Mycotoxin Affect On The Respiratory System
This Article is being worked on. Will have it organized and rewritten soon.
Strong lungs can give us better health. When we breathe deep, the blood is invigorated, the skin radiant and the thoughts clear.
Along with our skin, the respiratory system is one of the first organs that is assaulted by mycotoxins in our environment. This causes a variety of reactions as the respiratory system reacts to and attempts to remove these toxins. The surface of the lungs facilitates the transfer of compounds across its surface in both directions. It is the first point of contact for airborne xenobiotics. Xenobiotics (foreign chemicals) that enter the systemic circulation via the lungs have access to other tissues before they are metabolised by phase I and II enzymes of the liver. Orally ingested xenobiotics, in contrast, undergo the livers first pass effect giving the body a chance to transform them early-on before they cause damage.
Research suggests a role for environmental toxicants in the pathogenesis of lung diseases. This has lead to interest in xenobiotic metabolizing capacity or the lung. It is evident from the studies carried out to date CYP1A1, 1B1, 2A13, 2F1, 2S1 and 4B1 are preferentially expressed in the lung together with CYP2E1 and 3A5. Many phase II transformation pathways are also involved in the lungs biotransformational abilities of xenobiotics.
Mycotoxins along with other environmental pollutants can enter the lungs activating enzymes. This is thought to irritate, inflame, and open the tight junctions between the epithelial cells that prevents entry of environmental toxins. There is a breakdown of protein complexes in these tight junctions that allows entry of antigens, chemicals, and xenobiotics into the circulation which can lead to the formation of autoantibodies. These autoantibodies then cause a variety of systemic inflammatory responses through-out the body and a variety of symptoms. Mycotoxins appear to be getting through these tight junction barriers and causing reactions of an acute, subacute and chronic nature.
Some of the more acute and common reactions people with mold sensitivity notice are scratchy/sore throats, oral lesions (canker sores,herpetic), coughing, nasal/sinus congestion and runny noses. These tissues are constantly receiving air from our environment and it is no wonder that they react so quickly and show symptoms immediately or within 24 hours after a sensitive person is exposed to a water-damaged building. Two inflammatory markers that are often high in people with CIRS are MMP-9 and TGF-beta 1. (More data below on these biomarkers.) These markers are associated with respiratory inflammation/irritation/disease. There are many herbs and nutrients that can help decrease overall inflammation and lower these markers. See this link for treatment details.
Our respiratory system is set up to protect us from particulate matter, noxious fumes and such. It has a coating of mucus that protects the lungs surface. It catches particles in this mucus which acts as a barrier. Fine hairs called cilia that line the respiratory tract move the toxins out away from the lungs. It also protects us through an olfactory warning system. Many mold avoiders know this system well. You notice bad smells. You know when there is mold, hazardous chemicals or other odors around. As a person cleans the mycotoxins out of their body this olfactory alarm seems to get more sensitive. Don't get upset at this system. It is here to serve you. Additionally, the extreme olfactory sensitivity usually quiets down after months to a year for most folks. The mucus that our respiratory system produces is our friend in small amounts although it can be annoying when on overdrive. It is there to protect our delicate mucous membranes. The mucus catches particulate matter and the cilia move it out of the respiratory tract into the nose to be "blown out" or it ends up being dumped into the digestive tract. The mucus also acts as a barrier to protect our cells from damage.
It has been known for some time that people with chronic rhinosinusitis harbor numerous fungal organisms. Of the fungal organisms that have been observed such as Aspergillus, Chaetomium, Fusarium, Penicillium, and Trichoderma, many of these have the potential to produce mycotoxins. A research article review I read noted that in one study, both those with sinusitis and controls had equal prevalence of fungal organisms and that essentially everyone has nasal fungi. However, mycotoxins were not found in nasal washings from healthy controls, though they were in those previously exposed to a moldy environment.
See the research below which looks at low levels of mycotoxin and air particulate matter separately and then looks at them in combination. Notice that there was little reaction alone, but when low levels of these two respiratory irritants were combined they caused inflammation and damage.
Inflammatory Markers Seen In CIRS related to Lung Irritation/Damage
MMP-9 is an inflammatory marker than is sometimes elevated in people with CIRS
Matrix metallopeptidase 9 (MMP-9) is an enzyme. Proteins of the MMP9 family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes.
It has been implicated in pathogenesis of Chronic Obstructive Pulmonary Disease (COPD) by destruction of lung elastin, in rheumatoid arthritis, atherosclerosis, cardiomyopathy, and abdominal aortic aneurysm.
MMP-9 delivers inflammatory elements of of blood into subintimal spaces, where further delivery into solid organs (brain, lung, muscle, peripheral nerve and joint) is initiated.
TGF B-1 is an inflammatory marker than is often elevated in people with CIRS
Transforming growth factor-β1 is involved in maintenance of tissue homeostasis. TGF β-1 is often chronically over-expressed in disease states, including cancer, fibrosis and inflammation. It is moderately to extremely high in Chronic Inflammatory Response Syndrome due to water-damaged building (CIRS).
TGF b-1 is associated with various lung diseases. It is involved in pathogenesis of bronchopulmonary dysplasia, associated with lung fibrosis and asthma. It is elevated in premature infant respiratory distress after birth.
Prevention & Treatment
All people with mold issues should be under a treatment regime for CIRS.
Our lungs should be moist at all times. Too moist and we start coughing up phlegm. Too dry and we get a dry cough, loss of voice, and a dry throat and nasal passages. Generally acute inflammation brings on mucus and excess moisture while chronic inflammation of long duration can end up causing dryness.
We can protect our respiratory system by staying out of moldy environments. If you smell mold, leave the area. However, I realize this is not always possible. So,when in a moldy environment you can protect yourself by wearing masks. It is important to cover both the nose and the mouth well and to have equipment that keeps as much of the tiny mycotoxin particles out as possible. I have a write up on masks that you can read here.
Sometimes people know they will have to be in a moldy environment and they use cholestyramine or other binders and or VIP or supplements. I find an herbal mix of Echinacea/Osha/licorice is helpful. Now none of these things are perfect and often people still have reactions but they are lessened.
The general treatment protocols I list in the Treatment section are helpful for people with respiratory reactions to mold but the following information is specific to the respiratory tract rather than how to treat CIRS in general.
How to Protect and Support the Respiratory Tract in A Moldy Environment
Just as you take a shower after being in a moldy environment to wash it off your skin and hair, you should also wash your nasal passages and mouth if needed.
Irrigation of the nasal passages via a neti pot or even snorting saline/water after an exposure can be beneficial. Irrigating your mouth by gargling can also help prevent reactions. (Although your saliva washes a lot of debris down to the stomach fairly quickly.)
If the sinuses are closed and need to be opened up to allow them to drain, an herbal steam inhalation of peppermint works great. I wrote a blog on how this is done here.
People who have continual sinus/nasal inflammation/irritation from mold find using colloidal silver, and/or astringent herbs can be helpful. One mix that has been used successfully is colloidal silver and oregon grape root bark. Argentyn 23 and Sovereign Silver both seem to be colloidal silver brands that people get results from.
A tea is made by using a heaping teaspoon of root bark to 1 cup water and simmering it for 30 minutes with lid. Strain the tea and add 1/4 teaspoon salt and then use 1/4 cup tea with 1 Tablespoon colloidal silver as a wash. As an alternative, some folks use a colloidal nasal spray and make a tea to use separately. Some folks find the colloidal nasal spray by itself is fine or they just use the tea.
One reason for adding oregon grape is as a biofilm breake r. It has been noted that quite a few folks who have mold sensitivity also have a Multiple Antibiotic Resistant Coagulase Negative Staph (MARCoNS). These microbes create a biofilm and oregon grape helps break up biofilms. A spray called BEG spray which is an antibiotic spray is another choice of treating MARCoNS and may be necessary if the colloidal silver and oregon grape do not work. Not everyone with mold has MARCoNS but those who do often end up using BEG spray to kill the hard to kill microbes. Using oregon grape in addition to the BEG spray will help break up the biofilm the microbes create to protect them from the antibiotics in the BEG spray.
Another nasal spray used to wash and keep the nasal passages clear by mold folks is Xclear. My only concern with this product is that it contains grapefruit seed extract and I am not sure if it is one of the grapefruit seed extracts that has had chemicals used to extract it. For details on why grapefruit seed extract is a concern, go to my blog here.
If you like Xclear but don't want to use it with the preservative in it, simply make your own product up with Xylitol and saline.
Supporting the Lungs
We want our mucus and cilia to be working well as a first line of defense. If a person tends to be dry, has a dry cough, dry throat, lowered voice, this is probably indicative of a lack of moisture. This can be localized to the lungs or full body. If localized to the lungs, supportive herbs such as plantain, mucilaginous herbs can be used to support moisture. See the list below.
However, often this is a systemic problem that can be caused by organ issues in the kidneys or adrenals. In these cases the person is also thirsty, has dry skin, and may urinate a lot and may get a lot of static electrical shocks.
Additionally, food and drink should be examined. Any food or herb that acts as a diuretic
Do Not Consume Diuretic Food, Herbs or Medicines if you have an issue with dryness. They will add to the dryness.
Herbal diuretics would include but are not limited to:
- Boneset (Eupatorium perfoliatum)
• Burdock (Arctium lappa)
• Cleavers (Galium aparine)
• Corn silk (Zea mays)
• Couch grass (Elytrigia repens)
• Dandelion (Taraxacum officinalis)
• Elder (Sambucus nigra/canadensis)
• Garlic (Allium sativa)
• Gravel root (Eupatorium purpureum) - contains pyrrolizidine alkaloids
• Juniper (Juniperus communis)
• Linden flower (Tilia spp.)
• Nettle (Urtica dioica)
• Parsley (Petroselinum sativum/crispum)
• Yarrow (Achillea millefolium)
Additionally coffee, black and green tea, and alcohol are strong diuretics. So are melons. The inside rind of the melon has the stongest diuretic action of the melon.
Bitter herbs should not be used in this condition as it will cause more dryness.
Moistening Herbs and Food
Herbs and food that can help to promote fluid are almonds, american ginseng, coconut oil, codonopsis, eggs, cold water fish, fish oil, flaxseeds, jerusalem artichoke, jujubee dates, licorice, marshmallow, or wild mallows, milk and diary products in general (organic with full fat), oats, puslane, sea vegetables, sesame seeds and oil, schizandra,slippery elm, rehmannia, and saw palmetto. This is not a complete list. These are just a few ideas.
Vitamin D & Sunshine: In the lungs, deficiency of vitamin D is associated with accelerated decline in lung function. Chronic respiratory diseases associated with vitamin D deficiency include cystic fibrosis, interstitial lung disease and chronic obstructive pulmonary disease (COPD). Deficiency of vitamin D has also been associated with increased risk of respiratory infection from influenza A and Mycobacterium tuberculosis. Absence of Vitamin D receptors (VDR) in mouse lungs can lead to an early onset of emphysema/COPD because of chronic inflammation, immune dysregulation and lung destruction. As of yet, there is no report on VDR regulation of cell junction proteins in lungs like there is in the intestines, but this is also a possibility.
VDR activators, such as calcitriol, doxercalciferol, paricalcitol or alfacalcidol, are used to activate the vitamin D signaling pathways in the VDR. By the way, the VDR is affecting transcription of over 1000 genes that impact calcium and antimicrobial peptides.
Vitamin D is often found to be low in folks with mycotoxin issues.
Most patients who are treated for Mold Illness will have a low Vitamin D level rise to normal levels after treatment for CIRS even if you do not give them vitamin D during that the treatment.
If vitamin D is low, it may be beneficial to give vitamin D3 at least in the beginning of treatment until it is normalized. It may not normalize however and I have written below as to why vitamn D levels may not rise. In this case vitamin D may not be useful and some feel it may be counter-productive.
Vit D decreases levels of TGF-β and NF-kappaB. Monitor levels fof vitamin D for correct dosage.
There is a massive amount of research connecting low vitamin D levels to many disease processes. However, we do not know for sure that supplementation is working as we would wish it to, so sunshine is really the best way to go. Let the body decide what to make. I have found that some people with CIRS can easily react to the sun and I think it is due to the low MSH levels. Once the person removes themselves from mold and they use a sequestering agent to remove the mycotoxins they are usually able to go into the sun without getting terrible sunburns as well as other skin reactions they get from the sun. I have actually had three people report getting burnt through their clothing.
I would like to share some important data regarding vitamin D and the VDR but I have not yet written it up. However I would say that low levels of Vitamin D may be a protective response of the body. This may be a result and not a cause. It appears there may be an issue with a deffective microbiome due to pathogenic bug infiltration that causes high active vitamin D (calcitriol or 1,25(OH)(2)D(3) ) which then lowers the inactive major circulating form of Vitamin D3 (25-hydroxyvitamin D(3) or (25(OH)D(3)). Thus low vitamin D may not be the factor causing the issues. Possibly it is a result of issues going on in the body. Clearly, we don't know enough about this.
Some Docs are now taking both 25 hydroxy levels and 1,25 hydroxy levels and if the 1,25 is high and the 25 is low, they do not treat. If 25 is low and the 1,25 is low or normal they treat. If the 25 stays lower and the 1,25 goes up, treatment is often curtailed. There are some practitioners who are telling patients not to take vitamin D3, stay out of the sun so they do not raise the 25 or D3 level and at the same time they are giving pulsed doses of antibiotics to kill off microbes they believe are causing dysregulation of the VDR. Additionally they are giving a VDR agonist to stimulate the VDR. If you want to know more about this protocol is called the Marshall protocol. I would mention that some of the theories this protocol is based on is not well reaserched or researched by running computerized programs. However, the theory is very appealing and does explain a lot of things we have been noting. I am not on line with all the assumptions or the fact that the internal terrain as well as the external terrain is being ignored.
When the lungs are too dry or too moist they can get infectied by opportunistic bacteria. When there is lack of moisture, moistening herbs called demulcents can be used. This would include but is not limited to the following.
Examples of moistening herbs:
• Aloe vera - internal juicy part (not external skin area- which is bitter and has a laxative effect)
• Borage - Borago officinalis
• Chia seed - Salvia hispania
• Corn silk - Zea mays
• Fenugreek - Trigonella foenum-graecum
• Flax - Linum usitatissimum
• Guar - Cyamopsis tetragonolobus (ground endosperm)
• Marshmallow - Althea officinalis
• Oats - Avena sativa
• Okra - Abelmoschus esculentus
• Plantain - Plantago spp.
• Psyllium seeds - Plantago ovata
• Quince seed - Cydonia oblonga
• Slippery elm - Ulmus fulva/rubra
If there is an abundance of moisture it is generally better to use stimulating expectorants. These are safer than drying or diuretic herbs. However, it can depend on the situation. Some herbs have both qualities. Sometimes you need diuretics or drying herbs but many mold folks are too dry already.
Examples of stimulating or irritating expectorants:
• Elecampane (Inula helenium)
• Gumweed (Grindelia spp.)
• Horehound (Marrubium vulgare)
• Peppermint - Mentha piperita
• Poplar buds (Populus spp.)
• Thyme (Thymus vulgaris)
• Yerba santa (Eriodictyon californicum)
Examples of drying herbs.
See data on herbal diuretics and drying herbs above.
Sometimes an antimicrobial is needed:
• Calendula (Calendula officinalis)
• Cinnamon (Cinnamomum spp.)
• Echinacea (Echinacea spp.)
• Elecampane (Inula helenium)
• Garlic - fresh (Allium sativa)
• Goldenseal (Hydrastis canadensis)
• Horseradish (Armoracia rusticana)
• Myrrh (Commiphora myrrha)
• Old man’s beard (Usnea spp.)
• Oregon grape (Mahonia spp.)
• Oregano (Origanum vulgare)
• Thyme (Thymus vulgaris)
• Yarrow (Achillea millefolium)
Sometimes bronchodilators are needed:
• Anise (Pimpinella anisum)
• Chamomile (Matricaria recutita)
• Cramp bark (Viburnum opulus)
• Dong quai (Angelica sinensis)
• Elecampane (Inula helenium)
• Khella (Ammi visnaga)
• Peppermint (Mentha piperita)
• Osha (Ligusticum porteri)
• Thyme (Thymus vulgaris)
• Wild yam (Dioscorea villosa)
• Yarrow (Achillea millefolium)
• Yerba santa (Eriodictyon spp.)
Sometimes antiiflammatories are needed:
• Angelica - Angelica archangelica
• Calendula - Calendula officinalis
• Chamomile - Matricaria recutita
• Chickweed - Stellaria media
• Fennel - Foeniculum vulgare
• Fenugreek - Trigonella foenum-graecum
• Hyssop - Hyssopus officinalis
• Licorice - Glycyrrhiza glabra
• Linden - Tillia spp.
• Marshmallow - Althaea officinalis
• Turmeric - Curcuma longa
• Yarrow - Achillea millefolium
• Yucca - Yucca spp.
I have started to place research abstracts related to mold and the respiratory system here as I look up new articles. When I have time, I will add more and set this up in its own section with a link from here.
Toxicon. 2015 Aug 8;104:65-72. doi: 10.1016/j.toxicon.2015.08.008. [Epub ahead of print]
Synergistic inflammatory effect of PM10 with mycotoxin deoxynivalenol on human lung epithelial cells.
Capasso L1, Longhin E1, Caloni F2, Camatini M1, Gualtieri M3.
The presence of deoxynivalenol (DON), a mycotoxin produced by Fusarium species, has been reported worldwide in food and feedstuffs. Even though oral intake is the main route of exposure, DON inhalation is also of concern in workers and exposed population. Particulate matter (PM) is one of the most important causes of air quality detriment and it induces several adverse health effects. Therefore it is of primary importance to understand possible combined effects of DON and PM. The alveolar type II, A549, and the bronchial epithelial, BEAS-2B, cell lines were exposed for 24 h to different concentrations of DON (10-1000 ng/ml), PM10 (5 μg/cm2, sampled in summer or winter season), and a combination of these pollutants. Cell death, interleukins release and cell cycle alteration were analysed; protein array technique was also applied to evaluate proteins activation related to MAP-kinases cascade. Our results demonstrate that low doses of PM and DON used alone have scarce toxic effects, while induce cytotoxicity and inflammation when used in combination. This observation outlines the importance of investigation on the combined effects of air pollutants for their possible outcomes on human health.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Deoxynivalenol; Human pulmonary cells; Inflammation; In vitro; Particulate matter
PMID: 26263889 [PubMed - as supplied by publisher]
Eur J Immunol. 2014 Dec;44(12):3596-604. doi: 10.1002/eji.201444963. Epub 2014 Oct 29.
CD4(+) FoxP3(+) regulatory T cells suppress fatal T helper 2 cell immunity during pulmonary fungal infection.
Schulze B1, Piehler D, Eschke M, von Buttlar H, Köhler G, Sparwasser T, Alber G.
The opportunistic fungal pathogen Cryptococcus neoformans causes lung inflammation and fatal meningitis in immunocompromised patients. Regulatory T (Treg) cells play an important role in controlling immunity and homeostasis. However, their functional role during fungal infection is largely unknown. In this study, we investigated the role of Treg cells during experimental murine pulmonary C. neoformans infection. We show that the number of CD4(+) FoxP3(+) Treg cells in the lung increases significantly within the first 4 weeks after intranasal infection of BALB/c wild-type mice. To define the function of Treg cells we used DEREG mice allowing selective depletion of CD4(+) FoxP3(+) Treg cells by application of diphtheria toxin. In Treg cell-depleted mice, stronger pulmonary allergic inflammation with enhanced mucus production and pronounced eosinophilia, increased IgE production, and elevated fungal lung burden were found. This was accompanied by higher frequencies of GATA-3(+) T helper (Th) 2 cells with elevated capacity to produce interleukin (IL)-4, IL-5, and IL-13. In contrast, only a mild increase in the Th1-associated immune response unrelated to the fungal infection was observed. In conclusion, the data demonstrate that during fungal infection pulmonary Treg cells are induced and preferentially suppress Th2 cells thereby mediating enhanced fungal control.
© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Cryptococcus neoformans; Pulmonary fungal infection; Regulatory T (Treg) cells; Th2 immunity
PMID: 25187063 [PubMed - indexed for MEDLINE]
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