ArticleAmerican journal of physiology. Heart and circulatory physiology2021
Electronic cigarette solvents, pulmonary irritation, and endothelial dysfunction: role of acetaldehyde and formaldehyde.
Article in American journal of physiology. Heart and circulatory physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses 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
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- Clinical features, radiological findings, and mortality in patients with e-cigarette or vaping product use-associated lung injury: a systematic review and meta-analysis.BMC pulmonary medicine · 2026Pooled it
- Health Messaging Strategies for Vaping Prevention and Cessation Among Youth and Young Adults: A Systematic Review.Health communication · 2025Pooled it
- Electronic hookah (waterpipe) vaping reduces vascular endothelial function: the role of nicotine.American journal of physiology. Heart and circulatory physiology · 2024Trial
- Tobacco and marijuana induce adverse effects on cardiac function and platelet activity and reduce tissue preservation following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Article
- The Tie-2 agonist PMC-403 inhibits endothelial damage induced by e-cigarette vapor or LPS.Respiratory research · 2026Article
- Prevalence, perceived effects, and motivations for adolescent e-cigarette use: A cross-sectional study in the Paris region.Tobacco prevention & cessation · 2026Article
- Toxicity of humectants propylene glycol and vegetable glycerin in electronic nicotine delivery systems.Toxicology letters · 2025Review
- Exploring the Impact of E-cigarettes on Cardiovascular Health: Insights from Preclinical and Clinical Studies.Cardiovascular toxicology · 2025Review
- Chronic Pod-Mod E-Cigarette Aerosol Exposure Induces Aortic Dysfunction in Hypercholesterolemic Mice: Role of Oxidative Stress and Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Prevalence and health outcomes of combustible cigarettes and noncombustible nicotine or tobacco products: a nationwide cross-sectional study in South Korea.Preventive medicine reports · 2025Article
- The Impact of Maternal/In Utero Exposure of Novel Tobacco Products on the Offspring Cardiovascular Health.Cardiovascular toxicology · 2025Review
- Acute and Persistent Cardiovascular Effects of Menthol E-Cigarettes in Mice.Journal of the American Heart Association · 2025Article
- Role of the Transient Receptor Potential Ankyrin-1 in the Pulmonary, Vascular, and Systemic Effects of Short-Term Acrolein Inhalation in Mice: Implications for the Toxicity of Electronic Nicotine Delivery Systems.Cardiovascular toxicology · 2025Article
- Pregnancy and Postpartum Effects of Electronic Cigarettes on Maternal Health and Vascular Function in the Fourth Trimester.Cardiovascular toxicology · 2025Article
- A Review of the Toxicity of Ingredients in e-Cigarettes, Including Those Ingredients Having the FDA's "Generally Recognized as Safe (GRAS)" Regulatory Status for Use in Food.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2024Review
- Formaldehyde and the transient receptor potential ankyrin-1 contribute to electronic cigarette aerosol-induced endothelial dysfunction in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Influence of gestational window on offspring vascular health in rodents with in utero exposure to electronic cigarettes.The Journal of physiology · 2024Article
- An electron paramagnetic resonance time-course study of oxidative stress in the plasma of electronic cigarette exposed rats.Experimental physiology · 2024Article
- Evidence of premature vascular dysfunction in young adults who regularly use e-cigarettes and the impact of usage length.Angiogenesis · 2024Article
- Addressing Cardiovascular Toxicity Risk of Electronic Nicotine Delivery Systems in the Twenty-First Century: "What Are the Tools Needed for the Job?" and "Do We Have Them?"Cardiovascular toxicology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
After more than a decade of electronic cigarette (E-cig) use in the United States, uncertainty persists regarding E-cig use and long-term cardiopulmonary disease risk. As all E-cigs use propylene glycol and vegetable glycerin (PG-VG) and generate abundant saturated aldehydes, mice were exposed by inhalation to PG-VG-derived aerosol, formaldehyde (FA), acetaldehyde (AA), or filtered air. Biomarkers of exposure and cardiopulmonary injury were monitored by mass spectrometry (urine metabolites), radiotelemetry (respiratory reflexes), isometric myography (aorta), and flow cytometry (blood markers). Acute PG-VG exposure significantly affected multiple biomarkers including pulmonary reflex (decreased respiratory rate, -50%), endothelium-dependent relaxation (-61.8 ± 4.2%), decreased WBC (-47 ± 7%), and, increased RBC (+6 ± 1%) and hemoglobin (+4 ± 1%) versus air control group. Notably, FA exposure recapitulated the prominent effects of PG-VG aerosol on pulmonary irritant reflex and endothelial dysfunction, whereas AA exposure did not. To attempt to link PG-VG exposure with FA or AA exposure, urinary formate and acetate levels were measured by GC-MS. Although neither FA nor AA exposure altered excretion of their primary metabolite, formate or acetate, respectively, compared with air-exposed controls, PG-VG aerosol exposure significantly increased post-exposure urinary acetate but not formate. These data suggest that E-cig use may increase cardiopulmonary disease risk independent of the presence of nicotine and/or flavorings. This study indicates that FA levels in tobacco product-derived aerosols should be regulated to levels that do not induce biomarkers of cardiopulmonary harm. There remains a need for reliable biomarkers of exposure to inhaled FA and AA.
Indexed as
Identifiers
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.