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Department of
Thoracic Medicine, National Heart & Lung Institute, Dovehouse Street,
London SW3 6LY, UK
Correspondence to: Dr J A Nightingale
Received 20 May 1999; Returned to authors 21 July 1999; Revised version received 12 August 1999; Accepted for publication 27 August 1999
BACKGROUND
Nitric
oxide (NO) may have a role in the pathophysiology of tissue injury in
response to inhaled ozone in animals.
METHODSA double
blind, randomised, placebo controlled, crossover study was undertaken
to investigate the effects of inhaled ozone in 10 normal and 10 atopic
asthmatic volunteers. Subjects were exposed to 200 ppb ozone or clean
air for four hours with intermittent exercise, followed by hourly
measurement of spirometric parameters and exhaled NO for four hours.
Nasal NO and methacholine reactivity were measured and exhaled breath
condensate and induced sputum samples were collected four and 24 hours
after exposure.
RESULTSExposure
to ozone caused a fall in forced expiratory volume in one second
(FEV1) of 7% in normal subjects (p<0.05) and 9% in
asthmatic subjects (p<0.005). There was a 39% increase in sputum neutrophils at four hours in normal subjects (p<0.05) and a 35% increase at four hours in asthmatic subjects, remaining high at 24 hours (p<0.005 and p<0.05, respectively). There were no differences between normal and asthmatic subjects. There were no changes in methacholine reactivity, exhaled or nasal NO, nitrite levels in exhaled breath condensate, or sputum supernatant concentrations of
interleukin 8, tumour necrosis factor 
, or granulocyte-macrophage colony stimulating factor in either group.
CONCLUSIONSExposure
to 200 ppb ozone leads to a neutrophil inflammatory response in normal
and asthmatic subjects but no changes in exhaled NO or nitrite levels.
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