Cyclic exposure to ozone alters distal airway development in infant rhesus monkeys

Fanucchi, Michelle V.; Plopper, Charles G.; Evans, Michael J.; Hyde, Dallas M.; Winkle, Laura S. Van; Gershwin, Laurel J.; Schelegle, Edward S.

doi:10.1152/ajplung.00027.2006

Cited by 94 publications

(79 citation statements)

References 43 publications

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“…Additional subchronic and chronic ozone exposure studies (500 ppb) in rhesus monkeys have demonstrated structural changes in the distal and proximal airways (Fanucchi et al, 2006;Carey et al, 2011) and allergy-like patterns of response (increased globlet cells and eosinophils) to allergen and ozone co-challenges (Kajekar et al, 2007;Miller et al, 2009;van Winkle et al, 2010;Plopper et al, 2007). These studies would therefore seem to support the epidemiological observations that reported impaired lung growth (peak flow: Gauderman et al, 2002;FVC and FEV1: Rojas-Martinez et al, 2007) and a worsening of asthma symptoms in children with high ozone exposures (asthma incidence: McConnell et al, 2002;Islam et al, 2009;asthma medication usage: Millstein et al, 2004).…”

Section: Experimental and Panel Studiesmentioning

confidence: 99%

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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Section: Experimental and Panel Studiesmentioning

confidence: 99%

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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“…Although the nonrespiratory airways of rats and humans do not form additional branches postnatally, they exhibit proportional increases in length and diameter, the diameters of terminal bronchioles at 18 years of age in humans being about 2-fold those at 2 years of age and more than 5-fold those of a neonate (30,31). Whether early viral airway injury alters normal growth of conducting airways is not known, but a study of intermittent exposure of infant monkeys to ozone, a noninfectious airway insult, found that terminal bronchioles were significantly narrower and shorter in the ozone group (32).…”

Section: Discussionmentioning

confidence: 99%

Viral Bronchiolitis in Young Rats Causes Small Airway Lesions that Correlate with Reduced Lung Function

Sorkness

Szakaly

Rosenthal³

et al. 2013

Am J Respir Cell Mol Biol

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Viral illness with wheezing during infancy is associated with the inception of childhood asthma. Small airway dysfunction is a component of childhood asthma, but little is known about how viral illness at an early age may affect the structure and function of small airways. We used a well-characterized rat model of postbronchiolitis chronic airway dysfunction to address how postinfectious small airway lesions affect airway physiological function and if the structure/function correlates persist into maturity. Brown Norway rats were sham-or virus inoculated at 3 to 4 weeks of age and allowed to recover from the acute illness. At 3 to 14 months of age, physiology (respiratory system resistance, Newtonian resistance, tissue damping, and static lung volumes) was assessed in anesthetized, intubated rats. Serial lung sections revealed lesions in the terminal bronchioles that reduced luminal area and interrupted further branching, affecting 26% (range, 13-39%) of the small airways at 3 months of age and 22% (range, 6-40%) at 12 to 14 months of age. At 3 months of age (n ¼ 29 virus; n ¼ 7 sham), small airway lesions correlated with tissue damping (r s ¼ 0.69) but not with Newtonian resistance (r s ¼ 0.23), and Newtonian resistance was not elevated compared with control rats, indicating that distal airways were primarily responsible for the airflow obstruction. Older rats (n ¼ 7 virus; n ¼ 6 sham) had persistent small airway dysfunction and significantly increased Newtonian resistance in the postbronchiolitis group. We conclude that viral airway injury at an early age may induce small airway lesions that are associated quantitatively with small airway physiological dysfunction early on and that these defects persist into maturity.Keywords: asthma; lung growth and development; airway injury and repairSevere viral bronchiolitis and less severe wheezing viral illnesses occurring in the first 3 years of life have been associated strongly with an increased incidence of childhood-onset asthma (1, 2). However, the mechanisms by which early viral illnesses may induce asthma are not understood, and the fundamental question of whether the viral illness has a causative role in the development of persistent airway dysfunction in humans has not been resolved definitively (1-3). Recent data from the Childhood Origins of Asthma (COAST) birth cohort indicate that children with a history of rhinovirus-induced wheezing illness during the first 3 years of life have physiological and imaging evidence of altered small airway function at 9 to 10 years of age, suggesting that the small airways may be altered by antecedent respiratory viral illnesses in a subgroup of infants (4).The rat model of persistent airway dysfunction after viral respiratory illness at an early age (3-to 4-wk-old weanlings) has been a valuable tool for the study of mechanisms that may be relevant to childhood asthma that develops after viral bronchiolitis (5). This rat model shares many features with its human analog, including variable airway obstruction that persists at ...

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“…Recently, two important nonhuman primate models of respiratory syncytial virus (RSV) and bronchial asthma and RSV have been developed in the baboon and Rhesus monkey, respectively. These models are again important in reflecting physiological, immunological, and morphological similarities to human neonatal/pediatric diseases (27,58). Additionally, both are known to significantly impact lung function in affected children who survive preterm birth.…”

Section: Advantages Of the Baboon And Nonhuman Primate Modelsmentioning

confidence: 99%

Animal models of bronchopulmonary dysplasia. The preterm baboon models

Yoder

Coalson

2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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Yoder BA, Coalson JJ. Animal models of bronchopulmonary dysplasia. V. The preterm baboon models. Am J Physiol Lung Cell Mol Physiol 307: L970 -L977, 2014. First published October 3, 2014 doi:10.1152/ajplung.00171.2014.-Much of the progress in improved neonatal care, particularly management of underdeveloped preterm lungs, has been aided by investigations of multiple animal models, including the neonatal baboon (Papio species). In this article we highlight how the preterm baboon model at both 140 and 125 days gestation (term equivalent 185 days) has advanced our understanding and management of the immature human infant with neonatal lung disease. Not only is the 125-day baboon model extremely relevant to the condition of bronchopulmonary dysplasia but there are also critical neurodevelopmental and other end-organ pathological features associated with this model not fully discussed in this limited forum. We also describe efforts to incorporate perinatal infection into these preterm models, both fetal and neonatal, and particularly associated with Ureaplasma/Mycoplasma organisms. Efforts to rekindle the preterm primate model for future evaluations of therapies such as stem cell replacement, early lung recruitment interventions coupled with noninvasive surfactant and high-frequency nasal ventilation, and surfactant therapy coupled with antioxidant or anti-inflammatory medications, to name a few, should be undertaken.baboon; bronchopulmonary dysplasia; lung; preterm infant; ureaplasma OF THE NEARLY 4,000,000 annual births in the United States, ϳ1% (ϳ40,000) occur at Ͻ29-wk gestation. Advances in prenatal and neonatal care have contributed to marked improvements in survival rates for these extremely immature infants, with many centers reporting survival rates Ͼ90% for infants in the 25-to 28-wk range (71). However, increasing survival of these fragile infants has been accompanied by high rates of bronchopulmonary dysplasia (BPD), the most common morbidity affecting extremely preterm infants (66,71,96). Much of the progress in improved neonatal care, particularly management of underdeveloped preterm lungs, including approaches to mechanical ventilation, surfactant therapy, and application of noninvasive respiratory support, has been derived through investigations of multiple animal models, including the neonatal baboon (Papio species). In this article we will highlight how primate models, particularly the preterm baboon model at both 140 days and 125 days gestation (term equivalent 185 days), have advanced our understanding and management of the immature human infant with neonatal lung disease; identify limitations to this and other animal models in the quest to prevent BPD; and suggest future directions to improve animal modeling and translational research to further improve outcomes. 140-Day Model ("Old BPD")The first long-term animal model for neonatal BPD in the 140-day premature baboon was developed in the early 1980s (19,26). At that time surfactant replacement therapy had not been approved for human use. Additi...

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Cyclic exposure to ozone alters distal airway development in infant rhesus monkeys

Cited by 94 publications

References 43 publications

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

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

Viral Bronchiolitis in Young Rats Causes Small Airway Lesions that Correlate with Reduced Lung Function

Animal models of bronchopulmonary dysplasia. The preterm baboon models

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