interval (CI), 0.1–2.8] and a 0.9-mmHg increase in diastolic BP (95% CI, 0.2–1.6). We observed no evidence of statistical interaction between BC and any of the genetic variants examined and found no association between PM\(_{2.5}\) and BP. Conclusions: We observed positive associations between BP and BC, but not between BP and PM\(_{2.5}\), and found no evidence of effect modification of the association between BC and BP by gene variants related to antioxidative defense.
Published Version: doi://10.1289/ehp.0900591
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