Styrene Exposure Levels Research Articles

Associations of Occupational Styrene Exposure With Risk of Encephalopathy and Unspecified Dementia: A Long-Term Follow-up Study of Workers in the Reinforced Plastics Industry.

Exposure to industrial solvents has been associated with encephalopathy. Styrene is a neurotoxic industrial solvent, and we investigated the long-term risk of encephalopathy and unspecified dementia following styrene exposure. We followed 72,465 workers in the reinforced plastics industry in Denmark (1977–2011) and identified incident cases of encephalopathy (n = 228) and unspecified dementia (n = 565) in national registers. Individual styrene exposure levels were modeled from information on occupation, measurements of work place styrene levels, product, process, and years of employment. Adjusted analyses were performed using a discrete survival function. A positive trend for encephalopathy (P < 0.01) and a negative trend for unspecified dementia (P = 0.03) were seen with cumulative styrene exposure accrued during the recent period of up to 15 years. For unspecified dementia and the combination of unspecified dementia and encephalopathy, a positive trend was indicated when applying a 30-year exposure lag (P = 0.13 and P = 0.07). The risk patterns seen following recent exposure probably reflect diagnostic criteria for encephalopathy requiring recent industrial solvent exposure and referral bias rather than association with styrene exposure, while the increasing risk observed for unspecified dementia and the combination of encephalopathy and unspecified dementia following distant exposure indicates an increased risk of dementia following styrene exposure with a long latency period.

Environmental styrene exposure and neurologic symptoms in U.S. Gulf coast residents

BackgroundStyrene is an established neurotoxicant at occupational levels, but effects at levels relevant to the general population have not been studied. We examined the neurologic effects of environmental styrene exposure among U.S. Gulf coast residents. MethodsWe used National Air Toxics Assessment (NATA) 2011 estimates of ambient styrene concentrations to assign exposure levels for 21,962 non-diabetic Gulf state residents, and additionally measured blood styrene concentration in a subset of participants (n = 874). Neurologic symptoms, as well as detailed covariate information, were ascertained via telephone interview. We used log-binomial regression to estimate prevalence ratios (PR) and 95% confidence intervals (95% CI) for cross-sectional associations between both ambient and blood styrene levels and self-reported neurologic symptoms. We estimated associations independently for ten unique symptoms, as well as for the presence of any neurologic, central nervous system (CNS), or peripheral nervous system (PNS) symptoms. We also examined heterogeneity of associations with estimated ambient styrene levels by race and sex. ResultsOne-third of participants reported at least one neurologic symptom. The highest quartile of estimated ambient styrene was associated with one or more neurologic (PR, 1.12; 95% CI: 1.07,1.18), CNS (PR, 1.17; 95% CI: 1.11,1.25), and PNS (PR, 1.16; 95% CI: 1.09,1.25) symptom. Results were less consistent for biomarker analyses, but blood styrene level was suggestively associated with nausea (PR, 1.78; 95% CI: 1.04, 3.03). In stratified analyses, we observed the strongest effects among non-White participants. ConclusionsIncreasing estimated ambient styrene concentration was consistently associated with increased prevalence of neurologic symptoms. Associations between blood styrene levels and some neurologic symptoms were suggestive. Environmental styrene exposure levels may be sufficient to elicit symptomatic neurotoxic effects.

Lung disease associated with occupational styrene exposure.

Despite reports of pulmonary toxicity due to styrene, guidelines on acceptable styrene exposure levels have been based on risk of cancer and central nervous system and liver toxicity and not on respiratory effects. Many reports have linked exposure to styrene vapor in occupational settings to various forms of non-malignant pulmonary disorders including bronchiolitis, hypersensitivity pneumonitis, and occupational asthma. We report two cases in which the same tasks performed in a single workplace resulted in exposure to styrene vapor with subsequent development of acute respiratory symptoms associated with impaired gas exchange and imaging and histopathologic findings consistent with bronchiolitis and organizing pneumonia. Both patients gradually recovered once their workplace exposure to styrene was terminated. Clinicians, employers, and insurers should be aware of the potential for pulmonary toxicity from exposure to styrene.

Cooperativity in CYP2E1 metabolism of acetaminophen and styrene mixtures

Risk assessment for exposure to mixtures of drugs and pollutants relies heavily on in vitro characterization of their bioactivation and/or metabolism individually and extrapolation to mixtures assuming no interaction. Herein, we demonstrated that in vitro CYP2E1 metabolic activation of acetaminophen and styrene mixtures could not be explained through the Michaelis–Menten mechanism or any models relying on that premise. As a baseline for mixture studies with styrene, steady-state analysis of acetaminophen oxidation revealed a biphasic kinetic profile that was best described by negative cooperativity (Hill coefficient=0.72). The best-fit mechanism for this relationship involved two binding sites with differing affinities (Ks=830μM and Kss=32mM). Introduction of styrene inhibited that reaction less than predicted by simple competition and thus provided evidence for a cooperative mechanism within the mixture. Likewise, acetaminophen acted through a mixed-type inhibition mechanism to impact styrene epoxidation. In this case, acetaminophen competed with styrene for CYP2E1 (Ki=830μM and Ksi=180μM for catalytic and effector sites, respectively) and resulted in cooperative impacts on binding and catalysis. Based on modeling of in vivo clearance, cooperative interactions between acetaminophen and styrene resulted in profoundly increased styrene activation at low styrene exposure levels and therapeutic acetaminophen levels. Current Michaelis–Menten based toxicological models for mixtures such as styrene and acetaminophen would fail to detect this concentration-dependent relationship. Hence, future studies must assess the role of alternate CYP2E1 mechanisms in bioactivation of compounds to improve the accuracy of interpretations and predictions of toxicity.

Susceptibility of linear and nonlinear otoacoustic emission components to low-dose styrene exposure

Objective: To investigate potential susceptibility of active cochlear mechanisms to low-level styrene exposure by comparing TEOAEs in workers and controls. Design: Two advanced analysis techniques were applied to detect sub-clinical changes in linear and nonlinear cochlear mechanisms of OAE generation: the wavelet transform to decompose TEOAEs into time-frequency components and extract signal-to-noise ratio and latency of each component, and the bispectrum to detect and extract nonlinear TEOAE contributions as quadratic frequency couplings (QFCs). Study sample: Two cohorts of workers were examined: subjects exposed exclusively to styrene (N = 9), and subjects exposed to styrene and noise (N = 6). The control group was perfectly matched by age and sex to the exposed group. Results: Exposed subjects showed significantly lowered SNR in TEOAE components at mid-to-high frequencies (above 1.6 kHz) and a shift of QFC distribution towards lower frequencies than controls. No systematic differences were observed in latency. Conclusion: Low-level styrene exposure may have induced a modification of cochlear functionality as concerns linear and nonlinear OAE generation mechanisms. The lack of change in latency seems to suggest that the OAE components, where generation region and latency are tightly coupled, may not have been affected by styrene and noise exposure levels considered here.

Occupational Styrene Exposure Induces Stress-Responsive Genes Involved in Cytoprotective and Cytotoxic Activities

ObjectiveThe aim of this study was to evaluate the expression of a panel of genes involved in toxicology in response to styrene exposure at levels below the occupational standard setting.MethodsWorkers in a fiber glass boat industry were evaluated for a panel of stress- and toxicity-related genes and associated with biochemical parameters related to hepatic injury. Urinary styrene metabolites (MA+PGA) of subjects and environmental sampling data collected for air at workplace were used to estimate styrene exposure.ResultsExpression array analysis revealed massive upregulation of genes encoding stress-responsive proteins (HSPA1L, EGR1, IL-6, IL-1β, TNSF10 and TNFα) in the styrene-exposed group; the levels of cytokines released were further confirmed in serum. The exposed workers were then stratified by styrene exposure levels. EGR1 gene upregulation paralleled the expression and transcriptional protein levels of IL-6, TNSF10 and TNFα in styrene exposed workers, even at low level. The activation of the EGR1 pathway observed at low-styrene exposure was associated with a slight increase of hepatic markers found in highly exposed subjects, even though they were within normal range. The ALT and AST levels were not affected by alcohol consumption, and positively correlated with urinary styrene metabolites as evaluated by multiple regression analysis.ConclusionThe pro-inflammatory cytokines IL-6 and TNFα are the primary mediators of processes involved in the hepatic injury response and regeneration. Here, we show that styrene induced stress responsive genes involved in cytoprotection and cytotoxicity at low-exposure, that proceed to a mild subclinical hepatic toxicity at high-styrene exposure.

Low level occupational exposure to styrene: Its effects on DNA damage and DNA repair

The present study aimed to evaluate the effects of styrene exposure at levels below the recommended standards of the Threshold Limit Value (TLV-TWA(8)) of 20 ppm (ACGIH, 2004) in reinforced-fiberglass plastics workers. Study subjects comprised 50 exposed workers and 40 control subjects. The exposed workers were stratified by styrene exposure levels, i.e. group I (<10 ppm, <42.20 mg/m(3)), group II (10-20 ppm, 42.20-84.40 mg/m(3)), and group III (>20 ppm, >84.40 mg/m(3)). The mean styrene exposure levels of exposed workers were significantly higher than those of the control workers. Biomarkers of exposure to styrene, including blood styrene and the urinary metabolites, mandelic acid (MA) and phenylglyoxylic acid (PGA), were significantly increased with increasing levels of styrene exposure, but were not detected in the control group. DNA damage, such as DNA strand breaks, 8-hydroxydeoxyguanosine (8-OHdG), and DNA repair capacity, were used as biomarkers of early biological effects. DNA strand breaks and 8-OHdG/10(5)dG levels in peripheral leukocytes of exposed groups were significantly higher compared to the control group (P<0.05). In addition, DNA repair capacity, determined by the cytogenetic challenge assay, was lower in all exposed groups when compared to the control group (P<0.05). The expression of CYP2E1, which is involved in styrene metabolism, in all styrene exposed groups, was higher than that of the control group at a statistically significant level (P<0.05). Levels of expression of the DNA repair genes hOGG1 and XRCC1 were significantly higher in all exposed groups than in the control group (P<0.05). In addition to styrene contamination in ambient air, a trace amount of benzene was also found but, the correlation between benzene exposure and DNA damage or DNA repair capacity was not statistically significant. The results obtained from this study indicate an increase in genotoxic effects and thus health risk from occupational styrene exposure, even at levels below the recommended TLV-TWA(8) of 20 ppm.

DNA damage, DNA repair rates and mRNA expression levels of cell cycle genes (TP53, p21CDKN1A, BCL2 and BAX) with respect to occupational exposure to styrene

We studied the relationship between DNA damage, DNA repair rates and messenger RNA (mRNA) expression levels of cell cycle genes TP53, p21(CDKN1A), BCL2 and BAX in a group of 71 styrene-exposed workers and 51 control individuals. The exposure was assessed by measuring the concentration of styrene at workplace and in blood. Parameters of DNA damage [measured as single-strand breaks (SSBs) and endonuclease III-sensitive sites], γ-irradiation-specific DNA repair rates and mRNA levels of studied genes were analyzed in peripheral blood lymphocytes. The workers were divided into low (<50 mg/m³) and high (>50 mg/m³) styrene exposure groups. We found negative correlations between mRNA expression of TP53, BCL2, BAX and styrene exposure (P < 0.001 for all parameters). In contrast, p21(CDKN1A) mRNA expression significantly increased with increasing styrene exposure (P = 0.001). SSBs and endonuclease III-sensitive sites increased with increasing mRNA levels of TP53 (P < 0.001 for both) and BCL2 (P = 0.038, P = 0.002, respectively), whereas the same parameters decreased with increasing mRNA levels of p21(CDKN1A) (P < 0.001, P = 0.007, respectively). γ-Irradiation-specific DNA repair rates increased with p21(CDKN1A) mRNA levels up to the low exposure level (P = 0.044). Our study suggests a possible relationship between styrene exposure, DNA damage and transcript levels of key cell cycle genes.

Occupational styrene exposure, colour vision and contrast sensitivity: a cohort study with repeated measurements

Associations between occupational styrene exposures and impairment of visual functions were investigated with a view to answering three questions: (1) are the published findings for colour vision deficiencies and impaired contrast sensitivity to reproduce in a new study approach, (2) if such effects exist, are they related to current or chronic exposures and (3) if effects exist, are there reductions in the effects during an exposure-free period? Workers from a boat building plant were examined in groups of current low [n = 97, mean mandelic acid (MA) + phenylglyoxylic acid (PGA) = 51 mg/g creatinine], medium (n = 115, mean = 229 mg/g creatinine) and high (n = 30, mean = 977 mg/g creatinine) level exposure to styrene. Job tenure was about 6 years. In addition, subgroups chronically exposed to low-short (n = 34, lifetime weighted mean 200 mg/g creatinine for 6 years) and high-long (n = 17, mean = 660 mg/g creatinine, 15 years) styrene levels were analysed. The examinations were carried out during normal working days and during the company holidays. Colour vision was investigated with the Lanthony desaturated panel D-15d using the colour confusion index (CCI) as a relevant variable. Contrast sensitivity was investigated with the Vistech charts VCTS 6500 using frequency-related results as well as total scores as variables. Co-variance analyses with repeated measurements and multiple linear regressions were used for statistical analysis. There was no evidence of significant associations between exposure parameters and CCI. This is true for the analyses with all participants as well as for those with the subgroups with high-long versus low-short exposure. Thus, no exposure related changes in the relevant variables were found during the exposure-free period. The analyses for contrast sensitivity show similar results. The largest portions of the variances in both tests were explained by age. German as mother tongue covered a considerable portion of the CCI variances. Education, long-term alcohol use and job tenure explain only partly significant portions of the test variances exhibited. Both acute styrene exposure levels of 40 ppm (range of standard deviation up to 54 ppm) and long term exposures to 27 ppm (range of standard deviation up to 44 ppm with higher exposure levels in the past) for a period of about 15 years were not identified as causing elevated risks for the investigated parameters of colour vision and contrast sensitivity. This statement contradicts the published results for styrene-related colour vision deficiencies but it seems to be compatible with published results for contrast sensitivity due to styrene exposure.

Effects of styrene exposure on vibration perception threshold

Objectives We aimed to investigate whether styrene can affect the vibration perception threshold (VPT) and to examine the dose–effect relationship at current and past styrene exposure levels. Methods VPT was examined using a Vibrometer (TM-31A) for 67 subjects exposed to styrene in a fiberglass reinforced plastic boat plant and 151 non-exposed subjects. We selected 67 age-matched controls out of the non-exposed subjects for the analyses. End shift urinary metabolites of styrene were measured for evaluation of the dose–effect relationship for the past eight years and at the time of VPT measurement. The current exposure level was expressed by the end shift urinary mandelic acid (MA) and phenylglyoxylic acid (PGA) levels. Cumulative exposure index (CEI) were calculated based on the exposure frequency and urinary MA concentrations measured for the past eight years. Results The VPT of the exposed group was higher than that of non-exposed group. Multiple regression analysis revealed that past maximum exposure level and age were significant factors explaining the variation of VPT. Dose–effect relationship was recognized in upper limbs but not in lower limbs among exposure groups. When the exposed group was divided into high- and low-level groups for the past maximum exposure level by the cutoff point of MA 0.83 g/g cr (equivalent to 50 ppm in air) and compared to the control group, we found significant differences in the VPT in upper limbs, between the high-level exposed group and control group, and in lower limbs, between both of the high- and low-level exposed groups and the control group. Conclusion If the maximum concentration of styrene exposure exceeded 50 ppm in the past, effects of exposure to styrene on the VPT are likely to persist.

Company-Level, Semi-Quantitative Assessment of Occupational Styrene Exposure when Individual Data are not Available

In epidemiological research, self-reported information about determinants and levels of occupational exposures is difficult to obtain, especially if the disease under study has a high mortality rate or follow-up has exceeded several years. In this paper, we present a semi-quantitative exposure assessment strategy for nested case-control studies of styrene exposure among workers of the Danish reinforced plastics industry when no information on job title, task or other indicators of individual exposure were readily available from cases and controls. The strategy takes advantage of the variability in styrene exposure level and styrene exposure probability across companies. The study comprised 1522 cases of selected malignancies and neurodegenerative diseases and controls employed in 230 reinforced plastics companies and other related industries. Between 1960 and 1996, 3057 measurements of styrene exposure level obtained from 191 companies, were identified. Mixed effects models were used to estimate expected styrene exposure levels by production characteristics for all companies. Styrene exposure probability within each company was estimated for all but three cases and controls from the fraction of laminators, which was reported by a sample of 945 living colleagues of the cases and controls and by employers and dealers of plastic raw materials. The estimates were validated from a subset of 427 living cases and controls that reported their own work as laminators in the industry. We computed styrene exposure scores that integrated estimated styrene exposure level and styrene exposure probability. Product (boats), process (hand and spray lamination) and calendar year period were the major determinants of styrene exposure level. Within-company styrene exposure variability increased by calendar year and was accounted for when computing the styrene exposure scores. Exposure probability estimates based on colleagues' reports showed the highest predictive values in the validation test, which also indicated that up to 67% of the workers were correctly classified into a styrene-exposed job. Styrene exposure scores declined about 10-fold from the 1960s-1990s. This exposure assessment approach may be justified in other industries, and especially in industries dominated by small companies with simple exposure conditions.

Relation between colour vision loss and occupational styrene exposure level

Aims: To investigate the relation between colour vision loss and the exposure level of styrene. Exposure level included the current exposure concentration, past cumulative exposure, and the maximum exposure level...

Evaluation of genotoxic effects in a group of workers exposed to low levels of styrene

Occupational exposure to styrene was studied in a group of workers engaged in the production of fiberglass-reinforced plastics. Sister-chromatid exchanges (SCE), micronuclei (MN), and DNA damage (evaluated by means of comet assay) were measured in peripheral blood cells from the exposed workers and from a control population. Mandelic acid concentration, an indicator of styrene exposure level, was measured in urine samples collected at the end of the work shift. Average estimated values for styrene exposure were slightly below the threshold limit value (TLV®) of 20 ppm recommended by the American Conference of Governmental Industrial Hygienists. Significant increases ( P≤0.01) have been found for SCE and MN frequencies and comet tail length among exposed individuals, as well as significant decreases ( P≤0.01) in the proliferation indices, as compared with control population. High correlation has been obtained between endpoints evaluated and exposure length, and increased values of SCE and MN frequencies and comet tail length have been found among smokers only in the exposed population. The high correlation obtained among SCE and MN frequencies and comet tail length, and the increase of these parameters in the exposed group with regard to control group justify the use of these three biomarkers in the evaluation of genotoxic effects in human populations exposed to styrene.

Simultaneous high-performance liquid chromatographic determination of urinary mandelic and phenylglyoxylic acids as indirect evaluation of styrene exposure

Styrene is rapidly metabolised to mandelic acid (MA) and phenylglyoxylic acid (PGA), which are excreted in urine. In this work, we have developed a simple, sensitive and specific high-performance liquid chromatographic method with minor sample preparation procedures for the simultaneous determination of MA and PGA in urine of workers exposed to styrene. Moreover, urine samples from workers of two plastic factories were analysed, styrene exposure levels of the workers were estimated and data obtained from the two factories were compared.

Time to pregnancy among male workers of the reinforced plastics industry in Denmark, Italy and The Netherlands. ASCLEPIOS.

The relationship between occupational styrene exposure and male fecundity was examined. Among 1560 Danish, Italian, and Dutch reinforced plastics workers, 220 styrene-exposed workers and 382 unexposed referents who had fathered a child were identified. A total of 768 historical styrene measurements conducted in 1970-1996 in the study companies formed the basis for semiquantitative exposure assessment in combination with measurements of urinary styrene metabolite levels. All the subjects were interviewed about work conditions and other factors potentially related to reduced fecundity. Fecundity was measured as the reported time to pregnancy (number of months a couple needed to conceive their youngest child). A statistically nonsignificantly reduced fecundity was observed for the styrene-exposed workers [fecundity ratio 0.79, 95% confidence interval (95% CI) 0.59-1.05]. But no consistent pattern of a detrimental effect on fecundity was found when time to pregnancy was related to worktasks indicating higher styrene exposure levels or semiquantitative or quantitative measures of styrene exposure. The workers with high exposure showed a fecundity ratio of 1.09 (95% CI 0.69-1.72). It is unlikely that styrene exposure has a strong effect on male fecundity.

An Investigation of Factors Contributing to Styrene and Styrene-7,8-oxide Exposures in the Reinforced-Plastics Industry

During the manufacturing of reinforced plastics, large amounts of styrene and trace quantities of styrene-7,8-oxide (SO) are released. Since previous work suggests that inhalation of even small amounts of SO might be an important health risk, we investigated several possible factors contributing to styrene and SO exposure during the manufacture of reinforced plastics. Factors related to job type, worker and the type and quantity of styrene-containing resins were investigated using mixed-effects multiple linear regression models. Overall, SO exposure levels were positively correlated with styrene exposure levels. However, this correlation was statistically significant only among hand laminators who had the highest exposures to both styrene and SO. An important factor for predicting both styrene and SO concentrations was the type of resin used, while the quantity of resin consumed was predictive of styrene but not of SO exposure. Since SO exposure appears to be associated with factors other than coexposure to styrene, more effort should be placed on investigating emissions of SO per se. The type of mixed-models regression analysis employed in this study can be used for clarifying the underlying patterns for exposures to styrene and SO as well as for evaluating preventive measures. 1999 British Occupational Hygiene Society. Published by Elsevier Science Ltd. All rights reserved.

An Investigation of Factors Contributing to Styrene and Styrene-7,8-oxide Exposures in the Reinforced-Plastics Industry

During the manufacturing of reinforced plastics, large amounts of styrene and trace quantities of styrene-7,8-oxide (SO) are released. Since previous work suggests that inhalation of even small amounts of SO might be an important health risk, we investigated several possible factors contributing to styrene and SO exposure during the manufacture of reinforced plastics. Factors related to job type, worker and the type and quantity of styrene-containing resins were investigated using mixed-effects multiple linear regression models. Overall, SO exposure levels were positively correlated with styrene exposure levels. However, this correlation was statistically significant only among hand laminators who had the highest exposures to both styrene and SO. An important factor for predicting both styrene and SO concentrations was the type of resin used, while the quantity of resin consumed was predictive of styrene but not of SO exposure. Since SO exposure appears to be associated with factors other than coexposure to styrene, more effort should be placed on investigating emissions of SO per se. The type of mixed-models regression analysis employed in this study can be used for clarifying the underlying patterns for exposures to styrene and SO as well as for evaluating preventive measures. 1999 British Occupational Hygiene Society. Published by Elsevier Science Ltd. All rights reserved.

The Importance of Sampling Time and Coexposure to Acetone in the Biological Monitoring of Styrene-Exposed Workers

Abstract Forty-four workers exposed to styrene and acetone in the fiberglass industry were monitored on Monday and Thursday for 8 hours using passive dosimeters. The charcoal discs of the passive dosimeters were analyzed by gas chromatography. The 8-hour time-weighted average (TWA) exposure values ranged from 10 to 522 and 14 to 1581 mg/m3 on Monday and from 9 to 423 and 10 to 579 on Thursday for styrene and acetone, respectively. Urine samples were collected at the end of the work shift and before the start of the work shift the next morning (Tuesday and Friday). Mandelic acid and phenylglyoxylic acid were measured in the urine using a high pressure liquid chromatography method; values were expressed in milligrams/gram creatinine. Styrene TWA exposure values significantly correlated with the sum of metabolites at the end of the workday (r = 0.60 on Monday and r = 0.77 on Thursday) and also the next morning (r = 0.87 on Tuesday and r = 0.84 on Friday). Mandelic acid was always correlated with exposure better than phenylglyoxylic acid. A calculated styrene exposure level of 213 mg/m3 (American Conference of Governmental Industrial Hygienists threshold limit value) was associated with an excretion of metabolites (mandelic acid + phenylglyoxylic acid) higher on Thursday (921 mg/g creatinine) than on Monday (706 mg/g creatinine). The same observation was made on Friday (423 mg/g creatinine) as compared with Tuesday (315 mg/g creatinine). In conclusion, the threshold limit value of styrene was associated with different values of metabolites at the beginning and at the end of the workweek, and we must take this into account in establishing biological exposure indices. Moreover, our data show that the excretion of mandelic acid and phenylglyoxylic acid is not modified by simultaneous exposure of the workers to acetone.

A note on individual differences in the urinary excretion of optical enantiomers of styrene metabolites and of styrene-derived mercapturic acids in humans.

Urine samples from 20 male workers in the polyester industry exposed by inhalation to styrene concentrations ranging from 29 to 41 ppm were investigated. Excretion products of styrene metabolism, mandelic acid and mercapturic acids, were purified from the urine over an extraction column packed with Porapak Q, with subsequent ether elution. The optical enantiomers R- and S-mandelic acid were then determined by thin layer chromatography (TLC) using chiral plate material and selective staining with vanadium pentoxide. Quantitative analysis of these compounds was performed using commercial reference substances. Styrene-specific mercapturic acids were analyzed by a modified TLC method, using synthesized reference substances. The concentration of racemic mandelic acid in the individual urine samples ranged from 80 to 1610 mg/l, and the ratio of the R- and S-enantiomers ranged from 0.7 to 2.2. These individual variations are not explained by differences in individual styrene exposure levels, or by differences in the concentration of the urine samples (in relation to creatinine excretion). Styrene-specific mercapturic acids were detected in the urine of only 1 of the 20 workers, at a concentration much lower than expected from previous investigations by others in humans and laboratory animals, in which less specific analytical methods had been used. The results point to marked interindividual differences in metabolism of styrene, probably related to enzyme polymorphisms.

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.