Abstract P071: Moderate Exposure to Inorganic Arsenic in Drinking Water is Associated with Elevated Pulse Pressure: Results from Chihuahua, Mexico
Background: Though levels of arsenic >100 μg/L in drinking water have been consistently associated with increased risk of cardiovascular disease (CVD), evidence of an association at lower levels of exposure is more inconsistent. We used data from a cohort from Chihuahua Mexico to examine whether relatively low levels of arsenic in drinking water were associated with elevated pulse pressure, a marker linked to arterial stiffening and CVD risk.
Methods: We used concentrations of arsenic in household drinking water from 931 adults not taking hypertensive medication to examine the association between water arsenic categories as low as 25-50 μg/L and mean increases in systolic, diastolic and pulse pressure (systolic - diastolic pressure). We also examined the association between water arsenic categories and elevated pulse pressure, defined as >70 mm Hg. Associations between arsenic exposure and blood pressure measures were obtained from multivariable linear or logistic regression models that adjusted for age, gender, education level, ethnicity, BMI, waist circumference, smoking status and alcoholic beverage intake.
Results: After multivariable adjustment, compared to lower levels, water arsenic concentrations of 25-50 μg/L and above were associated with statistically significant increases in systolic blood pressure (SBP) and pulse pressure, but were not associated with diastolic blood pressure (DBP). Multivariable-adjusted associations [β (95% confidence interval)] with water arsenic concentrations of 25-50 μg/L were: 4.3 (1.2-7.4) mm Hg for SBP; 3.3 (0.8-5.7) mm Hg for pulse pressure; and 1.3 (-0.6-3.3) mm Hg for DBP. For elevated pulse pressure (16.1% of the sample), the association [odds ratio (95% CI)] with water arsenic levels of 25-50 μg/dL was 2.5 (1.3-4.9).
Conclusions: Results support potential adverse effects of exposure to moderate levels of arsenic in drinking water on CVD risk through pathways that may involve widening pulse pressure.
Author Disclosures: M.A. Mendez: None. C. González-Horta: None. B. Sánchez-Ramírez: None. L. Ballinas-Casarrubias: None. R. Hernández Cerón: None. D. Viniegra Morales: None. F. Baeza Terrazas: None. D. Gutiérrez-Torres: None. M. Ishida: None. Z. Drobna: None. J. Buse: None. G. García-Vargas: None. L. Del Razo: None. M. Stýblo1: None.
- © 2017 by American Heart Association, Inc.