There are limitations to our study, the main relating to use of a questionnaire-based assessment of OSA, since PSG is the gold standard to diagnose OSA. Prospective use of a costly technology such as PSG would have been prohibitive for this large study, but our results substantiate a need for such PSG-based studies. The SA-SDQ demonstrated high internal validity, good sensitivity, and specificity in a large sample of sleep study patients.19 Furthermore, this questionnaire has a high diagnostic value compared with other sleep apnea screening instruments.45 Second, the SA-SDQ has not been specifically validated in patients with asthma. In other primary non-lung disease patient populations, the SA-SDQ was found to be a good predictor for OSA on PSG46,47 such that lower cutoff scores than used herein have been proposed for use in these patients.47 However, when these lower cutoff scores were applied to a population of patients with another chronic lung condition (ie, pulmonary fibrosis), although a good correlation was noted between SA-SDQ score and OSA severity, this instrument did not perform as well as48 in the original validation study.19 These findings raise the possibility that the original cutoff scores,19 which we used in our study, may be more appropriate for patients with lung diseases. Further studies are necessary to validate this scale specifically in patients with asthma. A third limitation stems from the cross-sectional design, preventing any conclusion about causality. Although asthma also may be a risk factor for the development of OSA,49 our data, corroborated by other interventional studies7‐10 along with the magnitude of independent effects observed and the plausible mechanistic basis presented, suggest an effect of OSA on asthma control. It is also possible that our study population, which was based in a highly specialized clinic, may contribute to an underestimation of the true relationship of OSA with asthma control. The nose is the main breathing route during sleep, and nasal congestion is a well-established risk factor for OSA.50 A large proportion of our study subjects had a history of rhinitis, with the majority (91%) receiving at least one treatment at the time of survey. Such a high proportion of treatment use, through its effect, is a likely explanation for the “protective” association of rhinitis with asthma control. These observations suggest that this treatment effect also may have contributed to a reduction of the true OSA risk in this cohort and perhaps attenuated the impact of OSA on asthma control. Group analyses such as ours may not entirely describe control of asthma in individual patients, such as those with a poor perception of airway narrowing. Therefore, in such patients, using the full-version ACQ for determining its relationship with OSA risk may provide the best estimate of asthma control. Finally, none of the ACQ versions can separate between nocturnal from daytime asthma control. Because interventional studies for OSA in asthma have preferentially selected patients with nocturnal symptoms,7‐10 the OSA effect specifically on daytime asthma remains largely unknown. Understanding this relationship may have important implications on the mechanisms underlying this interaction and is worthy of future study.