J Youth Adolescence (2006) 35:717727
DOI 10.1007/s10964-006-9101-2
ORIGINAL PAPER
Pubertal Development, Choice of Friends, and Smoking Initiation
among Adolescent Males
Laurie A. Drapela Janet L. Gebelt Nick McRee
Received: 21 June 2005 / Accepted: 7 July 2005 / Published online: 22 July 2006


C Springer Science+Business Media, Inc. 2006
Abstract Prior research has indicated that pubertal devel-
opment and peer associations are important determinants of
adolescent smoking behavior. However, more remains to be
learned about why these variables matter or how they may
be related to one another in ways that lead to the initia-
tion of smoking. Using contractual data from the National
Longitudinal Study of Adolescent Health, we consider the
relationship between early pubertal development and associ-
ations with close friends who smoke, and smoking initiation
among male youths. The results of the study reveal a link
between advanced pubertal development and the initiation
of smoking among boys, but we discover that the effect is
indirect, mediated by a greater propensity of sexually ma-
ture males to forge friendships with peers who smoke. We
also find that this propensity is greatest among the youngest
adolescents in the sample, suggesting that the age of the re-
L. A. Drapela
(Ph.D., The University of Texas at Austin), is an Assistant
Professor at Washington State University at Vancouver. Her areas
of interest include juvenile delinquency and substance abuse.
Vancouver, WA, USA.
e-mail: Drapela@vancouver.wsu.edu
J. L. Gebelt
(Ph.D., Rutgers: The State University of New Jersey) is an
Assistant Professor at Westfield State College. Her area of interest
is adolescent identity development.
Westfield, MA 01086, USA.
e-mail: JGebelt@wsc.ma.edu
N. McRee (
)
(Ph.D., The University of Texas at Austin) is an Associate
Professor at the University of Portland. His areas of interest
include biosocial models of adolescent problem behavior.
Department of Social and Behavioral Sciences,
5000 N. Willamette Blvd., Portland, OR 97203, USA.
e-mail: mcree@up.edu
spondent conditions the effects of pubertal development on
the formation of friendships with peers who smoke.
Keywords Puberty . Peers . Smoking . National
Longitudinal Study of Adolescent Health
Smoking is a significant and growing public health risk
for adolescents. According to data from the 1999 National
Household Survey, almost 15% of all youths in the United
States aged 1217 smoke cigarettes (Kopstein, 2001). Moni-
toring the Future data show that more than one quarter of high
school students are regular smokers by the time they gradu-
ate (Johnston et al., 2003) and evidence from the Youth Risk
Behavior Surveillance Survey (Kann et al., 1999) suggests
that the proportion of teens who smoke regularly increased
over the last decade. These trends in adolescent smoking be-
havior are a source of concern to parents, schools, and health
officials because adolescent tobacco use is associated with
negative health and behavioral outcomes. Smoking in early
adolescence is strongly linked to habitual cigarette smok-
ing in adulthood (Chassin et al., 1990; USDHHS, 1994).
Moreover, youths who smoke cigarettes are more likely than
non-smokers to: (1) chew tobacco, smoke cigars, or consume
novelty cigarettes (e.g., clove cigarettes or bidis) (Gilpin
and Pierce, 2003); (2) have an earlier age at onset for al-
cohol and marijuana use (DuRant et al., 1999; Ellickson
et al., 1992; Simon et al., 1995); and (3) engage in fighting,
weapons use, and high-risk sexual behaviors (Simon et al.,
1995; USDHHS, 1994).
The negative consequences of smoking demand additional
research into the developmental and social factors that may
be associated with the decisions of youths to start smoking.
In this paper, we investigate the interrelationship between
pubertal development and peer associations in a study of
smoking initiation among adolescent males. We focus the
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current investigation on boys for two reasons. We are aware
of only one published study that has considered the longi-
tudinal effects of both pubertal development and peer as-
sociations on adolescent substance use, and this study only
considered girls (Stattin and Magnusson, 1990). Moreover,
there is evidence that boys may be more susceptible to the
social influence of peers who use tobacco than are females
(Simon et al., 1995). For reasons we elaborate below, we
speculate that the degree of male adolescents susceptibil-
ity to peer influence may be related to the timing of their
sexual development. As a result, early maturing males may
have an elevated likelihood of smoking initiation mainly be-
cause they differentially form associations with friends who
smoke.
Pubertal development and youth deviance
Two hypotheses concerning the relationship between pu-
bertal development and adolescent problem behavior have
emerged from the literatures of developmental psychology
and juvenile delinquency. One hypothesis has considered the
general issue of whether the timing of ones sexual matura-
tion is out-of-synch with that of ones peers. The idea is that
early or late sexual maturation results in elevated levels of
emotional stress (Brooks-Gunn et al., 1985), and increases
the likelihood that adolescents will engage in socially pro-
scribed behaviors (Caspi and Moffitt, 1991; Tschann et al.,
1994). According to this perspective, both early and late
maturing boys should engage in more proscribed behav-
iors (such as smoking) than should males who mature on
time.
By contrast, an early maturation hypothesis identifies
early puberty in particular as a critical developmental trajec-
tory to explain adolescent participation in proscribed conduct
(Brooks-Gunn et al., 1985). Several studies have investigated
the relationship between early pubertal development and
adolescent delinquency. For example, youths who are more
sexually developed than their peers are more likely to ex-
press a desire for autonomy and independence (Montemayor
and Hanson, 1985) and to report conflict with parents (Hill
et al., 1985a, 1985b). They also report earlier onset and more
frequent sexual activity (Flannery et al., 1993), delinquent
behavior (Felson and Haynie, 2002; Flannery et al., 1993;
Magnusson et al., 1986; Udry, 1988), and abuse of substances
such as alcohol and marijuana (Dick et al., 2000; Tschann
et al., 1994; Wichstrom, 2001; Wiesner and Ittel, 2002).
With respect to regular smoking, the early maturation
hypothesis has received a great deal of empirical support.
For instance, in their longitudinal study of German adoles-
cents, Wiesner and Ittel (2002) suggest that early maturing
youths show a higher than expected rate of substance use, and
that the effect is particularly pronounced for cigarette use.
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J Youth Adolescence (2006) 35:717727
Several additional studies support this conclusion, reporting
that early maturing youths are more likely to smoke than
their late maturing peers (Harrell et al., 1998; Martin et al.,
2001).
We identified one study (Wiesner and Ittel, 2002) that di-
rectly compared the maturational deviance and early matura-
tion hypotheses to explore the relationship between pubertal
timing and substance abuse in early adolescence. In that
study, the authors discovered that early sexual maturation,
not merely out-of-synch pubertal development, was associ-
ated with greater levels of cigarette consumption. However,
the question of how pubertal timing might be related to the
specific decision of youths to start smoking (versus regular
use, or number of cigarettes smoked) remains unclear.
Puberty, peer associations and youth smoking
Research reveals that youths tend to belong to friendship
groups with others who are similar to themselves (Kobus,
2003; Moody, 2001). Primary demographic characteristics
such as gender, race, and ethnicity appear to be the most
salient factors that shape friendship associations, followed
closely by similarity in behaviors, such as drug use (Kandel,
1978). In particular, the powerful effect of friends has been
convincingly demonstrated for youth smoking (Conrad et al.,
1992; Kobus, 2003; Oygard and Klepp, 1995). Adolescent
friendship groups tend to cluster around smoking behavior,
with smokers associating with other smokers while non-
smokers typically befriend other non-smokers (Eiser et al.,
1991; Ennett et al., 1994; Urberg et al., 1997). It is also
increasingly clear that children who forge friendships with
peers who smoke are likely to try smoking themselves (Fisher
and Bauman, 1988; Urberg et al., 1997).
If the development of friendships with peers who smoke
is a key factor in explaining adolescent initiation of smoking,
what influences nonsmoking youths to form friendships with
smokers in the first place? Stattin and Magnusson (1990) pro-
pose an interrelationship between pubertal development and
peer associations to explain smoking initiation. Their study,
a longitudinal investigation of Swedish adolescent girls, sug-
gests that the timing of pubertal development is linked to the
particular types of friends with which youths are likely to
associate. In particular, Stattin and Magnusson (1990) dis-
covered that the girls in their sample who matured earlier
than their peers were more likely to form friendships with
older youths, resulting in an accelerated trajectory toward a
more mature lifestyle, which included earlier experimenta-
tion with alcohol and tobacco. However, this study did not
consider whether this relationship holds true for male youths.
More generally, a convincing theoretical explanation for why
pubertal timing might be associated with the composition of
adolescent friendship networks is needed.
J Youth Adolescence (2006) 35:717727
We suggest that the publication of a developmental tax-
onomy by Terrie Moffitt (1993) may help to shed light on
this question. Moffitt theorizes the existence of two distinct
groups of youth offenders to differentiate delinquent or an-
tisocial activity committed by adolescents. In this paper we
are most interested in Moffitts (1993) conceptualization of
adolescence-limited delinquents, which represent most of the
population of youths who engage in delinquent and norm-
violative behavior during adolescence. Moffitt argues that the
transitory nature of adolescent antisocial activity for most
youths can be traced to the behavioral consequences of a
mismatch between sexual development and the attainment
of adult social status. Moffitt proposes that one of the conse-
quences of pubertal development is an increase in the desire
for personal autonomy and adult status. Because children
in modern societies typically are not afforded independence
at puberty, they become frustrated, and may therefore be
inclined to pursue non-approved pathways to autonomy.
Research hypotheses
Moffitts identification of a mismatch between sexual ma-
turity and social competence among adolescents provides
a powerful conceptual framework from which to explore
whether pubertal development and peer associations inter-
act in ways that contribute to smoking initiation. Her pro-
posal identifies sexual maturity as a prime mover for an
increasing interest in autonomy and independence among
adolescents. We suggest the perspective may contribute to
an understanding of smoking initiation among teens because
smoking behavior has been linked to an expression of auton-
omy among youths (Samdal et al., 2000). Equally important,
her theory specifies a mechanism through which a frustrated
desire for autonomy may be surmounted: imitation of delin-
quent peers. Applied to the present investigation, Moffitts
theory suggests that early pubertal development may pre-
cipitate smoking initiation mainly because it increases the
susceptibility of youths to the influence of peers who smoke.
To evaluate this argument, we analyze a large population
of young males drawn from a national longitudinal sample
of adolescents in the US. We hypothesize that compared to
youths in general, boys of advanced pubertal status would
have a greater number of close friends who smoke. We con-
sider whether this hypothesized association between early
pubertal development and peer smoking is contemporane-
ous or lagged by examining this relationship at two separate
waves of data collection.
Of course, pubertal development does not automatically
lead to negative behavior. As Piquero and Brezina (2001)
point out, the incidence of delinquent behavior varies among
an adolescent cohort, and a small minority of youths abstains
from prohibited conduct. One possible contributing factor to
719
this variability may be that the timing of ones pubertal devel-
opment shapes the experience of a maturity gap (Moffitt,
1993). Early developing adolescents may chafe under the
significant restrictions on autonomy typically imposed on
the very young, while late developers of the same age may
experience little or no frustration from similar impingements
on their independence. Given that younger children are typi-
cally afforded less autonomy than older youths, we speculate
that early puberty in younger children should be associated
with greater problem behavior. In other words, we suspect
that the effect of early sexual maturity on peer associations
may be conditional on the age of the child.
Finally, we turn our attention to the specific question of
smoking initiation. We isolate male youths in our sample
that had not smoked before initial wave of data collection,
and investigate whether early pubertal development and peer
associations predict whether those youths started smoking at
a later time.
Prior research has uncovered race and ethnic differences
in adolescent smoking prevalence (Kann et al., 1999; Unger
et al., 2001; USDHHS, 1994) and friendship patterns
(Kandel, 1978; Moody, 2001). We expect to confirm in our
data that white youths are more likely to smoke. Research
has also demonstrated a link between parent smoking and
the likelihood that youths will start smoking (Fleming et al.,
2002; Jackson et al., 1997; Melby et al., 1993). Accordingly,
we will control for the smoking behavior of parents in our
sample.
Method
This study relies on data collected from in-home surveys in
the first two waves (19951996) of the National Longitudinal
Study of Adolescent Health (henceforth, Add Health). The
Add Health study is a nationally representative, probability-
based survey of adolescents in grades 712. The sampling
design of Add Health has been described in detail elsewhere
(Bearman et al., 1997; Resnick et al., 1997). Briefly, 80
high schools were randomly selected from a roster of all
high schools in the United States stratified by enrollment, re-
gion, urbanicity, type of school, and racial/ethnic mix. Sub-
sequently, the largest feeder school (junior high or middle
school) was selected when one existed; thus, a total of 132
schools participated. Information on pubertal development,
peer associations, and several important control variables
was collected from adolescents at both waves of data collec-
tion. A parent of each respondent also completed a question-
naire at the first wave.
We limit our analyses to male adolescents between
the ages of 12 and 16 years because boys at these ages
show significant variation in pubertal development. We
focus on boys in the current investigation because there
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are significant gender differences observed in the timing of
sexual maturation (Ablassi, 1998; Tanner, 1962). Thus, the
meaning of being on-time differs by gender. As we noted
above, the only prior investigation to explicitly consider a
puberty-peers link to smoking behavior focused exclusively
on female adolescents (Stattin and Magnusson, 1990). After
restricting our focus to males who were between the ages of
12 and 16 at the first wave of data collection, and censoring
cases with missing values for our variables of interest, we
are left with a final sample of 3,958 respondents.
Outcome variables
Initiation of smoking behavior
This variable is constructed by considering respondents an-
swers about their smoking behavior in the Wave I and Wave II
in-home surveys. At the first wave, respondents were asked,
have you ever tried cigarette smoking, even just 1 or 2
puffs? In our sample of 3,958, 47% of respondents reported
never smoking (N = 1,853). Subjects were asked a similar
question at the second wave, but were asked whether they
had tried smoking since the month of the Wave I interview.
We construct a dichotomous smoking initiation variable by
identifying nonsmoking male youths at Wave I. Of the 1,853
nonsmokers at Wave I, 322 reported initiating smoking be-
havior between the first and second waves. The 322 respon-
dents who initiated smoking between the waves were coded
as 1; the remaining 1,531 youths who reported no smoking
initiation at either the first or the second wave were coded
as 0 (thus, this variable excludes subjects who reported any
smoking at Wave I).
Peer smoking
Prior research has demonstrated that ones closest friends
(compared to an adolescents larger friendship group) are
more influential for initiation of youth smoking (Urberg
et al., 1997). We employ two measures to tap smoking be-
havior of respondents best friends, drawn from each of the
in-home surveys. At each wave, respondents identified the
number of their three best friends who smoked at least one
cigarette a day. Responses range from 0 to 3.
Independent variables
Pubertal status
Our measures of self-reported pubertal status are derived
from variables commonly used to assess adolescent sex-
ual development (Petersen et al., 1988). Questions asked of
respondents at each wave included self-descriptions of the
amount of hair under the arms (1 to 5), thickness of facial
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J Youth Adolescence (2006) 35:717727
hair (1 to 4), deepening of the voice since grade school (1 to
5), and self-reported physical development compared to boys
of similar age (1 to 5). Previous research has demonstrated
that adolescent self-assessment of pubertal development is
strongly correlated with assessments made by parents or
medical professionals (Dorn et al., 1990). For each ques-
tion, higher values reflect a greater level of development.
The Chronbachs alpha statistics for the summed indices are
.65 for Wave I and .66 for Wave II. We use the summed pu-
berty indices to construct two dichotomous measures of early
pubertal development. For each wave, we standardized the
puberty index and then identified adolescents who were one
standard deviation or greater above the mean. These early
developing youths were coded as 1; the remaining youths
were coded as 0.
Recall that we also suspect that any observed effect of
pubertal development on peer associations and smoking ini-
tiation may be greatest among the youngest youths in our
sample. To consider this particular question, we isolate the
youngest but most developed children at Wave 1 with a mul-
tiplicative interaction term. The term (PD AGE) has two
constituent components: the age of the child and the di-
chotomous pubertal development measure. To avoid prob-
lems with collinearity, adolescents ages have been centered
about the sample mean.
Demographics and parent smoking
We include a dummy variable where respondents are coded
as 1 if they identified themselves as White (and selected no
other racial or ethnic identity); otherwise they were coded as
0. We also incorporate a measure of parent smoking (0 = no;
1 = yes), taken from the parent questionnaire administered
during Wave I.
The multistage cluster sampling design of the Add Health
study requires the use of a software package that can cor-
rect for design effects and unequal probability of subject
selection. Unless otherwise noted, all results are computed
using the STATA statistical software package which, when
used with appropriate sample weights, provides nonbiased
parameter estimates and standard errors (Chantala and Tabor,
1999).
Results
Weighted descriptive statistics for all variables used in this
study are presented in Table 1. The average age for our
sample at Wave I is 14 years. Approximately 69% of the
sample identified themselves as White. The mean value for
our smoking initiation variable is 19%. This means that of
the subjects in the sample who reported no smoking prior
to Wave I, approximately 1 in 5 engaged in some degree of
J Youth Adolescence (2006) 35:717727 721

Table 1 Descriptive statistics,

National Longitudinal Study of Variable Mean Standard deviation Min Max
Adolescent Healtha
Smoking Initiationb (Wave 1 = No/Wave 2 = .19 .38 0 1
Yes)
Age 14 1.19 12 16
White (1 = yes) .69 .50 0 1
Parents: Do you smoke? (1 = yes) .33 .45 0 1
Pubertal Development Indices:
Wave I 11 2.94 4 19
Wave II 12 3.01 4 19
Advanced Pubertal Development ( 1 STD):
Wave I .20 .40 0 1
a Wave II .15 .36 0 1
Descriptive statistics come
How many close friends smoke?
from the first two waves of the
study, 19951996. N = 3,958. Wave I .72 1.00 0 3
Wave II .91 1.09 0 3
b
N = 1,853.

smoking behavior by the second wave (about one year after
the first wave of data collection).
The mean number of best friends who smoked at Wave
I is 0.72, which increased to 0.91 at the second wave. Ad-
ditional analyses (not shown) demonstrated that at Wave
I about 40% of respondents reported having one or more
close friends who smoked. At Wave II, this proportion in-
creased to 48%. For subjects with changes in the number
of close friends who smoke, the typical difference in friend-
ship composition was rather small. For instance, less than
4% of the sample reported a shift from 0 to 3 close friends
who smoked between Waves I and II, and only 1.5% re-
ported 3 close friendships with smokers at Wave I but none at
Wave II.
Most of the adolescents in the sample experienced at least
some of the signs of physical development associated with
puberty. At both waves, the average physical development
score is located within the middle of the range for our
indices of puberty. The indices are also stable across the
two waves of data for a range of 4 to 19, the mean for
the Wave I scale is 11; for Wave II is it 12. Diagnostic
statistics indicate that both scales are essentially normally
distributed (skewness statistics for both scales are .05
and .20 respectively; kurtosis statistics are .29 and
.13, respectively). Approximately 20% of the sample had
reached an advanced level of pubertal development by Wave
I of the study (e.g., they are one standard deviation above
the mean for pubertal development). For Wave II, 15% of
the sample was identified as having an advanced pubertal
status.
The stability of the physical development scales and the
peer measures between the waves of data collection suggest
that these variables may be highly correlated. To investigate
this possibility, bivariate associations for the core variables
in our analyses are shown in Table 2. There are modest to
strong associations between the Wave I and Wave II pubertal
development scales (.63), and the Wave I and Wave II reports
of the number of respondents 3 best friends who smoked
(.51). Age of respondent has moderate to weak associations
with the pubertal development measures (.32 and .21, re-
spectively) and peer smoking variables (.17 and .13). Wave
I advanced pubertal status is also modestly correlated with
Wave II pubertal status (.45) and weakly associated with age
(.19).

Table 2 Zero-order correlation matrix for variables, add health (N = 3,958)

01 02 03 04 05 06 07 08 09 10

01 Age 1.00
02 White .05 1.00
03 Parent smoke .01 .08 1.00

04 Wave I Pubertal Development .32 .12 .01 1.00

05 Wave I Advanced Pubertal Development .19 .08 .02 .70 1.00
06 Wave I Advanced Pubertal Development Age .41 .02 .01 .28 .39 1.00
07 Wave II Pubertal Development .21 .18 .03 .63 .45 .22 1.00
08 Wave I Peer Smoking .17 .08 .13 .13 .10 .10 .06 1.00

09 Wave II Peer Smoking .13 .10 .15 .10 .09 .05 .08 .51 1.00
10 Smoking Initiation .01 .03 .04 .01 .01 .03 .06 .13 .31 1.00

p<.05; p<.01; p<.001.

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Table 3 Ordered logistic regression estimates of pubertal development on peer smokinga,b,c

Wave I Peer Wave II Peer Smoking

Smoking
Model 1 Model 2 Model 3 Model4 Model 5 Model
6

Age .37 .36 .25 .25 .10 .15

White .15 .15 .27 .26 .22 .23
Parent smoking .57 .57 .73 .73 .51 .51
Wave I Advanced Pubertal development .21 .20 .15 .06 .17
Wave II Advanced Pubertal development .23 .08
Wave I Peer smoking .97 .97
Wave I Advanced Pubertal Development .04 .30
Age
2 LOGL 4188.7 4188.6 4645.8 4643.7 4189.03 4182.06
Model chi square 147.04 147.17 117.25 119.41 409.63 421.72
Pseudo R2 .03 .03 .03 .03 .12 .12
a
Data: National Longitudinal Survey of Adolescent Health, 19951996.
b
Estimates shown are ordered logistic regression metric coefficients. Odds ratios are not shown.
c
N = 3,958.

p<.05; p<.01; p<.001.

Smoking initiation is not associated with respondent age
or pubertal development measured at the first wave. The cor-
relation between smoking initiation and Wave II pubertal
development is statistically significant but it is not substan-
tively meaningful (.06). At first glance, these data might
appear to contradict previous research that has identified a
relationship between pubertal development and adolescent
smoking (Harrell et al., 1998; Martin et al., 2001; Wiesner
and Ittel, 2002). However, it is important to keep in mind
that the present investigation is specifically concerned with
smoking initiation, not regular consumption of cigarettes,
which has been the focus of prior research.
Moreover, the failure to discern a bivariate association be-
tween the pubertal development measures and smoking ini-
tiation does not preclude the hypothesis we have advanced;
namely, that that the effect of sexual maturity on adoles-
cent decisions to start smoking may be indirect, through an
increased propensity of early developing youths to be influ-
enced by peers who smoke. Indeed, we observe a significant
association between youths who started smoking by Wave II
and respondents reports of the number of their three closest
peers who smoke at Wave II (.31).
Our search for the direct and indirect effects of pubertal
development on the number of close friends who smoke
is shown in Table 3. The models report the change in the
logged odds of a respondent reporting N + 1 best friends
who smoke, per unit of change in the selected independent
variables. In the first model, we consider the effect of Wave I
pubertal status on Wave I peer smoking, net of controls. The
model reveals that older children, and youths whose parents
self-reported that they smoked at Wave I were significantly
more likely to identify a greater number of best friends who
smoked. The race/ethnicity measure does not significantly
contribute to the predictive power of the model. Net of these
controls, advanced sexual maturity at Wave I significantly
increase the likelihood that respondents reported having a
greater number of best friends who smoked (.21, p < .05).
In model 2 we add to the previous model an interaction
term that is the product of the respondents age and Wave I
pubertal status. In our discussion of Moffitts (1993) theory
about the adolescent maturity gap, we speculated that the
effects of early sexual maturation on the propensity of youths
to seek out friendships with delinquent peers might vary as a
function of child age. Specifically, we hypothesized that the
effects of early pubertal development on associations with
peers who smoke might be greatest among the youngest
youths in our sample. In fact, no significant conditioning
effect of age on pubertal development is observed in model
2. At least for the Wave I cross-sectional data, we conclude
that early sexual maturity has a direct and non-conditional
association with the number of respondents best friends who
smoke.
A more accurate test of Moffitts maturity gap argument
(1993) may require longitudinal data. After all, the hypoth-
esis is that early puberty impels children to seek out friends
who flaunt age-specific prohibitions of conduct (such as un-
derage smoking), and these new associations in turn promote
initiation of proscribed behavior. This suggests that ones
level of pubertal development may influence the composi-
tion of ones friendship network at a later time. In Models
36 of Table 3, we assess the effects of advanced pubertal
development on friend selection at Wave II.
We discover that older respondents, respondents who
identify themselves as White, and respondents whose

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J Youth Adolescence (2006) 35:717727
Fig. 1 Expected probability of
youth at wave 2 reporting N + 1
close friends who smoke
parents smoke were significantly more likely to have a
greater number of close friends who smoked at Wave II.
Moreover, it appears that the effect of advanced puberty on
friend selection is contemporaneous rather than lagged be-
cause Wave I pubertal development does not significantly
affect Wave II friend selection (Model 3), but Wave II puber-
tal status does (.23, p < .05; Model 4). This contemporaneous
effect of Wave II pubertal development on friend selection
disappears once the number of close friends who smoked at
the prior wave of study is added to the model (Model 5).
These data suggest that the effect of advanced puberty on the
number of peers who smoke at Wave II is completely medi-
ated by the number of peers who smoked at the prior wave of
the study. Thus, the effects of advanced sexual maturity on
Wave II peer smoking appear to be indirect: advanced sexual
maturity at Wave I is positively associated with the number
of close friends who smoke at the first wave; and it is those
peers who have direct effects on Wave II smoking peers.
In Model 6 of Table 3, we revisit the possibility that
the effect of advanced sexual maturity on deviant peers is
conditioned by age. The results indicate that, indeed, the
effect of Wave I puberty on the number of best friends who
smoke at Wave II is conditioned by the age of respondent.
The significant, negative coefficient for the interaction term
723
suggests that the effect of advanced sexual development at
Wave I is greatest among the younger subjects in the sample.
Put another way, among youth who have experienced
advanced pubertal development, the younger the adolescent,
the greater the number of close friends who smoke. The
interaction between Wave II advanced pubertal status
and age never reached statistical significance; thus, this
term as well as our measure of Wave II advanced sexual
maturity were removed from the model for the sake of
parsimony.
In order to clarify our interpretation of the interaction
term, we graphed the predicted probabilities for advancing
into the next category of the number of close friends who
smoke by values of the advanced puberty-age interaction.
The three lines in Fig. 1 represent the probability that sex-
ually developed adolescents in the sample would report an
additional friend who smoked at wave II as a function of
their age.
The graph is consistent with our aforementioned under-
standing of the interaction term. Among the most sexu-
ally developed adolescents in the sample, twelve year olds
who had two best friends who smoked at wave I had a
.68 predicted probability of selecting an additional friend
who smoked at wave II. The probability for a comparable
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724 J Youth Adolescence (2006) 35:717727

Table 4 Logistic regression

estimates of smoking initiation Model 1 Model 2 Model 3 Model 4
on pubertal development,
Intercept 1.67 1.67 1.84 2.32
deviant peers, and age: waves
III (19951996)a,b,c,d Age .04 .06 .10 .11
White .05 .04 .05 .12
Parent smoking .30 .30 .22 .01
Wave I Advanced Pubertal Development .07 .10 .10 .20
Age Wave I Advanced Pubertal Development .20 .20 .19

Number of Friends who Smoke (Wave I) .41

Number of Friends who Smoke (Wave II) .86
2 LOGL 884.4 883.7 868.49 785.4
Model chi square 4.11 4.86 18.25 92.52
Pseudo R2 .004 .005 .02 .12
a
Data: National Longitudinal Survey of Adolescent Health.
b
Estimates shown are logistic regression metric coefficients. Odds ratios are not shown.
c
N = 1,853.
d
Due to collinearity, smoking peers from both waves cannot be included in the same model.

p < .05; p < .01; p < .001.

16 year-old youth at the upper range of pubertal development
was .39. The results were similar for sexually mature adoles-
cents with one best friend who smoked at the prior wave of
the study: the twelve year-olds had a .28 probability of adding
another smoking peer, whereas the sixteen year olds had a
.18 probability. Overall, our results suggest that pubertal de-
velopment has a lagged effect on the number of ones close
friends who smoke, and this lagged effect is only apparent in
longitudinal analyses. Additionally, it appears that a lagged
effect of advanced pubertal status is most intense among the
youngest adolescents who are more physically developed
than are their peers. These findings represent key evidence in
support of Moffitts (1993) argument about the causal order
between early sexual maturity and increased susceptibility
of youths to the behavior of their rule-flaunting peers.
Finally, we turn our attention to the issue of first onset of
smoking behavior. Recall that of the 3,958 adolescent males
in our sample, 1,853 did not report any cigarette smoking
at Wave I. By Wave II, 322 of these Wave I nonsmokers
reported some cigarette smoking. In Table 4, we consider
pubertal development and peer associations in terms of their
potential effects on initiation of smoking behavior. In partic-
ular, we use logistic regression to identify any direct, mediat-
ing, or conditioning effects of pubertal development and peer
smoking on the odds of smoking initiation between Waves
1 and 2.
In the first two models of Table 4, we consider the effects
of demographic variables, parent smoking, advanced puber-
tal development, and early puberty on the odds of smoking
initiation. None of the variables in either model significantly
affect the likelihood of smoking initiation. In Models 3 and 4,
we consider the effect of Wave I and Wave II peer smoking on
this form of deviant behavior. We find both contemporaneous
and lagged effects of smoking peers on smoking initiation
among respondents. (The two peer measures are not included
in the same model due to collinearity issues.) We considered
additional models that included interaction terms between
Wave II advanced puberty and age, but in no case did any of
the interactions prove significant (results not shown). Thus,
we conclude that the influence of advanced pubertal develop-
ment on smoking initiation appears to be indirect, expressed
through the number of close friends who smoke at Wave I.
This indirect effect is strongest among the youngest but most
sexually developed adolescents in the sample.
Discussion
We applied longitudinal data from a national sample of ado-
lescents to consider the relationship between advanced pu-
bertal development, peer associations, and smoking initiation
among male youths. We find that being more physically de-
veloped than ones peers has no direct effect on adolescent
boys uptake of cigarette smoking. Rather, we find that the
effects of puberty on smoking are indirect, mediated by the
number of the adolescents close friends who smoke.
A second important finding of this study is that the
effect of advanced pubertal development on the number of
smoking peers is most salient for the youngest adolescents
in the sample. Put another way, very young boys who are
more physically developed than their peers appear to be
more motivated to form close associations with friends who
smoke, and it is those friends who in turn support the initi-
ation of smoking. These results are consistent with Stattin
and Magnussons (1990) research showing that girls who
were more physically mature than their peers tended to form

Springer
J Youth Adolescence (2006) 35:717727
friendships with older adolescents. Associations with older
friends were related to an earlier age of onset for alcohol
and drug using behaviors among the early developing girls
in their sample. In our study, the conditional effect of age
on the puberty-deviant peers relationship is exclusively lon-
gitudinal in naturecontemporaneous interactions between
Wave II pubertal status and age affected neither Wave II
peer selection nor smoking initiation by Wave II. Due to
these mediating and conditioning effects, we conclude that
peer associations are a key link between adolescent pubertal
development and initiation of smoking.
Our research has implications for both the public health
and delinquency literatures. In terms of the public health
literature, our findings reinforce the conclusions of prior
research concerning the importance of pubertal develop-
ment as a determinant of smoking behavior (Andersson and
Magnusson, 1990; Aro and Taiple, 1987; Dick et al., 2000;
Harrell et al., 1998; Martin et al., 2001; Stattin and Mag-
nusson, 1990; Tschann et al., 1994; Wiesner and Ittel, 2002;
Wilson et al., 1994). What this study also contributes to the
smoking literature is an empirical basis for considering the
role of smoking peers especially close friends who smoke
in an association between pubertal development and smok-
ing initiation. Moreover, because the link between advanced
puberty and smoking initiation is lagged, we suggest that
longitudinal assessments of this relationship are needed in
order to avoid misspecifying analytical models of smoking
initiation.
Regarding the delinquency literature, the results of this
study are consistent with the elaboration of a causal chain
between pubertal development, peer associations and delin-
quency hypothesized by Terrie Moffitt (1993). Moffitt pro-
poses that advanced pubertal status motivates modern ado-
lescents to imitate the behavior of delinquents. Our findings
build upon this insight by demonstrating the importance of
close friendships (and not merely imitation of ones general
cohort of peers), which appear to precipitate the initiation of
problem behaviors such as smoking. Our results are consis-
tent with other studies that have examined this hypothesis for
other delinquent and antisocial adolescent behaviors (Felson
and Haynie, 2002; Piquero and Brezina, 2001).
Our findings take on greater theoretical importance when
one considers the age-graded nature of risk and protective
factors for delinquency. On the one hand, associations with
deviant peers are a critical risk factor, and research shows that
access to such peers may be a function of parental control. For
example, Warr (1993b) found that the greater the amount of
evening and weekend time parents spent with their children,
the weaker the effect of delinquent peers on an adolescents
delinquent behavior. Similarly, Piquero and Brezina (2001)
find that the greater the level of behavioral autonomy with
peers, the greater the effect of physical maturity on rebellious
delinquency. On the other hand, we did discover a strong
725
positive relationship between parent smoking and the number
of a youths close friends who smoke. An adolescent may
establish close friendships with peers who smoke not only
as a means of establishing behavioral autonomy but also
because they are modeling the smoking behavior of their own
parents (e.g., Akers, 2000). It is therefore possible that the
parental controls that might otherwise reduce the influence of
close friends (e.g., Warr, 1993b) will be attenuated if parents
themselves are smokers.
An additional dimension of future research underscores
a fundamental limitation of our study as well as Stattin and
Magnussons (1990) similar investigation of female youths.
Neither research team is directly measuring two key com-
ponents of Moffitts theory: adolescent frustration due to
the maturity gap and the particular mechanisms by which
adolescents model delinquent peers. We have emphasized
that youths opportunities to form and sustain friendships
with delinquent peers are a key consideration. How those
opportunities specifically translate into friendship selection
and modeling of peers is an area for future study. The re-
silience of friendships also deserves additional attention. If
Moffitt (1993) is correct, the friendships formed between
early maturing adolescents and their delinquent friends will
be attenuated when both groups desist from crime as they
age. However, there is some evidence that friendships among
deviant youth stand the test of time, persisting well into
early adulthood (e.g., Warrs (1993a) discussion of so-called
sticky friends). Future research should explore whether there
are lingering consequences of early sexual maturation on
friendships and proscribed conduct as youths enter early
adulthood.
Acknowledgment This research uses data from Add Health, a pro-
gram project designed by J.Richard Udry, Peter S. Bearman, and
Kathleen Mullan Harris, and funded by a grant P01-HD31921 from
the National Institute of Child Health and Human Development,
with cooperative funding from 17 other agencies. Special acknowl-
edgment is due Ronald R. Rindfuss and Barbara Entwisle for as-
sistance in the original design. Persons interested in obtaining data
files from Add Health should contact Add Health, Carolina Popu-
lation Center, 123 W. Franklin Street, Chapel Hill, NC 27516-2524
(www.cpc.unc.edu/addhealth/contract.html).
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