Aspergillus versicolor

Aspergillus versicolor is a slow-growing species whose colonies shift through a range of colours as they mature, which is where the name comes from. It is among the most commonly recovered Aspergillus species from indoor environments in surveys worldwide.

Indoors it turns up on damp gypsum board, on and behind wallpaper, and very consistently in floor, carpet, mattress and upholstered-furniture dust. It is an organism of persistent mild dampness rather than of catastrophe: the wall that is always a bit cold, the room that never quite dries out, the cavity with a small recurring condensation problem.

Reported minima for growth sit around 0.78 to 0.80 aw. That places it below the roughly 0.85 aw that many textbook indoor species need, and well above the extreme xerophiles at the dry end of this panel.

The practical meaning of 0.78 is that this species does not need liquid water. A surface in equilibrium with air at 78% relative humidity is enough. That describes a great many ordinary interior surfaces in a house with marginal ventilation, which is exactly why it is so commonly found.

It also explains why it is a poor indicator of an acute event. A burst pipe produces conditions far wetter than this species requires, and also produces the wet-end species that a burst pipe uniquely permits. Finding versicolor without those is more consistent with a slow problem than a sudden one.

Aspergillus versicolor is the major producer of sterigmatocystin, a compound that is a biosynthetic precursor of the aflatoxins and is itself classified as a carcinogen in laboratory study. Sterigmatocystin has been reported from mould-affected buildings and building materials, so this is not a purely theoretical association.

What follows from that, and what does not, matters. A species being capable of producing a mycotoxin is not evidence that it produced any. Production depends on substrate, water activity, temperature and the particular isolate, and a colony of versicolor may produce none. Detection of the organism is therefore not detection of the toxin.

Nor does presence of the toxin on a material establish an inhalation exposure at a dose relevant to health. The evidence reviews on dampness and health did not conclude that household mycotoxin exposure explains the outcomes they associated with damp buildings; they associated those outcomes with dampness. Stating anything stronger than that from a species identification is going beyond what the identification supports.

It points to sustained mild dampness, and it points at surfaces rather than at structure. The productive investigation is usually of the boring kind: where are the cold surfaces, where does moist air sit without moving, which rooms produce moisture and where does it go.

Because it is so common in dust, a low level in a dust panel is not by itself remarkable. What is informative is a level that stands out against the rest of the panel, and against what the building's construction era and climate would predict.

Remediation guidance from the EPA and the CDC turns on removing the moisture and the growth rather than on identifying the species, and that guidance applies here as it does anywhere on this panel. The species tells you what kind of moisture problem to look for. It does not change what fixing it involves.