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  • Title: New information on lead in dirt and dust as related to the childhood lead problem.
    Author: Haar GT, Aronow R.
    Journal: Environ Health Perspect; 1974 May; 7():83-9. PubMed ID: 4831152.
    Abstract:
    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.
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