Addictive Behaviors. Vol. 17, pp. 459--467, 1992
0306-4603/92 $5.00 + .00 Copyright © 1992 Pergamon Press Ltd.
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T H E I N T E R A C T I O N OF S O C I O L O G I C A L AND BIOLOGICAL FACTORS IN A D O L E S C E N T CIGARETI'E S M O K I N G KARL E. BAUMAN Department of Health Behavior and Health Education, The University of North Carolina at Chapel Hill
VANGIE A. FOSHEE Curriculum in Public Health Nursing, School of Public Health, The University of North Carolina at Chapel Hill
NANCY J. HALEY American Health Foundation Abstract - - This article considers the interaction of social and biological factors in the context of adolescent cigarette smoking. Parent and peer smoking are the sociological variables and testosterone is the biological indicator. The subjects are 212 males and females 12-14 years of age. The findings support the interaction model, suggesting that both sociological and biological factors are necessary for understanding adolescent smoking.
That smoking by parents and peers are among the most consistent and strongest correlates of smoking by adolescents often is considered evidence that social factors cause people to become cigarette smokers (Bell & Battjes, 1985; Best, Thomson, Santi, Smith, & Brown, 1988; Bonaguro & Bonaguro, 1989; Botvin & McAlister, 1982; Cleary, Hitchcock, Semmer, Flinchbaugh, & Pinney, 1988; Flay, d'Avernas, Best, Kersell, & Ryan, 1983; Glynn, 1981, 1984; Perry & Murray, 1985; U.S. Department of Health and Human Services, 1979, 1989). The correlations often are explained by reasoning that parents and friends who smoke portray norms and attitudes favorable to smoking, make cigarettes more readily available, or serve as models for smoking. A very different perspective is that cigarette smoking has a biological origin. Genetics has been given as an explanation for the tendency for smoking by children whose parents or older siblings also smoke (Hughes, 1986). Adoption and twin studies also suggest a biological basis for smoking onset (Eysenck, 1980; Hughes, 1986). In a comprehensive review of smoking and health by the Surgeon General of the United States (U.S. Department of Health and Human Services, 1979), two observations were offered to suggest that biological factors may be implicated in smoking initiation: (a) cigarette smoking increases sharply during adolescence, a period in the life cycle when dramatic physical changes occur, and (b) there are interrelationships among some personality characteristics, hormonal changes, and cigarette smoking. This evidence is indirect and the relationships could be spurious. Evidence more difficult to dismiss is the positive association between testosterone and smoking among boys and girls in early adolescence (Bauman, Foshee, Koch, Haley, & Downton, 1989). Testosterone, a hormone secreted by the ovaries and adrenal glands in females and by the testes in males, is the masculinizing hormone that stimulates body hair and musThis research was supported by Grant CA38392 from the National Cancer Institute of the National Institutes of Health. Thanks to Connie Padgett and J. Richard Udry for comments on earlier drafts of this paper. Requests for reprints should be sent to Karl E. Bauman, University of No. Carolina. Dept. of Health Behavior and Health Education, CB #7400, Rosenau Hall, Chapel Hill, NC 27599-7400. 459
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K . E . B A U M A N et al.
cle growth (Maroulis, 1981). How testosterone might lead to smoking is unknown and our present purpose excludes empirical examination of the explanation. We offer these speculations for the association. First, a major feature of adolescence is that it is when children first experiment with a wide range of adult behaviors. Perhaps the awareness of newly acquired adult physical characteristics that follows increased testosterone levels signals the onset of adolescence and a time to begin experimenting with adult behaviors, such as smoking. Second, a completely different line of explanation for the association between testosterone and smoking in adolescence is that testosterone and a wide variety of personality and behavioral characteristics are related (Baucom, Besch, & Callahan, 1985; Daitzman & Zuckerman, 1980; Doering et al.. 1975; Kemper, 1990; Olweus, Mattsson, Schalling, & Low, 1980; Persky, Smith, & Basu, 1971; Susman, Nottelmann, Inoff-Germain, Dorn, & Chrousos, 1987; Udry & Talbert, 1988) and also related to cigarette smoking (Cherry & Kiernan, 1976: Seltzer & Oechsli, 1985; U.S. Department of Health and Human Services, 1979). For example, sensation seeking, low socialization, and extraversion correlate positively with both smoking and testosterone (Zuckerman, 1991). Perhaps personality characteristics mediate the testosterone-smoking relationship. Third, biological factors may be the direct and proximate determinants of adolescent smoking. Whether these or other explanations account for the relationship between testosterone and smoking remain considerations for future research. In this study, we incorporate biological and social variables in an interaction model because it is common in social biology (Ehrhardt, 1985; Gove, 1985; Ladewig, Thoma, & Scanozi, 1988; Rowe & Osgood, 1984; Schuckit, 1980; Ud~' & Talbert, 1988). We view parent and peer smoking as interacting with testosterone to influence smoking. Our reasoning is that testosterone has the tendency to influence smoking onset through its impact on mediating factors, such as the development of adult physical characteristics or personality attributes, or it may have more proximate effects. Social variables, as reflected by friend and parent smoking, modify the influence: testosterone influences smoking only if the adolescent experiences norms and attitudes favorable toward smoking, cigarettes are readily available, or models support smoking. Another way of viewing the same interaction is to reason that social variables do not influence cigarette smoking onset until the consequences of testosterone (such as, personality, behavioral, or physical characteristics) have been realized. The purpose of this study is to determine whether parent or peer smoking and testosterone interact in their relationship to adolescent smoking. METHODS
In 1985, baseline data were collected for a field experiment to evaluate the impact of mass media campaigns on adolescent cigarette smoking (Bauman, LaPrelle, Brown, Koch, & Padgett, 1991). The data are from probability samples of adolescents 12-14 years of age in 10 Standard Metropolitan Statistical Areas of the southeast United States. Questionnaires with items on media use, smoking attitudes and behavior, and general social and psychological characteristics were self-administered to 2,102 adolescents in their homes. Recent smoking was measured by carbon monoxide in alveolar breath samples (Bauman & Koch, 1983). Each adolescent subject deposited 1.5 m of saliva into a vial. The saliva was frozen on the day of collection and stored until analysis for testosterone. Expense precluded obtaining testosterone values for all subjects. Testosterone was measured for the 71 sub-
Sociological and biological factors in adolescent smoking
461
jects who had smoked recently as indicated by having carbon monoxide >__ 9 ppm in their alveolar breath. One hundred fifty subjects were randomly selected from those with carbon monoxide < 9 ppm and their saliva was analyzed for testosterone. Our total sample, therefore, consists of 221 adolescents. Sample sizes vary slightly across analyses because of missing information. Coat-A-Count Total Testosterone measured free testosterone in saliva (Diagnostic Products Corporation, 1987). The original protocol was modified as follows because the samples were saliva rather than serum. (a) To remove debris, the samples were centrifuged for 2 min in an Eppendorf centrifuge at 11,500 revolutions per minute. (b) The assay was incubated for 3 h at 37"C. (c) The value for each sample was calculated as for serum, except that the result was divided by 9 to adjust for the larger volume used to analyze saliva. No serum samples were obtained for this study. Preliminary analyses revealed two extreme testosterone values for females and more variance for females than for males. The square root of the testosterone value was used to adjust for extreme values. To measure parent smoking, adolescents were asked how many cigarettes they thought each parent smoked in a day. A value of 0 was assigned if the parent did not smoke daily and a value of I if they did. The question was not asked about parents who did not live in the household. For example, subjects without fathers living in the household are excluded from analyses that involve father smoking. The adolescents also were asked how often they thought their best friend smoked cigarettes. A value of 0 was assigned if the best friend did not smoke and a value of I ifthey did. Adolescent smoking is measured with a commonly used four-category self-report measure that ranges from being a nonsmoker (code = 0) to smoking half a pack of cigarettes or more per week (code = 3) (National Cancer Institute, 1986). Subjects were told before completing the questionnaire that the alveolar breath and saliva samples would indicate their smoking behavior, a procedure that earlier studies show increases the validity of self-reports of smoking by adolescents (Bauman & Dent, 1982; Murray, O'Connell, Schmid, & Perry, 1987). We included four other variables in regression analyses to assure that they did not produce a spurious association between testosterone and smoking. Adolescent age (code 0 = age 12, code l = age 13, code 2 = age 14-15), race (code 0 = nonwhite, code l = white,), and sexual behavior (code 0 = virgin, code l = nonvirgin) were controlled because earlier studies found them related to both testosterone and cigarette smoking. Deviance also was controlled. Subjects were asked if they had ever drunk alcohol, cheated on a test, cut school or class, smoked marijuana, driven a car without permission, or stolen something worth more than $10. Positive responses were coded as 1 and negative and missing responses were coded as 0. Deviance was the number of items with code -- l divided by the number of items. Because the testosterone levels for males and females differ and because the social influence processes in the interaction models could vary substantially by gender, all analyses were conducted separately for males and females. FINDINGS
For males, there is a statistically significant interaction involving testosterone and friend smoking (Table 1). This interaction remains statistically significant when controlling for race, age, sexual behavior, and deviance. The interaction is in the predicted direction of (a) stronger relationships between friend smoking and adolescent smoking
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Table 1. SummaD' statistics from multiple regression analyses involving testosterone and parent and peer smoking with adolescent smoking as the dependent variable Male
Female
Independent variable
/3
p
n
/3
p
n
Testosterone (T) Mother smoking (M) T X M (uncontrolled) T X M (controlled) a
.01 .03 .00 .00
.13 .91 .79 .99
97 97 97 93
- .01 -.05 -.06 .05
.64 .88 .03* .05*
100 100 100 98
Testosterone (T) Father smoking (F) T × F (uncontrolled) T X F(controlled)"
.01 .18 .02 .02
.25 .56 .26 .18
82 82 82 79
.02 .16 .00 .04
.45 .71 .99 .22
82 82 82 80
Testosterone(T) Friend smoking (F) T X F(uncontrolled) T X F (controlled) a
.01 .35 .03 .02
.45 .18 .03* .04*
103 103 103 99
.01 1.28 .01 .03
.52 .00"* .69 .24
107 107 t07 101
*p < .05. **p < .01. aThe controls are race. age, sexual behavior, and deviance.
for males at the highest testosterone levels (Table 2) and (b) stronger relationships between testosterone and adolescent smoking for males whose friends smoke than for males whose friends do not smoke (Table 3). For males, there is no statistically significant interaction involving parent smoking and testosterone. Collinearity diagnostics indicated that the statistically insignificant interactions are not due to large correlations between the independent variables and the interaction terms. For females, there is a statistically significant interaction of mother smoking and testosterone in adolescent smoking that remains statistically significant when controlled for race, age, sexual behavior, and deviance (Table 1). The interactions are in the expected direction of (a) stronger relationships between mother and adolescent smoking for the highest testosterone levels (Table 2) and (b) a stronger relationship between testosterone and smoking for females whose mothers smoke than for females whose mothers do not smoke (Table 3). For females there are no interactions involving testosterone and father or friend smoking. Multicollinearity between the independent variables and the interaction terms do not produce statistical insignificance.
Table 2. Correlations between adolescent smoking and parent and peer smoking by testosterone Male testosterone
Female testosterone
Social referent
High
Medium
Low
High
Medium
Low
Mother (n) Father (n) Friend (n)
.03 (34) .34 (29) .52** (35)
-.01 (30) .27 (27) .52** (34)
-.01 (33) .16 (26) .39* (34)
.35* (34) .07 (26) .53** (34)
.45** (33) .09 (32) .77** (35)
-.09 (33) ,09 (24) .67** (34)
*p < .05. **p < .01.
Sociological and biological factors in adolescent smoking
463
Table 3. Correlations (Spearman p) between testosterone and adolescent smoking by parent and peer smoking Male Smoking
Female
P
(n)
Mother Yes
.20
(44)
No
.25
(53)
-.02
(53)
.37* .17
(39) (43)
.12 .20
(48) (34)
.38* .22
(35) (68)
.10 .19
(50) (53)
Father Yes No Friend Yes No
p
(n)
.34*
(47)
*p < .05.
DISCUSSION
AND
CONCLUSION
The biological and sociological variables interact in their relationship to adolescent smoking. The interaction varies, however, by adolescent gender and by whether the smoking of the mother, father, or friend is the referent. Possible explanations for the variation in interaction patterns are discussed here. Mother smoking and testosterone interact in relationship to daughter smoking, but there is no interaction between father smoking and testosterone. Differential parent influence might explain this. Females model mothers more than fathers (Jacklin, 1989; Mischel, 1966), mothers have the primary responsibility for child socialization, and mothers may be more involved than fathers in norm setting and in expressing attitudes related to smoking. Our findings that mother and daughter smoking are associated, but that father and daughter smoking are not (Table 2), are consistent with these propositions. Under these conditions, mother smoking and its association with other variables, such as norms, attitudes, and modeling, would be more effective than father smoking in modifying the influence of testosterone on daughter smoking. Testosterone and mother smoking interact with smoking for females but not for males. Perhaps this occurs because mothers influence daughters more than sons. Compared to males, for example, females are socialized to be more dependent on their mothers (Simmons & BIyth, 1987), they are more closely supervised (Clausen, 1968), they comply more to parental expectations and rules (Douvan & Adelson, 1966; Simmons & BIyth, 1987), and they are more accepting of mother control (Clausen, 1968). The correlations in Table 2 show that mother smoking is related to daughter smoking but not son smoking, which is consistent with the more general principle that mothers influence daughters more than sons. Perhaps differential influence by mothers on daughters and sons explains why mother smoking modifies the relationship between testosterone and smoking for daughters but not sons. Another possible explanation for the finding that mother smoking modifies the influence of testosterone on smoking by females but not males involves the interrelationship of three propositions. First, for children the ages of those in our sample, females are more physically developed than the males: the testosterone level of females has nearly peaked, whereas the testosterone of males will increase substantially during their next several years (Sizonenko, 1978) and females appear more physically mature than males
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(Petersen & Taylor, 1980; Sizonenko, 1978). Second, a child's physical development may activate the mother's socialization of her child specific to adolescent behaviors (Hamburg. 1974; Hill & Lynch, 1983), including the mother's expression to her child of norms and attitudes related to the child's smoking. Third, mothers who do not smoke may have more tendency than those who do smoke to express more unfavorable norms and attitudes toward smoking to their child. Therefore, among adolescents 12-14 years of age, testosterone may increase smoking for females whose mothers smoke but not for those whose mothers do not smoke, and this does not occur for males the same ages because relatively few of them have reached the stage of physical development necessary to activate their mother's socialization processes related to smoking. According to this reasoning, when the males in our sample are several years older they too may exhibit an interaction between their own smoking and the smoking of their mothers. A different line of reasoning for the interaction of testosterone with mother smoking for females but not males also is related to the age differential in puberty, but uses modeling to explain the gender difference in the interaction. Adolescents may associate puberty and smoking with adulthood, and puberty may increase the adolescent's attention to. and modeling of, parent behavior. Because more females than males had reached puberty, the females may have been more likely than the males to have modeled adult smoking. Friend smoking and testosterone interact with smoking by males but not smoking by females. Friend and adolescent smoking are associated for both genders in our sample (Table 2). suggesting that the difference is not explained by peers having more influence on males than females. Perhaps the stronger parental influence for females than males described above counteracts the influence of peers more for females than for males (Clausen, 1968). A limitation of our study is that the data are cross-sectional; panel data are more approporiate for many of our interpretations. We have reasoned, for example, that the association between friend and adolescent smoking reflects peer influence, but that association also indicates that adolescents who smoke are likely to choose friends who smoke (Fisher & Bauman, 1988). Similarly, we assume that parent smoking influences adolescent smoking, as suggested by the literature on the relationship between parent and adolescent smoking. It is possible, however, that child smoking influences parent smoking. Finally, no studies of adolescents allow definitive identification of the direction of the relationship between testosterone and smoking. The two experiments conducted with adults found that increasing smoking either decreases (Briggs, 1973) or does not change (Winternitz & Quillen, 1977) testosterone levels, supporting our assumption that testosterone is a cause rather than a consequence of smoking. However, the possibility remains that among adolescents smoking causes an increase in testosterone. Another possible limitation of our study is that we have considered the association between parent and adolescent smoking to reflect social factors even though it may be partially genetic (Hughes, 1986). Moreover, although the relationship between peer and adolescent smoking may be of social origin, it could be biological if parents smoke for genetic reasons and encourage friendships for their children on the basis of their behavioral preferences (Hansen et al., 1987). We are unable to remove all possible sources of confounding of biological and sociological factors in some of our measures and associations. Limitations of the measurement of testosterone include intra-individual (Dai et al., 1981; Mattsson, Schalling, Olweus, Low, & Svensson, 1980), daily (Dai et al., 1981;
Sociological and biological factors in adolescent smoking
465
Dotson, Robertson, & Tuchfeld, 1975), seasonal (Dai et al., 1981), and menstrual cycle (Udry, Talbert, & Morris, 1986) variation in testosterone. We obtained the saliva specimens when it was convenient to subjects, data collectors, and the time frame for our research plan. This procedure could have produced measures of testosterone that reduced the strength of their association with smoking, and we would have preferred more refined measurement. The correlation between testosterone and smoking under these conditions suggests that our findings are particularly robust. In conclusion, our findings suggest that the appropriate consideration of adolescent smoking requires recognition of the interaction of sociological and biological factors. The interactions vary by adolescent gender and whether the mother, father, or peer smokes. Future research is needed to test the explanations for the interactions, to explain exceptions to the interaction model, and to establish the directions of the relationships.
REFERENCES Baucom. D. H.. Besch. P. K., & Callahan. S. (1985). Relation between testosterone concentration, sex role identity, and personality among females. Journal of Personality and Social Psychology, 48, 1218-1226. Bauman. K. E., & Dent, C. W. (1982). Influence of an objective measure on self-reports of behavior. Journal of Applied Psychology, 67, 623-628. Baumano K. E., Foshee. V. A., Koch, G. G.. Haley, N. J., & Downton, M. 1. (1989). Testosterone and cigarette smoking in early adolescence. Journal of Behavioral Medicine, 12, 425-433. Bauman, K. E., & Koch, G. G. (1983). Validity of self-reports and descriptive and analytical conclusions: The case of cigarette smoking by adolescents and their mothers. American Journal ofEpidemiology, 118, 9098. Bauman. K. E., LaPrelle, J., Brown, J. D., Koch, G. G., & Padgett, C. A. ( 1991). The influence of three mass media campaigns on variables related to adolescent cigarette smoking: Results of a field experiment. A merican Journal of Public Health, 81, 597-604. Bell. C. S.. & Battjes. R. (1985). Prevention research: Deterring drug abuse among children and adolescents. Washington. DC: U.S. Government Printing Office. Best. J. A.. Thomson, S. J., Santi, S. M., Smith, E. A., & Brown, K. S. (1988). Preventing cigarette smoking among school children. Annual Review of Public Health. 9, 161-201. Bonaguro. E. W.. & Bonaguro, J. A. (1989). Tobacco use among adolescents: Directions for research. American Journal of Health Promotion, 4, 37-4 I. Botvin, G.. & McAlister, A. (1982). Cigarette smoking among children and adolescents: Causes and prevention. In C. B. Arnold (Ed.), Advances in disease prevention (pp. 222-249). New York: Springer. Briggs. M. H. (1973). Cigarette smoking and infertility in men. The Medical Journal ofA ustralia, 1, 616-617. Cherry. N.. & Kiernan, K. (1976). Personality scores and smoking behaviour: A longitudinal study. British Journal of Preventive and Social Medicine, 30, 123-131. Clausen. J. (1968). Sociali:ation and society. Boston: Little, Brown & Co. Clearl¢. P. D., Hitchcock, J. L., Semmer, N., Flinchbaugh, L. J., & Pinney, J. M. (1988). Adolescent smoking: Research and health policy. The Milbank Memorial Fund Quarterly, 66, 137-17 I. Dai. W. S.. Kuller. L. H., LaPorte, R. E., Gutai, J. P., Falvo-Gerard, L., & Caggiula, A. (1981). The epidemiology of plasma testosterone levels in middle-aged men. American JournalofEpidemiology, 114, 804816. Daitzman. R., & Zuckerman, M. (1980). Disinhibitory sensation seeking, personality and gonadal hormones. Personality and Individual Differences, 1, 103-110. Diagnostic Products Corporation. (1987). Coat-a-count: Total testosterone. Los Angeles, CA: Author. Doering. C. H., Brodie, K. H., Kraemer. H. C., Mops, R. H., Becker, H. B., & Hamburg, D. A. (1975). Negative affect and plasma testosterone: A longitudinal human study. Psychosomatic Medicine. 37, 484491. Dotson, L. E., Robertson, L. S., & Tuchfeld, B. (1975). Plasma alcohol, smoking, hormone concentrations and self-reported aggression: A study in a drinking situation. Journal of Studies on Alcohol. 36, 578-586. Douvan. E.. & Adelson, J. (1966). Tile adolescent experience. New York: Wiley. Ehrhardt. A. A. (1985). The psychobiology of gender. In A. S. Rossi (Ed). Gender and the life course (pp. 8196). New York: Aldine. Eysenck. H. J. (1980). The causes and effects of smoking. Beverly Hills, CA: Sage Publications.
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Fisher, L. A., & Bauman, K. E. (1988). Influence and selection in the friend-adolescent relationship: Findings from studies of adolescent smoking and drinking. Journal of Applied Social Psychology. 18, 289-314. Flay. B. R., d'Avernas, J. R., Best. J. A.. Kersell, M. W.. & Ryan, K. B. (1983). Cigarette smoking: Why young people do it and ways of preventing it. In P. J. McGrath & P. Firestone (Eds.), Pediatric and adolescent behavioral medicine: Issues in treatment (pp. 132-183). New York: Springer. Glynn. T. J. ( 1981 ). From family to peer: A review of transitions of influence among drug-using youth. Journal ~/"Youth and Adolescence. 10, 365-383. Glynn, T. J. (1984). Adolescent drug use and the family environment: A review. Journal ~?lDrttgIssues. 14, 271-295. Gore, W. R. (1985). The effect of age and gender on deviant behavior: A biopsychosocial perspective. In A. S. Rossi (Ed.), Gender and the life course (pp. 115-144). New York: Aldine. Hamburg. B. A. (1974). Early adolescence: A specific and stressful stage of the life cycle. In G. V. Coelbo. D. A. Hamburg, & J. E. Adams (Eds.). Coping and adaptation (pp. 101-124). New York: Basic Books. Hansen, W. B.. Graham, J. W., Sobel, J. L.. Shelton. D. R., Flay, B. R., & Johnson, C. A. (1987). The consistency of peer and parental influences on tobacco, alcohol, and marijuana use among young adolescents. Journal of Behavioral Medicine. 10, 559-579. Hill. J. P., & Lynch. M. E. (1983). The intensification of gender-related role expectations during early adolescence, In J. Brooks-Gunn & A. C. Petersen (Eds.), Girls at puberty: Biological and ps)'ehoh~giealperspeetives (pp. 201-228). New York: Plenum. Hughes, J. R. (1986). Genetics of smoking: A brief review. Behavior Therapy. 17, 335-345. Jacklin, C. N. (1989). Female and male: Issues of gender. American Psychologist. 44 (February), 127-133. Kemper, T. D. (1990). Social structure and testosterone. New Brunswick, N J: Rutgers University Press. Ladewig, B. H., Thoma, S. J., & Scanozi. J. H. (1988). Sociobiology and the family: A focus on the interplay between social science and biology. In E. E. Filsinger (Ed.). Biosocialperspectives on thefamily(pp. 173187). Newbury Park, CA: Sage. Maroulis. G. B. (1981). Evaluation and hirsutism and hyperandrogenemia. Fertility and Sterility. 36, 273305. Mattsson, A., Schalling, D., Olweus, D.. Low, H.. & Svensson, J. (1980). Plasma testosterone, aggressive behavior, and personality dimensions in young male delinquents. Journal ~['the American Academy ~g Child Psyehiato'. 19, 476-490. Mischel. W. (1966). A social-learning view of sex differences in behavior. In E. E. Maccoby (Ed.), The development of sex differemws (pp. 56-81 ). Stanford, CA: Stanford University Press. Murray, D. M., O'Connell, C. M., Schmid, L. A., & Perry, C. L. (1987). The validity of smoking self-reports by adolescents: A reexamination of the bogus pipeline procedure. Addictive Behaviors. 12, 7-15. National Cancer Institute. (1986). Smoking. tobacco, and cancer program: 1985 report. Bethesda, M D: U.S. Department of Health and Human Services. Olweus. D., Mattsson, A., Schalling, D,, & Low, H. (1980). Testosterone, aggression, physical, and personalit.~ dimensions in normal adolescent males. Psychosomatic Medicine. 42, 253-269. Perry, C. L., & Murray, D. M. (1985). The prevention of adolescent drug abuse: Implications from etiological, developmental, behavioral, and environmental models. Journal Q['Primao" Prevention. 6, 31-52. Persk.v, H., Smith. K. D., & Basu, G. K. ( 1971 ). Relation of psychologic measures ofaggression and hostilit3 to testosterone production in man. Psychosomatic Medicine. 33, 265-277. Petersen, A. C.. & Taylor, B. (1980). The biological approach to adolescence: Biological change and psychological adaptation. In J. Adelson (Ed.), Handbook of adolescent psyeholog.v (pp. 117-155). New York: Wiley. Rowe, D. C., & Osgood, D. W. (1984), Heredity and sociological theories of delinquency: A reconsideration. American Sociological Review. 49, 526-540. Schuckit, M. A. (1980). A theory of alcohol and drug abuse: A genetic approach. In D. J. Lettieri, M. Sayers, & H. W. Pearson (Eds.), Theories on drug abuse: Selected contemporao" perspectives (pp. 297-3021. Washington, DC: U.S. Government Printing Office. Seltzer, C. C.. & Oechsli, F. W. (1985). Psychosocial characteristics of adolescent smokers before they started smoking: Evidence of self-selection. Journal of Chronic Diseases. 38, 17-26. Simmons, R. G.. & Blyth, D. A. (1987). Moving into adolescence: The impact of pubertal change and school context. New York: Aldine De Gruyter. Sizonenko, P. C. (1978). Endocrinology in preadolescents and adolescents. American Journal of Diseases in Children. 132, 704-712. Susman, E. J., Nottelmann. E. D., lnoff-Germain, G., Dorn, L. D., & Chrousos. G. P. (1987). 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T H E I N T E R A C T I O N OF S O C I O L O G I C A L AND BIOLOGICAL FACTORS IN A D O L E S C E N T CIGARETI'E S M O K I N G KARL E. BAUMAN Department of Health Behavior and Health Education, The University of North Carolina at Chapel Hill
VANGIE A. FOSHEE Curriculum in Public Health Nursing, School of Public Health, The University of North Carolina at Chapel Hill
NANCY J. HALEY American Health Foundation Abstract - - This article considers the interaction of social and biological factors in the context of adolescent cigarette smoking. Parent and peer smoking are the sociological variables and testosterone is the biological indicator. The subjects are 212 males and females 12-14 years of age. The findings support the interaction model, suggesting that both sociological and biological factors are necessary for understanding adolescent smoking.
That smoking by parents and peers are among the most consistent and strongest correlates of smoking by adolescents often is considered evidence that social factors cause people to become cigarette smokers (Bell & Battjes, 1985; Best, Thomson, Santi, Smith, & Brown, 1988; Bonaguro & Bonaguro, 1989; Botvin & McAlister, 1982; Cleary, Hitchcock, Semmer, Flinchbaugh, & Pinney, 1988; Flay, d'Avernas, Best, Kersell, & Ryan, 1983; Glynn, 1981, 1984; Perry & Murray, 1985; U.S. Department of Health and Human Services, 1979, 1989). The correlations often are explained by reasoning that parents and friends who smoke portray norms and attitudes favorable to smoking, make cigarettes more readily available, or serve as models for smoking. A very different perspective is that cigarette smoking has a biological origin. Genetics has been given as an explanation for the tendency for smoking by children whose parents or older siblings also smoke (Hughes, 1986). Adoption and twin studies also suggest a biological basis for smoking onset (Eysenck, 1980; Hughes, 1986). In a comprehensive review of smoking and health by the Surgeon General of the United States (U.S. Department of Health and Human Services, 1979), two observations were offered to suggest that biological factors may be implicated in smoking initiation: (a) cigarette smoking increases sharply during adolescence, a period in the life cycle when dramatic physical changes occur, and (b) there are interrelationships among some personality characteristics, hormonal changes, and cigarette smoking. This evidence is indirect and the relationships could be spurious. Evidence more difficult to dismiss is the positive association between testosterone and smoking among boys and girls in early adolescence (Bauman, Foshee, Koch, Haley, & Downton, 1989). Testosterone, a hormone secreted by the ovaries and adrenal glands in females and by the testes in males, is the masculinizing hormone that stimulates body hair and musThis research was supported by Grant CA38392 from the National Cancer Institute of the National Institutes of Health. Thanks to Connie Padgett and J. Richard Udry for comments on earlier drafts of this paper. Requests for reprints should be sent to Karl E. Bauman, University of No. Carolina. Dept. of Health Behavior and Health Education, CB #7400, Rosenau Hall, Chapel Hill, NC 27599-7400. 459
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cle growth (Maroulis, 1981). How testosterone might lead to smoking is unknown and our present purpose excludes empirical examination of the explanation. We offer these speculations for the association. First, a major feature of adolescence is that it is when children first experiment with a wide range of adult behaviors. Perhaps the awareness of newly acquired adult physical characteristics that follows increased testosterone levels signals the onset of adolescence and a time to begin experimenting with adult behaviors, such as smoking. Second, a completely different line of explanation for the association between testosterone and smoking in adolescence is that testosterone and a wide variety of personality and behavioral characteristics are related (Baucom, Besch, & Callahan, 1985; Daitzman & Zuckerman, 1980; Doering et al.. 1975; Kemper, 1990; Olweus, Mattsson, Schalling, & Low, 1980; Persky, Smith, & Basu, 1971; Susman, Nottelmann, Inoff-Germain, Dorn, & Chrousos, 1987; Udry & Talbert, 1988) and also related to cigarette smoking (Cherry & Kiernan, 1976: Seltzer & Oechsli, 1985; U.S. Department of Health and Human Services, 1979). For example, sensation seeking, low socialization, and extraversion correlate positively with both smoking and testosterone (Zuckerman, 1991). Perhaps personality characteristics mediate the testosterone-smoking relationship. Third, biological factors may be the direct and proximate determinants of adolescent smoking. Whether these or other explanations account for the relationship between testosterone and smoking remain considerations for future research. In this study, we incorporate biological and social variables in an interaction model because it is common in social biology (Ehrhardt, 1985; Gove, 1985; Ladewig, Thoma, & Scanozi, 1988; Rowe & Osgood, 1984; Schuckit, 1980; Ud~' & Talbert, 1988). We view parent and peer smoking as interacting with testosterone to influence smoking. Our reasoning is that testosterone has the tendency to influence smoking onset through its impact on mediating factors, such as the development of adult physical characteristics or personality attributes, or it may have more proximate effects. Social variables, as reflected by friend and parent smoking, modify the influence: testosterone influences smoking only if the adolescent experiences norms and attitudes favorable toward smoking, cigarettes are readily available, or models support smoking. Another way of viewing the same interaction is to reason that social variables do not influence cigarette smoking onset until the consequences of testosterone (such as, personality, behavioral, or physical characteristics) have been realized. The purpose of this study is to determine whether parent or peer smoking and testosterone interact in their relationship to adolescent smoking. METHODS
In 1985, baseline data were collected for a field experiment to evaluate the impact of mass media campaigns on adolescent cigarette smoking (Bauman, LaPrelle, Brown, Koch, & Padgett, 1991). The data are from probability samples of adolescents 12-14 years of age in 10 Standard Metropolitan Statistical Areas of the southeast United States. Questionnaires with items on media use, smoking attitudes and behavior, and general social and psychological characteristics were self-administered to 2,102 adolescents in their homes. Recent smoking was measured by carbon monoxide in alveolar breath samples (Bauman & Koch, 1983). Each adolescent subject deposited 1.5 m of saliva into a vial. The saliva was frozen on the day of collection and stored until analysis for testosterone. Expense precluded obtaining testosterone values for all subjects. Testosterone was measured for the 71 sub-
Sociological and biological factors in adolescent smoking
461
jects who had smoked recently as indicated by having carbon monoxide >__ 9 ppm in their alveolar breath. One hundred fifty subjects were randomly selected from those with carbon monoxide < 9 ppm and their saliva was analyzed for testosterone. Our total sample, therefore, consists of 221 adolescents. Sample sizes vary slightly across analyses because of missing information. Coat-A-Count Total Testosterone measured free testosterone in saliva (Diagnostic Products Corporation, 1987). The original protocol was modified as follows because the samples were saliva rather than serum. (a) To remove debris, the samples were centrifuged for 2 min in an Eppendorf centrifuge at 11,500 revolutions per minute. (b) The assay was incubated for 3 h at 37"C. (c) The value for each sample was calculated as for serum, except that the result was divided by 9 to adjust for the larger volume used to analyze saliva. No serum samples were obtained for this study. Preliminary analyses revealed two extreme testosterone values for females and more variance for females than for males. The square root of the testosterone value was used to adjust for extreme values. To measure parent smoking, adolescents were asked how many cigarettes they thought each parent smoked in a day. A value of 0 was assigned if the parent did not smoke daily and a value of I if they did. The question was not asked about parents who did not live in the household. For example, subjects without fathers living in the household are excluded from analyses that involve father smoking. The adolescents also were asked how often they thought their best friend smoked cigarettes. A value of 0 was assigned if the best friend did not smoke and a value of I ifthey did. Adolescent smoking is measured with a commonly used four-category self-report measure that ranges from being a nonsmoker (code = 0) to smoking half a pack of cigarettes or more per week (code = 3) (National Cancer Institute, 1986). Subjects were told before completing the questionnaire that the alveolar breath and saliva samples would indicate their smoking behavior, a procedure that earlier studies show increases the validity of self-reports of smoking by adolescents (Bauman & Dent, 1982; Murray, O'Connell, Schmid, & Perry, 1987). We included four other variables in regression analyses to assure that they did not produce a spurious association between testosterone and smoking. Adolescent age (code 0 = age 12, code l = age 13, code 2 = age 14-15), race (code 0 = nonwhite, code l = white,), and sexual behavior (code 0 = virgin, code l = nonvirgin) were controlled because earlier studies found them related to both testosterone and cigarette smoking. Deviance also was controlled. Subjects were asked if they had ever drunk alcohol, cheated on a test, cut school or class, smoked marijuana, driven a car without permission, or stolen something worth more than $10. Positive responses were coded as 1 and negative and missing responses were coded as 0. Deviance was the number of items with code -- l divided by the number of items. Because the testosterone levels for males and females differ and because the social influence processes in the interaction models could vary substantially by gender, all analyses were conducted separately for males and females. FINDINGS
For males, there is a statistically significant interaction involving testosterone and friend smoking (Table 1). This interaction remains statistically significant when controlling for race, age, sexual behavior, and deviance. The interaction is in the predicted direction of (a) stronger relationships between friend smoking and adolescent smoking
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Table 1. SummaD' statistics from multiple regression analyses involving testosterone and parent and peer smoking with adolescent smoking as the dependent variable Male
Female
Independent variable
/3
p
n
/3
p
n
Testosterone (T) Mother smoking (M) T X M (uncontrolled) T X M (controlled) a
.01 .03 .00 .00
.13 .91 .79 .99
97 97 97 93
- .01 -.05 -.06 .05
.64 .88 .03* .05*
100 100 100 98
Testosterone (T) Father smoking (F) T × F (uncontrolled) T X F(controlled)"
.01 .18 .02 .02
.25 .56 .26 .18
82 82 82 79
.02 .16 .00 .04
.45 .71 .99 .22
82 82 82 80
Testosterone(T) Friend smoking (F) T X F(uncontrolled) T X F (controlled) a
.01 .35 .03 .02
.45 .18 .03* .04*
103 103 103 99
.01 1.28 .01 .03
.52 .00"* .69 .24
107 107 t07 101
*p < .05. **p < .01. aThe controls are race. age, sexual behavior, and deviance.
for males at the highest testosterone levels (Table 2) and (b) stronger relationships between testosterone and adolescent smoking for males whose friends smoke than for males whose friends do not smoke (Table 3). For males, there is no statistically significant interaction involving parent smoking and testosterone. Collinearity diagnostics indicated that the statistically insignificant interactions are not due to large correlations between the independent variables and the interaction terms. For females, there is a statistically significant interaction of mother smoking and testosterone in adolescent smoking that remains statistically significant when controlled for race, age, sexual behavior, and deviance (Table 1). The interactions are in the expected direction of (a) stronger relationships between mother and adolescent smoking for the highest testosterone levels (Table 2) and (b) a stronger relationship between testosterone and smoking for females whose mothers smoke than for females whose mothers do not smoke (Table 3). For females there are no interactions involving testosterone and father or friend smoking. Multicollinearity between the independent variables and the interaction terms do not produce statistical insignificance.
Table 2. Correlations between adolescent smoking and parent and peer smoking by testosterone Male testosterone
Female testosterone
Social referent
High
Medium
Low
High
Medium
Low
Mother (n) Father (n) Friend (n)
.03 (34) .34 (29) .52** (35)
-.01 (30) .27 (27) .52** (34)
-.01 (33) .16 (26) .39* (34)
.35* (34) .07 (26) .53** (34)
.45** (33) .09 (32) .77** (35)
-.09 (33) ,09 (24) .67** (34)
*p < .05. **p < .01.
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463
Table 3. Correlations (Spearman p) between testosterone and adolescent smoking by parent and peer smoking Male Smoking
Female
P
(n)
Mother Yes
.20
(44)
No
.25
(53)
-.02
(53)
.37* .17
(39) (43)
.12 .20
(48) (34)
.38* .22
(35) (68)
.10 .19
(50) (53)
Father Yes No Friend Yes No
p
(n)
.34*
(47)
*p < .05.
DISCUSSION
AND
CONCLUSION
The biological and sociological variables interact in their relationship to adolescent smoking. The interaction varies, however, by adolescent gender and by whether the smoking of the mother, father, or friend is the referent. Possible explanations for the variation in interaction patterns are discussed here. Mother smoking and testosterone interact in relationship to daughter smoking, but there is no interaction between father smoking and testosterone. Differential parent influence might explain this. Females model mothers more than fathers (Jacklin, 1989; Mischel, 1966), mothers have the primary responsibility for child socialization, and mothers may be more involved than fathers in norm setting and in expressing attitudes related to smoking. Our findings that mother and daughter smoking are associated, but that father and daughter smoking are not (Table 2), are consistent with these propositions. Under these conditions, mother smoking and its association with other variables, such as norms, attitudes, and modeling, would be more effective than father smoking in modifying the influence of testosterone on daughter smoking. Testosterone and mother smoking interact with smoking for females but not for males. Perhaps this occurs because mothers influence daughters more than sons. Compared to males, for example, females are socialized to be more dependent on their mothers (Simmons & BIyth, 1987), they are more closely supervised (Clausen, 1968), they comply more to parental expectations and rules (Douvan & Adelson, 1966; Simmons & BIyth, 1987), and they are more accepting of mother control (Clausen, 1968). The correlations in Table 2 show that mother smoking is related to daughter smoking but not son smoking, which is consistent with the more general principle that mothers influence daughters more than sons. Perhaps differential influence by mothers on daughters and sons explains why mother smoking modifies the relationship between testosterone and smoking for daughters but not sons. Another possible explanation for the finding that mother smoking modifies the influence of testosterone on smoking by females but not males involves the interrelationship of three propositions. First, for children the ages of those in our sample, females are more physically developed than the males: the testosterone level of females has nearly peaked, whereas the testosterone of males will increase substantially during their next several years (Sizonenko, 1978) and females appear more physically mature than males
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(Petersen & Taylor, 1980; Sizonenko, 1978). Second, a child's physical development may activate the mother's socialization of her child specific to adolescent behaviors (Hamburg. 1974; Hill & Lynch, 1983), including the mother's expression to her child of norms and attitudes related to the child's smoking. Third, mothers who do not smoke may have more tendency than those who do smoke to express more unfavorable norms and attitudes toward smoking to their child. Therefore, among adolescents 12-14 years of age, testosterone may increase smoking for females whose mothers smoke but not for those whose mothers do not smoke, and this does not occur for males the same ages because relatively few of them have reached the stage of physical development necessary to activate their mother's socialization processes related to smoking. According to this reasoning, when the males in our sample are several years older they too may exhibit an interaction between their own smoking and the smoking of their mothers. A different line of reasoning for the interaction of testosterone with mother smoking for females but not males also is related to the age differential in puberty, but uses modeling to explain the gender difference in the interaction. Adolescents may associate puberty and smoking with adulthood, and puberty may increase the adolescent's attention to. and modeling of, parent behavior. Because more females than males had reached puberty, the females may have been more likely than the males to have modeled adult smoking. Friend smoking and testosterone interact with smoking by males but not smoking by females. Friend and adolescent smoking are associated for both genders in our sample (Table 2). suggesting that the difference is not explained by peers having more influence on males than females. Perhaps the stronger parental influence for females than males described above counteracts the influence of peers more for females than for males (Clausen, 1968). A limitation of our study is that the data are cross-sectional; panel data are more approporiate for many of our interpretations. We have reasoned, for example, that the association between friend and adolescent smoking reflects peer influence, but that association also indicates that adolescents who smoke are likely to choose friends who smoke (Fisher & Bauman, 1988). Similarly, we assume that parent smoking influences adolescent smoking, as suggested by the literature on the relationship between parent and adolescent smoking. It is possible, however, that child smoking influences parent smoking. Finally, no studies of adolescents allow definitive identification of the direction of the relationship between testosterone and smoking. The two experiments conducted with adults found that increasing smoking either decreases (Briggs, 1973) or does not change (Winternitz & Quillen, 1977) testosterone levels, supporting our assumption that testosterone is a cause rather than a consequence of smoking. However, the possibility remains that among adolescents smoking causes an increase in testosterone. Another possible limitation of our study is that we have considered the association between parent and adolescent smoking to reflect social factors even though it may be partially genetic (Hughes, 1986). Moreover, although the relationship between peer and adolescent smoking may be of social origin, it could be biological if parents smoke for genetic reasons and encourage friendships for their children on the basis of their behavioral preferences (Hansen et al., 1987). We are unable to remove all possible sources of confounding of biological and sociological factors in some of our measures and associations. Limitations of the measurement of testosterone include intra-individual (Dai et al., 1981; Mattsson, Schalling, Olweus, Low, & Svensson, 1980), daily (Dai et al., 1981;
Sociological and biological factors in adolescent smoking
465
Dotson, Robertson, & Tuchfeld, 1975), seasonal (Dai et al., 1981), and menstrual cycle (Udry, Talbert, & Morris, 1986) variation in testosterone. We obtained the saliva specimens when it was convenient to subjects, data collectors, and the time frame for our research plan. This procedure could have produced measures of testosterone that reduced the strength of their association with smoking, and we would have preferred more refined measurement. The correlation between testosterone and smoking under these conditions suggests that our findings are particularly robust. In conclusion, our findings suggest that the appropriate consideration of adolescent smoking requires recognition of the interaction of sociological and biological factors. The interactions vary by adolescent gender and whether the mother, father, or peer smokes. Future research is needed to test the explanations for the interactions, to explain exceptions to the interaction model, and to establish the directions of the relationships.
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