Increased nitric oxide elimination from the airways after smoking cessation

Abstract

A B S T R A C TSmokers have been found to have low exhaled nitric oxide (NO) levels. The aim of the present study was to investigate where in the respiratory system the decrease in NO occurs, and whether this decrease was affected by smoking cessation. Measurements of exhaled NO were carried out in smokers (n l 20) and non-smoking control subjects (n l 30). In nine of the smokers, exhaled NO was analysed 1, 2 and 4 weeks after smoking cessation. The level of exhaled NO at a flow rate of 0.1 litre/s was significantly lower in smokers (4p2 p.p.b.) than in nonsmokers (7p5 p.p.b. ; P l 0.007). A calculation of the contributions from different areas of the lung showed that the NO flux from the airways was significantly lower (14p10 compared with 36p26 nl/min ; P l 0.0001) and the alveolar fraction was significantly higher (2.1p0.8 compared with 1.5p0.9 p.p.b. ; P l 0.006) in smokers than in non-smokers. Nine smoking subjects refrained from smoking for 4 weeks, and this resulted in increased NO flux from the airways of 28p17 nl/min, which was no longer significantly different from controls. In conclusion, endogenous production of NO in the airways is decreased in smokers, but can be restored to normal values by 4 weeks after cessation of smoking. Smokers have an increased alveolar fraction of NO, and this might be a diagnostic sign of lung damage. Thus NO monitoring can be used to indicate improvements when a smoker decides to stop smoking.

Time course of exhaled hydrogen peroxide and nitric oxide during chemotherapy

“…Smoking is known to lead to a reduction of FeNO levels, probably due to scavenging by ROS. After smoking cessation, FeNO levels rise over ,1-4 weeks [32]. The time of the start of the study, as well as the fall in FeNO level at day 8, did not favour the assumption that smoking cessation has biased FeNO measurements.…”

Smokers Have Reduced Nitric Oxide Production by Conducting Airways but Normal Levels in the Alveoli

“…The slope of the regression line equals NO production by the conducting airway (Vaw NO ). Högman et al, 2002aHögman et al, , 2002bSilkoff et al, 2000;Tsoukias et al, 1998). Because the variable Q E appears in both the horizontal and upright axes, the solution risks potential errors from mathematical coupling that can lead to erroneous conclusions (Archie, 1981;Ronco et al, 1991).…”

“…Other investigators have modeled the conducting airways to have a constant concentration of NO in the bronchial wall (Paw NO ) with NO diffusing into the lumen in proportion to the gradient between Paw NO and P E (Brindicci et al, 2005;Högman et al, 2002aHögman et al, , 2002bSilkoff et al, 2000;Tsoukias et al, 1998). Silkoff and co-workers (2000) calculated Paw NO and Daw NO from the regression line defined by plots of P E versus Q E P E /(P B -47).…”

“…Reduction of airway inflammation with inhaled corticosteroids normalizes elevated exhaled NO levels in asthmatics, and measurements of exhaled NO have been proposed as a method to monitor disease activity and response to therapy (Kharitonov et al, 1997). In contrast, cigarette smokers consistently show decreased levels of NO in their expired breath (Brindicci et al, 2005;Högman et al, 2002aHögman et al, , 2002bKharitonov et al, 1995;Persson et al, 1994). Because NO functions to destroy microorganisms and neoplastic cells (Lowenstein et al, 1992), the diminished levels observed in the lung of smokers may contribute to their increased incidence of pulmonary diseases.…”

“…In contrast, cigarette smokers consistently show decreased levels of NO in their expired breath (Brindicci et al, 2005; Högman et alPersson et al, 1994). Because NO functions to destroy microorganisms and neoplastic cells (Lowenstein et al, 1992), the diminished levels observed in the lung of smokers may contribute to their increased incidence of pulmonary diseases.During the past 8 yr, our group and others have published methods that distinguish the amount of NO being produced by the conducting airways (Vaw NO ) from the NO concentration in the alveoli (P ALV ) by measuring exhaled NO at different expiratory flow rates (Brindicci et al, 2005;Högman et al, 2002aHögman et al, , 2002bPietropaoli et al, 1999;Silkoff et al, 2000;Tsoukias et al, 1998). We have previously reported that multiplying P ALV by a separate measurement of the pulmonary alveolar diffusing capacity for NO (D LNO ) determines the amount of NO produced by the alveolar compartment that enters the airspaces (V LNO ) (Pietropaoli et al, 1999).…”