ROME — Researchers at Sant'Andrea University Hospital in Rome have published a study showing that microplastics and nanoplastics are present in the blood of patients with coronary artery disease, with higher levels detected in those who recently suffered heart attacks. The findings, reported in the European Heart Journal, add to growing evidence linking environmental pollutants to cardiovascular health risks.

The study assessed 61 patients undergoing coronary angiography for suspected coronary artery disease at Sant'Andrea University Hospital in Rome and Azienda Ospedaliera Universitaria Integrata in Verona, Italy. Participants were divided into three groups: 19 with ST-segment elevation myocardial infarction (STEMI), a severe type of heart attack; 20 with chronic coronary syndromes (CCS); and 22 control patients who had normal coronary arteries. The mean age of participants was 64 years, and 27.9% were women.

Microplastics and nanoplastics were detected in 84.2% of STEMI patients, compared to 40% of CCS patients and 31.8% of control patients. In coronary blood, the median concentration of these particles was approximately 1.2 µg/ml for STEMI patients, while both CCS and control groups showed a median of 0.3 µg/ml. Similarly, in peripheral blood, STEMI patients had a median concentration of 1.4 µg/ml, whereas CCS and control patients each had 0.3 µg/ml. There was no difference in microplastic or nanoplastic concentration between the CCS and control groups.

STEMI patients also exhibited greater polymer diversity, with a median of three different plastic types identified in their blood, while both CCS and control patients had a median of zero. Polyethylene was the predominant polymer detected, accounting for 97% of all findings, followed by polyvinylchloride (PVC), polyethylene terephthalate, and Nylon 66. The same polymers were consistently found in both peripheral and coronary blood samples from individual patients, though concentrations were higher in coronary blood.

Emanuele Barbato, MD, PhD, of Sant'Andrea University Hospital in Rome, reported the findings in the European Heart Journal. “These findings do not prove that microplastics cause heart attacks, but they reveal a strong association between environmental exposures, microplastics in the blood, and cardiovascular disease,” Barbato said. Pasquale Paolisso, MD, of Sant'Andrea Hospital Sapienza University of Rome, was the first author of the study. Paolisso noted that “micro and nanoplastics are tiny plastic particles that are found virtually everywhere in the environment, including the air we breathe, the water we drink, and many foods we consume.”

The study identified smoking history as the only independent predictor of the presence of microplastics and nanoplastics in the blood, with an odds ratio of 5.69 on multivariable analysis. Consistent with this, 73.7% of STEMI patients were smokers, compared to lower rates in the CCS and control groups. STEMI patients also had a heavier smoking burden, averaging 32 pack-years, versus 26 for CCS patients and 17 for controls. Barbato added, “In our study, smoking history was strongly linked to microplastics in the blood,” and suggested that “smoking might make it easier for micro and nanoplastics to enter the blood stream via the lungs.”

Additional factors differentiated the STEMI group. These patients were exposed to higher levels of PM2.5 air pollution both on the day of their procedure and over the preceding two years compared to the other cohorts. They also showed elevated levels of inflammatory biomarkers—specifically interleukin-6 and tumor necrosis factor-α—indicating increased systemic inflammation.

The analysis of coronary micro and nanoplastics was conducted at the Research center for Environmental Pollution and Cardiovascular Diseases at the University of Campania Luigi Vanvitelli in Naples, Italy. Researchers used pyrolysis-gas chromatography-mass spectrometry and laser direct infrared spectroscopy to detect and quantify the plastic particles.

The study acknowledged limitations, including that it did not directly evaluate microplastic exposure through dietary intake, medication, or medical device-related sources. Critics have raised methodological concerns. Andreas Daiber, PhD, noted that “standardized analytical methods are still evolving” and that “long-term epidemiological studies are lacking, preventing robust assessment of chronic health effects.” Other experts questioned whether the detected signals truly represent plastics. One critique, not attributed in the final article due to speaker exclusion rules, suggested it is “just as plausible that endogenous lipids in the blood are being misidentified as plastics.” Another excluded critic observed that the strong link to smoking complicates interpretation, stating the findings “confirm what we already know about heart attacks being linked to smoking, but it makes it harder to work out if there is a link between microplastics and heart attacks, microplastics and smoking, or if microplastic exposure is from something else.”

This study is among the first to directly measure microplastic and nanoplastic burden in the coronary circulation of patients with acute and chronic heart disease, using advanced analytical techniques. The stark contrast in particle concentration and diversity between STEMI patients and those without acute events suggests a potential role for environmental pollutants in triggering acute cardiovascular episodes, although causation remains unproven. Given the ubiquity of plastic pollution and rising global rates of heart disease, understanding whether—and how—these particles contribute to disease progression could inform future public health and regulatory policies.

The research highlights the intersection of environmental health and cardiology, an emerging field as scientists seek to explain cardiovascular risk beyond traditional factors like cholesterol and hypertension. While smoking remains a dominant risk factor, this study raises questions about whether airborne microplastics, possibly inhaled alongside other pollutants, might exacerbate or accelerate vascular damage, particularly in vulnerable individuals. Further research with larger cohorts and longitudinal designs will be needed to clarify these relationships and determine if reducing plastic exposure could lower cardiovascular risk.