MERCURY POISONING IN THE AMAZON: THE TIP OF THE ICEBERG Speaker : Dr. Jean Lebel, Senior Program Officer, Ecosystem Approaches to Human Health Program Initiative, International Development Research Centre (IDRC) E-mail : jlebel@idrc.ca

Introduction The Problem Why are Scientists concerned about Mercury? Discovering Another Source of Mercury Shedding New Light on the Health Effects of Methylmercury Pioneering Study Turning Research into Action A New Network for Mercury Research People living in the Amazon suffer from mercury poisoning as a result of eating contaminated fish. For years, mercury used in gold mining was thought to be the sole cause. Then a team of Brazilian and Canadian Researchers, funded by the International Development Research Centre (IDRC), took a fresh look at the problem. To their surprise, they found another, unanticipated source of mercury in the environment. Today, this ongoing investigation continues to shed new light on the relationship between human health and the ecosystem.

The problem

Over the past decade, an increasing number of studies have reported that fish in some rivers of the Amazon region are contaminated with mercury. Likewise, people who live along those rivers and depend on fish for a major part of their diet have relatively high levels of mercury in their hair (an indication of mercury exposure). Until recently, it was believed that the widespread mercury contamination resulted from the use of mercury to extract gold from the river's sediment and soil - a method used to this day.

Concerned about the effects of mercury on human health in the Amazon, scientists from the Federal University of Pará in Belém and the Université du Québec à Montréal (UQAM) teamed up in 1994 to explore the problem further. Their focus was Brazil's Tapajós River, where thousands of miners or garimpeiros have panned for gold in the last 30 years.

With support from the International Development Research Centre (IDRC), the team's initial research revealed the first surprise. Levels of mercury contamination were constant all along the Tapajós River, even hundreds of kilometres downstream from gold mining operations where one would expect mercury levels to be lower. Why? To find the answer to this puzzling question, IDRC provided additional funding to the team for what has become an intriguing, multi-disciplinary study.

Why are scientists concerned about mercury?

The presence of mercury in the food chain and its absorption by humans is universally recognized as a potential health hazard. Once mercury is released into rivers, lakes, and other aquatic environments, bacteria can transform the mercury into its organic form - highly toxic methylmercury. In this form it can be absorbed by the aquatic fauna, increasing in concentration (biomagnifying) as it moves up the food chain to fish and then to humans.

One of the best-known cases of methylmercury poisoning was discovered in 1956 in communities near Minamata Bay, Japan, where mercury discharged from a chemical plant accumulated in fish. Thousands of people who lived in the area and ate fish and shellfish from the bay developed symptoms of what came to be known as Minamata Disease. Symptoms of this disorder, which attacks the nervous system and brain, may include numbness of limbs and the area around the mouth, muscle weakness, an unsteady gait, tunnel vision, slurred speech, hearing loss, and abnormal behavior such as sudden fits of laughter. More aggravated symptoms include general paralysis, difficulty in swallowing, convulsions, and death. Methylmercury also cripples neural development in fetuses and passes much more readily into the brains of young children than adults.

Discovering another source of mercury

When the project began in 1994, the team's main focus was to find the source of mercury in the Tapajós River region, to understand how people in the area were being contaminated with mercury, and to examine its impact on their health.

The researchers set out for Brazil, intent on living like the people who dwell along the Tapajós River - eating fish twice a day. Within one three-week period, the concentration of methylmercury in their own hair doubled or tripled. They also began to sample levels of mercury in the water, sediment and soil at intervals along the river, starting at gold mining sites

and ending hundreds of kilometres away. They expected mercury levels to drop as distance increased from gold mining operations, but instead the concentrations were relatively constant. Moreover, there was essentially no difference in mercury exposure levels between villagers living 100 kilometres downstream and those residing 300 kilometres away from the gold-mining area. This raised suspicions that there must be another source of mercury, apart from gold mining. Mercury in the environment and water is always associated with the fine particulate matter because of the ability of metal to adsorb on them, and in a river these particles settle in the riverbed. So the team collected sediment cores all along the river and laboriously measured the levels of mercury every half centimetre. The most recent layers of sediment contained 1.5 to 3 times more mercury than layers of sediment deposited 40 years ago, even 400 kilometres downstream from the mines. Another examination of soils along the river bank revealed a higher concentration of mercury in surface soils. The team's conclusion: mercury had been released from the soil by the cutting and burning of trees along the river banks, which began 40 years ago when poor immigrants from northern Brazil began to colonize the Tapajós River basin.

"Slash and burn" agricultural practices in the region are responsible for the well publicized deforestation of 25,000 to 50,000 square kilometers of the Amazon per year (20% of the original surface has been deforested so far.) Since waterways are the major means of access to the region, deforestation is particularly apparent along their banks. Once the land is deforested, rain washes soil at the top of banks into the river. Mercury, which had naturally accumulated in these soils for up to 100,000 years, was washed into the river too. Along the Tapajós River, in some areas, up to 15 centimetres of surface soil have been lost. It is this process that may largely explain the increase in mercury in newly colonized watersheds of the Amazon.

In 1996, the team also discovered a link between the seasons and the amount of methylmercury in people living in one of the villages along the Tapajós River. It turned out that contamination was highest during the rainy season, when large carnivorous fish grew in number. This new correlation was of great interest to those who rely heavily on fish as part of their diet.

Shedding new light on the health effects of methylmercury

Although none of the people who lived along the Tapajós River displayed the severe clinical signs of Minamata disease, the team wanted to know whether the level of mercury contamination they experienced was having an impact on their health.

In the village of Brasília Legal, situated about 250 kilometres downstream from the most extensive gold-mining area of Brazil, they discovered that hair samples taken from adults contained an average mercury level of 15.9 micrograms per gram (15.9 parts per million). This amount of exposure is well below the threshold of 50 micrograms per gram considered "safe" by the World Health Organization (WHO). The WHO threshold is based on the lowest level at which scientists in previous studies have reported the first clinical signs of mercury poisoning in adults.

However, when the team conducted simple coordination and vision tests on the same people from Brasília Legal, it was clear that they had experienced a decline in their coordination, manual dexterity and certain visual functions — such as the ability to distinguish contrasting lines. In fact, the study revealed a direct relationship between declining coordination and increasing levels of methylmercury in people's hair. Eureka! Contrary to conventional wisdom, the team had discovered that mercury can damage human health even at levels well below accepted international safety standards.

Pioneering study

This study is one of the first to illustrate the harmful effects of low-level exposure, and is thus contributing to international discussions on the need to lower the WHO threshold for mercury exposure. In the meantime, no one knows whether the residents of Brasília Legal or other villages along the Tapajós will eventually develop any of the advanced neurological symptoms associated with methylmercury poisoning - including loss of peripheral vision and speech problems. The research serves as an early warning sign that more serious neurological problems could develop, but it is hoped that efforts to reduce mercury consumption in the region will reduce this likelihood. The same group of people from Brasília Legal will be tested again in the year 2000 to measure changes in mercury levels and to determine the impact of intervention projects on human exposure to mercury. The researchers may then have a better idea of whether impaired motor and visual function can improve if exposure to mercury is reduced.

Turning research into action

The Amazonian ecosystem is very complex - the foodchain, for example, is longer and more complex than any found in more northerly climes. For this reason, more research is needed to develop a complete picture of how mercury behaves in this environment. In the meantime, the team is working with community members to develop short, medium, and long-term solutions.

In the short term, the focus is on diet. Fortunately for the local people, who derive much of their protein from fish, reducing exposure to mercury does not mean giving up fish. There are more than 40 fish species in the river, each with varying amounts of mercury contamination.

So far, the team has collected and examined some 500 fish samples, taken from the same sites that local fishermen frequent. In the process they highlighted that herbivorous or plant-eating fish contain very little mercury, while predatory fish contain the most and omnivorous fish fall in between. Likewise, people who predominantly eat herbivorous fish were found to have less mercury than those who eat more predatory fish. Surprisingly, the juveniles of some species contained more mercury than the adults. The researchers also discovered seasonal variations in hair mercury levels, reflecting the different availability of fish species during the rainy and dry seasons.

Based on this new knowledge, the team has been working with community members to propose fish diets which contain a greater proportion of fish with low mercury levels. Women in the village suggested they could use a poster illustrating each species and where it falls in the range of mercury contamination.

In the medium term, scientists are also working with fishers to identify "hotspots" - areas in the river with conditions that highly favour the transformation of mercury into toxic methylmercury (methylation). A third, longer term area for intervention is to reduce the overall level of mercury in the environment. One solution being explored is reforestation and agriculture. In collaboration with local farmers, the team plans to test which type of trees are best able to reduce the leaching of natural mercury into the river. If they can find fruit trees that do the job, all the better, since they would provide another source of food.

A new network for mercury research

Building on this research, IDRC recently provided new funding for the establishment of an interdisciplinary network of researchers and a reference centre related to mercury contamination in the Amazon. The main goal is to gather existing scientific knowledge about the behaviour of mercury in the Amazon, its transmission in the food chain, and its neurotoxic and health impacts. This knowledge will then be used to develop concrete solutions to decrease mercury intake by local populations, to improve their general health conditions, and to reduce the level of methylmercury in the ecosystem. The reference center will be the first bank of standardized data on mercury in the Amazon - its sources and its impact on the food chain and human health. Eventually, this information will be made available to anyone through a web site. Human health and the environment: IDRC's multi-disciplinary approach

The investigation into the cause of mercury contamination in the Amazon is one of many projects being funded under the umbrella of IDRC's program initiative on "Ecosystem Approaches to Human Health." The goal of this initiative is to improve human health by supporting trans-disciplinary research on the structure and function of stressed ecosystems on which people depend for their lives and livelihoods. This knowledge can then be used to develop interventions and policies toward the better management of ecosystems in order to improve human health and well-being while simultaneously maintaining or improving the health of ecosystems as a whole.

Trans-disciplinary research offers a more holistic approach to understanding environmental problems and risks, and finding sustainable, cost-effective solutions. Today, the team that is exploring mercury contamination in the Amazon includes a neurotoxicologist, and specialists in ethnobotany, cytogenetics,sociology, biogeochemistry, the environment, and forestry from the Amazonian Federal University of Para (UFPa) in Belém, the UFPa outreach campus in Santarém, the Federal University of Rio de Janeiro, the University of Quebec at Montréal (UQAM), the Montréal Biodome, and the Grupo do Defencia do Amazona in Santarém. Another important element of this project is community involvement, in both the research and the development of solutions.

Copyright 1999 © International Development Research Centre, Ottawa, Canada media@idrc.ca | 10 June 1999 --------------------------------------------------------------------------------

MERCURY AND ITS MANY FORMS Topics on this page include: Elemental Mercury What are sources of exposure to elemental mercury? How toxic is elemental mercury? Can elemental mercury be dangerous? Inorganic Mercury What are the symptoms of inorganic mercury poisoning? Organic Mercury What is the most common source of organic mercury poisoning?

What are the signs and symptoms of organic mercury poisoning? How is mercury poisoning diagnosed and treated? How do I clean up a small spill of elemental mercury? How to safely and correctly clean up a small spill is more complicated Broken thermometers are the cause of numerous calls to the Poison Center. Thermometers with a silver line contain elemental mercury. Thermometers with a red or blue liquid do NOT contain mercury.

There is much misinformation about mercury, its various forms and its dangers. Three different types of mercury exist, varying in their levels of toxicity. They are elemental mercury, inorganic mercury and organic mercury.

Elemental mercuryMercury is an extremely heavy, odorless, silver colored liquid. Mercury exists as a natural element in the earth's crust. Elemental mercury is also known as metallic mercury, liquid mercury, liquid silver and quicksilver.

What are sources of exposure to elemental mercury?Sources of elemental mercury in the home include broken mercury thermometers, broken fluorescent light bulbs, dental amalgam fillings, mercury containing latex paints, extraction of gold from ore using mercury, and contaminated clothing from workers in thermometer making plants. Elemental mercury is also used as a Mexican folk medicine to treat "empacho," a chronic stomach disorder.

How toxic is elemental mercury?Of all the forms of mercury, elemental mercury is the most commonly swallowed form of mercury, usually from a broken thermometer. Fortunately, elemental mercury from a thermometer is not absorbed from the stomach and will not cause any poisoning in a healthy person.

In a healthy person, the slippery swallowed mercury will roll into the stomach, out in to the bowels and will be quickly eliminated without causing any symptoms. A person with severe inflammatory bowel disease or those with a fistula (hole or opening) in their gut may have problems with mercury if it is not all cleared out, resulting in prolonged exposure.

Handling liquid mercury for a very short period of time usually does not result in any problems. An allergic rash is possible, though. Mercury is not well absorbed across the skin so skin contact is not likely to cause mercury poisoning, especially with a brief one-time exposure. Even if a person has cuts in their skin, mercury is too heavy to be contained by a cut. Merely washing the wound well will wash the mercury out of the wound.

Can elemental mercury be dangerous?Inhalation of elemental mercury vapors is the main cause of toxicity, as mercury is well absorbed by the lungs. To develop problems by inhalation you need either a large one-time exposure or a long-term exposure. A small, one-time exposure is not likely to cause problems.

What are the symptoms?After a large, one-time inhalation exposure of mercury vapor, the lungs are the main target of mercury poisoning, although other symptoms develop as well.

Symptoms may develop within a few hours and include chills, metallic taste, mouth sores, swollen gums, nausea, vomiting, abdominal pain, diarrhea, headache, weakness, confusion, shortness of breath, cough, chest tightness, bronchitis, pneumonia and kidney damage.

How does long-term exposure differ from a short-term exposure?Long-term exposure (usually work-related) of inhaled vapors is generally more dangerous than a one-time short exposure. After long-term inhalation exposure, the nervous system is the main target of toxicity. Symptoms may occur within weeks but usually develop insidiously over a period of years.

Neurologic symptoms include tremors, headaches, short-term memory loss, incoordination, weakness, loss of appetite, altered sense of taste and smell, numbness and tingling in the hands and feet, insomnia, and excessive sweating. Psychiatric effects are also seen after long-term exposure.

Acrodynia can result from repeated exposures to mercury-containing latex paint fumes. Acrodynia is usually seen in younger children. The symptoms include chills, sweating, body rash, irritability, sleeplessness, leg cramps, swelling of the cheeks, nose, hands and feet, light-sensitivity to the eyes and peeling skin layers on the palms of the hands and soles of the feet.

Inorganic MercuryInorganic mercury compounds are known as "mercuric salts." Some of the mercuric salts include: mercuric chloride, mercuric iodide, mercuric nitrate, mercuric sulfide, yellow mercuric oxide, red mercuric oxide, ammoniated mercury, mercurous chloride and mercurous acetate.

What are sources of inorganic mercury compounds?Some folk medicines from outside the United States contain high amounts of mercury that can cause mercury poisoning. Two common mercury compounds are calomel and cinnabar.

Chinese herbal drugs with measurable amounts of mercury include: Tse Koo Choy Qing Fen Zhu-Sha Chen-Fen

Chinese herbal ball preparations containing both mercury and arsenic include: An Gong Niu Huang Wan Da Huo Luo Wan Dendrobium Moniliforme Night Sight pills Niu Huang Chiang Ya Wan Niu Huang Chiang Hsin Wan Ta Huo Lo Tan Tsai Tsao Wan

Indian and Mexican folk medications containing mercury include: Creme de Belleza-Manning Tainan Ping-tong Sin-chu

What are the symptoms of inorganic mercury poisoning?Inorganic mercuric salts are corrosive and they damage the kidneys. Following ingestion, symptoms include nausea, vomiting blood, burns and tissue death in the throat and stomach, abdominal pain, bloody diarrhea, decreased urination and kidney failure.

Long-term application of mercury-containing substances causes skin redness and staining of the skin. More severe symptoms include nerve damage resulting in weakness, numbness and tingling.

Organic Mercury

What are sources of organic mercury?Organic mercury compounds are found in a variety of products. They are used medically as fungicides and antibacterials. The most common organic mercury compounds in the home may well be mercurochrome (merbromin) and merthiolate (thimerosal), two common antiseptics. Fortunately, small ingestions by children rarely cause major problems.

What is the most common source of organic mercury poisoning?In the general population, the main source of mercury poisoning is the ingestion of mercury- contaminated food, usually fish. When lake, river or ocean water is contaminated with methyl-mercury compounds, the mercury accumulates and magnifies in the flesh of the fish. Organic mercury concentrations can be more than 1,000 times greater in the fish than in the surrounding water. People who eat fish as a main component of their diet may be at risk. If a river or lake is known to be polluted with mercury, fish eaters are warned to decrease their weekly intake of fish.

What are the signs and symptoms of organic mercury poisoning?Organic mercury compounds are very damaging. They are toxic by ingestion, inhalation, and skin and eye contact. These mercury compounds can attack all body systems. They can cause nausea, vomiting, lack of appetite, weight loss, abdominal pain, diarrhea, kidney failure, skin burns and irritation, respiratory distress, swollen gums and mouth sores, drooling, numbness and tingling in the lips, mouth, tongue, hands and feet, tremors and incoordination, vision and hearing loss, memory loss, personality changes and headache. Allergic reactions can also occur.

Methyl-mercury, usually from contaminated food, is very dangerous to pregnant women. Methyl-mercury causes profound mental retardation, cerebral palsy, seizures, spasticity, tremors, and incoordination, along with eye and hearing damage in the unborn baby as a result of the mother's exposure. Organic mercury passes into the breast milk as well.

How is mercury poisoning diagnosed and treated?Because the number of symptoms is so great and the variety of symptoms is so wide, anyone could pick out at least 2 or 3 symptoms at any given time. If you have any doubt and if you have been or are exposed to mercury compounds, see a physician and get tested. Testing is the only definite way to determine if mercury is the cause of the symptoms.

Mercury poisoning can be diagnosed by special blood and urine collection tests. If levels are high, there is treatment. Medication can be administered to help bind the mercury and increase elimination. Symptoms do not always correspond to blood mercury levels: Many patients with high levels do not have severe symptoms.

If mercury blood levels are going to be tested, it is important NOT to eat any seafood products for at least 30 hours before testing. Even a single meal of seafood can elevate mercury blood levels for as long as 20 to 30 hours after eating. Eating seafood will cause misleading high levels.

How do I clean up a small spill of elemental mercury?Many people have called the Poison Center asking how to clean up the mercury from a broken thermo-meter. There are several different ideas on how and how not to clean up the mercury beads. Experts agree on the ways NOT to clean up a spill:

Do not sweep the area with a broom. Sweeping breaks the mercury into smaller droplets, further contaminating the room and the broom.

Vacuuming vaporizes the mercury and increases the concentration of mercury in the air.

NOTE: If you are wearing gold jewelry, either remove the jewelry or wear good protective gloves. If the liquid mercury contacts the gold jewelry, the mercury bonds permanently to the gold and ruins it.

How to safely and correctly clean up a small spill is more complicatedStep One: Using a playing card, credit card or stiff piece of paper, gather up, scrape up or roll up the beads of mercury into one big bead or ball.

Then, several cleanup options are available:Option A: Using an eyedropper or other squeeze-bulb dropper, carefully suck the mercury droplets up.

Option B: Using a common penny, dip the penny into the mercury and let the mercury adhere or bond to the penny. This may require more than one penny.

Option C: Using duct (duck) tape, place the tape over the mercury ball or beads and lift the mercury off the surface.

Step Two: Place the mercury beads, mercury-coated pennies, or tape with the mercury beads into a zip-lock plastic bag. Seal the bag securely, tape it shut, wrap it in newspaper and dispose properly.

Two other, more complicated ways for cleaning up small spills require the use of granular zinc or sulfur powder. Granular zinc can be obtained from scientific supply houses and sulfur powder can be obtained at garden supply shops.

NOTE: It is important to know that using zinc granules will permanently stain carpets a dark gray that cannot be removed. Sulfur may stain carpets black, but this can often (but not always) be removed with carpet stain cleaners.

Step One: Dust on the zinc or sulfur powder and rub in well with a disposable whisk broom.

Step Two: Sweep up as much of the mixture as possible with the whisk broom.

Step Three: Vacuum up the residual matter with a vacuum cleaner and immediately discard the vacuum cleaner bag.

Step Four: If any mercury beads remain, repeat the process until none is present.

Step Five: Discard the whisk broom after use.

Regardless of the method used for cleanup, there is very little risk of danger if the area is well ventilated. A spill of a large amount of mercury that is not immediately cleaned up can present a problem as the mercury vaporizes and is breathed in by family members.

Call: 1-800-876-4766 anytime, anyplace in CaliforniaCalifornia Poison Control System

Mercury poisoning case being investigated

A woman, who has been using this product for more than 20 years, presented with signs of mercury poisoning. Subsequent investigation confirmed that the samples of ointment contained significant amounts of mercury. It is believed that the product was prescribed, for treatment of vitiligo, by a Chinese medicine practitioner ¼Ú ¥ü ¤å who is practising in Causeway Bay.

Mercury compounds mainly affect the nervous system and kidneys. Symptoms may include hand tremors, visual or hearing loss, memory deterioration, irritability, and difficulty with sleeping. Kidney damage can result in oedema, particularly in the ankles and legs. Gastrointestinal symptoms such as nausea, vomiting, and abdominal discomfort may also occur. Mercury can also pass from the mother to the foetus resulting in impaired brain development. Some neurological effects can be long-lasting, while other health effects are usually reversible.

If you have not used the ointment for more than 6 months, your body would have excreted most of the mercury. If you are concerned about your health, you may also seek medical advice from doctor.

MERCURY: A FACT SHEET FOR HEALTH

PROFESSIONALSMercury is probably best know as the silver liquid in thermometers. However, it has over 3000 industrial uses. Mercury and its compounds are widely distributed in the environment as a result of both natural and man-made activities. The utility, and the toxicity, of mercury have been known for centuries. New evidence demonstrates that even low levels of mercury exposure may be hazardous. The purpose of this document is to provide health professionals with updated information on mercury and guidance on preventing toxic exposures in health care workers and their clients.

HISTORY & REGULATIONSMercury occurs naturally in the environment as mercuric sulfide, also known as cinnabar. It is also present in some fossil fuels. Cinnabar has been refined for its mercury content since the 15th or 16th century B.C. Its health hazards have been known at least since the roman conquest of Spain. Due to the toxicity of mercury in cinnabar, criminals sentenced to work in quicksilver mines by the Romans had a life expectancy of only 3 years.

Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and cannot be broken down into less hazardous compounds. Elemental or inorganic forms can be transformed into organic (especially methylated) forms by biological systems. Not only are these methylated mercury compounds toxic, but highly bioaccumulative as well. The increase in mercury as it rises in the aquatic food chain results in relatively high levels of mercury in fish consumed by humans. Widespread poisoning of Japanese fisherman and their families occurred in Minamata, Japan in the 1950's as a result of consumption of methyl mercury contaminated fish. Today, we continue to be exposed to mercury in our diets, primarily from fish and shellfish. As a result, the U.S. Food and Drug Administration (FDA) has an action level for mercury of 1 part per million (ppm) in fish and the Michigan Department of Public Health issues fish consumption advisories to anglers when mercury levels exceed 0.5 ppm in fish tissue.

Widespread industrial production of mercury, along with lack of careful handling and disposal practices, has contributed to environmental contamination. The U.S. Environmental Protection Agency (EPA) has made efforts to regulate the continued release of mercury into the environment. EPA regulates industrial discharges to air and water, as well as regulating some aspects of mercury waste disposal. In 1976, EPA banned most pesticide uses of mercury - with the exceptions of fungicidal uses in paints and outdoor fabrics, and for control of Dutch Elm disease. In 1990, mercury use as a fungicide in interior latex paint was halted by the EPA. This action stemmed from requests by Michigan officials after a child was poisoned from over formulated mercury-containing paint used in his home. More recently, the use of mercury compounds in exterior latex paint has also been halted.

In addition to the early workers in the cinnabar mines, modern workers in industries using mercury are at risk from overexposure. The Occupational Safety and Health Administration (OSHA) has been reviewing the current occupational exposure standard of 0.1 mg/m3 (milligrams per cubic meter of air) to determine if they should reduce the 8 hour acceptable exposure limit to 0.05 mg/m3. Although no regulatory limit exists for airborne exposure to mercury outside of an occupational setting, the EPA suggests that 0.3 ug/m3 (micro-grams per cubic meter of air) of mercury is a no-effect level (or reference dose = Rfd) for chronic inhalation exposure.

USESDesirable properties such as the ability to alloy with most metals, liquidity at room temperature, ease of vaporizing and freezing, and electrical conductivity make mercury an important industrial metal. In 1973, U.S. consumption of mercury was 1900 metric tons. Primary among its over 3000 industrial uses are battery manufacturing and chlorine-alkali production. Paints and industrial instruments have also been among the major uses. Until paint manufacturers agreed to eliminate the use of mercury in interior paints, 480,000 pounds of mercury in paints and coatings were produced each year. Table 1 provides a list of mercury uses.

EXPOSURE SCENARIOSHumans come in contact with mercury through environmental, occupational or accidental exposure scenarios. An estimated 80% of utilized mercury is eventually released back into the environment. Because it is easily vaporized, air around chlorine-alkali plants, smelters, municipal incinerators, sewage treatment plants and even contaminated soils may contain increased levels of mercury. A primary route of exposure is through transport into surface waters, where mercury becomes biomagnified in fish tissues.

Workplace exposure to mercury occurs through inhalation of contaminated air, direct skin contact with liquid mercury, or oral exposure through contaminated hands, food, etc. A recent edition of the television show 60 Minutes highlighted concerns about mercury exposure in patients receiving silver dental fillings with mercury-containing amalgam. Insufficient scientific evidence exists at this time to either support or refute the claims that dental fillings may result in harmful exposure to mercury.

Accidents have resulted in several cases of mercury poisoning in Michigan in the past two years. Four members of a Lincoln Park family were killed after one member attempted to refine dental amalgam in his home while attempting to recover silver. High levels of mercury were found throughout the house, including wrapped food inside the freezer. The entire house had to be demolished and disposed of in a hazardous waste landfill.

A number of children have developed mercury poisoning after playing with small vials of mercury which they found at home or school. These children were hospitalized when symptoms became so severe that they could not longer walk. One contamination incident involved closing a school for weeks and entailed environmental investigation of residences, cars, school buses and day care centers.

METABOLISM & TOXICITYExposure to mercury can occur through inhalation, ingestion or dermal absorption. the amount of mercury absorbed by the body -and thus the degree of toxicity - is dependent upon the chemical form of mercury. For instance, ingested elemental mercury is only 0.01% absorbed, but methyl mercury is nearly 100% absorbed from the gastrointestinal tract. The biological half-life of mercury is 60 days. Thus, even though exposure is reduced, the body burden will remain for at least a few months. Elemental mercury is most hazardous when inhaled. Only about 25% of an inhaled dose is exhaled. Skin absorption of mercury vapor occurs, but at low levels (ex. 2.2% of the total dose). Dermal contact with liquid mercury can significantly increase biological levels. The primary focus of this article is elemental mercury, since that is the form of exposure to health care workers involved with mercury-containing instrument accidents.

In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury may cause acute or chronic health effects. Acute exposure (i.e., short term, high dose) is not as common today due to greater precautions and decreased handling. However, severe acute effects may include severe gastrointestinal damage, cardiovascular collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5 hours may cause headaches, salivation, metallic taste in the mouth, chills, cough, fever, tremors, abdominal cramps, diarrhea, nausea, vomiting, tightness in the chest, difficulty breathing, fatigue, or lung irritation. Symptoms may be delayed in onset for a number of hours.

Chronic effects include central nervous system effects, kidney damage and birth defects. Genetic damage is also suspected. Nervous system effects. These are the most critical effects of chronic mercury exposure from adult exposure as they are consistent and pronounced. some elemental mercury is dissolved in the blood and may be transported across the blood/brain barrier, oxidized and retained in brain tissue. Elimination from the brain is slow, resulting in nerve tissue accumulation. Symptoms of chronic mercury exposure on the nervous system include: Increased excitability, mental instability, tendency to weep, fine tremors of the hands and feet, and personality changes. The term "Mad as a Hatter" came from these symptoms which were a result of mercury exposure in workers manufacturing felt hats using a mercury-containing process.

Kidney effects: Kidney damage includes increased protein in the urine and may result in kidney failure at high dose exposure.

Birth defects: Neurologic damage from methyl mercury. The manifestations of mild exposure include delayed developmental milestones, altered muscle tone and tendon reflexes, and depressed intelligence.

Mercury exposure in children can cause a severe form of poisoning termed acrodynia. Acrodynia is evidenced by pain in the extremities, pinkness and peeling of the hands, feet and nose, irritability, sweating, rapid heartbeat and loss of mobility.

PRECAUTIONS FOR HEALTH CARE WORKERSSubstitutes for mercury-containing medical devices should be used whenever possible, e.g. thermometers and sphygmomanometers. When mercury devices must be used, special precautions should be taken. These devices should never be used on a cloth surface, such as upholstered chair or in a room with a carpeted floor. If a spill occurred in such an area, the upholstery or carpeting would need to be discarded as it could not be effectively decontaminated. Children should never be left unattended near these devices. If mercury thermometers are used, a mercury spill kit should be kept readily accessible. The kit should contain a sulfur powder to suppress volatilization and a collection device.

SPILL RESPONSEIf a spill occurs, evacuate the immediate area and ventilate as well as possible. An environmental consultant will need to be contacted for clean-up and disposal. DO NOT attempt to clean-up a mercury spill using rags or an ordinary vacuum. This will only serve to disperse the mercury and encourage volatilization. For further assistance, contact your local health department and/or the Michigan Department of Public Health, Division of Health Risk Assessment. For assistance with a large spill, call the Fire Department for assistance. For assistance with clean-up, you may look in your local phone book for environmental consultants. Table 2 contains a list of consultants known to respond to mercury spills.

DISPOSALThe best method of mercury disposal is reclamation. Attached is a list of agencies in Michigan that will take used mercury. Button batteries can be recycled at many jewelry stores and other retail outlets that sell batteries. Larger quantities of mercury will need to be disposed of by a licensed hazardous waste hauler. Contact the Michigan Department of Natural Resources, Waste Management Division for assistance with mercury disposal.

Hg Mercury

at. no. 80, at. wt. 200.61, metal, row 7, col. 2B, val. 1-2, orbits 2-8-18-32-18-2 The Problem With Mercury

{Merck Index - © 1952 by Merck & Co., Inc.}

Mercury, Quicksilver: Hg; at. wt. 200.61; at. no. 80; valence 1-2. Silver-white, heavy, mobile, liquid metal; slightly volatile at ordinary temp. d. 13.456. Solidif. at - 39° forming a tin-white, ductile, malleable mass which may be cut with a knife. b. 356.9°. When pure does not tarnish on exposure to air at ordinary temp., but when heated to near the boil. point slowly oxidizes to HgO. Forms alloys with most metals except iron and combines with sulfur at ordinary temp. Insoluble in and not attacked by H2O; soluble in dill. HNO3; not attacked by HCl or cold H2SO4; converted by heating with concentrated. H2SO4 into mercurous or mercuric sulfate, depending on the excess of the acid and time of heating. Poisonous! Mercury salts when heated with Na2CO3 yield metallic Hg and are reduced to metal by H2O2 in presence of an alkali hydroxide. Cu, Fe, Zn and many other metals ppt. metallic Hg from neutral or slightly acid solns. of mercury salts. Soluble ionized Mercuric salts give a yellow ppt. of HgO with NaOH and a red ppt. of HgI2 with alkali iodide. Mercurous salts give a black ppt. with alkali hydroxides and a white ppt. of calomel with HCl or soluble chlorides. They are slowly decomposed by sunlight. Use: In barometers, thermometers, thermostats, hydrometers, pyrometers; in mercury arc lamps producing ultraviolet rays, fluorescent lamps, mercury vapor lamps; manuf. all mercury salts, mirrors; as catalyst in oxidation of organic compounds; extracting gold and silver from ores; making amalgams, electric rectifiers, mercury fulminate, ammunition; In dental amalgams for filling teeth; in determining N by Kjeldahl method, for Millon's reagent; as cathode in electrolysis, electro analysis, exterior house paint, ceramics, and many other uses. Grades available: Reagent, N.F., technical. Toxicity: Readily absorbed via respiratory tract (elemental mercury vapor, mercury compound dusts), intact skin, and G.I. tract. Spilled and heated elemental mercury is particularly hazardous. Acute: Soluble salts have violent corrosive effects on skin and mucous membranes; severe nausea, vomiting, abdominal pain, bloody diarrhea; kidney damage; death usually within 10 days. Chronic: Inflammation of mouth and gums, swelling of salivary glands, excessive flow of saliva, loosening of teeth; kidney damage; muscle tremors, jerky gait, spasms of extremities; personality changes, discouragement, depression, irritability, nervousness, dementia, loss of motor coordination. {dementia - loss or impairment of mental powers due to organic causes.}

Mercury has been found to accumulate in vital organs and tissues, such as the liver, brain, and heart muscle. Major symptoms of mercury toxicity include Emotional Instability, tremors, gingivitis, and kidney failure. Some also believe mercury may be linked to multiple sclerosis and epileptic seizures. Further, its affect on the body's immune system is potentially devastating, possibly contributing to diseases such as leukemia and hematopoietic dycrasias. Recent studies have found that substantial amounts of mercury vapor are released from dental amalgam after chewing gum for just ten minutes. No governmental agency has established safe standards for mercury intake from dental amalgams. Some experts believe "there is No Safe Level of mercury exposure." Mercury exposure is of particular concern in the developing fetus and in children due to their low body weight. — Source —

The Problem with Mercury

Mercury Chemicals and Their UsesMeragidone Sodium

Used as diuretic Meralluride Sodium Solution (Mercuhydrin) Med. Use: Diuretic Merbak® -- see Acetomeroctol Med. Use: 1:1000 soln. as topical antiseptic Caution: May cause irritation if applied to mucous membranes or extensive wounds. Merbaphen (Novasurol) Med. Use: Has been used as a diuretic Merbromin Med. Use: Antiseptic for the skin as a 2 to 5% soln. and mucous membranes as a 1% soln. Mereaptoacetic Acid -- see Thioglycollic Acid ß- Mercaptoalanine - Cysteine 2- Mercaptobenzoic Acid -- see Thiosalicylic Acid 2- Mercapto- 4-hydroxypyrimidine -- see 2-Thiouracil Med. Use: Hyperthyroidism, thyrotoxicosis and thyroiditis. Toxicity: Leukopenia, granulocytopenia, drug fever, skin eruptions.

Mercaptomerin Sodium Med. Use: Diuretic 2- Mercapto- 4-pyrimidone -- see 2-Thiouracil Med. Use: Hyperthyroidism, thyrotoxicosis and thyroiditis. Toxicity: Leukopenia, granulocytopenia, drug fever, skin eruptions. Mercazole - Proposed as antithyroid Mercocresols (Mercresin) Med. Use: Antiseptic for minor superficial wounds and infections, preoperative preparation, mucous membranes and irrigation. Mercresin® -- see Mercocresols Med. Use: Antiseptic for minor superficial wounds and infections, preoperative preparation, mucous membranes and irrigation. Mercuhydrin® -- see Meralluride Sodium Solution Mercumatillin Sodium (Cumertilin Sodium) Mercupurin® -- see Mercurophylline Injection Mercuranine -- see Merbromin Med. Use: Antiseptic for the skin as a 2 to 5% soln. and mucous membranes as a 1% soln. Mercurial Ointment, Mild Med. Use: Has been used for pediculosis (Does not kill nits) Mercurial Ointment, Strong Med. Use: Has been used in syphilis Mercuric Acetate Use: Chiefly for mercuration of organic compounds. Mercuric Aminoacetate (Mercuris glycocollate) Mercuric |-Aminopropionate (Mercury-alanine) Mercuric Ammonium Chloride Vet. Use: As ointment in chronic eczema, parasitic skin diseases. Mercuric Arsenate Mercuric Asparaginate (Asparagin-mercury) Mercuric Atoxylate (Mercury arsanilate) Med. Use: Formerly in syphilis Mercuric Barium Bromide Mercuric Barium Iodide Use: As an aq. soln., known as Rohrbach's Soln., for separating minerals of different densities; also for microchemical detection of alkaloids. Mercuric Benzoate Mercuric Bromide Mercuric Cacodylate Mercuric Chloride (Mercury bichloride) Use: Preserving (kyanizing) wool and anatomical specimens; also embalming; disinfecting; browning and etching steel and iron; intensifier in photography; white reserve in fabric printing; tanning leather; electroplating aluminum; depolarizer for dry batteries; freeing gold from lead; magic photograms; mordant for rabbit and beaver furs; staining wood and vegetable ivory pink; Manuf. of ink for mercurography; treating seed potatoes; manuf. other mercury compounds. As an important reagent in anal. chemistry. Med. Use: Disinfectant for unabraded skin as a 1:1000 to 1:2000 soln. Toxicity: Corrosive to mucous membranes. Severe nausea, vomiting, abdominal pain, diarrhea, kidney damage, prostration. 1 g. is fatal in 50% of cases. Vet. Use: Caustic, antiseptic, general disinfectant; irritant in bony growth, spavin, etc. Caution: Undue absorption through skin or by licking may cause poisoning. DANGER! May Be Fatal If Swallowed. Do not breathe dust. Keep away from feed or food products. Wash thoroughly before eating or smoking. Mercuric Chloride Ammoniated (Ammoniated mercury) Med. Use: Has been used as a skin antiseptic particularly for impetigo contagiosa and parasitic skin diseases. Vet. Use: Skin antiseptic. Mercuric Chloride-Urea, Solution Mercuric Cuprous Iodide Use: For detecting overheating of machine bearings, etc., the red color changes to brownish-black at 60-70º and again becomes red on cooling. Mercuric Cyanide Med. Use: Antiseptic for use on skin as a 1:2000 soln. and mucous membranes as a 1:10,000 soln. Has been used in syphilis. Toxicity: Capable of causing mercury and cyanide poisoning. Mercuric Dichromate

Mercuric Diiodosalicylate Mercuric Formamide, Solution Mercuric Gallate Mercuric Glycocollate Mercuric Guaiacolsulfonate Mercuric Imidosuccinate -- see Mercuric Succinimide Med. Use: Has been used in syphilis. Mercuric Iodate Mercuic Iodide Red Use: In anal. chemistry for preparation of Nessler's Reagent. Med. Use: Formerly in syphilis Vet. Use: Blister ointment in exostoses bursal enlargement, etc. Caution: Avoid contact with hands. Mercuric Lactate Med. Use: Formerly in syphilis. Mercuric Naphtholate Mercuric Nitrate Use: Manuf. felt; mercury fulminate; destroying phylloxera. Mercuric Nitrate Ointment. Med. Use: Has been used in impetigo and parasitic skin diseases. Vet. Use: Stimulant in ulcers, ringworm, eczema, foot rot, chronic eye diseases. Caution: Undue absorption through skin or by licking may cause poisoning. Mercuric Oleate Med. Use: Has been used in parasitic skin diseases. Mercuric Oxide Red Use: In paints for ship's bottoms, diluting pigments for painting on porcelain, with graphite as depolarizer in dry batteries. In Kjeldahl nitrogen determination; and as reagent for citric acid, thiophene, glucose, aldehyde, urea, acetone. Med. Use: Has been used topically as a stimulant and antiseptic for chancres; chronic ulcers and fungus infections of the skin. Vet. Use: As Med. Use in fissured heels. Mercuric Oxide Yellow Use: Similar to that of the red oxide; in the manuf. of organic mercurials. In anal. chemistry for determining Zn or HCN; detecting acetic acid in formic acid, CO in gas mixtures. Med. Use: Antiseptic used chiefly for inflammation of the eyelids and conjunctiva as 1% (10,000 ppm) ointment.

Vet. Use: As Med. Use. In ringworm, eczema, indolent ulcers, chronic glandular enlargement. Mercuric Oxycyanide Violent poison! It explodes when touched with a flame or by percussion; hence for commerce it is made with an excess of mercuric cyanide which eliminates the danger of explosion. Use: As a 0.1% soln. (1,000 ppm) for sterilizing surgical instruments. Med. Use: 1:5000 soln. (200 ppm) as an antiseptic. Formerly in syphilis. Toxicity: Capable of causing mercury and cyanide poisoning. Mercuric Phenate Mercuric Phosphate Mercuric Potassium Cyanide Use: In manuf. of mirrors to prevent the silver coating from becoming yellow; as reagent in testing for free acids. Mercuric Potassium Iodide Med. Use: 1:100 to 1:10,000 soln. as a disinfectant. Mercuric Resorcinol-acetate (Resorcinol-mercury acetate) Mercuric Salicylate (Mercury subsalicylate) Med. Use: Extern. for parasitic and fungous skin diseases. Has been used in syphilis. Mercuric Silver Iodide Use: To detect overheating in journal bearings, etc., becoming blood-red at 40-50º and yellow again on cooling. Mercuric Stearate Mercuric Subsulfate (Turpeth mineral) Mercuric Succinate Mercuric Succinimide Med. Use: Has been used in syphilis. Mercuric Sulfate (Mercury bisulfate) Use: Filling for galvanic batteries; with NaCl for extracting gold and silver from roasted pyrites; as a reagent for wine coloring, barbital, and cystine.

Mercuric Sulfate Ethylenediamine -- see Sublamine® Mercuric Sulfide, Black (Ethiops mineral) Use: As pigment for horn, rubber, etc. Mercuric Sulfide, Red (Vermilion) Occurs in nature as the mineral cinnabar. {Bright scarlet-red; considered as a royal color in some cultures.} Use: For coloring plastics, sealing wax, and with FeSO4 for marking linen; also manuf. of fancy colored papers; as a pigment. Mercuric Sulfocyanate -- see Mercuric Thiocyanate Mercuric Sulfocyanide -- see Mercuric Thiocyanate. Mercuric Thiocyanate (Mercuric sulfocyanate or sulfocyanide) Use: For Pharaoh's serpents; intensifier in photography. Mercuric Tribromophenylacetate Med. Use: Formerly in syphilis and TB. Mercuric Zinc Cyanide Mercurin® (Mercuzan) Med. Use: Diuretic Mercurochrome® -- see Merbromin Mercurochrome-220 Soluble® -- see Merbromin. Mercurocol -- see Merbromin. Mercuro-iodohemol Med. Use: Formerly in syphilis. Mercurol (Mercury "Nucleate") Med. Use: Formerly in syphilis and as an antiseptic. Mercurome -- see Merbromin Mercurophage -- see Merbromin Mercurophen (Sodium hydroxymercuri-o-nitrophenolate) Med. Use: 1:2000 to 1:15,000 soln. as an antiseptic for skin and mucous membranes. Caution: Strong solns. to be applied for 1 min. only. Not effective for sporulating pathogens. Mercurophylline Injection (Mercuzanthin, Formerly known as Mercupurin) Med. Use: Diuretic Mercurosal® (Disodium hydroxymercuri-salicyloxyacetate) Mercurous Acetate Med. Use: Formerly for skin lesions of syphilis. Mercurous Benzoate Mercurous Bromide Mercurous Chlorate Mercurous Chloride Use: Dark-green Bengal lights; calomel paper; mixed with gold in painting on porcelain; for calomel electrodes. Med. Use: Has been used as a laxative, diuretic, and antiseptic. Vet. Use: Locally antiseptic, desiccant in moist eczema, canker, thrush, foot rot. In corneal ulcers, phlyctenular conjunctivitis. Orally, cathartic in horses, dogs, cats. Diuretic in cardiac hepatic diseases. Mercurous Chromate Use: Coloring porcelain and chinaware green. Mercurous Citrate Mercurous Iodide (Yellow mercury iodide; mercury protoiodide) Med. Use: Extern. as ointment in eye diseases. Formerly in syphilis. Mercurous Isovalerate Mercurous Lactate Mercurous Nitrate (Mercury protonitrate) Use: Fire gilding, blackening brass. {gilding - the art or process of applying gold leaf or a substance like gold to a surface.} Mercurus Nitrate Ammoniated (Hahnemann's soluble mercury) Mercurous Oxide (Mercury oxide black) Mercurous Phosphate (Schaeffer's phosphorated mercury) Med. Use: Formerly in syphilis Mercurous Sulfate Use: For making electric batteries; with zinc sulfate in the Clark standard cell and with cadmium sulfate in the standard Weston cell. Mercurous Tannate (Hydrargotin) Med. Use: Formerly in syphilis Mercurous Tartrate Mercury-Alanine -- see Mercuric |-Aminopropionate Mercury Arsanilate -- see Mercuric Atoxylate

Mercury Betanaphthol -- see Mercuric Naphtholate Mercury Bichloride -- see Mercuric Chloride Mercury Bichromate -- see Mercuric Dichromate Mercury Biniodide -- see Mercuric Iodide Red Mercury Bisulfate -- see Mercuric Sulfate Mercury Carbolate -- see Mercuric Phenate Mercury with Chalk (Gray power) Med. Use: Has been used as a laxative and antisyphilitic. Vet. Use: Has been used as a laxative for foals, caves, puppies. Mercury Colloidal Mercury Mass (Blue pill; blue mass) Med. Use: Cathartic {Cathartic - a medication for stimulating evacuation of the bowels.} Toxicity: Can cause systemic mercury poisoning. Vet. Use: Has been used as a laxative. Mercury Monochloride -- see Mercurous Chloride Mercury "Nucleate" -- see Mercurol Mercury Oxide Black -- see Mercurous Oxide Mercury Perchloride -- see Mercuric Chloride Mercury Pernitrate -- see Mercuric Nitrate Mercury Phenolate -- see Mercuric Phenate Mercury Potassium Iodide Solution (Channing's solution; solution potassium iodohydrargyrate) Med. Use: 1:100 to 1:10,000 soln. as an antiseptic. Mercury Protochloride -- see Mercurous Chloride Mercury Protoiodide -- see Mercurous Iodide Mercury Protonitrate -- see Mercurous Nitrate Mercury Sozoiodolate -- see Sozoiodole-Mercury Med. Use: Has been used in syphilis. Mercury Subchloride -- see Mercurous Chloride Mercury Subsalicylate -- see Mercuric Salicylate Mercuzan® -- see Mercurin Mercuzanthin® -- see Mercurophylline Injection Merdroxone Sodium -- Meragidone Sodium Merethoxylline Sodium (Dicurin Sodium) Med. Use: as a diuretic Meroxyl Med. Use: 1:200 to 1:1000 soln. as an antiseptic. Merphene -- see Phenylmercuric Nitrate, Basic Use: Antiseptic, germicide, fungicide. Phenol coefficient stated to be about 600 and relatively unaffected by organic matter. Med. Use: 1:1500 to 1:24,000 soln. as an antiseptic for extern. use. Merphenyl® Nitrate -- see Phenylmercuric Nitrate, Basic Mersalyl (Salyrgan) Med. Use: Mersalyl (2 parts) and theophylline (1 part) as a diuretic. Merthiolate® (Merthiolate Sodium; sodium ethylmercurithiosalicylate; Thimerosal; Thiomersalate) Med. Use: Antiseptic for surface tissues as a 1:1000 to 1:30,000 soln. or 1:1000 tincture. Caution: Not effective against sporulating organisms.

The Problem With MercuryThe problem is Mercury simply "Loves Sulfur" too much. So much so, that it will compete with other molecules

for Sulfur and can usually "steal" Sulfur out of other molecular structures, in effect killing them. Mercury (Hg) interacts with brain tubulin and disassembles microtubules that maintain neurite structure. -reference- If it can't steal Sulfur, Mercury will bond to the Sulfur atom the best it can. This usually prevents the molecule from performing its function. Sulfur is part of our blood cells as well as many other proteins and enzymes. Many systems in our bodies are very much like today's Industrial Assembly Lines. If one work station stops functioning the whole system can backup or get very crazy.

Hemoglobin (The oxygen carrying protein in red blood cells.)

(C738 H1,166 Fe N203 O208 S2)4 Enzymes perform very specialized functions within our body's chemical assembly line. It shouldn't be very hard to visualize the whole process going out of whack if someone doesn't show up for work. Imagine cars coming off the assembly line without tires, or headlights, or oil light sensors, or fuses — you get the idea. From our viewpoint, Enzymes are really "Hyper" little fellows. In the lab, they have been clocked doing Two Million Reactions Per Minute ! (2,000,000 /min.) That means in a 24-hour period, they can do their job 2,880,000,000 times. (Two Billion, Eight Hundred Eighty Million Reactions per Day) At that speed, these guys could count our national debt in only 1,875 days. (5.1 years)

Today a typical adult carries ten amalgams weighing a total of about ten grams, of which five grams is mercury. What little research there is on the rate at which mercury escapes amalgam suggests about half a gram of mercury will escape from these ten fillings over the ten-year life of these fillings, and most of this mercury will be absorbed by the bearer of the amalgams. To put a half-gram in context, consider these facts: Half a gram of mercury dropped into a ten-acre lake warrants the promulgation of a fish advisory for the lake in Minnesota; the tennis shoes with mercury in them that were banned by the Minnesota legislature in 1994 contained half a gram of mercury per shoe. -reference-

(0.5 gram in a 180 lb. body produces a concentration of 6.168 PPM. Compare this level, to the elements in the " Water of Life". —TRC—)

There are about 1,501,430,636,558,496,585,414 atoms in 0.5 grams of mercury. Each and every atom of mercury is able to disable an enzyme or other critical protein in your body. Over ten years, if the body fails to remove this mercury, a lot of damage can be done. Unfortunately, mercury has ways of "hiding in the body" and can be quite hard to remove. This 0.5 grams of mercury can produce a potential loss of 4,324,120,233,288,470,165,993,719,156,572 chemical reactions in your body. (Based on our lab example / over 10 years) That number of seconds equals 137,023,101,670,864,392,919,414.6 years ! As you can see, it is quite difficult to grasp the scale on which all these chemical reactions are occurring, and we are only considering one source of mercury and this one toxic atom. Mercury intoxication often produces a psychotic state resulting in hyper-excitability. The expression 'Mad as a Hatter' originates from the hat-makers of the 19th century who were chronically exposed to mercury compounds used in making felt and beaver hats. Mercury was also used to preserve leather and the furs for coats.

— MAD AS A HATTER —

Few people who use the phrase today realize that there's a story of human suffering behind it; the term actually derives from an early industrial occupational disease. Felt hats were once very popular in

North America and Europe; an example is the top hat. The best sorts were made from beaver fur, but cheaper ones used furs such as rabbit instead.

A complicated set of processes was needed to turn the fur into a finished hat. With the cheaper sorts of fur, an early step was to brush a solution of a mercury compound - usually mercurous nitrate - on to the fur to roughen the fibers and make them mat more easily, a process called carroting because it made the fur turn orange. Beaver fur had natural serrated edges that made this unnecessary, one reason why it was preferred, but the cost and scarcity of beaver meant that other furs had to be used.

Whatever the source of the fur, the fibers were then shaved off the skin and turned into felt; this was later immersed in a boiling acid solution to thicken and harden it. Finishing processes included steaming the hat to shape and ironing it. In all these steps, hatters working in poorly ventilated workshops would breathe in the mercury compounds and accumulate the metal in their bodies.

We now know that mercury is a cumulative poison that causes kidney and brain damage. Physical symptoms include trembling (known at the time as hatter's shakes), loosening of teeth, loss of co-ordination, and slurred speech; mental ones include irritability, loss of memory, depression, anxiety, and other personality changes. This was called mad hatter syndrome. — Source —

The people who then wore these "Fur Products" were also Poisoned !!!

Mercury is added to products to stop things from growing. Mercury was commonly added to exterior house paint until the late 1990's to keep mold from growing on the paint. Exterior paint is designed to "powder-off" instead of cracking and peeling, so the mercury enters the environment as a fine powder. (I highly recommend that you filter the air coming into your environment.)

Mercury is added at even higher levels to marine paint for ships. The object here is to keep barnacles off the hull. The solvents used in these paints continues to "out-gas" for many months, and are very good at carrying mercury into the body via the respiratory tract. Mercury is also used in ammunition and many explosives, especially military types. Studies have shown that toxic levels of lead can be detected in blood samples, after only a couple of hours of indoor target practice, in a poorly ventilated room. This study failed to measure mercury levels, but there is a direct relationship between the amount of lead absorbed and the amount of mercury absorbed by human bodies.

Cellular Immunity

Antibodies* contain sulfur and are therefore attacked by mercury — thereby destroying the body's natural disease defense system. [ * an·ti·bod·y n. A protein substance produced in the blood or tissues in response to a specific antigen, such as a bacterium or a toxin. Antibodies destroy or weaken bacteria and neutralize organic poisons, thus forming the basis of immunity. ] Major Immunoglobulin Classes Major Subclasses of Human IgG An antibody is about 1/700 the size of a red cell. The immune system needs to be able to create an enormous number of antibodies, e.g., perhaps 10 billion B lymphocytes, each able to produce more than 100 million different antibody proteins. Since humans have only about 100,000 genes, it becomes impossible for our genes to specify each one of these proteins. Newborn children receive specific environmental antibodies through nursing. (Mother's milk) Our bodies are constantly creating new antibodies in response to the many different life forms attacking our bodies. In cellular immunity, cells play the most important role in destroying foreign invaders. The cells involved are macrophages and the various subsets of T cells: helper CD4+ cells, suppressor CD8+ cells, cytotoxic T killer cells, and natural (NK) killer cells. Monokines and lymphokines secreted by macrophages and CD4+ helper cells, respectively, play an important role in directing and augmenting both cellular and humoral immune responses. — Reference —

It Should Be Obvious

No Amount of Mercury Can Be Considered Safe !

The following information was copied from this web page Table I: Summary Comparison of Traits of Autism & Mercury Poisoning

( ASD references in bold; Mercury Poisoning references in italics )Psychiatric Disturbances Social deficits, shyness, social withdrawal (1,2,130,131; 21,31,45,53,132 Repetitive, preservative, stereotypic behaviors; obsessive-compulsive tendencies (1,2,43,48,133; 20,33-35,132) Depression/depressive traits, mood swings, flat affect; impaired face recognition (14,15,17,103, 134,135; 19,21,24,26,31) Anxiety; schizoid tendencies; irrational fears (2,15,16; 21,27,29,31)

Irritability, aggression, temper tantrums (12,13,43; 18,21,22,25) Lacks eye contact; impaired visual fixation (HgP)/ problems in joint attention (ASD) (3,36,136,137; 18,19,34) Speech and Language Deficits Loss of speech, delayed language, failure to develop speech (1-3,138,139; 11,23,24,27,30,37) Dysarthria; articulation problems (3; 21,25,27,39) Speech comprehension deficits (3,4,140; 9,25,34,38) Verbalizing and word retrieval problems (HgP); echolalia, word use and pragmatic errors (ASD) (1,3,36; 21,27,70)

Sensory Abnormalities Abnormal sensation in mouth and extremities (2,49; 25,28,34,39) Sound sensitivity; mild to profound hearing loss (2,47,48; 19,23-25,39,40) Abnormal touch sensations; touch aversion (2,49; 23,24,45,53) Over-sensitivity to light; blurred vision (2,50,51; 18,23,31,34,45) Motor Disorders Flapping, myoclonal jerks, choreiform movements, circling, rocking, toe walking, unusual postures (2,3,43,44; 11,19,27,30,31,34,39) Deficits in eye-hand coordination; limb apraxia; intention tremors (HgP)/problems with intentional movement or imitation (ASD) (2,3,36,181; 25,29,32,38,70,87) Abnormal gait and posture, clumsiness and incoordination; difficulties sitting, lying, crawling, and walking; problem on one side of body (4,41,42,123; 18,25,31,34,39,45) Cognitive Impairments Borderline intelligence, mental retardation - some cases reversible (2,3,151,152; 19,25,31,39,70) Poor concentration, attention, response inhibition (HgP)/shifting attention (ASD) (4,36,153; 21,25,31,38,141) Uneven performance on IQ subtests; verbal IQ higher than performance IQ (3,4,36; 31,38) Poor short term, verbal, and auditory memory (36,140; 21,29,31,35,38,87,141) Poor visual and perceptual motor skills; impairment in simple reaction time (HgP)/ lower performance on timed tests (ASD) (4,140,181; 21,29,142) Deficits in understanding abstract ideas & symbolism; degeneration of higher mental powers (HgP)/sequencing, planning & organizing (ASD); difficulty carrying out complex commands (3,4,36,153; 9,18,37,57,142) Unusual Behaviors Self injurious behavior, e.g. head banging (3,154; 11,18,53) ADHD traits (2,36,155; 35,70) Agitation, unprovoked crying, grimacing, staring spells 3,154; 11,23,37,88) Sleep difficulties (2,156,157; 11,22,31) Physical Disturbances Hyper- or hypotonia; abnormal reflexes; decreased muscle strength, especially upper body; incontinence; problems chewing, swallowing (3,42,145,181; 19,27,31,32,39) Rashes, dermatitis, eczema, itching (107,146; 22,26,143) Diarrhea; abdominal pain/discomfort, constipation, "colitis" (107,147-149; 18,23,26,27,31,32) Anorexia; nausea (HgP)/vomiting (ASD); poor appetite (HgP)/restricted diet (ASD) (2,123; 18,22) Lesions of ileum and colon; increased gut permeability (147,150; 57,144)

Table II: Summary Comparison of Biological Abnormalitiesin Autism & Mercury Exposure

Mercury Exposure Autism Biochemistry Binds -SH groups; blocks sulfate transporter in intestines, kidneys (40,93) Low sulfate levels (91,92)

Reduces glutathione availability; inhibits enzymes of glutathione metabolism; glutathione needed in neurons, cells, and liver to detoxify heavy metals; reduces glutathione peroxidase and reductase (97,100,161,162)

Low levels of glutathione; decreased ability of liver to detoxify xenobiotics; abnormal glutathione peroxidase activity in erythrocytes (91,94,95)

Disrupts purine and pyrimidine metabolism (10,97,158,159)

Purine and pyrimidine metabolism errors lead to autistic features (2,101,102)

Disrupts mitochondrial activities, especially in brain (160,163,164)

Mitochondrial dysfunction, especially in brain (76,172)

Immune System

Sensitive individuals more likely to have allergies, asthma, autoimmune-like symptoms, especially rheumatoid-like ones (8,11,18,24,28,31,111,113)

More likely to have allergies and asthma; familial presence of autoimmune diseases, especially rheumatoid arthritis; IgA deficiencies (103,106-109,115)

Can produce an immune response in CNS; causes brain/MBP autoantibodies (18,111,165)

On-going immune response in CNS; brain/MBP autoantibodies present (104,105,109,110)

Causes overproduction of Th2 subset; kills/inhibits lymphocytes, T-cells, and monocytes; decreases NK T-cell activity; induces or suppresses IFNg & IL-2 (100,112,117-120,166)

Skewed immune-cell subset in the Th2 direction; decreased responses to T-cell mitogens; reduced NK T-cell function; increased IFNg & IL-12 (103,108,114-116,173,174)

CNS Structure Selectively targets brain areas unable to detoxify or reduce Hg-induced oxidative stress (40,56,161)

Specific areas of brain pathology; many functions spared (36)

Accumulates in amygdala, hippocampus, basal ganglia, cerebral cortex; damages Purkinje and granule cells in cerebellum; brain stem defects in some cases (10,34,40,70-73)

Pathology in amygdala, hippocampus, basal ganglia, cerebral cortex; damage to Purkinje and granule cells in cerebellum; brain stem defects in some cases (36,60-69)

Causes abnormal neuronal cytoarchitecture; disrupts neuronal migration, microtubules, and cell division; reduces NCAMs (10,28,57-59,161)

Neuronal disorganization; increased neuronal cell replication, increased glial cells; depressed expression of NCAMs (4,54,55)

Progressive microcephaly (24) Progressive microcephaly and macrocephaly (175)

Neuro-chemistry Prevents presynaptic serotonin release and inhibits serotonin transport; causes calcium disruptions (78,79,163,167,168)

Decreased serotonin synthesis in children; abnormal calcium metabolism (76,77,103,179)

Alters dopamine systems; peroxidine deficiency in rats resembles mercurialism in humans (8,80)

Either high or low dopamine levels; positive response to peroxidine, which lowers dopamine levels (2,177,178)

Elevates epinephrine and norepinephrine levels by blocking enzyme that degrades epinephrine (81,160)

Elevated norepinephrine and epinephrine (2)

Elevates glutamate (21,171) Elevated glutamate and aspartate (82,176) Leads to cortical acetylcholine deficiency; increases muscarinic receptor density in hippocampus and cerebellum (57,170)

Cortical acetylcholine deficiency; reduced muscarinic receptor binding in hippocampus (83)

Causes demyelinating neuropathy (22,169) Demyelination in brain (105) Neurophysiology Causes abnormal EEGs, epileptiform activity, variable patterns, e.g., subtle, low amplitude seizure activities (27,31,34,86-89)

Abnormal EEGs, epileptiform activity, variable patterns, including subtle, low amplitude seizure activities (2,4,84,85)

Causes abnormal vestibular nystagmus responses; loss of sense of position in space (9,19,34,70)

Abnormal vestibular nystagmus responses; loss of sense of position in space (27,180)

Results in autonomic disturbance: excessive sweating, poor circulation, elevated heart rate (11,18,31,45)

Autonomic disturbance: unusual sweating, poor circulation, elevated heart rate (17,180)

References

1 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Washington D.C.: American Psychiatric Association, 1994. 2 Gillberg C., Coleman M. The Biology of the Autistic Syndromes, 2nd edn. London: Mac Keith Press, 1992. 3 Filipek P., Accardo P., Baranek G., et al. The screening and diagnosis of autistic spectrum disorders. J Autism Dev Disord 1999; 29(6): 439-484. 4 Bailey A., Phillips W., Rutter M. Autism: towards an integration of clinical, genetic, neuro-psychological, and neurobiological perspectives. J Child Psychol Psychiatry 1996; 37(1): 89-126. 5 Suzuki T., Takemoto T. I., Kashiwazaki H., Miyama T., Metabolic fate of ethylmercury salts in man and animal. Mercury, Mercurials, and Mercaptans ,Ch 12; 209-233. Miller M. W., Clarkson T. W., eds. Springfield: Charles C. Thomas, 1973. 6 Halsey N. A. Perspective on the use of thimerosal-containing vaccines. Presentation at the National Vaccine Advisory Committee Workshop on Thimerosal and Vaccines, August 11-12, 1999. Institute of Vaccine Safety website;. 7 Egan, W. M. Thimerosal in Vaccines. Presentation to the FDA, September 14, 1999. 8 Gosselin R. E., Smith R. P., Hodge H. C. Mercury. Clinical Toxicology of Commercial Products, Section III, Therapeutic Index,5th edn. Baltimore: Williams & Wilkins, 1984: 262-271. 9 Dales L. D. The neurotoxicity of alkyl mercury compounds. Am J Med 1972; 53: 219-232. 10 Koos B. J., Longo L. D., Mercury toxicity in the pregnant woman, fetus, and newborn infant. Am J Obstet Gynecol 1976: 126(3): 390-406. 11 Warkany J., Hubbard D. H. Acrodynia and mercury. J Pediatrics 1953: 42; 365-386.

12 McDougle C. J., Brodkin E. S., Yeung P. P., Naylor S. T., Cohen D. J., Price L. H. Risperidone in adults with autism or pervasive developmental disorder. J Child Adolesc Psychopharmacol 1995; 5(4): 273-282. 13 Jaselskis C., Cook E., Fletcher K., Bennett L. Clonidine treatment of hyperactive and impulsive children with autistic disorder. J Clin Pharmacol 1992. 14 Piven J., Palmer P. Psychiatric disorder and the broad autism phenotype: evidence from a family study of multiple-incidence autism families. Am J Psychiatry 1999; 156(4): 557-563. 15 Clarke D., Baxter M., Perry D., Prasher V. The diagnosis of affective and psychotic disorders in adults with autism: seven case reports. Autism 1999; 3(2): 149-164. 16 Muris P., Steerneman P., Merckelbach H., Holdrinet I., Meesters C. Comorbid anxiety symptoms in children with pervasive developmental disorders. J Anxiety Disord 1998; 12(4): 387-393. 17 Wing L., Attwood A. Syndromes of autism and atypical development. Handbook of Autism and Pervasive Developmental Disorders. John Wiley & Sons, Inc. 1987: 3-19. 18 Fagala G. E.,Wigg C. L. Psychiatric manifestations of mercury poisoning. J Am Acad Child Adolesc Psychiatry 1992; 31(2): 306-311. 19 Kark R. A., Poskanzer D .C., Bullock J. D., Boylen G. Mercury poisoning and its treatment with N-acetyl-D., L-penicillamine. N Engl J Med 1971; 285: 10-16. 20 White R. F., Feldman R. G., Moss M. B., Proctor S. P. Magnetic resonance imaging (MRI), neurobehavioral testing, and toxic encephalopathy: two cases. Environ Res 1993; 61: 117-123. 21 O'Carroll R. E., Masterton G., Dougnall N., Ebmeier K. P. The neuropsychiatric sequelae of mercury poisoning: The Mad Hatters disease revisited. Br J Psychiatry 1995; 167(1): 95-98. 22 Florentine M. J., Sanfilippo II D. J. Grand rounds: elemental mercury poisoning. Clin Pharm 1991; 10: 213-221. 23 Amin-Zaki, L., Elhassani S., Majeed M. A., Clarkson T. W., Doherty R. A., Greenwood M., Intra-uterine methylmercury poisoning in Iraq. Pediatrics 1974; 54(5) 587-595. 24 Amin-Zaki L., Majeed M. A., Elhassani S. B., Clarkson T. W., Greenwood M. R., Doherty R. A., Prenatal methylmercury poisoning. Am J Disabled Child 1979; 133: 172-177. 25 Joselow M. M., Louria D. B., Browder A. A., Mercurialism: environmental and occupational aspects. Ann Intern Med 1972; 76: 119-130. 26 Smith D. Mental Effects of Mercury Poisoning. Presentation before the Section on Family Practice, Southern Medical Association, 71st Annual Scientific Assembly, November 6-9, 1977. 27 Lowell J. A., Burgess S., Shenoy S., Curci J. A., Peters M., Howard T. K. Mercury poisoning associated with high-dose hepatitis-B immune globulin administration after liver transplantation for chronic hepatitis B. Liver Transpl Surg 1996; 2(6): 475-478. 28 Clarkson, T. The toxicology of mercury. Crit Rev Clin Lab Sci 1997; 34(3): 369-403. 29 Camerino D., Cassito M.G., Desideri E., Angotzi G. Behavior of some psychological parameters of a population of a Hg extraction plant. Clin Toxicol 1981; 18(11): 1299-1309. 30 Snyder R. D. The involuntary movements of chronic mercury poisoning. Arch Neurol 1972; 26: 379-381. 31 Vroom F. Q., Greer M. Mercury vapor intoxication. Brain 1972; 95: 305-318. 32 Adams C. R., Ziegler D. K., Lin J. T. Mercury intoxication simulating amyotrophic lateral sclerosis. JAMA 1983; 250: 642-643. 33 Cuomo V., Ambrosi L., Annau Z., Cagiano R., Brunello N., Racagni G. Behavioural and neurochemical changes in offspring of rats exposed to methylmercury during gestation. Neuobehav Toxicol Teratol 1984; 6(3): 249-254. 34 Tsubaki T., Irukayama K., eds. Minamata Disease. Elsevier Scientific Publishing Co., 1977. 35 Elsner J. Testing strategies in behavioral teratology. III. Microanalysis of behavior. Neurobehav Toxicol Teratol 1986; 8: 573-584. 36 Dawson G. Brief report: neuropsychology of autism: a report on the state of the science. J Autism Dev Disord 1996; 26(2): 179-184. 37 Pierce P. E., Thompson J. F. MPH, Likosky W. H. MD, Nickey L. N. MD, Barhtel W. F., Hinman A. R. MD MPH. Alkyl mercury poisoning in humans. JAMA 1972; 220(11): 1439-1442. 38 Grandjean P., Weihe P., White R. F., Debes F. Cognitive performance of children prenatally exposed to "safe" levels of methylmercury. Environ Res 1998; 77(2): 165-172. 39 Amin-Zaki L., Majeed M. A., Clarkson T. W., Greenwood M. R. Methylmercury poisoning in Iraqi children: clinical observations over two years. British Medical Journal 1978; March 1: 613-616. 40 Clarkson T. W. Mercury: major issues in environmental health. Environ Health Perspect 1992; 100: 31-38. 41 Kugler B. The differentiation between autism and Asperger syndrome. Autism 1998; 2(1): 11-32. 42 Teitelbaum P., Teitelbaum O., Nye J., Fryman J., Maurer R. G. Movement analysis in infancy may be useful for early diagnosis of autism. Proc Natl Acad Sci U S A 1998; 95: 13982-13987. 43 Tsai L. Y. Brief report: comorbid psychiatric disorders of autistic disorder. J Autism Dev Disord 1996; 26(2): 159-164. 44 Cesaroni L., Garber M. Exploring the experience of autism through firsthand accounts. J Autism Dev Disord 1991; 21(3): 303-313. 45 Farnsworth D. Pink Disease Survey Results. Pink Disease Support Group Site, 1997;

46 Brasic J. R. Movements in autistic disorder. Med Hypoth 1999; 53: 48-49. 47 Rosenhall U., Nordin V., Sandstrom M., Ahlsen G., Gillberg C. Autism and hearing loss. J Autism Dev Disord 1999; 29(5): 349-358. 48 Roux S., Adrien J-L., Bruneau N., Malvy J., Barthelemy C. Behavior profiles within a population of 145 children with autism using the Behaviour Summarized Evaluation scale: influence of developmental age. Autism 1998; 2(4): 345-366. 49 Baranek G. Autism during infancy: a retrospective video analysis of sensory-motor and social behaviors and 9-12 months of age. J Autism Dev Disord 1999; 29(3): 213-224. 50 ONeill M., Jones R. S. P. Sensory-perceptual abnormalities in autism: a case for more research? J Autism Dev Disord 1997; 27(3): 283-293. 51 Sperry V. W. Family and personal section: from the inside out - a view of the world as seen by one with Asperger syndrome. Autism 1998; 2(1): 81-86 52 Cass H. Visual impairment and autism: current questions and future research. Autism 1998; 2(2): 117-138. 53 Manser N. Neville's (a Pinkie) Recollection of Pink Disease. Pink Disease Support Group; www.users.bigpond.com/difarnsworth. 54 Minshew N. J. Brief report: brain mechanisms in autism: functional and structural abnormalities. J Autism Dev Disord 1996; 26(2): 205-209. 55 Plioplys A. V., Hemmens S. E., Regan C. M. Expression of a neural cell adhesion molecule serum fragment is depressed in autism. J Neuropsychiatry Clin Neurosci 1990; 2(4): 413-417. 56 Sarafian T. A., Bredesen D. E., Verity M. A. Cellular resistance to methylmercury. Neurotoxicology 1996 Spring Abstract; 17(1): 27-36. 57 Hassett-Sipple B., Swartout J., Schoeny R. Vol. V. Health effects of mercury and mercury compounds. Mercury Study Report to Congress. Environmental Protection Agency (EPA), December 1997. 58 Pendergrass J. C., Haley B. E., Vimy M. J., Winfield S. A., Lorscheider F. L. Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brain. Neurotoxicology 1997; 18(2): 315-324. 59 Dey P. M., Gochfeld M., Reuhl K. R. Developmental methylmercury administration alters cerebellar PSA-NCAM expression and Golgi sialyltransferase activity. Brain Res 1999; 845(2): 139-151. 60 Courchesne E., et al. More evidence links autism, cerebellar defects. reviewed in Autism Research Review International 1994; 8(2): 1,7. 61 Ritvo E. R., Freeman B. J., Scheibel A. B., et al. Lower Purkinje cell counts in the cerebella of four autistic subjects: initial findings of the UCLA-NSAC Autopsy Research Report. Am J Psychiatry 1986; 143: 862-866. 62 Hoon A. H., Riess A. L. The mesial-temporal lobe and autism: case report and review. Dev Med Child Neurol 1992; 34: 252-265. 63 Piven J., Berthier M., Starkstein S., Nehme E., Pearlson G., Folstein S. Magnetic resonance imaging evidence for a defect of cerebral cortical development in autism. Am J Psychiatry 1990; 147(6): 734-739. 64 Abell F., Krams M., Ashburner J., et al. The neuroanatomy of autism: a voxel-based whole brain analysis of structural scans. Neuroreport 1999; 10(8): 1647-1651. 65 Aylward E. H., Minshew N. J., Goldstein G., et al. MRI volumes of amygdala and hippocampus in non-mentally retarded autistic adolescents and adults. Neurology 1999; 53(9): 2145-2150. 66 Otsuka H. Brain metabolites in the hippocampus-amygdala region and cerebellum in autism: an 1H-MR spectroscopy study. Neuroradiology 1999; July. 67 Sears L. L. An MRI study of the basal ganglia in autism. Prog Neuropsychopharmacol Biol Psychiatry 1999; May. 68 Hashimoto T., Tayama M., Murakawa K., et al. Development of the brainstem and cerebellum in autistic patients. J Autism Dev Disord 1995; 25(1): 1-18. 69 McClelland R. J., Eyre D., Watson D., Calvert J. A neurophysiological study of autistic children. Electroencephalogr Clin Neurophysiol 1985; 61: 16. 70 Davis L. E., Kornfeld M., Mooney H. S., et al. Methylmercury poisoning: long term clinical, radiological, toxicological, and pathological studies of an affected family. Ann Neurol 1994: 35(6): 680-688. 71 Larkfors L., Oskarsson A., Sundberg J., Ebendal T. Methylmercury induced alterations in the nerve growth factor level in the developing brain. Brain Res Dev Brain Res 1991; 62(2): 287-291. 72 Lorscheider F. L., Vimy M. J., Summers A. O. Mercury exposure from "silver" tooth fillings: emerging evidence questions a traditional dental paradigm. FASEB J 1995; 9: 504-508. 73 Magos L., Brown A. W., Sparrow S., Bailey E., Snowden R. T., Skipp W. R. The comparative toxicology of ethyl- and methylmercury. Arch Toxicol 1985; 57(4): 260-267. 74 Rolls E. T. Memory systems in the brain. Ann Rev Psychol 2000; 51: 599-630. 75 Bachevalier J. Medial temporal lobe structures: a review of clinical and experimental findings. Neuropsychologia 1994; 32: 627-648. 76 Chugani D. C., Muzik O., Behen M., et al. Developmental changes in brain serotonin synthesis capacity in autistic and nonautistic children. Ann Neurol 1999; 45. 77 Cook E. H. Autism: review of neurochemical investigation. Synapse 1990; 6: 292-308.

78 O Kusky J. R., Boyes B. E., McGeer E. G. Methylmercury-induced movement and postural disorders in developing rat: regional analysis of brain catecholamines and indoleamines. Brain Res 1988; 439(1-2): 138-146. 79 Nishio H., Nezasa K., Hirano J., Nakata Y. Effects of thimerosal, an organic sulfhydryl modifying agent, on serotonin transport activity into rabbit blood platelets. Neurochem Int 1996; 29(4): 391-396. 80 McKay S. J., Reynolds J. N., Racz W. J. Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatal slices. Can J Physiol Pharmacol 1986; 64(12): 1507-1514. 81 Hrdina P. D., Peters D. A., Singhal R. L. Effects of chronic exposure to cadmium, lead and mercury of brain biogenic amines in the rat. Research Communications in Chemistry, Pathology and Pharmacology 1976; 15(3): 483-493. 82 Moreno H., Borjas L., Arrieta A., et al. Clinical heterogeneity of the autistic syndrome: a study of 60 families (Spanish). Invest Clin 1992; 33(1): 13-31. 83 Perry E., Lee M., Court J., Perry R. Cholinergic Activities in Autism: Nicotinic and Muscarinic Receptor Abnormalities in the Cerebral Cortex. Presentation to Cure Autism Now, 2000. 84 Lewine magnetoenchalography in children with an autistic epileptiform regression. J Pediatrics 1999; 405-418. 85 Nass R., Gross A., Devinsky O. Autism and autistic epileptiform regression with occipital spikes. Dev Med Child Neurol 1998; 40(7): 453-8. 86 Brenner R. P, Snyder R. D. Late EEG finding and clinical status after organic mercury poisoning. Arch Neurol 1980; 37(5): 282-284. 87 Piikivi L., Tolonen U. EEG findings in chlor-alkali workers subject to low long term exposure to mercury vapor. Br J Ind Med 1989; 46(6): 370-375. 88 Rohyans J., Walson P. D., Wood G. A., MacDonald W. A. Mercury toxicity following merthiolate ear irrigations. J Pediatr 1984: 311-313. 89 Szasz A., Barna B., Szupera Z., et al. Chronic low-dose maternal exposure to methylmercury enhances epileptogenicity in developing rats. Int J Devl Neurosci 1999; 17(7): 733-742. 90 Scheyer R. D. Involvement of glutamate in human epileptic activities. Prog Brain Res 1998; 116, 359-369. 91 O Reilly B. A., Waring, R. Enzyme and sulfur oxidation deficiencies in autistic children with known food/chemical intolerances. Journal of Orthomolecular Medicine 1993; 4: 198-200. 92 Alberti A., Pirrone P., Elia M., Waring R. H., Romano C. Sulphation deficit in "low-functioning" autistic children: a pilot study. Biol Psychiatry 1999; 46(3): 420-4. 93 Markovich D., Knight D., Renal Na-Si cotransporter NaSi-1 is inhibited by heavy metals. American Journal of Renal Physiology 1998; 274(2): 283-289. 94 Golse B., Debray-Ritzen P., Durosay P., Puget K., Michelson A. M. Alterations in two enzymes: superoxide dismutase and glutathion peroxidase in developmental infantile psychosis. Rev Neurol (Paris) 1978; 134(11): 699-705. 95 Edelson S. B., Cantor D. S. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-563. 96 Fuchs J., Packer L., Zimmer G. Lipoic Acid in Health and Disease . Marcel Dekker, Inc., 1997 97 Williams M. V., Winters T., Waddell K. S. In vivo effects of Mercury (II) on deoxyuridine triphosphate nucleotidohydrolase, DNA polymerase (a,b), uracil-DNA glycosylase activities in cultured human cells: relationship to DNA damage, DNA repair, and cytotoxicity. Mol Pharmacol 1987; 31(2): 200-207. 98 Aukrust P., et al. Decreased levels of total and reduced glutathione in CD4+ lymphocytes in common variable immunodeficiency are associated with activation of the tumor necrosis factor system: possible immunopathogenic role of oxidative stress. Blood 1995;86(4): 1383-1391. 99 Jaffe J. S., et al. Functional abnormalities of CD8+ t cells define a unique subset of patients with common variable immunodeficiency. Blood 1993; 82(1): 192-201. 100 Shenker B. J., Guo T. L., Shapiro I. M. Low-level methylmercury exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial dysfunction. Environ Res 1998; Section A 77(2): 149-159. 101 Page T., Yu A., Fontanesi J., Nyhan W. L. Developmental disorder associated with increased cellular nucleotidase activity. Proc Natl Acad Sci U S A 1997; 94: 11601-11606. 102 Page T., Coleman M. Purine metabolism abnormalities in a hyperuricosuric subclass of autism. Biochim Biophys Acta 2000; 1500(3): 291-296. 103 Plioplys A. Autism: Biomedical Perspectives. Presentation for the Autism Society of America meeting, July 1989. 104 Connolly A. M., et al. Serum autoantibodies to brain in Landau-Kleffner variant, autism, and other neurologic disorders. J Pediatr 1999; 134(5): 607-613. 105 Singh V., Warren R., Odell J., Warren W., Cole P. Antibodies to myelin basic protein in children with autistic behavior. Brain Behav Immun 1993; 7(1): 97-103. 106 Comi A. M., Zimmerman A., et al. Familial clustering of autoimmune disorders and evaluation of medical risk factors in autism. J Child Neurol 1999; 14: 388-394. 107 Whiteley P., Rogers J., Shattock P. Clinical features associated with autism: observations of symptoms outside the diagnostic boundaries of autistic spectrum disorders. Autism 1998;2(4): 415-422.

108 Warren R. P., Margaretten N. C., Pace N. C., Foster A. Immune abnormalities in patients with autism. J Autism Dev Disord 1986; 16(2): 189-197. 109 Zimmerman A., Frye V. H., Potter N. T. Immunological aspects of autism. International Journal of Pediatrics 1993; 8: 199-204. 110 Weitzman A., Weisman R., Szekely G. A., Wijsenbeek H., Livni E. Abnormal immune response to brain tissue antigen in the syndrome of autism. Am J Psychiatry 1982; 139(11): 1462-1465. 111 Nielsen J. B., Hultman P. Experimental studies on genetically determined susceptibility to mercury-induced autoimmune response. Ren Fail 1999; 21(3&4): 343-348. 112 Hu H., Abedi-Valugerdi M., Moller G. Pretreatment of lymphocytes with mercury in vitro induces a response in T cells from genetically determined low-responders and a shift of the interleukin profile. Immunology 1997; 90: 198-204. 113 Al-Balaghi S., Möller E., Möller G., Abedi-Valugerdi M. Mercury induces polyclonal B cell activation, autoantibody production and renal immune complex deposits in young (NZB x NZW) F1 hybrids. Eur J Immunol 1996; 26(7): 1519-1526. 114 Warren R. P., Margaretten N. C., Foster A., Reduced natural killer cell activity in autism. J Am Acad Child Adolesc Psychiatry 1987; 26(3): 333-335. 115 Gupta S., Aggarwal S., Heads C., Brief report: dysregulated immune system in children with autism: beneficial effects of intravenous immune globulin on autistic characteristics, J Autism Dev Disord 1996; 26(4): 439-452. 116 Messahel S., Pheasant A. E., Pall H., Ahmed-Choudhury J., Sungum-Paliwal R. S., Vostanis P. Urinary levels of neopterin and biopterin in autism. Neurosci Lett 1998; 241(1): 17-20. 117 Johansson U., Hansson-Georgiadis H., Hultman P. The genotype determines the B cell response in mercury-treated mice. Int Arch Allergy Immunol 1998; 116(4): 295-305. 118 Bagenstose L. M., Salgame P., Monestier M. Murine mercury-induced autoimmunity: a model of chemically related autoimmunity in humans. Immunol Res 1999; 20(1): 67-78. 119 Hu H., Moller G., Abedi-Valugerdi M. Mechanism of mercury-induced autoimmunity: both T helper 1- and T helper 2-type responses are involved. Immunology 1999; 96(3): 348-357. 120 Ilback N. G. Effects of methyl mercury exposure on spleen and blood natural-killer (NK) cell-activity in the mouse. Toxicology 1991; 67(1): 117-124. 121 Mattsson J. R., Miller E., Alligood J. P., Koering J. E., Levin S. G. Early effects of methylmercury on the visual evoked response of the dog. Neurotoxicology 1981; 2(3): 499-514. 122 Redwood, L. Chelation case histories. Http://tlredwood.home.mindspring.com/case_studies.htm. 124 Gilberg C., Wing L. Autism: not an extremely rare disorder. Acta Psychiatr Scand 1999; 99(6); 399-406. 123 Kanner L. Autistic disturbances of affective contact. The Nervous Child 1942-1943; 2(3): 217-250. 125 Bristol M., Cohen D., Costello E., et al. State of the science in autism: report to the National Institutes of Health. J Autism Dev Disord 1996; 26(2): 121-157. 126 Prevalence of Autism in Brick Township, New Jersey, 1998: Community Report. Centers for Disease Control and Prevention, April 2000; www.cdc.gov/nceh/cddh/dd/rpttoc. 127 Sager. P. R., Aschner, M., Rodier, P. M. Persistent differential alteration in developing cerebellar cortex of male and female mice after methylmercury exposure. Dev Brain Res 1984; 12: 1-11. 128 Rossi A. D., Ahlbom E., Ogren S. O., Nicotera P., Ceccatelli S. Prenatal exposure to methylmercury alters locomotor activity of male but not female rats. Exp Brain Res 1997; 117(3): 428-436. 129 Uproar over a little-known preservative, thimerosal, jostles U.S. hepatitis B vaccination policy. 1999 Summer; 4(2). 130 Capps L., Kehres J., Sigman M. Conversational abilities among children with autism and children with developmental delays. Autism 1998; 2(4): 325-44. 131 Tonge B. J., Brereton A. V., Gray K. M., Einfeld S. L., Behavioural and emotional disturbance in high-functioning autism and Aspergers syndrome. Autism 1999; 3(2): 117-130. 132 Ross W. Donald, Gechman A., Sholiton M., Paul H. Alertness to neuropsychiatric manifestations. Compr Psychiatry 1977; 18(6): 595-598. 133 Howlin P. Outcome in adult life for more able individuals with autism or Asperger syndrome. Autism 2000; 4(1): 63-84. 134 Klin A., Sparrow S. S., de Bilt A., et al. A normed study of face recognition in autism and related disorders. J Aut Dev Disorders 1999; 29(6): 499-508. 135 DeLong G. R. Autism: new data suggest a new hypothesis. Neurology 1999; 52(5): 911-916. 136 Bernabei P., Camaioni L., Levi G. An evaluation of early development in children with autism and pervasive developmental disorders from home movies: preliminary findings. Autism 1998; 2(3): 243-258. 137 Baron-Cohen S., Allen J., Gillberg C. Can autism be detected at 18 months: the needle, the haystack, and the CHAT. Br J Psychiatry 1992; 161: 839-843. 138 Eisenmayer R., et al. Delayed language onset as a predictor of clinical symptoms in pervasive developmental disorders. J Autism Dev Disord 1998; 28(6): 527-533. 139 Prizant B. M. Brief report: communication, language, social, and emotional development. J Autism Dev Disord 1996; 26(2): 173-178.

140 Grandin T. The learning style of people with autism: an autobiography. Teaching Children with Autism. Kathleen Ann Quill, ed., 1995: 33-52. 141 Hua M. S., Huang C. C., Yang Y. J. Chronic elemental mercury intoxication: neuropsychological follow up case study. Brain Inj 1996; 10(5): 377-384. 142 Yeates K. O., Mortensen M. E. Acute and chronic neuropsychological consequences of mercury vapor poisoning in two early adolescents. J Clin Exp Neuropsychol 143 Aronow R., Fleischmann L. Mercury poisoning in children. Clin Pediatr 1976; 15(10): 936-945. 144 Watzl B., Abrahamse SL., Treptow-van Lishaut S., et al. Enhancement of ovalbumin-induced antibody production and mucosal mast cell response by mercury. Food Chem Toxicol 1999; 37(6): 627-637. 145 Church C., Coplan J. The high functioning autistic experience: birth to preteen years. J Pediatr Health Care 1995; 9: 22-29. 146 ONeill J. L. Through the Eyes of Aliens. Jessica Kingsley Publishers Ltd., 1999. 147 Deufemia P., Celli M., Finocchiaro R., et al. Abnormal intestinal permeability in children with autism. Acta Pædiatr 1996; 85: 1076-1079. 148 Horvath K., Papadimitriou J. C., Rabsztyn A., Drachenberg C., Tildon J. T. Gastrointestinal abnormalities in children with autistic disorder. J Pediatr 1999; 135(5): 559-563. 149 Wakefield A. J., Murch S. H., Anthony A., et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 1998; 351: 637-641. 150 Shattock P., Savery D. Autism as a Metabolic Disorder. Sunderland, UK: Autism Research Unit, University of Sunderland, 1997. 151 Edelson M. G., Schubert D. T., Edelson S. M. Factors predicting intelligence cores on the TONI in individuals with autism. Focus on Autism and Other Developmental Disabilities 1998; 13(1): 17-26. 152 Long term follow-up: early intervention effects lasting. ARI Newsletter, review 1993; 7(1): 1&6 153 Rumsey J. Conceptual problem-solving in highly verbal, nonretarded autistic men. J Autism Dev Disord 1985; 15(1): 23-36. 154 Gedye A. Anatomy of self-injurious, stereotypic, and aggressive movements: evidence for involuntary explanation. J Clin Psychol 1992; 48(6): 766-778. 155 Kim J. A., Szatmari P., Bryson S. E., Streiner D. L., Wilson F. J. The prevalence of anxiety and mood problems among children with autism and Asperger syndrome. <>2000; 4(2); 117-133. 156 Richdale A. L. Sleep problems in autism: prevalence, cause, and intervention. Dev Med Child Neurol 1999; 41(1): 60-66. 157 Stores G., Wiggs L. Abnormal sleeping patterns associated with autism: a brief review of research findings, assessment methods and treatment strategies. Autism 1998; 2(2): 157-170. 158 Sarafian T., Verity M..A. Altered patterns of protein phosphorylation and synthesis caused by methyl mercury in cerebellar granule cell culture. J Neurochem 1990; 55(3): 922-929. 159 Rosenspire A. J., Bodepudi S., Mathews M., McCabe M. J. Jr. Low levels of ionic mercury modulate protein tyrosine phosphorylation in lymphocytes. Int J Immunopharmacol 1998; 20(12): 697-707. 160 Rajanna B., Hobson M. Influence of mercury on uptake of [3H]dopamine and [3H]norepinephrine by rat braisynaptosomes. Toxicol Lett 1985; 27(1-3): 7-14. 161 Aschner M., Mullaney KJ., Wagoner D., Lash LH., Kimelberg HK. Intracellular glutathione (GSH) levels modulate mercuric chloride (MC)- and methylmercuric chloride (MeHgCl)-induced amino acid release from neonatal rat primary astrocytes cultures. Brain Res 1994; (664); 133-140. 162 Ashour H., Abdel-Rahman M., Khodair A. The mechanism of methyl mercury toxicity in isolated rat hepatocytes. Toxicol Lett 1993; 69(1): 87-96. 163 Atchison W. D., Hare M. F. Mechanisms of methylmercury-induced neurotoxicity, FASEB J 1994; 8(9): 622-629. 164 Faro L. R. F., Nascimento J. L. M., Alfonso M., Duran R., Acute administration of methylmercury changes in vivo dopamine release from rat striatum. Bull Environ Contam Toxicol 1998; 60: 632-638. 165 El-Fawal H. A., Waterman S. J., De Feo A., Shamy M. Y. Neuroimmunotoxicology: humoral assessment of neurotoxicity and autoimmune mechanisms. Environ Health Perspect 1999; 107(Suppl 5): 767-775. 166 Tan X. X., Tang C., Castoldi A. F., Manzo L., Costa L. G. Effects of inorganic and organic mercury on intracellular calcium levels in rat T lymphocytes. J Toxicol Environ Health 1993; 38(2): 159-170. 167 Elferink J. G. Thimerosal: a versatile sulfhydryl reagent, calcium mobilizer, and cell function-modulating agent. Gen Pharmacol 1999; 33(1): 1-6. 168 Atchison W. D., Joshi U., Thornburg J. E. Irreversible suppression of calcium entry into nerve terminals by methylmercury. J Pharmacol Exp Ther 1986; 238(2): 618-624. 169 Chu C. C., Huang C. C., Ryu S. J., Wu T. N. Chronic inorganic mercury induced peripheral neuropathy. Acta Neurol Scand 1998; 98(6): 461-465. 170 Coccini T., Randine G., Candura S. M., Nappi R. E., Prockop L. D., Manzo L. Low-level exposure to methylmercury modifies muscarinic cholinergic receptor binding characteristics in rat brain and lymphocytes: physiologic implications and new opportunities in biologic monitoring. Environ Health Perspect 2000; 108(1): 29-33.

171 Volterra A., Trotti D., Cassutti P., et al. High sensitivity of glutamate uptake to extracellular free arachidonic acid levels in rat cortical synaptosomes and astrocytes. J Neurochem 1992: 59(2): 600-606. 172 Lombard J. Autism: a mitochondrial disorder? Med Hypotheses 1998; 50(6): 497-500. 173 Gupta S., Aggarwal S., Rashanravan B., Lee T. Th1- and Th2-like cytokines in CD4+ and CD8+ T cells in autism. J Neuroimmunol 1998; 85(1): 106-109. 174 Singh V. K. Plasma increase of Interleuken-12 and Interferon-gamma. Pathological significance in autism. J Neuroimmunology 1996; 66: 143-145. 175 Fombonne E., Rogé B., Claverie J., Courty S., Frémolle J. Microcephaly and macrocephaly in autism. J Autism Dev Disord 1999; 29(2): 113-119. 176 Carlson M. L. Hypothesis: is infantile autism a hypoglutamatergic disorder? Relevance of glutamate - serotonin interactions for pharmacotherapy. J Neural Transm 1998; 105(4-5): 525-535. 177 Gillberg C., Svennerholm L. CSF monoamines in autistic syndromes and other pervasive dev. disorders of early childhood. Br J Psychiatry 1987; (151): 89-94. 178 Ernst M., Zametkin A. J., Matochik J. A., Pascualvaca D., Cohen R. M. Low medial prefrontal dopaminergic activity in autistic children. Lancet 1997; 350(9078): 638. 179 Leboyer M., Philippe A., Bouvard M., et al. Whole blood serotonin and plasma beta-endorphin in autistic probands and their first-degree relatives. Biol Psycatry 1999; 45(2): 158-163. 180 Ornitz E. M. Neurophysiologic studies of infantile autism. Handbook of Autism and Pervasive Developmental Disorders. John Wiley & Sons, Inc., 1987: 148-165. 181 Schuler A. L. Thinking in autism: differences in learning and development. Teaching Children with Autism. Kathleen Ann Quill, ed., 1995: 11-32

From The Web ...http://www.pp.okstate.edu/ehs/training/mercury.htm Exposure to any form of mercury on a repeated basis, or even from a single, very high exposure can lead to the disease of chronic mercury poisoning. There are three main symptoms:

1. Gum problems. The gums become soft and spongy, the teeth get loose, sores may develop, and there may be increased saliva.

2. Mood and mental changes. People with chronic mercury poisoning often have wide swings of mood, becoming irritable, frightened, depressed or excited very quickly for no apparent reason. Such people may become extremely upset at any criticism, lose all self-confidence, and become apathetic. Hallucinations, memory loss and inability to concentrate can occur.

3. Nervous system. The earliest and most frequent symptom is a fine tremor (shaking) of the hand. A tremor may also occur in the tongue and eyelids. Eventually this can progress to trouble balancing and walking.

http://www.townhall.westwood.ma.us/human/boh/index_boh.html Mercury is a neurotoxin. Exposure to high levels can cause permanent damage to the brain and kidneys, as well as causing harm to the developing fetus. Mercury accumulates in the brain and kidneys. Exposure to mercury can cause personality changes, tremors, changes in vision, loss of sensation and memory. Small amounts of mercury can have serious impact on the environment. Mercury evaporates easily and travels in the atmosphere, and is deposited into soil and water. The mercury that enters lakes, ponds rivers and oceans accumulates in fish tissue and concentrates as larger fish eat smaller fish.

http://www.algonet.se/~leif/fummwr19.html Villanacci JF et al. Mercury Poisoning Associated with Beauty Cream - Texas, New Mexico, and California, 1995 - 1996 MMWR 45(19):400-403 (1996) Mercury Poisoning — Continued The Texas Department of Health (TDH), New Mexico Department of Health (NMDH), and San Diego County Health Department (SDCHD) recently investigated three cases of mercury poisoning among persons who had used a beauty cream produced in Mexico. The investigations implicated the beauty cream as the source of the mercury. The cream, marketed as "Crema de Belleza - Manning," lists "calomel" (mercurous chloride) as an ingredient and was found to contain 6%-8% mercury by weight. This report summarizes the ongoing investigation of these and other possible cases. Case 1: In September 1995, a previously healthy 15-year-old boy who resided in Texas near the Mexico border had onset of fatigue, weakness, insomnia, myalgias of his extremities, severe headache, sore throat, cough, constipation, and paresthesias of his feet and hands. On September 16, a physician in Piedras Negras, Mexico, prescribed symptomatic treatment for the paresthesia and cough. Subsequent problems included loss of taste, weight loss of approximately 15 pounds, and progressive weakness in his arms and legs. A neurologist in Piedras Negras performed an electromyogram and measured nerve-conduction velocities that were consistent

with a demyelinating polyneuropathy. In early November 1995, the patient was evaluated at a hospital in San Antonio, Texas, where a magnetic resonance imaging (MRI) scan of his brain was normal. Findings on examination by a pediatric neurologist included intact cranial nerve function, diffusely decreased deep tendon reflexes, and mild weakness of the lower extremities. On November 3, his blood lead and urine arsenic levels were normal; however, a urine mercury level was 178 mg/L (normal range: 0-20 mg/L), and chelation therapy was initiated on December 7. TDH conducted an environmental assessment of the patient's home in mid-December and did not detect mercury in indoor air, indoor paint, or soil. Family members reported that they ate fish from Mexico once or twice per year and denied hobbies at home or school known to be associated with mercury exposure. However, a container of cream ("Crema de Belleza-Manning") that was used regularly by the patient for treatment of acne had "calomel" listed as an ingredient. Elevated mercury levels (approximately 6% by weight) were confirmed in that container and in a second previously unopened container of the cream. The patient had been using the cream daily since June and was advised to discontinue use. Case 2: In April 1996, a neurologist in El Paso, Texas, diagnosed mercury poisoning in a 35-year-old woman who resided in New Mexico; urinary mercury levels were 355 mg/g creatinine (normal: 0-25 mg/g creatinine). Beginning in September 1995, the patient had onset of symptoms progressing to paresthesias (left forearm, right leg, and ear), irritability, and insomnia by March 1996. A collaborative investigation by the NMDH and TDH indicated that the woman had used "Crema de Belleza-Manning" for approximately 10 years and had no other known exposures to mercury. She was immediately advised to discontinue use of the cream. Case 3: On May 7, 1996, SDCHD identified mercury poisoning in a 33-year-old woman who resided in San Diego, California; urinary mercury levels were 143 mg/g creatinine. During 1992-1996, the woman had had weekly severe migraine headaches of 3-4 days duration, irritability, fatigue, short-term memory loss, night blindness, and inability to eat products from tin cans because of overt metal taste. Since 1990, the patient had been using "Creme de Belleza-Manning" daily on her face, hands, and chest and had no other known exposures to mercury. She was immediately advised to discontinue use of the cream.

Follow-Up Investigation and Control Measures TDH and the California Department of Health Services (CDHS) are investigating additional cases of possible mercury poisoning related to the use of "Crema de Belleza-Manning."

On April 19, TDH issued press releases recommending that persons discontinue use of "Crema de Belleza-Manning" and that persons with potential manifestations of mercury poisoning or who were exposed to the product consult their physicians. Physicians were advised to contact local poison-control centers regarding the medical management of patients exposed to mercury.

In addition, because the cream is considered hazardous waste, TDH recommends that cream be disposed of in a manner consistent with the proper disposal of hazardous household waste such as batteries or paint. CDHS will issue similar recommendations. For disposal instructions, commercial retailers with remaining stock can contact Paul Thomas, U.S. Environmental Protection Agency, telephone (214) 665-6707.

During April 22-30, 1996, the Mexican Secretary of Health seized 35,000 containers of "Crema de Belleza-Manning" in the State of Tampaulipas, Mexico, for testing at the National Public Health Laboratory. Laboratory analyses confirmed high levels of mercury (approximately 8% by weight) in the cream. As a result, the Mexican Secretary of Health issued an epidemiologic alert to all northern border states of Mexico to enhance surveillance for cases of acute or chronic mercury intoxication.

Reported by: JF Villanacci, PhD, R Beauchamp, MD, DM Perrotta, PhD, Bur of Epidemiology; K Hendricks, MD, Bur of Communicable Disease Control; M Rodriguez, MD, Office of Border Health; RJ Dutton, PhD, Environmental and Consumer Health; K Sutton, MS, Public Health Region 8; J Duran, Public Health Region 9/10; DM Simpson, MD, State Epidemiologist, Texas Dept of Health. K Richards, Office of Border Health; D Nelson, Div of Epidemiology, Evaluation, and Planning; F Crespin, MD, Public Health Div; CM Sewell, DrPh, State Epidemiologist, New Mexico Dept of Health. M Bartzen, M Ginsberg, MD, San Diego County Health Dept, San Diego; L Senini, Office of Border Health, F Nava, S Richardson, S Waterman, MD, State Epidemiologist, California Dept of Health Svcs. MG Lombera, MD, MA Ruíz, MD, P Cravioto, MS, Director General of Epidemiology, Ministry of Health; O Saldate, National Laboratory of Public Health, Ministry of Health; G Flores, MD, Health Svcs of Tampaulipas, Mexico. Environmental Hazards Epidemiology Section, Health Studies Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health; Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note: Although the product associated with these three reported cases of mercury poisoning is sold primarily in Mexico, the ongoing investigation also is assessing reports that the product may be sold in the United States in

some border-area shops. Furthermore, some U.S. residents residing in the border-area frequently travel to Mexico to purchase pharmaceuticals for use in the United States. The product label is printed in Spanish and lists "calomel" (i.e., mercurous chloride) as an ingredient, but does not indicate the concentration. Because mercury compounds are readily absorbed through the skin, Food and Drug Administration regulations restrict the use of these compounds as cosmetic ingredients: specifically, mercury can be used only as a preservative in eye-area cosmetics at concentrations not exceeding 65 ppm (0.0065%); no effective and safe nonmercurial substitute preservative is available for use in such cosmetics.

Urinary mercury concentrations over 20 mg/L or over 25 mg/g creatinine have been associated with signs and symptoms of mercury poisoning. Chronic exposure to mercury salts can result in central nervous system toxicity, including personality changes; nervousness; irritability; tremors; weakness; fatigue; loss of memory; changes in or loss of hearing, vision, or taste ( 1 ); gingivitis; stomatitis; and excessive salivation. In children, mercury poisoning can result in the syndrome of acrodynia, which is characterized by severe leg cramps, irritability, paresthesias, excessive perspiration, pruritus, and painful redness and peeling of the palms of the hands and soles of the feet. Acute poisoning with mercury salts can result in a metallic taste, nausea, vomiting, bloody diarrhea, severe abdominal pain, and tenesmus. Renal damage may include acute tubular necrosis and excessive protein, casts, and red blood cells in the urine. Additional information about mercury poisoning is available from local poison-control centers.

Reference 1. Agency for Toxic Substances and Disease Registry. Toxicological profile for mercury. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Diseases Registry, May 1993.

http://www.calpoison.org/public/mercury.html

What are the signs and symptoms of organic mercury poisoning?

Organic mercury compounds are very damaging. They are toxic by ingestion, inhalation, and skin and eye contact. These mercury compounds can attack all body systems. They can cause nausea, vomiting, lack of appetite, weight loss, abdominal pain, diarrhea, kidney failure, skin burns and irritation, respiratory distress, swollen gums and mouth sores, drooling, numbness and tingling in the lips, mouth, tongue, hands and feet, tremors and incoordination, vision and hearing loss, memory loss, personality changes and headache. Allergic reactions can also occur.

How does long-term exposure differ from a short-term exposure?

Long-term exposure (usually work-related) of inhaled vapors is generally more dangerous than a one-time short exposure. After long-term inhalation exposure, the nervous system is the main target of toxicity. Symptoms may occur within weeks but usually develop insidiously over a period of years. Neurologic symptoms include tremors, headaches, short-term memory loss, incoordination, weakness, loss of appetite, altered sense of taste and smell, numbness and tingling in the hands and feet, insomnia, and excessive sweating. Psychiatric effects are also seen after long-term exposure. Acrodynia can result from repeated exposures to mercury-containing latex paint fumes. Acrodynia is usually seen in younger children. The symptoms include chills, sweating, body rash, irritability, sleeplessness, leg cramps, swelling of the cheeks, nose, hands and feet, light-sensitivity to the eyes and peeling skin layers on the palms of the hands and soles of the feet.

Methyl-mercury, usually from contaminated food, is very dangerous to pregnant women. Methyl-mercury causes profound mental retardation, cerebral palsy, seizures, spasticity, tremors, and incoordination, along with eye and hearing damage in the unborn baby as a result of the mother's exposure. Organic mercury passes into the breast milk as well.

How do I clean up a small spill of elemental mercury? Many people have called the Poison Center asking how to clean up the mercury from a broken thermometer. There are several different ideas on how and how not to clean up the mercury beads. Experts agree on the ways NOT to clean up a spill: Do not sweep the area with a broom. Sweeping breaks the mercury into smaller droplets, further contaminating the room and the broom. Vacuuming vaporizes the mercury and increases the concentration of mercury in the air. NOTE: If you are wearing gold jewelry, either remove the jewelry or wear good protective gloves. If the liquid mercury contacts the gold jewelry, the mercury bonds permanently to the gold and ruins it.

Mercury occurs naturally in the environment as mercuric sulfide, also known as cinnabar. It is also present in some fossil fuels. Cinnabar has been refined for its mercury content since the 15th or 16th century B.C. Its health hazards have been known at least since the roman conquest of Spain. Due to the toxicity of mercury in cinnabar, criminals sentenced to work in quicksilver mines by the Romans had a life expectancy of only 3 years.

Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and cannot be broken down into less hazardous compounds. Elemental or inorganic forms can be transformed into organic (especially methylated) forms by biological systems. Not only are these methylated mercury compounds toxic, but highly bioaccumulative as well. The increase in mercury as it rises in the aquatic food chain results in relatively high levels of mercury in fish consumed by humans. Widespread poisoning of Japanese fisherman and their families occurred in Minamata, Japan in the 1950's as a result of consumption of methyl mercury contaminated fish. Today, we continue to be exposed to mercury in our diets, primarily from fish and shellfish. As a result, the U.S. Food and Drug Administration (FDA) has an action level for mercury of 1 part per million (ppm) in fish and the Michigan Department of Public Health issues fish consumption advisories to anglers when mercury levels exceed 0.5 ppm in fish tissue.

Widespread industrial production of mercury, along with lack of careful handling and disposal practices, has contributed to environmental contamination. The U.S. Environmental Protection Agency (EPA) has made efforts to regulate the continued release of mercury into the environment. EPA regulates industrial discharges to air and water, as well as regulating some aspects of mercury waste disposal. In 1976, EPA banned most pesticide uses of mercury - with the exceptions of fungicidal uses in paints and outdoor fabrics, and for control of Dutch Elm disease. In 1990, mercury use as a fungicide in interior latex paint was halted by the EPA. This action stemmed from requests by Michigan officials after a child was poisoned from over formulated mercury-containing paint used in his home. More recently, the use of mercury compounds in exterior latex paint has also been halted.

In addition to the early workers in the cinnabar mines, modern workers in industries using mercury are at risk from overexposure. More than 0.5 parts per million of mercury in eggs is considered sufficient to prevent hatching. 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. 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). Mercury in blood may also be transferred to breast milk. 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. 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.