Pulmonary effects of inhaled ultrafine particles
Pulmonary effects of inhaled ultrafine particles
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DOI：
10.1007/s004200000185
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发表时间：
2000-11
影响因子：
3
通讯作者：
G. Oberdörster
中科院分区：
文献类型：
--
作者：
G. Oberdörster
介绍和目标：最近的流行病学研究表明，城市空气颗粒污染的增加与对人口中易受影响的部分，特别是对先前患有呼吸道和心血管疾病的老年人的不利健康影响之间存在联系。城市颗粒物由三种模态组成：超细颗粒物、堆积模态颗粒物（它们共同构成细颗粒物模态）和粗模态颗粒物。超细颗粒物（直径小于0.1 μm的颗粒物）对总质量的贡献很小，但数量非常高，在偶发事件中，城市空气中的超细颗粒物可达到数十万/cm 3。假设超细颗粒是因果关系参与不良反应中看到敏感的人是基于几项研究总结在此简要review.Methods和结果：啮齿动物的研究表明，超细颗粒给药到肺部引起更大的炎症反应比大颗粒，每给定的质量。表面性质（表面化学）似乎在超细颗粒毒性中起着重要作用。对超细颗粒的影响有贡献的是当作为单线态超细颗粒而不是作为聚集颗粒吸入时它们非常高的尺寸比沉积。超细颗粒物在肺中沉积后，很大程度上逃脱了肺泡巨噬细胞的监视，进入肺内。啮齿动物吸入低剂量含碳超细颗粒物6 h后可引起轻度肺部炎症。啮齿类动物的老年和受损/致敏的呼吸道可显著增加其对超细颗粒物的炎症效应的易感性，并且与年轻生物体相比，老年生物体似乎处于由这些颗粒物引起的氧化应激诱导的肺损伤的更高风险中。结果还表明，超细颗粒的影响，可以显着增强的气态共污染物，如O3.Conclusions：迄今为止进行的研究支持超细颗粒的假设。有必要进行更多的研究来评估反应的机制途径。
Introduction and Objectives: Recent epidemiological studies have shown an association between increased particulate urban air pollution and adverse health effects on susceptible parts of the population, in particular the elderly with pre-existing respiratory and cardiovascular diseases. Urban particles consist of three modes: ultrafine particles, accumulation mode particles (which together form the fine particle mode) and coarse mode particles. Ultrafine particles (those of <0.1 μm diameter) contribute very little to the overall mass, but are very high in number, which in episodic events can reach several hundred thousand/cm3in the urban air. The hypothesis that ultrafine particles are causally involved in adverse responses seen in sensitive humans is based on several studies summarized in this brief review.Methods and Results: Studies on rodents demonstrate that ultrafine particles administered to the lung cause a greater inflammatory response than do larger particles, per given mass. Surface properties (surface chemistry) appear to play an important role in ultrafine particle toxicity. Contributing to the effects of ultrafine particles is their very high size-specific deposition when inhaled as singlet ultrafine particles rather than as aggregated particles. It appears also that ultrafine particles, after deposition in the lung, largely escape alveolar macrophage surveillance and gain access to the pulmonary interstitium. Inhaled low doses of carbonaceous ultrafine particles can cause mild pulmonary inflammation in rodents after exposure for 6 h. Old age and a compromised/sensitized respiratory tract in rodents can increase their susceptibility to the inflammatory effects of ultrafine particles significantly, and it appears that the aged organism is at a higher risk of oxidative stress induced lung injury from these particles, compared with the young organism. Results also show that ultrafine particle effects can be significantly enhanced by a gaseous co-pollutant such as ozone.Conclusions: The studies performed so far support the ultrafine particle hypothesis. Additional studies are necessary to evaluate mechanistic pathways of responses.