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Polychlorinated biphenyl exposure and glucose metabolism in 9-year-old Danish children
Tina K Jensen1, Amalie G Timmermann, Laura I Rossing
1Department of Environmental Medicine (T.K.J., A.G.T., L.I.R., C.D., F.N., P.G.), Department of Sports Science and Clinical Biomechanics (M.R.L., A.G., L.B.A.), Institute of Public Health, University of Southern Denmark, DK-5000 Odense C, Denmark; and Department of Biostatistics (O.H.H., T.S.), University of Copenhagen, DK-1165 Copenhagen, Denmark.
Insights
Polychlorinated biphenyls (PCBs) exposure in children was inversely associated with serum insulin levels, not fasting glucose. This suggests PCBs may impact beta-cell function rather than insulin sensitivity.
Area of Science:
- Environmental Health
- Pediatric Endocrinology
- Toxicology
Background:
- Human exposure to polychlorinated biphenyls (PCBs) is linked to type 2 diabetes in adults.
- Investigating PCB effects on glucose metabolism in children is crucial for understanding long-term health risks.
Purpose of the Study:
- To determine the association between plasma PCB concentration and glucose metabolism markers in healthy children.
- To explore potential links between PCB exposure and insulin resistance or beta-cell function.
Main Methods:
- A cross-sectional study of 509 healthy Danish children aged 8-10 years.
- Measured plasma PCB congeners, serum glucose, and insulin.
- Calculated homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-B).
Main Results:
- PCBs were detected at low concentrations in children's plasma.
- Higher PCB levels showed a significant inverse association with serum insulin, but not fasting glucose.
- HOMA-B was inversely affected by increasing PCB exposure, suggesting potential beta-cell toxicity.
Conclusions:
- PCB exposure in children is strongly associated with lower serum insulin levels.
- Findings suggest PCBs may impair beta-cell function rather than peripheral insulin sensitivity.
- Further research is needed to confirm the impact of PCBs on beta-cell function and its long-term consequences.
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.
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