Black carbon exposure, oxidative stress genes, and blood pressure in a repeated-measures study.
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.


OBJECTIVE
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 < or = 2.5 microm (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.
Mordukhovich
Irina
I
Department of Epidemiology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina 27599, USA. irinam@email.unc.edu
Wilker
Elissa
E
Suh
Helen
H
Wright
Robert
R
Sparrow
David
D
Vokonas
Pantel S
PS
Schwartz
Joel
J
D000368:Aged; D000393:Air Pollutants / Q000009:adverse effects*; D000397:Air Pollution / Q000009:adverse effects; D001794:Blood Pressure / Q000187:drug effects*; D004781:Environmental Exposure; D014644:Genetic Variation; D006801:Humans; D008297:Male; D008875:Middle Aged; D015233:Models, Statistical; D018384:Oxidative Stress / Q000187:drug effects / Q000235:genetics; D052638:Particulate Matter / Q000633:toxicity; D053260:Soot / Q000633:toxicity*; D001335:Vehicle Emissions / Q000633:toxicity*
D000393:Air Pollutants; D052638:Particulate Matter; D053260:Soot; D001335:Vehicle Emissions