Re: Serious Breach of Ethics within the AIHA

[Guest guest]

Re: [iequality] Re: Serious Breach of Ethics within the AIHA

iequality/message/8175

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

Tue Sep 5, 2006 12:24 pm

Show Message Option

---------------------------------------------------------------------

-----------

View Source

Use Fixed Width Font

Unwrap Lines

---------------------------------------------------------------------

-----------

snk1955@...

snk1955

Offline

Send Email

Invite to 360°

Attachment(not stored)

Veritox 2000, Robbins, Swenson, Kelman, Neally, Gots.pdf

Type:

application/pdf

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.

REFERENCES

1. Squires, S.: Fungus Tied to Deaths of Cleveland Infants. The

Washington Post, Feb. 11, p. 7 (1997).

2. Searcey, D.: Mold May Delay Opening of School. Seattle Times,

Aug. 11 (1998).

3. Brettman, A.: Health Department Looking for New Home: Toxic

Mold Forces Imminent Closure; Of.cials Looking at 4-H Building

at Fairgrounds. The Daily News, Longview, WA, Oct. 17 (1996).

4. Lynch, K.: Deadly Mold is Found in Cellars of 2 Homes. The

Detroit News, Oct. 31 (1997).

5. Canino, T.: Mold Found at High School. North Lake Tahoe Bo

nanza, Dec. 24 (1998).

6. Fung, F.; , R.; , S.: Stachybotrys, a Mycotoxin-

Producing Fungus of Increasing Toxicologic Importance. Clin Tox

icol 36(1 & 2):79–86 (1998).

7. Burge, H.A.: Health Effects of Biological Contaminants. In: Indoor

Airand Human Health.pp.171–178,R.B.Gammage;B.A.Berven,

Eds. CRC Press/ Publishers, Boca Raton, FL (1996).

8. Tobin, R.S.; Baranowski, E.; Gilman, A.; et al.: Signi.cance of

Fungi in Indoor Air: Report of a Working Group. Can J Pub Health

78:1–32 (1987).

9. Creasia, D.A.; Thurman, J.D.; III, L.J.; et al.: Acute

Inhala

tion Toxicity of T-2 Mycotoxin in Mice. Fund Appl Toxicol 8:230–

235 (1987).

10. Creasia, D.A.; Thurman, J.D.; Wannemacher, R.W.; et al.: Acute

Inhalation Toxicity of T-2 Mycotoxin in the Rat and Guinea Pig.

Fund Appl Toxicol 14:54–59 (1990).

11. Marrs, T.C.; Edginton, J.A.G.; Price, P.N.; et al.: Acute

Toxicity of

T-2 Mycotoxin to the Guinea Pig by Inhalation and Subcutaneous

Routes. Br J Exp Path 67:259–268 (1986).

12. Pang, V.F.; Lambert, R.J.; Felsburg, P.J.; et al.: Experimental

T2

Toxicosis in Swine Following Inhalation Exposure: Clinical Signs

and Effects on Hematology, Serum Biochemistry, and Immune

Response. Fund Appl Toxicol 11:100–109 (1988).

13. Brinton, W.T.; Vastbinder, E.E.; Greene, J.W.; et al.: An

Outbreak

of Organic Dust Toxic Syndrome in a College Fraternity. JAMA

258:1210 –1212 (1987).

14. Croft, W.A.; Jarvis, B.B.; Yatawara, C.S.: Airborne Out

break of Trichothecene Toxicosis. Atmos Environ 20(3):549–552

(1986).

15. Di Paolo, N.; Guarnieri, A.; Garosi, G.; et al.: Inhaled

Mycotoxins

Lead to Acute Renal Failure. Nephrol Dial Transplant 9: Suppl.

4:116 –120 (1994).

16. Emanuel, D.A.; Wenzel, F.J.; Lawton, B.R.: Pulmonary Mycotox

icosis. Chest 67:293–297 (1975).

17. Malmberg, P.; Rask-Andersen, A.; Rosenhall, L.: Exposure to Mi

croorganisms Associated with Allergic Alveolitis and Febrile Re

actions to Mold Dust in Farmers. Chest 103:1202–1209 (1993).

18. Johanning, E.; Biagini, R.; Hull, D.L.; et al.: Health and

Immunol

ogy Study Following Exposure to Toxigenic Fungi (Stachybotrys

chartarum) in a Water-Damaged Of.ce Environment. Int Arch Oc

cup Environ Health 68:207–218 (1996).

19. Montana,E.;Etzel,R.A.;Allan,T.;etal.:EnvironmentalRiskFac

tors Associated with Pediatric Idiopathic Pulmonary Hemorrhage

and Hemosiderosis in a Cleveland Community. Pediatrics 99:1–8

(1997).

20. Dearborn, D.G.; Infeld, M.D.; , P.G.; et al.: Update: Pul

monary Hemorrhage/Hemosiderosis Among Infants-Cleveland,

Ohio, 1993 –1996. MMWR 46:33–35 (1997).

21. Hodgson,M.J.;Morey,P.;Leung,W.Y.;etal.:Building-Associated

Pulmonary Disease from Exposure to Stachybotrys Chartarum and

Aspergillus Versicolor. J Occup Environ Med 40:241–249 (1998).

22. opoulos, C.J.; Mims, C.W.: Introductory Mycology, 3rd ed.

Wiley & Sons, New York (1979).

23. Eppley, R.M.: Chemistry of Stachybotryotoxicosis. In: Mycotoxins

in Human and Animal Health, pp. 285–295, J.V. Rodricks; C.W.

Hesseltine; M.A. Mehlman, Eds. Pathotox Publishers, Inc., Park

Forest South, IL (1977).

24. Korpinen, E.L.; Kurkinen, M.; Nummi, M.; et al.: Studies on

Stachybotrys Alternans: III. Chromatographic Separation and Tis

sue Culture Toxicity Test of Stachybotrys Toxins. Acta Pathol Mi

crobiol Scand B Microbiol Immunol 82B:7–11 (1974).

HEALTH EFFECTS OF MYCOTOXINS IN INDOOR AIR: A CRITICAL REVIEW

25. Burge, H.A.; Otten, J.A.: Fungi. In: Bioaerosols: Assessment and

Control, pp. 19.1–19.13, J. Macher; H.A. Ammann; H.A. Burge;

et al., Eds. American Conference of Governmental Industrial Hy

gienists, Cincinnati, OH (1999).

26. Rom, W.N.: Environmental and Occupational Medicine. Little,

Brown and Co., Boston (1983).

27. , T.S.: Microbiology. W.B. Saunders Co., Philadelphia

(1998).

28. Ciegler, A.; , J.W.: Mycotoxins and Mycotoxicoses. Bio-

Science 30:512–515 (1980).

29. Jarvis, B.B.: Mycotoxins and Indoor Air Quality. In: Biological

Contaminants in Indoor Environments. pp. 201–214, P.R. Morey;

J.C. Feely; J.A. Otten, Eds. ASTM, Philadelphia (1990).

30. Pestka, J.J.; Bondy, G.S.: Alteration of Immune Function Fol

lowing Dietary Mycotoxin Exposure. Can J Physiol Pharmacol

68:1009 –1016 (1990).

31. D'Mello, J.P.: Handbook of Plant and Fungal Toxicants. CRC

Press, Boca Raton, FL (1997).

32. Schiefer, H.: Mycotoxins in Indoor Air: A Critical Toxicologi

cal Viewpoint. In: Indoor Air '90, Proceedings of the Fifth In

ternational Conference on Indoor Air and Climate. pp. 167–172.

Toronto, Canada (1990).

33. Hendry, K.M.; Cole, E.C.: A Review of Mycotoxins in Indoor Air.

J Toxicol Environ Health 38:183–198 (1993).

34. Wicklow, D.T.; Shotwell, O.L.: Intrafungal Distribution of Aa

toxins Among Conidia and Sclerotia of Aspergillus Flavus and

Aspergillus Parasiticus. Can J Microbiol 29:1–5 (1983).

35. Pasanen, A.-L.; Nikulin, M.; Tuomainen, M.; et al.: Laboratory

Experiments on Membrane Filter Sampling of Airborne Mycotox

ins Produced by Stachybotrys Atra Corda. Atmospheric Environ

27A:9–13 (1993).

36. Ciegler, A.; Bermeister, H.R.; Vesonder, F.R.; et al.:

Mycotoxins:

Occurrence in the Environment. In: Mycotoxins and N-Nitroso

Compounds:EnvironmentalRisks, pp. 1–50. R.C.Shank,Ed.CRC

Press, Inc., Boca Raton, FL (1981).

37. Linsell, C.A.: The Mycotoxins and Human Health Hazards. Pure

& Appl Chem 49:1765–1769 (1977).

38. Forgacs, J.: Mycotoxicoses. Adv Vet Sci 7:273–382 (1962).

39. Newberne, P.M.: Mycotoxins: Toxicity, Carcinogenicity, and the

Inuence of Various Nutritional Conditions. Environ Health Per

spect 9:1–32 (1974).

40. , A.W.: Mycotoxins: A Review of Biological Effects and

Their Role in Human Diseases. Clin Toxicol 17:45–83 (1980).

41. Kaminski, E.; Stawicki, S.; Wasowicz, E.: Volatile Flavour Com

pounds Produced by Molds of Aspergillus, Penicillium, and Fungi

Imperfecti. Appl Microbiol 27:1001–1004 (1974).

42. Pohland, A.E.: Mycotoxins in Review. Food Addit Contam

10(1):17–28 (1993).

43. Wyllie, T.; Morehouse, L., editors.: Mycotoxic Fungi, Mycotox

ins, Mycotoxicoses, an Encyclopedic Handbook, Vol. 3. Marcel

Dekker, Inc., New York (1978).

44. World Health Organization: Selected Mycotoxins: Ochratoxins,

Trichothecenes, Ergot. In: Environmental Health Criteria 105, pp.

73–16. WHO, Geneva (1990).

45. National Research Council: Protection Against Mycotoxins. Na

tional Academy Press, Washington, D.C. (1983).

46. Marasas, W.F.O.; , P.E.; Toussoun, T.A.: Toxic Fusarium

Species: Identity and Mycotoxicology. Pennsylvania State Univer

sity Press, University Park, PA (1984).

47. Hudler, G.W.: Magical Mushrooms, Mischievous Molds. Princeton

University Press, Princeton (1998).

48. Burg, W.R.; Shotwell, O.L.; Saltzman, B.E.: Measurements of Air

borne Aatoxins During the Handling of Contaminated Corn. Am

Ind Hyg Assoc J 42:1–11 (1981).

49. Jakab, G.J.; Hmieleski, R.R.; Zarba, A.; et al.: Respiratory Aa

toxicosis: Suppression of Pulmonary and Systemic Host Defenses

in Rats and Mice. Toxicol Appl Pharmacol 125:198–205 (1994).

50. Zarba, A.; Hmieleski, R.; Hemenway, D.R.; et al.: Aatoxin B1

DNA Adduct Formation in Rat Liver Following Exposure by

Aerosol Inhalation. Carcinogenesis 13(6):1031 –1033 (1992).

51. Louria, D.B.; Finkel, G.; , J.K.; et al.: Aatoxin-Induced

Tumors in Mice. Sabouraudia 12:371–375 (1974).

52. Bruce, R.D.: Risk Assessment for Aatoxin: II. Implications of

Human Epidemiology Data. Risk Analysis 10:561–569 (1990).

53. Jarvis, B.B.; Sorenson, W.G.; Hintikka, E.-L.; et al.: Study of

Toxin

Production by Isolates of Stachybotrys Chartarum and Memnon

iella Echinata Isolated During a Study of Pulmonary Hemosidero

sis in Infants. Appl Environ Microbiol 64(10):3620–3625 (1998).

54. Jarvis, B.B.; Lee, Y.-W.; Comezoglu, S.N.; et al.: Trichothecenes

Produced by Stachybotrys Atra from Eastern Europe. Appl Environ

Microbiol 51:915–918 (1986).

55. Forgacs, J.: Stachybotryotoxicosis. Microbial Toxins. In: Fungal

Toxins, pp. 95–128, S. Kadis; A. Ciegler; S.J. Ajl, Eds. Academic

Press, New York (1972).

56. Mirocha, C.J.; Pathre, S.V.; Christensen, C.M.: Chemistry of

Fusarium and Stachybotrys Mycotoxins. In: Mycotoxic Fungi, My

cotoxins, Mycotoxicoses: An Encyclopedic Handbooks, pp. 365–

420, T.D. Wyllie; L.G. Morehouse, Eds. Marcel Dekker, Inc., New

York (1977).

57. Nikulin, M.; Reijula, K.; Jarvis, B.B.; et al.: Experimental Lung

Mycotoxicosis in Mice Induced by Stachybotrys Atra. Int J Exp

Path 77:213–218 (1996).

58. Sumi, Y.; Nagura, H.; Takeuchi, M.; et al.: Granulomatous Lesions

in the Lung Induced by Inhalation of Mold Spores. Virchow Arch

424(6):661–668 (1994).

59. Sumi, Y.; Hamasaki, T.; Miyakawa, M.: Tumors and Other Le

sions Induced in Germ-Free Rats Exposed to Aspergillus Versicolor

Alone. Jpn J Cancer Res 78(5):480–486 (1987).

60. Ueno, Y.: Toxicological Features of T-2 Toxin and Related Tri

chothecenes. Fund Appl Toxicol 4:S124–S132 (1984).

61. Smoragiewicz, W.; Cossette, B.; Boutard, A.; et al.:

Trichothecene

Mycotoxins in the Dust of Ventilation Systems in Of.ce Buildings.

Int Arch Occup Environ Health 65:113–117 (1993).

62. Samson, R.A.; Flannigan, B.; Flannigan, M.E.; et al.: Health

Impli

cationsof FungiinIndoorEnvironments.AirQuality Monographs,

vol. 2. Elsevier, Amsterdam (1994).

63. Etzel, R.A.; Montana, E.; Sorenson, W.G.; et al.: Acute Pulmonary

Hemorrhage in Infants Associated with Exposure to Stachybotrys

Atra and Other Fungi. Arch Pediatr Adolesc Med 152:757–762

(1998).

64. Schlesinger, R.B.: Comparative Deposition of Inhaled Aerosols in

Experimental Animals and Humans: A Review. J Toxicol Environ

Health 15:197–214 (1985).

65. Nikulin, M.; Reijula, K.; Jarvis, B.B.; et al.: Effects of

Intranasal

Exposure to Spores of Stachybotrys Atra in Mice, Fund Appl Tox

icol 35:182–188 (1997).

66. Drobotko, V.G.: Stachybotryotoxicosis a New Disease of Horses

and Humans. Am Rev Soviet Med 2:238–242 (1945).

C. A. ROBBINS ET AL.

67. Emanuel, D.A.; Marx, J., Jr.; Ault, B.; et al.: Pulmonary Mycotox

icosis Revisited. Am J Ind Med 10:305–306 (1986).

68. Sigsgaard, T.; Pedersen, O.F.; Juul, S.; et al.: Respiratory

Disorders

and Atopy in Cotton, Wool, and Other Textile Mill Workers in

Denmark. Am J Ind Med 22(2):163–184 (1992).

69. Milton, D.K.: Bacterial Endotoxins: A Review of Health Effects

and Potential Impact in the Indoor Environment. In: Indoor Air and

Human Health, pp. 179–195, R.B. Gammage; B.A. Berven, Eds.

Pub., New York (1996).

70. Mouilleseaux, A.; Squinazi, F.: Airborne Fungi in Several Indoor

Environments.In:HealthImplicationsof FungiinIndoorEnviron

ments, pp. 155–168, R.A. Samson; B. Flannigan; M.E. Flannigan;

et al., Eds. Air Quality Monographs. Elsevier, Amsterdam (1994).

71. Lacey, J.; Crook, B.: Fungal and Actinomycete Spores as

Pollutants

of the Workplace and Occupational Allergens. Ann Occup Hyg

32:515 –533 (1988).

72. Wilkins, C.K.; Larsen, S.T.; Hammer, M.; et al.: Respiratory Ef

fects in Mice Exposed to Airborne Emissions from Stachybotrys

Chartarum and Implications for Risk Assessment. Pharmacol Tox

icol 83:112 –119 (1998).

73. Johanning, E.; Jarvis, B.B.; Morey, P.R.: Clinical-

Epidemiological

Investigations of Health Effects caused by Stachybotrys Atra Build

ing Contamination. In: Proceedings of Indoor Air '93, Health Ef

fects, pp. 225–230. Helsinki (1993).

74. Page, E.; Trout, D.: Mycotoxins and Building-Related Illness; Let

ter to the Editor. J Occup Environ Med 40(9):761–763 (1998).

75. Middleton, E.; , C.; Ellis, E.; et al., eds.: Allergy,

Principles

and Practice, vol. II. Mosby, St. Louis (1998).

76. Wallach, J.: Interpretation of Laboratory Medicine: A Synopsis of

LaboratoryMedicine.5th ed.Little,BrownandCo.,Boston (1992).

77. Kozak, P.P.; Gallup, J.; Cummins, L.H.; et al.: Currently

Available

Methods for Home Mold Surveys. II. Examples of Problem Homes

Surveyed. Ann Allergy 45:167–176 (1980).

78. Cassimos, C.D.; Chyrssanthopoulos, C.; Panagistidou, C.: Epi

demiologic Observations in Idiopathic Pulmonary Hemosiderosis.

J Pediatr 102:698–702 (1983).

79. Lowry, R.; Buick, B.; Riley, M.: Case Report: Idiopathic

Pulmonary

Haemosiderosis and Smoking. Ulster Med J 1:116–118 (1993).

80. Soergel, K.H.; Sommers, S.C.: Idiopathic Pulmonary Hemosidero

sis and Related Syndromes. Am J Med 32:499–511 (1962).

81. Sorenson, B.; Kullman, G.; Hintz, P.: NIOSH Health Hazard Eval

uation Report, HETA 95-0160-2471 . NIOSH, Cincinnati, Ohio

(1996).

82. Palmgren, U.; Strom, G.; Blomquist, G.; et al.: Collection of

Airborne Micro-Organisms on Nuclepore Filters: Estimation

and Analysis-CAMNEA-Method. J Appl Bacteriol 61:401–406

(1986).

83. Centers for Disease Control and Prevention Of.ce of the Director:

Update: Pulmonary Hemorrhage/Hemosiderosis Among Infants –

Cleveland, Ohio, 1993–1996. MMWR 49(9):180–184 (2000).

84. , J.D.; Eaton, D.L.; Guengerich, F.P.; et al.: Aatoxin B1

Activation inHuman Lung. Toxicol Appl Pharmacol 144(1):88–95

(1997).

85. Donnelly, P.J.; , R.E.K.; Ali, S.L.; et al.:

Biotransformation

of Aatoxin B1 in Human Lung. Carcinogenesis 17(11):2487 –

2494 (1996).

86. , R.B.; Van Nieuwenhuize, J.P.; Raatgever, J.W.; et al.: Aa

toxin Exposures in the Industrial Setting: An Epidemiological

Study of Mortality. Food Chem Toxic 22(1):39–43 (1984).

87. Olsen, J.H.; Dragsted, L.; Autrup, H.: Cancer Risk and Occupa

tional Exposure to Aatoxins in Denmark. Br J Cancer 58(3):392–

396 (1988).

88. Deger, G.E.: Aatoxin-Human Colon Carcinogenesis? Ann Inter

nal Med 85:204–205 (1975).

89. Dvorackova, I.; Pichova, V.: Pulmonary Interstitial Fibrosis with

Evidence of Aatoxin B1 in Lung Tissue. J Toxicol Environ Health

18(1):153–157 (1986).

90. Yike, I.; Allan, T.; Sorenson, W.G.; et al.: Highly Sensitive

Protein

Translation Assay for Trichothecene Toxicity in Airborne Partic

ulates: Comparison with Cytotoxicity Assays. Appl Environ Mi

crobiol 65(1):88–94 (1999).

91. Rao, C.Y.; Burge, H.A.; Chang, J.C.S.: Review of Quantitative

Standards and Guidelines for Fungi in Indoor Air. J Air Waste

Manage Assoc 46:899–908 (1996).

92. Haley, M.: Mold Attacks Bear Creek Station, Forces Fire.ghters.

The Woodinville Weekly 24(27):1 (1999).

93. Post, N.M.: Containing Noxious Mold. Engineering News Record,

May 3 (1999).

94. National Safety Council: Fundamentals of Industrial Hygiene, B.A.

Plog, Ed. Chicago (1988).

[Guest guest]

Re: [iequality] 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]

The year 2000 was an upsetting time. I had gone to Dr. Johanning and

got the evidence I needed after waiting 8 months for my appointment.

I desparately was trying to get a lawyer while working on my case and

also trying to get the help of doctors. Dr. Johanning had resigned

from the NY Environmental Center and he did call my local doctors,

but they would not give me the medication I needed. I had the best

insurance at the time, now I have none and feel like I am basically

waiting to die. They could see I was very ill but they didn't know

about mold illness. All the doctors kept saying yeast won't hurt

you. My case was thrown out cuz the court refused to give me more

time. Yeast in my body for so many years cannot be good. How were

we to get the proper help with creeps like this writing this crap.

--- In , " tigerpaw2c " <tigerpaw2c@...>

wrote:

>

> Re: [iequality] 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]

snk1955@... wrote:

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.

Sheer poetry!

-