Toxic
Metals: Emissions, Deposition, Health Effects, Controls & the relation
to incinerators, coal plants, acid rain, food, etc.
(
some
updates in 2023)
Heavy metals are naturally occurring
elements that have a high atomic weight and a density at least 5 times greater
than that of water. Their multiple industrial, domestic, agricultural,
medical
and technological applications along with emissions
from burning coal have led to their wide distribution in the environment and
food supply, raising concerns over their potential effects on human health and
the environment.
Mercury
in
dental
amalgam
is a hidden source of
global
mercury
pollution
, resulting from daily excretion of significant levels into
sewers
and
thus fresh and saltwater rivers and bays by people with amalgam fillings and
from dental offices and the illegal diversion of dental
mercury
into
the artisanal and small-scale gold mining sector, to
crematoria
emissions
from the deceased and s
sewage sludge
that
is sold to farmers. Even after the last
mercury
dental
amalgam
is placed, its toxic legacy will continue for decades,
because of its pervasive bioaccumulation in the environment. Government
regulatory agencies should make it mandatory to utilize available technologies,
not only in developing countries, but also in developed countries, to reduce
mercury
contamination.
(2.4)
These significant
mercury
sources result in air, water, and food contamination that consequently have a
negative impact on human health (2.4).
Their toxicity of toxic metals depends on several factors
including the dose, route of exposure, and chemical species, as well as the
age, gender, genetics, and nutritional status of exposed individuals. Because
of their high degree of toxicity, arsenic, lead, mercury, cadmium, and chromium
rank among the priority metals that are of public health significance (1a).
These metallic elements are considered systemic toxicants that are known to
induce multiple organ damage, even at lower levels of exposure. They are also
classified as human carcinogens (known or probable) according to the U.S.
Environmental Protection Agency, and the International Agency for Research on
Cancer. (2.2)
Exposure to these toxic heavy metals is common and low
levels of exposure are documented to cause chronic systemic oxidative stress,
mitochondrial dysfunction, and inflammation, which as shown
here
synergistically
cause
immune, cardiovascular, neurological, endocrine, allergy, and fertility
problems or conditions.
N
- acetylcysteine (NAC),
a precursor of glutathione, affords protection against lead-induced
cytotoxicity and oxidative stress (9.6d).
Long-Term
supplementation with the algae extract (Chlorella
and Fucus
sp
)
and
Aminosulphurate
Supplementation
modulate SOD-1 activity and decrease heavy metals (Hg
++
,
Sn) levels in patients with long-term dental titanium implants and/or
amalgam- fillings
restorations. (9.6c)
The original source
of much of the information for this review was the reading files or summary
articles of the State Pollution Control Agencies of Florida, Minnesota, and
Wisconsin, and the U.S. EPA from the 1980s and 90s, along with updates and newer
information from the
NIH
Pubmed
abstract
files and medical newsletters. This paper has been periodically updated since
that time until now.
The health effects of toxic metals are
synergistic
with
other toxic exposures s
uch
as
pesticides
, herbicides,&
other
endocrine
disrupting substances
like organochlorine compounds
, POP
s,
PAHs
,
PCBs, etc. There are also synergistic effects with the various types of
parasites, bacteria, viruses to which people have common exposures and commonly
become infected when the immune system is weakened by toxic exposures. Studies
have found considerable genetic variability in
susceptibility
to
toxic metals as well. The health effects caused
pesticides
and herbicides
include neurological conditions such as
Alz
.
Disease, ALS., Multiple Sclerosis,
Parkinson�s
, ADHD,
seizures, developmental conditions, etc. as well as
autoimmune
conditions
such as Diabetes, Rheumatoid Arthritis, Lupus, etc.
While there is considerable commonality to the health effects commonly caused
by the toxic metals, and effects are cumulative and
synergistic
with
other toxic exposures, this paper will concentrate on the health
effects of elemental mercury from amalgam fillings and toxic metals.
I. Health Effects of Toxic Metals (mercury, lead, cadmium,
chromium, etc.)
II. Mercury in Fish and the Food Chain of Lakes and Streams and
Bays
III. Effect of Toxic Metals on Forests and Plant Ecosystems
IV. Sources of Mercury Emissions and Mercury Content of Fuels
V. Emissions of Other Toxic Metals from Human Activities
VI. The Relation of Acidity and Acid Rain to Toxic Metal Impacts on
Aquatic Systems, Fish, the Food Chain, and Health
VII. European Experience with Mercury Emissions
VIII. Experience with Emissions Control Equipment for Toxic Metals and
Mercury Reduction Options
IX. Toxic Metals in Flue Ash and Bottom Ash
X. Heavy Metals and Drinking Water
XI. Toxic Metals from Sewer Plants and
Urban
Runof
Toxic metals
(mercury, lead, cadmium, aluminum, etc.) appear to be the number one
environmental health threat in Florida and most states currently and appear to
be seriously affecting thousands of Floridians, especially children and older
people (1-1.7,2,2.2, etc.). Toxic metals have been documented to
be neurotoxic, as well as reproductive and developmental toxins.
Occupational exposure to mercury and toxic metals are documented to commonly
cause chronic health conditions (1.8,1.9,2.2,9.8,46, etc.).
Synergistic effects
of multiple exposures (38) and
susceptibility factors
that reduce the bodies detoxification processes are a major reason
that some are affected by exposures more than others. A study found that for
low levels
of
lead
, cadmium, arsenic, and mercury,
combined exposure disrupted brain synaptic homeostasis even though the levels
of each were supposedly low safe levels (71).
Over 60 % of Florida lakes
and rivers tested last year by the Game and Fresh Water Fish Commission had
dangerous levels of mercury in the fish and food chain (33) and over 20%
of all U.S. lakes have similar warnings (64). High levels of mercury are
also being found in other wildlife such as frogs, turtles, raccoons,
alligators, etc. with many birds and an endangered Florida panther being killed
by high levels of mercury. Florida is one of a
growing list
of
at least 40 states and 4 Canadian provinces (20,64) with bans or limits on
eating fish from thousands of lakes or rivers with dangerously high levels of
mercury in fish. Europe has similar experience. Dangerous levels of
mercury have also been found in shark, tuna, sea
trout,
sailcat
, mackerel, bluefish, etc., as well as
toxic metals in shellfish (17a). Over 90% of the health risk to
the public (and animals) from toxic metals such as mercury (as well as
from dioxin) has been found to be related to such toxics that are bioaccumulating in
the food chain.
Mercury, cadmium, and lead
have been found to be
estrogenic chemicals
that disrupt the endocrine/reproductive/ hormonal
systems of animals at low levels of exposure, with serious adverse seen on
animals and humans (14.5,14.7). They are also well documented to be neurotoxic
and to commonly cause major chronic neurological conditions.
Lead
is a
persistent
toxic
metal
and associated with impairment of various body functions in occupational
workers. A study results (9.8a) revealed that lead-exposed workers had
significantly high BLLs, median (range), 29.1 (9.0-61.1)
microg/dL compared with controls, 8.3 (1.0-21.6) microg/dL.
IntraOcularPressure
was
associated with
blood
lead and
mercury levels (46).
Oxidative
stress (MDA, GGT) and inflammatory markers (high-sensitivity CRP) were
significantly increased.
Blood
pressure
was
raised, whereas hemoglobin was decreased in exposed group. Serum urea, uric
acid, phosphate, and ALT were significantly raised in lead-exposed workers.
Serum albumin, total proteins, and glomerular filtration rate (GFR) were
decreased.
Blood
lead
showed a significant positive correlation with serum GGT, MDA, CRP, urea,
creatinine, and uric acid. It was concluded that lead exposure increases
oxidative stress that correlates with adverse changes in hematological, renal,
and hepatic function in the occupational workers.
Elevated blood
lead
has positive correlation with oxidative stress, inflammatory and biochemical
markers that might be used to detect impairment in the body function in lead
exposed workers.
A meta-analysis of occupational exposures found that
lead exposure increased the risk for ALS and
Alzheimer�s
and
Parkinson�s
by at least 60% (9.8b). Other studies
found that lead causes hypertension (9.8,46).
The prominent mechanism of action
associated with the development of hypertension seems to be oxidative stress
and kidney damage for lead, while increased RAS activation links methylmercury
to hypertension (9.8d). Not only are heavy metals and arsenic associated with
high blood pressure, but phthalates are also; and all of these have
synergistic
effects
(9.8e). A meta-analysis found that
there was a significant positive association
between
mercury
and
hypertension and between
mercury
and BP (9.8f). Another study showed that the mean
values of Cd and Hg were significantly higher in scalp hair
and blood
samples
of hypertensive patients as compared with healthy controls, whereas Zn and Se
concentrations were found to be lower in hypertensive patients (9.8g). The
levels of both Hg & Cd were 2-3-folds higher in scalp hair
and blood
samples of non-hypertensive
smoker subjects as compared with nonsmoker controls. It was observed that
exposure of Toxic Elements via cigarette smoking may be synergistic with other
risk factors associated with hypertension. In a representative sample of
the Korean adult
population, blood
Manganese
level was associated with an increased risk of hypertension( 9.8h).
Urinary
concentrations of several phthalate metabolites at age 3 years, compared to
other time periods, were more strongly associated with decreased cognitive
abilities in a group of children
tested( 9.8e
).
Exposure to cadmium in the
jewelry industry is a significant source of occupational cadmium exposure.
Other occupational sources include the manufacture of nickel-cadmium batteries,
metal plating,
zinc
and lead refining, smelting of
cadmium and lead, and production of plastics(40b). Cadmium is also an
environmental pollutant that accumulates in leafy vegetables and plants,
including tobacco. Major toxicities anticipated from cadmium exposure involve the
renal, pulmonary, and, to a lesser extent, gastrointestinal systems. These
include the development of renal proximal tubular dysfunction, glomerular
damage with progressive renal disease, and respiratory symptoms including
pneumonitis and emphysema. Low-level cadmium exposure has also been associated
with increased urinary calcium excretion and direct bone toxicity, effects that
recent research suggests may result in the development of osteoporosis. The
body burden of cadmium, over half of which may reside in the kidneys, is most
often measured
through the use of
urinary cadmium
levels. Blood cadmium measurements generally reflect current or recent exposure
and are especially useful in cases with a short exposure period and only
minimal accumulation of cadmium in the kidneys. Both ss2-microglobulin and
alpha1-microglobulin serve as organ-specific, early-effect biomarkers of
tubular proteinuria and thus play a role in identifying early signs of
cadmium-induced renal damage in those with potential exposures(40b).
Cadmium (and mercury) has
been found to be a major cause of neurological dysfunction such as Alzheimer's
disease and other dementia (15.1,5,9.7d). Cadmium has also been
shown to be toxic to the testes and sperm at
fairly low
levels and to damage the placenta, which can cause damage or death to
the fetus (46).
A
study found that cadmium is significantly associated with metabolic syndrome
(40c).
A 2-fold increase in mercury concentrations at 16-
weeks
gestation
was associated with 0.83 point- higher BASC-2 anxiety scores. Maternal and cord
blood mercury concentrations at delivery were associated with parent-reported
anxiety at 8
years (9.7a). Among
boys with low level gestational lead exposure, a study found lower scores for
cognitive functions, along with increasing cord blood lead levels (9.7b).
Several studies have found Arsenic to be significantly associated with type 2
diabetes and other conditions (9.5a). Total urine arsenic was
associated with increased prevalence of type 2 diabetes, and since there
is a widespread exposure worldwide this finding supports the hypothesis that
low levels of exposure to inorganic arsenic in drinking water may
play a role in diabetes prevalence. Arsenic multifactorial
effects include accelerating birth and postnatal weight gains, elevated body
fat content, glucose intolerance, insulin resistance, and increased serum lipid
profile. Arsenic also elevated cord blood and placental, as well as
postnatal serum leptin levels. The data from human studies indicate an
association between inorganic arsenic exposure and the risk
of diabetes and obesity. �A study also found polymorphisms in
diabetes- related genes to be a factor in toxic effects (9.5a). Studies
(9.5b,61
b) support
the role of maternal
exposure to heavy toxic metals that persist longtime in the
environment as a risk factor for Gestational Diabetes Mellitus.
Mercury is
according to EPA the most toxic substance people commonly come in contact with
and is a common cause of
most chronic health conditions
, including
immune conditions
;
autoimmune conditions
,
cardiovascular
condtions
,
endocrine conditions
,
allergic conditions
,
neurological conditions
, etc. Dental amalgam is the
largest source of mercury
in most people who have amalgam fillings, with
continuous vaporization of
mercury
in
all who have amalgams, which is increased by
galvanic action of mixed
metals
in the mouth, and by common exposure to
EMF, wi-fi, and microwaves
which increases vaporization of dental amalgams. Some people are
more easily affected by mercury and toxic metals than others, due to metals
immune reactivity(16.2),
susceptibility factors
such as blood allele type or factors which reduce
people�s
natural detoxification ability, and
synergisms with other toxic
exposures
or EMF or wi-fi. Most people with any of these
chronic conditions who have dental amalgams usually
recover or significantly
improve
after safe amalgam
replacement with proper immune support (16.2, etc.). This is often also true
for those with
mixed
metals
such
as gold crowns, which are often placed over amalgam
fillings and have continuous mercury exposure, or titanium implants with
amalgams, or other metals (16.2). The metals people are found to be most
commonly immune reactive to are nickel, gold, palladium, mercury, and titanium
(16.2a). Blood lymphocyte immune reactivity tests are the most effective at
assessing such immune reactivity (16.2), but patch tests can also be used
though slightly less effective (16.2).
Most of the mercury in Florida lakes and soils is from atmospheric
deposition, and the main sources of air emissions are municipal incinerators,
medical waste incinerators, and coal combustion. Dental amalgam which is
the
largest source of mercury in sewers
is also a significant source in rivers, lakes, and fish
(14.9). A Dept. of Environmental Protection report said that past
tests indicate that Florida incinerators and power plants were emitting approx.
6 tons and 3.4 tons per year of mercury emissions to the Florida
environment. Such facilities also emit large volumes of lead,
cadmium, and other toxics. Of the approx. 6 tons of
mercury generated in Fla. by coal plants, approx. 50% appear to be as air
emissions with the rest going into the ash. Ash from incinerators and coal
plants is a large and continuing problem. There appear to be only minor
natural sources of mercury in Florida, other than recycling of previously
deposited mercury by plants, soils, etc. which is significant in some areas. Coal
plants from other states and oil combustion in Florida together appear to
deposit almost as much mercury as Fla. coal plants, but Florida plants also
affect other states.
Studies in Wisconsin and Canada indicated only one gram
of mercury per year deposited in an average sized lake (25 acres) is sufficient
to contaminate fish and the food chain at dangerous levels requiring a fish
consumption ban or limitation (18). The amount of mercury emissions
each year by incinerators and coal plants (36 grams/square mile) are
enough to uniformly deposit 16 grams and 20 grams per square mile respectively,
for each of the 53,800 square miles of Florida. These levels
each appear to be well above the level of deposition required to cause
dangerous levels of mercury in fish throughout the state (2.5 gm/
sm
)
,
especially in lakes with low acidity or low alkalinity like many of Florida's
lakes (1.5,1.6). The average level of deposition into Minnesota lakes with
mercury health warnings was 13 micrograms per square meter (34 grams per
square mile) and for
Florida
the average deposition throughout Florida in 2001 was 17.6
micrograms per square
meter( 1.5b
).
The levels of the toxic metals- mercury,
lead, cadmium, copper, selenium, arsenic, zinc, and silver are increasing
cumulatively in the environment due to atmospheric emissions from human
activity. Mercury levels in Minnesota, Wisconsin, Canada, and Sweden
were found to be increasing in sediments, soils, and fish at rates between 2%
and 5% per year. Levels in Florida have also been found to be
increasing by a Univ. of Florida study. Toxic metals were found in
water body sediments sampled at levels exceeding the FDEP toxics criteria in
30% of "reaches" sampled for mercury, 15% for cadmium, 20% for
copper, 15% for lead, etc. The higher rates were in areas with major emission
sources and in recent years. At this rate of increase, levels double
in as little as 10 years. Levels of toxic metals in soils and plants
in industrial areas were found to be doubling in many cases every 3 to 10
years. Mercury, lead, cadmium, and manganese are now being deposited
in some areas at levels toxic to humans as well as other animals and
plants. The other toxic metals previously listed are being deposited
at levels toxic to plants or other organisms.
High
levels of other toxic metals have also been found in drinking water, surface
water, sediments, and the food chain throughout Florida. Toxic metal air
emissions have been suggested to be a factor in high lung cancer rates of some
areas of North Florida. Toxic metals have been documented to cause large
numbers of learning disabilities, neurological disorders, vascular disease,
hormonal problem, reproductive problems, and kidney disease (5,1.8,14.7,27), as
well as being major factors in the promotion of cancer and birth defects
(7.5,7.6). Approximately 250,000 U.S. children are born each year
with birth defects diagnosed at or shortly after birth. Birth defects are the
leading cause of infant mortality in the United States. Congenital anomalies,
sudden infant death syndrome, and premature birth combined account for more
than 50% of all infant mortality (62).
According to Federal studies, thousands of
children appear to have their learning ability and health permanently adversely
affected in Florida each year. Because of this, all school systems were ordered
by EPA to have their water systems tested. Over 20% of
Leon county
school water fountains were found to have
dangerous levels of lead in the water, and higher levels were found in some
other counties. An EPA drinking water survey found that the average
lead level in drinking water in many areas of Florida was above the EPA
drinking water standard of 20 parts per billion, a level shown high enough to
cause significant health effects. A large
proportion of drinking water in some areas of Florida appears to have dangerous
levels of lead from pipes, solder joints, brass fixtures, or water
fountains.
The increase in toxic metals in water and
the food chain has been shown to be related to increased acidity of drinking
water and surface water. Additional sources of large amounts of metals in
bay, lake, or river sediments are sewer or industrial outfalls
and urban runoff.
I. Health Effects
of Toxic Metals (mercury, lead, cadmium, chromium, copper,
nickel, etc.)
1. The levels of the toxic metals-
mercury, lead, cadmium, copper, selenium, arsenic, zinc, and nickel are
increasing cumulatively in the environment due to atmospheric emissions from
human activities (1.9,2,2.1,16.3,1). Mercury, lead, cadmium,
nickel, and manganese are now being deposited through atmospheric emissions in
many areas at levels toxic to humans, as well as to other animals and
plants. The average annual percent increase in emissions of
these metals has ranged from 1.5% to 5% (2), with accumulation in soils and
plants in some industrial areas of the U.S. and Europe doubling in between 3 to
10 years and in many cases reaching levels known to cause critical health
problems. Studies of human bones have found a 500- fold increase in the
levels of toxic metals such as lead currently as opposed
to preindustrial times. A large British study
(15.1) found a statistically highly significant,
age related
increase in the levels of toxic metals (aluminum, mercury, arsenic, cadmium,
lead) accumulating in the British population, as measured in hair, blood, and
sweat samples. Increasing body burdens of these toxic metals have been found to
be widely accumulating in industrial country populations throughout life, with
increasingly significant adverse health effects due to this accumulation
as populations age. Brain function and kidney function are
being especially adversely affected in large segments of the population of
industrial countries over 40 years of age.
There has been a large increase in depression,
impulsivity, and dementia in the U.S. since 1945 (5,15.1) and toxic metals
such as lead, mercury, and cadmium have been found to adversely affect levels
of brain neurotransmitters resulting in these conditions
(3.1,9.3,9.7,15.1,5,1.8). A study in China found that toxic metal exposure
appears to be a significant factor in Schizophrenia (69). Studies have found
that
mercury
is often a factor in
schizophrenia
,
depression
,
mood disorders, etc.
Nutritional deprivation in the early stage of life
increases the risk of developing schizophrenia(69b). Oxidative stress,
disturbed thinking and irrational behavior which are common to schizophrenic
patients may be a result of changes in the levels of certain essential trace
metals. A study found Pb, Cd and Cr were significantly raised in newly
diagnosed drug free schizophrenic patients compared with controls. (60b) Fe and
Se were significantly reduced in newly diagnosed and medicated-schizophrenic
patients compared with controls.
Mercury
and other toxic metals block an enzyme needed to digest gluten in wheat
products and casein in most
cow�s
milk products. The
result is formation of
gluteomorphins
and
caseomorphins
,
which act
like morphine and contributes to autism, schizophrenia, and ADHD
.
Detoxification of toxic metals and avoidance of products with gluten (wheat)
and casein (milk) was found to be the
two most
effective treatments
in a large survey of parents of autistic
children by the Autism Research Institute, and likewise for other related
conditions such as ADHD,
depression
, mood disorders,
schizophrenia.
A study (72
)
used
data
from 389 mothers and children in a prospective pregnancy and birth cohort
study. They defined mean
prenatal
mercury
concentration
as the mean of total whole blood
mercury
concentrations in maternal samples collected at
16- and 26-weeks of gestation, delivery, and neonatal cord blood samples and
assessed parent-reported child behavior up to five times from two to 8 years of
age using the Behavioral Assessment System for Children (BASC-2)
. A 2-fold increase
in
mercury
concentrations
at 16-
weeks
gestation was associated
with 0.83 point (95% CI: 0.05, 1.62) higher BASC-2 anxiety scores. Maternal and
cord
blood mercury
concentrations
at delivery were associated with parent-reported anxiety at 8
years.
Coal ash, generated from coal combustion, is composed of
small particles containing metals and other elements, such as
metalloids. Components of coal ash include heavy metals like
lead, mercury, and arsenic. A study assessed health effects of living
close to a coal ash site
(73). Attention-deficit hyperactivity disorder, gastrointestinal
problems, difficulty falling asleep, frequent night awakenings, teeth grinding,
and complaint of leg cramps were significantly greater in the children living
near coal ash. The odds of allergies excluding
asthma, attention-deficit hyperactivity disorder,
gastrointestinal problems, difficulty falling asleep, frequent night
awakenings, sleep talking, and complaint of leg cramps were greater in children
living near coal ash compared to children not living near coal ash
(non-exposed). Several components of coal ash, such as heavy metals like
lead, mercury, and arsenic, may be associated with health and sleep
problems in children.
A study of
student�s
levels
of toxic metals found that diet pattern affects the level of toxic metals
(70a).
Dietary patterns were
defined using factor loading scores for 108 foods from a Semi-Quantitative Food
Frequency Questionnaire. A high blood Hg level was found in boys with a high
score in the 'fish' pattern, and in girls with a high score in 'fruit' pattern.
The concentration of Pb was related to the 'imprudent' pattern in
high school boys. The effect of the 'vegetable' pattern on high excretion of
urinary Cd was observed in low grade elementary and middle school students, and
the effect of the 'fruit' pattern on the urinary Cd was observed in high grade
elementary school students. Another study (70b) concluded that: considering the
serious contamination of some samples of raw and pasteurized milk by
Cd, Pb and Zn, a control of heavy metals content during the
whole production processing of milk must be applied. Oxidative stress (OS) is
an important consequence of exposure to toxic metals. A study (70c)
of Uruguayan school children found that arsenic concentrations were positively
associated with 8-OHdG concentrations, a marker for oxidative stress. In sum,
even at low-level, Arsenic exposure is associated with detectable oxidative
damage to the DNA.
2. The U.S. Center for
Disease Control ranks toxic metals as the number one environmental health
threat to children, adversely affecting millions of children in the U.S. each
year and thousands in Florida (1.7,2.3,1). According to an EPA/ATSDR
assessment, the toxic metals lead, mercury, and arsenic are the top 3 toxics
having the most adverse health effects on the public based on toxicity and
current exposure levels in the U.S. (1,9.3), with cadmium,
chromium
and nickel also highly listed. A National Academy
of Sciences Report (65) found that 50% of U.S. pregnancies result in birth
defects or neurological conditions or other chronic developmental problems.
Researchers have documented that the majority of these are due to
toxic exposures (5,7.5,14,5,14.7,1.8, etc.) According to
studies reviewed, over 16% of all children in the U.S. have had their learning
ability (
ADHD
, dyslexia,
autism
,
learning disabilities
) significantly adversely affected by toxic metals such
as lead, mercury, and cadmium; and over 60% of children in some urban
areas have been adversely affected (1.7,5,6,9,15.1,46,47). The toxic
metals have been documented to be reproductive and developmental toxins,
causing birth
defects
and damaging fetal development,
as well as neurological effects, developmental delays, learning disabilities,
and behavioral abnormalities in many otherwise normal-appearing children
(5,6,7.5,9.1,9.3,9.7,19,46,47,1.8). Other neurological
disorders are also increasing, partly due to exposure of millions of American
workers to neurotoxic substances such as toxic metals
and pesticides (15.1).
3. Lead poisoning is the most prevalent environmental
disease in the U.S along with mercury toxicity. According to an EPA
survey, over 10% of all Americans and over 20% of all black children under 2
carry unsafe levels of lead in their bodies (over 10 mcg/dl) (9). In
an urban east coast area, almost half of children tested in 1998 had lead
levels exceeding the federal blood levels guideline (54).
In a study of Inuit
children, cord blood mercury concentrations were associated with
higher
TeacherReportForm
(TRF)
symptom scores for attention problems and
DisruptiveBehaviorDisorders
(DBD)
scores consistent with ADHD. Current blood Pb concentrations were
associated with higher TRF symptom scores for externalizing problems and with
symptoms of ADHD (hyperactive-impulsive type) based on the
DBD( 7.5d
).
Lead is a leading cause of birth defects,
cardiovascular disease, hypertension, neurological disease, kidney disease,
learning disability, retardation, tooth cavities, etc. (2‑3,5,6 bc,8‑9,15.1,28,41). An
increased lead burden of 5 ug/L in the blood corresponded to an increase
in cavities of 80% (41). Lead also has been shown to depress the immune
system and increase cancer rates (1.3,9).
Metal genotoxicity
is caused by indirect mechanisms (49).
The
three predominant
mechanisms of cancer causality by toxic metals are: (1) interference with
cellular redox regulation and induction of oxidative stress, which may cause
oxidative DNA damage or trigger signaling cascades leading to stimulation of
cell growth; (2) inhibition of major DNA repair systems resulting in genomic
instability and accumulation of critical mutations; (3) deregulation of cell
proliferation by induction of signaling pathways or inactivation of growth
controls such as tumor suppressor genes. In addition, specific metal compounds
exhibit unique mechanisms such as interruption of cell-cell adhesion by
cadmium, direct DNA binding of trivalent chromium, and interaction of vanadate
with phosphate binding sites of protein phosphatases. The toxic metals mercury,
cadmium, arsenic, nickel, and lead have been documented to cause or be a factor
in causing
many types of cancer
. Studies have shown
most have toxic metal accumulations and test with detox is appropriate and
useful in recovering health. (9.6)
Federal studies indicate that exposure to lead in
the environment reduces the IQ of hundreds of thousands of U.S. children each
year and causes pregnancy complications to over 500,000 U.S. women
each year (2.3, 2.3). Children aged 7 to 11 with high levels of
lead in their bones were found to exhibit much higher levels of attention
problems, aggressive/violent behavior, and delinquency than those with lower
levels (5).
Nanoparticles affect immune functions,
causing different immune responses. Study data showed a statistically
significant increased level of the pro-inflammatory cytokine TNF-α in serum in
both exposed industry groups compared with office workers, as well as a higher
level of TNF-α in workers from the woodworking company compared with the
metalworking employees(9c). We found an elevated level of IL-6 in the exposed
groups as well as an elevated level of IL-8 in the nasal lavage in woodworking
employees after work.
A one-year sampling campaign of road dusts was carried out
at 10 distinct sites in the broader area of the city of Thessaloniki,
Greece
and concentrations of heavy metals (HMs)
along with magnetic susceptibility were evaluated(9d). Non-exhaust vehicular
emissions, oil/fuel combustion and industrial activities as major sources of
heavy metals accounted for approximately 73% of the total variance.
Concentration peaks in the urban cluster were observed for Cd, Mn, and Ni
coinciding with the port area. Based on multiple pollution indices, a severe
polluted area was revealed, while potential ecological risk index (RI)
indicated a high potential ecological risk with Cd being regarded as the
pollutant of high concern. The health risk assessment model indicated ingestion
as the major exposure pathway. For both adults and
children,
Cr
and Pb had the highest risk values,
mainly recorded in
the urban cluster underscoring the need of potential measures to reduce road
dust in urban environments(9d).
�Mercury also has been documented to cause,
cardiovascular
disease,
neurological
disease, and
other conditions
.� Study
results suggest that
angiotensin II
AT-1 receptors upregulation might play a key role in
the vascular damage induced by Hg exposure- by increasing oxidative stress and
probably by reducing NO bioavailability (38b). A study found
prolonged
intake of heavy metals (cobalt,
cadmium
and mercury) leads to the development of marked hemodynamic disturbances,
combined with a sharp increase in the level of lipid peroxidation products in
the blood(38c). Melatonin under intoxication by heavy metals significantly
reduced hypertensive effect of heavy metals on systemic hemodynamics,
which
together
with a reduction of lipid
peroxidation processes allows one to consider the activation of lipid
peroxidation as one of the major pathogenic factors in the development of
hemodynamic disorders in conditions of heavy metal poisoning.
Drinking
water is a major source of lead in humans according to
EPA. Other major sources are lead in old
paint, lead solder in cans, lead in soils from previous gasoline exhaust, lead
emissions from incinerators, and lead in food chain (1.2). EPA
studies show that hundreds of thousands of school children are being exposed to
dangerous levels of lead in drinking water from fountains at U.S. schools
(2.3, 2.3). Levels from gasoline exhaust and cans have decreased in
the U.S.,
but are
still extremely high
in some other countries.
Studies
have confirmed lead in drinking water is a major problem in Florida
(2.3). Millions of people are exposed to dangerous levels of lead
and other toxic metals through home drinking water which has absorbed lead or
other toxic metals from pipes,
solder
joints
,brass
fixtures,
etc.
according to EPA
(2.3,2.6). An EPA drinking water survey (2.3, 2.8) found that
the average lead level in drinking water in many areas of Florida was
above the EPA drinking water standard of 15 parts
per billion
( parts
per billion(ppb)., a level high enough to cause significant health
effects. Counties with a significant number of homes above the EPA
standard were Escambia, Brevard, Volusia, Lee, Broward, and Dade.
4. Lead has been shown to
be one of the most potent promoters of cancer and birth defects (2.2,
9). In a Swiss study of residents living on a busy roadside, a group
of residents having free blood lead removed by calcium EDTA treatment was
compared to a control group that did not. 17% of those not
having lead
removed
died of cancer while only 1.7% of those having lead removed died of cancer
(2.1).
A
Boston area study found lead to be a potent promoter of birth defects. The
study suggests that as much as 46% of all birth defects in the area
were facilitated by or related to level of lead in the blood of the
fetus. Low levels of lead were found to promote birth defects, with
a blood lead level of 6.3 micrograms per deciliter(mcg/dl) being associated
with an 87% increase of birth defects. A blood lead level of 15
mcg/dl had a 137% higher risk of birth defects relative to the group with
less than 0.7 mcg/dl (9). (1
mcg/dl=10ppb)
Toxic
metal exposures have been found to commonly cause miscarriages, stillbirths,
spontaneous abortions, and infertility (42,46). A study of African countries
found that high levels of the toxic metals mercury, cadmium, lead, arsenic, and
chromium caused higher miscarriage and stillbirth rates(42c).
In Nigeria(42c), pregnant women with high lead levels
(BLL>25 ug/dL) had a 42% higher risk of miscarriage than those with lower
lead levels, and similar for Egypt. High cadmium levels resulted in an 84%
increase in miscarriage risk and 9.5% higher risk for high mercury levels
compared to those with lower levels. Similar higher risk levels were also found
in other countries.
Cadmium has also been
found to be a promoter of sperm abnormalities, birth defects, uterine fibroids,
infertility, spontaneous abortions (1.5,3,42,46,51), lung and brain cancer
(40,49,40), and peripheral neuropathy. (56)
Epidemiological
studies have shown that there exists a correlation between cadmium exposure and
human cancers(40a). The evidence that cadmium and cadmium compounds are
probable human carcinogens is also supported by experimental studies reporting
induction of malignant tumors formation in multiple species of laboratory
animals exposed to these compounds. In vitro studies with mammalian cells have
also shown that cadmium is clastogenic. Study results indicate that
metallothioneins
and
heat shock proteins appear to be excellent candidates for biomarkers for
detecting cadmium-induced proteotoxic effects at the molecular and cellular
levels (40a).
5. Studies reviewed
suggest that exposure to toxic metals may account for as least 23% of learning
disabilities, 20% of all strokes and heart attacks, and in some areas be a
factor in over 40% of all birth defects. Primary exposure to lead is from
drinking water, auto and industrial emissions, and lead in
paint. Cadmium, mercury, chromium, arsenic, silver, copper, and
aluminum are other metals to which Floridians are commonly exposed in drinking
water or the food system (3).
Arsenic exposures
are very common and cause numerous types of toxic harm.
A comprehensive
analysis of published data indicates that arsenic exposure induces
cardiovascular diseases, developmental abnormalities, neurologic and
neurobehavioral disorders, diabetes, hearing loss, hematologic disorders, and
various types of cancer (50). Recent reports have pointed out that arsenic
poisoning appears to be one of the major public health problems of pandemic
nature. Acute and chronic exposure to arsenic has been reported in several
countries of the world where a large proportion of drinking water (groundwater)
is contaminated with high concentrations of arsenic. Research has also pointed
significantly higher standardized mortality rates for cancers of the bladder,
kidney, skin, liver, and colon in many areas of arsenic pollution (50). Arsenic
is often found at high levels in drinking water (50b).
6.
A
study showed that
developmental
lead
(Pb)
exposure since fetal period can cause lasting impairments in physiological
parameters. The
intermittent lead
exposure
causes adverse health effects,
i.e
,
hypertension, increased respiratory frequency and chemoreflex sensitivity,
baroreflex impairment, anxiety, decreased synaptic activity, neuroinflammation
and reactive gliosis, in some ways similar to a permanent exposure, however
some are lower-grade due to the shorter duration of exposure( 4.5a).
In a large national
study, blood
lead
levels (BLL) were significantly correlated with higher systolic BP among black
men and women, but not white or Mexican-American participants. BLLs
were significantly associated with higher diastolic BPs among white men and
women and black
men( 4.5b
). Black men in the
90th percentile
of blood
lead distribution� compared to
black men in the 10th percentile of
blood
lead distribution had a significant increase of
risk of having hypertension. In
addition, blood
cadmium
was significantly associated with hypertension
and systolic and diastolic
blood
.
Researchers at the
U.S. Public Health Service and at Harvard Univ. have found that blood pressure
in men increases significantly at 20 mcg/dl blood level compared to 10
mcg/dl (4.5).
Another study found a linear relation between
elevated blood lead and blood pressure down to 7 mcg/dl
(4.5). Other studies have also found both lead and
cadmium to be significant causes of high blood pressure, heart
attacks, and stroke (4.5 & 3). Another large national study (4.5e)
found
BLL
was associated with systolic BP in non-Hispanic whites and
with hypertension and systolic and diastolic BP in non-Hispanic blacks. BLL was
not associated with BP outcomes in Mexican Americans. Non-Hispanic white ALAD2
gene carriers in the highest BLL quartile (3.852.9 microg/dL) had a
significantly higher adjusted prevalence odds ratio for hypertension compared
with ALAD1 homozygous individuals. The study also found a significant
interaction between lead concentration and the ALAD2 allele in non-Hispanic
whites and non-Hispanic blacks in relation to systolic BP.
7. A study of school
children in Maryland found that both lead and cadmium had significant impacts
on learning ability. The group of children labeled gifted by teachers all had
low levels of blood lead, while all children with blood lead levels of 50 ppm or
more were in the very low achiever group. There was a very high correlation
between blood lead level and achievement group (5). These results
were also confirmed by
a recent
medical
studies published in The New England Journal of Medicine (6)
and other studies (2.6,5,6,15.1,46,47).
8. Exposure to the 5 heavy
metals tested for in a study of school children accounted for 23% of the
variation in test scores for reading, spelling and visual motor skills
(6,15.1). A Canadian study found that blood levels of five metals were able
to predict with a 98% accuracy which children were learning disabled
(7). Animals exposes to a very low-dose mixture of six metals displayed
severe growth retardation and other abnormalities in the exposed fetuses,
indicating a synergistic effect of the metals in combination (10.8,19.5).
9. Medical studies have
shown that low levels of lead in the blood of infants (as low as 6 mcg/dl)
have significant effects on
mental development and learning ability
. An
average level of 14.6 mcg/dl had serious
impacts (
8 , 8, 8, 2.6,5).
10. There is a significant
correlation between maternal blood lead level with birth weight and early
learning ability. Adverse effects were found as low as 8 micrograms
per deciliter (9 & 9.5 & 2.6).
11. A study of 14 to
19 year-
olds found
that the amount of lead
in the blood was the most important factor in hearing threshold levels in
children. Levels as low as 10 micrograms per deciliter had a
significant effect and there was no threshold level (8). The lead
blood level also was found to be a significant factor in the age at which a
child first sat up, walked, and spoke (8); as well as being related to
reductions in height of children (4.5).
12. A review of
studies involving cadmium suggest cadmium is as effective as lead at
causing high blood pressure and heart disease. Likewise, cadmium has
been found to produce learning disabilities and mental retardation in children
much like lead, as well as causing kidney damage (46d,40c), sperm
abnormalities, and sterility in men
(2,3,6,1.2,15.1,42b,47-51,46d). One study (53) found a
significant correlation between hair cadmium level and sporadic ALS (53). Cadmium
has also been found to bioaccumulate in the food chain and to be
reaching dangerous levels in shellfish and animals (28,3.3,1.2). Cadmium
has been found to be widely distributed in sediments of Florida's bays and
estuaries (3.3), Cd is acutely toxic to marine life at sediment levels as low
as 6.9 parts per trillion (parts per trillion(ppt) (3.3). Cadmium also
appears to be an endocrine system disrupter and to cause other biological harm
at lower levels (14.5). The FDEP NOEL (no observed effects level) is 1
part per million (ppm). The FDEP PEL (probable effects
level-lower limit of range associated with adverse biological effects) for
cadmium is 7.5 ppm. Cadmium levels is sediments of 4 harbor
areas in the Indian River Lagoon were found to be .6 to .8 ppm, with much
higher levels in several urban coastal areas (3.3,3.3). The U.S. EPA
(36c) toxics criterion for cadmium in seafood used in coastal monitoring
programs is 0.5 ppm. The FDEP NOEL for lead in sediments is
21 ppm and the PEL is 160 ppm, which are also exceeded in some
areas of Florida. The EPA toxics contaminant criteria for lead in seafood
is 0.5 ppm. The FDEP NOEL for copper of 28 ppm and for
chromium of 33 ppm are also exceeded in many areas of
Florida. The PEL for copper and chromium respectively are
170 ppm and 240 ppm (3.3). The EPA contaminant criteria for
copper in seafood is 15 ppm and for chromium is 1ppm. The
EPA criteria for zinc is 60 ppm.
13. European studies have
found a correlation between long‑term air exposure to cadmium levels in
industrialized urban areas with lowered kidney function
(12,15.1). Hundreds of thousands of people suffer from serious kidney
dysfunction due to cadmium (2,15.1). As a result of research
carried out by the Danish National Agency of Environmental Protection, the EEC
Council of Environmental Ministers has concluded that present environmental
levels of cadmium are potentially harmful, with harmful levels of cadmium
accumulating in the lungs, bone tissue, brain, and kidneys
(44). Cadmium (and mercury) has been found to be a major cause of
neurological dysfunction such as Alzheimer's disease and other dementia
(15.1, 5,9.7). Cadmium has also been shown to be toxic to the
testes and sperm at
fairly low
levels and to damage
the placenta, which can cause damage or death to the fetus (9.8,46).
Urinary cadmium (U-Cd) has been associated with decreased
peripheral bone mineral density (BMD) and osteoporosis(52a). In a large sample
of the U.S. population, women >or= 50 years of age with U-Cd levels between
0.50 and 1.00 microg/g creatinine were at 43% greater risk for hip-BMD-defined
osteoporosis, relative to those with levels <or= 0.50 microg/g.
A study (52b)
found
a
significant interaction between cadmium and menopause (p =
0.022). The results suggest negative effects of low-level cadmium exposure on
bone, possibly exerted via increased bone resorption, which seemed to be
intensified after menopause.
Significant
levels of cadmium have been found in the German food system. Sweden has
instituted a ban on many uses of cadmium such as for paint pigment, and other
European countries are considering such bans (3). Japanese studies
indicate the lungs, gastrointestinal system, and kidneys are especially
susceptible to cadmium poisoning. A daily intake of 200 ug of
cadmium was found to significantly increase kidney damage in humans. Normal
intake in diet is 50 to 80 ug (13). Cadmium from combustion emissions is
also accumulating in coastal estuaries and inland water-
body sediments
,
and is widespread in shellfish and other organisms. Cadmium is toxic
at relatively low levels and has serious impacts on the organisms in water
bodies that accumulate cadmium (4,1.2).
14. The heavy metals
(lead, mercury, cadmium) tend to concentrate in the air and in the food chain,
facilitating metal poisoning which is the most widespread environmental
disorder in the U.S. These heavy metals have also been found to be
endocrine systems disrupting chemicals having effects on the endocrine and
reproductive systems
similar to
the organochlorine chemicals (14,14.5,5). Estrogenic chemicals like
mercury have been found in Florida wildlife at levels that feminized males to
the extent of not being able to reproduce,
and also
had adverse effects on the female reproductive systems. Chromium is
also on the EPA Special Health Hazard Substance List because it is "a
cancer-causing agent and a mutagen"(1.1,51). Lungs & throat
are especially affected. (11.7& 1.1).
The soluble
hexavalent chromium Cr (VI) is an environmental contaminant widely recognized
to act as a carcinogen, mutagen and teratogen towards humans and animals. The
fate of chromium in the environment is dependent on its oxidation state.
Hexavalent chromium primarily enters the cells and undergoes metabolic
reduction to trivalent chromium, resulting in the formation of reactive oxygen
species together with oxidative tissue damage and a cascade of
cellular events (51).
15.
"The neurotoxicity of alkylmetals such
as
mercury
represents a major
environmental health problem which should be of international
concern."(1.7-1.9,9.3,9.7,17a,1,63) Mercury is found in 3 different
forms: elemental mercury vapor, inorganic mercury compounds, and organic
mercury. The organic methyl mercury form bioaccumulates to
very high levels in the food chain and readily crosses the brain membrane where
it can do severe irreversible damage (11,28,9.3,9.7,15.1,17a,
1.2). Fish and seafood are common sources of mercury in people, but other
sources of elemental mercury also result in methyl mercury since it is
commonly methylated by bacteria and yeasts in the mouth and
intestines to methyl mercury (1.8).
Dental
mercury amalgam
( silver
) fillings are
the
number one source
of
mercury in most who have amalgam fillings, (1.8,1.7) but this is also the
largest source of methyl mercury for many people since oral bacteria methylate
inorganic mercury to methylmercury. . Exposure levels for those with amalgam
fillings commonly
exceed
Gov
�t
health guidelines (1.8,1.7,1.2,), which is
0.2 ug/M3 for mercury vapor. Thousands also get harmful exposure levels
from occupational exposure such as working in dental offices
(1.8). Inhaled metallic mercury vapor
is able to
diffuse much more extensively into blood cells and various tissues
than inorganic mercury (57,1.8). Approx. 70% of
methyl mercury in consumed fish or food is absorbed and retained in the body.
The
Gov
�t
health guideline for organic mercury is
0.1 ug Hg /kg body weight (1.7). Mercury has been
extensively documented to have serious adverse health effects including brain
and neurological damage, kidney failure, birth defects, learning disabilities,
depression, impulsivity, etc.
(1.2,1.7,1.8,3,5,6,9.7,14.7,15.1,17a,17,19,63). Mercury has been
found to adversely affect the brain's neurotransmitter uptake of serotonin,
dopamine, acetylcholine, and norepinephrine which control the
body's neurologic functions (1.8,14.7). Low serotonin
levels have been shown to result in depression, anger, anxiety, aggression,
violence, insomnia, obesity, sexual deviance, and other impulse
disorders.
Epidemiological studies have found that human embryos are
highly susceptible to brain damage from prenatal exposure to mercury
(7.5,9.7,5,1.8,63). Levels in the fetus are usually higher than the blood level
of the mother, and significant levels of mercury are often found
in breast milk (7.5,9.2f,44b,1.8). Normal levels in breast milk range up to
1.0 ug/L Cd, 5 ug/L Pb, and 1.7 ug/L Hg, but
levels above this are commonly found.
Cadmium and mercury
was
detected in 100% and lead in 87%
of breast milk samples from Norwegian mothers (7.5e). Maternal seafood intake
alone explained 10% of variance in mercury exposure, while together with
amalgam fillings explained 46% of variance in Hg concentration in breast milk.
For Hg concentration in breast milk,
number of amalgam fillings
and
high fish consumption were significant predictors of mercury level.
ATSDR staff recommend screening levels for dangerous
effects of 5 ug/l Cd, 20 ug/L Pb, and
3.5 ug/L Hg(44b). Mercury has also been documented to
cause cellular DNA damage and cancer in animal studies (19b). Mercury has
been documented to be causing serious harm to birds, animals, and humans
(2,14.5,14.7,17a,17.4,18,19b, 28,33,1.8). Native Americans eating
fish on a regular basis have been found to have serious health effects. Over
100 Japanese died and many more were seriously affected neurologically where
infants suffered mental retardation, severe cerebral
palsy, incoordination, weakness, seizures, vision loss, etc. after eating
fish contaminated with 10 to 20 parts per million(ppm) methyl mercury (about
1000 micrograms per 1/4 pound serving) (9.4,18). A large cohort study of
occupationally exposed women found an increased risk of spontaneous abortion
and other pregnancy complications (7.5).
The World
Health Organization maximum safe level for human ingestion was based mostly on
acute toxicity and is 30 micrograms per day. The ATSDR/EPA MRL amounts to
between 3 to 7 micrograms per day (9.3,1.7,1.8). The average U.S.
average human intake for those with amalgam fillings is over 10 micrograms per
day, but most with several fillings have excretion levels of about 30
micrograms per day, and a study of a group in New York eating more than the
average amount of fish found many ingesting over 40 micrograms per
day. The Minnesota Dept. of Health recommends limiting the intake of
mercury to 15 micrograms per week, but this level is commonly
exceeded. Studies have shown Floridians eat more fish on average
than the amounts assumed in setting standards and most Gulf Coast saltwater
fish have levels of mercury above government health standards and levels
documented to often cause adverse health effects(17a).
Mercury Health and
Wildlife
Standards
:
The FDEP NOEL for mercury
of .1 ppm is also widely exceeded. The FDEP PEL for mercury is
1.4 ppm. The FDA action level for mercury in seafood is
1 ppm
(
59 ). The historic U.S. EPA mercury wildlife guideline,
adopted by most states including Florida, is
12 nanograms per Liter(ng/L) (1.5)
The mercury health
standard to protect human life is 0.3 parts per million(ppm) in
fish and
shellfish
and 7.9 ng/L for
rivers and 3.5 ng/L for lakes under default water
conditions. The EPA mercury wildlife standard (adopted only for
the Great Lakes and tributaries) is 1.3 ng/L and the corresponding human
health criteria is 3.1 ng/L (1.3).
(16) Tin,
thallium, platinum, and gold can also be methylated in water bodies
and sediments to very toxic methyl forms. The extremely toxic tin
compound used in marine paints, tributyltin, was found at levels above the
EPA toxics criteria (TBT>1ppb) in 39% of Fla. Gulf Coast
sediments tested (36c). In addition, the metalloids arsenic,
selenium, and tellurium can be converted to volatile products of
extreme toxicity (11,3.3). The EPA contaminant criteria
for selenium is 1ppm. For silver, the sediment NOEL is 0.5, which is
exceeded in some parts of the state (3.3), and the PEL is 2.5.
Arsenic
is on the EPA Special Health Hazard List because it is a potent Class A
carcinogen in humans (1.2,11.7), as well as being neurotoxic. An EPA
study of cancer incidence for different levels of arsenic in drinking water
found a dose related response for all types of cancer (11.3). The cancer
rate for people with drinking water levels of above .6 parts per million
arsenic
were approx. 3 times those for people drinking
water below .3 ppm arsenic, with large increases in cancers of
internal organs. According to U.S. EPA it also causes birth defects,
learning disabilities, damage to bone marrow, and other
health problems., and new studies estimate that drinking water
contaminated with arsenic at the current federal limit poses a 1 percent lifetime
risk of cancer- about the same as radon or tobacco smoke
(1.2,1.6). EPA staff have proposed lowering the drinking
water standard for arsenic substantially to 3 to 5 parts per
billion. Arsenic is acutely toxic to marine organisms but also has
other effects at lower levels including growth retardation and
reproductive failure (3.3). Arsenic is widely distributed in sediments in
some areas of Florida and bioaccumulates in the food chain.
The FDEP NOEL (no observed effect level) for arsenic is 8 ppm. The
FDEP sediment PEL is 64 ppm. The EPA contaminant criteria
(36c) for arsenic in seafood is 2 ppm.
17. Aluminum
is neurotoxic and appears to be a cause of Alzheimer's disease and
other neurological disorders (15.1). Yale Univ.
researchers found that a population of elderly with high aluminum levels had a
much greater incidence of neuropsychiatric deficits, including poor
memory and impaired visual motor coordination. A study in
Great Britain found that Alzheimer's disease was 50% higher in water districts
where the aluminum concentration in drinking water exceeded .11 mg/liter
compared to districts with less than .01 mg/ liter (15,15.1). Similar
findings are available for most developed countries, including the
U.S. Aluminum has also been shown to cause learning disabilities
in children (15.1). The rate of American's reported dying from
Alzheimer's disease has increased 1000% in the last decade (a portion of this
increase may be due to increased doctor awareness)
(15). Americans are widely exposed to aluminum through food
and medicines and vaccines, as well as breathing wind- blown
aluminum particulates (along with other toxic metals)
(15.1). Yale Univ. researchers estimate that over 100,000
deaths due to metallic pollution particulates occur in the U.S. each year, and
such particulate pollution is increasing in many
areas. Investigators found that the constituent metals and their
bioavailability determine the acute inflammatory response of PM samples in
lung tissue (30.5).
A summary of peer-reviewed scientific
literature on
aluminum
reproductive toxicity
by
Robert A. Yokel, Ph.D.
,
published in Critical Reviews in Toxicology,2023.
The
review found aluminum exposure can lead to adverse reproductive outcomes
in
male and female mammals.
Most
vaccines contain aluminum and aluminum has been found
to be a
significant
factor in
several
neurological conditions.
(
click
on links)
Aluminum is
widely dispersed in soils and is a major factor in the adverse effects on fish
and wildlife in acidified lakes (1.2e).
18. A significant positive
correlation was found between the level of nickel in drinking water and the
rate of bladder and lung cancer in men. The higher the level
of nickel in drinking water, the higher the cancer rate (16.1). Nickel
carbonyl is extremely toxic and is formed when nickel is burned in the
presence of carbon monoxide. Chronic low- level exposure can cause serious
lung damage, birth defects, kidney disease, lung cancer, etc. (16.1,16.3,28,1.2). Beryllium
which is released in fossil fuel combustion is highly toxic; chronic inhalation
exposure can cause lung degeneration, lung cancer, adrenal
gland
and immune system impairment, etc. (1.2)
The Federal safety
standard is 2 micrograms per cubic meter of air, but
some
exposed at levels
lower than this have had serious lung damage.
19. High levels of copper
over long periods can damage the brain, kidneys, cornea, etc. Copper
levels in drinking water (from copper pipes) exceeding EPA
standards were found in several Florida counties
including:
Orange, Seminole, Pasco, Duval, and Hillsboro (16a). Chromium
is neurotoxic and a class A human carcinogen (EPA,1.2).
20. Vanadium and beryllium have been shown to cause acute
and chronic respiratory disease, as well as causing other serious health
problems including cancer (28,29,29.4,29.2). Vanadium, an important
pollutant produced from anthropogenic activities, has been suggested to be
embryotoxic and fetotoxic in animal studies(29a). A study of a large group of
women in China (the Healthy Baby Cohort) was used to assess
the association of
prenatal exposure to vanadium with the risk of adverse birth outcomes in
babies
.
Urinary Ln-vanadium
concentrations were linearly associated with the risk of early-term delivery
(linear, p<0.0001) and being small for gestational age (linear, p=0.0027),
with adjusted ORs of 1-15 for early-term delivery and 1.12 for being small
for gestational age per unit increase in Ln-vanadium concentrations. The
findings reveal a relationship between prenatal exposure to higher levels of
vanadium and increased risk of adverse birth outcomes.
Vanadium causes lung
damage and inflammation by several mechanisms, including damage to pulmonary
alveolar, interruption of cytokine function, altered macrophage
and
Ifn
response,
etc. (29.2,32b,29.2) - resulting in lung damage lung
infections, bronchopulmonary disease, asthma, and lowered resistance
to infectious microorganisms. Vanadium is also cytotoxic causing
extensive cell death through toxic accumulation and free
radical inducement (29.5). Vanadium also causes extensive DNA damage
in cells and is a reproductive and developmental toxin (29.5b), as well as
a proven carcinogen (29.4,30.2). Vanadium is a major factor in lung damage
caused by PM10 particulates in oil fly ash air pollution (29,32).
Thallium
intoxication is characterized by the development of painful peripheral
neuropathy, alopecia(61c), mental disorders, and in severe cases, respiratory
failure
and death (61). Toxic optic neuropathy is also a
feature.
Opthalmologic
features of
thallium poisoning include optic neuropathy, blepharoptosis, lens
opacities,
and
opthalmoplegia
(61). Thallium
is common in coal plant emissions and phospho-
gympsum
waste
in
Florida.
Vaporized
ash from burned residual oils has been shown to cause serious lung injury and
respiratory disease by causing cellular death of immune suppressor
cell macrophages (32b). Such damage by small particles in the
urban air has been found to cause over 60,000 deaths per year from
lung damage (29.2). EPA studies and other studies have
determined that toxic metals in the dust are a major factor in the induced lung
damage, and that vanadium is a particularly toxic to such macrophages in
the lung (29,29.2,30.5). Investigators found that the
constituent metals and their bioavailability determine the acute inflammatory
response of PM samples in lung tissue
(30.5).
High
levels of manganese cause manganese madness and result in violent and
antisocial behavior (15.1). Studies have found a very
significant positive relationship between criminals convicted of violent crime
and the level of manganese in hair samples. Manganese has been found
to damage the male reproductive system resulting in infertility (10.2), to
damage normal hormone production, and to be toxic to the brain,
causing neurologic damage including reduced production of the brain
neurotransmitter dopamine and excess production of acetylcholine
(10.6). A population exposed to manganese in the water supply has
experienced severe neurologic and muscle control problems
(10.6).
20.5 A study
results
of
diabetes patients (9.2e) showed that the mean values
of Pb, Cd and, As were significantly higher in scalp hair samples of
smoker and non-smoker diabetic patients as compared to control subjects
(p<0.001). The concentration of understudy toxic metals was also high in
blood and urine samples of DM patients, but the difference was more significant
in smoker DM patients. These results are consistent with those obtained in
other studies (9.7b), confirming that toxic metals may play a role in the development
of diabetes mellitus. Studies have also shown that mercury exposure
causes
diabetes
.
Combinations of
toxic metals have synergistic effects that are associated with type 2 diabetes
and other conditions (9.2a-e). Associations between arsenic and
cadmium were reported for cardiovascular and kidney disease, type I and type
II diabetes, cognitive function, hypothyroidism, and increased prevalence
and mortality for lung and other cancers (9.2,38).
Study results
demonstrated that As and Cd exposure caused significant changes to the gut
microbiome and metabolome by affecting bile acids, amino acids and taxa
associated with metabolic health (37c). Inorganic Arsenic can increase DM risk
by impairing mitochondrial metabolism, one of the key steps in the regulation
of glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells (36
)
.
The results also
found that Manganese, like Arsenic, may inhibit GSIS by impairing mitochondrial
function, whereas Cd may target other mechanisms that regulate GSIS in β-cells.
Impairment of hepatic glucose homeostasis can also play a crucial role in the
pathogenesis of DM. Along with compromised function of pancreas and muscles,
diminished liver and kidney functions also contribute considerably to increase
the blood glucose level. These metals have potential to bring conformational
changes in these enzymes and make them inactive. Additionally, these metals
also disturb the hormonal balance, such as insulin, glucocorticoids and catecholamines; by
damaging pancreas and adrenal gland, respectively. Moreover, these metals also
enhance the production of reactive oxygen species and depress the
anti-oxidative defense mechanism with subsequent disruption of multiple organs
(37). Exposure to Endocrine Disrupting Chemicals (
EDCs
)
during fetal or early life can disrupt the development of both the immune
system and the pancreatic beta cells, potentially increasing susceptibility to
T1DM later in life. In addition, developmental exposure to some EDCs can affect
beta cell development and function, influencing insulin secretion. These
changes may increase stress on the beta cells and identify them as a target to
the immune system. Developmental exposure to EDCs that disrupt metabolism by
increasing insulin resistance or obesity may also stress the beta
cells. (7.7a,9.2,9.5). Other study data indicated that
taurine administration
could ameliorate
iAs
-induced insulin resistance through activating
PPARγ-mTORC2 signaling and subsequently inhibiting hepatic autophagy
(7.7b).
II. Mercury in Fish and the Food Chain of Lakes and Streams and Bays
21. Studies by Univ.
of Florida scientists have found that human activities are increasing the
quantity of mercury delivered to the atmosphere, soils, sediments, water
bodies, and food chain (17.1,1.5). Mercury accumulation rates in the
Everglades reached an average of 6.4 times higher than 1900, with most of the
increase since 1940. Atmospheric emissions are the largest source of
mercury in lakes, and the main sources of emissions are municipal incinerators,
medical waste incinerators, and coal combustion
(2,2.1,16.2-17,18,18.8,22,28,28.7,33,34,35). The rain in areas with
incinerators like Broward County has been found to be unusually high in
mercury, higher than industrial areas around Lake Michigan
(21d). Some pollution controls have been mandated for incinerators
to reduce levels from incinerators and the level of mercury in the everglades
appears to be declining some. Ozone pollution and reactive compounds containing
chlorine or
bromine
oxidise
elemental
mercury to inorganic mercury which is more readily
depositied
by rain
(16.3). Recent studies have found high levels of mercury in the rain
all over Florida and throughout
the U.S.
( 1.5). Over
a 6- year period, Florida rain samples ranged from
1.3 nanograms/Liter to 81.2 ng/L, depending on location and climatic
considerations, with an average of 12.6 ng/L (1.5). The level
of mercury in Florida rain sampled exceeded the EPA human health criterion for
Hg in lakes in over 97% of samples. Studies by EPA and municipal
sewer agencies have also shown that sewer sludge has significant levels of
mercury all over Florida, with the main sources being dental offices and
excretion by those with amalgam dental fillings (14.9). Studies by Oak
Ridge National Laboratory for FDEP have documented that mercury in sewer sludge
and landfills is methylated to methyl mercury by soil bacteria and
much of the mercury ends up in crops if land spread and in the atmosphere and
rain if not (14.9). Thus, mercury from dental amalgam is a major
source of methyl mercury in rain. Mercury from sewers is also a
significant source of mercury in rivers, lakes, bays, and fish (14.9).
22. Mercury
in Salt-Water Fish and Shellfish
Studies document that Florida Saltwater fish and shellfish
have high levels of mercury in large parts of the state
(60,16.3f,43,51,33). There are fish consumption warnings/limits for most
saltwater fish species in all coastal and estuarine waters (43) and for most
larger freshwater fish species in many water bodies (
43 ).There
a
also fish advisory limits for dioxin, PCBs, pesticides, heavy metals other than
mercury, and saxitoxin in some Florida water bodies(43). �Some
areas such as North Florida Bay and offshore Tampa Bay have had test levels
higher than most other areas (60). Based on the tests that have been
done, five saltwater species(king mackerel, black grouper,
florida
smoothhound
,
great white shark, tilefish) have average mercury levels on tested samples
higher than the FDA action level of 1 part per million (ppm) for fish
(60,16.3f,51); 17 species have average mercury test levels above the FDA
warning level(0.5 ppm) for mercury in fish(barracuda, black
drum, blacktip shark, bluefish, bonefish, bonnethead shark,
bull shark, cobia, snook, greater amberjack, jack crevalle, ladyfish,
lemon shark, red
drum,rock
bass,
spanish
mackeral
,
spotted bass, stone crab) , and 16 species of fish (blacknose shark, blue
crab,
gafftopsail
catfish, gag
grouper, grouper, gulf flounder, permit, red grouper, sand
trout, sheepshead, silver seatrout, southern flounder, tarpon,
tripletail, white bass, yellow bass, yellow jack), as well as crabs, oysters
and shrimp have average test levels near the warning level or some that tested
above the FDA action level(60,51) and all were above the EPA health criterion
of 0.3ppp (1.6). All of these have average levels of mercury above the U.S. EPA
health criterion for methylmercury of 0.3 ppm
(1.6). Studies (22.5) have also found that the level in most large
predator species on the Gulf Coast is higher than levels found to adversely
affect health (66,67) with mercury contamination being pervasive along the
whole coastal area, and that people who eat Gulf Coast fish at least once per
week usually have dangerous levels of mercury (16.3). 29% of a coastal sample
from Florida, Alabama, and Mississippi ate fish at least once per week
(16.3). Several studies including a large CDC study have found
those with higher levels of mercury have higher rates of
neurological
problems,
cardiovascular
proble
ms
, infertility, and
cancer
(66,67,41,1.8,27,14.7). Another
study found infertile couples were significantly more likely to have elevated
mercury levels than the infertile couples, which was the case for both men (35
percent versus 15 percent) and women (23 percent versus 4
percent). Furthermore, patients who reported eating high
levels of seafood showed a clear trend towards elevated mercury levels (67
a,f
), as did those with
several
mercury amalgam dental fillings
.
A California health clinic study reports that of a California
population that eats at least 2 servings of fish per week, 89% had levels
of mercury in the blood exceeding 5 micrograms per liter(ug/L), the level
considered the safety limit for mercury by U.S. EPA and the National Academy of
Sciences(67a). Over 50% had levels over
10 ug/L and 15% had levels over 20 ug/L. The
group had chronic health effects including depression, loss of scalp hair,
metallic taste, headaches, arthritic pain in joints, irritability,
tremors, and numbness and tingling in hands and feet. She also described
cognitive problems such as pronounced memory loss,
confusion
and difficulties in talking. In some cases, those problems were so severe they
interfered with the ability to earn a living or attend school. In all cases,
health effects improved after several months of avoiding eating
fish. Some women in the group were found to have transferred
excessive mercury to their infants solely through their breast milk. One
breast-fed baby had three times the EPA's safe level for mercury by the time he
was 4 months old; and another had 4 times the EPA safe level at 19
months. Some of the infants with high mercury levels suffered severe
neurological problems such
as autism
, and improved
when treated for mercury toxicity.
The Mobile Register studies (16.3) have also found
that fish and shellfish that feed near offshore oil and gas platforms have
significantly higher levels of mercury than other areas (16.3) due to mercury
used in drilling. Over 200 tons of mercury has been added to the Gulf through
drilling over the last 30 years. More fishing occurs near such platforms since
shellfish and fish tend to congregate in such areas. Other known major sources
of mercury throughout the coastal area are air emissions and sewer outfalls,
with some other large local industrial sites such as chlor-alkali
plants. Accumulation of atmospheric oxidants and mercury can cause
high levels of mercury deposition in coastal areas when activated by sunlight,
which can result in very high levels of mercury in fish and wild
life(
68).
The U.S. FDA recommends that pregnant
women entirely avoid eating shark, swordfish, king mackerel and tilefish
(59b), because a significant portion of these types of fish have mercury levels
above the FDA action level of 1 ppm. However
other studies
( 66,67)
including one by the National Academy of Sciences(63) have found the old FDA
action level of 1 ppm is obsolete and not adequate to protect the
public, as adverse effects have been found for those eating fish at least once
per week at average mercury levels below the FDA warning level
of � ppm(66).
Based on this a coalition of
organizations using the name Environmental
Working Group
( EWG)
did a large study to more fully assess mercury exposure effects and safety
limits(51). In addition to the FDA limits, EWG advises pregnant women, nursing
mothers and all women of childbearing age, should not eat tuna steaks, sea
bass, oysters from the Gulf Coast, marlin, halibut, pike, walleye, white
croaker, and
largemouth bass
( 51). And
that these women should eat no more than one meal per month combined of canned
tuna, mahi-mahi, blue mussel, Eastern oyster, cod, pollock, salmon from
the Great Lakes, blue crab from the Gulf of Mexico, wild channel catfish
and lake whitefish. The EWG analysis was based on 56,000 test results on
mercury in fish from 7 different government agencies, and toxicity studies by
U.S. CDC and National Academy of Sciences.
However
EWG
recognizes that fish is an important
health food with nutrients and essential fatty acids hard to substitute from
other sources. The following fish are safer choices for avoiding mercury
exposure: farmed trout or catfish, shrimp, fish sticks, wild Pacific salmon,
croaker, haddock, some varieties of flounder, and blue crab from the
mid-Atlantic. (51)
*******
22.5. Dangerous levels of mercury (above 1.5 ppm)
have been found in over one third of
the
sharkmeat
tested throughout the state of
Florida (17d). A survey conducted by the Minnesota Dept. Of
Agriculture of swordfish offered for sale in Minnesota grocery stores found
levels of methyl mercury that are higher than the Federal action guideline in
over half of the samples (19.7b). A joint health advisory warning of the danger
of
consuming
sharkmeat
was
issued by the Fla. Dept. of Agriculture and the Dept. of Health &
Rehabilitative Services (19.7). Florida commercial fishermen sold over 6.8
million pounds
of
sharkmeat
in
1989, 36% of the U.S. total. Health warnings have also been
issued by the Fla. Dept. of H.R.S. for sea trout, bluefish, king & Spanish
mackerel, catfish, ladyfish, etc. (33,17a), and other ocean fish such as tuna
and swordfish have high levels. Florida Bay cormorants have also been found to
have high levels of mercury (14).
23. Mercury in Fresh Water Fish and
Wildlife
Studies
have found that freshwater predator fish such as bass, pickerel, and bowfin
have high levels of mercury in most of the state, with fish consumption
warnings issued (60,33,17a,17,17b). Eight other species (alligator gar, black
crappie, white crappie, blue catfish, flathead catfish, brook trout, drum,
striped bass) have average test levels near the FDA warning level or some
tested above the FDA action level (60). Over 2
million acres of
Florida�s
surface waters
have fish with high levels of mercury, averaging above the FDA/EPA warning
level of 0.5 parts per million (33) and even more above the U.S. EPA mercury
health criterion of
0.3 ppm
(1.6). The
major source of mercury into these water bodies is air deposition that is
brought down in rain. A Florida emissions inventory found that the
major sources of atmospheric mercury were municipal solid waste combustors
(MSW), electric utility industry, and medical waste incinerators (33), but
incinerator emissions have been reduced in recent years. The most
vulnerable groups to mercury exposure are women who are pregnant or might
become pregnant, nursing mothers, and young children (65,59b,51,7.5,5).
These groups should limit consumption of freshwater fish to no more than one
meal per week (6 ounces of cooked fish for adults and 2 ounces of cooked fish
for young children). Other animal species that eat fish and crawfish, such
as cormorants, wading birds, raccoons, alligators,
mink,etc
. and panthers which eat
raccoons have also been found to have dangerous levels of mercury and are have
been adversely
affected(
1.5,17.4). Three panthers
along with many birds that eat fish have died from mercury poisoning and others
have very high levels of mercury (14,17.4).
The majority
of
Florida panthers in south Florida have high levels of mercury and
have had reproductive systems and hormone levels disrupted to the extent of not
being able to reproduce.
The majority of
male panthers were found to have estrogen levels higher than testosterone
levels due to estrogenic effects of the mercury and perhaps other estrogenic
chemicals in the fish (14).
23.5: Studies by the Wisconsin Dept.
of Natural Resources and Univ. of Wisconsin researchers (18.6,16.3,2.1) found
hundreds of lakes and streams in Wisconsin with mercury in fish at above the
recommended levels
for eating
, and concluded
the major source of the mercury appears to be air
emissions. They also found that one gram of mercury
deposition is enough to cause the need for a fish consumption limitation in a
25 acre lake, and that mercury concentrations of 2 parts per trillion(parts per
trillion(ppt) in lake water often result in concentrations in fish sufficient
to require consumption advisories(Watras,18.6 &16.3,18) Warnings on eating
fish have been issued for thousands of rivers and lakes throughout the U.S. and
Canada(64), for approx. 20 % of all U.S. lakes including all Great
Lakes.
The Minnesota Pollution Control Agency (MPCA)
has also found widespread dangerous levels
of mercury
( as
much as 4.5 micrograms per gram of fish) in 94% of the hundreds of lakes and
streams tested in Minnesota (18.8, 16.3). MPCA
studies estimated that virtually
all of
the mercury in
Minnesota lakes come from emissions, with the largest amount from incinerators
and coal plants (18,18.8). They concluded that mercury emissions are
a larger threat to
the states
water
resources than acid rain, though acidity level is also a factor
in the level of mercury and other toxic metals in fish (18.8).
Mercury
deposition levels on the surface of lakes in Minnesota were 12 to 14 micrograms
per square meter per year. Precipitation measurements in Minnesota
were found to have an average mercury concentration of
19 ppt. Levels in sediment in recent years are more than 3.5
times levels in sediment prior to 1900, and approx. 25% of the mercury
deposited in a lake catchment area is exported to the lake
(18.8). Mercury in the
area�s
atmosphere
has increased an average of 2% per year, compared to a 1.5% increase over the
N. Atlantic Ocean which also was found to be primarily due to manmade
emissions. Deposition levels were found to be increasing throughout
the area due to long range transport,
butwas
highest
near emission sources. Worldwide mercury atmospheric levels are now at least 3
times the level of 1900, and there is much more mercury in aquatic ecosystems
than in past times (20), as shown by analyses of polar ice cores, lake
sediment cores, and peat cores.
Because
of the widespread high levels of toxic metals in fish and the food chain in
Minnesota and neighboring Great Lakes states, Minnesota requires emissions
limits on lead and mercury for municipal incinerators. The
emission limit for mercury was .002 pounds per ton for a 1990
incinerator permitted (18.3). The most recent study recommended
emission limits should be no more than 50 pounds per year, whereas current EPA
limits are 20,000 pounds (18.8).
24. According to EPA spokesmen, Gary
Glass and Ray Morrison, mercury has been found to be entering the food chain
throughout the U.S. At least 40 states and 2 Canadian provinces have
limited or banned consumption of fish from thousands of affected lakes and
rivers in both the U.S. and Canada (16.3,33). Mercury has
been found to be adversely affecting loons, eagles, ospreys, otters, and mink
in the Great Lakes area (28).
Studies by the
Electric Power Research Institute, the research arm of the electric utility
industry, have confirmed that atmospheric deposition of mercury accounts for
most of the mercury accumulating in fish in seepage lakes and that increased
acidity enhances mercury accumulations in fish
(18). Approx. 90 % of the mercury in fish is methyl mercury,
the most toxic form to humans. Based on their research, EPRI
believes that most older estimates of mercury levels are inaccurate
and questionable, and that clean sampling/clean lab procedures are required for
accurate sampling of mercury. Reported mercury removal
levels by wet scrubbers have a very wide range, from 25% to 90%, but
all of
the reported data should be
considered questionable (18).
Municipal
waste and coal contain large amounts of toxic metals such as mercury, lead,
cadmium, etc.; large volumes of toxic metal emissions are occurring where
stringent controls on incinerator fuel sources and stack emissions are not in
effect (18.3) as they are in some European countries.
26. The toxic metals most dangerous to
people eating
fresh water
fish are those
that accumulate in the edible muscle of fish‑ including mercury, arsenic,
radioactive cesium, and to a lesser degree lead (19.9). Most
toxic metals such as lead, cadmium, aluminum, etc. accumulate primarily in
internal organs, fat, fins, and mucus under the skin (21).
II(b). Bioaccumulation of
Toxic Metals in Marine Fish and S
hellfish
27. Shellfish, especially oysters, accumulate lead,
mercury, cadmium, copper, silver, arsenic, and radioactive metal isotopes
(19.9,3.3). Oysters and other shellfish are accumulating increasing
amounts of toxic metals, with oysters often accumulating levels of cadmium,
lead, and arsenic dangerous to people and above the FDA recommended action
level or guideline level (59). The following table gives a summary
of some of the levels of toxic metals found in shellfish in Florida.
The data for the Indian River Lagoon
is for an area with lower levels of metals in sediments than some other urban
coastal areas in Florida. The FDA Action Level is the level at which
commercial seafood may be removed from sale; however, it is based primarily on
acute toxicity criterion and does not take into account that some of the metals
such as mercury, lead, and cadmium have been found to be endocrine system
disrupters at relatively low levels and several of the metals are carcinogenic, neurotoxic,
and
immunotoxic
. While
there is no FDA Action Level for arsenic
,
arsenic
is more acutely toxic than the other metals for which there is an action level
and arsenic is highly carcinogenic (11.7,1.1). The drinking water guideline for
arsenic is lower than those for mercury or cadmium. The EPA toxics
contaminant criteria for arsenic in seafood is 2 ppm (36c).
Range
of Toxic Metals Observed in Florida Shellfish (ppm-wet weight*)
Metal
Oysters
Clams
FDEP
1984 N.O.A.A 1983-
1992 FDEP
1984 I.R.L.
1992 FDA EPA source:
(3.9) source:
(3.7) source:(3.9) source:(3.7) Action Crit.
min/mean/max min
to max min/mean/max min to
max Level Level
Arsenic .
05/ 1.5/
7.8 1.0/
4.6/9.5 **
2 Cadmium
.10/ .48/
1.6 .70 to 5.1 .05/
.35/1.1 .01 to 0.15 1.0 0.5
Chromium .005/.15/ .64 .20 to
0.9 .06/.30/1.28 .03 to
0.08 11 1
Copper .50/
7.3/28.4 .50/1.5/4.7 1.0
to 4.0 15
Lead .005/.14/1.36 .10
to 1.6 .05/.67/6.5 .04 to
1.73 1.2 0.5
Mercury .
001/.017/.05 .10
to .16 .001/.02/.
04 .
001
to .018 1.0 1
Nickel .005/
.23/1.1 .06/.72/2.6
Selenium .10/ .36/
.67 .18/.45/1.0 1
Zinc 34/
205/
546 1
/ 12/ 25 1.7 to 53 60
* Indian River Lagoon data was
calculated dry weight basis. Since all other data shown here is wet
weight, the data for I.R.L. was converted to wet weight by assuming water
content of clams was 85%.
From the
table it is seen that the FDA Action level for cadmium and lead appear to be
often exceeded by oysters and clams from some polluted coastal areas of
Florida, and the EPA contaminant criteria for arsenic in seafood. This
could indicate that people eating seafood regularly from such a polluted area
could experience serious health problems over time. To date there has
apparently been no health warnings for shellfish comparable to the warnings for
mercury in freshwater fish, even though FDA Action levels may be exceeded by
similar levels. In a controlled study, oysters exposed to 10
micrograms per liter of cadmium in water accumulated
18 ppm of cadmium (3.9). None of the cadmium levels in the
limited surveys done in Florida have reached this level, but some areas of the
state have higher levels of cadmium in sediments than the sampled
areas. The Indian River Lagoon study (3.3) noted that areas
with the highest levels of metals in sediments were toxic to clams so no clams
in these locations could be sampled and all clam samples came from less
polluted sites. Mussels and crabs have been found to accumulate
cadmium inversely with the salinity or alkalinity of water (19.9).
The
Canadian Food and Drug Admin. has established 2 ppm as the
maximum safe concentration of lead in fish. Due to recent studies of
lead and learning disabilities, some researchers believe this level is too high
and a lower guideline is recommended by the FDA of 1ppm. As
seen from the sample data oysters often accumulate levels higher than this.
Levels of 2 micrograms per liter in water often mean levels in oysters of more
than 2 ppm (19.9). Some U.S. rivers have above 20
micrograms per liter of lead in some areas. Increased
acidity increases the availability of lead, and fish at PH 6.0 accumulate 3
times as much lead as at PH 7.5 for the same concentration of lead in water.
Arsenic
accumulates in shellfish and has been found at levels 20 times the EPA
guideline maximum contaminant level (19.9). The
toxic
arsenite
form is the primary form in
shellfish and the
most toxic form to people
. Radioactive
cesium is dangerous to people and is discharged from nuclear power
plants. Large amounts of radioactive isotopes are
discharged into Florida water bodies by coal plants and phosphate mining,
and have
been found in
shellfish. Toxic metals have been found in Florida shellfish in
several areas of the state (16.3e,3.3).
Crabs
and fish often accumulate high levels of copper which has an adverse effect on fish
survival, but
doesn’t usually affect people because
the accumulation is not primarily in muscle tissue. Oysters
and squid accumulate copper to dangerous levels; however, copper use
as an algicide and water weed killer is a common source and has been found
to cause elevated copper levels in water and sediments in some areas of the
state such as the Crystal River.
Atmospheric
metal emissions to oceans are significantly altering the marine cycle of the
toxic metals (2,2.1). Oceans near areas with high fossil fuel
combustion have much higher levels of mercury and other toxic metals, with
atmospheric emissions being the main source of mercury in coastal
waters. Mercury gets into ocean fish and shellfish similarly to
freshwater fish.
A high percentage of coastal bay and
estuarine sediments tested in Florida have been found to have significantly
elevated levels of toxic metals (36), and sediments in Gulf Coast areas
were found to be toxic to marine organisms in 9 percent of the estuarine area
(36b).
III. Effect of Toxic Metals on Forests
and Plant Ecosystems
28. Some metals are toxic to
nitrogen-fixing bacteria associated with root-systems of legumes
(28). Nitrogen and phosphorus cycling in soils can also be adversely
affected by some metals. In addition, litter decomposers can be destroyed
by some metals.
All of
these effects are
made worse by acidity.
29. Heavy metals from atmospheric emissions are
deposited on leaves and soils of forests and cropland. Crop plants
have been shown to directly absorb and retain mercury and other toxic metals
through leaf uptake (58,2). The interaction of the heavy
metals and acid deposition is a factor in the extensive forest decline
occurring throughout Europe and North America (20,
20.2). Increased levels of toxic metal emissions are leading to
rapid buildups of trace metals in soil and water and likewise to buildups in
plants and the food chain, especially in industrial areas and near large
emission sources (2). Levels in the U.S. and Europe with large
emission sources are currently doubling every 3 to 10 years. The
level in plants and crops has reached levels that damage plants and cause human
health damage in some areas (2) and is approaching such levels in many
other areas. The loading of the air and environment in urban
industrial areas with toxic metals is a major health concern for the next and
future generations, but the extent of metals emissions is so large and
widespread that even the air of the most remote areas of the arctic
and antarctica have significant levels (2).
The solubility of
aluminum in soils and other heavy metals (lead, cadmium, zinc, etc.) being
deposited on leaves and soils by air pollution increases with increasing
acidity. Canada has issued a health warning for Central Canada
against eating the livers or kidneys of game animals because of cadmium buildup
in the food chain (2). The main sources of such toxic metal
emissions are atmospheric emissions.
Mercury and other toxic metals have also
been found to be accumulating in the forest floor of European forests; the
humus of Swedish forest floors
are
estimated to
contain over 600 tons of mercury. Both inorganic and methyl
mercury are toxic to spruce seedlings, suppressing chlorophyll content and
interfering with uptake of nutrients. In many areas of Europe,
the mercury level is beyond the 0.5 ppm found to be toxic to forests
and is approaching this level in many other areas. The
accumulating mercury in forest floors was also found to be affecting watersheds
and to be cycling through the entire ecosystem (18d), adding to the
thousands of lakes with dangerous levels of mercury in the fish in
Scandinavia. Ozone pollution and reactive compounds containing
chlorine or bromine
oxidise
elemental
mercury to inorganic mercury which is
more readily deposited by rain( 16.3). Mercury
deposited in the soil has been found
by
Gov
�
t
studies to
be methylated to methylmercury by soil bacteria, with uptake by
plants and outgassing of methylmercury and elemental
mercury when the sun shines (14.9).
At 2 remote stands of Norway spruce showing
serious decline, lead contamination/uptake was significantly increased on the
exposed windward edge, and there was a negative correlation between lead levels
and shoot growth (20b). This indicates dry deposition is a major
factor in lead uptake by forests. However, cadmium did not have a similar
pattern and apparently cadmium deposition is primarily through rain. Toxic
clouds/fog having relatively high levels of toxic metals and very low PH have
been found to be a major factor in forest damage in mountainous areas of the
eastern U.S. and Europe (20).
Uptake of mercury by red
mangrove and natural decomposition of leaves appears to play a role in
bioaccumulation of mercury in the Everglades ecosystem. Particulate
plant detritus is a primary energy source for many aquatic animals, and 80% of
detritus in the main area of the Everglades is from red mangrove
(58). Particulate organic detritus enriched by mercury is subjecting
animals in their food web to higher levels of mercury. There
is a 10 to 4 enrichment in suspended detritus compared to undecomposed leaves,
and a 6 to 4 enrichment for river bottom detritus and peat
(58). Peat is known to accumulate mercury from emissions,
etc. Disturbance of peat soils by burning,
agriculture, drying, etc. is likely to release mercury into the
environment. This is likely to be a factor in high levels of
mercury in the Everglades (17.4).
IV. Sources of Mercury Emissions and Mercury Content of Fuels
30. There is consensus among researchers that airborne emissions are
the major source of mercury in most lakes (2,2.1,16.2‑17,17.1,18‑18.8, 22‑23.4,
28,28.7,33,34,35) and that incineration and coal combustion are the largest
sources in most areas. Researchers in Minnesota found a three to four‑fold
increase in mercury deposition in northern Minnesota since the mid 1800s
(18.8). A Dept. of Environmental Regulation Spokesman and emission studies
indicate that based on past tests, Florida municipal incinerators emit over 8
tons per year to the environment and medical waste incinerators over 4 tons per
year (17.1,17,35). Florida coal power plants appear to have
emissions of about 3 tons per year, with at least that amount in coal ash that
can have air, soil, or water impacts(17b). About this much
mercury emissions also comes from a combination of coal plants from other
states or oil burning power plants. A study
by
Dr
.John
Simmons(17d) estimated that several tons
per year of mercury emissions in South Florida comes from burning
sugarcane bagasse and related soil erosion, but this is largely
recycling of previously deposited mercury. C.S.
Volland
(18d) points out that Florida's high
temperatures and acidic soils high in chloride content make Florida's aquatic
ecosystem especially vulnerable to mercury.
31. Florida incinerators in 4 counties: Pinellas,
Hillsboro, Dade, and Palm Beach burned approx. 10,000 tons per day of garbage
in 1990. Sampling by the Dept. of Environmental Regulation
found that the Pinellas facility emitted 21 pounds of mercury per day
(19.7). Based on emissions tests at this and other Florida
facilities, the Florida facilities appear to be emitting approx. 9 tons of
mercury per year (and considerable other toxic metals and other toxics) (17.1,17,19.7,35).
(
see
Appendix) The type of pollution
controls on some of these units have been found not to be effective for
mercury on most existing incinerators. More stringent controls have been
mandated for most incinerators.
32. Based on coal combustion data from the U.S. Dept.
of Energy and assuming coal averages 0.28 ppm mercury, U.S. coal
burned each year contains approx. 250 tons of mercury‑ the majority of which
appears to be emitted into the
air. Electricity generators and coal
combustion are projected to increase approx. 30% over the next 20 years, with
corresponding increases in other air toxics unless counter measures
are implemented (28). A study of coal plant emissions at a
Tennessee Valley Authority facility (21.6) found that over 92% of mercury
emissions were elemental mercury, that the mercury remained in the plume for
long distances, and precipitation scavenging was the main mechanism of mercury
deposition from such emissions. However, depending on the
percent of chlorine or similar reactive constituents of the coal burned, as
much as 50% of mercury in coal plant plumes can be water soluble inorganic
forms which are more easily removed by controls
and also
have shorter residence times in the atmosphere.
The majority of
mercury in plumes after emission controls
appears to usually be elemental mercury. Much higher levels of mercury
deposition is found near point sources, though only a small fraction of total
mercury emissions are deposited
locally( 22
).
Tests for incinerators
indicated that mercuric chloride was the main form of mercury emitted, which
appears to be a much more localized deposition source. U.S. municipal
incinerators produce approx. 187 tons of mercury emissions per year (21). Hospital
and hazardous waste incinerators produce additional toxic metal emissions.
Approx. 800 tons of
mercury is mined in the U.S. each year (21.6). The following
table gives a breakout by the U.S. Bureau of Mines (18c) of the
approx. 1145 tons per year used in manufacturing in 1989:
Use tons percent
____________________________________________________________
soda/chlorine manuf. 328 28.7
batteries 208 18.2
latex paint 192 16.8
wiring/switches 160 14.0
instruments 68 5.9
other chemical
products 40 3.5
fluorescent lighting/ 36 3.1
mercury vapor
lights
dental supplies 36 3.1
other 76 6.6
33. Recent studies have raised considerable doubt about the accuracy of
past mercury level measurements from power plants, incinerators, or
natural sources (18,60). However, most studies reviewed
agreed manmade sources of mercury were much more significant on land areas than
natural sources (1.9,2,2.1,18.8,20.4, 21.5,22,57,28,28.7,34,60e4r
. They also
agreed that atmospheric fluxes from combustion of fossil fuels dwarf those from
other sources. The following table gives estimates of
emissions by natural sources, manmade sources, and biogenic recycling from the
articles reviewed:
Mercury emissions
source tons/year total
__________________________________ _________ _____
Natural sources
seasalt
spray
20
windblown dust 55
volcanic activity 75
rock weathering/soil outgassing* 500 650
* a significant portion of
soil outgassing is of mercury previously deposited
from manmade sources
Manmade sources
energy production 1200
waste incineration 750
wood combustion 270
other fossil fuel
combustion 600
mine operations 100
mercury related
manufacturing 100
smelting/refining 130
consumer products 50 3200
The referenced articles also give estimates of
additional man‑made source impacts directly to soils or aquatic systems of over
8000 tons from coal, incinerator, or wood ashes, manufacturing or industrial
effluent, sewage, mining/smelting, metal fabrication, etc. According to FDEP
staff, the average concentration of mercury found in limestone bedrock range
from 33 parts per billion(ppb) to 48 parts per billion(ppb), and the
effects of weathering processes appear negligible in Florida
(21). There is general agreement among the summary articles reviewed
on source of mercury that the major sources are continental and manmade sources
are the largest source in local industrial areas‑ amounting to as much as 90%
of emissions (1.9,2,2.1,9.3,18.8,22,57,28,34).
Not included separately in
either of the above lists is a source that is becoming more important‑ biogenic
recycling of toxic metals through the atmosphere and aquatic systems through
forest fires, muck farming, dredging, organic uptake and decomposition,
ocean/atmosphere interchange, watershed water cycling through soils
and
humus
,etc
. Biogenic and hydrological
cycling of mercury appear to be on the order of 4000 tons per year (22),
including the air/sea exchange amounting to approx. 2000 tons per
year. The air/sea exchange appears to not have a major impact on
continental areas, however manmade emissions are a major source of deposition
to oceans (2,2.1). Much of the mercury (and other toxic
metals) being biogenically recycled or emitted came from past
atmospheric emissions. Present background fluxes of mercury
appear to be from 3 to 6 times those
of preindustrial levels; present fluxes are the sum of
manmade and background fluxes. However, as Sweden has already
found out, even if most atmospheric emissions were ended, this supply of
mercury already in the biogenic system would continue to have an impact on
water bodies and the food chain.
Additional evidence for the
primary importance of manmade emissions on land areas is found in the
literature. Measurements have found mercury levels in
open oceans to be much lower than in coastal areas impacted by manmade and
continental sources (2,2.1,60,22). Estuarine waters
average at least twice as high in mercury level as coastal water, and coastal
waters sampled (2 to 10 nanograms per liter) had levels at least
twice as high as
open oceans
( 0.5 to
2 ng/l). Over 99% of mercury transfer at the ocean
boundary is vapor phase, with the majority being elemental
mercury. Although some high levels have been reported locally
in volcanically active ocean areas, studies reviewed (60, 22)
estimated the total contribution of submarine volcanism as very small compared
to input from rivers, coastal sources, and the atmosphere. The
highest levels in coastal waters were found in localized areas impacted by
sewer or industrial outfalls or rivers with such sources.
Rainwater in open ocean areas
was found to contain very small levels
of mercury
( <1 ng/l),
and approx. 10 % the average levels in coastal waters
(60,20b2,2.1). Mercury in levels over continental areas
average several times higher than over coastal waters and over 20 times higher
than over open ocean areas. Water soluble gaseous phases from
continental sources appear to make up a significant portion of mercury in
rainfall over oceans, especially in areas near continental areas with the
highest mercury in rainfall. Elemental mercury appears to be
oxidized by ozone or other oxidants and scavenged by rainfall slowly
(20.4). Levels of mercury in rainfall of the N.W. Atlantic Ocean, where
continental mercury sources are highest, are larger than over other oceans‑
consistent with the hypothesis that the largest sources of mercury are
continental (20.4). The highest levels of mercury in rainfall (over
60 ng/cubic meter) have been reported in areas with high levels of
atmospheric emissions (18.6‑18.8,20).
Studies in Minnesota,
Wisconsin, Canada, and Sweden offer additional support that manmade sources are
significant (18.3‑18.8, 21.6, 20, 18d, 21). These studies have found
levels of mercury increasing between 2% to 5% per year in
freshwater fish and sediments, with recent sediment layers
having much higher levels than sediments deposited before large manmade
emissions.
Over 80% of total mercury in
the atmosphere is volatile insoluble mercury vapor, primarily elemental mercury
which has an average residence time of several months and travels
long distances (20). This mercury vapor is relatively uniformly
distributed throughout the troposphere, with an average concentration of
2 nanograms per cubic meter in the northern hemisphere and 1 ng/m3 in
the
southern hemisphere
; with higher
levels near local sources or industrial areas‑ depending on distance and wind
direction from the source, emissions
levels,etc
.
The
non
elemental
vapor portion
(monomethyl and dimethyl mercury and mercury chloride) represent
more localized sources and has a much shorter average residence
time. This portion can be a considerably higher fraction of the
total in regions with local emission sources (20). At
temperatures above 70 degrees, a significant and increasing portion of
elemental or dimethyl mercury volatilizes from water (or soils), with
the air to water equilibrium point being over 30% and increasing with
temperature.
34. Generally coal from northern Appalachia, the Gulf
Coast, and Washington have the highest levels of mercury, ranging
from 0.20 to 0.30 parts per million
(
28). Western
coal ranges from 0.05 to 0.13 ppm, while Midwestern coal ranges from 0.09
to 0.17 ppm. Data is available by state or in some cases
by mine (28, Table B-2).
V. MANMADE EMISSIONS OF OTHER TOXIC METALS
35. There was consensus among a panel of experts
convened by a group of State governors to assess the impact of air toxics that
fossil fuel combustion was the main source of atmospheric concentrations of
trace metals (28). Aquatic systems and the food chain were
found to be most impacted by atmospheric trace metals. The majority
of impact on humans was through the food chain, primarily from fish or
shellfish, but toxic metals are also building up in soils, plants, crops, and
game animals
( 2). Average
airborne concentrations of most toxic metals in urban industrial areas are 5 to
100 times those of remote/non-industrial areas. Acidity was a major factor in
facilitating trace metals in the food chain.
Utilities and incinerators are the largest
source of mercury, cadmium, arsenic, chromium, and manganese emissions in the
U.S. (28,1.2). Fossil fuel combustion is also responsible for over
90% of nickel and beryllium emissions. Midwestern coal, especially Missouri and
Illinois, have very high levels of cadmium, nickel, and lead. Gulf
Coast coal is high in most trace metals. Coal from northern
Appalachia is high in arsenic, as well as mercury. Tobacco smoke is
also a major source of cadmium that is accumulating in people
(1.2).
36. Only mercury, arsenic, and selenium are naturally in
the vapor phase in the atmosphere, the rest being non‑volatile and entering the
atmosphere primarily from combustion or smelting. In addition
to large volumes of manmade emissions of the toxic volatile metals, there is
significant cycling of these metals deposited from past emissions (1.9,2.0).
The following table gives annual atmospheric emissions due to human activity
and average levels in precipitation:
Toxic
Metal Emissions
from Toxic Metal
in
Human
Activities Precipitation
(tons
per year
) (micrograms per
liter)
Urban( local
sources) Rural
____________________________________________________________
lead 2,000,000 34 8
cadmium 6,000 0.7 0.5
arsenic 86,000 5.8 0.3
chromium 103,000 3.2 0.9
nickel 108,000 12 2.4
copper 286,000 40 5.4
selenium 15,000
silver 5,500 3.2 0.5
tin 47,000
vanadium 231,000 40 9
zinc 924,000 34 30
Greatly increased levels of toxic metals
such as lead, copper, and zinc have been found in peat bogs, soils, and
sediments compared to preindustrial levels (2), and increasing levels
are being found in fish, oysters, shellfish, other organisms, and plants. This
applies to remote areas and remote lakes indicating atmospheric emissions as
the primary source. Levels of toxic metals in urban and rural areas
of the U.S. are higher than in remote areas of the world by a factor of over
10, with the highest levels in East Coast areas (2). As PH
decreases, the fraction of toxic metal compounds in water in more toxic forms
increases.
The level of arsenic, chromium, and radium
exceeded the health- based screening criteria of EPA
in
phosphogypsum
waste from the majority of sites
tested in Central Florida. Concentrations
of arsenic
,lead ,cadmium,chromium,fluoride,zinc, antimony,copper ,
and thallium exceeded health screening criteria in leachate from some
facilities, with arsenic exceeding the criteria at most facilities(13). Other
toxic metals exceeded the criterion for aquatic life.
VI. THE RELATION OF ACIDITY AND ACID RAIN TO TOXIC METAL IMPACTS ON
AQUATIC SYSTEMS, FISH, THE
FOOD CHAIN, AND HEALTH
37. Methyl mercury bioaccumulates in fish and food
chains; fish‑eating birds and fish‑eating mammals are being seriously
impacted in increasing numbers (16.3,17.4,17b,16.3,18.8). A consistent
feature of waters having a methylmercury problem is low PH (acidic)
or a steady flow of acid deposition (16.3,17b,18c,21). Mercury
concentrations in fish have been found to be inversely correlated
with lake PH, alkalinity, and calcium level.
Also the
permeability of biological membranes to
methyl mercury and to other divalent metal ions is inversely correlated to
water calcium concentration.
As PH decreases, the fraction of mercury in more
toxic forms increases (2).
At PH = 8, almost all of monomethyl mercury is in hydroxyl form
which is least
toxic;
whereas at PH = 6 or
less, an increasing fraction is methyl mercury, the most dangerous
form.
Likewise for
inorganic mercury at PH = 8, almost all mercury is in hydroxyl form;
whereas at PH = 6 or less, over 90% is mercury chloride‑ a more toxic
form.
Microbial net production of methyl mercury
at the sediment/water interface and in
the water
column
is more rapid in low PH waters (18c,21). Decreased Ph also decreases loss of
volatile mercury from lakes and increases mercury binding to particles‑ factors
enhancing the bioavailability of mercury for methylation (18c). Decreased
PH also reduces dissolved organic carbon, which inhibits buildup of methyl
mercury in fish. High temperature has been found to
promote methylation in lake sediments which peaks in summer. The
increased input
of mercury into water bodies in the last century has been a factor
in the increased methyl mercury in fish, with levels of deposition 3 to 5 times
the past century; however other factors previously mentioned cause differences
in net methylation of mercury and content of fish in individual
circumstances. In newly formed reservoirs, the decomposition of newly flooded
organic material stimulates methylation of mercury and appears to be
a predominant that is
increasing
mercury in fish in such water bodies (18c).
Some suggested amelioration strategies
(18c) to reduce mercury in fish include: reduction
in mercury emissions, reduction in acidification of lakes and streams,
manipulation of conditions affecting demethylation, addition of selenium
to
water bodies
, and addition
of lime/calcium source to water bodies.
38. There is
a clearcut
health
danger from acidification of water supplies. The solubility of
highly toxic metals such as lead, cadmium, and aluminum increases sharply
with decreasing PH. Acid water leaches metals from soil, lake sediment, metal
pipes, and solder joints‑all with clear danger to human
health. It also releases asbestos fiber from cement‑asbestos
pipes commonly used in public water systems (22 &23.3).
The adverse health effects of lead
are so well known that the presence of increased lead in drinking water being
found is a clear indication of a health problem, according to John Wood of the
Gray Freshwater Biological Institute in Navarre, Minn. (21) A
major new concern is the growing presence of aluminum in water due to acid
rain. Aluminum is the third most common element
on earth
,
but is insoluble in neutral or alkaline water. But aluminum becomes
increasingly solubilized as PH falls below 6.0, and the aluminum
salts formed become much
more toxic
( 21).
Because of acid rain the increase of dissolved aluminum in lakes is
absolutely massive
, according to researcher Pamela Stokes of
the Univ. of Ontario. Aluminum is toxic to
fish at only 100 parts
per billion
( parts
per billion(ppb) and much higher levels are being
observed. Adverse effects of aluminum on fish and birds
is becoming
common. A study on the
influence of PH on metal toxicity to fish found toxicity of aluminum increases
with decreases in PH, and the recent declines of east coast striped bass is
related to
decreasing PH
( 25). In
test, all fish died within 7 days at PH 5.5 or lower at any concentration of
aluminum tested. At PH 6.5, exposure to 100 micrograms
per liter
( parts per billion(ppb) of
aluminum resulted in 97% mortality by day 7. At PH 7.2, exposure to 300
micrograms per liter of aluminum resulted in all fish dead within 7 days.
Considerable evidence exists
supporting a relation between aluminum and humans having neurological disorders
such as
dementia,
Alzheimersdisease
,
Parkinson's disease, and amyotrophic lateral sclerosis, which are becoming more
common (22,21). Acidification also leads to a buildup of the more toxic form of
metalloids such as arsenic and selenium in water (21).
VII. European Experience with Mercury Emissions
39. Swedish and Danish studies found that mercury
deposition rates in densely settled areas of Scandinavia have increased by a
factor of 5 in this century, with most of the increase since
WWII; whereas
in remote areas deposition rates
increased by less than a factor of 2. They concluded
combustion emissions are the main source of the increased deposition rates
(21.6,20). Danish researchers have found that the principal source of mercury
in peat bogs is from air borne deposition. Natural input from rock
underneath is small due to limited capillary action of bogs (18d).
The mercury and other toxic metals
accumulating in Scandinavia's forest floors was found to be affecting
watersheds and to be cycling through the entire ecosystem (18d), adding to the
thousands of lakes with dangerous levels of mercury in the fish in
Scandinavia. In Sweden where mercury emissions have been severely
reduced, most of the input of mercury into freshwater lakes occurs by
the exchange of mercury from soils and forest floors, where over 600
tons has been estimated to have accumulated, in regions where acid
precipitation is severe (21).
Because of documentation of
dangerous levels of mercury and cadmium in the food chain and humans in some
areas of Europe
and
Europe
�s
widespread use of incinerators, several European
countries have placed bans or limitations on use of mercury and cadmium in
products such as batteries and paint (55)). They are also
developing emissions caps for mercury and other toxic metals. The Swedish
emission limit for mercury is 40 micrograms per cubic meter.
A study by the Swedish
Environmental Protection Board found that approx. 50% of mercury in the Swedish
environment was due to incinerator emissions
(55). Mercury emissions in Germany were found to be over 20
tons per year (24). Incineration and
wastewater
treatment
were
found to be the biggest sources of metals pollution
in Switzerland (12) along with crematoria (14.9). Heavy metals are
inevitably concentrated in current incineration plants to dangerous levels.
Studies in several European countries have found 35 to 60% of incinerator
emissions of mercury to be due to batteries (55),21,24). Both
Switzerland and Sweden have declared any battery containing over .025% cadmium
or mercury to be a hazardous waste and require labeling. The European
Commission is proposing a European-wide limitation on the mercury
content of batteries to go into effect in
1992(55)). Emissions of mercury due to batteries have
been declining due to such limitations; however, emissions of some other toxic
metals have increased due to the changes.
VIII. Experience with Emissions Control Equipment for
Toxic Metals and Mercury Reduction Options
40. Most air pollution controls such as dry scrubbers and
electrostatic filters have not been found to be effective at removing toxic
metal emissions such as mercury (17, 17.1, 17,9,
28,39). A study by the Minnesota Pollution Control Agency
concluded that mercury was not effectively removed in most incinerators that
have been tested (18.3). Advanced coal cleaning techniques remove
approx. 21% of mercury and 55% of lead (39), and electrostatic
precipitators remove
the majority of
most toxic metals
other than mercury and an average of 16% of mercury. Flue
gas desulfurization has a mercury removal range of 0 to 60% with a
median of 17% (39).
Sampling at Minnesota and California incinerators with dry
scrubbers and filters has found most mercury is not removed (often less
than 30%). Carefully maintained and monitored wet scrubbers
operating at low stack temperatures have been found to be able to control
emissions of most toxic metals other than mercury. Wet scrubbers
have been found to remove 10% to 65% of mercury depending on the fuel and
other conditions (18,39). However, operation of scrubbers below
300 degrees faces other problems where acid gases form or in combustion
processes where calcium and chlorine are present. Calcium chloride and other
such compounds readily absorb water and will blind the filter
bags. Also, many of these scrubbers or spray dry absorber/fabric
filter systems have been found to experience degradation of performance in
periods after startup and compliance/performance testing due to caking of
solids on filter fabrics, plugging of ash removal systems, and carryover of
liquids from the absorber vessel (22). The mercury
removal rate for such SDA/FF systems on mass burn incinerators ranged from 30
to 85% (22).
Most dry or semidry air pollution control systems
were not found to be effective at controlling mercury, arsenic, or selenium‑
without other more specific control mechanisms (18.3). One study
found a dry scrubber plus a baghouse was able to remove 75 to 85% of
mercury emissions, while dry scrubbers with electrostatic precipitators removed
only 35 to 45% of mercury (24). However, some researchers at state and
federal environmental regulation agencies as well as university researchers and
environmental group researchers indicate that no pollution control technology
has been found that effectively controls emissions from some toxic metals such
as mercury (21, 17, 21.6, 21). They also indicate that toxic
ash and dust are a serious health threat to those handling or working with it,
as well as a danger to groundwater and drinking water. Hundreds of other
toxic chemicals including highly dangerous dioxins, furans, and
chlorine/bromine compounds‑ as well as acid pollutants and greenhouse gases
have been found to be emitted by incinerators (21,29).
41. The amount of chlorine in fuel affects which forms of mercury are
generated and the success of removal by pollution
controls. Higher chlorine levels produce more
mercuric chloride‑ which is highly volatile but easier to control than
elemental mercury (23.2). Mercury in the flue gas of a coal
fired power plant was found to be almost totally elemental mercury due to lower
chlorine levels in the fuel (22,16.3). However higher
chlorine levels in incinerators which produce mercuric chlorides also produce
more volatile arsenic and chromium compounds which are more likely to escape
dry scrubbers or similar controls.
42. A group of toxic air emission experts assembled at
a workshop by State governors indicated that energy conservation measures are
the most cost- effective method of controlling trace metals such as mercury
and cadmium (28). Fuel switching to coal low in mercury or
cadmium was also very cost effective in specific
cases, since
coal from certain areas has much higher levels of mercury and cadmium than from
other regions. Western coal in general has less mercury than
eastern coal (34). Northern Appalachia coal and lignite from
the Gulf Coast and North Dakota have the highest levels of
mercury. Midwest and Gulf Coast coal has the highest levels of
cadmium, with extremely high levels in Missouri and Illinois.
Mercury emission levels
can be reduced 35 to 50% by switching from high mercury coal to lower
mercury coal (28, Table 3-1). Physical coal cleaning can reduce
mercury emissions approx. 30%, higher for some coals (28, Table 3-5).
Existing control
technologies mercury removal efficiencies range from almost none for hot-side
electrostatic precipitators (ESP) to 35 to 40 % for cold-side ESPs,
wet scrubbers,
and baghouses
( 28).
Among new technologies,
activated carbon used with scrubbers and ESP or baghouses appear to
remove 80 to 90% of mercury (28). Sodium hypochlorite with
scrubber, lignite coke NOx Technology, and Sulfur-Impregnated Alumina
and Carbon appear to have potential to remove over 95% of mercury from
emissions. However, mercury also tends to volatilize from waste
piles so net mercury removal is more questionable. Minnesota PCA estimates cost
of effective mercury control for coal plants or incinerators at $2500 to $5000
per pound. A policy study by MPCA recommended emission limits should
be no more than 50 pounds per year, much lower than current EPA
standards.
Physical coal cleaning
removes 25 to 69% of cadmium depending on chemical composition, and from 10 to
75% of other trace metals (28, Table 4-3). Baghouses are
highly effective at removing cadmium and most trace metals that are not
primarily in elemental vapor form such as mercury, arsenic, and
selenium. ESPs are more effective for large particle sizes.
IX. TOXIC METALS IN FLUE ASH AND BOTTOM ASH
43. Large volumes of most toxic metals are present in
both emissions and ash from municipal or hospital incinerators or from coal
power plants. Extensive information on content of waste ash and on
emissions is available from EPA, FDEP, the California Air Resources Board,
Environmental Defense Fund, Univ. of Florida researchers,
etc.(17,21,30,30b,30c). A listing of average metal content of coal
and coal ash from a TVA plant is given in Appendix 3. Coal plants produce
approx. 90 million tons per year of ash and 35 million tons of flue
gas
desulfurizationwastes
( 30). Coal
plants with scrubbers produce for each megawatt of power about 308 tons of fly
ash, 77 tons of bottom ash, and 364 tons
of
fluegas
desulfurization waste
for landfilling. Most coal ash laboratory tests have found
cadmium and arsenic at levels considered hazardous per EPA RCRA standards,
along with lower levels of other toxic metals (30). Toxic
constituents from coal combustion waste disposal sites have been detected in
both on-site and off-site ground and surface water. Where the depth
to groundwater is less than 30 feet, "there is a reasonably high potential
that leachate will reach groundwater unless extensive precautions are
taken" (30). The high PH that often characterizes Western coals
tends to cause the release of harmful toxic metals such as arsenic, selenium,
and manganese.
According to an article
in the Wall Street Journal (20), most municipal incinerators reduce volume
approx. 60
% ,
leaving 40% to
be landfilled. This article also found most to be expensive to
build and operate and to result in high garbage bills or expensive
energy. From California experience the bottom ash and fly ash
contain heavy metals and other pollutants such as dioxins at levels that make
it hazardous waste and subject to disposal costs at least twice that of normal
garbage. Other new technologies such as composting appear to
be safer environmentally than incineration
and also
much lower in cost (20).
44. Minnesota studies have found from 1% to 10% of ash
at mass burn facilities to be flue ash, while 30 to 40% of refuse
derived fuel (RDF) ash was fly ash (18.3). Minnesota tests have
found high levels of cadmium and other toxic metals in most mass burn
incinerator fly ash (see Table). RDF plant fly ash tended
to have lower levels of mercury due to pre‑sorting of
garbage. However, RDF plants were found to tend to have higher
emissions of dioxins and furans.
Toxic
Metals in Flue Ash of Incinerators (18.3)
Heavy
Metals
Metals in
Waste Metals in Flue Ash
(grams per ton) � ����
�( parts
per million)*
_____________________________________________________________
Lead 1500 30,000
Cadmium 20 2,000
Mercury 5 3,000
Copper 1000 3,000
Nickel 100 100
Zinc 3200 80,000
*
multiply
by 0.91 to convert to grams per ton
For incinerators with
scrubbers, the distribution of cadmium was 30% in the bottom ash, 62 to 65 % in
flue ash, and 5 to 8% as emissions (24). Toxic metals have been
found to be increasingly soluble in acidic
conditions. Cadmium was found to be 85%
soluble at a PH of 4.0. Flue ash tends to be alkaline which
reduces solubility of toxic metals such as cadmium, mercury, lead,
etc. However, high PH causes the release of harmful toxic
metals such as arsenic, selenium, and manganese, and exposure to acidic water
or rainfall over time can reduce the PH.
Nationally, tests have
found incinerator fly ash cadmium to exceed the EPA EP toxicity
standard 97% of the time (18.3 & 21). Combined bottom and fly ash exceeded
the cadmium toxicity standard 14% of the time. For
bottom ash only cadmium exceeded limits 2% of the time. RDF
plant fly ash in Minnesota tended to have lower levels of mercury due to pre‑sorting. Because
of their adverse experience with toxic metals, Minnesota requires all municipal
solid waste incinerators to test ash quarterly for leachable metals
via EPA Method 1312‑Synthetic Precipitation Leach Test for
Soils. Minnesota also requires ash to be disposed of in
permitted
monofills
with liners
and leachate collection systems (18.3).
45. A significant fraction of oxidized mercury added to
a soil sample is quickly reduced and volatilized
(22,20). The evaporation of mercury captured in soils or fly
ash escalates dramatically(exponentially) as surface temperature increases
above 70 degrees F (57,20). One study reported that over a
period of 14 days, from 10 to 15% of the mercury in fly ash from a fabric
filter evaporated at room temperature (22). Emission
levels of waste ash piles from
chloralkali
plants
have been found to be 25% as much as active plant
emissions. At a temperature of 86 degrees, an old
chloralkali
waste
pile was found to produce emissions in the vicinity approaching EPA ambient air
quality guidelines (57,20). This is a special
problem in Florida where dark fly ash often attains a temperature of 140
degrees.
X. Heavy Metals and Drinking Water
46. Researchers have found the levels of toxic metals in water due to
acidic pollutants are having serious and permanent adverse health effects
(2.8). Over 38 million Americans now drink water containing over 20
parts
per billion
( parts per
billion(ppb) lead(25.5). An EPA study estimates
that reducing lead content of water in homes to 20 parts per billion(ppb) would
bring an economic benefit over $1 billion and a net savings of over $800
million, as well as large scale reductions in health problems and learning
disabilities. Recent studies have concluded drinking water is
now the number one source of lead in the human blood stream (2.8 &
2). The largest source of lead and heavy metals in drinking
water is from the dissolving of lead or other heavy metals like cadmium and
copper from home drinking water pipes or lead
solder. The more acidic and softer drinking water
is,
the more
heavy metals
are absorbed. Heavy metals in some surface water used as drinking water
are also increasing (25 & 2).
According to EPA, lead in
drinking water is a special problem in Florida due to the high acidity of much
Florida drinking water, which causes more rapid absorption of lead and other
heavy metals from pipes
or soil
( 2.5). An
EPA survey of drinking water in 1986 (2.5,2.8) found that average lead levels
in drinking water in many areas of Florida were above the EPA
drinking water standard of 20 parts per billion(ppb)(mcg/dl); and that thousands
of Florida children have been drinking water with lead levels above the level
that studies by the U.S. Center for Disease Control and EPA
indicate
areenough
to
permanently adversely affect learning ability.
Thus EPA
ordered all school districts in Florida
to test their water for lead, and issued a health warning regarding lead in
drinking water in Florida. Several Florida
counties including Leon and Broward found water from over 20% of the school
drinking fountains to contain levels of lead that have been shown to cause
serious decreases in learning ability.
Over 50 % of home
drinking water tested in some areas of Florida also had dangerous levels of
lead. As seen from other studies, even levels of lead
considerably lower than the EPA standard and the average level of lead in
Florida drinking water have been shown to have serious health effects.
47. The Center for
Disease Control
( CDC)
standard for" excessive absorption" of lead by children is 25
mcg/dl.
However
the EPA
Clean Air Science Advisory Committee has recommended a reduction to 10
mcg/dl. Over 60% of U.S. children under 5 years of age exceed
this level, according to an EPA survey, and over 40% of adults
(9). As a beginning to reach the goal for blood lead
level, EPA has reduced the EPA drinking water standard to 15 parts
per billion(ppb) from 50 parts per
billion(
ppb )( 2.3). The
drinking water of approx. 40 million Americans exceeds 20 parts
per billion(ppb) lead (9).
48. The following table prepared under an EPA contract
and presented at a
New York workshop on
acid deposition
( 18.6)
obtained results very similar to
another study by Richards
and Moore
( 18.6.3). It
gives the estimated relation between lead concentrations in drinking water and
human blood levels:
Lead in Tap
Water Lead in Blood
Due to Water
(parts per
billion( ppb
) (mcg/dl)
‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑ ‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑
1 3.4
5 5.8
10 7.4
20 9.1
25 10.0
50 12.6
100 15.8
Although lead in drinking
water appears to currently be the number one cause of lead in human blood, it
is responsible for less than 50 % of lead in humans. Thus
lowering the EPA drinking water standard to 15 parts per billion(ppb) does not
appear sufficient to reduce the level of lead in people's blood who are
drinking water at the EPA standard to the blood lead level recommended by the
EPA Clean Air Scientific
Advisory Committee
( 10
mcg/dl). In fact lowering the standard to 10 parts
per billion(ppb) may not be sufficient to lower blood lead level to the
recommended level
( 26.5).
Similar conclusions had
also been
reached earlier
( Moore et al
in a 1980 EPA study & 26.5). Several
researchers have concluded that lowering standard near 5 parts
per billion(ppb) is necessary to ensure protection from significant
adverse
health effects
, and have
offered analyses supporting the cost effectiveness of such a lowering of the
standard (8). A study by Erik Jansson estimated that a
program resulting in an average blood lead reduction of 2 mcg/dl would save
approx. $6 billion in medical cost and reduce U.S. cancer deaths from approx.
22% of the population to about 20 % of the population (all else being
equal). Additional reductions would bring roughly
proportional savings (2.8).
XI. Toxic Metals from Sewer Plants and Urban Runoff
49.
Sewage treatment plants
and septic tanks are a major source of toxic metal discharges into
rivers, estuaries, and bays in the U.S. Mercury, lead, copper,
chromium, etc. have been found in sediments and the food chain in many areas
near sewer outfalls (27). Municipal sewer sludge in Rochester, N.Y.
averages 1.24 ppm mercury, with 6% being methyl mercury
(27).
Dental amalgam
has been found to be the largest source of
mercury in most sewers and sewer sludge, with
the 2 largest sources being dental office effluent and excretion
into sewers by those with dental amalgam fillings (14.9). Sewers are a major source
of mercury in water bodies, fish, and wildlife, with over 30% of U.S. lakes
having fish consumption warnings and similar for rivers and
bays. The average amalgam filling
has
�
gram of mercury
which is enough to contaminate all fish in a 10- acre lake to dangerous
levels(35a). All sewer sludge has high levels of mercury due to
dental amalgam which results in mercury in crops and methylation of
mercury by soil bacteria, with subsequent
outgasing
of
high
levels of mercury (14.9).
Use of sewer sludge on gardens and farms was
found to lead to buildup of mercury in the soil and uptake by
plants. Industrial and commercial discharges have been found to be poorly
monitored and enforced by most public sewer systems. Four types of
toxic metals and two banned pesticides were found in plant samples and
sediments taken from St. Joseph's Bay where large areas of sea grasses
are dying (57). Toxic metals have also been found
in sediments and the food chain in other coastal bays and lakes throughout
Florida, with an additional source of such toxics in sediments being
urban runoff (27.5).
References
(1)
ATSDR/EPA
Priority List for 20: Top 20 Hazardous Substances, Agency for Toxic Substances
and Disease Registry, U.S. Department of Health and Human Services,
2019,
https://www.atsdr.cdc.gov/SPL/
; & (b)
Toxicolological Profile,
Mercury
,
Lead,
Arsenic
,
Cadmium
,
&
(c)
Case Studies in
Environmental Medicine,
https://www.atsdr.cdc.gov/csem/csem.html
;
& (d) Minimum Risk Levels (
MRLs
), 2020,
(1.1)
ATSDR ToxFaQs for
Mercury
,
Lead
,
Arsenic
,
Cadmium
,
Aluminum
(b) Health Effects of Mercury,
https://www.atsdr.cdc.gov/mercury/docs/11-229617-E-508_HealthEffects.pdf
;
Other Toxics,
https://wwwn.cdc.gov/TSP/substances/ToxOrganSystems.aspx
;
(1.2)
U.S. Environmental
Protection Agency, Hazardous Air Pollutant Hazard Summary, Fact Sheets,
EPA: In Risk Information System, 2018,
https://www.epa.gov/environmental-topics/air-topics
:
& Human Health Risk Assessment,
https://www.epa.gov/risk/human-health-risk-assessment
; & Ecological Risk Assessment,
https://www.epa.gov/risk/ecological-risk-assessment
; &
Air Pollutant Facts
&
Mercury
Page,
www.epa.gov/mercury/information.htm#fact_sheets
;
&
EPA
Acid
Rain Program
, &
Surface Water Monitoring
&
Clean Air Status
Th
e Great Lakes Information Page
; &
Fish and Shellfish Advisories and Safe Eating Guidelines
,
Great Lakes Open Lakes
Trend Monitoring Program: Total Mercury,
https://www.epa.gov/great-lakes-monitoring/great-lakes-open-lakes-trend-monitoring-program-total-mercury
; &
Fish Tissue Data Collected by States for State Fish
Advisories,
https://fishadvisoryonline.epa.gov/FishTissue.aspx
; &
EPA, Indocrine Disruption,
https://www.epa.gov/endocrine-disruption
; & Lead in Drinking Water in Schools and Childcare
Facilities, 2017,
https://www.epa.gov/dwreginfo/lead-drinking-water-schools-and-childcare-facilities
;
(1.3) U.S. EPA, 40 CFR Part 132, Water Quality Criteria,
Wildlife Protection & Human Health, & Drinking Water Regulations,
https://www.epa.gov/regulatory-information-topic/regulatory-information-topic-water#drinking
;
& Environmental Mercury Laws,
https://www.epa.gov/mercury/environmental-laws-apply-mercury
;
& Environmental Lead Laws,
https://www.epa.gov/lead/lead-laws-and-regulations
;
(1.5)National
Wildlife Federation, Cycle of Harm:
Mercury�s
Pathway
from Rain to Fish in the Environment, May, ,
https://www.researchgate.net/publication/242778694_Mercury's_Pathway_from_Rain_to_Fish_in_the_Environment
;
& (b) NADP/Mercury Deposition Network, Total Mercury
Concentration,
http://nadp.slh.wisc.edu
; & Total Mercury Wet Deposition , 2017,
http://nadp.slh.wisc.edu/maplib/pdf/mdn/hg_dep_2017.pdf
;
(1.6)
Water Quality Criterion for the
Protection of Human Health: Methylmercury,
United States
Environmental Protection Agency, Office of
Water 4304 EPA-823-F-01-001,
https://www.epa.gov/environmental-topics/water-topics
; &
www.epa.gov/waterscience/criteria/methylmercury/factsheet.html
(1.7)
Agency for Toxic Substances and Disease Registry, U.S. Public
Health Service,
https://www.atsdr.cdc.gov/toxprofiledocs/index.html
;
Toxicological
Profile for Mercury
", 2017,
https://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=115&tid=24
; &
A Media Advisory,
https://www.atsdr.cdc.gov/substances/toxsubstance.asp?toxid=24
:
New MRLs for toxic substances,
https://www.atsdr.cdc.gov/minimalrisklevels/index.html
(1.8) B. Windham, annotated bibliography, Documentation of
Common Exposure Levels and Adverse Health Effects due to mercury
from amalgam fillings�; (over 2000 medical study or scientific
references)
www.myflcv.com/indexa.html
;
(1.9) U.S. EPA, Mercury
Study Report to Congress, Vol 1, 1997; & (
b)
Harmful
Interactions of Non- Essential Heavy
Metals with Cells of the Innate Immune System. J
Clinic ToxicolS3:005. Theron
AJ,
Tintinger
GR, Anderson R (2012)
(2
) A History of Global Metal Pollution
, 1996, J.O.
Nriagu
.
& Dr. B. Victor,
Heavy metal contamination of global environment
; 2013,
&
National Seminar on Impact of Toxic Metals, Minerals and
Solvents leading to Environmental Pollution
-
2014 Journal of Chemical and Pharmaceutical Sciences; �&
"Global
Metal Pollution- Poisoning the Biosphere", Environment, Vol 32,
No. 7, Sept. 1990,
J.O.Nriagu
;
& (b) Dr. John Winchester, FSU Dept. of Oceanography,
In J.M. Pacyna and B Ottar (editors), "Control and
Fate of Atmospheric Trace
Metals", Kluwer Academic Publishers, 1989, p311‑320;
& (c) "Trace Metals in Atmospheric
Deposition", Atmospheric Environment, Vol 16, #7, P167‑170,1982,
J.N. Galloway et al; & Mason RP, Fitzgerald WF, Morel FM, 1994, The
biogeochemical cycling of elemental mercury: Anthropogenic influences,
Geochimica
et
Cosmochimica
Acta,
58(15): 3191-8; & Nature, Vol 338, 2 March 1989.
(2.1)
"Mercury: Present and Future Concerns", Environmental Health
Perspective, Vol 96, p159-166, 1991. W.F. Fitzgerald & T.W.
Clarkson, & Blumer and Reich, Environment
International, Vol 3,1980; & M.N Weissman, Columbia Univ.,
Science News, 12-5-95, p391.
(2.2
)
Heavy
Metal Toxicity and the Environment,
Tchounwou
PB,
Sutton DJ, et al;
Molecular, Clinical and Environmental
Toxicology
pp 133-164 | .
doi
:
10.1007/978-3-7643-8340-4_6
(2.3)
Tallahassee Democrat, 11‑2‑90 & Tallahassee Democrat,
"Cut Lead Level in Water",5‑8‑91 & Florida Times Union,
"EPA Orders Reduction in Drinking Water Lead",
5‑8‑91; & The Atlanta Constitution, "CDC: Lead levels still
poisoning kids", Charles Seabrook, July
17,1990; & Center for Disease Control,
in Tallahassee Democrat, "Lead Poisoning", Dec 8,1992,
Section 3A; & "Lot of Lead found in School Water", Orlando
Sentinel, 4‑28‑89. & The Washington Post, "Dangerous Amounts of Lead
in Much
Drinking
Water
",Nov
6, 1986; A. Beasley, "The danger
within: Lead lurks in pipes", Orlando
Sentinel, 11-24-92 & Miami Herald,
11-2-92.
(2.4)
Mercury
Contamination from
Dental
Amalgam
.
Tibau
AV, Grube BD,
J Health
Pollut
.
2019
Jun 4;9(22):190612.
(2.5)
"Cadmium and Lead Content of Maternal and Newborn
Hair", Archives of Environmental Health, Oct 1981. G.
Huel
et
al,
(2.6
) A.
H.Perier
, Chief of Science & Technology, EPA
Drinking Water Office, in N.Y.Times,11‑17‑90; & J.M. Davis et al,
"Lead and Childhood Development", Nature, 1987, p297-300.
(2.8) R. Merchant, Florida Dept. of Environmental
Regulation, Interoffice Memorandum to R.S.
DeHan
,
Sept. 8,1987; & Birth Defects Prevention News, March 1986; &
Erik Jansson, National Network to Prevent Birth
Defects,"Comments
on EPA Draft
Proposal to Revise Standard for Lead in Drinking Water", Jan 15,
1988; & P.
Shabecoff
,
"EPA Mulls New Rules to Reduce Lead in Drinking
Water", New York Times, Nov 1986; & Dr.
R.Goyer
, Chairman of
Pathology Dept., Univ. of Western Ontario Medical School, NAPAP
Hearing, House Committee on Science, Space, and
Technology, April 27, 1988; & D. Worth et al,
"Lead in Tap Water", in D.R. Lyman et al,
Environmental
Lead
, Academic
Press, New York, 1981; & The Washington Post, "Dangerous
Amounts of Lead in Much Drinking Water", Nov
6,
1986.
(3) "Bone Lead Levels and Delinquent Behavior",
J. of the American Medical Association, Feb 7, 1996; 275: 363-369, H.L.
Needleman et al; & Science News, Vol149, Feb,10, 1996;
&
www.myflcv.com/violence.html
(3.1) "Psychometric
Evidence that Mercury May be an Etiological Factor in Depression,
Excessive Anger, and Anxiety", Psychological Reports, 74, p67-80,
1994,
R
.L.Siblerud
et al, & R.
Kotulak
,
"Probing the Violent Mind, Experts Monitor Toxic Chemical in Wake of
U.S. Crime Wave", Chicago
Tibune
,
1994; Archives of General Psychiatry, Jan 1994; &
www.myflcv.com/depress.html
;
(3.3) Florida Dept. of Environmental Protection,
Florida Coastal Sediment Contaminants Atlas
: A Summary of Coastal Sediment
Quality Surveys
, 2001; & Mac Donald Environmental
Sciences Ltd.,
Development of an Approach to the
Assessment
of Sediment Quality in Florida Coastal Waters
, FDEP, January 1993,
&
J.H.Trefry
et al, Marine
& Environmental Chemistry Laboratories, Fla.
Institue
of
Technology,
Toxic Substances
Survery
for
the Indian River Lagoon System,
Volume I:
Trace Metals in the Indian River Lagoon, SJWMD, Oct 1996.
(3.9)
D.C.Heil
, Fla. Dept. of Natural Resources, Division
of Marine Resources,
Evaluation of Trace Metal Monitoring in Florida
Shellfish,
March 1986, & FDEP, Toxic metal levels in
Florida shellfish, 1990; & Science News, Nov 6, 1986, P327‑. &
Trace metal residues in shellfish from Maryland waters,
1976�1980
(4)
"
Cadmium Hazards to Fish, Wildlife,
and
Invertibrates
",
U.S. Fish & Wildlife Service, Contamination Hazard Biological Report
85(1.2), 1987.
(4.5) (a) Intermittent
low-level lead exposure provokes anxiety, hypertension, autonomic
dysfunction and neuroinflammation.
Shvachiy
L
, Rocha
I et al;
Neurotoxicology.
2018 Aug 8; & (b)
Association of low-level blood lead and blood pressure in
NHANES 1999-2006.
Scinicaniello
F,
Murray HE et al;
Environ Res.
2011
Nov;111(8):1249-57; & (c) Biochemical effects of lead exposure on battery
manufacture workers with reference to blood pressure, calcium metabolism
and bone mineral density.
Dongre
NN,
Suryakar
, AN et al;
Indian J Clin
Biochem
.
2013
Jan;28(1):65-70; & (d) J. Schwartz et al (EPA), Pediatrics, March
1986; &"The Relationship Between Blood Lead Levels &
Blood Pressure", American Journal of
Epidemiology, Vol 121,1985. J.L. Pirkle et al;
& (e) Modification by ALAD of the association
between blood lead and blood pressure in the U.S.
population: results from the Third National Health and Nutrition Examination
Survey.
Scinicariello
F,
Yesupriya
A, et al;
Environ
Health
Perspect
.
2010
Feb;118(2):259-64.
(5)"
Nutrition, Environmental Toxins, and Computerized EEG
", Journal of
Learning Disabilities, May 1985. R.W. Thatcher et al; &
�Cognitive and
Behaviorial
Effects
of Toxic Metals�, Nov 2000; &
NUTRITION
TRACK: ENVIRONMENTAL TOXINS
, 2018; &
"Main and Interactive Effect of Metallic Toxins
on Classroom Behavior, Journal of Abnormal Child
Psychology, Vol 13,1985.
M.Marlowe
(6)
National Institute of Environmental Health Sciences, New England
Journal of
Medicine, Oct
, 1992 &
P.A.
Baghurst
et
al,
"
Environmental Exposure to Lead and Children's
Intelligence at Age of 7 Years
", New
England Journal of Medicine, October,
1992;
&
(b) Marlowe
M,
Errera
J,
Jacobs J.
Increased lead and cadmium burdens among mentally
retarded children
and
children with
borderline
intelligence. Am
J
Ment
Defic
1983 Mar;87(5):477-83; & (c)
Thatcher RW, Lester ML,
McAlaster
R,
Horst R. Effects of
low
levels of cadmium and lead on cognitive functioning in
children. Arch Environ Health 1982 May-Jun;37(3):159-66; &
(d)
Jiang HM,
Han GA, He ZL. Clinical significance of hair cadmium content in the
diagnosis of mental retardation of children. Chin Med
J
(
Engl
)
1990 Apr;103(4):331-4.
(7) R.O. Pihl et al, "
Hair element content in Learning Disabled Children
",
Science
,Vol
198,1977,p204‑6.
(7.5)
Steskal
V, Developmental
Effects of Prenatal and Neonatal Mercury Exposure, 2002,
www.melisa.org
; &
Effect of Low-Level Prenatal Mercury Exposure on Neonate
Neurobehavioral Development in China
, 2014, &
Mercury Exposure and
Children�s
Health,
2011;
& (d)
Prenatal methylmercury, postnatal lead exposure,
and evidence of attention deficit/hyperactivity disorder among Inuit children
in Arctic Quebec. Boucher O, Jacobson SW et al;
Environ
Health
Perspect
.
2012
Oct;120(10):1456-61. & (e)
Concentration of mercury, cadmium, and lead in breast milk from Norwegian
mothers: Association with dietary habits, amalgam and other factors,
Science of the Total Environment ,
Volume
677
, 10 August 2019, Pages 466-473.
(7.6
)
R.
Sikorsky et
al, "Women in Dental Surgeries:
Reproductive Hazards", Int Arch
Occup
Environ Health 59:551- 557, 1987;
&
www.myflcv.com/dental.html
;
(7.7
)
Developmental
Exposure to Endocrine Disrupting
Chemicals and Type 1 Diabetes Mellitus. Howard SG.
Front
Endocrinol (Lausanne).
2018 Sep 3;9:513; & (
b)
Taurine improves
low-level inorganic arsenic-induced insulin resistance by activating
PPARγ-mTORC2 signaling and inhibiting hepatic autophagy. Gao N, Yao X
et al;
J Cell
Physiol.
2019
Apr;234(4):5143-5152. & EDCs,
www.myflcv.com/endoDC.html
;
(8) D. Bellinger et al, New England Journal of
Medicine, Vol 316, No. 17, April 23,1987 &
Pediatrics, 87:219-227; 1991; & "The Relationship Between Prenatal
Exposure to Lead and Cognitive Anomalies:, J of the American
Medical Association, June 8 1984, H. Needleman et al,& "Long Term
Effects of Exposure to Low Doses of Lead in Childhood: An
11-year follow-up report�, New England J. of Medicine, 322:83-88,
1990 & "Low-Level Lead Exposure and the IQ of
Children, JAMA, 263:673-678,1990.& E.
Jannson
,
Birth Defect
Prevention News, Jan 19,1988.
(9) "Blood
Lead
Levels
in the U.S. Population", Journal of the American
Medical Association, 1994, 272: p277-283. Brody, D.J. et al, & Science
News, Sept 13, 1986, p164; & � The effect of different workplace
nanoparticles on the immune systems of employees.
Kurjane
N,
Zvagule
T,
et al;
J
Nanopart
Res.
2017;19(9):
320; & (d) Seasonal and spatial variations of magnetic susceptibility and
potentially toxic elements (PTEs) in road dusts of Thessaloniki city,
Greece: A one-year monitoring period.
Bourliva
A,
Kaniranis
N et al;
SciTotal
Environ.
2018 Oct
15;639:417
-427.
(9.1) "Reproductive and Developmental Toxicity of
Metals
",
Scandanavian
J.
of Work & Environmental Health, 11:145-154; 1985. T.W. Clarkson et al,
(9.2)
(
a
)
Associations of cumulative
exposure to heavy metal mixtures with obesity and its comorbidities among U.S.
adults in NHANES 2003-2014. Wang X, Park SK et al;
Environ Int.
2018 Dec;121(Pt 1):683-694;
& (b)
Heavy metal exposure causes changes in
the metabolic health-associated gut microbiome and metabolites. Li X,
Brejnrod
AD et al;
Environ Int.
2019 May;126: 454-467; & ( c
) Impact of in vitro heavy metal exposure on pancreatic β-cell
function. Dover EN, Patel
NY,
Styblo
M.
Toxicol
Lett
.
2018 Dec
15;299:137
-144; & (d)
Role of cadmium
and arsenic as
endocrine disruptors
in the metabolism of
carbohydrates: Inserting the association into perspectives. Sabir S, Akash MSH
et al;
Biomed
Pharmacother
.
2019
Mar
25;114:108802
; &
(e)
Evaluation of status of
toxic metals in biological samples of diabetes mellitus patients. Afridi
HI,
Kazi
TG, et al;
Diabetes
Res Clin
Pract
.
2008
May;80(2):280-8;
&
(
f)"Toxic
Effects of Metals", in
Casarett
and
Doull's
Toxicology: the Basic
Science of Poisons
, McGraw-Hill Inc., N.Y., 1993. R.A.
Goyer
et
al,
(9.4) "Fetal Methylmercury Poisoning",
Ann Neurol, 7:348-355,1980 D.O. Marsh et al; &
Congenital Minamata Disease:
Intrauterine Methylmercury Poisoning", Teratology, 18:285-288,
1978. H. Harada; & K.
Krafft
et
al, Univ. of
Cincinati
Medical
Center, Science News, 2/16/85.
(9.5) (
a)
Arsenic
exposure and prevalence of type
2 diabetes in US adults.
Navas-Acien
A,
Silbergeld
EK, et al;
JAMA.
2008
Aug 20;300(7):814-22;
&
Arsenic
exposure, diabetes-related genes
and diabetes prevalence in a general population from Spain.
Grau-Perez M,
Navas-Acien
A et al;
Environ
Pollut
.
2018
Apr;235:948
-955; &
The role
of arsenic in obesity and diabetes.
Farkhondeh
T,
Samarghandian
S
et al;
J Cell
Physiol.
2019
Jan 22; & (b)
Exposure to heavy
metals during pregnancy related to gestational diabetes mellitus in
diabetes-free mothers. Soomro MH,
Baiz
N,
et al;
Sci
Total Environ.
2019
Mar
15;656:870
-876.; & �
Association
between maternal urinary speciated arsenic concentrations and
gestational diabetes in a cohort of Canadian women. Ashley-Martin J,
Dobbs L, Ashley-Martin J,
Dodds
L
et al;
Environ Int.
2018 Dec;121(Pt 1):714-720
(9.6
)
Detoxification
:
Heavy Metals Testing and Chelation Therapy-Lyn Patrick, ND (DMSA for challenge
test & chelation or MCP
)- https://cdn.simplecast.com/audio/4ed1adc9-1b56-4d5d-a2fb-9106997393d4/episodes/6c148e92-bf66-424f-9431-e1a01dbf870d/audio/8773d9e9-9e26-4b2f-aec6-a2004e921e66/default_tc.mp3?aid=rss_feed&feed=1NYUFSRI
& (b)
Take Charge of Your Health (Testing &
Chelation of Heavy Metals) - Dr. Chris Shade - CEO of Quicksilver
Scientific
https://s115.podbean.com/pb/1860a0ddeed2ad45db31477355f265e8/60103875/data1/fs48/6936790/uploads/Take_Charge_1218208ati1.mp3?pbss=f02615a5-91d0-5c11-8e0e-81cca9f7c721
;
& (c)
The Long-Term Algae
Extract (
Chlorella and Fucus
sp
)
and
AminosulphurateSupplementation
Modulate
SOD-1 Activity and Decrease Heavy Metals (Hg
++
, Sn)
Levels in Patients with Long-Term Dental Titanium Implants and
Amalgam- Fillings
Restorations.
Antioxidants (Basel).
2019
Apr 16;8(4). Merino
JJ
;
& (d )
N
-acetyl-cysteine affords protection
against lead-induced cytotoxicity and oxidative stress in human liver carcinoma
(
HepG
2
)
cells. Int J Environ Res Public Health 4:132_
137,
Yedjou
GC,
TchounwouPB
(2008)
(9.7
)
(
a) Very low-level prenatal
mercury exposure and behaviors in children: the HOME Study. Patel NB, Xu Y et
al;
Environ Health.
2019
Jan 9;18(1):4; &. (b)
Sex-Dependent Impact of
Low-Level Lead Exposure during Prenatal Period on Child Psychomotor
Functions.
Polanska
K, Hanke W
et al;
Int J Environ Res Public Health.
2018 Oct 16;15(10
);
&
(d )
"Abnormal neuronal migration of
human fetal brain", Journal of
Neurophalogy
, Vol 37,
p719-733, 1978;
B.Choi
et
al, & National Academy of
Sciences,"Toxicological
Effects of
Methylmercury, & Dental and Health Facts, Vol 6, no.3,
October 1993.
http://books.nap.edu/books/0309071402/html/81.html;
(9.8) (a) Lead-induced oxidative stress adversely
affects health of the occupational workers. Khan DA, Qayyum S, et al;
Toxicol
Ind Health.
2008 Oct;24(9):611-8;
& (b) Occupational Exposures and Neurodegenerative Diseases-A
Systematic Literature Review and Meta-Analyses. Gunnarsson
LG,
Bodin
L.
Int J Environ Res Public Health.
2019 Jan 26;16(3); & (c
)
Low
-level
exposure to lead, blood pressure, and hypertension in a population-based
cohort.
Gambelunghe
A,
Sallsten
G, et al;
Environ Res.
2016 Aug;149: 157-163; &
(d) The mechanisms associated with the development of hypertension after
exposure to lead, mercury species or their mixtures differs with the
metal and the mixture ratio.
Wildermann
TM
,
Weber LP et al;
Toxicology.
2016
Jan
2;339:1
-8; & (e) Higher urinary heavy metal,
arsenic, and phthalate concentrations in people with high blood pressure:
US NHANES, 2009-2010. Shiue I.
Blood Press.
2014 Dec;23(6):363-
9;&
Identifying periods
of susceptibility to the impact of phthalates
on children's cognitive abilities. Li N, Chen A, et al;
Environ
Res.
2019
Mar 5;172: 604-614;
&
(f) Mercury Exposure, Blood Pressure, and Hypertension: A
Systematic Review and Dose-response Meta-analysis. Hu XF, Singh K, et al;
Environ
Health
Perspect
.
2018
Jul 31;126(7):076002; & (g) Assessment of toxic elements in the samples of
different cigarettes and their effect on the essential elemental status in the
biological samples of Irish hypertensive consumers. Afridi HI,
Talpur
FN, et al;
J Hum
Hypertens
.
2015
May;29(5):309-15; & (h) Relationship between blood manganese
and blood pressure in the Korean general population according to
KNHANES 2008. Lee BK, Kim Y.
Environ Res.
2011 Aug;111(6):797-803.
�(
10
) "Blood Lead, Hearing
Thresholds, and Neurobehavioral Development in Children and
Youth", Archives of Environmental Health, Vol42, No.2, June 1987. J.
Schwartz & D. Otto,
(10.2) "Fertility of Male workers Exposed to
Manganese", Am. J. of Ind Med 7:171-176; 1985.
R.Lauwerys
et al,
(10.6) B.A.
Lown
et
al,
Neurotoicology
, 5:119-131; 1984 & L.E.
Gray et al, J. of Tox Env Health 6:861-867; 1980; & C.J.
Kilburn, "Manganese, Malformations and Motor Disorders: Findings in a
Manganese-Exposed Population", Neurotoxicology, 8:421-430; 1987.
(10.8) H. Tsuchiya
et
al
,"Effects
of
Materal
Exposure to Six Heavy Metals
on Fetal Development", Env
Contam
Tox,
38:580-587; 1987.
(11) "Mechanisms for the Neurotoxicity and
Biosynthesis of Methylmercury", in "
Organotransitional
Metal
Chemistry, Plenum Publishing Corporation,
NY, NY, 1987. J.M. Wood,
(11.3
)
Chien
-Jen
Chen et al (for U.S. EPA), Lancet, Feb de20, 1988; & Science News,
Volume 141, page 253.
(11.7) New Jersey Dept. of Health, Hazardous Substance Fact
Sheet, 1987; & Electric Power Research Institute, EPRI
Journal, December
, 1994,
p5.
(12)
Hawley's Condensed Chemical
Dictionary
,
Van Nostrand Reinhold
Co., NY, NY,1987 N.I. Sax & R.J. Lewis. & J.
Haggin
,
Chemical and Engineering News, Sept 8, 1986.
�
(13)
U.S. EPA, Report to Congress on Special Wastes from Mineral
Mining, PB90-258492, July 1990,
https://www.epa.gov/radiation/report-congress-special-wastes-mineral-processing
; &
1985
Report to Congress on Wastes from the Extraction and Beneficiation of Metallic
Ores, Phosphate Rock, Asbestos and Overburden from Uranium Mining,
Copper
(PDF)
,
Gold
& Silver (PDF)
,
Lead
(PDF)
,
Uranium
(PDF)
,
Zinc
(PDF)
;
�
https://www.epa.gov/hw/report-congress-wastes-extraction-and-beneficiation-metallic-ores-phosphate-rock-asbestos
; &
U.S. EPA, Abandoned Mine Lands, 2018, Superfund
Sites,
https://www.epa.gov/superfund/search-superfund-documents
;
�(
14
)"Mercury Found in Dead Florida
Bay Cormorants", Tallahassee Democrat,1-15-95 &
"Are Environmental Hormones Emasculating Wildlife", Science
News, Vol 145, 1994, p25-27.
(14.5) "
Developmental Effects of Endocrine-Disrupting Chemicals
in Wildlife and Humans",
Environmental Health Perspectives, Vol 101(5), Oct 93; T. Colburn et
al, & WHO,
Endocrine
Disrupting
Chemicals
(EDCs),2018, & Hormone Health Network,
Endocrine Disrupting Chemicals
; 2018, & Endocrine Society,
Endocrine Disrupting Chemicals
, 2018; (NU)
& EWG,
Dirty Dozen Endocrine Disrupters
, 1028, Health effects of endocrine
disrupting chemicals, &
EDCs,
(14.9)
The
Environmental
effects of mercury from dental amalgam
affect
Everyone, B Windham (Ed),
2016. &
www.myflcv.com/damspr2.html
(15) University Health
News Daily,
Aluminum Linked to
Alzheimer�s
Disease
,
7 Pieces of Evidence
; &
C.N. Martyn et
al, "Geographical relation between Alzheimer's disease
and aluminum in drinking water", The Lancet, Jan 14,1989;
& Bowdler NC, Beasley DS. Behavioral effects of aluminum
ingestion.
Pharmacol
Biochem
Behav
1979
; 10:
505-512; & Trapp GA, Miner GD. Aluminum levels in
brain
in
Alzheimer
�s
Disease.
BiolPsychiatry
1978;
13: 709; & Munoz-Garcia et al,
"An immunocytochemical comparison
of cytoskeletal proteins in aluminum-induced and Alzheimer-type
neurofibrillary tangles.� Acta Neuropathology Vol 70,1986, p.243-248;
& Guest
J,et
al, "The
effects of aluminum on sodium-potassium-activated
adenosinetriphosphatase
activity
and choline uptake in rat brain synaptosomes" Biochemical
Pharmacology, Vol 29, 1980, p.141; Davison, A., et al.,
"Differences in the inhibitory effect of aluminum 3+ on the uptake of
dopamine by synaptosomes from forebrain and from striatum of the
rat", Biochemical Pharmacology, Vol 30, 1981,
p.3123-3125].��� (NU)
(
15.1)
Toxic Metal Syndrome
,
How Toxic Metals Can Affect Your Brain, Avery Publishing Group,
1995 H.R.
Casdorph
, &
4
Toxic Metals
,
Mercury, Lead, Cadmium, Aluminum; & Charles Moon et al, "Main and
Interactive
Effects of Metallic Pollutants on Cognitive Functioning,
Journal of
Learning Disabilities, April 1985; & Congressional Office of Technology
Assessment,
Poisons of the Nervous System
, Oct 1990; (NU)
�(16) "High levels of
copper in water also a danger", Orlando Sentinel, 11-24-92, A. Beasley;
& US EPA, The Week, March 20, 2019,
EPA
chief says unsafe water a bigger crisis than climate change
;
(16.1) J.O.
Nriagu
,
Nickel in the Environment
,
John Wiley & Sons,1987;
Drinking Water and Cancer Incidence in Iowa
", American Journal of
Epidemiology, P.
Isacson
et
al, 1985; 121:856‑859(nickel).
(16.2) LTT-MELISA is clinically relevant for detecting
and monitoring metal sensitivity. Valentine-Thon E, Muller K,
Guzzi
, et al;
Neuro
Endocrinol Lett.
2006
Dec;27 Suppl 1:17-24.; &
The
beneficial
effect of amalgam replacement on health in patients with
autoimmunity.
Prochazkova
J
, Stejskal VD, et al;
Neuro
Endocrinol
Lett.
2004 Jun;25(3):211-8; &
The
beneficial effect of amalgam replacement on health in patients with
autoimmunity.
Prochazkova
J
, Stejskal VD, et al;
Neuro
Endocrinol
Lett.
2004 Jun;25(3):211-8; & Increased frequency of
delayed type hypersensitivity to metals in patients with connective tissue
disease. Stejskal V, Reynolds T, Bjorklund G.
J Trace Elem Med Biol.
2015;31:230
-6. (SLE, SS, RA); & Metals as a common
trigger of inflammation resulting in non-specific symptoms: diagnosis and
treatment. Stejskal V.
Isr
Med
AssocJ
.
2014 Dec;16(12):753-8; &
Epidemiology
of nickel sensitivity: Retrospective cross-sectional analysis of
North American Contact Dermatitis Group data 1994-2014.
WarshawEM
et al;
J Am
Acad
Dermatol.
2019
Mar;80(3):701-
713.�
� (NU)
(16.3) J.
Raloff
,
"Mercurial Risks from Acids Reign", Science News, March
9,1991 & "Mercurial Airs: Tallying Who's to Blame",
Science News, 2-19-94, p119; Greg
Mierle
,
Dorset Research Center, Ontario, Canada, in (16.3); & E.B. Swain
et al, "Mercury in Fish from Northeastern Minnesota Lakes: Historical
Trends, Environmental Correlates, and Potential Sources", Journal of
the Minn. Academy of Science, Vol 55, #1, 1989; & James Weiner,
U.S. Fish & Wildlife Service National
Fisheries Contaminant Research Center, in (16.3); & J
Raloff
, Why the mercury falls, Science News, V 163,
Feb 1; & Driscoll CT et al, 1994, The mercury cycle and fish in the
Adirondack Lakes. Environ Sci & Tech, 28(3): 136-143,
& Associated Press, Miami Herald, Oct 29,1990; & (e) Florida Dept. of
Environmental Regulation,
Florida Water
QualityAssessment
305(b)
Technical Appendix
, annual report, several years; also
special DER reports on water bodies such as Horseshoe Bayou; &(f) Mobile
Register, Mercury Series (Aug 2001 to Mar 2002): Mercury Taints
Seafood,
www.al.com/specialreport/?mobileregister/mercuryinthewater.html
(17) (a)
Mercury in Florida freshwater and saltwater fish, levels, sources, health
effects,
www.myflcv.com/flhg.html
;
& (b)
Forrest Ware, Game and Fresh Water
Fish Commission,
Results of Tests for Mercury in Florida Bass
,
1990 & T.R. Lange, H.E. Royals, and L.L. Connor,
FG&FWFC,
Influence of Water Chemistry on
Mercury
Concentration in Largemouth Bass from Florida Lakes
, 1993; &
(c ) Tampa Tribune, "Keep the Mercury from Rising in Florida's Lakes and
Rivers", Oct 29, 1990 & The Orlando
Sentinel (Peter Mitchell), "Florida Struggling to Get Handle
on Mercury Pollution", 11‑11‑90; Tampa Tribune,
"The
Posion
from Our
Skies: Mercury Taints Rivers and Streams", 7‑3‑89 &
The Orlando Sentinel, "
Mercury�s
Threat
to State's Environment May Be Worse Than Expected", 6‑25‑1989; &
Federation scolds Florida for excessive mercury contamination,
Jim Tunstall, Media General News Service, May 30, 2003, WMBB
TV, Panama City
Florida, www.wmbb.com/frontpage/MGBE3FH6CGD.html; &
Report: Florida Rain Laden With Toxic Chemicals
Rain
Poses Threat To Wildlife, Humans
Gainesville
Sun
May 30, 2003
http://gainesvillesun.com/apps/pbcs.dll/article?AID=/20030530/LOCAL/305300005/1007;
& Report details mercury
pollution Mercury-laden rain contaminating fish,
group says ,By Bruce R,.≥≥
m,itchie
Democrat
Staff Writer, May 30, 2003,
www.tallahassee.com/mld/democrat/news/local/5973192.htm; & (d) Florida
Environments, May 1991 & Dr. Robert
Hueter
, Mote Marine Laboratory Center for
Shark Research, Sarasota, Florida, July 19,1994; & Tallahassee
Democrat, 5‑13‑91 & News‑Press,4‑14‑91 & D.K. Rogers,
"Danger in the Air", St. Petersburg Times, 11‑4‑90.
(17.1) Chuck Clark, Ft. Lauderdale Sun
Sentinel,"2 waste burners pose mercury risk", 11‑5‑90; &
FCIR,
Florida home to 7 air polluters
of EPA�s watch list,
& Univ. of Florida Dept. of Environmental Engineering, study by
J.Delfino
summarized
in: Florida Environments, August,
1992 & Brian Rood, Tallahassee
Democrat, June 6, 1994; & Dr. S.
Sundlof ,
Univ. of Florida
Vetinary
College,
Florida Environments, Oct 1993.
(17.4)
Florida Panther Interagency Committee,
Status Report:
Mercury
Contamination in Florida Panthers
, Dec 1989, &
C.F.Facemire
et al, �Reproductive
impairment in the Florida Panther�, Health Perspect,1995, 103
(Supp4):79-86; &
Jagoe
CH,
1998, Mercury in Alligators in the Southeastern U.S., Science of the
Total
Envirnonment
,
213:255-262, &
Esley
RM,
Mercury levels in alligator meat in south
Louisian
,
1999, Bull Environ
Contam
Toxicol
, 63: 598-603; & High Mercury in Wading
Birds; & High Mercury in Florida alligators
hppt://everglades.fiu.edu/taskforce/precursor/chapter10.html; &
Osowski
SL, 1995, The decline of mink in
Georgia, North Carolina, and S. Carolina: the Role of
Contaminants, Env
Contam
and
Toxicol
, 29:418-423; & Sepulveda MS et al, 1999,
Effects of mercury on health and first-year survival of free-ranging
great
eggrets
from southern
Florida, Archives Environ
Contam
and
Toxicol
, 37:369-376; &
M.Maretta
et al, "Effect of mercury on the
epithelium of the fowl testis", Vet Hung 1995, 43(1):153-6.
�(
18
) Electric Power Research
Institute,EPRI
Journal,
April/May 1990 & EPRI Technical Brief,
"Mercury in the Environment", 1993; & Weiner, JG et al, 1990,
Partitioning and
bioavailablity
of
mercury in an experimentally
acified
lake,
Environmental Toxicology and Chemistry, Vol 9: 909-918. &
J.W. Huckaby, Electric Power Research Institute, formal comments to
health effects section of the National Acid Precipitation Assessment
Program, March 1991; &
( c
) M.R.
Winfrey & J.W.M. Rudd, U.S.E.P.A., "Factors
Affecting Methylmercury Formation in Low
PH Lakes",
Envir
. Toxic. &
Chem. 1990 (DER RF) & "Mercury: An Atmospheric
Hitchhiker", Health and Environment, Vol 4, #4, May 1990;
& (d) Proceedings, "International Conference on Mercury as
an Environmental
Pollutant, Gavle Sweden,
June 11‑13,1990. see: "Mercury in the Swedish
Environment", Water, Air, & Soil Pollution, Vol 55,
1991. Kluwer Academic Publishers
�(
18.6) Wisconsin Dept. of Natural
Resources and Wisconsin Division of Health, "Health Advisory for
People Who Eat Sport Fish from Wisconsin Waters", 1987; &
C.J.
Watras
and
N.S. Bloom," Observations
of Methylmercury in Precipitation:, pp199‑207 &
C.J.Watras
and W.F. Fitzgerald, "Mercury
in Surficial Waters of Rural Wisconsin Lakes", pp223‑232, in
The Science of the Total Environment, Vol 87/88,1989; & New
York State Dept. of Environmental Conservation,
Workshop
Proceedings,
Acidic Deposition
,Feb
1985, prepared under EPA contract by Corvallis
Envir
. Research Lab.
(18.8) Minnesota Pollution Control
Agency,
Assessment
of Mercury Contamination
in Selected Minnesota
Lakes and
Streams,edited
by
Edward Swain, Division of Water Quality, St Paul, Mn, 1989.(DER
RF) & "Increasing Rate of Atmospheric Mercury
Deposition in
Midconinental
North America",
Science,Vol
257, Aug, 1992; & Minnesota
Pollution Control Agency, "Strategies for Reducing Mercury
in Minnesota", June 1994.
�(
19
) Lebel et al,
Neuroltoxicology,1996,17:157- & Envir.Res.,1998,79:20-32; & (b)
J.M.Gauthier
,
Environ.Tox
.&
Chem,Dec
1998 & Science
News, Vol 155,p56.
(19.5) Bemis
JC,
Seegal
RF; 2000, PCBs
and methylmercury alter intracellular calcium concentrations in
rat cerebellar granule cells. Neurotoxicology, 21(6):
1123-1134.
(19.7) Minnesota Dept. Of Agriculture,
News Release
:� Swordfish
Survery
Reveals Excess Levels of
Methyl Mercury,1995. (612-297-1629)
(19.9) EPA‑600/3‑78‑
103,
Metal
Bioaccumulation in Fishes and Aquatic
Invertebrates
,
1978.
(20) R. L. Burgess,
Editor( 1984
)
Effects
of Acidic Deposition on Forest Ecosystems in the Northeastern U.S.
,
College of Forestry, Syracuse University, Syracuse, N.Y. (DER RF); &
(b) F. Perce, "The Strange Death of
Europe�s
Trees",
New Scientist, Dec 4, 1986 &
L.W.Blank
, "A New Type of Forest
Decline in Germany", Nature, Vol 314, p311‑314, 1985. (DER RF);
& J.
Haggin
,
Chemical and Engineering News, Sept 8,1986; &
R.& B.
Fackhaus
,
"Distribution of Long Range Transported Lead
and Cadmium in Spruce Strands Affected by Forest Decline", The
Science of the Total Environment, 59(1987), p283‑290. (DER RF);
& S.
M.Siegel
et
al, "Temperature Determinants of Plant‑Soil‑Air Mercury
Relationships", Water, Air, & Soil Pollution, 40: 443(1988)
�(21) Law and Gordon, U.S. EPA,1979; & California Air
Resources Board Stationary Source Division, Air Pollution Control at
Resource Recovery Facilities, May 24, 1984; & EDF, Summary of
Incinerator Ash ssues,1989; & Alex
Green, Univ. of Florida, ICAAS‑SSRB; &
D.O. Reimann, Director, Garbage Incineration Plant, Bamberg,
Germany,
Mercury Output by Garbage Incineration
,
1986; & Associated Press, Miami, 3‑12‑91(in several Fla. papers) (DER RF);
& J.M. Wood, "Effects of Acidification on the Mobility of
Metals and Metalloids", Environmental Health Perspectives,
Vol 63,1985; & (d) U.S. EPA study, in Florida Environments, May
1994.
(22) "Mercury: Measuring and Managing Risk",
Environment, 1978;
& S.
E.Lindberg
,"Mercury Partitioning in a
Power Plant Plume and Its Influence on Atmospheric Removal Mechanism",
Atmospheric
Environment,Vol
14, p227‑231,1980;
& "Peat Bog Records of Atmospheric Mercury
Deposition" Nature, 293, P127‑129, 1981. P.
Pheiffer
‑Madsen; &
O.Lindquist
,"
Atmospheric Mercury‑ A Review", Tellus, 37B,p136,1985; & (b)
W.F. Fitzgerald, in: P.
Buat
‑Menard(editor
),
The
Role of Air‑Sea Exchange
in
Geochemical Cycling
,
Reidel
Publishing
Co.,1986; & Industry Mercury Group, National Environmental Protection
Board,
Mercury
in the Swedish Environment‑ Recent
Research on Causes, Consequences, and
Corrective
Methods
,1990; & J.G.T.
Bergstom
,
"Mercury Behavior in Flue Gases", Waste Management
and Research, 4:57, 1986; & S.E. Lindberg,
"Mercury Partitioning in a Power Plant Plume and Its Influence on
Atmospheric Removal Mechanisms", Atmospheric Environment, 14:227(1980);
& W.H. Ellison, "Status of German FGD and
DeNox
", in
Proceedings of
theThird
Annual Pittsburg Cola
Conference
,
Pittsburg,Pa
. 1986; & "Compare Performance
among waste‑to energy plant emissions‑control systems", Power (the
magazine of power‑generation technology, McGraw Hill, Jan 1991;
&
( 23
)� "Acid Rain/Air
Pollution: The Situation in Florida and the Southeast",
1998. & Acid Rain, effects
www.myflcv.com/newar.html
; 2015
(24) H.
Vogg
et
al, " The Specific Role of
Cadmium and Mercury in Municipal Solid Waste Incineration",
Waste Management and Research, Vol 4,1986; & (b) Medical
findings in nickel-cadmium battery workers.
Isr
J
Med Sci 1992 Aug-Sep;28(8-9):578-83. Bar-Sela S, Levy M, et al;
&Renal tubular function of cadmium exposed workers.
Ann
Acad
Med
Singapore 1992 Nov;21(6):756-9. Chia KS, Tan AL, et al
�(
25
) D.R. Buckler et al, "Influence
of PH on the Toxicity of Aluminum and other Inorganic Contaminants
to East Coast Striped Bass", Water, Air and Soil
Pollution, Vol35(1987), pp97‑106
(26) "Content and Chemical Form of Mercury and
Selenium in Soil, Sludge, and Compost", Water, Air, and Soil
Pollution, 22,1984. C.J.
Cappon
,
(27) ATSDR, Medical Management Guidelines for Mercury:
Cardiovascular Effects of Mercury,
www.atsdr.cdc.gov/MHMI/mmg46.html
(28)
Electric Utilities and Long-Range
Transport of Mercury and other Toxic Air
Pollutants
,
Center for Clean Air Policy
(independent policy research center organized by State governors), Nov 1991.
(28.7) E.A. Nater et al, "Regional Trends in
Mercury Distribution Across the Great Lakes", Nature, Vol 358,
July 9, 1992.
(
29
)
Association of adverse birth
outcomes with prenatal exposure to vanadium: a population-based cohort study.
Hu J, Xia W et al;
Lancet Planet
Health.
2017
Sep;1(6): e230-e241; & (
b)
Science
News, page 334, May 22, 1993; & Dr.
John Vandenberg, Director, U.S. EPA National Health and Environmental
Effects Research Laboratory, Research Triangle Park;
& Science News, Vol 153, Jan 31, 1998, p68;
(29.2) L.M. Pierce et al, Harvard School of Public
Health, Boston, Ma., �Vanadium Induced pulmonary
inflammation�, 1997: & M.D. Cohen et
al, �Vanadium effects on macrophages and IFN gamma binding�,
Toxicol
Appl
Pharmacol
,
1996 May, 138(1):110-120; &
J.Toxicol
Environ
Health Aug 1997, 51(6): 591-608; &
J.Cortijo
et
al, �Spasmogenic effects of vanadate in human
broncus
�, Br J
Pharmacol
Aug
1997, 121(7): 1339-1349; & Z. Yang, N.Y.Univ .
Medidal Center
,� Pulmaonaryimmunotoxicity of
inhaled ammonium metavanadate�,
Fundam
Appl
Toxicol
Oct 1996; 33(2): 254-263; & (b)
Science News, toxics in Incinerator emissions, 4‑6‑91, p212; & Science
News, 7‑5‑97, p6; & Cohen MD, Yang Z,
Zelikoff
JT,
Schlesinger RB. Pulmonary immunotoxicity of inhaled
ammonium metavanadate in Fisher 344 rats.
Fundam
Appl
Toxicol
1996 Oct;33(2):254‑263.
(29.4) A.M.
Cortizo
et
al, �Proliferative and morphological changes induced by
vandaium
compounds�,
Biometals
Apr 1997, 10(2):127-133; &
G.A.
Kerckaert
et
al, �Carcinogenic potential of
heavy metal compounds�,
Fundam
APPl
Toxicol
Nov,
1996, 34(1):67-72; & & X. Shi et al,
National Cancer Institute, �Vanadium(IV) mediated free radical
generation and DNA damage�, Toxicology Jan 1996;
106(1-3):27-38; & D.R. Lloyd et al, Chem Res
Toxicol
Apr 1997, 10(4): 393-400; &
P.
Ramierz
et
al,
Mutat
Res Jun
1997, 386(3):291-298; & (c )
Kerckaert
GA,
LeBoeuf
RA,
Isfort
RJ. Use
of the Syrian hamster embryo cell transformation assay for determining the
carcinogenic potential of heavy metal compounds.
Fundam
Appl
Toxicol
1996 Nov;34(1):67‑72; & Lewis
DF, Ioannides C, Parke DV. COMPACT and molecular
structure in toxicity assessment:
a prospective
evaluation of
30 chemicals currently being tested for rodent carcinogenicity by the
NCI/NTP. Environ
Health
Perspect
1996
Oct;104 Suppl 5:1011‑1016
(29.5
) K.
H.Sit
et al, Dept. Of Anatomy, Nat.
Univ. Of Singapore, �Induction of vanadium accumulation causing
cell suicide in human liver cells
�,
Experientai
Aug 1996, 52(8):778-785;
&
Biometals
Apr 1997,
10(2): 119-122; & (b) J.L. Domingo, �Vanadium: a review of the
reproductive and developmental toxicity�,
Reprod
Toxicol
May 1996, 10(3):175-182,
(30)
U.S.EPA,
Wastes
from the Combustion of Coal Power Plants
, Report to Congress, Feb
1988; & (b) U.S.EPA,
Municipal Waste Combustion Study,
Report
to Congress, EPA/530-5w-87-021a, June, 1987; & ( c ) Congressional
Office of Technology Assessment,
Facing Americas Trash
, OTA-0-424,
USGPO, Oct 1989.
(31) Bioavailable Transition Metals in Particulate
Matter Mediate Cardiopulmonary Injury in Healthy and Compromised Animal
Models. Environ
Health
Perspect
105
(Suppl 5): 1053-1060 (1997), Costa, D. L., and Dreher, K.L.
�(
32
) J.M.
Samet
et
al,
Univ. Of N. Carolina, Disruption of protein tyrosine phosphate;
& A.
Holian
et
al, Univ. Of Texas Health Science
Center, Environmental Health Perspectives, March 1998; & Science
News, Vol 153, Jan 31, 1998, Page 68.
�(
33) Florida Department of Health,
Bureau of Environmental Toxicology, Health Advisories for Mercury in Florida
Fish 1997; 10-15; & FDEP, Toxic metal levels in Florida shellfish,
1990; & Tom
Atkeson
,
Florida Dept. of Environmental Protection Mercury Coordinator, "Warning
Issued on High Mercury Levels in Sea Trout", Tallahassee
Democrat, 9-12-93 & "Mercury in Florida's
Environment", Dept. of Environmental Protection, Aug 18,
1994 & "Warning Issued for Coastal Water
Fish",Fla
. Dept. of H.R.S., Tallahassee
Democrat, 10-7-95 and 6-5-96, p10c; &� Thomas D.
Atkeson
,
FDEP Mercury Coordinator, South Florida Mercury Science Program, MERCURY IN
FLORIDA'S ENVIRONMENT,
www.dep.state.fl.us/labs/mercury/docs/flmercury.htm
�(
34
) Compliance Strategies
Review, An Executive Briefing on the Clean Air Act,
Fieldston
Publications, Vol 5,
No. 12, June 6, 1994.
(35) (a) Electric Power Research
Institute. Mercury in the Environment. Electric
EPRI Journal 1990; April, p5; & EPRI Technical Brief:
"Mercury in the Environment", 1993; &
Mercury Emissions to the Atmosphere in Florida: Final
Report for Dept. of Environmental Regulation, KBN Engineering and Applied
Sciences, Inc. Aug 1990
(36) Florida Dept. of Environmental
Protection,
Florida
Coastal Sediment Contaminants Atlas, 1994.
&(b) U.S.
EPA, Contaminated Sediments News (EPA-823-N94-003
), September
, 1994;
& (c) U.S. EPA, Environmental Monitoring and Assessment Program,
Estuaries: Louisianian Province
-1992
& 1991.
(37)
Association between inflammatory
marker, environmental lead exposure, and glutathione S-transferase gene.
Sirivarasai
J,
Wananukul
W,
et al;
Biomed Res
Int.
2013;2013:474963.
(38)
Combined
exposure to lead, inorganic mercury and methylmercury shows deviation
from additivity for cardiovascular toxicity in rats.
WildemannTM
, Weber LP et al;
J Appl
Toxicol
.
2015
Aug;35(8):918-26; & (b) Mercury-induced vascular dysfunction is
mediated by angiotensin II AT-1 receptor upregulation.
Rizzetti
DA, da Silva TM et al;
Environ Res.
2018 Apr;162: 287-296; &
(c) [Role of activation of lipid peroxidation in the mechanisms of
cardiovascular disease system under the action of heavy metals in the
experiment].
Mitsiev
AK
.
Patol
Fiziol
Eksp
Ter.
2015
Jan-Mar;59(1):60-4.
(39) U.S.
EPA,
Study
of Hazardous Air Pollutant Emissions from Utility Steam Generators
,
EPA Tech Transfer Network, EPA-453/R-96-013a, 919-541-5384; & (b)
Minnesota Pollution Control Agency,
Interim Report of the
Household
Battery Recycling and Disposal Study
, 990.
(40)
Cytotoxicity
and transcriptional activation of stress genes in human liver carcinoma cells
(HepG2) exposed to cadmium chloride.
Tchounwou
PB,
Ishaque
AB et al;
Mol Cell
Biochem
.
2001
Jun;222(1-2):21-8;
&
Mortality
and cancer morbidity among cadmium
exposed workers. Environ
Health
Perspect
1979; 28: 199‑204,
Kjellstrom
T, Friberg L,
Rahnster
D; & Risk factors
for meningioma in adults: a case-control study in northeast
China. Int J Cancer 1999 Oct 29;83(3):299-304. Hu J, Little
J, Xu T, et al. (b) Cadmium exposure and nephropathy in a
28-year-old female metals worker. Wittman R, Hu H.
Environ
Health
Perspect
.
2002
Dec;110(12):1261-6.: (c)
Blood cadmium, mercury, and lead and metabolic syndrome in South Korea:
2005-2010 Korean National Health and Nutrition Examination Survey. Am J Ind
Med. 2013 Jun;56(6):682-92. Lee BK, Kim Y.
(41) Third National Health and Nutrition
Examination Survey (NHANES III) Journal of American Medical Assoc., June
1999,
M
.Moss
; & Science
News, Vol 155, june26, 1999(25,000 children tested); &
Science News, 9/6/97, p149.
(42) I. Gerhard et al, The limits of hormone
substitution in pollutant exposure and fertility
disorders,
Zentralbl
Gynakol
,
1992, 114, 593‑602; & Association of Blood and Seminal
Plasma Cadmium and Lead Levels With Semen Quality in
Non-Occupationally Exposed Infertile Men in
Abakaliki
,
South East Nigeria.
Famurewa
AC
,
Ugwuia
El.
J
Family
Reprod
Health.
2017
Jun;11(2):97-103; & The environment and male reproduction: The effect
of cadmium exposure on reproductive function and its implication
in fertility. De Angelis C,
Galdiero
M
et al;
Reprod
Toxicol
.
2017 Oct;73:105-127;
& �
Heavy metals in miscarriages and stillbirths in developing
nations
;
Middle East Fertility Society Journal;
Volume 22, Issue 2,
June 2017, Pages 91-100.
(43)
Eating Guidelines for Fresh Water Fish
for Florida Waters (based on mercury levels), 2018, Table 1- p 1-50;
http://www.floridahealth.gov/programs-and-services/prevention/healthy-weight/nutrition/seafood-consumption/_documents/advisory-brochure.pdf
; & Table 2: Eating
Guidelines for Marine and Estuarine Fish from Florida Waters (based on mercury
levels) page 51-52; & Table 3: Eating Guidelines for species
from Florida Waters with Heavy Metals (other than mercury), Dioxin, Pesticides,
Polychlorinated biphenyls (PCBs), or
SaxitoxinContamination
page
53-54 �
(44) Concentrations of mercury, cadmium, and lead in brain
and kidney of second trimester fetuses and Infants. Journal of Trace
Elements in Medicine and
Biology 199
;10:61 ‑67.
Lutz E, Lind
B,
Herin
P,
Krakau
I, Bui TH,
Vahter
M.:
& (b) U.S. Department of Health, Division of Toxicology, Agency for
Toxic Substances and Disease Registry. Breast-feeding exposure
of infants to cadmium, lead, and mercury: a public health viewpoint.
Toxicol
Ind
Health
1997; 13(4):495-517.
Abadin
HG
, Hibbs BF, Pohl HR,
(45) FDEP, Waste Reduction,,2018,
https://floridadep.gov/waste/waste-reduction
; & & U.S. EPA, Reusing and
Reducing Basics, 2017,
https://www.epa.gov/recycle/reducing-and-reusing-basics
; & D. Morris and N.
Seldman
,
"Getting Rid of All the Garbage in the U.S.", Wall Street
Journal, April, 1986, reprinted in the Gainesville Sun, May 10, 1986;
& Ecological Monitoring and Assessment Network, ESC
News, Vol 1, No 4, Feb 1995.
(46)
(a) H.J. Mason,
"Occupational Cadmium Exposure and Testicular Endocrine Function",
Human & Experimental Toxicology,
9:91-94,1990; & (b) A. Levin et al, Fetal Toxicity of Cadmium in
Rats
Toxicol
Appl
Pharmacol
,
58:297-306;1981; & (c)
A.Levin
et
al, "Cadmium: Placental Mechanisms of Fetal Toxicity", Placenta,
3:303-318; 1981; &
S.E.Chia
et
al, Blood concentrations of metals and human semen parameters, Arch
Androl
1992; 29(2):177-83; & A global
perspective on cadmium pollution and toxicity in non-occupationally exposed
population.
Satarug
S, Baker
JR, et al:
Toxicol
Lett.
2003 Jan
31;137(1-2):65-83; & (d) Shukla GS, Singhal RL. The
present status of biological effects of toxic metals in the environment:
lead, cadmium, and manganese. Can
J
Physiol
Pharmacol
1984
Aug;62(8):1015-31.
(47) Lewis
M,
Worobey
J, Ramsay DS, McCormack
MK. Prenatal exposure to heavy metals: effect on childhood
cognitive skills and health status. Pediatrics 1992; 89(6 Pt 1):1010-15; &
Capel ID, Pinnock MH, Dorrell HM, Williams DC, Grant
EC. Comparison of concentrations of some trace, bulk, and toxic metals in
the hair of normal and
dyslexic
children
.Clin
Chem 1981
Jun;27(6):879-81
(48)
Associations of blood heavy
metal levels with intraocular pressure. Park S, Choi NK;
Ann Epidemiol.
2016
Aug;26(8): 546-550.e1
(49)
Carcinogenic metal compounds: recent
insight into molecular and cellular mechanisms.
Beyersmann
D,
Hartwig A;
Arch
Toxicol
.
2008
Aug;82(8):493-512;
&
Contribution
of metals to respiratory cancer.
Environ
Health
Perspect
1986
Dec;70: 71‑83, Peters JM, Thomas D, et al;
(50)
Arsenic
toxicity, mutagenesis, and carcinogenesis--a health risk assessment and
management approach.
Tchounwou
PB,
Centeno JA et al;
Mol
Cell Biochem.
2004
Jan;255(1-2):47-55; & (
b)
National
Research Council
(2001) Arsenic in drinking water. 2001 Update. Online available at
http://www.nap.edu/books/0309076293/html/
; &( c )
Tchounwou
PB,
Patlolla
AK,
Centeno JA (2003) Carcinogenic and systemic health effects associated with
arsenic
exposure�a
critical
review. Toxicol Pathol 31:575�588;
https://link.springer.com/chapter/10.1007%2F978-3-7643-8340-4_6
;
(51) Environmental Working Group - U.S. Public
Interest Research Group, What Women Should Know About Mercury Contamination in
Fish" Including Expanded List of Fish to Avoid,
www.ewg.org/pub/home/reports/brainfood/sidebar.html
;
(52) Urinary cadmium and osteoporosis in U.S. Women
>or= 50 years of age: NHANES 1988-1994 and 1999-2004. Gallagher CM, Kovach
JS et al;
Environ
Health
Perspect
.
2008
Oct;116(10):1338-43;
&
Cadmium
-induced effects on bone in a
population-based study of women.
Akesson
A,
Vahter
M, et al;
Environ Health
Perspect
.
2006
Jun;114(6):830-4.
(53) Lead, cadmium, and selenium in the blood of patients
with sporadic amyotrophic lateral sclerosis. Ital
J Neurol Sci 1997
Apr;18(2):87-92, Vinceti M, Guidetti D,
et al
; & �U.S. Congress,
House Select Committee on Aging,
Alzheimer's disease: Is
There
an Acid Rain Connection?
, U.S. Govt. Printing
Office,1983, CPN 98‑400.
(54) J.
D.Bogden
et al, Lead in Chickens,
Environmental Health Perspectives, June 1999.
(55) Minnesota Pollution Control
Agency,
The
Reduction
of Mercury in Batteries
and Household Wastes in
Europe
, 1990;
& (b) R.
Dumarey
and R.
Dams, "Selective Gathering of Mercury‑batteries: a Possible
Way to Lower Mercury Emissions from Incineration Plants",
Environmental Technology
Letters, Vol 6,1985.
(56) Cadmium: a possible etiological factor in
peripheral polyneuropathy. Neurotoxicology 1999
Feb;20(1):7-
16,
Viaene
MK,
Roels
HA, et al;
(57) U.S.E.P.A., C.C. Lee, "A Model Analysis of Metal
Partitioning", Journal of the American Pollution
Control Association,38(7): 941,1988; & S.E. Lindberg, "Emission
and Deposition of Atmospheric Mercury Vapor",
in
Lead
,
Mercury, Cadmium, and
Arsenic in the Environment
,
John Wiley & Sons, Ltd, NY, 1987, p91‑106; & A. Anderson,
The
Biochemistry of Mercury in the Environment
, North‑ Holland Biomedical
Press, p79‑106,1979.
(58) Florida Dept. of Natural Resources, in Tallahassee
Democrat, 10‑10‑
90 &
T.H.
Maugh
(
1984),
"Acid Rains Effect on
People", Science, Vol 226, 21 Dec 1984; & E.
Lindberg & C. Harris, "Mercury Enrichment in Estuarine Plant
Detritus" Marine Pollution Bulletin, June 1974. (DER
RF)
(59) U.S. Food and Drug
Administration. Action Levels for Poisonous or Deleterious
Substances in Human Food and Animal Feed.1999.
Http://vm.cfsan.fda.gov/~Ird/fdaact.html
; & U.S. Food and Drug
Administration, An Important Message for Pregnant Women and Women Who May
Become Pregnant About the Risks of Mercury in Fish, Jan 2001,
www.fda.gov/bbs/topics/ANSWERS/2001/advisory.html
; & U.S. EPA, "National
Advice for Women and Children on Mercury in Freshwater Fish",
https://www.epa.gov/fish-tech/state-territorial-and-tribal-fish-consumption-advisories
; &
U.S. EPA (fish Hg)
https://www.epa.gov/fish-tech/studies-fish-tissue-contamination
;
(60) W.F. Fitzgerald, "Distribution of
Mercury in Natural Waters", Dept. of Geology and Marine
Sciences Institute, Univ. of Connecticut, 1979 (DER RF) & D.E.R.,
Bureau of Surface Water Management, "Mercury, Largemouth Bass, and
Water Quality: A Preliminary Report", Jan 1990.(DER RF);
& U.S. Geological Survey, The Occurrence of Mercury in the
Fishery Resources of the Gulf of Mexico; http://mo.cr.usgs.gov/gmp/hg.cfm; & D.H.Adams, R.H.McMichael,
Florida Marine Research Institute, Technical Reports, Mercury Levels in Marine
and Estuarine Fishes of Florida, 2001; & Mississippi fish warnings,
www.deq.state.ms.us/newweb/homepages.nsf
; & "Enhanced
Bioaccumulation of Mercury, Cadmium, and lead in Low‑
Alkalinity Waters", Environmental Toxicology and
Chemistry, Vol 9,1990, p821‑823 (DER RF)
(61)
Ophthalmologic
features
of
thallium poisoning, Am J
Ophthalmol
1994 Feb 15 ;117(2):243-5;
& (b) Association between serum thallium in early pregnancy
and risk of gestational diabetes mellitus: The
Ma'anshan
birth
cohort study. Zhu B, Liang C et al;
J Trace Elem Med Biol.
2019
Mar;52: 151-156.
&
(
c) Alopecia and Associated Toxic Agents: A
Systematic Review. Yu
V,
Jahasz
M
et al;
Skin
Appendage
Disord
.
2018
Oct;4(4):245-260.
(62) Mechanisms Underlying Children's
Susceptibility to Environmental Toxicants. Environmental Health
Perspectives Volume 108, Supplement 1, March 2000. Elaine M.
Faustman
,
Susan M.
Silbernagel
,
Rafael A. Ponce.
(63) (a)National Research Council, Toxicological
Effects of Methyl mercury (2000), pp. 304-332: Risk Characterization and Public
Health Implications,
Nat'l
Academy Press
2000. www.nap.edu; & (b) U.S. Centers for Disease
Control ,
.
Mar 2001
, Blood and Hair
Mercury Levels in Young Children and Women of Childbearing Age ‑‑‑
United
States, 1999
www.cdc.gov/mmwr/preview/mmwrhtml/mm5008a2.htm & U.S.
CDC,
Second National Report on Human Exposure to
Environmental Chemicals
, www.cdc.gov/exposurereport/
(64) United States Environmental
Protection Agency, Office of Water, November 2000, The National Listing of Fish
and Wildlife Advisories: Summary of 1999 Data, EPA-823-F-00-
20, www.epa.gov/ost/fish/advisories/general.html
; & U.S. EPA, Office of Water, Mercury Update: Impact on Fish
Advisories-Fact Sheet, www.epa.gov/ost/fish/mercury.html; & New England
Governors and Eastern Canadian Premiers Environment Committee Mercury Action
Plan, June 1998.
(65) National Academy of Sciences, National
Research Council, Committee on Developmental
Toxicology,
Scientific
Frontiers in Developmental Toxicology and Risk Assessment,
June
1, 2000, 313 pages; & Evaluating Chemical and Other Agent Exposures for
Reproductive and Developmental Toxicity Subcommittee on Reproductive and
Developmental Toxicity, Committee on Toxicology, Board on Environmental Studies
and Toxicology, National Research Council National Academy Press, 262 pages, 6
x 9, 2001
(66) J.T. Salonen et al, "Intake of
mercury from fish and the risk of myocardial infarction and cardiovascular
disease in eastern Finnish men", Circulation, 1995; 91(3):645-55; &
Wisconsin Bureau of Public Health, Imported seabass as a source of
mercury exposure: a Wisconsin Case Study, Environ
Health
Perspect
1995, 103(6): 604-6;
(67) (a) J. Hightower, �
Methylmercury
Contaminmation
in Fish: Human Exposures
and Case Reports," Environmental Health
Perspectives; Nov 1, 2002; & (b) A
Oskarsson
et
al, Swedish National Food Administration, Mercury levels in hair from people
eating large quantities of Swedish freshwater fish.
Food
Addit
Contam
1990;
7(4):555-62; & (c) Preventive Medicine February 2002;34:221 -225; &(d) Dickman MD;
Leung KM, "Hong Kong subfertility links to mercury in human hair
and fish", Sci Total Environ, 1998,214:165-74; & Mercury
and organochlorine exposure from fish consumption in Hong Kong.
Chemosphere 1998 Aug;37(5):991-1015; &(
e)
Y
.Kinjo
et al,
"Cancer mortality in patients exposed to methyl mercury through fish
diet", J Epidemiol, 1996, 6(3):134-8; & (f) Choy C et al,
Seafood consumption linked to infertility, BJOG: An International Journal of
Obstetrics &
Gynaecology
2002
109:1121-5.
(68) Lindberg, S.E. . . . M.S. Landis, R.K.
Stevens,
et
al
.
2002. Dynamic oxidation of gaseous mercury in the arctic troposphere at
polar sunrise.
Environmental Science and
Technology
36
(March 15):1245-1256;
&
Steding
, D.J., and A.R.
Flegal
.
In
press. Mercury concentrations in coastal California precipitation:
Evidence of local and trans-Pacific fluxes of mercury to North America.
Journal
of Geophysical
Research
107
(D24):4764.
Abstract available at
http://dx.doi.org/10.1029/2002JD002081
& Science News, Oct 2018,� Value
of Clean Rivers and Lakes,�
https://www.sciencenews.org/blog/science-public/were-probably-undervaluing-healthy-lakes-and-rivers
;
(69) A comparative
study of the typical toxic metals in serum by patients of
schizophrenia and healthy controls in China. Ma J, Wang B, et al;
Psychiatry Res.
2018
Nov;269: 558-564; & (b )
Essential trace metals and
heavy metals in newly diagnosed schizophrenic patients and those on
anti-psychotic medication
;
J Res Med Sci.
2010 Sep-Oct; 15(5): 245�249.
(70)
Effect of dietary patterns on the
blood/urine concentration of the selected toxic metals (Cd,
Hg, Pb) in Korean children.
Yoo
BW,
Kim B et al;
Food
Sci
Biotechnol
.
2018
Feb 24;27(4):1227-1237; & (
b)
Human
Health Risk
Assessment of Cd, Cu, Pb and Zn through Consumption of Raw and
Pasteurized Cow's Milk.
Sobhanardakani
S.
Iran J
Public Health.
2018
Aug;47(8):1172-1180; & (c
)
Multiple
-metal exposure, diet, and oxidative
stress in Uruguayan school children.
Kordas
K,
Roy A,
Vahter
M, et al;
Environ Res.
2018 Oct;166: 507-515.
(71)
Lead, cadmium, arsenic, and mercury
combined exposure disrupted synaptic homeostasis through activating
the
Snk
-SPAR
pathway. Zhou F,
Xie
J, et al;
Ecotoxicol
Environ Saf
.
2018 Nov 15;163: 674-684.
(72)
Very low-level
prenatal mercury exposure and behaviors in children: the HOME Study.
Patel NB, Xu Y, et al;
Environ Health.
2019
Jan 9;18(1):4.
(73) Health of Children Living Near Coal Ash. Sears
CG,
Zierold
KM.
Glob
Pediatr
Health.
2017
Jul
25;4:2333794
X17720330.
*************
Major
Atmospheric Mercury Sources (partial list)
Estimated Estimated
Source
Fuel Controls
Fuel Emissions Emissions
Burned Rate
(4) pounds
1993
________________________________(Tons)______________________
Incinerators:
Pinellas
Co. MSW ESP 860,900 .
0074
lb
/ T( 1)
6371
Hillsborough Co
MSW ESP 421,500 .0056
lb
/T(1) 2360
McKay
Bay MSW ESP 295,312 .
0070
lb
/ T( 1)
2067
Pasco
County MSW DS/FF 322,794 .
0026
lb
/ T( 1) 839
Lee
County MSW DS/FF 305,000 .
0021
lb
/ T( 1) 640
Lake
County MSW DS/FF 164,000 .
0025
lb
/ T( 1) 410
Key
West
Incin
. MSW ESP 43,800 1.5 ppm 131
Dade Co.
Incin
.
RDF ESP 972,000 .
0024
lb
/ T( 1)
2333
South Broward Co
MSW DS/FF 1,554,000
* .
0017
lb
/T(1) 2007
North Broward Co
MSW DS/FF " .
0021
lb
/ T( 1) 946
Palm Beach
Co. RDF DS/ESP
730,000 .00036lb/
T( 1
) 263
Bay
Co Incin
. MSW ESP 159,120 .
0024 lb
/ T( 1) 382
Total 18,749
Tampa Elec. Plants
Big Bend 1,2,
3 Coal
ESP 3,900,000 .1575 ppm(2) 1228
Big Bend
4 Coal WS 1,400.000 .
063 ppm
( 3) 176
Gannon Coal
ESP 3,100,000
.1575 ppm(2) 976
Gannon
1 Oil
?
1.4
million
brl
21.4lb/
mbrl
30 Total
2410
Florida Power Plants
Crystal
River Coal
ESP 7,000,000
.1575 ppm(2) 2200
Oil
?
9.7
million
brl
21.4lb/
mbrl
200 Total
2400
Gulf Power Plants
Crist Coal
ESP 3,350,000
.1575 ppm(2)
1055
Smith Coal
ESP 1,200,000
.1575 ppm(2) 378
Scholz Coal ESP 150,000 .
1575 ppm
( 2) 47 Total
1480
JEA
Power Plants
Coal WS 3,700,000 .063 ppm(3) 466
Oil
?
8
million
brls
21.4lb/
mbrl
200 Total
666
Gainesville Plant
Coal ESP 670,000 .
1575 ppm
( 2) 211 Total
211
FPL
Power Plants
Oil ?
34.1
million
brls
21.4lb/
mbrl
720 Total
720
State
Total 7887
MSW= municipal solid waste (not all of
those in state are listed here)
ESP=
electrostatic precipitator
, FF =
Fabric Filter
WS= wet scrubber plus electrostatic
precipitator
DS= dry scrubber
(1) emission rate from KBN
Engineering, Inc.- emissions tests, 1992
(2) based on average mercury
in
Eastern coal
( KBN) with 25% removal
(3) based on average mercury
in
Eastern coal
( KBN) with 70%
removal
(4) MSW contains over 2000 tons of toxic metals
including lead, mercury, cadmium, chromium, nickel, aluminum, etc.
per 1 million tons of MSW. Waste burned in the over 300 medical
waste incinerators in Fla. which are also major sources
is similar. Coal
contains over 1000 tons of toxic metals per 1 million
tons
Appendix
1 �
Average
Toxic Metal Concentrations in Various Fuels
(
parts
per million)
Metal #6 Oil Eastern
Coal RDF/MSW Sewer
Sludge
___________________________________________________________________
Aluminum 17000
Arsenic 0.1 15 4 1
Barium 2600
Berylium
0.03 3
Cadmium 0.30 0.07-16 8 64
Chromium 0.14 23 80 1372
Copper 0.20 16 300 855
Lead 0.6 14 380 1160
Mercury 0.06 0.10-0.30 1
&
3 6
Manganese 0.16 80 170 128
Nickel 10.0 18 60 153
Selenium 3 1 2
Silver 0.3
Thallium 25
Thorium 3.1
Uranium 1.3-2.3
Vanadium 5.7 100 28 26
Zinc 0.8 40 600 1372
source‑ for Eastern
coal: average of averages quoted by
(1)
Radian
Corporation
,Estimating
Air Toxics
Emissisions
from Coal and Oil Combustion
Sources,
U.S. EPA, 1989(NTIS PB89-194229).
& (2) California Air Resources Board,
1989.
for all
other fuels
( 2)