烹调油烟多环芳烃暴露与职业接触人群DNA氧化性损伤

目的 通过调查不同组别厨师和非暴露组尿中8-羟基脱氧鸟苷(8-OHdG)的排泄量,研究8-OHdG和1-羟基芘(1-OHP)之间的关系.方法 采集不同组别厨师组(n=86)和非暴露对照组(n=36)的尿液样本,观察对象均为年龄22～28岁男性,并有相似的吸烟习惯.在采样之前24 h内,以问卷调查的形式对研究对象的身体健康状况、职业史、吸烟习惯和酒精消费量进行评估.冷藏尿液样本,随后通过高效液相色谱法分析8-OHdG和1-OHP水平.结果 对照组尿液中8-OHdG的排泄量(平均1.2μmo1/mol肌酐,n=36)与厨房里有排烟设备运转的厨师组相似(平均1.5 μmol/mol肌酐,n=45).与对照组相比,接触油烟而排烟设备没有运转的厨师组,其尿8-OHdG的排泄量明显增加(平均2.3 μmol/mol 肌酐,n=18).经多元回归分析,尿ln 1-OHP和ln 8-OHdG的水平仍然呈明显的正相关.结论 接触油烟中的多环芳烃(PAH)或其他化合物可能导致DNA氧化损伤.     

车间二氧化钛接触对职业人群氧化应激水平影响的定群研究

目的 了解职业人群吸入性二氧化钛颗粒的接触水平,探讨其对工人机体氧化应激水平的影响.方法 应用定群设计的研究方法 ,通过问卷调查了解某二氧化钛生产车间成品岗位7名工人的一般信息及职业接触史.观察前后分别采集工人外周静脉血10ml,同时,连续29 d每日班前班后30 min内各采集尿样30 ml(共60 ml),并测定工人每日二氧化钛接触量及车间环境温、湿度.乳胶免疫比浊法测定个体外周血清超敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)水平;酶联免疫吸附法(ELISA)测定尿8-羟基脱氧鸟苷(8-hydroxy-deoxyguanosine,8-OHdG)水平.结果 个体每日接触可吸入性二氧化钛颗粒平均浓度为(1. 194±1.015)mg/m3;观察前后血样中hs-CRP水平分别为(1.13±1.08)、(1.33±1.01)mg/L,差异未见统计学意义(t=-0.848,P=0.425);班前班后尿样中8-OHdG水平分别为(3.51±1.39)、(3.65±1.06)μmol/mol Cr.相关性分析显示,随着二氧化钛颗粒接触浓度的增加,8-OHdG水平班前班后差异呈增大趋势(r=0.192,t=2.09,P=0.039).经班次、工龄、年龄、体质指数(BMI)等调整后,单污染物模型分析未发现二氧化钛浓度与班前班后8-OHdG水平差异存在统计学意义(β=0.288,t=1.940,P=0.055).结论 职业场所可吸入二氧化钛颗粒在所研究浓度范围,尚未发现工人机体DNA氧化应激水平发生明显变化.     

Exposure to traffic exhausts and oxidative DNA damage

Aims: To assess the relations between exposure to traffic exhausts and indicators of oxidative DNA damage among highway toll station workers.

Methods: Cross-sectional study of 47 female highway toll station workers exposed to traffic exhausts and 27 female office workers as a reference group. Exposure assessment was based on average and cumulative traffic density and a biomarker of exposure, urinary 1-hydroxypyrene-glucuronide (1-OHPG). Urinary 8-hydroxydeoxyguanosine (8-OHdG) was used as a biomarker of oxidative DNA damage. Plasma nitric oxide (NO) was measured as an indicator of oxidative stress related to traffic exhaust exposure.

Results: The mean concentration of urinary 8-OHdG was substantially higher among the exposed non-smokers (13.6 µg/g creatinine) compared with the reference non-smokers (7.3 µg/g creatinine; difference 6.3, 95% CI 3.0 to 9.6). The mean concentration of NO among the exposed (48.0 µmol/l) was also higher compared with the reference non-smokers (37.6 µmol/l; difference 10.4, 95% CI –0.4 to 21.2). In linear regression adjusting for confounding, a change in log(8-OHdG) was statistically significantly related to a unit change in log(1-OHPG) (ß = 0.372, 95% CI 0.081 to 0.663).

Conclusions: Results indicate that exposure to traffic exhausts increases oxidative DNA damage. Urinary 8-OHdG is a promising biomarker of traffic exhaust induced oxidative stress.

     

<Emphasis Type="Italic">trans,trans</Emphasis>-Muconic acid excretion in relation to environmental exposure to benzene

OBJECTIVES: Potential environmental sources of benzene exposure, and intake of foods and beverages susceptible to being preserved with sorbic acid, were investigated in relation to their contribution to the inter-individual variation in background urinary trans,trans-muconic acid ( t,t-MA) excretion among subjects non-occupationally exposed to benzene. METHODS: We measured urinary t,t-MA excretion in 65 subjects, 34 women and 31 men. A spot sample of morning urine was collected for each subject 10-12 h after they had consumed their last meal. Questionnaire information was collected on diet and possible sources of environmental benzene exposure in the surroundings of the subjects' residences. For each subject, an estimate of the average daily intake of sorbic acid with diet was calculated, based on questionnaire information and laboratory data on samples of local food items. RESULTS: The t,t-MA geometric mean was significantly higher among women (28.7 vs 11.5 microg/g creatinine, P<0.05) and among smokers (37.6 vs 15.6 microg/g creatinine, P<0.05), and increased by years of education among women, but not among men. In the multivariate analysis, smoking was the only significant predictor of elevated t,t-MA excretion. In our study, the average estimated daily sorbic-acid intake with diet was 0.33 ppm (standard deviation: 0.28), and it did not show a correlation with t,t-MA excretion. Urban traffic and residence within 100 m of a fuel station also did not show an association with elevated t,t-MA values. CONCLUSIONS: Our study confirms that, among subjects non-occupationally exposed to benzene, smoking contributes significantly to increased background t,t-MA excretion. Further studies should be addressed to confirm our observation of elevated t,t-MA levels among women.     

Urinary 8-hydroxydeoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to ethylbenzene

This study assessed the relationships between ethylbenzene exposure and levels of 8-hydroxydeoxyguanosine (8-OHdG) among spray painters. Sixty-four male workers employed at a large shipyard were recruited for this investigation. Fifteen spray painters exposed to paint, together with two non-exposed groups, namely 19 sandblasting workers and 30 office staffs were selected as the subjects. Personal exposure to xylene and ethylbenzene in air were collected using diffusive samplers. Urine samples of the spray painters were collected after a month-long holiday leave and during the pre- and post-workshifts. Urine samples of sandblasting workers and office staffs were gathered after their shift. Urinary mandelic acid and methyl hippuric acid were used as biological indices of dose of ethylbenzene and xylene, respectively. Urinary 8-OHdG was used as biomarker of oxidative DNA damage. The post-workshift concentration of urinary 8-OHdG for 10 spray painters (30.3 ± 9.28 μg g(-1) creatinine) significantly exceeded that of holiday leave (7.20 ± 1.08 μg g(-1) creatinine; P = 0.001). The post-workshift concentration of urinary 8-OHdG was higher among 15 spray painters (29.0 ± 6.52 μg g(-1) creatinine) than sandblasting workers (9.14 ± 2.05 μg g(-1) creatinine; P = 0.01) and office staffs (8.35 ± 0.84 μg g(-1) creatinine; P = 0.007). A stepwise regression model revealed an 8.11 μg g(-1) creatinine increase per 1 p.p.m. increase in ethylbenzene [95% confidence interval (CI) 4.13-12.1]. A stepwise regression model revealed an increase of 6.04 μg g(-1) creatinine (95% CI 2.23-9.84) per 1 p.p.m. in ethylbenzene after adjustment of age (95% CI 2.23-9.84). This pilot study suggests that occupational exposure to paint increases oxidative DNA injury. Moreover, urinary 8-OHdG levels displayed greater DNA damage in spray painters compared to other unexposed groups and their holiday leave samples. A significant correlation was found between urinary 8-OHdG and the exposure to ethylbenzene. The ethylbenzene exposure could not explain all urinary 8-OHdG measured. Other components of paint deserve further investigation.     

吸烟和年龄对电子垃圾拆解工人尿液中8-羟基脱氧鸟苷的影响

目的 研究吸烟和年龄对电子垃圾拆解工人尿液中8-羟基脱氧鸟苷(8-hydroxy-2'-deoxyguanosine,8-OHdG)的影响.方法 采用固相萃取-高效液相色谱电化学检测器(SPE-HPLC-ECD)方法,检测64名电子垃圾拆解男性工人上班前和下班后尿液中8-OHdG浓度.按照吸烟情况和工人的年龄分别对数据进行统计分析.结果 相对于吸烟者(42名),不吸烟者(22名)尿中8-OHdG浓度明显的增高,上班前,不吸烟组的工人尿液中的8-OHdG浓度为(8.25±4.23)μmol/mol肌酐,吸烟组工人尿液中8-OHdG浓度为(5.44±1.18)μmol/mol肌酐,两者差异无统计学意义(t=-0.81,P=0.42).而在下班后,不吸烟组的工人尿液中的8-OHdG浓度为(43.12±16.19)μmol/mol肌酐,大约是吸烟组工人尿液中8-OHdG浓度[(14.82±2.51)μmol/mol肌酐]的3倍.经过1 d暴露下班后,吸烟和不吸烟工人尿液中的8-OHdG浓度差异具有统计学意义(t=-2.33,P<0.05).按照工人的年龄分组,上班前,19岁～(6名)、20岁～(22名)、30岁～(23名)、40～49岁(11名)组工人尿中8-OHdG浓度分别为(1.86±0.66)、(3.57±0.54)、(8.12±4.10)、(11.39±3.70)μmol/mol肌酐,组间差异没有统计学意义(F=0.98,P=0.41);但经过1 d的暴露,下班后,19岁～、20岁～、30岁～、40～49岁组工人尿中8-OHdG浓度分别为(4.19±2.85)、(19.89±5.26)、(28.89±14.61)、(34.94±12.50)μmol/mol肌酐,组间差异具有统计学意义(F=4.81,P=0.03).结论 吸烟对拆解工人尿中8-OHdG浓度有一定的抑制作用,尿中8-OHdG浓度随年龄增高而增加.     

Evaluation to the exposure to polycyclic aromatic hydrocarbons, benzene, toluene and xylenes in workers in a power plant fueled with heavy oil]

Occupational exposure to polycyclic aromatic hydrocarbons (PAHs) has been demonstrated in many industrial sectors. However, up to date there are few studies in the literature on PAH exposure in thermoelectric power plants. The study was aimed at the evaluation of personal exposure to PAHs in workers of a power plant fueled with heavy oil. Exposure to polycyclic aromatic hydrocarbons (PAHs) and to benzene, toluene and xylenes (BTX) was evaluated on power plant workers exposed to heavy fuel oil; the control group consisted of office workers of the same power plant. Altogether 39 subjects were studied, for a total of 84 days of monitoring. Personal environmental exposure, cutaneous exposure and urinary concentrations of 1-hydroxypyrene (1-OHP), trans,trans-muconic acid (TTMA) and nicotine were measured. Personal environmental exposure to PAHs was very low; only maintenance workers showed exposure to total carcinogenic PAHs significantly higher than controls (median levels 3.05 and 0.88 ng/m3 respectively). All workers showed very low levels of dermal exposure to PAHs (less than 1 ng). The median 1-OHP urinary concentrations were 0.16, 0.11 and 0.08 mumol/mol creatinine in the groups of exposed workers and 0.08 mumol/mol creatinine in the control group. Neither the exposed workers nor the controls showed a significant increase in 1-OHP urinary concentrations across the shift. The regression analysis showed a significant effect of cigarette smoking on urinary 1-OHP, while no association was observed between occupational exposure and diet. Personal environmental exposure levels to BTX were very low. TTMA urinary concentrations of the exposed subjects were similar to those of the controls. No significant increase in the TTMA urinary concentrations was observed across the shift and, as expected, smokers showed higher values than non-smokers. The study did not show a measurable intake of PAHs and BTX in power plant workers that could be ascribed to occupational exposure, thus confirming the efficacy of the protective measures in force.     

焦炉工人血清谷胱甘肽硫转移酶活力和尿8-羟基脱氧鸟苷水平

目的 探讨血清谷胱甘肽硫转移酶（GST）和尿8-羟基脱氧鸟苷（8-OHdG）作为焦炉工人多环芳烃（PAHs）暴露生物监测标志的可行性.方法 用高效液相色谱-电化学方法和试剂盒分别检测47名男性焦炉工和31名男性对照者尿8-OHdG水平和血清GST活力;尿1-羟基芘（1-OHP）作为PAHs接触的内暴露标志,采用碱水解-高效液相色谱方法分析.结果 焦炉工人尿1-OHP浓度的中位数（P25～P75）为[5.7（1.4～12.0）μmol/mol Cr],血清GST活力为[22.1（14.9～31.2）U/ml],尿8-O-HdG水平为[1.9（1.4～15.4）μmol/mol Cr],均高于对照组工人[3.0（0.5～6.4）μmol/mol Cr、13.1（9.5～16.7）U/ml、1.3（1.0～4.0）μmol/mol Cr],差异均有统计学意义（P＜0.05或P＜0.01）.以吸烟分层,两组工人尿1-OHP浓度和血清GST活力仅在吸烟者中、尿8-OHdG水平仅在非吸烟者中差异有统计学意义（均P＜0.01）.焦炉工人血清GST活力和尿1-OHP浓度呈正相关（rs=0.31,P＜0.01,n=78）.多元Logistic回归分析显示,与对照工人相比,焦炉工人血清GST活力＞16.7 U/ml和尿8-OHdG水平＞1.8 μmol/mol Cr的OR值分别为13.2和4.4;高体重指数是影响尿8-OHdG水平下降的独立因素.结论 焦炉工人血清GST活力增强和氧化性DNA损伤增加,吸烟和职业暴露有交互作用;血清GST有可能作为PAHs暴露评价的生物标志;尿8-OHdG检测有助于焦炉工肺癌危险度评价.     

Biological monitoring of polycyclic aromatic hydrocarbon exposure in a highly polluted area of Poland.

Air pollution in Poland and particularly in Silesia is among the worst in Europe. Many coal mines and coke oven plants are located in this area, representing a major source of carcinogenic polycyclic aromatic hydrocarbons (PAHs). We quantitated the PAH exposure level in air samples using personal sampling devices, collected urine samples from the same individuals, and measured 1-hydroxypyrene with high performance liquid chromatography. Samples were collected twice, once in February and once in September. Mean PAH level of samples collected at three different coke oven plants varied from 2.3 micrograms/m3 to 12.3 micrograms/m3; the lowest mean was in September. Mean levels of 0.15 micrograms/m3 (September) and 0.44 micrograms/m3 (February) were noted for the environmentally exposed group. Mean urinary 1-hydroxypyrene varied from 2.45 to 13.48 mumol/mol creatinine at the three coke oven plants. The corresponding variation between the three different environmentally exposed groups in Silesia was 0.41-1.54 mumol/mol creatinine. In the nonindustrialized area, the mean varied from 0.20 to 0.14 mumol/mol creatinine. Seasonal variation was found both at the coke oven plants and in the environmental exposed groups in Silesia. Both PAH levels and 1-hydroxypyrene varied seasonally among coke oven workers and the environmentally exposed group. Our study shows that PAH exposure in the industrialized area of Silesia is high compared to levels in Western Europe. 1-Hydroxypyrene excretion in environmentally exposed individuals in Poland is among the highest in Europe.     

Exposure to toluene increases the urinary excretion of D-glucaric acid

Workers at a printing plant exposed to low concentrations of toluene (43-401 mg/m3, median 155 mg/m3) had increased urinary D-glucaric acid (3.55-5.12 mmol/mol creatinine) excretion at the end of the shift compared with controls (2.45-3.35 mmol/mol creatinine). No increase was found after the summer holiday (1.92-2.89 mmol/mol creatinine) but excretion had increased two weeks later (4.05-5.55 mmol/mol creatinine). These changes in the excretion of D-glucaric acid were not correlated to levels of exposure, to changes of urinary hippuric acid and o-cresol half lives (three to eight hours), nor to o-cresol/hippuric acid concentration ratios when measured at the end of daily exposure. Since a significant intra and interindividual variability of urinary D-glucaric acid was found in all groups, urinary D-glucaric acid excretion is suitable to monitor group but not individual exposure.     

Exposure to toluene increases the urinary excretion of D-glucaric acid.

Workers at a printing plant exposed to low concentrations of toluene (43-401 mg/m3, median 155 mg/m3) had increased urinary D-glucaric acid (3.55-5.12 mmol/mol creatinine) excretion at the end of the shift compared with controls (2.45-3.35 mmol/mol creatinine). No increase was found after the summer holiday (1.92-2.89 mmol/mol creatinine) but excretion had increased two weeks later (4.05-5.55 mmol/mol creatinine). These changes in the excretion of D-glucaric acid were not correlated to levels of exposure, to changes of urinary hippuric acid and o-cresol half lives (three to eight hours), nor to o-cresol/hippuric acid concentration ratios when measured at the end of daily exposure. Since a significant intra and interindividual variability of urinary D-glucaric acid was found in all groups, urinary D-glucaric acid excretion is suitable to monitor group but not individual exposure.     

Methodological issues in biomonitoring of low level exposure to benzene

Data from a pilot study on unmetabolized benzene and trans,trans muconic acid (t,t-MA) excretion in filling station attendants and unexposed controls were used to afford methodological issues in the biomonitoring of low benzene exposures (around 0.1 ppm). Urinary concentrations of benzene and t,t-MA were measured by dynamic head-space capillary GC/FID and HPLC, respectively. The accuracy of the HPLC determination of t,t-MA was assessed in terms of inter- and intra-method reliability. The adequacy of urinary t,t-MA and benzene as biological markers of low benzene exposure was evaluated by analysing the relationship between personal exposure to benzene and biomarker excretion. Filling station attendants excreted significantly higher amounts of benzene, but not of t,t-MA, than controls. Adjusting for occupational benzene exposure, smokers excreted significantly higher amounts of t,t-MA, but not of unmetabolized benzene, than nonsmokers. A comparative analysis of the present and previously published biomonitoring surveys showed a good inter-study agreement regarding the amount of t,t-MA and unmetabolized benzene excreted (about 0.1-0.2 mg/l and 1-2 micrograms/l, respectively) per unit of exposure (0.1 ppm). For each biomarker, based on the distribution of parameters observed in the pilot study, we calculated the minimum sample size required to estimate the population mean with given confidence and precision.     

Chromium (VI) induced oxidative damage to DNA: increase of urinary 8-hydroxydeoxyguanosine concentrations (8-OHdG) among electroplating workers

Aims: To investigate the concentration of urinary 8-hydroxydeoxyguanosine (8-OHdG) among electroplating workers in Taiwan.

Methods: Fifty workers were selected from five chromium (Cr) electroplating plants in central Taiwan. The 20 control subjects were office workers with no previous exposure to Cr. Urinary 8-OHdG concentrations were determined using high performance liquid chromatography with electrochemical detection.

Results: Urinary 8-OHdG concentrations among Cr workers (1149.5 pmol/kg/day) were higher than those in the control group (730.2 pmol/kg/day). There was a positive correlation between urinary 8-OHdG concentrations and urinary Cr concentration (r = 0.447, p < 0.01), and urinary 8-OHdG correlated positively with airborne Cr concentration (r = 0.285). Using multiple regression analysis, the factors that affected urinary 8-OHdG concentrations were alcohol, the common cold, and high urinary Cr concentration. There was a high correlation of urinary 8-OHdG with both smoking and drinking, but multiple regression analysis showed that smoking was not a significant factor. Age and gender were also non-significant factors.

Conclusion: 8-OHdG, which is an indicator of oxidative DNA damage, was a sensitive biomarker for Cr exposure.

     

Biological monitoring of environmental exposure to PAHs in the vicinity of a S?derberg aluminium reduction plant.

OBJECTIVES: To assess environmental exposure to polycyclic aromatic hydrocarbons (PAHs) in the vicinity of a Söderberg aluminium reduction plant in Shawinigan, Canada with urinary 1-hydroxypyrene (1-OHP) as a biomarker. METHODS: Urine samples were collected from 20 non-occupationally exposed subjects living less than 500 m from the plant and from 20 controls living in Trois-Rivières, another industrial town 40 km from Shawinigan. Concentrations of 1-OHP were measured by high performance liquid chromatography (HPLC). RESULTS: Among controls, geometric mean (range) 1-OHP concentrations were 0.046 (0.012-0.116) mumol/mol creatinine in non-smokers and 0.125 (0.051-0.282) mumol/mol creatinine in smokers. Among exposed subjects, values were 0.103 (0.056-0.196) mumol/mol creatinine in non-smokers and 0.250 (0.112-0.448) mumol/mol creatinine in smokers. Excretion of 1-OHP was significantly higher in exposed subjects than in controls among non-smokers and smokers (P < 0.05). CONCLUSION: Based on urinary 1-OHP as a biomarker, it seems that living near an industrial point source of PAHs is associated with higher exposure. The health significance of this finding will require further investigation.     

Biological monitoring of occupational exposure to tetrahydrofuran

Occupational exposure to tetrahydrofuran (THF) was studied by analysis of environmental air, blood, alveolar air, and urine from 58 workers in a video tape manufacturing plant. Head space gas chromatography (GC) with an FID detector was used for determination of THF concentration in alveolar air, urine, and blood. Environmental exposure to THF was measured by personal sampling with a carbon felt passive dosimeter. When the end of shift urinary THF concentrations were compared with environmental time weighted average (TWA) values, urinary THF concentration corrected for specific gravity correlated well with THF concentration in air (r = 0.88), and uncorrected urinary THF concentration gave a similar result (r = 0.86). Correction for creatinine in urine weakened the correlation (r = 0.56). For exposure at the TWA concentration of 200 ppm the extrapolated concentration of THF was 33 mumol/l in blood and 111.9 mumol/l (61 mumol/g creatinine) or 109 mumol/l at a specific gravity of 1.018 in urine. The correlation between exposure to THF and its concentration in exhaled breath and blood was low (r = 0.61 and 0.68 respectively). Laboratory methodological considerations together with the good correlation between urinary THF concentration and the environmental concentration suggest that THF concentration in urine is a useful biological indicator of occupational exposure to THF.     

Biological monitoring of occupational exposure to tetrahydrofuran.

Occupational exposure to tetrahydrofuran (THF) was studied by analysis of environmental air, blood, alveolar air, and urine from 58 workers in a video tape manufacturing plant. Head space gas chromatography (GC) with an FID detector was used for determination of THF concentration in alveolar air, urine, and blood. Environmental exposure to THF was measured by personal sampling with a carbon felt passive dosimeter. When the end of shift urinary THF concentrations were compared with environmental time weighted average (TWA) values, urinary THF concentration corrected for specific gravity correlated well with THF concentration in air (r = 0.88), and uncorrected urinary THF concentration gave a similar result (r = 0.86). Correction for creatinine in urine weakened the correlation (r = 0.56). For exposure at the TWA concentration of 200 ppm the extrapolated concentration of THF was 33 mumol/l in blood and 111.9 mumol/l (61 mumol/g creatinine) or 109 mumol/l at a specific gravity of 1.018 in urine. The correlation between exposure to THF and its concentration in exhaled breath and blood was low (r = 0.61 and 0.68 respectively). Laboratory methodological considerations together with the good correlation between urinary THF concentration and the environmental concentration suggest that THF concentration in urine is a useful biological indicator of occupational exposure to THF.     

尿中苯巯基尿酸的高效液相色谱-质谱测定方法

目的 研制我国职业接触苯工人尿中苯巯基尿酸(SPMA)的生物限值.方法 在苯作业车间选择空气中苯浓度在32.5 mg/m~3以下接苯工人55人,应用个体采样器采集空气样品,用气相色谱法检测作业者个体苯接触水平,同时采集当日工人班后尿,应用高压液相色谱/质谱法(HPLC/MS)测定尿中SPMA含量以评价苯接触者的内暴露水平,内外暴露水平的比较用相对内暴露指数(RIE)加以评定.结果 接苯工人工作环境空气苯浓度范围为0.71～32.17 mg/m~3,几何平均浓度为6.98 mg/m~3,中位数为7.50 mg/m~3,尿中SPMA与个体苯暴露量存在良好的线性关系Y(μg/g Cr)=-8.625+18.367 X(mg/m~3),r=0.8035(P<0.01);将我国职业苯接触限值时间加权平均容许浓度(PC-TWA=6 mg/m~3)代入回归方程,推算工作班后尿中SPMA含量为101.58μg/g Cr.计算的RIE指数显示,接触1 mg/m~3苯可平均代谢转化为尿中SPMA 18.23 μg/g Cr,并且随接苯水平的上升其代谢转化效率呈下降趋势.结论 参考国外SPMA生物限值标准,建议我国职业接触苯生物限值班后尿中SPMA为100μg/gCr(47μmol/mol Cr).     

Urinary 1-hydroxypyrene-glucuronide as a biomarker of exposure to various vehicle exhausts among highway toll-station workers in Taipei, Taiwan

In this cross-sectional study, the authors evaluated urinary 1-hydroxypyrene-glucuronide (1-OHP-gluc) as a potential biomarker of exposure to various traffic exhausts. Subjects were 47 female highway toll-station workers and 27 female office workers in training for toll-station employment in Taipei, Taiwan. The mean concentration of urinary 1 -OHP-gluc was 0.117 micromol/mol creatinine in the exposed group and 0.073 micromol/mol creatinine in the reference group (difference in mean concentrations: 0.044 micromol/mol creatinine [95% confidence interval [CI]: 0.015, 0.072). In the lanes where tolls were collected from passenger cars, there was a significant relationship between cumulative traffic and 1-OHP-gluc concentration (i.e., average increase of 0.015 micromol/mol creatinine [95% CI: 0.003, 0.027] per 1,000 vehicles). The average increase for truck/bus lanes was similar to that identified for the car lanes (i.e., average increase of 0.011 micromol/mol creatinine [95% Cl: -0.024, 0.045] per 1,000 vehicles). The authors determined that exposure to various traffic exhausts increased the urinary concentration of 1-OHP-gluc in a dose-response pattern, which suggests that this chemical may be a useful biomarker for exposure to vehicle exhausts.     

Application of the urinary S-phenylmercapturic acid test as a biomarker for low levels of exposure to benzene in industry.

Recently, the determination of S-phenylmercapturic acid (S-PMA) in urine has been proposed as a suitable biomarker for the monitoring of low level exposures to benzene. In the study reported here, the test has been validated in 12 separate studies in chemical manufacturing plants, oil refineries, and natural gas production plants. Parameters studied were the urinary excretion characteristics of S-PMA, the specificity and the sensitivity of the assay, and the relations between exposures to airborne benzene and urinary S-PMA concentrations and between urinary phenol and S-PMA concentrations. The range of exposures to benzene was highest in workers in chemical manufacturing plants and in workers cleaning tanks or installations containing benzene as a component of natural gas condensate. Urinary S-PMA concentrations were measured up to 543 micrograms/g creatinine. Workers' exposures to benzene were lowest in oil refineries and S-PMA concentrations were comparable with those in smoking or nonsmoking control persons (most below the detection limit of 1 to 5 micrograms/g creatinine). In most workers S-PMA was excreted in a single phase and the highest S-PMA concentrations were at the end of an eight hour shift. The average half life of elimination was 9.0 (SD 4.5) hours (31 workers). Tentatively, in five workers a second phase of elimination was found with an average half life of 45 (SD 4) hours. A strong correlation was found between eight hour exposure to airborne benzene of 1 mg/m3 (0.3 ppm) and higher and urinary S-PMA concentrations in end of shift samples. It was calculated that an eight hour benzene exposure of 3.25 mg/m3 (1 ppm) corresponds to an average S-PMA concentration of 46 micrograms/g creatinine (95% confidence interval 41-50 micrograms/g creatinine). A strong correlation was also found between urinary phenol and S-PMA concentrations. At a urinary phenol concentration of 50 mg/g creatinine, corresponding to an eight hour benzene exposure of 32.5 mg/m3 (10 ppm), the average urinary S-PMA concentration was 383 micrograms/g creatinine. In conclusion, with the current sensitivity of the test, eight hour time weighted average benzene exposures of 1 mg/m3 (0.3 ppm) and higher can be measured.     

Urinary excretion of O-cresol and hippuric acid after toluene exposure in rotogravure printing

Summary In 62 male rotogravure printers, the time-weighted average (TWA) toluene exposure during one workweek ranged from 8 to 496 mg/m³ (median 96). Post-shift urinary excretion of hippuric acid showed a poor correlation with the air toluene concentration. Level of o-cresol excretion ranged from 0.08 to 2.37 mmol/mol creatinine and was associated with the exposure (r _s = 0.57, P<0.0001), although the variation was considerable. However, this metabolite was significantly influenced by smoking habits, both in the workers (0.34 vs 0.10 mmol/mol creatinine after adjustment to zero exposure for the smokers and non-smokers, respectively; P = 0.03) and in 21 unexposed controls (0.18 vs 0.06 mmol/mot creatinine; P = 0.002). The excretion of these metabolites was followed during vacation, when the workers were unexposed. The shared one-compartment half-time was 44h (± SE 30, 82). After 2–4 weeks of vacation, the concentration of o-cresol was significantly higher for the smokers than the non-smokers (0.14 vs 0.06 mmol/mol creatinine; P = 0.02).No smoking-associated difference was found for the urinary hippuric acid concentration. However, there was an association between alcohol consumption and hippuric acid excretion (P = 0.03); no such difference was shown for o-cresol. These results demonstrate that hippuric acid excretion is unsuitable for biological monitoring of toluene exposure when the exposure level is below 200 mg/m³. Also, in spite of the favourable excretion kinetics, the impact of smoking and the large interindividual variation warrant the same conclusion for o-cresol as a means of monitoring low level exposure in an individual worker.