Traffic-related air pollution and QT interval: modification by diabetes, obesity, and oxidative stress gene polymorphisms in the normative aging study.
BACKGROUND
Acute exposure to ambient air pollution has been associated with acute changes in cardiac outcomes, often within hours of exposure.


OBJECTIVE
We examined the effects of air pollutants on heart-rate-corrected QT interval (QTc), an electrocardiographic marker of ventricular repolarization, and whether these associations were modified by participant characteristics and genetic polymorphisms related to oxidative stress.


METHODS
We studied repeated measurements of QTc on 580 men from the Veterans Affairs Normative Aging Study (NAS) using mixed-effects models with random intercepts. We fitted a quadratic constrained distributed lag model to estimate the cumulative effect on QTc of ambient air pollutants including fine particulate matter <or= 2.5 microm in aerodynamic diameter (PM2.5), ozone (O3), black carbon (BC), nitrogen dioxide (NO2), carbon monoxide (CO), and sulfur dioxide (SO2) concentrations during the 10 hr before the visit. We genotyped polymorphisms related to oxidative stress and analyzed pollution-susceptibility score interactions using the genetic susceptibility score (GSS) method.


RESULTS
Ambient traffic pollutant concentrations were related to longer QTc. An interquartile range (IQR) change in BC cumulative during the 10 hr before the visit was associated with increased QTc [1.89 msec change; 95% confidence interval (CI), -0.16 to 3.93]. We found a similar association with QTc for an IQR change in 1-hr BC that occurred 4 hr before the visit (2.54 msec change; 95% CI, 0.28-4.80). We found increased QTc for IQR changes in NO2 and CO, but the change was statistically insignificant. In contrast, we found no association between QTc and PM2.5, SO2, and O3. The association between QTc and BC was stronger among participants who were obese, who had diabetes, who were nonsmokers, or who had higher GSSs.


CONCLUSIONS
Traffic-related pollutants may increase QTc among persons with diabetes, persons who are obese, and nonsmoking elderly individuals; the number of genetic variants related to oxidative stress increases this effect.
Baja
Emmanuel S
ES
Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115 , USA.
Schwartz
Joel D
JD
Wellenius
Gregory A
GA
Coull
Brent A
BA
Zanobetti
Antonella
A
Vokonas
Pantel S
PS
Suh
Helen H
HH
D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity*; D001794:Blood Pressure; D015992:Body Mass Index; D004562:Electrocardiography; D017353:Gene Deletion; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D008297:Male; D008404:Massachusetts; D015233:Models, Statistical; D018384:Oxidative Stress / Q000187:drug effects*; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity*; D001335:Vehicle Emissions / Q000032:analysis / Q000633:toxicity*; D016276:Ventricular Function / Q000187:drug effects*
D000393:Air Pollutants; D005982:Glutathione Transferase; D052638:Particulate Matter; D001335:Vehicle Emissions; C413545:glutathione S-transferase T1