BACKGROUND: Several investigators have reported an association of blood lead or bone lead with increased blood pressure and hypertension, but questions remain concerning whether these effects are acute or chronic in nature. METHODS: In this longitudinal study, we evaluated the relation of lead, measured in blood and tibia, to changes in blood pressure between 1994 and 1998. We studied 496 current and former employees of a chemical-manufacturing facility in the eastern United States who had previous occupational exposure to inorganic and organic lead. Cohort members who provided three or four blood pressure measurements during the study were included. RESULTS: Mean age at baseline was 55.8 years with a mean of 18 years since last occupational exposure to lead. Blood lead at baseline averaged 4.6 microg/dL (standard deviation [SD] = 2.6) or 0.22 micromole/Liter (SD = 0.13). Tibia lead at year three averaged 14.7-microg/gm (SD = 9.4) bone mineral. Change in systolic blood pressure during the study was associated with lead dose, with an average annual increase of 0.64 mmHg (standard error [SE] = 0.25), 0.73 mmHg (SE = 0.26), and 0.61 mmHg (SE = 0.27) for every standard deviation increase in blood lead at baseline, tibia lead at year three, or peak past tibia lead, respectively. CONCLUSIONS: The results support an etiologic role for lead in the elevation of systolic blood pressure among adult males and are consistent with both acute and chronic modes of action.
BACKGROUND: Several investigators have reported an association of blood lead or bone lead with increased blood pressure and hypertension, but questions remain concerning whether these effects are acute or chronic in nature. METHODS: In this longitudinal study, we evaluated the relation of lead, measured in blood and tibia, to changes in blood pressure between 1994 and 1998. We studied 496 current and former employees of a chemical-manufacturing facility in the eastern United States who had previous occupational exposure to inorganic and organic lead. Cohort members who provided three or four blood pressure measurements during the study were included. RESULTS: Mean age at baseline was 55.8 years with a mean of 18 years since last occupational exposure to lead. Blood lead at baseline averaged 4.6 microg/dL (standard deviation [SD] = 2.6) or 0.22 micromole/Liter (SD = 0.13). Tibia lead at year three averaged 14.7-microg/gm (SD = 9.4) bone mineral. Change in systolic blood pressure during the study was associated with lead dose, with an average annual increase of 0.64 mmHg (standard error [SE] = 0.25), 0.73 mmHg (SE = 0.26), and 0.61 mmHg (SE = 0.27) for every standard deviation increase in blood lead at baseline, tibia lead at year three, or peak past tibia lead, respectively. CONCLUSIONS: The results support an etiologic role for lead in the elevation of systolic blood pressure among adult males and are consistent with both acute and chronic modes of action.
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