An expanded receptor model was applied to identify and apportion the PM2.5 sources that were common to three different environments (personal, indoor: inside school, and outdoor: outside school) resulting in exposure to asthmatic children who attended a school in Denver, CO for children with moderate to severe asthma. Four resolved external sources and three internal sources were resolved from the PM2.5 data for three different environments. Secondary nitrate and motor vehicle emissions were the two largest external sources in this study. Cooking was the largest internal source. A significant influence of indoor smoking on daily personal exposures to particles was observed for those houses in which smokers reside and the environmental tobacco smoke contribution correlated with urinary cotinine levels in these urban schoolchildren. The influence of the high traffic flow outside the school on the indoor air quality was also observed. The identification and apportionment of these sources will support a subsequent investigation of the potency of air pollution sources on asthma severity in children and provide a better understanding of potential mechanisms of asthma exacerbation.