Virus-laden Aerosols Research Articles

Modeling of indoor airflow and dispersion of aerosols using immersed boundary and random flow generation methods

Numerical modeling of environmental flows involves complex geometry, moving bodies, multi-phase flow, and buoyant jet effects. An in-house CFD code has been developed using finite volume and immersed boundary methods. The transport and dispersion of virus-laden aerosols in a ventilated room is investigated by this numerical code. The uniqueness of this numerical code is that it can efficiently compute small-scale turbulent flow in which most commercial CFD software will suffer from large numerical error. Random flow generation (RFG) [33] is an ideal choice for small-scale turbulence for low-Reynolds number flow in a ventilated room. In addition, Lagrangian stochastic (LS) walk model is applied to directly compute probability density function (PDF) of aerosols and estimate the risk factor of aerosol dispersion from a point source. The present study focuses on aerosols with small diameter (<10 μm) in which the effects of evaporation on the dispersion of aerosols could be neglected. Different location of aerosol sources and a typical ventilation layout are discussed in detail. The numerical results with PDF yield more useful quantitative information to assess the risk area of virus transport in a ventilated room than that shown in random trajectories of particles as widely reported in the literature. This study provides valuable information for ventilation control strategies with respiratory protection, such as enhanced air exchange, air filtration rate, and improved airflow patterns to reduce indoor infection risk via airborne virus laden droplets.

Investigating a safe ventilation rate for the prevention of indoor SARS transmission: An attempt based on a simulation approach.

This paper identifies the “safe ventilation rate” for eliminating airborne viral infection and preventing cross-infection of severe acute respiratory syndrome (SARS) in a hospital-based setting. We used simulation approaches to reproduce three actual cases where groups of hospital occupants reported to be either infected or not infected when SARS patients were hospitalized in nearby rooms. Simulations using both computational fluid dynamics (CFD) and multi-zone models were carried out to understand the dilution level of SARS virus-laden aerosols during these scenarios. We also conducted a series of measurements to validate the simulations. The ventilation rates (dilution level) for infection and non-infection were determined based on these scenarios. The safe ventilation rate for eliminating airborne viral infection is to dilute the air emitted from a SARS patient by 10000 times with clean air. Dilution at lower volumes, specifically 1000 times, is insufficient for protecting non-infected people from SARS exposure and the risk of infection is very high. This study provides a methodology for investigating the necessary ventilation rate from an engineering viewpoint.

Temporal-Spatial Analysis of Severe Acute Respiratory Syndrome among Hospital Inpatients

Background. We report the temporal-spatial spread of severe acute respiratory syndrome (SARS) among inpatients in a hospital ward during a major nosocomial outbreak and discuss possible mechanisms for the outbreak. Methods. All inpatients who had stayed in the same ward as the initial index case patient for any duration before isolation were recruited into a cohort and followed up to document the occurrence of SARS. The normalized concentration of virus-laden aerosols at different locations of the ward was estimated by use of computational fluid dynamics modeling. The attack rates in the various subgroups stratified by bed location were calculated. Multivariate Cox proportional hazards regression was used to document important risk factors. Results. The overall attack rate of SARS was 41% (30 of 74 subjects). It was 65%, 52%, and 18% in the same bay, adjacent bay, and distant bays, respectively (P = .001). Computation fluid dynamics modeling indicated that the normalized concentration of virus-laden aerosols was highest in the same bay and lowest in the distant bays. Cox regression indicated that staying in the ward on 6 or 10 March entailed higher risk, as well as staying in the same or adjacent bays. The epidemic curve showed 2 peaks, and stratified analyses by bed location suggested >1 generation of spread. Conclusions. The temporal-spatial spread of SARS in the ward was consistent with airborne transmission, as modeled by use of computational fluid dynamics. Infected health care workers likely acted as secondary sources in the latter phase of the outbreak.

The potential spread of infection caused by aerosol contamination of surfaces after flushing a domestic toilet

To determine the level of aerosol formation and fallout within a toilet cubicle after flushing a toilet contaminated with indicator organisms at levels required to mimic pathogen shedding during infectious diarrhoea. A semisolid agar carrier containing either Serratia marcesens or MS2 bacteriophage was used to contaminate the sidewalls and bowl water of a domestic toilet to mimic the effects of soiling after an episode of acute diarrhoea. Viable counts were used to compare the numbers of Serratia adhering to the porcelain surfaces and those present in the bowl water before and after flushing the toilet. Air sampling and settle plates were used to determine the presence of bacteria or virus-laden aerosols within the toilet cubicle. After seeding there was a high level of contamination on the porcelain surfaces both under the rim and on the sides of the bowl. After a single flush there was a reduction of 2.0-3.0 log cycles cm(-2) for surface attached organisms. The number of micro-organisms in the bowl water was reduced by 2.0-3.0 log cycles ml(-1) after the first flush and following a second flush, a further reduction of c. 2.0 log cycles ml(-1) was achieved. Micro-organisms in the air were at the highest level immediately after the first flush (mean values, 1370 CFU m(-3) for Serratia and 2420 PFU m(-3) for MS2 page). Sequential flushing resulted in further distribution of micro-organisms into the air although the numbers declined after each flush. Serratia adhering to the sidewalls, as well as free-floating organisms in the toilet water, were responsible for the formation of bacterial aerosols. Although a single flush reduced the level of micro-organisms in the toilet bowl water when contaminated at concentrations reflecting pathogen shedding, large numbers of micro-organisms persisted on the toilet bowl surface and in the bowl water which were disseminated into the air by further flushes. Many individuals may be unaware of the risk of air-borne dissemination of microbes when flushing the toilet and the consequent surface contamination that may spread infection within the household, via direct surface-to-hand-to mouth contact. Some enteric viruses could persist in the air after toilet flushing and infection may be acquired after inhalation and swallowing.

Evidence of airborne transmission of the severe acute respiratory syndrome virus.

There is uncertainty about the mode of transmission of the severe acute respiratory syndrome (SARS) virus. We analyzed the temporal and spatial distributions of cases in a large community outbreak of SARS in Hong Kong and examined the correlation of these data with the three-dimensional spread of a virus-laden aerosol plume that was modeled using studies of airflow dynamics. We determined the distribution of the initial 187 cases of SARS in the Amoy Gardens housing complex in 2003 according to the date of onset and location of residence. We then studied the association between the location (building, floor, and direction the apartment unit faced) and the probability of infection using logistic regression. The spread of the airborne, virus-laden aerosols generated by the index patient was modeled with the use of airflow-dynamics studies, including studies performed with the use of computational fluid-dynamics and multizone modeling. The curves of the epidemic suggested a common source of the outbreak. All but 5 patients lived in seven buildings (A to G), and the index patient and more than half the other patients with SARS (99 patients) lived in building E. Residents of the floors at the middle and upper levels in building E were at a significantly higher risk than residents on lower floors; this finding is consistent with a rising plume of contaminated warm air in the air shaft generated from a middle-level apartment unit. The risks for the different units matched the virus concentrations predicted with the use of multizone modeling. The distribution of risk in buildings B, C, and D corresponded well with the three-dimensional spread of virus-laden aerosols predicted with the use of computational fluid-dynamics modeling. Airborne spread of the virus appears to explain this large community outbreak of SARS, and future efforts at prevention and control must take into consideration the potential for airborne spread of this virus.