Ramanathan Gajalakshmi, Yin Fen, Speck Mary, Tseng Chi-Hong, Brook Jeffrey R, Silverman Frances, Urch Bruce, Brook Robert D, Araujo Jesus A
Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, 10833 Le Conte Avenue, CHS 43-264, P.O. Box 951679, Los Angeles, CA, 90095, USA.
Division of Occupational and Environmental Health, Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada.
Part Fibre Toxicol. 2016 May 24;13(1):26. doi: 10.1186/s12989-016-0139-3.
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.
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.
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).
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.
暴露于环境颗粒物（PM）会增加发病率和死亡率。已表明，暴露于PM2.5（<2.5μm）和臭氧与人类颈动脉内膜中层厚度有关。动物研究支持空气污染与动脉粥样硬化之间的因果关系，并确定了PM对高密度脂蛋白（HDL）功能的不良影响。我们旨在确定短期暴露于PM2.5和/或臭氧是否会对人类HDL的抗氧化和抗炎能力产生影响。
在一项随机交叉研究中，受试者在4个不同时间点，每次间隔至少两周，分别暴露于细颗粒物浓度为150μg/m³的浓缩环境细颗粒物（CAP）、臭氧浓度为240μg/m³（120ppb）、PM2.5加臭氧浓度相似的环境中以及过滤空气中（FA），持续2小时。在暴露前（基线）、暴露后1小时和暴露后20小时采集血液。测定血浆HDL的抗氧化/抗炎能力和对氧磷酶活性。HDL的抗氧化/抗炎能力通过无细胞荧光测定法评估，并以HDL氧化指数（HOI）的单位表示。HOI的变化（ΔHOI）计算为从基线到暴露后1小时或20小时HOI的差值。
暴露后1小时，PM2.5与FA之间的ΔHOI有增大趋势（p = 0.18），但暴露后20小时无此趋势。当基线HOI较低（<1.5或<2.0）时，这种趋势变得显著（p <0.05），表明暴露后不久HDL的抗氧化/抗炎能力下降。在两个时间点，单独臭氧或与PM2.5联合使用对HOI变化均无显著影响。PM2.5导致的HOI变化与颗粒物质量浓度呈正趋势（p = 0.078），并与暴露期间收缩压的斜率显著相关（p = 0.005）。
短期暴露于浓缩的PM2.5会迅速影响HDL的抗氧化/抗炎功能，这可能表明颗粒物空气污染诱发有害心血管效应的潜在机制。
Zotero 插件