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PubMed2004

Cytogenetic markers, DNA single-strand breaks, urinary metabolites, and DNA repair rates in styrene-exposed lamination workers.

The effect of occupational exposure to styrene on frequencies of chromosomal aberrations and binucleated cells with micronuclei and on single-strand break levels in peripheral blood lymphocytes was studied in 86 reinforced plastic workers and 42 control individuals (including 16 maintenance workers with intermittent, low-dose exposure). In these individuals, the irradiation-specific DNA repair rates and the repair rates of 8-oxoguanines were investigated. We assessed the exposure by measuring the concentrations of styrene in air and in blood and of mandelic acid, phenylglyoxylic acid, 4-vinyl phenol conjugates and regioisomeric phenyl hydroxyethyl mercapturic acids in urine. All these parameters correlated with one another. No clear relationship was found between the styrene exposure and the frequencies of chromosomal aberrations. Binucleated cells with micronuclei were moderately related to the parameters of styrene exposure. We found a negative correlation between all exposure parameters and single-strand breaks. The positive correlation between exposure parameters and DNA repair rates suggests that particular DNA repair pathways may be induced by styrene exposure.

Adult↗
PubMed1976

Hepatic and extrahepatic metabolism of 14C-styrene oxide.

With 8-(14)C-styrene oxide as substrate, specific glutathione S-transferase and epoxide hydrase activities were determined in subcellular fractions of liver, lungs, kidney, and intestinal mucosa from rabbit, rat, and guinea pig. Liver had the highest enzyme activities in each species. Rat and guinea pig had higher glutathione S-transferase activity in both liver and kidney than rabbit. Rat testis also had appreciable glutathione S-transferase activity. The perinatal development of epoxide hydrase and glutathione S-transferase was followed in liver and several extrahepatic tissues of fetal and neonatal guinea pigs and rabbits. The rates at which enzyme activities reached adult levels in the extrahepatic tissues differed from the liver in both species. Epoxide hydrase and glutathione S-transferases developed at different rates in each organ, demonstrating that the relative importance of these two detoxifying pathways for styrene oxide may shift before and after birth. The effects of pretreating male and female rats with phenobarbital (PB), 1,2,3,4-dibenzanthracene (DBA), pregnenolone-16alpha-carbonitrile (PCN), or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on hepatic and extrahepatic epoxide hydrase and glutathione S-transferase activities toward styrene oxide were determined. PB increased both enzyme activities in liver of both sexes. PCN induced only glutathione S-transferase activity in female liver. Extrahepatic epoxide hydrase and glutathione S-transferase activities were unaffected except that TCDD doubled female renal epoxide hydrase activity and PB increased intestinal epoxide hydrase activity in both sexes. Styrene oxide biotransformation was studied in isolated, perfused rat liver and rabbit lung preparations. Conjugation with glutathione was a major metabolic pathway although significant amounts of diol were also formed in each instance. In rat liver, 27-40% of the administered styrene oxide was excreted via the bile mainly as S-(1-phenyl-2-hydroxyethyl)glutathione.

Aging↗
PubMed2000

Possible reproductive toxicity of styrene in peripubertal male mice.

Environmental estrogens (endocrine disruptive chemicals) have been shown to affect reproduction in wild life and it has been reported that maternal exposure to those chemicals has adverse effects on the male reproductive tract. However, little is known about the potential effects of prepubertal or pubertal exposure to environmental estrogens on the male reproductive tract. Here we examine plasma hormone levels of mice following 4-week oral administration of styrene. Plasma free testosterone levels were dramatically decreased following 4 weeks of styrene treatment compared with control group. No differences in plasma corticosterone and luteinizing hormone levels were seen between styrene and control groups. Thus, exposure to styrene around pubertal period may directly disrupt the male reproductive tract. These facts suggest that more detailed studies regarding assessment of the risk to the developing human testes from exposure to styrene and other environmental estrogens in prepubertal and pubertal period are warranted.

Animals↗
PubMed1981

Distribution, elimination and retention of styrene in rats.

In rats exposed to styrene for 4 hours, the rate constant of elimination and biological half life of styrene were 0.11 and about 6 hours for adipose tissue, and 0.3 to 0.4 and about 2 hours for the other tissues, respectively. The relative ratio of apparent distribution of styrene decreased in the order adipose tissue much greater than liver greater than brain greater than kidney greater than blood not equal to spleen greater than muscle. Almost the same results were obtained in the experiment by intraperitoneal injection of styrene. Repeated 4-hour exposures at about 700 ppm daily for five days caused the results similar to those in a single exposure. A trend of increase in concentration of styrene was observed in adipose tissue by 5 successive intraperitoneal injections every 6 hours at a dose of 350 mg/kg.

Animals↗
PubMed1988

In vitro effects of styrene on cytoskeletal apparatus: an immunocytochemical study.

Styrene is known as an organic solvent implicated in neurological disorders occurring in exposed workers. Our studies were focused on the effects of styrene on the cytoskeletal apparatus, involved in several toxic neuropathies. The cultured cells were considered as living systems useful to investigate the mechanisms of cytotoxicity. Preliminary results reported here were obtained on two different epithelial cell lines (CG5 and HEp-2) by immunocytochemical methods. Treatment with styrene at 0.04% and 0.08% for 24 and 48 hours, induced changes in cytoskeletal elements. In particular, styrene seemed to induce a decrease in number of cells adhering to the substrate and some alterations in microtubule assembly. Moreover, a rearrangement of the keratin filaments was observed while styrene did not seem to induce noticeable changes in actin filament network. Data obtained seem to confirm in vitro studies as a useful tool in toxicity assessment of xenobiotic compounds at subcellular levels.

Actin Cytoskeleton↗
PubMed1976

Disturbances in psychological functions of workers occupationally exposed to styrene.

The relationship between long-term occupational styrene exposure and disturbances in psychological functions was studied. The exposed group consisted of 98 male workers exposed to styrene in the manufacture of polyester plastic products, and the comparison group comprised 43 concrete reinforcement workers. The duration of exposure in years and the mean mandelic acid concentration in urine (five determinations during 5 weeks before the clinical examination) and the cumulative dose of exposure were used as the indicators of exposure. The psychological functions studied were intelligence, visuomotor speed, visuomotor accuracy, memory, vigilance, and psychomotor performance. Some personality test variables were also included. In a group comparison two variables (visuomotor inaccuracy and poor psychomotor performance) out of 20 showed statistically significant differences and characterized the styrene exposed group. These findings were confirmed when workers with low and high styrene exposure were compared. One variable measuring visuomotor speed and another measuring visual memory were related to the duration of exposure (R = 0.28, p less than 0.05). In a multiple regression analysis disturbances in visuomotor accuracy, poor psychomotor performance, and lowered vigilance proved to have some connection with a high mandelic acid concentration (R = 0.49, p less than 0.01). In addition workers with disturbances in visuomotor accuracy and slight disturbances in virumotor speed had higher mandelic acid concentrations when compared with those workers without any deterioration. The results indicate that disturbances in visuomotor accuracy and, to a lesser degree, in psychomotor performance are the main findings measured by test methods used in this study and related to one indicator of styrene exposure, mandelic acid concentration. The psychological methods used revealed subclinical symptoms related to exposure, and they should aid in making group diagnoses, e.g., when additional information is needed for the determination of the threshold limit value. The deterioration found in visuomotor accuracy could be related to lowered safety in work and traffic.

Adolescent↗
PubMedDate not supplied

Is the aged rat ear more susceptible to noise or styrene damage than the young ear?

Noise- and styrene-induced hearing and hair cell loss were studied in young (3 months) and aged (24-26 months) Long-Evans rats. The animals were exposed 6 h/d, 5 d/w for 4 weeks to (a) broadband noise centered at 8 kHz (92 or 97dB SPL), or b) styrene (700 ppm). Auditory sensitivity was tested by recording evoked potentials from the inferior colliculus. Histological analyses of the organ of Corti, stria vascularis, and the spiral ganglions were also performed. Aged controls showed outer hair cell (OHC) loss at the basal and apical regions of the organ of Corti, and an increase in pigmentation concomitant to a decrease in vascularization of the stria vascularis, along with elevated thresholds relative to young controls. The 92-dB noise caused similar threshold shifts in both age groups, whereas the 97-dB noise caused more threshold shifts in the aged group compared to the young group. Recovery of the hearing thresholds depended both on the intensity of the noise and on the age of the animals. Aged rats had minimal hair cell loss as a result of styrene exposure, whereas young animals showed significant OHC loss, particularly in third row. Despite significant loss of OHCs, the young subjects showed styrene-induced threshold shifts only at high frequencies. In summary, the data show that : (a) there is an influence of age on both noise-induced and styrene-induced threshold shift and hair cell loss in rats and (b) the cochlea appear to have a redundancy in the number of OHCs, thus threshold shift does not necessarily occur with significant OHC loss.

Aging↗
PubMed1987

Occupational asthma due to styrene: two case reports.

Two cases of occupational asthma due to styrene are described. The subjects complained of cough, breathlessness, and symptoms of asthma when coming into contact with styrene; in patient 1 the respiratory reaction was followed by a late cutaneous rash. The symptoms disappeared when the subjects were away from work on weekends or holidays. In both cases, inhalation challenge with styrene produced an immediate bronchospastic reaction which was followed by a late cutaneous rash in patient 1. Prior administration of disodium cromoglycate (40 mg from a spinhaler) prevented the respiratory reactions completely, but failed to prevent the late skin response in case 1. Styrene removal was followed by complete disappearance of the symptoms. We conclude that styrene can be a primary cause of occupational asthma.

Adult↗
PubMed1979

The fate of intratracheally instilled 3H-styrene oxide in the isolated perfused rat lungs.

The metabolism and covalent binding of intratracheally instilled 7-3H-styrene oxide in the isolated perfused lungs of control and cigarette smoke-exposed rats were investigated. After intratracheal instillation of 100 nmoles of 7-3H-styrene oxide the lungs were perfused for 16 min and the nonrecirculating perfusate was collected in two fractions: 0--8 min and 8--16 min. About 40 percent of the instilled dose was in the 0--8 min perfusion medium, mainly in the form of unmetabolized styrene oxide. However, the radioactivity in the 8--16 min perfusion medium and lung tissue itself was mainly in the form of water soluble metabolites, probably glutathione conjugates. The amount of styrene glycol was very small. Exposure of rat to cigarette smoke had no effect on the metabolism of styrene oxide or on the amount of covalent binding to the protein and nucleic acid fractions of the perfused lungs.

Animals↗
PubMed1978

Effects of inhalation and cutaneous exposure to styrene on drug metabolizing enzymes in the rat.

The effects of inhalation and cutaneous exposure to styrene on the drug metabolizing enzymes were studied in the rat. Rats were exposed eight hours per day, for seven successive days to 450 ppm concentration of styrene or received one cutaneous dose of styrene daily for seven consecutive days (0.5 and 3.0 g/kg). The animals were killed one day after the last dose. Styrene inhalation increased the activities of epoxide hydrase and UDPglucuronosyltransferase (4-methylumbelliferone as substrate) in liver (1.5- and 1.7-fold, respectively). Ethoxycoumarin deethylation was enhanced 1.7-fold in the kidney. The content of cytochrome P-450 in the liver and the activities of NADPH cytochrome c-reductase, benzpyrene hydroxylase and glutathione S-transferase in the liver and kidney were not altered. No changes in the enzyme activities were detected in the lung. Styrene depressed the epoxide hydrase activity in liver when administered cutaneously. No signs of enzyme induction could be seen after cutaneous administration.

Administration, Topical↗
PubMed1982

[Occupational risk after repeated skin exposure to styrene].

The use of styrene in the production and processing of polymers, varnishes and paints is a prerequisite for a broad skin contact with the solvent, hence conditions for occupational effect on the workers, manifested with frequent contact toxic dermatitis. That determined the scope of this work, aiming at the specifying of the occupational risk in case of repeated dermal contact with styrene. The experiment was carried out in the course of 28 days on 70 albino male rats, treated daily, dermally with 4 ml/kg and 8 ml/kg from the substance and on groups with a following 14--day rehabilitation. The following methods were used in the investigation: histological (H.E.), histochemical (Sudan III, Sudan schwartz and PAS-reactions under the control of alpha-amilase), enzyme-histochemical (activity of alkaline phosphatase, acid phosphatases, ATP, SDH, LDH and G16PDH) and electron microscopic. The repeated skin application of styrene was established to induce changes in the organism of the experimental animals, localized mainly in the liver and carrying the character of fatty dystrophia. The latter is directly proportional to the dose applied and the exposure duration. After a 14-day rehabilitation period, the dystrophia abates and the processes of proliferation and regeneration predominate in the organ, regardless of the enzyme disorders established in the oxidation-reduction processes of liver, with the higher styrene dose (8 ml/kg). The authors presume that the dynamic follow up of the adaptation mechanisms in liver, in case of repeated dermal contact with styrene, determines reversible tissue deviations in organism of the experimental animals, being dose-effect dependent. The authors are in the opinion that the occupational risk in production and processing of polystyrene is minimum when observing the sanitary instructions for safe contact.

Administration, Topical↗
PubMed1978

Effects of long-term oral administration of styrene to mice and rats.

Styrene monomer dissolved in olive oil was given orally to female O20 mice (1,350 mg/kg), C57 Bl mice (300 mg/kg) and BD IV rats (1,350 mg/kg) on the 17th day of gestation. Their offspring were treated weekly with styrene by stomach tube from the time of weaning throughout their life-span. The weekly doses used were 1,350 mg/kg for O20 mice, 300 mg/kg for C57 Bl mice, and 500 mg/kg for BD IV rats. Following the continuous oral administration of styrene for over 100 weeks, an increased and earlier appearance of lung tumors was observed in O20 mice. A few tumors rarely seen in controls were observed in BD IV styrene-treated rats, and a slightly increased incidence of liver tumors was found in C57 Bl mice. In both cases, however, the total incidence of tumors was not significantly different from that of the controls. The present results provide weak evidence of the carcinogenicity of styrene in one of the two strains of mice tested, when it is given at a high dose level.

Administration, Oral↗
PubMed1978

Possible metabolic interaction of styrene with organic solvents.

Excretion of metabolites of styrene (dose: 2.2 mmol/kg i.p.) in 24-h urine was suppressed when rats were coinjected intraperitoneally with either toluene or trichloroethylene (dose: 2.2--11.0 mmol/kg) in addition to styrene, while a coinjection of n-hexane, ethyl acetate, methylchloroform, or acetone at an equimolar dose was ineffective in all cases. Suppressive effects of toluene and trichloroethylene were further confirmed by 6-h vapor exposure to (a) 0 to 1,300 ppm of toluene in addition to 150--170 ppm of styrene and (b) 0 to 4,000 ppm of trichloroethylene together with 100 or 150 ppm of styrene. The relationship between the amounts of three metabolites (i.e., phenylglyoxylic, mandelic and hippuric acids) in urine and styrene concentration in air was also determined.

Air Pollutants↗
PubMed1980

The problem of negative results for styrene in the in vitro mutagenesis test with metabolic activation (microsomal assay):explanation by gas chromatographic analysis.

Mutagenic experiments in vitro were performed on yeast (S. pombe) with styrene with metabolic activation by adding at fixed times fresh mouse microsomes to the incubation mixture. Preceding studies with a single initial addition of microsomes were negative up to the maximal dose of 100 mM styrene for 60 min (5). The addition of fresh microsomes at the times 12, 24, 36 and 48 min in the presence of EDTA 40 mM resulted in an increased toxicity of styrene in vitro, but not in increased mutagenicity. Gas chromatographic determination of styrene oxide in the incubation mixture with 50 mM styrene revealed a concentration of active metabolite not capable of acting mutagenically.

Ascomycota↗
PubMed2003

Secondary ion and laser ablation mass spectrometry for the quantitative characterization of styrene-butadiene copolymers.

Styrene-butadiene copolymers were analyzed by static secondary ion mass spectrometry (S-SIMS) and laser ablation Fourier transform ion cyclotron resonance mass spectrometry (LA-FTICRMS) to obtain quantitative information based on specific ions. Silver deposition was performed on polystyrene, butadiene rubber and styrene-butadiene rubber. Under these experimental conditions, new secondary ions were detected, in particular silver-cationized butadiene [M(butadiene) - Ag](+) and styrene [M(styrene) - Ag](+) monomers. In contrast, LA-FTICRMS experiments did not require pretreatment. At high laser power density, UV photons (193, 266 and 355 nm) allowed the detection of styrene and butadiene monomers at m/z 104 and 54, respectively. The use of the observed ions by SIMS or LA-FTICRMS ensures that quantitative information on the relative distribution of each monomer is obtained. However, the silver coating thickness in the SIMS experiment seems to have an important influence on the quantitative information obtained. For LA-FTICRMS experiments, the best results are obtained at a wavelength of 355 nm.

Journal Article↗
PubMed1980

Kinetics of the inhibition of styrene oxide and benzo(a)pyrene-4,5-oxide hydration in rat liver microsomes by cadmium.

The kinetics of the inhibition by cadmium of styrene oxide and benzo(a)pyrene-4,5-oxide hydration were studied in a microsomal preparation from rat liver. Cadmium inhibited the hydration of styrene oxide in an apparently noncompetitive manner, whereas the inhibition of benzo(a)pyrene-4,5-oxide hydration showed a competitive mechanism. Styrene oxide inhibited the hydration of benzo(a)pyrene-4,5-oxide competitively and cyclohexene oxide inhibited the hydration of both styrene oxide and benzo(a)pyrene-4,5-oxide competitively. The present data suggest that cadmium is bound near the active centre of the enzyme. Occupation of this site by cadmium inhibits the enzymic hydration of the polycyclic benzo(a)pyrene-4,5-oxide molecule competitively, and that of the smaller monocyclic alkene oxide of styrene noncompetitively. The estimated Ki values were below 10 mu mol for hydration of both substrates indicating that cadmium is a very potent inhibitor of epoxide hydration.

Animals↗
PubMed2005

Swelling behavior of organoclays in styrene and exfoliation in nanocomposites.

Organoclays were prepared by cationic exchange of montmorillonite (MMT) with three commercial surfactants: octadecylamine (ODA), hexadecyltrimethylammonium bromide (HTAB), benzalkonium chloride (BAC), and an in-house synthesized surfactant, vinylbenzylalkyldimethylammonium chloride (VDAC). The swelling behaviors of organoclays in styrene were compared by wettability and rheology measurements. VDAC-MMT had the slowest capillary rise rate in styrene. The Washburn equation was found not suitable for the swellable organoclay powders. All organoclay-styrene and organoclay-toluene mixtures demonstrated yield stress. However, VDAC-MMT-styrene and VDAC-MMT-toluene mixtures showed significant higher yield stresses than the other organoclay mixtures. The wettability and rheology measurements indicate that VDAC-MMT bearing a styryl functional group has the strongest interaction with styrene monomer and toluene. In order to further evaluate the extent of swelling and the microstructure, polystyrene (PS)-clay nanocomposites were prepared by in situ polymerization. X-ray diffraction (XRD) and transmission electron microscopy (TEM) indicate that ODA and HTAB-MMT led to intercalated PS-clay nanocomposites, while VDAC-MMT formed exfoliated PS-clay nanocomposites.

Journal Article↗
PubMed2002

Styrene 7,8-oxide induces caspase activation and regular DNA fragmentation in neuronal cells.

Neurobehavioral changes have been described in workers occupationally exposed to styrene vapors. Alterations of neurotransmitters and loss of neurons have been observed in brains of styrene-exposed rats. However, the mechanisms of neuronal damage are not yet clearly understood. We have characterized the cellular alterations induced by the main reactive intermediate of styrene metabolism, styrene 7,8-oxide (SO) in the human neuroblastoma SK-N-MC cell line and primary culture of rat cerebellar granule cells (CGC). SK-N-MC cells exposed to SO (0.3-1 mM) displayed apoptotic morphology, together with chromatin condensation and DNA cleavage into high molecular weight fragments of regular size. These features were accompanied by the activation of class II caspases, as detected with the DEVD assay, by following the cleavage of the caspase-substrate poly (ADP-ribose) polymerase (PARP) and by detection of the active fragment of caspase-3. Pre-incubation of the cells with the caspase inhibitor z-VAD-fmk reduced the cellular damage induced by SO, suggesting that caspases play an important role in SO toxicity. Increased proteolysis by class II caspases was detected also in primary culture of CGC exposed to SO. In addition, the presence of the 150-kDa cleavage product of alpha-fodrin suggests a possible activation of calpains in SK-N-MC cells. Moreover, SO did not affect the level of expression of the p53 protein, even though it is known to cause DNA damage. The identified intracellular pathways affected by SO exposure provides end-points that can be used in future studies for the evaluation of the neurotoxic effect of styrene in vivo.

Carrier Proteins↗