Pulmonary function, bronchial reactivity, and epithelial permeability are response phenotypes to ozone and develop differentially in healthy humans

Que, Loretta G.; Stiles, Jane V.; Sundy, John S.; Foster, W. Michael

doi:10.1152/japplphysiol.00337.2011

Cited by 49 publications

(38 citation statements)

References 48 publications

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“…Despite the resolution of these responses, Sftpd 1/1 mice remain functionally compromised 72 hours after ozone inhalation. Thus, in these mice, Rn was significantly increased, with no apparent effect on the parenchyma, as measured by H and G. These findings are in accordance with reports of hyperreactivity in response to methacholine challenge after ozone exposure (4,32). Interestingly, at PEEPs both above and below the physiological level of 3 cm H 2 O, which represent hypoinflation and hyperinflation of the lung, respectively, a decrease in Rn was evident after ozone exposure.…”

Section: Discussionsupporting

confidence: 90%

“…Airway and tissue mechanics are also altered after ozone exposure. Thus, in humans, ozone inhalation leads to a deterioration of pulmonary function, as measured by decreases in respiratory frequency, forced expiratory volume in 1 second, and forced vital capacity, and increases in airway resistance (1,4,5). Ozone has been shown to exacerbate asthma and increase airway hyperreactivity (5, 6), and to contribute to increased morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD) (7,8).…”

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confidence: 99%

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Prolonged Injury and Altered Lung Function after Ozone Inhalation in Mice with Chronic Lung Inflammation

Groves

Gow

Massa

et al. 2012

Am J Respir Cell Mol Biol

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Surfactant protein-D (Sftpd) is a pulmonary collectin important in down-regulating macrophage inflammatory responses. In these experiments, we analyzed the effects of chronic macrophage inflammation attributable to loss of Sftpd on the persistence of ozoneinduced injury, macrophage activation, and altered functioning in the lung. Wild-type (Sftpd 1/1 ) and Sftpd 2/2 mice (aged 8 wk) were exposed to air or ozone (0.8 parts per million, 3 h). Bronchoalveolar lavage (BAL) fluid and tissue were collected 72 hours later. In Sftpd 2/2 mice, but not Sftpd 1/1 mice, increased BAL protein and nitrogen oxides were observed after ozone inhalation, indicating prolonged lung injury and oxidative stress. Increased numbers of macrophages were also present in BAL fluid and in histologic sections from Sftpd 2/2 mice. These cells were enlarged and foamy, suggesting that they were activated. This conclusion was supported by findings of increased BAL chemotactic activity, and increased expression of inducible nitric oxide synthase in lung macrophages. In both Sftpd 1/1 and Sftpd 2/2 mice, inhalation of ozone was associated with functional alterations in the lung. Although these alterations were limited to central airway mechanics in Sftpd 1/1 mice, both central airway and parenchymal mechanics were modified by ozone exposure in Sftpd 2/2 mice. The most notable changes were evident in resistance and elastance spectra and baseline lung function, and in lung responsiveness to changes in positive endexpiratory pressure. These data demonstrate that a loss of Sftpd is associated with prolonged lung injury, oxidative stress, and macrophage accumulation and activation in response to ozone, and with more extensive functional changes consistent with the loss of parenchymal integrity. Keywords: ozone; surfactant protein-D; macrophages; iNOS; lung functionOzone is a ubiquitous urban air pollutant generated as a component of photochemical smog. Inhaled ozone causes ozonation and the peroxidation of proteins and lipids in the epithelial lining fluid layer of the lung, resulting in the production of oxidized proteins, aldehydes, and free radicals, which can damage surrounding tissue (1, 2). This is accompanied by an accumulation of activated macrophages in the lung and the production of additional cytotoxic and proinflammatory mediators, including reactive oxygen and reactive nitrogen species (ROS and RNS, respectively) that contribute to tissue injury (3). Airway and tissue mechanics are also altered after ozone exposure. Thus, in humans, ozone inhalation leads to a deterioration of pulmonary function, as measured by decreases in respiratory frequency, forced expiratory volume in 1 second, and forced vital capacity, and increases in airway resistance (1,4,5). Ozone has been shown to exacerbate asthma and increase airway hyperreactivity (5, 6), and to contribute to increased morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD) (7,8). Similar alterations in lung function and increases in sensitivity to ozone have b...

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Prolonged Injury and Altered Lung Function after Ozone Inhalation in Mice with Chronic Lung Inflammation

Groves

Gow

Massa

et al. 2012

Am J Respir Cell Mol Biol

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“…Importantly, and consistent with earlier studies, the evidence presented since 2005 does not support a simple concordance between ozone-induced inflammation, lung function changes, pulmonary injury and cardiovascular effects (Que et al, 2011;Tank et al, 2011). It is therefore necessary that any discussion that implies thresholds for acute response end-points from human chamber studies is not interpreted in an overly simplistic manner.…”

Section: Experimental Studiessupporting

confidence: 54%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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“…A breach in the integrity of the epithelium would disrupt its barrier function and, consequently, increases airway responsiveness by facilitating the delivery of spasmogens to the ASM. In fact, association between epithelial permeability and airway responsiveness in humans has been previously reported (108); albeit this finding is not unanimous (197). Increased leakiness of the epithelium can be due to cellular damage and desquamation, which can be induced, for example, by eosinophil mobilization and activation into the airways.…”

Section: Epithelium Integritymentioning

confidence: 97%

Airway Smooth Muscle in Asthma Symptoms: Culprit but Maybe Innocent

Bossé¹,

Paré²,

Boss³

2012

Lung Diseases - Selected State of the Art Reviews

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Pulmonary function, bronchial reactivity, and epithelial permeability are response phenotypes to ozone and develop differentially in healthy humans

Cited by 49 publications

References 48 publications

Prolonged Injury and Altered Lung Function after Ozone Inhalation in Mice with Chronic Lung Inflammation

Prolonged Injury and Altered Lung Function after Ozone Inhalation in Mice with Chronic Lung Inflammation

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Airway Smooth Muscle in Asthma Symptoms: Culprit but Maybe Innocent

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