Objective: To determine the efficacy of biomedical risk assessment (eg, exhaled carbon monoxide (CO), or genetic susceptibility to lung cancer) as an aid for smoking cessation. Data sources: Cochrane Tobacco Addiction Group Specialized Register, Cochrane Central Register of Controlled Trials, Medline (1966-2004) and EMBASE (1980-2004. Study selection: Randomised controlled smoking cessation interventions using biomedical tests with at least 6 months follow-up. Data extraction: Two reviewers independently screened all search results (titles and abstracts) for possible inclusion. Each reviewer then extracted data from the selected studies, and assessed their methodological quality based on the CONSORT (Consolidated Standards of Reporting Trials) statement criteria. Data synthesis: Of 4049 retrieved references, eight trials were retained for data extraction and analysis. Three trials isolated the effect of exhaled CO on smoking cessation rates resulting in the following ORs and 95% CIs: 0.73 (0.38 to 1.39), 0.93 (0.62 to 1.41) and 1.18 (0.84 to 1.64). Measurement of exhaled CO and spirometry were used together in three trials, resulting in the following ORs (95% CI): 0.60 (0.25 to 1.46), 2.45 (0.73 to 8.25) and 3.50 (0.88 to 13.92). Spirometry results alone were used in one other trial with an OR (95% CI) of 1.21 (0.60 to 2.42). Ultrasonography of carotid and femoral arteries performed on light smokers gave an OR (95% CI) of 3.15 (1.06 to 9.31). Conclusions: Scarcity and limited quality of the current evidence does not support the hypothesis that biomedical risk assessment increases smoking cessation as compared with the standard treatment. D espite increasing scientific knowledge about health hazards due to cigarette consumption, there is, in many countries, an increase in the prevalence of smoking among young people.1 2 The gap between knowledge and smoking cessation has been attributed, partly, to smokers' underestimation of their personal risks of smoking-related illness. A possible strategy for increasing quit rates might be to provide a personalised feedback on the physical effects of smoking by physiological measurements. We can distinguish three different types of feedback: the first one explores biomarkers of smoking exposure (cotinine and carbon monoxide (CO)); the second one gives information on smokingrelated disease risk (eg, lung cancer susceptibility according to CYP2D6 genotyping) 5 ; and the third one depicts smokingrelated harm (eg, atherosclerotic plaque and impaired lung functions). 6 The rationale for such interventions is to promote risk awareness and motivation to accelerate changes in smoking-behaviour. Individual studies have provided conflicting data on the effect of physiological feedback. [9][10][11][12][13][14][15][16][17] We aimed to review the data on smoking cessation rates from controlled trials using feedback on the physiological effects of smoking or on the genetic susceptibility to smoking-related diseases. This article is a shortened version of our Cochrane review.