Burn pit particles trigger lung inflammation through immune activation

A new study from National Jewish Health helps explain how exposure to burn pit smoke and desert dust may damage the lungs of military service members deployed to regions such as Afghanistan and Iraq. The research, published in Free Radical Biology and Medicine(Opens in a new window), sheds light on why veterans exposed to these environments face higher rates of asthma and other long-term respiratory conditions.

Burn pits, which are used to dispose of waste during military operations, release tiny particles into the air. These particles can be inhaled deep into the lungs, but until now, scientists have not fully understood how they trigger lasting lung damage. In this study, researchers compared particulate matter collected from Afghanistan with similar desert dust from California to better understand their effects on lung immune cells.

The findings show that particles linked to burn pit exposure cause stronger inflammation and stress in lung immune cells than typical desert dust. These particles activate an immune response that can lead to ongoing inflammation and tissue damage, helping explain why some service members develop chronic breathing problems after deployment.

This study provides important insight into how deployment-related particulate matter affects immune cells in the lungs. Our findings identify the Toll-like Receptor 2 (TLR2) as a key mediator of inflammation caused by burn pit–associated particulate matter and suggest that targeting this pathway may offer new strategies to protect or treat individuals exposed during military service."

Brian Day, PhD, vice president of research and, director of the Office of Research Innovation at National Jewish Health, and principal investigator of the study

Using pre-clinical monocyte cell lines and primary bone marrow–derived macrophages, researchers evaluated how Afghanistan desert particulate matter (APM) and California desert particulate matter (CPM) affect immune signaling and inflammatory responses. They measured the production of nitric oxide, hydrogen peroxide and inflammatory cytokines, which are key drivers of lung inflammation and tissue damage.

The results showed that APM was significantly more toxic to macrophages than CPM, producing stronger oxidative stress and inflammatory responses. These findings suggest that deployment-related particulate exposure may place warfighters at heightened risk for long-term respiratory disease.

 Key findings include:

• APM triggered stronger nitric oxide and cytokine responses than CPM, indicating a more intense inflammatory reaction.
• Activation of TLR2 amplified inflammatory signaling, while blocking TLR2 reduced responses to APM exposure.
• APM increased pro-inflammatory (M1) macrophage markers, an effect that was diminished in macrophages lacking TLR2, highlighting the receptor's central role in driving inflammation.

The research represents a significant step toward understanding the biological basis of deployment-related respiratory disease. It provides new information to help guide future diagnostic and therapeutic approaches for affected veterans and service members.