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Acute eCig Vapor or SHS Exposure Induces Inflammatory Signaling in the Adult Murine Lung

The detrimental effects of exposure to tobacco smoke have been confirmed repeatedly over the last several decades. Primary smoking produces the greatest damage; however, secondhand smoke (SHS) is also notably detrimental. More recently the development of electronic cigarettes (eCigs) has introduced a new aspect to the study of smoke exposure. A heating element is used by eCigs to vaporize an oil‐based carrier that contains nicotine and various flavorings. eCig liquid and aerosols have been linked to increased cytotoxicity, inflammation, and production of reactive oxygen species. Negative effects on respiratory health have also been confirmed. Both tobacco smoke and eCig vapor have been found to alter cellular signaling and activate inflammatory responses. Of note, inflammatory pathways include signaling through receptors for advanced glycation end‐products (RAGE). Our objective in this study was to examine effects of acute exposure to eCig vapor compared to SHS in the murine lung. Wild type mice were exposed to vapor containing Apple or Cinnamon flavoring, or to SHS for a period of four days using a nose‐only delivery system (Scireq). Exposure consisted of 30 minutes of eCig vapor or SHS generated by three cigarettes over a period of 30 minutes. Control mice were exposed to room air. Animal use was in accordance with approved IACUC protocols at Brigham Young University. After exposure, lung tissue was collected: the left lung lobe was inflated for histological analysis, and the right lung lobes were snap frozen for protein and RNA analysis. H&E stained lung sections did not show changes in morphology and staining for pulmonary cell types using cell‐specific antibodies (SPC, CCSP, T1a and Fox J1) revealed evidence of cell population alterations potentially explaining increases in pro‐apoptotic cleaved caspase‐3 following exposure. Immunoblotting for RAGE and signaling intermediates activated by RAGE such as NF‐kB and pERK revealed differential expression following eCig or SHS exposure. These results indicate that activation of inflammatory signaling pathways occurs following an acute four‐day exposure. Such signaling in eCig vapor exposed mice has potential to lead to chronic inflammatory disease characteristics with longer exposures potentially leading to chronic obstructive disorders resulting from tobacco smoke exposure.