Background: High chronic exposure to inorganic arsenic may contribute to the development of hypertension. Limited information is available, however, on the association of low to moderate exposure to inorganic arsenic with blood pressure levels and hypertension. We investigated the association of exposure to inorganic arsenic (as measured in urine) with systolic and diastolic blood pressure levels and the prevalence of hypertension in US adults.
Methods: We studied 4167 adults 20 years of age or older who participated in the National Health and Nutrition Examination Survey (NHANES) from 2003 through 2008 and for whom total arsenic, dimethylarsinate (DMA), and arsenobetaine had been assessed in urine.
Results: The median (interquartile range) urine concentrations were 8.3 μg/L (4.2–17.1) for total arsenic, 3.6 μg/L (2.0–6.0) for DMA, and 1.4 μg/L (0.3–6.3) for arsenobetaine. The weighted prevalence of hypertension in the study population was 36%. After multivariable adjustment, a 2-fold increase in total arsenic was associated with a hypertension odds ratio of 0.98 (95% confidence interval = 0.86–1.11). A doubling of total arsenic minus arsenobetaine was associated with a hypertension OR of 1.03 (0.94–1.14) and a doubling of DMA concentrations was associated with a hypertension OR of 1.11 (0.99–1.24). Total arsenic, total arsenic minus arsenobetaine, or DMA levels were not associated with systolic or diastolic blood pressure.
Conclusions: At the low to moderate levels, typical of the US population, total arsenic, total arsenic minus arsenobetaine, and DMA concentrations in urine were not associated with the prevalence of hypertension or with systolic or diastolic blood pressure levels. A weak association of DMA with hypertension could not be ruled out.
From the Departments of aEpidemiology, bEnvironmental Health Sciences, and cWelch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; and dDepartment of Cardiovascular Epidemiology and Population Genetics, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Submitted 16 July 2010; accepted 17 September 2010; posted 5 January 2011.
Supported by the National Heart, Lung and Blood Institute (NHLBI) grant R01HL090863 and by the National Institute of Environmental Health Sciences grant R01ES015597.
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Correspondence: Ana Navas-Acien, Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, 615 N Wolfe St, Office W7033B, Baltimore, MD 21205. E-mail: firstname.lastname@example.org.