Abstract Introduction Globally and in the U.S., adolescents and young adults have the highest rates of e-cigarette use. There are chemical components in e-cigarette aerosols unique to this form of nicotine delivery system; thus, vaping may have unexpected repercussions on human health. Multiple studies in mice have demonstrated inflammatory changes and immunomodulation both locally in the lungs and systemically. Here, we describe the effect of chronic e-cigarette aerosol inhalation in adolescent non-human primates (NHP) on pulmonary inflammation. Methods Three male rhesus macaques (Macaca mulatta) aged 2-3 years were exposed to e-cigarette aerosols (JUULTM Virginia Tobacco, 59 mg/mL nicotine salts) for 60 min/day, 3 days/week for 25 weeks. Bronchoalveolar lavage (BAL), bronchial and nasal epithelial cell brushings, blood (PAXgene RNA), and plasma were obtained prior to exposure and after 4 and 6 months of e-cigarette aerosol exposure. At 24 hours before euthanasia, animals underwent sampling prior to lipopolysaccharide challenge in the right caudal lobe, and sample collection was repeated on the day of euthanasia. After euthanasia, tracheal and lung tissue were collected from each animal for histology. Control lung tissue was obtained from the biobank at UC Davis. Total RNA was isolated from blood, BAL cell pellets, bronchial cells, nasal epithelial cells, and lung tissue, and underwent RNA-seq at the UCSD IGM Genomics Center. Plasma samples were analyzed for metabolites using rapid liquid chromatography-mass spectrometry. Fixed and paraffin-embedded lung tissue were evaluated using standard stains (e.g., H Tobacco Related Disease Research Program (TRDRP) T34IR8251; VA Merit Awards 1I01BX006447 and 1I01BX004767; NIH NHLBI K24 HL155884 and R01 HL137052.
Karandashova et al. (Fri,) studied this question.