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|AMPA:||#x3b1;-amino-5-hydroxy-3-methyl-4-isoxazole propionic acid|
|CA1:||cornu ammonis 1|
|cGMP:||cyclic guanosine monophosphate|
|DIV:||days in vitro|
|GFP:||green fluorescent protein|
|GluR2:||glutamate receptor R2|
|MAPK:||mitogen-activated protein kinase|
|nNOS:||neuronal nitric oxide synthase|
|Rac1:||Ras-related C3 botulinum toxin substrate 1|
|SK3 channel:||small-conductance calcium-activated potassium channel|
|TBS:||electrical theta-burst stimulation|
|TM-agrin:||transmembrane form of agrin.|
|Modifying factor: Not applicable.|
|Animal to human dosimetric adjustment: Not applied. As noted, the cardiac sensitization model with the dog heart is considered a good model for humans.|
|Time scaling: Not applied. Cardiac sensitization is an exposure and blood concentration related threshold effect. Several studies have shown that blood concentrations of halocarbons do not increase greatly with time after 15 #x02013;55 min of exposure, and exposure duration did not influence the concentration at which the effect occurred.|
|Data adequacy: The study was well conducted and documented. Supporting data include both human and animal studies. Animal studies covered acute, subchronic, and chronic exposure durations and addressed systemic toxicity as well as neurotoxicity, reproductive and developmental effects, cardiac sensitization, genotoxicity, and carcinogenicity. Other effects in animal studies occurred at much higher concentrations or with repeated exposures; the latter are not relevant for setting short-term exposures. No deaths occurred in several species of animals exposed for various periods of time to concentrations less than those requiring supplemental oxygen (approximately 700,000 ppm).|
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