ArticleAllergy2026
Heat-Not-Burn Tobacco Aerosols Induce Immune Dysregulation and Barrier Disruption Comparable to Conventional Cigarettes.
Article in Allergy, 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.
- Neutrophilic asthma: advances in experimental models from pathogenesis to therapeutic translation.Molecular medicine (Cambridge, Mass.) · 2026Review
- The Impact of the Exposome on Epithelial Barriers: New Approach Methodologies for Translational Research.Thoracic research and practice · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors.
Funding
Abstract
backgroundHeat-not-burn (HnB) tobacco products are marketed as a safer alternative to conventional cigarettes (CC), yet their health effects remain controversial, largely based on industry-funded studies. We aimed to assess lung function in HnB and CC users and examine the mechanistic effects of HnB exposure using animal and in vitro models.
methodsSpirometry data from 650 non-smokers (NS), 293 CC smokers, and 49 HnB users enrolled in the Bialystok-PLUS cohort were analyzed. To investigate underlying mechanisms, a whole-body mouse exposure model was performed with HnB aerosol or 3R4F cigarette smoke, assessing lung transcriptomic profiles (by means of RNA sequencing), lung inflammation (by flow cytometry and histochemical staining), and barrier integrity (by using immunofluorescent staining). Moreover, an in vitro ALI-culture model of human airway epithelial cells was used to validate the mouse experiments. The effect of HnB and CC was assessed through cytotoxic effect (MTT and LDH), inflammatory responses (cytokine release by ELISA), and tight junction proteins (immunofluorescence staining).
resultSpirometric analysis (FEV1, FVC, VC) revealed no significant overall differences in lung function among HnB users, CC smokers, and non-smokers (NS) in the unadjusted comparison. However, subgroup analyses showed that younger (< 45 years) HnB users and those with shorter smoking histories (< 20 years) already exhibited significantly lower FEV1, FVC, and VC compared to NS and CC smokers. After adjustment for age and smoking-related covariates, HnB users displayed modest but significant reductions in static FEV1 and FVC relative to NS, while no adjusted differences were detected between HnB and CC groups, indicating comparable baseline ventilatory function. Both exposures in mice increased eosinophils and B cell counts by ~2-fold, while decreasing ST2
conclusionDespite different molecular impacts, HnB aerosol exposure induces a level of airway epithelial injury and immune cell infiltration comparable to CC smoke. Our findings challenged the narrative of HnB products being a harmless alternative and highlight their potential to cause significant lung pathology.
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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 Socratic graph.