Menzel D B
Department of Community and Environmental Medicine, University of California, Irvine 92717-1825.
Ann N Y Acad Sci. 1992 Sep 30;669:141-55. doi: 10.1111/j.1749-6632.1992.tb17095.x.
Although the evidence for oxidative stress for air pollution in the human lung is fragmentary, the hypothesis that oxidative stress is an important, if not the sole, mechanism of toxicity of oxidizing air pollutants and tobacco smoke is compelling and growing. First, biochemical mechanisms have been worked out for oxidation of lung lipids by the gas phase of cigarette smoke, NO2 and O3. The oxidation of lung lipids can be prevented by both vitamins C and E. Vitamin C is more effective in preventing oxidation by NO2, and vitamin E is more effective against O3. Second, multiple species of experimental animals develop lung disease similar to human bronchitis and emphysema from exposure to NO2 and O3, respectively. The development of these diseases occurs over a near lifetime exposure when the levels of NO2 or O3 are at near ambient air pollution values. Third, isolated human cells are protected against oxidative damage from NO2 and O3 by both vitamins C and E. Fourth, the vitamin C level in the lung either declines on exposure to NO2 for short-term exposures or increases on chronic cigarette smoke exposure. The effects of cigarette smoking on serum vitamin C is apparently complex and may be related to the daily intake of vitamin C as well as smoking. Serum vitamin C levels may be poor indicators of lung demands when daily vitamin C intakes are above 100 mg/day. Fifth, vitamin C supplementation protects against the effects of ambient levels of air pollution in adults as measured by histamine challenge. An augmented response to histamine challenge may represent increased lung permeability brought about by air pollution. In experimental animal and human experiments, the amount of vitamin C or E that afforded protection was in excess of the current recommended dietary allowance. Although animal studies do not provide evidence for complete protection against NO2 or O3, they do illustrate that current recommended daily allowances are inadequate for maximum protection against air pollution levels to which over 100 million Americans are exposed. The problem of air pollution and its effects on humans is truly of global concern. Air pollution is not restricted to North America or Japan where it was first recognized, but is a major public health problem in Europe as well. When data are available, air pollution probably will be shown to be a major public health problem in all urban areas of the world.(ABSTRACT TRUNCATED AT 400 WORDS)
尽管有关空气污染在人类肺部引发氧化应激的证据尚不完整，但氧化应激即便不是氧化性空气污染物和烟草烟雾毒性的唯一重要机制，也是重要机制之一，这一假说令人信服且越来越有影响力。首先，已经明确了香烟烟雾、二氧化氮和臭氧气相氧化肺脂质的生化机制。维生素C和维生素E都能防止肺脂质氧化。维生素C在防止二氧化氮氧化方面更有效，而维生素E对臭氧的防护效果更佳。其次，多种实验动物分别因接触二氧化氮和臭氧而患上类似于人类支气管炎和肺气肿的肺部疾病。当二氧化氮或臭氧的浓度接近环境空气污染值时，在接近终生接触的情况下会引发这些疾病。第三，维生素C和维生素E都能保护分离出的人体细胞免受二氧化氮和臭氧的氧化损伤。第四，短期接触二氧化氮会使肺部的维生素C水平下降，而长期接触香烟烟雾则会使其升高。吸烟对血清维生素C的影响显然很复杂，可能与维生素C的每日摄入量以及吸烟有关。当每日维生素C摄入量超过100毫克/天时，血清维生素C水平可能无法很好地反映肺部的需求。第五，补充维生素C可保护成年人免受环境空气污染的影响，这一点通过组胺激发试验得到了验证。对组胺激发试验反应增强可能表明空气污染导致肺通透性增加。在实验动物和人体实验中，起到保护作用的维生素C或E的量超过了目前推荐的膳食摄入量。尽管动物研究并未提供完全抵御二氧化氮或臭氧的证据，但它们确实表明，目前推荐的每日摄入量不足以最大程度地保护超过1亿美国人所接触的空气污染水平。空气污染及其对人类的影响问题确实是全球关注的问题。空气污染并不局限于最早认识到这一问题的北美或日本，在欧洲它也是一个重大的公共卫生问题。一旦有相关数据，空气污染可能会被证明是世界所有城市地区的一个重大公共卫生问题。（摘要截选至400字）
