The limitation of data concerning clinically relevant exposures to agents, including fungi, in the indoor environment has been identified as an important problem by scientists studying building-related illness (1, 2). Despite the attempts to objectively characterize fungal exposure, the recent study of lower respiratory illness (LRI) among children by Stark and colleagues (3) appears to have important limitations in exposure assessment. The method of defining fungal exposure used in that study places emphasis on specific fungal types, but does not allow for any characterization of the total fungal count in the areas being evaluated. As described in the study by Stark and colleagues (3), a home could have a "high fungal level" when persons in other homes could easily be exposed to greater concentrations of total fungi. For example, a home with an airborne Aspergillus level of 100 cfu/m3 but no other fungi would be considered to have a "high fungal level," whereas a home with an Aspergillus level of 37 cfu/m3, Cladosporium of 177 cfu/m3, and Penicillium of 130 cfu/m3 (mean airborne concentrations from the study, yet totaling 240 cfu/m3) would not be "high" because none of those concentrations exceed the 90th percentile. Given the uncertainties concerning mechanisms of illness related to fungi, misclassification bias would be an important consideration for this type of exposure assessment. We agree with the authors that another important limitation of their exposure assessment involves fungal samples being taken only once at the beginning of the survey, whereas information on the outcome measures were collected every 2 months for a year. It remains unclear whether there is any clinical relevance of measures of fungal exposure taken up to 12 months before LRI (or any other health effect). In the article by Stark and colleagues (3), there appears not to have been any assessment of exposure to environmental tobacco smoke (ETS), whether at home or in daycare settings. Because ETS is known to be associated with increased morbidity in children (4), some assessment of ETS among the study participants would be important. Finally, the authors draw conclusions concerning the relationship of measured fungal concentrations in houses with the presence or absence of water damage or visible mold in those houses. The methods of assessment of water damage/visible mold are not described, but the assessment appears to be based on parental self-report. We question the usefulness of such occupant self-report and suggest that an objective assessment of the indoor environment for moisture (perhaps using a moisture meter) would be more appropriate. In summary, problems with assessment of exposure to fungi in the indoor environment, such as those pointed out above, are certainly not unique to the study in question. However, it is important to point out these limitations because they call into question the ability of the authors to draw conclusions concerning (1) appropriate types of evaluation techniques for indoor environments (the need for fungal sampling) and (2) the relationship of illness to exposure to fungi in the indoor environment.