首页> 美国卫生研究院文献>British Journal of Industrial Medicine >Exposure of iron foundry workers to polycyclic aromatic hydrocarbons: benzo(a)pyrene-albumin adducts and 1-hydroxypyrene as biomarkers for exposure.
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Exposure of iron foundry workers to polycyclic aromatic hydrocarbons: benzo(a)pyrene-albumin adducts and 1-hydroxypyrene as biomarkers for exposure.

机译:铸造厂的工人暴露于多环芳烃中:苯并(a)re-白蛋白加合物和1-羟基py作为生物标记物进行暴露。

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摘要

Exposure to polycyclic aromatic hydrocarbons (PAHs) in foundry workers has been evaluated by determination of benzo(a)pyrene-serum albumin adducts and urinary 1-hydroxypyrene. Benzo(a)pyrene binding to albumin and 1-hydroxypyrene were quantitatively measured by enzyme linked immunosorbent assay (ELISA) and reverse phase high performance liquid chromatography (HPLC), respectively. 70 male foundry workers and 68 matched controls were investigated. High and low exposure groups were defined from breathing zone hygienic samples, consisting of 16 PAH compounds in particulate and gaseous phase. Mean total PAH was 10.40 micrograms/m3 in the breathing zone, and mean dust adsorbed PAH was 0.15 microgram/m. All carcinogenic PAH was adsorbed to dust. Median benzo(a)pyrene-albumin adduct concentrations (10-90% percentiles) were similar in foundry workers (smokers 0.55 (0.27-1.00) and non-smokers 0.58 (0.17-1.15)) pmol/mg albumin and age matched controls (smokers 0.57 (0.16-1.45) and non-smokers 0.70 (0.19-1.55) pmol/mg albumin). Median 1-hydroxypyrene concentrations were significantly higher (P < 0.0001) in smoking and non-smoking foundry workers (0.022 (0.006-0.075) and 0.027 (0.006-0.164)) mumol/mol creatinine than in smoking and non-smoking controls (0 (0-0.022) and 0 (0-0.010) mumol/mol creatinine). Dose-response relations between total PAH, pyrene, carcinogenic PAHs, and 1-hydroxypyrene for smokers, and polycyclic aromatic hydrocarbons adsorbed to dust for non-smokers are suggested. Exposure to PAHs adsorbed to dust showed an additive effect. There was no correlation between the concentrations of 1-hydroxypyrene and benzo(a)pyrene-albumin adducts. The change in 1-hydroxypyrene over a weekend was also studied. Friday morning median 1-hydroxypyrene concentrations were significantly higher in both smokers and non-smokers (0.021 (0-0.075) and 0.027 (0.06-0.164)) mumol/mol creatinine than Monday morning median concentrations (0.007 (0-0.021) and 0.008 (0-0.021) mumol/mol creatinine). Smoking did not affect the concentrations of 1-hydroxypyrene or benzo(a)pyrene-albumin adducts. These data suggest that 1-hydroxypyrene is a sensitive biomarker for low dose PAH exposure. Exposure to PAHs may be aetiologically related to increased risk of lung cancer in foundry workers.
机译:通过测定苯并(a)py-血清白蛋白加合物和尿中的1-羟基py,评估了铸造工人中多环芳烃的暴露水平。分别通过酶联免疫吸附测定(ELISA)和反相高效液相色谱(HPLC)定量测定与白蛋白和1-羟基py结合的苯并(a)measured。调查了70名男性铸造工人和68名相称的控制人员。高和低暴露组是从呼吸区卫生样品中定义的,该样品由16种呈颗粒状和气相的PAH化合物组成。呼吸区的平均总PAH为10.40微克/立方米,粉尘吸附的平均PAH为0.15微克/立方米。所有致癌的PAH均吸附在灰尘上。铸造工人(吸烟者0.55(0.27-1.00)和非吸烟者0.58(0.17-1.15))pmol / mg白蛋白和年龄匹配的对照组中苯并(a)-白蛋白加合物的中位数浓度(10-90%百分数)相似(吸烟者0.57(0.16-1.45)和非吸烟者0.70(0.19-1.55)pmol / mg白蛋白)。吸烟和不吸烟铸造工人的1-mol mol肌酐中位数比吸烟和不吸烟对照组的肌醇/摩尔肌酐显着更高(P <0.0001)(0.022(0.006-0.075)和0.027(0.006-0.164))(0 (0-0.022)和0(0-0.010)mumol / mol肌酐)。建议吸烟者的总PAH,pyr,致癌的PAH和1-羟基py与非吸烟者吸附在粉尘上的多环芳烃之间存在剂量反应关系。暴露于吸附在粉尘上的PAHs表现出累加效应。 1-羟基py和苯并(a)py-白蛋白加合物的浓度之间没有相关性。还研究了一个周末内1-羟基ne的变化。星期五上午吸烟者和非吸烟者的1-羟基py中位数浓度(0.021(0-0.075)和0.027(0.06-0.164))mumol / mol肌酐显着高于星期一早晨中位数浓度(0.007(0-0.021)和0.008 (0-0.021)mumol / mol肌酐)。吸烟不会影响1-羟基py或苯并(a)py-白蛋白加合物的浓度。这些数据表明1-羟基py是低剂量PAH暴露的敏感生物标志物。在病因上暴露可能与铸造厂工人患肺癌的风险增加有关。

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