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.