The Longitudinal Association of Lead with Blood Pressure

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, meas...

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Veröffentlicht in:Epidemiology (Cambridge, Mass.) Mass.), 2003-01, Vol.14 (1), p.30-36
Hauptverfasser: Glenn, Barbara S., Stewart, Walter F., Links, Jonathan M., Todd, Andrew C., Schwartz, Brian S.
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container_end_page 36
container_issue 1
container_start_page 30
container_title Epidemiology (Cambridge, Mass.)
container_volume 14
creator Glenn, Barbara S.
Stewart, Walter F.
Links, Jonathan M.
Todd, Andrew C.
Schwartz, Brian S.
description 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 μg/dL (standard deviation [SD] = 2.6) or 0.22 μmole/Liter (SD = 0.13). Tibia lead at year three averaged 14.7-μg/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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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 μg/dL (standard deviation [SD] = 2.6) or 0.22 μmole/Liter (SD = 0.13). Tibia lead at year three averaged 14.7-μg/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. 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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 μg/dL (standard deviation [SD] = 2.6) or 0.22 μmole/Liter (SD = 0.13). Tibia lead at year three averaged 14.7-μg/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.</description><subject>Adult</subject><subject>Biological markers</subject><subject>Blood</subject><subject>Blood Pressure</subject><subject>Bones</subject><subject>Cohort Studies</subject><subject>Cross-Sectional Studies</subject><subject>Diastolic blood pressure</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - epidemiology</subject><subject>Lead</subject><subject>Lead - adverse effects</subject><subject>Lead - blood</subject><subject>Lead - metabolism</subject><subject>Longitudinal Studies</subject><subject>Mid-Atlantic Region - epidemiology</subject><subject>Middle Aged</subject><subject>Occupational Exposure - adverse effects</subject><subject>Radiography</subject><subject>Risk Factors</subject><subject>Spectrometry, X-Ray Emission</subject><subject>Standard deviation</subject><subject>Systolic blood pressure</subject><subject>Tibia</subject><subject>Tibia - diagnostic imaging</subject><subject>Tibia - metabolism</subject><issn>1044-3983</issn><issn>1531-5487</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtOwzAQRS0EoqXwBwj5Bwx-JU6XpeIlRYJF95afJCWtKztRxd_jEigrvBnP6J6R5gAACb4leC7ucH6k5BWiGDNMcocOE3ICpqRgBBW8Eqf5jzlHbF6xCbhIaZ0TgpHiHEwILXKesymoVo2Dddi-t_1g263q4CKlYFrVt2ELg4e1Uxbu276B910IFr5Fl9IQ3SU486pL7uqnzsDq8WG1fEb169PLclEjw6kgSGmunSGm9M4YZahWhBfcaIGdr3ChK5bvodhSZkqimadeUIEt5worwy2bgWpca2JIKTovd7HdqPgpCZYHF_LXhTy6kN8uMnozortBb5z9A3-OzwE-Bvah611MH92wd1E2TnV9I_9znLHrEVunPsTjWiYwo6JkX5nmcf0</recordid><startdate>20030101</startdate><enddate>20030101</enddate><creator>Glenn, Barbara S.</creator><creator>Stewart, Walter F.</creator><creator>Links, Jonathan M.</creator><creator>Todd, Andrew C.</creator><creator>Schwartz, Brian S.</creator><general>Lippincott Williams &amp; Wilkins</general><general>Lippincott Williams &amp; Wilkins, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20030101</creationdate><title>The Longitudinal Association of Lead with Blood Pressure</title><author>Glenn, Barbara S. ; Stewart, Walter F. ; Links, Jonathan M. ; Todd, Andrew C. ; Schwartz, Brian S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4271-ab4bec1c6feccac2ba1454cb70ef805b8309720d23c61b3f2f7270d44a0ac4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Biological markers</topic><topic>Blood</topic><topic>Blood Pressure</topic><topic>Bones</topic><topic>Cohort Studies</topic><topic>Cross-Sectional Studies</topic><topic>Diastolic blood pressure</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - epidemiology</topic><topic>Lead</topic><topic>Lead - adverse effects</topic><topic>Lead - blood</topic><topic>Lead - metabolism</topic><topic>Longitudinal Studies</topic><topic>Mid-Atlantic Region - epidemiology</topic><topic>Middle Aged</topic><topic>Occupational Exposure - adverse effects</topic><topic>Radiography</topic><topic>Risk Factors</topic><topic>Spectrometry, X-Ray Emission</topic><topic>Standard deviation</topic><topic>Systolic blood pressure</topic><topic>Tibia</topic><topic>Tibia - diagnostic imaging</topic><topic>Tibia - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Glenn, Barbara S.</creatorcontrib><creatorcontrib>Stewart, Walter F.</creatorcontrib><creatorcontrib>Links, Jonathan M.</creatorcontrib><creatorcontrib>Todd, Andrew C.</creatorcontrib><creatorcontrib>Schwartz, Brian S.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Epidemiology (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Glenn, Barbara S.</au><au>Stewart, Walter F.</au><au>Links, Jonathan M.</au><au>Todd, Andrew C.</au><au>Schwartz, Brian S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Longitudinal Association of Lead with Blood Pressure</atitle><jtitle>Epidemiology (Cambridge, Mass.)</jtitle><addtitle>Epidemiology</addtitle><date>2003-01-01</date><risdate>2003</risdate><volume>14</volume><issue>1</issue><spage>30</spage><epage>36</epage><pages>30-36</pages><issn>1044-3983</issn><eissn>1531-5487</eissn><abstract>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 μg/dL (standard deviation [SD] = 2.6) or 0.22 μmole/Liter (SD = 0.13). Tibia lead at year three averaged 14.7-μg/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.</abstract><cop>United States</cop><pub>Lippincott Williams &amp; Wilkins</pub><pmid>12500043</pmid><doi>10.1097/00001648-200301000-00011</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source Jstor Complete Legacy; MEDLINE; Journals@Ovid Complete
subjects Adult
Biological markers
Blood
Blood Pressure
Bones
Cohort Studies
Cross-Sectional Studies
Diastolic blood pressure
Humans
Hypertension
Hypertension - epidemiology
Lead
Lead - adverse effects
Lead - blood
Lead - metabolism
Longitudinal Studies
Mid-Atlantic Region - epidemiology
Middle Aged
Occupational Exposure - adverse effects
Radiography
Risk Factors
Spectrometry, X-Ray Emission
Standard deviation
Systolic blood pressure
Tibia
Tibia - diagnostic imaging
Tibia - metabolism
title The Longitudinal Association of Lead with Blood Pressure
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