Department of Environmental Health, National Institute for Health and Welfare, Kuopio, Finland.
Environ Res. 2012 Jul;116:44-51. doi: 10.1016/j.envres.2012.04.004. Epub 2012 Apr 26.
Short-term exposure to ambient air pollution is associated with increased cardiovascular mortality and morbidity. This adverse health effect is suggested to be mediated by inflammatory processes. The purpose of this study was to determine if low levels of particulate matter, typical for smaller cities, are associated with acute systemic inflammation. Fifty-two elderly individuals with ischemic heart disease were followed for six months with biweekly clinical visits in the city of Kotka, Finland. Blood samples were collected for the determination of inflammatory markers interleukin (IL)-1β, IL-6, IL-8, IL-12, interferon (IFN)γ, C-reactive protein (CRP), fibrinogen, myeloperoxidase and white blood cell count. Particle number concentration and fine particle (particles with aerodynamic diameters <2.5 μm (PM(2.5))) as well as thoracic particle (particles with aerodynamic diameters <10 μm (PM(10))) mass concentration were measured daily at a fixed outdoor measurement site. Light-absorbance of PM(2.5) filter samples, an indicator of combustion derived particles, was measured with a smoke-stain reflectometer. In addition, personal exposure to PM(2.5) was measured with portable photometers. During the study period, wildfires in Eastern Europe led to a 12-day air pollution episode, which was excluded from the main analyses. Average ambient PM(2.5) concentration was 8.7 μg/m(3). Of the studied pollutants, PM(2.5) and absorbance were most strongly associated with increased levels of inflammatory markers; most notably with C-reactive protein and IL-12 within a few days of exposure. There was also some evidence of an effect of particulate air pollution on fibrinogen and myeloperoxidase. The concentration of IL-12 was considerably (227%) higher during than before the forest fire episode. These findings show that even low levels of particulate air pollution from urban sources are associated with acute systemic inflammation. Also particles from wildfires may exhibit pro-inflammatory effects.
短期暴露于环境空气中的污染物与心血管疾病死亡率和发病率增加有关。这种不良健康影响被认为是通过炎症过程介导的。本研究旨在确定较小城市中典型的低水平颗粒物是否与急性全身炎症有关。52 名患有缺血性心脏病的老年人在芬兰科特卡市接受了为期六个月的随访，每两周进行一次临床访视。采集血样以测定炎症标志物白细胞介素（IL）-1β、IL-6、IL-8、IL-12、干扰素（IFN）γ、C 反应蛋白（CRP）、纤维蛋白原、髓过氧化物酶和白细胞计数。每天在一个固定的户外测量点测量颗粒物数浓度和细颗粒物（空气动力学直径<2.5μm 的颗粒物（PM（2.5））以及胸颗粒物（空气动力学直径<10μm 的颗粒物（PM（10））质量浓度。使用烟雾反射计测量 PM（2.5）过滤器样品的光吸收，这是燃烧衍生颗粒的指标。此外，还使用便携式光度计测量个人 PM（2.5）暴露情况。在研究期间，东欧的野火导致了为期 12 天的空气污染事件，该事件被排除在主要分析之外。平均环境 PM（2.5）浓度为 8.7μg/m（3）。在所研究的污染物中，PM（2.5）和吸光度与炎症标志物水平升高最密切相关；尤其是在接触污染物后的几天内，与 CRP 和 IL-12 相关性最强。也有一些证据表明，颗粒物空气污染对纤维蛋白原和髓过氧化物酶也有影响。在森林火灾事件期间，IL-12 的浓度高出了约 227%。这些发现表明，即使是来自城市污染源的低水平颗粒物空气污染也与急性全身炎症有关。此外，野火产生的颗粒也可能具有促炎作用。
