Fetal cocaine exposure has proven to be an area of medicine that has generated more heat than light. Although many reports associate cocaine with a variety of isolated structural anomalies, there is no detectable syndromic clustering, raising doubts about a real causal association or a specific teratogenic action. Potential confounding variables, including the abuse of other drugs, pregnancy deprivations, and socially patterned maternal behaviors, have limited the reliability of observational studies, making it difficult to demonstrate effects solely attributable to cocaine. The clinical expression of in utero cocaine exposure is contextual, critically dependent on the biology/environment interplay. The present work summarizes the fetal structural anomalies that have been associated in the literature with cocaine use during pregnancy, and reviews the putative mechanisms of fetal impairment secondary to cocaine exposure. The final discussion of methodologic issues in cocaine epidemiology highlights the need for innovative approaches to assure that the myths conjured up about "crack babies" are replaced with reliable, high-quality scientific data.