There is almost universal agreement among leading experts at top medical institutions –Johns Hopkins, Harvard Medical School, the National Institutes of Health, Scripps and others –that our day-to-day exposure to environmental toxins — through the air we breathe and the chemicals we absorb through our skin — is a major trigger of autoimmune disease.
However, because most toxins are found in trace amounts, it has been difficult to gauge what effect they might be having on our health. Yet both lab animal and occupational studies of human beings provide us with disturbing insights into how even low exposures to chemicals can cause our immune systems to go haywire. For example, mice exposed to common pesticides – at levels four-fold lower than the level set as acceptable for humans by the EPA – are more susceptible to getting lupus than control mice. Mice that absorb low doses of trichloroethylene (TCE) – a chemical used in industrial degreasers, and that can be found in your dry-cleaning, household paint thinners, paint strippers, glues and adhesives – at levels deemed safe by the EPA, and equal to what a factory worker today might encounter, quickly develop autoimmune hepatitis. And low doses of PFOA, a breakdown chemical of Teflon – which can be found in nonstick cookware, car parts, flooring, computer chips, phone cables, Stainmaster carpet guard, upholstery, new clothing (particularly kids’ clothing), grease-resistant French fry boxes, the disposable cup of soup that you warm up in the microwave, and disposable coffee cups like the ones you get at your local coffee shop) — can be found in 96 percent of humans tested for it. In recent studies, immunotoxicologists have been unable to find a dose that didn’t alter the function of immune cells at each major step that the immune system takes in trying to protect us against foreign invaders.
Even tiny doses of BPA, a plastics building block used in everything from safety helmets, dental sealants, baby bottles, and eyeglass lenses to every-day processed food packaging, has been shown to change basic cellular function at levels currently present in blood samples taken from people as well as animals.
Proving an absolute link between chemicals and autoimmune disorders in humans is hardly easy. Researchers can expose rodents to low doses of chemicals and look for signs of autoimmune disease roughly six weeks to three months later. But in humans, a comparable time span between exposure and disease might be forty years. Indeed, lab work in longitudinal studies of people shows us that autoimmune diseases are often long, slow-brewing conditions that can quietly smolder in the body for a decade or more before actual symptoms of disease appear. Moreover, it may be that a combination of exposures rather than any acute single dose at a single time increases one’s risk of autoimmunity, conditions that are hard to replicate in animal studies.
I suspect that on some level we don’t want to face what all this research is telling us. We don’t want proof, because even if we agree that the soup of chemicals we’re all carrying around within us is harmful, what do we do about it? Talking about the autoimmune epidemic is a bit like talking about global warming before the movie An Inconvenient Truth was released. For the longest time, we couldn’t see, or didn’t want to see, that the smallest rise in temperature would melt the polar ice caps. Likewise, we don’t want to know that the ways we’re polluting our environment are also harming our bodies and causing our immune cells to go haywire. In the international medical world, the scientists who study autoimmune disease now call this epidemic “the global warming of women’s health.” Yet the reality that the environment plays a major role in triggering these diseases hasn’t yet trickled down to the rest of the population.

