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Microplastics: A Matter of the Heart (and Vascular System)
Summary
This review summarizes growing evidence that microplastics and nanoplastics can damage the heart and blood vessel system in both fish and mammals. In fish, plastic particles enter through the gills and trigger inflammation, disrupt blood chemistry, promote blood clots, and cause heart damage. In mammals, including humans, microplastics interact with blood cells and proteins, travel to the heart, and cause oxidative stress in heart muscle cells, raising concerns about long-term cardiovascular health effects.
Plastic use dramatically increased over the past few years. Besides obvious benefits, the consequent plastic waste and mismanagement in disposal have caused ecological problems. Plastic abandoned in the environment is prone to segregation, leading to the generation of microplastics (MPs) and nanoplastics (NPs), which can reach aquatic and terrestrial organisms. MPs/NPs in water can access fish's bodies through the gills, triggering an inflammatory response in loco. Furthermore, from the gills, plastic fragments can be transported within the circulatory system altering blood biochemical parameters and hormone levels and leading to compromised immunocompetence and angiogenesis. In addition, it was also possible to observe an unbalanced ROS production, damage in vascular structure, and enhanced thrombosis. MPs/NPs led to cardiotoxicity, pericardial oedema, and impaired heart rate in fish cardiac tissue. MPs/NPs effects on aquatic organisms pose serious health hazards and ecological consequences because they constitute the food chain for humans. Once present in the mammalian body, plastic particles can interact with circulating cells, eliciting an inflammatory response, with genotoxicity and cytotoxicity of immune cells, enhanced haemolysis, and endothelium adhesion. The interaction of MPs/NPs with plasma proteins allows their transport to distant organs, including the heart. As a consequence of plastic fragment internalisation into cardiomyocytes, oxidative stress was increased, and metabolic parameters were altered. In this scenario, myocardial damage, fibrosis and impaired electrophysiological values were observed. In summary, MPs/NPs are an environmental stressor for cardiac function in living organisms, and a risk assessment of their influence on the cardiovascular system certainly merits further analysis.