Contribution of lead from calcium supplements to blood lead.

We conducted a case-control study to determine the contribution of lead to blood from consumption of calcium supplements approximating the recommended daily intakes over a 6-month period. Subjects were males and females ages 21 to 47 years (geometric mean 32 years) with a geometric mean blood lead concentration of 2.5 microg/dL. They were subdivided into three groups. One treatment group (n = 8) was administered a complex calcium supplement (carbonate/phosphate/citrate) and the other treatment group (n = 7) calcium carbonate. The control group (n = 6) received no supplement. The lead isotopic compositions of the supplements were completely different from those of the blood of the subjects, allowing us easily to estimate contribution from the supplements. The daily lead dose from the supplements at 100% compliance was about 3 microg Pb. Three blood samples were taken at 2-month intervals before treatment to provide background values, and three were taken during treatment. Subjects in the treatment group were thus their own controls. Lead isotopic compositions for the complex supplement showed minimal change during treatment compared with pretreatment. Lead isotopic compositions in blood for the calcium carbonate supplement showed increases of up to 0.5% in the (206)Pb/(204)Pb ratio, and for all isotope ratios there was a statistically significant difference between baseline and treatment (p < 0.005). The change from baseline to treatment for the calcium carbonate supplement differed from that for both the control group and the group administered the complex supplement. Blood lead concentrations, however, showed minimal changes. Variations in blood lead levels over time did not differ significantly between groups. Our results are consistent with earlier investigations using radioactive and stable lead tracers, which showed minimal gastrointestinal absorption of lead in the presence of calcium (+/- phosphorus) in adults. Even though there is no discernible increase in blood lead concentration during treatment, there are significant changes in the isotopic composition of lead in blood arising from the calcium carbonate supplement, indicating a limited input of lead from diet into the blood. Because calcium carbonate is overwhelmingly the most popular calcium supplement, the changes we have observed merit further investigation. In addition, this type of study, combined with a duplicate diet, needs to be repeated for children, whose fractional absorption of lead is considerably higher than that of adults.

Longitudinal study of daily intake and excretion of lead in newly born infants.

As an adjunct to a study of lead mobilization during pregnancy and lactation, we have obtained estimates of the daily lead intake and excretion/intake for 15 newly born infants monitored for at least 6 months postpartum. The longitudinal data presented reflect the far lower levels of environmental contribution to lead in blood in the 1990's than that in the earlier studies from the 1970's and early 1980's, the last period for which such dietary information is available in newly born infants. Infants were breast-fed or formula-fed or both and, in the second quarter, were usually fed solid foods (beikost). Lead concentrations were as follows: lead in breast milk, ranged from 0.09 to 3.1 microg/kg with a geometric mean of 0.55 microg/kg, lead in infant formula ranged from 0.07 to 11.4 microg/kg with a geometric mean of 1.6 microg/kg, and lead in beikost ranged from 1.1 to 27 microg/kg with a geometric mean of 2.9 microg/kg. Daily lead intakes ranged from 0.04 to 0.83 microg/kg body weight/day with a geometric mean of 0.23 microg Pb/kg body weight/day, and excretion/intake ranged from 0.7 to 22 with a geometric mean of 2.6. There was no significant difference at the 5% level in lead concentration in daily intakes and excretion/intake for the first quarter versus the second quarter for this small number of subjects. Assuming that there was no contribution from environmental samples such as house dust and ambient air, the contribution of diet to blood has been estimated from lead isotopic measurements with the following ranges: for breast milk only as the dietary source, 40 to 65%; for breast milk and infant formula as the dietary sources, 15 to 70%; and for infant formula and beikost, 20 to 80%. The geometric mean value of the dietary contribution to blood over the 6-month period of approximately 35% is consistent with earlier estimates of uptake of lead in blood in newly born infants when environmental lead concentrations were much higher. Other sources such as air, soil, and dust are considered to contribute minimally to blood lead in these infants because of the low 206Pb/204Pb ratios in environmental media. Thus, we consider that the increased excretion over intake, along with other evidence, reflects mobilization of infant tissues arising especially from rapid bone turnover at this stage of life; the tissue lead has been identified isotopically in urine.

Dietary intakes of selected elements from longitudinal 6-day duplicate diets for pregnant and nonpregnant subjects and elemental concentrations of breast milk and infant formula.

As part of a longitudinal investigation into mobilization of lead from the maternal skeleton during pregnancy and lactation, we have determined the daily intake of selected elements (hereafter called micronutrients) for various subjects and compared these intakes with recommended and/or published intakes, especially those of the United States, through the U.S. National Health and Nutrition Examination Survey (NHANES). We also sought to ascertain whether there was any seasonal effect in the diets. Six-day duplicate diets were collected from 15 pregnant and 16 nonpregnant migrants to Australia, 6 pregnant Australian control subjects, and 8 children of nonpregnant migrants (6 to 11 years). Samples of breast milk and infant formula were also analyzed. Blended samples were analyzed by inductively coupled plasma mass spectrometry for the elements Ca, Cu, Fe, Mg, P, K, Na, Zn, Ba, Sr, and Pb. Daily intakes of micronutrients were only about half of the daily intake estimated for non-Hispanic white females and infants in the U.S. NHANES III. Estimates of daily intakes from breast milk were also considerably lower for the migrant and Australian infants compared with the values extracted from tables of food composition and dietary recall for non-Hispanic white infants in the U.S. NHANES III. For example, Ca was a factor of approximately 3 times lower, Fe approximately 50, and Zn approximately 4. We consider our estimates a reliable indication of the daily intakes for several reasons, including the collection of up to nine quarterly collections of 6-day duplicate diets and retention of subjects in a longitudinal prospective study. The low intakes of the essential elements such as Ca, Fe, and Zn in all these population groups are of potential concern from a public health viewpoint.

Urinary excretion of lead during pregnancy and postpartum.

We have compared lead isotopic ratios and lead concentrations in 53 spot urine and 59 24-h urine samples from 13 subjects covering the interval from pre-pregnancy through 180 days postpartum to estimate the amount of lead excreted in urine and renal clearance relative to blood. The total amount of lead excreted in 24-h urine samples ranges from 0.8 to 5.9 microg Pb with an arithmetic mean of 2.2+/-1.1 microg (geometric mean 1.90 microg). This compares with amounts of 0.9-10 microg of extra lead per day estimated to be released into blood from the skeleton during pregnancy and postpartum. There were no differences in excretion rates during the trimesters of pregnancy and between pregnancy and postpartum time periods. The renal clearance relative to blood ranged from 0.8 to 10 g/h (arithmetic mean 3.2+/-1.9; geometric mean 2.7). Renal clearance relative to blood was somewhat higher in trimesters 2 and 3 compared with postpartum 150-180 days (P = 0.004, 0.006, respectively). Reassessment of earlier published blood and dietary data for Australian pregnant controls indicates there is no increased gastrointestinal absorption of lead during pregnancy and postpartum. This differs from calcium, which shows increased absorption during late pregnancy. In light of the inconvenience of sampling and potential contamination at the low levels of lead found in most of these subjects, we do not consider the 24 h urines to provide sufficient useful information.

Urinary lead isotopes during pregnancy and postpartum indicate no preferential partitioning of endogenous lead into plasma.

We have compared lead isotopic ratios and lead concentrations in 51 matched blood and spot urine samples from 13 subjects covering the interval from before pregnancy through 180 days postpartum to evaluate whether mobilization of lead from the maternal skeleton is preferentially partitioned into plasma; we have used urine as an isotopic proxy for plasma. There was no statistically significant difference in the lead 206/lead 204 and lead 207/lead 206 ratios over pregnancy. The urine data for the postpartum period are in the opposite relationships to that predicted for a preferential partitioning hypothesis. These data provide no support for the hypothesis that lead released from the skeleton is preferentially partitioned into plasma.

Limited seasonality effects on blood lead for a small cohort of female adults and children.

Many blood lead surveys, especially during the 1970s and 1980s have shown variations of up to 35% in blood lead concentration, with higher values in summer over winter. We have monitored 13 adult females and seven children for periods from 348 to 1337 days as non-pregnant controls in a longitudinal study of mobilization of lead from the maternal skeletal during pregnancy and lactation. Samples of blood, 6-day duplicate diet and environmental samples were analyzed by high-precision thermal ionization mass spectrometry for lead isotope ratios and lead concentrations. There was no statistically significant difference between seasons for blood lead concentrations and dietary intake although there were small differences in the isotopic composition for blood. One explanation for the lack of a seasonal effect in blood lead of our cohort may be the absence of climatic extremes in Sydney. The minimal effects from seasonality observed in this cohort make this an especially useful cohort within which to study effects that could be obscured by seasonal factors.

Impact of diet on lead in blood and urine in female adults and relevance to mobilization of lead from bone stores.

We measured high precision lead isotope ratios and lead concentrations in blood, urine, and environmental samples to assess the significance of diet as a contributing factor to blood and urine lead levels in a cohort of 23 migrant women and 5 Australian-born women. We evaluated possible correlations between levels of dietary lead intake and changes observed in blood and urine lead levels and isotopic composition during pregnancy and postpartum. Mean blood lead concentrations for both groups were approximately 3 microg/dl. The concentration of lead in the diet was 5.8 +/- 3 microg Pb/kg [geometric mean (GM) 5.2] and mean daily dietary intake was 8.5 microg/kg/day (GM 7.4), with a range of 2-39 microg/kg/day. Analysis of 6-day duplicate dietary samples for individual subjects commonly showed major spikes in lead concentration and isotopic composition that were not reflected by associated changes in either blood lead concentration or isotopic composition. Changes in blood lead levels and isotopic composition observed during and after pregnancy could not be solely explained by dietary lead. These data are consistent with earlier conclusions that, in cases where levels of environmental lead exposure and dietary lead intake are low, skeletal contribution is the dominant contributor to blood lead, especially during pregnancy and postpartum.

Comparison of the rates of exchange of lead in the blood of newly born infants and their mothers with lead from their current environment.

Newly born infants (n = 15) were monitored for 6 months after birth or for longer periods to evaluate the changes in isotopic composition and lead concentration in infants as compared with that in women from the same population groups and to determine the clearance rates of lead from blood in the infants. These data represent the first published results for serial blood sampling in a relatively large cohort of newly born infants. Blood lead concentrations decrease from the cord to samples taken at 60 to 90 days and then increase by amounts varying from negligible to 166%. In spite of concern about individual susceptibility to lead pharmacokinetics, changes in isotopic ratio followed a smooth decrease over time for 9 of the 11 infants born to migrant parents, and the patterns of variation were quite reproducible. Data for 2 of 4 infants born to multigenerational Australian parents exhibited little change in isotopic ratio over time, and in the other two cases, the changes were attributed to diet. The rate of exchange (t1/2) for the migrant infants of lead in blood derived from the mother during pregnancy and the lead from the current environment was calculated by using a linear function and ranged from 65 to 131 (91+/-19, mean+/-SD) days. The half-lives for the exchange of skeletal and environmental lead for 7 of the 8 women before significant mobilization of lead from the maternal skeleton ranged from 50 to 66 (59+/-6) days. One explanation for the longer half-lives for infants as compared with the mothers may be the proportionally higher contribution of current environmental (Australian) lead in the infants at parturition. Exchanges of lead in infants are more complex than for the adults, reflecting inputs from sources such as maternal skeletal lead during breast feeding.

Relationships of lead in breast milk to lead in blood, urine, and diet of the infant and mother.

We have obtained stable lead isotope and lead concentration data from a longitudinal study of mobilization of lead from the maternal skeleton during pregnancy and lactation and in which the newly born infants were monitored for 6 months postpartum to evaluate the effects of the local environment on lead body burden of the infant. Samples of maternal and infant blood, urine, and diet and especially breast milk were measured for 21 mothers and 24 infants. Blood lead concentrations were less than 5 microg/dl in all except one subject. The mean lead concentration in breast milk +/- standard deviation was 0.73 +/- 0.70 microg/kg. In seven subjects for whom serial breast milk sampling was possible, the lead concentration varied by factors of from 2 to 4, and for three subjects there was an increase at or after 90 days postpartum. For the first 60-90 days postpartum, the contribution from breast milk to blood lead in the infants varied from 36 to 80%. Multiple linear regression analyses indicated statistically significant relationships for some of the variables of isotope ratios and lead concentrations between breast milk, blood, urine, and diet for infants and mothers. For example, the analyses revealed that both a mother's breast milk 207Pb/206Pb and 206Pb/204Pb ratios and lead concentration provide information to predict her infant's blood 207Pb/206Pb and 206Pb/204Pb ratios. The major sources of lead in breast milk are from the maternal bone and diet. An evaluation of breast milk lead concentrations published over the last 15 years indicates that studies in which the ratio of lead concentrations in breast milk to lead concentrations in whole maternal blood (Multiple>100) were greater than 15 should be viewed with caution because of potential contamination during sampling and/or laboratory analyses. Selected studies also appear to show a linear relationship between breast milk and maternal whole blood, with the percentage of lead in breast milk compared with whole blood of <3% in subjects with blood lead levels ranging from 2 to 34 microgram/dl. The levels of lead in breast milk are thus similar to those in plasma. Breast-fed infants are only at risk if the mother is exposed to high concentrations of contaminants either from endogenous sources such as the skeleton or exogenous sources.

Blood lead-urine lead relationships in adults and children.

To determine the potential for using instead of blood as an indicator of lead exposure, especially in infants, lead concentrations and high-precision lead isotopic measurements have been compared in venous blood and "spot" urine (n > 260 from 182 different subjects) collected within the same 24-h period. Physiological conditions for the children and most of the adults were considered to be in a steady-state between body stores and lead in the environment. In the case of some adults, conditions were initially not steady-state because exposure conditions changed (for example, subjects moved to a country with lead of different isotopic composition.) There was a high correlation (r2 = ) between the blood and urine measurements of the isotope ratios but about 10% of measurements were outliers--the blood and urine measurements were further apart than was consistent with the measurement error that was generally obtained. The discrepancy was usually found to be associated with the urine measurement and was attributed to contamination during sampling. Weekly urine and monthly blood monitoring of an adult male over a 24-month period showed and excellent correlations, although the standard deviations were about an order of magnitude higher than the precision measured for replicate analyses of a single blood or urine sample. "Spot" urine analyses for two male subjects gave excellent agreement with 24-h urine samples. Standard deviations of the spot analyses were of similar order to those in the 24-month monitored subject. In cases where female adults from Eastern Europe migrated to Australia, there was generally a more rapid exchange of skeletal lead with Australian environmental lead in urine compared with blood. These data do not support a differential partitioning of endogenous lead into the plasma. At this stage, isotopic measurements of urine can be used as a proxy for isotopic measurements in blood. However, lead concentrations in blood and in urine are only weakly related. Concentrations of lead in urine cannot serve to predict concentrations of lead in blood, particularly at the lower range of exposures, for example, at blood concentrations less than 10 microgram/d1.

Mobilization of lead from the skeleton during the postnatal period is larger than during pregnancy.

A cohort of 15 immigrant females to Australia and 7 native Australian controls were monitored on a monthly basis with high-precision lead isotopic methods during gestation and for 6 months after pregnancy to determine the extent of lead mobilization from the maternal skeleton. Quarterly environmental samples of house dust, drinking water, urban air, gasoline, and a 6-day duplicate diet were also measured. The geometric mean blood lead concentration for the immigrant females on arrival in Australia was 3.0 microg/dl (range: 1.9 to 20 microg/dl), and for the Australian controls was 3.1 gm/dl (range: 1.9 to 4.3 microg/dl). During gestation and after pregnancy, blood lead concentrations varied, with mean individual changes of -14% to 83%. For the immigrant subjects, the percentage change in blood lead concentration was significantly greater during the postpregnancy period than during the 2nd and 3rd trimesters (p < 0.001). Skeletal contribution to blood lead, based on the isotopic composition for the immigrant subjects, increased in an approximately linear manner during pregnancy. The mean increases for each individual during pregnancy varied from 26% to 99%. Skeletal lead contribution to blood lead was significantly greater (p < 0.001) during the postpregnancy period than during the 2nd and 3rd trimesters. The contribution of skeletal lead to blood lead during the postpregnancy period remained essentially constant at the increased level of lead mobilization, although the duration of breastfeeding varied from 1 week to more than 6 months. The increased contribution of skeletal lead to blood lead during the postpregnancy period is attributed to increased mobilization of lead from maternal skeletal stores during lactation. The increased contribution of skeletal lead both during pregnancy and in the postpregnancy period is consistent with increased bone resorption, and may be associated with an inadequate calcium intake observed in quarterly 6-day duplicate diets. Mobilization of skeletal lead stores represents a potentially important source of perinatal lead intake and accumulation in the developing fetus. Only two subjects consumed dietary supplements for calcium, and their mobilization of lead from the skeleton to the blood was the lowest of all the subjects. These two subjects' use of calcium supplements may have reduced mobilization of skeletal mineral stores to supply the calcium needs of pregnancy and lactation. Calcium supplementation may be an important means of limiting fetal exposure to lead.

Pregnancy increases mobilization of lead from maternal skeleton.

The question of the extent of lead mobilization from the maternal skeleton during pregnancy and lactation is one of the most outstanding problems of lead toxicity. We have undertaken a longitudinal cohort study in an urban environment of European female immigrants of child-bearing age (18 to 35 years) to Australia whose skeletal lead isotopic composition has been determined to be different from that in their current environment. The cohort was to consist of 100 immigrants anticipated to provide 20 pregnant subjects who would be compared with two groups of control subjects: a matched immigrant nonpregnant control group and second-generation Australian pregnant control subjects. Pregnant subjects also serve as their own controls for a comparison of changes during gestation with those before conception. High-precision lead isotopic compositions and lead concentrations are measured in maternal blood and urine prenatally, monthly during gestation, and postnatally for 6 months; they are also measured in infant blood and urine for 6 months; environmental measures are sampled quarterly for 6-day duplicate diet, house dust and water, and urban air and gasoline. Because of continuing public health concerns about lead exposure, interim findings from this cohort are being reported. To date there have been 13 conceptions in immigrant subjects, with 7 births, in addition to 3 conceptions in the Australian control group, with 2 births. PbBs have been generally low, with a geometric mean of 3.0 microg/dl, and have ranged from 1.9 to 20 microg/dl. Increases in PbB of approximately 20% during pregnancy have been detectable even in subjects with low blood lead levels. The skeletal contribution to blood lead level, based on isotopic measurements, has exhibited a mean increase (and standard deviation) of 31% +/- 19% with a range from 9% to 65%. Earlier studies that used lead concentrations only have suggested that blood lead levels increased only during the second half of pregnancy. This increase in blood lead levels has also been observed in the present study. However, in two subjects the increases in total blood lead were also detected in the first 2 months of pregnancy. Changes in isotopic composition and blood lead during gestation for Australian pregnant controls were negligible. The ratio of cord/maternal blood lead levels varied from 0.54 to 1.05, and the ratio for the isotopic composition was 0.993 to 1.002. Results of this study confirm that lead is mobilized from skeletal stores at an accelerated rate during pregnancy and is transferred to the fetus. These results also show that mobilization from long-term stores (i.e., bone) contributes significantly to blood lead levels during pregnancy. Furthermore, exposure of the fetus to lead during pregnancy has implications for interpretations of neurobehavioral disorders attributed to only postnatal exposure. Even after 800 days of residence in Australia, the contribution of European skeletal lead to blood lead in nonpregnant subjects can be on the order of 50%, but the current PbB may give no indication of the former high skeletal lead burden.

Dietary lead intakes for mother/child pairs and relevance to pharmacokinetic models.

Blood and environmental samples, including a quarterly 6-day duplicate diet, for nine mother/child pairs from Eastern Europe have been monitored for 12 to >24 months with high precision stable lead isotope analysis to evaluate the changes that occur when the subjects moved from one environment (Eastern Europe) to another with different stable lead isotopes (Australia). The children were between 6 and 11 years of age and the mothers were between 29 and 37 years of age. These data were compared with an Australian control mother/child pair, aged 31 and 6 years, respectively. A rationale for undertaking this study of mother/child pairs was to evaluate if there were differences in the patterns and clearance rates of lead from blood in children compared with their mothers. Blood lead concentrations ranged from 2.1 to 3.9 microg/dl in the children and between 1.8 and 4.5 microg/dl in the mothers, but the mean of differences between each mother and her child did not differ significantly from zero. Duplicate diets contained from 2.4 to 31.8 microg Pb/kg diet; the mean+/- standard deviation was 5.5 +/- 2.1 microg Pb/kg and total daily dietary intakes ranged from 1.6 to 21.3 microg/day. Mean daily dietary intakes relative to body weight showed that the intake for children was approximately double that for the mothers (0.218 vs. 0. 113 microg Pb/kg body weight/day). The correlations between blood lead concentration and mean daily dietary intake either relative to body weight or total dietary intake did not reach statistical significance (p>0.05). Estimation of the lead coming from skeletal (endogenous) sources relative to the contribution from environmental (exogenous) sources ranges from 8 to 70% for the mothers and 12 to 66% for the children. The difference between mothers and children is not statistically significant (p = 0.28). The children do not appear to achieve the Australian lead isotopic profile at a faster rate than their mothers. These data provide evidence that the absorption or uptake of lead from dietary sources is similar in adult females and children of the age in this study. In spite of lower bone lead and faster bone remodeling and recycling in children compared with adult females, we see no differences between the mothers and their children in overall contribution of tissue lead to blood lead. Results from this study suggest that fractional absorption of ingested lead by children 6-11 years of age is comparable with absorption patterns observed among adult females in the 29-37-year-old age range. Because pharmacokinetic models apply a 40-50% absorption even for 7-year-old children, further investigations on fractional absorption of ingested lead by young children are warranted. Further investigations are especially needed in younger children than those who were subjects in the current study, particularly children in the 1-3-year-old age range. In addition, the effect of nutritional status and patterns of food intake on children's lead absorption require investigation, particularly given the increased prevalence of marginal nutritional status among low-income populations that are at increased risk of elevated blood lead levels.

Importance of monitoring family members in establishing sources and pathways of lead in blood.

High precision lead isotope measurements were undertaken to establish the sources and pathways in blood and environmental samples of five families from the Broken Hill lead mining community, New South Wales, Australia. The five families were selected from 27 families investigated to illustrate the different sources and pathways of lead into blood and the importance of monitoring the whole family. The results illustrate that although the major source of lead is from the orebody, paint and petrol can be significant contributors to both house dust and blood leads. The results also show that the sources and pathways can be from the father's occupation and hence monitoring of families is important, especially in high risk locations. In two cases, the elevated blood leads in the children did not derive from their current residence but from other residences in the community.

Non-orebody sources are significant contributors to blood lead of some children with low to moderate lead exposure in a major lead mining community.

High precision lead isotope ratios in blood from 58 children aged 1-11 years from the Broken Hill lead mining community have been measured to determine the source and pathways of lead in their blood. Sources of lead are from the Pb-Zn-Ag orebody (lead), from paint and from petrol. Thirty-five of the 58 children (60%) had blood leads (PbB) > or = 0.72 micromol/l (15 microg/dl), the current level of 'personal exposure and source remediation/abatement' compared with a 'background' level of approximately 0.29 micromol/l (6 microg/dl), estimated from adult females who were generally mothers of the children. Six of 17 children aged 7 years or older, had PbBs > or = 0.72 micromol/l (15 microg/dl). Even though the orebody lead is the major contributor to PbB in Broken Hill children, of the 35 children whose PbB is > or = 0.72 microm/l (15 microg/dl), 12 (34%) have approximately 50% or more of their PbB derived from sources such as paint and petrol or both by isotopic identification. The identification of elevated PbB in older children is a concern, especially for females, as there is potential for release of endogenous lead during pregnancy and lactation.

Stable lead isotope profiles in smelter and general urban communities: a comparison of environmental and blood measures.

High-precision lead isotope ratios and lead concentrations have been compared statistically and graphically in women of child-bearing age (n = 77) from two smelter communities and one general urban community to evaluate the relative contributions to blood lead of tissue lead stores and lead from the contemporaneous environment (soil, floor dust, indoor airborne dust, water, food). Blood lead (PbB) contents were generally low (e.g. <10 µg dL(-1)). Statistically significant isotopic differences in blood and environmental samples were observed between the three cities although isotopic differences in blood for individual subjects living in close proximity (∼200 m radius) was as large as the differences within a city. No single environmental measure dominated the biological isotope profile and in many cases the low levels of blood lead meant that their isotopic profiles could be easily perturbed by relatively small changes of environmental exposure. Apportioning of sources using lead isotopes is possibly not feasible, nor cost effective, when blood lead levels are <5 µg dL(-1). Interpretations based on statistical analyses of city-wide data do not give the same conclusions as when the houses are considered individually. Aggregating data from multiple subjects in a study such as this obscures potentially useful information. Most of the measures employed in this study, and many other similar studies, are markers of only short-to-medium integration of lead exposure. Serial sampling of blood and longer sampling times, especially for household variables, should provide more meaningful information.

Contribution of tissue lead to blood lead in adult female subjects based on stable lead isotope methods.

Public health and medical recommendations on prevention of lead toxicity rely on use of blood lead concentrations to assess lead exposure and predict onset of adverse health effects. Blood lead levels have generally been thought to reflect recent environmental lead exposures. However, tissue lead stores are accumulated over a long time period (i.e., years). These tissue stores, primarily from bone, can be remobilized as part of both normal physiologic and pathologic processes. Although chemical analyses do not differentiate lead isotopes, mass spectrometric determinations can differentiate the quantities of stable lead isotopes present in particular samples (e.g., lead 207, lead 206, lead 204, and lead 208). Selected geographic locations may have distinct isotopic profiles. For example, on mainland Australia the 206Pb/204Pb ratios reported in both environmental lead sources and blood samples are typically less than 17.0. By contrast, stable lead isotope profiles in blood samples of adult women immigrating from Eastern Europe and the former Soviet Union usually have 206Pb/204Pb ratios greater than 17.5 and as high as 18.5 on entry into Australia. Longitudinal monitoring of blood samples to determine stable lead isotope profiles by mass spectrometry and chemical analyses of blood samples for total lead content were conducted over a 300-day period. These data show that between 45% and 70% of lead in blood comes from long-term tissue lead stores. Recognition that the predominant source of lead in blood was tissue stores rather than the contemporaneous environment should greatly modify recommendations on use of blood lead to monitor occupational or environmental interventions. In addition, internal biokinetics of lead, documented through presence of tissue lead in blood, underlie the long-term health risks of lead exposure. Transfer of lead to the fetus from maternal tissue stores represents a special area of concern.

Lead bioavailability in the environment of children: blood lead levels in children can be elevated in a mining community.

Lower blood lead averages in mining communities, compared with other child exposure settings, e.g., innercity areas of the United States and smelter communities, have been attributed to lower bioavailability of lead to children in the mining areas. Direct supporting evidence of the lower bioavailability has, however, generally been lacking. Elevated blood lead levels for approximately 85% of children with > 10 micrograms/dl have been reported from the Broken Hill mining community in Australia. Lead isotope, optical, and scanning electron microscope analyses on the lead species from soils and dusts show them to be derived mainly from weathered ore body material. Solubility tests using 0.1M HCl on the -53 + 38 microns fraction of soil and dust show the lead species to have a high degree of bioavailability. Ingestion of soil and dust, either directly or via mouthing activity, is the main source and pathway for elevated blood lead in children from this community.

Effect of plumbing systems on lead content of drinking water and contribution to lead body burden.

Stable lead isotopes and lead contents in drinking water from a number of Australian cities have been measured to determine the contribution of drinking water to body burden. Lead contents are generally < 2 micrograms/l and thus contribute an insignificant amount to the lead budget in humans in Australia. First-flush and running water samples taken at intervals of up to 10 min show that equilibrium is reached within 1 min or approximately 10 l by volume. There is, however, large variability in both lead content and isotopic composition within the first minute which brings into question the reliability of the recommended sampling time of 30 s. Extremely large isotopic differences between individual dwellings within the one city and between dwellings and the storage tanks for the water supply are attributed to differences in lead residing in the plumbing within the dwellings, usually from lead solder in brass fittings. Isotopic analysis of solder and water from two dwellings confirm this relationship.