Scientists have discovered that microplastics may be silently fueling heart disease.

Regular exposure to these ubiquitous tiny particles can speed up the development of atherosclerosis, a disease that narrows and hardens the arteries, according to researchers at the University of California, Riverside (UCR).

Microplastics are extremely small plastic fragments — usually less than 5 millimeters long— that come from the breakdown of larger plastic items or are intentionally manufactured for products such as cosmetics and cleaning agents. They are widespread in the environment, showing up in water, soil, and even in the air. People can ingest or inhale them, raising growing concerns about their potential effects on human health.

Atherosclerosis occurs when plaque — made up of fat, cholesterol, and other substances — builds up inside artery walls. This buildup restricts blood flow and increases the risk of heart attacks and strokes.

According to ScienceDaily, the UCR team discovered that only male mice developed severe atherosclerosis after being exposed to microplastics. The study, published in Environmental International, suggests that hormones or sex chromosomes may help protect females.

These findings support earlier studies that detected microplastics in human atherosclerotic plaques and linked higher levels of these particles with elevated cardiovascular risk. However, the new research takes the connection further by showing that microplastics may actively contribute to plaque formation rather than simply being present.

STUDY DETAILS

Lead researcher Changcheng Zhou, a professor of biomedical sciences at UCR’s School of Medicine, and his team fed both male and female mice a low-fat, low-cholesterol diet similar to what a health-conscious person might choose. The researchers then exposed the mice to microplastics at a dose of 10 milligrams per kilogram of body weight for nine weeks.

The results were striking: male mice developed 63% more plaque in the aortic root — the section of the artery connected to the heart — and 624% more plaque in the brachiocephalic artery, a major branch in the upper chest. Female mice did not show comparable plaque buildup.

Importantly, the mice did not gain weight or develop high cholesterol during the study, which ruled out traditional risk factors for atherosclerosis. Instead, the researchers found that microplastics altered certain types of cells involved in the disease. Endothelial cells, which line the inside of blood vessels, were particularly affected.

By using fluorescent microplastics, the researchers were able to track where the particles traveled. They found higher concentrations within the plaques and in the endothelial layer —findings that align with human studies.

"Our study provides some of the strongest evidence so far that microplastics may directly contribute to cardiovascular disease, not just correlate with it," Zhou said. "The surprising sex-specific effect — harming males but not females — could help researchers uncover protective factors or mechanisms that differ between men and women."