ArticleAmerican journal of respiratory cell and molecular biology2013
Radical-containing ultrafine particulate matter initiates epithelial-to-mesenchymal transitions in airway epithelial cells.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- A systematic review of environmentally persistent free radical (EPFR) formation, characteristics, and health effects: are there sufficient data for risk assessment?Journal of toxicology and environmental health. Part B, Critical reviews · 2026Pooled it
- AhR Activation at the Air-Blood Barrier Alters Systemic microRNA Release After Inhalation of Particulate Matter Containing Environmentally Persistent Free Radicals.Cardiovascular toxicology · 2025Article
- Regulatory mechanisms of haptoglobin on particulate matter-induced epithelial-to-mesenchymal transition in bronchial epithelial cells.Journal of thoracic disease · 2024Article
- Review
- Article
- Biochar-Derived Persistent Free Radicals: A Plethora of Environmental Applications in a Light and Shadows Scenario.Toxics · 2024Review
- Inhaled Microplastics and Airway Development: Concerning Evidence from Organoids.American journal of respiratory and critical care medicine · 2024Article
- Impact of particulate air pollution on airway injury and epithelial plasticity; underlying mechanisms.Frontiers in immunology · 2024Review
- Involvement and repair of epithelial barrier dysfunction in allergic diseases.Frontiers in immunology · 2024Review
- Environmentally persistent free radicals: Methods for combustion generation, whole-body inhalation and assessing cardiopulmonary consequences.Environmental pollution (Barking, Essex : 1987) · 2023Article
- Increased alveolar epithelial TRAF6 via autophagy-dependent TRIM37 degradation mediates particulate matter-induced lung metastasis.Autophagy · 2022Article
- Epithelial barrier hypothesis: Effect of the external exposome on the microbiome and epithelial barriers in allergic disease.Allergy · 2022Review
- Korean Red Ginseng and Ginsenoside Rg3 Suppress Asian Sand Dust-Induced Epithelial-Mesenchymal Transition in Nasal Epithelial Cells.Molecules (Basel, Switzerland) · 2022Article
- A critical review of environmentally persistent free radical (EPFR) solvent extraction methodology and retrieval efficiency.Chemosphere · 2021Review
- Particulate Matter (PMInternational journal of molecular sciences · 2021Article
- Association between particulate matter containing EPFRs and neutrophilic asthma through AhR and Th17.Respiratory research · 2021Article
- Loss of E-cadherin due to road dust PMEnvironmental science and pollution research international · 2021Article
- Air pollution and children's health-a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter.Environmental health and preventive medicine · 2021Review
- Effects of ozone and particulate matter on airway epithelial barrier structure and function: a review ofInhalation toxicology · 2021Review
- SARS-CoV-2 infection, COVID-19 pathogenesis, and exposure to air pollution: What is the connection?Annals of the New York Academy of Sciences · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Environmentally persistent free radicals (EPFRs) in combustion-generated particulate matter (PM) are capable of inducing pulmonary pathologies and contributing to the development of environmental asthma. In vivo exposure of infant rats to EPFRs demonstrates their ability to induce airway hyperresponsiveness to methacholine, a hallmark of asthma. However, the mechanisms by which combustion-derived EPFRs elicit in vivo responses remain elusive. In this study, we used a chemically defined EPFR consisting of approximately 0.2 μm amorphrous silica containing 3% cupric oxide with the organic pollutant 1,2-dichlorobenzene (DCB-230). DCB-230 possesses similar radical content to urban-collected EPFRs but offers several advantages, including lack of contaminants and chemical uniformity. DCB-230 was readily taken up by BEAS-2B and at high doses (200 μg/cm(2)) caused substantial necrosis. At low doses (20 μg/cm(2)), DCB-230 particles caused lysosomal membrane permeabilization, oxidative stress, and lipid peroxidation within 24 hours of exposure. During this period, BEAS-2B underwent epithelial-to-mesenchymal transition (EMT), including loss of epithelial cell morphology, decreased E-cadherin expression, and increased α-smooth muscle actin (α-SMA) and collagen I production. Similar results were observed in neonatal air-liquid interface culture (i.e., disruption of epithelial integrity and EMT). Acute exposure of infant mice to DCB-230 resulted in EMT, as confirmed by lineage tracing studies and evidenced by coexpression of epithelial E-cadherin and mesenchymal α-SMA proteins in airway cells and increased SNAI1 expression in the lungs. EMT in neonatal mouse lungs after EPFR exposure may provide an explanation for epidemiological evidence supporting PM exposure and increased risk of asthma.
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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.