Neurotoxicology and Teratology, Vol. 15, p. 289, 1993 0892-0362/93 $6.00 + .00 Printed in the U.S.A. All rights reserved. Copyright © 1993 Pergamon Press Ltd.

COMMENTARY

Does Cocaine Cause Birth Defects?

M I C H A E L W. C H U R C H

Department of Obstetrics and Gynecology, Fetal Alcohol Research Center, Wayne State University School of Medicine, Detroit, MI 48201

I AGREE with Dr. Don Hutchings' view that the literature on the effects of prenatal cocaine exposure in humans is rather mixed. As a possible explanation, he points out that terato- genic effects might be produced only in infants exposed to very high doses. He also mentions maternal polydrug abuse, poor maternal health, genetic or physiological susceptibility, as well as poor pre- and postnatal care as possible confound- ing variables that obfuscate our conclusions about cocaine's teratogenic and neurobehavioral effects.

It is also important to consider the differential influence of critical periods of exposure, maternal age, the target organs, and the long-term outcome. In terms of critical periods, co- caine exposure during the first trimester may cause one effect (e.g., limb reductions) while exposure during the third trimes- ter may cause another effect (e.g., cerebral infarcts). In terms of maternal age, an older women may metabolize cocaine more slowly than a younger woman, resulting in different levels of toxicity to the fetuses. In terms of target organs, it appears that the genitourinary tract is vulnerable to prenatal cocaine exposure. But it is possible that we have not looked carefully enough at other possible targets. For example, the animal literature suggests that the eye may be an important

target of cocaine's teratogenic effects. With regard to the long- term effects of prenatal cocaine exposure, we know very little. This is because the current generation of cocaine-exposed chil- dren is still very young. Yet a body of literature on fetal insult suggests that affected children often express different morbid- ities at different ages. For example, the poor reflexes seen in infants with Fetal Alcohol Syndrome usually disappear only to be replaced in older children by problems in cognition, social behavior, speech, and language. Because we know so little about these variables, it is still premature to draw f'mal conclusions about cocaine's teratogenic and neurobehavioral effects.

Animal studies have helped to provide some answers re- garding cocaine's effects by controlling for many of the con- founding variables found in the human literature. The animal studies, like the human literature, has produced evidence of growth retardation, placental abrnption, cerebral infarctions, increased pre- and postnatal mortality, limb/digit reductions and eye anomal ies- to name a few findings. But like the hu- man literature, the teratogenlc risk seems low in animal mod- els and seems to require high doses and individual suscepti- bility.

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