Exposure to persistent organic pollutants as potential risk factors for developing diabetes

Abstract

Persistent organic pollutants (POPs), such as dioxins, polychlorinated biphenyls (PCBs), and organochlorine pesticides (OCPs), which are synthetic chemicals or by-products with an intrinsic resistance to natural degradation processes, are released into the environment, resulting in the widespread dispersal and accumulation in the environment, as well as in human and ecological food chains. Due to their ubiquity in the environment and lipophilic properties, there is emerging concern over the potential risks of human exposure to POPs. Extensive growing evidence indicated that exposure to POPs might be strongly associated with increased risk of a worldwide epidemic of diabetes, especially type 2 diabetes, suggesting that POPs might play a key role in their pathogenesis. Based on summary of the related studies, this paper reviews the epidemiologic and experimental data that addresses the association between increased risk of diabetes and POP exposure, including dioxins, PCBs, OCPs, polybrominated flame retardants (PBFRs), and some environmental estrogens. The potential mechanisms whereby POPs cause diabetes were discussed, such as alterations in lipid metabolism, in glucose transport, in insulin signaling pathway, in steroid metabolism, and disruption of endocrine system, induction of tumor necrosis factor-α (TNF-α). However, with respect to diabetes, some of the evidence on POPs linked to risk of diabetes was suggestive of a direct or indirect association but was limited or inconclusive. Future research is urgently needed for determining the relative contribution of POPs to diabetes and elucidating the exact mechanisms.