Microplastics in food packaging may increase heart disease risk

By Dr. Chinta SidharthanReviewed by Lily Ramsey, LLMFeb 10 2025

New research reveals that microplastics, especially those from food containers, can damage blood vessels, triggering inflammation and cellular changes linked to cardiovascular disease.

​​​​​​​Study: Virgin and photo-degraded microplastics induce the activation of human vascular smooth muscle cells. Image Credit: Andrzej Rostek/Shutterstock.com

Could the plasticware we use for food be linked to heart damage? In a recent study published in Scientific Reports, a team of Italian scientists revealed that microplastics — especially those from food packaging — can trigger harmful changes in vascular cells, increasing the risk of heart disease.

The study found that exposure to these plastics may damage blood vessels, leading to serious health concerns.

Microplastic pollution

Microplastics are now an unavoidable part of our environment. These tiny plastic fragments, shed from packaging, textiles, and industrial waste, have been detected in human blood, lungs, and even the heart, and scientists are increasingly concerned about their potential health effects, particularly their impact on the cardiovascular system.

Studies have already linked microplastics to oxidative stress, inflammation, and tissue damage, but their direct role in heart disease remains unclear. Recently, researchers found microplastics in the arteries of patients undergoing surgery, raising fears that these pollutants may contribute to atherosclerosis and other vascular conditions.

However, the mechanisms through which microplastics could trigger the changes that lead to cardiovascular disease remain unclear.

The current study

The present study explored whether microplastics, including those naturally degraded by sunlight and environmental exposure, cause damage to vascular smooth muscle cells, which play a crucial role in maintaining healthy blood vessels.

To investigate the effects of microplastics on vascular health, the researchers studied human coronary artery smooth muscle cells (HCASMCs) exposed to polyethylene and polystyrene — two common plastics used in food packaging.

These microplastics were tested in both their "virgin" form and after being artificially aged to simulate environmental degradation. The team aimed to determine whether these plastics could trigger harmful cellular changes linked to cardiovascular disease.

The study involved several key experiments. The scientists first measured cell viability to assess how exposure to microplastics affected cell survival.

They also evaluated apoptosis, programmed cell death, and cytotoxicity by measuring markers such as p53 and B-cell lymphoma two modifying factor (BMF), known for their roles in stress response and cell death.

Migration assays were also conducted to see if microplastics altered the movement of smooth muscle cells, which is a crucial factor in the development of vascular diseases such as atherosclerosis.

Additionally, the researchers performed immunofluorescence analysis to detect changes in key proteins that signal phenotypic switching. In this process, smooth muscle cells shift from a healthy to a disease-prone state.

Specifically, they measured the levels of the contractile marker α-smooth muscle actin, galectin-3 (an inflammation marker), and Runt-related transcription factor 2 (RUNX-2), an osteogenic marker linked to vascular calcification.

Finally, they explored the role of microplastics in activating the inflammasome complex, a critical driver of inflammation in cardiovascular diseases.

Results

The study found that exposure to microplastics significantly affected vascular smooth muscle cells (VSMCs), leading to several harmful changes in the heart.

Cell viability was observed to have dropped across all groups exposed to microplastics, with aged polystyrene causing the greatest reduction. This suggests that environmental degradation makes these plastics even more toxic to human cells.

Markers of cell stress and death were also elevated. Levels of p53 and BMF, both associated with apoptosis, increased significantly in microplastic-treated cells, indicating that microplastics may promote programmed cell death.

Furthermore, the cytotoxicity tests confirmed that microplastics caused membrane damage, with lactate dehydrogenase release rising in treated samples.

Additionally, the migration assays revealed that microplastic exposure enhanced VSMC movement, a process linked to atherosclerosis. Cells exposed to microplastics, especially degraded polystyrene, showed increased migration, suggesting a shift toward a disease-associated phenotype.

Immunofluorescence analysis further confirmed these changes, where α-smooth muscle actin levels were observed to have decreased, and galectin-3 and RUNX-2 were upregulated.

These markers indicated that microplastics drive a transition from a healthy contractile state to a synthetic phenotype prone to vascular inflammation and calcification.

Most notably, microplastics activated the inflammasome complex, pointing to a heightened inflammatory response, a known contributor to cardiovascular diseases such as atherosclerosis. Aged microplastics intensified these effects, suggesting that environmentally weathered plastics may pose an even greater risk.

Overall, the study provided strong evidence that microplastics not only infiltrate the human vascular system but also actively contribute to cellular damage and inflammation, increasing the risk of cardiovascular disease.

Conclusions

To conclude, the findings showed that microplastics are more than just an environmental hazard — they may pose a serious threat to heart health.

This study highlighted how microplastics, particularly from food packaging, can trigger harmful changes in vascular cells, potentially leading to atherosclerosis and other cardiovascular conditions.

With plastic pollution on the rise, understanding and mitigating its health effects should be a priority for both researchers and policymakers.