One Year Language and Developmental Outcomes of Cocaine-Exposed Infants† 1336

Abstract

Prenatal cocaine exposure may have long-term negative effects on child developmental outcomes, but prior studies have been contradictory. We followed 408 infants (212 cocaine-exposed (CE) and 196 non-exposed (NCE)) to 6.5 and 12 months of age, administering the Bayley Mental (MDI) and Motor (PDI) Scales and, in a subset, the Preschool Language Scale (PLS). Maternal self-report interviews and infant meconium analyses quantified severity of cocaine exposure. Based on this drug information the cocaine-exposed infants were subdivided into heavy and light exposed groups. Bayley MDI's were lower for CE infants at 6 months (96 ± 8 vs. 98 ± 8, t (335) =-.2.3, p <.02), with GA controlled (p <.05), and at 12 months (94 ± 11 vs. 100 ± 12, t (280) = -4.3,p <.01). The CE infants' MDI's decreased over time, while NCE infants' did not. Mean PDI's did not differ. Twelve month MDI scores were also related to the amount of cocaine metabolites in meconium, i.e., cocaine(r = -.10, p <.09), benzoylecgonine (r =-.12, p <.05), and MOH benzoylecgonine (r = -.12,p <.05), and to the severity of cocaine use reported by the mother (r = -.17, p <.002). Severity of cocaine exposure predicted lower 12 month MDI after consideration of confounders, but was mediated by neonatal head circumference. On the PLS, heavy CE infants had a higher rate of mildly (39% vs. 24% and 23%, χ2 = 5.2,p <.07), and moderately delayed total language scores (17% vs. 6% and 6%, χ2 = 5.8, p <.05) than light CE or NCE infants, reflecting higher rates of mildly (43% vs. 20% and 24%,χ2 = 8.2, p <.02) and moderately delayed(11% vs. 2% and 4%, χ2 = 5.8, p <.06) expressive language skills. After controlling for confounders, there were trends for severity of alcohol and cocaine exposure to predict mild deficits and for cocaine exposure to predict moderate deficits (p <.05). These data indicate that fetal cocaine exposure predicts poorer cognitive and language development at 1 year with a dose-response relationship of biologic assays to cognitive outcomes.