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Ananth, Cande V. PhD, MPH; Smulian, John C. MD, MPH; Vintzileos, Anthony M. MD


Objective: To systematically review the literature and summarize the relationship between cigarette smoking and placental abruption, and to evaluate the joint influences of smoking and hypertensive disorders (chronic hypertension and preeclampsia) on the subsequent development of abruption.

Data Sources: We reviewed studies identified through a MEDLINE literature search between 1966 and 1997 and through studies cited in the references of published reports.

Methods of Study Selection: A total of 13 observational (seven case-control and six cohort) studies were identified which included a total of 1,358,083 pregnancies. We excluded case reports on placental abruption, and restricted the literature search to studies published in English. A meta-analysis was performed by computing pooled odds ratios based on random-effects models describing the association between placental abruption, smoking, and hypertensive disorders. Potential sources of heterogeneity among these studies were explored in detail.

Tabulation, Integration, and Results: The overall incidence of placental abruption was 0.64% (8724 of 1,358,623). Smoking was associated with a 90% increase in the risk of placental abruption (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.8, 2.0). This pattern was consistent by study design (case-control compared with cohort studies) and smoking prevalence (low compared with high prevalence, defined as less than 30% compared with 30% or more, respectively). However, the association was significantly (P < .001) stronger among the seven studies conducted outside the United States (OR 2.1, 95% CI 2.0, 2.2), compared with the six studies conducted in the United States (OR 1.6, 95% CI 1.5, 1.8). Pooled population attributable risk percentage for each stratum ranged between 15% and 25%, implying that 15–25% of placental abruption episodes are attributable to cigarette smoking. Data on the dose-response relationship between number of cigarettes smoked per day and the risk of abruption indicate that the OR increased with increasing number of cigarettes smoked. Furthermore, a meta-analysis of the joint effects of smoking and hypertension during pregnancy on the development of abruption identified two published studies, including 102,609 pregnancies. In the presence of smoking, the risk of abruption was further increased due to chronic hypertension, mild or severe preeclampsia, or chronic hypertension with superimposed preeclampsia.

Conclusion: Our meta-analyses showed an increased risk for placental abruption in relation to both cigarette smoking and hypertensive disorders during pregnancy. Because cigarette smoking is a modifiable risk factor, and hypertensive disorders are potentially treatable if diagnosed early in pregnancy, patient education, smoking cessation programs, and early prenatal care may be important factors in the prevention of placental abruption.

Placental abruption is defined as the premature separation of a normally implanted placenta before delivery.1 It occurs in 0.8–1.0% of all pregnancies,2 with much higher incidences among women with sudden uterine decompression, uterine tumors, short umbilical cord, pregnancies complicated by hypertensive disorders (including chronic hypertension, pregnancy-induced hypertension, and preeclampsia), premature rupture of membranes, oligohydramnios, and uterine infections such as chorioamnionitis. After an initial pregnancy complicated by abruption, the recurrence of this condition is almost 20 to 30 times greater in subsequent pregnancies.2 Finally, obstetric and lifestyle factors that significantly contribute to the increased incidence of placental abruptions include advanced maternal age, grand multiparity, cigarette smoking, and cocaine use.

Tobacco use during pregnancy has been associated with many adverse reproductive outcomes, including infertility, spontaneous abortion, low birth weight, pre-term delivery, and long-term physical and developmental disorders in infants. Although the deleterious effects of smoking on pregnancy outcomes are well described, evidence linking tobacco smoke to placental disorders, especially placental abruption, has been inconsistent among studies, and the relationship has not been completely investigated. This shortcoming is partly because of weaknesses in study design, inadequate sample sizes, and inconsistent definitions of placental abruption.2 Information on cigarette smoking in published studies is based exclusively on self-reported smoking behavior. Because there is a social stigma associated with smoking, these studies may have been hampered by significant underreporting of smoking behavior.

The objective of our study was to perform a systematic overview and meta-analysis of published studies on cigarette smoking and hypertensive disorders during pregnancy and the subsequent development of placental abruption. We also reviewed the literature to assess the dose-dependence relationship between the number of cigarettes smoked and the subsequent development of placental abruption. Ananth et al2 recently reported the results of a meta-analysis on the relationship between hypertensive disorders (chronic hypertension and mild and severe preeclampsia) and placental abruption. The present meta-analysis attempts to summarize the relationship between smoking and abruption, and the joint influences of smoking and hypertensive disorders on the subsequent development of placental abruption.

A meta-analysis comprising 1.4 million pregnancies indicates that cigarette smoking during pregnancy is associated with a two-fold increase in the risk for placental abruption.

Division of Epidemiology and Biostatistics, and the Division of Maternal-Fetal Medicine, The Center for Perinatal Health Initiatives, Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School/St. Peter's Medical Center, New Brunswick, New Jersey.

Address reprint requests to: Cande V. Ananth, PhD, MPH, Division of Epidemiology and Biostatistics, Department of Obstetrics and Gynecology, UMDNJ—Robert Wood Johnson Medical School, 125 Paterson Street, New Brunswick, NJ 08901-1977; E-mail:

Drs. Ananth and Smulian are supported, in part, by grant 029553 from the Robert Wood Johnson Foundation, awarded to the Center for Perinatal Health Initiatives.

Opinions, views and conclusions expressed in this paper are those of the authors and not those of the Robert Wood Johnson Foundation.

Received April 27, 1998. Received in revised form July 13, 1998. Accepted July 24, 1998.

© 1999 The American College of Obstetricians and Gynecologists