The authors of this paper were involved in sampling of three homes. Molds isolated and cultured from bulk samples obtained from the three homes revealed mycotoxins as follows: Home 1: satratoxins H and G, isosatratoxin F, roridin, 1-2, E and isororidin, epoxydolabellane A, MER 503; aflatoxin B, sterigmatocystin and cyclopanzoic acid; Home 2: roquefortine C, sterigmatocystin and 5-methyloxysterigmatocystin; and Home 3: sterigmatocystin, MER 503 and dolabellanes (Neville, P-K Jarvis unpublished reports).
An 18-month-old male child in one of the homes died from pulmonary bleeding. In the other two homes, two women and a 7-year-old boy developed permanent neurocognitive deficits as well as increased sensitivity to various odorous chemicals. The latter three had changes in quantitative electroencephalograms
(QEEG) involving the frontal cortex as well as other regions of their brains. The neurocognitive deficits were shown by testing performed by neuropsychologist Raymond Singer, PhD, Santa Fe, New Mexico.
Airborne macrocyclic trichothecenes in contaminated buildings, control buildings and outdoor air were investigated (Brasel et al, 2005a,b). The Quant Tox Kit manufactured by Envirologix was utilized to detect satratoxin G and H, verrucarin A, verracarol and isosatratoxin F by an ELISA method with roridin A as the control. Air samples were collected using a Spin Con PAS bioaerosol sample. The air samples were pulled through multistage polycarbonate filters of 5.0, 1.2 and 0.4 mm. The mycotoxins were present in all particulate fractions, particularly 0.4 to 1.2 mm.
Briefly, macrocyclic trichothecene concentrations present in the fine particle fractions ranged from <10 to >1300 pg/m3, significantly greater (p < .001) than detection in control buildings and outdoor air.
In addition, the trichothecenes were detected in the sera of symptomatic occupants of the same buildings vs controls (p < .05; Brasel et al, 2004). More recently, elevated macrocyclic trichothecenes were reported in flooded moldy dwellings in which S. chartarum was present (Charpin-Kadouch et al, 2006).
Additionally, Bloom et al (2007), using gas chromatography as well as HPL with tandem mass spectrometry, tested for the presence of trichothecenes (verrucarol, trichodermol, satratoxins G and H, trichodermol, gliotoxin, aflatoxins and sterigmatocystin) in building materials and dust from water-damaged buildings and homes. Of 62 samples, 45 were positive for mycotoxins, three of eight settled dust samples and five of eight air dust samples were positive for macrocyclic trichothecenes and sterigmatocystin.
Additionally, concentrations of various mycotoxins were as follows: building materials (gliotoxin at 0.43-1.12 pg/mg; sterigmatocystin at 4.9-50,000 pg/mg; trichodermol at 0.9-8700 pg/mg; verrucarol at 8.8-17,000 pg/mg and dust samples (aflatoxin B1 at 32.0-13,500 pg/cm2; sterigmatocystin at 3.6-
10,900 pg/cm2; trichodermol at 6.5-170 pg/cm2; verrucarol at 25-3,400 pg/cm2; gliotoxin at 400 pg/cm2).
In addition, verrucarol and sterigmatocystin were found in dust samples from Katrina homes (Bloom, 2008). Also, airborne satratoxin G and H were demonstrated in a contaminated home utilizing a 0.8-mm filter and LC-MS/MS (Gottschalk et al, 2008).
More recently, hydrophilic fungi and ergosterol were shown to be associated with respiratory illness in a water-damaged building (Park et al, 2008). Ergosterol is a biomarker for the assessment of mold damage (Foto et al, 2005; Hippelein and Rugamer, 2004).
In conclusion, mycotoxins in damp indoor environments become airborne in both large (spores, hyphae fragments) and fine particles. They are also present in bulk in dust samples from the same buildings. In conclusion, multiple mycotoxins, e.g., trichothecenes, aflatoxins, gliotoxin, are prevalent in water-damaged homes and buildings.
The epipolythiodioxopiperzines (ETP) are a class of fungal toxins produced by several different genera of mold (Gardiner et al, 2005). One of the most abundant ETP is gliotoxin produced by A. fumigatus, niger, terreus, flavus, Trichoderma virens, Penicillium spp. and C. albicans (Gardiner et al, 2005; Lewis et al, 2005b).
Gliotoxin is a virulence factor in invasive A. fumigatus in mice and probably for humans (Kupfahl et al, 2008; Lewis et al, 2005a,b; Sugui et al, 2007). Gliotoxin is an immunomodulating toxin with suppressive activity (Mullbacher et al, 1986; Sutton et al, 1994). It inhibits macrophage and polymorphonuclear cell function and generation of alloreactive cytotoxic T cell. The toxin inhibits the transcription factor, nuclear factor kappalight-chain-enhancer of activated B cells (NF-kB), an integral part of the inflammatory immune response and controls expression of some cytokines.
Finally, gliotoxin and other ETPs are mitochondrial poisons resulting in reduction of adenosine triphosphate (ATP) by hyper-polarization of the mitochondrial membrane and causing apoptosis (Gardiner et al, 2005; Pardo et al, 2006). Gliotoxin has been identified in the lungs and sera of mice and cancer patients with aspergillosis (Lewis et al, 2005a).
The percentage of Aspergillus species isolated from cancer patients with IA secrete gliotoxins as follows: A. fumigatus – 93%; A. niger – 75%; A. terres – 24%; and S. flavus – 4% (Lewis et al, 2005b). Moreover, the production of gliotoxin by clinical and environmental isolates of A. fumigatus has been confirmed in Germany and Austria (Kupfahl et al, 2008).
The percentage of A. fumigatus isolates that produced gliotoxin was clinical isolates – 98%; environmental isolates – 96%. The toxin was also detected in decreasing frequency in other isolated species: A. niger – 56%; A. terreus – 37%; and A. flavus – 13%.
In conclusion, these observations make it imperative that more attention should be paid to Aspergillus species as well as other genera of molds and their production of gliotoxin. The need for an increased awareness of these molds is apparent with respect to the exposure of humans who have risk factors of corticosteroid usage, COPD, diabetes mellitus, pre-existing illnesses as well as altered immune function, e.g., autoimmune diseases.