PURPOSE: It has been suggested that obesity is an inflammatory illness, and that this phenomena may contribute to the symptoms of dyspnea and wheeze. To determine if traditional markers of inflammation, are involved we measured the concentrations of exhaled nitric oxide (eNO) in obese (O) and contrasted them with normal (N) individuals.
METHODS: Thirty two O and 32 N individuals who were free of cardiopulmonary disease were recruited to provide sufficient power and determine a 30% difference in eNO between groups with an α of 0.05 and β of 0.20. Obesity was defined as a Body Mass Index (BMI) ≥ 30kg/M2.
RESULTS: Single breath eNO were obtained at flow rates of 30 and 250mL/sec through a chemiluminescence analyzer using flow restrictors to evaluate the airway (eNOair) and alveoli (eNOalv) levels. Spirometry was also recorded. Statistical comparisons were performed with unpaired t-tests, and chi square analysis. Obese subjects had a mean BMI of 45 ± 8 Kg/M2. Their forced vital capacity (FVC) was 80 ± 17% predicted. Normal subjects were leaner by design (BMI = 24 ± 3 Kg/M2, p=0.001), and their FVC averaged 95 ± 20% predicted (p= 0.002). The O group eNOair was 17.5 ± 11ppb, and eNOalv = 5.0 ± 4ppb. These values were significantly smaller than those found in N at identical flows (N eNOair = 26 ±14.2ppb; eNOalv = 8.0 ±5ppb, p= 0.006 for both).
CONCLUSION: These data demonstrate that O is not associated with increased levels of eNO from either airway walls or alveoli. Thus, airway inflammation does not appear to be a feature of this illness. Distinctions between groups may be due to lung volume induced differences in airway size and the resulting changes in the dynamics of the NO diffusion relationships.
CLINICAL IMPLICATIONS: The respiratory components of O are unlikely to respond to anti-inflammatory therapy.
DISCLOSURE: Javaad Khan, None.