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.
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.