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Black Mold: The Great Pretender

Black Mold TPby Chris D. Meletis, N.D.

Nothing is more frustrating than working with a patient who doesn’t seem to respond to any regimen we prescribe. In the case of these stubborn, unresolved health concerns—especially if they are respiratory, autoimmune or fatigue related or involve frequent headaches or joint pain—the cause may be something that’s often not even considered. I’m referring to black mold.

Understanding Black Mold

Black mold is the common name for a type of fungus known as Stachybotrys chartarum. It’s a greenish-black color and is usually slimy due to a wet layer on the top. If a colony’s water source goes dry, however, the mold can appear dry and powdery.

Approximately one-third of the S. chartarum isolates from the United States and Europe represent a chemotype that produces macrocyclic trichothecene mycotoxins,1 which are responsible for the mold’s health damaging effects and the reason why it’s called "toxic black mold".

Black mold grows on cellulose-based materials such as wood, ceiling tiles and dry wall, although it doesn’t grow as quickly or as easily as most molds.

In some cases, the mold isn’t visible because it’s growing on hidden surfaces, such as the backside of dry wall, wallpaper or paneling, the top of ceiling tiles and the underside of carpets and pads. When there are leaking or condensing pipes, hidden mold also can take over in pipe chases and utility tunnels. Condensation also can occur in walls behind furniture, drain pans inside air handling units, porous thermal or acoustic liners inside ductwork or roof materials above ceiling tiles.

Black mold is not the only harmful mold to grow inside houses. In fact, after Hurricane Katrina, another toxic mold, penicillium, was thought to be an equally prominent threat to flooded New Orleans homes.2

A Growing Health Threat

Black mold can occur anywhere throughout the country. And if your practice is located in the Northeast coastal United States, a discussion about black mold is especially timely since many of the houses flooded by Superstorm Sandy are at risk of developing black mold—and the occupants at risk of developing related health conditions.

Surprisingly, though, dry climates are as much at risk of mold invasion as wet climates. The mold that grows in desert regions can be especially tenacious, since it’s had to adapt to the drier air.

Once black mold takes hold in a house, its presence is often obvious due to an unpleasant odor that can be musty, moldy or even smell like urine. However, in some cases, people may mistake the odor for something else. For example, one contractor in Hawaii was renting a house with his wife. Two of the rooms in the house flooded twice during a very wet winter. After the flooding, the rooms smelled like cat urine. The couple just assumed the moisture brought out the smell caused by a cat owned by a previous tenant. When the contractor’s wife and mother-in-law became sick, they began to suspect the smell was really due to black mold.

The first negative health effects caused by black mold’s presence—especially in sensitive people who have mold sensitivities or allergies—may appear before the mold can be seen. Stachybotrys chartarum and other black fungi can’t be seen by the human eye until they form colonies of substantial size.

Mimics Many Diseases

Black mold is "the Great Pretender" because its effects on the body mirror many other diseases. Patients who already have asthma, COPD or a history of allergic rhinitis are the most vulnerable, and the restricted breathing caused by the black mold can result in respiratory failure, organ damage and, on rare occasions, death.

Molds have been strongly linked to the worsening of asthma, although it’s less clear whether they can contribute to the development of the disease. An estimated 21.8 million people have asthma in the United States and it’s thought that approximately 4.6 million cases may be attributed to dampness and mold exposure in the home.3

Symptoms of coughing, wheezing and shortness of breath are warning signs that breathing difficulties may escalate to respiratory failure. Even healthy people without mold allergies who breathe in the mold spores are at risk of respiratory problems related to the mold.

Symptoms in the eyes manifest as allergic conjunctivitis with red, watery and itchy eyes and usually appear immediately after exposure to the mold. Contact dermatitis also can occur in some patients who have mold allergies, but may take several days to appear. The skin may start to itch and a rash forms.

After mold exposure, fluid may accumulate in the nose and sinuses. Intense sneezing triggers migration of the fluid. This results in a runny nose, nasal itching, postnasal drip and congestion—symptoms that mimic hay fever. Many humans have antibodies to proteins produced by Stachybotrys chartarum, causing an allergic reaction that is likely responsible for the allergy symptoms after exposure to black mold.4

Repeated allergic reactions to mold can produce constant inflammation of the lung tissue (pneumonitis), which is characterized by fever, chills, coughing and difficulty breathing that begins a few hours after mold exposure. If the patient continues to be exposed to the mold, chronic breathing problems are accompanied by a loss of energy and weight. At this stage, repairing the tissue damaged by inflammation may be difficult or impossible. Gradually,this interferes with lung function.

People living in mold-infested homes are at an increased risk for another lung disease—sarcoidosis. In a study presented during CHEST 2012, the annual meeting of the American College of Chest Physicians, researchers tested 62 non-smoking sarcoidosis patients. Thirty-four of the subjects had extrapulmonary manifestations of the disease. The researchers tested the subjects for beta-glucan, an immune-modulating agent found in fungi, and accompanying inflammatory biomarkers, including interleukin (IL)-6, IL-10 and IL-12. The scientists also collected samples from 18 control subjects with no pulmonary disease or respiratory symptoms.

Levels of IL-6 and IL-12 were higher among subjects with sarcoidosis as compared with controls, and IL-12 was significantly higher among subjects with extrapulmonary manifestations. The researchers also found a significant relationship between beta-glucan and mold/ fungi levels in the home, leading them to conclude, "The results further support the hypothesis that exposure to fungi is important for the risk of sarcoidosis."5

Inhaling mold spores can also cause a fungal infection of the lung called aspergillosis, which is more likely to occur in people who have had prior lung damage from surgery, asthma or other lung conditions. The fungal lung infection may cause damage to the lung tissue, as well as blood clots. The infection may spread to other organs. Sometimes, symptoms resolve when people move out of mold-infested homes. Other times, the symptoms will remain long after exposure.

How Does it Exert Its Bad Effects?

Mycotoxins in the mold, which are carried on the spores and are also found throughout the entire mold colony, are responsible for the damaging health effects of black mold. Toxic black mold produces trichothecene mycotoxins, some of the most toxic and stable mycotoxins, which can take several years to break down and are extremely difficult to remove from homes. In one study, no remediation treatment could eliminate all the toxins from the damaged materials.6

One type of trichothecene mycotoxin produced in Stachybotrys chartarum is Satratoxin-G (SG), which has been shown to cause harmful respiratory effects in animals. In monkeys, whose nasal airways resemble those of humans, daily exposure to the SG mycotoxin for four days caused acute rhinitis, atrophy of the olfactory epithelium and programmed cell death (apoptosis) of olfactory sensory neurons.7

It is thought that, among other actions, macrocyclic trichothecenes might be able to damage DNA. In a study reported in 2007, researchers determined that aqueous extracts of trichothecene-producing S. chartarum spores caused DNA fragmentation in developing rat lung fibroblasts.8

Trichothecenes exposure also results in elevated expression of inflammatory markers such as TNF-, IL-6 and IL-1® and the chemokine macrophage-inflammatory protein-2 (MIP-2) in both the nasal airways and the adjacent olfactory bulb ofthe brain.9

The Bacterial Connection

In water-damaged homes and offices, bacteria often grow side-by-side with mold, exacerbating the negative health consequences. In a study published in 2012, researchers linked two specific strains of bacteria—Stenotrophomonas maltophilia and Mycobacterium—to indoor mold growing after water damage.10

Tests and Treatments

Black MoldTo determine if mold is the source of your patient’s health concerns, begin by asking the questions listed in Table 1.

Patients can also use an at-home mold test. When testing for mold at home, it’s best to get both an air sample and a surface sample. This is because when mold first starts growing on a surface, it may not be releasing many mold spores into the air. In this case, air sampling alone wouldn’t accurately portray the extent of mold growth. And during random surface sampling, the sample taken might not be from a surface where mold growth is at its worse or where it is releasing the most mold spores.

One at-home test kit for your patients to try is made by Pro-Lab (www.prolabinc.com/mold-kits.asp) and is available at Home Depot and Lowe’s.

If the presence of mold is confirmed, patients should be urged to move away from the mold-infested home, if possible.

If that’s not possible, a professional remediation company should be used to remove the mold.

The chosen company should be certified by: IICRC (Institute of Inspection, Cleaning and Restoration Certification), NORMI (National Organization of Remediators and Mold Inspectors), ACAC (American Council for Accredited Certification) or RIA (Restoration Industry Association). It’s also important to verify the remediator’s qualifications and insurance (liability as well as workman’s comp).

Everything that came in contact with mold should be thrown away. This includes mattresses, clothing that can’t be cleaned, pillows, etc. Only objects certified by an expert as clean should be kept. This is important because mold spores can’t be detected with the naked eye.

Other important steps include making sure the home’s ventilation system is clean and replacing carpet in the home, since it’s virtually impossible to completely clean all the mold spores out of the carpet. Investing in an air purification system that uses low levels of ozone also is a good idea.

Finally, modifying the diet to eliminate foods that weaken the immune system or cause cross-reactivity is another way to strengthen the body after exposure to black mold. People may become sensitized to black mold and therefore have an allergic reaction to various foods, especially those foods that are subject to getting moldy.

Black Mold Table 1

Critical Supplemental Support

Black MoldHealth problems may continue long after the mold source is removed from a patient’s life. That is why it’s important to use key nutritional supplements to support patients’ health both during and after mold exposure. Three important foundational supplements are probiotics, vitamin D and the immune-balancing, fermented yeast known as Saccharomyces cerevisiae.

Probiotics such as Lactobacillus strengthen the intestinal tract against fungus and increase immunity and respiratory health.11-12 Vitamin D was found to prevent allergy to Aspergillus fumigatus, a common mold that often causes allergy symptoms in asthmatics and patients with cystic fibrosis.13-14 The fermented yeast Saccharomyces cerevisiae strengthens secretory IgA, the protective coating on the mucous membranes, which helps create a mold-blocking shield and reduces allergic rhinitis symptoms.15

Addressing inflammation also is important in patients exposed to mold. Herbs such as Stephania tetrandra, Ocimum sanctum (holy basil), Zingiber officinale (ginger) and Boswellia serrata (frankincense) have been shown to decrease various inflammatory mediators.

Several studies have shown that ginger inhibits pro-inflammatory cytokines, including IL-1beta, IL-2, IL-12, TNF-alpha and interferon (IFN)-gamma.16 Similarly, holy basil leaf inhibits both COX and 5-LOX,17 and the boswellic acids derived from boswellia are potent inhibitors of the 5-LOX enzyme.18 The anti-inflammatory constituents tetrandrine and fangchinopne found in Stephania tetrandra have been shown to decrease IL-1beta, IL-6, IL-8 and TNF-alpha,19 as well as decrease leukotriene and prostaglandin generation.20

If the patient is reacting to the mold with hay-fever-like symptoms, a combination of quercetin, bromelain and vitamin C can provide antiallergy support.

Quercetin has inhibited allergen-stimulated histamine bursts from the body’s mast cells and basophils in preliminary trials of patients with allergic rhinitis.21 Similarly, bromelain, when taken on an empty stomach, stimulates anti-inflammatory prostaglandins and blocks proinflammatory prostaglandins.22-23

Vitamin C is another histamine blocker. Research shows that low plasma levels of this vitamin correspond to higher overall histamine levels—and that 2 grams of vitamin C supplementation per day can lower blood histamine measurements by as much as 38 percent within just one week.24

Finally, clear the mold toxins from the body by putting the patient on a good detoxification regimen and a fiber supplement.

Conclusion

We often don’t suspect black mold as the cause behind an illness. Yet, investigating whether this is the source of your patients’ health complaints will ensure you’re getting to the root of the problem, allowing you to tailor your treatments to the real reason for their poor health.

References:

1. Andersen B, et al. Mycologia. 2002;94:392-403.

2. Chew GL, et al. Environ Health Perspect. 2006 Dec;114(12):1883-9.

3. Mudarri D, et al. Indoor Air. 2007;17:226-35.

4. Shi C, et al. Int Arch Allergy Immunol. 2011;155(1):74-85.

5. http://www.chestnet.org/accp/article/ mold-exposure-home-could-increase-risk-sarcoidosis.

6. Peitzsch M, et al. J Environ Monit. 2012 Mar;14(3):908-15.

7. Carey SA, et al. Toxicol Pathol. 2012 Aug;40(6):887-98.

8. McCrae KC, et al. Pediatr Pulmonol. 2007;104(1):4-26.

9. http://toxsci.oxfordjournals.org/content/104/1/4.long#ref-109. 10. http://www.sciencedaily.com/releases/2012/06/120619230226.htm.

10. Rao JS, et al. Transl Psychiatry. 2012 Jul 3;2:e132.

11. Guo J, et al. Bioeng Bugs. 2012 Mar-Apr;3(2):104-13.

12. Abreu NA, et al. Sci Transl Med. 2012 Sep 12;4(151):151ra124.

13. Coughlan CA, et al. Am J Respir Crit Care Med. 2012 Nov 15;186(10):999-1007.

14. Kreindler JL, et al. J Clin Invest. 2010 Sep;120(9):3242-54.

15. Moyad MA, et al. Adv Ther. 2009;26(8):795-804.

16. Tripathi S, et al. BMC Complement Altern Med. 2008 Jan 3;8:1.

17. Singh S, et al. J Ethnopharmacol. 1996 Oct;54(1):19-26.

18. Uz T, et al. FASEB J. 1998;12:439-49.

19. Tak P, Firestein G. J Cpn Invest. 2001;107:7-11.

20. Teh BS, et al. Int J Immunopharmacol. 1990;12(3):321-6.

21. Pearce F, et al. J Allergy Clin Immunol. 1984;73:819-23.

22. Taussig S. Med Hypoth. 1980;99-104.