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Department of
Thoracic Medicine, Imperial College School of Medicine at the National
Heart and Lung Institute, Dovehouse Street, London SW3 6LY, UK
Correspondence to: Professor P J Barnes p.j.barnes{at}ic.ac.uk
Received 10 April 2000; Returned to authors 18 September 2000; Revised version received 17 November 2000; Accepted for publication 15 February 2001
BACKGROUND
Cigarette
smoking reduces the level of exhaled nitric oxide (NO) in healthy
subjects, although the mechanism is unclear. NO is a highly reactive
molecule which can be oxidised or complexed with other biomolecules,
depending on the microenvironment. The stable oxidation end products of
NO metabolism are nitrite and nitrate. This study investigated the
effect of smoking on NO metabolites in exhaled breath condensate.
METHODSFifteen
healthy current smokers were recruited together with 14 healthy
non-smokers. Measurement of exhaled NO, lung function, and collection
of exhaled breath condensate were performed. Nitrite, nitrite + nitrate, S-nitrosothiols, and nitrotyrosine levels were measured. The
effect of inhaling two cigarettes in smokers was also evaluated. The
mean level of exhaled NO in smokers was significantly lower than in
non-smokers (4.3 (0.3) ppb v 5.5 (0.5) ppb, p<0.05).
RESULTSThere was no
difference in the levels of nitrite, nitrite + nitrate,
S-nitrosothiols, and nitrotyrosine in the exhaled breath condensate at
the baseline visit between smokers and non-smokers. After smoking,
nitrite + nitrate levels were significantly but transiently increased
(from 20.2 (2.8) µM to 29.8 (3.4) µM, p<0.05). There was no
significant change in the levels of exhaled NO, nitrite, S-nitrosothiols, or nitrotyrosine 30 and 90 minutes after smoking.
CONCLUSIONSThese
findings suggest that acute smoking can increase the level of nitrate,
but not nitrite, S-nitrosothiols, or nitrotyrosine in breath
condensate. The deleterious effect of oxidant radicals induced by
smoking may contribute to the epithelial damage of airways seen in smokers.
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