Propylene is a colorless gas with a faint petroleum like odor. It is shipped as a liquefied gas under its own vapor pressure. For transportation it may be stenched. Contact with the liquid can cause frostbite. It is easily ignited. The vapors are heavier than air. Any leak can either be liquid or vapor. It can asphyxiate by the displacement of air. Under prolonged exposure to fire or intense heat the containers may rupture violently and rocket. It is used to make other chemicals. Can cause explosion.
A mixture under confinement in a glass pressure bottle at 20 °C polymerized explosively, the polymerization probably being initiated by access of light through the clear glass container. Such alkene-sulfur dioxide co-polymerizations will not occur above a ceiling temperature, different for each alkene.
...Exposure to 6 ppm propylene for 6 hours produced 160 ng propylene oxide per gram of blood in rats... 600 ppm propylene for 8 hours produced 740 ng propylene oxide per gram of blood. Both exposure concentrations reduced nasal and liver cytochrome P450 levels (to differing degrees).
Propylene oxide is produced during the first step of propylene metabolism. Epoxidation by a reconstituted cytochrome P450LM2 system including cytochrome P450 reductase proceeded with a concomitant, stereospecific (trans to the alkyl group) hydrogen/deuterium exchange from the aqueous phase when trans-1-deuterio-propylene in H2O or propylene in D2O (pH 7.4, 4 °C) was used. Both enantiomers of propylene oxide were found after incubation (37 °C, pH 7.4) of propylene with an NADPH-regenerating system and microsomes prepared from livers of male Wistar rats (control and phenobarbital-pretreated animals) and male NMRI/HAN mice (control, phenobarbital- and benzo[a]pyrene-pretreated animals). Epoxide hydrolase activity was inhibited in those incubates which contained trichloropropylene oxide. In incubations with liver microsomes of rats, about 30% of R- and about 70% of S-enantiomer were formed, whereas with mouse microsomes the amounts of the two enantiomers were nearly equal: R, 42-55%; S, 45-58%, depending on the pretreatment.
Alkylation of DNA at the N7 position of guanine was investigated in male CBA mice exposed to atmospheric propylene or uniformly labelled (14)C-propylene. The adduct levels were related to the concentration of propylene oxide (0.88 mmol/kg bw), calculated from the rate of propylene metabolism. Immediately after exposure to 107 MBq uniformly labelled (14)C-propylene (18.1 MBq/mmol propylene) for 7 hr in a closed exposure chamber, in which the atmospheric concentration-time course was measured after injection of a single dose into the chamber atmosphere, the mice were killed and 2-hydroxypropyl-DNA adducts were measured. The values were: liver, 3000 pmol/g DNA; kidney, 3000 pmol/g DNA; and spleen, 2000 pmol/g DNA.
... Exposure to 6 ppm propylene for 6 hours produced 160 ng propylene oxide per gram of blood in rats... 600 ppm propylene for 8 hours produced 740 ng propylene oxide per gram of blood. Both exposure concentrations reduced nasal and liver cytochrome P450 levels (to differing degrees).
IDENTIFICATION AND USE: Propylene is a colorless gas. It is used in manufacture of isopropyl alcohol, polypropylene, synthetic glycerol, acrylonitrile, propylene oxide, heptene, cumene, polymer gasoline, acrylic acid, vinyl resins, oxo chemicals. It is also used as aerosol propellant and component. Formerly used in dental surgery as temporary anesthetic. HUMAN STUDIES: In the gaseous state propylene is not irritating to the skin or eyes based on limited human studies. However, should skin or eye contact occur to this chemical in its liquid state, tissue freezing, severe cold burn, and/or frostbite may result. ANIMAL STUDIES: No adverse effects were observed in repeated dose inhalation toxicity studies in rodents at concentrations up to 10,000 ppm propylene, for 14 weeks. Furthermore, there was no evidence of carcinogenicity in rats or mice exposed to propylene concentrations as high as 10,000 ppm for up to 103 weeks. Inflammation of the nasal cavity was the only indication of toxicity observed following exposure of male rats to 5,000 and 10,000 ppm propylene and female rats exposed to 10,000 propylene for 103 weeks. These effects were not observed when rats were exposed to similar concentrations for 14 weeks. Mutagenic activity was observed in a single bacterial strain in the Ames assay in the presence of metabolic activation. Inhalation exposure of pregnant Wistar rats to propylene from implantation to one day prior to the expected day of parturition (days 6-19 p.c.) elicited no maternal toxicity, prenatal or developmental toxicity, or teratogenicity at all tested concentrations up to 10,000 ppm.
Evaluation: There is inadequate evidence in humans for the carcinogenicity of propylene. There is inadequate evidence in experimental animals for the carcinogenicity of propylene. Overall evaluation: Propylene is not classifiable as to its carcinogenicity to humans (Group 3).
Accumulation is /unlikely/ because of rapid removal from the body. ... A direct chemical interaction between propylene and biological media of the body is /also/ unlikely. Elimination occurs rapidly in an unaltered form through the lungs.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
丙烯吸入的药代动力学已经在雄性Sprague-Dawley大鼠和CBA小鼠在封闭暴露室中进行研究，其中在向室内空气中注入单剂量后，测量了大气浓度-时间过程。研究发现大鼠体内丙烯的吸收较低。由于吸收导致的清除，反映了丙烯从大气中转移到生物体中的速率，对于一只体重250克的大鼠，清除率为19毫升/分钟。这个值仅代表肺泡通气量（117毫升/分钟）的16%。吸入肺部的丙烯大部分又被呼出，没有进入血液成为全身可利用的物质。同一大鼠体内丙烯的最大积累，以整体动物：空气的热力学分配系数（Keq=Conc.animal/Conc.air）来衡量，仅为1.6。在浓度低于50 ppm[86 mg/m³]时，稳态下整体动物：空气中的浓度比甚至更小（0.7），这是由于代谢消除。在这些浓度下，发现了第一级动力学，并且相对于大气中的浓度，由于代谢导致的清除率在250克大鼠中计算为11毫升/分钟。因此，在稳态下，大约58%全身可利用的丙烯通过代谢消除，42%以未改变的物质通过呼出消除。对于小鼠尚未发布相应的数据。在大鼠和小鼠中，丙烯的代谢速率显示出饱和动力学，最大代谢速率（Vmax）分别为0.17 umol/(min x 250 g bw)[1.7 mg/(hr x kg bw)]和8 mg/(hr x kg bw)，Vmax/2的大气浓度分别为260 ppm（447 mg/m³）和800 ppm（1376 mg/m³）。
The pharmacokinetics of inhaled propylene have been investigated in male Sprague- Dawley rats and CBA mice in closed exposure chambers, in which the atmospheric concentration-time course was measured after injection of a single dose into the chamber atmosphere. The uptake of propylene into the body of rats has been found to be low. Clearance due to uptake, reflecting the rate of transfer of propylene from the atmosphere into the organism, was 19 mL/min for one rat weighing 250 g. This value represents only 16% of the alveolar ventilation (117 mL/min). Most propylene inhaled into the lungs is exhaled again and does not reach the blood to become systemically available. Maximal accumulation of propylene in the same rat, determined as the thermodynamic partition coefficient for whole body:air (Keq=Conc.animal/Conc.air), was only 1.6. At concentrations below 50 ppm [86 mg/cu m], the concentration ratio at steady-state whole body:air was even smaller (0.7), owing to metabolic elimination. At these concentrations, first-order kinetics were found, and clearance due to metabolism in relation to the concentration in the atmosphere was calculated to be 11 mL/min for a 250-g rat. Thus, at steady state, about 58% of systemically available propylene is eliminated metabolically and 42% is eliminated by exhalation as the unchanged substance. No corresponding data have been published for mice. In rats and mice, the rate of propylene metabolism showed saturation kinetics, with maximal metabolic rates (Vmax) of 0.17 umol/(min x 250 g bw) [1.7 mg/(hr x kg bw)] and 8 mg/(hr xkg bw) and atmospheric concentrations at Vmax/2 of 260 ppm (447 mg/cu m) and 800 ppm (1376 mg/cu m), respectively.
A physiological toxicokinetic (PT) model was developed for inhaled propylene gas (PE) in mouse, rat, and human. Metabolism was simulated to occur in the liver (90%) and in the richly perfused tissue group (10%). The partition coefficients tissue:air were determined in vitro using tissues of mice, rats, and humans. Most of the tissues have partition coefficients of around 0.5. Only adipose tissue displays a 10 times higher value. The partition coefficient blood:air in human is 0.44, about half of that in rodents. PE can accumulate in the organism only barely. For male B6C3F1 mice and male Fischer 344/N rats, parameters of PE metabolism were obtained from gas uptake experiments. Maximum rates of metabolism (V(maxmo)) were 110 umol/hr/kg in mice and 50.4 umol/hr/kg in rats. V(maxmo)/2 was reached in mice at 270 ppm and in rats at 400 ppm of atmospheric PE. Pretreatment of the animals with sodium diethyldithiocarbamate resulted in an almost complete inhibition of PE metabolism in both species. Preliminary toxicokinetic data on PE metabolism in humans were obtained in one volunteer who was exposed up to 4.5 hr to constant concentrations of 5 and 25 ppm PE. The PT model was used to calculate PE blood concentrations at steady state. At 25 ppm, the blood values were comparable across species, with 0.19, 0.32, and 0.34 umol/L for mouse, rat, and human, respectively. However, the corresponding rates of PE metabolism differed dramatically, being 8.3, 2.1, and 0.29 umol/hr/kg in mouse, rat, and human. For a repeated human exposure to 25 ppm PE in air (8 hr/day, 5 days/wk), PE concentrations in venous blood were simulated. The prediction demonstrates that PE is eliminated so rapidly that it cannot accumulate in the organism. For low exposure concentrations, it became obvious that the rate of uptake into blood by inhalation is limited by the blood flow through the lung and the rate of metabolism is limited by the blood flow through the metabolizing organs.
