ArticlePloS one2018
Particulate matter containing environmentally persistent free radicals induces AhR-dependent cytokine and reactive oxygen species production in human bronchial epithelial cells.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 65 citations in OpenAlex.
- Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Shifts in soil microbiome surrounding a thermal treatment facility for hazardous waste: the hidden impact of environmentally persistent free radicals.Environmental science. Processes & impacts · 2026Article
- Aryl hydrocarbon receptor in club cells drives Th17-mediated lung injury following inhalation exposure to environmentally persistent free radicals.Redox biology · 2026Article
- Persistent chemicals in particulate matter (PM) near a hazardous waste thermal treatment facility.Atmospheric pollution research · 2025Article
- AhR Activation at the Air-Blood Barrier Alters Systemic microRNA Release After Inhalation of Particulate Matter Containing Environmentally Persistent Free Radicals.Cardiovascular toxicology · 2025Article
- Environmentally persistent free radicals lead to selective inhibition of CYP1 monooxygenase activities, and increased production of reactive oxygen species by reaction uncoupling.Frontiers in public health · 2025Article
- Inhalation of particulate matter containing environmentally persistent free radicals induces endothelial dysfunction mediated via AhR activation at the air-blood interface.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Biochar-Derived Persistent Free Radicals: A Plethora of Environmental Applications in a Light and Shadows Scenario.Toxics · 2024Review
- Involvement and repair of epithelial barrier dysfunction in allergic diseases.Frontiers in immunology · 2024Review
- Adjuvant effect of inhaled particulate matter containing free radicals following house-dust mite induction of asthma in mice.Inhalation toxicology · 2023Article
- Inhaled toxicants and pulmonary lipid metabolism: biological consequences and therapeutic interventions.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Environmentally persistent free radicals: Methods for combustion generation, whole-body inhalation and assessing cardiopulmonary consequences.Environmental pollution (Barking, Essex : 1987) · 2023Article
- Airborne Exposure of the Cornea to PMInternational journal of molecular sciences · 2023Article
- Characteristics and Risk Assessment of Environmentally Persistent Free Radicals (EPFRs) of PMInternational journal of environmental research and public health · 2023Article
- Article
- Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Environmental Impacts on COVID-19: Mechanisms of Increased Susceptibility.Annals of global health · 2022Article
- Association between particulate matter containing EPFRs and neutrophilic asthma through AhR and Th17.Respiratory research · 2021Article
- Inhalation of particulate matter containing free radicals leads to decreased vascular responsiveness associated with an altered pulmonary function.American journal of physiology. Heart and circulatory physiology · 2021Article
- Effects of intranasal instillation of nanoparticulate matter in the olfactory bulb.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Particulate matter (PM) is emitted during the combustion of fuels and wastes. PM exposure exacerbates pulmonary diseases, and the mechanism may involve oxidative stress. At lower combustion temperatures such as occurs in the cool zone of a flame, aromatic compounds chemisorb to the surface of metal-oxide-containing PM, resulting in the formation of surface-stabilized environmentally persistent free radicals (EPFR). Prior studies showed that PM-containing EPFR redox cycle to produce reactive oxygen species (ROS), and after inhalation, EPFR induce pulmonary inflammation and oxidative stress. Our objective was to elucidate mechanisms linking EPFR-induced oxidant injury with increased cytokine production by pulmonary epithelial cells. We thus treated human bronchial epithelial cells with EPFR at sub-toxic doses and measured ROS and cytokine production. To assess aryl hydrocarbon receptor (AhR) activity, cells were transfected with a luciferase reporter for xenobiotic response element activation. To test whether cytokine production was dependent upon AhR activation or oxidative stress, some cells were co-treated with an antioxidant or an AhR antagonist. EPFR increased IL-6 release in an ROS and AhR- and oxidant-dependent manner. Moreover, EPFR induced an AhR activation that was dependent upon oxidant production, since antioxidant co-treatment blocked AhR activation. On the other hand, EPFR treatment increased a cellular ROS production that was at least partially attenuated by AhR knockdown using siRNA. While AhR activation was correlated with an increased expression of oxidant-producing enzymes like cytochrome P450 CYP1A1, it is possible that AhR activation is both a cause and effect of EPFR-induced ROS. Finally, lipid oxidation products also induced AhR activation. ROS-dependent AhR activation may be a mechanism for altered epithelial cell responses after EPFR exposure, potentially via formation of bioactive lipid or protein oxidation products.
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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.