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Alcohol Research & Health, Winter, 2000 by Marie D. Cornelius
Effects on Cognitive Function
Laboratory research with animals has shown that nicotine affects the CNS at exposure levels below those at which growth changes are evident (Slotkin 1998). For example, animal studies have shown associations between fetal nicotine exposure and increased loco-motor activity in male rat pups (Shacka et al. 1997); hyperactivity in rats associated with increased nicotine receptors in the brain (Tizabi et al. 1997); lower turnover of the brain chemicals dopamine and serotonin in the rat brain as a result of alterations in the release or removal of dopamine and serotonin from the synapse (Muneoka et al. 1997); and changes in the morphology of the hippocampus in rats (Roy and Sabherwal 1998).
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In the literature on humans, prenatal tobacco exposure has also been linked to CNS effects, including cognitive and neurobehavioral outcomes, although the reports are inconsistent. At birth, prenatal tobacco exposure has been associated with poorer auditory orientation and autonomic regulation (Picone et al. 1982) and increased tremors and startles (Fried and Makin 1987). In a recent race-matched study of cocaine-exposed and non-cocaine-exposed infants, neurological exams showed that prenatal tobacco exposure was significantly related to muscle tone abnormalities when controlling for other variables, including prenatal cocaine and ethanol exposure, head circumference, and prenatal care (Dempsey et al. 2000). The authors concluded that maternal cigarette smoking, rather than cocaine exposure, might be the major predictor of tone abnormalities.
Studies have also reported adverse effects of prenatal tobacco exposure on cognitive and behavioral development in older children. In one study, cognitive functioning at age 3 was higher among the children of mothers who quit smoking during pregnancy than among children whose mothers smoked throughout pregnancy (Sexton et al. 1990). Poor language development and lower cognitive scores have also been reported in 2- (Fried and Watkinson 1988), 3-, and 4-year-old (Fried and Watkinson 1990) children prenatally exposed to tobacco. When those children were 9 to 12 years old, prenatal tobacco exposure was negatively associated with language and reading abilities (Fried et al. 1997). In another analysis of this same cohort of 9 to 12 year-olds, prenatal tobacco exposure had a negative, dose-dependent association with visual perception after consideration of other potential prenatal risk factors and of pre- and post-natal secondhand smoke exposures (Fried and Watkinson 2000).
Other researchers (Baghurst et al. 1992; Fergusson and Lloyd 1991) have argued that initially significant associations between prenatal tobacco exposure and cognitive development were explained better by differences in social class and the home environment. For example, after controlling for socioeconomic and environmental differences, Eskenazi and Trupin (1995) failed to find consistent relationships between prenatal tobacco exposure and performance on the Raven Colored Matrices Test (Raven et al. 1986), a measure of nonverbal reasoning, or the Peabody Picture Vocabulary Test (PPVT) (Dunn and Dunn 1981). However, in the MHPCD study of adult mothers, prenatal tobacco exposure predicted deficits in visual memory and verbal learning scores on the Wide Range Assessment of Memory and Learning test (WRAML) (Sheslow and Adams 1990) (Cornelius et al. 1999c), and these associations remained after consideration of other factors, including socioeconomic status, maternal psychological status, home environment, other pr enatal substance exposures, and current maternal tobacco and other substance use.
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