Determination of plasma lead levels in normal subjects and in lead-exposed workers.

Lead levels in whole blood and in plasma were measured in 64 non-exposed and in 29 exposed subjects with signs and symptoms of varying severity. Lead was determined by atomic absorption spectrophotometry after chelation with ammonium pyrrolidine dithiocarbamate and extraction with methyl isobutyl ketone. The method has a sensitivity of 04 ,ug/l00 ml (0.02 ,umol/l) for whole blood and of 0-2 ,g/100 ml (0.01 O,mol/l) for plasma and is reliably accurate and precise. Plasma lead increases progressively and significantly with the increase of whole blood lead, while its relative percentage in the plasma remains practically constant at all concentrations in whole blood. In exposed subjects a highly significant correlation was found between lead in plasma and lead in urine (r = 0 549) but the correlation coefficient was higher for whole blood lead versus urinary lead (r = 0 938). Aminolevulinic acid excretion in urine appeared to be significantly related to plasma lead concentration (r = 0-563) but to a greater extent to whole blood levels (r = 0-801). There was no significant correlation between lead in plasma and the logarithm of aminolevulinic acid dehydratase. The hypothesis is advanced that plasma lead, the more biologically active fraction of the metal, could be related to different individual sensitivities which would condition the development of toxic effects in various organs at different levels of lead. Although normally considered to be a single compartment (Rabinowitz et al., 1976) blood contains lead (Pb) in two forms, a non-diffusible form bound to erythrocytes and a diffusible form in plasma. Because of the uneven distribution of the metal between red blood cells and plasma, two physiological pools may be considered to exist. The diffusible form, because of its greater bioavailability, is likely to influence lead concentration of the other compartments directly and, as a consequence, to produce critical effects in the various organs, with the possible exception of erythrokinetic effects. There is little information so far relating to plasma lead levels; this may be attributable either to the technical difficulties involved in their measurement or to the lack of evidence of correlation with whole blood concentrations (Ambrosi and Chiantera, 1962; Rosen et al., 1974) which are normally considered to be a good indication of the degree of lead exposure. Received for publication 22 February 1977 Accepted for publication 19 April 1977 21 Varying concentrations have been reported for serum lead: in adults, Ambrosi and Chiantera (1962) found levels ranging from 4-0 to 8-6 pug/100 ml (019-0-41 ,umol/l) in non-exposed subjects and from 5-0 to 13(),ug/100 ml (0 24-063 ,umol/l) in workers showing toxic effects, by using a dithizone method. Butt et al. (1964) by means of an emission spectrochemical technique, estimated lead values of 3 9, 2-7 and 2-8 ,ug/10O ml (0-19, 0-13 and 0(13 ,utmol/l) respectively in three non-exposed groups. Lloyd Davies and Rainsford (1967) reported figures of 1-2 ug (0-05-01 ,umol/l) of lead in serum of nonexposed subjects and of 3-4 Htg/100 ml (0-14-0-19 ,tmol/l) at whole blood values of 100 ,ug/100 ml (4-83 ,umol/l). In children, Robinson et al. (1958) found plasma concentrations varying from 0 to 9 0 ug/I100 ml (0-43 ,umol/l) by a dithizone method; Rosen et al. (1974) examining the blood of normal and lead-poisoned children by a flameless atomic absorption spectrophotometric technique (AAS) found lead levels ranging from 1 0 to 7(0 ,ug/100 ml (005-0(34 j,molfl), the mean concentration proving remarkably constant regardless ofwhole blood levels, haematocrit values and symptoms, and without group.bmj.com on October 28, 2017 Published by http://oem.bmj.com/ Downloaded from