#essay
Research Article
Is It Important to Prevent Early Exposure to Drugs and Alcohol Among Adolescents? Candice L. Odgers,1 Avshalom Caspi,2,3 Daniel S. Nagin,4 Alex R. Piquero,5 Wendy S. Slutske,6
Barry J. Milne,3 Nigel Dickson,7 Richie Poulton,7 and Terrie E. Moffitt2,3
1 University of California, Irvine;
2 Duke University;
3 Kings College London;
4 Carnegie Mellon University;
5 University of
Maryland; 6 University of Missouri-Columbia; and
7 University of Otago
ABSTRACT—Exposure to alcohol and illicit drugs during
early adolescence has been associated with poor outcomes
in adulthood. However, many adolescents with exposure to
these substances also have a history of conduct problems,
which raises the question of whether early exposure to
alcohol and drugs leads to poor outcomes only for those
adolescents who are already at risk. In a 30-year pro-
spective study, we tested whether there was evidence that
early substance exposure can be a causal factor for
adolescents’ future lives. After propensity-score matching,
early-exposed adolescents remained at an increased risk
for a number of poor outcomes. Approximately 50% of
adolescents exposed to alcohol and illicit drugs prior to age
15 had no conduct-problem history, yet were still at an
increased risk for adult substance dependence, herpes in-
fection, early pregnancy, and crime. Efforts to reduce or
delay early substance exposure may prevent a wide range
of adult health problems and should not be restricted to
adolescents who are already at risk.
Many adolescents experiment with drugs and alcohol, and
parents, teachers, and policymakers want to know the conse-
quences of adolescent substance use. Parents, in particular,
worry that their adolescents who use drugs or alcohol may suffer
long-term consequences, such as a dependence on drugs; be
drawn into risky sexual behaviors; contract sexually transmitted
diseases (STDs); fall behind in school; or get a criminal record.
Research has demonstrated that exposure to illicit drugs and
alcohol prior to age 15 statistically predicts substance disorders
in adulthood (Grant & Dawson, 1997; Hingson, Heeren, &
Winter, 2006). Exposure to these substances during adoles-
cence has also been linked to involvement in risky sexual
behaviors and STDs (Stueve & O’Donnell, 2005), early preg-
nancy (Ellickson, Tucker, & Klein, 2003), low educational
attainment (King, Meehan, Trim, & Chassin, 2006), and crime
(Elliott, Huizinga, & Menard, 1989). On the basis of this
evidence, the U.S. Surgeon General’s office has issued a call to
action to stop underage drinking (U.S. Department of Health and
Human Services, 2007), placing a special emphasis on risks to
youth who report drinking before the age of 15. However,
nagging doubts remain regarding whether substance use affects
adolescents’ later lives causally.
Critics of this recent policy stance allege that early exposure
to alcohol and drugs per se is not the cause of problems in ad-
olescents’ later lives (Peele, 2007). Indeed, research has re-
peatedly shown that adolescents who use substances in early
adolescence are also more likely than other adolescents to have
a childhood history of conduct problems, which itself predicts
the same adult outcomes (Moffitt, 2006). A recent review con-
cluded that adolescents at risk for developing substance-use
disorders are not ‘‘just normal adolescents who happen to be
experimenting with substances but, in many cases, are youths
with other . . . problems’’ (Armstrong & Costello, 2002, p. 1235).
Thus, parents, teachers, and policymakers are caught between
mixed messages: On the one hand, they are told that exposure to
drugs and alcohol prior to age 15 is harmful for adolescents and
should be prevented, and on the other hand, they are told that it
is normal for adolescents to try these substances and that the
majority will not become addicts or ruin their lives.
It is not practical or feasible to administer alcohol and drugs to
young adolescents in a randomized control trial in order to test
Address correspondence to Candice L. Odgers, Department of Psy- chology and Social Behavior, University of California, Irvine, 3361 Social Ecology Building II, Irvine, CA 92697-7085, e-mail: codgers@ uci.edu.
PSYCHOLOGICAL SCIENCE
Volume 19—Number 10 1037Copyright r 2008 Association for Psychological Science
the causal effect of substance use on adolescents’ future lives.
However, analytic strategies are now available to quantify
‘‘treatment’’ effects in observational studies when randomized
control trials are not a viable option (D’Agostino & D’Agostino,
2007; Stuart & Green, 2008). Such propensity-score methods
are designed to re-create the desirable features of experimental
designs by creating balance between exposed (‘‘treatment’’)
and nonexposed (‘‘control’’) groups that have formed naturally
over the course of an observational study (Haviland, Nagin, &
Rosenbaum, 2007).
Here we report the results of applying propensity-score
matching (Rosenbaum & Rubin, 1985) in a 30-year longitudinal
study to address a question of significant public-health impor-
tance that cannot be studied using randomized control trials.
Specifically, we asked whether there is evidence that early
exposure to illicit substances is a causal factor in adolescents’
future lives (‘‘are drugs bad for kids?’’), or whether adolescents
with a developmental history of conduct problems are simply
more likely than other adolescents to be exposed to alcohol and
illicit substances and to experience poor adult outcomes (‘‘do
bad kids do drugs?’’). At present, the extent to which a history of
conduct problems in childhood has confounded the association
between early substance exposure and adult outcomes is un-
clear. Researchers have called for prospective longitudinal
designs that are able to adequately account for childhood con-
duct problems (Hingson et al., 2006); however, to date, only a
handful of studies have met this criterion.
In the present study, adolescents’ developmental history of
conduct problems was assessed prospectively by multiple
informants. Assessments were made when the study members
were ages 7, 9, 11, and 13. Early substance exposure was de-
fined as frequent exposure to illicit substances prior to age 15.
Adolescents were then followed prospectively into adulthood
to assess the influence of early substance exposure on their adult
lives. We estimated two types of treatment effects to test whether
early substance exposure influenced adolescent’s adult lives.
First, we estimated the effect of early substance exposure on
adolescents’ adult outcomes across the entire birth cohort.
Propensity-score matching was applied to adjust treatment-
effect estimates for nonrandom assignment to the treatment
condition (in this case, defined as exposure to illicit substances
prior to age 15, which we term early exposure) and to facilitate
causal inference by ensuring that adolescents with early exposure
were balanced relative to those with no early exposure on key
background factors that might otherwise confound the results.
Second, we estimated group-specific treatment effects to test
whether early substance exposure is similarly dangerous for
all adolescents, or whether some adolescents’ developmental
history of conduct problems signals particular vulnerability to
early substance exposure. Developmental trajectories of con-
duct problems were defined previously in this cohort using
group-based trajectory modeling (Odgers et al., 2008); this work
isolated a group of children (66% of the cohort) who followed a
no-conduct-problem trajectory between the ages of 7 and 13.
Adolescents on this trajectory had very few deficits in childhood
and were less likely than their already-at-risk peers to experience
early substance exposure and poor adult outcomes. The question
for the majority of ordinary adolescents, therefore, was whether
adolescentswhohadno history of conduct problemswere protected
from any untoward effects of early substance exposure. By contrast,
the remaining 34% of the children in this cohort entered adoles-
cence with a history of conduct problems; these adolescents were
more likely (or had a higher propensity) than their normative peers
to experience early substance exposure and poor adult outcomes.
Thequestionforthissubgroupofalready-at-riskadolescents,there-
fore, was not whether they would go on to experience poor adult
outcomes, but rather whether early substance exposure placed an
additive burden on their already-compromised future lives.
METHOD
Participants
Participants were members of the Dunedin Multidisciplinary
Health and Development Study. The cohort of 1,037 children
(52% male) was constituted at 3 years of age, when investigators
enrolled 91% of children born consecutively between April
1972 and March 1973 in Dunedin, New Zealand. Cohort fami-
lies represent the full range of socioeconomic status in New
Zealand’s South Island and were primarily White. Follow-up
assessments were conducted, with informed consent, when the
cohort members were 5, 7, 9, 11, 13, 15, 18, 21, 26, and 32 years
of age; 96% of the living study members participated in the
age-32 assessment, which took place in 2003 through 2005.
Research ethics committees at the University of Otago, Duke
University, and Maudsley Hospital approved this research.
Early Exposure and Conduct-Problem Measures
Early Substance Exposure
At ages 13 and 15, study members reported on their frequency of
exposure to illicit substances during the past year. They reported
whether they had sniffed glue, gasoline, or other inhalants;
smoked cannabis; used any illegal drugs other than cannabis;
bought or drunk alcoholic drinks; or drunk alcoholic drinks
during school. Response options were 0, never; 1, once or twice;
and 2, multiple occasions. In total, 11.2% of the study members
were classified as being exposed to substances on multiple
occasions at age 13, age 15, or both; hereafter, we refer to these
study members as early-exposed adolescents. Alcohol was the
substance most commonly used by the young adolescents in our
cohort; 10% of study members were exposed to alcohol prior
to age 15, 5% were exposed to cannabis, and fewer than 2% were
exposed to inhalants or other drugs.
Conduct Problems
Self-, parent, and teacher reports were used to assess study
members’ conduct problems at ages 7, 9, 11, and 13 years. The
1038 Volume 19—Number 10
Early Exposure to Drugs and Alcohol
following six symptoms of conduct disorder, as defined by the
fourth edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM–IV; American Psychiatric Association, 1994),
were assessed as being present or absent at each age: physical
fighting, bullying other people, destroying property, telling lies,
truancy, and stealing. A composite score, ranging from 0 to 6,
was calculated to represent the number of different types of
conduct-problem behaviors each study member had engaged
in during the past year. As noted earlier, prior group-based
trajectory modeling isolated young adolescents following a no-
conduct-problem trajectory between the ages of 7 and 13 (65.7%
of the cohort; 74.1% of females and 57.9% of males). This group
represented a ‘‘pure,’’ or super-healthy, group in that the average
number of conduct-problem symptoms at each age was below 1.
Background Covariates
Psychometric properties of all background covariates in this
study have been reported in detail elsewhere (Moffitt, Caspi,
Rutter, & Silva, 2001), and all estimates of their reliability
exceeded .70. Background covariates were assessed prior to age
13, unless otherwise stated.
Family history of alcohol and drug disorders was assessed in
2003 through 2006 as part of the Dunedin Family Heath History
Study (DFHHS; Odgers et al., 2007). That study used the Family
History Screen (Weissman et al., 2000) to collect psychiatric-
history data about each study member’s biological parents,
grandparents, and siblings older than 10 years old. Ratings were
obtained from multiple informants. A family-liability score
was computed for each study member. This score indexed
the proportion of family members, across three generations, with
an alcohol or drug disorder.
Criminal conviction of a parent was also assessed through the
DFHHS; 25% of study members had at least one parent with a
criminal conviction.
Socioeconomic status (SES) was measured as the higher of the
father’s or mother’s occupation, as rated on a 6-point scale for
New Zealand (Elley & Irving, 1976); 21% of the families were
classified as low SES.
Maltreatment was measured using the following indicators:
rejecting mother-child interactions (as observed by staff mem-
bers), parental reports of harsh discipline, two or more changes
in primary caregiver, and retrospective self-reports of injurious
physical abuse or unwanted sexual contact. A study member was
considered to be maltreated if he or she had two or more indi-
cators of maltreatment (Caspi et al., 2002); on this basis, 9% of
the study members were classified as maltreated.
Mother’s IQ was tested using the SRA (Thurstone & Thurstone,
1973); scores were standardized (M 5 100, SD 5 15). Low mo-
ther’s IQ was defined as a standardized SRA score less than 85.
Child IQ was tested using the Wechsler Intelligence Scale
for Children–Revised (WISC-R; Wechsler, 1974); scores were
standardized (M 5 100, SD 5 15). Low child IQ was defined as a
standardized WISC-R score below 85.
Undercontrolled temperament was measured through staff
ratings. Ratings were made after observing the child in a 90-min
testing session with an unfamiliar examiner. Factor and cluster
analyses reduced these ratings to three temperament types,
including the undercontrolled type (Caspi & Silva, 1995).
Attention-deficit/hyperactivity disorder (ADHD) was measured
using the Diagnostic Interview Schedule for Children (Costello,
Edelbrock, Kalas, Kessler, & Klaric, 1982). Data obtained
when the study members were ages 5 to 15 were used to make
diagnoses according to the criteria of the third edition of
the Diagnostic and Statistical Manual of Mental Disorders
(DSM–III; American Psychiatric Association, 1980); diagnoses
were confirmed through parent or teacher report. Six percent of
study members met diagnostic criteria for ADHD.
Adult Outcomes
Substance-use disorders at age 32 were assessed from data
obtained in private structured interviews using the Diagnostic
Interview Schedule (Robins, Cottler, Bucholz, & Compton,
1995). Diagnoses were made according to DSM–IV criteria
(American Psychiatric Association, 1994). For this report,
substance dependence was defined as cannabis dependence,
dependence on other drugs, or alcohol dependence within the
past year. Dependence at age 32 signals a substance-use
problem serious enough to outlast early adulthood, a develop-
mental period when large numbers of young people can meet
criteria for substance disorders on a short-term basis.
Type 2 herpes infection at age 32 was assessed using blood
samples. Diagnoses were made on the basis of an indirect en-
zyme-linked immunosorbent assay (HerpeSelect s
2 ELISA
IgG, Focus Technologies, Cyprus, CA; Eberhart-Phillips et al.,
2001). Herpes infection was diagnosed using a cutoff value of
3.5, and any equivocal result (between 0.9 and 3.5) was resolved
using the Western Blot test (Ho, Field, Irving, Packham, &
Cunningham, 1993).
Early pregnancy was defined as having at least one pregnancy
prior to age 21 and was assessed by females’ self-report. The
failure to delay pregnancy until age 20 or 21 is associated with
economic costs and poor social consequences for both mothers
and children in contemporary cohorts (Maynard, 1996).
No educational qualifications was defined as ending second-
ary education prior to receiving qualifications and not returning
to earn qualifications by age 32. In New Zealand, students re-
ceive qualifications on the basis of national exams that almost
all students take by age 16; the results determine promotion in
secondary and technical schools and help people secure better
employment in the labor market (Miech, Caspi, Moffitt, Wright,
& Silva, 1999).
Number of criminal convictions between ages 17 and 32
was determined for each study member by searching the
computerized New Zealand Police database. Convictions for
nonviolent and violent crimes were included, but traffic con-
victions were not.
Volume 19—Number 10 1039
C.L. Odgers et al.
STATISTICAL ANALYSES
Analyses proceeded in four steps. First, because study members
were not randomly assigned to a substance-use condition,
potential selection biases were addressed by developing a
propensity score for early substance exposure. This score, e(x),
represented the conditional probability of early substance ex-
posure (z 5 1), versus no early substance exposure (z 5 0), given
a combination of key familial, social, and child covariates (x);
that is, e(x) represented P(z 5 1|x). Propensity scores were
calculated for all adolescents using a multivariate logistic re-
gression that included the 13 covariates listed in Table 1. The
c statistic for this model was .72 (95% confidence interval:
.67–.77), which indicates a fair-to-good ability to discriminate
between early-exposed and non-early-exposed adolescents.
The propensity scores ranged from .02 to .73.
Second, we used the STATA module PSMATCH2 (Leuven &
Sianesi, 2003–2006) to perform 3-to-1 nearest-neighbor pro-
pensity-score matching. Specifically, propensity scores were
used to match each early-exposed adolescent to 3 non-early-
exposed adolescents who had a similar probability of early
exposure.
Third, to determine whether early substance exposure influ-
enced adolescents’ later lives, we compared the adult outcomes
of early-exposed adolescents with the adult outcomes of
propensity-matched non-early-exposed adolescents.
Fourth, adolescents were stratified by their conduct-problem
history to estimate group-specific treatment effects. More spe-
cifically, we tested (a) whether early substance exposure pre-
sents a risk for the majority of adolescents, who have no conduct-
problem history (no-conduct-problem group), and (b) whether
adolescents with a prior history of conduct problems (conduct-
problem group) have a particular vulnerability to early substance
exposure.
RESULTS
Does Propensity-Score Matching Create Balance Between
Early- and Non-Early-Exposed Adolescents?
As Table 1 shows, early-exposed adolescents were well matched
to non-early-exposed adolescents following propensity-score
matching. Prior to propensity-score matching, the standardized
bias (SB) between groups ranged from �8% to 85% across the background covariates; the average SB was 17%. After propen-
sity-score matching, the SB between groups ranged from �6% to 8% across the background covariates, and the average SB
was 0%. We obtained a similar reduction in SB within the
conduct-problem subgroups after propensity-score matching:
TABLE 1
Risk Factors in Adolescents With Versus Without Early Substance Exposure, Before and After Propensity-Score
Matching
Risk factor
Before propensity-score matching After propensity-score matching
Mean score or prevalence Mean score or prevalence
No early exposure
Early exposure
SB (%)
No early exposure
Early exposure
SB (%)(n 5 813) (n 5 114) (n 5 342) (n 5 114)
Family history of alcohol or drug
disorder 0.14 0.21 43n 0.20 0.21 5
Conduct problems, age 7 1.65 1.90 16 1.97 1.90 �5 Conduct problems, age 9 1.47 1.75 18n 1.83 1.75 �6 Conduct problems, age 11 1.36 1.72 23n 1.79 1.72 �6 Conduct problems, age 13 1.31 2.49 85n 2.45 2.49 3
Parent criminal conviction (%) 25.0 31.8 16 29.3 31.8 6
Low socioeconomic status (%) 20.0 20.0 0 17.8 20.0 7
Maltreatment (%) 8.4 10.0 6 10.0 10.0 1
Low mother’s IQ (%) 14.1 18.1 11 15.7 18.0 8
Low child IQ (%) 13.1 15.2 6 16.3 15.2 �4 Undercontrolled temperament (%) 10.7 8.2 �8 9.1 8.2 �4 ADHD (%) 6.1 7.2 5 7.9 7.2 �3 Male (%) 50.6 51.8 3 53.3 51.8 �4 Average — — 17 — — 0
Note. The sample included 927 adolescents, categorized as early-exposed (i.e., exposed to alcohol or drugs on multiple occasions before age 15) and non-early-exposed (i.e., not exposed to alcohol or drugs on multiple occasions before age 15). Standardized bias (SB) between the treatment (exposed) group and the control (unexposed) group (subscripts T and C, respectively) was computed as follows: SB 5 MT � MC/
p [sT
2 1 sC 2)/2]. Negative values of SB indicate greater risk in the non-early-exposed group than in the early-exposed group. ADHD 5
attention-deficit/hyperactivity disorder. np < .10.
1040 Volume 19—Number 10
Early Exposure to Drugs and Alcohol
Within the no-conduct-problem subgroup, the average SB for
early- versus non-early-exposed adolescents was reduced from
2% to 1%, and within the conduct-problem subgroup, the aver-
age SB was reduced from 11% to 0%. For all analyses, the SB was
reduced to below 20% for each of the 13 covariates following
propensity-score matching, an indication of a high degree of
similarity in the distributions of the background covariates.
Does Early Substance Exposure Predict Poor Adult
Outcomes for Adolescents After Propensity-Score
Matching?
As Table 2 shows, early-exposed adolescents were at an increased
risk for the adult outcomes of substance dependence, herpes in-
fection, early pregnancy, failure to obtain educational qualifica-
tions, and criminal convictions. The adjusted effects after
propensity-score matching remained statistically significant for
all of these outcomes. Early-exposed adolescents were approxi-
mately 2 to 3 times more likely than non-early-exposed adoles-
cents to be substance dependent, to have herpes infection, to have
had an early pregnancy, and to have failed to obtain educational
qualifications; early-exposed adolescents also had significantly
more criminal convictions than non-early-exposed adolescents.
Does Early Substance Exposure Influence the Majority of
Ordinary Adolescents With No Prior History of Conduct
Problems?
As expected, early substance exposure was not a random event;
adolescents with a conduct-problem history were 2 times (odds
ratio 5 2.1, confidence interval 5 1.4–3.1) more likely to be
exposed to illicit substances prior to age 15, compared with ad-
olescents without a conduct-problem history. More specifically,
17.0% of adolescents with a conduct problem history, versus
9.1% of adolescents with no conduct-problem history, experi-
enced early substance exposure. Fifty-six of the 114 early-
exposed adolescents were assigned to the no-conduct-problem
subgroup; this means that approximately 50% of adolescents
exposed to substances prior to age 15 had no prior history of
conduct problems.
Table 3 presents the group-specific effects of early substance
exposure on adolescents’ adult outcomes. Adjusted effects after
propensity-score matching are presented separately for
adolescents with versus without a conduct-problem history. The
results in the table illustrate two main findings. First, after
propensity-score matching, ordinary adolescents without a
conduct-problem history were at an increased risk for adult
substance dependence, herpes infection, early pregnancy, and
criminal convictions if they had experienced early substance
exposure, although early substance exposure did not increase
risk for not finishing school in this subgroup. Second, early
substance exposure further elevated the risk for adult substance
dependence, early pregnancy, failure to obtain educational
qualifications, and criminal convictions—but not herpes in-
fection—among adolescents who were already at risk because of
their conduct-problem history.
Sensitivity Analyses
Are the effects of early substance exposure different for alcohol
versus illicit drugs? The substance most frequently used by
TABLE 2
Effects of Early Substance Exposure on Adolescents’ Adult Outcomes, Before and After Propensity-Score Matching
Adult outcome
Before propensity-score matching After propensity-score matching
Mean risk Mean risk
No early exposure
Early exposure Effect
size
No early exposure
Early exposure Effect
size(n 5 813) (n 5 114) (n 5 342) (n 5 114)
Substance dependence at age 32 (%) 11.1 28.8 3.25nn 14.7 28.8 2.25nn
(2.04–5.18) (1.35–3.73)
Herpes infection at age 32 (%) 17.0 28.0 1.90nn 16.1 28.0 2.02nn
(1.18–3.07) (1.18–3.44)
Early pregnancy (prior to age 21) a (%) 18.1 44.7 3.65nn 22.5 44.7 2.78nn
(1.93–6.86) (1.38–5.57)
No educational qualifications by age 32 (%) 14.7 32.1 2.74nn 19.3 32.1 1.97nn
(1.76–4.27) (1.22–3.19)
Number of criminal convictions between
ages 17 and 32 b
1.31 7.12 5.35nn 1.74 7.12 3.95nn
(2.85–10.05) (2.23–6.97)
Note. Study members were categorized as early-exposed (i.e., exposed to alcohol or drugs on multiple occasions before age 15) versus non- early-exposed (i.e., not exposed to alcohol or drugs on multiple occasions before age 15). The reported effect sizes are odds ratios for all outcomes except number of criminal convictions, for which incidence-rate ratios are reported. The numbers in parentheses are 95% confidence intervals. All findings remained statistically significant after adjustment of standard errors via bootstrapping in PSMATCH2. a Early pregnancy was estimated for females only and was defined as having at least one pregnancy prior to age 21; sex-specific propensity scores were used for this female-only analysis.
b Negative binomial regressions were applied to model incidence-rate ratios for the number
of criminal convictions. nnp < .05.
Volume 19—Number 10 1041
C.L. Odgers et al.
adolescents in our cohort was alcohol, and the vast majority of
early-exposed adolescents were exposed to alcohol. However,
65 of these adolescents were exposed to alcohol only and did not
use drugs. We tested whether adolescents exposed only to
alcohol differed from adolescents with no early substance ex-
posure. After propensity-score matching, early alcohol exposure
alone predicted a cumulative index of poor adult outcomes,
including substance dependence, herpes infection, failure to
obtain educational qualifications, and criminal convictions
(Cohen’s d 5 0.51, p < .01).
The remaining early-exposed adolescents (n 5 49) were ex-
posed to multiple substances. This reflects the reality of ado-
lescent substance use: It is extremely rare for a young adolescent
to specialize in the use of cannabis, inhalants, or any other illicit
drug. Rather, adolescents who use illicit drugs typically use
alcohol as well. After propensity-score matching, early poly-
substance exposure predicted a cumulative index of poor adult
outcomes (Cohen’s d 5 1.15, p <.01). Thus, although early
alcohol exposure alone was a significant predictor of adult
risk, early poly-substance exposure was associated with more
pronounced risk.
DISCUSSION
This application of propensity-score matching within a 30-year
prospective study helps to advance what is known about the
effects of early substance exposure in two ways. First, the prior
consensus in child psychology and psychiatry has been that
adolescents who go on to develop substance dependence are not
normal adolescents who are experimenting with substances, but
rather are highly likely to be adolescents with a prior history of
conduct problems (Armstrong & Costello, 2002). If this is the
case, the documented association between early substance
exposure and adult outcomes would not be due to exposure per
se, but instead would be the result of who is exposed (Wells,
Horwood, & Fergusson, 2004). Prior research has not resulted
in a consensus regarding the causal status of substance exposure
(Agrawal, Neale, Prescott, & Kendler, 2004; Kandel, 2003;
Lynskey et al., 2003; Prescott & Kendler, 1999). However,
results from this study are consistent with a causal effect of early
substance exposure among adolescents with no prior history
of conduct problems. That is, early-exposed adolescents with
no conduct-problem history, although they did not have an in-
creased risk of failing to complete school, were more likely than
their matched non-early-exposed counterparts to develop sub-
stance dependence, test positive for herpes, have an early
pregnancy, and be convicted of criminal offenses.
Second, findings from this prospective study support a causal
link between early substance exposure and a wide range of adult
outcomes. Propensity-score-adjusted effects indicate that early
substance exposure more than doubles the odds of adult
substance dependence, herpes infection, early pregnancy, and
criminal convictions. With a few notable exceptions (Brook,
Brook, Zhang, Cohen, & Whiteman, 2002; Dooley, Prause,
Ham-Rowbottom, & Emptage, 2005; Fergusson & Horwood,
1997; Wells et al., 2004), most prior tests of the association
between early substance exposure and adult outcomes have
been based on cross-sectional surveys of adults, which are
TABLE 3
Propensity-Adjusted Effects of Early Substance Exposure on Adolescents’ Adult Outcomes, for Adolescents With
Versus Without a Conduct-Problem History
Adult outcome
No conduct-problem history Some conduct-problem history
Mean risk Mean risk
No early exposure
Early exposure Effect
size
No early exposure
Early exposure Effect
size(n 5 168) (n 5 56) (n 5 165) (n 5 55)
Substance dependence at age 32 (%) 7.6 23.2 3.64nn 15.3 32.0 2.60nn
(1.57–8.45) (1.24–5.46)
Herpes infection at age 32 (%) 15.4 32.7 2.66nn 20.5 23.4 1.18
(1.26–5.60) (0.54–2.60)
Early pregnancy (prior to age 21) a (%) 12.3 34.4 3.75nn 35.9 69.2 4.02nn
(1.45–9.69) (1.04–15.46)
No educational qualifications by age 32 (%) 10.9 14.2 1.37 28.7 49.0 2.38nn
(0.56–3.34) (1.24–4.57)
Number of criminal convictions between
ages 17 and 32
0.65 1.59 2.86nn 2.52 13.12 4.96nn
(1.2–6.6) (2.5–10.0)
Note. Study members were categorized as early-exposed (i.e., exposed to alcohol or drugs on multiple occasions before age 15) and non- early-exposed (i.e., not exposed to alcohol or drugs on multiple occasions before age 15). The reported effect sizes are odds ratios for all outcomes except number of criminal convictions, for which incidence-rate ratios are reported. The numbers in parentheses are 95% confidence intervals. All findings remained statistically significant after adjustment of standard errors via bootstrapping in PSMATCH2. a The within-group treatment effects for pregnancy prior to age 21 are exploratory because each subgroup contained fewer than 50 early- exposed females. nnp < .05.
1042 Volume 19—Number 10
Early Exposure to Drugs and Alcohol
limited to retrospective recall of both childhood behaviors and
age of onset for substance use.
This study has limitations. First, although propensity-score
matching is designed to mimic the desirable features of ran-
domized control trials within observational studies, the lack
of random assignment to a treatment condition (which in this
case would have involved administering illicit drugs to children)
restricts an ideal test of causal association. Second, children
with conduct problems are a heterogeneous group; future studies
are required to estimate the impact of early substance exposure
separately for distinct subtypes of children with conduct prob-
lems. Third, this study was based on a single New Zealand
cohort and requires replication across ethnicities and cultures.
Fourth, the culture of drug and alcohol use among adolescents
has shifted over time. The cohort we studied was exposed to
substances for the first time in 1984 through 1987, which meant
that exposure was restricted mainly to alcohol and cannabis.
Ideally, a study would isolate the effects of specific types of
drugs on adolescents’ future lives. However, the reality is that,
aside from adolescents who are exposed to alcohol only, ado-
lescents exposed to substances prior to age 15 do not specialize
in their substance use. Only 1.2% of the cohort restricted their
substance use to cannabis prior to age 15, and less than 1% used
inhalants or other drugs exclusively. Therefore, we could not
examine the specific effects of cannabis, inhalants, or other
drugs separately, as the necessary groups of adolescents did not
exist. Research needs to examine the effects of other substances
that are now used more frequently by adolescents (e.g., cocaine,
ecstasy). Future studies should also be designed to include
a more rigorous assessment of early substance exposure based
on multiple informants and finer-grained measurement of the
precise timing and dosage of exposure.
With these limitations in mind, the implications of these re-
sults for public policy and prevention can be noted. With respect
to public policy, out results are consistent with the U.S. Surgeon
General’s call to action to prevent early substance exposure.
Results support the policy position that early substance expo-
sure poses independent risks for adolescents’ future lives; these
risks extend beyond the development of later substance de-
pendence, to include risks for herpes infection, early pregnancy,
and crime. With respect to prevention, it is important to note that
in our study, 50% of the adolescents exposed to substances
before age 15 did not have a prior history of conduct problems,
yet they experienced many of the same ill consequences as their
peers who were already at risk. This means that prevention
efforts should not focus solely on at-risk or conduct-problem
adolescents. Moreover, this research provides a rationale for
evaluating the cost-benefit ratios of substance-use prevention
programs separately for adolescents with versus without conduct
problems. In short, universal interventions are required to
ensure that all children—not only those entering early adoles-
cence on at at-risk trajectory—receive an adequate dose of
prevention.
Acknowledgments—This work was supported by the U.S.
National Institute of Mental Health (Grants MH45070 and
MH49414), the U.K. Medical Research Council (G0100527),
the William T. Grant Foundation, the Health Research Council
of New Zealand, and the National Institute on Drug Abuse
(Grant 1 P20 DA017589, awarded to the Duke University
Transdisciplinary Prevention Research Center). We thank the
Dunedin Multidisciplinary Health and Development Study
members and their families, the study unit’s research staff, and
study founder Phil Silva. We also thank the National Consortium
on Violence Research and Director Alfred Blumstein, as well
as the Center for Child and Family Policy and Director Kenneth
Dodge, for facilitating this research.
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1044 Volume 19—Number 10
Early Exposure to Drugs and Alcohol
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Created PDF documents can be opened with Acrobat and Adobe Reader 5.0 and later.) >> /Namespace [ (Adobe) (Common) (1.0) ] /OtherNamespaces [ << /AsReaderSpreads false /CropImagesToFrames true /ErrorControl /WarnAndContinue /FlattenerIgnoreSpreadOverrides false /IncludeGuidesGrids false /IncludeNonPrinting false /IncludeSlug false /Namespace [ (Adobe) (InDesign) (4.0) ] /OmitPlacedBitmaps false /OmitPlacedEPS false /OmitPlacedPDF false /SimulateOverprint /Legacy >> << /AddBleedMarks false /AddColorBars false /AddCropMarks false /AddPageInfo false /AddRegMarks false /ConvertColors /ConvertToCMYK /DestinationProfileName () /DestinationProfileSelector /DocumentCMYK /Downsample16BitImages true /FlattenerPreset << /PresetSelector /MediumResolution >> /FormElements false /GenerateStructure false /IncludeBookmarks false /IncludeHyperlinks false /IncludeInteractive false /IncludeLayers false /IncludeProfiles false /MultimediaHandling /UseObjectSettings /Namespace [ (Adobe) (CreativeSuite) (2.0) ] /PDFXOutputIntentProfileSelector /DocumentCMYK /PreserveEditing true /UntaggedCMYKHandling /LeaveUntagged /UntaggedRGBHandling /UseDocumentProfile /UseDocumentBleed false >> ] >> setdistillerparams << /HWResolution [1200 1200] /PageSize [612.000 792.000] >> setpagedevice