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. 1992 Sep;49(9):631–644. doi: 10.1136/oem.49.9.631

In vivo measurements of lead in bone at four anatomical sites: long term occupational and consequent endogenous exposure.

J Erkkilä 1, R Armstrong 1, V Riihimäki 1, D R Chettle 1, A Paakkari 1, M Scott 1, L Somervaille 1, J Starck 1, B Kock 1, A Aitio 1
PMCID: PMC1039308  PMID: 1390269

Abstract

Measurements of bone lead concentrations in the tibia, wrist, sternum, and calcaneus were performed in vivo by x ray fluorescence on active and retired lead workers from two acid battery factories, office personnel in the two factories under study, and control subjects. Altogether 171 persons were included. Lead concentrations in the tibia and ulna (representative of cortical bone) appeared to behave similarly with respect to time but the ulnar measurement was much less precise. In an analogous fashion, lead in the calcaneus and sternum (representative of trabecular bone) behaved in the same way, but sternal measurement was less precise. Groups occupationally exposed to lead were well separated from the office workers and the controls on the basis of calculated skeletal lead burdens, whereas the differences in blood lead concentrations were not as great, suggesting that the use of concentrations of lead in blood might seriously underestimate lead body burden. The exposures encountered in the study were modest, however. The mean blood lead value among active lead workers was 1.45 mumol l-1 and the mean tibial lead concentration 21.1 micrograms (g bone mineral)-1. The kinetics of lead in the tibia appeared to be noticeably different from that in the calcaneus. Tibial lead concentration increased consistently both as a function of intensity of exposure and of duration of exposure. Calcaneal lead concentration, by contrast, was strongly dependent on the intensity rather than duration of exposure. This indicated that the biological half life of lead in calcaneus was less than the seven to eight year periods into which the duration of exposure was split. Findings for retired workers clearly showed that endogenous exposure to lead arising from skeletal burdens accumulated over a working lifetime can easily produce the dominant contribution to systemic lead concentrations once occupational exposure has ceased.

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Selected References

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  1. Barry P. S. A comparison of concentrations of lead in human tissues. Br J Ind Med. 1975 May;32(2):119–139. doi: 10.1136/oem.32.2.119. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Batuman V., Wedeen R. P., Bogden J. D., Balestra D. J., Jones K., Schidlovsky G. Reducing bone lead content by chelation treatment in chronic lead poisoning: an in vivo X-ray fluorescence and bone biopsy study. Environ Res. 1989 Feb;48(1):70–75. doi: 10.1016/s0013-9351(89)80086-6. [DOI] [PubMed] [Google Scholar]
  3. Bigler R. E., Woodard H. Q. Skeletal distribution of mineralized bone tissue in humans. Health Phys. 1976 Sep;31(3):213–218. doi: 10.1097/00004032-197609000-00001. [DOI] [PubMed] [Google Scholar]
  4. Chettle D. R., Scott M. C., Somervaille L. J. Improvements in the precision of in vivo bone lead measurements. Phys Med Biol. 1989 Sep;34(9):1295–1300. doi: 10.1088/0031-9155/34/9/014. [DOI] [PubMed] [Google Scholar]
  5. Christoffersson J. O., Ahlgren L., Schütz A., Skerfving S., Mattsson S. Decrease of skeletal lead levels in man after end of occupational exposure. Arch Environ Health. 1986 Sep-Oct;41(5):312–318. doi: 10.1080/00039896.1986.9936703. [DOI] [PubMed] [Google Scholar]
  6. Christoffersson J. O., Schütz A., Ahlgren L., Haeger-Aronsen B., Mattsson S., Skerfving S. Lead in finger-bone analysed in vivo in active and retired lead workers. Am J Ind Med. 1984;6(6):447–457. doi: 10.1002/ajim.4700060608. [DOI] [PubMed] [Google Scholar]
  7. Haenninen H., Hernberg S., Mantere P., Vesanto R., Jalkanen M. Psychological performance of subjects with low exposure to lead. J Occup Med. 1978 Oct;20(10):683–689. [PubMed] [Google Scholar]
  8. Hernberg S., Tola S. The battle against occupational lead poisoning in Finland. Experiences during the 15-year period 1964--1978. Scand J Work Environ Health. 1979 Dec;5(4):336–344. doi: 10.5271/sjweh.2648. [DOI] [PubMed] [Google Scholar]
  9. Hu H., Milder F. L., Burger D. E. X-ray fluorescence measurements of lead burden in subjects with low-level community lead exposure. Arch Environ Health. 1990 Nov-Dec;45(6):335–341. doi: 10.1080/00039896.1990.10118752. [DOI] [PubMed] [Google Scholar]
  10. Landrigan P. J. Toxicity of lead at low dose. Br J Ind Med. 1989 Sep;46(9):593–596. doi: 10.1136/oem.46.9.593. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Rabinowitz M. B., Wetherill G. W., Kopple J. D. Kinetic analysis of lead metabolism in healthy humans. J Clin Invest. 1976 Aug;58(2):260–270. doi: 10.1172/JCI108467. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Schütz A., Skerfving S., Ranstam J., Christoffersson J. O. Kinetics of lead in blood after the end of occupational exposure. Scand J Work Environ Health. 1987 Jun;13(3):221–231. doi: 10.5271/sjweh.2059. [DOI] [PubMed] [Google Scholar]
  13. Seppäläinen A. M., Hernberg S. Subclinical lead neuropathy. Am J Ind Med. 1980;1(3-4):413–420. doi: 10.1002/ajim.4700010319. [DOI] [PubMed] [Google Scholar]
  14. Somervaille L. J., Chettle D. R., Scott M. C., Aufderheide A. C., Wallgren J. E., Wittmers L. E., Jr, Rapp G. R., Jr Comparison of two in vitro methods of bone lead analysis and the implications for in vivo measurements. Phys Med Biol. 1986 Nov;31(11):1267–1274. doi: 10.1088/0031-9155/31/11/008. [DOI] [PubMed] [Google Scholar]
  15. Somervaille L. J., Chettle D. R., Scott M. C. In vivo measurement of lead in bone using x-ray fluorescence. Phys Med Biol. 1985 Sep;30(9):929–943. doi: 10.1088/0031-9155/30/9/005. [DOI] [PubMed] [Google Scholar]
  16. Somervaille L. J., Chettle D. R., Scott M. C., Tennant D. R., McKiernan M. J., Skilbeck A., Trethowan W. N. In vivo tibia lead measurements as an index of cumulative exposure in occupationally exposed subjects. Br J Ind Med. 1988 Mar;45(3):174–181. doi: 10.1136/oem.45.3.174. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Somervaille L. J., Nilsson U., Chettle D. R., Tell I., Scott M. C., Schütz A., Mattsson S., Skerfving S. In vivo measurements of bone lead--a comparison of two x-ray fluorescence techniques used at three different bone sites. Phys Med Biol. 1989 Dec;34(12):1833–1845. doi: 10.1088/0031-9155/34/12/007. [DOI] [PubMed] [Google Scholar]
  18. Subramanian K. S., Meranger J. C. A rapid electrothermal atomic absorption spectrophotometric method for cadmium and lead in human whole blood. Clin Chem. 1981 Nov;27(11):1866–1871. [PubMed] [Google Scholar]
  19. Wielopolski L., Ellis K. J., Vaswani A. N., Cohn S. H., Greenberg A., Puschett J. B., Parkinson D. K., Fetterolf D. E., Landrigan P. J. In vivo bone lead measurements: a rapid monitoring method for cumulative lead exposure. Am J Ind Med. 1986;9(3):221–226. doi: 10.1002/ajim.4700090304. [DOI] [PubMed] [Google Scholar]
  20. Wittmers L. E., Jr, Aufderheide A. C., Wallgren J., Rapp G., Jr, Alich A. Lead in bone. IV. Distribution of lead in the human skeleton. Arch Environ Health. 1988 Nov-Dec;43(6):381–391. doi: 10.1080/00039896.1988.9935855. [DOI] [PubMed] [Google Scholar]
  21. Woodard H. Q., White D. R. Bone models for use in radiotherapy dosimetry. Br J Radiol. 1982 Apr;55(652):277–282. doi: 10.1259/0007-1285-55-652-277. [DOI] [PubMed] [Google Scholar]

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