Evaluation of exposure to polycyclic aromatic hydrocarbons in a coke production and a graphite electrode manufacturing plant: assessment of urinary excretion of 1-hydroxypyrene as a biological indicator of exposure.

OBJECTIVES--Characterisation of the airborne concentration of 13 polycyclic aromatic hydrocarbons (PAHs) at various workplaces in a graphite electrode and a coke production plant. Validation of the urinary excretion of 1-hydroxypyrene (hydroxypyrene) as a biological marker of exposure to PAH. DESIGN--Cross sectional study of workers exposed to PAHs (106 in the graphite electrode producing plant and 16 in the coke works). METHODS--Personal air sampling during at least six hours per workshift using a glass fibre filter and a Chromosorb 102 solid sorbent tube and analysis of PAHs by high performance liquid chromatography (HPLC) and spectrofluorometric detection (SFD). Collection of spot urine samples before and after the shift and analysis of 1-hydroxypyrene by HPLC and SFD. RESULTS--The workers most exposed to PAHs were those occupied at the topside area of the coke oven plant and those working in the blending and impregnation areas of the graphite electrode producing plant (mean airborne concentration of total PAHs: 199 and 223 micrograms/m3 respectively). Except for naphthalene and perylene, the relative proportion of the different PAHs did not differ between the plants. Pyrene concentration in air was highly correlated with the total airborne PAH concentration (r = 0.83, p < 0.0001) and the correlation coefficients between hydroxypyrene concentration in postshift urine samples and pyrene or total PAHs in air were 0.67 (p < 0.0001) and 0.72 (p < 0.0001) respectively. Excretion of hydroxypyrene doubled when the exposure to pyrene in air increased 10-fold. The half life for the urinary excretion of hydroxypyrene was around 18 hours (95% confidence interval 16.1-19.8). Smoking habits only explained 2.3% of the variance in hydroxypyrene excretion compared with 45% for the pyrene concentration in air. CONCLUSION--The determination of the urinary excretion of hydroxypyrene in postshift urine samples can be used as a suitable biomarker to assess individual exposure to PAHs in coke ovens and in graphite electrode manufacturing plants.     

Evaluation of exposure to polycyclic aromatic hydrocarbons in a coke production and a graphite electrode manufacturing plant: assessment of urinary excretion of 1-hydroxypyrene as a biological indicator of exposure.

OBJECTIVES--Characterisation of the airborne concentration of 13 polycyclic aromatic hydrocarbons (PAHs) at various workplaces in a graphite electrode and a coke production plant. Validation of the urinary excretion of 1-hydroxypyrene (hydroxypyrene) as a biological marker of exposure to PAH. DESIGN--Cross sectional study of workers exposed to PAHs (106 in the graphite electrode producing plant and 16 in the coke works). METHODS--Personal air sampling during at least six hours per workshift using a glass fibre filter and a Chromosorb 102 solid sorbent tube and analysis of PAHs by high performance liquid chromatography (HPLC) and spectrofluorometric detection (SFD). Collection of spot urine samples before and after the shift and analysis of 1-hydroxypyrene by HPLC and SFD. RESULTS--The workers most exposed to PAHs were those occupied at the topside area of the coke oven plant and those working in the blending and impregnation areas of the graphite electrode producing plant (mean airborne concentration of total PAHs: 199 and 223 micrograms/m3 respectively). Except for naphthalene and perylene, the relative proportion of the different PAHs did not differ between the plants. Pyrene concentration in air was highly correlated with the total airborne PAH concentration (r = 0.83, p < 0.0001) and the correlation coefficients between hydroxypyrene concentration in postshift urine samples and pyrene or total PAHs in air were 0.67 (p < 0.0001) and 0.72 (p < 0.0001) respectively. Excretion of hydroxypyrene doubled when the exposure to pyrene in air increased 10-fold. The half life for the urinary excretion of hydroxypyrene was around 18 hours (95% confidence interval 16.1-19.8). Smoking habits only explained 2.3% of the variance in hydroxypyrene excretion compared with 45% for the pyrene concentration in air. CONCLUSION--The determination of the urinary excretion of hydroxypyrene in postshift urine samples can be used as a suitable biomarker to assess individual exposure to PAHs in coke ovens and in graphite electrode manufacturing plants.     

Urinary methylhippuric acid isomer levels after occupational exposure to a xylene mixture

Summary The quantitative relationship between exposure to xylene vapor and urinary excretion of methylhippuric acid (MHA) isomers were studied in the second half of a working week. The participants in the study were 121 male workers engaged in dip-coating of metal parts who were predominantly exposed to three xylene isomers. The intensity of exposure measured by diffusive sampling during an 8-h shift was such that the geometric mean vapor concentration was 3.8 ppm for xylenes (0.8 ppm for o-xylene, 2.1 ppm for m-xylene, and 0.9 ppm for p-xylene), 0.8 ppm for toluene, and 0.9 ppm for ethylbenzene. Urine samples were collected at the end of the shift and analyzed for metabolities by HPLC. The statistical analysis showed that there is a linear relationship between the intensity of exposure to xylenes and the concentration of MHA in urine, that the regression line passes very close to the origin, and that the increment in observed (i.e., noncorrected) MHA concentrations as a function of increasing xylene concentration was 17.8 mg × 1^–1 ppm^–1. Further examination on the basis on individual xylene isomers showed that the slopes of the regression lines for o- and m-isomers were similar (i.e., 17.1 and 16.6 mg l^–1 ppm^–1, respectively), whereas that for p-xylene was larger (21.3 mg l^–1 ppm^–1).     

Genotoxic risk assessment in white blood cells of occupationally exposed workers before and after alteration of the polycyclic aromatic hydrocarbon (PAH) profile in the production material: comparison with PAH air and urinary metabolite levels

Objective: Workers in various industries can be exposed to polycyclic aromatic hydrocarbons (PAHs). The relationship between biomarkers of genotoxic risk, PAH compounds in air (ambient monitoring) and PAH metabolites in urine (internal exposure) were studied in 17 workers exposed to PAHs in a fireproof-material producing plant before and 3 months after the PAH profile was altered in the binding pitch. Methods: Two biomarkers of exposure, specific DNA adducts of (±)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE) and non-specific DNA adduct of 8-oxo-7,8-dihydro-2-deoxyguanosine (8-oxodGuo) were determined in white blood cells (WBCs). In addition, DNA strand breaks were analysed in lymphocytes by single-cell gel electrophoresis in a genotoxic risk assessment. Sixteen PAH compounds in air were determined by personal air sampling, and hydroxylated metabolites of phenanthrene, pyrene and naphthalene were determined in urine. Results: After substitution of the binding pitch the concentrations of benzo[a]pyrene in air decreased (P<0.01). No changes could be observed for pyrene, while levels of phenanthrene (P=0.0013) and naphthalene (P=0.0346) in air increased. Consequently, median DNA adduct rates of anti-BPDE decreased after alteration of the production material (from 0.9 to <0.5 adducts/10⁸ nucleotides). No changes in the excretion of 1-hydroxypyrene in urine could be determined, whereas increased levels of 1-, 2+9-, 3- and 4-hydroxyphenanthrene (P<0.0001) and 1-naphthol and 2-naphthol (P=0.0072) were found in urine. In addition, a statistically significant increase in DNA strand break frequencies (P<0.01) and elevated 8-oxodGuo adduct levels (P=0.7819, not statistically significant) were found in the WBCs of exposed workers 3 months after the PAH profile in the binding pitch had been altered. Conclusion: The results presented here show that the increased concentration of naphthalene and/or phenanthrene in the air at the work place could induce the formation of DNA strand breaks and alkali-labile sites in WBCs of exposed workers.     

Urinary excretion of phenols as an indicator of occupational exposure in the coke-plant industry

Objective: In the present study the relationship between the level of exposure to o-cresol and of 2,4- +2,5-, 3,4-, and 3,5-xylenols and the urinary excretion of their metabolites was examined. The mixed exposure to phenolic derivatives of exposed workers during their work shift was monitored by personal air sampling of the breathing-zone air and by measurements of phenol, o-cresol, and xylenol isomer concentrations in shift-end urine. Methods: The study subjects were 76 men working at a coke plant who were 22–58 years old and 34 nonexposed subjects. Concentrations of phenolic compounds were determined in the breathing-zone air during the work shift, whereas concentrations of phenol, cresol, and xylenol isomers were measured in urine collected after the work shift. Concentrations of phenols in air and urine were determined by gas chromatography with flame-ionization detection. Urine samples were extracted after acid hydrolysis of glucuronides and sulfates by solid-phase extraction. The gas chromatography-mass spectrometry method was applied to identify metabolites in urine samples. Results: The time-weighted average concentrations of phenol, cresol, and xylenol isomers detected in breathing-zone air showed that the exposure level of the workers was relatively low. The geometric mean values were as follows: 0.26 mg/m³ for phenol, 0.09 mg/m³ for o-cresol, 0.13 mg/m³ for p- and m-cresol, and 0.02–0.04 mg/m³ for xylenols at the tar-distillation process. Corresponding urinary concentrations were 10.39, 0.53, and 0.25–0.88 mg/g creatinine for phenol, o-cresol, and xylenol isomers, respectively. The correlation coefficients between the o-cresol and 2,4-, 2,5-, 3,4-, and 3,5-xylenol concentrations measured in urine and in the breathing-zone air were statistically significant, varying in the range of 0.54–0.74 for xylenol isomers and being 0.69 for o-cresol. Conclusion: We have found that the presence of o-cresol and xylenol isomers in urine can be used as a biomarker for phenol exposure. Analysis performed on workers at the tar-distillation process showed that they were exposed to relatively low concentrations of phenolic compounds. Received: 15 October 1996 / Accepted: 5 May 1997     

Distribution of Volatile Organic Compounds in Ambient Air of Tehran

Transportation sources have created a major hydrocarbon pollution problem in the ambient air of Tehran. The authors used a Carbotrap tube to determine volatile organic compounds in air. Such compounds can be desorbed thermally and analyzed with gas chromatography-mass spectrometry. Samples were obtained from 8 sites in Tehran at which traffic flow varied between 500 and 2,500 vehicles/hr. A total of 54 hydrocarbons were identified in the ambient air of Tehran, and the average measured concentrations of benzene, toluene, m- and p-xylene, ethyl benzene, and o-xylene were 127.6 μg/m³, 201.1 μg/m³, 110.7 μg/m³, 58.1 μg/m³, and 57.6 μg/m³, respectively (standard deviation = 3.8–51.7 μg/m³). Emissions of individual pollutants in south Tehran exceeded those in north Tehran, and these emissions were higher during the afternoon than during the morning. The geographical parameters and the photochemical reaction also played important roles in the pollution conditions.     

Tumor markers in serum,polyamines and modified nucleosides in urine,and cytogenetic aberrations in lymphocytes of workers exposed to polycyclic aromatic hydrocarbons

Some polycyclic aromatic hydrocarbons (PAHs) such as benzo(a)pyrene and benzo(a)anthracene are well-established genotoxic agents. Long-term exposure to PAHs may lead to proliferative cell disorders in humans, predominantly in the skin, lung, and bladder. The concentration of several tumor markers in serum, of polyamines and modified nucleosides in urine, and of cytogenetic endpoints in peripheral lymphocytes (sister-chromatid exchanges, high frequency cells [HFC], and micronuclei) were measured in 149 male workers exposed to PAHs in two coke oven and one graphite electrode plants, and in 137 controls. We have assessed whether these biomarkers were related to several parameters reflecting exposure to PAHs, i.e., the sum of the airborne concentration of 13 PAHs, 1-hydroxypyrene (1-OHP) concentration in postshift urine, ben-zo(a)pyrene-diolepoxide adducts to hemoglobin (BPDE-Hb adducts), and duration of exposure, taking also into account several possible confounding factors. HFC was the biomarker most consistently associated with the intensity of current exposure to PAHs. Smoking exerts an independent effect on the same parameter. On the basis of the logistic regression between the prevalence of abnormal HFC values and PAHs in air and 1-OHP in postshift urine found in nonsmokers, it is suggested that the latter should be kept below 6.4 μg/m³ and 2.7 μg/g creatinine, respectively. No relationship was found between the cytogenetic effects and BPDE-Hb adducts although both parameters are statistically correlated with the airborne PAH level. Some tumor markers in serum (carcinoembryonic antigen, tissue polypeptide antigen, sialic acid) and the urinary concentration of some polyamines were correlated with either PAHs in air or 1-OHP in urine. The associations, however, were very weak which suggests that these biomarkers have limited practical value for the health surveillance of groups of workers exposed to genotoxic PAHs. © 1995 Wiley-Liss, Inc.     

occupational exposure to aromatic hydrocarbons at a coke plant: Part II. Exposure assessment of volatile organic compounds

The objective of the study is to assess the external and internal exposures to aromatic hydrocarbons in the tar and oil naphthalene distillation processes at a coke plant. 69 workers engaged as operators in tar and oil naphthalene distillation processes and 25 non-exposed subjects were examined. Personal analyses of the benzene, toluene, xylene isomers, ethylbenzene, naphthalene, indan, indene and acenaphthene in the breathing zone air allowed us to determine the time weighted average exposure levels to the aromatic hydrocarbons listed above. The internal exposure was investigated by measurement of the urinary excretion of naphthols, 2-methylphenol and dimethylphenol isomers by means of gas chromatography with a flame ionization detection (GC/FID). Urine metabolites were extracted after enzymatic hydrolysis by solid-phase extraction with styrene-divinylbenzene resin. The time-weighted average concentrations of the hydrocarbons detected in the breathing zone air shows that the exposure levels of the workers are relatively low in comparison to the exposure limits. Statistically significant differences between average concentrations of aromatic hydrocarbons (benzene, toluene, xylene isomers) determined at the workplaces in the tar distillation department have been found. Concentrations of the naphthalene and acenaphthene detected in workers from the oil distillation department are higher that those from the tar distillation department. Concentrations of naphthols, 2-methoxyphenol and dimethylphenol isomers in the urine of occupationally exposed workers were significantly higher than those of non-exposed subjects. Concentrations of the 2-methoxyphenol and dimethylphenol isomers in urine were significantly higher for the tar distillation workers, whereas concentrations of naphthols were higher for the oil naphthalene distillation workers. Operators at the tar and naphthalene oil distillation processes are simultaneously exposed to a mixture of different hydrocarbons, mainly benzene and naphthalene homologues.     

Relationship between blood antioxidants and occupational exposure to polycyclic aromatic hydrocarbons in coke oven workers

Background We investigated if blood Cu⁺⁺/Zn⁺⁺ superoxide dismutase, glutathione peroxidase, and catalase activities are increased and total plasma antioxidant concentration is decreased in coke oven workers exposed to polycyclic aromatic hydrocarbons. Methods Ninety-six coke oven workers participated in the study. Nonexposed workers (n = 105) were randomly sampled among power plant workers in the same age range. The examination included a questionnaire on health status, occupational history, smoking, and dietary habits. Blood samples completed the examination. Coke oven workers were classified into low-, middle-, and high-exposure groups based on the benzo[a]pyrene (B[a]P) air concentrations and were further classified into the categories “topside” and “non-topside,” according to their proximity to the ovens. Results Erythrocyte glutathione peroxidase activity increased with age (r = 0.18, P = 0.061) in power plant workers, whereas plasma glutathione peroxidase activity decreased with age (r = −0.18, P = 0.068) and erythrocyte glutathione peroxidase activity was inversely correlated with the number of cigarettes per day (r = −0.28, P = 0.08) in coke oven workers. Comparison of blood antioxidant enzyme activities and total plasma antioxidant concentration between coke oven and power plant workers showed that erythrocyte glutathione peroxidase activity was significantly lower in coke oven workers, even after adjustment for potential confounding factors. No differences were found either in other blood antioxidant enzyme activities or in total plasma antioxidant concentration between coke oven and power plant workers. Moreover, no trends toward decreased glutathione peroxidase activity among the three subgroups of B[a]P exposure were observed, and no differences either in blood antioxidant enzyme activities or in total plasma antioxidant concentration between the two groups of job categories were found. Conclusions Production of reactive oxygen species seems not to be increased in coke oven workers. Am. J. Ind. Med. 34:272–279, 1998. © 1998 Wiley-Liss, Inc.     

Urinary 1-naphthol and 1-pyrenol as indicators of exposure to coal tar products

Chemical exposure of assemblers handling creosote-impregnated wood and of a single worker chiselling coal tar pitch layer was assessed by measuring airborne naphthalene and various polycyclic aromatic hydrocarbons (PAHs), and by measurement of urinary excretion of 1-naphthol and 1-pyrenol. The sum concentration of PAHs and of 4–6 aromatic ring-containing PAHs were high, 440 g/m³ and 290 g/m³, respectively, when chiselling. In the assembler's workplace, the PAH concentrations were about 1/50 of this value. Regarding airborne naphthalene concentrations the situation was reversed (assemblers, 1000 g/m³; chiseller, 160 g/m³). Correspondingly, the assemblers' urinary 1-napthol concentrations were 15–20 times higher than those of the chiseller. The urinary 1-pyrenol concentration of the chiseller was 2–4 times higher than among the assemblers. As the estimated pyrene inhalation doses among the assemblers could account for only about 2%–25% of the 24-h pyrenol excretion in urine, the skin was presumably the main route of uptake. For an assessment of the exposure to PAHs, air measurements, monitoring of metabolites in urine and preferably also data on the composition of the skin-contaminating product are needed.     

Occupational exposure to polycyclic aromatic hydrocarbons in a graphite-electrode producing plant: biological monitoring of 1-hydroxypyrene and monohydroxylated metabolites of phenanthrene

 Objective. The objective of this study was to assess external and internal exposure to polycyclic aromatic hydrocarbons (PAHs) of workers who are employed in a graphite-electrode producing plant. Additionally we wanted to contribute to the question of biological limit values in order to reduce exposure to tolerable levels. Methods. At five different working places 12 stationary and 16 personal air measurements were carried out to determine the concentrations of phenanthrene, fluoranthene, pyrene, benz[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[a]pyrene and dibenz[a, h]anthracene in air. In addition, we investigated the excretion of 1-, 2+9-, 3- and 4-hydroxyphenanthrene and of 1-hydroxypyrene in the urine of 67 workers by a very sensitive and practical high-performance liquid chromatographic (HPLC) method with fluorescence detection; 2- and 9-hydroxyphenanthrene could not be separated with our analytical method. Results. During the production of graphite electrodes significantly higher PAH exposures were found in the baking and impregnation area than in the crushing, graphitisation and conditioning area. The results of personal air measurements (mean values of the sum of eight PAHs) are: 29.3 (baking), 23.4 (impregnation), 5.2 (crushing), 1.3 (graphitisation) and 0.4 μg/m³ (conditioning). Stationary air measurements yielded similar concentrations. Workers employed in the baking and impregnation areas excreted the highest amount of PAH metabolites in urine. The 1-hydroxypyrene concentrations (median) were: 23.4 (baking), 22.0 (impregnation), 9.6 (crushing), 1.8 (graph itisation) and 2.3 μg/g creatinine (conditioning). The corresponding concentrations of the sum of monohydroxylated phenanthrene metabolites (median) were: 23.1, 36.0, 10.4, 4.6 and 7.6 μg/g creatinine. Within the monohydroxylated phenanthrene metabolites 3-hydroxyphenanthrene predominates with a percentage of 43%. Our results showed that a benzo[a]pyrene concentration in air of 2 μg/m³ would lead to 1-hydroxypyrene concentrations in urine of 20–74 μg/g creatinine. That means that corresponding values in the literature which lie between 4.4 and 6.2 μg/g creatinine are due to other conditions of exposure and cannot be applied to graphite-electrode producing plants. Conclusions. Although to date there are no obligatory biological exposure limits for metabolites of PAHs in urine, it must be concluded that the internal PAH exposure is too high at some work places in this plant, as is generally the case in graphite-electrode producing plants. This is probably caused by skin absorption of PAHs. So for the prevention of health hazards by PAH, internal exposure must be measured using biological monitoring. Although it has not been possible to establish biological exposure limits for PAHs until now, we suggest a reduction in skin contact with these substances and thereafter use of the 90th percentile of the results of biological monitoring as “action levels” for corrective measures. Received: 20 May 1996/Accepted: 18 July 1996     

Airborne exposure to polycyclic aromatic hydrocarbons (PAHs) and urinary excretion of 1-hydroxypyrene of carbon anode plant workers

Workers in plants producing carbon anodes for aluminium electrolysis are exposed to PAHs containing coal tar pitch volatiles, pitch and coke. The aim of this study was to evaluate the suitability of urinary 1-hydroxypyrene to characterize respiratory exposure to PAH, which is most relevant for assessing individual health risks. Six workers in a carbon anode plant volunteered to take part in a personal air sampling and a biological monitoring programme lasting five consecutive 8-h shifts to determine occupational exposure to airborne PAHs and urinary excretion of 1-hydroxypyrene. Exposure to total PAH for all worksites varied from 3.99 to 120.6 μg PAH m⁻³ and for benzo(a)pyrene (BaP) from 0.17 to 4.88 μg BaP m⁻³. The concentration of 1-hydroxypyrene in post- and pre-shift urine samples was in the range (0.5–61.8 μmol 1-OHP per mol creatinine) and depended on the worksite. The Spearman rank correlation test showed a low but significant (P < 0.05) correlation of urinary 1-hydroxypyrene in the post- and pre-shift samples with respiratory pyrene exposure. The quantitative aspects of biological monitoring for the evaluation of respiratory PAH exposure were tested with a pharmacokinetic model. On the basis of individual pyrene exposure, excretion of urinary 1-hydroxypyrene during the working week was calculated for each worker. The results presented in this investigation indicate that biological monitoring of the pyrene metabolite 1-hydroxypyrene is a useful indicator of a general PAH exposure, but cannot replace personal air sampling for assessing the lung cancer risk of individuals.     

尿中萘及其代谢产物作为焦炉工生物监测指标的研究

目的　探讨尿中萘及其代谢产物作为焦炉工生物监测指标的可行性。方法　在某焦化厂随机选取 2 8名焦炉工人和 2 2名对照个体 ,统一收集工作周末班后 2h尿 ,并使用调查表收集一般情况。采用顶空固相微提取结合气相色谱 -质谱联机方法 ,同时测定尿中萘和芘的水平 ,采用酶水解结合气相色谱 -质谱联机方法 ,同时测定样品中 1-萘酚、 2 -萘酚和 1-羟基芘的水平。使用多元线性回归分析不同工种和吸烟量对尿中这 5种多环芳烃生物标志物浓度的影响。结果　尿中萘、 1-萘酚、 2 -萘酚和 1-羟基芘的浓度呈炉顶工 >炉侧和炉底工 >对照个体的趋势 ,其中尿中 1-萘酚和 1-羟基芘的水平受工种的影响大于2 -萘酚 ;不同暴露水平组中 ,吸烟个体尿中 1-萘酚、 2 -萘酚和 1-羟基芘的浓度均大于不吸烟者 ,但吸烟对 2 -萘酚的影响最大。结论　尿中 1-萘酚和 2 -萘酚浓度均能够有效地反映个体短期多环芳烃暴露的内剂量水平 ,可用于焦炉工的生物监测。     

Urinary carcinogenic 4–6 ring polycyclic aromatic hydrocarbons in coke oven workers and in subjects belonging to the general population: Role of occupational and environmental exposure

AimA new solid phase microextraction–gas chromatography–mass spectrometry method (SPME–GC–MS) to detect urinary unmetabolized 3-, 6-ring polycyclic aromatic hydrocarbons (PAHs) was applied to coke oven workers and general population subjects with the aim to assess exposure to carcinogenic PAHs, to evaluate the role of occupational and environmental variables on PAHs levels, and to compare present results with those previously obtained with a less sensitive method.MethodsA total of 104 coke oven workers (CW) from Poland [recruited in 2000 (CW-2000; n = 55) and 2006 (CW-2006; n = 49)], and 45 control subjects from the same area, provided urine spot samples for measurement of 10 PAHs (from phenanthrene to benzo[g,h,i]perylene). The comparison between the two methods was performed only on CW-2000 subjects. Information regarding personal characteristics and job variables was collected by a questionnaire.ResultsThe new method enables the quantification of 5-, 6-ring PAHs; precision and accuracy were in the 7.3–20.8% and 89.4–110% range, respectively; in CW-2000 samples results obtained with the new and the old method were highly correlated (Lin's concordance correlation coefficients: from 0.790 to 0.965); the mean difference between measured PAHS increased with the molecular weight of the analytes (from +5 to +27%). Urinary PAHs were above or equal to the quantification limit, depending on the compound, in 67–100% (min–max), 26–100% and 6–100% of samples from CW-2000, CW-2006 and controls, respectively. Chrysene and benz[a]anthracene were the most abundant carcinogenic PAHs with median levels of 43.4, 13.4, and 2.3 ng/L and 45.9, 14.9, and 0.7 ng/L in CW-2000, CW-2006, and controls, respectively, while benzo[a]pyrene levels were 6.5, 0.7 and <0.5 ng/L. The multiple linear regression model showed that the determinants of exposure were the use of wood and/or coke for house heating for controls, and job title or the plant for CW-2006.ConclusionsUrinary benzo[a]pyrene and other carcinogenic PAHs were, for the first time, quantified in urine samples from both occupationally and environmentally exposed subjects. These results show that urinary PAHs can discriminate exposure at different levels. Moreover, the simultaneous determination of several PAHs allows for the development of excretion profiles to assess exposure to specific compounds.     

Aromatic DNA adducts in white blood cells of coke workers

Summary White blood cell DNA adducts were measured in coke workers, local controls and countryside controls using the ³²P-postlabelling technique. The method detected aromatic adducts including those formed by polycyclic aromatic hydrocarbons (PAHs). Coke workers are heavily exposed to PAHs particularly when working at the batteries. A difference in adduct levels was noted between the coke workers at the battery as compared to other jobs. The adduct levels in the non-battery were higher than those in the countryside controls.     

Urinary elimination of nickel and cobalt in relation to airborne nickel and cobalt exposures in a battery plant

Objective To estimate the relationship between Ni concentrations in the ambient air and in the urine, at a battery plant using nickel hydroxide. Methods Workers occupationally exposed to a mixture of nickel hydroxide, metallic cobalt and cobalt oxyhydroxide dust were studied during two consecutive workdays. Air levels of Ni and Co in total dust were determined by personal sampling in the breathing zone. Both metals in air were sampled by Teflon binder filters and analyzed by inductively coupled plasma absorption emission spectrophotometry. Urine was collected from 16 workers immediately before and after the work shift. Urinary Ni and Co concentrations were measured by electrothermal atomic absorption spectrometry. Results A poor correlation was seen between Co in the air and in post-shift urine (r = 0.491; P < 0.01), and no correlation was found between Ni in the air and in post-shift urine (r = 0.272; P = 0.15), probably due to the use of respiratory protection. The subjects were exposed to higher levels of Ni than Co (Ni (mg/m³) = −0.02 + 7.41 Co (mg/m³), r = 0.979, P < 0.0001). Thus, exposure to Co at 0.1 mg/m³ should produce a Ni level of 0.7 mg/m³. According to section XIII of the German list of MAK and BAT Values, a relationship between exposure to Co and urinary Co excretion, Co (μg/l) = 600 Co (mg/m³), has been established and the relationship between soluble or insoluble Ni salts in the air and Ni in urine was as follows: Ni (μg/l) = 10 + 600 Ni (mg/m³) or Ni (μg/l) = 7.5 + 75 Ni (mg/m³). Assuming nickel hydroxide to be soluble and to be insoluble, the Ni concentrations corresponding to Ni exposure at 0.7 mg/m³ were calculated as 430 and 60 μg Ni/l, respectively. Similarly, exposure to Co at 0.1 mg/m³ should result in Co urinary concentrations of 60 μg Co/l. On the other hand, a good correlation was found between Co and Ni in post-shift urine (Ni (μg/l) = 9.9 + 0.343 Co (μg/l), r = 0.833, P < 0.0001). On the basis of this relationship, the corresponding value found in our study was 0.343 × 60 μg Co/l + 9.9 = 30.5 μg Ni/l. This value was close to that calculated by the equation for a group of insoluble compounds, but about 14 times lower than that calculated by the equation for a group of soluble compounds. Conclusions Our results suggest that exposure to nickel hydroxide yields lower urine nickel concentrations than the very soluble nickel salts, and that the grouping of nickel hydroxide might be reevaluated. Therefore, to evaluate conclusively the relationship between nickel hydroxide dust in the air and Ni in post-shift urine, further studies are necessary.     

DNA single strand breakage, DNA adducts, and sister chromatid exchange in lymphocytes and phenanthrene and pyrene metabolites in urine of coke oven workers.

OBJECTIVES: To investigate the specificity of biological monitoring variables (excretion of phenanthrene and pyrene metabolites in urine) and the usefulness of some biomarkers of effect (alkaline filter elution, 32P postlabelling assay, measurement of sister chromatid exchange) in workers exposed to polycyclic aromatic hydrocarbons (PAHs). METHODS: 29 coke oven workers and a standardised control group were investigated for frequencies of DNA single strand breakage, DNA protein cross links (alkaline filter elution assay), sister chromatid exchange, and DNA adducts (32P postlabelling assay) in lymphocytes. Phenanthrene and pyrene metabolites were measured in 24 hour urine samples. 19 different PAHs (including benzo(a)pyrene, pyrene, and phenanthrene) were measured at the workplace by personal air monitoring. The GSTT1 activity in erythrocytes and lymphocyte subpopulations in blood was also measured. RESULTS: Concentrations of phenanthrene, pyrene, and benzo(a)pyrene in air correlated well with the concentration of total PAHs in air; they could be used for comparisons of different workplaces if the emission compositions were known. The measurement of phenanthrene metabolites in urine proved to be a better biological monitoring variable than the measurement of 1-hydroxypyrene. Significantly more DNA strand breaks in lymphocytes of coke oven workers were found (alkaline filter elution assay); the DNA adduct rate was not significantly increased in workers, but correlated with exposure to PAHs in a semiquantitative manner. The number of sister chromatid exchanges was lower in coke oven workers but this was not significant; thus counting sister chromatid exchanges was not a good variable for biomonitoring of coke oven workers. Also, indications for immunotoxic influences (changes in lymphocyte subpopulations) were found. CONCLUSIONS: The measurement of phenanthrene metabolites in urine seems to be a better biological monitoring variable for exposure to PAHs than measurement of hydroxypyrene. The alkaline filter elution assay proved to be the most sensitive biomarker for genotoxic damage, whereas the postlabelling assay was the only one with some specificity for DNA alterations caused by known compounds.     

Exposure to diesel engine exhausts and increase of urinary 8-hydroxy-2′-deoxyguanosine among Male tank maintenance workers in the Republic of Korea Army

This study was conducted to evaluate the exposure of diesel engine exhaust (DEE) and oxidative stress among tank maintenance workers in the Republic of Korea Army. Airborne concentrations of elemental carbon (EC), polycyclic aromatic hydrocarbons (PAHs), and metals were measured at two units. Urine analysis for 1-hydroxypyrene and 8-hydroxy-2′-deoxyguanosine (8-OHdG) was performed for tank maintenance workers from one unit (n=17). To compare the level of 8-OHdG, the analysis was performed in 17 unexposed controls. The airborne EC concentration was 8.6–24.3 µg/m³ in indoor unit. EC was not detected in the outdoor unit. As for the PAHs, trace −0.0004 mg/m³ of naphthalene was detected. I_TWA for 26 metals was calculated to be 0.009–0.027. The geometric mean urinary 1-hydroxypyrene was 0.08 µg/g creatinine. The geometric mean of 8-OHdG was 1.04 µg/g for the maintenance workers, while 0.45 µg/g for controls. The level of urinary 8-OHdG was significantly higher among maintenance workers in multivariate analysis. In conclusion, tank maintenance workers are exposed to various by-products from diesel engine combustion during work, and their level of oxidative stress marker was increased. Countermeasures for reducing hazardous substances in the military workplace are necessary.     

Humoral immunosuppression in men exposed to polycyclic aromatic hydrocarbons and related carcinogens in polluted environments.

We evaluated humoral immunity by measuring IgG, IgA, IgM, and IgE concentrations in 274 male workers in an iron foundry in Cracow, Poland. There were two groups: 199 coke oven workers and 76 cold-rolling mill workers. The groups were similar with respect to age, length of work (average 15 years), and smoking habits. Exposure to polycyclic aromatic hydrocarbons (PAHs), assessed by personal and area monitoring, ranged from 0.2 to 50 micrograms/m3 benzo[a]pyrene in coke plant workers and was of 3-5 magnitudes higher than in the cold-rolling mill employees. Comparison of the two groups revealed a marked depression of mean serum IgG and IgA in coke oven workers (p < 0.001, Student's unpaired t-test). In the same subjects, serum IgM had a tendency to decrease, whereas serum IgE showed a trend toward higher values. Thus, workers exposed chronically to complex mixtures of air pollutants, composed primarily of PAHs, develop immunosuppression. It remains to be established whether the immunosuppression described here is related to the frequent development of lung cancer reported in coke plant employees. Workers exposed chronically to PAHs should have serum immunoglobulins monitored regularly.     

Possible preferential metabolism of xylene isomers following occupational exposure to mixed xylenes

Objectives: Solvent exposures commonly involve mixtures of substances or mixtures of isomers of a single solvent. These may be metabolised through common pathways, resulting in the potential for metabolic interactions. These may then lead to accumulation of solvent or metabolic intermediates, some of which may be toxic. This paper describes a pilot study conducted to determine the correlation between airborne xylene isomers and the appearance of methylhippuric acid (MHA) isomers in urine of workers exposed mainly to xylene. The project also aimed to determine whether there is preferential metabolism of any isomer by comparison of the ratios of airborne isomers with the ratios of metabolite isomers appearing in urine. Subjects and methods: A total of 12 workers (11 male, 1 female) were recruited into this study, with 2 of the participants providing samples on more than one occasion. Workers included flooring contractors (5), printers (2), chemical manufacturers (2), histology technicians (2) and one householder using a xylene-based varnish. Subjects were aged between 24 and 48 years (37.6 ± 2.0 years; mean ± SEM). After giving informed consent, workers provided a prework and postwork urine sample on a midweek work day. Samples were stored frozen prior to analysis. Breathing-zone air samples were collected using personal air samplers at 50 ml/min. Solvents were trapped on activated-charcoal sampling tubes. Subjects wore pumps for 18–304 (178 ± 24) min on the same day on which urine samples were collected. Results: Xylene exposures ranged from 1.6 to over 7000 ppm. In all, 7 of 16 measurements exceeded the Australian TWA standard of 80 ppm. Two of the flooring contractors wore respiratory protective equipment (RPE) and the two histopathology technicians used workplace ventilation systems. Total urinary MHA output ranged from 10 to 8000 mmol/mol creatinine, with 6 of 16 samples exceeding the modified biological exposure index of 702 mmol/mol. Correlations between airborne concentrations of individual xylene isomers and their corresponding MHA isomers were poor but improved when workers using RPE were excluded from the analysis. Gradients of the regression lines (millimoles of MHA per mole of creatinine per parts per million of xylene) were 3.2 for o-isomers, 7.0 for p-isomers, and 14.4 for m-isomers. Comparisons of isomer ratios of xylene in air were made with the corresponding ratio of MHA isomers in urine. These revealed higher ratios of m-MHA to other MHA isomers than those of m-xylene to the other xylene isomers. The MHA isomer ratios were expected to be the same as the airborne xylene isomer ratios if there were no preferential elimination of any isomer. m-MHA appeared in urine in a greater proportion than would be predicted from the proportion of m-xylene detected in air. The time course of the appearance of MHA isomers in urine also suggests that interactions were taking place, with m-MHA appearing in high proportion in urine following several days of repeated heavy xylene exposure. On a single moderate exposure, m-MHA appeared initially in high proportion in the first few hours but was undetectable in urine after 18 h. p-MHA was detectable for up to 6 h after exposure, and o-MHA remained detectable after 18 h. Conclusions: This study suggests that excretion of m-MHA in urine is favoured over that of the other isomers following exposure to mixed xylenes. This is independent of airborne xylene isomer composition and suggests that the metabolism of m-xylene occurs preferentially to that of the other isomers. It is not clear at which step in the metabolism of xylene this preference occurs, although other work indicates that the initial oxidation of xylene to methylbenzyl alcohol by cytochrome P450 2E1 occurs at the same rate for each isomer. These findings suggest that there is potential for metabolic interactions between xylene isomers and that these may be the basis for xylene toxicity. Received: 11 May 1998 / Accepted: 15 October 1998