Elsevier

Alcohol

Volume 45, Issue 1, February 2011, Pages 73-79
Alcohol

Impact of prenatal alcohol consumption on placenta-associated syndromes

https://doi.org/10.1016/j.alcohol.2010.05.010Get rights and content

Abstract

The biology of placental and fetal development suggests that alcohol may play a significant role in increasing the risk of feto-infant morbidity and mortality, but study results are inconsistent and the mechanism remains poorly defined. Previous studies have not examined the risk of placenta-associated syndromes (PASs: defined as the occurrence of either placental abruption, placenta previa, preeclampsia, small for gestational age, preterm, or stillbirth) as a unique entity. Therefore, we sought to examine the relationship between prenatal alcohol use and the risk of PAS among singleton births in the Missouri maternally linked data files covering the period 1989–2005. Logistic regression with adjustment for intracluster correlation was used to generate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Compared with nondrinkers, drinkers were more likely to be smokers, 35 years of age or older, black, and multiparous. Drinkers had an increased risk of PAS (OR = 1.26, 95% CI = 1.22,1.31) when compared with their nondrinking counterparts. The risk of PAS was progressively amplified with increasing prenatal alcohol consumption (P for trend <.01). Women who reported consuming five or more alcoholic drinks per week had more than twofold increased risk of PASs, whereas women in the lowest drinking category (one to two drinks per week) had only a slight increased risk of PAS (OR = 1.09, 95% CI = 1.05, 1.14). Enhanced understanding of the mechanism by which prenatal alcohol consumption leads to PAS may aid in the development of more targeted interventions designed to prevent adverse pregnancy outcomes. Screening women for alcohol use may assist providers in protecting developing fetuses from the potential dangers of prenatal alcohol use.

Introduction

The placenta is critical for maternal–fetal exchange, and abnormalities (e.g., vascular lesions) are associated with adverse pregnancy outcomes and complications, such as placental abruption, placenta previa, preeclampsia, small for gestational age (SGA), preterm, or stillbirth (Khong, 2004). Because of their associations with vascular abnormalities, these feto-infant morbidities are believed to be placental in origin and are collectively known as placental-associated syndromes (Ray et al., 2005). These disorders are presumed to originate from diseased placental vessels and have previously been examined in aggregate to determine the risk of premature cardiovascular disease in women (Ray et al., 2005). Alcohol may contribute to the development of vascular lesions leading to adverse pregnancy outcomes as it readily crosses the placenta, and exposure causes dose-dependent placental vasoconstrictions and decreases in placental weight (Burd et al., 2007). Although only about 1.6% of pregnant women reported frequent drinking during pregnancy, an even greater percentage, about 12.5%, report consuming at least some alcohol during pregnancy (Floyd and Sidhu, 2004). Less than half of all reproductive aged women abstain from alcohol use (45.4%), an indication that exposure rates may be even higher, especially in early pregnancy before it is recognized (Floyd and Sidhu, 2004).

Previous studies of alcohol consumption during pregnancy and the various components of placenta-associated syndromes (PASs) have had inconsistent results (Aliyu et al., 2008, Henderson et al., 2007a, Yang et al., 2001). Nonetheless, the biology of placental and fetal development suggests that alcohol may play a significant role in increasing the risk of feto-infant morbidity and mortality. The placenta grows throughout pregnancy and this growth is accompanied by an increase in vasculature and trophoblast surface area (Myatt, 2006). Alcohol exposure may cause disruptions in these processes, resulting in impaired development and culminating in any number of feto-infant morbidities or mortality (Burd et al., 2007, Myatt, 2006). It is hypothesized that depending on the timing of the exposure, and the dose received, alcohol exposure can lead to PASs (Burd et al., 2007). However, while previous authors have considered associations between alcohol and adverse pregnancy outcomes, they have not examined PASs as a larger entity. Accordingly, we conducted this population-based study with the following objectives: (1) To examine the impact of prenatal alcohol use on the risk of PASs; and (2) To assess whether there is a dose–response relationship between the amount of alcohol consumed and the level of risk for PAS.

Section snippets

Materials and methods

We used the Missouri maternally linked cohort data files covering the period of 1989 through 2005. The Missouri vital record system is a reliable one that has been adopted as the “gold standard” to validate U.S. national data sets that involve matching and linking procedures (Martin et al., 2003). For the purpose of this study, we selected singleton births within the gestational age range of 20–44 weeks. On the basis of the previously published reports (McTigue et al., 2006, NHLBI Obesity

Results

A total of 1,312,505 singleton births were available for analysis. We excluded pregnancies before 20 weeks or beyond 44 weeks of gestation (70,803 or 5.4%) and records for which prenatal drinking (7,085), gestational age (7,559), and birth weight (333) values were missing (total = 14,990 or 1.2%). The final data set composed of a total of 1,226,685 singleton records, consisting of drinking (16,003 or 1.3%) and nondrinking gravidas (1,210,682 or 98.7%; the referent group).

Overall, the prevalence

Discussion

In this study, we found that the risk for PASs increases with increasing prenatal alcohol consumption. Women who reported consuming five or more alcoholic drinks per week had more than twofold increased risk of PASs. To our knowledge, previous studies have not examined PASs as a unique entity with the components sharing similar pathophysiologic pathways. Prior studies that have examined the individual components of PASs have found similar associations. For example, a study by Marbury et al.

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