Evidence map›Paper›PMID 41519495›Full record

ArticleToxicology in vitro : an international journal published in association with BIBRA2026

Vitamin E acetate and its aerosol activate aryl hydrocarbon receptor signaling and exacerbate inflammation in human U937-derived macrophages.

Xiaohan Li, Andrea Rossi, Thomas Haarmann-Stemmann, Elliot R Spindel, Jack C Connolly, Allison K Ehrlich, Kent E Pinkerton, Christoph F A Vogel

Abstract read
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In one paragraph

Article in Toxicology in vitro : an international journal published in association with BIBRA, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Xiaohan LiCenter for Health and the Environment, University of California, Davis, CA, USA; Department of Pediatrics, School of Medicine, University of California, Davis, CA, USA.
Andrea RossiLeibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Thomas Haarmann-StemmannLeibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.
Elliot R SpindelOregon Health Sciences University, Portland, OR, USA.
Jack C ConnollyCenter for Health and the Environment, University of California, Davis, CA, USA.
Allison K EhrlichDepartment of Environmental Toxicology, University of California, Davis, CA, USA.
Kent E PinkertonCenter for Health and the Environment, University of California, Davis, CA, USA; Department of Pediatrics, School of Medicine, University of California, Davis, CA, USA.
Christoph F A VogelCenter for Health and the Environment, University of California, Davis, CA, USA; Department of Environmental Toxicology, University of California, Davis, CA, USA. Electronic address: cfvogel@ucdavis.edu.

Funding

UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Irva Hertz-Picciotto · 2015 to 2026
$26.0M
The impact of Aryl hydrocarbon receptor signaling on Toll like receptor-mediated inflammationR01ES032827 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHRISTOPH F A VOGEL · 2022 to 2026
$1.7M
Ah-Receptor as a central mediator of immunomodulation in the tumor microenvironment of breast cancerR01ES036338 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI COLLEEN Ann SWEENEY, CHRISTOPH F A VOGEL · 2025 to 2026
$997k
NIEHS NIH HHS P30 ES023513NIEHS NIH HHS R01 ES032827NIEHS NIH HHS R01 ES036338
6 · The paper itself

Abstract

In 2019, a number of patients were hospitalized after the use of electronic cigarettes and displayed acute lung injuries. Such injury was categorized as e-cigarette or vaping associated lung injury (EVALI). Among these patients, Vitamin E acetate (VEA) was detected in most used electronic cigarette cartridges as well as the patients' bronchoalveolar lavage fluid, suggesting VEA to be a culprit of causing lung injury. Although further experiments verified the potential of VEA aerosol to cause cytotoxicity and lung injury, mechanisms of VEA aerosol toxicity are not well understood. In this study, we tested the toxicity of VEA, and its aerosol using a human macrophage model. VEA aerosols significantly induced oxidative stress as well as proinflammatory responses. In addition, the aerosol activated the aryl hydrocarbon receptor (AhR) signaling pathway, inducing CYP1A1 expression in human U937 monocyte-derived macrophages. Additionally, non-aerosolized VEA and VEA aerosol induce the expression of inflammatory markers such as interleukin (IL)-8 and cyclooxygenase (COX)-2 in an AhR-dependent manner as shown in CRISPR-cas9 AhR-knockout U937-derived human macrophages. These results suggest that VEA is an agonist for AhR and provide new potential mechanisms for lung injury induced by VEA aerosol inhalation via AhR activation in addition to the generation of oxidative stress.

Indexed as

AcetatesBasic Helix-Loop-Helix ProteinsMacrophagesReceptors, Aryl HydrocarbonVitamin EAerosolsCyclooxygenase 2Cytochrome P-450 CYP1A1HumansInflammationInterleukin-8Oxidative StressSignal TransductionU937 CellsAcetatesAerosolsAHR protein, humanBasic Helix-Loop-Helix ProteinsCyclooxygenase 2CYP1A1 protein, humanCytochrome P-450 CYP1A1Interleukin-8Receptors, Aryl HydrocarbonVitamin EAhRCOX-2EVALIIL-8InflammationOxidative stressVEA

Identifiers

PMID41519495
PMCPMC13317782

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Registered trials

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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.