Influence of Insoluble Aerosol Deposits on the Surface Activity of the Pulmonary Surfactant: A Possible Mechanism of Alveolar Clearance Retardation?

Pulmonary surfactant is believed to be involved in the alveolar clearance both due to its direct influence on the flow of the liquid alveolar hypophase and due to the stimulating effect on the alveolar macrophages activity. In the present work, interaction between aerosol particles and liquid material containing pulmonary surfactant was investigated in a model physicochemical system. Interfacial activity of the surfactant material used in clinical practice (Infasurf) was evaluated with the Pulsating Bubble Surfactometer (PBS). Dynamic surface properties were compared for the surfactant before and after contact with soot particles (MMAD: 0.3 microns, GSD: 1.56). Concentration of soot in the surfactant suspension was adjusted to 0.2 mg per ml and 1 mg per ml based on the calculations of maximum alveolar deposition for the particles of that size during 6 h inhalation at 2 harmful occupational concentrations: 750 mu g /m³ and 3.7 mg /m³, respectively. The average minimum surface tension measured under dynamic conditions was 3.2 mN /m for control surfactant, while for the surfactant mixed with soot it was equal to 4.5 and 6.8 mN /m for 0.2 mg soot per ml and 1 mg soot per ml, respectively. Other surfactant properties (hysteresis, stability index) determined from the experimental data confirmed surfactant inactivation. Results of the studies indicate that the amount and activity of the surfactant in the suspensions were reduced after contact with soot particles, probably due to adsorption of the surfactant molecules on solid particles characterized by a large interfacial area. Reduction of the activity of the surfactant in the presence of a significant number of airborne insoluble particles (e.g., soot), as suggested by this study, can lead to disturbance of the physiological role of the surfactant, including alveolar clearance. This physicochemical phenomenon can be considered as a contributing factor to alveolar clearance retardation in the overloaded lungs.