Gilliland F D, McConnell R, Peters J, Gong H
Department of Preventive Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA.
Environ Health Perspect. 1999 Jun;107 Suppl 3(Suppl 3):403-7. doi: 10.1289/ehp.99107s3403.
Acute respiratory health effects in children from exposure at current ambient levels of ozone are well documented; however, evidence for acute effects from other criteria pollutants such as nitrogen dioxide and respirable particles is inconsistent. Whether chronic effects result from long-term exposure to any of these pollutants during childhood is an important unresolved question. Establishing whether acute or chronic effects result from childhood exposure and identifying sensitive subgroups may require integration of biologic mechanisms of lung defenses, injury, and response into the study design and statistical models used in analyses. This review explores the theoretical basis for explaining such adverse effects in light of our contemporary understanding of mechanisms of lung injury and response at the cellular and molecular levels. The rapidly evolving understanding of the effects of air pollution on cellular and molecular levels presents an opportunity to develop and refine innovative biologically based hypotheses about the effects of childhood exposure. We hypothesize that children with low fruit and vegetable intake, low antioxidant levels, high polyunsaturated fat intake, or who have inherited certain alleles for genes involved in lung defenses and immune response regulation may be at increased risk for adverse effects. Because responses to air pollutants of interest are complex and involve a number of pathophysiologic processes, the magnitude of main effects of dietary factors, genes, and gene-environment interactions may be modest for individuals; however, each may make an important contribution to the population burden of preventable respiratory diseases.
儿童在当前环境臭氧水平下暴露所产生的急性呼吸道健康影响已有充分记录；然而，关于二氧化氮和可吸入颗粒物等其他标准污染物的急性影响的证据并不一致。儿童期长期接触这些污染物中的任何一种是否会导致慢性影响，是一个重要的未解决问题。确定儿童暴露是否会导致急性或慢性影响，并识别敏感亚组，可能需要将肺部防御、损伤和反应的生物学机制纳入研究设计和分析中使用的统计模型。本综述根据我们目前对细胞和分子水平上的肺损伤和反应机制的理解，探讨了解释此类不良反应的理论基础。对空气污染在细胞和分子水平上的影响的快速发展的理解，为开发和完善关于儿童暴露影响的基于生物学的创新假设提供了机会。我们假设，水果和蔬菜摄入量低、抗氧化剂水平低、多不饱和脂肪摄入量高，或遗传了参与肺部防御和免疫反应调节的某些基因等位基因的儿童，可能面临更大的不良反应风险。由于对感兴趣的空气污染物的反应很复杂，涉及许多病理生理过程，饮食因素、基因和基因-环境相互作用的主要影响程度对个体来说可能不大；然而，每一项都可能对可预防的呼吸道疾病的人群负担做出重要贡献。
