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     

Biological monitoring of occupational exposure to polycyclic aromatic hydrocarbons (PAH) by determination of monohydroxylated metabolites of phenanthrene and pyrene in urine

Objectives The aim of our study was to assess individual polycyclic aromatic hydrocarbon (PAH) exposure of workers coming from three different industrial branches by several parameters of external and internal exposure. By analysing the relationships between those markers the suitability of individual parameters [e.g. monohydroxylated phenanthrene (Phe) metabolites] for exposure surveillance should be evaluated. Methods The total study population consisted of 255 male workers (age: 19-62, mean: 39.61 years), who were employed in coke production (n = 40), production of graphite electrodes and special carbon products (92), or production of refractory materials (123), respectively. For each worker external PAH exposure was determined by personal air sampling of 16 PAH, including Phe, pyrene (Pyr) and benzo[a]pyrene (BaP). For determination of internal PAH exposure the excretion of the PAH metabolites 1-, 2 + 9-, 3-, 4-hydroxyphenanthrene and 1-hydroxypyrene was measured in post-shift urine samples of all workers. Results In the total study population median total PAH exposure and exposure to BaP were 30.62 and 0.27 μg/m3, respectively. A calculation of PAH profiles resulted in substantial branch-related variations with Phe being a major component. Considering all branches the median excretions of 1-hydroxypyrene and hydroxyphenanthrenes (sum) were 6.68 and 11.22 μg/g creatinine. A correlation analysis yielded a good correlation between total ambient PAH exposure and excretion of hydroxyphenanthrenes in urine (r = 0.662; P < 0.01), but no significant correlation between Phe metabolites and the carcinogenic BaP. For 1-hydroxypyrene and BaP a weak but significant association was found (r = 0.235; P < 0.01). Conclusions Considering the results of the correlation analysis hydroxyphenanthrenes in urine should reflect an uptake of lowly condensed volatile PAH rather than an incorporation of highly condensed PAH like BaP which should be reflected better by 1-hydroxypyrene. Therefore, the determination of hydroxyphenanthrenes in addition to the well-established marker 1-hydroxypyrene could offer some further information about the exposure situation at a particular work place.     

Urinary monohydroxylated phenanthrenes and hydroxypyrene – the effects of smoking habits and changes induced by smoking on monooxygenase-mediated metabolism

Objectives: Internal polycyclic aromatic hydrocarbon (PAH) exposure is usually studied by determining 1-hydroxypyrene in urine. In many studies, increased urinary levels of 1-hydroxypyrene have been found in smokers compared with non-smokers. The disadvantage of this procedure, however, is that it is based on only one substance. Therefore, in our study, urine specimens from smokers and non-smokers were tested for four monohydroxylated phenanthrenes in addition to 1-hydroxypyrene. Subjects and methods: Spot urine samples from 288 non-smokers and 100 smokers were analysed for 1-, 2-, 3- and 4-hydroxyphenanthrene and 1-hydroxypyrene by a very sensitive high performance liquid chromatography (HPLC) method with fluorescence detection. The detection limit of the method is 5 ng metabolite/l urine. The data were calculated on a creatinine basis (ng/g creatinine). Results: Highly significant differences and dose-response relationships with regard to cigarettes smoked per day were found for 2-, 3- and 4-hydroxyphenanthrene and 1-hydroxypyrene, but not for 1-hydroxyphenanthrene. When the ratio of the sum of hydroxyphenanthrenes to 1-hydroxypyrene, and the ratio of 1- and 2-/3- and 4-hydroxyphenanthrene were taken into consideration, significant negative dose-response relationships to the numbers of cigarettes smoked per day, were found. Conclusion: 1-Hydroxypyrene as well as 2-, 3- and 4-monohydroxylated phenanthrenes in urine may be used as parameters to detect PAH exposure from cigarette smoking. Moreover, 3,4-oxidation of phenanthrenes was found to be enhanced in smokers, with a significant dose-response relationship. This phenomenon is thought to be caused by an induction of the CYP 1A2 (or CYP 3A4) monooxygenase system in smokers. Therefore, it may be recommended that monohydroxylated phenanthrenes be analysed in order to assess the balance between the PAH-metabolising cytochrome isoforms, and the activity or induction of cytochrome P450 isoforms, respectively. Received: 12 May 2000 / Accepted: 1 November 2000     

Indoor exposure to polycyclic aromatic hydrocarbons and carbon monoxide in traditional houses in Burundi

Objectives: Wood combustion is used as a major energy source in African countries and could result in indoor, pollution-related health problems. This exploratory study was undertaken to estimate polycyclic aromatic hydrocarbon (PAH) and carbon monoxide exposure in individuals living in traditional rural houses in Burundi. Methods: Standard methods were used to determine indoor air concentrations of 12 PAHs, and carbon monoxide. The urinary excretion of 1-hydroxypyrene (1-OHP) was measured in occupants of traditional houses, and compared with that of individuals living in the town of Bujumbura, the capital of Burundi. Results: Mean airborne concentration of four volatile PAHs, naphthalene, fluorene, phenanthrene and acenaphthene, exceeded 1 μg/m³, and that of benzo(a)pyrene was 0.07 μg/m³. Naphthalene was by far the main PAH contaminant, with a mean concentration (±standard deviation) of 28.7 ± 23.4 μg/m³, representing on average 60–70% of total PAH concentration. Carbon monoxide mean concentration (±standard deviation) was 42 ± 31 mg/m³, and correlated with total PAH concentration. Geometric mean urinary 1-OHP excretion (range) in people living in traditional houses was 1.50 (0.26–15.62) μmol/mol creatinine, a value which is on average 30 times higher than that of people living in the capital (0.05 (0.009–0.17) μmol/mol creatinine). Conclusions: It appears that the substantially high concentrations of the studied contaminants constitute a potential health hazard to the rural population of Burundi. Received: 15 July 1999 / Accepted: 20 November 1999     

Urinary levels of 1-hydroxypyrene, 1-, 2-, 3-, and 4-hydroxyphenanthrene in females living in an industrial area of Germany

The concentrations of 1-hydroxypyrene (1-HOPYR), and 1-, 2-, 3-, and 4-hydroxyphenanthrene (HOPHE) as metabolites of pyrene and phenanthrene, were measured in urine samples collected from 124 housewives (27 smokers and 97 nonsmokers) living in Bottrop, an industrial city located in the Ruhr area in Germany. The urine samples were analyzed by a very sensitive and practical high-performance liquid chromatographic (HPLC) method using a two-column switching technique and a special precolumn packing material followed by fluorescence detection. The polycyclic aromatic hydrocarbon (PAH) metabolites are selectively enriched on the precolumn and separated from the matrix. Therefore, laborious clean-up steps were omitted. The above-mentioned PAH metabolites could be detected in all urine samples investigated. Smokers had significantly higher urine concentrations of 1-HOPYR (median 0.48 g/g creatinine), 3-HOPHE (median 0.61 g/g creatinine), 2-HOPHE (0.41 g/g creatinine) and 4-HOPHE (median 0.10 g/g creatinine) than non-smokers (median 0.15 g/g creatinine, 0.31 g/g creatinine, 0.31 g/g creatinine and 0.04g/g creatinine, respectively). The study shows that the influence of smoking is of such an order of magnitude that potential environmental exposure to PAH in this highly industrialized area is obscured by smoking habits. Furthermore, it can be concluded that the determination of 1-HOPYR, 1-, 2-, 3-, and 4-HOPHE in urine is a diagnostically useful method for the biological monitoring of persons environmentally exposed to PAH.     

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.     

Environmental exposure of small children to polycyclic aromatic hydrocarbons

Objectives: The aim of the study was to assess the intake (by various routes of exposure) of polycyclic aromatic hydrocarbons (PAH) by children living in a Czech city, and its effect on excretion of 1-hydroxypyrene (1-OHP) in summer and winter periods. Methods: Four groups of children (3–6 years old) were chosen: (1) two groups from a kindergarten situated in the city center with a higher traffic density (“polluted” area); (2) two groups from a kindergarten situated in a green zone of the same city (“non-polluted” area). Food consumption was recorded in all children and PAH intake from foodstuffs was estimated. Ambient air samples were collected from the playground and inside the kindergartens. Soil samples were collected too. Morning and evening urine samples were collected during sampling days. Results: In both seasons, the mean outdoor total PAH concentration (sum of 12 individual PAH) in the “polluted” area was approximately three-times higher than that in the “non-polluted” area. Indoor concentration in the “polluted” area was more than six-times higher than that in the “non-polluted” area in summer, and almost three-times higher in winter. The same trend was observed for pyrene and for the sum of carcinogenic PAH. The contribution to the total pyrene absorbed dose from food consumption was much more important than that from inhalation and from ingestion of soil dust. Significantly higher urinary concentrations of 1-OHP (evening samples) were found in children from the “polluted” kindergarten in both seasons. The number of significant relationships between 1-OHP and pyrene absorbed dose was weak. Conclusions: Food seems to be the main source of total pyrene and total PAH intake in small children, even under relatively higher air PAH exposure in the city. Estimated pyrene ingestion from soil had a negligible contribution to the total pyrene absorbed dose. Urinary 1-OHP seems to be an uncertain (non-sensitive) marker of the environmental inhalation exposure to pyrene (PAH) if the pollution of air by pyrene (PAH) is not excessive and the pyrene (PAH) dose by this route is much less than by ingestion. Usefulness of the urinary 1-OHP as an indicator of overall environmental exposure to PAH needs further investigation. Received: 18 September 2000 / Accepted: 20 February 2001     

Exposure to polycyclic aromatic hydrocarbons in occupational versus urban environmental air

To evaluate the balance between occupational and environmental exposure to suspended particulate matter (SPM) and polycyclic aromatic hydrocarbons (PAHs), comparison measurements were performed in a coal-fired power plant and the urban atmosphere from the town nearby. Methods: The analysis of SPM for PAH content was done according to a high-performance liquid chromatography (HPLC)-based method. The microscopic assessment was performed using scanning electron microscopy (SEM) by silver coverage of the samples derived by air filter. Results: Contrary to expectations, the results showed low levels of particle-bound PAHs in the occupational environment (<1 ng benzo(a)pyrene/m³ air) and high levels in urban air (range 80–1250 ng benzo(a)pyrene/m³). The SPM collected from the power plant exhibited non-respirable characteristics (particles larger than 10 μm), whereas urban SPM almost exclusively contained respirable airborne particles (<3 μm). Conclusions: The PAH burden, combined with the enhanced probability of respiratory absorption, confers a much greater hazard potential to the urban SPM. Under these conditions, in areas or countries in which old technologies remain in use, occupational exposure to SPM containing PAHs might represent a severe underestimation of the total risk as it does not take into account the background air pollution. Received: 6 December 1997 / Accepted: 12 June 1998     

Urinary cotinine concentration in flight attendants, in relation to exposure to environmental tobacco smoke during intercontinental flights

Objectives: To measure and compare the urinary cotinine concentration (U-cotinine) in non-smoking cabin attendants (C/A) working with the Scandinavian Airlines System, before and after work on intercontinental flights with exposure to environmental tobacco smoke (ETS). Methods: The study material consisted of 24 cabin attendants and one pilot, all volunteers and all without exposure to ETS in the home, working on 15 intercontinental flights. Information on age, gender and occupation was gathered, as well as possible sources of ETS exposure in other places, outside work and during previous flights, during a 3-day period prior to the investigation. Urine samples were taken before departure and after landing, on board, and were kept frozen (−20 °C) until analysis. Cotinine was analyzed by a previously developed gas chromatographic method, using mass spectrometry (MS) with selected-ion monitoring (SIM). The difference in U-cotinine before and after the flight was compared. Moreover, the change in U-cotinine during the flight was related to occupation (work in the forward or aft galley) and observed degree of smoking during each flight. Results: The median U-cotinine was 3.71 μg/g crea; 2.4 μg/l (unadjusted) (interquartile range 2.08–8.67 μg/g crea) before departure, and 6.37 μg/g crea; 7.1 μg/l (interquartile range 3.98–19 μg/g crea) after landing, a significant difference (P < 0.003). C/A in the aft galley had a significantly higher concentration of U-cotinine after landing than subjects working in the front of the aircraft (P=0.01). In C/A working in the aft galley, the median increase of U-cotinine was 3.67 μg/g crea; 3.2 μg/l (interquartile range 0.04–13.8 μg/g crea) during flight. In contrast, those seven subjects working in the forward part of the aircraft had no increase in U-cotinine during the flight (median increase 0.97 μg/g crea; 0.5 μg/l interquartile range 0.27–2.65 μg/g crea). Conclusion: Tobacco smoking in commercial aircraft may cause significant exposure to environmental tobacco smoke among C/A working in the aft galley, despite high air exchange rates and spatial separation between smokers and non-smokers. This agrees with earlier studies, as well as measurements on the aircraft, showing a higher degree of ETS-related air pollution in the aft galley than in the forward galley. The average cotinine concentration in urine was similar to that in other groups with occupational exposure to ETS, e.g., restaurant staff, police interrogators and office workers. Since smoking in commercial aircraft may result in an involuntary exposure to ETS among non-smokers, it should be avoided. Received: 1 February 1999 / Accepted: 29 May 1999     

Biomonitoring of manganese in blood, urine and axillary hair following low-dose exposure during the manufacture of dry cell batteries

Objectives: A cross-sectional study was carried out on 100 workers from three different workplace areas in a dry cell battery manufacturing plant and on 17 currently nonexposed referents, to examine the relationship between the external exposure to manganese dioxide (MnO₂) and the body burden of manganese in blood, urine and hair. Methods: Inhalable dust was measured gravimetrically after stationary active sampling. Manganese was analyzed in dust samples, blood, urine and axillary hair by atomic absorption spectro- metry. Results: The average air concentrations of manganese in the three workplace areas were 4 μg/m³ (range: 1–12 μg/m³), 40 μg/m³ (12–64 μg/m³) and 400 μg/m³ (137–794 μg/m³). Manganese in blood and axillary hair correlated with airborne manganese in group-based calculations but not on an individual level. The manganese concentrations varied between 3.2 μg/l and 25.8 μg/l in the blood (mean: 12.2 ± 4.8 μg/l) and between 0.4 μg/g and 49.6 μg/g in hair (mean: 6.2 ± 6.2 μg/g in the proximal sequence), respectively. The results for the nonexposed referents were 7.5 ± 2.7 μg/l (mean) in the blood (range: 2.6–15.1 μg/l) and 2.2 ± 1.8 μg/g (mean) in axillary hair (range: 0.4–6.2 μg/g). In these matrices, manganese differed significantly between the highly exposed workers and both the reference and the low-exposure group. Manganese in blood revealed the lowest background variance. No differences for manganese in urine were observed between workers (mean: 0.36 ± 0.42 μg/l, range: 0.1–2.2 μg/l) and referents (mean: 0.46 ± 0.47 μg/l, range: 0.1–1.7 μg/l). Conclusions: Manganese in blood is a specific and suitable parameter for the biomonitoring of MnO₂ exposure, although its validity is limited to group-based calculations. Urinary manganese failed to allow a differentiation between exposed workers and referents. The suitability of manganese analysis in hair for biomonitoring purposes suffers from a relatively great background variation as well as from analytical problems. Received: 11 December 1998 / Accepted: 17 July 1999     

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.     

Urinary hydroxy-metabolites of naphthalene,phenanthrene and pyrene as markers of exposure to diesel exhaust

Objective The objective of this study was to assess the exposure of bus-garage and waste-collection workers to polycyclic aromatic hydrocarbons (PAHs) derived from diesel exhaust by the measurement of levels of seven urinary PAH metabolites: 2-naphthol, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 3-hydroxyphenanthrene, 1+9-hydroxyphenanthrene, 4-hydroxyphenanthrene and 1-hydroxypyrene.Subjects and methods One urine sample from each of 46 control persons, and one pre-shift and two post-shift spot urine samples from 32 exposed workers were obtained in winter and in summer. The metabolites were analysed after enzymatic hydrolysis by high performance liquid chromatography (HPLC) with fluorescence detection.Results The sum of seven PAH metabolites (mean 3.94±3.40 and 5.60±6.37 mol/mol creatinine in winter and summer, respectively) was higher [P=0.01, degrees of freedom (df) =61.2 and P=0.01, df=67.6 in winter and summer, respectively] in the exposed group than in the control group (mean 3.18±3.99 and 3.03±2.01 mol/mol creatinine in winter and summer, respectively). The mean concentrations of 2-naphthol among exposed and controls ranged between 3.34 and 4.85 mol/mol creatinine and 2.51 and 2.58 mol/mol creatinine, respectively (P<0.01 in winter, P<0.03 in summer). The mean level of the hydroxyphenanthrenes in the samples of exposed workers was between 0.40 and 0.70 mol/mol creatinine and in the control samples 0.40–0.60 mol/mol creatinine. The concentration of 1-hydroxypyrene was higher among exposed workers in both pre-shift and post-shift samples (mean 0.10–0.15 mol/mol creatinine) than in control group (mean 0.05–0.06 mol/mol creatinine) in winter (P=0.002, df=78) and in summer (P<0.001, df=68).Conclusions The urinary hydroxy-metabolites of naphthalene, phenanthrene and pyrene showed low exposure to diesel-derived PAHs; however, it was higher in exposed workers than in control group. Urinary PAH monohydroxy-metabolites measured in this study did not correlate with the PAHs in the air samples, reported earlier, in 2002 and 2003.     

Biological monitoring of environmental exposure to polycyclic aromatic hydrocarbons in subjects living in the vicinity of a creosote impregnation plant

Objective: This study was undertaken to evaluate the environmental exposure to polycyclic aromatic hydrocarbons (PAHs) in nonsmoking adult subjects living in the vicinity of a creosote impregnation plant in Delson, Canada. Urinary metabolites of naphthalene, α- and β-naphthol, and pyrene metabolite 1-hydroxypyrene (1-OHP), were used as biomarkers of exposure. Methods: Morning and evening urine samples were collected in mid-August from 30 exposed individuals living at a distance of 50–360 m downwind of the plant and from a control group in the adjoining municipality residing at a distance of 1.9–2.7 km upwind of the plant. Metabolites were measured by gas chromatography/mass spectrometry. Results: Excretion values of α- and β-naphthol were significantly higher in the exposed group than in controls (P < 0.04), after accounting for possible confounding variables by multivariate analyses. The respective geometric mean concentrations (5th and 95th percentiles) of α-naphthol for the exposed and nonexposed groups were 2.04 (0.55–6.00) and 1.37 (0.39–7.02) μmol/mol creatinine for evening samples, and 2.49 (0.77–8.43) and 1.17 (0.37–6.88) μmol/mol creatinine for morning samples. Corresponding values for β-naphthol were 1.78 (0.82–3.67) and 1.36 (0.63–5.07) μmol/mol creatinine for evening samples, and 1.94 (1.03–4.96) and 1.08 (0.49–5.05) μmol/mol creatinine for morning samples. On the other hand, no significant difference in 1-OHP excretion was observed between the exposed and the control group (P>0.5). The respective geometric mean concentrations (5th and 95th percentiles) of 1-OHP for these groups were 0.05 (0.01–0.17) and 0.06 (0.01–0.48) μmol/mol creatinine for evening samples, and 0.05 (0.02–0.12) and 0.05 (0.01–0.42) μmol/mol creatinine for morning samples. Conclusions: The measurement of α- and β-naphthol urinary concentrations appears to be an approach sufficiently sensitive to reveal differences in low exposure levels of volatile PAHs due to creosote impregnation plant emissions. However, uptake of pyrene due to the plant was too small to contribute significantly to 1-OHP excretion. Received: 13 June 2000 / Accepted: 21 April 2001     

Quantification and Source Identification of Polycyclic Aromatic Hydrocarbons in Core Sediments from Sundarban Mangrove Wetland, India

The distribution and potential sources of 16 polycyclic aromatic hydrocarbons (PAHs) in sediment cores (<63 μm particle size) of the Sundarban mangrove wetland, northeastern coast of Bay of Bengal (India), were investigated by gas chromatography coupled to mass spectrometry. The total concentrations of 16 PAHs (∑₁₆PAHs) ranged from 132 to 2938 ng/g, with a mean of 634 ng/g, and the sum of 10 out of 16 priority PAHs (∑₁₀PAH) varied from 123 to 2441 ng/g, with a mean of 555 ng/g, and the 5 carcinogenic PAHs (benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, indeno[1,2,3-cd]pyrene, and dibenz[a,h]anthracene) accounted for 68–73% of the priority PAHs. Maximum concentrations of the sediment core were obtained at subsoil depth of 12–16 cm. The prevalence of four to six aromatic ring PAHs and cross-plots of specific isomer ratios such as phenanthrene/anthracene, fluoranthene/pyrene, and methylphenanthrenes/phenanthrene suggested the predominance of wood and coal combustion sources, the atmospheric deposition, and surface runoff to be the major transport pathways. A good correlation existed between the benzo[a]pyrene level and the total PAH concentrations, making this compound a potential molecular marker for PAH pollution. Total TEQ_S^carc values calculated for samples varied from 6.95 ng/g TEQ_S^carc to 119 ng/g TEQ_S^carc, with an average of 59 ng/g dry weight TEQ_S^carc. The baseline data can be used for regular monitoring, considering the industrial and agricultural growth around this coastal environment.     

Metabolites of Polycyclic Aromatic Hydrocarbons (PAHs) in Bile as Biomarkers of Pollution in European Eel (Anguilla anguilla) from German Rivers

In the light of the alarming decline of the European eel (Anguilla anguilla L.) population, there is an urgent need to define ecological indicators for eel habitat quality. Due to an increasing shortage of glass eels available for local stock enhancement, the decision of whether restocking is a valuable management tool to increase high-quality silver eel escapement to the sea needs to be evaluated. Organic contaminants, such as polycyclic aromatic hydrocarbons (PAHs), are among the major threats to fish in their habitat. Therefore, the aim of the investigation presented here was to examine metabolites of PAHs in eel bile as one possible marker for habitat quality. In total, 170 yellow eels were collected in the rivers Rhine, Ems, Weser, Elbe, Havel, Schlei, Eider, Trave, Warnow, Peene, Uecker, and Oder in 2009. PAH metabolites in eel bile were analyzed using high-performance liquid chromatography with fluorescence detection. Metabolites of pyrene and phenanthrene were investigated. Concentrations of PAH metabolites in eel bile varied significantly between several rivers, with the highest mean concentrations of 1-hydroxypyrene and 1-hydroxyphenanthrene in eel bile from the river Trave (2421 and 632 ng/ml). Moreover, huge differences in the ratio of 1-hydroxypyrene to 1-hydroxyphenanthrene, with the highest mean value in eel bile from the river Ems (7.43) and the lowest mean value in eel bile from the river Uecker (0.70), indicate different sources of PAH contamination. A comparative analysis of PAH-metabolite contamination of eels in different river systems is seen as a first step toward a classification of freshwater habitats for restocking purposes.     

Smoking and dietary intake of polycyclic aromatic hydrocarbons as sources of interindividual variability in the baseline excretion of 1-hydroxypyrene in urine

Summary Seventy-six male volunteers, who were not occupationally exposed to polycyclic aromatic hydrocarbons (PAHs), participated in a study on the effect of tobacco smoking, alcohol consumption, dietary PAH intake, age, and body fat content on the baseline excretion of 1-hydroxypyrene in urine. Major determinants of urinary 1-hydroxypyrene excretion were smoking, dietary PAH intake, and age. The mean 1-hydroxypyrene concentrations in the urine of the volunteers in this study ranged between 0.05 and 0.79 mol/mol creatinine. Smokers excreted on average 0.25 mol/mol creatinine (range: 0.10–0.79 mol/mol creatinine), and nonsmokers on average 0.12 mol/mol creatinine (range: 0.04–0.29 mol/mol creatinine). The average number of cigarettes smoked per day correlated well with urinary 1-hydroxypyrene concentrations (r _s = 0.67, P < 0.001). The consumption of PAH-containing food products and active smoking account for 99% of total pyrene intake. The effect of age on 1-hydroxypyrene excretion is probably caused by a lower creatinine excretion in the elderly. Passive smoking and fat content had a statistically significant, but negligible effect on urinary 1-hydroxypyrene excretion. Passive smoking and the inhalation of ambient air are relatively inimportant for total pyrene intake (both account for less than 1%). Neither the consumption of alcohol nor the inhalation of ambient air significantly affected urinary 1-hydroxypyrene excretion. It is concluded that when urinary 1-OH-pyrene excretion is used in the assessment of PAH exposure, one should particularly be aware of the interindividual variability of the baseline excretion of PAH metabolites due to tobacco smoking and dietary PAH intake.     

Urinary N -acetyl-β-glucosaminidase as an indicator of renal dysfunction in electroplating workers

Objectives: To investigate chromium-induced renal dysfunction in electroplating workers. Methods: A cross-sectional study was used to evaluate four biochemical markers of renal function. A total of 178 workers were divided into 3 comparable groups consisting of 34 hard-chrome plating workers, 98 nickel-chrome electroplating workers, and 46 aluminum anode-oxidation workers, who represented the reference group. Ambient and biological monitoring of urinary chromium were performed to measure exposure concentrations. Results: Overall, urinary chromium concentrations were highest among hard-chrome plating workers (geometric mean 2.44 μg/g creatinine), followed by nickel-chrome electroplating workers (0.31 μg/g creatinine) and aluminum workers (0.09 μg/g creatinine). Airborne chromium concentrations were also highest in the hard-chrome plating area (geometric mean 4.20 μg/m³), followed by the nickel-chrome electroplating area (0.58 μg/m³) and the aluminum area (0.43 μg/m³). A positive correlation was found between urinary chromium and airborne concentrations (r = 0.54, P < 0.01). Urinary concentrations of N-acetyl-β-d-glucosaminidase (NAG) were also highest among hard-chrome plating workers (geometric mean 4.9 IU/g creatinine), followed by nickel-chrome workers (3.4 IU/g creatinine) and aluminum workers (2.9 IU/g creatinine). The prevalence of “elevated” NAG (>7 IU/g creatinine) was significantly highest among hard-chrome plating workers (23.5%), then among nickel-chrome workers (7.1%) and aluminum workers (8.7%). Differences in β₂-microglobulin, total protein, and microalbumin were not significant. Conclusion: The author's evidence indicates that NAG is an early indicator of renal dysfunction in hard-chrome plating workers.     

Measured exposures by personal monitoring for respirable suspended particles and environmental tobacco smoke of housewives and office workers resident in Bremen, Germany

Objective : Exposures to respirable suspended particles (RSP) and environmental tobacco smoke (ETS) were assessed in Bremen, Germany, as part of a European air quality study. The range and level of personal exposures were assessed for housewives and office workers. Design : Nonsmokers were randomly selected from a representative sample of the population of Bremen. Housewives were recruited into one group primarily for assessment of exposures in the home and office workers, into a second group for assessment of the contribution of the workplace to overall exposure. Methods : A total of 190 subjects collected air samples from areas close to their breathing zone by wearing personal monitors for 24 h. Samples collected were analysed for RSP, ultraviolet-absorbing particulate matter (UVPM), fluorescing particulate matter (FPM), solanesol-related particulate matter (SolPM), nicotine and 3-ethenylpyridine (3-EP). Saliva cotinine levels for all subjects were also established. Results : Overall the levels found were quite low, with the majority of results being below the limit of quantification. Workers both living and working with smokers were exposed to the highest 24-h median quantities of RSP (789 μg) and ETS particles (128 μg) measured by FPM. The highest nicotine levels, based on median 24-h time-weighted average concentrations, were experienced by office workers working with smokers (0.69 μg m⁻³). These workers were also found to have␣the highest median cotinine levels (1.6 ng ml⁻¹). Conclusions: The most highly exposed workers, both living and working with smokers, would potentially inhale over 20 cigarette equivalents (CE) per annum as based on the upper decile levels. Housewives living with smokers could inhale up to 11 CE per annum as based on the upper decile levels. Locations outside the workplace, including the home, contribute most to overall RSP and ETS particle exposure. Consideration should be given to extending the personal monitoring period in cities where levels appear to be quite low. Received: 9 May 1997 / Accepted: 17 October 1997     

Comparison between blood and urinary toluene as biomarkers of exposure to toluene

Objectives: To compare blood toluene (TOL-B) and urinary toluene (TOL-U) as biomarkers of occupational exposure to toluene, and to set a suitable procedure for collection and handling of specimens. Method: An assay based on headspace solid-phase microextraction (SPME) was used both for the determination of toluene urine/air partition coefficient (λ_urine/air) and for the biological monitoring of exposure to toluene in 31 workers (group A) and in 116 non-occupationally exposed subjects (group B). Environmental toluene (TOL-A) was sampled during the work shift (group A) or during the 24 h before specimen collection (group B). Blood and urine specimens were collected at the end of the shift (group A) or in the morning (group B) and toluene was measured. Results: Toluene λ_urine/air was 3.3 ± 0.9. Based on the specimen/air partition coefficient, it was calculated that the vial in which the sample is collected had to be filled up to 85% of its volume with urine and 50% with blood in order to limit the loss of toluene in the air above the specimen to less than 5%. Environmental and biological monitoring of workers showed that the median personal exposure to toluene (TOL-A) during the work-shift was 80 mg/m³, the corresponding TOL-B was 82 μg/l and TOL-U was 13 μg/l. Personal exposure to toluene in environmentally exposed subjects was 0.05 mg/m³, TOL-B was 0.36 μg/l and TOL-U was 0.20 μg/l. A significant correlation (P < 0.05) was observed between TOL-B or TOL-U and TOL-A (Pearson's r=0.782 and 0.754) in workers, but not in controls. A significant correlation was found between TOL-U and TOL-B both in workers and in controls (r=0.845 and 0.681). Conclusion: The comparative evaluation of TOL-B and TOL-U showed that they can be considered to be equivalent biomarkers as regards their capacity to distinguish workers and controls and to correlate with exposure. However, considering that TOL-U does not require an invasive specimen collection, it appears to be a more convenient tool for the biological monitoring of exposure to toluene. Received: 20 October 1999 / Accepted: 4 March 2000     

A comparison of different lead biomarkers in their associations with lead-related symptoms

Objectives: To evaluate whether dimercaptosuccinic acid (DMSA) -chelatable lead, an estimate of current bioavailable lead stores, is a better predictor of lead-related symptoms than are other commonly used lead biomarkers. Methods: A total of 95 male lead workers from three lead industries (one secondary lead smelting facility, one polyvinyl chloride-stabilizer manufacturing plant, and one lead-acid storage battery factory), and 13 workers without occupational lead exposure recruited from an occupational health institute, were studied. Blood lead, blood zinc protoporphyrin (ZPP), 4 h DMSA-chelatable lead (after oral administration of 10 mg/kg DMSA), urine lead, and urinary δ-aminolevulinic acid levels were evaluated as predictors of 15 lead-related symptoms, assessed by self-administered questionnaire, with linear and logistic regression controlling for covariates. Total symptoms and symptoms in three categories (gastrointestinal, neuromuscular, and general) were evaluated. Results: The mean (SD) 4 h DMSA-chelatable lead level was 288.7 (167.7) μg, with a range from 32.4 to 789 μg in the 95 lead workers. The mean (SD) in the non-exposed subjects was 23.7 (11.5) μg with a range from 10.5 to 43.5 μg. Blood lead, blood ZPP, and spot urine lead levels ranged from 21.4 to 78.4 μg/dl, 40 to 331 μg/l, and 7.5 to 153.0 μg/l, respectively, in the lead workers, and from 4.0 to 7.2 μg/dl, 27 to 52 μg/l, and 2.9 to 15.5 μg/l in the non-exposed controls, respectively. The overall mean symptom score (SD), derived as the sum of 0 or 1 point for absence or presence of 15 symptoms, of the lead workers was 3.7 (2.0), compared to 1.2 (1.5) for the non-exposed workers. DMSA-chelatable lead was the best predictor of symptom scores in both crude and adjusted analyses, compared with the other biomarkers. Lead workers with DMSA-chelatable lead values greater than the median (260.5 μg) were 6.2 times more likely to have frequent tingling or numbness of the arms or legs and 3.3 times more likely to have muscle pain than subjects with lower chelatable lead values. Three symptoms (tingling or numbness of arm or leg, muscle pain, and feeling irritation at the slightest disturbance) evidenced a dose-dependent relationship with DMSA-chelatable lead levels. Conclusions: DMSA-chelatable lead was found to be the best predictor of lead-related symptoms, particularly of both total symptom scores and neuromuscular symptoms, than were the other other lead biomarkers. Received: 27 January 1999 / Accepted: 29 January 2000