ratory disease has been identified. The processes involved, such as inflammation and increased levels of oxidants, are not unique to tobacco-related respiratory diseases. Identifying unique biomarkers is further confounded by the heterogeneous nature of these diseases, the complex mixture that makes up tobacco smoke, and the range of individual susceptibilities to the harmful effects of tobacco smoke among users (see Chapter 11). In COPD, for example, the majority of smokers develop abnormal lung function (Camilli et al., 1987), but only 15–20% will develop symptomatic COPD (Fletcher and Peto, 1977). There appears to be no specific clinical or physiological feature to predict which smokers exhibit a rapid decline in lung function (Habib et al., 1987). The most widely used markers of tobacco-related respiratory diseases in population studies are symptom questionnaires and pulmonary function testing. These have well-known limitations of specificity and sensitivity, particularly for detecting the early effects of tobacco smoke on lungs (U.S. DHHS, 1989). Subtle effects of tobacco smoke exposure on the lung can be detected by sampling fluid in