Walking for two hours on a traffic-congested street reduced cardioprotective NO2-cLA levels compared to a park walk in COPD patients (0.0189 vs 0.0323 μg/g creatinine, p=0.03).
RCT (n=116)
Random order crossover
Does short-term exposure to traffic pollution alter cardiac electrophysiology and cardioprotective biomarker levels in adults with COPD, IHD, and healthy individuals?
Short-term exposure to traffic pollution induces adverse cardiac electrophysiological changes and reduces cardioprotective NO2-cLA levels, particularly in COPD patients, though inhaler use may attenuate these effects.
Absolute Event Rate: 0.0189% vs 0.0323%
p-value: p=0.03
• Individuals with COPD exhibited greater electrophysiological responses to traffic-related pollution compared to those with IHD and healthy individuals. • In populations COPD, who exhibited the lowest baseline levels of cardiac electrophy, NO 2 -FA levels increased compensatorily but declined most markedly after traffic pollution exposure. • Inhaler use in COPD patients was associated with attenuated electrocardiographic changes following traffic pollution exposure. Traffic pollution exposure has been associated with adverse cardiovascular outcomes, but determinants of individual susceptibility remain unclear. To explore whether disease status modifies traffic-related cardiac responses and to examine the cardioprotective role of nitro linoleic acids. In a crossover study, 39 chronic obstructive pulmonary disease (COPD) patients, 38 ischemic heart disease (IHD) patients, and 39 healthy participants walked for two hours on traffic-congested Oxford Street and in traffic-free Hyde Park, in random order, on separate days. Cardiac electrical activity, including heart rate, heart rate variability (HRV), QT interval, and ST-segment changes, was continuously monitored for 24 h. At 24 h following the walk, a urine void was collected and analyzed for nitro linoleic acid NO 2 -cLA (a cardioprotective marker). Mixed-effect models assessed pollution-related cardiac changes. In reference to walking in the park, participants following the street walk exhibited adverse cardiac changes, including increased heart rate, decreased HRV, shortened QT interval, and elevated ST-segment, with larger changes in some parameters observed in COPD participants, though between-group differences were not statistically significant. Among COPD participants, the cardiac effects were more pronounced in those who did not use inhaler medications than in those who used them. NO 2 -cLA concentrations were significantly lower in COPD participants after the street walk compared to after the park walk (0.0189 vs 0.0323 μg/g creatinine, p = 0.03). Increasing NO 2 -cLA concentrations were associated with increased pNN50 and QTc and decreased ST elevation. Among measured pollutants, ultrafine particles and black carbon were most elevated in the street and showed the strongest cardiac effects. Although between-group comparisons were not statistically significant, COPD patients showed numerically larger electrophysiological changes and reductions in NO 2 -cLA levels following short-term exposure to traffic pollution. Use of inhaler medications lessened these effects, suggesting a potential role of medication use in modifying pollution responses.
Meng et al. (Mon,) conducted a rct in Chronic obstructive pulmonary disease (COPD), ischemic heart disease (IHD), and healthy adults (n=116). Walking on a traffic-congested street vs. Walking in a traffic-free park was evaluated on NO2-cLA concentrations in COPD participants (p=0.03). Walking for two hours on a traffic-congested street reduced cardioprotective NO2-cLA levels compared to a park walk in COPD patients (0.0189 vs 0.0323 μg/g creatinine, p=0.03).