Author, year and country | Design | Study population | Air pollutant | Exposure | Outcome | Results | Main findings |
---|---|---|---|---|---|---|---|
Maiseyeu et al. 2014, United States [29] | Randomized double-blinded crossover study | Country: United States Age: 18–50 y (25.9 ± 6.6 y) Non-smoking adults without established CV disease or traditional CV risk factors n = 32 (16 female subjects) | PM10–2.5 | Coarse concentrated ambient particles (CAP) [76,2 ± 51,5 μg/m3] in a rural location and filtered air (FA) for 2 h. | HDL mediated cholesterol efflux capacity (CEC) HDL antioxidant capacity (measured as HDL oxidation index (HOI)) Paraoxonase (PON) activity | There were no significant differences detected in CEC metrics to HDL from subjects exposed 2 h or 20 h following CAP versus FA exposures. HOI and PON activity did not differ 20-h post-CAP versus FA, respectively. | Brief inhalation of high levels of coarse PM did not acutely impair several facets of HDL functionality (CEC, HOI, PON activity). |
Ramanathan et al. 2016, United States [30] | Randomized blinded crossover study | Country: Canada Age: 18–50 y (28 ± 9 y) Non-smoking adults without any risk for CV disease n = 30 (17 female subjects) | PM2.5 | PM2.5 targeted at 150 μg/m3for 2 h on 4 different occasions at least two weeks apart. | HDL antioxidant/ anti-inflammatory capacity measured as HDL oxidation index (HOI)) Paraoxonase (PON) activity | There was a trend towards bigger ΔHOI between PM2.5 and FA 1 h after exposures (p = 0.18) but not 20 h after. This trend became significant (p < 0.05) when baseline HOI was lower (< 1.5 or < 2.0), indicating decreased HDL antioxidant/anti-inflammatory capacity shortly after the exposures. No significant differences in the enzymatic activity of PON-1 was observed. | Exposure to concentrated PM2.5 induced swift effects on HDL anti-oxidative/anti-inflammatory capacity. Changes were, however, transient and of short duration. |