Level of prenatal cocaine exposure and scores on the Bayley Scales of Infant Development: modifying effects of caregiver, early intervention, and birth weight.

At the beginning of the cocaine epidemic, many predicted that children exposed to cocaine in utero would show lasting developmental impairments. However, peer-reviewed research does not find striking or consistent effects of prenatal cocaine exposure on developmental test scores in the first 2 years of life. Of the 11 studies using masked examiners to evaluate the impact of prenatal cocaine exposure on scores on the Bayley Scales of Infant Development (BSID),1,2 6 found no statistically significant effect,3– 8 including 1 study that classified infants according to mothers’ report of level of prenatal exposure.7 Among the 5 studies that did find adverse effects of prenatal cocaine exposure, effects differ by age of assessment and whether exposure to tobacco, alcohol, and marijuana, and other potential confounds were included in the analysis. In a sample of infants whose mothers entered drug treatment during pregnancy, the mean BSID Mental Developmental Index (MDI) and Psychomotor Developmental Index (PDI) scores of infants whose mothers used cocaine/alcohol/marijuana were lower at 6 months than infants whose mothers did not use these drugs, but identical to those of mothers who had used alcohol/marijuana without cocaine. These results suggest that there is no incremental detrimental impact of cocaine use on development quotients beyond that imposed by the concurrent use of alcohol/marijuana.9 No deleterious cocaine effects were detected in this sample on BSID scores at other assessment ages up to 24 months.9 Other investigators found a bivariate association of lower PDI scores at 3 months with prenatal cocaine exposure, but not after statistical control for potential confounds.10 In a sample confined to very low birth weight infants tested at ~ 16 months’ corrected age, a negative association with prenatal cocaine exposure was found with MDI and PDI, but in utero exposure to other psychoactive substances was not analytically controlled.11 A study that used the recently revised BSID II2 found no main effects of mothers’ reported level of prenatal cocaine exposure on MDI or PDI at 8 or 18 months.12 In posthoc comparisons, children whose mothers reported higher levels of prenatal cocaine use (2 or more days per week) were found to have significantly lower MDI scores at 18 months than those with no exposure.12 For infants who were unexposed or lightly exposed, higher environmental risk was also associated with a greater decline in MDI scores from 8 to 18 months.12 Singer et al13 found in a large sample a statistically significant decrement in BSID II MDI scores associated with prenatal cocaine exposure, with an increased risk of developmental delay among the exposed. This study contained a substantial number of very low birth weight infants who are excluded from other samples and did not measure whether subjects received developmental intervention. When adaptive behavior during the testing situation was measured by the Infant Behavior Record (IBR) of the BSID, 2 investigators found cocaine-exposed infants more listless than unexposed infants in bivariate analyses, but not after covariate control.3,11 Contextual factors may partially account for these discrepancies.14 Prenatal cocaine exposure may exert differing impacts on later developmental outcomes depending on the interaction of exposure with other biological and social factors. Discrepant findings are also susceptible to multiple possible methodologic explanations, including differences in study design, varying patterns of sample attrition, misclassification of exposed infants as unexposed because of inaccurate maternal report, and failure to address potential dose effects.15 If exposed infants are misclassified as unexposed, between-group differences may be missed. If lightly and heavily exposed infants are aggregated into a single category, cocaine effects that may occur only at higher or lower levels of prenatal exposure may be obscured.7 Testing meconium for drug metabolites presents a method of assessing prenatal cocaine exposure that enhances accurate identification of newborns exposed to cocaine prenatally, detecting more exposed infants than mothers’ report or peripartum urine assays from mothers or infants.16–19 Although not a precise reflection of the total grams of cocaine used by a mother during pregnancy or the gestational timing of use, the concentration of cocaine metabolites in meconium allows newborns to be rank ordered by their relative level of cocaine exposure. This rank order correlates with newborns’ birth weight, behavior, and risk of subependymal hemorrhage.20–23 The first goal of this analysis was to assess whether, after control of potential confounding variables, there is an independent association between the level of prenatal cocaine exposure (assessed by mothers’ self-report and/or assay of infants’ meconium) and infants’ scores on the BSID at 6, 12, and 24 months of age. The second goal was to determine which biological and social variables, individually and in interaction with each other, may moderate such an association if one is found.