Prenatal drug (cocaine, opiates,
alcohol) exposure
Messinger
Questions
What is Frank et al.'s thesis about the current scientific
literature (their major argument)? Describe typical levels of
medical and social risk (including other types of exposure) in
cocaine exposed children. Summarize findings from the
Maternal Lifestyle Study with respect to 4 month interaction,
18 month attachment, and Bayley mental, motor, and
behavioral development between 1 and three years. Describe
the bolded pathways leading 7-year behavior (CBCL)
problems in Lester et al. (2009). Do you see a potential
problem with any of those pathways? Describe the impact of
prenatal alcohol exposure on childhood behavior in Sood et
al. What is a dose-response effect? Is maternal prenatal
substance exposure child abuse? In your view, What
Messinger
substances would and would not constitute abuse?
Crack Babies: Twenty Years
Later
http://www.npr.org/templates/story/story.ph
p?storyId=126478643
 Encouraging news on babies born to
cocaine-abusing mothers - The New...
http://www.nytimes.com/2009/01/27/world/
americas/27iht

Messinger
Is maternal prenatal substance
exposure child abuse?
What substances would and would
not constitute abuse?
Overview (Frank)
Prenatal cocaine exposure does not appear
to have a uniquely detrimental impact on
the developing child
 Other risk factors – such as prenatal alcohol
exposure, premature birth, low maternal
education and socioeconomic status – have
at least equally detrimental impacts on the
developing child.

Messinger
Review of Prenatal Cocaine Exposure

Issues in the Study of Cocaine
Exposure
–
Findings Contamination
Preconceptions about the
population
 Blindness to exposure

–
Confounding factors
Low SES
 Co-occurring exposure to other
teratogens

–
Mattson
Prospective vs. Retrospective
A Review of the
Effects of Prenatal
Cocaine Exposure
Among School-Aged
Children

Messinger
Ackerman, J. P., Riggins, T., & Black, M. M. (2010). A
Review of the Effects of Prenatal Cocaine Exposure
Among School-Aged Children abstract. Pediatrics, 125(3),
554-565. doi: 10.1542/peds.2009-0637
Systematic Review of Prenatal Cocaine
Exposure and Adolescent Development
Stacy Buckingham-Howes, Sarah Shafer Berger, Laura A. Scaletti and Maureen M. Black





Messinger
27 studies representing 9 cohorts.
Of 11, 7 found small but significant differences with
small effect sizes.
8 examined cognition/school performance; 6 reported
significantly lower scores on language and memory
tasks among adolescents with PCE, with varying
effect sizes.
Most studies controlled for other prenatal exposures,
caregiving environment, and violence exposure.
Pediatrics 2013;131:e1917–e1936
How big of a problem?

45,000 (~1.1%) mothers report cocaine use
–
Higher if unmarried, not working, less educated
0.1% for opiate use
 18.8% (757,000) of mothers reported
alcohol use during pregnancy
 20.4% (820,000) reported cigarette use

•
Messinger
(NPHS ‘92-’93)
Messinger
Perceptions of cocaine exposure


Drug of poor (crack)
– Quick acting, highly addictive, cheap
Use during pregnancy - child abuse?
–


Teachers ‘know’ that exposed children perform
more poorly
Can you tell the difference?
–

Messinger
200 women prosecuted in 30 states since 1985
Final project experiment
Video
An early rush to judgement

Fetal development
–

Neonatal/perinatal outcome
–

SIDS, poor feeding, hypertonia, & irritability
Development (from anecdotal reports)
–
Messinger
Spontaneous abortion & prematurity
distractibility, hyperactivity, impulsivity,
aggressiveness, & language delays
Current scientific literature


“Among children aged 6 years or younger, there is
no convincing evidence that prenatal cocaine
exposure is associated with developmental toxic
effects that are different in severity, scope, or kind
from the sequelae of multiple other risk factors.
Many findings once thought to be specific effects
of in utero cocaine exposure are correlated with
other factors, including prenatal exposure to
tobacco, marijuana, or alcohol, and the quality of
the child's environment.”
•
Messinger
Frank, et al. (2001).
Design issues

Previous problems
–
Small sample sizes

Current solutions
–
Large sample

–
Lack of matching
–
Follow-up matching on

–
Messinger
Lack of statistical
controls
–
4 centers
gestational age, gender,
and race
Ability to statistically
control for associated
risks
Exposure defined
Cocaine: Admitted use during the maternal
hospital interview and/or cocaine
metabolites in meconium
 Opiates: Admitted use during the maternal
hospital interview and/or opiate metabolites
in meconium

–
Messinger
central laboratory gas chromatography/mass spectroscopy
Cocaine exposed neonates are
slightly smaller
Characteristics
Absolute
Cocaine/
Opiate
Difference
Gestational Age (Ballard)
-1 week
Adjusted
Cocaine
Difference at
GA > 32 Weeks
---
Birthweight (g)
-465 g
-168 g
Length (cm)
-2.4 cm
-.77 cm
Head Circum.(cm)
-1.4 cm
-.49 cm


No opiate differences
Smoking and heavy drinking also associated
with smaller size
Bada
Messinger
et al., 1991; Bauer et al., 1991
Risk for Central Nervous System/autonomic
Nervous System (CNS/ANS) Signs Bada et al., 2002




Cocaine  increased risk of manifesting a constellation of
CNS/ANS outcomes, OR (95% CI): 1.7 (1.2 to 2.2)
Opiate effect, OR (95% CI): 2.8 (2.1 to 3.7).
Opiate+Cocaine had additive effects, OR: 4.8 Smoking
also increased the risk OR (95% CI) of 1.3 (1.04 to 1.55)
less than half a pack per day ; 1.4 (1.2 to 1.6) half a pack
per day or more.
Cocaine or opiate exposure increases the risk for
manifesting a constellation of CNS/ANS outcomes even
after controlling for confounders
–
11,811 maternal/infant dyads were enrolled.

Messinger
Of 1185 EXP, meconium analysis confirmed exposure in 717 to
cocaine only, 100 to opiates, and 92 to opiates plus cocaine
High levels of medical / social risk

Present in both groups - higher in the exposed group
COCAINE/OPIATE
Birthweight (% < 2500 g)
Married (%)
Education <12 years (%)
Medicaid (% Yes)
Messinger
EXPOSED
COMPARISON
(N=658)
(N=730)
4190.00%
10.3
49.4
85
4170.00%
24.7
31.3
79.5
Tobacco, marijuana, & alcohol

Present in both groups - higher in the exposed group
Tobacco use (% Yes)
Marijuana use (% Yes)
Alcohol use (% Yes)
Cocaine use (% Yes)
Opiate use (% Yes)
Messinger
COCAINE/OPIATE
EXPOSED COMPARISON
(N=658)
(N=730)
82.8
28.3
37.8
9.1
73.3
48.5
91
0
17.1
0
1 month neurobehavioral exam


Simple comparisons (univariate)
Cocaine exposed show poorer movement quality
–

4.43 vs. 4.49
No consistent cocaine differences on measures of:
Attention, Arousal, Regulation, Handling,, Excitability,
Lethargy, Non-optimal Reflexes Asymmetrical reflexes,
Hypotonia, Hypertonia, or signs of Stress Abstinence
(Lester et al., 2002)
Messinger
Controlling for other risk factors

Cocaine exposed infants were
– less aroused
 (lower
–
less stable self-regulation
 (less
–
ability to regulate crying)
Small differences
 (e.g.

behavioral state)
.02-.07 on 7-point scale) (Lester et al., 2002)
Similar isolated reports of early state regulation
difficulties in the literature
Messinger
Differences while feeding?


No infant cocaine differences on sucking / feeding
But cocaine-using mothers were less flexible and
engaged; had shorter feeding sessions
–

Even when controlling for other risks
Opiate-exposed infants showed prolonged
sucking, fewer pauses, more feeding problems
(e.g., spitting up), and increased arousal
–
Their mothers showed increased feeding related
activity, independent of their infants’ feeding problems.
•
Messinger
LaGasse, Messinger et al., 2003
4 month face-to-face interaction


No differences in infant smiling & sociality.
Cocaine moms more negative
–
–

Heavy exposed caregiver infant-dyads
–
–


Messinger
More negative when infant neutral
More mismatched in general
Infants more passive negative
Dyad shows more negative matching
Even after controlling for other risk factors
Does this have a continuing effect?
No differences in free-play at 18
months (Miami)
Caregiver requests, toy offers, positive and
negative vocalizations, or sensitivity
 Toddler toy offers, looks to caregiver,
smiles, and joint attention bids;
 Dyadic variables indicating the proportion
of caregiver and toddler requests and toy
offers fulfilled by the other partner.

Messinger
No exposure attachment effects


Level of prenatal cocaine exposure not
significantly related to secure/insecure attachment
status, disorganized attachment status, or rated
level of felt security.
Foster care status also not associated with
attachment status.
–
But heavier prenatal cocaine exposure, in interaction
with contextual variables (public assistance or
multiparity) associated with a higher level of behavioral
disorganization, more avoidance of the caregiver, and
less crying.
•
Messinger
Beeghly et al (2003)
Cocaine summary




Cocaine exposed neonates are slightly smaller
than non-exposed infants.
Slight, scattered decrements in self-regulation
(after covariate control) at 1 month were not
detectable in infant feeding behavior, 4 month
interaction, or Bayley mental, motor, or behavioral
development between 1 and three years.
Although cocaine caregivers were less involved at
1 & 4 months, there were no differences in secure
attachment or quality of play at 18 months
Standardized measures of development?
Messinger
Mental (MDI) Cocaine Effects

Unadjusted MDI
96
93
No Cocaine
Cocaine
90
•

87
84
81
Cocaine exposure was
associated with an
average 1.6 point MDI
decrement
Not significant after
adjusting for
covariates.
–
78
1 Year
Messinger
2 Year
3 Year
(P = .0075).
Site, birth weight, SES,
vocabulary, maternal care.
Psychomotor (PDI) Opiate Effects
Unadjusted PDI

96
93

90
87
84
No Opiate
Opiate
81
78
1 Year
Messinger
2 Year
3 Year
Opiate exposure was
associated with an
average 4 point PDI
decrement (P = .0023).
Not significant after
adjusting for
covariates (P = .0361).
–
Site, birth weight, SES, HOME
Behavior Rating Scale (BRS)

Messinger
Neither cocaine (P = .799, 0.26 percentile
difference) nor opiate exposure (P = .075,
4.5 percentile difference) was associated
with overall differences in BRS ratings
Covariate Effects

Low infant birth weight associated with lower
overall MDI, PDI, and BRS,
–

Indices of higher quality caregiving associated
with higher BSID-II scores.
–
–
–
–

Messinger
but did not moderate cocaine or opiate exposure effects.
Higher HOME scores with higher PDI and BRS.
Higher vocabulary scores with higher MDI and BRS.
Consistent mother with higher MDI and PDI.
Poverty status associated with lower BRS.
Partially responsible for sharp decline in mental
performance after one year for all groups
•
(Messinger et al., 2003)
Standardized tests of cognitive
achievement, motor performance,
and language development
Often show no significant exposure effects
 Effects, when present, tend to be of small
magnitude

–
Messinger
Although Singer found cocaine deficits in
mental performance (and motor performance),
Frank did not.
Cognitive cocaine exposure deficit –
in some studies

“6-point deficit in Bayley Mental Scales of Infant
Development scores at 2 years, with cocaine-exposed
children twice as likely to have significant delay
(mental development index <80).”
–
Controlled for confounding variables

“Four hundred fifteen consecutively enrolled infants (218 cocaineexposed and 197 unexposed) identified from a high-risk, low–
socioeconomic status, primarily black (80%) population screened
through clinical interview and urine and meconium samples for drug
use.
–
–
Messinger
The retention rate was 94% at 2 years of age.
Singer et al., 2002
But not in all studies


No significant adverse main effects of level of
cocaine exposure on Mental Development (MDI),
Psychomotor Development (PDI), or Infant
Behavior Record.
Interactions:
–
–
heavily exposed children who received child-focused
early intervention – highest adjusted mean MDI scores
“heavier exposure group born at slightly lower
gestational age - higher mean MDI scores than other
children of that gestational age
–

Messinger
Although the sample was born at or near term interaction of
cocaine exposure and gestational age
Frank et al.
Interaction: child age & caregiver


The adjusted mean MDI of children in unrelated
foster care at 6 months was 8.2 points lower than
children of biological mothers, whereas it was 7.3
points higher at 24 months.
At 6 months, the adjusted MDI of children living
with a kinship caregiver was 15.5 points lower
than that of children living with their biological
mother,
–
effect no longer significant at 24 months

difference in means: 4.3 points.
Frank et al.
Messinger
Motor differences

Cocaine-exposed group performed significantly
less well on both the fine and the gross motor
development indices.
–
–
Mean scores for both groups were within the average
range on the gross motor index, but greater than 1
standard deviation below average on the fine motor
index.
There also was an effect of alcohol exposure on the
receipt and propulsion subscale.
•
Messinger
Arendt . . . . Singer (1999)
Cocaine summary



Cocaine exposed neonates are slightly smaller
than non-exposed infants.
Slight, scattered decrements in self-regulation
(after covariate control) at 1 month were not
detectable in infant feeding behavior, 4 month
interaction, or Bayley mental, motor, or behavioral
development between 1 and three years.
Although cocaine caregivers were less involved at
1 & 4 months, there were no differences in secure
attachment or quality of play at 18 months
Messinger
Conclusions
As in other studies, cocaine exposure had little
impact on developmental outcome
 Exposure differences that did exist were
small.
 Nevertheless, even small deficiencies in the
performance of older cocaine exposed
children remain a cause of social concern.

Messinger
Impact of Small Cocaine Effects:
A Meta-Analysis of Studies
Using School-Age Children
Measure
Effect (SEM)
Percent Increase Affected
< 2 SD
Children
Service Cost
IQ difference
(n=5)
3.26 (2.01)
IQ points
3.75
1.6x
1,688 14,062
$4-35
million
Expressive
Language
(n=5)
.60 (.29)
SD units
8.08
3.5x
3,636 30,300
$17-138
million
Messinger
(Lester et al., 1998)
7 Year MLS Follow-up
100
Predicted Mental Functioning Over Time
80
60
70
Predicted IQ
90
No Cocaine
Cocaine
1
2
3
4
Age (Years)
Messinger
5
6
7
The cocaine deficit increased as
children reached school age.



There was an overall cocaine related deficit of
1.45 IQ points (p<.02) (see Figure). However,
this deficit increased at older ages (p = 0.003).
At 4 ½ years of age, the deficit was 3.35 points,
while at 7 years it increased further to 4.4 points.
Lower birthweight, SES, and maternal vocabulary
were also associated with decreasing performance
with age.
–
Messinger
These risk factors were common and partially explain
the entire sample’s decrease in test scores with age.
Cocaine exposure influences
sustained attention at 3, 5 and 7
 Stable
cocaine-specific effect on
sustained attention processing.
 “Each standard deviation increase
in level of prenatal cocaine
exposure 16% standard
deviation increase in omission
error scores at 7.
–
Messinger
Bandstra ES, Morrow CE, Anthony JC, Accornero VH, Fried PA. Neurotoxicol
Teratol. 2001 23(6):545-59. Longitudinal investigation of task persistence and
sustained attention in children with prenatal cocaine exposure.
Subtle special ed effects at age 7

Prenatal cocaine exposure … effect on
individualized education plan, but only
when controlling for low IQ.
–
When low child IQ was not included in the
model, prenatal cocaine exposure had a
significant effect on support services.
 Male
gender, low birth weight, white race, and low
child IQ also predicted individualized education
plan. Low birth weight and low child IQ were
significant in all models
•
Messinger
Pediatrics. 2008 Jul;122(1):e83-91. Epub 2008. Effects of prenatal cocaine exposure on special
education in school-aged children. Levine TP, Liu J, Das A, Lester B, Lagasse L, Shankaran
S, Bada HS, Bauer CR, Higgins R.
Jury out?



Messinger
Differences associated with cocaine exposure and
other risk factors were associated with a widening
deficit in child IQ.
The impact of cocaine exposure became more
evident at later ages when demands for higherlevel cognition become more prevalent (e.g.,
school performance).
The, “jury is still out” on the long-term effects of
prenatal exposure.
Provisos

Compliance
–

High risk samples - high variability
–


Messinger
Difficulty in discerning specific effects
Generalizable only to similar high-risk samples
Multiple risks come together
–

Heaviest users
Polydrug use, low SES, low birth weight
Older kids
Unique?

Messinger
“There is no convincing evidence that
prenatal cocaine exposure is associated with
any developmental toxicity different in
severity, scope, or kind from the sequelae of
many other risk factors.” (Frank et al., 2001,
pp. 21-24)
Behavior Problems in Children With
Prenatal Substance Exposure
Messinger
What about other drugs?





Messinger
Prenatal tobacco exposure costs $263 million in
neonatal health costs alone
Alcohol is a known teratogen
High levels associated with fetal alcohol syndrome
Lower levels negatively affect cognitive
development through lifespan
In infancy, there is a dose-response relationship
between prenatal alcohol exposure (AA/day, 0 2+) and mental and motor development (Jacobson
et al., 1993).
Prenatal Alcohol



Alcohol impacts prenatal development by
impairing and altering the development of fetal
brain structures.
Extensive alcohol use during pregnancy is
associated with the altered facial characteristics,
reduced growth, and severe cognitive deficits of
Fetal Alcohol Syndrome.
Fetal Alcohol Syndrome (FAS).
–
Messinger
http://scan.missouri.org/~willowpd/EffectBaby/fas_cau
ses.html
Current issues
Improved identification of occurrence of
maltreatment
 Examination of its consequences

–

What determines effect of abuse?
Establishing adequate services and supports
for families and children to protect from
exploitation and harm
Continuum of Severity


Messinger
Prenatal alcohol exposure has been shown to
result in a broad spectrum of negative outcomes
for the developing child. The nature and degree of
such effects appear to fall along a continuum of
severity.
Where the child falls along this continuum
depends upon the timing, the extent, and the
chronicity of the prenatal exposure to alcohol
(Phelps & Grabowski, 1992).
Alcohol effects are dosedependent.



Messinger
“Readily apparent relationships between the
quantity of alcohol consumed and subsequent
deficits and problems in the child.
Less obvious effects of alcohol exposure include
reductions in general intelligence and verbal
learning as well as problems with social
functioning.
Attention problems, memory deficits, and motor
skills problems have been associated with habitual
social drinking by the expectant mother
throughout the pregnancy
Is alcohol use child maltreatment?

Prenatal exposure to alcohol affects one in
four births
–
one in twelve mothers reporting binge drinking
during the pregnancy
The Effects Of Prenatal Alcohol Exposure On Infant
Mental Development: A Meta-analytical Review

Fetal alcohol exposure at all three dosage levels
was associated with significantly lower MDI
scores among 12–13-month-olds.
–
–
1 drink, 1–1.99 drinks, and > 2 drinks per day among
6–8-, 12–13- and 18–26-month-olds.
effect not eliminated, when adjusted for covariates

Messinger
Testa, Quigley, & Das Eiden Alcohol and Alcoholism 38, 4,
295-304, 2003
12 Month effect
Messinger
Heavy Exposure

Messinger
Habitually heavy alcohol consumption (3
or more drinks per day) and/or one or
more first-trimester alcoholic binges has
been shown to raise the risks of global
developmental damage to the fetus
(Driscoll et al., 1990).
Prenatal alcohol  conduct disorder?
“Prenatal exposure to alcohol was
associated with higher levels of conductdisorder symptoms in offspring, even after
statistically controlling for the effects of
parental externalizing disorders (illicit
substance use disorders, alcohol
dependence, and antisocial/behavioral
disorders), prenatal nicotine exposure,
monozygosity, gestational age, and birth
Messinger weight.” Disney et al., 2008

Prenatal Alcohol Exposure and
Childhood Behavior at Age 6 to 7
Sood, B., V. Delaney-Black, et al. (2001). "Prenatal Alcohol Exposure
and Childhood Behavior at Age 6 to 7 Years: I. Dose-Response
Effect." Pediatrics 108(2): e34.
Messinger
Individual Differences

Among children with similar high levels of
prenatal alcohol exposure, some will
manifest severe FAS symptomatology,
some will manifest mild effects, and some
children will appear unaffected (Able &
Sokol, 1986; Phelps & Grabowski, 1992).
–
Messinger
Genetics?
Smoking: One in five women
reports using while pregnant
Prenatal exposure to cigarettes is associated
with premature birth, low birth weight, and
irritability in the newborn.
 Tobacco exposure is associated with lower
intelligence scores and higher risk for
attention deficit disorder in school age
children.

Messinger
Immediate postnatal smoking
effects
Smoking-exposed infants showed greater
need for handling and worse self-regulation
(P < .05) and trended toward greater
excitability and arousal (P < .10)
 Effects of maternal smoking during
pregnancy at 10 to 27 days are subtle and
consistent with increased need for external
intervention and poorer self-regulation.

•
Messinger
1: J Pediatr. 2009 Jan;154(1):10-6. Epub 2008 Nov 5. Maternal smoking
during pregnancy and newborn neurobehavior: effects at 10 to 27
days.Stroud LR, Paster RL, Papandonatos GD, Niaura R, Salisbury
AL, Battle C, Lagasse LL,Lester B.
Nicotine replacement therapy?
While “Nicotine replacement therapy [e.g.,
nicorettes] avoids exposure to the myriad
compounds present in tobacco smoke,
nicotine itself causes damage to the
developing nervous system. … Based on the
clear, adverse effects of nicotine on brain
development observed in human and animal
studies, we suggest that safer alternatives for
smoking cessation in pregnancy are badly
needed.
(Pauly
&
Slotkin,
2008)
Messinger
Methamphetamines

Prenatal methamphetamine use is associated
with fetal growth restriction after
adjusting for covariates
–
–
–
3.5 times more likely to be small for gestational
age (sga).
Tobacco 2 times more likely to be sga
Birthweight in the methamphetamine exposed
group was lower than the unexposed group.
•
Messinger

The Infant Development, Environment, andLifestyle Study: Effects of Prenatal Methamphetamine Exposure,
Polydrug Exposure, and Poverty on Intrauterine Growth. Lynne M. Smith, MDa, Linda L. LaGasse, PhDb,Chris
Derauf, MDc, Penny Grant, MDd,Rizwan Shah, MDe, Amelia Arria, PhDf,Marilyn Huestis, PhDg, William
Haning, MDh,Arthur Strauss, MDh, Sheri Della Grotta, MPHb,Jing Liu, PhDb and Barry M. Lester, PhDb.
PEDIATRICS Vol. 118 No. 3 September 2006, pp. 1149-1156
Effects of prenatal methamphetamine
exposure on behavioral and cognitive
findings at 7.5 years of age

After adjusting for covariates, children exposed to
methamphetamine had significantly higher cognitive
problems subscale scores than comparisons and were 2.8
times more likely to have cognitive problems scores that
were above average on the Conners' Parent Rating Scale–
Revised: Short Form. No association between prenatal
methamphetamine exposure and behavioral problems,
measured by the oppositional, hyperactivity, and attentiondeficit/hyperactivity disorder index subscales, were found.
•
Messinger
Diaz, S. D., Smith, L. M., LaGasse, L. L., Derauf, C., Newman, E.,
Shah, R., Arria, A., Huestis, M. A., Della Grotta, S., Dansereau, L.
M., Neal, C., & Lester, B. M. (2014).. J Pediatr, 164(6), 13331338. doi: 10.1016/j.jpeds.2014.01.053
Debate
Illicit drug use is uniquely toxic to the
infant
 Illicit prenatal drug use is child abuse and
should be prosecuted
 Licit and illicit drug use have comparable
effects on the infant
 Both should be prosecuted.

Messinger
Additional readings









Messinger
Frank, D. A., Augustyn, M., Knight, W. G., Pell, T., & Zuckerman, B. (2001). Growth, development,
and behavior in early childhood following prenatal cocaine exposure: A systematic review. Journal
of the American Medical Association, 285(12), 1613-1625.
Alessandri, S. M., Bendersky, M., & Lewis, M. (1998). Cognitive functioning in 8- to 18- month-old
drug-exposed infants. Developmental Psychology, 92(3), 565-573.
Alessandri, S. M., Sullivan, M. W., Imaizumi, S., & Lewis, M. (1993). Learning and emotional
responsivity in cocaine-exposed infants. Developmental Psychology, 29(6), 989-997.
Arendt, R., Angelopoulos, J., Salvator, A., & Singer, L. (1999). Motor Development of Cocaineexposed Children at Age Two Years. Pediatrics, 103(1), 86-92.
Bauer, C., Shankaran, S., Bada, H. S., Lester, B., Wright, L., Krause-Steinrauf, H., Smeriglio, V.,
Finnegan, L., Maza, P., & Verter, J. (2002). The Maternal Lifestyle Study: Drug exposure during
pregnancy and short-term maternal outcomes. American Journal of Obstetrics and Gynecology,
186(3), 487-495.
Bendersky, M., & Lewis, M. (1998). Arousal modulation in cocaine-exposed infants. Developmental
Psychology, 34(3), 555-564.
Dow-Edwards, D. (1993). The puzzle of cocaine's effects following maternal use during pregnancy:
Still unsolved. Neurotoxicology & Teratology, 15(5), 295-296.
Eiden, R. D., Lewis, A., & Young, S. C. a. E. (2002). Maternal cocaine use and infant behavior.
Infancy, 3(1), 77-96.
Eyler, F. D., Behnke, M., Conlon, M., Woods, N. S., & Wobie, K. (1998). Birth Outcome From a
Prospective, Matched Study of Prenatal Crack/Cocaine Use: II. Interactive and Dose Effects on
Neurobehavioral Assessment. Pediatrics, 101(2), 237-241.
Additional readings II
Jacobson, J. L., & Jacobson, S. W. (1995). Strategies for detecting the effects
of prenatal drug exposure: Lessons from research on alcohol. In M. Lewis &
M. Bendersky (Eds.), Mothers, babies, and cocaine: The role of toxins in
development. (1 ed., pp. 111-128). Hillsdale, NJ: Lawrence, Erlbaum
Associates, Publisher.
 Jacobson, J. L., & Jacobson, S. W. (1996). Methodological considerations in
behavioral toxicology in infants and children. Developmental Psychology,
32(3), 390-403.
 Jacobson, J. L., Jacobson, S. W., Sokol, R. J., Martier, S. S., & Ager, J. W.
(1993). Prenatal alcohol exposure and infant information processing ability.
Child Development, 64, 1706-1721.
 Jacobson, J. L., Jacobson, S. W., Sokol, R. J., Martier, S. S., & Kaplan-Estrin,
M. G. (1993). Teratogenic effects of alcohol on infant development.
Alcoholism: Clinical and experimental research, 17(1), 174-183.
 Jacobson, S. W., Fein, G. G., Jacobson, J. L., Schwartz, P. M., & Dowler, J. K.
(1984). Neonatal correlates of prenatal exposure to smoking, caffine and
alcohol. Infant Behavior and Development, 7, 253-265.
 Jacobson, S. W., Jacobson, J. L., Sokol, R. J., Martier, S. S., & Chiodo, L. M.
Messinger
(1996). New evidence for neurobehavioral effects of in utero cocaine

Additional readings III








Messinger
Lester, B. M., Boukydis, C. F. Z., & Twomey, J. E. (2000). Maternal substance abuse and child
outcome. In C. H. Zeanah, Jr. (Ed.), Handbook of infant mental health (pp. 161-175). New York,
NY: Guilford.
Lester, B. M., Freier, K., & LaGasse, L. (1995). Prenatal cocaine exposure and child outcome: What
do we really know? In M. Lewis & M. Bendersky (Eds.), Mothers, babies, and cocaine: The role of
toxins in development. (1 ed., pp. 19-39). Hillsdale, NJ: Lawrence Erlbaum Associates.
Mayes, L. C., Bornstein, M. H., Chawarska, K., & Granger, R. H. (1995). Information processing and
development assessments in 3-month-old infants exposed prenatally to cocaine. Pediatrics, 95(4),
539-545.
Mayes, L. C., Granger, R. H., Frank, M. A., Schottenfeld, R., & Bornstein, M. H. (1993).
Neurobehavioral profiles of neonates exposed to cocaine prenatally. Pediatrics, 91(4), 778-783.
Mayes, L. C. F., Thomas. (2001). Prenatal drug exposure and cognitive development. In R. J.
Sternberg & E. L. Grigorenko (Eds.), Environmental effects on cognitive abilities (pp. 189-219).
Mahwah, NJ: Lawrence Erlbaum Associates, Inc.
Singer, L. T., Arendt, R., Minnes, S., Farkas, K., Salvator, A., Kirchner, L., & Kliegman, R. (2002).
Cognitive and Motor Outcomes of Cocaine-Exposed Infants. Journal of the American Medical
Association, 287(5), 1952-1960.
Singer, L. T., Arendt, R., Minnes, S., Salvator, A., Siegel, A. C., & Lewis, B. A. (2001). Developing
language skills of cocaine-exposed infants. Pediatrics, 107(5), 1057-1064.
Tronick, E. Z., Frank, D. H., Cabral, H., Mirochnick, M., & Zuckerman, B. (1996). Late doseresponse effects of prenatal cocaine exposure on newborn neurobehavioral performance. Pediatrics,
98(1), 76-83.