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Bioaccumulation: Threats to Health in
North American Native Villages
Part I
(Adapted from (2000) Project WILD K-12 Curriculum and Activity Guide)
Objectives: Participants will be able to
1) give examples of ways toxic chemicals enter and accumulate in food chains
2) describe possible health consequences of eating foods high on food chains
Method: Participants become Macroinvertebrates (i.e, stoneflies, mayflies and caddisflies) Fish (i.e.,
trout), and Bears in a physical activity.
 One small paper bag for each Macroinvertebrate (see table on next page).
 30 small “food” tokens (2/3 white or plain; 1/3 colored) for each Macroinvertebrate. [These
could be white/plain & colored drinking straws, pipe cleaners, poker chips, dry dog food, paper
clips, small squares of card stock, etc.]
 Animal name tags for participants to wear around their necks. [These tags will have colored
yarn and a picture of the animal. Black yarn for Bear, gray yarn for Fish, pink or red or orange
yarn for Macroinvertebrates.]
 Large, clear area for doing the activity (classroom with tables/chairs removed to side, lobby or
hall of conference center, outside parking lot or field).
Key terms: toxic, food chain, bioconcentration, biomagnification, bioaccumulation.
Background: Many toxic chemicals have a way of persisting in the environment and often become
concentrated in unexpected and undesirable places – from food and water supplies to wildlife and
sometimes people, too.
Bioconcentration occurs when toxic chemicals are taken up directly from air, water, and soil and
stored in various tissues and organs in the body. Bioconcentration results in the storage of these
chemicals in organisms in higher concentrations than are normally found in the environment.
Biomagnification is the accumulation of a substance up the food chain by transfer of residues of the
substance in smaller organisms that are food for larger organisms in the chain. It generally refers to
the sequence of processes resulting in higher concentrations in organisms at higher levels in the
food chain (at higher trophic levels).
Bioaccumulation is the combined process of bioconcentration and biomagnification.
Bioaccumulation = Bioconcentration + Biomagnification.
Bioaccumulation = toxins taken up from air, water, soil, AND from the food an animal eats.
Its results can be far-reaching.
Adapted from (2000) Project WILD K-12 Curriculum and Activity Guide
Revised 5/7/07
1. Discuss the term “food chain” with the participants [definition: a sequence or “chain” of
living things in a community, based on one member of the community being eaten by the
next one up the chain, and so forth, to the top predator]
2. Divide the group into three teams (depending upon class size):
Class size
[The ideal distribution is multiplying by 3 as you go down the food chain.]
3. Distribute animal name tags to participants.
4. Give each “Macroinvertebrate” a small paper bag to represent the “stomach” of the animal.
5. Distribute the “food” tokens in the playing space [can be done ahead of time if space is
6. The Macroinvertebrates will be the first group to go looking for food, while the Fish and
Bears wait patiently on the sidelines [as predators watching their prey]. At the signal, the
Macroinvertebrates enter the playing area and collect as many food tokens as they can,
placing them in their stomachs. They must move quickly for they only have 30 seconds to
7. At the next signal, the Fish will enter the playing space to feed on the Macroinvertebrates by
tagging them. When this occurs, the Macroinvertebrates must hand their “stomachs” to the
Fish and then sit on the sidelines. [Time allotted for feeding: 15 seconds in classroom size
space, 30 seconds in larger area, up to 60 seconds on large playing field – adjust
accordingly.] Those who are uneaten remain in the playing area.
8. Finally, allow 15 to 60 seconds (based on playing space) for the Bears to hunt for Fish. The
same rules apply – those who are tagged and “eaten” must give up their “stomach” and sit
on the sidelines. During this hunt, the Fish may also hunt for the Macroinvertebrates.
9. At the end of the time, all participants come together and sit in a circle, bringing whatever
food bags they have with them.
10. Those who are “still alive” [“uneaten”] should empty out their bags and count the number of
white/plain food tokens they have and the number of colored tokens. Make a chart on the
board that indicates each organism and the contents of its “stomach.”
11. Inform the participants that the colored food pieces represent a toxic chemical. All
Macroinvertebrates having any amount of this chemical may now be considered dead. Any
Fish having colored pieces for more than half of their food tokens have also died as a result.
Adapted from (2000) Project WILD K-12 Curriculum and Activity Guide
Revised 5/7/07
The Bear with the highest number of colored pieces will not die, but it will have birth
defects in its offspring. The other Bears will not be visibly affected at this time.
12. Ask for observations from the participants about how the food chain seems to work and how
toxic substances can impact it. Introduce and discuss the terms “bioconcentration,”
“biomagnification,” and “bioaccumulation.” Discuss how these terms are different.
Bioaccumulation: Threats to Health in
North American Native Villages
Part II
(Adapted from (2003): Centre for Indigenous Peoples’ Nutrition and Environment,
Objectives: Participants will be able to
1) give examples of ways toxic chemicals enter and accumulate in food chains
2) describe possible health consequences of eating foods high on food chains
Method: Participants work in small groups to analyze cases of specific contaminants in northern
food chains and the health effects of these. Groups will report the details of their cases to the large
Materials: 3 case studies [including 2 community “plates”, contaminant information sheets, northern
food chain diagrams]
Key terms: mercury, cadmium, PCBs (PolyChlorinated Biphenyls)
1. Divide the class into 3 groups; assign one contaminant to each group.
 Group 1 = mercury
 Group 2 = cadmium
 Group 3 = PCBs
2. Groups have 15 minutes to read the background information and to examine the 2
community “plates.” Each group decides which community is most at-risk for their specific
3. Each group will then report back to the class on:
 the properties, biological impacts, and “location in the environment” of the contaminant
 their decision on the community most at-risk for high levels of that contaminant
Adapted from (2000) Project WILD K-12 Curriculum and Activity Guide
Revised 5/7/07
Community Plates for
Case Study Analysis
Let's consider examples of what women from two northern Aboriginal communities in Canada
reported eating over one year.
The "plates" you see below show the traditional foods most eaten by women; the relative
amount of each type of food is shown by the size of the piece on the plate.
Community 1
Community 2
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Bioconcentration of Contaminants
Bioconcentration: A long word that describes a simple idea - it is the build-up of something,
in this case, contaminants, in an animal's body. And it is one of the things that makes
contaminants a problem for wildlife.
Once the contaminant enters a tissue in the animal, it stays there. So if the animal continues to
live in an environment where contaminants are present, the contaminants will accumulate or
build up, over the lifetime of the animal. This means that if we compare the same species, say
whitefish, occupying the same habitat, say Great Slave Lake, younger whitefish will have a
lesser contaminant load than older whitefish.
Contaminants build up over time
The shaded fill represents contaminants
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Biomagnification of Contaminants
Biomagnification. It's the word scientists use to explain why animals that eat other animals
have higher levels of contaminants than animals that eat plants. Some contaminants are
persistent - once they are in the animal's body, they stay there for a long time. So when smaller
animals are eaten by bigger animals, all the contaminants stored in the smaller animals are then
passed on to the bigger animal.
The result of biomagnification is that animals at the "top" of their food chain have higher
contaminant levels than animals at the "bottom." In the example below, the tiny drifting plants
and animals will have much lower levels of contaminants than beluga.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Northern Food Chains for Case Study Analysis
Bowhead Whale
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
(Some populations of walrus eat seals, so there would be another layer in chain.)
Ringed Seal
Arctic cod, other fish
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Lake trout
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Canada Goose
Surf scoter
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Mercury in traditional foods
Mercury is a metal and like all metals, it is present naturally in rocks, soil and water.
Human activities, such as making paper, building dams and burning fuel, have increased the
amount of mercury in water, air and soil. In high doses, mercury is toxic to living things,
causing damage to the brain and nerves.
Mercury has been measured in many animals across the North. If you know a few facts about
mercury and are familiar with the food chains of animals, you will be able to accurately guess
where mercury can be found in your diet.
Just remember :
Mercury biomagnifies. This means there is more in animals with longer food
chains. For example, seals have more mercury than cod. Loche, pike and lake trout have more
mercury than whitefish. Loons have more mercury than geese or ptarmigan.
Mercury is usually higher in fish than in land animals.
Mercury builds up in whale skin. Skin (muktuk without blubber) from beluga
and narwhal will have more mercury than muscle or blubber.
Mercury does not build up in fat or blubber.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Health Risks from Mercury
Mercury in people
Have you ever been asked for a sample of your hair? It might have been
to measure mercury. This is a painless way to find out how much
mercury is in the body. Mercury gets into people's bodies from eating
foods that contain mercury. How much and what kind of food they eat
will determine their exposure to mercury. Levels of exposure are often
measured in hair and blood.
Since the 1970s, many people from Nunavut, Nunavik, northern Quebec, the NWT, Yukon,
Greenland, the Faroe Islands and southern Ontario have given their blood or hair so that their
exposure to mercury in the body could be measured. The highest levels were found in the
James Bay Cree and Inuit from eastern Canada, northern Quebec and Greenland. People who
eat fish and marine mammals have more mercury in their bodies than those who do not.
What are the effects of mercury on people's health?
The effects of mercury poisoning through food are known because of
industrial accidents that occurred in Japan in the 1950s. Fish became highly
polluted with mercury from industrial waste. (Fish had much higher levels of
mercury than animals from the Canadian north.) People ate the fish for months
before the pollution was discovered.
From the Japanese experience we learned that symptoms of mercury
poisoning may range from numbness and tingling sensations around lips,
fingers and toes to stumbling, difficulty speaking clearly, fatigue and inability
to concentrate.
Quite a lot is known about health problems from high-level exposure. But we still don't know
if there are health problems from low-level exposure. It is this kind of exposure that is more
common in the north. Low-level exposure is when there is less than 20 ppm of mercury in hair.
When people in a community have a higher level, health officials monitor them more closely.
They will want to find out where the mercury is coming from and if people's health is in
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
If there are health risks from low-level exposure they may not be like
those found in the Japanese study. People probably will not have
symptoms that are easily noticed. Specialized tests will be needed to
find the problems. Babies and children are more likely to be affected
than adults. This is because mercury can go from the mother's blood
into the baby's blood. Brain and nerve cells are formed and then grow
rapidly when a baby is developing in the womb and mercury can
damage these cells. Research is underway looking at the possible
dangers of mercury for the developing brain and nerves.
Should I continue to eat foods that contain mercury?
Some people are exposed to more than the guideline (safe) level of mercury. At the present
time, however, no one has been advised to reduce the amount of traditional food they eat. This
may change as more is learned about the risk of low-level exposure.
Cadmium in traditional food
Cadmium is a metal that is found naturally in bedrock, and in fresh and seawater. Most
types of food (traditional and market meats, vegetables, breads, dairy, etc.) contain some
cadmium, but organs (livers and kidneys) have the highest levels. Smoke from cigarettes
contains cadmium and smokers have more cadmium in their blood than nonsmokers. Longterm exposure to high levels of cadmium can cause permanent kidney damage.
Cadmium has been measured in many animals across the North. If you know a few facts about
cadmium you will be able to accurately guess where cadmium can be found in your diet.
Just remember:
Cadmium builds up in the kidneys and livers of animals.
Cadmium bioconcentrates. This means older animals will have higher levels than younger
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Cadmium does not biomagnify.
Animals that eat other animals do not have higher levels of cadmium than plant-eating animals.
People who eat liver or kidney from moose or caribou often (once a week) may go over the safe
level and need closer monitoring.
Generally, cigarette smoking contributed most to cadmium exposure, then market food and
finally traditional food. Most people had intakes well below the safe level. If regular
consumers of liver and kidney also smoked 1 pack of cigarettes per day, they would go over the
safe level. Smokers eating liver or kidney once a month or less would probably be getting less
than the guideline levels.
Seal meat is not high in cadmium, but if a lot is eaten, cadmium levels may be elevated.
Health risks from cadmium
Cadmium in people
To find out how much cadmium people are being exposed to, scientists measure it in blood.
Blood values have been studied in people from the US, southern Canada, Greenland, Nunavik,
Nunavut and the NWT. Smokers have more cadmium in their blood than non-smokers.
What are the effects of cadmium on people's health?
Long-term exposure to high levels of cadmium (higher than the guideline) can lead to
permanent kidney damage.
Who is most at risk from cadmium?
Those who may already have kidney problems, such as people with diabetes, and the elderly.
Should I continue to eat foods that contain cadmium?
In the past, advisories were issued warning people to limit consumption of liver and kidney
from moose and caribou in several regions in Canada. Dietary studies suggest that most people
are probably not eating enough of these organs on a regular basis to be a health risk.
Of course the healthiest way to decrease exposure to cadmium is to give up smoking!
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Itai-itai disease (Ouch-ouch disease)
The itai-itai disease (Japanese:イタイイタイ病, literally: ouch-ouch-disease) was the first
cadmium poisoning in the world in Toyama Prefecture, Japan in 1950. The cadmium poisoning
caused softening of the bones and kidney failures. The name of the disease comes from the
painful screams (Japanese: 痛い itai) due to the severe pain in the joints and the spine. The
cadmium was released in the rivers by mining companies in the mountains. The mining
companies were successfully sued for the damage. Itai-itai disease is known as one of the Four
Big Pollution Diseases of Japan.
Itai-itai disease was caused by cadmium poisoning due to mining in Toyama Prefecture. The
earliest records of mining for gold in the area date back to 710. Regular mining for silver
started in 1589, and soon thereafter, mining for lead, copper, and zinc began. Increased demand
for raw materials during the Russo-Japanese War and World War I, as well as new mining
technologies from Europe, increased the output of the mines, putting the Kamioka Mines in
Toyama among the world's top mines. Production increased even more before World War II.
Starting in 1910 and continuing through 1945, cadmium was released in significant quantities
by mining operations, and the disease first appeared around 1912. Prior to World War II the
mining, controlled by the Mitsui Mining and Smelting Co., Ltd., increased to satisfy the
wartime demand. This subsequently increased the pollution of the Jinzu River and its
tributaries. The river was used mainly for irrigation of rice fields, but also for drinking water,
washing, fishing, and other uses by downstream populations.
Due to the cadmium poisoning, the fish in the river started to die, and the rice irrigated with
river water did not grow well. The cadmium and other heavy metals accumulated at the bottom
of the river and in the water of the river. This water was then used to irrigate the rice fields. The
rice absorbed all heavy metals, but especially the cadmium. The cadmium accumulated in the
people eating contaminated rice. The population complained to the Mitsui Mining and Smelting
company about the pollution, which subsequently built a basin to store the mining waste water
before leading it into the river. This, however, was too little too late, and many people already
were very sick. The causes of the poisoning were not well understood, and up to 1946 it was
thought to be simply a regional disease, or possibly a type of bacteria. Medical tests started in
the 1940s and 1950s, searching for the cause of the disease. Initially, it was expected to be lead
poisoning due to the lead mining upstream. Only in 1955 did Dr. Ogino and his colleagues
suspect cadmium as the cause of the disease. Dr. Ogino also coined the term itai-itai disease.
The Toyama prefecture also started an investigation in 1961, determining that the Kamioka
Mining Station of the Mitsui Mining and Smelting company caused the cadmium pollution, and
that the worst affected areas were 30 km downstream of the mine. In 1968 the Ministry of
Health and Welfare issued a statement about the symptoms of the itai-itai disease caused by the
cadmium poisoning.
The reduction of the levels of cadmium in the water supply reduced the number of new disease
victims, and no new victim has been recorded since 1946. However, while the victims with the
worst symptoms came from the Toyama prefecture, the government also found victims in five
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
other prefectures. One of the main effects of this painful cadmium poisoning are very weak and
brittle bones, for details of the symptoms see Cadmium poisoning. The mines are still in
operation today.
Legal action
29 plaintiffs, consisting of nine victims and 20 family members of victims, sued the Mitsui
Mining and Smelting Co. in 1968 in the Toyama Prefectural court. In June 1971, the court
found the Mitsui Mining and Smelting Co. guilty. Subsequently, the company appealed to the
Nagoya District Court in Kanazawa, but the appeal was rejected in August 1972. The Mitsui
Mining and Smelting Co. agreed to pay for the medical care of the victims; finance the
monitoring of the water quality performed by the residents; and pay reparations to the victims
of the disease.
People who consider themselves victims of itai-itai disease have to contact the Japanese
Ministry of Health, Labor and Welfare to have their claims assessed. However, many victims
were not satisfied with government actions, and demanded a change in the official procedures.
This caused the government to review the criteria for recognizing a victim legally; the
government also reassessed the treatment of the disease. A person is considered to have the
itai-itai disease if he or she lived in the contaminated areas, has kidney dysfunctions, softening
of the bones, but no related heart problems. 184 victims have been legally recognized since
1967, of whom 54 were recognized in the period from 1980 to 2000. However, only 15 victims
were still alive as of 1993.
Economic costs
In 1992, the average annual health expense compensation was 743 million yen. Agricultural
damage was compensated with 1.75 billion yen per year, or a total of annually 2.518 billion
yen. Another 620 million yen were invested annually to reduce further pollution of the river.
PCBs in Traditional Food
PCBs is short for PolyChlorinated Biphenyls. They are a type of organochlorine
that was commonly used in electrical transformers; they are no longer produced in North
America. Although PCBs can be found near DEW-line sites, most of the PCBs in the North
come from other parts of the world, carried by winds and ocean currents. Very low levels
of PCBs are found in water and soil; higher levels are found in animals. Because of their
chemical nature, PCBs do not break down easily and so are passed up the food chain when a
small animal is eaten by a larger one.
PCBs have been measured in many animals across the North. If you know a few facts about
PCBs and are familiar with the food chains of animals, you will be able to accurately guess
where PCBs can be found in your diet.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Just remember:
They bioconcentrate. There will be more in older animals. In
mammals, older males will have more than older females since PCBs are lost through
They biomagnify. This means there will be more PCBs in animals high on the food
They are highest in fatty tissue. This means blubber and fat will have
more PCBs than muscle, skin or organs.
Health Risks from PCBs
PCBs in people
PCBs get into people's bodies from eating foods that contain PCBs. How much and what kind
of food they eat will determine their exposure to PCBs. PCBs have been measured in human
blood, milk and fat tissue in people from many places in the world including northern and
southern Canada, United States, Sweden and the Netherlands. Most everyone has some PCBs
in their body; people who eat a lot of fish, seafood, and marine mammals have higher levels.
What are the effects of PCBs on health?
A few studies have looked at the effects of PCB exposure from food on the health of children.
Some found that children who had been exposed to PCBs when they were in the womb
(through the mothers' diets) were slightly smaller at birth and had slower brain development
than children who had not been exposed. Other studies have not been able to confirm this.
Research in the Arctic suggests that exposure to PCBs and other related organochlorines, is
associated with more infectious disease and ear infections in children. However, many more
studies are needed before we can clearly say there are or are not health effects from low-level,
long-term exposure.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Who is most at risk from PCBs?
Babies (especially when they are developing in the womb) and young children.
Should I continue to eat foods that contain PCBs?
People in some communities are exposed to more than the guideline (safe) level of PCBs. At
the present time, however, none have been advised to reduce the amount of traditional food
they eat because the benefits are far more important than the risks. Breast milk is known to
contain PCBs, but the many well-established benefits of breast-feeding are more important than
the risks, which are not well-known.
Killer Whales Have Extremely High Levels of PCBs and DDT
Nancy Black1, Richard Ternullo1, and Marilyn Dahlheim2
Monterey Bay Cetacean Project
National Marine Mammal Laboratory, NMFS
In Ecosystems Observations for the Monterey Bay National Marine Sanctuary, 2003.
Killer whales feed and travel along the deep waters of Monterey Canyon, feeding upon diverse
prey in this extremely productive region. Top predators, they are highly intelligent whales with
culturally distinct patterns that live in family groups. Because of the close proximity of the
canyon to shore in Monterey Bay and our consistent year-round boat surveys, killer whales are
seen here more often than anywhere else along the California coast. Sightings are unpredictable
but occur year-round, providing us with a unique opportunity to study these animals in an open
ocean habitat.
At least three eco-types of killer whale occur in the eastern North Pacific: residents, transients,
and offshores. All three types have been seen in Monterey Bay. Each eco-type differs
genetically, in physical appearance, distribution patterns, vocalizations, and prey preferences.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
These types do not intermix even though they have overlapping ranges. Transient type whales
are most frequently sighted in Monterey Bay and prey on marine mammals – including gray
whale calves, California sea lions, elephant seals, harbor seals, Dall’s porpoise, Pacific whitesided dolphins, and common dolphins. Each whale is identified by its natural markings, and we
have identified 136 individuals to date.
Since 1987 we have studied the behavior and ecological patterns of these known transient killer
whales. We work with other researchers along the West Coast to look for re-sightings of
previously identified whales. This transient population ranges from southern California to
Southeast Alaska, although whales that occur in Monterey Bay are primarily seen in the coastal
waters of California.
Part of our research involves collecting a small amount of skin and blubber through biopsy
sampling from a research inflatable, with a permit through the National Marine Mammal
Laboratory, National Marine Fisheries Service (NMFS). Skin is used for genetic analysis, and
the blubber is used to determine levels of toxic chemicals. This research is being incorporated
into a project to compare persistent organic pollutants (POPs) from killer whales ranging from
Russia and the Aleutian Islands, through central and southeast Alaska and down the West Coast
to California. Gina Ylitalo, from the Northwest Fisheries Science Center, NMFS in Seattle,
analyzes the blubber samples for toxins.
POPs include PCBs (polychlorinated biphenyls) and DDT (dichlorodiphenyltrichloroethane),
which are highly stable organic compounds that were used (and are still used in some
countries) as pesticides or by industrial companies. POPs persist in the environment,
bioaccumulate through the food web, are fat-soluble, and are toxic to humans and animals. The
long-range atmospheric transport of these chemicals to regions where they have never been
produced represents a threat to the global environment. These chemicals are of particular
concern to species at the top of the food chain – most significantly, killer whales.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Figure 1. Eastern North Pacific killer whales: PCB concentrations
PCBs were first produced in the 1920s and were the most lethal chemicals dumped into the
environment. They were used as coolants and lubricants for electrical transformers and
capacitors and in various industrial products. Monsanto Company, a large North American
manufacturer of PCBs, made 635,000 metric tons before the ban in 1977. DDT is a pesticide
that was used in many countries to control mosquitoes and was also heavily used by farmers to
protect their crops. DDT was banned in the United States in 1972 but degrades slowly and
remains in rivers and ocean sediments. Heavy rains throughout California still flush the
chemicals into the oceans, and El Niño storms churn up sediments, releasing these chemicals.
The Montrose Chemical Corporation in southern California was one of the world’s largest
manufacturers of DDT and disposed of thousands of tons of DDT waste into the ocean between
1949 and 1970. Several other industries also discharged PCBs. These polluted waters, near the
Channel Islands, are the main breeding area for California sea lions, which are major prey for
killer whales. Since DDT was banned, levels in California sea lions have greatly decreased but
are still high compared to pinnipeds in other regions.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
The adult male killer whales sampled in Monterey Bay carry very high levels of POPs –
shockingly, the highest levels known for any marine mammal. Levels of PCBs in male
transients ranged from 750 to 1,600 micrograms/gram lipid weight and the highest DDT levels
were 8,700 micrograms/gram lipid weight. A female transient recently found dead off
Washington (an identified whale from our California catalog) contained about 1,000 parts PCB.
Comparatively, levels of PCBs from transient whales in British Columbia and Alaska, although
still high, average three to ten times lower. Since resident whales are fish eaters, it is expected
that their levels would be less than transients, but levels are still high enough to cause concern
(Figure 1). These high values are much greater than those known to affect the growth,
reproduction, and immune systems of harbor seals. As apex predators, killer whales typically
have smaller population sizes than those of their prey. As such, an outbreak of a virus or
disease could be disastrous to their survival if their immune systems are compromised.
California’s pinnipeds and cetaceans, prey of the transients, are all known to have relatively
high levels of POPs. Since transient killer whales are at the top of the food chain, they
bioaccumulate these toxins from their prey. Female whales offload some of the toxins to their
calves through milk, transferring up to 90 percent of their contaminants to their first born.
Females first reproduce at around fifteen years, but after the age of forty to fifty they are postreproductive and can then continue to accumulate these toxins. The males have no way of
offloading these chemicals and continue to accumulate them throughout their lives. Killer
whales are long-lived animals, with males living forty to fifty years and females, eighty to
ninety years. The shorter male lifespan could be due to higher toxins in their bodies.
Killer whales off California appear to be the most contaminated animals on earth and are
indicators of the health of the marine environment. Our long-term research will continue to
sample toxin levels from more individuals and to monitor this population and their survival
rates. Efforts to decrease these toxins worldwide and attempts to prevent continued
contamination of the oceans, including looking for source points and researching clean-up
methods, should increase.
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Cadmium toxicity threatening wildlife in Rocky Mountains
By Mark Floyd, 541-737-0788
SOURCE: Jim Larison, 541-737-8284
CORVALLIS, Ore. - An alarming number of white-tailed ptarmigan in a large region of the
southern Rocky Mountains are suffering from acute cadmium poisoning - an exposure to high
concentrations of the extremely toxic trace metal.
Scientists report in the journal Nature that 46 percent of the adult birds surveyed in a 10,000square kilometer area in south-central Colorado were found with cadmium accumulations in
their kidneys well above the toxic threshold of 100 parts per million.
Cadmium toxicity causes kidney and liver dysfunction, brittle bones, and adversely affects
reproduction and survival.
Lead author James R. Larison, an Oregon State University professor and alpine ecologist, said
the findings are not unlike those that linked the pesticide DDT to a problem of thin-eggshells in
the peregrine falcon three decades ago. The implications of the toxicity go beyond a single
"What we found in our study was that a particular genus of
plants - willows - were 'biomagnifying' or concentrating
cadmium," Larison said. "They act as biological pumps,
increasing the concentrations of cadmium by two orders of magnitude. Birds eat a lot of
willow, especially in the winter when other foods are scarce.
"They aren't the only creatures to eat willow, though," he added. "The possibility exists that
deer, elk, moose, snowshoe rabbits, beaver and other animals may face similar problems, just
as it is possible that other plants - including some vegetables - may have the same abilities to
biomagnify cadmium that willow does."
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site
Larison said the human health risk from eating ptarmigan likely is small, unless the internal
organs are consumed. But, he added, many people eat vegetables grown in the area and these
could pose a risk to human health. The former director of Sea Grant Communications at
Oregon State University, Larison has spent the past four years at Cornell University pursuing
his doctorate in ecology and evolutionary biology. His doctoral study was funded primarily by
the National Geographic Society. Other authors in the Nature article include Gene Likens,
director of the Institute for Ecosystem Studies in Millbrook, N.Y., John Fitzpatrick, director of
the Cornell University Laboratory of Ornithology, and J.G. Crock, a chemist with t he U.S.
Geological Survey.
The study focused on an expansive section of Colorado stretching from Denver and Fort
Collins to Durango known as an "ore belt." Larison, who has returned to the OSU faculty, said
abandoned mines throughout this area have "exacerbated the problem."
Though cadmium is natural to the area, he pointed out, mining tends to mobilize potentially
toxic metals. "Cadmium poisoning originally was discovered in Japan, with rice acting as a
biomagnifier," Larison said. "Elderly women in particular were affected with severe
osteomalacia - a condition not unlike osteoporosis. Trace amounts of cadmium can be found in
almost all soils, surface waters and plants, but human activities tend to concentrate it. Mining is
one obvious factor, but cadmium also is mobilized by certain industrial and agricultural
Once ingested, cadmium cannot easily be excreted from the body and accumulates, usually in
the kidneys and liver. The kidneys are responsible for calcium levels in the blood, Larison said,
and when cadmium levels rise and kidneys tubules fail, calcium levels drop. To compensate,
the body "borrows" calcium from bones. In Japan, elderly women eating a diet heavy in
cadmium-contaminated rice suffered from severe bone decalcification.
In Larison's study, 57 percent of the adult ptarmigan had damaged kidneys and their bones
contained 8 to 10 percent less calcium.
"We also found a number of birds with bone fractures," he said. "For every one we found, there
may have been others that did not survive long enough for us to discover them."
Cadmium toxicity in predators eating ptarmigan is a concern, Larison pointed out, because they
likely would eat the internal organs and the cadmium would then accumulate in their bodies as
well. Ptarmigan predators include eagles and hawks, as well as foxes and coyotes.
Though the Nature article focuses on one area in the Rocky Mountains, cadmium poisoning
potentially could occur elsewhere, Larison said.
"We happened to look at the effects just on white-tailed ptarmigan eating willows in Colorado,"
Larison said. "But there are some indications that the conditions for cadmium poisoning are
News & Communication Services Homepage Updated 12-July 2000
Adapted from (2003) Centre for Indigenous Peoples’ Nutrition and Environment web site