Jensen, Tina K.2; Timmermann, Amalie G.2; Rossing, Laura I.2; Ried-Larsen, Mathias2; Grontved, Anders2; Andersen, Lars B.2; Dalgaard, Christine2; Hansen, Oluf Kristian Højbjerg3; Scheike, Thomas3; Nielsen, Flemming2; Grandjean, Philippe2
1 Section of Biostatistics, Department of Public Health, Faculty of Health and Medical Sciences, Københavns Universitet2 unknown3 Section of Biostatistics, Department of Public Health, Faculty of Health and Medical Sciences, Københavns Universitet
Context: Human exposure to polychlorinated biphenyls (PCBs) has been associated to type 2 diabetes in adults. Objectives: To determine whether concurrent serum PCB concentration was associated with markers of glucose metabolism in healthy children. Design: Cross-sectional study. Settings and participants: A total of 771 healthy Danish third grade school children aged 8-10 years in the municipality of Odense were recruited in 1997 through a two-stage cluster sampling from 25 different schools stratified according to location and socioeconomic character; 509 (9.7±0.8 years, 53% girls) had adequate amounts available for PCB and analyses. Main outcome measures: Fasting plasma glucose and serum insulin were measured and a homeostasis assessment model of insulin resistance (HOMA-IR) and β-cell function (HOMA-B) calculated. Serum PCB congeners and other persistent compounds were measured and ΣPCB calculated. Results: PCBs were present in serum at low concentrations, median 0.19μ g/g lipid (interquartile range, IQR: 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<0.01), compared to the first quintile, but not with plasma glucose (p=0.45). 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 and pp-DDE. Conclusion: A strong inverse association between serum insulin and PCB exposure was found while fasting plasma 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 shown if lower HOMA-B is caused by destruction of β-cell reducing peripheral insulin resistance and thereby increase fasting plasma glucose as previously found.
Journal of Clinical Endocrinology and Metabolism, 2014, Vol 99, Issue 12