TY - JOUR
TI - Acute pulmonary effects of sidestream secondhand smoke at simulated car concentrations
AU - Vardavas, C.I.
AU - Anagnostopoulos, N.
AU - Kougias, M.
AU - Evangelopoulou, V.
AU - Connolly, G.N.
AU - Behrakis, P.K.
JO - Xenobiotica
PY - 2013
VL - 43
TODO - 6
SP - 509-513
PB - 
SN - 0049-8254, 1366-5928
TODO - 10.3109/00498254.2012.741272
TODO - nitric oxide, acute pulmonary disease;  adult;  airway reactance;  airway resistance;  article;  car;  clinical article;  environmental exposure;  fraction of exhaled nitric oxide;  human;  lung disease;  lung flow volume curve;  oscillometry;  particle size;  passive smoking;  pilot study;  respiratory tract parameters;  spirometry, Adult;  Airway Resistance;  Automobiles;  Humans;  Lung;  Middle Aged;  Respiration;  Tobacco Smoke Pollution;  Vehicle Emissions
TODO - 1. Exposure to secondhand smoke (SHS) can occur in many places; however, regulations banning smoking may reduce the sources of exposure to SHS to personal areas such as the family car, a source of brief but potently intense exposure. 2. Fifteen non-smoking volunteers were exposed to sidestream SHS concentrations of 5000 μg/m3, within a simulated car setting. The Fraction of Exhaled Nitric Oxide (FeNO) was calculated, dynamic flow volumes were assessed through spirometry; while airway impedance (Z), resistance (R), and reactance (X) was assessed through impulse oscillometry before and after exposure. 3. Exposure to sidestream SHS within this experimental condition did not affect dynamic flow volumes, however FENO decreased from 15.34 ppb to 11.15 ppb, (p < 0.001). Increases in airway resistance at R5Hz by 0.114 kPa/(L/s) (p = 0.002), at R10Hz by 0.093[kPa/(L/s)] (p = 0.006) and at R20Hz by 0.093[kPa/(L/s)] (p = 0.008) were noted. Correspondingly overall peripheral and central airway resistance was also found to increase by 40% (by 0.083 kPa/(L/s), p = 0.038) and 25% (by 0.045 kPa/(L/s), p = 0.047) respectively. 4.Brief but elevated exposure to sidestream SHS can alter airway resistance, and impedance indicating a potential additional mechanistic pathway between exposure to SHS and the development of respiratory disease. Further research is needed to verify these pilot results. © 2013 Informa UK, Ltd.
ER -