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PubMed2001

Identification of 1-adenine DNA adducts in workers occupationally exposed to styrene.

Styrene is an extensively used industrial chemical that has been classified as a possible human carcinogen. The possible carcinogenicity may be related to the covalent DNA binding properties of styrene 7,8-oxide, a major metabolite of styrene. We have developed a sensitive and a highly specific phosphorus-32-postlabeling method for the determination of 1-styrene 7,8-oxide-adenine DNA adducts. These adducts were analyzed in white blood cells from workers exposed to styrene at mean level of 76.2 mg/m3. Three of nine exposed workers showed adducts above the detection limit; the mean was 0.79 +/- 0.14 1-styrene 7,8-oxide-adenine DNA adducts/10(9) nucleotides. None of the 11 control cells showed adducts above the detection limit, which was 0.4 adducts/10(9) nucleotides. The results show a potential of 1-adenine DNA adducts for predicting risks in the workers exposed to styrene.

Adenine↗
PubMed2006

Cytogenetic biomarkers, urinary metabolites and metabolic gene polymorphisms in workers exposed to styrene.

The present study comprised a biomonitoring study in 95 workers occupationally exposed to styrene and 98 unexposed controls, employing an integrated approach involving biomarkers of exposure, effect, and susceptibility. Airborne styrene was evaluated at workplace, and urinary styrene metabolites, mandelic acid (MA), phenylglyoxylic acid (PGA), vinylphenols (VPTs) and phenylhydroxyethylmercapturic acids (PHEMAs), were measured as biomarkers of internal dose. Cytogenetic alterations were evaluated by analysing the frequency of chromosomal aberrations (CAs) and micronucleated binucleated cells (MNBN) in peripheral blood lymphocytes. The micronucleus assay was coupled with centromeric fluorescence in situ hybridization to distinguish micronuclei (MN) arising from chromosomal breakage (C- MN) from those harboring whole chromosomes (C+ MN). The possible influence of genetic polymorphisms of xenobiotic-metabolizing enzymes involved in styrene biotransformation (EPHX1, GSTT1, GSTM1, GSTP1) and NAT2 on the cytogenetic endpoints was investigated. The exposed workers showed a significantly higher frequency of MNBN (13.8+/-0.5% versus 9.2+/-0.4%; P<0.001) compared to control subjects. The effect appeared to concern both C- and C+ MN. A positive correlation was seen between the frequency of C+ MN and urinary level of MA+PGA (P<0.05) and VPTs (P<0.001). Chromosome-type CAs positively correlated with airborne styrene level and VPTs (P<0.05), whereas chromatid-type CAs correlated with PHEMAs (P<0.05). Workers bearing GSTM1 null genotype showed lowered levels of PHEMAs (P<0.001). The GSTT1 null genotype was associated with increased MNBN frequencies in the exposed workers (P<0.05) and the fast activity EPHX genotype with a moderate decrease in both MNBN and CAs in the controls. Our results suggest that occupational exposure to styrene has genotoxic effects that are potentiated by the GSTT1 gene deletion. These observations may have relevance considering the risk of lymphatic and haematopoietic malignancies tentatively associated with styrene exposure.

Chromosome Aberrations↗
PubMed1990

Microbial transformation of styrene by anaerobic consortia.

Methanogenic microbial consortia, originally enriched from anaerobic sewage sludge with ferulic acid or styrene (vinylbenzene) as sole organic carbon and energy sources, were used to study transformation of styrene under strictly anaerobic conditions. Styrene, which was added as the substrate in a range of concentrations from 0.1 to 10 mmol/l, was extensively degraded but no methane production was observed during incubation for eight months. The addition of yeast extract during the enrichment stage completely inhibited degradation of styrene. Gas chromatography (GC), gas chromatography/mass spectrometry (GC/MS), high performance liquid chromatography (HPLC) analyses of the culture fluid, and GC analyses of the anaerobic headspace, indicated that the transformation of this arylalkene was initiated through an oxidation-reduction reaction and that the favoured mechanism was most likely the addition of water across the double bond in the alkenyl side-chain. The degradation proceeded through to carbon dioxide, the final product. Benzoic acid and phenol were transient compounds found in highest concentrations in the spent culture fluid and are suggested as the key intermediates of the transformation process. The tentative routes of anaerobic transformation partially overlap with those previously proposed for aromatic hydrocarbons such as toluene. Several pure cultures, which were tentatively identified as Clostridium spp. and Enterobacter spp., were isolated from the styrene-degrading consortia. Two of these cultures were demonstrated to grow on styrene as sole carbon and energy source. Additionally, a pure culture of Enterobacter cloacae DG-6 (ATCC 35929) which had been isolated previously from the ferulate-degrading consortium, was shown to degrade styrene through to carbon dioxide.

Bacteria, Anaerobic↗
PubMed2005

Accumulation of polyhydroxyalkanoate from styrene and phenylacetic acid by Pseudomonas putida CA-3.

Pseudomonas putida CA-3 is capable of converting the aromatic hydrocarbon styrene, its metabolite phenylacetic acid, and glucose into polyhydroxyalkanoate (PHA) when a limiting concentration of nitrogen (as sodium ammonium phosphate) is supplied to the growth medium. PHA accumulation occurs to a low level when the nitrogen concentration drops below 26.8 mg/liter and increases rapidly once the nitrogen is no longer detectable in the growth medium. The depletion of nitrogen and the onset of PHA accumulation coincided with a decrease in the rate of substrate utilization and biochemical activity of whole cells grown on styrene, phenylacetic acid, and glucose. However, the efficiency of carbon conversion to PHA dramatically increased once the nitrogen concentration dropped below 26.8 mg/liter in the growth medium. When supplied with 67 mg of nitrogen/liter, the carbon-to-nitrogen (C:N) ratios that result in a maximum yield of PHA (grams of PHA per gram of carbon) for styrene, phenylacetic acid, and glucose are 28:1, 21:1, and 18:1, respectively. In cells grown on styrene and phenylacetic acid, decreasing the carbon-to-nitrogen ratio below 28:1 and 21:1, respectively, by increasing the nitrogen concentration and using a fixed carbon concentration leads to lower levels of PHA per cell and lower levels of PHA per batch of cells. Increasing the carbon-to-nitrogen ratio above 28:1 and 21:1 for cells grown on styrene and phenylacetic acid, respectively, by decreasing the nitrogen concentration and using a fixed carbon concentration increases the level of PHA per cell but results in a lower level of PHA per batch of cells. Increasing the carbon and nitrogen concentrations but maintaining the carbon-to-nitrogen ratio of 28:1 and 21:1 for cells grown on styrene and phenylacetic acid, respectively, results in an increase in the total PHA per batch of cells. The maximum yields for PHA from styrene, phenylacetic acid, and glucose are 0.11, 0.17, and 0.22 g of PHA per g of carbon, respectively.

Carbon↗
PubMed1994

An updated cohort mortality study of workers exposed to styrene in the reinforced plastics and composites industry.

Mortality data have been updated for a further 12 years for a cohort of workers in the reinforced plastics and composites industry with exposures to styrene monomer and other chemicals. The cohort consisted of 15,826 male and female employees who were exposed to styrene for at least six months between 1948 and 1977 at 30 participating manufacturing plants in the United States. A total of 1628 deaths were reported during the extended observation period, 1948-89. Mortality from several causes showed significant increases--namely, all causes, all cancers, oesophageal cancer, lung cancer, cancer of the cervix uteri, cancer of other female genital organs, hypertensive heart disease, certain non-malignant respiratory diseases, motor vehicle accidents, and homicides. When, however, mortality data were examined in terms of duration of employment, durations of styrene exposure, and cumulative styrene exposure no upward trend was detected in any of these causes of death. Most of the increases in mortality were among workers who were employed for only six months to a year or who had very low cumulative exposure (< 10 ppm-years). Therefore, the increased mortality was not likely to be related to exposure to styrene. Several explanations for the increased mortality are offered, including low socioeconomic class, smoking, and lifestyle factors characteristic of short term workers. There was no increased mortality from lymphatic and haematopoietic cancers overall or from any specific haematological malignancies. In particular, no increase in mortality from non-Hodgkin's lymphoma, Hodgkin's disease, multiple myeloma, or leukaemia was found. Furthermore, detailed exposure-response analyses did not show any relation between exposure to styrene and any of these haematological malignancies. The lack of an exposure-response relation further supports the conclusion that workers in the reinforced plastics industry in this study did not experience any increased risk of lymphatic and haematopoietic cancers as a result of their exposure to styrene.

Cause of Death↗
PubMed2001

Neurobehavioural changes and persistence of complaints in workers exposed to styrene in a polyester boat building plant: influence of exposure characteristics and microsomal epoxide hydrolase phenotype.

OBJECTIVES: To investigate neurobehavioural effects and the persistence of complaints in workers exposed to styrene relative to exposure characteristics and the enzyme microsomal epoxide hydrolase (mEH) activity. METHODS: A cross sectional study was performed in a retrospective cohort of workers of a polyester boat building plant 3 years after the main activity shut down in 1989. Workers still currently exposed to a much lower concentration of styrene in air than before (n=27) and formerly exposed workers (n=90) were compared with matched control workers (n=64). Currently and formerly exposed workers laminated 4700 and 3610 hours on average at mean exposure to styrene concentrations of 148 and 157 mg/m(3) respectively. A structured neurological anamnesis into former and present complaints, the NSC-60 questionnaire, and computer assisted neurobehavioural tests (NES) were administered. The mEH phenotype activity was measured in lymphocytes with a novel gas chromatography-mass spectroscopy (GC-MS) method. RESULTS: For the period before 1989, currently and formerly exposed workers reported more complaints than control workers which related well with the mean exposure to airborn styrene concentration (p=0.03). Most complaints disappeared after the end of exposure, although the chest, equilibrium, and somatic category scores of NSC-60 and the number of workers reporting diminished sense of smell remained increased in formerly exposed workers (p<or=0.05). Symbol-digit substitution and digit span forwards test results were worse in currently and formerly exposed workers (p<or=0.01). In the combined group of currently and formerly exposed workers, the symbol-digit substitution and colour-word vigilance results related well to duration of exposure (p<0.01 and p=0.03) and mEH phenotype activity (p=0.01 and p=0.05), whereas the digit span forwards results only showed associations of borderline significance (duration of exposure (p=0.08) and mEH phenotype activity (p=0.08)). CONCLUSION: Most subjective symptoms were reversible but some persisted after the end of exposure to styrene, whereas dysfunction of visuomotor performance and perceptual speed seemed to persist. Duration of exposure at lamination tasks and the interaction, duration of exposurexconcentration of exposure, were found to be the best predictors of worsening visuomotor and perceptual speed performances. Activity of the mEH phenotype may play a modulating part in styrene neurotoxicity. The results suggested that less than 10 years of exposure to atmospheric styrene at an average concentration of 155 mg/m(3) may result in persistent neurotoxic effects.

Adult↗
PubMed2001

Certain styrene oligomers have proliferative activity on MCF-7 human breast tumor cells and binding affinity for human estrogen receptor.

To examine the estrogenic activities of styrene oligomers, we carried out cell proliferation assays with estrogen-sensitive MCF-7 cells and competitive binding assays to human estrogen receptor [alpha] (hER[alpha]). The styrene oligomers tested were 1,3-diphenyl propane (SD-1), 2,4-diphenyl-1-butene (SD-2), cis-1,2-diphenyl cyclobutane (SD-3), trans-1,2-diphenyl cyclobutane (SD-4), 2,4,6-triphenyl-1-hexene (ST-1), 1a-phenyl-4a-(1'-phenylethyl)tetralin (ST-2), 1a-phenyl-4e-(1'-phenylethyl)tetralin (ST-3), 1e-phenyl-4a-(1'-phenylethyl)tetralin (ST-4), 1e-phenyl-4e-(1'-phenylethyl)tetralin (ST-5), 1e,3e,5a-triphenylcyclohexane (ST-6), and 1e,3e,5e-triphenylcyclohexane (ST-7). In the MCF-7 cell proliferation assay, styrene trimers (ST-1, ST-3, ST-4, and ST-5) had the highest proliferative activities of the compounds tested. The relative potency of these chemicals was 0.0002-0.0015%, which was comparable with that of bisphenol A (0.0001-0.0025%), and their relative proliferative effect was 51-104%. Styrene dimers (SD-3 and SD-4) also significantly increased the cell yields. However, SD-1, SD-2, ST-2, ST-6, and ST-7 had insignificant proliferative activities. The competitive binding assay revealed the binding affinity of some styrene oligomers for hER[alpha]. The order of their binding potency for hER[alpha] was as follows: ST-4 > ST-2 > ST-3 > ST-5 > ST-1 > SD-3 > SD-4 > SD-2 > SD-1. ST-6 and ST-7 did not appear to bind to hER[alpha]. The present studies indicate that styrene dimers SD-3 and SD-4 and styrene trimers ST-1, ST-3, ST-4, and ST-5 have estrogenic activity on MCF-7 cells and binding affinity for hER[alpha]. These compounds might be endocrine disrupters.

Binding, Competitive↗
PubMed2005

Effects of pregnancy, age and sex in the metabolism of styrene in rat liver in relation to the regulation of cytochrome P450 enzymes.

To elucidate the effect of maternal styrene exposure, which is due to various postnatal changes in the development and behavior of offspring, we investigated pregnancy-induced changes in the metabolism of styrene in rat liver in relation to the regulation of cytochrome P450 enzymes. We also examined age and sex-induced changes in the metabolism of styrene. Pregnancy appeared to exert a negative effect on cytochrome P450 content at the late stage, whereas microsomal protein content showed little change during pregnancy. Pregnancy significantly decreased the rate of formation of styrene glycol at the late stage. The percentage of remaining activity in microsomes exposed to anti-CYP2E1 was lower than that exposed to anti-CYP2C11/6 in pregnant and non-pregnant female rats and immature male rats, indicating that CYP2E1 contributes to the metabolism of styrene more than CYP2C11/6 in these rats. Although pregnancy seemed to decrease styrene metabolism, the contribution of CYP2E1 seemed to be slightly increasing. In conclusion, pregnancy clearly influences the metabolism of styrene as well as other characteristic factors such as age and sex. It is very important to elucidate the changes in specific P450 isozyme composition related to their characteristic modification and in their affinity for chemicals.

Age Factors↗
PubMed2006

Field study to explore possible effects of styrene on auditory function in exposed workers.

OBJECTIVES: We conducted this study to examine, whether occupational styrene exposures are associated with reduced hearing ability. METHODS: The auditory function was investigated by pure tone audiometry and registration of transitory evoked otoacoustic emissions (TEOAE) in 32 workers of a fibre-reinforced plastic boat building factory. Sixteen subjects were laminators (mean age: 41 yr (SD: 8)) and therefore regularly exposed to styrene with mean duration of exposure to styrene of 7.5 yr (SD 5.0). The tests were applied to a reference group of 16 workers (mean age: 39 yr (SD: 8)) who were not directly exposed to styrene but had a similar noise exposure. RESULTS: A few and isolated correlations between the parameters of hearing acuity and exposure indices, such as current internal styrene exposures (sum of MA and PGA) and duration of styrene exposure, were statistically significant, but no consistent association was found. CONCLUSION: The results of this study do not support the assumption of an ototoxic effect of chronic styrene exposure in workers.

Adult↗
PubMedDate not supplied

Vestibulo-oculomotor disturbances in humans exposed to styrene.

Several reports indicate that disturbances of the vestibulo-oculomotor ability are a manifestation of the toxic action on the central nervous system exerted by some industrial solvents. The aim of the present investigation was to examine the vestibulo-oculomotor system during exposure to styrene, which is extensively used in the production of plastics. Healthy volunteers were exposed to styrene for one hour. Rotatory and optokinetic nystagmus, visual suppression as well as speed, latency and accuracy of saccades were tested before, during, and one hour after the exposure. The pulmonary uptake and the blood level of the solvent were continuously analysed by gas chromatography. The styrene blood concentration was equivalent to that which may well be reached after serveral hours of hard work in an industrial environment with a concentration of styrene within permitted limits. No spontaneous nystagmus appeared. The rotatory and optokinetic nystagmus was not influenced by styrene. However, the speed of the saccade was significantly enhanced. The visual suppression was disturbed, shown by an increased gain after styrene exposure. The experiments thus indicate that styrene given to healthy test persons induced disturbances, thus consistent with the theory that some organic solvents block the cerebellar inhibition of the vestibulo-oculomotor system.

Adult↗
PubMed1976

Neurophysiological findings among workers occupationally exposed to styrene.

Ninety-six male workers occupationally exposured to styrene in 24 plants producing reinforced polyester plastic products were studied neurophysiologically. The mean age of the subjects was 29.6 +/- 7.4 years, and the duration of the exposure varied from 6 months to 14 years (mean 5.0 years). Mandelic acid concentration in the urine (mean of five values determined during five consecutive weeks) was used as the measure of exposure. The individual means of the mandelic acid concentrations varied from 7 to 4,715 mg/dm3 (median 808 mg/dm3). Neurotoxic effects of styrene exposure upon the central nervous system were revealed by abnormalities in the EEG. The overall prevalence of abnormal EEGs was 24% (23 out of 96), which is higher than that found among a normal population (p less than 0.05). Abnormal EEGs were found in one-third of the subjects with relevant styrene exposure (mandelic acid concentration over 700 mg/dm3), while low-level styrene exposure did not increase the prevalence of normal EEGs above that found in a normal population. Nerve conduction velocity measurements performed on 40 subjects did not reveal any definite relationship between neuropathy and styrene exposure. The EEG examination is useful in the investigation of the neurotoxic effects of styrene. Whenever a possibility exists of excessive styrene exposure or beginning poisoning, the workers should be submitted to an EEG examination.

Adolescent↗
PubMed2002

[A study on the adduct characteristics of styrene and DNA].

OBJECTIVE: To explore the adduct characteristics of styrene and DNA. METHODS: The adduct reactions between styrene, urinary mandalic acid(MA), phenylglyoxalic acid(PGA), mercapturic acid of styrene (UMA) and DNA were studied by ultraviolet spectral analysis. The SO-DNA adducts by 32P-post labeled method, the chemical structures of SO-DNA adducts by GC-MS and NMR were also studied. RESULTS: SO combined with DNA at O6, N2 positions of dGMP to form six adducts, but styrene, urinary mandalic acid, phenylglyoxalic acid and mercapturic acid of styrene did not react with DNA to form adduct. CONCLUSIONS: Styrene formed adduct with DNA through its active center metabolite--SO after entering the body. SO combined with DNA at O6, N2 positions of dGMP to form adducts. If these DNA adducts are not repaired or are mis-repaired before cell duplication, the gene mutation and chemical damage would happen. No adduct reactions are seen among other metabolites of styrene.

Acetylcysteine↗
PubMedDate not supplied

[Urinary excretion of 4-vinyl phenol after experimental and occupational exposure to styrene].

Aim of this study was to assess the importance and the role of a minor metabolic route of styrene metabolism, involving the oxidation of the arene moiety of styrene, by means of the characterization of the conjugated urinary metabolites of 4-vinylphenol (4-VP). 4-vinylphenol-glucuronide (4-VP-G) and -sulfate (4-VP-S) were measured by liquid chromatography tandem mass spectrometry (LC-MS/MS) from 174 workers belonging to three cohorts recruited in European countries, and from 26 volunteers exposed to 50 mg/m3 (11.8 ppm) of styrene for 8 h. The 4-VP conjugates represented about 0.5-1% of the total excretion of styrene metabolites. Both 4-VP-G and 4-VP-S are eliminated with a mono-phasic kinetic, the glucuronide being excreted faster (half-time, 2.2 +/- 0.2 h) than the sulfate (half-time 9.7 +/- 1.7 h). The urinary 4-VP was found to be significantly correlated both with airborne styrene (r = 0.607, p < 0.001) and the sum of MA and PGA (r = 0.903, p < 0.001 in 'end-of-shift' samples). A measurable background excretion of 4-VP was also found in all urine samples from controls not occupationally exposed to styrene. This background appears to be highly correlated to smoking (p < 0.001). Consequently, the use of 4-VP as a biomarker of styrene exposure is recommended for exposures exceeding 1 ppm.

Adult↗
PubMedDate not supplied

[Lymphocyte subpopulations in workers exposed occupationally to styrene].

In a group of 32 workers occupationally exposed to styrene, the distribution of lymphocyte subsets was investigated by automated flow cytometry. The group under study consisted of 22 male and 10 female workers aged 39.7, D.S. = 10 years and employed for 6.8 years in factories manufacturing glass fibre-reinforced plastics. A control group (12 males and 7 females) recruited according to the same selection criteria was simultaneously examined. Environmental and biological monitoring was used to characterize styrene exposure. In styrene-exposed workers, phenotypic analysis of peripheral blood revealed a reduced proportion of T helper lymphocytes and a relative increase in the T suppressor subset, leading to a significant inversion of the helper/suppressor ratio (0.92) among heavily exposed workers (greater than 50 ppm, 8h-TWA) as compared to less exposed workers and controls (1.37 and 1.43 respectively). The proportion of natural killer (NK) T lymphocytes was significantly increased among styrene workers. The proportion of B lymphocytes was unchanged as compared to the control group. Dose-response relationships were clearly apparent for the observed increases in the prevalence of abnormalities: none of control subjects showed more than 2 (out of 8) abnormal values as compared to 20 and 40% of styrene workers belonging respectively to the low and high exposure group (p less than 0.007). Only a minority of controls exhibited abnormally high levels of both NK and suppressor T lymphocytes (0-5%), the corresponding figures for styrene workers being 7-10% (low exposure) and 45% (high exposure). As a whole, the findings support the hypothesis of the immunotoxicity of styrene, which could be due either to direct effects on lymphocytes or to indirect mechanisms possibly mediated by neuroendocrine changes.

Adult↗
PubMed2006

[Effects of styrene on the dopaminergic transmitter content and monoamine oxidase activity in different sections of rat brain].

OBJECTIVE: To observe the effect on dopaminergic transmitter content and of monoamine oxidase (MAO) activity at dose of experiment in different sections of rat brain exposed bu acutely and subacutely styrene. METHODS: Rats were administrated orally with styrene of at dose of 600mg/kg for acute, 150, 300 and 600mg/kg for subacute experiment; recovery group were observed after 3 weeks exposure of styrene and intervened group were injected intraperitoneally at dose of 600mg/kg Levodopa (L-dopa) ; the urinary metabolites of styrene mandelic acid (MA) and phenylglyoxylic acid (PGA) were monitered as inner dosage, and the content of dopamine (DA) and activity of MAO were evaluated. RESULTS: The result indicated that the content of urinary MA and PGA were associated with dosage positively, and MA may be more sensitive as inner dosage of styrene exposure since the background of PGA. Levels of DA in retina, hypophysis and striatum were decreased after styrene exposure, the activities of MAO in hypophysis were increased and were reduced in retina and striatum. CONCLUSION: It was suggested dopaminergic system could be participated in styrene neurotoxicity.

Animals↗
PubMedDate not supplied

The distribution and pharmacokinetics of styrene monomer in rats by the pulmonary route.

Exposures (5 hr) of individual rats to atmospheres having styrene concentrations of from 50 to 2,000 ppm yield uptake blood profiles which show a continued and increasing absorption of styrene, proportional to the styrene atmospheric concentration, over the entire absorption period. Post-exposure elimination follows a dose-dependent two compartment model, similar to that observed after I.V. administration, although the initial stage of the elimination is more rapid and the terminal stage much slower than is observed in the I.V. case. A two-compartment pharmacokinetic model, with zeroth-order input, is proposed to interpret the uptake kinetics. Tissue concentrations of styrene in the heart, liver, lung, kidney, spleen, brain and perirenal fat show a different pattern of distribution as the dose increases. At all exposure concentrations the concentration of styrene in the perirenal fat is ten times that in any organ. At the lowest exposure concentration the kidney registered the highest concentration while a higher level of styrene is found in the liver, brain and kidney as the exposure level increases and for these tissues the concentration of styrene is always greater than that in the blood.

Animals↗
PubMed1978

Alcohol consumption and tolerance of workers exposed to styrene in relation to level of exposure and psychological symptoms and signs.

A group of 98 male workers occupationally exposed to styrene was interviewed for information on the amount and frequency of alcohol consumption and changes in consumption frequency and tolerance. Alcohol consumption and changes in consumption were not compared to any reference data, but the changes in tolerance were. The styrene-exposed workers revealed a lowered tolerance somewhat more often than the unexposed group. Neither the duration nor the intensity of styrene exposure was related to any of the alcohol "behavior" variables. The amount of over-time work in exposure had a slight relationship to high alcohol consumption, but the interpretation of this relationship remains undecided. Subjective symptoms, like hand tremor and difficulties in staying asleep, were associated with the alcohol "behavior" variables, but these two symptoms were unrelated to intensity of styrene exposure. Of the psychological functions studied, lowered visuomotor speed showed a slight relationship to high alcohol consumption. Visuomotor inaccuracy, which had proved to be related to a high intensity of styrene exposure, revealed no connection with the alcohol "behavior" variables. It was concluded that alcohol consumption among styrene-exposed workers is not related to the same psychological symptoms and signs as styrene exposure.

Adolescent↗
PubMed1978

Accumulation of styrene monomer and neurochemical effects of long-term inhalation exposure in rats.

A simplified compartment model indicated that fat styrene content might be used as an index of the whole body styrene burden. Intermittent exposure of adult male rats to 300 ppm 5 d a week, 6 h daily for 1 to 11 weeks showed an initial steady increase in the fat styrene content up to the 4th week and an exponential decrease thereafter. This phenomenon might have resulted from the enhancement of styrene oxidation due to the prolonged exposure. The effect of the increased oxidation on the body styrene burden is theoretically doubled after 9.1 weeks of exposure. Neurochemical effects after that time might have resulted from an increased binding of styrene oxide in the cellular macromolecules, e.g., to their sulfhydryl groups. The activity of the metabolite towards the cellular constituents could very well explain the increased proteolysis possibly caused by lysosomal labilization. The present data also lend support to the theory of the importance of metabolic activation to styrene and other solvent toxicity.

Adipose Tissue↗