TY - JOUR
T1 - Acute respiratory response to prolonged, moderate levels of sidestream tobacco smoke
AU - Willes, Stuart R.
AU - Fitzgerald, Thomas K.
AU - Permutt, Thomas
AU - Proud, David
AU - Haley, Nancy J.
AU - Bascom, Rebecca
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1998/2
Y1 - 1998/2
N2 - Environmental tobacco smoke (ETS) is a significant component of indoor air pollution yet the acute upper respiratory response has not been well studied. The goal of this study was to determine the response of healthy subjects to moderate levels of sidestream tobacco smoke (SS). Twenty-three subjects were challenged on 2 separate days to clean air or SS (2 h, 15 ppm carbon monoxide, at rest). Subjects completed symptom questionnaires, posterior rhinomanometry, and body plethysmography. Average total and differential cell counts and albumin concentration were determined on nasal lavage samples. The urinary cotinine: creatinine ratio was used as a biomarker of exposure. Following SS exposure, irritant and rhinitis symptoms increased, nasal resistance rose from 4.9 ± 0.4 to 6.3 ± 0.6 cm H2O/L/s and specific airway conductance decreased from 0.14 ± 0.01 to 0.13 ± 0.01 cm H2O−1 s−1. Total cell counts, neutrophils, and albumin were unchanged. An increased nasal congestive response did not correlate with an increased cotinine : creatinine ratio. A history of ETS rhinitis did not predict an increased group response to smoke, but individuals with the largest physiologic and inflammatory response were historically ETS sensitive. In summary, healthy normal subjects demonstrate nasal congestion with exposure to moderate levels of SS without evidence of increased nasal vascular permeability.
AB - Environmental tobacco smoke (ETS) is a significant component of indoor air pollution yet the acute upper respiratory response has not been well studied. The goal of this study was to determine the response of healthy subjects to moderate levels of sidestream tobacco smoke (SS). Twenty-three subjects were challenged on 2 separate days to clean air or SS (2 h, 15 ppm carbon monoxide, at rest). Subjects completed symptom questionnaires, posterior rhinomanometry, and body plethysmography. Average total and differential cell counts and albumin concentration were determined on nasal lavage samples. The urinary cotinine: creatinine ratio was used as a biomarker of exposure. Following SS exposure, irritant and rhinitis symptoms increased, nasal resistance rose from 4.9 ± 0.4 to 6.3 ± 0.6 cm H2O/L/s and specific airway conductance decreased from 0.14 ± 0.01 to 0.13 ± 0.01 cm H2O−1 s−1. Total cell counts, neutrophils, and albumin were unchanged. An increased nasal congestive response did not correlate with an increased cotinine : creatinine ratio. A history of ETS rhinitis did not predict an increased group response to smoke, but individuals with the largest physiologic and inflammatory response were historically ETS sensitive. In summary, healthy normal subjects demonstrate nasal congestion with exposure to moderate levels of SS without evidence of increased nasal vascular permeability.
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U2 - 10.1080/009841098159330
DO - 10.1080/009841098159330
M3 - Article
C2 - 9482351
AN - SCOPUS:0032488792
SN - 1528-7394
VL - 53
SP - 193
EP - 209
JO - Journal of Toxicology and Environmental Health - Part A
JF - Journal of Toxicology and Environmental Health - Part A
IS - 3
ER -