The current study examined the effectiveness of a brief, motivational intervention using biologically-based feedback to alter behavioral smoking outcomes. The intent was to build and strengthen motivation to quit through a personalized health risk assessment and brief motivational intervention, reduce common barriers to empirically validated treatment by offering free access to phone counseling which could be utilized anytime in the next year, and thereby increase treatment uptake and abstinence rates. The intervention was also purposefully designed to be applicable to all smokers, regardless of their readiness to quit. The experimental group did not exhibit higher levels of motivation to quit, greater use of the provided cessation treatment, or higher abstinence rates at either follow-up compared to the control group. In fact, controls reported a higher level of motivation to quit at one year, were more likely to have used pharmacotherapy at six months and had a higher 30 day PPA rate at 6 months.
An important question when the intervention does not have a statistically significant benefit is whether the intervention is ineffective or whether the trial lacked statistical power to detect the intervention effect. To answer this question, confidence intervals were examined for PPA and treatment utilization. Confidence intervals (CI) indicate what range of effects, both positive and negative, are consistent with the trial data. Based on the 95% CI of -7.8% to +3.6% for the difference (intervention minus control) in 7 day ITT PPA at 6 months, our results are consistent with the true underlying effect of the intervention lying somewhere between a 3.6% decrease and a 7.8% increase in abstinence rates. In other words, one can rule out that the intervention increased abstinence rates by more than 3.6%. In contrast, one cannot rule out that the intervention may have decreased abstinence rates by up to about 8%. Virtually identical results were seen at one year: the 95% CI was -7.7% to +4.1% for ITT 7 day PPA. The 95% CI for the proportion enrolling in the provided cessation counseling program at one year was -13.0% to 2.2%, indicating that the intervention benefit was at most 2.2%, but the data are consistent with up to a 13% reduction in the utilization rate. In sum, we can rule out all but small benefits due to the intervention.
Several explanations for the lack of an experimental intervention effect should be considered. These may be considered caveats or study limitations. First, counseling smokers about their increased risk of lung disease and CO exposure simply may not be an effective way to promote cessation, or if so, it may require more than a one-time, brief intervention to present and discuss these risks. It is well-documented that abstinence is correlated with intervention dose. 25
The current study provided access to intensive counseling, but more proactive outreach may be required to motivate smokers to take advantage of this resource. Next, the control group received an active intervention, designed to match the experimental treatment in terms of contact time, focus on smokers’ health, and access to self-help materials and subsequent counseling. By holding these features constant, the additional contribution of the personalized smoking-risk assessment could be better evaluated. However, it is possible that the control intervention had an important effect on motivation, treatment utilization, and abstinence, which would explain the apparent trend toward better outcomes in the control group. Based on a meta-analysis of the literature, the estimated abstinence rates when no advice to quit or intervention are provided is 7.9%, 25
compared to the 14% - 15% 7 day PPA ITT rates seen among controls in this trial. Thus, if a no-treatment intervention had been given to controls, a more robust intervention effect may have been seen. The lack of an experimental treatment effect could also have resulted from the population studied. If the population were restricted to smokers ready to quit, rather than all smokers, participants might have been more receptive to change, but this would defeat the important goal of identifying interventions which are effective among all
smokers, not simply the minority ready to take action. It is also possible that the experimental intervention undermined motivation and attempts to quit smoking, rather than promoting them. Telling some smokers they had no demonstrable evidence of lung impairment may have inadvertently reinforced continued smoking, dampening abstinence rates in the experimental group. If this occurred, the impact was not substantial enough to have caused a marked treatment group difference in cessation outcomes, but the possibility of an unintended impact among some participants must be considered. Finally, abstinence rates may have been inflated by self-report, since biochemical verification was not obtained, but there is no reason to expect a response bias favoring the control intervention, given the nature of the minimal intervention. Biochemical verification is not recommended in this type of minimal contact intervention and may, in fact, introduce a selection bias unrelated to smoking status.33
Moreover, prior research has shown that the rate of under-reporting of smoking, particularly for brief intervention studies, is minimal. 41-43
This study has a number of strengths, including its focus on action-oriented behavioral outcomes (treatment utilization and quitting smoking), inclusion of all smokers and not just those ready to quit, the use of treatment records to verify enrollment in the provided phone program, and a well-controlled intervention design. Additional detail on the intervention and measures used to ensure treatment fidelity are discussed elsewhere.31
The use of an active control may have obscured an intervention effect, but it was a reasonable comparison group since our goal was to identify the unique contribution of the personalized, biologically-based, smoking-risk feedback on outcomes. From this perspective, the intervention did not have a significant effect.
In sum, the present study found no support for adding a personalized health risk assessment emphasizing lung health and CO exposure to generic cessation advice and counseling for community-based smokers not otherwise seeking treatment. Despite this, it would be premature to conclude that personalized risk assessments and motivational counseling cannot be an effective part of an intervention for smoking cessation. Recent evidence shows that smokers newly diagnosed with stroke, cancer, lung disease, heart disease, or diabetes are 3.2 times more likely to quit smoking compared to smokers not receiving a recent health diagnosis.44
Similar results have been reported by others.45-47
Thus, there is something about a change in one's health status that can be motivating for smoking cessation. However, it may be that increased disease risk alone is not sufficient to lead to sustained behavior change for most smokers and the absence of demonstrable health effects may undermine efforts to quit. As such, targeting smokers with new or worsening medical conditions may be more a useful strategy for using health-related feedback to promote cessation.