Chlorobenzene appears as a colorless to clear, yellowish liquid with a sweet almond-like odor. Flash point 84°F. Practically insoluble in water and somewhat denser than water (9.2 lb / gal). Vapors heavier than air. Used to make pesticides, dyes, and other chemicals.
颜色/状态：
Colorless liquid
气味：
Faint, not unpleasant odor
蒸汽密度：
3.88 (NTP, 1992) (Relative to Air)
蒸汽压力：
12.0 mm Hg at 25 °C
亨利常数：
0.00 atm-m3/mole
大气OH速率常数：
7.70e-13 cm3/molecule*sec
自燃温度：
1099 °F (593 °C)
粘度：
0.806 mPa.s at 20 °C
腐蚀性：
Liquid chlorobenzene will attack some forms of plastics, rubber, and coatings
Output of mercapturic acid in man ... /from (14)C-labelled chlorobenzene/ was small ... Main metab of chlorobenzene ... accounting for about 70% of excreted radioactivity, was 4-chlorocatechol conjugated mainly with glucuronic acid & to lesser extent with sulfate.
In rats administered chlorobenzene by intraperitoneal injection, 33% of the administered dose was excreted in the urine, with p-chlorophenol as the major metabolite. Other metabolites included 4-chlorocatechol, o-chlorophenol, and m-chlorophenol.
The in vitro metabolites of chlorobenzene are o-chlorophenol, m-chlorophenol, and p-chlorophenol; the proportions differ according to the source of the mono-oxygenase system and its state of purity. The o- and p-chlorophenols result from isomerization of the intermediate 3- and 4-chlorobenzene oxides, respectively. The formation of m-chlorophenol appears to occur via a direct oxidative pathway. In vitro conjugation of the arene oxide with glutathione or hydration is not a significant pathway.
/The study investigated/ urinary metabolites of chlorobenzene in rats, mice, and rabbits. Rats were given oral doses of 0.3 mmol/kg, while all three species received intraperitoneal injections of 0.5, 1.0, or 2.0 mmol/kg. Urinary p-chlorophenylmercapturic acid, and 4-chlorocatechol, after hydrolysis of its conjugate, were reported. Other urinary metabolites /from rabbits/ included quinol, 3-chlorocatechol, and o- and m- chlorophenylmercapturic acids.
Chlorobenzene is known to be absorbed via ingestion and inhahation. As it is a lipophilic compound, chlorobenzene distributes preferentially to adipose tissue. It is metabolized by cytochrome P-450 enzymes into its major metabolite 4-chlorocatechol. Unchanged chlorobenzene is exhalted and its metabolites are excreted mainly in the urine. (L200)
IDENTIFICATION AND USE: Chlorobenzene is a colorless liquid with a characteristic penetrating, almond-like odor. It is used as an Intermediate in the manufacture of chloronitrobenzenes, oxide, DDT, and silicones; as a process solvent for methylene diisocyanate, adhesives, polishes, waxes, pharmaceutical products, paints, and natural rubber; as a degrading solvent; heat transfer medium; in textile processing; and tar and grease remover. HUMAN EXPOSURE AND TOXICITY: Dermal exposure to chlorobenzene for 1 hour resulted in burning pain, hyperemia, whealing, and erythema formation at the application site. Twelve hours postexposure, a minimal local vesiculation was seen. Continuous contact for a week may result in moderate erythema and slight superficial necrosis. Clinical symptoms included hyperpnea, ataxia, labored breathing, prostration, and death from respiratory paralysis. Humans occupationally exposed to chlorobenzene intermittently for up to 2 years at levels above current federal limits displayed signs of neurotoxicity including numbness, cyanosis (from depression of respiratory center), hyperesthesia, and muscle spasms. Early complaints included headache and irritation of the upper respiratory tract and mucosa of the eyes. Clinical examination of workers exposed to chlorobenzene in the manufacture of polyvinyl chloride showed that some workers reported nerve lesions, hepatitis, chronic gastritis with gastric juice hypoacidity, and bronchitis. Severe anemia and medullary aplasia in a 70 year old woman was related to her employment in hat making, which required the use of glue containing 70% chlorobenzene. A 2 year old boy swallowed 5 to 10 mL of Puran, a cleaning agent containing chlorobenzene and 2.5 hr after ingestion, lost consciousness and suffered vascular paralysis and heart failure. He survived, and the odor of chlorobenzene was present in breath and urine for 5 to 6 days. ANIMAL STUDIES: Chlorobenzene is lethal following acute, intermediate, and chronic oral exposures in animals. Neurological effects of chlorobenzene have also been reported in animals following inhalation. Acute inhalation exposure produced muscle spasms followed by /CNS depression/ in rabbits exposed to 5 mg/L chlorobenzene (1,090 ppm) or greater for 2 hours. Dermal contact resulted in moderate skin and eye irritant (tested in the guinea pig and rabbit, respectively). Single ip injections of chlorobenzene in rats resulted in time- and dose-dependent hepatotoxicity, including liver necrosis, increased liver weights, and increased serum enzyme activities with dose-dependent recovery. Systemic effects of single ip injections of chlorobenzene also included damage to the kidney, effects on bile and pancreatic flow, increased alanine aminotransferase (ALT) and centrilobular necrosis. Death occurred within 2 to 3 days after a single exposure to 4,000 mg/kg in corn oil by gavage in rats of both sexes, and in mice after a single exposure to 1,000 mg/kg. Administration of chlorobenzene by gavage resulted in dose-dependent chemical induced injuries to the liver (centrilobular hepatocellular degeneration and necrosis), kidney (necrosis of the proximal tubular epithelium), bone marrow (myeloid depletion), spleen (lymphoid depletion or necrosis) and thymus at doses > or = 250 mg/kg. Male and female mice exposed to chlorobenzene at 2500 mg/cu m daily, 7d/wk for 3 weeks showed loss of appetite, general emaciation, marked somnolence and weight loss; 5 animals died. Autopsy revealed fatty degeneration in the liver, leading to acute yellow atrophy. The majority of mice showed a decrease in white blood cell number with relative decrease in neutrophils and relative increase in lympocytes. Chronic exposure of mice to chlorobenzene at 100 mg/cu m daily for 3 months, showed increased agitation and motility and decreased white blood cell count with relative decrease in neutrophils and relative increase in lymphocytes. In a two-generation study in rats, chlorobenzene in concentrations up to 450 ppm did not adversely affect reproductive performance or fertility. Chlorobenzene was not mutagenic for Salmonella typhimurium strains TA98, TA100, TA1535, TA1537 or TA1538, with or without addition of rat liver or hamster liver homogenate. Chlorobenzene did not induce DNA damage in Escherichia coli strains WP2 uvr A+ rec A+ or WP100 uvr A- rec A- or S. typhimurium strains TA1978 uvr B+ or TA1538 uvr B-. Slight leukopenia and lymphocytosis occurred in mice exposed to chlorobenzene (0.1 mg/L) for 3 months. ECOTOXICITY STUDIES: Chlorobenzene was less hepatotoxic to trout than rats. This difference could not be totally accounted for by reduced absorption in trout. Chlorobenzenes caused significant increases in serum testosterone concentration in the crucian carps compared to the controls.
The reactive metabolites of chlorobenzene are believed to bind both liver and kidney proteins, causing direct damage. Chlorobenzene also activates nuclear factor-kappa B (NF-kappa B) and p38 mitogen-activated protein kinase, inducing the release of monocyte chemoattractant protein 1 (MCP-1) by lung epithelial cells, causing an inflammatory reponse. (T36, A141)
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
CLASSIFICATION: D; not classifiable as to human carcinogenicity. BASIS FOR CLASSIFICATION: No human data, inadequate animal data and predominantly negative genetic toxicity data in bacterial, yeast, and mouse lymphoma cells. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: Inadequate. /Based on former classification system/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A3; 已确认的动物致癌物，对人类的相关性未知。
A3; Confirmed animal carcinogen with unknown relevance to humans.
... 27% of /0.5 g/kg of body wt admin to rabbits/ was excreted unchanged in expired air; 25% appeared in the urine as glucuronide, 27% as an ethereal sulfate, & 20% as mercapturic acid. The recovery of admnistered radioactivity (99%) was nearly complete in this study.
Chlorobenzene is absorbed from the gastrointestinal tract. In a study with a single human volunteer, /it was/ reported that at least 31% of administered chlorobenzene was absorbed. In the same study, rats administered chlorobenzene absorbed at least 18% of the administered dose. Similar results were reported by /others/, who observed that in rabbits administered (14)C-labeled chlorobenzene, at least 22% of the administered chlorobenzene was absorbed.
... Chlorobenzene is absorbed through the lung and from the gastrointestinal tract. Because chlorobenzene is highly lipophilic and hydrophobic, it is thought to be distributed throughout total body water, with body lipids being a major deposition site.
Rats were exposed to (14)C-chlorobenzene vapor at concentrations of 100, 400, and 700 ppm for 8 hours. The plasma concentration-time profile for chlorobenzene on cessation of exposure, as estimated by respiratory elimination of radioactivity, indicated a two compartment elimination. Increase in exposure by a factor of seven (100-700 ppm) increased the total uptake of radioactivity by a factor of about 13. This increase in body burden was associated with a decrease in total body clearance, as indicated by an approximate four fold increase in the half-life of the central compartment. The proportion of the dose excreted via the lungs (which may be presumed to be largely, if not entirely, unchanged chlorobenzene) increased nonlinearly and the proportion eliminated by hepatic metabolism decreased. Increase in the dose of chlorobenzene was associated with a decrease in the proportion cleared as the mercapturic acid derivative. Of interest, the half-life of chlorobenzene was shorter at the 700 ppm exposure level when the animals were subjected to repeated treatment daily for 5 days, as compared with that of the single 700 ppm exposure animals, raising the possibility of induction of metabolic clearance. In agreement with this possibility, the proportion cleared by metabolism in the multi-exposed animals was increased, and the proportion excreted unchanged via the lung was decreased, as compared with the 700 ppm-single exposure animals.
Estimation of dioxin emission from fires in chemicals
摘要：
The formation of the 17 toxic 2,3,7,8-substituted PCDDs and PCDFs during combustion of selected chemicals were measured by high-resolution GC/MS. The 16 chemicals studied were commonly used chlorinated pesticides, industrial chemicals, and PVC. In a series of experiments carried out in a DIN 53,436 furnace, 2.5 g of these compounds were burned at 500 degrees C and 900 degrees C, respectively. The resultant yields ranged from 740 ng ITEQ/g for pentachlorophenol, to below 0.01 ng ITEQ/g for PVC and dichlobenil. The results show that some chemicals generate PCDD/F in very high possibly dangerous - amounts during burning, whereas others generate insignificant amounts. The influence of scale were studied for chlorobenzene and 4-chloro-3-nitro-benzoic acid in additional experiments, carried out in a cone calorimeter burning 20 g substance, and in ISO 9705 room test burning about 50 kg. A good agreement between the results for large and small scale indicated that formation of PCCD/F during a fire may be estimated from laboratory experiments. This suggest laboratory test may be used to screen for chemicals posing a hazard for release of PCDD/F during fires. (C) 1999 Elsevier Science Ltd. All rights reserved.
Aromatization of cyclohexenes and cyclohexadienes with selenium dioxide-trimethylsilyl polyphosphate
摘要：
Selenium dioxide is depolymerized and activated by trimethylsilyl polyphosphate in carbon tetrachloride. The reagent effectively aromatizes substituted cyclohexenes and cyclohexadienes under mild reaction conditions.
Novel processes for the preparation of adenosine compounds and intermediates thereto
申请人：——
公开号：US20030069423A1
公开（公告）日：2003-04-10
Novel processes for the preparation of adenosine compounds and intermediates thereto. The adenosine compounds prepared by the present processes may be useful as cardiovascular agents, more particularly as antihypertensive and anti-ischemic agents, as cardioprotective agents which ameliorate ischemic injury or myocardial infarct size consequent to myocardial ischemia, and as an antilipolytic agents which reduce plasma lipid levels, serum triglyceride levels, and plasma cholesterol levels. The present processes may offer improved yields, purity, ease of preparation and/or isolation of intermediates and final product, and more industrially useful reaction conditions and workability.
DISUBSTITUTED TRIFLUOROMETHYL PYRIMIDINONES AND THEIR USE
申请人：BAYER PHARMA AKTIENGESELLSCHAFT
公开号：US20160221965A1
公开（公告）日：2016-08-04
The present application relates to novel 2,5-disubstituted 6-(trifluoromethyl)pyrimidin-4(3H)-one derivatives, to processes for their preparation, to their use alone or in combinations for the treatment and/or prevention of diseases, and to their use for preparing medicaments for the treatment and/or prevention of diseases, in particular for treatment and/or prevention of cardiovascular, renal, inflammatory and fibrotic diseases.
[EN] IMIDAZOLE DERIVATIVES USEFUL AS INHIBITORS OF FAAH<br/>[FR] DÉRIVÉS IMIDAZOLE UTILES COMME INHIBITEURS DE LA FAAH
申请人：MERCK & CO INC
公开号：WO2009152025A1
公开（公告）日：2009-12-17
The present invention is directed to certain imidazole derivatives which are useful as inhibitors of Fatty Acid Amide Hydrolase (FAAH). The invention is also concerned with pharmaceutical formulations comprising these compounds as active ingredients and the use of the compounds and their formulations in the treatment of certain disorders, including osteoarthritis, rheumatoid arthritis, diabetic neuropathy, postherpetic neuralgia, skeletomuscular pain, and fibromyalgia, as well as acute pain, migraine, sleep disorder, Alzeimer Disease, and Parkinson's Disease.
[EN] 3-[(HYDRAZONO)METHYL]-N-(TETRAZOL-5-YL)-BENZAMIDE AND 3-[(HYDRAZONO)METHYL]-N-(1,3,4-OXADIAZOL-2-YL)-BENZAMIDE DERIVATIVES AS HERBICIDES<br/>[FR] DÉRIVÉS DE 3-[(HYDRAZONO))MÉTHYL]-N-(TÉTRAZOL-5-YL)-BENZAMIDE ET DE 3-[(HYDRAZONO)MÉTHYL]-N-(1,3,4-OXADIAZOL-2-YL)-BENZAMIDE UTILISÉS EN TANT QU'HERBICIDES
申请人：SYNGENTA CROP PROTECTION AG
公开号：WO2021013969A1
公开（公告）日：2021-01-28
The present invention related to compounds of Formula (I): or an agronomically acceptable salt thereof, wherein Q, R2, R3, R4, R5 and R6 are as described herein. The invention further relates to compositions comprising said compounds, to methods of controlling weeds using said compositions, and to the use of compounds of Formula (I) as a herbicide.
