Microbial toxins and eukaryotic cell toxicity from indoor building materials heavily colonized by fungi and bacteria were analyzed. The dominant colonizers at water-damaged sites of the building were Stachybotrys chartarum (10 3 to 10 5 visible conidia cm ؊2 ), Penicillium and Aspergillus species (10 4 CFU mg ؊1 ), gram-negative bacteria (10 4 CFU mg ؊1 ), and mycobacteria (10 3 CFU mg ؊1 ). The mycobacterial isolates were most similar to M. komossense, with 98% similarity of the complete 16S rDNA sequence. Limulus assay of water extracts prepared from a water-damaged gypsum liner revealed high contents of gram-negative endotoxin (17 ng mg ؊1 of E. coli lipopolysaccharide equivalents) and ␤-D-glucan (210 ng mg ؊1 of curdlan equivalents). High-performance liquid chromatography analysis of the methanol extracts showed that the water-damaged gypsum liner also contained satratoxin (17 ng mg ؊1 ). This methanol-extracted substance was 200 times more toxic to rabbit skin and fetus feline lung cells than extract of gypsum liner sampled from a non-water-damaged site. The same extract contained toxin(s) that paralyzed the motility of boar spermatozoa at extremely low concentrations; the 50% effective concentration was 0.3 g of dry solids per ml. This toxicity was not explainable by the amount of bacterial endotoxin, ␤-D-glucan, or satratoxin present in the same extract. The novel in vitro toxicity test that utilized boar spermatozoa as described in this article is convenient to perform and reproducible and was a useful tool for detecting toxins of microbial origin toward eukaryotic cells not detectable in building materials by the other methods.

A cluster of cases of pulmonary hemosiderosis among infants was reported in Cleveland, Ohio, during 1993 and 1994. These unusual cases appeared only in infants ranging in age from 1 to 8 months and were characterized by pulmonary hemorrhage, which caused the babies to cough up blood. A case-control study identified major home water damage (from plumbing leaks, roof leaks, or flooding) as a risk factor for development of pulmonary hemorrhage in these infants. Because of an interest in the possibility that trichothecene mycotoxins might be involved in this illness, a number of isolates ofStachybotrys chartarum were grown in the laboratory on rice, and extracts were prepared and analyzed both for cytotoxicity and for specific toxins. Two isolates of Memnoniella echinata, a fungus closely related to S. chartarum, were also included in these studies. S. chartarum isolates collected from the homes were shown to produce a number of highly toxic compounds, and the profiles of toxic compounds from M. echinata were similar; the most notable difference was the fact that the principal metabolites produced by M. echinatawere griseofulvins.

Stachybotrys atra is often isolated from building materials in houses with moisture problems. Spores of S. atra can contain mycotoxins which may lead to various symptoms in exposed residents in damp houses. The pathogenesis of S. atra-induced lung diseases has not been elucidated. The purpose of the present study was to investigate lung mycotoxicosis experimentally in mice after an intranasal exposure to spores of S. atra-fungus. One group of mice received one intranasal injection of spores of a toxic strain of S. atra (1 x 10(6) spores) and the other group spores of a less toxic strain. Spores of both strains contained spirolactones and spirolactams while the highly toxic strain contained also trichothecene mycotoxins, satratoxins. The spores containing satratoxins caused severe intra-alveolar, bronchiolar and interstitial inflammation with haemorrhagic exudative processes in the alveolar and bronchiolar lumen. A significant difference was observed in the severity of the lung damage caused by the two strains of S. atra. The spores without satratoxins induced a milder inflammation, so that the toxic compounds of S. atra-spores are most likely responsible for the severity of the lung injury.

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