Microplastics & Nanoplastics: Cardiovascular Challenges

Investigating any possible link between cardiovascular diseases (CVDs) and microplastics and nanoplastics has gained popularity in recent years.

These environmental synthetic polymer particles are extremely dangerous to human health.

The intricate interplay between microplastics/nanoplastics and CVDs is explored in depth, with emphasis on underlying mechanisms, clinical implications, and future research directions.

Overview

Plastic particles smaller than 5 millimeters and 100 nanometers, respectively, are known as microplastics and nanoplastics, and they have become ubiquitous environmental contaminants.

Because single-use plastic products are so widely available, are so simple to make, and require insufficient trash and recycling management, plastic pollution has become a major concern in recent decades.

Through the intake of contaminated food and drink, inhalation of contaminated air, dermal contact, and other means, humans are exposed to micro and nanoplastics of all sizes and types.

Humans can receive MPs and NPs from a variety of sources, including mussels, frequently eaten fish, commercial salt, sugar and honey, tea bags, and drinking water.

Unsurprisingly, pollutants can also be detected in bottled water, plastic water bottles, and large amounts of dust that have settled on plates after meals.

Moreover, it has been shown recently that NPs can infiltrate the food chain that feeds humans and livestock by way of plant ingestion. 

Plastic particles may directly induce toxicity by infiltrating plant cells. It has been shown that plant cells are capable of absorbing particles smaller than 0.1 μm, which could lead to their entry into the food chain and pose a significant hazard to higher creatures.

Research on the possible impacts of plastic pollution on human health, especially cardiovascular health, is just beginning, despite the well-established negative effects on ecosystems.

Mechanisms of Action

When ingested or inhaled, microplastics and nanoplastics can interact with biological systems due to their distinct physicochemical characteristics.

Inflammation, oxidative stress, endothelial dysfunction, and dysregulation of lipid metabolism are just a few of the possible pathways that these particles may contribute to the etiology of cardiovascular illnesses, according to recent studies.

Findings from Research: 

Important new information about the relationship between cardiovascular health outcomes and exposure to microplastics and nanoplastics has come from epidemiological studies.

According to these studies, there is a relationship between the amount of microplastic and nanoplastic in ambient samples and cardiovascular risk indicators such high blood pressure, atherosclerosis, and myocardial infarction.

A study found microplastics (shown by arrows) in a tissue sample taken from an artery belonging to a study participant.

In this study italian researchers studied 257 individuals with carotid artery disease, finding microplastics in the plaques of approximately 60% of patients.

After three years post-surgery, 20% of those with microplastics experienced adverse events like death, stroke, or heart attack, compared to only 7.5% of those without microplastics.

Even after adjusting for other risk factors, individuals with microplastics faced a 4½ times higher risk of heart attack, stroke, or death.

According to the results, Polyethylene was found in carotid artery plaque of 150 patients (58.4%), with an average concentration of 21.7±24.5 μg per milligram of plaque; additionally, 31 patients (12.1%) had detectable levels of polyvinyl chloride, averaging 5.2±2.4 μg per milligram of plaque.

Electron microscopy revealed visible foreign particles with jagged edges among plaque macrophages and scattered debris.

Radiographic analysis showed the presence of chlorine in some of these particles.

Patients with detectable micro and nanoplastics (MNPs) in their atheroma faced a significantly higher risk of experiencing a primary end-point event compared to those without these substances.

Investigations on mammals have revealed the deposition of plastic fragments in cardiac tissues, particularly after oral administration.

A study observed that Inhalation of multi-walled carbon nanotubes has been linked to endothelial damage in the heart.

Polystyrene microplastics (PS-MPs) were directly observed using transmission electron microscopy, and it was discovered that they had internalized in cardiomyocytes, indicating that they had been transported to the heart through the circulatory system.

At experimental doses of 5 and 50 mg/L of PS-MPs, the heart showed structural damage and significant myocardial apoptosis along with collagen synthesis.

Molecularly speaking, cardiac Troponin I and myocardial creatine-kinase MB-two significant indicators of myocardial injury—were significantly elevated upon exposure to PS-MPs at high concentrations (50 mg/L).

Furthermore, the assessment of oxidative stress demonstrated a reduction in an antioxidant molecule favoring pro-oxidation in the groups treated with 5 and 50 mg/L, as well as the activation of the Wnt/β-catenin signaling pathway, a fibrosis promoter, at the highest dose.

These findings imply that PS-MPs cause cardiotoxicity by inducing oxidative stress-driven cardiomyocyte apoptosis, which then transitions to Wnt/β-catenin-mediated cardiac fibrosis.

In a rat model, intravenous introduction of plastic microbeads resulted in pulmonary embolism and arterial hypotension.

In vitro cardiac contraction synchronization was achieved by fast internalization of positively charged PS-NPs at a concentration of 25 μg/mL into the ventricular myocytes of neonatal rats exposed to electrical pulses.

L-type calcium channel (LTCC) inhibition was seen as a result of a notable drop in intracellular calcium levels.

In the early period, contraction forces decreased as a result of this effect and a decline in the electrophysiological performance of newborn cardiomyocytes.

A decrease in baseline oxygen consumption rate and a marked impairment in glycolytic balance during the late phase affected ATP synthesis by lowering mitochondrial membrane potentials.

The biological effects of microplastics and nanoplastics on the cardiovascular system have been further clarified by experimental study employing in vitro and animal models.

These investigations have shown that these particles can cause endothelial dysfunction, trigger pro-inflammatory and pro-thrombotic reactions, and accelerate the formation of atherosclerotic plaques.

These findings underscore the significant risks posed by microplastic and nanoplastic pollution on cardiovascular health and the potential development of cardiovascular diseases.

Towards the Future: 

Comprehensive mitigation and prevention methods are needed due to the severe implications of microplastic-induced cardiovascular damage.

It is imperative for healthcare practitioners to acknowledge the possible cardiovascular hazards linked to microplastic exposure and include environmental health concerns into their therapeutic procedures.

To advance our understanding of micro and nanoplastic (MNP) impact on cardiovascular health, future investigations should delve into variables like particle size, exposure levels, surface properties, plastic varieties, dimensions, and concentrations aiming for more realistic scenarios.

It's crucial to monitor early signs of MNP-induced cardiovascular harm, such as fluctuations in heart rate and changes in cardiac enzyme levels, to unravel the mechanisms behind these effects and their links to cardiovascular diseases.

In the future, multidisciplinary studies are required to clarify the intricate connection between cardiovascular illnesses and microplastics and nanoplastics.

Conclusion:

A major public health concern is the association between cardiovascular illnesses and microplastics/nanoplastics.

Healthcare practitioners must continue to be watchful and proactive in treating the cardiovascular risks linked to plastic pollution as our awareness of this relationship develops.