Cystic Fibrosis (CF) is the most commonly inherited, life-shortening genetic condition amongst Caucasians, with an incidence of about 1 in 3,800 newborns and currently affecting about 30,000 Americans. It is chronically debilitating and the annual cost of medical care per person makes it a serious public health concern. Airway inflammation contributes to progressive pulmonary disease, the leading cause of morbidity and mortality in patients with Cystic Fibrosis. The mechanism by which the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene affects airway inflammation has not been fully elucidated to date; however, several mechanisms have been proposed. Despite the need for continued study in determining this mechanism, we do know that mutations in the CFTR gene ultimately result in bacterial colonization in the lungs, reduced mucociliary clearance and airway inflammation. Chronic airway inflammation results in continued assault on the lungs and progresses the course of the disease. Airway inflammation can be monitored through the use of bronchoalveolar lavage to evaluate the influx of neutrophils; however, routine bronchoscopy is an invasive procedure and is less than ideal for routine assessment. Exhaled gas as a marker for airway inflammation is useful in that it is minimally invasive and relatively easy to obtain. Some of the data on the clinical utility of exhaled gas measurements has been conflicting with regard to its efficacy in assessing airway inflammation. If exhaled gas measurements can be used to assess airway inflammation, they could provide a non-invasive alternative to monitor inflammation and do so more frequently than invasive methods, with the ultimate goal of being able to detect inflammation earlier with the intent of earlier treatment and possible reduction in progression of lung disease
