By National Research Council, Division on Earth and Life Studies, Board on Environmental Studies and Toxicology, Committee on Toxicology, Committee on Spacecraft Exposure Guidelines
NASA keeps an energetic curiosity within the environmental stipulations linked to dwelling and dealing in spacecraft and making a choice on risks that may adversely impact the healthiness and wellbeing and fitness of team individuals. regardless of significant engineering advances in controlling the spacecraft atmosphere, a few water and air illness is inevitable. numerous hundred chemical species usually are present in the closed setting of the spacecraft, and because the frequency, complexity, and period of human house flight elevate, settling on and realizing major health and wellbeing dangers becomes extra complex and extra severe for the good fortune of the missions.
To safeguard house crews from contaminants in potable and hygiene water, NASA asked that the nationwide learn Council NRC supply tips on tips on how to advance water publicity directions and for this reason evaluation NASA's improvement of the publicity guidance for particular chemical compounds. This publication offers spacecraft water publicity instructions (SWEGs) for antimony, benzene, ethylene glycol, methanol, methyl ethyl ketone, and propylene glycol.
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This trend had disappeared by 3 wk of treatment. In contrast, treatment of male B6C3F1 mice by gavage in corn oil at somewhat lower daily doses produced marked nephropathy. Larson et al. (1994c) found a dose-related acute tubular necrosis in the kidneys of male B6C3F1 mice after 4 d of treatment by gavage with chloroform at 0, 34, 90, 138, or 277 mg/kg/d in corn oil. After 3 wk of dosing, regenerating tubules were observed in the lower dose groups, while mice treated with 277 mg/kg/d had severe nephropathy characterized by degeneration, necrosis, and regeneration affecting all the proximal tubules.
1974b). Experimental depletion of hepatic GSH by pretreatment with diethyl maleate also resulted in centrilobular necrosis after exposure to chloroform (Brown et al. 1974b). In cytotoxicity studies at CIIT, freshly isolated hepatocytes cultured from B6C3F1 mice and F-344 rats were exposed to solutions of chloroform for up to 3 h. Concentration-dependent cytotoxicity (lactate dehydrogenase release) was seen in culture at concentrations higher than 1 millimolar (mM) (Ammann et al. 1998). Co-treatment with the cytochrome P-450 inhibitor 1-phenylimidazole prevented both cytolethality and GSH depletion, indicating that metabolism is necessary for chloroform-induced cytotoxicity.
3, 2, 10, 30, and 90 ppm for 6 h/d, 7 d/wk, for up to 13 wk and proposed that this should also be a NOAEL for liver cancer in female B6C3F1 mice. In other words, chloroform carcinogenicity should have a threshold if tumorigenesis is dependent on regenerative cell proliferation. This proposal was challenged in a 1998 study by Melnick et al. , tumorigenesis is not dependent on regenerative cell proliferation at low doses) and assert that this is therefore true for chloroform also (Melnick et al. 1998).