Maternal levels of dichlorodiphenyl-dichloroethylene (DDE) may increase weight and body mass index in adult female offspring

Wilfried Karmaus ^1*, Janet Rose Osuch ², Ihuoma Eneli ³, Lanay M Mudd ², Jessica Zhang ¹, Dorota Mikucki ², Pam Haan ² and Susan Davis ²

¹ University of South Carolina, United States
² Michigan State University, United States
³ Ohio State University, United States

^* To whom correspondence should be addressed. E-mail: karmaus{at}sc.edu.

Accepted 29 August 2008

Abstract

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: From the female parental generation (n=391) in the Michigan fisheater cohort, most of whom had repeated DDE and PCB determinations between 1973 and 1991, 259 mothers participated. We estimated prenatal exposure to PCBs and DDE by extrapolating maternal measurements to the time that the women gave birth. We identified 213 daughters who were 20-50 years of age in 2000. Of these, 83% 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 measures we used generalized estimating equations nested for repeated measurements (2001/02 and 2006/07) and for sharing the same mother. We controlled for maternal height and BMI and for daughters’ characteristics including age, birth weight, having been breastfed, and number of pregnancies.

Results: Maternal height and BMI were significant predictors of their daughters’ height, weight, and BMI. Low birth weight (<2,500 g) was significantly associated with reduced adult offspring weight and BMI. 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 below 1.502 µg/L, there was an increase in offspring BMI of 1.65 when prenatal DDE levels were between 1.502 – 2.9 µg/L and an increase of 2.88 if maternal serum DDE was greater than 2.9 µg/L. Prenatal PCB levels showed no effect.

Conclusion: Prenatal exposure to the estrogenic endocrine-disrupting chemical DDE may be one of the factors contributing to the epidemic of obesity in women.