Microplastics Linked to Increased Heart Disease Risk

A research team at the University of California, Riverside, has revealed that routine exposure to microplastics may accelerate the development of atherosclerosis, a condition linked to heart attacks and strokes.

The study focused on male mice, which demonstrated a significant increase in arterial plaque formation after exposure to microplastics. According to the lead researcher Changcheng Zhou, the findings underscore a notable difference in how male and female subjects respond to microplastic exposure, potentially influenced by biological factors such as sex hormones.

Microplastics are ubiquitous in our environment, found in food, drinking water, and even the air we breathe. Studies have detected these particles within human bodies, particularly in atherosclerotic plaques, but it has been unclear whether they directly contribute to arterial damage.

Zhou emphasized that while complete avoidance of microplastics is nearly impossible, minimizing exposure is critical. Suggested strategies include limiting plastic use in food and water containers, reducing single-use plastics, and avoiding highly processed foods.

In the study published in Environment International, LDLR-deficient mice were studied under a controlled diet, receiving daily doses of microplastics for nine weeks, reflecting realistic exposure levels.

The results indicated that male mice developed 63% more plaque in the aortic root and 624% more in the brachiocephalic artery compared to their female counterparts, who showed no significant change. Interestingly, weight and cholesterol levels remained stable in both sexes, suggesting that traditional risk factors for heart disease did not explain the increased arterial damage observed in males.

Further analysis revealed that microplastics disrupted the function of endothelial cells, which line the arteries and regulate important processes such as inflammation and circulation. The study utilized fluorescent microplastics, which were found within arterial plaques, indicating a direct association with plaque formation.

This suggests that microplastics may activate harmful gene pathways in endothelial cells, promoting atherosclerosis across species, as similar gene responses were recorded in both mice and human cells.

Zhou's research team plans to explore the reasons behind the sex-specific effects observed in their findings. They aim to investigate how different types and sizes of microplastics influence vascular cells and to understand the molecular mechanisms behind endothelial dysfunction.

As microplastic pollution continues to proliferate globally, the urgency to comprehend its health impacts, especially regarding heart disease, is paramount. This study highlights the pressing need to address plastic pollution as a significant public health concern, with broader implications for environmental policy and sustainability.