ArticleAmerican journal of physiology. Lung cellular and molecular physiology2024
Does vaping increase the likelihood of SARS-CoV-2 infection? Paradoxically yes and no.
Article in American journal of physiology. Lung cellular and molecular physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis.The European respiratory journal · 2024Pooled it
- Methylglyoxal and Glyoxal in High-Puff Disposable Electronic Cigarette Liquids: Unexpected Accumulation and Enhanced Cytotoxicity.ACS omega · 2026Article
- Vaping nicotine is associated with increased medically-attended COVID-19 in women of reproductive age in an integrated health system.Journal of thoracic disease · 2025Article
- Contextualizing Changes in e-Cigarette Use During the Early COVID-19 Pandemic and Accompanying Infodemic ("So Much Contradictory Evidence"): Qualitative Document Analysis of Reddit Forums.Journal of medical Internet research · 2025Article
- Menthol, a consumer product additive, adversely affects human embryonic stem cells via activation of TRPM8 and TRPA1 channels.Stem cells translational medicine · 2025Article
- E-cigarettes are not associated with post-acute COVID-19 syndrome among US adults.Scientific reports · 2025Article
- Acetaldehyde and methylglyoxal: comparative analysis of toxic electronic cigarette degradation products in 3D and 2D exposure systems using human bronchial epithelial models.Frontiers in toxicology · 2025Article
- Challenges in current inhalable tobacco toxicity assessment models: A narrative review.Tobacco induced diseases · 2024Review
- Establishing a Disease-in-a-Dish Model to Study SARS-CoV-2 Infection During Prenatal Development.Current protocols · 2023Article
- Endocytosis inhibitors block SARS-CoV-2 pseudoparticle infection of mink lung epithelium.Frontiers in microbiology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Data on the relationship between electronic cigarettes (ECs) and SARS-CoV-2 infection are limited and contradictory. Our objectives were to investigate the impact of EC aerosols on SARS-CoV-2 infection of human bronchial epithelial cells and identify the causative chemical(s). Fully differentiated human bronchial epithelial tissues (hBETs) were exposed at the air-liquid interface (ALI) to aerosols produced from JUUL "Virginia Tobacco" and BLU ECs, as well as nicotine, propylene glycol (PG), vegetable glycerin (VG), and benzoic acid, and infection was then evaluated with SARS-CoV-2 pseudoparticles. Pseudoparticle infection of hBETs increased with aerosols produced from PG/VG, PG/VG plus nicotine, or BLU ECs; however, JUUL EC aerosols did not increase infection compared with controls. Increased infection in PG/VG alone was due to enhanced endocytosis, whereas increased infection in PG/VG plus nicotine or in BLU ECs was caused by nicotine-induced elevation of the aerosol's pH, which correlated with increased transmembrane protease, serine 2 (TMPRSS2) activity. Notably, benzoic acid in JUUL aerosols mitigated the enhanced infection caused by PG/VG or nicotine, offering protection that lasted for at least 48 h after exposure. In conclusion, the study demonstrates that EC aerosols can impact susceptibility to SARS-CoV-2 infection depending on their specific ingredients. PG/VG alone or PG/VG plus nicotine enhanced infection through different mechanisms, whereas benzoic acid in JUUL aerosols mitigated the increased infection caused by certain ingredients. These findings highlight the complex relationship between ECs and SARS-CoV-2 susceptibility, emphasizing the importance of considering the specific aerosol ingredients when evaluating the potential effects of ECs on infection risk.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.