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My Latest Guest Editorial Article in Response to Lake Co. Record-Bee

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Author: R. Haney (---.dsl.scrm01.pacbell.net)

Date: 08-23-05 04:48

http://chat.osb.net/read.php?f=25 & i=2351 & t=2351

ALL:

About two weeks ago I was invited by Larson, Managing

Editor of the Lake County Record-Bee and Clear Lake Observer-

American to submit an article in response to the editorial comment

condemning environmental mold exposures written by a reader of the

Record-Bee, Darrell Watkins. (See: \ " Some Dimwitts Need an

Education, If That\'s Possible\ " ; K.C. 08-09-05)

Since it has not been accepted as of yet, nor have I heard any

response from the editor after speaking with her at length and

calling her again yesterday, I prefer not to take the chance that it

will not be accepted for print and left unsaid. So below is a copy

of the article I submitted for your review.

ARTICLE:

Guest Editorial, R. Haney

CEO, EnviroHealth Research & Consulting, Inc.

Rocklin, CA (E-mail: _Haney52@...)

" MOLDS—POLITICS—HUMANS: WHY MOLDS HAVE A LICENSE TO KILL! "

The American College of Occupational and Environmental Medicine

(ACOEM), the National Academy of Sciences, and other health field

disciplines continue to harbor the belief that inhalation of indoor

molds are in some manner physically different than molds and

mycotoxins encountered by the consumption of food products, and

therefore inhaled, they are not as dangerous as a " causative effect "

in human disease. Some of these nationally recognized entities offer

that inhaled mold spores do little more than cause respiratory

problems, e.g., asthma and allergic reactions. For instance, in

their October 27, 2002 ACOEM evidence-based statement,

titled " Adverse Human Health Effects Associated with Molds in the

Indoor Environment " , the College (a membership organization, and

clearly not an " academic medical institution " ) is quoted as

stating, " Current scientific evidence does not support the

proposition that human health has been adversely affected by inhaled

mycotoxins in the home, school, or office environment. " In fact the

primary authors of this " medical report " are not " medical

physicians " at all, they are both PhDs. Let's see if what is being

said about indoor mold exposures is true?

First, we must separate micro fungi (meaning molds and yeasts) from

the secondary chemicals that they produce. Harriet Ammann, PhD,

D.A.B.T., Senior Toxicologist Air Quality Program Washington State

Department of Ecology, perhaps explains this best in her article

about cytotoxic micro fungi and their secondary mycotoxins, " Is

Indoor Microfungi Contamination a Threat to Health? " (Ammann, 2001)

" Mycotoxins… are not essential to maintaining the life of the micro

fungi cell in a primary way (at least in a friendly world), such as

obtaining energy or synthesizing structural components,

informational molecules or enzymes. They are products whose function

seems to be to give micro fungi a competitive advantage over other

micro fungi species and bacteria. Mycotoxins are nearly all

cytotoxic, disrupting various cellular structures such as membranes,

and interfering with vital cellular processes such as protein, RNA

and DNA synthesis. Of course they are also toxic to the cells of

higher plants and animals, including humans. Mycotoxins vary in

specificity and potency for their target cells, cell structures or

cell processes by species and strain of the micro fungi that

produces them. Higher organisms are not specifically targeted by

mycotoxins, but seem to be caught in the crossfire of the

biochemical warfare among micro fungi species and micro fungi and

bacteria vying for the same ecological niche. "

Dr. Ammann's article further demonstrates with clarity the

difference in roles between weaker, " passive " micro fungi as

unattached spore unassociated with a colonized formation and those

directly inhaled after breaking loose from a pathogenic colony.

Citing specific studies by nationally respected researchers, Jarvis

(1990, 1995), Burge, and Yang (1995), Dr. Ammann states:

" Toxigenic micro fungi vary in their mycotoxin production depending

on the substrate on which they grow (Jarvis, 1990). The spores, with

which the toxins are primarily associated, are cast off in blooms

that vary with the micro fungi's diurnal, seasonal, and life cycle

stage (Harriet Burge, 1990; Yang, 1995). The presence of competitive

organisms may play a role, as some micro fungi grown in monoculture

in the laboratory lose their toxic potency (Jarvis, 1995). Until

relatively recently, micro fungi poisons were regarded with concern

primarily as contaminants in foods. More recently, concern has

arisen over exposure to multiple mycotoxins from a mixture of micro

fungi spores growing in wet indoor environments. " (Ammann, 2001)

Molds and yeasts don't always grow in a colony of a particular mold

or yeast species, nor are they always unhealthy for humans to

breathe in or touch. This is because most species are not pathogenic

until they become pathogenic. Pathogenic, or " disease causing " micro

fungi are those normally found in a colony, such as growing on a

wall, in the heating and air conditioning system, under a sink, on a

windowsill, in a bathtub, and in other indoor areas. Micro fungi

become pathogenic when their environment changes to where they

become chemically sensitive to their survival. This triggers

colonization for strength, nutrient search, and territorial gain in

order to continue the survival of their species.

The fortunate part of this for animals and humans is that the longer

micro fungi are airborne and away from other species the weaker they

become, and outside of a home, office, school in the natural

environment where ambient air is plentiful, the abundant amount of

oxygen involved in airflow, combined with ultraviolet rays of the

sun, and other natural resources keep micro fungi in a weakened

state enough not to hurt humans as they enter the human body. Even

inside the human body there are several biological methods for

keeping micro fungi at bay, i.e., a balanced pH level, a responsive

immune system, competent homeostasis, among the many defensive

biological factors. That's the good news. But over time pathogenic

micro fungi can cause serious health problems. The medical field

claims that all of this, especially relating to inhaled micro fungi

in an indoor environment is new science, and that the mycotoxins

that micro fungi excrete are not a health factor. Nothing could be

further from the truth!

The study of potentially dangerous mycotoxin poisoning in humans is

not new to the science community. A.V. Costantini, M.D. (retired),

is the former head of the World Health Organization Collaborating

Center for Mycotoxins in Food (Department of Clinical Chemistry,

School of Medicine, Albert Ludwigs University, Freiburg, Germany),

and member of the Clinical Professional Faculty (retired) University

of California, School of Medicine, San Francisco. In his

Fungalbionic© series of books on microfungi and disease Dr.

Costantini states:

" In the 1930s and 1940s, as many as 1,000 compounds, classifiable as

mycotoxins, were studied by the pharmacology industry as potential

antibiotics 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 a variety of 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, cause in humans. "

One such mycotoxin product known to cause death and severe health

problems in humans at high amounts, is referred to as Oxalic acid.

In his article, " Decomposition of Oxalate by Microorganisms, "

Professor N. Sahin, Mugla University, Turkey (1997) reports:

" Accumulation of oxalate by fungi (micro fungi), particularly in

Aspergillus, Penicillium and Mucor species is of such an order that

these fungi could be used for industrial fermentation for oxalate…

At high concentrations, oxalic acid causes death in humans and

animals due to its corrosive effects. In smaller amounts, oxalic

acid causes a variety of pathological disorders, including

hyperoxaluria, pyridoxine deficiency, cardiomyopathy, cardiac

conductance disorders, calcium oxalate stones and renal failure. "

What is really astonishing is that hospitals recognize pathogenic

micro fungi spores in an indoor environment as being deadly with

patient inhalation, yet the American College of Occupational and

Environmental Medicine tends to downplay the dangers of micro fungi.

Micro fungi in a hospital setting are dreaded more than bacteria and

viruses because once in the human body they are more aggressive and

harder to treat medically than these pathogens. There are more

ailing and immune compromised people living external of hospital

environments (that are " controlled " environments which can become

very deadly with few pathogenic micro fungi spores) than people

occupying " uncontrolled " home, office, and school environments. When

a person really takes the time to research about micro fungi and

mycotoxin release, the hypothesis presented by the ACOEM report does

not make a lot of logical sense.

According to Professor Wong, Ph.D., at the University of

Hawaii, Botany Department, " The successful treatment of fungal

diseases is more difficult to treat than those caused by bacteria.

Because bacteria are prokaryotes, the makeup of their cells are very

different than our own eukaryotic cells and pharmaceutical products,

such as antibiotics, can successfully destroy bacteria without

harming our cells, tissues, and organs. However, because fungi are

eukaryotes, finding a treatment that will kill the fungus and not

harm our own cells is more difficult. "

According to the land Department of Health & Mental Hygiene,

Community Health Administration (1999), " Although invasive

aspergillosis may be community acquired, most cases are nosocomial

in origin. Major outbreaks of invasive nosocomial Aspergillosis have

been reported associated with hospital construction, renovation and

maintenance, activities that allow spores to become airborne. "

It is interesting to learn what instructions medical students and

students destined for future laboratory work are being given prior

to working with micro fungi in university laboratory settings. In

her text, Introduction to Diagnostic Microbiology (1997), Associate

Professor and Director of Medial Laboratory Programs, Dannessa

Delost, M.S., M.T. (ASCP) of the Department of Allied Health,

College of Health and Human Services, Youngstown State University.

Professor Delost administrates the following health and safety

policies and procedures:

" Conidia and spores may remain dormant in the air or environment or

may be transported through the air to other locations. The spores of

pathogenic molds can be inhaled and enter the respiratory tract.

This is a common rout of infection, and because of this, it is

imperative to practice good laboratory safety when working in

mycology. All work, including the preparation of slides, plating and

transferring cultures, and any biochemical work, must be performed

in a biological safety cabinet. Because airborne conidia and spores

are readily released from a fungal culture, one should never smell a

fungal culture. Screw-cap test tubes should be used in place of test

tubes with a cotton, metal, or plastic lid. In addition, Petri

plates must be sealed tightly with either an oxygen-impermeable tape

or Parafilm. As always, gloves should be worn and any breaks or cuts

in the skin covered to prevent the transmission of fungal infection. "

The ACOEM report previously referred to states also that " Uncommon

allergic syndromes, allergic bronchopulmonary aspergillosis (ABPA),

and allergic fungal sinusitis (AFS), are briefly discussed for

completeness, although indoor mold has not been suggested as a

particular risk factor in the etiology of either. " According to B.

A. Cockrill, M.D. and C. A. Hales, M.D., Pulmonary and Critical Care

Unit, Partner\'s Asthma Center, Massachusetts General Hospital and

Harvard Medical School, Boston, Massachusetts, allergic

bronchopulmonary aspergillosis seems to have a lot to do with

inhalation:

" Allergic bronchopulmonary aspergillosis (ABPA) is a syndrome seen

in patients with asthma and cystic fibrosis. It is characterized by

chronic colonization of the airways with a ubiquitous fungus,

Aspergillus fumigatus. The clinical expression of ABPA results from

the complex interaction of chronic colonization of the airways with

A. fumigatus, host factors allowing this colonization, and the

host\'s genetically determined immune response. Clinically the

syndrome is characterized by recurrent episodes of wheezing, mucus

production, pulmonary infiltrates, and elevated levels of serum IgE.

Many patients develop central bronchiectasis, and a subset will go

on to end-stage fibrotic lung disease. It is thought that treatment

will prevent this progression. The mainstay of therapy remains oral

corticosteroids. "

So, the ACOEM, given this example would have us believe that all

inhalation is conducted externally of a home, office, or school

environment. In uncontrolled environments we would all have to stop

breathing for the ACOEM hypothesis to be true. Here is a given fact

with lots of science to back it up. The only people that are not

able to breathe in outside and inside environments are dead people.

Emphasis similar to the example given above is exercised for

allergic fungal sinusitis (AFS).

I believe that M. , M.D., and R. Perfect, M.D., both

professors of medicine at the Duke University Medical Center clearly

state the current position in medical science quite aptly:

" Fungal sinusitis encompasses a wide variety of fungal infections

that range from merely irritating to rapidly fatal. The frequent

inhalation of fungal spores into the lungs and sinuses creates

abundant opportunities to acquire fungal sinusitis. The efficiency

of the defense mechanisms of the upper airways prevent fungal

sinusitis from becoming more common. Nevertheless, fungal infections

of the sinuses appear to be underdiagnosed, partly because of lack

of awareness on the part of clinicians. "

In a study conducted at the Mayo Clinic in Rochester, Minnesota and

publicly released through the journal Mayo Clinic Proceedings on

September 9, 1999, the research of Jens Ponikau, M.D., and

colleagues found that 96% of the 210 chronic sinusitis patients

clinically evaluated were not suffering from bacterial infections as

medical experts had been assuming for years, but from a fungal

infection in the sinuses. Using new genetic identifying methods the

team of medical scientists identified 40 different species in the

combined study of patients with an average of 2.7 species per

patient. And of course since this research involved new tools of

molecular science there as been much controversy over the techniques

used in the study.

How does specific scientific research equate molds to human

diseases? When medical health experts refer to " lay press " they are

often inferring that what is reported is " unproven " or " junk

science " as opposed to having specific scientific merit. When this

relates to indoor micro fungi exposures adversely affecting health,

the medical field, insurance providers, and other entities standing

to lose money tend to separate pathogenic molds-- found in " immune

compromised " individuals --from people with " healthy immune systems "

who become ill from such exposures.

Many times scientific literature is non-specific in how it defines

physical illness due to micro fungi exposures. For instance, most

journal articles will indicate that a person who is adversely

affected by mold exposures " often has an underlying immune

deficiency such as… " or " rarely affecting a person who is immune

sufficient… " In these instances the words " often " and " rarely " are

meaningful words indeed. What these words clearly signify is

that " no one " in science knows for certain what triggers major

illnesses from mere exposures to pathogenic micro fungi, or when

such exposures start to chemically and/or genetically influence the

manifestation of the disease process.

To provide an example of this, a Journal of Aerosol

Science, " Bioaerosols and Occupational Lung Disease " (Lacey, J, J.

Dutkiewicz, March 1994) states:

" Infection may be aided by immunodeficiency caused by underlying

disease or therapeutic treatments or, perhaps, by mycotoxins. "

However, pathogenic micro fungi are molds and yeasts that are

actively excreting mycotoxins due to the fact that they are actively

attempting to decompose an area of the human body that has given

them chemical messages that it is weakening or dying. At least

research at the Department of Cell and Molecular Biology, Tulane

University, comes closer to this reality as a Clinical Microbiology

Reviews article titled " Mycotoxins " states:

" Primary pathogens affect otherwise healthy individuals with normal

immune systems. Opportunistic pathogens produce illness by taking

advantage of debilitated or immunocompromised hosts. The majority of

human mycoses are caused by opportunistic fungi. The mechanisms of

pathogenesis of both primary and opportunistic fungi are complex,

and medical mycologists have devoted considerable research energy

trying to identify the factors that distinguish fungal pathogens

from saprophytic and commensal species. Some infections remain

localized, while others progress to systemic infection. For many

mycoses, the ordinary portal of entry is through the pulmonary

tract, but direct inoculation through skin contact is not uncommon.

(, J., Klich, M., July 2003)

Micro fungi like many other forms of life in cellular evolution were

mutated from bacterial and other similar life forms, and as with

human cellular physiology eukaryotic cells of micro fungi are

stronger than their prokaryotic counterparts. Human cells are

stronger than bacteria, micro fungi, viruses, because cellular

development is based upon evolutional changes. The oldest species is

the weakest species due to the mutational changes that take place

over eons that allow species to survive and strengthen. We know this

in molecular and medical science simply because the Penicillin

mycotoxin extracted from the fungal species Penicillium notatum (and

later, P. Chrysogenum) is used to kill pathogenic (disease causing)

bacteria in animals and humans. As famed biologists Lynn Margulis

and Dorian Sagan aptly state in their work, " Microbial Microcosm " :

Far from leaving microorganisms behind on an evolutionary ladder, we

more complex creatures are both surrounded by them and composed of

them. New knowledge of biology alters our view of evolution as a

chronic, bloody competition among individuals and species. Life did

not take over the globe by combat, but by networking. Life forms

multiplied and grew more complex by co-opting others, not just by

killing them …

In the first two billion years of life on Earth, bacteria - the only

inhabitants - continuously transformed the planet\'s surface and

atmosphere and invented all life\'s essential, miniaturized chemical

systems. Their ancient biotechnology led to fermentation,

photosynthesis, oxygen breathing, and the fixation of atmospheric

nitrogen into proteins. It also led to worldwide crises of bacterial

population expansion, starvation, and pollution - long before the

dawn of larger forms of life…

Those who speak only for the special interests of human beings fail

to see how interdependent life on Earth really is. Without the

microbial life forms, we would sink in feces and choke on the carbon

dioxide we exhale. We cannot view evolutionary history in a balanced

manner if we think of it only as a four-billion-year preparation

for " higher " organisms, like humans. Most of life\'s history has

been microbial. We are recombinations of the metabolic processes of

bacteria that appeared before, during, and after the accumulation of

atmospheric oxygen some 2,000 million years ago... The ancient,

vast, and fundamental nature of our interdependence with other forms

of life may be humbling, but it provides a basis for facing the

future free of crippling delusions. Despite all our conceits, we are

as much exploited as exploiters, as much consumed as consumers. The

lesson of evolutionary history is that it will be through

conservation, interaction, and networking, not domination, that we

avert a premature end to our species.

We are not entering the 21st century of medical science; we are

living it! It is time to move our " intellectual society " of educated

PhDs, MDs, and all other humans who have challenged and surpassed

atomic age, space age, and computer age, and claimed to have entered

the age of Aquarius, to intellectually understand the world of

microbes and how we are as balanced with the earth as they are. It

is so incredibly ironic and perhaps even humbling in the last thirty

years since the inception of the field of Molecular Science, that we

as humans have the most integrated neural system in the universe and

are able to send men and women into space with its capacity to

construct logic from practically nothing, and yet tiny microbes that

have been waging ecological battles for billions of years with no

brain function whatsoever can fake out our biological system enough

to demoralize our intellect and destroy our lives. And, because we

have not quite figured out that human lives are more important than

our economic status, we can't quite grasp the meaning of our own

purpose within our own existence.

References:

1. Merck Manual, The. 17th Ed. (1999) " Systemic Fungal Diseases "

(Systemic Mycoses). Chapter 158, Page 1210.

2. , J. W., Klich M. (July 2003). Mycotoxins. Clinical

Microbiology Reviews, Vol. 16. No. 30893-8512/03. American Society

for Microbiology (p. 497-516) Retrieved October 26, 2004 at

http://www.cmr.asm.org/cgi/content/full/16/3/497

3. Webster's Ninth Collegiate Dictionary (1988). Page 783.

4. land Department of Health & Mental Hygiene, Community Health

Administration (1999). Guidelines for Prevention and Control of

Nosocomial Pulmonary Aspergillosis. Retrieved August 9, 2005 at

http://edcp.org/guidelines/aspers2.html

5. Delost, D. M. (1997). Introduction to Medical Mycology.

Introduction to Diagnostic Microbiology: A Text and Workbook. Mosby,

St. Louis, MO. 358

6. Ammann, H.M. (February 2001, Updated September 2003). Is Indoor-

Mold a Threat to Human Health. Washington State Department of

Health, Office of Environmental Assessments. Retrieved March 14,

2004 from http://www.allergyconsumerreview.com/mold-and-mildew-

allergy.html

7. National Academy of Sciences (May 25, 2004). News

Release: " Indoor Mold, Building Dampness Linked to Respiratory

Problems and Require Better Prevention; Evidence Does Not Support

Links to Wider Array of Illnesses " . Retrieved on August 10, 2005,

from http://www4.nationalacademies.org/news.nsf/isbn/0309091934?

OpenDocument

8. Moran, M. (July 26, 2000). Environmental Health Watch: Healthy

House. WebMD Medical News. Retrieved on April 16, 2003 from

http://www.ehw.org/Healthy_House/HH_Toxic_Mold.htm

9. ACOEM (October 27, 2002). Adverse Human Health Effects Associated

with Molds in the Indoor Environment. ACOEM Evidence-based

Statement. American College of Occupational and Environmental

Medicine. Retrieved on August 10, 2005, from

http://www.acoem.org/guidelines/article.asp?ID=52

10. Cockrill, B. A., Hales, C. A. (February 1999). Allergic

Bronchopulmonary Aspergillosis. Annual Review of Medicine, Vol. 50:

303-316 (Volume publication date February 1999)

(doi:10.1146/annurev.med.50.1.303), Pulmonary and Critical Care

Unit, Partner\'s Asthma Center, Massachusetts General Hospital and

Harvard Medical School, Boston, Massachusetts 02114. Retrieved on

August 10, 2005 from

http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.med.50.1.

303?journalCode=med

11. , G.M., Perfect, J.R. (October 31, 2003). Fungal Sinusitis.

Uptodate Patient Information. Retrieved on August 10, 2005, from

http://patients.uptodate.com/topic.asp?file=fung_inf/5646

12. Lacey, J., Dutkiewicz J., (March 1994). Bioaerosols and

Occupational Lung Disease. Institute of Arable Crops Research,

Rothamsted Experimental Station. Journal of Aerosol Science, Vol.

25. No. 8, Page 1371

13. Jarvis, B. (1995). Mycotoxins in the Air: Keep Your Buildings

Dry or the Bogeyman Will Get You. International Conference: Fungi

and Bacteria in Indoor Environments, Health Effects, Detection and

Remediation. Eckardt Johanning, Chin S. Yang, editors. Saratoga

Springs, NY

14. Ecohealth Environmental Change and Our Society: Glossary.

Retrieved July 28, 2005 at http://www.ecohealth101.org/glossary.html

15. The American Heritage® Dictionary of the English Language,

Fourth Edition Copyright © 2000 Published by Houghton Mifflin

Company.

16. Retrieved on July 28, 2005 at

http://www.emc.maricopa.edu/faculty/farabee/BIOBK/BiobookglossE. html

17. Retrieved on July 28, 2005 at

http://www.emc.maricopa.edu/faculty/farabee/BIOBK/BiobookglossPQ.

html

18. Retrieved on July 28, 2005 at

http://www.enchantedlearning.com/subjects/butterfly/glossary/indexed.

shtml

19. Margulis, L., Sagan, D. (1996). Microbial Microcosm. Retrieved

July 28, 2005 at http://www.context.org/ICLIB/IC34/Margulis.htm

20. Fox S.W. (May 12, 1997). My Scientific Discussion of Evolution

for the Pope and His Scientists. Retrieved July 28, 2005 at

file://C:\\DOCUME~1\\DOUGLA~1\\LOCALS~1\\Temp\\9BY8TCYV.htm

NOTE: Your comments concerning this article are most welcome.

R. Haney

EnviroHealth Research & Consulting, Inc.

E-mail: _Haney52@...

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