- A small 61-person study assessed the burden of microplastics and nanoplastics across the spectrum of coronary artery disease (CAD) via in vivo detection and quantification.
- STEMI patients were shown to harbor higher levels and more diversity of these plastic particles compared with chronic coronary syndrome and control cohorts.
- Micro- and nanoplastics detection frequently co-occurred with elevated inflammatory biomarkers, greater PM2.5 exposure, and smoking, suggesting a potential association between these environmental exposures and CAD.
Among people undergoing coronary angiography for suspected coronary artery disease (CAD), heart attack patients stood out for having higher microplastics and nanoplastics in their blood, a small Italian study found.
People with ST-segment elevation myocardial infarction (STEMI), chronic coronary syndromes (CCS), and normal coronary arteries had distinct findings when it came to blood sampled during the invasive procedures:
- Frequency of any detection of microplastics and nanoplastics: 84.2%, 40%, and 31.8%, respectively (P=0.002)
- Concentration of microplastics and nanoplastics in coronary blood: median ~1.2 µg/ml vs 0.3 µg/ml vs 0.3 µg/ml (P<0.001)
- Concentration of microplastics and nanoplastics in peripheral blood: median ~1.4 µg/ml vs 0.3 µg/ml vs 0.3 µg/ml (P<0.001)
- Polymer diversity: median of three polymers vs 0 vs 0 (P<0.001)
Polyethylene was the predominant polymer detected (97%), followed by polyvinylchloride (PVC), polyethylene terephthalate, and Nylon 66. The same polymers were consistently identified in peripheral and coronary blood samples from individual patients, with the highest concentrations in coronary blood (P<0.001), reported Emanuele Barbato, MD, PhD, of Sant’Andrea University Hospital in Rome, and colleagues 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,” said Barbato in a press release.
Indirect products of mass industrial processes, microplastics and nanoplastics are now ubiquitous in every environment on Earth, including air, water, soil, and food. These particles are increasingly found in human tissues and organs, raising concerns about their potential harms.
Yet the diversity in size and composition of these plastic particles has challenged research. Polyethylene, for example, comes in long linear chains and low- and high-density options, while PVC is a substantially denser thermoplastic.
“Standardized analytical methods are still evolving,” Andreas Daiber, PhD, and two colleagues of University Medical Center of the Johannes Gutenberg-University in Mainz, Germany, wrote in an accompanying editorial. “Long-term epidemiological studies are lacking, preventing robust assessment of chronic health effects. The fate of plastic particles within the human body, whether they accumulate, degrade, or are excreted, remains poorly understood. Furthermore, current experimental models often do not reflect real-world exposure conditions, where individuals are exposed to complex mixtures of particles and chemicals.”
What’s more, it is not clear that the lab methods really detected plastics in the first place, argued Kevin Thomas, PhD, of the University of Queensland in Brisbane. “Microplastics are notoriously challenging to measure in human blood, and based on recently published confidence levels, the results presented are presumptive of the presence of plastics at best,” Thomas said in a commentary submitted to the Science Media Centre.
“While the authors are to be commended for their efforts to control contamination, the study ignores findings that show that the pyrolysis-gas chromatography-mass spectrometry method … is not suitable for polyethylene and PVC, two of the main plastics detected. It is just as plausible that endogenous lipids in the blood are being misidentified as plastics,” Thomas contended.
Moreover, it was a challenge parsing out the sources of the plastics and any effect of modifiers based on the present report. Considering ambient exposure, the STEMI group also had greater exposures to air pollution (PM2.5), and microplastics and nanoplastics detection was more frequent among smokers and patients exposed to more PM2.5, Barbato’s team reported. However, smoking history was the only independent predictor of the presence of these plastics on multivariable analysis (OR 5.69, 95% CI 1.33-26.63).
“The present study addresses an urgent and emerging public health issue by investigating the association between MNPs [microplastics and nanoplastics], PM2.5, and smoking in CAD, both in the acute and chronic settings, potentially amplifying their damaging effects on cardiovascular health. MNPs, PM2.5, and smoking constitute potentially modifiable environmental risk factors for cardiovascular diseases, with significant implications for public health and cardiovascular disease prevention,” Barbato and colleagues concluded.
Their cross-sectional study included 61 consecutive patients undergoing coronary angiography for suspected CAD at two Italian centers.
Participants were split into STEMI (n=19) and CCS (n=20) groups, with peers showing normal coronary arteries serving as controls (n=22). Mean age was 64 years, and 27.9% were women. Smokers represented the majority of the cohort — reaching a high of 73.7% in the STEMI arm, which on average had a habit of 32 packs per year (compared with 26 with CCS and 17 with controls, P=0.003).
Peripheral and coronary blood samples were collected two or three times during the invasive procedures, stored in freezers, and sent to the core laboratory. Microplastics and nanoplastics in coronary and peripheral blood samples were evaluated using pyrolysis-gas chromatography-mass spectrometry and laser direct infrared spectroscopy.
There was no significant difference in microplastic or nanoplastic concentration between CCS and control groups.
Air pollution exposure data were collected on the day of the invasive procedure (acute exposure) and over the preceding 2 years (chronic exposure). STEMI patients were exposed to higher levels of PM2.5 both on the day of the invasive procedure (P=0.012) and over the preceding 2 years (P=0.010), compared with the other cohorts.
Additionally, STEMI patients showed higher levels of interleukin-6 and tumor necrosis factor-α, indicating increased systemic inflammation.
Study authors acknowledged that their findings should be considered exploratory given the small sample, and that minor differences existed in the methods used for collecting coronary blood samples across the study groups. In addition, the investigation did not directly evaluate microplastics exposure through dietary intake, medication-, or device-related sources.
Inherent also from its observational design is the study’s potential for confounding or reverse causation. For one, the high prevalence of smoking in the STEMI group, and smoking history in turn being the only independent predictor of microplastics, may be a point of concern with this analysis.
“This confirms 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,” said Ria Devereux, PhD, of the University of East London, in another statement to the Science Media Centre.
“Overall, this study is an important step forward, but much larger prospective studies with harmonized analytical methods and detailed exposure assessment are needed before firm conclusions can be drawn about the causal role of micro- and nanoplastics in cardiovascular disease,” said Thava Palanisami, PhD, of the University of Newcastle in New South Wales, Australia, also on the Science Media Centre.
