These epigenetic changes decreased the expression of mesenchymal peroxisome proliferator-activated receptor-γ, which is essential to lung development and repair, and this reduction resulted directly in the observed asthmatic phenotype. “Importantly, this study linked nicotine exposure during pregnancy to epigenetic modifications that cause multigenerational transmission of asthma,” the authors wrote. Follow-up research by the same authors further confirmed this association.
In addition, although animal studies have shown nicotine to decrease lung inflammation, it has also been found to reduce immune cell migration to infection sites, thus increasing the likelihood for the occurrence of the respiratory viral infections that often cause asthma exacerbations.8
In contrast to tobacco cigarettes, e-cig manufacturers use a wide variety of flavoring agents in e-liquids, and the use of these agents is currently unregulated. For example, a study published in 2014 identified 7764 unique flavors, with 242 new flavors introduced monthly over a 17-month period.9 Although data are scarce regarding the toxicity of these agents in the context of e-cigs specifically, some results have shed light on their potential risks.
The food-safe flavoring agent diacetyl (2,3butanedione) has been shown to induce acute-onset bronchiolitis obliterans in workers exposed to the aerosolized form of the chemical. A recent study detected diacetyl in 69.2% of e-cig products tested, and it was estimated that many of these products would result in greater exposures than the limit recommended by the National Institute for Occupational Safety and Health and the Centers for Disease Control.10
Other flavoring agents commonly used in e-cigs, such as cinnamaldehyde (cinnamon), menthol (mint), eugenol (clove), and limonene (citrus), have been established as transient receptor potential ankyrin 1 agonists, which have been implicated in the pathogenesis of asthma. There have been some case reports of mint-induced asthma as well as occupational asthma among workers who inhaled cinnamon dust.
“While e-cig use may help some [individuals with asthma] quit smoking, it is imperative that we continue addressing knowledge gaps to fully assess whether and how vaping e-cigs can significantly modify asthma and allergic airway disease,” the authors concluded.
- Amrock SM, Zakhar J, Zhou S, Weitzman M. Perception of e-cigarette harm and its correlation with use among US adolescents. Nicotine Tob Res. 2015;17(3):330-336.
- Clapp PW, Jaspers I. Electronic cigarettes: their constituents and potential links to asthma. Curr Allergy Asthma Rep. 2017;17(11):79.
- McNeill A, Brose L, Calder R, Hitchman S, Hajek P, McRobbie H. E-cigarettes: an evidence update. A report commissioned by Public Health England. London, UK: Public Health England; 2015.
- Fedele DA, Barnett TE, Dekevich D, Gibson-Young LM, Martinasek M, Jagger MA. Prevalence of and beliefs about electronic cigarettes and hookah among high school students with asthma. Ann Epidemiol. 2016;26(12):865-869.
- Varughese S, Teschke K, Brauer M, Chow Y, van Netten C, Kennedy SM. Effects of theatrical smokes and fogs on respiratory health in the entertainment industry. Am J Ind Med. 2005;47(5):411-418.
- Wang P, Chen W, Liao J, et al. A device-independent evaluation of carbonyl emissions from heated electronic cigarette solvents. PLoS One. 2017;12(1):e0169811.
- Rehan VK, Liu J, Naeem E, et al. Perinatal nicotine exposure induces asthma in second generation offspring. BMC Med. 2012;10:129.
- Razani-Boroujerdi S, Singh SP, Knall C, et al. Chronic nicotine inhibits inflammation and promotes influenza infection. Cell Immunol. 2004;230(1):1-9.
- Zhu SH, Sun JY, Bonnevie E, et al. Four hundred and sixty brands of e-cigarettes and counting: implications for product regulation. Tob Control. 2014;23(Suppl 3):iii3-iii9.
- Farsalinos KE, Kistler KA, Gillman G, Voudris V. Evaluation of electronic cigarette liquids and aerosol for the presence of selected inhalation toxins. Nicotine Tob Res. 2015;17(2):168-174.