Effects of Prenatal Exposure to Environmental Tobacco Smoke

by National Institute of Health

(Page 4 of 4)

Pregnant women who do not smoke but live with or spend time with smokers expose their children to environmental tobacco smoke. In a review of 25 epidemiological studies of the relationship between fetal growth and ETS exposure, all but one study reported a decrement in mean birth weight with ETS exposure. Martin and Bracken found that passive exposure to smoking during pregnancy was significantly correlated with lower birth weight among the children of nonsmoking women. Full-term newborns exposed only to passive smoke weighed 61 grams less than newborns not exposed to passive smoke and had a significantly increased risk of LBW. Data from the National Health Interview Survey showed that after controlling for potential confounding variables - including race, number of children, income, and maternal age - nonsmoking women with high exposure to passive smoke were 1.6 times more likely to have a LBW infant than were nonsmokers with low exposure.

Studies using biomarkers to measure passive exposure provide further evidence of an adverse effect on growth. For example, one study examined levels of cotinine (a product of nicotine metabolism) in pregnant nonsmokers and found that the infants of the passively exposed mothers weighed 108 grams less than infants of unexposed women, even after controlling for known birth-weightassociated covariates. Other studies have confirmed these findings.

Makin and colleagues examined the long-term effects of prenatal passive exposure on 6- to 9-year-olds and found that children of nonsmoking mothers generally performed better on tests of speech and language skills, intelligence, and visual-spatial abilities as well as on the mothers' ratings of behavior, compared with children whose mothers were active or passive smokers. The performance of children of passive smokers was found, in most areas, to be between that of the children of active smokers and nonsmokers.

Effects of Postnatal Exposure to Environmental Tobacco Smoke

Postnatal exposure to ETS has been significantly associated with an increased risk of SIDS. After considering the effects of socioeconomic status, prenatal care, prenatal tobacco exposure, birth weight, breast feeding, and routine infant sleeping position, Klonoff-Cohen and colleagues reported that children exposed to the smoking of more than 1 pack of cigarettes per day in a household were 22.7 times more likely than other children to develop sudden infant death syndrome. Blair and colleagues reported that the risk of SIDS increased with the number of cigarettes smoked per day in the household, ranging from 2.5 for 1 to 19 cigarettes per day to 7.6 for 40 or more cigarettes per day.

Cognitive and behavioral outcomes are also affected by postnatal exposure to passive smoke. Postnatal exposure to household smoke was reported to be associated with reduced IQ scores in 3- year-olds. However, the effects of prenatal exposure were not considered in this analysis. Eskenazi and Trupin reported that 5- year-olds who were environmentally exposed to tobacco smoke had significantly lower scores on the Raven test and PPVT and were rated as more active by their mothers. That analysis controlled for prenatal tobacco exposure.

Among 6- to 11-year-old children of nonsmoking mothers, McCartney and colleagues found that postnatal passive tobacco exposure resulted in scores on central auditory processing tasks that were similar to scores for children of mothers who were light smokers during pregnancy. In the MHPCD cohort of adolescent mothers and their 6-year-old children, passive tobacco exposure, measured by the child's urine cotinine levels, was significantly related to poorer scores on subtests of the Test of Language Development, thereby reflecting lower receptive language abilities.

Summary and Conclusions

Smoking during pregnancy has been associated significantly with a number of adverse effects on the growth, cognitive development, and behavior of the exposed child. However, because women who smoke during pregnancy are also likely to use alcohol or other drugs, researchers must account for these confounding factors in order to identify accurately the specific and unique role of tobacco exposure. In addition, even nonsmoking mothers can expose their children through environmental tobacco exposure. Compared with alcohol and other drug use, tobacco use is less likely to decline during pregnancy, and women who smoke during pregnancy are more likely to continue to smoke after delivery. This means that children who are prenatally exposed to tobacco are at higher risk for continued exposure to environmental tobacco smoke from the mother and from other household smokers.

Prenatal tobacco exposure has consistently been associated with deficits in weight, height, and head circumference at birth. In general, long-term studies that have controlled for other factors that affect growth, particularly prenatal alcohol exposure, have reported that these growth deficits are corrected by "catch-up" growth in early childhood. Other studies have indicated a disproportionate weight-to-height ratio with higher ponderal indices in infants and body mass indices in older children.

Recent research has noted a higher rate of behavioral problems among children who were prenatally exposed to tobacco. Higher rates of cognitive deficits, specifically in language, reading, and vocabulary, as well as poorer performances on tests of reasoning and memory have been reported. Researchers have also reported behavior problems, such as increased activity, inattention, impulsivity, opposition, and aggression. In addition, prenatal tobacco exposure has been associated with higher rates of delinquency and criminality in adolescence and adulthood, an outcome that is perhaps mediated by earlier behavior problems.

Heredity is an important factor to consider in the interpretation of these findings. A shared genetic component between the mother and child may represent a vulnerability to the characteristics that are associated with tobacco use. For example, prenatal tobacco exposure may result in more impulsive offspring, or women who are impulsive may be more likely to smoke and to produce more impulsive children. Data from animal studies demonstrate specific CNS changes resulting from prenatal nicotine exposure that may affect offspring behavior. Therefore, both genetic and teratological etiologies are most likely involved in the observed adverse outcomes.

The neurobehavioral effects of prenatal and postnatal tobacco exposure are subtle. They are not easily identified, and difficulties arise in demonstrating that many of the outcomes discussed in this review are "caused by" tobacco exposure. Nevertheless, we must continue identifying both short- and long-term effects of prenatal and postnatal tobacco exposure on the growth and neurobehavioral development of children. Future studies should consider the separate and combined effects of tobacco and alcohol exposure on the developing offspring and use study designs and methodologies that allow researchers to tease out the effects from both prenatal and postnatal time periods. Without an understanding of the exact mechanisms by which tobacco exposure affects the CNS, the causes of the cognitive and behavior problems associated with prenatal tobacco exposure will possibly be attributed to another exposure, to environmental factors, or to the character of the mother or child.

Recognition and clarification of the effects of tobacco exposure on the development of the child may also help improve understanding of the effects of prenatal exposure to alcohol and other drugs. In addition, this research will facilitate the development of interventions to prevent substance use during pregnancy and to treat children prenatally exposed to tobacco, alcohol, and other drugs.

About the Author

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