Glass Deborah C, Gray Christopher N, Jolley Damien J, Gibbons Carl, Sim Malcolm R, Fritschi Lin, Adams Geoffrey G, Bisby John A, Manuell Richard
Department of Epidemiology and Preventive Medicine, Central and Eastern Clinical School, The Alfred Hospital, Commercial Road, Melbourne, Victoria, Australia.
Epidemiology. 2003 Sep;14(5):569-77. doi: 10.1097/01.ede.0000082001.05563.e0.
Men who were part of an Australian petroleum industry cohort had previously been found to have an excess of lympho-hematopoietic cancer. Occupational benzene exposure is a possible cause of this excess.
We conducted a case-control study of lympho-hematopoietic cancer nested within the existing cohort study to examine the role of benzene exposure. Cases identified between 1981 and 1999 (N = 79) were age-matched to 5 control subjects from the cohort. We estimated each subject's benzene exposure using occupational histories, local site-specific information, and an algorithm using Australian petroleum industry monitoring data.
Matched analyses showed that the risk of leukemia was increased at cumulative exposures above 2 ppm-years and with intensity of exposure of highest exposed job over 0.8 ppm. Risk increased with higher exposures; for the 13 case-sets with greater than 8 ppm-years cumulative exposure, the odds ratio was 11.3 (95% confidence interval = 2.85-45.1). The risk of leukemia was not associated with start date or duration of employment. The association with type of workplace was explained by cumulative exposure. There is limited evidence that short-term high exposures carry more risk than the same amount of exposure spread over a longer period. The risks for acute nonlymphocytic leukemia and chronic lymphocytic leukemia were raised for the highest exposed workers. No association was found between non-Hodgkin lymphoma or multiple myeloma and benzene exposure, nor between tobacco or alcohol consumption and any of the cancers.
We found an excess risk of leukemia associated with cumulative benzene exposures and benzene exposure intensities that were considerably lower than reported in previous studies. No evidence was found of a threshold cumulative exposure below which there was no risk.
此前发现，澳大利亚石油行业队列中的男性患淋巴造血系统癌症的人数过多。职业性接触苯可能是导致这一情况的原因。
我们在现有的队列研究中开展了一项关于淋巴造血系统癌症的病例对照研究，以探究苯接触的作用。1981年至1999年间确诊的病例（N = 79）与队列中的5名对照对象进行年龄匹配。我们利用职业史、当地特定地点信息以及一种使用澳大利亚石油行业监测数据的算法，估算了每位受试者的苯接触量。
配对分析显示，累积接触量超过2 ppm - 年以及最高接触工作的接触强度超过0.8 ppm时，白血病风险会增加。风险随着接触量的增加而升高；对于累积接触量大于8 ppm - 年的13个病例组，比值比为11.3（95%置信区间 = 2.85 - 45.1）。白血病风险与开始工作日期或工作时长无关。与工作场所类型的关联可由累积接触量来解释。仅有有限的证据表明，短期高接触量比在较长时期内分散的相同接触量带来的风险更大。接触量最高的工人患急性非淋巴细胞白血病和慢性淋巴细胞白血病的风险升高。未发现非霍奇金淋巴瘤或多发性骨髓瘤与苯接触之间存在关联，也未发现吸烟或饮酒与任何一种癌症之间存在关联。
我们发现，白血病风险增加与累积苯接触量以及苯接触强度有关，且这些接触量和强度远低于此前研究报告的水平。未发现存在无风险的阈值累积接触量的证据。
