Maternal levels of dichlorodiphenyl-dichloroethylene (DDE) may increase weight and body mass index in adult female offspring
- 1Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, South Carolina, USA
- 2Departments of Surgery and Epidemiology, College of Human Medicine, Michigan State University, East Lansing, Michigan, USA
- 3Center for Healthy Weight and Nutrition, Department of Pediatrics, Nationwide Children’s Hospital, The Ohio State University, Columbus, Ohio, USA
- Dr Wilfried Karmaus, Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, 800 Sumter Street, Columbia, SC 29208-0001, USA;
- Accepted 29 August 2008
- Published Online First 5 December 2008
Objectives: To investigate the effect of prenatal exposure to polychlorinated biphenyls (PCBs) and dichlorodiphenyl-dichloroethylene (DDE) on weight, height and body mass index (BMI) in adult female offspring of the Michigan fisheater cohort examined between 1973 and 1991.
Methods: 259 mothers from the Michigan fisheater cohort were studied. Prenatal exposure to PCBs and DDE was estimated by extrapolating maternal measurements to the time that the women gave birth. 213 daughters aged 20–50 years in 2000 were identified and 83% of them participated in at least one of two repeated investigations in 2001/02 (n = 151) and 2006/07 (n = 129). To assess the effect of prenatal PCB and DDE exposure on anthropometric measurements, generalised estimating equations nested for repeated measurements (2001/02 and 2006/07) and for sharing the same mother were used. We controlled for maternal height and BMI and for daughters’ age, birth weight, having been breastfed and number of pregnancies.
Results: Maternal height and BMI were significant predictors of the daughters’ height, weight and BMI. Low birth weight (<2500 g) was significantly associated with reduced adult offspring weight and BMI. The weight and BMI of adult offspring were statistically significantly associated with the extrapolated prenatal DDE levels of their mothers. Controlling for confounders and compared to maternal DDE levels of <1.503 μg/l, offspring BMI was increased by 1.65 when prenatal DDE levels were 1.503–2.9 μg/l and by 2.88 if levels were >2.9 μg/l. Prenatal PCB levels showed no effect.
Conclusion: Prenatal exposure to the oestrogenic endocrine-disrupting chemical DDE may contribute to the obesity epidemic in women.
Funding: This research was supported by a grant from the Agency for Toxic Substances and Disease Registry (H75/ATH582536, R01 TS000007 and R01 TS000069)
Competing interests: None.