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      Effects of ozone exposure on human epithelial adenocarcinoma and normal fibroblasts cells

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          Abstract

          Previous studies show variable ozone cytotoxicity and genotoxicity in cell cultures, laboratory animals and humans directly exposed to tropospheric ozone. The aim of this study was therefore to investigate and compare the cyto and genotoxic effects of ozone using adenocarcinoma human alveolar basal epithelial cells A549 and normal human fibroblasts Hs27. A cell culture chamber with controlled atmosphere (a simulation reactor) was built to inject a flow of 120 ppb of ozone, which is two times the threshold value for the protection of human health, fixed by the EU legislation. Cell proliferation was evaluated by a luminescent cell viability assay while we assessed the genotoxic potential of ozone by the induction of micronuclei as well as evaluating DNA strand breaks by the induction of micronuclei evaluated by means of the cytokinesis-block micronucleus (CBMN) assay as well as evaluating DNA strand breaks by Alkaline Comet Assay (CA) or Comet Assay. A549 cells viability decreases significantly at 24 hours treatment with 120 ppb of O 3 while at 48 hours and 72 hours O 3 treated cells viability doesn’t differ in respect to the control. However a significative decrease of A549 viability is shown at 72 hours vs. 48 hours in both treated and not-treated cells. The viability trend in the Hs27 cells did not show any significant changes in treated samples compared to the control in all conditions. The two genotoxicity biomarkers, the micronucleus and the comet tests, showed in both the cell types exposed to ozone, a significant increase in the number of micronuclei and in the tail DNA % in respect to the control even if at different times/cell type. Moreover, we found that O 3 provokes genotoxic effects more evident in A549 cancer cells than in normal fibroblasts Hs27 ones. We applied a cell growth simulation model referred to ozone treated or not cell lines to confirm that the ozone exposure causes a slackening in the cells replication.

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          Chemical exposure-response relationship between air pollutants and reactive oxygen species in the human respiratory tract

          Pascale S. J. Lakey, Thomas Berkemeier, Haijie Tong … (2016)
          Air pollution can cause oxidative stress and adverse health effects such as asthma and other respiratory diseases, but the underlying chemical processes are not well characterized. Here we present chemical exposure-response relations between ambient concentrations of air pollutants and the production rates and concentrations of reactive oxygen species (ROS) in the epithelial lining fluid (ELF) of the human respiratory tract. In highly polluted environments, fine particulate matter (PM2.5) containing redox-active transition metals, quinones, and secondary organic aerosols can increase ROS concentrations in the ELF to levels characteristic for respiratory diseases. Ambient ozone readily saturates the ELF and can enhance oxidative stress by depleting antioxidants and surfactants. Chemical exposure-response relations provide a quantitative basis for assessing the relative importance of specific air pollutants in different regions of the world, showing that aerosol-induced epithelial ROS levels in polluted megacity air can be several orders of magnitude higher than in pristine rainforest air.
          Article 0 comments Cited 90 times – based on 0 reviews     Review now
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            Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects.

            T. Schmitt, R Devlin, Márcia M. Jardim … (2012)
            Recent epidemiology studies have reported associations between short-term ozone exposure and mortality. Such studies have previously reported associations between airborne particulate matter pollution and mortality, and support for a causal relationship has come from controlled-exposure studies that describe pathophysiological mechanisms by which particulate matter could induce acute mortality. In contrast, for ozone, almost no controlled-human-exposure studies have tested whether ozone exposure can modulate the cardiovascular system. Twenty-three young healthy individuals were exposed in a randomized crossover fashion to clean air and to 0.3-ppm ozone for 2 hours while intermittently exercising. Blood was obtained immediately before exposure, immediately afterward, and the next morning. Continuous Holter monitoring began immediately before exposure and continued for 24 hours. Lung function was performed immediately before and immediately after exposure, and bronchoalveolar lavage was performed 24 hours after exposure. Immediately after ozone exposure, we observed a 98.9% increase in interleukin-8, a 21.4% decrease in plasminogen activator inhibitor-1, a 51.3% decrease in the high-frequency component of heart rate variability, and a 1.2% increase in QT duration. Changes in interleukin-1B and plasminogen activator inhibitor-1 were apparent 24 hours after exposure. In agreement with previous studies, we also observed ozone-induced drops in lung function and an increase in pulmonary inflammation. This controlled-human-exposure study shows that ozone can cause an increase in vascular markers of inflammation and changes in markers of fibrinolysis and markers that affect autonomic control of heart rate and repolarization. We believe that these findings provide biological plausibility for the epidemiology studies that associate ozone exposure with mortality. URL: http://www.clinicaltrials.gov. Unique identifier: NCT01492517.
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              Mathematical modeling of tumor growth and treatment.

              Heiko Enderling, Mark Chaplain (2014)
              Using mathematical models to simulate dynamic biological processes has a long history. Over the past couple of decades or so, quantitative approaches have also made their way into cancer research. An increasing number of mathematical, physical, computational and engineering techniques have been applied to various aspects of tumor growth, with the ultimate goal of understanding the response of the cancer population to clinical intervention. So-called in silico trials that predict patient-specific response to various dose schedules or treatment combinations and sequencing are on the way to becoming an invaluable tool to optimize patient care. Herein we describe fundamentals of mathematical modeling of tumor growth and tumor-host interactions, and summarize some of the seminal and most prominent approaches.
              Article 0 comments Cited 48 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Anna Poma:
                ORCID: http://orcid.org/0000-0001-8627-6646
                Role: ConceptualizationRole: Data curationRole: Formal analysisRole: Funding acquisitionRole: InvestigationRole: Project administrationRole: ResourcesRole: SupervisionRole: Writing – original draftRole: Writing – review & editing
                Sabrina Colafarina: Role: Data curationRole: InvestigationRole: MethodologyRole: Software
                Eleonora Aruffo: Role: ConceptualizationRole: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: SoftwareRole: Writing – review & editing
                Osvaldo Zarivi: Role: Data curationRole: MethodologyRole: ResourcesRole: Software
                Antonella Bonfigli: Role: Formal analysisRole: MethodologyRole: Resources
                Sebastiano Di Bucchianico: Role: Data curation
                Piero Di Carlo: Role: ConceptualizationRole: Data curationRole: Formal analysisRole: Funding acquisitionRole: InvestigationRole: SoftwareRole: SupervisionRole: ValidationRole: Writing – original draftRole: Writing – review & editing
                Maria Rosaria Scarfi: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 8 September 2017
                Publication date Collection: 2017
                Volume: 12
                Issue: 9
                Electronic Location Identifier: e0184519
                Affiliations
                [1 ] Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
                [2 ] Department of Psychological, Health and Territorial Sciences, University "G. d'Annunzio" of Chieti-Pescara, Chieti, Italy
                [3 ] Centre of Excellence CETEMPS, University of L'Aquila, L'Aquila, Italy
                Consiglio Nazionale delle Ricerche, ITALY
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Author information
                http://orcid.org/0000-0001-8627-6646
                Article
                Publisher ID: PONE-D-17-23056
                DOI: 10.1371/journal.pone.0184519
                PMC ID: 5590931
                PubMed ID: 28886142
                SO-VID: f584d0d0-4727-4430-8f4f-50405e42e92e
                Copyright © © 2017 Poma et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 16 June 2017
                Date accepted : 27 August 2017
                Page count
                Figures: 6, Tables: 0, Pages: 14
                Funding
                Funded by: University of L'Aquila
                Award ID: RIA 2016
                Award Recipient :
                ORCID: http://orcid.org/0000-0001-8627-6646
                Funded by: CETEMPS L'Aquila
                Award Recipient :
                Funded by: Department of Psycological, Health and Territorial Sciences, University D'Annunzio Chieti Pescara
                Award ID: 2016-2017
                Award Recipient :
                The research funds of DiSPuTer (Department of Psychological, Health and Territorial Sciences, University "G. d'Annunzio" of Chieti-Pescara, Italy) have been supporting the work of EA and PDC and the research funds of Department of Life, Health and Environmental Sciences, University of L'Aquila, Italy have been supporting the work of AP, SC, AB and OZ. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Earth Sciences
                Subject: Atmospheric Science
                Subject: Atmospheric Chemistry
                Subject: Greenhouse Gases
                Subject: Ozone
                Subject: Physical Sciences
                Subject: Chemistry
                Subject: Environmental Chemistry
                Subject: Atmospheric Chemistry
                Subject: Greenhouse Gases
                Subject: Ozone
                Subject: Ecology and Environmental Sciences
                Subject: Environmental Chemistry
                Subject: Atmospheric Chemistry
                Subject: Greenhouse Gases
                Subject: Ozone
                Subject: Biology and Life Sciences
                Subject: Microbiology
                Subject: Protozoology
                Subject: Micronuclei
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cell Processes
                Subject: Cell Proliferation
                Subject: Research and Analysis Methods
                Subject: Bioassays and Physiological Analysis
                Subject: Cell Analysis
                Subject: Cell Viability Testing
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cellular Types
                Subject: Animal Cells
                Subject: Epithelial Cells
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Epithelium
                Subject: Epithelial Cells
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Epithelium
                Subject: Epithelial Cells
                Subject: Research and Analysis Methods
                Subject: Biological Cultures
                Subject: Cell Cultures
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cellular Types
                Subject: Animal Cells
                Subject: Connective Tissue Cells
                Subject: Fibroblasts
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Connective Tissue
                Subject: Connective Tissue Cells
                Subject: Fibroblasts
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Biological Tissue
                Subject: Connective Tissue
                Subject: Connective Tissue Cells
                Subject: Fibroblasts
                Subject: Medicine and Health Sciences
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Carcinomas
                Subject: Adenocarcinomas
                Custom metadata
                Data Availability All relevant data are within the paper and its Supporting Information files.

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                ScienceOpen disciplines: Uncategorized

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