Micro-nanoplastics and cardiovascular diseases: evidence and perspectives

Graphical Abstract Summary of the available knowledge relative to the possible role of micro- and nanoplastics (MNPs) in cardiovascular disease. Environmental and modelling studies suggest that air (both indoor and outdoor), water (both bottled and tap water), food, and cosmetic products are possible sources of exposures to MNPs in humans. Such MNPs can be absorbed through inhalation, ingestion, or even skin contacts, as suggested by animal models. Once reached the bloodstream, such MNPs might accumulate in multiple cardiovascular tissues, as evidenced by studies employing ex-vivo samples from humans. Here, they might promote the activation of a number of deleterious pathways promoting low-grade inflammation, oxidative stress, endothelial dysfunction, alteration of autophagy, and apoptosis, as proposed by experiments in vitro and in animal models. In humans, the presence of MNPs in carotid plaques is associated with the subsequent incidence of a composite of myocardial infarction, stroke, and all-cause mortality. Emerging evidence indicates that chemical exposures in the environment are overlooked drivers of cardiovascular diseases (CVD). Recent evidence suggests that micro- and nanoplastic (MNP) particles derived largely from the chemical or mechanical degradation of plastics might represent a novel CVD risk factor. Experimental data in preclinical models suggest that MNPs can foster oxidative stress, platelet aggregation, cell senescence, and inflammatory responses in endothelial and immune cells while promoting a range of cardiovascular and metabolic alterations that can lead to disease and premature death. In humans, MNPs derived from various plastics, including polyethylene and polyvinylchloride, have been detected in atherosclerotic plaques and other cardiovascular tissues, including pericardia, epicardial adipose tissues, pericardial adipose tissues, myocardia, and left atrial appendages. MNPs have measurable levels within thrombi and seem to accumulate preferentially within areas of vascular lesions. Their presence within carotid plaques is associated with subsequent increased incidence of cardiovascular events. To further investigate the possible causal role of MNPs in CVD, future studies should focus on large, prospective cohorts assessing the exposure of individuals to plastic-related pollution, the possible routes of absorption, the existence of a putative safety limit, the correspondence between exposure and accumulation in tissues, the timing between accumulation and CVD development, and the pathophysiological mechanisms instigated by pertinent concentrations of MNPs. Data from such studies would allow the design of preventive, or even therapeutic, strategies. Meanwhile, existing evidence suggests that reducing plastic production and use will produce benefits for the environment and for human health. This goal could be achieved through the UN Global Plastics Treaty that is currently in negotiation.