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MATERNAL SUBSTANCE ABUSE, CHILD DEVELOPMENT AND DRUG ENDANGERED CHILDREN
Claire D. Coles, Ph.D.
2010 Drug, DUI and Mental Health Court Conference May 18-20, 2010
Atlanta, Georgia
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Dr. Coles’ Affiliations
Fetal Alcohol Center, at the Marcus Center of Children’s Health Care of Atlanta
Departments of Psychiatry and Behavioral Sciences and Pediatrics, Emory University School of Medicine
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MANY, DIFFERENT, DEVELOPMENTAL AND BEHAVIOR PROBLEMS ARE NOTED IN CHILDREN AND ADOLESCENTS WHOSE PARENTS ABUSE DRUGS AND ALCOHOL
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Why are we concerned about the effects of substance use on neurodevelopment?
Prevalence of Substance Use by Pregnant Women
Teratogenic effects of exposure
Relationship between Substance Use and Postnatal Environmental problems
Behavior and Developmental Problems noted in Children of Substance Abusers
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Alcohol and Drugs in
PREGNANCY:
Mother
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Why the Concern for Prenatal Drug Exposure?
1 - 5% in U.S. have tried cocaine
10% of U.S. are alcoholics
20% of women smoke in pregnancy
40% of women report some alcohol use during pregnancy
60 - 80% of DFCS referrals in GA involve substance abuse; 78% nationwide
Estimates range from 0.6 to 31% prenatally exposed children
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Why the Concern for Prenatal Drug Exposure, continued
Exposure higher in some SES groups already at risk
Public belief that cocaine, methamphetamine and other drug exposure causes birth defects and developmental problems
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Reality?
The majority of women who use alcohol/drugs
in pregnancy, use more than one drug.
Cigarettes and alcohol the most common.
Next are marijuana and prescription drugs
Cocaine, maybe Methamphetamines, are next
Finally Opiates, like Heroin
Genetic loading? Antisocial personality?
And then there is the postnatal environment!
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Lifetime Prevalence (%) of Substance Use Reported by Young Women (18-25)
0
10
20
30
40
50
60
70
80
90
1972 1982 1992 2002
Alcohol
Cigarettes
Cocaine
SAMHSA, National Survey on Drug Use and Health, 2002
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Drug Use During Pregnancy
0
5
10
15
20
25
30
Marijuana Cocaine Other Alcohol Cigarettes
Ebrahim, SH, & Gfroerer, J (2003) Obstetrics and Gynecology, 101, p374-378
%
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0 5 10 15 20 25
Any illicit drug
Marijuana
Cocaine
Alcohol
Cigarettes
Hispanic
Whites
Afr-Amer
Percent of Women Using Drugs During
Pregnancy by Racial and Ethic Groups, 1992
NIDA
Notes
J/F
1995
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FACTORS INFLUENCING DRUG USE
A. EXTERNALIsolation
Poverty
Violent Crime
Drug Related Lifestyle
Unstable Family / Social
Environment
Inadequate Social Services
Solitary Caregiver or Provider
B. INTERNALPoor Coping Skills
Depression
Boredom
Anger
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ENVIRONMENTAL FACTORS:Social Problems Associated
With Substance Abuse
Poverty
Violent crime
Parent’s drug-related life style
Parent’s poor physical and mental health
Disorganized / dysfunctional families
Lack of stable social environment
Inadequate medical services
Inadequate social services
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MEDICAL PROBLEMS COMMONLY
ASSOCIATED WITH ALCOHOLISM
Liver: Alcoholic steatosis
(fatty liver)
Alcoholic hepatitis
and fibrosis
Cirrhosis
Cardiovascular
InjuryAlcoholic
cardiomyopathy
Hypertension
Hemorrhagic strokes
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Neurological disorders:
Wernicke - Korsakoff syndrome
Alcoholic dementia
Organic mental disorder
MEDICAL PROBLEMS COMMONLY
ASSOCIATED WITH ALCOHOLISM
Immune system impairment:
Cancers of mouth and upper respiratory tract
Liver cancer
Pancreatitis
From: “Effects of Alcohol on Health and Body Systems” (1993). Secretary of Health and
Human Services, 8th Special Report to the U.S. Congress on Alcohol and Health, Rockville,
MD., USDHHS, NIA, NIAAA, 1993.
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PSYCHIATRIC CONDITIONS OFTEN CO-MORBID
WITH ALCOHOL / DRUG ABUSE
Depression
Conduct Disorder
Personality Disorders:Antisocial Personality DisorderBorderline Personality Disorder
Posttraumatic Stress Disorder
Psychotic Conditions
Anxiety Disorders Sexual Dysfunction
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Figure 1: Survival Curve for Drinkers and
Nondrinkers
0.9
0.91
0.92
0.93
0.94
0.95
0.96
0.97
0.98
0.99
1
1.01
0 2 4 6 8 10 12 14 16 18 20
Years between Childbirth and Mother's Death
%
A
l
i
v
e
Alcohol
Control
41 (7%) of the
583 women were
deceased, 6
controls and 35
alcohol users ,
with alcohol
users
significantly
more likely to
die, X2 (1) =7.59, p<.006.
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ALCOHOLISM IN WOMEN VS. MENDifference in Signs Associated
with Alcohol Abuse
Fewer reports of academic / work difficulties
Less antisocial behavior
Fewer legal problems
Fewer DUI‟s, auto accidents
More physical problems
Spouse/partner leaves more often
More suicide attempts
More depression
More neurological damage
Roman, 1988; Tamerin et al., 1986
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ALCOHOLISM IN WOMEN
Effects on Reproductive Function
• Amenorrhea or severe oligomenorrhea
• Dysmenorrhea
• Anovulation/luteal phase dysfunction
• Increased premenstrual discomfort
• Spontaneous abortion
• Increased gynecological problems
• Fetal alcohol effects
• Sexual disorderMello, 1986
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Obstetrical Complications for Which Drug Abusing Women
Are at Increased Risk
Impaired Fertility
Spontaneous Abortion
Poor Maternal Weight Gain
Intrauterine Growth
Retardation (IURG)
Intrauterine Death
Placental Insufficiency
Retroplacental Hemorrhage
Abruptio Placenta
Septic Thrombophlebitis
Uterine Irritability
Preterm Labor & DeliveryPremature Rupture of
Membranes (PROM)AmnionitisPrecipitous LaborEmergency Caesarian
SectionIncreased Anesthesia
AdministrationForceps DeliveryFetal DistressPostpartum HemorrhageMaternal Mortality
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Economic Barriers
• lack of health insurance
• lack of transportation
• lack of caretakers for children
Limited Availability of Treatment Services
• lack of women-oriented treatment models
Individual Barriers
• Maternal psychopathology
• Family dysfunction
BARRIERS TO TREATMENT
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IDENTIFYING WOMEN AT RISK
Self Report Measures
Quantity / frequency indices
Forced choice ordinal scales
Time sampling
Diary
Open-ended response format
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How do we measure Drug Use?
Maternal Self Report.
Did you drink/use drugs in pregnancy?
How often did you use “crack”?
How many cigarettes do you smoke a day?
How many joints do you smoke?
How many drinks do you have on each occasion when you drink?
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How did we measure Drug Use?
Urine (EMIT) Screens
During prenatal care
At delivery
Postpartum
Infants in the nursery
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Alcohol and Drugs in
PREGNANCY:
Child
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POSSIBLE MECHANISMS OF DRUGS/ALCOHOL
IN PREGNANCY:
Teratogenic (Single Factor) Model
Teratogenic
SubstanceFetus
OutcomeSIDS
Fetal wastage
Behavioral
effects
Birth Defects
Growth
retardation
Coles, 1995,
Mother
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SOME POSSIBLE MECHANISMS OF EFFECTS
OF DRUGS/ALCOHOL IN PREGNANCY:
Toxic (interactive) Model
Toxic
Substance
Mother
Fetus
OUTCOMES
Reduced fertility
Fetal wastage
Preterm birth
Birth defects
Growth retardation
Behavior effects
SECONDARY OUTCOMESMedical & behavioral
problems
SIDSColes, 1995
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Prenatal Environment
Social Factors
Legal Issues
Prenatal Care
Substance Use & Abuse
Maternal Characteristics
Genetics
OUTCOMES• Reduced fertility• Fetal wastage• Preterm birth• Birth defects• Growth Retardation
MOTHER
FETUS SECONDARY OUTCOMES
• Developmental & Medical
Effects
• SIDS
POSTNATAL EVIRONMENT
Maternal Status/ Legal
issues/ Social Factors/
Nutrition/ Substance Use
Abuse/ Education / Social
Services/et cetera
MULTI-FACTOR MODEL
Coles, 1995
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MODEL OF ENVIRONMENTAL INFLUENCE
Greater Society
Social Supports
Family
Child
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TYPE OF DRUG EXPOSURE: Critical Periods of Development
Embryonic period (in weeks) Fetal period (in weeks)
3 4 5 6 7 8 9 16 20-36 38 40
FullTerm
Major morphological abnormalitiesPhysiological defects and minor
morphological abnormalities
Central Nervous System
Heart
Eyes
Limbs
Digestive System
PalateExternal Genitalia
EarsDevelopment and Descent of Thyroid
Adapted from The Developing Human by K. L. Moore, 1993
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PERINATAL COMPLICATIONS
SEEN IN DRUG EXPOSED NEONATES
Preterm birth, with associated
problems
Respiratory distress
Intraventricular hemorrhage (IVH)
Necrotizing endocolitis (NEC)
Asphyxia Neonatorum
Meconium staining
Meconium aspiration
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PERINATAL COMPLICATION SEEN INDRUG EXPOSED NEONATES
Pneumonia Hypoglycemia Hypocalcemia Tachypnea Apnea Respiratory alkalosis HyperbilirubinemiaRespiratory distress syndrome
(RDS)
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ENVIRONMENTAL FACTORS: Effects of Substance Abuse on Caretaking / SES
Death of parent
Loss of custody
Depressed mother
Neglect / Abandonment
Abuse
Inconsistent parenting
Failure of attachment
Failure to use social /
medical services
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AGENCIES INVOLVED
WITH EXPOSED CHILDREN
PRENATALWIC
Health CentersPrenatal Clinics
Physicians/MidwivesA&D Programs
INFANCY/PRESCHOOLWIC
HospitalsHealth Centers/Well Baby Clinics
High Risk Nurses
CourtsSocial Services AgenciesChild Protective ServicesCounty Welfare Agencies
Educational ProgramsTreatment ProgramsParenting Programs
SCHOOL AGECourts
SchoolsSpecial Education Programs
Hospital & Health CentersCounty Welfare Agencies
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Physical/
Health/MotorDevelopmental/
Cognitive
Behavioral/
Social
Academic/
Vocational
Alcohol and Drug Affected children
may have problems in the
following areas:
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What are the effects of various drugs?
Alcohol Global cognitive deficits Specific neurodevelopmental impact Academic deficits
Cocaine Arousal regulation Emotional development Executive Functioning
Smoking/Nicotine Auditory perception Language development Conduct Disorders
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Alcohol
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Prenatal Alcohol Exposure
Fetal Alcohol Syndrome (FAS)
Fetal Alcohol Spectrum Disorders (FASD)
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THE TIP OF THE ICEBERGFETAL ALCOHOL Spectrum Disorders
Partial FAS
Alcohol-related Birth Defects
Alcohol-related Neurobehavioral Effects
FAS 1 per 1000
5 per 1000
1 per 100
73,000 Alcohol-Affected Georgia Citizens , 0 to 21years
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How is FAS Diagnosed?
Prenatal Alcohol Exposure
Face
Growth
Brain
FAS
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Facial Features Microcephaly
Short palprebral fissure
Thin upper vermillion
Absent philtrum
Hypoplastic midface
Low nasal bridge
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Effect of Alcohol Exposure on Birth Weight
(N = 368)
3,300
3,200
3,100
3,000 -
2,900 -
2,800 -
2,700 -
0 --
Never
Drank
Stopped
Second
Trimester
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Controls,
n=7
Alcohol,
n=7
Coronal Sagittal Axial
Prenatal Alcohol Exposure Affects the Brain:White Matter in Young Adults (sMRI) Li, et al,
(2008) Brain Imaging and Behavior.
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(Neuro) Behavioral Outcomes Examined in FASD
General Cognitive/Learning Skills (IQ) Executive Functioning Skills Attentional regulation Memory,Planning and organization
Motor skills Visual/spatial skills Academic Achievement Adaptive Behavior Social Behavior Mental Health/Behavioral Disorders
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FAS Neurocognitive Deficits
FAS is associated with a clinically significant level of general intellectual impairment.
IQ range: 40-110; X=70’s across many studies of children with FAS
Deficits related to neurological damage
Additional clear, but unacknowledged, environmentalcomponent to functional deficits
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Effects on Educational Functioning
Global functioning- global limitations on learning abilities
Arousal regulation/Attention
Executive Functioning Skills-metacognition
Visual/Spatial Skills
Memory (or metamemory and strategy use)
Speed of processing
Specific deficits in math
Depression
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Is there a ‚Pattern‛ of Learning and Behavior that affects Education?
Although hard to find against this complicated background, patterns are emerging.
Cognitive: Both Global and Specific deficits
Behavior: “Arousal Dysregulation”.
Early deficits in motor and visual/motor
Commonly find secondary disabilities in achievement, behavior.
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Clinical Presentations 0 to 5 years Significantly Developmental Delayed with
complex medical histories. Asthma.
Behavioral disturbances with mild delays and significant histories of abuse/neglect.
Arousal dysregulation beginning with sleep problems progressing to behavior problems.
Need for PT, OT, Speech and social work services. More motor than other areas.
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Clinical Presentations: School Age
Mild Intellectual Disabilities (IQ=50 to 69) with significant physical findings. Occasionally lower.
Borderline IQs with history of foster care and specific learning deficits. Frequent behavior problems.
International adoption with emotional (attachment) problems and specific language disabilities. IQ varies.
Nonverbal learning disabilities. V/P split with significantly higher language than performance scores.
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ADHD and FASD
Many (many) children with FASD are diagnosed with ADHD.
Questionable diagnosis due to history of exposure, arousal dysregulation, parenting problems, custody issues.
In clinical observation, medications do not seem to improve outcomes. Little systematic research on this.
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Effects of Disadvantage on Development in Alcohol and Control Samples*
50
60
70
80
90
100
110
120
6 Mon 12 Mon 24 Mon 5 years 7 years 15 years
Norms SES Controls Alcohol
Ab
ility S
tan
dard
Sco
re
Child’ Age at Testing (*Various N’s)
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Source: Lynch, et al. (2003) Examining delinquency in adolescents differentially prenatally exposed to alcohol.J Stud Alcohol
Predicting Adolescent Delinquency (N=250)
Variable Std Beta t p
Life Stress .363 6.6 .000
Child Drug Use
.265 4.4 .000
Parenting: Supervision
-.222 -3.7 .000
Prenatal Exposure
.01 .16 .96,ns
However, it is
also widely
reported that
prenatal alcohol
exposure is
associated with
later criminal
behavior.
But most
studies didn’t
controlled for
environmental
factors.
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Specific Deficits:e.g., Math Disabilities
Math skills more impaired than language
Probably related to visual/spatial deficits
Probably related to executive functioning problems
Can be observed in preschool period and persists through adulthood
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Academic (WIAT) Scores for Exposure Groups
55
60
65
70
75
80
85
90
Reading Spelling Math
Control FAS-E Exposed Special Ed
Howell, et al, 2006
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SFr: Superiorfrontal
RMF: Rostralmiddlefrontal
CMF: Caudalmiddlefrontal
PTr: Parstriangularis
POr: Parsorbitalis
LOF: Lateralorbitofrontal
PrC: Precentral
PoC: Postcentral
SuM: Supramarginal
SPa: Superiorparietal
STe: Superiortemporal
ITe: Inferiortemporal
LOc: Lateraloccipital,
CAC: Caudalanteriorcingulate
PCu: Precuneus
Cun: Cuneus
PCa: Pericalcarine
Lin: Lingual
Fus: Fusiform
PHi: Parahippocampal
RAC: Rostralanteriorcingulate
IPa: Inferiorparietal
POp: Parsopercularis.
Chen, et al., (2008) Systematic Investigation of Volume Changes Induced by
Prenatal Alcohol Exposure in Cortical and Sub-cortical Regions, in review
Cortical regions exhibiting PAE effects
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Cbr: Cerebral Cortex
Cbe: Cerebellum Cortex
Tha: Thalamus Proper
Hip: Hippocampus
Put: Putamen
Pal: Pallidum
Amy: Amygdala
Cau: Caudate
Acu: Accumbens
Area.
R: Right Hemisphere,
L: Left Hemisphere.
Sub-cortical regions exhibiting PAE effects
Chen, et al., (2008) Systematic
Investigation of Volume Changes
Induced by Prenatal Alcohol
Exposure in Cortical and Sub-cortical
Regions, in review
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Why study corpus callosum (CC)? Agenesis of CC found at higher rate in FAS
patients
Previous studies have identified CC abnormalities (e.g., Riley et al, 1995, Johnson et al., 1996, Swayze
et al, 1997, Sowell et al, 2001, Bookstein et al. 2001)
Large, white matter tract often associated with efficiency of information processing
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. Segmentation of the corpus callosum (A), in which some
portions (1, 4 and 5) exhibited the general PAE effect (B). 1:
Anterior, 2: Mid-Anterior, 3: Central, 4: Mid-Posterior, 5:
Posterior.
Chen, et al., (2008) Systematic Investigation of Volume
Changes Induced by Prenatal Alcohol Exposure in Cortical
and Sub-cortical Regions, in review
Effects of Prenatal Alcohol Exposure on Corpus Callosum Volume
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LI, Coles, Lynch, & Hu, Human Brain Mapping, 2009
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Interhemispheric Transfer of Information Authors:
P. Santhanam1, X. Hu1, S.J. Peltier1, Z. Li1, C.D. Coles2, M.E. Lynch2
Experimental Design:
7 dysmorphic PAE, 7 non-dysmorphic PAE, 7 Controls: 20-24 yrs old from longitudinal cohort
PAE: identified by reported alcohol consumption by mother during pregnancy
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Results: ‘Same’ Condition
Controls Non-Dys PAE Dys PAE
Controls Non-Dys PAE Dys PAE
Left hand
response to
Same side
stimulation
(LS)
Right hand
response to
Same side
stimulation
(RS)
No significant difference seen between groups in the „same‟ condition
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Results: ‘Opposite’ ConditionControls Non-Dys PAE Dys PAE
Controls Non-Dys PAE Dys PAE
Left hand
response to
Opposite side
stimulation (LO)
Right hand
response to
Opposite side
stimulation (RO)
Significant difference between Dys-PAE and Control groups in
primary motor (arrows) and premotor areas
Significant difference between Dys-PAE and Control groups in premotor area
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Skeletonized FA difference between Control and Non-Dysmorphic PAE groups (green=skeleton, purple=anatomically defined ROI, pink=region of significant difference). Similar differences were seen between control and dysmorphic PAE groups. Santhanam, et al, 2009, in preparation.
Using TBSS for DTI analysis, voxel-wise statistics on the skeletonized FA data reveal subregions of the cingulum with significantly lower FA values in both PAE groups versus control subjects.
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Caudate
Pallidum Putamen
AmygdalaHippocampus
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Trial by Group
F(4,553)=2.3,
p<.006
Con vs Dys,
p<.03
vs EtOH,
<.08
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Verbal Selective Reminding-Total Recall (N=82)
Trial by Group
F(4,539)=1.65,
p=.06
Con vs Dys,
p<.01
vs EtOH,
NS
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Mediation Model
Assumptions:
1. Memory function is affected by prenatal alcohol exposure
2. Memory deficits are the result of alterations in brain associated with prenatal alcohol exposure
3. Regions of brain showing volumetic reductions in alcohol affected individuals will be found to mediate memory performance.
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Alternate Hypotheses
Direct effect Mediated effect
EtOH
Brain Volume
Recall EtOH
Brain Volume
Recall
IV must be related to DV; IV must be related to Mediator; Mediator must be related to DV.
If mediated, adding Mediator to equation must significantly reduced IV-DV correlation.
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Hippocampus Mediates effects of Alcohol Exposure
Dysmorphia Score
Spatial Learning
Slope
HippocampalVolume
b=-.03, SEb=.02, β=-.18,p<.10, ns
b=-56.6, SEb=.14.62 β=.38,p<.000
b=.000, SEb=.00, β=.26,p<.017
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Overall Conclusions: Alcohol
Evidence for persistent, global deficits even when SES and post natal environment accounted for.
In addition to global deficits, there may be specific cognitive problems in the following areas: Motor functioning, visual spatial skills, math, memory.
MRI (and fMRI) suggest neurological basis for behavioral findings.
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Cocaine
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Weight over first 8 years
0
10
20
30
40
50
60
70
80
Birth I year 2 years 8 years
Cocaine
Control
EBD
P
o
u
n
d
s
Child’s Age
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Mental Development Standard Scores and Cocaine Exposure
0
20
40
60
80
100
120
1 year 2 years 8 years
Cocaine
Control
EBD
Standard
Score
BSID MDI DAS
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CBCL Summary T-Scores at
8 Years
0
10
20
30
40
50
60
70
80
Total Externalizing Internalizing Sex Problems
Cocaine Control Behavior
T-Scores * *
* p<.000
* *
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Slope of Skin Conductance Level During Stressors
0
0.05
0.1
0.15
0.2
0.25
0.3
Controls Cocaine BD
Kable, Coles, Lynch, & Platzman (2008) Physiological responses to social and cognitive challenges in 8-year olds with a history of prenatal cocaine exposure. Dev Psychobiol 50, 251-265.
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Conclusions
The BD group demonstrated elevated heart rate across all conditions but no differences in change in HR as a function of stress
The BD group demonstrated a pattern of “hypo-responsiveness to stressors”
The cocaine group demonstrated a pattern of “hyper-responsiveness to stressors”
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Linda Mayes’ Neurochemical Regulatory Switch Hypothesis Cocaine alters reuptake of monoamines
(Norepinephrine, dopamine, & serotonin)
Neural regions involved in gating regulation of arousal by mesolimbic systems and prefrontal cortex involving executive mediation of arousal disrupted to that set point of the neurochemical regulatory switch is altered making cocaine-exposed children vulnerable to hyperarousal responses
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Bilateral Amygdala area(brain images) comparing activation between Cocaine exposed and Controls (bar graphs). Activation level is the produce of mean regression coefficient (representing the fMRI signal amplitude) and number of activated voxels in the ROI (representing the activation volume). With “NEU0” value as the baseline (zero). The error bars represent standard error.
Prenatal cocaine exposure and emotional arousal in adolescents: Neuroimaging and N-Back task
Li, Coles, Lynch, Hamann, Peltier, LsConte and Hu, (2008, submitted) Prenatal cocaine exposure alters emotional arousal regulation and its effects on working memory. In Review
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Left dorsal lateral prefrontal area(brain images) and the activation amount comparison between groups (bar graphs). As in the previous slide, there is an interaction between Condition (Neuo.Neg) and Exposure Group.
Cocaine exposed adolescents do not show the usual balance between cognitive and emotional arousal
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Cocaine does not have the same teratogenic effect as alcohol
No effects on growth
No effects on cognition
What about behavior?
It may affect psychophysiology (that is, arousal and attention).
Psychophysiology may interaction with environmental factors to produce developmental psychopathology.
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MATERNAL SMOKING: DEVELOPMENTAL CONSEQUENCES
•Behavior Disturbances
•Language Development
•Medical Consequences
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Medical Consequences
Lower Birthweight
SGA
Increased weight as older children and adults
Sudden Infant Death Syndrome (SIDS)
Respiratory problems in infancy
Asthma or aggravation of asthma symptoms
Otitis Media
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Studies of Behavior Problems Following Maternal Tobacco Use During Gestation
Reports of ADHD
Criminal Behavior in Young Adults (Brennan, Grekin,
& Mednick, 1999, Maternal smoking during pregnancy and adult male criminal outcomes. Arch Gen Psychia 56, 215.)
Developmental Psychopathology (Wakschlag,
Lahey, Loeber, Green, Gordon, & Leventhal (1997). Maternal smoking during pregnancy and the risk of conduct disorder in boys. Archives of General Psychiatry, 54(7), 670-6.)
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Auditory Processing and Language Development Fried (1998) Cigarette smoke exposure and
hearing loss, JAMA, 280, 963
Fried, O’Connell, Watkinson (1992) 60 and 72 month follow-up of children prenatally exposed to marijuana, cigarettes, and alcohol: Cognitive and language assessment. J Dev Beh Peds, 13, 383
Fried, Watkinson, & Siegel (1997) Reading and language in 9 to 12-year olds prenatally exposed to cigarettes and marijuana. Neurtox Teratol, 14, 299.
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Previous Links Between Maternal Smoking and Language Development
Early teratology studies found deficits in auditory habituation items of the Brazelton
Fried found deficits in language development among toddlers and preschoolers
Deficits in phonemic and phonetic processing in Middle Childhood
Fried: Suggested that prenatal tobacco smoke caused an auditory processing deficits
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Emory Language Development Study
Proposed looking at auditory processing skills and language development in children of smokers between 6-months and 2-years Using:
Bayley Scales of Infant Development , 2nd, 3rd Ed Sequence Inventory of Communication Development
(SCID) Natural Language Protocol for assessing phonetic
expression (tapes to Georgia State) (15 & 24 mos) Parent report of language development (MacArthur
CDI) ABERs and Information Processing Paradigm
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Early Language: % showing language delays on BSID Language Facet
0
5
10
15
20
25
30
35
40
45
50
% Language Delayed
Control
Low Dose
Hi Dose
*
*
* Linear trend,
p<.05
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CID/Words and Gestures: Number of Words Said and Understood
0
50
100
150
200
250
Said Understood
Control
Low Dose
Hi Dose
* *
*Linear trend, p<.006
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Effects of Multiple Risk Factors
Poverty Disability
Behavior
Disorder
Prenatal exposure
Family
Dysfunction
Other drug Use
Genetics
Poor Schools
Inadequate Medical Care
Bias
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Conclusions
Parental Substance Abuse, perhaps, particularly abuse by mothers, affects child development.
Effects are seen across a broad range, including motor, cognitive, behavioral, social and academic functioning.
It is clear that there are teratogenic effects (direct effects of the substances); however, many problems are the results of environmental and social factors, as well.
Prevention and treatment are both necessary.