The relationship between environmental lead and blood lead in children : a study in environmental epidemiology

This study deals with the relationship between environmental lead and blood lead in children.Chapter 1 provides a summary of the environmental health aspects of lead. The occurrence of lead in the environment and in man is described; children are discussed as a population at risk for undue lead absorption, and the exposure-response system is briefly outlined.Chapter 2 discusses a number of methodological issues in studies on the relationship between environmental lead and blood lead in children. Lead is present in various environmental media like air, soil and dust. From all these media, lead intake by children may occur, by inhalation or ingestion. The inhalation rate per kg body weight is larger in children than in adults, due to a higher metabolism. The ingestion of dust and dirt cannot be easily quantified; at present, measurement of the lead concentration in dust and dirt usually serves as a surrogate. The concentration of lead in blood has been the major dependent variable in studies on the relationship between environmental lead exposure and internal lead exposure. The concentration of lead in blood does not only depend on intake but also on the fractional absorption of lead from the gut, and on distribution and excretion patterns within the body. All of these vary with age. Nutritional factors are important as well, for example dietary calcium, iron, phosphorus and fat. Lead is not only present in the general environment but also in food and drinking water, both of which may act as predominant sources of lead intake. Lead in food originates in part from environmental pollution, and it is still debated how large this part actually is. Lead in drinking water usually originates from pipes or storage facilities. In the United States especially, lead from crumbling paint is an important source for children; paint lead does not seem to be of general importance in The Netherlands, however.The relationship between total lead intake and the concentration of lead in blood is usually given as a curvilinear downward function. The implication of this is that at low levels of exposure, a given increase of intake is expected to result in a stronger increase in blood lead concentrations than at high levels of exposure. In some studies, it has been customary to adjust relationships between air lead and blood lead for lead in other media. As lead in the air and lead in other media like soil and dust often originate from the same source or sources, such a procedure may under-estimate the impact of environmental lead on children's blood lead.It is difficult to measure the intake of lead from the environment by children exactly. Instead, the concentration of lead in one or more environmental media is usually measured as an index of exposure.Apart from being only approximations of actual lead intake from the environment, these concentrations also tend to have large temporal and spatial variations. A decomposition of total variation into within-subjects and between- subjects variation is a weans to estimate the reliability of exposure indicators. If the within-subjects variation of exposure indicators is large compared to the between- subjects variation, the impact of environmental lead exposure on blood lead will usually be underestimated in a regression analysis.Chapter 3 reviews a number of studies from which estimates of relationships between environmental lead and children's blood lead can be obtained. Aggregate relationships are emphasized, i.e. it is not attempted to estimate the separate contributions of inhalation, ingestion of soil, dust etc. as the available data usually do not permit such an analysis. Aggregate relationships are relationships in which different indicators of lead exposure are thought to represent all environmental exposure. When the concentration of lead in air is taken as an indicator, a blood lead/air lead slope of about 3-5 μg/100 ml per μg/m ³ is obtained. When the concentration of lead in soil, street dust or house dust is taken as an indicator, most blood lead/soil (dust) lead slopes are in the order of 5.0 - 10.0 μg/100 ml per g/kg.Although the ranges of the different types of estimates are wide, the review suggests that for children, lead intake from the environment constitutes a major part of total lead intake in quite a number of situations.Chapter 4 is a description of our study on environmental lead and blood lead in children living in Rotterdam, The Hague and Zoetermeer which was performed in 1981.Blood lead concentrations in children were different between city centers and suburbs. After adjustment for a number of confounders, more than half of the difference remained. Most probably, this was caused by differences in environmental lead pollution as most indicators of lead exposure were clearly different between city centers and suburbs. In a multiple regression analysis, most exposure indicators were significantly associated with the concentration of lead in blood, after adjustment for a number of confounders. Further analysis of the origins of lead in the environment suggested that in the area under investigation, vehicular traffic was the main source.When our study results were compared with those of others, the estimated impact of environmental lead on children's blood lead was somewhat higher than in most other studies, but the difference was not great, considering the wide range in estimates which was reported in chapter 3. Theoretically, the differences can be explained by the low level of exposure which was studied, and by the use of repeated exposure measurements. As indicated in chapter 2, a given exposure difference is expected to result in a larger blood lead difference at low overall levels of PbB than at a high overall level of PbB. Also, repetition of exposure measurements leads to a more precise estimate of exposure, and can theoretically be expected to result in a higher exposure impact estimate than when exposure is only measured once, as was the case in most studies reviewed in chapter 3.