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Prenatal cocaine exposure is associated with alterations in arousal regulation in response to stress in young children. However, relations between cocaine exposure and stress response in adolescence have not been examined. We examined salivary cortisol, self-reported emotion, heart rate, and blood pressure (BP) responses to the Trier Social Stress Test (TSST) in 49 prenatally cocaine and other drug exposed (PCE) and 33 non-cocaine-exposed (NCE) adolescents. PCE adolescents had higher cortisol levels before and after stress exposure than NCE adolescents. PCE girls showed an elevated anxiety response to stress (compared to NCE girls) and PCE boys showed a dampened diastolic BP response (compared to NCE boys). Girls showed higher anger response and lower pre-stress systolic BP than boys. Group differences were found controlling for potential confounding variables and were not moderated by caregiver-child relationship quality (although relationship quality predicted HPA axis and anxiety response). The findings suggest that prenatal drug exposure is associated with altered stress response in adolescence and that gender moderates this association., (Copyright © 2010 Elsevier Inc. All rights reserved.)

The theoretical framework for many of the early studies of prenatal cocaine exposure has been rooted in the basic concepts of teratology/developmental toxicology. Few have published longitudinal analyses of the complex interplay between the relative effects of prenatal cocaine exposure and perinatal and environmental factors on development. The purpose of this paper was to use structural equation modeling to describe the direct and indirect effects of prenatal drug exposure on developmental outcome from birth to age 6 months. Key variables considered for study include prenatal drug exposure, perinatal medical characteristics, maternal/caregiver/family characteristics, the home environment, and neurobehavioral outcomes. We prospectively enrolled 154 predominantly crack-using women. A priori exclusion criteria included: <18 years old, major illnesses diagnosed prior to pregnancy, chronic use of legal drugs, and any use of illicit drugs other than cocaine and marijuana. From the pool of noncocaine users, 154 subjects were matched to users on pregnancy risk, parity, race, and socioeconomic status. At the end of each trimester, experienced staff conducted private interviews prompting memory of amount and timing of past drug use. Urine specimens were collected at two unanticipated times; positive screens were confirmed by gas chromatography/mass spectroscopy. Measures analyzed include medical (birth) and developmental (birth, 1 month, 6 months) assessments, all performed by blinded evaluators, as well as caregiver characteristics and environmental factors (birth, 1 month). A series of four theoretical models was tested, one for each time point (birth, 1 month, 6 months) and a longitudinal model spanning birth to 6 months. Key findings include direct effects of prenatal cocaine exposure on development at birth in the birth model and on development at birth and 6 months in the longitudinal model. In addition, indirect effects of prenatal cocaine exposure were identified on development at birth, 1 month, and 6 months, mediated through the prenatal use of alcohol and tobacco and the birth head circumference. Implications of these and other findings, including the advantages and limitations of structural equation modeling, are discussed.

To assess teratogenic effects of cocaine exposure and maternal psychological distress on birth outcomes, we conducted a longitudinal prospective study of 415 infants (218 cocaine-exposed--CE, 197 nonexposed--NE). Drug exposure was determined through a combination of maternal self-report, urine, and meconium screens. Maternal psychological distress postpartum was evaluated through a standardized, normative, self-report assessment. An extensive set of confounding variables was controlled, including severity of exposure to alcohol, tobacco, marijuana and other drugs, maternal age, race, parity, number of prenatal care visits, educational, marital, and socioeconomic status, and verbal and nonverbal intelligence. CE infants were smaller on all birth parameters and more likely to be preterm, small for gestational age, and microcephalic than NE infants. Forty-one percent of cocaine users had clinically significant psychological symptoms, compared to 20% of a high-risk comparison group of noncocaine users. Consistent with a teratologic model, cocaine exposure independently predicted offspring birthweight, length, and head circumference. Maternal psychological distress self-reported postnatally also independently predicted head circumference. Tobacco, alcohol, and marijuana exposures were also significant independent predictors of some fetal growth parameters. In addition, maternal distress symptoms, which may be reflective of maternal mental health disorders or responses to stress, added significantly to the risk for poorer fetal growth.

The present study estimates the longitudinal effects of prenatal cocaine exposure on indicators of sustained attention processing at 3, 5 and 7 years of age in an urban sample of full-term African-American children (235 cocaine-exposed, 207 noncocaine-exposed). The sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview, urine and meconium toxicology assays. Sustained attention was measured at age 3 years using a standardized measure of task persistence during a challenging task [G.A. Morgan, N.A. Busch-Rossnagel, C.A. Maslin-Cole and R.J. Harmon, Individualized Assessment of Mastery Motivation: Manual for 15-36 Month Old Children, 1992.], and at ages 5 and 7 years using omission error scores from computerized continuous performance tasks (CPT) [L. Greenberg, R. Leark, T. Dupuy, C. Corman, C. Kindschi, M. Cenedela, Test of Variables of Attention (T.O.V.A. and T.O.V.A.-A.), 22, Universal Attention Disorders, Los Alamitos, CA, 1996; C.K. Conners, Conners' Continuous Performance Test (CPT), second ed., Multi-Health Systems, Canada, 1995.]. Findings from longitudinal GLM/GEE analyses of the three measured time points support a stable influence of prenatal cocaine exposure on indicators of sustained attention, after controlling for prenatal exposure to alcohol, marijuana, tobacco and over 20 additional medical and social-demographic covariates drawn from potentially confounding influences assessed at birth and later assessment visits (D=0.21; 95% CI=0.04, 0.38; P=.017). This effect was not mediated by fetal growth or gestational age and remained highly stable with increasing levels of covariate control. Separately, using the age 7 data, a structural equations model (SEM) was constructed combining all available self-report and bioassay data to measure magnitude of cocaine exposure in relationship to attention task performance. Results indicated a gradient of influence, with each standard deviation increase in the level of prenatal cocaine exposure relating to a 16% standard deviation increase in omission error scores at age 7. Overall findings support a stable cocaine-specific effect on indicators of sustained attention processing during the early childhood years. Results are discussed within the context of neurobiological and behavioral research linking prenatal cocaine exposure to long-lasting disruption of the brain systems subserving arousal and attention.

This study investigated infant neurobehavioral functioning during the newborn period in 334 full-term, African American neonates (187 cocaine exposed, 147 non-cocaine exposed) enrolled prospectively at birth, with documentation of drug exposure status through maternal interview and urine and meconium toxicology assays. Infants were assessed using the Brazelton Neonatal Behavioral Assessment Scale (BNBAS) during the newborn period (0-6 postnatal days). Findings from multivariate profile analyses support a consistent, modest effect of prenatal cocaine exposure on neurobehavioral functioning in full-term neonates. All of the BNBAS cluster scores, with the exception of abnormal reflexes, were similarly affected, sharing a common slope (D=-0.14; 95% CI=-0.27, -0.003; P=.046) representing a -0.14 point difference between cocaine-exposed and non-cocaine-exposed infants after controlling for prenatal exposure to alcohol, tobacco, and marijuana (ATM); maternal age, education, employment, primigravida status, and prenatal care visits; and infant sex and postnatal age in days. Fetal growth was also related to neurobehavioral functioning and, in part, mediated the relationship between cocaine exposure and the BNBAS cluster scores. Cocaine exposure during each trimester similarly influenced infant neurobehavioral profiles, with cocaine-associated deficits most pronounced in infants with exposure in all three trimesters. Results from qualitative and quantitative urine and meconium bioassay indicators further substantiated these results. Findings, while significant, represent modest effect sizes in full-term infants.