High amounts of methyl mercury in a person's blood can inhibit an enzyme that helps prevent atherosclerosis, researchers report in the journal Environmental Health Perspectives.
Many investigations have focused on the impacts of mercury contamination on aquatic habitats, but little has been done to establish baseline information on the mechanisms by which mercury is transported and transferred through terrestrial habitats. This lack of information greatly limits our understanding of the overall effects of atmospheric mercury deposition on ecosystems and associated wildlife and human health.
The most important organic mercury compound, in terms of human exposure, is methyl mercury. Methyl mercury exposure occurs primarily through the diet, with fish and fish products as the dominant source. Sources of past exposure to methyl mercury include fungicide-treated grains and meat from animals fed such grain. However, fungicides containing mercury are banned in many nations today, and this source of exposure is now negligible in these countries.
Mercury has been listed as a pollutant of concern to EPA's Great Waters Program due to its persistence in the environment, potential to bioaccumulate, and toxicity to humans and the environment.
A large number of human studies on the systemic effects of methyl mercury have been carried out. This is the result of two large scale poisoning incidents in Japan and Iraq and several epidemiologic studies investigating populations that consume large quantities of fish.
Oral exposure to methyl mercury has been observed to produce significant developmental effects in humans. Infants born to women who ingested high concentrations of methyl mercury exhibited CNS effects, such as mental retardation, ataxia, deafness, constriction of the visual field, blindness, and cerebral palsy. At lower methyl mercury concentrations, developmental delays and abnormal reflexes were noted.
Atherosclerosis is the buildup of plaque deposits along artery walls that can lead to vessel hardening and eventual blockage. This, in turn, can lead to heart attacks and other cardiac problems. The discovery helps explain how eating excessive amounts of mercury-containing seafood can increase the risk of cardiovascular disease.
Fish are generally considered a necessary part of a heart-healthy diet. However, research shows a link between eating large amounts of seafood – particularly items high in methyl mercury – and a higher risk for heart disease. Such a link has been found in populations – including certain Native American populations – that consume above average amounts of seafood.
methyl mercury is a pollutant that persists in the body and the environment. Certain fish species have high mercury levels and continue to be a large source of exposure for people. Elevated levels in the body can lead to well-known neurological and developmental problems, such as memory and attention troubles.
Less well known are its effects on the heart and circulatory system. For example, methyl mercury can alter patterns in heart rate and affect blood pressure. These effects may counteract the health benefits of a seafood diet when methyl mercury exposure is relatively high.
However, scientists don’t know exactly how methyl mercury affects cardiovascular health. A study of Inuit adults in Canada provides new evidence about the underlying process in humans, since fish and other seafood dominate the Inuit diet, and therefore, the population is highly exposed to methyl mercury.
Scientists measured and compared blood mercury concentrations and activity levels of an enzyme called paraoxonase (PON1). Lab studies show mercury hinders PON1 activity. PON1 is thought to protect against arterial disease by breaking down harmful oxidized lipid fats that, in turn, act on the low-density (LDL) and high-density (HDL) lipid components of cholesterol.
The scientists also measured blood concentrations of selenium, an essential element commonly found in seafood that is thought to protect against mercury toxicity.
As expected, blood mercury levels were linked to a decrease in PON1 enzyme activity, and thus, decreased protection against heart disease. In contrast, selenium levels were associated with increased enzyme activity.
These findings are among the first to present evidence of a process by which methyl mercury can lead to a higher risk of heart disease, and one way in which selenium may counteract this process.