职业性哮喘的推论。

P Cullinan, A J Newman Taylor
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引用次数: 6

摘要

职业性哮喘——由工作时吸入的某种物质引起的哮喘——为检查引起哮喘的更一般的环境原因提供了一个有效的模型。在许多情况下,在工作场所暴露于浓度相对容易测量的新型过敏原的可定义人群发展为与ige相关的哮喘和特征性嗜酸性支气管炎。精心设计的流行病学研究表明,IgE抗体和哮喘的发病率在接触的头一至两年最高;这种风险与空气中接触过敏原的强度直接相关。暴露与结果之间的关系被同时吸烟和基因型所改变,尽管后者相互作用的细节尚不清楚。症状、气道高反应性和气道炎症可在避免接触起始剂后持续数年。如果模型的相关性被接受,那么这些见解需要在职业性哮喘领域以及在一般环境中更广泛的哮喘领域进行测试和进一步调查。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inferences from occupational asthma.

Occupational asthma-asthma induced by an agent inhaled at work-provides a valid model for the examination of the more general environmental causes of asthma. In many instances, definable populations exposed to a novel allergen in the workplace at concentrations that are relatively easily measured develop IgE-associated asthma and characteristic eosinophilic bronchitis. Carefully designed epidemiological studies suggest that the incidence of IgE antibody and asthma is highest in the first one to two years of exposure; and that the risk is directly related to the intensity of airborne allergen exposure. The relationship between exposure and outcome is modified both by concurrent cigarette smoking and by genotype, although the details of this latter interaction remain unclear. Symptoms, airway hyper-responsiveness and airway inflammation may persist for several years after avoidance of exposure to the initiating agent. If the relevance of the model is accepted then these insights require testing and further investigation, both within the field of occupational asthma and, by extension, in the wider field of asthma in the general environment.

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