Do you know how many chemicals are in your body? At what levels? Probably not. Every two years, the U.S. Centers for Disease Control and Prevention measures the levels of some environmental contaminants in a group of people that represent the general U.S. population, and publishes its findings in the National Report on Human Exposures to Environmental Chemicals. For most of the chemicals measured, so little research has been done on them that we do not know if the exposures found constitute a health concern. The most recent report (from 2009) confirms widespread exposure to some commonly used industrial chemicals, including many discussed here. Note that this project only tests for a couple of hundred contaminants; over 80,000 chemicals are in use in the U.S., and approximately 1000-2000 new ones are introduced each year. The U.S. government does not require safety testing for new or existing chemicals, and we know very little about how they act in combination with each other. Of critical concern is the ability of chemicals to cross the placenta and influence fetal development (Vandenberg et al. 2009). Alarmingly, 99-100% of the pregnant women in this CDC sample have measurable levels of certain PCBs, organochlorine pesticides, PFCs, phenols, PBDEs, phthalates, polycyclic aromatic hydrocarbons (PAHs) and perchlorate in their bodies (Woodruff et al. 2011).

 

Scientists have long suspected that environmental toxicants could be involved in the development of type 1 diabetes, in part because certain drugs and chemicals could cause diabetes in laboratory animals. They have used these drugs, such as alloxan, streptozotocin (STZ), and cyclophosphamide to induce diabetes in animals for laboratory studies. Some other drugs have also been linked to the development of type 1 diabetes in humans. One example of a chemical inducing insulin-dependent diabetes in humans is the now-banned rat poison Vacor. In the late 1970s, a few people tried to kill themselves by eating Vacor, and ended up with diabetes instead. All of these compounds destroy beta cells, but all act via different mechanisms (Kraine and Tisch 1999). Vacor and STZ both target beta cells, but have also been found linked to type 1-related autoimmunity: Vacor in humans (Karam et al 1980) and STZ in primates (Wei et al 2011). Numerous environmental chemicals can target beta cells (Hectors et al 2011); can they somehow provoke an autoimmune attack? We don't know.

 

Surprisingly, only a very few studies have directly examined the ability of the contaminants we encounter in the environment to affect the development of type 1 diabetes (Howard and Lee 2011). Thus, for many contaminants described here, I also included studies associating them with other related diseases, such as gestational and type 2 diabetes or other autoimmune diseases. And, I incuded information on contaminants and how they can influence other factors that may influence the development of type 1 diabetes, such as increased insulin resistance or weight gain. I have also included information on contaminants that produce effects in the laboratory that could have ramifications for the development of type 1 diabetes, such as by inducing or accelerating autoimmunity, or affecting beta cells.

 

Sharp (2009) reviews the evidence that environmental toxics may contribute to the development of type 2 diabetes, focusing on Canadian Aboriginal people. Yet this review would be of interest to other communities, and may also be relevant for type 1. He concludes that some toxic chemicals interfere with the functioning of the beta cells, and affect insulin production, and that obesity is also linked to toxics (see the height and weight page). The accepted risk factors for diabetes, inculding diet, lifestyle, and genetics, do not fully explain the high rates of diabetes in First Nation peoples.

 

The evidence for individual contaminants or groups of contaminants is summarized on separate pages, organized by type of contaminant. The site navigation tool to the side or the links to the subpages below provide access to the individual pages.

The following list is a summary of the studies described on the specific contaminant pages. Please note that some of these associations have only been found in one or two studies; further research is required to confirm them. Further research is also necessary to look for any possible causes and effects, since "correlation does not imply causation." These associations, however, might provide suggestions as to which contaminants should be included in studies of type 1 diabetes.

    some air pollutants, PCBs, nitrate/nitrite/N-nitroso compounds, some heavy metals, radiation

    some air pollutants, arsenic, bisphenol A, cadmium, some pesticides, some persistent organic pollutants (including dioxin and PCBs), some flame retardants, selenium, phthalates, radiation

    some air pollutants, some phthalates, some persistent organic pollutants (including dioxin and PCBs), mercury, radiation

    some phthalates, some persistent organic pollutants, some heavy metals

    bisphenol A, some heavy metals, some phthalates, trichloroethylene, some persistent organic pollutants (including dioxin), nitrate/nitrite

    arsenic, bisphenol A and nonylphenol, cadmium, PCBs, dioxin, nitrate/nitrite, phthalates

    some air pollutants, bisphenol A, some persistent organic pollutants (including PCBs), some pesticides

    some air pollutants, bisphenol A, some persistent organic pollutants (including PCBs), some phthalates, some heavy metals, some pesticides, solvents

    mercury, trichloroethylene, some persistent organic pollutants (including PCBs), radiation