Does exposure to air pollution cause T wave alternans in subjects with no pre-existing cardiovascular disease?

BACKGROUND:

Epidemiological studies have assessed T wave alternans (TWA) as a possible mechanism to sudden cardiac death and arrhythmogenesity related to air pollution in high risk subjects and demonstrated increases in the value of TWA, but whether exposure to air pollution has an effect on TWA in healthy subjects is unclear. In this controlled human exposure study, we tested the hypothesis that exposure to concentrated ambient fine particles (CAP) and/or ozone (O3) would increase temporal dispersion of repolarization in healthy subjects.

METHODS:

In a randomized, crossover design, 40 healthy volunteers (22 female and 18 male; 18-50 years of age) were randomized to 2-hr controlled exposures to filtered air (FA), CAP (150 μg/m3), O3 (120 ppb), or combined CAP+O3. Continuous 12-lead ECG was recorded at rest (mean heart rate: 73.4 ± 11.37 beats/min.); TWA was computed by modified moving average (MMA) analysis with and without QRS alignment for the artifact free intervals of 20 beats along the V3 lead. Exposure-induced changes in the highest TWA value, TWAMax, between the start (first 5 min) and end (last five min) of exposure were calculated (ΔTWA-Max). TWA was adjusted for heart rate and ANOVA was employed to compare TWAMax in different exposure groups. ΔTWA-Max75 was defined as a binary variable and logistic regression was used to estimate the effect of pollution on the probability of ΔTWA-Max - 75th percentile.

RESULTS:

Results for lead V3 are shown in the table below. We did not find any significant difference in the odds of ΔTWAMax75 with QRS alignment (P = 0.69) between differentexposure groups. (Table presented).