4.3. Micro/nanoplastic particles in the human body

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For ethical reasons, it is not possible to study the effects of micro/nanoplastics on the human body directly with human clinical trials, since research in which certain test groups are deliberately exposed to (presumably) harmful effects cannot, of course, be conducted in humans. Therefore, the adverse effects of micro/nanoplastics on human health can only be inferred from in vitro test data. In such in vitro studies on human cells, size-dependent cell damage in macrophages and a dose-dependent increase in reactive oxygen species (ROS) in human brain and epithelial cell lines were observed when treated with nanoplastics. Oxidative processes in cells physiologically also generate oxygen free radicals. These free radicals are extremely reactive, they can easily trigger the production of more free radicals, creating a chain reaction. Excessive production of ROS can result in damage to proteins, nucleic acids (including inhibition of DNA repair enzymes, modified nucleotid bases, and fragmentation) and lipids (leading to lipid peroxidation). Therefore, the human body relies on an antioxidant protection system (including GSH, SOD, catalase, etc.) to eliminate reactive oxygen radicals. Depletion of these antioxidants can lead to cellular damage and pathological processes. An imbalance between generated radicals and the antioxidant system leads to oxidative stress. Excessive production of free radicals during oxidative stress is associated with the development of numerous diseases, such as neurological or cardiovascular diseases, as well as tumor development. Aminated nanoplastics induced cytotoxic effects, cell membrane damage, apoptosis and morphological changes in the lysosomes and mitochondria of human cells in vitro. Studies with human gastric adenocarcinoma cells have demonstrated that PS nanoparticles penetrate the cytosol, alter cell morphology and permeability, and induce inflammation. The expression of several genes related to inflammation and cell cycle regulation (c-Myc, ERK -1, Ki67, CCNE1, p38, p53, IL -8, IL -6) was found to be altered by PS nanoparticles. The upregulation of IL -8 and IL -6 cytokines gene expression plays an important role in gastric pathology. Moreover, PS nanoparticles were found to bind to coagulation factors VII and IX in vitro, leading to decreased activity [107]. Recently, an Italian research group reported that 5-10 µm microplastic particles were detected in the placentas of pregnant women [115]. The plastic particles studied are small enough to enter the bloodstream. According to experts, these particles or the chemicals they contain can cause long-term damage or compromise the immune system of the developing fetus.

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When considering human exposure to micro/nanoplastics, it is essential to account not only for the particles ingested or inhaled unintentionally (Chapter 4.6), but also for those generated from plastic degradation that intentionally enter the body. The use of PE implants, such as total joint replacements or prostheses may lead to the producion of wear and tear debris. A significant amount of PE particles has been found in the tissues surrounding aging PE implants, previously considered inert. Their presence seem to trigger local inflammation, bone resorption and, in the worst-case scenario, rejection of the implant [104].
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