Re: EUROPEAN RESPIRATORY REVIEW, 2007

December 27, 2007

You hit the nail right on the head! Especially since allergic

reaction aren't the only reactin of concern. There are plenty of non-

allergic reactions including asthma triggers and toxicity.

Carl Grimes

Healthy Habitats LLC

-----

> Since Mold won't go away, here's an idea ...Looks as if soon, there

> may be a medication that will just turn off the IgE - inflamatory

> stage, which is all well and good I would expect for anyone in an

> emergency situation....but, isn't a " REACTION " just that? You subject

> your body to something it isn't able to handle and WHAMO! It's the

> body's WARNING SYSTEM... So, I am... reading this right aren't I?

> They'll be developing a medication and soon you'll be able to inhale

> more of the bad stuff???? And shushhhh the body's SOS call

>

> http://err.ersjournals.com/cgi/content/full/16/104/61

>

> FAIR USE NOTICE:

>

December 28, 2007

Happru/All:

There is only one disturbing thing that I am reading with your comment. An IgE

reaction is not an " inflammatory stage. " Medically termed, it is the " allergen "

stage or an " allergenic response " as the Merck Manual indicates on Page 1015,

Para. 7, 17th Ed. Please, I am not mentioning this to demean your contributions

to this Board in any manner, and forgive me should I make you feel as such.

However, I am attempting to incorporate/contribute a bit more accuracy.

I wrote a paper in 2003 which I would like to share with you and others:

IMMUNOGLOBULIN TESTING

By R. Haney

It seems, there is a great deal of confusion and misunderstanding being

dispensed throughout the medical community concerning immunoglobulin testing and

its specific value and reliability. Recently I received a message from a friend

back east who was informed by a well respected Neurotoxicologist that this form

of testing, “only determines that a person was once exposed to a particular

allergen, and does not determine how current an exposure an allergen exposure

is, or when the person was first exposed.” Part of this statement is true,

medical science has very little to go on in determining when an initial exposure

to a particular allergen occurred, and so medical science must rely upon

first-hand accounts of patient histological reporting in order to guess, if

need.

Currently, blood-serum tests of immunoglobulin cells serve as a primary tool for

the detection of microfungi activity in the human body. Antibody proteins are

referred to medically as “immunoglobulins,” or “Ig.” All immunoglobulins have

many common structural features. The antibodies are made of protein “chains”

linked together by chemical bonds. These protein chains are termed as “heavy”

and “light” chains. There are five different classes of “heavy” immunoglobulin

molecule chains referred to collectively in classes as, IgA, IgD, IgE, IgM, and

IgG, respectively depending upon their specific functions and activities.

The class referred to as IgA, is a type of antibody that protects against

infections of mucous membranes lining the mouth (sputum), and is observed in the

airways, tears, nasal fluids, sweat, genito-urinary and gastro-intestinal

tracts, and lung secretions. This is the most common type of immunoglobulin

deficiency occurring in approximately 1 of every 400 humans. It protects against

bacterial and viral infections. (Primary Source: Mosby’s Medical Dictionary, 6th

Edition, 2002)

Very little is known about the specific purpose of the class referred to as IgD.

It is found in small amounts of serum tissue. However, IgD is mainly found on

the surface of B-lymphocytes (B-cells) developed though bone marrow and are

thought regulate B-cell function or development activity. IgD increases in

quantity during allergic reactions to milk, insulin, penicillin, and various

toxins. (Primary Source: Mosby’s Medical Dictionary)

The most studied class of immunoglobulin antibody is IgE, however its protective

role in humans is unclear. IgE is frequently increased in parasitic infestations

and atopic individuals (those with a hereditary predisposition to immediately

react hyper-allergically to the presence of a specific allergen). It is

concentrated in the lungs, skin, and mucous membranes.

The IgE antibody provides the primary defense mechanism against environmental

antigens and is believed to be responsive to IgA. IgE reacts with certain

antigens to trigger the release of chemical mediators that cause anaphylactic

hypersensitivity reactions characterized by wheal and flare. (Primary Source:

Mosby’s Medical Dictionary)

The class, IgG is the major antibody found in the blood that is able to

penetrate into human tissues. In tracking down antigens, it coats the germs in

its ability to attract and assist other immune defense cells seek and destroy

them. This protein molecule also maintains the longest attraction mechanisms of

the immune process, lasting up to 30 days in duration, and currently is the most

persuasive indicator in detecting invasive diseases, e.g., aspergillosis,

cancers, etc. It is synthesized in response to “invasions” by bacteria,

microfungi, and viruses. IgG crosses the placenta and protects the fetus

against red cell antigens and white cell antigens. (Primary Source: Mosby’s

Medical Dictionary)

The class, IgM is an antibody that remains in the bloodstream where it can kill

bacteria that enter the blood stream. Elevated levels of IgM are associated

with Waldenstrom’s Macrobulinemia, a cancer of mature plasma cells,

B-lymphocytes, that causes overproduction of monoclonal macroglobulin (IgM

antibody). It is sometimes called a lymphoplasmacytic disorder. It is the

largest antibody in molecular structure, is observed in circulating fluids, and

is the first immunoglobulin molecule produced, when the biological system of a

human is antigenically challenged. IgM triggers the increased production of

immunoglobulin G, and the complement fixation required for effective immune

response. It is the dominant antibody in the “ABO” blood group

incompatibilities. (Primary Source: Mosby’s Medical Dictionary)

Immunology is the branch of biomedical science concerned with the body's

response and protection against environmental agents that are foreign to the

organism; it is also concerned with the body's recognition of self and not self.

Immunology encompasses the study and function of the immune system,

immunization, organ transplantation, blood banking and immunopathology (diseases

of the immune system).

A foreign molecule (i.e. pollen) or molecule(s) on the surface of an infectious

agent (i.e. bacteria, fungus, virus, etc.) that elicits an immune response is

called an “immunogen.” These are also referred to as antigens. Antibodies are

one of nature's most brilliant solutions to the problem of antigens or " foreign "

material. Acquired immunity (relatively new in evolutionary terms - present only

in vertebrates) is initiated, as the name implies, by initial contact with the

foreign agent (immunization). The initial contact triggers a chain of events

that leads to the activation of certain cells (lymphocytes) and the production

of proteins (antibodies) with specificity against the foreign agent. Antibodies

attach themselves to antigens and start the immune response cascade that leads

ultimately to the neutralization of the foreign agent.

The IgG antibody is the predominant immunoglobulin of internal components such

as blood, cerebrospinal fluid and peritoneal fluid (fluid present in the

abdominal cavity). IgG is the only class of immunoglobulin that crosses the

placenta, conferring the mother's immunity on the fetus. IgG makes up 80% of the

total immunoglobulins. It is the smallest immunoglobulin, with a molecular

weight of 150 000 Daltons. Thus, it can readily diffuse out of the body's

circulation into the tissues. The synthesis of IgG is largely governed by

antigen stimulation, so that in germ free animals, IgG levels are very low but

rise rapidly on transfer to a normal environment.

IgG, IgM, IgA, IgE, and IgD can be subdivided into subclasses as well. They can

differ from one another in that portion of the molecule that binds specifically

to the respective antigen type- IgG for instance, that bind only to a “specific”

microfungi species, and an IgG type that bind to “another” specific type of

microfungi antigen. This of course can also apply to the IgM, IgA, IgE

immunoglobulin classes as well. (Primary Source: “Immunoglobulin Explanation”

Guy Sherwood, 2001)

The purpose in explaining the Ig testing process involving immunoglobulin

classifications is that many people observed as part of our microfungi

health-related research consistently demonstrate ELISA Ig testing which tends to

increase with each testing, if proper medical treatment is not sought, when a

person is adversely affected with a health conditions such as aspergillosis,

histoplasmosis, Coccidioidomycosis, etc.

Many medical professionals indicate that the symptoms of microfungi invasion in

humans subside as a person moves away from an infested environment into a

healthy environment. This is true to an extent as far as symptoms go, but

nothing has effectively stopped the invading microbes from continuing to

formulate into colonization. Thus, eventually as the human body weakens

symptoms tend to reappear later in life (e.g., respiratory problems and

sometimes more serious problems as acid reflux disease or pneumonia). This

tells me that pathogenic microfungi do not leave the human body willingly and

instead continue to grow subtly toward their eventual ability to cause human

disease development.

One problem is that colonized microfungi are rarely specifically tested for and

do not show up readily in normal blood tests. This is perhaps due to a

phenomenon referred to as “molecular mimicry.” Microfungi infestation in humans

is often overlooked in the medical profession because few physicians have the

time to actively monitor their patient’s complete medical history, and many

patients fear discussing fungal exposures with their doctor. A person is

medically observed, and his/her history reviewed in the doctor’s office for

perhaps 15 minutes or so, and then their file is usually “shelved” until the

doctor reads the patient chart again on their next visit- unless special testing

indicates a specific health issue exists.

In medical school, future physicians are rarely adequately trained to rule out

microfungi as a “causation” factor in the health symptoms of their patients-

specifically, they are not taught in-depth, the ecological methods microbes and

plant life use to negotiate and perpetuate their own survival. Current medical

dogma supports the theory that only seriously ill or immunocompromised patients

are subject to major health complications due to mold infestations. This view is

seriously flawed in its scope!

One person B.H., living in Arizona and monitored since 1999, with a high IgG

count for 9 microfungi species (previously on a medically-supervised treatment

program where antifungal drugs “were not prescribed,” and proper nutrient intake

and detoxification methods were the focus), clearly demonstrated increasing IgG

blood serum microfungi level reactions over several interval IgG antibody tests,

even though these same test also showed a dramatic lowering of mycotoxin

reactivity as the body was detoxified.

If microfungi are being extracted in the human immune process, under highly

controlled medical intervention, as they have been in this patient (i.e., his

removal from all microfungi infested environments, elimination of infested food

products with a medically monitored and restricted dieting regiment, and an

ongoing medically-controlled mycotoxin detoxification and nutritional infusion

process), we as observers, might expect a major decrease in the Ig levels of

this person as microfungi “die-off.” In this case, the exact opposite was

observed as IgG (whose cell life is approximately 30 days) levels for the

9-microfungi species actually increased to exceedingly high concentrations.

This poses a serious question. If IgG individual cell life expectancy is only 30

days, and repeatedly demonstrates a progressive decrease over the course of

proper medical treatment, how can doctors continue to believe that once exposed,

a patient’s immunoglobulin antibody levels will continue indicate exposure to

the antigen that was responsible. In other words, if all of the

cytotoxic/pathogenic microfungi were killed and a patient became completely

recovered how is it possible for the immune system to continue to produce IgG

antibody for the antigen? The answer of course is that it would not continue to

be produced. The flaw comes in the fact that once a person has been exposed to a

specific antigen the immune system now has the immune cell chemistry stored to

readily create more IgG antibody in response to the microbial invader, if the

IgE antibody fails success in its initial insurgence. The patient B.H., whom I

feared for the worse three years ago is now on proper antifungal medication, and

is demonstrating marked improvement to both his physical stamina and lowered

microfungi species Ig levels.

The Ig testing process confirms two major aspects of contention relating to

indoor microfungi exposures. First, those who are demonstrating long term

symptoms of cytotoxic and/or pathogenic microfungi exposures, once exposed, are

constantly incubating microfungi colonization.

Why? It due to the fact that body immunity is constantly being

antigenically-challenged by microfungi. Environmentally, microfungi survive and

grow unobstructed by a weakened biological biosphere that climatically is

controlled by an average 98.6oF degree temperature (actually demonstrates

“low-grade” reduction to 97-97.8oF degrees in long term exposed people), and

anywhere from a70% or greater, body fluid content.

This is prime territory for microbial growth, and since bacteria are a weaker

species ecologically and in the molecular evolutionary process of microbes on

earth, it would be normal for people exposed with cytotoxic and/or pathogenic

microfungi colonization to have little or no body flora left to control their

colonized growth patterns territorially, since nearly every living organism on

earth falls prey to the decomposing processes of microfungi in the “Carbon

Cycle.” The Ig testing process provides an excellent tool for confirming that

this process is taking place and is out of control while an animal or human are

still alive.

Additionally, high IgG levels confirm that inflammation is occurring at least

within a 30- day period and if consistent testing is involved, currently in the

living body. Inflammation is instigated by molecular agitation, leading to

friction, and ultimately inflammation. Excreted mycotoxins are definitely a

primary source of the inflammation process. Their cytotoxic chemicals (known

intracellular poisons) are pathogenically dispensed when sensitized to their

ecological niche, leading to only one scientifically observed conclusion, that

human cells are increasingly being genetically challenged, deformed, and killed

as long as the biochemistry of the human body is unable to successfully control

or ultimately destroy their antigenic invaders.

As stated earlier herein, medical science is also aware through a process of

“Molecular Mimicry” that microfungi, bacteria, and viruses are readily able and

capable of initiating this process, as described through research conducted on

the subject.

“What turns the T cells against the Self? Infection often precedes the onset of

autoimmune disease, and so scientists have closely scrutinized the tactics that

pathogens commonly employ to elude T cells. The answer appears to lie in

molecular mimicry, an evolutionary adaptation whereby viruses and bacteria [as

well as microfungi as decomposers] attempt to fool the body into granting them

free access. Such mimicry works by showing the immune system stretches of amino

acids that look like self.”

“An autoimmune response can begin even if the molecular mimicry is not quite

exact. Research at the Scripps Research Institute demonstrated that hepatitis B

virus polymerase shared a stretch of just six amino acids with a part of the

myelin basic protein molecule that causes EAE in rabbits.”

“When they immunized rabbits with this part of the virus, the animals developed

inflammation in their brains. This research suggests that molecular mimicry

between bacteria, or viruses [and microfungi], or bacteria, or viruses the self

may be critical in initiating autoimmune responses.” (Source: Scientific

American, September Issue, 1993, Pg. 109, L. Steinman, M.D., Ph.D., Article:

“Autoimmune Disease”)

If such is the case, then there is another serious flawed complication with the

normal blood testing process that medical doctors rely on currently for proper

diagnosis of an “unknown cause, unknown cure” human ailment. If the immune

system is not actively searching for specific microfungi because of molecular

mimicry, then how is it that Ig blood serum testing is able to determine the

levels of antibody to microbes, especially of a particular microfungi species.

The answer lies in that Ig tests do not- serum samples are exposed to specific

nutrients (media) that in effect “coax” specific microfungi species from the Ig

to feed upon and are incubated to form microfungi colonies. The colonies are

then counted. The forming of microfungi colonization actually clarifies the

specific microfungi species, which are observed via high-powered microscopy.

Microfungi can also be cultured from other sources, e.g., sputum, urine, bone

marrow and specimens from infected tissues. Tissue invasion verification of

microfungi type and level of disease process is presently the best confirmatory

method available.

I hope that this will provide you with additional insight in to the strange

world of immunoglobulins and generate more public interest in learning more

about Immunology.

God Bless and take care,

Doug Haney

EnviroHealth Research & Consulting, Inc.

Email: _Haney52@...

@...: happyru@...: Thu, 27 Dec 2007

23:39:41 +0000Subject: [] EUROPEAN RESPIRATORY REVIEW, 2007

Since Mold won't go away, here's an idea ...Looks as if soon, there may be a

medication that will just turn off the IgE - inflamatory stage, which is all

well and good I would expect for anyone in an emergency situation....but, isn't

a " REACTION " just that? You subject your body to something it isn't able to

handle and WHAMO! It's the body's WARNING SYSTEM... So, I am... reading this

right aren't I? They'll be developing a medication and soon you'll be able to

inhale more of the bad stuff???? And shushhhh the body's SOS

callhttp://err.ersjournals.com/cgi/content/full/16/104/61

_________________________________________________________________

Get the power of Windows + Web with the new Windows Live.

http://www.windowslive.com?ocid=TXT_TAGHM_Wave2_powerofwindows_122007

December 28, 2007

Doug,

Thank you very much for this post. It is one of the best I have even

seen on explaining the Ig panels. Very informative and easy to

understand. Now if we can only get the rest of our physicians to

grasp this information we would all be better off.

KC

>

> Happru/All:

>

> There is only one disturbing thing that I am reading with your

comment. An IgE reaction is not an " inflammatory stage. " Medically

termed, it is the " allergen " stage or an " allergenic response " as

the Merck Manual indicates on Page 1015, Para. 7, 17th Ed. Please,

I am not mentioning this to demean your contributions to this Board

in any manner, and forgive me should I make you feel as such.

However, I am attempting to incorporate/contribute a bit more

accuracy.

>

> I wrote a paper in 2003 which I would like to share with you and

others:

>

> IMMUNOGLOBULIN TESTING

> By R. Haney

>

> It seems, there is a great deal of confusion and misunderstanding

being dispensed throughout the medical community concerning

immunoglobulin testing and its specific value and reliability.

Recently I received a message from a friend back east who was

informed by a well respected Neurotoxicologist that this form of

testing, " only determines that a person was once exposed to a

particular allergen, and does not determine how current an exposure

an allergen exposure is, or when the person was first exposed. "

Part of this statement is true, medical science has very little to

go on in determining when an initial exposure to a particular

allergen occurred, and so medical science must rely upon first-hand

accounts of patient histological reporting in order to guess, if

need.

>

> Currently, blood-serum tests of immunoglobulin cells serve as a

primary tool for the detection of microfungi activity in the human

body. Antibody proteins are referred to medically

as " immunoglobulins, " or " Ig. " All immunoglobulins have many common

structural features. The antibodies are made of protein " chains "

linked together by chemical bonds. These protein chains are termed

as " heavy " and " light " chains. There are five different classes

of " heavy " immunoglobulin molecule chains referred to collectively

in classes as, IgA, IgD, IgE, IgM, and IgG, respectively depending

upon their specific functions and activities.

>

> The class referred to as IgA, is a type of antibody that protects

against infections of mucous membranes lining the mouth (sputum),

and is observed in the airways, tears, nasal fluids, sweat, genito-

urinary and gastro-intestinal tracts, and lung secretions. This is

the most common type of immunoglobulin deficiency occurring in

approximately 1 of every 400 humans. It protects against bacterial

and viral infections. (Primary Source: Mosby's Medical Dictionary,

6th Edition, 2002)

>

> Very little is known about the specific purpose of the class

referred to as IgD. It is found in small amounts of serum tissue.

However, IgD is mainly found on the surface of B-lymphocytes (B-

cells) developed though bone marrow and are thought regulate B-cell

function or development activity. IgD increases in quantity during

allergic reactions to milk, insulin, penicillin, and various toxins.

(Primary Source: Mosby's Medical Dictionary)

>

> The most studied class of immunoglobulin antibody is IgE, however

its protective role in humans is unclear. IgE is frequently

increased in parasitic infestations and atopic individuals (those

with a hereditary predisposition to immediately react hyper-

allergically to the presence of a specific allergen). It is

concentrated in the lungs, skin, and mucous membranes.

>

> The IgE antibody provides the primary defense mechanism against

environmental antigens and is believed to be responsive to IgA. IgE

reacts with certain antigens to trigger the release of chemical

mediators that cause anaphylactic hypersensitivity reactions

characterized by wheal and flare. (Primary Source: Mosby's Medical

Dictionary)

>

> The class, IgG is the major antibody found in the blood that is

able to penetrate into human tissues. In tracking down antigens, it

coats the germs in its ability to attract and assist other immune

defense cells seek and destroy them. This protein molecule also

maintains the longest attraction mechanisms of the immune process,

lasting up to 30 days in duration, and currently is the most

persuasive indicator in detecting invasive diseases, e.g.,

aspergillosis, cancers, etc. It is synthesized in response

to " invasions " by bacteria, microfungi, and viruses. IgG crosses

the placenta and protects the fetus against red cell antigens and

white cell antigens. (Primary Source: Mosby's Medical Dictionary)

> The class, IgM is an antibody that remains in the bloodstream

where it can kill bacteria that enter the blood stream. Elevated

levels of IgM are associated with Waldenstrom's Macrobulinemia, a

cancer of mature plasma cells, B-lymphocytes, that causes

overproduction of monoclonal macroglobulin (IgM antibody). It is

sometimes called a lymphoplasmacytic disorder. It is the largest

antibody in molecular structure, is observed in circulating fluids,

and is the first immunoglobulin molecule produced, when the

biological system of a human is antigenically challenged. IgM

triggers the increased production of immunoglobulin G, and the

complement fixation required for effective immune response. It is

the dominant antibody in the " ABO " blood group incompatibilities.

(Primary Source: Mosby's Medical Dictionary)

> Immunology is the branch of biomedical science concerned with the

body's response and protection against environmental agents that are

foreign to the organism; it is also concerned with the body's

recognition of self and not self. Immunology encompasses the study

and function of the immune system, immunization, organ

transplantation, blood banking and immunopathology (diseases of the

immune system).

> A foreign molecule (i.e. pollen) or molecule(s) on the surface of

an infectious agent (i.e. bacteria, fungus, virus, etc.) that

elicits an immune response is called an " immunogen. " These are also

referred to as antigens. Antibodies are one of nature's most

brilliant solutions to the problem of antigens or " foreign "

material. Acquired immunity (relatively new in evolutionary terms -

present only in vertebrates) is initiated, as the name implies, by

initial contact with the foreign agent (immunization). The initial

contact triggers a chain of events that leads to the activation of

certain cells (lymphocytes) and the production of proteins

(antibodies) with specificity against the foreign agent. Antibodies

attach themselves to antigens and start the immune response cascade

that leads ultimately to the neutralization of the foreign agent.

>

> The IgG antibody is the predominant immunoglobulin of internal

components such as blood, cerebrospinal fluid and peritoneal fluid

(fluid present in the abdominal cavity). IgG is the only class of

immunoglobulin that crosses the placenta, conferring the mother's

immunity on the fetus. IgG makes up 80% of the total

immunoglobulins. It is the smallest immunoglobulin, with a molecular

weight of 150 000 Daltons. Thus, it can readily diffuse out of the

body's circulation into the tissues. The synthesis of IgG is largely

governed by antigen stimulation, so that in germ free animals, IgG

levels are very low but rise rapidly on transfer to a normal

environment.

> IgG, IgM, IgA, IgE, and IgD can be subdivided into subclasses as

well. They can differ from one another in that portion of the

molecule that binds specifically to the respective antigen type- IgG

for instance, that bind only to a " specific " microfungi species, and

an IgG type that bind to " another " specific type of microfungi

antigen. This of course can also apply to the IgM, IgA, IgE

immunoglobulin classes as well. (Primary Source: " Immunoglobulin

Explanation " Guy Sherwood, 2001)

> The purpose in explaining the Ig testing process involving

immunoglobulin classifications is that many people observed as part

of our microfungi health-related research consistently demonstrate

ELISA Ig testing which tends to increase with each testing, if

proper medical treatment is not sought, when a person is adversely

affected with a health conditions such as aspergillosis,

histoplasmosis, Coccidioidomycosis, etc.

> Many medical professionals indicate that the symptoms of

microfungi invasion in humans subside as a person moves away from an

infested environment into a healthy environment. This is true to an

extent as far as symptoms go, but nothing has effectively stopped

the invading microbes from continuing to formulate into

colonization. Thus, eventually as the human body weakens symptoms

tend to reappear later in life (e.g., respiratory problems and

sometimes more serious problems as acid reflux disease or

pneumonia). This tells me that pathogenic microfungi do not leave

the human body willingly and instead continue to grow subtly toward

their eventual ability to cause human disease development.

> One problem is that colonized microfungi are rarely specifically

tested for and do not show up readily in normal blood tests. This is

perhaps due to a phenomenon referred to as " molecular mimicry. "

Microfungi infestation in humans is often overlooked in the medical

profession because few physicians have the time to actively monitor

their patient's complete medical history, and many patients fear

discussing fungal exposures with their doctor. A person is medically

observed, and his/her history reviewed in the doctor's office for

perhaps 15 minutes or so, and then their file is usually " shelved "

until the doctor reads the patient chart again on their next visit-

unless special testing indicates a specific health issue exists.

>

> In medical school, future physicians are rarely adequately trained

to rule out microfungi as a " causation " factor in the health

symptoms of their patients- specifically, they are not taught in-

depth, the ecological methods microbes and plant life use to

negotiate and perpetuate their own survival. Current medical dogma

supports the theory that only seriously ill or immunocompromised

patients are subject to major health complications due to mold

infestations. This view is seriously flawed in its scope!

> One person B.H., living in Arizona and monitored since 1999, with

a high IgG count for 9 microfungi species (previously on a medically-

supervised treatment program where antifungal drugs " were not

prescribed, " and proper nutrient intake and detoxification methods

were the focus), clearly demonstrated increasing IgG blood serum

microfungi level reactions over several interval IgG antibody tests,

even though these same test also showed a dramatic lowering of

mycotoxin reactivity as the body was detoxified.

> If microfungi are being extracted in the human immune process,

under highly controlled medical intervention, as they have been in

this patient (i.e., his removal from all microfungi infested

environments, elimination of infested food products with a medically

monitored and restricted dieting regiment, and an ongoing medically-

controlled mycotoxin detoxification and nutritional infusion

process), we as observers, might expect a major decrease in the Ig

levels of this person as microfungi " die-off. " In this case, the

exact opposite was observed as IgG (whose cell life is approximately

30 days) levels for the 9-microfungi species actually increased to

exceedingly high concentrations.

> This poses a serious question. If IgG individual cell life

expectancy is only 30 days, and repeatedly demonstrates a

progressive decrease over the course of proper medical treatment,

how can doctors continue to believe that once exposed, a patient's

immunoglobulin antibody levels will continue indicate exposure to

the antigen that was responsible. In other words, if all of the

cytotoxic/pathogenic microfungi were killed and a patient became

completely recovered how is it possible for the immune system to

continue to produce IgG antibody for the antigen? The answer of

course is that it would not continue to be produced. The flaw comes

in the fact that once a person has been exposed to a specific

antigen the immune system now has the immune cell chemistry stored

to readily create more IgG antibody in response to the microbial

invader, if the IgE antibody fails success in its initial

insurgence. The patient B.H., whom I feared for the worse three

years ago is now on proper antifungal medication, and is

demonstrating marked improvement to both his physical stamina and

lowered microfungi species Ig levels.

> The Ig testing process confirms two major aspects of contention

relating to indoor microfungi exposures. First, those who are

demonstrating long term symptoms of cytotoxic and/or pathogenic

microfungi exposures, once exposed, are constantly incubating

microfungi colonization.

>

> Why? It due to the fact that body immunity is constantly being

antigenically-challenged by microfungi. Environmentally, microfungi

survive and grow unobstructed by a weakened biological biosphere

that climatically is controlled by an average 98.6oF degree

temperature (actually demonstrates " low-grade " reduction to 97-

97.8oF degrees in long term exposed people), and anywhere from a70%

or greater, body fluid content.

> This is prime territory for microbial growth, and since bacteria

are a weaker species ecologically and in the molecular evolutionary

process of microbes on earth, it would be normal for people exposed

with cytotoxic and/or pathogenic microfungi colonization to have

little or no body flora left to control their colonized growth

patterns territorially, since nearly every living organism on earth

falls prey to the decomposing processes of microfungi in the " Carbon

Cycle. " The Ig testing process provides an excellent tool for

confirming that this process is taking place and is out of control

while an animal or human are still alive.

> Additionally, high IgG levels confirm that inflammation is

occurring at least within a 30- day period and if consistent testing

is involved, currently in the living body. Inflammation is

instigated by molecular agitation, leading to friction, and

ultimately inflammation. Excreted mycotoxins are definitely a

primary source of the inflammation process. Their cytotoxic

chemicals (known intracellular poisons) are pathogenically dispensed

when sensitized to their ecological niche, leading to only one

scientifically observed conclusion, that human cells are

increasingly being genetically challenged, deformed, and killed as

long as the biochemistry of the human body is unable to successfully

control or ultimately destroy their antigenic invaders.

> As stated earlier herein, medical science is also aware through a

process of " Molecular Mimicry " that microfungi, bacteria, and

viruses are readily able and capable of initiating this process, as

described through research conducted on the subject.

> " What turns the T cells against the Self? Infection often

precedes the onset of autoimmune disease, and so scientists have

closely scrutinized the tactics that pathogens commonly employ to

elude T cells. The answer appears to lie in molecular mimicry, an

evolutionary adaptation whereby viruses and bacteria [as well as

microfungi as decomposers] attempt to fool the body into granting

them free access. Such mimicry works by showing the immune system

stretches of amino acids that look like self. "

> " An autoimmune response can begin even if the molecular mimicry is

not quite exact. Research at the Scripps Research Institute

demonstrated that hepatitis B virus polymerase shared a stretch of

just six amino acids with a part of the myelin basic protein

molecule that causes EAE in rabbits. "

>

> " When they immunized rabbits with this part of the virus, the

animals developed inflammation in their brains. This research

suggests that molecular mimicry between bacteria, or viruses [and

microfungi], or bacteria, or viruses the self may be critical in

initiating autoimmune responses. " (Source: Scientific American,

September Issue, 1993, Pg. 109, L. Steinman, M.D., Ph.D.,

Article: " Autoimmune Disease " )

>

> If such is the case, then there is another serious flawed

complication with the normal blood testing process that medical

doctors rely on currently for proper diagnosis of an " unknown cause,

unknown cure " human ailment. If the immune system is not actively

searching for specific microfungi because of molecular mimicry, then

how is it that Ig blood serum testing is able to determine the

levels of antibody to microbes, especially of a particular

microfungi species. The answer lies in that Ig tests do not- serum

samples are exposed to specific nutrients (media) that in

effect " coax " specific microfungi species from the Ig to feed upon

and are incubated to form microfungi colonies. The colonies are then

counted. The forming of microfungi colonization actually clarifies

the specific microfungi species, which are observed via high-powered

microscopy. Microfungi can also be cultured from other sources,

e.g., sputum, urine, bone marrow and specimens from infected

tissues. Tissue invasion verification of microfungi type and level

of disease process is presently the best confirmatory method

available.

>

> I hope that this will provide you with additional insight in to

the strange world of immunoglobulins and generate more public

interest in learning more about Immunology.

>

> God Bless and take care,

>

> Doug Haney

> EnviroHealth Research & Consulting, Inc.

> Email: _Haney52@...

>

> @...: happyru@...: Thu, 27 Dec 2007 23:39:41

+0000Subject: [] EUROPEAN RESPIRATORY REVIEW, 2007

>

> Since Mold won't go away, here's an idea ...Looks as if soon,

there may be a medication that will just turn off the IgE -

inflamatory stage, which is all well and good I would expect for

anyone in an emergency situation....but, isn't a " REACTION " just

that? You subject your body to something it isn't able to handle and

WHAMO! It's the body's WARNING SYSTEM... So, I am... reading this

right aren't I? They'll be developing a medication and soon you'll

be able to inhale more of the bad stuff???? And shushhhh the body's

SOS callhttp://err.ersjournals.com/cgi/content/full/16/104/61

>

> _________________________________________________________________

> Get the power of Windows + Web with the new Windows Live.

> http://www.windowslive.com?

ocid=TXT_TAGHM_Wave2_powerofwindows_122007

>

December 28, 2007

Tahnk you, and it just shows to go ya... this MOLD illness makes it

so even a very simple article can get all messed up and warped in a

MOLD invaded brain.

Thanks again Mr. Haney

oh and PS... please let me know if you rec'vd my e-mail.

>

> Happru/All:

>

> There is only one disturbing thing that I am reading with your

comment. An IgE reaction is not an " inflammatory stage. " Medically

termed, it is the " allergen " stage or an " allergenic response " as the

Merck Manual indicates on Page 1015, Para. 7, 17th Ed. Please, I am

not mentioning this to demean your contributions to this Board in any

manner, and forgive me should I make you feel as such. However, I am

attempting to incorporate/contribute a bit more accuracy.

>

> I wrote a paper in 2003 which I would like to share with you and

others:

>

> IMMUNOGLOBULIN TESTING

> By R. Haney

>

> _________________________________________________________________

> Get the power of Windows + Web with the new Windows Live.

> http://www.windowslive.com?

ocid=TXT_TAGHM_Wave2_powerofwindows_122007

>

December 30, 2007

Doug: I was on the trip to Washington, D.C. as you stated in the

post below. However, I strongly feel that Sharon Kramer's work was

of greater benefit to the indoor mold problem than what we

accomplished. Also, the Air Traffic Control Towers litigation is on

the move. Both Dr. Lipsey and I are involved in this matter. All

litigation moves slowly. Finally, I remember on the trip that you

were promoting a fogging mixture of chemicals to be used in damp

indoor spaces to kill mold and bacteria. I just looked up the

California Pesticide Registration of this product at the request of

an individual who wanted information on its toxicology. The product

is a petroleum distillate of the diesel fuel and kerosene group. I

would not recommend this product under any condition, particularly

when occupants may have developed MCS or chemical hypersensitivity.

The product I am referring to is MDF 500, California Pesticide

Registration No. 218536 and 21548. The USEPA number is 80364-1 and

9036r-2. A registered pesticide is a pesticide. If I am wrong

please let me know. Jack D. Thrasher, Ph.D.

>

> KC: Hope yours and all who visit and appreciate the " Sickbuildings "

board have a very happy New Year. Thank you so very much for your

comments. A couple years ago I made some promises that we would have

some major developments wherein mold exposures and illness are

concerned. I believed then that this news would arise from the

massive mold exposure problems that Air Traffic Controllers are

continuing to face in Control Towers across the nation (which the FAA

has all but put on its very low priority list). I was one of four

original consulting experts on environmental health that had been

contacted for this arbitration/litigation process. I chose to depart

from that process, mainly due to the " snail pace " of the case. When a

team we organized to visit Washington DC in April 2007 to speak with

members of the Senate and Congress, the president of the Detroit

Metro Air Traffic Controller's Association chapter accompanied us.

Others who dedicated their time and own expenses to make the trip and

contribute greatly were Dr. Jack Thrasher (Expert Toxicologist, exp.,

environmental fungi and health), Dr. Dennis Hooper (Medical

Mycology/Genetic Researcher), Ms. Cheryl Bossio, Esq. (expert

plaintiff's attorney greatly experienced in litigating mold exposure

health-related cases), Overton, Esq. (who also is experienced

with mold and health litigation). These people have been working hard

either behind the scenes or publicly to bring about greatly needed

change. My thought then was that 2007 was going to be a positive-

explosive year for mold exposure victims. This visit WAS successful

in its own right, and Sharon Kramer's work to this regard has been

nothing less than exceptional, given the pressures and fiscal issues

facing her in her own litigation matter, but what has happened in

reality with all of our efforts in 2007, is that what we have

accomplished as set up 2008 as a banner year for mold victims. In

January several things will start to happen to demonstrate clearly

what I am telling you now. Look for news coming out of Sacramento,

California concerning this topic. And, remember all throughout 2008,

that you heard it here on " Sickbuildings " first. Sometime between

January 7-11, I will write " THE " post that I have been waiting to

write for over 11-years, AND I will guarantee that we will have some

delightful fun with all of those " naysayers " who have expressed the

views/writings that " mold exposures are not harmful. "

>

> God Bless and take care. Doug Haney

> EnviroHealth Research & Consulting, Inc.

> Email: _Haney52@...

>

> @...: tigerpaw2c@...: Sat, 29 Dec 2007 03:08:40

+0000Subject: [] Re: EUROPEAN RESPIRATORY REVIEW, 2007

>

> Doug,Thank you very much for this post. It is one of the best I

have even seen on explaining the Ig panels. Very informative and easy

to understand. Now if we can only get the rest of our physicians to

grasp this information we would all be better off. KC---

>

January 2, 2008

Doug: I did not mean to imply that we did not accomplish our goal.

I only meant to point out that Sharon Kramer has done outstanding

work in this area, particularly with the ongoing GA0 investigation.

She is to be commended.

I am surprised that you are not aware of the chemical compopsition of

MDF 500. There is at least three products with this registration.

One is known to release copious amounts of ammonia. However, all are

petroleum based. I do not recommend their use, partcularly where an

individual has chemical hypersensitivity. When it comes to this

illness some people are highly sensitive. The manufacturer and

registrar of these products do not warn regarding the issue of

chemical hypersensitivity. You may have used it successfully, but in

my experience many will not, particularly with respect to the diesel

fuel rating of these products. Jack D. Thrasher, Ph.D.

P.S. My left leg injury has pretty well healed. It has taken its

time to heal. I had a severe muscle pull in the left gastrocnemius

muscle that probably will never be 100% at my age.

>

> Dr. Thrasher:

>

> First, let me say that your wisdom and opinions have always been

held in the highest esteem with me, and continue as such. Second,

there is no question what so ever that Sharon Kramer's dedicated

service to mold exposed victims has been of unparalleled by our trip

to Washington, DC, or anything else. And our trip was not meant to

compete with anyone or boost anyone's ego. Our mission was clearly

spelled out: (Mission/Objective: extracted from the trip report.)

>

> WASHINGTON DC MISSION/OBJECTIVE

>

> Our primary focus was to educate federal lawmakers and special

interest groups as to the scientific facts relating to the complex

pathogenic environment to promote serious interest in order to enact

responsible legislation that will educate and guide fields involved

sufficiently to adequately protect the health and safety of American

citizens.

>

> The Politicians in Washington clearly demonstrated a proactive

interest in the welfare of the American public. They actively

listened and posed thoughtful questions in response to the material

presented.

>

> OUR CALL TO ARMS

>

> · Encouraged advanced medical training

> · Positively impact our fight against human disease.

> · Investigate dangerous and unhealthy exposures.

> · Investigate alleged fraudulent concealment, cohesion, and

unethical activity

> · Mandate monitoring with public reporting and accountability

> · Punish unethical destructive behavior against others and

publicly identify the perpetrators to discourage future such activity

>

> The team suggested consideration of classification of mold-related

diseases as " reportable diseases " by healthcare professionals or

facilities by the Centers for Disease Control and Prevention (CDC).,

Mold infections have proven to be more difficult to medically

diagnose and treat than bacteria or viruses despite the availability

genetic analysis to rapidly identify the disease.

>

> AUTHOR/COORDINATOR'S SUMMARY

>

> For eight years now, I have been planning a trip such as this. Each

person who joined our venture in Washington DC paid their own

expenses and were not sponsored by any other party. No conflict of

interest issues were present. The teams mission was to initiate

education as to the seriousness of health issues involving human

exposures.

> We did our best as a cohesive team, and everyone gave outstanding

presentations unified in the goal to help educate the decision makers

of our nation.

> There are forces that do not want laws assisting in the health,

safety, and prevention of indoor exposures to unhealthy environments

to come into effect in the United States. As we push forward and

demand full accountability and disclosure it becomes ever clearer who

the obstacles are behind the prevention of initiation of safety

measures with accountability for all Americans. We are truly fighting

a war of economy verses human quality, and the stakes are much higher

than other types of warfare because we are fighting invisible

entities within our own fold. I believe in the American way of life,

and that justice will endure.

>

> Dr. Thrasher, as I recall, you went further than any of us in your

dedication because you were in quite a bit of pain at the time, and

for that reason I consider your participation extraordinary. However,

I believe we did accomplish quite a bit as a result of that trip

because I have received several calls from congress and senate aids

since. To this regard, I do not believe that Sharon Kramer feels

anything but respect for our attention to mold exposure health

issues, and knowing her as I do, as we have spoken in the past, I

believe she feels as I do, that we are all in this effort together. I

would welcome many people to visit their political leaders and

personally do not care in the least who finally accomplishes the best

results as I care about public involvement more than anything. As I

have stated before, this public health problem involves a literal WAR

between the values of American economics and the sciences AND an

American public that has suffered greatly because the " cause and

effect " of exposures to indoor pathogenic microfungi and the

multitude of products with microfungi and microfungi produced

mycotoxins/MVOCs has been terribly neglected and maligned in regard

to human health and serious diseases. Beyond that scope of interest,

my personal work and efforts are simply part of the overall effort.

>

> Third: Dr. Thrasher, until this date, I had no idea of the deep

chemical composites of MDF-500. However, your recommendations or

not, I have found this to be the very best answer in killing and

sustaining the kill ratio of molds, bacteria, and viruses that the

government has ever produced as I have personally used it in my home

and on my patio area with exceptional results. It was used in a

surgical center in Roseville, CA with exceptional results as

monitored through standard remediation protocol. One year later, air

sampling demonstrated clearly that this product was highly

effective. All of your concerns regarding this product's can

certainly be answered much better by the manufacturing folks at

Modec, Inc., of Denver, CO. The reason I promoted it in Washington

DC, was that it was being used for remediation efforts in other

federal buildings, nationally by HASMAT teams coast to coast, had

been properly reviewed and registered by the CA EPA, and might be

useful in the Detroit Metro Control Tower situation, and at the

Walter Medical Hosptial. I will continue to suggest its use to

anyone who might find it useful. I suffer with MCS, sugar diabetes II

(mellitus II), polycystic kidney disease, severe GERD/acid reflux

disease, and have 10 species of microfungi at 4-7x the ranges

formerly posed by ImmunoSciences Laboratory, and this product's use

has done nothing after use in my own home to harm me in any manner.

In fact, this year I have felt better than in years past. I can only

speak for myself on this subject, but though I absolutely value your

opinions, on this one humbly, I submit that I have to waiver and will

look into your considerations to a greater degree.

>

> Fourth: Thank you for the update on the Detroit metro situation. I

am aware of that matter as well as several others around the country.

My point overall is that it moved too slowly for my involvement.

Prior to your commitment to it I had been reviewing this matter for

nearly a year, and that is precisely why I requested that you go to

Washington DC, to meet with my friend and then, Detroit Metro Air

Traffic Controllers chapter President, Mr. Sugent. I wanted him to

meet you and for you to hear of their plight first hand. Another

person who should be working with Controllers, nationwide and not

just in Detroit, is Dr. Hooper. I have all the faith in the world,

that with your expert assistance, and that of Dr. Lipsey (whom I also

hold in the highest of esteem), this matter will resolve sooner than

later, and that the mold exposed victims who have been made seriously

ill as a result of working there, will find effective medical

attention as a result.

>

> God Bless you and your work, and I wish you and yours the very best

New Year.

>

> With warmest regard,

>

> Doug Haney

>

> @...: toxicologist1@...: Mon, 31 Dec 2007 06:03:46

+0000Subject: [] Re: EUROPEAN RESPIRATORY REVIEW, 2007

>

> Doug: I was on the trip to Washington, D.C. as you stated in the

post below. However, I strongly feel that Sharon Kramer's work was of

greater benefit to the indoor mold problem than what we accomplished.

Also, the Air Traffic Control Towers litigation is on the move. Both

Dr. Lipsey and I are involved in this matter. All litigation moves

slowly. Finally, I remember on the trip that you were promoting a

fogging mixture of chemicals to be used in damp indoor spaces to kill

mold and bacteria. I just looked up the California Pesticide

Registration of this product at the request of an individual who

wanted information on its toxicology. The product is a petroleum

distillate of the diesel fuel and kerosene group. I would not

recommend this product under any condition, particularly when

occupants may have developed MCS or chemical hypersensitivity. The

product I am referring to is MDF 500, California Pesticide

Registration No. 218536 and 21548. The USEPA number is 80364-1 and

9036r-2. A registered pesticide is a pesticide. If I am wrong please

let me know. Jack D. Thrasher, Ph.D.--- In

, Haney <_Haney52@>

wrote:>> KC: Hope yours and all who visit and appreciate

the " Sickbuildings " board have a very happy New Year. Thank you so

very much for your comments. A couple years ago I made some promises

that we would have some major developments wherein mold exposures and

illness are concerned. I believed then that this news would arise

from the massive mold exposure problems that Air Traffic Controllers

are continuing to face in Control Towers across the nation (which the

FAA has all but put on its very low priority list). I was one of four