Re: Hypersensitivity pneumonitis~Toxic effects of mold exposure~Irritant effects of

[Guest guest]

Okay....I'll bite!

I was exposed to high levels of several types of molds. The one that I took

samples of was Stachybotrys. The idiot contractors doing the remodel of the

company, were scraping the mold off the walls sending the spores airborne. ALL

OVER THE PLACE!!!! Not at any time was any protective wear worn by anyone , nor

were we notified of the mold levels in the building.

Now what??????

Marcie

LymeAngl@... wrote:

Hypersensitivity pneumonitis

HP, also referred to as extrinsic allergic alveolitis, is a disease that

exists in acute, subacute, and chronic forms but with considerable overlap. It

is

an allergic disease in which the allergen is inhaled in the form of an organic

dust of bacterial, fungal, vegetable, or avian origin. Both sensitization and

the elicitation of the disease state generally require high-dose exposure,

prolonged exposure, or both to the causative allergen. Many cases are, in fact,

occupational because of this. There are reports of a similar, if not

identical, disease from workers exposed to inhaled chemicals, especially

isocyanates. A

few instances of the disease have been attributed to systemically

administered drugs.

HP is rare, and most cases have been reported in certain occupations, such as

farming, and in hobbyists, such as persons who raise pigeons. It is not a

reportable disease, and therefore prevalence and incidence are difficult to

estimate. The immunopathogenesis of the disease is believed to be cell-mediated

(delayed) hypersensitivity. Allergen-specific precipitins are often present in

serum and are important is establishing exposure. Precipitins might also play a

role in the mechanism of the acute phase of the disease. HP results in acute

episodes of noninfectious, immunologically mediated interstitial pneumonitis

(ie, alveolitis), which might eventually produce restrictive irreversible lung

disease.

The diagnosis requires a clinical and environmental history, relevant

physical examination findings, chest radiography or computed tomographic

scanning,

high-resolution computed tomographic scanning, pulmonary function testing,

bronchoalveolar lavage, and transbronchial or open lung biopsy. Specific

diagnosis

of the responsible allergen is performed by testing for IgG antibody to the

allergen extract, typically by testing for the presence of precipitins in the

Ouchterlony double-diffusion assay. In some instances provocation inhalation

challenge to the suspected allergen extract might be necessary to replicate

pertinent clinical and laboratory responses. Finally, a favorable response to

the

elimination of the inhaled antigen, administration of prednisone, or both is

confirmatory. Because a differential diagnosis covers a number of respiratory

diseases, an accurate diagnosis of HP demands that the clinical diagnosis be

ensured.

Exposure to domestic specific indoor fungal spores is an extremely unlikely

cause of HP, except in highly unusual circumstances, such as workplace

exposure.

Conclusions:

• HP is an uncommon but important disease that can occur as a result of mold

exposure, particularly in occupational settings with high levels of exposure.

Infection

Superficial mold infections (eg, tinea cruris, onychomycosis, and thrush) are

common in healthy individuals and result primarily from local changes in the

cutaneous or mucosal barrier, resident microflora, or both.24 and 25 These

infections are not the result of environmental exposure, except occasionally as

r

elated to certain animal vectors. Indeed, molds of the Malassezia genus are

resident on the vast majority of human subjects and only become evident as “

tinea versicolor†during periods of more exuberant growth. A limited number of

molds (eg, coccidiomycosis, histoplasmosis, and blastomycosis) are aggressive

pathogens in otherwise healthy persons. Acquisition of these infections is

generally related to specific outdoor activities-exposures. Individuals with

recognized primary and secondary immunodeficiency disorders are at increased

risk for

infection with a wide range of opportunistic fungi, with the risk varying

with the degree and nature of the specific immunodeficiency. Opportunistic

fungal

infections are typically associated with cellular rather than (isolated)

humoral immunodeficiencies. Generally, host factors, rather than environmental

exposure, are the critical factor in the development of opportunistic mold

infection in immunocompromised individuals because exposure to potential fungal

opportunistic pathogens (eg, Aspergillus species) is ubiquitous in normal

outdoor

and indoor environments. Accepted histologic and microbiologic methods should

be used to make the diagnosis of fungal infection.

Conclusions:

• Common superficial fungal infections are determined by local changes in the

skin barrier, resident microflora, or both.

• A very limited number of aggressive fungal pathogens can be acquired

through specific outdoor exposures.

• Host factors, rather then environmental exposure, are the main determinant

of opportunistic fungal infection.

Toxic effects of mold exposure

Ingestion

Ingestion of mycotoxins in large doses (generally on the order of a milligram

or more per kilogram of body weight) from spoiled or contaminated foods can

cause severe human illness.26 Toxicity from ingested mycotoxins is primarily a

concern in animal husbandry, although human outbreaks do occur occasionally

when starvation forces subjects to eat severely contaminated food. Specific

adverse effects from a given toxin generally occur in a narrower and

better-defined dose range than for immunologic or allergic effects that might

vary across

much broader dose ranges. Some mycotoxins, such as ocratoxins and aflatoxins,

are commonly found in food stuffs, including grain products and wines, and

peanut products, respectively, such that there are governmental regulations as

to

the amounts of allowable aflatoxin in foods.27 and 28 Acute high-intensity

occupational exposures to mixed bioaerosols have given rise to a clinical

picture

called “toxic dust syndrome.†The nature of the responsible agent or agents

in that condition remains undefined, and the observed adverse effects reported

have been transient. Such exposures are highly unlikely in nonoccupational

settings.

Toxicity caused by inhalation

The term mold toxicity as used here refers to the direct injurious effects of

mold-produced molecules, so-called mycotoxins, on cellular function. Toxicity

should not be used to refer to changes related to innate immune responses

(eg, nonspecific inflammation caused by mold particulates) or to adaptive immune

responses (eg, induction of IgE or IgG antibodies). Mycotoxins are

low-molecular-weight chemicals produced by molds that are secondary metabolites

unnecessary for the primary growth and reproduction of the organisms. In-depth

review

of the toxicology of mycotoxins and their potential for adverse health effects

can be found elsewhere.1 and 2 It is important to emphasize key principles of

toxicology relevant to patient concerns about possible toxic effects from mold

exposure.

Only certain mold species produce specific mycotoxins under specific

circumstances. Importantly, the mere presence of such a mold should not be taken

as

evidence that the mold was producing any mycotoxin. For a toxic effect to occur

in a subject, (1) the toxin must be present, (2) there must be a route of

exposure, and (3) the subject must receive a sufficient dose to have a toxic

effect. In the nonoccupational setting the potential route of exposure is

through

inhalation. Mycotoxins are not volatile and, if found in the respirable air,

are associated with mold spores or particulates. They are not cumulative toxins,

having half-lives ranging from hours to days depending on the specific

mycotoxin. Calculations for both acute and subacute exposures on the basis of

the

maximum amount of mycotoxins found per mold spore for various mycotoxins and the

levels at which adverse health effects are observed make it highly improbable

that home or office mycotoxin exposures would lead to a toxic adverse health

effects.1 and 29

Thus we agree with the American College of Occupational and Environmental

Medicine evidence-based statement and the Institute of Medicine draft, which

conclude that the evidence does not support the contention that

mycotoxin-mediated

disease (mycotoxicosis) occurs through inhalation in nonoccupational

settings. Furthermore, the contention that the presence of mycotoxins would give

rise

to a whole panoply of nonspecific complaints is not consistent with what is

known to occur; when a toxic dose is achieved (eg, through ingestion of spoiled

foods), there is a specific pattern of illness seen for specific mycotoxins.

Conclusions:

• The occurrence of mold-related toxicity (mycotoxicosis) from exposure to

inhaled mycotoxins in nonoccupational settings is not supported by the current

data, and its occurrence is improbable.

Irritant effects of mold exposure

The Occupational Health and Safety Administration defines an irritant as a

material causing “a reversible inflammatory effect on living tissue by

chemical

action at the site of contact.†Irritant effects are dose related, and the

effects are transient, disappearing when the exposure has decreased or ceased.

Molds produce a number of potentially irritating substances that can be

divided into volatile organic compounds (VOCs) and particulates (eg, spores,

hyphae

fragments, and their components). The threshold level of irritant response

depends on the intrinsic properties of the specific material involved, the level

plus length of exposure, and the innate sensitivity of the exposed tissues

(eg, the skin versus nasal mucosa).

VOCs made by molds (MVOCs) are responsible for their musty odor. MVOCs

include a wide range of alcohols, ketones, aldehydes, esters, carboxylic acids,

lactones, terpenes, sulfur and nitrogen compounds, and aliphatic and aromatic

hydrocarbons.30 Although levels causing irritant effects have been established

for

many VOCs, MVOC levels measured in damp buildings are usually at a level so

low (on the order of nanograms to micrograms per cubic meter) that exposure

would not be expected to cause complaints of irritation in human subjects.31

Because there are other sources of VOCs indoors, measurement of indoor airborne

concentrations of MVOCs is rarely done.

Mold particles (spores, hyphal fragments, and their structural components)

are not volatile. These structural mold compounds (particulates) have been

suggested to cause inflammation through deposition on mucus membranes of their

attached glucans and mannans. However, whether such effects occur clinically

remains unproved. In fact, subjects exposed to airborne concentrations of

between

215,000 and 1,460,000 mold spores/m3 at work showed no differences in

respiratory symptoms at work versus while on vacation nor was there evidence of

increased inflammatory markers in their nasal lavage fluids related to their

mold

exposure at work.32 Thus mold particulates generally found indoors, even in damp

buildings, are not likely to be irritating.

It should be emphasized that irritant effects involve the mucus membranes of

the eyes and upper and lower respiratory tracts and are transient, so that

symptoms or signs persisting weeks after exposure and those accompanied by

neurologic, cognitive, or systemic complaints (eg, chronic fatigue) should not

be

ascribed to irritant exposure.

[Guest guest]

BOY DOES THAT SOUND FAMILIAR, MARCIE--I HOPE YOU ARE GETTING BETTER?!

V.

Re: [] Hypersensitivity pneumonitis~Toxic effects of

mold exposure~Irritant effects of

Okay....I'll bite!

I was exposed to high levels of several types of molds. The one that I

took samples of was Stachybotrys. The idiot contractors doing the remodel of

the company, were scraping the mold off the walls sending the spores

airborne. ALL OVER THE PLACE!!!! Not at any time was any protective wear

worn by anyone , nor were we notified of the mold levels in the building.

Now what??????

Marcie

LymeAngl@... wrote:

Hypersensitivity pneumonitis

HP, also referred to as extrinsic allergic alveolitis, is a disease that

exists in acute, subacute, and chronic forms but with considerable overlap.

It is

an allergic disease in which the allergen is inhaled in the form of an

organic

dust of bacterial, fungal, vegetable, or avian origin. Both sensitization

and

the elicitation of the disease state generally require high-dose exposure,

prolonged exposure, or both to the causative allergen. Many cases are, in

fact,

occupational because of this. There are reports of a similar, if not

identical, disease from workers exposed to inhaled chemicals, especially

isocyanates. A

few instances of the disease have been attributed to systemically

administered drugs.

HP is rare, and most cases have been reported in certain occupations, such

as

farming, and in hobbyists, such as persons who raise pigeons. It is not a

reportable disease, and therefore prevalence and incidence are difficult to

estimate. The immunopathogenesis of the disease is believed to be

cell-mediated

(delayed) hypersensitivity. Allergen-specific precipitins are often present

in

serum and are important is establishing exposure. Precipitins might also

play a

role in the mechanism of the acute phase of the disease. HP results in acute

episodes of noninfectious, immunologically mediated interstitial pneumonitis

(ie, alveolitis), which might eventually produce restrictive irreversible

lung

disease.

The diagnosis requires a clinical and environmental history, relevant

physical examination findings, chest radiography or computed tomographic

scanning,

high-resolution computed tomographic scanning, pulmonary function testing,

bronchoalveolar lavage, and transbronchial or open lung biopsy. Specific

diagnosis

of the responsible allergen is performed by testing for IgG antibody to the

allergen extract, typically by testing for the presence of precipitins in

the

Ouchterlony double-diffusion assay. In some instances provocation inhalation

challenge to the suspected allergen extract might be necessary to replicate

pertinent clinical and laboratory responses. Finally, a favorable response

to the

elimination of the inhaled antigen, administration of prednisone, or both is

confirmatory. Because a differential diagnosis covers a number of

respiratory

diseases, an accurate diagnosis of HP demands that the clinical diagnosis be

ensured.

Exposure to domestic specific indoor fungal spores is an extremely unlikely

cause of HP, except in highly unusual circumstances, such as workplace

exposure.

Conclusions:

â?¢ HP is an uncommon but important disease that can occur as a result of

mold

exposure, particularly in occupational settings with high levels of

exposure.

Infection

Superficial mold infections (eg, tinea cruris, onychomycosis, and thrush)

are

common in healthy individuals and result primarily from local changes in the

cutaneous or mucosal barrier, resident microflora, or both.24 and 25 These

infections are not the result of environmental exposure, except occasionally

as r

elated to certain animal vectors. Indeed, molds of the Malassezia genus are

resident on the vast majority of human subjects and only become evident as

â?o

tinea versicolorâ? during periods of more exuberant growth. A limited

number of

molds (eg, coccidiomycosis, histoplasmosis, and blastomycosis) are

aggressive

pathogens in otherwise healthy persons. Acquisition of these infections is

generally related to specific outdoor activities-exposures. Individuals with

recognized primary and secondary immunodeficiency disorders are at increased

risk for

infection with a wide range of opportunistic fungi, with the risk varying

with the degree and nature of the specific immunodeficiency. Opportunistic

fungal

infections are typically associated with cellular rather than (isolated)

humoral immunodeficiencies. Generally, host factors, rather than

environmental

exposure, are the critical factor in the development of opportunistic mold

infection in immunocompromised individuals because exposure to potential

fungal

opportunistic pathogens (eg, Aspergillus species) is ubiquitous in normal

outdoor

and indoor environments. Accepted histologic and microbiologic methods

should

be used to make the diagnosis of fungal infection.

Conclusions:

â?¢ Common superficial fungal infections are determined by local changes in

the

skin barrier, resident microflora, or both.

â?¢ A very limited number of aggressive fungal pathogens can be acquired

through specific outdoor exposures.

â?¢ Host factors, rather then environmental exposure, are the main

determinant

of opportunistic fungal infection.

Toxic effects of mold exposure

Ingestion

Ingestion of mycotoxins in large doses (generally on the order of a

milligram

or more per kilogram of body weight) from spoiled or contaminated foods can

cause severe human illness.26 Toxicity from ingested mycotoxins is primarily

a

concern in animal husbandry, although human outbreaks do occur occasionally

when starvation forces subjects to eat severely contaminated food. Specific

adverse effects from a given toxin generally occur in a narrower and

better-defined dose range than for immunologic or allergic effects that

might vary across

much broader dose ranges. Some mycotoxins, such as ocratoxins and

aflatoxins,

are commonly found in food stuffs, including grain products and wines, and

peanut products, respectively, such that there are governmental regulations

as to

the amounts of allowable aflatoxin in foods.27 and 28 Acute high-intensity

occupational exposures to mixed bioaerosols have given rise to a clinical

picture

called â?otoxic dust syndrome.â? The nature of the responsible agent or

agents

in that condition remains undefined, and the observed adverse effects

reported

have been transient. Such exposures are highly unlikely in nonoccupational

settings.

Toxicity caused by inhalation

The term mold toxicity as used here refers to the direct injurious effects

of

mold-produced molecules, so-called mycotoxins, on cellular function.

Toxicity

should not be used to refer to changes related to innate immune responses

(eg, nonspecific inflammation caused by mold particulates) or to adaptive

immune

responses (eg, induction of IgE or IgG antibodies). Mycotoxins are

low-molecular-weight chemicals produced by molds that are secondary

metabolites

unnecessary for the primary growth and reproduction of the organisms.

In-depth review

of the toxicology of mycotoxins and their potential for adverse health

effects

can be found elsewhere.1 and 2 It is important to emphasize key principles

of

toxicology relevant to patient concerns about possible toxic effects from

mold

exposure.

Only certain mold species produce specific mycotoxins under specific

circumstances. Importantly, the mere presence of such a mold should not be

taken as

evidence that the mold was producing any mycotoxin. For a toxic effect to

occur

in a subject, (1) the toxin must be present, (2) there must be a route of

exposure, and (3) the subject must receive a sufficient dose to have a toxic

effect. In the nonoccupational setting the potential route of exposure is

through

inhalation. Mycotoxins are not volatile and, if found in the respirable air,

are associated with mold spores or particulates. They are not cumulative

toxins,

having half-lives ranging from hours to days depending on the specific

mycotoxin. Calculations for both acute and subacute exposures on the basis

of the

maximum amount of mycotoxins found per mold spore for various mycotoxins and

the

levels at which adverse health effects are observed make it highly

improbable

that home or office mycotoxin exposures would lead to a toxic adverse health

effects.1 and 29

Thus we agree with the American College of Occupational and Environmental

Medicine evidence-based statement and the Institute of Medicine draft, which

conclude that the evidence does not support the contention that

mycotoxin-mediated

disease (mycotoxicosis) occurs through inhalation in nonoccupational

settings. Furthermore, the contention that the presence of mycotoxins would

give rise

to a whole panoply of nonspecific complaints is not consistent with what is

known to occur; when a toxic dose is achieved (eg, through ingestion of

spoiled

foods), there is a specific pattern of illness seen for specific mycotoxins.

Conclusions:

â?¢ The occurrence of mold-related toxicity (mycotoxicosis) from exposure to

inhaled mycotoxins in nonoccupational settings is not supported by the

current

data, and its occurrence is improbable.

Irritant effects of mold exposure

The Occupational Health and Safety Administration defines an irritant as a

material causing â?oa reversible inflammatory effect on living tissue by

chemical

action at the site of contact.â? Irritant effects are dose related, and the

effects are transient, disappearing when the exposure has decreased or

ceased.

Molds produce a number of potentially irritating substances that can be

divided into volatile organic compounds (VOCs) and particulates (eg, spores,

hyphae

fragments, and their components). The threshold level of irritant response

depends on the intrinsic properties of the specific material involved, the

level

plus length of exposure, and the innate sensitivity of the exposed tissues

(eg, the skin versus nasal mucosa).

VOCs made by molds (MVOCs) are responsible for their musty odor. MVOCs

include a wide range of alcohols, ketones, aldehydes, esters, carboxylic

acids,

lactones, terpenes, sulfur and nitrogen compounds, and aliphatic and

aromatic

hydrocarbons.30 Although levels causing irritant effects have been

established for

many VOCs, MVOC levels measured in damp buildings are usually at a level so

low (on the order of nanograms to micrograms per cubic meter) that exposure

would not be expected to cause complaints of irritation in human subjects.31

Because there are other sources of VOCs indoors, measurement of indoor

airborne

concentrations of MVOCs is rarely done.

Mold particles (spores, hyphal fragments, and their structural components)

are not volatile. These structural mold compounds (particulates) have been

suggested to cause inflammation through deposition on mucus membranes of

their

attached glucans and mannans. However, whether such effects occur clinically

remains unproved. In fact, subjects exposed to airborne concentrations of

between

215,000 and 1,460,000 mold spores/m3 at work showed no differences in

respiratory symptoms at work versus while on vacation nor was there evidence

of

increased inflammatory markers in their nasal lavage fluids related to their

mold

exposure at work.32 Thus mold particulates generally found indoors, even in

damp

buildings, are not likely to be irritating.

It should be emphasized that irritant effects involve the mucus membranes of

the eyes and upper and lower respiratory tracts and are transient, so that

symptoms or signs persisting weeks after exposure and those accompanied by

neurologic, cognitive, or systemic complaints (eg, chronic fatigue) should

not be

ascribed to irritant exposure.

[Guest guest]

Not better yet and it is still a big long fight......will let you all know

soon.( I hope) Going for my 13th IVIG tomorrow.....YUCK!!!!!!

Marcie

<toria@...> wrote:

BOY DOES THAT SOUND FAMILIAR, MARCIE--I HOPE YOU ARE GETTING BETTER?!

V.

Re: [] Hypersensitivity pneumonitis~Toxic effects of

mold exposure~Irritant effects of

Okay....I'll bite!

I was exposed to high levels of several types of molds. The one that I

took samples of was Stachybotrys. The idiot contractors doing the remodel of

the company, were scraping the mold off the walls sending the spores

airborne. ALL OVER THE PLACE!!!! Not at any time was any protective wear

worn by anyone , nor were we notified of the mold levels in the building.

Now what??????

Marcie

LymeAngl@... wrote:

Hypersensitivity pneumonitis

HP, also referred to as extrinsic allergic alveolitis, is a disease that

exists in acute, subacute, and chronic forms but with considerable overlap.

It is

an allergic disease in which the allergen is inhaled in the form of an

organic

dust of bacterial, fungal, vegetable, or avian origin. Both sensitization

and

the elicitation of the disease state generally require high-dose exposure,

prolonged exposure, or both to the causative allergen. Many cases are, in

fact,

occupational because of this. There are reports of a similar, if not

identical, disease from workers exposed to inhaled chemicals, especially

isocyanates. A

few instances of the disease have been attributed to systemically

administered drugs.

HP is rare, and most cases have been reported in certain occupations, such

as

farming, and in hobbyists, such as persons who raise pigeons. It is not a

reportable disease, and therefore prevalence and incidence are difficult to

estimate. The immunopathogenesis of the disease is believed to be

cell-mediated

(delayed) hypersensitivity. Allergen-specific precipitins are often present

in

serum and are important is establishing exposure. Precipitins might also

play a

role in the mechanism of the acute phase of the disease. HP results in acute

episodes of noninfectious, immunologically mediated interstitial pneumonitis

(ie, alveolitis), which might eventually produce restrictive irreversible

lung

disease.

The diagnosis requires a clinical and environmental history, relevant

physical examination findings, chest radiography or computed tomographic

scanning,

high-resolution computed tomographic scanning, pulmonary function testing,

bronchoalveolar lavage, and transbronchial or open lung biopsy. Specific

diagnosis

of the responsible allergen is performed by testing for IgG antibody to the

allergen extract, typically by testing for the presence of precipitins in

the

Ouchterlony double-diffusion assay. In some instances provocation inhalation

challenge to the suspected allergen extract might be necessary to replicate

pertinent clinical and laboratory responses. Finally, a favorable response

to the

elimination of the inhaled antigen, administration of prednisone, or both is

confirmatory. Because a differential diagnosis covers a number of

respiratory

diseases, an accurate diagnosis of HP demands that the clinical diagnosis be

ensured.

Exposure to domestic specific indoor fungal spores is an extremely unlikely

cause of HP, except in highly unusual circumstances, such as workplace

exposure.

Conclusions:

â?¢ HP is an uncommon but important disease that can occur as a result of

mold

exposure, particularly in occupational settings with high levels of

exposure.

Infection

Superficial mold infections (eg, tinea cruris, onychomycosis, and thrush)

are

common in healthy individuals and result primarily from local changes in the

cutaneous or mucosal barrier, resident microflora, or both.24 and 25 These

infections are not the result of environmental exposure, except occasionally

as r

elated to certain animal vectors. Indeed, molds of the Malassezia genus are

resident on the vast majority of human subjects and only become evident as

â?o

tinea versicolorâ? during periods of more exuberant growth. A limited

number of

molds (eg, coccidiomycosis, histoplasmosis, and blastomycosis) are

aggressive

pathogens in otherwise healthy persons. Acquisition of these infections is

generally related to specific outdoor activities-exposures. Individuals with

recognized primary and secondary immunodeficiency disorders are at increased

risk for

infection with a wide range of opportunistic fungi, with the risk varying

with the degree and nature of the specific immunodeficiency. Opportunistic

fungal

infections are typically associated with cellular rather than (isolated)

humoral immunodeficiencies. Generally, host factors, rather than

environmental

exposure, are the critical factor in the development of opportunistic mold

infection in immunocompromised individuals because exposure to potential

fungal

opportunistic pathogens (eg, Aspergillus species) is ubiquitous in normal

outdoor

and indoor environments. Accepted histologic and microbiologic methods

should

be used to make the diagnosis of fungal infection.

Conclusions:

â?¢ Common superficial fungal infections are determined by local changes in

the

skin barrier, resident microflora, or both.

â?¢ A very limited number of aggressive fungal pathogens can be acquired

through specific outdoor exposures.

â?¢ Host factors, rather then environmental exposure, are the main

determinant

of opportunistic fungal infection.

Toxic effects of mold exposure

Ingestion

Ingestion of mycotoxins in large doses (generally on the order of a

milligram

or more per kilogram of body weight) from spoiled or contaminated foods can

cause severe human illness.26 Toxicity from ingested mycotoxins is primarily

a

concern in animal husbandry, although human outbreaks do occur occasionally

when starvation forces subjects to eat severely contaminated food. Specific

adverse effects from a given toxin generally occur in a narrower and

better-defined dose range than for immunologic or allergic effects that

might vary across

much broader dose ranges. Some mycotoxins, such as ocratoxins and

aflatoxins,

are commonly found in food stuffs, including grain products and wines, and

peanut products, respectively, such that there are governmental regulations

as to

the amounts of allowable aflatoxin in foods.27 and 28 Acute high-intensity

occupational exposures to mixed bioaerosols have given rise to a clinical

picture

called â?otoxic dust syndrome.â? The nature of the responsible agent or

agents

in that condition remains undefined, and the observed adverse effects

reported

have been transient. Such exposures are highly unlikely in nonoccupational

settings.

Toxicity caused by inhalation

The term mold toxicity as used here refers to the direct injurious effects

of

mold-produced molecules, so-called mycotoxins, on cellular function.

Toxicity

should not be used to refer to changes related to innate immune responses

(eg, nonspecific inflammation caused by mold particulates) or to adaptive

immune

responses (eg, induction of IgE or IgG antibodies). Mycotoxins are

low-molecular-weight chemicals produced by molds that are secondary

metabolites

unnecessary for the primary growth and reproduction of the organisms.

In-depth review

of the toxicology of mycotoxins and their potential for adverse health

effects

can be found elsewhere.1 and 2 It is important to emphasize key principles

of

toxicology relevant to patient concerns about possible toxic effects from

mold

exposure.

Only certain mold species produce specific mycotoxins under specific

circumstances. Importantly, the mere presence of such a mold should not be

taken as

evidence that the mold was producing any mycotoxin. For a toxic effect to

occur

in a subject, (1) the toxin must be present, (2) there must be a route of

exposure, and (3) the subject must receive a sufficient dose to have a toxic

effect. In the nonoccupational setting the potential route of exposure is

through

inhalation. Mycotoxins are not volatile and, if found in the respirable air,

are associated with mold spores or particulates. They are not cumulative

toxins,

having half-lives ranging from hours to days depending on the specific

mycotoxin. Calculations for both acute and subacute exposures on the basis

of the

maximum amount of mycotoxins found per mold spore for various mycotoxins and

the

levels at which adverse health effects are observed make it highly

improbable

that home or office mycotoxin exposures would lead to a toxic adverse health

effects.1 and 29

Thus we agree with the American College of Occupational and Environmental

Medicine evidence-based statement and the Institute of Medicine draft, which

conclude that the evidence does not support the contention that

mycotoxin-mediated

disease (mycotoxicosis) occurs through inhalation in nonoccupational

settings. Furthermore, the contention that the presence of mycotoxins would

give rise

to a whole panoply of nonspecific complaints is not consistent with what is

known to occur; when a toxic dose is achieved (eg, through ingestion of

spoiled

foods), there is a specific pattern of illness seen for specific mycotoxins.

Conclusions:

â?¢ The occurrence of mold-related toxicity (mycotoxicosis) from exposure to

inhaled mycotoxins in nonoccupational settings is not supported by the

current

data, and its occurrence is improbable.

Irritant effects of mold exposure

The Occupational Health and Safety Administration defines an irritant as a

material causing â?oa reversible inflammatory effect on living tissue by

chemical

action at the site of contact.â? Irritant effects are dose related, and the

effects are transient, disappearing when the exposure has decreased or

ceased.

Molds produce a number of potentially irritating substances that can be

divided into volatile organic compounds (VOCs) and particulates (eg, spores,

hyphae

fragments, and their components). The threshold level of irritant response

depends on the intrinsic properties of the specific material involved, the

level

plus length of exposure, and the innate sensitivity of the exposed tissues

(eg, the skin versus nasal mucosa).

VOCs made by molds (MVOCs) are responsible for their musty odor. MVOCs

include a wide range of alcohols, ketones, aldehydes, esters, carboxylic

acids,

lactones, terpenes, sulfur and nitrogen compounds, and aliphatic and

aromatic

hydrocarbons.30 Although levels causing irritant effects have been

established for

many VOCs, MVOC levels measured in damp buildings are usually at a level so

low (on the order of nanograms to micrograms per cubic meter) that exposure

would not be expected to cause complaints of irritation in human subjects.31

Because there are other sources of VOCs indoors, measurement of indoor

airborne

concentrations of MVOCs is rarely done.

Mold particles (spores, hyphal fragments, and their structural components)

are not volatile. These structural mold compounds (particulates) have been

suggested to cause inflammation through deposition on mucus membranes of

their

attached glucans and mannans. However, whether such effects occur clinically

remains unproved. In fact, subjects exposed to airborne concentrations of

between

215,000 and 1,460,000 mold spores/m3 at work showed no differences in

respiratory symptoms at work versus while on vacation nor was there evidence

of

increased inflammatory markers in their nasal lavage fluids related to their

mold

exposure at work.32 Thus mold particulates generally found indoors, even in

damp

buildings, are not likely to be irritating.

It should be emphasized that irritant effects involve the mucus membranes of

the eyes and upper and lower respiratory tracts and are transient, so that

symptoms or signs persisting weeks after exposure and those accompanied by

neurologic, cognitive, or systemic complaints (eg, chronic fatigue) should

not be

ascribed to irritant exposure.