NEW YORK MOLD ASSESSORS INC

 

 

Fungi found in dust and air samples- representative findingsa

Species% of houses where species was found in:

Dust samplesAir samples

Penicillium spp.8047

Rhizopus spp.73

Cladosporium cladosporioides (Fresen) de Vries678

Alternaria alternata (fr.) Keissler57Xb

Sterile isolates55

Aspergillus niger van Tieghem536

Penicillium viridicatum Westling396

Mucor spp.31X

Trichoderma viride (Pers.) ex Gray256

Ulocladium botrytis Preuss224

Penicillium fellutinum Biourge2014

Penicillium decumbens Thom1810

Cladosporium herbarum (Pers.) Link16

Paecilomyces variotii Bainier10

Phoma spp.10

Arthrinium spp.8

Aspergillus fumigatus Fresen.6

Aureobasidium pullulans (deBary) Arnaud6

Monilia sitophila Sacc.6

Paecilomyces spp.6

Periconia spp.6

Aspergillus candidus Link4

Aspergillus ochraceus Wilhelm4X

Aspergillus spp.48

Phialophora melinii (Nannf.) Conant4

Yeasts826

Aspergillus versicolor (Vuill.) TiraboschiXX

Basidiomycetes (clamp connections)XX

Cladosporium sp.X

Curvularia inaequalis (Shear) BoedijnX

Geotrichum candidum LinkXX

Penicillium aurantiogriseum DierckxX

Penicillium brevi-compactum DierckxX6

Penicillium chrysogenum ThomXX

Penicillium digitatum Sacc.XX

Penicillium janthinellum BiourgeX8

Penicillium lividum WestXX

Penicillium purpurogenum StollX

Penicillium rugulosum ThomXX

Penicillium simplicissimum (Oud.) ThomX

Stachybotrys atra CordaX

Thamnidium elegans Link.X

Torula herbarum (Pers.) Link ex GrayX

Verticladiella sp.X

 

Associations with Human Disease

The possible association of Stachybotrys species with human disease became apparent coincident with the equine epidemics. In areas of enzootic equine disease, humans, especially fodder-handlers and others who had close contact with musty straw, developed a dermatologic and respiratory syndrome (103, 104, 196, 229, 429, 434). Occasionally, individuals who used straw for fuel or bedding became ill (133). Close family members without such exposures, and even workers protected by clothing, did not become ill. Primary disease manifestations appeared on the skin, with dermatitis on the scrotum, medial thighs, axilla, and, less frequently, the hands and other areas. Lesions progressed from hyperemia to crusting exudates to necrosis, with subsequent resolution (429). Lesion location suggested that rather than direct contact, the lesions were due to aerosolization of the offending substances, with primary effects in dermal areas with abundant moisture and skin-to-skin contact. Some patients suffered erosions on the oral and gingival mucosa (7, 229). Respiratory symptoms were described, including catarrhal angina, bloody rhinitis, cough, throat pain, chest tightness, and occasional fever. Some patients experienced transient leukocytopenia. Subsequently, straw yielded S. alternans isolates that were toxic in a rabbit dermal toxicity test, producing areal fructifications. When applied to the skin of volunteers, the isolates produced the same local and systemic responses (104). A striking aspect of these observations is their significant difference from animal disease, both in symptoms (dermatologic versus systemic illness) and in the route of exposure (ingested versus aerosolized contact) (7, 360, 361).

Despite the association of Stachybotrys with animal and human disease, early researchers were unable to fulfill Koch's postulates with the fungus. There was no evidence that the fungus itself was a pathogen, and scientists could not transmit infection or disease by injection of tissue from affected animals (104). At most, injection of the fungus caused a local response but no systemic invasion (429). It was only with the identification and application of Stachybotrys toxins that the nature of the disease process was understood.

Mycotoxins from Stachybotrys

The mycotoxins responsible for many of the described effects of Stachybotrys were isolated in the 1940s during the aforementioned Russian equine outbreak and were found to have an empiric formula of C25H34O6 or C26H38O6, consistent with the trichothecene class of compounds (103, 104, 133). There are 148 natural trichothecenes alone (147). At least 40 of these are mycotoxins, produced mainly by Fusariumspecies (71). While trichothecenes are chemically diverse, they are all tricyclic sesquiterpenes with a 12,13-epoxy-trichothec-9-ene ring (187, 322), some of the best described of which are satratoxins F, G, and H, roriden E, verrucarin J, and trichoverrols A and B. The toxins have been isolated from a variety of substrates, including dust (satratoxins, trichoverrols, verrucarol, verrucarins, trichoverrins) and grain (T-2 toxin, nivalenol, and derivatives of others) (68). The most potent of these are T-2 toxin, diacetoxyscirpenol (DAS or anguidine), deoxynivalenol (vomitoxin), and fusarenon-X (Fig. ​(Fig.2).2). Sites of action include initiation of protein synthesis (scirpentriol, 15-acetoxyscirpendiol, DAS, verucarin A, and T-2 toxin) and elongation or termination (trichodermin, trichodermol, crotocol, trichothecolone, trichothecin, and verrucarol) (187, 258). Because of their potency in affecting protein synthesis, they may cause a predilection to other diseases, masking the underlying toxicosis (322, 337). As a result, many diagnoses were entertained before alimentary toxic aleukia (see below) was correctly linked to fusarial toxins (Table ​(Table4)4) (194). Stachybotrys species can produce spirolactams and spirolactones related to anticomplement components (188), phenylspirodrimanes which inhibit complement activation (275), cyclosporins (354), and endothelin receptor antagonists (287). There is also a beneficial trichothecene complex of antibiotics exerting phytotoxic, cytotoxic, and cytostatic properties (186) and recently described stachyflin compounds with potent antiviral activity (269). Trichothecenes resist sunlight, UV light, X-rays, heat (up to 120°C), and acids. They are readily destroyed by alkali, which allows for detoxification with sodium, potassium, calcium, or ammonium hydroxide or gaseous ammonia (28, 336). This has important ramifications for building remediation.

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FIG. 1.

Morphology of S. chartarum. (A) Representative section of damaged wallboard. Note the areas of black discoloration. (B) Pure culture of S. chartarum, initially obtained from contaminated wallboard (40× objective). (C) Higher-power view of the same culture as in panel B (100× oil objective). (D) Scanning electron micrograph of conidia at the tip of a conidiaphore. (E) Scanning electron micrograph of mature conidia. Slime has been removed by scanning electron microscope processing. Panels D and E are reprinted from Nelson, http://www.apsnet.org/online/feature/stachybotrys/ with permission.

TABLE 2.

Toxigenic species of mold isolated from indoor air of housesa

SpeciesToxins produced

Aspergillus flavusAflatoxins

Aspergillus fumigatusFumiclavines, fumigatoxin, fumigillin, fumitrems, gliotoxin

Aspergillus versicolorSterigmatocystin, versicolorin, aspercolorin, averufin, cyclopiazonic acid

Penicillium brevicompactumBrevianamide A, mycophenolic acid

Penicillium chrysogenumCitrinin, penicillic acid, PR-toxin, roquefortin C

Penicillium citrinumKojic acid, citrinin, citreoviridin

Penicillium corylophilumGliotoxin

Penicillium cyclopiumPenicillic acid

Penicillium expansumPatulin, citrinin

Penicillium fellutanumCitreoviridin, citrinin

Penicillium spinulosumSpinulosin

Penicillium viridicatumBrevianamide A, citrinin, mycophenolic acid, penicillic acid, viomellein, xanthomegnin

Stachybotrys chartarumRoridin E, satratoxin H, sporidesmin G, trichoverrins, verrucarol

Trichoderma virideGliotoxin, T-2 toxin, trichodermin, trichodermol, viridiol

aAdapted from reference 130 with permission of the publisher.

 

 

ASSOCIATION OF STACHYBOTRYS SPECIES WITH “SICK BUILDINGS”

Because of concerns of mold-induced building-related illness and the particular characteristics of Stachybotrys species, there has been growing concern about the health of occupants of Stachybotrys-“damaged” buildings (9, 79, 91, 133, 150, 157, 184, 188, 197, 241, 318, 423, 424). Many authors have reported ill effects in relation to Stachybotrys, although it is critical to note these reports are often associations rather than proof of causation. Hodgeson et al. (164) reported building-related illness in Florida; this was described as symptoms consisting of mucosal irritation, fatigue, headache, and chest tightness that occurred within weeks of moving into the affected building. The symptoms were purportedly caused by S. chartarum and A. versicolor, although a number of other species were seen. The authors identified mycotoxins including satratoxins G and H (see below) in moldy ceiling tiles, although the significance of these findings is unclear. While they concluded the symptom outbreak was likely a result of inhalation of fungal toxins, there was in fact no clear evidence (e.g., laboratory parameters) to support the claim. Tuomi et al. (420) examined Finnish buildings with water damage and identified a host of fungal organisms and mycotoxins (satratoxins G and H, T-2 toxin, and the aflatoxin precursor sterigmonisin) in bulk samples, although the relationship between the organisms and toxins was unclear, as explored below. Examining buildings with building-related illness complaints, Johanning et al. (197) isolated satratoxin H and spirocyclic lactones from water damaged material. The authors implied these mycotoxins were the cause of respiratory and immune problems, although, as we discuss below, the claims are questionable. Other authors have reported anecdotal cases of illness in which S. chartarum and mycotoxins have been isolated from building materials, but again there are few objective measurements of illness or clear etiologic links to the fungus (79). While authors claim the health effects are similar to past cases of stachybotryotoxicosis, such effects are often vague, poorly described, and clearly not the same as the serious illnesses of equine stachybotryotoxicosis and alimentary toxic aleukia described below.

One of the best studies of building-related illness showed minimal relation to Stachybotrys. Miller et al. (267) examined 50 Canadian homes in which the occupants had complaints of respiratory or allergic symptoms for which there was no explanation, although at the time of the study, occupants of only 6 houses had “building-related illnesses.” Looking at air exchange rate, moisture levels, and analyzing air and dust for fungus and fungal products in 37 of the homes, they found S. chartarum in only one house; analysis of the 6 “sick” houses did not indicate fungus-related disease. During parts of the year when windows are open, indoor fungi are comparable to outdoor species (Cladosporium, Alternaria, and Aureobasidium) (391). However, in this study, outdoor air spores were negligible and Penicillium and other soil fungi were most important. Toxigenic fungi included P. viridicatum, Trichoderma viride, P. decumbens, and A. versicolor. House dust usually contained “appreciable” amounts of filamentous fungi and yeast, and so it was expected that spores could be found in air, depending on the activity in the room.

Recently, there has been a great concern regarding exposure of school children in “contaminated schools,” sometimes resulting in building closures (367, 409, 414; Norris, ABC News online article). In fact schools may have lower mean viable mold spore counts than the students' homes (105). In one 22-month study of 48 schools in which there were concerns regarding indoor air quality and health (rhinitis and congestion which improved when the students were away from school), fewer than 50% of affected schools had fungal CFUs higher than outdoor air (72). In 11 schools where complaint areas had samples with the same organisms as outdoors, Stachybotrys was found, but only on surface swabs and not air specimens. The researchers did not look for other etiologies, nor were there objective measures of illness. Taskinen et al. (409, 410) also reported an increase in asthma in moisture- and mold-affected schools but presented no objective measurements of asthma and very limited immune data, including surprisingly low incidences of positive skin prick tests. Other authors have presented similar findings, reporting that “exposed” children had a higher prevalence of respiratory symptoms and infection, doctor visits, and antibiotic use, and got better post renovation (367). However despite claiming “[exposure]…increased the indoor air problems of the schools and affected the respiratory health of the children,” the study was neither controlled nor blinded, and presented no physical diagnosis or objective measures.

Other evidence suggests that Stachybotrys exposure is not responsible for these building-related episodes. Sudakin (404) examined water-damaged buildings in the Pacific Northwest, due to occupants' neurobehavioral and upper respiratory health complaints (there were no objective pulmonary data) and found S. chartarum in only 1 of 19 cellulose agar cultures from building materials; the fungus was not detected in any of the above samples. While employees felt better after being relocated, there was no evidence that Stachybotrys was a causative agent. Even when large amounts of fungus are detected, analysis often fails to show direct links between symptomatic residents and fungal growth (41). In studies reporting that exposure to home dampness and mold may be a risk factor for respiratory disease, other factors such as smoking may be more contributory (84). In buildings with moisture problems where mycotoxins have been identified, a variety of species are identified, and links between a particular organism and toxin often cannot be established (420).

Despite these problems and an almost complete lack of objective evidence to support guidelines, broad recommendations have been made concerning indoor mold exposure, acceptable air contamination limits, and remediation goals. The sources range from individual authors (267, 292) to the American Academy of Pediatrics (7a) to government agencies (15). Nikodemusz et al. (292) declared that microbial monitoring of air is important even though the organisms the author found were not pathogens. While Miller et al. (267) admit that their “data seriously call into question any attempt to set arbitrary standards for fungal CFU values,” they proposed that some fungi should be considered unacceptable, e.g., pathogens and certain toxigenic species such as S. chartarum, even though complete elimination would be untenable. The same authors stated that it is reasonable to assume there is a problem if a single species predominates with >50 CFU m−3; that <150 CFU m−3 is acceptable if there is a mix of benign species; and that there is no problem when up to 300 CFU of Cladosporium or other common phylloplane fungi m−3 is isolated. Notably there is no source material to support these assertions. The American Association of Pediatrics produced guidelines in the wake of the Cleveland IPH story (7a), again without substantial evidence. More moderate recommendations (while recognizing that the presence of fungi does not necessarily imply illness) would appear reasonable (240). These could include maintaining heating, ventilation, and air conditioning (HVAC) systems, controlling humidity, inspecting and repairing water damage and other sources of contamination, regularly cleaning the home environment with dust removal, cleaning carpets, removing visible mold growth, and formulating guidelines to standardize the levels of fungal and bacterial contamination.

There have been a number of media reports on the abandonment or destruction of buildings contaminated with S. chartarum (34; McFarlane, CNN online article; Moriarty, CBS News program). It is unlikely that such extreme measures are warranted. Methods are discussed further below, but it is important to note that individuals get better with remediation efforts (6, 72, 79, 191, 321, 367), although perhaps not always (164). Simple methods, including removing damaged material and spraying affected areas with bleach, are generally effective in controlling contamination and result in “clean” air samples (430). In some cases, temperature and humidity control may be adequate (142).

FUNGI AND FUNGAL TOXINS

Mycotoxins

Perhaps the earliest recorded cases of mycotoxicosis date to the Middle Ages with the description of “St. Anthony's Fire” or ignis sacer (sacred fire) due to ergotism from Claviceps purpurea (which can also be produced by some species of Penicillium, Aspergillus, and Rhizopus) (322, 382). By the 17th century, it was recognized that moldy rye produced the disease, and ergot alkaloids from fungi were identified as toxins in the 18th century (53, 69, 157). The source of ergot affects both the type of alkaloid produced and the clinical syndrome. There are two types of toxicity: C. purpura produces gangrenous ergotism, while C. fusiformis causes convulsive ergotism (discussed below). The disease is rare today due to food hygiene and the lability of the alkaloid toxins. That ergotism was produced by oral consumption is important, reflecting the fact that historically, mycotoxicosis has usually been associated with oral consumption of moldy grain (157). As discussed below, other routes of instillation result in significantly different types and degrees of toxicity.

Mycotoxins are diverse secondary metabolites produced by fungi growing on a variety of foodstuffs consumed by both animals and humans (Table ​(Table2)2) (76). Clinical toxicological syndromes caused by ingestion of large amounts of mycotoxins have been well characterized in animals and range from acute mortality to slow growth and reduced reproductive efficiency. The effects on humans are much less well characterized (Table ​(Table3)3) (76, 329). Outbreaks of various types of animal mycotoxicosis have occurred worldwide in livestock, including sweet clover poisoning, moldy- corn toxicosis, cornstalk disease, bovine hyperkeratosis, and poultry hemorrhagic syndrome (76, 133).

 

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NEW YORK MOLD ASSESSORS INC. MOLD INFORMATION

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MYCOTOXINS INFORMATION (GENERAL)

Toxigenic species of mold isolated from indoor air of housesa

SpeciesToxins produced

  • Aspergillus flavusAflatoxins
  • Aspergillus fumigatusFumiclavines, fumigatoxin, fumigillin, fumitrems, gliotoxin
  • Aspergillus versicolorSterigmatocystin, versicolorin, aspercolorin, averufin, cyclopiazonic acid
  • Penicillium brevicompactumBrevianamide A, mycophenolic acid
  • Penicillium chrysogenumCitrinin, penicillic acid, PR-toxin, roquefortin C
  • Penicillium citrinumKojic acid, citrinin, citreoviridin
  • Penicillium corylophilumGliotoxin
  • Penicillium cyclopiumPenicillic acid
  • Penicillium expansumPatulin, citrinin
  • Penicillium fellutanumCitreoviridin, citrinin
  • Penicillium spinulosumSpinulosin
  • Penicillium viridicatumBrevianamide A, citrinin, mycophenolic acid, penicillic acid, viomellein, xanthomegnin
  • Stachybotrys chartarumRoridin E, satratoxin H, sporidesmin G, trichoverrins, verrucarol
  • Trichoderma virideGliotoxin, T-2 toxin, trichodermin, trichodermol, viridiol

MOLD INDOORS INFORMATION

This is a subtitle

Mycotoxins

Perhaps the earliest recorded cases of mycotoxicosis date to the Middle Ages with the description of “St. Anthony's Fire” or ignis sacer (sacred fire) due to ergotism from Claviceps purpurea (which can also be produced by some species of Penicillium, Aspergillus, and Rhizopus) (322, 382). By the 17th century, it was recognized that moldy rye produced the disease, and ergot alkaloids from fungi were identified as toxins in the 18th century (53, 69, 157). The source of ergot affects both the type of alkaloid produced and the clinical syndrome. There are two types of toxicity: C. purpura produces gangrenous ergotism, while C. fusiformis causes convulsive ergotism (discussed below). The disease is rare today due to food hygiene and the lability of the alkaloid toxins. That ergotism was produced by oral consumption is important, reflecting the fact that historically, mycotoxicosis has usually been associated with oral consumption of moldy grain (157). As discussed below, other routes of instillation result in significantly different types and degrees of toxicity.

Mycotoxins are diverse secondary metabolites produced by fungi growing on a variety of foodstuffs consumed by both animals and humans (Table ​(Table2)2) (76). Clinical toxicological syndromes caused by ingestion of large amounts of mycotoxins have been well characterized in animals and range from acute mortality to slow growth and reduced reproductive efficiency. The effects on humans are much less well characterized (Table ​(Table3)3) (76, 329). Outbreaks of various types of animal mycotoxicosis have occurred worldwide in livestock, including sweet clover poisoning, moldy- corn toxicosis, cornstalk disease, bovine hyperkeratosis, and poultry hemorrhagic syndrome (76, 133).

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