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The impact of lead in soil and dust on blood lead concentrations in young children (i.e., 1-5 y of age, N = 202) and the risk of health effects were investigated in an urban and a mining area of Sweden. Blood, soil, and indoor dust, as well as information on lead-exposure factors, were collected. The blood lead concentrations (total range = 9-77 microg/l) the authors measured indicated a low risk for lead-induced health effects. Lead in soil (i.e., < 10-5,000 microg/g) and in dust (i.e., < 1-316 microg/g) had little effect on blood lead concentrations, given the present conditions and present concentration range--especially in the mining area. Urban children had significantly higher blood lead concentrations than children in the mining area, despite higher concentrations of lead in soil in the mining area. In the urban children, blood lead concentrations were influenced by parental smoking and lead in dust at day-care centers.

A capillary blood microsampling technique was tested among urban young children in Stockholm. Blood lead (BPb) and hemoglobin (Hb) concentrations were determined in capillary blood obtained by fingerstick from 41 children, 13-20 months old, and the accompanying parent. The quality control included control for lead (Pb) and cadmium (Cd) contamination of material and equipment used for blood sampling, washing procedures for the hands and fingers to be punctured, comparisons of Pb and Cd concentrations in blood obtained by fingerstick and by brachial vein puncture from the same individuals, analysis of external quality control samples for Pb and Cd in blood together with the collected samples, and evaluation of the analytical performance using linear regression analysis. The results showed that blood sampling material may contaminate the blood samples with amounts of Pb and Cd that would seriously influence the monitoring results in the low concentration range (< 100 micrograms Pb/L and < 1 microgram Cd/L). However, it is possible to obtain reliable BPb concentrations (> 10 micrograms Pb/L), but not BCd concentrations (< 1 microgram Cd/L), with the capillary blood microsampling technique tested provided that a strict quality control is applied. The sampling procedure tested was well accepted by the children and their parents. The children's median BPb concentration (27 micrograms/L; range 9-73 micrograms/L) was similar to the median BPb concentration of their parents (27 micrograms/L; range 7-74 micrograms/L). However, the correlation between child and parent BPb concentrations was poor (R2 = 0.20), which may indicate different sources to Pb exposure in children and parents.

Methods for determining personal exposure to lead and cadmium were tested in Stockholm in 1988. Lead and cadmium in breathing-zone air, 24-h duplicate diets, and feces of 15 nonsmoking women (27-46 years of age) were studied. Blood was collected at the beginning of and immediately after the test period (seven consecutive days). An extensive quality assurance program was included. Most technical problems were encountered in the 24-h collection of airborne particles. The pumps were noisy, and the batteries had to be recharged every 6-8 h. The lead and cadmium levels in feces were found to be useful indicators of the total ingested amounts of these metals. Because of the large day-to-day variation in the dietary intake of lead and cadmium, the sampling period for duplicate diets and feces should be at least 5-6 d.

Blood lead levels in 32 male chronic alcoholic patients were measured and related to drinking habits. An external reference group and a group with previous high alcohol consumption served as controls. Blood lead concentrations were significantly higher (P less than 0.05) in the group with current high alcohol consumption (mean +/- S.D.) (90 +/- 48 micrograms/l, n = 17) than in the external reference group (57 +/- 27 micrograms Pb/l, n = 35). The blood lead concentrations in the latter group were similar to those in the group with previous high alcohol consumption (55 +/- 20 micrograms Pb/l, n = 15). Patients with excessive consumption of wine only (average intake 2.61 wine/day, range 1.3-4.5 l/day) had particularly elevated blood lead concentrations (149 +/- 31 micrograms Pb/l, n = 5), whereas blood lead levels were close to the control value in patients with excessive consumption of spirits only (68 +/- 28 micrograms Pb/l, n = 7). Furthermore, within the external reference group blood lead levels were higher in those who regularly drank more than 0.51 of wine on several occasions each week (96 +/- 22 micrograms Pb/l, n = 6) than in those who consumed less wine (48 +/- 20 micrograms Pb/l, n = 29). In a recent study of table wines sold in Sweden the average lead concentration in 84 samples was found to be 73 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Lead concentrations in blood and brain were measured in rats exposed to lead via drinking water, 0.25% Pb (12 mM), and dithiocarbamate/thiuram derivatives administered by gavage singly or in combination for 6 weeks. Sodium salts of diethyldithiocarbamate (DEDTC) and dimethyldithiocarbamate (DMDTC) were given in doses of 0.2 mmol/kg and tetramethylthiuram disulfide (thiram) and tetraethylthiuram disulfide (disulfiram) in doses of 0.1 mmol/kg twice a week. In rats that received lead plus dithiocarbamate/thiuram derivatives lead concentrations in blood and brain were significantly increased; disulfiram being most effective in increasing lead levels, followed by thiram, DMDTC and DEDTC. In blood, lead levels were increased 3-fold and in brain almost 4-fold after treatment with lead plus disulfiram compared to treatment with lead alone. When rats were given DEDTC or thiram by gavage (0.1 mmol/kg/day 5 days a week for 2 weeks) after cessation of the lead treatment, there was no increase in blood lead levels but in thiram-treated rats brain lead concentration was increased 2.7-fold. In rats treated with DEDTC intraperitoneally after cessation of lead treatment, both blood and brain concentrations of lead were increased. This study suggests that combined exposure of lead and dithiocarbamate/thiuram derivatives causes a substantial increase in brain levels of lead which are not always reflected in increases of blood lead levels. This interaction effect ought to be taken into consideration when evaluating the health effects of environmental and occupational lead exposure.

The effects of early postnatal lead administration on the spontaneous activity of cerebellar Purkinje neurons were studied electrophysiologically in adult male Sprague-Dawley rats. Newborn rat litters were divided into three groups and injected daily from Day 1 to Day 20 after birth with 8 mg NaAc/kg, 1 mg PbAc/kg, or 8 mg PbAc/kg intraperitoneally. Purkinje neurons in all three groups showed regular and sustained discharge. However, the mean spontaneous firing rate was significantly lower in the 8-mg PbAc/kg group (26.13 +/- 1.28 Hz) compared to the NaAc controls (32.39 +/- 1.93, P greater than 0.01). Furthermore, the distribution of the firing rates of the Purkinje cells were different in the two groups, with an obvious loss of faster firing cells in the 8-mg PbAc/kg group. No differences were seen between the 1-mg PbAc/kg group and the NaAc controls. As the 8-mg PbAc/kg group weighed significantly less than the NaAc group, malnourished animals were produced by using oversized litters, to control for any changes caused by the lower body weight. However, when compared to concomitantly raised controls, no changes could be seen in Purkinje cell discharge in the malnourished animals. It is concluded that neonatal exposure to lead can cause permanent changes in spontaneous Purkinje cell discharge.

Lead and cadmium was determined in whole blood samples obtained from 473 nonoccupationally exposed adult persons in Sweden in 1980. Analyses were performed using atomic absorption spectrophotometry equipped with an electrothermal atomization unit. Accuracy of the analysis was confirmed by the analysis of quality control samples. Blood lead concentrations were shown to be significantly influenced by sex, smoking habits, and alcohol consumption. Current male smokers had a median blood lead level of 92 micrograms Pb/liter, as compared to 77 micrograms Pb/liter for nonsmokers. For females the corresponding values were 69 micrograms Pb/liter and 57 micrograms Pb/liter for current smokers and nonsmokers, respectively. Highly significant correlations were found between stated alcohol consumption and blood lead in most of the different sex and smoking categories. People living in apartments close to streets with heavy traffic in Stockholm had slightly, but not significantly, higher blood lead levels when compared to people living in areas of this city with low traffic density. Blood cadmium levels were very strongly affected by smoking habits. A significant correlation existed between the number of cigarettes consumed daily and blood cadmium concentration. The median blood cadmium level for nonsmoking males was 0.2 micrograms Cd/liter (less than or equal to 0.2, detection limit) and for females 0.3 micrograms Cd/liter. About 90% of all nonsmokers had cadmium concentrations in blood below 0.6 micrograms Cd/liter, whereas about 90% of the current male and female smokers had cadmium concentrations in blood of 0.6 micrograms Cd/liter or more.

A number of measures have been taken to decrease the spread of lead to ambient air and food. In a study of the effect of these and other preventive measures, blood samples from approximately 100 persons living in the inner city area of Stockholm were collected and analyzed for lead content on three different occasions, in 1980, 1983, and 1984. The same subjects were examined on at least two occasions and the analytical method, atomic absorption spectrophotometry, was carefully controlled by means of reference samples on each occasion. The blood lead levels decreased during the observation period. The average blood lead concentrations for all the examined persons were 0.37, 0.26, and 0.25 mumol/l for 1980, 1983, and 1984, respectively. The mean of the differences in individual blood lead levels for 1980 and 1984 was 0.12 mumol/l. This figure corresponds to an average decrease in blood lead of 34% for all the subjects examined in 1980. The decrease occurred mainly during the period 1980-1983 (mean 0.11 mumol/l) and, thereafter, was only slight for the period 1983-1984 (mean 0.01 mumol/l). Factors such as age, sex, and change of residence during the observation period did not influence the final results.

The effects of disulfiram (tetraethylthiuram disulfide) on blood and brain lead levels and on lead-induced changes in growth and cerebellar Purkinje neuron excitability were assessed in adult Sprague-Dawley rats. Disulfiram is metabolized to diethyldithiocarbamate, which forms a lipophilic complex with lead, and can thereby influence the tissue distribution of lead. Pregnant rats were exposed to 0.25% lead acetate or an equimolar amount of sodium acetate in the drinking water, and these treatments were continued for 4 weeks after birth. Half of the mothers from each group were given 0.1 mmole/kg disulfiram orally twice a week until parturition, after which the treatment was continued for 4 weeks in the respective pups in the form of subcutaneous injections. Although lead exposure markedly increased blood lead levels, the increase in brain lead levels was much more modest. Disulfiram markedly increased brain lead levels while blood lead levels in this group were only slightly elevated as compared to animals receiving lead alone. In addition, the lead + disulfiram group had depressed weight gain during maturation, and Purkinje neuron firing rates were reduced. The lead alone and disulfiram alone groups were not different from controls in these respects. These data suggest that disulfiram potentiates the adverse effects of lead on growth rates and on cerebellar Purkinje neuron function by facilitating the accumulation of lead in brain tissue.