ACOEM Mold Statement is up for review/ACOEM members may submit research

[Guest guest]

ACOEM Mold Statement is up for review/ACOEM members may submit

research

Dear Friends of SMH,

FYI, if you know of any research that can be submitted to ACOEM

..... via a member.

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

The following notice was just sent to our Physician, Researcher,

and Professional Friends of The Center for School Mold Help (SMH),

I thought you might want to know that the ACOEM Mold Statement is

up for review and you m may submit research, via an ACOEM member, it is

my understanding.

This is our article on the site:

ACOEM Mold Statement up for review/updating

The problematic ACOEM mold position

statement (see below) is under review for updating and ACOEM is

soliciting comments from its members. Physicians and researchers with

mold or damp-building related, peer-reviewed research published since

Sept. 2002 are encouraged to submit these, via an ACOEM member, to ACOEM,

through March 31, 2009. (SMH)

" ACOEM Employs New Technology in Review Process for

Position Statement on

Mold

http://acoem.org/moldstatement.aspx

As ACOEM begins the process of reviewing/updating its 2002 position

statement on Adverse Human Health Effects Associated with Molds in the

Indoor Environment it is employing the latest technology to ensure access

to

the broadest and most scientifically reliable (evidence-based) research.

This new technology enables members to submit relevant peer-reviewed

scientific reports published since September 2002 via the web. The 2002

statement was the focus of wide interest, and this technology will help

ensure the maximum opportunity for interested members to contribute to

the

updating of the statement. The submission and comment period will be open

until March 31, 2009. "

The ACOEM Mold Position Statement has been described, by some, to

allegedly be one of the main reasons that those sick from mold cannot

obtain medical care. Indeed, this statement is used in courtrooms by

defense, often. (SMH)

" The paper has become a key defense tool wielded by builders,

landlords and insurers in litigation. It has also been used to assuage

fears of parents following discovery of mold in schools. One point that

rarely emerges in these cases: The paper was written by people who

regularly are paid experts for the defense side in mold litigation.

The ACOEM doesn't disclose this, nor did its paper. The professional

society's president, Tee Guidotti, says no disclosure is needed because

the paper represents the consensus of its membership and is a statement

from the society, not the individual authors. " (Court of Opinion Amid

Suits Over Mold, Experts Wear Two Hats: Authors of Science Paper Often

Cited by Defense Also Help in Litigation, Jan. 9, 2007, Wall Street

Journal)

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ACOEM Mold Position Statement (current)

Adverse Human Health Effects Associated with Molds in the Indoor

Environment

Copyright © 2002 American College of Occupational and

Environmental Medicine http://acoem.org/guidelines.aspx?id=850

In recent years, the growth of molds in home, school, and office

environments has been cited as the cause of a wide variety of human

ailments and disabilities. So-called " toxic mold " has become a prominent

topic in the lay press and is increasingly the basis for litigation when

individuals, families, or building occupants believe they have been harmed

by exposure to indoor molds. This evidence-based statement from the

American College of Occupational and Environmental Medicine (ACOEM)

discusses the state of scientific knowledge as to the nature of

fungal-related illnesses while emphasizing the possible relationships to

indoor environments. Particular attention is given to the possible health

effects of mycotoxins, which give rise to much of the concern and

controversy surrounding indoor molds. Food-borne exposures, methods of

exposure assessment, and mold remediation procedures are

beyond the scope of this paper.

The fungi are eukaryotic, unicellular, or multicellular organisms that,

because they lack chlorophyll, are dependent upon external food sources.

Fungi are ubiquitous in all environments and play a vital role in the

Earth's ecology by decomposing organic matter. Familiar fungi include

yeasts, rusts, smuts, mushrooms, puffballs, and bracket fungi. Many

species of fungi live as commensal organisms in or on the surface of the

human body. " Mold " is the common term for multicellular fungi that grow as

a mat of intertwined microscopic filaments (hyphae). Exposure to molds and

other fungi and their spores is unavoidable except when the most stringent

of air filtration, isolation, and environmental sanitation measures are

observed, eg, in organ transplant isolation units.

Molds and other fungi may adversely affect human health through three

processes: 1) allergy; 2) infection; and 3) toxicity. One can estimate

that about 10% of the population has allergic antibodies to fungal

antigens. Only half of these, or 5%, would be expected to show clinical

illness. Furthermore, outdoor molds are generally more abundant and

important in airway allergic disease than indoor molds — leaving the

latter with an important, but minor overall role in allergic airway

disease. Allergic responses are most commonly experienced as allergic

asthma or allergic rhinitis ( " hay fever " ). A rare, but much more serious

immune-related condition, hypersensitivity pneumonitis (HP), may follow

exposure (usually occupational) to very high concentrations of fungal (and

other microbial) proteins.

Most fungi generally are not pathogenic to healthy humans. A number of

fungi commonly cause superficial infections involving the feet (tinea

pedis), groin (tinea cruris), dry body skin (tinea corporus), or nails

(tinea onchomycosis). A very limited number of pathogenic fungi — such

as Blastomyces, Coccidioides, Cryptococcus, and Histoplasma — infect

non-immunocompromised individuals. In contrast, persons with severely

impaired immune function, eg, cancer patients receiving chemotherapy,

organ transplant patients receiving immunosuppressive drugs, AIDS

patients, and patients with uncontrolled diabetes, are at significant

risk for more severe opportunistic fungal infection.

Some species of fungi, including some molds, are known to be capable of

producing secondary metabolites, or mycotoxins, some of which find a

valuable clinical use, eg, penicillin, cyclosporine. Serious veterinary

and human mycotoxicoses have been documented following ingestion of foods

heavily overgrown with molds. In agricultural settings, inhalation

exposure to high concentrations of mixed organic dusts — which include

bacteria, fungi, endotoxins, glucans, and mycotoxins — is associated with

organic dust toxic syndrome, an acute febrile illness. The present alarm

over human exposure to molds in the indoor environment derives from a

belief that inhalation exposures to mycotoxins cause numerous and varied,

but generally nonspecific, symptoms. Current scientific evidence does not

support the proposition that human health has been adversely affected by

inhaled mycotoxins in the

home, school, or office environment.

Allergy and other hypersensitivity reactions

Allergic and other hypersensitivity responses to indoor molds may be

immunoglobulin E (IgE) or immunoglobulin G (IgG) mediated, and both types

of response are associated with exposure to indoor molds. Uncommon

allergic syndromes, allergic bronchopulmonary aspergillosis (ABPA), and

allergic fungal sinusitus (AFS), are briefly discussed for completeness,

although indoor mold has not been suggested as a particular risk factor in

the etiology of either.

Immediate hypersensitivity: The most common form of hypersensitivity

to molds is immediate type hypersensitivity or IgE-mediated " allergy "

to fungal proteins. This reactivity can lead to allergic asthma or

allergic rhinitis that is triggered by breathing in mold spores or

hyphal fragments. Residential or office fungal exposures may be a

substantial factor in an individual's allergic airway disease depending

on the subject's profile of allergic sensitivity and the levels of

indoor exposures. Individuals with this type of mold allergy are

" atopic " individuals, ie, have allergic asthma, allergic rhinitis, or

atopic dermatitis and manifest allergic (IgE) antibodies to a wide

range of environmental proteins among which molds are only one

participant. These individuals generally will have allergic reactivity

against other important indoor and outdoor allergens such as

animal dander, dust mites, and weed, tree, and grass pollens. Among

the fungi, the most important indoor allergenic molds are Penicillium

and Aspergillus species.1 Outdoor molds, eg, Cladosporium and

Alternaria, as well as pollens, can often be found at high levels

indoors if there is access for outdoor air (eg, open windows).

About 40% of the population are atopic and express high levels of

allergic antibodies to inhalant allergens. Of these, 25%, or 10% of the

population, have allergic antibodies to common inhalant molds.2 Since

about half of persons with allergic antibodies will express clinical

disease from those antibodies, about 5% of the population is predicted

to have, at some time, allergic symptoms from molds. While indoor molds

are well-recognized allergens, outdoor molds are more generally

important.

A growing body of literature associates a variety of diagnosable

respiratory illnesses (asthma, wheezing, cough, phlegm, etc.),

particularly in children, with residence in damp or water-damaged homes

(see reviews 3-5). Recent studies have documented increased

inflammatory mediators in the nasal fluids of persons in damp buildings,

but found that mold spores themselves were not responsible for these

changes.6,7 While dampness may indicate potential mold growth, it is

also a likely indicator of dust mite infestation and bacterial growth.

The relative contribution of each is unknown, but mold, bacteria,

bacterial endotoxins, and dust mites can all play a role in the

reported spectrum of illnesses, and can all be minimized by control of

relative humidity and water intrusion.

Hypersensitivity pneumonitis (HP): HP results from exaggeration of

the normal IgG immune response against inhaled foreign (fungal or

other) proteins and is characterized by: 1) very high serum levels of

specific IgG proteins (classically detected in precipitin tests

performed as double diffusion tests); and 2) inhalation exposure to

very large quantities of fungal (or other) proteins.8 The resulting

interaction between the inhaled fungal proteins and fungal-directed

cell mediated and humoral (antibody) immune reactivity leads to an

intense local immune reaction recognized as HP. As opposed to immediate

hypersensitivity (IgE-mediated) reactions to mold proteins, HP is not

induced by normal or even modestly elevated levels of mold spores. Most

cases of HP result from occupational exposures, although cases have

also been attributed to pet birds, humidifiers, and

heating, ventilating, and air conditioning (HVAC) systems. The

predominant organisms in the latter two exposures are thermophilic

Actinomyces, which are not molds but rather are filamentous bacteria

that grow at high temperatures (116°F). The presence of high

levels of a specific antibody — generally demonstrated as the

presence of precipitating antibodies — is required to initiate HP,

but is not diagnostic of HP.9 More than half of the people who have

occupational exposure to high levels of a specific protein have such

precipitin antibodies, but do not have clinical disease.8 Many

laboratories now measure IgG to selected antigens by using solid phase

immunoassays, which are easier to perform and more quantitative than

precipitin (gel diffusion) assays. However, solid phase IgG levels that

are above the reference range do not carry the same

discriminatory power as do results of a precipitin test, which

requires much greater levels of antibody to be positive. Five percent

of the normal population have levels above the reference value for any

one tested material. Consequently, a panel of tests (eg, 10) has a high

probability of producing a false-positive result. Screening IgG

antibody titers to a host of mold and other antigens is not justified

unless there is a reasonable clinical suspicion for HP and should not

be used to screen for mold exposure.10

Uncommon allergic syndromes: Allergic bronchopulmonary aspergillosis

(ABPA) and allergic fungal sinusitis (AFS). 11 These conditions are

unusual variants of allergic (IgE-mediated) reactions in which fungi

actually grow within the patient's airway. ABPA is the classic form of

this syndrome, which occurs in allergic individuals who generally have

airway damage from previous illnesses leading to bronchial

irregularities that impair normal drainage, eg, bronchiectasis.12,13

Bronchial disease and old cavitary lung disease are predisposing

factors contributing to fungal colonization and the formation of

mycetomas. Aspergillus may colonize these areas without invading

adjacent tissues. Such fungal colonization is without adverse health

consequence unless the subject is allergic to the specific fungus that

has taken up residence, in which case there may be

ongoing allergic reactivity to fungal proteins released directly into

the body. Specific criteria have been recognized for some time for the

diagnosis of ABPA.14,15 As fungi other than Aspergillus may cause this

condition, the term " allergic bronchopulmonary mycosis " has been

suggested. It has more recently become appreciated that a similar

process may affect the sinuses — allergic fungal sinusitis (AFS).16

This condition also presents in subjects who have underlying allergic

disease and in whom, because of poor drainage, a fungus colonizes the

sinus cavity. Aspergillus and Curvularia are the most common

forms, although the number of fungal organisms involved continues to

increase. As with ABPA, the diagnosis of AFS has specific criteria that

should be used to make this diagnosis.17-19

Recommendations

Individuals with allergic airway disease should take steps to

minimize their exposure to molds and other airborne allergens, eg,

animal dander, dust mites, pollens. For these individuals, it is prudent

to take feasible steps that reduce exposure to aeroallergens and to

remediate sources of indoor mold amplification. Sensitized individuals

may need to keep windows closed, remove pets, use dust mite covers, use

high-quality vacuum cleaners, or filter outdoor air intakes to minimize

exposures to inhalant allergens. Humidification over 40% encourages

fungal and dust mite growth, so should be avoided. Where there is indoor

amplification of fungi, removal of the fungal source is a key measure to

be undertaken so as to decrease potential for indoor mold allergen

exposure.

ABPA and AFS are uncommon disorders while exposure is ubiquitous to

the fungal organisms involved. There is no evidence to link specific

exposures to fungi in home, school, or office settings to the

establishment of fungal colonization that leads to ABPA or AFS.

Once a diagnosis of HP is entertained in an appropriate clinical

setting and with appropriate laboratory support, it is important to

consider potential sources of inhaled antigen. If evaluation of the

occupational environment fails to disclose the source of antigens,

exposures in the home, school, or office should be investigated. Once

identified, the source of the mold or other inhaled foreign antigens

should be remediated.

Appropriate measures should be taken in industrial workplaces to

prevent mold growth, eg, in machining fluids and where stored organic

materials are handled such as in agricultural and grain processing

facilities. Engineering controls and personal protective equipment

should be used to reduce aerosol generation and minimize worker

exposures to aerosols.

Although it is not relevant to indoor mold exposure, it should be

mentioned that there is a belief among some health practitioners and

members of the public regarding a vague relationship between mold

colonization, molds in foods, and a “generalized mold hypersensitivity

state.†The condition was originally proposed as the “Chronic Candida

Syndrome†or “Candida Hypersensitivity Syndrome,†but now has been

generalized to other fungi. Adherents may claim that individuals are

“colonized†with the mold(s) to which they are sensitized and that they

react to these endogenous molds as well as to exposures in foods and other

materials that contain mold products. The proposed hypersensitivity is

determined by the presence of any of a host of non-specific symptoms plus

an elevated (or even normal) level of IgG to any of a host of molds. The

claim of mold colonization is

generally not supported with any evidence, eg, cultures or biopsies, to

demonstrate the actual presence of fungi in or on the subject. Instead,

proponents often claim colonization or infection based on the presence of

a wide variety of nonspecific symptoms and antibodies detected in

serologic tests that represent no more than past exposure to normal

environmental fungi. The existence of this disorder is not supported by

reliable scientific data.20,21

Infection An overview of fungi as human pathogens follows.

Exposure to molds indoors is generally not a specific risk factor in the

etiology of mycoses except under specific circumstances as discussed

below for individual types of infection.

Serious fungal infections: A very limited number of pathogenic fungi

such as Blastomyces, Coccidioides, Cryptococcus, and Histoplasma infect

normal subjects and may cause a fatal illness. However, fungal

infections in which there is deep tissue invasion are primarily

restricted to severely immunocompromised subjects, eg, patients with

lymphoproliferative disorders including acute leukemia, cancer patients

receiving intense chemotherapy, or persons undergoing bone marrow or

solid transplantation who get potent immunosuppressive drugs.22

Uncontrolled diabetics and persons with advanced AIDS are also at

increased risk. Concern is greatest when patients are necessarily in

the hospital during their most severe immunocompromise, at which time

intense measures are taken to avoid fungal, bacterial, and viral

infection.23 Outside the hospital, fungi, including

Aspergillus, are so ubiquitous that few recommendations can be made

beyond avoidance of known sources of indoor and outdoor amplification,

including indoor plants and flowers because vegetation is a natural

fungal growth medium.24,25 Candida albicans is a ubiquitous

commensal organism on humans that becomes an important pathogen for

immunocompromised subjects. However, it and other environmental fungi

discussed above that are pathogens in normals as well (eg, Cryptococcus

associated with bird droppings, Histoplasma associated with bat

droppings, Coccidioides endemic in the soil in the southwest US) are

not normally found growing in the office or residential environment,

although they can gain entry from outdoors. Extensive guidelines for

specific immunocompromised states can be found at the Centers for

Disease Control and Prevention (CDC) web site

at www.cdc.gov.

Superficial fungal infections: In contrast to serious internal

infections with fungi, superficial fungal infections on the skin or

mucosal surfaces are extremely common in normal subjects. These

superficial infections include infection of the feet (tinea pedis),

nails (tinea onychomycosis), groin (tinea cruris), dry body skin (tinea

corporis), and infection of the oral or vaginal mucosa. Some of the

common organisms involved, eg, Trychophyton rubrum, can be found

growing as an indoor mold. Others, such as Microsprum canis and T.

mentagrophytes can be found on indoor pets (eg, dogs, cats, rabbits,

and guinea pigs). As a common commensal on human mucosal surfaces, C.

albicans can be cultured from more than half of the population that has

no evidence of active infection. C. albicans infections are

particularly common when the normally resident microbial flora

at a mucosal site are removed by antibiotic use. Local factors such as

moisture in shoes or boots and in body creases and loss of epithelial

integrity are important in development of superficial fungal infections.

Pityriasis (Tinea) versicolor is a chronic asymptomatic infection of

the most superficial layers of the skin due to Pityriasis ovale (also

known as P. orbiculare and Malassesia furfur) manifest by patches of

skin with variable pigmentation. This is not a contagious condition and

thus is unrelated to exposures, but represents the overgrowth of normal

cutaneous fungal flora under favorable conditions.

Recommendations

Only individuals with the most severe forms of immunocompromise need

be concerned about the potential for opportunistic fungal infections.

These individuals should be advised to avoid recognizable fungal

reservoirs including, but not limited, to indoor environments where

there is uncontrolled mold growth. Outdoor areas contaminated by

specific materials such as pigeon droppings should be avoided as well as

nearby indoor locations where those sources may contaminate the intake

air.

Individuals with M. canis and T. mentagrophytes infections should

have their pets checked by a veterinarian. No other recommendations are

warranted relative to home, school, or office exposures in patients

with superficial fungal infections.

Toxicity Mycotoxins are “secondary metabolites†of fungi,

which is to say mycotoxins are not required for the growth and survival

of the fungal species (“toxigenic speciesâ€) that are capable of

producing them. The amount (if any) and type of mycotoxin produced is

dependent on a complex and poorly understood interaction of factors that

probably include nutrition, growth substrate, moisture, temperature,

maturity of the fungal colony, and competition from other

microorganisms.26-30 Additionally, even under the same conditions of

growth, the profile and quantity of mycotoxins produced by toxigenic

species can vary widely from one isolate to another.31-34 Thus, it does

not necessarily follow from the mere presence of a toxigenic species that

mycotoxins are also present.35-38 When produced, mycotoxins are

found in all parts of the fungal colony, including the hyphae,

mycelia, spores, and the substrate on which the colony grows. Mycotoxins

are relatively large molecules that are not significantly volatile;39,40

they do not evaporate or “off-gas†into the environment, nor do they

migrate through walls or floors independent of a particle. Thus, an

inhalation exposure to mycotoxins requires generation of an aerosol of

substrate, fungal fragments, or spores. Spores and fungal fragments do

not pass through the skin, but may cause irritation if there is contact

with large amounts of fungi or contaminated substrate material.41 In

contrast, microbial volatile organic compounds (MVOCs) are low molecular

weight alcohols, aldehydes, and ketones.42 Having very low odor

thresholds, MVOCs are responsible for the musty, disagreeable odor

associated with mold and mildew and they may be responsible for the

objectionable taste of spoiled foods.42,43

Most descriptions of human and veterinary poisonings from molds involve

eating moldy foods.41,43-46 Acute human intoxications have also been

attributed to inhalation exposures of agricultural workers to silage or

spoiled grain products that contained high concentrations of fungi,

bacteria, and organic debris with associated endotoxins, glucans, and

mycotoxins.47,48 Related conditions including “pulmonary

mycotoxicosis,†“grain fever,†and others are referred to more broadly as

“organic dust toxic syndrome†(ODTS).49 Exposures associated with

ODTS have been described as a “fog†of particulates50 or an initial

“thick airborne dust†that “worsened until it was no longer

possible to see across the room.â€51 Total microorganism counts have

ranged from 105-109 per cubic meter of air52 or even 109-1010 spores per

cubic meter,53,54 extreme conditions not

ordinarily encountered in the indoor home, school, or office

environment.

“Sick building syndrome,†or “non-specific building-related

illness,†represents a poorly defined set of symptoms (often sensory)

that are attributed to occupancy in a building. Investigation generally

finds no specific cause for the complaints, but they may be attributed to

fungal growth if it is found. The potential role of building-associated

exposure to molds and associated mycotoxins has been investigated,

particularly in instances when Stachybotrys chartarum (aka Stachybotrys

atra) was identified.55-58 Often referred to in the lay press by the

evocative, but meaningless terms, “toxic mold†or “fatal fungus,â€

S. chartarum elicits great concern when found in homes, schools, or

offices, although it is by no means the only mold found indoors that is

capable of producing mycotoxins.35,36,59,60 Recent critical reviews of

the literature35,61-67 concluded that

indoor airborne levels of microorganisms are only weakly correlated with

human disease or building-related symptoms and that a causal relationship

has not been established between these complaints and indoor exposures to

S. chartarum.

A 1993-1994 series of cases of pulmonary hemorrhage among infants in

Cleveland, Ohio, led to an investigation by the CDC and others. No causal

factors were suggested initially,68 but eventually these same

investigators proposed that the cause had been exposures in the home to

S. chartarum and suggested that very young infants might be unusually

vulnerable.69-71 However, subsequent detailed re-evaluations of the

original data by CDC and a panel of experts led to the conclusion that

these cases, now called " acute idiopathic pulmonary hemorrhage in

infants,â€72 had not been causally linked to S. chartarum exposure.73

If mycotoxins are to have human health effects, there must be an actual

presence of mycotoxins, a pathway of exposure from source to susceptible

person, and absorption of a toxic dose over a sufficiently short period of

time. As previously noted, the presence of mycotoxins cannot be presumed

from the mere presence of a toxigenic species. The pathway of exposure in

home, school, and office settings may be either dermal (eg, direct contact

with colonized building materials) or inhalation of aerosolized spores,

mycelial fragments, or contaminated substrates. Because mycotoxins are not

volatile, the airborne pathway requires active generation of that aerosol.

For toxicity to result, the concentration and duration of exposure must be

sufficient to deliver a toxic dose. What constitutes a toxic dose for

humans is not known at the present time, but some estimates can be made

that suggest

under what circumstances an intoxication by the airborne route might be

feasible.

Experimental data on the in vivo toxicity of mycotoxins are scant.

Frequently cited are the inhalation LC50 values determined for mice,

rats, and guinea pigs exposed for 10 minutes to T-2 toxin, a

trichothecene mycotoxin produced by Fusarium spp.74,75 Rats were most

sensitive in these studies, but there was no mortality in rats exposed to

1.0 mg T-2 toxin/m3. No data were found on T-2 concentrations in Fusarium

spores, but another trichothecene, satratoxin H, has been reported at a

concentration of 1.0 x 10-4 ng/spore in a “highly toxic†S.

chartarum strain s. 72.31 To provide perspective relative to T-2 toxin,

1.0 mg satratoxin H/m3 air would require 1010 (ten billion) of these s.

72 S. chartarum spores/m3.

In single-dose in vivo studies, S. chartarum spores have been

administered intranasally to mice31 or intratracheally to rats.76,77 High

doses (30 x 106 spores/kg and higher) produced pulmonary inflammation and

hemorrhage in both species. A range of doses were administered in the rat

studies and multiple, sensitive indices of effect were monitored,

demonstrating a graded dose response with 3 x 106 spores/kg being a clear

no-effect dose. Airborne S. chartarum spore concentrations that would

deliver a comparable dose of spores can be estimated by assuming that all

inhaled spores are retained and using standard default values for human

subpopulations of particular interest78 – very small infants,â€

school-age children,††and adults.†††The no-effect dose in

rats (3 x 106 spores/kg) corresponds to continuous 24-hour exposure to

2.1 x 106 spores/m3 for infants,

6.6 x 106 spores/m3 for a school-age child, or 15.3 x 106

spores/m3 for an adult.

That calculation clearly overestimates risk because it ignores the

impact of dose rate by implicitly assuming that the acute toxic effects

are the same whether a dose is delivered as a bolus intratracheal

instillation or gradually over 24 hours of inhalation exposure. In fact, a

cumulative dose delivered over a period of hours, days, or weeks is

expected to be less acutely toxic than a bolus dose, which would overwhelm

detoxification systems and lung clearance mechanisms. If the no-effect 3 x

106 spores/kg intratracheal bolus dose in rats is regarded as a 1-minute

administration (3 x 106 spores/kg/min), achieving the same dose rate in

humans (using the same default assumptions as previously) would require

airborne concentrations of 3.0 x 109 spores/m3 for an infant, 9.5 x 109

spores/m3 for a child, or 22.0 x 109 spores/m3 for an adult.

In a repeat-dose study, mice were given intranasal treatments twice

weekly for three weeks with “highly toxic†s. 72 S. chartarum spores

at doses of 4.6 x 106 or 4.6 x 104 spores/kg (cumulative doses over three

weeks of 2.8 x 107 or 2.8 x 105 spores/kg).79 The higher dose caused

severe inflammation with hemorrhage, while less severe inflammation, but

no hemorrhage was seen at the lower dose of s. 72 spores. Using the same

assumptions as previously (and again ignoring dose-rate implications),

airborne S. chartarum spore concentrations that would deliver the

non-hemorrhagic cumulative three-week dose of 2.8 x 105 spores/kg can be

estimated as 9.4 x 103 spores/m3 for infants, 29.3 x 103 spores/m3 for a

school-age child, and 68.0 x 103 spores/m3 for adults (assuming

exposure for 24 hours per day, 7 days per week, and 100% retention of

spores).

The preceding calculations suggest lower bound estimates of airborne

S. chartarum spore concentrations corresponding to essentially no-effect

acute and subchronic exposures. Those concentrations are not infeasible,

but they are improbable and inconsistent with reported spore

concentrations. For example, in data from 9,619 indoor air samples from

1,717 buildings, when S. chartarum was detected in indoor air (6% of the

buildings surveyed) the median airborne concentration was 12 CFU/m3 (95%

CI 12 to 118 CFU/m3).80

Recommendations

The presence of toxigenic molds within a home, school, or office

environment should not by itself be regarded as demonstrating that

mycotoxins were present or that occupants of that environment absorbed a

toxic dose of mycotoxins.

Indoor air samples with contemporaneous outdoor air samples can

assist in evaluating whether or not there is mold growth indoors; air

samples may also assist in evaluating the extent of potential indoor

exposure. Bulk, wipe, and wall cavity samples may indicate the presence

of mold, but do not contribute to characterization of exposures for

building occupants.

After the source of moisture that supports mold growth has been

eliminated, active mold growth can be eliminated. Colonized porous

materials, eg, clothing or upholstery, can be cleaned using appropriate

routine methods, eg, washing or dry cleaning clothing, and need not be

discarded unless cleaning fails to restore an acceptable appearance.

When patients associate health complaints with mold exposure,

treating physicians should evaluate all possible diagnoses, including

those unrelated to mold exposure, ie, consider a complete appropriate

differential diagnosis for the patient’s complaints. To the extent that

signs and symptoms are consistent with immune-mediated disease, immune

mechanisms should be investigated.

The possibility of a mycotoxicosis as an explanation for specific

signs and symptoms in a residential or general office setting should be

entertained only after accepted processes that are recognized to occur

have been appropriately excluded and when mold exposure is known to be

uncommonly high. If a diagnosis of mycotoxicosis is entertained,

specific signs and symptoms ascribed to mycotoxins should be consistent

with the potential mycotoxins present and their known biological effects

at the potential exposure levels involved.

Summary Molds are common and important allergens. About 5% of

individuals are predicted to have some allergic airway symptoms from molds

over their lifetime. However, it should be remembered that molds are not

dominant allergens and that the outdoor molds, rather than indoor ones,

are the most important. For almost all allergic individuals, the reactions

will be limited to rhinitis or asthma; sinusitis may occur secondarily due

to obstruction. Rarely do sensitized individuals develop uncommon

conditions such as ABPA or AFS. To reduce the risk of developing or

exacerbating allergies, mold should not be allowed to grow unchecked

indoors. When mold colonization is discovered in the home, school, or

office, it should be remediated after the source of the moisture that

supports its growth is identified and eliminated. Authoritative guidelines

for mold remediation are available.81-83

Fungi are rarely significant pathogens for humans. Superficial fungal

infections of the skin and nails are relatively common in normal

individuals, but those infections are readily treated and generally

resolve without complication. Fungal infections of deeper tissues are rare

and in general are limited to persons with severely impaired immune

systems. The leading pathogenic fungi for persons with nonimpaired immune

function, Blastomyces, Coccidioides, Cryptococcus, and Histoplasma, may

find their way indoors with outdoor air, but normally do not grow or

propagate indoors. Due to the ubiquity of fungi in the environment, it is

not possible to prevent immune-compromised individuals from being exposed

to molds and fungi outside the confines of hospital isolation units.

Some molds that propagate indoors may, under some conditions, produce

mycotoxins that can adversely affect living cells and organisms by a

variety of mechanisms. Adverse effects of molds and mycotoxins have been

recognized for centuries following ingestion of contaminated foods.

Occupational diseases are also recognized in association with inhalation

exposure to fungi, bacteria, and other organic matter, usually in

industrial or agricultural settings. Molds growing indoors are believed by

some to cause building-related symptoms. Despite a voluminous literature

on the subject, the causal association remains weak and unproven,

particularly with respect to causation by mycotoxins. One mold in

particular, Stachybotrys chartarum, is blamed for a diverse array of

maladies when it is found indoors. Despite its well-known ability to

produce mycotoxins under appropriate growth conditions,

years of intensive study have failed to establish exposure to S.

chartarum in home, school, or office environments as a cause of adverse

human health effects. 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.

Mold spores are present in all indoor environments and cannot be

eliminated from them. Normal building materials and furnishings provide

ample nutrition for many species of molds, but they can grow and amplify

indoors only when there is an adequate supply of moisture. Where mold

grows indoors there is an inappropriate source of water that must be

corrected before remediation of the mold colonization can succeed. Mold

growth in the home, school, or office environment should not be tolerated

because mold physically destroys the building materials on which it grows,

mold growth is unsightly and may produce offensive odors, and mold is

likely to sensitize and produce allergic responses in allergic

individuals. Except for persons with severely impaired immune systems,

indoor mold is not a source of fungal infections. Current scientific

evidence does not support the proposition that human

health has been adversely affected by inhaled mycotoxins in home,

school, or office environments.

____________________

Acknowledgments This ACOEM statement was prepared by D.

Hardin, PhD, Bruce J. Kelman, PhD, DABT, and Saxon, MD, under the

auspices of the ACOEM Council on Scientific Affairs. It was peer-reviewed

by the Council and its committees, and was approved by the ACOEM Board of

Directors on October 27, 2002. Dr. Hardin is the former Deputy Director of

NIOSH, Assistant Surgeon General (Retired), and Senior Consultant to

Global Tox, Inc, where Dr. Kelman is a Principal. Dr. Saxon is Professor

of Medicine at the School of Medicine, University of California at Los

Angeles. ____________________

†5th percentile body weight for 1-month-old male infants, 3.16 kg;

respiratory rate for infants under 1 year of age, 4.5 m3/day78

††50th percentile body weight for 6-year-old boys, 22 kg;

respiratory rate for children age 6-9, 10.0 m3/day78

†††50th percentile body weight for men aged 25-34 years, 77.5 kg;

respiratory rate for men age 19-65, 15.2 m3/day78

____________________

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

Results 1 - 16 of 16 5 10 15 20 25 30 50

1. ACOEM Mold Statement up for review/updating

(News/Latest)

The problematic ACOEM mold position statement (see below) is under

review for updating and ACOEM is soliciting comments from its members.

Physicians and researchers with mold or damp-building related,

2. Mold Science / Conflicts of Interest: Critique of ACOEM

Mold Statement & Letters to Editor

(News/Latest)

From: VOL 14/NO 4, OCT/DEC 2008 • www.ijoeh.com Conflicts of Interest

and the ACOEM Statement on Mold (Dr. Craner) VOL 15/NO 1, JAN/MAR 2009

• www.ijoeh.com (Letters to the Editor) Rea

3. Chemical-related sensitivity is associated with gene

variants

(Information/Multiple Chemical Sensitivities Info)

... (IEI). In a position paper from 1999 the American College of

Occupational and Environmental Medicine (ACOEM) stated that these terms refer to

recurrent non-specific symptoms from multiple organ sy...

4. Obama pledges schools upgrade in stimulus plan

(News/Latest)

...past, incorrect position papers on environmental illness caused by

mold, by medical associations such as ACOEM and AAAAI that now mislead

these physicians immediate respite for those suffering i...

5. Adverse Health Effects of Indoor Molds

(Information/Sick Building Symptoms)

...nnett J, Klich M. Mycotoxins. Clin Microbiol Rev 2003; 16(3):

497–516. [35] Hardin B, Kelman B, Saxon A. ACOEM evidence base statement.

Adverse health effects associated with molds in the indoor envir...

6. Mold-Sick Teacher presents at New York State Toxic Mold

Task Force Meeting

(News/Latest)

...ummary did not contain all of the most important findings, from

2004 - 2006, and unfortunately cites the ACOEM Position Paper, too soon to

reveal the accusations that it supports corporate inter...

7. CA Research Bureau (2006): Mold

(Information/Mold Education)

...ummary did not contain all of the most important findings, from

2004 - 2006, and unfortunately cites the ACOEM Position Paper, too soon to

reveal the accusations that it supports corporate inter...

8. ACOEM, Expose! Updated 3/08

(News/Latest)

...essing the problems of dangerous, damp buildings? Read the

accusations against ACOEM* by IJOEH**, the ACOEM response and IJOEH's

March, 2008 reply *American College of...

9. ACOEM, Expose! Updated 3/08

(Information/Mold Education)

...essing the problems of dangerous, damp buildings? Read the

accusations against ACOEM* by IJOEH**, the ACOEM response and IJOEH's

March, 2008 reply *American College of...

10. Adverse Health Effects of Indoor Molds

(Information/Mold Research)

...nnett J, Klich M. Mycotoxins. Clin Microbiol Rev 2003; 16(3):

497–516. [35] Hardin B, Kelman B, Saxon A. ACOEM evidence base statement.

Adverse health effects associated with molds in the indoor envir...

11. ACOEM, Expose! Updated 3/08

(Information/Sick Building Symptoms)

...essing the problems of dangerous, damp buildings? Read the

accusations against ACOEM* by IJOEH**, the ACOEM response and IJOEH's

March, 2008 reply *American College of...

12. Pathogenic References

(Information/Fungal Glossary)

...Green WR. Cornea. 1984-85;3(3):213-6. A 70-year-old white man

developed mycotic keratitis following phacoemulsification and intraocular lens

implantation. Extensive therapeutic surgery was necessar...

13. Pediatrics Health Effects

(News/Latest)

...l Academies Press; 2004 American College of Occupational and

Environmental Medicine. Available at: www.acoem.org/guidelines/article. Accessed

December 1, 2005 Brown CM, Redd SC, Damon SA; Centers ...

14. Wall Street Journal Reports Conflicts

(News/Latest)

...ied in part on a position paper from the American College of

Occupational and Environmental Medicine, or ACOEM. Citing a substance some molds

produce called mycotoxins, the paper said " scientific...

15. American Academy of Pediatrics Policy Statement on

Molds

(Information/Mold Research)

...l Academies Press; 2004 American College of Occupational and

Environmental Medicine. Available at: www.acoem.org/guidelines/article. Accessed

December 1, 2005 Brown CM, Redd SC, Damon SA; Centers ...

16. How should I protect workers remediating mold?

(Information/Admin FAQs)

... Health Effects Associated with Molds in the Indoor Environment.

[Online]. Available: http://www.acoem.org/guidelines/pdf/mold-10-27-02.pdf

American Conference of Governmental Industri...

Brinchman

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