Health Risks Due To Inhalation of Fungal Mycotoxins

Health Risks Due To Inhalation of Fungal Mycotoxins

By Dave Gallup

Chairman, EMLab P&K

“Toxic mold” caused a flurry of media attention during the last 10 years and the resulting fear of “toxic mold” was a significant driver in the rapid growth of fungal IAQ investigations. In past issues of the Environmental Reporter we have discussed some of the adverse health effects that can be caused by fungi including allergic responses, hypersensitivity pneumonitis, and microbial volatile organic compounds. In this issue, we will discuss “toxic mold” and the risk of inhalation exposure to fungal toxins in residential and office environments. We will also focus on Stachybotrys, with a bias towards providing counterarguments to some of the claims of extreme adverse health effects that many of you have probably read or heard about.

Background

Many mycotoxins are secondary metabolites of fungi, meaning that they are not required for growth of the organism producing them. They are produced under suboptimal conditions for the fungi, such as when nutrients are limited. Production can vary significantly from one isolate to another and is dependent upon a poorly understood combination of many factors probably including temperature (Fusarium tricintum produces significant amounts of toxin when the temperatures is less than 15°C and produces very little when it is warmer), nutrient sources, competition with other organisms, relative humidity, growth rate, and maturity of the fungi1,2. As a result, the mere presence of a toxigenic fungus, meaning a fungus that is capable of toxin production, does not assure that toxin is being produced at that location. Similarly, if a fungus is producing toxins in the field, that same organism may not produce toxins in the lab.

Mycotoxins have relatively high molecular weights and are not significantly volatile. Consequently, they are usually not airborne unless they are attached to a particle and there has been an aerosolization event and, as a result, significant exposure through inhalation is unusual.

Recognition of risk due to ingestion

Severe adverse health effects due to ingestion of moldy food are well documented in both humans and animals. Aflatoxin, one of the most well known fungal toxins in the IAQ community, has been classified as a type 1 carcinogen and is probably the most potent liver carcinogen for humans. In the 1960’s, over 100,000 turkeys were killed in England due to aflatoxin contaminated peanuts. Ergotism is a mycotoxin disease caused by ingestion of moldy rye. The mycotoxin was responsible for outbreaks of “St. Anthony’s Fire” in the middle ages2. Ingestion of ochratoxin from moldy food remains a significant risk for cancer in some underdeveloped countries. Risks due to ingestion of moldy food are well recognized by the scientific community and should be avoided.

Risks due to inhalation of mycotoxins

There is some evidence for adverse health effects to humans in occupational environments where the exposure to mycotoxins is intense. However the available evidence and research regarding adverse health effects due to inhalation of mycotoxins supports the hypothesis that the risk is low in normal residential and office environments. This is primarily because the dosage is so low. The amount of mycotoxin contained in fungal spores is tiny. A Stachybotrys spore is roughly 9.5 x 7.5 µm in size. This is a volume of 2.8 x 10-10cm3 per spore. Dust with 85% spores has been found to contain 9.5 nanogram (ng) of Satratoxin H (SH)/mg of dust, or 11ng/mg of spores. Note that one ng is just 0.000000001 grams. This yields 3.1×10-15 grams of toxin per spore3. The implications of this are sometimes overlooked. In February of this year, Environmental Health Perspective published an article showing that the no effect dose in mice for intranasal instillation of Satratoxin G (SG) was 5×10-6 grams/kilogram body weight and suggested that this was a low dose4. However, if we want to get a sense of what that means in the human model, and make the significant assumptions that the concentration of SG is the same as SH, that people have the same no effect dose as mice (this may be significantly off), and use a body weight of 70kg (154 pounds), then the no effect dose level for that person is 3.5×10-4 grams. Using 3.1×10-15 grams/spore, an intranasal instillation of 110 billion spores would be the no effect dose level.

Another way to look at this is to make a mathematical model using conservative assumptions. A crude risk assessment can be made using the following set of data and conservative assumptions3:

  • One nanogram of mycotoxin is enough to cause an adverse health effect in people. This is extraordinarily conservative. The European Commission Regulation on aflatoxins from 1999 required that total aflatoxin levels must be less than 4 micrograms/kg in products intended for human consumption5. That is more than 100 times higher than what we’re permitting in this mathematical model.
  • One Stachybotrys spore contains 3×10-15 grams of mycotoxin, as calculated above.
  • All the airborne spores have mycotoxin, are inhaled into the respiratory tract, all of the toxin is absorbed by the body, and accumulates over time with none of it being metabolized or broken down.
  • A person breathes 30 m3 of air per day and is in this environment all day. This is probably a “reasonably” conservative estimate using data from the California Air Resources Board6 and reasonable assumptions about average activity levels throughout the day.
  • A background level of 100 spores/m3 of Stachybotrys spores. Due to the stickiness of Stachybotrys spores, and their relatively fast settling rated, this is a conservative estimate since it would likely require an ongoing active disturbance of a source of Stachybotrys to maintain this level continuously.

Given the model above, it would take over 1,000 days for a person to reach the ten nanogram threshold. The above model provides support for an argument that the risk due to inhalation of fungal mycotoxins in normal office and residential environments is low. This is in contradiction to some of the anecdotal evidence that has been provided by the media. Both sets of data should be moderated by the fact that there are many other things to consider, such as the presence of other spores in the air besides Stachybotrys, the possible presence of other toxins in the air, non-exposure related effects such stress and psychological damage, etc. Taking these other factors into account is what makes fungal IAQ investigations challenging and interesting. Such investigations require skill, training, expertise, and compassion for our fellow human beings. Compassionate approaches require both that specific risks be identified, and that the absence of a specific risk is made clear.

Note that this is a complex topic and that due to space constraints this discussion is necessarily superficial and is not and should not be construed as medical or any other form of advice.

References:

1. Adverse Health Effects Associated with Molds in the Indoor Environment, American College of Occupational and Environmental Medicine, October 27, 2002.
2. D.M. Khun and M.A. Ghannooum, Indoor Mold, Toxigenic Fungi, and Stachybotyrs chartarum: Infectious Disease Perspective, Clinical Microbiology Reviews, January 2003, p144-172.
3. Adapted from Harriet A. Burge, Health Effects of Biological Contaminants, Indoor Air and Human Health, CRC Press, 1996, Chapter 10, p171-176.
4. Z. Islam, et. al., Satratoxin G from the Black Mold Stachybotrys chartarum Evokes Olfactory Sensory Neuron Loss and Inflammation in the Murine Nose and Brain, Environmental Health Perspectives, February 27, 2006.
5. http://www.micotoxinas.com.br/boletim34.pdf (PDF, 164kb)
6. Air Resources Board: How Much Air Do We Breathe?