TY - JOUR
T1 - Effect of ozone on bronchial reactivity in atopic and nonatopic subjects
AU - Holtzman, M. J.
AU - Cunningham, J. H.
AU - Sheller, J. R.
AU - Irsigler, G. B.
AU - Nadel, J. A.
AU - Boushey, H. A.
PY - 1979/12/1
Y1 - 1979/12/1
N2 - We studied the effect of exposure to ozone (0.6 ppm, 2 h) on bronchial reactivity in 16 otherwise healthy, nonsmoking subjects with normal pulmonary function. On the basis of medical history and allergen skin testing, 7 subjects were classified as nonatopic; 9, as atopic. Bronchial reactivity was assessed by measuring the increase in specific airway resistance (SRaw) produced by inhaling histamine or methacholine aerosol before and after sham exposure and after ozone exposure. Non-atopic subjects inhaled 10 breaths of histamine (16 mg/ml solution) and of methacholine (10 mg/ml solution); atopic subjects inhaled 10 breaths of histamine 98 mg/ml solution). In neither group of subjects was the response to histamine affected by sham exposure (p > 0.5). In the nonatopic subjects, the increase in SRaw produced by histamine (6.57 ± 1.43 cm H 2O/L/s x L, mean ± SEM) an by methacholine (8.94 ± 2.12 cm H 2O/L/s x L) after ozone exposure were significantly greater than after sham exposure (3.42 ± 0.64 and 3.62 ± 0.61 cm H 2O/L/s x L, respectively; p < 0.02). In the atopic subjects, the increase in SRaw produced by histamine after exposure to ozone (10.44 ± 3.32 cm H 2O/L/s x L) was also significantly greater than after sham exposure (4.02 ± 1.12 cm H 2O/L/s x L; p < 0.05). In each group, the increase in bronchial response to histamine or methacholine occurred at a time when baseline SRaw was not changed significantly by ozone exposure, and in each group, the increase in bronchial responses returned to control values by the following day. In both groups, premedication with atropine sulfate aerosol (0.1 mg/kg of body weight) decreased baseline SRaw and prevented the increase in bronchial response to histamine that occurred after ozone exposure. We conclude that brief exposure to 0.6 ppm of ozone increases bronchial reactivity via cholinergic, postganglionic pathways, and that inducibility of bronchial hyperreactivity by exposure to ozone is not related to atopy.
AB - We studied the effect of exposure to ozone (0.6 ppm, 2 h) on bronchial reactivity in 16 otherwise healthy, nonsmoking subjects with normal pulmonary function. On the basis of medical history and allergen skin testing, 7 subjects were classified as nonatopic; 9, as atopic. Bronchial reactivity was assessed by measuring the increase in specific airway resistance (SRaw) produced by inhaling histamine or methacholine aerosol before and after sham exposure and after ozone exposure. Non-atopic subjects inhaled 10 breaths of histamine (16 mg/ml solution) and of methacholine (10 mg/ml solution); atopic subjects inhaled 10 breaths of histamine 98 mg/ml solution). In neither group of subjects was the response to histamine affected by sham exposure (p > 0.5). In the nonatopic subjects, the increase in SRaw produced by histamine (6.57 ± 1.43 cm H 2O/L/s x L, mean ± SEM) an by methacholine (8.94 ± 2.12 cm H 2O/L/s x L) after ozone exposure were significantly greater than after sham exposure (3.42 ± 0.64 and 3.62 ± 0.61 cm H 2O/L/s x L, respectively; p < 0.02). In the atopic subjects, the increase in SRaw produced by histamine after exposure to ozone (10.44 ± 3.32 cm H 2O/L/s x L) was also significantly greater than after sham exposure (4.02 ± 1.12 cm H 2O/L/s x L; p < 0.05). In each group, the increase in bronchial response to histamine or methacholine occurred at a time when baseline SRaw was not changed significantly by ozone exposure, and in each group, the increase in bronchial responses returned to control values by the following day. In both groups, premedication with atropine sulfate aerosol (0.1 mg/kg of body weight) decreased baseline SRaw and prevented the increase in bronchial response to histamine that occurred after ozone exposure. We conclude that brief exposure to 0.6 ppm of ozone increases bronchial reactivity via cholinergic, postganglionic pathways, and that inducibility of bronchial hyperreactivity by exposure to ozone is not related to atopy.
UR - http://www.scopus.com/inward/record.url?scp=0018689985&partnerID=8YFLogxK
M3 - Article
C2 - 507522
AN - SCOPUS:0018689985
SN - 0003-0805
VL - 120
SP - 1059
EP - 1067
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 5
ER -