Skip Navigation


American Journal of Epidemiology Advance Access originally published online on June 4, 2007
American Journal of Epidemiology 2007 166(3):289-295; doi:10.1093/aje/kwm073
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
166/3/289    most recent
kwm073v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (5)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ananth, C. V.
Right arrow Articles by Cnattingius, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ananth, C. V.
Right arrow Articles by Cnattingius, S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

American Journal of Epidemiology © The Author 2007. Published by the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

ORIGINAL CONTRIBUTIONS

Influence of Maternal Smoking on Placental Abruption in Successive Pregnancies: A Population-based Prospective Cohort Study in Sweden

Cande V. Ananth1 and Sven Cnattingius2

1 Division of Epidemiology and Biostatistics, Department of Obstetrics, Gynecology, and Reproductive Sciences, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ
2 Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden

Correspondence to Professor Cande V. Ananth, Division of Epidemiology and Biostatistics, Department of Obstetrics, Gynecology, and Reproductive Sciences, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, 125 Paterson Street, New Brunswick, NJ 08901 (e-mail: cande.ananth{at}umdnj.edu).

Received for publication December 15, 2006. Accepted for publication January 31, 2007.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
The authors examined associations between cumulative smoking during a woman's first and second pregnancies and risk of placental abruption in the second pregnancy. They performed a population-based prospective cohort study of 526,690 women who delivered their first two consecutive singletons in Sweden in 1983–2001. Using logistic regression models, the authors found that, among women without placental abruption in the first pregnancy, smoking was associated with increased risk of abruption in the second pregnancy; however, this effect was confined to exposure occurring during the second pregnancy (adjusted odds ratio (OR) = 1.8, 95% confidence interval (CI): 1.4, 2.3) but not the first (adjusted OR = 1.1, 95% CI: 0.9, 1.3). Among women with a prior abruption, the risk of repeating abruption was increased irrespective of smoking habits. When women smoked during both pregnancies, there was an almost 11-fold increase in risk (adjusted OR = 10.9, 95% CI: 7.3, 16.3). These findings suggest that women who quit smoking before pregnancy may benefit from reduced risk of abruption. The observation that the recurrence of abruption is substantially increased regardless of changes in smoking habits suggests that factors other than smoking may influence the recurrence of placental abruption.

abruptio placentae; pregnancy; recurrence; risk; smoking


Abbreviations: ICD, International Classification of Diseases; SGA, small-for-gestational-age


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Approximately 10–20 percent of women in industrialized countries smoke during their pregnancies. During the past several decades, smoking during pregnancy has remained one of the most consistently reported—and modifiable—risk factors for an array of maternal and perinatal outcomes, including restricted fetal growth, preterm delivery, and placental abruption (1, 2).

Placental abruption is a devastating obstetric complication that is associated with excessively high rates of stillbirth, preterm birth, and reduced fetal growth (39). While the etiology of abruption remains largely speculative, risk factors associated with it include advanced maternal age, multiparity, cocaine use during pregnancy, preeclampsia, intrauterine infection, oligohydramnios, prolonged rupture of membranes, and prior abruption (818). Smoking during pregnancy has also been shown to be associated with abruption; relative risks range from 1.5 to 2.5, with a strong dose-dependent relation with amount smoked per day (1, 8, 17, 19, 20).

It remains unknown whether the toxic effect of maternal smoking on abruption risk is restricted to the pregnancy during which the mother smokes (i.e., a direct effect) or whether cumulative exposure to smoking across pregnancies confers increased risk (i.e., a cumulative effect). We tested these hypotheses in a large cohort of over half a million women with two consecutive singleton births.


    MATERIALS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Study design and cohort composition
The Swedish Medical Birth Register includes information prospectively collected during pregnancy, delivery, and the neonatal period on virtually all births in Sweden. From 1983 through 2001, 1.9 million singleton births were recorded in the Swedish Birth Register. Each woman is assigned a unique national registration number, enabling linkage of successive births to each woman within the register. Data on sociodemographic characteristics, reproductive history, and complications during pregnancy, delivery, and the neonatal period are prospectively collected beginning with the first antenatal visit. These data are forwarded to the Birth Register through copies of standardized individual antenatal, obstetric, and pediatric records. The current study was restricted to women who had delivered their first two consecutive singletons (526,690 women).

Data on smoking were ascertained by a midwife at the woman's first prenatal care visit, which occurs before the 15th week of gestation in over 95 percent of the pregnancies in Sweden (21). Mothers were categorized with regard to self-reported smoking as nonsmokers (including nondaily smoking), moderate smokers (1–9 cigarettes/day), or heavy smokers (≥10 cigarettes/day). Maternal age at first delivery was categorized as <25, 25–29, 30–34, or ≥35 years. Through linkage with the Education Register, number of years of formal education completed as of December 2001 was obtained from Statistics Sweden, and education was categorized as ≤11 years and ≥12 years. Interpregnancy interval was calculated as the number of months between the birth of the first child and the estimated date of conception of the following child, and was categorized as <5, 6–11, 12–23, 24–35, 36–47, or ≥48 completed months.

Gestational age was largely based on early second-trimester ultrasound examination, when available, or was estimated from the date of the last menstrual period. Early ultrasound examination gradually became increasingly common in Sweden during the 1980s and has been offered to all pregnant women since 1990. Approximately 95 percent of the women accept this procedure (22).

Complications arising during pregnancy and delivery were classified according to the International Classification of Diseases (ICD), Eighth (1983–1986), Ninth (1987–1996), or Tenth (since 1997) revision. Placental abruption was defined using ICD-8 codes 632.1 and 651.4, ICD-9 code 641C, and ICD-10 code O45; preeclampsia was defined using ICD-9 codes 642E–H and ICD-10 codes O11 and O14; and pregestational diabetes was defined using ICD-9 code 648A and ICD-10 codes O24.0–O24.3. Since the ICD-8 did not permit separation of nonproteinuric gestational hypertension from proteinuric gestational hypertension or separation of pregestational diabetes from gestational diabetes, we were unable to define preeclampsia or pregestational diabetes for births occurring between 1983 and 1986.

The study was approved by the ethics research committee at the Karolinska Institutet, Stockholm, Sweden.

Statistical analysis
Associations between maternal smoking and risk of abruption in the second pregnancy were evaluated using smoking as both an indicator (smoker or nonsmoker) and an ordinal factor categorized as nonsmoker, moderate smoker, and heavy smoker. We evaluated whether the association between smoking and abruption risk in the second pregnancy was one of a "direct" effect (i.e., confined to smoking exposure in the second pregnancy) or whether cumulative exposure (i.e., smoking in both the first and the second pregnancies) was associated with increased risk. This was accomplished by comparing risks with women categorized as a nonsmoker in both pregnancies (reference group), a smoker in the first pregnancy but not in the second pregnancy, a nonsmoker in the first pregnancy but a smoker in the second pregnancy, or a smoker in both pregnancies.

We used logistic regression analyses to evaluate associations between smoking habits and abruption risk. Odds ratios and 95 percent confidence intervals were derived from these models and were used to approximate relative risks. These logistic regression models were adjusted for two sets of factors: 1) covariates that included maternal age, education, interpregnancy interval, country of birth, and year of second delivery and 2) all of the confounders listed above, plus preeclampsia and pregestational diabetes in the second pregnancy and perinatal outcomes in the first pregnancy. Country of birth, obtained through linkage to the Migration Register, was stratified into Sweden, other Nordic countries (Denmark, Norway, Finland, and Iceland), and non-Nordic countries. To account for temporal changes in smoking prevalence and abruption, we adjusted all analyses by year of the second birth (grouped as 1983–1989, 1990–1993, 1994–1997, and 1998–2001).

Fetal and infant outcomes in the first pregnancy were hierarchically grouped as follows: 1) stillbirths occurring at ≥28 weeks; 2) very preterm (gestational age <32 weeks) small-for-gestational-age (SGA) births; 3) moderately preterm (gestational age 32–36 weeks) SGA births; 4) full-term (gestational age ≥37 weeks) SGA births; 5) very preterm non-SGA births; 6) moderately preterm non-SGA births; and 7) full-term non-SGA births. SGA birth was defined as a birth weight less than two standard deviations below the mean for gestational age, based on the Swedish reference curve (23).


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Rates of placental abruption in the first and second pregnancies were 0.49 percent and 0.41 percent, respectively. Women with an abruption in their first pregnancy were at a greater than 11-fold increased risk (odds ratio = 11.6, 95 percent confidence interval: 9.5, 14.1) of developing a recurrent abruption (table 1).


View this table:
[in this window]
[in a new window]

 
TABLE 1. Characteristics of women who delivered their first two singleton infants and associations with the risk of placental abruption in the second pregnancy, Sweden, 1983–2001

 
The association between changes in smoking habits in the first and second pregnancies and risk of placental abruption in the second pregnancy is shown in table 2. The effect of smoking on risk of abruption in the second pregnancy was largely confined to smoking in the second pregnancy. In comparison with women who were nonsmokers in both pregnancies, the risk of abruption in the second pregnancy increased with the amount smoked during the second pregnancy. Women who quit smoking before the second pregnancy had risks for abruption similar to those of women who were nonsmokers in both pregnancies.


View this table:
[in this window]
[in a new window]

 
TABLE 2. Smoking habits in two successive pregnancies and risk of placental abruption in the second pregnancy, Sweden, 1983–2001

 
We examined whether the association between maternal smoking habits in successive pregnancies and placental abruption in the second pregnancy persisted among women who did and did not experience abruption in their first pregnancy (table 3). Among women with no abruption in their first pregnancy, the risk of abruption in the second pregnancy increased when women initiated smoking in their second pregnancy or smoked during both pregnancies (as compared with nonsmoking in both pregnancies), while women who stopped smoking during their second pregnancy were not at increased risk of placental abruption. In contrast, among women who experienced abruption in the first pregnancy, the risk of recurrent abruption was high regardless of smoking habits in either the first or the second pregnancy. However, if women smoked during both their first and second pregnancies, the risk of abruption in the second pregnancy was almost 11-fold higher (odds ratio = 10.9, percent confidence interval: 7.3, 16.3) in comparison with women who remained nonsmokers in both of their pregnancies. Although these associations were significant, they deserve cautious interpretation owing to the fairly wide confidence intervals.


View this table:
[in this window]
[in a new window]

 
TABLE 3. Smoking habits in two successive pregnancies and risk of placental abruption in the second pregnancy among women with and without abruption in the first pregnancy, Sweden, 1983–2001

 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
We found that the risk of abruption in the second pregnancy is reduced when women quit smoking between their first and second pregnancies and is increased when women start smoking. These findings indicate that the adverse effect of maternal smoking on abruption risk is largely confined to a direct toxic effect of smoking exposure during pregnancy. Among women with a history of abruption, the risk of recurrent abruption is increased dramatically, even among nonsmokers and women who quit smoking, suggesting that other, unobserved determinants shape the risk of recurrent placental abruption.

In previous studies, investigators have consistently reported dose-response relations between maternal smoking and risk of abruption (1, 6, 8, 12). We found that a change in exposure to tobacco smoke between pregnancies influences the risk of abruption. The reduced risk of abruption in the second pregnancy when women stopped smoking between their first and second pregnancies suggests that the effect of maternal smoking on abruption risk is one that is probably transient.

Biologic interpretations
Microscopic studies of the placenta have suggested that tobacco use leads to vasoconstriction of the arterioles and placental underperfusion surrounding the site of implantation (24, 25). These two processes result in rigidity in arteries and consequently lead to decidual and maternal floor infarctions and hemorrhage, and eventually to abruption (26).

Biases and limitations
The findings of our study warrant some caution in interpretation, owing to a few limitations. Foremost among them is the fact that details regarding smoking habits, although ascertained prior to any untoward pregnancy outcome, were based entirely on maternal self-reporting early in pregnancy. Widely publicized information on the harmful effects of smoking may have caused some women to underreport their smoking (27). Furthermore, some smokers may have falsely reported that they were nonsmokers, and others may have quit smoking after their first prenatal care visit, after information about smoking was recorded (28). If anything, these limitations would have led to an underestimation of smoking-related risk of placental abruption. On the other hand, if a woman reported that she was a smoker early in pregnancy and then quit smoking shortly thereafter, this may have led to overestimation of the effects of smoking on abruption risk. Residual confounding due to unmeasured factors (e.g., passive exposure to tobacco smoke and use of drugs) may also have influenced our findings.

The validity of the diagnosis of placental abruption may be a concern. In Sweden, the definition of abruption is entrusted to clinicians. We are unaware of whether the low prevalence of reported abruption in the first and second pregnancies reflects the possibility that abruption is relatively less common in Sweden than in other countries (11, 29) or reflects a low sensitivity of the diagnosis. However, a quality study of the Swedish Medical Birth Registry showed minimal variability across hospitals with respect to the prevalence of abruption (30). More importantly, a previous validation study carried out in Sweden reported good correspondence between the diagnosis of abruption as reported by ICD codes and the clinical picture of abruption as documented in individual delivery records (31). The diagnosis of abruption in this study was based on ICD codes, and different versions of the ICD (ICD-8 through ICD-10) have been used over the years. However, we did not find that the prevalence of abruption was markedly influenced by year of birth, which also was included as a covariate in the analyses.

Strengths
The population-based nature of this study permits generalizability of findings across Sweden and perhaps to other countries as well. Since all Swedish residents have a unique national registration number, successive linkage of individual information from first pregnancies to second pregnancies was virtually complete. The population of pregnant women in Sweden is fairly homogeneous, with widespread availability of and access to prenatal care, which is regularly used by the vast majority of women (30). Ascertainment of smoking data and other data collection efforts were accomplished prospectively, precluding recall and selection biases.

The observation of an increased risk of recurrent abruption among women who stopped smoking during the second pregnancy, in comparison with women who were nonsmokers in both pregnancies, is intriguing. This suggests that other, unobserved factors—factors stronger than maternal smoking—may influence the risk of recurrent abruption. In searching for other causes of placental abruption, a strong genetic predisposition is one that may explain the 11-fold increased risk of recurrence of placental abruption (3234). Although large-scale studies evaluating a genetic predisposition to abruption are largely lacking, a study of maternal and fetal genes and imprinting of paternal alleles, as well as genetic effects modified through environmental exposures, may yield informative data on the problem of recurrent abruption.

Conclusions
These findings strongly suggest that there is a causal association between maternal smoking during pregnancy and risk of placental abruption. These data lend credence to the interpretation that the adverse impact of maternal smoking on increased risk of abruption is largely confined to the pregnancy in which the exposure occurs. Among women with no placental abruption in the first pregnancy, the observation that the risk of abruption in the second pregnancy diminishes when women quit smoking between pregnancies is encouraging. While primary prevention of smoking is best, intensive efforts to promulgate information regarding the harmful consequences of smoking in human reproduction should be encouraged.


    ACKNOWLEDGMENTS
 
This study was supported by grants from the Karolinska Institutet. Dr. Cande V. Ananth was partially supported by a grant (HD038902) from the US National Institutes of Health.

The authors thank Gunnar Petersson for providing the data set and Drs. Darios Getahun, Morgan R. Peltier, John C. Smulian, and Anthony Vintzileos for their comments on the manuscript.

Conflict of interest: none declared.


    References
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

  1. Ananth CV, Savitz DA, Luther ER. Maternal cigarette smoking as a risk factor for placental abruption, placenta previa, and uterine bleeding in pregnancy. Am J Epidemiol (1996) 144:881–9.[Abstract/Free Full Text]
  2. Ananth CV, Savitz DA, Williams MA. Placental abruption and its association with hypertension and prolonged rupture of membranes: a methodologic review and meta-analysis. Obstet Gynecol (1996) 88:309–18.[CrossRef][Web of Science][Medline]
  3. Ananth CV, Berkowitz GS, Savitz DA, et al. Placental abruption and adverse perinatal outcomes. JAMA (1999) 282:1646–51.[Abstract/Free Full Text]
  4. Ananth CV, Smulian JC, Srinivas N, et al. Risk of infant mortality among twins in relation to placental abruption: contributions of preterm birth and restricted fetal growth. Twin Res Hum Genet (2005) 8:524–31.[CrossRef][Web of Science][Medline]
  5. Ananth CV, Wilcox AJ. Placental abruption and perinatal mortality in the United States. Am J Epidemiol (2001) 153:332–7.[Abstract/Free Full Text]
  6. Kyrklund-Blomberg NB, Gennser G, Cnattingius S. Placental abruption and perinatal death. Paediatr Perinat Epidemiol (2001) 15:290–7.[CrossRef][Web of Science][Medline]
  7. Rasmussen S, Irgens LM, Bergsjo P, et al. Perinatal mortality and case fatality after placental abruption in Norway 1967 –1991. Acta Obstet Gynecol Scand (1996) 75:229–34.[Web of Science][Medline]
  8. Raymond EG, Mills JL. Placental abruption. Maternal risk factors and associated fetal conditions. Acta Obstet Gynecol Scand (1993) 72:633–9.[Web of Science][Medline]
  9. Kramer MS, Usher RH, Pollack R, et al. Etiologic determinants of abruptio placentae. Obstet Gynecol (1997) 89:221–6.[CrossRef][Web of Science][Medline]
  10. Ananth CV, Oyelese Y, Srinivas N, et al. Preterm premature rupture of membranes, intrauterine infection, and oligohydramnios: risk factors for placental abruption. Obstet Gynecol (2004) 104:71–7.[CrossRef][Web of Science][Medline]
  11. Ananth CV, Oyelese Y, Yeo L, et al. Placental abruption in the United States, 1979 through 2001: temporal trends and potential determinants. Am J Obstet Gynecol (2005) 192:191–8.[CrossRef][Web of Science][Medline]
  12. Ananth CV, Smulian JC, Demissie K, et al. Placental abruption among singleton and twin births in the United States: risk factor profiles. Am J Epidemiol (2001) 153:771–8.[Abstract/Free Full Text]
  13. Brink AL, Odendaal HJ. Risk factors for abruptio placentae. S Afr Med J (1987) 72:250–2.[Web of Science][Medline]
  14. Rasmussen S, Irgens LM, Dalaker K. A history of placental dysfunction and risk of placental abruption. Paediatr Perinat Epidemiol (1999) 13:9–21.[CrossRef][Web of Science][Medline]
  15. Rasmussen S, Irgens LM, Dalaker K. Outcome of pregnancies subsequent to placental abruption: a risk assessment. Acta Obstet Gynecol Scand (2000) 79:496–501.[CrossRef][Web of Science][Medline]
  16. Williams MA, Lieberman E, Mittendorf R, et al. Risk factors for abruptio placentae. Am J Epidemiol (1991) 134:965–72.[Abstract/Free Full Text]
  17. Williams MA, Mittendorf R, Monson RR. Chronic hypertension, cigarette smoking, and abruptio placentae. Epidemiology (1991) 2:450–3.[Web of Science][Medline]
  18. Lockwood CJ, Toti P, Arcuri F, et al. Mechanisms of abruption-induced premature rupture of the fetal membranes: thrombin-enhanced interleukin-8 expression in term decidua. Am J Pathol (2005) 167:1443–9.[Abstract/Free Full Text]
  19. Misra DP, Ananth CV. Risk factor profiles of placental abruption in first and second pregnancies: heterogeneous etiologies. J Clin Epidemiol (1999) 52:453–61.[CrossRef][Web of Science][Medline]
  20. Mortensen JT, Thulstrup AM, Larsen H, et al. Smoking, sex of the offspring, and risk of placental abruption, placenta previa, and preeclampsia: a population-based cohort study. Acta Obstet Gynecol Scand (2001) 80:894–8.[CrossRef][Web of Science][Medline]
  21. Lindmark G, Cnattingius S. The scientific basis of antenatal care. Report from a state-of-the-art conference. Acta Obstet Gynecol Scand (1991) 70:105–9.[Medline]
  22. Hogberg U, Larsson N. Early dating by ultrasound and perinatal outcome. A cohort study. Acta Obstet Gynecol Scand (1997) 76:907–12.[Web of Science][Medline]
  23. Marsal K, Persson PH, Larsen T, et al. Intrauterine growth curves based on ultrasonically estimated foetal weights. Acta Paediatr (1996) 85:843–8.[Web of Science][Medline]
  24. Christianson RE. Gross differences observed in the placentas of smokers and nonsmokers. Am J Epidemiol (1979) 110:178–87.[Abstract/Free Full Text]
  25. Spira A, Philippe E, Spira N, et al. Smoking during pregnancy and placental pathology. Biomedicine (1977) 27:266–70.[Web of Science][Medline]
  26. Ananth CV, Oyelese Y, Prasad V, et al. Evidence of placental abruption as a chronic process: associations with vaginal bleeding early in pregnancy and placental lesions. Eur J Obstet Gynecol Reprod Biol (2006) 128:15–21.[CrossRef][Web of Science][Medline]
  27. Lindqvist R, Aberg H. Locus of control in relation to smoking cessation during pregnancy. Scand J Public Health (2002) 30:30–5.[CrossRef][Web of Science][Medline]
  28. Cnattingius S. The epidemiology of smoking during pregnancy: smoking prevalence, maternal characteristics, and pregnancy outcomes. Nicotine Tob Res (2004) 6(suppl 2):S125–40.[Abstract]
  29. Rasmussen S, Irgens LM, Bergsjo P, et al. The occurrence of placental abruption in Norway 1967 –1991. Acta Obstet Gynecol Scand (1996) 75:222–8.[Web of Science][Medline]
  30. Cnattingius S, Ericson A, Gunnarskog J, et al. A quality study of a medical birth registry. Scand J Soc Med (1990) 18:143–8.[Web of Science][Medline]
  31. Karegard M, Gennser G. Incidence and recurrence rate of abruptio placentae in Sweden. Obstet Gynecol (1986) 67:523–8.[Web of Science][Medline]
  32. Kupferminc MJ. Thrombophilia and pregnancy. Curr Pharm Des (2005) 11:735–48.[CrossRef][Web of Science][Medline]
  33. Mousa HA, Alfirevic Z. Do placental lesions reflect thrombophilia state in women with adverse pregnancy outcome? Hum Reprod (2000) 15:1830–3.[Abstract/Free Full Text]
  34. Mousa HA, Alfirevic Z. Thrombophilia and adverse pregnancy outcome. Croat Med J (2001) 42:135–45.[Web of Science][Medline]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Am J EpidemiolHome page
S. M. Engel, T. M. Janevic, C. R. Stein, and D. A. Savitz
Maternal Smoking, Preeclampsia, and Infant Health Outcomes in New York City, 1995-2003
Am. J. Epidemiol., January 1, 2009; 169(1): 33 - 40.
[Abstract] [Full Text] [PDF]


Home page
Am J EpidemiolHome page
R. M. Nilsen, S. E. Vollset, S. A. Rasmussen, P. M. Ueland, and A. K. Daltveit
Folic Acid and Multivitamin Supplement Use and Risk of Placental Abruption: A Population-based Registry Study
Am. J. Epidemiol., April 1, 2008; 167(7): 867 - 874.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
166/3/289    most recent
kwm073v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (5)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ananth, C. V.
Right arrow Articles by Cnattingius, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ananth, C. V.
Right arrow Articles by Cnattingius, S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?