Brauer, Michael

The cardiovascular, respiratory, systemic, and autonomic responses to exercise in diesel exhaust

Digital Document

Purpose: To determine the cardiovascular, respiratory, systemic inflammatory, and autonomic nervous system responses to varying exercise intensities during exposure to diesel exhaust (DE), and to determine how DE exposure before exercise affects the cardio-respiratory system and subsequent exercise performance. Methods: Eighteen males performed six 30-minute trials, which included rest, low-intensity, and high-intensity cycling. Each trial was performed twice, once breathing filtered air (FA) and once breathing DE (300ug/m³ of PM₂.₅) with seven days between trials. Before, and following exercise, exhaled nitric oxide, pulmonary function, heart rate variability, flow-mediated dilation (FMD), complete blood count, endothelin-¹ , and plasma nitrite/nitrate (NOx) were measured. During exercise, minute ventilation (VE), oxygen consumption (VO₂), CO₂ production (VCO₂), respiratory exchange ratio (RER), and rating of perceived exertion (RPE) for lungs and legs were measured. In a second experiment, eight males were exposed to DE (300ug/m³ of PM₂.₅) or FA for 60-minutes, followed by an indoor 20-km cycling time trial. Pulmonary function was assessed before and after exposure and after exercise. Heart rate was measured during exposure and exercise performance was measured as mean power output during exercise. Results: In the first experiment, RER was significantly lower (0.94 vs. 0.96), and RPE significantly greater, in DE compared to FA (p<0.05). During low-intensity exercise, VE (44.5 vs. 40.5 L•min-¹ ), VO₂ (27.9 vs. 24.9 ml*kg*min-¹) and VCO₂ (25.9 vs. 23.6 ml*kg*min-¹) were significantly greater during DE (p<0.05). Following exercise in DE, plasma NOx significantly increased (p<0.05). On low-intensity exercise days, FMD/shear rate area under the curve (SRAUC) was significantly lower in DE compared to FA (9.7 x 10-⁵ vs. 11.7x10-⁵; p<0.05). In the second experiment, we found that pre-exercise exposure to DE did not impair exercise performance but attenuated exercise-induced bronchodilation and increased exercise heart rate (163.9 vs. 157.3bpm; p<0.05). Conclusion: Metabolic and endothelial responses to low- but not high-intensity cycling in DE differ from those in FA. Therefore, reducing exercise intensity during bouts of air pollution may have no benefit. Exposure to DE prior to exercise increased exercise heart rate and decreased exercise-induced bronchodilation. Consequently, encouraging individuals to minimize exposure to air pollution prior to exercise could be beneficial.

Background: Associations between air pollution and a multitude of health effects are now well established. Given ubiquitous exposure to some level of air pollution, the attributable health burden can be high, particularly for susceptible populations. oBjectives: An international multidisciplinary workshop was convened to discuss evidence of the effectiveness of actions to reduce health impacts of air pollution at both the community and indi- vidual level. The overall aim was to summarize current knowledge regarding air pollution exposure and health impacts leading to public health recommendations. discussion: During the workshop, experts reviewed the biological mechanisms of action of air pollu- tion in the initiation and progression of disease, as well as the state of the science regarding community and individual-level interventions. The workshop highlighted strategies to reduce individual baseline risk of conditions associated with increased susceptibility to the effects of air pollution and the need to better understand the role of exposure duration in disease progression, reversal, and adaptation. conclusion: We have identified two promising and largely unexplored strategies to address and mitigate air pollution–related health impacts: reducing individual baseline risk of cardiovascular disease and incorporating air pollution–related health impacts into land-use decisions.

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