A review and meta-analysis of outdoor air pollution and risk of childhood leukemia.
A review and meta-analysis of outdoor air pollution and risk of childhood leukemia.
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DOI：
10.1080/10590501.2015.1002999
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Vinceti M
中科院分区：
文献类型：
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作者：
Filippini T;Heck JE;Malagoli C;Del Giovane C;Vinceti M
白血病是影响儿童的最常见的恶性疾病。到目前为止，儿童白血病的病因仍在很大程度上未知。风险因素很少（遗传易感性、感染、电离辐射等）已经被明确确定，但它们似乎只能解释一小部分病例。更不确定的是其他环境风险因素的作用，如室内和室外空气污染。我们试图总结和量化交通相关空气污染与儿童白血病风险之间的关系，并根据暴露评估方法，研究质量，白血病亚型，研究时间段和大陆进行进一步检查结果。文献检索产生6项生态研究和20项病例对照研究后，我们根据纽卡斯尔-渥太华量表对研究进行评分。这些研究通过计算邻近道路或加油站附近的交通密度，或使用测量或模拟的二氧化氮和苯室外空气水平，评估了机动交通污染物对住宅的暴露。由于观察到了研究间的异质性，因此报告了随机效应汇总比值比（OR）和95%置信区间（CI）。只要有可能，我们还进行了分层分析，比较急性淋巴细胞白血病（ALL）和急性髓细胞白血病（AML）。将分析限于高质量研究（Newcastle-Ottawa量表≥ 7），使用交通密度作为暴露评估指标的研究显示，最高暴露类别中儿童白血病风险增加（OR=1.07，95%CI 0.93 - 1.24）。然而，我们观察到发表偏倚的证据。NO2暴露和苯暴露的OR分别为1.21（95%CI 0.97 - 1.52）和1.64（95%CI 0.91 - 2.95）。当按白血病类型分层时，基于NO2的ALL和AML的结果分别为1.21（95% CI 1.04 - 1.41）和1.06（95% CI 0.51 - 2.21）;基于苯的ALL和AML的结果分别为1.09（95% CI 0.67 - 1.77）和2.28（95% CI 1.09 - 4.75）。出生后阶段的估计值一般高于出生前阶段，欧洲研究的估计值高于北美研究的估计值。总的来说，我们的研究结果支持环境暴露于交通污染和儿童白血病风险之间的联系，特别是由于苯。
Leukemia is the most frequent malignant disease affecting children. To date, the etiology of childhood leukemia remains largely unknown. Few risk factors (genetic susceptibility, infections, ionizing radiation, etc.) have been clearly identified, but they appear to explain only a small proportion of cases. Considerably more uncertain is the role of other environmental risk factors, such as indoor and outdoor air pollution. We sought to summarize and quantify the association between traffic-related air pollution and risk of childhood leukemia, and further examined results according to method of exposure assessment, study quality, leukemia subtype, time period and continent where studies took place. After a literature search yielded 6 ecologic and 20 case-control studies, we scored the studies based upon the Newcastle-Ottawa Scale. The studies assessed residential exposure to pollutants from motorized traffic by computing traffic density in the neighboring roads or vicinity to petrol stations, or by using measured or modeled nitrogen dioxide and benzene outdoor air levels. Because heterogeneity across studies was observed, random-effects summary odds ratios (OR) and 95% confidence intervals (CI) were reported. Whenever possible we additionally conducted stratified analyses comparing acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). Limiting the analysis to high-quality studies (Newcastle-Ottawa Scale ≥ 7), those using traffic density as the exposure assessment metric showed an increase in childhood leukemia risk in the highest exposure category (OR=1.07, 95% CI 0.93 – 1.24). However, we observed evidence of publication bias. Results for NO2 exposure and benzene showed an OR of 1.21 (95% CI 0.97 – 1.52) and 1.64 (95% CI 0.91 – 2.95) respectively. When stratifying by leukemia type, the results based upon NO2 were 1.21 (95% CI 1.04 – 1.41) for ALL and 1.06 (95% CI 0.51 – 2.21) for AML; based upon benzene were 1.09 (95% CI 0.67 – 1.77) for ALL and 2.28 (95% CI 1.09 – 4.75) for AML. Estimates were generally higher for exposures in the postnatal period compared to the prenatal period, and for European studies compared to North American studies. Overall, our results support a link between ambient exposure to traffic pollution and childhood leukemia risk, particularly due to benzene.