By University of California
Riverside
December 28, 2025

Microplastics may be quietly invading arteries and accelerating heart disease, especially in males.

New research led by biomedical scientists at the University of California, Riverside suggests that routine contact with microplastics — tiny particles released from packaging, clothing, and many plastic products — may speed up atherosclerosis, a condition in which arteries become clogged and can lead to heart attacks and strokes. In this study, the harmful effects appeared only in male mice, offering fresh insight into how microplastics could influence heart health in humans.

“Our findings fit into a broader pattern seen in cardiovascular research, where males and females often respond differently,” said lead researcher Changcheng Zhou, a professor of biomedical sciences in the UCR School of Medicine. “Although the precise mechanism isn’t yet known, factors like sex chromosomes and hormones, particularly the protective effects of estrogen, may play a role.”
Microplastics Found Throughout the Body and Environment

Microplastics have become nearly impossible to avoid. They are present in food, drinking water, and the air, and have even been detected inside the human body. Recent studies involving people have found microplastics embedded in atherosclerotic plaques and have linked higher concentrations to an increased risk of cardiovascular disease. Until now, however, it was unclear whether these particles actively damage arteries or simply accompany disease.

“It’s nearly impossible to avoid microplastics completely,” Zhou said. “Still, the best strategy is to reduce exposure by limiting plastic use in food and water containers, reducing single-use plastics, and avoiding highly-processed foods. There are currently no effective ways to remove microplastics from the body, so minimizing exposure and maintaining overall cardiovascular health — through diet, exercise, and managing risk factors — remains essential.”
How the Mouse Study Was Designed

In a study published in Environment International, Zhou and his colleagues used a widely accepted animal model for heart disease research. The team studied LDLR-deficient mice, which are genetically prone to developing atherosclerosis. Both male and female mice were fed a low-fat, low-cholesterol diet comparable to what a lean and healthy person might consume.

Over a nine-week period, the mice received daily doses of microplastics (10 milligrams per kilogram of body weight). These exposure levels were chosen to reflect amounts considered environmentally relevant and similar to what humans could encounter through contaminated food and water.
Severe Plaque Buildup Seen Only in Males

The results showed a striking difference between sexes. In male mice, microplastic exposure greatly accelerated atherosclerosis. Plaque buildup increased by 63% in the aortic root, the portion of the aorta connected to the heart, and by 624% in the brachiocephalic artery, which branches from the aorta in the upper chest. Female mice exposed to the same conditions did not experience a significant increase in plaque formation.

Importantly, the microplastics did not cause the mice to gain weight or raise their cholesterol levels. The animals remained lean, and their blood lipid measurements stayed the same, indicating that the artery damage was not driven by classic risk factors such as obesity or high cholesterol.
Microplastics Disrupt Cells That Protect Blood Vessels

The researchers also discovered that microplastics interfered with the cells lining the arteries. Using single-cell RNA sequencing, a method that reveals which genes are active in individual cells, the team found changes in both the behavior and balance of several cell types involved in atherosclerosis. Endothelial cells — which form the inner lining of blood vessels and help control inflammation and blood flow — were affected most strongly.

“We found endothelial cells were the most affected by microplastic exposure,” Zhou said. “Since endothelial cells are the first to encounter circulating microplastics, their dysfunction can initiate inflammation and plaque formation.”
Particles Found Inside Plaques and Triggering Harmful Genes

In laboratory experiments, fluorescent microplastics were seen entering atherosclerotic plaques and accumulating within the endothelial layer. These findings align with recent human studies that have also identified microplastics inside arterial lesions.

The team further reported that microplastics activated damaging gene activity in endothelial cells taken from both mice and humans. Exposure triggered pro-atherogenic (plaque-promoting) genes in both species, suggesting a shared biological response to microplastic exposure.

“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.”
Why Males Are More Vulnerable and What Comes Next

Zhou and his colleagues note that additional research is needed to understand why males appear more susceptible to microplastic-related artery damage. The team plans to explore whether similar effects occur in people.

“We would like to investigate how different types or sizes of microplastics affect vascular cells,” Zhou said. “We will also look into the molecular mechanisms behind endothelial dysfunction and explore how microplastics affect male and female arteries differently. As microplastic pollution continues to rise worldwide, understanding its impacts on human health — including heart disease — is becoming more urgent than ever.”

Reference: “Microplastic exposure elicits sex-specific atherosclerosis development in lean low-density lipoprotein receptor-deficient mice” by Ting-An Lin, Jianfei Pan, Mya Nguyen, Qianyi Ma, Liang Sun, Sijie Tang, Matthew J. Campen, Hong Chen and Changcheng Zhou, 17 November 2025, Environment International.
DOI: 10.1016/j.envint.2025.109938
https://doi.org/10.1016/j.envint.2025.109938