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No legal habit has caused more morbidity and mortality than cigarette smoking which takes greater than 10 years away from the average smoker's life, being a major risk factor for the leading causes of mortality in both developed and low-income/middle-income countries, including coronary artery disease, cancers (especially lung cancer) and COPD.1–4 While cigarette smoking is increasing worldwide, we have made slow but steady progress in the USA reducing smoking prevalence to 18% of adults. Nicotine replacement therapy has assisted many smokers to quit; however, with the advent of electronic cigarettes (e-cigarettes), investigators began to wonder to what extent vaporised nicotine is responsible for disease pathogenesis beyond its addictive properties. Nicotine modulates inflammation causing both inflammatory cell apoptosis5 and inflammatory cell chemotaxis.6 There is growing evidence that e-cigarettes increase the risk for oxidative burden and inflammation in the lungs of mice.7 The study by Garcia-Arcos et al8 published in Thorax convincingly demonstrates that chronic exposure (4 months) of inhaled e-cigarettes in mice causes characteristic changes observed in COPD, including airway pathology, inflammation and emphysematous lung destruction.
Are preclinical models of COPD sufficient to consider regulating the use of e-cigarettes? Murine models of disease are often criticised for lack of …
Contributors Both authors contributed to the Editorial.
Funding National Heart, Lung, and Blood Institute (HL126711).
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
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