Arsenic in drinking water linked to LV thickening, hypertrophy

Drinking water contaminated with inorganic arsenic could increase young adults’ risk of CVD by thickening the heart’s left ventricular (LV) wall and triggering hypertrophy, researchers reported in Circulation: Cardiovascular Imaging May 7.

Arsenic, a toxic metalloid, is an established carcinogen that can be fatal to humans in excess doses, first author Gernot Pichler, MD, PhD, MSc, of Hospital Hietzing and the Heart Center Clinic Floridsdorf in Vienna, wrote in the journal. We know it’s found in food, soil, air and water—especially unregulated groundwater in both rural and suburban communities.

“The relationship of arsenic exposure with adverse cardiac outcomes is not fully understood,” Pichler and co-authors said. “Inorganic arsenic is related to hypertension and diabetes mellitus, the main risk factors for the development of cardiac dysfunction. It is unknown whether inorganic arsenic is related to cardiac structure and functioning or if the observed adverse outcomes are secondary to a worse cardiometabolic profile of arsenic-exposed individuals.”

Pichler and his team recruited 1,337 young adults from the Strong Heart Family Study, a long-running effort to study cardiovascular risk factors in American Indians. Nobody has studied the link between arsenic exposure and CV outcomes in the population to date, but the authors said the groundwater in many American Indian tribal communities is contaminated with the chemical.

None of the participants, who were on average 30 years old, had diabetes or CVD at baseline. Pichler et al. studied the size, shape and function of their hearts using echocardiography and measured arsenic exposure with urine samples, repeating echocardiography after a mean 5.6 years of follow-up.

The researchers found arsenic exposure in the American Indian communities they studied in Oklahoma, Arizona and North and South Dakota was higher than that in the general U.S. population but lower than averages in Mexico and Bangladesh. With a twofold increase in the amount of arsenic in a patient’s urine sample, the team identified a 47% greater chance of LV thickening as a whole and a 58% higher chance of LV thickening in patients with increased or high blood pressure.

In a related editorial, two U.K. scientists from the University of Cambridge, Rajiv Chowdhury, MBBS, PhD, and Kim van Daalen, BSc, MPhil, commended Pichler et al.’s work but noted some limitations. The study suffered from a lack of long-term follow-up, they said, and only considered one measure of arsenic exposure.

“Although commonly used as a biomarker, urinary arsenic reflects recent exposure, generally from the previous day,” Chowdhury and van Daalen wrote. “Due to a single measurement of arsenic in this study at baseline, statistical analysis cannot account for changes of arsenic exposure over time nor can a temporal relation (short-term and long-term) between arsenic exposure and outcome be conclusively established.”

They also said enrollees in the study were likely exposed to other co-occurring environmental metals in their water like cadmium, lead and selenium, which could have altered results. Certain interactions across co-occurring metal species—synergism, additivity and antagonism, for example—might confer CVD risk. Pichler’s team did incorporate tungsten and uranium in sensitivity analyses, but Chowdhury and van Daalen said a more comprehensive analysis of the interplay between different metals and how they affect CV risk is warranted.

“While this elegant analysis by Pichler et al. helps to clarify the observational associations of inorganic arsenic with LV geometry and function, it stimulates further complimentary work,” they wrote. “Such studies would be essential since CVD remains the single leading cause of adult premature death worldwide, and millions of individuals globally are exposed to arsenic and other metal contaminants.”