Peterson B, Saxon A
Hart and Louise Lyon Laboratory, USA.
Ann Allergy Asthma Immunol. 1996 Oct;77(4):263-8; quiz 269-70. doi: 10.1016/S1081-1206(10)63318-2.
Reading this article will enable the readers to recognize and evaluate i e potential relationship between allergic respiratory disease and polyaromatic hydrocarbons as air pollutants from industrial and automotive fuel sources. In this article we review the long-term trends in the prevalence of allergic airway diseases (rhinitis and asthma). We then examine the epidemiologic and other research data relating to the role that hydrocarbon fuel emissions may have had on allergic respiratory disease.
Published literature on the relationship between specific air pollutants and trends in allergic respiratory disease were reviewed. Reports of research on pollutant effects on allergic antibody (IgE) were also studied. In both cases, the Melvyl-Medline database since 1975 was used for literature searches. Older references were identified from the bibliographies of relevant articles and books and with the help of the rare books collection at UCLA's Louis M. Darling Biomedical library.
Examination of the historical record indicates that allergic rhinitis and allergic asthma have significantly increased in prevalence over the past two centuries. Although the reasons for this increase are not fully elucidated, epidemiologic data suggest that certain pollutants such as those produced from the burning of fossil fuels may have played an important role in the prevalence changes. Also important are studies showing that diesel exhaust, a prototypical fossil fuel, is able to enhance in vitro and in vivo IgE production.
Increased levels of the compounds resulting from fossil fuel combustion may be partly responsible for the increased prevalence of allergic respiratory disease. If the nature of these compounds and the mechanisms by which they exacerbate allergic disease can be identified, steps can be taken to reduce the production or the impact of these allergy producing compounds.
阅读本文将使读者能够认识和评估过敏性呼吸道疾病与作为工业和汽车燃料来源的空气污染物多环芳烃之间的潜在关系。在本文中，我们回顾了过敏性气道疾病（鼻炎和哮喘）患病率的长期趋势。然后，我们研究了与碳氢化合物燃料排放可能对过敏性呼吸道疾病产生的作用相关的流行病学及其他研究数据。
对已发表的关于特定空气污染物与过敏性呼吸道疾病趋势之间关系的文献进行了综述。还研究了关于污染物对过敏性抗体（IgE）影响的研究报告。在这两种情况下，均使用自1975年以来的Melvyl-Medline数据库进行文献检索。通过相关文章和书籍的参考文献以及加州大学洛杉矶分校路易斯·M·达林生物医学图书馆的善本书籍收藏，找到了更早期的参考文献。
对历史记录的研究表明，在过去两个世纪中，过敏性鼻炎和过敏性哮喘的患病率显著增加。尽管这种增加的原因尚未完全阐明，但流行病学数据表明，某些污染物，如化石燃料燃烧产生的污染物，可能在患病率变化中起了重要作用。同样重要的是，研究表明，柴油尾气作为典型的化石燃料，能够在体外和体内增强IgE的产生。
化石燃料燃烧产生的化合物水平升高可能部分导致了过敏性呼吸道疾病患病率的增加。如果能够确定这些化合物的性质及其加剧过敏性疾病的机制，就可以采取措施减少这些产生过敏的化合物的产生或影响。
