e cigarette, vaping, blu cigs

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In a Nutshell

  • Brief e-cigarette vapor exposure damaged the protective lining of human lung cells and triggered a stress response that led to cell death.
  • In hamsters, signs of lung cell stress and incomplete cellular repair were still present ten days after vaping exposure ended, even though the animals looked and acted healthy.
  • Hamsters pre-exposed to vapor had higher coronavirus levels in their airways and lower activity of genes that normally help fight viral infections.

It took only five days. Five days of vaping was enough to leave lung cells struggling to repair themselves more than a week after the last puff, and hamsters given the same short exposure still showed weaker antiviral defenses ten days on, even though the animals looked completely healthy.

Researchers from National Jewish Health, the University of Colorado, and Colorado State University, writing in the journal JCI Insight, wanted to know what vapor from e-cigarettes actually does to the deepest, most delicate parts of the lungs: the tiny air sacs and blood vessels where oxygen moves into the bloodstream. Working with human lung cells in the lab and with hamsters exposed to vapor from a popular nicotine vape product, they found that even brief exposure sets off a stress response that damages the lungs’ protective lining, jams up the cells’ internal cleanup system, and leaves hamsters carrying higher levels of a coronavirus after infection.

Timing is what stands out here. This wasn’t the result of years of heavy use. Human cells showed damage after just 24 hours of lab exposure. In hamsters, five days of vaping was enough to trigger changes in lung gene activity and immune defenses that stuck around long after the vaping stopped. A separate round of experiments showed those weakened defenses carried real consequences when a virus arrived.

How Scientists Tested Vaping’s Effect on the Lungs

Researchers started small, growing human lung cells in lab dishes, including cells that line blood vessels in the lungs and cells that line the small airways deep in the chest. They also used thin slices of real human lung tissue donated for research. These cells and tissues were exposed to vapor from a commercial nicotine vape product, at levels meant to mimic what a casual vaper might breathe in.

That exposure weakened the protective barrier these cells form, in some cases almost immediately. Researchers measured this by tracking electrical resistance across a layer of cells, a way of testing how “leaky” the barrier becomes. Higher vapor levels caused more damage, and the effect appeared in both blood vessel and airway cells.

To understand why, the team found that vaping activated a stress pathway inside cells called JNK signaling, which normally kicks in when cells encounter chemical irritants or other damage. Once triggered, it set off a chain reaction. Cells tried to clean up the damage through a process called autophagy, a kind of internal recycling system, but the process got stuck partway through. Instead of finishing the cycle, waste material piled up inside the cells, growth slowed, and some cells died off. When researchers blocked the JNK pathway with a drug, the barrier damage and the stalled cleanup process both improved, pointing to this pathway as a central driver of the injury.

Why Vaping Damage Lingers in the Lungs

To see whether this damage sticks around, researchers used golden Syrian hamsters, chosen because their small airways more closely resemble human lungs than a mouse’s and because they respond to respiratory viruses similarly to people. Researchers exposed the hamsters to vapor once a day for five days in a row, then left them alone for ten days before examining their lungs on day 15.

By that point, the hamsters looked completely normal. Their weight was stable, and the microscope showed no visible signs of illness or lung inflammation. But a closer look told a different story. Lung tissue showed a fourfold increase in a protein called p62, a marker that builds up when a cell’s cleanup process doesn’t finish properly, the same stalled process seen in the human cell experiments. This buildup appeared in both blood vessel and airway linings. Researchers also found cell death still happening in lung blood vessels a full ten days after the last vaping exposure.

Gene activity in the hamster lungs supported this: researchers counted roughly 200 genes turned up and about 300 turned down compared with unexposed animals, though many of these changes still need further confirmation. Many of the shifts pointed to the same JNK stress pathway identified in the lab dish experiments, along with signs of tissue remodeling and changes in immune-related genes.

Infographic showing how five days of vaping caused lingering lung cell stress and weakened antiviral defenses in hamsters.
Infographic by StudyFinds

Vaping Leaves Lungs Weaker Against Viruses

Given these immune changes, researchers next tested whether prior vaping affected how hamsters handled a real viral infection. Animals were exposed to vapor for five days, then infected with SARS-CoV-2, the virus that causes COVID-19, a few days later. Some animals were also given the flu virus beforehand to mimic a real-world scenario in which someone catches two respiratory illnesses close together.

Hamsters that had been exposed to vaping beforehand carried notably higher levels of SARS-CoV-2 in their airways than unexposed animals. Vapor exposure downregulates several genes involved in fighting viral infections, while increasing molecular signals tied to tissue remodeling and inflammatory pathways, even though the physical damage visible under the microscope was severe across all infected animals regardless of whether they had vaped.

Weight loss, a measure of how sick the infected animals became, told a more complicated story depending on sex. Female hamsters pre-exposed to vapor lost far more weight after SARS-CoV-2 infection than females that hadn’t vaped. Male hamsters showed the opposite pattern, losing less weight if they had been pre-exposed, though researchers caution that each sex group was small and this finding needs confirmation in future work. A prior flu infection seemed to offer some protection against the SARS-CoV-2 infection that followed, a known effect called viral interference, while vaping appeared to work against the body’s defenses, leaving more virus in the airways.

Why Vaping’s Lasting Lung Damage Matters

A few days of vaping left a mark on the lungs that outlasted the exposure itself, and that mark included a weaker ability to fight off a respiratory virus. A stress response that lingers quietly without obvious symptoms, paired with a dulled antiviral defense, complicates the common idea that vaping is harmless as long as someone isn’t coughing or wheezing. Lungs can look fine on the outside while cells inside are still working through an incomplete cleanup job, and animals that appear perfectly healthy can still be more vulnerable when a virus comes knocking.

Disclaimer: This research was conducted in laboratory human lung cells and in hamsters, not in people. Cell and animal findings do not always translate directly to humans, and more study is needed before drawing firm conclusions about how vaping affects human health.

Paper Notes

Limitations

The researchers noted several limitations. The study used a single commercial vape product containing nicotine, so it did not separate out whether the damage came from nicotine itself, from other chemical ingredients, or from flavoring compounds. Because of safety restrictions during the study, the researchers generated vapor from a condensate rather than fresh aerosol, meaning some short-lived chemical compounds present in real-time vaping may not have been captured. Each sex-specific group had few animals, and the researchers said the sex-based differences they observed will need confirmation in future studies. The study also did not examine how vaping affects flu-induced lung injury, since the flu was used only to model a dual-infection scenario alongside SARS-CoV-2.

Funding and Disclosures

The American Lung Association, the National Heart, Lung, and Blood Institute, and the Wollowick Chair for COPD Research at National Jewish Health supported this research. One of the authors, Irina Petrache, disclosed being a scientific co-founder and consultant for a company called Allinaire Therapeutics.

Publication Details

Paper Title: “E-cigarette exposure triggers distal lung cell injury, persistent lung stress response, and antiviral immune suppression”

Authors: Tanner C. Rivera, Kelly S. Schweitzer, Christina Cornell, Jordan Nall, Nicholas Egersdorf, Courtney Moeder, Riley A. Cooney, Eszter K. Vladar, Steve D. Groshong, Gregory P. Downey, James P. Bridges, Richard Bowen, Hong Wei Chu, and Irina Petrache. Tanner C. Rivera and Kelly S. Schweitzer share first authorship, and Irina Petrache served as the corresponding author ([email protected]).

Authors Affiliations: National Jewish Health, the University of Colorado Denver, and Colorado State University.

Journal: JCI Insight, 2026;11(18):e198757

DOI: https://doi.org/10.1172/jci.insight.198757

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