Haar G T, Aronow R
Environ Health Perspect. 1974 May;7:83-9. doi: 10.1289/ehp.74783.
It has been known for many years that the eating of leaded paint is the prime cause of lead poisoning and elevated blood leads of children living in deteriorated housing. Recently, there has been speculation that children may eat dirt and dust contaminated with lead exhausted from cars and that this amount of ingested lead is sufficient to contribute significantly to the childhood lead problem. This paper reports on a twopart study conducted to evaluate the validity of the dirt-and-dust hypotheses. The first part of the study was made to determine the source of lead in dirt to which children are normally exposed. Dirt samples were taken in old urban areas around 18 painted frame houses and 18 houses of brick construction. Samples also were taken around seven old frame farmhouses remote from traffic. Based on the fact that lead concentrations in the dirt were similar in city and rural yards at corresponding distances from the houses, it is clear that nearly all of the lead in dirt around these houses is due to paint from the houses. Lead antiknock additives are therefore not a significant contributor to the lead content of dirt around houses where children usually play. The second part of the study used a naturally occurring radioactive tracer (210)Pb to determine the relative amounts of dust and other lead-containing materials (e.g., paint) eaten by young children. This tracer is present in very low concentrations in paint and in significantly higher concentrations in fallout dust. Stable lead and (210)Pb were analyzed in fecal material from eight children suspected of having elevated body burdens of lead and ten children living in good housing where lead poisoning is not a problem. The normal children averaged 4 mug Pb/g dry feces, with a range of 2 to 7. Of the eight children suspected of having elevated lead body burdens, two had fecal lead values within the normal range. However, the remaining six were 4 to 400 times as high. Despite these differences in fecal lead between the two groups, the groups were essentially identified in the (210)Pb content of their feces. The "elevated" children averaged 0.040 pCi of (210)Pb dry feces, while the normal group averaged 0.044 pCi/g. The results provide sound evidence that these children suspected of elevated lead body burden were not ingesting dust or air-suspended particulate.
多年来人们都知道,食用含铅油漆是居住在破旧房屋中的儿童铅中毒和血铅升高的主要原因。最近,有人猜测儿童可能会食用被汽车排放的铅污染的泥土和灰尘,并且这种摄入的铅量足以对儿童铅问题产生重大影响。本文报道了一项分为两部分的研究,旨在评估泥土和灰尘假说的有效性。研究的第一部分是确定儿童通常接触的泥土中铅的来源。在18座涂漆框架房屋和18座砖混结构房屋周围的旧城区采集了泥土样本。还在远离交通的7座旧框架农舍周围采集了样本。基于在距房屋相应距离处城市和农村院子里泥土中铅浓度相似这一事实,很明显这些房屋周围泥土中的几乎所有铅都来自房屋的油漆。因此,铅抗爆添加剂对儿童通常玩耍的房屋周围泥土中的铅含量贡献不大。研究的第二部分使用一种天然存在的放射性示踪剂(210)Pb来确定幼儿食用的灰尘和其他含铅物质(如油漆)的相对量。这种示踪剂在油漆中的浓度非常低,而在沉降灰尘中的浓度要高得多。对8名疑似铅负荷升高的儿童和10名居住在铅中毒不是问题的良好住房中的儿童的粪便样本进行了稳定铅和(210)Pb分析。正常儿童的粪便干重平均含铅量为4微克/克,范围在2至7微克/克之间。在8名疑似铅负荷升高的儿童中,有两名儿童的粪便铅值在正常范围内。然而,其余6名儿童的粪便铅值高出正常范围4至400倍。尽管两组儿童的粪便铅含量存在这些差异,但两组儿童粪便中的(210)Pb含量基本相同。“铅负荷升高”组儿童的粪便干重平均含(210)Pb为0.040皮居里,而正常组平均为0.044皮居里/克。结果提供了有力证据,表明这些疑似铅负荷升高的儿童没有摄入灰尘或空气中悬浮的颗粒物。