Urinary 1-hydroxypyrene and polycyclic aromatic hydrocarbon exposure among asphalt paving workers

OBJECTIVES: Using urinary 1-hydroxypyrene (1-OHP) as a measure of total absorbed dose, the primary objective of this study was to evaluate the total effect of inhalation and dermal PAH exposures while considering other factors such as age, body mass index and smoking that may also have a significant effect on urinary 1-OHP. METHODS: The study population included two groups of highway construction workers: 20 paving workers and 6 milling workers. During multiple consecutive workshifts, personal air and dermal samples were collected from each worker and analyzed for pyrene. During the same work week, urine samples were collected pre-shift, post-shift and at bedtime each day and analyzed for 1-OHP. Distributed lag models were used to evaluate the independent effect of inhalation and dermal exposures that occurred at each of several preceding exposure periods and were used to identify the relevant period of influence for each pathway. RESULTS: The paving workers had inhalation (mean 0.3 micro g/m(3)) and dermal (5.7 ng/cm(2)) exposures to pyrene that were significantly higher than the milling workers. At pre-shift on Monday morning, following a weekend away from work, the pavers and millers had the same mean baseline urinary 1-OHP level of 0.4 micro g/g creatinine. The mean urinary 1-OHP levels among pavers increased significantly from pre-shift to post-shift during each work day, while the mean urinary 1-OHP levels among millers varied little and remained near the baseline level throughout the study period. Among pavers there was a clear increase in the pre-shift data during the work week, such that the average pre-shift level on day 4 (1.4 micro g/g creatinine) was 3.5 times higher than the average pre-shift results on day 1 (0.4 micro g/g creatinine). The results of the distributed lag model indicated that the impact of dermal exposure was approximately eight times the impact of inhalation exposure. Furthermore, dermal exposure that occurred during the preceding 32 h had a statistically significant effect on urinary 1-OHP, while the effect of inhalation exposure was not significant. CONCLUSIONS: We found that distributed lag models are a valuable tool for analyzing longitudinal biomarker data and our results indicate that dermal contact is the primary route of exposure to PAHs among asphalt paving workers. An exposure assessment of PAHs that does not consider dermal exposure may considerably underestimate cumulative exposure and control strategies aimed at reducing occupational exposure to asphalt-related PAHs should include an effort to reduce dermal exposure.     

Urinary 1-hydroxypyrene as a biomarker of polycyclic aromatic hydrocarbons exposure of workers on a contaminated site: influence of exposure conditions

The aim of the study was to determine the exposure levels of workers to polycyclic aromatic hydrocarbons on gasworks sites by the measurement of urinary 1-hydroxypyrene. Start-shift and end-shift urine samples were taken every day during an entire week (Monday to Friday), once in November and a second time in June. Four groups of workers were selected according to their activity. Increased exposure was only found among volunteers involved in the remediation of a site, 0.16 to 2.31 mumol/mol creatinine in non-smokers. The median of the non-smoker referent group was 0.02 mumol/mol creatinine (95% confidence interval, 0.01 to 0.04). Smokers had greater exposure levels than non-smokers in every group. Within and between variability was around 200%. Assessment of the exposure of persons on contaminated soil is possible, with the condition that the exposed subjects come in direct contact with the soil.     

Urinary 1-hydroxypyrene as a biomarker of internal dose of polycyclic aromatic hydrocarbons in carbon black workers

In this study, a total of 30 workers were selected, including eight wet pelletizing workers and 22 packaging workers. For all selected workers, urine samples were collected on the first day pre-shift, first day post-shift and fifth day post-shift, and their urinary 1-hydroxylpyrene levels (1-OHP) were determined (denoted as BM1pre, BM1post and BM5post, respectively). Personal respiratory exposures, including both inhalable particle-bound PAHs (Cinh) and gaseous PAHs (Cgas), together with dermal exposure to particle-bound PAHs (Cskin) were measured. Personal background information, including age, sex and smoking habit, was carefully registered. Pyrene exposure was statistically significantly correlated with exposure to PAHs and carcinogenic PAHs. Multiple linear regression analysis results showed that the BM1post values could not be explained by workers' exposures. For BM5post in packaging workers, both the regression model (R2 = 0.73) and the regression coefficients for Cgas, Cinh and Cskin were statistically significant (P < 0.05). For pelletizing workers, the R2 value was higher but was not statistically significant because of the smaller number of workers. The resultant regression coefficients for 'sex', 'smoking habit' and 'age' were statistically insignificant (P > 0.05), which could be because these variables made relatively small contributions to BM5post. In conclusion, this study suggests BM5post could be a suitable indicator for PAH exposures of carbon black workers, on the condition that both respiratory (including gaseous PAHs and particle-bound PAHs) and dermal exposures have been assessed.     

Urinary 1-hydroxypyrene as a comprehensive carcinogenic biomarker of exposure to polycyclic aromatic hydrocarbons: a cross-sectional study of coke oven workers in China

Purpose

Polycyclic aromatic hydrocarbons (PAHs) are multiple compounds that include many carcinogens. We conducted a cross-sectional study in steel plant workers in Anshan, China, to identify biomarkers that reflect the carcinogenicity of PAHs.

Methods

Subjects were 57 workers and 20 controls. Level of personal exposure to PAHs was measured using GC–MS. In accordance with the assessment methods defined by the United States Environmental Protection Agency (US EPA), 15 PAHs were selected for the analysis. For the measurement of urinary metabolites, urine samples were treated with β-glucuronidase and analyzed using HPLC with a fluorescence detector.

Results

The mean range of personal exposure to 15 PAHs (total PAHs) was 178.85, 47.08–1,329.45 (geometric mean, 5th and 95th percentile) μg/m³. Ten known urinary metabolites (1-hydroxynaphthalene, 2-hydroxynaphthalene, 2-hydroxyfluorene, 1-hydroxyphenanthrene, 3-hydroxyphenanthrene, 9-hydroxyphenanthrene, 1-hydroxypyrene, 3-hydroxybenz[a]anthracene, 6-hydroxychrysene, and 3-hydroxybenzo[a]pyrene) and four unknown peaks were detected. The highest correlation was between total PAHs and urinary 2-hydroxynaphthalene (Spearman r = 0.716, P < 0.01). Among the detected urinary metabolites, 2-hydroxyfluorene, 1-hydroxyphenanthrene, 3-hydroxyphenanthrene, and 1-hydroxypyrene were found to correlate significantly with the “Σ carcinogenic potency of PAHs” (sum of seven carcinogenic PAHs calculated from the levels of personal PAHs and relative potency factors), and with the greatest correlation found for 1-hydroxypyrene (Spearman r = 0.630, P < 0.01).

Conclusions

The analysis of personal exposure to 15 PAHs and 10 urinary metabolites, and calculation of Σ carcinogenic potency, indicated that urinary 1-hydroxypyrene was the most comprehensive carcinogenic biomarker of exposure to PAHs.     

尿中1-羟基芘作为焦炉工多环芳烃暴露生物监测指标的研究

目的探讨焦炉工外暴露等级与尿中1-羟基芘(1-OHPy)浓度的关系。方法以某焦化厂120名生产工人和30名非接触者为研究对象,收集班后6h尿,并收集个人信息,用高效液相法测定尿中1-羟基芘。结果尿中1-羟基芘浓度呈炉顶>炉侧>炉底>对照组的趋势。与外暴露呈显著相关性(r=0.653,P<0.01),同样外暴露条件下,吸烟者尿中1-羟基芘显著高于未吸烟者(P<0.05)。结论焦炉工尿中1-羟基芘水平与外暴露等级存在明显的相关性,可反映多环芳烃暴露个体的内剂量水平。     

职业多环芳烃暴露人群尿中生物标志物浓度水平

多环芳烃类化学物质因为其被熟知的致癌性而一直备受关注, 近来越来越多的学者意识到单一的接触生物标志物并不能完全代表暴露者体内的暴露水平。本研究就1999年以后15年间报道的职业环境中接触多环芳烃类物质的工人尿中接触生物标志物进行综述, 重点对其浓度水平进行描述, 为职业环境中多环芳烃类化学物质暴露的生物学检测提供理论依据。     

Exposure to polycyclic aromatic hydrocarbons in coal liquefaction workers: impact of a workwear policy on excretion of urinary 1-hydroxypyrene.

OBJECTIVE--This study was undertaken to assess whether contaminated personal clothing worn beneath a coverall (normal workwear) is a source of potentially significant dermal exposure to polycyclic aromatic hydrocarbons (PAHs) in coal liquefaction workers. METHODS--An intervention study was conducted over a two week period involving 10 workers that reflected the range of activities performed at the factory. A cross over design was used to examine the influence of normal workwear (personal clothing worn beneath a coverall) and intervention workwear (new coverall, shirt, trousers, underwear, socks, and boots) upon excretion of urinary 1-hydroxypyrene (1-OHP) and skin pad deposition of pyrene. RESULTS--The impact of intervention was noted in three ways: (1) A notable reduction (55%) in the mass of 1-OHP excreted on the first day of the intervention phase was found. The median reduction in mass excreted (22.7 nmol) was significant from zero at the 5% level; (95% confidence interval (95% CI) 9.5-40.8 nmol). (2) A notable reduction (82%) in skin pad deposition of pyrene on the first day of the intervention phase was found. The median reduction of 13.20 ng.cm-2 was significant from zero at the 5% level; (95% CI 7.3-26.4 ng.cm-2). (3) About a 50% reduction in 1-OHP concentration over the working week occurred during the intervention phase; an increase of 2.07 mumol/mol creatinine was found from the start to the end of the work period during the intervention phase compared with an increase of 4.06 mumol/mol creatinine during the normal phase. This reduction was not significant at the 5% level. CONCLUSION--The results indicate that on the first day of the working week investigated, significant reductions in absorbtion (as measured by excretion of urinary 1-OHP) and deposition of PAHs (as measured by skin pad deposition of pyrene) can be effected by improvements in workwear policy. The impact of the improved workwear regimen was also detected by reduction in spot urinary 1-OHP concentrations, although this effect was less pronounced. One implication of the findings is that exposure to PAHs may arise from workers' own contaminated personal clothing. As a consequence of this study an improved workwear policy has been implemented at the factory.     

Benchmark guideline for urinary 1-hydroxypyrene as biomarker of occupational exposure to polycyclic aromatic hydrocarbons

Many individual polycyclic aromatic hydrocarbons (PAH) are genotoxic carcinogens. One of the parent PAH, pyrene, undergoes simple metabolism to 1-hydroxypyrene. 1-Hydroxypyrene and its glucuronide are excreted in urine. Biological monitoring of exposure to PAH has rapidly been expanded since urinary 1-hydroxypyrene was suggested as a biological index of dose of pyrene. Since pyrene is always present in PAH mixtures, the biological indicator is not only an indicator of uptake of pyrene, but also an indirect indicator of all PAH. At present, several hundreds of papers reporting on urinary concentrations of 1-hydroxypyrene in workers' urine are available. It appeared that urinary 1-hydroxypyrene is a sound biomarker and that the analytical method is robust and non-laborious. Since epidemiological studies of cancer mortality related to long-term average urinary 1-hydroxypyrene concentration are lacking, a sound health-based limit value of 1-hydroxypyrene in urine cannot be set as yet. Since PAH exposure is widespread and the dermal uptake is substantial among exposed workers, an attempt was made to propose a three-level benchmark guideline for urinary 1-hydroxypyrene. The reference value as a 95th percentile in non-occupational exposed controls is 0.24 micromol mol(-1) creatinine and 0.76 micromol mol(-1) creatinine for non-smokers and smokers, respectively. This is the first level of the benchmark guideline. A no-biological-effect-level of 1-hydroxypyrene in urine of exposed workers was found at 1.4 micromol mol(-1) creatinine. It is the lowest reported level at which no genotoxic effects were found and therefore the estimate for the second level of the benchmark guideline. In two types of industry, coke ovens and primary aluminium production, the regression of airborne PAH concentrations and urinary 1-hydroxypyrene concentrations in exposed workers has been studied. The correlation of airborne concentrations and urinary 1-hydroxypyrene in urine of workers from coke ovens and in the primary aluminium industry was used to estimate the level of urinary 1-hydroxypyrene equal to the present occupational exposure limit (OEL) of PAH. The concentration of 1-hydroxypyrene in urine equal to the OEL is 2.3 micromol mol(-1) creatinine and 4.9 micromol mol(-1) creatinine, respectively, in these two industries. These latter values present the third level of the benchmark guideline.     

核仁区嗜银蛋白作为多环芳烃暴露效应标志的研究

目的研究焦炉工人外周血T淋巴细胞核仁区嗜银蛋白(AgNOR)是否可作为多环芳烃暴露的效应标志。方法选取52名焦化厂职工(按焦炉逸散物暴露水平分为高、中、低暴露组)和10名非职业多环芳烃暴露人员(对照组)作为研究对象。采集外周血,经培养、制片、银染,用核仁银染面积/细胞核面积(I/S)衡量T淋巴细胞AgNOR相对含量;同时检测尿1羟基芘的水平,作为接触多环芳烃的内暴露标志。结果高、中、低暴露组和对照组工人尿1羟基芘的平均浓度分别为(16.56±2.77)、(7.17±3.05)、(3.30±2.77)和(3.04±1.58)μmol/mol肌酐,高暴露组与低暴露组和对照组比较,差异有统计学意义;高、中、低暴露组和对照组工人T淋巴细胞AgNOR的I/S值分别为0.056±0.010、0.065±0.013、0.067±0.008和0.076±0.007,高暴露组与其他3组比较以及中、低暴露组与对照组比较,差异均有统计学意义。结论职业多环芳烃暴露可导致尿1羟基芘水平上升和外周血T淋巴细胞AgNOR相对含量下降,提示多环芳烃暴露可损伤T细胞免疫功能,AgNOR有可能作为多环芳烃暴露的效应标志。     

Urinary 1-hydroxypyrene as a biomarker of PAH exposure in 3-year-old Ukrainian children

Urinary 1-hydroxypyrene (1-OHP) is a biomarker of polycyclic aromatic hydrocarbon (PAH) exposure. We measured urinary 1-OHP in 48 children 3 years of age in Mariupol, Ukraine, who lived near a steel mill and coking facility and compared these with 1-OHP concentrations measured in 42 children of the same age living in the capital city of Kiev, Ukraine. Children living in Mariupol had significantly higher urinary 1-OHP and creatinine-adjusted urinary 1-OHP than did children living in Kiev (adjusted: 0.69 vs. 0.34 micromol/mol creatinine, p < 0.001; unadjusted: 0.42 vs. 0.30 ng/mL, p = 0.002). Combined, children in both cities exposed to environmental tobacco smoke in their homes had higher 1-OHP than did children not exposed (0.61 vs. 0.42 micromol/mol creatinine; p = 0.04; p = 0.07 after adjusting for city). In addition, no significant differences were seen with sex of the children. Our sample of children in Mariupol has the highest reported mean urinary 1-OHP concentrations in children studied to date, most likely due to their proximity to a large industrial point source of PAHs.     

Elimination of 1-hydroxypyrene after human volunteer exposure to polycyclic aromatic hydrocarbons

The aim of this study was to estimate the kinetics of 1-hydroxypyrene (1-HP) elimination after inhalation exposure to polycyclic aromatic hydrocarbons (PAHs). Samples of inhaled and exhaled air were collected on glass fiber filters backed with tubes filled with Amberlit XAD-2 resin. The filters were extracted by cyclohexane and Amberlit – by acetonitrile. Extracts for the determination of pyrene and benzo[a]pyrene (B[a]P) concentrations were analyzed by high-performance liquid chromatography (HPLC). 1-Hydroxypyrene in urine was determined after its preconcentration on a C-18 column (solid phase extraction method) using the same analytical technique. Five male volunteers were exposed for 6 h (two times, with a 1-month interval) to a PAH mixture at an aluminium plant. The volunteers were breathing at rest through facial mask equipped with a 1000-ml compensation container which allows collection of the exhaled air. Inhaled air samples were collected in the breathing zone of each volunteer. Urine samples were collected until the 71st hour after the onset of exposure. The average respiratory retention of pyrene was found to be 61%. The 1-HP elimination process could be described by one-compartment model with the half-live of 9.8 hour (95% CI 7.9–11.7 h). The simulation of 1-HP elimination in urine during a working week (4 days) indicates that the balance between absorption and elimination is achieved at the end of the second day. Received: 29 July 1996 / Accepted: 21 February 1997     

Urinary 1-hydroxypyrene levels in offshore workers

Objectives  

To compare differences in pre- and post-shift urinary 1-hydroxypyrene (1OHP) levels as a measure of internal dose of polycyclic aromatic hydrocarbons (PAHs) between two groups of oil production workers offshore assumed to be exposed to PAH, and to compare the exposed group to an unexposed control group.     

Leukocyte 8-hydroxydeoxyguanosine and aromatic DNA adduct in coke-oven workers with polycyclic aromatic hydrocarbon exposure

Objective To investigate the potential for exposure to polycyclic aromatic hydrocarbons (PAHs) to induce oxidative DNA damage, we conducted a cross-sectional study in coke-oven workers employed at an iron–steel factory.Methods The study population contained 119 coke-oven workers from different work areas of the oven and 38 controls. Personal information on age, employment duration, smoking habit and alcohol consumption was obtained at an interview. Leukocyte 8-hydroxydeoxyguanosine (8-OHdG) was measured by high performance liquid chromatography with electrochemical detection. Leukocyte aromatic DNA adducts as effective dose, and urinary 1-hydroxypyren as internal dose, were also measured, and used to analyze the relationship of 8-OHdG with other biomarkers for PAH exposure, tobacco smoke and alcohol consumption.Results The leukocyte 8-OHdG revealed a wide inter-individual variation. The highest 8-OHdG level was detected in bottom-workers of the coke-oven. There were significant differences among the four different work areas (P=0.02). We could not find significant correlation between 8-OHdG levels and urinary 1-hydroxypyrene, but a weakly positive correlation was found between 8-OHdG and leukocyte aromatic DNA adducts among all subjects (r=0.19 P=0.03). We could not observe any effect of smoking and alcohol drinking on 8-OHdG production.Conclusion We could not find clear evidence that PAH exposure induces oxidative DNA damage.     

Associations between exposure to polycyclic aromatic hydrocarbons and temporal change of urinary 1-hydroxypyrene levels in Taiwanese coke-oven workers

OBJECTIVES: Our aim is to analyze the association between polycyclic aromatic hydrocarbon (PAH) exposure and the temporal change of urinary 1-hydroxypyrene (1-OHP). METHODS: Two personal air samples, eight spot urine samples, and questionnaires were used to collect PAH exposure, urinary 1-OHP, demographic data, and environmental pollutants. RESULTS: Topside-oven workers had significantly higher levels of PAH exposure and 1-OHP than side-oven workers. Urinary 1-OHP was a biomarker for PAH exposure. In topside-oven workers, the trend of 1-OHP increased sharply and reached the top in the sixth day after work and declined dramatically on days off. In side-oven workers, such a trend was not found, and those who smoked showed a slight increase in urinary 1-OHP levels on days off. CONCLUSIONS: We suggest that the pattern of temporal change of urinary 1-OHP levels is different between topside-oven and side-oven workers.     

Exposure of iron foundry workers to polycyclic aromatic hydrocarbons: benzo(a)pyrene-albumin adducts and 1-hydroxypyrene as biomarkers for exposure.

Exposure to polycyclic aromatic hydrocarbons (PAHs) in foundry workers has been evaluated by determination of benzo(a)pyrene-serum albumin adducts and urinary 1-hydroxypyrene. Benzo(a)pyrene binding to albumin and 1-hydroxypyrene were quantitatively measured by enzyme linked immunosorbent assay (ELISA) and reverse phase high performance liquid chromatography (HPLC), respectively. 70 male foundry workers and 68 matched controls were investigated. High and low exposure groups were defined from breathing zone hygienic samples, consisting of 16 PAH compounds in particulate and gaseous phase. Mean total PAH was 10.40 micrograms/m3 in the breathing zone, and mean dust adsorbed PAH was 0.15 microgram/m. All carcinogenic PAH was adsorbed to dust. Median benzo(a)pyrene-albumin adduct concentrations (10-90% percentiles) were similar in foundry workers (smokers 0.55 (0.27-1.00) and non-smokers 0.58 (0.17-1.15)) pmol/mg albumin and age matched controls (smokers 0.57 (0.16-1.45) and non-smokers 0.70 (0.19-1.55) pmol/mg albumin). Median 1-hydroxypyrene concentrations were significantly higher (P < 0.0001) in smoking and non-smoking foundry workers (0.022 (0.006-0.075) and 0.027 (0.006-0.164)) mumol/mol creatinine than in smoking and non-smoking controls (0 (0-0.022) and 0 (0-0.010) mumol/mol creatinine). Dose-response relations between total PAH, pyrene, carcinogenic PAHs, and 1-hydroxypyrene for smokers, and polycyclic aromatic hydrocarbons adsorbed to dust for non-smokers are suggested. Exposure to PAHs adsorbed to dust showed an additive effect. There was no correlation between the concentrations of 1-hydroxypyrene and benzo(a)pyrene-albumin adducts. The change in 1-hydroxypyrene over a weekend was also studied. Friday morning median 1-hydroxypyrene concentrations were significantly higher in both smokers and non-smokers (0.021 (0-0.075) and 0.027 (0.06-0.164)) mumol/mol creatinine than Monday morning median concentrations (0.007 (0-0.021) and 0.008 (0-0.021) mumol/mol creatinine). Smoking did not affect the concentrations of 1-hydroxypyrene or benzo(a)pyrene-albumin adducts. These data suggest that 1-hydroxypyrene is a sensitive biomarker for low dose PAH exposure. Exposure to PAHs may be aetiologically related to increased risk of lung cancer in foundry workers.     

Urinary 1-hydroxypyrene concentrations in coke oven workers

OBJECTIVES: To investigate the relation of individual occupational exposure to total particulates benzene soluble fraction (BSF) of ambient air with urinary 1-hydroxypyrene (1-OHP) concentrations among coke oven workers in Taiwan. METHODS: 80 coke oven workers and 50 referents were monitored individually for the BSF of breathing zone air over three consecutive days. Exposures were categorised as high, medium, or low among coke oven workers based on exposure situations. The high exposure group (n = 18) worked over the oven. The medium and low exposure groups (n = 41 and n = 21) worked at the side of the oven for > 4 hours and < 4 hours a day, respectively. Urine was collected before the shift on the morning of day 1 and after the shift on the afternoon of day 3 to find the change of 1-OHP concentrations across the shift. RESULTS: The median (range) changes of urinary 1-OHP concentrations across the shift for various exposure situations (microgram/g creatinine) were as follows: high 182 (7 to 3168); medium 9 (-8 to 511); low 7 (-6 to 28); and referents 0.2 (-2 to 72). This change of urinary 1-OHP was highly associated with individual occupational exposure to the BSF in air (r = 0.74 and 0.64, p < 0.001). The regression model showed significant effects of individual exposures to the BSF and alcohol consumption on urinary postshift 1-OHP after adjusting for preshift 1-OHP in the total population (n = 130). More exposure to the BSF led to higher postshift 1-OHP (p < 0.001); current drinkers of > 120 g/week had lower urinary postshift 1-OHP than never and former drinkers (p = 0.01). A 10-fold increase in the average BSF in air resulted in about a 2.5-fold increase in postshift 1-OHP among the 80 coke oven workers. CONCLUSION: Urinary 1-OHP concentrations can be used as a good biomarker to assess individual exposure to the BSF in air. Alcohol drinking may modify the toxicokinetic pathway of the BSF; the effects of alcohol should be investigated further in occupational studies.

 

     

Significance of dermal and respiratory uptake in creosote workers: exposure to polycyclic aromatic hydrocarbons and urinary excretion of 1-hydroxypyrene.

OBJECTIVES--To evaluate workers' exposure in a creosote impregnation plant by means of ambient and biological monitoring. METHODS--Naphthalene (vapour phase) and 10 large molecular polycyclic aromatic hydrocarbons (PAHs) (particulate phase) were measured in the breathing zone air during an entire working week. 1-Hydroxypyrene (1-HP) was measured in 24 hour urine as a metabolite of the pyrene found in neat (dermal exposure) and airborne creosote. RESULTS--Naphthalene (0.4-4.2 mg/m3) showed 1000 times higher concentrations in air than did the particulate PAHs. In total, the geometric mean (range) of three to six ring PAHs was 4.8 (1.2-13.7) micrograms/m3; pyrene 0.86 (0.23-2.1) micrograms/m3, and benzo(a)pyrene 0.012 (0.01-0.05) micrograms/m3. There was no correlation between pyrene and gaseous naphthalene. The correlations between pyrene and the other nine particulate PAHs were strong, and gave a PAH profile that was similar in all air samples: r = 0.83 (three to six ring PAHs); r = 0.81 (three ring PAHs); r = 0.78 (four to six ring PAHs). Dermal exposure was probably very high in all workers, because the daily output of urinary 1-HP exceeded the daily uptake of inhaled pyrene by < or = 50-fold. Urinary 1-HP concentrations were very high, even on Monday mornings, when they were at their lowest (4-22 mumol/mol creatinine). 1-HP seldom showed any net increase over a workshift (except on Monday) due to its high concentrations (16 to 120 mumol/mol creatinine) in the morning samples. 1-HP was always lower at the end of the shift (19 to 85 mumol/mol creatinine) than in the evening (27 to 122), and the mean (SD) change over the working week (47 (18)) was greater than the change over Monday (35 (32)). The timing of 1-HP sampling is therefore very important. CONCLUSIONS--Urinary 1-HP proved to be a good biomarker of exposure to three to six ring PAHs but not to airborne naphthalene. Hence, biomonitoring based on 1-HP has to be completed with exposure assessment for naphthalene as a marker for creosote volatiles that mainly enter the body through the lungs.     

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.