Roles of Environmental Pollution and Pesticides in Diabetes and Obesity: The Epidemiological Evidence

Abstract There are several factors that contribute to the development of type 2 diabetes, such as obesity, sedentary lifestyle, and family history, which are widely accepted in the medical community. However, the role of environmental contaminants or pollutants in diabetes is not yet well understood. The strongest body of epidemiological evidence is that linking certain persistent organic pollutants (POPs) to diabetes. POPs include dioxins, furans, polychlorinated biphenyls (PCBs) and organochlorine pesticides. A metaanalysis of six studies of dioxins and furans produced a relative risk (RR) of 1.91 (95% CI 1.44–2.54) for diabetes when comparing the highest category versus the lowest category. A metaanalysis of 13 cross-sectional studies of PCBs and diabetes produced an RR of 2.90 (95% CI 2.14–3.92), and a metaanalysis of 8 prospective studies of PCBs and diabetes produced an RR of 1.65 (95% CI 1.16–2.34). Comparing the top versus the bottom tertile, a metaanalysis of any organochlorine pesticide and diabetes in 22 studies found a summary odds ratio of 1.68 (95% CI 1.37–2.07). Bisphenol A (BPA) is an endocrine disrupter that is found in many consumer products; human exposure is believed to be mainly from food product packaging containing BPA. A metaanalysis of BPA and type 2 diabetes, using five studies, produced a summary RR of 1.45 (95% CI 1.13–1.87) comparing the fourth quartile with the first quartile of urinary BPA. Phthalates are chemicals added to plastics to increase their flexibility, transparency, durability, and longevity. A metaanalysis of four studies produced a summary RR of 1.48 (95% CI 0.98–2.25) for diabetes when comparing the highest category of total phthalates with the lowest category. Although this summary RR is not significant, there is evidence that some individual phthalate metabolites are related to diabetes. Other environmental pollutants that have been studied include carbon monoxide, lead, nitrogen dioxide, ozone, particulate matter and sulfur dioxide in air pollution, and toxic heavy metals such as arsenic, cadmium, and mercury. Notably, a metaanalysis of 12 studies of arsenic in drinking water and type 2 diabetes had a pooled RR of 1.75 (95% CI 1.20–2.54). There is growing support for the “developmental obesogen” theory. It promotes the concept that certain chemicals may be capable of disrupting developmental processes related to metabolic homeostasis during early life and thus increasing the risk for obesity and other related metabolic diseases. However, most of the work relating environmental pollutants to obesity has produced inconsistent results. An exception is DDE (dichlorodiphenyldichloroethylene), a metabolite of dichlorodiphenyltrichloroethane. For DDE, there are seven studies showing positive associations with adiposity and two studies having null relationships.