Ann. occup. Hyg., Vol. 46, No. 2, pp. 229-235, 2002
© 2002 British Occupational Hygiene Society
Published by Oxford University Press
Article |
Urinary 1-Hydroxypyrene as a Biomarker of Internal Dose of Polycyclic Aromatic Hydrocarbons in Carbon Black Workers
1Graduate Institute of Environmental and Occupational Health, Medical College, National Cheng Kung University, 138, Sheng-Li Road, Tainan 70428; 2Southern Labor Inspectory Bureau, Council of Labor Affairs, Executive Yuan. Fl. 7, 386, Chi-Hsien 1st Road, Kaohsiung 80101; 3Department of Environmental Engineering, National Cheng Kung University, 1, University Road, Tainan 70101; 4Institute of Occupational Safety and Health, Council of Labor Affairs, Executive Yuan. 4F, 132, Sec. 3, Ming-Sheng E. Road, Taipei, Taiwan, ROC
Received 11 April 2001; in final form 23 July 2001.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSREFERENCES |
|---|
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.
Keywords: polycyclic aromatic hydrocarbons; 1-hydroxypyrene; carbon black; biological monitoring; pyrene
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSREFERENCES |
|---|
Carbon black is widely used by various industries, including the printing ink, paint, lacquer and rubber industries. The global consumption rate for carbon black was ~1 x 106 tons/yr in 1999 (Poliski, 1999). The consumption rate in Taiwan area was ~1.13 x 105 tons/yr in 1999, of which 1 x 105 tons (~90%) were produced domestically. According to the labor statistics published by the Taiwan government in 1995, ~18 500 workers were potentially exposed to carbon black in either the using or producing industries. The history of manufacture of carbon black has been well documented (Gardiner et al., 1992a). The manufacture involves the thermal combustion of feedstock oil; therefore, semi-volatile organic compounds, such as polycyclic aromatic hydrocarbons (PAHs; including both gaseous PAHs and particle-bound PAHs), are expected to be generated (Flenklach et al., 1988). To date, several PAH species have been classified into probable (2A) or possible (2B) human carcinogens (IARC, 1987). To help carbon black manufacturing industries to initiate an effective exposure abatement program in the future, it is important to know not only workers’ PAHs exposure levels, but also their corresponding internal doses.
Occupational exposures to carbon black for workers in manufacturing industries have been intensively studied by Gardiner et al. (Gardiner et al., 1996). Regarding the internal doses caused by carbon black exposures, only one study has been conducted that aimed to evaluate the feasibility of using urinary 1-hydroxpyrene (1-OHP) as an indicator for assessing the exposures of carbon black workers (Gardiner et al., 1992b). In this study, personal dust exposures (conducted over the whole shift) were used to replace the personal PAH exposures, and only five nonsmoking warehouse workers were investigated. The results showed that the levels of 1-OHP on days after Monday were higher than the level on Monday, which suggested that carbon black exposures could result in the increase of 1-OHP levels. Because of missing data, only the relationship between the week mean dust and week mean 1-OHP levels were examined. Correlation was not statistically significant. The authors explained that this might be due to insufficient individual exposure data to characterize workers’ mean 1-OHP excretions. Because PAHs are semi-volatile, workers might be exposed to not only the particle-bound PAHs but also gaseous PAHs, so dust exposure levels might not be representative of workers’ PAH exposures. In particular, the bioavailability of particle-bound PAHs could be very different from gaseous PAHs, and thus might have different half-lives to the excretion of 1-OHP (Wolff et al., 1989). From this, it is not so surprising to see that no correlation could be found in the above study. In addition to respiratory exposures, Jongeneelen et al. (Jongeneelen et al., 1988) indicated that workers’ internal doses might also be affected by dermal exposures. For coke oven workers, Van Rooij et al. (Van Rooij et al., 1993) reported that the skin contact accounted for ~75% (range = 28–95%) of the total absorbed pyrene. Therefore, it can be expected that taking both respiratory and dermal PAH exposures into account would lead to better explanations of workers" urinary 1-OHP concentrations.
According to a study conducted by Robertson and Smith (Robertson and Smith, 1994), workers in the pelletizing and packaging/stacking areas had the highest exposure levels in the carbon black manufacturing industries. Therefore, only the above two groups of workers were selected for this study. This study is part of our two earlier studies that focused on characterizing inhalable PAH exposure (Tsai et al., 2001a) and dermal PAH exposure (Tsai et al., 2001b) in carbon black workers. Here we summarize both respiratory and dermal PAH exposure assessments, but concentrate on the biological monitoring results used to describe the internal doses, to assess the suitability of using urinary 1-OHP levels when both respiratory and dermal exposure routes are involved.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSREFERENCES |
|---|
Subjects
All workers who performed their job mainly in either the wet pelletizing or packaging area were selected, including eight wet pelletizing workers and 22 packaging workers. The pelletizing workers not only worked in the pelletizing room for monitoring pelletizing machines, but also periodically collected pelletized carbon black for quality control. In addition, they visited the control room for setting and monitoring the operating conditions. The packaging workers worked at the packaging sites, charging carbon black and driving fork-lift trucks for stacking most of the time. However, they also performed other miscellaneous tasks outside the packaging area. For all selected workers, personal background information, including smoking habit, age, sex, body weight and height, were carefully registered and are summarized in Table 1.
|
Sampling strategy
Sampling for personal respiratory exposures
Personal air sampling was conducted on each selected worker for 8 h per day for 5 consecutive days. The sampling method was modified from Method 5515 of the US National Institute for Occupational Safety and Health (NIOSH, 1994). The sampling train contained a filter cassette (IOM personal sampler; SKC Inc., Eighty Four, PA) and was followed by a sorbent tube (washed XAD-2, 3.5 g/0.5 g) with a sampling flow rate of 2 l/min. After sampling, filter cassettes and sorbent tubes were sent to a laboratory for determination of the inhalable particle-bound PAH concentration (Cinh) and gaseous PAH concentration (Cgas), respectively.
Sampling for dermal exposures
A surrogate skin sampling technique was adopted to assess workers’ dermal exposures for 8 h per day for 5 consecutive days. Because of workers’ unwillingness, only two workers were selected from each exposure group. For each selected worker, nine exposure pads (each made of soft polypropylene, with a surface area of 100 cm2) were placed on the skin at nine designated body surface areas: the front head, neck/back, neck/front, back, chest, upper arm, lower arm, upper leg and lower leg. This method was proposed for assessing workers’ pesticide dermal exposure (WHO, 1986; US EPA, 1992), but its use has been extended to assess the exposure to various occupational hazards, including PAHs (Jongeneelen et al., 1988) and dichlorobenzidene (London et al., 1989). The exposure level of each selected worker was first converted to an 8 h exposure level based on his or her average daily dermal exposure duration during the week of work (see Table 1). Here, the daily dermal exposure duration for pelletizing workers was defined as the duration that workers performed their tasks in the pelletizing room, including monitoring the pelletizing machine and periodically collecting pelletized carbon black for quality control. For packaging workers, it was defined as the duration that workers performed their tasks in the packaging room for charging carbon black and driving fork-lift trucks for stacking. The 8 h exposure level was then further converted to the exposure of a standard man based on the body surface areas estimated for the standard man and the worker. Body surface area was estimated according to the Du Bois equation:
body surface area (cm2) = 2020 x height (m)0.725 x weight (kg)0.425
For the standard man, the values of 70 kg and 173 cm were adopted (ISO, 1990). Because only two workers were selected from each exposure group, the two estimated dermal exposure levels for the standard man were averaged and served as a basis for estimating the exposure level of each individual worker (Cskin).
Biological monitoring
Urine samples were collected at the first day pre-shift, first day post-shift and fifth day post-shift (BM1pre, BM1post and BM5post, respectively) to determine their 1-OHP content for each selected worker. A polyethylene bottle, first pretreated with 10% of nitric acid then rinsed with distilled water, was used to collect urine samples. During sampling, all workers were requested to wash their hands prior to urine collection to avoid contamination. Immediately after each urine sample was collected, a 5 ml aliquot was sent to an accredited laboratory to determine its creatinine contents and the rest was stored at –80°C until analysis.
Sample analysis
PAH analyses for air and dermal samples
Both air samples (including the filter cassette and XAD-2 sorbent tube) and dermal samples were analyzed to determine their PAH contents. All collected samples were placed in a solvent solution (a 1:1 vol/vol mixture of n-hexane and dichloromethane), then extracted in a Soxhlet extractor for 24 h. The extract was then concentrated, cleaned-up and re-concentrated to exactly 1.0 or 0.5 ml. PAH content were determined by using a gas chromatograph (GC) (Hewlett-Packard 5890A) with a mass selective detector (Hewlett-Packard 5972) and a computer workstation. The GC/mass spectrometer was equipped with a Hewlett-Packard capillary column (HP Ultra 2: 50 m x 0.32 mm x 0.17 µm) and an HP-7673A automatic sampler. The operating conditions were set as: injection volume = 1 µl; splitless injection temperature = 310°C; ion sources temperature = 310 °C; oven temperature from 50 to 100°C at 20°C /min, from 100 to 290 °C at 3°C /min, then hold at 290°C for 40 min. The masses of primary and secondary ions of PAHs were determined using the scan mode for pure PAH standards. Identification of PAHs was performed using the selected ion monitoring mode.
The concentrations of 21 PAH species were determined. These were naphthalene (Nap), acenaphthylene (AcPy), acenaphthene (Acp), fluorene (Flu), phenanthrene (PA), anthracene (Ant), fluoranthene (FL), pyrene (Pyr), cyclopenta[c,d]pyrene (CYC), benzo[a]anthracene (BaA), chrysene (CHR), benzo[b]fluoranthene (BbF), benzo[k]fluoranthene (BkF), benzo[e]pyrene (BeP), benzo[a]pyrene (BaP), perylene (PER), indeno[1,2,3,-c,d]pyrene (IND), dibenzo[a,h]anthracene (DBA), benzo[b]chrycene (BbC), benzo[g,h,i]perylene (BghiP) and coronene (COR). The detection limit of the method of the 21 PAHs (range = 0.022–0.935ng), recovery efficiencies (range = 0.759–1.070) and analyses of field blanks (no significant contamination) have been described in our earlier studies (Tsai et al., 2001a,b).
Analyses of urinary 1-OHP levels
Each urine sample was analyzed to determine its 1-OHP contents by using the HPLC method developed by Jongeneelen et al. (1987). Prior to analysis, a 10 ml urine sample was adjusted to pH 5.0 by adding a buffer solution of 1 N hydrochloric acid and 0.1 M acetate mixture to a final volume of 30 ml. Then, the sample was incubated for 24 h with 15 µl of glucoronidase-arylsulphatase (134 600 units/ml; Sigma, St Louis, MO; Lot 97H3386) at 37 ± 0.5°C in an electronically controlled rotary shaking bath (Shaker Bath Model 903; Hotech, Taichung, Taiwan). A sample purification and enrichment cartridge, packed with C18 reversed-phase liquid chromatograph material (500 mg/3 ml; Waters, Taunton, MA), was used to extract the metabolites. The flow rate of the treated urine passing through the cartridge was ~3 ml/min. The cartridge was washed with 10 ml of distilled water and 3 ml of 50% methanol in water. Final elution of 1-OHP was performed with 10 ml of methanol. The solution was evaporated to dryness and reconstituted with 2 ml of methanol. The HPLC system, consisting of a high-performance liquid chromatograph with an auto-injector (Hewlett-Packard 1100) and a fluorescence detector (Hewlett HP-1046A), was used in this study for quantification. The extracts (20 µl) were injected onto a 150 x 4.0 mm column (Supelco RP-18), with the column temperature at 40°C and a flow rate of 1.0 ml/min. The excitation wavelength (
ex) of the fluorescence detector was set to 241 nm and the emission wavelength (em) to 395 nm. The detection limit of the method was ~5.43 ng, obtained from seven repeated analyses at a concentration of 15.0 ng/dl. The reproducibility of the method was determined by repeated analysis of urine samples at concentrations ranging from 2.85 to 9.99 µg/dl, and was found to give variation coefficients ranging from 1.87 to 8.40%. To minimize the effect on the variation of the hydration states of workers, the urinary 1-OHP concentrations were calibrated by their corresponding creatinine concentrations (analyzed by an accredited laboratory in Taiwan) and were expressed as µg/g.creatinine.
|
RESULTS AND DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSREFERENCES |
|---|
Personal respiratory exposures
Detailed personal respiratory PAH exposures have been described in our earlier study (Tsai et al., 2001a) and thus are not repeated here. In this study, only the exposure levels of the individual compound pyrene, the sum of seven carcinogenic PAH compounds (
PAHcarci) and total PAHs were summarized. Here, the PAHcarci were defined as the sum of the concentrations of seven PAH compounds with toxic equivalent factors [TEFs; defined by Nisbet and LaGoy (Nisbet and LaGoy, 1992) by reference to the carcinogenic potency of BaP] > 0.01. These include BaP, CHR, BbF, BkF, IND, DBD and ANT. The total PAH exposure level was defined as the sum of the concentrations of the 21 analyzed PAH compounds. The exposure levels summarized in Table 2 include the range and arithmetic mean [AM; calculated according to the method of minimum variance unbiased estimate (MVUE) suggested by Attfield and Hewett (Attfield and Hewett, 1992)]. As shown in Table 2, the total PAH levels for respiratory exposures (= Cgas + Cinh) for pelletizing and packaging workers were 2.60 and 2.92 µg/m3, respectively. The result suggests that both exposure levels were lower than the REL-TWA value (= 100 µg/m3) recommended by US NIOSH. For pelletizing workers, the Cgas:Cinh ratios for pyrene, PAHcarci and total PAHs exposure levels were 1.06 (= 151/142), 0.77 (= 235/301) and 1.17 (= 1400/1200), respectively. For packaging workers, the ratios were 1.03 (= 129/125), 1.32 (= 348/264) and 0.82 (= 1320/1610), respectively. The above results suggest that both particle-bound and gaseous PAHs played an important role in workers’ PAH exposures.
|
Personal dermal exposures
Mean dermal exposure levels estimated for the standard man of both exposure groups have been described in detail in our earlier study (Tsai et al., 2001b). It was concluded that the mean pyrene,
PAHcarci and total PAH dermal exposure levels for pelletizing and packaging exposure workers were 0.112, 0.136 and 1.41 µg/kg body mass/day, and 0.137, 0.486 and 1.61 µg/kg body mass/day, respectively. In this study, the above mean dermal exposure levels were further converted to unit dermal exposure levels based on the Du Bois equation for estimating body surface area. The resultant unit pyrene, PAHcarci and total PAHs dermal exposure levels for the pelletizing workers and packaging workers were 10.90, 1.05 and 0.87 µg/100 cm2 body surface area/day and 12.45, 3.76 and 1.06 µg/100 cm2 body surface area/day, respectively (on an 8 h exposure basis). The dermal exposure levels for each individual worker (µg/day) were thus obtained based on his or her estimated body surface area and dermal exposure duration (see Table 1), and the resultant dermal exposures are summarized in Table 2. The results show that the estimated AM dermal exposure levels in pyrene, PAHcarci and total PAHs for pelletizing workers were 3.72, 7.15 and 46.4 µg/day, respectively, which were consistently lower than those for packaging workers (i.e. 7.22, 25.6 and 85.2 µg/day, respectively), reflecting the lower dermal exposure levels and durations for pelletizing workers.
1-Hydroxypyrene in urine
Table 3 summarizes the BM1pre, BM1post and BM5post urinary 1-OHP concentrations. The results clearly indicate that BM5post > BM1post > BM1pre in both exposure groups. Since both groups of workers were exposed to gaseous PAHs (Cg) and particle-bound PAHs (including Cinh and Cskin) simultaneously, it is necessary to examine the half-life of excretion of 1-OHP caused by both types of PAH exposure before explaining the above results. It has been suggested that the excretion of 1-OHP for gaseous PAH exposures is biphastic, with a half-life for the first phase of 6–34 h (Jongeneelen et al., 1990). This half-life suggests that it is plausible that both BM5post and BM1post should be greater than BM1pre. For inhalatory particle-bound PAH exposures, no half-life has been reported. However, Wolff et al. (Wolff et al., 1989) concluded that the removal rates of nitropyrene (Npyr) in the form of pure aerosol were much shorter than that absorbed by carbon black. Based on this, it can be expected that continuous exposure to particle-bound PAHs via inhalation might lead to the accumulation of PAHs in the human body, and eventually to BM5post > BM1post > BM1pre. At this stage, it might not be able to identify the impact of dermal PAH exposures on the excretion of 1-OHP, partly due to the intrinsic difference in personal hygiene (such as hand washing and showering habit during/after the workshift) among workers. Since pyrene could be absorbed via skin contact, the results obtained from this study could be theoretically plausible.
|
The relationship between urinary 1-OHP and personal PAH exposure levels
Theoretically, for a worker’s urinary 1-OHP level (i.e. the metabolite of the marker compound pyrene) to be used to assess the worker’s internal dose of PAHs, it is necessary for the worker’s pyrene exposure to be representative of the worker’s PAH exposure. For this, it is necessary to test the correlation between workers’ pyrene exposure levels and their corresponding total PAH exposure levels and
PAHcarci exposure levels. This was not possible for dermal exposure because the levels were corrected to the mean exposure level of the standard man (i.e. based on the exposure with the same PAH composition). In this study, Pearson correlation coefficients were calculated between workers’ exposure levels for pyrene, total PAHs and PAHcarci for both gaseous (Cgas) and particle-bound PAHs (Cinh) in both exposure groups. The results show all correlation coefficients were >0.71 (range = 0.71–0.83) (see Table 4). In all cases, the correlation coefficients were significant (Bonferroni-adjusted P < 0.002), so the results suggest that pyrene concentration could be regarded as a suitable indicator for both PAHcarci and total PAH exposures.
|
In this study, BM1post and BM5post were used as dependent variables in a multiple linear regression model in order to assess the effects of various independent variables (including Cg, Cinh and Cskin, worker’s smoking habit, sex and age) on the excretion of urinary 1-OHP. Tables 5 and 6 show the regression results for data obtained from pelletizing workers and packaging workers, respectively. For BM1post, the results show that no regression coefficients were statistically significant (P >> 0.05), and the regression model yielded an R2 of 0.00 for data collected from pelletizing workers (see Table 5). A similar result can also be seen for packaging workers (all regression coefficients with P >> 0.05), and although the regression model yielded a higher R2 (= 0.28), the F ratio (= 2.38) suggests no statistical significance of the regression model (P = 0.08) (see Table 6). The above results might be associated with the long half-life of particle-bound PAHs (which mean that various independent variables cannot explain the small variation in BM1post). For BM5post, the regression analysis yielded an R2 of 0.89 for pelletizing workers; however, neither regression coefficients (P >> 0.05) nor the model itself (F ratio = 15.0, P = 0.08) were statistically significant (see Table 5). Considering that only eight workers were included, the above results could be because data were inadequate to discriminate the contribution of each individual independent variable. For packaging workers (Table 6), since 22 workers were selected, it is not surprising to see that BM5post could be effectively explained by the regression model. The resultant regression coefficients for the independent variables Cgas, Cinh and Cskin were statistically significant (all P < 0.05). The regression coefficients obtained for the independent variables ‘sex’, ‘smoking habit’ and ‘age’ were not statistically significant, so their contribution to the excretion of 1-OHP is relatively small compared with Cgas, Cinh and Cskin. Similar results have also been found in other published studies (Buchet et al., 1992; Ny et al., 1993; Viau et al., 1995). In particular, Viau et al. (Viau et al., 1995) indicated that the contribution of ‘smoking’ on urinary 1-OHP was ~0.105 µg/g creatinine, compared with mean BM5post values for both pelletizing workers and packaging workers of 4.24 and 4.97 µg/g creatinine, respectively (see Table 3).
|
|
|
CONCLUSIONS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSREFERENCES |
|---|
This study shows that exposure to pyrene was statistically significantly correlated with exposure to all PAHs and carcinogenic PAHs, and the relationship with urinary 1-OHP levels indicates the possibility of using urinary 1-OHP levels to characterize workers’ internal doses of PAHs. Because particle-bound PAHs had a long half-life for the excretion of urinary 1-OHP, this study suggests that BM1post is not a feasible indicator. On the other hand, BM5post could be effectively explained by workers’ occupational exposures (including Cg, Cinh and Cskin). The effects of personal background information (including sex, smoking habit and age) on BM5post were not significant. This study suggests that BM5post could be a suitable indicator for internal doses of PAHs.
Acknowledgements—The authors wish to thank the National Science Council in Taiwan for funding this project (grant number: NSC-89-2314-B-006-168).
|
FOOTNOTES |
|---|
* Author to whom correspondence should be addressed. Tel: +886-6-2088391; fax: +886-6-2752484; e-mail: pjtsai{at}mail.ncku.edu.tw
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSREFERENCES |
|---|
Attfield MD, Hewett P. (1992) Exact expressions for the bias and variance of estimators of the mean of a lognormal distribution. Am Ind Hyg Assoc J; 53: 423–35.
Buchet JP, Gennart JP, Mercado-Calderon F, Delavignette JP, Cupers L, Lauwery R. (1992) Evaluation of exposure to polycyclic aromatic hydrocarbons in a coke production and graphite electrode manufacturing plants: assessment of urinary excretion of 1-hydroxypyrene as a biological indicator of exposure. Br J Ind Med; 49: 761–8.[Web of Science][Medline]
Flenklach M, Clary DW, Yuan T, Gardine CW, Stein SE. (1988) Production of polycyclic aromatic hydrocarbons in chlorine containing environments. Combust Sci Technol; 74: 283–92.
Gardiner K, Trethowan WN, Harrington JM, Calvert IA, Glass DC. (1992a) Occupational exposure to carbon black in its manufacture. Ann Occup Hyg; 36: 477–96.
Gardiner K, Hale KA, Calvert IA, Rice C, Harrington JM. (1992b) The suitability of the urinary metabolite 1-hydroxypyrene as an index of polynuclear aromatic hydrocarbon bioavailability from workers exposed to carbon black. Ann Occup Hyg; 36: 681–8.
Gardiner K, Calver IA, van Tongeren MJA, Harrington JM. (1996) Occupational exposure to carbon black in its manufacture: data from 1987–1992. Ann Occup Hyg; 40: 65–77.
IARC. (1987) IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans, supplement 7. Lyons: International Agency for Research on Cancer.
ISO. (1990) ISO 8996: Ergonomics-determination of metabolic heat production. Geneva: International Standard Organization.
Jongeneelen FJ, Anzion BM, Henderson PTh. (1987) Determination of hydroxlated metabolites of polycyclic aromatic hydrocarbons in urine. J Chromatogr; 413: 227–32.[Web of Science][Medline]
Jongeneelen FJ, Scheepers PJT, Groenendijk A, Van Aerts LA, Anzion RBM, Bos RP, Veestra SJ. (1988) Airborne concentrations, skin contamination, and urinary metabolite excretion of polycyclic aromatic hydrocarbons among paving workers exposed to coal tar derived road tars. Am Ind Hyg Assoc J; 49: 600–7.[Web of Science][Medline]
Jongeneelen FJ, van Leeuwen FE, Oosterink S, Anzion RBM, Van der Loop F, Bos RP, Van Veen HG. (1990) Ambient and biological monitoring of coke oven workers: determination of internal dose of PAHs. Br J Ind Med; 47: 454–61.[Web of Science][Medline]
London MA, Boiano JM, Lee SA. (1989) Exposure assessment of 3,3'-dicholorobenzidine. (DCB) at two chemical plants. Appl Ind Hyg; 4: 101–4.
NIOSH. (1994) Manual of analytical methods 5506: polynuclear aromatic hydrocarbons by HPLC. Washington DC: US Department of Health and Human Services, National Institute for Occupational Safety and Health.
Nisbet C, LaGoy P. (1992) Toxic equivalency factors. (TEFs) for polycyclic aromatic hydrocarbons. (PAHs). Regul Toxicol Pharmacol; 16: 290–300.[Web of Science][Medline]
Ny ET, Heederik H, Kromhout H, Jongeneelen F. (1993) The relationship between polycyclic aromatic hydrocarbons in air and in urine of workers in a Soderbeg potroom. Am Ind Hyg Assoc J; 54: 277–84.[Web of Science][Medline]
Poliski I. (1999) Carbon black: the state of art. Modern Paint Coat; 89: 40–1.
Robertson JM, Smith RG. (1994) Carbon black. In Patty’s industrial hygiene and toxicology. New York: John Wiley & Sons.
Tsai P-J, Shieh HY, Lee WJ, Lai SO. (2001a) Characteristics of the exposure profiles for workers exposed to airborne dusts and polycyclic aromatic hydrocarbons. (PAHs) in the carbon black manufacturing industry. J Occup Health; 43: 118–28.
Tsai P-J, Shieh HY, Lee WJ, Lai SO. (2001b) Health-risk assessment for workers exposure to polycyclic aromatic hydrocarbons in a carbon black manufacturing industry. Sci Total Environ; 278: 137–50.[Medline]
US EPA. (1992) Dermal exposure assessment: principles and applications. Washington DC: US Environmental Protection Administration, EPA/600/8-91/011B.
Van Rooij GM, Bodelier-Bade MM, Jogeneelen FJ. (1993) Estimation of individual dermal and respiratory uptake of polycyclic aromatic hydrocarbons in 12 coke oven workers. Br J Ind Med; 50: 623–32.[Web of Science][Medline]
Viau C, Vyskocil A, Martel L. (1995) Background urinary 1-hydroxypyrene levels in non-occupational exposed individual in the province of Quebec, Canada, and comparison with it excretion in workers exposed to PAH mixtures. Sci Total Environ; 163: 191–4.[Medline]
WHO. (1986) World Health Organization field surveys of exposure to pesticide protocol. Toxicol Lett; 33: 223–35.
Wolff RK, Sun JD, Barr EB, Rothenbergs J, Yeh HC. (1989) Lung retention and binding of. (14C)-1 nitropyrene when inhaled by F334 rats as a pure aerosol or adsorbed to carbon black particles. J Toxicol Environ Health; 26: 309–25.[Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||