Comparison of UV C light and chemicals for disinfection of surfaces in hospital isolation units.

OBJECTIVE: To determine the bactericidal effect on surfaces of ceiling- and wall-mounted UV C (UVC) light (wavelength, 254 nm) in isolation units, compared with standard hospital environmental cleaning and chemical disinfection during final disinfection after patients are treated for infections. DESIGN: Microbial samples were obtained from surfaces in isolation units (patient room, anteroom, and bathroom) before and after irradiation with UVC, chloramine disinfection, and standard hospital environmental cleaning. Samples were tested using standard contact plates. SETTING: Four identical, negative air-pressure isolation units (patient room, anteroom, and bathroom) with a defined number of ceiling- and wall-mounted UVC light units. The UVC distribution was monitored in one isolation unit after irradiation for approximately 40 minutes, corresponding to doses ranging from 160 J/m2 in a shadowed area to 19,230 J/m2 at the mostly highly exposed site (which is high enough to inactivate most bacterial organisms, including spores). RESULTS: UVC disinfection significantly reduced the number of bacteria on surfaces directly or indirectly exposed to UVC to a very low number, as did 5% chloramine disinfection alone (P<.001 for both). Completely shadowed areas in the isolation unit (eg, the bed rail, lockers, and mattresses) still required disinfection by chemicals. CONCLUSION: Disinfection with UVC light may significantly reduce environmental bacterial contamination and thereby protect the next patient housed in an isolation room. UVC disinfection may not be used alone but is a good addition to chemical disinfection.

Induction of multinucleated cells caused by UVA exposure in different stages of the cell cycle.

Fibroblasts of the line 3T3 from swiss albino mice were exposed to ultraviolet A (UVA) irradiation. The cells were synchronized by treatment with nocodazole and mitotic shake-off, and then exposed to UVA irradiation in different stages of the cell cycle. Their photosensitivity varied through the cell cycle, being greatest in the G2 phase. UVA irradiation was found to induce the formation of multinucleated cells. Cells in the G1 phase were found to be most prone to multinucleation 15 min after UVA irradiation, while cells exposed to UVA irradiation in S and G2 phases contained the largest fractions of multinucleated cells 24 h after treatment. The present results indicate that multinucleated cells are formed by fusion of two or more cells shortly after UVA irradiation of early G1 cells, while impairment of cytokinesis is a possible explanation for the delayed formation of multinucleated cells after irradiation in S and G2.

[Use of short wave ultraviolet radiation for disinfection in operating rooms]. / Bruk av kortbølget ultrafiolett stråling til desinfeksjon i operasjonsstuer.

Over a number of years, short wave ultraviolet radiation (UVC; 200-280 nm) has been used to disinfect air and surfaces in operating rooms, patient rooms, laboratories and so on, as well as air in ventilation ducts. Despite the well-documented effect of ultraviolet radiation on air quality, thus reducing the occurrence of infections, this technology has been relatively little used. One advantage of this method is that the UVC sources ensure a continuous reduction in the number of airborne microorganisms that are generated all the time. There are, however, some disadvantages with this method. Human exposure to ultraviolet C may cause keratoconjunctivitis and erythema and requires protection of the skin and the eyes of people exposed to levels above recommended exposure limits. However, by enclosing the UVC sources or by irradiating in the absence of human activity, human exposure is eliminated. These and other aspects concerning the use of short wave ultraviolet radiation as a disinfection agent in operating rooms are discussed in this article.

Early induction of binucleated cells by ultraviolet A (UVA) radiation: a possible role of microfilaments.

The effects of UVA (365 nm) radiation on the cellular distribution of F-actin and formation of binucleated cells have been studied using 3T3 Swiss albino mouse fibroblasts and V79 Chinese hamster fibroblasts. Ultraviolet A at biologically relevant fluences was found to disintegrate the actin filaments in the cells shortly (5 min) after irradiation, concomitant with the formation of cells with two nuclei. In 76-100% of the bi- and multinucleated cells the distribution of F-actin was clearly altered. Cells in GI phase of the cell cycle were most probably involved in the formation of binucleated cells. The disintegration of F-actin was presumably not due to depolymerization of F-actin to G-actin, as the amount of F-actin in the cells was unaltered after UVA exposure but rather due to direct breakage of the actin filaments. Ultraviolet B (297/302 nm) had no effect on the cellular distribution of microfilaments, not even at highly lethal fluences.

S phase arrest and induction of multinucleated cells after exposure to ultraviolet radiation.

The effects of UVA (365 nm) and UVB (297/302 nm) radiation on cellular proliferation, cell cycle progression, aneuploidy and multinucleus induction have been studied in two different fibroblast cell lines; V79 Chinese hamster lung fibroblasts and 3T3 Swiss albino mouse fibroblasts. UVA and UVB were found to inhibit proliferation of the cells in a fluence-dependent manner. This inhibition was due to a temporary accumulation of cells in the S phase of the cell cycle, as determined by flow cytometry of UV-irradiated V79 cells. The UVA- and UVB-induced S phase delay was observed a few hours after irradiation and by 48 h post-irradiation the cells had recovered from cell cycle arrest. For UVA, but not for UVB, the elongation of S phase was followed by a small accumulation of cells in the G2 phase. After exposure to UVA and a post-irradiation time long enough for the cells to recover from cell cycle arrest, a large proportion of the cells were polyploid, with two or more nuclei. Multinucleated cells were not, however, induced by UVB irradiation.

Effects of ultraviolet radiation on intercellular communication in V79 Chinese hamster fibroblasts.

The effects of ultraviolet (UV) radiation on gap junctional intercellular communication (GJIC) in V79 Chinese hamster fibroblasts were studied by means of a dye transfer assay. Intercellular communication was shown to be altered by UVB (297/302 nm) and UVA (365 nm) radiation, the effect depending on the wavelength of exposure and time between irradiation and microinjection of the dye in the dye transfer assay. Exposure to 297/302 nm radiation induced a reduction in intercellular communication 6 min after exposure. Incubation of the cells post-irradiation reversed the inhibition of GJIC. From 2 to 24 h after exposure an increase in GJIC over the control cells was seen, with a maximum at 8 h post-irradiation. UVA (365 nm) radiation, on the other hand, induced an increase in the intercellular communication 6 min after irradiation. Incubation of the cells post-irradiation led to a decrease in the number of communicating cells, with a minimum seen 4 h after exposure. The reduction in communication observed after exposure to UVB and UVA was not correlated with similar modifications in the gap junction protein connexin43 as found when exposing the cells to the tumour promoter 12-O-tetradecanoyl-phorbol-13-acetate. For the higher fluences of UVA, a decrease in immunorecognizable connexin43 was seen, concomitant with a markedly increased background of higher mol. wt compounds. This may be due to UVA-induced crosslinking of connexin43. No correlation was found between changes in communication induced by UV radiation and levels of cyclic AMP.

An action spectrum for UV-induced attachment of V79 Chinese hamster cells to a substratum.

When cells growing in monolayers are exposed to ultraviolet radiation (UV) their binding to the substratum is increased in strength. An action spectrum for such UV-induced binding was determined, using the time needed for trypsin-EDTA to detach the cells as a measure of the binding strength. This action spectrum was significantly different from the action spectrum for cell inactivation, which was also determined. At the shortest wavelengths (297/302, 313 nm) lethal fluences were needed to induce measurable binding while at the longest wavelengths (365, 405 nm) completely nonlethal fluences induced strong and persistent binding. Thus, different chromophores are involved in the two processes: while DNA may be the main chromophore for cell inactivation, other and unidentified chromophores may be more important for induction of increased cell binding to the substratum.