Re: Serious Breach of Ethics within the AIHA

[Guest guest]

Dear IEQuality Board Members,

To those of you who understand what I am saying and understand the significance of the need to go back and retract "endorsments" of junk science, I would like to thank all of you who have sent me off board posts regarding this matter. Is there any one of you willing to post your thoughts of this on board?

Sharon

[Guest guest]

Hey Tony,

You weren't one of the " gentlemen " to which my post below was

directed.

I remember when Coreen Robbins' 2000 paper appeared in AOEH, and I

also recall reading it with considerable interest. (It and the 2002

ACOEM " Evidence-Based Statement " are intertwined of course, as you

know.)

For example, at the time I found it troubling that Robbins' paper

described only three groups of adverse health effects associated

with fungi: allergic, infectious and toxic. Robbins, et al,

neglected to describe irritant effects, which are generally

trivialized, but which are strongly associated with inflammation.

Inflammation, in turn, is poorly understood and understudied, but

can have a profound effect on one's health status.

The journal EHP featured a fascinating article on inflammation that

describes the limits of our understanding in the December 2005 issue

(Environmental Health Perspectives, v113, n12, p A816-A821).

As a peer reviewer myself, I concur that the process helps weed out

the really bad and the mediocre. All I'm suggesting is that we as a

community need to (1) consider the source, and (2) critically

consider all that we read, whether it's peer-reviewed or not.

As scientists with the appropriate academic background and years of

experience in this line of work, it is the ability to do so that

sets some on this list - such as you - apart. For those who were

hydrogeologists, asbestos pump-jockeys, or other minimally-related

environmental specialists yesterday, and " certified IAQ experts "

today, that task may simply be out of reach.

Regards,

Wane

> >

> > > Sharon, your increasingly strident conspiracy theories are

> growing

> > > tiresome. The ACOEM paper was an excellent summary of existing

> > > knowledge at the time of publishing, and most of it remains

> entirely

> > > appropriate now. Their statement " Current scientific evidence

> does not

> > > support the proposition that human health has been adversely

> affected

> > > by inhaled mycotoxins " was indeed based on scant evidence,

> because

> > > *very little evidence was available, period*. I assume if that

> > > scientifically verifiable evidence becomes available, their

> position

> > > would change.

> <snip>

> > > Now, in the interest of carrying this debate forward to today

> rather

> > > than sniping at a 4 year old document, have you seen the August

> 2006

> > > issue of the Environmental Reporter, specifically the article

> > > * " **Mycotoxins: Continuing Review of the Literature " ?*

> > >

> > > An excerpt:

> > >

> > > So far, the animal studies reported in the literature verify

> that

> > > mycotoxins produced by some fungi that grow in indoor

> environments can

> > > produce changes in some physiological parameters in the

animals.

> Thus,

> > > very high doses of appropriate strains of /Stachybotrys

> chartarum/

> > > spores produce indicators of lung damage (Rosenblum et al.,

> 2006) and

> > > nasal irritation (Islam et al., 2006). The models that

> extrapolate

> > > these doses to human health effects indicate that the no effect

> level

> > > is much higher than any exposures that have been recorded in

> indoor

> > > environments. (Kelman et al., 2004) This review suggests that

> levels

> > > of /Stachybotrys/ spores, provided that they contain sufficient

> > > quantities of Satratoxin G and H could result in irritation if

> present

> > > in concentrations in excess of 2x10^-5 /m^3 (20,000

> spores/m^3 ). This

> > > concentration has not been reported for

> undisturbed /Stachybotrys/

> > > spores, but could be experienced by professional remediators.

> > >

> > > Comments, anyone?

> > >

> > >

> > > D. Carlson, CIAQC, CMRS

> > >

>

>

[Guest guest]

Carl:

thank you for your note of encouragement.

thanks as well for your off-list email message. I'm sure we'll be

talking more in the near future.

for purposes of this list, a couple of clarifications are in order:

1. perhaps you misconstrue my intent. my message was not so much in

support of Ms. Kramer's particular assertions as it was a suggestion

that all of us need to do our homework. even in the peer-reviewed

literature, appearances can be deceiving.

2. as I recall, the scientific method does not " begin with a

judgement [sic] " -- indeed, it must not begin there. rather, it

starts with an observation, which generates an hypothesis that is

challenged by experimentation, providing empirical data that

culminates in a conclusion (if all goes well). the conclusion in

turn serves to validate or perhaps modify the hypothesis.

the rest I haven't time to comment upon right now. let's do talk.

thanks again.

Wane

>

> Wane,

>

> You and I have our differences, but I will clearly and

emphatically

> state that your support of Sharon Kramer's assertions (below) is a

> commonality, not a difference.

>

> Although I am not qualified to critique the validity of scientific

> research and of the subsequent published studies, as you and

others

> are, I can say emphatically (based on my education, etc) that

proper

> procedure, foundation and logic, while necessary, are not

sufficient.

>

> Scientific inquiry always begins with a judgement, the conclusions

> can be affected by judgement, and application of the findings is

of

> course always based on judgement; all according to appropriate

> procedure and sometimes supported by law. As you clearly assert,

> common sense is also required.

>

> The process of a scientific experiment (as with any system) cannot

be

> self-validating. It must also stand on other principles such as

> independant verification.

>

> Remember the excitement of the claims of cold fusion, until they

> couldn't be independantly verified? Or the medical assertion that

> infants can't feel the pain of surgery, until someone investigated

> and could find only a single study in Britain from the 1920's?

When a

> claim tries to stand only on it's own and is then generally

accepted

> prior to independant verification, it can lead to the type of

> distortion and misuse that Sharon is asserting.

>

> Which begs the question: Has the study and the paper in question

been

> challanged by repeating the experiment? Independantly or otherwise?

>

> If not, then why is it being so wholeheartedly accepted and

honored

> as established science when the same authorities demand that

contrary

> studies await a mature body of independant verfication? (E.g. the

> more recent one indicating inflamation and brain cell death in

> murines from inhaled mycotoxins). If the ACOEM position cannot be

> independantly verified we may be at risk of supporting the " cold

> fusion " of our profession.

>

> Wane, I'm not qualified to determine where the truth lies in this

> matter, but I applaud your courage in taking the lead in this

> unpopular stand and for again demonstrating your passion for

finding

> the truth.

>

> Carl Grimes

> Healthy Habitats LLC

>

> -----

> > Gentlemen:

> >

> > I can't help but agree that Ms. Kramer sometimes gets a bit

carried

> > away. Her passion is driven by personal experience, as I'm sure

you

> > realize.

> >

> > But have you actually studied the ACOEM document? I don't mean

[Guest guest]

Group,

I am discussing sciences, research science coupled with the science of marketing. I am discussing how a paper, based on scant scientific foundation and not supported by any other study was unduly parlayed in stature and validity thru the use and abuse of journals and medical associations. What this has caused is an incorrect perception among the IAQ community, the medical community, the legal community and the public in general as to the validity of the seriousness of illnesses from excessive mold/mycotoxin exposure. The mantra of "not plausible" has no legitimate scientific foundation.

If you want to discuss it in scientific terms, then:

Let's look at the scientific foundation that has become the national medical understanding of the implausibility of illnesses caused by mycotoxin inhalation indoors.

Let look at how this position has been marketed to the IAQ communities, the medical communities and the courts.

Let's look in detail at the article published by the Journal of Applied Occupational and Environmental Health back in 2000. This is the one that is the SOLE foundation for the ACOEM mold statement of:

"Levels of exposure in the indoor environment, dose-response data in animals, and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations."

I see it as a guise of being presented as a review piece, when in reality, the conclusions of the paper are not founded upon anything being reviewed. The key conclusion (the one that whispers on thru medical journals) is only founded upon a rodent study with math extrapolations applied to deduce all human illness is not plausible.

The paper was authored by GlobalTox and ICTM. It is attached below in pdf form (for ease of reading) and text form (for ease of cutting and pasting)

You may view it differently, but if you all want to discuss the science in detail, I am more than willing to cooperate with your wishes.

The way I normally read these types of docs is to go down them line by line, word by word - just as I would a real estate contract.

I color code them as I go. Blue = agree, Green = I have some questions, Red = I know this is wrong.

And just like a real estate contract, 99.5% is accurate (Blue). .49 % need more clarification (Green) and .01% is blatantly incorrect (Red). The .01% is typically the critical aspect to the heart of the contract. The answer to why .01% is wrong (Red), can be found in the .49% of needs clarification (Green) .

To save time with this doc, let me just ask you all two questions:

1. Where within the attached document is the information that would support the ACOEM statement of "Levels of exposure in the indoor environment, dose-response data in animals, and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations." ?

2. What information within the document attached below substantiates the foundation of the document?

In other words:

Where is the scientific premise for the above ACOEM statement of "not plausible" within this document?

Sharon

Applied Occupational and Environmental Hygiene

Volume 15(10): 773 –784, 2000

Copyright °c2000 Applied Industrial Hygiene

1047-322X/00 $12.00 + .00

Health Effects of Mycotoxins in Indoor Air:

A Critical Review

Coreen A. Robbins,1 Lonie J. Swenson,1 Mark L. Nealley,2 E. Gots,2

and Bruce J. Kelman1

1GlobalTox, Inc.; 2International Center for Toxicology and Medicine, Inc.

Industrial hygienists (IHs) are called upon to investigate

exposures to mold in indoor environments, both residential

and commercial. Because exposure standards for molds or

mycotoxins do not exist, it is important for the industrial

hygienist to have a broad knowledge of the potential for ex

posure and health effects associated with mold in the indoor

environment.

This review focuses on the toxic effects of molds associated

with the production of mycotoxins, and the putative associ

ation between health effects due to mycotoxin exposure in

the indoor environment. This article contains background

information on molds and mycotoxins, and a brief summary

and review of animal exposure studies, case reports, and epi

demiological studies from the primary literature concern

ing inhalation of mycotoxins or potentially toxin-producing

molds. The relevance of the .ndings in the reviewed articles

to exposures to mold in indoor, non-agricultural environ

ments is discussed.

Although evidence was found of a relationship between

high levels of inhalation exposure or direct contact to mycoto

xin-containing molds or mycotoxins, and demonstrable ef

fects in animals and health effects in humans, the current lit

erature does not provide compelling evidence that exposure

at levels expected in most mold-contaminated indoor envi

ronments is likely to result in measurable health effects. Even

though there is general agreement that active mold growth

in indoor environments is unsanitary and must be corrected,

the point at which mold contamination becomes a threat to

health is unknown. Research and systematic .eld investiga

tion are needed to provide an understanding of the health im

plications of mycotoxin exposures in indoor environments.

Keywords Mold, Indoor Air, Mycotoxins

With increased media attention and public awareness about

mold in the indoor environment, both residential and commer

cial,(1¡5) industrial hygienists (IHs) are more frequently called

upon to investigate exposures to mold in these situations. The

IH is often asked to determine the presence or extent of mold

growth and to make recommendations about its remediation.

Often when these recommendations are made, there is an im

plicit assumption that signi.cant health effects may occur if the

mold is not removed. Headlines about “toxic molds” have el

evated the level of concern and response for certain species of

mold which are known to produce mycotoxins. In particular,

Stachybotrys chartarum (S. chartarum) has been the focus of

much attention.(6) Because exposure standards for molds or my

cotoxins do not exist, it is important for the IH to have a broad

knowledge of the potential for exposure and health effects asso

ciated with mold in indoor environments.

Large gaps remain in the knowledge base needed to con

duct quantitative risk assessments for inhaled mycotoxins.(7)

Although a great body of literature exists concerning the in

gestion of mycotoxins by animals, there are few such studies

of mycotoxin inhalation.(8) In addition, results of these inhala

tion toxicity studies are conicting, with some reporting greater

potency of mycotoxins via inhalation compared to other expo

sure routes,(9,10) and with others reporting different results.(11,12)

Case reports and studies of agricultural workers indicate that

certain health effects occur from inhalation of molds that are

due at least in part to mycotoxins;(13¡17) however, these expo

sures are orders of magnitude greater than the typical cases in

which mold is found growing in the indoor environment.(17)

There are several case reports and epidemiological articles in

which toxin-producing molds have been reported to be associ

ated with health effects in indoor environments.(18¡21) Although

aatoxin B1 (AFB1) is a well-studied mycotoxin, exposures to

AFB1-containing dusts have not been reported in indoor envi

ronments, and it is not known whether exposure to AFB1 poses

a health risk in indoor environments.

This review focuses on the toxic effects of molds associated

with the production of mycotoxins, and the putative association

between health effects due to mycotoxin exposure in the in

door environment. The “indoor environment” here includes the

C. A. ROBBINS ET AL.

interiors of of.ces, commercial buildings, and residences. This

articlecontains background information on moldsand mycotox

ins, and a brief summary and review of selected animal exposure

studies, case reports, and epidemiological articles from the pri

mary literature which concern inhalation of mycotoxins or po

tentially toxin-producing molds.Therelevanceof the .ndingsin

thesearticlestoexposurestomold intheindoor,non-agricultural

environments is discussed.

BACKGROUND

Molds are organisms in the kingdom of fungi (Myceteae).(22)

Unlike bacteria and algae, the cells of fungi have a nuclear en

velope and thus are eukaryotes. Fungi include molds, rusts,

smuts, and mushrooms, and some classi.cations include the

slime molds. Lichens are organisms that consist of a symbiotic

combination of a mold and algae.(22)

Fungi have no chlorophyll, and thus they are obligate or fac

ultative saprobes or parasites.(22) They reproduce typically by

spores, via sexual or asexual mechanisms. Spores are small,

propagating structures that can produce a new individual. Asex

ual spores are called conidia. With the exception of some slime

mold life stages, fungi have cell walls, and these almost always

contain chitin.

The classi.cation of fungi is based upon phylogeny, repro

ductive strategies, life cycle, cell structure, and morphology.

Their classi.cation is complex, because of the large number and

variety of organisms; indeed there is much disagreements about

the classi.cation among mycologists.(22) Three major divisions

of fungi are:(22)

² Gymnomycota: cellular and slime molds

² Mastigomycota: the “lower fungi” water molds

² Amastigomycota: the “true fungi” yeasts, molds, mildews,

cup fungi, rusts, smuts, bracket fungi, puffballs, and

mushrooms.

Classes in the division of Amastigomycota are of interest here

because all of the common toxin-producing molds are members,

and molds from these classes are commonly found in indoor en

vironments. The classes are the Zygomycetes, Ascomycetes,

Basidiomycetes, and Deuteromycetes. The .rst three classes

are grouped on the basis of different spore-producing struc

tures. The Deuteromycete class is a catch-all group that con

tains fungi for which the sexual state is unknown, hence the

name, “fungi imperfecti.” Once the sexual stage is known, the

fungi are categorized into one of the .rst three classes. Thus, a

single fungus may be classi.ed as a Deuteromycete and as an

Ascomycete. In fact, most Deuteromycete fungi are, or would

be, Ascomycete fungi, and include such familiar geni as Al

ternaria, Aspergillus, Stachybotrys, Penicillium, Cryptococcus,

Histoplasma, and Candida.(22) As a further complication, a sin

gle mold species may have more than one name. “Western

taxonomists”(23) consider Stachybotrys atra, S. alternans, and

S. chartarum to be the same organism.(24) This grouping will be

assumed here, with the three types represented by S. chartarum

because this name is used in the more recent articles reviewed

that include a reference to Stachybotrys. For a detailed discus

sion of the classes of molds in indoor air, see Burge, 1999.(25)

Health Effects of Molds in Indoor Air

Possible health effects associated with fungi generally fall

into one of three groups:

1. Allergic: sensitization and immune responses such as al

lergic rhinitis (hay fever), asthma, or hypersensitivity pne

umonitis.(26)

2. Infectious: growth of the fungus in or on the body, as with

aspergillosis or histoplasmosis.(27)

3. Toxic: disruption of cellular function and interaction with

DNA, as occurs with toxigenic effects, including aatoxin

induced cancer.(28)

Although the fungi clearly can effect human health in a va

riety of ways, discussion of the many diseases associated with

the fungi is beyond the scope of this review. This article focuses

on the toxic effects of molds associated with the production

of mycotoxins, and the putative association between health ef

fects due to mycotoxin exposure in the indoor environment. The

health effects discussed will be limited to those described in the

articles, which report associations between mycotoxin exposure

and health effects. The term mycotoxin is very general, and

here is de.ned as a mold-produced secondary metabolite that

is injurious to vertebrates upon ingestion, inhalation, or dermal

contact.(28¡30) Although the toxins from poisonous mushrooms

may be included in the general de.nition of mycotoxins, they

will not be considered here.

Mycotoxins

Mycotoxins exert their effect on organisms in many ways, in

cluding interference with cellular respiration, interference with

carbohydrate and lipid metabolism, and direct binding with DNA

and RNA.(31) In general, mycotoxinsarelarge, complex molecu

les, and thus are not volatile.(32) Mycotoxins have been shown

to occur in mycelia, spores, and the matrix in which molds

(33,34)

grow.

Mycotoxins consist of many diversecompoundsproduced by

a wide variety of molds.(31) A single mold species may produce

several different mycotoxins; and conversely, different mold

geni may produce the same mycotoxin.(28,31) For example, it is

known that several trichothecene mycotoxins are produced by S.

chartarum, and that the mycotoxin ochratoxin A is produced by

both Aspergillus and Penicillium species.(28) Mycotoxin produc

tion for a given species is highly dependent on growth conditions,

such as nutrient availability, temperature, and humidity.(29,35,36)

There are many molds that produce mycotoxins, and discussion

of their health effects on animals and humans are the subject of

numerous articles(28,37¡42) and texts(31,36,43¡46) and a complete

treatise or review of these is beyond the scope of this article.

HEALTH EFFECTS OF MYCOTOXINS IN INDOOR AIR: A CRITICAL REVIEW

Examples follow of just a few mycotoxins, the molds that pro

duce them, and their role in the history of human disease. An

interesting popular press historical account of the impact of the

kingdom fungi on human affairs was recently published.(47)

Aspergillus

Aatoxins are classic mycotoxins produced by Aspergillus

avus, A. niger, and A. parasiticus.(28) More than 13 aatoxin

compounds have been identi.ed, the most potent of which is

AFB1.(48) Not all strains of A. avus produce aatoxins, and

they are not produced until exponential growth of the colony

occurs.(48) Aspergillus avus grows best at 77 to 86±F, and at 80

to 85 percent humidity, but can produce mycotoxins from 54 to

106±F at a relative humidity (RH) of 99 percent.(48)

Foods that can be contaminated include peanuts, pecans,

peas, bread, cheese, rice, corn, barley, grain, sorghum, wheat,

and cotton seed. Aatoxins are also found in milk, eggs, and

livers of animals that have consumed contaminated feed.(36)

Aatoxins by the oral route can be teratogenic or carcino

genic in animals, with rats and trout being more sensitive than

mice and monkeys.(48) Animal studies indicate that inhaled aa

toxins are immunosuppressive(49) and may also be carcinogenic

by the inhalation route in animals.(50,51) The disease outbreak

that caused aatoxin to be identi.ed in the 1960s was “Turkey

X disease.”(28) Hundreds of thousands of turkeys died after eat

ing aatoxin-containing peanut meal. Ingestion of aatoxin has

been implicated in human liver cancer, with hepatitis B as a co

risk factor.(52) Aatoxins have also been indirectly associated

with liver cirrhosis and Reye’s syndrome.(36) Case reports of

inhalation exposure to laboratory workers have associated lung

disease and cancer with aatoxin exposure, and epidemiologi

cal studies suggest higher cancer rates in workers involved in

peanut processing.(48)

Fusarium, Stachybotrys chartarum, Memnoniella echinata,

and others

Trichothecenes have been isolated from cultures of molds in

cludingthoselistedabove.(28,53) Whiletheseorganismsarecapa

ble of producing other mycotoxins, the trichothecenes are highly

toxic, intensively studied, and include over 100 isolated com

pounds including: T-2 toxin, diacetoxyscirpenol (DAS), satra

toxins (satratoxins G and H have been extracted from straw bed

ding in animal disease outbreaks(54)), verrucarol, verrucarins,

trichoverrins, roridin E, and vomitoxin, to name a few.(31) The

main mechanism of action of the trichothecenes appears to be in

hibition of proteinsynthesis.(28) Symptomsof trichothecenepoi

soning include skin irritation, vomiting, anorexia, diarrhea, hem

orrhage, and convulsions, and, in some cases, death results.(28)

Fusarium sporotrichioides is thought to be the mold species

responsible for alimentary toxic aleukia (ATA).(36) The probable

mycotoxin was T-2 toxin. It is thought that the deaths of hun

dreds of thousands of people in the U.S.S.R. at the end of WWII

were caused by ingestion of grain left under winter snow.(46)

People were starving and ate the over-wintered cereal grains.

Ten percent of the population was affected; early symptoms of

gastroenteritis were followed a few months later by progres

sive bone marrow damage, leukopenia, pancytopenia, and death

due to hemorrhage. The outbreaks were originally thought to be

diphtheria or cholera, which have some similar symptoms.(37)

Stachybotrytoxicosis was .rst reported in 1931 in Eastern

Europe and Russia as a fatal hemorrhage disease of horses,

with farm workers and those using straw for bedding report

ing symptoms as well.(36,55) The moldy straw, which contained

S. chartarum and other fungi,(56) killed many horses and other

farm animals and caused dermatitis, bloody rhinitis, cough, and

severe respiratory tract irritation in exposed people.(39) Occu

pational stachybotrytoxicosis has been reported in farm work

ers, workers in cottonseed oil plants and grain elevators, and

workers at facilities for reprocessing moldy grain, processing

malt grain, textile mills using plant .bers, and binder twine

factories.(36) Symptoms included chest and upper respiratory

symptoms, fever, dermatitis, and leukopenia (in some cases).

Recently, associations have been reported for the presence of

Stachybotrys inindoor environmentswithpulmonary hemoside

rosis and hemorrhage in infants,20 and with other wide-ranging

health effects in adults.(14,21)

Penicillium

Penicillium produces a number of mycotoxins.(33) More than

a dozen species of Penicillium (and some species of Aspergillus)

produce ochratoxin A.(28) It can be teratogenic and has been

shown to cause kidney damage in experimental animals.(28) It

has been implicated in Balkan nephropathy, a chronic, fatal,

kidney disease of humans which occurs in the Balkan valley

(Bulgaria, Romania, and Yugoslavia).(28) It is hypothesized that

this disease is due to chronic exposures by ingestion of contam

inated foods.(28)

Alternaria

Alternaria is a ubiquitous mold.(22) Species of Alternaria

are known to produce approximately 125 secondary metabo

lites, one-quarter of which are toxic in animals or cell culture

systems.(31) Alternaria is an example of how large numbers of

mycotoxins may be produced by a single, common mold that is

generally considered benign. Although Alternaria has a role in

allergic disease, whether exposure to its mycotoxins has a sig

ni.cant role in human disease is not known. This also holds for

other molds and mycotoxins, because studies of the relationship

between inhalation exposure to mycotoxins of different mold

species and health effects are few.

Animal Inhalation Studies

Animal studies of inhalation of mycotoxin and mold spores

are included in this review because they are used as models

of human exposure and response, and they provide a mech

anism for comparing the toxicity of different compounds. A

great deal of literature existsabout mycotoxins infeed and food

stuffs. Because the main route of human and animal exposure

C. A. ROBBINS ET AL.

to mycotoxins is by ingestion, the vast majority of animal re

search on toxicity has been done with ingestion studies.(40) There

are few studies that examine the inhalation of mycotoxins or

toxin-producing molds.(8,57) and reportsfromsomedo not quan

tify exposure.(58¡60) Studies published by Creasia et al. (1987,

1990)(9,10) have been cited in support of the biological plausibil

ity of mycotoxin-related illness from indoor exposure(8,21,61¡63)

because their results indicate that mycotoxins are more toxic

when exposure occurs by inhalation rather than ingestion.

Studies have been conducted on the acute toxicity of T-2

toxin, a potent trichothecene, because of the potential for its use

in chemical warfare. In 1986, Marrs reported that for guinea

pigs, the T-2 toxin LD50 for aerosol exposure (4 mg/kg) was

about twice the LD50 for subcutaneous exposure (2 mg/kg), but

Marrs also reported that effects of acute inhalation and sub

cutaneous exposure to T2 toxin were quantitatively and qual

itatively similar.(11) In contrast, Creasia found later for guinea

pigs, that the T-2 toxin LD50 for aerosol exposure (0.4 mg/kg)

was one-third of the LD50 for intraperitoneal injections (LD50 =

1.2 mg/kg).(10) These conicting results may be due to the dura

tion of inhalation exposure for a given total dose. Marrs exposed

the guinea pigs for periods spanning 15 to 75 minutes, and noted

a decrease in toxicity when dose was delivered over the longer

time interval; Creasia exposed the guinea pigs for either 10 or

30 minutes. In the latter study, similarly exposed rats were even

more sensitive to inhalation of T-2 toxin, which was 20 times

more toxic than by the intraperitoneal route. In another study

by Creasia, the sensitivity of mice to inhaled T-2 toxin was sim

ilar to rats; and they too were more sensitive to exposures via

inhalation (LD50 = 0.94 mg/kg) than exposures via the dermal

(LD50 > 10 mg/kg) or injection (LD50 = 4.5 mg/kg) route.(9) In

a study of swine, Pang projected that the LD50 would be higher

by the inhalation route (>8 mg/kg, sub-lethal doses used only)

compared to intraveneous exposure (1.2 mg/kg).(12) Pang sug

gested that this apparent conict with Creasia’s results may be

due to differing susceptibilities of the animals, as well as dif

fering time intervals used for the aerosol exposure (pigs were

exposed for 45 to 61 minutes).

Aatoxins have been the subject of extensive research be

cause they are potent liver toxins and are carcinogenic by inges

tion exposure. They are found in a wide variety of crops used for

human and animal consumption. Studies of acute inhalation ex

posure (· 120 min) to puri.ed AFB1 in animals have shown the

formation of DNA adducts in the rat liver,(50) and suppression

of pulmonary and immune function in rats and mice.(49) Mice

exposed chronically (daily for one year) to aerosolized AFB1

had a 38 percent increase incidence of lymphatic leukemia.(51)

Even though these studies are limited, some general trends

are present. The results indicate that rats are more sensitive to

inhaled T-2 toxin, followed by mice and then swine. Guinea

pigs appear somewhere between the most sensitive (rats) and

least sensitive (swine) animals. It also appears that the toxicity

resulting from inhalation exposure is dependent on the time in

terval of exposure for a given total dose, with greater toxicity

for shorter exposures. This may be the result of more effective

clearance and or metabolism of T-2 toxin by the lung at the

lower airborne concentrations associated with longer exposure

intervals. Exposures did not result in pulmonary edema or gross

histopathological changes in the lung; although the latter effects

were seen in other organ systems.(9¡12) It has been suggested

that toxic effects are not seen in the lung because the toxin or

toxin and vehicle is rapidly absorbed by the lung and quickly

transported to other organs.(12)

Inhalation studies of mycotoxins in animals were designed to

measure acute effects at high exposure levels. These experimen

talexposuresand concomitanteffectsdo notrepresentexposures

to mycotoxins at chronic, low exposure levels from molds in in

door settings. However, the data show decreasing toxicity with

longer exposure for a given total dose, indicating that physio

logical mechanisms can mitigate the effect of exposure at low

levels. These results suggest the existence of a threshold for the

effects of mycotoxins.

These kinds of studies are useful in determining the range

of response for different animals for a particular toxin at differ

ent doses and exposure time intervals. However, they are only

indirectly useful in examining the issue of exposure to myco

toxins from inhalation of mold spores. Unlike a pure mycotoxin

aerosol, a mold spore is a complex assortment of chemicals that

may act as synergists or inhibitors in producing toxic effects. In

addition, the aerodynamic properties of mold spores (particles)

are likely to be different from an arti.cially generated myco

toxin aerosol. This will most likely cause different deposition

patterns in the respiratory tree, which will affect the amount and

location of the delivered dose and subsequent toxicity.(64)

In an effort to better model the effect of mycotoxins from

inhalation of spores, Nikulin injected mice intranasally with S.

chartarum spores.(57) Mice were injected once with 106 spores

in phosphate-buffere d saline (PBS) of one of two strains of S.

chartarum., s. 72, a highly toxic strain, or s. 29, a slightly toxic

strain (toxicity determined by cytotoxicity tests). Controls re

ceived PBS only. The s. 72 strain contained satratoxins. All mice

receiving spores developed lung inammation; however, there

was a signi.cant difference in the inammation changes between

the two strains. The changes in the s. 29-exposed mice were

signi.cantly milder than that produced by s. 72, and necrotic

changes were seen only in the s. 72-exposed animals.

In another experiment, mice were injected intranasally with

103 to106 sporesoflesstoxic (s.29)andmoretoxic (s.72)strains

of S. chartarum.(65) This treatment was repeated twice weekly

for three weeks. A relative increase in pulmonary inammation

(from “¡ ” for no inammation, to “+++” for extensive inam

mation) was reported as the intranasal dose was increased from

fewer spores (103) of the less-toxic strain, to greater numbers

(105) of spores of either strain. Severity of inammatory lung

changes was the same in mice instilled with 103 spores of s. 72

and 105 spores of s. 29. Inammation was not detected in an

imals receiving 103 of s. 29 spores. Hematological parameters

were generally similar between exposed and control animals;

HEALTH EFFECTS OF MYCOTOXINS IN INDOOR AIR: A CRITICAL REVIEW

however, unlike the studies with puri.ed mycotoxins, histolog

ical changes were seen only in the lungs of exposed animals.

These results highlight the importance of the delivery route

and vehicle of mycotoxins in inhalation exposure studies. The

signi.cance and applicability of the results to actual inhala

tion exposures is limited because of the small number of an

imals used, subjective grading of histological response, non-

physiological exposure technique (injection), and method of

spore quanti.cation in the dose. The report further highlights

that intranasal inoculation of large numbers of spores is un

likely to model the exposure of humans in even very moldy

environments.(57)

CASE REPORTS

Although case reports cannot be used to determine causation

for an environmental agent, they can sometimes be used to iden

tify factors that need further investigation. A number of case

reports are cited as showing links between exposure to inhala

tion of mold and mycotoxin-induced illness inhumans. Because

there are only a few reports of possible mycotoxin exposures in

indoor settings, several case reports from agricultural exposures

are included in this review. Although the exposure levels were

high and occurred in agricultural settings, data from these studies

may be relevant to human exposures in indoor environments.

In a review of stachybotrytoxicosis, Forgacs compiled ear

lier information of human exposure to Stachybotrys that had

been reported in the Soviet Union during the 1940s.(55) Most

of the persons affected had handled contaminated animal feed,

but some became ill after using contaminated straw for fuel

or mattress stuf.ng. Some of the scientists investigating ani

mal outbreaks also developed the toxicosis from contact with

straw that was naturally or arti.cially infected with Stachybotrys

alternans.(55,66) Straw contaminated with other molds did not

produce the toxicosis.(66) It was thought that exposure to tox

ins occurred via inhalation and dermal contact.(55) Symptoms

included dermatitis, primarily on the scrotum and in the axil

lary region, and, less often, on the hands and other body areas.

In addition to dermatitis, other symptoms reported were bloody

nose, cough, and complaints of throat pain, burning nasal pas

sages, and congestion in the chest. Some patients had elevated

body temperature, and some developed leukocytosis followed

by leukopenia. Patients recovered rapidly after exposure cessa

tion; however, upon subsequent exposure, the diseased recurred

with more serious sequelae.

In the often-cited 1986 report by Croft, a family reported cold

and u symptoms, sore throats, diarrhea, headaches, fatigue,

dermatitis, hair loss, and general malaise.(14) The self-reported

complaints were thought to be associated with massive growth

of mold in the HVAC system and on the ceiling of one room.

Although the air sample was not cultured, S. chartarum was

identi.ed from examination of spores, and trichothecenes were

extracted from materials taken from the house. There were no ob

jectively measured disease outcomes, and other possible causes

for the reported symptoms were not ruled out. Reported symp

toms ceased after the mold was removed. Although the symp

toms were attributed to S. chartarum, other molds or bioaerosols

were not ruled out as possible causes or contributors to symp

toms. The presence of other molds is likely because the water

in.ltration and mold growth had been occurring for four or .ve

years.

In 1987, Brinton reported an isolated epidemic of febrile ill

ness after a college fraternity party.(13) Moldy straw was used

on the oor in an enclosed room where the party was held. The

airborne dust was so thick that it obscured vision across the

room. Fifty-.ve of 67 partygoers developed fever, chills, cough,

shortness of breath, and chest and back pain after attending the

party. The risk for illness increased with increasing time spent

at the party. Serological tests did not implicate allergic or viral

causes. All of the partygoers recovered completely.

DiPaolo (1994) found ochratoxins in Aspergillus ochraceous

contaminated wheat that was suspected of causing acute respi

ratory symptoms and intestinal disturbances in a farmer and his

wife who had worked for eight hours sieving the grain.(15) The

woman also subsequently suffered acute renal failure possibly

due to the inhalation of mycotoxins from contaminated grain

dust. The couple recovered completely. The wheat was visibly

moldy and covered with dust that was described as acidic and

irritating. Several experimental animals subjected to air passing

through the contaminated grain died or showed organ damage.

The amount of ochratoxin on the grain or in the air owing

through it was not determined and control animals were not

used in this experiment.

Emanuel has followed dairy farmers who are thought to have

inhaled “massive amount of fungi” from handling moldy hay

or corn silage.(16,67) Typical symptoms after exposure include

chills, fever, dry cough, and inamed mucous membranes, with

some individuals later developing in.ltrates and interstitial dis

ease in the lungs. The authors ruled out allergies as the cause be

cause the farmers did not respond to antigen challenge and were

asymptomatic at lower re-exposures. Although .ve species of

mold were cultured from one case lung biopsy specimen, mea

surements of mycotoxins were not reported. Of the .ve fungi,

one was a Fusarium and another was from the genus Penicillium.

No bacteria were cultured. Lung histology showed a multi-focal

acute process in the terminal bronchioles, alveoli, and interstitial

cells. Emanuel has suggested that the symptoms and signs were

caused by massive exposure to fungi and bacteria, and that my

cotoxin, endotoxin, or other constituents were the causal agents.

Measurements of airborne mold were made for a series of

cases of farmers with and without symptoms of febrile reac

tions to inhaled mold dust, referred to as organic dust toxic syn

drome (ODTS), and allergic alveolitis (AA).(17) Organic dust

toxic syndrome is also referred to as silo unloader’s disease and

pulmonary mycotoxicosis. It requires intense exposure to air

borne dust and results in inuenza-like symptoms with leuko

cytosis and fever but does not require prior sensitization. Anti

bodies do not develop, and respiratory symptoms may or may

C. A. ROBBINS ET AL.

not occur, and there are usually no radiographic changes. Al

lergic alveolitis, also called hypersensitivity pneumonitis (HP),

will not be discussed in detail because it is primarily an allergic

response.

Exposure was evaluated within two weeks of medical con

sultation for ODTS or AA. Samples were collected during nor

mal farming (background ) and during handling of materials

associated with the reported illness or causing maximal (or

worst case) exposure in reference farms. There were 16 cases of

ODTS and 17 reference farmers. The average concentration was

1.3 § 1.3 £ 1010 spores/m3, and 1.2 § 2.0 £ 108 spores/m3, for

ODTS cases, and comparison farmers, respectively. The ODTS

response was associated with extreme exposure occurring on a

single day. There was no correlation of disease with spore type,

and the results support the hypothesis that common cell wall

componentsof microorganisms causethe“toxic” symptomsand

stimulate immune reactions.

Exposure measurements were unavailable for all but the

last(17) of these case reports. For the remaining reports, exposures

are presumed to be extremely high, based upon descriptions

of the conditions associated with exposure. The measurements

from Malmberg’s report indicate that exposures associated with

acute effects are indeed very high, in the range of 1010 spores/

m3.(17) In all the case reports, symptoms were temporally related

to exposure, but in most cases the contribution of bacterial en

dotoxin was not evaluated. Because inhaled bacterial endotoxin

has been shown to affect lung function(68) and is also associated

with febrile respiratory illness(69) it may have had a role in some

of these cases.

As a whole, case reports show that clinically important health

effects occur after exposure to conditions associated with high

levels of bioaerosols. Historical reports indicate that direct con

tact with Stachybotrys-contaminated straw results in health ef

fects. It is unlikely, though not impossible, that these extreme

exposure conditions would occur due to surface mold growth in

the indoor working or home environment.(70) Exposure to air

borne molds from surface contamination is dependent on the

degree of colonization of substrates, how much it is disturbed,

and the effectiveness of ventilation,(71) and requires an exposure

pathway from the affected area to the occupants.

In two reports,(14,66) the outbreaks are reported to be associ

ated with Stachybotrys, but the remaining cases are not reported

in association with a particular mold species. The health effects

in these case reports may be associated with mycotoxins, endo

toxins, other bioaerosol constituents, or a combination of these

components, and the contribution of each component to cases of

clinical illness remains to be elucidated.(17) Another important

common .nding among these reports is that symptoms ended

upon removal from exposure, and did not re-occur when high-

level exposures were avoided.

EPIDEMIOLOGICAL INVESTIGATIONS

There are few epidemiological investigations of inhaled my

cotoxins and disease in indoor air settings.(6,18,33,72) Although

some purport to show an association between inhaled myco

toxins and health effects,(18,21,63,73) some have been criticized as

nothaving adequatedatatosupportthisclaim.(6,74) Theevidence

for health effects in indoor air from mycotoxins associated with

S. chartarum was recently reviewed and includes the articles

summarized here.(6)

Johanning (1996) compared self-reported symptoms and

blood and immunology tests among 53 cases from a “prob

lem” building (a building with moisture problems and visible

mold growth) and 21 controls from a “non-complaint” building

(a building without known problems).(18) This study appears to

include results for 43 cases in this building reported previously

by Johanning et al., (1993)(73) thus, only the most recent article

is discussed here.(18) Cases were further divided into groups de

pending on whether they worked on the ground oor (n = 7), or

in the basement (n = 33), or sub-basement (n = 9) of the build

ing (four subjects without an assigned oor were excluded from

sub-group comparisons). The sub-basement had experienced

ooding, mold growth, and mold cleanup over several years

(unspeci.ed).Testsof theblood,serumchemistry, immunology/

antibodies, and lymphocyte enumeration and function were con

ducted for cases and controls. Results of air samples showed that

levels of airborne viable spores were similar on all levels of the

building, and these in turn were similar to outdoor concentra

tions. Elevated spore levels were found in the sub-basement, as

compared to the ground level and basement, when aggressive

sampling techniques were used. Several mycotoxins, including

satratoxin H, were found in bulk building material.

Results of 24 blood and immunological tests are reported

for comparisons between cases and controls, and among cases

according to building location (ground oor, basement, sub

basement). Results for a second comparison between controls

and cases, strati.ed by building location, are reported for white

blood cells(WBC),theproportionofCD3lymphocytes (CD3%),

and natural killer lymphocytes (NK). In thissecond comparison,

cases are strati.ed differently, as ground oor (n = 7), or base

ment plus sub-basement (n = 42) occupants.

In the .rst comparison, a signi.cant reduction was found

in the proportion of CD3 lymphocytes (a measure of the pro

portion of mature lymphocytes) for cases compared to controls

(cases = 73.5%, controls = 75.7%). No differences were found

for comparisons by work location. In the second comparison,

NK cells were higher for the new basement grouping (basement

plus sub-basement, p = 0.03); however, it is unclear whether

the difference is between cases and controls or between the two

case groups (ground oor, new basement). The .rst comparison

of total WBC did not show signi.cant differences. In the sec

ond comparison, the new basement group has the highest WBC

(p = 0.024); but again it is unclear whether the comparison

is being made between cases and controls or between the case

groups. There was no signi.cant difference between the number

of cases and controls with an immune response to S. chartarum,

Penicillium, or Apergillus antigens.

The CD3% levels and pokeweed mitogen (PWM) prolifera

tion scores were signi.cantly lower in cases reporting a history of

HEALTH EFFECTS OF MYCOTOXINS IN INDOOR AIR: A CRITICAL REVIEW

upper respiratory infections (p < 0.05). Signi.cant differences

were found for self-reports of lower respiratory, constitutional,

eye, and chronic fatigue symptoms. Among the building occu

pants, a larger proportion of sub-basement occupants reported

symptoms. The authors conclude that their results suggested an

immunecompetency dysfunction associatedwith prolonged and

intense toxigenic mold exposure.

The studied disease end points included reported symptoms

and reported excess of infections. Clinical evaluation or reviews

of records to con.rm the patient’s perceptions were not reported.

In a situation where a perceived hazard exists, the mold in this

case, symptoms may be over-reported and must be objectively

con.rmed before reported symptoms can be considered to re

liably represent the incidence of illness or disease. The level

of mold exposure was assigned based upon the presence and

amount of mold contamination reported. Whether exposure to

mycotoxins occurred in the studied population is not resolved,

and the authors state that there was no relationship between IgE

antibodies to S. chartarum and the reported symptoms. This

..nding does not support an exposure–disease relationship for S.

chartarum and reported symptoms and infections.

Toxins associated with S. chartarum are not known to affect

the CD3 population speci.cally; however, it is known that stress,

medications, and infection can all affect various component of

the T-cell population.(75) Because the cases reported more infec

tions, this could account for the change in the T-cell population.

Thus, whether the change in CD3% was caused by exposure to

mycotoxins cannot be determined from these data.

The meaning and importance of differences in the WBC is

uncertain. While the WBC was higher for the new basement

group (6.29 k/l l), the controls had higher counts (6.06 k/l l)

than ground oor cases (5.05 k/l l). More importantly, the re

ported values all fall within the normal range for adults.(76) This

same situation occurs with the NK counts, with the values for

new basement group (55.45) >controls (41.83) >ground oor

(23.59). This is inconsistent with an exposure–response effect

because exposures are expected to increase from controls <

ground oor < basement.

The major .nding of this study, a signi.cant association be

tween reported symptoms and building occupancy, may be due

to recall and reporting bias because conditions in the building

had been the subject of investigation and remediation prior to this

study. The clinical importance of the statistically different lab

oratory results is uncertain because the WBC values are within

the normal range for adults,(76) and these and the NK results do

not follow an exposure-related pattern. The basis for analyzing

the laboratory data after changing the case groups (combining

the basement and sub-basement cases) is not explained.

The issue of mycotoxins in indoor air received national media

attention after the reported association of S. chartarum in homes

with sick infants.(1) In 1994, eight cases of infant idiopathic

pulmonary hemorrhage and hemosiderosis (IPH) were reported

in Cleveland, Ohio.(77) Subsequently, the cases were investi

gated with the assistance of the Centers for Disease Control and

Prevention (CDC) and three separate articles were published that

examined the occurrence of IPH with environmental factors,(19)

and with the presence of mold and S. chartarum.(20,63) Risk fac

tors previously implicated in IPH include smoking, pesticide

exposure, and familial history of hemoptysis.(78¡80)

Testing for the presence of airborne Stachybotrys was con

ducted using a method based upon the method for collecting and

analyzing air samples for asbestos.(81) Samples were collected

on membrane .lters that were mounted on slides and cleared

with acetone vapor. Filters were examined with a phase-contrast

microscope, and S. chartarum was identi.ed by comparing the

image on the .lter to a photomicrograph of S. chartarum coni

dia. The CAMNEA method(82) was used to estimate viable air

borne mold concentration.(63) Samples were collected on Nucle

pore .lters, diluted and plated on growth media. Cultures were

examined and colonies were categorized as either Aspergillus,

Cladosporium, Penicillium, Stachybotrys, or other.(63) Surface

samples were collected from areas of suspected mold growth;

the scrapings were diluted and plated. Colonies were counted,

and results were expressed as CFU/g.(63)

The .rst report of thecase-control study included the original

eight cases, plus two more that appeared later, all compared to

30 controls.(20) Dearborn et al. (1997) reported that signi.cant

factors associated with IPH were male gender (p < 0.05) and liv

ing in a water-damaged home (OR = 16.3, CI = 2.6–in.nity).(20)

Other factors which were not statistically signi.cant included the

presence of smokers in the home (OR = 7.9, CI = 0.9 to 70.6),

and S. chartarum in the home (OR = 1.6, 1.0 to 30.8).(20) Tri

chothecenes were later recovered from cultures taken from case

and control homes.(53) In the report of environmental variables

(Montana et al., 1997), S. chartarum is not discussed; however,

the authors concluded that environmental risk factors may con

tribute to pulmonary hemorrhage.(19) In addition to the statis

tics reported by Dearborn, Montana reported that cases were

more likely to have a relative who coughed blood (OR = 33.14,

CI = 5.1–in.nity), and that casesand controls were signi.cantly

different in terms of gender and race (p < 0.05).(19) Nine of ten

cases were male and all were black, whereas half the controls

were male and 83 percent were black. Cases were also less likely

to have normal birth weight (p < 0.05), and none were breast-

fed (p = 0.04). Additional analyses of the case-control study

data were reported by Etzel et al. (1998).(63) The matched odds-

ratio for a change of 10 units in the mean concentration of S.

chartarum was 9.83 (CI = 1.08 to 3 £ 106). Higher concentra

tions of S. chartarum on surfaces in case homes (case homes,

20 £ 106 CFU/g, control homes, 7.0 £ 103 CFU/g) were also re

ported. Etzel concluded that infants with IPH were more likely

to live in homes with toxigenic S. chartarum and other fungi in

the indoor air.

The odds ratio for S. chartarum and IPH is not signi.cant

until the matched odds ratio analysis is used.(63) The utility of

the matched odds ratio analysis is uncertain, because the com

parison is made for units of 10 CFU/m3. It is dif.cult to in

terpret the outcome of a statistical test that is based upon the

C. A. ROBBINS ET AL.

comparisons of quantities that differ by less than the reported

limit of detection (LOD) of the method (70 CFU/m3).(81) The

interpretation of the study outcome is further complicated be

cause the duration, amount, and source of water damage was

not reported, and the extent of mold growth and the putative

exposure pathways are not described. Sampling results are not

likely to represent exposure conditions because the study was

conducted using “aggressive” techniques, and in many cases was

conducted months after the IPH was reported. The signi.cance

of differences between surface sample concentrations is dif.

cult to interpret because the quantities of mold scraped from an

area of suspected mold growth are not likely to represent overall

surface contamination in a home. The meaning of these surface

sample data in terms of exposure potential is unclear. The CDC

recently published a summary of an internal and external re

view of the investigation of mold exposure and IPH, and in it

concluded that the association between IPH and exposure to S.

chartarum “was not proven.”(83) However, the CDC will con

tinue to consider possible associations between IPH and many

other possible etiologies, including exposure to molds.

In 1998, Hodgson et al. reported the results of a study of

occupants of a courthouse in Florida that had previously had

extensive mold growth in its walls.(21) They evaluated question

naire results, lung function, and blood and immunology test

results among occupants of the courthouse and occupants from

other non-complaint buildings. Participants in the study included

14 courthouse occupants identi.ed by the workers’ compensa

tion carrier for examination; 197 questionnaire respondents from

which 30 cases reporting at least two interstitial lung disease

(ILD) symptoms were selected for the case-control study; and

47 courthouse volunteers who participated in a clinical screen

ing for building-related disease. The case-control study com

pared 24 cases selected from the questionnaire study to con

trols (n = 26) selected from two buildings thought to be free

of building-related disease. The case-control subjects under

went full pulmonary function testing and neuropsychological

testing.

Air and bulk material sampling was conducted in the com

plaint building but not in the control buildings. Satratoxins G

and H were isolated from ceiling tiles removed from the court

house. Air samples revealed lower viable spore levels indoors

compared to outdoors. Aspergillus versicolor and A. glaucus

were found indoors but not outdoors. Aggressive sampling re

sulted in indoor air spore concentrations ranging from 104 to

105 CFU/m3. Stachybotrys chartarum was found in air samples

collected while books were being handled, and was also found

in bulk samples of water-damaged ceiling tiles.

The 14 subjects identi.ed by the insurance carrier described

symptoms consistent with work-related asthma in three cases

(decreased FEF25¡75 in onea ), interstitial lung disease (ILD) in

one, and rhinitis that improved over weekends in six. Of 44 sub

aFEF25¡ 75 = forced expiratory ow of during the middle half of the FVC,

the average rate of ow during the middle two quarters of the forced expiratory

effort.(94)

jects from the clinical screening, 16 reported symptoms consis

tent with ILD, and had either single-breath carbon monoxide

diffusing capacity (DLCO), functional residual capacity (FRC),

or total lung capacity (TLC) less than 80 percent of predicted.

However, seven of the 16 subjects were smokers, and smoking

has been associated with ILD.(21) The questionnaire survey had a

90 percent response rate and was dominated by women (81.8%)

in lower-status job categories who were more likely to smoke.

Statistically signi.cant increased symptom reporting was found

for courthouse occupants for individual symptoms and grouped

symptom categories, except for wheezing. Symptoms of ILD

were reported more often among case building occupants.

In the case-control study, cases had signi.cantly higher lev

els of mean reserve volume (RV)/TLC ratios; however, ANOVA

indicated that the differences were due to smoking. Immunol

ogy panels did not provide useful information. Persons report

ing more than two symptoms had signi.cantly higher levels of

antibodies to Alternaria, A. fumigatus, pigeon serum, pigeon

droppings, and bovine serum, but not to the agents identi.ed

in the buildings. Results of neuropsychological testing showed

no difference in cognitive function; however, subjects with ILD

symptoms were more likely to endorse symptomatology reect

ing intense moods, anxiety, restlessness, irritability, and other

related symptoms.

There were two positive associations reported between court

house occupancy and outcome variable; (1) in the questionnaire

survey, symptoms of ILD were reported more often among case

building occupants; and, (2) statistically signi.cant increased

symptom reporting was found for courthouse occupants for in

dividual symptoms and grouped symptom categories, except for

wheezing. Results from objective measures of health (lung func

tion) or exposure (immune tests) do not appear to support an

association between exposure (building occupancy) and health

effects.

It is unclear whether the insurance exam participants, ques

tionnaire respondents, clinical screening, and case-control par

ticipants represented distinct groups, or if the groups overlapped

(except that three of 47 clinical screen subjects were removed

because they appeared in other groups). Thus, it is unclear how

many occupants participated in the study.

Selection and recall bias were likely to occur in this study be

cause the building had been undergoing mold remediation and

sampling prior to the study, and some occupants were actively in

volved in litigation concerning mold in the building and claimed

health effects. In addition, building occupants without symptom

complaints would be less likely to participate because subjects

were acquired by posting a memorandum describing the pur

pose of the investigation. Although the authors concluded that

a mycotoxin-induced effect was the most likely explanation for

increased symptoms in the problem building, support for this

conclusion is weak due to the limitations described above.

Epidemiological studies have linked ingestion of aatoxin

containing foods to liver cancer in humans. However, its exact

role in human liver cancer is unclear due to coincidence with

hepatitis B virus.(52,84) There is some evidence that the human

HEALTH EFFECTS OF MYCOTOXINS IN INDOOR AIR: A CRITICAL REVIEW

lung is also a target tissue for the action of AFB1,(84,85) but the

epidemiological data for AFB1 as a pulmonary carcinogen is

contradictory.(84) Workers exposed to potentially high levels of

AFB1-containing airborne dust from aatoxin-containing agri

cultural products have been studied. Two studies of workers

at a peanut-and linseed-processing plant (exposed to 0.04 to

2.5 l g AFB1 over a 45-hour week), showed higher incidences

of respiratory tumors compared to an unexposed cohort.(84,86)

No excess lung cancer risk was found in a study of proportion

ate risk of cancer in exposed (170 ng per day) livestock feed

processing plant workers; however, the workers had increased

risks of biliary and liver cancer.(87) There are also several case

reports linking AFB1 inhalation and human cancer.(88,89)

Although there are currently no published data regarding the

exposure to aatoxin-containing dusts in indoor environments,

they are included here because they are potent mycotoxins and

have been studied inother environments. It is not known ifexpo

sure to aatoxin-containing dusts in indoor environments poses

a health risk to building occupants. Sterigmatocystein, an aa

toxin precursor, has been detected in bulk samples in a mold-

contaminated building.(21)

DISCUSSION

Studies of animals exposed to puri.ed mycotoxins demon

strate their potency, but the evidence from these studies that

mycotoxins are more toxic via inhalation exposure is equivocal.

Studies of intratracheal instillation of mold spores indicate in

creased inammatory responseinthe lung duetothe presenceof

large numbers of toxic mold spores; however the applicability

of these results to human exposure in indoor environments is

limited due to the lack of comparability of the animal to human

physiology, arti.cial exposure route, high exposure level, and

the subjective grading of the response. Case reports indicate that

exposures to high levels of airborne molds (e.g. 1010 spores/m3)

and/or bioaerosols are associated with acute clinical illness,

which is likely due in part to mycotoxins. However, there is

no single mold genus that is consistently implicated in these

cases and there is evidence that many common molds can pro

ducetoxicmetabolites.(31) Epidemiologicalstudieswhich report

associations between health effects and exposure to mycotox

ins in indoor environments are limited, and generally do not

contain strong evidence to support this association. Although

there is evidence of a relationship between high levels of inhala

tion exposure or direct contact to mycotoxin-containing molds

or mycotoxins, and demonstrable effects in animals and health

effects in humans, the current literature does not provide com

pelling evidence that exposure at levels expected in most mold-

contaminated indoor environments are likely to result in mea

surable health effects.

More information is needed concerning the health effects

of exposure to molds, including putative toxigenic species, in

indoor environments. Studies of mold inhalation exposure us

ing animal models (animals having respiratory systems with

physiology similar to humans) could provide a better under

standing of the transport, fate, and toxic effects associated with

inhaling mycotoxin-containing mold particles. Extrapolation of

results from animal studies to human inhalation exposure is dif.

cult because of the exposure vehicle, exposure route, and type of

animal used. Studies have involved inhalation exposure to puri

..ed mycotoxin aerosols, rather than mycotoxin-containing mold

particles in different animals (rats, mice, guinea pigs, swine), or

have involved intratracheal instillation of mycotoxin-containing

mold particles in rodents, rather than inhalation exposure in

larger animals. This is limiting because the physiology of the

respiratory system of the mouse, rat, and guinea pig are not

similar to those of a human, and this affects the dose delivered

from a particular airborne exposure level due to differences in

terms of particle inhalation, deposition, and retention.(64) Al

though swine have lung physiology more similar to humans,

studies with them have been of inhalation exposure to puri.ed

mycotoxins, and this exposure is unlike inhalation exposure to

mycotoxins contained in or on a mold particle.

Epidemiological studies of exposure and health effects of

potentially highly exposed remediation workers may be useful.

This type of investigation is warranted on the basis of the histor

ical record of detecting sentinel health effects in highly exposed

populations. The ability of these studies to measure potential

health effects of mycotoxins will depend upon the development

of methods to quantify exposures to airborne mycotoxins.

There is a general need to develop better methods of estimat

ing exposure to molds that are relevant to the health effects of

interest. Improved methods are needed to accurately quantify

exposures to the irritant, allergenic, and toxic components (for

inhalation and dermal exposures) of molds. Currently, widely

available methods allow for quantitative estimates of airborne

viable or non-viable mold particles. Viable methods allow for

species identi.cation but do not include dead propagules that

may continue to have antigenic or toxigenic properties. Non

viable methods give an indication of the total antigenic burden

(since they include viable and non-viable propagules), but only

allow for putative identi.cation of some mold genera (and a few

to species). Neither method is useful for determining the my

cotoxin content of the sampled bioaerosol. Only recently has a

method been proposed to estimate trichothecene mycotoxins in

air samples,(90) and this technique remains to be validated. (Note

that this method does not measure trichothecenes directly, but

quanti.es the level of protein inhibition from material collected

on an air sample.) Standard methods for quantitative sampling

of surfaces do not yet exist; nor is there a model that would

allow the interpretation of surface sampling results to estimate

inhalation or dermal exposure. In current practice, standard sur

face sampling techniques for determining the “cleanliness” of

potentially mold-contaminated surfaces and objects are needed.

In addition to developing more standard sampling and analyt

ical techniques, there is a need to develop an empirical database

of typical indoor and outdoor molds (amounts and types, air

borne and surface) in non-problem buildings in different areas

C. A. ROBBINS ET AL.

of the country. Data collected in suspect buildings could ini

tially be compared to these control data to identify similarities

and differences that may be helpful in determining if a problem

exists.

Health-based exposure standards for molds(91) and mycotox

ins do not yet exist. While there is general agreement that active

mold growth in indoor environments is unsanitary and must be

corrected, the point at which mold contamination becomes a

threat to health is unknown. Better information about potential

health effectsand improved sampling techniqueswill help inde

termining what are the acceptable levels of exposures to mold

in indoor environments. In the future, this will help to determine

how clean an environment must be to avoid health effects, and

thus, provide guidance on when cleanup is required and “how

clean is clean.”

Whether molds such as Stachybotrys should be treated differ

ently than other molds, when considering cleanup or sampling

and exposures issues, is also a controversial subject. Cleanup and

repair of mold-contaminated buildings is often conducted using

asbestos abatement-like methods and clearance sampling.(92,93)

These procedures are often triggered, and sometimes build

ings are evacuated, because Stachybotrys has been found in the

building,(2,3) at times without regard to the extent of contamina

tion or exposure potential. The information about health effects

and exposure in the current scienti.c literature does not warrant

the use of more conservative measures for mold remediation

based on the presence of a particular species of mold. Instead, the

available data indicate that evacuation and immediate cleanup is

needed, regardless of the genus or species identi.ed, if contami

nation in indoor environments results in extremely high airborne

mold levels.

With or without mycotoxins, the issue of mold exposure is

important from a health standpoint, and can potentially effect

anyone in the indoor environment. Research and systematic

..eld investigation are needed to provide an understanding of

the health implications of mycotoxin exposures in indoor envi

ronments. The appropriateness of the amount of time, energy,

and other resources that will be spent in the future on controlling

exposures to mold in indoor environments will hinge upon the

accurate collection and dissemination of information about the

health risks associated with mold and mycotoxin exposures in

these environments.

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[Guest guest]

Hi !

Another great posting about this - thanks!

-

Klane, M.S.Ed., CIH, CHMM, CET

Klane's Education Information Training Hub (KEITH)

" Take a step in the right direction "

93 Norridgewock Road

Fairfield, Maine 04937-3116

207-453-KEITH (5348)

Fax:

@... www.TrainerMan.com

, wrote:

> Dear Group--

>

> I believe the following very closely describes the non-scientific

> approach Sharon takes when she communicates with this list. This is in

> addition of the underlying logical fallacies she uses in her

> arguments, such as :

>

> False Dilemma: two choices are given when in fact there are three options

>

> >From Ignorance: because something is not known to be true, it is

> assumed to be false

>

> Slippery Slope: a series of increasingly unacceptable consequences is

> drawn

>

> Complex Question: two unrelated points are conjoined as a single

> proposition

>

> Neveretheles, her " advocacy " adds a bit of excitement to this list.

>

>

> F. , Ph.D., MPH, D(ABMM), CIC, HEM

> Microbial Epidemiologist

> The Children's Hospital

> 1056 East 19th Ave. B-276

> Denver, Colorado 80218

>

> This excerpt is from Survivor Psychology: The Dark Side of a Mental

> Health Mission by , pp. 133-134. Upton Books and SIRS

> Mandarin, Boca Raton, FL. Copyright © 1995. Reprinted by permission.

> All rights reserved.

>

> The entire system of survivor psychology and recovery culture

> psychology is built on " true believer " logic. True believer logic is

> defined by Goldberg, author of When Wish Replaces Thought, as a

> system of fallacious and subjective arguments which " have no logical

> consistency, are discordant with the empirical evidence, and either

> fail to explain that which they claim to explain or offer explanations

> of that which does not exist. " This is the definition I have used for

> survivor logic as well.

>

> The basic principles of survivor logic are outlined below:

>

> Principle 1-Personalize the issues.

> The arguments are based on emotionally charged statements and " I

> messages. "

>

> Principle 2-The opposing argument becomes the proof.

> Hard evidence in support of the opposing viewpoint, or the lack of

> evidence for the belief is used as " evidence " and strengthens beliefs

> instead of challenging them.

>

> Principle 3-When confronted with logical discrepancies, revert to God,

> society or morality.

> When the evidence is stacked against the beliefs and the true believer

> is backed into a corner, they retreat behind their preferred social

> control modality-religion, political rhetoric and moral crusade

> monologues.

>

> Principle 4-When in doubt, abort further interaction or exploration of

> the issues by playing " Ain't it Awful " games while stepping up the

> intensity.

> When the true believer is backed into a corner, he or she often

> reverts to a favorite ideological or abortive interaction game (or

> plays all of them sequentially): God's Will; The Oppressor and the

> Oppressed; The Power of Evil and What Happens When Good People Do

> Nothing; Social Decline and Moral Decay; This Hurts Me as Much as It

> Hurts You; I Know This Is Hard to Believe-I Used to Be a Skeptic Too!;

> The Experts Know Best; Suicide; Revictimization; No Motive; and I'm

> Only Trying to Help.

>

> Principle 5-When all else fails, bring up denial and conspiracy theories.

>

>

> Re: Serious Breach of Ethics within the AIHA

>

> Steve,

>

> Can you cite for me the scientific foundation for the following statement

> within the ACOEM mold statement? I will give you a hint, it was picked

> paper

> of the year, 2000 by the AIHA. And....there is absolutely NO

> scientific paper

> that makes the same conclusion.

>

> " Levels of exposure in the indoor environment, dose-response data in

>

> animals, and dose-rate considerations suggest that delivery by the

> inhalation route of a toxic dose of mycotoxins in the indoor

> environment is

> highly unlikely at best, even for the hypothetically most vulnerable

> subpopulations. "

>

> Can you tell me how this statement within this document may still be

> impacting the misinformation over the science?

>

> I am working in today's world over this matter. And before the true

> science

> can accurately move forward, junk like this needs to be brought to

> light for

> what it really is. Its a defense argument meant for the courtroom. It

> has no

> scientific foundation and it has negatively impacted, and continues to

> negatively impact the scientific understanding as it stands today.

>

> So, one has to go back and correct the mistakes of yesterday in order to

> move forward with tomorrow. Sorry if I am boring you, but there are a

> lot of

> lives at stake here.

>

> Sharon

>

>

>

>

>

[Guest guest]

Thanks Wane:

Also:

1. You Stated:

" As a peer reviewer myself, I concur that the process helps weed out

the really bad and the mediocre. All I'm suggesting is that we as a

community need to (1) consider the source, and (2) critically

consider all that we read, whether it's peer-reviewed or not. "

My Comments:

Yes. It only weeds out bad and sometimes the mediocre - with perhaps the

exception of Nature which weeds out a lot.

Even if the Journal is " peer reviewed " , pieces or types of submittals may not be

formally or stringently peer reviewed. For instance, AIHA/ACGIH have the

Journal of Occuipational and Environmental Hygiene (JOEH) that has a section for

contuing education and case studies. Although very professionally done and

treviewed by at least one qualified person, it is not fully peer-reviewed.

Incidentally, the JOEH is no longer double-blind peer review. Another example

could be " Brief Communications " or " Short Communications " as in J Allergy which

historically have had only similar review. And of course, editorials are not

formally peer-reviewed.

Because of ethical issues recently (cloning for instance), journals are more

disclosing on the process and more investigative before publishing.

Tony

...........................................................................

" Tony " Havics, CHMM, CIH, PE

pH2, LLC

PO Box 34140

Indianapolis, IN 46234

cell

90% of Risk Management is knowing where to place the decimal point...any

consultant can give you the other 10%â„ 

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Re: Serious Breach of Ethics within the AIHA

Hey Tony,

You weren't one of the " gentlemen " to which my post below was

directed.

I remember when Coreen Robbins' 2000 paper appeared in AOEH, and I

also recall reading it with considerable interest. (It and the 2002

ACOEM " Evidence-Based Statement " are intertwined of course, as you

know.)

For example, at the time I found it troubling that Robbins' paper

described only three groups of adverse health effects associated

with fungi: allergic, infectious and toxic. Robbins, et al,

neglected to describe irritant effects, which are generally

trivialized, but which are strongly associated with inflammation.

Inflammation, in turn, is poorly understood and understudied, but

can have a profound effect on one's health status.

The journal EHP featured a fascinating article on inflammation that

describes the limits of our understanding in the December 2005 issue

(Environmental Health Perspectives, v113, n12, p A816-A821).

As a peer reviewer myself, I concur that the process helps weed out

the really bad and the mediocre. All I'm suggesting is that we as a

community need to (1) consider the source, and (2) critically

consider all that we read, whether it's peer-reviewed or not.

As scientists with the appropriate academic background and years of

experience in this line of work, it is the ability to do so that

sets some on this list - such as you - apart. For those who were

hydrogeologists, asbestos pump-jockeys, or other minimally-related

environmental specialists yesterday, and " certified IAQ experts "

today, that task may simply be out of reach.

Regards,

Wane

> >

> > > Sharon, your increasingly strident conspiracy theories are

> growing

> > > tiresome. The ACOEM paper was an excellent summary of existing

> > > knowledge at the time of publishing, and most of it remains

> entirely

> > > appropriate now. Their statement " Current scientific evidence

> does not

> > > support the proposition that human health has been adversely

> affected

> > > by inhaled mycotoxins " was indeed based on scant evidence,

> because

> > > *very little evidence was available, period*. I assume if that

> > > scientifically verifiable evidence becomes available, their

> position

> > > would change.

> <snip>

> > > Now, in the interest of carrying this debate forward to today

> rather

> > > than sniping at a 4 year old document, have you seen the August

> 2006

> > > issue of the Environmental Reporter, specifically the article

> > > * " **Mycotoxins: Continuing Review of the Literature " ?*

> > >

> > > An excerpt:

> > >

> > > So far, the animal studies reported in the literature verify

> that

> > > mycotoxins produced by some fungi that grow in indoor

> environments can

> > > produce changes in some physiological parameters in the

animals.

> Thus,

> > > very high doses of appropriate strains of /Stachybotrys

> chartarum/

> > > spores produce indicators of lung damage (Rosenblum et al.,

> 2006) and

> > > nasal irritation (Islam et al., 2006). The models that

> extrapolate

> > > these doses to human health effects indicate that the no effect

> level

> > > is much higher than any exposures that have been recorded in

> indoor

> > > environments. (Kelman et al., 2004) This review suggests that

> levels

> > > of /Stachybotrys/ spores, provided that they contain sufficient

> > > quantities of Satratoxin G and H could result in irritation if

> present

> > > in concentrations in excess of 2x10^-5 /m^3 (20,000

> spores/m^3 ). This

> > > concentration has not been reported for

> undisturbed /Stachybotrys/

> > > spores, but could be experienced by professional remediators.

> > >

> > > Comments, anyone?

> > >

> > >

> > > D. Carlson, CIAQC, CMRS

> > >

>

>

FAIR USE NOTICE:

This site contains copyrighted material the use of which has not always been

specifically authorized by the copyright owner. We are making such material

available in our efforts to advance understanding of environmental, political,

human rights, economic, democracy, scientific, and social justice issues, etc.

We believe this constitutes a 'fair use' of any such copyrighted material as

provided for in section 107 of the US Copyright Law. In accordance with Title 17

U.S.C. Section 107, the material on this site is distributed without profit to

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must obtain permission from the copyright owner.

[Guest guest]

Wane,

I stand corrected about support for Sharon Kramer vs support for

carefully evaluating peer-reviewed information.

As for the judgement issue on the scientific method, I agree that the

formal process starts with an observation that generates a hypothesis

to test, etc, rather than a judgement. However, the choice to pursue,

the choice of which observation to pursue and the choice of

hypothesis cannot be determined by the scientific method. They are

all chosen by judgement. Even what is noticed as an observation is

colored by belief, experience, intent, bias, luck, serendipity, etc

and does not necessarily derive purely from the scientific method. It

is in that sense that I say the scientific method begins with a

judgement.

Carl Grimes

Healthy Habitats LLC

-----

> Carl:

>

> thank you for your note of encouragement.

>

> thanks as well for your off-list email message. I'm sure we'll be

> talking more in the near future.

>

> for purposes of this list, a couple of clarifications are in order:

>

> 1. perhaps you misconstrue my intent. my message was not so much in

> support of Ms. Kramer's particular assertions as it was a suggestion

> that all of us need to do our homework. even in the peer-reviewed

> literature, appearances can be deceiving.

>

> 2. as I recall, the scientific method does not " begin with a

> judgement [sic] " -- indeed, it must not begin there. rather, it

> starts with an observation, which generates an hypothesis that is

> challenged by experimentation, providing empirical data that

> culminates in a conclusion (if all goes well). the conclusion in

> turn serves to validate or perhaps modify the hypothesis.

>

> the rest I haven't time to comment upon right now. let's do talk.

>

> thanks again.

>

> Wane

>

>

>

> >

> > Wane,

> >

> > You and I have our differences, but I will clearly and

> emphatically

> > state that your support of Sharon Kramer's assertions (below) is a

> > commonality, not a difference.

> >

> > Although I am not qualified to critique the validity of scientific

> > research and of the subsequent published studies, as you and

> others

> > are, I can say emphatically (based on my education, etc) that

> proper

> > procedure, foundation and logic, while necessary, are not

> sufficient.

> >

> > Scientific inquiry always begins with a judgement, the conclusions

> > can be affected by judgement, and application of the findings is

> of

> > course always based on judgement; all according to appropriate

> > procedure and sometimes supported by law. As you clearly assert,

> > common sense is also required.

> >

> > The process of a scientific experiment (as with any system) cannot

> be

> > self-validating. It must also stand on other principles such as

> > independant verification.

> >

> > Remember the excitement of the claims of cold fusion, until they

> > couldn't be independantly verified? Or the medical assertion that

> > infants can't feel the pain of surgery, until someone investigated

> > and could find only a single study in Britain from the 1920's?

> When a

> > claim tries to stand only on it's own and is then generally

> accepted

> > prior to independant verification, it can lead to the type of

> > distortion and misuse that Sharon is asserting.

> >

> > Which begs the question: Has the study and the paper in question

> been

> > challanged by repeating the experiment? Independantly or otherwise?

> >

> > If not, then why is it being so wholeheartedly accepted and

> honored

> > as established science when the same authorities demand that

> contrary

> > studies await a mature body of independant verfication? (E.g. the

> > more recent one indicating inflamation and brain cell death in

> > murines from inhaled mycotoxins). If the ACOEM position cannot be

> > independantly verified we may be at risk of supporting the " cold

> > fusion " of our profession.

> >

> > Wane, I'm not qualified to determine where the truth lies in this

> > matter, but I applaud your courage in taking the lead in this

> > unpopular stand and for again demonstrating your passion for

> finding

> > the truth.

> >

> > Carl Grimes

> > Healthy Habitats LLC

> >

> > -----

> > > Gentlemen:

> > >

> > > I can't help but agree that Ms. Kramer sometimes gets a bit

> carried

> > > away. Her passion is driven by personal experience, as I'm sure

> you

> > > realize.

> > >

> > > But have you actually studied the ACOEM document? I don't mean

>

>

>

>

>

>

>

>

>

> FAIR USE NOTICE:

>

> This site contains copyrighted material the use of which has not always been

specifically authorized by the copyright owner. We are making such material

available in our efforts to advance understanding of environmental, political,

human rights, economic, democracy, scientific, and social justice issues, etc.

We believe this constitutes a 'fair use' of any such copyrighted material as

provided for in section 107 of the US Copyright Law. In accordance with Title 17

U.S.C. Section 107, the material on this site is distributed without profit to

those who have expressed a prior interest in receiving the included information

for research and educational purposes. For more information go to:

http://www.law.cornell.edu/uscode/17/107.shtml. If you wish to use copyrighted

material from this site for purposes of your own that go beyond 'fair use', you

must obtain permission from the copyright owner.

>

[Guest guest]

It should be noted that the attached document is another review paper, not an original study.

It says "the current literature does not provide compelling evidence that exposure at levels expected in most mold-contaminated indoor environments are likely to result in measurable health effects."

It also calls strongly for more study, as we are all aware is needed, particularly in regard to dose-response data. I think it is obvious that if a different dose-response curve can be demonstrated, then the conclusions of this paper and the ACOEM paper must be visited again. The problem is the scarcity of such data. Sharon, are you aware of alternative studies regarding mycotoxin dose-response curves? (apologies in advance if you have previously brought such information to light, I don't have time to read every post)

D. Carlson, CIAQC, CMRS

Liesch Associates, Inc.

-----Original Message-----From: snk1955@... Sent: Tuesday, September 05, 2006 11:25 AMTo: iequality Subject: Re: Re: Serious Breach of Ethics within the AIHA

Group,

I am discussing sciences, research science coupled with the science of marketing. I am discussing how a paper, based on scant scientific foundation and not supported by any other study was unduly parlayed in stature and validity thru the use and abuse of journals and medical associations. What this has caused is an incorrect perception among the IAQ community, the medical community, the legal community and the public in general as to the validity of the seriousness of illnesses from excessive mold/mycotoxin exposure. The mantra of "not plausible" has no legitimate scientific foundation.

If you want to discuss it in scientific terms, then:

Let's look at the scientific foundation that has become the national medical understanding of the implausibility of illnesses caused by mycotoxin inhalation indoors.

Let look at how this position has been marketed to the IAQ communities, the medical communities and the courts.

Let's look in detail at the article published by the Journal of Applied Occupational and Environmental Health back in 2000. This is the one that is the SOLE foundation for the ACOEM mold statement of:

"Levels of exposure in the indoor environment, dose-response data in animals, and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations."

I see it as a guise of being presented as a review piece, when in reality, the conclusions of the paper are not founded upon anything being reviewed. The key conclusion (the one that whispers on thru medical journals) is only founded upon a rodent study with math extrapolations applied to deduce all human illness is not plausible.

The paper was authored by GlobalTox and ICTM. It is attached below in pdf form (for ease of reading) and text form (for ease of cutting and pasting)

You may view it differently, but if you all want to discuss the science in detail, I am more than willing to cooperate with your wishes.

The way I normally read these types of docs is to go down them line by line, word by word - just as I would a real estate contract.

I color code them as I go. Blue = agree, Green = I have some questions, Red = I know this is wrong.

And just like a real estate contract, 99.5% is accurate (Blue). .49 % need more clarification (Green) and .01% is blatantly incorrect (Red). The .01% is typically the critical aspect to the heart of the contract. The answer to why .01% is wrong (Red), can be found in the .49% of needs clarification (Green) .

To save time with this doc, let me just ask you all two questions:

1. Where within the attached document is the information that would support the ACOEM statement of "Levels of exposure in the indoor environment, dose-response data in animals, and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations." ?

2. What information within the document attached below substantiates the foundation of the document?

In other words:

Where is the scientific premise for the above ACOEM statement of "not plausible" within this document?

Sharon

[Guest guest]

Hi Steve,

Thanks for the reply.

It should be noted that the attached document is another review paper, not an original study.

Yes, that is exactly correct. The topic I am trying to discuss with you all is that the "not plausible one could become seriously ill from inhaling mycotoxins indoors" stance - that has been widely distributed and commonly accepted - is based solely on this document and 2 accompanying paper, all written by the same authors and their associates. No other authors, that I am aware, have come to this conclusion. So how did a mere review piece published within the journal of the AIHA become the accepted scientific understanding of the matter? This is the first document that implied what was known of human illness from mycotoxin exposure should be seperated into two catagories. 1. When people were exposed in a home, school or office. 2. When people were exposed anywhere else. This is where the science of marketing began to come in to the equation. Separate location of causation in order to limit liability. It says "the current literature does not provide compelling evidence that exposure at levels expected in most mold-contaminated indoor environments are likely to result in measurable health effects."

That's correct. Which is not synonymous with the occurrence of these illnesses is implausible. I would argue with the statement that "current literature does not support". There was much current literature available at the time this doc was written that was not part of the review. And many of the docs cited within the review indicate a knowledge that inhaling mycotoxins can indeed cause serious illness. But the gist of the doc is only if one is exposed anywhere but in a home, school or office.

But, again, that is not the point of this topic. The point is "current literature does not support" is in no way synonymous with "these illnesses are not plausible". Yet, based on this document, the wheels of denying human illness from indoor exposure, were set in motion. From there, the science of marketing took over. Will write of that tomorrow.

It also calls strongly for more study, as we are all aware is needed, particularly in regard to dose-response data. I think it is obvious that if a different dose-response curve can be demonstrated, then the conclusions of this paper and the ACOEM paper must be visited again.

Thank you. That is exactly what I have been trying to say. Its absolutely true much research is needed. But that does not mean there is any science that these illnesses are implausible. Nor, that there ever has been. Do you see the difference?

The problem is the scarcity of such data. Sharon, are you aware of alternative studies regarding mycotoxin dose-response curves? (apologies in advance if you have previously brought such information to light, I don't have time to read every post)

The problem with human mycotoxin exposure and trying to establish a dose-response curve is that there are too many variables involved to accomplish this - even in the rodents that are studied. Let alone extrapolated data to understand human illness. Many of the studies within the AIHA paper of the year 2000 discuss mechanistic work in an effort to better understand human toxicity. Nukilin, Cressia, etc.

The study that was recently discussed on this board by Dr. Rand, et al, is a clear indication of the insurmountable problems in attempting to establish concrete dose response data from mechanistic work alone in regard to mycotoxins. What the study found was that mycotoxins have various components that can cause illness, even in rodents. Exposing rodents to just one of the various components for varying times at varying levels and in varying combinations of time and levels, elicited varying symptoms.

Because molds do not produce mycotoxins all the time, Because mycotoxins have multiple components, Because humans who live and work within water damaged buildings are exposed at varying levels for varying amounts of time, Because of a need for at least a ten-fold margin of error with interspecies extrapolations, Because within water damaged building mycotoxins enter the body via inhalation, ingestion and dermal contact simultaniously,

Because there is evidence of a genetic component for human susceptibility in regard to mold/mycotoxins, There is no such thing as an concrete dose-response curve for understanding illness brought on by mycotoxin exposure within an indoor environment. And there never will be. It is not as simple to establish a dose-response curve for mycotoxin exposure within a water damaged building as it would be for something like, how much salt must a human eat to cause toxicity. If A + B = C and A is always a variable number, then C will always be a variable number. At that is the exact case with human mold/mycotoxin exposure within a water damaged building.

But the good news is rodent studies, even without the ability to apply extrapolations to human exposure to mycotoxins within an indoor environment are very valuable studies. They may not be much help in establishing a concrete dose-response curve. But there are MANY that indicate adverse health effects in rodents that are similar to adverse health effects in humans. These are the symptoms being reported by some exposed to mold/mycotoxins within water damaged buildings. Many epidemiological studies support the same evidence as is what is found within rodent studies.

An accurate dose response curve would be a wonderful thing to have in understanding human illness, but it is not necessary to understand that people are indeed becoming quite ill from mycotoxin exposure indoors. Nor should an accurate dose response curve be required before people are able to obtain medical treatment for their illnesses.

Which brings me back to the AIHA paper of the year 2000. Read it again. The studies it cites all discuss adverse human health effects from mycotoxins or rodent adverse health effects from mycotoxins. The paper then goes on to diss the epidemiological research of Dr. Johanning (who by the way, has been instrumental in helping the rescue workers of 911 overcome the "not plausible" of their illnesses). But nowhere in that entire document does it provide data that would clearly substantiate that human illness is not plausible from inhaling mycotoxins indoors. It does imply this without any scientific foundation for the implication.

One has to look at the political climate at the time this paper was accepted for publication within the journal of the AIHA. This paper was written in the year 2000. Litigation was heating up over the mold issue. The authors have a history of expert defense witness backgrounds, yet no background in rodent/mycotoxin research. This paper was designed to cast doubt on illnesses caused by indoor mold/mycotoxin exposure. It is what is known as "cigarette science". Attempt to cast doubt on proof of illness for the purpose of limiting financial liability. If you go onto the website of SourceWatch.Org, you can see this technique being duplicated again. Just search "GlobalTox TCE". The AIHA paper was the first document to set the bar high for the burden of proof before one could obtain medical help. This, like the Dearborn review, set the bar at a courtroom level. The precautionary principle afforded most illnesses, went out the courtroom window. It was a scary time for all involved. Melinda was quite vocal and raised the public awareness of illness. People who were sick and had no clue why (because their doctors certainly were not trained) began to make the connection on their own. It was known that construction standards and building materials were causing petri dish situations. The fear of the unknown from both a financial and physical aspect was rampant.

So for the AIHA to promote this paper by naming it paper of the year, some may have originally thought they were acting with noble intentions in an attempt to shut down the litigation and the confusion that was occurring in 2000. But, there is no way anyone with a scientific background could say this paper proved in any way, shape or form that illness from inhaling mycotoxins indoors is not plausible based on the information within this paper. And as is true with everything in life, the ends never justify the means. The means of promoting this document as science indicative of a lack of causation of illnesses has utterly ruined the health and lives of many, no matter how noble anyone's intentions were in the year 2000.

Tomorrow, I'll write more about what was done with this paper to further the medical mod mentality that is still with us, continues to stifle true medical understanding and to harm many even to this very day.

Sharon

[Guest guest]

Hi Steve,

Here is the spin sentence within the ACOEM doc. "Highly unlikely at best" is the actual quote in this one. The catch phrase at the end of the document needs to also be understood from a marketing standpoint.

"Levels of exposure in the indoor environment, dose-response data in animals, and dose-rate considerations suggest that delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations."

I am getting a little ahead of myself here, but what was done with the next phase of this paper is where the marketing really kicks in. The authors were getting more brazen with every document as nobody with any authority was stopping them on the promotion of their defense argument. Those in authority were backing them.

Below is the catch phrase of the translation of the ACOEM document. This is the one that was promoted by the United States Chamber of Commerce.

"A Scientific View of the Health Effects of Mold Hardin, PhD, Saxon MD, Correen Robbins, PhD, CIH and Bruce J. Kelman, Ph.D., DABT"

“Thus the notion that ‘toxic mold’ is an insidious secret ‘killer’ as so many media reports and trial lawyers would claim is ‘Junk Science’ unsupported by actual scientific study.â€

I want to go back to the ACOEM paper. But I will have to do it later today. I can explain what was done with it from a marketing standpoint and where there is a fundamental flaw within the ACOEM paper that promotes the concept of "not plausible".

But there are others on this board who can explain it in more scientific detail than I can as to the actual spinning of science to promote the not plausible concept. Wane? Tony? Greg?

Will write more later.

Sharon

[Guest guest]

Sharon, everything you are saying about the variables involved is true. However, the basic premise of the papers position on mycotoxin inhalation is:

A. (X) amount of mycotoxin is necessary to affect health (dose response).

B. Only a dose quantity substantially less than (X) amount of airborne mycotoxin is available via inhalation (available dose).

Therefore airborne mycotoxins, considered by themselves, do not seem able (or plausible, if you will) to affect health.

If either A or B can be demonstrated to be false, then the "Therefore" must be reassessed. I think studies of this are at least possible to do, though not easy. But to my knowledge, studies are not currently available that change A or B. Hopefully more studies are forthcoming that will confirm or change these rudimentary conclusions.

Regarding the semantic differences between "not plausible" and "does not support", I just looked at the ACOEM October 2002 paper and the AOEH 2000 paper in search of the "not plausible" statement in order to understand the context of the statement, but could not find it. Can you point to it for me? Apologies, as I am sure you have cited the reference before.

D. Carlson, CIAQC, CMRS

Liesch Associates, Inc.

-----Original Message-----From: snk1955@... Sent: Thursday, September 07, 2006 1:11 PMTo: iequality Subject: Re: Re: Serious Breach of Ethics within the AIHA

Hi Steve,

Thanks for the reply.

It should be noted that the attached document is another review paper, not an original study.

Yes, that is exactly correct. The topic I am trying to discuss with you all is that the "not plausible one could become seriously ill from inhaling mycotoxins indoors" stance - that has been widely distributed and commonly accepted - is based solely on this document and 2 accompanying paper, all written by the same authors and their associates. No other authors, that I am aware, have come to this conclusion. So how did a mere review piece published within the journal of the AIHA become the accepted scientific understanding of the matter? This is the first document that implied what was known of human illness from mycotoxin exposure should be seperated into two catagories. 1. When people were exposed in a home, school or office. 2. When people were exposed anywhere else. This is where the science of marketing began to come in to the equation. Separate location of causation in order to limit liability. It says "the current literature does not provide compelling evidence that exposure at levels expected in most mold-contaminated indoor environments are likely to result in measurable health effects."

That's correct. Which is not synonymous with the occurrence of these illnesses is implausible. I would argue with the statement that "current literature does not support". There was much current literature available at the time this doc was written that was not part of the review. And many of the docs cited within the review indicate a knowledge that inhaling mycotoxins can indeed cause serious illness. But the gist of the doc is only if one is exposed anywhere but in a home, school or office.

But, again, that is not the point of this topic. The point is "current literature does not support" is in no way synonymous with "these illnesses are not plausible". Yet, based on this document, the wheels of denying human illness from indoor exposure, were set in motion. From there, the science of marketing took over. Will write of that tomorrow.

It also calls strongly for more study, as we are all aware is needed, particularly in regard to dose-response data. I think it is obvious that if a different dose-response curve can be demonstrated, then the conclusions of this paper and the ACOEM paper must be visited again.

Thank you. That is exactly what I have been trying to say. Its absolutely true much research is needed. But that does not mean there is any science that these illnesses are implausible. Nor, that there ever has been. Do you see the difference?

The problem is the scarcity of such data. Sharon, are you aware of alternative studies regarding mycotoxin dose-response curves? (apologies in advance if you have previously brought such information to light, I don't have time to read every post)

The problem with human mycotoxin exposure and trying to establish a dose-response curve is that there are too many variables involved to accomplish this - even in the rodents that are studied. Let alone extrapolated data to understand human illness. Many of the studies within the AIHA paper of the year 2000 discuss mechanistic work in an effort to better understand human toxicity. Nukilin, Cressia, etc.

The study that was recently discussed on this board by Dr. Rand, et al, is a clear indication of the insurmountable problems in attempting to establish concrete dose response data from mechanistic work alone in regard to mycotoxins. What the study found was that mycotoxins have various components that can cause illness, even in rodents. Exposing rodents to just one of the various components for varying times at varying levels and in varying combinations of time and levels, elicited varying symptoms.

Because molds do not produce mycotoxins all the time, Because mycotoxins have multiple components, Because humans who live and work within water damaged buildings are exposed at varying levels for varying amounts of time, Because of a need for at least a ten-fold margin of error with interspecies extrapolations, Because within water damaged building mycotoxins enter the body via inhalation, ingestion and dermal contact simultaniously,

Because there is evidence of a genetic component for human susceptibility in regard to mold/mycotoxins, There is no such thing as an concrete dose-response curve for understanding illness brought on by mycotoxin exposure within an indoor environment. And there never will be. It is not as simple to establish a dose-response curve for mycotoxin exposure within a water damaged building as it would be for something like, how much salt must a human eat to cause toxicity. If A + B = C and A is always a variable number, then C will always be a variable number. At that is the exact case with human mold/mycotoxin exposure within a water damaged building.

But the good news is rodent studies, even without the ability to apply extrapolations to human exposure to mycotoxins within an indoor environment are very valuable studies. They may not be much help in establishing a concrete dose-response curve. But there are MANY that indicate adverse health effects in rodents that are similar to adverse health effects in humans. These are the symptoms being reported by some exposed to mold/mycotoxins within water damaged buildings. Many epidemiological studies support the same evidence as is what is found within rodent studies.

An accurate dose response curve would be a wonderful thing to have in understanding human illness, but it is not necessary to understand that people are indeed becoming quite ill from mycotoxin exposure indoors. Nor should an accurate dose response curve be required before people are able to obtain medical treatment for their illnesses.

Which brings me back to the AIHA paper of the year 2000. Read it again. The studies it cites all discuss adverse human health effects from mycotoxins or rodent adverse health effects from mycotoxins. The paper then goes on to diss the epidemiological research of Dr. Johanning (who by the way, has been instrumental in helping the rescue workers of 911 overcome the "not plausible" of their illnesses). But nowhere in that entire document does it provide data that would clearly substantiate that human illness is not plausible from inhaling mycotoxins indoors. It does imply this without any scientific foundation for the implication.

One has to look at the political climate at the time this paper was accepted for publication within the journal of the AIHA. This paper was written in the year 2000. Litigation was heating up over the mold issue. The authors have a history of expert defense witness backgrounds, yet no background in rodent/mycotoxin research. This paper was designed to cast doubt on illnesses caused by indoor mold/mycotoxin exposure. It is what is known as "cigarette science". Attempt to cast doubt on proof of illness for the purpose of limiting financial liability. If you go onto the website of SourceWatch.Org, you can see this technique being duplicated again. Just search "GlobalTox TCE". The AIHA paper was the first document to set the bar high for the burden of proof before one could obtain medical help. This, like the Dearborn review, set the bar at a courtroom level. The precautionary principle afforded most illnesses, went out the courtroom window. It was a scary time for all involved. Melinda was quite vocal and raised the public awareness of illness. People who were sick and had no clue why (because their doctors certainly were not trained) began to make the connection on their own. It was known that construction standards and building materials were causing petri dish situations. The fear of the unknown from both a financial and physical aspect was rampant.

So for the AIHA to promote this paper by naming it paper of the year, some may have originally thought they were acting with noble intentions in an attempt to shut down the litigation and the confusion that was occurring in 2000. But, there is no way anyone with a scientific background could say this paper proved in any way, shape or form that illness from inhaling mycotoxins indoors is not plausible based on the information within this paper. And as is true with everything in life, the ends never justify the means. The means of promoting this document as science indicative of a lack of causation of illnesses has utterly ruined the health and lives of many, no matter how noble anyone's intentions were in the year 2000.

Tomorrow, I'll write more about what was done with this paper to further the medical mod mentality that is still with us, continues to stifle true medical understanding and to harm many even to this very day.

Sharon

[Guest guest]

This horse

is dead already..can we move on

Re: Re:

Serious Breach of Ethics within the AIHA

Hi

Steve,

Here is

the spin sentence within the ACOEM doc. " Highly unlikely at

best " is the actual quote in this one. The catch phrase at the end

of the document needs to also be understood from a marketing standpoint.

" Levels of exposure in the indoor environment,

dose-response data in

animals, and dose-rate considerations suggest that delivery by the

inhalation route of a toxic dose of mycotoxins in the indoor environment is

highly unlikely at best, even for the hypothetically most

vulnerable

subpopulations. "

I am

getting a little ahead of myself here, but what was done with the next phase of

this paper is where the marketing really kicks in. The authors were

getting more brazen with every document as nobody with any authority

was stopping them on the promotion of their defense argument. Those

in authority were backing them.

Below is

the catch phrase of the translation of the ACOEM document. This is the

one that was promoted by the United States Chamber of Commerce.

" A

Scientific View of the Health Effects of Mold Hardin, PhD,

Saxon MD, Correen Robbins, PhD, CIH and Bruce J. Kelman, Ph.D.,

DABT "

“Thus

the notion that ‘toxic mold’ is an insidious secret ‘killer’ as so

many media reports and trial lawyers would claim is ‘Junk Science’

unsupported by actual scientific study.”

I want

to go back to the ACOEM paper. But I will have to do it later

today. I can explain what was done with it from a marketing standpoint

and where there is a fundamental flaw within the ACOEM paper that promotes

the concept of " not plausible " .

But

there are others on this board who can explain it in more scientific detail

than I can as to the actual spinning of science to promote the not plausible

concept. Wane? Tony? Greg?

Will

write more later.

Sharon

[Guest guest]

Hi Steve,

I will respond in blue:

Sharon, everything you are saying about the variables involved is true. However, the basic premise of the papers position on mycotoxin inhalation is:

A. (X) amount of mycotoxin is necessary to affect health (dose response).

a. No one has established (X) the minimum amount of mycotoxins a human must inhale in order to elicit symptoms of ill health. There is no minimum dose response established.

B. Only a dose quantity substantially less than (X) amount of airborne mycotoxin is available via inhalation (available dose).

b. Less than what? If there is no established minimum then there is no established number less than that.

Therefore airborne mycotoxins, considered by themselves, do not seem able (or plausible, if you will) to affect health.

The concept they have tried to portray is that they have been able to establish a threshold level that could never plausibly occur within a damp indoor environment to cause human illness.

If either A or B can be demonstrated to be false, then the "Therefore" must be reassessed.

A is false. There is no minimum amount known or established threshold level to cause human illness. Too many variables involved. So, B is also false.

I think studies of this are at least possible to do, though not easy.

I could be wrong, but I don't think so - or some scientist who actually has experience with mycotoxin research would have already done it. So let's look closely at what this erroneous information is based upon.

The year was early 2002. It was already being largely promoted that the absence of evidence within the Dearborn study meant evidence of absence. The AIHA was backing the "not plausible" stance, based on the Veritox, ICTM paper of the year 2000.

Physicians and IAQ pros were being told it was all hype and hysteria. (I know this one personally. By this time, I was living it) Many good papers came out such as the New York City Guidelines, but the medical aspects of papers that identified plausibility were quickly over powered by the association or CDC backed documents.

A lot of research within NIOSH/CDC Bacterial and Mycotic Disease dept, that had made great strides in the 90's all but came to a halt. Page and Trout were putting out documents regarding the lack of relevance of IgG, mycotoxins measurements, etc. Etzel left the CDC in disgust.

The terms mold, toxic mold, mycotoxins, mold toxins, Stachybotris were all synonymous in the eyes of the physicians who were denying the illnesses because they read somewhere that these illnesses were not plausible. But for some odd reason, people who were never liars before, were claiming they were sick. The lawsuits kept coming.

In early 2002, the ACOEM specifically brought in to their organization, Hardin, Kelman and Saxon for the purpose of writing their mold position statement. Hardin had recently retired from NIOSH and joined Kelman at Veritox (used to be GlobalTox). ACOEM had 6000 physician members, but for some reason Saxon, who was not a member, was the one they wanted to write their mold paper. Doctors, who were already members of ACOEM such as Johanning, Hodson, Dearborn, Harbut, etc and did have research/epidemiological experience with molds/mycotoxins/water damaged buildings were not asked or even permitted to participate in the peer review process. So you understand why this assoc was key in the matter, they are the occupational and environmental physicians that treat and evaluate injured workers on behalf of insurers or employers. (worker's compensation insurance physicians)

As Veritox had already written the AIHA's paper of the year 2000 that made the implication of "not plausible", it is easy to understand why these three were chosen to write the ACOEM mold statement. I have written a paper on this subject. Its called ACOEM Exposed, a case study in sham peer review and conflicts of interest. Its based a lot on the subpoenaed ACOEM emails at the time this paper was being drafted. They were calling it a defense argument as they were drafting it. If you want a copy, just send me an email.

So, its easy to understand that in the year 2002, when the ACOEM mold statement was written, that the industry beneficial stance of 'not plausible' was given precedence over the health and safety of the public. Not only was the unsubstantiated position not being called out for what it really was by authority, again it was being promoted by authority. All closely involved knew it was merely a defense argument.

This is getting to be a very long email. I will write of the slight of hand ratty rationale science tomorrow. Will end this email with a speech Dr. Johanning gave in 2004 before the Boston City Council.

Sharon

Dr.Johanning's speech in Boston I feel I am qualified to speak on this subject because I am anoccupational physician and I have worked in research and haveworked several government agencies such as EPA, CDC, & HUD. I have been involved with this issue for the past 15 years in NYC. We have had several symposiums and have brought scientists together 5 times who will be more than willing to collaborate our findings. Which have already been published. I know the Washington office of the Budget Management did a study of the structure and situations of schools and concluded that a third of the schools have serious Indoor Air Quality problems and that many of these are related to water intrusion.The press picked up on this issue many years ago, much more than the medical community I'm sad to say, and probably got the word out. I have seen over the last couple of years organized effects by the insurance industry and their advocates to defuse the issue and recently a report and some papers have come out on this issue saying we don't see a connection. I am a member ofthe American College of Occupational & Environmental Medicine.They state they have a so-called paper that concludes that we don't think the evidence that connects mold in particular, mold to adverse health effects. If you go and look how this paper was generated you will realize, and I have legal documents to prove this, that this wasn't an objective, free discussion within our membership. But rather a paper that was pushed in such a secret manner, was pushed through the committee in order to use that as a statement against doctors who think that there is a problem. Following this came the IOM paper and let me mention a couple ofnames here and documents that have come over the last couple of years, that makes it very difficult for doctors out there who don't know much about the issue to really educate themselves andif they are going to the internet or pick up a medical journal they would come up with papers which essentially conclude, we don't see a connection between the problems of mold exposure and indoor health quality problems and adverse effects. There are other papers out there and we should mention this and probably it's a little more removed from this. But Harriett Burge who was the group Harvard School of Public Health put together a group, to my knowledge, for the IOM two (2) years ago. She is thesame person who in 2002 also attended a meeting organized by Dr.Ron Gots, Globaltox in Washington which basically had all the leading defense experts there saying, we don't think there is a problem with mold. She also went to the press and media in the years 2002-2003 stating we don't think there is a problem. She chaired this committee, she called many of the member on the committee. Interesting enough the conclusion now of the report that came out recently that supported basically the CDC and many other people saying, we don't think there is a connection between toxic mold and many of the claims that people are doing. I think this process very undemocratic, secretive and that there was not enough public input and opportunity for doctors who are more involved with the research and care of patients to address these issues. I think we need to restudy this and to reconvene a group. I am a member of the MPha and feel they can doan objective look at this. There were only two physicians on this committee. Two physicians who had not really worked in this field. So a lot of the people whowere members of the committee, and they are very qualified and good minded people, but if you look at their publication record and if you look at some of their opinions that they had before theywent into the committee, you can already see that the conclusion that came out of it was not really based on what I would think is science and knowledge that is published in the papers. Several members of the IOM committee had written their opinion and it wassent to "higher-ups" to change, were not allowed to comment on the changes. But its a good start I think, but the conclusions are not based onthe facts, I would say. I think we have enough knowledge out thereand that's what the committee, the IOM committee chopped off their report. Knowing is not enough, we must apply.Living is not enough, we must do. Dr. Eckhart Johanning

[Guest guest]

Sharon and all,

I love the bantering about on this subject. However, where is it going?

It is going to be brought to public light soon. And yes, the document can be discredited. I know what I know and that is enough to show the deceit in science over the matter. But, I could use you alls help by running through this one more time to make sure I have all my facts straight. The next email I send is going to be discussing the specific reference papers and how they were applied. Not my strongest suit in this whole equation.

BTW , thanks for speaking up.

Sharon

Meaning, can the document be discredited if it is as ethically bad as you say it is and what credible group is doing this? My purpose for getting some form of closure, attorney’s waive this document in lawsuits as the premier proof that their isn’t a big deal with mold, toxins, etc., and the plaintiff and their experts must be crazy. (By the way, I do more defendant expert witness work than plaintiff).

Moffett

[Guest guest]

As the rhetoric of the approaching election season proves, the English language is a highly malleable format.

Great quote! Wish I had said that. Malleable, what a wonderful word. "The concept that it is implausible serious illness is not occurring after an atypical exposure to fungi has been harshly subjected to questionable scrutiny that is, at its best, described as malleable."

[Guest guest]

Hi Tony.

Blue is the old info. Red is yours. I will do this one in Green.

a. No one has established (X) the minimum amount of mycotoxins a human must inhale in order to elicit symptoms of ill health. There is no minimum dose response established.

There is very little data on humans for many agents.

We set limits on animal data all the time - that's the whole idea of not using humans.

Why aren't you complaining about other agents.

Because the discussion and the heart of the contention over the mold issue lays specifically about this particular agent. Why are you speaking in broad general terms?

B. Only a dose quantity substantially less than (X) amount of airborne mycotoxin is available via inhalation (available dose).

b. Less than what? If there is no established minimum then there is no established number less than that.

Therefore airborne mycotoxins, considered by themselves, do not seem able (or plausible, if you will) to affect health.

A NOAEL/LOAEL with a safety is usually the case (animal or human) applied based on historical variation in responses to a wide varierty of agents.

True. But again you are speaking in broad general terms. The subject of this discussion is that the threshold level purported to be established for Human mycotoxin inhalation within an indoor environment has some errors in the methodology and therefore its conclusions. However, even with the errors, it has been the gold standard widely used to deny that humans are becoming ill from mycotoxins indoors. In certain circles, medical primarily, it is a cornerstone concept that molds indoor do not cause human illness.

The concept they have tried to portray is that they have been able to establish a threshold level that could never plausibly occur within a damp indoor environment to cause human illness.

If either A or B can be demonstrated to be false, then the "Therefore" must be reassessed.

A is false. There is no minimum amount known or established threshold level to cause human illness. Too many variables involved. So, B is also false.

I think studies of this are at least possible to do, though not easy.

I could be wrong, but I don't think so - or some scientist who actually has experience with mycotoxin research would have already done it. So let's look closely at what this erroneous information is based upon.

You are wrong - it can be done - in humans and animals. Unfortunately, it's the ethical part on humans that is the problem.

Yes. I understand how this is a major stumbling block in establishing a legitimate threshold level, NOAEL/LOAEL. But, this should not be required before people are able to obtain medical treatment. The weight put on the need of this information and the inaccurate information that is currently widely accepted, is where the grind is that is stopping medical treatment.

Insurance companies (the ones with a lot to lose right now) won't fund the testing because (note: I've probed with cetain contacts requesting funding from a couple Co. for this) they will be appear as biased tests (paid for) and thus won't be usuable.

True, if not addressed and disclosed right up front. But I think it could be done. You would have to tread very carefully through the appearance of conflict of interest. Look at Clorox. They have funded some great studies that have concluded it takes more than bleach.

This sounds like it would be a huge project. Wouldn't you have to evaluate the various mycotoxins, the various components, the time of exposure, dermal, inhalation, etc, each individually? What would it take to do something like this? As this is the main point of contention within the relationship of the courtroom to the physician office, it would be fantastic to have more accurate information available on this point. Seems to me, one would almost have to publish a book with all the varying results that the situation would bring. Am I thinking correctly on that?

As an interesting counter to this bias, consider that many "professionals" that claim mold causing significant problems to normally healthy people at low levels are also making money from their stance. Bias works both ways, and thus one could claim that the results were biased on behalf of the FOR crowd (there is some evidence that this was done in the Cleveland Stachy events).

Yes, bias does work both ways. I can't comment on the Cleveland study as I have not looked at it in great detail. I know there is a new paper just published by Dr. Dearborn. But even if there was bias within the Dearborn study, it would justify the bias in the ACOEM paper and the way this has been misused as a weapon against the ill.

The year was early 2002. It was already being largely promoted that the absence of evidence within the Dearborn study meant evidence of absence. The AIHA

who is "the AIHA" and where is this "stance" in verbal recorded or written form?

1. You named the Veritox 2000 that implied it was not plausible as paper of the year. I would consider that a promotion of a particular concept. Wouldn't you?

2. AIHA gave credits for a teleweb "mold defense seminar" based primarily on the findings of the ACOEM mold statement. teleweb DVDs available from PNS-AIHA for short-term rental (viewing is $10 per ... February 16, 2005 with Hardin, Ed Light, Coreen Robbins. ...http://www.pnsaiha.org/Documents/seattle.htm

(will just pull out snippets of this info)

Toxicological and Occupational Medicine Perspective on Molds and Mycotoxins: Update and Implications for IH

Course Description"....The important points of the toxicity and health effects discussion from the recent position paper by the American College of Occupational and Environmental Medicine (ACOEM)... ...Implications for industrial hygiene practice as a result of the ACOEM paper will be presented, along with practical suggestions for addressing mold issues. ....The legal approach to claims of mold toxicity will be discussed, and the future of the “toxic mold†issue will be explored....

How does the American College of Occupational and Environmental Medicine characterize the evidence....

Industrial Hygiene Practice in Light of the 2003 American College of Occupational and Environmental Medicine Position Paper on Mold

Industrial Hygiene Practice For Indoor Mold: Hazard vs. Allergen?â€

Response to mold growth in buildings is now often based on hazardous material methodology

Such an approach is overly stringent where the risk of mycotoxicosis and opportunistic infection is negligible

A more realistic approach to mold assessment and remediation assumes mold is a common allergen

Current use of toxicological, exposure, and medical information in mold and mycotoxins cases in the U.S. court system.

Course Level:This is an intermediate level course.

Prerequisites:There are no prerequisites for this course.

Be aware of the events and publications that have likely resulted in the IH community’s treatment of mold as a hazardous materialUnderstand the potential health effects of mold, and the ACOEM’s position on the health effects of mold in the indoor environment, and the scientific/medical basis for it.Learn the basis for a practical approach to mold investigations and remediation based on the ACOEM’s statement about the potential health effects of mold.Understand where and to what extent occupational exposures to mycotoxins may occur, and the types of biomarkers and tests that can be used to test for those exposures.Appreciate the current approach in the legal community using scientific data in cases of alleged health effects due to mold exposure in indoor environments.

It's a great way to train multiple employees or a large group in a convenient and cost effective way!

These fully accredited courses allow IHs and OEHS professionals to obtain CMs, CEUs, and COCs on their own time in a comfortable atmosphere.

Presenters:Coreen Robbins, PhD, CIH Globaltox, Inc. D. Hardin, Ph.D. GlobalTox, Inc. Ed Light, CIH Building Dynamics

L. Sudakin, MD, MPH, FACMT, FACOEM Oregon State University V. Denham, Jr. Goldstein LLP

V. Denham, Jr., handles a wide range of litigation matters at the trial and appellate level. He chairs the Firm's Product Liability, Personal Injury, and Environmental practice group.

3. You have the overseer of the peer review process for the ACOEM mold statement as an advisor for the journal of the AIHA, Borak. This is the gentleman who was referring to it as a defense argument that would be garbage if they didn't accepted as the position of the ACOEM.

Tony, are you saying that members AIHA were not, by and large, of the opinion these illnesses are not plausible to be caused from an indoor environment? I can tell a difference in the perception just within the last year since I have joined this board. When I first came on here, it was common practice for some to make fun of those who just thought they were sick from mold.

Physicians and IAQ pros were being told it was all hype and hysteria. (I know this one personally. By this time, I was living it)

You'll have to admit - there is a lot more hype than reality.

Completely. The hype is that people are faking their illnesses just to get money from the poor stakeholder. The hype is that the best way to solve this problem is to deny these illnesses are real and just battle it out in court. The hype is that it is cheaper to keep the physicians in the dark about the illnesses, then it would be to train the doctors and inform the public.

Many good papers came out such as the New York City Guidelines, but the medical aspects of papers that identified plausibility were quickly over powered by the association or CDC backed documents.

A lot of research within NIOSH/CDC Bacterial and Mycotic Disease dept (who?? at NIOSH and what Dept?)

There is an old paper written in the year of 2003. It is a review of the ACOEM mold statement. Its cites much government research of illnesses caused by molds/mycotoxins prior to the year 2000. I have put a request in for the doc.

, that had made great strides in the 90's all but came to a halt. Page and Trout were putting out documents regarding the lack of relevance of IgG, mycotoxins measurements, etc. Etzel left the CDC in disgust.

The terms mold, toxic mold, mycotoxins, mold toxins, Stachybotris were all synonymous in the eyes of the physicians who were denying the illnesses because they read somewhere that these illnesses were not plausible. But for some odd reason, people who were never liars before, were claiming they were sick. The lawsuits kept coming.

In early 2002, the ACOEM specifically brought in to their organization, Hardin, Kelman and Saxon for the purpose of writing their mold position statement. Hardin had recently retired from NIOSH

( I thought you said above that there were great strides by NIOSH in the 90's - but how then would a NIOSH person take the opposite stance?)

Time and change in political climate.

and joined Kelman at Veritox (used to be GlobalTox). ACOEM had 6000 physician members, but for some reason Saxon, who was not a member, was the one they wanted to write their mold paper. Doctors, who were already members of ACOEM such as Johanning, Hodson, Dearborn, Harbut, etc and did have research/epidemiological experience with molds/mycotoxins/water damaged buildings were not asked or even permitted to participate in the peer review process (this is/was a problem - and it happens in opther organizations)

I know. It has been rampant in the past six years. Go on the Scirus search engine. Search the term Conflicts of Interest. It will turn your stomach.

. So you understand why this assoc was key in the matter, they are the occupational and environmental physicians that treat and evaluate injured workers on behalf of insurers or employers. (worker's compensation insurance physicians)

As Veritox had already written the AIHA's paper of the year 2000 that made the implication of "not plausible", it is easy to understand why these three were chosen to write the ACOEM mold statement. I have written a paper on this subject. Its called ACOEM Exposed, a case study in sham peer review and conflicts of interest. Its based a lot on the subpoenaed ACOEM emails at the time this paper was being drafted. They were calling it a defense argument as they were drafting it. If you want a copy, just send me an email.

So, its easy to understand that in the year 2002, when the ACOEM mold statement was written, that the industry (what industry, who?? - such a vague term)

See the US Chamber of Commerce teleconference July 17, 2003 when the "lay translation" of the ACOEM doc was presented. It was the insurance industry, the real estate industry, the mortgage industry, the building industry.

beneficial stance of 'not plausible' was given precedence over the health and safety of the public. Not only was the unsubstantiated position not being called out for what it really was by authority, again it was being promoted by authority. All closely involved knew it was merely a defense argument (note: I sem to recal that it is only defensive on "toxic" responses - not other responses, ortherwise why get rid of mold why not grow it inside?).

Because mold is bad structurally for a building is what has been widely promoted that the logical reason for ridding of mold. And one would not want to leave themselves open for liability by those nasty liars and whiners who will say they are ill in an attempt to get into your pocket book. But you are right. Not all aspects of the ACOEM mold statement are false. However, it is the entire concept of the doc based on a flawed and nonscientific application of mechanistic research that is the problem.

This is getting to be a very long email. I will write of the slight of hand ratty rationale science tomorrow. Will end this email with a speech Dr. Johanning gave in 2004 before the Boston City Council.

Sharon

Dr.Johanning's speech in Boston I feel I am qualified to speak on this subject because I am anoccupational physician and I have worked in research and haveworked several government agencies such as EPA, CDC, & HUD. I have been involved with this issue for the past 15 years in NYC. We have had several symposiums and have brought scientists together 5 times who will be more than willing to collaborate our findings. Which have already been published. I know the Washington office of the Budget Management did a study of the structure and situations of schools and concluded that a third of the schools have serious Indoor Air Quality problems and that many of these are related to water intrusion. (Where is this data and why isn't it published, could it be the IAQ is more poor ventilation and O & M?)

I have no idea what document he is discussing here.

The press picked up on this issue many years ago, much more than the medical community I'm sad to say, and probably got the word out. I have seen over the last couple of years organized effects by the insurance industry and their advocates to defuse the issue and recently a report and some papers have come out on this issue saying we don't see a connection. I am a member ofthe American College of Occupational & Environmental Medicine.They state they have a so-called paper that concludes that we don't think the evidence that connects mold in particular, mold to adverse health effects (note: He states that the emphasis is that the EVIDENCE does CONNECT MOLD to ADVERSE HEALTH EFFECTS - I don't see "not plausible" in his words - hummm).

I think you understand the concept of his presentation. The magic words of "not plausible" do not need to appear for a concept to be understood.

.. If you go and look how this paper was generated you will realize, and I have legal documents to prove this, that this wasn't an objective (policy papers never are)

, free discussion within our membership. But rather a paper that was pushed in such a secret manner, was pushed through the committee in order to use that as a statement against doctors who think that there is a problem. Following this came the IOM paper and let me mention a couple ofnames here and documents that have come over the last couple of years, that makes it very difficult for doctors out there who don't know much about the issue to really educate themselves andif they are going to the internet or pick up a medical journal they would come up with papers which essentially conclude, we don't see a connection between the problems of mold exposure and indoor health quality problems and adverse effects. (again no "Not plausible" but rather no "connection") There are other papers out there and we should mention this and probably it's a little more removed from this. But Harriett Burge who was the group Harvard School of Public Health put together a group, to my knowledge, for the IOM two (2) years ago. She is thesame person who in 2002 also attended a meeting organized by Dr.Ron Gots, Globaltox in Washington which basically had all the leading defense experts there saying, we don't think there is a problem with mold. She also went to the press and media in the years 2002-2003 stating we don't think there is a problem. She chaired this committee, she called many of the member on the committee. Interesting enough the conclusion now of the report that came out recently that supported basically the CDC and many other people saying, we don't think there is a connection between toxic mold and many of the claims that people are doing. I think this process very undemocratic (Nothing is democratic - it is republic at best despotism at worst) , secretive and that there was not enough public input (It is the ACOEM - not a public association - it is a policy statement for the members not by and for the public; It's use in the cimmunity is a different story) and opportunity for doctors who are more involved with the research and care of patients to address these issues. I think we need to restudy this and to reconvene a group. I am a member of the MPha and feel they can doan objective look at this. There were only two physicians on this committee (I have not been happy with a lot of physicians participation - I'd rather have a Nurse and an Epidemiologist over a physician many times - not to say that most are poor participants)

How bout a real estate agent? (no need for you to answer that one)

I want to make something very clear here. I have been writing much lately on this board that is not exactly flattering to the AIHA. If you go back to where we started discussing this (this go round), you will see I said "a few bad apples". I have been writing about the problems the ACOEM mold statement has caused for about 20 months.

Until recently, I never wrote much about the AIHA's involvement in the matter. I think the AIHA is an honorable organization. I think the vast majority of their work is toward helping to solve this problem. And I am one who has personally benefitted from the ethics of the AIHA. It was an AIHA member who refused to do what the insurance company was directing within my own home. It was an AIHA member who saved my daughter's life.

[Guest guest]

See below in RED

........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%â„ This message is from pH2. This message and any attachments may contain legally privileged or confidential information, and are intended only for the individual or entity identified above as the addressee. If you are not the addressee, or if this message has been addressed to you in error, you are not authorized to read, copy, or distribute this message and any attachments, and we ask that you please delete this message and attachments (including all copies) and notify the sender by return e-mail or by phone at . Delivery of this message and any attachments to any person other than the intended recipient(s) is not intended in any way to waive confidentiality or a privilege. All personal messages express views only of the sender, which are not to be attributed to pH2 and may not be copied or distributed without this statement.

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of snk1955@...Sent: Friday, September 08, 2006 7:20 PMTo: iequality Subject: Re: Re: Serious Breach of Ethics within the AIHA

Hi Steve,

I will respond in blue:

Sharon, everything you are saying about the variables involved is true. However, the basic premise of the papers position on mycotoxin inhalation is:

A. (X) amount of mycotoxin is necessary to affect health (dose response).

a. No one has established (X) the minimum amount of mycotoxins a human must inhale in order to elicit symptoms of ill health. There is no minimum dose response established.

There is very little data on humans for many agents.

We set limits on animal data all the time - that's the whole idea of not using humans.

Why aren't you complaining about other agents.

B. Only a dose quantity substantially less than (X) amount of airborne mycotoxin is available via inhalation (available dose).

b. Less than what? If there is no established minimum then there is no established number less than that.

Therefore airborne mycotoxins, considered by themselves, do not seem able (or plausible, if you will) to affect health.

A NOAEL/LOAEL with a safety is usually the case (animal or human) applied based on historical variation in responses to a wide varierty of agents.

The concept they have tried to portray is that they have been able to establish a threshold level that could never plausibly occur within a damp indoor environment to cause human illness.

If either A or B can be demonstrated to be false, then the "Therefore" must be reassessed.

A is false. There is no minimum amount known or established threshold level to cause human illness. Too many variables involved. So, B is also false.

I think studies of this are at least possible to do, though not easy.

I could be wrong, but I don't think so - or some scientist who actually has experience with mycotoxin research would have already done it. So let's look closely at what this erroneous information is based upon.

You are wrong - it can be done - in humans and animals. Unfortunately, it's the ethical part on humans that is the problem. Insurance companies (the ones with a lot to lose right now) won't fund the testing because (note: I've probed with cetaincontacts requesting funding from a couple Co. for this) they will be appear as biased tests (paid for) and thus won't be usuable. As an interesting counter to this bias, consider that many "professionals" that claim mold causing significant problems to normally healthy people at low levels are also making money from their stance. Bias works both ways, and thus one could claim that the results were biased on behalf of the FOR crowd (there is some evidence that this was done in the Cleveland Stachy events).

The year was early 2002. It was already being largely promoted that the absence of evidence within the Dearborn study meant evidence of absence. The AIHA

who is "the AIHA" and where is this "stance" in verbal recorded or written form?

was backing the "not plausible" stance, based on the Veritox, ICTM paper of the year 2000.

Physicians and IAQ pros were being told it was all hype and hysteria. (I know this one personally. By this time, I was living it)

You'll have to admit - there is a lot more hype than reality.

Many good papers came out such as the New York City Guidelines, but the medical aspects of papers that identified plausibility were quickly over powered by the association or CDC backed documents.

A lot of research within NIOSH/CDC Bacterial and Mycotic Disease dept (who?? at NIOSH and what Dept?) , that had made great strides in the 90's all but came to a halt. Page and Trout were putting out documents regarding the lack of relevance of IgG, mycotoxins measurements, etc. Etzel left the CDC in disgust.

The terms mold, toxic mold, mycotoxins, mold toxins, Stachybotris were all synonymous in the eyes of the physicians who were denying the illnesses because they read somewhere that these illnesses were not plausible. But for some odd reason, people who were never liars before, were claiming they were sick. The lawsuits kept coming.

In early 2002, the ACOEM specifically brought in to their organization, Hardin, Kelman and Saxon for the purpose of writing their mold position statement. Hardin had recently retired from NIOSH

( I thought you said above that there were great strides by NIOSH in the 90's - but how then would a NIOSH person take the opposite stance?)

and joined Kelman at Veritox (used to be GlobalTox). ACOEM had 6000 physician members, but for some reason Saxon, who was not a member, was the one they wanted to write their mold paper. Doctors, who were already members of ACOEM such as Johanning, Hodson, Dearborn, Harbut, etc and did have research/epidemiological experience with molds/mycotoxins/water damaged buildings were not asked or even permitted to participate in the peer review process (this is/was a problem - and it happens in opther organizations) . So you understand why this assoc was key in the matter, they are the occupational and environmental physicians that treat and evaluate injured workers on behalf of insurers or employers. (worker's compensation insurance physicians)

As Veritox had already written the AIHA's paper of the year 2000 that made the implication of "not plausible", it is easy to understand why these three were chosen to write the ACOEM mold statement. I have written a paper on this subject. Its called ACOEM Exposed, a case study in sham peer review and conflicts of interest. Its based a lot on the subpoenaed ACOEM emails at the time this paper was being drafted. They were calling it a defense argument as they were drafting it. If you want a copy, just send me an email.

So, its easy to understand that in the year 2002, when the ACOEM mold statement was written, that the industry (what industry, who?? - such a vague term) beneficial stance of 'not plausible' was given precedence over the health and safety of the public. Not only was the unsubstantiated position not being called out for what it really was by authority, again it was being promoted by authority. All closely involved knew it was merely a defense argument (note: I sem to recal that it is only defensive on "toxic" responses - not other responses, ortherwise why get rid of mold why not grow it inside?).

This is getting to be a very long email. I will write of the slight of hand ratty rationale science tomorrow. Will end this email with a speech Dr. Johanning gave in 2004 before the Boston City Council.

Sharon

Dr.Johanning's speech in Boston I feel I am qualified to speak on this subject because I am anoccupational physician and I have worked in research and haveworked several government agencies such as EPA, CDC, & HUD. I have been involved with this issue for the past 15 years in NYC. We have had several symposiums and have brought scientists together 5 times who will be more than willing to collaborate our findings. Which have already been published. I know the Washington office of the Budget Management did a study of the structure and situations of schools and concluded that a third of the schools have serious Indoor Air Quality problems and that many of these are related to water intrusion. (Where is this data and why isn't it published, could it be the IAQ is more poor ventilation and O & M?) The press picked up on this issue many years ago, much more than the medical community I'm sad to say, and probably got the word out. I have seen over the last couple of years organized effects by the insurance industry and their advocates to defuse the issue and recently a report and some papers have come out on this issue saying we don't see a connection. I am a member ofthe American College of Occupational & Environmental Medicine.They state they have a so-called paper that concludes that we don't think the evidence that connects mold in particular, mold to adverse health effects (note: He states that the emphasis is that the EVIDENCE does CONNECT MOLD to ADVERSE HEALTH EFFECTS - I don't see "not plausible" in his words - hummm).. If you go and look how this paper was generated you will realize, and I have legal documents to prove this, that this wasn't an objective (policy papers never are) , free discussion within our membership. But rather a paper that was pushed in such a secret manner, was pushed through the committee in order to use that as a statement against doctors who think that there is a problem. Following this came the IOM paper and let me mention a couple ofnames here and documents that have come over the last couple of years, that makes it very difficult for doctors out there who don't know much about the issue to really educate themselves andif they are going to the internet or pick up a medical journal they would come up with papers which essentially conclude, we don't see a connection between the problems of mold exposure and indoor health quality problems and adverse effects. (again no "Not plausible" but rather no "connection") There are other papers out there and we should mention this and probably it's a little more removed from this. But Harriett Burge who was the group Harvard School of Public Health put together a group, to my knowledge, for the IOM two (2) years ago. She is thesame person who in 2002 also attended a meeting organized by Dr.Ron Gots, Globaltox in Washington which basically had all the leading defense experts there saying, we don't think there is a problem with mold. She also went to the press and media in the years 2002-2003 stating we don't think there is a problem. She chaired this committee, she called many of the member on the committee. Interesting enough the conclusion now of the report that came out recently that supported basically the CDC and many other people saying, we don't think there is a connection between toxic mold and many of the claims that people are doing. I think this process very undemocratic (Nothing is democratic - it is republic at best despotism at worst) , secretive and that there was not enough public input (It is the ACOEM - not a public association - it is a policy statement for the members not by and for the public; It's use in the cimmunity is a different story) and opportunity for doctors who are more involved with the research and care of patients to address these issues. I think we need to restudy this and to reconvene a group. I am a member of the MPha and feel they can doan objective look at this. There were only two physicians on this committee (I have not been happy with a lot of physicians participation - I'd rather have a Nurse and an Epidemiologist over a physician many times - not to say that most are poor participants) . Two physicians who had not really worked in this field. So a lot of the people whowere members of the committee, and they are very qualified and good minded people, but if you look at their publication record and if you look at some of their opinions that they had before theywent into the committee, you can already see that the conclusion that came out of it was not really based on what I would think is science and knowledge that is published in the papers. Several members of the IOM committee had written their opinion and it wassent to "higher-ups" to change, were not allowed to comment on the changes. But its a good start I think, but the conclusions are not based onthe facts, I would say. I think we have enough knowledge out thereand that's what the committee, the IOM committee chopped off their report. Knowing is not enough, we must apply.Living is not enough, we must do. Dr. Eckhart Johanning

[Guest guest]

It is not the ACOEMs fault that lawyers are subverting the statements in the paper to further their case (although inevitable, I suppose). The phrase "typical allergic reactions" is not found in the paper. It says in fact "mold is likely to sensitize and produce allergic reactions in allergic individuals", no use of the word "typical".

The problem is that people (and most jurors) are pre-conditioned to believe that "allergies" can be nothing more than hay fever and the sniffles. This is flat out incorrect. Even the victims such as yourself are unwilling to acknowledge that their symptoms could be explainable by immune responses (allergies) because it doesn't sound as dire as "toxic mold". Most of us in this community know better, but the general public does not.

D. Carlson, CIAQC, CMRS

Liesch Associates, Inc.

-----Original Message-----From: snk1955@... Sent: Friday, September 08, 2006 7:33 PMTo: iequality Subject: Re: Re: Serious Breach of Ethics within the AIHA

In a message dated 9/8/2006 4:56:45 P.M. Pacific Standard Time, k.roegnerindustrial-solutions (DOT) net writes:

This horse is dead already..can we move on

That is the point . We can't move on until this mistake is undone. It is the bottleneck that keeps the legitimate science from freely moving forward.

Below is a court verdict in LA yesterday. Do you see how the "not plausible" mantra has such extreme monetary value to some pretty powerful industries? Do you see where the bottleneck is that is stopping people from being able to obtain proper medical treatment?

Judgment for Builder Rendered in Mold Bodily Injury Lawsuit

Thursday September 7, 7:44 pm ET

LOS ANGELES, Sept. 7 /PRNewswire/ -- Shea Homes was absolved of any liability for damages that a son Ranch family alleged had arisen out of mold exposure in their home. Jurors in the closely watched personal injury suit returned a defense verdict for Shea, the nation's largest private home builder, following a three week trial. The family of three claimed a host of bodily injuries from exposure to mold while living in a single family home that Shea had constructed. Although homeowners have asserted many claims for mold-caused damages, few have reached trial and yielded verdicts.

In this case, the Achin family sought in excess of $20 million (reduced to $5 million at trial) for various personal injuries. Prior to trial, the court eliminated many of their claims, finding that the general medical community has rejected any link between household mold and injuries other than typical allergic reactions in otherwise healthy people. After trial, the jury returned its verdict that Shea was not negligent, made no misrepresentations of fact and did not cause any harm to plaintiffs. The jury further found that Shea acted reasonably in responding to the family's initial warranty requests, and that the claims asserted were wholly unrelated to any actions of Shea. Several jurors commented post-trial that they thought Shea had done everything it could to work with the Achin family and avoid the litigation that transpired.

After the trial, several jurors expressed doubt with the plaintiffs' claims, and found their actions to be highly suspicious. "The jurors expressed their doubts that a little mold in a wall cavity could cause the harm that plaintiffs claimed," said defense attorney Dan Berman. Mr. Berman, a founding partner in the Los Angeles office of Wood, , Henning & Berman stated that, "This trial demonstrates that when all testimony comes into evidence, juries are able to separate the hype related to mold claims from reality."

Les , President of Shea Homes Southern California stated, "We are gratified by the jury's verdict. We would have preferred to have resolved this matter outside the court system, but we are prepared to defend the quality of our construction when necessary."

West Hollywood lawyer Witzer and Balaban represented the Achin family. Dan Berman and Stacey Blank represented Shea Homes Limited Partnership at trial, along with Schoenberg during the pre-trial motions.

[Guest guest]

It says in fact "mold is likely to sensitize and produce allergic reactions in allergic individuals", no use of the word "typical".

The problem is that people (and most jurors) are pre-conditioned to believe that "allergies" can be nothing more than hay fever and the sniffles. This is flat out incorrect. Even the victims such as yourself are unwilling to acknowledge that their symptoms could be explainable by immune responses (allergies) because it doesn't sound as dire as "toxic mold". Most of us in this community know better, but the general public does not.

D. Carlson, CIAQC, CMRS

Liesch Associates, Inc.

Steve,

Very well articulated, as usual. This is true in my experience as well. If there were truly a potential for an exposure that constituted a toxic dose, mold assessors and remediators would be expected to be at particularly high risk. There seems to be a lack of recognition on the part of some that the ranks of these occupations (which includes many of us on this List) are not being decimated by mold toxins. I know of a few professionals who have become sensitized. Indeed, the allergic effects are plenty bad enough and they can vary widely in manifested inflammatory and immune-related symptoms from one individual to another.

Apparently, there is an immune cascade effect, akin to an autoimmune reaction, that certain individuals with genetic susceptibility are experiencing when exposed to some "biotoxins". One of the genetic susceptibility markers according to some research (esp. Dr. Ritchie Shoemaker) is HLA-DR.

The dose makes the poison only in the sense that if there is no dose, there is no poison. Think about severe peanut allergies and the validity of the term "peanut toxins". The individual genetic susceptibility factor is clearly the key to assessing health effects attributed to inhalation of airborne mycotoxins. These purported mycotoxicosis-via-inhalation cases are extremely rare while mold and other bioaerosol allergies are quite prevalent. This is all perfectly consistent with mold being a known health risk and why we want to prevent and remediate mold contamination in indoor environments.

I agree that the use of scientific information from any source by attorneys on either side is another matter altogether and that there have been breaches of ethics (and science) all around. Sharon has caught some defense whores with their pants down. Good going, Sharon. Nice research and investigative reporting, too. They definitely messed with the wrong person when they SLAPPed her with a suit.

The ACOEM paper talks about the potential for exposure to a toxic dose of mycotoxins, not the immune effects. I don't ever recall seeing a statement anywhere that said that "all human illness from mold is not plausible" except in Sharon's posts.

Steve Temes

[Guest guest]

Mr. ,

I will say that Sharon is doing her best to get " so-called "

professionals to pay attention and lift their heads from the money

trough. She may not be as educated as some who argue but, she has

experience and most do not.

SLIPPERY SLOPE: The two rat studies (intratracheal installation of

Stachybotrys) done by Dr. Rao at Harvard with Harriet Burge as a co-

author show that mycotoxins and nothing else are responsible for the

health outcomes of the rats. Please read BOTH studies.

COMPLEX QUESTION: How can dose be derived from those studies since

the spores were counted with a hemocytometer at 200X magnification?

Most environmental labs use 400X magnification as the minimum level

of microscopy for mold. How much mycelial matter and fragments of

spores or conidia can you see at 200X magnification?

FALSE DILEMNA: Most of the medical community points to allergic

reactions that can be as severe as RADS for the lungs. They point

to common allergies like irritations of the skin, eyes, nose and

throat. I am amazed everyone is still behind the curve with hormone

disregulation.

CASE IN POINT: A patient of Dr. Ritchie Shoemaker has the usual

high leptin levels and low aMSH (alpha melanocyte stimulating

hormone) levels because leptin is not being converted into aMSH.

aMSH is a precursor to melatonin which is necessary for proper sleep

and works in conjuction with IGF (insulin growth hormone) or HGH

(human growth hormone) for the sake of argument. Melatonin is

supposed to be higher at night so we can sleep and lower in the day

when serotonin (carbohydrate craving) is higher all due to light

exposure - alledgedly.

This Shoemaker patient has a history of diabetes in the family tree

like many of Shoemaker's patients, along with sleep apnea. When the

Shoemaker patient takes melatonin pills, he/she can sleep like a

baby. If the melatonin is not taken, sleep is difficult at best.

The mold exposure came from an office building rented by the federal

government. These problems did not exist before exposure.

This patient verifies Dr. Ritchie Shoemaker's theories by the need

for melatonin to sleep.

I'm asking for the " so-called " professionals to think before they

advertise their " alledged " understanding of environmental illnesses.

Regards,

Greg Weatherman

aerobioLogical Solutions Inc.

Arlington VA 22202

gw@...

**********************************************************

>

> Dear Group--

>

> I believe the following very closely describes the non-scientific

approach Sharon takes when she communicates with this list. This is

in addition of the underlying logical fallacies she uses in her

arguments, such as :

>

> False Dilemma: two choices are given when in fact there are three

options

>

> From Ignorance: because something is not known to be true, it is

assumed to be false

>

> Slippery Slope: a series of increasingly unacceptable consequences

is drawn

>

> Complex Question: two unrelated points are conjoined as a single

proposition

>

> Neveretheles, her " advocacy " adds a bit of excitement to this list.

>

>

> F. , Ph.D., MPH, D(ABMM), CIC, HEM

> Microbial Epidemiologist

> The Children's Hospital

> 1056 East 19th Ave. B-276

> Denver, Colorado 80218

>

> This excerpt is from Survivor Psychology: The Dark Side of a

Mental Health Mission by , pp. 133-134. Upton Books and

SIRS Mandarin, Boca Raton, FL. Copyright © 1995. Reprinted by

permission. All rights reserved.

>

> The entire system of survivor psychology and recovery culture

psychology is built on " true believer " logic. True believer logic is

defined by Goldberg, author of When Wish Replaces Thought, as

a system of fallacious and subjective arguments which " have no

logical consistency, are discordant with the empirical evidence, and

either fail to explain that which they claim to explain or offer

explanations of that which does not exist. " This is the definition I

have used for survivor logic as well.

>

> The basic principles of survivor logic are outlined below:

>

> Principle 1-Personalize the issues.

> The arguments are based on emotionally charged statements and " I

messages. "

>

> Principle 2-The opposing argument becomes the proof.

> Hard evidence in support of the opposing viewpoint, or the lack of

evidence for the belief is used as " evidence " and strengthens

beliefs instead of challenging them.

>

> Principle 3-When confronted with logical discrepancies, revert to

God, society or morality.

> When the evidence is stacked against the beliefs and the true

believer is backed into a corner, they retreat behind their

preferred social control modality-religion, political rhetoric and

moral crusade monologues.

>

> Principle 4-When in doubt, abort further interaction or

exploration of the issues by playing " Ain't it Awful " games while

stepping up the intensity.

> When the true believer is backed into a corner, he or she often

reverts to a favorite ideological or abortive interaction game (or

plays all of them sequentially): God's Will; The Oppressor and the

Oppressed; The Power of Evil and What Happens When Good People Do

Nothing; Social Decline and Moral Decay; This Hurts Me as Much as It

Hurts You; I Know This Is Hard to Believe-I Used to Be a Skeptic

Too!; The Experts Know Best; Suicide; Revictimization; No Motive;

and I'm Only Trying to Help.

>

> Principle 5-When all else fails, bring up denial and conspiracy

theories.

>

>

> Re: Serious Breach of Ethics within the AIHA

>

> Steve,

>

> Can you cite for me the scientific foundation for the following

statement

> within the ACOEM mold statement? I will give you a hint, it was

picked paper

> of the year, 2000 by the AIHA. And....there is absolutely NO

scientific paper

> that makes the same conclusion.

>

> " Levels of exposure in the indoor environment, dose-response

data in

>

> animals, and dose-rate considerations suggest that delivery by the

> inhalation route of a toxic dose of mycotoxins in the indoor

environment is

> highly unlikely at best, even for the hypothetically most

vulnerable

> subpopulations. "

>

> Can you tell me how this statement within this document may still

be

> impacting the misinformation over the science?

>

> I am working in today's world over this matter. And before the

true science

> can accurately move forward, junk like this needs to be brought

to light for

> what it really is. Its a defense argument meant for the

courtroom. It has no

> scientific foundation and it has negatively impacted, and

continues to

> negatively impact the scientific understanding as it stands today.

>

> So, one has to go back and correct the mistakes of yesterday in

order to

> move forward with tomorrow. Sorry if I am boring you, but there

are a lot of

> lives at stake here.

>

> Sharon

>

>

>

>

>

[Guest guest]

Sharon is an advocate and not a scientifically based professional. She also has issues associated with family illnesses that she associates with mould. As such she is very biased in her views. No facts will change her mind as she is a true believer. She really should not be allowed to continue using this list as her personal soundingboard.

Dr. ,

I find this above statement to be quite insulting. Not to toot my own horn, but I have more to raise the national awareness of the legitimacy of these illnesses than most. I have moderated US Senate Staff Briefing. I have changed Conflict Interest policies within major medical associations. I have brought many physicians and researchers together to share their information in a new light. But mostly what I have done is to use my professional background to research and demonstrate how the marketing of a non-scientific concept has been carried out and used as a weapon against the ill.

And I would like to state right here and now, what I am discussing is far more scienfically founded than what you are attempting to state. What YOU, as a self professed professional, are attempting to argue is that one can take a rodent study, apply some extrapolated math and deduce all human illness is not plausible from mycotoxin exposure. Read your own words, then think about how ridiculous that concept really is. And then read the Chapter on Mycotoxins within the Damp Indoor Spaces and Mold Report. Tell me from there, who between the two of us is more adeptly discussing true scientific understanding of the matter.

Sharon

[Guest guest]

Greg—

Here is my response (in underline):

Mr. ,

I will say that Sharon is doing her best to get

" so-called "

professionals to pay attention and

lift their heads from the money

trough. She may not be as

educated as some who argue but, she has

experience and most do not.

Sharon is an advocate and

not a scientifically based professional. She also has issues associated with

family illnesses that she associates with mould. As such she is very biased in

her views. No facts will change her mind as she is a true believer. She really

should not be allowed to continue using this list as her personal soundingboard.

SLIPPERY SLOPE: The two rat

studies (intratracheal installation of

Stachybotrys) done by Dr. Rao at

Harvard with Harriet Burge as a co- author show that mycotoxins and nothing else are responsible for the

health outcomes of

the rats.

Please read BOTH studies.

I have read both studies. I have only one technical problem

with the studies and that is the use of methanol extracted spores. Methanol is

a good fixative and denatures proteins. The authors state that “Some glucans,

extracellular polysaccharides, lipids, and allergens, which can also cause inflammation,

may have been extracted or altered by the methanol. In addition, the methanol

treatment sterilized the spores. Thus, the lack of effects associated with the

methanol-extracted S. chartarum spores

cannot be attributed solely to the absence of mycotoxins.” These studies

are a good start.

COMPLEX QUESTION: How can dose

be derived from those studies since

the spores were counted with a hemocytometer

at 200X magnification?

Most environmental labs use 400X

magnification as the minimum level

of microscopy for mold. How

much mycelial matter and fragments of

spores or conidia can you see at

200X magnification?

It is easy to count

S. chartarum spores at 200X

magnification.

FALSE DILEMNA: Most of the

medical community points to allergic

reactions that can be as severe as

RADS for the lungs. They point

to common allergies like irritations

of the skin, eyes, nose and

throat. I am amazed everyone is still behind the curve with

hormone

disregulation.

There are many

diseases associated with hormone disregulation.

CASE IN POINT: A patient of

Dr. Ritchie Shoemaker has the usual

high leptin levels and low aMSH

(alpha melanocyte stimulating

hormone) levels because leptin is

not being converted into aMSH.

aMSH is a precursor to melatonin

which is necessary for proper sleep

and works in conjuction with IGF

(insulin growth hormone) or HGH

(human growth hormone) for the sake

of argument. Melatonin is

supposed to be higher at night so we

can sleep and lower in the day

when serotonin (carbohydrate

craving) is higher all due to light

exposure - alledgedly.

This Shoemaker patient has a history

of diabetes in the family tree

like many of Shoemaker's patients,

along with sleep apnea. When the

Shoemaker patient takes melatonin

pills, he/she can sleep like a

baby. If the melatonin is not

taken, sleep is difficult at best.

The mold exposure

came from an office building rented by the federal

government. These problems did not exist before exposure.

This patient

verifies Dr. Ritchie Shoemaker's theories by the need

for melatonin to

sleep.

Your very confusing

point is what?

Please see the following

web site (http://www.chronicneurotoxins.com/)

for an overview of Dr. Shoemaker’s bio-toxin theories. He is not exactly practicing

mainstream medicine. Please see the FDA warning letter to Dr. Shoemaker. ( http://www.fda.gov/foi/warning_letters/g4710d.htm)

I'm asking for the

" so-called " professionals to think before they

advertise their

" alledged " understanding of environmental illnesses.

I do not advertise

at all. Your company is actively involved in promoting the notion that mould remediation

is essential. You are also a promoter of Dr. Shoemaker’s ideas.

Dr. Burge knows

more about environmental illness than you or Dr. Shoemaker will ever know.

Cheers,

F. , Ph.D., MPH, D(ABMM), CIC, HEM

Microbial Epidemiologist

Children's Hospital

Department of Epidemiology B-276

1056 East 19th Ave.

Denver,

Colorado 80218

[Guest guest]

,

My posting was really addressed to everyone at large who reads this chatboard and holds themselves to be professionals for hire to the public in need.

I will address some of your points.

>> Greg-> > > > Here is my response (in underline):> Sharon is an advocate and not a scientifically based professional. She> also has issues associated with family illnesses that she associates> with mould. As such she is very biased in her views. No facts will> change her mind as she is a true believer. She really should not be> allowed to continue using this list as her personal soundingboard.

She raises good points even if she is not very scientific but, she is trying and learning. I see professionals make ludicrous statements all the time and nobody gives them the scarlet letter of "unscientific" like those Globaltox or Veritox folks deserve. I saw Sharon Kramer ask several questions at the Surgeon General's conference in Washington DC.

As far as a sounding board, I think she should keep doing what she is doing so long as she is "raising the level of conscienceness" - bad pun intended. This could also be an unofficial IAQA slogan for this year's conference in Nashville.

> SLIPPERY SLOPE: The two rat studies (intratracheal installation of > > Stachybotrys) done by Dr. Rao at Harvard with Harriet Burge as a co-> author show that mycotoxins and nothing else are responsible for the > > health outcomes of the rats. Please read BOTH studies.> > > > I have read both studies. I have only one technical problem with the> studies and that is the use of methanol extracted spores. Methanol is a> good fixative and denatures proteins. The authors state that "Some> glucans, extracellular polysaccharides, lipids, and allergens, which can> also cause inflammation, may have been extracted or altered by the> methanol. In addition, the methanol treatment sterilized the spores.> Thus, the lack of effects associated with the methanol-extracted S.> chartarum spores cannot be attributed solely to the absence of> mycotoxins." These studies are a good start.

POINT TAKEN WITH COMMENTS: There are some animal studies cited by Dr. Ritchie Shoemaker that show rats given lethal doses of fumonisin B (mycotoxin from Fusarium). One group was given fumonisin and all died. One group was given fumonisin B and cholestyramine and lived just like the control group. Glucans, extracellular polysaccharides, lipids, and allergens had nothing to do with the results. I would give a citation but, you need to go reread Dr. Shoemaker's papers.

His patients usually show real progress as they take cholestyramine for 2 weeks or more. I know some of his patients and the results are night and day. This medication is listed in the EPA medical handbook for removing neurotoxins like chlorpyrifos. Dr. Shoemaker was documented on the Discovery Health TV show for treating patients for pfisteria. He is used the same cholestyramine for that problems too. He was the runner-up for national MD of the year after that year. Curiously, he had a microscope but sends samples to microbiologists for their opinions. He does not claim to be a microbiologist or mycologist.

> COMPLEX QUESTION: How can dose be derived from those studies since > > the spores were counted with a hemocytometer at 200X magnification? > > Most environmental labs use 400X magnification as the minimum level > > of microscopy for mold. How much mycelial matter and fragments of > > spores or conidia can you see at 200X magnification?> > > > It is easy to count S. chartarum spores at 200X magnification.

See above for highlighed question not answered. Then go to the Texas Tech Study where they used an electron microscope for Stachybotrys particles (submicron) and showed the presence of mycotoxins. Ever wonder why qPCR is so much more reliable than spore traps? Ever wonder why there are more complaints after remediation than before? Maybe those HEPA filtered air cleaners are not doing the job all the time for all people.> > > > FALSE DILEMNA: Most of the medical community points to allergic > > reactions that can be as severe as RADS for the lungs. They point > > to common allergies like irritations of the skin, eyes, nose and > > throat. I am amazed everyone is still behind the curve with hormone > > disregulation.> > > > There are many diseases associated with hormone disregulation.>

Typical response for misdirection because the statement goes nowhere just like an ancient sophist. I keep a copy of The dialogues of Plato on my bookshelf.

Here is a medical wonder: Certain symptons can lead an MD to diagnose asthma even though there is no "allegedly" known cause of asthma. The moment a cause is known for a patient, the condition is then diagnosed as RADS. Medicine is littered with diagnoses with no known etiology or cause. MDs pump the patients full of drugs for the symptoms but fail to identify the cause and remove the source. If we claim the mantra of "source removal" for mold and IAQ, why do MDs get to "spray and go" - literally.

A few years ago, MDs were called quacks for suggesting agent orange exposure can lead to adult onset diabetes or type 2 diabetes. Now, the tide had shifted and the VA is investigating why so many Vietnam veterans have diabetes compared to any other subpopulations.

> > CASE IN POINT: A patient of Dr. Ritchie Shoemaker has the usual > > high leptin levels and low aMSH (alpha melanocyte stimulating > > hormone) levels because leptin is not being converted into aMSH. > > aMSH is a precursor to melatonin which is necessary for proper sleep > > and works in conjuction with IGF (insulin growth hormone) or HGH > > (human growth hormone) for the sake of argument. Melatonin is > > supposed to be higher at night so we can sleep and lower in the day > > when serotonin (carbohydrate craving) is higher all due to light > > exposure - alledgedly.> > > > This Shoemaker patient has a history of diabetes in the family tree > > like many of Shoemaker's patients, along with sleep apnea. When the > > Shoemaker patient takes melatonin pills, he/she can sleep like a > > baby. If the melatonin is not taken, sleep is difficult at best. > > The mold exposure came from an office building rented by the federal > > government. These problems did not exist before exposure.> > > > This patient verifies Dr. Ritchie Shoemaker's theories by the need > > for melatonin to sleep.> > > > Your very confusing point is what?> > > > Please see the following web site (http://www.chronicneurotoxins.com/)> for an overview of Dr. Shoemaker's bio-toxin theories. He is not exactly> practicing mainstream medicine. Please see the FDA warning letter to Dr.> Shoemaker. ( http://www.fda.gov/foi/warning_letters/g4710d.htm> <http://www.fda.gov/foi/warning_letters/g4710d.htm> )

I'm aware of the situation and you can hear the same story said in court and depositions: He gave a prescription for a product that is the same for dogs and people except the product literature insert is different. A mistake was made by the manufacturer not Dr. Shoemaker.> > > > I'm asking for the "so-called" professionals to think before they > > advertise their "alledged" understanding of environmental illnesses.> > > > I do not advertise at all. Your company is actively involved in> promoting the notion that mould remediation is essential. You are also a> promoter of Dr. Shoemaker's ideas.> > > > Dr. Burge knows more about environmental illness than you or Dr.> Shoemaker will ever know.

Dr. Burge needs to stop talking about health effects as if she is the last word on medicine. I do not hold a medical degree. Here is some easy information to support Dr. Shoemaker's theories and refute Harriet Burge's attempts to hold the floor a little longer than she should in a convention where she has little standing.

1. Patients must be screened for HLA genotypes before they are given "cyclosporin" to help recieve an organ like a liver or kidney. If they have an HLA genotype, they will develop type 2 diabetes or adult onset diabetes from the cylosporin medication (according to e-medicine). Cyclosporin is a naturally occuring mycotoxin produced by more than one form of mold.

2. A State researcher has shown an association between HLA genotypes and Gulf War syndrome. (Just interesting for thought.)

Dr. Shoemaker had thousands of patients and tests for allergic reactions like Ig-E. His data says their is no correlation for allergies but the effects are neurotoxic - immune system and nervous system. If you know how corticosteriods work, you should be able to figure it out - really.

On a more positive note: I have never seen Dr. Chin Yang or Dr. Steve Vespers claim to know medicine. They point to probabilities that need to be investigated. They are each peers to Harriet Burge.

I also note that Dr. Harriet K. Amman, toxicologist, put her name on Dr. Shoemaker's paper. She wrote the chapter on mycotoxins in the ACGIH book, Bioaerosols: Assessment & Control (1999). She obviously disagrees. She is a toxicologist not a microbiologist. Call me crazy but, I will go with the toxicologist. I'm sure Harriet Burge is a wonderful microbiologist and did a lot of research for allergic responses in Florida but, that is all. I would trust a veterinarian for race horses before I trusted a microbiologist when it comes to health effects.

Final note: Any paper that contains the name, Dr. Gots M.D., is suspect. I saw the NBC Dateline investigation where he and his firm were implicated in medical examiner services for State Farm Insurance involving medical claims from car wrecks. The paper cited by Phil Havics is dead in the water just because Dr. Gots is a co-author. I said it before today; Dr. Gots does his literature reviews at the 7-eleven comic book section.

Please don't take my comments personally. I'm doing my part to raise the level of conscienceness.

Regards,

Greg Weatherman

Arlington VA 22202

gw@...> > > > Cheers,> > > > > > > > > > F. , Ph.D., MPH, D(ABMM), CIC, HEM> > Microbial Epidemiologist> > Children's Hospital> > Department of Epidemiology B-276> > 1056 East 19th Ave.> > Denver, Colorado 80218> > > > > > >

[Guest guest]

Greg—

I have studied the web site of Dr

Shoemaker (aka “The Mold Warior” from past years).

This site ( http://www.chronicneurotoxins.com/index.cfm

) is full of pseudo-medical claims. I will let the reader decide for

themselves.

F.

, Ph.D., MPH, D(ABMM)

Microbial

Epidemiologist

Children's

Hospital

Department

of Epidemiology B-276

1056

East 19th Ave.

Denver, Colorado 80218

Re: Serious

Breach of Ethics within the AIHA

,

My posting was really addressed to

everyone at large who reads this chatboard and holds themselves to be

professionals for hire to the public in need.

I will address some of your points.

>

> Greg-

>

>

>

> Here is my response (in underline):

> Sharon is an advocate and not a scientifically based

professional. She

> also has issues associated with family illnesses that she associates

> with mould. As such she is very biased in her views. No facts will

> change her mind as she is a true believer. She really should not be

> allowed to continue using this list as her personal soundingboard.

She raises good points even

if she is not very scientific but, she is trying and learning. I

see professionals make ludicrous statements all the time and nobody gives them

the scarlet letter of " unscientific " like those Globaltox or Veritox

folks deserve. I saw Sharon Kramer ask several questions at the

Surgeon General's conference in Washington DC.

As far as a sounding board, I think

she should keep doing what she is doing so long as she is " raising the

level of conscienceness " - bad pun intended. This could also

be an unofficial IAQA slogan for this year's conference in Nashville.

> SLIPPERY SLOPE: The two rat studies

(intratracheal installation of

>

> Stachybotrys) done by Dr. Rao at Harvard with Harriet Burge as a co-

> author show that mycotoxins and nothing else are responsible for the

>

> health outcomes of the rats. Please read BOTH studies.

>

>

>

> I have read both studies. I have only one technical problem with the

> studies and that is the use of methanol extracted spores. Methanol is a

> good fixative and denatures proteins. The authors state that " Some

> glucans, extracellular polysaccharides, lipids, and allergens, which can

> also cause inflammation, may have been extracted or altered by the

> methanol. In addition, the methanol treatment sterilized the spores.

> Thus, the lack of effects associated with the methanol-extracted S.

> chartarum spores cannot be attributed solely to the absence of

> mycotoxins. " These studies are a good start.

POINT TAKEN WITH COMMENTS: There

are some animal studies cited by Dr. Ritchie Shoemaker that show rats given

lethal doses of fumonisin B (mycotoxin from Fusarium). One group was

given fumonisin and all died. One group was given fumonisin B and

cholestyramine and lived just like the control group. Glucans,

extracellular polysaccharides, lipids, and allergens had nothing to do with the

results. I would give a citation but, you need to go reread Dr.

Shoemaker's papers.

His patients usually show real progress

as they take cholestyramine for 2 weeks or more. I know some of his

patients and the results are night and day. This medication is

listed in the EPA medical handbook for removing neurotoxins like

chlorpyrifos. Dr. Shoemaker was documented on the Discovery Health TV

show for treating patients for pfisteria. He is used the same

cholestyramine for that problems too. He was the runner-up for national

MD of the year after that year. Curiously, he had a microscope but sends

samples to microbiologists for their opinions. He does not

claim to be a microbiologist or mycologist.

> COMPLEX QUESTION: How can dose be derived from

those studies since

>

> the spores were counted with a hemocytometer at 200X magnification?

>

> Most environmental labs use 400X magnification as the minimum level

>

> of microscopy for mold. How

much mycelial matter and fragments of

>

> spores or conidia can you see at 200X magnification?

>

>

>

> It is easy to count S. chartarum spores at 200X magnification.

See above for highlighed question not

answered. Then go to the Texas Tech Study where they used an electron

microscope for Stachybotrys particles (submicron) and showed the presence of

mycotoxins. Ever wonder why qPCR is so much more reliable than spore

traps? Ever wonder why there are more complaints after remediation than

before? Maybe those HEPA filtered air cleaners are not doing the job all

the time for all people.

>

>

>

> FALSE DILEMNA: Most of the medical community points to allergic

>

> reactions that can be as severe as RADS for the lungs. They point

>

> to common allergies like irritations of the skin, eyes, nose and

>

> throat. I am amazed everyone is still behind the curve with hormone

>

> disregulation.

>

>

>

> There are many diseases associated with hormone disregulation.

>

Typical response for

misdirection because the statement goes nowhere just like an ancient

sophist. I keep a copy of The dialogues of Plato on my bookshelf.

Here is a medical wonder: Certain

symptons can lead an MD to diagnose asthma even though there is

no " allegedly " known cause of asthma. The moment a

cause is known for a patient, the condition is then diagnosed as

RADS. Medicine is littered with diagnoses with no known etiology

or cause. MDs pump the patients full of drugs for the symptoms

but fail to identify the cause and remove the source. If we

claim the mantra of " source removal " for mold and IAQ, why do

MDs get to " spray and go " - literally.

A few years ago, MDs were called quacks

for suggesting agent orange exposure can lead to adult onset diabetes or

type 2 diabetes. Now, the tide had shifted and the VA is investigating

why so many Vietnam veterans have diabetes compared to

any other subpopulations.

>

> CASE IN POINT: A patient of Dr. Ritchie Shoemaker has the usual

>

> high leptin levels and low aMSH (alpha melanocyte stimulating

>

> hormone) levels because leptin is not being converted into aMSH.

>

> aMSH is a precursor to melatonin which is necessary for proper sleep

>

> and works in conjuction with IGF (insulin growth hormone) or HGH

>

> (human growth hormone) for the sake of argument. Melatonin is

>

> supposed to be higher at night so we can sleep and lower in the day

>

> when serotonin (carbohydrate craving) is higher all due to light

>

> exposure - alledgedly.

>

>

>

> This Shoemaker patient has a history of diabetes in the family tree

>

> like many of Shoemaker's patients, along with sleep apnea. When the

>

> Shoemaker patient takes melatonin pills, he/she can sleep like a

>

> baby. If the melatonin is not taken, sleep is difficult at best.

>

> The mold exposure came from an office building rented by the federal

>

> government. These problems did not exist before exposure.

>

>

>

> This patient verifies Dr. Ritchie Shoemaker's theories by the need

>

> for melatonin to sleep.

>

>

>

> Your very confusing point is what?

>

>

>

> Please see the following web site (http://www.chronicneurotoxins.com/)

> for an overview of Dr. Shoemaker's bio-toxin theories. He is not exactly

> practicing mainstream medicine. Please see the FDA warning letter to Dr.

> Shoemaker. ( http://www.fda.gov/foi/warning_letters/g4710d.htm

> <http://www.fda.gov/foi/warning_letters/g4710d.htm> )

I'm aware of the situation and you can

hear the same story said in court and depositions: He gave a prescription

for a product that is the same for dogs and people except the product

literature insert is different. A mistake was made by the manufacturer

not Dr. Shoemaker.

>

>

>

> I'm asking for the " so-called " professionals to think before

they

>

> advertise their " alledged " understanding of environmental

illnesses.

>

>

>

> I do not advertise at all. Your company is actively involved in

> promoting the notion that mould remediation is essential. You are also a

> promoter of Dr. Shoemaker's ideas.

>

>

>

> Dr. Burge knows more about environmental illness than you or Dr.

> Shoemaker will ever know.

Dr. Burge needs to stop talking about

health effects as if she is the last word on medicine. I do not hold a

medical degree. Here is some easy information to support Dr. Shoemaker's

theories and refute Harriet Burge's attempts to hold the floor a little longer

than she should in a convention where she has little standing.

1. Patients must be screened for

HLA genotypes before they are given " cyclosporin " to help recieve an

organ like a liver or kidney. If they have an HLA genotype, they will

develop type 2 diabetes or adult onset diabetes from the cylosporin medication

(according to e-medicine). Cyclosporin is a naturally occuring mycotoxin

produced by more than one form of mold.

2. A State researcher has

shown an association between HLA genotypes and Gulf War syndrome. (Just

interesting for thought.)

Dr. Shoemaker had thousands of patients

and tests for allergic reactions like Ig-E. His data says their is no

correlation for allergies but the effects are neurotoxic - immune system and

nervous system. If you know how corticosteriods work, you should be

able to figure it out - really.

On a more positive note: I have

never seen Dr. Chin Yang or Dr. Steve Vespers claim to know medicine.

They point to probabilities that need to be investigated. They are each

peers to Harriet Burge.

I also note that Dr. Harriet K. Amman,

toxicologist, put her name on Dr. Shoemaker's paper. She wrote the

chapter on mycotoxins in the ACGIH book, Bioaerosols: Assessment &

Control (1999). She obviously disagrees. She is a toxicologist

not a microbiologist. Call me crazy but, I will go with the

toxicologist. I'm sure Harriet Burge is a wonderful

microbiologist and did a lot of research for allergic responses in Florida but, that is all. I

would trust a veterinarian for race horses before I trusted a microbiologist

when it comes to health effects.

Final note: Any paper that

contains the name, Dr. Gots M.D., is suspect. I saw the NBC

Dateline investigation where he and his firm were implicated in medical

examiner services for State Farm Insurance involving medical claims from car wrecks.

The paper cited by Phil Havics is dead in the water just because Dr. Gots is a

co-author. I said it before today; Dr. Gots does his literature

reviews at the 7-eleven comic book section.

Please don't take my comments

personally. I'm doing my part to raise the level of conscienceness.

Regards,

Greg Weatherman

Arlington VA 22202

gw@...

>

>

>

> Cheers,

>

>

>

>

>

>

>

>

>

> F. , Ph.D., MPH, D(ABMM), CIC, HEM

>

> Microbial Epidemiologist

>

> Children's Hospital

>

> Department of Epidemiology B-276

>

> 1056 East 19th Ave.

>

> Denver, Colorado 80218

>

>

>

>

>

>

>

[Guest guest]

Greg:

Who is "Phil Havics " ?

and the paper has Gots as the last author - probably a necessity of association than actual participation.

Tony

........................................................................... "Tony" Havics, CHMM, CIH, PEpH2, LLCPO Box 34140Indianapolis, IN 46234 cell90% of Risk Management is knowing where to place the decimal point...any consultant can give you the other 10%â„ This message is from pH2. This message and any attachments may contain legally privileged or confidential information, and are intended only for the individual or entity identified above as the addressee. If you are not the addressee, or if this message has been addressed to you in error, you are not authorized to read, copy, or distribute this message and any attachments, and we ask that you please delete this message and attachments (including all copies) and notify the sender by return e-mail or by phone at . Delivery of this message and any attachments to any person other than the intended recipient(s) is not intended in any way to waive confidentiality or a privilege. All personal messages express views only of the sender, which are not to be attributed to pH2 and may not be copied or distributed without this statement.

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of , Sent: Tuesday, September 12, 2006 3:35 PMTo: iequality Subject: RE: Re: Serious Breach of Ethics within the AIHA

Greg—

I have studied the web site of Dr Shoemaker (aka “The Mold Warior†from past years).

This site ( http://www.chronicneurotoxins.com/index.cfm ) is full of pseudo-medical claims. I will let the reader decide for themselves.

F. , Ph.D., MPH, D(ABMM)

Microbial Epidemiologist

Children's Hospital

Department of Epidemiology B-276

1056 East 19th Ave.

Denver, Colorado 80218

-----Original Message-----From: iequality [mailto:iequality ] On Behalf Of Greg WeathermanSent: Tuesday, September 12, 2006 8:14 AMTo: iequality Subject: Re: Serious Breach of Ethics within the AIHA

,

My posting was really addressed to everyone at large who reads this chatboard and holds themselves to be professionals for hire to the public in need.

I will address some of your points.

>> Greg-> > > > Here is my response (in underline):> Sharon is an advocate and not a scientifically based professional. She> also has issues associated with family illnesses that she associates> with mould. As such she is very biased in her views. No facts will> change her mind as she is a true believer. She really should not be> allowed to continue using this list as her personal soundingboard.

She raises good points even if she is not very scientific but, she is trying and learning. I see professionals make ludicrous statements all the time and nobody gives them the scarlet letter of "unscientific" like those Globaltox or Veritox folks deserve. I saw Sharon Kramer ask several questions at the Surgeon General's conference in Washington DC.

As far as a sounding board, I think she should keep doing what she is doing so long as she is "raising the level of conscienceness" - bad pun intended. This could also be an unofficial IAQA slogan for this year's conference in Nashville.

> SLIPPERY SLOPE: The two rat studies (intratracheal installation of > > Stachybotrys) done by Dr. Rao at Harvard with Harriet Burge as a co-> author show that mycotoxins and nothing else are responsible for the > > health outcomes of the rats. Please read BOTH studies.> > > > I have read both studies. I have only one technical problem with the> studies and that is the use of methanol extracted spores. Methanol is a> good fixative and denatures proteins. The authors state that "Some> glucans, extracellular polysaccharides, lipids, and allergens, which can> also cause inflammation, may have been extracted or altered by the> methanol. In addition, the methanol treatment sterilized the spores.> Thus, the lack of effects associated with the methanol-extracted S.> chartarum spores cannot be attributed solely to the absence of> mycotoxins." These studies are a good start.

POINT TAKEN WITH COMMENTS: There are some animal studies cited by Dr. Ritchie Shoemaker that show rats given lethal doses of fumonisin B (mycotoxin from Fusarium). One group was given fumonisin and all died. One group was given fumonisin B and cholestyramine and lived just like the control group. Glucans, extracellular polysaccharides, lipids, and allergens had nothing to do with the results. I would give a citation but, you need to go reread Dr. Shoemaker's papers.

His patients usually show real progress as they take cholestyramine for 2 weeks or more. I know some of his patients and the results are night and day. This medication is listed in the EPA medical handbook for removing neurotoxins like chlorpyrifos. Dr. Shoemaker was documented on the Discovery Health TV show for treating patients for pfisteria. He is used the same cholestyramine for that problems too. He was the runner-up for national MD of the year after that year. Curiously, he had a microscope but sends samples to microbiologists for their opinions. He does not claim to be a microbiologist or mycologist.

> COMPLEX QUESTION: How can dose be derived from those studies since > > the spores were counted with a hemocytometer at 200X magnification? > > Most environmental labs use 400X magnification as the minimum level > > of microscopy for mold. How much mycelial matter and fragments of > > spores or conidia can you see at 200X magnification?> > > > It is easy to count S. chartarum spores at 200X magnification.

See above for highlighed question not answered. Then go to the Texas Tech Study where they used an electron microscope for Stachybotrys particles (submicron) and showed the presence of mycotoxins. Ever wonder why qPCR is so much more reliable than spore traps? Ever wonder why there are more complaints after remediation than before? Maybe those HEPA filtered air cleaners are not doing the job all the time for all people.> > > > FALSE DILEMNA: Most of the medical community points to allergic > > reactions that can be as severe as RADS for the lungs. They point > > to common allergies like irritations of the skin, eyes, nose and > > throat. I am amazed everyone is still behind the curve with hormone > > disregulation.> > > > There are many diseases associated with hormone disregulation.>

Typical response for misdirection because the statement goes nowhere just like an ancient sophist. I keep a copy of The dialogues of Plato on my bookshelf.

Here is a medical wonder: Certain symptons can lead an MD to diagnose asthma even though there is no "allegedly" known cause of asthma. The moment a cause is known for a patient, the condition is then diagnosed as RADS. Medicine is littered with diagnoses with no known etiology or cause. MDs pump the patients full of drugs for the symptoms but fail to identify the cause and remove the source. If we claim the mantra of "source removal" for mold and IAQ, why do MDs get to "spray and go" - literally.

A few years ago, MDs were called quacks for suggesting agent orange exposure can lead to adult onset diabetes or type 2 diabetes. Now, the tide had shifted and the VA is investigating why so many Vietnam veterans have diabetes compared to any other subpopulations.

> > CASE IN POINT: A patient of Dr. Ritchie Shoemaker has the usual > > high leptin levels and low aMSH (alpha melanocyte stimulating > > hormone) levels because leptin is not being converted into aMSH. > > aMSH is a precursor to melatonin which is necessary for proper sleep > > and works in conjuction with IGF (insulin growth hormone) or HGH > > (human growth hormone) for the sake of argument. Melatonin is > > supposed to be higher at night so we can sleep and lower in the day > > when serotonin (carbohydrate craving) is higher all due to light > > exposure - alledgedly.> > > > This Shoemaker patient has a history of diabetes in the family tree > > like many of Shoemaker's patients, along with sleep apnea. When the > > Shoemaker patient takes melatonin pills, he/she can sleep like a > > baby. If the melatonin is not taken, sleep is difficult at best. > > The mold exposure came from an office building rented by the federal > > government. These problems did not exist before exposure.> > > > This patient verifies Dr. Ritchie Shoemaker's theories by the need > > for melatonin to sleep.> > > > Your very confusing point is what?> > > > Please see the following web site (http://www.chronicneurotoxins.com/)> for an overview of Dr. Shoemaker's bio-toxin theories. He is not exactly> practicing mainstream medicine. Please see the FDA warning letter to Dr.> Shoemaker. ( http://www.fda.gov/foi/warning_letters/g4710d.htm> <http://www.fda.gov/foi/warning_letters/g4710d.htm> )

I'm aware of the situation and you can hear the same story said in court and depositions: He gave a prescription for a product that is the same for dogs and people except the product literature insert is different. A mistake was made by the manufacturer not Dr. Shoemaker.> > > > I'm asking for the "so-called" professionals to think before they > > advertise their "alledged" understanding of environmental illnesses.> > > > I do not advertise at all. Your company is actively involved in> promoting the notion that mould remediation is essential. You are also a> promoter of Dr. Shoemaker's ideas.> > > > Dr. Burge knows more about environmental illness than you or Dr.> Shoemaker will ever know.

Dr. Burge needs to stop talking about health effects as if she is the last word on medicine. I do not hold a medical degree. Here is some easy information to support Dr. Shoemaker's theories and refute Harriet Burge's attempts to hold the floor a little longer than she should in a convention where she has little standing.

1. Patients must be screened for HLA genotypes before they are given "cyclosporin" to help recieve an organ like a liver or kidney. If they have an HLA genotype, they will develop type 2 diabetes or adult onset diabetes from the cylosporin medication (according to e-medicine). Cyclosporin is a naturally occuring mycotoxin produced by more than one form of mold.

2. A State researcher has shown an association between HLA genotypes and Gulf War syndrome. (Just interesting for thought.)

Dr. Shoemaker had thousands of patients and tests for allergic reactions like Ig-E. His data says their is no correlation for allergies but the effects are neurotoxic - immune system and nervous system. If you know how corticosteriods work, you should be able to figure it out - really.

On a more positive note: I have never seen Dr. Chin Yang or Dr. Steve Vespers claim to know medicine. They point to probabilities that need to be investigated. They are each peers to Harriet Burge.

I also note that Dr. Harriet K. Amman, toxicologist, put her name on Dr. Shoemaker's paper. She wrote the chapter on mycotoxins in the ACGIH book, Bioaerosols: Assessment & Control (1999). She obviously disagrees. She is a toxicologist not a microbiologist. Call me crazy but, I will go with the toxicologist. I'm sure Harriet Burge is a wonderful microbiologist and did a lot of research for allergic responses in Florida but, that is all. I would trust a veterinarian for race horses before I trusted a microbiologist when it comes to health effects.

Final note: Any paper that contains the name, Dr. Gots M.D., is suspect. I saw the NBC Dateline investigation where he and his firm were implicated in medical examiner services for State Farm Insurance involving medical claims from car wrecks. The paper cited by Phil Havics is dead in the water just because Dr. Gots is a co-author. I said it before today; Dr. Gots does his literature reviews at the 7-eleven comic book section.

Please don't take my comments personally. I'm doing my part to raise the level of conscienceness.

Regards,

Greg Weatherman

Arlington VA 22202

gw@...> > > > Cheers,> > > > > > > > > > F. , Ph.D., MPH, D(ABMM), CIC, HEM> > Microbial Epidemiologist> > Children's Hospital> > Department of Epidemiology B-276> > 1056 East 19th Ave.> > Denver, Colorado 80218> > > > > > >