Skip to main content
NCBI home page
Environmental Health Perspectives logoLink to Environmental Health Perspectives
. 2002 Mar;110(3):263–268. doi: 10.1289/ehp.02110263

The relationship between lead in plasma and whole blood in women.

Donald Smith 1, Mauricio Hernandez-Avila 1, Martha Maria Téllez-Rojo 1, Adriana Mercado 1, Howard Hu 1
PMCID: PMC1240766  PMID: 11882477

Abstract

Studies have suggested that plasma lead levels may better reflect the toxicologically labile fraction of circulatory Pb that is more freely available for exchange with target tissues than do Pb levels in whole blood. Studies have also reported an apparent severalfold variation in the relative partitioning of Pb between whole blood and plasma (or serum) for a given whole-blood Pb level. This may reflect inherent differences in the plasma Pb/whole blood Pb partitioning among individuals and/or methodologic challenges associated with the collection and analyses of samples that generally contain < 1-2 ng total Pb. Here, we conducted a longitudinal assessment of the relationship between Pb in whole blood and plasma in environmentally exposed reproductive-age women (n = 63) living in Mexico City, Mexico. We collected whole blood and plasma samples using trace metal clean techniques and analyzed them for Pb using high-resolution inductively coupled plasma mass spectrometry. A subset of subjects provided repeated blood samples weekly for 4 consecutive weeks (n = 17 subjects) or every 1-2 months over a 9-month period (n = 14 subjects). Plasma Pb concentration was significantly positively associated with whole-blood Pb in a curvilinear fashion over the range of blood Pb values observed here (2.13-39.7 microg/dL). This relationship was best described by the function Plasma Pb = e (-2.392 + 0.0898 x blood Pb), where SE(coefficient) = 0.0054, SE(constant) = 0.063 (n = 63 subjects, n = 141 observations). Results from the short- and long-term repeated collection subjects indicated that the within- and between-subject variance components were not significantly different between the two subsets of subjects. The between-subjects component accounts for 78% of the variance in plasma Pb levels, while the residual variance (22%) may be attributed to other unmeasured factors. Collectively, this study demonstrates that plasma Pb measurements may be applied to general clinical settings, provided that established trace metal clean techniques are adopted. This study also shows that the relative (%) partitioning of whole-blood Pb in plasma naturally varies by a factor of about 2-4-fold among subjects at a given blood Pb level. Because Pb in the plasma is considered to more closely represent the fraction of Pb in the circulation that is readily exchanged with peripheral target tissues (e.g., brain, kidney, skeleton), the routine assessment of plasma Pb may provide a more meaningful measure of toxicologically available Pb.

Full Text

The Full Text of this article is available as a PDF (766.2 KB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Bergdahl I. A., Schütz A., Gerhardsson L., Jensen A., Skerfving S. Lead concentrations in human plasma, urine and whole blood. Scand J Work Environ Health. 1997 Oct;23(5):359–363. doi: 10.5271/sjweh.232. [DOI] [PubMed] [Google Scholar]
  2. Bergdahl I. A., Sheveleva M., Schütz A., Artamonova V. G., Skerfving S. Plasma and blood lead in humans: capacity-limited binding to delta-aminolevulinic acid dehydratase and other lead-binding components. Toxicol Sci. 1998 Dec;46(2):247–253. doi: 10.1006/toxs.1998.2535. [DOI] [PubMed] [Google Scholar]
  3. Bergdahl I. A., Vahter M., Counter S. A., Schütz A., Buchanan L. H., Ortega F., Laurell G., Skerfving S. Lead in plasma and whole blood from lead-exposed children. Environ Res. 1999 Jan;80(1):25–33. doi: 10.1006/enrs.1998.3880. [DOI] [PubMed] [Google Scholar]
  4. Cake K. M., Bowins R. J., Vaillancourt C., Gordon C. L., McNutt R. H., Laporte R., Webber C. E., Chettle D. R. Partition of circulating lead between serum and red cells is different for internal and external sources of lead. Am J Ind Med. 1996 May;29(5):440–445. doi: 10.1002/(SICI)1097-0274(199605)29:5<440::AID-AJIM2>3.0.CO;2-Q. [DOI] [PubMed] [Google Scholar]
  5. Finkelstein Y., Markowitz M. E., Rosen J. F. Low-level lead-induced neurotoxicity in children: an update on central nervous system effects. Brain Res Brain Res Rev. 1998 Jul;27(2):168–176. doi: 10.1016/s0165-0173(98)00011-3. [DOI] [PubMed] [Google Scholar]
  6. Flegal A. R., Smith D. R. Lead levels in preindustrial humans. N Engl J Med. 1992 May 7;326(19):1293–1294. [PubMed] [Google Scholar]
  7. Gulson B. L., Mahaffey K. R., Mizon K. J., Korsch M. J., Cameron M. A., Vimpani G. Contribution of tissue lead to blood lead in adult female subjects based on stable lead isotope methods. J Lab Clin Med. 1995 Jun;125(6):703–712. [PubMed] [Google Scholar]
  8. Gulson B. L., Mizon K. J., Palmer J. M., Korsch M. J., Patison N., Jameson C. W., Donnelly J. B. Urinary lead isotopes during pregnancy and postpartum indicate no preferential partitioning of endogenous lead into plasma. J Lab Clin Med. 2000 Sep;136(3):236–242. doi: 10.1067/mlc.2000.108751. [DOI] [PubMed] [Google Scholar]
  9. Hernández-Avila M., Smith D., Meneses F., Sanin L. H., Hu H. The influence of bone and blood lead on plasma lead levels in environmentally exposed adults. Environ Health Perspect. 1998 Aug;106(8):473–477. doi: 10.1289/ehp.106-1533211. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Hu H., Rabinowitz M., Smith D. Bone lead as a biological marker in epidemiologic studies of chronic toxicity: conceptual paradigms. Environ Health Perspect. 1998 Jan;106(1):1–8. doi: 10.1289/ehp.981061. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Leggett R. W. An age-specific kinetic model of lead metabolism in humans. Environ Health Perspect. 1993 Dec;101(7):598–616. doi: 10.1289/ehp.93101598. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Manton W. I., Cook J. D. High accuracy (stable isotope dilution) measurements of lead in serum and cerebrospinal fluid. Br J Ind Med. 1984 Aug;41(3):313–319. doi: 10.1136/oem.41.3.313. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Melman S. T., Nimeh J. W., Anbar R. D. Prevalence of elevated blood lead levels in an inner-city pediatric clinic population. Environ Health Perspect. 1998 Oct;106(10):655–657. doi: 10.1289/ehp.106-1533171. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Needleman H. L., Riess J. A., Tobin M. J., Biesecker G. E., Greenhouse J. B. Bone lead levels and delinquent behavior. JAMA. 1996 Feb 7;275(5):363–369. [PubMed] [Google Scholar]
  15. O'Flaherty E. J., Inskip M. J., Franklin C. A., Durbin P. W., Manton W. I., Baccanale C. L. Evaluation and modification of a physiologically based model of lead kinetics using data from a sequential isotope study in cynomolgus monkeys. Toxicol Appl Pharmacol. 1998 Mar;149(1):1–16. doi: 10.1006/taap.1997.8328. [DOI] [PubMed] [Google Scholar]
  16. O'Flaherty E. J., Inskip M. J., Yagminas A. P., Franklin C. A. Plasma and blood lead concentrations, lead absorption, and lead excretion in nonhuman primates. Toxicol Appl Pharmacol. 1996 May;138(1):121–130. doi: 10.1006/taap.1996.0105. [DOI] [PubMed] [Google Scholar]
  17. O'Flaherty E. J. Physiologically based models for bone-seeking elements. IV. Kinetics of lead disposition in humans. Toxicol Appl Pharmacol. 1993 Jan;118(1):16–29. doi: 10.1006/taap.1993.1004. [DOI] [PubMed] [Google Scholar]
  18. Pirkle J. L., Kaufmann R. B., Brody D. J., Hickman T., Gunter E. W., Paschal D. C. Exposure of the U.S. population to lead, 1991-1994. Environ Health Perspect. 1998 Nov;106(11):745–750. doi: 10.1289/ehp.98106745. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. 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]
  20. Schütz A., Bergdahl I. A., Ekholm A., Skerfving S. Measurement by ICP-MS of lead in plasma and whole blood of lead workers and controls. Occup Environ Med. 1996 Nov;53(11):736–740. doi: 10.1136/oem.53.11.736. [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Smith D. R., Flegal A. R. The public health implications of humans' natural levels of lead. Am J Public Health. 1992 Nov;82(11):1565–1566. doi: 10.2105/ajph.82.11.1565. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Smith D. R., Ilustre R. P., Osterloh J. D. Methodological considerations for the accurate determination of lead in human plasma and serum. Am J Ind Med. 1998 May;33(5):430–438. doi: 10.1002/(sici)1097-0274(199805)33:5<430::aid-ajim2>3.0.co;2-w. [DOI] [PubMed] [Google Scholar]
  23. Smith D. R., Osterloh J. D., Flegal A. R. Use of endogenous, stable lead isotopes to determine release of lead from the skeleton. Environ Health Perspect. 1996 Jan;104(1):60–66. doi: 10.1289/ehp.9610460. [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Smith D. R., Osterloh J. D., Niemeyer S., Flegal A. R. Stable isotope labeling of lead compartments in rats with ultralow lead concentrations. Environ Res. 1992 Apr;57(2):190–207. doi: 10.1016/s0013-9351(05)80079-9. [DOI] [PubMed] [Google Scholar]
  25. Wilson M. A., Johnston M. V., Goldstein G. W., Blue M. E. Neonatal lead exposure impairs development of rodent barrel field cortex. Proc Natl Acad Sci U S A. 2000 May 9;97(10):5540–5545. doi: 10.1073/pnas.97.10.5540. [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. deSilva P. E. Determination of lead in plasma and studies on its relationship to lead in erythrocytes. Br J Ind Med. 1981 Aug;38(3):209–217. doi: 10.1136/oem.38.3.209. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Environmental Health Perspectives are provided here courtesy of National Institute of Environmental Health Sciences

RESOURCES