Development of airway reactivity to nitrates in subjects with influenza

Although epidemiologic studies have found a correlation between increased symptoms in asthmatics and increased concentrations of atmospheric nitrates, acute short-term exposure to nitrates does not alter airway function in normal subjects or asymptomatic asthmatics. To examine the potential synergy between acute exposure to pollutant and acute respiratory infections, we studied the effects on the airways of acute exposure to nitrate during uncomplicated influenza A (H ₁N ₁) infections in 11 previously healthy adults. Subjects were studied at the time of acute illness and 1, 3, and 6 wk thereafter. By double blind randomization, each subject breathed an aerosol of either sodium chloride or sodium nitrate for an initial 16-min period and then breathed the other aerosol for 16 min 3 h later. The mass median aerodynamic diameter of the NaNO ₃ aerosol was 0.49 μm; the concentration, 7,000 μg/m ³. Deposition studies showed a mean retention of 45 to 50% for both inhaled aerosols. Compared to inhalation of sodium chloride, at initial examination and 1 wk later, exposure to sodium nitrate produced significant decreases in specific airway conductance (p<0.005) and partial expiratory flows at 40% of total lung capacity (p<0.05). By 3 wk, inhalation of sodium nitrate no longer produced changes in airway function. Unlike normal or asymptomatic asthmatic subjects, subjects with acute respiratory disease have airway constriction after acute exposure to nitrate. Because no significant constriction developed with exposure to sodium chloride at these times, the constriction is a specific effect of the sodium nitrate rather than a nonspecific response to the particles. Therefore, subjects with acute respiratory disease are susceptible to bronchoconstriction from specific air pollutants that normally do not influence airway function.