Objective Examined effects of prenatal cocaine exposure (PCE) on tobacco, alcohol, marijuana and cocaine use by age 15. Methods Adolescent (n = 358; 183 PCE, 175 non-prenatally cocaine exposed; NCE) drug use was assessed using urine, hair, and/or blood spot samples and self-report (Youth Risk Behavior Surveillance System; YRBSS) at ages 12 and 15. Logistic regression assessed effects of PCE on drug use controlling for other drug exposures, environment and blood lead levels (BLL). Results Adjusted percentages of drug use (PCE vs. NCE) were: tobacco 35% vs. 26% (p < .04), marijuana 33% vs. 23% (p < .04), alcohol 40% vs. 35% (p < .01), and any drugs 59% vs. 50% (p < .005). PCE adolescents were twice as likely to use tobacco (OR = 2.02, 95% CI = 1.05–3.90, p < .04), 2.2 times more likely to use alcohol (OR = 2.16, 95% CI = 1.21–3.87, p < .01) and 1.8 times more likely to use marijuana (OR = 1.81, 95% CI = 1.02–3.22, p < .04) than NCE adolescents. A race-by-cocaine-exposure interaction (p < .01) indicated PCE non-African American adolescents had greater probability of tobacco use (65%) than NCE non-African American youth (21%). PCE was associated with any drug use (OR = 2.16, CI = 1.26–3.69, p < .005), while higher BLL predicted alcohol use (p < .001). Violence exposure was a predictor of tobacco (p < .002), marijuana (p < .0007) and any drug (p < .04). Conclusions PCE and exposure to violence increased the likelihood of tobacco, marijuana or any drug use by age 15, while PCE and higher early BLL predicted alcohol use. Prevention efforts should target high risk groups prior to substance use initiation.

The effect of prenatal cocaine exposure (PCE) on externalizing behavior and substance use related problems at 15 years of age was examined. Participants consisted of 358 adolescents (183 PCE, 175 non-cocaine exposed (NCE)), primarily African-American and of low socioeconomic status, prospectively enrolled in a longitudinal study from birth. Regression analyses indicated that the amount of PCE was associated with higher externalizing behavioral problems (β=.15, p=.02). Adolescents with PCE were also 2.8 times (95% CI=1.38–5.56) more likely to have substance use related problems than their NCE counterparts. No differences between PCE adolescents in non-kinship adoptive or foster care (n=44) and PCE adolescents in maternal/relative care (n=139) were found in externalizing behavior or in the likelihood of substance use related problems. Findings demonstrate teratologic effects of PCE persisting into adolescence. PCE is a reliable marker for the potential development of problem behaviors in adolescence, including substance use related problems.

Differences in caregiver reported executive function in 12-year-old children who were prenatally exposed to cocaine (PCE) compared to children who were not prenatally exposed to cocaine (NCE) were assessed. One hundred and sixty-nine PCE and 169 NCE, primarily African-American, low socioeconomic status children participated in a prospective longitudinal study. The Behavior Rating Inventory of Executive Function (BRIEF) Parent Form was administered. Two broadband BRIEF scores (Behavioral Regulation Index (BRI) and Metacognition Index (MI)) and a summary Global Executive Composite (GEC) were computed. Multiple and logistic regression analyses were used to assess the effects of amount of PCE on executive function, controlling for covariates including caregiver (rater) psychological distress, child’s gender and other prenatal drug exposure variables. After adjustment for covariates, amount of PCE was associated with the GEC and two MI subscales, Plan/Organize and Monitor, with heavier exposure associated with more problems of executive function. An amount of PCE by gender interaction revealed amount of PCE effects in other remaining subscales of the MI (Initiate, Working Memory, and Organization of Materials) only among girls. Head circumference did not mediate the effects of cocaine on outcomes. Higher current caregiver psychological distress levels were independently associated with poorer ratings on the executive function scales. Assessment and targeted interventions to improve metacognitive processes are recommended for girls who were prenatally exposed to cocaine.

Background Prenatal cocaine exposure (PCE) is associated with increased risk for externalizing behavior problems; childhood externalizing behavior problems are linked with subsequent early sexual behavior. The present study examined the effects of PCE on early sexual initiation (sexual intercourse prior to age 15) and whether externalizing behavior in preadolescence mediated the relationship. Methods Three hundred fifty-four (180 PCE and 174 non-cocaine exposed; 192 girls, 142 boys), primarily African-American, low socioeconomic status, 15-year old adolescents participated in a prospective longitudinal study. Adolescents’ sexual behavior was assessed at 15 years using the Youth Risk Behavior Surveillance System. Externalizing behavior was assessed at 12 years using the Youth Self-Report. Results Logistic regression models indicated that adolescents with PCE (n=69, 38%) were 2.2 times more likely (95% CI= 1.2 – 4.1, p < .01) to engage in early sexual intercourse than non-exposed peers (n=49, 28%) controlling for covariates. This relationship was fully mediated by self-reported externalizing behavior in girls but not in boys, suggesting childhood externalizing behavior as a gender moderated mediator. Blood lead level during preschool years was also related to a greater likelihood of early sexual intercourse (OR=2.6, 95% CI=1.4 – 4.7, p < .002). Greater parental monitoring decreased the likelihood of early sexual intercourse, while violence exposure increased the risk. Conclusions PCE is related to early sexual intercourse, and externalizing behavior problems mediate PCE effects in female adolescents. Interventions targeting externalizing behavior may reduce early sexual initiation and thereby reduce HIV risk behaviors and early, unplanned pregnancy in girls with PCE.

Purpose In this study, the authors aimed to examine the long-term effects of prenatal cocaine exposure (PCE) on the language development of 12-year-old children using a prospective design, controlling for confounding prenatal drug exposure and environmental factors. Method Children who were exposed to cocaine in utero (PCE; n = 183) and children who were not exposed to cocaine (i.e., no cocaine exposure [NCE]; n = 181) were followed prospectively from birth to 12 years of age and were compared on language subtests of the Test of Language Development—Intermediate, Third Edition (Hammill & Newcomer, 1997b), and phonological processing as measured by the Comprehensive Test of Phonological Processing (Wagner & Torgesen, 1999). The authors evaluated the relationship of PCE to language development through a multivariate analysis of covariance and regression analyses while controlling for confounders. Results Results show that PCE has small effects on specific aspects of language, including syntax and phonological processing. The caregiver variables of lower maternal vocabulary, more psychological symptoms, and a poorer home environment also had consistent effects on language and phonological processing scores. Conclusions These findings suggest that PCE continues to have small, subtle effects on specific aspects of language at age 12 years. Phonological processing skills were significantly related to the reading outcomes of letter–word identification, reading fluency, and reading comprehension, indicating that PCE also has small but lasting effects on the language skills that are related to later literacy skills.

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Prenatal cocaine exposure (PCE) may increase adolescent substance use through alterations of neurotransmitter systems affecting fetal brain development. The relationship between PCE and substance use at 15 and 17 years was examined. Subjects (365: 186 PCE; 179 non-cocaine exposed (NCE)) supplied biologic and self-report data using the Youth Risk Behavior Surveillance System (YRBSS) and Computerized Diagnostic Interview Schedule for Children (C-DISC 4) at ages 15 and 17. The relationship between PCE and substance use was assessed using General Estimating Equation (GEE) analyses controlling for confounding factors including violence exposure and preschool lead level. Teens with PCE vs. NCE teens were 2 times more likely to use tobacco (OR = 2.1; 95% CI 1.21–3.63; p < .001) and marijuana (OR = 1.85; CI 1.18–2.91; p < .001) and have a substance use disorder at age 17 (OR = 2.51; CI 1.00–6.28; p < .05). Evaluation of PCE status by gender revealed an association between PCE and marijuana use that was more pronounced for boys than girls at 17 years. Violence exposure was also a significant predictor of alcohol (p < .001), tobacco (p < .05), and marijuana (p < .0006) use and substance abuse/dependence (p < .01). Externalizing behavior at age 12 fully mediated the effects of PCE on substance use disorder at age 17 and partially mediated effects of PCE on tobacco use, but did not mediate effects on marijuana use. The percentage of substance use reported increased between 15 and 17 years, with no differences between the PCE and NCE groups. Data suggest specialized drug use prevention measures for children with PCE may benefit this high risk group.