In the United States, a record number of teens picked up a vaping habit in 2018. Outcry surrounding all those new vapers has prompted concerns about the habit that affects health and confusion over exactly what happens to the body when a person starts to vape. Now, early research suggests that, while the changes are small, just vaping for a month can alter the lungs.
This pilot study, published Tuesday in Cancer Prevention Research, examined people who had never vaped before. The driving idea behind this experiment was to see what happens to the lung tissue of people who have just started to vape — even if the liquid they vape has no nicotine or THC. In that way, they could show how vaping itself, not necessarily the complex components in each cartridge, can impact the lungs.
Overall, the research team discovered that the lungs of people in the vaping group did see some small changes in inflammation over the course of four weeks, though the change wasn’t statistically significant compared to the control group.
Peter Shields, M.D., a lung cancer researcher and the study’s senior author, explains that this result implies there’s a small baseline level of inflammation caused by vaping itself, though nothing too drastic. He adds that the additional stuff that goes into the liquid — like THC, nicotine, or flavors — may enhance the risk and make the habit dangerous in the long term.
“The implication of this study is that longer-term use, increased daily use, and the addition of flavors and nicotine may promote additional inflammation,” Shield says.
Since July 26, over 1,200 cases of a “vaping-related illness” have captured the country’s attention. The illness is now, according to CDC guidance, called EVALI, or e-cigarette, or vaping product use-associated lung injury.
Instead, this study looks at what happens in the lungs when you fill them with a vaporized product. It’s not so much about what’s in the cartridge as it is about what vaping does to the lungs in general. But, as the authors interpret their findings, they’ve highlighted just how important it is to consider what is actually in that cartridge.
In the experiment, Shields and his team asked 30 people who had never vaped before to agree to pick up the habit. For four weeks, they vaped twice each day, taking 20 puffs over the course of an hour. Again, there was no nicotine, THC, or flavoring compounds in the liquid used in these experiments. But it was comprised of either 50 percent propylene glycol (PG) or 50 percent vegetable glycerin (VG) — ingredients that are often included within e-liquids.
Vaping that PG or VG formula still caused the lungs to mount a small immune response (which is where the inflammation came from), though as the authors amend, that inflammation was still very small. There was also a significant link between the amount of propylene glycol that was found in the participant’s urine samples and how much inflammation there was in their lungs. That draws a tenuous connection between the ingredients and the inflammation.
But in the wider scale of research into how nicotine, PG, and VG all interact in e-liquids, the authors argue that their results actually somewhat vindicate PG and VG — at least when it comes to inflammation in the lungs. Other studies have raised concerns about the effects of PG on things like blood pressure. These findings, however, “support the hypothesis that large-magnitude changes in expression are likely not to occur from inhaling PG and VG, at least after one month of use.”
In other words, the bigger changes to the lungs may come back to the increasingly important effects of nicotine or flavoring additives, which is a direction that scientists will have to pursue as we try to figure out what’s safe to vape and what isn’t.
E-cig use is continuing to increase, particularly among youth never-smokers, and is used by some smokers to quit. The acute and chronic toxicity of e-cig use is unclear generally in the context of increasing reports of inflammatory-type pneumonia in some e-cig users. To assess lung effects of e-cigs without nicotine or flavors, we conducted a pilot study with serial bronchoscopies over 4 weeks in 30 never-smokers, randomized either to a four-week intervention with the use of e-cigs containing only 50% propylene glycol (PG) and 50% vegetable glycerine (VG) or to a no-use control group. Compliance to the e-cig intervention was assessed by participants sending daily puff counts and by urinary propylene glycol (PG). Inflammatory cell counts and cytokines were determined in bronchoalveolar lavage (BAL) fluids. Genome-wide expression, microRNA, and mRNA were determined from bronchial epithelial cells. There were no significant differences in changes of BAL inflammatory cell counts or cytokines between baseline and follow-up, comparing the control and e-cig groups. However, in the intervention but not the control group, change in urinary PG as a marker of e-cig use and inhalation, was significantly correlated with change in cell counts (cell concentrations, macrophages, and lymphocytes) and cytokines (IL-8, IL-13, and TNF-α), although the absolute magnitude of changes was small. There were no significant changes in mRNA or microRNA gene expression. Although limited by study size and duration, this is the first experimental demonstration of an impact of e-cig use on inflammation in the human lung among never-smokers.