Donaldson Ken, Stone Vicki
ELEGI Colt Laboratory, Medical School, University of Edinburgh, Scotland.
Ann Ist Super Sanita. 2003;39(3):405-10.
PM10 is a complex mixture of particles and we have focused here on the ultrafine component, i.e. particles with a diameter of less than 100 nm. In PM10 this fraction is mostly composed of combustion-derived, carbon-centred particles with associated hydrocarbons and metals. Progress in understanding the effects of ultrafine particles in the lungs has been achieved largely through the use of surrogate particles such as ultrafine carbon black and titanium dioxide. Using these types of particles, ultrafines have been shown to cause oxidative stress and pro-inflammatory effects in a number of in vivo and in vitro models. The mechanisms of the generation of the oxidative stress is not understood, but appears to be related to the large particle surface area in some way. Modulation of calcium signalling also appears to be involved in the stimulation of cytokine release by macrophages in response to ultrafines. Effects of PM10 are seen on cardiovascular mortality and morbidity, as well as on the lung. Although the role of ultrafine particles in these effects are not well understood there are plausible pathways that remain to be explored.
可吸入颗粒物（PM10）是一种复杂的颗粒混合物，我们在此重点关注其超细成分，即直径小于100纳米的颗粒。在PM10中，这一部分主要由燃烧产生的、以碳为中心的颗粒以及相关的碳氢化合物和金属组成。在理解超细颗粒对肺部影响方面取得的进展，很大程度上是通过使用替代颗粒，如超细炭黑和二氧化钛实现的。使用这类颗粒，已证明超细颗粒在许多体内和体外模型中会引起氧化应激和促炎作用。氧化应激产生的机制尚不清楚，但似乎在某种程度上与颗粒的大表面积有关。钙信号的调节似乎也参与了巨噬细胞对超细颗粒作出反应时细胞因子释放的刺激过程。PM10对心血管疾病的死亡率和发病率以及肺部均有影响。尽管超细颗粒在这些影响中所起的作用尚未完全了解，但仍有一些合理的途径有待探索。
