Acute Exposure to Diesel Exhaust Increases Muscle Sympathetic Nerve Activity in Humans

Abstract

Background Diesel exhaust (DE) emissions are a major contributor to ambient air pollution and are strongly associated with cardiovascular morbidity and mortality. Exposure to traffic‐related particulate matter is linked with acute adverse cardiovascular events; however, the mechanisms are not fully understood. We examined the role of the autonomic nervous system during exposure to DE that has previously only been indirectly investigated. Methods and Results Using microneurography, we measured muscle sympathetic nerve activity (MSNA) directly in the peroneal nerve of 16 healthy individuals. MSNA, heart rate, and respiration were recorded while subjects rested breathing filtered air, filtered air with an exposure mask, and standardized diluted DE (300 µg/m 3 ) through the exposure mask. Heart rate variability was assessed from an ECG. DE inhalation rapidly causes an increase in number of MSNA bursts as well as the size of bursts within 10 minutes, peaking by 30 minutes ( P <0.001), compared with baseline filtered air with an exposure mask. No significant changes occurred in heart rate variability indices during DE exposure; however, MSNA frequency correlated negatively with total power ( r 2 =0.294, P =0.03) and low frequency ( r 2 =0.258, P =0.045). Heart rate correlated positively with MSNA frequency ( r 2 =0.268, P =0.04) and the change in percentage of larger bursts (burst amplitude, height >50% of the maximum burst) from filtered air with an exposure mask ( r 2 =0.368, P =0.013). Conclusions Our study provides direct evidence for the rapid modulation of the autonomic nervous system after exposure to DE, with an increase in MSNA. The quick increase in sympathetic outflow may explain the strong epidemiological data associating traffic‐related particulate matter to acute adverse cardiovascular events such as myocardial infarction. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02892279.

Air pollution and cardiovascular disease: the Paul Wood Lecture, British Cardiovascular Society 2021

“…Indeed, Rankin et al observed that short-term acute exposure to diesel exhaust causes a rapid increase muscle sympathetic nerve activity in healthy volunteers. This provides further support for the hypothesis that sympathetic nervous system modulation underlies some of the cardiovascular effects of air pollution 33…”

Associations between short-term exposure to PM2.5and cardiomyocyte injury in myocardial infarction survivors in North Carolina

“…Despite the evidence that air pollution may cause continual damage to cardiac tissue, only a few studies have used cardiac specific troponins to investigate the damage that air pollution may cause outside of an MI. In a study of patients who underwent a cardiac catheterisation, short-term PM 2.5 exposure was associated with significant increases in troponin T. Similar results for cardiac troponin I have been observed in both an observational study of healthy, young adults12 as well as a controlled exposure study of diesel exhaust particulates 13…”

“…Imbalances within the autonomic nervous system, particularly increased sympathetic activity, can cause myocardial tissue damage 25–27. In a controlled exposure study of healthy volunteers, authors observed that short-term exposure to diesel exhaust directly increased the activity of the sympathetic nervous system 13. Another mechanism may be increased oxidative stress and inflammation which has been proposed as one of the central hallmarks of exposure to environmental pollutants 28.…”

Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution

“…Thus, some studies have emphasized the role of different AR subtypes in mediating pulmonary and cardiovascular effects of air pollutants; however, the cellular mechanisms, and how pollutant exposure results in increased circulating ligands for ARs, are just beginning to emerge. Although the role of sympathetic activation in mediating cardiovascular effects has been established [107,108], and epidemiological studies have shown associations between circulating catecholamines and air pollution [91], the mechanisms of central regulation mediating the release of catecholamines responsible for activating ARs have yet to be demonstrated in ambient PM studies.…”