Mercury: Assessing the environmental burden of disease at national and local levels

Environmental burden of disease series, No. 16

Overview

This document provides a review of the health effects of elemental, inorganic, and Methylmercury and methods for estimating the burden of disease for methylmercury. Elemental mercury can cause a variety of health effects. Methylmercury has been associated with adult neurological problems, and there is some evidence that methylmercury exposure affects the adult cardiovascular system. However, the data for these effects are insufficient for a quantitative analysis. As a result, the quantitative aspect of this report focuses on the neurodevelopmental toxicity of methylmercury.

 Cognitive deficits in infants are represented as IQ point deficits caused by prenatal exposure to methylmercury. The disease burden is assessed using the distribution of hair mercury concentrations among pregnant women or women of childbearing age as a measure of infant exposure. Although small IQ deficits may not be visible on an individual basis, they can be significant in a population with high exposure or among those affected by endemic diseases that impair neurological function. IQ deficits have the greatest population impact among children with IQ scores just above 69 points, for whom lowered IQ score would result in mild mental retardation (defined as an IQ between 50 and 69 points). The rate of mild mental retardation caused by methylmercury-related IQ loss and the resulting number of disability-adjusted life years (DALYs) lost are calculated from the exposure distribution. DALYs measure the health impact in a population as the number of healthy years of life lost based on the severity and length of the illness.

This report estimates the disease burden for several populations, including subsistence fishers, sport fishers, and indigenous communities near industrial and mining activities. The incidence rate for mild mental retardation is estimated to be as high as 17.37 per 1000 infants born among a subsistence fishing population in the Amazon, resulting in a loss of 202.8 disability-adjusted life years per 1000 infants. Due to the lack of exposure data from representative populations in the various regions throughout the world, the global burden of disease could not be estimated. Quantification of the disease burden in subpopulations for which exposure is known, however, provides an important basis for targeting populations at risk for significant health deficits.

Because elemental mercury can be transported long distances in air, regions with little or no mercury emissions may have high environmental mercury levels. Minimizing the amount of mercury emitted into the environment to reduce methylmercury concentrations in fish and seafood requires global cooperation. Furthermore, some elemental mercury is emitted as a result of natural processes (e.g. volcanoes, forest fires). Thus, reducing the consumption of seafood with high methylmercury concentrations is the most direct way to reduce the risk of methylmercury-related cognitive deficits in a highly exposed population. However, consumption recommendations must also consider the nutritional value of fish and shellfish, particularly in populations without access to alternative sources of protein.

Additionally, there is evidence that omega-3 fatty acids in fish and shellfish have a beneficial effect on neurodevelopment. The risks and benefits of fish consumption depend on the amount and species of fish consumed and must be weighed carefully for each subgroup in the population.

Editors
Poulin, Jessie, Gibb, Herman, Prüss-Üstün, Annette & World Health Organization
Number of pages
60
Reference numbers
ISBN: 9789241596572
Copyright
World Health Organization. All rights reserved