Electronic cigarettes (e-cigarettes) have been widely considered as an alternative to combustible cigarettes. However, the effects and mechanisms of e-cigarette aerosol on respiratory system function need to be fully elucidated, and in vivo studies can be used to evaluate e-cigarettes aerosol (ECA) vs. combustible cigarette smoke (CCS).

Thirty-two specific pathogen-free male C57BL/6 mice (eight weeks old) were randomly divided into four groups, including the air exposure (sham) group, an ECA low-dose (ECAL) group, an ECA high-dose (ECAH) group, and a CCS exposure group. Mice were orally and nasally exposed to the corresponding CCS and ECA, and compared with the differences induced in the mouse model. Changes in the trachea, lungs, tissue inflammation levels, and proteome of the lung were measured and analysed.

It was found that CCS exposure resulted in pathological changes in the airways and lungs, with decreased lung functions and increased levels of inflammation, whereas the ECAS exposure produced significantly less effects at equivalent nicotine levels. Proteomic analysis showed that CCS had more differentially expressed genes and complex regulatory mechanisms relative to ECAL and ECAH.

In this study different nicotine dose levels were selected and conducted a 10-week subchronic inhalation toxicity experiment was conducted. The results support the hypothesis that e-cigarettes aerosols have less harmful effects on the respiratory system than combustible cigarette smoke at the same nicotine dose under the animal model used, providing additional evidence for the relative safety of e-cigarettes.