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Principles of Metal Toxicity

Essential Metals

Low concentrations are needed for good health. High


concentrations are toxic.

Chromium (Cr)

Copper (Cu)

Zinc (Zn)

Nickel (Ni)

Manganese (Mn)

Selenium
(Se)

Essential metals are also called trace metals because they are required in trace
amounts by humans and other organisms. But "too much of a good thing"
leads to adverse impacts on health (Wright and Welbourn (2002)).

The following graph (Wright and Welbourn (2002)) shows the relationship
between the concentration of an essential metal and the growth rate of the
organism. If the metal concentration is too low, then the organism will not
grow at a healthy rate. If the metal concentration is in the "essential" range,
this is sufficient to meet the growth needs of the organism. However, if the
essential concentration is exceeded, the metal will be toxic to the organism
and the growth rate will decrease.

Silver and Gold Toxicity - Heap-Leap Extraction


Diagram of the heap-leach extraction process used at many gold mines.

Non-Essential Metals

These are metals that are not required in trace amounts by humans and
other organisms. They have no known function for maintenance of health.

Cadmium (Cd)

Lead (Pb)

Mercury (Hg)

Tin (Sn)

Silver (Ag)

Gold (Au)

Aluminium (Al)

Arsenic
(As)

(Wright and Welbourn (2002)).


Metal Toxicity

Metal toxicity produces adverse biological effects on an


organism's

survival

activity

growth

metabolism

reproduction

Metals can have lethal effects (directly kill the organism) or sublethal effects
(harm the organism but do not directly kill it). Adverse effects on an organism's
activity, growth, metabolism, and reproduction are examples of sublethal
effects. Metabolism refers to the process of obtaining energy from nutrients.

Toxicity Measurements

LC50 (lethal concentration 50) - causes death in


50% of the organisms in an exposed
population.

EC50 (effective concentration 50) -


causes nonlethal negative effect in 50%
of exposed organisms.

IC50 (inhibitory concentration


50) - specific type of EC50

The lower the LC50, EC50


or IC50, the more toxic
the metal.

An example of an EC50 is the concentration of a metal that causes reduced


growth in 50% of exposed organisms. IC50 is the concentration of a metal that
causes an inhibitory effect in 50% of exposed organisms, e.g., inhibition of the
activity of an enzyme (a protein that catalyzes metabolic reactions) (Landis and
Yu (2003)).
For example, Metal A has LC50 of 6 mg/liter (parts per million - ppm) and Metal
B has LC50 of 30 ppm. Which one is more toxic? Metal A is more toxic than
Metal B because a lower concentration of Metal A kills 50% of the exposed
organisms.

Dose - Response Curve

Graph that describes the response of an


organism, population or biological community
to a range of concentrations of a toxic
chemical.

Cumulative mortality is plotted at each


concentration or dose.

Result is S-shaped (sigmoid)


curve.

The following graph (Landis and Yu (2003)) shows the relationship between the
concentration (dose) of a toxic chemical and the percent mortality in the
exposed population. LD50 (lethal dose 50) is the same concept as LC50. To
determine what concentration of the toxic chemical kills 50% of the exposed
organisms, draw a line from the 50% point on the Y-axis to its intersection with
the curve and then draw a line from that intersection point to the X-axis. If the
unit of measurement on the X-axis were ppm, the LD50/LC50 would be
approximately 3.5 ppm.

Suggested Exercise

A Daphnia population was exposed for 24 hours to increasing concentrations of


Metal X. Using the data given above, plot a dose-response curve and determine
the LC50 for this metal.

Note - The correct answer for this exercise is 17.5 ppm. Any result between 17
and 18 ppm is acceptable.

Modes of Action of Toxic Metals

Destruction or disruption of cellular structure.

Direct chemical combination with


cellular constituent.

Effect on enzymes.

Secondary action as
result of the presence of
a metal.

Endocrine
disruption.

(Landis and Yu (2003), Cunningham and Cunningham (2004), Colburn,


Dumanoski, and Myers (1997)).

Destruction or Disruption of Cellular Structure

Metal injures an organ (e.g., brain, bones, liver, kidneys,


gills, lungs) by causing structural damage (lesions) to the
tissues of the organ. (A tissue is a group of cells that
perform a similar function. An organ is a group of tissues
that perform a similar function).

For example, the organic form of mercury causes structural damage to the
brain. Cadmium and aluminum cause structural damage to the bones (Landis
and Yu (2003), Bradl (2005), Wright and Welbourn (2002)).

Direct Chemical Combination with Cellular Constituent

Can lead to impaired function.

Metallothionen is a protein that is


involved in the transport and selective
storage of Cd.

Cd binds to metallothionen and


accumulates in kidneys.

The organ might still have normal structure, but abnormal function. For
example, when Cd accumulates in the kidneys, it prevents the kidneys from
doing their job of filtering urea from the blood and returning nutrients to the
blood (Landis and Yu (2003), Bradl (2005), Wright and Welbourn (2002)).

Effect on Enzymes

Enzymes are proteins that catalyze metabolic reactions.


Metal may:

Inhibit enzyme.

Inactivate cofactor required for enzyme


activity e.g., may complete with
cofactor for active site on enzyme.

Metals such as Hg, Pb, and Cd can attach to the sulfhydryl (SH) group on an
enzyme, forming a covalent bond with the sulfur atom. This will lead to
inactivation of the enzyme if the SH group is the active site of the enzyme. The
following equation (Landis and Yu (2003)) illustrates how Pb can inactivate an
enzyme (Enz).

2 Enz-SH + Pb+2 Enz-S-Pb-S-Enz + 2H+

Many enzymes require cofactors, often cations, for their activity. Cd replaces
Zn in some enzymes (Landis and Yu (2003)).

Secondary Action as a Result of the Presence of a Metal

Metal binds to carcinogen, enters cells, and alters cell


metabolism.

A carcinogen is a chemical that causes cancer. Metals can promote the action
of carcinogens or can cause cancer on their own (Landis and Yu (2003)).

Endocrine Disruption

Metals disrupt the effects of some hormones.

Hormones are regulatory molecules produced by


endocrine glands and that fit precisely to
proteins called receptors.

Examples - thyroxine, insulin, estrogen,


testosterone.

A toxic chemical:

Mimics the hormone.

Blocks the hormone.

Alters the
metabolism of the
hormone.

Modifies
the level of
hormone
receptors.

(Cunningham and Cunningham (2004), Colburn, Dumanoski, and Myers


(1997)). Endocrine glands are ductless glands. Examples are the thyroid gland,
pancreas, ovaries, and testes. When a hormone is produced by an endocrine
gland, the hormone enters the bloodstream and can affect organs throughout
the organism.

Endocrine disruption has led to decreased fertility in many species of animals


and to male fish having characteristics of female fish and vice versa. For
example, if a toxic chemical mimics the hormone estrogen or blocks the
hormone testosterone, a male fish may develop vitellogenin, an egg yolk
protein that is normally found only in female fish (Colburn, Dumanoski, and
Myers (1997)).

Metal Exposure Pathways in Fish

gills - diffusion across membranes into


bloodstream

skin - diffusion into bloodstream

drinking metal-polluted water

ingestion of sediments

food chain

In order for a metal to have a toxic effect, it needs to somehow get into the
body of the exposed organism. There are several pathways by which fish and
humans are exposed to metals. In addition to diffusion into the bloodstream
via the gills or skin, fish can be exposed by drinking water or eating sediments
that are polluted with the metal, or eating other animals or plants that have
been exposed to the metal and, therefore, contain the metal in their tissues
(Wright and Welbourn (2002)).

Gills

Respiratory organs with large surface area for


oxygen and carbon dioxide exchange and
regulation of salts.

Thin membranes composed of lipids


(fats) and proteins.

Dissolved metals diffuse across


gill membranes into
bloodstream.

Membrane proteins may


transport metals.

Mucus-secreting
cells in gill
membranes may
bind metals.

Sodium and potassium salts are regulated via the gills. These salts are called
electrolytes and are needed for normal functioning of the nervous and
circulatory systems (Wright and Welbourn (2002)).

Metal Exposure Pathways in Humans

lungs - inhaled particulates

skin

drinking metal-polluted water

food chain - eating


shellfish, finfish, rice,
and other plants grown
in water

The pathways for human exposure to metals are analogous to the pathways for
fish exposure to metals. We humans are exposed to metals via diffusion into
the bloodstream from our lungs and skin, via drinking water that is polluted
(contaminated) with the metal, and via eating other animals or plants that
have been exposed to the metal (Wright and Welbourn (2002)).
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Principles of Metal Toxicity - Essential Metals

Schematic representation of a dose-response to an essential metal.

Principles of Metal Toxicity - Dose-Response Curve


Tabla 1: curva dosis - respuesta, el ejercicio

Concentracin (partes por mil millones -


% Mortalidad Acumulada
ppb)
5 3

10 10

15 22

20 75

25 90

30 95

35 97

40 100

r
Tabla 1: curva dosis - respuesta, el ejercicio

Factors Affecting Metal Toxicity

concentration

mode and time of exposure

chemical factors

interaction of metals

water temperature

biological
factors

(Wright and Welbourn (2002)). The toxicity of a given metal depends on many
existing chemical, physical, and biological factors at the time and location of
discharge of the metal. Each of these factors will now be discussed in more
detail.
Bioconcentration (Bioaccumulation)

Increase in concentration of a metal in an


organism compared to its concentration in
water or sediments.

Animals such as shellfish that live in


sediments are especially vulnerable.

All metals undergo


bioconcentration.

The concentration of a given metal in the water column or sediments of a


waterbody (e.g., estuary, river, stream, lake) is not by itself a good predictor of
the metal's toxicity. The phenomena of bioconcentration (also called
bioaccumulation) and biomagnification (also called ecological magnification)
affect what happens to the concentration of the metal inside an organism
(Wright and Welbourn (2002)).

Bioconcentration Factor (BCF)

Concentration of a metal in a plant or animal


divided by the concentration of the metal in
water or sediments.

Example - A metal is found at 700


micrograms per gram (ppm) in a fish
compared to 7 ppm in the river water.
BCF for that metal = 100.

(Wright and Welbourn (2002)). The concentration of a metal in water or


sediments may seem too low to cause toxic effects. However, once the metal
enters a target organism, the concentration will be much higher and may now
be high enough to cause toxic effects.

Biomagnification (Ecological Magnification)

Increase in concentration of metals in


successively higher trophic levels of a food
chain.

Predators have higher concentrations


than their prey.
Animals at top of food chain
(humans, other large mammals)
have very high concentrations.

Pertains to Hg and
possibly Cd, Mn, and Se.

(Wright and Welbourn (2002)). The concentration of a metal in algae at the


bottom of the food chain may seem too low to have toxic effects. However, for
some metals, this concentration increases at each trophic level and, therefore,
may be high enough to cause toxic effects in secondary consumers such as fish
and tertiary consumers such as humans.

The following diagram (source: NWETC) illustrates biomagnification of a toxic


chemical in the food chain. Green squares indicate the concentration of the
chemical. The toxic chemical was originally in the air and then entered the
waterbody via precipitation. This process is called atmospheric deposition. The
lower left corner of the diagram shows that the concentration is higher in the
shellfish than in their prey (phytoplankton and zooplankton). The center and
right corners of the diagram show that the concentration of the toxic chemical
is further magnified in the fish that eat the shellfish and even higher in the
seals that eat the fish. The bear, who is the top consumer in this food chain,
has the highest levels of the toxic chemical in its body.

Exposure Mode and Time


Exposure to high concentrations (levels) often
results in acute effects.

Exposure to low concentrations may


result in chronic effects.

The longer the exposure time,


the more detrimental the
effects.

Continuous exposure is
more detrimental than
intermittent exposure.

Acute effects are those that occur in a short period of time (e.g., a few hours or
days). Chronic effects are effects that occur in a longer period of time. Both
acute effects and chronic effects can be lethal or sublethal. If an organism is
exposed intermittently to a metal, the organism may be able to recover in
between exposure periods. This is why intermittent exposure is less
detrimental than continuous exposure (Landis and Yu (2003)).

Chemical Factors

speciation

pH

alkalinity

salinity

hardness

particulates

(Wright and Welbourn (2002)). Many chemical factors at the time and location
of discharge of a metal will influence its toxicity. Each of these factors will now
be discussed in more detail.

Speciation

Refers to different chemical forms in which a


metal exists.
Can include the neutral element, ions,
and organic forms (metal combines
with groups containing carbon).

Speciation affects
bioavailability.

Bioavailability

It is the availability of a
metal to enter and
affect a biological
system.

The
concentration of
a metal is not a
good predictor of
its biological
effect.

Metal
must be
in a form
that can
be "seen"
by the
biological
system
(e.g.,
dissolved)
and must
interact
with
surface or
interior of
cells.

In general, the most bioavailable form of metals is the free ion. Therefore, the
toxicity of metals correlates directly with concentrations of the free metal ion
rather than with concentrations of the total metal or metal complexes (Bradl
(2005), Wright and Welbourn (2002)).

Speciation Examples

Dissolved Al is bioavailable and toxic. Al(OH)3 is


not bioavailable because it is bound to soil and
sediments.

Cr+6 is more bioavailable and more toxic


than Cr+3 (illustrated in the film Erin
Brockovich).

Organic Hg is more bioavailable


and more toxic than elemental
Hg or inorganic Hg.

(Bradl (2005), Wright and Welbourn (2002)).

In the film Erin Brockovich, the Pacific Gas & Electric utility company in the
eastern California desert used hexavalent chromium (Cr+6) as an anti-corrosive
agent in cooling water. The cooling water was discharged to unlined ponds and
percolated through the soil into groundwater which was the drinking water
and swimming pool water supply for the people in the town of Hinkley. Over
500 people suffered adverse health impacts as a result of long-term exposure,
in some cases for 20-30 years. The film is based on a true story and is highly
recommended.

pH

Metals are more toxic at lower pH.

H+ affects speciation of metals in water


(e.g., Al and Cu).

Lower pH releases metals from


sediments. Higher pH binds
metals in sediments.

pH<5 increases
permeability of cells in
gill membranes, causing
loss of electrolytes
(sodium, potassium, and
chloride ions).

Lower pH promotes the formation of the more bioavailable species of a metal,


thereby contributing to higher toxicity of the metal (Wright and Welbourn
(2002)).

Alkalinity

Buffering capacity of water (alkalinity) affects


vulnerability of an aquatic ecosystem to ARD.

Depends on concentration of several


anions, e.g., carbonate, bicarbonate,
hydroxide.

In general, metals are less toxic


in a buffered waterbody.

A buffered waterbody will have a higher pH. Therefore, if ARD is discharged to


a buffered waterbody, the effluent will be neutralized and the metals in it will
be less toxic (Wright and Welbourn (2002)).

Salinity

Metals are more toxic in freshwater than in


saltwater because they are more bioavailable
in freshwater.

Salinity affects chemical speciation.

For example, Cd+2 is the most


bioavailable form of Cd and
predominates in freshwater. In
more saline water, Cd forms
chloride complexes which are
less bioavailable, and therefore,
less toxic.

(Wright and Welbourn (2002)).

Water Hardness (Ca+2)

U.S. Environmental Protection Agency (EPA) definitions:

soft water = 0 - 75 mg/L (ppm) Ca+2

moderately hard water = 76 - 150 mg/L


Ca+2

hard water = 151 - 300 mg/L


Ca+2

very hard water = >300


mg/L Ca+2
Ca+2 is a principal component of water hardness. The U.S. EPA defines hardness
in terms of CaCO3 equivalents (Wright and Welbourn (2002)).

Metals are more toxic in soft water and less


toxic in hard water.

Ca+2 has a protective effect on and in


cells.

Canada, U.S., and Europe base


water quality criteria for metals
on hardness. Criteria are stricter
for soft water.

Another reason why metals are less toxic in hard water than in soft water is
that hardness is usually correlated with higher pH and higher alkalinity, which
affect speciation of metals (Wright and Welbourn (2002)).

Role of Particulates

More distribution of metals in fine (silty)


sediments than coarse (sandy) sediments due
to larger surface area of fine sediments.

Bioavailability is affected by the


presence or absence of oxygen in
sediments. Some metals (Cd, Cu, Zn, Ni)
are more soluble in presence of oxygen
and therefore more toxic.

(Wright and Welbourn (2002)).

Interaction of Metals

Additivity (1+1=2) - two metals have twice the


effect of either metal.

Synergism (1+1=3) - two metals have


more than twice the effect of either
metal (e.g., Cd and Cu, Cd and Cr, Cu
and Ag, Zn and Ag, Se and Ag, Cu and
Au).

Antagonism (1+1=1.5) - two


metals have less than twice the
effect of either metal (e.g., Zn
and Cd, Zn and Pb, Se and Hg,
Se and Cd, Se and As, Cd and
Hg).

When metals interact synergistically, the combined effect is greater than what
would be predicted by just adding the effects of each of the metals in the
mixture. When metals interact antagonistically, the combined effect is less
than what would be predicted by just adding the effects of each of the metals
in the mixture. One metal partially cancels out the toxic effect of another metal
(Wright and Welbourn (2002), Landis and Yu (2003)).

Water Temperature

Metal toxicity increase as water temperature


increases.

Q10 = 2 (metabolism rate in cold-


blooded animals doubles with every
10C increase in water temperature).

Increased respiratory rate,


membrane permeability, and
absorption rates.

Humans, other mammals, and birds are warm-blooded animals. This means
that we maintain a constant body temperature, regardless of the temperature
in the surrounding air or water. By contrast, fish and shellfish are cold-blooded
animals. This means that their body temperature changes as the water
temperature changes. If the water temperature increases, the body
temperature of a fish or shellfish will increase. The resulting increased
respiratory rate (rate of oxygen uptake), increased permeability of gill
membranes, and increased absorption rates through the skin and the digestive
tract will lead to increased exposure of the organism to toxic metals (Wright
and Welbourn (2002), Landis and Yu (2003)).

Impacts of Exposure Time on Temperature Effects

Exposure time can be more important than temperature in


affecting toxicity.

Higher Zn toxicity in Atlantic salmon at 19C


than at 3C after one day of exposure, based
on LC50

Higher Zn toxicity at 3C than at 19C


after two weeks of exposure, based on
LC50

When Atlantic salmon were exposed to Zn for one day, the toxicity of the Zn
was greater at the higher temperature. This means that the LC50 for Zn was
lower at 19C than at 3C. This is what would be expected, per the previous
discussion of temperature effects. However, when Atlantic salmon were
exposed to Zn for two weeks, the toxicity of the Zn was greater at the lower
temperature. The 19C LC50 remained the same, but the 3C LC50 decreased
approximately sixfold. Therefore, caution must be used when interpreting
temperature effects from acute toxicity tests (Hodson and Sprague (1975)).

Biological Factors

species and individual differences

age/body size

nutritional status

persistence

biotransformation

detoxification

(Wright and Welbourn (2002), Landis and Yu (2003)). Many biological factors at
the time and location of discharge of a metal will influence its toxicity. Each of
these factors will now be discussed in more detail.

Species and Individual Differences

Aquatic animals are more sensitive than


aquatic plants.

Daphnids (water fleas) are among the


most sensitive freshwater crustaceans.

Shrimp are the most sensitive


marine crustaceans.
Salmon and trout are
the most sensitive fish.

There are
individual
differences in
sensitivity within
each species.

(Wright and Welbourn (2002)). The most sensitive species will have the lowest
LC50 measurements for any given metal.

Age/Body Size

Larval and juvenile stages of fish are more sensitive than


adults.

They have a larger surface area/volume ratio,


therefore, a faster toxic chemical uptake per
unit weight.

They have higher breathing and


metabolic rates, therefore, a faster and
more extensive uptake of toxic
chemicals.

Young animals lack completely


developed detoxification
enzyme systems.

(Wright and Welbourn (2002)). Larvae are newly hatched or newly born fish.

Nutritional Status

Nutritional status of exposed organism affects


its ability to metabolize or detoxify metals.

Poor nutritional status may impair


removal of pollutants from the
organism, leading to increased toxicity.

Dietary fats may delay or


enhance absorption of metals
(e.g., high fat diets increase Pb
absorption and retention).
(Landis and Yu (2003)).

Persistence

Metals are persistent in organisms.

The biological half-life is the time


required for 50% of the dose of the
metal to be eliminated from the
organism.

Some metals (e.g., Cd, Pb, Hg)


have long half-lives in mammals
and can cause serious long-term
effects.

(Wright and Welbourn (2002)). If the biological half-life of a particular metal is


one year, this means that 50% of the dose of the metal will be eliminated from
the organism and 50% of the dose will remain in the organism after one year.
After two years, 50% of the remaining dose (75% of the original dose) will have
been eliminated from the organism and 25% of the original dose will remain.
After three years, 50% of the remaining dose (87.5% of the original dose) will
have been eliminated from the organism and 12.5% of the original dose will
remain. If the biological half-life of a metal is many years, then the metal will
never be entirely eliminated from the organism and the metal may have more
serious long-term harmful effects than a metal that is less persistent.

Biotransformation

Biotransformation is the alteration of a toxic


chemical by an organism.

The toxicity of the chemical can be


increased or decreased.

Examples - Transformation of
inorganic Hg to organic Hg
increases Hg toxicity. But
transformation of inorganic As
to organic As decreases As
toxicity.

In fish and in humans, biotransformation occurs most frequently in the liver


and kidneys (Landis and Yu (2003)). One of the main roles of the liver is to
metabolize foreign chemicals to which the organism is exposed. In addition to
excreting urine, the kidneys function to excrete foreign chemicals from the
body of an organism.
Detoxification of Metals

Overview

Detoxification can occur if metal is excreted


from the body rapidly or is stored in an inert
form.

Excretion can be enhanced if metal is


metabolized to another form (e.g.,
methylmercury to inorganic mercury).

If a metal undergoes biotransformation to a form that is more soluble in water,


then the new form of the metal will be excreted in the urine of the exposed
animal and the metal will be less toxic than in its original form (Landis and Yu
(2003)).

Metallothionen

Metallothionen is a low molecular weight


protein that is capable of binding some metals
(in the +2 ion form) and decreasing their
toxicity.

Exposure to metals induces


metallothionen in most tissues.

Metallothionen is produced in the largest quantities in the liver and kidney,


which as previously mentioned, are the major sites of biotransformation of
toxic chemicals in fish and in humans (Wright and Welbourn (2002), Landis and
Yu (2003)).

hidden
.

Review #1
The randomly selected multiple-choice questions below are designed to review your understanding of
the material covered in the preceding sessions.

This review is currently set to practice mode. If you have already registered and been approved for
certification then you should Exit Course and re-enter before proceeding.

Each question below has one or more correct responses. Your selection of a response is immediately
marked correct or not.
Q1. Metals are more toxic in saltwater than in freshwater because of the salinity?

True?

False?

Q2. An aquatic biological community and its physical environment can be considered as an
ecosystem.

True?

False?

Q3. Salmon are more vulnerable than other fish because they are in contact with a wider
range of human activities.

True?

False?

Q4. Photosynthesis by green plants is an example of ... (select one only)

primary productivity?

tertiary consumerism?

anadromy?

Q5. Continuous exposure of organisms to toxic metals is more detrimental than


intermittent exposure?

True?

False?

Q6. Which of the following are significant sources of metal discharge into the
environment?

mining?

agriculture?

pulp and paper production?


urban waste?

coal combustion?

highway de-icing?

Q7. Which of the following metal exposure pathways are common to both humans and
fish? (select one or more)

lungs

skin

drinking water

food chain

gills

Q8. Water with a pH of 5 is ... (select one only)

acidic?

neutral?

alkaline?

Q9. Which of the following is the correct term for an increase in concentration of metals in
successively higher trophic levels of a food chain is ... (select one only)

bioaccumulation?

biomagnification?

bioconcentration?

Q10. Select the metals that qualify as essential metals from the following list (select one or
more).

aluminum?

chromium?
zinc?

nickel?

arsenic?

mercury?

selenium?

Q11. The term 'bioconcentration' is defined as ... (select one only)

an increase in concentration of a metal in an organism compared to its


concentration in water or sediments?

an increase in concentration of metals in successively higher trophic levels


of a food chain?

Q12. Which of the following forms of mercury (Hg) is the most toxic? (select one only)

elemental mercury?

organic mercury?

inorganic mercury?

Q13. The most biologically diverse ecosystems are to be found in ... (select one or more)

oceans?

fresh water lakes?

wetlands?

estuaries?

seashores?

swamps?

Q14. In an ecological context, the concept of a 'population' includes all of the biological
species that live in the same area at the same time.
True?

False?

Q15. Production of acid rock drainage (ARD) is catalyzed by the presence of bacteria.

True?

False?

Q16. Metals from rocks and mineral ores can be released into the environment by ...
(select one or more)

erosion?

weathering?

mining?

mineral processing?

Q17. Which of the following are valid properties of metals? (select one or more)

dissolve in water?

form positive ions (anions)?

form negative ions (cations)?

good conductors of electricity?

generally solid at normal temperatures?

always form acidic oxides?

Q18. What percentage of the world's liquid freshwater is represented by groundwater?


(select one only)

75%?

53%?

95%?
Click to see how well you did on this review.

Introduction

This part of the course will focus on the properties and uses of specific metals that are
mined or byproducts of mining in Canada and other countries, and the toxic effects of these
metals on fish, other aquatic organisms, and humans. We will cover some of the specific
characteristics of Cr, Cd, Pb, Hg, Cu, and Zn.

Chromium Properties

Cr is the 7th most abundant element on Earth.

It occurs in nine different oxidation states (valences) from


-2 to +6. Trivalent (+3) ion and hexavalent (+6) ion are the
most important.

Exposure pathways - inhalation of windblown


dusts, absorption through skin, drinking
contaminated water, and eating contaminated
food.

It is an essential trace element.

Needed for carbohydrate


metabolism.

Becomes toxic at higher


concentrations.

Cr+6 is much more


toxic than Cr+3. U.S.
EPA criteria for
protection of aquatic
life are much stricter
for Cr+6.

Synergism
between Cr
and Cd.
Humans are exposed to Cr via inhalation of windblown dusts. Humans and fish
are exposed to Cr via absorption through the skin, drinking water that is
contaminated with Cr, and eating other organisms that are contaminated with
Cr. Fish are also exposed to Cr via their gills (Bradl (2005), Wright and
Welbourn (2002)).

Canadian water quality guidelines for protection of aquatic life are stricter for
freshwater than saltwater because of the greater toxicity of metals in
freshwater and are stricter for Cr+6 (hexavalent Cr) than for Cr+3 (trivalent Cr).
The Cr+6 guidelines are 1 ppb for freshwater and 1.5 ppb for saltwater,
compared to 8.9 ppb for freshwater and 56 ppb for saltwater for Cr +3. When Cr
and Cd are present in the same waterbody, each metal increases the toxicity of
the other so that their combined toxic effects are greater than the sum of their
individual toxic effects (Wright and Welbourn (2002)).

Chromium Uses

manufacturing of alloys - e.g., elbow and knee


implants

hardening of steel

pigments

textiles and leather tanning

wood treatment

electronic
equipment

(Bradl (2005), Wright and Welbourn (2002)).

Bioconcentration (Bioaccumulation)

High in benthic (bottom-dwelling) fish and


shellfish, e.g., BCF = 2622 in brown bullhead
muscle, and 86-192 in oysters, mussels, and
soft-shell clams.

High in phytoplankton (BCF = 2300) and


zooplankton (BCF = 1900).

There is no evidence of
biomagnification in food chains.

(Wright and Welbourn (2002), Puget Sound Water Quality Authority (1988)).

Chromium Toxicity Factors

Cr is more toxic to aquatic organisms in soft water than


hard water.

Fathead minnow LC50 = 3 ppm (3,000 ppb) in


soft water and 72 ppm (72,000 ppb) in hard
water.

Goldfish LC50 = 18 ppm in soft water


and 133 ppm in hard water.

Rotifer (a zooplankton) LC50 =


3.1 ppm in soft water and 15
ppm in hard water.

(Puget Sound Water Quality Authority (1988), Taub (2004)). The comparative
LC50 values indicate that the fathead minnow is a more sensitive fish species to
the toxic effects of Cr than goldfish.

Cr toxicity to aquatic organisms increases as


water temperature increases.

Cr toxicity increases as pH decreases.

Cr toxicity increases as salinity


decreases.

(Wright and Welbourn (2002)). These factors illustrate the general principles of
metal toxicity.

Impacts of Chromium on Aquatic Organisms

Inhibits growth of algae - 62 ppb Cr+6

Inhibits fish growth - 16 ppb Cr+6


reduces growth of chinook salmon.
Sublethal effects may become
lethal effects, e.g., smaller fish
may be more vulnerable to
predators.

(Taub (2004)). Chinook salmon are more sensitive than algae to the toxic
effects of hexavalent Cr because a lower concentration of hexavalent
chromium reduces growth in the salmon. This is consistent with the overall
finding that aquatic animals are more sensitive to metals than are aquatic
plants. Although reducing the growth of a plant or animal is not directly lethal,
the smaller size increases the vulnerability of the organism to predators. What
begins as a sublethal effect of a metal may end up as a lethal effect.

Chromium Effects on Humans

Toxicity Story

In 1965, an alloy manufacturing company discharged Cr


to a well that was used by 155 people in a village in
China.

Cr has adverse effects on human health when its


concentration in drinking water is higher than 5
ppm.

Cr concentration in well water was 20


ppm.

Villagers' illnesses were:

mouth ulcers

digestive system problems

abnormal blood
cells

increased
incidence of
lung and
stomach
cancer
(1970-1978)

People who lived


closest to Cr
source had the
highest rates of
illness.

(Taub (2004)).

Other Human Health Effects of Chromium

kidney damage - tissue death and abnormal


function

nosebleeds

deformed spine

low white blood cell


counts, depressed
immune defense system

miscarriages

(Bradl (2005), Wright and Welbourn (2002)).

These health effects were seen in the film Erin Brockovich. The film is a true
story about the exposure of the residents of Hinkley, California to Cr+6 in
groundwater that was used for drinking water. Pacific Gas & Electric, the local
utility company, used Cr+6 as an anti-corrosion agent in cooling towers. Effluent
from the cooling towers was discharged to unlined ponds, from where the Cr +6
leached into groundwater that supplied drinking water and swimming pool
water for this community in the California desert. Over 500 people experienced
the health problems described above, as well as several types of cancer. Babies
were born with deformed spines. Many people had been exposed to Cr+6 for
over 30 years.

Erin Brockovich, a clerk at a law firm, investigated the health problems and
established the association with exposure to Cr+6. Her work resulted in a major
lawsuit against the utility company, with financial compensation paid to every
resident of Hinkley who had suffered ill health from exposure to Cr +6. An
employee of the utility company had been ordered to destroy company
records, but instead gave the information to Ms. Brockovich.

The film illustrates that one person can make a difference, it is possible to
make changes from within a company, and it is less expensive to prevent
pollution than to discharge pollutants and then clean up the polluted site.

Cadmium Properties
Cd is in the same family of the periodic table as
Zn and can replace Zn in some enzymes.

Bioavailability depends on presence of


Cd ion (valence = +2).

Cd is more toxic in freshwater


than saltwater because it
combines with chlorides in
saltwater to form molecule that
is less available from solution.

(Bradl (2005), Wright and Welbourn (2002)).

Cadmium Occurence and Sources

Common by-product of mining and smelting


for Zn, Pb, and other nonferrous metals.

7000 metric tonnes/year of Cd released


into air, mainly from mining.

1750 metric tonnes/year of Cd


released into aquatic
environment from industrial
effluent.

(Bradl (2005), Wright and Welbourn (2002)).

Cadmium Uses

Ni/Cd batteries

pigments

anti-corrosive metal coatings

plastic stabilisers

alloys

control
rods and
shields in
nuclear
reactors

(Bradl (2005), Landis and Yu (2003), Wright and Welbourn (2002)).

Cadmium Levels in Water and Sediments

Unpolluted freshwater - up to 3 mg/kg (parts


per million - ppm).

Freshwater near Cd sources - up to


1,000 ppm.

Concentrations in sediment are


at least 10 times as high as in
water.

(Bradl (2005)).

Cadmium Bioconcentration from Water - High BCFs

marine and freshwater plants - 1000

marine invertebrates - 250,000

marine and freshwater fish -


3000

freshwater invertebrates
- 4000

(Taub (2004)).

Cadmium Biomagnification

Fish and shellfish have higher Cd


concentrations than do zooplankton and algae.

Human exposure to Cd is mostly


dietborne.

Cd concentrations in fish and


humans are highest in liver,
kidneys, and bones.

(Bradl (2005), Landis and Yu (2003), Wright and Welbourn (2002)). The higher
concentrations of Cd in fish and shellfish compared with zooplankton and algae
suggests biomagnification of Cd in the food chain. However, there are mixed
opinions in the scientific literature about whether biomagnification of Cd
occurs. Accumulation of Cd in the liver, kidneys, and bones of fish and humans
suggests that the toxic effects of Cd are most severe in these organs.

Cadmium Effects on Aquatic Organisms

Impairs aquatic plant growth - this affects the


entire ecosystem.

Impairs functioning of renal (kidney)


tubules in fish.

Skeletal deformities in fish - Cd can


replace calcium in bones.

Effects can be directly or


indirectly lethal.

Cellular damage
observed in
hepatopancreas of
marine crustaceans
exposed to Cd.

Sublethal Cd
exposure
during
embryonic
and larval
developmen
t reduced
long-term
survival and
growth,
which can
cause long-
term
changes in
population
structure.

(Bradl (2005), Landis and Yu (2003), Wright and Welbourn (2002)). Green
plants are at the base of all food chains and food webs. All other biological
productivity is dependent on primary productivity. When aquatic plants that
are exposed to Cd do not grow normally, there will be less food available for
aquatic animals.

Skeletal deformities in fish can result in impaired ability of the fish to find food
and to avoid predators; hence, this sublethal effect of Cd can become a lethal
effect.

The hepatopancreas is a combination of liver and pancreas and therefore has


both digestive and metabolic functions which may be damaged by prolonged
exposure to Cd. Reduced long-term survival and growth were observed in the
marine isopod (a group of marine invertebrates) Idotea baltica. Males showed
greater sensitivity than females to Cd toxicity. Some individual animals were
more sensitive to the toxic effects of Cd than others. Differential survival of Cd-
exposed isopods can result in long-term changes in population structure
(Wright and Welbourn (2002)).

Cadmium Effects on Human Health

Cd half-life is 20 to 30 years.

20% of Cd is stored in liver and 30% is stored in kidneys.

Chronic Cd exposure causes kidney damage by inhibiting


enzymes responsible for resorption processes in kidney tubules.
Glucose and protein are excreted in the urine rather than
resorbed into the bloodstream.

Cd can become detoxified by binding with


metallothionens in liver.

But excessive concentration of Cd can prevent it


from being detoxified.

Cd can be released from liver as Cd-


metallothionen, and accumulate in
kidneys where metallothionen is
degraded and toxic Cd is released.

Skeletal deformities and bone loss


- Cd blocks vitamin D synthesis.

Anemia - indicates kidney


damage.

Generalized pain.

Carcinogenic
(can cause
cancer).

(Wright and Welbourn (2002)). The long biological half-life of Cd means that
exposed humans will never be able to get rid of all of the Cd in their bodies. It
will take 20 to 30 years to get rid of 50% of the Cd, 40-60 years to get rid of
75% of the Cd, and 60-90 years to get rid of 87.5% of the Cd.

If the concentration of Cd is high, the metallothionen detoxification system can


become overwhelmed and the excess Cd will be available to produce adverse
effects on the liver and/or kidneys (Landis and Yu (2003), Wright and Welbourn
(2002)).

Cadmium Story

Itai-Itai Disease

In the 1950s, people living in Fuchu, Japan


(near the city of Toyoma in Jintsu River Basin)
complained of joint, bone, and muscle pains
and also had symptoms of severe kidney
dysfunction.

Itai-itai (ouch-ouch) disease resulted in


deaths of some residents.

Causes:

Kamioka Mine, located 40


kilometers upstream of Fuchu,
had discharged untreated
effluent containing Cd, to rice
paddies since the 1920s.

Rice plants absorb Cd


easily.

People ate
contaminated
rice.

(Bradl (2005), Landis and Yu (2003), Wright and Welbourn (2002)).

Dietborne Cadmium Levels

Cd is toxic to people when the daily intake is


250 to 300 micrograms.

Rice farmers were eating 600 to 1000


micrograms of Cd daily - some for up to
30 years.

This illustrates that metal toxicity is higher with continuous exposure than
intermittent exposure to a metal.

In order to discontinue human exposure to Cd-contaminated rice, the surface


soil in the rice paddies was covered with 25 centimeters of uncontaminated
soil and several soil amendments were applied. After these remedial actions
were taken, the Cd concentrations in the rice decreased to less than 0.1
milligram per kilogram (less than 0.1 ppb), which is the usual Cd concentration
in rice that is grown in unpolluted paddies (Bradl (2005), Landis and Yu (2003)).

The effects listed above were observed in the people who had itai-itai disease.
Vitamin D is a cofactor, necessary for the deposition of calcium in bones. By
blocking Vitamin D synthesis, Cd prevents the bones from having a normal
amount of calcium. The bones become soft (osteomalacia) or brittle
(osteoporosis). The International Agency for Research on Cancer has classified
Cd as a Category I (human) Carcinogen (Bradl (2005), Landis and Yu (2003),
Wright and Welbourn (2002)).

hidden

Lead Toxicity
Uses of Lead

plumbing

rechargeable batteries

cable sheathing

shot and ammunition

solder (seams of canned foods)

shields for protection against


radioactive materials

insecticides

paint pigments
(past)

gasoline
additive
(past)

The history of the human use of Pb goes back for more than 5,000 years. Pb
occurs naturally in the earth's crust, often in association with sulfur, and is easy
to find and mine. The ancient Romans mined Pb extensively, mostly from
deposits in England and Spain. Because Pb is resistant to corrosion and
discoloration, early uses of it included pipes for the collection, transport, and
distribution of water and containers for the storage of food and beverages.
Chronic Pb poisoning among the ruling classes may have contributed to the
decline of the Roman Empire. Although the use of Pb in drinking water pipes
has been largely discontinued in developed countries, old buildings in older
cities in the U.S. still use Pb-based systems (Wright and Welbourn (2002),
Angier (2007)).

Pb has been used in paint pigments because it imparts brightness to the color;
furthermore, Pb-based paints cling well to wood (Angier, (2007)). Pb is still
used in paint pigments in developing countries; some products are then
exported back to developed countries. For example, wooden toy trains
manufactured in China and exported to the U.S. have bright red and yellow
paint coatings that contain lead. The U.S. based toy maker, RC2 Corporation,
recently recalled 1.5 million of these toy trains (Warren (2007)). Inexpensive
children's jewelry manufactured in China also contains lead-based paint. In the
past three years, the U.S. Consumer Product Safety Commission recalled
17,901,020 pieces of this jewelry (Lipton and Story (2007)). Mattel, the world's
largest toy company, has recalled 436,000 toy cars made in China because they
are covered with Pb paint. Laboratory tests conducted by the Center for
Environmental Health, a nonprofit organization in Oakland, California, have
found that some Chinese-made vinyl baby bibs sold at Toys "R" Us stores are
contaminated with Pb at levels up to 1800 ppm (1.8 parts per thousand =
0.18%). Pb can end up in vinyl by being added as an inexpensive stabilizer; Pb
can also come from pigments used to add color or can come from recycled
vinyl, which may have had Pb in it from its earlier use (Story and Barboza
(2007)).

Mobilisation of Lead

Smelting of Pb ore.

Smelting of Cu and Zn ore.

Pb dust is released into the air


and can then be deposited in
waterbodies and sediments.

Long-range transport of
Pb is causing
bioaccumulation in
remote aquatic
ecosystems such as
Arctic lakes and seas.

The average concentration of Pb in the Earth's crust is 20 ppm. The usual


valence of Pb is +2, found in inorganic compounds such as PbSO 4 and PbCO3. Pb
can also exist in the +4 or -4 valence, forming organic compounds such as
tetraethyl Pb. This highly versatile metal can be mobilised and enter the
aquatic environment from several sources (Cunningham and Cunningham
(2004), Landis and Yu (2003), Wright and Welbourn (2002)).

Human Exposure Pathways

Inhalation of Pb dust.

Drinking water.

Eating contaminated food -


Acidic foods and juices will
solubilise Pb from containers.

Eating leaded paint


(children) that flakes off
walls of old buildings.

(Bradl (2005), Landis and Yu (2003), Wright and Welbourn (2002)).

Impacts on Human Health

Pb accumulates and persists in bones and teeth,


which function as reservoirs for releasing Pb into
bloodstream.

Half-life of Pb in bones = 20 years.

Pb toxicity is higher when diet is


deficient in Ca.

Pb exposure can be assessed


by measuring Pb
concentration in blood.

250 ppb was


considered "safe"
until the 1970s. This
is not "safe" for
children.

50-100 ppb is
the
recommende
d guideline for
"safe"
concentration
in children.

But
wheth
er
there
is a
thresh
old for
effects
is
unkno
wn.
Although Pb does not directly harm bones and teeth, it remains in these organs
for a long time and is released into the bloodstream, where it then travels to
target organs such as the brain and the bone marrow (the organ that produces
blood cells). As is the case with Cd, the long biological half-life of Pb in bones
means that people who are exposed to Pb will never completely get rid of it.
People who do not get enough calcium in their diets will accumulate more lead
in their bones, with the consequence of greater lead toxicity (Bradl (2005),
Landis and Yu (2003), Wright and Welbourn (2002), World Health Organisation
(1995)).

Neurological Impacts

"Subtle" effects occur in absence of symptoms


of overt Pb poisoning.

Hyperactivity, poor attention span, and


low IQ, especially in children.

Detroit, Michigan study of 5000


children with elevated blood Pb
levels - high percentage were in
special education classes.

(Bradl (2005), Cunningham and Cunningham (2004), Landis and Yu (2003),


Wright and Welbourn (2002)).

Mechanism of Toxicity:

It mimics Ca.

Interferes with Ca transport across


membranes of neurons (nerve cells).

The result is inhibited


neurotransmission.

Ca transport across membranes of neurons is a necessary step in the


transmission of nervous system "messages" and, therefore, in the normal
functioning of the nervous system (Landis and Yu (2003)).

Physiological and Biochemical Impacts

Inhibits enzymes that are needed for


haemoglobin synthesis (e.g., ALAD =
aminolaevulinic acid dehydratase).
The result is anaemia (found in children
with blood Pb >400 ppb).

Severely damages kidney


function.

Teratogen (causes birth


defects).

Haemoglobin is an iron-containing protein found in red blood cells; it binds


with oxygen and transports oxygen to all the cells in the human body. Two key
enzymes involved in haemoglobin synthesis are ALAD and ferrochelatase.
When these enzymes are inhibited and the synthesis of haemoglobin is
disrupted, then there is insufficient transport of oxygen and anaemia is the
result. Anaemia was observed as a consequence of Pb exposure during the
time of the Roman Empire; the Roman engineer Vitruvius noted that men who
worked in Pb smelters had abnormally pale complexions (Angier (2007)).
Children who have anaemia fatigue easily and are less able to learn well.

In summary, Pb has a wide range of toxic effects on humans including


subcellular, physiological, and behavioural. The developing foetus and children
under the age of six are most vulnerable to the toxic effects of Pb. Assessing
the risk of very low levels of exposure to Pb is challenging, especially for young
children. Pb can cross the placenta, resulting in miscarriages, stillbirths, and
birth defects including neurological damage (Bradl (2005), Landis and Yu
(2003), Wright and Welbourn (2002)). After it infiltrates a cell, Pb distorts
protein molecules and has a particularly severe effect on transcription factors,
proteins that control when genes flick on and off. Genetic timing is critical
curing embryonic development. Even modest exposure to Pb might therefore
corrupt the whole script of a developing brain (Angier (2007)).

Exposure Pathways in Aquatic Biota

Absorption through gills.

Drinking Pb-contaminated water.

Eating Pb-contaminated prey.

Eating Pb-contaminated
sediments - Pb
compounds (PbS, PbCO3,
PbSO4) do not dissolve
well in water, but adsorb
(bind to) sediments.
Pb is not reactive
in water or
sediments. It
remains in the
form or
compound in
which it enters
the water or
sediments.

(Landis and Yu (2003), Wright and Welbourn (2002)).

Surface Water Concentrations

Background Pb levels: 0.5 ppb in freshwater,


0.001 to 0.004 ppb in seawater.

Pb levels downstream of ARD from


abandoned coal mines: 6,600 to
811,000 ppb.

(Jaworski (1978), Paulson and Feely (1985), Schut et al. (1986)).

Bioconcentration

Aquatic organisms bioconcentrate Pb.

Pb does NOT biomagnify. Its


concentration decreases at higher
trophic levels in food chains.

Pb concentrations are higher in


acidic water than in water with
neutral or alkaline pH.

Pb accumulates in skin,
bones, kidneys, and liver
of fish rather than
muscle.

(Wright and Welbourn (2002)).


The ability of aquatic organisms to bioconcentrate lead means that the
concentration of lead in the tissues of these organisms will be higher than the
concentration of Pb in the water or sediments. It is good news for people that
Pb does not accumulate in the muscle (edible) tissue of fish. This makes Pb less
problematic via this route of exposure. However, people who eat the whole
fish and wildlife (who, of course, eat the whole fish) can potentially be exposed
to high concentrations of Pb.

Lead BCFs

freshwater invertebrates: 499-1700

brook trout (a finfish species): 42

blue gill (a finfish species) 45

mussels: 2570

oysters: 1400

Note that Pb bioconcentrates more in shellfish than in finfish because many Pb


compounds are not highly soluble in water, they are found at higher
concentrations in the sediments at the bottom of a waterbody (Taub (2004)).

Shellfish are more likely than finfish to inhabit or burrow in the sediments,
where they are exposed to higher concentrations of Pb.

Impacts on Aquatic Organisms

Algae

Adverse effects when Pb level is higher than 500 ppb:

Inhibits enzymes needed for photosynthesis.

Reduces absorption of water.

Interferes with cell division and


respiration.

Inhibits growth.

(Taub (2004)). When less photosynthesis takes place, the algae will produce
less food and therefore will not grow as much. Decreased primary productivity
means less food for animals; this has repercussions for the entire ecosystem.
Fish

Adverse effects when Pb level is higher than 50 ppb:

Embryos and fry are more sensitive to toxic


effects of Pb than are adults.

Pb is more toxic at lower pH and in soft


(low alkalinity) water.

Adverse effects on gill function


in fish exposed in lab to 0.1-500
ppm Pb.

(Wright and Welbourn (2002), Taub (2004)). As is the case with other metals,
the toxicity of Pb to fish depends in part on the species. Goldfish are relatively
resistant to Pb because they can excrete Pb via their gills (Landis and Yu
(2003)).

Birds

Chronic exposure to Pb causes:

Impaired growth.

Reproductive effects - reduced egg


clutch size, inadequate calcium
deposition in eggshells.

Pb substitutes for Ca in bird eggshells (Wright and Welbourn (2003)).

Mercury Toxicity

Introduction

Hg is an interesting metal from the viewpoint of toxicity because it is the


organic form (methylmercury) that is the most toxic. In addition to the topics
covered for other metals, we will also focus on factors affecting methylation of
mercury from inorganic to organic forms.

Hg is known to biomagnify in food chains (Wright and Welbourn (2002)). This


property is illustrated in the Minamata Bay story, which will be discussed.
Sources

Natural (50 ppb in Earth's crust) - volcanic


eruptions, erosion of soils containing Hg.

Hg mining and smelting.

Gold mining - 130 tonnes of Hg


per year are deposited in the
Amazon River and its
tributaries.

Cu and Pb smelting
(byproduct).

(Bradl (2005), Cunningham and Cunningham (2004), Landis and Yu (2003),


Wright and Welbourn (2002)).

Artisanal (informal) miners in developing countries such as the countries of the


Amazon River Basin use Hg to trap Au and separate it from sediments, and
then boil off the Hg with a blowtorch. This process and the human health
issues that result from it will be described in more detail in the section on the
Global Mercury Project.

Uses

Historical Uses

Hg was mined at least 2000 years ago in


Spanish Almaden mines, which are the largest
producers of Hg today.

The use of HgS (cinnabar) as pigment


for red ink in China goes back 3000
years.

(Wright and Welbourn (2002)).

Current Uses

thermometers
barometers

batteries

fluorescent tubes and other


electrical equipment

dental amalgam

pulp and paper


industry

gold
extracti
on
(artisan
al
mining)

(Bradl (2005), Wright and Welbourn (2002)).

Hg is the only common metal that is liquid at room temperature. It is useful in


thermometers because of its ability to expand uniformly over its liquid
temperature range (-39oC to 357oC) and is useful in electrical equipment
because of its good electrical conductivity (Landis and Yu (2003)).

Chemical Speciation

elemental Hg/metallic Hg (Hg0)

divalent inorganic Hg (Hg+2)

organic Hg (methylmercury)

(Wright and Welbourn (2002)).

Elemental Mercury

It is liquid at room temperature.

Volatilises (vaporizes) readily.

Does not dissolve well in water.


These properties of elemental mercury mean that it is not bioavailable to
aquatic organisms (Wright and Welbourn (2002)).

Inorganic Mercury

Forms salts with various anions.

Mercuric salts are slightly soluble in


water.

Hg+2 associates with particles


and water in the atmosphere.

(Wright and Welbourn (2002)).

Organic Mercury

Formed in aquatic ecosystems by methylation of


inorganic Hg from Vitamin B12 (methylcobalamin)
by bacteria.

L5Co-CH3 + Hg+2 = L5Co+ + CH3Hg+

Methylation takes place at the


interface between water and
sediments.

Monomethylmercury
(CH3Hg+) is stable and
dissolves well in water.

Dimethylmercury
(CH3)2Hg is less
stable and less
water-soluble.

Monomethylmercury is more bioavailable and therefore more toxic than


dimethylmercury (Wright and Welbourn (2002)).

Monomethylmercury Toxicity

It is the most toxic and persistent form of Hg.

Moves readily across biological


membranes and is lipophilic.

Bioaccumulates in fish muscle


tissue.

Has the longest


biological half-life (70
days in humans vs. 6
days for inorganic Hg,
170 days in pike).

A lipophilic (literally "fat-loving") compound is a compound that can dissolve in


fatty tissues. Organic compounds have this property, which explains their
ability to cross cell membranes (such as gill membranes that are comprised of
proteins and lipids) and to persist in fatty tissues of organisms rather than
being excreted (Wright and Welbourn (2002)).

Factors Affecting Methylation

Low pH

Stimulates CH3Hg+ production.

Increases proportion of total Hg


available for methylation due to
increased binding of Hg to particulates
and decreased evaporation of Hg from
water.

Because monomethylmercury is the most toxic form of Hg, factors that


increase methylation will increase Hg toxicity. When the pH of a waterbody is
low, there is more binding of Hg to particulates in the water column or
sediments and less Hg is lost from water by evaporation than at neutral or
alkaline conditions (Wright and Welbourn (2002)).

High Dissolved Organic Carbon (DOC)

Promotes methylation, often in combination


with low pH.

Responsible for high levels of


methylmercury in fish in reservoirs,
even at pristine locations.

3.5 ppm Hg in northern pike in


LaGrande-2 reservoir in
Quebec.

High DOC is often combined with low pH under natural conditions. Therefore,
it can be difficult to assess the separate respective roles of these two factors in
methylation. The water in wetlands is often acidic with a large amount of
organic matter. As a result, wetlands frequently export methylmercury to lakes
and rivers (Wright and Welbourn (2002)).

Reservoirs are created when a terrestrial site is flooded and converted to an


aquatic system, often for hydroelectric projects. The DOC in the vegetation in
the original terrestrial ecosystem stimulates microbial methylation of the
naturally occurring Hg. The methylation, combined with biomagnification,
results in unacceptably high Hg levels in predatory fish. For example, in the
LaGrande-2 reservoir, the Hg levels in northern pike were approximately five
times higher than those in unflooded natural environments (James Bay
Mercury Committee (1993)). The advisory level for fish consumption is 0.5 ppm
Hg in Canada (Watras and Huckabee (1994)).

Exposure Pathways

Atmospheric - Hg can be transported long distances to


remote aquatic ecosystems.

Hg enters aquatic ecosystems from atmosphere


as wet and dry deposition.

Bacteria transform it to CH3Hg+.

Bioconcentration from water and


sediments.

BCF = 100 for marine algae


and 225,000 for northern
pike.

Biomagnification up
the food chain -
Humans are
exposed by eating
contaminated fish.

(Wright and Welbourn (2002)).


Biomagnification in Remote Ontario Lake

Hg levels were higher


in clams than in the
sediment in which
they live, higher in
smelt than in clams,
higher in bass and
pike than in the smelt that they eat, and
highest in otters and marine birds which are
the top predators in this food web.

The advisory level for fish consumption


is 0.5 ppm Hg.

Hg level in bass was 0.58 ppm.


Hg level in pike was 1.01 ppm.

Hg underwent bioconcentration in the organisms in the lake. Although Hg was


undetectable in the lake water, it does not mean that Hg was absent. It means
that the concentration of Hg was too low to be measured by the available
analytical methods. Hg underwent bioconcentration and therefore was
detected in organisms in the lake. Hg underwent biomagnification; its
concentration increased at each higher level in the food chain (Wren et al.
(1983)).

Factors Affecting Mercury Levels in Fish

Size (age) of fish - Larger and older fish have higher


levels of Hg than smaller and younger fish.

Species - Predators have higher levels than


fish species lower in food chain (e.g., higher
levels in walleye than pumpkinseed).

Water temperature - More Hg is


concentrated in summer than in
winter.

pH of lake water - Hg levels


are higher in acid lakes than in
lakes with higher pH.

Water softness - Hg
levels are higher in
softwater than
hardwater.

Antagonism -
Hg and Se, Hg
and Cd.

Larger and older fish have had more time in which to accumulate lipophilic
methylmercury in their tissues than smaller and younger fish. Additionally,
larger fish and predatory fish eat further up on the food chain, which means
that they are exposed to and therefore accumulate higher concentrations of
methylmercury in their tissues. As it was explained previously, the body
temperature of a given fish is the same as the water temperature. The
metabolic rate is higher when the water temperature is higher; hence, more
methylmercury will bioaccumulate in fish tissues (Wright and Welbourn
(2002)). The 96-hour LC50 for freshwater crayfish was found to be 0.79 ppb at
20C, 0.35 ppb at 24C, and 0.14 ppb at 28C (Del Ramo et al. (1987)).

Also, more methylation of inorganic mercury to methylmercury occurs when


the pH of lake water is acidic. Se and Cd are able to protect organisms from Hg
uptake and toxicity, but the physiological basis for this interaction is unclear. It
is possible that Se binds with methylmercury, thereby preventing the
methylmercury from binding with SH groups on enzymes and inhibiting enzyme
activity (Landis and Yu (2003)).

This graph shows the influence of fish size, species,


and trophic level on the concentration of mercury in
two species of fish from Lake St. Clair in Ontario,
Canada. This lake has been affected by industrial
releases of mercury. Walleye are larger fish than
pumpkinseed and feed at a higher trophic level; hence, more biomagnification
of mercury has taken place in their tissues. About half of the walleye as well as
the larger pumpkinseed had mercury concentrations that exceeded the human
health guideline of 0.5 ppm (Ontario Ministry of the Environment (1992)).

Impacts of Methylmercury on Fish and Wildlife

Fish are relatively insensitive to toxic effects of


CH3Hg+.

Can tolerate 10 times as much CH3Hg+ as


humans and are more tolerant of CH3Hg+ than
wildlife predators.

Storage of CH3Hg+ in muscle tissue may


detoxify CH3Hg+ and/or reduce
exposure of brain tissue to it.

If CH3Hg+ levels are high


enough, then there will be
adverse impacts.

Decreased hatching rate


of fish and bird eggs.

Impaired growth
and
development.

Death -
When
mink
from
Ontario
and
Quebec
ate fish
containin
g 0.9-1.0
ppm
CH3Hg+,
at least
50% of
the
exposed
populatio
n died.

Decreased hatching rate and impaired growth and development can lead to
severe adverse effects at the population and ecosystem levels (Wright and
Welbourn (2002)).

Minamata Bay Story

Overview

Minamata Bay is located on Kyushu Island, in


southern Japan.

In the 1950s, fishermen, their families,


and seabirds were stricken with
mysterious neurological illness.

Some babies were born with


Minamata Disease although
their mothers did not always
show symptoms.

High concentrations of
total Hg were found in
fish and shellfish in the
bay.

Median
concentration in
fish was 11 mg/g
(11,000 ppm = 11
parts per
thousand = 1.1
percent).

Hg source
was
traced to
discharge
of
industrial
waste
from
upstream
factory.

Minamata Disease occurred during the same time period as Itai-Itai Disease
from the toxic effects of Cd. Minamata Disease in newborn babies, but not in
their mothers, suggests that Hg crosses the placenta; this may function as a
detoxification mechanism for pregnant women (Bradl (2005), Landis and Yu
(2003), Wright and Welbourn (2002)).

Landis and Yu (2003) contrast this extremely high concentration (11,000 ppm)
of Hg in Minamata Bay fish with the current Canadian advisory level of 0.5
ppm.

History

In 1907, the Chisso chemical manufacturing


company (acetaldehyde and vinyl chloride)
was built.

In 1932, mercuric oxide (HgO) was used


as a catalyst.

In the 1950s, a strange


neurological disease affected
the fishing community and
there were fewer fish in the
bay.

In 1959, scientists
discovered that there
was a link between
CH3Hg+ and Minamata
Disease (more than 700
cases had been
identified).

(Bradl (2005), Landis and Yu (2003), Wright and Welbourn (2002)).

What Happened in Minamata Bay?

Chisso discharged industrial waste to the bay.

Bacteria transformed Hg+2 to CH3Hg+.

Seabirds and people ate fish.

CH3Hg+ level at top of


the food chain is
thousands or millions of
times higher than in
water.

(Bradl (2005), Landis and Yu (2003), Wright and Welbourn (2002)).

Chisso Reaction

Company did not listen to fishermen, because:

Fishermen were poor.

Fishermen were not part of the major


economic community.

Chisso employees did not have


the Minamata Disease.

Chisso employees were working with inorganic Hg and were not exposed to
methylmercury. They did not rely on Minamata Bay fish for a major part of
their diet. The Chisso Company managers said that there was no proof that the
mercury used in the manufacturing process had caused Minamata Disease;
after all, their employees were not ill. Eventually, the company did accept
responsibility (Wright and Welbourn (2003)).

What Actions Were Taken?

Toxic sediments were dredged from Minamata


Bay.

It was an imperfect solution because it


was expensive and had disposal issues.

Compensation was offered to


2,265 victims (but another
15,000 people developed
Minamata Disease).

Finally, in 1997,
Minamata Bay was
declared "clean."

In 1968, the Chisso Company stopped using mercuric oxide as a catalyst in the
production of acetaldehyde. This eliminated the source of mercury that had
been discharged to Minamata Bay for over three decades. However, the
sediments at the bottom of Minamata Bay were still contaminated with high
levels of methylmercury.

From 1974 to 1990, the local government and the Chisso Company partnered
in funding the dredging of 1,510,000 cubic meters of sediment from Minamata
Bay. The work was carried out by using four cutterless suction dredges, a newly
developed type of dredging equipment that minimizes re-suspension of
sediments. The dredged sediments were disposed of in a landfill that had an
area of 2,000,000 square meters and that was enclosed by a highly watertight
revetment. The dredged material was covered with a sandproof membrane,
lightweight ash earth, and mountain soil. As a result of the dredging, 58
hectares of land were reclaimed from the inner area of the bay (Yoshinaga
(1995)).
Impacts of Methylmercury on Human Health

Structural Damage to Brain:

impaired hand-eye coordination

memory and speech loss

poor performance on
intelligence tests

blurred vision, blindness

muscle
weakening and
spasms

death

Children and developing fetuses are at higher


risk because the brain is still developing.

CH3Hg+ is teratogen. Babies are born


with twisted arms and legs.

Lower concentrations of CH3Hg+


than previously thought (10
ppm instead of 50 ppm) can
cause brain damage and birth
defects.

Long-term exposure to
Hg causes kidney
damage.

The U.S.
Environmental
Protection
Agency has
classified
inorganic Hg and
CH3Hg+ as
possible human
carcinogens.

Methylmercury is a neurotoxin; its target organ is the brain (Bradl (2005),


Landis and Yu (2003), Wright and Welbourn (2002)). Kidney damage occurs at
concentrations higher than those that produce neurological symptoms (Bradl
(2005), Wright and Welbourn (2002)).

Mechanism of Mercury Toxicity

Inhibition of enzyme activity - Hg binds with


sulfhydryl (SH) groups in enzymes.

Affects metabolism of sodium and


potassium.

Decreases DNA content of cells.

Adversely affects mitosis


(cell division).

The ultimate effects of Hg in the human body are inhibition of enzyme activity
and cell damage. Methylmercury displaces hydrogen ions from SH groups, as
shown in the following equation (Landis and Yu (2003)):
RSH + CH3Hg+ R-S-Hg-CH3 + H+

Mercury affects the metabolism of sodium and potassium by increasing the


permeability of potassium. Sodium and potassium are electrolytes needed for
the normal functioning of the cardiovascular and nervous systems. Decreasing
the DNA content of cells and adversely affecting cell division can lead to birth
defects and cancer (Landis and Yu (2003)).

Regulatory Aspects in Canada

Water quality guideline for Hg is 0.1 ppb for


protection of aquatic life and 1.0 ppb for
drinking water.

Sediment quality guideline for Hg is


0.13 ppm dry weight.

Food intake criterion for Hg is


<0.5 ppm fresh weight (before
cooking).

(Watras and Huckabee (1994)).

Unsafe Fish
The following species of fish accumulate exceptionally high concentrations of
Hg in their edible (muscle) tissue and should be avoided or eaten rarely. This is
especially true for pregnant women and for children (Canada's Seafood Guide,
Washington State Department of Health (2006)).

Chilean sea bass

Halibut (Atlantic)

Mackerel

Monkfish

Orange roughy

Rockfish/snapper

Shark

Sturgeon

Swordfish

Tilefish

Tuna
steak
Toxicidad Mercury - biomagnificacin en remoto lago Ontario

Este diagrama muestra concentraciones crecientes (en partes por milln) de mercurio
con niveles trficos ms altos en un remoto lago Ontario softwater (Wren et al. (1983)).

La toxicidad del mercurio - Factores que afectan los niveles de mercurio en el pescado
Relacin entre la concentracin de mercurio y la longitud del pez.

The Global Mercury Project

Introduction

This session is an overview of the Global Mercury Project (GMP), a


collaborative initiative between the United Nations International Development
Organization (UNIDO) and the University of British Columbia (UBC) Norman B.
Keevil Institute of Mining Engineering.

The project, which aims at reducing mercury pollution


in artisanal gold mining sites, began in six countries in
August 2002: Brazil, Sudan, Tanzania, Zimbabwe, Laos,
and Indonesia. In the past five years, eight other
countries have been added: Ecuador, Venezuela,
Suriname, Senegal, Guinea, Ghana, Mozambique, and
Cambodia.
Dr. Marcello M. Veiga, the Chief Technical Advisor for the GMP and Associate
Professor of Mining Engineering at UBC, provided the information for this
section of the course.

(Gunson et al. (2006), UNIDO Global Mercury Project (2006), Veiga and Baker
(2004), Veiga et al. (2006)).

Artisanal and Small-Scale Miners

The term artisanal and small-scale miners


(ASM) encompasses all small, medium,
informal, legal and illegal miners who use
rudimentary processes to extract gold and
other minerals from secondary and primary
ores.

10 to 15 million artisanal
miners are producing 600-
800 tonnes Au/year in more
than 60 countries.

About 50 to 100
million people are
directly and indirectly involved in
artisanal gold mining.

Why Miners Use Hg

Mercury amalgamation is an ancient technique but


still useful for artisanal gold miners.

Main reasons why Hg is widely used by ASM:

Easy to be used.

Cheap (1kg Hg = 1g
Au).

Very accessible.

Miners are not aware of


the risks.
In many ASM sites, Hg is sold in pharmacies in vials for "dental use". Anyone
can buy it and no questions are asked. Hg in developing countries is from
developed countries. In 2000, the Netherlands shipped 245 tonnes of Hg to 18
countries, mostly in Latin America and the Caribbean region. Spain shipped 774
tonnes, the U.K. shipped 200 tonnes, and Germany shipped 105 tonnes. In
2006, the U.S. shipped 350 tonnes of Hg to developing countries. Most of this
Hg is of low quality - not suitable for electronics but good for ASM.

Main Findings

The first phase of the GMP was an assessment of the environmental and
human health impacts of the use of Hg in Au mining.

Hg-contaminated tailings are submitted to cyanidation in So Chico,


Brazil:

Carnivorous fish, average = 4.16 ppm Hg

Non-carnivorous, average = 1.33 ppm


Hg

60% of fish > 0.5 ppm Hg

One fish sample had 22


ppm Hg

Exposure of the Hg-contaminated tailings to cyanide solubilises the Hg; it can


then be methylated more easily. Hg-contaminated tailings are also very mobile
and have been transported more than 200 kilometers downstream in the
Tapajs River, Brazil. The Hg then undergoes methylation and bioaccumulation
downstream.

Problems with Hg Vapor


This photo shows the
exposure of a baby to
Hg vapours. As
indicated previously,
babies and young
children are most
vulnerable to the
toxic effects of Hg.

Retorted Au (still with Hg) is sold to gold shops


and melted: Hg vapour is released in the
villages.

Retorted Au contains 2% to 5% Hg.

Solutions

The first phase was dedicated to environmental and human


health impact assessment. The second part of the GMP
project focuses on developing and implementing actions to
reduce the Hg exposure of artisanal Au miners and their
families:

Education of miners and communities.

Promote and improve gravity


concentration.

Reduction/elimination of Hg
emissions and exposure of
miners and communities.

Solutions Being Introduced

In the short-term, actions need to be taken to reduce Hg use and emissions. In


the long-term, another method of mining Au needs to replace Hg
amalgamation.
Education/Training

Miners cannot afford to stop their activities to


"be educated."

Miners learn by example.

Miners must decide what is


good or not for themselves ...
not us.

M
i
n
e
rs move from one site to
another.

GMP innovation:
Transportable
Demonstration
Units (TDU) (see
figure.)

There are economic and cultural challenges involved in educating artisanal Au


miners about the dangers of Hg amalgamation and how to reduce exposure to
Hg. The miners need to continue to earn a living. They need to decide what
actions to take, not have foreign "experts" tell them what to do. Miners are
very mobile; they go where the Au is. Therefore, the GMP takes the education
to the miners at the various locations where ASM is practised.

The trainers are local people, who then train their families, friends, and
neighbors.
Following are examples of actions that are underway to reduce Hg emissions
and Hg exposure of artisanal Au miners and their families.

Eliminating Copper-Amalgamating Plates

Amalgamation of the whole ore is the main


cause of mercury pollution in nearby
waterbodies because this process generates
tailings with high levels of mercury and the
tailings are often poorly stored. Furthermore,
the tailings are often submitted to cyanidation
(addition of cyanide compounds in order to help dissolve the gold).
Cyanidation of mercury-contaminated tailings exacerbates methylation
of inorganic mercury to methylmercury. Eliminating copper-
amalgamating plates will help to reduce the large losses of mercury to
the environment from whole ore amalgamation.

(Veiga et al. (2006)).

Activating Hg Before Amalgamation

Increase coalescence = reduces Hg flouring = less Hg loss with tailings

Reducing % Mercury in Amalgam

Some of the mercury added to the amalgamation process does not


combine with gold and therefore must be removed. As shown in the
picture on the left, miners usually squeeze off the excess mercury
through a piece of fabric. A better way to remove excess mercury from
amalgam involves transferring the amalgam to a cup made of steel,
porcelain or polyvinyl chloride (PVC) covered with a piece of fabric, and
placing the cup in a centrifuge, as shown in the diagram in the middle.
Running the centrifuge for one or two minutes removes the excess
mercury.

The resulting amalgam has more gold and less than 20% mercury. This
mechanical procedure eliminates exposure of the miners to mercury
through their skin. The picture on the right shows the use of a bicycle
wheel as an improvised centrifuge. Two PVC tubes forming two cups
connected to each other with a piece of fabric in the middle are
strongly joined together with clamps. The assembly is attached to a
bicycle wheel, which is rotated for one or two minutes to force the
excess mercury through the fabric of the second cup.
(Veiga et al. (2006)).

Home-Made Retort Using Kitchen Bowls

After gold is amalgamated with mercury, the amalgam must be heated above
360C to separate out the mercury. When heated, mercury becomes volatile
leaving the gold behind in a solid state. Burning amalgam in an open pan
exposes the miners and their families to mercury vapour. The use of retorts
prevents this exposure by condensing the mercury vapour in a contained
space; the liquid mercury can then be reused.

The picture below shows a retort that has been made with metallic and glass
bowls found in local markets. The amalgam is placed in a small metal bowl,
which fits into a hole made in a larger metal bowl. A glass bowl is used as a
cover. Wet sand is added to seal the retort and prevent loss of mercury vapour
to the air. Mercury evaporates and condenses on the walls of the glass cover,
dripping onto the sand.

(Veiga et al. (2006)).

Measuring Hg Escaping from Kitchen Bowl Retorts

When burning amalgam in open air, miners are


exposed to Hg levels around 50,000 g/m3

When using the kitchen bowl: 0.4


g/m3

WHO guideline for worker's


exposure = 25 g/m3

When gold is melted, residual


mercury is released in populated
environments. When the amalgam is
retorted, the resulting gold is melted
to rid it of impurities. The melting
occurs in village gold shops, at home
or at the mine site.
(Gunson et al. (2006))

Prototype description

The picture below is a diagram of a rudimentary fume hood. When gold is


melted, residual mercury vapours are extracted. The fan blows the mercury
vapours out into the air. (Veiga et al. (2006))

Reducing emissions from gold shops

The pictures below show a more sophisticated fume hood that extracts and
contains the residual mercury. The fume hood includes a metallic condenser
and an activated charcoal filter. Less than 2% of the residual mercury will be
released into the air. (Veiga et al. (2006))

Brochures and Posters (health)


Mercury hazard and solutions

Why Hg is a hazard and what people


can do to protect themselves

Maternal and baby health

Related
health
issues

H
IV/AIDS and other
diseases

Water and sanitation

Nutrition

These are examples of educational posters, focusing on groups most at risk


(e.g., children).

Success of the Train-the-Trainer Model

The GMP Team trained local miners on the use of retorts to reduce Hg
exposure. Later in the day, the local workers were teaching others in the
community.

Conclusions
Artisanal mining is a poverty-driven activity (in more than 60 countries).

The number of ASM is increasing with gold price and more women and children are involved.

Hg emissions from artisanal and small-scale gold mining (ASM) are increasing.

Important to introduce immediately MEASURES to reduce exposure and emissions.

Amalgamating copper plates must be BANNED.

Cyanidation of Hg-contaminated tailings must STOP.

Tailings with Hg must be properly disposed of.

In June 2005 the European Community decided to stop mercury trade by 2011, but what about USA,
Canada and Japan?

It is needed to show alternatives to artisanal gold miners not just stop their access to Hg.

UNIDO Commitment: reduce 50% Hg in ASM by 2017.

Next GMP is aiming to reach at least 20 countries: 5 or 6 years

Monitoring and Solutions will be implemented simultaneously


Suggested Exercise

Mercury from an artisanal mine has been discharged into River X. Describe the
combination of factors that would produce the worst case scenario for impacts
to aquatic organisms in the river and for impacts to humans.

hidden
The Global Mercury Project - Solutions Being Introduced

Short-term and long-term solutions

The Global Mercury Project - TDU

TDU

El Proyecto Mundial del Mercurio - La eliminacin de amalgama de cobre Placas


Mineral de oro se amalgama con mercurio utilizando una placa de cobre (Venezuela,
2003)

The Global Mercury Project - Activating Hg

The Global Mercury Project - Reducing % Mercury in Amalgam


Manual squeeze of mercury (Indonesia, 2001)

El Proyecto Mundial del Mercurio - La reduccin de mercurio en las amalgamas%

Reducir el mercurio en la amalgama de 40% a 20%, utilizando tazas de PVC.

The Global Mercury Project - Reducing % Mercury in Amalgam

An improvised centrifuge using a bicycle wheel.

El Proyecto Mundial del Mercurio - Home-Made Retort


Equipos Todos los das, disponible se puede utilizar con eficacia para reducir la
exposicin al Hg vapor (Repblica Democrtica Popular Lao, 2003).

The Global Mercury Project - Prototype Description

Hg is contained by the fume hood

El Proyecto Mundial del Mercurio - Reduccin de las Emisiones


Indonesia 2006: 10 tiendas de oro en Galangan ya ha adoptado la nueva campana de
humos.

The Global Mercury Project - Reducing Emissions

Indonesia 2006: > 98% of Hg abatement


.
Copper and Zinc Toxicity

Properties of Copper

It is found in metallic form and as compounds


in ores, e.g., copper pyrites (CuFeS2) and
malachite [CuCO3.Cu(OH)2].

Valences: Cu+1 (cuprous) and Cu+2


(cupric).

Moderately soluble in water.

Cu binds to sediments
and organic matter.

Exposure
pathways: eating
contaminated
food, drinking
contaminated
water, inhaling
Cu dust.

(Bradl (2005), Wright and Welbourn (2002)). People who work in Cu mines can
experience continuous exposure to Cu dust.

Copper - Essential Element

In low concentrations (5-20 ppm), Cu is an essential trace


nutrient for all organisms and has a role in:

Normal haemoglobin and haemocyanin


formation.

Normal carbohydrate metabolism.

Normal functioning of more


than 30 enzymes.

Healthy hair in humans.

In high concentrations (>20


ppm), Cu is toxic.

Cu is present in normal human serum (the liquid part of blood) at


concentrations of 120 -140 ppb; signs of toxicity will be seen if its
concentration rises significantly above this (Bradl (2005), Wright and Welbourn
(2002)).

Haemocyanin is the pigment that binds with oxygen and transports it to cells of
invertebrate animals such as shellfish.

Uses of Copper

alloys (bronze and brass)

tools

ornaments

jewelry

coins

storage vessels for food and


beverages

electrical wiring

electroplating

algicides,
fungicides,
and
molluscicide
s

Cu has been known to humans for at least 6000 years. Its uses reflect its
malleability, ductility, and electrical conductivity (Bradl (2005), Wright and
Welbourn (2002)).

The use of Cu to kill algae, fungi, and molluscs demonstrates that it is highly
toxic to aquatic organisms.

Copper Concentrations in Water and Sediments


unpolluted freshwater: 0.001-0.1 ppb

unpolluted seawater: 0.03-0.6 ppb

water polluted by mine tailings:


50-100 ppb

sediments polluted by
mine tailings: 7000 ppm
(7,000,000 ppb)

(Wright and Welbourn (2002)).

Copper BCFs in Water

aquatic plants - 1000

algae - 2400

aquatic insects - 546

freshwater invertebrates
- 1000

freshwater fish -
200

oysters -
28,000

(Taub (2004)). The ability of oysters to filter materials from large volumes of
water contributes to the high bioconcentration factor for Cu in this species.

Copper Biomagnification

Cu does NOT biomagnify.

Concentration in fish is lower than in


algae.

Cu is highly toxic to aquatic


organisms.

Fish and crustaceans are


10-100 times more
sensitive to Cu than are
mammals. Algae are
1000 times more
sensitive to Cu than are
mammals.

The lower toxicity of Cu to mammals is due to the ability of mammals to


detoxify Cu in the liver and kidney (Forstner and Witmann (1979), Hodson et al.
(1979), Wright and Welbourn (2002)).

Factors Affecting Copper Bioavailability and Toxicity

Free Cu+2 is the most bioavailable and toxic


form. The formation of complexes with organic
compounds in sediments decreases Cu
bioavailability.

Lower pH increases bioavailability.

Cu is less toxic in hardwater


than softwater.

Species, size, and life


stage affect toxicity.

Copper is less toxic in marine than in freshwater ecosystems because it forms


complexes with amino acids that are present in seawater. These complexes are
less toxic than free Cu+2. The lower toxicity of Cu in hardwater compared to
softwater is due to the protective effects of Ca ions on and in living cells
(Wright and Welbourn (2002)).

Species Sensitivity to Copper

Coho salmon LC50 for 96 hours of exposure to


Cu is 60-74 ppb.

Rainbow trout LC50 for 96 hours of


exposure to Cu is 250-680 ppb.
(Taub (2004)). Coho salmon is more sensitive to toxic effects, because a lower
concentration (60-74 ppb compared with 250-680 ppb) of Cu will kill half of the
exposed fish.

Copper Effects on Shellfish

Individual effects: lower rates of metabolism in


clams.

Population effects : lower production


of sperm and eggs in sea scallops
exposed to 10-20 ppb Cu.

(Taub (2004)). Although individual sea scallops might not be harmed by Cu, the
adverse effects of Cu on reproduction will lead to smaller populations of sea
scallops in subsequent generations.

Copper Effects on Finfish

Reduced sperm and egg production.

Abnormalities in newly hatched fish.

Reduced survival of young fish.

Prevention of successful migration.

Reduced appetite and food intake.

Reduced growth.

Gills become frayed and lose


their ability to regulate
transport of salts into and
out of fish.

Kidney damage.

Deformed
vertebrae
and fin rays.

Fin or
tail
erosio
n.

(Taub (2004)). Cu is toxic to both individual finfish and to finfish populations.


Relatively low concentrations of Cu can have profound effects on aquatic
ecosystems by reducing the reproductive potential of the finfish in those
ecosystems. Reduced appetite and food intake contribute to reduced growth
of finfish. These are examples of sublethal effects that are eventually lethal;
smaller or weaker fish will be less resistant to disease and to predation.

(Bradl (2005), Taub (2004)). Salts such as sodium chloride and potassium
chloride are important for the normal functioning of the cardiovascular and
nervous systems. Deformed vertebrae and fin rays, and eroded fins and tails
will prevent finfish from swimming normally, which, in turn, will prevent them
from finding food and avoiding predators.

Examples

Fathead Minnows

Decreased growth.

Early hatching of eggs, smaller fry (baby


fish).

Decreased percentage survival


of fry (621 ppb Cu).

Increased percentage of
abnormalities in newly
hatched fry (338 ppb
Cu).

(Taub (2004)).

Butterfish

Acute toxicity test - Butterfish were exposed to


250 ppb Cu for 24 hours.

Subacute toxicity test - Butterfish were


exposed to 25 ppb Cu for 7 days and
returned to normal water for 48 hours.
After 7 day exposure, highest
level of Cu was found in liver,
then kidneys, gills, and muscles.

Cu caused structural
damage to liver, kidneys,
and gills.

Tissues were
altered more
severely in 7 day
exposure group
than in 24 hour
exposure group.

Tissues
regenerat
ed during
48 hour
recovery
period.

(Jiraungkoorskul and Sahaphong (2007)). These findings illustrate the principle


that longer and continuous exposure to a toxic metal will harm an organism
more than short-term exposure because the organism does not have the
opportunity to recover.

Sublethal Effects of Copper on Rainbow Trout

Rainbow trout show stress at very low copper levels (1.4


ppb).

Hyperactivity.

Increased levels of cortisol in blood.

Synthesis of metallothionens in
liver.

(Taub (2004)). Cortisol is a hormone that is secreted in response to stress.

Ecosystem Effects of Copper


Decreased algae growth.

Disappearance of "good" insects (such


as mayflies) and appearance of other
insects that tolerate water pollution.

These changes will affect which


species of fish are present.

Changing one part of an ecosystem


will affect the entire ecosystem.

(Taub (2004)). Cu compounds are effective algicides (Wright and Welbourn


(2002)); therefore, it is not surprising that the discharge of Cu to an aquatic
ecosystem leads to decreased algae growth. Some insects such as mayflies are
indicators of water quality because they are found in unpolluted waterbodies
(Odum (1971)).

Copper Effects on Humans

Low toxicity in humans: metallothionens


detoxify Cu in liver and kidneys; availability of
Cu is low in many foods.

Drinking water standards for Cu are


based on taste, not on risk of toxicity.

The low availability of Cu in many foods can be attributed to the tendency of


Cu to bind with organic matter (Wright and Welbourn (2002)).

Copper Standards

Ontario drinking water objective: 1 ppm.

Canadian federal guidelines for


protection of aquatic life: 2 ppb for
softwater, 3 ppb for moderately
hardwater, 4 ppb for hardwater.

Water that has a CaCO3 concentration of 0 to 120 ppm is characterized as


softwater. If the CaCO3 concentration is greater than 120 but less than 180
ppm, then the water is characterized as moderately hard. If the CaCO3
concentration is greater than 180 ppm, then the water is characterized as hard
(Nriagu (1980)).

Properties of Zinc

It is found in metallic form and as Zn


compounds, e.g., Zn(OH)2, ZnO, ZnS.

The bioavailable form is Zn+2.

Adsorbs to sediments.

Exposure pathways -
deposition from air into
water, eating food and
sediments, and drinking
water that contains Zn.

(Bradl (2005), National Academy of Sciences (1979)).

Zinc - Essential Element

In low concentrations, Zn is an essential nutrient for all


organisms.

Healthy immune defense system.

Normal functioning of cell membranes.

Normal growth and


development.

Cofactor in enzymes
associated with DNA and
protein synthesis.

In high concentrations, zinc is


toxic.

There is a wide margin between normal dietary intake and the toxic level of Zn
in humans (Bradl (2005), National Academy of Sciences (1979)).
Uses of Zinc

automobile industry, e.g., manufacture of tires

protective coatings for iron and steel

batteries

antiseptics and ointments

paints and varnishes

rubber products.

electrical and electronic


equipment

fertilizer

wood
preserva
tive

(Bradl (2005), National Academy of Sciences (1979)). The uses of Zn, especially
in the automobile industry, paints and varnishes, fertilizers, and wood
preservatives, suggest that Zn is a common component of stormwater runoff in
both urban and agricultural areas.

Zinc Concentrations in Water and Fish

Average concentration in unpolluted


freshwater = 15 ppb.

Average concentration in unpolluted


seawater = 5 ppb.

Higher concentrations in fish


downstream of mining sites in
U.S.

Brown trout: 72 - 130 ppm

White sucker: 61 - 139 ppm

Carp: 320 - 1321 ppm


(Bradl (2005), Taub (2004)).

Zinc BCFs in Water

marine algae - 1000

freshwater plants - 4000

freshwater invertebrates -
40,000

freshwater fish - 1000

oysters - 24,000

tuna - 500
to 700

(Taub (2004)). These BCFs show that Zn bioaccumulates readily in aquatic


organisms, especially invertebrate filter feeders.

Biomagnification of Zinc

Zn does not biomagnify at higher trophic


levels.

Zn levels are lower in fish than in algae.

Zn is more toxic to aquatic


organisms than to humans.
Metallothionens detoxify Zn in
liver and kidney.

(National Academy of Sciences (1979)). The toxicity of Zn is similar to the


toxicity of Cu in that aquatic organisms are impacted more than humans.

Zinc Effects on Fish

Individual Effects of Zinc

Accumulates in gills, liver, and kidneys, but not


muscle.

Causes structural damage to gills, liver,


and kidneys.

Stress response in rainbow


trout: hyperactivity, increased
blood cortisol levels, synthesis
of metallothionens in liver.

(Taub (2004)). It is good news for people that Zn does not accumulate in the
muscle tissue of fish. This makes Zn less problematic via this route of exposure.
However, people who eat the whole fish and wildlife (who, of course, eat the
whole fish) can potentially be exposed to high concentrations of Zn.

Ecosystem Effects of Zinc

Population effects: decreased spawning in


rainbow trout.

Community effects: altered benthic


species; therefore, altered fish species.

(Taub (2004)). When the composition of the benthic community changes, the
species that feed on benthic organisms will change. This is another example of
how altering one part of an ecosystem has ripple effects throughout the entire
ecosystem.

Zinc Standards

Federal and Ontario drinking water guideline =


5 ppm, based on taste not human health
protection.

Federal guideline for protection of


aquatic life in freshwater = 30 ppb.

The Canadian federal guideline for protection of aquatic life in freshwater is an


order of magnitude more lenient (10 times more lenient) for Zn than for Cu.
This indicates that Cu is more toxic to aquatic life.
Coho Pre-Spawn Mortality

63-89% of adult coho salmon in urban Puget


Sound streams die before spawning.

Coho enter small streams following fall


storm events and are exposed to high
concentrations of pollutants from
urban stormwater runoff.

Cu and Zn are likely


contributors.

(Feist et al. (2007)).

Nickel and Tin Toxicity

Introduction

This part of the course will continue with the properties and uses of specific heavy metals
that are mined or byproducts of mining in Canada and other countries, and the toxic effects
of these metals on fish, other aquatic organisms, and humans. We will focus on nickel, tin,
silver, gold, aluminum, manganese, arsenic, and selenium and then compare the relative
toxicities of all the metals that have been covered in this course.

Nickel Level and Properties

1.5 ppb in unpolluted seawater.

0.2-10 ppb in pristine rivers, streams,


and lakes.

6.4 ppm (6400 ppb) in surface


water near Ni mines and
smelters.

Can be transported in air


to remote aquatic
ecosystems.
Essential element
for some plants
and animals -
found in some
enzymes.

(Bradl (2005), Wright and Welbourn (2002)).

Uses of Nickel

Ni-Cd batteries

stainless steel production

jewelry

electroplating

pigments and glazes for


ceramics

electronic equipment

shipbuilding,
automotive,
and
aeronautical
industries

(Bradl (2005), Wright and Welbourn (2002)).

Nickel Bioaccumulation

Nickel bioaccumulates in aquatic organisms


but does not biomagnify up the food chain.

BCFs in aquatic organisms range from


100 to 5,000 on a dry weight of tissue
to water basis.

(Chau and Kulikovsky-Codeiro (1995), Environment Canada (1994)).


Nickel Toxicity to Aquatic Biota

Reduced growth rates of algae and aquatic


macrophytes when exposed to nickel
concentrations of 0.5-2.0 ppm.

Delays hatching and increases embryo


mortality in fish.

Decreased growth in
invertebrates and fish.

More toxic in softwater


than hardwater.

Aquatic plant and


animal species
vary in their
sensitivity to Ni.

Blue-green algae are more sensitive than green algae to the toxic effects of Ni
(Taub, 2004). Certain molluscs and crustaceans (e.g., Daphnia) are relatively
sensitive to Ni and are, therefore, not found at Ni-contaminated sites (Chau
and Kulikovsky-Codeiro (1995), Environment Canada (1994)). This is another
example of how a pollutant can alter an entire ecosystem.

Ni toxicity to freshwater species can be masked by the presence of other


metals in water polluted by mining, electroplating, and stainless steel
production (Kszos et al. (1992)). Chronic effects of Ni exposure occur at Ni
concentrations that are up to two orders of magnitude lower than
concentrations that cause acute effects (Azeez and Banerjee (1991), Kszos et al.
(1992)). Long-term exposure of fish to low levels of Ni may result in reduced
deposition of Ca in the bones and in asphyxiation (Moore (1991)).

Nickel Toxicity to Humans

Exposure routes - inhalation (primary),


ingestion of food and water (secondary).

Particulate Ni is persistent in human


lung and nasal tissue. Its biological half-
life is 3 to 4 years.

Reacts directly with DNA and


may cause lung and nasal
passage cancer.

Inhalation of Ni compounds such as nickel carbonyl (Ni(CO)4), nickel sulfide


(Ni2S3), nickel oxide (NiO), and nickel trioxide (Ni2O3) leads to inflammation of
lung tissue, pulmonary edema (accumulation of fluid in the lungs), asthma, and
liver damage (Bradl (2005), Wright and Welbourn (2002)).

Acute toxicity: Ni(CO)4 is most toxic, then


particulate Ni compounds, then water-soluble
Ni compounds.

Chronic toxicity: Particulates are most


toxic. Water-soluble Ni compounds are
least toxic.

Ni(CO)4, a gas, has higher acute toxicity than particulate Ni because it is highly
lipid soluble and the kinetics of gas phase delivery to lung tissue are much
faster than incorporation of particulates into cells (Wright and Welbourn
(2002)). Free Ni+2 is the ultimate toxic form of Ni in cells. Soluble Ni compounds
are less toxic than particulate Ni compounds because the water-soluble
compounds have a faster biological turnover. Once they are inside cells,
particulate Ni compounds react directly with DNA to produce DNA damage
(Nieboer et al. (1988)).

Nickel Standards

Canadian water quality objective for Ni in


freshwater ranges from 25-150 ppb,
depending on water hardness.

Lower values are for softer waters.

U.S. criteria are similar and are


also hardness-related.

(Chau and Kulikovsky-Codeiro (1995), Environment Canada (1994)).

Tin Uses

Inorganic Tin
Sn0, Sn+2, Sn+4.

protective coating agent

cans (tinplate)

automotive and aerospace


industries (Zn-Sn and Cd-Sn
alloys)

Sn is found as the pure metal (Sn0) and as stannous (Sn+2) and stannic (Sn+4) ions
(Bradl (2005)).

Organotins

Tributyltin (TBT)

antifouling paints on boats

agricultural fungicides

molluscicides

TBT is the most commonly used organotin compound (Wright and Welbourn
(2002)).

Tin Exposure Pathways

Aquatic Organisms

atmospheric deposition - Sn particles can


travel long distances.

gills

drinking Sn-polluted water

sediments

food chain

(Wright and Welbourn (2002)).


Humans

Skin absorption from water.

Food chain - ingestion of contaminated


shellfish and finfish.

Butyltin compounds have been


found in human blood,
indicating exposure to these
substances.

(Kannan et al. (1999)).

Tin Concentrations in Aquatic Environment

<0.005 ppb for inorganic Sn.

Elevated concentrations of organotins


in the past: 0.026-0.091 ppb near
California coast, 0.2-3.3 ppb in Lake
Michigan, 0.3 ppb in Rhine River.

4-8 ppm in fish.

(Magos (1986)).

Tin Bioaccumulation and Biomagnification

Sn bioaccumulates but does not biomagnify in


food web.

Sn is metabolized more rapidly by


higher trophic level organisms than by
organisms lower down in food chain.

TBT absorbs strongly to


particulate matter in water
column and to sediments and is
persistent in aquatic organisms.
(Taub (2004)).

Tin BCFs in Water

Daphnia: 200

oysters: 1000-5000

freshwater mussels: 47,000


(winter), 62,000 (summer)

marine mussels: 10,500

marine molluscs
and fish: 1500-
6000

BCFs
higher at
pH 8 than
pH 5

(Taub (2004)).

Tin Toxicity

Inorganic Sn compounds (chlorides, oxides,


sulfides) have low solubility and poor
absorption, therefore, low bioavailability and
low toxicity.

Bacteria methylate inorganic Sn to


organotin compounds.

TBT is most toxic form, with low


concentrations adversely
impacting aquatic organisms.

(Bradl (2005), Wright and Welbourn (2002)).

History of TBT Use


Through the 1960s, TBT became increasingly
popular as an active ingredient in antifouling
paints.

Worldwide consumption of these


paints increased from 5000 to 35,000
metric tonnes from 1965 to 1980.

TBT levels ranged from 0.01-


0.10 ppb in estuaries and urban
bays, and reached 1.0 ppb in
harbours and marinas.

(Wright and Welbourn (2002)).

During the late 1970s and early 1980s,


unnatural shell thickening and poor
reproductive success in oysters were linked to
high TBT concentrations near boat moorings.

Coastal TBT contamination contributed


to decline in native oyster fishery on
the east coast of England in the 1970s.

Laboratory experiments showed that very low TBT levels (0.002-0.008 ppb) had
adverse effects on oysters (Alzieu and Portman (1984)).

TBT

Impacts on Aquatic Organisms

0.29 ppb caused high death rate of


zooplankton in Chesapeake Bay.

0.016 ppb caused sublethal effects.

2.7 ppb is 96-hour LC50 for


fathead minnows.

TBT concentrations are


the highest in fish liver
and kidneys.
(Taub (2004)). Fathead minnows are very sensitive to the toxic effects of TBT.
Uptake of TBT in the liver and kidneys of fish indicates that the fish is
attempting to detoxify and excrete these compounds. However, TBT is
lipophilic and, therefore, biologically persistent.

liver, kidney, and retinal lesions

skin inflammation

abnormal numbers of blood cells

immuno-suppression in snails and


molluscs

abnormal moulting in
prawns

reproductive failure
and population
decline

endocrine
disruption -
imposex

(Oberdorster and Cheek (2001), Taub (2004)).

Imposex

Imposex is the development of male sex


organs in 150 species of female molluscs
exposed to TBT.

Examples - 0.002 ppb TBT caused


imposex in dog whelk; 0.001 ppb TBT
caused imposex in snails.

Female molluscs develop a vas deferens and penis, and the female genital duct
becomes blocked (Oberdorster and Cheek (2001), Gibbs and Bryan (1986)).

Another organotin compound that can induce imposex in molluscs, is


triphenyltin, which is used in antifouling paints and as an agricultural fungicide
(Horiguchi et al. (1997)).

Possible Mechanisms
TBT inhibits conversion of testosterone to
female sex hormone estradiol.

TBT inhibits metabolism of


testosterone to compounds that can be
excreted.

In either case, TBT is functioning as an endocrine disrupter, leading to


increased testosterone levels in the female molluscs (Beltin et al. (1996), Ronis
and Mason (1996)).

Restrictions on TBT Use

Began in late 1980s in U.K. and France, then in


Canada and the U.S.

Restrict TBT content of antifouling


paints, leaching rate, and size of vessels
to which paints can be applied.

Exemptions for large ships (>25


meters in length).

Not enforced in
developing countries.

(Wright and Welbourn (2002)).

Effect of Restrictions on TBT Use

Recovery of sensitive species, e.g., increases in


oyster populations in France.

Decreased TBT concentrations in urban


bay sediments (e.g., San Diego Bay).

(Alzieu (1986), Taub (2004)).

TBT Standards (U.S. EPA)


Acute Toxic Effects on Aquatic Life:

freshwater - 0.46 ppb

saltwater - 0.42 ppb

Chronic Toxic Effects on Aquatic Life:

freshwater - 0.072 ppb

saltwater - 0.0074 ppb

(U.S. Environmental Protection Agency (2002)). In contrast to other metals, the


organic form of Sn is more toxic in saltwater than in freshwater.

Silver and Gold Toxicity

Uses of Silver

photographic film and paper

electrical conductors

alloys and solders

batteries

jewelry

coins

mirrors

dental
amalgam
s

(Purcell and Peters (1998)).

Silver Properties
Found as Ag0 and Ag+1.

The most important forms of Ag are


metallic Ag, Ag2S (argentite), AgCl
(hornsilver).

Found in ores of Ag, Pb, Pb-Zn,


Cu, and Cu-Ni.

Released to air in
particulate form.

Enters aquatic
environment as
sulfides,
chlorides, and
soluble organic
complexes.

Ag is normally present at very low concentrations (<0.001 ppb) in aquatic


ecosystems because it forms insoluble compounds such as sulfides which then
accumulate in sediments (Purcell and Peters (1998)).

Silver Impacts on Aquatic Organisms

Ag+1 is very toxic to fish and shellfish.

Essential metals (Cu, Se, Zn) have


synergistic effect on accumulation of
Ag in fish and oysters.

Binds to specific sites on or in


gills and interferes with enzyme
involved in Na+ transport,
resulting in decreased Na+ levels
in blood.

(Langston and Bebianno (1998), Purcell and Peters (1998)). As indicated


previously, Na+ is an important electrolyte for the normal functioning of the
cardiovascular and nervous systems.

Silver toxicity has been demonstrated with lab


experiments: death, decreased biomass in
plants, altered reproduction in animals.

LC50 ranges from 6.5-70 ppb for


freshwater fish.

(Bradl (2005), Purcell and Peters (1998)).

Silver Bioavailability

The highest bioavailability and toxicity occur under the


following conditions:

presence of Ag+1

soft water

low pH

absence or low
concentration of Cl-

absence or low
concentration of
dissolved organic
carbon

When Ag binds with Cl- or with dissolved organic carbon, the resulting
complexes have low water solubility and are therefore less bioavailable (Bradl
(2005), Hogstrand and Wood (1998)).

Silver Impacts on Humans

Relatively nontoxic - easily excreted in


perspiration, urine, and faeces.

Some accumulation in hair and bones.

Can cause skin discoloration,


which is a cosmetic rather than
a toxic problem.
(Bradl (2005), Purcell and Peters (1998)).

Silver Standards

Environment Canada guideline for protection


of aquatic life = 0.1 ppb.

U.S. Environmental Protection Agency


criteria for protection of aquatic life
vary with water hardness: 1.2 ppb in
soft water and 13 ppb in hard water.

(Purcell and Peters (1998)).

Gold Properties and Uses

Found as Au0, Au+1, Au+3.

Au compounds are stable in water.

Au+3 is the most toxic form.

Uses: coins, jewelry,


pharmaceuticals
(treatment of
rheumatoid arthritis).

(Eisler (2004)).

Toxicity of Gold to Aquatic Organisms

Marine diatoms, 0.1 ppm Au, 21 days - showed


decreased chlorophyll concentrations and
decreased rate of photosynthesis.

LC50 for 96 hours of exposure in


estuarine killifish was 0.8 ppm. Au was
less toxic than Ag or Hg, but more toxic
than Cd, As, Al, Cu, Zn, Cr or Ni.
Au interacts synergistically with
Cu.

(Eisler (2004)).

Impacts of Gold in Humans

Overall Au toxicity to humans is low.

Au accumulates in kidneys. Side effect


of arthritis treatment can be
inflammation of kidneys.

(Eisler (2004)).

Gold Toxicity Related to Mining Processes

Most Au toxicity problems are related to


processes used to extract Au from its ore
rather than direct effects of Au.

Use of Hg to extract Au - artisanal


mining

Cyanidation/heap-leach
extraction - common extraction
process in Au mines in Canada
and the U.S.

(Cunningham and Cunningham (2004)). The effects of Hg amalgamation in


artisanal Au mining were discussed earlier in the course. We will now focus on
the toxic effects of cyanidation in Au mining.

Heap-Leach Extraction
Piles of crushed ore
are heaped on an
impervious pad and
sprayed with a dilute
alkaline-cyanide
solution, such as
sodium cyanide or potassium cyanide.

The cyanide (CN-) solution percolates


through the heap and dissolves gold
from the ore.

Au-containing solution is
pumped to processing plant
that removes Au by electrolysis.

Excess CN- is stored for


reprocessing in ponds.

If there is a leak
in the supposedly
impervious pad
or if the CN-
solution overtops
the storage
ponds, then
cyanide can be
discharged to
groundwater or
to nearby surface
waterbodies.

(Cunningham and Cunningham (2004)).

Cyanidation Problems

CN- solution can enter groundwater and


surface water from leaks in heap pad or from
open ponds behind earthen dams.

Some mine operators abandon site


after Au is recovered and leave leaking
ponds of CN- (e.g., Summitville Mine in
Colorado).

Okanogan Highlands Alliance -


NGO that monitors
environmental review process
for proposed CN- leach Au
mines in Washington State.

(Cunningham and Cunningham (2004)). The "impervious" pads are not always
impervious in practice. CN- can spill from the open ponds and enter
downstream lakes and rivers.

Cyanide Properties

CN- is anion with carbon and nitrogen atoms


joined by triple bond.

CN- does not persist like toxic metals


and does not bioaccumulate in food
chains.

CN- toxicity is instant or acute


and leaves little residual trace
after it reacts.

It is difficult to analyse
after a mining spill how
much and what type of
CN- has been spilled.

(Lenntech, Moran (2004)).

Toxicity of Cyanide to Aquatic Organisms

Fish and aquatic invertebrates are especially


sensitive to CN-.

CN- prevents cells from using oxygen by


inhibiting the enzyme cytochrome
oxidase, causing the animal to
suffocate.
20-76 ppb CN- causes death of
many fish.

>200 ppb CN- is rapidly


toxic to most fish
species.

30-100 ppb CN- is


lethal to
invertebrates.

(Eisler (1991)). Finfish are somewhat more sensitive to CN- toxicity than are
shellfish and other invertebrate animals. CN- does not prevent oxygen from
entering the body of an animal or from binding with haemoglobin or
haemocyanin. Although a normal amount of oxygen may be delivered to the
cells of the animal, the CN- prevents the cells from using the oxygen.

Sublethal Effects of Cyanide on Aquatic Organisms

5.0-7.2 ppb CN- has sublethal toxic impacts on fish; 18-43


ppb CN- has similar impacts on aquatic invertebrates. Some
of the effects are:

reduced swimming performance

decreased reproductive success

developmental abnormalities in
embryos

disrupted respiration

decreased
growth

(Eisler et al. (1999)). Reduced swimming performance, disrupted respiration,


and decreased growth can indirectly become lethal effects because the
affected animals will be less able to forage for food, metabolize food, and
escape predators. Decreased reproductive success and developmental
abnormalities in embryos have negative repercussions for the population.

Factors Affecting Cyanide Toxicity


More toxic in water with low dissolved oxygen
levels.

More toxic in water with acidic pH.

More toxic in warmer water.

Large interspecies
variation in sensitivity.

(Eisler et al. (1999)).

Cyanide Spills

Baia Mine (Romania)

In 2000, two accidents at the Baia Mine in


Romania resulted in cyanide spills: Heavy
snow, followed by heavy rain, caused tailings
dam to break. Large volumes of mine waste
slurry and CN- from the gold mine entered the
Danube River and flowed into the Black Sea.

There were extensive fish kills in


Romania and other countries
downstream of spill.

First spill killed 1200 tonnes of


fish in Danube River and
endangered birds feeding on
fish within a national park.

In Hungary, spill caused


a five kilometer carpet
of dead fish and left 25%
of the population
without drinking water.

The adverse
impact on the
fishing industry
had adverse
impacts on local
communities,
economies, and
tourism.

The human population downstream of the spills was impacted by losing


sources of drinking water and income (UNEP/OCHA (2000a), UNEP/OCHA
(2000b), Cunningham (2005)).

Rapu Rapu (Phillipines)

Two CN- spills at a gold mine in October 2005


caused death of several kilograms of fish and
shellfish.

People were afraid to eat local fish


afterwards and stopped fishing in the
area. Local fishing industry was hurt.

(Rapu Rapu Fact Finding Commission (2006)). Again, the spills impacted a food
source for the local people as well as the local economy.

Toxicity of Cyanide to Humans

CN- compounds are absorbed through


inhalation, ingestion or skin contact, and are
distributed throughout the body via the
bloodstream.

Hydrogen cyanide (HCN) gas is


biological weapon, used in Nazi death
camps in World War II.

5 ml of a 2% CN- solution is
lethal.

(Lenntech, Moran (2004)).

Personal Story

When I (Dr. Fran Solomon) was a graduate student in


fisheries at the University of Washington (Seattle), I was
conducting an experiment on the effects of potassium
cyanide (KCN) on enzyme activity in the liver tissue of fish. I
needed to pipette 3 ml of the KCN solution. Instead of
using a bulb to pipette the solution, I put the 10 ml pipette
in my mouth and was in the process of sucking 3 ml of the
solution into the pipette when my major professor walked
into the lab and inquired why I was not using the bulb. I
responded that I did not have time to use the bulb; using
the pipette like a straw was faster. He said "you know that
KCN is very toxic; a little bit can kill a person." I asked him
how much KCN would be lethal. He did not give me the
answer; rather, he required me to figure it out. Based on
the concentration of the KCN solution and the gram
molecular weight of KCN, I determined that if I had
swallowed 2 ml of the solution I would have been dead.
This experience reinforced for me the toxicity of CN- and
was an example of excellent teaching on the part of my
major professor!

Silver and Gold Toxicity - Heap-Leap Extraction

Diagram of the heap-leach extraction process used at many gold mines.

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