Introduction

Infertility as a Global Health Concern

Infertility is a growing global health issue affecting millions of individuals and couples. Over the past 50 years, fertility rates have declined significantly, with sperm counts decreasing by more than 59% in North America, Europe, Australia, and New Zealand.1 Between 1990 and 2011, the global miscarriage rate increased by 2%,2 and an estimated 48 million couples and 186 million individuals worldwide struggle with infertility.3 Sub-Saharan Africa and South Asia bear a disproportionate burden, with infertility prevalence rates remaining high.3,4

While genetic, anatomical, and behavioral factors contribute to infertility, environmental exposures have emerged as critical but underexplored determinants of reproductive health.5 Factors such as endocrine-disrupting chemicals (EDCs), microplastics, and pollutants have been linked to declining fertility.6 Among these environmental toxins, mycotoxins—secondary metabolites produced by fungi—are of increasing concern, though their impact on human fertility has received limited attention.

Mycotoxins and Reproductive Health

Mycotoxins, harmful compounds produced by fungi such as Aspergillus, Fusarium, and Penicillium, commonly contaminate food and agricultural products. These toxins are well known for their carcinogenic, immunotoxic, and hepatotoxic effects,7 but emerging evidence suggests they may also impair reproductive health. Studies indicate that exposure to mycotoxins such as ochratoxin A (OTA) and zearalenone (ZEA) can disrupt hormone regulation, impair gametogenesis, and cause direct cellular toxicity to reproductive tissues.8 Understanding their role in infertility is essential, given the widespread presence of mycotoxins in food supplies, particularly in regions with warm climates and high agricultural contamination.

This review examines mycotoxin exposure’s mechanisms, evidence, and clinical implications on reproductive health. It synthesizes findings from human epidemiological studies and animal models to assess the extent of mycotoxins’ impact on fertility and highlights potential strategies for mitigating their harmful effects.

Mycotoxins: Definition, Sources, and Significance

Major Mycotoxin-Producing Genera & Types

Mycotoxins are toxic secondary metabolites produced by fungi, primarily Fusarium, Aspergillus, and Penicillium, with additional contributions from Alternaria, Claviceps, and Stachybotrys.9–11 These naturally occurring toxins contaminate food and agricultural products, posing serious health risks to humans and animals.9,10,12,13 Table 1 shows the major mycotoxins-producing genera with their sources and contamination of various foods.

Table 1.Major Mycotoxin-Producing Genera, Sources and Exposure
Mycotoxin Producing Fungi Common Sources Health Risks
Ochratoxin A (OTA) Aspergillus, Penicillium Cereals, coffee, dried fruits Endocrine disruption, nephrotoxicity
Zearalenone (ZEA) Fusarium Grains, maize Estrogenic effects, reproductive toxicity
Aflatoxins Aspergillus Peanuts, maize, dairy Carcinogenicity, immune suppression
Fumonisins Fusarium Corn, maize Neural tube defects, hepatotoxicity

Key Mycotoxins & their Sources

1. Fusarium Mycotoxins

Fumonisins (FBs), Zearalenone (ZEA), and Trichothecenes (DON, T-2, HT-2) are the three common mycotoxins belonging to this group. These are commonly found in grains, maize, and animal feed, often contaminating crops before and after harvest,14,15 particularly in warm climates (e.g., Africa). ZEA, is a non-steroidal oestrogenic mycotoxin that has biological effects even at low doses and disrupts endocrine function, impacting fertility even at low doses.16–18 Certain climates are more prone to contamination since Fusarium mycotoxin synthesis requires a temperature of about 25°C.19–21 For the above reasons, African nations tend to have greater levels of mycotoxin contamination.22,23

2. Aspergillus Mycotoxins

Aflatoxins (Afs) are highly toxic and carcinogenic mycotoxins produced by Aspergillus species, contaminating various crops such as corn, wheat, soybeans, peanuts, and dried fruits during storage and transport under specific temperature conditions.24,25 These toxins also affect livestock feed, leading to contamination of food products like nuts, vegetables, fish, poultry meat, coffee, and tea24,26). AFB1, AFB2, AFG1, and AFG2 are the most toxic, causing aflatoxicosis with documented reproductive toxicity.27,28

3. Penicillium Mycotoxins

Penicillium species contribute to contamination through Ochratoxins (OTA), Patulin (PAT), Mycophenolic Acid (MPA).29,30 These are commonly found in cereals, coffee, and dried fruits, colonizing commodities and foods during drying and storage particularly in developed countries.14,15 OTA exposure has been linked to significant male fertility issues, specifically impacting sperm viability and morphology.30,31

Prevalence and Global Exposure

Mycotoxin contamination is a global issue, with serious health and economic consequences and higher prevalence in humid climates that favor fungal growth.22 The Food and Agriculture Organisation (FAO) estimates that mycotoxins contaminate about 25% of agricultural goods worldwide each year, resulting in serious health issues and financial losses27,32,33

Mycotoxin exposure is widespread in developing nations, with high contamination levels reported in Africa and Asia.23,34 Regional factors like temperature, humidity, and poor hygiene influence mycotoxin prevalence.35 In African countries, an estimated 4 million people are exposed to high mycotoxin levels, affecting immune function and leading to teratogenic, mutagenic, and carcinogenic effects.22,23,36 Studies have reported widespread mycotoxin contamination in staple foods across Tunisia (96%), Morocco (50%), and Lebanon, with exposure levels exceeding toxicological reference values.37,38 In wealthy nations, contaminated buildings are more frequently the source of OTA exposure than dietary elements.39 The presence of mycotoxins in processed feeds across Asia, America, and Europe highlights and emphasizes the global scale of the issue (Figure 1). Table 2 summarizes global contamination data and highlights regions with higher exposure risks & table 2a outlines the key aspects of mycotoxin contamination, exposure, and health effects.

Table 2.Prevalence of Mycotoxin Contamination in Different Regions
Region/Country Mycotoxin Prevalence of Contamination Products Affected Health Impact Reference
Tunisia Beauvericin, Nivalenol 96% of staple foods Cereals, grains, legumes Immune system suppression, carcinogenic risk Serrano et al.34
Morocco Beauvericin, Nivalenol 50% of staple foods Wheat, barley, rice Carcinogenic effects, compromised fertility Serrano et al.37
Ghana Aflatoxin B1 High in maize, groundnuts Maize, peanuts, other grains Miscarriage, low birth weight, developmental defects Shuaib et al.40
Lebanon Ochratoxin A (OTA) and deoxynivalenol (DON) High levels in food products Dried fruits, coffee, cereals Increased cancer risk, kidney toxicity, infertility Raad et al.38
Sub-Saharan Africa Various mycotoxins High levels across countries Maize, sorghum, animal feed Immune suppression, increased infertility rates Darwish et al.22
Table 2a.Summary of the key aspects of mycotoxin contamination, exposure, and health effects
Aspect Key Findings References
Global Contamination Mycotoxins contaminate approximately 25% rate of the global food supply. Song et al.41; Alhelaisi et al.42; Park et al.43
Prevalence in Tested Samples Recent studies suggest 60-80% of tested food samples contain detectable mycotoxins. Song et al.41; Eskola et al.44
Factors Influencing Contamination Improved detection methods and climate change contribute to increased contamination. Magan et al.45
Toxic Effects Mycotoxins can cause carcinogenic, mutagenic, teratogenic, estrogenic, immunotoxic, nephrotoxic, and neurotoxic effects. Unicsovics et al.46
Major Health Concerns Long-term low-level exposure to carcinogenic mycotoxins like aflatoxins, ochratoxin A, zearalenone, and fumonisins poses a major health risk. Khoury et al.47; Unicsovics et al.46
Reproductive Health Impact Mycotoxins disrupt hormonal function due to their structural similarity with reproductive hormones, leading to fertility issues in both males and females. Sayed et al.48
Figure 1
Figure 1.Regional Mycotoxin Contamination Levels

This bar chart illustrates the estimated mycotoxin contamination levels across different global regions. The data are derived from studies reporting staple food contamination and associated health risks. Sub-Saharan Africa exhibits the highest contamination levels (90%), predominantly due to aflatoxin and fumonisin presence in maize and groundnuts. North Africa follows with 80%, where wheat, barley, and rice are frequently contaminated. The Middle East (75%) faces high ochratoxin A and deoxynivalenol exposure, while South Asia (70%) has significant risks linked to maternal health. Southeast Asia (65%) and Latin America (60%) report contamination in livestock feed, maize, and coffee, with implications for reproductive toxicity and cancer risks.

Health Risks & Reproductive Effects

OTA exposure adversely affects both male and female reproduction. In males, it significantly reduces sperm viability and morphology, causing DNA damage and leading to defects such as larger heads, coiled tails, and decapitation, impairs motility and fertilization.31 Other Penicillium-derived toxins, such as patulin (PAT) and mycophenolic acid (MPA), also cause systemic and reproductive harm.49,50

ZEA mimics estrogen, leading to hormonal imbalances, menstrual irregularities, and fertility issues. Chronic exposure to mycotoxins has been associated with miscarriage, fetal growth restriction, and developmental defects. Even in low concentrations, Fusarium toxins in animal feed have biological effects. OTAs cause cellular damage through apoptosis, protein synthesis inhibition, and DNA damage, and their long half-life leads to inconsistent excretion patterns.

Bioaccumulation and Metabolism

After ingestion, mycotoxins are absorbed through the gastrointestinal tract and undergo metabolic biotransformation in the liver.51 The liver processes mycotoxins through Phase I metabolism, where cytochrome P450 enzymes convert them into reactive intermediates.52,53 In Phase II metabolism, these intermediates by products are transported by the bloodstream, to several organs, including the reproductive system, that may have systemic effects. Once metabolized, they undergo conjugation with molecules such as glucuronic acid, making them more water-soluble for excretion primarily through the kidneys or via bile into the intestines, where they may be further broken down by gut microbiota and eliminated in faeces.52,53

Some mycotoxins bioaccumulate in reproductive tissues, where they disrupt hormone balance, impair gametogenesis, and cause cellular damage. For example, zearalenone (ZEA) mimics estrogen, binding to estrogen receptors in the ovaries and testes, leading to hormonal imbalances and infertility.8 Table 3 summarizes the absorption, metabolism, and excretion processes of mycotoxins and their impact on reproductive organs.

Table 3.Summary of Mycotoxin Metabolism in Humans
Mycotoxin Absorption Metabolism (Phase I & II) Excretion Impact on Reproductive Organs Study
Zearalenone (ZEA) Absorbed through the GI tract Metabolized in the liver, converted to conjugates Excreted through urine and feces Mimics estrogen, affects ovarian and testicular function Zheng et al.54
Ochratoxin A (OTA) Absorbed via gastrointestinal system Phase I metabolism by cytochrome P450 enzymes Excreted in urine, long half-life Reduces sperm viability, alters ovarian steroidogenesis Chakraborty et al.31
Aflatoxin B1 Absorbed through GI tract Phase I oxidation, Phase II conjugation Excreted in bile and urine Impairs testicular function, reduces sperm motility Ibeh et al.55
Deoxynivalenol (DON) Absorbed via gastrointestinal tract Liver metabolism to less toxic metabolites Excreted via urine Alters ovarian function, disrupts steroid hormone production Guerrero-Netro et al.56

Methodology

A comprehensive literature search was conducted in November 2024 using four major electronic databases: PubMed, Google Scholar, EMBASE, and Web of Science. The aim was to identify studies on mycotoxins and their impact on human reproductive health. Only English-language publications were considered, covering research published between 1960 and 2024.

The search strategy included multiple keywords, such as:

  • “Mycotoxins AND human health,”

  • “Aflatoxins AND human reproduction,”

  • “Zearalenone AND endocrine disruption,”

  • “Mycotoxins AND infertility,”

  • “Mycotoxins AND detoxification.”

Relevant studies were selected based on study quality, methodological rigor, and relevance to reproductive health. Both human and animal studies were considered. Data was extracted to analyse mycotoxin exposure, reproductive toxicity, and potential mechanisms of action. Risk of bias and study limitations were also assessed. A total of 150 studies were identified and included in this review.

Results

A total of 150 studies were reviewed to evaluate the impact of mycotoxins on reproductive health. Findings indicate that exposure to mycotoxins through contaminated food is associated with hormonal disruption, decreased fertility, and adverse pregnancy outcomes.

1. Mycotoxin Exposure and Infertility

In a human study, OTA was detected in 70% of infertile men, with concentrations 10 times higher than in fertile men.57 Zearalenone (ZEA), an estrogenic mycotoxin, was linked to early puberty and menstrual irregularities in studies of adolescent girls.58 Aflatoxins were found in 60% of semen samples from infertile men, correlating with low sperm count and motility.55

2. Mycotoxins and Hormonal Disruption

ZEA mimics estrogen and alters testosterone levels, leading to decreased sperm production in male rodents.54 Exposure to OTA reduced sperm viability and caused morphological abnormalities, including coiled tails and enlarged heads.31 In vitro studies suggest that DON (deoxynivalenol) disrupts ovarian steroidogenesis, impairing progesterone and estradiol synthesis.56

3. Pregnancy and Fetal Development Risks

Women with high aflatoxin exposure had higher rates of miscarriage and preterm birth.40 A cohort study in Ghana found a strong correlation between maternal aflatoxin exposure and low birth weight.59 Fumonisins in maize were linked to neural tube defects in new-borns.60

These findings underscore the need for stricter food safety regulations and public awareness campaigns to mitigate mycotoxin exposure and reproductive health risks. Table 4 summarizes key studies, their findings, and the specific mycotoxins and reproductive health impacts observed.

Table 4.Mycotoxin Exposure and Reproductive Health: Study Results Summary
Study Mycotoxin Population Exposure Outcome Reproductive Health Impact Reference
Uriah et al.57 Aflatoxin B1 Infertile men High levels of AFB1 in semen Lower sperm count and motility Ibeh et al.55
Massart et al.58 Zearalenone (ZEA) Adolescent girls Early puberty and menstrual irregularities Disrupted hormone balance, early puberty Massart et al.58
Chakraborty et al.31 Ochratoxin A (OTA) Male rodents OTA exposure in drinking water Reduced sperm viability, coiled tails, enlarged heads Chakraborty et al.31
Zheng et al.54 Zearalenone (ZEA) Male rodents ZEA exposure in diet Lower testosterone, decreased sperm production Zheng et al.54
Shuaib et al.40 Aflatoxins Pregnant women (Ghana) Aflatoxin exposure in food Higher miscarriage and preterm birth rates Shuaib et al.40
Turner et al.59 Aflatoxins Pregnant women (Ghana) Aflatoxin exposure in food Low birth weight, developmental issues in offspring Turner et al.59

Discussion

Impact on Human Health and Fertility

Although direct human data on mycotoxin exposure and infertility remain limited, existing evidence strongly suggests that certain mycotoxins, particularly ochratoxin A (OTA) and zearalenone (ZEA), exert significant effects on reproductive health. OTA is known to inhibit protein synthesis, induce apoptosis through mitochondrial membrane potential loss, and cause DNA damage via adduct formation, leading to decreased fertility in both males and females.61 Due to its long half-life and inconsistent excretion, OTA can have prolonged biological effects. In males, OTA exposure leads to sperm abnormalities, including decapitation, coiled tails, and enlarged heads, which collectively impair sperm motility and reduce fertilization rates.31

ZEA, a nonsteroidal estrogenic compound, mimics endogenous hormones, disrupting endocrine function and contributing to reproductive disorders. This mycotoxin binds to estrogen receptors, altering normal hormonal signaling and leading to fertility issues in both sexes.

Hormonal Disruption by Mycotoxins

Impact on Female Reproduction

ZEA and aflatoxins (AF) are classified as endocrine-disrupting chemicals (EDCs), which interfere with hormone biosynthesis, transport, metabolism, receptor interactions, and feedback regulation.62 These disruptions can occur from fetal development through adulthood, causing lifelong reproductive consequences.63,64

ZEA disrupts the hypothalamic-pituitary-gonadal (HPG) axis by binding to estrogen receptors, mimicking endogenous estrogens, and altering hormonal balance.65 This disruption manifests as ovulation disorders, menstrual irregularities, polycystic ovarian syndrome (PCOS), premature ovarian failure (POF), and endometriosis.66–68

EDCs impair hormones like insulin and insulin-like growth factors, essential for growth, while enhancing glucocorticoid activity, further disrupting growth processes.68 Other hormones, such as growth hormones and thyroid hormones, are also affected, leading to growth abnormalities or delayed puberty.69 Epidemiological studies have linked ZEA exposure to early puberty and estrogen imbalances in girls. Studies from Turkey, Hungary, and Italy report significantly elevated serum ZEA levels (18.9–103 µg/L) in girls experiencing precocious puberty.58,70,71 Similar findings in Lebanese girls indicate early breast development and shortened growth periods.72,73 In addition to impeding ovarian folliculogenesis, it has been implicated in conditions such as endometriosis, polycystic ovarian syndrome (PCOS), and premature ovarian failure (POF) affecting conception and pregnancy maintenance.66

ZEA adversely disrupts the synthesis and release of sex hormones such as testosterone, progesterone, and estradiol and has been shown to have a detrimental impact on reproduction, leading to infertility in both sexes.54

Impact on Male Reproduction

Mycotoxins also detrimentally affect male reproduction. Exposure to mycotoxins, particularly zearalenone (ZEA), has been linked to reproductive issues. ZEA exposure can cause precocious puberty in boys under nine.69,74 ZEA and aflatoxins impair testosterone production, sperm motility, and spermatogenesis through oxidative stress and hormonal dysregulation.75 ZEA disrupts the release of luteinizing hormone (LH), lowering testosterone synthesis by Leydig cells and negatively affecting sperm production.76

Aflatoxin B1 (AFB1) exposure has been linked to male infertility. It has been detected in the blood and semen of infertile males exposed to contaminated diets, causing atrophy of spermatogenic tubules, germ cell layer destruction, and termination of spermatogenesis.57,77,78 Nigerian infertile men exhibited significantly higher semen AFB1 concentrations (60–148 ng/mL) compared to fertile men (0–5 ng/mL), correlating with reduced sperm count and motility.79 Uriah et al.57 found similar results, with AFB1 levels in infertile men exceeding WHO safety limits. Table 5 outlines the specific mycotoxins and their hormonal effects on reproductive organs (e.g., ovaries, testes).

Table 5.Role of Specific multiple mycotoxins (ZEA, OTA, AFB1, DON) and their specific impacts on male vs. female fertility.
Mycotoxin Male Reproductive Effects Female Reproductive Effects
Zearalenone (ZEA) Decreased testosterone, impaired spermatogenesis, increased oxidative stress Estrogenic activity → menstrual disorders, PCOS, premature ovarian failure (POF)
Ochratoxin A (OTA) Sperm abnormalities (coiled tails, enlarged heads), mitochondrial dysfunction Impaired ovarian steroidogenesis, disrupted menstrual cycle
Aflatoxin B1 (AFB1) Decreased sperm count & motility, Leydig cell dysfunction Increased miscarriage risk, hormonal imbalance
Deoxynivalenol (DON) Reduced sperm viability, testicular toxicity Ovarian toxicity, impaired follicle development

Gametogenesis Impairment

Mycotoxins such as aflatoxins and ochratoxins generate reactive oxygen species (ROS), leading to oxidative stress, lipid peroxidation, mitochondrial dysfunction, and DNA damage in gametes.80,81 These toxic effects disrupt spermatogenesis in males and folliculogenesis in females.56

In animal models, mycotoxin exposure has been linked to reduced sperm motility and compromised oocyte quality.82–84 Deoxynivalenol (DON) exposure has been shown to trigger autophagy-mediated apoptosis in granulosa cells, reducing progesterone and estradiol production and impairing oocyte maturation.85 ZEA decreases key steroidogenesis enzymes (aromatase, P450scc, 3βHSD), increasing follicular atresia and reducing fertility.86 Table 6 concisely summarizes key reproductive outcomes associated with specific mycotoxins.

Table 6.Statistical Summary of Reproductive Effects of Mycotoxin Exposure
Mycotoxin Reproductive Outcome Effect on Male Reproductive Health Effect on Female Reproductive Health Study
Zearalenone (ZEA) Disrupts hormonal balance Decreased sperm motility, low testosterone Menstrual irregularities, ovarian dysfunction Zheng et al.54
Ochratoxin A (OTA) Reduced sperm count and motility Increased sperm abnormalities (coiled tails, enlarged heads) Impaired oocyte quality and fertilization Chakraborty et al.31
Aflatoxin B1 Low sperm count, reduced motility Testicular atrophy, germ cell loss Reduced fertility, hormonal imbalance Ibeh et al.79
Deoxynivalenol (DON) Disruption in spermatogenesis Low sperm production Impaired oocyte maturation, autophagy in granulosa cells Guerrero-Netro et al.56
Fumonisins Reduced fertility Reduced testosterone production Neural tube defects in offspring Missmer et al.60

Uterine and Placental Toxicity

Pregnant women and their unborn children are particularly vulnerable to mycotoxin exposure.87–89 Studies suggest that mycotoxins cross the placental barrier, causing fetal toxicity, growth restriction, and birth defects.87

Prenatal exposure to aflatoxins is associated with malnutrition and adverse birth outcomes, especially during the critical first 1,000 days of life.89,90 These include fetal growth restriction, neonatal jaundice, preterm birth, and increased miscarriage risk.40,59,91–93 In maize-consuming populations, fumonisin exposure has been linked to neural tube and urogenital defects in the fetuses and maternal hypertension, and preeclampsia.60,94,95 Additionally, maternal blood samples from Bangladesh revealed high mycotoxin levels, further emphasizing the risk of transplacental toxicity.96–98

Mechanisms of Reproductive Toxicity

Mycotoxin-induced reproductive toxicity operates through multiple pathways:

Mitochondrial Dysfunction

Mycotoxins interfere with mitochondrial activity, reducing ATP production and triggering apoptosis.99,100 This has been linked to pro-apoptotic genes (Bak and Bax) and anti-apoptotic genes (Bcl-XL, Bcl-2) regulating mitochondria-dependent apoptosis.99 Excessive levels of aflatoxin B1 (AFB1) produce energy blockages by interfering with mitochondrial biogenesis, hence interfering with Leydig cell function that exacerbates sperm failure and infertility.101,102 AFB1 compromises mitochondrial structure and function by reducing membrane potential, causing calcium build-up, and inducing oxidative stress, indirectly impairing mitochondrial activity.103 Reactive oxygen species (ROS) production triggered by mycotoxins increases mitochondrial membrane permeability, releasing pro-apoptotic proteins and activating the apoptotic cascade, which results in germ-cell apoptosis and DNA fragmentation.100,104

Hormonal Disruption

Mycotoxins mimic or inhibit sex hormone function, impairing endocrine regulation and fertility.98 Aflatoxin disrupts and inhibits steroidogenic enzymes that impact cholesterol utilization and testosterone production.105,106 This hormonal dysregulation impairs testicular function and spermatogenesis, impacting the quality of sperm production. Table 7 shows a summary of the mechanism of different mycotoxins affecting hormone disruption.

Table 7.Hormonal Disruption by Mycotoxins: A Summary of Mechanisms
Mycotoxin Hormonal Effect Affected Organ(s) Mechanism of Action Study
Zearalenone (ZEA) Estrogenic effect (mimics estrogen) Ovaries, testes Binds to estrogen receptors, alters hormonal balance Zheng et al.54
Ochratoxin A (OTA) Reduces testosterone, disrupts sperm function Testes, ovaries Inhibits protein synthesis, damages sperm morphology Chakraborty et al.31
Aflatoxin B1 Disrupts testosterone production, lowers sperm motility Testes Interferes with steroidogenic enzymes, damages seminiferous tubules Uriah et al.57
Deoxynivalenol (DON) Disrupts ovarian steroidogenesis Ovaries Reduces progesterone and estradiol synthesis Guerrero-Netro et al.56

Oxidative Stress

Reproductive health is disrupted, and germ cell loss is worsened by factors like oxidative stress-producing ROS. Mycotoxin causes increased ROS production, and damages sperm and oocytes, leading to compromised fertility.107,108

Placental Toxicity

Mycotoxins disrupt placental function, impairing fetal growth and increasing pregnancy complications.109 These negative consequences have been linked to mechanisms such as intestinal inflammation, decreased placental function, dysregulated pro-inflammatory cytokines, and organ damage.109 For instance, by increasing liver toxicity and fetal hemoglobin breakdown, aflatoxins may worsen newborn jaundice.92,93,108,110 Known mechanisms of mycotoxin toxicity include immune suppression, disruption of ribosomal protein synthesis, hormone dysregulation, and erythrocyte apoptosis, leading to fetal toxicity, inflammation, and hypoxia.111 However, limited knowledge exists regarding the effects of lesser-known mycotoxins and their combinations on adverse pregnancy outcomes.

Conclusion

This review highlights the strong association between mycotoxin exposure and reproductive toxicity. Evidence from epidemiological and animal studies suggests that mycotoxins significantly disrupt hormonal balance, gametogenesis, and fetal development. Given the severity of these risks, proactive measures are needed:

  1. Strengthening Food Safety Regulations: Ensuring proper storage and contamination control in food production.

  2. Improving Public Awareness: Educating consumers about the risks of contaminated food and dietary choices.

  3. Advancing Research: Large-scale human biomonitoring studies are required to assess long-term exposure risks and develop targeted interventions.

Mycotoxin-induced reproductive toxicity is a significant but often overlooked public health issue. Addressing this challenge requires interdisciplinary efforts, combining toxicology, epidemiology, and food safety initiatives to safeguard reproductive health globally.

Funding Statement

No external funding was needed for this manuscript.

Competing Interest

None

Submission declaration

  • The manuscript has never been published before.

  • There are no other publications considering it.

  • The publication is approved, either expressly or implicitly, by all authors.

CRediT Authorship Contribution Statement

Conceptualization. Yasmin Sajjad, Joseph Dib
Software: Solmaz Sajjad
Writing – original draft; Yasmin Sajjad, Solmaz Sajjad
Writing – review and editing: Joseph Dib, M. Fakih, Hussain, Marwa, Narmeen, Yasmin Sajjad

Declaration of generative AI and AI-assisted technologies in the writing process

Statement: During the preparation of this work, the author(s) used chat GPT to format, make grammatical corrections, rephrasing & structure the manuscript. After using this tool, the author(s) reviewed and edited the content as needed and take(s) full responsibility for the content of the published article.