1,1-Difluoroethylene (or vinylidene fluoride) is a colorless gas which is flammable in the ranges of 5.5 to 21%. It is toxic by inhalation and contact. It is slightly soluble in water and soluble in alcohol and ether. Under prolonged exposure to fire or intense heat the containers may rupture violently and rocket.
颜色/状态：
Colorless gas
气味：
Nearly odorless
闪点：
Flammable gas
溶解度：
Water solubility = 6.3 cu cm/100 g at 25 °C and 10 kPa
In 10.3 L closed containers with oxygen replenishment and carbon dioxide removal, and stocked with 3 rats, the rates of Vinylidene fluoride metab was 1% that of vinyl chloride.
Metabolism proceeded very slowly and was saturable at exposure concentrations of about 260 mg/cu m (100 ppm). The maximal metabolic rate was 1% that of vinyl chloride and less than 20% that of vinyl fluoride. Exposure of rats to vinylidene fluoride has been reported to result in some increase in the urinary excretion of fluoride.
Like other halogenated C1 and C2 compounds that are biotransformed to reactive metabolites, vinylidene fluoride causes changes in rat intermediary metabolism which lead to increased exhalation of acetone.
No epidemiological data relevant to the carcinogenicity of vinylidene fluoride were available. There is inadequate evidence for the carcinogenicity of vinylidene fluoride in experimental animals. Overall evaluation Vinylidene fluoride is not classifiable as to its carcinogenicity to humans (Group 3).
IARC Monographs:Volume 39: (1986) Some Chemicals Used in Plastics and Elastomers
Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)
Volume 71: (1999) Re-evaluation of Some Organic Chemicals, Hydrazine and Hydrogen Peroxide (Part 1, Part 2, Part 3)
来源:International Agency for Research on Cancer (IARC)
Inhalation comparatively studied. Metabolic elimination was saturable, dose-dependent process. Elimination determined by zero-order law at atmospheric concn above point of saturation, and otherwise by normal first-order kinetics.
... Concentrations of vinylidene fluoride were measured in blood of /B6C3F1/ mice during 6 hr exposures to nominal concentrations of 250, 3750 or 15,000 ppm vinylidene fluoride. A physiological model developed to simulate blood levels of /this cmpd/ in rats was adapted for mice by incorporating physiologically realistic parameters for mice where appropriate ( alveolar ventilation, cardiac output, blood flow to organs, and organ volumes) and by assuming that chemical specific parameters such as tissue/blood partition coefficients determined for rats could also be applied to mice. Measured steady state levels of vinylidene fluoride in blood of mice increased with increasing exposure concn. For both the 15,000 and 3750 ppm vinylidene fluoride exposures, the experimentally determined data fell within the 95% confidence interval predicted by the physiological model. For the 250 ppm vinylidene fluoride exposure, the experimentally determined values /for this cmpd/ in blood were lower than what was predicted by the model. Model predictions indicated that for mice, as observed for rats, levels of vinylidene fluoride would rise very rapidly, reaching steady state within minutes of exposure, and that at the end of exposure, blood levels will decline rapidly. At the two lowest concn, ... no vinylidene fluoride /could be detected/ in blood taken 15 min or longer after cessation of exposure, suggesting that the post exposure levels were at or below the limit of detection which was 4 ug/vinylidene fluoride/ml blood. For the 15,000 ppm exposure vinylidene fluoride could be detected in blood up to 15 min post exposure.
A physiological model was developed to describe the uptake of vinylidene fluoride in male F344/N rats exposed /to the cmpd/ for 6 hr at a concentrations ranging from 27 to 16,000 ppm in a nose only exposure system. The steady state concn of vinylidene fluoride in blood increased linearly with increases in the exposure concn. ... Rise to steady state concentrations was rapid, occurring within 15 min. Rapid decreases following the end of exposures were also noted. Vinylidene fluoride had very limited solubility in tissues with varying lipid and aqueous content. Predictions based on the model developed indicate that while the total amount of /cmpd/ metabolized increased with increasing exposure concn, this increase was not linearly related to exposure concn. Even though the blood levels of vinylidene fluoride increased linearly with increasing concn, the amount of vinylidene fluoride metabolized per 6 hr exposure approached a maximum at about 2000 ppm.
Defluorination and cytochrome p450 loss induced by fluoroethenes and fluorochloroethenes were studied in vitro. Hepatic microsomes were isolated from male Sprague-Dawley rats, some of which had been pretreated with sodium phenobarbital or beta-naphthoflavone. These were incubated with 1,1-difluoroethene, 2-chloro-1,1-difluoroethene, trifluoroethene or trifluorochloroethene. The effects of structure on fluoride release and cytochrome p450 and heme loss were investigated. Near maximal release of fluoride occurred in microsomes from phenobarbital treated rats. The greatest release occurred with 2-chloro-1,1-difluoroethene, followed by trifluorochloroethene, trifluoroethene and 1,1-difluoroethene in that order. The amounts of fluoride released were 2.4 to 4 times that released from untreated microsomes. beta-Naphthoflavone caused a slight inhibition of fluoride release from all compounds, relative to microsomes from untreated rats. Trifluoroethene caused the greatest loss of cytochrome and heme from microsomes, followed by 2-chloro-1,1-difluoroethene, trifluoroethene, and 1,1-difluoroethene in that order. /Results indicate/ that fluoroethenes and chloroethenes are cytochrome p450 substrates that effectively inactivate cytochrome p450 isozymes. The ability to undergo these reactions, however, depends on the degree and nature of their halogen substituents.
