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3 Reasons a “Safe Level” for Mold is Unscientific

Respiratory exposure to indoor biological contamination—such as mold, bacteria, and volatile organic compounds—exerts toxic and inflammatory effects. A common question in mold litigation is what constitutes a “safe level” of toxic mold contamination. This question cannot be answered with a hard cut-off without being in error.

The Centers for Disease Control, as well as the World Health Organization do not provide cut-off levels for safety on commercial mold testing, such as air sampling. As the WHO wrote:

“As the relations between dampness, microbial exposure and health effects cannot be quantified precisely, no quantitative health-based guideline values or thresholds can be recommended for acceptable levels of contamination with microorganisms. Instead, it is recommended that dampness and mould-related problems be prevented. When they occur, they should be remediated because they increase the risk of hazardous exposure to microbes and chemicals.”

This article will elaborate upon three reasons that a hard cut-off for a safe mold level is impossible to establish.

Reason 1: Commercial mold testing provides unreliable estimates of overall microbial exposure.

A common mistake is to presume that the result of an air sample (or other testing methodology) provides a precise and comprehensive representation of indoor air quality. The reality is each test offers only partial information.

Consider that room air sampling only assesses whole intact mold spores, but does not measure harmful mold fragments, which outnumber the spores by at least 300 times.

Or how a swab sample for mold is, by its inherent design, not intended to measure toxic bacteria, such as Actinomyces, which significantly contribute to health hazards. Over thirty triggering foreign molecules have been identified in the biological structure of mold and bacteria, along with harmful metabolic products, such as toxins.

It is therefore not reasonable to use a single commercial mold test to represent the cumulative building hazard level. Like the Harvard applicant evaluation, building assessment is a holistic process.

Reason 2: Immune injury is not a dose-dependent relationship.

In medicine, a dose-dependent relationship is a predictable correlation between a given exposure and its effect on health. The level of a medication. The right amount of water to drink. The safe level of vitamin A. These examples feature dose-dependent relationships.

Consider how a vitamin is ineffective at too low a dose, health promoting within a range, and toxic beyond a cut-off.

But there are exposures that are not dose-dependent as well. Consider how, for an individual with an allergy, the scent of peanut oil can send him to the emergency room, but his dining companion can eat a whole can of Planter’s® with no harm—there is not a general predictable dose-dependent response.

As with allergy, the type of inflammation that occurs with exposure to water-damaged buildings is not dose dependent. This type of inflammation is known as innate immune activation and occurs when the body detects triggering foreign molecules from inhaled biological contaminants and other noxious elements in the air.

As medical expert and environmental specialist Dr. Scott McMahon writes:

“The immune system is not a linear system; it functions through a series of cascades that amplify geometrically.”

How violently an individual responds depends upon immune priming–a phenomenon by which repeated exposures to indoor air pollution increases the body response over time. Biologist Jamie Lichtenstein has found that, in a test tube, immune cells from mold-exposed subjects showed massive increases in the levels of cytokines and chemokines when exposed to mold spores or mold toxins compared with the immune cells from healthy controls.

Lichtenstein concluded:

“Molds may induce persistent changes in inflammatory and immune responses.”

Reason 3: Genetics influence risk.

How a body responds to toxic and inflammatory agents depends upon genetics as well. Consider the Human Leukocyte Antigen (HLA), a cluster of genes that is involved in over 100 metabolic and autoimmune diseases, including the strongest known genetic association to lupus.

In the syndrome of mold-related innate immune activation, Chronic Inflammatory Response Syndrome, the HLA is an important predictor of this condition.

A vulnerable HLA type is present in about 25% of the population, but constitute over 75% of the patients under the care of Chronic Inflammatory Response Syndrome clinicians. Since the development of Chronic Inflammatory Response Syndrome and other immune responses features a genetic element, what is safe for one building occupant would not be safe for another.


Heseltine, Elisabeth, and Jerome Rosen, eds. “WHO guidelines for indoor air quality: dampness and mould.” (2009).

Shoemaker, Ritchie C., James Louis Schaller, and Patti Schmidt. Mold Warriors: Fighting America’s Hidden Health Threat. Gateway Press, 2005.

Górny, Rafał L., et al. “Fungal fragments as indoor air biocontaminants.” Applied and environmental microbiology 68.7 (2002): 3522-3531.

Bakhru, Aruna, ed. Nutrition and Integrative Medicine for Clinicians: Volume Two. CRC Press, 2023.

Rosenblum Lichtenstein JH, Hsu Y-H, Gavin IM, Donaghey TC, Molina RM, Thompson KJ, et al. (2015) Environmental Mold and Mycotoxin Exposures Elicit Specific Cytokine and Chemokine Responses.