Molds in food and health risks

Evidence Review

Aflatoxin B1 as a liver carcinogen (Hamid et al., 2013)

Hamid and colleagues reviewed the global distribution and mechanistic evidence for aflatoxin B1 as a cause of hepatocellular carcinoma (HCC), focusing on sub-Saharan Africa and Southeast Asia where both aflatoxin exposure and liver cancer rates are high [1]. The review summarized the molecular pathway to carcinogenesis: after ingestion, AFB1 is metabolized in the liver to AFB1-8,9-epoxide, a reactive intermediate that forms bulky DNA adducts. These adducts cause characteristic G-to-T transversions in codon 249 of the TP53 tumor suppressor gene — a mutation signature so specific to AFB1 that it has been used as a molecular epidemiology marker in human studies. When hepatitis B virus (HBV) infection coexists with high AFB1 exposure, the two act synergistically — the combined relative risk of HCC is not merely additive but multiplicative.

IARC classified AFB1 as Group 1 (carcinogenic to humans) based on sufficient evidence from both animal studies and human epidemiology. Population-attributable fraction estimates suggest AFB1 contributes to 4.6–28.2% of all HCC cases globally, with the highest burden in Africa and Southeast Asia where regulatory limits are weakly enforced and staple diets are corn- and groundnut-heavy. In North American and European populations where food safety monitoring is robust and peanut products are rigorously tested, individual exposure from any single contaminated product is far less likely, but cumulative exposure across multiple products over years remains the primary concern.

Ochratoxin A in coffee: global exposure data (Massahi et al., 2024)

This 2024 systematic review by Massahi et al. synthesized worldwide data on ochratoxin A across all coffee product categories including green coffee, roasted beans, ground coffee, instant coffee, and espresso [2]. Key findings:

• OTA was detected in virtually all coffee categories worldwide, though at concentrations that varied enormously by origin, processing, and form
• Wet-processed (washed) green coffees showed consistently lower OTA levels than natural-processed coffees — a finding attributed to the fermentation and washing steps that remove the Aspergillus spores on the outer bean layers before drying
• Roasting significantly reduces OTA compared to green coffee, with darker roasts achieving greater reduction (estimated 40–80% OTA reduction depending on bean type and roast profile)
• Instant coffee showed among the lowest OTA levels per serving due to dilution during manufacturing and high-temperature processing steps
• Human health risk assessment found that for average consumers in most countries, estimated daily intake remained below the tolerable daily intake (TDI) established by EFSA (17 ng/kg body weight/day). However, heavy coffee drinkers — more than 4 cups daily — approached meaningful percentages of the TDI from coffee alone, not counting contribution from cereals, wine, and dried fruits

The authors noted significant heterogeneity across studies due to differing sampling methods, detection limits, and geographic origins, and recommended further biomonitoring studies to better characterize aggregate exposure.

Systematic review of mycotoxin exposure and human cancer risk (Claeys et al., 2020)

This comprehensive systematic review by Claeys et al. searched epidemiological databases for studies directly linking dietary mycotoxin exposure to human cancer incidence, mortality, or biomarkers [3]. Of the studies meeting inclusion criteria:

• The strongest and most consistent evidence concerned aflatoxins and hepatocellular carcinoma — the association is considered established at the epidemiological level, especially in populations with high hepatitis B prevalence where the synergistic interaction amplifies risk substantially
• For ochratoxin A, the evidence is suggestive but limited — most human data rely on cross-sectional biomarker studies rather than prospective cohorts, making causal inference difficult
• Fumonisins and esophageal cancer showed an association in studies from high-exposure regions (parts of southern Africa and China where corn is a dietary staple and processing is minimal), though confounding by other factors makes definitive attribution challenging
• The authors identified a major evidence gap: most prospective cohort studies with long-term cancer follow-up have not routinely measured dietary mycotoxin exposure, meaning the epidemiological database is thinner than for other dietary carcinogens like aflatoxin in high-incidence settings

The review concluded that reducing aflatoxin exposure remains the highest-priority public health intervention among the mycotoxins, particularly in low- and middle-income countries, and that food safety programs targeting maximum limits in grain staples have measurable population-level impact.

Human biomonitoring in a real-world exposure scenario (Kyei et al., 2022)

Kyei and colleagues conducted urinary biomonitoring in 350 pregnant women in rural Bangladesh — a population with high dietary dependence on rice, wheat, and legumes — measuring metabolites of multiple mycotoxins simultaneously to characterize co-exposure patterns [4]. This is methodologically important because most laboratory and regulatory studies examine single mycotoxins in isolation, while real human exposure involves simultaneous contamination of the diet across multiple compounds.

Key findings from the Bangladesh cohort:

• Aflatoxin B1 (measured as AFB1-lysine adduct in blood) was detected in 97% of participants, indicating near-universal exposure in this food environment
• Fumonisins and DON were detected in the majority of participants
• Co-exposure to three or more mycotoxins simultaneously was common, not exceptional
• The magnitude of exposure correlated with consumption frequency of specific food groups — corn, wheat products, and legumes were the strongest predictors of higher total mycotoxin load

The authors noted that existing tolerable daily intake values are derived from single-compound toxicity data and may underestimate risk for the combined exposures that are typical in real diets. This remains a recognized limitation in regulatory risk assessment frameworks globally, including those of the FDA and EFSA.

Reduction strategies during storage (Chulze, 2010)

Chulze reviewed the evidence on post-harvest strategies to limit aflatoxin and fumonisin accumulation in stored maize [5]. The review covered physical, chemical, and biological interventions applicable at the storage stage — the point where the largest preventable increases in contamination occur after harvest:

• Moisture and temperature control — the most evidence-backed intervention. Maintaining moisture below 13.5% and temperatures below 18°C essentially halts Aspergillus flavus growth and toxin production. In humid tropical environments, achieving this requires active drying infrastructure, not just ambient storage.
• Hermetic (airtight) storage — grain stored in sealed containers with modified atmosphere (low oxygen) shows substantially lower mycotoxin accumulation than open storage over equivalent time periods
• Sorting and selection — removing visually damaged, shriveled, or discolored kernels before storage removes a disproportionate share of the contamination, since mycotoxin levels cluster in damaged and insect-attacked grain
• Chemical fumigants and biological controls — several interventions (atoxigenic Aspergillus strains as competitive biocontrol, ammonia treatment, ozone fumigation) showed promise but had implementation barriers for smallholder settings

For consumers, the household-level takeaways from the storage literature are clear: proper storage conditions matter far more than whether a food was organically or conventionally grown. A well-stored conventional peanut has substantially lower mycotoxin risk than an organically grown one stored improperly in warm, humid conditions.

Overall evidence assessment

The risk from mycotoxins in food is real and well-established — aflatoxin B1 in particular holds the strongest evidence base of any naturally occurring food carcinogen. The key contextual factors:

Regulatory frameworks are meaningful. In the United States, European Union, and other countries with robust food safety monitoring, maximum limits for aflatoxins in peanuts, corn, tree nuts, and related products are enforced, and surveillance data generally show compliance. This provides a significant baseline level of consumer protection compared to regions with weaker enforcement.

Exposure is cumulative and continuous. Mycotoxins are not acute poisoning risks at typical dietary levels — the concern is chronic, low-level accumulation over years and decades. This makes the risk invisible in daily life but meaningful over a lifetime, particularly for people who eat corn-heavy, peanut-heavy, or grain-heavy diets without variety.

Co-exposure adds uncharacterized risk. The evidence that simultaneous exposure to multiple mycotoxins is the norm rather than the exception — and that combined effects may be more than additive — suggests that aggregate dietary mycotoxin exposure has not been fully characterized by existing single-compound regulatory frameworks [4].

Practical mitigation is feasible. Unlike some food contaminants that are difficult to avoid, mycotoxin exposure is meaningfully modifiable through food storage habits, purchasing choices, dietary variety, and coffee processing preferences — actionable interventions well within an individual's control.