Association between iron deficiency and blood lead level in a longitudinal analysis of children followed in an urban primary care clinic.
Association between iron deficiency and blood lead level in a longitudinal analysis of children followed in an urban primary care clinic.
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DOI：
10.1067/mpd.2003.mpd0344
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发表时间：
2003
期刊：
影响因子：
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通讯作者：
R. Wright;Shirng-Wern Tsaih;J. Schwartz;Rosalind J Wright;Howard Hu
中科院分区：
文献类型：
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作者：
R. Wright;Shirng-Wern Tsaih;J. Schwartz;Rosalind J Wright;Howard Hu
目的 确定缺铁 (ID) 是否与铅中毒存在纵向相关性。研究设计 测定了 1,275 名儿童的血铅水平、血红蛋白、平均红细胞体积 (MCV)、红细胞分布宽度 (RDW)、保险状况和年龄。如果年龄 >/=2 岁，则 ID 定义为 MCV 14.5，如果年龄为 14.5。使用二分法 >/=0.48 microm/L (10 microg/dL) 的二次就诊血铅水平作为结果构建逻辑回归模型。结果 第二次就诊时预测铅中毒的基线 ID 比值比 (OR) 为 4.12（95% CI，1.96-8.65）。在第二个模型中，使用两次就诊时均补充铁的儿童作为参考组，对于两次就诊时均患有 ID 的儿童，第二次就诊时预测铅中毒的 OR 为 5.54（95% CI，2.25-13.62）。对于第一次就诊时缺铁、第二次就诊时补充铁剂的儿童，OR 为 2.73（95% CI，0.90-8.27）；对于第一次就诊时铁充足、第二次就诊时缺铁的儿童，OR 为 0.81（95% CI，0.10-6.30）。结论 ID 与随后的铅中毒有关。这些数据与缺铁儿童铅吸收增加的生物学机制一致。
OBJECTIVE To determine if iron deficiency (ID) is longitudinally associated with lead poisoning. STUDY DESIGN Blood lead levels, hemoglobin, mean corpuscular volume (MCV), red cell distribution width (RDW), insurance status, and age were determined for 1,275 children. ID was defined as MCV 14.5 if age was 14.5 if age was >/=2 years. Logistic regression models were constructed by using the second-visit blood lead levels dichotomized at >/=0.48 microm/L (10 microg/dL) as the outcome. RESULTS The odds ratio (OR) for baseline ID predicting lead poisoning at the second visit was 4.12 (95% CI, 1.96-8.65). In the second model, using children who were iron-replete at both visits as the referent group, for children with ID at both visits, the OR for predicting lead poisoning at the second visit was 5.54 (95% CI, 2.25-13.62). For children with ID at the first visit and iron-replete at the second visit, the OR was 2.73 (95% CI, 0.90-8.27), and for children iron-replete at the first visit and ID at the second visit, the OR was 0.81 (95% CI, 0.10-6.30). CONCLUSIONS ID is associated with subsequent lead poisoning. These data are consistent with a biological mechanism of increased lead absorption among iron deficient children.