Effects of urban fine particulate matter and ozone on HDL functionality

BACKGROUND: Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM(2.5) (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM(2.5) and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans. METHODS: Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM(2.5) targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM(2.5) plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures. RESULTS: There was a trend towards bigger ΔHOI between PM(2.5) 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 anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM(2.5) on the change in HOI at both time points. The change in HOI due to PM(2.5) showed a positive trend with particle mass concentration (p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures (p = 0.005). CONCLUSIONS: Brief exposures to concentrated PM(2.5) elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12989-016-0139-3) contains supplementary material, which is available to authorized users.