MycoTOX
The MycoTOX panel quantifies nine urinary mycotoxin metabolites—aflatoxin M1, ochratoxin A, sterigmatocystin, roridin E, verrucarin A, gliotoxin, zearalenone, T-2 toxin, and citrinin—using LC-MS/MS, reflecting recent exposure to moulds in water-damaged buildings or contaminated food.
9
Biomarkers
Urine (random)
Sample
10–14 business days
Turnaround
No
Fasting
What is the MycoTOX test?
The MycoTOX panel quantifies urinary metabolites of nine mycotoxins produced by moulds commonly found in water-damaged buildings, contaminated food, and occupational settings. Mycotoxins are secondary metabolites with diverse toxic mechanisms — hepatotoxicity, nephrotoxicity, immunosuppression, endocrine disruption, and inhibition of protein synthesis — and exposure is implicated in a spectrum of chronic health complaints in environmental and functional medicine. Practitioners order this panel when clinical suspicion points to mould-related illness: patients with chronic respiratory symptoms, cognitive complaints, fatigue, or multi-system dysfunction following exposure to damp indoor environments, or when dietary sources of mycotoxin contamination are suspected. The test provides a snapshot of recent exposure — mycotoxins are cleared over days to weeks — and results are interpreted alongside environmental assessment, symptom patterns, and other markers of inflammation or immune dysregulation rather than as stand-alone diagnostics.
What does the MycoTOX test measure?
Aflatoxin M1 is the hydroxylated metabolite of aflatoxin B1, produced primarily by Aspergillus species that contaminate grains, nuts, and animal feed. Following ingestion, hepatic cytochrome P450 enzymes convert aflatoxin B1 to M1, which is then renally excreted. Aflatoxins are potent hepatotoxins and carcinogens; chronic exposure is linked to hepatocellular carcinoma, particularly in regions with endemic hepatitis B.
Urinary aflatoxin M1 reflects recent dietary or environmental exposure to aflatoxin-contaminated food or mould-infested indoor environments. Elevation prompts investigation of food sources, storage conditions, and occupational or residential mould contamination.
Ochratoxin A is a nephrotoxic mycotoxin produced by Aspergillus and Penicillium species, often found in stored cereals, coffee, dried fruit, and wine. It is absorbed from the gastrointestinal tract, undergoes enterohepatic recirculation, and is slowly eliminated via the kidneys, with a half-life of several days in humans.
Urinary ochratoxin A indicates recent exposure and may correlate with chronic kidney disease risk, immune suppression, and possible carcinogenic effects. Persistent elevation warrants environmental assessment and dietary modification.
Sterigmatocystin is a precursor in the biosynthetic pathway of aflatoxins, produced by Aspergillus versicolor and related species. It is found in mouldy grains, cheese, and damp indoor environments. Sterigmatocystin is hepatotoxic and classified as a probable human carcinogen.
Detection signals mould exposure, often from water-damaged buildings or contaminated food. It is a marker used in environmental medicine to assess the burden of indoor mould and guide remediation.
Roridin E is a macrocyclic trichothecene mycotoxin produced by Stachybotrys chartarum (black mould) and Myrothecium species. Trichothecenes inhibit protein synthesis and are potent irritants of mucous membranes, skin, and the gastrointestinal and respiratory tracts.
Urinary roridin E is used as a biomarker of exposure to Stachybotrys in water-damaged indoor environments. Symptoms attributed to such exposure include respiratory complaints, neurological symptoms, and immune dysregulation, though causation remains contested.
Verrucarin A is another macrocyclic trichothecene from Stachybotrys and Myrothecium. It shares the protein-synthesis-inhibiting mechanism of other trichothecenes and is considered one of the more toxic members of this class.
Presence in urine suggests exposure to black mould or related species, typically in damp, poorly ventilated buildings. Interpretation is combined with other trichothecene markers and clinical context.
Gliotoxin is an immunosuppressive epidithiodioxopiperazine mycotoxin produced by Aspergillus fumigatus and other species. It inhibits T-cell activation, induces apoptosis, and disrupts phagocyte function. In invasive aspergillosis, elevated gliotoxin is associated with immune evasion.
Urinary gliotoxin may reflect chronic Aspergillus colonisation, invasive infection in immunocompromised hosts, or environmental exposure. It is used in functional and environmental medicine to assess mould-related immune burden.
Zearalenone is a resorcylic acid lactone mycotoxin produced by Fusarium species that contaminate maize, wheat, and other cereals. It has oestrogenic activity, binding to oestrogen receptors and disrupting reproductive and endocrine function in livestock and potentially humans.
Urinary zearalenone indicates dietary or environmental exposure. It is investigated in cases of unexplained oestrogenic symptoms, infertility, or hormone-sensitive conditions, particularly when environmental mould or grain contamination is suspected.
T-2 toxin is a type A trichothecene produced by Fusarium sporotrichioides and related species, found in mouldy cereals. It is highly cytotoxic, inhibiting protein synthesis and causing bone marrow suppression, gastrointestinal haemorrhage, and dermal necrosis in acute poisoning.
Detection in urine suggests dietary contamination or occupational exposure to mouldy grain. T-2 toxin is associated with alimentary toxic aleukia in severe outbreaks and is monitored in functional medicine as part of mycotoxin burden assessment.
Citrinin is a nephrotoxic mycotoxin produced by Penicillium, Aspergillus, and Monascus species, often found in stored cereals, rice, and fermented products. It damages renal tubular cells and has been implicated in endemic Balkan nephropathy in combination with ochratoxin A.
Urinary citrinin reflects dietary or environmental exposure and is a marker of potential renal injury risk. It is included in comprehensive mycotoxin panels to assess cumulative nephrotoxic burden.
Why is the MycoTOX test ordered?
- Investigation of chronic respiratory symptoms, sinusitis, or asthma exacerbations in patients living or working in water-damaged buildings
- Assessment of neurological or cognitive complaints — brain fog, headache, memory impairment — attributed to possible mould exposure
- Evaluation of unexplained fatigue, joint pain, or multi-system symptoms in individuals with known or suspected environmental mould exposure
- Screening patients with chronic inflammatory or immune dysregulation syndromes when environmental toxin burden is part of the differential
- Baseline and follow-up monitoring during mould remediation or relocation from contaminated environments, to document clearance of mycotoxins
- Investigation of hormone-sensitive conditions or unexplained oestrogenic symptoms when dietary or environmental zearalenone exposure is suspected
- Occupational health assessment of agricultural workers, grain handlers, or building inspectors with potential chronic mycotoxin exposure
- Functional-medicine evaluation of patients on elimination or detoxification protocols targeting environmental toxins
Sample collection and turnaround
Sample type
Urine (random)
Fasting required
No
Collection method
At-home collection kit
Turnaround
10–14 business days
Collection notes
The patient collects a mid-stream random urine sample at home using the sterile container provided in the kit. First morning void is often preferred for creatinine stability, but random collection is acceptable. Withhold mycotoxin binders (activated charcoal, bentonite, cholestyramine) for 48–72 hours before collection if baseline exposure assessment is the goal. Collect in a clean, dry environment away from visible mould. Seal the specimen and return via the prepaid shipping label; avoid delays, as some mycotoxins degrade at room temperature.
Specimen requirements
Minimum 10 mL random urine in the provided sterile container. Record collection time. Specimen should be frozen if shipment is delayed beyond 24 hours. Creatinine is measured in parallel to normalise concentrations.
What can affect MycoTOX results?
Food-borne mycotoxins are absorbed and renally excreted; recent consumption of contaminated products can elevate urinary levels independent of environmental mould exposure.
Mycotoxins have varied half-lives; some clear within days, so a single random urine may miss episodic exposure, and serial or first-morning-void collections may improve sensitivity.
Impaired renal clearance prolongs mycotoxin half-life, while dilute urine lowers creatinine-corrected concentrations; results are normalised to creatinine, but extremes of hydration or renal disease affect interpretation.
Genetic polymorphisms in phase I and phase II detoxification enzymes, gut permeability, and microbiome composition alter mycotoxin bioavailability and clearance, so urinary levels reflect both exposure and individual handling.
Activated charcoal, bentonite clay, cholestyramine, and other binders can reduce gastrointestinal absorption of mycotoxins, lowering urinary excretion; withhold binders for 48–72 hours before collection if baseline exposure is being assessed.
Collection in a visibly mould-contaminated bathroom or use of a non-sterile container can theoretically introduce external mycotoxin contamination, though this is rare; follow kit instructions carefully.
What do MycoTOX results mean?
Elevated
Elevation of one or more mycotoxins indicates recent exposure via inhalation, ingestion, or dermal contact. Aflatoxin and ochratoxin point to dietary sources or Aspergillus environmental contamination; trichothecenes (roridin, verrucarin, T-2) suggest Stachybotrys or Fusarium; gliotoxin implicates Aspergillus; zearalenone indicates Fusarium-contaminated grain or environmental exposure; citrinin and sterigmatocystin reflect Penicillium or Aspergillus. Multiple elevations suggest cumulative exposure from a contaminated environment. Results must be paired with environmental inspection, symptom correlation, and follow-up after remediation or dietary change to establish clinical relevance.
Normal
Results within reference ranges suggest no detectable recent exposure to the panel's mycotoxins. In patients with persistent symptoms attributed to mould, consider retesting after suspected re-exposure, evaluating other biotoxins or inflammatory markers, or broadening the differential to non-mould aetiologies.
Reduced
Low or non-detectable levels indicate no recent significant exposure to the tested mycotoxins, or effective clearance following remediation. They do not exclude past exposure, sensitivity to other unmeasured mycotoxins, or non-mycotoxin-related illness.
Note: This panel detects urinary metabolites, not tissue burden or cumulative lifetime exposure; mycotoxins clear over days to weeks, so timing matters. Reference ranges are derived from populations without known exposure and are not universal diagnostic thresholds. The clinical significance of low-level detections in the absence of corroborating symptoms or environmental findings is uncertain. Interpretation should be cautious and multidisciplinary, integrating environmental hygiene, symptom patterns, and response to remediation rather than relying on laboratory values alone.
Frequently asked questions
The panel quantifies nine mycotoxins: aflatoxin M1, ochratoxin A, sterigmatocystin, roridin E, verrucarin A, gliotoxin, zearalenone, T-2 toxin, and citrinin. Each reflects exposure to specific mould species common in water-damaged buildings or contaminated food.
How to access the MycoTOX test
The MycoTOX reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: October 7, 2026
Last reviewed: October 7, 2026
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- Pestka JJ, Smolinski AT. Deoxynivalenol: toxicology and potential effects on humans. J Toxicol Environ Health B Crit Rev. (2005)
- Hope J. A review of the mechanism of injury and treatment approaches for illness resulting from exposure to water-damaged buildings, mold, and mycotoxins. ScientificWorldJournal. (2013)
- Straus DC. The possible role of fungal contamination in sick building syndrome. Front Biosci (Elite Ed). (2011)
- European Food Safety Authority (EFSA) Panel on Contaminants in the Food Chain. Scientific opinion on the risks for public health related to the presence of zearalenone in food. (2011)
- International Agency for Research on Cancer (IARC) monographs on aflatoxins and ochratoxin A. (2012)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.