Soluble in acetone, ethanol, chloroform, ether (U.S. EPA, 1985), and other organic solvents
including bromoform, carbon tetrachloride, methylene chloride, trichloroethylene, and tetrachloroethylene.
Trichloroethylene appears as a clear colorless volatile liquid having a chloroform-like odor. Denser than water and is slightly soluble in water. Noncombustible. Used as a solvent, fumigant, in the manufacture of other chemicals, and for many other uses.
... We collected urine from Hartley male and female guinea pigs 24 hours after intracutaneous injection of trichloroethylene (TRI), trichloroethanol (TCE) or trichloroacetic acid (TCA) during a guinea pig maximization test and measured the urinary metabolites by gas chromatography-mass spectrometry. After TRI treatment, the amount of TCA was significantly greater in females than males, while there was no sex difference in the total amount (TCA + TCE). TCA was only detected in urine after TCA treatment. Interestingly, not only TCE but also TCA was detected in urine of both sexes after TCE treatment, and the amount of TCA was also greater in females than males. An additional experiment showed that TCE treatment did not result in the detection of urinary TCA in cytochrome P450 (CYP)2E1-null mice TCE but did in wild-type mice, suggesting the involvement of CYP2E1 in the metabolism from TCE to TCA. The constitutive expression of CYP2E1 in the liver of guinea pigs was greater in females than males. The sex difference in urinary TCA excretion after TRI and TCE treatments may be due to variation of the constitutive expression of CYP2E1.
Toxicological interactions with drugs have the potential to modulate the toxicity of trichloroethylene (TCE). Our objective is to identify metabolic interactions between TCE and 14 widely used drugs in human suspended hepatocytes and characterize the strongest using microsomal assays. Changes in concentrations of TCE and its metabolites were measured by headspace GC-MS. Results with hepatocytes show that amoxicillin, cimetidine, ibuprofen, mefenamic acid and ranitidine caused no significant interactions. Naproxen and salicylic acid showed to increase both TCE metabolites levels, whereas acetaminophen, carbamazepine and erythromycin rather decreased them. Finally, diclofenac, gliclazide, sulphasalazine and valproic acid had an impact on the levels of only one metabolite. Among the 14 tested drugs, 5 presented the most potent interactions and were selected for confirmation with microsomes, namely naproxen, salicylic acid, acetaminophen, carbamazepine and valproic acid. Characterization in human microsomes confirmed interaction with naproxen by competitively inhibiting trichloroethanol (TCOH) glucuronidation (Ki=2.329 mM). Inhibition of TCOH formation was also confirmed for carbamazepine (partial non-competitive with Ki=70 uM). Interactions with human microsomes were not observed with salicylic acid and acetaminophen, similar to prior results in rat material. For valproic acid, interactions with microsomes were observed in rat but not in human. Inhibition patterns were shown to be similar in human and rat hepatocytes, but some differences in mechanisms were noted in microsomal material between species. ...
... In this study we have compared the renal toxicity of TCE and /its major metabolite trichloroethanol/ (TCE-OH) in rats to try and ascertain whether the glutathione pathway or formic aciduria can account for the toxicity. Male rats were given TCE (500 mg/kg/day) or TCE-OH at (100 mg/kg/day) /by oral gavage/ for 12 weeks and the extent of renal injury measured at several time points using biomarkers of nephrotoxicity and prior to termination assessing renal tubule cell proliferation. The extent of formic aciduria was also determined at several time points, while renal pathology and plasma urea and creatinine were determined at the end of the study. TCE produced a very mild increase in biomarkers of renal injury, total protein, and glucose over the first two weeks of exposure and increased Kim-1 and NAG in urine after 1 and 5 weeks exposure, while TCE-OH did not produce a consistent increase in these biomarkers in urine. However, both chemicals produced a marked and sustained increase in the excretion of formic acid in urine to a very similar extent. The activity of methionine synthase in the liver of TCE and TCE-OH treated rats was inhibited by about 50% indicative of a block in folate synthesis. Both renal pathology and renal tubule cell proliferation were reduced after TCE and TCE-OH treatment compared to controls. Our findings do not clearly identify the pathway which is responsible for the renal toxicity of TCE but do provide some support for metabolism via glutathione conjugation.
Extraplacental membranes define the gestational compartment and provide a barrier to infectious microorganisms ascending the gravid female reproductive tract. We tested the hypothesis that bioactive metabolites of trichloroethylene (TCE) decrease pathogen-stimulated innate immune response of extraplacental membranes. Extraplacental membranes were cultured for 4, 8, and 24 hr with the TCE metabolites trichloroacetate (TCA) or S-(1,2-dichlorovinyl)-l-cysteine (DCVC) in the absence or presence of lipoteichoic acid (LTA) or lipopolysaccharide (LPS) to simulate infection. In addition, membranes were cocultured with DCVC and Group B Streptococcus (GBS). DCVC (5-50 uM) significantly inhibited LTA-, LPS-, and GBS-stimulated cytokine release from tissue cultures as early as 4 hr (P </= 0.05). In contrast, TCA (up to 500 uM) did not inhibit LTA-stimulated cytokine release from tissue punches. Because cytokines are important mediators for host response to infectious microorganisms these findings suggest that TCE exposure could potentially modify susceptibility to infection during pregnancy.
IDENTIFICATION AND USE: Trichloroethylene (TCE) is a colorless liquid (unless dyed blue). The major use of TCE is in metal cleaning or degreasing. TCE was used earlier as an extraction solvent for natural fats and oils, such as palm, coconut and soya bean oils. It was also an extraction solvent for spices, hops and the decaffeination of coffee. The United States Food and Drug Administration banned these uses of trichloroethylene. Its use in cosmetic and drug products was also discontinued. It was also used as both an anesthetic and an analgesic in obstetrics. HUMAN EXPOSURE AND TOXICITY: Potential symptoms of overexposure are headache, vertigo, visual disturbance, fatigue, giddiness, tremors, somnolence, nausea and vomiting, irritation of eyes and skin, dermatitis, cardiac arrhythmias, paresthesia, liver injury. Death has occurred at very high concentrations (10,000 ppm) and was associated with cardiac arrhythmia and massive liver damage. Workers chronically exposed to levels between 38 and 172 ppm reported symptoms of sleepiness, dizziness, headache, and nausea, but no apparent trigeminal nerve disorders. In a study of Dutch workers regularly exposed to no more than 35 ppm, investigators found no trigeminal nerve impairment as measured by blink reflex, but did observe a significant association between years of exposure and masseter reflex, which is another measure of trigeminal nerve function. Increased micronucleus frequency is associated with occupational TCE exposure. TCE exerts genotoxic effects in HepG2 cells. In Tier I cancer incidence cohort studies, TCE exposure was associated with an increased risk of kidney cancer. Liver cancer incidence was elevated in most of the Tier I cancer incidence studies. Maternal residential proximity to industrial emissions of chlorinated solvents might be associated with selected birth defects in offspring, especially among older mothers. ANIMAL STUDIES: Studies on the longer-term toxicity of TCE in rats and mice exposed orally and by inhalation showed consistent increases in relative liver weight and associated histopathological and biochemical changes. The effects described in kidney included increased relative weights in mice exposed continuously to > 75 ppm (> 390 mg/cu m) TCE for 30 days and renal dysfunction in the absence of marked histopathological changes in rats exposed to > 50 ppm (> 260 mg/cu m) for 12 weeks. In rats exposed to TCE by gavage (50 or 250 mg/kg, once daily, 4 to 5 days/week for 52 weeks) there was a dose-related increase in the incidence of leukemia (immunoblastic lymphosarcomas) in males. No increase was noted in the tumor incidence of females. In TCE exposed rat and mice (7 hours/day, 5 days/week for 104 weeks at 50, 150, or 450 ppm), tumors were found mainly in the hematopoietic system, lungs, and mammary glands of mice and in the pituitary and mammary glands of rats. Administration of TCE in the diet of mice and rats at concentrations equivalent to doses of up to 300 mg/kg bw per day for two generations resulted in marginal effects on testicular weight and on survival of pups of both the F1 and F2 generations at the highest dose. In general, TCE and most of its major metabolites are not potent genotoxicants in a broad range of bacterial, lower eukaryotic, and in vitro and in vivo mammalian test systems. In mammalian cell-culture studies, TCE did not induce chromosomal aberrations in Chinese hamster ovary (CHO) cells, unscheduled DNA synthesis in rat hepatocytes, but it did induce sister chromatid exchange in CHO cells, gene mutations in mouse lymphoma cells, and morphological transformation of rat embryo cells. In rodent in vivo studies, TCE did not induce unscheduled DNA synthesis, sister chromatid exchange, dominant lethal mutations, or chromosomal aberrations. TCE gave mixed results for DNA single-strand breaks or alkali-labile sites in mouse liver and positive results for micronucleus formation in mice. ECOTOXICITY STUDIES: TCE had effects on genes and proteins related to metabolism, reproduction, and growth in D. magna. Exposure of goldfish (Carassius auratus) to 0.1 mg/L TCE for >/= 60 days in a static-renewal test resulted in significantly reduced body weight and altered histopathology. Affected fathead minnows, 31 days old, in toxicant concentrations ranging from 8.43-77.3 mg/L, lost schooling behavior, swam in a corkscrew/spiral pattern near the surface, were hyperactive and hemorrhaging. TCE induced chlorosis (bleaching of needles), necrosis (death of needles), and premature needle loss over 2 decades in fir (Abies alba), Norway spruce (Picea abies), beech (Fagus silvatica), and other tree species.
The toxic and carcinogenic effects of trichloroethylene are believed to be caused mainly by its metabolites, including trichloroacetic acid, dichloroacetic acid, and chloral hydrate. The nephrotoxicity and nephrocarcinogenicity of TRI have been attributed to glutathione conjunction, which forms reactive, sulfur-containing metabolites. Dichloroacetic acid is known to inhibit pyruvate dehydrogenase kinase, while chloral hydrate inhibits alcohol dehydrogenase. Studies in rodents have shown that neurotoxic effects may be caused by trichloroethylene's incorporation into brain membranes or ability to alter the fatty acid pattern of brain phospholipids and amino acids. One of the mechanisms of trichloroethylene's carcinogenicity is believed to be the peroxisome proliferation induced by its metabolites. (L14, T12, A46)
Overall Evaluation: Group 1: Carcinogenic to humans. Based on sufficient epidemiological evidence for cancer of the kidney, with strong mechanistic support from studies in experimental animals and exposed humans. The epidemiological data also identified limited evidence for an association with liver cancer and non-Hodgkin lymphoma. The Working Group also noted that the data for trichloroethylene are very informative with regard to demonstrating tumor-site concordance between humans and experimental animals; several rare cancers were observed in animals in the absence of common "background" tumors.
Blood and urine samples were collected in 1990 from 10 people working in four dry cleaning shops in Croatia, where trichloroethylene was used as the cleaning solvent. The concentration of trichloroethylene in the air was 25-40 ppm [134-215 mg/cu m]. The mean blood levels of trichloroethylene were 0.38 umol/L [50 ug/L] on Monday morning (range, 0.15- 3.58 umol/L) (20-70 ug/L) and 3.39 umol/L [445 ug/L] on Wednesday afternoon (range, 0.46- 12.71 umol/L (60-1670 ug/L]. ...
TCE is rapidly absorbed into the systemic circulation via the oral and inhalation routes. The majority of TCE undergoes oxidation in the liver by CYPs, with a small proportion being conjugated with glutathione (GSH) via glutathione S-transferases (GSTs). Thus, two distinct metabolic pathways exist for TCE. ... TCE may be oxidized to yield one of three initial metabolites: chloral, TCE-epoxide, and dichloroacetylchloride. These metabolites rapidly undergo oxidation and/or reduction to yield trichloroacetate (TCA) and trichloroethanol (TCOH), the major end products of the oxidative pathway. TCOH is either oxidized to TCA or glucuronidated. TCOH glucuronide is excreted via the urine and bile. That in the bile may undergo enterohepatic recirculation by hydrolysis to TCOH in the gut, with reabsorption and the possibility of conversion to TCA. TCA accumulates in the body due to strong plasma protein binding and slow excretion. In contrast, blood levels of DCA, formed by TCA dechlorination or from TCOH, are very low or nondetectable in humans. Relatively small amounts of TCE can be conjugated in the liver with GSH to form S-(1,2-dichlorovinyl)glutathione (DCVG). DCVG is then effluxed from the hepatocyte into plasma and bile for translocation to the kidney and small intestine, respectively. The plasma DCVG is intrarenally converted by gamma-glutamyltransferase and dipeptidases to the cysteine conjugate S-(1,2-dichlorovinyl)-L-cysteine (DCVC). The DCVG secreted into the bile can undergo extrarenal processing to DCVC, that is subsequently delivered to the kidney by enterohepatic recirculation. DCVC represents a branch point in the pathway. It may be detoxified through N-acetylation or bioactivated to reactive thiols via renal beta-lyase located in renal proximal tubular cells (or to a lesser extent, bioactivated to DCVC sulfoxide via flavin-containing monooxygenases).
TCE is rapidly and extensively absorbed by all routes of environmental exposure, including oral ingestion, inhalation and skin contact. Absorbed TCE is distributed throughout the body, where it can accumulate in fat and other tissues.
... The pharmacokinetics of trichloroethylene (TCE) in male Sprague-Dawley (S-D) rats were characterized (1) during and after inhalation exposure to 50 or 500 ppm TCE, (2) following administration of 8 mg/kg TCE PO, and (3) following intra-arterial injection of 8 mg/kg TCE. Blood and tissues (including liver, kidney, fat, skeletal muscle, heart, spleen, gastrointestinal tract, and brain) were collected at selected time-points from 5 min up to 24 hr post initial exposure. The fat compartment was modified to be diffusion-limited to predict the observed slow release of TCE from the fat. The addition of a deep liver compartment was necessary to accurately predict the slower hepatic clearance of TCE for all three exposure routes. Simulations of liver concentrations following gavage of male B6C3F1 mice with 300-2000 mg/kg TCE were also improved with the addition of a deep liver compartment. Liver predictions were calibrated and validated using a cross-validation technique novel to PBPK modeling. Splitting of compartments did not significantly affect predictions of TCE concentrations in the liver, fat, or venous blood. ...
[EN] CATALYST AND PROCESS USING THE CATALYST FOR MANUFACTURING FLUORINATED HYDROCARBONS<br/>[FR] CATALYSEUR ET PROCÉDÉ UTILISANT LE CATALYSEUR POUR LA FABRICATION D'HYDROCARBURES FLUORÉS
申请人：MEXICHEM FLUOR SA DE CV
公开号：WO2018046928A1
公开（公告）日：2018-03-15
A catalyst comprising chromia and at least one additional metal or compound thereof and wherein the catalyst has a total pore volume of greater than 0.3 cm3/g and the mean pore diameter is greater than or equal to 90 Å, wherein the total pore volume is measured by N2 adsorption porosimetry and the mean pore diameter is measured by N2 BET adsorption porosimetry, and wherein the at least one additional metal is selected from Li, Na, K, Ca, Mg, Cs, Sc, Al, Y, Ti, Zr, Hf, V, Nb, Ta, Cr, Mo, W, Mn, Re, Fe, Ru, Co, Rh, Ir, Ni, Pd, In, Pt, Cu, Ag, Au, Zn, La, Ce and mixtures thereof.
Halocarbon Encapsulation via Halogen···π Interactions in a Bispyrazole-Based Cryptand
作者：Ashish Verma、Kapil Tomar、Parimal K. Bharadwaj
DOI：10.1021/acs.cgd.8b01471
日期：2019.1.2
structures clearly revealed that halogen bonding (C–Cl/Br···π (pyrazole)) and hydrogen bonding (C–H···π(pyrazole)) interactions played a key role in stabilizing the halogenated guests inside the hydrophobic cavity of cryptand. At the same time, the cage is efficiently able to exclude hydrophilic solvent molecules, like, water and methanol, suggesting the hydrophobic nature of the cavity. Due to the comparably
一种新的基于bispyrazole膨胀穴状配体经由具有160埃的内部腔体的席夫碱缩合反应合成3用疏水性性质。穴状分子具有富电子的多个吡唑环，可增强与客体分子的弱非共价相互作用。研究了穴状配体的主客体能力，用于包封最不活泼的卤素键供体分子（具有较小的σ孔大小），即CH 2 Cl 2，CHCl 3，CCl 4，C 2 HCl 3，C 2 H 4 Cl 2和C 2 H 4 Br 2。晶体结构分析清楚地表明，卤素键（C–Cl / Br··π（吡唑））和氢键（CH–··π（吡唑））的相互作用在稳定卤代物内部起着关键作用。穴状的疏水腔。同时，该笼子能够有效地排除亲水性溶剂分子，例如水和甲醇，表明该腔体具有疏水性。由于C 2 H 4 Br 2中的σ孔相对较大，因此它显示出与主体穴体最强的卤素键相互作用，而CH 2 Cl 2的相互作用最弱。σ孔尺寸最小的宾客。此外，穴状体能够根据客人的大小调节其中央腔。对于C
Flash Chemistry Using Trichlorovinyllithium: Switching the Reaction Pathways by High-resolution Reaction Time Control
作者：Aiichiro Nagaki、Yusuke Takahashi、Andrea Henseler、Chika Matsuo、Jun-ichi Yoshida
DOI：10.1246/cl.140980
日期：2015.2.5
High-resolution reaction time control in flow microreactors enables the reaction-pathway switching of trichlorovinyllithium generated by the H/Li exchange of trichloroethene. The method was successfully applied to the synthesis of 1,1,2-trichloroalkenes, 1-chloroalkynes, and unsymmetrically disubstituted ethynes.
Synthesis and Singlet Oxygen Reactivity of 1,2-Diaryloxyethenes and Selected Sulfur and Nitrogen Analogs
作者：Gregory Nkepang、Praveen K. Pogula、Moses Bio、Youngjae You
DOI：10.1111/j.1751-1097.2012.01095.x
日期：2012.5
oxygen‐mediated drug release. Even though 1,2‐diaryloxyethenes look very simple, their synthesis was not an easy task. Previous methods are limited to symmetric molecules, lengthy step and low yield. We report on a facile synthetic method not only for 1,2‐diaryloxyethenes but also their sulfur and nitrogenanalogs in yields ranging from 40 to 90% with more than 90% purity at the vinylation reaction
A novel entry to xanthones by an intramolecular Diels-Alder reaction involving 2-(1,2-dichlorovinyloxy) aryl dienones
作者：Katerina Otrubova、Anne E. Fitzgerald、Neelakandha S. Mani
DOI：10.1016/j.tet.2018.08.007
日期：2018.9
of syntheticmethods are described in the literature for the preparation of xanthones—a prominent class of tricyclic molecules that occur widely in nature. Majority of these reported methods involve linking the two aromatic rings and forming the central pyrone ring using a variety of classical and non-classical cyclization strategies. In a conceptually different approach, we describe here a new xanthone
