Fetal alcohol and drug effects

Alcohol and drug use by pregnant women are harmful to the developing embryo and fetus. Teasing apart the specific contributions of each substance to adverse child outcome, however, proves difficult in practice. The risks to the neonate include intra-uterine growth retardation, birth defects, altered neurobehavior, and withdrawal symptoms. Subsequent behavior, development, and neurologic function may also be impaired.

Maternal cigarette smoking carries the greatest risk of impaired fetal growth of any of the substances discussed herein and has been linked to subsequent externalizing behaviors. Alcohol is a well-established teratogen. Heavy exposure to alcohol in a subset of infants is associated with fetal alcohol syndrome (FAS). Mental retardation is one of the main sequelae of alcohol exposure in utero. Fetal marijuana exposure has no consistent effect on outcome. Prenatal cocaine exposure has not been shown to have any detrimental effect on cognition, except as mediated through cocaine effects on head size. Although fetal cocaine exposure has been linked to numerous abnormalities in arousal, attention, and neurologic and neurophysiological function, most such effects appear to be self-limited and restricted to early infancy and childhood. Opiate exposure elicits a well-described withdrawal syndrome affecting central nervous, autonomic, and gastrointestinal systems, which is most severe among methadone-exposed infants.

Most adverse effects of prenatal drug exposure are self-limited, with catch-up growth and resolution of withdrawal and of prior neurobehavioral abnormalities noted over time. The exception is alcohol, which is linked to life-long impairments (i.e., mental retardation and microcephaly) and possibly cigarette-related behavioral effects. The absence of tangible evidence of detrimental long-term cocaine effects may reflect limitations in the methodology used to identify children at greatest risk for adverse outcome.