A direct approach to limit airborne viral transmissions is to inactivate them within a short time of their production. Germicidal ultraviolet light, typically at 254 nm, is effective in this context but, used directly, can be a health hazard to skin and eyes. By contrast, far-UVC light (207–222 nm) efficiently kills pathogens potentially without harm to exposed human tissues. We previously demonstrated that 222-nm far-UVC light efficiently kills airborne influenza virus and we extend those studies to explore far-UVC efficacy against airborne human coronaviruses alpha HCoV-229E and beta HCoV-OC43. Low doses of 1.7 and 1.2 mJ/cm2 inactivated 99.9% of aerosolized coronavirus 229E and OC43, respectively. As all human coronaviruses have similar genomic sizes, far-UVC light would be expected to show similar inactivation efficiency against other human coronaviruses including SARS-CoV-2. Based on the beta-HCoV-OC43 results, continuous far-UVC exposure in occupied public locations at the current regulatory exposure limit (~3 mJ/cm2/hour) would result in ~90% viral inactivation in ~8 minutes, 95% in ~11 minutes, 99% in ~16 minutes and 99.9% inactivation in ~25 minutes. Thus while staying within current regulatory dose limits, low-dose-rate far-UVC exposure can potentially safely provide a major reduction in the ambient level of airborne coronaviruses in occupied public locations.
Coronavirus disease 2019 (COVID-19) was first reported in December 2019 and then characterized as a pandemic by the World Health Organization on March 11, 2020. Despite extensive efforts to contain the spread of the disease, it has spread worldwide with over 5.3 million confirmed cases and over 340,000 confirmed deaths as of May 25, 20201. Transmission of SARS-CoV-2, the beta coronavirus causing COVID-19, is believed to be both through direct contact and airborne routes, and studies of SARS-CoV-2 stability have shown viability in aerosols for at least 3 hours2. Given the rapid spread of the disease, including through asymptomatic carriers3, it is of clear importance to explore practical mitigation technologies that can inactivate the airborne virus in public locations and thus limit airborne transmission.
Ultraviolet (UV) light exposure is a direct antimicrobial approach4 and its effectiveness against different strains of airborne viruses has long been established5. The most commonly employed type of UV light for germicidal applications is a low pressure mercury-vapor arc lamp, emitting around 254 nm; more recently xenon lamp technology has been used, which emits broad UV spectrum6. However, while these lamps can be used to disinfect unoccupied spaces, direct exposure to conventional germicidal UV lamps in occupied public spaces is not possible since direct exposure to these germicidal lamp wavelengths can be a health hazard, both to the skin and eye7,8,9,10.
By contrast far-UVC light (207 to 222 nm) has been shown to be as efficient as conventional germicidal UV light in killing microorganisms11, but studies to date12,13,14,15 suggest that these wavelengths do not cause the human health issues associated with direct exposure to conventional germicidal UV light. In short (see below) the reason is that far-UVC light has a range in biological materials of less than a few micrometers, and thus it cannot reach living human cells in the skin or eyes, being absorbed in the skin stratum corneum or the ocular tear layer. But because viruses (and bacteria) are extremely small, far-UVC light can still penetrate and kill them. Thus far-UVC light potentially has about the same highly effective germicidal properties of UV light, but without the associated human health risks12,13,14,15. Several groups have thus proposed that far-UVC light (207 or 222 nm), which can be generated using inexpensive excimer lamps, is a potential safe and efficient anti-microbial technology12,13,14,15,16,17,18 which can be deployed in occupied public locations.
The biophysically-based mechanistic basis to this far-UVC approach12 is that light in this wavelength range has a very limited penetration depth. Specifically, far-UVC light (207–222 nm) is very strongly absorbed by proteins through the peptide bond, and other biomolecules19,20, so its ability to penetrate biological materials is very limited compared with, for example, 254 nm (or higher) conventional germicidal UV light21,22. This limited penetration is still much larger than the size of viruses and bacteria, so far-UVC light is as efficient in killing these pathogens as conventional germicidal UV light12,13,14. However, unlike germicidal UV light, far-UVC light cannot penetrate either the human stratum corneum (the outer dead-cell skin layer), nor the ocular tear layer, nor even the cytoplasm of individual human cells. Thus, far-UVC light cannot reach or damage living cells in the human skin or the human eye, in contrast to the conventional germicidal UV light which can reach these sensitive cells7,8,9,10.
In summary far-UVC light is anticipated to have about the same anti-microbial properties as conventional germicidal UV light, but without producing the corresponding health effects. Should this be the case, far-UVC light has the potential to be used in occupied public settings to prevent the airborne person-to-person transmission of pathogens such as coronaviruses.
We have previously shown that a very small dose (2 mJ/cm2) of far-UVC light at 222 nm was highly efficient in inactivating aerosolized H1N1 influenza virus23. In this work we explore the efficacy of 222 nm light against two airborne human coronaviruses: alpha HCoV-229E and beta HCoV-OC43. Both were isolated over 50 years ago and are endemic to the human population, causing 15–30% of respiratory tract infections each year24. Like SARS-CoV-2, the HCoV-OC43 virus is from the beta genus25.
Here we measured the efficiency with which far-UVC light inactivates these two human coronaviruses when exposed in aerosol droplets of sizes similar to those generated during sneezing and coughing26. As all coronaviruses have comparable physical and genomic size, a critical determinant of radiation response27, we hypothesized that both viruses would respond similarly to far-UVC light, and indeed that all coronaviruses will respond similarly.
Inactivation of human coronaviruses after exposure to 222 nm light in aerosols infectivity assay
We used a standard approach to measure viral inactivation, assaying coronavirus infectivity in human host cells (normal lung cells), in this case after exposure in aerosols to different doses of far-UVC light. We quantified virus infectivity with the 50% tissue culture infectious dose TCID50 assay28, and estimated the corresponding plaque forming units (PFU)/ml using the conversion PFU/ml = 0.7 TCID50 29. Figure 1 shows the fractional survival of aerosolized coronaviruses HCoV-229E and HCoV-OC43 expressed as PFUUV/PFUcontrols as a function of the incident 222-nm dose. Robust linear regression (Table 1) using iterated reweighted least squares30 indicated that the survival of both genera alpha and beta is consistent with a classical exponential UV disinfection model (R2 = 0.86 for HCoV-229E and R2 = 0.78 for HCoV-OC43). For the alpha coronavirus HCoV-229E, the inactivation rate constant (susceptibility rate) was k = 4.1 cm2/mJ (95% confidence intervals (C.I.) 2.5–4.8) which corresponds to an inactivation cross-section (or the dose required to kill 90% of the exposed viruses) of D90 = 0.56 mJ/cm2. Similarly, the susceptibility rate for the beta coronavirus HCoV-OC43 was k = 5.9 cm2/mJ (95% C.I. 3.8–7.1) which corresponds to an inactivation cross section of D90 = 0.39 mJ/cm2.