Abstract
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.