摘要：Ba c k g r o u n d: Epide miological studies have assessed T-wa ve a lterna ns (TWA) as a possible mechanism of cardiac arrhythmias related to air pollution in high-risk subjects and have reported associations with increased TWA magnitude.oB j e c t i v e: In this controlled human exposure study, we assessed the impact of exposure to concen-trated ambient particulate matter (CAP) and ozone (O3) on T-wave alternans in resting volunteers without preexisting cardiovascular disease.Me t h o d s: Seventeen participants without preexisting cardiovascular disease were randomized to fil-tered air (FA), CAP (150 μg/m3), O3(120 ppb), or combined CAP + O3exposures for 2 hr. Continuous electrocardiograms (ECGs) were recorded at rest and T-wave alternans (TWA) was computed by modi-fied moving average analysis with QRS alignment for the artifact-free intervals of 20 beats along the V2 and V5 leads. Exposure-induced changes in the highest TWA magnitude (TWAMax) were estimated for the first and last 5 min of each exposure (TWAMax_Early and TWAMax_Late respectively). .TWAMax(Late–Early) were compared among exposure groups using analysis of variance.re s u l t s: Mean ± SD values for .TWAMaxwere –2.1 ± 0.4, –2.7 ± 1.1, –1.9 ± 1.5, and –1.2 ± 1.5 in FA, CAP, O3, and CAP + O3exposure groups, respectively. No significant differences were observed between pollutant exposures and FA.co n c l u s i o n: In our study of 17 volunteers who had no preexisting cardiovascular disease, we did not observe significant changes in T-wave alternans after 2-hr exposures to CAP, O3, or combined CAP + O3. This finding, however, does not preclude the possibility of pollution-related effects on TWA at elevated heart rates, such as during exercise, or the possibility of delayed responses
