Air pollution spurs inflammation in heart failure patients

Results from the Intermountain Health study, presented on Saturday at the American Heart Association's 2024 Scientific Sessions international conference in Chicago, found that two inflammatory markers -; CCL27 (C-C motif chemokine ligand 27) and IL-18 (interleukin 18) -; were elevated in heart failure patients who were exposed to poor air quality, but did not change in those without heart disease.

This indicates that such air pollution events put more strain on the bodies of patients who already have heart problems.

While previous research has shown that people with some chronic health conditions, like heart failure, coronary disease, asthma, and COPD, struggle during spikes in air pollution, the new Intermountain Health study demonstrates that cardiac inflammation levels specifically rise in people with heart disease during periods of poor air quality.

Benjamin Horne, PhD, principal investigator of the study and professor of research at Intermountain HealthThese biomarkers rose in response to air pollution in people who already had heart disease, but not in patients who were heart disease free, showing that heart failure patients are not as able to adapt to changes in the environment."

For the retrospective study, Intermountain Health researchers worked with scientists at Stanford University and the Harvard School of Public Health to examine the blood of patients enrolled in the Intermountain INSPIRE registry, which collects blood and other biological samples, medical information and laboratory data from healthy individuals and those who have been diagnosed with a variety of medical conditions.

Researchers specifically looked at blood tests for 115 different proteins that are signs of increased inflammation in the body.

They then examined blood draws of 44 patients with heart failure with preserved ejection fraction, and 35 people without heart disease. Some blood was drawn on days with low air pollution, where ambient PM_2.5 levels were under 7 micrograms per cubic meter (μg/m³) of air; those test results were compared to draws done in other people on days when air pollution spiked to PM_2.5 levels of 20 μg/m³ or over.

These spikes were caused by either wildfire smoke in the summer, or during a winter inversion, where air pollution is trapped when warm air holds pollution closer to the ground.

Researchers found that two inflammatory markers -; CCL27 and IL-18 -; were elevated in heart failure patients, but did not change in those without heart disease, indicating that such air pollution events put more strain on the bodies of patients who already have heart problems.

These findings "give us some information about mechanisms in people with heart failure who are having inflammation and suggest they're not as capable in responding to acute inflammation as people who are healthy," said Dr. Horne.

He added that the results from the study suggest that heart failure patients need to take extra precautions during times when air pollution is high.

"It's important that individuals with known heart disease, including those diagnosed with heart failure, need to be especially cautious during periods of poor air quality. This includes exercising indoors, making sure to take their prescribed medications, and avoiding areas like roadways and highways where there's a lot more traffic and pollution," he said.

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