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Lead Exposure and Conventional and Ambulatory Blood PressureA Prospective Population Study
Jan A. Staessen, MD, PhD;
Harry Roels, PhD;
Robert Fagard, MD, PhD;
PheeCad Investigators;
Antoon Amery;
Leszek Bieniaszewski;
Christopher J. Bulpitt;
Hilde Celis;
Primoz Dolenc;
Robert Fagard;
Paul Lijnen;
Victor Petrov;
Lutgarde Thijs;
Jan A. Staessen;
Alfred Bernard;
Jean-Pierre Buchet;
Robert R. Lauwerys;
Harry Roels, Md;
Francis Dondeyne;
Dirk Wildemeersch
JAMA. 1996;275(20):1563-1570.
Abstract
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Objective.
—To evaluate in a prospective fashion the association between low-level lead exposure and blood pressure.
Design.
—Prospective cohort study.
Setting.
—General population.
Participants.
—A random population sample (N=728; 49% men; age range, 20-82 years) was studied in Belgium for 1985 through 1989 and reexamined for 1991 through 1995.
Mean Outcome Measures.
—At baseline and follow-up, blood pressure was measured by conventional sphygmomanometry (15 total readings) and at followup also by 24-hour ambulatory monitoring. Lead exposure was estimated from blood lead and zinc protoporphyrin concentrations. Multivariate analyses controlled for sex, age, body mass index, smoking and drinking habits, physical activity, exposure at work, social class, menopausal status, use of medications (antihypertensive medication, oral contraceptives, hormonal replacement therapy), hematocrit or hemoglobin, serum total calcium concentration, 24-hour urinary sodium and potassium excretion, and  -glutamyltransferase activity.
Results.
—At baseline, mean (SD) systolic/diastolic conventional blood pressure was 130 (17)/77 (9) mm Hg. The mean blood lead concentration was 0.42 µmol/L (8.7 µg/dL), and the mean zinc protoporphyrin concentration was 1.0 µg per gram of hemoglobin. Over the 5.2-year median follow-up, the mean blood lead concentration dropped by 32% (0.14 µmol/L [2.9 µg/dL]) (P<.001). Small but significant (P<.01) changes occurred in systolic (-1.5 mm Hg) and diastolic (+1.7 mm Hg) conventional blood pressure and in zinc protoporphyrin concentration (+0.5 µg per gram of hemoglobin). Over the follow-up period, no consistent associations emerged between the changes in conventional blood pressure and in blood lead or zinc protoporphyrin concentrations. In addition, after adjustment for sex, age, and body mass index, blood lead and zinc protoporphyrin concentrations at baseline did not predict the development of hypertension in 47 patients (risk ratio for doubling of the initial lead concentration, 1.2; 95% confidence interval, 0.7-2.0). In a time-integrated analysis in which each person was characterized by all available measurements, conventional blood pressure did not correlate with blood lead or zinc protoporphyrin concentrations in a consistent manner. Similarly, the mean (SD) 24-hour blood pressure at follow-up (119[11]/71 [8] mm Hg; N=684) did not show a consistent relationship with blood lead or zinc protoporphyrin concentrations at baseline or at follow-up.
Conclusions.
—Lead exposure at the intensity studied (<1.45 µmol/L [<30 µg/dL]) was not consistently associated with increased conventional or 24-hour blood pressure in the general population or with increased risk of hypertension. These findings argue against the hypothesis that current lead exposure levels are associated with excess cardiovascular morbidity and mortality caused by hypertension. (JAMA. 1996;275:1563-1570)
Author Affiliations
Hypertension and Cardiovascular Rehabilitation Unit, Department of Molecular and Cardiovascular Research, University of Leuven (Belgium); Industrial Toxicology and Occupational Medicine Unit, University of Louvain, Brussels, Belgium; Provincial Health Inspectorate, Ministry of the Flemish Community, Hasselt, Belgium.
From the Hypertension and Cardiovascular Rehabilitation Unit, Department of Molecular and Cardiovascular Research, University of Leuven (Belgium) (Drs Staessen and Fagard), and the Industrial Toxicology and Occupational Medicine Unit, University of Louvain, Brussels, Belgium (Dr Roels). A complete list of the PheeCad Investigators appears at the end of the article.
Footnotes
Reprints: Jan A. Staessen, MD, PhD, Klinisch Laboratorium Hypertensie, Inwendige Geneeskunde-Cardiologie, UZ Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.
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