Adelaide Lang

Effects of prenatal cocaine/polydrug exposure on substance use by age 15

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.

Externalizing behavior and substance use related problems at 15 years in prenatally cocaine exposed adolescents

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/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.

Pathways to adolescent sexual risk behaviors: Effects of prenatal cocaine exposure

BACKGROUND To assess the impact of prenatal cocaine exposure (PCE) on adolescent sexual risk behaviors. Externalizing behavior, teen substance use, and early sexual intercourse were examined as pathways mediating the effects of PCE on sexual risk behaviors. METHODS Adolescents (N=364; 185 PCE, 179 non-cocaine exposure (NCE); 205 girls, 159 boys), primarily African-American and of low socioeconomic status, were prospectively enrolled in a longitudinal study at birth. Risky sexual behaviors were assessed at ages 15 and 17. Externalizing behavior at 12 years was assessed with the Youth Self-Report. Substance use, via self-report and biologic assays, and early (before age 15) sexual intercourse were assessed at age 15. Path analyses with the weighted least squares estimator with mean and variance adjustments were performed. RESULTS The final structural equation model-based path model, χ(2)=31.97 (df=27), p=.23, CFI=.99, TLI=.99, RMSEA=.021, WRMR=.695, indicated a direct effect of PCE on sexual risk behavior (β=.16, p=.02). Although PCE was related to greater externalizing behavior (β=.14, p=.009), which in turn, predicted early sexual intercourse (β=.16, p=.03), leading to sexual risk behavior (β=.44, p<.001), bootstrapping indicated a non-significant indirect effect (β=.01, p>.10). Substance use was correlated with early sexual intercourse (r=.60, p<.001) and predicted sexual risk behavior by age 17 (β=.31, p=.01). CONCLUSIONS Prenatal cocaine exposure was related to more engagement in sexual risk behaviors, suggesting the importance of reducing substance use among pregnant women as a means of prevention of offspring substance use and sexual risk behavior.

Executive function in children with prenatal cocaine exposure (12–15 years)

PURPOSE Prenatal exposure to cocaine (PCE) may alter areas of the brain dense with monoamine receptors such as the prefrontal cortex and negatively affect cognitive processes implicated in executive function (EF). This study investigated the effects of PCE on EF at 12 and 15years. METHODS EF was examined in 189 PCE and 183 non-cocaine exposed (NCE) children who were primarily African American and of low socioeconomic status. Caregivers rated their child on the Behavior Rating Inventory of Executive Function (BRIEF) at ages 12 and 15. The BRIEF includes two summary scales and eight subscales: Behavioral Regulation Index (BRI) (Inhibit, Shift, and Emotion) and Metacognition Index (MI) (Monitor, Working Memory, Plan/Organize, Organization of Materials and Task Completion). Two additional measures were included at age 15 (BRIEF Self-Report and the CANTAB Stockings of Cambridge (SOC)). RESULTS Girls with PCE were perceived by caregivers to have more behavioral regulation problems at age 12 (p<0.005) and more metacognitive problems at age 12 (p<0.003) than NCE females, but there was no association for males. PCE girls improved in behavioral regulation (p<0.05) and metacognition (p<0.04) from 12 to 15years compared to NCE girls based on caregiver report. By self-report PCE was associated with problems of inhibition (p<0.006). Girls with PCE performed more poorly on number of moves to complete the SOC, requiring planning and problem solving, than NCE girls. CONCLUSION Prenatally cocaine exposed girls were perceived by caregivers as having problems of behavioral regulation, and by self-report, inhibitory control problems. Girls with PCE also performed more poorly on a task of planning and problem solving at age 15 which corresponded to caregiver report at age 12. Early assessment and remediation of these weaknesses in girls may improve school performance and behavior associated with poor EF.

The association of prenatal cocaine exposure, externalizing behavior and adolescent substance use

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.

Blood lead levels and longitudinal language outcomes in children from 4 to 12 years

OBJECTIVES In this study, the authors aimed to examine the association of a range of blood lead levels on language skills assessed at 4, 6, 10 and 12 years of age using a prospective longitudinal design controlling for potential confounding variables including maternal vocabulary, caregivers psychological distress and symptomatology, childs race and prenatal drug exposure. METHODS The participants (N = 278) were a subsample of a large longitudinal study that examined the association of prenatal drug exposure on children who were followed prospectively from birth and assessed for receptive and expressive language skills at 4, 6, 10 and 12 years of age. Blood lead levels were determined at 4-years of age by atomic absorption spectrometry. A mixed model approach with restricted maximum likelihood procedures was used to assess the association of lead on language outcomes. RESULTS Longitudinal mixed model analyses suggested a negative effect of lead exposure on both receptive and expressive language, with the adverse outcomes of lead exposure appearing to become more prominent at 10 and 12 years. Higher caregiver vocabulary was positively associated with childs language scores whereas caregiver psychological distress appeared to negatively affect language scores. Prenatal drug exposure was not related to the effects of lead on language skills. CONCLUSIONS These findings suggest that elevated blood lead levels occurring early in life may be associated with poorer language skills at older ages. A language rich environment may minimize the negative influence of early lead exposure on language skills, with psychological distress seemingly exacerbating the negative outcome.

Prenatal and concurrent cocaine, alcohol, marijuana, and tobacco effects on adolescent cognition and attention

BACKGROUND Prenatal cocaine/polydrug exposure (PCE) may increase vulnerability to substance use disorders due to associated cognitive deficits. We examined whether neurocognitive deficits in executive functions and attention observed in PCE children persisted to adolescence when compared to non-cocaine/polydrug (NCE) children, and whether adolescent substance use (tobacco, alcohol, marijuana) was also associated with neurocognitive deficits. METHODS 354 (180 PCE, 174 NCE) adolescents in a longitudinal study from birth were administered the Wechsler Intelligence Scales for Children - IV (WISC-IV), and the Integrated Visual and Auditory Continuous Performance Test (IVA/CPT) at age 15.5. Assessments of prenatal exposure to cocaine, alcohol, marijuana, and tobacco and measures of use at age 15.5 were taken. Confounding factors measured included lead, the caregiving environment, and violence exposure. Relationships between drug use and prenatal exposures on outcomes were assessed through multiple regression. RESULTS Adolescents with PCE had deficits in Perceptual Reasoning IQ and visual attention. Prenatal alcohol exposure predicted verbal and working memory IQ and visual and auditory attention deficits. Adolescent tobacco, alcohol, and marijuana use predicted attention in addition to PCE, lead and the caregiving environment. CONCLUSION Prenatal cocaine and alcohol exposure and adolescent use of substances are associated with neurocognitive deficits known to increase vulnerability to SUDs.

In Utero Exposure to Nicotine, Cocaine, and Amphetamines

Nicotine, cocaine, and amphetamines (methamphetamine, amphetamine, and 3,4, methylenedioxymethamphetamine, “MDMA/Ecstasy”) are all psychomotor stimulants, a class of drugs in which significant sensorimotor activation occurs in response to drug administration. Effects on child developmental outcome are important to consider given their widespread use during pregnancy, but gaps in the research literature are striking, with only a few studies on amphetamines. Prenatal stimulant exposure exerts physiologic stress on the pregnancy and increases chances of birth complications and intrauterine growth restriction. Brain imaging data support structural and functional differences attributable to prenatal stimulant exposure. Prenatal nicotine exposure has a small negative effect on overall IQ in a dose–response relationship while prenatal cocaine exposure has no overall effect on IQ but specific effects on visual-perceptual reasoning, executive function, language, and behavior. Prenatal methamphetamine exposure is related to motor, behavioral, and specific cognitive deficits in the preschool years. Similar deficits in motor development were found in a well-controlled study of MDMA exposed children to 2 years. Prenatal nicotine and cocaine exposure are associated with decreased academic performance, attention and executive function problems, language deficits, increased externalizing behaviors, and teen substance use. Data on prenatal amphetamine exposure is sparse but suggest problems in executive skills and internalizing behaviors. In sum, prenatal stimulant exposure interferes with development, educational attainment, and risk for teen substance abuse. Early developmental assessment and intervention for identified weaknesses are recommended.