Interesting question. Here's what Wikipedia says about the use of aspergillus in foods consumed by humans:
>Other species are important in commercial microbial fermentations. For example, alcoholic beverages such as Japanese sake are often made from rice or other starchy ingredients (like manioc), rather than from grapes or malted barley. Typical microorganisms used to make alcohol, such as yeasts of the genus Saccharomyces, cannot ferment these starches, and so koji mold such as Aspergillus oryzae is used to break down the starches into simpler sugars.
>Members of the genus are also sources of natural products that can be used in the development of medications to treat human disease.
>Perhaps the largest application of A. niger is as the major source of citric acid; this organism accounts for over 99% of global citric acid production, or more than 1.4 million tonnes per annum. A. niger is also commonly used for the production of native and foreign enzymes, including glucose oxidase and hen egg white lysozyme. In these instances, the culture is rarely grown on a solid substrate, although this is still common practice in Japan, but is more often grown as a submerged culture in a bioreactor. In this way, the most important parameters can be strictly controlled, and maximal productivity can be achieved. It also makes it far easier to separate the chemical or enzyme of importance from the medium, and is therefore far more cost-effective.
Aspergillus and other toxic molds also are present as contaminants in many foods we eat. Corn and peanuts usually are measurably contaminated, and other grains can be as well. The government regulates and checks the amounts that are present, but (I once read) increased the limits about a decade ago. Standards also are not met in all instances.
Back before I knew that toxic mold was an issue for me, I used to be diligent about avoiding foods that were bothersome to me. I used something called the "Pulse Test," developed by Arthur Coca, M.D., (there's an inexpensive book on this) to gauge my reactions. The test involves taking the pulse, eating a large amount of the suspect food, and then taking the pulse again at 30-minute intervals thereafter. He says that problematic foods will cause a jump in the pulse rate within 90 minutes after consumption.
I found that certain foods did cause my pulse rate to jump, in some cases from 70 to 110. When this happened, I avoided those foods. This did make a substantial difference in my illness.
Eventually I did enough experimentation to find some peculiarities. One experiment showed that a bowl of popcorn made my pulse jump, whereas a goodly amount of fresh corn did not. Another suggested that Whole Foods organic oatmeal was problematic, whereas McCann's Irish Oatmeal did not.
When I look back, I think that in many cases I was responding to the contaminants in the foods rather than the foods themselves. The foods that made my pulse jump were only loosely overlapped with the ones that blood tests identified as ones I should be sensitive to. Toxic mold is rarely present in fresh produce (it grows during the periods of storage in silos), and I've heard that standards in Europe are stricter than those in the U.S.
Not all toxic mold is equally bad. It's my impression that Stachybotrys and other trichothecene-producing molds are the most problematic for us. Aspergillus inherently is much less toxic.
However, the reaction of at least some CFSers to toxic molds is so strong that tiny amounts of any mold toxin can set it off. I think that this was what was happening prior to avoidance.
When I first got unmasked from the mold, I found myself reacting strongly to almost all buildings. Not all buildings have Stachy in them, and in most cases my symptoms tended to be different than the ones I got from my house (which had Stachy). Most buildings do have a bit of the milder toxic molds (such as aspergillus) in them, but to my knowledge don't have much Stachy.
Erik's and my reactivities were the same when I visited him. This makes me believe that I was perhaps reacting a bit to Aspergillus, but much much more so to Stachy and other trichothecene-producing molds. (See his comments below on his own reactions.)
Over the past 2 1/2 years, my mold reactivity has gone way down. Now I can go in most buildings without incident. I also can eat anything I want without continuing to feel well. Only occasionally do I go in a building that has any effect on me (and that usually is just irritability).
So I think that now, my reactivity to Stachy has gone down a lot, and my reactivity to most other toxic molds is basically non-existent.
(What I am still reacting to now is a substance that is present mostly outside and very very occasionally in particularly bad buildings. I think that this is some sort of aquatic biotoxin such as cyanobacteria, and that I actually am a "severe biotoxin responder" rather than a "severe mold responder." Hopefully research eventually will make this more clear.)
What I'd thus like to suggest is that if CFSers are severe mold responders, they may indeed be responding to foods that have aspergillus and other mildly toxic molds in them, even if the amounts are not enough to bother normal people.
However, insofar as people indeed are responding to those foods, they might do well to suspect that they're responding to mold in the external environment as well. That's especially the case since inhaled trichothecenes are much worse than ingested ones (that's the consensus of those of us who are unmasked, and research studies suggest that as well), and since toxic molds in our environments are far more objectively damaging than the ones we encounter in foods.
When no doctors would help me to figure this mold problem out, I hired a mycologist to accompany me to various mold colonies so I could assess my reaction and have the offending one identified.
When we got to a black mold on some joists, I stuck my finger in it.
He said, "I wouldn't do that if I were you!”
And I replied, "This stuff? This isn't the one that is bothering me or I'd be slammed by now. Hell, I'll eat this mold on my peanut butter sandwich for lunch. This isn't the stuff.”
And that one was "Aspergillus Niger.”
Then we moved on to Penicillium, and that didn't do it either.
Finally we hit a mold which, when disturbed, put me down for the count. And as I was dropping to the floor, I said, "THAT'S THE ONE.”
Stachy, of course.
Nothing like self testing when doctors refuse to help.
No question about the results.
I have a woodbox in my MECU rig, to feed the fireplace.
The wood is covered with Aspergillus.... Niger, probably.
Doesn't seem to give me any trouble at all.
Amuzie CJ, Harkema JR, Pestka JJ. Tissue distribution and proinflammatory cytokine induction by the trichothecene deoxynivalenol in the mouse: comparison of nasal vs. oral exposure. Toxicology. 2008 Jun 3;248(1):39-44. PMID: 18433975
Competitive direct ELISA revealed that, regardless of exposure route, DON concentrations in plasma, spleen, liver, lung and kidney were maximal within 15-30 min and declined by 75-90% after 120 min. However, plasma and tissue DON concentrations were 1.5-3 times higher following intranasal exposure as compared to oral exposure.
In contrast, inductions of IL-1beta, IL-6 and TNF-alpha mRNAs in nasally exposed mice were 2-10, 2-5 and 2-4 times greater, respectively, than those in the tissues of orally exposed mice.
Taken together, these data suggest that DON was more toxic to the mouse when nasally exposed than when orally exposed, and that this might relate to greater tissue burden of the toxin.