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肥胖与哮喘在低收入、城市、少数族裔人群中的关联。

Associations between obesity and asthma in a low-income, urban, minority population.

机构信息

Division of Environmental and Occupational Health Sciences, University of Illinois at Chicago School of Public Health, Chicago, IL 60612, USA.

出版信息

Ann Allergy Asthma Immunol. 2013 May;110(5):340-6. doi: 10.1016/j.anai.2013.02.001. Epub 2013 Feb 28.

Abstract

BACKGROUND

Community-based studies of obesity, asthma, biomarkers of oxidative stress, and adipokines among low-income, urban, minority populations are lacking. Oxidative stress, perhaps modulated by adipokines, may increase airway inflammation in obese individuals.

OBJECTIVES

To characterize associations between obesity and asthma in a low-income, urban, minority community and evaluate adipokines, biomarkers of inflammation, and oxidant-antioxidant balance in association with asthma and obesity.

METHODS

A door-to-door evaluation of asthma and obesity prevalence was performed in a low-income housing development. Nonsmoking adults and children underwent additional evaluation, including allergy skin testing, and measures of serum adipokines, and indicators of oxidative stress in blood and exhaled breath.

RESULTS

The prevalences of current asthma and a body mass index in the 85th percentile or higher were 15.8% and 35.3%, respectively, among 350 nonsmokers older than 4 years. Asthma and obesity were not associated with one another (odds ratio, 1.0; 95% confidence interval, 0.55-1.84). Among 116 nonsmoking participants who underwent biomarker evaluation, obesity was not associated with exhaled nitric oxide. In multivariate logistic models that adjusted for age category, sex, and a body mass index in 85th percentile or higher, leptin concentrations in the highest quartile were associated with asthma (odds ratio, 8.34; 95% confidence interval, 1.29-50.2) but not with atopy. Adiponectin was associated with total antioxidant capacity in exhaled breath.

CONCLUSION

Asthma and obesity, although both common in a low-income, minority community, were not associated with one another. Nevertheless, adipokines were associated with asthma status and with markers of oxidative stress in the lungs, providing some support for an adipokine-inflammatory mechanistic link between the two conditions.

摘要

背景

在低收入、城市、少数族裔人群中,缺乏关于肥胖、哮喘、氧化应激生物标志物和脂肪因子的社区研究。氧化应激可能通过脂肪因子调节,从而增加肥胖个体的气道炎症。

目的

在低收入、城市、少数族裔社区中描述肥胖与哮喘之间的关联,并评估与哮喘和肥胖相关的脂肪因子、炎症标志物和氧化应激平衡的生物标志物。

方法

对一个低收入住房开发区进行了哮喘和肥胖患病率的上门评估。不吸烟的成年人和儿童接受了额外的评估,包括过敏皮肤测试,以及血清脂肪因子和血液及呼气中氧化应激指标的测量。

结果

在 350 名年龄大于 4 岁的不吸烟人群中,当前哮喘和体重指数在第 85 百分位数或更高的患病率分别为 15.8%和 35.3%。哮喘和肥胖之间没有关联(比值比,1.0;95%置信区间,0.55-1.84)。在 116 名接受生物标志物评估的不吸烟参与者中,肥胖与呼气一氧化氮无关。在多变量逻辑回归模型中,根据年龄类别、性别和体重指数在第 85 百分位数或更高进行调整,最高四分位数的瘦素浓度与哮喘相关(比值比,8.34;95%置信区间,1.29-50.2),但与过敏无关。脂联素与呼气中总抗氧化能力相关。

结论

尽管哮喘和肥胖在低收入、少数族裔社区中都很常见,但它们之间没有关联。然而,脂肪因子与哮喘状态和肺部氧化应激标志物相关,为这两种情况之间的脂肪因子-炎症机制联系提供了一些支持。

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