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21-510: When combined with a fluorescent dye like 9,10-bis(phenylethynyl)anthracene , a solvent (such as diethyl phthalate ), and a weak base (usually sodium acetate or sodium salicylate ), and hydrogen peroxide , the mixture will start a chemiluminescent reaction to glow a fluorescent green color. Red, yellow and blue colors can be made by replacing the 9,10-bis(phenylethynyl)anthracene with rhodamine B , rubrene and 9,10-diphenylanthracene respectively. The above fluorescent dyes absorb much of

42-540: A POISON CENTER or doctor/physician. If Inhaled : Remove person to fresh air and keep comfortable for breathing.Call a POISON CENTER or doctor/physician. In case of unconsciousness place patient stably in side position for transportation. Environmental Safety and Waste Management Recommendations Must not be disposed of together with household garbage. Do not allow product to reach sewage system. Disposal must be made according to official regulations. : Do not allow to enter sewers/ surface or ground water. If there

63-483: A by-product of triethylamine hydrochloride. The triethylamine hydrochloride can be dissolved in water, methanol or ethanol, so the product is more purified. After washing it can be recrystallized from ethyl acetate. Human Safety Recommendations Use only outdoors or in a well-ventilated area. Wear protective gloves/protective clothing/eye protection/face protection. If on skin (or hair): Take off immediately all contaminated clothing. Rinse skin with water/shower. Call

84-445: Is a spill, it is recommended to absorb with liquid-binding material (sand, diatomite, acid binders, universal binders, sawdust) then dispose of as 'hazardous waste'. Diethyl phthalate Diethyl phthalate ( DEP ) is a phthalate ester . It occurs as a colourless liquid without significant odour but has a bitter, disagreeable taste. It is more dense than water and insoluble in water; hence, it sinks in water. Diethyl phthalate

105-610: Is not known for a specific species. The chronic toxicity of toxicants is useful information to know in determining water quality guidelines, but this information is not always easily obtained. Chronic toxicity tests can be costly and difficult, due to challenges in keeping control organisms alive, maintaining water quality, retaining constant chemical exposures, and the sheer time required for tests. Because of this, acute toxicity tests are more commonly employed, and ACRs and AFs are used to estimate chronic toxicity of toxicants to organisms. There are many factors that can increase or decrease

126-646: Is produced by the reaction of ethanol with phthalic anhydride , in the presence of a strong acid catalyst : It finds some use as a specialist plasticiser in PVC , it has also been used as a blender and fixative in perfume . Biodegradation of DEP in soil occurs by sequential hydrolysis of the two diethyl chains of the phthalate to produce monoethyl phthalate, followed by phthalic acid. This reaction occurs very slowly in an abiotic environment. Thus there exists an alternative pathway of biodegradation which includes transesterification or demethylation by microorganisms, if

147-587: Is sometimes called the chronic value (CV) and defined as “the concentration (threshold) at which chronic effects are first observed”. The predicted no effects concentration (PNEC) is calculated from toxicity tests to determine the concentration that is not thought to cause adverse effects to aquatic organisms. Determination of aquatic PNEC values requires toxicity test results from freshwater fish (e.g. ‘‘Pimephales promelas’’), freshwater invertebrates (e.g. ‘‘Daphnia magna’’), and freshwater algae (e.g. ‘‘Raphidocelis subcapitata’’) The probable effects concentration (PEC),

168-549: The biotic ligand model (BLM). Chronic toxicity will vary with differences in organisms, including species, size, and age. Certain species are more susceptible to toxic effects, as shown in species sensitivity distributions (SSDs). Certain life stages are more susceptible to adverse effects, which is why early life stage (ELS) toxicity tests are performed for certain aquatic species. In addition, other physical factors, like organism size, can lead to differences in response to toxicants. Water quality guidelines are determined based on

189-407: The activity of chitobiase in the epidermis and hepatopancreas . Chitobiase plays an important role in degradation of the old chitin exoskeleton during the pre- moult phase. When pregnant rats were treated with diethyl phthalate, it became evident that certain doses caused skeletal malformations, whereas the untreated control group showed no resorptions . The amount of skeletal malformations

210-621: The chronic toxicity of different contaminants, and usually last at least 10% of an organism's lifespan. Results of aquatic chronic toxicity tests can be used to determine water quality guidelines and regulations for protection of aquatic organisms. Chronic toxicity is the development of adverse effects as the result of long term exposure to a toxicant or other stressor. It can manifest as direct lethality but more commonly refers to sublethal endpoints such as decreased growth, reduced reproduction, or behavioral changes such as impacted swimming performance. Chronic toxicity tests are performed to determine

231-600: The concentration predicted to be in the environment, is compared with the PNEC in risk assessment. The PEC takes into account both acute and chronic exposures to toxicants. The acute to chronic ratio (ACR) allows for an estimation of Chronic toxicity using acute toxicity data. It is calculated by dividing the LC50 by the MATC. The inverse of this (MATC/LC50) is termed the application factor (AF). AFs can be used when chronic toxicity data

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252-467: The control. The lowest observed effects concentration (LOEC) is the lowest concentration of those tested that produced a statistically significant difference from the control. NOECs and LOECs can be derived from both acute and chronic tests and are used by agencies to set water quality standards. The maximum acceptable toxicant concentration (MATC) is calculated as the geometric mean of the NOEC and LOEC. MATC

273-486: The development of adverse effects as a result of long term exposure to a contaminant or other stressor, is an important aspect of aquatic toxicology . Adverse effects associated with chronic toxicity can be directly lethal but are more commonly sublethal, including changes in growth, reproduction, or behavior. Chronic toxicity is in contrast to acute toxicity , which occurs over a shorter period of time to higher concentrations. Various toxicity tests can be performed to assess

294-635: The diversity of the alkyl side chains of PAEs. Little is known about the chronic toxicity of diethyl phthalate, but existing information suggests only a low toxic potential. Studies suggest that some phthalates affect male reproductive development via inhibition of androgen biosynthesis. In rats, for instance, repeated administration of DEP results in loss of germ cell populations in the testis . However, diethyl phthalate does not alter sexual differentiation in male rats. Dose response experiments in fiddler crabs have shown that seven-day exposure to diethyl phthalate at 50 mg/L significantly inhibited

315-408: The energy produced during the decomposition of the oxalate ester, and convert that energy into light energy which is observed as the characteristic glow in products such as glowsticks . TCPO can be prepared from a solution of 2,4,6-trichlorophenol in a solution of dry toluene by reaction with oxalyl chloride in the presence of a base such as triethylamine . This method produces crude TCPO with

336-487: The long term toxicity potential of toxicants or other stressors, commonly to aquatic organisms. Examples of common aquatic chronic toxicity test organisms, durations, and endpoints include: Results from chronic toxicity tests can be used to calculate values that can be used for determining water quality standards. These include: The no observed effects concentration (NOEC) is determined as the highest tested concentration that shows no statistically significant difference from

357-403: The risk from a mixture of phthalates or phthalates and other anti-androgens, may not be accurately assessed studying one chemical at a time. The same may be said about risks from several exposure routes together. Humans are exposed to phthalates by multiple exposure routes (predominantly dermal), while toxicological testing is done via oral exposure. Chronic toxicity Chronic toxicity ,

378-485: The soil is also contaminated with methanol , that would produce another three intermediate compounds, ethyl methyl phthalate, dimethyl phthalate and monomethyl phthalate. This biodegradation has been observed in several soil bacteria . Some bacteria with these abilities have specific enzymes involved in the degradation of phthalic acid esters such as phthalate oxygenase, phthalate dioxygenase, phthalate dehydrogenase and phthalate decarboxylase. The developed intermediates of

399-438: The toxicity of toxicants or stressors, making interpretation of test results difficult. These can be chemical, biological, or toxicological. Water chemistry plays an important role in the toxicity of certain toxicants. This includes pH, salinity, water hardness, conductivity, temperature, and amounts of dissolved organic carbon (DOC) For instance, the toxicity of copper is decreased with increasing amounts of DOC, as described by

420-440: The transesterification or demethylation, ethyl methyl phthalate and dimethyl phthalate, enhance the toxic effect and are able to disrupt the membrane of microorganisms. Recent studies show that DEP, a phthalic acid ester (PAE), is enzymatically hydrolyzed to its monoesters by pancreatic cholesterol esterase (CEase) in pigs and cows. These mammalian pancreatic CEases have been found to be nonspecific for degradation in relation to

441-402: Was highest at highest dose. In a following study it was found that both phthalate diesters and their metabolic products were present in each of these compartments, suggesting that the toxicity in embryos and fetuses could be the result of a direct effect. Some data suggest that exposure to multiple phthalates at low doses significantly increases the risk in a dose additive manner. Therefore,

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