The recent coronavirus disease , caused by SARS-CoV-2, is inarguably the most challenging coronavirus outbreak relative to the previous outbreaks involving SARS-CoV and MERS-CoV. With the number of COVID-19 cases now exceeding 2 million worldwide, it is apparent that (i) transmission of SARS-CoV-2 is very high and (ii) there are large variations in disease severity, one component of which may be genetic variability in the response to the virus. Controlling current rates of infection and combating future waves require a better understanding of the routes of exposure to SARS-CoV-2 and the underlying genomic susceptibility to this disease. In this mini-review, we highlight possible genetic determinants of COVID-19 and the contribution of aerosol exposure as a potentially important transmission route of SARS-CoV-2.

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The outbreak of COVID-19, and its current resurgence in the United States has resulted in a shortage of isolation rooms within many U.S. hospitals admitting COVID-19-positive cases. As a result, hospital systems, especially those at an epicenter of this outbreak, have initiated task forces to identify and implement various approaches to increase their isolation capacities. This paper describes an innovative temporary anteroom in addition to a portable air purifier unit to turn a general patient room into an isolation space. Using an aerosolization system with a surrogate oil-based substance, we evaluated the effectiveness of the temporary plastic anteroom and the portable air purifier unit. Moreover, the optimal location of the portable unit, as well as the effect of negative pressurization and door opening on the containment of surrogate aerosols were assessed. Results suggested that the temporary anteroom alone could prevent the migration of nearly 98% of the surrogate aerosols into the adjacent corridor. Also, it was shown that the best location of a single portable air purifier unit is inside the isolation room and near the patient's bed. The outcome of this paper can be widely used by hospital facilities managers when attempting to retrofit a general patient room into an airborne infection isolation room.

Our findings suggest that glutathione-related oxidative burden may be more strongly associated with lung cancer mortality than PM2.5 mass concentrations.

Airborne fine particle mass concentrations (PM2.5) are used for ambient air quality management worldwide based in part on known cardiorespiratory health effects. While oxidative stress is generally thought to be an important mechanism in determining these effects, relatively few studies have specifically examined how oxidant defence may impact susceptibility to particulate air pollution. Here we review studies that explore the impact of polymorphisms in anti-oxidant related genes or anti-oxidant supplementation on PM2.5-induced cardiorespiratory outcomes in an effort to summarize existing evidence related to oxidative stress defence and the health effects of PM2.5. Recent studies of PM-oxidative burden were also examined. In total, nine studies were identified and reviewed and existing evidence generally suggests that oxidant defence may modify the impact of PM2.5 exposure on various health outcomes, particularly heart rate variability (a measure of autonomic function) which was the most common outcome examined in the studies reviewed. Few studies examined interactions between PM2.5 and oxidant defence for respiratory outcomes, and in general studies focused primarily on acute health effects. Therefore, further evaluation of the potential modifying role of oxidant defence in PM2.5-induced health effects is required, particularly for chronic outcomes. Similarly, while an exposure metric that captures the ability of PM2.5 to cause oxidative stress may offer advantages over traditional mass concentration measurements, little epidemiological evidence is currently available to evaluate the potential benefits of such an approach. Therefore, further evaluation is required to determine how this metric may be incorporated in ambient air quality management.

Between-city differences in glutathione-related oxidative potential may modify the impact of PM2.5 on acute respiratory illnesses at low PM2.5 concentrations. This may explain in part how small changes in ambient PM2.5 mass concentrations can contribute to acute respiratory morbidity in low-pollution environments.

Most studies of road dust composition have sampled a very wide range of particle sizes, but from the perspective of respiratory exposure to resuspended dusts, it is the PM10 fraction which is of most importance. The PM10 fraction of road dust samples was collected at two sites in Birmingham, UK (major highway and road tunnel) and one site in New Delhi, India. Dust loadings were found to be much higher for New Delhi compared to Birmingham, while concentrations of several species were much higher in the case of Birmingham. Detailed chemical source profiles were prepared for both cities and previously generated empirical factors for source attribution to brake wear, tyre wear, and crustal dust were successfully applied to the UK sites. However, 100% of the mass for the Indian site could not be accounted for using these factors. This study highlights the need for generation of local empirical estimation factors for non-exhaust vehicle emissions. A limited number of bulk road dust and brake pad samples were also characterized. Oxidative potential (OP) was also determined for a limited number of PM10 and bulk road dust samples, and Cu was found to be a factor significantly associated with OP in PM10 and bulk road dust.