Humans commonly exhale aerosols comprised of small droplets of airway-lining fluid during normal breathing. These ''exhaled bioaerosols'' may carry airborne pathogens and thereby magnify the spread of certain infectious diseases, such as influenza, tuberculosis, and severe acute respiratory syndrome. We hypothesize that, by altering lung airway surface properties through an inhaled nontoxic aerosol, we might substantially diminish the number of exhaled bioaerosol droplets and thereby provide a simple means to potentially mitigate the spread of airborne infectious disease independently of the identity of the airborne pathogen or the nature of any specific therapy. We find that some normal human subjects expire many more bioaerosol particles than other individuals during quiet breathing and therefore bear the burden of production of exhaled bioaerosols. Administering nebulized isotonic saline to these ''high-producer'' individuals diminishes the number of exhaled bioaerosol particles expired by 72.10 ؎ 8.19% for up to 6 h. In vitro and in vivo experiments with saline and surfactants suggest that the mechanism of action of the nebulized saline relates to modification of the physical properties of the airway-lining fluid, notably surface tension.drug delivery ͉ lung ͉ infectious disease ͉ influenza I t has long been understood that exhaled bioaerosol particles provide an important vector for the spread of certain infectious diseases (1, 2). Viruses known to spread from humans and͞or animals through breathing, sneezing, and coughing include measles, influenza virus (3, 4), adenovirus (5), African swine fever virus (6), foot and mouth disease virus (7), varicellazoster virus (chicken pox) (8), infectious bronchitis virus (9), and smallpox, among others (10). Airborne bacteria include anthrax, Escherichia coli (11), Klebsiella pneumoniae (12), Francisella tularensis (13), and tuberculosis (14). Normal mouth breathing (more than coughing, nose breathing, or talking) has been observed to produce the largest number of airborne droplets (15,16). These droplets are primarily Ͻ1 m in size, because larger droplets tend to be filtered out of the expired air by the lungs (16). Given the variable dimensions of common viral and bacterial pathogens (Ϸ25 nm to 5 m), the ability of exhaled bioaerosol droplets of a given size to carry pathogen obviously varies with pathogen type. Bioaerosols seem to form by the passage of air, during inhalation and exhalation, over the mucus layer lining the lungs (17) or possibly through the reopening of closed small airways, destabilizing the mucus surface through an interplay of surface tension and viscous forces to form small airborne droplets, as has been simulated in vitro via ''cough machine '' experiments (18). In this study, we aimed to explore the ability to transiently diminish the number of exhaled bioaerosol droplets in normal human subjects by delivery of a simple, safe, liquid aerosol. We also aimed to understand the mechanism of the effect of the inhaled aerosol through in vitro cough...

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