Isophorone, determination

Abscisin II is a plant hormone which accelerates (in interaction with other factors) the abscission of young fruit of cotton. It can accelerate leaf senescence and abscission, inhibit flowering, and induce dormancy. It has no activity as an auxin or a gibberellin but counteracts the action of these hormones. Abscisin II was isolated from the acid fraction of an acetone extract by chromatographic procedures guided by an abscission bioassay. Its structure was determined from elemental analysis, mass spectrum, and infrared, ultraviolet, and nuclear magnetic resonance spectra. Comparisons of these with relevant spectra of isophorone and sorbic acid derivatives confirmed that abscisin II is 3-methyl-5-(1-hydroxy-4-oxo-2, 6, 6-trimethyl-2-cyclohexen-l-yl)-c s, trans-2, 4-pen-tadienoic acid. This carbon skeleton is shown to be unique among the known sesquiterpenes. 

Determination of Certain Nitroaromatics and Isophorone in Municipal and Industrial Discharges using LLE and GC... 

Isomerization of jS-isophorone to a-isophorone has been represented as a model reaction for the characterization of solid bases 106,107). The reaction involves the loss of a hydrogen atom from the position a to the carbonyl group, giving an allylic carbanion stabilized by conjugation, which can isomerize to a species corresponding to the carbanion of a-isophorone (Scheme 9). In this reaction, zero-order kinetics has been observed at 308 K for many bases, and consequently the initial rate of the reaction is equal to the rate constant. The rate of isomerization has been used to measure the total number of active sites on a series of solid bases. Figueras et al. (106,107) showed that the number of basic sites determined by CO2 adsorption on various calcined double-layered hydroxides was proportional to the rate constants for S-isophorone isomerization (Fig. 3), confirming that the reaction can be used as a useful tool for the determination of acid-base characteristics of oxide catalysts. 

IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO ISOPHORONE ... 

No medical test is known to determine human exposure to isophorone. A few studies in rats and rabbits have shown that isophorone and its metabolites can be found in the urine of these animals, so it may be possible to find a method for testing the urine of humans to determine exposure to isophorone. It is not known, however, whether such a measurement would predict how much exposure had occurred or the possible health effects. For more information see Chapter 2. 

The Environmental Protection Agency (EPA) has determined that the level of isophorone in natural waters (lakes, streams) should be limited to 5.2 parts isophorone per million parts of water (5.2 ppm) to protect human health from the harmful effects of isophorone from drinking the water and from eating contaminated fish and other animals found in the water. The Occupational Safety and Health Administration (OSHA) has set a permissible exposure limit of 4 parts of isophorone per million parts of workroom air (4 ppm) during an 8-hour work shift to protect workers. The National Institute for Occupational Safety and Health (NIOSH) recommends that the amount in workroom air be limited to 4 ppm averaged over a 10-hour work shift. Further information on government recommendations can be found in Chapter 7. 

As part of an intermediate duration study, in which rats were exposed to 500 ppm isophorone in air, Dutertre-Catella (1976) mated exposed males with exposed females, control males with exposed females, exposed males with control females, and control males with control females after 3 months of exposure. Exposure of females continued throughout gestation, and they were allowed to deliver. No differences in pregnancy rate or litter size and no abnormalities in pups were found. The pups were not examined for internal malformations therefore, this study was inadequate to determine developmental effects of isophorone. 

The oral LDso of isophorone was reported as 3450 mg/kg in male rats (Hazleton Labs 1964) and 2104-2150 mg/kg in female rats (Smyth et al. 1969, 1970). LDso values of 2700 200 mg/kg for male rats, 2100 200 mg/kg for female rats, and 2200 200 mg/kg for male mice also were reported by Dutertre-Catella (1976). The value reported by Hazleton Labs (1964) was estimated because the mortality data did not lend itself to statistical analysis. Furthermore, the doses were widely spaced, and the animals were fasted for only 3-4 hours before dosing, which could have interfered with gastrointestinal absorption of isophorone. Necropsy of rats that died revealed congestion of the lungs, kidneys, adrenals, and pancreas, and gastrointestinal inflammation. Necropsy of rats that survived the 14-day observation period revealed no effects. The studies by Smyth et al. (1969, 1970) were determinations of the joint toxic action of 27 pairs of industrial solvents (see Section 2.7 on Interactions with other chemicals), but the details of the individual LDs° determinations and the cause of death were not provided. Nevertheless, the values for isophorone were reproducible in the two studies by Smyth et al. (1969, 1970). The reason for the sex difference... 

Hazleton Labs (1964) reported that the dermal LDso of isophorone in rabbits was greater than 3160 mg/kg, the highest dose tested. In this study, the area of application was occluded for 24 hours. Union Carbide (1968), however, reported 1.5 mL/kg (1384 mg/kg) as the dermal LDso in rabbits, but no details of the determination were provided. Therefore, it is not possible to reconcile these contradictory reports. Dutertre-Catella (1976) estimated a dermal LDso of 1200 mg/kg in rabbits. The LDso was difficult to determine with precision because some rabbits died within 6 hours of application and the method requires that the chemical remain on the skin for 24 hours. The rabbits that did not die within 6 hours recovered and were not harmed by doses up to 4000 mg/kg. The dermal LDso js indicated on Table 2-3. When 0.1 or 0.2 mL isophorone was applied to the shaved skin of rats for 8 weeks, 20% of the males but none of the females died (Dutertre-Catella 1976) (Table 2-3). No studies were located regarding death of animals following chronic duration exposure to isophorone. 

Chronic exposure of mice by gavage to isophorone at 250 mg/kg/day resulted in hyperkeratosis of the forestomach (NTP 1986), an effect that may also be related to the irritating effect on mucous membranes. Although there is no tissue in man that is precisely analogous to the mouse forestomach and the effects of oral exposure of humans to isophorone are not known, ingestion of isophorone could result in gastrointestinal irritation. The minimum concentration of isophorone in water or food necessary to produce the irritation cannot be determined from the available data in animals. 

Experimental studies in humans have attempted to determine the inhalation thresholds for odor detection and eye, nose, and throat irritation. Reports on humans occupationally exposed to isophorone also indicate that isophorone is irritating to the skin, eye, nose, and throat, and may cause symptoms of dizziness, fatigue, and malaise. 

Thus, structure-activity relationships developed to estimate levels in biological media based on the partitioning properties of a chemical may not provide accurate information for isophorone. Furthermore, only one bioaccumulation study was available. In this study, which indicated a low potential for bioaccumulation, fish were exposed to isophorone in water rather than in food. From these data, it appears that food chain bioaccumulation may be occurring, and a clearer understanding of the potential for this would aid in determining how levels in the environment affect the food chain and potentially impact on human exposure levels. 

No studies were located regarding the transformation of isophorone in soils. Based on the information presented above and the lack of any monitoring data that report isophorone in groundwater or soils (except for hazardous waste sites), it appears that isophorone may not be discharged to soils in large amounts, and the small amounts that are deposited may degrade rapidly in soil. Another explanation, however, is that there is a lack of studies determining isophorone content in soil. 

Isophorone was detected in the Delaware River in the winter only in the summer, biodegradation or other processes (e.g., sorption) may have removed it from the water column. Isophorone has been detected in the sediments of Lake Pontchartrain, which is located in the delta plain of the Mississippi River. Its presence probably is due to the many industries that are situated along the Mississippi River and use the river water as process water. Levels of isophorone in surface waters range from a trace to 100 ppb however, this range represents only a few determinations. 

Exposure Levels in Environmental Media. Environmental monitoring data are not available for soil and air, and the data available for water, sediments, and biota are not sufficient to determine ambient concentrations. These data would be helpful in determining the ambient concentrations of isophorone so that exposure estimates of the general population and the bioconcentration factor of this chemical in aquatic organisms can be made. 

Methods for Biomarkers of Exposure. No methods are available for the analysis of isophorone biomarkers of exposure in biological materials. If a method for the determination of the level of a specific biomarker were available in a biological medium, it could be used to indicate the level of exposure and the possible resultant health effect. 

Shafer KH. 1982. Determination of nitroaromatic compounds and isophorone in industrial and municipal waste waters. U.S. EPA, Off Res Dev, 1-71. 

Nitroaromatics and Isophorone (Method 609). The GC column used for determination of these compounds is essentially the same as that used for the pesticides and PCBs. Nitrobenzene and isophorone are determined at 85 °C by using a FID. 2,6-Dinitrotoluene and 2,4-dinitrotoluene are determined at 145 °C by using an EC detector. 

The effect of curing on the diffusion of polymer and the curing agent is studied for the system of hydroxyl-terminated polybutadiene (R-45-M)/isophorone disso-cyanate (IPDI). Both components contribute to the echo intensity and the plot of In P(x)/I(0)] vs (G5)2 (A — 5/3) consists of two exponentials (Eq. (22)) the fast component (the steep intial slope) is attributed to the IPDI, and the long component to the R-45-M. The dependence of both diffusion constants on the curing time is shown in Fig. 19. The accuracy for Dfast data is less pronounced than for the polymer D(Mn), because only the first few data points are relevant for its determination. Furthermore, the low tail of the R-45-M molecular weight distribution nearly coin-... 

Figure 6.6 Evolution of tan 8 during polyurethane synthesis at 110°C, at different angular frequencies,

Figure 9.1 Rate constant for isophorone isomerization at 308 K as a function of the number of sites determined by C02 adsorption for a series of basic solids ( ) KF ( ) Mg(La)0 (a) Mg(Al)0 and ( ) Ba(Al)0. Reprinted from Journal of Catalysis, vol. 211, Figueras et al., Isophorone isomerization as model reaction for the characterization of solid bases application to the determination of the number of sites, pp. 144-149, Copyright (2002), with permission from Elsevier...

Kinetic studies of the reaction of CO2 with radical anions generated from dialkyl fumarates and maleates showed that C-C bond formation was the rate-determining step. The pseudo first-order rate constants, kco2, for fumarate radical anions in C02-saturated DMF were found to vary between 0.35 and 1.5 s and to decrease in the same order as observed for dimerization [218]. Rate constants for maleates (kco2 varied from 32.0 s to 18.0 s ) were higher. Rather slow is the coupling of CO2 with the 4-keto isophorone in MeCN (k co2 = 0-35 s ) [219]. 

Sharping, G., Dalene, M., and Tinnerberg, H., Biological monitoring of hexamethylene-diisocyanate and isophorone-diisocyanate by the determination of hexamethylene-diamine and isophorone-diamine in hydrolyzed urine using liquid-chromatography and mass-spectrometry. Analyst, 119, 2051-2055, 1994. 

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