Abstract
BackgroundPrenatal exposure to persistent organic pollutants (POPs), may influence offspring weight gain. More prospective epidemiological studies are needed to compliment the growing body of evidence from animal studies.MethodsSerum from 412 pregnant Norwegian and Swedish women participating in a Scandinavian prospective cohort study were collected in 1986–88, and analyses of two perfluoroalkyl substances (PFASs) and five organochlorines (OCs) were conducted. We used linear and logistic regression models with 95% confidence intervals (CIs) to evaluate the associations between maternal serum POP concentrations at 17–20 weeks of gestation and child overweight/obesity (body mass index (BMI) ≥ 85th percentile) at 5-year follow-up. Results were further stratified by country after testing for effect modification. We also assessed potential non-monotonic dose-response (NMDR) relationships.ResultsIn adjusted linear models, we observed increased BMI-for-age-and-sex z-score (β = 0.18, 95% CI: 0.01–0.35), and increased triceps skinfold z-score (β = 0.15, 95% CI: 0.02–0.27) in children at 5-year follow-up per ln-unit increase in maternal serum perfluorooctane sulfonate (PFOS) concentrations. We observed increased odds for child overweight/obesity (BMI ≥ 85th percentile) for each ln-unit increase in maternal serum PFOS levels (adjusted OR: 2.04, 95% CI: 1.11–3.74), with stronger odds among Norwegian children (OR: 2.96, 95% CI: 1.42–6.15). We found similar associations between maternal serum perfluorooctanoate (PFOA) concentrations and child overweight/obesity. We found indications of NMDR relationships between PFOS and polychlorinated biphenyl (PCB) 153 and child overweight/obesity among Swedish children.ConclusionWe found positive associations between maternal serum PFAS concentrations and child overweight/obesity at 5-year follow-up, particularly among Norwegian participants. We observed some evidence for NMDR relationships among Swedish participants.
Highlights
Prenatal exposure to persistent organic pollutants (POPs), may influence offspring weight gain
We aimed to evaluate the associations between maternal serum POP concentrations in early pregnancy and offspring anthropometry, including child overweight/obesity at 5-year follow-up
All high-risk pregnancies resulting in an small for gestational age (SGA) birth, and a 10% random sample of the study population were invited for follow-up when children were five years of age (n = 791)
Summary
Prenatal exposure to persistent organic pollutants (POPs), may influence offspring weight gain. From 1990 to 2010, the global estimated prevalence of overweight and obesity among preschool children increased from 4.2% to 6.7% [1]. This trend is expected to continue, and the World Health Organization (WHO) predicts that 60 million preschool children worldwide (9.1%) will be overweight or obese by 2020 [1]. An increasing body of evidence suggests that in utero exposure to endocrine disrupting chemicals (EDCs) may contribute to obesity development in children and adults [3, 4]. Animal and in vitro studies suggest that EDCs may cause obesity through interference with lipid metabolism to promote fat storage, by altering the metabolic set points, or modifying hormonal control of appetite and satiety [4]. Obesity may be programmed in the intrauterine period, and fetal exposure to certain EDCs may modify the epigenome of stem cells to preferentially produce more adipocytes at the cost of bone [5]
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