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Peat et al1 have contributed a helpful review to the debate on techniques for measuring asthma in population studies. However, they have endorsed airway hyperresponsiveness (AHR) while neatly sidestepping the issue of what test they are discussing. Inhaled provocation tests used in epidemiological work have included histamine, methacholine, hypertonic saline, cold air, and adenosine. Exercise provocation tests have also been used. Peat et al have previously shown that exercise and histamine challenges may define different groups of children,2 and we have shown that longer term repeatability of a free running exercise provocation test is poor within a childhood population.3 In adults quite considerable within subject variability in PD20 to methacholine has been observed during a 1 year period,4 and a childhood population study found that methacholine PD20 varied by >4 doubling doses within the course of a year in 33% of the subjects.5
We would suggest that more care should be taken to define the precise measure of AHR used before comments can be made about its sensitivity and specificity in an epidemiological survey. The medium term temporal variation in AHR seen by a number of researchers is another measure which may make it difficult to make useful comparisons between populations.
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Authors' reply
Primhak and Powell make the valid point that the presence of airway hyperresponsiveness (AHR) is not an absolute attribute. Abnormal AHR represents one end of a continuum of responsiveness. Furthermore, the distribution of that continuum varies according to the nature of the direct or indirect stimulus that is applied.
In our studies, referred to in the review, we have defined abnormal airway responsiveness as a decline of more than 20% in forced expiratory volume in 1 second (FEV1) after inhalation of a cumulative dose of histamine of ≤3.9 μmol. Using this criterion, the presence of AHR is a useful marker of airway abnormality consistent with asthma in epidemiological studies1 and is also predictive of the subsequent course of the disease.2 We acknowledge that other criteria for the presence of AHR have not been evaluated as extensively in epidemiological studies. However, there is evidence that at least some indirect agonists, such as non-isotonic aerosols and exercise, also have a high level of specificity but only moderate sensitivity as markers of asthma symptoms.3,4