The Contribution of Declines in Blood Lead Levels to Reductions in Blood Pressure Levels: Longitudinal Evidence in the Strong Heart Family Study.

American Indians Strong Heart Study cardiovascular disease lead

Journal

Journal of the American Heart Association
ISSN: 2047-9980
Titre abrégé: J Am Heart Assoc
Pays: England
ID NLM: 101580524

Informations de publication

Date de publication:
11 Jan 2024
Historique:
medline: 11 1 2024
pubmed: 11 1 2024
entrez: 11 1 2024
Statut: aheadofprint

Résumé

Chronic lead exposure is associated with both subclinical and clinical cardiovascular disease. We evaluated whether declines in blood lead were associated with changes in systolic and diastolic blood pressure in adult American Indian participants from the SHFS (Strong Heart Family Study). Lead in whole blood was measured in 285 SHFS participants in 1997 to 1999 and 2006 to 2009. Blood pressure and measures of cardiac geometry and function were obtained in 2001 to 2003 and 2006 to 2009. We used generalized estimating equations to evaluate the association of declines in blood lead with changes in blood pressure; cardiac function and geometry measures were considered secondary. Mean blood lead was 2.04 μg/dL at baseline. After ≈10 years, mean decline in blood lead was 0.67 μg/dL. In fully adjusted models, the mean difference in systolic blood pressure comparing the highest to lowest tertile of decline (>0.91 versus <0.27 μg/dL) in blood lead was -7.08 mm Hg (95% CI, -13.16 to -1.00). A significant nonlinear association between declines in blood lead and declines in systolic blood pressure was detected, with significant linear associations where blood lead decline was 0.1 μg/dL or higher. Declines in blood lead were nonsignificantly associated with declines in diastolic blood pressure and significantly associated with declines in interventricular septum thickness. Declines in blood lead levels in American Indian adults, even when small (0.1-1.0 μg/dL), were associated with reductions in systolic blood pressure. These findings suggest the need to further study the cardiovascular impacts of reducing lead exposures and the importance of lead exposure prevention.

Sections du résumé

BACKGROUND BACKGROUND
Chronic lead exposure is associated with both subclinical and clinical cardiovascular disease. We evaluated whether declines in blood lead were associated with changes in systolic and diastolic blood pressure in adult American Indian participants from the SHFS (Strong Heart Family Study).
METHODS AND RESULTS RESULTS
Lead in whole blood was measured in 285 SHFS participants in 1997 to 1999 and 2006 to 2009. Blood pressure and measures of cardiac geometry and function were obtained in 2001 to 2003 and 2006 to 2009. We used generalized estimating equations to evaluate the association of declines in blood lead with changes in blood pressure; cardiac function and geometry measures were considered secondary. Mean blood lead was 2.04 μg/dL at baseline. After ≈10 years, mean decline in blood lead was 0.67 μg/dL. In fully adjusted models, the mean difference in systolic blood pressure comparing the highest to lowest tertile of decline (>0.91 versus <0.27 μg/dL) in blood lead was -7.08 mm Hg (95% CI, -13.16 to -1.00). A significant nonlinear association between declines in blood lead and declines in systolic blood pressure was detected, with significant linear associations where blood lead decline was 0.1 μg/dL or higher. Declines in blood lead were nonsignificantly associated with declines in diastolic blood pressure and significantly associated with declines in interventricular septum thickness.
CONCLUSIONS CONCLUSIONS
Declines in blood lead levels in American Indian adults, even when small (0.1-1.0 μg/dL), were associated with reductions in systolic blood pressure. These findings suggest the need to further study the cardiovascular impacts of reducing lead exposures and the importance of lead exposure prevention.

Identifiants

pubmed: 38205795
doi: 10.1161/JAHA.123.031256
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e031256

Auteurs

Wil Lieberman-Cribbin (W)

Department of Environmental Health Sciences Columbia University Mailman School of Public Health New York NY USA.

Zheng Li (Z)

Office of Capacity Development and Applied Prevention Science, Agency for Toxic Substances and Disease Registry Atlanta GA USA.

Michael Lewin (M)

Office of Community Health and Hazard Assessment, Agency for Toxic Substances and Disease Registry Atlanta GA USA.

Patricia Ruiz (P)

Office of Innovation and Analytics, Agency for Toxic Substances and Disease Registry Atlanta GA USA.

Jeffery M Jarrett (JM)

Division for Laboratory Sciences Centers for Disease Control and Prevention Atlanta GA USA.

Shelley A Cole (SA)

Population Health Program Texas Biomedical Research Institute San Antonio TX USA.

Allison Kupsco (A)

Department of Environmental Health Sciences Columbia University Mailman School of Public Health New York NY USA.

Marcia O'Leary (M)

Missouri Breaks Research Industries Research, Inc. Eagle Butte SD USA.

Gernot Pichler (G)

Department of Cardiology Karl Landsteiner Institute for Cardiovascular and Critical Care Research, Clinic Floridsdorf Vienna Austria.

Daichi Shimbo (D)

Division of Cardiology Columbia University Irving Medical Center New York NY USA.

Richard B Devereux (RB)

Weill Cornell Medical College New York NY USA.

Jason G Umans (JG)

MedStar Health Research Institute Hyattsville MD USA.
Georgetown-Howard Universities Center for Clinical and Translational Science Washington DC USA.

Ana Navas-Acien (A)

Department of Environmental Health Sciences Columbia University Mailman School of Public Health New York NY USA.

Anne E Nigra (AE)

Department of Environmental Health Sciences Columbia University Mailman School of Public Health New York NY USA.

Classifications MeSH