Several studies have examined longitudinal associations of blood pressure change or hypertension incidence with lead concentration in blood or bone. It is not clear whether the observed associations reflect an immediate response to lead as a consequence of recent dose or rather are a persistent effect of cumulative dose over a lifetime.
We followed 575 subjects in a lead-exposed occupational cohort in South Korea between October 1997 and June 2001. We used generalized estimating equation models to evaluate blood pressure change between study visits in relation to tibia lead concentrations at each prior visit and concurrent changes in blood lead. The modeling strategy summarized the longitudinal association of blood pressure with cumulative lead dose or changes in recent lead dose.
On average, participants were 41 years old at baseline and had worked 8.5 years in lead-exposed jobs. At baseline, the average ± standard deviation for blood lead was 31.4 ± 14.2 μg/dL, and for tibia lead, it was 38.4 ± 42.9 μg/g bone mineral. Change in systolic blood pressure during the study was associated with concurrent blood lead change, with an average annual increase of 0.9 (95% confidence interval = 0.1 to 1.6) mm Hg for every 10-μg/dL increase in blood lead per year.
The findings in this relatively young population of current and former lead workers suggest that systolic blood pressure responds to lead dose through acute pathways in addition to the effects of cumulative injury.
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From the *Office of Research and Development, U.S. Environmental Protection Agency, Washington, DC; the †Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; the ‡Institute of Industrial Medicine, Soonchunhyang University, Chonan, South Korea; the §Department of Community and Preventive Medicine, Mount Sinai Medical Center, New York, NY; the ∥Division of Occupational and Environmental Health, Department of Environmental Health Sciences and the ¶Department of Epidemiology, Johns Hopkins Bloomberg School of Hygiene and Public Health, Baltimore, MD; and the **Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD.
Submitted 3 March 2005; accepted 21 March 2006.
The views expressed are the author’s own and do not reflect official U.S. EPA Policy.
Supported by grant ES07198 (Dr. Schwartz) from the National Institute of Environmental Health Sciences.
Supplemental material for this article is available with the online version of the journal at www.epidem.com; click on “Article Plus.”
Correspondence: Barbara S. Glenn, Office of Research and Development, U.S. Environmental Protection Agency, 1600 Pennsylvania Avenue, NW (8723F), Washington, DC 20460. E-mail firstname.lastname@example.org.