An examination of the time course from human dietary exposure to polycyclic aromatic hydrocarbons to urinary elimination of 1-hydroxypyrene.

The significance of diet as an exposure route for polycyclic aromatic hydrocarbons (PAHs) and the associated kinetics of urinary 1-hydroxypyrene (1-OHPY) elimination were examined through a controlled human exposure study. Results showed that a 100 to 250-fold increase in a dietary benzo(a)pyrene (BaP) dose paralleled a four to 12-fold increase in urinary 1-OHPy elimination. Mean elimination rates during minimal exposure periods ranged from 6 to 17 ng/h whereas peak elimination rates of 60 to 189 ng/h were seen after a meal high in PAHs. A biexponential model fitted to a limited number of urinary 1-OHPY elimination points gave mean kinetic parameter estimates for t1/2 of 4.4 hours and tmax of 6.3 hours. It is concluded that dietary exposure to PAHs is potentially as substantial as some occupational exposures and therefore requires consideration in studies of exposure to PAHs. The dietary control strategies and the kinetic parameters defined in this investigation provide data for the control of this exposure route when examining other sources of exposure.     

Inhalation and dietary exposure to polycyclic aromatic hydrocarbons and urinary 1-hydroxypyrene in non-smoking university students

Objective To examine which exposure pathway, dietary or inhalation, contribute more to the exposure to, and/or internal dose of, polycyclic aromatic hydrocarbons (PAHs) of non-smoking Japanese. Methods Duplicated diet, personal air samples and 24-h urine were collected from14 non-smoking male university students without occupational exposure and the concentrations of PAHs in diet and air and that of 1-hydroxypyrene (1-OHP) in urine were measured with HPLC-fluorescence detector. Results Daily dietary exposure contributed more than 90% of the total (diet + inhalation) daily exposure level for pyrene (diet/inhalation: 757/1.2 ng/day), benzo[k]fluoranthene (25/1.7 ng/day) and benzo[a]pyrene (91/2.1 ng/day). Urinary excretion of 1-OHP (median: 37 ng/day) was statistically significantly correlated only with dietary PAHs exposure level but not with inhalation. Conclusion Countermeasures to lower PAHs levels in atmosphere has been successful in Japan and more attention should be directed to dietary exposure to PAHs for reducing cancer risk in general population.     

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     

Risk assessment of occupational exposure to polycyclic aromatic hydrocarbons by means of urinary1-hydroxypyrene

Polycyclic aromatic hydrocarbons have mutagenic and carcinogenic properties and some of them are classified as probable or possible human carcinogens. Aim of this study was to evaluate the genotoxic risk in workers exposed to diesel exaust. Environmental and biological monitoring exposure to polycyclic aromatic hydrocarbons was carried out on fifty-two workers exposed to diesel exhaust. Urinary 1-hydroxypyrene was employed as a biomarker of internal dose. Significant urinary 1-hydroxypyrene differences between smokers and non-smokers were found. Twenty per cent of urinary 1-hydroxypyrene values exceeded benchmark level for genotoxic effect, while the results of environmental monitoring excluded the existence of exposure to polycyclic aromatic hydrocarbons. In the absence of greater knowledge about the relationship between urinary 1-hydroxypyrene and genotoxic effects under the conditions of very low exposure, extreme caution is recommended when this biomarker of internal dose is employed as an indicator of genotoxic risk.     

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.     

Assessment of exposure to polycyclic aromatic hydrocarbons in engine rooms by measurement of urinary 1-hydroxypyrene.

OBJECTIVE: Machinists have an increased risk of lung cancer and bladder cancer, and this may be caused by exposure to carcinogenic compounds such as asbestos and polycyclic aromatic hydrocarbons (PAHs) in the engine room. The aim of this study was to investigate the exposure of engine room personnel to PAHs, with 1-hydroxypyrene in urine as a biomarker. METHODS: Urine samples from engine room personnel (n = 51) on 10 ships arriving in different harbours were collected, as well as urine samples from a similar number of unexposed controls (n = 47) on the same ships. Urinary 1-hydroxypyrene was quantitatively measured by high performance liquid chromatography. The exposure to PAHs was estimated by a questionnaire answered by the engine room personnel. On two ships, air monitoring of PAHs in the engine room was performed at sea. Both personal monitoring and area monitoring were performed. The compounds were analysed by gas chromatography of two types (with a flame ionisation detector and with a mass spectrometer). RESULTS: Significantly more 1-hydroxypyrene was found in urine of personnel who had been working in the engine room for the past 24 hours, than in that of the unexposed seamen. The highest concentrations of 1-hydroxypyrene were found among engine room personnel who had experienced oil contamination of the skin during their work in the engine room. Stepwise logistic regression analysis showed a significant relation between the concentrations of 1-hydroxypyrene, smoking, and estimated exposure to PAHs. No PAHs were detected in the air samples. CONCLUSION: Engine room personnel who experience skin exposure to oil and oil products are exposed to PAHs during their work. This indicates that dermal uptake of PAHs is the major route of exposure.     

Exposure to polycyclic aromatic hydrocarbons in petrochemical industries by measurement of urinary 1-hydroxypyrene.

Biological monitoring of exposure of workers to polycyclic aromatic hydrocarbons (PAHs) in petrochemical industries was performed by the measurement of urinary excretion of 1-hydroxypyrene. In 121 of the 462 workers studied (both smokers and non-smokers) who had had no recent occupational exposure to PAHs a median 1-hydroxypyrene concentration of 0.21 micrograms/g creatinine was found. The upper limit of the 95% confidence interval in these workers of 0.99 micrograms/g creatinine was used as the upper normal value for industrial workers. Urinary 1-hydroxypyrene concentrations were measured in workers involved in manufacture and maintenance operations in oil refineries (13 studies in eight different settings), in workers manufacturing or handling products containing PAHs in chemical plants (five studies in three settings) and laboratories (four studies), and in workers digging soil contaminated with PAHs (three studies). In most studies in oil refineries 1-hydroxypyrene concentrations were only marginally greater than the values measured in the 121 workers with no recent occupational exposure to PAHs. This was also the case in maintenance operations with higher potential exposure to PAHs, indicating that personal protection equipment was generally adequate to prevent excessive exposure. The studies in chemical plants also showed that exposure to PAHs is low. An exception was the workers engaged in the production of needle coke from ethylene cracker residue, where increased urinary 1-hydroxypyrene concentrations were measured. The excretion of 1-hydroxypyrene by the operators and maintenance workers of this plant was investigated in relation to potential methods of exposure to PAHs. Dermal and inhalatory exposure were both significant determinants of exposure to PAHs.     

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.     

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.     

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.     

Simulation of urinary excretion of 1-hydroxypyrene in various scenarios of exposure to polycyclic aromatic hydrocarbons with a generic, cross-chemical predictive PBTK-model

Introduction

A physiologically based toxicokinetic (PBTK) model can predict blood and urine concentrations, given a certain exposure scenario of inhalation, dermal and/or oral exposure. The recently developed PBTK-model IndusChemFate is a unified model that mimics the uptake, distribution, metabolism and elimination of a chemical in a reference human of 70?kg. Prediction of the uptake by inhalation is governed by pulmonary exchange to blood. Oral uptake is simulated as a bolus dose that is taken up at a first-order rate. Dermal uptake is estimated by the use of a novel dermal physiologically based module that considers dermal deposition rate and duration of deposition. Moreover, evaporation during skin contact is fully accounted for and related to the volatility of the substance. Partitioning of the chemical and metabolite(s) over blood and tissues is estimated by a Quantitative Structure–Property Relationship (QSPR) algorithm. The aim of this study was to test the generic PBTK-model by comparing measured urinary levels of 1-hydroxypyrene in various inhalation and dermal exposure scenarios with the result of model simulations.

Experimental

In the last three decades, numerous biomonitoring studies of PAH-exposed humans were published that used the bioindicator 1-hydroxypyrene (1-OH-pyrene) in urine. Longitudinal studies that encompass both dosimetry and biomonitoring with repeated sampling in time were selected to test the accuracy of the PBTK-model by comparing the reported concentrations of 1-OHP in urine with the model-predicted values. Two controlled human volunteer studies and three field studies of workers exposed to polycyclic aromatic hydrocarbons (PAH) were included.

Results

The urinary pyrene-metabolite levels of a controlled human inhalation study, a transdermal uptake study of bitumen fume, efficacy of respirator use in electrode paste workers, cokery workers in shale oil industry and a longitudinal study of five coke liquefaction workers were compared to the PBTK-predicted values. The simulations showed that the model-predicted concentrations of urinary pyrene and metabolites over time, as well as peak-concentrations and total excreted amount in different exposure scenarios of inhalation and transdermal exposure were in all comparisons within an order of magnitude. The model predicts that only a very small fraction is excreted in urine as parent pyrene and as free 1-OH-pyrene. The predominant urinary metabolite is 1-OH-pyrene-glucuronide. Enterohepatic circulation of 1-OH-pyrene-glucuronide seems the reason of the delayed release from the body.

Conclusions

It appeared that urinary excretion of pyrene and pyrene-metabolites in humans is predictable with the PBTK-model. The model outcomes have a satisfying accuracy for early testing, in so-called 1st tier simulations and in range finding. This newly developed generic PBTK-model IndusChemFate is a tool that can be used to do early explorations of the significance of uptake of pyrene in the human body following industrial or environmental exposure scenarios. And it can be used to optimize the sampling time and urine sampling frequency of a biomonitoring program.     

Assessment of occupational exposure to aromatic polycyclic hydrocarbons determining urinary levels of 1-pyrenol

In conformity with Italian law 626/94, occupational exposure to Polycyclic Aromatic Hydrocarbons (PAH) in several types of work environments was assessed by analysing urinary levels of 1-pyrenol. A total of 231 non-smokers exposed to PAH (82 workers, employed in two different thermoelectric power plants using combustible oil (30 subjects from plant A and 52 from plant B), 18 subjects working for a company recovering exhausted oils, 12 working on rubber production, 10 on road surface asphalting operations, 22 working in the anodizing section of an aluminium plant, 27 chimney-sweeps, and 60 coke-oven workers (30 topside workers, and 30 doing other jobs)) were enrolled. There were also 53 non-smoker control subjects, not occupationally exposed to PAH. Current smokers were excluded, since smoking is an important confounding factor when occupational exposure to low PAH concentrations are monitored. Confounding factors, i.e., diet and passive smoking, were checked by means of a questionnaire which, in addition to personal data and habits, also requested specific details about the type of diet followed and possible exposure to passive smoking during the 24-hour period preceding urine collection. In controls, exposure to PAH in the diet significantly increased 1-pyrenol levels in urine: in subjects introducing > or = 1 microgram of pyrene with the diet, the mean urinary level of 1-pyrenol was significantly higher than that introduced with < 1 microgram (high versus low dietary intake, mean +/- SD, 0.08 +/- 0.13 and 0.04 +/- 0.06 1-pyrenol mumoles/mole of creatinine, respectively; Mann-Whitney U-test Z = 2.67, p < 0.01). Conversely, passive smoking did not influence 1-pyrenol levels. In the overall population (controls and exposed), multiple linear regression analysis showed that levels of urinary 1-pyrenol were significantly influenced by occupational exposure to PAH in asphalt workers, anodizing plant workers, chimney-sweeps, and coke-oven workers, both those working at the top side of the oven and those doing other jobs (t = 2.19, p = 0.02; t = 2.56, p = 0.01; t = 5.25, p = 0.001; t = 3.34, p = 0.001; t = 7.82, p = 0.001, respectively; F = 9.7, p < 0.01), but not in power plant workers in contact with combustible oils, workers recovering exhausted oils, or rubber production workers. Diet and passive smoking did not influence urinary 1-pyrenol levels in the entire sample population. This biomarker also allowed an assessment of exposure levels among certainly exposed subjects. The percentage of subjects with urinary 1-pyrenol values higher than the 99th percentile of the reference population (0.67 mumoles 1-pyrenol/mole of creatinine) was significantly higher than that of controls in asphalt workers (20%), anodizing plant workers (14%), chimney-sweeps (13%) and coke-oven workers (33%) (chi-square test: asphalt workers = 6.1, p = 0.01; anodizing plant workers = 4.3, p = 0.04; chimney-sweeps = 7.1, p = 0.008; coke-oven workers with other duties = 4.4, p = 0.04; top side workers = 16.5, p < 0.001). In chimney sweeps and top side workers, respectively 2 and 4 subjects (7% and 13%) exceeded the precautionary level of 1.4 mumoles 1-pyrenol/mole of creatinine; of these, 1 chimney sweep and 3 top side workers (4% and 10%) exceeded the recommended biological threshold of 2.3 mumoles 1-pyrenol/mole of creatinine.     

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.     

An assessment of occupational exposure to polycyclic aromatic hydrocarbons in the UK

A cross-industry occupational hygiene survey was commissioned by the Health and Safety Executive (HSE) to determine the levels of polycyclic aromatic hydrocarbon (PAH) exposure in UK industry and to determine if one or more target analytes were suitable as markers for assessing total exposure to PAHs. There were no broadly applicable UK exposure standards for assessing total exposure to PAHs. Until 1993 a guidance value for assessing exposure in coke ovens only, where PAH exposure is known to be the highest, was based on gravimetric analysis of cyclohexane-soluble material. Biological monitoring based on urinary 1-hydroxypyrene (1-OHP) is widely reported to be an effective indicator of exposure by both dermal and inhalation routes but there was no UK guidance value. The survey involved an occupational hygiene study of 25 sites using both airborne monitoring of a total of 17 individual PAHs and biological monitoring. The results showed 8 h TWA levels of total PAH in air ranged from 0.4 to 1912.6 microg m(-3) with a GM of 15.8 microg m(-3). The profile of PAHs was dominated by naphthalene, the most volatile 2-ring PAH. Airborne benzo(a)pyrene (BaP) correlated well (r(2) = 0.971) with levels of carcinogenic 4-6 ring PAHs and was an effective marker of exposure for all industries where significant particle bound PAH levels were found and, in particular, for CTPV exposure. The 8 h TWA levels of BaP ranged from <0.01 to 6.21 microg m(-3) with a GM of 0.036 microg m(-3); 90% were <0.75 microg m(-3) and 95% were <2.0 microg m(-3). Two hundred and eighteen urine samples collected from different workers at the end of shift and 213 samples collected pre-shift next day were analysed for 1-OHP. Levels of 1-OHP in end-of-shift samples were generally higher than those in pre-shift-next-day samples and showed a good correlation (r(2) = 0.768) to airborne BaP levels if samples from workers using respiratory protection or with significant dermal exposure were excluded. Urinary 1-OHP in end-of-shift samples ranged from the limit of detection (0.5 micromol mol(-1) creatinine) to 60 micromol mol(-1) creatinine with a mean of 2.49 micromol mol(-1) and a 90th percentile value of 6.7 micromol mol(-1) creatinine. The highest 1-OHP levels were found in samples from workers impregnating timber with creosote where exposure was dominated by naphthalene. If the 11 samples from these workers were excluded from the dataset, the 90% value for end-of-shift urine samples was 4 micromol mol(-1) creatinine (n = 207) and this value has since been adopted by the HSE as a biological monitoring benchmark value.     

Evaluation of worker exposure to polycyclic aromatic hydrocarbons

A sampling and analytical method was selected to determine the physical and chemical nature of worker exposure to polycyclic aromatic hydrocarbons (PAH). It consists of filter and sorbent tube sampling followed by benzene extraction and analysis of 12 different PAHs with a gas chromatograph connected to a mass spectrometer. This method has undergone extensive field trials. Sampling temperature, inorganic and organic interferences have an effect on the results as they do on the standard gravimetric method of benzene-solubles. A combination of the gravimetric method and the particulate and gaseous concentration profile of 12 PAHs is necessary to obtain an informative evaluation of worker exposure. This approach was used to demonstrate that workers in paving and roofing operations and on some worksites in the steel and silicon carbide industries show an exposure profile that suggests minimal health risk and is largely different from the exposure of workers in aluminum refineries, refractory brick laying and most other worksites in the silicon carbide industry.     

Assessment of exposure to polycyclic aromatic hydrocarbons in police in Florence, Italy, through personal air sampling and biological monitoring of the urinary metabolite 1-hydroxypyrene

In this study, the authors evaluated exposure to airborne polycyclic aromatic hydrocarbons (PAHs) in workers exposed to exhaust gas from cars, and they assessed the efficiency of urinary 1-hydroxypyrene as an indicator of exposure to pyrene and PAHs. The authors selected 2 groups of police who worked in 2 areas in the city of Florence: 1 group was highly exposed to high-density traffic emissions during the winter and summer of 1997, and the 2nd group experienced low exposure to traffic emissions during the same period. Ambient monitoring was achieved with personal sampling of airborne PAHs during each workshift. Eight hydrocarbons were used as indicators of pollution caused by PAHs (e.g., pyrene, benzo[a]pyrene, benzo[a]anthracene, dibenzo[a,h]anthracene). Biological monitoring was performed through dosing of 1-hydroxypyrene (pyrene metabolite) in urine samples taken at the end of each workshift. The ambient monitoring revealed that PAH concentrations were influenced by both season of sampling and varying intensities of traffic in the different areas. The median concentration of benzo[a]pyrene in winter was twice as high in the high-density traffic area as in the low-density traffic area (i.e., 4.1 ng/m3 versus 1.8 ng/m3). In summer, the high-density traffic area experienced benzo[a]pyrene concentrations that were 6 times higher than in the low-density traffic area (i.e., 1.2 ng/m3 versus 0.2 ng/m3). Benzo[a]pyrene was also correlated highly (r(s) = .92, p < .0001) with the mixture of total PAHs analyzed, thus confirming its function as a good indicator of exposure to PAHs in an urban environment. Levels of urinary 1-hydroxypyrene appeared to be generally influenced by the intensity of traffic, especially during the winter (i.e., median value in winter was 199.2 ng/gm creatinine in the high-density traffic area and 120.5 ng/gm creatinine in the low-density traffic area). An analysis of the general data revealed that 1-hydroxypyrene was, to some degree, related to pyrene, benzo[a]pyrene, and airborne total PAHs, whereas analysis of separate data for the area and the season revealed an emergence of a closer correlation during the winter in the high-traffic area. Therefore, 1 -hydroxypyrene can be considered a good biological indicator of exposure to airborne PAHs in the urban environment, especially in winter and in high-density traffic areas.     

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.