A growing body of evidence suggests the potential harm of vaping electronic cigarettes has been underestimated. While e-cigarette advertisements claim the devices can help people quit smoking cigarettes, research shows that they also targeted non-smoker teens, and scientists are discovering that e-cigarettes can cause serious harm on their own.
Adding to this evidence is a study released Thursday in the American Journal of Respiratory and Critical Care Medicine. Scientists from the University of North Carolina, Chapel Hill found that, in a sample of 14 vapers, all those individuals had elevated levels of protease enzymes in their lungs. High levels of protease enzymes are known to cause lung condition called emphysema, which is commonly found among people who smoke cigarettes.
This evidence suggests that vaping can provoke the same cellular response as cigarette smoking. Emphysema involves the gradual damage of lung tissue, causing shortness of breath. According to senior author Robert Tarran, Ph.D., a professor at the UNC School of Medicine, these findings indicate “that vaping may not be safer than cigarette smoking.”
The study involved 41 subjects, who were divided into groups of e-cigarette vapers, cigarette smokers, and nonsmokers. Each individual underwent a bronchoscopy, a procedure in which physicians closely examine an individual’s lungs and air passages. All subjects were also asked to report how often they smoke or vape presently, as well as how much they’ve smoked or vaped in the past. Nine of the 14 vapers had previously smoked tobacco but had switched to e-cigarettes for at least 6 months prior to the bronchoscopy. The researchers additionally measured the subjects for serum levels of nicotine, as well as the nicotine metabolites cotinine and hydroxycotinine, in an effort to confirm tobacco and vape use.
The team observed that the protease levels were “significantly elevated” in the groups of smokers and vapers but not in the group of nonsmokers, suggesting that vaping and smoking may both promote emphysema.
This, the second part of the study indicates, is likely because they both include the consumption of nicotine.
When the scientists administered nicotine to cultured immune cells, these cells began to overproduce the proteases. Higher levels of nicotine were linked to higher levels of overproduction. It’s hypothesized that this overproduction of protease enzymes damages the lung’s air sac structures, leading to the development of emphysema.
This study comes a day after the CDC announced that 16 states have reported 153 cases of serious, vaping-related respiratory illnesses over the past two months. It is not yet clear what is causing these illnesses — all that is known is that the victims have either vaped nicotine or tetrahydrocannabinol (THC). A different team of scientists also announced on Wednesday that vaping flavored e-liquids can cause significant changes in blood flow in the femoral artery.
In 2018, England’s public health agency claimed that vaping is at least 95 percent safer than smoking. However, as more researchers investigate the matter, it’s unclear whether that claim is accurate. According to the American Lung Association and the Centers for Disease Control and Prevention, youth e-cigarette use should be categorized as an “epidemic”: E-cigarette use by middle and high school students increased by 900 percent between 2011 and 2015. While the debate over whether e-cigarettes are effective at helping people quit cigarettes continues, it’s increasingly clear that they are not a healthy choice.
Proteolysis is a key aspect of the lung’s innate immune system. Proteases, including neutrophil elastase and matrix metalloproteases (MMPs), modulate cell signaling, inflammation, tissue remodeling and leukocyte recruitment via cleavage of their target proteins. Excessive proteolysis occurs with chronic tobacco use and is causative for bronchiectasis and emphysema. The effect of e-cigarettes (vaping) on proteolysis is unknown. Objectives: We used protease levels as biomarkers of harm to determine the impact of vaping on the lung. Methods: We performed research bronchoscopies on healthy non-smokers, cigarette smokers and e-cigarette users (vapers) and determined protease levels in bronchoalveolar lavage (BAL). In parallel, we studied the effects of e-cigarette components on protease secretion in isolated human blood neutrophils and BAL-derived macrophages. We also analyzed the nicotine concentration in induced sputum and BAL. Measurements and Main Results: Neutrophil elastase, MMP-2 and MMP-9 activities/protein levels were equally elevated in both vapers’ and smokers’ BAL relative to non-smokers. In contrast, antiprotease levels were unchanged. We also found that exposure of isolated neutrophils and macrophages to nicotine elicited dose-dependent increases in protease release. After vaping, measurable levels of nicotine were detectable in sputum and BAL, which corresponded to the EC50s for protease release seen in immune cells. Conclusions: We conclude that vaping induces nicotine-dependent protease release from resident pulmonary immune cells. Thus, chronic vaping disrupts the protease-antiprotease balance by increasing proteolysis in lung, which may place vapers at risk of developing chronic lung disease. These data indicate that vaping may not be safer than tobacco smoking.