Toxic Metals: Emissions, Deposition, Health Effects, Controls & the relation to incinerators, coal plants, acid rain, food, etc.


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 ewage 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 - acetyl-cysteine (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,61b)  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, 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).  

  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  signalling  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  uptatke  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). 




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.




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.


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  are enough 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).



(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, ; & (b)  Toxicolological Profile,  Mercury , Lead, Arsenic , Cadmium , (c)   Case Studies in Environmental Medicine, ; & (d) Minimum Risk Levels ( MRLs ), 2020, 

(1.1)      ATSDR  ToxFaQs  for Mercury , Lead ,   Arsenic , Cadmium , Aluminum

(b) Health Effects of Mercury, ;

Other Toxics, ;

(1.2)  U.S. Environmental Protection Agency, Hazardous Air Pollutant Hazard Summary, Fact Sheets, EPA: In Risk    Information System, 2018, : & Human Health Risk Assessment, ; & Ecological Risk Assessment, ; &  Air Pollutant Facts &

Mercury Page,

 & 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, ; & 

Fish Tissue Data Collected by States for State Fish Advisories, ; & 

EPA, Indocrine Disruption, ; & Lead in Drinking Water in Schools and Childcare Facilities, 2017, ;

(1.3) U.S. EPA, 40 CFR Part 132, Water Quality Criteria, Wildlife Protection & Human Health, & Drinking Water Regulations, ;

& Environmental Mercury Laws,

& Environmental Lead Laws, ;

(1.5)National Wildlife Federation, Cycle of Harm: Mercury’s Pathway from Rain to Fish in the Environment,  May, ,'s_Pathway_from_Rain_to_Fish_in_the_Environment

& (b) NADP/Mercury Deposition Network, Total Mercury Concentration, ; & Total Mercury Wet Deposition , 2017, ;

(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, ; &

(1.7) Agency for Toxic Substances and Disease Registry, U.S. Public Health Service, ;

  Toxicological Profile for Mercury ", 2017, ; & 

A Media Advisory,

 New MRLs for toxic substances,

(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)

(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; &

(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; & ;

(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, ; &  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; & ;

(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, ;

(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;   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; Sci Total 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 ) -

& (b) Take Charge of Your Health (Testing & Chelation of Heavy Metals) - Dr. Chris Shade - CEO of Quicksilver Scientific ; & (c) The Long-Term 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   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.;  

(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, ; & 
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) ; &  U.S. EPA, Abandoned Mine Lands, 2018, Superfund Sites, ;

�( 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. &

(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.  NriaguNickel 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,

(17) (a) Mercury in Florida freshwater and saltwater fish, levels, sources, health effects, ;   & (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,;  & Report: Florida Rain Laden With Toxic Chemicals     Rain Poses Threat To Wildlife, Humans     Gainesville Sun     May 30, 2003; & Report details mercury pollution    Mercury-laden rain contaminating fish, group says ,By Bruce R,.≥≥  m,itchie  Democrat Staff Writer, May 30, 2003,; & (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://; &  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 CyclingReidel  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   ConferencePittsburg,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 ; 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,

 (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.UnivMedidal  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,

�( 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; ; & 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, ; & & U.S. EPA, Reusing and Reducing Basics, 2017, ; & 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 ; &( 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; ;

(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, ;

(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:// ; & 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, ; & U.S. EPA, "National Advice for Women and Children on Mercury in Freshwater Fish", ; &

U.S. EPA (fish Hg)

 (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;; & 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, ; & "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.; & (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         &  U.S. CDC,  

Second National Report on Human Exposure to Environmental  Chemicals,

(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, ;  & U.S. EPA, Office of Water, Mercury Update: Impact on Fish Advisories-Fact Sheet,; & 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

& Science News, Oct 2018,�  Value of Clean Rivers and Lakes,� ;

(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;4:2333794X17720330. 


           Major Atmospheric Mercury Sources (partial list)

                                        Estimated   Estimated

Source         Fuel  Controls     Fuel   Emissions   Emissions   

                                             Burned  Rate  (4)    pounds     




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



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)