Snoring in children is increasingly being recognized as a highly prevalent condition, and indicates the presence of heightened upper airway resistance during sleep. In this paper, we present evidence to support the hypothesis that local inflammatory processes within the upper airway contribute to the pathophysiology of adenotonsillar hypertrophy and altered reflexes potentially leading to increased propensity for upper airway obstruction during sleep. Furthermore, the cumulative evidence supporting multiorgan morbidity for sleep-disordered breathing (SDB) is reviewed, and a unified hypothesis of a triple risk model proposing oxidative-inflammatory mechanisms as mediating the morbid consequences of SDB is presented. This hypothetical working model incorporates both dose-dependent disease severity components, as well as environmental and genetic elements of susceptibility.