Genetic and environmental contributions to initiation of cigarette smoking in young African-American and European-American women
Introduction
More than one-third of 12th graders (17–18-year olds) in the U.S. report smoking at least one cigarette during the last year (Johnston et al., 2014) and approximately one in three adolescents who try cigarettes will progress from experimentation to regular smoking (Choi et al., 1997, Flint et al., 1998). The rate of cigarette use among adolescents is currently as high for girls as boys (Johnston et al., 2014) and according to the 2014 Report of the Surgeon General (U.S. Department of Health and Human Services, 2014), smoking related disease risks for women now equal those for men, highlighting the importance of identifying mechanisms underlying early smoking behaviors in adolescent girls and young women.
Genetic factors play a major role in the development and persistence of smoking behaviors. The heritability of regular smoking (generally defined as smoking 100 or more cigarettes over the lifetime) has been estimated from twin studies to be between 50% and 80% (Agrawal et al., 2005, Kendler et al., 1999, True et al., 1997, Vink et al., 2005), although studies that have found sex differences have reported somewhat lower estimates for women: 32–46% (Broms et al., 2006, Hamilton et al., 2006, Madden et al., 2004). Genetic contributions to the earliest stage of smoking, experimentation with cigarettes or initiation of smoking (i.e., ever smoking a cigarette), have not been as extensively investigated, but heritability estimates of smoking initiation are in the same range as those for regular smoking (Hardie et al., 2006, Maes et al., 2004, Maes et al., 2006, Seglem et al., 2015). The estimated contribution of shared environment – environmental influences that make members of a twin pair alike, such as common peers and parenting – to initiation of smoking is less consistent across studies but appears to vary systematically by age. For example, in Seglem et al.’s study of 12–18 year-old twins (2015) and Boomsma et al.’s study of 13–22 year-old twins (1994), shared environment accounted for 56% and 59%, respectively, of variance in smoking initiation, whereas neither Maes et al. (2004) nor Hardie et al. (2006) found any evidence for shared environmental influences in their studies based on middle aged twins.
The twin studies to date have been instrumental in developing etiological models of smoking initiation in individuals of European ancestry but have only rarely examined smoking behaviors in African Americans. Differences in smoking behaviors between African Americans and European Americans are well documented. There is consistent evidence that the lifetime prevalence of smoking (Hu et al., 2006, Lawrence et al., 2007) and risk for progression to regular smoking (Griesler et al., 2002, Kandel et al., 2004, Vega et al., 2007) are lower in African Americans than European Americans. African Americans also initiate smoking at an older age (Andreski and Breslau, 1993, Duncan et al., 2012, Mickens et al., 2010) and continue to smoke later into adulthood (Moon-Howard, 2003).
We are aware of only one large-scale twin study to examine smoking behaviors in African Americans, an earlier investigation by our group (Sartor et al., 2009) that was based exclusively on African-American (AA) young women. Consistent with prior studies based on adults of European ancestry, 62% of variance in initiation of smoking (ever smoking a cigarette) was attributable to genetics and the remainder to unique – also known as individual-specific – environmental influences (i.e., environmental influences not shared by family members); shared environment was not implicated. Although an important step toward improving our understanding of liability to smoking initiation among African Americans, in the absence of European-American (EA) participants, a direct comparison between racial/ethnic groups in the relative influence of genetic vs. environmental factors could not be made. The current study, which integrated data from female participants in a high-risk family study (52% AA) with data from female twin study participants (14% AA), was designed to test for differences between AA and EA young women in the relative contribution of genetic, shared environmental, and individual-specific environmental influences on initiation of cigarette smoking.
Section snippets
Methods
Data were drawn from the Missouri Adolescent Female Twin Study (MOAFTS) and the Missouri Family Study (MOFAM). Both studies were approved by Washington University's Human Research Protections Office. MOFAM was also approved by the Ethics Board of the State Department of Health and Senior Services (which was not required at the time that MOAFTS started).
Sibling pair correlations
Sibling pair correlations, calculated separately for AA and EA participants, are shown in Table 1. For MZ and DZ twin pairs (but not non-twin sibling pairs), correlations were lower in AA than EA participants, suggestive of an overall lesser degree of familial influence on initiation among AA than EA young women.
However, the correlations suggested the presence of genetic factors in both AA and EA subsamples. For African Americans, the DZ and non-twin sibling correlations were about half the
Discussion
The current investigation applied a twin-sibling modeling approach to identifying possible sources of distinctions in liability of AA vs. EA adolescent girls and young women to initiation of cigarette smoking. By expanding on our previous study based exclusively on AA twins (Sartor et al., 2009) through the incorporation of EA participants and integration of non-twin sibling pairs, we were able to detect racial/ethnic differences in the total contribution of familial influences to smoking
Role of funding sources
Funding for this study was provided by grants AA090022, AA011998, AA012640, AA017688, AA017915, AA017921, AA021492, and AA023549 from the National Institute on Alcohol Abuse and Alcoholism, grant DA23668 from the National Institute on Drug Abuse, grant HD049024 from the National Institute of Child Health and Human Development, and a grant from the Robert E. Leet and Clara Guthrie Patterson Trust.
The National Institutes of Health and the Robert E. Leet and Clara Guthrie Patterson Trust had no
Contributors
Dr. Sartor conducted the literature searches and wrote the first draft of the manuscript, Dr. Grant conducted the statistical analyses, and Dr. Agrawal provided consultation on analyses. Drs. Bucholz, Heath, and Madden designed the studies from which data were drawn and oversaw data collection. All authors provided input on the study design and edited the manuscript. All authors have approved the final manuscript.
Conflicts of interest
We have no conflicts of interest to declare.
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