Human exposure to styrene

Summary An industrial hygiene study of 10 glassfiber reinforced polyester plants (including 90 workers) was undertaken to investigate the styrene exposure in this industry and to estimate biological limit values (BLV's) for the urinary metabolites of styrene: mandelic (MA) and phenylglyoxylic acids (PGA). Time weighted average (TWA) styrene exposures were found ranging from 2 to 200 ppm. The urinary elimination of metabolites correlated well with exposure and the BLV's corresponding to an 8-h exposure at 100 ppm were consistent with earlier laboratory findings (end-of-shift sample: MA 1640, PGA 510, MA + PGA 2150; next-morning sample: MA 330, PGA 330, MA + PGA 660 mg/g creat.). Total metabolites (MA + PGA) in the next-morning sample or mandelic acid in the end-of-shift sample are recommended for routine monitoring of exposure to styrene. The study revealed the need for further research on how to reduce styrene exposure in this industry.     

Biological monitoring of occupational exposure to tetrahydrofuran

Occupational exposure to tetrahydrofuran (THF) was studied by analysis of environmental air, blood, alveolar air, and urine from 58 workers in a video tape manufacturing plant. Head space gas chromatography (GC) with an FID detector was used for determination of THF concentration in alveolar air, urine, and blood. Environmental exposure to THF was measured by personal sampling with a carbon felt passive dosimeter. When the end of shift urinary THF concentrations were compared with environmental time weighted average (TWA) values, urinary THF concentration corrected for specific gravity correlated well with THF concentration in air (r = 0.88), and uncorrected urinary THF concentration gave a similar result (r = 0.86). Correction for creatinine in urine weakened the correlation (r = 0.56). For exposure at the TWA concentration of 200 ppm the extrapolated concentration of THF was 33 mumol/l in blood and 111.9 mumol/l (61 mumol/g creatinine) or 109 mumol/l at a specific gravity of 1.018 in urine. The correlation between exposure to THF and its concentration in exhaled breath and blood was low (r = 0.61 and 0.68 respectively). Laboratory methodological considerations together with the good correlation between urinary THF concentration and the environmental concentration suggest that THF concentration in urine is a useful biological indicator of occupational exposure to THF.     

Biological monitoring of occupational exposure to tetrahydrofuran.

Occupational exposure to tetrahydrofuran (THF) was studied by analysis of environmental air, blood, alveolar air, and urine from 58 workers in a video tape manufacturing plant. Head space gas chromatography (GC) with an FID detector was used for determination of THF concentration in alveolar air, urine, and blood. Environmental exposure to THF was measured by personal sampling with a carbon felt passive dosimeter. When the end of shift urinary THF concentrations were compared with environmental time weighted average (TWA) values, urinary THF concentration corrected for specific gravity correlated well with THF concentration in air (r = 0.88), and uncorrected urinary THF concentration gave a similar result (r = 0.86). Correction for creatinine in urine weakened the correlation (r = 0.56). For exposure at the TWA concentration of 200 ppm the extrapolated concentration of THF was 33 mumol/l in blood and 111.9 mumol/l (61 mumol/g creatinine) or 109 mumol/l at a specific gravity of 1.018 in urine. The correlation between exposure to THF and its concentration in exhaled breath and blood was low (r = 0.61 and 0.68 respectively). Laboratory methodological considerations together with the good correlation between urinary THF concentration and the environmental concentration suggest that THF concentration in urine is a useful biological indicator of occupational exposure to THF.     

Monitoring of exposure to cyclohexanone through the analysis of breath and urine.

Occupational exposure to cyclohexanone was studied for 59 workers through the analysis of environmental air, alveolar air, and urinary cyclohexanol. Environmental cyclohexanone exposure was measured by personal sampling with a carbon-felt passive dosimeter. Cyclohexanone in alveolar air and cyclohexanol in urine were determined with gas chromatography with a flame ionization detector. The end-of-shift urinary cyclohexanol levels correlated well with the time-weighted average environmental cyclohexanone values (r = 0.66). Urinary cyclohexanol corrected for creatinine correlated best with cyclohexanone in air (r = 0.77); when corrected for specific gravity, it gave a similar correlation coefficient (r = 0.73). When the time-weighted average of the exposure was 25 ppm, the corresponding calculated concentration for urinary cyclohexanol was 54.5 mg/1, 23.3 mg/g of creatinine, or 43.5 mg/l at a specific gravity of 1.018. The relationship between cyclohexanone exposure and its concentration in exhaled breath was found to be poorer than that for cyclohexanone exposure and the urinary metabolite (r = 0.51).     

Kinetics of styrene urinary metabolites: a study in a low-level occupational exposure setting in Singapore

Summary Biological monitoring of styrene exposure commonly involves measurement of styrene metabolites, mainly mandelic acid (MA) and phenylglyoxylic acid (PGA), in the urine of exposed subjects. Previous studies on the kinetics of styrene metabolites in urine were mostly conducted in a controlled environment on subjects exposed to high concentrations of styrene. In this study, we examined subjects exposed to low levels of styrene in a fiber-reinforced plastics (FRP) plant to see whether the excretion kinetics of styrene metabolites are similar under field conditions. Eight healthy Chinese male volunteers were exposed to styrene for 4 h with a mean environmental concentration of 11 ppm. Urine samples were collected continuously for 20 h after termination of the exposure and concentrations of urinary MA and PCA were determined. The results showed that MA was rapidly excreted in urine after the exposure, with a half-life of 2.1 h or 1.9 h when corrected with urine creatinine. The excretion of PGA followed that of MA and the half-life was 8.1 h or 5.1 h after correction with creatinine. The half-lives are considerably shorter compared to those in previous reports, suggesting that environmental factors, exposure conditions, or ethnic differences may affect the excretion kinetics of styrene metabolites. The fast excretion of styrene metabolites is also consistent with the observation that urine MA and PGA levels correlated better with the half-day time-weighted average (TWA) concentration of environmental styrene than with the whole-day TWA concentration. Our findings thus underscore the need for information on excretion kinetics in order to develop an appropriate biological monitoring scheme for specific exposure settings and subjects.     

Biological monitoring of occupational exposure to methyl ethyl ketone

Summary This study was conducted to evaluate the usefulness of three commonly used methods of biological monitoring for worker exposed to methyl ethyl ketone (MEK) under field conditions using blood, breath and urine. Environmental MEK exposures were measured by personal sampling with carbon-felt dosimeters. The correlation coefficient (r) between the time-weighted average (TWA) MEK concentration in air and the MEK concentration in blood collected at the end of the work shift was 0.85. The correlation coefficient between the TWA MEK level in air and the concentration exhaled in the breath of workers at the end of the work shift was 0.71. The end-of-shift urinary MEK excretion correlated best with the environmental concentration (r = 0.89). Correlations became lower after urine samples had been corrected for urinary creatinine (r = 0.83) or specific gravity (r = 0.73). After 8 h exposure to 200 ppm MEK, the corresponding end-of-shift urinary excretion was 5.11ol/l or 4.11 mg/g creatinine. This value is higher than that previously found in some studies, the difference probably being due to the physical acitivites of the present workers and their extensive skin contact with the solvent. The kinetics of inhaled MEK was also studied in eight subjects. Breath and urine samples were collected during the 8-h work shift on 2 consecutive Mondays. The results showed that urinary MEK excretion rose steadily until the end of exposure, whereas the MEK concentration in exhaled air varied markedly throughout the day. These findings suggest that the determination of MEK levels in end-of-shift urine samples appears to be the most reliable biological indicator of occupational exposure.     

Biological monitoring of styrene: a review

Recent literature about the biological monitoring of styrene-exposed workers is reviewed. Styrene primarily exhibits its toxicity on the central and peripheral nervous systems, although its mutagenicity and chromosome damaging ability also may be relevant. Uptake, transformation and excretion of styrene show that beside the usual biological indicators, such as urinary mandelic and phenylglyoxylic acids (main metabolites), other indicators also may be of interest. These include styrene in expired air, in blood or in urine. Moreover, intermediate or final metabolites such as styrene glycol or mandelic acid in blood also have been proven to be useful in the interpretation of individual values. The most widely used analytical methods for these indicators are gas or high performance liquid chromatography. Correlations between exposure and the different biological indicators mentioned above show that the most reliable indicators are mandelic acid (MA) in urine sampled at the end of the work shift (but not the first day of the week) and the sum of mandelic and phenylglyoxylic acids (MA + PGA) in urine sampled 16 hr after exposure (before the next shift). The biological exposure limit values corresponding to the threshold limit value-time-weighted average (TLV-TWA) of 50 ppm of styrene are 850 mg MA/g creatinine in the end-of-shift sample and 330 mg MA + PGA/g creatinine in the next-morning sample. Other biological indexes, such as styrene glycol (phenyl ethylene glycol) in blood or styrene in urine, look promising but require further research in field situations.     

Neuroendocrine effects of styrene on occupationally exposed workers

The serum levels of prolactin (PRL), human growth hormone (HGH), thyroid-stimulating hormone (TSH), and the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured in 30 females exposed to about 130 (range 65-300) ppm of styrene in the air and in 30 age-matched referents to show whether styrene exposure influences the dopaminergic tuberoinfundibular system (TIDA). The exposed subjects' serum levels of PRL were more than double the reference values and were significantly related to the urinary excretion of styrene metabolites, ie, to the sum of mandelic acid (MA) and phenylglyoxylic acid (PGA) in the "next-morning" urine spot sample. Such a relationship still proved to be statistically significant after the removal of the effects of age and duration of exposure with the method of partial correlation. The serum concentrations of HGH in the exposed workers were also higher than in the reference group. Though within the reference levels, the TSH values of the exposed subjects were significantly related to the urinary excretion of MA and PGA. These results are consistent with the dose-dependent depletion in tuberoinfundibular dopamine after experimental styrene exposure of rabbits.     

苯乙烯生物标志物的研究

目的 研究苯乙烯的生物标志物，为苯乙烯的生物监测提供理论依据。方法 采用高效液相色谱法对苯乙醇酸(MA)、苯乙醛酸(PGA)、苯乙烯巯基尿酸(MUA)进行监浏。结果 晨尿中MA、PGA、MUA和苯乙烯接触浓度间相关关系分别为y＝2．58x 70．82，y＝1．66. 37．42，y＝0．05x 0．555;班末尿中MA、PGA、MUA和苯乙烯接触浓度间相关关系分别为y＝1．85x 89．02，y=1．33x 4．32，y＝0．04x |0．68，均呈良好的相关性。结论 晨尿及班末尿中的MA、PGA、MUA测定均可作为苯乙烯的生物监测指标。     

Biological monitoring of styrene exposure and possible interference of acetone co-exposure

 The object of this study is the evaluation of some of the toxicokinetic effects of exposure to low concentrations of styrene, and the possible influence of simultaneous exposure to acetone. To this end we studied 19 workmen simultaneously exposed to both solvents. During a week of 4-h work shifts, the workmen underwent daily personal environmental monitoring and the collection of urine samples, at both the beginning and the end of the work period, for the determination of mandelic acid (MA) and phenylglyoxylic acid (PGA). The presence of the solvents in the atmosphere was evaluated using passive personal monitoring and gas chromatography. Average exposure to styrene and acetone were respectively 72.2 mg/m³ and 225.7 mg/m³. MA and PGA were quantified by high-performance liquid chromatography (HPLC). The daily urinary concentration averages, both at commencement and at the end of work shifts, of both the metabolites studied and of the sum of the two, were in statistically significant linear correlation with the average daily styrene exposure. Concentrations of MA and PGA in urine samples collected at the start of the work shift averaged 61.5 mg/g creatinine and 45.2 mg/g creatinine respectively, representing 41% and 72% of those at the end of the work shift which were 148.3 and 62.6 mg/g creatinine, respectively. With equal exposure to styrene, the average urinary concentrations of MA and PGA at both the beginning and end of the work shift increased significantly (P<0.001) during the working week. Moreover, we found that with equal exposure to styrene, urinary excretion of MA, PGA and MA+PGA at the end of the shift was inversely correlated with the intensity of acetone exposure (r=0.4659, 0.3410 and 0.4542 respectively, P<0.001). In conclusion, these results express slower urinary kinetics of styrene metabolites than is usually described in the literature, and favor a tendency to accumulate MA and PGA in the organism as a consequence of the retardation of urinary excretion kinetics. Acetone apparently represents one of the determining factors in this interference. Received: 3 July 1996/Accepted: 20 September 1996     

Application of a single-compartment model for estimation of styrene uptake from measurements of urinary excretion of mandelic and phenylglyoxylic acids after occupational exposure

In biological monitoring of styrene, the exposure is usually related to the urinary concentration of mandelic (MA) and/or phenylglyoxylic (PGA) acids in a urine sample taken after the workshift or on following morning. To study this relationship further, a single-compartment mathematical model was developed by which measured occupational repetitive uptake of styrene during a working day was related to measured excretion rates of the urinary metabolites. The model was used in practice to calculate the unknown uptake (dose) from MA and PGA excretion analyzed in urine samples. For comparison, a styrene limit dose was calculated from the exposure limit. Analytical results of samples from plastic boat builders were compared with the limit values.     

Exposure-effect and exposure-response relationships between occupational exposure to styrene and neuropsychological functions

A neuropsychological test battery was administered to 50 workers exposed to styrene and to 50 sex-, intelligence-, and age-matched controls. The main styrene metabolites, ie, mandelic acid (MA) and phenylglyoxylic acid (PGA), were measured as exposure indices in the urine collected on Saturday mornings, just before neuropsychological testing. Exposure-response and exposure-effect relationships were found between the intensity of the exposure (as reflected by the sum of MA and PGA) and the scores of the neuropsychological tests. Verbal learning skills were significantly impaired in workers with a sum of MA and PGA higher than 150 mmole/mole creatinine, corresponding to styrene airborne concentrations higher than 25 ppm (mean daily exposure). Logical memory and visuo-constructive abilities were shown to be significantly affected in workers with MA and PGA higher than 300 mmole/mole creatinine, corresponding to exposure levels of more than 50 ppm of styrene in air.     

Toxicokinetics of methyl tert-butyl ether (MTBE) and tert-amyl methyl ether (TAME) in humans, and implications to their biological monitoring

Healthy male volunteers were exposed via inhalation to gasoline oxygenates methyl tert-butyl ether (MTBE) or tert-amyl methyl ether (TAME). The 4-hr exposures were carried out in a dynamic chamber at 25 and 75 ppm for MTBE and at 15 and 50 ppm for TAME. The overall mean pulmonary retention of MTBE was 43 +/- 2.6%; the corresponding mean for TAME was 51 +/- 3.9%. Approximately 52% of the absorbed dose of MTBE was exhaled within 44 hr following the exposure; for TAME, the corresponding figure was 30%. MTBE and TAME in blood and exhaled air reached their highest concentrations at the end of exposure, whereas the concentrations of the metabolites tert-butanol (TBA) and tert-amyl alcohol (TAA) concentrations were highest 0.5-1 hr after the exposure and then declined slowly. Two consecutive half-times were observed for the disappearance of MTBE and TAME from blood and exhaled air. The half-times for MTBE in blood were about 1.7 and 3.8 hr and those for TAME 1.2 and 4.9 hr. For TAA, a single half-time of about 6 hr best described the disappearance from blood and exhaled air; for TBA, the disappearance was slow and seemed to follow zero-order kinetics for 24 hr. In urine, maximal concentrations of MTBE and TAME were observed toward the end of exposure or slightly (< or = 1 hr) after the exposure and showed half-times of about 4 hr and 8 hr, respectively. Urinary concentrations of TAA followed first-order kinetics with a half-time of about 8 hr, whereas the disappearance of TBA was slower and showed zero-order kinetics at concentrations above approx. 10 micro mol/L. Approximately 0.2% of the inhaled dose of MTBE and 0.1% of the dose of TAME was excreted unchanged in urine, whereas the urinary excretion of free TBA and TAA was 1.2% and 0.3% within 48 hr. The blood/air and oil/blood partition coefficients, determined in vitro, were 20 and 14 for MTBE and 20 and 37 for TAME. By intrapolation from the two experimental exposure concentrations, biomonitoring action limits corresponding to an 8-hr time-weighted average (TWA) exposure of 50 ppm was estimated to be 20 micro mol/L for post-shift urinary MTBE, 1 mu mol/L for exhaled air MTBE in a post-shift sample, and 30 micro mol/L for urinary TBA in a next-morning specimen. For TAME and TAA, concentrations corresponding to an 8-hr TWA exposure at 20 ppm were estimated to be 6 micro mol/L (TAME in post-shift urine), 0.2 micro mol/L (TAME in post-shift exhaled air), and 3 micro mol/L (TAA in next morning urine).     

Metabolic interferences in subjects occupationally exposed to binary styrene-acetone mixtures

Objective: To investigate the excretion of styrene metabolites (mandelic acid, MA, and phenylglyoxylic acid, PGA) in workers employed in plastic manufacturing to verify the possible influence of coexposure to acetone on styrene metabolism. Methods: This study was carried out on 50 workers employed in 3 factories producing polyester buttons. The workers were divided into three groups according to three different levels of acetone exposure. The trend of excretion for metabolites was examined during and after work shifts. Styrene and acetone were monitored on Thursday during the entire work shift by passive dosimeters placed on the lapel of the workers' uniforms, desorbed by carbon disulfide, and analyzed by gas chromatography. Biological monitoring was performed by determination of the urinary metabolites of styrene in urine samples collected on Thursday at the middle and the end of the work shift. MA and PGA were determined by a high-pressure liquid chromatographic method. Results: The styrene concentrations ranged between 16 and 439 mg/m³, and in ten samples they exceeded the TLV-TWA (213 mg/m³). The acetone concentration ranged between 15 and 700 mg/m³ (TLV-TWA 1780 mg/m³), with the mean value being 208 mg/m³. During cleaning operations higher exposures to acetone demonstrated, with concentrations ranging between 500 and 3400 mg/m³. The amounts of MA and PGA determined at the end of workshifts did not significantly differ between the groups with different levels of acetone coexposure. Analysis of variance (ANOVA) between the groups confirmed that MA and PGA excretion did not significantly differ, although the metabolite values measured on the “morning of the day after” appeared higher in those groups with high levels of acetone exposure and were related to the average airborne concentrations of the solvent. In addition, the range and degree of correlation between styrene in air and biological levels of metabolites were modified by coexposure to acetone. Conclusions: Our data demonstrate that amounts of MA and PGA did not differ in groups with different levels of acetone exposure, but when the acetone air concentration increased the degree of correlation between styrene and MA and PGA decreased. Furthermore, coexposure to acetone levels similar to those described herein may hamper the use of urinary metabolites for the assessment of exposure to styrene, especially on an individual basis. Received: 23 January 1998 / Accepted: 29 May 1998     

Albumin and hemoglobin adducts as biomarkers of exposure to styrene in fiberglass-reinforced-plastics workers

Objective: The purpose of this work was to compare levels of styrene-7,8-oxide (SO) adducts of albumin (Alb) and hemoglobin (Hb) with those of two urinary metabolites of styrene, mandelic acid (MA) and phenylglyoxylic acid (PGA), among workers exposed to styrene in the reinforced-plastics industry and in unexposed subjects. We also wished to determine whether cigarette smoking influenced adduct levels among these subjects. Methods: A group of 22 male workers was selected on basis of an expectedly high level of exposure to styrene, and a group of 15 controls was selected from hospital blood donors and hospital staff. In the exposed group, MA and PGA were quantified by high-performance liquid chromatography (HPLC) analysis of urine samples collected prior to the work shift. The SO adducts were cleaved from cysteine residues by reaction with Raney nickel to give 1-phenylethanol (1-PE) and 2-phenylethanol (2-PE), which, after derivatization, were measured using gas chromatography-mass spectrometry (GC-MS) in the negative-chemical-ionization (NCI) mode. Results: The estimated mean levels of MA and MA+PGA were 74 and 159 mg/g creatinine, respectively. Using the levels of urinary metabolites, an average styrene concentration of about 100 mg/m³ in the workplace air was estimated. The mean levels of 2-PE and 1-PE adducts in exposed workers were 2.84 and 0.60 nmol/g Alb and 5.44 and 0.43 nmol/g Hb, respectively. When subjects were stratified by level of urinary metabolites [zero (controls), low-level exposure (MA+PGA ≤159 mg/g creatinine), and high-level exposure (MA+PGA> 159 mg/g creatinine)] and smoking status (smokers versus nonsmokers), a difference in Alb adduct levels was found among the groups (2-PE P=0.002, 1-PE P=0.052). The difference in 2-PE-Alb levels was related to exposure category, to smoking status, and to their interaction. Correlations at or near a 0.05 level of significance were observed among the workers (n=22) between individual levels of SO-protein adducts and MA+PGA (2-PE Alb, r=0.54, 2-PE Hb, r=0.40). Conclusion: Our data suggest that only exposure to relatively high levels of styrene allows a clear relationship to be detected between styrene exposure and SO adducts, due in part to the effects of cigarette consumption and to the high background levels of these adducts observed in unexposed subjects. Received: 3 February 1997 / Accepted: 9 June 1997     

Exposure assessment for study of olfactory function in workers exposed to styrene in the reinforced-plastics industry

BACKGROUND: This study was undertaken in conjunction with an evaluation of the olfactory function of 52 persons exposed to styrene vapors to provide quantitative styrene exposure histories of each subject for use in the interpretation of the results of olfactory function testing. METHODS: Current and historic exposures were investigated. Historic exposures were reconstructed from employment records and measurements of styrene exposure made in the subject facilities over the last 15 years. Current exposures were estimated for every exposed subject though personal air sampling and through pre- and post-shift measurements of urinary metabolites of styrene. RESULTS: The study population had been employed in the reinforced-plastics industry for an average of 12.2 +/- 7.4 years. Their mean 8-hr time weighted average (TWA) respirator-corrected annual average styrene exposure was 12.6 +/- 10.4 ppm; mean cumulative exposure was 156 +/- 80 ppm-years. The current respirator-corrected 8-hr TWA average exposure was 15.1 +/- 12.0 ppm. The mean post-shift urinary mandelic and phenylglyoxylic acid (PGA) concentrations were 580 +/- 1,300 and 170 +/- 360 mg/g creatinine, respectively and were highly correlated with air concentrations of styrene. CONCLUSIONS: This quantitative exposure evaluation has provided a well-characterized population, with documented exposure histories stable over time and in the range suitable for the purposes of the associated study of olfactory function.     

Biological exposure limits estimated from relations between occupational styrene exposure during a workweek and excretion of mandelic and phenylglyoxylic acids in urine

Summary Styrene exposure of 18 workers in fiber-glass reinforced plastic industries was measured for 30-min periods throughout each workday for a week. The styrene uptake was estimated using pulmonary ventilation measurements. All urine voidings were collected separately and the styrene metabolites, mandelic acid (MA) and phenylglyoxylic acid (PGA) were determined. The relationship between both exposure and uptake versus excretion of these metabolites was studied. Styrene metabolite concentrations and excretion rates (with 95% tolerance limits) were calculated to correspond to a constant 8-h exposure at the Swedish exposure limit level (25 ppm) or an uptake of an exposure limit related styrene dose (6.3 mmol). The tightest tolerance limits were obtained for excretion rate of MA + PGA per 24 h. The calculated biological exposure limit was 3.4 (± 0.7) mmol MA + PGA/24 h for a dose of 6.3 mmol styrene.     

Biological monitoring of fluctuating occupational exposures to styrene

Nine workers occupationally exposed to styrene producing refrigerator lorries were analyzed. The styrene exposure was monitored 8 hours a day, for 5 days a week, for 1 week. We collected from workers a urine sample before and after each work shift. Moreover, alveolar air samples were obtained at the end of all work shifts. On Thursday afternoon and on Friday morning blood samples were taken from workers. The relationship between styrene exposure and biological data is reported and discussed. Alveolar, urinary and blood concentrations of styrene were comparable, suggesting similar kinetics. Biological styrene concentrations were significantly correlated with the mean daily environmental concentrations, but higher correlation coefficients were found with afternoon exposures. A narrow linear relationship between alveolar (Y) and urinary (X) styrene concentrations was found (Y = 0.359; r = 0.8579; n = 45; p less than 0.001). Urinary concentrations of mandelic acid (Y) confirmed a good relationship with the mean styrene exposure (X) (Y = 2.7 x +169; r = 0.4677 n = 45; p less than 0.01).     

Monitoring of occupational exposure to tetrachloroethene by analysis for unmetabolized tetrachloroethene in blood and urine in comparison with urinalysis for trichloroacetic acid

Objective: The present study was initiated to examine a quantitative relationship between tetrachloroethene (TETRA) in blood and urine with TETRA in air, and to compare TETRA in blood or urine with trichloroacetic acid (TCA) in urine as exposure markers. Methods: In total, 44 workers (exposed to TETRA during automated, continuous cloth-degreasing operations), and ten non-exposed subjects volunteered to participate in the study. The exposure to vapor was monitored by diffusive sampling. The amounts of TETRA and TCA in end-of-shift blood and urine samples were measured by either head-space gas chromatography (HS-GC) or automated methylation followed by HS-GC. The correlation was examined by regression analysis. Results: The maximum time-weighted average (TWA) concentration for TETRA-exposure was 46 ppm. Regression analysis for correlation of TETRA in blood, TETRA in urine and TCA in urine, with TETRA in air, showed that the coefficient was largest for the correlation between TETRA in air and TETRA in blood. The TETRA in blood, in urine and in air correlated mutually, whereas TCA in urine correlated more closely with TETRA in blood than with TETRA in urine. The TCA values determined by colorimetry and by the GC method were very similar. The biological marker levels at a hypothetical exposure of 25 ppm TETRA were substantially higher in the present study than were the levels reported in the literature. Possible reasons are discussed. Conclusions: Blood TETRA is the best marker of occupational exposure to TETRA, being superior to the traditional marker, urinary TCA. Received: 11 October 1999 / Accepted: 3 December 1999     

Effects on the kidney of occupational exposure to styrene

Objectives: To elucidate the extent of nephrotoxicity of long-term occupational exposure to styrene. Methods: In all 10 styrene-exposed workers (employed, mean age 12.6 years) and 15 nonexposed workers were studied. Each participant collected multiple overnight and end-of-shift urine samples. The sum of the urinary concentrations of mandelic acid and phenylglyoxylic acid (MAP) was determined to assess the absorbed dose of styrene. The urinary parameters alanine aminopeptidase (AAP), β-galactosidase (βGAL), N-acetyl-β-d-glucosaminidase (NAG), retinol-binding protein (RBP), and albumin (ALB) were determined to assess the effects on renal function and integrity. Results: The median concentration of MAP in urine was 175 mg/g urinary creatinine (CREAT-U; range 72–496 mg/g). The 8-h time-weighted average (8-h TWA) exposure to styrene was estimated from the urinary concentration of MAP and ranged from 21 to 405 mg/m³. RBP showed a borderline correlation with the dose of styrene. ALB in end-of-shift urine samples showed a borderline correlation with the absorbed dose of styrene. Conclusions: From the borderline correlation of RBP with the dose of styrene it was concluded that there might be a slight effect on the tubuli. The borderline correlation of ALB with the dose of styrene, together with the observation that five values were above the reference limit of the laboratory, suggests an effect on this parameter. Received: 10 March 1997 / Accepted: 9 June 1997