Various mediators of inflammation have been suggested as being important in the pathogenesis of asthma. These include histamine, acetylcholine, bradykinin, adenosine, prostaglandins D2 and F2 alpha, thromboxane A2, leukotrienes, PAF and, more recently, various cytokines. Intervention in the action of these mediators is proposed to offer therapeutic benefit, and recent advances in drug therapy have centred on two main approaches. Specific and potent leukotriene antagonists and inhibitors of leukotriene biosynthesis have emerged, and their effects against allergen challenge, cold-air- and exercise-induced bronchospasm and aspirin-sensitive asthma have been evaluated. A small number of studies have also been conducted in clinical asthma, with both acute and long-term (up to 20 weeks) efficacy studies being reported. A considerable degree of inter-individual variation is seen in the degree of protection afforded by leukotriene intervention. The extent to which inhibiting one set of inflammatory mediators can be expected to attenuate the asthmatic response can be questioned. As yet, there is no way of distinguishing leukotriene-related asthma from other types. It is likely, however, that leukotriene intervention may be useful in some patients with specific forms of the disease; for example, aspirin-sensitive asthma. Leukotriene intervention is unlikely to replace inhaled corticosteroids in the treatment of asthma, and its position in the guidelines for the management of asthma remain unclear thus far.