Despite containing fewer toxicants, cannabis vape aerosol triggered the same inflammatory, cancer, and stress gene pathways in human bronchial cells as cannabis smoke — challenging the assumption that vaping is meaningfully safer at the cellular level.
Read this if you switched from smoking to vaping cannabis assuming it's much safer — at the cellular level, the biological response is more similar than the marketing suggests.
What the researchers found
The shift from smoking to vaping cannabis is driven largely by the belief that vaping is safer. This study tested that assumption at the molecular level by comparing what cannabis smoke extract (CaSE) and cannabis vape extract (CaVE) actually do to human bronchial epithelial cells.
The chemical analysis confirmed what other studies have found: cannabis vape aerosol contained fewer toxicants than smoke. But here's the twist — both CaSE and CaVE still contained teratogens, carcinogens, and respiratory toxicants. Vaping reduces the dose of these compounds; it doesn't eliminate them.
More importantly, when the researchers looked at what happened inside the cells, the gene expression patterns were remarkably similar. RNA sequencing revealed that both smoke and vape extracts significantly upregulated genes in pathways related to inflammation, cancer, and cellular stress. Both also downregulated pathways involved in lipid synthesis and metabolism. The transcriptional response — what the cells were actually doing at the molecular level — was largely the same regardless of whether the exposure came from smoke or vapor.
Targeted metabolomics added another layer: both exposures caused significant changes in metabolites involved in inflammatory and oxidative stress pathways. The receptor-mediated activity of both extracts was primarily driven by THC concentration, suggesting that THC itself — present in both smoke and vapor — may be responsible for much of the biological response.
The implication is sobering: while vaping exposes the lungs to fewer chemical toxicants, the cellular and molecular response may be just as harmful.
Why it matters
The cannabis industry and many public health messages position vaping as harm reduction. This study suggests that at the cellular level, the harm reduction may be more limited than assumed. If the inflammatory, cancer, and stress pathways activated by vaping are the same as those activated by smoking, the long-term health consequences may converge even if the acute chemical exposure differs.
The numbers in context
Cannabis vape aerosol contained fewer toxicants than smoke (chemical analysis). Both CaSE and CaVE contained teratogens, carcinogens, and respiratory toxicants. RNA sequencing: both upregulated inflammation, cancer, and stress pathways. Both downregulated lipid synthesis pathways. Receptor activity primarily driven by THC concentration in both extracts. Metabolomic changes in inflammatory and oxidative stress metabolites from both exposures.
How the study worked
Comparison of cannabis smoke extract (CaSE) and cannabis vape extract (CaVE) using: chemical analysis (HPLC and GC/MS), BRET-based biosensor for receptor-mediated activity, RNA sequencing for transcriptomic changes, and targeted metabolomics — all in human bronchial epithelial cells. Assessed inflammatory pathways, cancer-related gene expression, cellular stress responses, and metabolite changes.
Who was studied
Human bronchial epithelial cells were used for analysis.
What this study cannot tell us
In vitro study — cell culture exposure doesn't replicate the complex dynamics of actual lungs (airway clearance, immune response, tissue repair). The concentrations of CaSE and CaVE used on cells may not reflect real-world exposure levels. Single cell type (bronchial epithelium) doesn't capture the full respiratory tract response. Acute exposure only — chronic effects of repeated low-level vaping exposure aren't addressed. The specific cannabis products and vaping devices used may not represent the full market.
How to read the evidence
In vitro study using multiple rigorous analytical methods (RNA-seq, metabolomics, chemical analysis). Strong molecular-level evidence, but cell culture findings don't directly predict clinical outcomes in living lungs.
When this study was published
Published in 2025. This is among the first studies to compare cannabis smoke and vape at the transcriptomic level in human cells.
The bigger picture
This directly challenges the vaping harm reduction narrative from RTHC-00110 (lung health review) and complicates RTHC-00122 (route-specific effects). While gross chemical exposure is lower with vaping, this cellular-level study suggests the biological damage pathways are similar. Combined with RTHC-00128 (comparable respiratory symptoms from cannabis and nicotine vaping), the evidence is building that cannabis vaping isn't as safe as commonly perceived — at least for the lungs.
Replication
Not stated in abstract.
Funding
Not reported in abstract.
Conflicts of interest
Not reported in abstract.
Questions still open
- If the transcriptomic response is similar, why do clinical studies show fewer respiratory symptoms with vaping? Is the difference between smoking and vaping a matter of degree (lower dose of the same damage) or timing (slower accumulation with vaping)? Would the cancer pathway activation translate to actual increased cancer risk with long-term vaping? Does vaping temperature affect which pathways are activated?
Read the original research
Cannabis vaping elicits transcriptomic and metabolomic changes involved in inflammatory, oxidative stress, and cancer pathways in human bronchial epithelial cells.
American journal of physiology. Lung cellular and molecular physiology, 328(3), L478-L496
The American Journal of Physiology is a reputable journal focusing on physiological research.
Citation
Arlen, Maddison T; Patterson, Stephanie J; Page, Michelle K; Liu, Rui; Caruana, Vincenza; Wilson, Emily T; Laporte, Stéphane A; Goniewicz, Maciej L; Harris, Cory S; Eidelman, David H; Baglole, Carolyn J. (2025). Cannabis vaping elicits transcriptomic and metabolomic changes involved in inflammatory, oxidative stress, and cancer pathways in human bronchial epithelial cells.. American journal of physiology. Lung cellular and molecular physiology, 328(3), L478-L496. https://doi.org/10.1152/ajplung.00131.2024
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