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Olfactory neuron loss and inflammation measured in mice after intranasal satratoxin G
Intranasal satratoxin G in mice was reported to cause dose-dependent olfactory sensory neuron loss, rhinitis, and cytokine expression extending to the olfactory bulb.
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This library reports what studies found. An entry describes a study's design, its findings in its own terms, and its limits. Nothing here is a claim about what a Sage Co. home does, delivers, or prevents.
Last reviewed August 30, 2026.
What they studied
- Mice given intranasal satratoxin G at graded single doses and in repeated low doses.
- Histopathology of nasal airways and olfactory bulb.
- Measurement of proinflammatory cytokine gene expression.
What they found
- Dose-dependent apoptosis of olfactory sensory neurons was reported.
- Acute rhinitis and proinflammatory cytokine expression were reported in the nasal airways and olfactory bulb.
- Repeated low-dose exposure was reported to produce cumulative effects comparable to single high doses.
What this study does not establish
- An animal study using purified toxin, not building air.
- Instilled doses are not equivalent to inhaled residential exposures.
- Findings do not establish human neurological outcomes.
- This entry reports the study. It is not a statement about any building Sage Co. designs or constructs.
Source
Islam Z, Harkema JR, Pestka JJ (2006). Satratoxin G from the black mold Stachybotrys chartarum evokes olfactory sensory neuron loss and inflammation in the murine nose and brain. Environmental Health Perspectives 114(7):1099–1107.
satratoxinanimal modelolfactoryinflammation
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