By National Research Council, Division on Engineering and Physical Sciences, Board on Environmental Studies and Toxicology, Committee on Toxicology, Subcommittee on Acute Exposure Guideline Levels
This file reports files on acute publicity instruction degrees (AEGLs) for nerve brokers GA (tabun), GB (sarin), GD (soman), GD, and VX, sulfur mustard, diborane, and methyl isocyanate. The records have been constructed by way of the nationwide Advisory Committee on Acute publicity instruction degrees for harmful chemical substances (NAC). The subcommittee concludes that the AEGLs built in these records are scientifically legitimate conclusions according to facts reviewed by means of NAC and are in step with the NRC stories on constructing acute publicity guide levels.
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Additional info for Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 3
Over GD 7-19, mean maternal body-weight gain was reduced in dams exposed to DMF at 150 ppm compared with controls, and dams in the 450-ppm group lost weight. Mean maternal body-weight gain over the entire study period of GD 0-29 was also decreased in dams from the 150- and 450-ppm groups compared with controls. Developmental toxicity was evident in the 450-ppm group because of significant reductions in mean fetal body weight compared with weight in the concurrent controls and significant increases in the litter incidence of total external malformations, total skeletal variations, and total malformations (external, soft tissue, and skeletal combined).
1. Acute Lethality No acute lethality data in humans were found in the searched literature. 2. 1. Controlled Exposures DMF has a faint amine odor (Budavari et al. 1996). 47 to 100 ppm (EPA 1992). 47-ppm concentration was the threshold for recognition; no data were provided for the 100-ppm concentration. Trochimowicz et al. 2 ppm; they stated that less than 50% of distracted individuals could perceive odor at the Threshold Limit Value (TLV) of 10 ppm. 2. The studies were conducted to assess metabolism, and no adverse effects of inhaled DMF exposure were reported at the concentrations and durations of exposure examined.
1998; McCarver et al. 1998), and increased CYP2E1 levels increase the toxic metabolites of DMF; (2) prior consumption of ethanol can exacerbate DMF toxicity in individuals; (3) on the basis of the proposed mechanism of action, detoxification of the reactive intermediate is partly dependent on conjugation with glutathione; therefore, if glutathione levels are depleted for other reasons, the potential exists for greater exposure to the reactive intermediate; and (4) because DMF exposure can result in hepatotoxicity, individuals with chronic liver disease may be at increased risk.