Prenatal Exposure to Persistent Organic Pollutants and Risk of Obesity in the Offspring: RHEA Mother-Child Cohort in Crete, Greece

Abstract

Background: The environmental obesogen hypothesis suggests that prenatal or early life exposure to certain endocrine disrupting chemicals such as persistent organic pollutants (POPs) may cause permanent physiological changes predisposing to later increased fat mass and obesity. Aims: We examined whether in utero exposure to low levels of different POPs is associated with postnatal growth and obesity rates in preschool children in the RHEA mother-child cohort in Crete, Greece. Methods: We included 700 mothers and their children from the Rhea study. Concentrations of several polychlorinated biphenyls (PCBs) and other organochlorine compounds (dichlorodiphenyl dichloroethene [DDE], and hexachlorobenzene [HCB]) were determined in 1st trimester maternal serum by triple quadrupole mass spectrometry. Rapid growth at the first 6 months of life was defined as a weight gain Z score >0.67. Age- and sex-specific Z scores for body mass index (BMI) were calculated at 4 years. Abdominal obesity was defined as waist circumference =90th percentile of national reference curves. Multiple linear and log Poisson regression models were used to examine the associations between exposures and continuous and binary outcomes respectively. Results: 36% of the children were rapid growers at 6 months and 21% were overweight/obese at 4 years. Geometric mean HCB, DDE and PCBs serum concentrations in pregnant women were 89, 2036 and 319 pg/ml respectively. Prenatal HCB exposure was associated with both increased risk of rapid growth at the first 6 months of life (RR= 1.97 [95% CI: 1.01 to 3.85] and overweight/obesity at 4 years (RR= 1.13 [95% CI: 0.98 to 1.30]. Prenatal DDE exposure was associated with increased risk of abdominal obesity at 4 years of age (RR= 2.09 [95% CI: 1.04 to 4.21]. Prenatal exposure to PCBs was not related to any of the examined outcomes. Conclusions: Prenatal exposure to even low levels of DDE and HCB may increase the risk of rapid postnatal growth and obesity in childhood.