Effects of urban fine particulate matter and ozone on HDL functionality

Abstract

BackgroundExposures 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.MethodsSubjects were exposed to fine concentrated ambient fine particles (CAP) with PM2.5 targeted at 150 μg/m3, ozone targeted at 240 μg/m3 (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.ResultsThere 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).ConclusionsBrief 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0139-3) contains supplementary material, which is available to authorized users.

Effect of Ambient Fine Particulate Matter Air Pollution and Colder Outdoor Temperatures on High-Density Lipoprotein Function

“…Animals exposed to high PM levels developed a blunted HDL anti-oxidant capacity 16,17 . In our prior study, acute exposure to concentrated PM 2.5 prompted a similar response in a subset of adults 18 . As far as we are aware, the lack of impact on CEC following a 2-hour exposure to coarse PM is the only previous study to evaluate the effect of any air pollutant on this endpoint 19 .…”

Increased Cardiac Sympathetic Activity and Oxidative Stress in Habitual Electronic Cigarette Users

“…Blood was drawn into preiced heparinized vacutainers and placed on ice. Blood was centrifuged to separate into plasma samples, which were frozen at −80°C in a cryopreservative solution 20 for later analysis for the following antioxidant parameters: (1) LDL oxidizability, indicative of susceptibility of apolipoprotein B–containing lipoproteins to oxidation as previously reported, 21 (2) high-density lipoprotein (HDL) antioxidant/anti-inflammatory capacity, expressed as an HDL antioxidant index, which assesses the ability of HDL to inhibit LDL oxidation monitored by conversion of a nonfluorescent dihydrodichlorofluorescein probe into the fluorescent dichlorofluorescein, performed as previously reported, 22,23 and (3) paraoxonase-1 activity, a protective ester hydrolase enzyme associated with HDL in blood that prevents the formation of oxidized LDL, 24 assayed by its ability to hydrolyze paraoxonsubstrate, 23 described in detail in the eMethods in the Supplement.…”

Cardiovascular effects of air pollution

“…Activation of endothelial cells following air pollution exposure is characterized by the release of proinflammatory adhesion molecules, such as vascular cell adhesion molecule-1 and monocyte chemotactic protein-1, which ensure monocyte recruitment and their differentiation into macrophages in the subendothelial space [2,49]. Furthermore, air pollution is associated with impairment of antiatherogenic molecules, such as high-density lipoprotein [53]. A reduced high-density lipoprotein antioxidant capacity was also found in an animal study, with ultra-fine particles having a larger effect compared with PM 2.5 [49].…”