Chapter 1. Introduction
Fungi inhabit nearly all terrestrial environments. In this regard, the interiors of human dwellings and workspaces are no exception. The mould flora of human-inhabited indoor environments consists of a distinctive group of organisms that collectively are not normally encountered elsewhere. The biology and taxonomy of selected members of the fungal flora of household dust are the focus of the research and discussion presented in this thesis.
Household dust itself is not a substance which evokes a rich sense of practical or historical importance aside from its relentless contribution to the stereotypical plight of suburban housewives obsessed with its elimination. Shakespeare used dust as a metaphor to evoke the cyclical nature of life, and the fact that neither class nor creed exempts us from this binding cycle. The spirit of Shakespeare’s metaphor provides a fitting framework within which to study the substance itself, as a thriving and complex community comprising a vast diversity of organisms whose lives secretly parallel our own.
The biology of house dust
Dust formation occurs as a result of the ongoing elutriation of airborne organic and inorganic particulate matter that originates from a multiplicity of indoor and outdoor sources. House dust is a fibrous material composed primarily of a matrix of textile fibres, hairs and shed epithelial debris (Bronswijk, 1981). The majority of particles comprising household dust fall within the size range from 10-3 to 1 mm (ibid.). Airborne particles smaller than this (e.g. smoke, fumes, etc.) tend to behave as a colloidal system and do not sediment efficiently even in still air due to their relative buoyancy; thus, their presence within dust is often a function of filtration, diffusion or electrostatic effects (Cox and Wathes, 1995).
The large daily influx of organic debris to the dust of inhabited houses provides a rich primary nutrient source that supports an intricate microcommunity encompassing three kingdoms of organisms: animals (arthropods, and to some extent larger animals such as rodents, etc.), bacteria and fungi (Bronswijk, 1981; Harvey and May, 1990; Harving et al., 1993; Hay et al., 1992a, 1992b; Miyamoto et al., 1969; Samson and Lustgraaf, 1978; Sinha et al., 1970). The fibrous nature of a stable dust matt composed predominantly of hygroscopic fibres acts to harvest atmospheric moisture and simultaneously provides shelter from desiccation for the organisms contained within. While the variety of fibres themselves (particularly cellulosic fibres) may serve as sources of carbon nutrition for the heterotrophic dust inhabitants, a more readily available source of organic carbon and nitrogen comes from food crumbs and excoriated epithelia. Although the latter makes up a considerable mass-fraction of house dust, its microbial availability is largely limited to non-keratin proteins and lipids due to the refractory nature of keratin itself (Currah, 1985). Plant pollens arising from the phylloplane are likely to provide additional nutritional input to the house dust ecosystem (Bronswijk, 1981). Bronswijk (1981) compiled a list of taxa of different groups of dust-borne organisms based on reports by numerous workers. The fauna in her inventory included isopods (5 taxa), roaches (47 taxa), lepismatids (8 taxa), psocopterans (20 taxa) and mites (147 taxa), while the microbiota was dominated by fungi (163 taxa) with only few bacterial taxa (8).
Interactions between mites and fungi
Bronswijk (1981) speculated considerably on trophic interactions between microarthropods and fungi within dust-bound habitats. She suggested that xerophilic fungi, notably Wallemia sebi and members of the Aspergillus glaucus series were responsible for the hydrolysis of fats in dustborne dander, facilitating the consumption of these materials by various mite species. Bronswijk (1981) further proposed that Acremonium, Penicillium and Scopulariopsis along with mesophilic species of Aspergillus provided food for oribatid mites by the colonization of crumbs and other food debris. Samson and Lustgraaf (1978) demonstrated an association between Dermatophagoides pteronyssinus and the microfungi Aspergillus penicillioides and Eurotium halophilicumwhereby these fungi frequently co-occurred with certain dust-borne mite species, and the mites preferred consuming materials upon which the fungi had grown. Hay and co-workers (1992a) showed antigenic cross-reactivity between Aspergillus penicillioides and the mite D. pteronyssinus, however these workers later suggested that this mite-fungus associate may have been an artifact of laboratory culture conditions under which the mites were reared (Hay et al., 1992b)¹.
Fungi in household dust
The fungal component of dust biodiversity probably remains underestimated since only a few studies to date have provided thorough mycological characterizations of house dust (Davies, 1960; Gravesen, 1978a; Lustgraaf and Bronswijk, 1977; Ostrowski, 1999; Schober, 1991). An analysis of dust from 60 households in the Netherlands by Hoekstra and co-workers (1994) revealed 108 fungal species in 54 genera using V8 juice agar and Dichloran 18 % glycerol agar (DG18) as isolation media. Species recovery showed temporal variation in samples taken 6 wks apart. Also, considerable variation was observed according to the isolation media used. A similar study by Ostrowski (1999) from 219 households in the Netherlands reported 143 fungal taxa of which 113 were also observed in air samples taken from kitchen areas, where the highest level of fungal species diversity was observed.
Innumerable reservoirs of fungal material exist outdoors that may contribute to the fungal burden of indoor air and dust according to the continuous input of outdoor air into indoor environments. Levels of phylloplane fungal spores in indoor air are typically correlated with prevailing weather conditions, including wind speed and precipitation that are responsible for mediating spore release in the outdoor environment (Ingold, 1965; Li and Kendrick, 1994, 1995). As such, surveys of fungi from indoor air and dust usually demonstrate the presence of phylloplane taxa that are qualitatively similar to outdoor air albeit at lower levels (Abdel-Hafez et al., 1993; Bunnag et al., 1982; Calvo et al., 1980; Dillon et al., 1996; Ebner et al., 1992).
Fungal propagules in household dust can be divided into two ecological categories according to their origin. Dustborne fungi may be 1) active inhabitants of dust (autochthonic sensu Bronswijk, 1981); or, 2) they may be imported, as passive entrants from other sources (allochthonic ibid.; see also Cohen et al., 1935; Davies, 1960; Gravesen, 1978; Morey, 1990). Davies (1960) reported dust-bound concentrations of viable fungal propagules in excess of 300 CFU/mg. The magnitude of this concentration prompted Bronswijk (1981) to infer that this dust-bound spora could not have been imported and must have been produced within the dust. Even when fungi are not produced within dust proper, an indoor fungal amplification site produces a characteristic pattern of species distribution in indoor air and consequently house dust.
Indoor sources of dust mycobiota
Indoor fungal growth contributes to disproportionately high spore levels in indoor air relative to those observed in outdoor air (Agrawak et al., 1988; Berk et al., 1957; Grant et al., 1989). Furthermore, when a fungal amplifier is local, the composition of the indoor fungal flora usually differs qualitatively, in being dominated by a single or few abundant species which may not be components of the background flora (Giddings, 1986; Miller, 1992; Miller et al., 1988; Moriyama et al., 1992). For instance, Cladosporium sphaerospermum is a frequent colonist of indoor finishes as a consequence of excessive indoor relative humidity (Burge and Otten, 1999). This species has a proclivity for many characteristically refractile substrates such as oil-based paints, and polymeric decorative finishes (e.g. vinyl wall coverings) (Domsch et al., 1980). Interestingly, Cl. sphaerospermum is a comparatively rare component of outdoor air flora where species such as Cl. herbarum and Cl. cladosporioides typically dominate (Burge and Otten, 1999). Despite the abundance of Mycosphaerella and its Cladosporium anamorphs in outdoor epiphyllous habitats and consequently as spora in outdoor air (Farr et al., 1989; Ho et al., 1999), Cl. sphaerospermum is comparably rare in these habitats and even low levels of this fungus in indoor air are unusual and strongly indicate active indoor fungal growth.
Indoor plantings can also serve as reservoirs of fungal material (Burge et al., 1982; Summerbell, 1992). Summerbell and co-workers (1989) examined soils from potted plants in hospital wards and found a large number of potential human pathogenic fungi including Aspergillus fumigatus and Scedosporium apiospermum, an anamorph of Pseudallescheria boydii. Although these workers did not investigate airborne concentrations of these fungi related to their presence in soil, based upon the results of Kaitzis (1977) and Smith and co-workers (1988) Summerbell and colleagues theorized that activites such as watering were likely to cause spore release. The recognition and elimination of indoor amplifiers of opportunistic human pathogenic fungi within the hospital environment are important in the reduction of nosocomial infection. Aspergillus fumigatus and A. flavus are of particular concern because these fungi are frequent agents of pulmonary aspergillosis especially in immunocompromised patients such as organ recipients and HIV patients (Summerbell, 1998).
Penicillium in indoor environments
Perhaps the most famous of all indoor fungi was made so in a 10 page paper written in 1929 by Alexander Fleming, which described the inhibition of several groups of cocciform bacteria by a fungus in the genus Penicillium. This fungus, identified for Fleming by St. Mary’s Hospital mycologist Charles La Touche as P. rubrum Grassberger-Stoll ex. Biourge, was sent by Fleming to Harold Raistrick at the University of London, who in turn sent it to Charles Thom of the US Department of Agriculture in Peoria, Illinois (Fleming, 1929; Gray, 1959; Howard, 1994). Thom (1930) considered Fleming’s isolate to be P. notatum, a species described by Westling (1911) from the branches of Hyssopus L. (Lamiaceae) in Norway. Over a decade after Fleming’s discovery, Ernst Chain and Howard Florey isolated the active principal, penicillin, and demonstrated its success in clinical trials, a collective achievement for which the three shared the Nobel Prize for Physiology and Medicine in 1945 (Howard, 1994).
The discovery of penicillin ranks as one of the most significant events in the history of medicine and possibly of human civilization and has been the subject of much discussion (Hare, 1970; MacFarlane, 1979, 1984; Williams, 1984). Fleming’s pivotal role in the penicillin story has been described as a most remarkable case of serendipity, since the vast majority of Penicillia produce metabolites with profound mammalian toxicity (Gray, 1959; Samson et al., 1996). Others have alleged that this discovery was inevitable. From knowledge of the substrate of Westling’s (1911) species P. notatum, Selwyn (1980) and later Lowe and Elander (1983) inferred the naïve use of penicillin from the following passage of the Old Testament Book of Psalms:
“Purge me with hyssop, and I shall be clean, wash me, and I shall be whiter than snow.
(Psalms 51:7)
Similarly, a passage from the Third Book of Moses describes a treatment for leprosy²:
“This is the law of the leper in the day of his cleansing… He shall take… the cedarwood, and the scarlet and the hyssop, and shall dip them… in the blood of the bird… And he shall sprinkle upon him that is to be cleansed from the leprosy…
(Lev. 14:2-7)
Certainly the habitat of P. chrysogenum is not restricted to Hyssopus, as this fungus is known from a vast range of outdoor substrates (Domsch et al., 1980; Pitt and Hocking, 1999). Despite the ubiquitous nature of P. chrysogenum outdoors, however, it remains poorly represented in samples of outdoor air where typical phylloplane fungi such as Alternaria, Aureobasidium, Cladosporium, Epicoccum and Ulocladium dominate (Dillon et al., 1996; Scott et al., 1999b; Tobin et al., 1987). Indoors, P. chrysogenum is typically the most commonly occurring airborne and dustborne species of this genus (Abdel-Hafez et al., 1986; Mallea et al., 1982; Summerbell et al., 1992). Certainly an important factor in the establishment of high indoor levels of P. chrysogenum is its role as an agent of food spoilage. Pitt and Hocking (1999) indicated that P. chrysogenum was the most common species of this genus associated with food contamination, known from numerous fruits, vegetables, cereals, meats and dairy products (Domsch et al., 1980; Pitt and Hocking, 1999; Samson et al., 1996). Indeed, most high penicillin-producing strains of this species were derived from a single isolate obtained from cantaloupe (Gray, 1956; Lowe and Elander, 1983; Raper and Thom, 1949). The growth of P. chrysogenum on wooden food-shipping crates has also been responsible for the tainting of foodstuffs by the release of chloroanisole produced during the breakdown of phenolic wood preservatives (Pitt and Hocking, 1999; Hill et al., 1995). Frisvad and Gravesen (1994) speculated that the indoor abundance of this species could not be explained by its occurrence on foodstuffs alone, and suggested that the somewhat xerophilic nature of both P. chrysogenum and P. brevicompactum may facilitate their colonization of other indoor substrates such as wood and paint. Adan and Samson (1994) listed P. chrysogenum as a common colonist of acrylic-based paint finishes, noting that this species exhibited growth at relative humidities as low as 79 %. This species is also known from wallpaper, textiles, broadloom, visual art and optical lenses (Samson et al., 1994). Similarly, P. brevicompactum is known from a wide range of indoor substrates including foods, building materials and decorative finishes (Adan and Samson, 1994; Domsch et al., 1981; Scott et al., 1999a).
Many of the microfungi that are routinely observed as colonists on indoor finishes and construction materials, such as Aspergillus, Paecilomyces, Penicillium and Scopulariopsis species tend to grow at relatively low water activity often on refractile substrates (Samson et al., 1996). These genera form the core of the group commonly refered to as “domicile fungi” owing to their inordinate abundance in the air and dust of residential interiors. While these fungi are common agents of structural deterioration in North America, the dry rot fungus Serpula lacrimans remains the principal agent of structural decay in Britain and Northern Europe (Singh, 1994). Similarly, the importance of indoor exposure to fungal spores indoors in the development of allergic asthma is greater in North America than in Europe, where dust mite and dander exposures are the primary exposure risk factors for this disease (Beaumont et al., 1985; Flannigan and Miller, 1994).
Health effects attributed to indoor fungal exposures
Although environmental fungal reservoirs have rarely been implicated in human infection (Burge, 1989; Miller, 1992; Summerbell et al., 1992), their presence has long been accepted as an important risk factor to respiratory morbidity (Dillon et al., 1996). Human exposure to indoor fungi has been implicated in the etiology of a multiplicity of health problems that ranges from allergies and respiratory diseases to toxicoses and neoplastic diseases. To the extent that fungi are involved in these processes, the inhalation or ingestion of fungal cellular debris is thought to be the principal route of exposure. Ancillary products of mould growth such as volatile organic metabolites (e.g. alcohols) or volatile breakdown products from extracellular processes (e.g. formaldehyde) may contribute to symptoms of illness or discomfort independent of exposure to fungal biomass (Miller, 1992). The diversity in clinical scope of building-related illnesses makes their diagnosis difficult. Similarly, the identification and localization of agents that may contribute to decreased indoor air quality (IAQ) is often problematic. Over the past 30 years, “Sick Building Syndrome”, in which the air quality in a building is compromised as a result of biological or chemical pollutants, has been recognized as a serious, modern threat to public health (Mishra et al., 1992; Su et al., 1992; Tobin et al., 1987).
The role of indoor fungi in irritative disorders (i.e. primarily non-infective diseases such as allergy and asthma) has long been recognised (Al-Doory, 1984; Cohen et al., 1935; Flannigan et al., 1991; Gravesen, 1979; Reymann and Schwartz, 1946). Bioaerosols of fungal origin, consisting of spores and hyphal fragments are readily respirable, and are potent elicitors of bronchial irritation and allergy (Brunekreef et al., 1989; Burge, 1990a; Dales et al., 1991a, 1991b; Platt et al., 1989; Sakamoto et al., 1989; Samet et al., 1988; Sherman and Merksamer, 1964; Strachan et al., 1990).
Allergic rhinitis and sinusitis
Type I allergic syndromes
Concern regarding human exposure to mould aerosols in indoor environments is mainly related to direct mucosal irritation and elicitation of an IgE-mediated hypersensitivity response that precipitates rhinitis and upper airways irritation, eye irritation and frequently sinusitis that characteristize allergic syndromes (Pope et al., 1993). The symptoms of allergy are not manifested until sensitisation in which an individual incurs repeated exposures to the antagonistic agent. During this process, antigen-specific IgE is produced that attaches to receptors on mast cells that are concentrated on gastric and respiratory mucosa. In a sensitised individual, the IgE on mast cells binds to antigen following exposure, mediating mast cell rupture, histamine release and the ensuant hypersensitivity response (Guyton, 1982). The principal fungal allergens are either high molecular weight carbohydrates (e.g. beta 1-3 glucans) or water soluble glycoproteins (such as enzymes) (ibid.). Typically, these compounds are sequestered within fungal spores or secreted into fungus-contaminated debris. These allergens become airborne which when these materials are aerosolized. A link between respiratory exposure to fungal material and seasonal allergy was first proposed in 1873 by Blackley who demonstrated the provocation of allergic respiratory symptoms by exposure to Penicillium spores (fide Nilsby, 1949). Latgé and Paris (1991) listed 106 fungal genera with members documented to elicit allergy, although it is likely that the true number is actually much larger (Li, 1994). Although the principal allergenic vehicles of fungal allergies are spores and other cellular debris, the culprit allergens are not always constitutively present in these materials. Savolainen and co-workers (1990) suggested that certain allergenic enzymes may only be produced upon germination. Exposure to these compounds requires inhalation of germinable propagules, followed by germination on upper respiratory tract mucosa.
Dust mites and allergy
Other notable biological elicitors of similar allergic cascades include plant pollens (particularly Ambrosia spp. in northern temperate North America fide Jelks, 1994), and so-called “dust mites”, typically of the genus Dermatophagiodes (especially D. pteronyssinus and D. farinae, Bronswijk, 1981). Considerable research has examined the relationship of dust mite allergen exposure to clinical allergy. Bronswijk (1981) provides an excellent review of this work. Dust mite sensitisation in domestic settings appears to be influenced by additional biotic agents. Miyamoto and colleagues (1969) showed allergenic cross-reactivity between domestic dust mites and other biological sensitizers including dust and fungi. It is likely that this cross-reactivity is a consequence of correlated exposures because mites often occur together with fungi on water-damaged indoor materials (Bronswijk, 1981)³. The feces of dust mites are considerably allergenic because of the large content of partially digested food materials and intact digestive enzymes (Tovey et al., 1981). In addition, mite fecal pellets often contain large numbers of intact and partially degraded fungal spores because these materials are a preferred food of many dustborne mite taxa (Samson and Lustgraaf, 1978).
Hypersensitivity syndromes
Extrinsic allergic alveolitis, or hypersensitivity pneumonitis (HP) is an acute inflammatory reaction of the lower airways upon exposure to an agent to which a sensitivity has developed from prior exposure. Hypersensitivity pneumonitis involves cell-mediated immunity (Type IV allergic response), in contrast to Type I allergic syndromes that are IgE-mediated, and thus may exist independently of the latter. Numerous environmental antigens have been implicated as elicitors of HP, including fungal aerosols. The majority of case literature on fungus-mediated HP involve occupational exposures where exposures to mould aerosol exceed background by several orders of magnitude. Furthermore, these exposures often involve a stable, low species diversity related to a particular substrate or process. Although the clinical presentation of these disorders is relatively uniform, a florid nomenclature has developed based primarily on the particular occupation or the sensitising agent implicated (see Table 1-1). In non-industrial, non-agricultural settings, some case reports suggest that sufficiently high airborne levels of otherwise innocuous fungal particulates have caused HP where patients exhibited pneumonia-like symptoms following even low exposures to irritant agents (Jacob et al., 1989; Pepys, 1969; Samet et al., 1988; Weissman and Schuyler, 1991). Four of the hypersensitivity pneumonitides in Table 1-1 have been reported from indoor environments: Humidifier Lung (fungal etiologic agents includePenicillium spp. and Cephalosporium [=Acremonium] spp.), Cephalosporium HP (Cephalosporium spp.), Housewife’s lung (Penicillium expansum) and Japanese Summer-Type HP (probable etiologic agent Trichosporon cutaneum) (Pope et al., 1993).
Asthma
Asthma is a disease characterized by reversible airway obstruction triggered by any of a number of provocation agents, including allergens, cold and exercise stress, and relieved by the inhalation of aerosolised beta-adrenergic antagonists (Hunninghake and Richardson, 1998; Pope et al., 1993). Asthmatic conditions are loosely categorized as 1) allergic asthma, with typical onset at an early age in patients with positive skin tests to common allergens or a family history of allergy; and, 2) idiosyncratic asthma, where onset is usually later in life, in the absence of immunological allergic predisposition, family history indicators or comorbid stimuli such as smoking. Asthma symptoms include wheezing, usually accompanied by dyspnea (shortness of breath) and cough, often in a episodic pattern with intermittent or extended periods of remission. For over a decade, it has been quite clear that the presence of moulds (as indicated by dampness) in housing exerts an adverse effect on the respiratory health of children (Martin et al., 1987; Platt et al., 1989). Strachan and co-workers (1988; 1990) showed an increase in symptoms of wheezing in children living in mouldy homes in Edinburgh, Scotland; however, these workers found little quantitative difference in the airborne mycoflora of households in which asthmatic children lived, as measured by viable sampling. These workers postulated that the disagreement between objective measurement of airborne mould levels and subjective assessment of housing conditions by occupants indicated a reporting bias in which asthmatics were more likely to report mould conditions than non-asthmatics. A Canadian cross-sectional study of over 13,000 children by Dales and colleagues (1991a) also showed a significant increase in respiratory symptoms according to reported mould or damp conditions in housing. These workers suggested that short-term indoor air samples (“grab samples”) such as those employed by Strachan and co-workers (1988; 1990) were not necessarily reflective of longer-term conditions, due to the periodic nature of spore release. An earlier US-based cross-sectional study (“The Harvard Six-Cities Study”, Brunekreef et al., 1989) showed a significantly lower prevalence of wheeze than the Edinburgh study, yet demonstrated a comparable odds ratio between this symptom and mouldy housing conditions, suggesting that wheeze may have been over-reported in the study by Strachan and co-workers (1988). In their review of asthma trends, Pope and co-workers (1993) noted that the magnitude of allergen exposure increased the potential for allergic sensitisation, and was both a risk factor for lowered age of asthma onset as well as increased disease severity. Furthermore, these workers proposed a recent increase in asthma morbidity and mortality as reflected by hospital admission statistics.
Table 1-1: Selected hypersensitivity pneumonitides with probable microbial etiologies
| DISEASE | SOURCE | PROBABLE ALLERGEN |
| Bagassosis | Mouldy bagasse (sugar cane) | Thermophilic actinomycetes |
| Cephalosporium HP | Basement sewage contamination | Cephalosporium spp. (=Acremonium) |
| Cheese washer’s lung | Mouldy cheese | Penicillium casei (=P. roquefortii) |
| Compost lung | Compost | Aspergillus spp. |
| Familial HP | Contaminated wood dust in walls | Bacillus subtilis |
| Farmer’s lung | Mouldy hay, grain or silage | Aspergillus fumigatus and thermophilic actinomycetes |
| Hot tub lung | Mould on ceiling | Cladosporium spp. |
| Housewife’s lung | Moldy wooden flooring | Penicillium expansum and other moulds |
| Humidifier/ Air-conditioner lung | Contaminated water or coils in humidifiers and air-conditioners | Aureobasidium pullulans,Cephalosporium spp., Penicilliumspp. and thermophilic actinomycetes |
| Japanese summer house HP | Bird droppings, house dust | Trichosporon cutaneum |
| Lycoperdonosis | Puffballs | Lycoperdon spp. |
| Malt worker’s lung | Mouldy barley | Aspergillus fumigatus or As. clavatus |
| Maple bark disease | Maple bark | Cryptostroma corticale |
| Mushroom worker’s lung | Mushroom compost | Thermophilic actinomycetes and other microorganisms |
| Potato riddler’s lung | Mouldy hay around potatoes | Aspergillus spp. and thermophilic actinomycetes |
| Sauna taker’s lung | Contaminated sauna water | Cladosporium spp. and others |
| Suberosis | Mouldy cork dust | unknown |
| Tap water lung | Contaminated tap water | unknown |
| Thatched roof disease | Dried grasses and other leaves | Sacchoromonospora viridis |
| Tobacco worker’s disease | Mouldy tobacco | Aspergillus spp. |
| Winegrower’s lung | Mouldy grapes | Botrytis cinerea |
| Wood trimmer’s disease | Contaminated wood trimmings | Rhizopus spp. and Mucor spp. |
| Woodman’s disease | Oak and maple trees | Penicillium spp. |
| Woodworker’s lung | Oak, cedar and mahogany dusts, pine and spruce pulp | Alternaria spp. and wood dust |
SOURCES: Hunninghake and Richardson (1998); Park et al. (1994); Pope et al. (1993)
Mycotoxins
In addition to their roles as irritants and allergens, many fungi produce toxic chemical constituents (Kendrick, 1992; Miller, 1992; Wyllie and Morehouse, 1977). Samson and co-workers (1996) defined mycotoxins as “fungal secondary metabolites that in small concentrations are toxic to vertebrates and other animals when introduced via a natural route”. These compounds are non-volatile and may be sequestered in spores and vegetative mycelium or secreted into the growth substrate. The mechanism of toxicity of many mycotoxins involves interference with various aspects of cell metabolism, producing neurotoxic, carcinogenic or teratogenic effects (Rylander, 1999). Other toxic fungal metabolites such as the cyclosporins exert potent and specific toxicity on the cellular immune system (Hawksworth et al., 1995); however, most mycotoxins are known to possess immunosuppressant properties that vary according to the compound (Flannigan and Miller, 1994). Indeed, the toxicity of certain fungal metabolites such as aflatoxin, ranks them among the most potently toxic, immunosuppressive and carcinogenic substances known (ibid.). There is unambiguous evidence that ingestion exposure as well as exposures by the inhalation pathway have been correlated with outbreaks of human and animal mycotoxicoses (Abdel-Hafez and Shoreit, 1985; Burg et al., 1982; Croft et al., 1986; Hintikka, 1978; Jarvis, 1986; Norbäck et al., 1990; Sorenson et al., 1987; Schiefer, 1986). Several common mycotoxigenic indoor fungi and their respective toxins are listed in Table 1-2.
TABLE 1-2: Mycotoxins of significance produced by indoor fungi
| MYCOTOXIN | PRIMARY HEALTH EFFECT | FUNGAL PRODUCERS |
| Aflatoxins | Carcinogens, hepatotoxins | Aspergillus flavus
As. parasiticus |
| Citrinin | Nephrotoxin | Penicillium citrinum
Pe. verrucosum |
| Cyclosporin | Immunosuppressant | Tolypocladium inflatum |
| Fumonisins | Carcinogens, neurotoxins | Fusarium moniliforme (=F. verticillioides)
F. proliferatum |
| Ochratoxin A | Carcinogen | As. ochraceus
Pe. verrucosum |
| Patulin | Protein synthesis inhibitor, nephrotoxin | As. terreus
Paecilomyces variotii Pe. expansum Pe. griseofulvum Pe. roquefortii |
| Sterigmatocystin | Carcinogen, hepatotoxin | As. nidulans
As versicolor Chaetomium spp. |
| Trichothecenes, macrocyclic | ||
| > Satratoxins | Protein synthesis inhibitors | Stachybotrys chartarum
Myrothecium spp. |
| Trichothecenes, non-macrocyclic | ||
| > Deoxynivalenol (vomitoxin) | Emetic | F. cerealis
F. culmorum F. graminearum |
| > T-2 toxin | Hemorrhagic, emetic, carcinogen | F. sporotrichioides |
| Verrucosidin | Neurotoxin | Pe. aurantiogriseum group |
| Xanthomegnin | Hepatotoxin, nephrotoxin | As. ochraceus
Pe. aurantiogriseum group |
| Zeralenone | Estrogenic | Fusarium spp. |
SOURCES: Burge and Ammann (1999); Rodricks et al. (1977); Samson et al. (1996)
Volatile fungal metabolites
During exponential growth, many fungi release low molecular weight, volatile organic compounds (VOCs) as products of secondary metabolism. These compounds comprise a great diversity of chemical structure, including ketones, aldehydes and alcohols as well as moderately to highly modified aromatics and aliphatics. Cultural studies of some common household moulds suggests that the composition of VOCs remains qualitatively stable over a range of growth media and conditions (Sunesson et al., 1995). Furthermore, the presence of certain marker compounds common to multiple species, such as 3-methylfuran, may be monitored as a proxy for the presence of a fungal amplifier (Sunesson et al., 1995). This method has been suggested as a means of monitoring fungal contamination in grain storage facilities (Börjesson et al., 1989; 1990; 1992; 1993). Limited evidence suggests that exposure to low concentrations of VOCs may induce respiratory irritation independent of exposure to allergenic particulate (Koren et al., 1992). Volatile organic compounds may also arise through indirect metabolic effects. A well-known example of this is the fungal degradation of urea formaldehyde foam insulation. Fungal colonization of this material results in the cleavage of urea from the polymer, presumably to serve as a carbon or nitrogen source for primary metabolism. During this process formaldehyde is evolved as a derivative, contributing to a decline in IAQ (Bissett, 1987).
Objectives of the current study
The present study was conceived with two primary objectives. First, this investigation shall characterize the fungal biodiversity of house dust. This work shall investigate correlations between dustborne fungal species, and examine the ecological similar of positively associated taxa based on the hypothesis that positively associated dustborne fungi are likely to share habitat characteristics. From this, a second hypothesis follows that mechanisms that permit the entry or concentration a given species will tend to facilitate the entry of other positively correlated taxa. A second objective of this research if to assess the extent of genotypic variability in two dustborne Penicillia, P. brevicompactum and P. chrysogenum. The goal of this work shall be to examine the extent of clonality within these two species, and to determine if the observed patterns of genotypic variation support the current species concepts.
[1] I have observed dramatic overgrowths on the cadavers of predatory mites (Macrochaelidae) from composting marine seaweeds incubated in moist chamber culture by a mould species that compared to P. olsonii. Similarly, fungus-feeding mites occurring as inquilines in laboratory cultures of leaf-cutting ants of the tribe Attini often become overgrown by Penicillium spp., when incubated under damp chamber conditions. In the latter case, it is reasonably clear that Penicillia are uncommon allochthonous members of the fungal flora of the fungal gardens of leaf-cutting ants. The colonisation of these mites by Penicillium is most likely an artefact of high arthropod population density under unnatural conditions of laboratory culture, and neither supports an hypothetical role for Penicillium in the mite lifecycles nor suggests that Penicillium is important in the nutrient cycling of this system.
[2] In biblical translations and allusions, leprosy refers to any disfiguring skin disease, whose cause was not necessarily limited to Hansen’s bacillus, Mycobacterium leprae (Brown, 1993).
[3] It is common to observe dense mite colonization on superficial fungal growth on wall surfaces, especially where Cl. sphaerospermum has disfigured the finished sides of exterior walls pursuant to excessive indoor relative humidity during the winter months. In such cases, elevated mite populations are a predictable consequence. Indeed, by gauging the level of mite activity on a fungus-contaminated surface it is often possible to determine the time-course of contamination, since mite populations do not generally develop until 3-6 months after the emergence of fungal growth (data not presented).
