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EC number: 433-480-9 | CAS number: 623-53-0
Short description of key information on bioaccumulation potential result: Single oral administration to rats at 5000 mg/kg rapidly produced signs of lethargy, ataxia, hunched posture, disturbed respiration etc. (evident from 1 hour post-dose) but these proved transient, resolving by day 2 post-dose. Acute inhalation exposure of rats at 17.6 mg/l produced similarly rapid onset of transient reactions (disturbed respiration, hunched posture, piloerection) which had resolved by day 2 post-exposure.An acute oral toxicity study of the close analogue diethyl carbonate also found rapid-onset but transient signs of sedation, which the investigators speculated might be related to metabolic conversion of the test substance to ethanol. In an oral subacute toxicity test of methyl ethyl carbonate, rats dosed at 1000 mg/kg/day showed no signs of adverse reaction (males) or only hunched posture plus cases of transient, post-dose salivation (females). No clear evidence of toxicity and no effects in body tissues/organs were seen.The close analogue diethyl carbonate also showed low repeat-dose toxicity: in a chronic mouse toxicity/carcinogenicity study, 1000 ppm in drinking water (approximately equal to 140 mg/kg/day) proved to be the NOAEL.The close analogue dimethyl carbonate is said to be hydrolysed to methanol and carbon dioxide. Also, it is known that organic carbonates are a substrate for liver esterases, leading to hydrolysis and release of carbon dioxide (e.g. action of porcine liver esterase on diphenyl carbonate, described in various publications including US Patent 4892811, 1990).
The evidence of rapid-onset signs of sedation and/or ataxia, disturbed respiration, etc. following acute exposure in rats suggests significant absorption may occur but the subsequent early recoveries, plus indications of low subacute or chronic toxicity, suggest significant metabolic detoxification. This is compatible with a hypothesis of hydrolysis to ethanol and methanol and carbon dioxide mediated by hepatic enzymes (e.g. esterases), with subsequent bioelimination via normal metabolic and excretory pathways.
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