Antimony Levels Linked to Higher Blood Pressure, PAH Severity: Study

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by Steve Bryson, PhD |

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A dropper squirts blood alongside four half-filled tubes.

Higher levels of the metal antimony were found in the bloodstream of adults with pulmonary arterial hypertension (PAH) than those without the condition, a pilot study reported.

Elevated antimony levels also correlated with higher blood pressure in the pulmonary arteries and reduced heart function.

The pilot study, “Plasma Level of Antimony Correlates with Pulmonary Arterial Hypertension Severity,” was published in Current Research in Toxicology.

In PAH, narrowing of the pulmonary arteries, the blood vessels that carry blood through the lungs, leads to high blood pressure, or hypertension. This makes the heart’s right ventricle work harder to pump blood through the body.

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The condition has many potential causes, including heart abnormalities, viral infections, connective tissue disorders, and certain medicines. Exposure to environmental pollution and heavy metals have also been associated with lung disease.

Antimony is a gray metalloid element that’s been used for centuries in medicines and cosmetics in its natural form stibnite. Metallic antimony is currently used in metal alloys with lead and tin in products such as solders, bullets, ball bearings, and batteries. Antimony trioxide form is a major component of flame retardants.

In animal models, exposure to antimony had adverse effects on heart function, but its impact on PAH is unknown.

The aim of the pilot study, which recruited participants from the University of Louisville PH center, was to examine antimony levels in PAH patients without a known history of occupational exposure. Levels were then compared to PAH assessments related to future outcomes (prognosis).

The study included 20 people with PAH, with a mean age of 57.6, of whom 80% were women. A control group of 10 people without PAH was added, it had a younger mean age of 37.1, and 60% were women.

The underlying cause of PAH was unknown (idiopathic) in six patients, while five had connective tissue disease, three had congenital disease, two were due to sarcoidosis, and two because of medicines. One PAH case was caused by a liver disease complication, while another was due to common variable immunodeficiency, a disorder marked by low antibody levels.

Blood tests revealed antimony levels were significantly higher in PAH patients compared to controls — a mean of 1.3 vs. 0.7 nanograms per milliliter (ng/ml) of blood. Similar results were seen in blood plasma (2.6 vs. 1.5 ng/ml), the liquid portion of the blood that remains once cells are removed. No significant differences were observed in urine levels.

Blood and plasma antimony levels were significantly higher in PAH with or without a known cause compared to controls. Although antimony was higher in idiopathic-PAH compared to PAH with a known cause, the difference did not reach statistical significance, which “could be related to the small sample size in each group,” the researchers wrote.

The team noted that higher antimony levels in PAH patients might be related to medications that alter antimony’s elimination from the body or co-exposure with an unidentified toxin that may predispose some people to PAH.

The researchers then compared antimony levels in people with PAH to their assessments of heart function and blood pressure.

High antimony levels in the plasma were significantly related to lower cardiac output and cardiac index, two measures of heart function, and reduced mixed venous oxygen saturation — the oxygen content of the blood that returns to the heart from the body — a marker for blood circulation. Elevated antimony also significantly correlated with a higher mean right atrial pressure — the blood pressure in the upper-right chamber of the heart — and pulmonary vascular resistance, the resistance to blood flow within the pulmonary arteries.

Based on these findings, the team hypothesized that environmental antimony exposure potentially led to right heart impairment due to calcium dysfunction and/or oxidative stress, cellular damage caused by an excess of reactive oxygen-containing molecules.

The researchers said the small sample size, along with not exploring these mechanisms were limitations of the study, and called for more studies in larger patient populations to validate and understand the implications of their findings.