This summer, mysterious vaping related illnesses have raised fears about unintended consequences from the habit. But as seasons turn and flu season begins to set in, new research suggests that vaping will continue to put people at risk for illness. Early-stage research shows that e-liquids, even without nicotine, can cause buildup in the lungs that takes a toll in more than one way.
This Wednesday, a team of scientists at Baylor University published a mouse study in the Journal of Clinical Investigation that showed how vaping can cause fat particles to build up in the lungs, and what happens when they end up there. Those accumulated fats, the authors note, not only may pose their own risks, but make it easier for the flu to take hold in the body.
Though vaping was originally posited to be safer than traditional smoking, vaping’s unique risks are starting to poke holes in that story. One of these biggest holes is the emergence of over 215 possible cases of “vaping related illnesses” under CDC investigation. In those cases, the underlying cause is still unclear, though one condition that’s been reported in vapers in Utah, and elsewhere is called lipoid pneumonia, which occurs when fat particles build up in lung tissues.
Although her experiment was done on mice, lead study author and Baylor College of Medicine pulmonologist Farrah Kheradmand, Ph.D., tells Inverse that she believes her findings hold important insight into vaping’s unique risks.
“Because the function of immune cells in most mammals is similar, and there are a number of ‘lipoid pneumonia cases’ described in recent news outlets, what we show in mice which described how lipids accumulate in lung immune cells is highly relevant to humans,” says Kheradmand.
Kheradmand’s experiment involved four groups of mice who were exposed to either cigarette smoke, e-cigarette vapor with nicotine, vapor without nicotine, or just plan air for four months. In a statement, they likened this level of vapor exposure to picking up the habit as a teen and continuing it five decades into life.
Kheradmand and her team saw that compared to smokers, the vaping mice showed no signs of emphysema in their lung tissue (this line of research is ongoing, though, and other studies have found evidence of emphysema). But they did show that even in the non-nicotine group, lipids were clogging up alveolar macrophages, guardian cells that protect the tiny air sacs in the lungs.
Kheradmand saw that these guardian cells were clogged with lipids, and when she infected the mice with influenza A, the clogged cells were impaired in their ability to fight the virus off.
Where did these lipids come from? Here, Kheradmand points to two components, one or both of which are found in almost every e-liquid: vegetable glycerol and propylene glycol. She and her team suspect that exposure to these two substances can upset the natural function of surfactant, an oozy liquid-like substance that also protects the lungs, leading to lipid accumulation in the lungs.
Their results suggest that continuous vaping can “upset” the homeostasis of surfactant, which naturally contains both lipids and proteins. These results suggest chronic exposure to vapor (even nicotine-free vapor) allows those lipids build up in abnormal ways. This, Kheradmand adds, suggests that some of the basic components of e-liquids may come with unintended consequences.
“It is important for the public to know that above and beyond added flavors and/or nicotine, the solvents used (also known as e-juice) are harmful in the lungs,” says Kheradmand.
As it stands, these early results hint at a big downside for vapers who contract the flu this fall. But on a much larger scale, they begin to explain some of the unique ways that vaping may affect the lungs that we’re only just beginning to uncover.
Electronic nicotine delivery systems (ENDS) or e-cigarettes have emerged as a popular recreational tool among adolescents and adults. Although the use of ENDS is often promoted as a safer alternative to conventional cigarettes, few comprehensive studies have assessed the long-term effects of vaporized nicotine and its associated solvents, propylene glycol (PG) and vegetable glycerin (VG). Here, we show that compared with smoke exposure, mice receiving ENDS vapor for 4 months failed to develop pulmonary inflammation or emphysema. However, ENDS exposure, independent of nicotine, altered lung lipid homeostasis in alveolar macrophages and epithelial cells. Comprehensive lipidomic and structural analyses of the lungs revealed aberrant phospholipids in alveolar macrophages and increased surfactant-associated phospholipids in the airway. In addition to ENDS-induced lipid deposition, chronic ENDS vapor exposure downregulated innate immunity against viral pathogens in resident macrophages. Moreover, independent of nicotine, ENDS-exposed mice infected with influenza demonstrated enhanced lung inflammation and tissue damage. Together, our findings reveal that chronic e-cigarette vapor aberrantly alters the physiology of lung epithelial cells and resident immune cells and promotes poor response to infectious challenge. Notably, alterations in lipid homeostasis and immune impairment are independent of nicotine, thereby warranting more extensive investigations of the vehicle solvents used in e-cigarettes.