el_hayek.qxd

Mercury Contamination in Arctic Canada:

Possible Implications for Aboriginal Health

Youssef H. El-Hayek

Abstract

Methylmercury is a potent neurotoxin found at elevated

concentrations in both the Arctic ecosystem and tissues of

the local Aboriginal inhabitants. Combined studies of

ecological contamination with the possible implications

for human health, have made this one of the largest

environmental research projects in Canadian history.

Recent scientific advances have revolutionized the

understanding of the global mercury cycle. The major

source of mercury exposure is through the consumption of

locally derived food sources. Mercury tissue

concentrations are reaching alarming levels in some

Aboriginal communities. Studies on both animals and

humans have provided compelling evidence suggesting

that methylmercury contamination induces neurological

defects. Cognitive defects have been noted in children

exposed congenitally in several other seafood-consuming

communities around the world. Defects in motor function

have been observed in both adults and children in Inuit

Communities. Furthermore, environmental mercury has

been linked to both autism and Alzheimer disease.

Aboriginals are currently exposed to methylmercury in

addition to several other environmental toxins. This may

have serious repercussions for neurodevelopment and

health in this population.

Mercury and the Environment of Arctic Canada

The Northern Contaminants Program (NCP)

Approximately 7.5% of Canada's aboriginal population inhabits the Arctic

region in the northern part of the country, where they comprise just over half

of the combined population (Statistics Canada, 2001). The lives of these

JOURNAL ON DEVELOPMENTAL DISABILITIES, VOLUME 13 NUMBER 1, 2007

56,000 people are linked to the local environment, particularly through the

consumption of traditional foods (Van Oostdam et al, 2005). Mercury

contamination as a possible health concern was initially raised in the early

1970s, following contamination of fish due to effluents from chlor-alkali

plants in northern Ontario. Similar concerns were later recapitulated in

several other communities (CACAR, 2003). Moreover, early studies in the

mid-80s indicated that the Arctic ecosystem harbored unusually high levels

of contaminants such as persistent organic pollutants, radionucleotides, and

heavy metals including mercury (Wong, 1986). In response to such

concerns, the Department of Indian Affairs and Northern Development

established the Northern Contaminants Program (NCP) in partnership with

Federal and Territorial Departments, Aboriginal organizations, and

University researchers (CACAR, 2003). Since its conception in 1991 the

NCP has focused on determining the levels and sources of contaminants in

the Arctic, and assessing the possible impacts and risks towards human

health.

The Mercury Cycle in the Arctic Ecosystem

The initiatives of the NCP, in conjunction with the development of more

sophisticated instrumentation, have lead to a scientific revolution in our

understanding of the global mercury cycle (CACAR, 2003). Mercury exists

in three states: elemental mercury, inorganic mercury salts, and organic

mercury. In aquatic environments, inorganic mercury is converted to the

more toxic organic state, otherwise known as methylmercury (MeHg).

Methylmercury is found at elevated concentrations in the tissues of aquatic

animals in the Arctic (Lockhart & Evans, 2000; Wagemann et al., 1995).

When a contaminant enters the food web, it is passed on from prey to

predator, and in the process successively increases in concentration. Animals

higher up the food web are therefore at a higher risk for exposure. This

process is known as biomagnification or bioaccumulation. Once it enters the

food chain, mercury is biomagnified as methylmercury (Atwell et al., 1995),

and results in global human exposure primarily through the consumption of

contaminated fish (WHO, 1990).

Although the process of biomagnification enhances exposure levels, it is the

physiochemical reactions of mercury in the air and water that ultimately

determine the amount that enters the food web. Natural sources of mercury

from local rocks and soils have remained steady for decades, while human-

made, or anthropogenic sources are on the rise (CACAR, 2003).

Anthropogenic emissions from fossil fuel consumption, waste incineration,

chlor-alkali plants and metal smelting and processing release elemental

EL-HAYEK

mercury in a gaseous state into the atmosphere (Pacyna & Keeler, 1995).

Once in the atmosphere, gaseous mercury is capable of long-range transport

in air currents (Schroeder and Munthe, 1998), which can reach isolated

environments such as the Arctic from industrial regions such as Europe,

Asia, and North America.

Canadian researchers have recently characterized a staggering discovery

known as atmospheric mercury depletion events (MDEs) at Alert, Nunavut

and Kuujjuarapik, Quebec (Schroeder et al., 1998; 1999a). During the polar

sunrise in the spring after approximately five months of darkness,

atmospheric mercury levels drop drastically. During this sudden exposure to

solar radiation, atmospheric mercury is converted into a more reactive,

oxidized form (Schroeder et al., 1999b), which deposits more easily in the

snow (Schroeder et al., 2000). The occurrence of MDEs in the springtime

correlates with the preparation of plants and animals for peak summertime

activity possibly enhancing exposure. Approximately 60% of the mercury

that reaches lakes and rivers flows out and 25% falls to the bottom and, and

current data suggests that, at least in some areas, the levels of mercury in

lake sediments are increasing (CACAR, 2003).

Mercury Exposure Levels

Aboriginal Perspectives on Food

For us to be fully healthy, we must have our foods, recognizing the

benefits they bring. Contaminants do not affect our souls. Avoiding

our food from fear does. (Egede, 1995)

Exposure to mercury in Aboriginal communities occurs primarily through

the consumption of traditional country foods (Van Oostdam, 2005). Country

food refers to mammals, waterfowl/ seabirds, fish, and vegetation harvested

from the local flora and fauna. The attitudes towards the collection,

consumption, and trade of traditional food are different to those in Western

life. Food is an integral part of the community, with social, cultural,

economic and spiritual ramifications (Wheatly, 1996). Data from 1,721

interviews collected from five Inuit areas illustrated that traditional food is

perceived to provide cultural and economic benefits in addition to basic

nutrition (Kuhnlein et al., 2000). Cultural aspects aside, it would cost

approximately 55 million dollars to purchase equivalent amounts of imported

food, which is well above the 10,000 dollar aboriginal average household

income (Usher & Wenzel, 1989). Despite the date of the previously

MERCURY CONTAMINATION IN ARCTIC CANADA

mentioned study, it illustrates that a major economic drawback would be

associated with avoiding locally derived food sources. It is therefore apparent

that exposure to contaminants such as mercury can be potentially confounded

by socio-demographic, economic, and cultural factors.

Intake Levels and Guidelines

The major global source of MeHg exposure is through the consumption of

contaminated fish (WHO, 1990). In aboriginal communities, exposure may

also arise through the consumption of other local animals such as seals, polar

bears, narwhal muktuk, and caribou (Kuhnlein et al., 2000). Metals such as

mercury accumulate mostly in the internal organs of animals such as the liver

and kidney (Chan et al., 1995). The WHO has specified a guideline for the

provisional tolerable daily intake (pTDI) for total mercury (0.71μg/kg/day)

and methylmercury (0.47μg/kg/day) (WHO, 1978). Health Canada has also

issued a methylmercury pTDI of 0.2μg/kg/day for children and women of

childbearing age (Health Canada, 1998). The U.S Environmental Protection

Agency has established a MeHg dose of 0.1μg/kg/day for pregnant mothers

(U.S. Environmental Protection Agency, 1997).

Mercury intake levels for various populations have been compiled based on

a comparison of dietary surveys with the known mercury content of various

foods. Care should be taken in interpreting these values since much of the

available data is based on total mercury levels, not the more toxic organic

form. This has important implications as certain species such as fish contain

mostly MeHg while sea mammals contain mostly inorganic mercury

(Wagemann, 1997). Furthermore, recent reconstructions of MeHg intakes

using mathematical models based on biomarkers have illustrated that dietary

surveys may have overestimated intake values (Gosselin et al., 2005).

Finally, it should be understood that the data represent an average for the

population. As in any statistical distribution, a few individuals may be

exceeding the mean value by a large magnitude. Data from dietary surveys

indicate that the Inuit have the highest intakes of mercury with levels close

to the pTDI (Kuhnlein, 2001), while other groups have intake levels well

below the pTDI. The data suggests that Inuit children and women of

childbearing age may be exceeding the pTDI.

Tissue Levels and Guidelines

The Medical Services Branch of Health Canada, the First Nations and Inuit

Health Branch (FNIHB), the Cree Board of Health and Social Services, and

the Government of the Northwest Territories (GNWT) have accumulated a

EL-HAYEK

wealth of data on tissue mercury levels. The combined efforts of these and

other agencies have made this one the largest contamination research

projects in Canadian history.

There are two commonly used biomarkers to assess mercury tissue levels:

mercury levels in hair and mercury levels in maternal/umbilical cord blood.

Health Canada has issued ranged guidelines for methylmercury blood levels

(Health Canada, 1979). Levels below 20μg/L are acceptable, while those

between 20 and 100μg/L are at increasing risk, and above 100μg/L

considered at risk. More recently, the USA issued a benchmark level of

58μg/L and a recommended maternal level of 5.8μg/L (NRC, 2000).

The blood levels mirror intake levels, in that Inuit mothers are exceeding

both Canadian and US guidelines, while no Caucasian, Dene, or Metis

mothers exceed the lower guideline of 5.8μg/L (Butler & Walker, 2005).

Within Inuit regions, Nunavik appears to have the highest proportion of

mothers exceeding recommended guidelines (Figure.1). It should be noted

that mercury concentrates on the fetal side of the placental circulation so

umbilical cord levels would be 1.5 to 1.8 times higher than in maternal blood

(Van Oostdam et al., 2005). The general historical trend is that the

percentage of Inuit mothers exceeding blood guidelines is on the decline

(Van Oostdam, 2005). However, issues regarding the statistical sampling of

historical accounts have been raised (Van Oostdam, 1999).

Figure 1. Maternal contaminant levels in Arctic Canada: Total mercury

(

g/L plasma)

Figure reprinted from (Van Oostdam et al, 2005) with permission from Elsevier

MERCURY CONTAMINATION IN ARCTIC CANADA

Dene/Métis (1.4)

Inuit - Nunavik

(10.4)

Inuit - Baffin (6.7)

Inuit - Inuvuk (2.1)

Inuit - Kitikmeot (3.4)

Caucasian (0.9)

Other (1.3)

Inuit - Kivalliq (3.7)

Mercury and the Nervous System

Toxicity of Mercury

Once ingested, 90% of MeHg is absorbed across the gastrointestinal tract.

Once in the blood stream it can easily cross the normally protective blood

brain barrier, due to its lipophilic nature (Mendola et al., 2002). It can be

transferred from mother to fetus via the placenta (Kajiwara et al., 1996), and

to infants through lactation (Sakamoto et al., 2002). Methylmercury is a

neurotoxin that can induce severe, irreversible damage to the central nervous

system (Philbert et al., 2000). Although the mechanisms remain to be fully

elucidated, it appears that a major neurotoxic effect involves oxidative stress

through the increased production of reactive oxygen species (ROS).

Methylmercury also alters cell proliferation, differentiation, and migration

(Mendola et al., 2002). These processes are crucial to the well-orchestrated

and highly organized process of brain development.

A number of factors can potentially modulate the effect produced a

neurotoxic agent such as MeHg. One obvious factor is dose, or the

concentration that the nervous system is subjected to. Another would be the

extent of exposure time. When dealing with low-level exposures, however,

there may be more subtle factors involved. One such factor is the time point

of exposure during development. Brain development proceeds in a very

tightly regulated, highly organized pattern. Slight perturbations in this

process may have profound consequences for the immature brain. On the

other hand, a fully mature brain may be less vulnerable. Consequently, low-

level exposure may induce different defects in prenatal, neonatal, adolescent,

or adult nervous systems. Furthermore, subtle defects early in CNS

development may not become apparent until relatively late stages of life.

This is known as the Barker Hypothesis, which postulates that, certain

parameters in early life, such as low birth weight or small head

circumference induced by malnutrition, are indicators for disease

development in later life (Osmond & Barker, 2000). In 2003, this hypothesis

was expanded to include environmental toxins and brain development

(Landrigan et al., 2005). This hypothesis is similar to that of "Silent

Damage" (Weis & Reuhl, 1994). It has been postulated that the early

exposures to neurotoxic chemicals reduces the number of neurons in critical

brain areas, which becomes magnified later in life due to the aging process.

This for example, includes a well-documented correlation between early life

exposures to pesticides and Parkinson disease (Landrigan et al., 2005).

EL-HAYEK

Acute Poisoning

The horrific neurotoxic effects of high level MeHg exposure are well

characterized through catastrophic events of mass poisoning. On two

separate occasions in Japan, fish become contaminated with MeHg from

local industrial discharge (Tsubaki, 1977). The first event occurred in the

1950s at Minamata Bay, and resulted in severe developmental defects

including cerebral palsy, microcephaly, blindness, and seizures in children

exposed during pregnancy (Goto, 2000). This has been dubbed Congenital

Minamata Disease. A similar episode occurred in Niigata, Japan in the

1960s. Based on lessons learned in Minamata, abortion was recommended

for pregnant mothers exhibiting high hair mercury levels (Tsubaki, 1977). In

exposed adults, the primary effect seems to be a targeted loss of neurons in

areas of the brain involved in vision, motor function, as well as the

disruption of sensory nerves (Reviewed in Castoldi et al., 2001).

Consequently, acute exposure during adulthood induced defects such as

hearing loss, muscle weakness, mental deterioration, and visual

abnormalities. In 1971, accidental consumption of seed grains treated with a

mercury containing fungicide resulted in hundreds of deaths in Iraq, with

thousands becoming clinically ill. Children exposed during pregnancy

exhibited higher frequencies of mental retardation, blindness, seizures, and

other neurological defects (Marsh et al., 1987). Three major conclusions can

be drawn from these unfortunate events. Firstly, high levels of MeHg can

have a devastating effect on both the developing and mature nervous

systems. Secondly, acute poisoning induces damage to several brain areas,

resulting in a broad spectrum of clinical manifestations. Thirdly, exposures

of the developing fetus to MeHg results in more severe neurological defects

than exposures in later life.

Low Level Exposure

Animal Studies

As mentioned above, the acute neurotoxic effects of MeHg have been well

documented. The effects of chronic low-level exposure are somewhat more

controversial. Animal models have several advantages over human studies,

the most important of which being that it permits testing in a controlled

environment. This facilitates data interpretation by reducing the potential

confounding effects of environmental factors such as diet or genetic

variations. The results from animal models are mixed (Reviewed in Rice,

1996). The major drawback being difficulty in distinguishing between

MERCURY CONTAMINATION IN ARCTIC CANADA

defects in sensory/motor functions from defects in cognition, or

"intelligence". Rodents and monkeys exposed developmentally to MeHg

seem to display difficulty in performing simple tasks. This difficulty appears

to be more related to sensory or motor deficits rather than a direct defect in

cognitive aptitude. In one series of experiments, Macaque monkeys exposed

to MeHg during pregnancy displayed infantile alterations in visual

recognition tasks that are believed to assess cognitive function. However,

this same group of monkeys was not impaired on similar tests later in life.

In a separate series experiments no cognitive deficits were found in monkeys

exposed, but visual and somatosensory defects were recorded. In one study,

five monkeys were dosed from birth to seven years of age with 50μg/kg/day

of MeHg (Rice, 1998). These monkeys displayed defects in auditory, visual,

and somatosensory function at age 20 years. The monkeys were then tested

for defects in speed of information processing, which is highly correlated

with IQ in humans. A button pushing test in response to a visual stimulus

experiment was set up to distinguish between reaction time (information

processing) and motor time (speed of movement). Since no significant

difference was observed between the reaction times in the experimental and

control groups, and the authors concluded that cognitive defects were not

impaired. Care should be exercised in interpreting these results since which

is that five monkeys is hardly a large enough group to develop a statistical

population. Despite the inconsistency in animal models a few conclusions

may drawn with respect to low-level exposure. First, it is likely that

developmental exposure can induce sensory and motor defects; however,

evidence for direct cognitive defects is more controversial. Second,

although a controlled scientific environment is a necessity, it is

nonetheless a simplistic model of a much larger, genetically heterogeneous

human population. Third, these experiments do not take into account the

possible additive effect of exposure to multiple environmental

neurotoxins, as is the case in Arctic Canada (Van Oostdam, 2005), which

may have additive effects.

Congenital Exposure in Humans

A number of human studies have been carried out to address the issue of

development defects following congenital exposure to low levels of MeHg

through maternal consumption of contaminated seafood (Castoldi et al.,

2001; Myers & Davidson, 2000). None of these studies have identified

mental retardation or other severe development defects. However, it is

ambitious to expect that such small sample sizes would have the sensitivity

to detect increases in rare outcomes such as mental retardation.

EL-HAYEK

Consequently, researchers have focused on more identifying subtle signals

of neurological damage and developmental delay, which are anticipated to

be more likely prevalent as a consequence of low-level developmental

exposure. Table 1 compares known MeHg biomarkers in various

populations including those in Canada. Note the wide variation in levels,

illustrated in the range column. In general, the results of human studies

mirror those seen in animals, in that there are inconsistencies. However, the

data supporting cognitive defects are relatively more conclusive. Cognition

is usually assessed by subjecting patients to standard tests that assess

aptitude in areas such as language, memory, and attention. The National

Research Council of the National Academy of Sciences (NAS) recently

reviewed some of these studies and concluded that the evidence supporting

neurodevelopmetal defects associated with methylmercury through

contaminated seafood is compelling (NRC, 2000).

Table 1. Comparison of mercury (total) concentrations in Nunavik with

those observed in other cohorts.

Cohort Medium Years N Geometric Range Interquartile

(reference) mean range

(continued)

MERCURY CONTAMINATION IN ARCTIC CANADA

Nunavik

Inuit

Cord blood

(μg/L)

1996-

2000

18.595 2.8-97.0 12.0-27.2

Maternal

blood (μg/L)

1993-

1995

10.4130 2.6-44.2 6.6-17.0

Maternal

hair (μg/g)

1992 3.7123

0.3-14.0

2.5-6.2

Southern

Quebec

Cord blood

(μg/L)

1977-

1978

1.01108

0.9-1.0

James Bay

Cree

Women hair,

not pregnant

(μg/g)

1981 2.570 max=19.0

USA Women hair,

not pregnant

(μg/g)

1981

0.36

1274 0.14-0.90

Northern

Quebec

Cree

Maternal

hair (μg/g)

6.0

215

5.2

0.24

1546 0.09-0.62

Canada

Table 1. (cont’d)

Cohort Medium Years N Geometric Range Interquartile

(reference) mean range

Table reprinted from (Van Oostdam et al, 2005) with permission from Elsevier.

Original source: (Muckle et al, 2005b)

The average Hg concentration was reported in nmol/L, this concentration was

divided by 5 to transform to

g/L.

95% confidence interval.

Women aged between 15 and 39 years old.

Arithmetic mean.

Standard deviation.

Among seafood consumers.

Among non-seafood consumers.

In New Zealand, maternal exposure to MeHg, primarily through the

consumption of contaminated fish, resulted in a lower performance on

neurobehavioral tests in children at age 4 (Kjellstrom et al., 1986) and age 6

(Kjellstrom et al., 1989). At age 4, children exhibited abnormal test scores

on the Denver Developmental Screening Test. Higher incidences of

premature birth and low birth weight was also reported. At age 6, children

EL-HAYEK

Seychelles Island

Main

study

Maternal

hair (μg/g)

1989-

1990

5.9740 0-25 6.0

Pilot

study

Maternal

hair (μg/g)

6.6789 0.6-36.4 6.1

New

Zealand

Maternal

hair (μg/g)

1978-

1984

8.3

935 6.0-86.0

Greenland,

Disko Bay

Cord blood

(μg/L)

1994-

1996

25.3178 2.4-181.0

Maternal

blood (μg/L)

1994-

1996

12.8180 1.9-75.6

Faroe Islands

First

Cohort

Cord blood

(μg/L)

1986-

1987

22.9894 13.4-41.3

Maternal

hair (μg/g)

1994-

1995

4.3914 2.6-7.7

Second

cohort

Cord blood

(μg/L)

20.4163 1.9-102.0 11.8-40.0

Maternal

hair (μg/g)

4.1144 0.4-16.3 2.5-7.4

displayed poorer scores on the Wechsler Intelligence Scale for Children-

Revised and in the Test of Language Development. However, the

experimenters also found that social class and ethnic group affected scores.

In both incidences, defects were correlated to higher levels of mercury in

maternal hair.

A larger study in the Faroe Islands assessed the effects of maternal exposure

through the consumption of contaminated fish and pilot whale (Grandjean et

al., 1997). At seven years of age, the children were subjected to several

neurobehavioral and sensory-motor tests. Defects were observed in verbal

memory, language, attention, motor function, and visual-spatial abilities.

Clinical testing revealed that the children had no apparent physiological

defects, and were otherwise healthy. The same experimenters later found

that these defects were also associated with umbilical cord mercury levels.

Curiously, no evidence for a threshold hair level was found in these studies,

with mothers exhibiting a broad range of levels. This population is also

exposed to relatively high levels of PCBs, particularly through the

consumption of whale meat. However, corrections for PCB cord blood

levels suggested that concomitant exposure could not explain the mercury

related defects, and that there was no additive effect between these two

environmental contaminants (Budtz-Jorgensen, 1999). Another study

conducted in the Faroe Islands correlated a decreased neurologic optimality

score in 182 neonates to cord blood mercury levels (Steuerwald et al., 2000).

Maternal hair mercury levels were also found to be associated with

neurobehavioral defects in 351 children in Amazonian communities in

Brazil (Grandjean et al., 1999a). Gold mining in the Amazon Basin has

released mercury into rivers, and subsequently contaminates fish in

downstream areas.

The results of two other major epidemiological studies did not report any

effects of prenatal MeHg on neurobehavioral function. In the Republic of the

Seychelles over 700 mother-children pairs were examined (Davidson et al.,

1998). Deep sea and reef fish consumption is the source of MeHg for this

population. Six age appropriate neurobehavioral tests were implemented on

children age 66 months. Adverse effects were controversially noted in the

pilot study; however, the main study, in which the covariates were better

controlled, revealed no apparent neurobehavioral defects associated with

maternal MeHg. The average maternal total mercury hair levels were

intermediate between those recorded in the Faroe Islands and New Zealand.

The authors of the Seychelles study recently reported that two of the 21

neurobehavioral endpoints examined at 9 years of age were correlated to

MeHg exposure, but that this was probably due to chance as a consequence

MERCURY CONTAMINATION IN ARCTIC CANADA

of multiple analyses (Myers, 2003). The mercury levels in local fish were

comparable to those found in the United States (Mahaffey & Rice, 1997),

suggesting that the higher hair mercury levels were due to a greater

consumption of fish, rather than higher contamination in the environment.

Another smaller study on 131 infant-mother pairs in Mancora, Peru

similarly found no neurodevelopmental anomalies.

The Seychelles, New Zealand, and Faroe Islands studies were all reviewed

by the NAS. Despite the negative results in the Seychelles, the NAS still

concluded that the evidence was compelling. Several factors were suggested

to account for the apparent inconsistencies in findings between these studies

(NRC, 2000). Differences in age at testing, the end points assessed, the

source of mercury, and the pattern of exposure could all account for the

differences between the results of the Faroe Island and the Seychelles

studies. The exposure and experimental designs, however, were similar in

the New Zealand and Seychelles study. Although it is curious that the pilot

study found neurobehavioral effects in the Seychelles, differences in

environmental and genetic factors may have also played a role.

Referring to Table 1, the Inuit of Disko Bay, Greenland have the highest

maternal and cord blood levels. Similar, but lower levels are found in the

Seychelles, Faroe Islands, New Zealand, and Nunavik regions. Lower levels

are found across Caucasian Southern Quebec and U.S. populations. Given

the compelling evidence that mercury contamination during pregnancy can

cause neurodevelopmental defects, and that those aboriginal populations

such as the Inuit harbor comparable maternal and cord levels, it seems

reasonable to assume that such populations are at risk. Prospective

longitudinal studies on the neurobehavioral effects of MeHg and other

contaminants on Aboriginal populations have been ongoing since 1997

(Muckle et al., 2001a & 2001b). The exposure data have already been

published and statistical analysis of the possible neurodevelopment defects

are currently being undertaken and will be available soon.

Postnatal Exposure in Humans

The previous section addresses defects in cognitive functions. A recent study

addressed the possible effects of postnatal MeHg exposure on neuromoter

function in Inuit preschool children (Muckle et al., 2005). Blood mercury

levels are an indicator for very recent exposure, within 1 or 2 months (WHO,

1976). The authors found that blood mercury levels at the time of testing

were associated with tremor amplitude in pointing tasks. Additionally, 234

EL-HAYEK

Quebec Cree children aged 12 to 30 months revealed abnormal tendon

reflexes (McKeown-Eyssen et al., 1983). However, the abnormality was

only correlated with blood mercury levels in males, and no evidence was

observed relating increasing amounts of maternal hair mercury and

abnormal tendon reflexes. Beuter and colleagues found a similar correlation

between methylmercury exposure and static/ kinetic tremors in Quebec Cree

adults (Beuter & Edwards, 1998; Beuter et al 1999a, Beuter et al., 1999). At

mercury hair levels higher than 24ug/g, eye-hand coordination was also

impaired in this group. Furthermore, adult Brazilian Amazon dwellers were

found to be at increased risk for defects in arm movement and manual

dexterity (Lebel et al., 1998).

In 1977, 306 Quebec Cree adults were analyzed for the possible

neurological defects associated with chronic low-level exposure in response

to litigation against 15 mining and industrial companies (Koffman et al.,

1979). The authors found no correlation between MeHg levels and

neurological problems. Recently, these data were reanalyzed using different

statistical methods (Auger et al., 2005). Instead of using an overall

neurological score, which may exclude subtle defects, the authors examined

several possible neurological outcomes independently. The authors

performed several tests for cognitive impairment, reflexes, and sensory-

motor functions, and found only a correlation with tremor. There are several

problems characteristically associated with studies of this type – for

example, bias of subjects who have something to gain, such as a winning a

lawsuit or public recognition. Other possible confounding factors include

alcohol usage, which is known to induce neurological defects including

tremor. The most difficult complication is attempting to assess whether the

tremors are associated with chronic low-level postnatal exposure, or delayed

neurotoxicity from prenatal exposure. Delayed neurotoxicity is well

established in response to acute poisoning in Minamata patients, in which

patients over the age of 40 years exhibit difficulties in performing daily

activities (Kinjo et al., 1993). Auger and coworkers found the strongest

association of tremors with average mercury levels along the hair shaft

(Auger et al., 2005). These levels are believed to be a good indicator of long-

term exposure, as opposed to peak levels along the shaft or scalp hair, which

are believed to represent fluctuations of past exposure. However, similar to

the Brazilian study, tremor development was associated with age in that

younger adults exhibited the response exclusively. Thus, it is possible that

induction of tremors in adults may be a delayed neurotoxic consequence of

low level congenital exposure correlated to historical time points such as

industrialization of these rural areas.

MERCURY CONTAMINATION IN ARCTIC CANADA

It has been suggested that elemental mercury exposure, particularly through

dental amalgams, may be a risk factor for Alzheimer Disease (AD)

(reviewed in Mutter et al., 2004). Patients with sporadic AD have a gene

known as apolipoprotein E4 that is expressed in the brain. This compound

may have a reduced ability to bind metals such as mercury, which may in

turn increase the risk of AD development. As discussed previously, fish

eating populations are exposed primarily to organic rather than elemental

mercury. A study on 474 Baltimore residents aged 50 to 70 years exposed to

mercury primarily through contaminated fish, however, revealed no

association between blood mercury levels and neurobehavioral performance

(Weil et al., 2005). This study has some limitations (Mutter and Naumann,

2005), the most serious of which is that blood methylmercury levels

represent only recent exposures, and do not take into consideration exposure

throughout life or during development.

In summary, there is currently no compelling evidence to suggest a

correlation for cognitive defects with respect to chronic or acute low-level

exposures in adult fish eating populations. This is supported by the fact that

in the Faroe Islands the blood mercury levels at seven years of age were

generally uncorrelated with neurobehavioural deficits, except in the area of

performance on memory for visuospatial information (Grandjean, 1999b).

This indicates that cognitive impairment is likely a function of congenital

but not recent exposure. There may be neuromotor deficits associated with

chronic low-level exposure, as indicated by previously mentioned studies;

however, it is not absolutely clear whether theses effects are due to some

form of delayed neurotoxicity associated with prenatal exposure.

Mercury and Autism

Autism is the most severe of the Autism Spectrum Disorders (ASD). It is

characterized by impairments in social interaction, difficulties in

communication, and repetitive or stereotyped behavioral patterns. Autism

was first described in 1943, and by 1995 the National Institutes of Health

had reported a prevalence of 1 in 500 (Bristol et al., 1996). The exact

etiology of ASD is unknown, however, it is clear that development is subject

to both genetic and environmental factors. For example, genetically

identical twins have only a 60 % concordance rate in disease expression (Le

Couteur, et al., 1996).

From the 1930s to 2001, a preservative known as thimerosal was commonly

added to childhood vaccines. Thimerosal contains a slightly different form

of organic mercury known as ethylmercury. It was proposed that exposure to

EL-HAYEK

ethylmercury may contribute to the pathogenesis of ASD (Bernard et al.,

2001; Bernard et al., 2002). Support for this hypothesis was based on

temporal associations between onsets and prevalence of ASD with the

introduction of ethylmercury into vaccines. Furthermore, autistic patients

exhibited elevated levels of mercury in biological samples such as urine.

Finally, the effects of low-level exposure to organic mercury in fish eating

populations induces neurobehavioral defects characteristic of ASD.

However, despite these correlations, the current viewpoint of the scientific

community does not support this hypothesis. The conclusions of both the

Institute of Medicine and the World Health Organization are that thimerosal

does not cause neurobehavioural defects (IOM, 2004). However, the subject

remains controversial with advocates of the thimerosal hypothesis vocally

accusing the scientific community of covering up evidence (Kennedy, 2005).

Although the link between ASD and thimerosal is tenuous, a recent study

has implicated environmentally released mercury as a risk factor (Palmer et

al., 2006). The state of Texas has the fourth highest release rates of

environmental mercury in the US. Investigators have found that, on average,

a 61 % increase in the rate of autism among school children is associated

with each 1000 lbs. of environmentally released mercury. The results of this

study do not prove a causal relationship between environmental mercury and

ASD. It is nonetheless a first step, with more detailed studies at the

individual rather than ecological level required. None of the previously

mentioned studies on fish eating populations has identified severe

developmental disorders such as autism. It remains to be seen whether

exposure to environmental mercury is a risk factor for ASD in aboriginal

populations in Canada.

Outlook and Conclusions

Nutritional Benefits of Traditional Foods

Traditional country foods are of high nutritional benefit, providing a good

source of vitamins, minerals, lipids, and proteins (Van Oostdam, 1999).

Consumption of these foods has been associated with lower levels of

saturated fat and carbohydrates (Kuhnlein et al., 2004). Health benefits from

consuming 1-2 servings of fish a day have been well documented

(Kromhout et al., 1995). Consumption of fish more than 4 times per week

during pregnancy may actually improve cognitive functions in children

(Daniels et al., 2004). Thus, the risks associated with mercury exposure

should be carefully weighed against the benefits (Kuhnlein et al., 2000).

MERCURY CONTAMINATION IN ARCTIC CANADA

This risk benefit assessment should be assessed for different populations,

which may have different eating habits. For example, caribou are currently

the main source of mercury exposure for Inuit communities, which are the

most highly exposed population (Kuhnlein et al., 2000). It would therefore

seem unreasonable to advise against fish consumption in this population,

given the benefits. However, a reduction in caribou consumption may be

warranted, although the health benefits of this animal are currently unknown

(Van Oostdam, 2005).

Possible Implications of Climate Change

It is become abundantly clear that the activities of the human race are

inducing environmental changes on a global scale. Greenhouse gases and

aerosols are being released into the atmosphere causing global warming,

with the 1990s likely the warmest decade of the millennium (IPCC, 2001).

The marine food webs are being disrupted (Pauly et al., 1998) and the

hydrological cycle is being altered by excessive damming (Dynesius and

Nilsson, 1994).

Current understanding of the possible implications of climate change are not

well understood; however, speculation is rampant in the scientific

communities. Global mercury levels in the atmosphere have more than

doubled since the dawn of industry (Lamborg et al., 2002). The process of

biomagnification makes aquatic environments the most vulnerable,

especially in the Arctic due to mercury depletion events. Although global

mercury emissions are decreasing, levels are on the rise in the Arctic, with

climate change being a possible cause (CACAR, 2003). Several possible

factors may contribute to alterations of environmental mercury levels

(CACAR, 2003). For example, the loss of permafrost is expected to occur

with global warming. This would increase the amount of wetlands,

enhancing the influx of soils and organic materials into lakes and rivers,

which may concurrently increase mercury levels. Animals reliant on the

permafrost are already being found in different areas. The shift in animal

species may alter exposure patterns of local communities, and possibly

lengthen food chains enhancing biomagnification. Arctic oscillations are a

natural phenomenon that result in the reversal of ocean and air currents into

the north. Climate change is expected to increase the frequency and strength

of these oscillations, which may increase the amounts of mercury brought

into the Canada Basin from industrial regions such as Russia. Changes in the

amount of sea ice and general salinity are also predicted to have effects.

EL-HAYEK

Careful analysis of the neurological effects of mercury contamination can

potentially be confounded by alterations of the mercury cycle in the

environment, which itself may be influenced by global climate change. All

longitudinal studies of human health implications represent static images of

mercury contamination through an environment which may have very well

changed since the time of initial measurements. As mentioned earlier, it is

the physiochemical and biological properties of mercury that ultimately

define exposure, not just the consumption of traditional foods. With the

environment constantly evolving due to human activities, mercury exposure

levels may fluctuate in an unpredictable fashion.

Conclusions

The evidence from cellular, animal and human studies all indicate that

methylmercury can induce irreparable damage to the nervous system.

Mercury and several other environmental contaminants are currently found

in the arctic biota, and are contaminating traditional aboriginal foods

sources. These contaminants are found in the tissues of the Aboriginal

inhabitants, in some cases at alarming levels. Evidence from studies of

seafood consuming communities around the globe strongly suggests that

methylmercury can induce neurodevelopmental and motor defects in

exposed populations. Studies are currently underway to completely assess

the health impacts of mercury contamination in the Arctic. However, with

the possibilities of confounding factors such as delayed neurotoxicity,

climate change, and exposures to multiple contaminants, an in depth

understanding of the effects on health is highly optimistic. The seemingly

inexorable link between the Aboriginal people and their local environment

may have social, cultural, spiritual, and nutritional ramifications; yet it may

paradoxically have serious repercussions for their survival and future in

Arctic Canada.

References

Atwell, L., Hobson, K.A., & Welch, H.E. (1995). Biomagnification and bioaccumulation of

mercury in an Arctic marine food web: Insights from stable nitrogen analysis. Canadian

Journal of Fisheries and Aquatic Science, 55, 1114-1121.

Auger, N., Kofman, O., Kosatsky, T., & Armstrong, B. (2005). Low-level methylmercury

exposure as a risk factor for neurologic abnormalities in adults. Neurotoxicology, 26(2),

149-57.

Bernard, S., Enayati, A., Redwood, L., Roger, H., & Binstock, T. (2001) Autism: a novel form

of mercury poisoning. Medical Hypotheses, 56(4), 462-71.

MERCURY CONTAMINATION IN ARCTIC CANADA

Bernard, S., Enayati, A., Roger, H., Binstock, T., Redwood, L. (2002). The role of mercury in

the pathogenesis of autism. Molecular Psychiatry, 7 (Suppl 2.) S42-3.

Beuter, A., & Edwards, R. (1998). Tremor in Cree subjects exposed to methylmercury: A

preliminary study. Neurotoxicology and Teratology, 20, 581-589.

Beuter, A., de Geoffroy, A., & Edwards, R. (1999a). Quantitative analysis of rapid pointing

movements in Cree subjects exposed to mercury and in subjects with neurological

deficits. Environmental Research, 80, 50-63.

Beuter, A., de Geoffroy, A., & Edwards, R. (1999b). Analysis of rapid alternating movements

in Cree subjects exposed to methylmercury and in subjects with neurological deficits.

Environmental Research, 80, 64-79.

Bristol, M.M., Cohen, D.J., Costello, E.J., Denckla, M., Eckberg, T.J., Kallen, R., et al. (1996).

State of the science in autism: report to the National Institutes Health Journal of Autism

and Developmental Disorders. 26(2), 121-54.

Butler Walker, J., Houseman, J., Seddon, L., McMullen, E., Tofflemire, C., et al. (2006).

Maternal and umbilical cord levels of mercury, lead, cadmium and essential trace

elements in Arctic Canada. Environmental Research, 100(3), 295-318.

Budtz-Jorgensen, E., Keiding N., Grandjean, P., & White, R.F. (1999). Methylmercury

neurotoxicity independent of PCB exposure. Environmental Health Perspectives, 107.

A236-A237.

CACAR Canadian Arctic Contaminants Assessment Report (2003), Department of Indian

Affairs and Northern Development, Ottawa, Ontario, Canada. Retrieved online February,

5, 2006, from http://www.ainc-inac.gc.ca/ncp/pub/index_e.html.

Castoldi, A.F., Coccinin, T., Ceccatelli, S., & Manzo, L. (2001). Neurotoxicity and molecular

effects of methylmercury. Brain Research Bulletin. 55(2),197-203.

Chan H.M., Kim C., Khoday K., Receveur, O., & Kuhnlein H.V. (1995), Assessment of dietary

exposure to trace metals in Baffin Inuit food samples. Environmental Health Perspectives,

103(7-8), 740-746.

Daniels, J.L., Longnecker, M.P., Rowland, A.S., & Golding, J. (2004) Fish intake during

pregnancy and early cognitive development of offspring. Epidemiology, 15(4), 394-402.

Davidson, P.W., Myers, G., Cox, C., Axtell, C., Shamlaye, C., Sloane-Reeves, J., Cernichiari,

E., Needham, L., Choi, A., Wang, Y., Berlin, M., & Clarkson, T.W. (1998). Effects of

prenatal and postnatal methylmercury exposure from fish consumption on

neurodevelopment. Outcomes at 66 months of age in the Seychelles Child Developmental

Study. Journal of the American Medical Association, 280, 701-707.

Despres, C., Beuter, A., Richer, F., Poitras, K., Veilleux, A., Ayotte, P., Dewailly, E., Saint-

Amour, D., & Muckle, G. (2005). Neuromotor functions in Inuit preschool children

exposed to Pb, PCBs, and Hg. Neurotoxicology and Teratology, 27(2):245-57.

Dynesius, M., & Nilsson, C. (1994). Fragmentation and flow regulation of river systems in the

northern third of the world. Science 266, 753-761.

Egede, I. (1995). Inuit food and Inuit health: Contaminants in perspective. Presentation to Inuit

Circumpolar Conference, Seventh General Assembly, Nome, Alaska. July.

EL-HAYEK

Gosselin, N.H., Brunet, R.C., Carrier, G., Bouchard, M., Feeley, M. (2005) Reconstruction of

methylmercury intakes in indigenous populations from biomarker data. Journal of

Exposure Analysis and Environmental Epidemiology, 2005. 1-11

Goto, CS. (2000). Heavy metal intoxication. In Behrman, R. E., Kliegman, R. E., Jenson, H.

B., (Eds.). Nelson textbook of pediatrics. Philadelphia: WB Saunders Company.

Grandjean, P., Weihe, P., White, R.F., Debes, F., Araki, S., Yokoyama, K., et al. (1997).

Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury.

Neurotoxicology and Teratology, 19, 417-428.

Grandjean, P., White, R.F., Nielsen, A., Cleary, D., & de Oliveira Santos, E.C. (1999a).

Methylmercury neurotoxicity in Amazonian children downstream from gold mining.

Environmental Health Perspectives, 107, 587-591.

Grandjean, P., Budtz-Jorgensen, E., White, R.F., Jorgensen, P.J., Weihe P., & Debes, F. (1999b).

Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7

years. American Journal of Epidemiology, 150(3), 301-305.

Health Canada (1979). Methylmercury in Canada: Exposure of First Nations and Inuit

residents to methylmercury in the Canadian environment (Vol. 1). Medical Services

Branch, Department of National Health and Welfare. Ottawa, Ontario, Canada

Health Canada (1998). Food directorate memo on re-evaluation of mercury TDI Ottawa,

Ontario:Author.

Intergovernmental Panel on Climate Change. IPCC (2001) Third assessment report - Climate

change 2001. Retrieved online February 20, 2006 from http://www.ipcc.ch/

Institute of Medicine (IOM). Immunization safety review: Vaccines and autism. National

Academies Press, Washington, DC, 2004.

Kajiwara, Y., Yasutake, A., Adachi, T., & Hirayama K. (1996). Methylmercury transport across

the placenta via neutral amino acid carrier. Archives of Toxicology, 70(5), 310-314.

Kennedy, R.F, Jr. (2005). Retrieved online February 5,2005 from http://www.rollingstone.com/

politics/story~/id/7395411.

Kinjo, Y., Higashi, H., Nakano, A.,Sakamoto, M., & Sakai, R. (1993). Profile of subjective

complaints and activities of daily living among current patients with Minamata disease

after three decades. Environmental Research, 63 (2) 241-251.

Kjellstrom, T., Kennedy, P., Wallis, S., & Mantell, C. (1986). Physical and mental development

of children with prenatal exposure to mercury from fish. Stage 1. Preliminary tests at age

4. National Swedish Environmental Protection Board, Report 3080, Solna, Sweden; 1986.

Kjellstrom, T., Kennedy, P., Wallis, S., Stewart, A., Friberg, L., Lind, B., et al. (1989). Physical

and mental development of children with prenatal exposure to mercury from fish. Stage

2. Interviews and psychological tests at age 6. National Swedish Environmental

Protection Board, Report 3642, Solna, Sweden.

MERCURY CONTAMINATION IN ARCTIC CANADA

Kofman, O., Simard, D., Marsh, D. (1979). Mercury intoxication of the nervous system in

Canada (Chronic Minamata Disease). Abstract in: Le Journal Canadien des Sciences

Neurologiques 1979;6(3);397; Presented at XIV Canadian Congress of Neurological

Sciences. Halifax (NS), 1979; The V Panamerican Congress of Neurology. Caracas

(Venezuela), 1979; and the 12th World Congress of Neurology. Kyoto (Japan), 1981;

Clinical and Toxicological Assessment of a Northwest Quebec Population for Possible

Methylmercury Intoxication. John P. Robarts Research Library, University of Toronto,

Ontario, Canada, 1980.

Kromhout, D., Feskens, E.J.M., & Bowles, C.H.. The protective effect of a small amount of fish

on coronary heart disease mortality in an elderly population. International Journal of

Epidemiology, 24(2), 340-344.

Kuhnlein, H.V., Receveur, O., Chan, H.M., & Loring, E. (2000). Assessment of dietary

benefit/risk in Inuit communities. Centre for Indigenous Peoples' Nutrition and

Environment (CINE): Ste-Anne-de-Bellevue, Québec.

Kuhnlein, H.V., Receveur, O., & Chan, H.M. (2001). Traditional food systems research with

Canadian indigenous peoples. International Journal of Circumpolar Health, 60(2), 112-

122.

Kuhnlein, H.V., Receveur, O., Soueida, R., & Egeland, G.M. (2004). Arctic indigenous peoples

experience the nutrition transition with changing dietary patterns and obesity. Journal of

Nutrition, 134, 1447-1453.

Lamborg, C.H., Fitzgerald, W.F., O'Donnell, J., & Torgerson, T. (2002). A non-steady-state

compartmental model of global-scale mercury biogeochemistry with interhemispheric

gradients. Geochimica et Cosmochimica Acta, 66, 1105-1118.

Le Couteur, A., Bailey, A., Goode, S., Pickles, A., Robertson, S., Gottesman, I., & Rutter, M.

(1996). A broader phenotype of autism: the clinical spectrum in twins. Journal of Child

Psychology and Psychiatry, and Applied Disciplines, 37(7), 785-801.

Lebel, J., Mergler, D., Branches, F., Lucotte, M., Amorim, M., Larribe, & F., Dolbec., J. (1998).

Neurotoxic effects of low-level methylmercury contamination in the Amazonian Basin.

Environmental Research, 79, 20-32

Landrigan, P.J., Sonanwane, B., Butler, R.N., Trasande, L., Callan, R., & Droller D. (2005)

Early environmental origins of neurodegenerative disease in later life. Environmental

Health Perspectives, 113(9), 1230-3.

Lockhart, W.L., & Evans, M (2000). Mercury in fish from stock surveys of lakes in the western

Northwest Territories: Investigations into the factors affecting mercury levels. In:

Synopsis of Research Conducted Under the 1999/2000 Northern Contaminants Program.

Indian and Northern Affairs Canada, Ottawa, ON.

Mahaffey, K. R., & Rice, G. E. (1997). An assessment of exposure to mercury in the United

States, Volume IV: Mercury Study Report to Congress. Washington, DC: US

Environmental Protection Agency. Document EPA-452/R-97-006; 1997.

Marsh, D.O., Clarkson, T.W., Cox, C., Myers, G.J., Amin-Zaki, L., & Al-Tikriti, S. (1987). Fetal

methylmercury poisoning. Relationship between concentration in single strands of

maternal hair and child effects. Archives of Neurology, 44(10), 1017-22.

EL-HAYEK

McKeown-Eyssen, G.E., Ruedy, J., & Neims, A. (1983). Methyl mercury in northern Quebec:

II. Neurologic findings in children. American Journal of Epidemiology, 118, 470-479.

Mendola, P., Selevan, S.G., Gutter, S., & Rice, D. (2002).Environmental factors associated with

a spectrum of neurodevelopmental deficits. Mental Retardation and Developmental

Disabilities Research Reviews, 8(3):188-97.

Muckle, G., Ayotte, P., Dewailly, É., Jacobson, S.W., & Jacobson, J.L. (2001a). Determinants of

polychlorinated biphenyls and methylmercury exposure in Inuit women of childbearing

age. Environmental Health Perspectives, 109(9),957-963.

Muckle, G., Ayotte, P., Dewailly, É., Jacobson, S.W., & Jacobson, J.L. (2001b) Prenatal

exposure of the northern Québec Inuit infants to environmental contaminants.

Environmental Health Perspectives, 109(12), 1291-1299.

Mutter, J., Naumann, J., Sadaghiani, C., Schneider, C., Walach, H. (2004). Alzheimer

disease:mercury as a pathogentic factor and apolipoprotein E as a moderator.

Neuroendocrinology Letters, 25(5), 331-339.

Mutter, J., & Naumann, J. (2005). Blood mercury levels and neurobehavior. Journal of the

American Medical Association, 294(6), 679.

Myers, G.L., & Davidson, P.W. (2000) Does methylmercury have a role in causing

developmental disabilities in children? Environmental Health Perspectives, 108(Suppl. 3)

413-20.

Myers, G.J., Davidson, P.W., Cox, C., Shamlaye, C.F., Palumbo, D., Cernichiari E., et al.

(2003). Prenatal methylmercury exposure from ocean fish consumption in the Seychelles

child development study. Lancet, 361,1686-1692.

National Research Council. (2000). Toxicological effects of methylmercury. National Academy

Press: Washington, DC.

Osmond, C., & Barker, D. (2000). Fetal, infant, and childhood growth are predictors of

coronary heart disease, diabetes, and hypertension in adult men and women.

Environmental Health Perspectives, 108(Suppl. 3), 545-553.

Pacyna, J.M., & Keeler, G.J. (1995). Sources of mercury to the Arctic. Water, Air, Soil Pollution,

80, 621-63.

Palmer, R.F., Blanchard, S., Stein, Z., Mandell, D., & Miller, C. (2006). Environmental mercury

release, special education rates, and autism disorder: An ecological study of Texas. Health

and Place, 12(2), 203-209.

Pauly, D., Palomares, M.L., Fooese, R., Sa-a, P., Vakily, M., Preikshot, D., & Wallace, S.

(2001). Fishing down Canadian aquatic food webs. Canadian Journal of Fisheries and

Aquatic Sciences, 58, 51-62.

Philbert, M.A., Billingsley, M.L., & Reuhl K.R. (2000). Mechanisms of injury in the central

nervous system. Toxicologic Pathology, 28, 43-53.

Rice, D.C. (1996). Sensory and cognitive effects of developmental methylmercury exposure in

monkeys, and a comparison to effects in rodents. Neurotoxicology, 17, 139-154.

MERCURY CONTAMINATION IN ARCTIC CANADA

Rice, D.C. (1998). Lack of effect of methylmercury exposure from birth to adulthood on

information processing speed in the monkey. Neurotoxicology and Teratology, 20(3),

275-83.

Sakamoto, M., Kubota, M., Matsumoto, S., Nakano, A., and Akagi, H. (2002). Declining risk

of methylmercury exposure to infants during lactation. Environmental Research, 90(3),

185-189.

Schroeder, W.H., & Munthe, J. (1998). Atmospheric mercury – An overview. Atmospheric

Environment, 32(5), 809-822.

Schroeder, W.H., Anlauf, K.G., Barrie, L.A., Lu, J.Y., Steffen, A., & Schneeberger, D.R. (1998).

Arctic springtime depletion of mercury. Nature, 394, 331-332.

Schroeder, W.H., Anlauf, K.G., Barrie, L.A., Steffen, A., & Lu, J.Y. (1999a). Depletion of

Mercury Vapour in the Arctic Troposphere after Polar Sunrise. In: Proceedings of the

1998 EUROTRAC Symposium on Transport and Chemical Transformation in the

Troposphere; Garmisch-Partenkirchen, pp. 358-362.

Schroeder, W.H., Steffen, A., Lu, J.Y., Blanchard, P., & Barrie, L.A.(1999b). Mercury

measurements at Alert. In: Synopsis of Research Conducted under the 1998-1999

Northern Contaminants Program, (pp. 49-53). Indian and Northern Affairs Canada:

Ottawa, ON.

Schroeder, W.H., Steffen, A., Lu, J.Y., & Barrie, L.A. (2000). Mercury measurements at Alert.

In: Synopsis of research conducted under the 1999-2000 Northern Contaminants

Program, (pp.137-141). Indian and Northern Affairs Canada: Ottawa, ON.

Statistics Canada (2001) Profile of Canada's Aboriginal population. Custom Database

(Adapted from 1996 data). Ottawa, Ontario: Author.

Steuerwald, U., Weihe, P., Jorgensen, P.J., Bjerve, K., Brock, J., Heinzow, B., et al. (2000)

Maternal seafood diet, methylmercury exposure and neonatal neurologic function.

Journal of Pediatrics, 136, 599-605.

Tsubaki, T., & Irukayam K (1977). Methylmercury poisoning in Minamata and Niigata, Japan.

In Minamata Disease, (pp. 57-95). Tokyo: Kodansha Ltd.

U.S. Environmental Protection Agency (1997). Mercury study report to Congress, Volume V:

Health effects of mercury and mercury compounds. EPA-452/R-97-007. Washington, DC:

Author.

Usher, P.J., & Wenzel, G. (1989). Socio-economic aspects of harvesting. In: Keeping on the

land: a study of the feasibility of a comprehensive wildlife support programme in the

northwest territories. Canadian Arctic Resources Committee, Ottawa, Ontario, Canada.

Van Oostdam, J., Gilman, A., Dewailly, É., Usher, P., Wheatley, B., & Kuhnlein, H. (1999)

Human health implications of environmental contaminants in Arctic Canada: A review.

The Science of the Total Environment, 230, 1-282.

Van Oostdam, J., Donaldson S.G., Feeley M., Arnold D., Ayotte P., Bondy G., Chan L., Dewaily

E., Furgal C.M., Kuhnlein H., Loring E., Muckle G., Myles E., Receveur O., Tracy B., Gill

U., & Kalhok, S. (2005). Human health implications of environmental contaminants in

Arctic Canada: A review. The Science of the Total Environment, 351-352, 165-246.

EL-HAYEK

Wagemann, R., Lockhart, W.L., Welch, H., & Innes, S. (1995). Arctic marine mammals as

integrators and indicators of mercury in the Arctic. Water, Air, and Soil Pollution, 80, 683-

693.

Wagemann, R., Trebacz, E., Boila, G., & Lockhart, W.L. (1997). Mercury species in the liver of

ringed seals. The Science of Total Environment, 261(1-3), 21-32.

Weil, M., Bressler, J., Parsons, P., Bolla, K., Glass, T., Schwartz, B. (2005). Blood mercury

levels and neurobehavioral function. Journal of the American Medical Association,

293(15), 1875-1882.

Weiss, B., & Reuhl, K. (1994). Delayed neurotoxicity: A silent toxicity. In: Principles of

Neurotoxicology, (pp. 765-784). Marcel Dekker, New York

Wheatley, M.A. (1996). The Importance of Social and Cultural Effects of Mercury on

Aboriginal Peoples. Neurotoxicology, 17(1), 251-256.

Wong, M. (1986). Chemical residues in fish and wildlife harvested in Northern Canada.

Environmental Studies Vol. 46. Department of Indian Affairs and Northern Development:

Ottawa, Canada.

WHO (1976). World Health Organization. Environmental Health Criteria 1: Mercury. Geneva:

Author.

WHO (1978). World Health Organization. Summary of toxicological data of certain food

additives and contaminants. Twenty-second Report of the Joint FAO/WHO Expert

Committee on Food Additives. WHO Additive Series. No. 13..

WHO (1990). World Health Organization. Methylmecury, Vol. 101. World Health Organization,

International Program on Chemical Safety, Geneva, Switzerland.

Correspondence

Youssef H. El-Hayek

Toronto Western Hospital

Room: mcl-14-413

399 Bathurst Street

Toronto, ON

M5T 2S8

[email protected]

MERCURY CONTAMINATION IN ARCTIC CANADA

JOURNAL ON DEVELOPMENTAL DISABILITIES