title: Effect of acute ozone induced airway inflammation on human sympathetic nerve traffic: a randomized, placebo controlled, crossover study.
abstract: BACKGROUND
  Ozone 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.
  
  
  RESULTS
  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
  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.
authors.affiliation: Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany. tank.jens@mh-hannover.de
authors.forename: Jens
authors.initials: J
authors.lastname: Tank
authors.forename: Heike
authors.initials: H
authors.lastname: Biller
authors.forename: Karsten
authors.initials: K
authors.lastname: Heusser
authors.forename: Olaf
authors.initials: O
authors.lastname: Holz
authors.forename: André
authors.initials: A
authors.lastname: Diedrich
authors.forename: Theodor
authors.initials: T
authors.lastname: Framke
authors.forename: Armin
authors.initials: A
authors.lastname: Koch
authors.forename: Anika
authors.initials: A
authors.lastname: Grosshennig
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Koch
authors.forename: Norbert
authors.initials: N
authors.lastname: Krug
authors.forename: Jens
authors.initials: J
authors.lastname: Jordan
authors.forename: Jens M
authors.initials: JM
authors.lastname: Hohlfeld
mesh_terms: D000328:Adult; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002452:Cell Count; D015331:Cohort Studies; D018592:Cross-Over Studies; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D019570:Inhalation Exposure; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000294:innervation; D010126:Ozone / Q000008:administration & dosage / Q000494:pharmacology*; D010919:Placebos; D011014:Pneumonia / Q000139:chemically induced* / Q000503:physiopathology; D013183:Sputum / Q000166:cytology; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D055815:Young Adult
chemical_list: D010919:Placebos; D010126:Ozone