Serving Substance Abuse Professionals Since 1993

Last Update: 6.10.08

C O R K O N L I N E

powerpoint presentations
CORK database search
resource materials
bibliographies
clinical tools
user services
newsletters
about cork
home

CORK Bibliography: Developmental Effects of Prenatal Drug Exposure

37 citations. October 2007 to present

Prepared: September 2008

Adnams CM; Sorour P; Kalberg WO; Kodituwakku P; Perold MD; Kotze A et al. Language and literacy outcomes from a pilot intervention study for children with fetal alcohol spectrum disorders in South Africa. Alcohol 41(6): 403-414, 2007. (44 refs.)

This pilot study investigated the efficacy of a classroom language and literacy intervention in children with fetal alcohol spectrum disorders (FASD) in the Western Cape Province of South Africa. The study forms part of a larger, ongoing study that includes metacognitive and family support interventions in addition to language and literacy training (LLT). For the LLT study, 65 nine-year-old children identified as either FASD or not prenatally exposed to alcohol, were recruited. Forty children with FASD were randomly assigned to either a LLT intervention group or FASD control group (FASD-C). Twenty-five nonalcohol-exposed children were randomly selected as nonexposed controls (NONEXP-C). Prior to intervention and after nine school-term months of treatment, general scholastic tests, teacher and parent questionnaires, classroom observations and specific language and literacy tests were administered to the participants. The nine months assessment reflects the midpoint and the first assessment stage of the overall study. At initial diagnosis and prior to commencement of the interventions, participants with FASD were significantly weaker than NONEXP-C children in reading, spelling, addition, subtraction, phonological awareness, and other tests of early literacy. Teachers rated a range of adaptive behaviors of children with FASD as significantly worse than NONEXP-C. Mean scholastic and language and literacy scores for all groups showed improvement over baseline scores after 9 months of intervention. The mean test scores of children with FASD remained lower than those of NONEXP-C. Comparison of mean baseline to postintervention score changes between the LLT, FASD-C, and NONEXP-C groups revealed that although there were no significant gains by the LLT intervention group over control groups on the general scholastic assessment battery, significantly greater improvements occurred in the LLT intervention group compared to the FASD-C group in specific categories of language and early literacy. These categories were syllable manipulation, letter sound knowledge, written letters, word reading and nonword reading, and spelling. In spite of cognitive and classroom behavioral difficulties, children with FASD from a vulnerable environment demonstrated significant cognitive improvements in specific areas targeted by classroom interventions. To our knowledge, this is the first report of a systematic classroom intervention and resultant cognitive response in children with FASD.

Bennett DS; Bendersky M; Lewis M. Children's cognitive ability from 4 to 9 years old as a function of prenatal cocaine exposure, environmental risk, and maternal verbal intelligence. Developmental Psychology 44(4): 919-928, 2008. (81 refs.)

This study examined the effects of prenatal cocaine exposure, environmental risk, and maternal verbal intelligence on children's cognitive ability. Gender and age were examined as moderators of potential cocaine exposure effects. The Stanford-Binet IV intelligence test was administered to 23 1 children (91 cocaine exposed, 140 unexposed) at ages 4, 6, and 9 years. Neonatal medical risk and other prenatal exposures (alcohol, cigarettes, and marijuana) were also examined for their unique effects on child IQ. Mixed models analysis indicated that prenatal cocaine exposure interacted with gender, as cocaine-exposed boys had lower composite IQ scores. Age at assessment did not moderate this relation, indicating that cocaine-exposed boys had lower IQs across this age period. A stimulating home environment and high maternal verbal IQ also predicted higher composite IQ scores. Cocaine-exposed boys had lower scores on the Abstract[Visual Reasoning subscale, with trends for lower scores on the Short-Term Memory and Verbal Reasoning subscales, as exposure effects were observed across domains. The findings indicate that cocaine exposure continues to place children at risk for mild cognitive deficits into preadolescence. Possible mechanisms for the Exposure X Gender interaction are discussed.

Bennett D; Bendersky M; Lewis M. Preadolescent health risk behavior as a function of prenatal cocaine exposure and gender. Journal of Developmental and Behavioral Pediatrics 28(6): 467-472, 2007. (37 refs.)

Objective: To examine the effect of prenatal cocaine exposure on health risk behaviors during preadolescence. Methods: The present study examined prenatal cocaine exposure, gender, and environmental risk as predictors of self-reported substance use, aggression, and a disregard for safety precautions on the Youth Risk Behavior Survey in a sample of 10.5 year olds (n = 154, including 60 who were prenatally exposed to cocaine). Results: Gender tended to moderate the effects of prenatal cocaine exposure because exposure effects were found for boys but not girls. Boys who were prenatally exposed to cocaine reported engaging in more high-risk behavior. In examining individual outcomes, cocaine exposed boys had the highest scores for aggression, substance use, and a disregard for safety precautions, although these differences were significant only for the composite health risk behavior measure. Conclusions: The findings extend earlier work showing that prenatal cocaine exposure places boys at risk for problems of inhibitory control, emotional regulation, and antisocial behavior. Research is needed to examine whether the effects of prenatal cocaine on health risk behaviors persist into adolescence, when such behaviors tend to increase.

Burns L; Mattick RP; Wallace C. Smoking patterns and outcomes in a population of pregnant women with other substance use disorders. Nicotine & Tobacco Research 10(6): 969-974, 2008. (38 refs.)

Using a retrospective cross-sectional study design, we examined smoking patterns and associated neonatal outcomes in infants born to women with a diagnosis of a substance use disorder in pregnancy. Antenatal and birth admissions were linked to midwives data on pregnancy care, services, and outcomes over a 5-year period (1998-2002). Birth admissions were flagged as positive for drug use where a birth admission or any pregnancy admission for that birth involved a cannabis-, opioid-, stimulant-, or alcohol-related ICD-10AM code. There were 4,346 live births to women with a substance-related diagnosis in pregnancy. Women with a substance-related diagnosis (the drug group) had an adjusted odds ratio for smoking during pregnancy of 10.8 (95% CI=9.9-11.7) relative to women without a substance-related diagnosis (the non-drug group). Women in the drug group also were heavier smokers; 26% smoked 1-10 cigarettes/day and 56% smoked more than 10 cigarettes/day compared with 8% in both groups in the non-drug group. Relative to the drug group, the adjusted odds ratio for quitting smoking during pregnancy in the non-drug group was 3.1 (95% CI=2.3-4.3). Among women in the drug group, any smoking significantly increased the risk of poor fetal growth, prematurity, and admission to the special care nursery. In conclusion, innovative and effective strategies for tobacco cessation should target pregnant women as a high priority. Further research should identify the models of tobacco cessation most suited to women who also use other substances during pregnancy.

Button TMM; Maughan B; McGuffin P. The relationship of maternal smoking to psychological problems in the offspring. Early Human Development 83(11): 727-732, 2007. (28 refs.)

There is strong evidence for an association between maternal smoking in pregnancy and psychological problems in offspring. The problems most frequently associated are attention problems, hyperactivity, and conduct problems, although there is some evidence for an association with substance use problems as well. The nature of this association is unclear, but it is likely the result of a number of different mechanisms. Animal studies provide evidence for a causal relationship, in which exposure to nicotine has detrimental effects on foetal development. Other studies suggest that factors that correlate with maternal prenatal smoking may be the real risk factors for behavioural problems, although evidence that the associations remain after controlling for such risks goes some way to dispel this as the only explanation. Finally, maternal prenatal smoking may index underlying psychological problems in the mother that are inherited by the offspring. In all likelihood, a combination of these mechanisms may contribute to observed relationships between prenatal smoking and offspring psychological problems. Now that the association is well established, future research needs to focus more strongly on disentangling underlying mechanisms. Although animal studies demonstrate a casual retationship, it appears from other research that this may not be the whole story in human samples. Furthermore, the relationship may only exist under certain conditions (i.e. against a certain genetic background), and this possibility warrants further examination, particularly in relation to other genetic risks, and outcomes other than ADHD. Application of the children-of-twins design may also cast further light on the processes involved.

Carter RC; Jacobson SW; Molteno CD; Jacobson JL. Fetal alcohol exposure, iron-deficiency anemia, and infant growth. Pediatrics 120(3): 559-567, 2007. (29 refs.)

OBJECTIVES. Our goals were to determine whether prenatal alcohol exposure is associated with an increased incidence of iron-deficiency anemia in infancy and to compare effects of fetal alcohol exposure and iron-deficiency anemia on infant growth. We also tested whether effects of fetal alcohol exposure on growth are mediated or moderated by iron-deficiency anemia. METHODS. A total of 96 infants born to mothers from the Coloured (mixed ancestry) community in Cape Town, South Africa, were recruited prenatally; 42 mothers drank heavily during pregnancy, and 54 abstained or drank small amounts of alcohol. Growth was assessed at birth and 6.5 and 12 months, and iron-deficiency anemia was assessed at 6.5 or 12 months. RESULTS. Infants whose mothers binge drank during pregnancy (>= 4 drinks per occasion) were 3.6 times more likely to be diagnosed with iron-deficiency anemia at 12 months than were infants whose mothers did not binge drink. Prenatal alcohol exposure was associated with reduced weight at birth, 6.5 months, and 12 months and with shorter length at 6.5 and 12 months. Iron-deficiency anemia was related to reduced 12-month weight and head circumference and to slower growth velocity between 6 and 12 months. The effects of prenatal alcohol on weight were not mediated by iron-deficiency anemia; however, they were seen primarily in infants with iron-deficiency anemia. CONCLUSIONS. The association of maternal binge drinking with an increased incidence of iron-deficiency anemia may reflect disruption of accumulation of fetal iron stores or postnatal deficiencies in iron uptake, absorption, or intake. Moreover, iron deficiency seems to exacerbate the prenatal alcohol effects on growth.

Chaplin TM; Fahy T; Sinha R; Mayes LC. Young children's emotional arousal and self-regulation in a frustrating task: Effects of gender and prenatal cocaine exposure. (meeting abstract). Journal of Women's Health & Gender-based Medicine 16(8): 1114-1114, 2007. (0 refs.)

Chiriboga CA; Kuhn L; Wasserman GA. Prenatal cocaine exposures and dose-related cocaine effects on infant tone and behavior. Neurotoxicology and Teratology 29(3): 323-330, 2007. (53 refs.)

Background: In experimental models, prenatal cocaine exposure has been found to perturb monoaminergic development. In humans, numerous studies have sought clinical correlates, but few have focused on dose-related effects, especially as regards neurologic function beyond the neonatal period. Objective: To assess whether prenatal cocaine exposure has adverse effects on infant neurologic, developmental and behavioral outcomes and whether any effects are dose-dependent. Design/Methods: Infants (398) were enrolled at birth from an urban hospital. Drug exposure was ascertained with biomarkers in hair (n=395), urine (n = 170) and meconium (n = 109). Children were followed prospectively and 286 (72%) were evaluated blind to drug exposure at 6 months of age with the Bayley scales, Fagan Scale of Infant Intelligence and a standardized neurological examination. Results: Certain neurological findings increased significantly by the amount of cocaine detected in maternal hair, e.g. abnormality of tone, as indicated by extensor posture was detected among 28% of cocaine-unexposed infants, 43% of infants exposed to lower and 48% exposed to higher cocaine levels in maternal hair (p<0.009). Persistent fisting increased in a similar dose-dependent manner. These associations persisted in adjusted analyses. Prenatal cocaine exposure was not associated with developmental scores (mental, motor or novelty preference) but was associated with lower orientation scores in adjusted analyses. Conclusions: At 6 months of age, prenatal cocaine exposure was associated with abnormalities of tone and posture and with lower orientation scores. Perturbations in monoaminergic systems by cocaine exposure during fetal development may explain the observed neurological and behavioral symptoms. Whether such findings in infancy increase the risk of later neurobehavioral problems requires further study.

Cornelius MD; Goldschmidt L; DeGenna N; Day NL. Smoking during teenage pregnancies: Effects on behavioral problems in offspring. Nicotine & Tobacco Research 9(7): 739-750, 2007. (104 refs.)

We prospectively examined the relationship between prenatal tobacco exposure (PTE) and child behavior in a birth cohort of 357 offspring of teenage mothers. PTE was defined as any exposure across pregnancy and, in separate analyses, exposure within each trimester. Outcomes included measures of behavior problems, activity, and attention. On average, the children were 6.4 years of age, 48% were females, and 69% were Black. Data on maternal tobacco and other substance use were collected prenatally and postnatally: 46% of the mothers smoked in the first trimester and 58(% smoked 6 years later. Child urinary cotinine measured exposure to environmental tobacco smoke (ETS). Stepwise multiple regressions were run. PTE predicted significantly increased offspring activity; impulsivity; and aggression, externalizing, and total behavior problems in step 1. PTE remained a significant predictor of increased activity when maternal psychological characteristics, home environment, and ETS were added. The results were similar when PTE was examined by trimesters, although later pregnancy tobacco exposure predicted the most behavioral outcomes. In the final model, PTE (all three trimesters) and PTE (second trimester) were significant predictors of increased activity and attention problems, respectively. Other predictors of child behavior included maternal anxiety, depression, hostility, and home environment. ETS was not a significant predictor of child behavior when PTE was considered. Smoking during pregnancy among adolescents is a significant predictor of increased activity and attention problems in their offspring after controlling for covariates in the prenatal and current environments. Smoking cessation interventions are recommended for this population to avoid the effects of PTE on the offspring of pregnant adolescents. This is particularly important because these mothers will likely become pregnant again and many will increase their level of tobacco use as they mature.

D'Onofrio BM; Van Hulle CA; Waldman ID; Rodgers JL; Harden KP; Rathouz PJ et al. Smoking during pregnancy and offspring externalizing problems: An exploration of genetic and environmental confounds. Development and Psychopathology 20(1): 139-164, 2008. (80 refs.)

Previous studies have documented that smoking during pregnancy (SDP) is associated with offspring externalizing problems, even when measured covariates were used to control for possible confounds. However, the association may be because of nonmeasured environmental and genetic factors that increase risk for offspring externalizing problems. The current project used the National Longitudinal Survey of Youth and their children, ages 4-10 years, to explore the relations between SDP and offspring conduct problems (CPs), oppositional defiant problems (ODPs), and attention-deficit/hyperactivity problems (ADHPs) using methodological and statistical controls for confounds. When offspring were compared to their own siblings who differed in their exposure to prenatal nicotine, there was no effect of SDP on offspring CP and ODP. This suggests that SDP does not have a causal effect on offspring CP and ODP. There was a small association between SDP and ADHP, consistent with a causal effect of SDP, but the magnitude of the association was greatly reduced by methodological and statistical controls. Genetically informed analyses suggest that unmeasured environmental variables influencing both SDP and offspring externalizing behaviors account for the previously observed associations. That is, the current analyses imply that important unidentified environmental factors account for the association between SDP and offspring externalizing problems, not teratogenic effects of SDP.

Henderson J; Kesmodel U; Gray R. Systematic review of the fetal effects of prenatal binge-drinking. (review). Journal of Epidemiology and Community Health 61(12): 1069-1073, 2007. (27 refs.)

Objective: The effects of binge-drinking during pregnancy on the fetus and child have been an increasing concern for clinicians and policy-makers. This study reviews the available evidence from human observational studies. Design: Systematic review of observational studies. Population: Pregnant women or women who are trying to become pregnant. Methods: A computerised search strategy was run in Medline, Embase, Cinahl and Psychinfo for the years 1970-2005. Titles and abstracts were read by two researchers for eligibility. Eligible papers were then obtained and read in full by two researchers to decide on inclusion. The papers were assessed for quality using the Newcastle-Ottawa Quality Assessment Scales and data were extracted. Main outcome measures: Adverse outcomes considered in this study included miscarriage; stillbirth; intrauterine growth restriction; prematurity; birth-weight; small for gestational age at birth; and birth defects, including fetal alcohol syndrome and neurodevelopmental effects. Results: The search resulted in 3630 titles and abstracts, which were narrowed down to 14 relevant papers. There were no consistently significant effects of alcohol on any of the outcomes considered. There was a possible effect on neurodevelopment. Many of the reported studies had methodological weaknesses despite being assessed as having reasonable quality. Conclusions: This systematic review found no convincing evidence of adverse effects of prenatal binge-drinking, except possibly on neurodevelopmental outcomes.

Herrmann M; King K; Weitzman M. Prenatal tobacco smoke and postnatal secondhand smoke exposure and child neurodevelopment. (review). Current Opinion in Pediatrics 20(2): 184-190, 2008. (112 refs.)

Purpose To review the recent scientific literature examining the association of prenatal tobacco and postnatal secondhand smoke exposure and child neurodevelopment. Recent findings Low birth weight and decreased in-utero brain growth are two of multiple potential etiologic pathways proposed as mediating the effects of prenatal tobacco smoke exposure on child neurodevelopment. These negative effects of prenatal exposure have been consistently demonstrated in animal models, and in humans have been found as early as the newborn period. The literature on both prenatal and postnatal exposure is remarkably consistent in showing associations with increased rates of behavior problems, including irritability, oppositional defiant behavior, conduct disorders and attention deficit hyperactivity disorder. A more rudimentary literature also suggests deficits in intelligence quotient. Recent studies have focused on elucidating the complex interaction among tobacco exposure, genetics and environmental factors. Questions still remain about the relative roles of prenatal vs. postnatal exposure and the potential role of genetic and social confounders, limiting the ability to infer a causal nature to these associations at this time. The consistency of findings across studies is, however, highly suggestive of a causal relationship between environmental tobacco exposure and adverse behavioral and cognitive outcomes in children. Summary Prenatal tobacco and postnatal secondhand smoke exposure is consistently associated with problems in multiple domains of children's neurodevelopment and behavior.

Huijbregts SCJ; Warren AJ; de Sonneville LMJ; Swaab-Barneveld H. Hot and cool forms of inhibitory control and externalizing behavior in children of mothers who smoked during pregnancy: An exploratory study. Journal of Abnormal Child Psychology 36(3): 323-333, 2008. (73 refs.)

This study examined whether children exposed to prenatal smoking show deficits in "hot" and/or "cool" executive functioning (EF). Hot EF is involved in regulation of affect and motivation, whereas cool EF is involved in handling abstract, decontextualized problems. Forty 7 to 9-year-old children (15 exposed to prenatal smoking, 25 non-exposed) performed two computerized tasks. The Sustained Attention Dots (SA-Dots) Task (as a measure of "cool" inhibitory control) requires 400 non-dominant hand and 200 dominant hand responses. Inhibitory control of the prepotent response is required for dominant hand responses. The Delay Frustration Task (DeFT) (as a measure of "hot" inhibitory control) consists of 55 simple maths exercises. On a number of trials delays are introduced before the next question appears on the screen. The extent of response-button pressing during delays indicates frustration-induced inhibitory control. Prenatally exposed children showed poorer inhibitory control in the DeFT than non-exposed children. A dose-response relationship was also observed. In addition, prenatally exposed children had significantly higher (dose-dependent) conduct problem- and hyperactivity-inattention scores. There were no significant group differences in inhibitory control scores from the SA-Dots. These results indicate that children exposed to prenatal smoking are at higher risk of hot but not cool executive function deficits.

Jones AS. Maternal alcohol abuse/dependence, children's behavior problems, and home environment: Estimates from the National Longitudinal Survey of Youth using propensity score matching. Journal of Studies on Alcohol and Drugs 68(2): 266-275, 2007. (65 refs.)

Objective: Propensity score (PS) matching was used to investigate the relationship between maternal alcohol abuse (AA) and alcohol dependence (AD), based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria and three child outcomes: child behavior problems and two characteristics of the child's home environment as measured by the Home Observation and Measurement of the Environment-Short Form, cognitive stimulation and emotional support. Method: A cohort of children (N = 2,193; 49% female) whose mothers were drawn from the 1994 National Longitudinal Survey of Youth were stratified by gender and matched on maternal propensity to exhibit AA or AD. Results: After matching, sons of mothers with AA/ AD had higher behavior problem scores (p <= .05), and daughters of mothers with AA/AD lived in homes with significantly less emotional support (p <= 05) and cognitive stimulation (p :<= .005). Results were robust to alternative specifications of PS regressions. Conclusions: The findings suggest that policies aimed at reducing AA and AD among young adult women with children are justified. PS matched results also suggest that school counselors and mental health providers who encounter young boys with elevated behavior problems should consider maternal AA/AD as one possible causal factor. Future research should be directed toward understanding the trajectory of these outcomes and their sequelae over the child's life cycle and toward developing improved methods of identifying and intervening with at-risk children of both genders and their mothers.

Julvez J; Ribas-Fito N; Torrent M; Forns M; Garcia-Esteban R; Sunyer J. Maternal smoking habits and cognitive development of children at age 4 years in a population-based birth cohort. International Journal of Epidemiology 36(4): 825-832, 2007. (44 refs.)

Background: Active maternal smoking during pregnancy has been associated with a higher risk of behavioural disorders in children, but a few cohort studies measuring smoking data prospectively have studied its specific effects on the cognitive abilities of pre-schoolers. Method: A birth cohort was set up in Menorca Island in 1997 within the Asthma Multicenter Infants Cohort Study. A total of 420 (87% of those eligible) children had complete data for final analyses at age 4 years. Interviewer-administered questionnaires were completed by mothers during the third trimester of pregnancy and then every year up to age 4 years of their child. A standardized version of the McCarthy Scales of Children's Abilities (MCSA) was used to evaluate the child's motor and cognitive capabilities. Multivariable regressions were used with MCSA`s assessed outcomes adjusting for: home location, maternal alcohol consumption, mother's social class and level of education during pregnancy, parity, marital status, father's education level, child's gender, birth weight and height, breastfeeding duration, passive smoking, school season, age during test administration and evaluator (psychologist). Results: A high global consistency in maternal smoking habits was found (total agreement= 88.7%). Maternal social class and education level were inversely associated with maternal smoking behaviour. Maternal smoking during pregnancy (in cig./day) was associated with a decrease (in points) of children's global cognitive score [beta=-0.60, (95% CI: -1.10; -0.09)]; as wen as global cognitive sub-areas like verbal score [beta = -0.59, (95% CI: -1.11; -0.07)]; quantitative score [beta=-0.57, (95% CI: -1.08; -0.06)]; executive function score [beta = -0.71, (95% CI: -1.23; -0.20)]; and working memory score [beta=-0.46, (95% CI: -0.92; -0.01)]. Conclusion: Our findings suggest an association with maternal smoking during pregnancy and lowered cognitive development in children at age 4 years.

Kable JA; Coles CD; Lynch ME; Platzman K. Physiological responses to social and cognitive challenges in 8-year olds with a history of prenatal cocaine exposure. Developmental Psychobiology 50(3): 251-265, 2008. (76 refs.)

Cocaine-exposed infants have been found to have altered arousal responses but little is known about such responses in later childhood. Physiological responses to stressors were used to assess the arousal modulation of school-aged, cocaine-exposed children (n = 73) and two contrast groups, socioeconomically-matched controls (n = 58) and children with behavioral disturbance (n = 35). The behaviorally disturbed group had the highest heart rate across conditions but demonstrated a pattern of hyporesponsiveness to the stressors. They had the smallest decrement in skin conductance response at baseline and the least recovery of skin conductance response following exposure to stressors. Cocaine-exposed children demonstrated greater acceleratory responses to the stressors as indexed by their skin conductance level and were intermediate between the socioeconomically-matched controls and children with behavioral disturbance in recovery of skin conductance response following stressors. Altered arousal responses associated with prenatal cocaine exposure persisted into middle childhood but were different from those found in behaviorally disturbed children.

Lewis BA; Kirchner HL; Short EJ; Minnes S; Weishampel P; Satayathum S et al. Prenatal cocaine and tobacco effects on children's language trajectories. Pediatrics 120(1): E78-E85, 2007. (37 refs.)

OBJECTIVE. The objective of this study was to examine the effects of prenatal cocaine and polydrug exposure on language development of preschool children using a prospective longitudinal model, controlling for confounders. METHODS. Children who were exposed to cocaine in utero (n = 209) and nonexposed children (n = 189) were followed prospectively at birth and at 1, 2, 4, and 6 years of age and were compared on receptive, expressive, and total language scores across time using random coefficient models, controlling for confounders. RESULTS. A significant, stable effect of cocaine exposure on language development was observed over time for all language domains, with cocaine exposure related to poorer language performance. Cigarette exposure was related to lower receptive language scores. Environmental influences on language scores were also observed. Both the cocaine-exposed and nonexposed children declined in language performance over time. CONCLUSIONS. Prenatal cocaine exposure has a stable negative effect on language skills during the first 6 years of life. Both cocaine-exposed and nonexposed children showed decreased language growth over time; however, cocaine-exposed children demonstrated linguistic deficits compared with nonexposed peers and did not catch up. Cigarette and environmental influences were also noted.

Lumeng JC; Cabral HJ; Gannon K; Heeren T; Frank DA. Pre-natal exposures to cocaine and alcohol and physical growth patterns to age 8 years. Neurotoxicology and Teratology 29(4): 446-457, 2007. (53 refs.)

Two hundred and two primarily African American/Caribbean children (classified by maternal report and infant meconium, as 38 heavier, 74 lighter and 89 not cocaine-exposed) were measured repeatedly from birth to age 8 years to assess whether there is an independent effect of pre-natal cocaine exposure on physical growth patterns. Children with fetal alcohol syndrome identifiable at birth were excluded. At birth, cocaine and alcohol exposures were significantly and independently associated with lower weight, length and head circumference in cross-sectional multiple regression analyses. The relationship over time of pre-natal exposures to weight, height, and head circumference was then examined by multiple linear regression using mixed linear models including covariates: child's gestational age, gender, ethnicity, age at assessment, current caregiver, birth mother's use of alcohol, marijuana and tobacco during the pregnancy and pre-pregnancy weight (for child's weight) and height (for child's height and head circumference). The cocaine effects did not persist beyond infancy in piecewise linear mixed models, but a significant and independent negative effect of pre-natal alcohol exposure persisted for weight, height, and head circumference. Catch-up growth in cocaine-exposed infants occurred primarily by 6 months of age for all growth parameters, with some small fluctuations in growth rates in the preschool age range but no detectable differences between heavier versus unexposed nor lighter versus unexposed thereafter. reserved.

MacArthur AC; McBride ML; Spinelli JJ; Tamaro S; Gallagher RP; Theriault G et al. Risk of childhood leukemia associated with parental smoking and alcohol consumption prior to conception and during pregnancy: the cross-Canada childhood leukemia study. Cancer Causes and Control 19(3): 283-295, 2008. (45 refs.)

Objective As part of a larger case-control study, the authors evaluated risk of childhood leukemia relative to parental self-reported smoking and alcohol consumption. Methods Children 0-14 years of age diagnosed with leukemia between 1990 and 1994 were ascertained through population-based sources at the time of diagnosis. For each participating case, an age, gender, and area-matched control was randomly selected from provincial government health insurance rolls. Risk factor information was obtained through personal interviews with each child's parents. Conditional logistic regression models were used to examine risk of leukemia associated with parental smoking and drinking. Results Maternal alcohol consumption prior to conception (OR = 1.37, 95% CI, 0.99-1.90) and during pregnancy (OR = 1.39, 95% CI, 1.01-1.93) was associated with an excess risk of childhood leukemia, with a positive dose-response trend for increasing weekly consumption (p< 0.05). Similar results were observed for children diagnosed with acute lymphoblastic leukemia (ALL). Odds ratios for maternal cigarette smoking before and during pregnancy were consistently elevated above one, but not statistically significant. No relationship was observed with paternal drinking or smoking in the perinatal period. Conclusion Our study suggests that maternal alcohol drinking before or during pregnancy may contribute to an increased risk of childhood leukemia.

Marques PR; Pokorni JL; Long T; Teti LO. Maternal depression and cognitive features of 9-year-old children prenatally-exposed to cocaine. American Journal of Drug and Alcohol Abuse 33(1): 45-61, 2007. (22 refs.)

This study evaluated cocaine exposure and maternal characteristics as competing predictors of school-age cognitive, achievement, and language performance. One group of 47 exposed 9-year-old children were first studied in an earlier prenatal study. A non-exposed contrast group (n = 46) served as a reference. Maternal measures included: IQ, psychopathology, drugs, demographics, and environment. Child intelligence, language, and achievement scores were inversely related to maternal IQ and depression scores, with cocaine exposure significant secondary or tertiary predictors for many children. Verbal IQ scores of exposed children strongly reflected maternal depression (r = .54) but no such relationship was found among the non-exposed cohort (r = .00).

Mcgee CL; Fryer SL; Bjorkquist OA; Mattson SN; Riley EP. Deficits in social problem solving in adolescents with prenatal exposure to alcohol. American Journal of Drug and Alcohol Abuse 34(4): 423-431, 2008. (18 refs.)

This study evaluated the social problem solving skills of adolescents with histories of prenatal alcohol exposure. Adolescents (28 alcohol-exposed, 15 controls) completed a standardized questionnaire of social problem solving, and caregivers completed a parent-report measure of executive functioning. Both questionnaires were mailed to families, and caregivers were asked to recruit a non-exposed control. Results suggest that alcohol-exposed adolescents have substantial impairments in their abilities to solve problems in their everyday life, even in the absence of mental retardation. Such impairments are likely to have a significant impact on social and academic functioning and reflect their need for critical services otherwise unavailable to them.

Mcgee CL; Riley EP. Social and behavioral functioning in individuals with prenatal alcohol exposure. International Journal on Disability and Human Development 6(4): 369-382, 2007. (67 refs.)

Prenatal exposure to alcohol can lead to long-term impairments in cognition and behavior and represents a major public health concern. This paper reviews studies examining the social and behavioral functioning of individuals with prenatal alcohol exposure. Social and behavioral functioning are important domains for study because deficits in these areas can lead to problems in everyday functioning and to maladjustment in later life. Most research with individuals with prenatal alcohol exposure has used caregiver or self-report questionnaires or semi-structured interviews to sample behavior. The vast majority of studies indicate significant difficulties with interpersonal functioning, internalizing and externalizing behavior problems, and high rates of psychopathology. Recent intervention studies conducted with individuals with prenatal alcohol exposure have shown promising results in improving the social skills and behavioral functioning in this population. Finally, this paper concludes with recommendations for future studies in this area.

Milner AD; Rao H; Greenough A. The effects of antenatal smoking on lung function and respiratory symptoms in infants and children. Early Human Development 83(11): 707-711, 2007. (42 refs.)

We highlight evidence demonstrating antenatal smoking exposure is an important risk factor for increased respiratory symptoms and lung function abnormalities in infants and children. Epidemiological. studies have demonstrated an excess both of wheezing in the first two years after birth and asthma and persistent wheezing in older children. Lung function testing in children exposed to antenatal smoking has demonstrated a reduction in airway function. Antenatal exposure of nicotine to animal models results in pulmonary hypoplasia, fewer but larger alveoli and altered airway morphology. Pulmonary function testing, however, has not demonstrated that infant tung volume is affected by antenatal smoking exposure, other than due to the expected effect of smoking on somatic growth, but there is an adverse effect on airway development. There is no evidence that antenatal smoking exposure increases bronchial hyperreactivity, rather it may be associated with a diminished response to both bronchoconstrictors; and bronchodilators in infants.

Mizutani T; Suzuki K; Kondo N; Yamagata Z. Association of maternal lifestyles including smoking during pregnancy with childhood obesity. Obesity 15(12): 3133-3139, 2007. (32 refs.)

Objective: To examine the extent to which maternal smoking during early pregnancy and other prepregnancy lifestyle habits are associated with obesity and overweight in 5-year-old Japanese children. Research Method and Procedures: We studied 1417 mother-child pairs enrolled in Project Enzan-a prospective cohort study. The dependent variables, childhood overweight and obesity, were defined with an international cut-off value. Maternal smoking during early pregnancy and other prepregnancy lifestyle habits were used as independent variables. Results: Maternal smoking habits were associated with overweight in the 5-year-old children [adjusted odds ratio (OR): 2.15; 95% confidence interval (CI): 1.12 to 4.11]. Maternal sleep duration of >= 8 h/d negatively affected childhood overweight (adjusted OR: 0.71; 95 % CI: 0.49 to 1.04). Children whose mothers skipped breakfast were likely to become overweight (adjusted OR: 1.78; 95% CI: 1.14 to 2.77). The results of childhood obesity analysis were similar to those of childhood overweight analysis. Discussion: The results of this study suggest that there are effects of smoking during early pregnancy and other maternal lifestyle habits on the onset of childhood obesity in Japan. Therefore, interventions in maternal lifestyle habits are required to prevent childhood obesity, and these interventions should be initiated before pregnancy.

Paus T; Nawazkhan I; Leonard G; Perron M; Pike GB; Pitiot A et al. Corpus callosum in adolescent offspring exposed prenatally to maternal cigarette smoking. Neuroimage 40(2): 435-441, 2008. (60 refs.)

Teratogens, such as alcohol or anti-epileptic drugs, affect the size of the corpus callosum. Here we report findings obtained in a case-control study that investigated possible effects of teratogens contained in cigarette smoke on the size and structural properties of this structure. We recruited and scanned with magnetic resonance imaging a total of 408 adolescents (12 to 18 years of age); a subsample of 300 adolescents is considered in this report. Cases (n=146) were exposed to maternal cigarette smoking during pregnancy; non-exposed controls (n=154) were matched to cases by maternal education. We measured the size of corpus callosum (CC) and its sections (corrected for brain size), as well as mean values of magnetization-transfer ratio (MTR) in each CC section. Corpus callosum, and especially its posterior part, was smaller in the exposed vs. non-exposed female adolescents; no significant effects were found in males. Exposed and non-exposed subjects did not differ in the MTR-based index of myelination in either gender in any CC section. Given the lack of exposure effect on the myelination index, this finding might reflect a lower number of inter-hemispheric connections in female offspring of mothers who smoked during pregnancy.

Pulsifer MB; Butz AM; Foran MO; Belcher HME. Prenatal drug exposure: Effects on cognitive functioning at 5 years of age. Clinical Pediatrics 47(1): 58-65, 2008. (37 refs.)

The goal of this cross-sectional study was to compare cognitive functioning at age 5 years in prenatal drug-exposed children with nondrug-exposed children from a comparable inner-city environment. Children with prenatal drug exposure scored significantly lower on measures of language, school readiness skills, impulse control, and visual attention span/sequencing than controls matched for age and socioeconomic status. Intelligence, visual-motor, manual dexterity, and sustained attention scores were not significantly different between groups. The total sample scored significantly below the normative mean on standardized measures of intelligence, language, school readiness, visual-motor skills, impulse control, and sustained attention, with 40% scoring at least I standard deviation below the mean (IQ < 85) on a measure of intelligence. Findings suggest that children with prenatal drug exposure are at increased risk for learning and attention problems and are in need of close developmental surveillance and possible intervention to support school success and improve behavioral outcome.

Richardson GA; Goldschmidt L; Larkby C. Effects of prenatal cocaine exposure on growth: A longitudinal analysis. Pediatrics 120(4): e1017-e1027, 2007. (58 refs.)

OBJECTIVE. There has been a limited amount of research on the long-term effects of prenatal cocaine exposure on growth of the infant, and there has been no use of longitudinal growth models. We investigated the effects of prenatal cocaine exposure on offspring growth from 1 through 10 years of age by using a repeated-measures growth-curve model. METHODS. Women were enrolled from a prenatal clinic and interviewed at the end of each trimester of pregnancy about their cocaine, crack, alcohol, marijuana, tobacco, and other drug use. Fifty percent of the women were white, and 50% were black. Follow-up assessments occurred at 1, 3, 7, and 10 years of age. RESULTS. Cross-sectional analyses showed that children exposed to cocaine during the first trimester (n = 99) were smaller on all growth parameters at 7 and 10 years, but not at 1 or 3 years, than the children who were not exposed to cocaine during the first trimester (n = 125). The longitudinal analyses indicated that the growth curves for the 2 groups diverged over time: children who were prenatally exposed to cocaine grew at a slower rate than children who were not exposed. These analyses controlled for other factors associated with child growth. CONCLUSIONS. To our knowledge, this is the first study of the long-term effects of prenatal cocaine exposure to conduct longitudinal growth-curve analyses using 4 time points in childhood. Children who were exposed to cocaine during the first trimester grew at a slower rate than those who were not exposed. These findings indicate that prenatal cocaine exposure has a lasting effect on child development.

Rodriguez A; Miettunen J; Henriksen TB; Olsen J; Obel C; Taanila A et al. Maternal adiposity prior to pregnancy is associated with ADHD symptoms in offspring: Evidence from three prospective pregnancy cohorts. International Journal of Obesity 32(3): 550-557, 2008. (44 refs.)

Objectives: We examine whether pregnancy weight (pre-pregnancy body mass index (BMI) and/or weight gain) is related to core symptoms of attention deficit hyperactivity disorder (ADHD) in school-age offspring. Design: Follow-up of prospective pregnancy cohorts from Sweden, Denmark and Finland within the Nordic Network on ADHD. Methods: Maternal pregnancy and delivery data were collected prospectively. Teachers rated inattention and hyperactivity symptoms in offspring. High scores were defined as at least one core symptom rated as 'severe' and two as 'present' (approximately 10% of children scored in this range). Logistic regression and latent class analyses were used to examine maternal pregnancy weight in relation to children's ADHD core symptoms. Results: Teacher rated 12 556 school-aged children. Gestational weight gain outside of the Institute of Medicine guidelines was not related to ADHD symptoms (below recommendations: odds ratio (OR): 0.96; 95% confidence interval (CI): 0.81, 1.14; above recommendations: OR: 0.98; 95% CI: 0.82, 1.16). To examine various patterns of pre-pregnancy BMI and weight gain, we used latent class analysis and found significant associations between classes that included pre-pregnancy overweight or obesity and a high ADHD symptom score in offspring, ORs ranged between 1.37 (95% CI: 1.07, 1.75) and 1.89 (95% CI: 1.13, 3.15) adjusted for gestational age, birth weight, weight gain, pregnancy smoking, maternal age, maternal education, child gender, family structure and cohort country of origin. Children of women who were both overweight and gained a large amount of weight during gestation had a 2-fold risk of ADHD symptoms (OR: 2.10, 95% CI: 1.19, 3.72) compared to normal-weight women. Conclusions: We show for the first time that pre-pregnancy BMI is associated with ADHD symptoms in children. Our results are of public health significance if the associations are causal and will then add ADHD symptoms in offspring to the list of deleterious outcomes related to overweight and obesity in the prenatal period.

Salihu HM; Wilson RE. Epidemiology of prenatal smoking and perinatal outcomes. Early Human Development 83(11): 713-720, 2007. (58 refs.)

During the previous two decades smoking among pregnant women in the developed world declined by about 60-75%. Nevertheless, prenatal smoking remains a common habit and accounts for a significant proportion of fetal morbidity and mortality through both a direct (fetal) and an indirect (placental) effect. The most important smoking-induced placental. pathology is placental abruption with reported risk estimates ranging from 1.4 to 4.0. It is almost a consensus that prenatal smoking is a causative factor for placental abruption. Although the evidence is less compelling, smoking mothers are at an increased risk for placenta previa and placenta-previa-accreta combination. There is no association between maternal smoking and the syndrome of idiopathic uterine bleeding. The relationship between maternal smoking and fetal growth is causal, and includes significant reduction in growth of head circumference, abdominal circumference and femur length, with the largest reduction in size observed for femur length. Prenatal smoking is associated with a 20-30% higher likelihood for stillbirth, a 40% elevation in the risk for infant mortality and a 2-fold increase in the incidence of SIDS. Conclusion: Despite a temporal decline in maternal smoking, it still accounts for significant feto-infant morbidity and mortality, and efforts to discourage prenatal smoking need to be intensified.

Schempf AH. Illicit drug use and neonatal outcomes: A critical review. Obstetrical & Gynecological Survey 62(11): 749-757, 2007. (88 refs.)

Although the neonatal consequences of tobacco and alcohol exposure are well established, the evidence related to prenatal illicit drug use is less consistent despite prevalent views to the contrary. The many social, psychosocial, behavioral, and biomedical risk factors for adverse birth outcomes associated with illicit drug use complicate the evaluation of neonatal effects. Placing emphasis on recent research, this review summarizes the epidemiologic literature on the neonatal impact of marijuana, opiate, and cocaine use. Of these drugs, cocaine use is most consistently related to fetal growth decrements and dose-response effects have been observed. However, studies to date have largely failed to control for associated social, psychosocial, and contextual factors. Additional recommendations for future research are provided. It is likely that interventions will need to address the factors surrounding drug use to greatly improve neonatal outcomes (e.g., social circumstances, poor nutrition, stress, infections).

Sheinkopf SJ; Lagasse LL; Lester BM; Liu J; Seifer R; Bauer CR et al. Vagal tone as a resilience factor in children with prenatal cocaine exposure. Development and Psychopathology 19(3): 649-673, 2007. (82 refs.)

Studies have investigated the potential effects of prenatal cocaine exposure (CE) on children's development. However, few studies have examined predictors of resilient outcomes in this population. We examined vagal tone (VT) as a resilience factor in prenatal CE. Utilizing data from the Maternal Lifestyle Study, a cumulative risk index was derived for children with and without prenatal CE. Presence of CE and other prenatal drugs was summed with postnatal risks in infancy to Yield a 15-item risk index. Preschool cognitive outcomes, problem behaviors, and adaptive behaviors were measured. VT was assessed during an infant exam at I month and toy exploration at 36 months. We included children with complete physiologic data (217 CE. 333 non-CE). Children were classified having consistently high, consistently low, or fluctuating. VT at 1 and 36 months. Children were also classified as high versus low risk. High-risk children had lower IQ scores. more problem behaviors, and lower ratings of adaptive behaviors than low-risk children. A significant risk by VT-stability interaction indicated that for high-risk children, those with stable low VT had higher ratings of adaptive behaviors at 36 months. This is consistent with theory linking reduced VT during tasks to adaptive regulation and indicates that such regulatory functioning may serve as a protective factor in prenatal CE.

Streissguth A. Offspring effects of prenatal alcohol exposure from birth to 25 years: The Seattle prospective longitudinal study. Journal of Clinical Psychology in Medical Settings 14(2): 81-101, 2007. (72 refs.)

Before alcohol was generally known to cause birth defects, National Institute on Alcohol Abuse and Alcoholism in 1974 began funding a population-based Seattle study on alcohol use and pregnancy outcome. Women receiving prenatal care by mid-pregnancy were recruited (N = 1,529) and interviewed at home. Approximately 500 offspring exposed to a range of alcohol levels were examined on 11 occasions between day 1 and 25 years. Neuropsychological and neurobehavioral performance measures are correlated with prenatal alcohol dose, without substantial confounding by socio-demographic or rearing conditions, smoking, nutrition, or other drugs. Deficits in attention, arithmetic skill, spatial-visual memory, and IQ, as well as increased alcohol problems and psychiatric disorders are among offspring outcomes correlated at several ages with maternal drinking during and before pregnancy recognition. Findings are not confined to women who believed they had alcohol problems. Not all exposed offspring appear affected.

Topley J; Windsor D; Williams R. Behavioural, developmental and child protection outcomes following exposure to Class A drugs in pregnancy. Child Care, Health and Development 34(1): 71-76, 2008. (11 refs.)

Background: The long-term consequences of intrauterine exposure to Class A drugs are still relatively undocumented, and much of the literature relates to the North American experience, where cocaine use predominates. In Britain, heroin and amphetamine use is more common and, within Britain, patterns of drug use vary. Clearly the long-term educational and welfare needs of these children will be enhanced if the behavioural, developmental and child-care outcomes are known. This study attempts to explore some of these issues. Methods The developmental, behavioural and child protection outcomes in a group of 62 children exposed to Class A drugs in utero were investigated when the children were in full-time schooling. Results: Seventy-four per cent (46/62) of the children at the time of the study had no educational or behavioural problems, and 11 (17.7%) were receiving extra support in school. No child had a statement of special educational need. Twelve (19.3%) were reported to have behaviour and concentration problems, and in four cases, this was attributed to poor-quality parenting at the time of the study. Three of the 12 children had fetal alcohol syndrome. Twenty-six (42%) children were placed on the Child Protection Register, and care orders or residence orders were granted for 22 (35.5%) of those who were placed on the register. All of the 22 children went into substitute care at some stage. Of these children, nine were adopted and 10 were placed permanently with other family members. Ten of the 62 (16.1%) children at the time of the study were of concern to professionals for child protection reasons, and four of them were on the Child Protection Register. Conclusions: This study suggests we can be reasonably optimistic about the developmental and behavioural outcomes for children exposed to Class A drugs in utero. Over 50% required an intervention by social services, and 31% were in substitute care at the time of the study. There were continuing child protection concerns in 16% at school entry.

Traves C; College O; Cararach V; Gual A; De Tejada BM; Lopez-Tejero MD. Clinical approach to intestinal maturation in neonates prenatally exposed to alcohol. Alcohol and Alcoholism 42(5): 407-412, 2007. (54 refs.)

Aim: The need for a non-invasive diagnosis of the effects of ethanol in utero on the development of the intestine in humans led us to look for a serum marker of the structural integrity of the intestine. We propose apolipoprotein A-IV (apoA-IV) as a possible candidate. In humans this protein is synthesized only by intestinal mucosa, it is expressed in the enterocyte of the foetus from 20 weeks of gestation, and it is released to the blood stream after synthesis. Methods: We measured the levels of apoA-IV in the umbilical cord serum of neonates whose mothers had consumed alcohol during pregnancy and neonates born to women who had not (controls).The gestational age at delivery of the cases studied ranged from 36 to 42 weeks. ELISA and Western blot analysis were used. Results: There was no difference in the mean body weight of neonates from either group. Nevertheless, exposure to ethanol in utero significantly reduced (by about 30%) the apoA-IV levels in serum at birth, regardless of body weight. Conclusion: Our findings suggest that circulating apoA-IV levels could be used as a clinical marker of the prenatal effects of ethanol on the structural integrity of the intestine. Neonatal diagnosis of these intestinal effects could improve post-natal outcome.

Walhovd KB; Moe V; Slinning K; Due-Tonnessen P; Bjornerud A; Dale AM et al. Volumetric cerebral characteristics of children exposed to opiates and other substances in utero. Neuroimage 36(4): 1331-1344, 2007. (54 refs.)

Morphometric cerebral characteristics were studied in children with prenatal poly-substance exposure (n = 14) compared to controls (n = 14) without such exposure. Ten of the substance-exposed children were born to mothers who used opiates (heroin) throughout the pregnancy. Groups were compared across 16 brain measures: cortical gray matter, cerebral white matter, hippocampus, amygdala, thalamus, accumbens area, caudate, putamen, pallidum, brainstem, cerebellar cortex, cerebellar white matter, lateral ventricles, inferior lateral ventricles, and the 3rd and 4th ventricles. In addition, continuous measurement of thickness across the entire cortical mantle was performed. Volumetric characteristics were correlated with ability and questionnaire assessments 2 years prior to scan. Compared to controls, the substance-exposed children had smaller intracranial and brain volumes, including smaller cerebral cortex, amygdala, accumbens area, putamen, pallidum, brainstem, cerebellar cortex, cerebellar white matter, and inferior lateral ventricles, and thinner cortex of the right anterior cingulate and lateral orbitofrontal cortex. Pallidum and putamen appeared especially reduced in the subgroup exposed to opiates. Only volumes of the right anterior cingulate, the right lateral orbitofrontal cortex and the accumbens area, showed some association with ability and questionnaire measures. The sample studied is rare and hence small, so conclusions cannot be drawn with certainty. Morphometric group differences were observed, but associations with previous behavioral assessment were generally weak. Some of the volumetric differences, particularly thinner cortex in part of the right lateral orbitofrontal cortex, may be moderately involved in cognitive and behavioral difficulties more frequently experienced by opiate and polysubstance-exposed children.

Weinberg J; Sliwowska JH; Lan N; Hellemans KGC. Prenatal alcohol exposure: Foetal programming, the hypothalamic-pituitary-adrenal axis and sex differences in outcome. Journal of Neuroendocrinology {Dartmouth e-journal} 20(4): 470-488, 2008. (221 refs.)

Prenatal exposure to alcohol has adverse effects on offspring neuroendocrine and behavioural functions. Alcohol readily crosses the placenta, thus directly affecting developing foetal endocrine organs. In addition, alcohol-induced changes in maternal endocrine function can disrupt the normal hormonal interactions between the pregnant female and foetal systems, altering the normal hormone balance and, indirectly, affecting the development of foetal metabolic, physiological and endocrine functions. The present review focuses on the adverse effects of prenatal alcohol exposure on offspring neuroendocrine function, with particular emphasis on the hypothalamic-pituitary-adrenal (HPA) axis, a key player in the stress response. The HPA axis is highly susceptible to programming during foetal and neonatal development. Here, we review data demonstrating that alcohol exposure in utero programmes the foetal HPA axis such that HPA tone is increased throughout life. Importantly, we show that, although alterations in HPA responsiveness and regulation are robust phenomena, occurring in both male and female offspring, sexually dimorphic effects of alcohol are frequently observed. We present updated findings on possible mechanisms underlying differential effects of alcohol on male and female offspring, with special emphasis on effects at different levels of the HPA axis, and on modulatory influences of the hypothalamic-pituitary-gonadal hormones and serotonin. Finally, possible mechanisms underlying foetal programming of the HPA axis, and the long-term implications of increased exposure to endogenous glucocorticoids for offspring vulnerability to illnesses or disorders later in life are discussed.

Weiss SJ; Jonn-Seed MS; Harris-Muchell C. The contribution of fetal drug exposure to temperament: Potential teratogenic effects on neuropsychiatric risk. (review). Journal of Child Psychology and Psychiatry 48(8): 773-784, 2007. (137 refs.)

Background: Preliminary evidence indicates that fetal drug exposure may be associated with alterations in temperament. However, studies often do not dissociate the potential effects of drug exposure from other perinatal or environmental factors that could influence temperament phenotypes. Methods: High risk children (n = 120) were followed from birth to 6 months of age to determine the effects of fetal drug exposure on temperament, after controlling for the child's gender, gestational age, medical morbidity, ethnicity, and maltreatment as well as the mother's stress, income adequacy, and quality of caregiving. Methods included medical chart review, questionnaires, and videotapes of mother-child interaction. Results: Preliminary analyses indicated that fetal drug exposure was associated with both distractibility and intensity of children's responses to the environment at 6 months of age. After adjusting for potentially confounding variables, drug exposure accounted for 12% of the variance in distractibility but was not a significant predictor in the regression model for intensity. Conclusions: Findings suggest that drug-exposed children may experience difficulty sustaining their focus of attention and be more easily distracted by environmental stimuli than non-drug-exposed children. Results converge with previous research to implicate cortical hyperarousal, stemming from teratogenic effects on the dopaminergic system during fetal development.