In my last post, I mentioned the possible role of persistent organic pollutants (POPs) as one of the theories explaining the alarming rise in the incidence of type 1 diabetes around the globe. The effects of environmental chemicals (both natural and human-produced) are of great concern within the endocrine community today. I decided to review the current information about this growing problem more closely, and share my impressions with you. The U.S. environmental protection agency (EPA) website describes POPs as follows:
Persistent organic pollutants (POPs) are toxic chemicals that adversely affect human health and the environment around the world. They persist for long periods of time in the environment and can accumulate and pass from one species to the next through the food chain.
POPs can be produced either by intentionally produced chemicals currently or once used in agriculture, disease control, manufacturing, or industrial processes. OR
POPs can be unintentionally produced by chemicals, such as dioxins, that result from some industrial processes and from combustion.
POPs are lipophilic meaning that they have a strong attraction to fat and accumulate in fat stores in the body. They do not evaporate easily and are resistant to physical or chemical destruction. POPs amass in high concentrations throughout the food web. In other words, they are a force to be reckoned with and can be transported long distances via air, water and migratory species of animals and birds—even into regions where they have never been used before. The half-life (the time required for 50% of the chemical to be completely destroyed) for these chemicals is estimated between an astonishing 7-10 years!
I’ve listed the EPA’s Dirty Dozen POPs from their website here. Most of these compounds were pesticides used in the past. For example, Aldrin, a now prohibited pesticide in the US, was used to kill soil insects such as termites and grasshoppers in order to protect corn and potato crops. Several of these chemicals, such as dioxins, have been widely investigated for links to obesity and diabetes.
The effects of POPs on animals has been known for a while based on information from the US Great Lakes. POPs exposures in animals in that area were associated with reproductive problems and cancer. A recent experimental exposure study in rats using the POP 2,3,7,8-tetrachlorodibenzo-p-dioxin (the main chemical in Agent Orange) yielded interesting results. Rats fed a diet of fish, intentionally contaminated with this POP, had reduced insulin response and production compared to unexposed rats. The implication of the study being that diabetes risk is increased with this POP exposure.
The evidence for the link between POPs and diabetes in humans has not yet been clearly demonstrated. Research studies investigating the link fall between two categories. The first category of studies examined groups of people that have known high POP exposure. The second category of studies looked at a broad, cross-section of the population for abnormal POP levels and diabetes.
A 1997 study focused on veterans exposed to Agent Orange. In a comparison of non-exposed veterans in a similar field of operation, to exposed veterans showed several abnormalities related to diabetes risk including a one and a half fold higher risk for diabetes and a three fold higher risk for abnormal insulin levels. A more recent 2009 study in Taiwan examined people living near a dioxin contaminated industrial site. The study found rising risk for insulin resistance (a risk factor for type 2 diabetes) associated with higher levels of POPs detected in the blood.
A cross-section study associated with the 1999-2002 National Health and Examination Survey (NHANES) analyzed blood concentrations of six different POPs (several from the dirty dozen list above) and the prevalence of diabetes. The incidence of diabetes, mainly type 2 diabetes, was more than five times higher in groups with higher concentrations of POPs. It is important to not that the authors of the cross-sectional paper caution readers that their information doesn’t show a clear cause link between POPs and diabetes.
I maintain a similar opinion regarding POPs and diabetes. The research data on POPs and diabetes risk deals almost exclusively with type 2 diabetes and obesity risk, which are not the same as type 1 diabetes (pediatric) with its autoimmune based destruction of insulin producing beta-cells. I have expanded my knowledge from the research I have done to prepare this post, realize there is still much to learn and understand. I plan to continue to watch, with great interest, as new research is published on the subject of POPs and endocrine health.
In the interest of protecting human health, especially of our youngest population, I encourage efforts in support of limiting the production of new POPs as well as clean-up of existing POPs from the environment. I look forward to hearing from you.