Young adults who vape or smoke cigarettes already show measurable damage to their blood vessels and reduced exercise capacity, even after relatively short periods of use, according to a peer-reviewed study of 75 healthy, active people aged 18 to 30. The research, which compared 25 exclusive e-cigarette users, 25 combustible-cigarette smokers, and 25 never-users, each with at least 18 months of use history, found that both vaping and smoking cut fitness levels by roughly 15 percent. Separate laboratory and animal studies point to a mechanism that does not depend on nicotine at all, raising hard questions about the safety claims that have long surrounded flavored and nicotine-free vape products.
Blood vessel and lung damage in young vapers and smokers
The central finding comes from a study published in a European respiratory journal and accessible via this clinical report. Researchers recruited 75 healthy, active young adults and divided them into three equal groups: exclusive e-cigarette users, combustible-cigarette smokers, and people who had never used either product. All participants in the vaping and smoking groups had logged at least 18 months of regular use. The team measured brachial artery flow-mediated dilatation, or FMD, using Doppler ultrasound, a standard clinical technique for assessing how well blood vessels expand in response to increased blood flow. Both e-cigarette users and cigarette smokers showed impaired vessel expansion compared with nonusers.
Exercise testing revealed a parallel decline. Ventilatory efficiency, a measure of how effectively the lungs exchange oxygen during physical effort, was lower in both user groups. The combined vascular and respiratory deficits translated into a roughly 15 percent reduction in cardiorespiratory fitness among vapers and smokers alike. That gap appeared despite the fact that all participants were young, otherwise healthy, and physically active, conditions that would normally mask early organ damage. In practical terms, vapers and smokers reached exhaustion sooner and processed oxygen less efficiently than their peers who had never used nicotine products.
Although the study was not designed to pinpoint which components of e-cigarette aerosol or cigarette smoke caused the damage, the similar magnitude of impairment in both user groups undercuts the notion that vaping is benign for cardiovascular and respiratory health, at least in the short to medium term. The authors noted that the observed deficits in FMD are comparable to those seen in older adults with early cardiovascular risk factors, suggesting that vaping and smoking may accelerate vascular aging in people still in their twenties.
Airway irritation, not nicotine, may drive vascular harm
A separate line of NIH-funded research offers a possible explanation for why e-cigarettes produce vascular effects similar to combustible tobacco, even when nicotine is absent. Endothelial-cell experiments showed that exposure to e-cigarette aerosol reduced the release of nitric oxide, a molecule that signals blood vessels to relax and widen. When nitric oxide drops, arteries stiffen, and the cardiovascular system works harder during exercise.
Animal studies published in a vascular biology journal tested whether a specific chemical in smoke or vapor was responsible. The answer pointed instead to a general airway-irritation pathway: inhaled particles trigger sensory nerves in the airways, which send signals through the vagus nerve to blood vessels throughout the body. That vagal reflex impairs endothelial function regardless of whether the aerosol contains nicotine, tar, or flavoring agents. The finding suggests that the physical act of inhaling heated aerosol, not any single additive, is enough to weaken vascular health.
This mechanism carries particular weight for adolescents whose lungs are still developing. Ongoing airway growth could amplify the vagal-mediated response, potentially producing faster declines in exercise capacity among teenagers than among adults in their twenties. A pilot study targeting adolescent vapers found measurable changes in airway resistance and nasal epithelial gene-expression patterns that mirror lower-airway inflammation and weakened cilia function, according to research published in the respiratory cell biology literature. Those gene-expression shifts serve as a biological proxy for damage deeper in the lungs, where direct tissue sampling is impractical in young research subjects.
Laboratory work on cultured human airway cells reinforced the concern. Repeated exposures to nicotine-free e-cigarette aerosols impaired airway protective functions, including cilia movement and epithelial barrier integrity, with quantified drops in transepithelial electrical resistance after repeated sessions, according to a study indexed at a PubMed database. The barrier breakdown means inhaled particles and pathogens face less resistance reaching deeper lung tissue, a deficit that compounds with each vaping session. Together, these mechanistic findings align with the human data showing reduced vascular function and exercise capacity in young adult users.
Gaps in adolescent data and what parents should watch
The strongest clinical evidence so far comes from adults aged 18 to 30, not from younger teenagers. The ERJ Open Research study used groups of 25 people each, a sample size large enough to detect group-level differences in FMD and ventilatory efficiency but too small to capture the full range of individual variation. Exact statistical details for all measures in the e-cigarette cohort have not been fully reported in public summaries, and no primary adolescent dataset includes direct information about specific device types, flavors, or patterns of dual use with combustible cigarettes. That leaves important questions about dose–response relationships and whether certain products pose higher risks than others.
The mechanistic evidence, while consistent across cell, animal, and limited human studies, still stops short of proving long-term outcomes such as heart attack, stroke, or chronic lung disease in people who only vape and never smoke. Most participants in the adult cohorts had relatively short use histories, often under three years, and the adolescent studies rely on indirect markers like gene expression and airway resistance rather than hard clinical endpoints. Researchers also caution that lifestyle factors-such as alcohol use, environmental pollution, and physical activity patterns-can interact with vaping in ways that are not yet fully understood.
For parents and caregivers, the current evidence supports a cautious, prevention-focused approach. Signs that warrant attention include new or unexplained shortness of breath during sports, chest tightness or palpitations, frequent coughing or throat irritation, and a noticeable drop in stamina compared with prior seasons or peers. While these symptoms are not specific to vaping, they may signal that the cardiovascular and respiratory systems are under strain. Clinicians can evaluate lung function, oxygen uptake during exercise, and, when appropriate, vascular health, though sophisticated measures like FMD are usually reserved for research settings.
Open conversations about vaping should emphasize that “nicotine-free” or “just flavor” products are not risk-free, given the emerging evidence that airway irritation alone can trigger systemic vascular effects. Parents may find it helpful to frame the issue in terms of performance: even in healthy young adults, regular vaping is associated with measurable losses in endurance and efficiency, which can affect sports, dance, and other physical activities that many teenagers value. For adolescents already using e-cigarettes, reducing frequency, avoiding deep inhalation, and seeking support for quitting may limit further damage, though definitive data on reversibility are still lacking.
Researchers are calling for larger, longer-term studies that follow adolescents and young adults over time, track specific products and usage patterns, and link early biological changes to later clinical outcomes. Until those data arrive, the convergence of human, animal, and cellular evidence points in a consistent direction: inhaling heated aerosols-whether from cigarettes or e-cigarettes-can impair blood vessels and lungs well before visible disease appears. For a generation that often sees vaping as a harmless habit, the message from the lab and the clinic is increasingly clear: early use leaves a physiological footprint that may be difficult to erase.
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*This article was researched with the help of AI, with human editors creating the final content.
