Skip to main content
SpringerLink
Log in

Chronic Low-Level Lead Exposure

Its Role in the Pathogenesis of Hypertension

  • Concepts in Toxicology Review
  • Published:
Medical Toxicology and Adverse Drug Experience Aims and scope Submit manuscript

Summary

Lead is a common element in the earth’s crust, serving useful purposes in industry, but serving no purpose in the human body. Increase in blood pressure is an important public health problem with numerous factors contributing to many facets of the disease. The relationship of lead exposure and increased blood pressure has long been considered, but only recently critically investigated. Reports of subtle changes in calcium metabolism and renal function, as well as in vitro studies examining end-arteriolar smooth muscle contractility, link lead exposure and increased blood pressure.

This paper critically examines the evidence associating chronic low-level lead exposure and increased blood pressure. The review focuses on epidemiological, clinical, and toxicological data. The epidemiological evidence is consistent with low-level exposure to lead causing an elevation in blood pressure. The strength of that association, and the doseresponse characteristics, are less certain. Individual resistance and susceptibility could affect the degree of blood pressure elevation.

The results of animal and in vitro studies are consistent with the epidemiological evidence, and suggest biologically plausible mechanisms for the association. The most probable mechanisms are intracellular pertubations in calcium metabolism mediated by direct lead effects at the end-arteriole, and indirect effects via renal dysfunction. Better indices of lead exposure and lead activity are needed to quantify these effects in humans. New and safer methods of chelating lead suggest interesting approaches for studying the relationship between lead and hypertension. This link could have significant implications in determining what constitutes a ‘safe’ level of environmental lead exposure, and whether a proportion of essential hypertension could be ‘cured’ by chelation therapy.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  • Ahlgren L, Haeger-Aronsen B, Mattsson S, Schutz A. In-vivo determination of lead in the skeleton after occupational exposure to lead. British Journal of Industrial Medicine 37: 109–113, 1980

    PubMed  CAS  Google Scholar 

  • Ahlgren L, Liden K, Mattsson S, Tejning S. X-ray fluorescence analysis of lead in human skeleton in vivo. Scandinavian Journal of Work, Environment and Health 2: 82–86, 1976

    PubMed  CAS  Google Scholar 

  • Ahlgren L, Mattsson S. An x-ray fluorescence technique for in vivo determination of lead concentration in a bone matrix. Physics in Medicine and Biology 24: 136–145, 1979

    PubMed  CAS  Google Scholar 

  • Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, et al. Chronological trend in blood lead levels between 1976 and 1980. New England Journal of Medicine 308: 1373–1377, 1983

    PubMed  CAS  Google Scholar 

  • Aviv A, John E, Bernstein L, Goldsmith DI, Spitzer A. Lead intoxication during development: its late effects on kidney function and blood pressure. Kidney International 17: 430–437, 1980

    PubMed  CAS  Google Scholar 

  • Batuman V, Landy E, Maesaka JK, Wedeen RP. Contribution of lead to hypertension with renal impairment. New England Journal of Medicine 309: 17–21, 1983

    PubMed  CAS  Google Scholar 

  • Beevers DG, Cruickshank JK, Yeoman WB, Carter GF, Goldberg A, et al. Blood-lead and cadmium in human hypertension. Journal of Environmental Pathology and Toxicology 4: 251–260, 1980

    PubMed  CAS  Google Scholar 

  • Beevers DG, Erskine E, Robertson M, Beattie AD, Goldberg A, et al. Blood-lead and hypertension. Lancet 2: 1–3, 1976

    PubMed  CAS  Google Scholar 

  • Belknap EL. Clinical studies on lead absorption in the human. III. Blood pressure observations. Journal of Industrial Hygiene and Toxicology 18: 380–390, 1936

    CAS  Google Scholar 

  • Bennett WM. Lead nephropathy. Kidney International 28: 212–220, 1985

    PubMed  CAS  Google Scholar 

  • Berkson J. Limitations of the application of fourfold table analysis to hospital data. Biometrics 2: 47–53, 1946

    PubMed  CAS  Google Scholar 

  • Blackman SS. Intranuclear inclusion bodies in the kidney and liver caused by lead poisoning. Bulletin of the Johns Hopkins Hospital 58: 384–403, 1936

    Google Scholar 

  • Blaustein MP. Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a hypothesis. American Journal of Physiology 232: C165–C173, 1977

    PubMed  CAS  Google Scholar 

  • Boscolo P, Galli G, Iannaccone A, Martino F, Porcelli G, et al. Plasma renin activity and urinary kallikrein excretion in lead-exposed workers as related to hypertension and nephropathy. Life Sciences 28: 175–184, 1981

    PubMed  CAS  Google Scholar 

  • Boscolo P, Porcelli G, Cecchetti G, Salimei E, Iannaccone A. Urinary kallikrein activity of workers exposed to lead. British Journal of Industrial Medicine 35: 226–229, 1978

    PubMed  CAS  Google Scholar 

  • Boscolo P, Porcelli G, Menini E, Finelli VN. EDTA plus zinc as therapy of lead intoxication: preliminary results. Medicina del Lavoro 74: 370–375, 1983

    PubMed  CAS  Google Scholar 

  • Boscolo P, Salimei E, Adamo A, Porcelli B. Effects of environmental lead levels on the urinary kallikrein excretion of exposed workers. Life Sciences 20: 1715–1722. 1977

    PubMed  CAS  Google Scholar 

  • Bruschi G, Bruschi ME, Caroppo M, Orlandini G, Spaggiari M, et al. Cytoplasmic free (Ca++) is increased in the platelets of spontaneously hypertensive rats and essential hypertensive patients. Clinical Science 68: 179–184, 1985

    PubMed  CAS  Google Scholar 

  • Bulpitt CJ, Hodes C, Everitt MG. The relationship between blood pressure and biochemical risk factors in a general population. British Journal of Preventive and Social Medicine 30: 158–162, 1976

    PubMed  CAS  Google Scholar 

  • Campbell BC, Beattie AD, Elliott HL, Goldberg A, Moore MR, et al. Occupational lead exposure and renin release. Archives of Environmental Health 34: 439–443, 1979

    PubMed  CAS  Google Scholar 

  • Campbell BC, Beattie AD, Moore MR, Goldberg A, Reid AG. Renal insufficiency associated with excessive lead exposure. British Medical Journal 1: 482–485, 1977

    PubMed  CAS  Google Scholar 

  • Campbell BC, Elliott HL, Meredith PA. Lead exposure and renal failure: does renal insufficiency influence lead kinetics? Toxicology Letters 9: 121–124, 1981

    PubMed  CAS  Google Scholar 

  • Campbell BC, Meredith PA, Scott JJC. Lead exposure and changes in the renin-angiotensin-aldosterone system in man. Toxicology Letters 25: 25–32, 1985

    PubMed  CAS  Google Scholar 

  • Carmignani M, Boscolo P, Ripanti G, Finelli VN. Effects of chronic exposure to cadmium and/or lead on some neurohumoral mechanisms regulating cardiovascular function in the rat. International Conference on Heavy Metals in the Environment 1: 557–560, 1983

    CAS  Google Scholar 

  • Cheung JY, Bonventre JV, Malis CD, Leaf A. Calcium and ischemic injury. New England Journal of Medicine 314: 1670–1676, 1986

    PubMed  CAS  Google Scholar 

  • Chmielnicka J, Komsta-Szumska E, Szymanska JA. Arginase and kallikrein activities as biochemical indices of occupational exposure to lead. British Journal of Industrial Medicine 38: 175–178, 1981

    PubMed  CAS  Google Scholar 

  • Christoffersson JO, Schutz A, Ahlgren L, Haeger-Aronsen B, Mattsson S, et al. Lead in finger-bone analysed in vivo in active and retired lead workers. American Journal of Industrial Medicine 6: 447–457, 1984

    PubMed  CAS  Google Scholar 

  • Cohn JN. Calcium, vascular smooth muscle, and calcium entry blockers in hypertension. Annals of Internal Medicine 98 (Part 2): 806–809, 1983

    PubMed  CAS  Google Scholar 

  • Cooper WC, Wong O, Kheifets L. Mortality among employees of lead battery plants and lead-producing plants, 1947–1980. Scandinavian Journal of Work, Environment and Health 11: 331–345, 1985

    PubMed  CAS  Google Scholar 

  • Cottier VP, Kunz HA, Zollinger HU. Experimenteller beitrag zur Frage der Bleihypertonie. Helvetica Medica Acta 20: 443–449, 1953

    PubMed  CAS  Google Scholar 

  • Council of the Queensland Branch of the British Medical Association. An historical account of the occurrence and causation of lead poisoning among Queensland children. Medical Journal of Australia 1: 148–152, 1922

    Google Scholar 

  • Cramer K, Dahlberg L. Incidence of hypertension among lead workers: a follow-up study based on regular control over 20 years. British Journal of Industrial Medicine 23: 101–104, 1966

    PubMed  CAS  Google Scholar 

  • Cramer K, Goyer RA, Jagenburg R, Wilson MH. Renal ultra-structure, renal function, and parameters of lead toxicity in workers with different periods of lead exposure. British Journal of Industrial Medicine 31: 113–127, 1974

    PubMed  CAS  Google Scholar 

  • Craswell PW, Price J, Boyle PD, et al. Chronic renal failure with gout: a marker of chronic lead poisoning. Kidney International 26: 319–323, 1984

    PubMed  CAS  Google Scholar 

  • Croll DG. The incidence of chronic nephritis amongst young people in Queensland. Medical Journal of Australia 2: 144–145, 1929

    Google Scholar 

  • David OJ, Wintrob HL, Arcoleo CG. Blood lead stability. Archives of Environmental Health 37: 147–150, 1982

    PubMed  CAS  Google Scholar 

  • Davies JM. Long term mortality study of chromate pigment workers who suffered lead poisoning. British Journal of Industrial Medicine 41: 170–178, 1984

    PubMed  CAS  Google Scholar 

  • Delves HT, Sherlock JC, Quinn MJ. Temporal stability of blood lead concentrations in adults exposed only to environmental lead. Human Toxicology 3: 279–288, 1984

    PubMed  CAS  Google Scholar 

  • Diaz-Rivera RS, Horn RC. Postmortem studies on hypertensive rats chronically intoxicated with lead acetate. Proceedings of the Society for Experimental Biology and Medicine 59: 161–163, 1945

    CAS  Google Scholar 

  • Dingwall-Fordyce I, Lane RE. A follow-up study of lead workers. British Journal of Industrial Medicine 20: 313–315, 1963

    PubMed  CAS  Google Scholar 

  • Dreessen WC. Health of lead-exposed storage battery workers. Journal of Industrial Hygiene and Toxicology 25: 60–70, 1943

    CAS  Google Scholar 

  • Dreessen WC, Edwards TI, Reinhart WH, Page RT, Webster SH, et al. The control of the lead hazard in the storage battery industry. Public Health Bulletin No. 262, US Government Printing Office, Washington DC, 1941

    Google Scholar 

  • Elinder CG, Friberg L, Lind B, Nilsson B, Svartengren M, et al. Decreased blood lead levels in residents of Stockholm for the period 1980–1984. Scandinavian Journal of Work, Environment, and Health 12: 114–120, 1986

    CAS  Google Scholar 

  • Emmerson BT, Lecky DS. The lead content of bone in subjects without recognized past lead exposure and in patients with renal disease. Australasian Annals of Medicine 12: 139–142, 1963

    Google Scholar 

  • Engel H. Uber die Gesundheitsgefahrdung bei der Verarbeitung von metallischem Blei mit besonderer Berucksichtigung der Bleiloterei. Schriften Aus Dem Gesamtgebiet Der Gewerbehygiene, Vol. 13, Der Deutschen Gesellschaft fur Gewerbehygiene. J. Springer, Berlin, 1925

  • Erne P, Bolli P, Burgisser E, Buhler FR. Correlation of platelet calcium with blood pressure. New England Journal of Medicine 310: 1084–1088, 1984

    PubMed  CAS  Google Scholar 

  • Fairley KD. A review of the evidence relating to lead as an aetiological agent in chronic nephritis in Queensland. Medical Journal of Australia 1: 600–606, 1934

    Google Scholar 

  • Favalli L, Chiari MC, Piccinini F, Rozza A. Experimental investigations on the contraction induced by lead in arterial smooth muscle. Acta Pharmacologica et Toxicologica 41 (Suppl. II): 412–420, 1977

    PubMed  CAS  Google Scholar 

  • Filo RS, Bohr DF, Ruegg JC. Glycerinated skeletal and smooth muscle: calcium and magnesium dependence. Science 147: 1581–1583, 1965

    PubMed  CAS  Google Scholar 

  • Fleischer N, Mouw DR, Vander AJ. Chronic effects of lead on renin and renal sodium excretion. Journal of Laboratory and Clinical Medicine 95: 759–770, 1980

    PubMed  CAS  Google Scholar 

  • Fouts PJ, Page IH. The effect of chronic lead poisoning on arterial blood pressure in dogs. American Heart Journal 24: 329–331, 1942

    CAS  Google Scholar 

  • Fowler BA, Kimmel CA, Woods JS, McConnell EE, Grant LD. Chronic low-level lead toxicity in the rat: HI. An integrated assessment of long-term toxicity with special reference to the kidney. Toxicology and Applied Pharmacology 56: 59–77, 1980

    CAS  Google Scholar 

  • Garay RP, Meyer P. A new test showing abnormal net Na+and K+fluxes in erythrocytes of essential hypertensive patients. Lancet 1: 349–353, 1979

    PubMed  CAS  Google Scholar 

  • Garcia-Palmieri MR, Costas R, Cruz-Vidal M, Sorlie PD, Tillotson J, et al. Milk consumption, calcium intake, and decreased hypertension in Puerto Rico: Puerto Rico Heart Health Program Study. Hypertension 6: 322–328, 1984

    PubMed  CAS  Google Scholar 

  • Genest J. Volume hormones and blood pressure. Annals of Internal Medicine 98 (Part 2): 774–749, 1983

    Google Scholar 

  • Goldman JM, Vander AJ, Mouw DR, Keiser J, Nicholls MG. Multiple short-term effects of lead on the renin-angiotensin system. Journal of Laboratory and Clinical Medicine 97: 251–263, 1981

    PubMed  CAS  Google Scholar 

  • Goldstein GW. Lead encephalopathy: the significance of lead inhibition of calcium uptake by brain mitochondria. Brain Research 136: 185–188, 1977

    PubMed  CAS  Google Scholar 

  • Goldstein GW, Ar D. Lead activates calmodulin sensitive processes. Life Sciences 33: 1001–1006, 1983

    PubMed  CAS  Google Scholar 

  • Gonick HC, Khalil-Manesh F, Raghavan SRV, Weiler E. Characterization of human erythrocyte lead-binding protein. International Conference on Heavy Metals in the Environment 1: 313–316, 1985

    CAS  Google Scholar 

  • Goyer RA. Lead and the kidney. Current Topics in Pathology 55: 147–176, 1971

    PubMed  CAS  Google Scholar 

  • Goyer RA, Leonard DL, Moore JF, Rhyne B, Krigman MR. Lead dosage and the role of the intranuclear inclusion body. Archives of Environmental Health 20: 705–711, 1970a

    PubMed  CAS  Google Scholar 

  • Goyer RA, May P, Cates MM, Krigman MR. Lead and protein content of isolated intranuclear inclusion bodies from kidneys of lead-poisoned rats. Laboratory Investigation 22: 245–250, 1970b

    PubMed  CAS  Google Scholar 

  • Goyer RA, Moore JF. Cellular effects of lead. Advances in Experimental Medicine and Biology 48: 447–462, 1974

    PubMed  CAS  Google Scholar 

  • Goyer RA, Wilson MH. Lead-induced inclusion bodies: results of ethylenediaminetetraacetic acid treatment. Laboratory Investigation 32: 149–156, 1975

    PubMed  CAS  Google Scholar 

  • Graziano JH. Role of 2,3-dimercaptosuccinic acid in the treatment of heavy metal poisoning. Medical Toxicology 1: 155–162, 1986

    PubMed  CAS  Google Scholar 

  • Graziano JH, Siris ES, LoIacono N, Silverberg SJ, Turgeon L. 2,3-Dimercaptosuccinic acid as an antidote for lead intoxication. Clinical Pharmacology and Therapeutics 37: 431–438, 1985

    PubMed  CAS  Google Scholar 

  • Griffith JQ, Lindauer MA. The effect of chronic lead poisoning on arterial blood pressure in rats. American Heart Journal 28: 295–297, 1944

    Google Scholar 

  • Guazzi MD, Polese A, Fiorentini C, Bartorelli A, Moruzzi P. Treatment of hypertension with calcium antagonists: review. Hypertension 5 (Suppl. II): 85–95, 1983

    Google Scholar 

  • Habermann E, Crowell K, Janicki P. Lead and other metals can substitute for Ca++in calmodulin. Archives of Toxicology 54: 61–70, 1983

    PubMed  CAS  Google Scholar 

  • Hammond PB, Beliles RP. Metals. In Doull et al. (Eds) Casarett and Doull’s toxicology: the basic science of poisons, 2nd ed., pp. 409–467, Macmillan Publishing Co., Inc., New York, 1980

    Google Scholar 

  • Harlan WR, Landis JR, Schmouder RL, Goldstein NG, Harlan LC. Blood lead and blood pressure relationship in the adolescent and adult US population. Journal of the American Medical Association 253: 530–534, 1985

    PubMed  CAS  Google Scholar 

  • Harlan WR, Hull AL, Schmouder RL, Landis JR, Thompson FE, et al. Blood pressure and nutrition in adults: the National Health and Nutrition Examination Survey. American Journal of Epidemiology 120: 17–28, 1984

    PubMed  CAS  Google Scholar 

  • Harris LI. A clinical study of the frequency of lead, turpentine and benzin poisoning in four hundred painters. Archives of Internal Medicine 22: 129–156, 1918

    Google Scholar 

  • Hasan J, Vihko V, Hernberg S. Deficient red cell membrane (Na++ K+)-ATPase in lead poisoning. Archives of Environmental Health 14: 313–318, 1967

    PubMed  CAS  Google Scholar 

  • Hawthorne VM, Greaves DA, Beevers DG. Blood pressure in a Scottish town. British Medical Journal 3: 600–603, 1974

    PubMed  CAS  Google Scholar 

  • Heath H, Callaway CW. Calcium tablets for hypertension? Annals of Internal Medicine 103: 946–947, 1985

    PubMed  Google Scholar 

  • Henderson DA. A follow-up of cases of plumbism in children. Australasian Annals of Medicine 3: 219–224, 1954

    PubMed  CAS  Google Scholar 

  • Henderson DA. Chronic nephritis in Queensland. Australasian Annals of Medicine 4: 163–177, 1955

    PubMed  CAS  Google Scholar 

  • Henderson DA, Inglis JA. The lead content of bone in chronic Bright’s disease. Australasian Annals of Medicine 6: 145–154, 1957

    PubMed  CAS  Google Scholar 

  • Hinton D, Cresswell BCL, Janus ED, Malpress WA. Industrial lead exposure: a review of blood lead levels in South Island industries, 1974–83. New Zealand Medical Journal 97: 769–773, 1984

    PubMed  CAS  Google Scholar 

  • Hopper JL, Balderas A, Mathews JD. Analysis of variation in blood lead levels in Melbourne families. Medical Journal of Australia 2: 573–576, 1982

    PubMed  CAS  Google Scholar 

  • Hryhorczuk DO, Rabinowitz MB, Hessl SM, Hoffman D, Hogan MM, et al. Elimination kinetics of blood lead in workers with chronic lead intoxication. American Journal of Industrial Medicine 8: 33–42, 1985

    PubMed  CAS  Google Scholar 

  • Iannaccone A, Carmignani M, Boscolo P. Neurogenic and humoral mechanisms in arterial hypertension of chronically lead-exposed rats. Medicina del Lavoro 1: 13–21, 1981a

    Google Scholar 

  • Iannaccone A, Carmignani M, Boscolo P. Reattivita cardiovascolare nel ratto dopo cronica exposizione a cadmio o piombo. Annali dell Istituto Superiore di Sanita 17: 655–660, 1981b

    PubMed  CAS  Google Scholar 

  • Iannaccone A, Porcelli G, Boscolo P, Ranieri M. Urinary kallikrein excretion in lead intoxication. Life Sciences 16: 820, 1975

    Google Scholar 

  • Ibels LS, Pollock CA. Lead intoxication. Medical Toxicology 1: 387–410, 1986

    PubMed  CAS  Google Scholar 

  • Kapoor SC, van Rossum GDV. Effects of Pb++added in vitro on Ca++movements in isolated mitochondria and slices of rat kidney cortex. Biochemical Pharmacology 33: 1771–1778, 1984

    PubMed  CAS  Google Scholar 

  • Karai I, Fukumoto K, Horiguchi S. An increase in Na+/K+-ATPase activity of erythrocyte membranes in workers employed in a lead refining factory. British Journal of Industrial Medicine 39: 290–294, 1982

    PubMed  CAS  Google Scholar 

  • Karai I, Lee SI, Horiguchi S, Fukumoto K, et al. Combined effects of lead and EDTA on Na+, K+-ATPase activity of erythrocyte membranes. Journal of Toxicology and Environmental Health 12: 721–730, 1983

    PubMed  CAS  Google Scholar 

  • Keiser JA, Vander AJ, Germain CL. Effects of lead on the secretion and disappearance of renin in rabbits. Toxicology and Applied Pharmacology 69: 117–126, 1983a

    PubMed  CAS  Google Scholar 

  • Keiser JA, Vander AJ, Germain CL. Clearance of renin in unanesthetized rats: effects of chronic lead exposure. Toxicology and Applied Pharmacology 69: 127–137, 1983b

    PubMed  CAS  Google Scholar 

  • Kesteloot H, Geboers J. Calcium and blood pressure. Lancet 1: 813–815, 1982

    PubMed  CAS  Google Scholar 

  • Khera AK, Wibberley DG, Edwards KW, Waldron HA. Cadmium and lead levels in blood and urine in a series of cardiovascular and normotensive patients. International Journal of Environmental Studies 14: 309–312, 1980

    Google Scholar 

  • Kijewski H, Lowitz HD. Der Nachweis von Blei als Hydrid in Knochenbiopsieproben von Patienten mit langen zurückliegenden Bleivergiftungen. Archives of Toxicology 50: 301–311, 1982

    PubMed  CAS  Google Scholar 

  • Kirkby H, Gyntelberg F. Blood pressure and other cardiovascular risk factors of long-term exposure to lead. Scandinavian Journal of Work, Environment and Health 11: 15–19, 1985

    PubMed  CAS  Google Scholar 

  • Kok FJ, Vandenbroucke JP, van der Heide-Vessel C, van der Heide RM. Dietary sodium, calcium, and potassium, and blood pressure. American Journal of Epidemiology 123: 1043–1048, 1986

    PubMed  CAS  Google Scholar 

  • Kopp SJ, Perry HM, Glonek T, Erlanger M, Perry EF, et al. Cardiac physiologic-metabolic changes after chronic low-level heavy metal feeding. American Journal of Physiology 239: H22–H30, 1980

    PubMed  CAS  Google Scholar 

  • Kromhout D, Bosschieter EB, de Lezenne Coulander C. Potassium, calcium, alcohol intake and blood pressure: the Zutphen Study. American Journal of Clinical Nutrition 41: 1299–1304, 1985

    PubMed  CAS  Google Scholar 

  • Lancereaux E. Nephrite et arthrite saturnines: coincidences de ces affections; parallele avec la nephrite et l’arthrite goutteuses. Transactions of the International Medical Congress 7: 193–202, 1881

    Google Scholar 

  • Lanerolle P de, Nishikawa M, Yost DA, Adelstein RS. Increased phosphorylation of myosin light chain kinase after an increase in cyclic AMP in intact smooth muscle. Science 223: 1415–1417, 1984

    PubMed  Google Scholar 

  • Lilis R, Dumitriu C, Roventa A, Nestorescu B, Pilat L. Renal function in chronic lead poisoning. Medicina del Lavoro 58: 506–512, 1967

    PubMed  CAS  Google Scholar 

  • Lilis R, Fischbein A, Eisinger J, Blumberg WE, Diamond S, et al. Prevalence of lead disease among secondary lead smelter workers and biological indicators of lead exposure. Environmental Research 14: 255–285. 1977

    PubMed  CAS  Google Scholar 

  • Lilis R, Gavrilescu N, Nestorescu B, Dumitriu C, Roventa A. Nephropathy in chronic lead poisoning. British Journal of Industrial Medicine 25: 196–202, 1968

    PubMed  CAS  Google Scholar 

  • Lorimer G. Saturnine gout, and its distinguishing marks. British Medical Journal 2: 163, 1886

    PubMed  CAS  Google Scholar 

  • Mahomed FA. Chronic Blight’s disease without albuminuria. Guy’s Hospital Reports 25 (Series 3): 295–418, 1881

    Google Scholar 

  • Malcom D, Barnett HAR. A mortality study of lead workers 1925–76. British Journal of Industrial Medicine 39: 404–410, 1982

    Google Scholar 

  • Malpress WA, Janus ED, Hinton D. Blood lead levels in the New Zealand population: preliminary communication. New Zealand Medical Journal 97: 868–869, 1984

    PubMed  CAS  Google Scholar 

  • Marcus AH. The body burden of lead: comparison of mathematical models for accumulation. Environmental Research 19: 79–90, 1979

    PubMed  CAS  Google Scholar 

  • Mayers MR. A study of the lead line, arteriosclerosis, and hypertension in 381 lead workers. Journal of Industrial Hygiene and Toxicology 9: 239–250, 1927

    Google Scholar 

  • McAllister RG, Michelakis AM, Sandstead HH. Plasma renin activity in chronic plumbism. Archives of Internal Medicine 127: 919–923, 1971

    PubMed  Google Scholar 

  • McCarron DA. Low serum concentrations of ionized calcium in patients with hypertension. New England Journal of Medicine 307: 226–228, 1982

    PubMed  CAS  Google Scholar 

  • McCarron DA. Calcium and magnesium nutrition in human hypertension. Annals of Internal Medicine 98 (Part 2): 800–805, 1983

    PubMed  CAS  Google Scholar 

  • McCarron DA. Calcium in the pathogenesis and therapy of human hypertension. American Journal of Medicine 78 (Suppl. 2B): 27–34, 1985

    PubMed  CAS  Google Scholar 

  • McCarron DA, Morris CD. Blood pressure response to oral calcium in persons with mild to moderate hypertension. Annals of Internal Medicine 103: 825–831, 1985

    PubMed  CAS  Google Scholar 

  • McCarron DA, Morris CD, Cole C. Dietary calcium in human hypertension. Science 217: 267–269, 1982

    PubMed  CAS  Google Scholar 

  • McCarron DA, Morris CD, Henry HJ, Stanton JL. Blood pressure and nutrient intake in the United States. Science 224: 1392–1398, 1984

    PubMed  CAS  Google Scholar 

  • McCarron DA, Stanton J, Henry H, Morris C. Assessment of nutritional correlates of blood pressure. Annals of Internal Medicine 98 (Part 2): 715–719, 1983

    PubMed  CAS  Google Scholar 

  • McMichael AJ, Johnson HM. Long-term mortality profile of heavily-exposed lead smelter workers. Journal of Occupational Medicine 24: 375–378, 1982

    PubMed  CAS  Google Scholar 

  • Meredith PA, Campbell CB, Blower A, Derkx FHM, Reid JL. The effects of lead on the renin-angiotensin system. Xenobiotica 15: 521–528, 1985

    PubMed  CAS  Google Scholar 

  • Moore JF, Goyer RA. Lead-induced inclusion bodies: composition and probable role in lead metabolism. Environmental Health Perspectives 7: 121–127, 1974

    PubMed  CAS  Google Scholar 

  • Moreau T, Orssaud G, Juguet B, Busquet G. Lettre-a-l’editeur: plombemie et pression arterielle: premiers resultats d’une enquete transversale de 431 sujet de sexe masculin. Revue d’Epidemiologie et de Sante Publique 30: 395–397, 1982

    PubMed  CAS  Google Scholar 

  • Morgan JM. Chelation therapy in lead nephropathy. Southern Medical Journal 68: 1001–1006, 1975

    PubMed  CAS  Google Scholar 

  • Morgan JM, Hartley MW, Miller RE. Nephropathy in chronic lead poisoning. Archives of Internal Medicine 118: 17–29, 1966

    PubMed  CAS  Google Scholar 

  • Nye LJJ. An investigation of the extraordinary incidence of chronic nephritis in young people in Queensland. Medical Journal of Australia 2: 145–158, 1929

    Google Scholar 

  • Orssaud G, Claude JR, Moreau T, Lellouch J, et al. Blood lead concentration and blood pressure. British Medical Journal 290: 244, 1985

    PubMed  CAS  Google Scholar 

  • Padilla F, Shapiro AP, Jensen WN. Effect of chronic lead intoxication on blood pressure in the rat. American Journal of the Medical Sciences 258: 359–365, 1969

    PubMed  CAS  Google Scholar 

  • Pardoe AU. Renal function in lead poisoning. British Journal of Pharmacology and Chemotherapy 7: 349–357, 1952

    PubMed  CAS  Google Scholar 

  • Parr DR, Harris EJ. The effect of lead on the calcium-handling capacity of rat heart mitochondria. Biochemical Journal 158: 289–294, 1976

    PubMed  CAS  Google Scholar 

  • Peitzman SJ, Bodison W, Ellis I. Moonshine drinking among hypertensive veterans in Philadelphia. Archives of Internal Medicine 145: 632–634, 1985

    PubMed  CAS  Google Scholar 

  • Perry HM, Erlanger MW. Pressor effects of chronically feeding cadmium and lead together. In Hemphill (Ed.) Trace substances in environmental health, Vol. 12, pp. 268–275, University of Missouri, Columbia, 1978

    Google Scholar 

  • Piccinini F, Favalli L, Chiari MC. Experimental investigations on the contraction induced by lead in arterial smooth muscle. Toxicology 8: 43–51, 1977

    PubMed  CAS  Google Scholar 

  • Pirkle JL, Schwartz J, Landis JR, Harlan WR. The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. American Journal of Epidemiology 121: 246–258, 1985

    PubMed  CAS  Google Scholar 

  • Pocock SJ, Shaper AG, Ashby D, Delves T, Whitehead TP. Blood lead concentration, blood pressure, and renal function. British Medical Journal 289: 872–874, 1984

    PubMed  CAS  Google Scholar 

  • Porcelli G, Boscolo P, Finelli VN, Di Iorio M, Iannaccone A. Effect of chelation therapy of plumbism on urinary prokallikrein, kallikrein and kininase activities. In Fritz et al. (Eds) Recent progress on kinins, pp. 627–630, Birkhauser Verlag, Boston, 1982

    Google Scholar 

  • Postnov YV, Orlov SN. Cell membrane alteration as a source of primary hypertension. Journal of Hypertension 2: 1–6, 1984

    PubMed  CAS  Google Scholar 

  • Postnov YV, Orlov SN, Shevchenko A, Adler AM. Altered sodium permeability, calcium binding and Na-K-ATPase activity in the red blood cell membrane in essential hypertension. Pflugers Archiv 371: 263–269, 1977

    PubMed  CAS  Google Scholar 

  • Pounds JG. Effect of lead intoxication on calcium homeostasis and calcium-mediated cell function: a review. Neurotoxicology 5: 295–332, 1984

    PubMed  CAS  Google Scholar 

  • Pounds JG, Wright R, Morrison D, Casciano DA. Effect of lead on calcium homeostasis in the isolated rat hepatocyte. Toxicology and Applied Pharmacology 63: 389–401, 1982

    PubMed  CAS  Google Scholar 

  • Raghavan SRV, Culver BD, Gonick HC. Erythrocyte lead-binding protein after occupational exposure: I. Relationship to lead toxicity. Environmental Research 22: 264–270, 1980

    CAS  Google Scholar 

  • Raghavan SRV, Culver BD, Gonick HC. Erythrocyte lead-binding protein after occupational exposure. II. Influence on lead inhibition of membrane Na+, K+-Adenosinetriphosphatase. Journal of Toxicology and Environmental Health 7: 561–568, 1981

    CAS  Google Scholar 

  • Raghavan SRV, Gonick HC. Isolation of low-molecular-weight lead-binding protein from human erythrocytes. Proceedings of the Society for Experimental Biology and Medicine 155: 164–167, 1977

    PubMed  CAS  Google Scholar 

  • Rappaport SM. Smoothing of exposure variability at the receptor: implications for health standards. Annals of Occupational Hygiene 29: 201–214, 1985

    PubMed  CAS  Google Scholar 

  • Rasmussen H. Cellular calcium metabolism. Annals of Internal Medicine 98 (Part 2): 809–816, 1983

    PubMed  CAS  Google Scholar 

  • Revis NW, Zinsmeister AR, Bull R. Atherosclerosis and hypertension induction by lead and cadmium ions: an effect prevented by calcium ion. Proceedings of the National Academy of Sciences (USA) 78: 6494–6498, 1981

    CAS  Google Scholar 

  • Rosen JF. The metabolism of lead in isolated bone cell populations: interactions between lead and calcium. Toxicology and Applied Pharmacology 71: 101–112, 1983

    PubMed  CAS  Google Scholar 

  • Sandstead HH, Michelakis AM, Temple TE. Lead intoxication: its effect on the renin-aldosterone response to sodium deprivation. Archives of Environmental Health 20: 356–363, 1970

    PubMed  CAS  Google Scholar 

  • Sawyer RA, Waggoner RW, Erickson AA. Science News. Science (Suppl.)90: 11, 1939

    Google Scholar 

  • Schwartz J. The relationship between blood lead levels and blood pressure. Presentation to the Royal Society of Canada Commission on Lead in the Environment, US Environmental Protection Agency, Washington DC, 1985

    Google Scholar 

  • Secchi GC, Alessio L, Cambiaghi G. Na+/K+-ATPase activity of erythrocyte membranes. Archives of Environmental Health 27: 399–400, 1973

    PubMed  CAS  Google Scholar 

  • Selevan SG, Landrigan PJ, Stern FB, Jones JH. Mortality of lead smelter workers. American Journal of Epidemiology 122: 673–683, 1985

    PubMed  CAS  Google Scholar 

  • Shaper AG, Pocock SJ, Walker M, Cohen NM, Wale CJ, et al. British regional heart study: cardiovascular risk factors in middle-aged men in 24 towns. British Medical Journal 283: 179–186, 1981

    PubMed  CAS  Google Scholar 

  • Smith WM. Epidemiology of hypertension. Medical Clinics of North America 61: 467–486, 1977

    PubMed  CAS  Google Scholar 

  • Sparrow D, Sharrett AR, Garvey AJ, Craun GF, Silbert JE. Trace metals in drinking water: lack of influence on blood pressure. Journal of Chronic Diseases 37: 59–65, 1984

    PubMed  CAS  Google Scholar 

  • Staessen J, Bulpitt CJ, Roels H, Bernard A, Fagard R, et al. Urinary cadmium and lead concentrations and their relation to blood pressure in a population with low exposure. British Journal of Industrial Medicine 41: 241–248, 1984

    PubMed  CAS  Google Scholar 

  • Symposium Proceedings. Nutrition and blood pressure control: current status of dietary factors and hypertension. Annals of Internal Medicine 98 (Part 2): 697–890, 1983

    Google Scholar 

  • Teleky L. A note on blood pressure in lead poisoning. Journal of Industrial Hygiene and Toxicology 19: 1–5, 1937

    CAS  Google Scholar 

  • Trefry JH, Metz S, Trocine RP, Nelsen TA. A decline in lead transport by the Mississippi River. Science 230: 439–441, 1985

    PubMed  CAS  Google Scholar 

  • Victery W, Vander AJ, Markel H, Katzman L, Shulak JM, et al. Lead exposure, begun in utero, decreases renin and angiotensin II in adult rats. Proceedings of the Society for Experimental Biology and Medicine 170: 63–67, 1982a

    PubMed  CAS  Google Scholar 

  • Victery W, Vander AJ, Schoeps P, Germain C. Plasma renin is increased in young rats exposed to lead in utero and during nursing. Proceedings of the Society for Experimental Biology and Medicine 172: 1–7, 1983

    PubMed  CAS  Google Scholar 

  • Victery W, Vander AJ, Shulak JM, Schoeps P, Julius S. Lead, hypertension, and the renin-angiotensin system in rats. Journal of Laboratory and Clinical Medicine 99: 354–362, 1982b

    PubMed  CAS  Google Scholar 

  • Vigdortchik NA. Lead intoxication in the etiology of hypertonia. Journal of Industrial Hygiene and Toxicology 17: 1–6, 1935

    Google Scholar 

  • Vitale LF, Joselow MM, Wedeen RP, Pawlow M. Blood lead — an inadequate measure of occupational exposure. Journal of Occupational Medicine 17: 155–156, 1975

    PubMed  CAS  Google Scholar 

  • Voors AW, Johnson WD, Shuman MS. Additive statistical effects of cadmium and lead on heart-related disease in a North Carolina autopsy series. Archives of Environmental Health 37: 98–102, 1982

    PubMed  CAS  Google Scholar 

  • Wambach G, Helber A, Bonner G, Hummerich W. Natrium-Kalium-Adenosintriphosphatase-Aktivität in Erythrozytenghosts von Patienten mit essentieller Hypertonie. Klinische Wochenschrift 57: 169–172, 1979

    PubMed  CAS  Google Scholar 

  • Webb RC, Bhalla RC. Altered calcium sequestration by subcellular fractions of vascular smooth muscle from spontaneously hypertensive rats. Journal of Molecular and Cellular Cardiology 8: 651–661, 1976

    PubMed  CAS  Google Scholar 

  • Webb RC, Winquist RJ, Victery W, Vander AJ. In vivo and in vitro effects of lead on vascular reactivity in rats. American Journal of Physiology 241: H211–H216, 1981

    PubMed  CAS  Google Scholar 

  • Wedeen RP. Lead nephrotoxicity. In Porter (Ed.) Nephrotoxic mechanisms of drugs and environmental toxins, pp. 255–265, Plenum, New York, 1982a

    Google Scholar 

  • Wedeen RP. The role of lead in renal failure. Clinical and Experimental Dialysis and Apheresis 6: 113–146, 1982b

    PubMed  CAS  Google Scholar 

  • Wedeen RP, Mallik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Archives of Internal Medicine 139: 53–57, 1979

    PubMed  CAS  Google Scholar 

  • Weiss ST, Munoz A, Stein A, Sparrow D, Speizer FE. The relationship of blood lead to blood pressure in a longitudinal study of working men. American Journal of Epidemiology 123: 800–808, 1986

    PubMed  CAS  Google Scholar 

  • Westerman MP, Pfitzer E, Ellis LD, Jensen WN. Concentrations of lead in bone in plumbism. New England Journal of Medicine 273: 1246–1250, 1965

    PubMed  CAS  Google Scholar 

  • Wielopolski L, Ellis KJ, Vaswani AN, Cohn SH, Greenberg A, et al. In vivo bone lead measurements: a rapid monitoring method for cumulative lead exposure. American Journal of Industrial Medicine 9: 221–226, 1986

    PubMed  CAS  Google Scholar 

  • Williams BJ, Griffith WH, Albrecht CM, Pirch JH, Hejtmancik MR. Effects of chronic lead treatment on some cardiovascular responses to norepinephrine in the rat. Toxicology and Applied Pharmacology 40: 407–413, 1977

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. University of California, Berkeley, USA

    Dan S. Sharp,  Charles E. Becker (Professor of Medicine) & Allan H. Smith

  2. San Francisco General Hospital Medical Center, University of California, Building 30, 5th Floor, 1001 Potrero Avenue, San Francisco, CA, 94110, USA

    Dan S. Sharp,  Charles E. Becker (Professor of Medicine) & Allan H. Smith

Authors
  1. Dan S. Sharp
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Charles E. Becker
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Allan H. Smith
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Sharp, D.S., Becker, C.E. & Smith, A.H. Chronic Low-Level Lead Exposure. Med Toxicol Adverse Drug Exp 2, 210–232 (1987). https://doi.org/10.1007/BF03259865

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF03259865

Keywords

Search

Navigation