Journal of Applied Physiology, Vol 46, Issue 1 189-196, Copyright © 1979 by American Physiological Society
Airway reactivity to nitrates in normal and mild asthmatic subjects
M. J. Utell, A. J. Swinburne, R. W. Hyde, D. M. Speers, F. R. Gibb and P. E. Morrow
Epidemiologic studies have reported increased symptoms in young asthmatics
when atmospheric pollutants containing nitrates and sulfates are elevated.
To determine if inorganic nitrate pollutants cause increased airway
reactivity in humans, 10 normal volunteers and 11 mild asthmatics inhaled a
sodium nitrate (NaNO3) aerosol with an aerodynamic diameter of 0.46 micron
at a concentration of 7,000 microgram/m3, a level 100--1,000 times greater
than reported urban levels for nitrates. A sodium chloride (NaCl) aerosol
of similar characteristics served as a control. By double-blind
randomization, each subject breathed NaCl or NaNO3 for a 16-min period and
again 2--4 h later. Deposition studies showed 32--78% retention of the
inhaled aerosol. Functional residual capacity, airway resistance, forced
vital capacity, 1-s forced expiratory volume, and maximum and partial
expiratory flow rates at 60 and 40% of total lung capacity did not
significantly change during or after exposure. All subjects remained
asymptomatic. To establish if aerosol exposure increased reactivity to a
known bronchoconstrictor, subjects inhaled 0.025--1.0% carbachol following
the 16-min exposure. Although prior inhalation of NaNO3 or NaCl aerosols
did not significantly alter the effect of carbachol on pulmonary function,
two asthmatics demonstrated mild potentiation of the carbachol
bronchoconstrictor response after nitrate exposure. These results suggest
that in normal subjects and mild asthmatics short-term NaNO3 exposure does
not alter pulmonary function.
