TOXIC HEAVY METALS SOURCES AND EFFECTS

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TOXIC HEAVY METALS:  SOURCES AND EFFECTS

Heavy metal toxins contribute to a variety of adverse health effects. There

exist over 20 different heavy metal toxins that can impact human health and

each toxin will produce different behavioral, physiological, and cognitive

changes in an exposed individual. The degree to which a system, organ, tissue,

or cell is affected by a heavy metal toxin depends on the toxin itself and the

individual's degree of exposure to the toxin. Here are presented just 5 of the

many hazardous metal toxins that are commonly encountered by humans. Each of

these metals affects an individual in such a way that its respective

accumulation within the body leads to a decline in the mental, cognitive, and

physical health of the individual. The specific sources of exposure, where the

metals tend to be deposited and the adverse health effects of each metal are

identified below.

1. Aluminum

Sources of exposure: Aluminum is a naturally occurring metal that has been

utilized by humans for a number of years. It is the third most abumdant element in the earth's crust (approximately 8% of

the crust is composed of aluminum compounds) and is apparent is small

quantities (from 3-2400 ppb) in seawater (Venugopal

and Luckey, 1978). Incidences of acid rain on the

planet have increased the availability of aluminum to various biological

systems. Acid rain is able to dissolve aluminum compounds that are naturally

found in soil and rock, thus increasing their prevalence in soils and fresh-

and salt-water sources. Because of this, aluminum concentrations can be seen in

various fresh and salt-water marine life, and in

plants that have been grown in aluminum laden soil. Humans have processed

aluminum compounds for years, and its use is apparent in many different forms

of industry. Because of its many industrial and commercial uses, aluminum is

consumed and/or handled by many individuals on a daily basis. Today aluminum

can be found in cookware, aluminum foil, dental cements, dentures, leather

tanning preparations, antacids, antiperspirants, appliances, baking powder,

buffered aspirin, building materials, canned acidic foods, food additives,

lipsticks, construction materials (the automotive, aviation and electrical

industries all use aluminum compounds for various uses), prescription and

over-the-counter drugs (anti-diarrhea agents, hemorrhoid medications, vaginal

douches), dialysates, vaccines, processed cheese,

paints, toothpaste, fireworks and " softened " and normal tap water

(ATSDR 1990, Wills and Savory, 1985). Aluminum has been found in at least 489

of the 1,416 (34%) National Priorities List (NPL) sites

identified by the Environmental Protection Agency (EPA) (ATSDR 1995).

Target

tissues: Aluminum accumulates in the brain, muscles, liver lungs, bones,

kidneys, skin, reproductive organs and stomach (ATSDR 1990, Wills and Savory,

1985). Depending on the source of exposure, aluminum can be absorbed through

the gastrointestinal (GI) tract or the lungs. Absorption through the GI tract

is slow, due primarily to pH factors, but once absorbed it is distributed to

the bones, liver, testes, brain and soft tissues. Following aluminum

inhalation, deposition occurs primarily within the lungs (Venugopal

and Luckey, 1978).

Signs and Symptoms: Aluminum toxicity can produce a number of clinical signs

and symptoms. Common are excessive headaches, abnormal heart rhythm, depression, numbness of the hands and feet and blurred

vision (Kilburn and Warshaw, 1993). Aluminum toxicity

has been shown to produce impairment in choice reaction time, long-term memory,

psychomotor speed, and recall in affected individuals as compared to controls

(Wills and Savory 1985). Animal studies have shown similar impairment in locomotor activity/response and spatial learning in rats

receiving dietary aluminum for a period of 12 weeks (Commissaris

et al., 1982). In a study conducted with patients receiving dialysis for renal

failure, aluminum was believed to be a causal agent in the development of

dialysis encephalopathy (or " dialysis dementia " ), a special form of

bone disease known as osteomalacic dialysis osteodystrophy, and anemia (Wills and Savory, 1985). In

this study, individuals had been receiving concentrations of aluminum directly

from their dialysate. Similarly, long-term hemo-dialysis patients have exhibited a progressive

neurological syndrome that includes speech disorders, dementia, myoclonus and encephalopathy (Perl

and Brody, 1980). Evidence suggests that inhaled aluminum may contribute to the

development of pulmonary fibrosis and, to a lesser degree, pulmonary granulomatosis (ATSDR 1990).

Aluminum may be involved in a myriad of neurodegenerative diseases. Dr.

McLaughlin, MD, F.R.C.P., a professor of physiology and medicine and the

director of the Centre for Research in Neurodegenerative Diseases at the University

of Toronto, states:

" Concentrations of aluminum that are toxic to many biochemical processes

are found in at least ten human neurological conditions " (Crapper-McLachlan 1980). Recent studies suggest that aluminum may

be involved in the progression of Alzheimer's Diseae,

Parkinson's disease, Guam ALS-PD complex, " Dialysis dementia " ,

Amyotrophic Lateral Sclerosis (ALS), senile and presenile

dementia, neurofibrillary tangles, clumsiness of

movements, staggering when walking and an inability to pronounce words properly

(Berkum 1986; Goyer 1991;

Shore and Wyatt, 1983). To date, however, we do not completely understand the

role that aluminum plays in the progression of such human degenerative

syndromes.

Chronic aluminum exposure has contributed directly to hepatic failure, renal

failure, and dementia (Arieff et al., 1979). Other

symptoms that have been observed in individuals with high internal

concentrations of aluminum are colic, convulsions, esophagitis,

gastroenteritis, kidney damage, liver dysfunction, loss of appetite, loss of

balance, muscle pain, psychosis, shortness of breath, weakness, and fatigue

(ATSDR 1990). Behavioral difficulties among schoolchildren have also been

correlated with elevated levels of aluminum and other neuro-toxic

heavy metals (Goyer 1991). And, aluminum toxicity may

also cause birth defects in new-borns (ATSDR 1990).

Medical

tests for aluminum screening: Blood, urine, feces, hair, and fingernails.

2. Arsenic 

Sources of exposure: The use of this toxic element in numerous industrial

processes has resulted in its presence in many biological and ecological

systems. Ground, surface, and drinking water are susceptible to arsenic

poisoning from the use of arsenic in smelting, refining, galvanizing and power

plants; environmental contaminants like pesticides, herbicides, insecticides,

fungicides, desiccants, wood preservatives, and animal feed additives; and

human made hazardous waste sites, chemical wastes and antibiotics. Arsenic

concentrations are apparent in the air as a result of the burning of arsenic

containing materials such as wood, coal, metal alloys, and arsenic waste (ATSDR

1989; Morton and Caron, 1989). Arsenic concentrations can also be found in

specialty glass, defoliants, marine life (primarily fish and shellfish) and

riot-control gas (Hine et al., 1977). Arsenic is

present in at least 781 of the 1,300 (60%) NPL sites as identified by the EPA

(RAIS 1992).

Target

tissues: Many arsenic compounds are readily absorbed through the GI tract when

delivered orally in humans. Absorption within the lungs is dependent upon the

size of the arsenic compound, and it is believed that much of the inhaled

arsenic is later absorbed through the stomach after (respiratory) mucocillary clearance (ATSDR 1989). After the absorption of

arsenic compounds, the primary areas of distribution are the liver, kidneys,

lung, spleen, aorta, and skin. Arsenic compounds are also readily deposited in

the hair and nails (U.S. EPA, 1984).

Signs and

Symptoms: Arsenic is a highly toxic element that has been used historically for

purposes of suicide and homicide. Its health effects are well known and

multiform. Acute exposure to arsenic compounds can cause nausea, anorexia,

vomiting, abdominal pain, muscle cramps, diarrhea and burning of the mouth and

throat (ATSDR 1989). Garlic-like breath, malaise, and fatigue have also been

seen in individuals exposed to an acute dose of arsenic, while contact

dermatitis, skin lesions and skin irritation are seen in individuals whom come

into direct tactile contact with arsenic compounds (Feldman et al., 1979). A

large, acute oral dose has caused tachycardia, acute encephalopathy, congestive

heart failure, stupor, convulsions, paralysis, coma and even death (Morton and

Caron 1989). Animal studies have shown similar acute effects when arsenic

compounds were delivered orally to Rhesus monkeys (Heywood and Sortwell, 1979). Repeat exposure to arsenic compounds have

been shown to lead to the development of peripheral neuropathy, encephalopathy,

cardiovascular distress, peripheral vascular disease, EEG abnormalities, Raynaud's phenomenon, gangrene of the lower legs

( " Black foot disease " ), acrocyanosis,

increased vasopastic reactivity in the fingers,

kidney and liver damage, hypertension, myocardial infarction, anemia and leukopenia (ATSDR 1989; Blom et

al., 1985; Feldman et al., 1979; Heyman et al., 1956;

Hine et al., 1977; Langerkvist

et al., 1986; Morton and Caron, 1989). Other chronic effects of arsenic

intoxication are skin abnormalities (darkening of the skin and the appearance

of small " corns " or " warts " on the palms, soles, and

torso), neurotoxic effects, chronic respiratory

diseases (pharyngitits, laryngitis, pulmonary insufficiency), neurological disorders, dementia,

cognitive impairment, hearing loss and cardiovascular disease (Blom et al., 1985; and Pease, 1965; Morton and Caron,

1989). A significantly higher percentage of spontaneous abortions has been shown in a population living near a copper smelting

plant; lower birth weights of babies born to this same population are seen, and

an abnormal percentage of male to female births is also apparent, suggesting

that arsenic affects babies in utero (Nordstrom et

al., 1979).

Studies have shown close associations between both inhaled and ingested arsenic

and cancer rates. Cancers of the skin, liver, respiratory tract and

gastrointestinal tract are well documented in regards to arsenic exposure (IARC

1980; Lee-Feldstein 1989). Several arsenic compounds have been classified by

the US Environmental Protection Agency as a Class A- Human Carcinogen (IARC

1987).

Medical

test for arsenic screening: Urine (best), hair and fingernails.

3. Copper

Sources

of exposure: Copper occurs naturally in elemental form and as a component of

many different compounds. The most toxic form of copper is thought to be that

in the divalent state, cupric (Cu2+). Because of its high electrical

conductivity, copper is used extensively in the manufacturing of electrical

equipment and different metallic alloys. Copper is released into the

environment primarily through mining, sewage treatment plants, solid waste

disposal, welding and electroplating processes, electrical wiring materials,

plumbing supplies (pipes, faucets, braces, and various forms of tubing), and

agricultural processes (ATSDR 1990a). It is present in the air and water due to

natural discharges like volcanic eruptions and windblown dust. Drinking water

sources become contaminated with copper primarily because of its use in many

different types of plumbing supplies. It is a common component of fungicides

and algaecides, and agricultural use of copper for these purposes can result in

its presence in soil, ground water, farm animals (grazing animals like cows,

horses, etc.) and many forms of produce (ATSDR 1990a). Copper is also present

in ceramics, jewelry, monies (coins) and pyrotechnics (ACGIH 1986). Though

copper is an essential trace element required by the body for normal

physiological processes, increased exposure to copper containing substances can

result in copper toxicity and a wide variety of complications.

Target

tissues: Absorption of copper occurs through the lungs, gastrointestinal tract

and skin (U.S. EPA, 1987). The degree to which copper is absorbed in the

gastrointestinal tract largely depends upon its chemical state and the presence

of other compounds, like zinc (U.S.A.F., 1990). Once absorbed, copper is

distributed primarily to the liver, kidneys, spleen, heart, lungs, stomach,

intestines, nails, and hair. Individuals with copper toxicity show an

abnormally high level of copper in the liver, kidneys, brain, eyes and bones

(ATSDR 1990a).

Signs and

symptoms: Acute toxicity of ingested copper is characterized by abdominal pain,

diarrhea, vomiting, tachycardia and a metallic taste in the mouth. Continued

ingestion of copper compounds can cause cirrhosis and other debilitating liver

conditions (Mueller-Hoecker et al., 1989). Inhaled

copper dust or fumes can produce eye and respiratory tract irritation,

headaches, vertigo, drowsiness, chills, fever, aching muscles and discoloration

of the skin and hair in humans (U.S.A.F., 1990). Vineyard workers exposed to

copper fumes for a long period of time developed pulmonary fibrosis and granulomas of the lungs, liver impairment and liver disease

(cirrhosis, fibrosis, and various morphological changes). Similar results were

obtained in animals chronically exposed to copper containing dust and fumes

(Johansson et al., 1984; Stockinger 1981). Further

animal studies on copper toxicity have shown varying degrees of liver and

kidney damage (necrosis of the kidney; sclerosis, necrosis, and cirrhosis of

the liver), decreased total weight, brain weight and red blood cell count,

increased platelet counts and the presence of gastric ulcers (Kline et al.,

1977; Rana and Kumar, 1978). Copper also appears to

affect reproduction and development in humans and animals. Offspring of

hamsters that received copper sulfate injections while pregnant exhibited

increased incidences of hernias, encephalopathy, abnormal spinal curvature and spina bifida (Ferm and Hanlon,

1974). Sperm motility also appears to be compromised by the presence of copper

in human spermatozoa (Battersby and Morton, 1982).

Chronic exposure to copper can produce numerous physiological and behavioral

disturbances. Copper toxicity has been characterized in patients with 's Disease, a genetic disorder that causes an abnormal

accumulation of copper in body tissue. 's disease is fatal unless treated

in time. Manifestations of 's Disease include

brain damage and progressive demylination, psychiatric

disturbances-- depression, suicidal tendencies and aggressive behavior--

hemolytic anemia, cirrhosis of the liver, motor dysfunction and corneal

opacities (ATSDR 1990a; Goyer, 1991a; U.S. EPA,

1987). Some patients may also experience poor coordination, tremors, disturbed

gait, muscle rigidity, and myocardial infarction (ATSDR 1990a).

Medical tests for copper screening: Blood, urine, and hair.

4. Lead

Sources of exposure: Lead is the 5th most utilized metal in the U.S.

It is mined extensively in Missouri,

Colorado, Idaho,

and Utah and is used for the

production of ammunition, bearing metals, brass materials, solder, ballasts,

tubes, containers, gasoline products, ceramics, and weights (ATSDR 1993). Human

exposure to lead occurs primarily through drinking water, airborne

lead-containing particulates and lead-based paints. Several industrial

processes create lead dust/fumes, resulting in its presence in the air. Mining, smelting and manufacturing processes, the burning of fossil

fuels (especially lead-based gasoline) and municipal waste and incorrect

removal of lead-based paint results in airborne lead concentrations.

After lead is airborne for a period of ten days, it falls to the ground and

becomes distributed in soils and water sources (fresh and salt water, surface

and well water, and drinking water). However, the primary source of lead in

drinking water is from lead-based plumbing materials (U.S. EPA, 1989). The

corrosion of such materials will lead to increased concentrations of lead in

municipal drinking water. Lead from water and airborne sources have been shown

to accumulate in agricultural areas, leading to increased concentrations in

agricultural produce and farm animals (ATSDR 1993). Cigarette smoke is also a

significant source of lead exposure; people whom smoke tobacco, or breath in

tobacco smoke, may be exposed to higher levels of lead than people whom are not

exposed to cigarette smoke (RAIS 1994).

Target

tissues: Lead is absorbed into the body following inhalation or ingestion.

Children absorb lead much more efficiently than adults do after exposure, and

ingested lead is more readily absorbed in a fasting individual (U.S.EPA 1986).

Over 90% of inhaled lead is absorbed directly into the blood. After lead is

absorbed into the body, it circulates in the blood stream and distributes

primarily in the soft tissues (kidneys, brain and muscle) and bone. Adults

distribute about 95% of their total body lead to their bones, while children

distribute about 73% of their total body lead to their bones (U.S. EPA, 1986a).

Signs and

Symptoms: Lead is one of the most toxic elements naturally occurring on Earth.

High concentrations of lead can cause irreversible brain damage

(encephalopathy), seizure, coma and death if not treated immediately (U.S. EPA,

1986). The Central Nervous System (CNS) becomes severely damaged at blood lead

concentrations starting at 40mcg/dL, causing a reduction in nerve conduction

velocities and neuritis (ATSDR 1993). Neuropsychological impairment has been

shown to occur in individuals exposed to moderate levels of lead. Evidence

suggests that lead may cause fatigue, irritability, information processing

difficulties, memory problems, a reduction in sensory

and motor reaction times, decision making impairment, and lapses in concentration

(Ehle and McKee, 1990). At blood concentrations above 70 mcg/dL, lead has been

shown to cause anemia, characterized by a reduction in hemoglobin levels, and erythropoiesis-- a shortened life span of red blood cells (Goyer, 1988; US EPA 1986a). In adults, lead is very

detrimental to the cardiovascular system. Occupationally exposed individuals

tend to have higher blood pressure than normal controls (Pocock

et al., 1984; Harlan et al., 1985; Landis and Flegal,

1988), and are at an increased risk for cardiovascular disease, myocardial

infarction, and stroke (US EPA, 1990). The kidneys are targets of lead toxicity

and prone to impairment at moderate to high levels of lead concentrations.

Kidney disease, both acute and chronic nephropathy, is a characteristic of lead

toxicity (Goyer, 1988). Kidney impairment can be seen

in morphological changes in the kidney epithelium, increases in the excretion

rates of many different compounds, reductions in glomerular

filtration rate, progressive glomerular, arterial,

and arteriolar sclerosis, and an altered plasma albumin ratio (Goyer, 1985, 1988; Landigran,

1989). Chronic nephropathy has lead to increased death rates among

occupationally exposed individuals as compared to controls in studies by Selevan et al. (1975) and et al. (1985). Other

signs/symptoms of lead toxicity include gastrointestinal disturbances-abdominal

pain, cramps, constipation, anorexia and weight loss-immunosuppression,

and slight liver impairment (ATSDR, 1993; US EPA, 1986a).

Children are susceptible to the most damaging effects of lead toxicity. Ample

literature exists that shows just how damaging lead is

to children. Prenatal and postnatal development are

compromised significantly by the presence of lead in the body. At blood lead

concentrations of 80-100 mcg/dL, severe

encephalopathy occurs. Those children who survive lead-induced encephalopathy

typically suffer permanent brain damage marked by mental retardation and

numerous behavioral impairments. These children also suffer slower neural conduction

velocities, peripheral neuropathy, cognitive impairment, and personality

disorders (US EPA 1986a). Tuthill (1996) has found

that hair lead levels in children were positively correlated with

attention-deficit and hyperactive behavior. Numerous studies have implicated

lead as a causal agent in the deterioration of cognitive functioning in

children. Studies by Schroeder and Hawk (1986), Burchfield et al. (1980), Otto

et al. (1981, 1982), and Munoz et al. (1993) have shown IQ deficits in children

with blood lead concentrations from 6-70 mcg/dL.

Longitudinal studies have given further evidence that lead affects intelligence

in exposed children. Studies by Vimpani et al.

(1989), Mc et al. (1988) and Wigg et al.

(1988) have shown decreased performance on intelligence tests in lead exposed

school children. One study has correlated lower socio-economic status with

childhood lead poisoning 50 years after lead exposure (White et al., 1993).

Maternal blood lead concentrations and prenatal lead exposure appear to be

strong predictors of cognitive performance in offspring. Prenatal exposure may

also cause birth defects, miscarriage, spontaneous abortion and underdeveloped

babies (Goyer, 1988; Mc et al., 1988; US EPA

1986d). Lead not only appears to affect cognitive development of young

children, but also other areas of neuropsychological function. Young children

exposed to lead may exhibit mental retardation, learning difficulties,

shortened attention spans (ADHD), increased behavioral problems (aggressive

behaviors) and reduced physical growth (Bellinger, D.

et al., 1990, 1992). Lead has been determined by many health experts to be the

#1 threat to developing children in our industrial societies.

Medical

test for lead screening: Blood, urine, and hair.

5. Mercury

Sources of exposure: Mercury occurs primarily in two forms: organic mercury and

inorganic mercury. Inorganic mercury occurs when elemental mercury is combined

with chlorine, sulfur, or oxygen. Inorganic mercury and elemental mercury are

both toxins that can produce a wide range of adverse health affects. Inorganic

mercury is used in thermometers, barometers, dental fillings, batteries,

electrical wiring and switches, fluorescent light bulbs, pesticides,

fungicides, vaccines, paint, skin-tightening creams, vapors from spills,

antiseptic creams, pharmaceutical drugs and ointments (ATSDR, 1989a). Inorganic

mercury vapor is at high concentrations near chlorine-alkali plants, smelters,

municipal incinerators and sewage treatment plants. The organic form occurs

when mercury is combined with carbon. The most common form of organic mercury

is methyl mercury, which is produced primarily by small organisms in water and

soil when they are exposed to inorganic mercury. Humans also have the ability

to convert inorganic mercury to an organic form once it has become absorbed

into the bloodstream. Organic mercury is known to bioaccumulate--

or pass up the food chain due an organism's inability

to process and eliminate it. It is found primarily in marine life (fish), and

can often be found in produce and farm animals, processed grains and dairy

products, and surface, salt-, and fresh water sources (ATSDR, 1989a; Brenner

and Snyder, 1980). Occupational exposure to mercury containing compounds

presents a significant health risk to individuals. Dentists, painters,

fisherman, electricians, pharmaceutical/laboratories workers, farmers, factory

workers, miners, chemists and beauticians are just some of the professions

chronically exposed to mercury compounds.

Target

tissues: The absorption and distribution of mercury compounds depends largely

upon its chemical state. Organic mercury compounds are absorbed from the

gastrointestinal tract more readily than inorganic mercury compounds, with the

latter being very poorly absorbed. After absorption in the gastrointestinal

tract, organic mercury is readily distributed throughout the body but tends to

concentrate in the brain and kidneys (Goyer, 1991b).

Approximately 80% of mercury vapor is absorbed directly through the lungs and

distributed primarily to the CNS and the kidneys (Friberg

and Nordberg, 1973). Inorganic and organic forms of mercury have also been seen

in the red blood cells, liver, muscle tissue, and gall bladder ( et

al., 1991, Dutczak et al., 1991, ATSDR 1989a).

Signs and

symptoms: Mercury exposure can result in a wide variety of human health

conditions. The degree of impairment and the clinical manifestations that

accompany mercury exposure largely depend upon its chemical state and the route

of exposure. While inorganic mercury compounds are considered less toxic than

organic mercury compounds (primarily due to difficulties in absorption),

inorganic mercury that is absorbed is readily converted to an organic form by

physiological processes in the liver.

The acute ingestion of inorganic mercury salts may cause gastrointestinal

disorders such as abdominal pain, vomiting, diarrhea, and hemorrhage (ATSD

1989a). Repeated and prolongued exposure has resulted

in severe disturbances in the central nervous system, gastrointestinal tract,

kidneys, and liver. Daivs et al. (1974) reported

dementia, colitis, and renal failure in individuals chronically poisoned due to

the ingestion of an inorganic mercury containing laxative. Inhaled inorganic

mercury can cause a wide range of clinical complications in individuals

including corrosive bronchitis, interstitial pneumonitis,

renal disorders, fatigue, insomnia, loss of memory, excitability, chest pains,

impairment of pulmonary function and gingivitis (Goyer

1991b, ATSDR 1989a). Chronic inhalation of inorganic mercury compounds may

result in a reduction of sensory and motor nerve function, depression, visual

and/or auditory hallucinations, muscular tremors, sleep disorders, alterations

in autonomic function (heart rate, blood pressure, reflexes), impaired visuomotor coordination, speech disorders, dementia, coma

and death (son 1989; Goyer 1991b; Fawyer et al. 1983; Piikivi and Hanninen 1989; and Ngim et al.

1992). Ngim et al. (1992) have shown that a group of

dentists exposed to mercury vapors occupationally perform significantly worse

in neurobehavioral tests that measure motor speed, visual scanning, visuomotor coordination and concentration, verbal memory

and visual memory. Kishi et al. (1993) have found

that smelter workers exposed to inorganic mercury compounds continue to

experience neurological symptoms-tremors, headaches, slurred speech-senile

symptoms and diminished mental capacities eighteen years after the cessation of

mercury exposure.

Our understanding of the effects of methyl mercury poisoning comes primarily

from epidemic poisonings in Iraq and Japan. In iraq,

more than 6,000 individuals were hospitalized and 459 died as a result of

methyl mercury poisoning. Adults experienced symptoms including parasthesia, visual disorders, ataxia, fatigue, tremor,

hearing disorders (deafness) and coma (Bakir et al.,

1973; Mottet, Shaw, and Burbacher,

1985). Neuropahtologic observations of exposed

individuals have shown irreversible brain damage including neuronal necrosis,

cerebral edema, gliosis, and cerebral atrophy (Mottet, Shaw, and Burbacher,

1985). Iraqi children poisoned through the consumption of methyl mercury

containing food products (grains treated with mercury containing fungicides)

exhibited nervous system impairment, visual and auditory disorders, weakness,

marked motor and cognitive impairment, and emotional disturbances (Bakir et al., 1973; Bakir et al.,

1978). Individuals in Japan experienced many of these same symptoms after the

ingestion of fish containing large amounts of methyl mercury. Similarly,

autopsies conducted on deceased Japanese in the Minamata

Bay have shown pronounced brain lesions, cerebral atrophy, edema, and gliosis in the deeper fissures (sulci)

of the brain, such as in the visual cortex (Takeuchi 1968). The Japan and Iraq

epidemics have clearly established mercury as an agent that can disrupt

developmental processes in the unborn, and infantile, individual. Methyl

mercury can pass through the placental barrier and produce many deleterious

effects on the unborn fetus (Mottet, Shaw and Burbacher 1985). Children born to mercury poisoned mothers

were of smaller total weight, had decreased brain weights at birth, had fewer

nerve cells in the cerebral cortex, and experienced an abnormal pattern of

neuronal migration (Choi et al. 1978; Takeuchi 1968, Amin-Zake et al. 1974). Of those children that survived the

epidemic, many experienced severe developmental effects like impaired motor and

mental function, hearing loss, and blindness throughout their childhood (Amin-Zaki et al. 1974). Researchers have also observed a

heightened incidence of cerebral palsy in children born to mothers in the Minamata Bay (Matsumoto, Koya,

and Takeuchi 1965).

Mercury has recently been implicated as being a contributing factor to the

increasing prevalence of autism in American children. The Autism Research

Institute has focused on mercury containing vaccines (TMS) and their

relationship to autism. Over 2 million individuals are affected with autism, a

neurodevelopment syndrome that typically produces impairment in sociality,

communication, and sensory/perceptual processes, and recent evidence has found

a positive correlation between complications seen in autistics and

complications seen in mercury poisoned individuals (Bernard et al., 2000).

While it is difficult to ascribe causation in this case, it should not be

altogether dismissed. Mercury poisoning has been implicated in the development

of many other human dysfunctional states for many years. Among these are

cerebral palsy, amyotrophic lateral sclerosis, Parkinson's disease, psychosis,

and chronic fatigue syndrome ( et al., 1983; Bernard et al., 2000; Dales

1972).

Facts About

Mercury

1. Mercury is the most toxic non-radioactive element on

Earth.

2. A silver colored mercury amalgam filling normally contains

52% mercury

3. On average, amalgam filling weighs 1 gram and contains 1/2

gram of mercury

4. The typical adult carries ten amalgam fillings containing

about 5 grams of mercury

5. 1/2 gram of mercury in a ten acre lake would warrant

issuance of a fish advisory for the lake

6. Running shoes with mercury lights in their heels were

banned by the Minnesota Legislature in 1994 because they contained a 1/2 gram

of mercury in them and this was considered dangerous to public health

7. The use of mercury amalgams has been banned and are on a

scheduled phaseout in Germany, Austria, Denmark and

Sweden

8. A proposition passed in California in 1994 requires a

warning in dental offices using mercury amalgam stating that " the people

of the state of California have determined that the use of mercury in dental

amalgam causes birth defects and other health problems " The proposition

also requires that permission must be obtained from a patient before placing

hazardous material in the mouth. (The new law is being contested by the ADA and

California Dental Association and is tied up in Federal Court)

9. Legislation is now being proposed in Minnesota for a similar " Informed

Consent " legislation for all dental patients.

For

specific information regarding the source and effects of heavy metals not

listed above:  Antimony, Beryllium,

Bismuth, Cadmium, Nickel, Platinum, Thallium, Thorium, Tin, Tungsten, and Uranium,

please contact BioMark.

References:

ACGIH (American Conference of Governmental Industrial

Hygienists).

1986. Copper. In: Documentation of the Threshold Limit Values and Biological

Exposure Indices, 5th ed. ACGIH, Cincinnati, OH, p. 146.

, C.R., Ziegler, D.K., and Lin, J.T.

1983. Mercury intoxication simulating Amyotrophic Lateral Sclerosis.

JAMA 250: 642-643.

Amin-Zaki,

L., S. Elhassani, M.A. Majeed,

T. W. son, R.A. Doherty and M. Greenwood. 1974. Intra-uterine methylmercury poisoning. Pediatrics 54:587-595.

Arieff, A.L., , J.D., Armstrong, D., and Lazarowitz, V.C. 1979. Dementia, renal

failure, and brain aluminum. Ann. Intern. Med. 90: 741-747.

Bernard, S., Enayati, A., Redwood,

L., and Bistock, T. 2000. Autism: A novel form

of mercury poisoning. The Aurtism

Research Institute. http://www.autism.com/ari/mercury.html.

ATSDR (Agency for Toxic Substances and Disease Registry). 1989. Toxicological

Profile for Arsenic. Agency for Toxic Substances and Disease

Registry, U.S. Public Health Service,

Atlanta, GA. ATSDR/TP-88/02.

ATSDR (Agency for Toxic Substances and Disease Registry). 1989a.

Toxicological Profile for Mercury. ATSDR/U.S. Public

Health Service.

ATSDR (Agency for Toxic Substances and Disease Registry). 1990. Toxicological

Profile for Aluminum. Agency for Toxic Substances and Disease

Registry, U.S. Public Health Service,

Atlanta, GA ATSDR/TP-88/01.

ATSDR (Agency for Toxic Substances and Disease Registry). 1990a.

Toxicological Profile for Copper. Prepared by Syracuse

Research Corporation for ATSDR, U.S. Public Health Service

under Contract 88-0608-2. ATSDR/TP-90-08.

ATSDR (Agency for Toxic Substances and disease Registry). 1993. Toxicological

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