This current study also showed that childhood obesity in the absence of SDB and asthma and allergy did not result in increased eNO levels. This is an important finding, because it has been suggested that this could be one of the mechanisms linking obesity with asthma. Indeed, asthma is the most common chronic illness in childhood, with its prevalence and severity still increasing in developed countries over the last few decades. The cause of the increase in asthma is probably multifactorial, with allergic sensitization, lifestyle changes, and genetics emerging as important determinants.21 Almost in parallel with this rise in asthma prevalence has been the epidemic increase in the prevalence of childhood obesity. This has led to the hypothesis that obesity could be a risk factor for the development of asthma. Various longitudinal studies14–18 in children and adolescents have shown an association between obesity and asthma, but the mechanisms explaining this association remain unclear.19 It is proposed that the obesity-related systemic inflammatory state leads to increased levels of proinflammatory mediators, which could potentially influence airway smooth muscle.20,21 Leung et al22 studied 92 asthmatic children and 23 control subjects. Although mean eNO and leukotriene B4 levels were higher in asthmatic patients, obesity itself was not associated with any alteration in these markers in asthmatic patients. Furthermore, these inflammatory marker levels did not differ between asthmatic patients in the highest and lowest quartiles of weight-for-height z score.22 Santamaria et al38 also failed to find any association between eNO level and obesity in children with and without asthma. The results of these studies indicate that eNO levels are not different between normal-weight and obese children. These findings do not suggest a role for airway inflammation in obesity, so that factors other than airway inflammation are likely responsible for the development of asthma in obese subjects. One could hypothesize that obstructive SDB could contribute to the link between childhood obesity and asthma. It has indeed been proposed39 that there is also a significant overlap between SDB and asthma, as airway obstruction, inflammation, and obesity are implicated in the development of both diseases. Our findings indicate that overweight subjects with habitual snoring have lower values of FEV1, FEV1/VC ratio, and MEF50 compared to their peers with normal sleep study findings. Unfortunately, our present study was underpowered to demonstrate a similar difference between the OSAS group and the group with normal sleep study findings (differences for FEV1 and MEF50 between both groups resulted in p = 0.1). Zerah-Lancner et al40 found similar evidence in obese adults with OSAS, adjusting for adiposity. Although there have been studies41,42 evaluating both lung function and SDB in obese children and adolescents, they did not report an association between obstructive SDB and smaller airway obstruction. Therefore, our present report warrants further studies with more extensive lung function techniques (eg, body plethysmography and airway resistance testing) on the association between obstructive SDB and lower airway dysfunction, as it could partly explain the association between obesity and asthma in children.