Effect of Maternal Smoking on Fetal Catecholamine Concentrations at Birth

Abstract

The aim of this study was to compare catecholamine concentrations in the fetal umbilical artery cord blood from the offspring of smokers versus the offspring of nonsmokers. Pregnant women who were self-identified as smokers (Ն10 cigarettes per day throughout pregnancy) or nonsmokers were recruited for study participation. Maternal blood was collected for cotinine concentrations. Umbilical artery cord blood was collected at delivery for arterial pH and catecholamine concentrations. Cord blood was obtained from 51 subjects, including 21 smokers and 30 nonsmokers. Median epinephrine concentrations [304 pg/mL versus 597 pg/mL (Mann-Whitney U ϭ 170; p ϭ 0.006)] and median norepinephrine concentrations [3148 pg/mL versus 6558 pg/mL (Mann-Whitney U ϭ 191; p ϭ 0.006)] were significantly lower in smokers compared with nonsmokers, respectively. After controlling for gestational age, route of delivery, and arterial pH, log-transformed epinephrine concentrations between smokers and nonsmokers were statistically significant (p ϭ 0.03), with a similar trend for log-transformed norepinephrine concentrations (p ϭ 0.07). Analyses of the data using cotinine Ͻ20 ng/mL to classify nonsmokers also showed differences in epinephrine concentrations between groups (p ϭ 0.02). These results are consistent with results from animal studies showing that catecholamine concentrations may be affected by prenatal nicotine exposure. Further studies are needed to validate these findings and to examine the specific mechanism by which these differences may arise. Maternal smoking is one of the most important causes of poor pregnancy outcomes in developed countries. Maternal smoking increases the risk of spontaneous abortion, low birth weight, premature delivery, and infant death from perinatal disorders and from SIDS (1-3). One of the most dramatic effects of maternal smoking is a tripling of the risk of SIDS, a tragic syndrome that claims thousands of infant lives each year (1). Although the epidemiologic association between smoking and these disorders is well established, the mechanism by which smoking contributes to these health risks is not well understood.SIDS may result from cardiorespiratory failure of the infant during a hypoxic episode, as in sleep apnea (4). If this is the case, animal research suggests that smoking could contribute to the increased risk of SIDS through changes in cell differentiation within the adrenal medulla. The ability to survive hypoxic challenge requires responses mediated by circulating catecholamines, which the fetal or neonatal adrenal medulla does via an autonomous mechanism that is independent of CNS innervation (5). This mechanism disappears with further cell differentiation, triggered by the development of innervation, and the consequent stimulation of the nicotinic cholinergic receptors on the chromaffin cells by the neurotransmitter, acetylcholine (6). Nicotine mimics acetylcholine, leading to premature loss of the fetal/neonatal response. Consistent with this hypothesis, the offspring of pregnant rats adm...

Prenatal and Adolescent Exposure to Tobacco Smoke Modulates the Development of White Matter Microstructure

“…In addition to myelination, FA increases reflect maturational increases in cell packing density, fiber diameter, and directional coherence (Beaulieu and Allen, 1994;Shimony et al, 1999;Beaulieu, 2002). Thus, observed group differences are consistent with previous evidence that stimulation of nAChRs by nicotine may disrupt neurodevelopment by disrupting the trophic actions of acetylcholine (Slotkin, 1998;Oncken et al, 2003). FA increases were most extensive in adolescent smokers with and without prenatal exposure.…”

Interrelations between maternal smoking during pregnancy, birth weight and sociodemographic factors in the prediction of early cognitive abilities

“…For example, several studies have shown lower autonomic arousal and vigilance levels in children of mothers who smoked during pregnancy (Horne, Franco, Adamson, Groswasser, & Kahn, 2004;Kristjansson et al, 1989;Raine, 2002). Measures of arousal and vigilance might be specifically sensitive to prenatal smoking, because without continued nicotinic intake after birth, the increased number of nicotinic cholinergic receptor binding sites that have been formed as a consequence of in utero-nicotine exposure may be understimulated (Oncken et al, 2003;Raine, 2002;Slotkin et al, 2005). …”

Critical Review

“…Significantly lowered levels of catecholamines found in umbilical cord blood in response to hypoxemia during parturition may explain the increased perinatal morbidity and mortality associated with smoking during pregnancy (Oncken et al, 2002). A blunted catecholamine response to hypoxic stress with a greater risk of death to offspring was also observed in rats receiving nicotine throughout gestation.…”