This test is most useful if any of these apply to you.
STC (sterigmatocystin) is one of the lesser-known cousins of aflatoxin, a fungal toxin classified by the International Agency for Research on Cancer as a possible human carcinogen. It hides in foods you eat regularly, such as grains, coffee, cheese, nuts, and spices, and in the dust of damp buildings.
Measuring it in your urine gives you a window into your recent exposure to a substance that animal studies link to liver damage, kidney damage, and DNA injury. This is a research-grade marker without an official clinical cutoff, so the value comes from spotting unexpected exposure and watching how your numbers move over time.
Sterigmatocystin is not made by your body. It is a chemical produced by certain molds, mainly Aspergillus versicolor and Aspergillus nidulans. It is also a biological precursor of aflatoxin B1, one of the most potent natural cancer-causing substances known, sitting two enzymatic steps upstream of aflatoxin B1 in the same fungal pathway.
These molds grow on stored crops and in water-damaged buildings. Surveys around the world have detected sterigmatocystin in grains, corn, bread, cheese, spices, coffee, soybeans, nuts, animal feed, and silage. It also turns up in indoor dust in damp or poorly ventilated spaces, including a study of school classrooms in Malaysia where it was measurable in settled classroom dust.
The International Agency for Research on Cancer has placed sterigmatocystin in Group 2B, meaning it is considered a possible human carcinogen. That label comes mostly from animal and laboratory cell research. In those studies, sterigmatocystin damages liver and kidney cells, forms attachments to DNA called adducts, triggers oxidative damage (when reactive molecules harm cells), disrupts the energy-producing parts of cells (mitochondria), and pushes cells toward programmed death.
Human evidence is thinner but growing. Biomonitoring studies have found that sterigmatocystin is detectable in the blood and urine of healthy people in Europe, suggesting low-level exposure is widespread. What the marker on your test tells you is not whether you have a disease, but whether you are being exposed at a level your body is absorbing and excreting.
In animal studies, the liver and kidney are the two organs most consistently injured by sterigmatocystin. It can damage liver cells directly and has produced liver tumors in long-term animal experiments. Direct human evidence linking sterigmatocystin exposure to liver or kidney disease is limited, so the concern is mechanistic rather than proven.
If you already have liver or kidney conditions, an ongoing exposure picked up by this test is one variable worth removing from the picture while you investigate other drivers.
Beyond the IARC Group 2B classification, animal research has linked sterigmatocystin to lung tumors in mice, and laboratory studies on cultured human lung cells have shown disruption of cell cycle progression and other changes associated with cancer development. These findings come from animal and cell-culture work, not from human cohort studies, so they should be read as warning signals rather than proven risks.
Sterigmatocystin also rarely shows up alone. Biomonitoring data show it commonly appears together with aflatoxins, ochratoxin A, fumonisins, and other mold toxins. Combined exposures are harder to study but may matter more than any single toxin in isolation.
A 2020 biomonitoring study in Spain found measurable sterigmatocystin in about 86% of adult plasma samples after the lab used enzymes to break apart the bound, conjugated forms of the toxin. That high detection rate suggests broad, low-level exposure across the population, and shows that much of the sterigmatocystin in the body circulates in modified forms produced by your liver. Studies measuring sterigmatocystin in plasma (a related but different specimen than the urine measured by this test) help illustrate exposure patterns even though the matrix differs.
A separate study of Spanish children found the toxin in roughly 99% of plasma samples after similar enzyme treatment, with mean levels around 1.3 to 1.5 ng/mL. In Nigerian breast milk, sterigmatocystin was rare, appearing in 1 of 22 samples at about 1.2 ng/L. In waste recycling facilities, airborne sterigmatocystin was measurable but below 1 ng/m3, a level that the study authors judged as not posing a significant additional health risk to workers.
This test detects sterigmatocystin in your urine and reports the amount relative to creatinine (a waste product your kidneys filter at a steady rate). Pegging the number to creatinine adjusts for how concentrated or diluted your urine sample is, so a result from a thirsty morning and a well-hydrated afternoon become comparable.
A detectable result means your body has recently absorbed and is excreting sterigmatocystin. It does not by itself diagnose any disease. Most of what is known about safe versus harmful levels still comes from animal research and modeled human risk estimates rather than direct human outcome studies.
Sterigmatocystin is an emerging-research biomarker. There is no agreed clinical reference range, and the published exposure data (about 1 to 2 ng/mL in plasma in European children) come from descriptive population studies, not diagnostic thresholds. That means a single result on its own cannot tell you whether you are at imminent risk.
The useful question is not just whether the toxin is present, but how much is present compared to your last test, and whether other mycotoxins on the same panel are also elevated. Patterns and changes carry more weight than any single reading.
Because exposure is intermittent and depends on what you ate, where you slept, and which building you spent time in over the past few days, a single sterigmatocystin reading is a snapshot, not a sentence. Two readings months apart tell you whether your exposure is acute and one-off (something you ate that week) or chronic and ongoing (a moldy pantry, a damp office, repeated contaminated foods).
A sensible cadence is to get a baseline, retest in 3 to 6 months if you make changes to your diet or environment, and retest annually thereafter. If your first result is high, retesting after a few weeks of changes is the only way to know whether what you did worked.
If your sterigmatocystin shows up unexpectedly high, the next move depends on what else is on your panel and in your life. First, look at the other mycotoxins measured alongside it. A broad pattern of elevations across multiple mycotoxins points toward an environmental source (mold in your home or workplace) more than any single food. A spike limited to sterigmatocystin alone is more consistent with a recent dietary source.
Consider companion testing of liver enzymes (ALT, AST, GGT) and kidney function (creatinine, cystatin C, eGFR) to see whether your body shows signs of strain. If you live or work in a building you suspect of water damage, an environmental mold assessment of dust or air can confirm the source. For repeated high readings, an environmental medicine specialist can help you map exposure pathways and a hepatologist can help you monitor liver health over time.
Sterigmatocystin is best interpreted alongside these tests.
Sterigmatocystin is included in these pre-built panels.