Angela Gambelunghe1, Gerd Sallsten2, Yan Borné3, Niklas Forsgard4, Bo Hedblad5, Peter Nilsson6, Björn Fagerberg7, Gunnar Engström8, Lars Barregard9. 1. Department of Medicine, Section of Occupational Medicine and Toxicology, University of Perugia, Italy. Electronic address: angela.gambelunghe@unipg.it. 2. Department of Occupational and Environmental Medicine, University of Gothenburg, Sweden. Electronic address: gerd.sallsten@amm.gu.se. 3. Cardiovascular Epidemiology, Department of Clinical Sciences in Malmö, Lund University, and Skåne University Hospital, Malmö, Sweden. Electronic address: yan.borne@med.lu.se. 4. Department of Clinical Sciences in Malmö, Lund University and Skåne University Hospital, Sweden. Electronic address: niklas.forsgard@vgregion.se. 5. Cardiovascular Epidemiology, Department of Clinical Sciences in Malmö, Lund University, and Skåne University Hospital, Malmö, Sweden. Electronic address: bo.hedblad@med.lu.se. 6. Department of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden. Electronic address: peter.nilsson@med.lu.se. 7. Department of Molecular and Clinical Medicine, Wallenberg Laboratory for Cardiovascular and Metabolic Research, University of Gothenburg, and Sahlgrenska University Hospital, Sweden. Electronic address: bjoern.fagerberg@wlab.gu.se. 8. Cardiovascular Epidemiology, Department of Clinical Sciences in Malmö, Lund University, and Skåne University Hospital, Malmö, Sweden. Electronic address: gunnar.engstrom@med.lu.se. 9. Department of Occupational and Environmental Medicine, University of Gothenburg, Sweden. Electronic address: lars.barregard@amm.gu.se.
Abstract
BACKGROUND: Environmental lead exposure is a possible causative factor for increased blood pressure and hypertension, but large studies at low-level exposure are scarce, and results inconsistent. OBJECTIVE: We aimed to examine the effects of environmental exposure to lead in a large population-based sample. METHODS: We assessed associations between blood lead and systolic/diastolic blood pressure and hypertension in 4452 individuals (46-67 years) living in Malmö, Sweden, in 1991-1994. Blood pressure was measured using a mercury sphygmomanometer after 10min supine rest. Hypertension was defined as high systolic (≥140mmHg) or diastolic (≥90mmHg) blood pressure and/or current use of antihypertensive medication. Blood lead was calculated from lead in erythrocytes and haematocrit. Multivariable associations between blood lead and blood pressure or hypertension were assessed by linear and logistic regression. Two-thirds of the cohort was re-examined 16 years later. RESULTS: At baseline, mean blood pressure was 141/87mmHg, 16% used antihypertensive medication, 63% had hypertension, and mean blood lead was 28µg/L. Blood lead in the fourth quartile was associated with significantly higher systolic and diastolic blood pressure (point estimates: 1-2mmHg) and increased prevalence of hypertension (odds ratio: 1.3, 95% confidence interval: 1.1-1.5) versus the other quartiles after adjustment for sex, age, smoking, alcohol, waist circumference, and education. Associations were also significant with blood lead as a continuous variable. Blood lead at baseline, having a half-life of about one month, was not associated with antihypertensive treatment at the 16-year follow-up. CONCLUSIONS: Low-level lead exposure increases blood pressure and may increase the risk of hypertension.
BACKGROUND: Environmental lead exposure is a possible causative factor for increased blood pressure and hypertension, but large studies at low-level exposure are scarce, and results inconsistent. OBJECTIVE: We aimed to examine the effects of environmental exposure to lead in a large population-based sample. METHODS: We assessed associations between blood lead and systolic/diastolic blood pressure and hypertension in 4452 individuals (46-67 years) living in Malmö, Sweden, in 1991-1994. Blood pressure was measured using a mercury sphygmomanometer after 10min supine rest. Hypertension was defined as high systolic (≥140mmHg) or diastolic (≥90mmHg) blood pressure and/or current use of antihypertensive medication. Blood lead was calculated from lead in erythrocytes and haematocrit. Multivariable associations between blood lead and blood pressure or hypertension were assessed by linear and logistic regression. Two-thirds of the cohort was re-examined 16 years later. RESULTS: At baseline, mean blood pressure was 141/87mmHg, 16% used antihypertensive medication, 63% had hypertension, and mean blood lead was 28µg/L. Blood lead in the fourth quartile was associated with significantly higher systolic and diastolic blood pressure (point estimates: 1-2mmHg) and increased prevalence of hypertension (odds ratio: 1.3, 95% confidence interval: 1.1-1.5) versus the other quartiles after adjustment for sex, age, smoking, alcohol, waist circumference, and education. Associations were also significant with blood lead as a continuous variable. Blood lead at baseline, having a half-life of about one month, was not associated with antihypertensive treatment at the 16-year follow-up. CONCLUSIONS: Low-level lead exposure increases blood pressure and may increase the risk of hypertension.
Authors: Catherine M Bulka; Molly Scannell Bryan; Victoria W Persky; Martha L Daviglus; Ramon A Durazo-Arvizu; Faruque Parvez; Vesna Slavkovich; Joseph H Graziano; Tariqul Islam; John A Baron; Habibul Ahsan; Maria Argos Journal: Environ Pollut Date: 2019-02-07 Impact factor: 9.988
Authors: Katarzyna Gajewska; Marzena Laskowska; Agostinho Almeida; Edgar Pinto; Katarzyna Skórzyńska-Dziduszko; Anna Błażewicz Journal: Molecules Date: 2021-05-20 Impact factor: 4.411