Although the use of tobacco cigarettes in the United States is on the decline, the use of electronic cigarettes (e-cigs) has steadily increased since their introduction to the US market in 2007. E-cigs are especially popular among teenagers and young adults, who reportedly view them as less harmful than conventional cigarettes. A 2015 study found that roughly 34% of adolescents who had heard of e-cigs, and 72% of those who had tried e-cigs, perceived them to be less harmful comparatively.1
There are numerous types of e-cig products, such as vape pens and e-hookahs, but each is a battery-operated device that delivers “nicotine, flavorings, and other constituents to the user by heating flavored e-cig liquid (e-liquid) solutions to temperatures sufficient to form aerosols,” explained the authors of a recent review published in Current Allergy and Asthma Reports.2 “Inhalation of e-cig aerosols (commonly referred to as e-cig vapor) provides the sensation of smoking and desired nicotine effect without combusting tobacco.”
Some experts have suggested that tobacco smokers with asthma should switch to e-cigs to decrease smoking-related exacerbations. Such recommendations, along with public health messages stating that e-cigs are less harmful than tobacco cigarettes, have likely influenced public perceptions of their relative safety.3 Indeed, various findings show a higher prevalence of usage in adolescents with vs without asthma in the United States and elsewhere.4
Safety comparisons between e-cigs and tobacco cigarettes often focus on differences in the constituents found in the latter. “However, e-cig aerosols are poorly characterized complex mixtures of inert and reactive chemicals, and it is unclear whether long-term inhalation will improve or worsen asthma,” the authors wrote.
Recent evidence indicates that e-cigs can lead to respiratory damage via mechanisms similar to those of conventional cigarettes, as well as through additional mechanisms. The present review explored how the inhalation of the following compounds present in e-cig aerosols may influence the development or exacerbation of asthma.
Propylene Glycol (PG) and Vegetable Glycerin (VG)
PG and VG, the main components of e-liquids, are considered generally safe by the US Food and Drug Administration for oral consumption; however, the effects of inhaling these compounds repeatedly in aerosolized form have not been established. Some findings indicate that acute exposure has no significant effect on lung function, fraction of exhaled nitric oxide, or serum C-reactive protein levels in individuals with or without asthma.
Other results, however, show that long-term exposure may have more serious consequences. An earlier study found significantly lower forced expiratory volume in 1 second and forced vital capacity values in entertainment industry employees consistently exposed to PG-based theatrical fog, compared with nonentertainment industry controls.5 In addition, lower lung function was observed in entertainment industry employees who often worked within 10 feet of the fog source vs those employees who worked further away.
“An emerging concern is that thermal decomposition of PG and VG results in the formation of carbonyl compounds with known inhalational toxicity and irritant properties,” the authors noted, especially with newer-generation e-cig devices that allow users to increase the temperature of the heating coil, which results in a larger amount of aerosol per puff. A study published in 2017 reported that vaping at high temperatures (≥215° C) can pyrolyze PG and VG into reactive carbonyls, including formaldehyde, acetaldehyde, and acrolein, all of which have been implicated in the development and exacerbation of asthma.6
Researchers recently found that injecting pregnant rats with a daily dose of nicotine (comparable to that typically consumed by habitual smokers), “altered histone acetylation in the testes, ovaries, and lung tissues of F1 offspring and resulted in an asthmatic phenotype,” and “mating of the F1 rats produced similar epigenetic alterations and an asthmatic phenotype in both the male and female F2 offspring,” despite the F2 offspring’s lack of direct nicotine exposure, according to the current paper.7