mold article

[Guest guest]

from this web page: http://www3.sympatico.ca/ross.fraser/9.htm Significance of Molds

in Indoor Proliferation

There are a surprising number of mechanisms by which molds proliferating within public buildings or homes may adversely affect human occupants:

A. Allergenicity

1. Type 1 allergies (immediate type hypersensitivity).

Fungi may cause allergic rhinitis similar to that caused by pollen grains, and, after asthmatics become allergically sensitized to one or more of them, they may trigger asthma attacks. Most asthmatics have multiple allergies.

2. Type 3 allergies (delayed type hypersensitivity)

In certain susceptible individuals, after prolonged, heavy exposure, fungi may cause hypersensitivity pneumonitis (allergic alveolitis), characterized by wheeze, shortness of breath, cough, chest tightness, and in some prolonged cases, pulmonary fibrosis.

There has been a custom of giving each new subtype of hypersensitivity pneumonitis (HP) an evocative medical nickname, such as farmer's lung, maple bark stripper's disease, and so on. "Humidifier fever" is the most common such name associated with indoor mold proliferation, since HP is often associated with contaminated humidifiers. HP has also, however, been reported from indoor mold proliferations on structural or furnishing elements, such as walls or shower curtains. An HP patient should have strong serum precipitins specific to the fungus (or bacterium or protozoan) which is causing the reaction. Bronchioalveolar lavage or biopsy will usually show elevated numbers of eosinophil cells, showing eosinophilic immune activation.

3. Allergic bronchopulmonary aspergillosis (ABPA) or other allergic bronchopulmonary mycosis

Persons who have been asthmatic for many years may progress to have their bronchial passages colonized by a fungus, usually Aspergillus fumigatus, but sometimes another organism such as Bipolaris hawaiiensis, Wangiella dermatitidis, or Pseudallescheria boydii. Constant allergic response helps to maintain the fungal colonization, and first-line therapy is often with steroids: bringing down the level of inflammation may result in elimination of the colonizing organism. Some studies have made tentative links between exacerbations of ABPA and moldy houses. Cystic fibrosis patients also may get allergic bronchopulmonary mycosis.

4. Allergic mycotic sinusitis.

A colonizing infection of mucus adhering to the sinus walls. Very similar to ABPA otherwise, except that patients need not necessarily have had asthma or cystic fibrosis. To date no discrete connection with indoor mold proliferation has been shown in any individual cases, but that may be from lack of investigation.

B. Chemical irritation

Several epidemiological studies have shown that non-specific respiratory symptoms in both non-allergic and allergic persons are linked to excess building moisture and mold growth (1). In fact, the difference in response between the two groups of persons appears not to be significant. This means that there is very likely to be a non-allergic mechanism behind the irritation reported. At the same time, there is a body of literature concerning relatively intense toxin-like effects exerted by moldy materials on workers who have disturbed or have been exposed to substantial quantities. In addition, liver cancer has been epidemiologically linked to occupational respiratory exposure to the fungal toxin group known as the aflatoxins (from Aspergillus flavus and close relatives). Animal model experiments have shown that inhaled aflatoxin forms DNA adducts (places where the toxin alters DNA by binding to it) in the lungs and in the liver.

1. Mycotoxin effects.

One candidate for the agent of the direct chemical effects apparently exerted by respiratory or other contact with molds is the mycotoxins. The class of small fungal secondary metabolites which has been given the name "mycotoxins" is definitely known to include many compounds which are highly toxic to vertebrates (such as humans). Most of the well characterized toxic effects are from animal feeding situations, either natural mycotoxicosis outbreaks caused by contaminated animal feed, or laboratory experiments based on feeding (or connected artificial experimental situations such as parenteral injection of purified toxins into experimental animals). Ingestion of mycotoxin-contaminated foods by humans results in similar symptoms. Toxic effects have also been found in laboratory experiments in which animals are exposed to mycotoxins via the respiratory tract. In cases involving humans and airborne exposure, the most suggestive of a direct mycotoxin effect are those in which heavily mold-exposed workers develop severe symptoms reminiscent of animal mycotoxicoses or contaminated-food mycotoxicoses. The link between inhaled aflatoxin and liver cancer has already been mentioned.

As another example, classic stachybotryotoxicosis, described mostly from agricultural workers who handled or disturbed large quantities of material (usually hay or straw) contaminated by Stachybotrys chartarum, was characterized by "cough, rhinitis, burning sensation in the mouth, (throat) and nasal passages, and cutaneous irritation at (points) of toxin contact" (2). Nosebleeds were also common, and tracheal bleeding was occasionally reported. Whether such mycotoxin effects explain the symptoms seen in common building exposures has been disputed. It has been pointed out that, although the mycotoxins are often associated with disseminating fungal conidia, the quantities present may not be sufficient to explain the effects observed (3), at least not in terms of classic toxicosis. A number of mycotoxins orconidia of mycotoxigenic fungi, however, have also been shown to have effects such as activation of pulmonary alveolar macrophages (PAMs), DNA fragmentation in PAMs, inhibition of the oxidative burst killing mechanism in PAMs, and slowing of respiratory ciliary beat (e.g., 4). Such interactions with immune mechanisms may explain some symptoms not explained by toxicosis. Careful study of occupants of contaminated buildings suggests an association between inhalation of toxigenic fungi and nonspecific respiratory symptoms (5)

Recently, indoor Stachybotrys chartarum (= S. atra) mold infestation has been strongly implicated in an outbreak of pulmonary haemorrhage in infants around 1 yr old in the Cleveland area (6). The affected infants were almost all from impoverished African-American households in which rooms had been affected by river floods or severe, unfixed water leaks. Very large amounts of S. chartarum or, rarely, closely related species were found in the affected dwellings, and high counts were often found in air sampling. In this case, the effect seems most likely to have been straightforward toxicosis. The most probable model to explain the weakening of lungs by the mold exposure lies in the well known inhibition of protein synthesis by the mold's trichothecene mycotoxins. Infant lungs at that age are growing very rapidly in proportion to the growth occurring in the rest of the body, and the correct elasticity and integrity of developing alveoli and bronchi is endowed by proper elaboration of collagen connective tissue proteins. Protein synthesis inhibition by trichothecenes probably dangerously impedes this process, leading to weakening of the lungs. Such weakening is seen in pathology as pulmonary hemosiderosis, a condition in which PAMs (lung "white blood cells" devoted to scavenging foreign and out-of-place material) have scavenged a large number of red blood cells that have leaked into the lungs, and have converted the iron in blood haemoglobin to a distinct "non-haem" form that can be stained by pathologists' prussian blue staining procedures. Affected infants show such hemosiderosis in biopsies and autopsies. A secondary irritation such as cigarette smoking may be necessary to provoke an episode of massive pulmonary bleeding.

2. Glucan effects.

Beta-1,3-glucan is a major structural component of almost all fungal cell walls. It is a polymer of glucose similar to cellulose, but with less tendency to be found in strands. It bears considerable structural similarity to very toxic molecules known as endotoxins secreted by some bacteria, particularly some gram-negative organisms. This similarity caused an endotoxin expert, Dr. Ragnar Rylander, to investigate it as a possible candidate for the chemically irritating component found in mold conidia. It was found to activate PAMs, possibly making the lungs hyperreactive to a wide variety of foreign materials (7). Also, in double-blind inhalation exposure trials conducted with human volunteers, exposure correlated significantly with some non-specific respiratory symptoms. The most strongly correlating symptom, however, was headache. The contribution of glucans to indoor mold irritation is still under investigation; glucan effects may add to or synergize mycotoxin effects, or may be mistaken for mycotoxin effects in fungi where the actual amount of mycotoxin present in conidia is not sufficient to cause symptoms.

3. Volatile chemical effects

Most molds, especially those with dry conidia, produce volatile odor constituents. In a few cases, these are fruity or flowery and may be adapted to attract arthropod dispersers (e.g. insects carrying the mold conidia to new growth sites). Usually they are musty or earthy and are probably adapted to deter grazing and feeding invertebrates and vertebrates, or at least to give a distinct "not food" odor to mold colonies and their underlying nutritional substrates. A few such volatiles have been found to be directly irritating to vertebrates. Apart from experiencing such direct physiological irritation, humans and other vertebrates may be adapted to avoid such odors, and there may be a legitimate "psychological" objection to their presence in rooms. Mold growth in buildings may be accompanied by the growth of Streptomyces species, which usually have very strong earthy volatile odours. In addition, in very wet materials, copious bacteria may grow and may emit typical rotten or sour smelling odour molecules.

C. Invasive pathogenesis.

Of the regularly occurring indoor mold proliferation species, only a few have significant potential as opportunistic pathogens, and even these usually require a relatively strongly immunocompromised patient before they can be regarded as dangerous. Warm, moist environments, such as dirty heating ducts affected by condensation, or vanes and other apparati near heating system humidifiers, may grow Aspergillus fumigatus, the best known opportunistic mold fungus. This species also tends to occur in potted plant soils, particularly where these have not been exchanged for fresh soils (e.g., by repotting) for several years. Usually, a patient needs to have a relatively high degree of neutropenia (deficit in neutrophil type white blood cells, an essential component of the immune system) before he or she is seriously threatened with invasive disease by this organism. Most such patients are persons taking leukemia chemotherapy or drugs designed to prevent rejection of transplanted organs. Occasionally other predisposing factors are found, such as heavy, prolonged corticosteroid use. AIDS patients are at little risk for such diseases unless they develop lymphomas or are taking potentially neutropenia-inducing drugs such as ganciclovir. In recent years, because of the emergence of antibiotic-resistant bacteria in hospitals, some hospitals have begun to send severely neutropenic patients home. These patients are at high risk of infection by indoor infestations of A. fumigatus, A. niger, A. nidulans, A. flavus, A. terreus, Pseudallescheria boydii, Fusarium solani, F. oxysporum, F. moniliforme, F. proliferatum, and some other species. People who do not have these specific immunocompromising conditions, however, are not at significant risk of invasive disease from any of these fungi (with the possible exception of P. boydii punctured into the dermis or the eye).

Note that many members of the public, especially those advised by practitioners of various alternative medicines, often incorrectly assert that their immune systems are compromised. Such assertions should not be taken at face value until convincing detail about actual predisposing conditions is disclosed.

D. Community effects

Fungally colonized materials often support a large population of arthropods, usually fungivorous (fungus-eating) mites, but also other arthropods such as booklice, millipedes and beetles (a recent sticky tape sample sent to this author from the wall of a moldy house contained a lawn of Cladosporium which was being grazed on by the drugstore beetle, Stegobium panacaea. The insect's faecal deposits consisted entirely of mold conidia). The growth of the house dust mite, Dermatophagoides pteronyssimus, in carpets,mattresses and dust accumulations may be stimulated by growth of xerotolerant (drought-tolerant) aspergilli such as A. glaucus on human skin scale litter and other dry household organic particulates. Arthropod body parts and faeces may be highly allergenic, and house dust mite in particular is well known to be highly irritating to most asthmatic children.

1. Dales R.E., Zwanenburg H., Burnett R., lin C.A. 1991. Respiratory health effects of home dampness and molds among Canadian children. Am. J. Epidemiol. 134: 196-203.

2. Hintikka E.-L. 1978. Human stachybotryotoxicosis. In Mycotoxic fungi, mycotoxins, mycotoxicoses. An encyclopedic handbook. Vol. 3. Edited by T.D. Wyllie and L.G. Morehouse. Marcel Dekker, New York/Basel. pp. 87-89.

3. Burge H.A. 1996. Health effects of biological contaminants. In Indoor air and human health. Edited by R.B. Gammage and B.A. Berven. CRC Press/ Publishers, Boca Raton, FL., p. 175.

4. Jakab G.J., Hmielski R.R, Zarba A. et al. 1994. Respiratory aflatoxicosis: suppression of pulmonary and systemic host defenses in rats and mice. Toxicol. Appl. Pharmacol. 125: 198-205.

5. Hodgson M.J., Morey P., Leung W.Y. et al. 1998. Building associated pulmonary disease from exposure to Stachybotrys charatrum and Aspergillus versicolor. J. Occup. Environ. Med. 40: 241-249.

6. Dearborn D.G., Infeld M.D., P.G. et al. 1997. Update: pulmonary hemorrhage/hemosiderosis among infants -- Cleveland, Ohio, 1993-1996. Morbidity and Mortality Weekly Rpt. 46: 33-35.

7. Fogelmark B, Sjostrand M, and Rylander R. 1994. Pulmonary inflammation induced by repeated inhalations of beta (1,3)-D-glucan and endotoxin. Int. J. Exp. Pathol. 75: 85-90.

How to Find, and How Not to Find,Molds in Indoor Proliferations

Scientific ideals die hard. For at least four decades, there existed a scientific ideal that went more or less as follows: in order to determine the significance of indoor molds, first build a perfect air sampling device. Then use it to count either the total spores and conidia, for direct microscopic techniques, or the colony forming units (CFU), for culturing techniques, of molds in the building where excessive mold growth was suspected. Compare the numbers of molds you detected with a pre-existing standard threshold level above which the number of mold propagules is known to be unacceptable. This standard benchmark will have been calculated by comparing problem buildings with non-problem buildings. In buildings exceeding the air sampling benchmark, go looking for the mold sources and remediate them.

The problems with this doggedly pursued strategy were many. Here are a few:

-- there was no possibility of building a perfect air sampler. Non-viable samplers, depending on direct microscopy, rendered impracticable the accurate counting of small, nondescript propagules such as Aspergillus conidia. Yet some research studies showed that up to 50% of the mold propagules in air were dead, so that viable samplers tended to underestimate numbers. This was especially true with Stachybotrys, for which often 3% or fewer of the conidia in indoor air were viable in culturing techniques. Yet, dead conidia appeared to be just as irritating as live ones.

-- outdoor air mold counts fluctuated drastically over the year, making the setting of threshold benchmark mold count levels for indoor environments very difficult. The techniques used had no way of separating material produced indoors from that produced outdoors unless laborious identification studies wereconducted on dozens or hundreds of fungal colonies, and species on the outdoor list were subtracted from the indoor list. In the decades where the air sampling/counting ideal was pursued, benchmarks that were proposed were highly arbitrary, and the need for further research was cited routinely.

--often the mold colonies could be seen growing on the wall (or in the air system, or other places). This posed a quandary. If the number of colonies in indoor air sampling were below the published benchmark, should these molds simply be dismissed as insignificant and left to keep on growing? Could spending money cleaning such an insignificant problem be justified? If workers or tenants still complained that the molds were bothering them, were such people just being combative or neurotic? What if new workers or tenants also began to voice the same complaints?

-- the ideal was rather dependent on all molds being more or less of the same significance, so that they could all be counted together. But there was increasing evidence that some molds were far more irritating than others. Each mold was a biological species with its own array of allergenic proteins and potentially irritating toxins. When it became clear that a single Stachybotrys colony from indoors (which probably represented the presence of an additional 30 or more dead conidia in the same sample, and signalled, for example, a biochemically irritating forest of mold in the basement derived from a water leak) was actually more indicative of an air quality problem than 200 Cladosporium colonies which came into the house from the park across the street, it became pretty obvious that simply counting CFU was inadequate.

-- viable air sampling, especially with the more accurate machines, tended to take only a brief "snapshot" of the molds present in the air. The length of exposure was limited by need not to have colonies overgrowing one another. (With bacterial sampling, this problem was diminished by using liquid impingers that air could be bubbled through. These were of dubious efficacy, however, with highly water-repellent mold conidia.) But the actual presence in the air of mold conidia or spores was highly dependent on room activity, air currents, humidity, whether the door to the basement (or crawlspace, or attic hatch, or moldy closet) was open or closed, etc., not to mention the weather outdoors, time of day, wind speed, degree of maturity of nearby vegetation, occurrence of spore-mobilizing disturbances such as crop harvesting or compost turning, and so on.

--different individual people vary in their responsiveness to molds. Even if testing people's responses to different levels of molds were possible (lab experiments along these lines would be considered experimenting on humans, and would likely be regarded as ethically inadmissable), it would be difficult to decide what kind of person to use as a standard for devising benchmark levels. The most sensitive? This might be someone claiming sensitivity to almost everything in the environment, binding everyone else to an unlivable standard. The least sensitive? That would please almost no one except the occasional curmudgeon who had smoked off most of his/her airway epithelium. The average person? That ought, in theory, to leave about half the population dissatisfied, assuming a bell curve of mold response. This sort of strategy reaches the acme of its difficulty when you incorporate the possibility that different people might have different levels of reaction to different mold species. Finding the ideal benchmark population for Cladosporium cladosporioides proliferation might not help at all in assessing Stachybotrys chartarum proliferation.

Finally, an alternative strategy was mooted. This was based on the following propositions:

--mold amplifiers (proliferation sites) indoors are often eminently findable by room inspection or other simple techniques (e.g., sticky tape examination of dust from within heating ducts.) If not, air sampling can be used as an exploratory device to detect which molds are unusually well represented in indoor but not outdoor samples. This usage makes air sampling an auxiliary tool which can be used in the effort to physically locate indoor amplifiers, rather than an arbiter of the acceptability of mold propagule levels.

-- some molds are more irritating than others. Recognition of species involved in amplification is often important, whereas overall aerial counts are unlikely to be.

-- despite the differences in significance of different mold species, it is hard to justify allowing any mold amplifiers to persist indoors. Usually they indicate a moisture control problem that is also causing other damage or economic loss: for example, mold around a windowsill in an area of temperate climate often indicates poor heat seal and condensation, meaning that energy is being lost and the support for the windowframe is probably rotting; mold on a poorly insulated wall in winter in a chilly climate indicates voluminous energy loss; mold in the basement indicates either leaks or floods that are causing active destruction of structural materials, or foundation cracks/porosity that threatens every biodegradable item in the basement, whether clothing, shoes or suitcases, with destruction through excess humidity; mold on waterstained ceiling tiles or on rippled wallboard under the window indicates major leaks damaging the building, and so on.

Now here's another key piece of logic: if the mold amplifier is quite large, clearly it may be a major irritation or allergy problem, and it probably indicates a major underlying building problem as well. For the sake of the building, as well as for the human sufferers, it's worth remediating. But if the mold amplifier is small--well, it may be of negligible health significance, but then again, if it's that small, it probably is very easy to clean up. And most likely any underlying problem it represents is minor in scale and easy to remedy.

These principles came together in the following recommendation, taken from Health Canada's Fungal contamination in public buildings: a guide to recognition and management (1): " The visible presence of fungi on mouldy ceiling tiles, humidifiers, diffusers, air supply ducts, or other surfaces (including microscopically visible fungi in humidifiers) requires investigation and remedial action regardless of the airborne spore load." People working in actual cases--for example, industrial hygienists and public health inspectors--have reported that this recommendation is very effective in solving problems in the field. If the occasional building owner is recommended to clean up a mold amplifier even though its connection to health complaints is uncertain, he or she can have the satisfaction of knowing that following the recommendation will solve a problem of some kind. Even if a significant respiratory health problem is not solved, at least some sort of pernicious building maintenance problem is resolved, one that otherwise probably would have gotten worse. After all, leaving moldy materials around a building is rather like leaving moldy materials at the back of your refrigerator--it's negligence slowly giving rise to filth. It's very hard to defend.Stalking moldA full-scale guide to searching for indoor mold is given by Davies et al. (1). You can get that guide free, off the web, at the following (incredibly lengthy) URL:

http://www.hc-sc.gc.ca/datahpb/dataehd/English/catalog/bch_pubs/fungal_contamination.htm

Once you are at the appropriate web page, you will need to click on the Adobe Acrobat icon to download this free text handling software if you have not done so already. The full document is 76 pages, so have a little paper on hand if you are printing.

The basic synopsis, especially for ordinary cases, is as follows:

1. Look for sources of building moisture damage. Ask building owners and occupants where moisture problems have been observed. Have there been any leaks? Are there any stained ceiling tiles? And so on. Ask if any areas are especially noted for respiratory irritation or musty odours. Ask if there are any previously flooded, malodorous carpets. If the building has an air handling system, ask to see plenums, humidifying systems and any other readily inspected portions of the system. Ask for details about how the system is constructed and insulated, and how it is maintained. Remember in northerly areas that any poorly insulated cold spots may grow mold. Also, bear in mind that virtually any surface within a duct will accrete a microbial biofilm, so that fibreglass insulation, for example, will grow molds in humid ducts even though the glass itself is inert.

In warm, humid places or seasons, cold water pipes may be a condensation hazard. Such pipes tend to drip condensation water constantly unless they have been shielded with pipe insulation. Pools of condensation water can form inside false ceilings when unshielded pipes are present. Therefore, a person called in to analyse buildings for mold growth should consider inquiring about whether or not hidden cold water pipes are insulated.

Desert and prairie parts of North America may be too dry to have this problem, but in eastern North America it occurs all the way from Florida to north of Lake Superior.

Earthen or poured concrete basement floors (or ground floors if there is no basement) are notorious sources of evaporation water, leading to very humid atmospheres in areas of moist climate. Basement floors where concrete has been poured over a plastic or tar moisture barrier are often exempt from this problem. Where concrete is simply poured over the ground, however, its porousness permits evaporation to issue through it, and natural subsidence leads to cracks which augment the amount of evaporation. The same thing may happen with poured concrete basement walls that have been installed without a moisture barrier. Earthen crawlspaces or root cellars connected to the basement or house may be sources of problem humidity.

Vinyl wallpaper, which traps moisture behind it, is a notorious fomenter of mold problems in humid parts of North America.

Attics or rooms which have become bird or bat nesting sites and contain guano deposits are a special problem. They may contain hazardous, virulently pathogenic fungi and should be dealt with by a specialist. If your state or provincial public health lab says you are in a geographic area where Histoplasma, Blastomyces or Coccidioides is known or suspected to be endemic, do not enter rooms with significant guano deposition unless you are wearing full asbestos gear with HEPA filter respirator. Follow asbestos protocols, such as discarding disposable coveralls into a sealed bag, bagging your clothing for thorough washing, and showering immediately while still wearing your respirator mask, before putting on fresh clothing.

Even outside endemic areas for the above-mentioned fungi, do not significantly disturb and aerosolize indoor bird or bat guano deposits, as they may contain the ubiquitous virulent opportunistic pathogen Cryptococcus neoformans. Although inhalation of a large inoculum of this organism is ordinarily needed before one becomes infected (e.g., with cryptococcal pneumonia or meningitis), immunocompromised people and a few unlucky otherwise-healthy people may become infected after exposure to a small number of cells, perhaps only one.

In the tropics, it may be so humid that all exposed organic material will become moldy. For example, most humid tropical areas have libraries in which all the books have moldy spines. To my knowledge, only air conditioning or mechanical dehumidification is likely to control this problem. I know of no magic spray-on material that will significantly deter molds over a prolonged period of time without also imperilling the health of humans.

2. Examine suspect places for visible mold growth. Look especially for black, grey-brown, grey-green or pink mold areas. Gently pull back rippled, water damaged wallpaper or wallboard paper in order to look at what molds may be underneath. If ducts are suspect, dab a little sticky tape into their interiors to sample the materials adhering to their surfaces. When you find suspected mold growth, impress it onto sticky tape (cellulose-acetate, e.g., Scotch brand) and examine it under the microscope. Under the microscope, make sure you see not just conspicuous dark conidial types but also less conspicuous hyaline conidia, especially small, roundish conidia in chains, signifying the presence of Penicillium or Aspergillus. Look also for arthropods, their exoskeletal fragments, and their faecal pellets. Fungivorous (fungus-eating) mite pellets are rounded and usually full of conidia. Booklouse, beetle and millipede faeces, at least when found in mold infestations, resemble short, broken cylindrical columns composed of masses of conidia. Sometimes arthropod pellets will contain interesting mold elements not seen directly on the material sampled. For example, a health inspector recently sent me a tape impression from fibreglass insulation-covering paper in a house with problematic leaks. The paper surface itself had only a little Cladosporium on it, but booklouse and mite faeces scattered here and there were full of Stachybotrys conidia. Evidently there was a great deal of Stachybotrys within easy mite walking distance (i.e., within a few inches), most likely on the interior surface of the same paper. There were probably some minute cracks that the animals used to go back and forth from one side of the paper to the other.

3. If there are continued complaints and mustiness but no mold is found, consider whether or not there are any clues to where hidden mold may be. If building occupants remember a substantial leak or flood (or similar incident, e.g., fire extinguished with water) in a certain area, consider inspecting the wall, ceiling or floor interior at that place. The exterior of the damaged area may have been superficially repaired, leaving all the interior problems intact. Take out a ceiling tile or cut a 4- to 8-inch inspection port into the suspect area. The same may be done in areas where wallboard or ceiling tiles have become watermarked but the exterior is not actually moldy. The interior space, which forms a sheltered humid chamber facilitating fungal proliferation, as well as a conduit for leaks, is far more likely to be grossly moldy than the exposed exterior is. There is actually plenty of airflow between wall and ceiling/floor interiors and the inhabited parts of rooms, especially at the joins, so molds inside structural interior spaces are frequently sources of problems for building occupants.

If there is no strong clue to where mold may be, this is the best time to try air sampling. Analyse culture plates or strips in comparison to an outdoor air control to determine if there is an unusual mold buildup in the building. If there is, look up the mold's general habitat characters in a reference work such as the Compendium of soil fungi (2). Use the information given as a clue to what sort of indoor microhabitat you will find the mold growing in. It is best to use a medium such as DG18 (dichloran 18% glycerol) (3) that both osmotolerant fungi (drought-tolerating fungi such as Aspergillus glaucus) and mesophilic fungi (fungi such as Stachybotrys requiring high moisture levels) are known to grow on.In addition to viable air sampling, non-viable air sampling may be used (e.g., Rotorod). It will detect significant dead elements such as effete Stachybotrys conidia. An alternative to this non-viable air sampling is direct microscopy of settled dust, e.g., from shelf surfaces. Dust from floors that are frequently walked on with shod feet may be difficult to analyse because of the deposition of outdoor mold spora elements. Be aware that old library books may exude a musty odour which in my experience often seems not to be significantly associated with molds. Anyone who can tell me what this odour derives from will have my undying gratitude. I assume it may have something to do with the inherent self-destructiveness of modern acid papers. Library staff may find it quite oppressive and call in fungal analysts.

1. Davies, R., R.C. Summerbell, D. Haldane, et al. 1995. Fungal contamination in public buildings: A guide to recognition and management. Environmental Health Directorate, Health Canada, Ottawa, ON.

2. Domsch, K.H., Gams, W., , T.-H. 1980 (reprint 1993). Compendium of soil fungi. IHW Verlag, Eching, Germany.

3. Pitt J.I. and Hocking A.D. Fungi and food spoilage. Academic Press, Sydney, New York, San Diego, Orlando. p. 40.

Some Molds and Their Toxins

(Note: these molds were displayed in a National Laboratory Training Network teaching workshop. Not all are from indoor environments: some are strictly from contaminated grain or similar crop-related material.)

A. Stachybotrys chartarum

Morphology: Colonies in culture growing around 1.5 cm in 7 days on potato dextrose agar (PDA), pale at first but soon dark brownish black with conidial masses; a yellow-brown to dark brown soluble pigment may be secreted into the agar. Conidiophores simple or branched near the base, pale at the base but becoming more intensely black toward the apex, with an apical whorl of 4-10 inflated, bottle-shaped phialides. (On natural substrates these phialides soon evanesce after conidial formation and may not be seen). Conidia formed in slimy masses at first, soon drying, hyaline and often smooth when first formed, then becoming olivaceous black, coarsely roughened with dark warts, ellipsoidal, 7 - 12 X 4 - 6 µm.

Toxins:

1. Trichothecenes: Satratoxins, e.g., satratoxin H. Members of the macrocyclic trichothecene group of mycotoxins. Major toxic mechanism of this group appears to be inhibition of peptidyl transferase activity necessary for protein synthesis(1). Toxic effects:

--contact irritation, leading to mucous membrane irritation (sore throat, inflammation of conjunctiva around the eye; in heavy exposures, "catarrhal angina" or burning throat/upper airways, sometimes haemorrhaging lesions of the nasal passages or trachea) associated with airborne material; vesicular skin lesions (contact dermatitis) associated with the handling of contaminated materials (2).

-- immunodepression, known mostly from farm animals exposed to contaminated material but also relatively minor effects along these lines preliminarily demonstrated for humans in an infested office building by Johanning et al. (3). Specific immune deficits known from animal studies include depressed T or B lymphocyte activity, suppressed immunoglobulin and antibody production, reduced complement or interferon activity, impaired macrophage-effector cell function, impaired neutrophil chemotaxis and phagocytosis, pulmonary alveolar macrophage defects and inhibited phagocytosis.

2. Cyclosporins.

These compounds are immunosuppressive, and are well known from the medical applications of cyclosporin A (from the mold Tolypocladium inflatum), e.g., in prevention of rejection of transplanted tissues. The recently discovered cyclosporin-like compound from S. chartarum is distinct (4).

3. Stachybotryolactone and stachybotryolactam (a spirolactone and a spirolactam compound, respectively). These toxins may antagonize the complement pathways which normally target foreign elements for destruction by the immune system (5)

B. Memnoniella echinata

Morphology: very similar to S. chartarum, except that the conidia are borne in chains, not slimy masses, and they are nearly globose, 3 - 6 µm in diameter.

Toxins:

1. Trichothecenes: trichodermol and trichodermin. These compounds were first identified as secondary metabolites of Trichoderma viride. They are known to be toxic to cultured cells at concentrations of 5 ug/ml, mainly due to a high binding affinity for the 60S ribosomal protein (1). Overall, however, they are significantly less toxic than trichothecenes such as satratoxin H, T-2 toxin and deoxynivalenol.

2. Griseofulvins. This well known class of antifungal metabolites is mainly known from the commercially available anti-dermatophyte drug griseofulvin, originally from Penicillium griseofulvum. M. echinata produces two similar compounds.

C. Myrothecium verrucaria

Morphology: Colonies are white to pale pinkish-brown at first, soon dotted and then progressively covered with sporodochia, seen as slimy, shiny greenish black slightly elevated tufts. Sporodochia are composed of a dense tuft of erect penicillate branches giving rise at their apices to whorls of long, thin (10.5-14.5 X 1.5 - 2.0 µm) phialides. Conidia formed in slimy matrix, dark green in transmitted light, broadly spindle shaped to oat-shaped, with a pointed apex and a truncate base, 6.5 - 8 X 2.0 - 3.5 µm. The apex has a nearly invisible, funnel shaped appendage visible only in certain special stains or phase contrast (7).

Toxins:

1. Trichothecenes: Verrucarins and roridins. Members of the macrocyclic trichothecene group of mycotoxins. These are among the most toxic of all trichothecenes, cytotoxic at 0.003 - 0.005 ug/ml and with a mouse intraperitoneal LD50 (dose lethal to 50% of animals when injected into the body cavity) of 0.5 mg/kg (this is an order of magnitude more toxic than the most toxic common Fusarium trichothecene, T-2 toxin). They cause severe disease in animals on the rare occasions they are encountered (8).

D. Myrothecium roridum

Morphology: very similar to M. verrucaria, except that conidia are short-cylindrical, 5.5 - 7 X 1.5 - 2.0 µm.

Toxins:

1. Trichothecenes: verrucarins, roridins, mytoxins, myrotoxins, roritoxins. Highly toxic (see comments above for M. verrucaria), causing severe animal disease when encountered in moldy feed. The most dramatic cases of disease are in horses and pigs and are recorded from the former Soviet Union. M. roridum is referred to under a now-disused synonymous name, Dendrodochium toxicum.

E. Trichoderma viride

Morphology: Colonies pale, very fast growing, 5 - 8 cm on PDA at 7 days, thinly cottony, soon giving rise to white sporodochial tufts which turn green as conidia develop. Sporodochia roughly pyramidal, with long branches near base and shorter ones above; branches rebranch at right angles to the main axis or nearly so, usually in whorls or opposed pairs, and also bear lateral phialides in the same whorled or paired configuration, as well as terminal whorls of phialides. Conidia are rounded, usually 3.6 - 4.5 µm in diameter, usually distinctly roughened but sometimes only slightly so.

Toxins:

1. Trichothecenes: trichodermin. See comments under Memnoniella echinata, above.

2. Cyclic peptides: trichotoxin A. This is a protein-like cyclic peptide with mammalian toxicity.

F. Trichoderma harzianum

Morphology: as T. viride, except that conidia are smooth, not rough walled.

G. Trichoderma pseudokoningii

Morphology: much as the Trichoderma species mentioned above, except for a couple of noteworthy differences. Firstly, sporodochial branches lack the regularly whorled, pyramidal morphology seen in the species above. Phialides and branches tend to diverge singly, and the overall construction of the conidiophore is more linear than pyramidal. In other words, where T. viride and T. harzianum produce sporodochia with something of the form of a perfect little Christmas tree, T. pseudokoningii looks more like a scraggly little light-deprived forest understory tree in its pattern of differentiation. The other difference is that the conidia are smooth-walled and short-cylindrical, 3 - 4.8 X 1.9 - 2.8 µm. A closely related species, T. koningii, has similar conidia but has the whorled-pyramidal sporodochial construction seen in T. viride.

H. Fusarium sporotrichoides

Morphology: Colonies around 8.5 - 9.5 cm in diameter after 7 days on PDA, cottony, yellow, reddish, red-brown or red-purple with whitish aerial mycelium overlaid. Conidiophores branching, bearing phialides which often make fork-like proliferations at the tip as new secondary phialidic necks are produced. Microconidia ranging from subglobose and 5 - 7 µm in diameter to pear or spindle shaped, mostly 6 - 11 X 3 - 4 µm, usually unicellular, sometimes bicellular. Macroconidia slightly curved, 3 - 5 septate, thin, 30 - 45 X 3.5 - 5.5. µm. Chlamydospores abundant, yellow-brown, usually in chains.

Toxins:

1. Trichothecenes: a variety, most prominently T-2 toxin, HT-2 toxin, neosolaniol and fusarenon-X. These are strongly toxic compounds. Like the macrocyclic trichothecenes mentioned above, their primary toxic mechanism is the inhibition of protein synthesis at the level of the ribosome. For the most part, their effects are known from instances in which humans or animals ate contaminated grain, or from laboratory animal or in vitro studies. The major effects observed include "vomiting; inflammation; diarrhea; cellular damage of the bone marrow, thymus, spleen and mucous membranes of the intestines; and depression of circulating white blood cells." (9)

Humans who have eaten contaminated grain develop "alimentary toxic aleukia," which begins with burning sensations of the mouth, throat, esophagus and stomach, continues with vomiting, diarrhea and gastric cramps, and finally progresses to severe leukopenia (drop in white blood cell count), which renders the patient susceptible to infections. Death may result.

Skin contact with material laden with these trichothecenes induces contact dermatitis, and in stronger exposures lesions may be necrotizing (that is, may contain dead tissue, a significant risk factor for the development of bacterial infections).

Effects on immune system components apart from the above-mentioned killing of thymus and spleen cells include inhibition of lymphocyte proliferation responses (e.g., mitogen response) and disruption and lysis of alveolar macrophages.

Coagulation factors in the blood (except fibrinogen) are also significantly depressed.

Trichothecenes in general seem to have little carcinogenicity, but when consumed or administered in pregnancy may have some teratogenicity (inducing deformed offspring) or abortifacient properties.

2. Zearalenone: a few isolates of F. sporotrichoides have been verified as producing this toxin (10). This compound is an estrogen mimic, most commonly causing vulvovaginitis (swelling and reddening of the vulva) in gilts (young female pigs) and sows which have consumed contaminated feed. This condition sometimes leads to vaginal or rectal prolapse. Common results include reduced litter size, loss of pregnancy, and poor milk production in affected swine. Males may be feminized to some extent. Similar syndromes occur in cattle and sheep fed zearalenone-contaminated grain (11).

I. Fusarium culmorum

Morphology: colonies are very rapidly growing, exceeding 9 cm after 7 days on PDA, aerial mycelium whitish to yellow or tan, substrate mycelium and reverse carmine to intensely red brown. According to Domsch et al. (7), the aerial mycelium is very hydrophobic (difficult to wet), unlike that of the similar species F. graminearum. Phialides are monophialides: that is, they do not proliferate at the tips to form multiple fertile necks. Microconidia are absent. Macroconidia are distinctly stout, mostly 5-septate and 30 - 50 X 5 - 7.5 µm. Chlamydospores are abundant, brownish, in chains or in clumps.

The species can be distinguished with some difficulty from the similar F. graminearum and F. crookwellense. F. graminearum has macroconidia with relatively parallel dorsal and ventral sides, while the "back" of the F. culmorum macroconidium is strongly bowed or arched. The catch is that this character is best seen on carnation leaf agar (12), a medium usually only used by the most specialized fusariologists. In addition, isolates in good condition (i.e., isolates either freshly obtained from nature or retaining the characters of freshly isolated cultures) of F. culmorum, on PDA, often conidiate abundantly around the point of inoculation, while F. graminearum in good condition does not do so. The condition is mentioned because Fusarium species frequently deteriorate after a few subcultures, and slimy, profusely macroconidial (pionnotal) colonies are one type of degeneration seen. Such degenerate isolates produce masses of conidia all over the colony surface, regardless of which species they belong to.

F. crookwellense tends to have the same conidiation at the point of inoculation that F. culmorum has. It also has macroconidia with relatively strongly curved dorsa, compared to those of F. graminearum, just as F. culmorum does. According to Burgess et al. (13) "the macroconidia (of F. crookwellense) are longer and not as wide as those of F. culmorum...(and) in contrast to the conspicuous foot at the end of the basal cell of an F. crookwellense macroconidium, that of F. culmorum is less obvious." A comparison of the photos published by et al. (12) makes this more clear than descriptive text does.

Toxins:

1. Trichothecenes: The major compound produced is deoxynivalenol (vomitoxin). This toxin is somewhat less toxic than the compounds listed for F. sporotrichoides, above, but causes a serious feed refusal and emesis (vomiting) syndrome in animals fed contaminated feed, especially pigs.

J. Fusarium poae

Colonies fast growing, exceeding 9 cm after 7 days on PDA, with white to pink aerial mycelium and red agar surface and reverse, and with a distinct odour suggesting peaches. Phialides are monophialides, short (6 - 18 µm) and blunt, in clusters. Microconidia predominantly globose to broadly pyriform, with a basal apiculus, 6 - 10 X 5.5 - 7.5 µm. Macroconidia relatively sparse, 2 - 3 septate, 18 - 38 X 3.8 - 7.0 µm, occasionally longer and with up to 5 septa. Well defined chlamydospores not present, but there are some thickened portions of hyphae which are reminiscent of chlamydospores.

Toxins:

1. Trichothecenes: Although a variety of trichothecenes have been attributed to this species in the past, the careful reassessment of Marasas et al. (10) found only diacetoxyscirpenol produced in significant quantity by a large number of cultures. This compound is slightly less toxic than T-2 toxin, but in general has effects similar to those described for the toxins of F. porotrichoides, above. F. poae has been held by some scientists in the former Soviet Union to be particularly involved with bone deformity in animals and people who have eaten contaminated material. The identification, however, of the isolates used to draw these conclusions needs to be re-investigated before this attribution can be confirmed. A human disease, Kashin-Beck disease, has been described based on characteristic bone deformities seen in populations in affected areas. Although F. poae contamination has been proposed as etiologic in this disease, other theories have also been put forward and the final resolution of the matter is not clear.

K. Fusarium equiseti (sexual state Gibberella intricans)

Colonies 7 - 8 cm after 7 days on PDA, yellowish, ochre or buff finally becoming yellow-brown to brown, but never red. Phialides are monophialides, often in densely branching penicillate tufts. Microconidia absent. Macroconidia usually distinguished by extension of the apical cell into a pronounced beak; either nearly straight or strongly curved, 3 - 5 septate, with basal cell extended as a distinct pedicel, 30 - 50 (-65) X 4.0 - 5.0 µm. Chlamydospores abundantly produced, in chains.

Toxins:

1. Trichothecenes: Most commonly diacetoxyscirpenol (see F. poae), and in at least some strains also T-2 toxin, fusarenon-X and neosolaniol (see F sporotrichoides) are produced.

L. Fusarium moniliforme.

Morphology: Colony reverse usually pale purple; microconidia club-shaped with flat (truncate) basal end, seen in a 10X observation of undisturbed colony on low-sugar media to be formed all or partly in chains rather than slimy heads, phialides mostly under 30 µm, not proliferating (forking) at the tips. Chlamydospores not found.

Toxins:

1. Fumonisins: These toxins were first described in 1984 after a concerted search for the cause of equine leukoencephalomalacia, a disease of horses in which brain tissue is damaged and horses show ataxia (inability to coordinate walking), facial and other paralysis, partial blindness, lethargy or excitement, and in later stages lameness, inability to stand, seizures and death. After the purification of fumonisins, the disease was induced in horses with purified material, confirming the etiologic role of the mycotoxin. Liquefactive necrosis of white matter areas of brain tissue is the main pathological sign seen. Hepatotoxicity is also seen. Experimental animals often experience hepatotoxicity, nephrotoxicity or both; rats have also been shown to experience necrosis of stomach mucosa and myocardium. Liver cancers are induced. Fumonisins are also among the chief suspects for the agent(s) of elevated levels of esophageal cancer in certain parts of the world (14).

M. Fusarium proliferatum.

Morphology: much like F. moniliforme but older phialides proliferate (fork) extensively near the apex. Proliferating phialides can be very difficult to find in colonies younger than 7 days. Chlamydospores not found.

Toxins: fumonisins (see F. moniliforme)

N. Fusarium oxysporum.

Morphology: Colony reverse usually purple or pale; microconidia ellipsoidal, sometimes curved, produced in slimy heads not chains, phialides producing microconidia are mostly under 20 µm, often quite short and broad, not proliferating (forking) at the tips. Macroconidia rather sharply pointed and hooked over at the apex. Chlamydospores often found, seldom abundant.

Toxins: the picture of which toxins may be produced by the majority of F. oxysporum isolates is unclear.

O. Fusarium solani.

Morphology: Colony reverse usually pale tea-brown or pale, sometimes reddish-brown to purplish (especially on cycloheximide medium); microconidia ellipsoidal, macroconidia with ends more blunt than those of other species (but don't rely on this character alone); phialides producing microconidia are thin and elongate, often 20 - 40 µm long (best single character to look for to distinguish from F. oxysporum), not proliferating (forking) at the tips; chlamydospores often abundant, rough.

Toxins:

1. Naphthaquinone pigments. These pigments are not currently regarded to be mycotoxins significantly affecting humans or animals.

P. Alternaria alternata

Colonies fast growing, usually 6 cm in 7 days on PDA, most often woolly but occasionally flat and granular with heavy sporulation. Colour of the colonies is usually dull olive grey to olivaceous brown-black from the beginning, but some colonies begin pale greyish pink and turn dark only after some days or weeks of incubation. Conidiophores are nondescript erect stalks up to 50 µm long with a pore at the apex, or proliferating sympodially to form a series of a few pores on successively produced extensions. Conidia formed in long and sometimes branching chains (which are entirely disrupted in wet microscopic mounts), muriform (that is, with multiple cells and with septa produced in both the long and cross directions) ellipsoidal to egg shaped or more commonly hand-grenade or pear shaped, with the apical cells tapered into a distinct conical beak usually making up around 1/4 to 1/3 of the total conidial length, 18 - 63 X 7 - 18 µm.

Toxins: Alternaria has a unique group of mycotoxins, including alternariols, altenuenes, altertoxins, tenuazonic acid, and AAL toxins. Alternariols and altenuenes are weakly toxic to mice and are cytotoxic (toxic to cultured human cell lines) in vitro at concentrations between 6 and 28 ug/ml (15). Altertoxins and the related compound stemphyltoxin-III, also produced by Alternaria, are mutagenic. Tenuazonic acid appears to inhibit protein synthesis by preventing newly formed protein molecules from detaching from the ribosomes on which they formed. It is lethally toxic to young birds, and in administration to animals produced effects such as "salivation, emesis (vomiting), anorexia (avoidance of eating), erythema (red skin flush), gastrointestinal haemorrhage, convulsions, increase in packed cell volume (an immune parameter) and many other effects" (15). AAL toxins appear to have limited toxic effects against some cultured mammalian cell lines, but are mainly of significance in invasions of plants by Alternaria phytopathogens.

Q. Cladosporium cladosporioides

Colonies around 3 cm in 7 days on PDA, olivaceous grey-green to olivaceous brown, reverse olivaceous black. Conidiophores branching widely and giving rise to numerous clusters of blastoconidia in branching chains, with larger conidia near the base of the chain and smaller conidia near the apex. Conidia 1- or rarely 2-celled, mostly smooth walled or minutely roughened, bluntly forked near the apex if they have given rise to 2 or more apical daughter cells or chains, or ellipsoidal to lemon shaped if they have not, 3 - 7 (-11) X 2 -4 (-5) µm, with cicatrized (darkened), slightly protuberant scars at the places where they have been attached to other conidia or the conidiophore.

Toxins: the antifungal compound cladosporin is produced, as well as emodin, an anthraquinoid pigment compound which on breakdown in vitro by hepatic microsomes forms 2-hydroxyemodin, a mutagenic and cytotoxic product, and some other compounds of lower toxicity. Cultures fed to mice appeared to result in the death of the mice from hemolytic jaundice and renal failure (16). There has been no evidence so far, however, of a toxic effect associated with inhalation of conidia, e.g. in indoor mold proliferation cases.

R. Cladosporium sphaerospermum

Morphology: similar to C. cladosporioides but with conidia, especially those formed near the ends of chains, much more strongly rounded 3 - 4 (- 7) µm in diameter. Typical isolates have strongly roughened conidia, but some smooth-conidial types are seen. Probably consists of a complex of similar species.

Toxins: toxic effects have been noted, e.g., against chicken embryos, but chemicals responsible have not been thoroughly characterized. Not regarded as a highly toxic organism.

S. Cladosporium herbarum

Morphology: similar to C. cladosporioides except that:

-- conidiophores have distinct "geniculate elongations", that is, places where they have thickened up and produced one or more conidiogenous apertures, but then the conidiophore has continued to grow out at a slight angle, making a knee-joint-like bend (whence the term "geniculate") which technically constitutes a sympodial proliferation. Long, mature conidiophores may have a number of geniculate bends along their lengths.

-- conidia are larger and more often 2-celled; one-celled conidia are 5.5 - 13 X 3.5 - 6 µm, distinctly roughened.

Toxins: so far, not considered significantly toxic to humans.

T. Ulocladium spp.

Colonies usually fast growing and dark olivaceous brown to olivaceous black, mostly flat and granular with heavy conidiation. Conidiophores are upright branches with numerous zigzagging bends in the apical region typical of sympodial proliferation, the vertex of each bend with a small, conidium-producing, darkened pore. Conidia usually broadly rounded at the apical end and bluntly conical at the base, formed singly in most species.

In one species (U. chartarum), conidia are formed in short chains of 2 - 10, but never in long chains like Alternaria. In U. chartarum, short outgrowths resembling filament tips, called "false beaks," may protrude out of the conidia and connect them to their daughter conidia within the chains; these should not be confused with the true beaks of Alternaria, which are not outgrowths but rather extended and tapered areas integrated into the actual form of the conidia themselves. This, however, may prove to be a somewhat difficult character, and an easier way to distinguish U. chartarum from A. alternata is usually to see the strongly zigzagging conidiophores of the Ulocladium, as opposed to the very simple, usually single-pored (and therefore often difficult to detect in squash mounts, especially from woolly textured colonies) conidiophores of A. alternata.

Toxins: although most filamentous fungi have secondary metabolites that are toxic to some other form of life, there seems to have been little investigation of Ulocladium to detect such materials.

1. Ueno Y. 1983. Trichothecenes--chemical, biological and toxicological aspects. Developments in food science 4. Elsevier, Amsterdam, p. 135-194.

2. Hintikka E.-L. 1978. Human stachybotryotoxicosis. In Mycotoxic fungi, mycotoxins, mycotoxicoses. An encyclopedic handbook. Vol. 3. Edited by T.D. Wyllie and L.G. Morehouse. Marcel Dekker, New York/Basel. pp. 87-89.

3. Johanning, E., Biagini R., Hull D. et al. 1996. Health and immunology study following exposure to toxigenic fungi (Stachybotrys chartarum) in a water-damaged office environment. Internat. Arch. Occup. Environ. Health 68: 207-218.

4. Sakamoto K., Tsujii E., Miyauchi M. et al. 1993. FR 901459, a novel immunosuppressant isolated from Stachybotrys chartarum No. 19392. Taxonomy of the producing organism, fermentation, isolation, physico-chemical properties and biological activities. J. Antibiotics 46: 1788-1798 (erratum 47: C-1).

5. Jarvis B.B., Salemme J., Morais A. 1995. Stachybotrys toxins. Natural Toxins 3: 10-16.

7. Domsch, K.H., Gams, W., , T.-H. 1980 (reprint 1993). Compendium of soil fungi. IHW Verlag, Eching, Germany.

8. DiMenna, M.E., Mortimer, P.H, White E.P. 1977. In Mycotoxic fungi, mycotoxins, mycotoxicoses. An encyclopedic handbook. Vol. 1. Edited by T.D. Wyllie and L.G. Morehouse. Marcel Dekker, New York/Basel. pp. 107-110.

9. Sharma R.P. and Kim Y.-W. 1991. Trichothecenes. In Mycotoxins and phytoalexins. Edited by R.P. Sharma and D.K. Salunkhe. CRC Press, Boca Raton FL, pp. 339-358.

10. Marasas, W.F.O., P.E., Toussoun T.A. 1984. Toxigenic Fusarium species. Identity and mycotoxicology. Pennsylvania State University Press, University Park, PA.

11. Prelusky D.B., Rotter B.A., and Rotter R.G. 1994. Toxicology of mycotoxins. In Mycotoxins in grain. Compounds other than aflatoxin. Edited by J.D. and H.L. Trenholm, Eagan Press, St. , Minn., pp. 359-403.

12. P.E., Toussoun T.A., and Marasas, W.F.O. 1983. Fusarium species. An illustrated manual for identification. Pennsylvania State University Press, University Park, PA.

13. Burgess L.W., P.E., Toussoun T.A. 1982. Characterization, geographic distribution and ecology of Fusarium crookwellense sp. nov. Trans. Br. Mycol. Soc. 79: 497-505.

14. Beardall J.M and J.D. 1994. Diseases in humans with mycotoxins as possible causes. In Mycotoxins in grain. Compounds other than aflatoxin. Edited by J.D. and H.L. Trenholm, Eagan Press, St. , Minn., pp. 487-539.

15. Visconti A and Sibilia B. 1994. Alternaria toxins. In Mycotoxins in grain. Compounds other than aflatoxin. Edited by J.D. and H.L. Trenholm, Eagan Press, St. , Minn., pp. 315-336.

16. Daunter B and Greenshields R.N. 1973. Toxicity of Cladosporium cladosporioides. J. Gen. Microbiol. 75: xv (Roman numeral 15).

This site designed and maintained by Sextant Software Inc. © 2000 .

[Guest guest]

----- Original Message ----- From: barkwell

Barkwell's

Sent: Saturday, April 27, 2002 10:53 AM

Subject: mold article

Airborne Fungi in Indoor Environments

In the News

Estelle Levetin, PhDUniversity of Tulsa

Fungal spores, commonly called mold spores, are a normal component of the outdoor air. They are present in the atmosphere anytime that the ground is not covered with ice or snow. The spores are discharged from fungi growing as saprophytes (existing on dead or decaying organic matter is the soil or elsewhere in the environment) or parasites (infecting living tissues - most are plant pathogens). Many species of fungi are found as leaf surface microorganisms where they exist on organic matter produced by the plant. Concentrations outdoors can be high, especially in the late summer or fall. We have occasionally recorded hourly concentrations in Tulsa above 100,000 spores per cubic meter of air.The air in many indoor environments also contains spores; however, indoors we speak of these spores as contaminants. Actually the outdoor air may be the source of the spores whenever fresh air is introduced. In addition, many indoor locations may serve as amplification sites for the growth of fungi. Such sites include carpeting, upholstered furniture, showers, shower curtains, other bathroom fixtures, potted plants, and the soil around potted plants. Anytime moisture or even high humidity is available, spores can germinate and fungi can grow and produce thousands of new spores utilizing organic material in these sites. In buildings with central HVAC (heating, ventilation, and air conditioning) systems, properly maintained in-system or in-duct filters should remove many of the spores present. Many instances are known where the HVAC system itself served as an amplification and dissemination site for fungal spores. In these cases fungi have been found growing on air filters as well as in the ducts. This can often be prevented by routine maintenance.

There are no set levels of airborne fungi, which can be regarded as safe. Much depends on the out door concentration and also depends on the types of spores present indoors. Each office, each, building, or each home must be considered as a separate and unique case. Generally indoor concentrations that are less than 25% of outdoor levels are considered low when the fungi present are typical outdoor types.

Many fungal spores (possibly all) are allergenic, capable of causing allergic responses in susceptible individuals. A small group of fungi are also human pathogens. While many human pathogens just cause mild or annoying conditions, such as athlete's foot and ringworm, other human pathogens can cause severe and debilitating diseases.

Some fungi produce mycotoxins, which can be present within the spores and inhaled with the spores. Mycotoxins are potent compounds. Many are carcinogens, and others can impare the immune system. There has been a great deal of interest in the past few years on mycotoxins in indoor air. The following provides some background information on fungi commonly found in air samples:· Acremonium - common soil fungus. Occurs indoors in wet environments on a variety of substrates. Considered allergenic but not well studied.· Alternaria - common fungal genus especially in outdoor environments; worldwide it is often the second most common mold spore genus. It is a common saprophyte, leaf surface organism, and plant pathogens. Alternaria spores are highly allergenic. This is seldom found at high levels indoors. · Ascospores - spores produced by the sexual stage of many fungi. Usually from outdoor sources with the exception being Chaetomium which readily occurs on indoor substrates. Suspect allergens but not well studied.· Aspergillus - common fungal genus, especially in indoor environments. In nature this typically occurs in the soil. Various species of Aspergillus have been implicated in aspergillosis, a serious and persistent lung infection. Other species of Aspergillus are known to produce mycotoxins. Also known to be allergenic. · Aureobasidium - commonly occurring black yeast. In the natural environment it is found on leaf surfaces, indoors it is common where moisture accumulates such as kitchens and bathrooms. · Basidiospores - spore produced by mushrooms, bracket fungi, puffballs and similar higher fungi. Common in the outdoor environment and introduced indoors with outdoor air. Indoor sources of basidiospores are from dry rot. Many basidiospores are allergenic.· Chaetomium - common fungus found indoors and outdoors. Readily colonizes cellulose-based materials and is commonly found on sheet rock and other indoor substrates. Allergenicity is not known. Some species produce mycotoxins but these have not been well studied.· Cladosporium - common fungal genus occurring both indoors and outdoors. Spores of Cladosporium are the most abundant outdoor spore type and have a worldwide distribution. The fungus normally exists as a saprophyte or weak plant pathogen, but a few species of Cladosporium have been reported as human pathogens. The spores are known to be allergenic.· Curvularia - a fungus whose spores are often present in the outdoor air. It occurs as a saprophyte and plant pathogen. Although little is known, it is assumed to be allergenic and also can be a cause of fungal sinusitis.· Drechslera-type - several genera of very similar fungi including the genera Drechslera, Bipolaris, Helminthosporium, and Exserohilum. The fungi are either plant pathogens or saprobes in the natural environment. They are known to be allergenic and can also cause fungal sinusitis.· Epicoccum - a common saprophyte both indoors and outdoors. Epicoccum can grow on many substrates indoors. At times the outdoor concentrations are high in agricultural areas. Known to be allergenic and possibly cross react with Alternaria.· Fusarium - a common saprophyte and important plant pathogen. It normally is found in the soil but can be introduced indoors. Indoors it is often found in the bathroom or other areas with moisture. Some species of Fusarium produce mycotoxins.· Memnoniella - a soil fungus in the natural environment. Indoors it is found on cellulose-based materials that have gotten wet. Allergenic status not known. It is closely related to Stachybotrys and often occurs with it. It is known to produce mycotoxins.· Myrothecium - a soil fungus in the natural environment occurring on cellulose-based materials. Capable of forming mycotoxins similar to those from Stachybotrys· Non-sporulating - many fungi do not reproduce in culture because they require specialized environmental conditions. Without spores it is not possible to identify fungal colonies. · Paecilomyces - widespread genus occasionally found indoors. Able to grow on a number of indoor substrates. Similar to Penicillium. Considered to be allergenic and able to form mycotoxins. Not distinguishable from Penicillium on total spore samples· Penicillium - common fungal genus, especially in indoor environments. Found in water damaged buildings and homes. Also common on foodstuffs. In nature this typically occurs in the soil. Known to be allergenic. Some species of Penicillium are also known to produce mycotoxins. · Phoma - soil fungus, common on plant material. Indoors found on walls, ceiling tiles, shower curtains. Known to be allergenic but the spores are not readily dispersed by air currents. · Pithomyces - common saprophyte that is prevalent outdoors especially during summer and fall. Occasionally found indoors.· Rhizopus - common saprophyte that grows on a variety of substrates, especially spoiled food. Allergenic· Smut spores - spores produced by smut fungi, common plant pathogens that are especially prominent on cereals and other grasses. Very common in the outdoor atmosphere almost year round. These can be introduced indoors with outdoor air. Spores are allergenic but not well studied.· Stachybotrys - a soil fungus in the natural environment. Commonly found indoors on wet materials containing cellulose, such as wallboard, jute, wicker, straw baskets, and other paper materials. Some consider it to be allergenic although little is known. Able to produce mycotoxins.

General References on Bioaerosols

1. Burge, H. (Ed). 1995. Bioaerosols, Publishers, Boca Raton.

2. , C.S. 1987. The Aerobiological Pathway of Microorganisms, Wiley & Sons, New York.

3. , P.H. 1973. The Microbiology of the Atmosphere, 2nd ed., Halstead Press, New York

4. Lacey, J. 1991. Aerobiology and health: the role of airborne fungal spores in respiratory disease, p. 157-186. In D.L. Hawksworth (ed), Frontiers in Mycology, C.A.B. International, Kew, United Kingdom

5. Lacey, J. and J. Venette. 1995. Outdoor Air Sampling Techniques, p. 407-471. In C.S. and C.M.Wathes (ed), Bioaerosols Handbook. Publishers, Boca Raton, FL

6. Levetin, E. 1995. "Fungi". In: Bioaerosols, ed. H. Burge, Publishers, Boca Raton pp: 87-120.

7. Macher, J. (Ed). 1999. Bioaerosols: Assessment and Control, ACGIH, Cincinnati

Useful Links

CDC- Center for Disease Control

EPA - Environmental Protection Agency

Remediation and Clean Up

EPA Mold Resources

California Dept of Health Services

Indoor Air Quality Info Sheet

Stachybotrys Info Sheet

Washington Dept of Health

Dr. Malloch - University of Toronto

Doctor Fungus Home Page

Environmental Microbiology Lab - Description of commonly occurring fungal genera

[Guest guest]

Well said,Pat.

I could not believe the dribble that this " specialist " was writing about

mold. I also am dealing with workplace exposure. I have developed chronic

sinusitis,asthma,GERD,multiple chemical

sensitivity,hypertrygliceride,hoarseness,fatigue,etc. all within the past

five years of working here.

This past Jan. I complained of the chronic water intrusion in our locker area

at work. The area was tested to shut me up. Four months later after repeated

requests I received the test

results--Stachybotrys,Aspergillus,Pencillium,Chaemotium,etc. identified by

swabs. Testing done with two visits. The first was onsite exam and swabs. Two

weeks later air quality done.Apparantly,the air quality showed the spore

count less than outside. Strange that across the hall in the Operating Room

there were no spores at all noted. Because of the air quality showing less

spores the hospital has deemed that there is no problem.

I have been fighting this air quality stuff all summer and with the help of

coworkers was able to persuade the management to have a consultation done.

The consultant was from WSHA( Washington State L & I ). He was very thorough

and graciously called me after the test. He said he couldn't care less about

the air. He wanted the mold infested area cleaned up, including removing the

lockers to get to the drywall, pulling up the rug and repairing the cracked

cement which is the foundation over our heads.There is a lawn over the cement

which gets saturated every winter.

Two weeks ago we had another " air quality " meeting where it was agreed that

the cement would be fixed plus other areas.Today I read the minutes of the

meeting where it was stated that the air was OK and the moisture problem

would be taken care of. Not one mention of the four letter " M " word.I think

that if they uttered the word mold they would panic.

I have been told by the personnel director that I have no right to ask

questions and that the problem will be handled. I have no right to know how

or when. I was also told that I read too much and ask too many questions. I

was accused of contacting the Union. I am management and not protected by

union. I was then interrogated by her, my OR Director and the Employee Health

nurse to find out who called the Union who was now starting to make

inquiries. I refused to answer them and told them even if I knew I would not

divulge who the person was. The staff has a right to contact their

representatives.

My pulmonlogist and Occ/med doc have told me to find another job which I will

as soon as I can find a safe place to go. I have put in an L & I claim which

the L & I rep told me would probably be denied by the doctor. The L & I rep

told me to continue and petition as I have a legitimate claim. I am sure the

hospital thinks I am a pain in the butt.

The other staff is finally getting stirred up and contacting OSHA. This whole

thing about the air levels drives me nuts. I found out that the air filters

were changed the night before these inspections. I have also read that air

quality is not considered an indicator of an ongoing problem if there is

visible mold.

When I asked why we had a carpet in the locker room which has been saturated

repeatedly for 10 years I was told by my director that she thought it would

look nicer. We are the only area with a carpet.

Many people sick. I am sick of this cover-up. They act like the employees do

not have any rights to know about their environment.

Eileen B.

[Guest guest]

http://www.bizjournals.com/houston/stories/2002/07/29/editorial3.html

I'm sorry, but your article can't put a bandage on the booboos of mold

victims. I live in NY and have been sick for 3 years with NO

compensation at all *yet* even though I was stricken in the workplace.

http://www.presenting.net/sbs/sbsstory.html

I don't care what the credentials are of this misinformed doctor. He

needs a refresher course in modern medicine - as do most physicians.

Texans have every reason to be aware of and to be able to avoid being

struck down with mycotoxins from Stachybotrys mold. The abundance of

rain and flooding are sure to bring to light many cases of illness

from this. Many people may not realize why they are stricken with

cancer (yes, it's highly carcinogenic), MS, lupus, respiratory

problems, tremors, skin problems, etc. This problem was even addressed

in the Bible in Leviticus with advice on how to get rid of the mold.

To see most of the symptoms that it can cause, go to this survey

results page:

http://www.presenting.net/sbs/cgi-bin/survey/MasterSurvey.cgi?display=sbssurvey

You asked how this issue has grown to be a major consumer crisis

today. How about moldy wet lumber being used to build new homes,

sheetrock in homes (mold loves cellulose) as fodder for the mold, air

tight homes and businesses recirculating the spores and mycotoxins?

This doctor who states a " resounding NO " to whether mold can cause

memory loss, fatigue or brain damage needs to call Dr. Gordon from Mt.

Sinai Hospital in NY. As a last resort, he should live in a

contaminated home for a while. I'm not talking about a home that's

falling apart. I'm talking about a very nice looking home that appears

spotless. Perhaps he does live in a contaminated home and does have

brain damage himself. Who knows. It was 2 years after quitting my job

that I noticed an almost abrupt change for the better in my cognitive

functioning.

Toxic mold is no longer just an agriculture or food issue.

Stachybotrys is an airborne biowarfare weapon. How about aspergillus, Doc? That

can be fatal to humans if inhaled. It's very difficult to cure.

Regarding relocation apartments, houses and motels, some victims

cannot stay in them because the premises are also infected. Some

victims are staying in tents! Some victims leave with nothing but the

clothes on their backs and give up all of their personal possessions,

some of which can never be replaced.

Enough said.

Pat

[Guest guest]

Way to go Pat!

This misinformed doctor (Marshall) sounds like a spokesman for the

building, and insurance industry. I am a victim myself of the

massively contaminated places that Mr. Marshall says do not affect

us. There are two issues that he conveniently failed to address.

First, since the mid 70's buildings have been turned into closed

systems - ones that control the air we breathe and the environment we

live and work in daily. In doing so the building industry tried to

fool " Mother Nature, " and as we all know it is not nice to fool

Mother Nature. Second, he fails to address the problems that most

scientists agree on. That is that some people are more susceptible

to the toxic affects of these bad environments.

The issue of the closed systems came about because of the energy

crisis of the 70's. Building contractors are building totally closed

systems and building management is trying to do natures job. That is

control the environment - for cost reasons, of course. These types

of buildings, be it a home or a business is going to get worse and

worse. In theory, the closed system might be workable. However, as

we all know, mistakes are made, whether unintentional or not. Let

one thing go wrong with this system, and the entire building becomes

massively contaminated - a literal breeding ground for molds,

mildews, and other toxic contaminants.

The second issue concerns the supposedly healthy individual not being

affected whereas the people that are more susceptible to these

unhealthy effects, may be affected. This issue was not dealt with.

Let me express my opinion on this issue. Those healthy ones, are

still laying in wait for the long term affects which are assuredly to

show up in time. How long - who knows. We do know however is that

we have been affected, and it makes me quite mad when I read a so-

called doctor saying that " It absolutely is not a problem. "

Our world is in for a Major Plague, if something is not done!

>

http://www.bizjournals.com/houston/stories/2002/07/29/editorial3.html

>

> I'm sorry, but your article can't put a bandage on the booboos of

mold

> victims. I live in NY and have been sick for 3 years with NO

> compensation at all *yet* even though I was stricken in the

workplace.

>

> http://www.presenting.net/sbs/sbsstory.html

>

> I don't care what the credentials are of this misinformed doctor. He

> needs a refresher course in modern medicine - as do most physicians.

>

> Texans have every reason to be aware of and to be able to avoid

being

> struck down with mycotoxins from Stachybotrys mold. The abundance of

> rain and flooding are sure to bring to light many cases of illness

> from this. Many people may not realize why they are stricken with

> cancer (yes, it's highly carcinogenic), MS, lupus, respiratory

> problems, tremors, skin problems, etc. This problem was even

addressed

> in the Bible in Leviticus with advice on how to get rid of the mold.

> To see most of the symptoms that it can cause, go to this survey

> results page:

>

> http://www.presenting.net/sbs/cgi-bin/survey/MasterSurvey.cgi?

display=sbssurvey

>

> You asked how this issue has grown to be a major consumer crisis

> today. How about moldy wet lumber being used to build new homes,

> sheetrock in homes (mold loves cellulose) as fodder for the mold,

air

> tight homes and businesses recirculating the spores and mycotoxins?

>

> This doctor who states a " resounding NO " to whether mold can cause

> memory loss, fatigue or brain damage needs to call Dr. Gordon from

Mt.

> Sinai Hospital in NY. As a last resort, he should live in a

> contaminated home for a while. I'm not talking about a home that's

> falling apart. I'm talking about a very nice looking home that

appears

> spotless. Perhaps he does live in a contaminated home and does have

> brain damage himself. Who knows. It was 2 years after quitting my

job

> that I noticed an almost abrupt change for the better in my

cognitive

> functioning.

>

> Toxic mold is no longer just an agriculture or food issue.

> Stachybotrys is an airborne biowarfare weapon. How about

aspergillus, Doc? That

> can be fatal to humans if inhaled. It's very difficult to cure.

>

> Regarding relocation apartments, houses and motels, some victims

> cannot stay in them because the premises are also infected. Some

> victims are staying in tents! Some victims leave with nothing but

the

> clothes on their backs and give up all of their personal

possessions,

> some of which can never be replaced.

>

> Enough said.

>

> Pat

[Guest guest]

I agree with the comments about this Doctor who wrote that mold is OK as it

is everywhere. He probably does work for or with the building & insurance

industries.

When I complained about mold at work and the implications for affected

coworkers and the potential for others to be affected management agreed to a

meeting. At this meeting there was a doctor present with a stethoscope draped

around his neck. He was introduced as a mold specialist. He disputed all of

my concerns. I countered with proof for each topic with the research and

documentation in front of me. No one else had done any research or at least

had references present. His jaw dropped on many occasions at that meeting.

A few days later I found out that he is a Ph.D. who works in the laboratory.

I am as respectful of his doctorate as I would be of a physician but why

would they deem it necessary to falsely represent him?

Eileen

[Guest guest]

Apparently Dr. Marsall is unaware of our Coalition and

Foundation, wherein we have documented hundreds of

cases of Toxic Mold and related illnesses. I hear the

woes and tears of this people almost daily by email

and phone. DR. MARSHALL YOU CAN'T HAVE THAT MANY

PEOPLE WITH THE SAME SYMPTOMS, THE SAME MOLD PROBLEMS

AND NOT HAVE THE SAME DIAGNOSIS! Most of these have

had the blood tests so they know it is Toxic Mold. I

think it rather silly his opinion, since Dr. Marshall

knows that Texas has flooded twice in San and

Austin area in the last few years. Bad building,

shoddy work, houses built of straw, floods, torrential

rain, drought, and El Nino have played havoc with

humidity levels, fungi and bacterium.

I don't think Dr. Marshall said exactly what these

patients ARE suffering from. Allergic reactions, yes,

too be expected,but that's not the whole of it,

especially with long term exposure and massive

amounts. That is why I intend to visit my favorite

place,Congress, this coming year. Anyone else takers

to tell your story to Congress let me know and we will

charter us a ride! I guess the OTHER SIDE has to have

A doctor on their side! Ha!

Dr. Marshall has not had to deal with the Death from

complications of Mold exposure, that I have, as

President of NTMC.

If you haven't joined us yet, as a member,now is the

time, the topic is bound to be a heated one in the

next few years to come!

National Toxic Mold Coalition and Foundation

NTMCPresident

website:ntmc0.tripod.com

When the children cry, the whole world cries with

them!

--- lmac562002 <triggerpom@...> wrote:

> Way to go Pat!

>

> This misinformed doctor (Marshall) sounds like a

> spokesman for the

> building, and insurance industry. I am a victim

> myself of the

> massively contaminated places that Mr. Marshall says

> do not affect

> us. There are two issues that he conveniently

> failed to address.

> First, since the mid 70's buildings have been turned

> into closed

> systems - ones that control the air we breathe and

> the environment we

> live and work in daily. In doing so the building

> industry tried to

> fool " Mother Nature, " and as we all know it is not

> nice to fool

> Mother Nature. Second, he fails to address the

> problems that most

> scientists agree on. That is that some people are

> more susceptible

> to the toxic affects of these bad environments.

>

> The issue of the closed systems came about because

> of the energy

> crisis of the 70's. Building contractors are

> building totally closed

> systems and building management is trying to do

> natures job. That is

> control the environment - for cost reasons, of

> course. These types

> of buildings, be it a home or a business is going to

> get worse and

> worse. In theory, the closed system might be

> workable. However, as

> we all know, mistakes are made, whether

> unintentional or not. Let

> one thing go wrong with this system, and the entire

> building becomes

> massively contaminated - a literal breeding ground

> for molds,

> mildews, and other toxic contaminants.

>

> The second issue concerns the supposedly healthy

> individual not being

> affected whereas the people that are more

> susceptible to these

> unhealthy effects, may be affected. This issue was

> not dealt with.

> Let me express my opinion on this issue. Those

> healthy ones, are

> still laying in wait for the long term affects which

> are assuredly to

> show up in time. How long - who knows. We do know

> however is that

> we have been affected, and it makes me quite mad

> when I read a so-

> called doctor saying that " It absolutely is not a

> problem. "

>

> Our world is in for a Major Plague, if something is

> not done!

>

>

>

>

>

> >

>

http://www.bizjournals.com/houston/stories/2002/07/29/editorial3.html

> >

> > I'm sorry, but your article can't put a bandage on

> the booboos of

> mold

> > victims. I live in NY and have been sick for 3

> years with NO

> > compensation at all *yet* even though I was

> stricken in the

> workplace.

> >

> > http://www.presenting.net/sbs/sbsstory.html

> >

> > I don't care what the credentials are of this

> misinformed doctor. He

> > needs a refresher course in modern medicine - as

> do most physicians.

> >

> > Texans have every reason to be aware of and to be

> able to avoid

> being

> > struck down with mycotoxins from Stachybotrys

> mold. The abundance of

> > rain and flooding are sure to bring to light many

> cases of illness

> > from this. Many people may not realize why they

> are stricken with

> > cancer (yes, it's highly carcinogenic), MS, lupus,

> respiratory

> > problems, tremors, skin problems, etc. This

> problem was even

> addressed

> > in the Bible in Leviticus with advice on how to

> get rid of the mold.

> > To see most of the symptoms that it can cause, go

> to this survey

> > results page:

> >

> >

>

http://www.presenting.net/sbs/cgi-bin/survey/MasterSurvey.cgi?

> display=sbssurvey

> >

> > You asked how this issue has grown to be a major

> consumer crisis

> > today. How about moldy wet lumber being used to

> build new homes,

> > sheetrock in homes (mold loves cellulose) as

> fodder for the mold,

> air

> > tight homes and businesses recirculating the

> spores and mycotoxins?

> >

> > This doctor who states a " resounding NO " to

> whether mold can cause

> > memory loss, fatigue or brain damage needs to call

> Dr. Gordon from

> Mt.

> > Sinai Hospital in NY. As a last resort, he should

> live in a

> > contaminated home for a while. I'm not talking

> about a home that's

> > falling apart. I'm talking about a very nice

> looking home that

> appears

> > spotless. Perhaps he does live in a contaminated

> home and does have

> > brain damage himself. Who knows. It was 2 years

> after quitting my

> job

> > that I noticed an almost abrupt change for the

> better in my

> cognitive

> > functioning.

> >

> > Toxic mold is no longer just an agriculture or

> food issue.

> > Stachybotrys is an airborne biowarfare weapon. How

> about

> aspergillus, Doc? That

> > can be fatal to humans if inhaled. It's very

> difficult to cure.

> >

> > Regarding relocation apartments, houses and

> motels, some victims

> > cannot stay in them because the premises are also

> infected. Some

> > victims are staying in tents! Some victims leave

> with nothing but

> the

> > clothes on their backs and give up all of their

> personal

> possessions,

> > some of which can never be replaced.

> >

> > Enough said.

> >

> > Pat

>

>

__________________________________________________

[Guest guest]

Tackling a mold problem

Carol

" The Little Mad Nutritional Scientist "

www.hometown.aol.com/willowlee53

[Guest guest]

Jeff, great article. Sorry you have lost so much due

to the mold, and also the school district evading

their responsibilities. It seems to be happening to

so many mold victims. My mold was in my condo, I have

100 color photos of the mold, but they are still

saying I didn't have mold? Keep up your fighting

spirit and try to get your health back!

Judi

--- billyslongtimefan <billyslongtimefan@...>

wrote:

> If you are interested, go to phoenixnewtimes.com I

> am the guy the

> article is about.

>

>

>

>

>

>

__________________________________

Music Unlimited

Access over 1 million songs. Try it free.

http://music./unlimited/