1,1,1-trichloroethane appears as a colorless liquid with a sweet, pleasant odor. May irritate skin, eyes and mucous membranes. In high concentrations the vapors may have a narcotic effect. Nonflammable, but may decompose and emit toxic chloride fumes if exposed to high temperatures. Used as a solvent.
颜色/状态：
Colorless liquid
气味：
... Mild chloroform-like odor
沸点：
74.0 °C
熔点：
-30.4 °C
闪点：
greater than 200 °F (NTP, 1992)
溶解度：
In water, 1,290 mg/L at 25 °C
密度：
1.3376 at 20 °C/4 °C
蒸汽密度：
4.6 (NTP, 1992) (Relative to Air)
蒸汽压力：
124 mm Hg at 25 °C
亨利常数：
0.02 atm-m3/mole
大气OH速率常数：
9.43e-15 cm3/molecule*sec
自燃温度：
932 °F (500 °C) (closed cup)
分解：
Thermal decomposition of 1,1,1-trichloroethane occurs below 260 °C, while large amounts of hydrogen chloride and trace amount of phosgene form at temperatures above that level.
粘度：
0.00086 Pa.s at 20 °C
腐蚀性：
Readily corrodes aluminum and aluminum alloys
燃烧热：
4700 BTU/LB= 2600 CAL/G= 110X10+5 J/KG
汽化热：
32.50 kJ/mol at 25 °C
表面张力：
0.02518 N/m at 25 °C
电离电位：
11.00 eV
气味阈值：
The odor may be noticeable at concentrations near 100 ppm, well below those known to cause physiological response. However, the odor at 500 ppm and even 1000 ppm is not so unpleasant as to discourage exposure. The odor has been described as strong and unpleasant at 1500-2000 ppm. It has been reported that female test subjects exposed to 350 ppm objected to the odor; however, this has not been an industrial problem.
Metabolism appears to play a relatively minor role in the overall disposition of absorbed 1,1,1-trichloroethane in humans. Less than 10% of the absorbed dose is metabolized; a large fraction is excreted unchanged in exhaled air, regardless of the route of exposure. The major metabolites of 1,1,1-trichloroethane are water-soluble trichloroethanol and its glucuronide conjugate, trichloroacetic acid and carbon dioxide. The total amount of trichloroethanol and trichloroacetic acid excreted in urine accounts for 77% of the predicted amount of metabolized 1,1,1-trichloroethane. Excretion of trichloroethanol and trichloroacetic acid in urine is slow in relation to exhalation of 1,1,1-trichloroethane and these metabolites may accumulate with repeated exposure.
Metabolism following oral exposure is similar to metabolism following inhalation exposure. ... Approximately 3% of a dose ingested in drinking water by rats was metabolized and excreted as CO2 in expired air or as metabolites in urine. Mice metabolized 1,1,1-trichloroethane more extensively than rats. This is consistent with the metabolic differences between rats and mice following inhalation exposure, ... .
The data on 1,1,1-trichloroethane metabolism by animals are consistent with the human data. Approximately 90% of the inhaled dose is excreted unchanged in expired air, while the remainder is eliminated as CO2 in expired air and as trichloroethanol and trichloroacetic acid in the urine. A similar pattern of metabolism and subsequent excretion occurred in acutely and chronically exposed mice; the majority of 1,1,1-trichloroethane was excreted unchanged in the expired air and a small percentage was metabolized.
Metabolism has been shown to be saturable in animals over a range of exposure levels of 150-1500 ppm (820-8200 mg/cu m); thus, as the exposure level and absorbed dose increase, metabolism will contribute less to overall elimination of 1,1,1-trichloroethane.
The lungs excrete most of an absorbed dose unchanged. Small amounts are metabolized to trichloroacetic acid and trichloroethanol, which are excreted by the kidney. Chronic accumulation probably does not occur, although repeated exposure induces hepatic p450 mixed-function oxidase enzymes.
IDENTIFICATION AND USE: 1,1,1-Trichloroethane is a colorless liquid with a mild sweet odor. It is used as a cleaning solvent, as a chemical intermediate to produce vinylidene chloride, and as a propellant in aerosol cans. The EPA lists it as an inert pesticide ingredient, approved for nonfood use only. HUMAN EXPOSURE AND TOXICITY: The findings in human volunteers indicate that the urinary concentration of 1,1,1-trichloroethane can be used as an appropriate biological exposure indicator. Neurological response effects have been shown in acute exposure studies at 900 to 1000 ppm were reduced coordination, and inhalation of 1700 ppm or repeated inhalation of 500 ppm over 5 days reduced Romberg's test performance. Inhalation of very high 1,1,1-trichloroethane concentrations for a short period can produce severe cardiac arrhythmias and death in humans. Arrhythmias are thought to be produced indirectly by 1,1,1-trichloroethane by sensitization of the heart to epinephrine. In addition, reduced blood pressure, occasionally severe, has been reported in humans following brief exposure to high concentrations. Early symptoms may include mild eye and nasal discomfort and impairment of equilibrium and coordination. Increased lassitude and headache occur with heavier exposures and in severe poisoning progressive CNS depression occurs. Hepatotoxicity may not become manifest until near-anesthetic levels are reached. Nausea is apparently not common. Several deaths have occurred following industrial exposure in confined spaces and also in the context of solvent abuse. A 44 year old female with complaints of apparent work related perioral tingling and burning, and hand and foot discomfort was evaluated. After she was removed from work, the oral and hand symptoms disappeared, but she was left with sensations of burning and cramping in her feet which made it difficult to walk or stand for prolonged periods of time. Physical examination revealed decreased vibration sensitivity in both big toes. She had normal tendon reflexes, no evidence of muscle atrophy or weakness was seen. Testing of evoked potential, electromyographic, and motor nerve conduction velocity yielded normal results. The sensory nerve conduction velocity testing revealed, reduced amplitudes of sural sensory responses bilaterally and normal conduction velocities. This was diagnostic of a toxic axonopathy. The patient reported that she had been employed for the past 18 months as a hydraulic pump dismantler and parts cleaner. She typically spent half of her workday using a degreasing agent that was essentially 1,1,1-trichloroethane. She used protective gloves and a respirator, but she reported that they frequently leaked. She was permanently removed from work. Within 6 months, her symptoms had almost completely disappeared. Repeat sensory nerve conductance testing indicated a 32% improvement in the response. ANIMAL STUDIES: Rats were less affected by the solvents when they were tested in highly motivating situations, for example, rewarded for rapid or correct responding or escape from electrical shock, compared with less motivating circumstances. When tested in tasks with low-motivational contingencies, the dose-effect curves of humans (reaction times) and rats (electrophysiological responses to visual stimuli) were not significantly different. However, on an exploratory follow-up analysis, humans were less sensitive than rats. Dose-equivalence curves were derived for extrapolating to human effects from rat data. Carcinogenicity of 1,1,1-trichloroethane was examined by an inhalation exposure of rats and mice of both sexes at 0, 200, 800 or 3200 ppm for 6 hr/d, 5 d/week for 104 weeks. In male rats, the incidences of bronchiolo-alveolar adenomas and peritoneal mesotheliomas were significantly increased in the 800 and 3200 ppm-exposed groups, respectively. In female rats, the tumor incidences were not increased in any organs. 1,1,1-Trichloroethane did not induce unscheduled DNA synthesis in rat primary hepatocytes. It showed inconclusive evidence of gene mutation at the tk locus in mouse lymphoma L5178Y cells in the presence of an exogenous metabolic activation system. Results for induction of sister chromatid exchanges were also inconclusive. 1,1,1-Trichloroethane increased the frequency of chromosomal aberrations in Chinese hamster ovary cell cultures and induced morphological transformation in rat and virally-enhanced Syrian hamster embryo cells in vitro. 1,1,1-Trichloroethane did induce mutations in S. typhimurium strains TA100 and TA1535 in the presence or absence of exogenous metabolic activation. It induced reverse mutations in Escherichia coli in the presence of exogenous metabolic activation in one of three studies. It did not induce DNA damage, gene conversion, mutation or aneuploidy in Saccharomyces cerevisiae. It did not induce genetic crossing-over or aneuploidy in Aspergillus nidulans, mutation in Tradescantia or sex-linked recessive lethal mutation in Drosophila melanogaster. ECOTOXICITY STUDIES: 1,1,1-Trichloroethane was tested in aquatic species and plants without significant toxic effects.
1,1,1-Trichloroethane is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌性证据
癌症分类：D组 不可归入人类致癌性类别
Cancer Classification: Group D Not Classifiable as to Human Carcinogenicity
Evaluation: There is inadequate evidence for the carcinogenicity of 1,1,1-trichloroethane in humans. There is inadequate evidence for the carcinogenicity of 1,1,1-trichloroethane in experimental animals. Overall evaluation: 1,1,1-Trichloroethane is not classifiable as to its carcinogenicity to humans (Group 3).
1,1,1-Trichloroethane is rapidly taken up by humans after inhalation exposure. Experimental data collected in human subjects indicate that absorption of 1,1,1-trichloroethane is nearly complete following a single breath exposure, and that a steady-state lung retention of 25-30% in humans is achieved within 1-3 hours of continuous exposure. Steady-state blood levels are approximately 5-6 times that of alveolar air and increase with increasing air concentration, increasing alveolar ventilation and cardiac output. The percentage uptake of inhaled 1,1,1-trichloroethane decreased rapidly from approximately 95% at the beginning /single breath/ of a four-hour exposure to 30% at the end /steady state/.
The absorption of 1,1,1-trichloroethane by the skin in humans has been shown to be dependent on the duration of exposure and the area of skin exposed. 1,1,1-Trichloroethane vapours are absorbed through exposed skin to some extent, although absorption through the respiratory tract is expected to predominate during whole-body exposure to vapours. A quantitative examination of the relative magnitudes of percutaneous and respiratory absorption indicated that a whole-body exposure to 600 ppm (3280 mg/cu m) 1,1,1- trichloroethane for over 3.5 hours was equivalent to an inhalation exposure of only 0.6 ppm (3.3 mg/cu m) over the same time period.
After cessation of inhalation exposure, 1,1,1-trichloroethane is rapidly eliminated from the blood; 60-80% is eliminated within two hours after exposure and more than 95-99% within 50 hours.
Expired air concentrations after topical application of TCE or continuous immersion of the hand for 30 minutes were 0.5 ppm and 10 ppm respectively at 30 minutes post-exposure. In contrast, respiratory exposure for a similar time to levels sufficient to cause only mild symptoms, i.e. 910 ppm, was associated with expired air concentrations of around 35 ppm at 30 minutes post-exposure. The skin is therefore a considerably less significant route of absorption than the lung. ... Peak alveolar levels of 45 ppm /were estimated/ after immersion of both hands in TCE for 30 minutes, similar to peak levels observed after respiratory exposure of the same duration to 100-500 ppm in air. Penetration is less with topical application than after total immersion by a factor of about 20. They concluded that provided the solvent is not confined beneath an impermeable barrier there is little likelihood that toxic amounts will be absorbed during normal industrial use. The vapor itself is not absorbed in significant amounts through the skin.
Trichloroethane is rapidly absorbed through both the lungs and gastrointestinal tract, but cutaneous absorption probably is too slow to produce significant toxicity unless trapped against the skin by an impermeable barrier.
A convergentpairedelectrolysis catalyzed by a B12 complex for the one-pot synthesis of a tertiary amide from organic trichlorides (R-CCl3) has been developed. Various readily available organic trichlorides, such as benzotrichloride and its derivatives, chloroform, dichlorodiphenyltrichloroethane (DDT), trichloro-2,2,2-trifluoroethane (CFC-113a), and trichloroacetonitrile (CNCCl3), were converted
A manufacturing process for making hydrofluorocarbons (HFCs), by reacting a hydrochlorocarbon and HF in a liquid phase catalytic reactor using a large mole ratio of HF to hydrochlorocarbon to minimize formation of high boiling by-products and improve HF consumption and hydrofluorocarbon yields.
The reactivity of (LCN)2Sn (1) (where LCN is 2-(N,N-dimethylaminomethyl)phenyl-) towards various substrates containing E–Cl bond(s) has been studied (E = C, Si, Ge and Sn). Alkyl chlorides like chloroform or dichloromethane reacts with 1 to form (LCN)2SnCl2 and unidentified by-products in poor yields. The reaction of benzoyl chloride with 1 at low temperature yielded a thermally unstable product (LCN)2Sn(Cl)C(O)Ph
Through an original superelectrophile-promoted difluoroethylation in superacid, CF2-Me aromatic amines can be synthesized directly and regioselectivity. Applied to simple substrates, natural alkaloids and active pharmaceutical ingredients, this method offers an alternative for the late-stage synthesis of aryl methyl ethers bioisosters.
Substituted heterocyclylisoquinolinium salts and compositions and method
申请人：Sterling Winthrop Inc.
公开号：US05569655A1
公开（公告）日：1996-10-29
Substitutued heterocyclylisoquinolinium salts, pharmaceutical compositions containing them and methods for the treatment or prevention of neurodegenerative disorders or neurotoxic injuries utilizing them.
