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The Effect of Blood on the Anitiviral Activity of Sodium Hypochlorite, a Phenolic, and a Quaternary Ammonium Compound
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Abstract(back to top)
OBJECTIVE. To assess the virucidal activity of three disinfectants (sodium hypochlorite, a phenolic, and a quaternary ammonium compound) in the presence and absence of blood.
METHODS. Disinfectants at varying concentrations (hypochlorite: 5,000, 500, or 50 ppm; phenolic: 1:10 or 1:128 dilution; quaternary ammonium compound: 1:10 or 1:128 dilution) were added to either saline or whole blood (final concentration, 80% or 20% blood) and mixed. Test organisms included an attenuated vaccine strain of poliovirus type 1 (prototype for relatively resistant hydrophilic viruses) and herpes simplex virus (HSV) type 1 (prototype for relatively susceptible lipophilic viruses). Virus was added to create a viral‐blood suspension. Viral survival was tested at room temperature at the following times: 0, 15 seconds, 30 seconds, 1 minute, 2 minutes, 5 minutes, and 10 minutes. A neutralizer stopped the reaction, and virus was assayed using a plaque technique.
RESULTS. In the absence of blood, complete inactivation of HSV was achieved within 30 seconds with 5,000 (1:10 dilution of bleach) and 500 (1:100 dilution of bleach) ppm chlorine, 1:10 and 1:128 diluted phenolic (use dilution), and 1:10 and 1:128 diluted quaternary ammonium compound (use dilution). In the presence of 80% blood, only 5,000 ppm hypochlorite, 1:10 phenolic, and 1:10 or 1:128 quaternary ammonium compound were effective. In the absence of blood, complete inactivation of polio was achieved within 30 seconds by 5,000 and 500 ppm chlorine and 1:10 quaternary ammonium compound. In the presence of 80% blood, no solution tested was capable of completely inactivating poliovirus within 10 minutes.
CONCLUSIONS. Our data suggest that, in the absence of visible blood, environmental surfaces may be disinfected with a diluted hypochlorite solution (1:10 or 1:100), a phenolic, or a quaternary ammonium compound. Based on our studies using HSV, which has similar susceptibilities to disinfectants as human immunodeficiency virus (HIV), phenolics at their use dilution and 1:100 diluted hypochlorite are unlikely to inactivate HIV or hepatitis B virus reliably in the presence of blood. Hypochlorite at a final concentration of 5,000 ppm (1:10 dilution) should be used to decontaminate blood spills, but, even after decontamination, care should be used to avoid sharps injuries.
Bibliographic Information(back to top)
- The Effect of Blood on the Anitiviral Activity of Sodium Hypochlorite, a Phenolic, and a Quaternary Ammonium Compound
- David J. Weber , MD, MPH, Susan L. Barbee , MS, MSPH, Mark D. Sobsey , PhD and William A. Rutala , PhD, MPH
- Infection Control and Hospital Epidemiology
- Vol. 20, No. 12 (December 1999) (pp. 821-827)
Notes and References(back to top)
This item contains 1 note(s).
Notes
From the Division of Infectious Diseases, University of North Carolina (UNC) School of Medicine (Drs. Weber, Barbee, and Rutala), Department of Hospital Epidemiology, UNC Hospitals (Drs. Weber and Rutala), and Departments of Epidemiology (Dr. Weber), and Environmental Sciences (Dr. Sobsey), UNC School of Public Health, Chapel Hill, North Carolina.Address reprint requests to David Jay Weber, MD, MPH, 547 Burnett‐Womack Building, CB #7030, Division of Infectious Diseases, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599‐7030.This study was supported in part by the Statewide Program for Infection Control and Epidemiology. The authors wish to thank Newman C. Aguiar, Douglas A. Wait, and Dorothy L. Thompson for their technical assistance. Dr. Steven Bachenheimer kindly provided the herpes simplex virus and VERO cell line and helpful advice. UNC animal surgery provided the blood.99‐OA‐028. Weber DJ, Barbee SL, Sobsey MD, Rutala WA. The effect of blood on the antiviral activity of sodium hypochlorite, a phenolic, and a quaternary ammonium compound. Infect Control Hosp Epidemiol 1999;20:821‐827.
Items Citing this Item (back to top)
1 item(s) in JSTOR cite this item
- William A. Rutala , PhD, MPH; David J. Weber , MD, MPHVol. 31, No. 12 (December 2010) pp. 1306-1308Stable URL: http://www.jstor.org/stable/10.1086/657580