Two percent LBG and 2 mM Borax were chosen as representative mucus simulants and were in the literature range of 0.4–2% and 1–3 mM ( 18). Baker) to locust bean gum (LBG) in distilled water mixture (2% wt/vol Fluka) and mixing for 1 min, pipetting onto the trough mimetic and allowing 30 min for proper crosslinking. Mucus mimetics for bioaerosol formation in the simulated cough machine were prepared by adding a small amount of concentrated sodium tetraborate in distilled water solution (Na 2B 4O 7, 50 g/liter J.T. Aqueous solutions for aerosolization were prepared either as a 0.9% isotonic saline formulation or as a 7:3 wt/wt mixture of DPPC and POPG suspended at 100 mg/ml in 0.9% saline.
1,2-Dipalmitoyl- sn-glycero-3-phosphocholine (DPPC) and 1-palmitoyl-2-oleoyl- sn-glycero-3-phosphoglycerol (POPG) were purchased from Genzyme. We also aimed to understand the mechanism of the effect of the inhaled aerosol through in vitro cough machine experiments. 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. 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). Given the variable dimensions of common viral and bacterial pathogens (≈25 nm to 5 μm), the ability of exhaled bioaerosol droplets of a given size to carry pathogen obviously varies with pathogen type. These droplets are primarily <1 μm in size, because larger droplets tend to be filtered out of the expired air by the lungs ( 16). Normal mouth breathing (more than coughing, nose breathing, or talking) has been observed to produce the largest number of airborne droplets ( 15, 16). Airborne bacteria include anthrax, Escherichia coli ( 11), Klebsiella pneumoniae ( 12), Francisella tularensis ( 13), and tuberculosis ( 14). Viruses known to spread from humans and/or 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), varicella-zoster virus (chicken pox) ( 8), infectious bronchitis virus ( 9), and smallpox, among others ( 10). It has long been understood that exhaled bioaerosol particles provide an important vector for the spread of certain infectious diseases ( 1, 2).
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. 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. 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. 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. 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. Humans commonly exhale aerosols comprised of small droplets of airway-lining fluid during normal breathing.