Skip header and navigation

3 records – page 1 of 1.

Coarse Fraction Particle Matter and Exhaled Nitric Oxide in Non-Asthmatic Children.

https://arctichealth.org/en/permalink/ahliterature283704
Source
Int J Environ Res Public Health. 2016 Jun 22;13(6)
Publication Type
Article
Date
Jun-22-2016
Author
Hanne Krage Carlsen
Peter Boman
Bodil Björ
Anna-Carin Olin
Bertil Forsberg
Source
Int J Environ Res Public Health. 2016 Jun 22;13(6)
Date
Jun-22-2016
Language
English
Publication Type
Article
Keywords
Air Pollutants - analysis
Child
Exhalation - physiology
Female
Humans
Inflammation - etiology - physiopathology
Male
Models, Theoretical
Nitric Oxide - analysis
Particulate Matter - adverse effects - analysis
Sweden
Abstract
Coarse particle matter, PMcoarse, is associated with increased respiratory morbidity and mortality. The aim of this study was to investigate the association between short-term changes in PMcoarse and sub-clininal airway inflammation in children. Healthy children aged 11 years from two northern Swedish elementary schools underwent fraction of exhaled nitrogen oxide (FENO) measurements to determine levels of airway inflammation twice weekly during the study period from 11 April-6 June 2011. Daily exposure to PMcoarse, PM2.5, NO2, NOx, NO and O3 and birch pollen was estimated. Multiple linear regression was used. Personal covariates were included as fixed effects and subjects were included as a random effect. In total, 95 children participated in the study, and in all 493 FENO measurements were made. The mean level of PMcoarse was 16.1 µg/m³ (range 4.1-42.3), and that of O3 was 75.0 µg/m³ (range: 51.3-106.3). That of NO2 was 17.0 µg/m³ (range: 4.7-31.3), NOx was 82.1 µg/m³ (range: 13.3-165.3), and NO was 65 µg/m³ (range: 8.7-138.4) during the study period. In multi-pollutant models an interquartile range increase in 24 h PMcoarse was associated with increases in FENO by between 6.9 ppb (95% confidence interval 0.0-14) and 7.3 ppb (95% confidence interval 0.4-14.9). PMcoarse was associated with an increase in FENO, indicating sub-clinical airway inflammation in healthy children.
Notes
Cites: Environ Health. 2013 Apr 20;12:3623602059
Cites: Occup Environ Med. 2011 Aug;68(8):551-621045215
Cites: Occup Environ Med. 2015 Apr;72(4):284-9325475111
Cites: Am J Respir Crit Care Med. 2010 Feb 15;181(4):324-720007926
Cites: J Allergy Clin Immunol. 2012 Jan;129(1):232-9.e1-722055874
Cites: Environ Int. 2014 Dec;73:440-625244707
Cites: Eur Respir J. 2011 Mar;37(3):523-3120634264
Cites: Curr Opin Pulm Med. 2014 Jan;20(1):53-924275926
Cites: Environ Int. 2001 Oct;27(4):335-4011686645
Cites: Respir Med. 2014 Jun;108(6):830-4124636813
Cites: Environ Health Perspect. 2011 Oct;119(10):1472-721708511
Cites: Eur Respir J. 2005 Aug;26(2):309-1816055881
Cites: J Asthma. 2013 Nov;50(9):983-923931679
Cites: Environ Health Perspect. 2012 Mar;120(3):437-4421896396
Cites: Am J Respir Crit Care Med. 2007 Dec 15;176(12):1236-4217641154
Cites: Occup Environ Med. 2014 Jul;71(7):507-1324696513
Cites: J Toxicol Environ Health A. 2007 Feb 1;70(3-4):270-417365589
Cites: Curr Environ Health Rep. 2014 Aug 8;1:258-27425152864
Cites: Occup Environ Med. 1997 Dec;54(12):888-949470897
Cites: Environ Health Perspect. 2008 Jun;116(6):832-818560490
Cites: Environ Health Perspect. 2009 Apr;117(4):668-7419440509
Cites: Arch Environ Health. 2001 Mar-Apr;56(2):167-7411339681
Cites: Int Arch Occup Environ Health. 2002 Jun;75(5):348-5311981674
Cites: J Allergy Clin Immunol. 2013 Jan;131(1):87-93.e1-523199600
Cites: Environ Health Perspect. 2005 Apr;113(4):499-50315811822
Cites: Eur Respir J. 2016 Mar;47(3):751-6826846832
Cites: JAMA. 2003 Nov 19;290(19):2546-714625330
Cites: Environ Health Perspect. 2013 Nov-Dec;121(11-12):1357-6424076757
Cites: J Toxicol Environ Health A. 2010;73(4):272-8320077297
Cites: Environ Health Perspect. 2008 Oct;116(10):1423-718941589
Cites: Epidemiology. 2014 Jan;25(1):79-8724213146
Cites: Int J Hyg Environ Health. 2014 Apr-May;217(4-5):483-9124210257
Cites: Int Arch Allergy Immunol. 2003 Jun;131(2):127-3712811021
Cites: Environ Health Perspect. 2012 Mar;120(3):431-622182596
Cites: Environ Health Perspect. 2014 Jan;122(1):107-1324149084
PubMed ID
27338437 View in PubMed
Less detail

Effect of interleukin-1 beta on airway hyperresponsiveness and inflammation in sensitized and nonsensitized Brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature57706
Source
J Allergy Clin Immunol. 1994 Feb;93(2):464-9
Publication Type
Article
Date
Feb-1994
Author
H. Tsukagoshi
T. Sakamoto
W. Xu
P J Barnes
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, Royal Brompton Hospital, London, England.
Source
J Allergy Clin Immunol. 1994 Feb;93(2):464-9
Date
Feb-1994
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Airway Resistance - drug effects - physiology
Animals
Bradykinin - pharmacology
Bronchial Hyperreactivity - etiology - pathology - physiopathology
Bronchoalveolar Lavage Fluid - cytology
Immunization
Inflammation - etiology - physiopathology
Interleukin-1 - pharmacology
Male
Ovalbumin - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Time Factors
Abstract
Airway responsiveness (AR) to inhaled acetylcholine and bradykinin and inflammatory cell recruitment in bronchoalveolar lavage fluid (BALF) were studied in inbred male Brown-Norway rats actively sensitized to ovalbumin and later given 500 U interleukin-1 beta (IL-1 beta) intratracheally. We examined animals 14 to 21 days after initial sensitization at 18 to 24 hours after the intratracheal administration of IL-1 beta. We evaluated AR to acetylcholine as -log PC200, which is -log10 transformation of provocative concentration of acetylcholine producing 200% increase in lung resistance, and to bradykinin as percent increase in lung resistance. BALF was examined as an index of inflammatory changes within the lung. Although there was no significant difference in baseline lung resistance, nonsensitized and sensitized animals that were given IL-1 beta demonstrated a significant increase of AR to bradykinin at 18 to 24 hours and a significant increase of neutrophil counts in BALF, which was already observed by 4 to 6 hours. There was a significant correlation between AR to bradykinin and neutrophil counts in BALF in all animals (r = 0.644; p
PubMed ID
8120273 View in PubMed
Less detail

The gut as a potential trigger of exercise-induced inflammatory responses.

https://arctichealth.org/en/permalink/ahliterature203749
Source
Can J Physiol Pharmacol. 1998 May;76(5):479-84
Publication Type
Article
Date
May-1998
Author
J C Marshall
Author Affiliation
Department of Surgery, University of Toronto, Ontario, Canada. jmarshall@torhosp.toronto.on.ca
Source
Can J Physiol Pharmacol. 1998 May;76(5):479-84
Date
May-1998
Language
English
Publication Type
Article
Keywords
Animals
Cytokines - metabolism
Digestive System - immunology - microbiology
Endotoxins - metabolism
Exercise - physiology
Host-Parasite Interactions
Humans
Inflammation - etiology - physiopathology
Ischemia - etiology - immunology
Liver - immunology
Systemic Inflammatory Response Syndrome - etiology - immunology
Abstract
Multiple lines of evidence support the hypothesis that ischemia-induced impairment of normal gut barrier function, with loss of the normal tonic counterinflammatory influence of the gut immune system, contributes to the expression of uncontrolled inflammation in critically ill victims of trauma and overwhelming infection. The clinical syndrome known as the systemic inflammatory response syndrome (SIRS), which embodies uncontrolled inflammation in trauma and sepsis, is reproduced in its entirety by vigourous exercise, raising the possibility that the gut may also play a role in exercise-induced inflammation. Both strenuous exercise and systemic sepsis result in impairment of the normal gut barrier to luminal microorganisms, and result in elevated circulating levels of bacterial endotoxin. Under normal circumstances, the immune tissues of the gut-liver axis inhibit the expression of a host response to foodstuffs in the gut lumen, or to the indigenous microbial flora of the gut wall. This influence is an active, energy-requiring process. Both strenuous exercise and critical illness are associated with gut ischemia, providing a common biologic basis for the initiation of a dysregulated inflammatory response. Although direct evidence supporting or refuting the hypothesis that the gut can serve as a trigger for systemic inflammation following strenuous exercise is sparse, the similarities in the clinical manifestations of SIRS and exercise, and the promising results of prophylactic or therapeutic gut-directed strategies in critical illness, suggest that similar approaches may provide benefit for individuals engaged in extreme physical exercise.
PubMed ID
9839072 View in PubMed
Less detail