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PubMed1989

Effects of postnatal low-levels of exposure to styrene on behavior and development in rats.

Three groups of rats were exposed by inhalation to either clean air (control group) or styrene monomer at 25 and 50 ppm (styrene-exposed groups) for 7 h/day, 6 day/week, from 1 to 48 days of age. Compared to control group, Styrene-exposed groups showed significant delay in the following developmental indices: body weight gain, appearance of pinna detachment and incisor eruption. With respect to open-field activity, the styrene groups indicated longer latency to enter the field, less number of squares crossed and fewer rearings than those of controls. In the avoidance behavior aspect, the styrene groups attained less achievement level in avoidance rates than that of the control group. Dose-related trends were found between the two exposed groups in body weight increment, exploratory and avoidance behavior. Sex differences were seen on these factors also. These results suggest that at postnatal exposure of low-levels to styrene affects behavior and development in rats.

Animals↗
PubMed1981

Styrene epoxide intermediate as a possible stimulant of lymphocytic function.

Mice treated with styrene showed an increased lymphocyte transformation in splenic cell cultures. The effects were observed both on spontaneous transformation and phytomitogen induced blast formation. Addition of styrene oxide directly to splenic cultures, but not of styrene, increased blast formation at low concentrations but was cytotoxic at high concentrations. In this test system styrene exhibited a generalized immunostimulation. In vitro data suggest that this effect of styrene is mediated possibly through its conversion to styrene oxide, its transient metabolic intermediate.

Animals↗
PubMed1985

Urinary elimination of styrene in experimental and occupational exposure.

Twenty human volunteers were exposed to styrene vapor at 273-1 654 mumol/m3 (28.4-172.3 mg/m3) for a period of 1 to 3 h at rest (15 cases) and during light physical exercise (5 cases). Subsequently 51 workers occupationally exposed to styrene were studied during a workweek (median value 1 138 mumol/m3, geometric standard deviation 2.23). As expected, the relative uptake averaged about 65%, and the ratio of the alveolar concentration to the time-weighted average of the environmental concentration averaged about 0.15. Both in the experimentally exposed subjects and in the occupationally exposed workers the urinary styrene concentration showed a linear relationship to the corresponding environmental time-weighted average concentration. The correlation coefficients of the regression lines ranged between 0.88 (occupationally exposed group) and more than 0.93 (experimentally exposed groups). The regression coefficients were closely linked to the amount of styrene taken up and to the exposure times. The findings show that the urinary styrene concentration can be used as an appropriate biological exposure indicator whose meaning differs from that of other suggested indices. As an example, in occupationally exposed subjects performing moderate work the urinary styrene concentration corresponding to the time-weighted average of the threshold limit value is 815 nmol/l, and the 95% lower confidence limit (biological threshold) is 740 nmol/l.

Adult↗
PubMed1976

Urinary mandelic acid concentration after occupational exposure to styrene and its use as a biological exposure test.

Excretion of mandelic acid from workers in the reinforced polyester plastic industry was studied with the determination of urinary mandelic acid concentrations. The styrene exposure level at the workplaces was evaluated with measurements of the styrene concentration in the ambient air. Three different groups (I, II and III) were studied. In group I [n=9, median of the time-weighted average (TWA) of exposure = 23 ppmof styrene, postexposure observation period = 64 h] two excretion slopes were observed, the first with a median half-time of 9.4 h (postexposure period 0--18 h) and a second with a median half-time of 16.6 h (postexposure period 19--64 h). For group II (n=9, median TWA exposure = 248 ppm, postexposure observation period = 15 h) a half-time of 6.4 h was found. These results suggest that the excretion rate of mandelic acid is dependent on the styrene exposure level. In addition the mandelic acid concentrations of 29 workers (group III) before and after the work shift were analyzed. The urinary mandelic acid concentrations of groups I, II and III, sampled immediately after the 8-h work shift, correlated with the 8-h TWA of styrene exposure (n=47, r=0.93). Accordingly about 2,300 mg of mandelic acid per gram of creatinine corresponded to 100 ppm of styrene.

Air Pollutants, Occupational↗
PubMed1999

Mortality from nonmalignant diseases of the respiratory, genitourinary and nervous systems among workers exposed to styrene in the reinforced plastics and composites industry in the United States.

OBJECTIVES: Mortality from diseases of the nervous system and nonmalignant diseases of the respiratory and genitourinary systems was examined for workers exposed to styrene. METHODS: Altogether 15,826 styrene-exposed workers in 30 plants in the reinforced plastics and composites industry were included. Vital status was ascertained through 31 December 1989. Individual exposure estimates were developed based on job functions, existing industrial hygiene data, process changes, engineering controls, work practices, and the use of personal protective equipment. Analyses were based on cause-specific standardized mortality ratios (SMR) and the Cox proportional hazards model. Mortality data were analyzed by latency, duration of exposure, average exposure, cumulative exposure, and process category. RESULTS: For diseases of the nervous system, the SMR was 0.56 [95% confidence interval (95% CI) 0.31-0.95]. Mortality from nonmalignant genitourinary diseases was not increased (SMR 0.87, 95% CI 0.46-1.50). Latency, duration of exposure, average exposure, cumulative exposure, and process category showed no association between styrene exposure and these 2 types of disease. A small increase in mortality from nonmalignant respiratory diseases was found (SMR 1.21, 95% CI 0.98-1.47), mainly due to "other nonmalignant respiratory diseases" (SMR 1.40, 95% CI 1.04-1.84). The highest increase occurred for short exposure duration (SMR 1.79 for <1 year's exposure) or low exposure (SMR 2.15 for <10 ppm-years); there were no increased risks in the high exposure categories. The Cox proportional hazard model revealed no association between styrene exposure and the diseases. CONCLUSIONS: No relationship was found between mortality from any of the diseases examined and any of the styrene exposure indices. The findings were compared with those reported in a European study of styrene-exposed workers.

Cohort Studies↗
PubMed1999

Change in semen quality and sperm chromatin structure following occupational styrene exposure. ASCLEPIOS.

OBJECTIVES: Organic solvents have been suspected to exert detrimental effects on human spermiogenesis. Styrene, which is both mutagenic and neurotoxic, was selected as a suitable organic solvent for further assessment of a possible effect on semen quality and sperm DNA damage. SUBJECTS AND METHODS: Semen samples were collected from 23 reinforced plastics workers at the time of employment and after 6 months of styrene exposure and from 21 nonexposed farmers. Intra-individual changes in conventional semen parameters and sperm-DNA denaturation patterns were related to the internal dose of styrene exposure as measured by postshift urinary mandelic acid. RESULTS: A statistically significant decline in sperm density was seen during styrene exposure from 63.5 to 46.0 million sperm/ml, whereas no decline was seen in the nonexposed subjects. The total sperm count was almost halved from an initial value of 175 million sperm/ejaculate. However, no relationship was apparent when the sperm parameters were related to internal levels of exposure. However, an exposure-response relationship was shown for DNA-denaturation patterns, but the numbers were small. CONCLUSION: A declining sperm count following styrene exposure is suggested. However, the findings of the internal and external comparisons are inconsistent, and this may be due to the high intraindividual variability of semen parameters and the limited study size but may also be attributable to a weak internal exposure gradient. Spermatogenesis may be vulnerable to styrene exposure. However, due to the small numbers these findings are only preliminary.

Adult↗
PubMedDate not supplied

Evaluation of a possible styrene-induced damage to the haematopoietic tissues in the rat.

The aim of this study was to determine a possible risk of malignancies in the haematopoietic tissues of rats treated with styrene, either by injection or by inhalation. Two experiments were carried out: in the first (acute treatment), 12 male rats were treated intraperitoneally with different doses of styrene (40 mg/Kg/2 ml/die and 400 mg/Kg/2 ml/die) for 3 consecutive days. A control group (6 rats) was administered corn oil 2 ml/kg/die for the same period of time. In the second experiment (chronic treatment), 12 male rats were exposed to styrene inhalation (300 ppm/6 hour day/5 days a week for 2 weeks) for 3 weeks and sacrificed at the end of the experiment or after 3 weeks. The rats treated with the highest doses of styrene by injection (400 mg/kg, acute treatment) showed a hyperactivity of the erythropoietic series while the granulocytopoietic series was at the normal value. The rats exposed to 300 ppm styrene vapour (chronic treatment) showed a statistically significant increase in erythropoietic cells (basophilic, polychromatophilic and orthochromatic erythroblasts). A temporary block of immature cells of the granulocytopoietic series was also evident. These results indicate an alteration of the erythropoietic series independently of method of administration. However, these findings do not show a possible risk of preleukemic or leukemic disorders in rats exposed or treated with styrene.

Administration, Inhalation↗
PubMed2003

Styrene exposure and ischemic heart disease: a case-cohort study.

Epidemiologic studies have consistently reported increased daily mortality and hospital admissions for ischemic heart disease related to daily changes in ambient particulate levels. One theory is that substances adhering to particulates might have a cardiovascular effect. Styrene has been found in very low doses in air and has chemical characteristics that would cause adherence to particles. Industrial studies have found an increase in cardiovascular disease among styrene-exposed workers. To explore a possible dose-response relation between styrene exposure and ischemic heart disease, the authors of this case-cohort study included 498 cases that died from ischemic heart disease and a 15% random sample (n = 997) of all male workers who were employed during 1943-1984 in two styrene-butadiene rubber-manufacturing plants in the United States. Proportional hazards models showed that recent styrene exposure was significantly associated with acute ischemic heart disease death among active workers. The relative hazard of death from acute ischemic heart disease for exposure during the most recent 2 years among active workers with 2 or more years of employment was 2.95 (95% confidence interval: 1.02, 8.57) at a time-weighted styrene concentration of 0.2-<0.3 ppm and 4.30 (95% confidence interval: 1.56, 11.84) at >or=0.3 ppm for the same exposure period, respectively.

Acute Disease↗
PubMed2006

Estrogenic reduction of styrene monomer degraded by Phanerochaete chrysosporium KFRI 20742.

The characteristic biodegradation of monomeric styrene by Phanerochaete chrysosporium KFRI 20742, Trametes versicolor KFRI 20251 and Daldinia concentrica KFRI 40-1 was carried out to examine the resistance, its degradation efficiency and metabolites analysis. The estrogenic reduction effect of styrene by the fungi was also evaluated. The mycelium growth of fungi differentiated depending on the concentration levels of styrene. Additionally P. chrysosporium KFRI 20742 showed superior mycelium growth at less than 200 mg/l, while D. concentrica KFRI 40-1 was more than 200 mg/l. The degradation efficiency reached 99% during one day of incubation for all the fungi. Both manganese-dependent peroxidase and laccase activities in liquid medium were the highest at the initial stage of incubation, whereas the lowest was after the addition of styrene. However, both activities were gradually recovered after. The major metabolites of styrene by P. chrysosporium KFRI 20742 were 2-phenyl ethanol, benzoic acid, cyclohexadiene-1,4-dione, butanol and succinic acid. From one to seven days of incubating the fungi, the expression of pS2 mRNA widely known as an estrogen response gene was decreased down to the level of baseline after one day. Also, the estrogenic effect of styrene completely disappeared after treatment with supernatant of P. chrysosporium KFRI 20742 from one week of culture down to the levels of vehicle.

Basidiomycota↗
PubMedDate not supplied

[Chronic exposure to styrene and psychiatric symptomatology: a case-control descriptive study].

BACKGROUND: Although the acute psychiatric consequences exerted by Styrene and other aromatic hydrocarbons are abundantly described, the effects produced by a low-dosages chronic exposure are not known, in spite of the wide employment in the field of industrial production. The aim of this study is to evaluate the psychiatric symptoms in a group of subjects exposed to styrene in comparison with a control group, not exposed to the substance. SUBJECTS AND METHODS: Twenty two qualified workers, divided into 11 subjects in charge of welding and resin tapping exposed to styrene, and 11 not exposed to neurotoxic substances, were evaluated through the Symptom Check List Revised (SCL-90-R), a scale for the global self-evaluation of psychiatric symptomatology. RESULTS: The statistical tests, herein utilized, showed a significant prevalence for the dimensions somatization and psychoticism in the exposed subjects to styrene as compared to the non-exposed subjects. CONCLUSIONS: The results of this study, although limited by the paucity of the sample, emphasize the importance of an early diagnosis and evaluation of the clinical predictors in subjects exposed to styrene. The relatively low concentration levels of styrene in the working area of the subjects exposed underlines the opportunity to arrange preventive evaluation strategies for a prompt intervention in those cases with a clear syndromic presentation.

Adult↗
PubMed1986

Reproductive toxicology of inhaled styrene oxide in rats and rabbits.

Experiments were performed to evaluate reproductive and developmental toxicology in rats and rabbits exposed to styrene oxide by inhalation. Female rats were exposed to 100 or 300 ppm styrene oxide or to filtered air for 7 h/day, 5 days/week for 3 weeks. Extensive mortality occurred in rats that received prolonged exposure to 100 ppm styrene oxide while 300 ppm was rapidly lethal. As a result exposures were terminated in this latter group and the group was eliminated from further study. The rats of the 0 and 100 ppm groups were then mated and exposed to 0 or 100 ppm styrene oxide daily through 18 days of gestation (dg). Female rabbits were artificially inseminated and exposed for 7 h daily to 0, 15, or 50 ppm styrene oxide through 24 dg. Both of these lower concentrations used for exposure of the rabbits produced mortality of does. The rats were killed at 20 dg and the rabbits at 30 dg. Pregnant animals were examined for toxic changes including altered tissue weights and histopathologic effects. Litters were evaluated using several measures of embryotoxicity, and live fetuses were examined for external, visceral, and skeletal malformations. Exposure during gestation appeared to increase preimplantation loss in rats, and tended to increase the incidence of resorptions in rabbits. In both species, fetal weights and crown-rump lengths were reduced by gestational exposure. The incidences of ossification defects of the sternebrae aned occipital bones were increased by gestational exposure of rats to styrene oxide. These results indicate that inhalation exposures at these concentrations produce reproductive and development toxicity, as well as maternal toxicity.

Abnormalities, Drug-Induced↗
PubMed1981

Induction of nuclear styrene monooxygenase and epoxide hydrolase in rat liver.

The apparent Km and Vmax of styrene monooxygenase and styrene epoxide hydrolase were determined in intact nuclear preparations from male rat liver after in vivo treatment with phenobarbital and beta-naphthoflavone, which are known to induce microsomal cytochrome P-450 and cytochrome P-448 respectively. Treatment with phenobarbital does not alter the apparent Km, but greatly increases the Vmax of both nuclear styrene monooxygenase and styrene epoxide hydrolase. Almost the same pattern is observed for styrene monooxygenase after treatment with beta-naphthoflavone, whereas the same treatment slightly increases both the Vmax and Km value of styrene epoxide hydrolase.

Animals↗
PubMed1997

Styrene oxide DNA adducts: in vitro reaction and sensitive detection of modified oligonucleotides using capillary zone electrophoresis interfaced to electrospray mass spectrometry.

Styrene is one of the most important synthetic chemicals in the world and is subject to investigations concerning carcinogenicity and mutagenicity due to the active metabolite, styrene-7,8-oxide. This epoxide shows a tendency to react, among others, with DNA and DNA constituents. The in vitro reaction of styrene oxide with DNA was investigated by cleaving incubated calf thymus DNA with two different enzymes, namely Benzonase and alkaline phosphatase, to obtain oligonucleotides of the type n-nucleotide-(n-1)-phosphate with chain length from 2 to 8 bases. Alkylated and nonalkylated nucleotides were separated in groups according to their chain length using capillary zone electrophoresis and were detected with electrospray mass spectrometry. This improvement in sensitivity made it possible to obtain new information about the reaction of styrene oxide with DNA, especially to detect unknown reaction products. The results indicate that primarily purine bases were alkylated by styrene oxide before pyrimidine bases, which react with higher concentrations of styrene oxide. This means that in addition to the already reported adducts in DNA at the N-7-, O6- and N2-position of guanine also adducts at the nucleophilic sites of adenine can be found using mass spectrometry. We anticipate for the future this procedure will allow us to investigate base sequence specific reactions as well as interactions from xenobiotics and cytostatic drugs, since reaction products would directly be detectable.

Adenine↗
PubMed2005

Surface modification of crosslinked poly(styrene-divinyl benzene) micrometer-sized particles of narrow size distribution by ozonolysis.

Micrometer-sized polystyrene template particles of narrow size distribution were prepared by dispersion polymerization of styrene in 2-methoxyethanol. Uniform micrometer-sized polystyrene/crosslinked poly(styrene-divinyl benzene) composite particles were formed by a single-step swelling process of the template particles with styrene, divinyl benzene and benzoyl peroxide, followed by polymerization at 70 degrees C. Uniform micrometer-sized crosslinked poly(styrene-divinyl benzene) particles of higher surface area were produced by dissolution of the template polystyrene part of the former composite particles with N,N-dimethylformamide. Hydroperoxide conjugated crosslinked poly(styrene-divinyl benzene) particles were produced by ozonolysis of these particles. The effect of ozonolysis conditions, such as exposure time and flow rate of the ozone, on the hydroperoxide conjugation to the crosslinked particles was also studied. Functionalization of the crosslinked poly(styrene-divinyl benzene) particles was performed by graft polymerization of vinylic monomers such as acrylonitrile and chloromethylstyrene on the hydroperoxide conjugated crosslinked particles. This was accomplished by raising the temperature (e.g., 70 degrees C) of deairated acetonitrile dispersions containing the hydroperoxide conjugated particles and the vinylic monomers. The influence of various polymerization parameters on the grafting yield, e.g., monomer concentration, conjugated hydroperoxide concentration, and temperature, was also elucidated.

Journal Article↗
PubMed1996

Styrene oxide adducts in an oligodeoxynucleotide containing the human N-ras codon 12 sequence: structural refinement of the minor groove R(12,2)- and S(12,2)-alpha-(N2-guanyl) stereoisomers from 1H NMR.

The structures of the (R)- and (S)-alpha-(N2-guanyl)styrene oxide adducts at X6 in d(GGCAGXTGGTG).d(CACCACCTGCC), encompassing codon 12 of the human n-ras protooncogene (underlined), were refined from 1H NMR data. These were the R(12,2) and S(12,2) adducts. For the R(12,2) adduct, upfield chemical shifts were observed for the T7 H6, H1', and N3H resonances. At 30 degrees C, R-SOG 6 N1H, T7 N3H, and T10 N3H disappeared due to exchange with solvent. For the S(12,2) adduct, S-SOG6 H1' shifted upfield 0.33 ppm, but all imino resonances were observed. The styrene methylene protons were nonequivalent for both adducts, suggesting hydrogen bonding between the hydroxyl and C18 O2 or O4' in the R(12,2) adduct and C17 O2 in the S(12,2) adduct. The styrene aromatic protons appeared as three signals in the R(12,2) adduct and as two signals in the S(12,2) adduct, suggesting rapid rotation of the styrene ring on the NMR time scale. NOE data revealed that the phenyl ring was oriented in the 3'-direction relative to R-SOG6 for the R(12,2) adduct and in the 5'-direction relative to S-SOG6 for the S(12,2) adduct. A total of 253 and 221 interproton distances were obtained from relaxation matrix analyses of the R(12,2) and S(12,2) adducts, respectively. NOE-restrained molecular dynamics calculations converged with root mean square deviations of 0.8-1.2 A for the R(12,2) adduct and 0.82-1.4 A for the S(12,2) adduct. Complete relaxation matrix analyses of the nine inner base pairs yielded sixth root residual indices between calculated and experimental NOE intensities of 8.8 x 10(-2) for the R(12,2) adduct and 7.9 x 10(-2) for the S(12,2) adduct. The refined structure for the R(12,2) adduct showed a 0.4 A increase in the stretch of R-SOG6.C17 and T7.A16, and a 1-2 A widening of the minor groove at and adjacent to the SO lesion, with the styrene ring oriented edgewise in the minor groove. Smaller minor groove disturbances were observed for the S(12,2) adduct, which had the styrene ring oriented flat in the minor groove. No DNA bending was predicted by the calculated structures.

Base Sequence↗
PubMed1996

Major groove (S)-alpha-(N6-adenyl)styrene oxide adducts in an oligodeoxynucleotide containing the human N-ras codon 61 sequence: conformations of the S(61,2) and S(61,3) sequence isomers from 1H NMR.

The (S)-alpha-(N6-adenyl)styrene oxide adducts at positions X6 in d(CGGACXAGAAG). d(CTTCTTGTCCG) and X7 in d(CGGACAXGAAG).d(CTTCTTGTCCG), incorporating codons 60, 61 (underlined), and 62 of the human n-ras protooncogene, were examined by 1H NMR. These were the S(61,2) and S(61,3) adducts. Chemical shift perturbations were in the 3'-direction from the sites of adduction; upfield changes associated with the styrene aromatic ring current were noted for S-SOA6 H2 and H1', T16 N3H, H6, and CH3 resonances in the S(61,2) oligomer. In the S(61,3) oligomer, S-SOA7 H1', T16 H1', C15 N4Ha, and H5 shifted upfield. The styrene aromatic rings flipped rapidly on the NMR time scale; under these conditions the ortho and meta aromatic protons were equivalent. A sequence effect, in which the S(61,2) adduct equilibrated between two conformers, while the S(61,3) adduct exhibited only a single conformation, was observed. Potential energy minimization of the S(61,2) adduct major conformation yielded a structure in which the styrene ring was oriented in the 3'-direction and interacted primarily with the complementary strand. For the S(61,3) adduct, 291 restraints were obtained from NOE data at three mixing times using relaxation matrix analysis. The emergent structures refined to an average rms difference of 1.3 A, determined by pairwise analysis. These were compared to NOE intensity data; the calculated sixth root residual index was 9.2 x 10-2 at 250 ms. In the refined structure, the styrene ring was also oriented in the 3'-direction and interacted with the complementary strand. The minor conformation of the S(61,2) adduct was not identified. These results contrasted with the diastereomeric R(61,2) and R(61,3) adducts, which underwent slow ring flips on the NMR time scale and for which small sequence effects involving the minimum energy conformation of the styrene ring were observed.

Adenine↗
PubMed2005

Living copolymerization of ethylene with styrene catalyzed by (cyclopentadienyl)(ketimide)titanium(IV) complex--MAO catalyst system.

The copolymerization of ethylene with styrene by Cp*TiCl2(N=CtBu2) (Cp* = C5Me5) took place in a living manner in the presence of methylaluminoxane (MAO) cocatalyst, although the homopolymerization of neither ethylene nor styrene proceeded in a living manner. Both the cyclopentadienyl fragment (Cp') and the anionic donor ligand (X) in Cp'TiCl2(X) directly affect the copolymerization behavior, the catalytic activities, as well as the styrene incorporation; only the above set showed a living copolymerization. No styrene repeating units were observed in the resultant poly(ethylene-co-styrene)s, suggesting that a certain degree of the styrene insertion inhibited the chain transfer in this catalysis.

Journal Article↗
PubMed2004

Metabolism and toxicity of the styrene metabolite 4-vinylphenol in CYP2E1 knockout mice.

4-vinylphenol (4-VP) is a minor metabolite of styrene and is several times more potent as a hepatotoxicant and pneumotoxicant than is either the parent compound or the major metabolite of styrene, styrene oxide. 4-VP is metabolized primarily by CYP2E1 and CYP2F2. To further elucidate the possible role of 4-VP in styrene-induced toxicity and the importance of its metabolism by CYP2E1, the metabolism of 4-VP and its hepatotoxicity and pneumotoxicity were compared in wild-type and CYP2E1 knockout mice. There were no marked differences between the wild-type and knockout mice in the rates of microsomal metabolism of 4-VP in either liver or lung. This unexpected result mimics previous findings with styrene metabolism in wild-type and knockout mice. When mice were administered 100 mg/kg 4-VP ip, the knockout mice were more susceptible to hepatotoxicity, as measured by increases in serum sorbitol dehydrogenase activity, than were the wild-type mice. There was no significant difference in the pneumotoxicity between the two strains. The data suggest that, as for styrene, additional cytochromes P-450 are involved in the metabolism of 4-VP.

Animals↗