The authors examined 223 children at age 4 years for the effects of prenatal cocaine exposure, exposure to other substances, maternal and environmental risk factors, and neonatal medical problems on IQ, externalizing problems, and internalizing problems. Regression analyses showed that maternal verbal IQ and low environmental risk predicted child IQ. Cocaine exposure negatively predicted children's overall IQ and verbal reasoning scores, but only for boys. Cocaine exposure also predicted poorer short-term memory. Maternal harsh discipline, maternal depressive symptoms, and increased environmental risk predicted externalizing problems. In contrast, only maternal depressive symptoms predicted internalizing problems. These findings indicate that early exposure to substances is largely unrelated to subsequent IQ or adjustment, particularly for girls. Two important attributes studied in preschool-age children are intelligence and emotionalbehavioral adjustment. By age 4 years, IQ scores are relatively stable and predict academic success during the first few years of elementary school (Kaplan, 1996; Sameroff, Seifer, Baldwin, & Baldwin, 1993). Similarly, externalizing and internalizing problems also exhibit significant stability by age 4, and externalizing problems, in particular, predict later academic and social problems (

The impact of 2 environmental and 2 biological risk measures was studied in 175 preterm children. Levels of family risk, which included family composition, support, and interaction variables, and social class, as well as increases or decreases in family risk over the 1st year of life, were examined with intraventricular hemorrhage (IVH) and other neonatal medical complications as predictors of cognitive and motor outcomes in the 2nd year of life. Family risk, early medical risk, and the Family Risk X IVH interaction emerged as significant predictors of later development. Family risk had less impact on subjects at highest medical risk. Different regression equations for each outcome underscored the specificity of environmental effects on developmental outcomes.The environmental context in which a child is raised has long been recognized as crucial to determining developmental outcome in any number of domains. Wachs (1991) has enumerated three historical stages of research on the impact of the environment on development. In the earliest stage, studies determined that variability in the environment was related to variability in development. The environment was characterized by global, social address variables, such as socioeconomic status (SES), which do not affect the child directly. In the second stage, studies characterized by an exploration of the relation between more specific environmental variables, such as parental responsivity and variety of stimulation, and developmental outcome were examined (Lewis & Goldberg, 1969). In the third stage, the most recent research addressed the importance of organismenvironment interactions in understanding the complex relation between environmental, individual characteristics and development.Early studies found SES to be strongly related to developmental outcomes in normal and high-risk samples (

Cocaine exposure, being male, and a high-risk environment were all predictive of aggressive behavior at 5 years. It is this group of exposed boys at high environmental risk that is most likely to show continued aggression over time.

The ability to modulate arousal is a critical skill with wide-ranging implications for development. In this study, the authors examined arousal regulation as a function of levels of prenatal cocaine exposure in 107 infants at 4 months of age using a "still-face" procedure. Facial expressions were coded. A greater percentage of heavily cocaine-exposed infants, compared with those who were unexposed to cocaine, showed less enjoyment during en face play with their mothers and continued to show negative expressions during the resumption of play following a period when the interaction was interrupted. This finding was independent of other substance exposure, neonatal medical condition, environmental risk, maternal contingent responsivity, and concurrent maternal sensitivity and vocalizations.

Examined the effect of prenatal alcohol and cigarette exposure on infant adrenocortical reactivity to stress at 2 and 6 months of age. Cortisol response (pre- to poststressor increase) at 2 months was lower for the exposed than nonexposed infants, whereas cortisol response at 6 months did not differ between the exposed and nonexposed infants. The 2-month group difference in cortisol response reflected a higher prestressor cortisol level in the exposed infants.

This study examined the cognitive functioning in 236 infants at 8 and 18 months of age. Thirty-seven infants were heavily exposed to cocaine in-utero, 30 were lightly exposed, and 169 were not exposed to cocaine. Cognitive functioning was evaluated with the Bayley Scales of Infant Development (2nd ed.; N. Bayley, 1993) at both ages. Infant information processing was also assessed with an infantcontrolled habituation procedure. Results indicated that (a) infants of cocaine-abusing women had higher neonatal medical and environmental risk scores; (b) at 8 months, exposure groups did not differ in Psychomotor Development Index, Mental Development Index (MDI) scores, or recovery to a novel stimulus; and (c) infants heavily exposed to cocaine or high environmental risk had a decrease in MDI scores from 8 to 18 months. These results were obtained when neonatal medical and environmental risk, as well as polydrug exposure, were controlled.In examining whether prenatal exposure to cocaine impairs later cognitive functioning, research on humans continues to provide equivocal results. The ambiguous nature of outcome findings is due to methodological problems typically associated with behavioral toxicology research. In studies in which researchers are attempting to find relations between prenatal cocaine and some aspect of postnatal development, researchers must contend with a host of methodological problems, including (a) the potential confounding effects of other substances of abuse and poor maternal health and nutrition, (b) sensitive and valid measurement of infant outcome behaviors, and (c) differential effects of the postnatal child-rearing environment (e.g.,

Individual differences in emotion knowledge were examined among 188 4-year-old, predominantly African American children. Cognitive ability and negative emotionality, maternal characteristics (parenting, verbal intelligence, and depressive symptoms), environmental risk, and child sex were examined as predictors of emotion knowledge. Regression analyses indicated that cognitively skilled children who resided in relatively low risk environments with verbally intelligent mothers possessed greater emotion knowledge. Proximal (4-year) child cognitive ability was a stronger predictor than distal (2-year) cognitive ability. Positive parenting at 4 years was correlated with child emotion knowledge, but this relation disappeared when parenting was examined in the context of other predictors. These findings highlight the potential role of child cognitive ability, along with environmental risk and maternal verbal intelligence, in children's emotion knowledge and demonstrate the importance of examining a variety of predictors for their unique contribution to emotion knowledge.

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 231 children (91 cocaine exposed, 140 unexposed) at 4, 6, and 9 years of age. 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 of 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 by gender interaction are discussed. Keywordsprenatal cocaine exposure; environmental risk; gender differences; intelligence Prenatal cocaine exposure has been hypothesized to adversely affect children's cognitive development, possibly through its effect on developing neurotransmitter systems critical to neuronal differentiation and brain structure formation (Harvey, 2004;Morrow, Elsworth, & Roth, 2003). More specifically, cocaine has been found to block the reuptake of monoaminergic neurotransmitters, which may disrupt the development of neuronal circuitry in the fetus Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at http://www.apa.org/journals/dev/ 2 Values in Figure 1 are based on predicted mean scores for a particular hypothetical individual based on the model coefficients. Values were calculated directly as the inner product of the model coefficient vector and a vector of scores on all of the variables in the model. (Lidow, 1995;Mayes, 1999). Cocaine exposure also may cause vasoconstriction of cerebral blood vessels, producing a hypoxic condition in the brain that precipitates decreased fetal growth and nutrition (Kurth et al., 1993;van de Bor, Walther, & Sims, 1990). Collectively, these findings suggest that prenatal cocaine exposure is a risk factor for impaired central nervous system...