Clearing The Air on Mold & Mycotoxins

By Jason Earle, Founder & CEO, GOT MOLD?

5/20/2026

Key Takeaways

AIR MATTERS

Indoor air quality is foundational.

You breathe 20,000+ times every day and spend over 90% of your life indoors.

It is your single largest environmental exposure by orders of magnitude.

It either supports your health — or undermines it — more than almost anything else in your daily environment.

MOLD IS A MOISTURE PROBLEM

Mold is natural. Indoor moisture problems are not.

Mold is nature’s great recycler.

Problems begin when moisture allows it to grow indoors.

Mold needs:

Spores
Moisture
Oxygen
Food source
Proper temperature

Mold control = moisture control

THE 24–72 HOUR WINDOW

Water damage becomes a mold problem fast.

First 24–48 Hours

Easier cleanup
Lower cost
Lower exposure risk
Less disruption

After 72 Hours

Costs rise dramatically
Insurance coverage is extremely limited
Greater health and contamination risk
Mold amplification becomes much more likely
Specialized remediation is often required

MOLD EXPOSURE IS MORE THAN MYCOTOXINS

Indoor mold environments may contain:

Spores
Microbial VOCs (mVOCs/musty odors)
Allergens
Fragments
Bacteria
Mycotoxins (in some cases)

Only a small percentage of molds produce mycotoxins, and the research is clear: most human mycotoxin exposure comes from food — not buildings.

WHY PEOPLE FEEL SYMPTOMS SO QUICKLY

Your body is sensing the environment in real time.

One important system involved is the trigeminal nerve — a major sensory nerve in the face that helps detect airborne irritants and environmental threats.

It works alongside your sense of smell, but is often more sensitive.

The trigeminal system can respond to:

Microbial byproducts
Airborne irritants and particulates
Chemicals/fragrances/VOCs
Smoke

Importantly:

Detection can occur below odor threshold
Symptoms do not automatically mean “toxicity”

Common symptoms include:

Headaches
Brain fog
Burning eyes
Sinus irritation
Fatigue
Nervous system activation
Downstream effects: inflammation, immune activation

THE PATTERN

Small exposure → fast signal → amplified response.

Common pattern:

Symptoms begin shortly after entering a building
Persist during exposure
Improve upon leaving
Return upon re-exposure

This is often driven by neurogenic inflammation — a nervous system-mediated inflammatory response triggered by environmental signaling.

MUSTY ODORS MATTER

mVOCs are biological signals.

Microbial VOCs (mVOCs) are gases released during microbial growth.

Research has associated mVOCs with many symptoms blamed on mycotoxins:

Allergic reactions
Inflammation
Auto-immune disease
Gut dysregulation
Headaches
Nausea
Dizziness
Fatigue
Brain fog
Increased asthma risk

MYCOTOXIN CONFUSION

Important facts:

Only a small percentage of molds produce mycotoxins
Production occurs under specific stress conditions
Most mycotoxin exposure comes from food
Mycotoxins generally do not become airborne independently

Symptoms alone cannot determine causation.

URINE MYCOTOXIN TESTING

Detection does not equal causation.

Urine mycotoxin testing has become one of the most misunderstood tools in the mold world.

A positive urine result does not automatically prove:

A building problem
Ongoing indoor exposure
“Toxic mold illness”
Mold colonization
That symptoms are being caused by mold

Important context:

Most human mycotoxin exposure comes from food
Mycotoxins are common in the global food supply
Many are durable, fat-soluble, and biologically persistent
Detection alone cannot determine the source

Common mistake:

Symptoms + urine panel + ERMI score does not automatically equal:

“Your house is making you sick.”

Without proper environmental context, these tests are highly vulnerable to:

Confirmation bias
Overinterpretation
Misattribution
Fear-based decision making

The environment still has to be investigated properly.

WHY CONTEXT MATTERS

No single test tells the whole story.

Proper interpretation requires:

Visual observations
Spore counts
Odors
Building history
Moisture history
Symptoms
Current environmental conditions

Context matters.

WHEN TO HIRE A PROFESSIONAL

Not every mold issue requires major remediation.

However, professional evaluation should be considered when:

Visible growth covers more than a small isolated area
There is persistent moisture, dampness, or repeated leaks
Musty odors persist without an obvious source
Symptoms reliably improve outside the environment
Water damage involved HVAC systems, crawlspaces, or wall cavities
Flooding or major water intrusion occurred
Hidden mold is suspected despite low or normal spore counts
Occupants are medically vulnerable or highly sensitive

A qualified inspector should focus primarily on:

Moisture detection
Building science
Source identification
Environmental context

—not fear-based interpretation of isolated test results.

COMMONLY MISUSED METHODS

These tools are frequently overinterpreted or used without proper context:

Urine panels
Petri dish tests
Misapplied ERMI/HERTSMI scoring
Instant mold tests
Swabs
Pen-style tests

THE ERMI PROBLEM

ERMI was designed as a research tool — not a diagnostic tool.

Key limitations:

Only 36 species
Ignores building context
Prone to misleading interpretations
Uses a limited targeted MSqPCR approach
Developed as a research tool by EPA researchers
The EPA does not recommend ERMI for routine public use in homes or buildings

PCR VS NGS

Targeted PCR asks:

“Is this specific organism here?”

NGS asks:

“What is actually here?”

Whole-community analysis provides broader environmental context and pattern recognition.

COMING SOON

The Mycobiome (MCT) Dust Test

Based on HUD-funded Yale research.

Uses:

Next-Generation Sequencing (NGS)
AI/ML pattern analysis
Whole-community fungal assessment
Evaluates up to 230,000 taxa vs. just 36 species

Goal:

Better environmental interpretation through pattern recognition and analysis of the entire fungal ecology.

WHAT A GOOD INVESTIGATION LOOKS LIKE

Indoor environmental investigations are not about finding a single “bad mold.”

They are about understanding:

Moisture dynamics
Building history
Air quality
Hidden contamination
Occupant patterns
Environmental context

A proper assessment may involve:

Visual inspection
Moisture mapping
Infrared imaging
Humidity evaluation
HVAC assessment
Spore trap air sampling
Surface sampling where appropriate
Odor evaluation
Dust analysis
Building history review

No single test result should ever be interpreted in isolation.

The goal is pattern recognition and contextual understanding.

REMEDIATION: WHAT ACTUALLY MATTERS

The purpose of remediation is not sterilization.

The goal is to:

Correct the moisture problem
Remove contaminated materials
Restore a normal indoor ecology

Proper remediation generally includes:

Identifying and correcting the water source
Containment when appropriate
Removal of damaged porous materials
HEPA vacuuming
Detailed cleaning of surfaces and contents
Drying the structure properly
Post-remediation verification when necessary

Important:

Dead mold can still remain allergenic and inflammatory.

For this reason, remediation is primarily about:

Removal
Cleaning
Moisture correction

—not simply “killing mold.”

REMEDIATION RED FLAGS

Be cautious of approaches heavily focused on:

Fogging
Ozone
Fragrances
Routine biocide spraying
Encapsulating visible mold without removal
Extreme tear-outs without confirmed moisture damage
Fear-based sales tactics
Overreliance on ERMI scores or urine mycotoxin tests alone

The focus should remain on:

Identifying moisture
Correcting water intrusion
Removing damaged materials
Restoring healthy indoor conditions

PREVENTION: THE CLEAN & DRY PRINCIPLE

Healthy buildings are not sterile buildings.

They are buildings that stay:

Clean
Dry
Ventilated
Well maintained

Prevention strategies include:

Addressing leaks quickly
Monitoring humidity
Using bathroom and kitchen exhaust ventilation
Managing drainage around the structure
Drying wet materials rapidly
Using dehumidification where necessary
Inspecting vulnerable areas periodically
Using leak detectors in high-risk areas

Moisture that persists eventually becomes biology.

HOW PEOPLE ACTUALLY GET BETTER

After 25 years of investigations, one pattern stands out:

Air. Food. Attitude.

Air

Reducing or eliminating exposure to:

Mold
Dampness
VOCs
Water-damaged environments

Food

Many people report improvement with dietary changes such as:

Reducing sugar
Reducing ultra-processed foods
Prioritizing whole, nutrient-dense foods

Attitude

Supporting the nervous system through:

Neural retraining (e.g., Primal Trust, DNRS, and others)
Stress reduction
Nervous system regulation
Better sleep and recovery

The environment matters first.

THE FAST FOUR – Intake Questionnaire

Ask yourself:

Are you aware of any mold or moisture issues in your home?
Is there a history of leaks, dampness, or water damage?
Do you feel better when you leave the building?
Is there a musty or damp smell?

GOT MOLD? LET’S FIND OUT.

The GOT MOLD? Test Kit Includes:

Professional air sampling
World-class lab analysis at Eurofins
Clear, intuitive reporting
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Starting at just $199, everything included!

If you would like to try a GOT MOLD? Test Kit, go to www.gotmold.com and enter code TRIAL50 at checkout for 50% off, or click here. Expires May 25, 2026.

ARTICLES

LINKS

Main site

www.gotmold.com

Free Resources

Mycobiome (MCT) Dust Test

To register for early access and updates, click here.

Suggested Reading

REFERENCES & CITATIONS

I. Building Dampness, Mold, and Population-Level Health Signals

Ponikau, J. U., Sherris, D. A., Kern, E. B., Homburger, H. A., Frigas, E., Gaffey, T. A., & Roberts, G. D. (1999). The diagnosis and incidence of allergic fungal sinusitis. Mayo Clinic Proceedings, 74(9), 877–884.
https://doi.org/10.4065/74.9.877

Fisk, W. J., Lei-Gomez, Q., & Mendell, M. J. (2007). Meta-analyses of the associations of respiratory health effects with dampness and mold in homes. Indoor Air, 17(4), 284–296.
https://doi.org/10.1111/j.1600-0668.2007.00475.x

Mudarri, D., & Fisk, W. J. (2007). Public health and economic impact of dampness and mold. Indoor Air, 17(3), 226–235.
https://doi.org/10.1111/j.1600-0668.2007.00474.x

Shenassa, E. D., Daskalakis, C., Liebhaber, A., Braubach, M., & Brown, M. (2007). Dampness and mold in the home and depression: An examination of mold-related illness and perceived control of one’s home as possible depression pathways. American Journal of Public Health, 97(10), 1893–1899.
https://doi.org/10.2105/AJPH.2006.093773

Lawrence Berkeley National Laboratory. Prevalence of Building Dampness.
https://iaqscience.lbl.gov/prevalence-building-dampness

II. Fungal Volatile Organic Compounds (mVOCs): Source, Emissions, and Airborne Exposure

Morath, S. U., Hung, R., & Bennett, J. W. (2012). Fungal volatile organic compounds: A review with emphasis on their biotechnological potential. Fungal Biology Reviews, 26(2–3), 73–83.
https://doi.org/10.1016/j.fbr.2012.07.001

Hung, R., Lee, S., & Bennett, J. W. (2015). Fungal volatile organic compounds and their role in ecosystems. Applied Microbiology and Biotechnology, 99, 3395–3405.
https://doi.org/10.1007/s00253-015-6494-4

Inamdar, A. A., Masurekar, P., & Bennett, J. W. (2014). Volatile organic compounds from fungi isolated after Hurricane Katrina induce developmental defects and apoptosis in a Drosophila melanogaster model. Environmental Toxicology, 29(12), 1345–1356.
https://doi.org/10.1002/tox.21933

Macedo, G. E., Vieira, P. B., Rodrigues, N. R., Gomes, K. K., Martins, I. K., Franco, J. L., & Posser, T. (2020). Fungal compound 1-octen-3-ol induces mitochondrial morphological alterations and respiration dysfunctions in Drosophila melanogaster. Ecotoxicology and Environmental Safety, 206, 111232.
https://doi.org/10.1016/j.ecoenv.2020.111232

Bennett, J. W. (2015). Are some fungal volatile organic compounds (VOCs) mycotoxins? Toxins, 7(9), 3785–3804.
https://doi.org/10.3390/toxins7093785

Bennett, J. W. (2015). Silver linings: A personal memoir about Hurricane Katrina and fungal volatiles. Frontiers in Microbiology, 6, 206.
https://doi.org/10.3389/fmicb.2015.00206

Andersen, B., Dosen, I., Lewinska, A. M., & Nielsen, K. F. (2017). Pre-contamination of new gypsum wallboard with potentially harmful fungal species. Indoor Air, 27(1), 6–12.
https://doi.org/10.1111/ina.12298

Tabbal, S., El Aroussi, B., Bouchard, M., Marchand, G., & Haddad, S. (2022). A new headspace solid-phase microextraction coupled with gas chromatography-tandem mass spectrometry method for the simultaneous quantification of 21 microbial volatile organic compounds in urine and blood. Chemosphere, 293, 133901.
https://doi.org/10.1016/j.chemosphere.2022.133901

III. Airborne Chemical Exposure & Trigeminal Activation

Mølhave, L., Bach, B., & Pedersen, O. F. (1986). Human reactions to low concentrations of volatile organic compounds. Environment International, 12(1–4), 167–175.
https://doi.org/10.1016/0160-4120(86)90005-0

Mølhave, L. (1991). Volatile organic compounds, indoor air quality and health. Indoor Air, 1(4), 357–376.
https://doi.org/10.1111/j.1600-0668.1991.00001.x

Cometto-Muñiz, J. E., & Cain, W. S. (1995). Relative sensitivity of the ocular trigeminal, nasal trigeminal, and olfactory systems to airborne chemicals. Chemical Senses, 20(2), 191–198.
https://doi.org/10.1093/chemse/20.2.191

IV. Environmental Chemosensation & Sensory Detection

Simons, C. T., & Carstens, E. (2008). Chemesthesis. In The Senses: A Comprehensive Reference. Elsevier.
https://www.sciencedirect.com/topics/neuroscience/chemesthesis

Slack, J. P. (2016). Molecular pharmacology of chemesthesis. In Chemosensory Transduction. Elsevier.
https://doi.org/10.1016/B978-0-12-801694-7.00021-4

Green, B. G. (2012). Chemesthesis and the chemical senses as components of a “chemofensor complex.” Chemical Senses, 37(3), 201–206.
https://doi.org/10.1093/chemse/bjr119

Gerhold, K. A., & Bautista, D. M. (2009). Molecular and cellular mechanisms of trigeminal chemosensation. Annals of the New York Academy of Sciences, 1170, 184–189.
https://doi.org/10.1111/j.1749-6632.2009.04359.x

Bessac, B. F., & Jordt, S.-E. (2008). Breathtaking TRP channels: TRPA1 and TRPV1 in airway chemosensation and reflex control. Physiology (Bethesda), 23, 360–370.
https://doi.org/10.1152/physiol.00026.2008

Nassenstein, C., Kwong, K., Taylor-Clark, T., Kollarik, M., Macglashan, D. W., Braun, A., & Undem, B. J. (2008). Expression and function of the ion channel TRPA1 in vagal afferent nerves innervating mouse lungs. The Journal of Physiology, 586(6), 1595–1604.
https://doi.org/10.1113/jphysiol.2007.148379

V. Environmental Irritants & Dose-Dependent Activation

National Research Council (US) Committee on Toxicology. (1986). Organic solvents and the central nervous system. National Academies Press (US).
https://www.ncbi.nlm.nih.gov/books/NBK215642/

Inoue, T., & Bryant, B. P. (2005). Multiple types of sensory neurons respond to irritating volatile organic compounds (VOCs): Calcium fluorimetry of trigeminal ganglion neurons. Pain, 117(1–2), 193–203.
https://doi.org/10.1016/j.pain.2005.06.012

VI. Neurogenic Inflammation & Local Tissue Response

Meggs, W. J. (2007). Neurogenic inflammation and sensitivity to environmental chemicals. Pharmacology & Therapeutics, 113(2), 281–292.
https://doi.org/10.1016/j.pharmthera.2006.08.001

Holzer, P. (2006). Neurogenic inflammation: Mechanisms and implications for health and disease. European Journal of Pharmacology, 533(1–3), 182–193.
https://doi.org/10.1016/j.ejphar.2005.08.044

O’Connor, T. M., O’Connell, J., O’Brien, D. I., Goode, T., Bredin, C. P., & Shanahan, F. (2004). The role of substance P in inflammatory disease. Journal of Cellular Physiology, 201(2), 167–180.
https://doi.org/10.1002/jcp.20061

VII. Neuro-Immune Integration & Reflex Pathways

Chiu, I. M., Heesters, B. A., Ghasemlou, N., Von Hehn, C. A., Zhao, F., Tran, J., Wainger, B., Strominger, A., Muralidharan, S., Horswill, A. R., Bubeck Wardenburg, J., Hwang, S. W., Carroll, M. C., & Woolf, C. J. (2013). Bacteria activate sensory neurons that modulate pain and inflammation. Nature, 501(7465), 52–57.
https://doi.org/10.1038/nature12479

Pavlov, V. A., & Tracey, K. J. (2012). The vagus nerve and the inflammatory reflex—linking immunity and metabolism. Nature Reviews Endocrinology, 8(12), 743–754.
https://doi.org/10.1038/nrendo.2012.189

VIII. Central Processing, Sensitization & Modulation

Ji, R.-R., Nackley, A., Huh, Y., Terrando, N., & Maixner, W. (2018). Neuroinflammation and central sensitization in chronic and widespread pain. Anesthesiology, 129(2), 343–366.
https://doi.org/10.1097/ALN.0000000000002130

Hummel, T., Croy, I., & Sinding, C. (2023). Chemosensation in anxiety: The trigeminal system matters. Chemical Senses.
https://doi.org/10.1093/chemse/bjad010

IX. Clinical Phenomena: Environmental Intolerance

Binkley, K. E. (2023). Multiple chemical sensitivity/idiopathic environmental intolerance: A practical approach to diagnosis and management. Journal of Allergy and Clinical Immunology: In Practice, 11(12), 3645–3649.
https://doi.org/10.1016/j.jaip.2023.08.039

Molot, J., Sears, M. R., & Anisman, H. (2023). Multiple chemical sensitivity: It’s time to catch up to the science. Neuroscience & Biobehavioral Reviews.
https://doi.org/10.1016/j.neubiorev.2023.105094