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PubMed1996

Determination of albumin and hemoglobin adducts in workers exposed to styrene and styrene oxide.

Hemoglobin and albumin adducts of the carcinogen styrene-7,8-oxide (SO) were measured in 48 workers exposed to both styrene and SO in a boat manufacturing plant. Personal exposures to both substances were measured repeatedly over the course of 1 year (styrene:0.9-235 mg/m3 with a mean of 64.3 mg/m3 for 48 subjects; S0: 13.4-525 mu g/m3 with a mean of 159 mu g/m3 for 20 subjects). Cysteine and carboxylic acid adducts of SO with hemoglobin and albumin were assayed on one or more occasions for each subject. The proteins were subjected to base hydrolysis to release styrene glycol, representing carboxylic acid-bound SO, and were then treated with Raney nickel to release 1-phenylethanol and 2-phenylethanol, representing cysteine-bound SO. These three analytes were extracted, derivatized, and analyzed by gas chromatography-mass spectrometry. No evidence was found of any exposure-related increase in hemoglobin adducts. In contrast, albumin adducts were found to increase with exposures to either styrene or SO, the latter apparently being more important. This suggests that exposure to low levels of SO in the air may be important among workers in the reinforced plastics industry. Significant levels of SO adducts of albumin and hemoglobin were also detected in proteins obtained from persons without occupational exposure to styrene or to SO. This finding opens the possibility that SO is either a dietary or an environmental contaminant or is produced endogenously.

Air Pollutants, Occupational↗
PubMed1978

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↗
PubMed1983

Single-strand breaks in DNA of various organs of mice induced by styrene and styrene oxide.

Styrene and its metabolite styrene oxide were given i.p. to mice. The induction of single-strand breaks (SSB) in DNA was studied with the DNA unwinding technique. The level of SSB in kidney-DNA was a linear function of the dose for both substances. Styrene and styrene oxide induced an increase in the level of SSB in DNA of kidney, liver, lung, testis and brain 1 h after administration. After 24 h the damage remained on an enhanced level in liver, lung and testis after styrene oxide administration and in all organs except liver after styrene administration.

Animals↗
PubMed1983

Styrene oxidation to styrene oxide coupled with arachidonic acid oxidation by soybean lipoxygenase.

Styrene was co-oxidated to styrene oxide during soybean lipoxygenase catalyzed formation of arachidonic acid lipid peroxides. Styrene oxidation showed linear dependence on the amount of enzyme and on arachidonic acid concentration, and saturation kinetics with styrene concentration. Styrene oxide formation was dependent on the lipid substrate used and was inhibited by antioxidants. Lipid peroxides appear to be able to support styrene oxidation when produced from rat liver microsomes.

Animals↗
PubMed2004

Occupational exposure to styrene: modulation of cytogenetic damage and levels of urinary metabolites of styrene by polymorphisms in genes CYP2E1, EPHX1, GSTM1, GSTT1 and GSTP1.

Styrene is widely used in the production of various plastics, synthetic rubber and resins. The aim of this study was to evaluate if individual polymorphisms in xenobiotic metabolizing enzymes, related with the metabolic fate of styrene, could modify individual susceptibility to the possible genotoxic effects of the styrene exposure. Twenty-eight reinforced plastic workers and 28 control subjects were studied. In the selected population the urinary styrene metabolites mandelic (MA) and phenylglyoxylic (PGA) acids were quantified, sister chromatid exchanges (SCE) and micronuclei (MN) were assessed in peripheral lymphocytes and all the subjects were genotyped for GSTM1, GSTT1 (gene deletions), GSTP1 (codon 105 ile==>val), EPHX1 (codons 113 tyr==>his and 139 his==>arg) and CYP2E1 (DraI polymorphism in intron 6). The results obtained showed a significant difference between the levels of SCE, but not in MN levels, in exposed workers as compared with the control group. The GSTP1 and CYP2E1 individual genotypes modulate the baseline levels of SCE that are lower in non-wild type individuals for both polymorphisms. The GSTM1 null individuals with low levels of exposure have significantly higher urinary levels of MA+PGA. The present data seem to suggest that apart from the methodology usually used for monitoring populations occupationally exposed to styrene (urinary metabolites and biomarkers of early biological effects) the analysis of individual genotypes associated with the metabolic fate of styrene should also be carried out in order to evaluate the individual genetic susceptibility of exposed populations.

Adolescent↗
PubMed1976

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↗
PubMed1978

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↗
PubMed2000

Production of enantiopure styrene oxide by recombinant Escherichia coli synthesizing a two-component styrene monooxygenase.

A whole cell biocatalytic process was developed to enable the efficient oxidation of styrene to chiral (S)-styrene oxide with an enantiomeric excess better than 99%. Recombinant Escherichia coli cells were employed to express the genes styAB encoding the styrene monooxygenase of Pseudomonas sp. strain VLB120 from an expression plasmid utilizing the alk regulatory system of P. oleovorans GPo1. The strains reached specific activities of up to 70 U* (g cell dry weight)(-1) in shake-flask experiments with glucose as the carbon source. An efficient two-liquid phase fed-batch process was established for the production of (S)-styrene oxide with hexadecane as an apolar carrier solvent and a nutrient feed consisting of glucose, magnesium sulfate, and yeast extract. Engineering of the phase fraction and the composition of organic phase and feed led to a 2-L scale process with maximal volumetric productivities of 2.2 g (S)-styrene oxide per liter liquid volume per hour. This optimized process was based completely on defined medium and used bis(2-ethylhexyl)phthalate as the apolar carrier solvent, which together with substrate and inducer consisted of 50% of the total liquid volume. Using this system, we were able to produce per liter liquid volume 11 g of enantiopure (S)-styrene oxide in 10 h.

Base Sequence↗
PubMed1995

A note on individual differences in the urinary excretion of optical enantiomers of styrene metabolites and of styrene-derived mercapturic acids in humans.

Urine samples from 20 male workers in the polyester industry exposed by inhalation to styrene concentrations ranging from 29 to 41 ppm were investigated. Excretion products of styrene metabolism, mandelic acid and mercapturic acids, were purified from the urine over an extraction column packed with Porapak Q, with subsequent ether elution. The optical enantiomers R- and S-mandelic acid were then determined by thin layer chromatography (TLC) using chiral plate material and selective staining with vanadium pentoxide. Quantitative analysis of these compounds was performed using commercial reference substances. Styrene-specific mercapturic acids were analyzed by a modified TLC method, using synthesized reference substances. The concentration of racemic mandelic acid in the individual urine samples ranged from 80 to 1610 mg/l, and the ratio of the R- and S-enantiomers ranged from 0.7 to 2.2. These individual variations are not explained by differences in individual styrene exposure levels, or by differences in the concentration of the urine samples (in relation to creatinine excretion). Styrene-specific mercapturic acids were detected in the urine of only 1 of the 20 workers, at a concentration much lower than expected from previous investigations by others in humans and laboratory animals, in which less specific analytical methods had been used. The results point to marked interindividual differences in metabolism of styrene, probably related to enzyme polymorphisms.

Acetylcysteine↗
PubMed1983

Styrene oxidation to styrene oxide by hydroxyl radicals produced during reaction of xanthine with xanthine oxidase in the presence of Fe3+.

Styrene was oxidized to styrene oxide during reaction of xanthine (X) with xanthine oxidase (XO) in the presence of Fe3+. This reaction showed a dose-dependent requirement of iron and was inhibited by superoxide dismutase (SOD) and catalase, indicating that both the superoxide anion and H2O2 were essential. Styrene oxide production was inhibited by hydroxyl radical scavengers indicating that this reactive oxygen intermediate could be the proximal oxidant involved in styrene oxidation to styrene oxide.

Chemical Phenomena↗
PubMed2004

Study of the inclusion processes of styrene and alpha-methyl-styrene in beta-cyclodextrin.

The inclusion complexes of styrene and alpha-methyl-styrene with beta-cyclodextrin (beta-CD) were investigated by using [1H] NMR titration in solution and X-ray diffraction (XRD) analysis, thermo-gravimetric analysis (TGA), elemental analysis (EA) in the solid state. The inclusion process has been studied by using PM3 quantum-mechanical semi-empirical method. The calculated results are in agreed with the experimental data. All results show that alpha-methyl-styrene has stronger interaction with beta-cyclodextrin than styrene does, so the complex of beta-CD-alpha-methyl-styrene is more stable.

Cyclodextrins↗
PubMed1988

Long-term carcinogenicity bioassays on styrene administered by inhalation, ingestion and injection and styrene oxide administered by ingestion in Sprague-Dawley rats, and para-methylstyrene administered by ingestion in Sprague-Dawley rats and Swiss mice.

Styrene was administered to Sprague-Dawley rats by inhalation (300, 100, 50, 25, 10 and 0 ppm, 4 hours daily, 5 days weekly, for 52 weeks); by gavage (250, 50 and 0 mg/kg b.w. in olive oil, once daily, 4-5 days weekly, for 52 weeks), by intraperitoneal injection (50 and 0 mg in olive oil, four times at 2-month intervals), by subcutaneous injection (50 and 0 mg in olive oil, once). Styrene oxide was administered to Sprague-Dawley rats by gavage as styrene (250, 50 and 0 mg/kg b.w. in olive oil, once daily, 4-5 days weekly, for 52 weeks). The animals were kept under observation until spontaneous death. Para-methylstyrene was also administered by gavage to Sprague-Dawley rats at 500, 250, 50, 10 and 0 mg/kg b.w., and to Swiss mice at 250, 50, 10 and 0 mg/kg b.w., in olive oil, once daily, 5 days weekly, for 108 weeks and 78 weeks, respectively. The study was terminated when the survival rate reached 50% in at least one experimental group. Styrene, when given by inhalation, was found to cause an increase in total (benign and malignant) and malignant mammary tumors. Styrene oxide produced a high incidence of tumors in the forestomach (papillomas, acanthomas, and in situ and invasive squamous cell carcinomas). Para-methylstyrene was not shown to be carcinogenic.

Administration, Inhalation↗
PubMed1982

Studies on metabolism and toxicity of styrene. V. The metabolism of styrene, racemic, (R)-(+)-, and (S)-(--)-phenyloxiranes in the rat.

Metabolism of styrene, racemic phenyloxirane, (R)-(+)-, and (S)-(--)-phenyloxiranes in rats has been described. The animals excreted phenylethanediol, mandelic acid, phenylglyoxylic acid, and two regioisomeric mercapturic acids in their urine after the intraperitoneal injection of the phenyloxiranes as well as styrene. The mercapturic acids were identified as N-acetyl-S-(1-phenyl-2-hydroxyethyl)cysteine (MA-1) and N-acetyl-S-(2-phenyl-2-hydroxyethyl)cysteine (MA-2). The ratios of the mercapturic acids to the other metabolites excreted in the urine were 1 to 1.8 and 1 to 1.5 for styrene and racemic phenyloxirane, respectively. A remarkable stereoselectivity was observed in the excretion of both types of the metabolites when optically active phenyloxiranes were administered. The rate of excretion of the mercapturic acids was 2.5 times higher than that of the other metabolites when the (R)-oxirane was injected, but the reverse was the case in the (S)-oxirane. The mercapturic acid, MA-1, was excreted at higher rate than the isomer, MA-2, on the administration of styrene and the phenyloxiranes. The most significant regioselectivity in the excretion of MA's was observed when styrene and (S)-phenyloxirane were administered.

Acetylcysteine↗
PubMed1984

Cytogenetic analysis of human peripheral blood lymphocytes in culture exposed in vitro to styrene and styrene oxide.

Styrene and styrene oxide mutagenicity was tested in cultured human lymphocytes treated in vitro with various concentrations of test agents. Styrene alone was found mutagenic at the highest concentration used (5 X 10(-4) mol. l-1, combined with the alkylating agent THIO-TEPA it did not affect the chromosome aberration yield. Exposure to styrene oxide gave a positive result showing a clear-cut dose-effect relationship within the concentration range 5 X 10(-6) to 1 X 10(-3) mol. l-1. In combination with THIO-TEPA its effect on chromosome aberration yields was additive. Styrene oxide proved also to be a very potent inducer of sister chromatid exchanges (SCE) within the concentration range 5 X 10(-6) to 1 X 10(-3) mol. l-1 tested. Combined with THIO-TEPA it exhibited a distinct additive effect in the production of SCEs.

Adult↗
PubMed1994

Quantitative determination of styrene in blood and mandelic acid in urine of the occupationally styrene-exposed workers.

The concentration of styrene in blood of the occupationally styrene-exposed workers was checked by gas chromatographic headspace analysis. Mandelic acd in urine, that is a major metabolite of styrene, and hippuric acid were also analyzed by high performance liquid chromatography. For the biological monitoring of styrene-exposed workers, the routine method of the quantitative determination of styrene and its metabolites in the biological samples were studied.

Chromatography, Gas↗
PubMed1977

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↗
PubMed2002

DNA adducts of styrene-7,8-oxide in target and non-target organs for tumor induction in rat and mouse after repeated inhalation exposure to styrene.

Styrene by inhalation had been shown to increase the lung tumor incidence in mice at 20 ppm and higher, but was not carcinogenic in rats at up to 1000 ppm. Styrene-7,8-oxide, the major metabolic intermediate, has weak electrophilic reactivity. Therefore, DNA adduct formation was expected at a low level and a 32P-postlabeling method for a determination of the two regioisomeric 2'-deoxyguanosyl-O6-adducts at the alpha(7)- and beta(8)-positions had been established. The first question was whether DNA adducts could be measured in the rat at the end of the 2 years exposure of a bioassay for carcinogenicity, even though tumor incidence was not increased. Liver samples of male and female CD rats were available for DNA adduct analysis. Adducts were above the limit of detection only in the highest dose group (1000 ppm), with median levels of 9 and 8 adducts per 10(7) nucleotides in males and females, respectively (sum of alpha- and beta-adducts). The result indicates that the rat liver tolerated a relatively high steady-state level of styrene-induced DNA adducts without detectable increase in tumor formation. The second question was whether different DNA adduct levels in the lung of rats and mice could account for the species difference in tumor incidence. Groups of female CD-1 mice were exposed for 2 weeks to 0, 40, and 160 ppm styrene (6h per day; 5 days per week), female CD rats were exposed to 0 and 500 ppm. In none of the lung DNA samples were adducts above a limit of detection of 1 adduct per 10(7) DNA nucleotides. The data indicate that species- and organ-specific tumor induction by styrene is not reflected by DNA adduct levels determined in tissue homogenate. The particular susceptibility of the mouse lung might have to be based on other reactive metabolites and DNA adducts, indirect DNA damage and/or cell-type specific toxicity and tumor promotion.

Administration, Inhalation↗
PubMed1999

Protein adducts as dosimeters of human exposure to styrene, styrene-7,8-oxide, and benzene.

Cysteinyl adducts of hemoglobin (Hb) and albumin (Alb) formed via reactions with reactive species were measured in 48 subjects exposed to styrene (0.24-55.2 ppm) and to styrene-7,8-oxide (SO) (2.65-107 ppb) in a factory producing boats in the USA. Hb and Alb adducts were also investigated among 88 workers exposed to benzene (0-138 ppm) in several Chinese factories. The particular adducts were S-(2-hydroxy-1-phenylethyl) cysteine, from reactions of SO with Alb (designated SO-Alb), and S-phenylcysteine, from reactions of the CYP450 benzene metabolite, benzene oxide (BO), with Hb and Alb (designated BO-Hb and BO-Alb, respectively). The relationships between adduct levels and exposures were investigated in both studies. The estimated slopes varied considerably among the particular combinations of adduct and agent to which the workers were exposed, ranging from 0.815 pmol BO-Hb/g Hb per ppm benzene to 24400 pmol SO-Alb/g Alb per ppm SO. We used these estimated slopes, along with kinetic constants, to predict the systemic doses of SO and BO in humans per mg of styrene, SO or benzene per kg body weight, under certain assumptions. Using RX to signify the particular electrophile (SO or BO) the doses of RX to the blood per unit of dose varied between 2.21 and 4110 nM RX-h/mg agent per kg b.w. The dose of RX to the blood arising from inhalation of SO was almost 2000 times that of styrene (i.e. 4110 vs. 2.21 nM RX/mg agent per kg b.w.) and 430-781 times that of benzene (i.e. 4110 vs. 5.26-9.55 nM RX/mg agent per kg b.w.), depending upon the study. Comparable estimates of the blood dose of BO were obtained from adducts of Hb and Alb and two independent studies of BO-Alb yielded similar dose estimates. These results point to the utility of protein adducts as dosimeters of reactive electrophilic species in occupational studies. Finally, significant levels of background adducts of SO and BO with Hb and Alb were observed among workers, among control subjects and in commercial human proteins. Levels of these background adducts were too great to have arisen from non-occupational exposures to styrene or benzene or from cigarette smoking.

Air Pollutants↗