The objectives of this study were 1) to assess whether there is an independent association between the level of prenatal cocaine exposure and infants’ developmental test scores after control of potential confounding variables; and 2) if such an association exists, to determine which biological and social variables, individually and in interaction with each other, may modify it.
In a prospective, longitudinal study of 203 urban term infants, 3 cocaine exposure groups were defined by maternal report and infant meconium assay: unexposed, heavier cocaine exposure (> 75th percentile self-reported days of use or meconium benzoylecognine concentration), or lighter cocaine exposure (all others). Examiners, masked to exposure history, tested infants at 6, 12, and 24 months of age with the Bayley Scales of Infant Development.
The final mixed linear regression model included as fixed covariates level of prenatal exposure to cocaine, alcohol, and cigarettes; prenatal marijuana exposure; gestational age and birth weight z score for gestational age; and gender. Age at test, caregiver at time of each test (biological mother, kinship caregiver, unrelated foster caregiver), and any previous child-focused early intervention were included as time-dependent covariates. There were no significant adverse main effects of level of cocaine exposure on Mental Development Index (MDI), Psychomotor Development Index (PDI), or Infant Behavior Record. Child-focused early intervention interacted with level of cocaine exposure such that heavily exposed children who received such intervention showed higher adjusted mean MDI scores than all other groups. Although the sample was born at or near term, there was also a significant interaction of cocaine exposure and gestational age on MDI scores, with those in the heavier exposure group born at slightly lower gestational age having higher mean MDI scores compared with other children born at that gestational age.
There was also a significant interaction on MDI between child’s age and caregiver. At 6 months, the adjusted MDI of children living with a kinship caregiver was 15.5 points lower than that of children living with their biological mother, but this effect was diminished and was no longer significant at 24 months (difference in means: 4.3 points). The adjusted mean MDI of children in unrelated foster care at 6 months was 8.2 points lower than children of biological mothers, whereas it was 7.3 points higher at 24 months.
Early intervention attenuated the age-related decline in PDI scores for all groups. Birth weight < 10th percentile was associated with lower PDI scores for children with heavier cocaine exposure and with lower MDI scores for all groups.
Heavier prenatal cocaine exposure is not an independent risk factor for depressed scores on the Bayley Scales of Infant Development up to 24 months of age when term infants are compared with lighter exposed or unexposed infants of the same demographic background. Cocaine-exposed infants with birth weight below the 10th percentile for gestational age and gender and those placed with kinship caregivers are at increased risk for less optimal developmental outcomes. Pediatric clinicians should refer cocaine-exposed children to the child-focused developmental interventions available for all children at developmental risk.