The Effect of Environmental Chemicals on Insulin Production: Implications for All Types of Diabetes

Sarah Howard
Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group

In a recent review, published in the leading diabetes journal Diabetologia, Hectors et al. (2011) describe how numerous environmental chemicals affect the insulin-producing beta cells of the pancreas. These effects, the authors argue, may be significant in the development of type 2 diabetes. Chemicals like bisphenol A, PCBs, dioxin, organophosphorous pesticides, arsenic, heavy metals, and others, can all affect how the beta cells function, and can interfere with their capacity to secrete insulin.

In type 2 diabetes, both insulin resistance—the body’s inability to respond correctly to insulin—and beta cell malfunction contribute to the disease. The inability of the beta cells to produce enough insulin leads to high blood glucose levels, and eventually diabetes (in many people with type 2, insulin production is higher than normal, to compensate for the insulin resistance—but it is still inadequate to bring blood glucose under control).   

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Dioxin – Scientific Analysis

This letter is reprinted with permission from the Environmental Working Group, a CHE partner. See the original letter with full science analysis on EWG’s website.  

Dr. Timothy Buckley, Chair
Dioxin Review Panel
Science Advisory Board
Environmental Protection Agency (EPA)
Washington, DC

Dear Dr. Buckley,

Twenty-five years after publishing its first assessment of dioxin, a common industrial pollutant and food contaminant, the Environmental Protection Agency (EPA) has yet to establish a safe daily dose for human exposure to this potent chemical.

Dioxin (2,3,7,8-Tetrachlorodibenzo-p-dioxin, also known as 2,3,7,8-TCDD, or TCDD) may well be one of the most-studied of all chemical pollutants. The U.S. National Toxicology Program has listed dioxin as a known human carcinogen since 2001 (NTP 2005), and the U.S. Environmental Protection Agency has proposed to do the same (EPA 2010a). There is a large and persuasive body of research dating from the 1950s showing that dioxin undermines fetal development, damages the reproductive and immune systems and causes severe skin ailments and other disorders.

As U.S. industrial data demonstrate, dioxin is released from municipal waste incinerators; industrial and military hazardous waste treatment facilities; pesticide manufacturing and paper bleaching plants; and a wide range of other industrial processes. In the 1970s, dioxin was identified as a contaminant in Agent Orange, the notorious defoliant deployed by the U.S. during the Vietnam War and blamed for diabetes and other diseases among exposed personnel (Chamie 2008; Cranmer 2000; Gupta 2006).

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State of the Evidence: What Is the Connection between Chemicals & Breast Cancer?

The Breast Cancer Fund and Breast Cancer Action
edited by Nancy Evans

Breast cancer rates have been climbing steadily in the United States and other industrialized countries since the 1940s. Billions of dollars have been spent in an effort to stem this unrelenting tide, yet more than 50 percent of breast cancer cases remain unexplained by the characteristics and risk factors associated with the disease.

Ionizing radiation is the only proven environmental cause of human breast cancer. But powerful circumstantial evidence indicates that some of the 85,000 synthetic chemicals in use today are responsible for many of the unexplained cases of the disease. While scientists have not yet developed an ideal method for linking chemical exposures to breast cancer, several types of research – experimental, body burden and ecological studies – provide strong evidence of the connection between chemicals and breast cancer.

Because the types of evidence vary, the strength of the evidence linking chemicals and breast cancer also varies. The strongest evidence linking chemicals to breast cancer – based on the fact that lifetime exposure to natural estrogens increases the risk of breast cancer – concerns natural and synthetic estrogens, including drugs like diethylstilbestrol (DES), plastic additives like bisphenol-A (BPA), polyvinyl chloride (PVC) (found in many consumer products), dieldrin and some pesticides. Other synthetic substances strongly linked to breast cancer through experimental evidence are organic solvents (used in many manufacturing processes, including the manufacture of computer components), polycyclic aromatic hydrocarbons (PAHs) (created in soot and fumes from burning diesel, fuels or cigarettes) and 1,3 butadiene (a by-product of internal combustion engines).

There are also chemicals for which the evidence indicates a probable but less certain link to breast cancer. These chemicals include dioxin (created when plastics or other materials containing chlorine are burned), the pesticide DDT (dichloro-diphenyl-trichloroethane) and its metabolite DDE, and PCBs (polychlorinated biphenyls), previously used in the manufacture of electrical equipment and other industrial and consumer products.

Finally, there is evidence of chemicals that affect how the body functions in ways that suggest a possible link between these substances and breast cancer. These chemicals include the insecticide heptachlor and phthalates, used to make plastic soft and flexible.

We clearly have major gaps in our current knowledge about the links between breast cancer and the environment. Therefore, we need to focus our research efforts in areas that are most likely to provide useful information for framing public policies related to chemical exposures and our health. The types of research most likely to produce useful evidence will be those examining (1) workplace exposures, (2) household exposures and (3) breast milk as a marker for human contamination.

While we pursue the research that will lead to more definitive answers, the existing evidence linking chemicals to breast cancer demands that we act now as a society to begin removing many of these substances from our environment. Considerable resources are spent encouraging women to make changes in their personal lives in an effort to reduce their risk of breast cancer. But breast cancer is not just a personal tragedy; it is a public health crisis that demands action by society as a whole.

This crisis must be addressed by beginning now to implement the precautionary principle. Under this principle, evidence of harm, rather than definitive proof of harm, is the trigger for policy action. In addition, the precautionary principle mandates that the burden of proof with regard to chemicals rests with the manufacturers to demonstrate that the substances are safe, rather than with the public to show that they are harmful. Finally, the precautionary principle rests on the democratic principle that government officials are obligated to serve the public’s interest in human health and environmental protection.

The following 5-point plan will help us reduce the risk of breast cancer and ultimately end the epidemic:

  1. PHASE OUT TOXIC CHEMICALS that are omnipresent in the lives of so many people.
  2. ENACT “SUNSHINE” LAWS AND ENFORCE EXISTING ENVIRONMENTAL PROTECTION LAWS to reduce the use of toxics by requiring companies to report how many tons of chemicals they use.
  3. PRACTICE HEALTHY PURCHASING, with local, state and federal governments leading the way in purchasing environmentally preferable products, thereby creating an example for individuals to follow.
  4. OFFER CORPORATE INCENTIVES that encourage businesses to eliminate the use of harmful chemicals in their products and processes.
  5. MONITOR BREAST MILK through a comprehensive community program that identifies the chemicals present in breast milk, establishes links to geographic areas and initiates a plan to eliminate these contaminants.

We ignore at our peril the increasing evidence that chemicals are contributing to the rising tide of breast cancer. The obligation to understand this evidence, and begin to address it through the implementation of public policies that put health first, rests with all of us. It is in our power to change the course we are on. Now is the time.

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