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Environmental Tobacco Smoke and Risk of Spontaneous Abortion

George, Lena*; Granath, Fredrik†; Johansson, Anna L. V.*; Annerén, Göran‡; Cnattingius, Sven*

doi: 10.1097/01.ede.0000229984.53726.33
Original Article

Background: Studies of exposure to environmental tobacco smoke (ETS) and risk of spontaneous abortion are limited to a few studies of self-reported exposure, and the results have been inconsistent. The aim of this study was to investigate risk of early spontaneous abortion related to ETS and active smoking as defined by plasma cotinine levels.

Methods: We conducted a population-based case–control study in Uppsala County, Sweden, between January 1996 and December 1998. Cases were 463 women with spontaneous abortion at 6 to 12 completed weeks of gestation, and controls were 864 pregnant women matched to cases according to the week of gestation. Exposure status was defined by plasma cotinine concentrations: nonexposed, <0.1 ng/mL; ETS-exposed, 0.1–15 ng/mL; and exposed to active smoking, >15 ng/mL. Multivariable analysis was used to estimate the relative risk of spontaneous abortion associated with exposure to ETS and active smoking.

Results: Nineteen percent of controls and 24% of cases were classified as having been exposed to ETS. Compared with nonexposed women, risk of spontaneous abortion was increased among both ETS-exposed women (adjusted odds ratio = 1.67; 95% confidence interval = 1.17–2.38) and active smokers (2.11; 1.36–3.27). We could not show a differential effect of exposure to ETS or active smoking between normal and abnormal fetal karyotype abortions.

Conclusions: Nonsmoking pregnant women exposed to ETS may be at increased risk of spontaneous abortion. Given the high prevalence of ETS exposure, the public health consequences of passive smoking regarding early fetal loss may be substantial.

From the *Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; the †Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden; and the ‡Department of Clinical Genetics, The Rudbeck Laboratory, Uppsala University Children's Hospital, Uppsala, Sweden.

Submitted 2 January 2006; accepted 15 May 2006.

Supported by the International Epidemiology Institute through a grant from the National Soft Drink Association.

Editors’ note: A commentary on this article appears on page 492.

Correspondence: Lena George, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, PO Box 281, SE-171 77 Stockholm, Sweden. E-mail:

© 2006 Lippincott Williams & Wilkins, Inc.