title: Impact of prenatal alcohol consumption on placenta-associated syndromes.
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.
authors.affiliation: The Chiles Center for Healthy Mothers and Babies, University of South Florida, 3111 E. Fletcher Avenue, Tampa, FL 33613, USA. hamisu.salihu@gmail.com
authors.forename: Hamisu M
authors.initials: HM
authors.lastname: Salihu
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Kornosky
authors.forename: O'Neil
authors.initials: O
authors.lastname: Lynch
authors.forename: Amina P
authors.initials: AP
authors.lastname: Alio
authors.forename: Euna M
authors.initials: EM
authors.lastname: August
authors.forename: Phillip J
authors.initials: PJ
authors.lastname: Marty
mesh_terms: D000037:Abruptio Placentae / Q000453:epidemiology; D000328:Adult; D044383:Black People; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000008:administration & dosage / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D016015:Logistic Models; D008423:Maternal Age; D010922:Placenta Diseases / Q000139:chemically induced / Q000453:epidemiology* / Q000517:prevention & control; D010923:Placenta Previa / Q000453:epidemiology; D011225:Pre-Eclampsia / Q000453:epidemiology; D011247:Pregnancy; D047928:Premature Birth / Q000453:epidemiology; D012307:Risk Factors; D050497:Stillbirth; D044465:White People
chemical_list: D000431:Ethanol