Perinatal Factors Associated with Cardiovascular Disease Risk among Preschool-Age Children in the United States: An Analysis of 1999–2008 NHANES Data

We examined the relationships between selected perinatal and early infancy factors (maternal smoking during pregnancy, infant low birthweight, breastfeeding, and early introduction of solid foods [<6 months of age] and increased BMI [≥85th, ≥95th percentiles for age, sex]), waist circumference (WC), C-reactive protein (CRP), triglycerides, total cholesterol, low-density lipoprotein (LDL) cholesterol, non-high-density lipoprotein (HDL) cholesterol, and decreased HDL cholesterol during early childhood. The population-based sample included 3,644 3-to-6-year-old Non-Hispanic White (NHW), Hispanic, and Non-Hispanic Black (NHB) children who participated in the 1999–2008 National Health and Nutrition Examination Surveys. Analysis showed that breastfeeding was significantly protective against early childhood obesity (OR 0.43, 95% CI, 0.27–0.69) and the highest quintile for WC (OR 0.58, 95% CI, 0.37–0.32) among NHW, and against the highest quintile of non-HDL cholesterol among NHB (OR 0.56, 95% CI, 0.32–0.98). Additionally, NHW children were significantly more likely to be obese (OR 2.22, 95% CI 1.30–3.78) and have higher CRP levels (OR 1.63, 95% CI, 1.05–2.51) if their mothers smoked during pregnancy. These results support the observation that breastfeeding may be protective against early childhood obesity while maternal smoking during pregnancy is a risk factor for obesity and increased CRP levels among NHW young children

Assessing Latent Effects of Prenatal Cocaine Exposure on Growth and Risk of Cardiometabolic Disease in Late Adolescence: Design and Methods

Prenatal cocaine exposure has been linked to neurocognitive and developmental outcomes throughout childhood. The cardiovascular toxicity of cocaine is also markedly increased in pregnancy, but it is unknown whether this toxicity affects anthropometric growth and the development of cardiometabolic disease risk factors in the offspring across the lifespan. During the early 1990s, the Miami Prenatal Cocaine Study enrolled a cohort of 476 African American children (253 cocaine-exposed, 223 non-cocaine-exposed) and their biological mothers at delivery in a prospective, longitudinal study. The MPCS has collected 12 prior waves of multidomain data on over 400 infants and their mothers/alternate caregivers through mid-adolescence and is now embarking on an additional wave of data collection at ages 18-19 years. We describe here the analytical methods for examining the relationship between prenatal cocaine exposure, anthropometric growth, and cardiometabolic disease risk factors in late adolescence in this minority, urban cohort. Findings from this investigation should inform both the fields of substance use and cardiovascular research about subsequent risks of cocaine ingestion during pregnancy in offspring

Cocaine-related maternal death

Hemodynamic overload, cardiac ischemia, and arrhythmia are postulated to originate from "sex-cocaine" syndrome resulting in maternal and fetal death. High concentrations of cocaine and metabolites in maternal blood, urine, and nasal secretions confirmed recent ingestion. Changes in the maternal life-style may have contributed to the poor pregnancy outcome

Prenatal cocaine exposure: An examination of childhood externalizing and internalizing behavior problems at age 7 years

Aim – This study examines the relationship between prenatal cocaine exposure and parent-reported child behavior problems at age 7 years. Methods – Data are from 407 African-American children (210 cocaine-exposed, 197 non-cocaine-exposed) enrolled prospectively at birth in a longitudinal study on the neurodevelopmental consequences of in utero exposure to cocaine. Prenatal cocaine exposure was assessed at delivery through maternal self-report and bioassays (maternal and infant urine and infant meconium). The Achenbach Child Behavior Checklist (CBCL), a measure of childhood externalizing and internalizing behavior problems, was completed by the child's current primary caregiver during an assessment visit scheduled when the child was seven years old. Results – Structural equation and GLM/GEE models disclosed no association linking prenatal cocaine exposure status or level of cocaine exposure to child behavior (CBCL Externalizing and Internalizing scores or the eight CBCL sub-scale scores). Conclusions – This evidence, based on standardized ratings by the current primary caregiver, fails to support hypothesized cocaine-associated behavioral problems in school-aged children with in utero cocaine exposure. A next step in this line of research is to secure standardized ratings from other informants (e.g., teachers, youth self-report). Declaration of Interest: This research was conducted in the context of an ongoing longitudinal study funded by the National Institutes of Health National Institute on Drug Abuse (R01 DA 06556). Support was also provided by a NIDA career development award (K01 DA 16720), a NIDA research training award (T32 DA 07292), the General Clinical Research Center (MOI RR 16587), and the Health Foundation of South Florida

Behavioral outcome of preschoolers exposed prenatally to cocaine: Role of maternal behavioral health

OBJECTIVE: To examine the impact of prenatal cocaine exposure and maternal behavioral health (recent drug use and psychological functioning) on child behavior at age 5 years. METHOD: In this longitudinal investigation, maternal report of child behavior was assessed using the Achenbach Child Behavior Checklist (CBCL) in 140 cocaine-exposed and 181 noncocaine-exposed (61 alcohol, tobacco, and/or marijuana-exposed, and 120 nondrug-exposed) low-income, African American children. Structural equation modeling was used to estimate suspected causal relationships between indicators of maternal behavioral health at 5-year follow-up, according to self-report on a modified Addiction Severity Index (ASI) and CBCL scores. RESULTS: Prenatal cocaine exposure was not related to child behavior at age 5. Recent maternal drug use and psychological functioning had relationships with CBCL Internalizing and Externalizing scores. However, when considered within a combined model, only maternal psychological functioning remained significant. CONCLUSIONS: Findings highlight the importance of maternal functioning in the behavioral outcome of children exposed prenatally to cocaine

Rapid cocaine screening of urine in a newborn nursery

A rapid cocaine screening test, the Abuscreen OnTrak assay, was compared with the EMIT (enzyme-multiplied immunoassay technique) screening test to determine relative accuracy in 450 newborn infants sequentially tested for urinary cocaine during a 6-week period at a large urban hospital. The Abuscreen Ontrak screen had a sensitivity of 96% and a specificity of 100%

Estimated effects of in utero cocaine exposure on language development through early adolescence

The potential longitudinal effects of prenatal cocaine exposure (PCE) on language functioning were estimated from early childhood through early adolescence in a large, well-retained urban sample of 451 full-term children (242 cocaine-exposed, 209 non-cocaine-exposed) participating in the Miami Prenatal Cocaine Study (MPCS). The sample was enrolled prospectively at birth, with documentation of prenatal drug exposure status through maternal interview, and toxicology assays of maternal and infant urine, and infant meconium. Age-appropriate versions of the Clinical Evaluation of Language Fundamentals (CELF) were used to measure total, expressive, and receptive language at ages 3, 5, and 12 years. Longitudinal latent growth curve (LLGC) modeling of the data revealed an association between PCE (measured dichotomously as yes/no) and lower functioning in expressive and total language scores, after considering other sources of variation including child's age at testing, sex, prenatal exposure to alcohol, marijuana, and tobacco, and additional medical and social-demographic covariates. Analyses of level of PCE showed a gradient, i.e. dose-dependent, relationship between PCE level and expressive, receptive, and total language scores in the models controlling for age, child's sex, and other prenatal drug exposures. With additional covariate control these findings were most stable for the total language score. The evidence supports an inference about an enduring stable cocaine-specific effect on children's language abilities, with no effect on language growth over time in the longitudinal trajectory of language development

Longitudinal investigation of task persistence and sustained attention in children with prenatal cocaine exposure

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