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PubMed1995

Immunological changes among workers occupationally exposed to styrene.

The functional status of the immune system was investigated in a group of 71 workers exposed to styrene and in 65 control subjects, recruited according to the same selection criteria and comparable as to sex, age, and confounding variables. Air and biological monitoring were used to characterize styrene exposure (median of the main urinary metabolites in the "next-morning" spot samples: 106 mg/g creatinine). Phenotypic analysis of peripheral blood lymphocytes (PBL) by automated flow cytometry revealed a reduced proportion of T lymphocyte subsets (CD3+, CD4+ and CD4+45+), with no changes in CD8+, and a higher proportion of B lymphocytes (CD19+) among styrene-exposed workers. The exposed workers showed a higher proportion of activation markers, namely DR and interleukin-2 receptors (CD25). Immunoglobulin subclasses were comparable in the two groups. An increased prevalence of abnormally low values was apparent for CD2+, CD3+, CD4+, CD4+45+ and CD11b subsets among workers exposed to styrene, whereas CD19+, DR+ and CD25+ showed an increased prevalence of abnormally high values. Natural killer-related phenotypes (CD56+, CD56+16+, and CD56+16-) were more expressed among styrene workers, with average increase of 30%. However, the frequency distribution of the lytic activity of natural killer cells against K-562 target cells was shifted towards lower values in the exposed workers as compared to control subjects. Dose-response relationships between indices of internal dose and prevalence of abnormal values were detectable for T lymphocyte subsets, NK phenotypes, and activation markers. These findings suggest that moderate exposure to styrene is associated with an altered distribution of lymphocyte subsets.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Pharmacokinetic interaction between 1,3-butadiene and styrene in Sprague-Dawley rats.

Gas uptake studies were carried out to evaluate kinetic interactions between 1,3-butadiene and styrene in Sprague-Dawley rats. The animals were co-exposed by inhalation to a mixture of 1,3-butadiene between 20 and 6000 ppm (v/v) and styrene between 0 and 500 ppm. The data demonstrate that metabolism of 1,3-butadiene was partially inhibited by styrene. The inhibition was competitive at atmospheric concentrations of styrene up to 90 ppm. Higher concentrations of styrene resulted in a small additional inhibition only. The apparent Michaelis-Menten constant for 1,3-butadiene, related to the average concentration in the organism of the animals, was Kmapp = 1.17 +/- 0.37 (mumol/l of tissue) and the corresponding atmospheric concentration at steady state was 560 ppm. The inhibition constant of styrene was found to be Ki = 0.23 +/- 0.30 (mumol/l of tissue). The maximal metabolic rate for 1,3-butadiene was 230 +/- 10 (mu/kg/h).

Air↗
PubMed1997

Biological monitoring of styrene exposure and possible interference of acetone co-exposure.

The object of this study is the evaluation of some of the toxicokinetic effects of exposure to low concentrations of styrene, and the possible influence of simultaneous exposure to acetone. To this end we studied 19 workmen simultaneously exposed to both solvents. During a week of 4-h work shifts, the workmen underwent daily personal environmental monitoring and the collection of urine samples, at both the beginning and the end of the work period, for the determination of mandelic acid (MA) and phenylglyoxylic acid (PGA). The presence of the solvents in the atmosphere was evaluated using passive personal monitoring and gas chromatography. Average exposure to styrene and acetone were respectively 72.2 mg/m3 and 225.7 mg/m3. MA and PGA were quantified by high-performance liquid chromatography (HPLC). The daily urinary concentration averages, both at commencement and at the end of work shifts, of both the metabolites studied and of the sum of the two were in statistically significant linear correlation with the average daily styrene exposure. Concentrations of MA and PGA in urine samples collected at the start of the work shift averaged 61.5 mg/g creatinine and 45.2 mg/g creatinine respectively, representing 41% and 72% of those at the endo of the work shift which were 148.3 and 62.6 mg/g creatinine, respectively. With equal exposure to styrene, the average urinary concentrations of MA and PGA at both the beginning and end of the work shift increased significantly (P < 0.001) during the working week. Moreover, we found that with equal exposure to styrene, urinary excretion of MA, PGA and MA + PGA at the end of the shift was inversely correlated with the intensity of acetone exposure (r = 0.4659, 0.3410 and 0.542 respectively, P < 0.001). In conclusion, these results express slower urinary kinetics of styrene metabolites than is usually described in the literature, and favor a tendency to accumulate MA and PGA in the organism as a consequence of the retardation of urinary excretion kinetics. Acetone apparently represents one of the determining factors in this interference.

Acetone↗
PubMed1983

Enhancement of lipid peroxidation in rat liver on acute exposure to styrene and acrylamide a consequence of glutathione depletion.

Lipid peroxidation, glutathione level and activity of glutathione-S-transferase were studied in liver and brain of rats 4 and 3 h after a single i.p. administration of 0, 25, 75, 100 mg/kg acrylamide or 0, 50, 100, 200, 600 mg/kg styrene, respectively. In liver both acrylamide and styrene caused an increase in lipid peroxidation and decrease in glutathione contents and activity of glutathione-S-transferase in a dose dependent manner, while in brain only acrylamide produced a decrease in glutathione content. The decrease in glutathione content was not always associated with increase of lipid peroxidation. The enhancement of lipid peroxidation occurred only when glutathione contents were depleted to certain critical levels. No effect of acrylamide or styrene was seen on lipid peroxidation under in vitro conditions. The addition of glutathione in the incubation mixture significantly inhibited the rate of lipid peroxidation of liver homogenates of acrylamide and styrene treated animals. The results suggest that enhancement of lipid peroxidation in liver on exposure to acrylamide or styrene is a consequence of depletion of glutathione to certain critical levels. The inhibition of glutathione-S-transferase activity by acrylamide and styrene suggests that detoxication of these neurotoxic compounds could be suppressed following acute exposure.

Acrylamide↗
PubMed1992

Host resistance assays as predictive models in styrene immunomodulation.

Three infection models namely an oncogenic virus Encephalomyocarditis (EMCV), a rodent strain of malaria, Plasmodium berghei, and a rodent hookworm parasite, Nippostrongylus brasiliensis, were used to confirm the in vivo immunotoxic potential of styrene reported in our previous communication. The altered host resistance to these challenge infections was evaluated in rodents pre-treated with 0, 0.02, 0.03 or 0.05 x LD50 dose of styrene (5 days/week) for 4 weeks. Significantly increased mortality in mice was observed at the various tested dose levels of styrene when challenged with EMCV. Similarly the results obtained in the malaria infection model indicated increased blood parasitaemia as well as significantly enhanced mortality in styrene-treated animals. Also the rejection of N. brasiliensis was also found to be significantly impaired in animals treated with a higher dose of styrene. These results indicate that the exposure of rodents to styrene can markedly impair host resistance which may have biological significance.

Adjuvants, Immunologic↗
PubMed1995

Migration of styrene from polystyrene foam food-contact articles.

Polystyrene foam is used in many food-contact articles such as plates, cups, bowls, egg cartons, meat trays and hinged 'carryout' containers. In most of these applications the food is in contact with the article for a relatively short period of time at mild temperatures (up to 130 degrees F), or for longer periods of time at refrigerated temperatures (40 degrees F). The extent of migration of residual styrene from foam articles under these conditions is of interest in order to predict potential exposure of consumers to styrene from food-contact polymers. Studies of styrene migration from all polystyrene foam articles except egg cartons were completed using food oil as the simulant. Results showed that the amount of styrene migrating from the various food-contact articles made with thermoformed polystyrene sheet into food oil was proportional to the square root of time of exposure. The mean diffusion coefficients derived from these data, assuming the migration was Fickian in nature, showed a linear relationship between the log of the diffusion coefficient and the inverse of the absolute temperature of exposure from 70 to 150 degrees F (21-66 degrees C). The mean diffusion coefficients ranged from about 4.5E-11 cm2/s at 70 degrees F to 3.4E-9 cm2/s at 150 degrees F. Among the four thermoformed articles exposed to food oil, the diffusion coefficients varied by a factor of four or less at a given temperature. The migration of styrene from egg cartons was examined using conditions simulating 'typical' exposure temperature and time with 8% ethanol as the simulant (31 days at 40 degrees F (4 degrees C)). No migration of styrene was observed under this condition, with a detection limit of < 0.01 micrograms/cm2.

Diffusion↗
PubMed1987

Studies on the subchronic nephrotoxic potential of styrene in Sprague-Dawley rats.

The nephrotoxic potential low non-toxic dose of styrene was studied in male Sprague-Dawley rats. Groups of rats received i.p. injections of styrene in corn oil at doses 0, 2.9, and 5.8 mmol/kg once daily, 5 days/week for 6 consecutive weeks. After collection of urine for 0-24 and 24-48 h following the end of the treatment, the rats were sacrificed. A significant increase in the excreted urinary volume was noticed at 5.8 mmol styrene during 0-24 and 24-48 h, relative to control, whereas urinary concentrations of gamma-glutamyl transpeptidase and glucose were significantly elevated during the 24-48-h period. Urinary activity of N-acetyl-beta-D-glucosaminidase was increased at the higher dose of styrene during 0-24 and 24-48 h. The capacity of renal cortical slices to accumulate p-aminohippurate was significantly reduced 48 h after the exposure to any dose of styrene. Electron microscopic examination of renal cortex 48 h after the exposure to a higher dose revealed the presence of enlarged mitochondria having more electron dense matrix. The data suggest that subchronic exposure to a very low non-toxic dose of styrene may have the potential to elicit nephrotoxicity preferentially in the proximal tubular region of the rat kidney.

Animals↗
PubMed1996

Effects of ethanol administration on cerebral non-protein sulfhydryl content in rats exposed to styrene vapour.

Glutathione (GSH) and other non-protein sulfhydryls (NPS) are known to protect cells from oxidative stress and from potentially toxic electrophiles formed by biotransformation of xenobiotics. This study examined the effect of a simultaneous administration of styrene and ethanol on NPS content and lipid peroxidation in rat liver and brain. Hepatic cytochrome P450 and cytochrome b5 content, aniline hydroxylase and aminopyrine N-demethylase activities as well as the two major urinary metabolites of styrene, mandelic and phenylglyoxylic acids were also measured. Groups of rats given ethanol for 3 weeks in a liquid diet were exposed, starting from the second week, to 326 ppm of styrene (6 h daily, 5 days a week, for 2 weeks). In control pair-fed animals, styrene produced about 30% depletion of brain NPS and 50% depletion of hepatic NPS. Subchronic ethanol treatment did not affect hepatic NPS levels, but caused 23% depletion of brain NPS. Concomitant administration of ethanol and styrene caused a NPS depletion in brain tissue in the order of 60%. These results suggest that in the rat, simultaneous exposure to ethanol and styrene may lead to considerable depletion of brain NPS. This effect is seen when both compounds are given on a subchronic basis, a situation which better resembles possible human exposure.

Administration, Inhalation↗
PubMed1996

Pharmacokinetic model describing the disposition of butadiene and styrene in mice.

Coexposure to 1,3-butadiene (BD) and styrene occurs in the workplace of many polymer industries. The reactive epoxide metabolites of both compounds are responsible for their genotoxicity. A physiologically based pharmacokinetic (PBPK) model was developed to describe the simultaneous disposition of BD and styrene in mice coexposed by inhalation. A model with one oxidative pathway and competition between BD and styrene was compared with a model with two oxidation pathways for both BD and styrene. The different PBPK models were used to simulate the observed rate of BD metabolism and blood concentration of styrene from 8-h inhalation exposures of mice to mixtures of BD and styrene. The model with two oxidative pathways more accurately simulated the observed inhibition of BD uptake in coexposed mice.

Animals↗
PubMed1992

Neurochemical effects in rats following gestational exposure to styrene.

Styrene was evaluated for the reproductive effects of pregnant rats and the neurochemical effects in the offspring of rats exposed during gestation. Pregnant Wistar rats were exposed to 0, 50, or 300 ppm styrene for 6 h/day during days 7 to 21 of gestation. No significant differences in the number of offspring delivered were observed between the exposed and control groups. Body weights at 1 day of age of the offspring whose mothers were exposed to styrene were significantly lower than those of the control group. Although, there were neither statistically significant differences of protein contents nor brain weights among styrene-exposed and their control offsprings of rats, analyses of neurotransmitter studies showed dose-dependent decreases of neuroamines, especially 5-HT (serotonin) and its metabolite 5HIAA (5-hydroxyindoleacetic acid) in the newborn offspring of styrene-exposed rats. The results suggest that gestational exposure to styrene at these concentrations does not produce apparent reproductive toxicity but affects the body weight of pups and causes lowering of the neurotransmitter levels in the brain.

Administration, Inhalation↗
PubMed1995

An investigation of the association between exposure to styrene and hearing loss.

The importance of the association between advancing age and hearing loss is well recognized. Further, prolonged significant noise exposures are also known to result in permanent hearing loss. However, little is known of the contribution of industrial chemical exposures to hearing loss. Information available, from both animal and human studies, raises the possibility that certain aromatic hydrocarbons are ototoxic. The purpose of this study was to assess whether occupational styrene exposure causes hearing loss in a group of workers in the fiber-reinforced plastics manufacturing industry. The hearing acuity of 299 subjects was determined, using pure-tone screening audiometry, at the beginning of a single workshift and again at the end of the shift. On the same day, the personal, time-weighted average exposures of each subject to both styrene and noise were measured. In addition, information on the following factors was obtained from each participant: previous work history, including exposures to noise and chemicals; use of personal protective equipment for noise or solvents; personal and family history of hearing problems; and smoking history. Current exposures together with work histories were used to construct lifetime noise and styrene exposure indices. No conclusive evidence was found for a chronic styrene-induced effect on hearing acuity, when both noise and styrene lifetime exposures were taken into account. As expected, age and noise exposures were highly important variables, both positively associated with hearing loss. In addition, the detrimental effect of noise exposure on hearing acuity was found to be strengthened with increased age. Noise and styrene exposures were highly correlated, clearly illustrating the importance of considering all associated variables in analysis of such data. No evidence was found for a relationship between smoking, recreational noise, solvent exposures, and hearing loss.

Aging↗
PubMed1992

Styrene in adipose tissue of nonoccupationally exposed persons.

Given a styrene tissue/blood partition coefficient of ca. 39 and a relatively low perfusion rate of ca. 0.03 ml/min-g tissue, adipose tissue provides a useful physiologically damped integrative measure of environmental exposure. Styrene in the adipose tissue of nonoccupationally exposed individuals was measured for the first time. Tissue samples obtained from elective surgery patients and postmortem donors were analyzed by capillary gas chromatography and found to contain 1.12 +/- 1.06 (mean +/- SD) ppm styrene. Using these measured tissue levels and an apparent clearance of styrene (defined as the ratio of blood clearance to adipose tissue/blood partition coefficient), environmental intake of styrene was estimated to be 2.23 mg/hr, corresponding to an inhaled concentration of 1.96 mg/m3 (476 ppb). This value is two to three orders of magnitude higher than typical breathing zone air measurements, indicating additional undiscovered sources of styrene exposure.

Adipose Tissue↗
PubMedDate not supplied

Compositional analysis of samples of thermoset polyester and migration of ethylbenzene and styrene from thermoset polyester into pork during cooking.

The levels of ethylbenzene, styrene, benzene and benzaldehyde in samples of thermoset polyester were determined by dynamic headspace/gas chromatography. Styrene was present at levels from 50 to 1400 mg kg-1, ethylbenzene up to 25 mg kg-1 and benzaldehyde up to 180 mg kg-1. Benzene levels were usually less than 1 mg kg-1, but one article contained 19 mg kg-1. Levels of styrene dimers and trimers were estimated using size exclusion chromatography followed by gas chromatographic (GC) analysis and were present at approximately 100 mg kg-1 and 700 mg kg-1 respectively. The principal identified constituents of solvent extracts were stearic and palmitic acids, present at a combined level of nearly 1% by weight of the plastic. Styrene was shown to be produced by thermal depolymerization at temperatures of 175 degrees C and above. The migration of ethylbenzene and styrene into belly pork cooked in thermoset polyester dishes for 1.5 h at 175 degrees C was measured by Likens-Nickerson extraction of the cooked meat and GC/MS analysis of the extracts. Migration ranged from 6 to 2400 micrograms kg-1 for styrene and from < 6 to 34 micrograms kg-1 for ethylbenzene.

Animals↗
PubMed1984

Contact allergy to styrene and related chemicals.

One patient, sensitive to styrene, cross-reacted at patch testing to 2-,3-and 4-vinyltoluene (2-,3-and 4-methylstyrene) and to the metabolites styrene epoxide and 4-vinylphenol (4-hydroxy-styrene). It is assumed that styrene is a prohapten metabolized in the skin by aryl hydrocarbon hydroxylase (AHH) to styrene epoxide acting as the true hapten. Styrene occurs in nature and as a synthetic product. Vinyltoluenes (methylstyrenes) occur as synthetic products in plastics. 4-vinylphenol (4-hydroxystyrene) occurs frequently in different ciders, wines, foods and berries, e.g. cloudberry.

Dermatitis, Atopic↗
PubMed1992

Styrene formation by the decomposition by Pichia carsonii of trans-cinnamic acid added to a ground fish product.

It is not well known how the formation of styrene by microorganisms can occur in foods. In this study, we described and characterized the production of styrene by a yeast isolated from chikuwa fish paste. The styrene was not detected in fresh and normal food products nor in the food package's plastic film. The food containing styrene contained cinnamic acid as an antimicrobial agent and spice, and it was contaminated by 5.4 x 10(6) CFU of a yeast per gram. On the basis of morphological and biochemical features, the yeast isolated was determined to be a strain of Pichia carsonii, now designated strain CHI. Strain CHI, which was able to grow on cinnamic acid, had the ability to form styrene from trans-cinnamic acid via trans-p-coumaric and caffeic acids. The MIC of trans-cinnamic acid against strain CHI was 230 micrograms/ml. Strain CHI thrived well at pH 5.0 and 26.0 degrees C and was tolerant to 20% NaCl. Styrene was subsequently produced in ground fish meat containing cinnamic acid into which strain CHI had been inoculated. The yeast was found to be an environmental contaminant in food processing plants of the chikuwa manufacturer.

Biodegradation, Environmental↗
PubMed1996

Exposure to styrene and mortality from nonmalignant diseases of the genitourinary system.

OBJECTIVES: A historical cohort study was carried out to investigate mortality from nonmalignant diseases of the genitourinary system among workers in the reinforced plastics industry, where high workroom concentrations of styrene are encountered. METHODS: The external comparisons in this report were based on an average of 12.6 years of retrospective follow-up of 35 443 workers who were first employed in the reinforced plastics industry during 1945-1991 and were known to have been exposed to styrene in their work. For the internal comparisons, 2641 subjects with incomplete occupational histories were excluded, leaving 32 802 subjects. Previous individual exposure histories to styrene were reconstructed through job histories and environmental and biological monitoring data. RESULTS: Mortality from nonmalignant diseases of the genitourinary system (N = 20) was associated with average exposure to styrene (P for trend 0.05). Weaker increasing trends in risk were seen for time since first exposure and cumulative exposure, while no increase was identified for duration of exposure. There was a significant increasing trend in mortality from nephritis and nephrosis (N = 5), associated with an increasing average level of exposure to styrene (P for trend 0.03). No clear trend was observed for time since first exposure, duration of exposure, or cumulative exposure. CONCLUSIONS: In this large cohort study of workers exposed to styrene, mortality from nonmalignant diseases of the genitourinary system increased as the average intensity of exposure increased. This finding indicates that other data should be scrutinized.

Air Pollutants, Occupational↗
PubMed1989

Stereoselectivity of styrene oxidation in microsomes and in purified cytochrome P-450 enzymes from rat liver.

The stereochemistry of the cytochrome P-450(P-450)-dependent oxidation of styrene to styrene 7,8-oxide (SO) enantiomers was evaluated with rat hepatic microsomes and with individual rat liver P-450 enzymes in reconstituted monooxygenase systems. The stereoselectivity of the monooxygenase reaction with styrene was determined by high-performance liquid chromatographic analysis of the glutathione conjugates formed quantitatively from SO, the product of the monooxygenase reaction. Hepatic microsomes from control rats oxidized styrene at a rate of 13.1 +/- 4.5 nmol/min/nmol of P-450 and with a ratio of the amount of the (R)-styrene 7,8-oxide enantiomer to the amount of the (S)-styrene 7,8-oxide enantiomer (R/S) SO ratio of 0.65 +/- 0.1. These values were determined under incubation conditions in which epoxide hydrolase activity was inhibited by cyclohexene oxide, and at least 95% of the SO formed was converted enzymatically to glutathione conjugates. Treatment of rats i.p. with phenobarbital (PB) or beta-naphthoflavone (beta NF) caused changes in both parameters. Whereas the rates of oxidation in hepatic microsomes prepared from PB-treated rats was unchanged at 15.4 +/- 7.5 nmol/min/nmol of P-450 and decreased in hepatic microsomes from beta NF-treated rats to 9.4 +/- 2.8 nmol/min/nmol of P-450, the preference for formation of the R-enantiomer increased as the R/S ratio changed to 0.92 +/- 0.1 for PB and 1.25 +/- 0.1 for beta NF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Cooxidation of styrene by horseradish peroxidase and glutathione.

Styrene is oxidized to styrene oxide and benzaldehyde in the presence of glutathione, horseradish peroxidase, and hydrogen peroxide. Styrene oxide is not formed if any one of these reaction components is omitted or if oxygen is exluded from the reaction. The oxygen atom in the styrene oxide derives from molecular oxygen rather than from hydrogen peroxide. Oxidation of trans[1-3H]styrene yields the epoxide in which the deuterium stereochemistry is completely scrambled. The results indicate that the glutathione thiyl radical directly or indirectly activates molecular oxygen to a species that cooxidizes styrene. The one-electron oxidation of glutathione thus may promote the cooxidation of physiological substrates.

Glutathione↗