The impact of e-cigarette use on the inflammatory state and function of the lungs is not well understood. Here we review the latest studies on the impact of short and long term e-cigarette aerosol inhalation on molecular pathways, cellular recruitment, gas exchange and airway physiology. Inflammatory cytokines IL-6 and IL-8 were increased by e-cigarette exposures, and a variety of immune cells were recruited to the parenchyma and airways across models. While there are few consistent signals across in vitro, in vivo and human studies, due to the multitude of different e-devices and the combination of chemicals within different aerosols generated, it is clear that use of e-cigarettes does alter the inflammatory state and function of the lungs with both acute and chronic use. This is evidenced by the multitude of inflammatory lung diseases already tied to e-cigarette use, but the causal chemicals are primarily remain at large.

E-cigarette aerosols are exceedingly different from conventional tobacco smoke, containing dozens of chemicals not found in cigarette smoke. It is highly likely that chronic use of e-cigarettes will induce pathological changes in both the heart and lungs. Here we review human and animal studies published to date and summarize the cardiopulmonary physiological changes caused by vaping. In terms of cardiac physiology, acute exposure to e-cigarette aerosols in human subjects led to increased blood pressure and heart rate, similar to traditional cigarettes. Chronic exposure to e-cigarette aerosols using animal models caused increased arterial stiffness, vascular endothelial changes, increased angiogenesis, cardiorenal fibrosis and increased atherosclerotic plaque formation. Pulmonary physiology is also affected by e-cigarette aerosol inhalation, with increased airway reactivity, airway obstruction, inflammation and emphysema. Research thus far demonstrates that the heart and lung undergo numerous changes in response to e-cigarette use, and disease development will depend on how those changes combine with both environmental and genetic factors. E-cigarettes have been advertised as a healthy alternative to cigarette smoking, and users are under the impression that vaping of e-cigarettes is harmless, but these claims that e-cigarettes are safer and healthier are not based on evidence. Data from both humans and animal models are consistent in demonstrating that vaping of e-cigarettes causes health effects both similar to and disparate from those of cigarette smoking. Further work is needed to define the long-term cardiopulmonary effects of e-cigarette use in humans.

It is widely known that cigarette smoke damages host defenses and increases susceptibility to bacterial infections. Pseudomonas aeruginosa, a Gram-negative bacterium that commonly colonizes the airways of smokers and patients with chronic lung disease, can cause pneumonia and sepsis and can trigger exacerbations of lung diseases. Pseudomonas aeruginosa colonizing airways is consistently exposed to inhaled cigarette smoke. Here, we investigated whether cigarette smoke alters the ability of this clinically significant microbe to bypass host defenses and cause invasive disease. We found that cigarette smoke extract (CSE) exposure enhances resistance to human neutrophil killing, but this increase in pathogenicity was not due to resistance to neutrophil extracellular traps. Instead, Pseudomonas aeruginosa exposed to CSE (CSE-PSA) had increased resistance to oxidative stress, which correlated with increased expression of tpx, a gene essential for defense against oxidative stress. In addition, exposure to CSE induced enhanced biofilm formation and resistance to the antibiotic levofloxacin. Finally, CSE-PSA had increased virulence in a model of pneumonia, with 0% of mice infected with CSE-PSA alive at day 6, while 28% of controls survived. Altogether, these data show that cigarette smoke alters the phenotype of P. aeruginosa, increasing virulence and making it less susceptible to killing by neutrophils and more capable of causing invasive disease. These findings provide further explanation of the refractory nature of respiratory illnesses in smokers and highlight cigarette smoking as a potential driver of virulence in this important airway pathogen.

While health effects of conventional tobacco are well defined, data on vaping devices, including one of the most popular e-cigarettes which have high nicotine levels, are less established. Prior acute e-cigarette studies have demonstrated inflammatory and cardiopulmonary physiology changes while chronic studies have demonstrated extra-pulmonary effects, including neurotransmitter alterations in reward pathways. In this study we investigated the impact of inhalation of aerosols produced from pod-based, flavored e-cigarettes (JUUL) aerosols three times daily for 3 months on inflammatory markers in the brain, lung, heart, and colon. JUUL aerosol exposure induced upregulation of cytokine and chemokine gene expression and increased HMGB1 and RAGE in the nucleus accumbens in the central nervous system. Inflammatory gene expression increased in the colon, while gene expression was more broadly altered by e-cigarette aerosol inhalation in the lung. Cardiopulmonary inflammatory responses to acute lung injury with lipopolysaccharide were exacerbated in the heart. Flavor-specific findings were detected across these studies. Our findings suggest that daily e-cigarette use may cause neuroinflammation, which may contribute to behavioral changes and mood disorders. In addition, e-cigarette use may cause gut inflammation, which has been tied to poor systemic health, and cardiac inflammation, which leads to cardiovascular disease.