Objective Relationships were examined between persistent organic pollutants (POPs) and incident type 2 diabetes, end-stage renal disease (ESRD) and mortality.
Methods In a nested case–control study, 300 persons without diabetes had baseline examinations between 1969 and 1974; 149 developed diabetes (cases) and 151 remained non-diabetic (controls) during 8.0 and 23.1 years of follow-up, respectively. POPs were measured at baseline. ORs for diabetes were computed by logistic regression analysis. The cases were followed from diabetes onset to ESRD, death or 2013. HRs for ESRD and mortality were computed by cause-specific hazard models. Patterns of association were explored using principal components analysis.
Results PCB151 increased the odds for incident diabetes, whereas hexachlorobenzene (HCB) was protective after adjusting for age, sex, body mass index, sample storage characteristics, glucose and lipid levels. Associations between incident diabetes and polychlorinatedbiphenyl (PCB) or persistent pesticide (PST) components were mostly positive but non-significant. Among the cases, 29 developed ESRD and 48 died without ESRD. PCB28, PCB49 and PCB44 increased the risk of ESRD after adjusting for baseline demographic and clinical characteristics. Several PCBs and PSTs increased the risk of death without ESRD. The principal components analysis identified PCBs with low-chlorine load positively associated with ESRD and death without ESRD, and several PSTs associated with death without ESRD.
Conclusions Most POPs were positively but not significantly associated with incident diabetes. PCB151 was significantly predictive and HCB was significantly protective for diabetes. Among participants with diabetes, low-chlorine PCBs increase the risk of ESRD and death without ESRD, whereas several PSTs predict death without ESRD.
- Diabetes mellitus
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Parts of this article were presented at the 72nd Scientific Sessions of the American Diabetes Association, June 8–12, 2012, Philadelphia, Pennsylvania.
Contributors BAG, MEP, CCM, RGN and DEW contributed to the study design, data analysis, data interpretation and manuscript preparation. BAG, MEP, RGN and KMB contributed to manuscript preparation. RLH and WCK contributed to the study design, data interpretation and manuscript preparation. MEP is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Funding This work was supported by the Intramural Program of the National Institute of Diabetes and Digestive and Kidney Diseases and by an inter-agency agreement between the Centers for Disease Control and Prevention and the National Institute of Diabetes and Digestive and Kidney Diseases (094FED4907651).
Disclaimer The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the National Institutes of Health or the Centers for Disease Control and Prevention.
Competing interests None declared.
Patient consent Each participant gave informed consent or assent.
Provenance and peer review Not commissioned; externally peer reviewed.
Correction notice This paper has been updated since it first published online. In table 1 the median age for the control group has been corrected to 21.0 (15.2-37.3).
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