Environmental tobacco smoke, parental atopy, and childhood asthma
Environmental tobacco smoke, parental atopy, and childhood asthma
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DOI：
10.2307/3455031
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发表时间：
2001-06-01
影响因子：
10.4
通讯作者：
Magnus, P
中科院分区：
文献类型：
--
作者：
Jaakkola, JJK;Nafstad, P;Magnus, P
我们假设哮喘的一般倾向和暴露于环境烟草烟雾对儿童哮喘风险的联合作用大于基于其独立作用的预期。我们对出生于挪威奥斯陆的2,531名儿童进行了一项基于人群的4年队列研究。我们收集了儿童出生时以及6个月、12个月、18个月、24个月和4岁时的健康和环境暴露信息。关注的结果是前2年的支气管阻塞和4岁时的哮喘。父母特应性定义为母亲或父亲哮喘或花粉热病史。暴露于环境烟草烟雾的定义的基础上，家庭吸烟者在出生时的问卷信息。在调整混杂因素的logistic回归分析中，父母特应性单独增加了支气管阻塞[比值比1.62; 95%置信区间（CI）1.10-2.40]和哮喘（1.61; 95% CI，1.08-2.54）的风险。在父母没有过敏反应的儿童中，暴露于环境烟草烟雾对支气管阻塞（1.29; 95%CI，0.88-1.89）和哮喘（0.84; 95%CI，0.53-1.34）的影响很小。父母存在特应性和暴露对支气管阻塞（2.88; 95%CI，1.91-4.32）和哮喘（2.68; 95%CI，1.70-4.22）均有显著影响。研究结果与假设的父母特应性和暴露于环境烟草烟雾的联合作用一致。这一现象被称为遗传结构对环境暴露的效应修饰，或基因与环境的相互作用，表明某些遗传标记可能指示对环境因素的易感性。
We hypothesized that the joint effect of generic propensity to asthma and exposure to environmental tobacco smoke on the risk of childhood asthma is greater than expected on the basis of their independent effects. We performed a population-based 4-year cohort study of 2,531 children born in Oslo, Norway. We collected information on the child's health and environmental exposures at birth and when the child was 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma at the age of 4 years. Parental atopy was defined as a history of maternal or paternal asthma or hay fever. Exposure to environmental tobacco smoke was defined on the basis of questionnaire information on household smokers at birth. In logistic regression analysis adjusting for confounding, parental atopy alone increased the risk of bronchial obstruction [odds ratio 1.62; 95% confidence interval (CI) 1.10-2.40] and asthma (1.61; 95% CI, 1.08-2.54). In children without parental atopy, there was little effect of exposure to environmental tobacco smoke on bronchial obstruction (1.29; 95% CI, 0.88-1.89) and asthma (0.84; 95% CI, 0.53-1.34). The presence of parental atopy and exposure had a substantial effect both on bronchial obstruction (2.88; 95% CI, 1.91-4.32) and asthma (2.68; 95% CI, 1.70-4.22). The results are consistent with the hypothesized joint effect of parental atopy and exposure to environmental tobacco smoke. This phenomenon-denoted as effect modification of environmental exposure by genetic constitution, or gene by environment interaction-suggests that some genetic markers could indicate susceptibility to environmental factors.