To 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/SIGNIFICANCE: Our 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.