Various hypotheses have been proposed to explain the spread of the SARS virus in the Amoy Gardens outbreak. The investigation by the government of the Hong Kong Special Administrative Region suggested that the index patient infected a small group of residents in building E and that the infection subsequently spread to the other residents in that building through the sewage-disposal system, person-to-person contact, and the use of communal facilities such as elevators and staircases. These infected residents subsequently transmitted the disease to others both within and outside building E through person-to-person contact and by contaminating the environment.

An investigative team from the World Health Organization (WHO) found that traps in the floor drains in many of the housing units seemed not to have been filled with water for long periods; the seals in the traps thus dried out, and as a result, a connection was opened to the vertical soil stack (drainage pipe).7 The investigative team suggested that an exhaust fan that was running behind a closed door in the bathroom could have drawn fine droplets or aerosols from the soil stack into the bathroom through the unsealed floor drain and thereby contaminated the bathroom. The exhaust fan could have transported contaminated droplets or aerosols from the bathroom into the air shaft. These contaminated droplets or aerosols could have been carried upward by the natural air current and could have entered other apartment units, even units several floors away from the source of infection, if the virus-laden aerosols had reached an open window. The WHO report did not provide an explanation for the spread of the infection from building E to the other buildings.

We concur with the WHO hypothesis regarding the source of infection and the mechanism of the initial spread of the virus-contaminated aerosols. With the use of a mock-up of the drainage system in experimental studies at the Hydraulics Laboratory of the University of Hong Kong, we found that huge numbers of aerosols were generated by the hydraulic action in vertical soil stacks when toilets were flushed. The drainage pipes for various units within a single building were not directly connected, and the drainage pipes for all the buildings were not connected until they met underground. Hence, the spread of infection through the sewage system, which was suggested in the government's report, could explain only cases that developed in unit 7 of building E but not cases that developed in other units in that building and in other buildings.

Cases of infection began to occur in buildings B, C, and D only one to three days after the first cases occurred in building E. In the majority of the cases in buildings C and D, the first symptoms appeared within a period of three days (March 24 to 26), coinciding with the peak of the epidemic in building E. This finding suggested that these cases were more likely to have developed from exposure to a common source than from person-to-person contact, as was suggested in the government report.6 Riley et al. showed that the persons who became ill in the outbreak were likely to have been infected during a very short period (±1 day) around March 19, 2003.22 Our analysis also showed that the peak exposure would have occurred on approximately March 19 and 20, if a modal incubation period of about four to five days was assumed.23

Members of the management and security staff of Amoy Gardens, who worked on the ground floor in each building 24 hours a day and would probably have had frequent person-to-person contact with the residents, were not affected by the virus. Likewise, there were no cases reported among staff members in the large shopping center in the Amoy Gardens estate. The spatial distribution of the affected apartment units (in which there were cases of infection) could not be explained by random person-to-person contact. We believe that such contact probably occurred in the latter part of the epidemic and that the number of cases and therefore the number of units affected by this means was likely to have been small.

Ng put forward the theory that roof rats were both amplifiers and distributors of the SARS-associated coronavirus,9 but this theory is not supported by the epidemiologic distribution of cases; the middle-level floors were affected more than the upper floors, and certain units were affected more than others in the same building. Roof rats are by nature territorial, and they therefore could not be responsible for the rapid and efficient spread of the infection from a single building, building E, to other buildings. The main flaw in this hypothesis is that it does not explain the steep decline in the epidemic curve after the peak, because there was no sudden disappearance of roof rats or massive deaths among them.

The epidemic curve supports the hypothesis of a common source of the outbreak in Amoy Gardens, and the spatial distribution of the cases conformed to the hypothesis that virus-laden aerosols spread from a single source (the index apartment unit), as shown in our model made with the use of airflow-dynamics data. The delay of one to three days in the onset of the epidemic in buildings B, C, and D might be explained by a lower effective viral load in the aerosols as the plume became progressively diluted. A delay in the onset of symptoms was also observed among cases in the apartment units of building E that did not border the index air shaft. With regard to cases with an onset of symptoms within the first three days of the outbreak, all except one occurred in unit 7 (Ad) and unit 8 (Ab), which lined the air shaft nearest the index unit. The predominant direction of the wind blowing from unit 7 toward unit 8 could explain why residents in unit 8 on the various floors were more affected than those in unit 7.

The dilution of the viral load as the plume traveled upward might explain why residents on the middle floors were more affected than those on the upper floors. In apartment unit 5 (Dc) and unit 6 (Da) there were fewer cases of infection, because these units were upwind of the index air shaft and therefore received the lowest normalized viral concentrations. The unit directions (i.e., the directions the front and side windows faced) and floor levels that were associated with higher risk in buildings C and D corresponded well to the results of the airflow modeling, which showed the contaminated plume passing through the space between buildings C and D at middle-level floors. For building B, apartment units that faced building E appeared to have a higher risk of infection.

The extremely high concentrations of the SARS-associated coronavirus found in the feces and urine of the index patient, coupled with the aerosolization due to hydraulic action inside the drainage pipes (vertical soil stacks), most likely generated huge numbers of virus-laden aerosols. The concentration of the aerosols decayed as the plume traveled away from the source, and the decay corresponded to lower attack rates (and, possibly, to a longer incubation period) in other apartment units of building E and in other buildings. The concentration of virus in respiratory secretions was found to be much lower than the concentrations in urine and stool, and this difference might explain the need for close contact with the index cases in some nosocomial outbreaks of SARS.24

In summary, our epidemiologic analysis, experimental studies, and airflow simulations support the probability of an airborne spread of the SARS virus in the outbreak in Amoy Gardens. Virus-laden aerosols generated in the vertical soil stack of unit 7 in building E returned to the bathroom through the dried-up seals of the floor-drain traps and then entered the air shaft, probably by means of suction created by an exhaust fan. The aerosols moved upward owing to the buoyancy of the warm, humid air within the air shaft and could enter apartment units that bordered the air shaft on the upper floors because of the negative pressure created by the exhaust fans or the action of wind flows around the building. The horizontal spread of infection to other units in building E was by movement of the air between apartment units. After the plume reached the top of the air shaft in building E, the virus was spread to some units at certain heights in buildings B, C, and D by the action of a predominant northeasterly wind.

Our hypothesis adequately explains the temporal and spatial distribution of cases of SARS. This hypothesis remains to be confirmed by further analytic epidemiologic, environmental, and experimental studies and should have important public health implications for the prevention and control of SARS, should the disease recur.