The adverse effects of plastics on the environment, wildlife, and human health have been extensively studied, yet their production remains unavoidable due to the lack of viable alternatives. Environmental fragmentation of larger plastic particles generates microplastics (MPs, 0.1-5000 μm) and nanoplastics (NPs, 1-100 nm), which can enter the bloodstream through inhalation or ingestion. This review examines whether MPs and NPs influence blood pressure. To address this question, relevant studies were analyzed based on predefined criteria. Due to anatomical barriers and microcirculatory dynamics, only NPs and small MPs are expected to enter the bloodstream under physiological conditions, although pathological states may alter this. In vitro research indicates that MPs and NPs negatively affect erythrocytes and endothelial cells, while rodent models suggest potential cardiovascular effects. Plastic particles and fibers have been detected in human blood, thrombi, atherosclerotic plaques, and various tissues. However, validated data on plastic particle-related blood pressure changes remain lacking. Despite limitations in their applicability to human physiology, preclinical models suggest that MPs and NPs circulate in the bloodstream, interact with blood cells, and contribute to vascular damage. Mechanisms such as endothelial injury, platelet activation, inflammation, and MPs/NPs accumulation in atherosclerotic plaques may contribute to blood pressure elevation but are unlikely to be the exclusive cause of hypertension. Further research is needed to clarify the role of plastic particles in blood pressure regulation. Standardized detection methods, real-world scenario-related models, and targeted human studies are essential to assessing cardiovascular risks associated with MP and NP exposure.

Microplastic particles are ubiquitous in our environment, having entered the air, the water, the soil, and ultimately our food chain. Owing to their small size, these particles can potentially enter the bloodstream and accumulate in the organs. To detect microplastics using existing methods, they must first be isolated. The aim of this study was to develop a non-destructive method for efficiently and affordably isolating plastic particles. We investigated the digestion of kidney, lung, liver, and brain samples from pigs. Kidney samples were analyzed using light microscopy after incubation with proteinase K, pepsin/pancreatin, and 10% potassium hydroxide (KOH) solution. Various KOH:tissue ratios were employed for the digestion of lung, liver, and brain samples. Additionally, we examined the effect of 10% KOH solution on added polystyrene microplastics using scanning electron microscopy. Our findings revealed that a 10% KOH solution is the most suitable for dissolving diverse organ samples, while enzymatic methods require further refinement. Moreover, we demonstrated that commonly used 1 µm polystyrene particles remain unaffected by 10% KOH solution even after 76 h of incubation. Digestion by KOH offers a simple and cost-effective approach for processing organ samples and holds potential for isolating plastic particles from meat products.

The global microplastic pollution issue, as a result of the indispensable usage of microplastics in building materials, packaged food, medical products and consumer goods, poses significant health problems for the population. These small particles can penetrate intact cell barriers in the intestines and alveoli, thereby entering the bloodstream. The aim of this pilot study was to investigate the effects of reduced plastic consumption on blood pressure. Eight adult and healthy participants abstained from consuming commercially produced bottled beverages and restricted their primary fluid intake to tap water. Blood pressure was measured on both sides before, after 14 days and after 28 to 30 days of this partial plastic diet. Women exhibit a significant change in systolic blood pressure on the right arm after 2 and 4 weeks, while the left arm demonstrates no significant changes in blood pressure. On the contrary, in men, systolic blood pressure values on both arms show no significant alterations, attributable to the high variability across the three participants. Moreover, no significant differences in systolic blood pressure were observed when analysing the entire cohort. Significant findings are evident only at the two-week mark for diastolic blood pressure for all participants in both arms. When considering diastolic blood pressure separately for women and men, men again show no significant changes in blood pressure on either arm. However, women exhibit a significant decrease in diastolic blood pressure on the left arm after 2 weeks and a statistically significant decline in diastolic blood pressure on the right arm after both 2 and 4 weeks. The results of the study suggest, for the first time, that a reduction in plastic use could potentially lower blood pressure, probably due to the reduced volume of plastic particles in the bloodstream. To confirm this hypothesis, a larger sample of male and female participants must be examined, ideally with the monitoring of plastic concentration in the blood.

Nanoplastics (NPs) and microplastics (MPs) have recently been identified in human blood, kidney tissue, and urine, reflecting systemic exposure to environmental plastic contamination. As plastic particles can induce cellular damage, particle-related impairment of renal perfusion and filtration can be considered a hypothetical mechanism that could influence systemic blood pressure. The aim of this review was to evaluate current evidence on the effects of plastic particles on renal function and their potential implications for systemic blood pressure. For this purpose, current evidence from in vitro experiments, mouse and rat studies, and emerging human data on the nephrotoxic effects of NPs and MPs was examined, and potential mechanistic pathways linking renal injury to blood pressure regulation were discussed. Across experimental models, exposure to NPs and MPs induces oxidative stress, inflammatory responses, and structural damage to renal cells. These alterations may impair glomerular filtration and contribute to glomerulosclerosis and interstitial fibrosis. In adenine-induced chronic kidney disease (CKD) rat models, prolonged MP exposure has been associated with elevated serum creatinine and urea concentrations, albuminuria, histological evidence of fibrosis, and exacerbation of arterial hypertension. Renal localization and persistence of plastic particles depend on particle size, shape, surface chemistry, and exposure dose. In human kidney tissue and urine, plastic particles in the micrometer range have been detected across multiple studies. However, a direct association between their presence and any functional renal impairment has not yet been demonstrated in humans. Although a direct causal link between environmental plastic exposure, renal impairment, and hypertension has not yet been demonstrated in humans, current experimental evidence points to biological processes such as oxidative stress, inflammation, and vascular dysfunction. Long-term low-level exposure may therefore represent a hypothetical contributing factor to subtle changes in kidney function and blood pressure, though this remains to be demonstrated in humans.

Plastic particles have been detected in almost all areas of the human body. Consequently, the impact of nano- and microplastics has been investigated in various cell and animal models, mainly using polystyrene (PS) spheres. The objective of this study was to examine the effects of 100 nm and 1 µm PS spheres on human erythrocytes. Erythrocytes were isolated from human blood and incubated in protein-free medium with 0-100 µg/mL PS particles for up to 20 h. Cell counts and erythrocyte morphology were subsequently assessed by light microscopy. Compared with controls, 100 µg/mL of either 100 nm or 1 µm PS spheres did not alter cell number. In contrast, 100 nm spheres induced echinocyte formation, consistent with hydrophobic membrane interaction. At 1-100 µg/mL, 1 µm spheres showed minimal interaction and no morphological changes. Notably, combined exposure to both sizes induced erythrocyte aggregation at 100 µg/mL, accompanied by additional echinocyte formation. These findings confirm the effects of 100 nm PS nanospheres on erythrocytes but contradict previous reports on 1 µm microspheres, which here exhibited little membrane interaction. Aggregation as a cellular response to size-mixed particles illustrates distinct size-dependent effects under identical conditions. Moreover, these results underline the importance of standardised assay conditions to ensure comparability across studies. Although the applied concentrations exceed those expected from typical environmental exposure, inhaled and ingested particles in real-world settings also vary in size. When differences in shape and polymer composition are additionally considered, the variability of potential cellular responses in vivo may substantially increase.