Electronic Cigarette Exposure: Inflammatory and Immunological Implications in Structural Lung Cells and the Potential Public Health Consequences

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Electronic cigarettes have rapidly become the consumer preferred alternative to tobacco cigarettes, but very little is known about the harms associated with their use. Electronic cigarettes are often proposed as a cessation device from a harm reduction standpoint, but this overlooks the lack of evidence for reduced harms and the numerous new vapers who have never smoked that are exposed to harms they otherwise would have avoided. Studies within this thesis provide essential evidence in the harm reduction debate. In Chapter 3 we surveyed perceptions of young Australians towards E-cigarettes. We hypothesised that they would believe E-cigarettes to be less harmful than tobacco cigarettes, and that they would be misinformed about E-cigarette regulations in Australia due to a lack of education from regulatory bodies. In Chapters 4, 5 and 6 of this thesis we used in vitro models of exposure to determine potential health risks associated with E-cigarette use. Chronic obstructive pulmonary disease (COPD) patients have been identified as a high-risk population of E-cigarette users, hence our studies focused on the potential effect E-cigarette exposure may have on mechanisms related to the underlying pathophysiology of COPD. In Chapter 4, we developed an in vitro E-cigarette exposure model to determine the cytotoxic and inflammatory effects of E-cigarette exposure in COPD and non-COPD primary human airway smooth muscle cells. In this study we confirmed earlier suspicions on cytotoxicity and provided the first evidence that COPD cells are hyper-responsive to E-cigarettes. In Chapter 5 we provided the first evidence that E-cigarettes have the potential to induce cellular senescence. This finding gives further support to avoiding use of E-cigarettes in COPD patients, given the role cellular senescence plays in COPD pathophysiology. In Chapter 6 we provided evidence that combined cigarette and E-cigarette use is significantly more harmful than using either product alone. Furthermore, we found that the inflammatory response induced by dual exposure was glucocorticoid resistant. Glucocorticoid resistance is one of the hallmarks of COPD, and thought to contribute to uncontrolled inflammation in pre-COPD (symptomatic smokers) so dual use should be avoided. Importantly, this thesis elucidates pathological harms associated with E-vapour exposure. The evidence provided in the studies within this thesis should be used to inform clinicians, researchers and patients on the harms associated with E-cigarette use to improve clinical outcomes in terms of morbidity and mortality in COPD.
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