Effects of urban fine particulate matter and ozone on HDL functionality

Abstract

Background: Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM2.5 (<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 PM2.5 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 PM2.5 targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM2.5 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 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 anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM2.5 on the change in HOI at both time points. The change in HOI due to PM2.5 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 PM2.5 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.

Keywords: Air pollution; Cardiovascular; Fine particulate matter; HDL function; HDL oxidant index (HOI); High density lipoprotein (HDL); Ozone.

Fig. 1

Particle chemical composition of (a) PM_2.5 and (b) PM_2.5 + Ozone exposures. Both PM_2.5 and PM_2.5 + Ozone exposure aerosols had similar particle chemical composition, which was performed as described in Methods

Fig. 2

Effect of PM_2.5 exposure on HDL antioxidant and anti-inflammatory function. a Change in HOI from before and 1 h after exposures. b Change in HOI from before and 20 h after exposures. c and d HOI from before and 1 h after exposures are shown in a subset where average pre HOI is <1.5 (c) and <2.0 (d). FA = filtered air

Fig. 3

Association between PM_2.5 mass concentration and ΔHOI. The PM_2.5 mass concentration showed a trend to associate with ΔHOI 1 h after exposure (a) but not 20 h after exposure (b)

Fig. 4

ΔHOI associates with systolic BP slope. Change in HOI 1 h after exposure was significantly associated with the systolic BP change observed during the 2 h exposure (a). ΔHOI after exposure did not correlate with diastolic BP slope (b)