Experts reveal how plastic particles lodged in arteries could heighten heart disease risk, demanding urgent attention from clinicians and policymakers.
Microplastics and nanoplastics: tiny threats for cardiovascular diseases? Image Credit: Shutterstock
In a recent article published in the journal Cardiovascular Research, researchers discussed whether nanoplastics (NPs) and microplastics (MPs) are emerging risk factors for cardiovascular diseases (CVDs).
The ubiquity of plastics has led to an environmental crisis with profound health implications. While plastics were initially regarded as revolutionary materials due to their durability and versatility, they have become pervasive pollutants that fragment into NPs and MPs and infiltrate the food chain, ecosystem, and the human body. NPs and MPs have been detected in several human tissues, including the brain, blood, liver, lungs, placenta, and atheroma.
The authors first reported that NPs and MPs accumulate in atherosclerotic plaques in a prior NEJM cohort study, which is associated with a higher risk of cardiovascular disease. In particular, individuals with detectable NPs and MPs in their plaques had an exact 4.5-fold increased risk of major adverse cardiovascular events (MACEs) than those without. These findings, along with preclinical evidence, suggest that NPs and MPs play an active role in promoting MACE or atherogenesis.
Furthermore, NPs and MPs may act as carriers of toxic substances, such as pesticides, herbicides, and heavy metals, which can damage the cardiovascular system. Indirect mechanisms such as gut microbiota dysregulation have also been proposed. This raises new and urgent cardiovascular research questions and challenges the conventional view of atherosclerosis by introducing a novel risk factor. However, longitudinal human studies establishing causality are currently lacking, and extensive studies with diverse populations are needed to corroborate these findings.
Implications for translational and clinical research
The presence of NPs and MPs in atherosclerotic plaques highlights an emergent risk factor and might require integration into prevention strategies. While cardiovascular risk factors, including smoking, hypertension, hyperlipidemia, and obesity, are well established, environmental pollutants and their role in CVDs have gained substantial attention in recent years.
While the toxic effects of air pollution have long been linked to higher cardiovascular mortality, the discovery that NPs and MPs may have comparable effects implies that cardiovascular medicine must broaden its focus also to include environmental cardiology. Whether NPs and MPs directly contribute to plaque destabilization or formation, or their presence is simply an environmental exposure marker, remains unknown. The complexity of measuring and dosing MPs and NPs limits comparability across studies.
In preclinical models, NPs and MPs have been found to induce endothelial dysfunction, oxidative stress, apoptosis, pyroptosis, and vascular inflammation, suggesting that they might not be mere bystanders. Another fundamental question is how NPs and MPs enter the vascular system and build up in plaques. Although potential routes include inhalation of airborne particles, ingestion via contaminated water and food, and absorption through the skin, which sources are more relevant remains unclear. Uncertainty also exists about which particle sizes and polymer types are most pathogenic, with early hypotheses suggesting that nanoplastics may penetrate biological barriers more readily.
Prevention strategies and therapeutic perspectives
Addressing the cardiovascular impact of plastics necessitates both primary and secondary prevention strategies. Primary prevention efforts should focus on decreasing the contamination of plastics in the environment and in humans. However, this poses a significant economic and political challenge, with current regulatory measures described as weak, and legacy contamination is expected to persist for at least a century even if production were to stop today. Secondary prevention strategies should aim at alleviating the effects of NPs and MPs in the human body.
Current anti-atherosclerotic therapies may offer some protection if a role for NPs and MPs in inflammation, apoptosis, and endothelial dysfunction is substantiated in humans. Drugs such as statins, glucagon-like peptide 1 receptor agonists (GLP-1 RAs), sodium-glucose cotransporter 2 (SGLT2) inhibitors, and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors may counteract vascular inflammation, even if they do not address the root cause. In addition, exploratory strategies to enhance gastrointestinal elimination are being considered, including dietary fibres, probiotics, and bile-acid sequestrants.
Concluding remarks
Together, NPs and MPs represent an unprecedented challenge in CVD. They may emerge as a novel cardiovascular risk factor if their role in CVD development and atherogenesis is confirmed. A multidisciplinary approach, incorporating public health, molecular biology, epidemiology, and pharmacology, may be necessary to address this issue. Overall, cardiovascular medicine should adapt to the challenges posed by these new environmental threats.