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3100. Nitrosamines out of the frying pan
Processingaids femurs of male rats were studied after ip or oral administration of AF-2. Significant increases in the incidence of chromosomal aberrations were first apparent 4 hr after ip injection of 240mg AF-Z/kg, the incidence reaching a maximum after 6 hr and returning to control levels within 24 hr. A dose response was observed when chromosomal aberrations were scored 6 hr after ip administration of 4-240 mg AF-Z/kg, a 9% incidence of aberrations being produced by the maximum dose compared with 1, 2 and 5% incidences in control animals and those given 15 and 120 mg AF-Z/kg, respectively.Similar results were obtained when AF-2 was given by gavage, but 34 times the ip doses were necessaryto elicit quantitatively similar degrees of chromosomal damage. The aberrations were shown to be basically similar to those induced by the carcinogen 7,12-dimethylbenz[alanthracene in terms of morphology and chromosomal distribution of breaks and gaps. This experiment clearly showed the ability of AF-2 to damage DNA in Go, and it is reported that the carcinogenicity of AF-2 has since been demonstrated by the production of stomach tumours in mice fed AF-2. A small increase in tumour incidence was also recorded in mice exposed to AF-2 during the foetal and neonatal stages (ibid 1976, 14, 645). As a result of these findings, there has been a complete ban on the use of AF-2 in food in Japan since October 1974. 3100. Nitrosamines
out of the frying pan
Sen, N. P., Donaldson, B., Seaman, S., Iyengar, J. R. & Miles, W. F. (1976). Inhibition of nitrosamine formation in fried bacon by propyl gallate and L-ascorby1 palmitate. J. agric. Fd Chem. 24, 397. The occurrence of highly carcinogenic nitrosamines in food products and their formation by the action of nitrosating agents on normal food and body constituents has been reviewed recently (Cooper. Fd Cosmet. Toxicol. 1976. 14, 205). The inhibition by ascor-
by1 palmitate of the production of nitrosamines during the frying of bacon (ibid 1976, 14, 167) has now been investigated further by the authors cited above. Strips of bacon were sprayed with 5 ml of a solution containing about 1000 ppm of one of the following food additives: piopyl gallate (PG), L-ascorbyl palmitate (AP), piperazine hydrate, Sodium ascorbate, or nitrosoproline (NPro). After spraying, the samples were left for 30-60min at room temperature before. being fried to a ‘well-done’ stage. Control samples were not sprayed before cooking. Nitrosopyrrolidine (NPyr) was extracted with methylene chloride from the cooked bacon and cooked-out fat, analysed by a combination of thin-layer chromatography and fluorimetry, and confirmed by gas-liquid chromatography-mass spectrometry. For most brands of bacon tested, PG, AP and piperazine hydrate inhibited the formation of NPyr in the cooked bacon by more than 70%, with sodium ascorbate inhibiting the formation to a lesser extent. The addition of cysteine or sodium ascorbate along with PG gave results similar to those obtained with PG alone. When lard or non-nitrite bacon (bacon prepared without nitrite) was cooked alone no NPyr was formed, but when either was cooked with NPro, levels of NPyr between 0.04 and 0.06 ppm were detected. AP, PG and piperazine hydrate had no observable effect on the yield of NPyr from NPro, which suggested that these additives inhibited NPyr formation in normal cooked bacon by interfering with reactions other than the decarboxylation of NPro. Small residual amounts of NPyr in the additivetreated bacon after cooking probably originated from NPro present before cooking. The authors conclude that nitrosation reactions occurring during the cooking of bacon play a much greater part in the formation of NPyr than has been thought. As AP and PG are approved food additives, the addition of these to bacon before or after curing may be acceptable, but the feasibility of this treatment has not yet been determined.
PROCESSING 3101. Polydimethylsiloxane
in the environment
Hobbs, E. J., Keplinger, M. L. & Calandra, J. C. (1975). Toxicity of polydimethylsiloxanes in certain environmental systems.Enuir. Res. 10, 397. Polydimethylsiloxanes (PDMSs) are effective antifoam agents used in the processing of certain foods such as bread and cake, in the manufacture of drugs and cosmetics and in a variety of other industrial applications. In earlier studies, members of this class showed no toxicity to the rabbit or rat (Cited in F.C.‘I 1967, 5, 263) and were not carcinogenic in the mouse (Cutler et al. Fd Comet. Toxicol. 1974, 12, 443). The wide use of these compounds, however, and the possibility of their releaseinto the environment, combined with their resistanceto biodegradation, prompted the further study cited above. Various Dow Corning PDMS fluids were studied for their toxicity, persistenceand accumulation under
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different environmental conditions. In a simulated sewage digestor, [i4C]PDMS produced no 14C02 and, after 70 days, all the radioactivity was found on the filtered particulate matter, suggesting that no biodegradation or incorporation of PDMS by sewage bacteria had occurred. The toxicity of the fluids to daphnia, fresh-water fish, marine species, mallard ducks, bobwhite quail and domestic chickens was very low. Residues in the fresh-water bluegill sunfish exposed to [14C]PDMS in water for up to 31 days were low and highly variable (0.00-0.76 ppm in the tissue with exposures to 1 or 10ppm) and showed no correlation with either duration or level of exposure. Since PDMS was shown to be deposited on the walls of the aquaria, the 14C activity detected may have been due to surface contamination rather than to cellular uptake of the silicone. In white Leghorn chickens fed PDMS at dietary levelsup to 1000 ppm, neither egg production, quality
out of the frying pan
Sen, N. P., Donaldson, B., Seaman, S., Iyengar, J. R. & Miles, W. F. (1976). Inhibition of nitrosamine formation in fried bacon by propyl gallate and L-ascorby1 palmitate. J. agric. Fd Chem. 24, 397. The occurrence of highly carcinogenic nitrosamines in food products and their formation by the action of nitrosating agents on normal food and body constituents has been reviewed recently (Cooper. Fd Cosmet. Toxicol. 1976. 14, 205). The inhibition by ascor-
by1 palmitate of the production of nitrosamines during the frying of bacon (ibid 1976, 14, 167) has now been investigated further by the authors cited above. Strips of bacon were sprayed with 5 ml of a solution containing about 1000 ppm of one of the following food additives: piopyl gallate (PG), L-ascorbyl palmitate (AP), piperazine hydrate, Sodium ascorbate, or nitrosoproline (NPro). After spraying, the samples were left for 30-60min at room temperature before. being fried to a ‘well-done’ stage. Control samples were not sprayed before cooking. Nitrosopyrrolidine (NPyr) was extracted with methylene chloride from the cooked bacon and cooked-out fat, analysed by a combination of thin-layer chromatography and fluorimetry, and confirmed by gas-liquid chromatography-mass spectrometry. For most brands of bacon tested, PG, AP and piperazine hydrate inhibited the formation of NPyr in the cooked bacon by more than 70%, with sodium ascorbate inhibiting the formation to a lesser extent. The addition of cysteine or sodium ascorbate along with PG gave results similar to those obtained with PG alone. When lard or non-nitrite bacon (bacon prepared without nitrite) was cooked alone no NPyr was formed, but when either was cooked with NPro, levels of NPyr between 0.04 and 0.06 ppm were detected. AP, PG and piperazine hydrate had no observable effect on the yield of NPyr from NPro, which suggested that these additives inhibited NPyr formation in normal cooked bacon by interfering with reactions other than the decarboxylation of NPro. Small residual amounts of NPyr in the additivetreated bacon after cooking probably originated from NPro present before cooking. The authors conclude that nitrosation reactions occurring during the cooking of bacon play a much greater part in the formation of NPyr than has been thought. As AP and PG are approved food additives, the addition of these to bacon before or after curing may be acceptable, but the feasibility of this treatment has not yet been determined.
PROCESSING 3101. Polydimethylsiloxane
in the environment
Hobbs, E. J., Keplinger, M. L. & Calandra, J. C. (1975). Toxicity of polydimethylsiloxanes in certain environmental systems.Enuir. Res. 10, 397. Polydimethylsiloxanes (PDMSs) are effective antifoam agents used in the processing of certain foods such as bread and cake, in the manufacture of drugs and cosmetics and in a variety of other industrial applications. In earlier studies, members of this class showed no toxicity to the rabbit or rat (Cited in F.C.‘I 1967, 5, 263) and were not carcinogenic in the mouse (Cutler et al. Fd Comet. Toxicol. 1974, 12, 443). The wide use of these compounds, however, and the possibility of their releaseinto the environment, combined with their resistanceto biodegradation, prompted the further study cited above. Various Dow Corning PDMS fluids were studied for their toxicity, persistenceand accumulation under
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AIDS
different environmental conditions. In a simulated sewage digestor, [i4C]PDMS produced no 14C02 and, after 70 days, all the radioactivity was found on the filtered particulate matter, suggesting that no biodegradation or incorporation of PDMS by sewage bacteria had occurred. The toxicity of the fluids to daphnia, fresh-water fish, marine species, mallard ducks, bobwhite quail and domestic chickens was very low. Residues in the fresh-water bluegill sunfish exposed to [14C]PDMS in water for up to 31 days were low and highly variable (0.00-0.76 ppm in the tissue with exposures to 1 or 10ppm) and showed no correlation with either duration or level of exposure. Since PDMS was shown to be deposited on the walls of the aquaria, the 14C activity detected may have been due to surface contamination rather than to cellular uptake of the silicone. In white Leghorn chickens fed PDMS at dietary levelsup to 1000 ppm, neither egg production, quality