Impact of Exposure Error on the Relationship Between Traffic-Related Air Pollution and Heart Rate Variability (HRV)

Abstract

Listen

Translate article

TM6-O-05 Introduction: Numerous studies have shown associations between ambient fine particle (PM2.5) concentrations and heart rate variability (HRV). Previously, we reported results examining the association between ambient pollution and HRV for 18 individuals with chronic obstructive pulmonary disease (COPD) and 12 individuals with a myocardial infarction (MI). We found ambient concentrations of PM2.5 and the traffic-related elemental carbon (EC) and nitrogen dioxide (NO2) to have no effects on HRV among all individuals. When analyzed by subgroup, ambient PM2.5 was shown to result in significant increases in SDNN for COPD participants and nonsignificant decreases in MI participants. For EC and NO2, associations with SDNN showed similar, nonsignificant trends for COPD and MI participants. Other measures of HRV, including the parasympathetic indicators, r-MSSD, PNN50, and HF/LF, showed insignificant associations with all ambient measures. Methods: We compare pollutant-associated changes in HRV using ambient concentrations and personal exposures, which were measured for each participant 24 hours prior to each HRV measurement. Personal exposures to PM2.5, sulfate (SO42−), EC, and NO2 were measured using our multipollutant exposure monitor. Corresponding ambient concentrations were assessed using the average pollutant concentration measured at metropolitan Atlanta stationary ambient monitoring sites. The association between 24-hour ambient concentrations and personal exposures and HRV was examined using linear mixed-effects models (LME). Results: Similar to 24-hour ambient PM2.5 concentrations, 24-hour personal PM2.5 exposures were generally not significantly associated with any of the HRV measures. In contrast, personal EC and NO2 exposures averaged over the 24 hours prior to the HRV measurements were significantly associated with decreased HRV, particularly in rMSSD, PNN50, and HF, and with increased LF/HF. Among all participants, RMSSD decreased by 10.97% (95% CI, −18.00 to −3.34) for an IQR change in personal EC exposures (0.81 μg/m3). The magnitude of these associations was substantially stronger than those observed for corresponding 24-hour ambient concentrations and was strongest in MI participants. For example, an IQR change of 0.75 μg/m3 in personal EC exposures was associated with an overall 13.47% (95% CI, −23.81 to −1.73) decrease in RMSSD for MI participants as compared with a 7.53% (95% CI, −16.14 to 1.96) decrease in RMSSD for COPD participants. Similar findings were shown for NO2 and other HRV measures. Discussion and Conclusions: Results indicate decreased vagal tone in response to traffic pollutant exposures, which can best be detected with more precise measures of traffic pollutant exposures.