Through the Shadowlands

by Julie Rehmeyer

  The potential for insurance claims by homeowners maintaining that they were sickened by mold exposure is astronomical. The prospect of a peer-reviewed scientific article demonstrating a clear association between Stachybotrys and human illness must have kept plenty of insurance agents awake at night, and also made attorneys salivate. Also, everyone is aware that the insurance industry donates a great deal of money to finance political campaigns. The CDC is a government agency. I presume, then, that somebody made a phone call from Washington, DC, to Atlanta [the location of CDC headquarters] and told the CDC to shut those meddling scientists down in Ohio.

  This possibility seemed even more plausible when I learned that a few months before the CDC initiated its 1999 reinvestigation of the Cleveland babies, the agency got a new director: Jeffrey Koplan, who came to the agency from the research arm of Prudential, a large insurance company.

  Very slowly, scientists have prevailed in bringing down the ACOEM and AAAAI statements. In 2015, ACOEM removed the statement from its Web site, largely due to the efforts of Michael Hodgson, former head of occupational health at the US Veterans Health Administration, who had joined the organization’s board. He told me that he argued, “We can’t do this. We’re making ourselves a laughingstock. The science simply doesn’t support it.” The AAAAI statement expired as official policy in 2011 but was not retracted. It was only replaced with a new statement affirming the respiratory dangers of mold in 2016. The US Chamber of Commerce has never sent a revised paper to judges. No one from ACOEM, AAAAI, or the Chamber of Commerce answered my e-mails asking for comment.

  The ACOEM statement and its progeny shut down one mold-related court case after another. And in the long run, the cases stopped being filed at all because of the riders insurance companies added to their policies that excluded mold from coverage.

  Learning all this, I felt as if my brain were quietly exploding. A scientific organization put out a statement that was contrary to science, and scientists couldn’t get it removed for 12 years! How could that happen?

  And if respected organizations could sow doubt about whether mold is a significant risk factor for asthma—a link that had been observed in the very first textbook on asthma ever written, in 1698—what hope did I have that science would come to understand my weird illness?

  CHAPTER 20

  CRAZY NEUROLOGICAL PEOPLE

  None of my research so far had shed much light on what I really wanted to know—what was going on in my body. The question burned for me: What was the mechanism?

  I had learned enough to understand the mechanism for ordinary respiratory effects. Compounds in mold itself could trigger both allergies and inflammation.

  But for neurological effects like mine, the mechanism wasn’t so clear. There was an obvious suspect, though: mycotoxins. After all, these mold toxins were known to kill brain cells. There were other plausible culprits in the great airborne stew floating around in moldy buildings—volatile organic compounds, bacteria, bacterial toxins, particulates, manufactured chemicals, some combination thereof—but none of those were known to be powerful neurotoxins, as some mycotoxins are. So everyone seemed to focus on mycotoxins as the most likely culprit.

  The 2004 National Academy of Medicine (NAM) report gave good reasons for worry about the impact of airborne mycotoxins on our health. Humans absorb mycotoxins through their lungs and skin as well as through their guts, and for some mycotoxins, breathing them is as toxic as mainlining them straight into a vein—and 20 times as toxic as eating them. Mycotoxins had been found in human blood, tissue, and breast milk. (Breast milk was especially alarming since babies are more vulnerable.) In animals, mycotoxins had been shown to be toxic to the lungs, the skin, the gut, the liver, the kidneys, and the brain, and even low-level exposure to mycotoxins depressed animals’ immune systems, leaving them susceptible to infection. The report said that research on mycotoxins from Stachybotrys chartarum in particular “suggests that effects in humans may be biologically plausible.”

  But the report sounded aggravated with the insufficiency of the science. Over and over, it called for more research on the toxic effects of mold. By the umpteenth call, the statement had come to take on a pleading tone to my ear.

  It had been a decade since the NAM report was issued, though, so I wondered if the report’s call for more research on mycotoxins had been heeded. To find out, I asked the author of the toxicity chapter of the NAM report, Harriet Ammann, a former senior toxicologist with the Washington State Department of Health. Overall, how strong was the evidence that mycotoxins caused non-respiratory problems now?

  “I think the evidence is quite strong,” Ammann told me, “much stronger than in 2003.” My heart leapt.

  Ammann explained that one of the biggest arguments against problems from mycotoxins had been that many researchers didn’t think you could breathe enough of them in to poison you. But recently, they’d realized they’d been calculating exposure levels the wrong way. They’d been collecting air from moldy buildings and then counted the number of intact spores, which, like plant seeds, can germinate into new mold colonies. They then calculated the amount of mycotoxin each spore could carry, and the total quantity of mycotoxins seemed awfully low. Admittedly, nobody really knew how much mycotoxin it took to poison people, especially people who were exposed day after day and month after month. But still, this had made many researchers skeptical.

  It turned out, though, that whole spores weren’t the only things that mattered. Mycotoxins also oozed onto broken spores and tiny fragments of the mold itself and surrounding dust, all of which could float in the air. When environmental health researcher Tiina Reponen of the University of Cincinnati looked for these fragments, she found between 1,000 and 1,000,000 times more of them than intact spores.

  So our potential exposure to mycotoxins was vastly greater than previously thought. Furthermore, these fragments were far more dangerous. These smaller particles have more surface area to soak up the toxins and can penetrate deeper into our lungs, delivering their loads of mycotoxins, irritants, and allergens into the bloodstream more efficiently.

  Reponen’s work solved another puzzle too: Buildings that made people sick hadn’t seemed to be consistently moldier than buildings that didn’t. But that was when researchers were only counting spores—once Reponen counted the fragments and dust, she found that the more of it present in a building, the sicker people got.

  Another major advance was that we now had objective evidence for neurological impacts from mold. People who had lived in moldy buildings had poorer balance, slower reaction times, slower reflexes, weaker memories, and other problems, compared with those without known mold exposure. In addition, a Polish study had shown a 10 percent drop in IQ among children who lived in moldy homes for two or more years, after controlling for other factors.

  Furthermore, researchers had begun to realize that air pollution as a whole could cause systemic effects, not just the respiratory ones they’d long recognized. It had recently been linked to diabetes, heart disease, and dementia. The mechanisms for these associations were unclear, but many researchers fingered inflammation as a likely culprit.

  For my own symptoms, inflammation always struck me as a plausible culprit, at least in part. When I woke up in the morning, before my coffee enema or sauna, my face was usually swollen, sometimes so much so that I could barely see. It also seemed plausible that inflammation of the brain and spinal cord played a role in my walking problems. Neuroinflammation was known or suspected to be integral to Alzheimer’s, Parkinson’s, and multiple sclerosis. I knew that inflammation could happen fast, since severely allergic people can go into anaphylactic shock, with its massive inflammation, within seconds of an exposure. But could it really resolve as quickly as my symptoms could, vanishing when I stepped into a shower?

  Ammann pointed me to another key discovery that, I thought, might possibly explain the shower phenomenon, at least better than anything else I’d come up with. Mycotoxins can travel from ou
r noses, along our olfactory nerves, and straight into the brain, James Pestka of Michigan State University and his colleagues had found.Ch20-1 This route acts as a molecular version of TSA PreCheck, speeding mycotoxins past the blood-brain barrier that ordinarily would flag them as potential terrorists. When monkeys breathed mycotoxins from Stachybotrys chartarum, they lost their sense of smell, neurons in their olfactory bulbs died, and their brains grew inflamed. Similar particles, studies had shown, could travel past the olfactory bulbs to the rest of the brain.

  Whether this happens in humans from quantities of mycotoxins they absorb in moldy buildings wasn’t clear—the monkeys received very large doses. But repeated exposures had a vicious cumulative effect: Monkeys who received five micrograms of the toxin each day for four days showed even more damage than ones who received 20 micrograms once. It may be, then, that breathing still smaller quantities day after day could be similarly harmful.

  I doubted that mycotoxins were killing neurons in my brain, since I hadn’t lost my sense of smell and most of my symptoms could be swiftly reversed.Ch20-2 But neuroinflammation fit. I also thought this mechanism might apply to me in another way: Perhaps the mycotoxins were traveling up my olfactory nerve and causing some of my neurons to fire in some pathological way, and that was producing my semi-paralysis. Some mycotoxins could cause neurons to fire, I’d learned, so that didn’t seem like too big a stretch.

  That might explain both the quickness of my reactions and the quickness of their resolution. Research suggested that molecules might be able to travel along the olfactory pathway very quickly—certainly within minutes, possibly within seconds. And perhaps when a shower rinsed the mycotoxins away, the abnormal firing of my neurons stopped too.

  I learned of another mechanism that might result in neuroinflammation: Our immune systems come preprogrammed by evolution to detect some pathogens people have been exposed to for millions of years—including bits of the cell walls of mold spores. That means that when we breathe in mold, our immune systems may become convinced that they’re under attack, triggering inflammation and flulike symptoms. Cheryl Harding of Hunter College developed the hypothesis that this immune response could be driving inflammation in the brain as well, causing the neurological problems people report. She exposed mice to the cell walls of mold spores and found that they grew more anxious and forgetful, and they also had signs of inflammation in their brains. When the mice were exposed to intact Stachybotrys spores, complete with their mycotoxins, many of the effects were even stronger.

  I was astonished to read of a third, entirely new mechanism that had been discovered as well: The gases that give mold its characteristic smell may damage us. Joan Bennett of Rutgers University pumped a volatile organic compound (which, roughly speaking, is the type of gas we smell, commonly abbreviated VOC) from mold into a chamber filled with fruit flies, and the flies staggered and shook like Parkinson’s patients. When Bennett treated them with L-dopa, a standard Parkinson’s drug, they recovered. She also found that the mold VOCs killed human cells in a petri dish.

  I didn’t have Parkinson’s of course, but there are many mold VOCs, and perhaps one of them caused my particular flavor of nervous system problem. Buildings didn’t have to smell of mold to do me in, but our noses can’t detect every VOC out there. And thinking of the compound as a kind of scentless smell made some sense. I thought about how it could be nearly impossible to get rid of the reek in the house of a heavy smoker, how the smell could follow them around like a cloud. Perhaps that explained how difficult it was to decontaminate objects that had been in a moldy house for a long time.

  Of course, these theories about my reactions were all only possibilities, probably far more likely to be wrong than right. My theories were particularly tenuous because it was unclear whether people living or working in moldy buildings were actually harmed via any of these mechanisms—the work was preliminary, and the doses were unrealistically high. But I found it pretty incredible that we were finding entirely new mechanisms mold could use to hurt us.

  Especially because we were finding them even when we were barely looking. When I talked to Pestka, Harding, and Bennett, the researchers who had uncovered these new mechanisms, all reported they had given up their research because they couldn’t get funding to continue it. They had each repeatedly sent grant applications to the NIH that had been denied, and they’d concluded that the NIH was simply not interested in research into non-respiratory effects of mold. Pestka had returned to studying ingested mycotoxins. Harding had retired but was continuing work to finish and publish her research. Bennett had turned to studying the positive effects of mold VOCs (including a promising treatment for white nose syndrome in bats).

  Some mold researchers were getting funded, though—the ones studying respiratory effects. So I turned to them, figuring they must have some perspective on the range of possible impacts of mold. I often found, though, that as soon as the words “mycotoxin” or “neurological” passed through my mouth, I felt as though I could hear their eyes rolling through the telephone. Many adamantly argued that there weren’t enough mycotoxins in the air in moldy buildings to make people sick.

  “They’re just not there!” barked Jay Portnoy, the researcher whose name was falsely put on the AAAAI report. “We looked, and they’re not there!” Despite asking repeatedly, I couldn’t get him to cite a single study to back up his claim. I asked him about the study showing that airborne dust and mold fragments could carry vastly great loads of mycotoxins than spores alone, but he simply repeated his irritated dismissals. And when I asked him about the AAAAI report, he sighed, said it happened so long ago he could barely remember the details, and said it was “just a snafu.” He seemed angrier at the activists who had complained about the report than he was at his colleagues who had hijacked his name to prop up a statement he disagreed with.

  What the hell? I thought. Maybe he’s just having a bad day.

  Next I turned to David Miller of Carleton University in Ottowa, perhaps the foremost researcher on indoor air quality. In the mid-1980s, when workers in entire office buildings suddenly complained of feeling ill at work, Miller had been called in to investigate. He had patiently put together the clues linking the complaints to toxins trapped in the air of tightly sealed buildings, including VOCs, concentrated outdoor pollutants, and mold. He and his colleagues had raised the alarm, helping to change building practices around the world. This guy, I figured, must have a broad perspective on what’s going on.

  Miller was no less dubious about mycotoxins than Portnoy, though he was far friendlier. To get sick from mycotoxins, he said, you’d have to do “something stupid,” like carrying badly moldy boxes right up to your chest, so the mycotoxins would get shaken loose and breathed right in (though, as with Portnoy, I couldn’t get him to give me any citations to back up this claimCh20-3). Yes, he said, mycotoxinsCh20-4 could contribute to asthma—he himself had shown that—but their role was minor. The more significant danger, he argued, was the mold itself, rather than the toxins it produced. Proteins in mold could both irritate the lungs and cause an immune response.

  “What about neurological effects?” I asked. “Can mold, rather than mycotoxins, explain them?” Then Miller grew hesitant. He said that mold can cause allergies, and allergies can wind up the immune system and leave people feeling muddle-headed, but beyond that, he couldn’t identify a plausible mechanism through which ordinary moldy buildings could cause neurological effects.

  Still, Miller didn’t deny that neurological problems might occur in mold-exposed patients. He’d certainly heard people complain about it. Whenever he oversaw the remediation of a moldy building, he said, at the end, a couple of people continued to complain they were sickened by the building even when everyone else felt fine in it. Some of those outliers even reported that if they handled a single piece of paper that had been in the building before its remediation, their symptoms would flare up again.Ch20-5

  Now that sounds familiar, I thought. And sud
denly I confronted a decision: Was I going to fess up to being one of those folks?

  I’d been through this with other researchers. Once I divulged my secret, our nice, easy, relaxed conversations about their research suddenly became stiff and awkward. They’d started to measure their words carefully and then quickly tried to get off the phone. But, I reminded myself, data is data. I’d had the experiences I’d had, whether they fit into a tidy theory or not. If I stayed silent about them, it felt like I’d be turning them into something shameful.

  So I came out: I was one of those crazy neurological people. Then I told Miller about my washcloth experiment, partly to salvage my scientific creds. I described the placebo control and double-blinding and how just breathing through a contaminated washcloth crippled me. What did he make of that? If he didn’t think mycotoxins could do that, what could?

  Miller’s affable voice stayed even but became more careful. Perhaps, he suggested, I had at some point been exposed to multiple chemicals in a building at once, not just mold, and it was the combination of chemicals that had done me in. I was excited—I’d read that some evidence suggested that these combined exposures could be worse than the sum of their parts. Maybe he can point to other chemicals that can produce my symptoms! But when I asked, he said no. He just thought a combined effect was more biologically plausible than mold alone.

  Then he delicately suggested another explanation: “conditioned immunity.” If you give a mouse an allergen mixed with almond extract (with its distinctive smell), the mouse will of course react to the allergen. But if you do this again and again, slowly reducing the level of the allergen to nothing while maintaining the almond scent, the mouse will end up having an allergic reaction to the almond extract alone. That’s conditioned immunity, he explained.