Biomedical risk assessment as an aid for smoking cessation.
BACKGROUND
A possible strategy for increasing smoking cessation rates could be to provide smokers who have contact with healthcare systems with feedback on the biomedical or potential future effects of smoking, e.g. measurement of exhaled carbon monoxide (CO), lung function, or genetic susceptibility to lung cancer. We reviewed systematically data on smoking cessation rates from controlled trials that used biomedical risk assessment and feedback.


OBJECTIVE
To determine the efficacy of biomedical risk assessment provided in addition to various levels of counselling, as a contributing aid to smoking cessation.


METHODS
We systematically searched he Cochrane Collaboration Tobacco Addiction Group Specialized Register, Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (1966 to 2004), and EMBASE (1980 to 2004). We combined methodological terms with terms related to smoking cessation counselling and biomedical measurements.


METHODS
Inclusion criteria were: a randomized controlled trial design; subjects participating in smoking cessation interventions; interventions based on a biomedical test to increase motivation to quit; control groups receiving all other components of intervention; an outcome of smoking cessation rate at least six months after the start of the intervention.


METHODS
Two assessors independently conducted data extraction on each paper, with disagreements resolved by consensus.


RESULTS
From 4049 retrieved references, we selected 170 for full text assessment. We retained eight trials for data extraction and analysis. One of the eight used CO alone and CO + Genetic Susceptibility as two different intervention groups, giving rise to three possible comparisons. Three of the trials isolated the effect of exhaled CO on smoking cessation rates resulting in the following odds ratios (ORs) and 95% confidence intervals (95% CI): 0.73 (0.38 to 1.39), 0.93 (0.62 to 1.41), and 1.18 (0.84 to 1.64). Combining CO measurement with genetic susceptibility gave an OR of 0.58 (0.29 to 1.19). Exhaled CO measurement and spirometry were used together in three trials, resulting in the following ORs (95% CI): 0.6 (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 of 1.21 (0.60 to 2.42). Two trials used other motivational feedback measures, with an OR of 0.80 (0.39 to 1.65) for genetic susceptibility to lung cancer alone, and 3.15 (1.06 to 9.31) for ultrasonography of carotid and femoral arteries performed in light smokers (average 10 to 12 cigarettes a day).


CONCLUSIONS
Due to the scarcity of evidence of sufficient quality, we can make no definitive statements about the effectiveness of biomedical risk assessment as an aid for smoking cessation. Current evidence of lower quality does not however support the hypothesis that biomedical risk assessment increases smoking cessation in comparison with standard treatment. Only two studies were similar enough in term of recruitment, setting, and intervention to allow pooling of data and meta-analysis.
Bize
R
R
University Institute of Social and Preventive Medicine, Health Care Evaluation Unit and Prevention Unit, 17 Rue du Bugnon, Lausanne, Switzerland 1005. Raphael.Bize@hospvd.ch
Burnand
B
B
Mueller
Y
Y
Cornuz
J
J
D001676:Biofeedback, Psychology / Q000379:methods*; D001944:Breath Tests; D002248:Carbon Monoxide / Q000032:analysis; D020022:Genetic Predisposition to Disease; D006801:Humans; D016032:Randomized Controlled Trials as Topic; D018570:Risk Assessment; D012907:Smoking / Q000009:adverse effects* / Q000378:metabolism; D016540:Smoking Cessation / Q000379:methods / Q000523:psychology*; D013147:Spirometry
D002248:Carbon Monoxide