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环境烟草烟雾、室内过敏原与儿童哮喘。

Environmental tobacco smoke, indoor allergens, and childhood asthma.

作者信息

Gold D R

机构信息

Channing Laboratory, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

出版信息

Environ Health Perspect. 2000 Aug;108 Suppl 4(Suppl 4):643-51. doi: 10.1289/ehp.00108s4643.

Abstract

Both environmental tobacco smoke and indoor allergens can exacerbate already established childhood albeit primarily through quite disparate mechanisms. In infancy and childhood, environmental tobacco smoke (ETS) exposure is associated with measures of decreased flow in the airways, bronchial hyperresponsiveness, and increased respiratory infections, but the relationship between ETS and allergy is poorly understood. Indoor allergens from dust mite, cockroach, and cat can be associated with asthma exacerbation in children sensitized to the specific allergens. The precise role of either ETS or indoor allergens in the development of asthma is less well understood. The strong and consistent association between ETS and asthma development in young children may relate to both prenatal and postnatal influences on airway caliber or bronchial responsiveness. Dust mite allergen levels predict asthma in children sensitized to dust mite. The tendency to develop specific IgE antibodies to allergens (sensitization) is associated with and may be preceded by the development of a T-helper (Th)2 profile of cytokine release. The importance of either ETS or indoor allergens in the differentiation of T cells into a Th2-type profile of cytokine release or in the localization of immediate-type allergic responses to the lung is unknown. This article evaluates the strength of the evidence that ETS or indoor allergens influence asthma exacerbation and asthma development in children. We also selectively review data for the effectiveness of allergen reduction in reducing asthma symptoms and present a potential research agenda regarding these two broad areas of environmental exposure and their relationship to childhood asthma.

摘要

环境烟草烟雾和室内过敏原都可使已有的儿童疾病恶化,尽管其主要作用机制截然不同。在婴儿期和儿童期,接触环境烟草烟雾(ETS)与气道气流减少、支气管高反应性及呼吸道感染增加有关,但ETS与过敏之间的关系尚不清楚。来自尘螨、蟑螂和猫的室内过敏原可使对特定过敏原致敏的儿童哮喘加重。ETS或室内过敏原在哮喘发病中的具体作用尚不太明确。幼儿中ETS与哮喘发病之间强烈且持续的关联可能与产前和产后对气道管径或支气管反应性的影响有关。尘螨过敏原水平可预测对尘螨致敏儿童的哮喘发病情况。对过敏原产生特异性IgE抗体(致敏)的倾向与细胞因子释放的辅助性T细胞(Th)2型谱的形成有关,且可能先于此过程。ETS或室内过敏原在T细胞分化为细胞因子释放的Th2型谱或速发型过敏反应在肺部定位中的重要性尚不清楚。本文评估了ETS或室内过敏原影响儿童哮喘加重和哮喘发病的证据强度。我们还选择性地回顾了减少过敏原对减轻哮喘症状有效性的数据,并提出了一个关于这两个广泛的环境暴露领域及其与儿童哮喘关系的潜在研究议程。

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