Longitudinal Associations of Exposure to Perfluoroalkylated Substances in Childhood and Adolescence and Indicators of Adiposity and Glucose Metabolism 6 and 12 Years Later: The European Youth Heart Study.

OBJECTIVE: To investigate the long-term association of exposure to perfluoroalkylated substances, including perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA), during childhood (9 years) and adolescence (15 years) on indicators of adiposity and glucose metabolism in adolescence (15 years) and young adulthood (21 years). Secondarily, we aim to clarify the degree of tracking of exposure from childhood into young adulthood. RESEARCH DESIGN AND METHODS: Data derived from a large multicenter prospective cohort study, in which the same participants have been observed from childhood (N = 590), during adolescence (N = 444), and into young adulthood (N = 369). Stored plasma samples were analyzed for PFOS and PFOA. Indicators of adiposity comprising body height, body weight, sum of four skinfolds, and waist circumference, as well as indicators of glucose metabolism, comprising fasting blood glucose, triglyceride, and insulin levels, ß-cell function, and insulin resistance, have been collected at all study waves. Multiple linear regression was applied in order to model earlier exposure on later outcome while controlling for baseline outcome levels, sex, age, and socioeconomic factors. RESULTS: Childhood exposure to PFOS was associated with indicators of adiposity at 15 years of age that are displayed in elevated BMI, skinfold thickness, and waist circumference, as well as increased skinfold thickness and waist circumference at 21 years of age. PFOA exposure in childhood was associated with decreased ß-cell function at 15 years of age. We did not observe associations between exposure during adolescence and indicators of adiposity and glucose metabolism in young adulthood. CONCLUSIONS: This study found evidence for childhood exposure to PFOS and PFOA predicting adiposity at 15 and 21 years of age and impaired ß-cell function at 15 years of age, respectively.

Polychlorinated biphenyl exposure and glucose metabolism in 9-year-old Danish children.

CONTEXT: Human exposure to polychlorinated biphenyls (PCBs) has been associated to type 2 diabetes in adults. OBJECTIVE: We aimed to determine whether concurrent plasma PCB concentration was associated with markers of glucose metabolism in healthy children. SETTING AND DESIGN: Cross-sectional study of 771 healthy Danish third grade school children ages 8-10 years in the municipality of Odense were recruited in 1997 through a two-stage cluster sampling from 25 schools stratified according to location and socioeconomic character; 509 (9.7 ± 0.8 y, 53% girls) had adequate amounts available for PCB analyses. OUTCOME MEASURES: Fasting serum glucose and insulin were measured and a homeostasis assessment model of insulin resistance (HOMA-IR) and ß-cell function (HOMA-B) calculated. Plasma PCB congeners and other persistent compounds were measured and ΣPCB calculated. RESULTS: PCBs were present in plasma at low concentrations, median, 0.19 µg/g lipid (interquartile range, 0.12-0.31). After adjustment for putative confounding factors, the second, third, fourth, and fifth quintiles of total PCB were significantly inversely associated with serum insulin (-14.6%, -21.7%, -18.9%, -23.1%, P trend < .01), compared with the first quintile, but not with serum glucose (P = .45). HOMA-IR and HOMA-B were affected in the same direction due to the declining insulin levels with increasing PCB exposure. Similar results were found for individual PCB congeners, for ßHCB (hexachlorobenzen) and pp-DDE (dichlorodiphenyldichloroethylene). CONCLUSIONS: A strong inverse association between serum insulin and PCB exposure was found while fasting glucose remained within the expected narrow range. Our findings suggest that PCB may not exert effect through decreased peripheral insulin sensitivity, as seen in obese and low-fit children, but rather through a toxicity to ß-cells. It remains to be demonstrated whether lower HOMA-B is caused by destruction of ß-cell-reducing peripheral insulin resistance and thereby increase fasting glucose as previously found.