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Health Effects of Moulds (Molds): State of Knowledge

Caoimhín P. Connell
Forensic Industrial Hygienist

In spite of the recent media hype over the presence of mould (mold) in residences and the workplace, there is virtually no scientific or medical data that supports the level of fear and concern generated by misleading and sensationalized news reports.

All houses, offices, and workplaces have mould. All houses and workplaces contain the dreaded “toxic black mould” (a nonsensical term invented by the news media). Virtually every human, in virtually every location on earth inhales hundreds to hundreds of thousands of mould spores and mould fragments on a daily basis. And yet, contrary to common belief, there is currently no evidence that the presence of these moulds and the exposures to the same poses the threat to the health of members of the general public as suggested by irresponsible journalists, and dramatic news reports largely devoid of objective facts.

Ignoring for a moment that virtually all "mould tests" and all "mould samples" are completely invalid, and uninterpretable and cannot be used for decision making, indoor moulds almost always get the initial blame for complaints about indoor air quality. However, in the Summer of 2011, the US Department of Labor, OSHA published the guidelines Indoor Air Quality in Commercial and Institutional Buildings1, wherein OSHA referenced the Indoor Air Quality Investigation protocol in its Technical Manual and points out that all microbial contaminants combined (including viruses, fungi, mould, bacteria, nematodes, amoeba, pollen, dander, and mites) were found to be the primary sources of indoor air quality problems only 5% of the time. The unwarranted fear is propagated by a variety of “mould remediators” and “mould inspectors” who usually have no legitimate knowledge in mould or mycology but prey off the public’s fear and perform nonsensical and invalid mould “testing.”

In July of 2009, the World Health Organization (WHO) published its position paper 2on indoor moulds and Indoor Air Quality. Contrary to what many people in the mould remediation business want to believe, the WHO guidelines reinforced the findings of the 2004 Institute of Medicine mould study group. In that study, the IOM stated there was insufficient evidence to find a causal association between the presence of moulds and any of the claimed adverse health effects. That is, after reviewing the global scientific and medical literature, the IOM could not find sufficient evidence to support the argument that the normal presence of mould in residences and workplaces caused any adverse health effects.

These findings are consistent with other notable organizations, such as the “Health Alert” published by University Health Publishing and John Hopkins Medicine who state: 3

Popular reports about the health effects of mold are likely to include the term “toxic mold.” But that term can be misleading, the experts say. They point out that only certain mold spores produce toxins, and only under certain circumstances. Just because a particular mold can produce toxins doesn’t mean it will. Even if the mold is producing toxins, a person must breathe in a sufficient dose to be affected. It is highly unlikely that you could inhale enough mold in your home or office to receive a toxic dose.

The WHO and the IOM, however, both concluded there was an association between damp living spaces and some adverse health effects. The unfounded assumption by those unfamiliar with the studies presume that mould was responsible for the association, however, this is not the case. Although it is well established that there exists an “association” between damp in buildings and a slight increase in observed adverse health effects, it is also well established that no one has been able to conclusively demonstrate that the association is exclusively due to the presence of mould. WHO and the IOM note that dust mites, Bacteria, termites, protozoans, endotoxins, VOCs, formaldehyde, pesticides, viral survival and generally poor ventilation are similarly associated with damp, and these factors, too, are considered to be part of the etiological backdrop. As such, in the remediation of water damage, the stress is placed on correcting “damp” and not on removing mould.

The common misconception is that when water damage occurs, and/or mould is found to be present, it is imperative to find and remove the mould. However, this position is promoted mostly by companies who make a living from removing mould (including “hidden” mould), and therefore, the more mould they remove, the more money they make! Otherwise, there is no compelling reason to do any remediation beyond correcting the water damage, and (as part of that correction), address any remaining visible mould. The notion that “hidden mould” presents a significant threat to human health or the quality of indoor air, is a myth. All studies performed to date have demonstrated that mould hidden in walls, do not adversely impact the air quality in the occupied space.

Indeed, leaving mould contaminated surfaces inside a property following a remediation is not only unavoidable, it actually constitutes part of the decision making process incorporated in such texts as the so-called “Green Book” 4 and the WHO study, wherein WHO states:

The main challenge of field investigations is to decide which contaminated materials should be removed and which can be left in building assemblies with a reasonably low risk of indoor climate problems.

Far too many homeowners and property managers spend needless thousands of dollars of wasted financial resources unnecessarily tracking down and eliminating mould under the misconception that such removal is standard practice and is necessary to ensure good indoor air quality. In general, the removal of mould is considered to be acceptable when it is limited to that which is visible and/or known to be present and constitutes a problem due to aesthetic considerations. In general: 5

However, removal based on the mere fact of its presence, or based on nonspecific symptoms that are not related to mold exposure, is often not appropriate.

Similarly, other notable researchers have also concluded the same: : 6

…it is reasonable to infer that small amounts of mold enclosed in walls, floors, or ceilings will not have a large impact on the indoor air quality.

Studies and investigations performed by this author (Connell), consistent with other researchers, have not observed a correlation between mould hidden in walls and a degradation of indoor air quality or a correlation between mould hidden in walls and an increase in spore counts in occupied spaces.

Finally, we have encountered several poorly trained remediators and “mould consultants” who claim they need to find the hidden mould to pass the “final clearance sampling tests” following a mould remediation project. However, in short, there is no such thing as “clearance testing” for molds. No such tests, as commonly conducted, are scientifically valid, and none stand up to scientific scrutiny. The “Green-Book” for example, addresses “final clearance sampling” thusly:

18.5.2 Current mold remediation guidelines support the concept that project success depends on verification primarily through inspection that visible mold growth and associated debris and dust were appropriately removed. 7, 8, 9

The AIHA publication continues with:

The primary objective of mold remediation, based on based on guidelines published between 199310 and 200411, 12 is to remove visible mold growth and return material surfaces to a satisfactory condition.

And the section concludes with:

A difficulty associated with using air sampling as the primary means of achieving final clearance is the absence of numerical guidelines for airborne fungi and for bioaerosols in general. 13, 14, 15 IOM16, concluded that, although there is an association between respiratory health effects and dampness, the exact causal agents of irritation and respiratory disease are obscure. Thus, from a health effects viewpoint it remains uncertain whether the EHS investigator should sample during final clearance for total spores, culturable spores, hyphal fragments, specific allergens, glucans, endotoxins, or other agents.

Microorganisms are ubiquitous in our environment and within and upon the human body. There is no place on the planet Earth (or even in space 17) that man can go and avoid microorganisms. It is known that these organisms are present in every house on the planet to some extent, and a vast amount of data across the globe has firmly established the presence of airborne microbials. According to OSHA, 18 the Centers for Disease Control, (National Institute of Occupational Safety and Health) reported that during its investigations of reports of poor indoor air quality, microbiological contamination was suspected in only 5% of the cases.

In "healthy" air, it is very common to encounter moulds and/or Bacteria such as Aspergillus (including A. fumigatus and A. terreus), Pullularia, Stachybotrys atra, Acremonium, Aspergillus and Penicillium.

Moulds and Fungi

The Fungi
Depending on the reference, there may be as many as 1.5 million different species of fungi 19 on Earth; approximately 70,000 different species have been fully described.

In spite of their apparently small size, the Fungi include some of the largest living organisms on the planet. One such fungus, a single organism belonging to Armillaria, is estimated to cover over 1,500 acres and weighs in at over 4,400 tons. 20

Moulds are any kind of fungi that at some point in their lives grow extended appendages called "hyphae;" moulds are filamentous fungi. The hyphae form mats called "mycelium" which are usually easily seen with the naked eye. Therefore, all moulds are fungi, but not all fungi are moulds. Since the distinction between moulds and fungi is based on morphological characteristics, even some yeasts (another type of fungus), at some point in their development, may be considered to be a mould at that point and a yeast at other stages.

The Fungi are found on humans, in and on houseplants, in wine, beer, cheese, and maple syrup. We encounter fungi directly in our diets such as when we eat fungi like the Morchella esculenta; Agaricus bisporus; and perhaps the most famous of all - the French truffle: Tuber magnatum. Virtually every tree, houseplant, and bush probably is aided into full health by the mycorrhizae moulds which are intractably bound about its roots; and without which many plants could not survive.

Several studies have been conducted concerning the prevalence of moulds in "normal, clean" homes. In one study, 21 the authors reported finding that median levels of fungi identified in carpets (primarily from schools) in five states ranged from 10,000 colony forming units per gram of material (CFU/g) to 100,000 CFU/g except in Washington State, where median concentrations exceeded 100,000 CFU/g. It is also important to know that the commonly used unit of fungal concentrations in carpets and on surfaces -CFU/g - is grossly misunderstood by virtually all "certified mould experts" who do not realize that a reading of say 50,000 CFUs/g does not necessarily indicate an higher fungal density than that indicated by, say, 10,000 CFUs/g. These units (CFUs/g) are for the convenience of the laboratory and to be germane for fungal quantification, they need to be converted into useful values and slightly different units by the consultant before they can actually be used to denote a fungal population. Nevertheless, for the purposes of comparison, we will use the unit here; in another very large study, 22 a total of 243 bulk samples were collected from 30 "problem" buildings and 5 "control" (clean) buildings. The average concentration of fungi in the carpets in the problem buildings was 1,844,000 CFU/g. In the control (healthy) buildings, the average concentration was 30,256 CFU/g. Even in this study, one of the samples from the control buildings contained 100,000 CFU/g. In my experience, it is not uncommon to find fungal concentrations in excess of 50,000 CFU/g in healthy buildings.

(Certified mould inspectors are not actually certified in anything, and usually have virtually no legitimate training or knowledge in mycology, aerobiology or microbiology. The “certification” process is not recognized, and certificates are frequently nothing more than what the inspector has printed off their own computer. As a general rule, “certified mold inspectors” represent the lowest quality inspection and assessment services, and usually lack scientific foundation, in favor of the more lucrative “toxic” mould agenda. For a discussion of mould and its occurrence in properties complete with many photographs, visit our “Habits” page.)

Other researchers 23 have identified 1,000,000 CFU/g of dust or material as a "contamination indicator." Of the 1,000,000 CFU/g level, the US Department of Labor, Occupational Safety and Health Administration (OSHA) states: 24

Levels in excess of the above do not necessarily imply that the conditions are unsafe or hazardous. The type and concentrations of the airborne microorganisms will determine the hazard to employees.

Probably the most important part of OSHA's comments is that OSHA explicitly recognizes the importance of the airborne biota in the decision making process, rather than bulk sampling results.

Using an emerging technology called quantitative polymerase chain reaction analysis, qPCR, other studies have shown an excess of 10 million spores per gram of dust may be present in healthy houses.25,26

FACTs has collected hundreds of air samples from a variety of occupied spaces from Boston to Bakersfield and from Montana to Mexico. In our work, we see that for a northern latitude approximating the central portion of the U.S, clean- healthy houses typically have a "closed building" spore count (expressed as a statistic known as the MVUE) of no more than 500 spores per cubic meter of air with a 15% probability that any one randomly collected sample will exceed 1,000 spores per cubic meter of air. It is impossible to know the spore count of a house based on two or three samples (let alone one sample), and there is no scientific validity to correlate indoor samples to outdoor samples in closed building conditions. (That is - it is inappropriate to state that indoor levels are elevated based on the outdoor concentrations, for close-building conditions). For a discussion of "normal" spore concentrations and sampling issues, click here. For a discussion on why almost all mould testing is invalid, click here.

Therefore, once one recognizes that all carpets in homes contain fungi (often at very high concentrations), one realizes that the importance of such contamination is far less significant than elevated airborne fungal spores. And one must recognize that all homes contain "toxic moulds" on surfaces and in the air.

Allergic Reactions
It has been estimated that between 10% and 20% of the U.S. population exhibits an allergic reaction to something and up to 6% of the general population have a respiratory allergy to fungi. 27 Similarly, the prevalence of respiratory allergy to fungi is estimated to be between 20 to 30% in atopic (allergy-predisposed) individuals. 28

There are four general classifications of allergic responses, the response most germane to indoor moulds is the Type I "anaphylactic" response since it is this type of reaction that is the vastly predominate health hazard associated with indoor moulds. 29 Briefly, anaphylaxis (and other hypersensitivities) arise when an individual's immune system "recognizes" a particular molecular fragment (called an "epitope") of a compound (usually a protein). The immune system launches an inappropriate full-scale "attack" against what is probably an otherwise harmless agent (or indeed a person's own cellular protein).

Because an individual's response to an allergen is very different from person to person, it is difficult to determine an acceptable concentration of that allergen for the population as a whole. The concentration of an allergen needed to elicit a response so serious that a sensitive individual may die may be thousands of times lower than that needed to invoke so much as a sniffle in an equally healthy, but non-sensitized person.

Anaphylaxis is commonly known for its extreme manifestation called "anaphylactic shock." However, anaphylaxis also occurs in degrees; wherein "shock" is the most extreme anaphylactic reaction, and actually has a slightly different mechanism associated with its manifestation. Other milder forms of anaphylactic reactions such as those which occur in "hay fever" are more common.

Celery, lobster, peanuts, and an host of other common foods can make the sensitive person uncomfortable, ill or even kill a person who exhibits a hypersensitivity to any particular common food. Yet, we do not speak of "toxic peanuts" or "toxic milk," etc. Indeed, even the term "toxic mould" is a meaningless term,30 used mostly by the press and by individuals who are not familiar with mycology or toxicology. It is thought that, in theory, virtually all moulds have the potential to all degrees of anaphylaxis (including anaphylactic shock) following exposure. The common mushroom can be as toxic as the deadly Amanita mushroom to the person who is allergic to it. Therefore, all moulds have the potential to be "toxic moulds." However, as recent as November 2002, a prestigious medical organization 31 reported that indoor moulds, compared to outdoor moulds, were considered only a minor, (albeit important) factor in the development of allergic airway disease. Similarly, it has been reported elsewhere 32 that indoor exposures to cats, dust mites and cockroaches probably causes more health problems than do indoor moulds.

Similarly, many very common moulds including Stachybotrys atra produce compounds toxic to competing moulds and are designed to enhance the competitive edge of the organism producing the compound. Many of these compounds, called "mycotoxins," are also toxic to humans.

Probably the most studied and best known of these mycotoxins is the very common antibiotic penicillin which was originally isolated from the mould Penicillium. Some of the most common moulds on the planet, such as certain species of Fusarium, produce mycotoxins (such as the "aflatoxins" that are produced by the genus Aspergillus). Yet we humans have managed to live with Fusarium and Aspergillus for millennia with only very rare episodes of reported illnesses. Indeed, in a study by the Mayo Clinic, Aspergilli including A. clavatus, A. flavus (which produces a powerful carcinogen) A. fumigatus, and A. niger were colonized in the nasal passages of 43% of healthy volunteers.32a

Diseases which are the result of fungal infection are generally given the term "mycoses." Diseases which are the result of illnesses caused by the mycotoxins are called "mycotoxicoses." Histoplasmosis and cryptococcosis are examples of fungal infections. But, apart from a few fungi which attack human skin (athlete's foot, jock itch, sporotrichosis, etc.) fungi rarely infect man or other animals.33

Some fungal diseases however are endemic in the American population such as coccidioidomycosis. One of the most highly endemic regions in the U.S. is in the San Joaquin Valley of California and thus the eponym "San Joaquin Valley Disease" or "Valley Fever." The infection, although usually asymptomatic, is virtually universal in the endemic areas where perhaps as many as 80% of those residing in an endemic area become affected 34 within five years of initial residency. 35

Yet in spite of its huge impact on society, it is curious that the popular media has not given Valley Fever or jock itch the same notoriety as other "toxic indoor moulds" and has not turned Coccidioides immitis into the household name the way it did with Stachybotrys. The fact of the matter is that headlines about "athlete's foot" don't sell newspapers like "toxic mould" headlines. In writing about the current public concern about indoor moulds, Dr. Emil J. Bardana, Jr., M.D. of the Oregon Health Sciences University in Portland, OR stated: 36

This contemporary public health problem has frequently been discussed in the media and cyberspace without the benefit of scientific peer review. As a result, there has been distortion and exaggeration of the facts, and promotion of a brand of "toxic terror" among the population; ie, "babies dying of black mould exposure" is much more dramatic and fear-evoking than "babies dying of unknown causes."

Toxic Mould and Public Perception
That "toxic moulds" and other fungi and Bacteria exist in all of our homes and food to some degree is an absolute fact. Recent media reports usually center on now discredited reports of reported mould related illnesses. The media reports have frequently used as examples early reports of mould related illnesses cited by the U.S Department of Health and Human Services, Centers for Disease Control (CDC). Occasionally, "scientific" information presented in the popular media does not reflect current scientific thought, and tends to present information in a manner which sensationalizes the risks. A similar situation was seen in the late 1990's when the popular media sensationalized the proposed role of a mould called Scopulariopsis as causing Sudden Infant Death Syndrome. Follow-up studies failed to support the proposal. The news media was heavily criticized in medical literature for "…allowing their enthusiasm for a sensational story to overshadow cautious and careful reporting." 37

The flagship study which launched the American public into the realm of the "toxic mould" issue was a report in 1994 by the U.S. Centers for Disease Control titled "Acute Pulmonary Hemorrhage/Hemosiderosis Among Infants --Cleveland, January 1993-November 1994." 38 The CDC report implicated household moulds in general and a mould called Stachybotrys atra in particular as the causative agent for a disease observed in infants (acute idiopathic pulmonary hemosiderosis, or AIPH). However, the CDC report was criticized in scientific circles because its conclusions were not well supported by the underlying data.

In the CDC report, proper consideration was not given to alternate explanations of the occurrence of the observed disease. Potential epidemiological confounders and contradicting information was ignored by the report. For example, the presence of Stachybotrys spores in air samples taken from the "contaminated" houses was measured by two mycologists, who, based on their professional judgment, could only find agreement on the existence of Stachybotrys in the samples 56% of the time. 39 That is, in approximately half the samples, the two mycologists could not agree on the presence, absence or occurrence of the organism. This speaks to the issue of confidence in the data used to support the CDC's conclusions about "toxic mould" as the cause of the illness seen in the diseased children.

Also as reported by the CDC in their report, in 91% of the air samples obtained in the control homes (the non-contaminated homes which were used to compare the results), the measured concentration of Stachybotrys was below the level of detection (which seems to support the claim that Stachybotrys was not present in those homes.) But not reported by the CDC in their original report was the fact that in 81% of the air samples collected in the "contaminated" homes, the measured concentration of Stachybotrys was also below the level of detection, making the mean concentration of the organism an unreliable estimate of exposure. Indeed, in one "contaminated" air sample, the CDC admitted that it "potentially inflated" 40 (meaning "fabricated false data") a laboratory report which reported zero CFU/m3 of Stachybotrys, 41 but the CDC reported the value in the literature as 4 CFU/m3, thus falsely arguing that Stachybotrys was present in the sample at a concentration above the detection limit, when in fact Stachybotrys was not present in the sample above the detection limit.

Surface sampling showed that 43% of the "clean" (uncontaminated) homes, did in fact contain Stachybotrys. 42 There is some indication in the literature that if a sufficient number of samples are collected, the presence of Stachybotrys may be found in all houses.

As finally admitted by the CDC in March of 2000, the initial CDC report was not readily accepted by the scientific community. Unfortunately, the study had already been picked up by the popular media and quickly disseminated to the American public, resulting in several emergency (and possibly unnecessary) closures of buildings. In their final report on the issue of toxic mould 43 as the cause of the pulmonary illness observed in the earlier episodes, the CDC concluded that they had been mistaken in reporting that "toxic moulds" in general and Stachybotrys in particular were the cause for the observed illnesses. In the March 2000 statement, the CDC stated:

Both groups of reviewers concluded that the available evidence does not substantiate the [earlier] reported epidemiologic associations—between household water damage and AIPH or between household fungi and AIPH —or any inferences regarding causality.

However, retractions of this kind are not as exciting as reports of "toxic moulds" killing young children and the popular media failed to place the CDC retraction in the same light as the original alarming report. Therefore, most of the American public still believes that "toxic moulds" in general and Stachybotrys in particular are unequivocally an indoor hazard.

In fact, neither Stachybotrys nor any of the suspected mycotoxins were actually isolated from specimens taken from any of the infants. 44 However, it is important to remember that infection of the infants was not the only issue considered. The potential presence of mycotoxin from the organism in the air was what was at issue -- not infection or allergy, but a response to a toxin. There is no scientific basis for there being sufficient mycotoxin in the air to produce such a response, but that has been the general theme in a number of papers.

In fact, as recent as June of 2000 at the School of Public Health, Harvard University in Boston, Dr. Harriet Burge, Professor of Microbiology at Harvard, lectured that, to her knowledge, not a single case of confirmed mycotoxicosis due to indoor air had yet been reported. (Dr. Burge recognized the valid role of moulds in producing other indoor air complaints.) Dr. Burge is also a key author of several scientific texts on microbials including the 1999 American Conference of Governmental Industrial Hygiene manual titled Bioaerosols: Assessment and Control. During a professional conference in April of 2002 in Austin, Dr. Burge cautioned professionals in the field to avoid using the inappropriate terms "toxic moulds" and "pathogenic moulds" to describe indoor moulds and indoor mould exposures in an effort to curtail unwarranted public fears.

The state-of-the-art guidance document on fungal remediation is thought by many to be the Guidelines on Assessment and Remediation of Fungi in Indoor Environments which was published by the New York City Department of Health, Bureau of Environmental & Occupational Disease Epidemiology in April of 2000. According to those guidelines:

There are only a limited number of documented cases of health problems from indoor exposure to fungi.

The guidelines continue with:

The presence of fungi on building materials as identified by a visual assessment or by bulk/surface sampling results does not necessitate that people will be exposed or exhibit health effects. In order for humans to be exposed indoors, fungal spores, fragments, or metabolites must be released into the air and inhaled, physically contacted (dermal exposure), or ingested.

However, even Stachybotrys atra, which is probably the most maligned and feared indoor mould, is not as "toxic" as the media portray. The trichothecene mycotoxin which has given Stachybotrys a bad name is produced by only about a third of the species of Stachybotrys.45

Furthermore, the mycotoxins are not always produced by the organisms that do occasionally produce the compound; the mycotoxin is only produced under very specific stress conditions. Furthermore, the mycotoxin, when it is produced, is only produced in the spores and the spores are not readily removed from the main organism. It takes an unusual amount of mechanical effort to make the spores become airborne. The spores, when they are shaken loose, are so large they settle out within about 10 minutes 46 and so do not remain airborne for very long. Thus for a significant dose to occur, the recipient must be located in the immediate vicinity where the organism is being heavily disturbed. Finally, since there is only approximately 3 femtograms of toxin per spore, 47 it would take over 300,000 spores in a rodent's lungs to produce the one nanogram of toxin conservatively estimated as the quantity of toxin needed to make the animal ill. Based on these considerations, a human would have to be exposed for 100 continuous eight-hour days at 1,000 Stachybotrys atra spores per cubic meter to get the required amount of toxin.48

It is for this reason, that Dr. Vincent Miller, a researcher in the field of indoor moulds, stated: 49

Based on this model, it becomes apparent that most exposures to mold contaminated buildings would not be expected to cause adverse health effects.

These thoughts were echoed by Dr. Burge, who recently wrote: 50

These types of exposure are extremely rare and occur primarily in agricultural situations. Even for cancer, consistent exposure to levels higher than in the vast majority of homes and office/school workplaces would be necessary. These effects have only marginally been documented in agricultural situations. In general then, one can reassure patients that the symptoms they are experiencing, although real, are probably not associated with mycotoxin exposure. With the mycotoxin issue set aside, one can then proceed to a more likely diagnosis.

And also echoed by the American College of Occupational and Environmental Medicine who, in November 2002, issued a peer reviewed Evidence Based Statement, 51 wherein they made the observation that:

...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.

Due to the minute quantities of Stachybotrys located in most homes we visit, we usually find it unnecessary to determine if the species present in the homes are trichothecene producers. That is, significant quantities of the mycotoxin could not be produced by the extremely small quantities of Stachybotrys present.

Assessment of Dose and Exposure
Dose, not presence, is the key issue at stake. Several high profile studies exist which have been often quoted as describing a link between indoor moulds and illnesses. However, in most of those studies the actual human exposures were never quantified, making dose/response estimates unreliable. Many of the researchers in such studies assumed that there must have been unusual exposures based on visual indicators of moulds or water damage, sometimes even self reported conditions. Reliance on subjective exposure assessments provided by untrained parties outside of any standardized protocol produces exposure data that are very weak. Conclusions about mould exposures based on those data are not well supported by the data. For example, in the Finnish Jaakkola52 study claiming to establish a link between indoor moulds/dampness and asthma, the authors never quantified any aspect of dampness or mould for the "exposed" population, but relied on self reported exposures to dampness and mould. Researchers with the Danish research program "Mould in Buildings" (DAMIB) actually measured dusts and moulds and found no evidence of adverse health effects associated with mouldy or damp buildings. In a study53 of 525 teachers in a variety of mouldy, damp, and "healthy" buildings, the researchers found that complaints and physiological responses were actually higher in the dry "control" buildings than in the damp mouldy buildings:

In conclusion, exposure to damp and mouldy buildings at whole school level does not seem to influence irritative or lung symptoms or lung function at spirometry. Bronchial reactivity is higher in dry than in wet buildings indicating a possible bronchiolar irritation, which might be related to dust with or without moulds. Further analyses are needed to evaluate this hypothesis.

Another high-profile study 54 (Hodgson et al) is often referred to in the popular press as being a study that conclusively demonstrates a link between indoor mould exposures and illnesses. Shortly after the Hodgson paper came out, we spoke with Dr. Jarvis,55 co-author of the paper and Professor at the University of Maryland concerning the work. Dr. Jarvis informed me that in their study, they never actually measured the concentration of mycotoxins in the air during the study. Not usually reported by the press was a single sentence the authors used to qualify their findings when they stated:

The authors remain unsure whether toxins from Aspergillus species, Penicillium, or Stachybotrys may represent the primary cause. [of the observed illnesses]

In a more recent high-profile study, 56 (which we refer to here as the EHP study), purporting to be the first actual documented case of hypersensitivity pneumonitis (HP) resulting from ordinary residential exposures to mould had very serious flaws undermining the study (and subsequent causal link).

For a start, for indoor mould exposures to be translatable into quantitative information germane to the dynamics of indoor air associated illness, the mould must be predominantly airborne. Therefore, in a study which purports to make a link between "ordinary residential exposure" to airborne moulds and the onset of HP (an illness associated with inhaled triggers), one would have thought that the researchers would have sampled the air in the home to find out what the exposures were. In fact, in the EHP study, not one single air sample was collected. No samples were collected for moulds, fungi, endotoxins, or any other potential HP trigger. Instead, the researchers took bulk carpet samples. Unfortunately, it has been very well established and reported in the peer reviewed papers 57,58 that there is no correlation between carpet concentrations and air concentrations. Thus, the authors of the study did not even confirm that there was an "ordinary" exposure, let alone attempt to quantify it.

Furthermore, the woman involved in the study had massive self-administrated exposures to pyrethrin and permethrin insecticides in her home. It was estimated that the woman had emptied up to 40 aerosols cans of insecticide in her home to control a flea infestation in her house. The researchers themselves admit the exposure may have been a "contributing factor." It is possible that the very high exposures to the insecticide may equally have been exclusively responsible for the onset of the observed HP.

The researchers assumed exposure to indoor moulds based on the fact that the woman coincidentally had serum-precipitating antibodies for two of the several species of fungi found in her home. In fact, the woman's antibody response could have easily been due to an exposure to the organisms when she was a little girl, playing in her mother's garden. The researchers themselves recognized this fundamental drawback in their study and even stated so in their report when they admit:

The presence of serum-precipitating antibodies is evidence of prior exposure and antibody response to a substance, but does not confirm whether the disease was caused by the material.

In all, the study in question has other serious drawbacks such as:

1) The researchers never established or quantified airborne exposure, thus making a critical and necessary dose/response correlation possible. Without this information, one cannot make a reliable statement on causation.

2) The researchers claimed the subject's symptoms diminished when the woman moved to a new, "cleaner" dwelling. However, the researchers entirely failed to confirm the absence of moulds in the "clean" home where the woman moved when the symptoms ceased. The reality is that the mould exposures in her "clean" home could have been 5, 10, 20 or a 100 times higher than in the "dirty" home.

3) The researchers overlook all other confounders, exposures and potential exposures and such as the exposure to 40 cans of insecticide, endotoxins, TB exposure, the flea infestation that was reported in the woman's home, and a host of other possible factors that could overwhelm the mould issue into obscurity.

Other researchers 59 purporting to have observed an association between HP and indoor mould exposures have been somewhat more diligent in the application of good science in their investigations by considering (and arguably establishing) temporal and spatial relations with the onset of symptomology with the suspected house. However, even in this study, the authors used an airborne assessment technique that is incapable of proper enumeration of airborne organisms and the actual human exposures to the organisms was never quantified and the etiological agent was presumed, not demonstrated. One of the authors (Thornton) informed me 60that the word "Probable" in the title of the paper was inserted by the referees of the medical journal who felt a lesser degree of confidence in the causality than did the authors.

Work by Jacobs, et al61,62 is occasionally cited as evidence of HP as a result of exposures to indoor moulds. However, in both of the Jacobs studies referenced here, too many confounders (endotoxins, Mycobacterium/Avium complex, ozone, smoking, beta-glucans, etc) exist to view the studies as conclusive. Furthermore, proper quantification of exposures was not performed in either of the cited papers, rendering an exposure-response relationship unreliable. However, a strength found in the first Jacobs paper referenced was the fact that the researchers confirmed physiological hypersensitivity to suspected etiological agents. Nevertheless, the subject continued to be exposed to the agents in outdoor air without deleterious response, suggesting the suspected agents were not responsible for the HP.

Several reports 63 in the literature implicate moulds as causative agents in indoor air complaints. However, in each case, without exception, the association was assumed rather than demonstrated. That is, building staff complained of discomforts, and moulds were identified (or in some cases simply reported to be present); therefore the authors assumed the moulds must have been responsible. We have been unable to locate literature wherein fully documented cases of air concentrations of trichothecene laden Stachybotrys spores have been present in concentrations high enough or long enough to produce sufficient trichothecene to cause illness in humans.

This epidemiological drawback was the underlying theme in a recent (May 25, 2004) publication by the Institute of Medicine, National Academies of Science. 64 That document is a very large, almost 400 page compendium that, due to its complex language and structure, is certainly going to be fodder for misinterpretation. However, in essence the IOM report states that of the 21 categories of illnesses reported by other researchers as being possibly due to indoor moulds, no evidence of causation was found for any of the claims. The document also deals in a very realistic manner with the weaknesses of bias found in a large percentage of scientific and medical papers which initially reported finding causation.

Some researchers, however, quantified the dose and have attempted to clinically establish a dose-response relationship between airborne spores and adverse effects. One team 65 investigating Stachybotrys identified an LD50 (dose-based inhalation concentration resulting in death in 50% of the test population) of 2.7E5 spores per gram body weight. For a seventy kilogram individual, that would equate to a total body burden of 18,900,000,000 spores. In a home that contained an extremely elevated Stachybotrys spore count of say, 200 Stachybotrys spores per cubic meter of air, a person would have to spend 10,822 years in the house (24 hours per day, seven days per week) to receive the necessary dose.

Similarly, work done by another team in 2000 66 reported potentially adverse (but possibly insignificant) pulmonary effects following instillation of Stachybotrys spores. But the authors used concentrations so large, the authors themselves admitted that animals were unlikely to be capable of actually inhaling such huge doses. Again, at the doses used in the study, a human would have to spend over one thousand years in the contaminated atmosphere to receive an equivalent dose. Although the work was important and useful, the study had other serious flaws that detracted from the overall weight of the conclusions which were not particularly germane to normal indoor exposures.

In general, the academic, scientific, and medical communities generally do not support the current high profile concerns regarding indoor moulds.

Dr. Abba Terr M.D. as early as 2001, summed up the medical field's opinion in a peer-reviewed journal when he wrote: 67

No convincing cases of human allergic disease or infection from this mould [Stachybotrys] have been published. [He concluded] The current public concern for adverse health effects from inhalation of Stachybotrys spores in water-damaged buildings is not supported by published reports in the medical literature.

Members of the CDC also performed a review of the available medical literature regarding moulds and mycotoxin exposures in the indoor environment, and in the peer reviewed journal for the American Industrial Hygiene Association, the authors concluded: 68

This review of the literature indicates that there is inadequate evidence to support the conclusion that exposure to mycotoxins in the indoor (nonindustrial) environment is causally related to symptoms or illness among building occupants.

In a similar literature review by Frederick Fung with the Sharp Rees-Stealy Medical Group and University of California San Diego, Dr. Fung reported in the Journal of Clinical Toxicology 69 that:

A critical review of papers, reports, and studies on Stachybotrys mycotoxins revealed only descriptive reports of suspected animal and human poisoning secondary to consumption of mould contaminated foods. No studies of good toxicologic and epidemiologic designs answer whether airborne mycotoxins produced by Stachybotrys could produce specific human toxicity.

Dr. Burge also performed a review 70 of available literature and her assertion was: The review yielded many studies of the role of fungi in allergic disease, but none that systematically documented such a role for mycotoxins or fungal volatiles. Many case studies were found, but none of these unequivocally document a cause/effect relationship between mycotoxin exposure by inhalation and human disease in residential, school, or office settings.

Dr. Burge concluded:

The review led to the conclusion that that the primary result from fungal exposure is allergic disease, and that the evidence for inhalation disease resulting from mycotoxin exposure in residential and office settings is extremely weak.

Finally, perhaps one of the most thorough and comprehensive reviews of contemporary literature on the subject (replete with 465 references) was the Kuhn and Ghannoum review71 which concluded that

While many papers suggest a similar relationship between Stachybotrys and human disease, the studies nearly uniformly suffer from significant methodological flaws, making their findings inconclusive. As a result, we have not found supportive evidence for serious illness due to Stachybotrys exposure in the contemporary environment.

As we continue to study the fungal loading in occupied environments we are ever vigilant for new information, and remain objective in the evaluation of the information.

About the Author
Mr. Connell is an Industrial Hygienist with Forensic Applications Consulting Technologies, Inc., and possesses specialized knowledge in several areas of industrial hygiene including toxicology, indoor microbiology, microbial assessments, chemical exposures, analytical chemistry, and indoor air quality (IAQ).

Mr. Connell has been a continuously practicing Industrial Hygienist since 1987. Prior to entering the Industrial Hygiene field, he had approximately ten years experience as an analytical chemist in analytical and research laboratories in the United States and in Ireland.

Mr. Connell regularly performs legitimate mold "testing" (mold assessments) around the U.S. and has performed approximately 900 mould and microbial assessments during the last 25 years. Mr. Connell has performed microbial investigations in a number of litigious cases and for such highly acclaimed organizations as the National Center for Atmospheric Research (where Mr. Connell has served as the contract Industrial Hygienist for approximately ten years). He has been qualified as an expert witness in Federal Court (Philadelphia)72 on the lack of scientific validity of common mould sampling and testing used by “certified” mould inspectors. He has similarly been used as an expert witness in mould issues in Federal Criminal Court73 (US Bureau of Alcohol Tobacco and Firearms, in Federal Court, District of Colorado) and has provided testimony in several indoor air and mould related cases.

Mr. Connell’s clients have included the U.S. Geological Survey, Health and Human Services, Federal Bureau of Prisons, and the National Institute of Standards and Technology.

Mr. Connell is a member of the American Industrial Hygiene Association (AIHA), the American Conference of Governmental Industrial Hygienists (ACGIH), the Property Care Association (England) and the Occupational Hygiene Society of Ireland, and he currently serves on three International Standards Committees including ASTM D22.08 – Indoor Air (whose task is to develop and write internally accepted indoor and building mould assessment standards); ASTM E50 Committee (Environmental Assessment & Risk Management), and ASTM E30.05 Forensic Sciences committee. Mr. Connell serves as an Industrial Hygiene Subject Matter Expert for the Federally funded Inter Agency Board (Health, Medical Responder Safety Subgroup).

Mr. Connell is an internationally recognized expert on indoor microbial issues and has lectured on risk assessment, sampling and toxicology at the university level. He has been a guest lecturer for the PCA (Huntingdon, England), University of Vermont, (Johnson Conference) University of Arizona (Arizona Health Sciences Center, Zuckerman College of Public Health), University of Colorado, and the Environmental Information Association. He has presented papers on the statistical variations associated with indoor mould sampling including the international symposium on indoor mould at the International Johnson Conference at the University of Vermont where he served as Committee Chairman on the Mold Health Effects Committee.

1 US Department of Labor, OSHA Indoor Air Quality in Commercial and Institutional Buildings OSHA 3430-04 (2011)

2 Damp, Indoor Spaces and Health World Health Organization Guidelines For Indoor Air Quality Dampness And Mould (ISBN 798 92 890 4168 3) WHO Regional Office for Europe, Scherfigsvej 8, DK-2100 Copenhagen Ø, Denmark

3 John Hopkins Medicine, Health Alerts - Lung Disorders Special Report: 9 Common Mold Myths May 22, 2008, (http://www.johnshopkinshealthalerts.com/reports/lung_disorders/2012-1.html)

4 Recognition, Evaluation and Control of Indoor Mold (Prezant B, Weekes DM, Miller JD – Editors), American Industrial Hygiene Association, August 2008

5 Burge, H. Can Mold Be Safely Left Inside Walls? The Environmental Reporter, Vol. 3, No. 11, November 2005

6 Robbins C, Morrell J; Mold, Housing and Wood (Article prepared for the Western Wood Products Association), Jan 2006.

7 Health Canada: Fungal Contamination in Public Buildings: Health Effects and Investigation Methods. Health Canada, Ottawa, ON (2004)

8 Canadian Construction Association; Mould Guidelines for the Canadian Construction Industry; CCA; Ottawa, ON; 2004

9 Guidelines on Assessment and Remediation of Fungi in Indoor Environment; New York City Department of Health, Bureau of Environmental & Occupational Disease Epidemiology, 2000

10 Guidelines on Assessment and Remediation of Fungi in Indoor Environment; New York City Department of Health, Bureau of Environmental & Occupational Disease Epidemiology, 2000

11 Health Canada: Fungal Contamination in Public Buildings: Health Effects and Investigation Methods. Health Canada, Ottawa, ON (2004)

12 Canadian Construction Association; Mould Guidelines for the Canadian Construction Industry; CCA; Ottawa, ON; 2004

13 US Environmental Protection Agency, in its booklet “Mold Remediation in Schools and Commercial Buildings, EPA 402-K-01-001 March 2001 (updated 6/25/01)

14 American Conference of Governmental Industrial Hygienists, (ACGIH), Data Interpretation, In Bioaerosols: Assessment and Control, Macher J (Ed), Cincinnati OH, 1999

15 Storey E; et al Guidance for Clinicians on the Recognition and Management of Health Effects Related to Mold Exposure and Moisture Indoors, Farmington CT, University of Conn. Health Center, 2004

16 Institute of Medicine (IOM) Damp Indoor Spaces and Health, DC, IOM, 2004

17A host of microbial "stowaways" were recovered from the space shuttle and the MIR.

18 OSHA Technical Manual, Section III, Chapter 2, (C)(3)(1)(a)

19 Hawksworth, D. L., Kirk P.M., Sutton B.C. et al. 1995. Ainsworth and Bisby's Dictionary of the Fungi (8th Ed.). CAB International, Wallingford, United Kingdom.

20 I have estimated the weight by referencing a similar fungus in Michigan (a member of Armillaria bulbosa) which covered 37 acres and weighed 110 tons.

21 Burge, H.A., Burge, W. Mullenburg, M. Distribution of Culterable Fungi in Carpet Dust Samples Across the USA, Journal of Allergy and Clinical Immunology, Vol. I, Jan. 1993, page 326

22 Scott. R.J, Hodgson M, Prevalence Of Fungi In Carpet Dust Samples (Presented in a poster session of the Third International Conference on Fungi, Mycotoxins, and Bioaerosols in Saratoga Springs, New York, October, 1998.)

23 Brief, R. S. and T. Bernath. Indoor Pollution: Guidelines for Prevention and Control of Microbiological Respiratory Hazards Associated with Air Conditioning and Ventilation System. Applied Industrial Hygiene. 3(1):5-10, 1988.

24 The OSHA Technical Manual (SECTION III: CHAPTER 2)

25 Vesper SJ, Varma M, Wymer LJ, Dearborn DG et al Quantitative Polymerase Chain Reaction Analysis of Fungi in Dust From Homes of Infants Who Developed Idiopathic Pulmonary Hemorrhaging Journal of Occ. Environ. Medicine Vol. 46 No. 6, June 2004, p. 596-601

26 Meklin T, Haugland RA, Reponen T, Varma M, et al, Quantitative PCR Analysis of House Dust Can Reveal Abnormal Mold Conditions J. Environ. Monit., 2004, 6 (7), 615 – 620

27 Horner, W. E. Helbling, A. Lehrer, S. B. Fungal Allergens Clinical microbiology reviews. April 1 1995, Vol. 8 No. 2, p. 161

28 Horner, W. E. Helbling, A. Lehrer, S. B. Fungal Allergens Clinical microbiology reviews. April 1 1995, Vol. 8 No. 2, p. 161

29 Burge, H.A. Fungi: toxic killers or unavoidable nuisances? Annals of Allergy Asthma Immunology 2001; 87(Supp l):52-56

30 Hardin, B.D., Kelman B.J, Saxon, A. Adverse Human Health Effects Associated with Molds in the Indoor Environment Evidence Based Statement of the American College of Occupational and Environmental Medicine, prepared under the auspices of the ACOEM Council on Scientific Affairs. Peer-reviewed by the Council and its committees, and approved on October 27, 2002.

31 Hardin, B.D., Kelman B.J, Saxon, A. Adverse Human Health Effects Associated with Molds in the Indoor Environment Evidence Based Statement of the American College of Occupational and Environmental Medicine, prepared under the auspices of the ACOEM Council on Scientific Affairs. Peer-reviewed by the Council and its committees, and approved on October 27, 2002.

32 Horner WE, Helbling JE, et al Fungal Allergens Clinical Microbiology Reviews, April 1995, p. 163

32a Ponikau JN, Sherris DA, Kern EB, Homburger HA, et al The Diagnosis and Incidence of Allergic Fungal Sinusitis, Mayo Clin Proc, September 1999, Vol 74

33 Maldelin T.M.; Madelin M.F. Biological Analysis of Fungi and Associated Molds Bioaerosols Handbook, Edited by Cox and Wathes, Second Ed, 1995

34 Brock T.; Madigan, M.; et al Biology of Microorganisms, 7thEd. Prentice Hall Books.

35 Gales M, Phillips, C; Coccidioidomycosis--A Mycotic Infection on the Rise, Clinician Reviews 7(4):71-84, 1997; Clinicians Publishing Group and Williams & Wilkin

36 Bardana, E.J. The environment and allergic disease: Annals of Allergy Asthma Immunology 2001; 87(Supp l):52-56

37 Editorial Staff SIDS theory: from hype to reality. The lancet. DEC 09 1995 v 346 n 8989 Page: 1503

38 Dearborn DG, et al. Acute Pulmonary Hemorrhage/Hemosiderosis Among Infants — Cleveland, January 1993–November 1994. MMWR December 09, 1994 / 43(48);881-883

39 Sudikin, Daniel. Sudakin, Daniel, L Special Article: Stachybotrys chartarum: Current Knowledge of Its Role in Disease, MedScape General Medicine, February 29, 2000

40 Update: Pulmonary Hemorrhage/Hemosiderosis Among Infants — Cleveland, Ohio, 1993–1996 Morbidity and Mortality Weekly Report, Centers for Disease Control, Vol. 49, No. 9, March 10, 2

41 CFU/m3 means Colony Forming Units of Stachybotrys present in each cubic meter of sampled air

42 Etzel RA, Montana E, et al Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra and other fungi. Arch Pediatr Adolesc Med. 1998;152:757-762.

43 Update: Pulmonary Hemorrhage/Hemosiderosis Among Infants — Cleveland, Ohio, 1993–1996 Morbidity and Mortality Weekly Report, Centers for Disease Control, Vol. 49, No. 9, March 10, 2000

44 Update: Pulmonary Hemorrhage/Hemosiderosis Among Infants — Cleveland, Ohio, 1993–1996 Morbidity and Mortality Weekly Report, Centers for Disease Control, Vol. 49, No. 9, March 10, 2000

45 Personal conversation between Caoimhin P. Connell and Bruce Jarvis, PhD, Professor of Chemistry and Biochemistry University of Maryland at College Park, October 27, 2000.

46 Personal Lecture notes of Caoimhin P. Connell (Lecture by Dr. H Burge, Harvard School of Public Health, Boston, Mass. May 2000).

47 Personal communication between Caoimhin P. Connell and Dr. Bruce Jarvis, (referencing Sorenson, W.G.; Frazer D.G; Jarvis, B, Simpson J, and Robinson, V. 1987. Trichothecene mycotoxins in aerosolized conidia of Stachybotrys atra. Applied Environmental Microbiology 53:1370-1375.

48 Miller R.V; Martinez-Miller, C; Bolin, V A Risk Assessment Model for Mycotoxin-Producing Molds On Human Health In Indoor Environments. AeroTech Monitor, Vol. 3 No. 1, 2000.

49 Miller R.V; Martinez-Miller, C; Bolin, V A Risk Assessment Model for Mycotoxin-Producing Molds On Human Health In Indoor Environments. AeroTech Monitor, Vol. 3 No. 1, 2000.

50 Burge, H.A, Fungi: toxic killers or unavoidable nuisances? Annals of Allergy Asthma Immunology 2001; 87(Supp l):52-56

51 Hardin, B.D., Kelman B.J, Saxon, A. Adverse Human Health Effects Associated with Molds in the Indoor Environment Peer-reviewed by the Council and its committees, and approved on October 27, 2002.

52 Jaakkola MS, Nordman H, Piipari R, et al; Indoor Dampness and Moulds and Development of Adult-Onset Asthma: A Population Based Incident Case-Control Study Environmental Health Perspectives Vol 10, No. 5, May 2002

53 NE Ebbehoj, AL Svensson, HW Meyer, O Valbjorn, LUNG FUNCTION AND SYMPTOMS IN DAMP AND MOULDY BUILDINGS, (Joint investigation of the Department of Occupational and Environmental Medicine, Bispebjerg Hospital, Copenhagen, Denmark and the Danish Building Research Institute, Horsholm, Denmark.) Proceedings: Indoor Air 2002

54 Hodgson MJ, Morey P, Wing-Yang L, et al, Building- Associated Pulmonary Disease From Exposure to Stachybotrys chartarum and Aspergillus versicolor. Journal of Occupational and Environmental Medicine, Vol. 40, No. 3, 1998

55 Personal conversation between Caoimhin P. Connell and Bruce Jarvis, PhD, Professor of Chemistry and Biochemistry University of Maryland at College Park, October 27, 2000.

56 Apostolakos M.J., Rossmoore H., and Beckett W.S. Hypersensitivity Pneumonitis from Ordinary Residential Exposures, Environmental Health Perspectives, Volume 109, No.9 Sept 2001

57 Verhoeff A., Annals of Allergy Asthma and Immunology (1997)

58 Burge H. Journal of Allergy and Clinical Immunology (January 1993, Vol. 91).

59 Stone, CA, Johnson GC, Thornton JD, et al.Leucogyrophana pinastri, a Wood Decay Fungus as a Probable Cause of an Extrinsic Allergic Alveolitis Syndrome, Australian, New Zealand Journal of Medicine, Vol 19, 1989 p. 727- 729

60 Personal communication between Dr. Johnson and Caoimhin P. Connell May 3, 2003

61 Jacobs, RL; Andrews CP; Jacobs, FO; Hypersensitivity Pneumonitis Treated with an Electrostatic Dust Filter Ann. Of Internal Med. V 110, No.2 Jan. 1989 p.115

62 Jacobs, RL; Thorner, RE; Holcomb, JR; et al. Hypersensitivity Pneumonitis Caused by Cladosporium in an Enclosed Hot-Tub Area Ann. Of Internal Med. V105, 1986 p.204

63 Dales RE, Zwanenburg, et al Respiratory Health Effects of Home Dampness and Moulds among Canadian Children American Journal of Epidemiology Vol. 134, No. 2, 1991

64 Institute of Medicine, National Academies of Science, Damp Indoor Spaces and Health Committee on Damp Indoor Spaces and Health, ISBN 0-309-09193-4, May 25 2004

65 Peraica M; Radic B; Lucic A; Pavlovic M Toxic effects of mycotoxins in humans.Bull World Health Organ 1999;77(9):754-66 (ISSN: 0042-9686)

66 Rao, C.Y., H.A. Burge and J.D. Brain. The time course of responses to intratracheally instilled toxic Stachybotrys chartarum spores in rats. Mycopathologia 149: 27-34, 2000.

67 Terr, A. I. Stachybotrys: relevance to human disease Annals of Allergy Asthma and Immunology (87, Supp l: 57-63), 2001

68 Page, EH; Trout, D.B, The Role of Stachybotrys Mycotoxins in Building-Related Illness Journal of the American Industrial Hygiene Association, September, 2001

69 Fung F, Clark R, Williams S, Stachybotrys, a Mycotoxin-Producing Fungus of Increasing Toxicologic Importance; Clinical Toxicology 36 (1&2)79-86, 1998)

70 Burge H. A, Fungi: toxic killers or unavoidable nuisances? Annals of Allergy Asthma Immunology 2001; 87(Supp l):52-56

71 Kuhn, DM, Ghannoum MA; Indoor Mold, Toxigenic Fungi, and Stachybotrys chartarum: Infectious Disease Perspective Clinical Microbiology Reviews, Vol 16, No 1, Jan 2003, pp. 144-172

72 220 W. Rittenhouse Square Condominium Association v. Myrna Stolker. Philadelphia CCP April Term 2009 No. 02446, Honorable Gary F. Di Vito presiding (May 2012)

73 US v. Stylio Trachanas Case No. 2011VR00678, DJJ-12W-USA13-0136, July 9, 2012

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