Original Research Communications – general

ABSTRACT approximately 60% of an oral dose of 100_ug of ²⁰³Pb was retained in 85 fasting subjects with no difference noted between males and females. Body retention was proportional to dose up to 400_ug of lead. It was not related to the capacity to absorb iron or to the size of body iron stores, nor was it affected by the simultaneous ingestion of a 10-fold molar excess of iron. The effect of several dietary factors was also determined. Lead retention was lowered by eating food, slightly increased by ingestion of fat, but way unaffected by the administration of lactose or a 10-fold molar excess of zinc, cobalt, or calcium. One chelating agent, ascorbic acid, slightly lowered lead retention, whereas another agent ethylenediaminetetraacetic acid, produced a marked reduction. Several of these results suggest that human gastrointestinal lead absorption behaves differently to that of rodents. In particular, human lead retention was found to be unrelated to iron absorption or to body iron stores. Am J Clin Nutr 1982;36:823-829.

Introduction

 Nutritional factors are thought to play an important role in lead poisoning (1). Studies in animals have shown that the gastrointestinal absorption of lead is increased by dietary components such as citrate, ascorbate, amino acids, vitamin D (3,4) , protein and fat (5), and lactose (6) and lowered by cations such as iron (7,8), calcium (9), zinc, (10), and magnesium (11). Nutritional iron deficiency in laboratory animals also enhances lead absorption and promotes lead toxicity, thereby giving concern that pregnant women and young children may be susceptible to dietary lead (1). The purpose of the present work was to study possible lead-iron interactions in people (1,7,8), and secondarily to examine the modulating role of some dietary factors. We have measured the body retention of an oral dose of ²⁰³Pb in 85 human subjects and examined the influence of: 1) lead dose; 2) variation in iron-absorbing ability; 3) a meal, including the carbohydrate, fat and mineral components; and 4) chelating agents.

Our results indicate that lead retention in humans may not follow the pattern established by previous work in rodents.

Healthy volunteers (mean age 25, range 18 to 48yr) gave informed written consent for the investigations and ethical acceptability of the research was approved by The University of Western Ontario Health Sciences Standing Committee on Human Research. Each volunteer was given three test drinks of ²⁰³Pb at monthly intervals, once to establish a control retention value and twice more to measure the effect of factors added to the test dose.

* * * *  . . be excluded because the urine of these subjects was not available for counting.

The results of our study with young adults may not be relevant to lead retention in children. It is currently thought that iron deficiency may partly account for the vulnerability of children to lead toxicity (1). Although our results provide no evidence to support this concept, the mechanism of lead absorption in children may differ from that in young adults. The fact that fasting does increase lead retention may be important in determining lead exposure in children. Children may ingest lead from dirt, dust, etc, at times during the day when little food is present in their stomachs. Consequently, absorption of lead could be high, contributing to the well-known predisposition of children to lead toxicity (35).

In summary, the present work shows that the gastrointestinal absorption of lead in humans is proportional to the dose administered and it is not correlated with the level of iron absorption or with body iron stores. Human lead retention also differs in several other ways from lead absorption in laboratory animals. These include the inhibitory effect of EDTA and the lack of effect of selected metals and lactose. Although experiments with animals may give useful data concerning lead absorption, caution should be exercised in extrapolating the results of these studies to humans.

References