Asthma is a clinical entity characterised by a combination of three features: airway obstruction with spontaneous and/or pharmacological reversibility, increased airway responsiveness (BHR), and airway inflammation.1 ,2 Asthma originates with airway inflammation which results in the pathological process and ultimately culminates in symptoms.2

Airway inflammation has been considered the primary event leading to airway obstruction and hyperresponsiveness.2 The principal pathological features of asthma include thickening and disorganisation of the tissues of the airway wall with epithelial shedding, deposition of collagen under the basement membrane, hypertrophy/hyperplasia of the smooth muscle, epithelial damage, occlusion of airways by secretion, and infiltration of eosinophils and T lymphocytes.1 The investigation into the mechanisms involved in the pathogenesis of asthma has been hampered by difficulties in gaining direct access to asthmatic airways for evaluating the inflammatory process. Until recently it has not been possible in clinical practice to measure inflammation directly, and the presence or absence of airway inflammation has been assumed from symptoms, measurement of BHR, and the effect of treatment. The introduction of a method of sputum analysis3 ,4 which is a non-invasive safe tool for analysing the cellular and biochemical component of the airway secretions has allowed the direct measurement of airway inflammation in asthma.3-5 In fact, measurement of induced sputum has been shown to be a repeatable,6 ,7 valid,7 ,8and feasible4 ,5 method for assessing eosinophilic airway inflammation.

Despite many studies of the possible association between the three features that characterise chronic bronchial asthma using sputum parameters as a measure of airway inflammation,4 ,7-34the interrelations between the sputum cytological and biochemical profile and clinical or functional parameters in asthma remain a matter of debate. This raises the question whether sputum analysis is a useful …