砷暴露母子砷代谢特点及DNA损伤差异

目的通过尿中各种形态砷水平，探讨高砷暴露下儿童砷代谢特点；测定尿中8-羟基脱氧鸟苷（8-O-HdG）水平。初步探讨砷暴露对儿童DNA的损伤情况；并比较砷暴露对儿童与成人的不同影响。方法以氢化物发生．冷原子捕获．原子吸收分光光度法测定尿中各种砷化物的含量；以试剂盒法测定尿8-OHdG水平。结果砷暴露组妇女和儿童尿中无机砷（iAs）、二甲基砷（MMA）、甲基砷（DMA）及总砷（tAs）水平均显著高于对照组；砷暴露母子间，子女尿中iAs、DMA、tAs及DMA／tAs水平显著高于其母亲，而MMA／（MMA＋DMA）显著低于其母亲。母子间8-O-HdG水平差异无统计学意义。结论高砷暴露下，儿童二甲基化能力高于成人，DNA氧化损伤与成人相比不明显。     

2型糖尿病患者血尿酸和尿白蛋白排泄率的关系

目的 评价2型糖尿病患者血尿酸和尿白蛋白排泄率（UAER）之间的相关性。方法 将356例2型糖尿病患者依据UAER进行分组：UAER〈20μg／min为无白蛋白尿组（182例），UAER20-199μg／min为微量白蛋白尿组（120例），UAER≥200μg／min为大量白蛋白尿组（54例），并对血尿酸、UAER及相关临床资料进行分析。结果 无白蛋白尿组、微量白蛋白尿组、大量白蛋白尿组的平均血尿酸水平分别为（268±77）μmol／L、（298±90）μmol／L、（363±113）μmol／L（P〈0．05）。将血尿酸值从小到大排序，四分位后分别为（220±36）μmol／L（107-255μmol／L）、（287±24）μmol／L（256-315μmol／L）、（333±54）μmol／L（316-363μmol／L）、（416±65）μmol／L（364-613μmol／L），相应的白蛋白尿（包括微量白蛋白尿和大量白蛋白尿）的患病率分别为32．5％、46．2％、48．7％、59．2％（P〈0．01）。Pearson相关分析发现，UAER与血尿酸呈正相关（r=0．221，P〈0．05），另外还与体重指数、血甘油三酯呈正相关。调整年龄、性别、体重指数、高血压病史、胰岛素应用、吸烟、糖尿病病程、收缩压、舒张压、空腹血糖、血总胆固醇、血甘油三酯等因素后，血尿酸是白蛋白尿的独立危险因素（OR=1．56，P〈0．01）。结论 2型糖尿病患者血尿酸与UAER独立相关。     

内蒙地区水砷和人体血、尿砷含量的测定

目的：通过对内蒙地区（对照区和患病区）的水砷和人体血、尿砷含量的测定，进一步了解内蒙巴盟地区砷地方病对人体的危害及暴露水平。方法：0．5ml血样，5．0ml尿样用4＋1HNO3＋HCIO4消化，用原子荧光分光光度计测定，水样用石墨炉原子吸收法进行测定。结果：对照区人群血砷、尿砷含量的几何均值分别为1．98μg／L和11．02μg／L，病区血砷、尿砷含量的几何均值分别为16．04μg／L和135．64μg／L，病区地区人群血、尿砷明显高于对照区人群血砷、尿砷含量。对照地区水中砷含量为0．0151mg／L，病区水中砷含量为0．268mg／L，病区水砷含量明显高于对照区水砷含量。结论：本试验报告的方法灵敏度高，测定结果准确，适合对大批量样品进行流行病学调查。     

内蒙古不同浓度砷暴露人群尿砷代谢产物研究

目的 测定内蒙古地区饮用高砷水人群尿砷代谢产物，探讨不同人群砷代谢的特点。方法 采用氢化物发生原子吸收分光光度法检测尿中不同形态的砷代谢产物。结果 2个暴露组人群尿中无机砷（iAs，inorganic arserlic）、甲基砷（MMA，monomethylarsine）、二甲基砷（DMA．dimethylarsine）和总砷（TAs，total arserlic）均高于对照组（P〈0．05）；同样砷暴露水平下，尿中各形态砷含量及其相对比在不同性别问的差异均无统计学意义（P〉0．05），儿童DMA／MMA和DMA％高于成人（P〈0．05），MMA％低于成人（P〈0．05）；2个暴露组儿童、成人分别与对照组比较，暴露组MMA／ias、DMA／MMA、DMA／iAs、DMA％显降低（P〈0．05），而iAs％、MMA％显增高（P〈0．05）；高暴露组与低暴露组相比，儿童DMA／MMA、DMA／iAs、DMA％显增高（P〈0．05），iAs％、MMA％显降低（P〈0．05）。结论 相同砷暴露水平下，男女对砷的甲基化能力无差别，儿童二甲基化能力高于成人。高砷暴露可能降低人群对砷的生物甲基化能力。[编按]     

亚急性与慢性砷暴露人群尿砷和8-羟基脱氧鸟苷含量的比较

目的比较亚急性与慢性砷暴露人群尿砷水平、砷形态分布和DNA氧化损伤的情况。方法选择2004年12月阜新市亚急性砷中毒事件发生时阜新市中心医院收治的65名男性患者(年龄为20～62岁,水砷含量达48.5 mg/L,连续暴露4～7 d)为亚急性砷暴露组,慢性高砷(男性72人,年龄为18～73岁,水砷浓度为0.24 mg/L,暴露6 a)、低砷暴露人群(男性40人,年龄为18～60岁,水砷浓度为0.02 mg/L,暴露10 a,无砷中毒相关临床症状)均选自内蒙古呼和浩特市周边砷暴露区。采集亚急性砷暴露人群确诊入院且未采取治疗措施时的尿样,采集慢性砷暴露人群即时尿样。采用超低温捕集-氢化物发生-原子吸收分光光度法测定尿中不同形态砷含量,用酶联免疫法分析尿8-羟基脱氧鸟苷(8-OHdG)水平。结果3种不同砷暴露人群尿中总砷水平和不同形态砷水平均随着砷暴露剂量的升高呈升高趋势:亚急性砷暴露组>慢性高砷暴露组>慢性低砷暴露组,且差异均有统计学意义(P<0.05)。各组尿中无机砷、一甲基砷和二甲基砷含量占总砷含量的构成比(iAs%,MMA%和DMA%)间比较,差异均有统计学意义(P<0.05)。iAs%和MMA%在亚急性砷暴...     

砷职业暴露员工尿中价态砷含量与健康相关因素的分析

目的通过职业砷暴露水平与尿中总砷（TAs）和尿价态砷含量的测定,初步分析体内砷代谢产物（价态砷）与健康相关生化指标之间的关联性。方法选择2家有色金属冶炼企业砷暴露作业工人（暴露组）137人,其中砷暴露锡冶炼组97人、铅冶炼组40人。对照组为无砷接触者42人。暴露组及对照组均进行健康监护及收集晨尿,行尿中TAs及尿价态砷含量测定,并检测作业场所空气中砷及其化学物浓度,进行尿中TAs、价态砷与健康相关因素之间的相关分析。结果两厂砷暴露工作环境空气中含TAs浓度（中位数）为0．30（0．01—1．35）mg／m3。其中铅冶炼厂砷浓度为0．46（0．01—1．03）mg／m3,锡冶炼厂砷浓度为0．26（0．06—1．35）mg／m3。暴露组的TAs、二甲苯呻酸监（DMA）含量与对照组比较,差异有统计学意义（P〈0．01）;暴露组TAs与DMA之间呈正相关（相关系数r=0．693,P〈0．01）;DMA与丙氨酸转氨酶、天冬氨酸转氨酶（ALT、AST）之间呈正相关关系（r=0．148,P〈0．05、r=0．268,P〈0．01）、与血常规RBC、HGB呈负相关（r=-0．165,P=0．038、r=-0．149,P=0．015）。结论砷暴露作业工人在无机砷较高浓度下作业,体内无机砷甲基化后主要的代谢产物为DMA与MMA,且价态砷特别是DMA与TAs、ALT、AST呈正相关、与RBC、HGB呈负相关,说明DMA对肝细胞、红细胞存在一定损害作用。     

急性早幼粒白血病(APL)病人服用硫化砷后的血尿发砷测定

目的 :通过对急性早幼粒白血病 (APL)病人服用硫化砷后的血、尿及发中砷浓度进行测定 ,对急性早幼粒白血病人服用硫化砷后体内砷吸收及蓄积水平进行评估。方法 :氢化物 -原子吸收法。结果 :服药期病例服用硫化砷 1 .5 g以上 ,服药 8d以上 ,血砷平均水平为 5 3 .0±2 2 .5 (n=48) μg/L(1 4.7～ 1 40 .4μg/L) ,尿砷平均水平为 1 73 3 .6± 1 3 6 5 .9(n=44) μg/L(3 92 .6～ 6 847.1μg/L) ,尿砷排出量为 3 .93± 2 .44(n=3 2 ) mg/d(1 .1 4～ 1 1 .8mg/d)。停药期病例 ,停药 8d以上 ,血砷平均水平为 1 5 .3± 8.8(n=5 7)μg/L(2 .0～ 43 .5μg/L) ,尿砷平均水平为 2 3 2 .9± 2 5 7.3 (n=5 2 )μg/L (8.8～ 1 1 6 0 .7μg/L) ,尿砷排出量为 0 .3 3± 0 .3 0 (n=3 2 )mg/d(0 .0 1 9～ 1 .3 mg/d)。服药期病例血砷水平、尿砷水平及尿砷排出量水平均明显高于停药期病例 (P<0 .0 1 )。结论 :服用硫化砷 1 .5 g以上 ,服药 8d以上的服药期病例砷的吸收量为5 .6 1± 3 .48mg/d,停药 8d以上的停药期病例仍有部分砷蓄积于体内     

职业性镉接触工人尿镉含量的影响因素

目的分析镉接触工人的尿镉含量的影响因素。方法选取无锡某电池厂的镉接触工人437名为接触组,另选取782名未接触镉的工人作为对照组,分析2组人群的尿镉含量水平,同时对此镍镉电池厂进行劳动卫生学调查。结果工作场所中镉及其化合物的短时间接触浓度范围为0．002～3．058mg／m3,超标率为87．5％。接触组尿镉含量（中位数1．4300μmol／mol肌酐）明显高于对照组（中位数0．7300μmol／mol肌酐）,高浓度接触组的尿镉含量（中位数1．7500μmol／mol肌酐）明显高于低浓度接触组（中位数1．2450μmol／mol肌酐）,高浓度接触组的尿镉异常率（6．40％）也明显高于低浓度接触组（2．14％）。对照组和接触组中女性尿镉含量明显高于男性;多元线性回归分析结果显示,车间空气中镉暴露水平、工龄和年龄与尿镉含量的相关系数依次为0．851、0．630和0．038。结论工作场所中镉及其化合物浓度超标、工龄的增加是尿镉含量升高的主要因素,降低工作场所空气中镉及其化合物的浓度至职业接触限值以下和减少接触时间是预防慢性镉中毒的关键。     

无机砷对Chang肝细胞株血红素单加氧酶-1 mRNA和蛋白表达的诱导作用

[目的]观察亚砷酸钠（sodium arsenite,NaAsO2）对Chang肝细胞株血红素单加氧酶-1（heme oxygenase-1,HO-1）mRNA和蛋白表达的诱导作用。[方法]以5μmol／L和10μmol／L的NaAsO2作用Chang肝细胞株2、6、12h和24h,分别用逆转录-聚合酶链反应（RT-PCR）和Western Blot法检测细胞内HO-1的mRNA和蛋白表达情况。[结果]5μmol／L和10μmol／LNaAs02暴露2h开始出现HO-1mRNA的诱导表达;6h的表达水平明显高于对照组和2h暴露组（P〈0．01）。其中,10μmol／LNaAsO2暴露12h和24h的mRNA表达均明显高于该浓度的6h暴露组（P〈0．01）;但24h的HO-1 mRNA表达水平与12h组相比没有明显升高。NaAsO2暴露诱导的HO-1蛋白表达则从6h开始出现,12h组明显高于6h组,24h组明显高于12h组（均P〈0．01）;5μmol／L和10μmol／L NaAsO2分别暴露6、12h和24h的HO-1蛋白表达量分别是对照组的2．80、9．34、18．15和3．97、12．92、23．29倍;此外,10μmol/LNaAsO2暴露12h和24h的HO-1 mRNA和蛋白表达均明显高于对应时间的5μmol／L组（P〈0．01）。[结论]NaAsO2暴露能够有效和持续性诱导Chang肝细胞株HO-1的mRNA和蛋白表达,是无机砷暴露的一种细胞保护性适应性反应。     

医学科技期刊中常见的法定计量单位（一）

法定计量单位是国家强制推行的标准,我们一定要遵照执行。下面是目前科技期刊中较常出现的旧制单位,希望作者不要再用（括号内是法定计量单位）。血铅（铁、砷）：μ/dl（μmol／L）;血钾：mEq／L（mmol／L）;肌酐：mg／dl（μmol／L）;尿素氮：mg／dl（mmol／L）;尿素：Mg／d（mmol／L）;尿铅：mg/L（μmol／L）;     

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.     

Variations in arsenic methylation capacity and oxidative DNA lesions over a 2-year period in a high arsenic-exposed population

Objective  To assess long-term variations in arsenic methylation and oxidative DNA lesions of chronic high arsenic-exposed populations. Methods  A follow-up study was conducted in 64 chronic high arsenic-exposed subjects from 2004 to 2006. Urinary arsenic species and 8-hydroxydeoxyguanine were measured. Results  Percentages of urinary inorganic arsenic, monomethylarsonate and urinary 8-hydroxydeoxyguanine (8-OHdG) level were significantly higher, but the percentage of dimethylarsinate, the primary methylation index (PMI) and secondary methylation index (SMI) was lower in the ninth year of arsenic exposure compared with the seventh year. Substantial differences in relative arsenic methylation capacity were observed between the seventh and ninth year. Percentages of arsenic species, PMI and SMI were significantly correlated between siblings, and between parents and children. Conclusions  Arsenic methylation may decrease, but oxidative DNA lesions may increase with the increase of cumulative arsenic exposure level. Both genetic and environmental factors may contribute to variability in arsenic methylation.     

Urinary PAH metabolites influenced by genetic polymorphisms of GSTM1 in male hospital incinerator workers

Hospital waste incinerator workers are exposed to various pyrolysis products including polycyclic aromatic hydrocarbons (PAHs). We evaluated their exposure by assessing urinary 1-hydroxypyrene glucuronide (1-OHPG), as an internal dose of PAH exposure. The potential effect of genetic polymorphisms of GSTM1/T1 involved in PAH metabolisms was also investigated. Pre- and post-shift samples were collected from 28 hospital incinerator workers. Urinary 1-OHPG was assayed by synchronous fluorescence spectroscopy (SFS) after immunoaffinity purification with the monoclonal antibody 8E11. Genotypes of GSTM1/T1 were assessed by PCR-based methods. Information on smoking habits and use of personal protective equipment were collected by means of a self-administered questionnaire. The Mann-Whitney test was used to compare group means of these biomarkers. Urinary 1-OHPG levels were similar in pre- and post-shift urine samples. The arithmetic mean concentrations of urinary 1-OHPG were 0.16 +/- 0.04 micromol/mol creatinine pre-shift and 0.19 +/- 0.09 micromol/mol creatinine post-shift, but urinary 1-OHPG levels were significantly higher in individuals with the GSTM1 null genotype than with the GSTM1 present genotype (p=0.05, by Mann-Whitney test). Our results suggest that the urinary 1-OHPG levels in hospital waste incinerator workers may be modified by the GSTM1 genotype, but these findings remain to be confirmed in future studies involving larger sample sizes.     

Elevated levels of urinary 8-hydroxy-2 -deoxyguanosine, lymphocytic micronuclei, and serum glutathione S-transferase in workers exposed to coke oven emissions

To investigate associations among occupational exposure to coke oven emissions (COEs), oxidative stress, cytogenotoxic effects, change in the metabolizing enzyme glutathione S-transferase (GST), and internal levels of polycyclic aromatic hydrocarbons (PAHs) in coke oven workers, we recruited 47 male coke oven workers and 31 male control subjects from a coke oven plant in northern China. We measured the levels of 1-hydroxypyrene (1-OHP) and 8-hydroxy-2 -deoxyguanosine (8-OHdG) in urine, micronucleated binucleated cells (BNMNs) in peripheral blood lymphocyte, and GST in serum. Our results showed that the group exposed to COEs had significantly increased levels of 1-OHP [median 5.7; interquartile range (IQR), 1.4-12.0 micromol/mol creatinine] compared with the control group (3; 0.5-6.4 micromol/mol creatinine). In addition, the median levels (IQR) of 8-OHdG, BNMNs, and GST were markedly increased in the exposed [1.9 (1.4-15.4) micromol/mol creatinine; 6 (2-8) per thousand ; 22.1 (14.9-31.2) U/L, respectively] compared with controls [1.3 (1.0-4.0) micromol/mol creatinine, 2 (0-4) per thousand; and 13.1 (9.5-16.7) U/L, respectively]. These results appeared to be modified by smoking. However, multivariate logistic regression analysis revealed that exposure to COEs had the highest odds ratio among variables analyzed and that smoking was not a significant confounder of the levels of studied biomarkers. Overall, the present findings suggest that COE exposure led to increased internal PAH burden, genetic damage, oxidative stress, and GST activity. The consequences of the changes in these biomarkers, such as risk of cancer, warrant further investigations.     

Porphyrin status in aluminum foundry workers exposed to hexachlorobenzene and octachlorostyrene.

The possible interference of hexachlorobenzene and octachlorostyrene (i.e., thermal byproducts from hexachloroethane in aluminum degassing) with porphyrin metabolism was investigated in exposed workers. Urine specimens from 9 male aluminum foundry workers (i.e., smelters) at 6 different companies and from 18 controls-matched for sex, age, residence, and socioeconomic status-were analyzed for total porphyrins and porphyrin isomers. Workers exposed to hexachlorobenzene and octachlorostyrene had a statistically significant increase in urinary total porphyrins, compared with controls (mean +/- standard deviation: 13.63 +/- 11.13 micromol/mol creatinine and 6.24 +/- 3.84 micromol/mol creatinine, respectively; p = .02). The authors attributed the results mainly to differences in excretion of coproporphyrins-notably coproporphyrin III. Erythrocyte uroporphyrinogen decarboxylase activity was similar in both groups. There was a high correlation between levels of hexachlorobenzene and octachlorostyrene, respectively, in plasma and urinary excretion of porphyrins; these findings, however, relied heavily on 1 subject for whom extreme values were obtained. The results indicated that occupational exposure to hexachlorobenzene and octachlorostyrene in aluminum degassing with hexachloroethane may affect porphyrin metabolism in a manner consistent with early secondary coproporphyrinuria-the first recognized step in the development of chronic hepatic porphyria. It was also noted that changes remained detectable some years after exposure ceased.     

职业砷接触工人某些遗传毒性指标的变化

目的探讨职业砷接触工人某些遗传毒性指标的变化。方法选择云南某砒霜厂40人为接触组,当地无明显毒物接触史28人为对照组,检测并评价外周血淋巴细胞微核细胞率、微核率、彗星试验拖尾率和尾长,以及尿中总砷、有机砷水平。结果接触组外周血淋巴细胞微核细胞率、微核率、彗星试验拖尾率、尾长均极显著高于对照组(P<0.01)。尿中总砷、有机砷浓度也高于对照组(均低于0.02mg/L)。微核细胞率和微核率随有机砷浓度、工龄乘积增加有升高趋势(rs=0.356,P=0.024;rs=0.347,P=0.028)。结论职业性砷暴露可导致外周血淋巴细胞染色体和DNA损伤。     

江西省职业接触砷生物限值研制

目的研制江西省职业接触砷的生物限值。方法对接触砷危害的作业工人进行健康检查和尿砷检测,并结合国内外文献资料进行综合分析。结果对400名接触砷的职业工人进行尿砷测定,结果显示,尿总砷平均值为0．20mg／L,标准差为0．12mg／L,95％上限值为0．40mg／L。36名非职业接触人员尿总砷平均值为0．04mg／L,标准差为O．02mg／L,职业人群与非职业人群差异具有统计学意义（P〈0．01）。职业健康检查结果发现,9人出现砷斑等皮肤样病变。通过工作场所空气中砷及其化合物浓度测定,结合几例砷中毒患者的临床资料和国内外文献,经综合分析,提出江西省尿砷的职业接触限值。结论砷的生物指标较多,经综合分析,课题组认为以尿总砷作为判断指标更为科学合理,建议江西省职业接触砷的生物限值为尿总砷0．40mg／L。     

Increased levels of 8-hydroxy-2 -deoxyguanosine attributable to carcinogenic metal exposure among schoolchildren

Arsenic, chromium, and nickel are reported in several epidemiologic studies to be associated with lung cancer. However, the health effects of arsenic, chromium, and nickel exposures are equivocal for children. Therefore, we performed a cross-sectional study to investigate possible associations between the internal concentrations of arsenic, chromium, and nickel and the level of oxidative stress to DNA in children. We measured urinary levels of arsenic, chromium, and nickel for 142 nonsmoking children using atomic absorption spectrometry. As a biomarker for oxidative stress, urinary 8-hydroxy-2 -deoxyguanosine (8-OHdG) levels were analyzed with an enzyme-linked immunosorbent assay kit. The median urinary 8-OHdG level for our subjects was 11.7 ng/mg creatinine. No obvious relationship between the levels of urinary nickel and 8-OHdG was found. Multiple linear regression analysis showed that children with higher urinary chromium had greater urinary 8-OHdG than did those with lower urinary chromium. Similarly, subjects with higher urinary arsenic had greater urinary 8-OHdG than did those with lower urinary arsenic. Furthermore, children with both high urinary arsenic and high urinary chromium had the highest 8-OHdG levels (mean +/- SE, 16.0 +/- 1.3; vs. low arsenic/low chromium, p < 0.01) in urine, followed by those with low arsenic/high chromium (13.7 +/- 1.6; vs. low arsenic/low chromium, p = 0.25), high arsenic/low chromium (12.9 +/- 1.6 vs. low arsenic/low chromium, p = 0.52), and low arsenic/low chromium (11.5 +/- 1.3); the trend was significant (p < 0.001). Thus, environmental carcinogenic metal exposure to chromium and arsenic may play an important role in oxidative DNA damage to children.     

尿邻甲酚作为接触甲苯生物监测指标的探讨

目的探讨尿邻甲酚作为接触甲苯生物监测指标的可能性。方法建立柱前衍生高效液相色谱法测定人体尿中邻甲酚,且使用该方法测定非职业及职业接触甲苯人群尿中邻甲酚水平,并进行接触评定。结果甲苯接触者尿邻甲酚水平为(2.61±1.94)mg/L,明显高于对照组[(0.32±0.23)mg/L],差异有显著性(P<0.001),且接触甲苯工人班后尿邻甲酚水平比班前明显升高,最高可达29倍。接触甲苯者尿邻甲酚水平与个体接触甲苯浓度明显相关(r=0.6295,P<0.01)。结论尿邻甲酚可以作为接触甲苯的生物监测指标。     

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

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