Results

The characteristics of the study population are given in table 1. The three ethnic groups that made up most of the study sample (non-Hispanic whites, non-Hispanic blacks, and Mexican Americans) were represented in similar proportions. Approximately half of all subjects were atopic, while 9% had had asthma at some time. Mean BMI was 18.5 kg/m² (range 7.3–37.2; 1st quartile 7.3–15.4; 2nd quartile 15.5–17.1; 3rd quartile 17.2–20.4; 4th quartile 20.5–37.2). The prevalence of asthma, wheeze in the past 12 months, hay fever, and atopy rose significantly with increasing BMI (table 2).

Having been breastfed was found to be inversely related to BMI as reported previously.11 After adjustment for potential confounding factors such as age, sex, ethnicity, household size, and exposure to passive smoke, a significant positive association between BMI and the asthma outcomes remained (table 3). Additional controlling for birth weight (which was assessed only in children <12 years of age) or breast feeding status (which was assessed only in children <6 years of age) did not change the results (data not shown). With stratification for ethnicity and sex, no effect modification for the relation between BMI and asthma was seen (data not shown). When other measures such as waist circumference, arm circumference, and thigh skinfold were used as indicators of obesity, similar results were obtained (data not shown).

Atopic sensitisation, as assessed by skin prick tests, was only weakly and non-significantly positively related to BMI after adjustment for confounding. With further controlling for birth weight the association disappeared (data not shown). Moreover, in non-asthmatic children, BMI was not related to hay fever and atopy (data not shown). Finally, no significant association of BMI with serum eosinophil counts was seen (table 3). When the association between asthma and BMI was further adjusted for atopy, the effect of BMI remained virtually unchanged (data not shown). No interaction between atopy and BMI was found.

No relation between BMI and the number of episodes of wheeze in the past 12 months was found (table 3). However, the number of emergency room visits because of asthma was positively related to BMI. Among asthmatics only, BMI was inversely associated with the number of episodes of wheeze but not with the number of emergency room visits because of wheeze (data not shown). Time spent watching TV was not related to asthma (β=0.03, p=0.4) or atopy (β=–0.03, p=0.1), and the frequency of exercising per week was also not associated with asthma (data not shown).

Discussion

A high BMI was associated with an increasing prevalence of asthma in a representative sample of the US population aged 4–17 years after controlling for potential confounding factors such as sex, ethnicity, age, household size, passive smoke exposure, birth weight, and breast feeding status. No effect modification by sex or ethnic group was seen. In contrast, atopy was not related to BMI. The lack of correlation with television viewing hours or frequency of physical exercise suggests that it is obesity per se, and not lack of exercise, that is the issue.

The cross sectional design of this study does not allow an assessment of the timing of exposure in relation to the occurrence of asthma or atopy. Thus, the relation between BMI and asthma may reflect the predisposition of an asthmatic subject to gain weight because of reduced exercise tolerance rather than a causal association between a high BMI and the inception of asthma. However, no association between the number of episodes of wheezing in the past 12 months and BMI was found. In addition, longitudinal data for adults suggest that increases in BMI predict the development of asthma in nurses16 and in children.17 It therefore seems highly unlikely that asthma leads to obesity.

Increasing BMI was related to several measures of asthma, but not to atopy assessed as skin test reactivity. A lack of association between eosinophil counts and BMI suggests that the effects of increased BMI may be mediated through factors other than the induction of allergic eosinophilic inflammation of the airway epithelium. An increasing body of literature suggests that obesity is a proinflammatory state.18 Studies in animal models indicate that increased levels of leptin, IL-6, and IL-1 (all proinflammatory cytokines) may contribute to and upregulate inflammation in the airway, independent of an allergic mechanism.18 Studies of prior National Health and Nutrition Examination surveys showed that individuals with a high BMI have increased peripheral blood leucocyte counts which also may reflect an upregulation of inflammatory processes.

Mechanical properties of the respiratory system associated with obesity, such as diminished tidal lung expansion in overweight individuals, may partially account for these results. Reduced tidal lung expansion compromises force fluctuations acting on the airways. Impaired force fluctuations result in greater contractile responses of airway smooth muscle,19 thereby potentially causing increased airway responsiveness, a hallmark of asthma. Although airway responsiveness was not assessed in NHANES III, a previous study of Taiwanese adolescents6 clearly showed a positive effect of BMI, not only on the prevalence of asthma, but also on the presence of airway responsiveness as assessed by methacholine challenge. In the Normative Aging Study20 physiological studies suggesting that increases in obesity are associated with increases in methacholine airway responsiveness in adults are consistent with the mechanical impact of obesity on airway smooth muscle.

A strong association between asthma and atopy has been found in clinical studies where over 80% of asthmatic children react to one or more environmental allergens in skin prick tests.2 On a population level, however, the relation between asthma and atopic sensitisation is much less clear. In some regions of the world, such as rural China and rural Ethiopia, the prevalence of asthma is low and is unrelated to the prevalence of atopy, whereas in westernised areas the prevalence of asthma is higher and closely linked to a high prevalence of atopy.21 This discrepancy points to the importance of distinct factors in determining the incidence of asthma and atopy.

We showed in a German survey11 that prolonged breast feeding is a protective factor against childhood overweight and obesity. These data have been reproduced in this study which shows an increased risk of obesity in children not breastfed for at least 5 months. Recent studies have suggested a protective role of breast feeding against asthma.14 ,22 If prolonged breast feeding resulted in less obesity, then increased BMI might be an intermediate step in a causal pathway leading from shortened nursing to the development of asthma. However, the results of multivariate analyses including breast feeding do not support this notion. Breast feeding was no longer a significant predictor of asthma once BMI was introduced into the model. However, this may be because the intermediate variable (BMI) was included in the regression.

BMI may therefore be an independent risk factor for the development of asthma in both sexes and across ethnic groups. Appropriate strategies for the reduction of body weight in children may contribute to a reduced incidence of asthma in childhood.