Arsenic - A Fatal Complication for Pandemic Flu - MUST READ

[St Michael]

Re: Argentina has the world?s highest rate of deaths associated with swine flu infections

I wonder if the arsenic might account for the high rates of renal failure being seen in severe Mexican and Argentinian cases?

eMedicine Specialties
Toxicity, Arsenic

Pathophysiology

Arsenic exists in metalloid, arsenite (trivalent), and arsenate (pentavalent) valences and in arsine gas. The inorganic (trivalent) compound is absorbed more readily than the organic (pentavalent) forms because of its high lipid solubility. Absorption primarily occurs through the gastrointestinal tract; however, some absorption occurs through the skin. Once arsenic is in the body, it binds to hemoglobin, plasma proteins, and leukocytes and is redistributed to the liver, kidney, lung, spleen, and intestines. Over a period of weeks, deposits may be found in skin, hair, nails, bone, muscle, and even nervous tissue.

Arsenic produces cellular damage through a variety of mechanisms. Arsenic binds to enzyme sulfhydryl groups and forms a stable ring, which deactivates the enzyme. The process of deactivating the enzyme causes widespread endothelial cell damage, vasodilation, and leakage of plasma. Massive transudation of fluid into the bowel lumen, mucosal vesicle formation, and tissue sloughing may result in large gastrointestinal fluid losses. Arsenic binds to dihydrolipoic acid, a pyruvate dehydrogenase cofactor, blocking the conversion of pyruvate to acetyl coenzyme A and inhibiting gluconeogenesis. Arsenic competes with phosphates for adenosine triphosphate, forming adenosine diphosphate monoarsine, causing the loss of high-energy bonds.

In some forms, arsenic is caustic, exerting a direct toxic effect on blood vessels and large organs. Long-term exposure results in nerve damage and may lead to lung, skin, or liver cancer. Once inhaled, arsine gas combines with hemoglobin in RBCs, causing severe hemolysis and anemia. Patients develop hemoglobinuria and hematuria within several hours of exposure.
Frequency
United States

Approximately 1000 cases of arsenic exposure are reported annually. Many more cases of chronic arsenic exposure probably go unreported.
International

Thousands of people are exposed to arsenic in the form of contaminated drinking water, foodstuffs, and industrial pollution.
Mortality/Morbidity

* Acute arsenic intoxication resulting in a fatality is rare. Survivors may have severe disabilities secondary to organ damage.
* Chronic exposure, from weeks to months, can have devastating effects. Patients may develop encephalopathy, painful paresthesias, myocarditis, pericarditis, peripheral vascular disease (ie, blackfoot disease), lung cancer, renal failure, anemia, brittle nails exhibiting Mees lines, or hyperpigmentation (especially of the eyelids, neck, axillae, and groin).

[Shannon Bennett]

Re: Argentina has the world?s highest rate of deaths associated with swine flu infections

I wouldn't be one bit surprised St. Michael. Beginning to feel like an 'aha' moment. The renal failure is now explained.

http://water.usgs.gov/nawqa/trace/pu...W_vol38no4.pdf Arsenic in Ground Water of the United States: Occurence and Geochemistry Alan H Welch, D. B. Westjohn. Dennis R. Helsel and Richard B Wanty

The foregoing link gives a general description of high levels of naturally occurring arsenic in well water.

[sharon sanders]

Re: Woods Hole Scientists Link Influenza A (H1N1) Susceptibility to Arsenic Exposure

Arsenic round the world: a review
Badal Kumar Mandal, Kazuo T. Suzuki *
Graduate School of Pharmaceutical Sciences, Chiba Uniersity, Chiba 263 -8522, Japan
Received 7 December 2001; received in revised form 8 February 2002


4.1.1. Taiwan incident

The arsenic contamination incident in well water
on the south-west coast of Taiwan (1961?
1985) is well known [278?280]. The population of
endemic area is about 140,000. In the villages
surveyed, the arsenic content of the well water
examined, ranges from 0.01 to 1.82 mg l−1. Most
of the well water in the endemic area has arsenic
content around 0.4?0.6 mg l−1. The predominant
arsenic species in the well waters is iAsIII with an
average iAsIII to iAsV ratio of 2.6. Chronic arsenicism
is observed in a population of 40,421 in 37
villages, and 7418 cases of hyperpigmentation,
2868 of keratosis, 360 of BFD patients [281], and
some cases of cancer (liver, lung, skin, prostate,
bladder, kidney) [281?285] are observed. The
source material of the arsenic is likely to be
pyretic material or black shale occurring in underlying
geological strata [278]. It is thought at beginning
that arsenic alone is responsible for BFD
of the area [286]. The discovery in 1975 of fluorescent
compounds in these well waters leads to the
isolation of humic substances, which in combination
with arsenic is thought to be probable cause
for the BFD [287]. To save the people of the
Taiwan endemic areas, a water treatment plant is
run to remove arsenic from groundwater before
use.

4.1.2. Antofagasta, Chile incident

About 130,000 inhabitants of the city has been
drinking supplied water with high content of arsenic
(0.8 mg l−1) for 12 years from 1959 to 1970
[288]. The source of the high arsenic content in
water is the Tocance River, of which water comes
from the Andes Mountain at an altitude of 3000
m and is brought 300 km to Antofagasta. At the
beginning of 1960s, the first dermatological manifestation
was noted, especially in children [288].
Peripheral vascular manifestations in these children
included Raynaud?s syndrome, ischemia of
the tongue, hemiplegia with partial occlusion of
the carotid artery, mesenteric arterial thrombosis
and myocardial ischemia. One autopsy showed
hyperplasia of the arterial media. In a survey of
27,088 school children, 12% are found to have the
cutaneous changes of arsenicism, one-fourth to
one-third of these has suggestive systematic symptoms.
Eleven percent has acrocyanosis. Of the
Antofagastan residents, 144 have abnormal skin
pigmentation, compared with none in the 98 control
subjects. Recent studies [212,289] also document
arsenic-induced skin lesions, and increased
bladder and lung cancer mortality in Northern
Chile.
To save the people, a water treatment plant is
run to remove arsenic from drinking water before
use. The sources of arsenic have been reported as
quaternary volcanogenic sediments, minerals and
soil [290]. Samples taken from 23 locations at
Aracamenan settlements near Calama range from
less than 100 to more than 800 g As l−1. Most
of the arsenic is present as arsenate, but some
arsenite is also determined. Five soils irrigated
with high arsenic waters range from 86 to 446 mg
As kg−1 compared to 64 mg As kg−1 in one
control sample.

4.1.3. West Bengal-India incident

Around 1978 various aspects of arsenic groundwater
contamination and arsenicosis among people
in some villages of West Bengal first came to
the notice of Government of West Bengal [291].
Several recent studies [22,63,67,151,291?294] report
that about 6 million people of 2600 villages
in 74 arsenic-affected blocks of West Bengal, India
are in risk and 8500 (9.8%) out of 86,000
people examined are suffering from arsenicosis,
while the source is oxidation of arsenic rich pyrite
or anoxic reduction of ferric iron hydroxides in
the sediments to ferrous iron and thereby releasing
the adsorbed arsenic to groundwater.

4.1.4. Mexico incident

Chronic arsenic exposure via drinking water is
reported in six areas of Region Lagunera, situated
in the central part of North Mexico with a population
of 200,000 during 1963?1983 [295]. The
range of total arsenic concentrations is 0.008?
0.624 mg l−1, and concentrations greater than
0.05 mg l−1 are found in 50% of them. Most of
the arsenic is in inorganic form and pentavalent
arsenic is the predominant species in 93% of the
samples [61]. In 36% of the rest samples, however,
variable percentages (20?50%), of trivalent arsenic
are found. It is also observed that high
concentrations of fluoride in the range of 0.5?3.7
mg l−1 and concentrations greater than 1.5 mg
l−1 are found in 20% of the analysed samples
[296].
The symptoms observed in this area are cutaneous
manifestations (skin pigmentation changes,
keratosis and skin cancer), peripheral vascular
disease (BFD), gastrointestinal disturbances and
alteration in the coporphyrin/uroporphyrin excretion
ratio [297]. It is found that the proportion of
individuals (per age group) affected with cutaneous
lesion increase with age until the age of 50.
The shortest is 8 years for hypopigmentation, 12
years for hyperpigmentation and palmo-planter
keratosis, 25 years for papular keratosis and 38
years for ulcerative lesions [298]. The source of
arsenic is assumed to be geological (volcanic sediment)
[61].

4.1.5. Argentina incident

Similar incident of arsenic contamination in
groundwater is also reported in Monte Quemado
of Cordoba province, north of Argentina [62].
The occurrence of endemic arsenical skin disease
and cancer is first recognized in 1955. Total population
of the endemic area is about 10,000. From
the observations in the Cordoba, it is concluded
[62,209] that the regular intake of drinking water
containing more than 0.1 mg l−1 of arsenic leads
to clearly recognizable signs of intoxication and
ultimately might develop into skin cancer. Biagini
followed 116 patients with clear signs of chronic
arsenic disease over a number of years [299]. After
15 years of follow-up, 78 had died, 24 from cancer
(i.e. 30.7% of total deaths). In Monte Quemado,
the problem seems to be ultimately solved by
building a canal that supplies the town with arsenic
free water from Salta province.

Again, elevated concentrations of arsenic in
surface waters, shallow wells and thermal springs
are reported from the Salta and Jujay provinces in
northwestern Argentina [300]. This natural contamination
is related to Tertiary-Quaternary volcanic
deposits, together with post-volcanic geysers
and thermal springs. Waters abstracted for drinking
supplies for the population of 5000 in the
town of San Antonio de los Cobres ranges from
0.47 to 0.77 mg l−1. Thermal springs range from
0.05 to 9.9 mg l−1 of arsenic.

A strong natural contamination of groundwater
with arsenic and selenium is reported in the
Pampa Province of Cordoba, southeast Argentina.
The arsenic content of nearly 50% of the
water samples from this area ranges from 0.1 to
0.316 mg l−1 with a maximum value of 3.81 mg
l−1 [64,301]. Groundwater contamination is
caused from loess, which differed in composition
to loess from Europe, Asia and North America
[64], with arsenic concentrations ranging from 5.5
to 37.3 mg kg−1, and rhyolitic volcanic glass
ranging from 6.8 to 10.4 mg kg−1.

4.1.6. Millard County, Utah, USA incident

West Millard County is a desert area with low
population density and around 250 people drinking
well water of arsenic content between 0.18 and
0.21 mg l−1 and the predominant arsenic species
is arsenate (86% As5+) [302]. Participants are
examined for specific signs of arsenic toxicity including
palmer and plantar (palms and soles)
keratoses, diffuse palmer and plantar hyperkeratoses
and skin suggestive of arsenic toxicity is
rare, with only 12 of 149 participants having any
signs associated with arsenic ingestion. Participants
from Deseret have the highest average arsenic
in urine concern of 0.211 mg l−1 (n=40)
and that of Hinckley participants have 0.175 mg
l−1 (n=95) compared to control from Delta of
0.048 mg l−1 (n=99). The highest average arsenic
concentration in hair is 1.21 mg kg−1 (n=80)
from Hinckley residents and that of Deseret residents
is 1.09 mg kg−1 (n=37) compared to control
from Delta of 0.32 mg kg−1 (n=68). Lewis
et al. [303] recently reports hypertensive heart
disease, nephritis, nephrosis, and prostate cancer
among the people of the arsenic-affected areas in
Utah.

4.1.7. Lane County, Western Oregon, USA
incident

Well water in Central Lane County [304], located
in Western Oregon about midway between
the Colombia river and the northern boundary of
California gets contaminated with arsenic during
November 1962?March 1963. The concentration
range of arsenic in wells is 0.05?1.7 mg l−1. Wells
in Eugene, Creswell, and Grove districts in Central
Lane County which were known to yield
arsenic rich groundwater are in an area underlain
by a particular group of sedimentary and volcanic
rocks, which geologists have named the Fisher
formation [305]. The largest concentrations of
arsenic are found in samples from the Creswell
district.

4.1.8. Lessen County, California, USA incident

In the Lessen County, California, similar arsenic
poisoning in well water is observed. The
range of arsenic in the well water is 0.05?1.4 mg
l−1. It is found that arsenic is present in drinking
water above 0.05 (0.03) mg l−1 and an increased
level of arsenic in their hairs reflects body
burden due to arsenic exposure [306].

4.1.9. Ontario, Canada incident

In 1937, Wyllie [307] reported that water from
some deep wells in Rocky Mountain areas of
Ontario, Canada were known to contain large
amounts of arsenic. The source of arsenic in well
water is ferrous arsenate where arsenic in water
varies from 0.10 to 0.41 mg l−1 as As2O3. Preliminary
experiments show that arsenic as arsenate is
the primary source of arsenic, which contaminated
the well water. One person died of arsenic
dermatosis. The whole family members of the
victim died are also afflicted due to this arsenic
poisoning.

4.1.10. Nova Scotia, Canada incident

In 1976, several wells in Halifax County, Nova
Scotia are contaminated with arsenic [308] with
concentration greater than 3 mg l−1. More than
50 families have been affected due to arsenic
poisoning [309]. Recently, Boyle et al. [310] reports
also occurrences of elevated arsenic concentrations
in bedrock groundwaters used for
individual and municipal water supplies in the
mainland coast of southern British Columbia,
Canada.

4.1.11. Hungary incident

In Hungary also similar arsenic contamination
in the well water is observed [311,312] in the years
1941?1983. The amount of arsenic present in the
well water is in the range of 0.06?4.00 mg l−1.
Recently, concentrations of arsenic above 50 g
l−1 are identified in groundwaters from alluvial
sediments associated with the River Danube in
the southern part of the Great Hungarian Plain.
Concentrations up to 150 g l−1 (average 32 g
l−1, 85 samples) are found by Varsa?nyi et al. [54].
The Plain, some 110,000 km2 in area, consists of a
thick sequence of subsiding Quaternary sedi
ments. The groundwaters have highest arsenic
concentrations in the lowest parts of the basin,
where the sediment is fine-grained [54]. A few
thousand people are affected and several symptoms
of arsenic poisoning viz, melanosis, hyperkeratosis,
skin cancer, internal cancer, bronchitis,
gastroenteritis, haematologic abnormalities are
found among them [313].

4.1.12. New Zealand incident

In 1939, Grimmet and McIntosh described arsenic
contamination of groundwater and the resulting
effects on the health of livestock [314].
Later on in 1961, high levels of arsenic were
found in water from areas of thermal activity.
Thermal waters in New Zealand contain up to 8.5
mg As l−1 [315]. Aggett and Aspell [316] studied
the chemical forms of arsenic in water samples. In
the geothermal bores, more than 90% of the arsenic
is present in the trivalent form.

4.1.13. Poland incident

A small case is observed in Poland in 1898 [317]
with some skin cancer among the arsenic affected
persons. It is interesting to note that there is no
published data on this incident.

4.1.14. Fairbanks, Alaska incident

In the well water, spring of Fairbanks, Alaska,
arsenic is found above 0.05 mg l−1. The study is
initiated to evaluate the arsenic content of streams
and groundwaters of the Pedro-Dome Cleary
Summit area approximately 30 km north of Fairbanks,
Alaska in the heart of the historic Fairbanks
Mining District. Arsenic is associated with
gold mineralization here and is believed to reach
the water of the area through weathering of arsenic
containing rocks.

The arsenic concentrations in 53 water samples
from wells and springs range from less than 0.005
to 0.07 mg l−1. Eighty percent of the samples
contain less than 0.01 mg l−1 and 95% of the
samples contained less than 0.05 mg l−1 [318].
The arsenic levels in 243 well water range from
less than 0.05 to greater than 0.10 mg l−1. About
28% of the samples contain arsenic less than 0.05
mg l−1, 40% of the samples contained less than
0.10 mg l−1 and about 20% of the samples contain
greater than 0.10 mg l−1. Well water arsenic
concentrations in the Ester Dome study area
range from less than 1.0 to 14 mg l−1 and for the
study population range from less than 1.0 to 2.45
mg l−1 with a mean of 0.224 mg l−1. An epidemiological
study was made in 1976 [319], which
suggested no clinical or haematological abnormalities
among these people. Urine arsenic levels
above 0.02 mg l−1 are found in 130/198 (66%),
hair arsenic levels above 1 mg kg−1 occur in
74/181 (41%) and nail arsenic levels above 4 mg
kg−1 in 49/132 (37%) of the study population.

4.1.15. Sri lanka incident

In a clinical study of 13 cases of polyneuropathy
connected with arsenic poisoning, in Srilanka,
Senanayake et al. [320] found Mee?s line, i.e.
transverse white bands across finger nails, to be
the constant feature at least 6 weeks after the
onset of initial symptoms. In seven of these cases,
the source of arsenic was contaminated well water,
four others had a long history of consuming
illicit liquor.

4.1.16. Spain incident

Manzano and Tellow summarized their experiences
in treating arsenic poisoning caused by well
water in certain areas of Spain [321].

4.1.17. China incident

During the 1980s, the endemic arsenicosis was
found successively in many areas on mainland
China such as Xinjiang Uygur A. R., Inner Mongolia,
Shanxi, Liaoning, Jilin, Ningxia, Qinghai,
and Henan provinces [322?328]. The arsenic concentration
in the groundwater in these affected
areas is in the range of 220?2000 g l−1 with the
highest level at 4440 g l−1. Consequently, a large
sector of the rural population has been exposed to
chronic arsenic poisoning (CAP) resulting from
consuming well water with naturally occurring
high levels of arsenic during the past decades. At
present, the population exposed to high amounts
of arsenic is estimated to be over 2 million and
more than 20,000 arsenicosis patients are confirmed
[328]. The water of the deep-wells, however
contains fluoride and arsenic [323]. Fluorosis was
first found in the 1970s and arsenicism in 1980.
One of the characteristics of the Kuitun case is the
fact that there are three groups of patients among
the residents who drank the same well water for a
long time. Namely, one group suffers from fluorosis,
the second group from arsenicism and the
third group from both fluorosis and arsenicism
combined.

The cause of contamination is considered to be
geological. Major clinical symptoms observed are
keratosis, pigmentation, melanosis or leucoderma
on the skin, often accompanied with peripheral
neuritis, gastroenteritis, and hypertrophy of the
liver, bronchitis or cardiac infarction. At later
stages skin cancer and gangrene are also found.
Feng et al. [329] recently reports DNA damage in
buccal epithelial cells from individuals from this
arsenic-affected area. Various measures are taken
to supply clean water.

4.1.18. Northern India incident

In Ropar, Manimajra, Chandigarh, N. Garh,
Patiala and Ambala around Chandigarh of Punjab
and Haryana of India, the arsenic concentration
in water from wells and springs were higher
than the WHO limit of safety for human consumption
[330] with 0.05?0.545 mg l−1 of arsenic.
Cirrhosis (adult and childhood), non-cirrhotic
portal fibrosis and extra hepatic portal vein obstruction
in adults are very common in India and
suggests that consumption of arsenic-contaminated
water may have some role in the pathogenesis
of these clinical states [331]. The patients who
consumed the water containing arsenic 0.545 mg
l−1 throughout life are suffering from non-cirrhotic
portal fibrosis (N.C.P.F.), whereas their
two relatives consuming same water reveal gross
splenomegaly, but with normal liver function tests
[332]. The source of arsenic is still unknown.

4.1.19. Bangladesh incident

Several recent studies [23,216,292,333] report
that about 25 million people of 2000 villages in
178 arsenic-affected blocks of Bangladesh are in
risk and 3695 (20.6%) out of 17,896 people examined
are suffering from arsenicosis, while the
source is oxidation of arsenic rich pyrite or anoxic
reduction of ferric iron hydroxides in the sediments
to ferrous iron and thereby releasing the
adsorbed arsenic to groundwater. To combat the
situation, Bangladesh need a proper utilization of
its vast surface and rainwater resources and
proper watershed management.

4.1.20. Fallon, Neada Incident

In 1984, Viz et al. [334] were unable to detect
any increase in chromosomal aberrations or sister
chromatid exchange in residents of Fallon, Nevada,
where drinking water contained about 0.10
mg As l−1. From literature it is found that the
health status of these arsenic exposed populations
is not adversely affected [335].

4.1.21. Fukuoka Prefecture, Japan incident

In March 1994, arsenic over the permissible
level for drinking use (0.01 mg l−1) is detected in
well waters in the southern region of Fukuoka
Prefecture, Japan [71]. The highest concentration
found is 0.293 mg l−1, being quite high compared
to other arsenic-containing well waters reported in
Japan as a geological process. The mechanisms of
arsenite/arsenate elution from the soil proposed
are which involved: (i) anion exchange with OH−;
and (ii) reductive labialization of arsenic through
conversion of arsenate to arsenite.

4.1.22. New Hampshire, USA incident

Arsenic concentrations are measured in 992
drinking water samples collected from New
Hampshire households and in randomly selected
households, concentrations ranged from 0.0003
to 180 g l−1, with water from domestic wells
containing significantly more arsenic than water
from municipal sources. Water samples from
drilled bedrock wells have the highest arsenic
concentrations, while samples from surficial wells
has the lowest arsenic concentrations. The authors
[336] suggested that much of the groundwater
arsenic in New Hampshire was derived from
weathering of bedrock materials and not from
anthropogenic contamination. The spatial distribution
of elevated arsenic concentrations (50
g l−1) correlates with Late-Devonian Concordtype
granite bedrock. Analysis of rock digests
indicates arsenic concentrations up to 60 mg kg−1
in pegmatites, with much lower values in surrounding
schists and granites.

4.1.23. Vietnam incident

This is the first publication on arsenic contamination
of the Red alluvial tract (Mekong delta
region) in the city of Hanoi and in the surrounding
rural districts [72]. The contamination levels
vary from 1 to 3050 g l−1 in rural groundwater
samples from private small-scale tube-wells with
an average arsenic concentration of 159 g l−1. In
a highly affected rural area, the groundwater used
directly as drinking water has an average concentration
of 430 g l−1. Analysis of raw groundwater
pumped from the lower aquifer for the Hanoi
water supply show arsenic levels of 240?320 g
l−1 in three of eight treatment plants and 37?82
g l−1 in another five plants. Aeration and sand
filtration that are applied in the treatment plants
for iron removal lowers the arsenic concentrations
to levels of 25?91 g l−1, but 50% remains above
the Vietnamese Standard of 50 g l−1. The arsenic
in the sediments may be associated with iron
oxyhydroxides and releases to the groundwater by
reductive dissolution of iron. The high arsenic
concentrations found in the tube-wells (48%
above 50 g l−1 and 20% above 150 g l−1)
indicate that several million people consuming
untreated groundwater may be at a considerable
risk of CAP. No people were found in these
affected regions with symptoms of chronic arsenic
toxicity.

4.2. Arsenic contamination from industrial sources

4.2.1. Ronphibun, Thailand incident

In 1987, the skin manifestation of CAP was
first diagnosed among the residents of Ronphibun
district, Nakorn Srithammarat Province [337]. It
is seen that 85% of all reported of CAP are from
Ronphibun sub-district of Ronphibun district.
Most cases are of relatively mild disease, with
21.6%, however having very significant lesions
[338]. Rophibun district has eight sub-districts
and 65 villages with a population of 14,085. Three
out of 14 villages of Ronphibun sub-district with
19.9% of the population of the sub-district account
for 60.9% of the cases. These villages use
water with drains from the high-contaminated
area of Suan Jun and Ronna Mountains. Their
attack rate is 8.8 times, the rate in the remainder
of the sub-district. This area has 0.1% arsenopyrite.

Recently, Oshikawa et al. [339] reports the
long-term changes in arsenical skin lesions among
this population. At many sites, the arsenic content
of water exceeds by 8?100 times the 0.05 mg l−1
concentration, which is the accepted safety level
set down by WHO for occasional exposure [15].

4.2.2. Mindanao Island, Philippines incident

Soon after the construction of a geothermal
power plant on Mt. Apo started in January 1992,
people living downstream along the Matingao and
Marbol rivers which run through the construction
site, complained of symptoms such as eruption,
headache or stomach-ache. An environmental investigation
carried out in August 1993, which
revealed that river water downstream of the construction
site contained 0.1 mg l−1 of arsenic and
hair samples of some residents showed high concentrations
of mercury and manganese as well as
arsenic [340]. As a result, the construction of the
geothermal power plant is suspected as the cause
of arsenic contamination. In 1995, a medical survey
of 39 residents who had rashes on their skin
reveals that a few of them are suspected to be
patients suffering from CAP [341].

4.2.3. Nakajo, Japan incident

Waste water from a factory producing arsenic
sulfide contaminated nearby well water in Nakajo,
Japan in 1960 [342,343]. In this place a very small
number of people drank the well water, which was
contaminated with arsenic (0.025?4.00 mg l−1).
Melanosis, hyperkeratosis, cardiovascular disease,
hepatopathy, haematologic abnormalities were
observed among the residents of Nakajo.

4.2.4. Toroku and Matsuo, Japan incident

Toroku is a small mountain village to the north
of Miyazaki prefecture with a population of
about 300 where arsenious acid was produced by
roasting arsenopyrite ore from 1920 to 1962 [344].
Similarly, Matsuo is a small mountain village in
the north of Miyazaki prefecture. Here, white
arsenic was produced by calcinating arsenopyrite
at very primitive stone-made furnaces for nearly
half a century since about 1920. In this system
about 10% or more of As2O3 was lost as fumes
through the refining process. The arsenic-rich remains
of calcinated ore were dumped into the
river. Many mine workers and nearby residents
died from acute and sub-acute arsenic poisoning.
A 6-year follow-up study reveals a high prevalence
of malignant neoplasms especially in respiratory
tract, which was the main cause of death
in the patient [345]. A total of 147 persons are
examined in the study. Out of them, 125 are
diagnosed as CAP. A total of 58 malignant skin
tumors are noted out of 125 patients with skin
lesions of CAP and out of these 58 malignant skin
tumors, 51 occur on trunk and times. The appearance
of multiple malignant tumors was noted in
24 cases (58.5%), including 15 cases of double
cancers. The phenomenon is noted in 14 cases
(42.4%) among cases of malignant skin tumor.
Multiple Bowen?s disease is found in 12 cases
(37.5%). As of 1995, there were 153 patients in
Toroku and 64 in Matsuo who are recognized by
the government as suffering from CAP [346].

4.2.5. Other incidents in Japan

A severe cutaneous manifestations of CAP are
detected in seven out of 28 male Japanese workers,
who are exposed to arsenic in the form of lead
arsenate and Ca3AsO4 in the manufacture of insecticides
[347]. The lesions are symmetric punctuated
palmo-planter hyperkeratosis and bronze
hyper-pigmentation.

A retrospecific cohort study of a Japanese population
in between 1954 and 1959 used well water
contaminated with arsenic from a dye factory.
During the follow-up period until 1987, there
were 18 deaths from cancer, of which seven from
lung cancer and six in the high exposure group
[348].

4.2.6. P.N. Mitra Lane, Behala, Calcutta, India
incident

Arsenic contamination episode in residential
area of Behala, Calcutta during 1969?1989 is well
known [68,92,349]. The concentration of arsenic
in the tube-well water varies from 0.05 to 58 mg
l−1. Chronic arsenic toxicity, resulting from
household use of arsenic contaminated water occurs
in 53 out of 79 members (67% of 17 families)
residing near this factory area within age range
1?69 years. Typical skin manifestations are found
in all of them but pulmonary symptoms are
present in 40% and neurological symptoms in 65%
of cases. Hematomegaly (2?6 cm) is found in 80%
of cases and splenomegaly (1.5?2.6 cm) in 35% of
cases. A few died due to arsenicosis.

4.2.7. Rajnandgaon district, Madhya Pradesh,
India incident

Arsenic contamination of groundwater in
Koudikasa village of Rajnandgaon district, Madhya
Pradesh-India with a population of 1.5 million
was reported first on 1999 [350]. Most of the
villagers of Koudikasa used water from a forest
dug-well (0.52 mg As l−1) along with a PHED
tube-well (0.88 mg As l−1). Out of the total
number of adults (150 nos.) and children (58 nos.)
examined at random, 42 and 9%, respectively,
have arsenical skin lesions. The source of arsenic
contamination is speculated to be due to percolation
of gold and uranium mine?s tailings.

4.2.8. Australia incident

In Australia, old stocks of lead arsenate, that
was used as pesticides prior to 1970 remained in
sheds and caused chronic poisoning among the
workers [351].

4.2.9. Czechosloakia incident

People living near a plant burning arsenic contaminated
coal containing 900?1500 mg As kg−1
was responsible for the episode [352].

4.2.10. Toronto, Ontario, Canada incident

Vegetation and soil samples collected in 1974 in
the vicinities of two secondary lead smelters located
in a large urban area near Toronto, Ontario,
Canada showed arsenic concentrations over
30 times higher than normal urban background
levels of arsenic in unwashed plant foliage and
200 times higher than normal soil which were
found about 200 m away from the smelters. A
large number of people were found suffering from
arsenic toxicity in this region [353].

[sharon sanders]

Re: Woods Hole Scientists Link Influenza A (H1N1) Susceptibility to Arsenic Exposure

Arsenic round the world: a review
Badal Kumar Mandal, Kazuo T. Suzuki *
Graduate School of Pharmaceutical Sciences, Chiba Uniersity, Chiba 263 -8522, Japan
Received 7 December 2001; received in revised form 8 February 2002


4.2.11. Greece incident

Systematic sampling of soils and dusts in and
around the ancient lead mining and smelting site
at Lavrion, Greece, indicated extensive contamination
with arsenic as well as lead and had instigated
studies into possible health implications to
the local community [354]. Concentrations of arsenic
in garden soils and house dusts were ranged
up to 14,800 and 3800 mg kg−1, respectively.

4.2.12. Ghana incident

Arsenic in drinking water from streams, shallow
wells and boreholes in the Obuasi gold-mining
area of Ghana ranges from 0.002 to 0.175
mg l−1. The main source of pollution is due to
mining activities and oxidation of naturally occurring
sulfide minerals, predominantly arsenopyrite
(FeAsS). Some of the water samples have high
arsenite content. Soils are leached kaolinite?muscovite
laterites overlying saprolite [355]. It is reported
that in the saprolite, arsenopyrite appears
to have been replaced by secondary As- and Febearing
minerals, including scorodite
(FeAsO4?2H2O), arsenolite and arsenates [356].

4.2.13. USA incident

The serious incident of air pollution by arsenic
from copper smelters in the U.S. is recorded in
Anaconda, Montana [357,358] with the rate of
emissions of arsenic trioxide of 16,884 kg per day.
Although no atmospheric concentrations are in
record, edible plants contain arsenic trioxide up to
482 g g−1, causing serious health hazard surrounding
the area. Mortality from ischemic heart
disease is significantly increased among arsenic
exposed workers of this smelter [359]. The initial
1938?1963 mortality analysis of workers at the
copper smelter at Anaconda, Montana, demonstrated
a more than threefold excess respiratory
cancer ratio, with an excess risk as high as high as
eightfold among heavily exposed men who had
worked there 8 years or more [360]. A serious
incident of air pollution by arsenic also occurs in
a small Western town near a gold-smelter, USA
manufacturing 36 tons of arsenic trioxide per day
[361].
Some studies [362,363] involved a copper smelting
plant at Tacoma in the state of Washington
that produced As2O3 as a by-product. The plant
had an average employment of 904 during the
years 1944?1960 when a total of 229 deaths were
reported among active plant employees, 38 of the
death were classified as exposed to arsenic. Out of
these six died of cancer, including three cases of
cancer of the respiratory tract.
In literature [364], Perham was a town of 1900
situated on the agricultural area of western Minnesota,
USA and a core sample to a depth of 20
cm revealed 3000 parts per million (mg l−1) of
arsenic. The symptoms of sub-acute or chronic
arsenic intoxication were confirmed to the three
persons out of 13 with the highest intake.

4.2.14. British incident

In 1910 and 1943, a British plant manufactured
a sodium arsenite sheep dip [365,366]. The factory
was in a small county town within a specific birth
and death registration sub-district. Here 75 deaths
are reported among factory workers 22 (29%) due
to cancer.

4.2.15. Southern Rhodesia incident

There was excess lung cancer mortality among
southern Rhodesia miners of gold bearing ores
containing large amounts of arsenic [367].

4.2.16. Torreon, Mexico incident

In the city of Torreon, Mexico, Espinosa Gonzalez
[368] reported the presence of arsenic in
drinking water from a deep well range from 4 to
6 mg l−1. In Silesia, Mexico the concentration of
arsenic in spring water arose through leaching of
arsenic wastes from mining operations (coal
preparations wastes and fly ash from coal-fired
power plants) into spring water leading to contamination
[369].

4.2.17. Northern Sweden incident

At the Ronnskar smelter in northern Sweden,
ores with a high arsenic content were handled.
Women employed in the plant as well as those
who lived nearby deliver babies having significantly
lower weight than those delivered by
women who are not so exposed [231]. Among
those same women, the frequency of spontaneous
abortion is generally higher with closer proximity
of residence to the smelter [232]. Although residential
proximity to the Ronnskar smelter has no
effect on the incidence of congenital malforma
tions, pregnancies during which the mother had
worked at the smelter are significantly more apt to
babies with single or multiple malformations, particularly
urogenital malformations or hip-joint
dislocation [231].

4.2.18. Armadale, central Scotland incident

In Armadale, a town in central Scotland
[370,371] having population 7000, the standardized
mortality ratio (SMR) for respiratory cancer
are high and high sex-ratios of births were observed
during 1969?1973 which was due to arsenic
contamination from a steel foundry located
in that area. The arsenic concentrations in soil
samples in Armadale were higher (52?64 g g−1)
than those in the white burn soils.

4.2.19. Srednogorie, Bulgaria incident

Heavy air pollution as well as high arsenic
contamination of soil occur due to copper smelter
located in close vicinity to the Srednogorie [372]
with a population of 32,000 inhabitants and constituted
the largest metallurgical center in Bulgaria.
The smelter started operation in 1959 and
had been processing high arsenic containing
sulfide ores, mainly from Tjelopet ch causing contamination
of Topolnitza river water having arsenic
concentration of 0.75?1.5 mg l−1 during the
time period of 1987?1990. The aerial emission is
estimated at 50?100 tons per year. Exposure to
the general population is mostly by inhalation and
partly by ingestion of locally produced food products,
like vegetables. Several health hazards are
observed around the area of the exposed population
with high arsenic content in hair, nails and
urine.

[zimagail]

Re: Argentina has the world?s highest rate of deaths associated with swine flu infections



Two comments regarding arsenic and increased death rates.
1. Chaco may have a high arsenic level but that is not where the deaths are concentrated. Last I checked there were only 3 cases in Chaco.
2. Chile and Argentina both are mined heavily for gold, silver and copper, all extracted with arsenic.

[Giuseppe]

Re: Argentina has the world?s highest rate of deaths associated with swine flu infections

I am not completely persuaded about the statement points Argentina as the country with the higher case-fatality rate.

Argentina 1587 - 26 / 99 - 3 [CFR=16,38 x 1,000]
Australia 4090 - 7 / 52 - 0 [CFR=1,71]
Brazil 680 - 1 / 228 - 1 [CFR=1,47]
Canada 7983 - 25 / 208 - 4 [CFR=3,13]
Chile 6211 - 12 / 1025 - 5 [CFR=1,93]
Colombia 93 - 2 / 5 - 0 [CFR=21,5]
Costa Rica 279 - 2 / 24 - 1 [CFR=7,16]
Dominican Republic 108 - 2 / 0 - 0 [CFR=18,51]
Mexico 8680 - 116 / 401 - 0 [CFR=13,36]
Philippines 861 - 1 / 0 - 0 [CFR=1,16]
Spain 717 - 1 / 176 - 1 [CFR=1,39]
Thailand 1414 - 3 / 640 - 3 [CFR=2,12]
United Kingdom 6538 - 3 / 2288 - 2 [CFR=0,45]
Uruguay 195 - 1 / 0 - 1 [CFR=5,12]

From Latest WHO case count update http://www.who.int/csr/don/2009_07_01a/en/index.html


There should be several biases in epidemiological surveillance.

What's about recent dengue hemorrhagic fever outbreaks in south America?

Are there data about incidence of dengue in regions currently badly hit by H1N1?

[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6V78-4H7TCVM-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=945378200&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=186a8ce9a62a1c8ea33b9d459f1a190f

doi:10.1016/j.scitotenv.2005.09.005


Copyright © 2005 Elsevier B.V. All rights reserved.


Occurrence of arsenic contamination in Canada: Sources, behavior and distribution
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<!-- refMsg -->Suiling Wang^a and Catherine N. Mulligan^,^a^,

<!-- authorsNoEnt -->^aDepartment of Building, Civil and Environmental Engineering, Concordia University, 1455 de Maisonneuve Boulevard W., EV 006-187, Montreal, QC, Canada H3G 1M8

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<!-- articleText -->
Received 16 February 2005;
<!-- articleText -->revised 2 September 2005;
<!-- articleText -->accepted 2 September 2005.
<!-- articleText -->Available online 3 October 2005.
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<!-- articleText -->Abstract

Recently there has been increasing anxieties concerning arsenic related problems. Occurrence of arsenic contamination has been reported worldwide. In Canada, the main natural arsenic sources are weathering and erosion of arsenic-containing rocks and soil, while tailings from historic and recent gold mine operations and wood preservative facilities are the principal anthropogenic sources. Across Canada, the 24-h average concentration of arsenic in the atmosphere is generally less than 0.3 μg/m³. Arsenic concentrations in natural uncontaminated soil and sediments range from 4 to 150 mg/kg. In uncontaminated surface and ground waters, the arsenic concentration ranges from 0.001 to 0.005 mg/L. As a result of anthropogenic inputs, elevated arsenic levels, above ten to thousand times the Interim Maximum Acceptable Concentration (IMAC), have been reported in air, soil and sediment, surface water and groundwater, and biota in several regions. Most arsenic is of toxic inorganic forms. It is critical to recognize that such contamination imposes serious harmful effects on various aquatic and terrestrial organisms and human health ultimately. Serious incidences of acute and chronic arsenic poisonings have been revealed. Through examination of the available literature, screening and selecting existing data, this paper provides an analysis of the currently available information on recognized problem areas, and an overview of current knowledge of the principal hydrogeochemical processes of arsenic transportation and transformation. However, a more detailed understanding of local sources of arsenic and mechanisms of arsenic release is required. More extensive studies will be required for building practical guidance on avoiding and reducing arsenic contamination. Bioremediation and hyperaccumulation are emerging innovative technologies for the remediation of arsenic contaminated sites. Natural attenuation may be utilized as a potential in situ remedial option. Further investigations are needed to evaluate its applicability.

<!-- articleText -->Keywords: Arsenic; Speciation; Biota; Canada; Mining; Soil; Sediments; Water

<!-- articleText -->Article Outline

<dl><dt>1. Introduction </dt><dt>2. Arsenic sources </dt><dl><dt>2.1. Natural sources </dt><dt>2.2. Anthropogenic sources </dt><dl><dt>2.2.1. Mining residues </dt><dt>2.2.2. Industrial emissions </dt><dt>2.2.3. Wood preserving </dt><dt>2.2.4. Coal combustion </dt><dt>2.2.5. Arsenical pesticides</dt></dl></dl><dt>3. Arsenic in air </dt><dl><dt>3.1. Reported concentrations </dt><dt>3.2. Arsenic species in air </dt><dt>3.3. Atmospheric deposition of arsenic</dt></dl><dt>4. Arsenic in soil and sediments </dt><dl><dt>4.1. Reported concentrations </dt><dl><dt>4.1.1. Soil </dt><dt>4.1.2. Sediments</dt></dl><dt>4.2. Arsenic species in soil and sediments </dt><dt>4.3. Arsenic association with solid phases </dt><dt>4.4. Mineral dissolution induced arsenic release</dt></dl><dt>5. Arsenic in water </dt><dl><dt>5.1. Reported arsenic concentrations </dt><dl><dt>5.1.1. Surface water </dt><dt>5.1.2. Groundwater </dt><dt>5.1.3. Porewater </dt><dt>5.1.4. Geothermal fluid </dt><dt>5.1.5. Seasonal variation</dt></dl><dt>5.2. Main arsenic species in water </dt><dt>5.3. Arsenic sorption behavior in water</dt></dl><dt>6. Arsenic in biota </dt><dl><dt>6.1. Arsenic uptake </dt><dt>6.2. Reported arsenic concentrations </dt><dt>6.3. Implications for arsenic remediation technologies </dt><dl><dt>6.3.1. Hyperaccumulation </dt><dt>6.3.2. Microbially mediated mobilization </dt><dt>6.3.3. Natural attenuation </dt><dt>6.3.4. Other technologies</dt></dl></dl><dt>7. Conclusions and recommendations </dt><dt>References</dt></dl>
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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 1. Canadian arsenic production, 1885–1990 (modified from Cranstone, 2001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2. A simplified diagram of arsenic cycle.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 3. Arsenic release from NPRI reporting facilities, 1994–2001 (data sources: NPRI online database).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 4. The Eh–pH diagram for arsenic at 25 &#176;C and 101.3 kPa (modified from Ferguson and Gavis, 1972).

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Table 1. Estimated fluxes of arsenic transfer

(Mackenzie et al., 1979).

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Table 2. Arsenic concentrations measured in six mine tailings

(Wang and Mulligan, 2004a).

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Table 3. Arsenic concentrations in Canadian air

^a 24-h maximum concentrations.
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Table 4. Arsenic concentrations in Canadian soil


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Table 5. Arsenic concentrations in Canadian sediments


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Table 6. Arsenic concentrations in Canadian waters


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Corresponding author. Tel.: +1 514 848 2424x7925; fax: +1 514 848 7965.

[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

Interesting, many Inuit mothers have very high levels of contamination.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6V78-4HK5SJN-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=945387823&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0f11866494ac3a354c2f6653b7fe1c4a

doi:10.1016/j.scitotenv.2005.03.034


Crown copyright &#169; 2005 Published by Elsevier B.V.
Review

Human health implications of environmental contaminants in Arctic Canada: A review
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References and further reading may be available for this article. To view references and further reading you must purchase this article.


<!-- refMsg -->J. Van Oostdam^a^,^,, S.G. Donaldson^a^,^b, M. Feeley^c, D. Arnold^c, P. Ayotte^d, G. Bondy^c, L. Chan^e, &#201;. Dewaily^d, C.M. Furgal^f, H. Kuhnlein^e, E. Loring^g, G. Muckle^h, E. Mylesⁱ, O. Receveur^j, B. Tracy^k, U. Gill^l and S. Kalhok^m

<!-- authorsNoEnt -->^aEnvironmental Contaminants Bureau, Safe Environments Program, Health Canada, Rm 4-046, BMO Building, 269 Laurier Avenue W., AL4904B, Ottawa, ON, Canada K1A 0K9
^bCarleton University, 1125 Coloney By Drive, Ottawa, ON, Canada K1S 5B6
^cHealth Canada, Food Directorate, Bureau of Chemical Safety, Banting Research Center, Tunney's Pasture, Ottawa, ON, Canada K1A 0L2
^dUnit&#233; de recherche en sant&#233; publique (Centre hospitalier universitaire de Qu&#233;bec - Centre hospitalier de l'Universit&#233; Laval), Universit&#233; Laval, 945 Ave Wolfe, Ste. Foy, Qu&#233;bec, Canada G1V 5B3
^eCentre for Indigenous Peoples' Nutrition and Environment, Macdonald Campus of McGill University, 21,111 Lakeshore Road, Ste.-Anne-de-Bellevue, Quebec, Canada H9X 3V9
^fD&#233;partment Science Politique et Unit&#233; de recherche en sant&#233; publique (Centre hospitalier universitaire de Qu&#233;bec - Centre hospitalier de l'Universit&#233; Laval), Universit&#233; Laval, 945 Ave Wolfe, Ste. Foy, Qu&#233;bec, Canada G1V 5B3
^gEnvironmental Contaminants Research Division, Inuit Tapiriit Kanatami, 170 Laurier Avenue West, 12th Floor, Ottawa, ON, Canada, K1P 5V5
^h&#201;cole de psychologie et Unit&#233; de recherche en sant&#233; publique (Centre hospitalier universitaire de Qu&#233;bec - Centre hospitalier de l'Universit&#233; Laval), Universit&#233; Laval, Ste Foy, Qu&#233;bec, Canada G1K 7P4
ⁱAXYS Environmental Consulting Ltd., Suite 300, 805 8th Ave SW, Calgary, Alberta, Canada T2P 1H7
^jFacult&#233; de Medicin, Nutrition, Universit&#233; de Montreal, CP6128, Succursale Centre Ville Montreal, QC, Canada H3C 3J7
^kHealth Canada, Environmental Health Directorate, Radiation Protection Bureau, 775 Brookfield Road, AL 6302D1, Ottawa, ON, Canada K1A 0L2
^lHealth Canada, Health Products and Food Branch, 2nd Floor, Qualicum Twr A, 2936 Baseline, AL 3302C Nepean, ON, Canada K1A 0K9
^mIndian and Northern Affairs, Northern Science and Contaminants Research Directorate, 10 Wellington Street, Gatineau, Quebec, Canada K1A 0H4

<!-- authorsNoEnt -->
<!-- articleText -->
Accepted 30 March 2005.
<!-- articleText -->Available online 16 November 2005.
<!-- articleText -->


<!-- articleText -->Abstract

The objectives of this paper are to: assess the impact of exposure to current levels of environmental contaminants in the Canadian Arctic on human health; identify the data and knowledge gaps that need to be filled by future human health research and monitoring; examine how these issues have changed since our first assessment [Van Oostdam, J., Gilman, A., Dewailly, &#201;., Usher, P., Wheatley, B., Kuhnlein, H. et al., 1999. Human health implications of environmental contaminants in Arctic Canada: a review. Sci Total Environ 230, 1–82]. The primary exposure pathway for contaminants for various organochlorines (OCs) and toxic metals is through the traditional northern diet. Exposures tend to be higher in the eastern than the western Canadian Arctic. In recent dietary surveys among five Inuit regions, mean intakes by 20- to 40-year-old adults in Baffin, Kivalliq and Inuvialuit communities exceeded the provisional tolerable daily intakes (pTDIs) for the OCs, chlordane and toxaphene. The most recent findings in NWT and Nunavut indicate that almost half of the blood samples from Inuit mothers exceeded the level of concern value of 5 μg/L for PCBs, but none exceeded the action level of 100 μg/L. For Dene/M&#233;tis and Caucasians of the Northwest Territories exposure to OCs are mostly below this level of concern. Based on the exceedances of the pTDI and of various blood guidelines, mercury and to a lesser extent lead (from the use of lead shot in hunting game) are also concerns among Arctic peoples. The developing foetus is likely to be more sensitive to the effects of OCs and metals than adults, and is the age groups of greatest risk in the Arctic. Studies of infant development in Nunavik have linked deficits in immune function, an increase in childhood respiratory infections and birth weight to prenatal exposure to OCs. Balancing the risks and benefits of a diet of country foods is very difficult. The nutritional benefits of country food and its contribution to the total diet are substantial. Country food contributes significantly more protein, iron and zinc to the diets of consumers than southern/market foods. The increase in obesity, diabetes and cardiovascular disease has been linked to a shift away from a country food diet and a less active lifestyle. These foods are an integral component of good health among Aboriginal peoples. The social, cultural, spiritual, nutritional and economic benefits of these foods must be considered in concert with the risks of exposure to environmental contaminants through their exposure. Consequently, the contamination of country food raises problems which go far beyond the usual confines of public health and cannot be resolved simply by risk-based health advisories or food substitutions alone. All decisions should involve the community and consider many aspects of socio-cultural stability to arrive at a decision that will be the most protective and least detrimental to the communities.

<!-- articleText -->Keywords: Arctic regions; Environmental monitoring; PCBs; Organochlorines; Mercury; Maternal; Infant; Monitoring environmental pollution; Northern populations; Public health; Risk factors; Risk-benefit management

<!-- articleText -->Article Outline

<dl><dt>1. Introduction </dt><dl><dt>1.1. Aboriginal peoples of Canada </dt><dt>1.2. Aboriginal perspectives on food and health </dt><dt>1.3. Factors that contribute to Aboriginal Northerners' exposure to country food contamination </dt><dt>1.4. Evaluation of research in CACAR and application to benefit and risk assessment/management </dt><dt>1.5. Research ethics</dt></dl><dt>2. Exposure assessment </dt><dl><dt>2.1. Country food consumption in the Arctic </dt><dt>2.2. Contaminant levels in people and their relationship to traditional food diets </dt><dl><dt>2.2.1. Tissue levels of contaminant results </dt><dt>2.2.2. Levels of mercury in hair and blood </dt><dt>2.2.3. Population groups and studies </dt><dt>2.2.4. Maternal hair </dt><dt>2.2.5. Maternal/cord blood </dt><dt>2.2.6. Levels of selenium in maternal blood </dt><dt>2.2.7. Levels of lead in maternal blood </dt><dt>2.2.8. Levels of cadmium in maternal blood </dt><dt>2.2.9. Radionuclide exposure </dt><dl><dt>2.2.9.1. Radiocesium </dt><dt>2.2.9.2. Lead-210 and polonium-210 </dt><dt>2.2.9.3. Summary of radionuclide exposures</dt></dl></dl><dt>2.3. Trends in traditional/country food dietary intakes and contaminant exposures</dt></dl><dt>3. Toxicology </dt><dl><dt>3.1. Priority contaminants </dt><dl><dt>3.1.1. Toxaphene </dt><dl><dt>3.1.1.1. Discussion</dt></dl><dt>3.1.2. Chlordane </dt><dl><dt>3.1.2.1. Discussion</dt></dl></dl><dt>3.2. Toxicological effects induced by exposure to food-chain contaminant mixtures </dt><dl><dt>3.2.1. Discussion</dt></dl><dt>3.3. Contaminant and dietary nutrient interactions </dt><dl><dt>3.3.1. Discussion</dt></dl></dl><dt>4. Epidemiology and human biomarkers </dt><dl><dt>4.1. Immune system function </dt><dl><dt>4.1.1. Clinical outcomes </dt><dt>4.1.2. Biomarkers </dt><dl><dt>4.1.2.1. Lymphocyte subsets and immunoglobulins </dt><dt>4.1.2.2. Antibody response following vaccination </dt><dt>4.1.2.3. Complement system </dt><dt>4.1.2.4. Cytokine production by Th1/Th2 Cells </dt><dt>4.1.2.5. Vitamin A status</dt></dl></dl><dt>4.2. Neurodevelopment </dt><dl><dt>4.2.1. Clinical outcomes </dt><dl><dt>4.2.1.1. Polychlorinated biphenyls (PCBs) </dt><dt>4.2.1.2. Methylmercury</dt></dl><dt>4.2.2. Biomarkers of developmental effects </dt><dl><dt>4.2.2.1. Cytochrome P4501A1 induction and DNA adduct formation </dt><dt>4.2.2.2. Thyroid hormones</dt></dl></dl><dt>4.3. Sex hormone disruption </dt><dl><dt>4.3.1. Clinical outcomes </dt><dl><dt>4.3.1.1. Sexual maturation of newborn males </dt><dt>4.3.1.2. Environmental risk factors for osteoporosis</dt></dl><dt>4.3.2. Hormonal biomarkers </dt><dl><dt>4.3.2.1. Hormone profiles</dt></dl></dl><dt>4.4. Oxidative stress</dt></dl><dt>5. Risk-benefit characterization, assessment and advice </dt><dl><dt>5.1. Contaminant exposure risks </dt><dl><dt>5.1.1. Contaminant intakes </dt><dl><dt>5.1.1.1. Persistent organic pollutants </dt><dt>5.1.1.2. Metals—mercury, cadmium, and lead </dt><dt>5.1.1.3. Contaminant tissue levels and guidelines</dt></dl></dl><dt>5.2. Special considerations for risk management in Arctic communities </dt><dl><dt>5.2.1. Nutritional benefits</dt></dl><dt>5.3. Social, cultural, spiritual and economic benefits of country food </dt><dt>5.4. Assessment of perceptions of risks, benefits and safety of country foods </dt><dl><dt>5.4.1. Perceptions of risks in the north </dt><dt>5.4.2. Research on the perceptions of food-chain contamination in the north </dt><dt>5.4.3. Impacts of these perceptions</dt></dl><dt>5.5. Risk-benefit characterization </dt><dl><dt>5.5.1. Risk management frameworks </dt><dt>5.5.2. Problem identification and context </dt><dt>5.5.3. Risk and benefit assessment </dt><dl><dt>5.5.3.1. Risk assessment </dt><dt>5.5.3.2. Benefit assessment</dt></dl><dt>5.5.4. Risk characterization </dt><dt>5.5.5. Assumptions/uncertainties of concern </dt><dt>5.5.6. Weighing benefits and risks—challenges in practice </dt><dt>5.5.7. Option analysis/evaluation </dt><dt>5.5.8. Selecting a risk management option </dt><dt>5.5.9. Implementation </dt><dt>5.5.10. Monitoring and evaluating the decision</dt></dl><dt>5.6. Risk and benefit communication</dt></dl><dt>6. Conclusions </dt><dl><dt>6.1. Aboriginal perspectives on food and health and interpretation of research results </dt><dt>6.2. Exposure assessment </dt><dt>6.3. Toxicology </dt><dt>6.4. Epidemiology and biomarkers </dt><dt>6.5. Risk and benefit characterization, assessment and advice</dt></dl><dt>7. Knowledge gaps </dt><dl><dt>7.1. Exposure assessment </dt><dt>7.2. Toxicology </dt><dt>7.3. Epidemiology </dt><dt>7.4. Risk and benefit characterization, assessment and advice</dt></dl><dt>Acknowledgements </dt><dt>References</dt></dl>
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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 1.1.1. General locations of Arctic cultural groups (adapted from Van Oostdam et al., 1999).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 1.1.2. Age distribution of Canadian Arctic population by ethnicity.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.1.1. Communities participating in CINE dietary assessments.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.1.2. Percentage of energy from traditional/country foods in the Yukon, Dene and M&#233;tis, and Inuit communities.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.1. Contaminant studies in the Northwest Territories, Nunavut, and Nunavik.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.2. Maternal contaminant levels in Arctic Canada: oxychlordane (μg/L plasma).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.3. Maternal contaminant levels in Arctic Canada: hexachlorobenzene (μg/L plasma).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.4. Maternal contaminant levels in Arctic Canada: total toxaphene (μg/L plasma).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.5. Maternal contaminant levels in Arctic Canada: β-hexachlorocyclohexane (μg/L plasma).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.6. Maternal contaminant levels in Arctic Canada: p,p′-DDE (μg/L plasma).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.7. Maternal contaminant levels in Arctic Canada: PCBs (as Aroclor 1260) (μg/L plasma).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.8. Adjusted mean organochlorine (OC) concentrations according of the year of birth: (a) PCBs; (b) DDE; (c) HCB; (d) oxychlordane (Dallaire et al., 2003a).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.9. Maternal contaminant levels in Arctic Canada: total mercury (μg/L plasma).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2.2.10. Adjusted mean metal concentrations according to the year of birth for (a) lead and (b) mercury (Dallaire et al., 2003a).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 4.1.1. Distribution of PCB 153 concentration in cord serum or plasma, 10 studies (Longnecker et al., 2003).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5.1.1. Mean intakes of chlordane, toxaphene, and mercury in northern Canada (μg/kg/day) (Kuhnlein et al., 2001b).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5.1.2. Mean intakes of toxaphene and chlordane in different regions (ages 20–40 years) (Chan et al., in preparation(a)).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5.1.3. Mean intakes of toxaphene and chlordane among different age groups in Baffin (Chan et al., in preparation(a)).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5.1.4. Maternal blood guideline exceedances for PCBs as Aroclor 1260 in Arctic Canada, by region and ethnicity (Van Oostdam, 2001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5.1.5. Mean intake of total mercury in different regions (μg/kg/day) (Chan et al., in preparation(b)).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5.1.6. Maternal blood guideline exceedances for organic mercury in Arctic Canada, by region and ethnicity (Van Oostdam, 2001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5.5.1. Framework for environmental health risk management (Presidential/Congressional Commission on Risk Assessment and Risk Management, 1997a and Presidential/Congressional Commission on Risk Assessment and Risk Management, 1997b).

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Table 1.1.1 Aboriginal peoples: population size and proportion of the total population in each region of Arctic Canada, 1996

Source: Statistics Canada (2001).
^a Data presented in this table are for those who identify with one or more Aboriginal groups (Metis, Inuit, or North American Indian).
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Table 2.1.1 Five country/traditional food items most often consumed (yearly average of days per week)

Source: Kuhnlein (2002).

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Table 2.2.1 Mean levels of organochlorine pesticides in maternal blood, by region and ethnic group (geometric means, range, μg/L plasma)

NA = Not available; nd = not detected.
^a Source: Butler Walker et al. (2003).
^b Source: Muckle, 2000 and Muckle et al., 2001b.
^c N = 25.
^d N = 42.
^e Four composites (n = 12, 12, 12 and 14; Seddon, 1996).
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Table 2.2.2 Mean levels of PCBs in maternal blood, by region and ethnic group (geometric means, range, μg/L plasma)

NA = Not available; nd = not detected.
^a Source: Butler Walker et al. (2003).
^b Source: Muckle (2000) and Muckle et al., 2001a and Muckle et al., 2001b.
^c Aroclor 1260 = 5.2 (PCB 153 + 138) (Weber, 2002).
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Table 2.2.3 Dioxins and furans and PCBs in maternal blood

^a TEQs = toxic equivalents.
^b D + F = dioxins and furans.
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Table 2.2.4 Cord and maternal contaminants (lipid weight basis)

Source: Van Oostdam (2001).
Abbreviations: B-HCH, beta-hexachlorocyclohexane; PCBs, polychlorinated biphenyls.
^a Sample size: cord–maternal pairs.
^b Concentration (μg/kg lipid, arithmetic mean).
^c Cord/maternal blood (paired data only).
^d Pearson's correlations.
^e Statistical significance of cord/maternal Pearson's correlations.
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Table 2.2.5 Worldwide comparisons of maternal blood levels of PCBs (Aroclor 1260) and β-HCH (geometric means, μg/L plasma)

^a Source: Butler Walker et al. (2003).
^b Source: Muckle (2000) and Muckle et al., 2001a and Muckle et al., 2001b.
^c Source: Deutch (2001).
^d Source: Deutch and Hansen (2000).
^e Source: Klopov et al. (1998).
^f Source: Klopov (2000), Klopov and Shepovalnikov (2000), and Klopov and Tchachchine (2001).
^g Source: Odland (2001).
^h Source: Sharma and Bhatnagar (1996).
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Table 2.2.6 Current and historic levels^a of mercury in maternal hair (μg/g)

Source: Snider and Gill (2001).
LOD: below analytical method detection limits (0.4 μg/g).
^a Peak exposure levels reported as parts per million (ppm) in hair.
^b GSD: Geometric mean standard deviation.
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Table 2.2.7 Mean concentrations of metals in maternal blood, by ethnicity and region (geometric mean (range), μg/L whole blood)

NA = Not available; nd = not detected.
^a Source: Butler Walker et al. (2005).
^b Source: Muckle et al., 2001a and Muckle et al., 2001b.
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Table 2.2.8 Worldwide comparisons of maternal blood mercury levels (μg/L whole blood) for women living in arctic regions

^a GM: geometric mean.
^b GSD: geometric standard deviation.
^c Source: Bjerregaard and Hansen (2000).
^d Source: AMAP (1998).
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Table 2.2.9 Radionuclide levels in caribou meat and people in the Canadian Arctic, and resulting radiation doses to people

Source: Tracy and Kramer (2000).
^a Doses based on measured whole-body concentrations of ¹³⁷Cs (Tracy et al., 1997).
^b Doses based on estimated caribou consumption in a typical northern diet and on human metabolic parameters. The higher ²¹⁰Po doses in the 1960s is not based on any changes in environmental levels of ²¹⁰Po but on an estimated higher consumption of caribou meat at that time (Tracy and Kramer, 2000).
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Table 3.1.1 Relative percent contribution to chlordane total

^a Buchert et al. (1989).
^b Marine mammal blubber average, 1993–1994.
^c As heptachlor epoxide.
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Table 3.1.2 Chlordane-induced mortality in sub-acute studies

Bondy et al., 2000 and Bondy et al., 2003.

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Table 3.2.1 Composition of the organochlorine mixture

Source: Ayotte (2001).
^a Mixture containing 2,4,4′-trichlorobiphenyl (320 mg), 2,2′,4,4′-tetrachlorobiphenyl (256 mg), 3,3′,4,4′-tetrachlorobiphenyl (1.4 mg), 3,3′,4,4′,5-pentachlorobiphenyl (6.7 mg), Aroclor 1254 (12.8 g), and Aroclor 1260 (19.2 g).
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Table 3.2.2 Composition of complex mixture based on human blood residues

Source: Bowers et al. (2003).
^a Containing PCBs 28, 52, 99, 101, 105, 118, 128, 138, 153, 156, 170, 180, 183, 187.
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Table 3.2.3 Comparison of PBTK-derived TDIs to estimated contaminant intakes

Source: Chan et al., 1997 and Chan et al., 2000. ND—not determined.

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Table 4.2.1 Comparison of mercury (total) concentrations in Nunavik with those observed in other cohorts

Source: Muckle et al. (2001b).
^a The average Hg concentration was reported in nmol/L, this concentrations was divided by 5 to transform to μg/L.
^b 95% confidence interval.
^c Women aged between 15 and 39 years old.
^d Arithmetic mean.
^e Standard deviation.
^f Among seafood consumers.
^g Among non-seafood consumers.
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Table 5.1.1 Sources of organochlorines in the Baffin Region (percent contribution)

Source: Kuhnlein and Receveur (2001).
^a Percent by weight of each species contributing to the traditional diet.
^b Percent of each contaminant contributed by each food.
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Table 5.1.2 Proportionate contributions of three main food sources of chlordane and toxaphene, in five Inuit regions, by food item

Source: Kuhnlein and Receveur (2001).

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Table 5.1.3 Population distribution of organochlorine intake in Qikiqtarjuaq (μg/kg bw/day)

Source: Kuhnlein and Receveur (2001).

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Table 5.1.4 Comparison of daily intake of selected contaminants in Qikiqtarjuaq in 1987–1988 and 1998–1999

^a Source: Kuhnlein et al. (1995a) and Chan et al. (1997).
^b Source: Kuhnlein et al. (2000).
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Table 5.1.5 Proportionate contributions of three main food sources of total mercury, and total mercury concentrations by food item in five Inuit regions

Source: Kuhnlein and Receveur (2001).

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Table 5.1.6 Population distribution of heavy metal intake in Qikiqtarjuaq (μg/kg bw/day)

Source: Kuhnlein and Receveur (2001).

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Table 5.1.7 Blood guideline exceedances for methyl mercury, lead, and cadmium in Arctic Canada, by region and ethnicity

NA = Not available.
^a Based on US EPA 1999 re-evaluation of methyl mercury.
^b Increasing risk range is 20–100 μg/L, Health Canada.
^c Guideline value of 5 μg/L is for occupational exposure.
^d Source: Butler Walker et al. (2005).
^e Source: Ayotte (2001).
^f ≥ 5.8 μg/L value.
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Table 5.2.1 Percent energy from macronutrients on days with or without traditional/country food (least square means &#177; S.E.M.)

Source: Kuhnlein et al. (2004).
 Different from with TF, p < 0.01.
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Table 5.2.2 Top three sources of selected nutrients from 24-h recalls (fall and late winter combined) in five Inuit regions

Source: Kuhnlein and Receveur (2001).

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Table 5.2.3 Reported daily fish consumption by gender and age group in three recent dietary surveys among Canadian Arctic indigenous peoples^a

Data adapted from Receveur et al., 1996 and Receveur et al., 1998a and Kuhnlein et al. (2000).
^a Estimates obtained by averaging food intake over all 24-h recalls collected in two seasons (Sep–Nov and Feb–Apr).
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Corresponding author. Tel.: +1 613 941 3570.

[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

http://www.questia.com/googleScholar.qst;jsessionid=KLkGg7WX91N0t9pYRQZGYQ4gyNBHMgSkqwvTrBt7y9l0yPL3Hg0h!657527082!497993468?docId=5009311075

Mapping of Arsenic Content and Distribution in Groundwater in the Southeast Pampa, Argentina

Journal article by J.D. Paoloni, M.E. Sequeira, C.E. Fiorentino; Journal of Environmental Health, Vol. 67, 2005


Journal Article Excerpt

<TABLE id=rightTable border=0 cellSpacing=0 cellPadding=0><TBODY><TR><TD class=3text width=2></TD><TD class=3text>

Mapping of Arsenic Content and Distribution in Groundwater in the Southeast Pampa, Argentina.

by J.D. Paoloni , M.E. Sequeira , C.E. Fiorentino

Introduction
The relationship between groundwater and the chemical, physical, and kinetic processes affecting the various rock and sediment components could be the reason for the appearance of arsenic in some sources of water supply (Toth, 2000). The content in water depends more on speciation than on the amount of arsenic present in the environment (Bhumbla & Keefer, 1994). Upper, or phreatic groundwater, tends to be highly mineralized water containing considerable amounts of arsenic, fluoride, boron, vanadium, and other minerals.
According to the World Health Organization (WHO, 1998), the carcinogenic effect of ingesting water containing inorganic arsenic above the recommended maximum level of 0.01 milligrams per liter (mg/L) is well demonstrated and is reflected in an increased incidence of skin cancer in humans.
Morras, Blanco, and Paoloni (2000) reported excessive levels of arsenic in the groundwater of the Chaco-pampa region in Argentina. A study by Sastre, Rodriguez, Varillas, & Salim (1997), surveyed a population that had resided in the Salta Chaco (northwest Argentina) for over 10 years and found that 8.6 percent of those surveyed were suffering from chronic regional endemic hydro-arsenism (CREHA).
Volcanic ash in quaternary sediments in the pampa plains of north La Pampa Province, Argentina, show high concentrations of arsenic (7 to 12 mg/L), as well as other oligoelements (Nicolli, Smedley, & Tullio, 1997; Smedley, Nicolli, Macdonald, Barros, & Tullio, 2002).
A considerable number of studies have been undertaken in Argentina on high arsenic content in water a...


</TD><TD width=2></TD></TR></TBODY></TABLE>
End of free preview...

[Shannon Bennett]

Re: Discussion, high H1N1 CFR and elevated arsenic

Zimagail argues in post 7 that arsenic levels are not high in the city of Buenos Aries. While that may be true, the higher levels in other parts of the country coupled with the extremely high migration of people from outlying areas into Buenos Aries, where the levels are above the recommended rate, may explain the anomaly.

Two comments regarding arsenic and increased death rates.
1. Chaco may have a high arsenic level but that is not where the deaths are concentrated. Last I checked there were only 3 cases in Chaco.
2. Chile and Argentina both are mined heavily for gold, silver and copper, all extracted with arsenic.

[sharon sanders]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

I moved posts to this thread to solve a software problem on the other Arsenic discussion thread. Please post to this one. Thanks!

[AlaskaDenise]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

Here's an article that includes costs to remove arsenic from water systems. It's an issue in some populated areas of Alaska.

http://www.adn.com/news/alaska/matsu/story/644794.html

(snipped)

According to the EPA, 967 water systems nationwide serving more than 1.3 million people were out of compliance with the new arsenic rule as of December 2008. That list includes eight water systems in Alaska affecting more than 1,400 people, most located in the Valley.

"Engineering estimates for remediation can run $50,000 to $100,000," Winkler said.

The cost of treatment depends on a lot of factors, he said. For some, a new well is the least-expensive answer. For others, more intensive treatment like installing a filtration system is required. The federal standards do not apply to private wells, but homeowners can likely treat the problem for between $400 and $4,000, Winkler said.

.....a system that sprays air into the water and filters it would be the backup plan. The estimated price tag would be around $100,000,

.

[Shannon Bennett]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

We have some evidence of elevated levels of arsenic in three of the areas hardest hit with CFR from H1N1. Why does an elevated arsenic level result in a higher CFR for H1N1 patients?

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WXH-4DXBB1R-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=945432827&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=7c366b5d39c29f7aec21579b6706b8d5

doi:10.1016/j.taap.2004.08.010


Copyright &#169; 2004 Elsevier Inc. All rights reserved.


Implications of oxidative stress and hepatic cytokine (TNF-α and IL-6) response in the pathogenesis of hepatic collagenesis in chronic arsenic toxicity
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References and further reading may be available for this article. To view references and further reading you must purchase this article.


<!-- refMsg -->Subhankar Das, Amal Santra, Sarbari Lahiri and D.N. Guha Mazumder^,

<!-- authorsNoEnt -->Institute of Post Graduate Medical Education and Research, Kolkata, India

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Received 23 June 2004;
<!-- articleText -->accepted 23 August 2004.
<!-- articleText -->Available online 30 November 2004.
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<!-- articleText -->Abstract

Introduction:

Noncirrhotic portal fibrosis has been reported to occur in humans due to prolonged intake of arsenic contaminated water. Further, oxystress and hepatic fibrosis have been demonstrated by us in chronic arsenic induced hepatic damage in murine model. Cytokines like tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) are suspected to play a role in hepatic collagenesis. The present study has been carried out to find out whether increased oxystress and cytokine response are associated with increased accumulation of collagen in the liver due to prolonged arsenic exposure and these follow a dose–response relationship.
Methods:

Male BALB/c mice were given orally 200 μl of water containing arsenic in a dose of 50, 100, and 150 μg/mouse/day for 6 days a week (experimental group) or arsenic-free water (<0.01 μg/l, control group) for 3, 6, 9 and 12 months. Hepatic glutathione (GSH), protein sulfhydryl (PSH), glutathione peroxidase (GPx), Catalase, lipid peroxidation (LPx), protein carbonyl (PC), interleukin (IL-6), tumor necrosis factor (TNF-α), arsenic and collagen content in the liver were estimated from sacrificed animals.
Results:

Significant increase of lipid peroxidation and protein oxidation in the liver associated with depletion of hepatic thiols (GSH, PSH), and antioxidant enzymes (GPx, Catalase) occurred in mice due to prolonged arsenic exposure in a dose-dependent manner. Significant elevation of hepatic collagen occurred at 9 and 12 months in all the groups associated with significant elevation of TNF-α and IL-6. However, arsenic level in the liver increased progressively from 3 months onwards. There was a positive correlation between the hepatic arsenic level and collagen content (r = 0.8007), LPx (r = 0.779) and IL-6 (r = 0.7801). Further, there was a significant negative correlation between GSH and TNF-α (r = −0.5336)) and LPx (r = −0.644).
Conclusion:

Increasing dose and duration of arsenic exposure in mice cause progressive increase of oxystress and elevation of cytokines associated with increasing level of collagen in the liver.

<!-- articleText -->Keywords: Arsenic; Hepatotoxicity; Proinflammatory cytokines; Oxystress

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<dl><dt>Introduction </dt><dt>Materials and methods </dt><dl><dt>Experimental protocol </dt><dt>Estimation of hepatic thiol </dt><dt>Estimation of protein oxidation </dt><dt>Estimation of hepatic catalase and glutathione peroxidase (GSH-Px) </dt><dt>Estimation of hepatic lipid peroxidation (LPx) </dt><dt>Estimation of tissue collagen content </dt><dt>Estimation of cytokines </dt><dt>Estimation of hepatic arsenic (As) content </dt><dt>Estimation of protein </dt><dt>Statistical analysis</dt></dl><dt>Results </dt><dl><dt>Effect of chronic arsenic exposure on Hepatic Thiol </dt><dt>Effect on hepatic glutathione peroxidase (GSH-Px) and hepatic Catalase activity </dt><dt>Effect on hepatic lipid peroxidation </dt><dt>Glutathione (GSH) vs. lipid peroxidation (LPx) </dt><dt>Effect on hepatic protein carbonyl (PC) </dt><dt>Effect on hepatic collagen content </dt><dt>Correlation of hepatic collagen content with lipid peroxidation (LPx) and protein oxidation </dt><dt>Effect on hepatic arsenic </dt><dt>Correlation of hepatic arsenic content with lipid peroxidation and hepatic collagen level </dt><dt>Effect on Hepatic TNF-α and hepatic IL-6 </dt><dt>Glutathione (GSH) vs. tumor necrosis factor (TNF-α) </dt><dt>Hepatic IL-6 vs. hepatic collagen</dt></dl><dt>Discussion </dt><dt>Acknowledgements </dt><dt>References</dt></dl>
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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 1. Data showing inverse correlation between GSH and LPx in the liver of control and experimental animals (r = −0.644, P < 0.001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 2. Concentration of total collagen in liver of control and experimental animals. Results are mean &#177; SD. a = P < 0.05, l = P < 0.001, sample size (n) = 10 in each group.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 3. Data showing positive correlation between hepatic collagen content and MDA level of control and experimental animals (r = 0.7177, P < 0.001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 4. Data showing positive correlation between the levels of protein oxidation and collagen content in the liver of control and experimental animals (r = 0.8149, P < 0.001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 5. Hepatic arsenic (As) content of the control and experimental animals at different months of As feeding. Results are mean &#177; SD. l = P < 0.001, Sample size (n) = 10 in each group.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 6. Data showing positive correlation between hepatic arsenic level and lipid peroxidation of control and experimental animals (r = 0.779, P < 0.001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 7. Data showing positive correlation between the concentration of arsenic and collagen in the liver of control and experimental animals (r = 0.8007, P < 0.001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 8. Concentration of TNF-α in the liver of control and experimental animals during different months of arsenic exposure. Results are mean &#177; SD. a = P < 0.05, d = P < 0.01, l = P < 0.001, sample size (n) = 10 in each group.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 9. Concentration of IL-6 in the liver of control and experimental animals. Results are mean &#177; SD. d = P < 0.01, l = P < 0.001, sample size (n) = 10 in each group.

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 10. Data showing inverse correlation between GSH and TNF-α level in the liver of control and experimental animals (r = −0.5336, P < 0.001).

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<table><tbody><tr><td width="10%"></td></tr></tbody></table>Fig. 11. Data showing positive correlation between IL-6 and collagen content in the liver of control and experimental animals (r = 0.7801, P < 0.001).

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Table 1. Results of various components of antioxidant defense system during increasing dose and duration of arsenic (As) feeding in mice

Results are mean &#177; SD. α = P < 0.05., β = P < 0.02, δ = P < 0.01, λ = P < 0.001, Sample size (n) = 10 in each group.

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Corresponding author. 37/C, Block B, New Alipur, Kolkata-700053, India. Fax: +91 033 24751799.

[AlaskaDenise]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

What's the best immediate solution? Selenium?

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[Shannon Bennett]

Re: Discussion - Arsenic, A Fatal Complication for Pandemic Flu?

I have lost my satellite connection. It will not be repaired until Saturday. Until then I am limited to a dial-up connection which will severely limit my ability to do more research.

As for the selenium, extreme caution needs to be taken as selenium toxicity may be irreversible and deadly. How much you are getting is dependent on soils in your area. Some places such as Kesterson in the Central Valley of California have extremely high amounts while the central plains of the U.S. have very low levels. Food grown in each of those areas will reflect how much is ingested.