Oxidative stress: Its role in air pollution and adverse health effects
Oxidative stress: Its role in air pollution and adverse health effects
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DOI：
10.1136/oem.60.8.612
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发表时间：
2003-08-01
影响因子：
4.9
通讯作者：
Kelly, FJ
中科院分区：
文献类型：
--
作者：
Kelly, FJ
人们越来越关注空气污染对人类健康的不利影响。流行病学研究表明，心血管发病率、肺功能下降、住院率和死亡率增加与空气中光化学和颗粒污染物浓度之间存在明显关联。人体暴露室对特定污染物的研究表明，在一小部分（10-20%）健康个体中，短期暴露可导致正常人体气道出现急性炎症效应。长期暴露于空气污染的后果更难以获得，但普遍认为要严重得多。对儿童和成人的研究表明，接触二氧化氮和二氧化硫等微粒与支气管炎症状有关。此外，接触微粒与儿童肺功能发育减慢有关，如果家庭搬迁到微粒浓度较低的地区，这种情况会逆转。与任何有毒挑战一样，显而易见的解决方案是消除或至少将问题的根源降低到可接受的水平。近年来，许多国家的空气污染水平有所下降，另有几个国家采取了进一步降低浓度的措施。然而，即使在中期，这些实际措施也不太可能完全消除这个问题。因此，一段时间以来人们已经认识到，有必要提高我们对空气污染对生物系统影响的理解。例如，更好地了解空气污染引起健康问题的潜在机制，将有助于采取更有针对性的办法，消除空气污染中毒性最大的成分，并可能提供一种手段，降低个人对空气污染的敏感性。由于最近在许多不同国家进行的研究，使用了一系列不同的方法，氧化应激已被确定为引起关注的空气污染物毒性作用的统一特征。氧化应激，要么是由于暴露于氧化剂增加，要么是由于抗氧化防御能力下降，似乎会触发一些氧化还原敏感信号通路。现在有大量证据表明，暴露于污染事件后产生的肺部炎症反应是通过氧化信号通路介导的。此外，一个人对污染的敏感性似乎部分与他们的肺部抗氧化防御有关。什么是氧化应激？
Increasing concern exists over the adverse effects of air pollution on human health. Epidemiological studies have shown a clear association between cardiovascular morbidity, decreased lung function, increased hospital admissions, mortality, and airborne concentrations of photochemical and particulate pollutants. Human exposure chamber studies of specific pollutants have shown that short term exposure leads to an acute inflammatory effect on normal human airways in a small (10–20%) proportion of healthy individuals. The consequences of long term exposure to air pollution are more difficult to access but are generally believed to be much worse. Studies in both children and adults have shown that exposure to particulates, nitrogen dioxide and sulphur dioxide, are associated with symptoms of bronchitis. Moreover, exposure to particulates has been related to reduced lung function growth in children and is reversed if the family relocates to a area with lower particulate concentrations.As with any toxic challenge the obvious solution is to remove, or at least decrease to an acceptable level, the source of trouble. In many countries, air pollution levels have fallen in recent years, while additional measures are in place in several more to decrease concentrations further. It is unlikely however, that these practical measures will completely eliminate the problem, even in the medium term. As a consequence, it has been recognised for some time that there is also a need to improve our understanding of the impact of air pollution on biological systems. For example, a better appreciation of the mechanisms underlying air pollution induced health problems would allow a more targeted approach to remove the most toxic components of air pollution, and could possibly provide a means to decrease individual sensitivity to air pollution. As a consequence of recent research undertaken in a number of different countries, using a range of different approaches, oxidative stress has been identified as a unifying feature underlying the toxic actions of the air pollutants that are causing concern. Oxidative stress, resulting from either increased exposure to oxidants or the presence of decreased antioxidant defences, seems to trigger a number of redox sensitive signalling pathways. There is now a strong body of evidence to indicate that the pulmonary inflammatory response that arises following exposure to a pollution episode, is mediated via oxidant signalling pathways. Moreover, it appears likely that an individual’s sensitivity to pollution is related, in part, to their pulmonary antioxidant defences. c WHAT IS OXIDATIVE STRESS?