The inflammatory basis of asthma is now beyond dispute and even mild asthmatics exhibit mast cell degranulation, eosinophil infiltration and increases in mononuclear cells in airway mucosal biopsies. The chronic nature of this endobronchial inflammation may cause damage to ciliated epithelium, which, coupled with laying down of cross-linked collagen within the airway wall, leads to partly irreversible airway obstruction. Corticosteroids, which are potent anti-inflammatory agents, decrease bronchial hyperresponsiveness and the clinical manifestations of asthma. Although inhaled corticosteroids produce fewer side-effects, the use of low-dose (10 mg or less) oral treatment may be recommended for patients unable financially to afford inhaled corticosteroids or who are unable to use them effectively. Other anti-inflammatory drugs, including methotrexate, cyclosporin and the newer leukotriene inhibitors, are not yet in general use and may provide new pharmacological approaches to the treatment of asthma in the near future. In all but the mildest asthma, strategies aimed at preventing and decreasing bronchial inflammation should be the primary aim of treatment. The physician should refrain from prescribing only beta 2-agonists to new asthmatics and patients must be educated to increase understanding of the benefits of preventive rather than symptomatic forms of treatment for this chronic disease.