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Early-life exposures to persistent organic pollutants in relation to overweight in preschool children.

ABSTRACT: Current knowledge on obesogenic effects of persistent organic pollutants (POPs) is equivocal. We therefore evaluated the associations between early-life POP exposures and body mass index (BMI) in 444 Faroese children born in 2007-2009. POPs were measured in maternal 2-week postpartum serum and child age-5 serum. Linear regression and generalised linear models assessed the associations with continuous and dichotomous BMI z-scores, respectively, at ages 18 months and/or 5 years. Maternal serum concentrations of HCB, PFOS and PFOA were associated with increased BMI z-scores and/or overweight risk (i.e. BMI z-score?85th WHO percentile). No clear association was found for maternal serum-PCBs, p,p'-DDE, PFHxS, PFNA and PFDA. In cross-sectional analyses, we observed a pattern of inverse associations between child serum-POPs and BMI z-scores at age 5, perhaps due to reverse causation that requires attention in future prospective analyses. Findings in this recent cohort support a role of maternal exposure to endocrine disruptors in the childhood obesity epidemic.

SUBMITTER: Karlsen M

PROVIDER: S-EPMC5290287 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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Early-life exposures to persistent organic pollutants in relation to overweight in preschool children.

Karlsen Martina M Grandjean Philippe P Weihe Pal P Steuerwald Ulrike U Oulhote Youssef Y Valvi Damaskini D

Reproductive toxicology (Elmsford, N.Y.) 20160803

Current knowledge on obesogenic effects of persistent organic pollutants (POPs) is equivocal. We therefore evaluated the associations between early-life POP exposures and body mass index (BMI) in 444 Faroese children born in 2007-2009. POPs were measured in maternal 2-week postpartum serum and child age-5 serum. Linear regression and generalised linear models assessed the associations with continuous and dichotomous BMI z-scores, respectively, at ages 18 months and/or 5 years. Maternal serum con ...[more]

PMID: 27496715

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Project description:The incidence of neurodevelopmental and neurodegenerative diseases worldwide has dramatically increased over the last decades. Although the aetiology remains uncertain, evidence is now growing that exposure to persistent organic pollutants during sensitive neurodevelopmental periods such as early life may be a strong risk factor, predisposing the individual to disease development later in life. Epidemiological studies have associated environmentally persistent organic pollutant exposure to brain disorders including neuropathies, cognitive, motor, and sensory impairments; neurodevelopmental disorders such as autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD); and neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). In many ways, this expands the classical "Developmental Origins of Health and Disease" paradigm to include exposure to pollutants. This model has been refined over the years to give the current "three-hit" model that considers the individual's genetic factors as a first "hit." It has an immediate interaction with the early-life exposome (including persistent organic pollutants) that can be considered to be a second "hit." Together, these first two "hits" produce a quiescent or latent phenotype, most probably encoded in the epigenome, which has become susceptible to a third environmental "hit" in later life. It is only after the third "hit" that the increased risk of disease symptoms is crystallised. However, if the individual is exposed to a different environment in later life, they would be expected to remain healthy. In this review, we examine the effect of exposure to persistent organic pollutants and particulate matters in early life and the relationship to subsequent neurodevelopmental and neurodegenerative disorders. The roles of those environmental factors which may affect epigenetic DNA methylation and therefore influence normal neurodevelopment are then evaluated.

Project description:ObjectiveEndocrine-disrupting chemicals (EDCs) adversely affect human health. Our objective was to determine the association of EDC exposure with earlier age of menopause.MethodsCross-sectional survey using National Health and Nutrition Examination Survey (NHANES) data from 1999 to 2008 (n = 31,575 females). Eligible participants included: menopausal women >30 years of age; not currently pregnant, breastfeeding, using hormonal contraception; no history of bilateral oophorectomy or hysterectomy. Exposures, defined by serum lipid and urine creatinine-adjusted measures of EDCs, data were analyzed: > 90th percentile of the EDC distribution among all women, log-transformed EDC level, and decile of EDC level. Multi linear regression models considered complex survey design characteristics and adjusted for age, race/ethnicity, smoking, body mass index. EDCs were stratified into long (>1 year), short, and unknown half-lives; principle analyses were performed on those with long half-lives as well as phthalates, known reproductive toxicants. Secondary analysis determined whether the odds of being menopausal increased with EDC exposure among women aged 45-55 years.FindingsThis analysis examined 111 EDCs and focused on known reproductive toxicants or chemicals with half-lives >1 year. Women with high levels of ?-hexachlorocyclohexane, mirex, p,p'-DDE, 1,2,3,4,6,7,8-heptachlorodibenzofuran, mono-(2-ethyl-5-hydroxyhexyl) and mono-(2-ethyl-5-oxohexyl) phthalate, polychlorinated biphenyl congeners -70, -99, -105, -118, -138, -153, -156, -170, and -183 had mean ages of menopause 1.9 to 3.8 years earlier than women with lower levels of these chemicals. EDC-exposed women were up to 6 times more likely to be menopausal than non-exposed women.ConclusionsThis study of a representative sample of US women documents an association between EDCs and earlier age at menopause. We identified 15 EDCs that warrant closer evaluation because of their persistence and potential detrimental effects on ovarian function. Earlier menopause can alter the quantity and quality of a woman's life and has profound implications for fertility, human reproduction, and our global society.

Project description:BackgroundAnimal and human studies suggest certain persistent organic pollutants (POPs) may impact glucose metabolism; however, few epidemiologic studies have examined environmental determinants of glycemic outcomes during pregnancy. Our objective is to evaluate associations between exposures to individual and mixture of POPs and measures of prenatal fasting glucose, insulin, and insulin resistance during pregnancy in overweight women.MethodsA cohort of overweight and obese pregnant women (N = 95) was recruited from California. Blood samples were collected during late first or second trimester (median = 16 weeks' gestation; range = 10-24 weeks). Exposures included serum concentrations of polybrominated diphenyl ethers (PBDEs) and hydroxylated metabolites (OH-PBDEs), polychlorinated biphenyls (PCBs), and poly- and perfluoroalkyl substances (PFASs). Outcomes included serum concentrations of fasting plasma glucose, fasting plasma insulin, and calculated homeostatic model assessment of insulin resistance (HOMA-IR). Generalized linear models were used to evaluate cross-sectional associations between individual and aggregate POPs and mean percent difference in fasting glucose, fasting insulin, and HOMA-IR. Bayesian kernel machine regression (BKMR) was used to assess the relative importance of each exposure to the association with our outcomes, using conditional and group posterior inclusion probabilities (PIPs).ResultsStudy participants were racially/ethnically diverse and nearly half were below the federal poverty level. Across PBDEs and OH-PBDEs, the direction of associations with fasting glucose, fasting insulin and HOMA-IR were varied. A doubling of PCB-138, PCB-153, PCB-180, and ∑PCBs concentrations was associated with a 2.10% mmol/L (95%CI: 0.49%, 3.74%), 2.10% mmol/L (95%CI: -0.14%, 4.39%), 2.10% mmol/L (95%CI: 0.12%, 4.12%), and 2.81% mmol/L (95%CI: 0.38%, 5.31%) increase in fasting glucose, respectively. Exposure to individual PCBs was positively associated with both fasting insulin and HOMA-IR. All PFAS were inversely associated with fasting glucose, fasting insulin, and HOMA-IR. In BKMR models of fasting glucose, all four chemical classes were important contributors to the overall mixture, with PFASs identified as the most important contributor.DiscussionPrenatal PCB exposure was positively associated while certain PBDE and PFAS analytes were inversely associated with fasting glucose concentrations in overweight women. Further examination of the relationship between POPs exposure and glycemic functioning in a larger study population of women during pregnancy is warranted.

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Early-life exposures to persistent organic pollutants in relation to overweight in preschool children.

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Early-life exposures to persistent organic pollutants in relation to overweight in preschool children.

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