[Studies on industrial styrene poisoning. (Part VI) Styrene concentrations in alveolar air and blood of styrene workers and styrene exposed animals (author's transl)].
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Animals↗
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Mutagenic action of styrene and its metabolites. II. Genotoxic activity of styrene, styrene oxide, styrene glycol and benzoic acid tested with the SOS chromotest.
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Alkaline Phosphatase↗
[Inhibition of delta-aminolevulinic acid dehydratase by styrene and styrene oxide].
Effects of styrene and styrene oxide on delta-aminolevulinic acid dehydratase in rats were investigated, in vivo and in vitro. In the in vivo study, rats were exposed to styrene or styrene oxide intraperitoneally for seven days. delta-Aminolevulinic acid dehydratase in the erythrocyte was inhibited by both styrene and styrene oxide. The inhibition by styrene oxide had a clear dose-response relationship, but that by styrene did not. In the liver, however, these substances did not inhibit delta-aminolevulinic acid dehydratase. In the in vitro study, styrene oxide inhibited delta-aminolevulinic acid dehydratase both in the erythrocyte and in the liver, but styrene failed to inhibit it. These results suggest that styrene is metabolized to styrene oxide, and this metabolite inhibits delta-aminolevulinic acid dehydratase. It is also thought that the discrepancy of inhibition between the erythrocyte and the liver is due to a difference of distribution and metabolism of the substances.
Animals↗
In vitro transformation and tumor promotion studies of styrene and styrene oxide.
The carcinogenic properties of styrene and styrene oxide were investigated using C3H/10T1/2C18 cells as a test system. In vitro transformation was not observed for either of the two chemicals; however, styrene oxide at three different concentrations enhanced the morphological transformation in the two-stage transformation assay. 0.1, 1 and 10 microM styrene oxide added twice weekly resulted in 32.4, 26.8 and 31.4 per cent of the dishes with one or more type III foci. Styrene and styrene oxide were only slightly toxic to the cells at the concentrations used. Styrene oxide did not affect the growth rate of the C3H/10T1/2 cells at 10 microM. However, 100 microM styrene oxide added to logarithmically growing cells caused a significant decrease in growth rate within 24 to 48 h. The tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate inhibited DNA synthesis approximately 60% 8 h after initiation of treatment. When styrene oxide at concentrations up to 100 microM was tested in a similar experiment, however, no significant effect was observed. Total RNA synthesis increased by 70% 1.5 h after initiation of treatment at 1 microM styrene oxide; this effect was not seen after 24 h. Styrene oxide at concentrations of 1 and 0.1 microM stimulated the incorporation of [3H]choline into cells by approximately 20% during a 2 h incubation, the major site of incorporation being the nuclear-associated endoplasmic reticulum.
Animals↗
Sub-chronic effects of styrene and styrene oxide on lipid peroxidation and the metabolism of glutathione in rat liver and brain.
Sub-chronic effects of styrene and styrene oxide on lipid peroxidation, glutathione contents and glutathione reductase activities in the liver and brain were examined after intraperitoneal administration to rats 3 times a week for 7 weeks. Styrene (300, 400 and 500 mg/kg) and styrene oxide (200 and 300 mg/kg) increased lipid peroxidation in the liver after 7 weeks of treatment. Hepatic lipid peroxidation in the rats treated with a higher dose of styrene oxide (400 mg/kg) was significantly enhanced even after 2 weeks of treatment. On the other hand, no change in lipid peroxidation was observed in the brain under the above conditions. Neither glutathione contents nor glutathione reductase activities in the liver and brain were altered at 40 h after the last of these sub-chronic treatments. To elucidate the cause of lipid peroxidation, the time courses of glutathione content after treatment with either styrene or styrene oxide (300 mg/kg) were studied in more detail. Significant decreases in both the GSH and GSSG contents were detected shortly after these treatments and the levels recovered to the control values at 40 h in these organs, although the changes were less significant in the brain of rats treated with styrene. These results suggest that enhancement of lipid peroxidation in the liver after treatment with styrene or styrene oxide was a consequence of repeated depletions of glutathione to certain critical levels and delayed recovery of lipid peroxides.
Animals↗
Biological indicators of exposure in styrene polymerization workers. Styrene in blood and adipose tissue and mandelic and phenylglyoxylic acids in urine.
The concentrations of mandelic and phenylglyoxylic acids, urinary metabolites of styrene, and styrene in blood were determined for 491 styrene polymerization workers. Styrene in subcutaneous fat was determined for 25 workers. The levels of styrene exposure were estimated to be less than 10 ppm, and urinary metabolite and blood styrene concentrations indicated that significant recent exposure (within 4 h) had occurred among workers in areas of styrene polymerization and styrene monomer production. Styrene analysis of subcutaneous fat suggested that the monomer may have been present for as long as 3 d after exposure, a time when urinary metabolites and blood styrene were almost invariably undetectable. All three biological parameters were correlated with recency of exposure and estimated intensity of exposure within job categories.
Adipose Tissue↗
Bacterial degradation of styrene involving a novel flavin adenine dinucleotide-dependent styrene monooxygenase.
By using styrene as the sole source of carbon and energy in concentrations of 10 to 500 microM, 14 strains of aerobic bacteria and two strains of fungi were isolated from various soil and water samples. In cell extracts of 11 of the bacterial isolates, a novel flavin adenine dinucleotide-requiring styrene monooxygenase activity that oxidized styrene to styrene oxide (phenyl oxirane) was detected. In one bacterial strain (S5), styrene metabolism was studied in more detail. In addition to styrene monooxygenase, cell extracts from strain S5 contained styrene oxide isomerase and phenylacetaldehyde dehydrogenase activities. A pathway for styrene degradation via styrene oxide and phenylacetaldehyde to phenylacetic acid is proposed.
Bacteria↗
A very sensitive gas chromatographic method for the evaluation of styrene oxidase and styrene oxide hydratase activities.
Styrene is a compound widely used in the manufacture of polystyrenic plastics and it has recently been shown to exert mutagenic effects after metabolic activation into styrene oxide by the microsomal mixed function oxidases; this oxide is further converted into inactive styrene glycol. In order to investigate the relative importance of activation and desactivation processes of styrene, we developed a gas chromatographic method which enables us to simultaneously measure styrene oxide and styrene glycol formed after incubation of styrene with microsomal preparations from different tissues. After selective extraction of the two compounds from the incubation mixture, they are derivatized with pentafluorobenzoyl chloride and measured by gas chromatography using an electron capture detector. The high sensitivity of the method, which allows 0.01 ng of both compounds to be measured, as well as its selectiveity, has permitted us to adequately evaluate the kinetic parameters of styrene oxidase and styrene oxide hydratase activities, as well as their modifications under the influence of various pretreatments of the animals.
Animals↗
Cytogenetic effects of styrene and styrene oxide.
Styrene and styrene oxide induce various cytogenetic effects, similar in both human lymphocytes in vitro and onion root-tip cells in vivo. Styrene appears to cause chromosome breakage in both systems, and in Allium it shows a strong c-mitotic effect. Styrene oxide, on the other hand, seems to destroy the tertiary folding of the chromatin. Cytotoxicity of styrene oxide is very high (complete mitotic inhibition occurs on 0.03% v/v) in human lymphocytes, whereas, in Allium, styrene is slightly more toxic than styrene oxide. Styrene glycol, a further metabolite of styrene oxide, does not cause mitotic inhibition.
Cells, Cultured↗
[Studies on industrial styrene poisoning (Part VIII). Distribution and elimination of styrene in rats exposed to styrene (author's transl)].
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Animals↗
[Studies on industrial styrene poisoning (Part IX). Distribution of styrene in tissues of rats by repeated exposures and intraperitoneal administrations of styrene (author's transl)].
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Animals↗
A study on the mutagenic activity of styrene and styrene oxide.
Styrene oxide is multagenic, without metabolic activation, to S. typhimurium strains TA 1535 and TA 100, which have been devised to detect mutagens causing base-pair substitutions. Styrene seems to be mutagenic toward the same strains, but only after metabolic activation. The toxicity of both styrene and styrene oxide make the construction of reliable dose-response curves rather difficult. Diethylmaleate and 3,3,3-trichloropropene oxide enhanced the mutagenicity of styrene oxide in the presence of homogenate; this result indicates the participation of epoxide hydratase and glutathione S-oxide transferase in the metabolism of styrene oxide. These two chemicals did not influence the mutagenic activity of styrene. Styrene glycol and 4-tert-butyl-brenzcatechin were not mutagenic to any of the strains studied. Results show that further, more detailed experimental and, possibly, epidemiologic studies are warranted.
Animals↗
Cytogenetic effects of styrene and styrene oxide on human lymphocytes and Allium cepa.
Styrene and styrene oxide induce cytogenetic effects already at very low concentrations (0.01% v/v or even less); the effects are similar in both in vitro human lymphocytes and in vivo onion root tip cells (Allium cepa L.). It is characteristic that styrene treatment is more potent in causing chromosome breakage in both systems. In Allium styrene induced inhibition of mitotic spindle action as revealed by a strong c-mitotic effect. Also the number of micronuclei and nuclear bridges increased in both test systems, especially after styrene oxide treatment. Furthermore, the metaphase chromosome morphology in the cells treated with styrene oxide was strongly affected. In both systems, chromosome destruction was observed, or else the chromosome material was decondensed and resulted in a characteristic fuzzy appearance of Allium chromosomes or a banded appearance of human lymphocyte chromosomes. A specific effect of styrene oxide on the chromosomal proteins is thus suggested. The data obtained from the autoradiographic studies with Allium support the idea that [7--3H] styrene oxide binds irreversibly to the cytoplasmic and nuclear macromolecules.
Autoradiography↗
Effect of in vitro exposure to styrene, styrene oxide, and other structurally related compounds on murine cell-mediated immunity.
Spleen cells from C57BL/6 mice were exposed to nontoxic doses of styrene, styrene oxide, styrene glycol, allylbenzene, ethylbenzene and toluene. None of these compounds except allylbenzene showed any great suppression or stimulation of the cytotoxic-T lymphocyte response. Allylbenzene was a strong suppressor of the cytotoxic-T lymphocyte response but, like the other compounds, had no effect on natural cytotoxicity. Styrene glycol, ethylbenzene and toluene also did not suppress natural killer cell activity. In contrast, styrene, styrene oxide and allylbenzene were strong suppressors of natural killer cell activity. The natural killer cell inhibition caused by styrene oxide did not occur if treatment was performed at 0 degree C instead of 37 degrees C, and was reversed by the addition of 5 mM glutathione or a 30 min recovery period at 37 degrees C. The natural killer cell suppression caused by allylbenzene was not reversed by these methods. These compounds may be causing natural killer cell suppression by different mechanisms, depending on the compound under study, and on whether these compounds contain a double bond or an epoxide moiety.
Animals↗
Organ distribution and nervous system binding of styrene and styrene oxide.
Ten adult male rats were injected intraperitoneally with 460 mumol of styrene oxide with radioactive label. Fifteen similar rats were injected similarly with 577 mumol of styrene. The distribution of styrene in central nervous system, blood, liver, lungs, kidneys and duodenum was studied 3, 6 and 24 h after the injection while the same studies were done with styrene oxide 3 and 6 h after the injection. The liver, brain, kidney and duodenal contents of styrene and styrene oxide were higher than that in blood, lungs and spinal cord while the macromolecule-associated styrene oxide in the central nervous system was small. The removal of injected compounds was slow between 3 and 6 h after the injection in the organ systems although lipid-soluble compounds tended to diminish in brain more rapidly than the total radioactivity.
Animals↗
Blood styrene and urinary metabolites in styrene polymerisation.
The results of the analysis of blood and urine samples for styrene and its metabolites in 491 workers in a styrene polymerisation plant in the United States are reported. The levels of exposure to styrene were estimated to be less than 10 ppm, but nevertheless styrene and metabolites were detectable in more than 50% of workers in polymerisation jobs, within 4 h of exposure. Workers involved in the manufacture and purification of styrene from ethyl benzene also had detectable blood styrene and urinary metabolites in 83% of recently exposed subjects. The relationship between styrene in blood and in subcutaneous fat and urinary metabolites as pharmacokinetic variables is discussed.
Chemical Industry↗
Styrene and styrene oxide concentrations in the air during the lamination process in the reinforced plastics industry.
Styrene and styrene oxide concentrations were measured during the lamination process in the reinforced plastics industry. The mean concentration of styrene in the personal samples was 130 ppm, the highest value measured being 350 ppm. The average concentration for styrene oxide alone was 0.1 ppm, whereas the corresponding measurement for styrene oxide and its decomposition products combined was 0.7 ppm. In comparison then, the concentrations of styrene oxide and its derivatives were much lower (about 0.5% of the total) than those of styrene.
Air↗
Inhibitory characteristics of styrene & styrene oxide on Na+,K+ activated adenosine triphosphatase.
Styrene, an important ingredient of plastic, is reported to cause it neurotoxic effects through its important metabolite styrene oxide. Na+, K+ -ATPase (NKA), an important enzyme in the neurotransmission processes, is found to be inhibited by styrene (200 mg/kg) and styrene oxide (55 mg/Kg) by 15 and 45% respectively. Kinetic evaluations show that Km values, number of interaction sites and rate of reaction, with respect to K+ ions, decreased in styrene oxide treated NKA samples. However, high Km values of Na+ sites suggest for low affinity with respect to Na+ ions. Na+ and K+ ion activation, ATP hydrolysis and ouabain titration patterns indicate for a conformational change in NKA mainly due to styrene oxide.
Administration, Oral↗