We assessed the relationship between bronchial hyperresponsiveness (BH
R) and the onset of wheezing 5 years later, by epidemiological analysi
s of 194 working men without asthma or wheezing at the first examinati
on. In 1985/1986 and 1990/1991, subjects answered a British Medical Re
search Council questionnaire and performed lung function measurements
and methacholine challenge tests (total dose 6 mg). BHR was measured i
n three ways: (1) FEV(1) fall greater than or equal to 20% (PD20+); (2
) the two-point response slope expressed as percentage decline of FEV(
1)/dose, and (3) a four-parameter model: FEV(1) at dose (d)/prechallen
ge FEV(1) = ONE-k(d-delta)(+)(alpha), where 'k' is the slope of the re
lative variation of FEV(1) with the dose, 'delta' the threshold dose,
and 'alpha' a shape factor. In the 13 new wheezers, the mean values of
the two-point slope and of k were significantly increased, and the pr
oportion of reactors was almost threefold (the latter was not statisti
cally significant). Among nonsmokers, delta was significantly lower in
new wheezers than in the others, whereas the slope and k had similar
mean values. Among smokers, new wheezers had increased mean values for
the slope and k, and an increased proportion of reactors, whereas del
ta was not decreased. Thus, BHR was a significant predictor of wheezin
g, independent of the method of analysis. Moreover, the model distingu
ished between two components of bronchial response: wheezing was predi
cted by sensitivity (delta) in nonsmokers, and by reactivity (k) in sm
okers.