1,721,020 research outputs found
The effect of pre-exercise diesel exhaust exposure on cycling performance and cardio-respiratory variables
No full textPurpose: To determine the effect of pre-exercise exposure to diesel exhaust (DE) on 20-km cycling performance, pulmonary function, and cardio-respiratory variables during exercise.
Methods: Eight endurance-trained males participated in the study. Test days consisted of a 60-min exposure to either filtered air (FA) or DE, followed by a 20 km cycling time trial. Exposures to DE were at a concentration of 300 µg/m3 of PM2.5. Forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) were measured before and after exposure, and after exercise. Oxygen consumption (VO2) and carbon dioxide production (VCO2), minute ventilation (VE), tidal volume (VT), breathing frequency (FB), heart rate and oxyhemoglobin saturation (SpO2), were collected during the time trials. The effect of condition on time trial duration, an order effect, and mean cardio-respiratory variables were each analysed using paired T-tests. Repeated-measures ANOVA were used to assess the effect of DE exposure on pulmonary function.
Results: There was a main effect of condition (FA vs. DE) on the change in FEV1 from baseline, and in exercise heart rate. Post hoc tests revealed that exercise-induced bronchodilation was significantly attenuated following DE compared to FA. There were no main effects of condition on 20 km cycling performance, or VO2, VCO2, VE, VT, FB and SpO2 during a 20 km time trial.
Conclusion: A 60-min exposure to DE prior to exercise significantly attenuated exercise-induced bronchodilation and significantly increased heart rate during exercise. Pre-exercise exposure to diesel exhaust did not significantly impair 20 km cycling time trial performance.Peer reviewedFinal article publishedAir pollutionpulmonary functionparticulate matterheart rateexercise performanc
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
The pulmonary and autonomic effects of high-intensity and low-intensity exercise in diesel exhaust
Full text linkBackground
Exposure to air pollution impairs aspects of pulmonary and autonomic function and causes pulmonary inflammation. However, how exercising in air pollution affects these indices is poorly understood. Therefore, the purpose of this study was to determine the effects of low-intensity and high-intensity cycling with diesel exhaust (DE) exposure on pulmonary function, heart rate variability (HRV), fraction of exhaled nitric oxide (FeNO), norepinephrine and symptoms.
Methods
Eighteen males performed 30-min trials of low-intensity or high-intensity cycling (30 and 60% of power at VO2peak) or a resting control condition. For each subject, each trial was performed once breathing filtered air (FA) and once breathing DE (300μg/m3 of PM2.5, six trials in total). Pulmonary function, FeNO, HRV, norepinephrine and symptoms were measured prior to, immediately post, 1 h and 2 h post-exposure. Data were analyzed using repeated-measures ANOVA.
Results
Throat and chest symptoms were significantly greater immediately following DE exposure than following FA (p < 0.05). FeNO significantly increased 1 h following high-intensity exercise in DE (21.9 (2.4) vs. 19.3 (2.2) ppb) and FA (22.7 (1.7) vs. 19.9 (1.4)); however, there were no differences between the exposure conditions. All HRV indices significantly decreased following high-intensity exercise (p < 0.05) in DE and FA. The exception to this pattern was LF (nu) and LF/HF ratio, which significantly increased following high-intensity exercise (p < 0.05). Plasma norepinephrine (NE) significantly increased following high-intensity exercise in DE and FA, and this increase was greater than following rest and low-intensity exercise (p < 0.05). DE exposure did not modify any effects of exercise intensity on HRV or norepinephrine.
Conclusions
Healthy individuals may not experience greater acute pulmonary and autonomic effects from exercising in DE compared to FA; therefore, it is unclear if such individuals will benefit from reducing vigorous activity on days with high concentrations on particulate matter.Peer reviewedPulmonary functionFeNOAir pollutionNorepinephrineExercise intensit
Concentration-dependent effects of diesel exhaust exposure on the human proteome and airways : a double-blinded, crossover study
No full textAir pollution, to which diesel exhaust (DE) is a salient contributor in urban and occupational environments, is a leading contributor to premature mortality and morbidity worldwide. Concentration-responses (C-Rs) are a useful way to assess the magnitude and impact of air pollution exposure using external exposure surrogates and internal response markers. However, concentration-dependent health effects, which are potential markers of the response to DE exposure, are relatively unexplored in controlled human exposures where environmental confounders are limited. To investigate the C-R for DE across a broad range of exposure levels, we conducted a double-blinded crossover controlled human exposure study. Healthy non-smokers aged 19 – 49 were exposed to filtered air (FA) and DE standardized to 20, 50, and 150 µg/m³ PM₂.₅ in randomized order for 4h at the Air Pollution Exposure Laboratory. Before and up to 24h post-exposure, we measured lung function and airway responsiveness to methacholine using spirometry, airway inflammation using fractional exhaled nitric oxide (FeNO) and nasal epithelial lining fluid, symptoms using visual analog score questionnaires, and circulating proteins in blood using proteomics and immunoassays. Linear mixed effects models, repeated measures correlations and sparse partial least squares discriminant analyses were applied for statistical analysis. We identified concentration-dependent alterations in the proteome, which were enriched in complement activation and regulation pathways. Complement factor I was confirmed as significantly decreased by DE, with a potential threshold between 50-150 µg/m³ PM₂.₅. Complement factor I was correlated with changes in airway responsiveness, lung function and nasal cytokines. Although DE had no significant effect on lung function and airway responsiveness, it induced a concentration-dependent increase in FeNO, with a potential threshold between 50-150 µg/m³ PM₂.₅. DE induced a significant increase in symptoms, driven by eye and constitutional symptoms, with a potential threshold below 150 µg/m³ PM₂.₅. Symptoms were correlated with airway inflammation. Taken together, these findings are consistent with concentration-dependent inflammation in the airways and blood that is associated with clinically relevant endpoints, with potential effects thresholds as low as 50 µg/m³ PM₂.₅. My research corroborates known mechanisms of air pollution effects, while advancing novel concentration-dependent endpoints that may be useful markers for biomonitoring.Medicine, Faculty ofMedicine, Department ofGraduat
Investigation of air pollution interventions in airway epithelial cells
No full textAir pollution is a pervasive and global problem, with 99% of the world’s population living in areas that exceed the World Health Organization exposure guidelines. Although public policies and legislation continue to lower anthropomorphic emissions, and engineering solutions such as air purifiers work to limit personal exposures, few therapeutic strategies exist to limit the cellular effects of air pollution. To address this issue, I evaluated multiple approaches to counteracting air pollution-induced oxidative stress and inflammation using several in vitro models of particulate matter (PM) exposure on human lung epithelial cells. Using immortalized and primary human epithelial cells exposed to PM, I showed that two antioxidants, tetrahydrocurcumin and quercetin, significantly attenuated cellular reactive oxygen species (ROS) and inflammatory mediator release. Next, I examined the utility of modulating lung epithelial cell responses to PM by priming them with omega-3 fatty acids, precursors of specialised pro-resolving mediators. I demonstrated that docosahexaenoic acid significantly decreased PM-induced pro-inflammatory mediator release and cellular ROS. Finally, I noted that suppressing inflammation in the lungs has been associated with increased susceptibility to viral infections, an association also observed with air pollution exposures. Thus, I investigated the effect of exposing human epithelial cells to air pollution, as well as their treatment with a corticosteroid, a common medication used to control inflammation, on rhinovirus infectivity. I demonstrated that pre-exposure of epithelial cells to the corticosteroid fluticasone propionate and PM synergistically increased rhinovirus levels, suppressed host defence responses, and increased levels of the rhinovirus entry receptor. In summary, this thesis’ investigation of air pollution interventions and possible consequences both provides novel therapeutic options and identifies a potential risk, evidence that collectively may inform comprehensive strategies to mitigate the risk associated with air pollution exposure.Medicine, Faculty ofMedicine, Department ofGraduat
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
The effect of low and high-intensity cycling in diesel exhaust on flow-mediated dilation, circulating NOx, endothelin-1 and blood pressure
Full text linkINTRODUCTION:
Exposure to air pollution impairs aspects of endothelial function such as flow-mediated dilation (FMD). Outdoor exercisers are frequently exposed to air pollution, but how exercising in air pollution affects endothelial function and how these effects are modified by exercise intensity are poorly understood.
OBJECTIVES:
Therefore, the purpose of this study was to determine the effects of low-intensity and high-intensity cycling with diesel exhaust (DE) exposure on FMD, blood pressure, plasma nitrite and nitrate (NOx) and endothelin-1.
METHODS:
Eighteen males performed 30-minute trials of low or high-intensity cycling (30% and 60% of power at VO2peak) or a resting control condition. For each subject, each trial was performed once while breathing filtered air (FA) and once while breathing DE (300ug/m3 of PM2.5, six trials in total). Preceding exposure, immediately post-exposure, 1 hour and 2 hours post-exposure, FMD, blood pressure and plasma endothelin-1 and NOx concentrations were measured. Data were analyzed using repeated-measures ANOVA and linear mixed model.
RESULTS:
Following exercise in DE, plasma NOx significantly increased and was significantly greater than FA (p<0.05). Two hours following DE exposure, endothelin-1 was significantly less than FA (p = 0.037) but exercise intensity did not modify this response. DE exposure did not affect FMD or blood pressure.
CONCLUSION:
Our results suggest that exercising in DE did not adversely affect plasma NOX, endothelin-1, FMD and blood pressure. Therefore, recommendations for healthy individuals to moderate or avoid exercise during bouts of high pollution appear to have no acute protective effect.Peer reviewedFinal article published
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