Janitz Amanda E, Campbell Janis E, Magzamen Sheryl, Pate Anne, Stoner Julie A, Peck Jennifer D
Department of Biostatistics and Epidemiology, College of Public Health, University of Oklahoma Health Sciences Center, 801 NE 13th St., CHB 309, Oklahoma City, OK 73104, USA.
Department of Environmental and Radiological Health Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, 1681 Campus Delivery, Fort Collins, CO 80523, USA.
Environ Res. 2017 Oct;158:167-173. doi: 10.1016/j.envres.2017.06.015. Epub 2017 Jun 20.
Although childhood cancer is a leading cause of childhood mortality in the US, evidence regarding the etiology is lacking. The goal of this study was to evaluate the association between benzene, a known carcinogen, and childhood acute leukemia.
We conducted a case-control study including cases diagnosed with acute leukemia between 1997 and 2012 (n = 307) from the Oklahoma Central Cancer Registry and controls matched on week of birth from birth certificates (n = 1013). We used conditional logistic regression to evaluate the association between benzene, measured with the 2005 National-Scale Air Toxics Assessment (NATA) at census tract of the birth residence, and childhood acute leukemia.
We observed no differences in benzene exposure overall between cases and controls. However, when stratified by year of birth, cases born from 2005 to 2010 had a three-fold increased unadjusted odds of elevated exposure compared to controls born in this same time period (4th Quartile OR: 3.53, 95% CI: 1.35, 9.27). Furthermore, the estimates for children with acute myeloid leukemia (AML) were stronger than those with acute lymphoid leukemia, though not statistically significant.
While we did not observe an association between benzene and childhood leukemia overall, our results suggest that acute leukemia is associated with increased benzene exposure among more recent births, and children with AML may have increased benzene exposure at birth. Using the NATA estimates allowed us to assess a specific pollutant at the census tract level, providing an advantage over monitor or point source data. Our study, however, cannot rule out the possibility that benzene may be a marker of other traffic-related exposures and temporal misclassification may explain the lack of an association among earlier births.
尽管儿童癌症是美国儿童死亡的主要原因之一,但关于其病因的证据仍然不足。本研究的目的是评估已知致癌物苯与儿童急性白血病之间的关联。
我们进行了一项病例对照研究,纳入了1997年至2012年间在俄克拉荷马州中央癌症登记处诊断为急性白血病的病例(n = 307),以及根据出生证明按出生周匹配的对照(n = 1013)。我们使用条件逻辑回归来评估苯(通过2005年国家尺度空气毒物评估(NATA)在出生居住地的普查区进行测量)与儿童急性白血病之间的关联。
我们观察到病例组和对照组在总体苯暴露方面没有差异。然而,按出生年份分层时,2005年至2010年出生的病例与同期出生的对照组相比,未调整的高暴露几率增加了三倍(第四四分位数比值比:3.53,95%置信区间:1.35,9.27)。此外,急性髓系白血病(AML)患儿的估计值比急性淋巴细胞白血病患儿更强,尽管无统计学意义。
虽然我们总体上未观察到苯与儿童白血病之间的关联,但我们的结果表明,急性白血病与近期出生儿童中苯暴露增加有关,AML患儿在出生时可能有更高的苯暴露。使用NATA估计值使我们能够在普查区层面评估特定污染物,这比监测器或点源数据具有优势,但我们的研究不能排除苯可能是其他交通相关暴露的标志物以及时间错误分类可能解释早期出生儿童中缺乏关联的可能性。