Nanoplastic and microplastic in arterial plaque is associated with a higher risk of cardiovascular events Original paper

In this cohort study, participants with microplastics and nanoplastics in their carotid artery plaque had a 353% higher risk of cardiovascular events and death compared to participants without these plastics in their plaque.

The association between the presence of microplastics and nanoplastics (MNPs) in atherosclerotic plaques and cardiovascular events (heart attack or stroke) or death.

257 participants (average age of 73; 75% men, 25% women) with high-grade stenosis (more than 70% narrowing) of the carotid artery, the main artery that supplies blood to the brain.

All the participants were undergoing an endarterectomy, a surgery to remove the atherosclerosis plaque build-up causing the stenosis.

A cohort study was conducted in which carotid plaque samples were collected and analyzed for MNPs, and the participants were monitored for the incidence of cardiovascular events over a mean follow-up of 34 months.

The primary outcome was a composite of heart attack, stroke, or death from any cause. The secondary outcomes included biomarkers of inflammation (interleukin-8, interleukin 1-beta, tumor necrosis factor α, interleukin-6), lymphocyte and macrophage infiltration (indicators of inflammation and atherosclerosis progression), and collagen content (an indicator of plaque stability).

More than half of the participants (58%) had a detectable amount of polyethylene in their carotid plaque, and 31 of those participants (12%) also had detectable amounts of polyvinyl chloride (PVC). Polyethylene is the most common plastic in the world, found in food packaging and medical equipment. PVC is another common plastic.

Participants with MNPs in their plaque had a 353% higher risk of experiencing cardiovascular events or death, when adjusted for cardiovascular disease risk factors (e.g., age, sex, lipid profile, diabetes), compared to participants who did not have MNPs in their plaque.

The association between nanoplastic and microplastic in artery plaque and cardiovascular disease events or death

Primary endpoint events were heart attack, stroke, and death.

The amount of polyethylene MNPs present in plaques was positively correlated with the expression levels of markers of inflammation, as well as lymphocyte and macrophage infiltration, and inversely correlated with collagen content.

Plastic use is out of control.^[3] Of the almost 10,000 million metric tons of plastic estimated to have been produced from 1950 to today, approximately 80% has accumulated in landfills and the environment, and less than 10% has been recycled.^[4][5]

It’s difficult to characterize the plastic problem. Several models suggest there will be large future increases in plastic waste, but the numbers cited are often hard to grasp. (What does a million metric tons look like?) Although people are becoming more aware of the issue, whether through taxes on single use plastics like plastic grocery bags or media coverage of issues like the Great Pacific Garbage Patch, awareness alone is often not as powerful for behavioral change as a direct threat to health.^{[6][7][8][9][10][11]} In other words, people will care more readily when the problem affects them personally.

The enormous environmental threat of plastic pollution has been well documented for some time, specifically the disruption of soil, sediment, and aquatic ecosystems, and changes to carbon and nutrient cycles.^[12] However, the issue gained more attention when endocrine-disrupting chemicals like bisphenol A and phthalates became a research focus. MNPs can carry and release endocrine-disrupting chemicals that have potential effects on endocrine function because they can mimic or block hormones and their actions, but most of this research has been conducted in animal models.^[13] With unclear implications for human health, the threat may not seem serious or direct enough for people to make changes.^[14] Despite the mounting evidence for the burden caused by plastic pollution, evidence around plastic exposure and human health implications is still limited, policies on plastic production, consumption, and waste management are lacking, and the circular economy model (recycling, seemingly the only sustainable way to use plastics) is not embraced enough.^[15]

The most recent data collected and research conducted in the field of plastic pollution and its health implications demonstrate just how ubiquitous and harmful the breakdown products of plastics can be. As plastics break down into MNPs, they can be unknowingly ingested or inhaled.^[16] MNPs have been detected in air, water, soil, food (including fish, seafood, salt, honey, and rice) human tissues (e.g., placenta, lungs), breast milk, urine, and blood.^[1] Once in the body, MNPs are suspected of interacting with tissues and organs in many negative ways. Based on preclinical research, microplastics exposure may lead to cell death/damage, oxidative stress, and inflammation.^[16] MNPs may also alter gut microbiome diversity, composition, and metabolism, potentially through effects on gut barrier function.^[17] Again, most of the data driving these conclusions come from studies using human cells or animal models, but more applicable evidence is generated every day.

Routes of absorption, distribution, and excretion of microplastics and nanoplastics in the body

The study under review is noteworthy because it aligns with several of the conclusions from cell and animal model studies. The greater risk of cardiovascular events and death associated with plastic exposure supports the toxicity of MNPs, while the correlations with inflammatory biomarkers provide a compelling mechanism. Correlation does not prove causation, but using samples from the circulatory system in this study design is likely the best evidence available, short of an unethical plastic feeding intervention trial. With more data like these, researchers may be able to understand dose-response relationships and how MNPs may compare to other risk factors for chronic disease and death.

Although this study aims in the right direction for understanding the severity and directness of the threat of MNPs on humans, it still had some limitations. The authors did not monitor important related factors like diet and socioeconomic status. This is important because certain foods, including many highly processed foods, are possible sources of MNPs.^[18] Various highly processed foods are linked to chronic disease, and this may be related to factors other than MNPs and further complicate the interpretation of direct effects from MNPs on cardiovascular health and death. Could MNPs just be a marker of a poorer diet? More research is needed to account for such confounders.

Overall, plastic production and pollution are high and likely present a threat to environmental and human health.^[17] Although most data has previously come from cell and animal models, human studies are beginning to show how potentially harmful MNPs can be. There are hundreds, even thousands, of factors involved in this immense issue, and data availability and risk perception only cover a small part, so even a bit of clarity around these few aspects may help with necessary behavior modifications.^[3][4] How well the narrative of plastic pollution’s influence on human health is communicated, and how the public perceives the threat and risk of MNPs, will help decide how and whether the issue is addressed.

Microplastics are typically defined as plastic particles 1 μm to 5 mm in size. Nanoplastics are typically defined as plastic particles 1 nm to less than 1 μm in size.^[1]

An infarct is a small localized area of dead tissue resulting from interrupted blood supply. A myocardial infarction (heart attack) occurs when the supply of blood to the heart is interrupted, whereas a stroke occurs when the supply of blood to the brain is interrupted. The biggest difference is the speed of tissue death and permanent function loss, and full recovery from a moderate to large stroke is rare.^[2]