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Diesel Exhaust Exposure Increases Muscle Sympathetic Nerve Activity - A Human Exposure Study
Description
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A6197 - Diesel Exhaust Exposure Increases Muscle Sympathetic Nerve Activity - A Human Exposure Study
Author Block: G. Rankin1, M. Kabele1, T. Sandstrom1, R. Brown2, V. G. Macefield2, J. A. Bosson1; 1Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden, 2School of Medicine, Western Sydney University, Sydney, Australia.
Rationale
Air pollution, in particular particulate matter (PM), is a global environmental problem and public health concern, with diesel exhaust emissions being a major contributor. Air pollution has been increasingly linked to pulmonary and cardiovascular morbidity and mortality. The WHO now attributes approximately 70-80 % of the seven million premature deaths caused by air pollution to stroke and heart disease. Short-term exposure to low-level increases in PM has been associated with increased risk of myocardial infarction. It has been previously shown that even in healthy individuals, diesel exhaust exposure causes endothelial dysfunction, increased thrombogenicity and decreased heart rate variability.
Due to the rapid onset of cardiovascular events post-exposure to air pollution, we hypothesize that autonomic control of the heart and cardiovascular system may be altered and a contributing mechanism to cardiovascular events in at risk groups. Microneurography is a powerful research tool that can be used to record efferent activity from unmyelinated C-fibers, allowing for the assessment of sympathetic outflow. We hypothesize that muscle sympathetic nerve activity (MSNA) will increase after diesel exhaust exposure.
Methods
We measured MSNA from a muscle fascicle of the common peroneal nerve of 16 healthy male volunteers exposed to diluted diesel exhaust (idling engine, ~300µg/m3), via a modified CPAP mask.
Spontaneous MSNA was recorded for 1 hour. Two 10-minute baseline measurements were conducted; breathing filtered air (baseline) and breathing filtered air with the exposure mask on (mask baseline). Filtered air was then switched to diesel exhaust and subjects were exposed for 40 minutes. The median 5-minutes for every 10 minutes of recording was analyzed and MSNA expressed as burst incidence (bursts/100 heart beats), burst frequency (bursts/min) and normalized burst amplitude (size of burst normalized to largest recorded burst within analyzed recordings).
Results
Statistically significant increases in MSNA burst frequency and incidence were seen within 10 minutes of diesel exhaust exposure and gradually increased as exposure continued, reaching a peak after a 30-minute exposure. Burst amplitude also increased after exposure. There was no significant difference between MSNA outcomes between baseline and mask baseline.
Conclusions
This study indicates that inhalation of diesel exhaust quickly triggers the autonomic nervous system, with a shift to increase sympathetic outflow. This provides a possible mechanism to explain the strong epidemiological evidence linking acute cardiovascular events following exposure to combustion-derived air pollutants.
Author Block: G. Rankin1, M. Kabele1, T. Sandstrom1, R. Brown2, V. G. Macefield2, J. A. Bosson1; 1Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden, 2School of Medicine, Western Sydney University, Sydney, Australia.
Rationale
Air pollution, in particular particulate matter (PM), is a global environmental problem and public health concern, with diesel exhaust emissions being a major contributor. Air pollution has been increasingly linked to pulmonary and cardiovascular morbidity and mortality. The WHO now attributes approximately 70-80 % of the seven million premature deaths caused by air pollution to stroke and heart disease. Short-term exposure to low-level increases in PM has been associated with increased risk of myocardial infarction. It has been previously shown that even in healthy individuals, diesel exhaust exposure causes endothelial dysfunction, increased thrombogenicity and decreased heart rate variability.
Due to the rapid onset of cardiovascular events post-exposure to air pollution, we hypothesize that autonomic control of the heart and cardiovascular system may be altered and a contributing mechanism to cardiovascular events in at risk groups. Microneurography is a powerful research tool that can be used to record efferent activity from unmyelinated C-fibers, allowing for the assessment of sympathetic outflow. We hypothesize that muscle sympathetic nerve activity (MSNA) will increase after diesel exhaust exposure.
Methods
We measured MSNA from a muscle fascicle of the common peroneal nerve of 16 healthy male volunteers exposed to diluted diesel exhaust (idling engine, ~300µg/m3), via a modified CPAP mask.
Spontaneous MSNA was recorded for 1 hour. Two 10-minute baseline measurements were conducted; breathing filtered air (baseline) and breathing filtered air with the exposure mask on (mask baseline). Filtered air was then switched to diesel exhaust and subjects were exposed for 40 minutes. The median 5-minutes for every 10 minutes of recording was analyzed and MSNA expressed as burst incidence (bursts/100 heart beats), burst frequency (bursts/min) and normalized burst amplitude (size of burst normalized to largest recorded burst within analyzed recordings).
Results
Statistically significant increases in MSNA burst frequency and incidence were seen within 10 minutes of diesel exhaust exposure and gradually increased as exposure continued, reaching a peak after a 30-minute exposure. Burst amplitude also increased after exposure. There was no significant difference between MSNA outcomes between baseline and mask baseline.
Conclusions
This study indicates that inhalation of diesel exhaust quickly triggers the autonomic nervous system, with a shift to increase sympathetic outflow. This provides a possible mechanism to explain the strong epidemiological evidence linking acute cardiovascular events following exposure to combustion-derived air pollutants.
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