Inhalation of a nebulised extract of flax dust caused a fall in specific airway conductance (sGaw) in human subjects that typically reached its nadir 1h postexposure. Recovery was rapid, return of sGaw to baseline values occurring within 3h. This airway response was abolished by prior treatment with the calcium channel blocker, verapamil. However, neither indomethacin (a cyclo-oxygenase inhibitor) nor ketoconazole (an inhibitor of leukotriene release in guinea pig lung) was able to influence the effect of the inhaled dust extract. Cromoglycate was able to slightly attenuate the response of the subjects to the inhaled material but the potent and relatively selective H(1)-receptor antagonists, terfenadine and loratadine, markedly antagonised the airway change induced by the nebulised flax dust extract. In vitro, the flax dust extract was able to release histamine from lung tissue more effectively than equivalent concentrations of either cotton dust or E.coli endotoxin.

It is concluded that the airway response to inhaled flax dust extract arises from bronchiolar smooth muscle contraction. While the present evidence does not necessarily exclude a role for arachidonic acid metabolites in this phenomenon, it is suggested that the release of histamine locally in the lung may be involved.