Exposure to Tobacco Smoke in Utero and Subsequent Plasma Lipids, ApoB, and CRP among Adult Women in the MoBa Cohort
Lea A. Cupul‑Uicab,1 Rolv Skjaerven,2,3 Kjell Haug,2 Gregory S. Travlos,4 Ralph E. Wilson,4 Merete Eggesbø,5 Jane A. Hoppin,1 Kristina W. Whitworth,1 and Matthew P. Longnecker1
1Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA; 2Department of Public Health and Primary Health Care, University of Bergen, Bergen, Norway; 3Medical Birth Registry of Norway, Norwegian Institute of Public Health, Bergen, Norway; 4Cellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA; 5Department of Genes and Environment, Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway
Background: Recent findings suggest that maternal smoking during pregnancy may play a role in the development of metabolic alterations in offspring during childhood. However, whether such exposure increases the risk of developing similar metabolic alterations during adulthood is uncertain.
Objective: We evaluated the association of in utero exposure to maternal tobacco smoke with plasma lipids, apolipoprotein B (apoB), and C-reactive protein (CRP) in adulthood.
Methods: The study was based on a subsample of the Norwegian Mother and Child Cohort Study (MoBa) and included 479 pregnant women with plasma lipids, apoB, and CRP measurements. Information on in utero exposure to tobacco smoke, personal smoking, and other factors were obtained from the women by a self-completed questionnaire at enrollment, at approximately 17 weeks of gestation.
Results: Women exposed to tobacco smoke in utero had higher triglycerides [10.7% higher; 95% confidence interval (CI): 3.9, 17.9] and lower high-density lipoprotein cholesterol (HDL) (–1.9 mg/dL; 95% CI: –4.3, 0.5) compared with unexposed women, after adjusting for age, physical activity, education, personal smoking, and current body mass index (BMI). Exposed women were also more likely to have triglycerides ≥ 200 mg/dL [adjusted odds ratio (aOR) = 2.5; 95% CI: 1.3, 5.1] and HDL < 50 mg/dL (aOR = 2.3; 95% CI: 1.1, 5.0). Low-density lipoprotein cholesterol, total cholesterol, and apoB were not associated with the exposure. CRP was increased among exposed women; however, after adjustment for BMI, the association was completely attenuated.
Conclusions: In this population, in utero exposure to tobacco smoke was associated with high triglycerides and low HDL in adulthood, 18–44 years after exposure.
Key words: clinical chemistry, C-reactive protein, metabolic syndrome, plasma lipids, prenatal exposure delayed effects, smoking, women.
Environ Health Perspect 120:1532–1537 (2012). http://dx.doi.org/10.1289/ehp.1104563 [Online 19 July 2012]
Address correspondence to L.A. Cupul-Uicab, National Institute of Environmental Health Sciences, MD A3-05, 111 TW Alexander Dr., Research Triangle Park, NC 27709 USA. Telephone: (919) 541-3630. Fax: (919) 541-2511. E-mail: email@example.com
Supplemental Material is available online (http://dx.doi.org/10.1289/ehp.1104563).
We are grateful to all the participating families in Norway who take part in this ongoing cohort study.
This research was supported in part by the Intramural Research Program of the National Institutes of Health (NIH), National Institute of Environmental Health Sciences (NIEHS). The Norwegian Mother and Child Cohort Study is supported by the Norwegian Ministry of Health, contract N01-ES-75558 with the NIH/NIEHS, NIH/National Institute of Neurological Disorders and Stroke (grant 1 UO1 NS 047537-01), and the Norwegian Research Council/FUGE (grant 151918/S10).
The authors declare they have no actual or potential competing financial interests.
Received 30 September 2011; Accepted 19 July 2012; Online 19 July 2012.
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