Omland O, Sherson D, Hansen A M, Sigsgaard T, Autrup H, Overgaard E
Department of Occupational Medicine, Aarhus University Hospital, Denmark.
Occup Environ Med. 1994 Aug;51(8):513-8. doi: 10.1136/oem.51.8.513.
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.
通过测定苯并(a)芘-血清白蛋白加合物和尿中1-羟基芘，对铸造工人接触多环芳烃(PAHs)的情况进行了评估。分别采用酶联免疫吸附测定(ELISA)和反相高效液相色谱(HPLC)对苯并(a)芘与白蛋白的结合及1-羟基芘进行定量测定。对70名男性铸造工人和68名匹配的对照组进行了调查。根据呼吸带卫生样本确定高暴露组和低暴露组，样本中含有16种颗粒相和气态相的PAH化合物。呼吸带中PAH的平均总量为10.40微克/立方米，粉尘吸附PAH的平均量为0.15微克/米。所有致癌性PAH均吸附在粉尘上。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白蛋白与年龄匹配的对照组（吸烟者0.57(0.16 - 1.45)和非吸烟者0.70(0.19 - 1.55)）pmol/mg白蛋白的苯并(a)芘-白蛋白加合物浓度中位数（第10 - 90百分位数）相似。吸烟和不吸烟的铸造工人尿中1-羟基芘浓度中位数（0.022(0.006 - 0.075)和0.027(0.006 - 0.164)）μmol/mol肌酐显著高于吸烟和不吸烟的对照组（0(0 - 0.022)和0(0 - 0.010)）μmol/mol肌酐（P < 0.0001）。提示吸烟者的总PAH、芘、致癌性PAHs与1-羟基芘之间以及非吸烟者的粉尘吸附多环芳烃之间存在剂量-反应关系。接触吸附在粉尘上的PAHs显示出相加效应。1-羟基芘浓度与苯并(a)芘-白蛋白加合物浓度之间无相关性。还研究了周末期间1-羟基芘的变化情况。周五上午吸烟和不吸烟的工人1-羟基芘浓度中位数（0.021(0 - 0.075)和0.027(0.06 - 0.164)）μmol/mol肌酐均显著高于周一上午的浓度中位数（0.007(0 - 0.021)和0.008(0 -
