Chemicals as an emerging risk factor in developing type-2 diabetes: a short history

February 21, 2011 at 5:17 pm | Posted in Feature Articles | 3 Comments

“… obese persons that do not have elevated POPs are not at elevated risk of diabetes, suggesting that the POPs rather than the obesity per se is responsible for the association.

Evidence is emerging that persistent organic pollutants, even at background levels in populations, act in conjunction with obesity to cause type-2 diabetes.

You may be surprised by these words, written by Professor David Carpenter, Director of the Institute for Health and the Environment at the University of Albany, New York, in a review summarising the significance of studies examining a potential role for environmental pollutants in the onset of type-2 diabetes (Carpenter 2008).

In England, approximately 5% of men and 4% of women have been diagnosed with diabetes (Health Survey for England). In some states of the US, as much as 12.7% of the adult population is diagnosed as diabetic (Kaiser State Health Facts). Because many cases of diabetes go undiagnosed, the real incidence rates are thought to be higher.

Diabetes is a group of metabolic diseases in which a person’s blood sugar levels are too high. There are two main types of diabetes. Type-1 diabetes results from the body’s failure to produce insulin. Type-2 diabetes results from cells in the body losing the ability to respond to insulin, and is sometimes combined with insufficient insulin production.

Type-1 diabetes is caused by an autoimmune reaction that results in the destruction of the insulin-producing cells in the pancreas. It tends to develop early in life and is much rarer than type-2 diabetes. Type-2 diabetes becomes more common as people grow older.

Type-2 diabetes is of particular concern because incidence of the condition is increasing at an alarming rate. Although confirmatory data is not yet available, risk projections (Zimmet et al. 2001) have estimated that between 2001 and 2010, global incidence rates could have increased by 46%. North America could see an increase of 23%, Latin America of 44% and Africa of 50%.

There is also evidence that the age of onset for type-2 diabetes is coming down. Mean age at diagnosis in the US decreased from 52.0 to 46.0 years between 1988 and 2000 (Koopman et al. 2005). It was already clear by 2001 that type-2 diabetes was no longer an adult disease, with children as young as eight years old being diagnosed (Brosnan et al. 2001).

Going beyond the established risk factors

The main factors identified as responsible for diabetes are an aging population with a genetic predisposition towards diabetes, combined with changes associated with a so-called “modern” lifestyle such as low physical activity, obesity and eating more foods high in animal fats.

Human epidemiological studies are, however, challenging the completeness of this picture of the causes of the disease: researchers are finding consistent correlations between an elevated risk of type-2 diabetes and the presence in people of persistent organic pollutants (POPs) such as DDT, PCBs and dioxins. An earlier study found that levels of PCBs among subjects with diabetes were 30% higher than in the control subjects (Longnecker et al. 2001).

In 2006 Professor Duk-Hee Lee of the School of Medicine at Kyungpook National University, Korea, pushed the hypothesis further. On the basis of her own research finding “unusually strong” associations between POPs exposure and diabetes (Lee et al. 2006a), Lee speculated that obesity may not be sufficient for developing type-2 diabetes but, in addition, exposure to POPs was necessary to initiate the disease (Lee et al. 2006b). These levels could be as low as the background levels to which everyone is already exposed.

Because Lee’s epidemiological research at the time was only cross-sectional, however, she could not at that time draw any conclusions about the direction of causation: either elevated POPs levels caused diabetes in obese people, or obese people with diabetes metabolised POPs differently leading to elevated levels of the chemicals in their body. Which it was, Lee could not say. Indeed, before 2006 not one single prospective study had been carried out to test whether or not body burden of POPs was associated with type-2 diabetes.

Since 2006 three studies have confirmed the direction of causation, showing that POPs exposure in obese people causes type-2 diabetes, rather than the other way around. These are a study conducted by the U.S. Centers for Disease Control and Prevention, which found people with the highest levels of exposure to six POPs were 38 times more likely to have diabetes than those with the lowest exposure (Turyk et al. 2009), a study by Lee herself (Lee et al. 2010) and a further study of Swedish women (Rignell-Hydbom et al. 2009).

The need to reduce POPs exposure in food

Lee’s 2010 study is arguably the most provocative. Besides providing evidence that type-2 diabetes is caused by more factors than obesity alone, if correct then her findings have two profound implications: firstly, that current type-2 diabetes epidemiology may be badly confounded by POPs exposure; and secondly, that extremely low concentrations of pollutants are sufficient to initiate diabetes in obese people.

The implications are related because Lee found that exposure to background levels of POPs is sufficient to substantially raise the risk of diabetes. “The problem is the doses are so low that the control groups used in the epidemiological studies are already being exposed to levels of POPs which significantly increase the risk of developing diabetes,” explains Carpenter.

This would mean that current epidemiology which associates obesity with type-2 diabetes is not able to rule out a causal role for POPs. Instead, it can only tell us that obesity raises risk in conjunction with whatever factors (such as POPs exposure) occur simultaneously in obese people. If such a role could be confirmed, it would amount to a significant breakthrough in understanding the causes of diabetes and mark out a clear course of action.

Carpenter believes that heritage contaminants such as PCBs are still present at extraordinarily high levels, even though they were banned as long as 40 years ago, and points to food as the major source of exposure.

POPs such as PCBs, flame retardants and dioxins are recirculated in commercial food production through animal feed, as animals and fish are fed animal and fish fats to accelerate growth. Fish oils and fish meals are the animal feeds most heavily contaminated with dioxin, followed by animal fats, according to the EU Feeding Fats Safety research project.

As a result, animal foods contribute 80% to total human dioxin exposure and are the primary route for dioxin into food systems. As a result the EU is currently funding research into reducing POPs load in animal feed. There is already evidence that switching to purified feed can reduce POPs levels in salmon by 51-82% (Berntssen et al. 2010), while switching to non-animal feeds would likely be even more effective in reducing human exposure to POPs.

Absence of medical attention

The precise extent of the contribution of POPs to diabetes is not yet known. However, Carpenter says: “There aren’t any very good explanations for the marked increase in diabetes, except it is paralleled by the rise in obesity. If one accepts that obesity is not the only risk factor, then the […] emerging issue of chemicals that might promote diabetes or obesity looks interesting.”

Given the pressure rising rates of diabetes are already exerting on healthcare, coupled with the looming threat of an aging population for which this problem is only likely to get worse, one could ask why the issue is not yet widely discussed?

“In general it is very hard to get this sort of thing published in the medical literature,” says Carpenter. “The clinical community needs to understand there are about 12 compelling studies in the area.”

For now, Lee’s two papers from 2006 are almost the only ones published in medical journals; most studies looking at the issue are published in environmental health journals, and these do not have wide readership among the medical community.

“Most physicians are so busy treating patients they don’t give a thought to what might have caused diabetes; they think someone who has diabetes has just not exercised and has eaten too much,” says Carpenter, who has a medical degree himself. “They have no understanding of the role of these chemical exposures: education about chemicals as potential causes of diabetes for physicians is absolutely critical.”


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  1. I agree that this is an important topic that should get more attention. The National Toxicology Program recently held a workshop on the role of environmental chemicals in the development of diabetes and obesity, and reviewed the scientific evidence for a possible link (online at The chemicals of concern are not only POPs but also bisphenol A, heavy metals, phthalates, and other endocrine disrupting compounds.

    I also summarize the evidence linking diabetes to chemicals at my website,

    Note that there are a few inaccuracies in the article above, specifically in the paragraph beginning with “Since 2006…” The CDC did not conduct any of these studies; some of Dr. Lee’s studies were based on CDC data. The “38 times more likely” number is from Lee’s original 2006 study. Dr. Turyk did her own study, finding DDE associated with diabetes development over time. But otherwise, the points are valid, and the evidence is growing.

    The Collaborative on Health and the Environment will be following up on this issue: see and please email me if you would like to learn more or be involved (see my website).

    • Thanks very much for posting the clarifications. It’s good to hear that CHE will be following up on this – we’ll look forward to that. As for other chemicals, we will likely return to this issue in the near future – there was simply too much to cover in one piece so we focused in on POPs. We’ll be in touch, I’m sure!

  2. The issue of a diabetes epidemic has some characteristics like that of the cancer epidemic. It is a chronic, noninfectious disease which used to be rare. The evidence is finally being taken seriously that much of the cancer epidemic can be blamed on toxic exposures, and I suspect that logically the same is true of diabetes. Likewise, autism — for the same reasons, and probably ADHD too. Unfortunately the polluters hold the power here, as does the pharmaceutical industry which rakes in the profits from both epidemics, guaranteeing there won’t be swift action to address the problem.

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