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Severity of Prenatal Cocaine Exposure and Child Language Functioning Through Age 7 Years: a Longitudinal Latent Growth Curve Analysis

Emmalee S. Bandstra, M.D., April L. Vogel, Ph.D., Connie E. Morrow, Ph.D., Lihua Xue, M.S. M.A., James C. Anthony, Ph.D.

First Published: 03 January 2004     DIO: 10.1081/JA-120027765

Department of Pediatrics, University of Miami School of Medicine, Miami, Florida 33101, USA. 


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The current study estimates the longitudinal effects of severity of prenatal cocaine exposure on language functioning in an urban sample of full-term African-American children (200 cocaine-exposed, 176 noncocaine-exposed) through age 7 years. The Miami Prenatal Cocaine Study 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. Language functioning was measured at ages 3 and 5 years using the Clinical Evaluation of Language Fundamentals–Preschool (CELF-P) and at age 7 years using the Core Language Domain of the NEPSY: A Developmental Neuropsychological Assessment. Longitudinal latent growth curve analyses were used to examine two components of language functioning, a more stable aptitude for language performance and a time-varying trajectory of language development, across the three time points and their relationship to varying levels of prenatal cocaine exposure. Severity of prenatal cocaine exposure was characterized using a latent construct combining maternal self-report of cocaine use during pregnancy by trimesters and maternal and infant bioassays, allowing all available information to be taken into account. The association between severity of exposure and language functioning was examined within a model including factors for fetal growth, gestational age, and IQ as intercorrelated response variables and child’s age, gender, and prenatal alcohol, tobacco, and marijuana exposure as covariates. Results indicated that greater severity of prenatal cocaine exposure was associated with greater deficits within the more stable aptitude for language performance (D = −0.071, 95% CI = −0.133, −0.009; p = 0.026). There was no relationship between severity of prenatal cocaine exposure and the time-varying trajectory of language development. The observed cocaine-associated deficit was independent of multiple alternative suspected sources of variation in language performance, including other potential responses to prenatal cocaine exposure, such as child’s intellectual functioning, and other birth and postnatal influences, including language stimulation in the home environment.


In the late 1980s and early 1990s, the United States experienced an “epidemic” of cocaine-exposed deliveries due to the burgeoning numbers of women of childbearing age who were using cocaine and crack cocaine. The phenomenon of “cocaine abuse” by pregnant women received widespread media attention due to observations of serious, life-endangering consequences for the mother and fetus. Known catastrophic cardiovascular and central nervous system effects of cocaine use in adults clearly raised concerns that maternal use of cocaine, especially crack cocaine, would cause long-term, irreparable damage to the developing infant and young child. However, numerous limitations in study design among the earliest published studies on the effects of in-utero cocaine exposure have been noted, and results have been inconsistent for most aspects of infant and child developmental outcomes. In an attempt to curtail inappropriate labeling of cocaine-exposed children, perinatal “drug abuse” researchers urged the application of scientifically rigorous prospective study designs with sufficient samples to answer the analytic questions.

Early language development is one of the major domains of investigative interest in perinatal “drug abuse” research since it may impair long-term social adaptation and academic success. Cocaine may affect language development through alterations in the developing monoaminergic neurotransmitter systems and through indirect pathways related to cocaine-associated maternal hypertension, decreased uterine blood flow, fetal vasoconstriction, and hypoxemia, and nutritional deficiencies.

Keywords: Prenatal cocaine exposure, Language performance

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