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Beyond Classic Carcinogens: Micro- and Nanoplastics (MNPs) as Pervasive Factors in Cancer Risk
Summary
This review pulls together existing research suggesting that tiny plastic particles (microplastics), which are now found throughout our environment and even inside our bodies, may do more than just pollute — they might contribute to cancer by causing inflammation, cell damage, and harmful changes to our genes. While this doesn't prove microplastics cause cancer, it highlights a concerning new area of research worth watching, especially since these particles are so widespread in our food, water, and air that avoiding them entirely is nearly impossible.
Cancer is attributed to being caused by multiple genetic, epigenetic, and various direct and indirect environmental factors. Microplastics are defined as pieces of plastic that are smaller than five millimeters. Microplastics have been emphasized as ubiquitous environmental contaminants found in terrestrial and aquatic systems, food webs, and the human body. Moreover, microplastics can bind to environmentally harmful pollutants, heavy metals, and refractory organic pollutants that can aggravate the biological effects of these pollutants. Microplastics are suggested to induce chronic inflammation, oxidative stress, and genotoxicity by adsorbing and modifying the biomolecules in the biological systems. Oxidative stress, inflammation, and chemical-induced genetic and epigenetic changes in cancer cells and cancer-associated cells are considered as crucial processes in the development, progression, and therapeutic outcome of cancer. Among numerous tumor-promoting environmental factors, preclinical and clinical evaluations of how microplastics contribute to cellular and non-cellular pro-tumorigenic mechanisms like inflammation, genomic instability, and epigenetic modulation are emerging. This review will contribute to a better understanding of microplastics as additional environmental components apart from established carcinogens and genotoxic substances that directly or indirectly influence the pro-tumor microenvironment.