Over the years, the vaste expansion of plastic manufacturing has dramatically increased the environmental impact of microplastics [MPs] and nanoplastics [NPs], making them a threat to marine and terrestrial biota because they contain endocrine disrupting chemicals [EDCs] and other harmful compounds. MPs and NPs have deleteriouse impacts on mammalian endocrine components such as hypothalamus, pituitary, thyroid, adrenal, testes, and ovaries. MPs and NPs absorb and act as a transport medium for harmful chemicals such as bisphenols, phthalates, polybrominated diphenyl ether, polychlorinated biphenyl ether, organotin, perfluorinated compounds, dioxins, polycyclic aromatic hydrocarbons, organic contaminants, and heavy metals, which are commonly used as additives in plastic production. As the EDCs are not covalently bonded to plastics, they can easily leach into milk, water, and other liquids affecting the endocrine system of mammals upon exposure. The toxicity induced by MPs and NPs is size-dependent, as smaller particles have better absorption capacity and larger surface area, releasing more EDC and toxic chemicals. Various EDCs contained or carried by MPs and NPs share structural similarities with specific hormone receptors; hence they interfere with normal hormone receptors, altering the hormonal action of the endocrine glands. This review demonstrates size-dependent MPs’ bioaccumulation, distribution, and translocation with potential hazards to the endocrine gland. We reviewed that MPs and NPs disrupt hypothalamic-pituitary axes, including the hypothalamic-pituitary-thyroid/adrenal/testicular/ovarian axis leading to oxidative stress, reproductive toxicity, neurotoxicity, cytotoxicity, developmental abnormalities, decreased sperm quality, and immunotoxicity. The direct consequences of MPs and NPs on the thyroid, testis, and ovaries are documented. Still, studies need to be carried out to identify the direct effects of MPs and NPs on the hypothalamus, pituitary, and adrenal glands.

Introduction: Microbial contamination remains a vital challenge across the food production chain, particularly due to mycotoxins—secondary metabolites produced by several genera of fungi such as Aspergillus, Fusarium, Alternaria, and Penicillium. These toxins, including aflatoxins, fumonisins, ochratoxins, and trichothecenes (nivalenol, deoxynivalenol, T2, HT-2). These contaminants pose severe risks to human and animal health, with their potential to produce a variety of different toxic effects. Notably, up to 50% of global cereal production is affected by mycotoxin contamination, leading to significant economic losses. Current research focuses on innovative technologies to mitigate mycotoxins, with cold atmospheric pressure plasma emerging as a promising decontamination method.Method: This systematic review aimed at describing recent advances in the application of cold atmospheric plasma for the decontamination of toxigenic fungi and mycotoxins.Results and discussion: Cold atmospheric plasma offers a sustainable and cost effective solution to preserve food quality while inactivating toxigenic fungi and degrading mycotoxins. Through the generation of reactive oxygen and nitrogen species, cold plasma disrupts fungal cell integrity, hinders spore germination, and inhibits toxin biosynthesis. Additionally, cold atmospheric plasma-driven degradation of mycotoxins involves structural modifications, breaking key molecular bonds that reduce toxicity. The effectiveness of cold plasma depends on operational parameters and the specific characteristics of the treated food, with notable efficacy in degrading aflatoxin B₁ and deoxynivalenol by converting them into less toxic substances and inhibiting their spores and DNA responsible for their biosynthesis. While the data demonstrates that cold atmospheric plasma has minimal impact on food composition, further research is needed to fully assess the nature of the degradation products of mycotoxins, its influence on food quality attributes and to optimize application strategies for different products.

In this review, the intricate issue about the occurrence levels of mycotoxins in foods is discussed aiming to underline the main knowledge gaps on the persistence of these toxicants in the food production system. Mycotoxins have been a key challenge to the food industry, economic growth, and consumers’ health. Despite a breadth of studies over the past decades, the persistence of mycotoxins in foods remain an overlooked concern that urges exploration. Therefore, we aimed to concisely underline the matter and provide possible biochemical and metabolic details that can be relevant to the food sector and overall public health. We also stress the application of computational modeling, high-throughput omics, and high-resolution imaging approaches, which can provide insights into the structural and physicochemical characteristics and the metabolic activities which occur in a stored cereal grain’s embryo and endosperm and their relationship with storage fungi and mycotoxins on a cellular level. In addition, there is a need for extensive collaborative network and funding, which will play a key role in finding effective solutions against the persistence of mycotoxins at the genetic and molecular to metabolic levels in the food system.

This study aimed to conduct a first evaluation of maternal exposure to mycotoxins during pregnancy in Brazil through quantification of biomarkers in liver and serum samples from stillborn and neonates autopsied in the Clinical Hospital of Ribeirão Preto, state of São Paulo. Liver tissue (n = 43) and serum (n = 38) samples were collected from 43 patients and analyzed for biomarkers of aflatoxins (AFs), ochratoxin A (OTA), fumonisins (FBs), zearalenone (ZEN), deoxynivalenol (DON), T-2 and HT-2 toxins by ultra-performance liquid chromatography coupled to tandem mass spectrometry. In total, 9 samples of liver (20.9%) and 33 serum (86.8%) had quantifiable levels of mycotoxins. In liver samples, aflatoxin M₁ (AFM₁) was quantified in two samples (median level: 0.38 ng/g), while four samples had OTA residues (median: 0.31 ng/g) and one contained ZEN (3.6 ng/g). Compared with liver tissue, serum samples had higher occurrence rates of mycotoxins, particularly AFM₁, OTA and ZEN. Nineteen serum samples (50%) contained 2–4 types of mycotoxins, indicating an effective transplacental transfer of major mycotoxins during pregnancy. Median levels of AFM₁, OTA, FB₁, ZEN, DON, T-2 and HT-2 toxins in serum samples were 0.48, 3.39, 30.6, 10.53, 5.71, 2.85 and 10.84 ng/mL, respectively. The most frequent cause of death was extreme prematurity (33% of cases), followed by preterm premature rupture of membranes (16% of cases) and morphological abnormalities (42% of cases). Results of this trial suggest potential associations between dietary mycotoxins and congenital anomalies. Further research should clarify the transplacental transfer of mycotoxins and their association with toxic effects during human prenatal development.