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[Linking Evidence ...] [Toxic Effects ...] [Molds, Mycotoxins ...] [The Killer Within Us ...]
Presented to
World Safety Organization
17th International Environmental Safety & Health Conference& Exposition
November 3 - 5, 2003
Conference Theme: "Safety & Health In
the Changing Environment."
ABSTRACT
A mycotoxin is a highly toxic principle
produced by molds or fungi. One type, the aflatoxins, is a member of the
tricothecene group produced by the fusarium fungus. This has been
identified in samples of the so-called "yellow rain" in Southeast Asia,
where it is said to have been the cause of many deaths among war refugees.
Its presence there is subject to some conjecture, since the Fusarium
fungus cannot germinate in the humid environment of that area. There is
substantial evidence (blood tests, autopsies, and contaminated gas masks)
that the former U.S.S.R. have used such lethal agents in Afghanistan, just
as many other countries have used these lethal agents throughout the dawn
of history. The human body once exposed to a mycotoxin runs a triple risk
to its toxic effects. The triple risk factors are direct toxic effect of
the mycotoxin, acquisition of mutated RNAi from the mycotoxin's parent
fungus and creation of an internal biofilm, which will harbor a toxic soup
of disease.
INTRODUCTION
Mycotoxins represent an important
class of xenobiotics (in terms of morbidity), which cause renal injury in
humans and food animals.1
They are not the indigenous microorganisms of man. The flora and fauna
indigenous to man are often referred to simply as normal flora. In
this context, "flora" denotes all microscopic life forms and "normal"
becomes a statistical term. One must not equate normal with nonpathogenic,
for many organisms found on and in the body can pose problems under
conditions such as the following:
- Deterioration of the host's defense
mechanisms.
- Relocation of microorganisms, when an
organism finds its way to another area of the body previously
uninhabited by it.
- A disturbance of the "normal flora."
Normal floras are commonly referred
to as amphibionts, ranging from commensals to pathogens. The amphibionts
are obligately parasitic on man and other animals but are not obligately
pathogenic. They are encountered at least as often in the absence of
disease as in its presence. The indigenous microorganisms may flourish in
the general region of tissue damage and contribute to the disease state as
opportunists, rather than primary etiological agents. Thus, these
organisms may be implicated although Koch's postulates would not
necessarily hold true.2
Amphibiont Sites
As a rule, few or no microorganisms are
found in the following anatomical locations: blood, larynx, trachea, nasal
sinuses, bronchi, esophagus, stomach, upper intestinal tract, upper
urinary tract (including the posterior urethra), and posterior genital
tract (passage above cervix included). However, in studies with animals,
notably dogs and rabbits, microorganisms from the mouth and throat regions
and from the lower intestine were found in the blood and other tissues
after these animals were subjected to various types of physical or mental
stress and trauma. In particular, Clostridium perfringes (one of
the causative agents of gas gangrene) has been isolated from the "healthy"
tissues of these animals.
The regions of the body that constitute the
major habitats for indigenous microorganisms include the skin and
contiguous mucous membranes, conjunctivae, upper respiratory tract
(oral-pharynx included), mouth, lower intestine, external genitalia,
anterior urethra, and vagina. It will become apparent that each habitat
has certain characteristics, which allow a different overall range of
microorganisms to thrive. These differences can be categorized into the
following three types of environment:
- Extremely high levels of both moisture
and nutrients, as in the lower intestines and the mouth.
- A high level of moisture and a low level
of nutrients, as with mucous membranes.
- A low level of moisture and a moderate
level of nutrients, as on the skin.
Other variables include availability of
oxygen, pH, temperature, and relative exposures to contaminants and
ventilation.
Numbers of total aerobic and anaerobic
bacteria in certain anatomical regions:
- Lower intestine - approximately
100 billion microorganisms per gram of fecal matter.
- Mouth - approximately 1 billion
microorganisms per ml of saliva.
- Nose - approximately 20,000
microorganisms per ml of nasal washing.
- Skin
- approximately 1 million microorganisms per cm2;
this value is dependent upon the skin surface tested.
Development of the indigenous flora begins
with the normal birth process, since the infant has been bathed during the
ingestion period in a sterile amniotic fluid. As the baby passes through
the birth canal it begins to pick up organisms, many of which may remain
with it for its lifetime. Additional microorganisms are acquired by the
infant as a consequence of coming into contact with the air of the
environment and with hospital personnel. Such organisms may be transient
in nature, or may become permanent members of the flora.
Appreciable numbers of bacteria have been
cultured from the mouths of infants within 6 to 10 hours of birth and in
the feces within 10 to 20 hours.
The human body has various anatomical organ
areas, each anatomical area varies in relation to pH, oxygen content,
nutrients, and moisture as well as bactericidal factors, thus different
organisms will predominate. While the amphibionts persist in their
respective locations, saprophytic as well as many parasitic microorganisms
are destroyed or excreted. These locations can change as a consequence of
changes brought about by the maturation process of the individual, e.g.,
hormonal regulation, alteration in dietary habits, chemical exposure, IAQ
buildings, AIDS and chemotherapy.
The indigenous fungi are primarily
saprophytes of soil, which show preference for a parasitic habitat.
Because of their primary saprophytic role, it may appear questionable to
call them amphibionts. However, according to Rosenbury, an amphibiont may
be considered to be any organism, which is ". . . encountered in one or
more typical indigenous locations frequently, and distinctly more
frequently, than in the adjacent environment." On this basis, and
according to the propositions that an organism routinely isolated from the
body in the absence of disease may be indigenous, fungi are included, even
though they rarely are indigenous to the human body.2,
3
WHAT ARE FUNGI?
Fungi are single cell living forms of life,
which inhabit the land, air, and waters of our planet, earth. They are
everywhere in our environment, soil and home.
They are more highly developed than
bacteria and viruses. They are composed of many more species than are
found in other microorganisms. It is estimated that there are over 500,000
different species.
Fungi have been on earth several billion
years and, quite remarkably, have had little genetic change over that
period of time. They are survivalists. They can change their form from
rapidly growing to no growth for thousands of years, such as seen in their
living spores which have been found in Egyptian tombs. They secrete and
make a poisonous toxin called a mycotoxin.
Single fungi cells can only be seen under
the microscope but a colony of these cells makes a visible presence in the
form of mushrooms, toadstools and molds on food and other habitats.
While plants, animals and humans are
alive and well, the fungi around us are unable to overcome the natural
defense mechanisms which higher forms of life possess. But once death
overtakes the living, the fungi are the principle undertakers and
managers: they reduce all that have ever lived into the molecules from
which they were assembled. Biologists call this the carbon cycle while
theologist call it "from dust to dust."4, 5
However, there is one exception to this
simple balanced equation of life and death and that is that the fungi can
attack the living while they are alive.
At its most simplistic perspective, one has
many fungi entering the intestinal tract, the nose and lungs, and organs
exposed to the world at large. We generally do not develop an infection
from these intruders. However, a person might contract a fungal infection
such as "athlete's foot" or a "ring worm" on the skin.
At the opposite extreme is the patient with
AIDS who faces death-threatening major fungal infections because that
person's immune system has lost its effectiveness against fungi. In
between the extremes are fungal infections associated with diseases such
as diabetes, cancer and other conditions including cross infections
amongst humans.
Forturnately, the average person does not
succumb to a serious fungal infection such as Candida albicans
(yeast) and average life into the 70's.
All humans are colonized by
Candida albicans and normal healthy persons do not die from this
organism. This organism plays a very little role in causing human
diseases. It has been known to have tremendous elevated growth patterns in
individuals who have been diagnosed as being multichemical sensitive or
acutely poisoned from exposure to hazardous materials, such as urethane,
carbamates, nitrogen mustards and other compounds. It is interesting to
note that these same chemicals are known to be extrinsic mutagenic agents
in both fungi and human genes.6 This type of extrinsic mutagenic activity
by chemicals is also known as a "directed mutation."7
(See Table 1-1.)
Mycotoxins may be friends or foe. There are
as many as 1,000 compounds, classifiable as mycotoxins, where studied by
the pharmaceutical industry as potential antibiotics in the 1930's and
1940's only to be discarded as being too toxic for higher life forms to be
of value in treating bacterial diseases in humans. Little, if any of the
discarded data was published. Yet, what these toxicity studies actually
documented was the existence of a large number of fungal-derived toxins,
which caused serious, target organ injury in various animal models.
Obviously, in retrospect, what was being
seen was the pathology produced by the mycotoxins, in order to understand
this toxicity, one only has to look at what some of these mycotoxins, used
as medications, causes in humans:
The mycotoxin cyclosporin used for
transplantation causes cancer and atherosclerosis, complete with
hyperlipidemia in ALL humans who have received it. Many others develop
gout and other diseases.
As a friend, the study of such fungal
metabolites gave us penicillin at the beginning, which was replaced by a
chemical cyanamide man made compound from 1945 to present day. Quite later
on cyclosporin, the most potent immuno-suppressant transplantation drug,
lovastatin, and the other "statins", which have revolutionized the
treatment of hyperlipidemia and atherosclerosis. The latter group is quite
interesting in that they were initially developed as anti-fungal agents
which just happened to have an effect in lowering blood levels of low
density lipoproteins (commonly refereed to as "bad cholesterol").
The members of this group of drugs are
joined by another anti-fungal antibiotic, griseofulvin, which is also a
remarkably efficient anti-atherosclerosis drug. All of this goes a long
way to confirm the fungal etiology of atherosclerosis. This appears to be
a quite valid conclusion since all of the other effective anti-cholesterol
and/or anti-atherosclerotic therapeutic modalities share nothing in common
except that they possess anti-fungal and/or anti-mycotoxin activity.
Diseases of unknown etiology, which respond to anti-fungal-effective
drugs, suggest the probability that they have a fungal origin,
particularly when there is no other proven explanation as to how the drug
is working. Table 2-2 provides a number of human diseases, which so
respond and suggest a fungal or mycotoxin origin.
ENVIRONMENT, FOOD CHAIN and STORED FOOD
Fungi grow all over this planet. They
are found in the soil, on trees and in water. Their spores travel
throughout the lands by the winds from the four corners of our world.
Biosensor testing conducted by the U.S. military has resulted in an
increase population of Aspergillus niger on homes, trees and other
materials in various areas of the United States of America.8
Over the last decade, starting in the
1990's, research has implicated many toxin-producing fungi, such as
Stachybotrys, Penicillim, Aspergillus and Fusarium
species, to indoor air quality problems and building related
illnesses. Inhalation of mycotoxin producing fungi in contaminated
buildings is the most significant exposure, however, dermal contact form
handling contaminated materials and the chance of ingesting toxin
containing spores through eating, drinking and smoking is likely to
increase exposure in a contaminated environment. Recent advances in
technology have given laboratories the ability to test for specific
mycotoxins without employing cost-prohibitive gas chromatography or high
performance liquid chromatography techniques. Currently, surface, bulk,
food and feeds, and air samples can be analyzed relatively inexpensively
for mycotoxins.
Homes that have been damaged by water
or have had improper construction of ventilations systems have become
infected with fungal overgrowth and biofilms, which resulted in bacteria,
algae and fungi growing together as a communal colony with microtubules
connecting to each other to exchange nutrients. Thus, creating the most
toxic forms of mycotoxins, endotoxins, and exotoxins with the potential of
forming DNA plasmids in mycoplasma, with mutated RNAi sub-mutated forms of
fungi genes.9, 10
The most toxic forms of fungi,
mycotoxin is coming from our food itself, which is characteristically
present in stored and fermented food. Pesticides used on cereals as a
fungicide, such as benomyl have potentated the mycotoxin in selective
genes. In 1987 at Yale University, Karl Hager and Mike Plamann performed a
very important study, which was based on the plasmid pH303 and its
derivatives integrated at his-3 by a single crossover. When introduced to
benomyl, the mutant allele of his-3(1-234-723) was present in the genome,
and its mutation was mapped to be somewhere downstream of the Sall
restriction site. A cloning will occur at a higher transformation
frequency using linear than using circular DNA, and the transformation
frequencies are independent of the mating type of the host.11
If food is loaded with fungi, then the
myctoxin concept is fully operative and the disease-producing potential is
more than obvious.
This important question of how much
fungal colonization of food exists is answered by the most recent reported
mycological study of some quite representative foods; corn kernels,
peanuts, cashew nuts and copra (dried coconut). Table 3-3 demonstrates the
remarkable degree of fungal colonization of the interior of corn kernels
and peanuts.12
Humans who eat these foods are ingesting
both the toxicogenic fungi and their mycotoxins. These fungi are capable
of surviving in the intestinal stream where they may continue to produce
their toxins.
Similarly, animals fed fungal
colonized/mycotoxic feed are not only at risk of developing mycotoxicoses,
their meat and their fat, constitute another vehicle for human exposure to
excessive mycotoxin intake. Animal fat is increasingly being documented to
be a major risk factor for a number of human cancers and atherosclerosis.
It must be noted that fat, stores polycyclic organic xenobiotics and they
are highly lipid soluble. They concentrate in fat depots, which results in
low plasma levels and extended half-lives. These same compounds are known
to cause distinct mutations. When cattle were accidentally fed
contaminated feed in Michigan by PBB's in 1973, these compounds became
stored first in fat deposits of the cows and then, via milk fat,
bioaccumulated in fat stores of the people of Michigan, where PBB's can
still be detected. While there is no known effect of PBB's at the storage
site, this store is a potential hazard since mobilization during
starvation or other stress could lead to efflux into the bloodstream with
subsequent redistribution and toxicity. Similarly, patients treated for
acute exposure to organophosporous pesticides may be released from the
hospital and later suffer a relapse due to mobilization of the insecticide
from fat stores.13
Mycotoxins have been documented to cause a
number of specific types of diseases and very specific organ lesions both
in animals and in humans. Table 4-4 provides a summary of some of this
documentation.
DISEASES ASSOCIATED WITH VARIOUS MYCOTOXINS
Aflatoxin
- Aflatoxin is one of the most potent
carcinogens known to man and has been linked to a wide variety of human
health problems. The FDA has established maximum allowable levels of
total aflatoxin in food commodities at 20 parts per billion. The maximum
level for milk products is even lower at 0.5 parts per billion.
Primarily Aspergillus species fungi produce aflatoxin.
Ochratoxin
- Ochratoxin is primarily produced by
species of Penicillim and Aspergillus. Ochratoxin is
damaging to the kidneys and liver and is also a suspected carcinogen.
There is also evidence that it impairs the immune system.
T-2 Toxin
- T-2 Toxin is trichothecene produced by
species of Fusarium and is one of the more deadly toxins. If
ingested in sufficient quantity, T-2 toxin can severely damage the
entire digestive tract and cause rapid death due to internal hemorrhage.
T-2 has been implicated in the human diseases alimentary toxi aleukia
and pulmonary hemosiderosis. Damage caused by T-2 toxin is often
permanent.
Fumonisin
- Fumonisin is a toxin associated with
species of Fusarium. Fumonisisn is commonly found in corn and
corn-based products, with recent outbreaks of veterinary mycotoxicosis
occurring in Arizona, Indiana, Kentucky, North Carolina, South Carolina,
Texas and Virginia. The animals most affected were horses and swine,
resulting in dozens of deaths. Fumonisin toxin causes "crazy horse
disease", or leukoencephalomalcia, a liquefaction of the brain. Symptoms
include blindness, head butting and pressing, constant circling and
ataxia, followed by death. Chronic low-level exposure in humans has been
linked to esophageal cancer. The American Association of Veterinary
Laboratory Diagnosticians (AAVLD) advisory levels for fumonisin is horse
feed is 5 ppm.
Vomitoxin or Deoxynivalenol (DON)
- Vomitoxin, chemically known as
Deoxynivalenol, a tricothecene mycotoxin, is produced by several species
of Fusarium. Vomitoxin has been associated with outbreaks of
acute gastrointestinal illness in humans. The FDA advisory level for
vomitoxin for human consumption is 1 ppm.
Zearalenone
- Zearalenone is also a mycotoxin produced
by Fusarium molds. Zearalenone toxin is similar in chemical
structure to the female sex hormone estrogen and targets the
reproductive organs.
Citrinin
- Citrinin is a nephrotoxin produced by
Penicillium and Aspergillus species. Renal damage,
vasodilatation, and bronchial constriction are some of the health
effects associated with this toxin.
Alternariol
- Alternariol cytotoxic compound derived
from Alternia alternata.
Satratoxin H
- Satratoxin H is a macrocyclic
tricothecene produced by Stachybotrys chartaru, Trichoderma
viridi and other fungi. High doses or chronic low doses are lethal.
This toxin is abortogenic in animals and is believed to alter immune
system function and makes affected individuals more susceptible to
opportunistic infection.
Gliotoxin
- Gliotoxin is an immunosuppressive toxin
produced by species of Alternaria, Penicillium and
Aspergillus.
Patulin
- Patulin is a mycotoxin produced by
Penicillium, Aspergillus and a number of other genera of
fungi. It is believed to cause hemorrhaging in the brain and lungs and
is usually associated with apple and grape spoilage.
Sterigmatocystin
- Sterigmatocystin is a nephrotoxin
and a hepatotoxin produced by Aspergillus versicolor. This toxin
is also considered to be carcinogenic. Other mycotoxins include -
Penicillic acid, roquefortine, cyclopiazonic acid, verrucosidin,
rubratoxins A and B, PR toxin, luteoskyrin, cychlochlorotine, rugulosin,
erythroskyrine, secalonic acid D, viridicatumtoxin, kojic acid,
xanthomegnin, viomellein, chaetroglobosin C, echinulin, flavoglaucin,
versicolorin A, austamid, maltayzine, aspergillic acid, paspaline,
aflatrem, fumagillin nigragilin, chlamydosporol, iscotrichodermin and
many more. As previously discussed there are many mycotoxins that can
cause adverse health effects and even death in humans. These synergistic
effects of exposure to multiple mycotoxins simultaneously are very
poorly understood. Even more poorly understood are the by-products of
mycotoxin degradation, particularly under the influence of strong
oxidizing agents such as sodium hypochlorite and/or ozone, agents
frequently used or misused by hazardous materials personnel or
remediation remediators in industry. More research is required in this
field to better understand the relationship of fungal contamination,
relative humidity, temperature and ventilation in fungal growth in
buildings and on building substrates as they relate to disease.14
VOLATILE FUNGAL METABOLITES
During exponential growth, many fungi
release low molecular weight, volatile organic compounds (VOCs) as
products of secondary metabolism. These compounds comprise a great
diversity of chemical structure, including ketones, aldehydes, and
alcohols as well as moderately to highly modified aromatics and aliphatics.
Cultural studies of some common household molds suggest that the
composition of VOCs remains qualitatively stable over a range of growth
media and conditions. Furthermore, the presence of certain marker
compounds common to multiple species, such as 3-methylfuran, may be
monitored as a proxy for the presence of a fungal amplifier.14
This method has been suggested as a means of monitoring fungal
contamination in grain storage facilities. Limited evidence suggests that
exposure to low concentrations of VOCs may induce respiratory irritation
independent of exposure to allergenic particulate. Volatile organic
compounds may also arise through indirect metabolic effects. A well-known
example of this is the fungal degradtion of urea formaldehyde foam
insulation. Fungal colonization of this material results in the cleavage
of urea from the polymer, presumably to serve as a carbon or nitrogen
source for primary metabolism. During this process formaldehyde is evolved
as a derivative, contributing to a decline in Indoor Air Quality.12
INTEGRATIVE HEALTH CARE TREATMENT
Many fungi, mycotoxins, and their VOC's are
at a level of detection within the human body that is very hard to
determine at relatively low costs. Tissue samples of blood, urine and even
direct organ/tissue biopsy will determine the presence of a fungi,
mycotoxin and/or their VOC's. To kill fungi and remove other substances it
is necessary to look at a variety of treatment modalities. Current,
anti-fungal formulations have been developed to address specific fungal
infections. In many cases it is very hard for the healthcare provider and
physician to determine what species of fungi was present that created what
specific mycotoxin, which is a billion dollar revenue to the
pharmaceutical industry.
In AIDS patient's fungal infections have
been observed in tissue biopsy reports to be growing within the tissue and
this causes great health risks to the patient. The use of far infrared as
a treating modality can address the electromagnetic spectrum in micron and
micrometers (nano level), which would be an ideal choice, in treating
fungal infected patients. The far infrared segment of the electromagnetic
spectrum occurs just below, or "infra" to, red light as the next lowest
energy band. This band of light is as the next lowest energy band. This
band of light is not visible to human eyes but can be seen by special
cameras that translate infrared into visible colors. We can, however, feel
this type of light, which we perceive as heat. The sun produces most of
its energy in the infrared segment of the spectrum. Our atmosphere has a
"window" in it that allows infrared rays-in the 7 to 14 micron bands, with
peak output at 10 microns.
Our tissues normally produce infrared
energy for warmth and tissue repair. Tissue production of infrared energy
is associated with a variety of healing responses. At times the infrared
energy in our tissues may require a boost to higher level to ensure the
fullest healing possible for tissue repair. Body tissues that need an
infrared boost selectively absorb infrared rays, after boosting a tissue's
infrared energy; the remaining rays pass onward harmlessly. This
phenomenon is called "resonant absorption." Our bodies radiate infrared
energy through the skin at 3 to 50 microns, with most output at 9.4
microns. Our palms emit infrared energy too, from 8 to 14 microns. Palm
healing, an ancient tradition in China, has used the healing properties of
infrared rays for 3,000 years. Yogis in India also employ palm healing and
recommended it especially for relieving eyestrain.
An MPS Capsule from MPS, Inc. Seoul,
Korea, which generates far infrared energy from special carbon fibers
manufactured by Daiugin and high gem graded jade balls with far infrared
proprietary technology; may be a future solution for individuals suffering
from fungal infections. Its dome generates temperatures as high as 1650F
and the spinal column area as high as 1480F.
These temperatures are known to kill fungi and release VOCs that have a
lower melting point, like benzene at 810F.15,
16
The use of activated charcoal has
been recognized by the U.S. Environmental Protection Agency in their text,
Recognition and Management of Pesticide Poisonings, 4th Edition, in
absorbing volatile organic compounds (VOCs), which are the same type of
compounds found in fungal metabolites.17
Activated charcoal is made from burnt coconut husk. It is able to absorb
at a minimum 35 % of the VOCs found in the intestinal tract from
reabsorbing into the blood stream. It does not absorb in other areas of
the body were VOC's may accumulate, such as in the lungs, brain, liver and
fat. Research conducted at the Korean Atomic Institute have shown that Kuh
Sung YLS-95 (Trade Marks Bio-Oaky & Oaky Smoky) a liquid yielding high
plant infrared, which is made from oak wood charcoal vinegar is highly
effective in significantly reducing carbon tetrachloride in rats and
ethanol in humans within one hour after exposure.18
CONCLUSION:
One could test the validity of how
poisonous mycotoxins are by eating a handful of poison mushrooms, a
species of fungus. However, it would be less fatal to realize that many
forms of fungus produce mycotoxins, which are chemical substances that are
toxic to man and other life forms. In addition, fungi produce volatile
organic compounds (VOCs), which may bind to fat within in your body and
cause internal re-exposure to the toxic effects of these compounds.
Current, integrative technologies in the health care area have produced
far infrared MPS Capsules and Kuh Sung YLS-95 (Trade Mark Bio-Oaky & Oaky
Smoky) that will kill fungus and neutralize VOC's in other tissue organs
within the human body respectfully. These technologies may be the answer
to current biological weapons of mass destruction and the risk of exposure
to biological pesticides by killing these microorganisms at micron
(0.000,001) and nano (0.000,000,001) levels within our human body.
Cellular detoxification and its remediation are on the break of a new
horizon through terahertz, far infrared and subnano technologies.
TABLES:
TABLE 1-1: A partial list of known
extrinsic mutagenic agents. Taken from Levitan, Max and Ashley Montagu.
Textbook of Human Genetics. Oxford University Press. New York. (c) 1971,
pgs. 671 & 672.
- Radiations
- A. Ionizing, X-rays, alpha particles,
beta particles, gamma rays, Neutrons (various speeds), cosmic rays.
- B. Non-ionizing, ultraviolet light
(0.014-0.315 u), near-visible light (0.320-0.400 u)
- Temperature changes
- Heat, heat shocks, cold shock.
- Chemicals
- A. Compounds related to DNA or RNA
bases adenine (purine), 2-amino purine (purine analogue),
5-bromouracil (pyrimidine analogue), caffeine (purine), 2,6-diamino
purine (purine analogue), theobromide (purine analogue), formaldehyde
(known to react with purines and pyrimidines), nitrous oxide (known to
react with purines and pyrimidines) deoxyribonuclease (DNA metabolic
enzymes).
- B. Alkylating agents (mustard gases
and related compounds), nitrogen mustards, sulfur mustards, ethylene
oxide, ethyl methyl sulfates, halogenated and not, diethyl and
dimethyl sulfate, diepoxybutane.
- C. Acridine dyes, acridine orange,
acriflavine, proflavine.
- D. Carcinogens, 1,2,5,6
dibenzanthracene, methyl cholanthene, benzpyrene, beta-naphthylamine.
- E. Inorganic salts, copper sulfate,
ferrous chloride, manganous chloride.
- F. Organic acids, acetic acid,
carbolic acid (phenol) and related compounds, formic acid, and lactic
acid.
- G. Inorganic acids, boric acid.
- H. Others, ammonia, colchicines,
hydrogen peroxide, necrosine, neutral red (in the presence of light),
sodium desoxycholate, triazine, urethane and certain other carbamates.
TABLE 2-2: Fungal Mycotoxin Postulated Diseases.
COLCHICINE-RESPONSIVEM
| Acute Gouty Arthritis |
Alcoholic Cirrhosis |
| Familial Mediterranean Fever |
Mollaret's Meningitis |
| Belchet's Syndrome |
Psoriasis |
| Thrombocytopenic Purpura |
Chronic Lymphocytic Leukemia |
| Amyloidosis North African |
Leukocytoclastic Vasculitis |
| Sarcoid Arthritis |
|
GRISEOFULVIN-RESPONSIVE
| Atherosclerosis (Angina) |
Systemic Sclerosis |
| Raynaud's Syndrome/Disease |
Shoulder-Hand Syndrome |
ALLOPURINOL-RESPONSIVE
| Sarcoidosis |
Oxalate Nephrolithopathy |
| Idiopathic Respiratory |
Distress Syndrome/Newborns |
| Rheumatoid Arthritis (some) |
Calcium Pyrophosphatopathy |
| Hyperlipidemia |
Inflammatory Bowel Disease |
COLCHICINE PREVENTS IN EXPERIMENTAL
ANIMALS
| Atherosclerosis |
Casein Indusce Amyloidosis |
| Cushing's Disease |
|
NYSTATIN-RESPONSIVE
| Psoriasis |
Inflammatory Bowel Disease |
| Hyperactivity Syndrome |
Multiple Sclerosis |
| Duchenne's Muscular Dystrophy |
|
KETOCONAZOLE-RESPONSIVE
| Inflammatory Bowel Disease |
Disseminated Vascular |
| Coagulation |
Idiopathic Female Infertility |
| Precocious Puberty in Boys |
Hyper-Low Density |
| L poproteinemia |
Hyperaldosteronism aldosteronism |
| Prostrate Carcinoma |
|
Note: The anti-fungal nature of colchicines
and allopurinol has been fully documented.
TABLE 3-3: Food from farmers, middlemen, and retail outlets in
Bangkok, Thailand. Note: Surface was sterilized prior to fungal study.
Taken from Pilt JL, Hocking AD, Bhudhasamai K, Miscamble BF, Wheeler EKP:
The Normal Mycoflora of Commodities from Thailand, part 1 Nuts and
Oilseeds. International Journal Food Microbiology 20:211-226, 1993.
| CORN |
PEANUTS |
Acremonium siricium
Aspergillus flavus
Aspergillus niger
Aspergillus tamarii
Aspergillus wentii
Bipolaris maydis
Chaetomium globosum
Chaetomium funicola
Chaetomium spp.
Curvularia lunata
Eurotium amstelodami
Eurotium chevalieri
Eurotium rubrum
Fusarium moniliforme
Fusarium proliferatum
Fusarium semitectum
Nigrospora oryzae
Penicillium citrinum
Penicillium pinophilum
Penicillium raistrickii
Phoma spp.
Rhizoctonia solani
Rhizopus oryzae
Rhisopus arrhizus
Trichoderma harzianum |
Aspergillus candir
Aspergillus flavus
Aspergillus niger
Aspergillus tamarii
Aspergillus wentii
Chaetomium globosum
Chaetomium funicola
Chaetomium spp.
Eurotium amstelodami
Eurotium chevalien
Eurotium repens
Eurotium rubrum
Fusarium equiseti
Fusarium semitectum
Fusarium solani
Lasiodiplodia theobromae
Macrophomina phaseolina
Nigrospora oryzae
Penicillium aethiopicum
Penicillium citrinum
Penicillium funiculosum
Penicillium glabrum
Penicillium janthinellum
Penicillium olsonii
Rhizopus oryzae |
TABLE 4-4: Mycotoxicoses in which Experimental and Epidemiological
Data Suggesting Human Involvement
| DISEASE |
SPECIES |
FOOD/FEED |
MYCOTOXIN |
| Gout/Hyper-uricema |
Fowl |
Moldy Corn |
Oosporein |
| |
Fowl |
Barley |
Ochratoxin |
| |
Chicks |
|
Kojic acid |
| |
Chickens |
|
Oxalic acid |
| |
Pigeons |
|
Alloxan |
| |
Rats |
|
Yeast |
| |
Primate |
|
Aflatoxin |
| |
Man |
|
Cyclosporin |
| |
Man |
|
Penicillin |
| |
Man |
Beer/Wine/Bread |
Multiple |
| |
Man |
Meat Products |
Multiple |
|
Man |
Rye |
Ergotamine
|
| Atherososclerosis/ |
Sheep |
|
Sporidesmin |
| Hyperlipidemia |
Man |
|
Cyclosporin |
| |
Primates |
|
Fumonisin |
| |
|
|
Ergot
|
| Cardiac Ischemia with Arrhythmias |
Rabbit |
|
Citreoviridin/ Penicillium
|
| Hypertension |
Man |
|
Alcohol |
|
Rabbit |
|
T-2 Toxin
|
| Multiple Sclerosis |
Man(?) |
|
Ergot
|
| Pulmonary Hypertension |
Swine |
|
T-2 Toxin
|
| Scleroderma |
Man |
|
Amanita
|
| Diabetes |
Man |
|
Crytococcus/ Alloxan
|
| Crohn's Disease |
Man |
Fermentation |
S.cerversisae
|
| Lung Cancer |
Man |
Tobacco |
Fusarium
|
| Esophageal carcinoma |
Man |
|
Fusarium
|
| Breast Cancer |
Man |
Fermentation |
S. cervesisae
|
| Endometrial CA |
Man |
|
Fusarium
|
| Colon CA |
Man |
|
Fusarium
|
| Hepatocellular carcinoma |
Man |
Cereals, grains, peanuts |
Aspergillus
|
| Hepatoma |
Man |
|
Aflatoxin
|
| Cardiomyopathy |
Man |
Fermentation |
Alcohol
|
| Osteoporosis |
Man |
Fermentation |
Alcohol
|
Alimentary toxic aleukia
(ATA or septic angina) |
Man |
Cereals, grains (toxic bread) |
Fusarium trichiodes
|
| Dendrodochio-toxicosis |
Horse, Man |
Fodder (skin contact, inhaled fodder
particles) |
Dendrodochium toxicum
|
| Kashin Beck Disease, "Urov Disease" |
Man |
Cereal grains |
Fusarium trichiodes
|
| Stachybotryo-toxicsis |
Man, Horse, Other Livestock |
Hay, cereal grains, fodder (skin
contact, inhaled haydust) |
Stachybotris atra
|
| Cardiac beriberi |
Man |
Rice |
Fusarium
|
| Ergotism |
Man, Animals |
Rye, Cereal grains |
Claviceps purpurea
|
| Balkan-nephropathy |
Man |
Cereal, grains |
Penicillium
|
| IGA Nephropathy |
Mice |
Grains |
Vomitoxin
|
| Reye's Syndrome |
Man |
Cereal, grains |
Aspergillus |
REFERENCES:
- Haschek, Wanda M. and Colin G. Rousseaux
(Eds). Handbook of Toxicologic Pathology. Academic Press, Inc.
Harcourt Brace Jovanovich, Publishers. New York. (c) 1991, pg.338.
- Wistreich, Ph.D., George A. and Max D.
Lechtman, Ph.D. Microbiology and Human Disease, Second Edition.
Glencoe Press, a Division of Benziger Bruce & Glecoe, Inc. Beverly
Hills. (c) 1973. pg. 403-405.
- Rose, N.R., Milgrom. F., and Van Oss,
C.J. (Eds.): Principles of Immunology. Macmillan Publishing Co.,
Inc., New York, (c) 1973.
- Holy Bible, King James Version.
Oxford Press. London. (c) 1998.
- Fungalbionics,
http://www.mold-help.org/definition_of_fungalbioncs.htm. (c)
7/16/02.
- Levitan, Max and Ashley Montagu.
Textbook of Human Genetics. Oxford University Press. New York. (c)
1971, pgs. 671 & 672.
- Fungi,
http://mold-help.org/fungi.mycotoxins.currentreseach.htm (c)
7/16/02.
- Chemtrails and Barium.
http://www.inchem.org/documents/ehc/ehc/ehc107.htm
http://www.carnicom.com/precip1.htm
http://www.carnicom.com/spectra2.htm
http://www.carnicom.com/spectra1.htm
- U.S. Patent 4,530,834 (Bayer). U.S.
Patent Office. Washington, D.C. "Biological Pesticides: Fungi to the
Rescue, " Research: The Bayer Scientific Magazine, 1989, pgs. 22-31.
- Lau, Nelson C. and David P. Bartel.
Censors of the Genome. Scientific America. New York. August 2003,
pgs. 35-41.
- Vogt, Donna U. Congressional Research
Service Report for Congress. The Delaney Dilemma: Regulating
Pesticide Residues in Foods - Seminar Proceedings, March 6, 1993.
Science Policy Research Division. The National Council for Science and
the Environment. Washington, D.C. May 19, 1993.
-
http://www.mold-survivor.com/hiddemold.htm (c) 7/16/2002.
- Hascheck, Wanda M. and Colin G.
Rousseaux (Eds.). Handbook of Toxicologic Pathology. Academic
Press, Inc. Harcourt Brace Jovanovich, Publishers. (c) 1991, pg. 54.
- Johnson, Ph.D., Douglas E,
Principal, IE3,
International Consultant in HVAC Remediation and Sick Buildings, Branden,
Florida.
- Kim, Jong Ki., President. Renew Your
Health with MPS: State-of-the-art Capsule-style Therapy Bed. MPS
Global, Inc., Los Angeles, California. (c) 2003
- Lewis, Sr., Richard J. Hawley's
Condensed Chemical Dictionary, 13th Edition. John Wiley & Sons, Inc.
(c) 1997. Definition VOC's, pg. 1174.
- Morgan, M.D., Ph.D., Donald P. (Ed.).
U.S. EPA Document (EPA-540/9-88-001: Recognition and Management of
Pesticide Poisonings, 4th Edition. Health Effects Division, Office of
Pesticide Programs, United Stats Environmental Protection Agency,
Washington, D.C. U.S. Government Printing Office. Washington, D.C.
(c)1989 pg. 9.
- Yoo, Yong-Woon. Study on Effects of Kuh
Sung YLS-95. Manufacturer: Guh Sung Bio Co., Ltd. Korea Atomic Hospital.
Seoul, Korea. (c) 2001
Dr. Hildegarde Staninger
Health Life
3130 Wilshire Blvd., Suite 408
Los Angeles, CA 90010
Telephone: 213-383-9120
Fax: 213-383-9780
High levels of fungi in an indoor
environment as compared to normal outdoor levels are of particular
concern.
In the event that fungal contamination is
determined within a dwelling, a professional investigation is essential to
thoroughly evaluate the occupant space and determine appropriate clean-up
measures.
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ALL molds
reproduce by making "spores." Mold spores are microscopic and
only become visible when individual spores accumulate. According to the
United States EPA, these microscopic particles continuously move through
indoor and outdoor air. When mold spores find moisture indoors, they may
"begin growing and digesting whatever they are growing on in order to
survive."
Molds gradually destroy whatever they are
growing on.
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