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The chemical structure of fumonisin B1.[citation needed]

Fumonisin refers to any one of a class of related chemical structures, the fumonisins, that constitute a group of fungal mycotoxins originally identified with genus Fusarium, a mycotoxin known for its contamination of infested corn seed[1][better source needed] (as well as other plants and foodstuffs[citation needed]), the infecting species, in particular, being within Fusarium's Liseola section.[2] As shown in the example in the figure (of fumonisin B1), members of the family are composed of a central "chai[n] of about 20 carbons", and bear an "acidic ester, acetylamino and sometimes other substituents".[1][better source needed] The fumonisins inhibit ceramide synthetase an enzyme[clarification needed] that converts sphingolipids to ceramides.[1]

Family background

[edit]

As of 2000, 15 different fumonisins had been reported, and other minor metabolites have been characterized.[3][needs update] More specifically, the term refers primarily to the family of compounds that includes the widely studied fumonisins B1, B2, B3, and B4, as well as others.[citation needed] As chemical agents, the fumonisins are distinct[citation needed] from the large family of Fusarium trichothecene (T-2-type) mycotoxins,[4] and from the Fusarium estrogenic metabolite, zearalenone, an F-2-type mycotoxin.[5]

In 2015, a unique supposed class of non-aminated fumonisins was reported on grapes infected with Aspergillus welwitschiae, where toxicities have not yet been established.[6][non-primary source needed]

Mechanisms of toxicity

[edit]

The fumonisins inhibit ceramide synthetase (sphingosine N-acyltransferase), an enzyme[clarification needed] that converts sphingolipids to ceramides.[1][better source needed]

Other research

[edit]

Suggestion has appeared that the fumonisins are not genotoxic, and so might belong to the peroxisome proliferator class of non-genotoxic carcinogens.[7][needs update]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Fumonisin

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from Grokipedia
Fumonisins are a family of mycotoxins produced by fungi, particularly Fusarium verticillioides and Fusarium proliferatum, which contaminate cereal crops such as , , and during growth or storage under warm, humid conditions. These toxins, with fumonisin B1 (FB1) being the most abundant and potent analog, feature a backbone modified by tricarballylic acid groups, rendering them chemically stable during . Globally, fumonisins affect approximately 25–50% of crops, leading to significant agricultural losses and posing risks to and human health. In animals, exposure to fumonisins causes severe toxic effects, including equine leukoencephalomalacia (a fatal disorder in horses), porcine pulmonary edema (fluid accumulation in swine lungs), and hepatotoxicity or in various species through inhibition of ceramide synthase, disrupting sphingolipid metabolism. In humans, epidemiological studies link high dietary intake—primarily from maize-based staples in regions like , , and parts of —to esophageal cancer, defects in newborns, and stunted growth in children, with FB1 classified as a Group 2B possible by the International Agency for Research on Cancer (IARC). The Joint FAO/WHO Expert Committee on Food Additives has established a provisional maximum tolerable daily intake (PMTDI) of 2 μg/kg body weight per day to mitigate these risks. Regulatory bodies monitor fumonisin levels in food and feed to protect ; for instance, the U.S. Food and Drug Administration (FDA) provides guidance limits of 2–4 ppm in human foods and 5–100 ppm in animal feeds, depending on the product. Management strategies emphasize prevention through , resistant varieties (e.g., Bt hybrids), proper drying and storage of grains, and post-harvest interventions like sorting, , or enzymatic detoxification using tools such as FUMzyme. Despite these measures, contamination remains a challenge in developing regions, underscoring the need for integrated approaches combining agricultural practices, surveillance, and dietary diversification.

Discovery and Nomenclature

Discovery

Fumonisins were first isolated in 1988 from corn cultures of the fungus Fusarium moniliforme (now known as Fusarium verticillioides) strain MRC 826 by a team led by Willem C. A. Gelderblom and Paul G. Thiel at the Programme on Mycotoxins and Experimental Carcinogenesis, Medical Research Council, in Tygerberg, South Africa. This strain had been previously implicated in outbreaks of equine leukoencephalomalacia (ELEM), a fatal neurological disease in horses, prompting the investigation using a short-term rat liver cancer initiation-promotion bioassay to identify bioactive compounds. The isolation yielded two major compounds, later characterized as novel mycotoxins. The toxins were named fumonisin B₁ (FB₁) and fumonisin B₂ (FB₂) due to their production by , with FB₁ identified as the primary component exhibiting hepatocarcinogenic and hepatotoxic effects in rats. Structural elucidation confirmed FB₁ as a diester of a tricarballylic acid and a long-chain amino , distinguishing it from previously known Fusarium mycotoxins. Early characterization involved collaborative efforts between the South African team and researchers from the (USDA), who analyzed similar isolates from U.S. corn samples to confirm toxin production across strains. In the early 1990s, fumonisins were confirmed as the causative agents of porcine (PPE), a lethal in swine, following U.S. outbreaks linked to moldy corn feed; experimental dosing with FB₁-containing cultures reproduced the condition, with symptoms appearing within days. This milestone built on 1990 reports associating F. moniliforme isolates from PPE cases with fumonisin production. In 2002, the International Agency for Research on Cancer (IARC) classified fumonisin B₁ as a Group 2B possible human carcinogen based on sufficient evidence of carcinogenicity in experimental animals and limited human data.

Classification and Types

Fumonisins are a group of mycotoxins produced primarily by species, classified into four main series—A, B, C, and P—based on variations in their backbone structure, functional groups, and modifications. The B series (FB) represents the most prevalent and well-studied group, consisting of analogs such as FB1, FB2, FB3, and FB4, which share a 20-carbon aminopolyol backbone with two tricarballylic (TCA) esterified to hydroxyl groups at C14 and C15. These analogs differ primarily in their patterns along the backbone: FB1 possesses hydroxyl groups at C3, C5, and C10, while FB2 lacks the hydroxyl at C10, FB3 lacks it at C5, and FB4 lacks both. The A series (FA) analogs, such as FA1 and FA2, are N-acetyl derivatives of the B series, featuring an on the amino terminus at C2, and they may exhibit different patterns. In contrast, the P series (FP) includes analogs with a modified terminal group at the C2 position, such as a 3-hydroxypyrrolidine moiety replacing the aminomethyl group of the B series, while the C series (FC) is distinguished by a shortened 19-carbon backbone lacking the adjacent to the compared to the B series. These less common series, particularly the A and P types, are typically produced by modified or specific strains under certain conditions. In naturally contaminated samples, such as maize, the B series dominates, with FB1 comprising 70–80% of the total fumonisins, FB2 accounting for 15–25%, and FB3 making up 3–8%, reflecting their relative production efficiencies in fungal cultures. The A, C, and P series analogs occur at much lower levels, often below detectable thresholds in standard agricultural samples, underscoring the prominence of the B series in environmental and food safety contexts.

Chemical Structure and Properties

Molecular Structure

Fumonisins are a family of mycotoxins characterized by a linear backbone consisting of 20 carbon atoms in the case of the prototypical fumonisin B1 (FB1), which mimics the structure of the sphingoid base sphinganine. This backbone is an aminopolyhydroxyalkane with an amino group at the C-2 position and hydroxyl groups at C-3, C-5, C-10, C-14, and C-15, enabling its interference with metabolism. The molecular formula of FB1 is C34H59NO15, reflecting its diester structure formed by the attachment of two tricarballylic acid (propane-1,2,3-tricarboxylic acid) side chains to the hydroxyl groups at C-14 and C-15 of the backbone. These tricarballylic esters are critical functional groups that contribute to the molecule's polarity and , with the linkages involving the 1-carboxy groups of the acids and the specified backbone hydroxyls. The overall architecture positions the free amino group and hydroxyls to structurally resemble free sphinganine and its derivatives, facilitating in biochemical pathways. FB1 serves as the primary structural representative of the B-series fumonisins, with congeners such as FB2 differing by the absence of a hydroxyl group at C-10. The core 20-carbon chain and tricarballylic side chains are conserved across major variants, underscoring the shared molecular scaffold responsible for their toxicological profile.

Physical and Chemical Properties

Fumonisins, exemplified by the predominant fumonisin B1 (FB1), manifest as a to off-white hygroscopic crystalline . This physical form arises from their polar molecular architecture, facilitating moisture absorption under ambient conditions. The molecular weight of FB1 is 721.8 Da, a value consistent across analytical characterizations that underscores its classification as a high-molecular-weight . FB1 demonstrates high solubility in , exceeding 20 mg/mL at , attributed to its ionic amino and multiple groups that promote hydration and dissolution. In contrast, it exhibits low solubility in non-polar solvents like or , reflecting the molecule's hydrophilic nature driven by these polar functional groups. The pKa values for FB1 are approximately 3.5 for the tricarballylic acid moieties and 9.2–9.3 for the primary , influencing its ionization and behavior in aqueous environments across physiological ranges. Regarding stability, fumonisins are notably thermostable, enduring temperatures up to 100°C during typical without significant degradation, as evidenced by retention in cooked products. However, they undergo and degradation under strong alkaline conditions, such as pH >10, where the linkages in the side chains are cleaved, reducing . FB1 shows weak inherent UV absorption, with detection often relying on derivatization for enhanced signal at wavelengths around 390–410 nm.

Biosynthesis

Producing Fungi

Fumonisins are primarily produced by certain species within the fungal genus , particularly Fusarium verticillioides (formerly known as F. moniliforme) and F. proliferatum, which are the most prolific and commonly associated producers due to their high toxin yields and frequent occurrence in agricultural settings. These species generate fumonisins such as FB1 and FB2 through polyketide synthase-mediated pathways, with F. verticillioides capable of producing up to 17,900 mg/kg of FB1 under optimal conditions. Ecologically, F. verticillioides and F. proliferatum serve dual roles as endophytes and pathogens in (Zea mays), colonizing tissues asymptomatically as endophytes while also inciting diseases like ear rot when conditions favor . They exhibit a global distribution, thriving in warm, humid environments such as , the , and tropical regions of and , where maize cultivation predominates. In addition to the primary producers, minor fumonisin production has been documented in species like F. nygamai and F. napiforme, though their contributions are less significant and often limited to specific geographic isolates. Strain variability is notable, with toxigenic strains possessing the —responsible for fumonisin —contrasting non-toxigenic ones that lack this cluster or produce negligible amounts, leading to genetic clustering within sections such as Liseola. This variability influences the reliability of fumonisin detection in field populations, where less than 50% of isolates from secondary species may be toxigenic.

Biosynthetic Pathway

The fumonisin biosynthetic pathway is encoded by a consisting of 17 contiguous genes, designated FUM1 and FUM6 through FUM21, located on the chromosomes of species such as verticillioides. This cluster orchestrates the production of fumonisins through coordinated expression of enzymes involved in assembly and subsequent modifications. The primary host for this pathway is verticillioides, where the cluster enables synthesis during infection of kernels. The pathway initiates with the iterative condensation of units by the encoded by FUM1, which assembles a linear chain backbone consisting of approximately 18 carbons. This chain undergoes further modifications, including the addition of an group via the aminotransferase activity of FUM8, which transfers an amino group from to form the aminopolyol essential for fumonisin activity. Subsequent steps involve the esterification of tricarballylic acid moieties to hydroxyl groups on the backbone, catalyzed by enzymes encoded by FUM10 ( synthetase), FUM14 ( synthetase-like condensation domain), and FUM15 (hydroxylase), resulting in the characteristic tricarballylic ester side chains. These reactions proceed iteratively, with FB1 emerging as the predominant product due to the efficiency of the hydroxylations and esterifications at key positions. Regulation of the pathway occurs primarily at the transcriptional level, with expression of the FUM cluster regulated in response to carbon sources such as glucose and , with sucrose repressing production under certain conditions. This nutrient-dependent control ensures that fumonisin production aligns with favorable growth conditions in the host plant environment.

Occurrence and Contamination

In Crops and Environment

Fumonisins primarily contaminate kernels, where they are produced by species such as Fusarium verticillioides and F. proliferatum during pre- and post-harvest stages. In infested fields, total fumonisin concentrations can reach up to 100 ppm, particularly in regions with favorable conditions for fungal growth, though average levels in commercial often range from 1 to 5 ppm. These mycotoxins accumulate mainly in the pericarp and germ of the kernel, leading to widespread contamination in maize-based agricultural products. Globally, fumonisin incidence is highest in major maize-producing areas, with hotspots including the Midwest , where up to 50% of samples exceed regulatory thresholds in drought-affected years; , reporting a positive rate of 87% in new-season maize from 2017–2021; , particularly in northern Italian fields, with frequent detections; and , linked to historical outbreaks from contaminated maize consumption. extends beyond raw grain, carrying over into where fumonisins persist at levels of 0.5–10 ppm, and into processed foods such as tortillas, where during reduces but does not eliminate total fumonisins, retaining 40–50% of original concentrations. Estimates suggest that 25–50% of global and maize products are affected to varying degrees. While is the dominant substrate, fumonisins occur in trace amounts in other cereals like , , and , typically below 1 ppm and far less prevalent than in maize. In , contamination is generally low to medium, with levels rarely exceeding 2 ppm in commercial production areas, and in , detections are sporadic and associated with co-infestation by species. Fumonisins exhibit environmental persistence, remaining stable in and residues for extended periods, which facilitates year-to-year cycles as propagules overwinter in stubble and debris. This residue-bound stability contributes to recurring infections in subsequent crops, with studies showing fumonisin residues detectable in field soils at concentrations up to 0.1–1 ppm even after harvest. Such persistence underscores the role of and residue management in breaking cycles.

Factors Influencing Production

Fumonisins are primarily produced by species, such as Fusarium verticillioides and Fusarium proliferatum, with environmental conditions playing a critical role in modulating toxin levels in . Temperature and are key climatic factors influencing production; optimal fumonisin synthesis occurs at 25–30°C and a (a_w) of 0.98, where fungal growth and toxin biosynthesis are maximized on substrates. stress further exacerbates production by compromising plant defenses, increasing susceptibility to infection and elevating fumonisin concentrations during kernel development. Agronomic practices also significantly affect fumonisin yields. Insect damage, particularly from the (Ostrinia nubilalis), creates entry wounds in maize ears and stalks, facilitating colonization and substantially higher toxin accumulation compared to undamaged plants. Similarly, elevated nitrogen fertilization rates, such as those exceeding 200 kg ha⁻¹, enhance fumonisin production by promoting lush plant growth that indirectly supports fungal proliferation, though excessive rates can sometimes stress plants and amplify contamination. Post-harvest handling influences fumonisin levels through storage conditions. Moisture contents above 15% in stored grains foster growth and toxin production, as these levels correspond to a_w values permissive for fungal activity, leading to rapid contamination if not controlled. Emerging global trends linked to , including warmer temperatures and erratic precipitation, are projected to heighten fumonisin risks in maize-producing regions by extending favorable conditions for throughout the growing and storage seasons.

Toxicology and Health Effects

Mechanism of Action

Fumonisins, particularly fumonisin B1 (FB1), exert their toxicity primarily by inhibiting synthase, a key enzyme in that catalyzes the N-acylation of sphinganine or with fatty to form dihydroceramide or , respectively. This inhibition blocks de novo synthesis, resulting in the accumulation of sphinganine and its 1-phosphate derivative, while depleting levels of complex such as , , and glycosphingolipids. The structural of FB1 to sphingoid bases like sphinganine enables this interference in the biosynthetic pathway. FB1 binds competitively to the of ceramide synthase, occupying the substrate-binding pocket and preventing the normal interaction of sphinganine and . In mammalian cells, this binding exhibits an in the range of 1-10 μM, with variations depending on the specific ceramide synthase isoform and tissue, such as approximately 7 μM in neuronal cells and 0.1 μM in rat liver microsomes. The disruption of sphingolipid homeostasis leads to several downstream cellular consequences. Depletion of complex compromises integrity and fluidity, impairing and membrane-associated functions. Accumulated sphingoid bases, such as sphinganine, promote by activating pathways involving and calcium signaling. Additionally, the inhibition indirectly interferes with metabolism by compromising glycosylphosphatidylinositol (GPI)-anchored proteins essential for folate transporters, thereby reducing uptake and utilization in cells.

Effects in Animals

Fumonisins, particularly fumonisin B1 (FB1), are highly toxic to , primarily manifesting as equine leukoencephalomalacia (ELEM), a fatal characterized by in the of the . Horses ingesting feed contaminated with FB1 at concentrations exceeding 10 ppm develop symptoms including , head pressing, circling, and depression, often progressing to and death within 1 to 3 days of onset. In confirmed cases from 1989 to 1990, FB1 levels in implicated feeds ranged from less than 1 ppm to 126 ppm, with the majority surpassing 10 ppm across various feed types such as corn, screenings, and pelleted rations. Experimental feeding of naturally contaminated rations at 44 ppm and 88 ppm FB1 induced ELEM in horses after 30 to 60 days of exposure, confirming the mycotoxin's role in lesion formation. This condition arises from FB1's inhibition of , disrupting essential for neural integrity. In swine, fumonisins induce porcine pulmonary edema (PPE), a syndrome involving acute accumulation of fluid in the lungs and hydrothorax, leading to respiratory distress, , and sudden death. Feeds contaminated at 20 to 360 ppm FB1 have been associated with outbreaks of PPE, where mortality rates in affected herds reached up to 20%, particularly in growing pigs exposed for several days to weeks. Experimental studies demonstrate that FB1 concentrations of 175 ppm in diets provoke severe within 5 to 7 days, accompanied by elevated pulmonary artery pressure, reduced , and left-sided . Lower levels, such as 101 ppm, elevate serum liver enzymes and cause hepatic , while 23 ppm induces histologic liver damage, highlighting dose-dependent multi-organ effects in pigs. Fumonisins exhibit toxicity across other animal species, with rats showing pronounced hepatotoxicity including apoptosis, necrosis, and proliferation of hepatocytes at dietary FB1 levels as low as 23 ppm. In poultry, exposure to FB1 results in reproductive impairments such as decreased egg production and hatchability, alongside reduced growth rates at concentrations exceeding 50 ppm in feed. Acute toxicity studies in mice report an intraperitoneal LD50 for FB1 of approximately 15 mg/kg body weight, underscoring its potential for rapid systemic effects in rodents.

Effects in Humans

Fumonisins, particularly fumonisin B1 (FB1), have been epidemiologically linked to increased incidence of in regions with high consumption, such as in and certain areas in . In , studies in high-risk areas showed correlations between chronic consumption of moldy corn contaminated with verticillioides and rates, with estimated daily intakes ranging from 14 to 440 μg/kg body weight in affected populations. Similarly, in China's and Linxian regions, elevated FB1 levels in home-grown corn (up to 1,108 μg/kg) were associated with higher risk, where dietary exposure from contaminated grains contributed to the disease burden in maize-dependent communities. These associations are supported by prospective cohort studies measuring urinary biomarkers as indicators of fumonisin exposure. Maternal exposure to fumonisins has been implicated in elevated risks of defects (NTDs) in , notably in populations along the -Mexico border and in parts of . In , a 1990–1991 cluster of NTDs among Mexican-American women consuming corn tortillas was linked to fumonisin contamination in , with exposure levels proportionate to risk up to a threshold beyond which fetal lethality may occur, potentially through disruption of transport and metabolism. In , similar patterns emerged in Province, where high intake and fumonisin presence correlated with NTD incidence, and maternal exposure interfered with -dependent closure, as evidenced by altered profiles in exposed individuals. models corroborate these human risks, demonstrating dose-dependent NTDs in via comparable mechanisms. Acute effects of fumonisin exposure in humans are rare and typically limited to gastrointestinal distress, such as and , observed at high single doses from heavily contaminated , though no large-scale outbreaks have been documented. For chronic exposure, the Joint FAO/WHO Expert Committee on Food Additives (JECFA) established a provisional maximum tolerable daily intake of 2 μg/kg body weight per day for fumonisins B1, B2, and B3 combined, based on no-observed-adverse-effect levels for in animal studies extrapolated to humans, emphasizing the need to minimize long-term intake to prevent potential carcinogenic and developmental risks.

Detection and Analysis

Analytical Methods

Analytical methods for fumonisin detection primarily rely on chromatographic and techniques, enabling precise identification and quantification in contaminated samples such as and feed. (HPLC) with detection remains a standard approach, particularly after post-column derivatization to enhance sensitivity, as fumonisins exhibit weak native due to their . In HPLC-fluorescence detection (HPLC-FLD), samples are typically extracted with methanol-water mixtures, cleaned up via , and derivatized with o-phthaldialdehyde (OPA) to form fluorescent isoindoles, followed by separation on a reversed-phase C18 column using a methanol-phosphate mobile phase. This method achieves limits of detection (LOD) in the range of 0.04–0.13 µg/kg for major analogs like fumonisin B1 (FB1) and B2 (FB2), with limits of quantification (LOQ) around 2.7–3.0 µg/kg, and recovery rates often exceeding 95%. HPLC-FLD provides high specificity for individual fumonisin analogs but requires skilled operation and derivatization steps, making it suitable for confirmatory analysis in laboratories. Liquid chromatography tandem mass spectrometry (LC-MS/MS) has emerged as the gold standard for multi-mycotoxin screening, offering simultaneous detection of fumonisins alongside other toxins without derivatization, leveraging in positive mode for structural confirmation via multiple reaction monitoring. Extraction protocols similar to HPLC are used, often with acetonitrile-water-formic acid, followed by optional cleanup; typical LODs range from 0.001–1 µg/kg (1–1000 ng/g) in food matrices like , with LOQs of 0.01–10 µg/kg and recoveries of 80–115%. This technique excels in sensitivity and selectivity, enabling trace-level detection in complex samples, though it demands expensive instrumentation and expertise. Immunoassays, such as enzyme-linked immunosorbent assay (), provide rapid, cost-effective screening alternatives, utilizing antibodies specific to fumonisin structures for competitive binding formats. Commercial ELISA kits, like AgraQuant, involve methanol-water extraction and colorimetric detection at 450 nm, achieving LODs of approximately 0.2–0.5 ppm (200–500 µg/kg) and recoveries near 100%, though they may overestimate total fumonisins due to among analogs. While less accurate than for precise quantification, ELISA's speed (under 2 hours) and portability make it ideal for field or high-throughput testing, often serving as a preliminary step before confirmatory methods. Emerging methods, including aptamer-based biosensors and microfluidic assays, aim for real-time, on-site detection by exploiting aptamers that bind fumonisins with high affinity, integrated with or electrochemical readouts. For instance, aptamer-linked assays on microfluidic platforms achieve LODs below 1 ng/mL for FB1, offering advantages in portability and reduced sample volume over traditional methods. These innovations, such as surface-enhanced aptasensors, provide rapid results (under 30 minutes) and sensitivities comparable to LC-MS/MS, with potential for multiplexed monitoring in resource-limited settings.

Sampling and Quantification

Effective sampling of fumonisins in grains, particularly , requires composite strategies to account for the heterogeneous distribution of contamination, which can lead to significant variability in results. For whole , a recommended approach involves collecting 50 increments of 100 g each to form a minimum 5 kg bulk sample, while maize on the cob necessitates sampling 50 cobs for at least 7.5 kg; processed products like or meal use 10 increments of 100 g for a 1 kg sample. In practical settings, such as truckloads, a 6-foot spiral hand probe is used to gather a minimum 5-pound aggregate sample following USDA representative patterns, with larger loads like train cars requiring at least 10 pounds collected during movement via augering at intervals. Stratified methods, including thorough mixing and subsampling from multiple pile locations, reduce variability by minimizing bias from localized hotspots of infection. Sample preparation begins with dividing the bulk sample—typically 45 kg—into 1.1 kg test portions using riffle division, followed by in a Romer mill to ensure at least 70% of particles pass a . Extraction employs solvent-based methods, commonly methanol-water mixtures (70:30 or 80:20 v/v), to solubilize fumonisins from 25 g subsamples, achieving efficient recovery. Cleanup often involves immunoaffinity columns to isolate fumonisins B1 and B2 from matrix interferences, with reported recovery rates ranging from 79% to 102% at spiking levels of 150–250 μg/kg in corn products. These steps maintain recoveries between 80% and 110% across various matrices, supporting reliable downstream . Quantification focuses on total fumonisin levels, calculated as the sum of FB1, FB2, and FB3 concentrations, often determined via HPLC or following extraction. In heterogeneous matrices like corn, uncertainty is dominated by sampling variance, with a (CV) of 16.6% at 2 mg/kg, contributing to an overall test CV of 21% when including preparation (9.1%) and analysis (9.7%) variances. This highlights the need for standardized protocols to ensure representative assessments in contaminated lots.

Regulation and Risk Management

Regulatory Limits

Regulatory limits for fumonisins have been established by major international and national authorities to mitigate risks associated with exposure, particularly the potential for and carcinogenicity in s and animals. In the United States, the (FDA) issued guidance in 2001 recommending maximum levels of total fumonisins (FB1 + FB2 + FB3) at 2–4 ppm in uncooked corn products intended for consumption, such as degermed dry-milled products (2 ppm), whole or partially degermed dry-milled products (4 ppm), and dry-milled corn bran (4 ppm); these levels remain in effect as reaffirmed in subsequent FDA oversight documents through the 2020s. For animal feeds, the FDA advises limits of 5 ppm in corn and corn by-products destined for equine and rabbits, and 20 ppm for (resulting in no more than 10 ppm in the total ration for ), with higher thresholds for less sensitive species like ruminants (up to 30 ppm in the ration). In the , Commission Regulation (EU) 2023/915 sets maximum levels for the sum of fumonisins B1 and B2 ranging from 0.2 to 1.4 mg/kg (wet weight) in -based foods, including 0.2 mg/kg in processed cereal-based baby foods containing , 0.8 mg/kg in -based breakfast cereals and snacks, 1.0 mg/kg in for final consumers and certain milling products, and 1.4 mg/kg in other milling products not for direct consumption; unprocessed grains are limited to 4.0 mg/kg. This regulation, effective from 2023 and consolidated as of 2025, repealed the prior EC No 1881/2006 while maintaining similar thresholds for fumonisins to ensure consumer safety. The Commission has established maximum levels for total fumonisins (FB1 + FB2 + FB3) at 4 mg/kg in unprocessed and 2 mg/kg in and maize meal, adopted in updates to the General Standard for Contaminants and Toxins in Food and Feed (CXS 193-1995) as of 2024 to facilitate while protecting . The Joint FAO/WHO Expert Committee on Food Additives (JECFA) established a group provisional maximum tolerable daily intake (PMTDI) of 2 μg/kg body weight per day for fumonisins B1, B2, and B3 (alone or combined), based on a from equine studies extrapolated to humans; this value has been reaffirmed in JECFA evaluations through 2025 with no major revisions despite ongoing monitoring of emerging exposure data.

Prevention and Control Strategies

Cultural practices play a crucial role in minimizing fumonisin contamination during production. Crop rotation with non-host crops, such as , reduces inoculum in the soil, thereby limiting fungal infection and subsequent toxin production. Planting resistant hybrids, including Bt maize varieties that express insecticidal proteins, decreases ear damage from pests like the , which serves as a vector for Fusarium verticillioides, resulting in fumonisin levels up to 90% lower compared to susceptible varieties. Timely harvest at physiological maturity, before prolonged exposure to environmental stresses like , further prevents stress-induced fungal proliferation and toxin accumulation. Post-harvest handling is essential for preventing further fumonisin development and reducing existing contamination. Rapid drying of harvested to below 14% moisture content inhibits fungal growth and biosynthesis during storage. Sorting and removal of damaged or discolored kernels can eliminate up to 75% of contaminated grains, as these are primary sites of . For , chemical treatments such as ammoniation have been employed to partially detoxify fumonisins, though efficacy varies and it is more commonly used in combination with other methods. Biocontrol strategies offer environmentally friendly alternatives for fumonisin management. Application of non-toxigenic strains, such as F. oxysporum variants like "Fusaclean," competes with toxigenic species for resources, reducing fumonisin production by up to 80% in field trials. Integration of these approaches into Hazard Analysis and Critical Control Points (HACCP) systems along the ensures systematic monitoring and intervention at key stages, from farming to , to maintain low contamination levels. Recent advances in 2024-2025 include AI-enhanced monitoring, such as coupled with artificial neural networks for real-time detection of fumonisin in , enabling proactive adjustments.

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