ArticleToxicological sciences : an official journal of the Society of Toxicology2018
Ultrafine Particulate Matter Combined With Ozone Exacerbates Lung Injury in Mature Adult Rats With Cardiovascular Disease.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Subchronic pulmonary toxicity of ambient particles containing cement production-related elements.Toxicology reports · 2023Article
- The bio-distribution, clearance pathways, and toxicity mechanisms of ambient ultrafine particles.Eco-Environment & Health · 2023Review
- Lung-gut axis of microbiome alterations following co-exposure to ultrafine carbon black and ozone.Particle and fibre toxicology · 2023Article
- Aerosol physicochemical determinants of carbon black and ozone inhalation co-exposure induced pulmonary toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- The pro-inflammatory effects of combined exposure to diesel exhaust particles and mineral particles in human bronchial epithelial cells.Particle and fibre toxicology · 2022Article
- Modeling of Temporal Exposure to the Ambient Environment and Eczema Severity.JID innovations : skin science from molecules to population health · 2022Article
- Transcriptomics of single dose and repeated carbon black and ozone inhalation co-exposure highlight progressive pulmonary mitochondrial dysfunction.Particle and fibre toxicology · 2021Article
- Oxidized carbon black nanoparticles induce endothelial damage through C-X-C chemokine receptor 3-mediated pathway.Redox biology · 2021Article
- Air Pollution-Induced Autonomic Modulation.Physiology (Bethesda, Md.) · 2020Review
- Oxidative stress pathways of air pollution mediated toxicity: Recent insights.Redox biology · 2020Review
- Lung macrophages: current understanding of their roles in Ozone-induced lung diseases.Critical reviews in toxicology · 2020Review
- Susceptibility Variations in Air Pollution Health Effects: Incorporating Neuroendocrine Activation.Toxicologic pathology · 2019Article
- Associations of ambient PMInternational journal of biometeorology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Particulate matter (PM) and ozone (O3) are dominant air pollutants that contribute to development and exacerbation of multiple cardiopulmonary diseases. Mature adults with cardiovascular disease (CVD) are particularly susceptible to air pollution-related cardiopulmonary morbidities and mortalities. The aim was to investigate the biologic potency of ultrafine particulate matter (UFPM) combined with O3 in the lungs of mature adult normotensive and spontaneously hypertensive (SH) Wistar-Kyoto rats. Conscious, mature adult male normal Wistar-Kyoto (NW) and SH rats were exposed to one of the following atmospheres: filtered air (FA); UFPM (∼ 250 μg/m3); O3 (1.0 ppm); or UFPM + O3 (∼ 250 μg/m3 + 1.0 ppm) combined for 6 h, followed by an 8 h FA recovery period. Lung sections were evaluated for lesions in the large airways, terminal bronchiolar/alveolar duct regions, alveolar parenchyma, and vasculature. NW and SH rats were similarly affected by the combined-pollutant exposure, displaying severe injury in both large and small airways. SH rats were particularly susceptible to O3 exposure, exhibiting increased injury scores in terminal bronchioles and epithelial degeneration in large airways. UFPM-exposure groups had minimal histologic changes. The chemical composition of UFPM was altered by the addition of O3, indicating that ozonolysis promoted compound degradation. O3 increased the biologic potency of UFPM, resulting in greater lung injury following exposure. Pathologic manifestations of CVD may confer susceptibility to air pollution by impairing normal lung defenses and responses to exposure.
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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.