ArticleExperimental physiology2026
The effects of e-cigarette use on asthma severity in adult BALB/c mice.
Article in Experimental physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- The effects of e-cigarette use on asthma severity in adult BALB/c mice.Experimental physiology · 2026Article
- The testosterone paradox in asthma.Frontiers in allergy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Electronic cigarettes (e-cigarettes) are often perceived to be a less harmful alternative to tobacco cigarettes. Potentially due to this perception, they are used by people with pre-existing respiratory conditions, such as asthma, who otherwise would not smoke. Despite this, there are few studies exploring the health effects of e-cigarette use on pre-existing asthma. In this study, a house dust mite-induced allergic-airways disease phenotype was generated in adult BALB/c mice over 7 weeks. For the last 2 weeks of this period, mice were also exposed to either medical air, or tobacco smoke or e-cigarette aerosol (with or without nicotine) for 2 h/day. Twenty-four hours later, respiratory parameters including lung volume/function and responsiveness to methacholine were assessed. Biological samples were taken for analysis of pulmonary cellular inflammation and mediator levels, serum IgE and lung/airway structure. There were complex effects of exposure on respiratory outcomes. For example, tobacco smoke-exposed mice of both sexes were the most responsive to methacholine but had suppressed total cellular and eosinophilic inflammation. Female e-cigarette aerosol-exposed mice had impaired parenchymal mechanics at functional residual capacity compared with tobacco smoke-exposed mice, irrespective of nicotine. Interferon γ levels were suppressed in both e-cigarette-exposed groups. There was no effect of any exposure on IgE or lung structural parameters. E-cigarette aerosol exposure exacerbated aspects of an allergic airways disease phenotype in mice. This suggests that asthmatics should exercise increased caution if thinking of using e-cigarettes.
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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.