Chlorofluorocarbons
Chlorofluorocarbons, Methane
Ethane
Aerosol Propellants
Chlorofluorocarbons, Ethane
Hydrocarbons, Fluorinated
DDT
The kidney as a novel target tissue for protein adduct formation associated with metabolism of halothane and the candidate chlorofluorocarbon replacement 2,2-dichloro-1,1,1-trifluoroethane. (1/7)
Hydrochlorofluorocarbons (HCFCs) have been identified as chemical replacements of the widely used chlorofluorocarbons (CFCs) that are implicated in stratospheric ozone depletion. Many HCFCs are structural analogues of the anesthetic agent halothane and may follow a common pathway of biotransformation and formation of adducts to protein-centered and other cellular nucleophiles. Exposure of rats to a single dose of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) or of the candidate CFC substitute HCFC 123 (2,2-dichloro-1,1,1-trifluoroethane) led to the formation of trifluoroacetylated protein adducts (CF3CO-proteins) not only in the liver, but also in the kidney as a novel target tissue for protein trifluoroacetylation. CF3CO-proteins in the kidney amounted to about 5% of those formed in the liver of the same animal. The amount of CF3CO-proteins formed within the kidney was roughly reflected by the capacity of metabolism of halothane or HCFC 123 by rat kidney microsomes in vitro which amounted to about 10% of that observed with liver microsomes. By immunohistochemistry, CF3CO-proteins in the kidney were mainly localized in the tubular segments of the cortex. In the liver, the density of CF3CO-proteins decreased from the central vein towards the portal triad. In vitro incubation of rat liver microsomes with halothane or HCFC 123 resulted in extensive formation of CF3CO-proteins and reproduced faithfully the pattern of liver CF3CO-proteins obtained in vivo. CF3CO-proteins generated in vitro were immunochemically not discernible from those generated in vivo. Glutathione (5 mM) and cysteine (5 mM) virtually abolished CF3CO-protein formation; the release of Br- from halothane and Cl- from HCFC 123 was reduced to much lesser a degree. S-Methyl-glutathione, N-acetyl-cysteine, methionine, and N-acetyl-methionine only slightly affected the formation of CF3CO-proteins or metabolism of either substrate. The data suggest that metabolism and concomitant CF3CO-protein formation of halothane or of candidate CFC replacements like HCFC 123 is not restricted to the liver but also takes place in the kidney. Furthermore, an in vitro system for CF3CO-protein formation has been developed and used to show that protein-centered and glutathione-centered nucleophilic sites compete for intermediates of metabolism of halothane or of HCFC 123. (+info)Tissue acylation by the chlorofluorocarbon substitute 2,2-dichloro-1,1,1-trifluoroethane. (2/7)
Hydrochlorofluorocarbons (HCFCs) are being developed as substitutes for ozone-depleting chlorofluorocarbons (CFCs); because widespread human exposure to HCFCs may be expected, it is important to evaluate their toxicities thoroughly. Here we report studies on the bioactivation of the CFC substitute 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123) to an electrophilic intermediate that reacts covalently with liver proteins. HCFC-123 and its analog halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) were studied in rats by 19F NMR spectroscopy, and we found that a trifluoroacetylated lysine adduct was formed with liver proteins. Also, the pattern of proteins immunoreactive with hapten-specific anti-trifluoroacetylprotein antibodies was identical in livers of HCFC-123- and halothane-exposed rats. Because halothane causes an idiosyncratic, and sometimes fatal, hepatitis that is associated with an immune response against several trifluoroacetylated liver proteins, the present findings raise the possibility that humans exposed to HCFC-123 or structurally related HCFCs may be at risk of developing an immunologically mediated hepatitis. (+info)Modified extraction procedure for gas-liquid chromatography applied to the identification of anaerobic bacteria. (3/7)
Chloroform and ether commonly are used as solvents to extract metabolic organic acids for analysis by gas-liquid chromatography in the identification of anaerobic bacteria. Because these solvents are potentially hazardous to personnel, modified extraction procedures involving the use of a safer solvent, methyl tert-butyl ether were developed which remained both simple to perform and effective for organism identification. (+info)Hepatotoxicity in guinea pigs following acute inhalation exposure to 1,1-dichloro-2,2,2-trifluoroethane. (4/7)
Groups of 10 male Hartley guinea pigs were exposed to 3.0, 2.0, 1.0, or 0.1% (v/v) 1,1-Dichloro-2,2,2-trifluoroethane (HCFC-123) or 1.0% (v/v) halothane by inhalation for 4 hr. A sixth group of 10 guinea pigs received only air. All animals were sacrificed 48 hr postexposure. Gross and histopathologic examination of the liver, heart, and kidney and routine hematology and clinical chemistry analyses [including isocitrate dehydrogenase (ICDH)] were done on all guinea pigs. Lesions related to HCFC-123 and halothane exposure were limited to the liver and included centrolobular vacuolar (fatty) change, multifocal random degeneration and necrosis, and centrolobular degeneration and necrosis. These lesions were observed in 90-100% of the exposed animals and were absent in the air-only controls. There was significant individual animal variation in susceptibility to both HCFC-123 and halothane, resulting in a spectrum of histologic lesions and clinical chemistry values within each exposure group. Alanine aminotransferase, aspartate aminotransferase, and ICDH were the most significant predictors of hepatocellular damage. Similarities in the response between halothane and HCFC-123 in this guinea pig model suggests that humans susceptible to halothane-induced hepatitis may be susceptible to HCFC-123 by a common mechanism of toxicity. (+info)Microbial degradation of hydrochlorofluorocarbons (CHCl2F and CHCl2CF3) in soils and sediments. (5/7)
The ability of microorganisms to degrade trace levels of the hydrochlorofluorocarbons HCFC-21 and HCFC-123 was investigated. Methanotroph-linked oxidation of HCFC-21 was observed in aerobic soils, and anaerobic degradation of HCFC-21 occurred in freshwater and salt marsh sediments. Microbial degradation of HCFC-123 was observed in anoxic freshwater and salt marsh sediments, and the recovery of 1,1,1-trifluoro-2-chloroethane indicated the involvement of reductive dechlorination. No degradation of HCFC-123 was observed in aerobic soils. In some experiments, HCFCs were degraded at low (parts per billion) concentrations, raising the possibility that bacteria in nature remove HCFCs from the atmosphere. (+info)Toxicology of chlorofluorocarbon replacements. (6/7)
Chlorofluorocarbons (CFCs) are stable in the atmosphere and may reach the stratosphere. They are cleaved by UV-radiation in the stratosphere to yield chlorine radicals, which are thought to interfere with the catalytic cycle of ozone formation and destruction and deplete stratospheric ozone concentrations. Due to potential adverse health effects of ozone depletion, chlorofluorocarbon replacements with much lower or absent ozone depleting potential are developed. The toxicology of these compounds that represent chlorofluorohydrocarbons (HCFCs) or fluorohydrocarbons (HFCs) has been intensively studied. All compounds investigated (1, 1-dichloro-1-fluoroethane [HCFC-141b], 1,1,1,2-tetrafluoroethane [HFC-134a], pentafluoroethane [HFC-125], 1-chloro- 1,2,2,2-tetrafluoroethane [HCFC-124], and 1,1-dichloro-2,2,2-trifluoroethane [HCFC-123]) show only a low potential for skin and eye irritation. Chronic adverse effects on the liver (HCFC-123) and the testes (HCFC-141b and HCFC-134a), including tumor formation, were observed in long-term inhalation studies in rodents using very high concentrations of these CFC replacements. All CFC replacements are, to varying extents, biotransformed in the organism, mainly by cytochrome P450-catalyzed oxidation of C-H bonds. The formed acyl halides are hydrolyzed to give excretable carboxylic acids; halogenated aldehydes that are formed may be further oxidized to halogenated carboxylic acids or reduced to halogenated alcohols, which are excretory metabolites in urine from rodents exposed experimentally to CFC replacements. The chronic toxicity of the CFC replacements studied is unlikely to be of relevance for humans exposed during production and application of CFC replacements. (+info)Metabolism of 1,1-dichloro-1-fluoroethane (HCFC-141b) in human volunteers. (7/7)
Human subjects were exposed by inhalation to 250, 500, and 1000 ppm 1,1-dichloro-1-fluoroethane (HCFC-141b) for 4 hr, and urine samples were collected from 0-4, 4-12, and 12-24 hr for metabolite analysis. 19F nuclear magnetic resonance spectroscopic analysis of urine samples from exposed subjects showed that 2,2-dichloro-2-fluoroethyl glucuronide and dichlorofluoroacetic acid were the major and minor metabolites, respectively, of HCFC-141b. Urinary 2, 2-dichloro-2-fluoroethyl glucuronide was hydrolyzed to 2, 2-dichloro-2-fluoroethanol by incubation with beta-glucuronidase, and the released 2,2-dichloro-2-fluoroethanol was quantified by gas chromatography/mass spectrometry. Concentrations of 2, 2-dichloro-2-fluoroethanol were highest in the urine samples collected 4-12 hr after exposure, but 2,2-dichloro-2-fluoroethanol was also detected in the samples collected 0-4 and 12-24 hr after exposure. Exposure concentration-dependent excretion of 2, 2-dichloro-2-fluoroethanol, obtained by hydrolysis of 2, 2-dichloro-2-fluoroethyl glucuronide, was observed in seven of the eight subjects studied. In conclusion, HCFC-141b is metabolized in human subjects to 2,2-dichloro-2-fluoroethanol, which is conjugated with glucuronic acid and excreted as its glucuronide in urine in a time- and exposure concentration-dependent manner. (+info)Chlorofluorocarbons (CFCs) are synthetic, volatile organic compounds that consist of carbon atoms, chlorine atoms, and fluorine atoms. They were widely used in various applications such as refrigerants, aerosol propellants, solvents, and fire extinguishing agents due to their non-toxicity, non-flammability, and chemical stability.
However, CFCs have been found to contribute significantly to the depletion of the Earth's ozone layer when released into the atmosphere. This is because they are stable enough to reach the upper atmosphere, where they react with ultraviolet radiation to release chlorine atoms that can destroy ozone molecules. As a result, the production and use of CFCs have been phased out under the Montreal Protocol, an international treaty aimed at protecting the ozone layer.
Chlorofluorocarbons (CFCs) and methane are both greenhouse gases that contribute to global warming and climate change. However, they are distinct substances with different chemical structures and sources.
Chlorofluorocarbons (CFCs) are synthetic compounds made up of carbon, chlorine, and fluorine atoms. They were commonly used in refrigerants, aerosol sprays, and foam blowing agents until they were phased out due to their harmful effects on the ozone layer. CFCs have high global warming potential, meaning that they trap heat in the atmosphere many times more effectively than carbon dioxide.
Methane, on the other hand, is a naturally occurring gas made up of one carbon atom and four hydrogen atoms (CH4). It is produced by the decomposition of organic matter, such as in landfills, wetlands, and the digestive tracts of animals like cattle. Methane is also released during the extraction and transportation of fossil fuels like coal, oil, and natural gas. While methane has a shorter lifespan in the atmosphere than CFCs, it is an even more potent greenhouse gas, trapping heat at a rate 25 times greater than carbon dioxide over a 100-year period.
Therefore, while both CFCs and methane are harmful to the climate, they are distinct substances with different sources and impacts.
Ethane is not a medical term, but it is a chemical compound that is part of the human environment. Ethane is a hydrocarbon, which means it contains only hydrogen and carbon atoms. Specifically, ethane is made up of two carbon atoms and six hydrogen atoms (C2H6). It is a colorless gas at room temperature and has no smell or taste.
In the context of human health, ethane is not considered to be harmful in small amounts. However, exposure to high levels of ethane can cause respiratory irritation and other symptoms. Ethane is also a greenhouse gas, which means that it contributes to global warming when released into the atmosphere.
Ethane is produced naturally during the breakdown of organic matter, such as plants and animals. It is also produced in small amounts during the digestion of food in the human body. However, most ethane used in industry is extracted from natural gas and petroleum deposits. Ethane is used as a fuel and as a raw material in the production of plastics and other chemicals.
Aerosol propellants are substances used to expel aerosolized particles from a container. They are typically gases that are stored under pressure in a container and, when the container is opened or activated, the gas expands and forces the contents out through a small opening. The most commonly used aerosol propellants are hydrocarbons such as butane and propane, although fluorinated hydrocarbons such as difluoroethane and tetrafluoroethane are also used. Aerosol propellants can be found in various products including medical inhalers, cosmetics, and food products. It is important to handle aerosol propellants with care, as they can be flammable or harmful if inhaled or ingested.
Chlorofluorocarbons (CFCs) are a group of synthetic chemicals that were commonly used in refrigerants, aerosol propellants, and foam blowing agents. They consist of carbon atoms bonded to chlorine and fluorine atoms. CFCs are known to contribute to the depletion of the ozone layer in the Earth's atmosphere.
CFC-12, also known as dichlorodifluoromethane, is a specific type of CFC with the chemical formula CF~2Cl2. It was widely used as a refrigerant and aerosol propellant before being phased out due to its ozone-depleting properties.
On the other hand, ethane (C2H6) is a hydrocarbon consisting of two carbon atoms and six hydrogen atoms. It is a colorless gas with a faint sweet odor and is commonly found in natural gas. Ethane is not a CFC and does not contain chlorine or fluorine atoms.
Therefore, there is no medical definition for "Chlorofluorocarbons, Ethane" as it is a combination of two unrelated terms.
Fluorinated hydrocarbons are organic compounds that contain fluorine and carbon atoms. These compounds can be classified into two main groups: fluorocarbons (which consist only of fluorine and carbon) and fluorinated aliphatic or aromatic hydrocarbons (which contain hydrogen in addition to fluorine and carbon).
Fluorocarbons are further divided into three categories: fully fluorinated compounds (perfluorocarbons, PFCs), partially fluorinated compounds (hydrochlorofluorocarbons, HCFCs, and hydrofluorocarbons, HFCs), and chlorofluorocarbons (CFCs). These compounds have been widely used as refrigerants, aerosol propellants, fire extinguishing agents, and cleaning solvents due to their chemical stability, low toxicity, and non-flammability.
Fluorinated aliphatic or aromatic hydrocarbons are organic compounds that contain fluorine, carbon, and hydrogen atoms. Examples include fluorinated alcohols, ethers, amines, and halogenated compounds. These compounds have a wide range of applications in industry, medicine, and research due to their unique chemical properties.
It is important to note that some fluorinated hydrocarbons can contribute to the depletion of the ozone layer and global warming, making it essential to regulate their use and production.
DDT (dichlorodiphenyltrichloroethane) is a synthetic insecticide that was widely used in the mid-20th century to control agricultural pests and vector-borne diseases such as malaria. It belongs to a class of chemicals called organochlorines, which are known for their persistence in the environment and potential for bioaccumulation in the food chain.
DDT was first synthesized in 1874, but its insecticidal properties were not discovered until 1939. Its use as an insecticide became widespread during World War II, when it was used to control typhus and malaria-carrying lice and mosquitoes among troops. After the war, DDT was widely adopted for agricultural and public health purposes.
However, concerns about the environmental and human health effects of DDT led to its ban or severe restriction in many countries starting in the 1970s. The United States banned the use of DDT for most purposes in 1972, and the Stockholm Convention on Persistent Organic Pollutants (POPs) prohibited its production and use globally in 2004, except in cases where there is a risk of vector-borne diseases.
DDT has been linked to several health problems, including reproductive effects, developmental toxicity, neurotoxicity, and endocrine disruption. It is also highly persistent in the environment, with a half-life of up to 15 years in soil and up to 30 years in water. This means that DDT can accumulate in the food chain, posing risks to wildlife and humans who consume contaminated food or water.
In summary, DDT is a synthetic insecticide that was widely used in the mid-20th century but has been banned or restricted in many countries due to its environmental and health effects. It belongs to a class of chemicals called organochlorines, which are known for their persistence in the environment and potential for bioaccumulation in the food chain. DDT has been linked to several health problems, including reproductive effects, developmental toxicity, neurotoxicity, and endocrine disruption.
Dichlorodiphenyldichloroethane (DDT) is a synthetic insecticide that was widely used in the 20th century to control agricultural pests and vector-borne diseases such as malaria. It is a colorless, odorless crystalline solid with a weak sweetish taste. DDT has high toxicity to many insects, but relatively low toxicity to mammals and birds. However, its persistence in the environment and bioaccumulation in the food chain have raised significant environmental and health concerns.
DDT was first synthesized in 1874, but its insecticidal properties were not discovered until 1939. During World War II, it was used extensively to control typhus and malaria-carrying mosquitoes, saving countless lives. After the war, DDT became a popular agricultural pesticide, leading to widespread use in agriculture and public health programs.
However, in the 1960s, studies began to reveal the negative impacts of DDT on wildlife, particularly birds. Rachel Carson's book "Silent Spring" (1962) brought these issues to public attention and helped launch the modern environmental movement. Research showed that DDT caused thinning of eggshells in birds, leading to reproductive failure and population declines.
In 1972, the United States banned the use of DDT for most purposes due to its environmental persistence, bioaccumulation, and toxicity to wildlife. Many other countries followed suit, and international agreements were established to limit its production and use. However, DDT is still used in some countries to control vector-borne diseases such as malaria, despite concerns about its long-term impacts on human health and the environment.
DDT has been linked to several potential health effects in humans, including cancer, reproductive problems, and developmental issues. However, the evidence for these risks is not conclusive, and more research is needed to fully understand the potential health impacts of DDT exposure.