# Acute E-Cigarette Aerosol Condensate Exposure Disrupts the Transcriptome and Proteome Profiles of Human Bronchial Epithelial BEAS-2B Cells

## TL;DR

This study shows that short-term exposure to e-cigarette aerosol condensates harms human bronchial cells by disrupting their genetic and protein activity, causing cellular stress.

## Contribution

The study reveals novel insights into how e-cigarette aerosol condensates affect cellular homeostasis and proteostasis in bronchial epithelial cells.

## Key findings

- E-cigarette aerosol condensates altered transcriptome and proteome profiles in BEAS-2B cells.
- Nicotine- and flavor-containing condensates caused changes in lipid, lysosome content, and actin formation.
- Exposure induced irreversible protein modifications, indicating harmful effects on cellular function.

## Abstract

The growing popularity of electronic cigarettes (e-cigarettes) necessitates a better understanding of their biological effects. In this study, we aimed to evaluate the effects of e-cigarette aerosol condensates generated from either e-cigarette carrier liquid alone or with e-cigarette liquid with nicotine and flavor on bronchial epithelial cells. BEAS-2B cells were exposed to e-cigarettes for 24 h, and transcriptional and proteomic profiling, including assessment of protein modifications, was performed. Additionally, cell-based assays were used to evaluate mitochondrial function, rate of protein synthesis, lysosomal signal, lipid droplet quantity and actin formation. Our findings reveal that short-term exposure to both types of aerosol condensates altered transcriptome and proteome profiles, disrupting cellular homeostasis in BEAS-2B cells through impaired proteostasis and mitochondrial function in response to both types of condensates. Changes in lipid and lysosome content, as well as a reduction in polymerized actin, were observed with nicotine- and flavor-containing condensate. E-cigarette exposure also induced irreversible protein modifications, including different chemical derivatives (25 out of 49 in nicotine/flavor condensate; 20 out of 48 in nicotine/flavor-free condensate; 4 out of 35 in control), suggesting their particularly harmful effect. Together, these findings point to early-onset cellular stress and impaired lung epithelial fitness caused by acute e-cigarette exposure.