Objective. The objectives of this study were to estimate the effect of prenatal cocaine exposure on fetal growth and gestational age after controlling for exposure to alcohol, tobacco, and marijuana and other covariates; to evaluate whether prenatal cocaine exposure has a disproportionate adverse effect on head circumference compared with overall somatic growth; and to assess whether the effect of prenatal cocaine exposure on fetal growth is mediated by cocaine’s suspected effect on gestational age.

Methods. The study population includes 476 neonates participating in the Miami Prenatal Cocaine Study, a longitudinal follow-up of in utero cocaine exposure. The sample, restricted to full-term neonates born to African-American inner-city mothers, included 253 infants exposed prenatally to cocaine (with or without alcohol, tobacco, or marijuana exposure) and 223 non–cocaine-exposed infants, of whom 147 were drug-free and 76 were exposed to varying combinations of alcohol, tobacco, or marijuana.

Results. Evidence based on structural equations and multiple regression models supports a hypothesis of cocaine-associated fetal growth deficits (0.63 standard deviation) and an independent mild effect on gestational age (0.33 standard deviation). There was no evidence of a disproportionate adverse effect on birth head circumference once the impact on overall growth was estimated. There was evidence that some but not all of the cocaine effect on fetal growth was direct and some was indirect, acting via an intermediate influence of cocaine on gestational age.

Conclusions. Cocaine-associated growth deficits, symmetrical and partially mediated by gestational age, were observed in this sample of inner-city African-American full-term infants prospectively enrolled at birth. Long-term implications will be the subject of future reports from this longitudinal investigation.

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