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higher prevalence than Blacks (Geronimus, Neidert, & Bound,
1993; Johnston, O’Malley, Bachman, & Schulenberg, 2009).
Thus, it is not clear whether the associations between pubertal
timing and smoking are the same for White and Black
Cigarette smoking continues to be a significant public health
problem and is the most preventable cause of death in the United
States. The earlier smoking is initiated, the greater the risk of
developing smoking-related cancer. Women face increased
health risks from smoking compared with men. Approximately
178,000 women died from smoking-related diseases each year
(1995–1999), dying an average of 14.5 years earlier than non-
smokers (Centers for Disease Control, 2002). Adolescents are
also at risk for smoking-related health issues, such as respiratory
problems and early atherosclerotic lesions (a risk for cardiovas-
cular disease; Elders, 1997; Prokhorov, Emmons, Pallonen, &
Tsoh, 1996). Furthermore, a significant number of adolescents
smoke. In 2007, 20% of high school students in a nationwide
survey reported smoking in the past 30 days (Eaton et al.,
Adolescence is a crucial period for considering the implica-
tions of smoking initiation. Of adult smokers, 80%–90% began
smoking in adolescence (Kessler et al., 1996). Early smoking is
not only associated with continued cigarette use but also associ-
ated with increased risk of future drug use and other substance
use disorders (Lewinsohn, Rohde, & Brown, 1999). Typically,
cigarette use does not peak until later adolescence (Jackson,
Sher, Cooper, & Wood, 2002); however, early involvement,
especially use by age 11–13 years, has been found to predict sub-
stance use and abuse in later adolescence and adulthood (Sung,
Erkanli, Angold, & Costello, 2004). Thus, identifying factors
associated with early substance use is important for understand-
ing how initiation begins and may be prevented (Foshee et al.,
Pubertal timing is one factor found to affect the initiation
and prolonged use of substances. In particular, there is a strong
association between early pubertal timing and early use of ciga-
rettes for men and women (Bratberg, Nilsen, Holmen, & Vatten,
2007; Dick et al., 2000; Wilson et al., 1994). Adolescents with
Introduction: The purpose of this study was to examine
whether (a) early pubertal timing effects on smoking onset
existed for both White and Black girls and (b) whether the as-
sociation between pubertal timing and smoking onset was
moderated by race.
Methods: Participants included 264 girls (14.9 ± 2.2 years,
164 White, and 100 Black) at the baseline report of a longitu-
dinal study of whom 153 reported smoking and age at first
Results: Kaplan–Meier analysis stratified by racial group
showed a significant difference between the pubertal timing
groups for Black girls only. After accounting for covariates using
Cox regression, there was no significant interaction between
pubertal timing and racial group. There was a main effect of
pubertal timing indicating that late maturers were at significantly
lower risk for smoking initiation compared with the early and
on-time groups, but the early and on-time groups were not sig-
nificantly different from each other.
Discussion: Results point to equal risk of early smoking onset
for early and on-time maturers of both racial groups, indicating
the need for smoking prevention in early adolescence for both
White and Black females.
There is substantial evidence that early pubertal timing is associ-
ated with higher rates and earlier initiation of substance use
(Dick, Rose, Viken, & Kaprio, 2000; Ge, Jin, et al., 2006), par-
ticularly in girls. While early timing is related to earlier onset of
cigarette use (Wilson et al., 1994), there is limited research that
examines whether this association differs by race. Black girls
enter puberty earlier than White girls (Biro et al., 2006; Chumlea
et al., 2003), which may put them at higher risk for substance
use. However, racial disparities are noted in tobacco use with
White adolescents initiating at an earlier age and having a
Pubertal timing and smoking initiation in
adolescent females: Differences by race
Sonya Negriff, Ph.D.,1 Lorah D. Dorn, Ph.D.,1,2 & Bin Huang, Ph.D.2,3
1 Department of Pediatrics, Division of Adolescent Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH
2 University of Cincinnati College of Medicine, Cincinnati, OH
3 Center for Epidemiology and Biostatistics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH
Corresponding Author: Sonya Negriff, Ph.D., School of Social Work, University of Southern California, 3375 South Hoover Suite
E204, Los Angeles, CA 90089, USA. Telephone: 213-821-2206; Fax: 213-740-8905; E-mail: firstname.lastname@example.org
Received November 20, 2009; accepted April 17, 2010
Nicotine & Tobacco Research, Volume 12, Number 7 (July 2010)
early pubertal timing were twice as likely to try cigarettes
compared with those who were not early maturers (Westling,
Andrews, Hampson, & Peterson, 2008). Similarly, early
maturing boys and girls had significantly greater likelihood and
higher prevalence of smoking compared with average and late-
developing peers (Simon, Wardle, Jarvis, Steggles, & Cartwright,
2003; van Jaarsveld, Fidler, Simon, & Wardle, 2007). Within
women, early developers were 2.5 times more likely to have
tried cigarettes (Lanza & Collins, 2002) or smoked their first
cigarette about 7 months earlier than girls with later puberty
(Wilson et al.). Similarly, Tschann et al. (1994) found that
34% of early maturers initiated smoking at younger than 12
years of age. Thus, because girls are beginning to smoke at
younger ages and more go on to be regular smokers (Galanti,
Rosendahl, Post, & Gilljam, 2001; U.S. Department of Health
and Human Services, 2001), particular attention should be
paid to the factors associated with early initiation of smoking
in adolescent females.
Race is also associated with variation in cigarette use. Blacks
have lower cigarette initiation rates than Whites (Johnson &
Hoffmann, 2000), and the age of smoking onset is significantly
later in Blacks than Whites (Geronimus et al., 1993; Harrell,
Bangdiwala, Deng, Webb, & Bradley, 1998). Additionally, risk
factors for smoking (e.g., family and peer cigarette use, per-
ceived availability of cigarettes) were less prevalent among
Black than among White youth, while regular smoking was
more prevalent among White than among Black adolescents
(Robinson & Klesges, 1997). Although Blacks are at lower risk
for cigarette use in adolescence, by adulthood, the smoking
prevalence rates are comparable with Whites, yet Blacks have
higher lung cancer rates (U.S. Department of Health and
Human Services, 1998).
Although there is extensive evidence that early pubertal tim-
ing is related to early cigarette use and higher rates of smoking,
no studies have examined this association for Black adolescents.
Based on the literature, it was expected that early pubertal timing
would be associated with earlier age at first cigarette for White
adolescents; however, there is little empirical guidance re-
garding whether this association would be the same for Black
girls because there are no studies that have compared pubertal
timing effects on smoking onset by race. Therefore, the purpose
of this study was to determine (a) whether early pubertal timing
effects on age at smoking onset existed for both White and Black
girls and (b) whether the association between pubertal timing
and age at smoking onset was moderated by race.
The participants were girls enrolled in a longitudinal study on
smoking, mood, and its impact on bone and reproductive
health in adolescent girls (N = 264). Participants were primarily
White (62.1%) or Black (32.6%). The remaining 5.3% of the girls
were biracial or other race/ethnicities and were combined with
the Black group. Participants were recruited from an urban teen
health center and the surrounding community. Data for the
present study were from the first assessment, which took place
from December 2003 to October 2007. Girls were enrolled in
the study by age cohorts (11, 13, 15, and 17 years) based on the
cross-sequential design (Miyazaki & Raudenbush, 2000), and
an eligibility questionnaire based on five previously defined
levels of smoking experience ranging from “not even a puff”
to daily smoking. Smoking categories were based on modifica-
tions to the methods of Mayhew, Flay, and Mott (2000) and
consisted of (a) “Never-smoker,” defined as zero puffs of a
cigarette across the lifetime; (b) one puff to two cigarettes in
lifetime; (c) smoked 3–99 cigarettes or more than 100 but
none in the last 30 days; (d) smoked more than 100 cigarettes
in lifetime and 1–19 days of the last 30 days; and (e) smoked
more than 100 cigarettes and 20–30 days of the last 30 days.
Exclusion criteria were (a) pregnancy or breast feeding within
the past 6 months, (b) primary amenorrhea (>16 years) or sec-
ondary amenorrhea (<6 cycles/year), (c) body mass index less
than the first percentile or body weight greater than 300
pounds, (d) medication/medical disorder influencing bone
health, and (e) psychological disabilities impairing compre-
hension or compliance. This study received approval from the
hospital’s institutional review board.
Participants came to an urban children’s hospital for study
visits. After consent and assent were obtained, the parent was
directed to a separate room to complete questionnaires. The
adolescent then had a physical examination, during which time,
a standardized interview was conducted focusing on menstrual
history. Other procedures followed but were not the focus of
this paper. The protocol also included the Diagnostic Interview
Schedule for Children, which assessed cigarette use.
Age at menarche (in years and months) was obtained through
a clinician interview with the adolescent. Early, on-time, and
late timing groups were created based on the sample distribu-
tion of age at menarche within White and Black racial groups
in this study. Plus and minus 1 SD away from the mean is typ-
ically used as cutoffs for timing groups (Ge, Brody, Conger,
Simons, & McBride-Murray, 2006). Thus, girls who were 1 SD
or more below the mean (within their racial group) were cod-
ed as early timing, and those who were 1 SD or more above the
mean were coded as late timing. Remaining girls were coded as
At Time 1, 210 (80%) of the sample were menarcheal. For
the remaining 54 premenarcheal girls, age at menarche was
obtained from a subsequent data collection timepoint. Six pre-
menarcheal girls withdrew before the Year 2 visit and thus could
not be assigned to a timing group. At Year 4, there were three
girls who had not reached menarche. However, based on our
criterion and their chronological age, they were placed in the
late timing group.
Age at first cigarette
Age at first cigarette was defined as “how old were you the first
time you smoked a cigarette?” that was entered in years. This
was obtained from the Diagnostic Interview Schedule for
Children version VI (DISC; Shaffer, Fisher, Lucas, Dulcan, &
Schwab-Stone, 2000). The DISC is a computerized structured
diagnostic interview to assess mental health symptoms and
Pubertal timing and smoking onset
The covariates (socioeconomic status [SES], age, friend smok-
ing, and parental smoking) were chosen based on evidence that
these variables are associated with the dependent variable (age
at smoking initiation). The Hollingshead scale was used as an
index of SES (Hollingshead, 1976) with higher scores indicating
higher SES. Parent smoking was assessed by the question “are
there any parents or step-parents who live in the home that
smoke” (0 = no and 1 = yes). Friends’ smoking was assessed by
the girls’ report of whether they had one or more close friends
who were regular smokers (0 = no and 1 = yes).
To examine group differences in age at smoking onset separately
by pubertal timing and racial group, analysis of covariance
(ANCOVA) was conducted. Age at first cigarette was entered as
the dependent variable, and racial group was entered as an inde-
pendent variable. Covariates included age, SES, parental smok-
ing, and friend smoking. Next, pubertal timing group was
entered as the independent variable with the same dependent
variable and covariates as the previous analysis with the inclu-
sion of race.
The primary aims were conducted using survival analysis,
which estimates the time to a terminal event (“smoking onset”)
and the proportion “surviving” within each event period. This
analytic technique is used when a large proportion of the
participants have not yet had the “event” occur during the data
collection period. Thus, using traditional methods such as
regression would bias the results by excluding all those who
have not initiated the event in question (Singer & Willett, 1991).
Because of the nature of the dependent variable (age at smoking
initiation), there is inherently a large number of individuals
who do not have information on this variable (referred to as
censored observations). However, survival analysis is designed
to deal with censored observations, which would be problem-
atic in most other statistical approaches. To examine pubertal
timing effects on smoking onset for White and Black girls,
Kaplan–Meier analysis was used with pubertal timing group as
the between groups factor and stratified by race (White vs.
Black). This analysis produces median ages for age at first ciga-
rette by timing group and race. The log-rank test was used to
examine differences in the survival curves for each pubertal tim-
ing group stratified by race. To examine racial differences in
survival curves within pubertal timing groups, Kaplan–Meier
analysis was used with racial group as the between-groups
factor, stratified by pubertal timing group.
Cox regression was used to examine whether the associa-
tion between pubertal timing and smoking onset was moderat-
ed by race. The covariates were entered in the first block,
pubertal timing and race entered in the second block, and the
interaction term entered in the third block. A significant chi-
square change indicated whether the interaction term account-
ed for significant variance in the model above that of the
Descriptive statistics appear in Table 1. There were 153 girls
who reported smoking and thus also reported age at first ciga-
rette. Of those who reported an age at first cigarette, the mean
age was 12.24 years (SD = 2.56 years) and the median age was
13 years. Key variables were examined within pubertal timing
and race groups adjusting for stated covariates. ANCOVA
revealed no significant difference between White (adjusted M =
12.20) and Black (adjusted M = 12.67) groups on the mean age
of smoking initiation, F (1, 138) = 1.16, p = .28. For timing
group, post-hoc pairwise comparisons indicated a mean differ-
ence between the early (adjusted M = 11.38) and late (adjusted
M = 13.83) timing groups (p = .00) and the on-time (adjusted
M = 12.22) and late groups (p = .00) but no difference between
the early and on-time groups (p = .13).
Survival curves by racial group and
pubertal timing group
For the racial groups, 42.4% of the White group and 41.4% of
the Black group were censored in their age of onset of smok-
ing (i.e., those who had not started smoking). The
median survival time was 14 years for both racial groups (95%
CI = 13.49–14.51 years for White group and 13.32–14.68 years
for Black group). For the pubertal timing groups, 35.9% of the
early, 43.4% of the on-time, and 37.8% of the late groups were cen-
sored in their age of onset of smoking. The median survival
times were 14 years (95% CI = 12.67–15.33) for the early group,
Table 1. Descriptive statistics by pubertal timing and racial group in 264 adolescent girls
Pubertal timing groupRacial group
EarlyOn-time LateWhite Black
Mean age in years (SD)
Mean SES (SD)
Mean age at menarche in years (SD)
Percent that have never smoked
Percent that had friends who smoke
Percent that had parents who smoke
Note. SES = socioeconomic status. For the White group, the cutoffs for the early and late groups were 11.52 and 13.74 years, respectively, whereas
for the Black group, the cutoffs were 10.67 and 13.34 years, respectively.
Nicotine & Tobacco Research, Volume 12, Number 7 (July 2010)
14 years (95% CI = 13.46–14.54) for the on-time group, and
15 years (95% CI = 13.89–16.11) for the late group (see Figure 1).
The log-rank test was used to examine differences in the sur-
vival curves by pubertal timing group stratified by race. With-
in the White group, the median age at smoking onset was
14 years (95% CI = 12.88–15.12) for the early maturers,
13 years (95% CI = 12.37–13.63) for the on-time, and 14 years
(95% CI = 12.44–15.57) for the late timing groups. Pairwise
comparisons showed no significant differences between puber-
tal timing groups. For the Black group, the median age at
smoking onset was 12 years (95% CI = 10.59–13.41) for the early
maturers, 14 years (95% CI = 13.39–14.61) for the on-time,
and 15 years (95% CI = 13.98–16.02) for the late timing
group. Pairwise comparisons within the Black group showed
that early maturers had the youngest age at smoking onset
compared with on-time (c2 = 4.50, p = .03) and late maturers
(c2 = 6.42, p = .01). Kaplan–Meier survival estimates were also
computed between racial groups stratified by pubertal timing
group, but there were no significant differences, indicating
that within each timing group (early, on-time, and late), the
White and Black girls were not significantly different in the age
at smoking onset. Most importantly, within the early pubertal
timing group, the White (median age = 14, 95% CI = 12.88–
15.12) and Black (median age = 12, 95% CI = 10.59–13.41)
groups were not significantly different in the age at smoking
onset (p = .13).
Interaction effect between racial group
and pubertal timing on age at first
Using on-time puberty and Black group as the reference vari-
ables, there were no significant interactions (controlling for age,
SES, friend smoking, and parental smoking). Therefore, the in-
teraction terms were dropped, and the main effect of pubertal
timing was examined. Racial group, age, SES, parental smoking,
and friend smoking were entered in the first block, followed by
pubertal timing group in the second block. The block in which
pubertal timing was added improved the overall fit of the model
(Dc2 (2) = 6.67, p = .04) above the fit of the model with only the
first block of variables (c2 (7) = 40.42, p = .00). Several of the
covariates were significant: higher SES reduced the risk of smoking
onset (hazard ratio [HR] = 0.99, 95% CI = .97-1.00), whereas
parent and friend smoking increased the risk by 1.63 (95%
CI = 1.11–2.39) and two times (95% CI = 1.33–3.01), respectively.
However, racial group did not significantly increase the risk of
smoking initiation (HR = 1.37, 95% CI = 0.94–1.96). Of pri-
mary interest was the significant effect of pubertal timing group.
Being early or on-time increased the hazard of smoking initia-
tion in the next year by 1.94 (95% CI = 1.10–3.43) and 1.62
(95% CI = 1.04–2.57) times, respectively, over those in the late
pubertal timing group. However, the risk for smoking initiation
was not significantly different for early and on-time groups
Figure 1. Kaplan–Meier estimates of the number of participants who will experience the terminal event (smoking initiation) by the next event
period. Analyses completed by pubertal timing group for (a) White and (b) Black groups showed significant differences between pubertal timing
groups only for the Black group. Within Black girls, early maturers were significantly younger at first cigarette use than on-time or late maturers, as
shown by the distinct lines for each group with very little overlap. Censored data refer to those who have not experienced the event (smoking).
Pubertal timing and smoking onset
(HR = 1.19, 95% CI = 0.75–1.89). The results showed that after
adjusting for the covariates, there was no significant interaction
effect between racial group and pubertal timing on smoking ini-
tiation, although there appeared to be racial group differences
in the Kaplan–Meier analysis. There was a main effect of pubertal
timing for the total sample showing that late timing was associ-
ated with the lowest risk for smoking initiation (Figure 2).
The present study examined the association between pubertal
timing and age at first cigarette in a large sample of White and
Black adolescent females. When Black and White groups were
examined separately, early pubertal timing was associated with
earlier age of smoking initiation in Black girls only. This was
counter to expectations as most of the literature focuses on
White samples and the findings between early timing and sub-
stance use are well supported (Dick et al., 2000; Lanza & Collins,
2002; Westling et al., 2008). However, when race was tested as a
moderator, there was not a significant interaction between ra-
cial group and pubertal timing, but there was a main effect of
pubertal timing. Most studies have found that only early timing
is associated with increased substance use. For example, girls
with early puberty reported a younger age of first cigarette than
those with later puberty (Wilson et al., 1994) and were 1.5 times
more likely to smoke (Bratberg, Nilsen, Holmen, & Vatten, 2005).
However, we found that early and on-time groups were at in-
creased risk for early smoking initiation compared with the late
Although previous research has demonstrated that White
adolescents initiate smoking earlier, smoke more, and progress
to becoming regular smokers more rapidly than Black adoles-
cents (Harrell et al., 1998; Kandel, Kiros, Schaffran, & Hu,
2004), our study shows that a racial disparity may not exist
when assessing the effect of pubertal timing on smoking behav-
ior. Late timing for both Whites and Blacks seems to be protec-
tive against early smoking initiation. Smoking behavior in
adolescents, and especially early age at initiation, is particularly
important when examining long-term smoking and health
consequences. Youth who begin smoking in lower grades are
more likely to be adult smokers (Chassin, Presson, Sherman, &
Edwards, 1990). Additionally, age of smoking initiation is a
significant factor for failure in cessation attempts (Khuder,
Dayal, & Mutgi, 1999). These findings point to targeting early
and on-time maturers for smoking prevention programs in
adolescence. Furthermore, because pubertal timing is occurring
earlier for contemporary adolescents than in the past, targeting
early and on-time maturers at younger ages may be important.
There are several possible explanations for the differences
between our results and other studies. First, variability in how
pubertal timing was determined across the studies may yield
differences in timing classifications. We used age at menarche,
which is an event later in puberty, whereas other studies used
ratings of secondary sexual characteristics (e.g., breast and
pubic hair development). Although menarche and secondary
sexual characteristics are associated, the data suggest only a
moderate correlation between the two, thus introducing a po-
tential source of error (Biro et al., 2006). Second, the majority
of the participants were in mid- to late adolescence when it
becomes more likely that they will have tried smoking. Several
studies have found evidence of a “catch-up” effect when
assessing older adolescents. Specifically, late maturing females
between 16 and 18.5 years caught up to their early and on-time
maturing peers in their alcohol use (Dick et al., 2000). Thus, in
early adolescence, early timing may be important in predicting
substance use, while later in adolescence, girls with on-time de-
velopment may be using substances as much as the early matur-
ers. It is also possible that in late adolescence, pubertal timing
effects may be negligible (Stattin & Magnusson, 1990) with the
host of other influences that may be more salient for substance
use. However, the age at onset of cigarette use is still important
as it influences prolonged substance use into adulthood
(Faulkner, Escobedo, Zhu, Chrismon, & Merritt, 1996; Grant &
One limitation of this study may be that our dependent
variable was age of first cigarette, which may not necessarily
Figure 2. Survival functions for age at first cigarette by pubertal timing group via Cox regression. Analysis accounted for the effects of age, race,
SES, parent smoking, and friend smoking. The early and on-time groups are not significantly different from each other, but both are significantly
different from the late group. This is indicated in the graph by the overlapping survival curves for the early and on-time group but the distinct curve
for the late group.
Nicotine & Tobacco Research, Volume 12, Number 7 (July 2010)
reflect continued smoking. An individual may try a cigarette but
then not smoke ever again. However, in the present sample, 68%
of those who reported an age at first cigarette have continued to
smoke. Thus, like other studies (Lewinsohn et al., 1999; Sung et
al., 2004), we find that age at first cigarette is an important con-
sideration when assessing future smoking, and intervening early
is essential for prevention of long-tem health problems.
A second limitation is that self-report was used for age at
menarche and age at first cigarette. Although it is impossible to
check the veracity of the reported ages, it is probable that for
these events, the adolescent is the most accurate reporter. When
our study is completed, we will be able to assess the reliability of
reports across time for the age of smoking initiation and age at
menarche. The number of girls who had not yet smoked might
be viewed as a limitation; however, survival analysis accommo-
dates large amounts of censored data, utilizing the maximum
amount of available information from censored data for analy-
sis (Singer & Willett, 1991).
An additional limitation may be the sample size for this
study. Due to the nature of the pubertal timing variable, there
will inherently be more participants in the on-time group than
in the early or late groups. However, many studies have used
this variable with similar distributions and sample sizes to the
current study, thus our confidence is increased. Additionally,
because this was a secondary data analysis, we may have limited
statistical power, particularly in examining interaction terms.
The nonsignificant interaction effect may be due to difficulties
with unequal cell sizes and creating categorical variables from
continuous ones as well as lack of power (Aguinis, Boik, &
Pierce, 2001; Frazier, Tix, & Barron, 2004). However, we feel
confident that the cell sizes are adequate for the analyses, and
the findings are valid and show some novel associations between
pubertal timing, smoking onset, and race.
Other factors that were not measured in this study can in-
fluence smoking behavior, such as early dating and parental
monitoring (Fidler, West, Jarvis, & Wardle, 2006; Westling
et al., 2008). However, the inclusion of parent and friends smok-
ing did account for two large influences on smoking. Other
studies found that friend smoking was related to smoking initia-
tion among Whites but not Blacks (Headen, Bauman, Deane,
& Koch, 1991) and parent smoking contributed to the onset of
daily smoking in their teenagers (Hill, Hawkins, Catalano,
Abbott, & Guo, 2005). In the present study, parent smoking was
related to age at first cigarette with having a parent who smokes
increasing the risk by 1.6 times. Thus, to reduce the risk for
daily smoking in adolescents, it may be important to encourage
parents to stop or reduce smoking.
Cross-sectional studies have inherent limitations in being
unable to unravel causal pathways. Additionally, because we
have not observed all the participants through the period of
highest risk for smoking initiation, we lose some information
about those defined as censored. Some of the girls who enrolled
as nonsmokers at the time of the assessment may eventually ini-
tiate smoking, but we have no way of knowing when that critical
age may be for every individual. Several studies have examined
smoking initiation data using survival analysis, and they provide
useful information about the risks (Andreeva, Krasovsky, &
Semenova, 2007; Chen, Unger, & Johnson, 1999). One study
found that after age 14, the risk of new smoking initiation
decreases (Unger & Chen, 1999). The majority of the sample is
older than 14 years, and thus, we may be more certain that we
are capturing the accurate risk model for smoking initiation. In
the future, we can examine the smoking onset age for all girls up
to age 17 and assess the reliability of age at smoking onset from
the subsequent yearly visits.
Overall, our results indicate that early and on-time pubertal
development increases the risk for early smoking onset in adoles-
cent girls. Contrary to expectations, we did not find racial differ-
ences in this association, indicating that late timing may be
protective for both White and Black girls. Our study shows that a
racial disparity may not exist when assessing the effect of pubertal
timing on smoking behavior for White and Black adolescents.
However, possible differences should be examined for other racial
minority groups. Additionally, this result provides evidence for
the importance of assessing puberty in studies of substance use.
While there are clearly multiple factors that contribute to the etiol-
ogy and maintenance of substance use, we show that omitting pu-
berty is overlooking a substantial influence on early substance use.
Future models should aim to incorporate these numerous influ-
ences, including a reliable measure of puberty so that we can better
understand these complex relationships and work toward the pre-
vention of prolonged substance use.
This work was supported by the National Institute of Drug
Abuse (grant number R01 DA 16402) to LDD, Principal Inves-
tigator; the National Center for Research Resources at the
National Institutes of Health (USPHS grant UL1RR026314);
and National Research Service Award Training grant
1T32PE10027 from the National Institutes of Health.
Declaration of Interests
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