Acrolein concentrations

On the second startup no ignition in the bottom occurred, but it was observed here also that a significant drop in oxygen concentration occurred between the reactor bottom and the heat exchanger, without loss of acrolein concentration. The homogeneous reaction also produced acrolein, just in much lower selectivity. Then, on the third day of... 

Spectrophotometric determination with 4-hexylresorcinol and a fluorometric method with m-aminophenol are the most commonly used procedures for the determination of acrolein. However, gas chromatography and high-performance liquid chromatography procedures are also used (USEPA 1980 Kissel etal. 1981 Nishikawa and Hayakawa 1986). Acrolein concentrations in rainwater between 4 and 200 pg/L can be measured rapidly (less than 80 min) without interference from related compounds the method involves acrolein bromination and analysis by gas chromatography with electron capture detection (Nishikawa and Hayakawa 1986). Kissel etal. (1981) emphasize that water samples from potential acrolein treatment systems require the use of water from that system in preparing blanks, controls, and standards and that acrolein measurements should be made at the anticipated use concentrations. 

Degradation and evaporation seem to be the major pathways for acrolein loss in water smaller amounts are lost through absorption and uptake by aquatic organisms and sediments (USEPA 1980 Reinert and Rodgers 1987). The half-time persistence of acrolein in freshwater is 38 h at pH 8.6 and 50 h at pH 6.6 degradation is more rapid when initial acrolein concentrations are less than 3000 pg/L (Bowmer and Higgins 1976). Nordone et al. (1998) show a half-time persistence of 2.9 to 11.3 h at initial nominal concentrations of 20 pg/L, and 27.1 to 27.8 h at 101 pg/L. At pH 5, acrolein reacts by reversible hydrolysis to produce an equilibrium mixture with 92% beta-hydroxy-... 

Surface Water. In canal water, the initial acrolein concentration of 100 pg/L was reduced to 90, 50 and 30 pg/L at 5, 10, and 15 miles downstream. No explanation was given for the decrease in concentration, e.g., volatilization, chemical hydrolysis, dilution, etc. (Bartley and Gangstad, 1974). 

The simulation shows that acroleine is the most difficult to isolate. If not removed in C-1A it will be found in the top of C-2 and further in the end product The column C-1A is designed with a ratio stripping/rectificahon 3 1 to ensure over 99.9% HCN recovery. Despite a Rvalue of 1.7 the acroleine concentrates in the middle of the stripping zone, from which a quantitative removal by a large side stream or secondary recovery column is not efficient. The best solution is chemical conversion in heavies. 

Furthermore from the animal data available, no species appears to be especially sensitive to acrolein since similar effects were seen in all species tested with comparable acrolein concentrations. The highest NOAEL values and all reliable LOAEL values for respiratory effects in each species and duration category are recorded in Table 2-1 and plotted in Figure 2-1. 

Only two studies in animals were located that examined the carcinogenic potential of acrolein after inhalation exposure. Feron and Kruysse (1977) exposed hamsters to a single acrolein concentration of 4.0 ppm for 7 hours/day, 5 days/week for 52 weeks and found no evidence of respiratory tract tumors or tumors in other tissues and organs. However, this study is considered to be of too short duration to determine carcinogenicity. Le Bouffant et al. (1980) exposed rats for 10-18 months to 8 ppm acrolein for 1 hour/day, 7 days/week and reported no evidence of tumors in the respiratory tract or in other tissues and organs. 

The kinetics of acrolein oxidation is of first order with respect to acrolein, which can be easily understood by the competition of strongly adsorbed acrylic acid and less strongly adsorbed acrolein. The reduced rate of acrolein oxidation at elevated acrolein concentration is interpreted by adsorption of acrolein on reduced sites and consequently described by a negative reaction order with respect to acrolein in the reoxidation term r(02). In this context the independence of the acrolein oxidation rate from acrylic acid concentration is surprising. This result may be understood by the reaction mechanism proposed by T.V. Andrushkevich in which formed acrylate anions are shifted to sites on vanadium cations and after protonation are desorbed as acrylic acid. Parallel to the protonation the reduced sites are reoxidized. 

Concerning the molecular products of butenedial photolysis (Figure 3), the yield of 2(5H)-furanone is well predicted by the simulation, glyoxal and maleic anhydride are overpredicted while the CO yield in the simulation is much lower than observed experimentally. In MCMv3.1 glyoxal and CO are formed as co-products (Figure 4), but this is not consistent with the different yields of these products observed experimentally. Thuener et al. (2003) include a different source of CO in their proposed mechanism, i.e. direct formation fi om photolysis with a yield of 20%. A possible co-product for direct CO production is acrolein formed by an H-shift and C-C cleavage. The acrolein concentration was below the detection limit of the measurement technique, and its maximum yield was estimated to be 10%. No other direct photolysis products were observed and it was not possible to positively determine the mechanism and co-products for CO formation. 

After a 40-hour continuous exposure to a low acrolein concentration (2.1 ppm), an increased activity of the alkaline phosphatase was observed. The exposure to 4 ppm for 4, 8 and 20 hours resulted in increased values of the alkaline phosphates of the liver as compared to controls — 135, 222 and 253%, respectively. The activity of the liver alkaline phosphatases and tyrosine-ketoglutanate transaminases were increased in rats 5 to 10 hours after an injection or inhalation of acrolein. The results of research indicate the irritating effect of acrolein in stimulating the pituitary-adrenal system, which induces a hypersecretion of glucocorticoids conditioning the induction or stimulation of the synthesis of larger amounts of protein enzymes of the liver. 

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