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Matern Child Health J (2011) 15:670676

DOI 10.1007/s10995-010-0615-6

Alcohol Consumption During Pregnancy and Risk of Placental

Abruption and Placenta Previa
Muktar H. Aliyu ONeil Lynch Philip N. Nana
Amina P. Alio Ronee E. Wilson Phillip J. Marty

Roger Zoorob Hamisu M. Salihu

Published online: 1 May 2010

Springer Science+Business Media, LLC 2010

Abstract The purpose of this study was to examine the outcome defined as the occurrence of either or both lesions.
association between prenatal alcohol consumption and the Multivariate logistic regression was used to generate
occurrence of placental abruption and placenta previa in a adjusted odd ratios, with non-drinking mothers as the ref-
population-based sample. We used linked birth data files to erent category. Women who consumed alcohol during
conduct a retrospective cohort study of singleton deliveries pregnancy had a 33% greater likelihood for placental
in the state of Missouri during the period 1989 through abruption during pregnancy (adjusted odds ratio (OR), 95%
2005 (n = 1,221,310). The main outcomes of interest were confidence interval (CI) = 1.33 [1.161.54]). No associa-
placenta previa, placental abruption and a composite tion was observed between prenatal alcohol use and the
risk of placenta previa. Alcohol consumption in pregnancy
M. H. Aliyu was positively related to the occurrence of either or both
Department of Preventive Medicine, Institute for Global Health, placental conditions (adjusted OR [95% CI] = 1.29 [1.14
Vanderbilt University, Nashville, TN, USA 1.45]). Mothers who consumed alcohol during pregnancy
were at elevated risk of experiencing placental abruption,
O. Lynch
Department of Mathematics, Minnesota State University but not placenta previa. Our findings underscore the need
Moorhead, Moorhead, MN, USA for screening and behavioral counseling interventions to
e-mail: combat alcohol use by pregnant women and women of
childbearing age.
P. N. Nana
Department of Obstetrics and Gynecology, University
of Yaounde 1, Yaounde, Cameroon Keywords Alcohol  Placenta previa 
Placental abruption  Population-based study
A. P. Alio  H. M. Salihu (&)
Department of Family and Community Health, Center for
Research and Evaluation, Lawton and Rhea Chiles Center,
For Healthy Mothers and Babies, University of South Florida, Introduction
3111 E. Fletcher Avenue, Tampa, FL 33613, USA
Maternal alcohol use during pregnancy is a leading pre-
R. E. Wilson ventable cause of fetal malformations, neurodevelopmental
Department of Epidemiology and Biostatistics, University abnormalities and perinatal mortality [13]. One of the
of South Florida, Tampa, FL, USA pathways by which alcohol is postulated to exert its
inhibitory effects on fetal development is via impaired
P. J. Marty
The Chiles Center for Healthy Mothers and Babies, University placentation [4]. The two important placental pathologies
of South Florida, Tampa, FL, USA include placenta previa and placental abruption, both of
e-mail: which are precursors of perinatal mortality and morbidity.
Placental abruption accounts for up to a third of all peri-
R. Zoorob
Southeast Fetal Alcohol Research and Training Center, natal deaths [5, 6], mostly due to its detrimental effects
Meharry Medical College, Nashville, TN, USA on length of gestation and fetal growth [7, 8]. Similarly,

Matern Child Health J (2011) 15:670676 671

placenta previa is a major contributor to fetal growth training data set of 52,683 pairs of records. Weights of an
restriction, preterm delivery and perinatal mortality [9, 10]. individual variable were calculated as follows:
There is lack of consensus regarding the association
Wa log2 j1 =N1 =j2 =N2 
between maternal alcohol use and placental abruption.
Whereas some published reports suggest a positive asso- where Wa = weight for agreement, j1 = agreement in the
ciation [1114], others do not [15]. In the case of placenta first training dataset, N1 = number in the first training
previa, a lack of association with maternal alcohol use has dataset, j2 = agreement in the second training dataset,
been the usual finding [10, 16]. Few studies have analyzed N2 = number in the second training dataset.
the association between prenatal alcohol use and placental Wd log2 d1 =N1 =d2 =N2 
abruption and placenta previa together within the same
cohort. These two placental pathologies are believed to where Wd = weight for disagreement, d1 = disagreement
have a shared etiology [14], as mothers with a prior history in the first training dataset, N1 = number in the first
of placental abruption have an increased predisposition to training dataset, d2 = disagreement in the second training
developing placenta previa in subsequent pregnancies [17], dataset, N2 = number in the second training dataset.
and vice versa [18, 19]. In consideration of this common Correct and incorrect match weights were assigned to
origin theory, we set out to examine the association each pair of records and then summed up. Linkages with a
between prenatal alcohol consumption and the occurrence score\-5 were rejected. A quality of agreement indicator,
of placental abruption and placenta previa among a large based on the level of agreement of birth outcome, maternal
representative sample of singleton births to mothers in the first and family name, year and month of birth and race,
state of Missouri during the period 1989 through 2005. was then assigned to the remaining linkages and a priority
indicator was then assigned. The highest priority was given
to records with a high linkage weight that matched exactly
Materials and Methods on month and year of birth, maternal family and first
names. The lowest priority was given to records with no
We utilized the Missouri maternally linked cohort data files agreement on maternal first and family names, and inter-
covering the period 1989 through 2005. The Missouri Vital mediate priority levels for linkage for those records in
Record System is a central registry of all Missouri births, between. The quality of agreement and priority indicators
infant deaths and fetal deaths. The system is a reliable one were used to assess the validity of potential linkages,
that has been adopted as gold standard to validate US. especially those to multiple earlier births. For multiple
national datasets that involve matching and linking pro- linkages, the most likely potential linkage based on the
cedures [20]. The dataset used for this study has previously score and quality of agreement indicator was accepted.
been validated through a linkage system that we describe as Paternal last name and zip code of residence could change
follows: between pregnancies and two summary weights were cal-
A probabilistic linkage method was used in the linking culated: one with paternal name and zip code and one
process of the Missouri data files longitudinally using a without; the higher sum was used. A family indicator
multi-stage algorithm. The method is dependent on the variable to define sibship groups was then assigned.
calculation of a weighted score for every possible pair of For the purpose of this study we selected singleton live
records that reflects the likelihood that they belong to the births within the gestational age range of 2044 weeks.
same person. A computer program was employed to Based on previously published reports [21] we assigned
compare a combination of variables from two files, giving women to the following drinking categories: class I drinker
a separate weight to each value that matches or mis- (12 drinks per week); class 2 drinker (34 drinks per
matches. The weights for a pair of records are summed up week); class 3 drinker (C5 drinks per week). We used non-
and this represents the relative likelihood of both records drinking mothers as the referent category. The exposure of
belonging to the same person. Although the summing interest, namely, alcohol intake during pregnancy, was
assumes that the weights for each field are independent, measured at delivery through direct questioning of the
there is usually some dependence between fields. mother regarding the number of alcohol drinks consumed
Initially, the linkage weights were calculated using two per week. There was no biomarker confirmation of the
training datasets. The weights for a correct match came from maternal self-reported number of drinks consumed.
the exact linkage of first and family name, month and year of Although the Missouri dataset has been validated in terms
birth in a training data set of 52,683 pairs of births with a of the accuracy of its linkage procedure as being highly
previous live birth in 1983 or 1985. These exact links were successful and complete [22], validation of alcohol intake
assumed to be correct. The weights for an incorrect match as an isolated measure has not been formally performed.
came from a computer-generated random linkage of a Nonetheless, previous studies on alcohol and birth

672 Matern Child Health J (2011) 15:670676

outcomes using the same dataset reported results that were plausibility. These variables included maternal age, parity,
consistent with the literature [3, 23]. race, smoking, education, marital status, adequacy of pre-
The main outcomes of interest were placenta previa, natal care, gender of the infant and year of birth. We
placental abruption and a composite outcome defined as the constructed the regression models and assessed goodness-
occurrence of either lesion. Placenta previa is defined as an of-fit of the regression models using the 2 log likelihood
obstetric complication in which the placenta is attached to ratio test. We estimated the significance of main effects by
the uterine wall close to or covering the cervix. It can means of the Wald test, and assessed doseresponse using
sometimes occur in the later part of the first trimester, but the chi-square test for linear trend [28].
usually during the second or third. It is a leading cause of Adjusted estimates were derived in all cases by using
vaginal bleeding. Placental abruption is defined as a con- non-drinking gravidas as the referent category. All tests of
dition where all or part of the placenta has pulled away hypothesis were two-tailed with a type 1 error rate fixed at
from the uterine wall, disrupting the flow of blood and 5 percent. SAS version 9.1 (SAS Institute, Cary, NC) was
oxygen to the fetus. Small abruptions can heal, but larger used to perform all analyses. This study was approved by
ones can cause fetal distress or death. the Office of the Institutional Review Board at the Uni-
Gestational age was based on the interval between the last versity of South Florida.
menstrual period and the date of delivery of the baby (95
percent of cases). When the menstrual estimate of gestational
age was inconsistent with the birth weight (e.g., very low Results
birth weight at term), a clinical estimate of gestational age on
the vital records was used instead [24, 25]. A total of 1,304,557 singleton births were available for
Socio-demographic characteristics were captured by analysis. We excluded pregnancies before 20 weeks or
maternal self-report. The distribution of the following beyond 44 weeks of gestation (69,424 or 5.3 percent) and
selected characteristics was compared between drinking records for which prenatal drinking (6,897), gestational age
and non-drinking mothers to assess differences in baseline (6,559), birth weight (216) values were missing (total =
characteristics: maternal age, parity, race, education, mar- 13,823 or 1.1 percent). The final dataset comprised a total of
ital status and adequacy of prenatal care. Adequacy of 1,221,310 singleton records, consisting of drinking (15,911
prenatal care was assessed using the revised graduated or 1.3 percent) and non-drinking gravidas (1,205,399 or 98.7
index algorithm, which has been found to be more accurate percent; the referent group).
than several others, especially in describing the level of Overall, the prevalence of prenatal drinking was 1.3%.
prenatal care utilization among groups that are high-risk Figure 1 illustrates trend of the prevalence of prenatal
[26, 27]. This index assesses the adequacy of care based on drinking during pregnancy in the study population over
when the trimester prenatal care begun, number of visits, the course of the study while (Table 1) shows frequency
and the gestational age of the infant at birth. In this study, comparison between drinking and non-drinking mothers
inadequate prenatal care utilization refers to women who with respect to selected socio-demographic characteristics.
either had missing prenatal care information, had prenatal Overall, alcohol consumption among pregnant women
care but the level was considered sub-optimal, or mothers declined considerably from 16.8% in 1989 to 2.2% in 2005.
who had no prenatal care at all. We performed crude fre- Those gravidas who did not abstain during pregnancy were
quency comparisons between the two groups for the pres- more likely to be older, black, multiparous and to have
ence of common obstetric complications, namely, anemia, smoked during pregnancy. Drinking mothers were also less
insulin-dependent diabetes mellitus, other types of diabetes likely to be married, to have received adequate prenatal care
mellitus, chronic hypertension, preeclampsia, eclampsia, and to have attained high school education than their non-
abruption placenta and placenta previa. drinking counterparts.
Table 2 displays the prevalence of common medical and
obstetric complications among mothers in the study. The
Statistical Analysis overall prevalence of pregnancy complication was 10.9%
(N = 133,652) distributed as follows: drinkers (N = 1,444
Chi-square test was used to assess differences in socio- or 9.1%) and non-drinkers (132,208 or 11.0%) [P \ 0.01].
demographic characteristics and maternal pregnancy Of the obstetric complications, anemia, placenta previa and
complications between the two groups (Drinking/Non- placental abruption were more likely among drinkers while
drinking). We used logistic regression models to generate pre-eclampsia, eclampsia, insulin dependent diabetes, other
adjusted odd ratios and their 95 percent confidence inter- forms of diabetes and chronic hypertension were more
vals. The covariates in our models were selected a priori common among mothers who were non-drinkers during
based on previously published literature and biologic pregnancy.

Matern Child Health J (2011) 15:670676 673

Fig. 1 Crude rates of the

prevalence of maternal alcohol
consumption during pregnancy
by year, Missouri, 19892005

Table 1 Comparison of
Non-drinker Drinker P-value
selected socio-demographic
(N = 1,205,399)% (N = 15,911)%
characteristics by prenatal
drinking status, Missouri, Maternal age
C35 years 9.83 18.47 \0.0001
Multiparous 58.80 68.66 \0.0001
Black 14.99 21.24 \0.0001
White 82.58 77.54
C12 years 80.49 78.05 \0.0001
Yes 19.42 52.44 \0.0001
Yes 67.84 59.54 \0.0001
Adequate prenatal care
Yes 50.94 39.40 \0.0001

There were 4,582 (0.4%) infants born to mothers who Women who consumed alcohol during pregnancy had a
were diagnosed with placenta previa and 9,349 (0.8%) 33% greater likelihood for placental abruption during
diagnosed with placental abruption in the study population. pregnancy (adjusted OR = 1.33 [95% CI: 1.161.54]).
Figure 2 is an illustration of the distribution of rates of When the risk of placental abruption was analyzed by
placenta previa and placental abruption and the composite severity of drinking, a J-shaped trend was observed with a
outcome by prenatal drinking status. peak among those in the most severe category (class 3) and
The crude estimates for the association between prenatal a trough among moderate drinkers (class 2). These obser-
drinking, placenta previa, placental abruption as well as the vations were similar for the composite outcome measure.
composite outcome measure did not differ from the By contrast, no association was seen between alcohol use
adjusted estimates therefore only the latter are summarized in pregnancy and the risk of placenta previa (Table 3).
in Table 3. Overall, we detected an association between Although there was an indication of increased risk for
alcohol consumption during pregnancy and placental placenta previa in drinkers, the risk estimates failed to
abruption as well as the composite outcome measure. reach statistical significance.

674 Matern Child Health J (2011) 15:670676

Table 2 Prevalence of
Non-drinker Drinker P-value
common medical/obstetric
(N = 1,205,399) n (%) (N = 15,911) n (%)
complications among mothers
by prenatal drinking status, Anemia
Missouri, 19892005
Yes 17,420(1.45) 252(1.58) \0.0029
Insulin-dependent diabetes
Yes 8,862(0.74) 49(0.31) \0.0001
Other forms of diabetes
Yes 27,363(2.27) 258(1.62) \0.0001
Chronic hypertension
Yes 11,421(0.95) 119(0.75) \0.0003
Yes 55,600(4.61) 473(2.97) \0.0001
Yes 1,194(0.10) 10(0.06) \0.0029
Placental abruption
Yes 9,152(0.76) 197(1.24) \0.0001
Placenta previa
Yes 4,496(0.37) 86(0.54) \0.0006

Fig. 2 Crude rates of placenta

previa, placental abruption and
composite outcome by prenatal
drinking status, Missouri,

Discussion alcohol use during pregnancy. This discrepancy in results is

not surprising, because unlike our population-based study
The objective of this study was to describe the association with almost complete ascertainment of alcohol use (99%
between alcohol consumption and risk of placental abrup- complete) and adequate sample size, the Kramer et al. [15]
tion and/or placenta previa in a large population-based report was drawn from a relatively small (n = 36,875),
cohort of singleton deliveries (n = 1,221,310). Our prin- hospital-based cohort with substantial missing data for
cipal finding was that mothers who consumed alcohol alcohol use.
during pregnancy were at elevated risk of experiencing The lack of association between alcohol use in preg-
placental abruption, but not placenta previa. This finding is nancy and placenta previa is fairly well-established [8, 10].
consistent with previous reports that alcohol intake during Our inability to demonstrate an association between pla-
pregnancy increases the risk of placental abruption centa previa and prenatal alcohol use is therefore in con-
[1113]. On the other hand, our result is at variance with a formity with this trend. More specifically, the dual finding
cohort study from Canada, in which no significant associ- of an association between prenatal alcohol consumption
ation was observed between placental abruption and and placental abruption, but not placenta previa replicates

Matern Child Health J (2011) 15:670676 675

Table 3 Adjusted odd ratio for the association between prenatal alcohol ingestion and placenta previa and placental abruption
Placenta previa (N = 4,582) Placental abruption (N = 9,349) Composite outcome (N = 13,718)
Number of cases Adj. OR (95% CI) Number of cases Adj. OR (95% CI) Number of cases Adj. OR (95% CI)

Non-drinker N = 4,496 Referent N = 9,152 Referent N = 13,439 Referent

Drinker N = 86 1.19 (0.951.47) N = 197 1.33 (1.161.54) N = 279 1.29 (1.141.45)
Class 1 (12 drinks/week) N = 64 1.11 (0.871.43) N = 144 1.28 (1.081.51) N = 205 1.22 (1.061.41)
Class 2 (34 drinks/week) N = 11 1.37 (0.762.49) N = 19 1.09 (0.691.72) N = 29 1.15 (0.801.67)
Class 3 (C5 drinks/week) N = 11 1.58 (0.872.86) N = 34 1.98 (1.402.80) N = 45 1.89 (1.402.56)
Adj. OR = adjusted odds ratio. Non-drinker: number of drinks per week = 0; drinker: number of drinks per week [ 0. Adjusted estimates were
generated after controlling for the effects of maternal age, parity, race, smoking, education, marital status, adequacy of prenatal care, gender of
the infant and year of birth
P for trend \0.01

findings from a similar large population-based cohort [14] the effect of these factors on risk of placental abruption or
and others [10, 29]. placenta previa in our cohort.
The pathway by which alcohol predisposes to placental The strengths of this study include the large sample size,
abruption is not fully understood, but can be postulated on population-based design and high response rate (*99%
the basis of what we know about the effects of alcohol on complete information on the exposure variable i.e., alcohol
placentation and placental development in animal models. consumption). These merits enhance the external validity of
Alcohol impairs the physiological conversion of uterine our findings and reduce the risk of bias arising from sample
arteries into high-flow, low resistance placental vessels, a selection, a source of concern in data derived from individual
crucial process for adequate placentation and placental health facilities. Another strength is our adjustment for a
development [4, 30]. Alcohol also increases the production wide range of important confounding factors, thereby
of prostaglandins and other inflammatory cytokines [31], ensuring that any associations we detect in this study rep-
which might explain the increased necrosis and thrombi resent independent relationships between the exposure var-
formation seen within the labyrinthine and spongiotroph- iable (prenatal alcohol use) and our defined outcomes.
oblast layers of the alcohol-exposed placenta [4, 32]. The In summary, we found an elevated risk of placental
net effect of these changes would be the creation of an abruption but not placenta previa among women who
environment that is conducive to the detachment of the consumed alcohol during pregnancy. Although our data
placenta before delivery. show that alcohol consumption during pregnancy is
In interpreting the findings from this study, a number of declining there are still many women who fail to abstain
limitations should be considered. Underreporting of alco- during pregnancy thus this information adds to the con-
hol intake is a recognized phenomenon in pregnant women, temporary literature on the detrimental effects of alcohol
especially if ascertainment of alcohol use was based on use in pregnancy and will be useful in screening and
maternal recall in the postnatal period [12, 33]. However, behavioral counseling interventions to combat alcohol use
misclassification of prenatal alcohol use because of retro- by pregnant women and women of childbearing age.
spective data collection is uncommon [3437]. In addition,
the net effect of underreporting would be to bias our results
toward the null. That we still report elevated risks of pla-
cental abruption strengthens the validity of our findings. References
Misclassification of placental abruption and placenta previa
on the birth certificate is also possible, but not highly likely 1. Sokol, R. J., Delaney-Black, V., & Nordstrom, B. (2003). Fetal
[14]. However, as with alcohol use, any misclassification of alcohol spectrum disorder. The journal of the American Medical
Association, 290, 29962999.
placental pathology is likely to be nondifferential and to
2. OLeary, C. M., Nassar, N., Kurinczuk, J. J., & Bower, C. (2009).
yield conservative risk estimates [38]. Another limitation is The effect of maternal alcohol consumption on fetal growth and
our database did not include information on the timing of preterm birth. An international journal of obstetrics and gynae-
alcohol use or pattern of consumption (e.g., binge drink- cology, 116, 390400.
3. Aliyu, M. H., Wilson, R. E., Zoorob, R., Chakrabarty, S., Alio, A.
ing). In addition, risk factors commonly associated with
P., Kirby, R. S., et al. (2008). Alcohol consumption during
alcohol abuse, such as illicit drug use and HIV status, were pregnancy and the risk of early stillbirth among singletons.
also unavailable. We are therefore, unable to comment on Alcohol, 42, 369374.

676 Matern Child Health J (2011) 15:670676

4. Gundogan, F., Elwood, G., Longato, L., Tong, M., Feijoo, A., and risk of stillbirth and death in the first year of life. American
Carlson, R. I., et al. (2008). Impaired placentation in fetal alcohol Journal of Epidemiology, 155, 305312.
syndrome. Placenta, 29, 148157. 22. Herman, A. A., McCarthy, B. J., Bakewell, J. M., et al. (1997). Data
5. Ananth, C. V., & Wilcox, A. J. (2001). Placental abruption and linkage methods used in maternally-linked birth and infant death
perinatal mortality in the United States. American Journal of surveillance data sets from the United States (Georgia, Missouri,
Epidemiology, 153, 332337. Utah and Washington State), Israel, Norway, Scotland and Western
6. Rasmussen, S., Irgens, L. M., & Dalaker, K. (2000). Outcome of Australia. Paediatric and Perinatal Epidemiology, 11, 522.
pregnancies subsequent to placental abruption: a risk assessment. 23. Aliyu, M. H., Wilson, R. E., Zoorob, R., et al. (2009). Prenatal
Acta Obstetricia et Gynecologica Scandinavica, 79, 496501. alcohol consumption and fetal growth restriction: potentiation
7. Salihu, H. M., Bekan, B., Aliyu, M. H., Rouse, D. J., Kirby, R. S., effect by concomitant smoking. Nicotine & Tobacco Research,
& Alexander, G. R. (2005). Perinatal mortality associated with 11, 3643.
abruptio placenta in singletons and multiples. American Journal 24. Alexander, G. R., Himes, J. H., Kaufman, R. B., Mor, J., &
of Obstetrics and Gynecology, 193, 198203. Kogan, M. (1996). A United States national reference for fetal
8. Ananth, C. V., Smulian, J. C., Demissie, K., Vintzileos, A. M., & growth. Obstetrics and Gynecology, 87, 163168.
Knuppel, R. A. (2001). Placental abruption among singleton and 25. Taffel, S., Johnson, D., & Heuser, R. (1982). A method of
twin births in the United States: Risk factor profiles. American imputing length of gestation on birth certificates. Vital and Health
Journal of Epidemiology, 153, 771778. Statistics. Series 2, Data Evaluation and Methods Research, 93,
9. Ananth, C. V., Demissie, K., Smulian, J. C., & Vintzileos, A. M. 111.
(2001). Relationship among placenta previa, fetal growth 26. Alexander, G. R., & Cornely, D. A. (1987). Prenatal care utili-
restriction, and preterm delivery: A population-based study. zation: Its measurement and relationship to pregnancy outcome.
Obstetrics and Gynecology, 98, 299306. American Journal of Preventive Medicine, 3, 243253.
10. Salihu, H. M., Li, Q., Rouse, D. J., & Alexander, G. R. (2003). 27. Alexander, G. R., & Kotelchuck, M. (1996). Quantifying the
Placenta previa: neonatal death after live births in the United adequacy of prenatal care: A comparison of indices. Public
States. American Journal of Obstetrics and Gynecology, 188, Health Reports, 111(5), 408418.
13051309. 28. Clayton, D., & Hills, M. (1993). Statistical models in epidemi-
11. Tikkanen, M., Nuutila, M., Hiilesmaa, V., Paavonen, J., & ology. Oxford: Oxford University Press.
Ylikorkala, O. (2006). Clinical presentation and risk factors of 29. Ananth, C. V., Smulian, J. C., & Vintzileos, A. M. (2003). The
placental abruption. Acta Obstetricia et Gynecologica Scandi- effect of placenta previa on neonatal mortality: A population-
navica, 85, 700705. based study in the United States, 1989 through 1997. American
12. Marbury, M. C., Linn, S., Monson, R., Schoenbaum, S., Journal of Obstetrics and Gynecology, 188, 12991304.
Stubblefield, P. G., & Ryan, K. J. (1983). The association of 30. Naeye, R. L. (1989). Pregnancy hypertension, placental evi-
alcohol consumption with outcome of pregnancy. American dences of low uteroplacental blood flow, and spontaneous pre-
Journal of Public Health, 73, 11651168. mature delivery. Human Pathology, 20, 441444.
13. Halmesmaki, E. (1988). Alcohol counselling of 85 pregnant 31. Ylikorkala, O., Halmesmaki, E., & Viinikka, L. (1988). Urinary
problem drinkers: Effect on drinking and fetal outcome. British prostacyclin and thromboxane metabolites in drinking pregnant
Journal of Obstetrics and Gynaecology, 95, 243247. women and in their infants: Relations to the fetal alcohol effects.
14. Yang, Q., Wen, S. W., Phillips, K., Oppenheimer, L., Black, D., Obstetrics and Gynecology, 71, 6166.
& Walker, M. C. (2009). Comparison of maternal risk factors 32. Jones, P. J., Leichter, J., & Lee, M. (1981). Placental blood flow
between placental abruption and placenta previa. American in rats fed alcohol before and during gestation. Life Sciences, 29,
Journal of Perinatology, 26, 279286. 11531159.
15. Kramer, M. S., Usher, R. H., Pollack, R., Boyd, M., & Usher, S. 33. Little, R. E., Mandell, W., & Schultz, F. A. (1977). Consequences
(1997). Etiologic determinants of abruptio placentae. Obstetrics of retrospective measurement of alcohol consumption. Journal of
and Gynecology, 89, 221226. studies on alcohol, 38, 17771780.
16. Ananth, C. V., Demissie, K., Smulian, J. C., & Vintzileos, A. M. 34. Jacobson, S. W., Chiodo, L. M., Sokol, R. J., & Jacobson, J. L.
(2003). Placenta previa in singleton and twin births in the United (2002). Validity of maternal report of prenatal alcohol, cocaine,
States, 1989 through 1998: A comparison of risk factor profiles and smoking in relation to neurobehavioral outcome. Pediatrics,
and associated conditions. American Journal of Obstetrics and 109, 815825.
Gynecology, 188, 275281. 35. Greene, T., Ernhart, C. B., Martier, S., Sokol, R., & Ager, J.
17. Rasmussen, S., Albrechtsen, S., & Dalaker, K. (2000). Obstetric (1990). Prenatal alcohol exposure and language development.
history and the risk of placenta previa. Acta Obstetricia et Alcoholism, Clinical and Experimental Research, 14, 937945.
Gynecologica Scandinavica, 79, 502507. 36. da Costa Pereira, A., Olsen, J., & Ogston, S. (1993). Variability
18. Iyasu, S., Saftlas, A. K., Rowley, D. L., Koonin, L. M., Lawson, of self reported measures of alcohol consumption: implications
H. W., & Atrash, H. K. (1993). The epidemiology of placenta for the association between drinking in pregnancy and birth
previa in the United States, 1979 through 1987. American Journal weight. Journal of Epidemiology and Community Health, 47,
of Obstetrics and Gynecology, 168, 14241429. 326330.
19. Sheiner, E., Shoham-Vardi, I., Hallak, M., Hershkowitz, R., Katz, 37. Verkerk, P. H., Buitendijk, S. E., & Verloove-Vanhorick, S. P.
M., & Mazor, M. (2001). Placenta previa: Obstetric risk factors (1994). Differential misclassification of alcohol and cigarette
and pregnancy outcome. The Journal of maternal-fetal medicine, consumption by pregnancy outcome. International Journal of
10, 414419. Epidemiology, 23, 12181225.
20. Martin, J., Curtin, S., Saulnier, M., & Mousavi, J. (2003). 38. Morgenstern, H., & Thomas, D. (1993). Principles of study
Development of the matched multiple birth file. 19951998 design in environmental epidemiology. Environmental Health
matched multiple birth dataset. NCHS CD-ROM series 21, no. Perspectives, 101, 2338.
13a. Hyattsville, MD: National Center for Health Statistics.
21. Kensmodel, U., Wisborg, K., Olsen, S. F., Henriksen, T. B., &
Secher, N. J. (2002). Moderate alcohol intake during pregnancy

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