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.