Cigarette smoking prospectively predicts retarded physical growth among female adolescents

Journal of Adolescent Health 37 (2005) 363–370

Original article

Cigarette smoking prospectively predicts retarded physical growth among female adolescents Eric Stice, Ph.D.*, and Erin E. Martinez, B.A. Department of Psychology, University of Texas at Austin, Austin, Texas Manuscript received April 9, 2004; manuscript accepted October 15, 2004.

Abstract

Purpose: This study tested the hypothesis that cigarette smoking retards physical development during early adolescence among girls. Methods: A school-recruited sample of adolescent girls (N ⫽ 496) completed surveys assessing smoking behaviors and related variables as well as direct measures of height and weight annually over 3-years. Analyses tested whether smoking trajectories and initial smoking correlated with changes in physical growth over time. Results: Relative to persistent nonsmoking, persistent smoking was associated with reduced growth in height, weight, and body mass index (BMI). Initiation of smoking, relative to persistent nonsmoking, was associated with reduced growth in weight and BMI but not height. Smoking cessation, relative to persistent smoking, was associated with increased gains in weight and BMI but not height. Results also documented a prospective dose-response relation of initial smoking quantity and frequency to subsequent growth retardation in height, weight, and BMI. Conclusions: Findings are generally consistent with the assertion that smoking in early adolescence retards physical development among adolescent girls. © 2005 Society for Adolescent Medicine. All rights reserved.

Keywords:

Adolescence; Growth retardation; Health behavior; Smoking

Although the adverse health consequences of smoking in adulthood are well documented [1], less attention has been devoted to the possible health consequences of smoking during adolescence. Given that early adolescence represents an intense period of physical development [2,3], youth of this age may be particularly vulnerable to factors that impede growth. Therefore it seems prudent to examine the possible effects of cigarette smoking on health and development during this period. The general consensus that cigarette smoking results in appetite suppression and weight loss [4] raises the possibility that this behavior retards physical development during adolescence, a period characterized by marked physical growth [2,3,5]. Several lines of indirect evidence regarding the detriments of smoking in gestation, childhood, adoles*Address correspondence to: Eric Stice, 1715 Franklin Boulevard, Eugene, OR 97403. E-mail address: [email protected]

cence, and adulthood provide support for this possibility. First, maternal smoking during the neonatal period is associated with growth retardation in human beings [6,7]. Experiments have also verified that exposing pregnant rats to cigarette smoke causes retarded physical development in the fetus during gestation [8]. Second, passive exposure to second-hand cigarette smoke during childhood is associated with growth retardation [9,10]. Experiments have similarly indicated that exposure to cigarette smoke results in growth retardation in developing rat pups [11]. Third, endorsement of the belief that smoking causes weight loss is associated with adolescent cigarette use [4,12,13]. Furthermore, weight concerns and body dissatisfaction predict smoking initiation during middle adolescence [14,15]. Fourth, adolescent and adult smokers are shorter and weigh less than nonsmokers [16,17]. There is also some prospective evidence that smoking initiation results in attenuated weight gain over time in adults [16,18], although other studies have not observed this relation [19,20].

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There are several theoretical accounts that could explain a relation between cigarette smoking and retarded growth in weight and height. First, smoking may curtail physical development, because it reduces the efficiency of energy utilization [11,21]. In theory, nicotine ingestion results in less efficient routes of caloric storage, decreased rate of caloric storage, and increased caloric utilization and excretion. Specifically, nicotine causes activation of the sympathetic nervous system, which in turn increases the activity of energy expenditure substrate cycles and thus results in decreased caloric storage [22]. Second, smoking may also attenuate physical growth, because it increases metabolic rate and thermogenesis [23,24]. Finally, the putative appetite suppressant effects of smoking that lead to decreased caloric intake may also result in diminished growth rate [8,11]. However, this last theory is difficult to reconcile with the inconsistent effects of chronic smoking on caloric intake [22]. Despite the indirect evidence and plausible theoretical accounts, a comprehensive literature search did not identify any research that has prospectively tested whether smoking is associated with retarded physical development during adolescence. As noted, it is crucial to address this question, because early adolescence is one of the most intense periods of physical development [2,3] and therefore factors that impede growth are of particular relevance. Thus this study first tested the hypothesis that persistent smoking would be associated with smaller increases in height, weight, and body mass index (BMI) relative to persistent nonsmoking. Second, this study tested whether smoking initiation would be associated with attenuated increases in these growth parameters relative to persistent nonsmoking. Third, this study tested whether smoking cessation would be associated with greater increases in these growth parameters relative to persistent smoking. The final purpose was to test the hypothesis that there would be a dose-response relation between initial smoking quantity and frequency, and subsequent retardation in these 3 growth parameters over the following 1 year.

school graduate (2%) to graduate degree (11%), with a mode of college graduate (29%). Procedures

Methods

The study was described to parents and participants as an investigation of adolescent mental and physical health. An active parental consent procedure was used to recruit participants. First, an informed consent letter describing the study was sent to parents of eligible girls from the schools; a second mailing was sent to nonresponders after 2 weeks. Adolescent assent was secured immediately before data collection. This resulted in an average participation rate of 56% of eligible students, which is similar to that of other school-recruited samples that used active consent procedures and involved structured interviews (e.g., 61% for Lewinsohn et al. [26]). The ethnic composition of the sample was representative of the ethnic composition of the schools from which we recruited (2% Asian or Pacific Islanders; 8% African-Americans, 65% Caucasians, 21% Hispanics; 4% “Other” or mixed racial heritage). In addition, the educational attainment of parents (a proxy for socioeconomic status) was similar to census data for comparably aged adults (grade school graduate, 3%; high school graduate, 30%; college graduate, 25%; graduate degree, 8%). The median BMI score in our sample (19.9 kg/m2) closely approximated the median BMI score (18.8 kg/m2) from a large representative national sample [2]. The BMI divides weight by height (squared) to control for variations in weight due to height, and is thus considered a measure of relative weight. Participants completed a questionnaire, participated in a structured psychiatric interview, and had their weight and height measured by female research assistants at baseline (T0) and at 1-year (T1) and 2-year (T2) follow-up. Extensively trained female clinical assessors with an M.A. or Ph.D. degree in psychology conducted all interviews. Assessments took place on school campuses, at project offices, or at participants’ homes. Girls received a $15.00 gift certificate to a local book and music store as compensation for their participation. The institutional review board at the University of Texas at Austin approved this project.

Participants

Measures

Participants were 496 adolescent girls from 4 public (82%) and 4 private (18%) middle schools in a metropolitan area of the southwestern United States. This study focused exclusively on girls, because data were drawn from a project investigating the risk factors for eating disorders, which are extremely rare in boys [25]. Adolescent girls ranged in age from 11 to 15 years (mode ⫽ 13) at baseline. The sample was composed of 2% Asian or Pacific Islanders, 7% AfricanAmericans, 68% Caucasians, 18% Hispanics, 1% Native Americans, and 4% who specified “Other” or mixed racial heritage. Average parental education ranged from grade

Cigarette smoking. Items adapted from Johnston et al. [27] were used to assess frequency and intensity of cigarette use. At each of the 3 assessments adolescents reported their frequency of cigarette use during the past year, using a 7-point response scale with the following options: never, a few times, 1 to 3 times a month, 1 to 2 times a week, 3 to 4 times a week, and 5 to 7 times a week. They also reported the average number of cigarettes smoked daily, using a 6-point response scale with the following options: 0, 1 to 2, 3 to 8, 9 to 14, 15 to 20, and 21 or more. Pilot testing (N ⫽ 38) revealed 1-month test-retest coefficients of .92 for the

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smoking frequency item and .91 for the smoking quantity item. Research has verified that self-reported smoking shows high agreement with bioassay measures [28,29]. More generally, research suggests that self-reports of substance use are the most reliable and valid measure of this behavior [30,31]. Physical growth parameters. Adolescent height was measured to the nearest millimeter, using portable direct-reading stadiometers (Shorr Productions, Olney, MD). Participants were measured without shoes and with the body positioned such that the heels and buttocks were against the vertical support of the stadiometer and the head aligned so that the auditory canal and the lower rim of the orbit were in a horizontal plane. Body weight was assessed to the nearest 0.1 kg using digital scales (Model 770 digital scale; Seca, Weatherford, Texas), with the participants wearing light indoor clothing without shoes or coats. Two measures of height and weight were obtained and averaged for analyses. Body mass index scores [32] were also generated for each participant. The validity of the BMI is supported in that it correlates with direct measures of total body fat, such as dual-energy x-ray absorptiometry, and with health measures, such as adverse lipoprotein profiles, atherosclerotic lesions, and serum insulin levels in adolescent samples [32,33]. The BMI has also been found to be temporally reliable (1-year test-retest coefficient ⫽ .92) [34]. Body mass index scores from the current study also evidenced excellent temporal reliability (average 1-year test-retest coefficient ⫽ .94). Statistical methods First, descriptive data on the prevalence of smoking at each assessment point and results from attrition analyses that tested whether participants who provided complete data differed from those who did not on baseline variables are reported. Next, independent sample t tests investigated whether persistent smokers showed smaller increases in height, weight, and BMI than did persistent nonsmokers, whether adolescents who initiated smoking showed attenuated increases in these growth parameters relative to persistent nonsmokers, and whether adolescents who stopped smoking showed greater increases in these growth parameters than persistent smokers did. Finally, linear regression models tested whether there would be a dose-response relation between initial smoking quantity and frequency and subsequent retardation in the growth parameters. Results Preliminary analyses Of the 496 participants at T0, 403 (81%) reported no smoking in the past year, 37 (7%) reported less than daily smoking, 53 (11%) reported daily smoking and 3 (1%) did not provide smoking frequency data. (For a participant to be

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classified as a daily smoker, they had to endorse the 5 to 7 times a week response on the smoking frequency item and report smoking at least 1 to 2 cigarettes on the number of cigarettes smoked daily item.) At T1, 378 respondents (76%) reported no smoking in the past year, 50 (10%) reported less than daily smoking, 54 (11%) reported daily smoking, 4 (1%) did not complete the smoking frequency question, and 10 did not provide data at T1 (2%). At T2, 359 respondents (72%) reported no smoking in the past year, 56 (11%) reported less than daily smoking, 62 (13%) reported daily smoking, 9 (2%) did not complete the smoking frequency question, and 10 did not provide data at T2 (2%). Adolescents classified as less than daily smokers (intermittent smokers) reported smoking on average less than 1 cigarette per month (range, a few times, to 1 to 2 times per week in the past year); daily smokers reported an average intake of 3 to 8 cigarettes per day (range, 1 to 2, to 15 to 20 cigarettes per day in the past year). These rates of smoking are generally consistent with those observed in other largescale studies [35–37], which provides further evidence that this sample is representative. For example, the 11% rate of daily smoking in our sample at T0 was similar to the 10% rate observed by Johnston et al. [36] in their large national sample. Of the initial 496 participants, 10 (2%) did not provide data at T1 and an additional 10 (2%) did not provide data at T2, although only 4 participants did not provide data at either T1 or T2 (1%). Attrition analyses verified that the participants who did not provide data at T1 or T2 did not differ significantly from the remaining participants in terms of demographic factors, smoking rates, or anthropomorphic data (all p values ⬎ .10), suggesting that attrition should not bias parameter estimates. Relation of smoking to change in physical growth parameters To address the first 3 study aims, participants were classified into smoking trajectory groups based on self-reported smoking frequency at each of the 3 annual assessments. Analyses focused on onset, persistence, and cessation of daily smoking, because it was unlikely that the smoking rates observed in the infrequent smokers would have any perceptible effect on physiology; most reported smoking less than 1 cigarette per month in the past year. Because of the relatively small number of adolescents who reported onset, persistence, and cessation of daily smoking, those who evidenced these smoking trajectories between T0 and T1 or between T1 and T2 were classified together to maximize statistical power. (For participants who showed these rare smoking trajectories, i.e., onset, persistence, or cessation, over both time windows, e.g., persistence from both T0 to T1 and from T1 to T2, or onset from T0 to T1 and persistence from T1 to T2), one of the time windows was randomly selected for use in these analyses.) Thus partici-

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Table 1 Change in Growth Parameters Over 1-Year Study for 4 Smoking Trajectory Groups Smoking trajectory groups

Change in growth parameters over 1-year period Height (cm)

Persistent nonsmokers (n ⫽ 302) Smoking initiators (n ⫽ 55) Smoking terminators (n ⫽ 37) Persistent smokers (n ⫽ 35)

Weight (kg)

Body mass

Mean

SD

Mean

SD

Mean

SD

2.14a 1.81 1.24 1.41b

1.73 2.36 1.45 1.62

2.89a 1.84b 3.39 1.35b

2.36 5.56 4.78 3.98

.59a .19b .93 .17b

.78 2.06 1.88 1.46

Note: Means within same column with different subscripts are significantly different (p ⬍ .05).

pants who reported daily smoking at both T0 and T1 or at both T1 and T2 were classified as persistent smokers (n ⫽ 35). Participants were classified as smoking initiators if they denied smoking at T0 and reported daily smoking at T1 or denied smoking at T1 and reported daily smoking at T2 (n ⫽ 55). Participants were classified as smoking terminators if they reported daily smoking at T0 and no smoking at T1 or reported daily smoking at T1 and no smoking at T2 (n ⫽ 37). Finally, participants were classified as persistent nonsmokers if they reported no smoking at T0, T1, and T2 (n ⫽ 302). It is important to note that 47 participants could not be classified into 1 of these 4 smoking trajectory groups, because they reported intermittent (nondaily) smoking but never showed onset, persistence, or cessation of daily smoking (e.g., reported persistent intermittent smoking, change from daily smoking to intermittent smoking, or change from intermittent smoking to daily smoking), and were excluded from the trajectory analyses. We decided to exclude the intermittent smokers from the smoking trajectory groups because it seemed unlikely that an average of less than 1 cigarette per month would have any perceptible effect on physical growth. (It should be noted that the pattern of findings was similar, i.e., no significant effect became nonsignificant or vice versa, when the intermittent smokers were grouped with the nonsmokers in the analyses.) The remaining 20 participants did not have sufficiently complete smoking data across assessment waves to permit classification into one of the smoking trajectory groups, either because they did not provide any data at an assessment point or simply did not complete certain smoking items. To test the hypothesis that adolescent smoking would be associated with retarded physical growth, independent sample t tests were used to compare the changes in height, weight, and BMI over the 1-year period of adolescents who were persistent nonsmokers with those who were persistent smokers. Analyses focused on change in the growth parameters during the 1-year interval of the particular smoking trajectory under investigation (e.g., for adolescents who were classified as persistent smokers from T1 to T2, the growth parameters reflected change over this same period). Change scores (e.g., T1 height to T0 height) were computed to reflect increases or decreases in each of these criteria, wherein higher positive scores signaled greater increases in

each growth parameter. Consistent with hypotheses, persistent smokers showed significantly retarded gains in height (t [1/335] ⫽ 2.38, p ⫽ .018, r ⫽ ⫺.13), weight (t [1/335] ⫽ 3.33, p ⬍ .001, r ⫽ ⫺.18), and BMI (t [1/335] ⫽ 2.71, p ⫽ .007, r ⫽ ⫺.15) over the 1-year period relative to persistent nonsmokers. Changes in height, weight, and BMI for adolescents in the 4 smoking trajectory groups are presented in Table 1. Persistent smoking was associated with a 34% reduction in growth in height, a 53% reduction in growth in weight, and a 71% reduction in growth in BMI relative to the growth parameters observed in the persistent nonsmoking group. To test the hypothesis that initiation of adolescent smoking would be associated with growth retardation, t tests compared changes in height, weight, and BMI over the 1-year period of persistent nonsmokers with smoking initiators. As hypothesized (Table 1), adolescents who initiated daily smoking showed significantly less increases in weight (t [1/354] ⫽ 2.32, p ⫽ .021, r ⫽ ⫺.12) and BMI (t [1/354] ⫽ 2.53, p ⫽ .011, r ⫽ ⫺.13) over the 1-year period relative to persistent nonsmokers. However, there were no significant differences in growth in height for these 2 groups (t [1/354] ⫽ 1.22, p ⫽ .225, r ⫽ ⫺.06). Smoking initiation was associated with a 36% reduction in weight increase and a 68% reduction in BMI increase relative to the growth observed in the persistent nonsmoking group. To test the hypothesis that termination of smoking would be associated with increased growth relative to that observed in persistent smokers, t tests compared changes in height, weight, and BMI over the 1-year period for smoking terminators with persistent smokers. Smoking termination (Table 1), relative to smoking persistence, was associated with marginally significant increases in weight (t [1/70] ⫽ 1.96, p ⫽ .054, r ⫽ ⫺.23) and BMI (t [1/70] ⫽ 1.90, p ⫽ .061, r ⫽ ⫺.22), although it was not associated with significant changes in height (t [1/70] ⫽ .47, p ⫽ .639, r ⫽ ⫺.05). Smoking termination was associated with a 251% increase in weight and a 547% increase in BMI relative to the growth parameters observed in the persistent smoking group. In an effort to determine whether the gains in weight and BMI associated with smoking cessation reflected unhealthy weight gain or developmentally appropriate growth, we reestimated these 2 models, excluding overweight ado-

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lescents (as defined by BMI ⬎25 at any time point [33]). Results indicated that the effects were slightly larger when the overweight adolescents were excluded, which provides some evidence that smoking cessation results in healthy weight regain. To test whether any potential confounds explain these effects, all models were reestimated controlling for ethnicity, parental education, timing of menarche, age, dietary intake of high-fat foods, and initial levels of the growth parameters BMI, weight, and height. (Fat intake was assessed with 18 items adapted from the Fat-Related Diet Habits Questionnaire [38]. Participants indicated how frequently they ate common high-fat foods during the past month, using a 5-point scale ranging from never or almost never to 5 or more times a week; items were averaged. This adapted scale evidenced internal consistency [␣ ⫽ .79] and 1-week test-retest reliability [r ⫽ .90] in a pilot study, and internal consistency [␣ ⫽ .81] and 1-year test-retest reliability [r ⫽ .57] in the current study.) These analysis of covariance models indicated that when these factors were used as covariates in the analyses described above, all of the significant effects remained significant and none of the nonsignificant effects became significant. Furthermore, analyses also indicated that the 4 smoking trajectory groups did not evidence significant differences in terms of timing of menarche, which implies that the rate of physical development in these groups should be similar on the basis of maturational timing. Test of prospective dose-response relation between smoking and growth To test whether there was a prospective dose-response relation of initial smoking to growth retardation in height, weight, and BMI over the study period, the T1 to T0 change scores for the 3 growth parameters were regressed on T0 smoking quantity and frequency variables using linear regression models with data from the complete sample. Results confirmed that there was a consistent prospective doseresponse relation of initial smoking quantity and frequency to subsequent growth retardation in height, weight, and BMI over the study period. Table 2 shows the correlation coefficients reflecting the magnitude of these linear relations. Multiple regression analyses confirmed that each of these effects remained significant when ethnicity, parental education, timing of menarche, age, dietary intake of high-fat foods, and initial levels of the growth parameters were used as covariates, which suggests that these factors are not potential confounds that explain the effects. Discussion The overarching goal of this study was to test the hypothesis that smoking is associated with retarded physical development during early adolescence. In the first set of analyses, persistent smokers showed significantly smaller

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Table 2 Correlation Coefficients Reflecting Dose-Response Relations Between Initial Smoking Intensity and Physical Growth Parameters Over 1-Year Study Smoking intensity at T0 Frequency of cigarette smoking Number of cigarettes smoked daily

Change in growth parameters over 1 year Height

Weight

Body mass

⫺.18*

⫺.16†

⫺.23*

⫺.16‡

⫺.13‡

⫺.20*

* p ⬍ .0001. p ⬍ .001. ‡ p ⬍ .01. †

gains in height, weight, and BMI over the study period relative to persistent nonsmokers. Persistent smoking was associated with a 34% reduction in growth in height, a 53% reduction in growth in weight, and a 71% reduction in growth in BMI over 1 year. On average, persistent smokers gained almost 1 cm less in height and 1.5 kg less in weight over the 1 year. Separate analyses also provided consistent evidence of a statistically significant prospective doseresponse relation of initial smoking quantity and frequency to subsequent retardation in height, weight, and BMI gains. These effects cannot be attributed to initial differences in physical development across the 4 smoking trajectory groups, because all effects remained significant in models that controlled for initial growth parameters, initial age, timing of menarche, and intake of high-fat foods, as well as for ethnicity and parental education. Furthermore, the 4 smoking trajectory groups did not differ in terms of timing of menarche, and therefore should be similar in terms of potential for physical growth. Thus it is not simply the case that these effects resulted because shorter, leaner, or more developmentally advanced adolescents were more likely to smoke cigarettes. However, the nonexperimental design cannot rule out other potential third variable explanations for the relations. Ethical considerations preclude an experiment involving random assignment to a smoking condition. Within this context, it should be noted that any underreporting of cigarette use by adolescents would only serve to attenuate effect sizes. Thus these estimates might be a conservative estimate of the magnitude of the relation between adolescent smoking and growth retardation. Our study findings suggest that cigarette smoking results in retarded physical development during early adolescence. Nonetheless, these findings do converge with the evidence that exposure to second-hand cigarette smoke is associated with growth retardation during childhood [9,10]. The finding that adolescent smoking appears to result in retarded physical development is concerning, given that approximately 10% of adolescents are daily smokers [36]. Although the effect sizes were relatively small in magnitude and the growth retardation per year of persistent smoking is not large, the cumulative effects on of smoking over several

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years could be clinically relevant. Based on the data shown in Table 1, the average adolescent who smoked for 5 years would be 3.6 cm shorter and would weigh 7.7 kg less than an adolescent who did not smoke over this period. Separate analyses suggested that smoking initiation, relative to persistent nonsmoking, was associated with marginally significant attenuations in growth in weight and BMI. Smoking initiation was associated with a 36% reduction in growth in weight and a 68% reduction in growth in BMI relative to persistent nonsmoking. However, smoking initiation was not related to significant attenuations in height. Although these effects were generally consistent with expectations, they were smaller than the effects of persistent smoking. One possible explanation for the smaller effects is that the “dose” of cigarette exposure may have varied among adolescents who reported onset of daily smoking. For example, some of these youth may have recently started smoking, whereas others might have smoked for nearly a year. This heterogeneity of exposure might have resulted in a larger error term and attenuated statistical power to detect effects. Similar heterogeneity likely existed among the adolescents who reported smoking cessation, which may explain why the effects for smoking cessation were also smaller in magnitude compared with the effects of persistent smoking (see below). Future research should collect more detailed information on the timing of smoking onset when examining the possible effects of onset and cessation on physical growth. This pattern of findings seems to suggest that it is persistent daily smoking, rather than less consistent smoking patterns, that shows the strongest relation to retarded physical growth. This is reminiscent of the apparent effect of psychostimulant medication, which also results in sympathetic arousal, on growth retardation. Research indicates that persistent administration of psychostimulant medications is associated with retarded physical development, effects that can be reversed with medication holidays, that is, periods when the medication is discontinued [39]. Another set of analyses suggested that smoking cessation was associated with significant increases in weight and BMI but not height, relative to the growth observed in persistent smokers. Smoking cessation was associated with a 241% increase in weight and a 547% increase in BMI compared with the changes in these growth parameters in the persistent smoking group. These findings are consonant with the evidence from the adult literature indicating that smoking cessation is consistently associated with weight gain [16]. However, it is important to remember that the participants in the current study were still undergoing physical development [2]. The finding that gains in weight and BMI observed in the smoking cessation group were less than those observed in the persistent nonsmoking group seems to provide further evidence that smoking leads to retardation of physical growth, as opposed to an unhealthy increase in adiposity. The post hoc analyses indicated that weight and

BMI gains associated with smoking cessation were stronger when overweight and obese adolescents were excluded from the analyses provides further evidence that smoking cessation contributes to healthy weight regain rather than onset of clinically harmful levels of adiposity. Several limitations of this study should be considered when interpreting these results. First, the sample sizes were relatively small for some of the smoking trajectory groups. Although we had sufficient power to detect effects, greater confidence could have been placed in the stability of the parameter estimates with a larger sample size. Second, it would have been preferable to have observed younger participants over a longer period to more clearly document the longer term growth retardation associated with smoking during early adolescence. Third, because we did not include boys in our sample, it is not clear whether smoking is associated with growth retardation in adolescent boys. However, that boys experience their puberty-related growth spurt later than girls suggests that smoking-related growth retardation may be even more pronounced in boys. Fourth, although our results indicate growth retardation in early adolescence, this may represent a temporary delay in growth. Based on the present findings, we cannot conclude that the retardation would persist throughout the entire period of adolescence. Fifth, self-report measures were used to assess adolescent smoking. Although evidence suggests that self-reported smoking shows excellent concordance with bioassay measures [28], greater confidence could be placed in the findings if we had included such measures or a bogus pipeline procedure. Finally, there were a number of potential confounds that should have been assessed and controlled statistically in the analyses, particularly degree of pubertal development (Tanner ratings) and a detailed assessment of dietary intake. In terms of directions for future research, it will be important to attempt to replicate these findings in an independent study that addresses the previously noted methodologic shortcomings of this study. In addition, it would be useful for prospective research to examine the possible effects of smoking on neurologic and organ development during early adolescence. Because nonexperimental studies cannot rule out third variable explanations for observed relations, it would also be interesting to test whether successful smoking prevention programs that are evaluated in randomized trials produce elevated physical growth in intervention participants relative to control participants. Finally, research should attempt to elucidate the mediational processes that explain the relation between smoking and retarded physical development (e.g., decreased caloric utilization vs increased metabolic rate vs appetite suppression). In conclusion, our results suggest that persistent smoking is associated with retarded height, weight, and BMI development during early adolescence and indicate that there is a dose-response relation between initial smoking intensity and retardation of these 3 growth parameters. There is also

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evidence that smoking initiation, relative to persistent nonsmoking, is associated with reduced growth in weight and BMI but not height and that smoking cessation, relative to persistent smoking, is associated with increased growth in weight and BMI but not height. Collectively, the findings provide support for the assertion that smoking in early adolescence results in retarded physical development. Acknowledgments This research was supported by a career award (MH01708) and a research grant (MH/DK61957) from the National Institutes of Health. Thanks go to Gabriela Redwine, Heather Shaw, and Mark Myers for their thoughtful input regarding this manuscript. We would also like to express our gratitude to the project research assistants, Anne Appel, Allison Chase, Sarah Kate Bearman, Natalie McKee, Susan Stormer, Ariel Trost, and Katy Whitenton; a multitude of undergraduate volunteers; the Austin Independent School District; and the participants who made this study possible. References [1] Preventing tobacco use among young people: a report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Office on Smoking and Health, 1994. [2] Hammer LD, Kraemer HC, Wilson DM, et al. Standardized percentile curves of body-mass index for children and adolescents. Am J Dis Child 1991;145:259 – 63. [3] Tanner JM. Fetus into man. Cambridge, MA: Harvard University Press, 1978. [4] Camp DE, Klesges RC, Relyea G. The relationship between body weight concerns and adolescent smoking. Health Psychol 1993;1:24 – 32. [5] Connolly SD, Paikoff RL, Buchanan CM. Puberty: the interplay of biological and psychosocial processes in adolescence. In: Adams GR, Montemayor R, Gullotta TP, eds. Psychosocial development during adolescence. Thousand Oaks, CA: Sage, 1996:259 –99. [6] Davies DP, Gray OP, Ellwood PC, Abernethy M. Cigarette smoking in pregnancy: associations with maternal weight gain and fetal growth. Lancet 1976;1:385–7. [7] Lindley AA, Gray RH, Herman AA, Becker S. Maternal cigarette smoking during pregnancy and infant ponderal index at birth in the Swedish Medical Birth Register. Am J Public Health 2000;90:420 –3. [8] Bassi JA, Rosso P, Moessinger AC, et al. Fetal growth retardation due to maternal tobacco smoke exposure in the rat. Pediatr Res 1984;18: 127–30. [9] Ferris BG, Ware JH, Berkey CS, et al. Effects of passive smoking on health of children. Environ Health Perspect 1985;62:289 –95. [10] Rona RJ, Chinn S, Florey CD. Exposure to cigarette smoking and childrens’ growth. Int J Epidemiol 1985;14:402–9. [11] Wagner-Srdar SA, Levine AS, Morley JE, et al. Effects of cigarette smoke and nicotine on feeding and energy. Physiol Behav 1984;32: 389 –95. [12] Chesley EB, Roberts TA, Auinger P, et al. Longitudinal impact of weight-related intentions with the initiation and maintenance of smoking among adolescents. J Adolesc Health 2004;34:130. [13] Fulkerson JA, French SA. Cigarette smoking for weight loss or control among adolescents: gender and racial/ethnic differences. J Adolesc Health 2003;32:306 –13.

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