There is worldwide increasing awareness of the human and socioeconomic impact of chronic obstructive pulmonary disease (COPD) which is a major cause of morbidity and mortality.1 Even though its pathogenesis in industrialised countries is linked to a well known cause—namely, tobacco smoking—it is not envisaged that this knowledge will lead to breakthroughs in the prevention of this disease during the years to come. Hence, current efforts are mainly directed towards improving the diagnosis and management of patients with COPD.1

During the past decade it has been recognised that the pathophysiology of COPD includes (multiple) inflammatory pathways within the airways and lung parenchyma. Apart from the emphysematous lesions, smokers with chronic airflow limitation usually have increased submucosal glands, some degree of epithelial shedding, and an increase in the amount of airway smooth muscle.2 However, the most important pathological changes are found within the small airways where the inflammation is characterised by increased numbers of macrophages, mast cells,3 neutrophils, and CD8+ T cells,4together with increased expression of growth factors such as transforming growth factor β (TGF-β).5 Most of these abnormalities can be detected in bronchial biopsy specimens from the large airways6 and are related to the severity of airflow limitation.7

It is not therefore unexpected that attempts have been made to detect and monitor such inflammatory changes in COPD by non-invasive techniques. The first valuable step has been made by using the measurement of airway hyperresponsiveness to methacholine8which, indeed, provides complementary information to symptoms and lung function on the course and prognosis of the disease. More recent efforts concentrate on cellular or soluble markers of inflammation in induced sputum9 or molecular markers in exhaled air.10 ,11 Is there a need to monitor inflammatory activity in COPD and, if …