Abstract
Many modern pesticides have endocrine disrupting abilities and early-life exposure may affect growth and disease risk later in life. Previously, we reported associations between prenatal pesticide exposure and higher childhood body fat content measured by anthropometry. The associations were affected by child PON1 Q192R genotype. We aimed to study whether prenatal pesticide exposure was still associated with body fat content and distribution in the children at puberty and the potential impact of both maternal and child PON1 Q192R genotype. In this prospective cohort study of 247 children born by occupationally exposed or unexposed women (greenhouse workers and controls) two follow-up examinations (age 10-15 and 11-16years) including simple anthropometry, skinfold measurements, pubertal staging and blood sampling were performed. Total and regional fat% was determined by dual X-ray absorptiometry (DXA) at age 10-15. Prenatal pesticide exposure was associated with increased total, android, and gynoid fat percentage (DXA) at age 10-15years after adjustment for sex, socioeconomic status, and puberty (all β=0.5 standard deviation score (SDS) p<0.05). Stratified by sex, the associations were significant in girls (total fat: β=0.7 SDS, android-gynoid ratio: β=0.1, both p<0.05), but not in boys. Carrying the R-allele (child or mother, separately, or both) augmented the differences between exposed and unexposed children (total fat: β=1.0 SDS, β=0.8 SDS, p<0.05, respectively, and β=1.2 SDS, p<0.01). No exposure-related differences were found if either the child or mother had the QQ wild-type. At age 11-16, exposed children tended to have a higher total fat% estimated by skinfolds than unexposed children (p=0.06). No significant associations between prenatal exposure and body mass index or waist circumference were found. Prenatal pesticide exposure was associated with higher adolescent body fat content, including android fat deposition, independent of puberty. Girls appeared more susceptible than boys. Furthermore, the association depended on maternal and child PON1 Q192R genotype.
Highlights
Endocrine disrupting chemicals (EDCs), including some pesticides, are chemicals that can interfere with the endocrine system
Prenatal pesticide exposure was associated with higher adolescent body fat content, including android fat deposition, independent of puberty
We have reported that the associations between prenatal pesticide exposure and body fat content were found in those children who had a common genetic variant, a glutamine (Q) to arginine (R) substitution, at position 192 in the coding region of the paraoxonase 1 (PON1) gene (Andersen et al, 2012)
Summary
Endocrine disrupting chemicals (EDCs), including some pesticides, are chemicals that can interfere with the endocrine system. Some EDCs may affect endocrine pathways responsible for adipose tissue differentiation (adipogenesis) or endocrine function of adipocytes (secretion of adipocytokines that are key regulators of energy balance and insulin sensitivity) (Janesick et al, 2011). Early-life exposure to such chemicals may alter metabolic programming of adipose tissue with permanent endocrine dysfunction and increased risk of metabolic diseases, including overweight, later in life (Perera et al, 2011;Stel et al, 2015;Tang-Peronard et al, 2011). Higher child- and adulthood body mass index (BMI) has been associated with early-life exposure to persistent organochlorine pesticides such as DDT and hexachlorobenzene (Karmaus et al, 2009;Smink et al, 2008;Valvi et al, 2012) but potential associations between exposure to modern pesticides and adipose tissue accumulation has not been examined. Many modern pesticides have endocrine disrupting abilities and early life exposure may affect growth and disease risk later in life.
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