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The intensification of microplastics (MPs) pollution has emerged as a formidable environmental challenge, with profound global implications. The pervasive presence of MPs across a multitude of environmental mediums, such as the atmosphere, soil, and oceans, extends to commonplace items, culminating in widespread human ingestion and accumulation via channels like food, water, and air. In the domestic realm, kitchens have become significant epicenters for MPs pollution. A plethora of kitchen utensils, encompassing coated non-stick pans, plastic cutting boards, and disposable utensils, are known to release substantial quantities of MPs particles in everyday use, which can then be ingested alongside food. This paper conducts a thorough examination of contemporary research addressing the release of MPs from kitchen utensils during usage and focuses on the health risks associated with MPs ingestion, as well as the myriad factors influencing the release of MPs in kitchen utensils. Leveraging the insights derived from this analysis, this paper proposes a series of strategic recommendations and measures targeted at mitigating the production of MPs in kitchen settings. These initiatives are designed not solely to diminish the release of MPs but also to enhance public awareness regarding this pressing environmental concern. By adopting more informed practices in kitchens, we can significantly contribute to the reduction of the environmental burden of MPs pollution, thus safeguarding both human health and the ecological system.

Hydrogen sulfide (H2S), a highly toxic gas, has become a polluting gas that cannot be ignored, while H2S exposure results in acute or chronic poisoning or even death in humans or animals and plants, but the relevant mechanisms remain poorly understood. In this study, 9-day-old zebrafish larvae were exposed continuously to culture medium containing 30 μM survival rate was counted on H2S, and our results indicated that H2S exposure increased intracellular ROS, Ca2+, NO and MDA contents and decreased SOD activity, meaning that H2S caused oxidative stress in embryo-larval stages of zebrafish. Furthermore, we found that transgenic zebrafish (cms Tg/+ AB) displayed a lower fluorescence intensity, and cytochrome c oxidase (COX) activity and JC-1 monomer fluorescence ratio increased under H2S treatment conditions. These findings indicated that H2S caused mitochondrial dysfunction. Moreover, in this experiment, after H2S treatment, the increase of apoptotic cells, activity of caspase 3 and transcription of typical apoptosis-associated genes including BCL2 associated agonist of cell death (Bad), and BCL2 associated X apoptosis (Baxa) and so on were found, which suggested that H2S caused apoptosis in zebrafish larvae. Therefore, our data meant that H2S-traggered oxidative stress mediate mitochondrial dysfunction, thus triggering apoptosis. In conclusion, oxidative stress triggered H2S-induced apoptosis via mitochondria pathway in embryo-larval stages of zebrafish.