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were loosely grouped as British, Indian, Arabic, African, European and South American with
one to fifteen children in each group.
we prospectively elected to enter into the database a positive or negative response to the
questions and not categorise answers any further. We therefore did not investigate possible
dose-response relationships for atopy (personal or family), passive smoking or presence of
pets. For example, we did not try to quantify the numbers of cigarettes smoked by the one or
more household smokers and look at the exhaled NO levels in this group. Likewise we did not
quantify the number of atopic responses within the family and see if there was any correlation
between atopy severity and exhaled No. This was for a number of reasons' Firstly, as
mentioned we were relying on questionnaire data which could be variably accurate' Secondly,
in the straight .positive and negative' categorisation of responses there were no significant
differences that I thought should be further investigated in this setting. Thirdly, the numbers
with a positive response to one of these areas ranged from eleven to nineteen so the numbers
were becoming small. Finally, it would have been difficult with these small numbers to
quantify one response in exclusion of other responses. At the time, our sample of 39 children
was the largest study in this area of research but the lack of findings of these factors that
might cause some degree of airway inflammation may be secondary to lack of numbers
causing a type two statistical error.
Despite the questionnaire and normal lung function, we had one boy who was an outlier with
direct peak No ot l97.2ppb and t-piece peak No of l4l.2ppb which was 73ppb and 43ppb
higher than the next highest result. On history, he occasionally wheezed with viral infections
and, following parental permission had 2OVo fall in FEV1 at2 mglml histamine on challenge'
It is possible he had mild asthma or was on the extreme of the normal range of ainuay
reactivity. He was a European boy with no personal or family history, from a non-pet owning'
non-smoking household.
By time of publication of this study, other investigators during the same period had also
begun to examine the measurement of NO in children, both in normal subjects and those who
with a range of respiratory diseases. In the main, the control children studied had no
respiratory disease, were on no medications and usually were recorded to have no upper
respiratory tract infection for between two and six weeks prior to the studies' Unfortunately'
as mentioned in the previous chapters, with all the early research each individual research
group developed their own techniques and thus every group utilised a different method of
measurement. As with the adult data, the absolute results in the healthy children differed
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