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controls. Kharitinov et al reported levels of 283ppb in 6l asthmatics compared to 67 controls
at 80.2ppb when measured with single exhalations (Kharitonov, Yates et al. 1994). Persson et
al measuring mixed exhaled air found levels of 10.3ppb in 23 asthmatics compared to 20
controls at 8.4ppb (Persson, Zetterstrom et al. 1994). Massaro et al using a similar technique
found levels of l3.2ppb in five asthmatics compared to five controls at 4.7ppb (Massaro,
Mehta et al. 1996). Robbins et al measured single exhalations and a reservoir collection in 18
asthmatics and 91 controls, reporting significant differences between the groups with both
techniques, of l74ppb compared to l05.5ppb and 27.2ppb compared to 14.5ppb @obbins,
Floreani et al. 1996). Alving et al demonstrated no overlap between their control group with a
range of 5-l6ppb and their asthmatic group who had a range measured at 2l-3lppb (Alving,
Weitzberg et al. 1993). Martin et al also found significant differences between 18 control
subjects and 32 patients with allergic rhinitis when measured by single exhalation with
ll.lppb compared to l6.3ppb, following a ten second breath-hold at 15.6ppb compared to
34.0ppb and following a 60 second breath-hold at 32.lppb and 62ppb (Martin, Bryden et al.
1996). Massaro demonstrated that the NO levels were even higher at 13.9ppb during a period
of acute asthma in seven patients requiring emergency department treatment. A reduction of
NO began after 48 hours which soon became indistinguishable from control NO levels at
6.2ppb (Massaro, Gaston et al. 1995). Kharitinov et al showed a reduction from 203ppb to
120ppb over three weeks in eleven asthmatic patients and an increase on their mean FEVr as
percent predicted from92Vo to 99Vo after commencing 800pgs budesonide dipropionate twice
per day, with no corresponding change when the same patients were randomised to placebo
(Kharitonov, Yates et al. 1996). As by far the greatest amounts of NO in vitro were shown to
be produced from iNOS stimulation, these high levels in asthma were hypothesised by these
groups to be a measure of airway inflammation (Barnes 1993; Barnes and Kharitonov 1996).
Following measurement of exhaled NO in healthy children, I was then interested to assess
whether these same findings as had been documented in adults could be found in children
with asthma.
8.5.2 The asthmatic subjects
The children were recruited from the paediatric respiratory or asthma outpatient clinics at the
Royal Brompton Hospital where I was seeing patients. Five children were also enrolled from
the Park Walk Primary School (four on bronchodilators only and one on regular IHCS therapy
who was subsequently also seen in the asthma clinic). They were presented with the same
questionnaire as used for the control children. Following informed consent from their parent/s
or caregiver/s, the children were enrolled if:
t92