A 50-year follow-up of childhood plumbism. Hypertension, renal function, and hemoglobin levels among survivors.

A group of 192 subjects with well-documented lead poisoning in 1930 to 1942 were identified in this pilot study. Thirty-five of 72 survivors traced to a Boston area address and 22 age-, sex-, race-, and neighborhood-matched controls were recruited into a clinical study. One matched subject with plumbism had grossly abnormal renal function and an elevated blood lead level of an unclear cause. Among the remaining 21 matched pairs, the risk of hypertension was significantly higher in subjects with plumbism (relative risk, 7.0; 95% confidence interval, 1.2 to 42.3). Mean adjusted creatinine clearance rates for subjects with plumbism, however, were significantly higher than those of controls and supranormal in comparison to rates predicted for sex and age. Subjects with plumbism had significantly lower hemoglobin concentrations and hematocrit readings than the controls. Blood lead and serum creatinine levels were low for both groups. These results suggest that survivors of childhood lead poisoning have an increased risk of clinically significant hypertension developing in the setting of supranormal creatinine clearance rates.

[1]  P. Landrigan,et al.  Lead-induced anemia: dose-response relationships and evidence for a threshold. , 1990, American journal of public health.

[2]  P. Landrigan Toxicity of lead at low dose. , 1989, British journal of industrial medicine.

[3]  H. Needleman The persistent threat of lead: a singular opportunity. , 1989, American journal of public health.

[4]  E. Silbergeld,et al.  Lead and osteoporosis: mobilization of lead from bone in postmenopausal women. , 1988, Environmental research.

[5]  J. F. Rosen The Toxicological Importance of Lead in Bone: The Evolution and Potential Uses of Bone Lead Measurements by X-Ray Fluorescence to Evaluate Treatment Outcomes in Moderately Lead Toxic Children , 1988 .

[6]  J. V. van Hemmen,et al.  Occupational exposure to lead and blood pressure: a study in 105 workers. , 1987, American journal of industrial medicine.

[7]  F. Speizer,et al.  The relationship of blood lead to blood pressure in a longitudinal study of working men. , 1986, American journal of epidemiology.

[8]  P. D. Jong,et al.  Sickle cell nephropathy: New insights into its pathophysiology , 1985 .

[9]  R. Cohn,et al.  Renal function 9 to 17 years after childhood lead poisoning. , 1985 .

[10]  A. H. Marcus,et al.  Multicompartment kinetic models for lead. I. Bone diffusion models for long-term retention. , 1985, Environmental Research.

[11]  P. Meredith,et al.  Lead exposure and changes in the renin-angiotensin-aldosterone system in man. , 1985, Toxicology letters.

[12]  F. Gyntelberg,et al.  Blood pressure and other cardiovascular risk factors of long-term exposure to lead. , 1985, Scandinavian journal of work, environment & health.

[13]  J R Landis,et al.  Blood lead and blood pressure. Relationship in the adolescent and adult US population. , 1985, JAMA.

[14]  J. Lellouch,et al.  Blood lead concentration and blood pressure. , 1985, British medical journal.

[15]  S. Araki,et al.  Behavior of lead and zinc in plasma, erythrocytes, and urine and ALAD in erythrocytes following intravenous infusion of CaEDTA in lead workers. , 1984, Archives of environmental health.

[16]  V. Batuman,et al.  Contribution of lead to hypertension with renal impairment. , 1983, The New England journal of medicine.

[17]  A. Steenhout Kinetics of lead storage in teeth and bones: an epidemiologic approach. , 1982, Archives of environmental health.

[18]  D. Gompertz Assessment of risk by biological monitoring. , 1981, British journal of industrial medicine.

[19]  P. Barry Concentrations of lead in the tissues of children. , 1981, British journal of industrial medicine.

[20]  M. Carmignani,et al.  Neurogenic and humoral mechanisms in arterial hypertension of chronically lead-exposed rats. , 1981, La Medicina del lavoro.

[21]  R. Doherty,et al.  Bone lead mobilization in lactating mice and lead transfer to suckling offspring. , 1980, Toxicology and applied pharmacology.

[22]  G. Wetherill,et al.  Kinetic analysis of lead metabolism in healthy humans. , 1976, The Journal of clinical investigation.

[23]  A. H. Norris,et al.  Age-Adjusted Standards for Creatinine Clearance , 1976 .

[24]  P. Barry A comparison of concentrations of lead in human tissues. , 1975, British journal of industrial medicine.

[25]  R. Goyer,et al.  Renal ultrastructure, renal function, and parameters of lead toxicity in workers with different periods of lead exposure , 1974, British journal of industrial medicine.

[26]  George W. Wetherill,et al.  Lead Metabolism in the Normal Human: Stable Isotope Studies , 1973, Science.

[27]  L. W. Statius van Eps,et al.  [Sickle cell nephropathy]. , 1973, Nederlands tijdschrift voor geneeskunde.

[28]  Goyer Ra Lead and the kidney. , 1971 .

[29]  L. Tepper RENAL FUNCTION SUBSEQUENT TO CHILDHOOD PLUMBISM. , 1963, Archives of environmental health.

[30]  A. Pardoe Renal function in lead poisoning. , 1952, British journal of pharmacology and chemotherapy.

[31]  L. Nye An Investigation of the Extraordinary Incidence of Chronic Nephritis in Young People in Queensland. , 1929 .