Tiny plastic particles that are now everywhere in daily life may be doing far more damage to the heart than previously believed. A new study from the University of California, Riverside has found that microplastics can burrow into blood vessels and dramatically accelerate the development of heart disease, at least in male mice. The findings suggest that microplastics may actively damage arteries rather than simply being passive contaminants found alongside disease.
Microplastics are released from everyday items such as food packaging, synthetic clothing, and disposable plastic products. They have already been detected in human blood, organs, and even inside arterial plaques. Until now, scientists were unsure whether these particles played a direct role in cardiovascular disease. This research provides some of the strongest evidence yet that they do.
The study was led by Changcheng Zhou, a professor of biomedical sciences at UC Riverside’s School of Medicine. His team discovered that regular exposure to microplastics significantly worsened atherosclerosis, a condition where fatty plaques build up inside arteries and increase the risk of heart attacks and strokes. Strikingly, this effect was seen only in male mice, highlighting important biological differences in how males and females respond to environmental pollutants.
According to Zhou, sex-based differences are common in cardiovascular research. Hormones such as estrogen may offer protective effects in females, though the exact mechanism behind the male-specific damage observed in this study is still unclear.
To investigate the impact of microplastics, researchers used LDL receptor–deficient mice, a well-established model for studying heart disease. Both male and female mice were fed a low-fat, low-cholesterol diet similar to that of a healthy human. Over nine weeks, the mice were given daily doses of microplastics at levels considered environmentally relevant and comparable to potential human exposure through food and drinking water.
The results were dramatic. Male mice exposed to microplastics showed a 63 percent increase in plaque buildup in the aortic root near the heart, and an astonishing 624 percent increase in the brachiocephalic artery, a major vessel supplying blood to the head and arms. Female mice exposed to the same conditions showed no significant increase in plaque formation.
Importantly, the microplastics did not cause weight gain or changes in cholesterol levels. The mice remained lean, and their blood lipid profiles stayed stable. This indicates that the damage was not driven by traditional risk factors like obesity or high cholesterol, but by the particles themselves.
Further analysis revealed that microplastics disrupted endothelial cells, which line the inside of blood vessels and play a crucial role in regulating blood flow and inflammation. Using advanced single-cell RNA sequencing, the researchers found that microplastics altered gene activity in these cells, pushing them toward a state that promotes inflammation and plaque formation.
Laboratory experiments showed fluorescent microplastic particles entering arterial plaques and accumulating within the endothelial layer. This mirrors recent findings in human studies, where microplastics have also been found embedded in atherosclerotic lesions.
The team also tested endothelial cells from both mice and humans and found that microplastics activated genes known to promote atherosclerosis in both species. This suggests that the biological response seen in mice may also occur in humans.
Zhou emphasized that completely avoiding microplastics is nearly impossible, given their widespread presence in the environment. However, reducing exposure by limiting plastic food containers, avoiding single-use plastics, and cutting back on highly processed foods may help lower risk. At present, there are no known ways to remove microplastics from the human body.
The researchers now plan to explore why males are more vulnerable and whether different sizes or types of microplastics cause varying levels of damage. As plastic pollution continues to rise globally, understanding its long-term impact on human health, especially heart disease, has become increasingly urgent.
The study was published in the journal Environment International and was supported in part by funding from the National Institutes of Health.