交通排气装置,炼油厂和工业设施是美国环境保护署(U.S.EPA)确定的空气有毒物质的主要来源,因为它们对人类健康有潜在的风险。在子宫内和生命早期暴露于空气中的有毒物质,如苯和1,3-丁二烯,这是成年人中已知的致血剂,可能在儿童白血病中起病因学作用,儿童白血病包括大多数儿科癌症。我们进行了一项基于人群的病例对照研究,以检查苯的个体影响,1,3-丁二烯和多环有机物质(POM)的周围居住空气中的急性淋巴细胞白血病(ALL),从1995年至2011年在得克萨斯州5岁以下的儿童中诊断。
将得克萨斯州癌症登记病例与出生记录联系起来,然后按出生月份和年份与10个基于人群的对照进行频率匹配。从出生证明中提取母婴特征,以获取有关潜在混杂因素的信息。苯的建模估计,通过将出生证明中的地理编码的产妇地址与美国EPA国家规模的空气毒物评估数据相关联,以进行单污染物和共污染物统计分析,从而分配了人口普查区水平的1,3-丁二烯和POM暴露。混合效应逻辑回归模型用于评估空气中毒与儿童白血病之间的关联。
在调整后的单一污染物模型中,与最低四分位数的母亲相比,环境空气暴露最高的母亲患儿童白血病的几率为POM的1.11(95%CI:0.94-1.32),苯的1.17(95%CI:0.98-1.39)和1,3-丁二烯的1.29(95%CI:1.08-1.52)。在共污染物模型中,1,3-丁二烯的儿童白血病的比值比仍然升高,但苯和POM的比值接近零值.
我们在单一和共污染物模型中观察到1,3-丁二烯和儿童白血病之间的正相关,而在共污染物模型中,苯和POM的单一污染物模型的效应估计减少。早期接触1,3-丁二烯而不是苯或POM似乎会增加儿童早期急性淋巴细胞白血病的风险。
Traffic exhaust, refineries and industrial facilities are major sources of air toxics identified by the U.S. Environmental Protection Agency (U.S. EPA) for their potential risk to human health. In utero and early life exposures to air toxics such as benzene and 1,3-butadiene, which are known leukemogens in adults, may play an etiologic role in childhood leukemia that comprises the majority of pediatric cancers. We conducted a population based
case-control study to examine individual effects of benzene, 1,3-butadiene and polycyclic organic matter (POM) in ambient residential air on acute lymphocytic leukemia (ALL) diagnosed in children under age 5 years in Texas from 1995-2011.
Texas Cancer Registry cases were linked to birth records and then were frequency matched by birth month and year to 10 population-based controls. Maternal and infant characteristics from birth certificates were abstracted to obtain information about potential confounders. Modelled estimates of benzene, 1,3-butadiene and POM exposures at the census tract level were assigned by linking geocoded maternal addresses from birth certificates to U.S. EPA National-Scale Air Toxics Assessment data for single and co-pollutant statistical analyses. Mixed-effects logistic regression models were applied to evaluate associations between air toxics and childhood leukemia.
In adjusted single pollutant models, odds of childhood leukemia among mothers with the highest ambient air exposures compared to those in the lowest quartile were 1.11 (95 % CI: 0.94-1.32) for POM, 1.17 (95 % CI: 0.98-1.39) for benzene and 1.29 (95 % CI: 1.08-1.52) for 1,3-butadiene. In co-pollutant models, odds ratios for childhood leukemia remained elevated for 1,3-butadiene but were close to the null value for benzene and POM.
We observed positive associations between 1,3-butadiene and childhood leukemia in single and co-pollutant models whereas effect estimates from single pollutant models were diminished for benzene and POM in co-pollutant models. Early life exposure to 1,3-butadiene rather than benzene or POM appears to increase early childhood risk of acute lymphocytic leukemia.