Rising Concern About the Carcinogenetic Role of Micro-Nanoplastics

Abstract

In recent years, awareness regarding micro-nanoplastics' (MNPs) potential effects on human health has progressively increased. Despite a large body of evidence regarding the origin and distribution of MNPs in the environment, their impact on human health remains to be determined. In this context, there is a major need to address their potential carcinogenic risks, since MNPs could hypothetically mediate direct and indirect carcinogenic effects, the latter mediated by particle-linked chemical carcinogens. Currently, evidence in this field is scarce and heterogeneous, but the reported increased incidence of malignant tumors among younger populations, together with the ubiquitous environmental abundance of MNPs, are rising a global concern regarding the possible role of MNPs in the development and progression of cancer. In this review, we provide an overview of the currently available evidence in eco-toxicology, as well as methods for the identification and characterization of environmental MNP particulates and their health-associated risks, with a focus on cancer. In addition, we suggest possible routes for future research in order to unravel the carcinogenetic potential of MNP exposure and to understand prognostic and preventive implications of intratumoral MNPs.

Keywords: cancer; cancerogenesis; cancerogenicity; carcinogenic; carcinogenicity; ecotoxicology; microplastics; nanoplastics; tumor.

Figure 1

MNP environmental recirculation. Once emitted into the environment, MNPs have the capability to continuously recirculate through air suspension, soil penetration and sea emission, entering the water cycle. Sea natant MNPs can be ingested by marine organisms, persisting in the marine food chain. In addition, airborne MNPs can precipitate within rain, penetrating in soil and reaching underwater, rivers and lakes.

Figure 2

Hallmarks of cancer related to MNPs. Current evidence regarding the role of MNPs in cancer initiation and promotion is linked mainly to the capability of MNPs to induce metabolic stress through the induction of ROS, fostering immune infiltration and chronic inflammation since their persistence in cancer cells and macrophages. The inability of intracellular lytic enzymes of mononuclear phagocytes to process MNPs induces a “frustrated” phenotype that can cause uncontrolled cell death, further sustaining inflammatory processes. Moreover, MNP-exposed cancer cells showe an augmented capacity of invasion and metastatization in preclinical models. Finally, genomic instability could be the result of intricated cytotoxic and genotoxic damage triggered by the presence of MNPs, which needs to be further elucidated. Faded sections indicate that poor or no evidence is available in demonstrating a potential effect in those specific hallmarks.