Effects of brief and intermediate exposures to sulfate submicron aerosols and sulfate injections and cardiopulmonary function of dogs and tracheal mucous velocity of sheep.

Pulmonary mechanics of anesthetized dogs were not changed or were minimally altered by breathing the following compounds as submicron aerosols in concentrations up to 17.3 mg/m3 for 7.5 min: (1) sodium chloride (as a control), (2) sodium sulfate, (3) ammonium sulfate, (4) zinc sulfate, (5) zinc ammonium sulfate, (6) ammonium bisulfate, (7) aluminum sulfate, (8) manganese sulfate, (9) nickel sulfate, (10) copper sulfate, (11) ferrous sulfate, and (12) ferric sulfate. Submicron aerosols of these compounds in concentrations of 4.1-8.8 mg/m3, administered for 4 h to anesthetized dogs, did not affect mechanics of breathing, hemodynamics, and arterial blood gases. In conscious sheep, tracheal mucous velocity was not altered by exposure to the submicron aerosols of the sulfate compounds. None of these compounds, injected iv in a dose of 1 mg, had adverse effects on mechanics of breathing, pulmonary and systemic hemodynamics, or arterial blood gases. In 100-mg injections, zinc sulfate and zinc ammonium sulfate produced a fall in cardiac output, systemic hypotension, hypoxemia, and metabolic acidosis. Copper sulfate at this dose produced pulmonary hypertension, a fall in cardiac output, hypoxemia, respiratory acidosis, and a decrease of specific total respiratory conductance. It is concluded that submicron aerosols of sulfate salts do not have adverse cardiopulmonary effects when administered in high concentrations for up to 4 h. However, prolonged exposure to high concentrations of zinc sulfate, zinc ammonium sulfate, and copper sulfate aerosols should be carefully monitored because of the possibility that lower levels of these compounds in the bloodstream for long time period might have adverse cardiopulmonary effects.

Effects of sulfuric acid aerosol on cardiopulmonary function of dogs, sheep, and humans.

Submicronic aerosol of sulfuric acid (H2SO4) originates from the burning of fossil fuels and discharge of vapor from the automobile engine equipped with the catalytic converter. This study was conducted to determine whether brief exposure to this aerosol in high concentrations adversely affects the cardiopulmonary system. In all studies, submicronic aerosol of sodium chloride was used as a control. Anesthetized dogs that breathed H2SO4 aerosol in concentrations up to 8 mg per m3 showed no effects on respiratory resistance, static lung compliance, and functional residual capacity. A 4-hour exposure to H2SO4 aerosol (4 mg per m3) produced no significant changes in mechanics of breathing, functional residual capacity, pulmonary and systemic arterial blood pressures, cardiac output, heart rate, and arterial blood gas tensions. Conscious sheep that breathed H2SO4 aerosol in concentrations up to 14 mg per m3 for 20 min had no alteration of tracheal mucous velocity in an immediate 3-hour follow-up period or 5 to 10 days later. Conscious sheep that breathed H2SO4 aerosol (4 mg per m3) for 4 hours had no significant alteration of tracheal mucous velocity immediately and 2 hours thereafter. Both normal and asthmatic adults breathing H2SO4 aerosol in concentrations up to 1 mg per m3 for 10 min showed no significant alteration of lung volumes, distribution of ventilation, ear oximetry, dynamic mechanics of breathing, oscillation mechanics of the chest-lung system, pulmonary capillary blood flow, diffusing capacity, O2 consumption, and pulmonary tissue volume. No delayed effects in pulmonary function nor exacerbation of bronchial asthma were observe during a follow-up period of a few weeks. The present study indicates that single exposure to submicronic H2SO4 aerosol does not produce an immediate or a delayed adverse effect on cardiopulmonary function in anesthetized dogs, conscious sheep, and normal and asthmatic adults.