Arsenic in Drinking Water May Change Heart Structure

May 8, 2019

Drinking water that is contaminated with arsenic may lead to thickening of the heart’s main pumping chamber in young adults, according to a new study by researchers at Columbia University Mailman School of Public Health. This structural change increases the risk for future heart problems. The findings are published online in Circulation: Cardiovascular Imaging, an American Heart Association journal.
The researchers reviewed data from the Strong Heart Family Study, a study evaluating cardiovascular risk factors among young American Indian adults from Oklahoma, Arizona, and North and South Dakota. Arsenic exposure was measured in urine samples from 1,337 adults (average age 31 years, 61 percent female) and the size, shape, and function of their hearts were assessed using ultrasound (echocardiography). None of the participants had diabetes or heart disease at the start of the five-year study.
“People drinking water from private wells, which are not regulated, need to be aware that arsenic may increase the risk for cardiovascular disease. Testing those wells is a critical first step to take action and prevent exposure,” said Ana Navas-Acien, PhD, professor of environmental health sciences at Columbia Mailman School, and senior author.
People are most frequently exposed to arsenic, a toxic metal, through drinking water in areas where groundwater is contaminated, including many American Indian tribal communities and other rural and suburban communities in the United States. Previously, several studies have shown that arsenic exposure raises the risk of heart disease and its risk factors, including high blood pressure and diabetes. This is the first study to review the question in young adults.
Overall, arsenic exposure was higher than in the general United States population but lower than that found in other studies conducted in Mexico and Bangladesh. With a two-fold increase in arsenic in the urine, the researchers found:

  • 47 percent greater chance of thickening of the heart’s main pumping chamber (left ventricle) in the group as a whole; and
  • 58 percent greater chance of thickening of the left ventricle in participants with increased or high blood pressure (blood pressure at least 120/80 mm Hg or using pressure-lowering medication)

“The stronger association in subjects with elevated blood pressure suggests that individuals with pre-clinical heart disease might be more prone to the toxic effects of arsenic on the heart,” said Gernot Pichler, MD, PhD, and medical specialist for Internal Medicine, Department of Cardiology at Hospital Hietzing/Heart Center Clinic Floridsdorf in Vienna, Austria, and a visiting scholar in the Department of Environmental Health Sciences at Columbia Mailman School.
Although this study was performed in tribal populations in the north, central, and southwestern United States, the results are likely to be generalizable to millions of people in other rural locations exposed to low or moderate levels of arsenic in their water. The study also had only one measure of arsenic exposure and did not include long-term follow-up of the participants.
“The study raises the question of whether the changes in heart structure are reversible if exposure is reduced. Some changes have occurred in water sources in the study communities, and it will be important to check the potential health impact of reducing arsenic exposure,” Pichler said.
“Observational studies like this one are critical since cardiovascular disease remains the single leading cause of adult premature death worldwide and millions of individuals globally are exposed to arsenic and other metal contaminants,” noted Navas-Acien.
Co-authors are Maria Grau-Perez, Columbia Mailman School and Institute for Biomedical Research INCLIVA, Valencia, Spain; Maria Tellez-Plaza, Institute for Biomedical Research INCLIVA, Spain and Johns Hopkins Bloomberg School of Public Health; Jason G. Umans, MedStar Health Research Institute, and Georgetown University; Lyle G. Best, Missouri Breaks Industries Research, Inc; Shelley Cole, Texas Biomedical Research Institute; Walter Goessler, University of Graz, Austria; Kevin A. Francesconi, University of Graz, Austria; Jonathan Newman, New York University School of Medicine; Josep Redon, Institute for Biomedical Research INCLIVA, Spain; and Richard B. Devereux, Weill Cornell Medical College.
The study was supported by the National Institute of Environmental Health Sciences (ES021367, ES025216, ES010349, ES009089), the National Heart, Lung, and Blood Institute (HL41642, HL41652, HL41654, HL65520, HL65521), and grants HL109315, HL109301, HL109284, HL109282, HL109319, and HL090863.