Alcohol, tobacco and marijuana use among pregnant teenagers: 6-year follow-up of offspring growth effects

Abstract

This prospective study evaluated the relations between maternal alcohol, tobacco and marijuana use during pregnancy and children's growth at 6 years. In this cohort of pregnant teenagers and their offspring, mothers were recruited from an urban prenatal clinic between 1990 and 1995, and observed from their fourth prenatal month. At the delivery assessment, there were 413 live-born singletons. At the 6-year visit, 345 children and mothers were evaluated. Prenatal alcohol and marijuana exposure were significantly associated with growth deficits, after controlling statistically for other prenatal substance use, current maternal substance use, current environmental tobacco exposure (ETS) and sociodemographic and growth-related covariates. There was a significant negative association between the second and third trimester alcohol exposure and offspring height. Third trimester alcohol exposure predicted reduced skinfold thickness. Exposure to any prenatal marijuana in the second trimester was significantly associated with shorter stature. First trimester tobacco exposure was associated with increased skinfold thickness among the 6-year-olds. The effects of prenatal alcohol exposure on growth at birth persisted in older children despite a low level of exposure during gestation. Effects of prenatal marijuana exposure on reduced height were not anticipated and occurred only when use was categorized as any/none. These data are consistent with an emerging body of evidence indicating that, by contrast to the growth deficits associated with smoking during pregnancy, which are evident at birth, the shorter stature associated with prenatal alcohol exposure continues to be evident during childhood.

Introduction

Previous research on the effects of prenatal substance exposure has focused almost exclusively on populations of adults and their offspring, despite the fact that adolescent substance use and adolescent pregnancy are prevalent [36], [48]. Compared with adult pregnant women, pregnant adolescents use drugs at lower levels and more sporadically [5], [6], [9]. However, offspring of adolescents are at increased risk for prematurity, morbidity and growth retardation independent of sociodemographic factors and prenatal substance exposure [25], [37], [43]. Thus, offspring of adolescents are a vulnerable population.

Growth retardation is a cardinal feature in the diagnosis of Fetal Alcohol Syndrome (FAS). Children with FAS and fetal alcohol effects are smaller at birth and these growth deficits continue through adulthood [42], [46]. Growth deficits have been reported at birth at lower levels of alcohol exposure among those with no morphologic features of FAS among offspring of adult women at the Maternal Health Practices and Child Development (MHPCD) project [14]. In this same cohort, the effect of alcohol on growth was detected at 8 months [16], 18 months [13], 36 months [18], 6 years [15] and 10 years [19]. Growth deficits related to prenatal alcohol exposure have also been reported among 6- and 13-month-olds [35] and among 5-year-olds [3]. Other studies, however, have not found growth effects on follow-up [26], [39] or beyond 8 months of age [41].

Maternal smoking during pregnancy has long been considered an important risk factor for low birth weight. This association was first reported in 1957 and has been proven in numerous subsequent studies [10], [21], [44], [47], [48]. The longer-term effects of prenatal tobacco exposure on the growth of exposed offspring are not as clear. Rantakallio [41] found that exposed offspring were shorter at age 14, and Fogelman and Manor [22] reported decreased height at 7, 11 and 23 years of age. In the latter study, the differences in height at age 23 were mediated by birth weight. These studies did not control for the offspring's passive exposure to tobacco smoke or their exposure to alcohol, however. Fox et al. [23] studied the height and weight of 714 3-year-old children. The children of women who quit smoking during pregnancy were heavier and taller than those of women who did not quit. Adjustment for postpartum exposure to tobacco smoke reduced the difference in the children's weight, but had little effect on the differences in height.

Other studies have not found that growth retardation is associated with prenatal tobacco exposure over the long-term [26], [32]. Recently, it was argued that the association between prenatal tobacco use and reduced height at 6 and 13 months postpartum was actually attributable to prenatal exposure to alcohol [35], highlighting the importance of controlling for the effects of other drugs. In a MHPCD study of adult mothers and their offspring [12], there was a significant inverse relation between tobacco use and weight, length and head circumference at birth, after controlling for prenatal alcohol and other drug exposures and current maternal tobacco use. By a 6-year follow-up, however, prenatal tobacco exposure was not related to any growth reductions [15]. Vik et al. [49] also found that the reductions in birth weight that were attributed to prenatal tobacco exposure were no longer evident among 5-year-old children. Recently, Fried et al. [27] reported that adolescents who were prenatally exposed to heavy smoking were heavier than those not exposed.

There are fewer studies that have examined the effects of prenatal marijuana exposure on growth. Most, but not all, studies have found that prenatal marijuana exposure does not have a negative association with growth after potential confounds are controlled. In a report from a MHPCD cohort of children of adult women, there was a correlation between marijuana exposure in the first 2 months of pregnancy and decreased length at birth. This effect did not persist at later follow-ups [12], [15]. Several other studies have reported negative effects of prenatal exposure to marijuana on neonatal growth [33], [50]. In the Ottawa Prenatal Prospective Study [27], a trend of smaller head circumference in children exposed to daily marijuana use in utero was found at 1, 2, 3, 4 and 6 years of age, and was statistically significant when the children were early adolescents.

No previous study has examined the long-term effects of prenatal alcohol, tobacco or marijuana exposure on the growth of offspring of teenagers. In an earlier analyses of growth outcomes at birth from the current study cohort, second trimester alcohol exposure was significantly related to smaller head and chest circumferences, and lower birth weight [8]. Prenatal tobacco exposure significantly predicted lower birth weight, length, head and chest circumferences, and ponderal index [10]. Prenatal marijuana exposure was significantly related to earlier gestational age, but was not related to any growth outcomes at birth [10].

The purpose of the current study is to examine the long-term effects of prenatal alcohol, tobacco and marijuana use among teenage women on the growth of their offspring at age 6 years. We hypothesized that the growth deficits at birth that were related to prenatal alcohol exposure [8] would be measurable at age 6 and that growth deficits at birth that were related to prenatal tobacco exposure [10] would not be measurable at age 6. We hypothesized that, with respect to prenatal marijuana exposure, there would be no growth deficits at age 6, as there were no growth deficits at birth [10].