Microplastics may be silently fueling heart disease by damaging the very cells that keep arteries healthy.
University of California - Riverside
A research team at the University of California, Riverside
has found that routine exposure to microplastics -- tiny pieces released from
packaging, fabrics, and common consumer plastics -- may speed up the formation
of atherosclerosis, the artery-narrowing condition associated with heart
attacks and strokes. The effect appeared only in male mice, offering new
insight into how microplastics may influence cardiovascular health in people.
"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 Environment and the Body
Microplastics are found widely in the modern environment,
including in food, drinking water, and the air. They have also been detected
inside the human body. Recent clinical studies have identified microplastics in
atherosclerotic plaques and associated higher concentrations with elevated
cardiovascular risk, although it was not clear whether these particles directly
cause arterial injury.
"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."
Study Design Using a Heart Disease Mouse Model
In their paper published in Environment
International, Zhou and colleagues describe their use of LDLR-deficient
mice, a common model for examining atherosclerosis. Both male and female mice
were placed on a low-fat, low-cholesterol diet similar to what a lean and
healthy person might eat.
The team then administered microplastics daily (10
milligrams per kilogram of body weight) for nine weeks. This amount reflects
levels that could realistically be encountered through contaminated food and
water.
Microplastics Intensify Plaque Formation in Male Mice
The results showed a sharp increase in atherosclerosis, but
only in males. Male mice exposed to microplastics developed 63% more plaque in
the aortic root, the segment of the aorta connected to the heart, and 624% more
plaque in the brachiocephalic artery, a major vessel branching from the aorta
in the upper chest. Female mice exposed to the same conditions did not show
significant plaque progression.
The researchers confirmed that microplastics did not cause
weight gain or increased cholesterol in either sex. The mice stayed lean, and
their lipid profiles remained unchanged, indicating that traditional risk
factors such as obesity or high cholesterol did not explain the heightened
arterial damage.
Disruption of Artery-Lining Cells
The study also showed that microplastics interfered with the
function and makeup of cells lining the arteries. Using single-cell RNA
sequencing, which identifies gene activity in individual cells, the researchers
observed that microplastics altered several cell types involved in
atherosclerosis. Endothelial cells -- the cells that form the inner lining of
blood vessels and help regulate inflammation and circulation -- were affected
the most.
"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."
Microplastics Enter Arterial Plaques and Alter Gene
Activity
Fluorescent microplastics used in the study were found
inside plaques and concentrated within the endothelial layer, consistent with
reports from human samples that have revealed microplastics in arterial
lesions.
Another key observation was that microplastics activated
harmful gene pathways in endothelial cells from both mice and humans. This
included genes associated with pro-atherogenic (plaque-promoting) activity,
suggesting that microplastics trigger similar biological responses across
species.
"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."
Future Research on Sex Differences and Microplastic Types
Zhou and his team emphasize that more work is needed to
determine why males appear more susceptible. The group plans to investigate
whether humans show similar patterns.
"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."
Zhou conducted the study with collaborators from UCR, Boston
Children's Hospital and Harvard Medical School in Massachusetts, and the
University of New Mexico Health Sciences.
The work received partial support from the National
Institutes of Health.
The title of the paper is "Microplastic exposure elicits sex-specific atherosclerosis development in lean low-density lipoprotein receptor-deficient mice."
