The Autoimmune Epidemic: Bodies Gone Haywire in a World Out of Balance--and the Cutting-Edge Science that Promises Hope (No Series) (8 page)

Meanwhile, we know far less than we need to about the direct effect of these chemicals on the immune system. While chemical companies have to divulge information if their chemicals have been found to be carcinogenic in lab testing, no such testing and reporting are required on whether chemicals act as autogens and damage the human immune system. While debates brew between the chemical industry, which argues that these exposures are safe for humans, and the growing number of scientists investigating their damaging effects, recent published studies on PBDEs have not been reassuring. The CDC’s website now informs concerned consumers that PBDEs may indeed impair the cells of the immune system in animal studies.

Let’s look at some of the other culprits Becky encountered in her day, such as Teflon, pesticides, and plastics. At breakfast, Becky’s favorite no-hassle, stick-free Teflon pan is sending up gaseous fumes. Teflon is manufactured with a chemical known as perfluorooctanoic acid, or PFOA—as are other nonstick cookware, car parts, flooring, computer chips, phone cables, Stainmaster carpet guard, upholstery, clothing, grease-resistant french fry boxes, and disposable coffee cups like the ones you get at your local coffee shop. PFOA can also now be found in blood samples of 96 percent of people in the United States. It does not break down in the environment and has a half-life of 4.4 years in humans.

A chemical’s half-life is important because it is the measure of how long it takes a pollutant to break down to half of its initial amount. Because we are constantly exposed to PFOA, it always resides within us—we never have a chance to break down, metabolize, and excrete all that we are exposed to. As with PBDEs, we do not know much about what PFOA does in or to the body. In 2005, the Environmental Protection Agency (EPA) determined that even low-level exposure to PFOA poses “a potential risk of developmental and other adverse effects” on human health. In one recent and provocative paper from Stockholm University’s Unit for Biochemical Toxicology, investigators were unable to find a dose that
didn’t
alter the function of our immune cells at each major step that the immune system takes in mounting a defense to protect us against foreign antigens. Despite such evidence, manufacturers of the chemical maintain that PFOA does not pose a health risk to humans, citing a lack of sufficient evidence.

Consider now the strawberries and cantaloupe Becky prepares for breakfast. Prior to arriving on her daughter’s plate they have been sprayed repeatedly with insecticides to help protect their skins from pests both in the field and during transit to Becky’s local grocery store, where she bought them wholly unblemished. Back on the farm, this cantaloupe, like most cantaloupes, was treated with organochlorine pesticides—in this case, a type known as endosulfan. Commonly used today on melons, traces of endosulfan are found in the food we eat more than any other pesticide. In one recent study—which found that 100 percent of pregnant women now carry numerous pesticides in their placentas—endosulfan was found to be present at the highest concentration of any organochlorine pesticide. Like PFOA, organochlorine pesticides such as endosulfan also affect the immune system. Indeed, if you were to do a search on “endosulfan and immune system” on the National Library of Medicine’s Internet database, PubMed, you would receive twenty hits detailing the link between endosulfan and immune system dysfunction. While a few well-known organochlorine insecticides that are notoriously injurious to animals—DDT, for example—have been banned in the United States, even these persist for decades in the soil in which our fruits and vegetables are grown and in our water, meanwhile accumulating up the food chain (which is why traces of DDT can be found in the steaks Becky has yet to cook for dinner).

Hundreds of other pesticides and insecticides remain in regular use, including herbicides such as atrazine (which Becky’s lawn company sprays on her yard), and termiticides (which the local pest-control company uses to liberally spray the foundation, cracks, and crevices of Becky’s house every year). For the dog, there is tick and flea killer: more pesticides. In the Mount Sinai study examining what chemicals are found in the average American, every single participant carried detectable levels of pesticides that have been banned, like DDT, as well as a wide range of pesticides in liberal use today. A mixture of twenty-one pesticides was found in the umbilical cord blood of every single newborn baby tested.

Immunologists, meanwhile, are trying to ascertain what happens to the immune systems of lab mice when they expose them to organochlorine pesticides such as DDT and methoxychlor, the latter having been manufactured as a safer replacement for DDT and now being used widely on food crops, home gardens, and as flea and tick control on pets. They do not like what they see.

In a 2005 study, six researchers at the University of Florida College of Medicine in Gainesville set out to discover whether mice exposed to organochlorine pesticides would be more prone to develop autoimmune disease. Mice have long been known to possess the genetic potential to develop autoimmunity; like some 25 percent of humans, certain mice possess more of the genes that make them susceptible to autoimmune diseases such as lupus—that is, if and when they meet up with the right environmental trigger. Since autoimmune disease primarily affects women, over the past twenty years researchers have used female mice as the litmus-test lab animal for determining whether a chemical pollutant might cause or exacerbate autoimmune disease. The disease most easily distinguishable in mice is lupus—which means that the gold standard in the laboratory for ascertaining whether a pollutant might cause autoimmunity in humans is to see if it causes lupus in genetically-at-risk female mice.

Every single one of the female mice that the Gainsville team exposed to organochlorine pesticides rapidly developed the autoimmune disease lupus, while none of the mice in the control group did. The presence of these pesticides “markedly influenced” the progression of autoimmune disease, resulting in elevated levels of lupus autoantibodies. “It is worthwhile noting,” say the study’s authors, that the lower dose of the organochlorine pesticide methoxychlor that mice were exposed to was “4-fold lower” than the level set by the Environmental Protection Agency as acceptable. This suggests, say the authors, that the commonly used pesticide methoxychlor might stimulate autoimmunity at a much lower dose than doses necessary to cause other adverse health effects, and is “therefore of particular interest for risk assessment.”

Pesticide manufacturers dismiss the idea that pesticides pose health risks, arguing that it is an extrapolation to say that a given exposure that leads to disease in mice will do the same in humans. Yet occupational studies that link groups of people who work with pesticides to higher rates of autoimmune disease tell us that such an association clearly exists. In one 2007 study, researchers studied data from over 300,000 death certificates in 26 states over a 14-year period to examine the association between a person’s occupational exposures and their risk of dying from a systemic autoimmune disease such as lupus, rheumatoid arthritis, or scleroderma. Their findings were stark: farmers who worked with crops—and who were therefore more exposed to pesticides—were more likely to die from an autoimmune disease. In another study, rural farmers who had a lifetime exposure to organochlorine pesticides had a greater likelihood of having a high antinuclear antibody, or ANA, count—the telltale diagnostic sign that the immune system is turning against the organs and tissue of the body itself in the autoimmune disease lupus. In yet another research finding, farmers who reported mixing pesticides for agricultural work were significantly more likely to suffer from lupus. Despite such danger signals, in the United States we apply greater quantities of pesticides, such as the weed killer atrazine, to suburban tracts than to agricultural land. Just think back again to Becky, who pulled into her suburban driveway just as the lawn company was pulling away after spraying the crabgrass and dandelions.

Throughout Becky’s day, we can trace chemical triggers that tax her immune system and those of her children. As Becky and her children prepare to cross the street in the morning, they are blasted with microparticle bursts of exhaust from a diesel bus, then a truck. Within that diesel exhaust exist a host of extremely small particles that are well absorbed by the body, where they move from the lungs to enter the bloodstream. There is mounting evidence that this air pollution we inhale may cause an erratic response in our immune cells, leading to an elevated death rate of immune cells in some laboratory tests, exacerbating autoimmune disease or leading to immune-system dysfunction in others. Recent studies also show that mice exposed to fine particles of pollution at concentration levels equal to those found in the air in major metropolitan areas are more likely to develop atherosclerosis, which researchers now believe involves an autoimmune response.

One of the most potent by-products of exhaust fumes is dioxin, which is carried into the air by the fuel combustion of diesel trucks and buses. Dioxin is also produced through the industrial manufacturing of bleached fibers for paper and textiles, in the production of wood preservatives, chlorinated pesticides and herbicides, and in the manufacturing process of virtually every type of plastic and bleached or resin-coated food packaging that you can find lining the aisles of your neighborhood supermarket. We each receive some small, additional daily dose of dioxin through our steady diet of seafood, meat, and dairy. Like DDT and PCBs, when dioxins are released into the atmosphere (as they are in manufacturing, as well as through the burning of trash, hospital debris, and trees), they become attached to particles and fall back down to earth, where they are consumed by fish and other animals and concentrated and stored in their fat—before eventually ending up on our dinner plates. All nine people tested by Mount Sinai researchers tested positive for blood levels of dioxin, and every infant’s cord blood carried dioxin.

Dioxin is a recognized immune suppressor. It has long been known to cross the placenta from animals to their unborn and is increasingly linked to cancer and developmental effects. But recently researchers have observed that dioxin may work in more complex ways on the immune system as well—not only by suppressing immune cells, but by overcoming control mechanisms that should prevent an autoimmune response. In lab studies, when female rodents are exposed to dioxin during gestation, their offspring go on to develop autoimmune disease after being born. Other research is examining the role everyday exposure to dioxin may play in increasing the likelihood that an autoimmune response will be set in motion in general.

One of the complex aspects of understanding how autoimmunity works—and why chemicals can act as autogens, triggering autoimmune disease—involves comprehending the intricate way in which immune cells are schooled. T cells are made in the bone marrow. From the bone marrow they move to the thymus, a butterfly-shaped organ situated over the heart in the center of the upper chest, right behind your sternum, or breastbone. It is in the thymus that T cells mature before they enter your bloodstream. You might think of the thymus, in fact, as a kind of a military training school—one housing both an undergraduate training school for cadets as well as an officer training school. Millions of T cells are “educated” in your thymus to perform specific roles—such as, say, to recognize and eradicate an infiltrating influenza-A germ or food-borne bacteria like salmonella from your body, as well as hundreds of other antigens with which your body may come into contact. Some of the cells in the thymus, however, undergo a more sophisticated sort of education—a kind of officer training program if you will. They are schooled, instead, in a different class altogether and become regulatory T cells. Regulatory T cells do pretty much what their name implies: they act as the senior officers of the other T cells, in this case ensuring that educated T cells will not mistake the body for a foreign antigen and turn against the body’s own organs or tissue as they diligently scour the body for invading agents. You might think of them as the officers who make sure that T cells perform their military training exercises just right.

Scientists aren’t completely sure how, in a perfectly healthy immune system, these teacher or regulatory T cells neutralize other T cells so that they almost never erroneously target your own tissue in an autoimmune response (or, as scientists put it, so that all T cells stay “tolerant” of your body’s own cells). They do know, however, that when regulatory T cells lack a proper education, or when regulatory T cells are not formed in sufficient quantity in the thymus, antigen-seeking T cells can be suddenly freed to wreak havoc in the body, turning on both foreign antigens and body tissue at will, with nothing to tell them to stop.

Understanding the way in which T cells work in the body is key to comprehending why chemicals such as dioxin and PCBs, as well as other substances, can be so damaging to the immune system and lead to autoimmunity. There are several things that can cause the thymus to atrophy, or decrease in size, which in turn leads to an insufficient number of these regulatory T cells being educated to keep an eye on other T cells. Pregnancy is one of them—which may be why so many women develop autoimmune disease after the birth of a child. Exposure to a number of contaminants such as dioxin and PCBs is another.

Indeed, environmental exposures to dioxin and PCBs—at amounts as low as five times the average level that most of us come into contact with in our day-to-day lives—can cause the thymus to shrink as much as 80 percent. When that shrinkage happens, the number of regulatory or “officer” T cells decreases, and there are no longer as many of them to keep the “cadet” T cells in line. The immune system becomes unsupervised—which can trigger acts of friendly fire in the systems and organs almost anywhere in the body.