Home Contact Us Search Toxic Exposure Study Trust  Foundation

Environmental Hg

Mercury Neurotoxicity Alzheimer's & Hg AD & Mercury Neurites & Hg Hg Induced AD Rep. Burton & Amalgam Hg Nephrotoxicity Heart Disease & Hg Dentist's Hg Exposure Crematoria & Hg Amalgam Hg Release Published Studies Hg Abstracts Dr. Haley On Amalgam Hg Press Releases AD Pathology & Hg ADA & Amalgam Amalgam Safe Baratz Testimony Amalgam Make Up Hg Exposure Amyloid & Metals Amalgam & TMJ Hg Free Dentists Amalgam Quotes Hg Points of View Hg Free Patents Toxic Hg Species Amalgam Lawsuits Antibiotic Resistance Amalgam Economics Amalgam vs. Composites Amalgam Debate Safety & Treatment Amalgam Protest Federal Agencies Mercury Measurement CA Dental Board Fish & Mercury Dr. Haley Responds Ban Hg Petition Dr. Vimy Responds Mercury Links Amalgam & Cavitites Amalgam & Hg Waste Hg in Medicines Rep. Watson & CDA Amalgam Waste Black Caucus Mercury Links States Fight Hg Toxic Teeth

Mercury Toxicity
Environmental Hg
Nutritional Hg Toxicity
Hg Toxicity Summary
Mercury-General
Global Pollutant
Mercury Problem
Inorganic Mercury
Methylmercury A
Dimethylmercury
Methylmercury B
Hg Properties
Mercury Review
Hg Resources
Hg Fact Sheet
 

Mercury in the Environment


Excerpts from an article entitled

MERCURY IN MASSACHUSETTS: AN EVALUATION OF SOURCES, EMISSIONS, IMPACTS AND CONTROLS

by C. Mark Smith
Massachusettes Department of Environmental Protection (MA DEP)
Office of Research and Standards
E-mail: C.Mark.Smith@state.ma.us

Last Updated August 8, 1996

Chapter 1 - Introduction

Why is Mercury a Problem?

Mercury is a metal that is commonly found in the environment in several forms, all of which are toxic. Depending on its exact chemical form and the dose received, people or wildlife exposed to mercury can suffer serious adverse health effects. Mercury in the environment is derived from both natural sources and human activities. Mercury is mobile and widely dispersed in the biosphere and persists once released. "Organic" (carbon-containing) mercury compounds, such as methyl mercury, are of particular concern because they can become concentrated in living organisms, such as fish.

Mercury is an important environmental concern in Massachusetts and across the country. Extensive fish monitoring programs in Massachusetts and other states have led to some disturbing findings regarding mercury. For many waterbodies in the Northeast, concentrations of methyl mercury in large freshwater fish were found to be above levels currently considered to be safe for regular consumption. These findings have led several states, including Massachusetts, to issue statewide health advisories warning pregnant women to avoid eating native freshwater fish. Pregnant women are of special concern because methyl mercury can cross the placenta and is particularly toxic to developing fetuses. Warnings that citizens should refrain from eating fish from many specific waterbodies have also been issued across the Northeast with 37 such advisories in MA alone.

Such advisories minimize potential health risks from mercury but also indicate a need to further reduce sources of mercury pollution. Ultimately, the only way to achieve this is to identify controllable sources of mercury and to then take steps to reduce them. MADEP is committed to this goal which can be achieved in many ways, including actions that every citizen can take.

Both State and Federal regulatory agencies have taken many recent steps to better delineate and reduce mercury risks. Several reports by the United States Environmental Protection Agency (USEPA) have assessed possible sources of mercury in the environment on a national scale. The potential adverse health effects of mercury have also been extensively considered in recent scientific publications.

These efforts, including analyses presented herein, have helped to clarify our understanding of mercury risks and sources and have pointed to many steps that can be taken to reduce mercury releases. For example, as is discussed in Chapter 3 of this report, disposal of mercury containing products such as batteries, certain types of electric light fixtures, thermostats and thermometers in municipal solid waste can lead to substantial emissions of mercury to the environment.

Chapter 2 - Mercury: Forms, Fate & Effects

This chapter provides an overview of the forms, fates, and effects of mercury in the environment. It first discusses the forms of mercury, and their chemical and physical properties. Next it describes the cycling of mercury, its transformations, and the sources of mercury on a national and worldwide level. Next, the methods available and commonly used to measure mercury are described, along with the issues that must be considered in assessing monitoring data. Finally, the effects of mercury on human and ecological health are discussed.

Mercury Forms and Fates

Background

Mercury is a naturally-occurring metal, traces of which occur in rocks of the earth's crust. Mercury has three possible "valence states", or conditions of electrical charge. The uncharged metallic or elemental mercury (Hg0), the form commonly used in thermometers, readily vaporizes from its liquid state, and is the most common form of mercury in the atmosphere. Long-range transport of mercury through the atmosphere consists primarily of mercury in the elemental form (Mitra, 1986). Limited amounts of elemental mercury may be found in soils and water. In soils and surface waters, mercury predominantly exists in the mercuric (Hg++- with a double positive electrical charge), and mercurous (Hg+- with a single positive charge) states, as ions with varying solubility. Mercuric chloride, a simple salt, is the predominant form in many surface waters (Mitra, 1986).

Mercury can form many stable complexes with organic (carbon-containing) compounds. Methyl mercury is a toxic, organic mercury compound that is fairly soluble in water. Dimethyl mercury, another organic mercury compound, is much less soluble. Inorganic mercury can be methylated by microorganisms indigenous to soils, sediments, fresh water, and salt water, to form organic mercury. Almost all of the mercury found in animal tissues is in the form of methyl mercury (WHO, 1989).

MERCURY

CHEMICAL SYMBOL: Hg
(based on its ancient name: Hydragyrum

Elemental Mercury
        Hg 0
Inorganic Mercury
        Hg +1 or Hg +2
Organic Mercury
        compounds such as:
                Methyl mercury - HgCH3+
                Dimethyl mercury - Hg(CH3)2
                 Thimerosal

Mercury undergoes two predominant types of chemical transformations: 1) oxidation-reduction, and 2) methylation-demethylation (see Figure 2-1). In oxidation, for example, mercury present in its uncharged form (Hg0) is converted to a higher valence state (e.g. Hg+1 ). Reduction is the reverse of this process occurring through the addition of electrons. In methylation, elemental mercury adds an organic "methyl group" or hydrocarbon (CH3) group, which is lost in demethylation. Both transformations can occur in either direction.

Copy of hgtransform.gif (2719 bytes)

Probably the best known properties of elemental mercury are its low viscosity and its ability to form highly mobile droplets on surfaces. Low viscosity accounts for the way mercury droplets amalgamate into one when they collide. The high mobility of mercury may be the origin of its nickname, "quicksilver". Early Greek civilization recognized this metal's properties of quickness and embodied them in the messenger god Mercury, whom they elevated to the Pantheon. The planet Mercury, with its quick 88-day year and silver-white luster, epitomizes the reverence universally held for this element by ancient civilizations.

Mercury has a high surface tension, forming spherical droplets when the liquid is released. Though the mercury molecules within the droplets are stable, the molecules on the surface of the droplet are highly unstable, and readily vaporize. The boiling point of mercury is approximately 357°C (675°F). Essentially, all elemental mercury will exist as a vapor at temperatures above this level. Its high surface tension, uniform volume of expansion make mercury ideal for use in thermometers, barometers and other measuring devices.

PHYSICAL STATES OF MERCURY
    (atomic number: 80, atomic weight: 200.6)

Elemental mercury is a silver-white, heavy, mobile, liquid metal at ambient temperatures.

Other forms of mercury such as mercuric acetate and mercuric chloride are white, heavy powders or crystal solids. (US Dept. HHS, 1989)

Mercury is a relatively poor metallic conductor of electricity, yet it is often used in electronic devices such as switches and thermostats, when a liquid conductor is required and because its weight forms a positive seal. The ability of liquid mercury to conduct heat is responsible for the use of mercury as a coolant. The strongly toxic compounds of mercury have been exploited for bactericides, fungicides and insecticides, and its brilliant hues have lead to mercury use in paints (Mitra, 1986; ATSDR, 1994). It is also an excellent preservative and disinfectant, accounting for its presence in many chemical reagents and medical applications in forms such as mercurochrome and Thimerosal.

Elemental Mercury is Insoluble
Thus, raindrops, running water and moisture are not good sinks for mercury vapor.

Mercury is Affected by Temperature
Mercury vaporizes more easily as temperature rises; at high temperatures essentially all mercury will exist as a vapor.

Environmental Fate of Mercury: Cycling & Transformation in the Environment

All substances undergo cycling and transformations in the environment, but this is particularly so for mercury. Mercury's ability to exist in several physical states and chemical forms at commonly-encountered conditions of temperature and pressure, and propensity to undergo biological transformations, means that it is subject to complex and difficult-to-predict changes in concentration and form. Environmental monitoring studies thus must consider a variety of physical changes, geochemical reactions, and biochemical interactions in an attempt to understand the specific local conditions that contribute to mercury levels found in different environmental media and living things. 

Mercury released into the environment can either stay close to its source for long periods, or be widely dispersed on a regional or even world-wide basis. Mercury concentrations in seawater, air and in human hair are higher in the northern hemisphere than the southern hemisphere (Mitra, 1986). The greater industrialization in the north is probably responsible for the higher levels; the stratospheric air circulation system leads to the re-deposition of pollutants from the mid-latitude industrial northern hemisphere in the same hemisphere.

Although the precise compositions will vary based on the locations sampled, in general, greater than 50% of the total amount of mercury in air exists in the elemental form, with a few percent attributable to particulate ore and the remaining percentage being comprised of a variety of other mercury compounds (Johnson and Braman, 1974). Atmospheric mercury concentrations have been measured in industrial, rural, residential, and aquatic areas. Levels are higher over industrial areas. Estimates of the residence times of various forms of mercury in the atmosphere vary from about five to ninety days (Airey, 1982; Mitra, 1986) to as long as three years (WHO, 1990). Atmospheric mercury concentrations over Greenland, polar regions and the open ocean exhibit little variation, indicating that anthropogenic, or human-caused, sources contribute to the higher levels found over the continental landmass areas (Mitra, 1986).

The vaporization rate of mercury approximately doubles for every 10 degrees Centigrade increase in temperature. The saturation level of mercury in air increases logarithmically with increasing temperature. Thus, seasonal, daily and latitudinal changes in ambient air levels occur (Mitra, 1986).

Evidence consisting of before-and-after measurements suggests that rain washes some mercury out of the atmosphere (Fogg and Fitzgerald, 1979). However, in industrial zones that use mercury or where mercury is a by-product of manufacturing, more mercury may be precipitated by dry fall-out than by rainfall (Dams et. al., 1970). Rain is more effective at removing particulate mercury than mercury vapor, because raindrops, running water and moisture are not good sinks, or storage media, for elemental mercury.

The presence of mercury in snow fields in Greenland indicates that snow also removes mercury from the atmosphere (Weiss et. al, 1971). Mercury enters soils by way of rain and snowfall, dry fallout from the atmosphere, the disposal of sewage sludge, improper disposal of mercuric hazardous wastes (formerly much more common than at present), landfilling of solid waste, and the agricultural use of mercury-containing pesticides.

Ionized forms of mercury are strongly adsorbed (held by surface particles) by soils and sediments and is desorbed (released) slowly (Mitra, 1986). Clay minerals adsorb mercury maximally at pH 6. Iron oxides also adsorb mercury in neutral soils. In acid soils, most mercury is adsorbed by organic matter. Microbial activity may then metabolize some part of the mercury, releasing it into the soil gas. When organic matter is not present, mercury becomes relatively more mobile in acid soils, and evaporation to the atmosphere or leaching of mercury to groundwater occurs (Mitra, 1986).

Once released to the atmosphere, mercury is distributed to the earth's surface including soils, wetlands, lakes, and oceans. It can then undergo chemical transformations including oxidation, reduction, methylation, and demethylation (see Figure 2-1). Biological processes play an important part in these transformations; depending on local conditions, bacteria may ultimately convert some of the deposited mercury to methyl mercury, which is taken up by organisms through ingestion and absorption (Press & Siever, 1978).

METHYLATION OF MERCURY

Methylation, the addition of (-CH3) may occur in water, sediments or soil. Fish accumulate methyl mercury directly from the water in which they live or from prey.   In water and sediments the amount of methylation is affected by:
    1.the amount of dissolved oxygen present;
    2.the amount of sulfur present;
    3.the pH of the water or sediment; and,
    4.the presence of particles of clay or organic material.

Where the amount of oxygen is limited, as in deeper layers of the surface water or sediments, more methyl mercury is formed. The presence of sulfur may be important because it is thought that sulfate-dependent bacteria are involved in the methylation process. Low pH is associated with an increase in methylation. (This means that methylation may occur more readily in water affected by acid rain.) If clay particles are present in the water, the mercury may attach to the particles, and may not be as available for methylation.

Methyl mercury may also be formed in soil. As in lakes, rivers, or sediments, the oxygen and sulfur levels and the pH may affect the amount of methylation that occurs. Methyl mercury formed in the soil may be transported to surface water as runoff and ultimately enter lakes, ponds or the ocean.

The concentrations of different forms of mercury found in soil, water, or air, or in living things, is the result of the amount of releases, how they have been transported, and how the mercury is transformed. Figure 2-2 displays the overall process of cycling of mercury through the environment.

Figure 2-2. Cycling and Transformation of Mercury in the Environment

Copy of hgcycling.gif (35909 bytes)

Erosion, rainfall and leaching transport mercury from land surfaces to streams, lakes and oceans. Streams that cut through mercury deposits contribute elevated amounts of mercury to the stream environment. Thermal springs and mine drainage also contain significant amounts.

While it circulates in the environment and changes its form, mercury is persistent and is not biodegradable. It tends to accumulate in sediments - in rivers, streams, lakes and the ocean. Mercury can even accumulate in sewer pipes which can lead to long-term releases of mercury to municipal wastewater that may continue even after the original source has been eliminated. Mercury can thus be hard to control, once released. Furthermore, once present in a biological system, mercury can be passed up the food chain, "bioaccumulating" (increasing its concentrations) accordingly. Larger, older individuals build it up in their tissues with increasing age and thus the total concentration of mercury in a higher predator can be substantial. Because of mercury's combined qualities of potential toxicity, environmental persistence, and potential for bioaccumulation, this metal is a particularly insidious and difficult pollutant to manage.

Sources of Mercury

There are many sources of mercury inputs to the biosphere. Natural sources are significant contributors, clearly greater than man-made inputs in some areas, especially those where high concentrations of mercury exist in surficial ores. The contribution of mercury to the biosphere associated with human activities is a matter of great debate. In part, this is because it is difficult to separate mercury that was originally derived from past human releases from new natural inputs. In any case, many scientists believe that the flux of human-derived mercury into the atmosphere is at least on par with, and probably exceeds, by up to two- to four-fold, natural sources of this metal (Terry Haines, University of Maine; USEPA, 1991; Hovart, 1993; USEPA, 1995). Reports that the typical mercury content of lakes has increased by two- to seven times since industrialization (Nriagu, 1979; Swedish, EPA, 1991), and that the deposition of mercury has increased significantly in the mid-continental United States (Swain et. al. 1992) support this contention.

Natural Sources of Mercury

Mercury is one of the natural elements that make up our solar system. It is present in the sun, solar winds and solar flares and has been detected in meteorites and moon rocks (Mitra, 1986). On the earth, naturally occurring mercury deposits are generally found as Cinnabar (HgS) and this is the most important mercury ore. The mercury content of cinnabar exceeds is 86% This vermilion-red sulfide mineral ore occurs in quantity at relatively few locations (see text box below) (Mitra, 1986). Its associations with recent volcanic rocks and hot springs suggests a deep crustal or mantle source.

CINNABAR (Mercury Ore) DEPOSITS

Important mining localities include:
Almaden, Spain; Idria, Yugoslavia; Huancavelica, southern Peru

In the United States, large deposits occur in:
New Almaden, California New Idria, California.

Minable quantities of cinnabar are found in:
Nevada; Utah; Oregon; Arkansas; Idaho; Texas

No deposits of cinnabar have been identified in Massachusetts. (Hurlbut & Klein, 1977). However certain shales and granite that are found in MA have higher than average levels of mercury.

Inorganic mercury occurs in small amounts in many rocks. Granite contains about 0.2 parts per million (ppm) mercury (Press and Siever, 1978). Other crustal rocks generally contain less than half that amount. The mercury in rocks steadily contributes small amounts of this metal to the atmosphere and natural waters by ordinary weathering processes. Volcanic sources also disperse mercury vapor into the atmosphere. Atmospheric mercury levels measured at Kilauea and Mauna Loa volcanoes in Hawaii commonly show the same order of magnitude as Icelandic volcanoes, between 10 and 25 micrograms per cubic meter (µg/m3). Normal values in air (Mitra, 1986) are about 3 nanograms per cubic meter (ng/m3).

Soils and sediments may also contain mercury. The mercury content of sedimentary rocks such as shale, which were deposited long before humans existed, signifies that at least some of the mercury in modern sediments is natural in origin. More recent sediments will also contain mercury derived from manmade sources.

Mercury leaches into surface and groundwaters from natural sources, and it is distributed into the oceans through the mid-oceanic ridges and rift systems. Most natural waters contain a few parts per billion (ppb) mercury. Freshwater concentrations have been reported as high as 0.07 ppm (Hem, 1970). Some fraction of the mercury in natural waters may be converted to an organic form, methyl mercury which is the form most harmful to higher organisms (WHO, 1989).

MEASUREMENT OF CONCENTRATIONS IN AIR

Concentrations of chemicals in air are measured in units of:

the mass of chemical (milligrams, micrograms, nanograms, or picograms) per volume of air (cubic meters).

1 milligram (mg) = 1/1,000 gram
1 microgram (µg) = 1/1,000,000 gram
1 nanogram (ng) = 1/1,000,000,000 gram
1 picogram (pg) = 1/1,000,000,000,000 gram

One cubic meter (m3) = 35.31 cubic feet.

Mercury Sources Associated with Human Activities

The unique properties of mercury have resulted in a long history of use by the enterprising human race. The mercury ore cinnabar has been found smeared on Neolithic skulls. In about 2000 BC, mercury pigment was used on a tomb which was discovered on an island in the Mediterranean (Mitra, 1986). Today, its presence in batteries and thermometers establishes a place for mercury in every household.

Many thousands of tons of mercury have been mined during the past 50 years for use in electrical equipment, chemical processing plants, chlor-alkali plants, and pesticides. Mining essentially results in an accelerated weathering process, by which much more mercury than normal is released from rocks. Much of the mercury used in manufacturing subsequently escapes into natural waters and the atmosphere.

Mercury is used in a number of consumer and commercial products. Some of these products are more commonly recognized as containing mercury than others. Mercury is found in varying amounts in batteries, fluorescent and high intensity light bulbs, thermometers, thermostats, and light switches. Mercury is also used to make chlorine and caustic soda and certain types of dental fillings. Some paints and pesticides made in the United States used to contain mercury (as a preservative and fungicide) but no longer do as a result of voluntary and required bans. Thus, citizens, hospitals, dental offices, farmers, builders, and certain types of manufacturing operations all use and eventually discard products containing mercury into the municipal solid waste stream. Following disposal the mercury in these items may ultimately be released into a landfill or the atmosphere following combustion in a waste combustor. More detailed discussions of these various sources and quantitative estimates of their total contribution of mercury to MSW can be found in Chapter 3 and Appendix F.

In addition to mercury emissions associated with disposal and incineration of municipal wastes, mercury is also released into the atmosphere by the burning of fossil fuels such as coal and oil, medical wastes, and wood. Releases also occur:
1.when products containing mercury, such as fluorescent lights, are broken;
2.from volatilization during laboratory and industrial uses;
3.during cremation of human bodies, due to mercury use in amalgam fillings; and,
4.in the purification, or roasting, of ores.

In addition to industrial activities, worldwide agriculture and mining have also contributed major amounts of mercury to soils, water and air.

Measurement of Mercury Levels in the Environment

To assess how much mercury is present in the air, water, and other environmental media samples are taken and analyzed for this metal using a variety of scientific methods. Some of these are described in more detail in Appendix C. Sampling for mercury is not always a simple matter, and it is important to understand some of the key sampling issues to appropriately interpret the available data.

One important issue is ensuring that samples are "clean" - that what is being measured is what is present in the environment, and not the result of sample contamination (i.e. traces of mercury in the sampling or analytical containers). Improvements in trace-metal-free, "clean hands" methods in sampling, handling and processing materials for mercury analysis are thought to be responsible for some of the apparent decreases in environmental concentrations reported in recent publications. Formerly, sample contamination problems interfered with the accurate measurement of the low levels of mercury generally found in environmental media. For example, the measured mercury concentration in Vandercook Lake, Wisconsin, decreased from more than 200 nanograms per liter (ng/L) in 1983, to about 50 ng/L in 1985-1986, to 0.5 ng/L in 1986 as progressively cleaner techniques for sample collection and handling were adopted (Zillioux et. al., 1993). Such analytical contamination of samples presents a major uncertainty when comparing mercury concentrations between different studies (especially older investigations) and over time. In contrast, measurements of mercury emissions from specific sources have, in general, been less impacted by this problem since the concentrations are usually higher.

Another important concern in sampling is the availability of testing methods that can measure mercury in particular forms in various media, especially in trace (low) concentrations. If an appropriate measurement technique is not available it is easy to assume that a material is not present.

Measurement of mercury in water and soils is commonly done using methods specified by USEPA, such as Standard Methods for the Evaluation of Water and Wastewater (USEPA, 1986). A now-commonly-specified method used to measure mercury in water is the cold-vapor method, which can detect mercury down to levels of one parts per billion (ppb) depending on the features of the sample "matrix" (background medium or the soil or water from which the sample is taken). This and other methods afford high sensitivity, but where the sample matrix is not conducive to a low detection limit, it may not be possible to determine with certainty if very low or trace concentrations are present.

Most monitoring studies of atmospheric mercury have focused on deposition of this metal to water bodies and soils via dry and wet deposition (see text box on next page). For example, the Maine Department of Environmental Protection, in conjunction with the University of Maine, has initiated an International Toxics Monitoring Program to study mercury deposition in snow and rain, as well as mercury in freshwater fish from northeastern lakes (Haines, 1994).

Direct monitoring for trace levels of mercury in the ambient air is not now commonly performed, nor are there generally accepted methods available for making such measurements. Such techniques are just now becoming available and are seeing limited use in research projects. The following presents a brief summary of key issues relating to ambient monitoring of atmospheric mercury concentrations. Appendix C provides a more detailed discussion of sampling procedures, analytical methods, quality control issues, siting issues for ambient monitoring efforts, and approximate costs associated with such studies.

The development of ambient air and depositional monitoring techniques for mercury is mainly being spurred by concerns over mercury inputs to water bodies and its subsequent uptake by fish. Until recently, most monitoring for metals in the ambient air has been done using modifications of the Federal Reference Method for the Determination of Lead in Suspended Particulate Matter, which is found in the Code of Federal Regulations (CFR), 40 CFR Part 50, Appendix G. This method has been routinely employed to measure lead, which is a criteria air pollutant, and can be adapted to measure other metals as well. Limitations of the method include its relative insensitivity and sampling primarily of particulate-phase mercury. The method calls for the procurement of particulate samples on glass fiber filters using a high volume sampler with subsequent acid digestion and analysis by an atomic absorption (AA) or inductively coupled argon plasma emission spectroscopy (ICAP). Although the Federal Register lists 70 ng/m3 as the lower detection limit for the standard method, enhanced analytical methods can be used for special monitoring studies and have achieved detection limits below 2 ng/m3.

Mercury commonly occurs in the environment in vapor (Hg0), particulate and organic forms. The approach noted above may underestimate total mercury somewhat as it is of limited effectiveness with respect to vapor phase metals. Although organic mercury species are considered to be very toxic, due to chemical characteristics, they are not expected to be found in detectable concentrations in the ambient air and are generally not analyzed for.

DRY DEPOSITION VS. WET DEPOSITION

Dry Deposition

Dry deposition of atmospheric chemicals refers to any physical removal process that does not involve precipitation. These physical processes include:

  1. gravitational settling-settling of the chemical due to its mass or the mass of any paticulates to which it may be adsorbed
  2. impaction-when air containing particles moves past a stationary object such as a building, some of the particles collide with the object and settle out
  3. adsorption -gaseous chemicals may be adsorbed by liquid surfaces or by solid surfaces such as vegetation or soil

Wet Deposition

Wet deposition of atmospheric chemicals refers to removal processes associated with precipitation.

  1. dissolving in rain droplets-occurs with gaseous chemicals
  2. incorporation in rain droplets or ice crystals-may occur with solids

Generally, environmental or "ambient" background levels are consistently lower than those measurable using traditionally available techniques as noted above. Information regarding mercury at these lower concentration ranges would help to delineate air source contributions and overall atmospheric deposition rates of mercury to terrestrial and aquatic environments. However, no comprehensive ambient mercury monitoring studies have been conducted by the MADEP in Massachusetts, and few such studies have been undertaken by others in the state or nationwide.

Air monitoring and deposition studies for mercury have been performed primarily in rural locations. These generally show vapor phase mercury to be in the 1 to 10 ng/m3 and particulate mercury to be 10 to 100 picograms per cubic meter (pg/m3). This indicates that, in rural areas, vapor phase mercury is likely to constitute from 95 to 99% of the total with the remainder being particulate phase mercury. A study being conducted in the Lake Champlain Basin, Vermont, has estimated an annual wet deposition of 15 micrograms per square meter (µg/m2).

Biological Effects

Human Health Effects

Mercury compounds are of concern because of their potential to act as poisons. A large amount of scientific data about mercury toxicity exists. Several excellent reviews have been published on the health effects of mercury (for example, see Clarkson et al., 1988; Goyer, 1991; ATSDR, 1992; WHO, 1976, 1989, 1990 and 1991). This section presents a brief overview of the toxicity of mercury and is not meant to be an exhaustive analysis. For additional information please refer to the reviews noted above or to Appendix D, which presents a more detailed technical summary of the effects observed after human exposures to mercury.

Depending on the chemical form and the dose received, mercury can be toxic to both humans and wildlife. In people, toxic doses of mercury can cause developmental effects in the fetus, as well as effects on the kidney and the nervous system in children and adults (Stern, 1993; WHO, 1990; ATSDR, 1994). As is discussed in more detail in the following section, wildlife such as bald eagles, kingfishers, otter and mink that feed on fish are particularly at risk because of the potential for methyl mercury to bioaccumulate in freshwater fish. Methyl mercury has a high bioconcentration factor which means that it will accumulate in living organisms such as fish.

Bioconcentration factors (BCFs) are simple ratios between the concentration of mercury in an organism and the concentration in the medium to which the organism was exposed (WHO, 1989). For methyl mercury , BCFs of from 10,000-100,000 have been reported.

In wildlife, mercury-related effects on the central nervous system and reproductive system have been reported (Heinz, 1976; Wobeser et al, 1976), effects consistent with those observed in humans.

The symptoms associated with mercury poisoning can be complex. In part, this is because mercury exists in a number of different chemical forms and the toxicity of each of these differs. Further complicating the picture is the fact that these forms can be converted from one to another in the environment and in the body. Thus, although the exact symptoms caused by mercury poisoning will depend on the precise chemical form involved, some overlap in symptoms can occur, especially at higher levels of exposure.

Mercury can be toxic when inhaled, eaten, or when placed on the skin. At low concentrations, it may seem to have no effect but signs of toxicity may develop later or become noticeable with continued exposure. Toxicity in humans is evidenced by loss of feeling or a burning sensation in arms and legs, psychological effects, loss of memory, loss of vision, loss of hearing, paralysis, congenital malformations, kidney toxicity, and death. Prenatal toxicity can result in a child with normal appearance at birth but who later exhibits a developmental delay in the ability to walk and/or talk. Because of the long latent period for observable effects, the need for treatment may be recognized too late.

The amount of mercury taken into the body largely determines whether health effects will occur following exposures. At very low exposure levels, such as those that might occur from mercury leaching from a modest number of amalgam dental fillings or from an exposure that might result from wiping up a spill from a small broken thermometer, no adverse effects are usually noted (note that vacuuming mercury can lead to more significant exposures; by breaking the mercury up into smaller droplets and increasing air flow over them, vacuuming can increase volatilization and dispersion of mercury and thus increase the potential for exposure).

At the other extreme, high level exposures to mercury can cause serious effects or even be lethal. Such exposures do not typically occur in Massachusetts or elsewhere in the US and are generally only observed in isolated poisoning incidents. Several historical examples of epidemic mercury poisonings in other parts of the world, however, provide classic examples of investigative epidemiology and toxicology and serve to highlight the reasons why regulators are concerned about mercury.

For example, in a tragic episode in Iraq in 1971-1972, over 400 people died after ingesting large amounts of organic mercury in bread that was accidentally made with grain treated with a mercury-containing fungicide (Marsh et al, 1987; Bakir et al, 1973). In a second well known disaster which occurred from 1953-1960, many people living near Minamata Bay in Japan were severely poisoned by eating fish containing methylated mercury (Takeuchi, 1975; Tamashiro et al, 1985). In this case the bay was polluted by mercury from local industries, a practice now prevented by environmental regulations. Methyl mercury accumulated in marine organisms in the bay, including fish. These same fish were a primary source of food for many people in the area. In addition to many deaths, these exposures to mercury also caused a variety of other problems including neurological and developmental deficits in children exposed in the womb.

Effects on the brain and nervous system are frequently seen with high level exposures to mercury and can be quite severe. In the 18th century, mercury was used in the manufacture of fashionable felt hats. Workers involved in this trade handled mercury-laden skins and many were severely poisoned; while handling the furs, they would inadvertently inhale large amounts of mercury. These poisoned workers exhibited severe, and sometimes bizarre, psychological and behavioral symptoms. The term "mad as a hatter" was coined as a result of these poisonings.

Fortunately, exposures to mercury in Massachusetts, and the developed world in general, are well below those associated with such acute, severe effects. None-the-less, longer-term exposures to more modest levels of mercury can present unacceptable risks to susceptible groups including infants and fetuses.

In the United States a potentially significant route of exposure to mercury is from consumption of freshwater fish, which bioaccumulate methyl mercury, caught from contaminated waterbodies (certain larger predatory saltwater species such as shark may also contain elevated levels of mercury). Depending on how many contaminated fish one consumes, mercury exposures via this pathway can present a significant risk.

In contrast, inhalation exposures to mercury are generally not of concern since ambient air concentrations are typically low, ranging from 2 to 20 ng/m3 (ATSDR, 1993). Additionally, in Massachusetts no public drinking water supplies have been identified that are contaminated with significant amounts of mercury.

It is important to note that other potentially significant exposures to mercury can occur which are not related to environmental contamination. For example, exposures can occur in the home following accidental release of mercury or its intentional dispersion, as occurs during reported ceremonial/religious uses of this metal by certain groups of Caribbean descent including, for example, practitioners of Santeria and Espiritisimo, who may sprinkle elemental mercury around a dwelling or in an automobile to ward off evil spirits or to enhance positive forces. Some groups may also use mercury as a home remedy to treat certain ailments (Connecticut Department of Public Health, Division of Environmental Epidemiology and Occupational Health, personal communication).

ORGANIC MERCURY POISONING- CASES OF CONTAMINATION OF FOOD WITH HIGH LEVELS OF METHYL MERCURY

Descriptions and analyses of symptoms are found in reports of several poisoning episodes where foods became inadvertently contaminated with high levels of methyl mercury.

In Iraq, seed grain treated with a methyl mercury pesticide was mistakenly used to make bread that was a major source of food. Methyl mercury concentrations in the bread were estimated to average approximately 9 milligrams per kilogram (mg/kg) or 9 ppm.

In Japan, fish containing high levels of methyl mercury were a major food source. In Minamata Bay, Japan, estimated concentrations of methyl mercury in marine products ranged from 5.6 ppm to 35.7 ppm.

In the United States, in Alamogordo, New Mexico, a farm family was poisoned by eating meat from a pig that had been fed grain treated with methyl mercury fungicide. Exposure in this case was likely to have been very high.

Adverse effects have been found to be persistent in survivors of all major epidemics of methyl mercury poisoning. Effects often developed long after the exposure had ceased.

In the Iraq epidemic and in the United States family exposed by eating pork, follow-up studies showed that serious effects (quadriplegia, mental defect, loss of vision, etc.) persisted for the duration of follow-up or until death. Mercury remained in the brain over this period of time as well.

In both situations, methyl mercury had been ingested for as little as 3 months (at high levels). Medical attention, including chelation therapy, had been provided to the family in the United States.

With respect to fish contamination, methyl mercury has been found at unsafe levels in freshwater fish from many lakes and ponds in the Northeast. [Endnote 1] In MA alone, fish consumption advisories have been issued by the MADPH for 37 waterbodies due to mercury and a Statewide advisory warning pregnant women of the potential dangers of eating any freshwater fish caught from MA waterbodies has been issued. Nationwide, more than thirty states currently have freshwater fish consumption advisories in place for at least some waterbodies due to elevated levels of methyl mercury.

In general, consumption of larger sized predatory fish from species such as largemouth bass will pose greater risks- because these fish are both older and at the top of the food chain they will have accumulated more methyl mercury than younger, smaller fish. It is also important to note that freshly stocked trout that are part of the Massachusetts Division of Fisheries and Wildlife fish stocking program do not contain elevated amounts of mercury. These fish are grown in hatcheries, fed fish food containing low levels of mercury and generally do not live long enough after release to bioaccumulate elevated amounts of methyl mercury.

In Massachusetts, fish monitoring and fish consumption advisories currently in place have reduced the potential for harm from this pathway. Such fish contamination may, however, still present a risk to those who are unaware of the problem, do not heed the warnings or depend on freshwater fish as regular source of food. Contamination also diminishes the overall quality of the Massachusetts environment by reducing recreational and subsistence fishing opportunities.

The health risks of mercury at low levels of exposure remain uncertain and this is an area of considerable ongoing scientific investigation and debate (ATSDR, 1994; Stern, 1993; Marsh, et al 1995a; 1995b; Weiss, 1995). Fetuses, infants and small children, however, appear to be particularly sensitive to mercury. For prenatal exposures, effects may not be apparent at birth but may only reveal themselves later in childhood as delays or deficits in language, cognitive and motor skill development. Current research suggests that potentially important neurological and behavioral effects may be caused by exposures of a fetus to methyl mercury during pregnancy (ATSDR, 1994; Stern, 1993; WHO, 1990). The MADPH has established a trigger level of 0.50 ppm for methyl mercury in fish, a level at which pregnant women are advised to avoid consuming the fish in question. [Endnote 2] For fish with mercury levels between 0.5 - 1 ppm people are warned to limit their consumption of the affected fish and at levels above 1 ppm MADPH urges that everyone avoid eating the fish.

However, it is important to re-emphasize that the precise level at which demonstrably adverse effects occur remains highly uncertain. Two recent studies of children exposed to mercury via fish consumption have yielded conflicting results regarding the hazard posed by mercury in fish. In both studies, children living on islands where fish are regularly eaten were studied. No clearly adverse effects were reported among approximately 1,500 Seychelles islander children who were studied to the age of 5.5 years (see NeuroToxicology, V16, 1995). In publications on this study, the mercury concentrations of the fish consumed were not specifically given but they are reported to have been generally below levels deemed to be of concern by the USFDA and MADPH (presented at the Boston Risk Assessment Group (BRAG) seminar on May 8, 1996 by Dr. Philip Davidson one of the lead authors of the Seychelles Island mercury study). In any case, although reassuring in that clearly adverse effects were not seen, the reported results of this study must be interpreted cautiously. First of all, new analyses of the data suggest potentially deleterious effects may have occurred among some children (Dr. Philip Davidson, BRAG seminar, 1996). Secondly, the study has yet to be completed; additional assessments of the children, including tests that are more sensitive indicators of neurological effects, remain to be analyzed and/or completed. Further complicating this issue is a second study soon to be published, which has been reported to have detected significant effects in 1,000 children exposed to mercury and, potentially, other contaminants in the Faroe Islands. MADEP as well as other State and Federal regulatory agencies will continue to keep abreast of these studies to determine whether any changes to current health guidelines or exposure standards are warranted.

Ecological Effects of Mercury

Many more studies have been published on the effects of mercury on human health than on its effects on ecosystems. Ecosystems encompass the functional relationships between organisms and their physical environment. They include energy flow through food chains, and pathways through which chemical elements essential to life move through a complex network (Ehrlich & Ehrlich, 1970). Groups of living organisms interact within an ecosystem, giving it a certain amount of resilience to stress. If, for example, mercury is present in an ecosystem at high enough levels to cause the local extinction of eagles that live on fish, another predator species may assume the eagles' place on the food chain. The ecosystem persists, but the populations within it are less diverse, and possibly less specialized. Contaminants with a global distribution like mercury may cause impacts over a widespread geographic area.

The study of ecosystem effects of mercury typically has been reduced to studying its effects on individual species. Published studies generally fall into two categories: laboratory investigations and field studies. Laboratory studies tend to focus on individual species and show that organisms can absorb mercury compounds from their food as well as directly from the water, soil or sediments in which they live. Aquatic invertebrates bioconcentrate mercury at a much higher rate than fish, and plants have variable rates of bioconcentration depending on the species.

Effects of mercury on organisms in the laboratory do not directly correspond to field effects. Natural conditions introduce many variables that confound results. For instance, sediments can partition mercury from the water, lessening exposure to organisms in the water column. Changing temperatures and pH levels affect bioconcentration as well. The spectrum of other chemicals that occur in nature affect mercury interactions with sediments, water and organisms (WHO, 1989). In spite of these limitations,
such studies do, however, provide insight into the types of effects mercury may cause in wildlife and their potential magnitude.

Mercury is accumulated by aquatic organisms of all types and, in its methylated form, is the most common contaminant in freshwater fish (ATSDR, 1994; USEPA, 1992). Fish kills have occurred in cases of severe mercury contamination, such as occurred in Minamata Bay in Japan. Freshwater microorganisms can also be very sensitive to mercury contamination.

Field studies indicate that tissue concentrations of mercury in marine and freshwater fish increase with size. Monitoring of winter flounder, lobster and bivalves from coastal Massachusetts shows that mercury levels in these marine species are lower than concentrations in freshwater fish (Schwartz, et. al. 1995). Marine predators, particularly those that grow to large sizes, such as sharks, have been found to exhibit high mercury levels. Marine species that do not grow to large sizes and have short lives (e.g. many flounder) are generally lower in mercury than predatory freshwater species.

The long-term ecological effects of elevated mercury in fish are not presently known. In theory, the effects could be critical to the survival of species whose diet consists mainly of other fish.

Fish-eating birds have higher concentrations of mercury than other birds. Studies of mercury in feathers from Maine eagles, conducted by the United States Fish and Wildlife Service (USFWS) show that coastal eagles have a lower body burden of mercury than eagles that live inland and feed on freshwater fish. In areas where methyl mercury fungicides are used, seed-eating birds and small mammals and their predators can have high mercury concentrations (WHO, 1989).

Environmental Monitoring of Biological Effects

Extensive studies of mercury in the aquatic environment are underway at colleges and universities throughout the world. In the United States, a large number of studies are also supported by private industries and conducted by environmental consultants. State and federal environmental agencies support and conduct environmental monitoring studies. Many large ecosystems are presently being studied. For example, the Great Waters Study represents a concerted effort led by USEPA to assess the quality of large water bodies in the United States; mercury is one of several chemicals being considered. The International Toxics Monitoring Program investigates mercury in waterbodies in eastern Canada and New England. The Everglades, the Great Lakes, Lake Champlain, the Chesapeake Bay, large areas in Alaska, the Rocky Mountains and the Canadian Shield are additional examples of places where ecosystem-scale mercury monitoring projects have been initiated. Government agencies on the federal and state levels, scientists, and students from colleges and universities often join forces to perform these studies.

Tissue concentrations of mercury in fish and invertebrates are extensively available in the literature. Associated sediment and water quality data are also often available. Assessment of trophic pathways by means of radioisotope tagging is a recent trend in monitoring strategies. Aquatic studies are well-developed due in part to human exploitation of fish as a food supply. The National Study of Chemical Residues in Fish, published by USEPA's Office of Science and Technology, reports mercury detection in fish tissue at 92% of the 388 test locations. Measured concentrations ranged up to 1.77 parts per million, with 2% of the sites greater than 1 part per million. Most of the higher concentrations were in the Northeast (USEPA, 1992). Results of fish monitoring studies in Massachusetts will be discussed in detail in Chapter 4.

Terrestrial studies of mercury in the environment include studies of birds, mammals, invertebrates, soil microorganisms, plants, air and soils. A multitude of terrestrial investigations have been conducted on mercury in birds. Tissue mercury concentrations, often organ-specific, are widely available. Feathers are often used to measure mercury levels, thereby sparing the bird; evidence shows that significant adverse effects may occur at levels as low as 13 parts per million (WHO, 1976).

Studies of mercury levels in Maine eagles have been conducted by the US Fish and Wildlife Service. Data from these studies (Linda Welch, US Fish and Wildlife Service, personal communication) indicate that inland eagles have high levels of mercury in their feathers (an average of 20 parts per million, and as high as 37 parts per million in six to eight week-old fledgling eagles). The 'background" level in feathers is estimated to range from 2 to 3 parts per million. Mercury in eggs was greater than 0.5 parts per million in some cases. More than 0.5 parts per million of mercury in eggs is considered sufficient to prevent hatching. Freshwater fish make up 75% of the diet of inland eagles. Coastal eagles show much lower levels of mercury in feathers and eggs, suggesting that their prey along the coast of Maine contain lower concentrations of methyl mercury.

Testing Massachusetts eagles for mercury is underway in conjunction with the highly successful program to reestablish these raptors in the Quabbin Reservoir area, conducted by the Massachusetts Division of Fisheries and Wildlife. No effects of mercury have been observed, but mercury sampling is not far enough along to offer insights into possible effects on the health and fitness of eagle populations (Bill Davis, MA Division of Fisheries and Wildlife, personal communication). The population of eagles in Massachusetts is young, so perhaps the birds have not lived long enough to bioaccumulate significant levels of mercury.

One of the leading causes of death in eagles is collisions with buildings, cars, power lines, and the like. It has been proposed that an excess of mercury, which can lead to neurological impairment, may have contributed to an observed increase in eagle collisions in recent years, although other factors such as an increase in the absolute numbers of eagles in more highly developed regions of the country are also likely to be involved (Kenneth Carr, US Fish and Wildlife Service, personal communication).

Small mammal studies in the laboratory and in field situations demonstrate that mammals are particularly vulnerable to mercury, probably due to its neurotoxic effects and the high trophic position of mammals in the food chain. Mink show sublethal effects on a diet containing 5 to 10 ppm mercury, including loss of balance and coordination, anorexia, and weight loss (Wren et. al., 1987). Some of the test animals died. Small mammals sampled from fields sown with mercury-treated grain also died. Mercury poisoning was suspected as the possible cause of death of at least one Florida panther, and environmental mercury may have contributed to the severe population decline experienced by this endangered wild cat (Roelke, 1990).

Plants have also been studied for mercury accumulation. Sensitivities were species-specific, but in general, plants accumulate mercury as readily as other organisms. Aquatic plants are more efficient accumulators than terrestrial plants (John, 1972; WHO, 1989).

Terrestrial invertebrates also concentrate mercury. This observation has led to the suggestion that earthworms be used as a means to bioremediate soils contaminated with mercury (WHO, 1989).

Assessing the amount of the risk to human and ecological health from exposure to mercury, especially where organisms such as large fish and other species high on the food chain concentrate mercury, is central to determining the needed level of control of mercury emissions. The standards presently in place, how these standards are established, and the use of risk assessment in evaluating mercury hazards will be discussed in Chapter 5. To provide a picture of what is known about mercury releases in
MA, this report next assess State-wide mercury sources (Chapter 3). Chapter 4 then summarizes the results of monitoring studies in Massachusetts.

Endnotes:

1.    In these situations the water itself does not contain harmful amounts of methyl mercury; swimming, bathing and drinking these waters is thus generally safe.

2.    At this level, consumption of 4.6 ounces of fish a day would lead to a maternal mercury exposure of about 65 ug/day, a level approximately equal to that associated with a significant risk of adverse effects among those exposed in utero during the Iraq epidemic.

APPENDIX D -Mercury Toxicity: Technical Overview

Introduction

Several review articles have been published on health effects of mercury (for example, see Clarkson et al., 1988; Goyer, 1991; ATSDR, 1992; WHO, 1976, 1989, 1990 and 1991). The following section is not meant to be a duplication of these extensive technical reviews; rather, it is a brief summary of the effects observed after human exposures to mercury in its three most prevalent forms:

  • metallic mercury
  • inorganic mercury
  • organic (containing carbon) mercury compounds.

The mode of entry of these forms of mercury into the body, their distribution within the body, and the conversion of one form to another by metabolic processes in the body all influence the type and extent of toxicity observed. These factors are discussed below.

Fate of Mercury after Contact

The toxicity of a chemical is determined by the dose or amount taken into the body. The specific effects further depend on the amount or concentration that reaches specific organs, such as the brain or kidneys, that are sensitive to poisoning by the chemical. Factors that affect the amount of mercury reaching an organ are the rate at which it enters the bloodstream (its absorption efficiency) through the skin, the lungs or the gastrointestinal system; the rate at which it is distributed to the different body organs; and changes in its chemical structure that may occur in the different organs due to metabolism.

Mercury can exist in several different forms: metallic mercury, the type found in many thermometers, has no electrical charge (it is neutral); inorganic mercury is positively charged at a level of either +1 or +2; organic mercury is a complex of mercury with carbon containing compounds. Both the charge and chemical form of mercury affect how it is absorbed and transported in the body. Uncharged mercury can move into cells readily; mercury that has a charge is largely prevented from passing across barrier membranes such as the blood brain barrier and the placenta, unless it is carried through as part of another molecule. Organic mercury compounds can accumulate in living organisms such as fish.

The distribution and toxicity of mercury in the body is complex since any one of the three chemical forms can be changed to all of the others.

Metallic mercury (Hg0) can be changed to positively charged inorganic forms (Hg+1 ands Hg+2 ) as a result of a chemical process known as oxidation.

Inorganic forms of mercury can be changed to metallic mercury by a process called reduction or can be combined with a carbon atom (as the carbon in a methyl group -CH3) to form organic mercury compounds.

Copy of hgtransform.gif (2719 bytes)

Organic mercury compounds can themselves be metabolized so that the carbon is removed from the mercury.

In the body, conversion to the charged, inorganic form predominates but other transformations can occur.

Each chemical form of mercury produces a specific set of toxic symptoms. Complex patterns of effects may be observed, however, due to conversions of the initial form into the others in the body. For example, inorganic mercury (positively charged form) is highly toxic to the kidney. Since it is charged it does not readily pass through the blood brain barrier and thus is less toxic to the brain. Inorganic mercury is itself not readily transformed into the uncharged forms in the body. In contrast, metallic and organic mercury can more readily cause brain damage since they can pass through the protective blood-brain barrier. At high exposure levels the favored conversion of these forms of mercury to the inorganic form cannot sufficiently minimize the toxic accumulation of mercury in the brain. These compounds can also cause kidney toxicity in part because they are readily
transformed to inorganic mercury in the body. Thus, exposure to all three forms of mercury can result in kidney toxicity while brain toxicity is not commonly seen following exposures to inorganic mercury.

Tables 1 and 2 summarize the absorption, distribution, and metabolism of these three forms of mercury; a brief discussion follows.

Table 1. Extent of absorption of mercury after contact by different routes

  Extent of Absorption by Route of Contact
Form of Mercury Ingestion Dermal Contact Inhalation
Metallic (e.g. the form in thermometers) Very low for liquid form Moderate for vaporized form High for vaporized form
Inorganic (e.g. sometimes used in health and beauty products) Low to moderate (higher in infants and children) Low to moderate Low to moderate
Organic (e.g. methyl Hg; the predominant form found in fish) High Low to moderate High

Table 2. Fate of mercury in the body

Form of Mercury Mercury Retained in: Transformed to other forms: Whole body half-life (months) Excreted primarily in:
Metallic Kidney (most) Brain
Fetus
Liver
Inorganic (generally favored) 1 to 2 Feces (most)
Breath
Urine
Inorganic
Kidney (most)
Liver
(Brain if high intake results in large amounts being transformed)
Metallic and Organic  (generally less
favored)
1.5 to 2 Urine (most)
Feces
Hair
Milk
Organic (methyl compounds) Kidney (most)
Brain
Fetus
Liver
Muscle
Inorganic  (generally favored) 2 or 4 Feces (most)
Urine
Hair
Milk

Metallic mercury

Exposure to metallic mercury is primarily to vaporized mercury in industrial settings with some exposure to vaporized dental amalgam and to liquid mercury from spillage in the home. Spillage at home may occur if a mercury containing thermometer or thermostat is broken; the silvery metallic mercury will evaporate. As a vapor, it is well-absorbed into the blood and highly toxic when either inhaled or in contact with skin.

In the blood, metallic mercury may remain in plasma where it can be transported to organs such as the brain. It may also enter red blood cells, where it is readily transformed to the inorganic form. Inorganic mercury can either return to the blood plasma and combine with carrier proteins there or remain in the red blood cell.

Inorganic mercury does not readily enter or pass out of the brain nor do appreciable amounts pass between a pregnant woman's blood and blood of the fetus. Thus, metallic mercury that is transformed to inorganic mercury in either the brain or the fetus accumulates there. Mercury may also accumulate in the kidney as a result of its binding to sensitive tissue sites.

Other chemicals in the body can alter the rate of transformation from metallic mercury to inorganic mercury and the distribution to different body organs. Ethanol inhibits the conversion and seems to be protective against the accumulation of inorganic mercury in the brain. Results of studies on exposed human populations which use alcohol cannot be used to predict tolerable exposure levels for populations which have little or no alcohol intake (such as young children).

After absorption, the vaporized metallic mercury is excreted in the breath with trace amounts going to urine and feces. Once transformed to inorganic mercury, excretion is through urine and feces. After it is absorbed into the body the amount of metallic mercury present is reduced by half every 1-2 months (half-life). Larger amounts of mercury in the body (body burdens) take longer to be removed than smaller amounts. Different organs release accumulated mercury at different rates; brain and kidney have been found to retain mercury for a lifetime.

Inorganic mercury

Inorganic mercury can occur at two charge levels: mercuric (Hg+2) and mercurous (Hg+1). Both are toxic to humans, but effects of the doubly charged form tend to be more severe.

Absorption after ingestion is appreciable for both forms; ingestion and entry through the skin are the main ways inorganic mercury enters the body. Accidental poisoning from ingestion and skin application has been reported as a result of long-term use of mercurous compounds sometimes found in health and beauty preparations including some laxatives, skin-lightening creams, and baby teething powders.

Once absorbed into the bloodstream, inorganic mercury combines with proteins in the plasma or enters the red blood cells. It does not readily pass into the brain or fetus but may enter into other body organs. The liver is a major site of metabolism for mercury, and all mercury absorbed from the stomach and intestine is carried in blood directly to the liver. Inorganic mercury is transformed at a relatively low rate to both metallic and organic forms, allowing for the possibility of toxic effects from these forms following high level exposures to inorganic mercury. Some of the inorganic mercury may also be combined with other chemicals in liver bile; it is then carried in bile to the intestine and excreted in feces. If it leaves the liver in the bloodstream, it can then go to other organs, including the kidney. In the kidney, much of the plasma mercury is quickly absorbed into the kidney and excreted in urine. However, some may bind to cells in the kidney, persisting there for even a lifetime. Mercury in blood may also be transferred to breast milk or deposited in hair.

The concentration of inorganic mercury in the kidney is directly related to the amount taken in. The concentration of mercury in urine is usually measured to estimate the extent of a recent exposure.

While as much as 90% of ingested inorganic mercury can be unabsorbed and thus excreted within a few days of exposure, the half-life of the portion that is absorbed is approximately 2 months.

Organic mercury

Organic forms of mercury used as pesticides have been previous sources of widespread exposure of both humans and wildlife. Presently, human exposure is primarily due to eating foods containing methyl mercury, such as fish and shellfish. Human consumption of fish eating predators (some bird species, raccoons, and aquatic mammals such as seals and whales) results in a higher exposure rate since mercury is concentrated in their tissue after they eat contaminated fish and shellfish.

Methyl mercury in food is almost completely absorbed into blood. Once absorbed, most methyl mercury is transferred to the red blood cells; the rest is bound by carrier molecules in the plasma. This distribution is relatively stable so the concentration in blood is a useful indicator of the extent of a recent or ongoing exposure.

Because of the retention in red blood cells, methyl mercury in blood is slowly transferred to other organs; this transfer continues even after ingestion of contaminated food ends. Mercury absorbed into the bloodstream from the stomach and intestine goes to the liver, where it may be metabolized to inorganic mercury (and subsequently excreted as described above); combined with bile chemicals directly and excreted; or, combined with bile chemicals and reabsorbed from the intestine. This recirculation between intestine and liver continues until the organic mercury is excreted or released from the liver into the bloodstream.

Methyl mercury in the bloodstream can enter the brain and cross the placenta. Once in these and other organs, methyl mercury can be metabolized to other inorganic forms that become concentrated in the brain or fetus. Thus, even when blood mercury levels are decreasing, concentrations in the brain and fetus may still be high or even be increasing. Methyl mercury also persists in muscle tissue; because of this, ingestion of animals which have taken in methyl mercury can result in methyl mercury poisoning.

Methyl mercury is also transferred from blood to milk and hair. The concentration of mercury in milk is lower than in the mother's plasma, and most of the mercury in milk is in the inorganic form. In contrast, mercury is concentrated in hair, the ratio of hair methyl mercury to blood methyl mercury ranging from 200 to 1 to 300 to 1. The hair concentration can be used as an indicator of previous mercury exposures, for example during pregnancy, even if there were no obvious signs of exposure at the time of occurrence.

For most people, a period of approximately two months is required to clear half of an absorbed quantity of methyl mercury from the body. However, this may require about 4 months in some people, possibly because of genetic differences. This prolonged retention could put these people and their fetuses at greater risk of toxic effects.

Treatment of mercury poisoning by modifying its fate in the body

The chemical form, extent of exposure and entry into the body, the rate of change from one form to another, and the rate of removal from the body all affect the type and severity of symptoms seen after mercury poisoning. In general, medical treatment immediately after exposure involves the removal of mercury from blood by the administration of substances which will bind mercury and carry it out of the body. This form of treatment is know as chelation therapy. If treatment is delayed until mercury is concentrated or trapped in sensitive organs (e.g., the brain and the fetus), attempts to remove it will not be successful.

This type of treatment may not be protective in those who are exposed to high concentrations of mercury since it could cause release of mercury from less sensitive organs to blood; once in blood, there is a risk of mercury being transported to more sensitive tissues such as the brain.

Other therapeutic approaches utilize substances that bind mercury in the intestine so that it does not enter (or re-enter) the blood. This may be useful in speeding the removal of methyl mercury which is cycling between the liver and the intestine. Mercury in the brain is not appreciably removed by either approach.

Toxic Effects

Mercury can be toxic when inhaled, eaten, or when placed on the skin. At low concentrations, it may seem to have no effect but signs of toxicity may develop later or become noticeable with continued exposure. Toxicity in humans is evidenced by loss of feeling or a burning sensation in arms and legs, psychological effects, loss of memory, loss of vision, loss of hearing, paralysis, congenital malformations, kidney toxicity, and death. Prenatal toxicity can result in a child with normal appearance at birth but who later exhibits a developmental delay in the ability to walk and/or talk. Because of the long latent period for observable effects, the need for treatment may be recognized too late.

With respect to the potential for mercury compounds to cause cancer considerable uncertainty exists. In spite of the large numbers of people exposed to mercury epidemiological studies addressing the carcinogenicity of mercury are relatively few and are limited in their ability to detect an effect due the small numbers of people actually studied in any one investigation; possible exposures to other carcinogens and poor mercury exposure information also limit the confidence in these studies. Overall these human studies have not demonstrated a clear association between mercury and cancer. Additional research in this area is clearly needed. In addition to a sparse data base on humans, relatively few cancer studies have been performed under standard laboratory procedures. Those studies which have been completed suggest that exposure to inorganic forms of mercury might increase kidney, forestomach, thyroid, and lymphoid tissue tumors in some rodents. Animal studies also suggest that organic mercury compounds may cause kidney tumors at high levels of exposure where significant kidney toxicity occurs.

At this time the USEPA has proposed to classify methyl mercury and inorganic mercury as EPA Group C compounds (possible human carcinogens). Metallic mercury was deemed to be not classifiable due to insufficient data (EPA Group D). These classifications are currently under review.

Limited evidence suggests that mercury may decrease the body's defenses against cancer cells and infectious agents by depressing the immune system. Other studies have demonstrated the ability of mercury to cause chromosomal effects, an outcome that is frequently associated with transformation of normal cells to cancer cells. Further work on this aspect of mercury toxicity is needed.

When exposure is limited to one form of mercury, a characteristic set of toxic effects usually appears. However, as each chemical form can be metabolized to the others, a subset of clinical signs related to other forms can appear if high enough concentrations in the body are reached.

Table 3 lists the body organs and functions most affected by either the inhalation, ingestion, or dermal contact routes of exposure. These effects have been noted in both humans and animals except as indicated. Areas of the Table for which there are inadequate data to form a conclusion are left blank.

Metallic mercury

Metallic mercury toxicity is most usually a result of exposure to the vaporized form. A brief exposure to a high concentration in air results in toxicity to the lung--chest pain, bronchitis, pneumonitis. If the air concentration is lower, there may be no early signs of toxic effects because the vaporized mercury is cleared from the lungs to the blood or by exhaling. Poisoning from inhaled metallic mercury can also occur after a chronic low level exposure. Three cardinal signs of this type of exposure are
excitability (erethism), tremors, and gingivitis.

Excitability and tremors are results of the deposition of mercury in the nervous system. There is a rapid transfer of the vaporized form from blood to the brain; transformation of metallic mercury to the inorganic form in the brain results in accumulation. Both forms may be toxic while in the brain. Unsteadiness and tremor when trying to move or to hold objects (intention tremor) and various manifestations of excitability can develop after a long latent period.

Table 3. Organs and functions affected after exposure to various forms of mercury

Toxic effects Vaporized Metallic Mercury Inorganic Mercury Organic Mercury (Methylated)
Prenatal exposure effects in nervous system Yes (limited data from animals) Yes (animals) Yes
Postnatal exposure effects:
Nervous system Yes Yes Yes
Kidney Yes Yes Yes
Cardiovascular system Yes Yes (animals) Yes (animals)
Gastrointestinal system Yes Yes Yes
Lungs Yes    
Muscle Yes   Yes
Liver Yes    
Blood cell count Yes    
Skin and eyes Yes Yes Yes
Fertility Yes Yes Yes
Immune system Yes Yes (animals) Yes (animals)
Genetic Yes Yes Yes
Pancreas     Yes (extensive data from Japan populations)
Thyroid Yes (limited data)
   
Cancer   Yes (limited data from animals) Yes (limited data from animals)

The unsteadiness is seen most dramatically when the patient is asked in the clinic to hold both arms out to the side for three minutes. The patient is unable to do so, and will begin to flap the arms to relieve the stress (seagull sign). The psychological signs include insomnia, loss of appetite, shyness, emotional instability, and memory loss. Some reversal of these effects may occur upon removal from contact with mercury. With continued exposure, more severe tremor and muscle spasms as well as death may result.

Literature reports of incidents of mercury vapor toxicity include another type seen mainly in children--acrodynia (also known as Swift's disease or pink disease). In this disease, which occurs infrequently even among children exposed there is weight loss, loss of appetite, irritability, muscle weakness, learning disorders, and redness (hence "pink") and peeling of skin on fingers and toes. Children have most frequently shown these symptoms when calomel (a substance containing inorganic mercury) was used as a soothing agent on their teething rings. The same symptoms have been seen in children exposed to mercury vapor from contaminated floors or carpeting. Since the symptoms from inhaled mercury were accompanied by high urinary excretion rates and were the same symptoms as seen after calomel exposure, it may be that they were related to the transformation of metallic mercury to the inorganic form. It is thought that these signs may be the result of an autoimmune reaction against tissue containing mercury.

Studies of workers exposed to mercury have found that tremors and an abnormal walking gait occurred after chronic (1-5 years) exposure to 0.076 mg vaporized mercury per cubic meter of air. Mild tremors occurred at 0.026 mg/cu.m. Immune deficiency occurred in those exposed to as little as 0.106 mg/cu.m. (effects summarized by ATSDR). These numbers indicate that the toxic effects of inhaled mercury can occur at low concentrations.

A current epidemic of metallic mercury poisoning is going on now in the Amazon Rain Forest (described in Branches et al., 1993) among native people employed as gold miners. In Brazil alone, over a million miners are directly exposed to mercury vapors in the gold extraction process. Many others are exposed in the refinement and working of gold contaminated with mercury. Both sets of workers display signs of metallic mercury toxicity and excrete mercury in urine, but the gold shop workers have higher blood levels. Medical investigators studying these workers suggest that they may suffer increased levels of exposure resulting from vaporization of mercury as the contaminated gold is heated indoors.

The exposed miners and gold workers studied to date have all been adult men. No instances of exposed pregnant women have been described. In one case an individual studied, who did not work with gold at all, was found to have had a high blood mercury level. It was subsequently discovered that he lived above a gold shop and was almost certainly poisoned by mercury vapors from that source. Since these residents are also part of the exposed population and could include pregnant women, future investigations may extend to these families.

Inorganic mercury

Inorganic mercury toxicity can result from ingestion or direct skin contact with inorganic mercury or it can occur as a result of transformation of metallic mercury to inorganic mercury in the body. Poisoning has also resulted in the past when mercury containing calomel was used on teething rings; when mercury soaps and creams were applied as skin lighteners; or when laxatives containing inorganic mercury were taken chronically. Somewhat different signs of toxicity result depending on whether the mercury is in the mercuric (+2) or mercurous (+1) form.

Taken in a high dose (over 10 percent in water), mercuric chloride produces severe abdominal cramps, bloody diarrhea, and suppression of urine. Death of important tubule cells in the kidney also occurs after exposure to this form of mercury. Loss of these cells results in kidney malfunction including release of essential plasma proteins into urine (albuminuria) and excessive retention of water in the body tissues (edema). Death can result from shock and kidney failure within 24 hours, but if the patient is otherwise stabilized and placed on dialysis, the kidney may eventually repair itself using the surviving cells.

Ingestion of lower concentrations of mercuric chloride in water or food can result in an autoimmune reaction to kidney cells altered by exposure to mercury. The first signs are an inflammation of the glomerulus (the location where plasma fluids are filtered to the urinary tract); the body then further reacts immunologically to the degraded cells, causing further damage.

Mercurous compounds are less toxic than mercuric compounds. Calomel (mercurous chloride) was used in medicine; placed on gums of teething children to reduce pain; and was used as a skin lotion. Adverse responses to this form of mercury is thought to result from an immune reaction in the skin. Symptoms include a reddish skin and rash (leading to the common name of "pink disease"), fever, swollen lymph nodes and spleen, and peeling hands and feet. Mercurous compounds have also been used in the treatment of syphilis, as purgatives, and as both internal and external disinfectants. Toxicity and even death, generally as a result of kidney failure, have resulted from long-term use or misuse of these substances. Current regulations on prescription drugs and consumer products have decreased this type of exposure.

Organic mercury

Poisonings by organic mercury have occurred primarily as the result of contamination of food with methyl mercury. Extensive descriptions and analyses of symptoms have been described in reports on several widespread poisoning episodes where foods became inadvertently contaminated with high levels of methyl mercury. Studies have also been made of people exposed to more modest levels of methyl mercury in food. Some of the more extensive documentation of mercury effects in people include studies on populations in the following regions:

Iraq (Bakir, et al., 1973), where grain treated with a methyl mercury pesticide was mistakenly used to make bread that was a major source of food;

Japan (Takeuchi, 1975), Canada (McKeown-Eyssen et al., 1983 reports) and New Zealand (Kjellstrom, et al. 1986, 1989) where fish containing methyl mercury was a major food source;

the Faroe Islands (Grandjean et al., 1992; Dalgard, 1994), where mercury containing fish and whale meat are important sources of food;

the Mediterranean Basin (Franchie et al., 1994) where fishermen and their families are exposed to varying amounts of mercury from fish;

the United States (Davis et al., 1994) where a farm family was seriously affected by eating meat from a pig that had been fed methyl mercury treated grain.

In all cases, the severity of symptoms was increased when the food was either more highly contaminated or eaten in larger quantities. In adults, the first signs of toxicity included abnormal sensation (tingling or numbness) in arms and legs. This effect was correlated with a cumulative intake of 25-40 mg methyl mercury and 5 ug of mercury in a gram of hair (hair to blood ratio of approximately 250 to 1). An average daily intake of 3-7 ug methyl mercury per kilogram body weight could be expected to produce such effects. Other early effects included blurred vision and a general feeling of malaise.

At higher mercury exposure levels and correspondingly higher body burdens, additional symptoms appeared. These included: loss of coordination of gait (ataxia); slurred speech (dysarthria); loss of peripheral vision; loss of hearing; coma; kidney failure; loss of memory; abnormal blood sugar; and quadriplegia. Symptoms were due to toxic effects on the brain, peripheral nerves, pancreas, immune system, and kidneys. In addition, in some people, genetic changes were observed in lymphocytes, suggesting that such changes could also occur in other tissues, including the reproductive organs.

The evidence from numerous epidemiological studies indicates that the fetus is very sensitive to mercury. The children of women exposed to methyl mercury during pregnancy may show signs of toxic effects either at birth or later in childhood. Some mothers who had a hair concentration of 6 ug of mercury per gram of hair (6 ug Hg/g hair) or higher during pregnancy had children who, compared to those not so exposed to mercury, started walking and talking later in life and who scored lower in tests designed to measure other physical and mental development. Children whose mothers had even higher maternal exposure levels (hair mercury concentrations of up to 400 ug/g), were affected with a greater frequency and suffered more severe symptoms. These included mental retardation, cerebral palsy and a high degree of irritability and sensitivity to touch.

Comparison of the doses needed for adult toxicity and fetal toxicity is difficult since the fetus preferentially accumulates methyl mercury; the ratio of mercury in fetal blood to maternal blood is about 5:1. Thus, the fetus is exposed to a greater overall concentration of methyl mercury than the mother. Additionally, there may also be a greater rate of transfer of mercury to the brain in the fetus. Pregnant women may therefor show little if any adverse effect following mercury exposure but still have an affected child.

Because methyl mercury is secreted into breast milk, nursing infants of mothers exposed to mercury only after pregnancy can also be exposed to methyl mercury. Children exposed in this way have been shown to have methyl mercury in their blood; since few children were observed in these studies, and none followed through full development to adults, it is not possible to determine the effects of this type of exposure. Available data, however, suggest that effects of exposure after birth are less severe than effects from a prenatal exposure.

Adverse effects have been found to be persistent in survivors of all major epidemics of methyl mercury poisoning. In the Iraq epidemic and in the United States family exposed by eating pork, follow-up studies showed that serious effects (quadriplegia, mental defect, loss of vision, etc.) persisted for the duration of follow-up or until death; mercury remained in the brain over this period of time as well. In both situations, methyl mercury had been ingested for as little as 3 months (at high levels); medical attention, including chelation therapy, had been provided to the family in the United States.

Because of the seriousness of the effects associated with methyl mercury poisoning, their insidious onset, and the persistence of symptoms, environmental and public health professionals have focused their efforts on preventing exposures, especially of the fetus. As early as 1976, the World Health Organization (WHO, 1976) recommended that no more than 0.3 mg total methyl mercury be ingested per week. Other agencies have recommended limits for allowable daily intakes of mercury in its various forms or have set limits for concentrations in air, water, food, and other environmental media. A recent evaluation of data on methyl mercury resulted in the suggestion that the reference dose (the daily dose likely to be without significant adverse effects) for a chronic (long-term) exposure to this organo-metal should be somewhat lower than the previous value recommended by the USEPA (Stern, 1993). This and other data on mercury intake were evaluated by USEPA which recently lowered its recommended reference dose to 0.1 ug/kg/day from its earlier value of 0.3 ug/kg/day.

It is important to note, however, that the hazard of low doses of mercury, especially attributable to fish containing methyl mercury, is a matter of considerable controversy. Two recent studies on fairly large numbers of children exposed to mercury in utero are especially relevant. Results, which have not yet been published, from a study conducted on children living in the Faroe Islands, report an association between mercury exposure and developmental effects in the children studied (Science Scope, p. 10045, Science [271], 1996). In contrast, a second study, discussed below, did not detect any clearly adverse effects among children living on the Seychelles Islands. This extensive study, although not conclusive, is reassuring with respect to consumption of fish containing low levels of mercury. However, additional analysis of data derived from further follow-up of these children remains to be completed, making it premature to draw final conclusions regarding this investigation. Because of the quality and potential significance of this study, it is more extensively discussed below.

Seychelles Island Study

Previous reports by others (e.g., Grandjean, et al., 1992; Kjellstrom et al., 1986, 1989) have suggested that children born to women who eat fish or whale meat contaminated with organic mercury during pregnancy run a risk of delayed neurological development. Other studies showed that the average daily intake of organic mercury could be estimated by analyzing the amount of mercury deposited in the growing hair shaft during the exposure period (e.g., Cox et al., 1989). Data from an epidemic of organomercury poisoning caused by ingestion of pesticide-treated grain was used to determine that a 5% risk of developmental defects was associated with maternal hair concentrations as low as 10-20 ug/g (WHO, 1990).

The results of these studies were confounded because exposure to mercury from other sources could affect the outcome. Scientists at Rochester University conducted an international search for a population that was free of exposure to mercury from industrial sources, in which women were not exposed extensively to other factors influencing rate of fetal development (such as alcohol and tobacco), which had accessible quality medical institutions, which had a high rate of schooling and tracking of the children, which was stable and amenable to the study, and which had a high rate of local fish consumption. In addition, the investigators looked for a population that had methylmercury in hair below 20 ug/g.

The Seychelles Islands was chosen as the optimal site for the study. An extensive epidemiological study on the relationship between mercury content of mother's hair and fetal health was conducted in the Seychelles Islands by an international team of scientists. The details of the design of a pilot and full study; results after 66 months of observation in the pilot study; and results after 29 months in the full study are reported in several articles of one issue of the journal NeuroToxicology (1995; Issue16(4)).

At the Seychelles Islands, fish from reefs are eaten daily as a source of protein. These fish have relatively low mercury content, many species being below 0.1 ug Hg per g fish (wet weight). However, most women in this study ate 10-14 fish meals per week a considerably higher rate than seen with most US citizens. No estimates of the average daily dose of mercury were provided in these reports. In the pilot study on 789 mother-infant pairs, the methylmercury deposited in mother's hair during pregnancy ranged from 0.59 ppm to 36.4 ppm, with a median concentration of 6.6 ppm.

International neonatal physical developmental indices were used, including birth weight and other physical measurements, Apgar scores, and gestational age to investigate potential mercury related effects. The Revised Denver Developmental Screening Test (DDST-R) was given to children between the ages of 5 and 109 weeks of age; this measures motor, perceptual, and cognitive development at an early age. Results of the DDST-R are scored as normal, questionable and abnormal. If the questionable category is grouped with the abnormal scores, a positive association between mercury levels and developmental effects is observed. If grouped with the normal scores the study is negative for mercury effect.

Two hundred and seventeen children whose mothers had a median hair mercury content of 7.1 ppm were again evaluated at 66 months using additional psychological testing procedures for that age. Standard assessment procedures (Endnote 1) on cognitive, sensory, language, and comprehension abilities were adapted to avoid cultural and language bias. Physical examinations were conducted periodically as usual during childhood and the medical records were available for inclusion in the study.

The pilot study provided suggestive evidence of an association between mercury content of hair and fetal development. A slight negative correlation was found between hair mercury and these scores; it was not statistically significant. Five children had General Cognitive Index scores less than 60; 3 had clinical deficiencies in fine motor coordination, hearing, and language similar to what was seen in other children exposed to methylmercury prenatally when the mothers ate contaminated fish (Minamata study). The authors considered the possibility that a examination of a larger population might give different results.

The main study on 740 children over 66 months is still in progress. In this group, the mothers' hair mercury ranged from 0.5 to 26.7 ppm, with a median of 5.9 ppm, during pregnancy. Developmental tests with additional endpoints were added to those previously administered in order to expand the sensitivity of the testing. (Endnote 2) Observations at 6.5, 19 and 29 months were analyzed and are discussed in the currently published reports.

There was no association between mother's hair mercury content and childhood development scores at any of the observation times to date. At 19 and 29 months, one endpoint-- activity level of the male children-- was decreased as maternal hair mercury level increased. Other factors influencing this measurement, such as parental attention, other children in the family, etc., are hard to control and the authors are cautious in assigning weight to this in the absence of other findings. A highly significant association was, however, recently reported for this endpoint among certain women in the study (Philip Davidson, Boston Risk Assessment Group seminar, May 8, 1996).

Other evidence on mercury exposure of the infants in the Seychelles comes from autopsy data. Brain tissue has been routinely preserved for mercury analysis. Although the neonatal deaths are not strictly from the study group, they represent children of the same general population. Brain tissues from autopsies on infants in Rochester were also analyzed as controls. Neither the Rochester nor the Seychelles children had displayed symptoms of neurological deficiencies before death.

Tissue from 32 Seychelles children was examined for content of mercury. The data ranged from 50 to 250 ppb, representing mainly methylmercury. Brains from 12 children from Rochester were similarly analyzed and found to contain less than 50 ppb mercury (with one unexplainable exception). Histological observations on the Seychelles tissues showed no abnormality in cerebral or cerebella cortical organization; other changes were not indicative of mercury effect since the same features were present in the Rochester control tissue. These results, although limited in extent, suggest that the islanders were in fact exposed to greater overall amounts of mercury compared to US citizens. It is not clear, however, that the metabolism and distribution of methylmercury in this population would be the same. Toxic effects may relate to the dose rate and timing of exposure rather than the total dose received.

In conclusion, the Seychelles Island study has not detected any clearly significant association between mercury and developmental effects in a large population of children exposed via consumption of fish bearing low levels of this metal. Follow-up of these children continues and the investigators will be reporting additional results in the future. The fact that the study is not yet completed combined with questions over the applicability of the study to episodic exposures to fish more heavily contaminated with mercury suggest that it is premature to draw any firm conclusions based on this work at this time.


 

For another good review on the fate of mercury released into the environment see mercury.pdf.  Unfortunately, this review does not consider the contribution of the mercury amalgam fillings on the human body burden nor does it discuss the toxic effects mercury amalgam fillings on the human body.

Back Home Up Next