2015
DOI: 10.1186/s12989-016-0139-3
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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.M… Show more

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Cited by 48 publications
(38 citation statements)
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“…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 .…”
Section: Discussionmentioning
confidence: 54%
“…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 .…”
Section: Discussionmentioning
confidence: 54%
“…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.…”
Section: Methodsmentioning
confidence: 99%
“…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].…”
Section: Pathophysiological Evidencementioning
confidence: 99%