Impacts of Traffic-Related and Woodsmoke Air Pollution on Endothelial Function and Systemic Inflammation

Abstract

Background: Evidence links combustion-generated particulate matter (PM) with cardiovascular morbidity. Both traffic-related air pollution (TRAP) and residential wood combustion (RWC) may be important, but few studies have compared their impacts. Aims: We evaluated the effects of HEPA filtration and indoor PM2.5 on reactive hyperemia index (RHI) and inflammation (C-reactive protein [CRP] and IL-6) among individuals residing in Vancouver areas impacted by either TRAP or RWC. We aimed to test HEPA efficacy and to introduce similar PM2.5 exposure contrasts in all homes. Methods: In this randomized, single-blind crossover study we enrolled 83 healthy adults (44 homes), from the general population. Each home was monitored over two consecutive weeks (one with HEPA and one with “placebo” filtration). RHI was measured after each week and blood samples were collected at baseline and after each week. Effects were estimated from mixed models with PM2.5 effects reported per median within-home contrast (2.4 µg/m3). Results: This analysis included 51 participants with complete PM2.5, RHI, and blood measurements. Participants in TRAP- (N=34) and RWC-impacted areas (N=17) had similar BMI, baseline CRP, time spent at home, and PM2.5 levels, but TRAP-exposed participants were younger. HEPA filters reduced average indoor PM2.5 levels by 39%, and 92% of homes had reductions, but in intent to treat analysis filtration was not associated with changes in cardiovascular outcomes. PM2.5 was not associated with CRP in the full population; however, PM2.5 reductions were associated with lower CRP among TRAP-impacted (19.2% decrease, 95% CI: 3.2%–37.4%) but not RWC-impacted (11.6% increase, -37.3%–23.5%) participants. There were no associations with RHI or IL-6. Conclusions: Indoor PM2.5 reductions were associated with decreases in CRP, a marker of systemic inflammation, only among those in areas impacted by TRAP. This supports the hypothesis that traffic-related PM2.5 has greater inflammatory effects than other combustion PM.