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Environmental Exposures and Health Issues

Friday, 19 November 2010 04:27
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                     Mycotox Pty Ltd
Phone: 1300 046 442    
 
 
            Indoor Environmental Quality (IEQ)-A Real Health Issue
 
                                         David Lark, Vince Neil
 
Research reports and increased discussion (19) in the medical literature in those countries who’s health specialists appear not to be suppressed by commercial entities have brought greater attention to public health concerns associated with  human exposure to an ever broadening range of indoor toxins(20), including those admitted from the outside air but more importantly those released from building products, plus those generated as a result of indoor bacterial and/or fungal/mould activity where that ecology has been exacerbated in water damaged buildings. Some of these products can be a cause of oxidative stress. (It's has been shown hydrolysis products from fungi/mould do cause oxidative stress (21)).

 

 

 

 
Leading microbiologist from the Hebrew University, Professor Isaac Ginsburg, said: “Today we are aware of around 100 conditions resulting from oxidation. Tibetan herbal preparations are particularly important for the future because we are at the end of the era of antibiotics. Inflammations and oxidative processes are usually caused by a broad spectrum of harmful substances, this is why they have to be treated by multi-compound preparations. There is not one omnipotent substance that could do this.”
 
 
It has been reported that many kinds of fungi and their fungal-associated products have the potential to disrupt human molecular biochemistry and physiology, resulting in various types of acute and chronic affliction.
 
Fungi/Mould by products found as indoor environmental contaminants are only part of the total exposure and are not the only components which can lead to health concerns. Testing shows that Bacterial activity is also a major component of this environmental soup, producing their own by-products.
 
 Moisture which is found when there is a fungal/bacterial concern, also further promotes an unhealthy indoor environment, as well as MVOC’s, there are also elevated VOC’s due to moisture affecting building products, glues, and floor coverings which maybe breaking down and releasing their own by products/gases as well, in any chemical soup there are numerous cumulative or synergistic reactions of these combined by products.
 
 The affects of these reactions have yet to be defined but an example of synergistic reactions was established by Professor Isaac Ginsburg and he has shown when subtoxic amounts of ethanol were combined either with subtoxic amounts of glucose oxidase-generated hydrogen peroxide, or with mixtures of peroxide and with 2,2′-Azobis (2-amidinopropane)HCl (AAPH)-generated peroxyl radical. A further enhancement of cytotoxicity occurred when subtoxic amounts of trypsin were added to mixtures of all three agents. (20).
 
It has been noted in IAQ testing where moisture has affected some indoor environments that ethanol can be one of the major components of the resultant Volatile Organic Compounds- also where fungi has developed trypsin is normally produced in the majority of all fungal fruiting bodies, so that Professor’s Ginsburg’s
findings may have greater importance in relation to indoor exposures/environmental health, where there have been or is a current water ingress
 
 As environmental health has not been a focus for medical education, nor has the funding being readily available to develop the much needed research in this area some clinicians are not fully aware of the scope of mould/fungal-related health problems and are inadequately equipped to investigate and manage possible cases of mould exposure. As a result, manifestations of mould-related illness often remain misdiagnosed and ineffectually treated.
 
 It is important for physicians to be aware of the pathogenesis, the manifestations, the investigations and the management of possible mould exposure.
 
 
Mold elements can also directly infect some tissues and cause mycotic or fungal-related pathological and inflammatory illness, particularly when impaired circulation or immune compromise exists [4].
 
Molds, yeasts and other fungal organisms can invade the tissues of both immunocompromised and normal individuals, establishing an infectious state that is often difficult to clinically manage.
 
While serious infections by fungal microorganisms such as Pneumocystis generally afflict immunocompromised patients, fungi such as Histoplasmosis, Cryptococcus, Blastomyces and Coccidioides can also infect immunocompetent people.
 
Although acute sinusitis, for example, is often bacterial or viral in nature, the ever-increasing problem of chronic sinus infections is often due to inflammation of the mucous membranes induced by fungal elements (including mould) and the associated eosinophilic response
 
Exposure to biochemical products of mould
 
There are a number of ways that moulds induce infirmity this can be through the
production, absorption and dissemination of toxic and immunogenic by-products manufactured by the mould.
 Fungal biochemical products may include chemical Mycotoxins [5], enzymes [6], solvents [7], polysaccharides [8], microbial volatile organic compounds [1] and other by-products.
 
These biochemical compounds may be released into the air and inhaled, but some by-products such as aflatoxins (very potent carcinogens and hepatotoxins produced by some Aspergillus species) can also be ingested in foods.
As fungal particles less than 10 ?m in diameter are respirable, Mycotoxins (including Ochratoxin, sterigmatocystin and trichothecenes) may contaminate
indoor dust in mouldy buildings, leading to inhalation and absorption [9.10].
 
They may provoke local irritation, may induce hypersensitivity or may disseminate within the body to cause biochemical alternation of inherent physiology.
In addition to inciting sensitivity reactions, these dispersed chemical compounds can alter cell and tissue functions in a myriad of ways. For example, some mould by-products, including beta glucans, have the potential to cause immune-related illness by inducing immune suppression or modulation [11, 12]; other by-products are directly hormone-disrupting [2], nephrotoxic [13], genotoxic [2], or carcinogenic [14].
 
Some mould by products secrete enzymes that may induce thrombosis or infarction [15], while others employ multiple mechanisms to induce tissue damage with resultant illness [16].
 
 For example, some Mycotoxins, including a class known as trichothecenes, are released by moulds such as Stachybotrys and Fusarium and have enormous cytotoxic ability as potent inhibitors of DNA, RNA and protein synthesis [17]. Tricothecene Mycotoxins are under close study in animal models because of concern about utilization in biological warfare due to their lethal potential and
the inability to detect them on post-mortem examination.
 
 
The Cancer Assumption due to Microbial and Chemical Exposure
 
 
Cancer a multi step, multi-mechanism process
 
 
The initiation phase (DNA damage and mutagenesis)
 
 1. Studies and research have shown that no chemicals can initiate or mutate stem cells in human body at doses or concentrations that would not kill the individual (UV light is the only exception) James Trosko Ph.D./Genetics/Radiation-
Centre for Integrative Toxicology/ College of Human Medicine, Michigan State University.
 
2. Initiation can and does occur spontaneously every time a cell divides (errors of DNA replication) in other words we have “initiated” cells in our bodies regardless of any exposure or in layman’s terms “we are ready to go just waiting for an exposure bus to take us down a disease pathway”.
 
3.Tumour promoting chemicals or toxic agents like but not limited to DHEA, Ionizing radiation, Fungal Mycotoxins, bacterial Toxins, DDT, TPA, PBB’s, TCDD plus hundreds of other chemicals, growth factors, hormones can and do down regulate the GJIC. Understanding the critical role that gap junctions play in growth regulation, differentiation and apoptosis will provide new therapeutic insights (Lander, E.S et.al. (2001) nature, 409, 860-921/ Venter, J>C.et.al.2001 Science, 291, 1304-1351)
 
4. All promoters worked via inducing intra-cellular signalling, which in turn down regulated gap junctional intercellular communication (GJIC).
 
5. GJIC has been speculated to be necessary for the regulation of growth control, differentiation and apoptosis of normal progenitor cells. Most if not all of tumour cells have dysfunctional homologous or heterologous GJIC (RJ Ruch Gap junctions as Targets for Cancer Chemoprevention and Chemotherapy).
Cancer cells are characterized by the lack of growth control, inability to terminally differentiate or apoptose under normal conditions and have extended or immortalized life spans. (J.E TROSKO/ Michigan State University)
 
6. It’s an assumption but Gap Junction Function maybe used as a bio marker for Cancer-(Venter,J.C, et.al.2001) If we accept this then the following testing could also in conjunction ,become bio markers for Cancer.
 
 a. Glutathione deficiency
 
 b. Elevated oxidative stress
 
 c. If there is a glutathione deficiency then Glutathione S Transferase gene testing  
may show if a promotion exposure has suppressed or deleted the family of                                                         genes which   support the function of glutathione production in blood and tissue.
 
 d. Further research is then required to determine what is the most successful way to switch a suppressed gene or family of genes” back on”- is it simply the removal of those promoters which would appear to have initiated the suppression and if there is gene deletion of some of that gene family by removing the promoter will that allow those remaining family genes to be able to support the additional/required glutathione levels or is it a matter of supplementation?
 
 
7. As the initiation in the cancer step appears to be the result of an irreversible mechanism but in animal studies the promotion affect appears to be an interruptible or even a reversible step will then the deletion, removal or dilution of those promotional events or exposures lead to cancer or tumour regression. If there is the slightest possibility that these results could be established then shouldn’t we be looking at the next step?
 
 
8. Why aren’t we testing for indoor environmental toxin promoters in Breast Cancer Clusters and other Clusters?
 
There is increasing recognition that the air we breathe and the environment we live in are profound determinants of health and well-being [18]. Various researchers and organizations have begun to draw attention to the widespread
problem of indoor mould/bacterial growth resulting from damp conditions.
 In a paper entitled Toxic effects of indoor mould, for example, the American Academy of Paediatrics recently emphasized the urgent need to “eliminate water problems and to reduce the growth of indoor moulds” [3]. As moulds/fungi appear to be prevalent etiologic determinants of assorted health problems, physicians should become familiar with the wide range of afflictions and chronic health complaints that may result from this type of fungal exposure and have a working understanding of appropriate investigations and management protocols.
 
 Indoor Environmental Toxins are not just fungal but can include, bacterial, chemicals used in cleaning, pest control, low levels of ionizing radiation in the work place, as well, occupants may have exposure levels in their home which could cause an additive or synergistic promotion within certain “initiated” cells.
 
If environmental testing is carried out and various promoting agents/toxic chemicals or biologically accept concentrations of exposures are found in an Indoor Environment then reduction of that exposure may reduce the chance of additional promotional or current promotional events, which in turn may actually reduce the chances of a Cancer or other diseases developing.
 
9. If promoter toxins/agents are found in an indoor environment and occupants have Glutathione Deficiency, Elevated Oxidative stress or showing GST gene suppression when those identified toxins/agents are removed, along with Glutathione supplementation in occupants which are showing deficiencies, retesting for those markers may be a way of starting to validating a cause and effect from exposure to identified toxins/agents in an indoor occupied space.
 
 
References
 
 [1] BrandtM, BrownC, Burkhart J, BurtonN, Cox-Ganser J, Damon S, et al.
Mold Prevention Strategies and Possible Health Effects in the Aftermath
Of Hurricanes and Major Floods. MMWR Recomm Rep 2006; 55:1–27
[R0B].
[2] Johanning E. Indoor moisture and mould-related health problems.
Allerg Immunol (Paris) 2004; 36(5):182–5.
[3] American Academy of Pediatrics — Committee on Environmental H.
Toxic effects of indoor molds. Pediatrics 1998;101(4 Pt 1):712–4.
 (11):1181–7.
[4] Fleming RV,Walsh TJ, Anaissie EJ. Emerging and less common fungal
pathogens. Infect Dis Clin North Am 2002;16(4):915–33 [vi–vii].
factors of Candida species. Biol Chem 2002;383(7–8):1087–93.
 [5] Tuomi T, Reijula K, Johnsson T, Hemminki K, Hintikka EL, Lindroos
O, et al. Mycotoxins in crude building materials from water-damaged
buildings. Appl Environ Microbiol 2000;66(5):1899–904.
[6] Monod M, Capoccia S, Lechenne B, Zaugg C, Holdom M, Jousson O.
Secreted proteases frompathogenic fungi. Int JMed Microbiol 2002;292
(5–6):405–19.
[7] Claeson AS, Levin JO, Blomquist G, Sunesson AL. Volatile
metabolites from microorganisms grown on humid building materials
and synthetic media. J Environ Monit 2002;4(5):667–72.
[8] Douwes J, van der Sluis B, Doekes G, van Leusden F, Wijnands L,
van Strien R, et al. Fungal extracellular polysaccharides in house
dust as a marker for exposure to fungi: relations with culturable fungi,
reported home dampness, and respiratory symptoms. J Allergy Clin
Immunol 1999;103(3 Pt 1):494–500.
[9] Nielsen KF. Mycotoxin production by indoor molds. Fungal Genet
Biol 2003;39:103–17.
[10] Engelhart S, Loock A, Skutlarek D, Sagunski H, Lommel A, Farbe M,
et al. Occurrence of toxigenic Aspergillus versicolor isolates and
sterigmatocystin in carpet dust from damp indoor environments. Appl
Environ Microbiol 2002;68: 3886–90.
[11] Bondy GS, Pestka JJ. Immunomodulation by fungal toxins. J Toxicol
Environ Health B Crit Rev 2000;3(2):109–43.
[11] Berek L, Petri IB,MesterhazyA, Teren J,Molnar J. Effects ofmycotoxins
on human immune functions in vitro. Toxicol In Vitro 2001;15(1):
25–30.
[13] Pfohl-Leszkowicz A, Petkova-Bocharova T, Chernozemsky IN,
Castegnaro M. Balkan endemic nephropathy and associated urinary
tract tumours: a review on aetiological causes and the potential role of
mycotoxins. Food Addit Contam 2002;19(3):282–302.
[14] Dominguez-Malagon H, Gaytan-Graham S. Hepatocellular carcinoma:
an update. Ultrastruct Pathol 2001;25(6):497–516.
[15] Kordula T, Banbula A, Macomson J, Travis J. Isolation and properties
of stachyrase A, a chymotrypsin-like serine proteinase from Stachybotrys
chartarum. Infect Immun 2002;70(1):419–21.
[16] Bhatnagar D, Yu J, Ehrlich KC. Toxins of filamentous fungi. Chem
Immunol 2002;81:167–206.
[17] Hymery N, Sibiril Y, Parent-Massin D. In vitro effects of
trichothecenes on human dendritic cells. Toxicol In Vitro 2006;20(6):
899–909.
[18] Genuis SJ. The chemical erosion of human health: adverse environmental
exposure and in-utero pollution — determinants of congenital
disorders and chronic disease. J Perinat Med 2006;34:185–95.
(19) European Journal of Internal Medicine 18(2007)516-523. Stephan J. Genuis- Faculty of Medicine at the University of Alberta, Canada
20 .Ethanol synergises with hydrogen peroxide- Free Radical Biology and Medicine Vol 16 Issue 2 Feb 1994
21.Biodegradation of Dipropyl phthalate and toxicity of its degradation products- Arch Microbial(2005) 184:25-31 Do1 10.007
      

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Last Updated on Friday, 19 November 2010 05:01