Abstract
BackgroundOzone concentrations in ambient air are related to cardiopulmonary perturbations in the aging population. Increased central sympathetic nerve activity induced by local airway inflammation may be one possible mechanism.Methodology/Principal FindingsTo elucidate this issue further, we performed a randomized, double-blind, cross-over study, including 14 healthy subjects (3 females, age 22–47 years), who underwent a 3 h exposure with intermittent exercise to either ozone (250 ppb) or clean air. Induced sputum was collected 3 h after exposure. Nineteen to 22 hours after exposure, we recorded ECG, finger blood pressure, brachial blood pressure, respiration, cardiac output, and muscle sympathetic nerve activity (MSNA) at rest, during deep breathing, maximum-inspiratory breath hold, and a Valsalva maneuver. While the ozone exposure induced the expected airway inflammation, as indicated by a significant increase in sputum neutrophils, we did not detect a significant estimated treatment effect adjusted for period on cardiovascular measurements. Resting heart rate (clean air: 59±2, ozone 60±2 bpm), blood pressure (clean air: 121±3/71±2 mmHg; ozone: 121±2/71±2 mmHg), cardiac output (clean air: 7.42±0.29 mmHg; ozone: 7.98±0.60 l/min), and plasma norepinephrine levels (clean air: 213±21 pg/ml; ozone: 202±16 pg/ml), were similar on both study days. No difference of resting MSNA was observed between ozone and air exposure (air: 23±2, ozone: 23±2 bursts/min). Maximum MSNA obtained at the end of apnea (air: 44±4, ozone: 48±4 bursts/min) and during the phase II of the Valsalva maneuver (air: 64±5, ozone: 57±6 bursts/min) was similar.Conclusions/SignificanceOur study suggests that acute ozone-induced airway inflammation does not increase resting sympathetic nerve traffic in healthy subjects, an observation that is relevant for environmental health. However, we can not exclude that chronic airway inflammation may contribute to sympathetic activation.
Highlights
Based on large epidemiological studies, the World Health Organization estimated that air pollution is the 13th leading cause of mortality worldwide.[1]
We challenged healthy volunteers with ozone in a double blind, randomized, and crossover fashion to test the hypothesis that neutrophilic airway inflammation induced by acute ozone exposure is accompanied by increased muscle sympathetic nerve activity
6 hours after the start of challenge (n = 14) was increased after ozone compared to clean air (estimated treatment effect adjusted for period: 16%, 95% CI: 4.06% to 28.22%, p,0.05), indicating the presence of neutrophilic airway inflammation
Summary
Based on large epidemiological studies, the World Health Organization estimated that air pollution is the 13th leading cause of mortality worldwide.[1] A large proportion of the excess mortality can be attributed to cardiovascular deaths.[2] Long term exposure to fine particles and to ozone were associated with an increased cardiopulmonary mortality.[3] Short term exposure to air pollutants is sufficient to elicit changes in cardiovascular and pulmonary function in healthy subjects[4] and in patients[5]. A similar mechanism could contribute to sympathetic activation in patients with chronic obstructive pulmonary disease[16] or asthma.[17] We challenged healthy volunteers with ozone in a double blind, randomized, and crossover fashion to test the hypothesis that neutrophilic airway inflammation induced by acute ozone exposure is accompanied by increased muscle sympathetic nerve activity. Increased central sympathetic nerve activity induced by local airway inflammation may be one possible mechanism
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