What mycotoxins are tested in cannabis, and what produces them?
Five mycotoxins are currently regulated in most licensed cannabis markets:
Aflatoxins B1, B2, G1, G2: produced primarily by Aspergillus flavus and Aspergillus parasiticus. Aflatoxins are among the most potent naturally occurring carcinogens identified. Aflatoxin B1 in particular is classified as a Group 1 carcinogen by the International Agency for Research on Cancer. Acute exposure at high levels causes liver failure; chronic low-level exposure is associated with liver cancer and immune suppression. The FDA action level for aflatoxins in food is 20 ppb (µg/kg); most state cannabis programs adopt this same threshold.
Ochratoxin A: produced by Aspergillus ochraceus, Aspergillus carbonarius, and various Penicillium species. Ochratoxin A is a nephrotoxin that damages kidneys and is classified as a possible human carcinogen (Group 2B, IARC). It is the most frequently detected mycotoxin in cannabis compliance testing across multi-state data, though detections rarely exceed action limits. Most programs set the limit at 20 ppb, matching food safety standards.
Research published in ScienceDirect (2025) found that ochratoxin A was the most commonly detected mycotoxin in both flower and concentrate compliance testing across eleven states, but the overall failure rate remained low (<0.02%). This data suggests that regulated mycotoxin failures are uncommon under normal conditions, but also that ochratoxin A is present in measurable quantities more often than Aspergillus-specific failures might suggest.
Why do mycotoxins survive processing and remediation?
The critical property of mycotoxins that separates them from living organisms is their chemical stability. Unlike bacteria or mold spores, which can be inactivated by heat, radiation, or oxidizing chemistry, mycotoxins are resistant to the temperatures and processes that inactivate microorganisms.
Research confirms that aflatoxins require temperatures up to 250°C with extended exposure for significant reduction in lipid matrices, temperatures not reached during normal cannabis processing or use. Ochratoxin A showed no significant reduction after baking at 244°C for 25 minutes in dough matrices. The temperatures reached during cannabis combustion may inactivate some mycotoxins in the consumed fraction, but mycotoxins on cannabis surfaces and in inflorescence tissue accumulate during the production phase regardless.
Irradiation reduces viable Aspergillus counts and disrupts biosynthetic genes for toxin production, but research confirms that residual mycotoxin concentrations persist in irradiated samples. A batch remediated to pass Aspergillus microbial testing may still carry surface-level mycotoxin residues if colonization occurred before remediation.
This is why mycotoxin risk management requires preventing Aspergillus colonization during the grow, not treating the product after the fact.
What is the relationship between Aspergillus testing and mycotoxin testing?
They are related but measure different things, and passing one does not guarantee passing the other.
Aspergillus testing (presence/absence in most programs) detects whether living or recently viable Aspergillus DNA is present in the sample. A positive result means Aspergillus was present at some point. It does not directly measure whether mycotoxins were produced.
Mycotoxin testing measures the actual chemical concentration of aflatoxins and ochratoxin A in the product, regardless of whether viable Aspergillus is currently detectable. A product can pass Aspergillus testing (because the mold was killed) while still failing mycotoxin testing (because the toxins it produced remain).
Conversely, a product can have detectable Aspergillus at sub-action-level counts and low or undetectable mycotoxin concentrations; Aspergillus produces mycotoxins under specific conditions (particularly at water activity above 0.80 on substrate), and its presence does not automatically mean toxin production occurred.
The implication for operators: Aspergillus and mycotoxin panels answer different questions. Both should be understood on the COA, not treated as redundant.
What conditions drive mycotoxin accumulation on cannabis?
Mycotoxin production is not an automatic consequence of mold presence. The conditions that promote it:
Water activity above 0.80 on substrate. Aspergillus mycotoxin production requires sufficient available moisture. Cannabis flower below 0.65 to 0.70 aw is a poor substrate for mycotoxin accumulation, which is why drying to appropriate water activity is protective not just for TYM counts but for mycotoxin risk.
Extended exposure time. Mycotoxins accumulate over time as the mold colony grows and metabolizes. A brief Aspergillus presence on a product that is quickly dried to safe water activity produces less toxin than one that remains above the 0.80 aw threshold for extended periods.
Dense inflorescence with moisture retention. Dense bud structures maintain internal water activity above the room ambient even when surface conditions appear dry. The microclimate inside a dense inflorescence can remain above Aspergillus activation threshold while the room humidity appears controlled.
Damaged or stressed plant material. Aspergillus colonization initiates more readily on damaged tissue: physical wounds, pest damage, or senescing material provides entry points and substrate that intact, healthy tissue resists.
What about Fusarium mycotoxins? Why aren't they tested?
The regulatory gap around Fusarium mycotoxins is one of the most significant unaddressed risks in current cannabis testing programs. Research published in PMC (2025) evaluated seized cannabis samples from Arizona and California and found Fusarium-derived mycotoxins, including trichothecenes, fumonisins, and zearalenone, present in samples where no regulated mycotoxin (aflatoxin or ochratoxin A) was detected.
As of 2026, no U.S. state requires testing for Fusarium-derived mycotoxins in cannabis. The research notes this explicitly: Fusarium species infect cannabis inflorescences and show potential for mycotoxin production, but current testing requirements do not capture them. For operators growing in Fusarium-positive environments, this gap means that mycotoxin risk from that contamination pathway is not measured by the COA.