RIVERSIDE, Calif. — A recent study conducted by biomedical scientists at the University of California, Riverside, reveals that exposure to microplastics may significantly accelerate atherosclerosis in male mice. This artery-clogging process is a precursor to heart attacks and strokes, raising concerns about cardiovascular health in humans. The study, published in Environment International, highlights a gender-specific impact, with harmful effects observed only in male mice.
“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 at 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.”
Understanding Microplastics and Cardiovascular Health
Microplastics, tiny fragments originating from packaging, clothing, and numerous plastic products, are pervasive in the environment. They have been detected in food, water, air, and even inside the human body. Recent human studies have identified microplastics in atherosclerotic plaques, correlating higher levels with increased cardiovascular disease risk. However, the direct contribution of microplastics to artery damage was unclear until now.
“It’s nearly impossible to avoid microplastics completely,” Zhou noted. “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.”
The Study’s Methodology and Findings
Zhou and his team utilized a well-established mouse model for heart disease research: LDLR-deficient mice, which are prone to developing atherosclerosis. Both male and female mice were fed a low-fat, low-cholesterol diet, akin to a lean, healthy human diet. Over nine weeks, the mice received daily doses of microplastics (10 milligrams per kilogram of body weight), levels deemed environmentally relevant and similar to human exposure through contaminated food and water.
“In male mice, microplastic exposure increased plaque buildup by 63% in the aortic root and 624% in the brachiocephalic artery,” Zhou reported. “In female mice, the same exposure did not significantly worsen plaque formation.”
The study noted that microplastics did not cause obesity or raise cholesterol levels in the mice. The subjects remained lean, and their blood lipid levels were unchanged, indicating that increased artery damage was not due to traditional risk factors like weight gain or high cholesterol.
Impact on Arterial Cells
Further investigation revealed that microplastics altered key cells lining the arteries. Using single-cell RNA sequencing, the team found that microplastics disrupted the activity and proportions of several cell types involved in atherosclerosis, particularly endothelial cells, which line blood vessels and regulate inflammation and blood flow.
“We found endothelial cells were the most affected by microplastic exposure,” Zhou explained. “Since endothelial cells are the first to encounter circulating microplastics, their dysfunction can initiate inflammation and plaque formation.”
Fluorescent microplastics were observed entering plaques and localizing within the endothelial layer, consistent with recent human studies showing microplastics in arterial lesions. Moreover, microplastics triggered harmful gene activity in both mouse and human endothelial cells, activating pro-atherogenic genes, suggesting a shared biological response.
Implications and Future Research
“Our study provides some of the strongest evidence so far that microplastics may directly contribute to cardiovascular disease, not just correlate with it,” Zhou stated. “The surprising sex-specific effect — harming males but not females — could help researchers uncover protective factors or mechanisms that differ between men and women.”
Zhou and his team acknowledge the need for further research to understand why males are more vulnerable. They plan to investigate how different types or sizes of microplastics affect vascular cells and explore the molecular mechanisms behind endothelial dysfunction. As microplastic pollution continues to rise globally, understanding its impacts on human health, including heart disease, is becoming increasingly urgent.
The study was supported by grants from the National Institutes of Health and involved collaboration with colleagues at UCR, Boston Children’s Hospital, Harvard Medical School, and the University of New Mexico Health Sciences.
The University of California, Riverside, is a doctoral research university known for its groundbreaking exploration of critical issues. Reflecting California’s diverse culture, UCR enrolls over 26,000 students and has a significant economic impact, contributing more than $2.7 billion annually to the U.S. economy. For more information, visit www.ucr.edu.
