[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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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↗
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↗
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↗
Induction of sister chromatid exchanges by styrene and its presumed metabolite styrene oxide in the presence of rat liver homogenate.
Styrene and its metabolite styrene oxide were tested for their ability to induce sister chromatid exchanges (SCE) in CHO cells. Styrene oxide appeared to be a potent inducer of SCE. Styrene itself did not increase the number of SCE per metaphase, even in the presence of a metabolic activation system. The metabolic activation system decreased the SCE induction caused by styrene oxide. Induction of SCE by styrene in the presence of metabolic activation occurred when cyclohexene oxide was used as an inhibitor of the enzyme epoxide hydrase.
Animals↗
Microsomal styrene mono-oxygenase and styrene epoxide hydrase activities in rats.
1. Styrene epoxide formation and styrene epoxide hydration have been studied in liver, lung, kidney, heart, spleen and brain of female and male rats. 2. Styrene epoxide formation is NADPH-dependent although it is enhanced when NADH is added together with NADP. This enzymic activity is inhibited by metyrapone and SKF 525-A but not by the effective inhibitors of epoxide hydrase, 1,2-epoxy-3,3,3-trichloropropene and cyclohexene oxide. 3. Known inducers of liver microsomal mono-oxygenases show a different activity on the two enzymes. Phenobarbital increases both formation and hydration of styrene epoxide; and carbamazepine increase the hydration but not the formation of styrene epoxide; a steroid contraceptive combination (lynestrenol+ mestranol) increases styrene epoxide formation while it inhibits epoxide hydrase; 3-methylcholanthrene does not affect either of the activities.
Animals↗
Mutagenicity of industrial compounds. VII. Styrene and styrene oxide: II. Point mutations, chromosome aberrations and DNA repair induction analyses.
The possible genetic effects produced by styrene have been investigated by means of different methodologies in several biological organisms: (a) the induction of point mutation has been investigated in Salmonella typhimurium (reverse mutation), in the yeast Schizosaccharomyces pombe (forward mutation), both in vitro and in vivo, in the host-mediated assay of mice, and in the Chinese hamster cell line grown in vitro (V-79) (forward mutation); (b) the induction of chromosome mutation has been investigated in vivo, in mice, through the analysis of the presence of chromosome aberrations in bone marrow cells of treated animals; (c) the production of DNA (deoxyribonucleic acid) damage and the stimulation of DNA repair synthesis have been evaluated from measurements of unscheduled DNA synthesis in a heteroploid human cell line (EUE) and gene-conversion produced in the yeast Saccharomyces cerevisiae treated in vitro and in vivo (host-mediated assay). All the in vitro studies have been developed by the testing of the styrene in the presence of a metabolic activating system obtained with a mouse liver microsomal preparation. Styrene oxide, one of the in vivo metabolites of styrene with electrophilic properties towards DNA molecules, have also been tested in similar systems. Styrene was not mutagenic in all the systems tested; styrene oxide, on the contrary, was shown to be an active mutagen, independently of the genetic system under evaluation.
Animals↗
Toxicity of styrene and styrene oxide on chick embryos.
Styrene and styrene oxide were injected into the air space of fertilized chicken eggs at different times during an incubation period of 14 days. The toxicity of styrene and styrene oxide when injected on the fourth day of incubation revealed an LD50 of 40 mumol/egg and 1.5 mumol/egg, respectively. Malformations were found in 0-20% of the embryos, but never in the controls. The results obtained point to a need for further experimental, and possibly epidemiologic, studies on the consequences of styrene exposure.
Animals↗
Microbial transformations of styrene and [14C] styrene in soil and enrichment cultures.
Two different mechanisms were responsible for the disappearance of styrene in enrichment cultures: (i) a mixed population of microorganisms, capable of utilizing styrene as a sole carbon source, oxidized this substrate to phenylethanol and phenylacetic acid; (ii) the culture also mediated polymerization of the monomer to low-molecular-weight styrene oligomers. This chemical reaction probably occurred as the result of microbial degradation of butylcatechol, an antioxidant polymerization inhibitor present in commercial styrene. The resultant polymer material was subsequently metabolized. In soil incubation studies, 14CO2 evolution from applied [8-14C] styrene was used to estimate microbial degradation. Approximately 90 percent of the labeled carbon was evolved from a 0.2 percent addition, and about 75 percent was lost from the 0.5 percent application over a 16-week period.
Bacteria↗
Mutagenicity of industrial compounds: styrene and its possible metabolite styrene oxide.
Styrene and its presumed metabolite, styrene oxide, were tested for their mutagenic effect on a forward mutation system of yeast and of Chinese hamster cells, and on a gene-conversion system of yeast. Experiments with liver microsomal preparations and host-mediated assay with yeast were also carried out. Styrene oxide was mutagenic in all test systems. Styrene was mutagenic only in the host-mediated assay.
Adenine↗
Embryotoxicity and teratogenicity of styrene and styrene oxide on chick embryos enhanced by trichloropropylene oxide.
The effects of TCPO (trichloropropylene oxide) on the embryotoxicity and teratogenicity of styrene and styrene oxide and chick embryos were investigated. The compounds were injected into the air space of the eggs in a total volume of 25 microliter on the third day of embryogenesis. TCPO increased embryotoxicity and teratogenicity of styrene and styrene oxide. Our results present evidence that the epoxides possess embryotoxic and teratogenic properties in chick embryos.
Abnormalities, Drug-Induced↗