Breathing ozone disrupts gut-like microbes in the airways, weakens barriers, and sparks inflammation, which sends damaging signals to the liver to cause fat buildup and cell injury.


RT’s Three Key Takeaways:

  1. Lung–Liver Axis Identified — Researchers at Fudan University showed that ozone exposure disrupts the lung microbiome, driving inflammation and barrier damage that in turn trigger liver injury and metabolic dysfunction.
  2. Systemic Harm Beyond the Lungs — In mice, 30 days of ozone exposure caused lung inflammation, microbial imbalance, and ferroptosis-linked liver damage, revealing ozone’s reach far beyond respiratory illness.
  3. Public Health Implications — The study highlights ozone as a systemic pollutant and calls for stricter air quality standards, while also pointing to potential interventions such as microbial therapies and antioxidants.


Ozone pollution is rising worldwide, frequently exceeding safety thresholds in urban centers and industrial regions. Its health risks are well-documented: breathing ozone can worsen asthma, damage airways, and increase the risk of cardiovascular and neurological disorders. Toxicological studies further suggest that ozone generates reactive oxygen species and breaks down protective lung barriers. At the same time, researchers have observed links between ozone exposure and systemic metabolic problems, such as lipid disorders and oxidative stress. Yet the exact biological connections between respiratory exposure and distant organ damage remain elusive. Because of these challenges, it is essential to investigate how ozone crosses organ boundaries and aggravates systemic injury.

A team from Fudan University and collaborating institutions has revealed how ozone exerts multi-organ effects by disturbing the delicate dialogue between the lungs and liver. Their findings, published in Frontiers of Environmental Science & Engineering, show that mice exposed to ozone for 30 days developed not only lung injury but also liver dysfunction driven by microbial imbalance. By identifying the lung–liver axis as a critical pathway, the study provides fresh insight into how a common pollutant can silently compromise human health far beyond the respiratory system.

In controlled experiments, mice were exposed to ozone at concentrations mirroring polluted cities. Lung tissue analyses revealed congestion, inflammation, and weakened antioxidant defenses. Key protective genes such as Sod2 and Ucp2 were suppressed, while inflammatory markers like Il-1β and Il-18 rose sharply. Tight junction proteins including Occludin declined, pointing to compromised barrier integrity.

The lung microbiome also shifted dramatically: diversity dropped, beneficial bacteria dwindled, and harmful taxa associated with inflammation flourished. These microbial disruptions correlated closely with altered immune gene expression, suggesting a direct link between dysbiosis and pulmonary injury.

The damage did not stop there. Despite normal food intake, exposed mice gained less weight and developed liver abnormalities, including necrosis and lipid accumulation. Biochemical tests showed spikes in aspartate aminotransferase (AST), malondialdehyde (MDA), and iron ions, alongside depleted glutathione. Lipidomic profiling confirmed signs of ferroptosis, a type of cell death tied to oxidative imbalance. Mediation analysis revealed that lung injury and microbial changes played a central role in liver lipid dysregulation, firmly establishing the lung–liver axis as the bridge through which ozone spreads its harm.

“Ozone has traditionally been viewed as a respiratory hazard, but our work shows its influence reaches much further,” said Dr. Dan Li, corresponding author of the study. “By altering the lung microbiome, ozone triggers a chain of events that culminates in liver injury and metabolic disruption. This hidden lung–liver communication sheds light on how environmental exposures can ripple through the body. Recognizing this pathway is essential for understanding the true scope of ozone’s health risks and for designing effective strategies to protect vulnerable populations.”

The findings underscore the need to view ozone not just as a cause of coughing or asthma, but as a systemic pollutant capable of undermining multiple organs. By uncovering the role of the lung microbiome in mediating liver damage, the study opens new possibilities for interventions—ranging from microbial therapies and antioxidants to targeted policies that curb ozone emissions. It also provides a scientific rationale for more stringent air quality standards worldwide. Ultimately, protecting public health will require not only reducing ozone levels but also addressing the subtle biological connections through which pollutants exert their harm.