Substance use among pregnant women continues to be a major public health concern, posing potential risk to their drug-exposed children as well as burdens on society. This review is intended to discuss the most recent literature regarding the association between in utero cocaine exposure and developmental and behavioral outcomes from birth through adolescence across various domains of functioning (growth, neurobiology, intelligence, academic achievement, language, executive functioning, behavioral regulation and psychopathology). In addition, methodological limitations, associated biological, sociodemographic and environmental risk factors and future directions in this area of research are discussed. Given the large number of exposed children in the child welfare system and the increased need for medical, mental health and special education services within this population, more definitively documenting associations between prenatal cocaine exposure and later child outcomes is essential in order to be able to prospectively address the many significant public health, economic and public policy implications.
Substance use among pregnant women continues to be a major public health concern, posing risk to child development as well as imposing financial and social burdens on society via increased need for medical and social services. Recent US estimates indicated that 5.1% of pregnant women 15 to 44 years of age reported recent illicit drug use.1 Additional reports indicated that ∼32% of pregnant women who admitted illicit drug use also reported concomitant alcohol and tobacco use,2 with up to 1 million infants exposed in utero to licit and/or illicit drugs each year.3, 4 Estimates of multiple drug use during pregnancy tend to be even higher in individual high-risk research studies. Although these statistics reflect the need for public concern surrounding substance use during pregnancy, it is especially important to keep in mind that the aforementioned statistics are only estimates and that underreporting of substance use is common among all individuals including pregnant women, likely given the social and legal implications of their disclosure. Thus, the true prevalence of substance use during pregnancy may be expected to be higher than what has been reported.
Cocaine currently remains one of the most commonly abused illicit drugs in the United States. Cocaine induces euphoria by increasing dopamine release within the central nervous system, subsequently enhancing the potential for the user's ongoing drug-seeking and/or using behaviors.5, 6 Cocaine dependence is often associated with social and environmental disadvantage and high stress levels.7 Over the past two decades, cocaine use during pregnancy has received focused attention, with initial reports suggesting the potential for teratogenic effects of prenatal exposure on the developing fetus. However, many of these reports generated exaggerated and eventually unsubstantiated concerns regarding a hypothesized ‘crack baby syndrome’. As a result, several large prospective studies were initiated to assess the short- and/or long-term outcomes of children with prenatal cocaine exposure (PCE),8, 9, 10, 11, 12, 13, 14, 15 many of which continue to investigate potential biological and environmental vulnerabilities in exposed populations from birth into adolescence and young adulthood.
Although continued concern persists surrounding the impact of PCE, actual prevalence rates of PCE remain unclear. Historically, the prevalence of cocaine use during pregnancy had declined from previous years to an estimated 1.1% of women under age 44 years based on the last national survey data that were reported in 1992.16 A later report indicated that of an estimated 2.8% of women who used illicit drugs during pregnancy, 10% reported cocaine use.17 Ostrea et al.18 also demonstrated evidence of underreporting within this population. Of the ∼1300 women in their sample who tested positive for cocaine use during pregnancy, only 11% of the mothers admitted use through self-report. The lack of recent national data on prevalence rates and the problem of underreporting make it difficult to ascertain the true impact of PCE on our society today. Despite unclear prevalence rates, the issue of maternal substance use during pregnancy continues to constitute a significant public health concern. More specifically, substance abuse affects the health of not only the mother but also the exposed child, increasing the potential need for medical, social and special education services for the family. In addition, societal burdens include increased financial expense to society to support continued access to such services.
The objectives of this review are: (1) to examine the pathways by which PCE may influence short- and long-term developmental and behavioral functioning; (2) to highlight recent reports on outcomes of exposed children across various functional domains (physical growth, neurobiology, intelligence, academic achievement, need for special education, language skills, executive functioning, behavioral regulation and psychopathology); (3) to assess the impact of intervening biological, sociodemographic and environmental risk factors that confound the ability to determine specific fetal drug-exposure effects as time elapses; and (4) to discuss limitations within this body of research and address potential avenues for future research within this population.
PCE: potential pathways of influence
The direct and/or indirect pathways by which PCE may affect both development and behavior have been described. A major emphasis has been to determine the specific acute effects of PCE on developing brain structure and function as well as assessing the potential long-term developmental impact of such alterations. Cocaine readily crosses the placenta, thereby potentially directly affecting neuronal maturation and increasing the risk for central nervous system disruptions during fetal development.19 The magnitude of these effects will depend upon the dosage, timing and/or duration of exposure. For instance, higher doses of PCE have been shown to increase dopamine activity in utero, thereby increasing tolerance to the substance as well as the potential for substance abuse later in life.20 Fetal animal studies have shown that PCE can affect levels of neurotransmitters, resulting in subsequent alterations in brain development.21, 22, 23
Specific areas of the human brain, such as the frontal lobes that are involved with the regulation of attention, impulsivity and stress response, have been reported to be particularly vulnerable to PCE, with preliminary neuroimaging studies in humans revealing specific morphologic changes in these areas.19, 24 These prenatal disruptions in the developmental programming of an infant's behavioral regulatory system, in combination with the lifestyle that often accompanies drug-using women (for example, continued drug use after pregnancy, increased likelihood of compromised caregiving and dysfunctional environments), enhance the exposed child's vulnerability to maladaptive development and behavior later in life.25, 26
Literature review: developmental and behavioral functioning associated with PCE
Effects on child physical growth
Although reports of physical growth deficits among infants with PCE have been disputed,27 recent well-controlled prospective studies suggest that PCE does in fact affect fetal physical growth, resulting in an increased likelihood of premature delivery and generalized growth retardation (that is, decreased birth weight, shorter length and smaller head circumference).28, 29, 30, 31, 32 This may, in part, be mediated by the negative impact of cocaine on placental and uterine blood flow. Mayes et al.30 reported that infants with PCE had lower birth weights and smaller head sizes when compared with noncocaine-exposed infants or infants exposed only to alcohol, tobacco or marijuana. Shankaran et al.31 corroborated these growth deficits with evidence that lower levels of PCE increased the risk for low birth weight, whereas moderate exposure increased the risk for smaller head circumference.
Growth deficits involving weight, length and head circumference remain the most consistent finding. No consistent patterns of dysmorphology have been identified in well-controlled, long-term studies of infants with PCE.33, 34 This area of investigation remains heavily confounded by the simultaneous use of other substances (for example, alcohol, tobacco and marijuana) during pregnancy for which substantial evidence exists regarding their association with both dysmorphology and growth abnormalities.34, 35, 36, 37 However, even after controlling for these multiple drug exposures, growth suppression among cocaine-exposed children has been shown to persist beyond infancy, specifically regarding weight for height ratio and height.34 Compared with nonexposed controls, evidence of slower growth rates has been reported among exposed children through age 10 years.28, 38 Children who were born full term and who had the highest levels of PCE were reported to have a higher body mass index at age 9 years.39 High cocaine use, which has been associated with early undernutrition, may be a factor in the later development of obesity.39 Because early physical growth deficits have been associated with a negative impact on later motor development, cognitive functioning, metabolic processes, physical activity and social outcomes in diverse populations,28, 40 continued long-term follow-up of children with PCE is needed to identify mechanisms that result in abnormal growth and other dysfunctional outcomes in adolescents and young adults.
Intelligence, academic achievement and need for special education
Although there is consistent evidence of poorer cognitive performance in children with PCE, there is also a general consensus that PCE alone does not independently lower global intelligence. However, associated risk factors (for example, low birth weight, prematurity, low caregiver intelligence and lower quality home environment) have all been shown to contribute to less optimal intellectual performance in cocaine-exposed children.41, 42, 43, 44, 45, 46, 47, 48 Not surprisingly, many of these same risk factors have been shown to be associated with less optimal school performance among children with PCE. As with a lack of evidence that PCE directly affects intelligence, PCE has not been shown to be directly associated with child academic performance.45, 49, 50 Instead, evidence indicates that children who share common demographic risk factors (for example, inner-city environment, low socioeconomic status (SES)) tend to exhibit substandard performance regardless of their prenatal drug exposure status.49, 50 Overall, the poor sociodemographic characteristics of the prototypic pregnant drug abuser appear to have a much greater effect on intellectual functioning and school performance than the actual exposure to cocaine itself. It is essential that research assessing these drug exposure effects take into account the limited sociodemographic diversity of these samples.
The increased need for special education services has become a topic of major concern given the documented suboptimal school performance in high-risk populations. A recent report of low-SES, African-American children estimated that cocaine-exposed children were 2.8 times more likely than nonexposed peers to have a learning disability at age 7 years despite comparable performance on standardized intelligence measures.14 Additionally, in a more ethnically diverse sample who were entering the school system, PCE was associated with an increased need for an individualized education plan as well as for specialized support services.51 Levine et al.51 noted that PCE alone was estimated to account for an additional cost of over 26 million dollars per year in special education services in the United States.
Although PCE is not often found to be independently associated with intelligence, recent studies of children between toddlerhood and elementary school age have reported main effects of PCE on language skills, even after controlling for multiple social, medical and environmental risk factors.52, 53, 54, 55, 56, 57 More specifically, exposed children scored an average of 2 to 10 points below nonexposed children on language measures. Additional risk factors—such as ethnic minority status, female gender, fetal growth deficits, residing in maternal/relative care versus out-of-home placement, low maternal intelligence, education, or language ability and amount or duration of cocaine use—have also been shown to moderate the association between PCE and child language skills.13, 48, 53, 54, 57, 58, 59 Although longitudinal models have demonstrated significant declines in the language performance of exposed children through age 6 years,55 more recent evidence suggests a general improvement in the receptive language of exposed children through age 17 years.60 Better language functioning outcomes were associated with being reared in more stimulating home environments in this adolescent sample. Although the direct negative impact of PCE on language acquisition may dissipate over time for children raised in an enriched environment, other sociodemographic risk factors may, in part, explain the persistence of language deficits that have been observed in these complex high-risk populations.
Neuroimaging techniques have proven particularly valuable in examining the neural circuitry of the adult drug user as well as in the child who has experienced in utero exposure. Recent reports suggest an association between PCE and abnormalities in both brain structure and function.12, 19, 24, 61, 62, 63, 64, 65, 66 Sheinkopf et al.24 reported differences in the activation of specific brain regions including the right inferior frontal cortex and the temporal and occipital regions among school-aged children with PCE. Among adolescents, recent neuroimaging evidence suggests a long-term effect of PCE on the arousal regulation system with implications for the regulation of attention and impulsivity in exposed youth.67
The potential intrauterine fetal stress caused by maternal cocaine use and its high-risk correlates may also disrupt the infant's developing stress response system altering how physiology interacts with the extrauterine environment.68 More specifically, PCE may constitute a chronic stress that disrupts developmental programming in utero by prolonging fetal exposure to elevated cortisol levels, a stress hormone released by the adrenal gland. Elevated cortisol exposure may, in turn, alter how the child's neuroendocrine system responds to various stressful events in the extrauterine environment.20 Downregulation of the stress response system as a result of chronic stress exposure in utero may negatively affect attention regulation, motivation, immune system functioning and sleep cycles as well as increase the risk for the onset of stress-related diseases.69 In addition, other specific areas of the human brain (for example, the hippocampus and amygdala) that regulate emotional functioning have also been shown to be sensitive to stress hormones.70 The potential impact of a chronically disordered stress physiology on the ultimate functional outcomes of older children and adolescents who have PCE is currently an area of research emphasis.
There have been few studies measuring cortisol levels in cohorts of children with PCE. Infant studies have reported somewhat inconsistent findings with reports of both lower71 and elevated72 levels of basal cortisol levels in exposed infants. In addition, there is evidence of a suppressed cortisol response following a stressful event when compared with nonexposed infants (that is, lower cortisol reactivity)73 and heightened cortisol reactivity in male infants with PCE.74 Results have also been somewhat contradictory in older children. Lester et al.75 reported blunted cortisol reactivity in preadolescents with the strongest effects observed in cocaine-exposed children who were exposed to domestic violence. However, Chaplin et al.76 reported elevated cortisol levels in both baseline and reactivity measures among adolescents with PCE. Additional evidence has been reported suggesting that preadolescents with high levels of PCE exhibited flattened patterns of change in cortisol levels between evening and morning, controlling for related sociodemographic and environmental factors.77 In this sample, black race and caregiver depression were also associated with diurnal patterns. Overall, findings suggest that PCE may contribute to over- or under-regulation of the exposed child's stress response system and that related risk factors (for example, domestic violence, caregiver psychopathology) may moderate this association. Given the potential long-term impact of altered stress regulation on areas such as attention regulation and onset of stress-related diseases, understanding how chronic stressors (PCE and other associated environmental risk factors) interact to alter normal neuroendocrine physiology remains an important area of ongoing investigations.
Executive function represents a broad set of cognitive abilities that include working memory, inhibitory control, information processing, cognitive flexibility, problem solving, attention and planning. Prenatal substance exposure has been associated with less optimal executive functioning in cohort samples ranging from infancy to young adulthood.10, 78, 79, 80, 81, 82 Within samples of children with PCE specifically, both independent and moderated associations between PCE and specific executive function deficits (for example, inhibitory control, visual-perceptual ability and attention) have been reported.10, 78, 79, 81, 83, 84, 85 As in other areas reported to be affected by PCE, independent cocaine effects appear to be subtle, with evidence suggesting that it is the caregiving environment that accounts for a majority of the variance.10 Other studies have demonstrated stronger cocaine-specific effects. For instance, children with heavy PCE were reported to display less optimal inhibitory control when compared with children with light or no exposure.81 In addition, longer response latencies and variation in brain activation patterns have been observed in 8-year-old exposed children during an executive function task when compared with nonexposed children.86 As children age, control of executive functioning increases in complexity, especially with regard to decision making. Thus, executive function deficits have important long-term implications for the decision-making abilities of exposed adolescents and young adults, which may be particularly important regarding decisions to engage in inappropriate and/or risky behaviors (for example, early drug use or sexual experimentation).
Behavioral regulation difficulties
Associations between PCE and subsequent behavior regulation have been observed as early as the first year of life with cocaine-exposed infants demonstrating deficits in self-regulation, heightened excitability, increased attention problems, more passive-withdrawn negative affect, lower task orientation, decreased adaptability and increased fussiness,87, 88, 89, 90, 91, 92 although not all deficits are solely influenced by PCE.46, 56, 91 Prenatal drug exposure (including but not limited to cocaine) and associated sociodemographic and environmental risk factors remain a substantial concern regarding their impact on early infant behavior. Exposed infants have been shown to display clinically aberrant behavior profiles and may require special attention to prevent long-term behavioral disruptions.93
Among school-aged children, studies have traditionally assessed internalizing and externalizing behaviors via parent and/or teacher report. Associations between PCE and internalizing behavior problems (for example, social withdrawal, somatic complaints, anxiety and depression) are often moderated by factors such as gender, prenatal polydrug exposure and nonrelative foster care placement in exposed school-age samples.94, 95, 96 As with internalizing behavior, externalizing behaviors problems (behaviors directed outward/towards other people; for example, delinquency and aggressiveness) have also been observed among children with PCE, with observed effects often moderated by related sociodemographic or environmental factors. Such moderators include child gender, low SES, exposure to domestic violence, caregiver depression, lower quality home environments, child's living situation and prenatal exposure to alcohol and tobacco.94, 95, 97, 98, 99, 100, 101 A recent study utilizing sophisticated statistical modeling to assess cumulative risks associated with PCE and later behavior problems reported evidence for multiple pathways through which prenatal substance exposure may increase risk for later behavior problems.102 These findings suggest both direct effects and indirect pathways by which alterations in neurobehavioral regulation can affect later behavioral expression.
As children enter adolescence, increased risk-taking behaviors have been an area of interest and concern. Risk-taking behaviors typically involve behaviors that are potentially damaging to one's health, such as substance use, precocious/risky sexual behavior, driving dangerously and delinquent behaviors (for example, stealing, fighting and truancy).103 Increased willingness to engage in these risk-taking behaviors has been associated with living in high-risk social and cultural environments,104, 105 but the etiology of such behaviors has not been thoroughly addressed in adolescents with PCE. Thus, on-going longitudinal studies of adolescents and young adults with PCE are essential to help better understand risk-taking behaviors in this population.
Delinquent behaviors, in particular, have been observed in predominantly low-SES populations of youths born to substance abusing mothers, including youth with PCE.9, 96, 99, 100, 106 Such deviant behaviors (for example, aggression, disregard for safety precautions and substance use) have been most prevalent in males, both exposed and nonexposed.9, 96, 106, 107 Prenatal nicotine exposure and childhood exposure to violence have also been associated with self-reported delinquent behaviors among exposed adolescents; however, no direct effect of PCE have been confirmed.108 In general population surveys, deviant social behavior among youths aged 12 to 17 years has been associated with the use of illicit drugs.109 These observations reinforce concerns about the impact of PCE and other associated environmental risk factors on increasing deviant social behaviors and substance abuse among exposed youth as well as increasing potential for involvement with the criminal justice system.
These risk conditions clearly increase the opportunity for young adolescents to experiment with drugs, with reports indicating that they are ∼2.4 to 4 times more likely to develop an established substance use disorder during adolescence.110, 111 The specific impact of PCE, however, in increasing the risk of early-onset drug use and abuse during adolescence is less clear. Alterations observed in fetal brain development and programming associated with PCE may increase the risk for compulsive behaviors that underlie drug addiction;20 however, relatively few reports have been able to document this association as children who have participated in most longitudinal studies of PCE are only now reaching adolescence. A recent report in adolescents demonstrated an association between higher levels of PCE and an increased likelihood of using both licit and illicit substances, most commonly alcohol and marijuana.11 In addition, a higher level of exposure to violence between middle childhood and adolescence was associated with an increased incidence of substance use. Extended long-term follow-up studies are necessary to specifically identify the potential residual effects of PCE on later patterns of addictive behavior. In addition to self-report of drug use/risk-seeking behaviors, comprehensive neuroimaging assessments will be essential to more definitively identify structural and functional alterations in the central nervous system of these high-risk populations.
PCE has been associated with symptoms of later psychopathology, including attention deficit hyperactivity disorder,95 oppositional defiant disorder,95, 99 depression112 and anxiety.113 An increased likelihood of suicidal ideation was reported in a sample of urban, predominantly low-SES children with PCE who had reported elevated depressive symptoms, emotional distress and exposure to violence.112 However, a direct cocaine effect was not documented. Similarly, another study of preadolescents found no direct association between PCE and child depression, but reported an increased risk for depressive symptoms among children who had a history of abuse or who had caregivers with psychiatric problems.99
This association between PCE and later psychological symptomology among exposed children may be attributed, in part, to the vulnerability of the brain during fetal development. Variation in dosage, duration and/or timing of PCE (for example, during critical periods of brain development) may disrupt the typical developmental process of certain brain regions.20 Such affected areas include those that regulate attention, impulse control and behavioral response (for example, prefrontal cortex, limbic cortex). Deviations in a child's ability to appropriately perform these functions have been related to the later onset of mental health disorders. Although symptoms of attention deficit hyperactivity disorder, oppositional defiant disorder and depression have been observed in children with PCE up to age 11 years, additional environmental risk factors (for example, exposure to violence, caregiver psychopathology and low SES) also contribute to the etiology of these symptoms in exposed children.99, 112 Longitudinal research is needed to better understand and explain the interactive role of genetic, neurobiological and environmental factors in determining the presentation of these disorders in children with PCE. Additional concerns persist regarding a potential increased risk for the development of antisocial behaviors and early addictive behaviors as these children enter adolescence and early adulthood.
Uncertain PCE prevalence rates confounded by opposing reports in the literature have clouded attempts to define specific cocaine-related effects on child outcomes. The lack of consistent methodological approaches across studies of PCE likely contributes to much of this inconsistency.25, 114, 115 For example, a large proportion of study cohorts consist of low-SES, urban, ethnic minority participants. This limits the generalizability of study findings to a more diverse population. In addition, issues with matching criteria for control samples, inclusion of varying proportions of preterm infants in study samples and inadequate sample sizes have been other factors that contribute to inconsistencies in the research literature. Premature birth, in particular, has known effects on child development (for example, growth, developmental and behavioral difficulties) that may confound effects of PCE in studies that do not adequately control for this variable. Another significant methodological concern in PCE studies involves variation in drug screening/identification techniques (for example, maternal self-report vs. more objective, biologic confirmations utilizing urine, meconium or hair). The advantage of biologic confirmation of substance exposure far outweighs reliance on maternal self-report given the demonstrated high prevalence of underreporting. Other issues that may influence the consistency and accuracy of study findings include differences in assessment ages, increased attrition over time with drug-using cohorts and variation in statistical control variables used (for example, environmental risk factors, premature birth, continued maternal substance use). Even when samples are carefully selected and numerous control variables are considered, there remain many social and environmental variables that confound high-risk, drug-using behaviors, thereby making it difficult to isolate independent drug-related group differences. In addition, the lack of adequately controlling for comorbid legal and illegal drug use in statistical analyses limits both the ability to identify an independent association between any single exposure variable and a specific behavior/outcome as well as complicates the interpretation of observed effects.27
Given that biological, sociodemographic and/or environmental risk factors often coexist in youth with PCE, multidimensional statistical approaches are necessary in order to effectively discriminate the influences of PCE as opposed to these other contextual variables as they affect later child developmental and behavioral functioning. Such variables include gender,9, 39, 116 low birth weight,46, 58 low SES,99 low quality of home environments,47, 94 maternal age,28, 55 lower maternal education/intelligence,56, 91, 95 caregiver instability and/or foster care placement,45, 117 an increased number of individuals in the household,47 caregiver functioning/psychopathology,91, 99, 101 violence exposure94, 99 and the comorbid and/or continued use of other drugs (alcohol, tobacco, marijuana, opiates) by caregivers.79, 100 Recognition of these confounds and their potential interaction with PCE is essential for the interpretability and generalizability of study findings to larger populations. Thus, utilization of multivariate statistical approaches (multiple regression, structural equation models, longitudinal growth models, moderation analyses, cumulative stress models) facilitate stronger statistical control over confounding variables and, in turn, enhance the ability to examine trajectories of improvement/decline over time and help to untangle how combinations of multiple risk factors influence the development of child maladjustment.55, 77, 100, 102, 116 Such approaches are essential in longitudinal studies as sociodemographic and environmental factors become increasingly more influential on child outcomes as more time elapses from the PCE.
Conclusions and future directions
This review, as with others,27, 118, 119, 120, 121, 122 clearly emphasizes the complexity of determining the independent and interactive effects of early drug exposure and associated risk factors on various areas of development. Although there is a general consensus that PCE does influence certain aspects of the growth and development of infants, children and adolescents, projections regarding the severity and prevalence of teratogenic effects that were anticipated over two decades ago have not materialized (for example, ‘crack baby syndrome’). In recent years, interest has been redirected from examining growth deficits, acute medical outcomes and early neurodevelopmental functioning in exposed infants and toddlers to addressing the potential (and often more subtle) associations between PCE and later developmental and behavioral patterns in school-age children and adolescents. Overall, the wide array of research reports on these later outcomes suggests that illicit drug exposure is only one of many complex interacting factors (for example, genetics, parenting styles, environment, sociodemographics) that both acutely and chronically influence the drug-using mother and her child.
In addition, some factors may be more important than others with regard to certain specific child outcomes. For instance, dosage effects of PCE (amount/duration) may be more influential on child neurobiology (such as stress hormone regulation) and certain aspects of executive functioning. Child gender is another one of several factors that has been specifically shown to moderate the association of PCE with certain later child behavior problems. Similarly, the quality of the child's home environment is associated with child outcomes related to intelligence, academic achievement, language skills and executive functioning above and beyond PCE. Exposure to violence has also become an increasingly important focus within youth with PCE as evidence has demonstrated that this environmental variable has significant implications on youth stress responsivity, behavioral problems, delinquency, substance use and psychopathology. Thus, the influence of individual characteristics, as well as the family's lifestyle, becomes increasingly important to consider over time. Ideally, continued research will examine which developmental and behavioral patterns persist as longitudinal studies involving older children, adolescents and young adults are completed and more complex statistical techniques are employed.
Furthermore, research in this area will ideally inform clinical practice with high-risk populations of children with prenatal substance exposure. More specifically, recommendations for clinical care of exposed infants may emphasize coordinating medical care that monitors infant physical health, growth and nutrition. Other important clinical considerations may include making referrals as needed for substance abuse treatment for mothers and providing early intervention services that may facilitate optimal development for the children as well as their families. Given the increased need for special education services among this high-risk population, clinicians and service providers may also need to pay particular attention to the potential need for school preparation services or special education services. The earlier children receive such services, the more likely efforts can be made to prevent later or persistent school difficulties. Another area of concern is the potential risk for exposed youth (especially boys) to develop externalizing problems (for example, delinquency, oppositional defiance) and internalizing problems (for example, depression, anxiety, suicidal ideation) in later childhood and adolescence. In such cases, it is essential that medical and mental health providers be cognizant of the potential risk of in utero drug exposure and related environmental risk factors that may put these children at increased need for mental health and social services for the individual and/or their family in order to prevent long-term problems such as substance abuse, mental health disorders and involvement with the criminal justice system.
Overall, research in the area of prenatal drug exposure is essential for several reasons. Many questions persist within this body of research with regard to clearly distinguishing the direct and indirect pathways of influence on youth outcomes with regard to PCE and other related risk factors. Continued research in conjunction with multivariate statistical techniques will help researchers examine longitudinal trajectories, mediating or moderating factors and to statistically control for many of the prenatal and postnatal variables known to influence long-term outcomes in this population. Given the large number of exposed children in the child welfare system (for example, foster care) as well as the increased need for medical, mental health and special education services within this population,114 more definitively documenting associations between PCE and later developmental and behavioral outcomes is essential in order to be able to prospectively address the many significant public health, economic and public policy implications.
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This review was supported in part by the National Institute on Drug Abuse (NIDA) through cooperative agreement 5U10DA024118-03 and an interagency agreement with the National Institute of Mental Health (NIMH).
The authors declare no conflict of interest.
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Lambert, B., Bauer, C. Developmental and behavioral consequences of prenatal cocaine exposure: a review. J Perinatol 32, 819–828 (2012). https://doi.org/10.1038/jp.2012.90
- high-risk population
- prenatal exposure
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