(Symbolbild). Microplastics enter the human body through air, drinking water, and food and have been found in almost all organs. A Roman study has now measured these particles directly at the site of a heart attack. Concentrations differ significantly between patient groups.
(Photo: © Forschung und Wissen)
Blood samples taken directly from the coronary arteries of heart attack patients reveal concerning findings. Researchers from Rome found significantly higher concentrations of microplastics in patients suffering from severe heart attacks compared to heart-healthy individuals. At the same time, inflammatory markers in the same blood were measurably higher, indicating a possible connection between plastic particles and cardiovascular conditions.
Microplastics are defined as plastic particles smaller than five millimeters, originating from the breakdown of packaging, tire wear, textiles, and ubiquitous consumer products. Even smaller fragments under one micrometer are classified as nanoplastics and can surpass biological barriers that larger particles cannot. Humans are estimated to ingest tens of thousands to over 100,000 of these particles annually through air, drinking water, and food. Initially considered biologically inert because plastics are chemically stable and not metabolized in the body, the presence of microplastics in the bloodstream has been documented multiple times, sparking debate over their health implications. However, it remained unclear whether this burden left measurable traces in the body or merely reflected environmental pollution.
The coronary arteries supply oxygenated blood to the heart muscle, making them critical to heart attack events. When these arteries become constricted due to deposits of fats, connective tissue, and calcium, a condition known as atherosclerosis occurs. If a deposit ruptures and forms a blood clot, blood flow ceases abruptly, leading to the death of heart muscle tissue. Inflammation has been recognized as a driving force for many years, destabilizing these deposits. Animal studies have shown that plastic particles can promote chronic inflammation and contribute to deposits in blood vessels. However, whether this mechanism similarly manifests in humans under realistic conditions remained unresolved, and this new study aims to fill that gap.
Blood from Coronary Arteries Shows Clear Differences
A team from the Sant’Andrea University Hospital, led by Pasquale Paolisso, collected blood not from the arm vein but directly from the coronary arteries—the site of the disease. They examined 39 patients with chronically narrowed coronary arteries or severe heart attacks, alongside 21 heart-healthy individuals serving as controls. The analysis published in the European Heart Journal revealed a tiered picture among the three groups that seemed unlikely to have occurred by chance. Microplastics were detected in 84% of heart attack patients, 40% of those with chronic disease, and 31.8% in the control group. Moreover, the measured concentration was significantly higher among heart attack patients, with a wider variety of plastic types found, particularly polyethylene, which is commonly used in packaging.
Inflammatory Markers Support the Suspicions
From the same coronary blood, researchers additionally measured several inflammatory markers and found elevated levels of the cytokine Interleukin-6 in heart attack patients. This marker regulates the acute inflammatory response and stimulates the liver to produce C-reactive protein, making it an important marker in cardiology for inflammatory vascular processes. The combination of higher particle load and elevated inflammatory activity in the same location suggests a locally inflammatory environment. Andreas Daiber, a molecular cardiology professor at the University Medical Center Mainz who was not involved in the study, agrees with this interpretation, noting the interplay of epidemiological, clinical, and mechanistic evidence. For German readers, this situation is significant as similar exposure routes apply, and cardiovascular diseases remain the leading cause of death.
Smoking and Pollution Increase Particle Uptake
An intriguing question arises as to why some individuals are more affected than others. Most patients with elevated particle levels in their coronary blood lived in areas where fine particulate matter exceeded the World Health Organization’s guideline of 15 micrograms per cubic meter of air for more than a year. Furthermore, a strong correlation with smoking emerged, as particles were found in all heart attack patients with a history of smoking, but none in the non-smoking control group. A plausible mechanism is indirect, as cigarette smoke weakens the mucosal barrier of the airways, allowing particles to enter the bloodstream more easily. Research has indicated that microplastics can induce cellular changes in lung tissue, considered early signs of pathological processes. Air pollution may exert similar effects.
The study’s implications have clear limits, which the authors themselves acknowledge. Only 61 individuals were assessed at a single point in time, and the blood samples were collected post-heart attack, not before. Thus, it is challenging to determine whether the particles contributed to the event or if the event itself and its treatment influenced the measurements. Emanuele Barbato, the study leader from Sapienza University in Rome, emphasizes that the results do not prove a causal relationship but demonstrate a strong association between environmental exposure, blood particle load, and cardiovascular diseases. The true advancement lies in the study design, as this is the first time measurements were made at the target organ itself. Larger prospective cohorts are needed to establish whether the burden precedes the event. Additionally, the finding that airborne microplastics increase health risks suggests that risk factors should be considered collectively.
European Heart Journal, Study on nano- and microplastics in coronary blood; doi:10.1093/eurheartj/ehag447
