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Growth, development, and behavior in early childhood following prenatal cocaine exposure: a systematic review
D A Frank1, M Augustyn, W G Knight
1Boston University School of Medicine, Boston, MA 02118-2393, USA. dafrank@bu.edu
Insights
Prenatal cocaine exposure in children up to age 6 shows no convincing evidence of unique developmental harm. Other factors like tobacco and environment play significant roles.
Area of Science:
- Developmental Psychology
- Neuroscience
- Public Health
Background:
- Public perception and policy often view prenatal cocaine exposure as uniquely harmful.
- Recent studies challenge the notion of catastrophic effects of in utero cocaine exposure.
Purpose of the Study:
- To critically review outcomes in early childhood following prenatal cocaine exposure.
- To examine effects across physical growth, cognition, language, motor skills, and behavior/attention.
Main Methods:
- Systematic literature search of MEDLINE and Psychological Abstracts (1984-2000).
- Inclusion of peer-reviewed English-language studies with comparison groups and prospective, masked assessments.
- Exclusion of studies with significant co-exposures to opiates, amphetamines, phencyclidine, or HIV.
Main Results:
- No consistent negative associations found between prenatal cocaine exposure and physical growth, cognitive scores, or language skills.
- Motor skill deficits observed up to 7 months, potentially linked to tobacco exposure.
- No independent cocaine effects on standardized behavioral reports; preliminary findings suggest impacts on attention and emotional expressivity.
Conclusions:
- No convincing evidence indicates prenatal cocaine exposure causes unique developmental toxicity in children up to age 6.
- Observed effects are often correlated with other risk factors like tobacco, marijuana, alcohol exposure, and environmental quality.
- Further research is needed to replicate preliminary neurological findings.
Context:
Despite recent studies that failed to show catastrophic effects of prenatal cocaine exposure, popular attitudes and public policies still reflect the belief that cocaine is a uniquely dangerous teratogen.
Objective:
To critically review outcomes in early childhood after prenatal cocaine exposure in 5 domains: physical growth; cognition; language skills; motor skills; and behavior, attention, affect, and neurophysiology.
Data Sources:
Search of MEDLINE and Psychological Abstracts from 1984 to October 2000.
Study Selection:
Studies selected for detailed review (1) were published in a peer-reviewed English-language journal; (2) included a comparison group; (3) recruited samples prospectively in the perinatal period; (4) used masked assessment; and (5) did not include a substantial proportion of subjects exposed in utero to opiates, amphetamines, phencyclidine, or maternal human immunodeficiency virus infection.
Data Extraction:
Thirty-six of 74 articles met criteria and were reviewed by 3 authors. Disagreements were resolved by consensus.
Data Synthesis:
After controlling for confounders, there was no consistent negative association between prenatal cocaine exposure and physical growth, developmental test scores, or receptive or expressive language. Less optimal motor scores have been found up to age 7 months but not thereafter, and may reflect heavy tobacco exposure. No independent cocaine effects have been shown on standardized parent and teacher reports of child behavior scored by accepted criteria. Experimental paradigms and novel statistical manipulations of standard instruments suggest an association between prenatal cocaine exposure and decreased attentiveness and emotional expressivity, as well as differences on neurophysiologic and attentional/affective findings.
Conclusions:
Among children aged 6 years or younger, there is no convincing evidence that prenatal cocaine exposure is associated with developmental toxic effects that are different in severity, scope, or kind from the sequelae of multiple other risk factors. Many findings once thought to be specific effects of in utero cocaine exposure are correlated with other factors, including prenatal exposure to tobacco, marijuana, or alcohol, and the quality of the child's environment. Further replication is required of preliminary neurologic findings.
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