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Microplastics (MPs) contaminate the global marine and terrestrial ecosystems. This environmental contamination can enter the food chain, with MPs found in drinking water, fishery products and other food categories. Consequently, ingestion is considered the main route of human exposure to MPs. Concerns exist on the potential of MPs to act as vectors for pathogenic bacteria, possibly threatening microbial food safety.Starting from the current evidence on foodborne pathogens associated with MPs, we review the state of knowledge on the putative role of MPs in enhancing harmful bacterial traits and transporting them to humans. Finally, we focus on the simultaneous uptake of MPs and pathogens in the human gut.Overall, we identify major knowledge gaps, both on the mechanisms and the possible health outcomes. The scarce and inconclusive results regarding the effect of MPs on microbial virulence and evolution, together with the insufficient knowledge about the attachment of microbial toxins to MPs, highlight the need for further studies. We conclude that biofilm-coated MPs in foodstuffs may pose several risks to food safety, but further research will be essential to determine the extent of their effect on human health

Fumonisin B1 (FB1) and aflatoxin B1 (AFB1) are frequent contaminants of staple foods such as maize. Oral exposure to these toxins poses health hazards by disrupting cellular signaling. However, little is known regarding the multifaced mitochondrial dysfunction-linked toxicity of FB1 and AFB1. Here, we show that after exposure to FB1 and AFB1, mitochondrial respiration significantly decreased by measuring the oxygen consumption rate (OCR), mitochondrial membrane potential (MMP) and reactive oxygen species (ROS). The current work shows that the integrity of mitochondria (MMP and ROS), that is the central component of cell apoptosis, is disrupted by FB1 and AFB1 in undifferentiated Caco-2 and HepG2 cells as in vitro models for human intestine and liver, respectively. It hypothesizes that FB1 and AFB1 could disrupt the mitochondrial electron transport chain (ETC) to induce mitochondrial dysfunction and break the balance of transferring H+between the mitochondrial inner membrane and mitochondrial matrix, however, the proton leak is not increasing and, as a result, ATP synthesis is blocked. At the sub-toxic exposure of 1.0μg/mL for 24 h, i.e., a viability of 95% in Caco-2 and HepG2 cells, the mitochondrial respiration was, however, stimulated. This suggests that the treated cells could reserve energy for mitochondrial respiration with the exposure of FB1 and AFB1, which could be a survival advantage.