Inhalation of 0.30 ppm nitrogen dioxide potentiates exercise-induced bronchospasm in asthmatics

Bauer, MA; Utell, MJ; Morrow, PE; Speers, DM; Gibb, FR

HERO ID

35081

Reference Type

Journal Article

Year

1986

Language

English

PMID

3789520

HERO ID 35081
In Press No
Year 1986
Title Inhalation of 0.30 ppm nitrogen dioxide potentiates exercise-induced bronchospasm in asthmatics
Authors Bauer, MA; Utell, MJ; Morrow, PE; Speers, DM; Gibb, FR
Journal American Review of Respiratory Disease
Volume 134
Issue 6
Page Numbers 1203-1208
Abstract Epidemiologic studies support an association among elevated levels of nitrogen dioxide (NO2), increased respiratory symptoms, and alterations in lung function. To determine if low level NO2 inhalation potentiates exercise-induced bronchospasm, 15 asthmatic subjects, defined by airway constriction with cold air provocation, inhaled 0.30 ppm (560 micrograms/m3) NO2 for 30 min. All asthmatics inhaled either air or 0.30 ppm NO2 via a mouthpiece for 20 min at rest followed by 10 min of exercise on a bicycle ergometer at a workload of 300 kpm/min, producing a 3-fold or greater increase in minute ventilation. Our studies showed 72 +/- 2 (SE)% deposition of inhaled NO2 at rest and 87 +/- 1% deposition with exercise (p less than 0.001). Nitrogen dioxide inhalation at rest resulted in no significant change in pulmonary function. Nitrogen dioxide inhalation plus exercise compared to control (air) exposure plus exercise produced significantly greater reductions in FEV (p less than 0.01) and partial expiratory flow rates at 60% of total lung capacity (p less than 0.05). One hour after completion of NO2 exposure and exercise, pulmonary function had returned to baseline values. To determine if NO2 exposure caused increased reactivity to a known bronchoconstrictor, asthmatic subjects inhaled cold air (range: -11 +/- 2 degrees C) at 3 successive rates of isocapnic ventilation. The response to cold air was expressed as the respiratory heat exchange required to reduce the FEV by 10% (PD10RHE). Prior NO2 exposure potentiated the fall in FEV, PD10RHE, and specific airway conductance (p less than 0.05) after isocapnic cold air hyperventilation, compared to the control exposure. These data indicate that 0.30 ppm NO2 inhalation potentiates exercise-induced bronchospasm and airway hyperreactivity after cold air provocation in asthmatic subjects.
Doi 10.1164/arrd.1986.134.6.1203
Pmid 3789520
Wosid WOS:A1986F249800019
Is Certified Translation No
Dupe Override No
Comments ECRIB. 1986a in 082,15, 082,16, 242,02, 242,04 and 242,05.Am. Rev. Respir. Dis. 134: 1203-1208.
Is Public Yes
Language Text English
Is Qa No