On a molecular level, the mouths of 25 otherwise healthy participants who use electronic cigarettes daily closely resemble those of patients with gum disease, according to a study published in the May 29 issue of Science Advances.
The research finds that e-cigarettes trigger a proinflammatory response, coating friendly bacteria in the mouth with a biofilm layer that makes them unrecognizable to the body and prevents the sequential colonization of other bacteria that form a healthy community. This disrupts the fine-tuned balance between the oral microbiome and the body's immune system — which remains mostly unchanged throughout life in healthy individuals — with concerning long-term health implications.
"We chose subjects for the study who do everything right," said Purnima Kumar, a professor at the College of Dentistry at The Ohio State University and an author on the study. "They eat healthy, they have normal body weight, they have no systemic disease. I am an oral surgeon, and when these patients sit in my chair, I wouldn't be clued in to think that something is the matter. It is all happening at the molecular level."
E-cigarettes are battery-powered devices that often contain nicotine, flavorings, propylene glycol, glycerol and other chemicals. Unlike tobacco, this mixture is heated rather than burned, producing a vapor that the user inhales. These products have gained recent popularity among Americans, with 6% of the country's population — including 2.5 million high schoolers — puffing on the products nine years after their introduction to the United States. These devices are also the form of nicotine most often used by teens in the United States, in part due to the ease with which they can be concealed from adults and beliefs that they are safer than cigarettes.
While more than 2,800 Americans had been hospitalized due to lung injuries associated with e-cigarette use by February 2020 — with 68 confirmed deaths — much still remains unknown about how the potentially toxic substances in vaping devices may deteriorate health over time.
This was not an issue that Kumar and her colleagues originally planned to investigate. The team had received funding to conduct a smoking cessation study, in which they hoped to learn how long smokers must quit before their oral microbiomes begin to return to normal. After struggling to get their patients to quit, Kumar and colleagues initially suggested they try e-cigarettes, which were fairly new on the market at the time.
"When we looked into it more, we thought to ourselves, 'wait a minute, are we asking them to quit smoking using another device that could impact the mouth?'" Kumar recalled. "So we started studying e-cigarettes."
To develop early insights into how e-cigarettes affect the oral microbiome, Sukirth Ganesan, a Ph.D. student at The Ohio State University Division of Periodontology at the time of this research and the lead author of the study, and colleagues recruited 123 otherwise healthy individuals in their 20s and 30s, including 25 smokers, 25 nonsmokers, 20 e-cigarette users, 25 former smokers currently using e-cigarettes, and 28 smokers who also use e-cigarettes.
The researchers then created a catalog of bacterial genes in the microbial communities of e-cigarette users based on plaque samples collected from their teeth, finding that genes encoding biofilm, cell wall, and extracellular matrix created an environment of stress within the mouth.
"Healthy commensal bacteria in the mouth look beautiful, almost like popcorn festoons for Christmas trees," said Kumar. "But by the time you start using an e-cigarette, they look like they have been encased in concrete. Suddenly, your body sees these bacteria cloaked in the biofilm layer and it doesn't recognize them as friends anymore. When we looked at the host immune response, we found a huge proinflammatory response — it was absolutely off the charts."
To identify the culprit behind this inflammation, the researchers searched for differences between e-cigarette users who indulged in different levels of nicotine or preferred different kinds of flavoring agents, including berry or fruit, candy, tobacco, mint and menthol. They found that molecular-level variations were not tied to nicotine concentrations or flavoring preferences — they arose primarily based on duration of e-cigarette use. After further testing, the team deduced that the glycol or glycerol that carry the nicotine and flavors in all e-cigarettes appears to be driving the body's proinflammatory response.
When Kumar and colleagues compared the oral microbiomes of e-cigarette users who had been vaping for 14 months or less with those of tobacco smokers who had been smoking for five years or more, they found that smoking and vaping appear to stimulate two completely different inflammatory pathways. E-cigarettes produce inflammation faster than tobacco cigarettes, and their molecular profile dominates in participants who either used e-cigarettes to quit smoking or engaged in both activities.
"E-cigarettes create such a powerful perturbation of the system that in a game of rock-paper-scissors, e-cigarette beats smoking," said Kumar.
After gaining a glimpse into the unseen effects of e-cigarettes on the body, Kumar and colleagues plan to investigate how bacteria break down vaping aerosols in the body — perhaps metabolizing them into extra harmful components — as well as how they impact wound healing in the mouth. Most importantly, the researchers hope to learn how quickly the microbial community begins to shift after e-cigarette use begins.
"I am hoping this research will drive some level of policymaking about the harm we are seeing, challenging the popular perception that e-cigarettes provide a safer alternative to smoking," said Kumar. "If we can see changes in people who are otherwise healthy and have nothing wrong with them, then we should start seriously considering why would you put their lives and their well-being at risk."
[Credit for associated image: Lindsay Fox/ Flickr]