the amount of oxygen and nutrients available to the fetus through several mechanisms. Additionally, smoking reduces the mother's appetite, and carbon monoxide from cigarette smoke crosses the placenta, increasing fetal carboxyhemoglobin levels (Werler et al., 1985). Those mechanisms are associated with retarding intrauterine growth in an apparent doseresponse relationship; the more cigarettes smoked, the lower is the birth weight (Zuckerman, 1991).6 Maternal cigarette smoking is also linked to higher rates of negative outcomes, including spontaneous abortions (Risch et al., 1988), stillbirths and perinatal death (Cnattingius et al., 1988; Malloy et al., 1988), and sudden infant death syndrome (SIDS) (Werler et al., 1985; Kandall and Gaines, 1991; Fried, 1992). Additionally, other toxins in cigarettes, including cadmium, lead, and thiocyanate, may also have adverse effects on the developing fetus (Kuhnert, 1991).

Nicotine may affect fetal brain development both indirectly (through nicotine-associated hypoxia) and directly (through specific nicotinic receptors) (Slotkin, 1992). In animal models, it appears that there is a lower dose threshold for adverse effects of fetal nicotine exposure on neuronal development than on overall growth (Slotkin, 1992). The literature regarding later neuro-behavioral outcomes in nicotine-exposed infants and children is not as extensive or as conclusive as those studies regarding pregnancy and birth outcomes (Fried, 1992). One study has found that maternal smoking during pregnancy, when postnatal smoking was controlled, selectively increased the probability that female children would smoke as adolescents and would continue to smoke (Kandel et al., 1994). There is suggestive evidence of a relationship between maternal smoking and later adverse developmental outcomes, including effects on attention and auditory responsiveness (Fried and Watkinson, 1988, 1990). However, those effects, if any, have a small attributable risk.

Prenatal Alcohol Exposure

Alcohol in high doses is a potentially potent teratogen associated with a range of consequences, including congenital anomalies and neurodevelopmental impairments (reviewed in IOM, 1995). In high doses, alcohol acts as a direct neuroteratogen, affecting all aspects of fetal growth (including brain growth, structure, and function) through mechanisms

6  

Intrauterine growth retardation (IUGR) can be caused by a number of factors including undernutrition and is associated postnatally with impaired neuromotor performance, including decreased motor maturity, poor state control, and abnormal reflexes (Tronick and Beeghly, 1992). Studies have reported long-term consequences of IUGR, including language delay and poor academic performance, but a direct cause-effect relationship for long-term effects is still considered inconclusive.



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