Abstract
Lead remains one of the most significant occupational and environmental hazards world-wide, despite major efforts to ban its use in gasoline and paints. While environmental exposures have generally fallen in countries such as Canada and the US, occupational exposures remain significant. Workers are exposed in major industries, such as mining, battery manufacture, and electronics; environmental exposures result from emissions to air from stationary sources such as smelters and incinerators, contamination of drinking water from lead plumbing, contact with lead based paint, and leaching of lead from ceramics and glassware. Over the past 10 years, many countries have adopted public health guidance to prevent lead poisoning in children, using current epidemiological and toxicological information to set a blood lead level of 10 mcg/dL as an indicator of potentially toxic exposures. However, occupational guidelines and standards adopted to prevent adult lead toxicity have not been changed for over 20 years. In most developed countries, occupational exposures are set to prevent blood lead elevations above 40 or 50 mcg/dL. These exposures are clearly unsafe since effects on neurological, renal, and nervous system functions have been documented in adults with these levels of lead in blood (WHO, 1990)
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
REFERENCES
Alexander, B.H., Checkoway, H., van Netten, C., Kaufman, J.D., Vaughan, T.L., Mueller, B.A., Faustman, E.M., 1996, Paternal occupational lead exposure and pregnancy outcome. Int J Occup Environ Health. 2:280–285.
Anderson, L.M, Kasprzak, K.S., and Rice, J.M., 1994, Preconception exposure of males and neoplasia in their progeny: effects of metals and consideration of mechanisms, in: Male-mediated developmental toxicity, A.F. Olshan and D.R. Mattison, eds., Plenum Press, New York, 129–140.
Balhorn, R., 1990, Mammalian protamines: Structure and molecular interactions, in; Molecular Biology of Chromosome Function, K.W. Adolph, ed., Springer, New York, 366–395.
Balhorn, R., Reed, S., and Tanphaichitr, N., 1988, Aberrant protamine l/protamine2 ratios in sperm of infertile human males. Experientia. 44:52–55.
Bal, W., Jezowska-Bojczuk, M., and Kasprzak, K.S., 1997, Binding of nickel(II) and copper (II) to the Nterminal sequence of human protamine HP2. Chem Res Toxicol. 10:906–914.
Bartolomei, M.S. and Tilghman, S.M., 1997, Genomic imprinting in mammals. Annu Rev Genet. 31:493–525.
Bianchi, F., Rousseaux-Prevost, R., Sautiere, P., and Rosseaux, J., 1992, P2 protamines from human sperm are zinc-finger proteins with one Cys2/His2 motif. Biochem Biophys Res Commun. 182:540–547.
Brady, K., Herrera, Y., and Zenick, H., 1975, Influence of paternal lead exposure on subsequent learning ability of offspring. Pharmacol Biochem Behav. 3:561–565.
CDC, 1999, Adult blood lead epidemiology and surveillance — United States, second and third quarters, 1998, and annual 1994-1997. MMWR. 48:213–223.
De Yebra, L., Ballescá, J.L., Vanrell, J.A., Corzett, M., Balhorn, R., and Oliva, R., 1998, Detection of P2 precursors in the sperm cells of infertile patients who have reduced protamine P2 levels. Fertil Steril. 69:755–759.
Faustman, E. and Olshan, A., 1993, Male-mediated developmental toxicity. Annu Rev Public Health. 14:159–181.
Foster, W.G., McMahon, A., and Rice, D.C., 1996, Sperm chromatin structure is altered in cynomolgus monkeys with environmentally relevant blood lead levels. Toxicol Ind Health. 12:723–735.
Gandley, R.E., Anderson, L.D., and Silbergeld, E.K., 1999, Lead: Male-mediated effects on reproduction and development in the rat. Environ Res. 80:355–363.
Gatewood, J.M., Schroth, G.P., Schmid, C.W., and Bradbury, E.M., 1990, Zinc-induced secondary structure transitions in human sperm protamines. J Biol Chem. 265:20667–20672.
Georgiades, P., Watkins, M., Burton, G.J., and Ferguson-Smith, A.C., 2001, Roles of genomic imprinting and the zygotic genome in placental development. Proc Natl Acad Sci USA. 98:4522–4527.
Goering, P.L., 1993, Lead-protein interactions as a basis for lead toxicity. Neurotoxicology. 14:45–60.
Hanas, J.S., Rodgers, J.S., Bantle, J.A., and Cheng, Y.G., 1999, Lead inhibition of DNA-binding mechanism of Cys(2)His(2) zinc finger proteins. Mol Pharmacol. 56:982–988.
Hartwig, A., 1994, Role of DNA repair inhibition in lead-and cadmium-induced genotoxicity: a review. Environ Health Perspect. 1-2:45–50.
Hernández-Ochoa, I., García-Vargas, G., Morán-Martínez, J., Rubio-Andrade, M., Vera, E., López-Carillo, L., Cebrián, M., and Quintanilla-Vega, B., 2001, Semen quality in environmentally metal-exposed men in northern México. The Toxicologist. 60:386.
Irgens, A., Kruger, K., Skorve, A.H., and Irgens, L.M., 2000, Birth defects and paternal occupational exposure. Hypotheses tested in a record linkage based dataset. Acta Obstet Gynecol Scand. 79:465–470.
Ishihara, K., Alkondon, M., Montes, J.G., and Albuquerque, E.X., 1995, Ontogenically related properties of N-methyl-D-aspartate receptors in rat hippocampal neurons and the age-specific sensitivity of developing neurons to lead. J Pharmacol ExpTherap. 273:1459–1470.
Jedrusik, M.A. and Schulze, E., 2001, A single histone H l isoform (H1.1) is essential for chromatin silencing and germ line development in Caenorhabditis elegans. Development. 128:1069–1080.
Johansson, L. and Pellicciari, C.E., 1988, Lead-induced changes in the stabilization of the mouse sperm chromatin. Toxicology. 51:11–24.
Johansson, L., and Wide, M., 1986, Long-term exposure of the male mouse to lead: effects on fertility. Environ Res. 41:481–487.
Johnson, F.M., 1998, The genetic effects of environmental lead. Mutat Res. 410:123–140.
Kristensen, P., Irgens, L.M., Daltveit, A.K., and Andersen, A., Perinatal outcome among children of men exposed to lead and organic solvents in the printing industry. Am J Epidemiol. 137:134–144.
Kuhlmann, A.C., McGlothan, J.L., and Guilarte, T.R., 1997, Developmental lead exposure causes spatial learning deficits in adult rats. Neurosci Lett. 233:101–104.
Kvist, U., 1980, Importance of spermatozoal zinc as temporary inhibitor of sperm nuclear chromatin decondensation ability in man. Acta Physiol Scand. 109:79–84.
Lancranjan, I., Popescu, H.I., Gavanescu, O., Klepsch, I., and Serbanescu, M., 1975, Reproductive ability of workmen occupationally exposed to lead. Arch Environ Health 30:396–401.
McDiarmid, M.A. and Weaver, V., 1993, Fouling one’s own nest revisited. Am J Ind Med. 24:1–9.
Morrison, J.H., 1993, Differential vulnerability, connectivity, and cell typology. Neurobiol Aging. 14:51–54
Murphy, S.K. and Jirtle, R.L., 2000, Imprinted genes as potential genetic and epigenetic toxicologie targets. Environ Health Perspect. 108(Suppl 1):5–11.
Nihei, M.K., Desmond, NX., McGlothan, J.L., Kuhlmann, A.C., and Guilarte, T.R., 2000, N-methyl-Daspartate receptor subunit changes are associated with lead-induced deficits of long-term potentiation and spatial learning. Neuroscience. 99:233–242.
Oldereid, N.B., Thomassen, Y., Attramadal, A., Olaisen, B., and Purvis, K, 1993, Concentrations of lead, cadmium and zinc in the tissues of reproductive organs of men. J Reprod Fertil. 99:421–425.
Olshan, A.F., Teschke, K., and Baird, P.A., 1991, Paternal occupation and congenital anomalies in offspring. Am J Ind Med. 20:447–475.
Perreault, S.D., Naish, S.J., and Zirkin, B.R., 1987, The timing of hamster sperm nuclear decondensation and male pronucleus formation is related to sperm nuclear disulfide bond content. Biol Reprod. 36:239–244.
Quintanilla-Vega, B., Hoover, D.J., Bal, W., Silbergeld, E.K., Waalkes, M.P., and Anderson, L.D., 2000, Lead interaction with human protamine (HP2) as a mechanism of male reproductive toxicity. Chem Res Toxicol. 13:594–600.
Razmiafshari, M, Kao, J., d’Avignon, A., and Zawia, N.H., 2001, NMR identification of heavy metalbinding sites in a synthetic zinc finger peptide: toxicological implications for the interactions of xenobiotic metals with zinc finger proteins. Toxicol Appl Pharmacol. 172:1–10.
Silbergeld, E.K., 1992, Neurological perspective on lead toxicity, in: Human Lead Exposure, H. Needleman, ed., CRC Press, Boca Raton, FL, 89–103.
Silbergeld, E.K., Akkerman, M., Fowler, B.A., Albuquerque, E.X., and Alkondon, M., 1991, Lead: malemediated effects on reproduction and neurological development. Toxicology. 11:235.
Silbergeld, E.K., Landrigan, P.J., Froines, J.R., and Pfeffer, R.M., 1991, The occupational lead standard: a goal unachieved, a process in need of repair, New Solutions Spring:20–30.
Silbergeld, E.K., Waalkes, M., and Rice, J.M., 2000, Lead as a carcinogen: experimental evidence and mechanisms of action. Am J Ind Med. 28:316–323.
Stowe, V.M. and Goycr, R., 1971, Reproductive ability and progeny of F1 lead-toxic rats. Fertil Steril. 22:755–760.
Trasler, J.M. and Doerksen, T, 1999, Teratogen update: paternal exposures—reproducive risks. Teratology. 60:161–172.
Tycko, B., Trasler, J., Bestor, T., 1997, Genomic imprinting: gametic mechanisms and somatic consequences. J Androl. 18:480–486.
Uzych, L., 1985, Teratogenesis and mutagenesis associated with the exposure of human males to lead: A review. Yale J Biol Med. 58:9–17.
Viskum, S., Rabjerg, L., Jorgensen, P.J., and Grandjean, P., 1999, Improvement in semen quality associated with decreasing occupational lead exposure. Am J Ind Med. 35:257–263.
Waalkes, M.P., Diwan, B.A., Ward, J.M., Devor, D.E., Goyer, R.A., 1995, Renal tubular tumors and atypical hyperplasias in B6C3F1 mine exposed to lead acetate during gestation and lactation occur with minimal chronic nephropathy. Cancer Res. 55:5265–5271.
WHO, IPCS, 1990, Inorganic Lead, World Health Organization: Geneva.
Wiekowski, M., Miranda, M., and DePamphilis, M.L., 1991, Regulation of gene expression in preimplantation mouse embryos: Effects of the zygotic clock and the first mitosis on promoter and enhancer activities. Dev Biol. 147:403–414.
Wilson, M.A., Johnston, M.V., Goldstein, G.W., and Blue, M.E., 2000, Neonatal lead exposure impairs development of rodent barrel field cortex. Proc Natl Acad Sci USA. 97:5540–5545.
Winder, C., 1989, Reproductive and chromosomal effects of occupational exposure to lead in the male. Reprod Toxicol. 3:221–233.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2003 Springer Science+Business Media New York
About this chapter
Cite this chapter
Silbergeld, E.K., Quintanilla-Vega, B., Gandley, R.E. (2003). Mechanisms of Male Mediated Developmental Toxicity Induced by Lead. In: Robaire, B., Hales, B.F. (eds) Advances in Male Mediated Developmental Toxicity. Advances in Experimental Medicine and Biology, vol 518. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9190-4_4
Download citation
DOI: https://doi.org/10.1007/978-1-4419-9190-4_4
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-4829-0
Online ISBN: 978-1-4419-9190-4
eBook Packages: Springer Book Archive