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4 Toxic Effects of Fungi and Bacteria Although a great deal of attention has focused on the effects of bacteria and fungi mediated by allergic responses, these microorganisms also cause nonallergic responses. Studies of health effects associated with exposure to bacteria and fungi show that respiratory and other effects that resemble allergic responses occur in nonatopic persons. In addition, outcomes not generally associated with an allergic response--including nervous-system effects, suppression of the immune response, hemorrhage in the mucous membranes of the intestinal and respiratory tracts, rheumatoid disease, and loss of appetite--have been reported in people who work or live in build- ings that have microbial growth. This chapter discusses the available ex- perimental data on those nonallergic biologic effects. It first discusses the bioavailability of the toxic components of fungi and bacteria and the routes of exposure to them and then summarizes the results of research on various toxic effects--respiratory, immunotoxic, neurotoxic, sensory, dermal, and carcinogenic--seen in studies of microbial contaminants found indoors. It does not address possible toxic effects of nonmicrobial chemicals released under damp conditions by building components, furniture, and other items in buildings; chemical releases from such materials are discussed in Chapter 2. Except for a few studies on cancer, toxicologic studies of mycotoxins are acute or short-term studies that use high exposure concentrations to reveal immediate effects in small populations of animals. Chronic studies that use lower exposure concentrations and approximate human exposure more closely have not been done except for a small number of cancer studies. 125
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126 DAMP INDOOR SPACES AND HEALTH Chapter 5 discusses human health effects and includes some case reports relevant to toxic end points. CONSIDERATIONS IN EVALUATING THE EVIDENCE Most of the information reviewed in this chapter is derived from stud- ies in vitro (that is, studies in an artificial environment, such as a test tube or a culture medium) or animal studies. In vitro studies, as explained below, are not suitable for human risk assessment. Risk can be extrapolated from animal studies to human health effects only if chronic animal exposures have produced sufficient information to establish no-observed-adverse- effect levels (NOAELs) and lowest-observed-adverse-effect levels (LOAELs). Extrapolation of risk exposure from animal experiments must always take into account species differences between animals and humans, sensitivities of vulnerable human populations, and gaps in animal data. Risk assessment requires not only hazard identification but also dose-response evaluation and exposure assessment in humans whose risk is being evaluated. Esti- mates of exposures of humans to spores, bacteria, microbial fragments, and dust that contains mycotoxins are inherently imprecise and imperfect; bio- markers of exposure to toxins are few, and exposures to single or multiple mycotoxins carried by such agents have not been measured indoors. Thus results of animal studies cannot be used by themselves to draw conclusions about human health effects. However, animal studies are important in identifying hazardous substances, defining their target organs or systems and their routes of exposure, and elucidating their toxicokinetics and toxico- dynamics, the mechanisms that account for biologic effects, and the me- tabolism and excretion of toxic substances. Animal studies are also useful for generating hypotheses that can be tested through studies of human health outcomes in controlled exposures, clinical studies, or epidemiologic investigations, and they are useful for risk assessment that informs regula- tory and policy decisions. BIOAVAILABILITY AND ROUTE OF EXPOSURE Issues That Affect Bioavailability Some molds found in damp indoor spaces can produce mycotoxins. Table 4-1 lists a number of mycotoxins and the organisms that produce them. Bacteria can also produce toxins. Although there has not been a large amount of research conducted on the effects of those toxins in the context of their growth in damp buildings, mycotoxins and bacterial toxins have been studied for several decades because of their role in outbreaks of illness associated with the ingestion of moldy food (Etzel, 2002). More recently,
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TABLE 4-1 Some Mycotoxins and the Microorganisms That Produce Them Microorganisms That Chemical Compound Produce Mycotoxins References Ergot alkaloids Claviceps purpurea, species of Sorensen, 1993; Larsen Aspergillus, Rhizopus, Penicillium et al., 2001 Substituted coumarins, for example, Several species of Aspergillus, Penicillium van Walbeek et al., 1969; aflatoxins from Aspergillus flavus, Sorensen, 1993 Aspergillus parasiticus; ochratoxins Quinones, for example, citrinins Several species of Aspergillus, Penicillium Sorenson, 1993; Malmstrom et al., 2000 Anthoquinones, for example, rugulosin Penicillium islandicum Trichothecenes (sesquiterpenes with Fusarium and Stachybotrys species Etzel, 2002 trichothecene skeleton, olefinic group at C-9, 10, epoxy at C-12, 13), for example, T-2 toxin; DON (deoxynivalenol or vomitoxin) Macrocyclic trichothecenes (having carbon Stachybotrys, Myrothecium, others Sorensen, 1993; Jarvis, 1991 chain between C-4 and 15 in ester or ether linkage, for example, satratoxins G, H; verrucarins B, J; trichoverrins A, B) Substituted furans, for example, citreoviridin Penicillium citreoviride Nishie et al., 1988 Epipolythiodioxopiperazines, for example, At least six species of Aspergillus, Waring and Beaver, 1996 gliotoxin Penicillium Lactones, lactams, for example, patulin, Penicillium, Stachybotrys Jarvis et al., 1995, 1998 stachybotrylactones, stachybotrylactams Estrogenic compounds, for example, Many species of Fusarium Betina, 1989; Kuiper- 127 zearalenone Goodman et al., 1987
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128 DAMP INDOOR SPACES AND HEALTH concerns that toxins from microorganisms that grow in damp indoor envi- ronments may play a role in illnesses reportedly associated with living or working in damp buildings have focused attention on the adverse health effects of inhaling mycotoxins. The degree to which a toxin can harm tissues varies with a number of factors, including the chemical nature of the toxin, the route of entry into the body, the amount to which the target organism and organ are exposed, and the susceptibility of the target species (Coulombe, 1993; Eaton and Klaassen, 2001; Filtenborg et al., 1983; Vesper and Vesper, 2002). Inter- species differences in susceptibility can result from differences in absorp- tion, distribution, metabolism, excretion, and the effectiveness of a toxin at its receptor (site of action) (Eaton and Klaassen, 2001; Fink-Gremmels, 1999; Russell, 1996). Once produced, mycotoxins must be airborne to be inhaled. Mycotox- ins are found in and on the spores of molds that produce them, on hyphal fragments, and in dust from substrates on which mold grows and carpet dust (Englehart et al., 2002; Górny et al., 2002; Larsen and Frisvad, 1994; Sorenson, 1993, 1995; Sorenson et al., 1987). They are exuded into the substrate on which a microbial agent is growing, for instance, growth medium in the laboratory and gypsum board, wood, paper, and other building materials in damp or wet buildings (Andersen et al., 2002; Andersson et al., 1997; Buttner et al., 2001; Gravesen and Nielsen, 1999; Nieminen et al., 2002). Mycotoxins have also been isolated from dust sampled in moldy buildings that did not contain mold spores (Englehart et al., 2002; Gravesen et al., 1999; Nielsen et al., 1998). Mycotoxins are found in and on materials that can be aerosolized as particles, so such aerosols can become a source of mycotoxin exposure. But particles are not the only vehicle of exposure to mycotoxins. Mycotoxins are not generally thought to be volatile (Jarvis et al., 1995), but some, such as sesquiterpenes, are semivolatile, and others are at least partially water-soluble and thus able to enter the air in droplet aerosols (Harrach et al., 1982; Peltola et al., 1999, 2002). The bioavailability of aerosols (including mold spores, contaminated dust, bacteria, and microbial fragments) in the respiratory tract after inha- lation depends in part on the size of the particles formed, because their size determines where they are deposited in the respiratory tract and this deter- mines bioavailability. Figure 4-1 shows the relationship between spore di- ameter and respiratory deposition of a number of mold genera. Figure 4-2 shows the percentage of inhaled spores that are deposited in the respirable (alveolar) area of the lung. The size of mold spores depends on the species that produce them. Spores of genera that use the air pathway for dispersion, including Aspergillus and Penicillium, are in the range of 12 µm and are respirable. Some molds (such as Stachybotrys chartarum and Memnoniella echinata) that do not spread their spores through aerosol dispersion are wet
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TOXIC EFFECTS OF FUNGI AND BACTERIA 129 0.8 70 0.7 Lung Respiratory Area Deposition 60 Deposition Coefficient Average Spore Diameter ( µm) 0.6 Average Spore Diameter 50 (Decimal Percent) 0.5 40 0.4 30 0.3 20 0.2 0.1 10 0 0 Arthirinium Aspergillus Penicillium Cladosporium Fusarium Paecilomyces Aureobasidium Curvularia Memnoniella Botrytis Stachybotrys Ulocladium Pithomyces Alternaria Bipolaris Dreschlera Epicoccum Oidium Peronospora Stemphyllium Genus FIGURE 4-1 Spore-deposition coefficients of mold genera in indoor environments. SOURCE: Miller et al., 2001. 100 % Spores Deposited in Respirable 80 Area of Lung 60 40 20 0 0 1 2 3 4 5 6 7 8 10 Spore size (µm) FIGURE 4-2 Percentage of inhaled spores that are deposited in respirable (alveo- lar) area of lung. SOURCE: Miller et al., 2001.
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130 DAMP INDOOR SPACES AND HEALTH and slimy during sporulation; once dry, the spores can be dispersed into air through disturbance of contaminated surfaces and are of inhalable size (5 7 µm) (Sorenson et al., 1987). Such bacteria as Streptomyces californicus isolated from damp indoor spaces are about 1 µm in diameter and can reach the lower airways and alveoli when inhaled (Jussila et al., 2001). Furthermore, Wainman and colleagues (2000) have shown that semivolatile chemicals, such as terpenes and limonene (which can be produced by molds that also produce trichothecene mycotoxins and are also often used indoors as cleaning solvents) react with ozone in indoor air and form particles of a respirable size, 0.20.3 µm diameter. Apart from particle size, determining the bioavailability of mycotoxins found on or in particles is complicated because even toxins from spores that lodge in the nasal mucous membranes can damage cells locally or be ab- sorbed into the systemic circulation (Morgan et al., 1993). Lipid-soluble toxins pass readily through membranes, and the degree of their absorption depends on the blood supply to the tissue (Rozman and Klaassen, 1996). The bioavailability of mycotoxins and bacterial toxins also depends on residence time and clearance mechanisms. Many mycotoxins affect resi- dence time and clearance by inhibiting phagocytic activity of macrophages or reducing ciliary beat rate (Amitani et al., 1995; Coulombe et al., 1991; Jakab et al., 1994; Sorenson and Simpson, 1986; Sorenson et al., 1986; Wilson et al., 1990). The toxic effect of spores and other particles on alveolar macrophages can impair the ability of these cells to protect against not only mycotoxins but also other bacteria and infectious particles. Slowed ciliary clearance allows longer residence time in the airway and increases the time for absorption of toxins from mold spores, fragments, or dust (Coulombe et al., 1991). Because the respiratory system is the primary route of entry for gases and particles suspended in air, determination of exposure to air contaminants is complicated because air contains a mixture of substances and the concentra- tion of individual toxicants changes with time and location in the exposure mixture. That is particularly true for toxic compounds originating in micro- bial contaminants of indoor spaces, because growth and metabolism of microbial organisms introduce additional variables into the exposure para- digm. Difficulties in measuring microorganisms and their products hinder the accurate determination of human exposure to them. Chapter 3 discusses the methods used and the difficulties in measuring such exposures. Experimental Data Because inhalation appears to be an important route of exposure for humans, determining the bioavailability of mycotoxins after inhalation expo- sure is important for determining the relationship between damp indoor
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TOXIC EFFECTS OF FUNGI AND BACTERIA 131 spaces and human health. However, compared with ingestion, relatively few animal experiments have been performed with the inhalation pathway. Some of the studies that have been conducted indicate that acute inhalation expo- sure, at least of some toxicants, is at least as toxic as exposure by intravenous injection and is more toxic than ingestion or parenteral exposure. Ueno (1984a) found that inhalation, skin, and parenteral exposure of newborn, young, and older mice to T-2 toxin--a trichothecene mycotoxin produced by Fusarium species whose LD50 (the lowest dose that kills half the animals that receive it) does not vary much across animal species (Ueno, 1980)--directly affected capillaries, increasing their permeability and lead- ing to intestinal bleeding, diarrhea, and death. However, some ingestion of the toxin might have occurred because of grooming behavior of the animals after it was deposited on their skin. The authors also noted that newborn and young animals were much more susceptible to the mycotoxin than the older mice. Marrs et al. (1986), using head-only exposures, compared the acute inhalation toxicity of T-2 toxin in guinea pigs, which tend to be sensitive to respiratory irritants, with effects of subcutaneous administration. Respira- tory rate and minute volume were measured with whole-body plethysmog- raphy. The inhaled dose was estimated by using the concentration of T-2- fluorescein-complexed aerosol collected on a filter at 1.0 L/min. The lethal concentration (LCt50), the air concentration lethal to 50% of the exposed group of animals, was determined by using a range of concentrations and exposure durations. The corresponding dose at which 50% of the exposed group dies (LD50) was estimated from the LCt50. Another group of animals received subcutaneous injections of doses of T-2 toxin ranging from 0.5 to 4.0 mg/kg. The LD50 estimated from the inhalation exposure was about twice that of the subcutaneous LD50 values, but the authors noted that only about half the inhalation dose was retained. Taking the low retention into account, the lethal dose after inhalation was similar to that by subcutane- ous injection. The types of effects on the gastrointestinal tract were similar for the two routes of exposure and are thought to be mediated systemically. The estimated LD50s were also similar to those seen by DeNicola et al. (1978) after oral dosing, and similar gastrointestinal effects have been seen in other oral-exposure studies and appear to be largely independent of route of administration (Ueno, 1984a,b). Creasia et al. (1987) exposed young adult and mature mice to T-2 toxin by inhalation for 10 min. Tremors, stilted gait, and, in some animals, prostration were observed. Animals in the highest-dose group died 5 h after exposure. After 24 h, the LCt50s were 0.08 ± 0.04 and 0.325 ± 0.010 mg/L of air for young and mature mice, respectively. The corresponding LD50s were 0.24 and 0.94 mg/kg. When those results are compared with results of other studies, inhalation exposure was about 510 times more potent than
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132 DAMP INDOOR SPACES AND HEALTH intraperitoneal administration, which had a reported LD50 of about 4.5 mg/ kg (Bamburg, 1976; Creasia et al., 1987), and at least 10 times more potent than dermal application, which had a reported LD50 of at least 10 mg/kg (Schiefer and Hancock, 1984). Creasia et al. (1990) conducted a nose-only, acute inhalation study of the effects of a 10-min exposure to T-2 toxin in rats and guinea pigs. Respiratory-tract lesions were minimal, and lesions to organs were similar to those described after following systemic administration. LCt50s were 0.02 and 0.21 mg/L of air for rats and guinea pigs, respectively. Deposition dose was measured by extraction of toxin from sacrificed animals, and LD50 of 0.05 and 0.4 mg/kg, respectively, were estimated. In that study, inhalation exposure to T-2 was about 20 times as toxic in rats and twice as toxic in guinea pigs as in studies of intraperitoneally administered T-2 toxin (LD50, 1 mg/kg in the rat; and 12 mg/kg in the guinea pig. Coulombe et al. (1991) administered 3H-labeled aflatoxin B1 (AFB1) adsorbed to grain dust or in its crystalline form intratracheally to male rats and sampled blood and tissue at selected intervals for 3 weeks to determine the pharmacokinetics of this toxin. After absorption, distribution followed a two-compartment model, with an initial rapid-distribution phase fol- lowed by a slower phase. The rate of absorption from the dust-associated dose was much lower for the first 90 min and the time to peak plasma concentration was much longer (12 vs 2 h) than for the crystalline form. Clearance was identical in the two groups. At 3 h, there was a substantially greater amount of AFB1-DNA adducts in the trachea and lung of the dust group. Retention of dust-associated carcinogens in the lung is an important factor in pulmonary carcinogenesis; it presumably increases the time during which metabolically active cells of the respiratory epithelium capable of transforming procarcinogens to carcinogens are in contact with the car- cinogen. In the liver, however, the DNA binding was greater for the crystal- line group at 3 h and at 3 days. Zarba et al. (1992) found that nose-only inhalation exposure of rats to aerosolized grain dust that contained AFB1 resulted in a linear dose-response relationship (correlation coefficient, 0.96) between time of exposure and AFB1-DNA adducts for 20, 40, 60, and 120 min of exposure. Adduct formation in the lung was not determined. Dermal absorption of mycotoxins varies. When toxins in excised hu- man skin were tested, the relative penetration rate of toxins dissolved in methanol was T-2 > diacetoxyscirpenol (DAS) > satratoxin H (a tricho- thecene mycotoxin found in Stachybotrys) > AFB1 (Kemppainen et al., 1988). Systemic toxicity after dermal exposure to a mycotoxin depends on its rate of absorption, relative blood flow to skin area, and the potency of the compound and its metabolites. Of the trichothecenes studied in vivo, relative local and systemic toxicity measured by skin irritation and lethality, respectively, is T-2 > DAS verrucarin. In vitro studies are fairly consistent
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TOXIC EFFECTS OF FUNGI AND BACTERIA 133 with in vivo penetration studies, although the potency of both T-2 and verrucarin is greater than that of DAS (Kemppainen et al., 1988). Kemp- painen and colleagues (1988) showed that both aflatoxins and tricho- thecenes can be absorbed through the skin. Dermal absorption is slow, but increases with the concentration of toxin, with coexposure to solvents (such as DMSO) that enhance penetration, and when the application site is oc- cluded with clothing or wraps. Joffe and Ungar (1969) showed that aflatox- ins applied to the skin of rabbits penetrated the stratum corneum and caused changes in the epidermis and dermis. Experiments in newborn, young, and adult mice (Ueno, 1984a,b) and in vitro experiments (Kemppainen et al., 1988) have demonstrated skin penetration of tricho- thecenes. Kemppainen et al. (1984) showed with 3H-T-2 toxin that T-2 toxin adsorbed onto corn dust can partition and penetrate excised human and guinea pig skin; this indicates that mycotoxin on dust is available for absorption via skin. Those studies indicate that toxins found in damp in- door spaces are bioavailable to people through inhalation and dermal expo- sure, with the more potent route of exposure depending on the compound. The extent of exposure that occurs in damp indoor spaces, however, has not been studied. TOXIC EFFECTS OF INDOOR MOLDS AND BACTERIA Exposure to various mold products--including volatile and semivolatile organic compounds and mycotoxins--and components of and substances produced by bacteria that grow in damp environments has been implicated in a variety of biologic and health effects. This section discusses irritation and inflammation of mucous membranes, respiratory effects, immuno- toxicity, neurotoxicity, sensory irritation (irritation of nerve endings of the common chemical sense), dermotoxicity, and carcinogenic effects attrib- uted to such exposure. Mucous Membrane Irritation and Inflammation Exposure to microorganisms and their products can irritate mucous membranes, such as those of the eyes and respiratory tract, and lead to inflammation via an immune response. Such immune responses are impor- tant in normal host defenses, but chronic or excessive release of inflamma- tory mediators can cause damage to the lung and other adverse effects (Jussila et al., 2003). Immune responses triggered by exposure to microorganisms and their products include increased production of inflammatory mediators, such as cytokines (for example, tumor-necrosis factor [TNF] and interleukin-6 [IL-6]), reactive oxygen species, and, indirectly, nitric oxide (NO) via the
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134 DAMP INDOOR SPACES AND HEALTH induction of nitric oxide synthetase (iNOS) (Hirvonen et al., 1997a,b; Huttunen et al., 2003; Ruotsolainen et al., 1995). Different bacteria evoke different cellular responses. For example, Staphylococcus evokes a response from alveolar macrophages, and Pseudomonas evokes a neutrophil response (Rehm et al., 1980). Mold spores and fragments affect the inflammatory response differently (Hirvonen et al., 1999). A number of in vitro, animal, and human studies that have investigated the irritation and inflammation responses to exposure to microorganisms and molds commonly found in damp indoor spaces are discussed below. In Vitro Experiments In vitro experiments use animal or human cell lines or primary cell cultures to explore mechanisms of toxicity for specific target tissues or cells. Although toxic exposure of cells and tissues in vitro does not provide information about homeostasis or defenses involved in the responses of an intact animal to exposure by various routes, such studies can avoid some uncertainties of extrapolation from animal to human models, can provide specific, repeatable, precise measures of target-cell effects, and can help to determine their mechanisms (Pitt, 2000). Hirvonen et al. (1997a) tested the ability of Streptomyces annulatus and S. californicus--both gram-positive bacteria--and the fungi Candida, Aspergillus, Cladosporium, and Stachybotrys to activate the mouse mac- rophage cell line RAW264.7. All the microorganisms were isolated from moldy houses, and no endotoxin contamination was detected in the cell suspensions. Both bacterial species substantially induced the iNOS enzyme and increased NO, TNF, and IL-6 production in a dose-dependent man- ner within 24 h. Only Stachybotrys affected cell viability. Hirvonen et al. (1997b) compared the effect of Streptomyces species on macrophages with the macrophage response produced by the gram-positive Bacillus sp. and Micrococcus luteus, which are common airborne bacteria in normal houses, and the gram-negative bacterium Pseudomonas fluores- cens, a known activator of macrophages. All Streptomyces species tested were able to induce substantial amounts of TNF and IL-6 and to induce the expression of iNOS and later NO; Bacillus sp. and Micrococcus luteus, commonly found in houses without dampness problems, did not. None of the bacteria affected cell viability, but endotoxin LPS and Pseudomonas fluorescens substantially reduced cell viability within 4 h. For Streptomy- ces, some factor other than NO production seemed to be required to initiate apoptosis, but the induction of proinflammatory mediators may play a role in inflammation related to exposure. Huttenen et al. (2000) studied inflammatory responses of RAW 264.7
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TOXIC EFFECTS OF FUNGI AND BACTERIA 135 macrophages to three mycobacteria isolated from a moldy building: non- pathogenic Mycobacterium terrae and potentially pathogenic M. avium- complex and M. scrofulaceum. All the bacterial species tested induced time- and dose-dependent production of NO, IL-6, and TNF, but IL-1 and IL-10 production was not detected. Reactive oxygen species (ROSs) were increased at the highest doses. The level of response differed widely across species. The nonpathogenic M. terrae was the most potent inducer, and M. avium-complex was the least potent; both pathogenic and nonpathogenic bacteria apparently activate inflammatory processes. Hirvonen et al. (2001) exposed RAW 264.7 macrophages to Strepto- myces annulatus spores isolated from a moldy building and then grown on 15 growth media to determine whether growth conditions affected a micro- organism's ability to induce inflammatory mediators. After 24 h, bacteria from all growth media induced iNOS in macrophages to some extent; the amount of NO produced ranged from 4.2 to 39.2 µM, depending on the growth medium. ROSs were induced only by the highest dose of S. annul- atus grown on glycerol-arginine agar. Cytokine production (IL-6 and TNF) depended on the growth medium. Viability of the RAW 264.7 macro- phages varied widely (from 11% to 96%), depending on the growth me- dium on which the S. annulatus was grown. Murtoniemi et al. (2002) tested the effects of three molds (Stachybotrys chartarum, Aspergillus versicolor, and Penicillium spinulosum) and one gram- positive bacterium (Streptomyces californicus) isolated from water-damaged buildings and then grown on different wetted plasterboard cores and liners. Both liners and cores of plasterboard supported microbial growth; all species grew earlier on the core than on the liner material. Penicillium grew only on the plasterboard cores. Aspergillus and Streptomyces grown on those build- ing materials were the most potent of the microorganisms in inducing the production of NO and IL-6 in RAW 264.7 macrophages; Stachybotrys spores did not induce NO nor IL-6 but did induce abundant TNF production. Aspergillus also produced high concentrations of TNF, and both Aspergil- lus and Stachybotrys were potently cytotoxic. Nielsen et al. (2001) examined the cytotoxicity of 20 Stachybotrys isolates from water-damaged buildings and their ability to induce inflam- matory mediators in RAW 264.7 macrophages. Eleven of the isolates pro- duced satratoxin and were highly cytotoxic to macrophages. Isolates that produced atranone were not cytotoxic but induced inflammatory mediators (ROS, NO, IL-6, and TNF at doses of 106 spores/mL). Pure atranone B and atranone D did not elicit such a response. It should be noted that 30 40% of Stachybotrys strains isolated from buildings produce satratoxin (Jarvis et al., 1998).
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