Inhaled microplastics suppress pulmonary macrophages critical to the immune system

Microplastics are ubiquitous in the environment, and we all routinely inhale these tiny pollutants. Now new research published at the ATS 2025 International Conference has found that inhaled microplastics suppress pulmonary macrophages, a type of white blood cell found in the lungs that are critical to the immune system.

The findings shed new light on the mechanisms through which microplastic exposure leads to long-term disruption of immune function and increases risk of cancer and other diseases. These risks aren't limited to the lungs but can affect the entire body.

For me, it's a bit eye opening that although microplastics aren't the most dangerous agent we may encounter, they are far from benign. Respiratory microplastics disseminate systemically after passing through the lung and negatively affect macrophage function. Overall, these may have detrimental effects on any and all organ systems and contribute to a number of diseases."

Adam Soloff, PhD, associate professor of cardiothoracic surgery, University of Pittsburgh and first author of the study

Macrophages are the most abundant immune cell of the lung and play a critical role. These cells work as immune housekeepers, devouring pathogens and maintaining tissue homeostasis. They also clear away dead lung cells, which can cause chronic inflammation when they're left to accumulate.

For the study, researchers cultured macrophages with polystyrene microplastics at different sizes and concentrations. They also exposed mice to inhaled microplastics and then measured the effects on the animals' macrophage function.

They found that within 24 hours of exposure to microplastics of any size, the macrophages showed a reduced ability to surround and absorb other bacteria, a critical process called phagocytosis. Microplastic particles were readily detected in the liver, spleen and colon with trace amounts in the brain and kidney for up to a week after being inhaled.

Researchers also found that the drug Acadesine, an AMP kinase activator, was able to partially restore macrophage function after microplastic exposures.

Dr. Soloff said the results were surprising.

"When we first started to discuss these microplastic exposures, I was sure that the macrophages would just eat (phagocytose) and digest them (lysosomally process), and that would be the end of it," he said. "I was really surprised to see that not only did the macrophages struggle to break down the plastics in vitro, but macrophages in the lung retained these particles over time as well."

In addition to driving public health measures to reduce the use of plastics overall, the findings could support the use of drugs like Acadesine in at-risk populations.

"Given the poor air quality in so many places around the world, you could imagine that developing a low-cost, low-side-effect therapeutic to restore pulmonary macrophage function may be an important tool to combat increasing rates of lung disease," Dr. Soloff said.

Next, the team will examine microplastic exposure in lung tissues from patients, with a long-term goal of establishing biomarkers for lung disease and lung cancer risk that could be used to trigger early screening or intervention.