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From exposure to oncogenesis: a review on the multifaceted roles of microplastics in tumor initiation and progression

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This review examined the evidence linking microplastic exposure to tumor initiation and progression, covering physical, chemical, and inflammatory mechanisms by which MPs may promote oncogenesis. The authors conclude that while current evidence is largely preclinical, accumulating data warrant serious concern about microplastics as environmental carcinogens.

Body Systems
Models
Study Type In vivo

BACKGROUND: Microplastics (MPs) are pervasive environmental pollutants that pose significant health risks. While their prevalence in ecosystems is well-established, their accumulation in the human body and potential role in tumorigenesis demand further investigation. This review examines the potential links between MPs exposure and tumor development, providing a comprehensive analysis of their pathways from environmental sources to human exposure and the mechanisms by which they may exert their effects. MAIN BODY: MPs not only serve as carriers for other pollutants, thereby amplifying exposure risks, but also accumulate in human tissues, disrupting cellular homeostasis through various pathways, such as oxidative stress induction, organelle damage, physical barrier disruption, and chronic inflammation. Recent studies suggest that MPs may influence the tumor microenvironment, potentially facilitating tumor progression through immune–metabolic reprogramming. Although epidemiological studies indicate a correlation between exposure and chronic disease the precise mechanisms underlying their in vivo accumulation and the complete carcinogenic process remain unclear. CONCLUSIONS: Therefore, this review aims to establish a scientific basis for evaluating the health risks posed by MPs and for developing effective control strategies. Given that the comprehension of MPs toxicity is still in its early stages, future research must prioritize elucidating the influence of exposure concentration, particle characteristics, and individual susceptibility to fully define the oncogenic threat posed by these pollutants.

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