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Mold illness is perhaps the original indoor environmental illness. It existed well before the advent of indoor cooking and the resultant smoke inhalation illnesses that followed. Noted in the Bible, indoor mold is treated as a sickness of both body and spirit. The remediation of indoor mold delineated in the good book offers a peek toward its perceived threat in that day, requiring removed materials be taken to 'an unclean location outside of town' so as not to harm either the inhabitants nor the village.1
OSHA estimates that over a quarter of all buildings in the US have sustained water damage, including institutional buildings such as public schools and even hospitals. Water-damaged buildings are found to host molds that affect human health.2-4 In addition, water-damaged buildings have elevated fungal and microbial diversity in dust samples, affirming the concept of biofilm.5,6 This diversity increases the biologic and toxic load on the inhabitants. Many of the indoor molds that thrive on water-damaged building materials form toxins as a competitive advantage over neighboring fungi. One study showed sixty-six percent of water-damaged building materials contained mold toxins.7 Typically, the longer-standing the moisture issue, the more diverse and severe the mold and mold toxin danger.
Therefore, indoor molds pose two threats – the spore and the toxin, referred to as mycotoxins. When detected, mold spores are a generally accepted cause of illness. Spores are typically large enough to trigger local respiratory system irritation and an immune response whereas mycotoxins can bypass our clearance systems undetected and enter the bloodstream via the alveoli where the body must manage them as an environmental toxin. Further contrasting the two threats from mold, spore exposure leads to the generally accepted Type I hypersensitivity reactions commonly associated with mold exposure, such as allergic rhinitis, asthma, and hypersensitivity pneumonitis, whereas mycotoxin illnesses are less understood and are often diagnosed improperly as other conditions. For instance, a ten-year follow-up study on workplace molds identified associations between past or current presence of mold in the workplace and sick-building syndrome, a medical enigma diagnosis.8 According to a hurricane Katrina study of water-damaged homes, molds and dangerous mycotoxins were detected inside the homes five months after the water had receded. Based on their findings, the authors "emphasize the importance for returning residents and remediation workers to…use adequate personal protective equipment."9
There is an under-recognized third threat – spore fragments. Mold spore fragments are formed at a ratio of 500:1 fragment to spore, whose rate can increase when molds are disrupted during clean-up. Fragments can range from nanoparticle size to 3 microns and are missed by conventional environmental testing methods which only detect spores. The human respiratory system can clear fragments greater than 2 microns in size in the secondary bronchi. Anything smaller bypasses the mucociliary clearance system at the terminal bronchi and can be adsorbed into the lung tissue. Fragments may be the culprit behind sinus irritation, airway remodeling, and colonization (discussed later). Fragments also secrete mycotoxins.
We are already familiar with mycotoxins. Alcohol formed from brewer's yeast is a popularly ingested mycotoxin. Taken in controlled doses, it can cause desirable physiologic effects. Taken in excess, it can be deadly. We are also familiar with St. Anthony's fire, gangrene caused by a mycotoxin called ergot from the Claviceps purpurea fungus which grew on stored grains, primarily rye. This same mycotoxin was to later be blamed for the mysterious and frightening changes seen in the young women of Salem who processed the infected grain. These women became poisoned by the toxin and appeared possessed. Ergot causes small vessel vasculitis of the CNS and GI systems, creating the convulsions and wrenching blamed as witchcraft.
Mycotoxins are highly lipophilic toxins in nanoparticle size of less than 0.01 microns (or 10 nanometers). They have a wide structural and biosynthetic diversity and are responsible for the smell of 'must' or mildew as they are aerosolized or secreted onto the growth substrate by the mold spore or spore fragment. Their lipid solubility and small size lend to their toxicity. Not only can they be inhaled via the lungs, they can be absorbed through the nasal mucosa and the dermis and taken into enterocytes in the gastrointestinal system where certain strains can induce apoptosis of the intestinal epithelial cells.10 It is important to understand that if it is possible to smell mycotoxin 'must' or mildew, it is highly likely these toxins are being absorbed into the body. And conversely, it is important to learn that many toxic molds cannot be detected by scent alone since they may exist behind walls and underneath materials such as flooring.
Mycotoxins have well-established negative human impacts. These impacts are so reliable in fact that they're being used in oncology for their apoptotic activity and have been weaponized. A comprehensive review article investigating the mechanism of injury of mycotoxins found them to have diverse and synergistic actions.11 Mycotoxins are potent nerve toxins to both central and peripheral nervous system. They are highly inflammatory to lung tissue, causing airway remodeling with chronic exposure. Mycotoxins cause mitochondrial stress and damage via Nrf2 activation (an oxidation thermostat inside the cell) and eventual depletion.12 Mycotoxins are responsible for immune suppression and modulation. They impair immune host defenses, reduce natural-killer cell function, and reduce lymphocyte count and function. Consistent with other environmental toxins, mold mycotoxins must be detoxified in the liver via the cytochrome p450 system in Phase I detoxification. In Phase II, mycotoxins are detoxified via glutathione-S-transferase conjugation with reduced glutathione, therefore glutathione depletion is a common finding with mold and mycotoxin exposed patients.13 Certain polymorphisms increase a person's susceptibility to mycotoxins.14
Some mycotoxins have been shown to cross the blood-brain barrier and reduce its integrity leading to blood-brain barrier compromise. During inhalation exposure, mycotoxins travel the olfactory nerve to the hippocampus and frontal lobe. A patient of the author, for instance, with a decade-long exposure to toxic black mold developed cancer in exactly those two locations in the brain. Many mycotoxins can cross the placenta and are shown to bioactivate in utero, making them teratogenic. They are also found in breast milk. In summary mold mycotoxins are neurotoxic, nephrotoxic, hepatotoxic, hepatocarcinogenic, tera-togenic, and carcinogenic. Table 1 lists mycotoxins of concern of which we are currently aware, however research is ongoing. This is not to be considered an exhaustive list.
Table 1: Known Mycotoxins and Sources
Mycotoxin Mold source
Aflatoxin Aspergillus flavus, A. parasiticus
Chaetoglobosin A,C Chaetomium globosum
Gliotoxin Aspergillus fumigatus
Ochratoxin A Aspergillus ochraseus, A. niger, Penicillium verrucosum,
P. nordicum, P. chrysogenum
Trichothecenes Stachybotrys chartarum, Trichoderma viridae, Fusarium spp
Conditions associated with mycotoxin exposure range from EENT to dermatology to gastroenterology to immunology and beyond. Most commonly seen symptoms other than chronic sinusitis and respiratory distress are anxiety, insomnia, tinnitus, peripheral neuropathies, interstitial lung disease, interstitial cystitis, nephritis, dysbiosis, bloating, chronic fatigue syndrome, and acquired immune deficiency of the T- and B-cells to name a few. If all other factors have been ruled-out for infertility patients, consider mold toxicity.
While mycotoxins are more of a concern than spores from a toxicity perspective, people that are chronically exposed and immune depleted can also host actual spore colonies. The colonies of spores primarily reside in the sinuses, with a minute percentage residing in lungs, brain, and intestines. A study on rhinosinusitis surgical patients found that those with sinus biofilm had both more severe disease pre-surgically and worse outcomes including persistent infections post-surgically.15
Colonization is different than infection. Aspergillosis of the lungs, a very serious fungal infection of the lungs seen in immunodeficient patients, is a deadly condition. In contrast, colonization can exist undetected without the person falling terribly ill. Colonized spores don't invade the bloodstream. White counts may fall rather than rise, so it isn't easily discovered on labs. Currently, colonization's impact on health is a controversial concept. Infectious disease doctors differ in their opinion on whether these colonies create disease beyond the sinuses, if at all. Normal controls in multiple studies on chronic rhinosinusitis patients find fungal spores in nasal washings, leading to the conclusion that everyone is hosting fungus in their sinuses. The difference, it appears, is whether these colonies are forming mycotoxins and whether the person had been exposed to a water-damaged building.16 Even though fungal DNA may be detected in normal controls, mycotoxins are not. Mycotoxins are only found in nasal washings of sick patients.17 And even though normal controls in chronic rhinosinusitis studies find fungi that form mycotoxins in the sinuses, it's a false assumption to believe that some fungal colonies aren't having a negative impact on whole health. This misunderstanding of mycotoxin illness is where medicine is currently falling short. Mold illness is more than spore illness. It's also a toxicity illness, a mycotoxicity illness. These patients are 'vertically sick' rather than 'horizontally sick'. As discussed earlier, respiratory illness is not the only presentation of mold-related illness.
Now that we have the ability to easily test for the presence of mycotoxins in the body, it is becoming increasingly simpler to identify which colonies are harming human health and which are 'normal' findings. One study of chronic fatigue patients found that 93% were positive for at least one mycotoxin detected in urine, and almost 30% had more than one mycotoxin present, while normal controls had no detectable mycotoxins.18 Despite the controversy, acknowledging the presence of morbidity-contributing fungal colonies in mold-exposed patients has revolutionized treatments for these patients.
Regarding treatment, Dr. Walter Crinnion teaches, the first three treatment rules for the toxic patient are: 1) Avoidance, 2) Avoidance, 3) Avoidance.19 Mold-sensitized patients must be removed from the water-damaged building environment and its contents. This means, for some patients, taking no possessions from the water-damaged structure. In most environmental illnesses, avoidance is an effective first step. But in the case of mold toxicity and intranasal colonization, the patient brings the problem with him. An occupational study looking at remediation of a water-damaged office building found that outcomes were better if employees were removed during remediation, but simply removing employees from the building didn't ameliorate all symptoms.20 This further affirms the concept of colonization and the need for intranasal directed treatment. With every inhalation or pass of blood through the capillaries beneath the colony, mycotoxins can be absorbed. Other explanations for the findings in this study are residual fragments from clean-up, increased mycotoxin production as mold reacts to danger,21 and mycotoxin off-gassing from porous materials. A certified building biologist is a powerful ally in helping mold-exposed patients find the cause of their illness and stay protected during remediation.
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