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Microplastics, ranging from 1 micron to 5 mm in size, ubiquitous environmental pollutants, arise from diverse sources such as industrial processes, personal care products, textiles, and urban runoff, permeating air, soil, freshwater, sediment, and marine environments. Human exposure occurs through ingestion, inhalation, and dermal contact, leading to health concerns including oxidative stress, metabolic disruption, and immune modulation, with potential direct links to lung, skin, and digestive cancers. While direct evidence linking microplastics to lymphoma remains elusive, therefore we hypothesized that bloodstream's immediate exposure post-entry suggests a plausible indirect link. This review explores mechanisms around our hypothesis by which microplastics might contribute to lymphoma, encompassing inflammation, oxidative stress, immune dysregulation, endocrine disruption, and genotoxicity. Understanding these pathways is crucial given lymphoma's global impact. Future research warrants comprehensive epidemiological studies and interdisciplinary approaches, integrating epidemiology, experimental research, and computational modeling to elucidate the association between microplastics and lymphoma.
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Kumar et al. (2025) studied this question.
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