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.
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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
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.