We tested the survival of the Wa strain of human rotavirus on the hands of volunteers and also studied infectious virus transfer between animate and inanimate (stainless steel disks) surfaces. The virus was diluted in a 10% suspension of feces, and 10 ,ul (1 x 103 to 4 x 104 PFU) was placed on each of the four fingerpads of the left hand. One milliliter of 20% tryptose phosphate broth in Earle balanced salt solution was used for virus elution from each fingerpad, and the hands were disinfected with 70% ethanol before they were washed with an antiseptic soap and water. At 20, 60, and 260 min after inoculation, approximately 57, 43, and 7%, respectively, of the input infectious virus could be recovered. For virus transfer, the inoculum (2 x 104 to 8 x 104 PFU) was allowed to dry, and the donor surface was kept in contact with the recipient surface for 10 s at a pressure of approximately 1 kg/cm2. At 20 and 60 min after virus inoculation, 16.1 and 1.8%, respectively, of the input infectious virus could be transferred from the contaminated hand to a clean disk; when a clean hand was pressed against a contaminated disk, virus transfer was 16.8 and 1.6%, respectively. Contact between a contaminated and a clean hand 20 and 60 min after virus inoculation resulted in the transfer of 6.6 and 2.8%, respectively, of the input infectious virus. human hands in the spread of rotaviral infections. These findings indicate the potential vehicular role for * Corresponding author. Mass.) with Eagle minimal essential medium (EMEM; Flow Laboratories, Inc., Rockville, Md.) with 5% fetal calf serum and gentamicin (Cidomycin; Roussel, Montreal, Quebec, Canada) at a final concentration of 50 p.g/ml. The seeded plates were sealed in plastic bags (Philips, Toronto, Ontario, Canada) and incubated at 37°C for 48 h for monolayer

Hands often become contaminated with respiratory viruses, either directly or through contact with contaminated surfaces. Spread of such viruses could then occur by touching the nasal mucosa or the conjunctivae. In this quantitative study, we compared the survival of mucin-suspended human parainfluenza virus 3 (HPIV-3) and rhinovirus 14 (RV-14) and the transfer of the viruses to and from the fingers of adult volunteers. When each finger pad was contaminated with 10 ,ul of either HPIV-3 (1.3 x 105 to 5.5 x 105 PFU) or RV-14 (2.1 x 10' to 1.1 x 10 PFU), <1.0% of HPIV-3 and 37.8% of RV-14 remained viable after 1 h; after 3 h, nearly 16% of RV-14 could still be detected, whereas HPIV-3 became undetectable. Tests on the potential spread of viruses from contaminated hands or surfaces were conducted 20 min after contamination of the donor surface by pressing together donor and recipient surfaces for 5 s. Transfer of HPIV-3 from finger to finger or finger to metal disk could not be detected, but 1.5% of infectious HPIV-3 was transferred from disk to finger. Irrespective of the type of donor or recipient surface, 0.7 to 0.9% of RV-14 was transferred. The relatively rapid loss of HPIV-3 infectivity on hands suggests that their role in the direct spread of parainfluenza viruses is limited. However, the findings of this study further reinforce the view that hands can be vehicles for rhinovirus colds. These results also suggest a role for nonporous environmental surfaces in the contamination of hands with respiratory viruses.

Ten antiseptic formulations, an unmedicated liquid soap, and tap water alone were compared for their capacities to eliminate human rotavirus from the finger pads of adult volunteers; three of the antiseptics, the soap, and the tap water alone were also tested against Escherichia coli. A fecal suspension of virus or bacterium was placed on each finger pad and air dried. The contaminated site was exposed to the test product for 10 s, rinsed in tap water, and dried on a paper towel. The residual virus or bacterium was then eluted. Selected agents were also tested by an analogous whole-hand method by which the entire palm surfaces of both hands were contaminated. Alcohols (70%) alone or with Savlon reduced the virus titer by >99%, whereas the reductions by Proviodine, Dettol, and Hibisol ranged from 95 to 97%. Aqueous solutions of chlorhexidine gluconate were significantly less effective for virus removal or inactivation than 70% alcohol solutions. Furthermore, Savlon in water (1:200) was found to be much less effective in eliminating the virus (80.6%) than the bacterium (98.9%). The tap water alone and the soap reduced the virus titers by 83.6 and 72.5% and the bacterial titers by 90 and 68.7%, respectively. The results of the whole-hand method agreed well with those of the finger pad protocol. We conclude that the finger pad method is a suitable model for testing the in vivo efficacy of hand-washing agents and emphasize the need for using appropriate test viruses and bacteria.

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The impact of troposphere ozone (O(3)), the major oxidant in photochemical smog, on the overall wellbeing of skin is of considerable interest. To date, limited information is available on the impact of O(3) on human skin. Using a specially designed O(3) exposure chamber, we provide the first evidence that exposure of human skin to O(3) (0.8 ppm, 2-h time-weighted average) significantly reduced vitamin E by 70% and concomitantly increased lipid hydroperoxides by 2.3 fold in the superficial stratum corneum (SC). Although the dose of O(3) used here reduced the resident microflora population by 50% and created a state of oxidative stress within the SC, it did not affect several key enzymes involved in SC homeostasis including the redox-sensitive transglutaminase and the SC tryptic (KLK5) and chymotryptic (KLK7) proteases. Importantly, no signs of skin dryness or erythema were observed. We hypothesize that the limited effects of low doses of O(3) on SC function is attributable to several factors including: (i) protection provided by the anti-oxidant defence system; (ii) inability of O(3) to penetrate the SC; and (iii) limited water available to catalyse the Criegee reaction. Although chronic exposure to O(3) may produce a different outcome than that reported here, our data suggest that exposure to environmentally relevant doses of O(3), at best, induces a moderate state of oxidative stress, without producing a visible clinical response. In our opinion, exposure of skin to UV radiation is a much more significant threat than exposure to ground-level O(3).

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