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

Abstract

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 β-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 βHCB (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 β-cells. It remains to be demonstrated whether lower HOMA-B is caused by destruction of β-cell-reducing peripheral insulin resistance and thereby increase fasting glucose as previously found.