
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Short Communication |
1 National Human Genome Research Institute, Bethesda, Maryland; 2 Duke Comprehensive Cancer Center, Durham, North Carolina; and 3 North Carolina Central University, Chapel Hill, North Carolina
Requests for reprints: Colleen M. McBride, Social and Behavioral Research Branch, National Human Genome Research Institute, NIH, Room 4E08, Building 2, 2 Center Drive, Bethesda, MD 20892. Phone: 301-594-6788; Fax: 301-480-3108. E-mail: cmcbride{at}mail.nih.gov
| Abstract |
|---|
|
|
|---|
| Introduction |
|---|
|
|
|---|
African Americans who start smoking are less likely to quit smoking than Whites, making primary prevention of tobacco use an important public health priority (1). Moreover, because African American youth tend to adopt smoking at later ages, college settings may be optimal for evaluating primary prevention interventions (1, 2). Culturally targeted tobacco marketing and youth's optimistic perspectives about the chances of becoming nicotine dependent or experiencing the harms of tobacco use conspire against primary prevention efforts (1, 3). Smokers commonly perceive themselves to be less vulnerable to smoking-related harms than the generalized smoker, and this bias may be more accentuated among young smokers (4, 5).
Personalized risk feedback based on genetic markers of susceptibility to smoking-related harms could be used to dissuade young adults from experimenting with cigarette smoking. However, theoretical models of motivated reasoning and resistance to persuasion tell us that individuals are not passive recipients of risk information (6). Thus, greater personalization of risk information might increase the threat of risk messages and prompt self-defensively motivated processing of feedback. Moreover, these conceptual models suggest that smokers' interpretations of and responses to genetic susceptibility feedback will be moderated by factors, such as beliefs about the role of genetics in smoking-related disease risk, and their expectations about the test result. Smokers may respond more defensively to risk feedback, denoting higher risk if they believe that genetics plays a big role in disease development.
Although currently there are no clinically valid tests available to indicate susceptibility to lung cancer, >20 genes have been identified that are involved in the metabolism of nicotine and detoxification of carcinogens that cause lung cancer (7). The most consistent results implicate a common polymorphism in GSTM1, a gene in the family of glutathione S-transferases (EC 2.5.1.18), involved in signaling enzymes to metabolize a broad range of carcinogens (8). DNA adducts of tobacco smoke constituents in smokers with GSTM1-null genotype have been found to be higher than those in smokers with non-null genotype (9-11). These findings suggest that this type of genetic feedback may become available in the coming years.
This report describes data collected as part of a pilot study to explore the feasibility of evaluating a genetic susceptibility feedback intervention with African American college freshmen "at risk" of becoming regular cigarette smokers. The data was analyzed to assess the extent to which these young adults' beliefs about the association between genetics and lung cancer influence their expectations about test results if they were to undergo a hypothetical test for genetic susceptibility and, in turn, their interest in such testing.
| Materials and Methods |
|---|
|
|
|---|
Baseline Screening Survey
Demographics. Student's gender, date of birth, race, year in school, and whether or not they lived on campus were assessed.
Use of Cigarettes. Students were asked whether they had ever tried cigarette smoking, even a few puffs (no/yes), whether they had smoked in the last 30 and the last 7 days, and for each, the approximate number of cigarettes they had smoked on the days they smoked.
Susceptibility to Smoking. Three questions assessed susceptibility to smoking (12): (a) Do you think you will try a cigarette soon (no/yes)? (b) If one of your best friends were to offer you a cigarette, would you smoke it? (c) At any time during the next year, do you think you will smoke a cigarette? The response options for questions b and c were as follows: definitely yes, probably yes, probably not, and definitely not. Participants were deemed susceptible if they responded other than "no" to the first question and/or gave a response to question b or c other than "definitely not (12)." This screening tool has been shown in prospective studies to predict advancement in stage of adoption of cigarette smoking (12).
Genetic Measures
Three questions about genetic risk and related testing were included in the end-of-school year telephone survey (survey 2). Students were asked to rate the extent to which they believed that lung cancer was due to genetics on a scale from 0% to 100%, where 0% indicated genes are not at all involved and 100% indicated that genes were completely the cause of lung cancer. Level of interest in a "new genetic test that can tell whether someone is at higher or lower risk of getting lung cancer if they smoke" was assessed on a scale from 1 to 7, where 1 was not at all interested and 7 was extremely interested. Lastly, students' were asked if they were to have the genetic test, what they expected their results would show. Response options were higher risk or lower risk than other people.
| Results |
|---|
|
|
|---|
Of this 150 selected, 83% (n = 126) completed the first survey; 76% (95 of 125) completed survey 2 and comprise the sample for this report. Completion rates for survey 2 in the four "at-risk" groups described above were 79%, 84%, 70%, and 71%, respectively. Of those who completed survey 2, the majority was female, lived on campus, and the average age was 20 (SD, 2.6); just over half had experimented with smoking (Table 1).
|
Interest in testing was stronger among students who believed genetics plays a greater role in development of lung cancer (r = 0.22, P < 0.05) and among those who expected their result to show higher than average risk for lung cancer (r = 0.27, P < 0.05; Table 2). Additionally, those who believed genetics plays a greater role in lung cance P < 0.001).
|
|
| Discussion |
|---|
|
|
|---|
These results raise questions about how young at-risk smokers will respond to genetic susceptibility feedback if tested. Susceptibility testing for the GSTM1 null/null variant for example will identify
50% to 60% to be in the lower risk group. Thus, if tested, fully a quarter of these young adults would receive results, indicating that they were not at as high risk as they expected. Receipt of results discordant with expectations may motivate individuals to be biased in their processing of risk information (e.g., generalizing lower risk results for lung cancer to other smoking-related health outcomes; refs. 15, 16). Alternatively, results that confirm expectations may lead to fatalism about the benefits of not smoking, if individuals overestimate the role of genetics in determining risk.
It is notable that our sample of Black college freshmen expressed moderately high interest in undergoing the hypothetical genetic test. However, hypothetical scenarios that assess interest in or intention to be tested may overestimate interest in genetic testing (e.g., see ref. 17). It is likely that fewer of those at risk of becoming smokers would actually avail themselves of testing. It has been suggested that African Americans may be less enthusiastic about genetic testing when compared with Whites (18). However, we found that African Americans adults receiving care at a community clinic were very interested in genetic susceptibility testing for lung cancer (19). Similarly, others have found African American college students to hold generally positive attitudes towards medical applications of genetic testing and screening (20).
This small pilot study has several limitations. The genetic-related constructs were assessed using single items. The testing scenario was very general and did not provide specific details about the genetic test. For example, the brief narrative lacked any social contextual descriptors and, as such, may not have prompted critical review of the broader implications of such testing. Accordingly, we did not collect data on perceptions of stigmatization, insurance discrimination, or the scientific basis or validity of such testing. It is also noteworthy that more students who had experimented with smoking did not complete the end-of-year survey. This may have attenuated associations between smoking experimentation and other variables. The relatively small sample size limited power to explore interesting interactions among variables. The sample also was homogeneous with respect to race, education, and other demographics.
Despite these limitations, this study raises questions about the use of genetic susceptibility testing to motivate preventive behaviors that could be explored in future research with larger and more diverse samples. This research is important to pursue now as we anticipate the ways in which genetic susceptibility testing might be used in health promotion and public health interventions (21).
| Acknowledgments |
|---|
| Footnotes |
|---|
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 4/19/05; revised 7/11/05; accepted 9/21/05.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
S. C. Sanderson, S. E. Humphries, C. Hubbart, E. Hughes, M. J. Jarvis, and J. Wardle Psychological and Behavioural Impact of Genetic Testing Smokers for Lung Cancer Risk: A Phase II Exploratory Trial J Health Psychol, May 1, 2008; 13(4): 481 - 494. [Abstract] [PDF] |
||||
![]() |
J. Audrain-McGovern, C. Hughes Halbert, D. Rodriguez, L. H. Epstein, and K. P. Tercyak Predictors of Participation in a Smoking Cessation Program among Young Adult Smokers Cancer Epidemiol. Biomarkers Prev., March 1, 2007; 16(3): 617 - 619. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |