Traffic-related air pollution exposures and changes in heart rate variability in Mexico City: a panel study

Abstract

Background: While air pollution exposures have been linked to cardiovascular outcomes, the contribution from acute gas and particle traffic-related pollutants remains unclear. Using a panel study design with repeated measures, we examined associations between personal exposures to traffic-related air pollutants in Mexico City and changes in heart rate variability (HRV) in a population of researchers aged 22 to 56 years.

Methods: Participants were monitored for approximately 9.5 hours for eight days while operating a mobile laboratory van designed to characterize traffic pollutants while driving in traffic and "chasing" diesel buses. We examined the association between HRV parameters (standard deviation of normal-to-normal intervals (SDNN), power in high frequency (HF) and low frequency (LF), and the LF/HF ratio) and the 5-minute maximum (or average in the case of PM(2.5)) and 30-, 60-, and 90-minute moving averages of air pollutants (PM(2.5), O(3), CO, CO(2), NO(2), NO(x), and formaldehyde) using single- and two-pollutant linear mixed-effects models.

Results: Short-term exposure to traffic-related emissions was associated with statistically significant acute changes in HRV. Gaseous pollutants - particularly ozone - were associated with reductions in time and frequency domain components (α = 0.05), while significant positive associations were observed between PM(2.5) and SDNN, HF, and LF. For ozone and formaldehyde, negative associations typically increased in magnitude and significance with increasing averaging periods. The associations for CO, CO(2), NO(2), and NO(x) were similar with statistically significant associations observed for SDNN, but not HF or LF. In contrast, PM(2.5) increased these HRV parameters.

Conclusions: Results revealed an association between traffic-related PM exposures and acute changes in HRV in a middle-aged population when PM exposures were relatively low (14 μg/m(3)) and demonstrate heterogeneity in the effects of different pollutants, with declines in HRV - especially HF - with ozone and formaldehyde exposures, and increases in HRV with PM(2.5) exposure. Given that exposure to traffic-related emissions is associated with increased risk of cardiovascular morbidity and mortality, understanding the mechanisms by which traffic-related emissions can cause cardiovascular disease has significant public health relevance.

Figure 1

a. Point estimates and 95% confidence intervals for PM_2.5. Positive associations were observed for PM_2.5 and SDNN, HF and LF. A negative association was observed for the LF/HF ratio. The largest increase observed wasa 7.7% (95% CI: 2.3 to 13.3) increase in HF per IQR 90-min PM_2.5 (8.34 μg/m³). Figure 1b. Point estimates and 95% confidence intervals for CO and CO2. The largest declines in SDNN were 4.2% (95% CI: 1.8 to 6.5) per IQR 30-min CO (10 ppm) and 4.1% (95% CI: 1.8 to 6.3) per IQR 60-min CO2 (104 ppm). Figure 1c. Point estimates and 95% confidence intervals for NO¬2 and NOx. The associations for CO, CO2, NO2 and NOx (which were all correlated) were similar with statistically significant associations observed for SDNN and, in a few instances, the LF/HF ratio, but not HF or LF. The influence of averaging period differed for each pollutant. The largest declines in SDNN for each pollutant were a 3.9% (95% CI: 1.7 to 6.1) per IQR 60-min NO2 (155ppb), and 4.4% (95% CI: 2.2 to 6.5) per IQR 30-min NOx (240 ppb). Figure 1d. Point estimates and 95% confidence intervals for ozone and formaldehyde. Associations increased in magnitude and significance with increasing averaging periods for all HRV parameters except the LF/HF ratio. The largest effects were observed for HF, including a 16% (95% CI: 9.0 to 23.4) decline per IQR 90-min ozone (65 ppb) and a 12% (95% CI: 3.1 to 20.3) decline per IQR 90-min formaldehyde (34 ppb).