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Lower respiratory tract infections originate from multiple aerosol sources, varying from droplets erupting from bursting bubbles in a toilet or those produced by human speech. A key component of the aerosol-based infection pathway—from source to potential host—is the survival of the pathogen during aerosolization. Due to their finite-time instability, pinch-off processes occurring during aerosolization have the potential to rapidly accelerate the fluid into focused regions of these droplets, stress objects therein, and if powerful enough, disrupt biological life. However, the extent that a pathogen will be exposed to damaging hydrodynamic stressors during the aerosolization process is unknown. Here we compute the probability that particulates will be exposed to a hydrodynamic stressor during the generation of droplets that range in size from one to 100 microns. For example, particulates in water droplets less than 5 μm have a 50% chance of being subjected to an energy dissipation rate in excess of 10(11) W/m(3), hydrodynamic stresses in excess of 10(4) Pa, and strain rates in excess of 10(7) s(−1), values known to damage certain biological cells. Using a combination of numerical simulations and self-similar dynamics, we show how the exposure within a droplet can be generally predicted from its size, surface tension, and density, even across different aerosolization mechanisms. Collectively, these results introduce aerosol agitation as a potential factor in pathogen transmission and implicate the pinch-off singularity flow as setting the distribution of hydrodynamic stressors experienced within the droplet.

The global Coronavirus Disease (COVID-19) pandemic caused by the SARS-CoV-2 virus has raised many urgent questions about the transmission of this disease, including the possible roles of aerosols c...

When infectious epidemics occur, they can be perpetuated within health care settings, potentially resulting in severe health care workforce absenteeism, morbidity, mortality, and economic losses. The ventilation system configuration of an airborne infection isolation room is one factor that can play a role in protecting health care workers from infectious patient bioaerosols. Though commonly associated with airborne infectious diseases, the airborne infection isolation room design can also impact other transmission routes such as short-range airborne as well as fomite and contact transmission routes that are impacted by contagion concentration and recirculation. This article presents a computational fluid dynamics study on the influence of the ventilation configuration on the possible flow path of bioaerosol dispersal behavior in a mock airborne infection isolation room. At first, a mock airborne infection isolation room was modeled that has the room geometry and layout, ventilation parameters, and pressurization corresponding to that of a traditional ceiling-mounted ventilation arrangement observed in existing hospitals. An alternate ventilation configuration was then modeled to retain the linear supply diffuser in the original mock airborne infection isolation room but interchanging the square supply and exhaust locations to place the exhaust closer to the patient source and allow clean air from supply vents to flow in clean-to-dirty flow paths, originating in uncontaminated parts of the room prior to entering the contaminated patient's air space. The modeled alternate airborne infection isolation room ventilation rate was 12 air changes per hour. Two human breathing models were used to simulate a source patient and a receiving health care worker. A patient cough cycle was introduced into the simulation, and the airborne infection dispersal was tracked in time using a multi-phase flow simulation approach. The results from the alternate configuration revealed that the cough aerosols were pulled by the exhaust vent without encountering the health care worker by 0.93 s after patient coughs and the particles were controlled as the aerosols' flow path was uninterrupted by an air particle streamline from patient to the ceiling exhaust venting out cough aerosols. However, not all the aerosols were vented out of the room. The remaining cough aerosols entered the health care worker's breathing zone by 0.98 s. This resulted in one of the critical stages in terms of the health care worker's exposure to airborne virus and presented the opportunity for the health care worker to suffer adverse health effects from the inhalation of cough aerosols. Within 2 s, the cough aerosols reentered and recirculated within the patient and health care worker's surroundings resulting in pockets of old contaminated air. By this time, coalescence losses decreased as the aerosol were no longer in very close proximity and their movement was primarily influenced by the airborne infection isolation room airflow patterns. In the patient and health care worker's area away from the supply, the fresh air supply failed to reach this part of the room to quickly dilute the cough aerosol concentration. The exhaust was also found to have minimal effect upon cough aerosol removal, except for those areas with high exhaust velocities, very close to the exhaust grill. Within 5-20 s after a patient's cough, the aerosols tended to break up to form smaller sized aerosols of less than one micron diameter. They remained airborne and entrained back into the supply air stream, spreading into the entire room. The suspended aerosols resulted in the floating time of more than 21 s in the room due to one cough cycle. The duration of airborne contagion in the room and its prolonged exposure to the health care worker is likely to happen due to successive coughing cycles. Hence, the evaluated alternate airborne infection isolation room is not effective in removing at least 38% particles exposed to health care worker within the first second of a patient's cough.