The Autoimmune Epidemic: Bodies Gone Haywire in a World Out of Balance--and the Cutting-Edge Science that Promises Hope (No Series) (12 page)

Were Jan’s blood clots exacerbated by the air pollution through which she and Dave drove and biked for three solid days? To say yes would be mere supposition. As we have seen, the steps connecting exposure (one on that scale of one to ten) to disease (ten), are still blurry at best. At numbers four, five, and six, we cannot go back in time and travel with Jan’s cells to say definitively what prompted Jan’s sudden and rapid onset of antiphospholipid antibody syndrome or prove whether those forest fires had a thing to do with it.

It is all supposition, yes, but it is a very good guess.

THE STORY IN THE NUMBERS

If you were to look today at a chart detailing incidence rates of autoimmune disease versus heart disease and cancer, you would see that while cancer and heart disease rates are, more or less, flatlining, autoimmune diseases are continuing in a steady upward climb. This raises some interesting questions. If an estimated 25 percent of people around the globe carry genes that make them susceptible to autoimmune disease, and if 8.5 percent of Americans already suffer from one or more autoimmune diseases—and if subtle, chronic exposures to the chemicals in our industrialized world are, as we know, playing a role in rising disease rates—how long will it take before an autoimmune disease breaks out in the remaining genetically susceptible Americans? Detectable levels of man-made chemical agents found in nursing mothers’ breast milk have risen significantly over the past several decades—and they continue to rise dramatically. What is the threshold of chemical exposure at which an autoimmune reaction will be triggered in all who carry the genetic propensity?

Today, the National Institutes of Health spends only $591.2 million on autoimmune research annually—about one-sixth of the $3 billion spent on AIDS/HIV, which affects fewer than nine hundred thousand Americans. Cancer research claims ten times the annual research funding of autoimmune disease, although cancer affects less than half as many people. Despite the fact that autoimmune disease is the number-two cause of chronic illness and, on average, slices fifteen years off a patient’s life, the level of autoimmune research funding is less than 2.2 percent of the National Institutes of Health budget. A report by the Institute of Medicine states that the United States still lags behind other countries in research into the processes and contaminants involved in autoimmunity.

Many of the contaminants discussed early in this chapter have been so little tested that we have no real idea as to what role they may be playing in rising autoimmunity rates. PFOA, for example, has barely been studied at all. Despite the fact that it is found in 96 percent of people and the chemical has a half-life of 4.4 years in the human body, and even though the one piece of research that we have on PFOA has shown it to be a potent immune suppressor, the Environmental Protection Agency does not require scientists to perform further study on this or any other chemical that has shown signs of toxicity in laboratory testing. While Japan recently spent $135 million on a research program identifying some seventy chemicals as endocrine disruptors, the total U.S. budget in 2003, 2004, and 2005 to study endocrine disruptors was less than $15 million for all three years combined.

According to Kathleen Gilbert, the current climate for funding federal research into how toxins affect the immune system has never been more dismal. The problem is twofold. First, the success rate for federal research grants for new investigators has decreased from 22.5 percent in 1998 to 16.8 percent in 2004. Second, as the result of recent restructuring, there are few toxicologists on the grant-review committees that evaluate these new grant applications. This makes it less likely that grants involving environmental toxicants will receive a high priority. These two factors combined make it very difficult to obtain and maintain funding for immunotoxicology research. “It would take an environmentally enlightened political climate to restore research funding and cleanup efforts at levels equal to the challenge,” says Gilbert.

At the end of the 2005 conference Workshop on Lupus and the Environment: Disease Development, Progression and Flares, the National Institutes of Health asked scientists to provide suggestions for drafting what is known as a request for applications, or RFA. An RFA is a kind of clarion call from NIH that asks researchers to submit grant proposals in a specific area in need of more investigation—in this case the RFA is, should it ever get approval and difficult-to-find funding, to be used for researching autoimmune disease and environmental triggers more deeply. Yet to date, the National Institutes of Health has still not issued the request for researchers to submit applications for grants to investigate environmental triggers of autoimmunity.

Today, eighty thousand chemicals are registered for use in the United States and the U.S. Environmental Protection Agency approves an estimated seventeen hundred more a year with very little screening. We often assume that if no warning has appeared stating that a chemical is harmful, that must mean it’s benign, when nothing could be further from the case. The 1976 Toxic Substances Control Act requires that new chemical compounds be tested for negative health effects before approval only if evidence of potential harm already exists—which is rarely the case for brand new chemicals. The FDA approves about 90 percent of these new compounds without restrictions.

And so, a great debate continues to rage in the scientific and political arena about what the growing number of studies linking environmental contaminants to autoimmunity collectively means, what the implications are, and—as we shall see in further chapters—what actions should be taken, if any.

Jumping ahead with the research that does exist in order to claim that the invisible chemicals around us are causing or exacerbating a rise in autoimmunity is the kind of connecting-of-dots and blame-the-environment speculation that makes many politicians crazy, and that chemical-industry publicists routinely deem as toothless.

In Arkansas, Gilbert is now deepening her research to see what the exact mechanisms are by which TCE activates T cells. “Industry interest seems to center on designing drugs to stop those T cells from activating after exposures,” says Gilbert. “But what bothers me is that no one is talking about cleaning up the environment to help prevent these exposures in the first place.”

Science, as a whole, does not make sudden leaps. Even when a body of research begins to form an arrow pointing in one clear direction, the standard scientific line remains predictably the same. At the end of almost every published paper appear the words “more data is needed to further our understanding.”

Perhaps there is no better place to examine the ramifications of waiting too long for irrefutable proof of the role that environmental contaminants play in today’s autoimmune epidemic than in the city of Buffalo, New York, where for far too long, residents, researchers, and society looked the other way.

T
ry this exercise the next time you can spare a minute. Go to the web address http://www.epa.gov/enviro/emef and enter in zip code 14211 in the space provided. Now watch as your computer monitor morphs into a complex map of small green and black squares, each demarcating a hazardous-waste or toxic-release site within a few square blocks in Buffalo, New York. Take particular note of the number of black squares; each signifies a multihazard site—a combination of hazardous, toxic, and/or Superfund-classified substances and chemicals found at the locale. You might blink twice to think how foolhardy it would be for anyone to live smack in the heart of 14211 in the East Ferry neighborhood of Buffalo—it’s just that toxic.

But in the mid-1980s the unusual number of residents in the East Ferry community who were falling ill with lupus and other debilitating autoimmune diseases had no clue about the toxic waste simmering within the soil, pavement, and streams around their homes and schools. The chemicals that had been seeping into the neighborhood from abandoned industrial-waste sites for decades hadn’t yet been charted on any government website.

In 1980, Betty Jean Grant, a thirty-two-year-old African-American woman, and her husband, George, decided to open up a mom and pop store at 1055 East Ferry Street in Buffalo, N.Y. Serving the predominately African-American neighborhoods of East Ferry and next-door Delavan-Grider—zip code 14215—Grant’s Variety Shop would meet local residents’ needs, offering them milk, bread, and Afrocentric health-care products as well as items needed on the fly, like, say, a box of nails. Born and bred in Tennessee, and one of sixteen children, Betty Jean Grant possessed a general fondness for talking to people, and after having lived in Buffalo for ten years, she knew exactly what her neighbors’ daily wants were and how far they had to walk or drive to purchase such everyday conveniences. Grant’s Variety Shop quickly became, she says, “just like those neighborhood corner stores down South where people come in to see each other, talk, and socialize—and leave with a bit of food.”

Amidst all that talking and listening, Grant got to know local residents—and know them well. In 1986, after having listened carefully to customers’ woes for years, she began to divine a pattern in the stories they told that made her increasingly uneasy.

At first, it seemed no more than an isolated, tragic tale that could happen in any community. Karen Johnson,
*
a local teenager who often popped into Grant’s store on her way home from school, stopped coming by. She lived only a block away at 428 Moselle Street, and Grant hadn’t seen her in weeks. Grant heard one day that Karen had been diagnosed with the autoimmune disease lupus. A month later Karen died. She was eighteen years old.

She seemed to disappear overnight. And in a manner of speaking, Karen had. When lupus goes undiagnosed, the disease—which afflicts approximately 1.5 million Americans, or roughly one in two hundred people—can shift from mild periods when chronic symptoms seem barely present to a suddenly life-threatening crisis overnight. In lupus, deranged immune fighter cells, triggered into acts of self-sabotage by a combination of genetic predisposition and environmental triggers, can turn against virtually any organ or tissue, including the joints, kidneys, heart, lungs, brain, blood, or skin, inflicting severe pain, inflammation, and cellular damage.

If the illness is caught before the body’s rogue immune system significantly advances its attack, patients can work with their doctors toward a relatively decent outcome. To be diagnosed requires having an experienced physician who is also educated enough about the disease to detect lupus’s complex, often intermittent symptoms and make the judgment call to run specific blood tests. The primary test, known as an ANA, looks for unusual antibodies detectable in the blood called antinuclear antibodies, which are able to bind with the nuclei of tissue and organ cells and inflict damage. A high ANA warns doctors that a patient’s antibodies may indeed be turning against their own tissue, alerting physicians to the possibility of lupus as well as other connective-tissue diseases such as rheumatoid arthritis and scleroderma.

Although no new U.S. Food and Drug Administration–approved drugs have been developed for lupus in more than forty years, with the help of steroids and immune-suppressing drugs used to treat organ-transplant patients, those with lupus can control flares of their illness. Patients might always have to manage chronic pain and excessive fatigue, but life can often be reasonably good. However, left undiagnosed and untreated too long—as was the case with Karen Johnson—patients can experience sudden, serious organ damage and die. And nowhere was such a preventable and heartrending scenario more likely to occur than in the economically underprivileged African-American neighborhood of East Ferry in Buffalo, where few could afford regular preventative medical visits, quality medical care, and diagnostic tests for an emerging illness, much less the necessary interventions and medications for treatment.

Not long after Karen’s death, her thirteen-year-old next-door neighbor, Devonne,
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who lived at 426 Moselle, came into the store looking exhausted and depressed. Surmising that Devonne was low because of Karen’s death, Grant asked her if she was doing okay. Devonne looked up and said, “Mrs. Grant, I just found out that I have lupus too.”

Grant, a former nurse’s aid, knew what a devastating disease lupus could be. “I just didn’t know what to say to Devonne,” she recalls. “It seemed to me a very odd and sad coincidence that two teenage girls living right next door to each other would be struck with lupus at nearly the same time.”

Three months later a thirty-eight-year-old woman named Linda Winston,
*
who lived at 378 Moselle—almost across the street from Devonne—came into the store and told Grant that she was having a hard time because she couldn’t go out in the sunshine anymore. Her doctor had just diagnosed her with lupus. Sunlight made the disease flare.

“Right then a warning bell went off in my head,” says Grant. “Something just didn’t sound right to me.” Then, a few weeks later, Grant found out that one more woman living on Moselle Street was sick with the same autoimmune disease.

The next week there were five. A woman who lived three streets over from Moselle came in to say she’d been diagnosed with lupus as well.

That was it for Grant. “Five in a single block?” She called the City of Buffalo Department of Public Works and relayed her concerns to an official in the water department. Grant wanted to know, “Could our water be contaminated? Could something toxic in this area be causing multiple cases of lupus in a one-block radius?” A brusque answer shot back: absolutely not.

“I had no specifics,” Grant says. “Just stories, like straws I was trying to pull together from out of the air.” Twice she called different department heads at the Erie County Department of Health, only to be met with a more vehement response. “They told me, ‘Look, lady, you’re being paranoid, you’re creating a fantasy, looking for something that just isn’t there,’” she says. After making a few more phone calls, Grant was told point-blank to “stop creating a conspiracy theory.”

In the ensuing years, more and more cases of lupus would quietly emerge among people living in the East Ferry and Delavan-Grider neighborhoods, as would incidences of other autoimmune diseases such as rheumatoid arthritis, scleroderma, multiple sclerosis, Hashimoto’s thyroiditis, Sjögren’s syndrome, antiphospholipid antibody syndrome, Graves’ disease, type 1 diabetes, and myasthenia gravis. Most of those afflicted, however, would remain unaware of how many others were falling ill with similar autoimmune diseases—much less why.

Fifteen-year-old LaShekia Chatman
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was one of these young women. In 1992 she was about to go through a kind of hell no teenager should ever have to experience. LaShekia had grown up pretty much like any American city kid, in a white two-story with sky blue trim on the corner of Mapleridge and Deerfield, four blocks north of 537 East Delavan. She worked hard for A’s and B’s in school and in fifth grade was tapped for Buffalo’s gifted and talented program, City Honors School. By her freshman year of high school she performed on the cheerleading squad, starred in
Godspell
, and began an African step dancing group. She was well loved up and down her block by grown-ups and kids alike—including by her friend Kayla Jordan,
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with whom she played from the time she was a toddler.

At the age of fifteen, however, she began to experience muscle pain, joint aches, and a constant fatigue that she likens, looking back, to “that feeling you have during those first few hours when you’re getting the flu but you don’t know yet what’s wrong with you.” LaShekia’s flulike malaise lasted for weeks. As one month passed and then two, LaShekia’s mother worried that her daughter’s problems stemmed from something more serious than the normal wear and tear that comes with being an overachieving teen. Their pediatrician ran a battery of blood tests and discovered that LaShekia had Epstein-Barr virus, or EBV, a fairly common viral infection. Also known as mononucleosis, EBV could hit teenagers especially hard. At last, her family assumed, they’d discovered what was dragging LaShekia down.

Several months after mono ought to have run its natural course, however, LaShekia was no better. Her bone-deep lethargy was worsening. She noticed other small, worrisome signs. LaShekia would get a minuscule cut on her hand and the wound wouldn’t heal for weeks. She came down with one cold after another, until it seemed as if she’d been born with a raw throat and flooded sinuses. It hurt just to walk; LaShekia felt as if small ash fires smoldered in every joint. The pediatric practice reassured LaShekia’s mother that it could take a good amount of time for a fifteen-year-old to get back on her feet after mononucleosis.

LaShekia spent several days a week unable to go to school, struggling to keep up with homework from bed. Half a year slipped by this way in illness, as time often will when an undetected autoimmune disease mounts its attack, and LaShekia was not improving. The pediatrician agreed that they needed to run more tests and sent the Chatmans to a local rheumatologist to investigate LaShekia’s joint pain. This time, a new diagnosis emerged. LaShekia’s blood work revealed what is known as a “high sed rate.” Blood sedimentation rates, or sed rates, are lab tests that gauge how fast red blood cells fall to the bottom of a glass test tube. How fast they fall tells doctors, as a crude sort of measure, whether there might be inflammation going on in the body. The higher the rate at which the red blood cells fall, the more inflammation there is.

LaShekia’s sed rate was sky high. Bone X-rays confirmed that LaShekia’s joints were badly inflamed. The two findings together pointed to the diagnosis of juvenile rheumatoid arthritis, known for short as JRA. In JRA, as in all autoimmune diseases, fighter cells in the arsenal of the body’s exquisitely synchronized immune system, what we might think of as the body’s central intelligence agency—which normally safeguard us against dangerous infiltrators such as viruses, bacteria, or environmental toxins—skew off kilter. Instead of defending the body, a faction of fighter cells become akin to rogue agents, activating other cells to destroy healthy cells and tissue. In this case, fighter cells, or T cells, were activating autoantibodies, antibodies directed against self, to destroy the lining of LaShekia’s joints. The result, for LaShekia, was the kind of burning pain, swelling, and inflammation from which JRA patients so often suffer.

Upsetting as a diagnosis of JRA was, however, the Chatmans—LaShekia, her mom, dad, and grandmother—were happy finally to have something to work with. LaShekia started taking Tylenol for joint pain, with the hope that she would begin to feel better. For a while she did, although her physical improvement, if any, was slight.

In 1995, at the age of eighteen, LaShekia set off for Pace University in New York City, hoping to be the first college graduate in her family. Despite her physical setbacks, she had managed to graduate from high school with the rest of her class. She got as far as Halloween during her freshman year at Pace, when it became clear that her physical torpor was worsening. She had lost significant weight. Twice since she had left for university, LaShekia had blacked out and ended up in New York Downtown Hospital’s emergency room. Her mother worried that the stresses of college life were too much for her daughter and insisted that she return home to Buffalo.

LaShekia, who stands five foot six, had dropped to an emaciated ninety-five pounds by the time she returned home. Her long ebony hair had noticeably thinned, and her once-glowing brown complexion was lackluster and sallow. LaShekia recalls that when her mother saw her she was so upset that “she locked herself in the bathroom for nearly an hour. She said she had to finish her shower, but I could hear her in there crying, trying to hide from me how scared she was.”

LaShekia’s rheumatologist, whom she saw a few days later, couldn’t fathom what was happening; he sent LaShekia to Buffalo’s Roswell Park Cancer Institute to rule out any sort of cancer. In between stays in Roswell for tests, LaShekia would come home for a week or so. She was so weak and in such acute pain she couldn’t walk to the bathroom, turn a doorknob, or bear the pressure of her body’s weight against the mattress. When she did manage to sleep it was for a few fitful hours, only to awake in a pool of sweat. Her hair was falling out on her pillow, and the bright light of the outdoors made her wince. LaShekia’s mother, Renita, recalls feeling as though she were watching her daughter “die before my eyes.”

LaShekia sometimes overheard her mother speaking in hushed, worried tones with her friend Kayla’s mom over coffee at the Chatmans’ kitchen table. The two moms were close friends and had more in common than they might have liked: like LaShekia, Kayla had been growing increasingly unwell. For months, Kayla had been experiencing severe lethargy and debilitating headaches. Then she woke one morning and had trouble seeing out of her right eye. Kayla had seen several local doctors who, despite the severity of her symptoms, had been unable to discern what was wrong with her.