What does this research mean for the field?

Chronic inhalation of e-cigarette aerosols induces significant immunomodulatory proteomic changes in both systemic circulation and the lungs that are associated with the development of chronic diseases. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research aims to evaluate the health effects of chronic e-cigarette exposure on Rhesus macaques.

May 20, 2026

B26-25 Targeted Proteomic Profiling of Plasma and Bronchoalveolar Lavage From Rhesus Macaques Chronically Exposed to E-cigarette Aerosol Identifies Changes Commonly Associated With Chronic Diseases

Key Points

This research aims to evaluate the health effects of chronic e-cigarette exposure on Rhesus macaques.
Three adolescent male Rhesus macaques were exposed to JUUL e-cigarettes for 25 weeks.
Plasma and bronchoalveolar lavage samples were collected and analyzed for immunomodulatory proteins.
Statistical analyses were performed using paired t-tests with necessary corrections.
Significant decreases in E-selectin (suggesting decreased leukocyte adhesion) and CD40 ligand were observed in plasma after 6 months.
Increased levels of FGF-21 were found, indicating potential links to obesity and metabolic syndrome.
In bronchoalveolar lavage, reductions in VEGF and MIP-1α were noted, related to respiratory diseases and immune function.

Abstract

Abstract Introduction The use of electronic cigarettes (e-cigarettes) has rapidly increased in popularity. Particularly concerning are the high rates of e-cigarette use among youth and young adults. Currently, 4th-generation e-cigarettes in the form of pod-based or disposable devices are the most popular. However, there are limited data on the long-term health effects of e-cigarette vaping, highlighting an need for more research. Our lab has previously demonstrated that 4th-generation devices have immunomodulatory effects following sub-chronic exposures in mice. Here, we seek to determine the impact of chronic e-cigarette exposure on the systemic circulation and lung using a highly physiologic non human primate (NHP) model. Methods Three adolescent male Rhesus macaques (2-3 years old) were exposed to JUUL Virginia Tobacco (59mg/mL nicotinic salts) using a 4-second puff profile with 2 puffs/minute, for 1 hour, 3 days/week, for a total of 25 weeks using an aerosol mask. Bronchoalveolar lavage (BAL) was collected from the left and right lung at baseline and end of exposures. Plasma was collected at baseline, 4 months, and at time of harvest. Soluble immune mediators in plasma at baseline and 6 months were quantified using NUcleic acid Linked Immuno-Sandwich Assay (NULISAseq) Inflammation Panel. A 24-plex multiplex ELISA (MesoScale Discovery) was used for quantifying mediators in BAL. NULISA Protein Quantification (NPQ) units from NULISAseq were log2-transformed and analyzed using a paired t-test with Benjamini-Hochberg correction. Protein concentrations from the 24-plex multiplex ELISA were log2-transformed and compared using a paired t-test as well. Results NHP plasma samples exhibited 50% detection using the human NULISAseq panel. Of the detectable proteins in plasma, E-selectin (suggesting decreased leukocyte adhesion), CD40 ligand (immunodeficiency), CCL5 (periodontitis and thrombocytopenia), IL-5 (CAD and heart failure), and lipocalin-2 (type II diabetes) were found to be significantly decreased after 6 months of e-cigarette exposure, while FGF-21 (obesity, type II diabetes, metabolic syndrome, fatty liver disease) was increased. In BAL, VEGF (IPF, COPD, and ARDS) and MIP-1α (cancer, immunosuppression of T cells) were significantly lowered by e-cigarette exposure. Conclusion Here, we demonstrate that chronic inhalation of e-cigarette aerosols by NHP Rhesus macaques leads to immunomodulatory effects in both the systemic circulation and lung. These changes are highly concerning for the development of serious medical conditions such as diabetes, cardiovascular disease, IPF, COPD, and cancer. Future studies are needed to understand nicotine-dependent and independent mechanisms of immune dysregulation. This abstract is funded by: UC Davis NHP Pilot Award, NIH NHLBI T32 HL166127, NIH NHLBI K24 HL155884, VA Merit I01 BX006447, TRDRP T30IP0965, TRDRP T34IR8251

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