Brief vaping exposure triggers lasting lung injury and weakens defenses against viruses, study finds

DENVER — A brief burst of vaping is enough to injure the deepest, most delicate tissue of the lung and leave it less able to fight off respiratory viruses for at least ten days afterward, according to a study published by researchers at National Jewish Health. The findings, drawn from human lung cells and an animal model, are among the most detailed evidence yet that e-cigarette exposure does not merely irritate the airways but can set off a cascade of cellular injury deep in the lung's gas-exchange region, with consequences that outlast the vaping itself.

The study was published in JCI Insight, a journal of the American Society for Clinical Investigation, under the title "E-cigarette exposure triggers distal lung cell injury, persistent lung stress response, and anti-viral immune suppression." It was led by researchers at National Jewish Health and the University of Colorado Denver, with additional collaborators at Colorado State University. The senior author, Dr. Irina Petrache, chief of pulmonary, critical care and sleep medicine at National Jewish Health, said the work targeted a part of the lung that earlier vaping research had largely overlooked.

What the study found

Rather than focusing on the large airways, where most prior vaping research has concentrated, the team examined the distal lung: the microvascular and small-airway tissue where oxygen actually crosses into the bloodstream. Using primary human lung microvascular endothelial cells, small airway epithelial cells, and precision-cut human lung tissue slices, the researchers exposed the tissue to e-cigarette vapor condensate and tracked what happened over the following days.

Within 24 hours, exposed cells showed a weakened barrier function, increased cellular stress, and signs that their internal waste-clearance system — a process called autophagy — had become clogged rather than cleared. Cell growth and repair slowed, and more cells died than in unexposed tissue. The damage traced back to a stress-signaling pathway known as JNK; when the researchers chemically blocked that pathway in the lab, the cells' barrier function recovered and the buildup of waste proteins eased, pointing to JNK signaling as the mechanical driver of the injury rather than a side effect of it.

To see whether the damage would heal on its own, the team turned to Golden Syrian hamsters, which were exposed to nebulized vapor from JUUL pods for five consecutive days and then given ten days to recover before their lung tissue was examined. The injury markers were still present on day fifteen, ten days after the last exposure. Hamsters that had been pre-exposed to vapor and then infected with SARS-CoV-2 carried significantly higher viral loads than animals that had not vaped, and their lung tissue showed suppressed activity in several genes that normally help the body fight viral infection.

How we got here

The study extends a body of research into e-cigarette, or vaping, product use-associated lung injury, the syndrome identified by the Centers for Disease Control and Prevention after a 2019 outbreak that hospitalized more than 2,800 people in the United States and killed 68. That outbreak was eventually linked largely to vitamin E acetate in illicit THC vaping products, and the acute crisis faded by early 2020. But it left pulmonologists with an unanswered question: what, if anything, does routine e-cigarette use, without any contaminated additive, do to the lung over time, and does that damage persist once a person stops.

Much of the subsequent research examined the central and conducting airways, which are easier to sample and visualize than the lung's distal regions. The National Jewish Health group designed its study specifically to probe the thin-walled vessels and small airways at the edge of the gas-exchange surface, using a combination of human cell culture, intact human lung tissue slices and a live-animal infection model, an approach the authors said let them trace both the initial injury and its immunological aftermath in ways that single-method studies could not.

Who is affected

The population most directly implicated is the millions of Americans, many of them adolescents and young adults, who vape regularly. Government survey data analyzed by the Food and Drug Administration found that 5.2 percent of middle and high school students reported current e-cigarette use in 2025, down sharply from a peak of more than 5 million youth users in 2019, but that among those who still vape, the pattern has shifted toward heavier, more frequent use: the share of young e-cigarette users vaping daily rose from 9.4 percent in 2014 to 35.4 percent in 2025. It is that pattern of repeated, sustained exposure, rather than occasional use, that the Colorado researchers said is most relevant to their findings, since their hamster model showed injury markers compounding with repeated daily exposure and persisting well after the exposure stopped.

The study also found differences by sex. In hamsters coinfected with SARS-CoV-2 after vapor exposure, females lost significantly more body weight during infection than unexposed females, while males showed comparatively less weight loss, and female animals with both vapor exposure and infection had reduced lung macrophage counts. The authors said the sex-specific pattern warrants further investigation rather than firm conclusions, given the limits of translating a hamster model to human physiology.

Reaction and what happens next

In the National Jewish Health announcement, Dr. Petrache described the significance of locating injury in the lung's deepest structures:

"Even short-term vaping exposure can initiate injury in the deepest and most delicate regions of the lung. Importantly, some effects persisted after exposure ended."

The research team and the journal were explicit that the findings, built on cell culture and a hamster model, require confirmation in human studies before they can be translated into clinical guidance or policy. Hamsters are a common model for respiratory virus research because their airway physiology responds to influenza and SARS-CoV-2 in ways that mice do not, but they are not a perfect proxy for how a human vaper's lungs would respond over months or years of real-world use, with varying device types, e-liquid formulations and nicotine concentrations.

The authors said their next step is to examine whether the same JNK-driven injury pathway can be identified in people who vape regularly, through biomarkers in blood, breath condensate or bronchoscopy samples, and whether the pathway offers a target for pharmacological intervention. Because an existing class of JNK inhibitors is already in development for other inflammatory conditions, the researchers suggested the mechanism they identified could, if confirmed in humans, point toward a treatment strategy rather than only a warning. In the meantime, the finding that cellular damage and antiviral suppression outlasted the vaping exposure itself, by at least ten days in the animal model, is likely to feature in ongoing regulatory and public health debates over e-cigarette marketing and youth access as the FDA and state health agencies continue to track use patterns through future rounds of the National Youth Tobacco Survey.