In 14 retired lead workers, followed for over 18 years after end of exposure, repeated analyses of lead levels in finger bone by an in vivo X-ray fluorescence method revealed a decrease of lead concentration. The data were analysed using an exponential retention model. For the whole group the biological half-time was 16 (asymptotic 95% confidence interval, CI 12,23) years. The median of the estimated bone lead levels at the end of exposure was 85 micrograms.g-1 above the "background" (3 micrograms.g-1). A simultaneous follow-up of blood lead levels displayed a decrease, which could be described by a tri-exponential retention model with group half-times of 34 (CI 29,41) days, 1.2 (CI 0.9,1.8) years, and 13 (CI 10,18) years, respectively. The median of the estimated blood lead levels at the end of exposure for the three components were 0.49, 0.61, and 1.1 mumol.l-1 above the "background" (0.38-0.56 mumol.l-1), respectively. The well-documented decrease of lead exposure in the general population over the years, urged the use of a decreasing "background" of blood lead during the time of the study. The slowest of the three components represented the skeleton (probably mainly cortical bone), as did mainly probably also the intermediate one (trabecular bone). The data show the rather slow turnover of lead in the skeleton, the usefulnes of in vivo skeletal lead measurements as a long-term exposure index, and the importance of bone as a source of "endogenous" lead exposure.

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.

Samples of vertebral bone were obtained by skeletal biopsy and lead concentrations were determined by atomic absorption spectroscopy. The median level of lead in bone in 27 active lead workers was 29 micrograms/g wet weight (range 2-155), corresponding to 370 micrograms/g calcium (range 30-1,120). In 9 retired workers, the corresponding levels were 19 micrograms/g (5-76) and 250 micrograms/g calcium (60-700); in 14 reference subjects without occupational exposure, 1.3 micrograms/g (1-4) and 13 micrograms/g calcium (8-40). The bone lead content rose with time of exposure. Comparison of levels in vertebra with those in fingerbone, as measured by in vivo x-ray fluorescence in the same subjects, strongly suggested the presence of lead pools with different kinetics. The accumulation pattern, as well as the relation between levels in vertebra and fingerbone, suggests a much shorter half-time of lead in the mainly trabecular vertebral bone as compared to the mainly cortical fingerbone. Further, there was an association between vertebral and blood lead levels in the retired workers, which shows a considerable endogenous lead exposure from the skeletal pool.

Lead levels in finger bone were monitored using an in vivo X-ray fluorescence technique in retired lead workers. Eight subjects followed for 2-5 yr directly after end of exposure all displayed a decrease. Their average half-time was 7 (range 3-15) yr. In a second group of six persons, followed from year 7 to year 13 after finishing lead work, a decrease was seen in all but one. The average half-time for this group was 8 (range 2 infinity) yr. The mean value for both groups was 7 yr. The results show that there is a decrease of lead in bone after the end of exposure and that it is considerably faster than estimated earlier from various data on lead metabolism.