E-cigarette vapor exposure, independent nicotine, was shown to alter lipid homeostasis and immunity impairment in mice, warranting further investigation into these vaping solvents.
Exposure to e-cigarette vapors, independent of nicotine, disrupted normal lung function in mice and diminished the ability of their lung’s immune cells to respond to viral infection, according to a study published this week in the Journal of Clinical Investigation.1
Electronic nicotine delivery systems (ENDS), or e-cigarettes, are promoted as a safer alternative to normal cigarettes and have become increasingly popular among teens and adults. Researchers sought to assess the long-term effects of ENDS nicotine delivery as a vapor, composed of solvents such as propylene glycol (PG) and vegetable glycerin (VG), on the respiratory tract and its local immune functions. These compounds have been recognized by the FDA as generally safe for use as direct food additives, but its long-term impact as a vapor has not been studied.2
Researchers utilized a murine model of chronic inhalation exposure to assess and compare the effect on lung cellular function by conventional tobacco smoke and ENDS components. Four groups of mice were examined across a 4-month time span, an exposure regiment equivalent to a person who had smoked from their teenage years to ages 40-49:
Research revealed that mice who were chronically exposed to cigarette smoke or ENDS vapors with nicotine had significantly damaged lungs and excessive inflammation similar to that found in human smokers with emphysema. While mice who were administered solely vaping solvents (no nicotine) did not replicate lung inflammation or emphysema, researchers observed abnormal accumulation of lipids within resident macrophages in the lung. Researchers then infected this group of mice with the flu virus and compared them to the air-exposed group.
Evidence associated harmful effects by vaporized ENDS products, independent of nicotine, with the alveolar-lining fluid and the lung. These vaping solvents altered the lung lipoprotein biology in alveolar type 2 pneumocytes and impaired the physiology of alveolar macrophages. Corresponding author Farrah Kheradmand, MD, a pulmonologist and professor of medicine at Baylor College of Medicine, in a statement highlighted the importance of these macrophages that reside in the lung as “these cells represent the first line of defense against viral infections such as those caused by influenza virus."
The ENDS solvent-only exposed mice exhibited a delayed immune responsiveness and persistent lung inflammation when compared with the air-exposed group. “Our experimental findings reveal that, independent of nicotine, chronic inhalation e-cigarette vapors disrupts normal murine lung function and reduces the ability of resident immune cells to respond to infection, increasing the susceptibility to diseases such as influenza,” said Kheradmand.
Researchers noted that more extensive investigations into the vaping solvents present in e-cigarettes are warranted.