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Researchers using cardiac MRI have found that long-term exposure to air pollution is associated with early signs of heart damage, according to a study that was published today in Radiology, a journal of the Radiological Society of North America (RSNA). The research indicates that fine particulate matter in the air may contribute to diffuse myocardial fibrosis, a form of scarring in the heart muscle that can precede heart failure.

Cardiovascular disease is the leading cause of death worldwide. There is a large body of evidence linking poor air quality with cardiovascular disease. However, the underlying changes in the heart resulting from air pollution exposure are unclear.

We know that if you’re exposed to air pollution, you’re at higher risk of cardiac disease, including higher risk of having a heart attack. We wanted to understand what drives this increased risk at the tissue level.”

Kate Hanneman, M.D., M.P.H., study’s senior author, Department of Medical Imaging at the Temerty Faculty of Medicine, University of Toronto and University Health Network in Toronto

Dr. Hanneman and colleagues used cardiac MRI, a noninvasive imaging technique, to quantify myocardial fibrosis and assess its association with long-term exposure to particles known as PM_2.5. At 2.5 micrometers in diameter or less, PM_2.5 particles are small enough to enter the bloodstream through the lungs. Common sources include vehicle exhaust, industrial emissions and wildfire smoke.

The researchers wanted to evaluate the effects of air pollution on both healthy people and those with heart disease, so the study group included 201 healthy controls and 493 patients with dilated cardiomyopathy, a disease that makes it more difficult for the heart to pump blood.

Higher long-term exposure to fine particulate air pollution was linked with higher levels of myocardial fibrosis in both the patients with cardiomyopathy and the controls, suggesting that myocardial fibrosis may be an underlying mechanism by which air pollution leads to cardiovascular complications. The largest effects were seen in women, smokers and patients with hypertension.

The study adds to growing evidence that air pollution is a cardiovascular risk factor, contributing to residual risk not accounted for by conventional clinical predictors such as smoking or hypertension.

“Even modest increases in air pollution levels appear to have measurable effects on the heart,” Dr. Hanneman said. “Our study suggests that air quality may play a significant role in changes to heart structure, potentially setting the stage for future cardiovascular disease.”

Knowing a patient’s long-term air pollution exposure history could help refine heart disease risk assessment and address the health inequities that air pollution contributes to both in level of exposure and effect. For instance, Dr. Hanneman said, if an individual works outside in an area with poor air quality, healthcare providers could incorporate that exposure history into heart disease risk assessment.

The air pollution exposure levels of the patients in the study were below many of the global air quality guidelines, reinforcing that there are no safe exposure limits.

“Public health measures are needed to further reduce long-term air pollution exposure,” Dr. Hanneman said. “There have been improvements in air quality over the past decade, both in Canada and the United States, but we still have a long way to go.”

In addition to illuminating the links between air pollution and myocardial fibrosis, the study highlights the important role that radiologists will play in research and clinical developments going forward.

“Medical imaging can be used as a tool to understand environmental effects on a patient’s health,” Dr. Hanneman said. “As radiologists, we have a tremendous opportunity to use imaging to identify and quantify some of the health effects of environmental exposures in various organ systems.”

GABA, or gamma-aminobutyric acid, is an amino acid functioning as the principal inhibitory neurotransmitter that can act on the brain to slow or stop the reception of certain signals to the brain, leading to a calmer and more relaxed state. Low GABA levels in the brain have been associated with neurological disorders and diseases like depression, Alzheimer’s or epilepsy. Recently, there has been a push towards understanding more about the gut’s influence on mood, behavior and mental health, as well as what foods might fuel or hinder a healthy mind. Researchers set to work on determining whether brain GABA levels can be increased through dietary additions with the aim of modulating the gut bacteria present in an individual to bypass the blood-brain barrier, a barrier in which it is not proven yet GABA can pass through.

Results were published in npj Science of Food in April 2025.

The relationship between the gut and brain is not necessarily a newly established one, but one that is gaining more attention and influence in how science looks at treating the body more holistically. The two systems communicate effectively, but researchers wanted to know the answer of just how directly these two systems can pass information: can an increase in gut-derived GABA directly cause an increase in the levels of brain GABA?

Researchers confirmed a direct association between gut GABA, brain GABA and the gut microbiota through trials on mice. There are still no solid results on whether or not gut microbiota-derived GABA can cross the blood-brain barrier and directly increase brain GABA. However, further studies do indicate a potential for other pathways to cause an increase in brain GABA elevation, such as stimulation through the Vagus nerve or hormonal pathways.

Our study suggests that prebiotics have the ability to prevent or treat those brain diseases by increasing brain GABA levels via promoting gut GABA production through modulating gut microbiota.”

Thunatchaporn Kumrungsee, study corresponding author, associate professor at Hiroshima University’s Graduate School of Integrated Sciences for Life

In trials done on mice, researchers found the fructo-oligosaccarides (FOS), non-digestible oligosaccharides, and Aspergillus-derived enzymes, lipase and protease, as prebiotics that have shown effective in elevation brain GABA through the influence on the gut. FOS appeared to have a significant increase on the mice’s brain GABA in both the cortex and hippocampus, both sites where GABA acts to reduce excitability and induce a sense of calmness. Additionally, FOS and enzyme supplementation also raised homocarnosine levels in the hippocampus.

“Food factors such as prebiotics and fungi-derived enzymes with prebiotic-liked effects have an ability to increase brain GABA and homocarnosine, a GABA-containing brain-specific peptide, which can possibly in turn enhance brain health through gut microbiota modulation,” said Kumrungsee.

Homocarnosine appears to also be linked to some of the same brain diseases, with a previous study by Kumrungsee indicating homocarnosine-deficient mice were more prone to exhibiting depression-like behaviors and instances of hyperactivity.

Despite a lack of confirmed data on an increase in GABA in the brain derived directly from gut microbiota, there is good reason to believe prebiotic consumption might increase the brain’s GABA levels, as shown in the study. Researchers still need to unravel the mechanism by which the gut might influence the brain and what pathway might be responsible. Once clarified, the next goal is to figure out if the prebiotic treatment used in the study can be further employed for the treatment of GABA-related diseases, like epilepsy or depression.

Jason D. Braga, Norihisa Kato, Noriyuki Yanaka and Thanutchaporn Kumrungsee of the Program of Food and AgriLife Science at Hiroshima University with Jason D. Braga also of the Institute of Food Science and Technology at Cavite State University, Yongshou Yang of the School of Life Sciences at Anhui University, Kyoichi Nishio, Masasumi Okada, Manabu Kuroda and Shotaro Yamaguchi of Amano Enzyme Inc. and Thunatchaporn Kumrungsee of Smart Agriculture at Hiroshima University contributed to this research.

This research was made possible by the Japanese Society of Functional Fermented Foods and Enzyme Supplements, the Danone Institute of Japan Foundation research grant, the Japanese Ministry of Education, Culture, Sports, Science and Technology, and Amano Enzyme Inc.