HEAVY METALS 1

ASSIGNMENT # 2
ENVIRONMENTAL SCIENCES
CHEMISTRY

TOPIC:
DESCRIBE THE HEAVY AND TOXIC
METALS IN THE ENVIRONMENT (LEAD, MERCURY,
CHROMIUM AND ARSENIC).

ASSIGNED BY:
Dr. TAHSEEN AMAN

ASSIGNED TO:
AMNA ADIL

MAJOR:
FOOD SCIENCES (SEMESTER 1)
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FOOD SCIENCES (SEMESTER 1)
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There are 35 metals that concern us because of occupational or residential exposure; 23 of these
are the heavy elements or "heavy metals": antimony, arsenic, bismuth, cadmium, cerium, chromium,
cobalt, copper, gallium, gold, iron, lead, manganese, mercury, nickel, platinum, silver, tellurium,
thallium, tin, uranium, vanadium, and zinc (Glanze 1996). Interestingly, small amounts of these
elements are common in our environment and diet and are actually necessary for good health, but
large amounts of any of them may cause acute or chronic toxicity (poisoning). Heavy metal toxicity
can result in damaged or reduced mental and central nervous function, lower energy levels, and
damage to blood composition, lungs, kidneys, liver, and other vital organs. Long-term exposure may
result in slowly progressing physical, muscular, and neurological degenerative processes that mimic
Alzheimer's disease, Parkinson's disease, muscular dystrophy, and multiple sclerosis. Allergies are
not uncommon and repeated long-term contact with some metals or their compounds may even cause
cancer (International Occupational Safety and Health Information Centre 1999).

For some heavy metals, toxic levels can be just above the background concentrations naturally
found in nature. Therefore, it is important for us to inform ourselves about the heavy metals and to
take protective measures against excessive exposure. In most parts of the United States, heavy
metal toxicity is an uncommon medical condition; however, it is a clinically significant condition when
it does occur. If unrecognized or inappropriately treated, toxicity can result in significant illness
and reduced quality of life (Ferner 2001). For persons who suspect that they or someone in their
household might have heavy metal toxicity, testing is essential. Appropriate conventional and
natural medical procedures may need to be pursued (Dupler 2001).

The association of symptoms indicative of acute toxicity is not difficult to recognize because the
symptoms are usually severe, rapid in onset, and associated with a known exposure or ingestion
(Ferner 2001): cramping, nausea, and vomiting; pain; sweating; headaches; difficulty breathing;
impaired cognitive, motor, and language skills; mania; and convulsions. The symptoms of toxicity
resulting from chronic exposure (impaired cognitive, motor, and language skills; learning difficulties;
nervousness and emotional instability; and insomnia, nausea, lethargy, and feeling ill) are also easily
recognized; however, they are much more difficult to associate with their cause. Symptoms of
chronic exposure are very similar to symptoms of other health conditions and often develop slowly
over months or even years. Sometimes the symptoms of chronic exposure actually abate from time
to time, leading the person to postpone seeking treatment, thinking the symptoms are related to
something else.

Definition of a Heavy Metal

"Heavy metals" are chemical elements with a specific gravity that is at least 5 times the specific
gravity of water. The specific gravity of water is 1 at 4°C (39°F). Simply stated, specific gravity is
a measure of density of a given amount of a solid substance when it is compared to an equal amount
of water. Some well-known toxic metallic elements with a specific gravity that is 5 or more times

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that of water are arsenic, 5.7; cadmium, 8.65; iron, 7.9; lead, 11.34; and mercury, 13.546 (Lide
1992).

Beneficial Heavy Metals

In small quantities, certain heavy metals are nutritionally essential for a healthy life. Some of these
are referred to as the trace elements (e.g., iron, copper, manganese, and zinc). These elements, or
some form of them, are commonly found naturally in foodstuffs, in fruits and vegetables, and in
commercially available multivitamin products (International Occupational Safety and Health
Information Centre 1999). Diagnostic medical applications include direct injection of gallium during
radiological procedures, dosing with chromium in parenteral nutrition mixtures, and the use of lead
as a radiation shield around x-ray equipment (Roberts 1999). Heavy metals are also common in
industrial applications such as in the manufacture of pesticides, batteries, alloys, electroplated
metal parts, textile dyes, steel, and so forth. (International Occupational Safety and Heath
Information Centre 1999). Many of these products are in our homes and actually add to our quality
of life when properly used.

Toxic Heavy Metals

Heavy metals become toxic when they are not metabolized by the body and accumulate in the soft
tissues. Heavy metals may enter the human body through food, water, air, or absorption through
the skin when they come in contact with humans in agriculture and in manufacturing, pharmaceutical,
industrial, or residential settings. Industrial exposure accounts for a common route of exposure for
adults. Ingestion is the most common route of exposure in children (Roberts 1999). Children may
develop toxic levels from the normal hand-to-mouth activity of small children who come in contact
with contaminated soil or by actually eating objects that are not food (dirt or paint chips) (Dupler
2001). Less common routes of exposure are during a radiological procedure, from inappropriate
dosing or monitoring during intravenous (parenteral) nutrition, from a broken thermometer (Smith
et al. 1997), or from a suicide or homicide attempt (Lupton et al. 1985).

As a rule, acute poisoning is more likely to result from inhalation or skin contact of dust, fumes or
vapors, or materials in the workplace. However, lesser levels of contamination may occur in
residential settings, particularly in older homes with lead paint or old plumbing (International
Occupational Safety and Health Information Centre 1999). The Agency for Toxic Substances and
Disease Registry (ATSDR) in Atlanta, Georgia, (a part of the U.S. Department of Health and Human
Services) was established by congressional mandate to perform specific functions concerning
adverse human health effects and diminished quality of life associated with exposure to hazardous
substances. The ATSDR is responsible for assessment of waste sites and providing health
information concerning hazardous substances, response to emergency release situations, and
education and training concerning hazardous substances (ATSDR Mission Statement, November 7,
2001). In cooperation with the U.S. Environmental Protection Agency, the ATSDR has compiled a

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Priority List for 2001 called the "Top 20 Hazardous Substances." The heavy metals arsenic (1), lead
(2), mercury (3), and cadmium (7) appear on this list.

COMMONLY ENCOUNTERED TOXIC HEAVY METALS

 Arsenic
 Lead
 Mercury
 Chromium
As noted earlier, there are 35 metals of concern, with 23 of them called the heavy metals. Toxicity
can result from any of these metals. This protocol will address the metals that are most likely
encountered in our daily environment. Briefly covered will be four metals that are included in the
ATSDR's "Top 20 Hazardous Substances" list. Iron and aluminum will also be discussed even though
they do not appear on the ATSDR's list.

Arsenic
Arsenic is the most common cause of acute heavy metal poisoning in adults and is number 1 on the
ATSDR's "Top 20 List." Arsenic is released into the environment by the smelting process of copper,
zinc, and lead, as well as by the manufacturing of chemicals and glasses. Arsine gas is a common
byproduct produced by the manufacturing of pesticides that contain arsenic. Arsenic may be also
be found in water supplies worldwide, leading to exposure of shellfish, cod, and haddock. Other
sources are paints, rat poisoning, fungicides, and wood preservatives. Target organs are the blood,
kidneys, and central nervous, digestive, and skin systems.

Health and Toxicology

Exposure to arsenic can induce adverse health effects and can occur in a number of ways. For
example, primary copper, lead smelters and chemical manufactures release arsenic into the
atmosphere (Klaasen and Watkins III, 2003). Drinking water sources usually contain a few
micrograms of arsenic per liter or less. Large amounts of arsenic can be found in seafood (Klaasen
and Watkins III, 2003). Occupational settings also can serve as a source of arsenic exposure. In
fact, many U.S. workers at factories that produce pesticides, herbicides and other agricultural
products are exposed to arsenic (Klaasen and Watkins III, 2003). Smeltering industries are also
sources for high levels of arsenic fumes (Klaasen and Watkins III, 2003). These industries typically

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account for the excessive spread of arsenic in the environment. Arsenic is a metal that can
generate multiple adverse health effects because of the many chemical forms it takes on. For
example, arsenic can appear in inorganic or organic form.

Arsenic trioxide, sodium arsenite, and arsenic trichloride are the most common inorganic trivalent
arsenic compounds (Klaasen and Watkins III, 2003). Neurotoxiciy of both the peripheral and
central nervous systems may be due to inorganic arsenic compounds.

Neurotoxicity usually begins with sensory changes, muscle tenderness, followed by progressive
weakness from the proximal to distal muscle groups (Klaasen and Watkins III, 2003).

Organic forms of arsenic also may be in trivalent or pentavalent forms and may even occur in
methylated forms as a result of biomethylation in soil, fresh water and sea water in humans
(Klaasen and Watkins III, 2003). Pentavalent inorganic forms of arsenic include arsenic pentoxide,
arsenic acid, and arsenates, such as lead arsenate. Pentavalent arsenic forms affect human enzyme
activity (Klaasen and Watkins III, 2003).

Acute illnesses from arsenic exposure consist of fever, anorexia, melanosis, cardiac arrhythmia, and
eventually cardiovascular failure (Klaasen and Watkins III, 2003). A few days after exposure to
arsenic, anemia, and granulocyopenia will appear in the body (Klaasen and Watkins III, 2003).
Exposure to arsenic can inhibit succinic dehydrogenase activity and uncouples oxidative
phosphorylation. Uncoupled oxidative phosphorylation is process that results in the stimulation of
mitochondrial ATPase activity (Klaasen and Watkins III, 2003). Inhibition of mitochondria function
also can be caused by arsenic exposure. Mitochondria functions can be inhibited two ways: arsenic
can compete with a phosphate during oxidative phosphorlation and by inhibiting the reduction of
NAD (Klaasen and Watkins III, 2003). Inhibition of mitochondria respiration results in a decrease
in cellular production of ATP. The ingestion of large doses (70-180 mg) of arsenic may cause fatal
health problems. Chronic exposure to arsenic produces changes in skin epithelium. One to two weeks
of exposure results in sensory loss in the peripheral nervous system. Trivalent compounds of arsenic
are the most toxic forms of arsenic (Klaasen and Watkins III, 2003). High doses of inorganic
arsenic compounds given to a pregnant experimental animal resulted in various malformations in the
fetuses and offspring. However, these effects have not been recognized in humans with excessive
occupational exposures to arsenic (Klaasen and Watkins III, 2003). Studies show a possible
association between inhalation exposure to arsenic and skin and lung cancer. Some studies indicate
that arsenic causes cancer of internal organs from oral digestion (Klaasen and Watkins III, 2003).

Acute toxicity

Most cases of acute arsenic poisoning occur from accidental ingestion of insecticides or pesticides
and less commonly from attempted suicide. Small amounts (<5 mg) result in vomiting and diarrhoea
but resolve in 12 hours and treatment is reported not to be necessary.44 The lethal dose of arsenic

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in acute poisoning ranges from 100 mg to 300 mg.The Risk Assessment Information System
database states “The acute lethal dose of inorganic arsenic to humans has been estimated to be
about 0.6 mg/kg/day”. A 23 year old male who ingested 8 g of arsenic survived for eight days. A
student who consumed 30 g of arsenic sought help after 15 hours and survived 48 hours but died
despite gastric lavage and treatment with British anti-lewisite (an arsenic antidote) and
haemodialysis. Depending on the quantity consumed, death usually occurs within 24 hours to four
days.

The clinical features initially invariably relate to the gastrointestinal system and are nausea,
vomiting, colicky abdominal pain, and profuse watery diarrhoea. The abdominal pain may be severe
and mimic an acute abdomen. Excessive salivation occurs50 and may be the presenting complaint in
the absence of other gastrointestinal symptoms. Other clinical features are acute psychosis, a
diffuse skin rash, toxic cardiomyopathy, and seizures. Diarrhoea attributed to increased
permeability of the blood vessels is a dominant feature. The voluminous watery stools are described
as “choleroid diarrhoea”. In cholera the stools are described as “rice water”, but in acute arsenic
poisoning, because of blood in the gastrointestinal tract, the term“bloody rice water” diarrhoea is
used. The cause of death is massive fluid loss due to secretion from the gastrointestinal tract
eventuating in severe dehydration, reduced circulating blood volume, and consequent circulatory
collapse. On postmortem examination oesophagitis, gastritis, and hepatic steatosis are reported.

Haematological abnormalities reported are haemaglobinuria, intravascular coagulation, bone marrow

depression, severe pancytopenia, and normocytic normochromic anaemia and basophilic stippling.52–
54 Renal failure was reported in four of eight sailors exposed to arsine.53 Respiratory failure and
pulmonary oedema are common features of acute poisoning.

The most frequent neurological manifestation is peripheral neuropathy that may last for as long as
two years.47 55 56 The peripheral neuropathy may lead to rapid, severe ascending weakness,
similar to Guillain-Barré syndrome, requiring mechanical ventilation.52 Encephalopathy is a common
manifestation and the possibility of arsenic toxicity must be considered if the aetiology of
encephalopathy is uncertain.

Encephalopathy has occurred after intravenous administration of arsphenamines. The basis for the
encephalopathy is thought to be due to haemorrhage. Metabolic changes with acute arsenic
poisoning are reported. Acidosis has occurred in a single patient47 and hypoglycaemia and
hypocalcaemia in cattle. In acute poisoning the best indicator of recent ingestion (1–2 days) is
urinary arsenic concentration.

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Chronic toxicity

Neuropathy may be the first sign of chronic arsenic toxicity. Skin lesions and peripheral neuropathy
are the hallmarks of arsenic ingestion, and their presence should result in an aggressive search for
this etiology. Neuropathy can occur insidiously in chronic toxicity without other apparent symptoms.
However, careful evaluation usually reveals signs of multiorgan and multisystem involvement such as
anemia, leukopenia, skin changes, or elevated liver function tests. Hyperpigmentation and
hyperkeratosis are delayed hallmarks of chronic arsenic exposure. Anemia often accompanies skin
lesions in patients chronically poisoned by arsenic.

Manifestations of chronic arsenic ingestion depend on both the intensity and duration of exposure.
An intense exposure of several milligrams a day results in anemia, neuropathy, and hepatotoxicity
within a few weeks to months. Hematologic and neurologic signs may occur after a similar latency
period. Skin lesions, however, take longer to manifest (3 to 7 years for pigmentation changes and
keratoses; up to 40 years for skin cancer) and may occur after lower doses than those causing
neuropathy or anemia.

Lung cancer and skin cancer are serious long-term concerns in cases of chronic arsenic exposure.

Chronic arsenic dust inhalation may be accompanied by upper respiratory symptoms, nasal
perforation, and lung cancer; however, since permissible workplace arsenic levels have been lowered,
these conditions are rarely encountered in workers.

• Absorbed arsenic accumulates in the liver, kidneys, heart and lungs, with smaller amounts in the
muscles, nervous system, gastrointestinal tract, spleen, and lungs.

• Arsenic is deposited in the keratin-rich tissues: nails, hair, and skin.

• Mee’s lines occur in the fingernails and toenails.

• The most serious consequence is malignant change in almost all organs of the body.

• Dermatological changes are common, such as hyperpigmentation and both palmar and solar
keratoses.

• There is increased risk of cardiovascular disease, peripheral vascular disease, respiratory disease,
diabetes mellitus, and neutropenia.

• Effective treatment of chronic arsenic toxicity is not yet established.

Box 1: Industrial sources

Lead
Lead is number 2 on the ATSDR's "Top 20 List." Lead accounts for most of the cases of pediatric
heavy metal poisoning (Roberts 1999). It is a very soft metal and was used in pipes, drains, and

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soldering materials for many years. Millions of homes built before 1940 still contain lead (e.g., in
painted surfaces), leading to chronic exposure from weathering, flaking, chalking, and dust. Every
year, industry produces about 2.5 million tons of lead throughout the world. Most of this lead is
used for batteries. The remainder is used for cable coverings, plumbing, ammunition, and fuel
additives. Other uses are as paint pigments and in PVC plastics, x-ray shielding, crystal glass
production, and pesticides. Target organs are the bones, brain, blood, kidneys, and thyroid gland
(International Occupational Safety and Health Information Centre 1999; ATSDR ToxFAQs for
Lead).

Health and toxicology

Lead is commonly found in industrial settings and lead exposure has the tendency to cause adverse
health effects. The adverse health effects induced by lead exposure are dependent on two
important components: dose (how much of a contaminant ) and duration (how long there has been
contact with the contaminant ) (ATSDR, 1999). Exposure to lead can occur from eating and drinking
contaminated water or breathing in high levels of lead (ATSDR, 1999). Children are exposed to lead
through eating lead based paint chips or through skin absorption while playing in lead contaminated
soil. This hazardous material enters the air we breathe, the water we drink, and the plants and
animals we consume. Lead is a health problem for communities that reside near acidic water
supplies. Acidic water can cause lead to leach into our drinking water supply from lead pipes, leaded
solder, and brass faucets. The EPA reports that more than 99% of the public’s drinking water
contains less than 0.05 parts per million of lead, which is the maximum contaminant level for lead
(ATSDR, 1999). Refining facilities, brass foundries, rubber refineries, and steel welding operations
are settings in which exposure to lead to optimal. The Agency for Toxic Substances and Disease
Registry (ATSDR) states between 0.5 and 1.5 million workers are exposed to lead at the work place.
More than 200,000 workers in California alone are exposed to lead (ATSDR, 1999). This suggests
that many people, especially blue-collar workers, are disproportionately exposed to lead and suffer
adversely from health problems because of it. Once lead has entered the blood stream, it flows to
various parts of the body. Lead most commonly enters the body through ingestion, and then travels
to the lungs then swiftly through the blood stream to other parts of the body. Lead does not
change form once it enters the body. Lead in the blood stream travels to the soft tissues of the
body, such as the liver, kidneys, lungs, brain, spleen, muscles, and heart. Over time, lead particles
have the ability to move into the bones and teeth. Lead impairs communication between cells and
modification of neuronal circuitry (Curtis D. Klassmen and John B. Watkins 111, 2003). ATSDR
reports that 94% of the total amount of lead in the body is contained in bones and teeth. For
children, 73% of lead in their body is stored in their bones (ATSDR, 1999). Lead that enters the
bones can remain there for decades. However, over time, lead that is stored in the bones can
reenter the blood stream and organs.

Excretion of lead occurs through urine and feces when it is not stored in the bones. ATSDR reports
that 99% of the amount of lead absorbed in an adult’s body will leave the body through waste within

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a couple of weeks. In contrast, only 32% of the lead absorbed by children’s bodies leaves as waste.
Means of exposure determine if the lead entering the body will be removed or accumulate in the
body tissues, especially within the bone (ATSDR, 1999).

Lead toxicity usually begins with the nervous system in both adults and children. Exposure to lead
can cause weakness in fingers, wrists, or ankles. Studies show long-term exposure to lead at work
can lead to decreased performance. High levels of lead can cause damage to the brain, kidney, and
can cause anemia in both adults and children. large amounts of lead may develop blood anemia,
kidney damage, colic, muscle weakness, and brain damage. These combined health effects can cause
death in children. However, low levels of lead contamination can also cause detrimental effects to
the blood and brain of a child. Pregnant women can experience a miscarriage if exposed to high
levels of lead during pregnancy (ATSDR, 1999). High levels of lead can also damage organs that are
responsible for sperm production. Consistent and long exposures to lead can potentially produce
noxious health effects.

Acute toxicity

In acute poisoning, typical neurological signs are pain, muscle weakness, paraesthesia, and, rarely,
symptoms associated with encephalitis. Abdominal pain, nausea, vomiting, diarrhea, and constipation
are other acute symptoms. Lead’s effects on the mouth include astringency and a metallic taste.
Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common
in acute poisoning. Absorption of large amounts of lead over a short time can cause shock
(insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract.
Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin
in the urine. Damage to kidneys can cause changes in urination such as output. People who survive
acute poisoning often go on to display symptoms of chronic poisoning.

Chronic toxicity

Chronic poisoning usually presents with symptoms affecting multiple systems, but is associated with
three main types of symptoms: gastrointestinal, neuromuscular, and neurological. Central nervous
system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal
symptoms usually result from exposure over longer periods. Signs of chronic exposure include loss
of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination,
and numbness and tingling in the extremities. Fatigue, problems with sleep, headaches, stupor,
slurred speech, and anemia are also found in chronic lead poisoning. A "lead hue" of the skin with
pallor is another feature. A blue line along the gum, with bluish black edging to the teeth is another
indication of chronic lead poisoning. Children with chronic poisoning may refuse to play or may have
hyperkinetic or aggressive behavior disorder.

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Mercury
Number 3 on ATSDR's "Top 20 List" is mercury. Mercury is generated naturally in the environment
from the degassing of the earth's crust, from volcanic emissions. It exists in three forms:
elemental mercury and organic and inorganic mercury. Mining operations, chloralkali plants, and
paper industries are significant producers of mercury (Goyer 1996). Atmospheric mercury is
dispersed across the globe by winds and returns to the earth in rainfall, accumulating in aquatic
food chains and fish in lakes (Clarkson 1990). Mercury compounds were added to paint as a
fungicide until 1990. These compounds are now banned; however, old paint supplies and surfaces
painted with these old supplies still exist. Mercury continues to be used in thermometers,
thermostats, and dental amalgam. (Many researchers suspect dental amalgam as being a possible
source of mercury toxicity [Omura et al. 1996; O'Brien 2001].) Medicines, such as mercurochrome
and merthiolate, are still available. Algaecides and childhood vaccines are also potential sources.
Inhalation is the most frequent cause of exposure to mercury. The organic form is readily absorbed
in the gastrointestinal tract (90-100%); lesser but still significant amounts of inorganic mercury are
absorbed in the gastrointestinal tract (7-15%). Target organs are the brain and kidneys (Roberts
1999; ATSDR ToxFAQs for Mercury).

Health and Toxicology

Metallic mercury has been found at 714 hazardous waste sites in the United States (ATSDR, 1999).
The abundance of mercury present within these contaminated sites causes health and environmental
problems to surrounding ecosystems. Chronic exposure to mercury can cause detrimental effects to
human health and the environment. Exposure to mercury can come from a number of different
routes, such as through dental amalgam fillings, household products, fluorescent light bulbs, broken
thermometers, and industrial settings. Exposure to methyl mercury by these routes can cause
health problems. A major source of exposure to methyl mercury comes from the consumption of
fish. Methyl mercury is the most toxic species of mercury because it possesses a high adsorption
rate to membranes. Neurotoxic health effects are common after exposure to methyl mercury.
Pregnant women who consume large amounts of fish or who are exposed to high levels of mercury
are at an increased risk of exposing their fetus to methyl mercury. Therefore hospitals and clinics
advise pregnant women to limit the amount of fish they consume. Physical symptoms of methyl
mercury exposure can be identified by paresthensia and numbness in the fingers and toes.
Difficulty swallowing and clumsiness—called ataxia—are also symptoms of methyl mercury exposure
(ATSDR, 1999). After ataxia sets in, neurasthenia can occur, followed by fatigue and an inability to
concentrate. As methyl mercury continues to poison the body, tremors and vision and hearing loss
develop. The final stage of methyl mercury poisoning is coma followed by death (ATSDR, 1999).
Methyl mercury is a substance that should be addressed with caution and advisory because of its
harmful health effects. Mercury in the form of mercuric chloride is an example of a mercuric salt.
Oral ingestion of mercuric salts is said to cause severe abdominal cramps and bloody diarrhea

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(Klaasen and Watkins III, 2003). These symptoms are usually accompanied by corrosive ulceration
and necrosis of the gastrointestinal tract and renal failure within 24 hours of proximal tubular
epithelium necrosis. Any great exposure to mercury leads to the intake of mercury by various
organs of the body. Once mercury is absorbed into the body, its elemental or metallic form is
oxidized forming divalent mercury. Mercury vapor absorbed through inhalation penetrates the
body’s red blood cells and is transformed to divalent mercury (Klaassen and Watkins III, 2003). A
portion of inhaled mercury vapor in the form of metallic mercury is transported to more distal
tissues where transformation may occur. Inhalation of mercury vapor at high levels may produce an
acute, corrosive bronchitis and interstitial pneumonitis. With increased exposure to mercury, the
body’s system begins to show physical signs of effects. For example, the fingers begin to tremor
followed by memory loss; severe depression become s apparent after long exposure to mercury.
Mercury toxicity can also cause severe salivation and gingivitis (Klaasen and Watkins III, 2003).

The clinical presentation of mercury toxicity can manifest in a variety of ways, depending on the
nature of the exposure, the intensity of the exposure, and the chemical form. Acute toxicity
usually is related to the inhalation of elemental mercury or ingestion of inorganic mercury. Exposure
to organic mercury leads to chronic toxicity and, occasionally, acute toxicity.

Acute toxicity

Acute exposure caused by inhaled elemental mercury can lead to pulmonary symptoms. Initial
signs and symptoms, such as fever, chills, shortness of breath, metallic taste, and pleuritic chest
pain, may be confused with metal fume fever. Other possible symptoms could include stomatitis,
lethargy, confusion, and vomiting. In addition, elemental mercury can also be injected causing a life-
threatening pulmonary embolism.

Chronic and intense acute exposure causes cutaneous and neurological symptoms. The classic triad
found in chronic toxicity is tremors, gingivitis, and erethism (ie, a constellation of neuropsychiatric
findings that includes insomnia, shyness, memory loss, emotional instability, depression, anorexia,
vasomotor disturbance, uncontrolled perspiration, and blushing).

Additional findings may include headache, visual disturbance (eg, tunnel vision), peripheral
neuropathy, salivation, insomnia, and ataxia.

Without a complete history, mercury toxicity, especially in elderly individuals, can be misdiagnosed
as Parkinson disease, senile dementia, metabolic encephalopathy, depression, or Alzheimer disease.

Elemental mercury has poor GI absorption and, therefore, oral or rectal exposure to elemental
mercury from a thermometer should have no toxic effect. Dental amalgams also contain elemental
mercury. Dental professionals who are in contact with amalgam must follow specific guidelines to
avoid exposure to toxic amounts of aerosolized elemental mercury. Patients with dental amalgam

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fillings have slightly elevated levels in their urine, but these findings have not correlated with any
systemic disease.

Inorganic mercury or mercuric salt exposure mainly occurs through the oral and GI tract. Its
corrosive properties account for most of the acute signs and symptoms of inorganic mercury or
mercuric salt toxicity. The acute presentation can include ashen-gray mucous membranes secondary
to precipitation of mercuric salts, hematochezia, vomiting, severe abdominal pain, and hypovolemic
shock. Systemic effects usually begin several hours postingestion and may last several days. These
effects include metallic taste, stomatitis, gingival irritation, foul breath, loosening of teeth, and
renal tubular necrosis leading to oliguria or anuria”.

Chronic toxicity

Chronic exposure usually results from prolonged occupational exposure to elemental mercury that is
converted into the inorganic form, topical application of mercurial salves, and the chronic use of
diuretics or cathartics.

Chronic exposure results in renal failure, dementia, and acrodynia.

Acrodynia, known as Pink disease and considered to be a mercury allergy, presents with erythema of
the palms and soles, edema of the hands and feet, desquamating rash, hair loss, pruritus,
diaphoresis, tachycardia, hypertension, photophobia, irritability, anorexia, insomnia, poor muscle
tone, and constipation or diarrhea.

Acrodynia does not present in everyone who is exposed to inorganic mercury, but it is an indicator
of widespread disease.

Organic mercury poisoning usually results from ingestion of contaminated food. The long chain and
aryl forms of organic mercury have similar characteristics of inorganic mercury toxicity.

The onset of symptoms usually is delayed (days to weeks) after exposure.

Organic mercury targets enzymes, and the depletion of these enzymes must occur before the onset
of symptoms.

Symptoms related to toxicity are typically neurological, such as visual disturbance (eg, scotomata,
visual field constriction), ataxia, paresthesias (early signs), hearing loss, dysarthria, mental
deterioration, muscle tremor, movement disorders, and, with severe exposure, paralysis, and death.

Organic mercury targets specific sites in the brain, including the cerebral cortex (especially visual
cortex), motor and sensory centers (precentral and postcentral cortex), auditory center (temporal
cortex), and cerebellum.

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All forms of mercury are toxic to the fetus, but methylmercury most readily passes through the
placenta. Even with an asymptomatic patient, maternal exposure can lead to spontaneous abortion or
retardation.

Chromium
Chromium and its compounds are ubiquitous in the environment. A large number of animal and human
1-5
studies have shown the effect of cromium and its compoundS on health . Trivalent chromium (Cr
III), an essential metabolic trace nutrient, is noticeably less toxic than hexavalent chromium (Cr
6,7
VI), which can cause skin ulceration, perforation of the nasal septum and lung cancer . Public
health concern has mounted, recently about environmental and occupational exposures to toxic
elements such as lead, arsenic, mercury, cadmium and chromium and there is special attention from
the National Environmental agencies. In Thailand, a few studies to investigate the effects of
8,9
chromium and its compounds on human health were reported . The present review gives an
overview of the effects of chromium on the human health.

Physical and chemical properties

Chromium is a steel-gray luminous metallic element, atomic number 24, and its physicochemical
properties include atomic weight, 51.996; specific gravity, 7.20; melting point, 1,900°C and boiling
point, 2,642°C. Chromium metal reacts with diluted hydrochloric acid and sulfuric acid, but not with
nitric acid. This metal has a valency of 0, II, III, V or VI, and a wide range of chromium alloy and
inorganic compounds as shown in Table 1. Elemental chromium (valency 0) does not occur naturally.
The majority of chromium in nature is Cr (III) and Cr (VI). Trivalent chromium is an essential trace
element necessary for the formation of glucose tolerance factor and the metabolism of insulin.
Hexavalent chromium is a strong oxidizing agent.

Acute toxicity

Acute poisoning likely occurs through the oral route. Ingestion of hexavalent chromium may cause
both local and systemic involvement,

which include intense gastrointestinal irritation or ulceration and corrosion, epigastric pain, nausea,
vomiting, diarrhea, vertigo, fever, muscle cramps, hemorrhagic diathesis, toxic nephritis, renal
failure, intravascular hemolysis, circulatory collapse, peripheral vascular collapse, liver damage,
acute multi-system shock, coma, and even death. The severity of the involvement depends on the
dose. In addition, acute chromic acid exposure produces local inflammation, 6 ulceration of the skin
and hypersensitivity dermatitis while, in severe cases, systemic toxicity can occur. Inhalation
exposure in occupational workers with chromate spray paint, zinc chromate primer paint, chromic
acid vapor and Cr (VI) fumes can cause bronchial asthma; pulmonary edema, pneumoconiosis, and
metal fume fever.

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FOOD SCIENCES (SEMESTER 1)
 HEAVY METALS 14

Chronic toxicity

The essential features of chronic effects of Cr (III) and Cr (VI) are changes in the skin, mucous
membrane, allergic dermal and bronco-pulmonary effects.

- Skin irritation may result from contact with chromic acid, sodium or potassium dichromate or
ammonium dichromate. The major problem is ulcers, often called chrome holes or chrome sores. The
ulcers are commonly located at the nailroot area, finger webs, the backs of the hands and the
forearms.

- Perforation of the nasal septum is one of the main chronic effects in workers who have contacted
with chromate, chrome plating and chromic acid. An additional consequence of the effect on the
nasal mucous membrane is a loss of the sense of smell.

- Chromium is one of the most common skin sensitizers among occupational workers, involved in
cement handling, leather tanning, and chromium plating. Dermal exposure of chromium produces
irritant and allergic contact dermatitis. It is observed that keratinocytes are the first target cells
affected by chromium in causing contact dermatiti.

- The International Agency for Research on Cancer (IARC) and The US Toxicology Program
recognize hexavalent chromium as a known human carcinogen. The increased risk of lung cancer is
associated with the inhalation of Cr (VI) in the occupational setting, primarily in population of
workers refining chromite ore or producing chromate pigments. The risk of lung cancer following
exposure to Cr (VI) increases with the duration of exposure; the mean latency period ranges from
13 to 30 years.

Heavy Metal Sources General Symptoms That May

Arsenic Chemical processing plants,
cigarette smoke, drinking
water, fungicides, meats and
seafood, metal foundries, ore
smelting plants, pesticides, pol-
luted air, specialty glass
products, weed killers, wood
preservatives, etc.
Lead Air pollution, ammunition, auto
exhaust, batteries, containers
for corrosives, contaminated
soil, cosmetics, fertilizers,
Manifest
Extremely poisonous as well as
colorless and odorless, arsenic
can enter the body through the
mouth, lungs and skin. Arsenic
toxicity seems to
predominantly affect the skin,
lungs and gastrointestinal
system, and may cause nervous
disorders, deteriorated motor
coordination, respiratory
diseases, and kidney damage as
well as cancers of the skin,
liver, bladder and lungs.
Lead is a naturally-occurring
neurotoxin. Although many
leadcontaining products (such
as gasoline and house paints)

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FOOD SCIENCES (SEMESTER 1)

foods (if grown in lead-
contaminated soil), hair dyes,
insecticides, lead-based paints,
lead-glazed pottery, pesticides,
solder, tobacco smoke, water
(if transported via lead pipes),
etc.
Mercury Air pollution, barometers,
batteries, cosmetics, dental
amalgam fillings, freshwater
fish (such as bass and trout),
fungicides, insecticides,
laxatives, paints, pesticides,
saltwater fish (such as tuna
and swordfish), shellfish, tap
and well water, thermometers,
thermostats, vaccines, etc.
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FOOD SCIENCES (SEMESTER 1)
HEAVY METALS 15
were banned in the 1970s,
contamination still occurs today
mostly by drinking
leadcontaminated water,
breathing lead-polluted air, and
living in or near older painted
buildings and certain toxic
industrial areas. Lead toxicity
primarily targets the nervous
system, kidneys, bones, heart
and blood, and poses greatest
risk to infants, young children
and pregnant women. It can
affect fetal development, delay
growth, and may also cause
attention deficit disorder,
learning disabilities, behavioral
defects, and other
developmental problems.
Both poisonous and dangerous,
mercury is found throughout
our environments in many forms
and also in many household
items. Mercury often
permeates the ground we walk
on, and is also found in some
childhood vaccines today
because of its use as a
preserva¬tive. Mercury as used
in dental fillings is the primary
source of toxic exposure, and
in vapor form accounts for the
majority of all expo¬sures (via
inhalation). Mercury toxicity
can affect the central nervous
system, kidneys and liver.
Research suggests that this
heavy metal may also
contribute to autism and
multiple sclerosis.
 HEAVY METALS 16

References:

 http://www.lef.org/protocols/prtcl-156.shtml
 http://en.wikipedia.org/wiki/Lead_poisoning#Acute_poisoning
 http://heavy metal\Five Most Common Toxic Heavy Metals.mht
 Agency for Toxic Substances and Disease Registry, ATSDR. 1999.
http://www.atsdr.cdc.gov.
 Cynthia R. Evanko, Ph.D., and David A. Dzo mbak, Ph.D. Remediation of Metals-Contaminated
Soil and Groundwater. GWRTAC. October 1997. www.gwrtac.org.
 http://www.naturalrussia.com/pdfs/Mercury_toxicity.pdf
 http://www.atsdr.cdc.gov/csem/arsenic/clinical_evaluation.html
 http://digital.library.adelaide.edu.au/dspace/bitstream/2440/9980/1/hdl_9980.pdf
 http://www.ra2.mahidol.ac.th/journal/files/Vol26_No2_61.pdf

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FOOD SCIENCES (SEMESTER 1)