In 75 active lead workers the median lead level in finger-bone (bone-Pb), as determined in vivo by an X-ray fluorescence method, was 43 micrograms/g (range less than 20-122). In 32 retired workers the median level was even higher, 59 micrograms/g (range less than 20-135), which indicates a slow turnover rate of lead in finger-bone. This was confirmed in 18 of the "active" workers, in whom bone-Pb was studied in connection with an exposure-free period. In spite of a significant decrease in blood-lead levels (B-Pb), no systematic change of bone-Pb occurred. There was an increase of bone-Pb with time of employment, but with a large interindividual variation. No association was found between bone-Pb and present B-Pb in the active lead workers. However, in the retired ones, B-Pb rose with increasing bone-Pb. The bone-lead pool thus causes an "internal" lead exposure.

The concentrations of lead in the phalanges and in the blood were determined in 22 subjects who had formerly been exposed to lead in a storage battery plant, which had been closed for seven years. The bone lead concentration was measured in vivo using an x-ray fluorescence technique in which two 57Co y-ray sources were used for generating the characteristic x-rays of lead, which were measured with a Ge(Li) detector. In three subjects the variation of the lead concentration along the forefinger was measured together with the lead concentration in the tibia. The measured lead concentrations in the phalanges were between 20 lug/g (our detection limit) and 118 ,ug/g. The lead concentration in the phalanges was found to increase with the length of employment, but no simple relation was found between the lead concentrations in the blood and in the phalanges. The decrease in the blood lead concentration after the cessation of exposure was followed in four subjects. Seven years after exposure had ended, the blood lead concentration was found to be more dependent on the daily intake of lead than on the release of lead from the skeleton. These experimental results could be explained by a two-compartment model using exchange rates given in publications. This model has also been used to calculate the blood lead concentration that could be achieved after a sudden release of lead from the skeleton.The skeleton contains about 90-95% of the total body burden of lead.'2 Measurements of the lead concentration in the skeleton are therefore of fundamental importance for estimating the total body burden of lead. In earlier publications3-5 we have reported the in-vivo detection of lead in the skeleton of lead workers using x-ray fluorescence analysis. This paper deals with a comparison between the lead concentrations in the blood and in the skeleton as determined in the phalanges by x-ray fluorescence analysis in vivo. The determinations were carried out on subjects whose occupational exposure to lead had ended seven years before the study. Materials and methodsTwenty-two men aged between 27 and 75 years (mean 57), who had earlier worked in a storage Received 9 May 1979 Accepted 4 June 1979 battery plant for periods from 0-8 to 45 years (mean 22) were studied. At the time of the measurements the factory had been closed for seven years, since which time none of the subjects studied had been occupationally exposed to lead. Blood samples for determination of the lead content were collected at the time of the in-vivo measurement and analysed by atomic absorption spectrophotometry.6 For some of the subjects studied, the variation in the blood lead concentration had also been followed during the first year after the closing down of the factory.In our determination of lead in the skeleton the lowest detection limit (20 ,ug

Delta-aminolevulinic acid dehydratase (ALAD) is an enzyme involved in the biosynthesis of heme, in which it catalyzes the condensation of two molecules of delta-aminolevulinic acid to one molecule of porphobilinogen. It is a sulfhydryl enzyme, which means, among other things, that its activity is inhibited by many heavy metals. In the present investigation rabbits were given either zinc or lead or both. Zinc had a strong activating effect on ALAD in vivo, and the inhibitory effect of lead was almost completely eliminated. A close positive correlation was found between ALAD in the red blood cells and zinc in the plasma, but there was no correlation between ALAD and zinc in the red blood cells. These observations are of particular interest in the light of recent findings, suggesting that zinc is an essential metal for ALAD.

Hager-Aronsen, Birgitta (1971). Brit. J. industr. Med., 28, 52-58. An assessment of the laboratory tests used to monitor the exposure of lead workers. In order to ascertain which laboratory tests are valuable for the monitoring of lead workers, 168 men exposed to lead at eight factories were examined for lead (Pb), protoporphyrin (PP), haemoglobin (Hb), and basophilic stippling of red cells (BSC) in the blood and for 3-aminolevulinic acid (ALA) and coproporphyrin (CP) in the urine.The counting of BSC and the determination of PP in the blood are both complicated and time-consuming procedures. As they do not offer any particular advantages in the detection or evaluation of lead poisoning they are considered as less suitable.The concentration of Pb in the blood reflects the absorption of the lead but not its effect. This is certainly a disadvantage.A highly significant, negative correlation was found between Hb in the blood and ALA in the urine.The concentrations of ALA and CP in the urine are both good indicators of the degree of lead poisoning. The former is more specific and more sensitive and is therefore considered the most suitable test for the biochemical monitoring of lead workers. A simple, safe, and quick method is recommended.Determinations of Hb and Pb in the blood may be useful as supplementary methods in the evaluation of lead poisoning but are, in our experience, only seldom needed.

No abstract

No abstract

It has been known for some years that lead and some other metals such as mercury and silver have an inhibitory action on the activity of δ-aminolaevulinic acid dehydratase (ALAD) in red blood cells. Zinc in small concentrations has likewise an inhibitory effect on ALAD, while, in higher concentrations, this metal gives a significant increase in the activity of ALAD in red blood cells. This was shown in in vitro as well as in vivo studies.

No abstract