Failure Analysis Results and Corrective Actions Implemented for the EMU 3011 Water in the Helmet Mishap

During EVA (Extravehicular Activity) No. 23 aboard the ISS (International Space Station) on 07/16/2013 water entered the EMU (Extravehicular Mobility Unit) helmet resulting in the termination of the EVA (Extravehicular Activity) approximately 1-hour after it began. It was estimated that 1.5-L of water had migrated up the ventilation loop into the helmet, adversely impacting the astronauts hearing, vision and verbal communication. Subsequent on-board testing and ground-based TT and E (Test, Tear-down and Evaluation) of the affected EMU hardware components led to the determination that the proximate cause of the mishap was blockage of all water separator drum holes with a mixture of silica and silicates. The blockages caused a failure of the water separator function which resulted in EMU cooling water spilling into the ventilation loop, around the circulating fan, and ultimately pushing into the helmet. The root cause of the failure was determined to be ground-processing short-comings of the ALCLR (Airlock Cooling Loop Recovery) Ion Filter Beds which led to various levels of contaminants being introduced into the Filters before they left the ground. Those contaminants were thereafter introduced into the EMU hardware on-orbit during ALCLR scrubbing operations. This paper summarizes the failure analysis results along with identified process, hardware and operational corrective actions that were implemented as a result of findings from this investigation

Failure Analysis Results and Corrective Actions Implemented for the Extravehicular Mobility Unit 3011 Water in the Helmet Mishap

Water entered the Extravehicular Mobility Unit (EMU) helmet during extravehicular activity (EVA) no. 23 aboard the International Space Station on July 16, 2013, resulting in the termination of the EVA approximately 1 hour after it began. It was estimated that 1.5 liters of water had migrated up the ventilation loop into the helmet, adversely impacting the astronaut's hearing, vision, and verbal communication. Subsequent on-board testing and ground-based test, tear-down, and evaluation of the affected EMU hardware components determined that the proximate cause of the mishap was blockage of all water separator drum holes with a mixture of silica and silicates. The blockages caused a failure of the water separator degassing function, which resulted in EMU cooling water spilling into the ventilation loop, migrating around the circulating fan, and ultimately pushing into the helmet. The root cause of the failure was determined to be ground-processing shortcomings of the Airlock Cooling Loop Recovery (ALCLR) Ion Filter Beds, which led to various levels of contaminants being introduced into the filters before they left the ground. Those contaminants were thereafter introduced into the EMU hardware on-orbit during ALCLR scrubbing operations. This paper summarizes the failure analysis results along with identified process, hardware, and operational corrective actions that were implemented as a result of findings from this investigation

An Evaluation of Technology to Remove Problematic Organic Compounds from the International Space Station Potable Water

Since activation of the Water Processor Assembly (WPA) on the International Space Station (ISS) in November of 2008, there have been three events in which the TOC (Total Organic Carbon) in the product water has increased to approximately 3 mg/L and has subsequently recovered. Analysis of the product water in 2010 identified the primary component of the TOC as dimethylsilanediol (DMSD). An investigation into the fate of DMSD in the WPA ultimately determined that replacement of both Multifiltration (MF) Beds is the solution to recovering product water quality. The MF Beds were designed to ensure that ionic breakthrough occurs before organic breakthrough. However, DMSD saturated both MF Beds in the series, requiring removal and replacement of both MF Beds with significant life remaining. Analysis of the MF Beds determined that the adsorbent was not effectively removing DMSD, trimethylsilanol, various polydimethylsiloxanes, or dimethylsulfone. Coupled with the fact that the current adsorbent is now obsolete, the authors evaluated various media to identify a replacement adsorbent as well as media with greater capacity for these problematic organic contaminants. This paper provides the results and recommendations of this collaborative study

Adefovir dipivoxil for wait-listed and post-liver transplantation patients with lamivudine-resistant hepatitis B: Final long-term results

Wait-listed (n = 226) or post-liver transplantation (n = 241) chronic hepatitis B (CHB) patients with lamivudine-resistant hepatitis B virus (HBV) were treated with adefovir dipivoxil for a median of 39 and 99 weeks, respectively. Among wait-listed patients, serum HBV DNA levels became undetectable (<l,000 copies/mL) in 59% and 65% at weeks 48 and 96, respectively. After 48 weeks, alanine aminotransferase (ALT), albumin, bilirubin, and prothrombin time normalized in 77%, 76%, 60%, and 84% of wait-listed patients, respectively. Among postransplantation patients, serum HBV DNA levels became undetectable in 40% and 65% at weeks 48 and 96, respectively. After 48 weeks, ALT, albumin, bilirubin, and prothrombin time normalized in 51%, 81%. 76%, and 56% of posttransplantation patients, respectively. Among wait-listed patients who underwent on-study liver transplantation, protection from graft reinfection over a median of 35 weeks was similar among parents who did (n = 34) or did not (n = 23) receive hepatitis B immunoglobulin (HBIg). Hepatitis B surface antigen was detected on the first measurement only in 6% and 9% of patiends who did or did not receive HBIg, respectively. Serum HBV DNA was detected on consecutive visits in 6% and 0% of patients who did or did not receive HBIg, respectively. Treatment-related adverse events led to discontinuation of adefovir dipivoxil in 4% of patients. Cumulative probabilities of resistance were 0%, 2%, and 2% at weeks 48, 96, and 144, respectively. In conclusion, adefovir dipivoxil is effective and safe at wait-listed or posttransplantation CHB patients with lamivudine-resistant HBV and prevents graft reinfection with or without HBIg. © 2007 AASLD

Adefovir dipivoxil for wait-listed and post-liver transplantation patients with lamivudine-resistant hepatitis B : final long-term results

Wait-listed (n = 226) or post-liver transplantation (n = 241) chronic hepatitis B (CHB) patients with lamivudine-resistant hepatitis B virus (HBV) were treated with adefovir dipivoxil for a median of 39 and 99 weeks, respectively. Among wait-listed patients, serum HBV DNA levels became undetectable (<1,000 copies/mL) in 59% and 65% at weeks 48 and 96, respectively. After 48 weeks, alanine aminotransferase (ALT), albumin, bilirubin, and prothrombin time normalized in 77%, 76%, 60%, and 84% of wait-listed patients, respectively. Among posttransplantation patients, serum HBV DNA levels became undetectable in 40% and 65% at weeks 48 and 96, respectively. After 48 weeks, ALT, albumin, bilirubin, and prothrombin time normalized in 51%, 81%, 76%, and 56% of posttransplantation patients, respectively. Among wait-listed patients who underwent on-study liver transplantation, protection from graft reinfection over a median of 35 weeks was similar among patients who did (n = 34) or did not (n = 23) receive hepatitis B immunoglobulin (HBIg). Hepatitis B surface antigen was detected on the first measurement only in 6% and 9% of patients who did or did not receive HBIg, respectively. Serum HBV DNA was detected on consecutive visits in 6% and 0% of patients who did or did not receive HBIg, respectively. Treatment-related adverse events led to discontinuation of adefovir dipivoxil in 4% of patients. Cumulative probabilities of resistance were 0%, 2%, and 2% at weeks 48, 96, and 144, respectively. In conclusion, adefovir dipivoxil is effective and safe in wait-listed or posttransplantation CHB patients with lamivudine-resistant HBV and prevents graft reinfection with or without HBIg