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PubMed1997

Indigo formation by microorganisms expressing styrene monooxygenase activity.

The transformation of indole to indigo by microorganisms expressing styrene monooxygenase (SMO) has been studied. Styrene and indole are structurally very similar, and thus we looked at a variety of styrene-degrading strains for indole transformation to indigo. Two strains, Pseudomonas putida S12 and CA-3, gave a blue color on solid media when grown in the presence of indole. Indole induces its own transformation on solid media but is a poor inducer in liquid media. Styrene is the best inducer of indole transformation in both strains. Arginine represses styrene consumption and indigo formation rates in P. putida S12 compared to phenylacetic acid-grown cells, while the opposite effect is seen for P. putida CA-3. Characterization of an SMO- and styrene oxide isomerase (SOI)-negative transposon mutant of P. putida CA-3 and an SOI-negative N-methyl-N'-nitro-N-nitrosoguanidine mutant of P. putida S12 reveals the involvement of both SMO and SOI in indole transformation to indigo. Both strains stoichiometrically produce high-purity indigo from indole.

Indigo Carmine↗
PubMed1983

Styrene oxide metabolism in rhesus monkey liver: enzyme activities in subcellular fractions and in isolated hepatocytes.

The activity and the kinetic behavior of expoxide hydrolase were studied in various subcellular fractions of rhesus monkey liver isolated by differential centrifugation. The purity of the fractions was estimated by morphometric electron microscopy. Hydrolase activity was measured by a specific radiometric assay with [7-3H]styrene oxide as substrate. All isolated subcellular fractions catalyzed the hydration of styrene oxide at a significant rate. With a saturating concentration of substrate (1 mM), the enzymatic activity (nanomole of product per minute per milligram of protein; mean +/- S.E.) turned out to be 1.51 +/- 0.45 (nuclear fraction), 3.50 +/- 1.11 (mitochondrial fraction), 14.8 +/- 2.26 (microsomal fraction) and 1.69 +/- 0.37 (soluble fraction). The hydrolase obeyed Michaelis-Menten kinetics in each fraction. Vmax (nanomole per minute per milligram; mean +/- S.E.) was 1.64 +/- 0.65 (nuclear fraction) 3.87 +/- 1.71 (mitochondrial fraction), 19.8 +/- 5.4 (microsomal fraction) and 2.72 +/- 1.36 (soluble fraction). The Km (millimole; mean +/- S.E.) values in the fractions were 0.09 +/- 0.02, 0.07 +/- 0.01, 0.23 +/- 0.15 and 0.64 +/- 0.40, respectively. The metabolism of styrene oxide was also studied in isolated hepatocytes from rhesus monkey. These cells hydrated the substrate easily whereas the conjugation of styrene oxide with glutathione was not measurable. Our results show that epoxide hydrolase is present in all subcellular fractions of the rhesus monkey liver. Styrene oxide is preferentially metabolized by hydration to styrene glycol in the isolated hepatocytes of this species and no conjugation with glutathione was found under the incubation conditions used.

Animals↗
PubMed1983

Chromosome aberrations and sister chromatid exchanges in styrene-exposed workers with reference to their smoking habits.

The incidences of chromosome aberrations and the frequencies of sister chromatid exchanges (SCE) were investigated in cultured lymphocytes of 18 styrene-exposed workers in comparison with six controls. There was a marginal increase in the incidence of structural chromosomal aberrations in first-division metaphases in the styrene-exposed workers, as compared with the nonexposed controls. However, there was no difference in SCE frequencies. When each group was divided into smokers and nonsmokers, styrene-exposed smokers tended to have higher SCE frequencies than styrene-exposed nonsmokers. Furthermore, cell proliferation was inhibited in styrene-exposed workers (both smokers and nonsmokers) and control smokers.

Adolescent↗
PubMed1986

Degeneration and regeneration of respiratory mucosa of rats after exposure to styrene.

The recovery process of pathological changes in the respiratory mucosa following exposure to styrene were experimentally studied to improve the understanding of the respiratory toxicity of styrene. Thirty male SD rats were exposed to 150 ppm or 1000 ppm of styrene for 4 h a day over 3 weeks (5 days a week). They were killed for examination at 1 day or 12 weeks after completion of the exposure sequence. Bilateral mucosal samples from the nasal septum and the trachea of the animals were examined for ciliary activity and subjected to electron microscopy. Complete functional and morphological recovery of the nasal and tracheal mucosa was observed at the 12th week post-exposure to 150 ppm of styrene. After exposure to 1000 ppm of styrene, almost normal function and morphology of the tracheal mucosa was found at the 12th week post-exposure, but the nasal mucosa continued to show decreased ciliary activity and an affected morphology.

Animals↗
PubMed1995

Effects of methanol on styrene metabolism among workers occupationally exposed at low concentrations.

A survey was conducted in the second half of a work week on 39 male workers who were occupationally exposed to styrene in combination with methanol and methyl acetate during the production of plastic buttons. Time-weighted average exposure during an 8-h shift to styrene (Sty-A) and methyl acetate was monitored by carbon cloth-equipped personal samplers and to methanol by water-equipped ones. Urine samples were collected near the end of the shift and analyzed for mandelic (MA-U) and phenylglyoxylic acids (PhGA-U) by HPLC. Geometric mean styrene concentration was 12.4 ppm (micrograms/g) with the maximum of 46 ppm, whereas the values for methanol and methyl acetate in combination were 23.5 ppm and 229 ppm, respectively. The relationship of MA-U and PhGA-U with Sty-A was examined by linear regression analysis. The equations for the regression lines were compared with the results from a previous survey (Ikeda et al. 1983) in which workers were exposed only to styrene, and the methods employed were identical with that in the present study. The comparison showed no evidence to suggest that styrene metabolism is suppressed by coexposure to methanol and methyl acetate at low concentrations below the current occupational exposure limit of 200 ppm.

Acetates↗
PubMed1984

Regional alterations of brain catecholamines by styrene exposure in rabbits.

The regional distribution of dopamine, norepinephrine and homovanillic acid was assessed in adult male rabbits exposed to styrene vapours. The turnover of dopamine and norepinephrine was also measured in several brain regions by the decay in endogenous catecholamines after inhibition of tyrosine hydroxylase by alpha-methyl-p-tyrosine. Styrene exposure produced a marked and dose-dependent decrease in striatal and tuberoinfundibular dopamine, associated with a consistent increase in homovanillic acid content in the same regions. Norepinephrine levels were unaffected by styrene exposure. The observed increase in catabolism of dopamine cannot be explained by the turnover time, which was not significantly different in the exposed as compared to the control rabbits. Competition of a styrene metabolite with dopamine for the vesicular storage capacity or a selective destruction of dopaminergic terminals are suggested as the possible mechanisms for styrene neurotoxicity.

Animals↗
PubMed1993

Biological monitoring of workers exposed to styrene and acetone.

Twenty-two workers exposed to styrene and acetone in two fiberglass industries were monitored on Monday and Thursday for 8 hours using passive dosimeters. Urine samples were collected at the end of the workshift and before the start of the work on the next morning (Tuesday and Friday). The charcoal disks of the passive dosimeters were analysed by gas-chromatography. Mandelic acid (MA) and phenylglyoxylic acid (PGA) were measured using a HPLC method; values were expressed in mg/g of creatinine. The 8-h TWA exposure values for styrene and acetone ranged respectively from 22 to 522 mg/m3 and 40-1581 mg/m3 on Monday; 25-423 mg/m3 and 55-579 mg/m3 on Thursday. Styrene TWA exposure values significantly correlate with the sum of metabolites at the end of workday (r = 0.70 on Monday and r = 0.95 on Thursday) and also at the next morning (r = 0.86 on Tuesday and r = 0.85 on Friday). A styrene exposure level of 213 mg/m3 (ACGIH-TLV) was associated with an excretion of metabolites (MA+PGA) higher on Thursday (803 mg/g creat) than on Monday (570 mg/g creat). The same result was found on Friday (459 mg/g creat) compared with Tuesday (305 mg/g creat). Moreover our data show that the simultaneous exposure to acetone does not modify the excretion of MA. In conclusion the TLV of styrene is associated with different values of metabolites at the beginning and at the end of the work-week.

Acetone↗
PubMed1996

Otoneurological study in workers exposed to styrene in the fiberglass industry.

Twenty workers exposed to styrene and acetone in small fiberglass factories were monitored for 8 h using passive dosimeters. Urine samples were collected at the end of the workshift and before the start of work on the next morning. The 8-h time-weighted average exposure values for styrene and acetone ranged from 14 to 416 mg/m3 and from 70 to 277 mg/m3, respectively. The sum of styrene metabolites, mandelic acid and phenylglyoxylic acid (MA + PGA), in the next-morning urine samples ranged from 81 to 943 mg/g creatinine. Different test sensitivity was identified in the otoneurological battery: it was low for audiometric tests and ABR, and relatively high for vestibular tests. The vestibular system seems partially sensitive to the toxic effects of styrene in the absence of clinical signs and symptoms. The actual exposure levels for styrene cannot be considered devoid of functional subclinical consequences.

Acetone↗
PubMed1990

Hematological findings among styrene-exposed workers in the reinforced plastics industry.

A cross-sectional survey of hematological parameters was carried out among 221 workers exposed to styrene in the reinforced plastics industry and 104 controls. Styrene exposure was assessed in both groups by monitoring urinary excretion of styrene metabolites (i.e. mandelic and phenylglyoxylic acids) in post-shift urinary samples collected over five consecutive days. Blood tests were performed with the same counter for all subjects. Information on factors liable to affect hematological parameters was collected from personal questionnaires completed by the workers. Urinary excretion of styrene metabolites varied from 15 to 3740 mg/g creatinine. Exposed subjects exhibited significantly lower mean values of neutrophils and mean corpuscular hemoglobin concentration (MCHC) than controls, and significantly higher mean values for monocytes and mean corpuscular volume. A dose-effect relationship was found for MCHC which decreased with urinary metabolite concentrations. These results remained statistically significant for all parameters after adjustment for age, sex, tobacco and alcohol consumption, place of residence (rural or urban) and time of blood sampling (morning or afternoon) with the exception of neutrophils whose relationship with exposure was essentially explained by smoking. These results are suggestive of a direct effect of styrene-exposure--in the range considered--on the statistical distribution of some hematological parameters.

Adult↗
PubMed1993

Biological monitoring of styrene in the reinforced plastics industry in Emilia Romagna, Italy.

Biological monitoring of styrene exposure among workers in the reinforced plastics industry is widely implemented in the region of Emilia Romagna, Italy. More than 18,000 urine samples measurements of the main metabolites of styrene, mandelic (MA) and phenylglyoxylic acid, were retrieved for the period 1978-1990, and 4689 values of MA in postshift urine samples were analyzed for various variables thought to influence styrene exposure. The job performed was found to be the most important predictor of styrene exposure. Hand laminators had the highest exposure (mean MA 682 mg/g creatinine); spray laminators showed lower values (404 mg/g), while levels in semiautomatic process operators (243 mg/g) were only slightly higher than in nonprocess workers (186 mg/g). The use of ventilation resulted in lower exposure, but differences in average values were not particularly wide. Exposure decreased weakly during the study period in all work categories, but the percentage of measurements exceeding the current biological limit value (900 mg/g creatinine, 1300 mg/l corrected for density) is still very high (20% of measurements among hand laminators in 1990). These results indicate that the control measures implemented are only partially effective for the prevention of styrene exposure.

Automation↗
PubMed1994

Cytogenetic analysis of lymphocytes from fiberglass-reinforced plastics workers occupationally exposed to styrene.

In this study a group of 52 workers employed in a plant manufacturing fiberglass-reinforced plastic (FRP) pipes and cisterns, and therefore daily exposed to styrene, were monitored. As a control group 24 non-exposed workers from another factory producing and repairing pallets volunteered to participate. The airborne styrene during the monitoring ranged from 2.2 to 110.1 mg/m3. As a metabolic marker for styrene exposure mandelic acid was measured in the urine and ranged from 11 to 649 mg/g creatinine. From 43 exposed and 15 control workers sister-chromatid exchanges (SCE) and high frequency cell (HFC) data and from 49 exposed and 23 control workers micronucleus (MN) data from peripheral lymphocytes are reported. Although the two groups of workers could clearly be distinguished on the basis of the airborne styrene concentrations and urinary mandelic acid concentrations no differences in any of the cytogenetic markers were found. Correlations between the cytogenetic data and the level of airborne styrene concentrations or urinary mandelic acid levels could also not be demonstrated. Otherwise, smoking increased the SCE frequency. Grouping the workers according to smoking habits showed a statistically significant difference in SCE. Moreover, levels of urinary thiocyanate (SCN), which can be used as a metabolic marker for smoking, showed a significant positive correlation with the number of SCE. This indicates that SCE is a sensitive biomarker and might still be useful in biomonitoring. However, only chronic exposures over a long period would probably be detectable. In this study, where exposure was rather low and the number of working years was small (mean of 2.9 years), cytogenetic effects are probably too low or rare to be detectable with any assay.

Adult↗
PubMed1991

Biomarkers in styrene-exposed boatbuilders.

14 fiberglass-reinforced plastics (FRP) boatbuilders were compared with 9 unexposed controls with respect to several chemical specific and nonspecific biomarkers measured in peripheral blood. Biomarkers included styrene-hemoglobin adducts (styrene-Hb), sister-chromatid exchanges (SCEs), micronuclei (MN), single-strand breaks (SSBs) and N-acetoxy-2-acetylaminofluorene-induced DNA binding (NA-AAF binding) as a measure of susceptibility to DNA damage. Workers' exposures averaged 11 ppm (8-h TWA; geometric mean) and ranged from 0.6 to 44 p.p.m. Mandelic acid levels were measured in end-of-shift urine samples and reflected an average styrene exposure equivalent to 15 p.p.m. There was a large though not significant difference in levels of styrene-Hb adducts among exposed workers and controls, largely the consequence of a single heavily-exposed individual with an extremely high level of adducts. Significant differences between biomarker levels in exposed workers and controls were observed with MN, SSBs and NA-AAF binding. No significant differences were seen in mean levels of SCEs nor in the incidence of cells with a high frequency of SCEs. The data suggest that exposure to levels of styrene in occupational settings near or below the current OSHA standard (50 p.p.m.) can induce damage at the cellular/molecular level. Appropriately-selected panels of biomarkers can be useful in identifying potentially harmful exposures.

Acetoxyacetylaminofluorene↗
PubMed1993

Effects of different styrene metabolites on cytotoxicity, sister-chromatid exchanges and cell-cycle kinetics in human whole blood lymphocytes in vitro.

5 metabolites of styrene were tested in vitro for their cytotoxic effects, induction of SCEs and changes in cell-cycle progression in cultured human blood lymphocytes. Fresh heparinized peripheral blood (0.3 ml) from normal volunteers was cultured for a total of 72 h in 5 ml of RPMI 1640 medium containing 10% fetal calf serum, 0.1% garamycine, 1% glutamine and 1% phytohaemagglutinin. Styrene-7,8-oxide (SO), styrene glycol (SG), phenylglyoxylic acid (PGA), S-[1,2-phenyl-2-hydroxyethyl]-glutathione (PEG) (a glutathione conjugate of styrene oxide), N-acetyl-S-[1,2-phenyl-2-hydroxyethyl]-cysteine (NAPEC) in dimethyl sulfoxide (DMSO) were injected into the cultures 36 h after initial culture, so that the exposure time for these metabolites was 36 h. The final concentration of SO was 100 microM and those of the other metabolites were 500 microM. 24 h before harvest, BrdU (10 micrograms/ml) was added into the cultures for assessing cytogenetic endpoints. SO showed significant induction of SCEs and cell-cycle delay as well as a significant decline of cell survival. The same phenomena, but of less magnitude, were also observed with NAPEC, a cysteine derivative of SO. On the other hand, SG, PGA and PEG failed to produce any significant changes of these endpoints compared to the control. Thus, the present results have demonstrated that, in addition to SO, NAPEC possesses some cytogenotoxic potential and hence, these two metabolites together could contribute to the genotoxicity of styrene in human blood lymphocytes.

Cell Cycle↗
PubMed1986

Reduced synthesis of 5-aminolevulinate dehydratase in styrene-treated rats.

5-Aminolevulinate dehydratase (porphobilinogen synthase; 5-aminolevulinate hydro-lyase, EC 4.2.1.24) preparations purified from rat liver and erythrocytes are indistinguishable in terms of molecular weight, subunit size, immunoreactivity, amino-acid composition and kinetic properties, suggesting that the enzyme from liver and erythrocytes are identical. Intraperitoneal injection of styrene to rats decreased 5-aminolevulinate dehydratase activity in both erythrocyte (to 8% of the control) and the liver (to 40% of the control). Studies utilizing polysome-directed cell-free translation indicated that hepatic synthesis of the enzyme was inhibited by styrene at the transcriptional level. In vitro addition of styrene 7,8-oxide, a major intermediate of styrene, to purified 5-aminolevulinate dehydratase resulted in a loss of immunoassayable enzyme protein to less than 1% of the untreated control. These findings suggest that the decrease in 5-aminolevulinate dehydratase caused by in vivo treatment of styrene is partially due to a transcription-dependent decrease in the enzyme synthesis, and partially to post-translational alteration of the structure of the enzyme protein.

Animals↗
PubMed1985

Chronic toxicity and three-generation reproduction study of styrene monomer in the drinking water of rats.

Chronic toxicity and reproductive performance were evaluated in groups of rats receiving styrene monomer in their drinking water at nominal concentrations of 0, 125, or 250 ppm. Fifty male and 70 female rats in each test group and 76 males and 104 females in the control group were placed on a 2-year study and followed for observations of general health which included measurement of body weight, food and water consumption, hemograms, clinical chemistries, urinalysis, and histopathological examination. Ten males and 20 females from each group in the study were mated to produce F1 pups. These pups were subsequently mated to produce three generations of offspring, all maintained on styrene-treated drinking water. For each generation, the following were evaluated: fertility, litter size, pup viability, pup survival, sex ratio, pup body weight, weanling liver and kidney weight, and marrow cytogenetics. Except for a statistically significant reduction in water consumption for styrene-treated rats, no treatment-related changes, including mortality patterns, were reported for animals in the chronic study. The data evaluated for reproductive performance also showed no evidence of styrene-related changes. It was concluded that the administration of styrene in the drinking water of rats for 2 years produced no deleterious dose-related effects or decrements in reproductive performance.

Animals↗
PubMed1988

The effects of occupational exposure to styrene on high-frequency hearing thresholds.

Subchronic exposure to styrene has been reported to produce high-frequency hearing loss in rats. In humans, hearing thresholds for higher frequencies (greater than 8 kHz) are also more vulnerable to ototoxic drugs than those at lower frequencies. Since hearing loss at frequencies above 8 kHz does not seem to play a role in speech processing, hearing loss at frequencies above 8 kHz in workers exposed to styrene or other solvents might easily escape detection. Therefore, hearing thresholds were evaluated at frequencies up to 16 kHz in workers exposed to styrene and compared to those of a control group of unexposed workers. The airborne concentrations of styrene typically did not exceed 150 mg/m3 although individual exposures did, at times, reach higher values (up to 700 mg/m3). In accordance with the literature, an age-dependent increase in hearing thresholds at high frequencies was found. Compared to controls, workers exposed to styrene did not appear to demonstrate an aggravated age-dependent decrease in hearing high frequencies. A comparison, however, within the experimental group between the least exposed and the most exposed workers revealed a statistically significant difference on hearing thresholds at high frequencies.

Adult↗
PubMedDate not supplied

Effect of prenatal exposure to styrene on the neurobehavioral development, activity, motor coordination, and learning behavior of rats.

Maternal Wistar rats were exposed via inhalation to 0, 50, or 300 ppm styrene for 6 h/day during gestation days 7 to 21, and offspring were subsequently evaluated in several neurobehavioral tests. Preliminary results with a small number of litters revealed significant dose-dependent effects in tests performed prior to weaning (surface righting, pivoting locomotion, and bar holding), as well as in tests performed after weaning (motor coordination, open-field behavior, and motor activity). Exposure to low concentrations of styrene (50 ppm) caused disturbances in motor coordination in addition to delaying some motor and reflex developments. Large doses (300 ppm) led to changes in open-field behavior and increases in spontaneous activity in addition to the delay in neurobehavioral developments. Exposure of dams to styrene did not clearly affect the learning behavior of the offspring. It was also observed that age played a role in the differences in styrene's effects on neurobehavioral function. Only subtle effects were found in both open-field behavior and motor-coordination function when compared with control rats at 120 days of age. These results suggest that the functional neurobehavioral development of progeny of dams exposed to styrene (or other solvents) should be further investigated.

Animals↗
PubMed1997

Comparison of styrene-7,8-oxide adducts formed via reaction with cysteine, N-terminal valine and carboxylic acid residues in human, mouse and rat hemoglobin.

The reactive metabolite of styrene, styrene-7,8-oxide (SO), reacts with a variety of nucleophilic sites in hemoglobin (Hb) to form SO-Hb adducts. Following the in vitro incubation of SO with blood from humans, NMRI mice and Sprague-Dawley rats, the second-order reaction rate constants were determined for the reaction of SO with cysteine (through both the alpha- and beta-carbons of SO), N-terminal valine (through the beta-carbon of SO), and carboxylic acid (presumably through both the alpha- and beta-carbons of SO) residues in Hb. The rate constants for cysteine adducts vary dramatically between species [2.04, 10.7, 133 L (mol Hb)-1 h-1 (alpha binding) for humans, mice and rats, respectively] and [0.078, 2.16, 20.4 L (mol Hb)-1 h-1 (beta binding), respectively]. The considerably higher rate of reaction with cysteine in rat Hb probably reflects the presence of an additional cysteine residue at position beta 125. Although the rate constants for valine adducts (1.82, 0.80, 0.29 L (mol Hb)-1 h-1, respectively) and COOH adducts (3.55, 1.94, 2.37 L (mol Hb)-1 h-1, respectively) are much more consistent, the inter-species differences are statistically significant for the reaction of SO with the N-terminal valine of Hb. Following the i.p. administration of styrene to mice and styrene and SO to rats, the levels of adducts at each of these sites were used in conjunction with the calculated rate constants to predict the integrated blood doses of SO. While the SO doses predicted from cysteine and valine adducts were very similar, that based upon COOH-binding was significantly different, presumably due to the instability of SO-COOH adducts. This research affirms the use of both cysteine and valine adducts, but not carboxylic acid adducts, as biomarkers of exposure to styrene and SO.

Animals↗