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Fluoride: The Ultimate Cluster Flux Folder 2B

Fluoride: The Ultimate Cluster Flux Folder 2B

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Published by violakitty4124
Information on fluoride and those connected with it.
This collection is dedicated to those who wrote the original works and
made them available on the internet. I have spent countless hours
searching for information on fluoride and it is my wish, by assembling
these works, to enable others to save time looking and make available
more time for them to ‘do’.
Folder 2B
Information on fluoride and those connected with it.
This collection is dedicated to those who wrote the original works and
made them available on the internet. I have spent countless hours
searching for information on fluoride and it is my wish, by assembling
these works, to enable others to save time looking and make available
more time for them to ‘do’.
Folder 2B

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Published by: violakitty4124 on Mar 15, 2009
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Fluoride: The Ultimate Cluster-Flux

And the Players Involved A Compilation of Documents and Articles Relating to Fluoride

This collection is dedicated to those who wrote the original works and made them available on the internet. I have spent countless hours searching for information on fluoride and it is my wish, by assembling these works, to enable others to save time looking and make available more time for them to ‘do’. If you are sickened and appalled by the approved use of fluoride in food, beverage and other consumer products then I ask that you spread this knowledge on to others and contact your local representatives in the

hopes that one day fluoride will be more strictly regulated or, banned altogether. These documents are listed in roughly the order I found them. It would be nearly impossible to group them in some kind of order since they are all linked together – a cluster-flux of monumental proportions. I would like to thank (or curse) Christopher Bryson whose excellent book, The Fluoride Deception, opened my eyes to fluoride and started me on this journey of uncovering the truth. For more information on fluoride, I would recommend the Fluoride Action Network (FAN) http://www.fluoridealert.org/ as a good place to start.

NOTICE In accordance with Title 17 U.S.C., section 107, some material on this web site is provided without permission from the copyright owner, only for purposes of criticism, comment, news reporting, teaching, scholarship and research under the "fair use" provisions of federal copyright laws. These materials may not be distributed further, except for "fair use" non-profit educational purposes, without permission of the copyright owner.

http://gulfwarcouncil.com/gulf_war_illness_explained_in_th.htm

Gulf War Illness Explained in the Simplest Terms
Gulf War Illness Explained in the Simplest Terms

By: Jim Phelps Copyright 2005

The 1991 Persian Gulf War still affects hundreds of thousands of American Veterans from the "toxic soup" that cut some 30 years off many of their life-spans. There has been much discussion of the toxic soup's components that have taken the terrible toll on those exposed. The significant toxic exposures were aluminum and mercury in vaccines, the Depleted Uranium from munitions, the oil well fires, the nerve gases that hydrolyses to hydrogen fluoride, DEET, PB, high chlorine in drinking water, methanol from "Nutrasweet" soft drinks, and other insecticides. All these varied toxic materials leave many people mystified as to what are the main components driving the long term illnesses showing up in many of the hundreds of thousands of people sent into the Gulf War zone and others that never entered the war zone who also became sick from only the vaccines. The question becomes what is the common factor that connects all these persons leading to this similar illness pattern. There were some immediate effects due to consumption of high amounts of Nutrasweet beverages in the hot climates that put many soldiers well over the safe levels of methanol, which began some of the nervous system damage. This was made worse by damage to repair enzymes like SOD, due to varied chemical exposures that lowered this essential enzyme. The common factor that connects to all the illness is not a mystery and is a well known effect, but one that is suppressed. The

common mechanism is the loss of enzymes in the human body and the main two involved are glurathione (GSH) and SuperOxide Dimutase (SOD). Glutathione is the main enzyme that clears many toxic metals from the body and without it being at full potential toxic metals concentrations rise in the body leading to increases in free radical damage to cells via reactive oxygen damage (ROS). SOD is responsible for repair of the ROS damage to the cells. So, the main problem is both the loss of the mechanism that clears the toxic material and the loss of the mechanism that repairs the damage due to rise in the toxic materials driving high rates of ROS damage. The other key enzyme is one called RNase L which is damaged by the high free radical effects from the toxic metals interaction with cell mitochondria. The RNase L enzyme is the key one that controls viral infections (and also mycoplasma, bacteria) within cells. High radiation generation of free radicals also damages this same enzyme class and results in viral infections that are typically controlled with these enzymes. Inner cell infections like mycoplasmas can appear that require antibiotics to control. GSH and SOD also care for the brain and pass easily into the brain tissues. The GSH clears the brain of toxic metals, like mercury and lead, and the SOD tries to heal the damage caused by the toxic metals substituting into cell processes that lead to ROS damage. The "brain fog" or "foggy thinking" that associates with Gulf War Illness is a direct result of lowered levels of GSH and SOD in the body and is a first order sign for this type mechanism being of prime importance. The prime causes of reduced GSH and SOD are toxic materials like HF (hydrogen fluoride), AlFx, DEET, mercury, PCB, chlorine, insecticides, and a lack of vegetables and fruits in diets. Everyone in the US today has some degree of GSH and SOD suppression and the problem worsens with age. Many of these toxic materials highly retain in the body and the leading problems come from mercury, PCBs, and fluorides. The mercury component and the bad diets lead many vets to get many of the Gulf War Illness symptoms just due to the many killed vaccines they received that employed mercury.

The reduction of the clearance of toxic metals due to GSH is easily observed in the population as it plays a direct role in why hair turns gray. Grey hair is caused principally by rising levels of Hg or mercury in the body being incorporated into the hair follicles causing the loss of pigment from the higher cellular ROS problems. Grey hair has higher levels of mercury in it than pigmented hair strands and the effect helps to pull some mercury from tissues. Grey hair for many people begins in areas of the chin and face, where the highest concentrations of mercury tend to accumulate in tissues from mercury dental fillings. With increasing age the gray hair can affect most of the head's hair. This is a common example of the effects of reduced GSH and SOD enzymes that happens with age and rise of internal retention of PCB, pesticides, HF, and Hg that act to damage GSH and SOD production. The enzyme GSH removes toxic metals from the brain and tissues by combining the toxic metals with sulfur and then an excretion pathway via the bile into the feces and out of the body. As GSH levels in the body fall from chemical poisoning effects it places more of a load on the kidney pathway of excretion. The toxic metals loading on the kidney can become too large easily and damage the renal tubule cells leading to less excretion rate and an acid shift of the blood that enhances the toxic metals retention problems. The failure of the GSH pathway to remove metals from the body and the damage of the kidney pathway to remove metals from the body produces a rise in toxic metal retention in the body, high ROS levels, and very high risk for cancer and all the immune linked illnesses. The failure of the kidney pathway to remove toxic metals generally shows with porphyria in the urine. Vets that came to the war zone were exposed to HF from nerve gas demolition plumes of hydrogen fluoride enzyme system poisons drifting into their breathing air space that damaged the GSH and SOD levels. Vets were also exposed to DEET, oil hydrocarbons, and insecticide sprays the also damaged GSH and SOD levels. The net result of this long term poisoning effect is a slow rise in the toxic metals (Hg, Pb, Al, Cd, etc.) concentrations in the body and a slow decline of the beneficial trace metals (Zn, Mg, Se, Cu, etc.) in the body that support the formation of GSH and SOD. One can even look at the recovery regimen that GWI researcher named Dr.

Garth Nicholson recommends and find he recommends minerals and other factors that boost these beneficial trace elements and GSH and SOD. Nicholson was the first to spot mycoplasma effects in GWI, and the mycoplasma problems are also common to radiation exposures due to high levels of ROS damage to RNase L cellular enzymes in the body generated by high radiation. This basic mechanism for illness is common to the Chronic Fatigue Syndrome (CFS) and the illnesses of the DOE gas diffusion plant workers. The most damage to the GSH and SOD in these cases is due to the rise of fluoride and HF exposures that lead to the upset of the metals metabolism in the body. The health damage is due to high levels of ROS that lead to health problems that look like they are caused by internal radiation free radical damage. The rise of the toxic metals and the acid pH shifts in the blood lead to kidney cell damage that has the appearance of DU type heavy metals poisoning. When the body's pH goes into the acid domain the metals retention is high and the ROS damage to cells extreme and usually results in cancer virus activation. In areas like Oak Ridge where high levels of chemicals like HF kill off the GSH and SOD enzyme clearance of mercury from the body one finds higher rates of thyroid damage. High levels of mercury are well associated with hypothyroidism and Hashimoto's Thyroiditis. Sometimes the thyroid effects in Oak Ridge have the appearance of hyperthyroidism when there is too much cadmium and the high free radical damage due to loss of SOD. It is a very similar effect that damages the kidneys that potentiates toxic metals retention. The worst effect from GWI comes from the fluoride and aluminum vaccine effects that spontaneously form AlFx compounds that mimic the pituitary hormone TSH. The AlFx compound then determines the levels of thyorid gland and liver T-3 and T-4, which program the energy levels in the mitochondria of every cell in the body. It is this effect that results in the depletion of the GSH levels needed in all the cells of the body. This effect causes the night sweats that are common to both people with CFS and GWS. It also causes the loss of restful sleep and the inability to sleep because the cells won't power down like they would under the control of the pituitary gland.

It is this thyroid hormone mimic problem that lies at the very heart of GWI, because so little of a chemical can cause such a global effect on all cells in the body. The effect that is produced is like that of hyperthyroidism, which leaves people very tired, often sleepless, and will little cellular GSH. The standard thyroid test using TSH results in misdiagnosis of hypothyroidism because these persons will test low for TSH and be uncommonly tired. This effect leads to the confusion on GWS by many doctors and it also leads to ways to cover up the health problems by testing only for TSH. Only the Thyroid Panel tests begin to show the T-3 and T-4 high level problems that the AlFx compound causes in the GWI equation. The key to the AlFx TSH hormone mimic effect is that AlFx compounds don't follow the night and day amplitude and pulse fluctuations of the normal pituitary TSH. The AlFx compounds have drastically different bonding characteristics to TSH receptor sites of cells due to the fact that highly electronegative fluorine is involved in the site bonding. This effect results in a nearly permanent bond to the receptor sites for TSH, which highly upsets the normal thyroid hormone regulation process. It is this effect that depletes the GSH in every cell in the body and why the Al and F contamination effects are often the worst on GSH levels and the illness processes. The bottom line is that 10 days of war took 30 plus years off the lives of hundreds of thousands of US soldiers that entered this conflict. Hundreds of thousands of Vets were exposed to some of the most retained chemical poisons on the planet that killed their GSH and SOD levels leading to health problems about like those of a 60-year-old female. Some have brain injury so severe from the toxic metals effects on the brain that look like the seizures of Minimata Disease. Gone was their prime of life and health and 2030 year old people were suddenly given the health of life outlook for an elderly person. If one considers the typical life span these days as being 75 years, then the loss of 30 years from the life span of each of the 800,000 people in the Gulf War means 400,000 people effectively died from this toxic soup war zone. The American Government appears interested in offering up DU as the principle reason for all the rise of cancers in Iraq after the war. This benefits the US because it conceals the main issue of wide

ranging chemical damage effects from blown up oil wells and oil refineries that used HF and the oil products that damage the GSH and SOD in the human body. There is no possible way that the use of DU in Iraq has caused the wide spread illness effects in the civilian populations. On the other hand, there is little doubt that DU is directly involved in affecting the health of persons that cleaned up DU hits on vehicles, those that stirred up the DU dusts hunting war souvenirs, and some of the Iraq population in close proximity to high level DU contamination. DU oxide dusts of the nano-meter size particles easily gain entry to the body via skin and via lung and has toxic characteristics similar to mercury. The DU issue is being politicized to hide the very much larger problems of chemical effects on GSH and SOD. The chemical damage factor to GSH and SOD causes the DU retention time in the body (or the biological half-life) and ROS damage to be greater, and the same effect applies to all other toxic metals. All of the studies for DU's biological half life is done on healthy animals with normal levels of GSH and SOD, and without the mercury toxicity effect on renal cells. When chemical damage to the GSH and SOD levels in the body is included for the increased toxic metals damage to kidney calls, the biological half-life of DU and other metals is made much longer. The use of mercury in vaccines helped to impair kidney cells and the damage is high as mercury also suppresses GSH and SOD. All the GWI studies that use the single challenge DU exposure for the biological half-life numbers that don't include the chemical damage to the enzyme clearance of toxic metals are in error. With the reduction of GSH and the bile pathway comes high loading of the renal cells with DU, Hg, and other toxic metals that damage these cells and set up higher levels of toxic metals retention in the body due to highly impacted losses of the two main clearance mechanisms. The DU armor on US tanks is sandwiched between sheets of aluminum and when the material is hit, not only DU dusts come off but Aluminum dusts do also. The aluminum dusts pose an even worse health risk than the DU, because they form the AlFx compounds in the body that upset the TSH pituitary regulation process and the prime factor that triggers GWS via GSH depletion. These exposures would add on top of the aluminum in the vaccine exposures.

The War in Iraq also is one of political affectations, rather than any real threats against the US. Bush-41 holds a huge interest in the Kuwait oil fields and he was the first US operation to open up Kuwait's oil fields. Iraq was considered a threat to Israel and the Jews. Government engineered the Iraq conflicts for Israel's interests and not those of the US. In so doing, persons have killed some 400,000 effective lives in the US and cost the US trillions of dollars for the interests of a foreign power that has little interest in the US other than trickery to promote their own group aggrandizement interests. Big oil person Condi Rice, who was trained by Madeline Albright's father in Denver, Co., is part of the Jewish problems. Oil is being used by Israel to leverage US into doing their bidding. Even the 911 event was about Israel's agents helping to facilitate the WTC attacks and helping the Arab factions pull off the attacks. The pattern that has gone on since the times of JFK's death fits the Mossad Logo that Reads: "By Way Of Deception Thou Shalt Do War" The Persian Gulf Wars are all about the concepts of deceit and treachery and this method is being used to conceal the main health effects of GSH and SOD damage via chemical effects on enzymes. The effect is most pronounced for hydrogen fluoride systemic poisoning effects on enzymes using metals. This simple and very basic of effects is the principle damage vector to most all persons health in the US and the very roots of the system of profits for the AMA based medical system. When this very basic system for cause and effect on health becomes exposed, large parts of the medical system in the US will be tossed aside as being too expensive and insensible. Again, the main cause of Gulf War Illness and the very war itself is about politics and money and not about any mystery causation. The very roots of the GOP dominated industry is on the very verge of being found out for the degrees to which they have abandoned citizens health to favor making uranium, aluminum, and other strategic metals to gain control via wars. Long ago the US decided to cover up this major cause of ill health in the US and use AMA medicines to mask the symptoms and control the damage factors. The Rockefeller based AMA and big oil is right in the middle of the cover-ups. Even religion, which is highly GOP oriented, is being

used to help cover up the health associations from toxic emissions that appear in the biblical times. The very same diversion tactics have been used in Oak Ridge to conceal the HF dominated health damage to workers and area residents health. In Oak Ridge radiation and heavy metals are played up as the direct cause for what is causing everyone's health problems. The real problem is a two step progression due to chemical damage from HF, PCB, and Hg to enzymes GSH and SOD leading to factors that look like radiation damage effects to cell enzymes that regulate viruses and cause the rise of toxic metal retention. Oak Ridge uses deception to protect themselves from the massive lawsuits and the Govt. payout for the health damage their operations have caused to a large area in and around Oak Ridge. The local medical system uses the large-scale cover up of the problems as a reason to make great profits treating all the additional illnesses and dispensing large amounts of drugs to those affected. Oak Ridge has long had an understanding with the local medical community that they won't disclose the main causes of illnesses or diseases, if they associate in any way to the DOE operations in Oak Ridge. It is this same system of ultimate deceit and treachery used to fool the citizens that has been extended to those veterans of the Gulf Wars and the people of Iraq and other sites where the toxic soup factors have become extreme. Both GSH and SOD are liver oriented enzymes and required in every cell to work properly. GWI's prime cause and effect leads off with chemical damage to the liver's production of GSH and SOD. When this liver enzyme system is chemically poisoned the body's toxic metal load begins to increase and as this occurs these toxic metals interact with the cell mitochondria that then causes the increase in the ROS levels within the cells. It makes perfect since that these two areas would become the first affected, as these are the most vulnerable areas for chemical and metal poisoning effects on the body. The very same effect occurs with aging, as levels of these enzyme poisons rises in the body with age. Even the factors of high rates of ALS seen in the GW vets is directly associated with the GSH and SOD enzymes. ALS is associated with upsets of copper and manganese that form these enzymes. The problems of Mad Cow and Prion linked illnesses are caused by these same factors. Mad Cow effects come from a

systemic shift toward Mn-SOD from the Cu-Zn-SOD, and loss of Mn dependent enzymes that cleave viral RNA within cells. When sulfur bearing compounds like DMSO are applied to Mad Cow affected brain tissues, the plaques dissipate, and DMSO appears to act as GSH in supplying the sulfur to remove the toxic metals from the brain that attract the SOD needed for myelin repair. For those of you who want to look more deeply into the issues of how GWI and CFS are well association let me recommend reading this better documented piece at: "http://www.doewatch.com/cfs.html" and see this for more fluorine details: "http://www.doewatch.com/f.html" This health problem's main vector from damage to GSH and SOD has been long known back in time and is part of the story of Prometheus and damage to the liver from exposure to volcanic emissions, HF. Hercules rescued Prometheus from liver damage problems is the heart of this same health damage vector. If one notes, the Prometheus figure is part of Rockefeller Center in New York City, and this same mechanism is what makes the doctors of the Rockefeller AMA based system their wealth. The main problem of GWI is the greed of GOP oriented system of AMA profiteering by suppression of how industry poisons the GSH and SOD liver enzymes leading to immune related illnesses in the population. The Prometheus story is the Greek version of health effects from nature's emission of toxic materials, but versions of the same theme carry back in time to the stories of Noah and Moses, and their very similar volcanic associated health effects. The major problem blocking the real story on GWI being told by the US Govt. is all about near total corruption in US politics and the US version of religion based on alterations from the truths of the old biblical narratives. This is an effort to make the real story public, as we survive in each other's care. The real story here is about being dutiful toward the people of the US and not its corrupted operations that attempt to deceive the people from the truth. It is these untruths in religion and cover ups in health that are at the very roots of the terrorism equation, which Israel and the GOP exploit to the harm of every citizen in the US.

The People of America have never been so disenfranchised from control of their Govt. nor the US Constitution as threatened as now from this corrupted political and religion process. The entire US system is at risk from these cover-ups in health linked to industry emissions and racketeering process used to hide the massive problems.

REFERENCE CITATIONS: Title Role of glutathione and hepatic glutathione S-transferase in the biliary excretion of methyl mercury, cadmium and zinc: a study with enzyme inducers and glutathione depletors. Author Gregus Z; Varga F Source Acta Pharmacol Toxicol (Copenh), 56(5):398-403 1985 May Abstract The effect of hepatic glutathione (GSH) depletion and enzyme induction on hepatic glutathione S-transferase (GST) activity, biliary excretion of GSH, methyl mercury, cadmium and zinc was studied in rats. The GSH depletors, methyl iodide and diethyl maleate, did not influence hepatic GST activity but, depending on the substrate used, benzo(a)pyrene, phenobarbital, pregnenolone16 alpha-carbonitrile (PCN) and trans-stilbene oxide (TSO)

increased it by 16-33, 44-89, 53-97 and 208-279%, respectively. GSH depletors decreased (-88%), benzo(a)pyrene and TSO did not affect, phenobarbital and PCN increased (+113 and +149%) the transport of GSH into bile. The biliary excretion of methyl mercury, cadmium and zinc was reduced by GSH depletors (-97, -74 and 93%), and enhanced by phenobarbital (+139, +280 and +220%) and PCN (+150, +121 and +160%). Treatment with benzo(a)pyrene and TSO did not affect the excretion of methyl mercury and zinc into bile, but decreased that of cadmium. These results do not provide evidence for the role of hepatic GST but strongly support the importance of biliary GSH excretion in the hepatobiliary transport of methyl mercury, cadmium and zinc. It is assumed that phenobarbital and PCN enhance the biliary excretion of these metals by increasing the transport of GSH, the carrier molecule, from liver to bile.

Title Effect of lipoic acid on biliary excretion of glutathione and metals. Author Gregus Z; Stein AF; Varga F; Klaassen CD Address Department of Pharmacology' University Medical School of P]ecs' Hungary. Source Toxicol Appl Pharmacol, 114(1):88-96 1992 May Abstract Several metals are excreted in bile as glutathione complexes' and their biliary excretion is facilitated by increased hepatobiliary transport of glutathione. The present study analyzed the effect of lipoic acid (LA; thioctic acid; 37.5-300 mumol/kg' iv)' an endogenous disulfide which can be reduced in vivo to a dithiol' on

the hepatobiliary disposition of glutathione-related thiols and the biliary excretion of metals (10 mumol/kg' iv) in rats. Administration of LA enhanced the biliary excretion of reduced glutathione in a dose-dependent fashion. Despite increasing glutathione output' LA (150 mumol/kg' iv) did not increase' but rather decreased' the biliary excretion of methylmercury' cadmium' zinc' and copper' which are transported into bile in a glutathione-dependent manner' as indicated by a marked reduction in their biliary excretion after diethyl maleate-induced glutathione depletion. In contrast' biliary excretion of inorganic mercury' which is minimally affected by glutathione depletion' was dramatically enhanced (12- to 37-fold) by LA administration. Following inJection of LA' the concentrations of endogenous disulfides in arterial blood plasma (e.g.' cystine' glutathione disulfide' cysteine-glutathione' proteincysteine' and protein-glutathione mixed disulfides) were considerably diminished' while the levels of endogenous thiols (e.g.' glutathione and cysteine) were increased. This finding indicates that LA' probably after enzymatic conversion to dihydrolipoic acid' can reduce endogenous disulfides to thiols. It appears that LA induces the transport of glutathione into bile by the temporary formation of dihydrolipoic acid-glutathione mixed disulfide' which after being translocated into bile is cleaved to LA and reduced glutathione. Because the glutathione molecule thus transported into bile cannot complex metals at the thiol group' this might be the mechanism for the observed failure of the LA-induced increase in biliary excretion of glutathione to enhance the hepatobiliary transport of metals that are transported into bile as glutathione complexes (i.e.' methylmercury' cadmium' zinc' and copper). The observations also raise the possibility that endogenous dihydrolipoic acid' by forming a stable complex with mercuric ion' may play the role of a carrier molecule in the hepatobiliary transport of inorganic mercury.

Title Biliary secretion of glutathione and of glutathione-metal complexes. Author Ballatori N; Clarkson TW Source Fundam Appl Toxicol, 5(5):816-31 1985 Oct Abstract As bile is the main route of elimination of many metals, a large number of studies have been directed toward the characterization of the hepatobiliary transport of both endogenous and exogenous metals. Although some progress has been made, we still know little of the basic mechanisms involved in the hepatocellular uptake of metals, in their intracellular translocation and metabolism, or in their transport into bile. Our recent studies have focused on the last step in the hepatobiliary transport of mercury, namely, the secretion of the metal from liver cells into bile. The rate of secretion of methyl and inorganic mercury into bile was low in suckling rats and rapidly increased to adult rates soon after weaning. These changes closely followed similar developmental changes in the biliary secretion of reduced glutathione (GSH). When GSH secretion into bile was completely inhibited, without changing hepatic levels of GSH or mercury, mercury secretion was also completely blocked. mercury secretion paralleled individual and sex-related differences in GSH secretion. At the same time, the secretion of mercury was independent of bile flow, of the thiol and mercury concentration gradients between bile and liver cells, and of those between bile and plasma. Our results, therefore, indicate a close coupling between the secretion of mercury and that of GSH. These in vivo findings, along with in vitro studies by others in vesicles isolated from the canalicular membrane of the liver cell, indicate a carrier-mediated transport system for GSH, but the nature of the linkage of this transport system with mercury secretion is not yet fully established. Our data and those in the literature are consistent with the involvement of at least two steps in the movement of mercury from liver cells to bile--the formation of a mercury-glutathione complex in the liver cell, followed by the secretion of this complex through a process closely linked to GSH secretion. The identification of GSH as an endogenous complexing

agent in the transport of metals between tissues and body fluids now permits the design of therapeutic strategies aimed at exploiting this transport vehicle to effect the removal of metals via physiological routes of excretion. The present discussion considers the role of GSH in the hepatobiliary transport of metals. In doing so, a brief review is given of current understanding of hepatic GSH metabolism and transport.

Diagnosis: Environmental Toxic Pathway Analysis and Immune System Cytokine Modality Provide Key Insight into Chronic Fatigue Syndrome Mechanism and Etiology of Varied Pathogen Driven Illnesses.

By: J. E. Phelps Copyright 2005 Abstract:

The cytokine signature of chronic fatigue syndrome (CFS) is similar to that seen in chemical injury, Gulf War Syndrome (GWS), and Human Immunodeficiency Virus (HIV). CFS is shown to have a Th2 cytokine humoral modality from the shut down of the Th1 cellular defense. Th2 is an allergic antibody biased mode that takes precedence as the Th1 cellular mode that regulates pathogen infection internal to cells is exhausted.

Illnesses for Department Of Energy gas diffusion plant workers have this modality and many similarities to CFS due to similar toxic exposures. This report investigates the stance that toxic materials drive disease and presents an underlying common mechanism that has been overlooked and more recently suppressed. The report will show that there are new highs in toxic induced immune damage that lead to extreme free radical damage from toxic metals retention, then a proliferation of unregulated pathogens that further damage health. Analysis of the toxic pathways of nuclear industry toxic metals point to cytokine signatures that offer key insight into progression of these cytokine activations leading to long term CFS. Beryllium metal cytokine factors are presented as a model for other toxic metals and chemicals that form insoluble products in the lymph nodes due to shut down of GSH and SOD clearance enzymes which then leads to long term cytokine triggering and shutting down the macrophage pathogen destruction function. The beryllium-fluoride G-protein model is then expanded into a general model for other toxic metals and fluorides that damage GSH and SOD and share biological concentration of cytokine triggering toxic materials build up in the lymph nodes. This effect leads to continual cytokine triggering and toxic damage to the macrophage cells that perform pathogen destruction and antigen presentation function. The discussion also takes into account the time line of scientific discoveries that have allowed these insights into CFS since its recent popularized discovery in the mid 1980's. Key points that will be considered are the Gprotein mimic effects of beryllium and aluminum when compounded with fluorine that mode lock the lymph node dendritic cells when GSH and SOD are suppressed. Then the effect of fluoride compound breakdown that sequesters increasing fluorine atom concentrations in the bone marrow that in turn robs immune cell formation of essential metals for enzyme protection. The depletion of GSH will lead to discovery of problems with the global sulfur cycle from ozone hole effects damaging the DMS levels needed to support hepatic clearance of toxic metals and prevent hypethyroid type shifts and metabolic acidosis leading to CFS and other immune system illnesses. This report is a comprehensive and broad based discussion illustrated with practical examples and referenced to peer reviewed scientific journals to show the key effect in CFS and human immune health.

The human immune system is a complex system of dynamic cells with many cytokine feedback factors that have been explored in the last decade to reveal many of the mechanisms for illness. The

immune defense takes on two distinct modes as set up by the stimulation of T helper cells, as triggered from the lymph nodes. The cellular Th1 immune system profile is one designed to control pathogens internal to cells and the humoral Th2 system response controls external cell pathogens.[1] Study of the cell factors and cytokine signaling yields an understanding of how these factors lead to and control many illnesses, including chronic fatigue syndrome (CFS). This report outlines a cellular mechanism and a toxic pathway for damage to the immune system by analysis of the cellular cytokine response from toxic damage, which then leads to more progressive disease factors from loss of pathogen regulation. This discussion will time line the discovery of CFS, correlate toxic environmental factors with CFS, and connect the cell mechanisms to the prime factors driving the CFS immune dysfunction process. The nuclear weapon materials research offers key insight into the toxic pathways and cellular responses that lead to these theories and conclusions. This report reflects my research into viral and immune system effects since 1980, with direct experience from the Oak Ridge, Tennessee nuclear site. I, as an ORNL Sr. Staff, proposed that fluoride in bone had an insoluble precipitate effect, a metals speciation, on the essential trace metals for immune cells formed in the bone mass. The effects of fluoride forming Gproteins would lock up and shut down the lymph node immune defense process. Fluoride is a potent enzyme poison due to its affinity toward trace metals. This key effect has not been reported by ORNL and has been suppressed since 1986 due to Oak Ridge liabilities from toxic HF emissions. Presenting a key finding on fluoride toxic effect and its cumulative mechanism in a public forum is the purpose of this report. This report is principally concerned with the lymph system, its cytokine signaling, and how it responds to toxic exposure. Cell and lymph system response is nothing new as even snake venom toxin drives cytokine response and nitrogen oxide (NO) generation.[2] Snake bites require light tourniquet pressure to prevent circulation of snake venom in the lymph system and around the body leading to death in some cases. Many biological toxins are handled well by the lymph system, but many toxic materials enter the same pathways and cause serious problems

due to insolubility problems of mineralization or turning to stone in these critical zones. Oddly enough, it has been suggested that the symbolic imagery connected with the Virgin Mary icon standing with foot placed on a snake emanating from the Earth and the snake biting the apple as symbolism for contamination from the Earth's lower regions connected to disease and illness. Religion symbolism from Noah is connected to the largest land mass volcano on the Earth and the toxic emanations to health effects on man and animals. Religion and Revelations even speak to the asteroid called "wormwood" that poisoned the planet with volcanic like toxins from the heat of interactions from land impacts, or caused massive floods when they impacted oceans. This report will take a multi-disciplined investigation, using volcanology, asteroid terminal event toxic releases, history, religion, nuclear plants, wars, and toxic research to look more deeply into these health effects. From the nuclear weapons production, Oak Ridge is one of the most chemically impacted industry sites in the U.S. and many toxic linked illness patterns are evident. The toxic material research studies from the nuclear industry and Oak Ridge health problems provide a clear and unique view for some of the mechanisms for toxic driven immune activation in illnesses. These studies, that are well known in the nuclear plants, will be used to illustrate and prove the process of toxic induced immune illnesses. Toxic material pathways into the human body, how they retain or concentrate with time, and vector to different organ systems play pivotal roles in disease etiology. Some of these toxic material pathways directly affect the immune system resistance and lead to viral disease etiology. Examining these patterns and how they overlap CFS is the focus of this report. The term "CFS" (or CFIDS) made its national appearance in the mid 1980's with the investigations of Dr. Paul Cheney concerning sick persons in the area of Lake Tahoe, on the California and Nevada border. Most of these CFS persons were fine one day and came down with mononucleosis like illness the next, with flu like symptoms persisting. In 1999, Cheney described the illness as one that depleted glutathione, used much ATP, and showed a very significant up regulation in an enzymatic pathway known as the 25A RNase L.[3] Looking for toxic exposure factors, the waters of

Lake Tahoe are pristine, but the area is of volcanic origin that contaminate some wells and soils with volcanic materials. Well waters are often contaminated with higher levels of arsenic, manganese, radium, radon, and fluoride than surface waters. South Lake Tahoe has public water supplies from wells that have metal contamination, often associated with volcanic zones or mining. South Lake Tahoe water reports have specific caution for immune compromised persons because of these pollutants.[4] Cheney's CFS Tahoe cluster diagnosis was made possible by detection of new chemical bio-markers, but CFS is not new as it appears to be symptomatically reported in 1750 and in other terms in earlier periods.[5] It is also speculated that the biblical story of Jesus healing the person by the well is even earlier evidence of the illness. The Cheney / Tahoe mononucleosis like illness is associated with swollen lymph node from activation of EBV, HHV6, and other viral pathogens that are associated with follow on disease factors, like MS.[6, 7] Glutathione (GSH) depletion is associated with the cellular oxidant repair process and detoxification of tissues and it is lowered by chemical and pathogen damage to mitochondria of cells that manufacture ATP.[8, 9] Lowered GSH can hasten cell apoptosis and is an indicator in chronic disease, cancer, arthritis, and rapid aging.[10, 11, 12, 13, 14, 15] Glutathione is important in liver detoxification and in maintaining the mucosa cells that line the intestine.[16, 17] Selenium associated Glutathion depletion drives shifts in cytokine mode from Th1 to Th2.[18] The "2-5A RNase L" enzyme is part of the activation process for the Th1 interferon cytokine that inhibits viral replication in cells.[19] 2-5A RNase L is also important in the control of HIV replication.[20] These bio-markers point out that control of viral pathogens in the body have been compromised. The mechanism from just these indicators is not well defined, but these are indicators of immune cell toxic effects. There is a enzyme chimera effect for CFS associated 2-5A RNase L where persons with CFS produce a 37 kDa enzyme inside their white blood cells, where normal persons produce a slower but more effective 83 kDa enzyme. The lighter weight enzyme is faster in dissemination, but less effective in killing viral components. The damage to the RNase L enzyme follows damage to GSH and SOD, which clears toxic

metals that damage mitochondial function, produce excessive ROS generation, and reduce ATP production. The appearance of this lighter weight chimera of the 2-5A RNase L enzyme sets up the factor for viral infections and in white cells not being controlled. The 37 kDa enzyme does not kill viral presence inside cells, nor does it kill many of the white cells. This is the key to transmission for the viral spreading in the white cells of the immune system and infecting many cells in the body. The rise in the RNase L causes damage to the mitochondria and ATP production. It also sets up the causation for the high levels of NO in the cells that damage the mtDNA. This effect sets up the debilitating fatigue connected with CFS that follows directly upon the RNase L chimera. The principle question then becomes what causes this enzyme of the white cells formed in the bone marrow to mutate into a lesser effective enzyme. The basic mechanism of cell enzymes that police viral and pathogen infections inside the cells is also seen from high radiation effects. Typically the high ROS produced by external gamma radiation will result in cell infection problems that are treated with antibiotics. Mycoplasma's, viruse's, and bacteria's become problems when RNase L becomes less effective due to high rates of ROS damage. The very same effect on RNase L can be had from the loss of GSH and SOD due to chemical factors acting on G-protein channels shutting down its production. In this way, chemical induced free radical damage and radiation induced free radical damage are the same and additive toward damage to the RNase L. Cancer tumors occur from the activation of endogenous DNA viruses and the mutations of those viruses the radiation induces. Vaccines also included cancer viruse like SV-40, which can become active when cells loose their RNase L enzyme protection. When the Rnase L enzyme is impaired by free radical damage, cancer viruses can proliferate and even produce their own GSH and SOD to promote their growth. Cancer viruses also promote cytokine TNFa which sets up higher blood circulation that helps the tumors grow more rapidly. Cancer virus and tumors proliferate only with ROS damage to the RNase L enzymes impair the process that causes cell apoptosis or death AND when the back up system of Th1 cytokine signaling impairs the macrophage and T-cell protection system. Both failures often hinge on damage

to GSH and SOD from chemicals affecting the GSH G-protein channel. Cheney's patients were from an extinct volcanic zone with contaminates in well water. From the study of volcanology, we know volcanic zones have many of the toxic fluorides and metals problems associated with mining and operation of Department Of Energy (DOE) plants that emit metals and fluorides.[21, 22, 23] Volcanoes have more explosive power from H2S than nuclear weapons and produce toxic fallout and contamination problems with acids, toxic metals, and toxic halogen compounds [i.e.: calcium fluoride, hydrogen fluoride, hydrogen chloride]. Meteor events also present toxic emissions like those from volcanoes and these same factors play dominant roles in species survival. Meteors that hit the oceans cause massive waves as in the times of Moses flood, and those that hit the land mass produce huge levels of very toxic acids like HF. The Earth, for many millennia, was bathed in distilled waters from the heat of the sun that produced a thin layer of less toxic soils on the planets surface and clean surface waters. Mining, industry, and well drilling often compromise this natural toxic isolation process and lead to health problems in man. Volcanoes and glacial effects have long been associated with essential trace metals availability in soils. Soils in the US and other areas have been highly depleted of these essential trace metals by over farming, over grazing, and by acid rain effects. Before man's energy needs the chemical speciation and solubility factors for these trace metals was determined by sulfur from volcanic emissions. As man's energy needs have become dominate; the hydrochloric, carbonic, and nitric acid effects have grossly upset the metals speciation from that of sulfur dominated. This highly affects grazing animals health that are highly coupled to the soils via the grass uptake of these trace metals. The change in metal speciation puts more toxic and dangerous metals into the grazing animal's diets and with this effect comes the "mad cow," scrappie, and prion linked problems we see today. One can easily find cattle being highly affected by toxic aluminum, increased manganese, mercury, and other metals offset. In the US, the practice of feeding cows bone meal had to be stopped because the bone sequestered

these toxic metals and fluorides and this was linked to the prion formation. Toxic emissions from volcanoes have been associated to biomarkers such as porphirine and porphyrins, which are diagnostic indicators of toxic cell damage effects from metals and chemicals.[24] Porphyrin is the killing chemical inside NK cells and when these cells are destroyed it releases higher rates of the porphyrins in the blood. CFS causes lowered NK cell population and this is a result of their porphyrin content and RNase L ineffectivity toward viral infections. Persistent toxic gas emissions of volcanoes kill animals and cause long term defoliation of downwind areas. This is often connected to chemical damage effects to GSH and SOD enzymes, which increases retention of toxic metals and ROS damage in cells. Mining and smelting operations often cause similar problems with acid run off contaminating soil and water with metals and fluoride. It should be noted that century's earlier volcanic zones were connected with rapid spread of disease. An example is the Hawaiian Islands and their native residents weakened immune resistance to measles, syphilis, and other diseases, as Europeans traded and socialized with them. It is noted in history that in this population disease spread incredibly fast and devastated the islands inhabitants, which suggested their immune resistance was degraded by their volcanic environment. Volcanic eruptions are even postulated to have caused the downfall of the Egyptian City of Memphis from massive plagues. It was these early associations that connected toxic material to the weakening of the immune protection system making persons vulnerable to opportunistic infection and endogenous viruses in the body, as well as exogenous viral transmission. These early observations suggested CFS had environmental and industrial linked toxic contamination origins. In other centuries toxic metals such as arsenic, lead, and mercury were associated with health effects. Lead was connected to the neurological hearing illnesses that Beethoven experienced and even associated with the demise of the Roman empire due to the lead food storage methods.[25] Lead promotes a Th1 type cytokine response and tumor necrosis factor alpha (TNFa) that will activate the macrophage's and pull particulate into the lymph nodes.[26] The leading Th1 cytokine called TNFa promotes macrophage

activation. Persistent triggering of Th1 inflammatory cytokines by toxic materials is linked to CFS factors like headache, fever, myalgia, fatigue, and are toxic in high doses. Here the pathway was via food supply with absorption via stomach and gut and retention of metal oxides in the local lymph nodes. Toxic metal retention and damage to the immune system is associated with cancer vulnerability.[27, 28, 29] The effects of arsenic in well water are associated with the rising cancer rates in India. It was attempted to improve the biologically polluted, surface public water supplies in India via drilling wells, but this resulted in high arsenic public water. Arsenic is well connected to lung, bladder, and skin cancer, but is a treatment for liver cancer that impairs the mitochondria of cancer cells.[30, 31] A similar attempt to avoid biologically contaminated surface water in Africa presented wells with high fluoride content. How these toxic materials distribute in the body organs and inner cell effect is important to immune resistance. A dominate factor for metals retention and lymph node build up is linked to chemical damage to two essential enzymes, GSH and SOD, which convert metals to sulfides and excrete them via the liver's bile pathway. A metal oxide analogy from the mining industry is connected to the mechanism of a controversial anti-cancer drug called laetrile. In special mining practices, cyanide chemicals are combined with insoluble metal oxides in a process called in-situ mining to form extractable soluble metal products. The cyanide radical makes metal oxides soluble via replacement of the oxygen radical. The cyanide radical is unique in its ability to render metal oxides soluble and the effect is used in mining for various metals and in the electroplating process. Some enzyme processes mimic this effect in human chemistry. Cyanide radicals are also drawn into the lymph nodes, where the increased probability to react with metal oxides may reduce their concentration. Lessening the lymph node concentrations of insoluble metals then linked to the anticancer effect by restoring lymph node cell function. It is suggested that the biblical symbolism of turning to stone is a version of these metal oxide ore minerals forming stone and impairing the lymph system. The function of the immune system is central to the control of cancer viruses, yet many studies are done with only the cancer tumor cells in mind. The laetrile studies omit the immune system effects and the metal loading effects in the lymph nodes.

Many B vitamins are also cyanide involved compounds that may play a role in the metal detoxification process. Vitamin B-17 and laetrile share the cyanide radical. Many grains contain B-17 and over processing of foods tend to denature the natural beneficial content. These vitamin processes are highly controlled by the GSH enzyme's availability. Food processing and cooking often deplete food of vitamins, enzymes, and cyanide compounds. In the last 50 years, the industrial dominance of metals in immune damage has been replaced by more dominant chemicals, such as fluorides.[32, 33] This makes the effects of laetrile of lesser benefit in cancer treatment. When fluoride enters the picture, damage to the GSH and SOD process become dominate in the toxic metal retention and ROS cellular damage process. These simple observations began my thesis for the mechanism for disease from the impact of toxic metals on cells in the early 1980s. These observations qualify that many toxic metals are linked to disease, now it remains to determine what quantity and what processes are involved. It was observed that many toxic heavy metals damage cells and activates immune system response. The toxic cell damage triggers cytokine production and T-cells that kill the damaged cell with hyper-oxygen products and trigger macrophage's, which clean up the material and process it with hyper-oxygen reduction chemistry.[34] The process results in the accumulation of insoluble metal oxides in the macrophage region of lymph nodes and can be seen in data from many toxic metals. This biological accumulation of toxic metals is seen in the research data for beryllium, silicon, plutonium, uranium, and other insoluble metal oxides.[35, 36, 37] The effect is very clear in research for lung damage from airborne toxic metals pathways to lung that activate the lung inflammatory immune response. Toxic materials in the lung activate the cytokine production of TNFa that promote macrophage's, and can be seen with radiation and for toxic metals. [38, 39, 40] Cytokine TNFa is directly delivered to the mitochondria of cells and involved in apoptosis / necrosis.[41] The mitochondria of cells play important roles in cell energy production and hormonal and cytokine messaging. Beryllium is the most detailed studied toxic metal and makes an excellent example for the model of how a toxic metal activates the immune system.[42] Beryllium workers can become sensitive to

beryllium and become sensitized to breathing it as determined by a lymphocyte proliferation test. With any addition exposures persons can acquire a fatal disease called chronic beryllium disease, where the lungs cells are damaged by continual inflammation. This is often mediated with steroid inhaler medication. The disease is often mis-diagnosed as asthma initially due to similarity of symptoms. Beryllium is taken into the lymph nodes via the action of macrophages and as the lymph concentration builds it triggers the lymph nodes to make T-cells and B-lymphocytes in response to the toxic beryllium metal.[43] As the concentration in the lymph nodes builds the insoluble metal oxides retain long term and keep the local lung lymph system triggered long term in the Th1 inflammation mode. In this Th1 State the lung uses much glutathione for cell repair processes.[44] The key element for beryllium disease is that beryllium-fluoride compounds are the worst and this effect is tied to the issue of their BeFx G-protein effects toward shutting down GSH and SOD production within cells. The effect shuts down the prime clearance enzyme for the beryllium and the cell ROS repair process. The air pathway for beryllium used in the nuclear weapons business is a well developed model for the immune activation process, and shows a local process that is highly related to indicators seen in CFS. Sensitization to beryllium compounds happens after cells in the lymph nodes undergo blast cell transformation. It is clear that beryllium concentrations of beryllium toxic metal in lymph nodes set up the cytokine triggering of the immune system. Beryllium and fluoride can combine either in manufacturing processes or spontaneously inside the human body. Beryllium and fluorine combine to form dangerous BeFx and AlFx compounds that mimic G-protein triggers for human immune cells. The fluorine atom is the most electronegative of the elements and when bonded to these cell sites it cannot be undone. The vaccine business uses a similar technique with vaccine adjuvants made from aluminum [aluminum hydroxide (alum), aluminum phosphate], which forms an AlFx complex that also mimic the G-protein trigger effects.[45, 46, 47] Here the effect seeks to program the lymph node dendritic cells for long term memory of the vaccine and shift to Th-2 cytokine dominance. It is this effect that tends to lock on the immune system memory and set up long term immune sensitivity

to metals like beryllium, and cause the immune system's tolerance for varied pathogens to become negatively affected. Man's industrial effects have produced a systemic shift in the nature of the planet's processes that have resulted in a serious problem for the immune system. The rise of HCl in the environment has freed more aluminum into the food chain, and man uses aluminum in many places from salt and baking powder to vaccines and toothpaste. Fluoride has risen in the environment and into man due to similar aspects. Fluoride in the body tends to spontaneously interact with trace metals and can form the AlFx compounds that trigger the cellular G-protein channels that shut down GSH and SOD production. Man has also introduced dioxin, PCB, Hg, DDT and other chemicals that have risen in man's body and that interfere with the G-protein channel that regulates GSH and SOD cell production. 80% of the drugs make in the US are directed at controlling G-protein channels in cells that correct for these toxic induced effects on GSH and SOD. It is a multi-trillion dollar industry, where one system pollutes and causes illnesses, which the other attempts to correct for the toxic induced damages using pharmacology methods. Other toxic metals cause the same problems at concentrations lower than that needed to kill the cells directly, as long term cytokine activation causes serious health problems.[48] As the metals concentrations build in the lymph nodes the TNFa cytokine causes necrosis of the macrophage and other lymph nodes cells and continual generation of activated T and B cells. If the lymph node concentrations get too high this disables the pathogen destruction function of macrophages. Beryllium oxide particles principally involves the local lung lymph nodes, but other toxic metals that are more soluble and enter the body via air or food chain can impair lymph nodes near the intestine or all the lymph nodes at once. As the macrophages are disabled it leaves cell fragment products scattered around the tissues that then bias the system toward a Th2 response in the long term. Th2 modality excretes IL-10, which further shuts down the macrophage function and exasperates the effect. This leaves the body vulnerable to inner cell viruses and other pathogens such as mycoplasma. Metal prosthetic joints in the body further illustrate the effect of metal particulate concentrating into the lymph nodes and this

triggering inflammatory cells that loosen the bone with high levels of peroxides.[49, 50] Metal particles of less than 1 micron can be carried into the lymph nodes via the macrophage's and concentrate there.[51] The lungs are sensitive to many different metal particles that can also set up the Th1 inflammation mode. The effect is intensified if the particles from airborne exposure have an acid like coating that is insoluble. Regulations have attempted to mediate these toxic particle exposures, but has made further poor choices. Gasoline refining eliminated lead in the 1980's because of this effect on the population and replaced it with hydrogen fluoride (HF), which has even worse cumulative factors and time integral dose effect on the macrophage function. Rising levels of pesticides in food and water, rising industrial emissions of HF all combine to contribute to effects of GSH and SOD reduction leading to toxic metal retention that trigger the cytokines and lead to CFS cytokine Th2 modality in the long term. The worsening environmental metal effects can be seen in even the surface waters of the Great Lakes with their increasing levels of toxic metals that can damage the immune system, produce allergy, increases susceptibility to disease, and autoimmune disorders.[52] Even pollution of rivers from fluorides added to public water supplies harm salmon.[53] Animals and man can be highly affected by toxic metals and their phagocytosis cell ability severely impaired by low concentrations of metals, while NK cell activity is not impaired.[54] It is these poorly controlled pollutants that drive increasing rates of CFS, cancer, and many immune linked illnesses. The key etiology of the toxic accumulation effect can be anticipated by the function of oxygen based chemistry of stationary macrophage's in the lymph nodes acting with the mobile macrophage's carrying toxic cell material from around the body to these local lymph zones. This is an often overlooked important and key effect to have build up of insoluble toxic material directly in the critical signaling network of lymph nodes that keeps the immune system cytokine triggered and supply high oxidative stress directly in the lymph nodes. This effect can lead to toxic metals damaging the ability of the body to control pathogens and even to rising viral presence in the body from endogenous and exogenous sources.[55, 56] For air pollutants the lungs nodes are most affected and for food and water pollution the stomach and

intestine nodes are the principle effect zones. A pivotal role is carried by the proper function of the lymph node pathogen regulation mechanism. Simple local inflammatory activation of the immune system results in increased glutathione to aid in DNA repair, and long term global activation results in depletion of glutathione. Decreased levels of glutathione promote cell apoptosis / necrosis. Toxic's that damage the liver cause a lack of glutathione for DNA repair. The importance of a cell organelle called the mitochondria was better defined with respect to disease mechanisms in the mid 1980's with its critical role as the cell energy mechanism and the source of ATP.[57] These organelles were small cells within cells with bacterial like DNA that were vulnerable to oxidation effect, metals, and oxidative halogens.[58] GSH plays a strong role in the production of ATP and mtDNA repair from oxidative damage.[59, 60] CFS is well connected to lowered ATP levels.[61] Mitochondrial damage is connected to nerve damage and aging.[62, 63] Mitochondria is how the body converts stored fat into energy and damage to these areas of cells is linked to weight gain and obesity factors that are high in the US. Fluorides have the capacity to affect the thyroid T-3 hormone production and modify cellular ATP production throughout the body as well as diminish mitochondrial numbers in cells.[64] Depletion of ATP is connected to the Th1 to Th2 switch seen in CFS and other diseases.[65] High concentrations of toxic metals and fluorides in the lymph nodes will highly impact the mitochondria of these cells. This leave little doubt that the worst case for mitochondria damage due to toxic concentrations is the lymph nodes and that this process is directly connected to CFS and other immune dysfunction illnesses. The role of GSH and SOD and the involvement with mitochondria and ATP explains the issue of "radiation hormesis." Radiation hormesis was seen in areas like Japan after the bombs were dropped and it promoted more rapid tree growth as shown by tree growth ring data. The increase in radiation in the area promoted the cells and its feedback systems to call for more SOD to be produced to handle the free radical damage effects. SOD and GSH go hand in hand in plants and to increase SOD the GSH levels are naturally increased as well. The high GSH levels cleared the toxic metals from the cells to greater extents that promoted less

destructive mitochondria interaction from the metals and greater amounts of ATP generation. The higher levels of ATP promoted more rapid cell growth and is the interaction mechanism for radiation hormesis. The enzymes GSH and SOD are also the prime clearance and repair mechanism for the brain. Altered levels of GSH and SOD are tied to all of the mental illness problems, and also to factors of Alzheimer's, Parkinson's, and etc. It is well known that the metal lithium is used in the treatment for mental illnesses and what the lithium drugs promote is higher levels of SOD being made in the cells to repair the ROS damage to cells. The ROS damage to cells stems from toxic metals like mercury or the combination of aluminum and fluorine forming the AlFx type G-protein. The lithium atoms are believed to interact with other metals in the G-protein channels that direct the production of SOD by the cells. This process of lithium on SOD appears to not up-regulate the GSH levels needed to clear the brain of the toxic metals, so the lithium drugs have to be used often to control the mental illness. One of the prime CFS symptoms is that of frequent diarrhea and this again is associated with the levels of GSH and SOD in the cells of the gut walls. Persons with CFS and GWI generally have impaired levels of GSH and SOD enzymes. This effect is made much worse in the local area of the gut when these persons drink excessive levels of sugar-laden colas or other sugary foods. Processed sugar is a GSH and SOD antagonist and this promotes high levels of free radical damage to the cells of the gut wall. The high rates of free radical damage causes the gut cells to sluff-off with lots of water much as a blister type effect from a burn. The same type effect occurs from the radiation intestinal death effects for acute radiation doses that make the same levels of ROS damage to the cells. The extreme damage from the high levels of ROS damage also cause damage to the blood vessels in the colon and cause bleeding hemorrhoid problems and loss of blood and essential trace metals. The high levels of ROS damage in these local cells also damages the Mn dependent 2-5A RNase L enzyme resulting in lots of local cells having active viral infection problems that involve the local lymph system. The problems of reduction in the cell production of GSH and SOD well define the mechanism of

problems like persistent diarrhea and even the issue of loss of cognitive abilities from similar problems in the brain. These intestinal effects are even spoken of in the Biblical Narrative with recognition of guts like stinking sulfur bogs. The Biblical Narratives also speak to the use of the plant called "Aloe Vera" as a type of medicine. Aloe Vera has very high levels of both the enzymes GSH and SOD. The high levels of SOD in the plant is why it is often used so effectively to treat burns, as it corrects for the free radical damage effects to cells. Persons seeking to correct for the free radical damage of their intestinal tract often consume Aloe Vera juice. Another interesting association from the free radical effect produced from the loss of GSH and SOD from toxic materials exposures is that of nitric oxide production being increased. Rising levels of nitric oxide (NO) in the tissues promote sexual arousal and this is the effect produced by the drug called "Viagra." When the Manhattan Project was begun in the 1940s the plants in Oak Ridge had such a problem with workers having sex on the job that all the plants office and lab area frosted glass were changed to clear glass to cut down on these problems in the work force. The NO effect was particularly strong at the plants that released large amounts of hydrogen fluoride (K-25 and Y-12), that cuts GSH and SOD production via the combination with aluminum forming the AlFx G-protein. There is extensive evidence from the Manhattan Project and from the US Dept. of Energy (DOE) on the problems associated with toxic releases affecting the cellular levels of GSH and SOD leading to illnesses. Oak Ridge is an interesting place to study the effects of GSH and SOD suppression via occupation chemical exposures, as it has so many toxic materials that fall into this class of enzyme damaging chemicals. Oak Ridge lost some 2 million pounds of mercury from its lithium operations and this affects both workers and a large area into which the mercury escaped. Oak Ridge lost huge amounts of PCBs into area creek and burned PCBs to release dioxin. Oak Ridge and the local TVA power plants released huge amounts of hydrogen fluoride into plant and town areas. All of these pollutants are well known to damage the production of GSH and SOD, and often the workers in specific areas have health problems from the particular workplace chemical toxic of interest.

The collective sum of all these chemical agents that damage GSH and SOD is the reason the Oak Ridge area is highly affected by chemical injury problems. Toxic metal and fluoride releases are connected to the Oak Ridge K-25 gas diffusion plant and a number of workers were noted to be affected by symptoms similar to chronic fatigue syndrome. Gas diffusion plant workers with CFS like symptoms number in the hundreds. The K-25 gaseous diffusion plant lost huge amounts of toxic hydrogen fluoride (HF) to the air of the plant and region and was discovered by questioning workers about processes and releases. Other HF releases from the X-10 "Molten Salt Reactor Experiment" and the Y-12 UF-4 "Salt Shop" operations provided similarly affected workers and correlation to HF toxic effect due to cumulative low level exposures. The large losses of the K-25 plant exposed not only workers, but also downwind residents of the plant to fluorides. Fluorides were highly suspected as area pine trees, which are very vulnerable to fluorides, were showing impact. Fluorides damage the GSH and SOD enzymes of pine trees and acts much like dioxin, which works via this enzyme process to create ROS damage in plants. There was both air / lung pathway effects, soil contamination / food pathways into the gastrointestinal system, and ground and surface water pathways into communities. These pathways for fluorides connected them with the CFS like symptoms and asthma seen in workers and communities. Asthma is directly connected to reduced GSH and SOD. The workers had high levels of calcium that is indicative of fluoride exposure.[66] They also had high retention of metals and high porphyrin. Fluorides tend to be accumulated (integrated) over a lifetime and the same net dose occurs from a ten-unit dose over one year or that of a one unit dose over ten years. Fluorides cause some of the worst damage to the immune system with very low concentrations. Industrial fluoride emission in Germany in the late 1800s was perhaps the first chemical to produce worker and community health problems. Fluoride is connected to renal stone formation via insoluble calcium fluoride formation, much like what happens with metals in lymph nodes.[67] Veterinarians warn against using fluoride toothpaste on animals and with the knowledge of the lymph node effects fluoride tooth pastes and fluoridated public water become dangerous to

public health. Industrial fluoride emission was linked to asthma and to arthritis.[68, 69, 70] Fluoride workers also show their cytokine response biased toward the Th2 in the long term.[71] Fluorides impair the macrophage's at very low concentrations and the effect is strongest in the lymph nodes from the insoluble product effect that is often combined with metals and free radical synergy effects.[72, 73, 74, 75] Fluorides cause swelling of the mitochondria indicating damage to ATP processes.[76] Hydrogen fluoride sets off inflammation in lungs.[77, 78] Fluorides toxic effects set up the same mechanism as seen in the beryllium model. Fluorides are pulled into the lymph nodes and the affinity of fluoride for calcium produces an insoluble precipitate that is similar to the effects caused by the insoluble metals. The effect sets up TNFa and hyper-oxygen damage that locally lowers glutathione in the lymph cells. TNFa promotes viral RNA replication. Increasing viral infection in the type I macrophage's promotes more TNFa and this is multiplied by the repeating effect of cells in the lymph system. This activation of the Th1 process also sets up a switch to Th2 mode slowly as the macrophage's stop working and foreign cell products accumulate in the tissues that trigger the Th2 mode. Th2 suppressor effects on Th1, impaired ATP, glutathione, and other effects contribute to the mode switch.[79] Th2 mode involves IL-10 that further depresses and shuts down the macrophage action and locks in the Th2 mode. This lymph node / mitochondria impact thesis became a toxic pathway mechanism for immune dysfunction in 1986 that explained the process for all immune linked diseases and even aging / longevity factors. The thesis was that insoluble toxic material, metals and fluoride predominately, accumulated in the lymph nodes and disabled this pathogen destruction mechanism and the toxic presence set up a continuous cytokine response in the lymph system that keeps the immune system triggered and allows pathogen presence.[80] In the early stages of viral activation, a Th1 profile with TNFa is often seen and in a normal immune response these levels control the virus.[81] Internal cell viruses such as EBV, CMV, HHV-6, mycoplasma, cancer viruses, HIV, and etc. can run out of control with a system biased toward Th2. The toxic material concentrations triggered the inflammation effects that cause cell apoptosis, necrosis, consume glutathione, etc. Add in pathogenic components and the outcome is further

modified. HIV spends cell energy and promotes TNFa and IL-10, which helps in the demise of T-cells as the disease progresses due principally to the loss of macrophage activity from the IL-10.[82] The 1991 Gulf War exposed thousands of veterans to various toxic materials that have long retention in the body and set up the same conditions as the toxic metal effects in the lymph nodes. Many of these Gulf War Veterans experience the symptoms of CFS and multiple chemical sensitivity (MCS).[83] Gulf War persons were exposed to HF via hydrolysis of sarin and soman nerve gases, to glutathione depleting insecticides and oil emissions, and to toxic metals from vaccines (Al and Hg) and DU. They also are biased toward the Th2 profiles because of the similarity to the industrial pollution that drives CFS. They were exposed to toxic metals in the form of DU and mercury preservative in Th2 promoting vaccines. They were exposed to halogens in the form of bromine from PB tablets, excessive chlorides from water treatment, various pesticides, and fluorides from nerve gases.[84] Recent studies have shown that those exposed to chemicals have brain damage.[85] CFS affected persons also show brain damage.[86] Gulf War Syndrome (GWS) persons also have fibromyalgia similar to CFS.[87] The pain is driven by loss of sodium channel and ATP in nerve cells, and the calcium rich myelin of nerves is high in fluoride and metal retention that drives this effect. It is not a single chemical factor analysis that solves the illness toxic driven equation, but various toxins acting in the same pathway to disable the lymph system's critical enzymes (GSH, SOD, RNase L) that best explains GWS. This war was the toxic equivalent of hell that dosed many there with 30 years of industrial and environmental pollutants that aged them with health effects to 60 years old females. There is one central etiology mechanism involving chemical damage to GSH and SOD levels leading to increased toxic metals retention in the lymph nodes and cells triggering the cytokine response. The immune dysfunction comes from multiple contaminates acting via a common mechanism that allow varied illness outcomes as determined by exogenous and endogenous viral predisposition's and other opportunistic pathogens. Food processing and preparation play a strong role in the vitamin and free radical effects in the intestine that affect these cells and their local lymph nodes. Foods processing and cooking destroy

most of the nutrients in food. Raw and uncooked living vegetable foods supply more vitamins, as compared to cooked vegetables or fried food.[88, 89, 90] Cooked food has long been associated with delivery of free radicals from foodstuffs to the stomach and intestines and this effect causes some excess production of white blood cells, called digestive leukosis. High temperature fried food supplies the most free radical content and highest toxic exposure due to bio-concentration in the food chain. Raw and uncooked foods don't produce these free radical effects and provide better delivery of enzymes and vitamins, as well as fiber to detoxify the system. Raw food diets aid in mediation of CFS, cancers, and other immune illnesses because of these vitamin and reduced free radical factors. Raw vegetables supply glutathione that helps to keep the metals clearance of tissues and brain working to avoid the build up of toxic metals due to increased biological half-life of the toxic metals from glutathione impairment. The raw food verses cooked food is also involved with the biblical issues of Genesis. Animal foods add a level of bio-concentration of toxic material from airborne contamination of the animal food chain. Cooking vegetables or animal products produces free radicals from the pollutants and pesticides that can retain more easily in the body. Vegan diets also make the intestine more basic, which results in less immune activation and less absorption of toxic metals. A shift of the blood pH toward acid contributes to higher toxic metals retention because it impairs the rate of metals clearance by the kidney. Because of these effects, the raw uncooked vegan diet is connected toward effective intervention for fibromyalgia, rheumatoid, heart, and cancer.[91, 92, 93, 94, 95, 96] Vegan diets also alter the fecal bacteria levels and bacterial fatty acid generation.[97, 98] The toxic load and nutrient supply in the intestines is highly associated with immune illnesses and long term effects result in leaking gut syndromes. The quick heating pasteurization of milk also produces toxic effect.[99] Raw food diets promote illness recovery. One must acknowledge that most produce in the US is still short of the needed beneficial trace metals that have been depleted by poor farming methods, even in the organic farming realms. Serious persons should shift diets to include sea vegetables to enhance their essential trace metals nutrients.

Raw and uncooked vegetables promote better coupling of the human nutrient absorption systems for uptake of the essential trace metals (selenium, zinc, copper), which help to form the immune repair system with enzymes (GSH, SOD, RNase L) and also helps to remove fluorine from the body and bone mass. Soils in the US have become increasing depleted of these essential trace metals due to acid rain and over-farming without replacement of these metals. Glacial and volcanic effects placed these essential trace elements there, and the effects of industrial acid rains remove or worsen their availability to the food chain. The depletion of these trace metals sets up a rise in the rate of fluorine retention in the bone masses, where the immune system cells are formed. This effect starves the immune system cells formed in the bone mass of the essential metals needed for proper cell DNA repair and resistance against pathogen infections. This effect of fluorine rising in the bone mass is directly connected to the HIV infection process via loss of manganese. The effect also sets up the shrinkage of the thymus gland from these metals depletion effects on the immune cells. Plant cells and enzymes closely match those in animals and humans, and prove useful in helping return some of the enzyme functions in fluoride affected persons. It sometimes takes 10 years of toxic exposures from materials like fluoride to set up the cellular stress conditions that make for CFS. It also takes around 10 more years to turn around the bone burden of fluoride and get the cellular damage and enzyme processes back up to near normal. The bone retention of fluoride sets up a very long recovery period for those that chose to successfully modify their nutrition and healthy eating habits. There is more that supports the conclusion that the toxic loading in the lymph nodes shut down the monocytes / macrophage's and is the pivotal problem with HIV.[100] HIV transmission and infections appear most prevalently in the intestine and its local lymph system. Here the toxic load of the food and water chain come into play with cytokine factors and lymph node effect. The intestinal region is the most affected from cooked food free radicals and the uptake of toxics in the food and water chain. Regions in Africa with the highest fluoride in well water and food have the largest problem with HIV transmission.[101, 102, 103, 104,

105, 106] Many of the high fluoride regions follow the east African Rift Valley zone that is lined with volcano and seismic zones. In many of these areas the persons have frosty white teeth from dental fluorosis and many are disabled by age 40. This is significant because fluoride toxic effects set up cytokine profiles that HIV transmission and growth require with TNFa in the lymph nodes and loss of macrophage / monocyte performance driving Th2 bias in the intestines and body as a whole.[107] The TNFa cytokine promotes the viral proliferation of HIV.[108] The rise of fluorides in the body is the principle trigger for HIV infections due to the fluoride in the bone mass upsetting the beneficial trace metal concentrations for cellular enzymes. HIV affects the 2-5A RNase L enzyme pathway in cells, so the fatigue associated with CFS is altered when HIV enters the equation. Fluoride in the bone mass robs the immune cells that form there of the essential metal manganese that is needed to block reverse transcripion of HIV in cells.[109] This effect sets up the high rates of infectivity in the lymph systems immune cells by HIV, with the virus setting up the higher rates of TNFa that promote rapid growth. HIV is highly sequestered in the lymph nodes of the gut region, where the highest exposure due to fluorides and metals affects the lymph nodes and bone mass. The high level of mtDNA damage from metals promotes excessive NO production and damage factors. HIV, as it infects more cells in the body, sets up its own cytokine signatures that become the additional factors on top of the toxic effects that keep it from being regulated. HIV also produces IL-10, which suppresses macrophage action.[110] Impaired monocyte / macrophage function is highly associated to HIV progression and pathology for other viral infection.[111] Rising IL-10 levels that suppress macrophage action directly connect to the loss of CD-4+ T cells.[112] These T-cells are preferentially attacked due to the gp120 bonding site on T-cells that promotes HIV cellular transmission into these cells. The early AZT treatment acted more to destroy cell mitochondria than to oppose HIV replication.[113, 114] HIV always involves activation of other viruses and these can worsen the cytokine activation and AIDS progressions.[115] HHV-7 is often activated in HIV infected persons and the lymph nodes are seen to be the site of reactivation.[116] This leaves little doubt that

the failing lymph node effects play a central role in HIV proliferation. This can also be seen in the case of cancer viruses where the failing lymph node cellular regulation allows cancer metastasis of lymph nodes and helps to spread the cancer viral infection. The same effect also spreads HIV and other viruses, rather than regulate and destroy them. The HAART treatment for HIV lowers the AZT dose and avoids using TNFa mechanisms that promotes HIV transcription and this has almost rendered HIV a chronic survivable disease, with many having near normal lifespan with non-detectable HIV in their blood. The principle problem with HIV and the immune system is that TNFa triggers it and loss of manganese sustains its replication. The key factor is macrophage and monocyte enzyme performance for regulation of HIV, with the exposure to fluorides dominating this performance in many countries. The dominate effects of the fluorine atom's affinity toward metals in the body is easily established via the fluorine deposition rates in the bone mass and other calcium rich tissues. Fluoride absorbs into the calcium phosphate or hydroxyapatite of the bone mass, as well as the hydroxyapatite in the pineal gland, where the serotonin / melatonin hormone process is antagonistically affected. Fluorides rise in the bone mass contributes to the depletion of selenium needed for making the enzyme Se-glutathione and the copper and zinc needed to produce Cu-Zn superoxide dismutases or SOD. [117, 118, 119] Fluoride antagonism toward selenium also upsets the thyroid autoimmune hormone process. [120, 121] The depletion of these enzymes contributes toward the retention of toxic metals (Hg, Cd, Al) from acid rain effects on soil and food chain uptake. The retention of these toxic metals damages the cellular mtDNA and ATP production levels of cells due to the mutated enzyme RNase L. Fluoride's affinity toward beneficial trace metals damages literally 100s of enzyme processes that lead eventually toward poor health, illness, and death. GSH or Se-glutathione supplies a sulfur atom for toxic metals to bind that renders to them the same solubility factors as were dominate when the Earth's metals were formed from volcanic dominated sulfur releases. The effects of HCl dominated Acid Rain are upsetting the soils metals speciation and increasing the levels of metals availability from the change from the sulfur domination.

This results in damage to the Cu-Zn SOD as metallic elements like manganese compete against the copper-zinc. The combination of rising fluoride and acid rain set up loss of GSH and change of metals speciation for the SOD that sets up the problems leading to prion and mad cow problems. Chemicals like DMSO that supply sulfur atoms to bind metals deep into tissues and the brain have been shown to reverse the manganese amyloid plaques associated with prion diseases. The UV and Ozone Hole problem has severely upset the global sulfur cycle upon which the Se-GSH system depends for adequate sulfur. The ocean plankton levels have been reduced which causes an increase in the global CO-2 levels and a loss of DMS that is formed from the process that regulates cloud formation. The loss of cloud seeding by the DMS causes the bulk of the global warming problem via loss of reflective clouds for the IR radiation reflection. Plankton are the world's largest CO-2 sink and the largest system that places sulfur into the human and animal food chain. When the DMS is impacted by UV radiation, it lowers the DMS, DMSO, and MSM pathway into the human chain to supply the levels of sulfur needed by GSH in the liver and cells to remove toxic metals from the body. This systemic loss of sulfur stores causes a metabolic acidosis and hyperthyroid shift in the population that results in CFS and many other immune illnesses. Mad Cow or BSE is characterized by plaques with high levels of manganese. The mitichondria when under toxic stress makes MnSOD, that is the reason for these plaques and tangles in the brain. The high levels of toxic metals in the brain due to loss of GSH stimulates the increased Mn-SOD variant. The mitochondrial processes taking up all the cellular manganese depletes that needed to make the enzymes to protect the cell from internal viral activation. Viral protective enzymes like 2-5A RNase L require manganese to do their job as does interferon that protects cells from viral infection. The fluoride damage to the enzyme processes like Se-glutathione (GSH) and others like it set up factors that result in retention of the toxic metals such as mercury, cadmium, lead, nickel, and others. [122] This results in the appearance of persons with high fluorine effects having heavy metal poisoning. The fluoride effect driving the retention of metals like mercury add dramatically toward the

nervous system damage and loss of T-cells. The loss of GSH and other clearing enzymes results in a see-saw like effect where the beneficial trace elements such as selenium, zinc, magnesium, and copper are depleted and the harmful metals like mercury, lead, cadmium are increased. [123, 124, 125] Such observations often lead to chelation type therapy, which needs to be done carefully with reintroduction of beneficial mineral cocktails and keeping GSH levels preserved or increasing. This type effect is readily seen in the DOE K-25 gas diffusion plant workers exposed to HF associated with Oak Ridge, Tennessee. Hydrogen Fluoride (and other fluoride compounds) taken into the body will spontaneously form aluminum compounds that are similar to the pesticide called cryolite. Cryolite insecticide works by upsetting the trace metals metabolism within cells. Every man, woman, and child on this planet is being affected by this chemical insecticide forming inside the bodies and damaging their metals metabolism and in the long term. It is a dominant effect that results in death by a process like the novel called "Arsenic and Old Lace." Placing a safer metal into the blood circulation by adding titanium dioxide to the food chain is being used to offset this formation of the Al-F compound effect on human and animal health. The reduction of GSH for removing toxic metals via the bile pathway shifts toxic metals into the kidneys and slows the clearance of all toxic metals due to the pH effects on clearance of metals by kidney cells, which promotes blood pH shifts toward metabolic acidosis. Kidney damage and heart damage go hand in hand because of this relationship with build up of toxic metals within the body due to loss of GSH levels. Heart disease and kidney disease always go hand in hand, as high blood pressure from arterial disease causes renal failure. The cholesterol build up on arteries is directly associated with toxic metals / fluorides adhering to the arterial walls and the cholesterol repair mechanism attempting to repair the problems. These are processes that are the normal outcome of old age, but the onset of these old age factors is a direct function of the GSH impairment from both natural and industrial exposures. Cancers and the neurological outcomes are the outcome of the same process of loss of GSH and SOD with age due to environmental accumulation.

Heart disease yields an interesting association with salt, because doctors recommend to stop to control blood pressure. The problem with table salt is that it has aluminum silicate added to keep it flowing. The blood has a high concentration of salt on the order of seawater concentration, so dietary salt is not going to be what causes the high blood pressure reaction. Aluminum will combine with fluoride in the blood making the AlFx compound that lowers GSH and provokes the build up of metals in heart cell mitochondria and high rates of ROS production. The administration of nitro-glycerin for heart pain promotes the production of SOD in the heart cells and the neutralization of the ROS within the cells. A very similar effect happens in the brain with metals accumulation that causes increased ROS and the metal lithium being used to trigger increased SOD to counter mental disorders. Ending the use of salt with aluminum hydroxide acts to lower the kidney stress factors from toxic metals accumulation and lowers blood pressure. This effect is very telling of the sensitivity of the body to aluminum / fluoride affecting GSH levels. The aluminum in salt and aluminum in baking power observations began to break the secrets of CFS in the 1980s at ORNL. CFS and GWI symptoms like "night sweats" are easily explained once one finds that the AlFx G-protein effect mimics the TSH hormone generated by the pituitary gland. When the AlFx levels formed from the foods a person consumed during the day exceed the levels of TSH hormone from the pituitary then the cells can't power down at night from the dynamic control of the mitochondria by the pituitary TSH and thyroid process. Likewise, other symptoms like inability to sleep or get rested sleep could be explained. What they were experiencing was the effect of hyperthyroidism, which involves extreme tiredness, inability to sleep, and loss of GSH. It is this running full power 24 hours a day that exhausts the supply of GSH in cells. The body intentionally powers down at night to replenish GSH and do cell repair processes and this cannot happen when TSH mimic compounds like AlFx take control over thyroid hormone levels. The characteristics of the AlFx compound in the mimic of TSH is a very destructive method, as the fluorine component of the compound causes a bond that does not clear as does the normal

TSH. The highly electronegative effects of fluorine causes the AlFx to bond long term to receptor sites of cells. This process highly upsets the normal pulse and amplitude processes of the pituitary control via TSH on the thyroid hormone generation. The characteristics of the AlFx compounds to form almost permanent bonds to the receptor sites for TSH highly damages the cellular repair processes and GSH levels within cells. The heart of the problems with the AlFx compound is that it doesn't follow day and night variation of normal TSH and the fluorine component of AlFx forms a nearly permanent bond to TSH receptor sites, which causes severe thyroid hormone regulation problems. This is why the AlFx compounds play a dominant role in cellular GSH depletion throughout the body and human health. One of the problems in detection and diagnosis of this effect is that doctors will only run simple TSH tests for thyroid function, which will often show up as low when the AlFx compounds are driving the over production of thyroid hormones. When the doctor sees a low TSH he declares the person as having hypothyroidism, when just the direct opposite is the case. The doctors need to run the "Total Thyroid Panel" type test to get a better idea of what is happening with T-3 and T-4 and see if things like AlFx and other thyroid affecting chemicals are causing problems. This is part and parcel for how the AMA doctors avoid exposing the industry that poison people via this process. The American population has been poisoning itself with this low level of aluminum and fluoride in the food chain. The incidence of common colds, flu, and fever are strongly correlated with high much flour and salt with aluminum content enters their diets. The duration of colds, flu, and fever was correlated with diet and the time of clearance of these materials from the gut. This effect was similar to the night sweat effects seen in CFS and GWS, which stemmed from the highly abnormal thyroid hormone mimic effect of AlFx compounds. It was found that fever and sudden recovery would trace the elimination of these food materials from the gut. It was also found that persons that consumed too much aluminum in flour and salt exhibited higher rates of heart problems. They exhibited early brown spots on their skin similar to liver spots that warn of liver damage, and they had degenerative mental problems that resembled ADD and dyslexia. It became clear there were ways

to avoid colds and flu, and that Americans have been poisoning themselves chronically from the rising Al and F effect in their food chain. Environmental legislation has slowed some of the toxic effects from the chemicals that damage GSH and SOD enzyme levels. The Government has not been clear as to why DDT, PCB, Dioxin, and varied chemicals have been banned, but the major reason has been to slow down the toxins that damage GSH and SOD enzymes. It is a case of not enough or soon enough, as the problems continue to mount. Eating fish has been suggested to be limited to once a week over the same problems with mercury. The current trend is that industry is being protected, while the citizens have been increasing affected. The systemic health problems due to these many chemicals and damage GSH and SOD enzymes show up clearly in areas like Oak Ridge and the HF toxic releases and Al vaccine problems from the Gulf War. The analysis of the trace metals factors leads again to the metals speciation shifts due to fluorine's presence in the body and bone marrow. Here the issues of the Old World belief in the trace metal copper being linked to eternal life come into play. Copper is grouped with silver and gold in the valence column of the Periodic Table. Examination of the elemental gold reveals that in its Gold +0 metallic state that it very non-reactive with most ions, with exceptions being mercury via the amalgam effect and fluorine due to the high electronegative effect. Gold colloid particles would become a sort of "teflon bullet" and be able to migrate past brain and cellular membranes and become effective in the removal of mercury from the tissues and brain, as well as aid in the removal of fluorine itself. This concept stems from ancient alchemical texts and the science arts from Egypt and plays a strong role in early religious beliefs and practices leading toward higher brain functioning and longevity. Similar concepts called "acupuncture" for pain therapy using metallic needles of copper, silver, and gold inserted into tissues are associated with the same fluorine and mercury removal concept. These concepts are applicable toward treatment for CFS and other fluorine induced illnesses. It is these factors that set the stage for the appearance of CFS in volcanic zones like the Lake Tahoe region, as found by Cheney. The loss of ATP, the depletion of GSH, and the appearance of

multiple endogenous viruses in the body are the direct result of the synergistic effects of rising fluorides on the beneficial trace metals needed for the proper functioning of the human immune system. Fluorides in the body cause the loss of the beneficial trace metals required for proper enzyme protection of cells, and the rise of the toxic metals that damage mtDNA and ATP production. The effects set up increased rates of cellular damage from NO and other oxidation effects (ROS). The net result is called Chronic Fatigue Syndrome. The mechanism is common too not only CFS, but to HIV infectivity and the process leading to cancers. Fluoride causes acidosis of the body and with this comes even greater loss of ability to clear toxic metals by the kidneys and the high levels of metals damage that set up cancer by loss of immune system regulation. This analysis process leads to a new more inclusive model for total oxidative stress for cells that involves radiation induced oxidative stress directly, chemicals that alter thyroid hormones and lower GSH and SOD, and exposures to toxic metals that set up high rates of mitochondria malfunction and production of ROS. The total oxidative stress model for cells predicts that the AlFx and mercury interaction as thyroid hormones and the GSH and SOD depletion with age dominated pre-industry health effects. The postindustrial effects must include the PCBs, DDT, Dioxin, Hg, and others that similarly alter thyroid response and reduce the GSH and SOD protective enzymes. When the "Total Oxidative Stress Model" is used, which includes the loss of GSH and SOD and its clearance mechanism for toxic metals in the body, then the biological sciences correctly models the cellular protective enzyme health mechanism. This process then accurately models the failure mechanisms for CFS, Cancer, AIDS, MS, BSE / mad cow, Scrapie, Alzheimer's, Kidney / Heart Disease, and etc. In Conclusion, immune system diseases are caused by poor environmental, industrial, and agricultural practices bringing toxic material into contact with the air, food and water chain leading to animals and humans. The principle toxic offenders are fluorides (HF) and its halogen family relatives, closely followed by toxic metals (Hg), and chemicals (dioxin, PCB, DDT) that impact GSH and SOD. The leading damage vector is via GSH and SOD enzymes leading to toxic metals damage to the cell mitochondria of lymph

node macrophage cells of the Th1 driven cellular defense immune system. The failing of the Mn dependent RNase L enzyme leaves cells infected with the pathogens seen in chemical plant workers, CFS, GWS, MCS, and HIV. The critical or processional pivotal event leading to this is the accumulation of toxic products in the lymph nodes and fluoride in the bone mass that robs the immune cells of essential DNA and mtDNA repair enzymes. This effect produces the net aging effect of the body, as it sets the net cellular degradation from unregulated pathogens. The effect is largely being driven by the loss of the Global Sulfur Cycle and the DMS, DMSO, and MSM availability to the food chain leading to not only a rise in CFS, but all immune illnesses globally.

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Author:

The author formed and directs the Magnum-Opus Project to correct and expose the wrongs the Manhattan Project and the abuses of openness in national security. He is former Senior Development Staff of Oak Ridge National Laboratory and has direct experience with some of the most toxic materials from the nuclear industry. He worked on toxic site remediation, radiation detection, invented the USRADS survey system, and won ORNL significant event award. He discovered high levels of hydrogen fluoride emissions from the gas diffusion plants and noticed the link to CFS like illnesses in the worker and local community populations. He defined the basic mechanism for cancer, CFS, and HIV in national security circles in the 1980's. He claims his inspiration for the discovery came from the icon imagery of volcanism connected to the story of the Ark and the environmental imagery associated with Mary controlling the poisons from the Earth entering the food chain. The ultimate of the inspiration came from the understanding of the Global Sulfur Cycle and how this associated to the story of a volcanic mountain near an oil field of Midian, Saudi Arabia and how this process formed DMS. Author says enzyme, bone, and lymph immune system mechanism information was suppressed for more than two decades by industry control of research, negligence on the part of CDC,

ATSDR, and EPA, and criminal cover up on the part of the DOE. He purposely chose public publication of his work to express the need for preventive and alternative medicine to take a more balanced stance against AMA and pharmaceutical based dominance and excessive profiteering in medicine.

RETROSPECTIVE: The process of discovery of the principle failure system in Human Health. The aftermath for the Manhattan Project is the fitting setting for the discovery of the principle failure mechanism leading to cancer, CFS, immune illnesses, and AIDS. The Manhattan Project discovered early on the acute effects of radiation due to ROS forming in the marrow death, intestinal death, and nervous system death effects. The studies in Oak Ridge also found that sub-lethal radiation exposures lead to the need for antibiotics to protect the person from the immune system loosing its ability to protect against viruses, mycoplasma, and other infections. The 1980s brought on the problems of AIDS and HIV nearly simultaneously, and the research in this period identified the loss of glutatione (GSH) and superoxide dimutase (SOD) enzymes connected with CFS. The glutathione metals clearance mechanism also pinned down that toxic metals upset the cell mitochondria processes leading to high rates of ROS from the mitochondria ATP production. CFS would involve endogenous DNA viruses, HIV exogenous retrovirus from monkeys, and cancer the radiation mutation of activated endogenous viruses. The entire process for CFS, AIDS, and cancer was uniquely defined by three simple enzymes: Se-GSH, Mn-SOD, and Mn dependent 2-5A RNase L. In the 1980s, Jim Phelps was the first at Oak Ridge to correctly flag all the problems of the Ozone Hole or the UV problem in upsetting both the Global Warming factors and the Global Sulfur Cycle of the planet. The largest CO-2 sink on the planet is the ocean's plankton and the UV was impairing and killing the plankton's CO-2

conversion process. The plankton process is also part of the global Sulfur Cycle that supplies DMS into the atmosphere that places DMSO and MSM into the human and animal food chain. These place sulfur into the food, which is in turn used to make the Se-GSH to clean the body of toxic metals. DMS also supports cloud seeding that acts as a sunscreen for heat from the sun and regulates the Earth's temperature. The loss of DMS levels directly drives global warming and the loss of immunity in humans and animals. The higher levels of retained metals in the body due to loss of the hepatic phase II elimination of toxic metals sets up a slow shift toward hyperthyroidism like problems due to the AlFx effects and this process sets up a metabolic acidosis that slows the kidney clearance of aluminum and other metals. The rise of the toxic metals within cells causes mitochondria ROS generation to rise and greater demand on Mn-SOD to compensate, and upsets of the Mn dependent 2-5A RNase L generation. With the discovery of the function of the 2-5A RNase L enzyme in controlling the internal cell viral infections the association of the metals induced ROS and the radiation induced ROS paths crossing paths became highly evident. The discovery that these three enzymes dominated the failings of the immune system from either radiation or toxic metals was fully discovered in the mid1980s at Oak Ridge National Laboratory by Jim Phelps. Jim Phelps' discovery of this principle mechanism for illnesses began when his father became sick while working as a uranium machinist at the Y-12 plant and was highly exposed to PCBs used as a uranium cutting tool coolant. This lead to gall bladder problems, which are directly connected with PCB exposures. The Y-12 managers moved Jim Phelps father from the dirty PCB uranium cutting operations to the cleaner Y-12 9201-1 buildings operation. Jim Phelps' Division at ORNL designed the TSCA incinerator for the K-25 plant in the 1980s and he discovered the issues behind the need to ban PCBs and Dioxin were due to cumulative damage effects to the enzymes GSH and SOD, which eventually leads to free radical damage to the RNase L enzyme's effectiveness and viral infection problems within cells. Jim Phelps' dad came down

with Parkinson's and had to take early retirement from Y-12, and the mechanism of glutathione was the main clearance mechanism for toxic metals and chemicals from the brain. Jim Phelps quickly spotted this as associated with his father's progressive illness pattern from his occupation exposures at Y-12. Jim Phelps' dad also worked on the K-25 improvement program which exposed him to aluminum parts run in a fluoride chemical process, which made an extremely dangerous AlF3 coat on these parts. This exposed his father to one of the most dangerous of the Oak Ridge toxic insecticide effects that mimic the TSH pituitary hormone and upsets the GSH and SOD levels in cells. His dad had multiple toxic insults [PCBs, then AlFx] to the same enzyme systems that protect the body and brain from toxic injury. This was the process that cracked the issue that Harold Hodge spotted in 1944 about the F factor causing health problems in those exposed to UF-6. The AlFx problems were now exposed, and the process via which they caused illnesses in the work force. With that mechanism defined, it was a short time before the problems of hydrogen fluoride (HF) and other toxins were identified as upsetting the GSH and SOD levels. HF effects were quickly connected to the high rates of thyroid illness seen in the work force due to accumulation of mercury in the thyroid gland leading to thyroid cancer like problems normally associated with radiation damage. These were the natural order of events that lead to the major discovery for the causes of cancers, CFS, immune disorders, and even AIDS in the mid-1980s at the Oak Ridge National Laboratory by Jim Phelps. Jim Phelps was the first to connect that HF emissions from the Oak Ridge plants impacted GSH and SOD, and that this effect was becoming worse on a national scale from coal plant emissions of HF. The effect was leading to problems of "Mad Cow" and "BSE" in even grazing animals. Jim Phelps proposed the mediation factor by spraying titanium dioxide from planes to offset the problem in grazing animals. This idea became the start of the so called "Chemtrails" activities and top secret compartmented research at LANL on the rising

problem in animals. Jim Phelps also discovered an atmospheric injection vector involving HF and H2SO4 in combination with hydrocarbons in the air that dominated the global warming effects. Jim Phelps discovery that all of medicine comes down to damage factors from environment and industry to these three principle enzymes proved highly embarrassing to the Govt., Industry, and AMA; to the point that the AMA styled medicine could be forced out of business and charged with malpractice on a national scale. This began the massive cover up for this discovery that could well change the world, if it became public knowledge. Jim Phelps' discovery not only showed that the common cold could be made extinct, but that man could be made to have the Biblical longevity of Genesis. His discovery even impacted the interpretations for religion and exposed massive problems there. The discovery of the toxic metals mechanism has strong links to religion, as the Egyptians were into metals mining. They were the first to use copper for water pipes, while the Romans used lead pipes and poisoned themselves into self-destruction. Also in these times, Joseph of Aramea held tin mines in the UK, and the socalled "white lead" made a highly safe metal for use in cookware and food storage. "Tin lined" copper cookware (Gérard Leclerc, etc.) is still in use today and is some of the finest and most expensive of French cookware. In these old world cultures the use of mercury, which is the worst of the worst of toxic metals, in the mining for gold via an amalgamation process made Kings and Rulers rich. It was not in the interest of the powers of those times to expose that mercury made these gold miners sick, so that information was suppressed. Vatican and Jewish religious interpretations of issues like eternal life were suppressed in those times as they played the game that kept them and their rulers in gold. The US plays the same games today in the cover ups on health connected with processing aluminum, a strategic metal. Aluminum uses fluoride to process it to metal and the AlFx health effect on GSH and SOD appears there strongly. Similarly the strategic metal Uranium production for bombs uses lots of Fluorine and coal power that released mercury and HF. This too causes serious AlFx health problems. And the list goes on into the cover-ups on PCBs,

Dioxin, DDT, and all the other chemicals that suppress the GSH and SOD enzymes needed for health and longevity. The knowledge of the GSH, SOD, and Mn based viral protection enzymes is literally the issue of how to attain very long longevity by avoidance of toxic metals and chemicals. This is the theme of the eternal life part of religion and elements from the story of Genesis. Moses was educated in Egypt by what some term the Egyptian School of Mysteries or what might better be termed the school of the natural orders of the world. They knew well the power of metals to heal and to make ill. There was one special metal that had the ultimate power to heal and produce clarity of mind, expanded cognitive powers, the realm of divine thought. Gold Colloids were part of the story of Moses and the Manna. Later, Jesus and Joseph lived in Egypt and were exposed to these same teachings. Jesus was termed a magician and had unusual powers to heal people. In those times the knowledge of natural processes and the health problems linked to fluoride and toxic metals effects would be the ultimate in health knowledge. This knowledge is still the ultimate in health conservation today. It is this knowledge that appears connected to the graduated learning needed to attain that associated with the Holy Grail. The Masons Organization (Scottish Rite Temple) still practice part of this ancient Egyptian School of Mysteries type teachings in their progressing up their orders. They seek to imitate the knowledge and attainments from Old Egypt that lead to Jesus' divine level of knowledge. So, one can now see that the information of how health is affected by toxic metals can play a strong role in the interpretations and misinterpretations of the church on the true story of what Jesus was about. Jesus was also said to be an Essene and this faction also practices a version of the divine knowledge keeping from the Egyptian Mystery School knowledge base. It is for this association that many of these illnesses connected with this failure mechanism are called "mystery illnesses;" CFS, GWS, Gas Diffusion Worker Illness, Cancer, ALS, etc. The illnesses represent no mystery, as the mechanism for them is well known.

To acknowledge the mechanism for these illnesses is to open up Pandora's Box and to expose the very serious problems in religion, both in Judaism and Catholicism, as well as the problems of modern medicine that make their entire profits from this health failure mechanism. One of the most prized metals in Egypt was copper and was associated with eternal life and the symbolism of the Ankh (The first religious Cross). Later, gold took over as the leading metal for health, as its colloid form could remove fluoride and mercury from the body and brain. The ultimate powers of the Ark of Moses were closely associated with this metal's healing power and how to make it. Thus, one can see why the corrupted power of religion and government in the US attempt to keep these associations a mystery for the public at large. Keeping the mechanism a mystery allows industry to pollute and harm health of large populations, while others make money from treatment of the illnesses induced. Doing such is a crime against humanity and racketeering beyond the wildest imagination. Those associated with such deception are assigned the definition of anti-Christ. It is these three enzymes that form a sort of Holy Trinity for man's existence on this planet, and the inner sanctum for why Jesus was so special in the realm of religion. With the knowledge of the Final Diagnosis report in hand, the real issues of religion come into view. It is part of the story of Jesus' Revelations. The bottom line is that places like Oak Ridge released hydrogen fluoride, which combines with aluminum in the body to form a toxic compound like the insect poison called cryolite, sodium aluminum fluoride. Cryolite's pesticide mechanism works by upsetting the trace metals metabolisms within cells, and this is exactly the problem seen in Oak Ridge and elsewhere with the mysterious illnesses and diseases. It affects every man, woman, and child on this planet and is directly connected with killing them in the long term. This same effect is the trigger mechanism for Gulf War Syndrome, and all that and much more could have been averted if Oak Ridge

was not a criminal entity seeking to cover ups its many mistakes and toll on human life.

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The interface between science and society: water fluoridation as a case study, Bundaberg 1952-57†
HF Akers and SAT Porter*
Between 1945 and 1954, the concept of adjusting the fluoride content in reticulated water supplies (henceforth referred to as water fluoridation) for the partial prevention of dental caries was in its infancy. While Australia’s peak scientific body, the National Health and Medical Research Council (NHMRC) had conditionally endorsed this public health measure in December 1953, two factors hampered prospects for its implementation in Queensland.1 First was a political legacy arising from the widely publicised impact of naturally over-fluoridated water on sheep in the western parts of the State. This caused public confusion and concern when the biological impact of the continual ingestion of naturally over-fluoridated water on sheep was extrapolated to the fluoridation of community water

Bundaberg ca 1951. (Picture Queensland Collection, State Library of Queensland)
†This article has been peer reviewed. *Mr Harry F Akers is a PhD student at The University of Queensland’s School of Dentistry, Turbot St, Brisbane. Dr Suzette AT Porter is the Director of Clinical Placements and the Coordinator of Community Dentistry at The University of Queensland’s School of Dentistry, Turbot St, Brisbane.

2

Figure 1 Professor SF Lumb to Director General, 2 March 1954. (Reproduced courtesy of The University of Queensland School of Dentistry)

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supplies. While Queensland’s agrarian bureaucracy had perceived natural artesian fluoride as a post-1945 threat to the pastoral industry, major veterinary issues had been largely resolved by 1953.3 The second factor was a legitimate scientific hesitancy due to contemporaneous concerns about human fluid homeostasis (compensation mechanism). Queensland’s tropical and subtropical climates meant fluid intakes were likely to be higher than those of the more temperate climates in the southern States. In November 1954, the NHMRC addressed this issue with implementation protocols that modified bioavailable (active) fluoride concentrations to allow for potentially higher fluid intake in parts of Queensland.4 In this era, the ravages of the caries epidemic were obvious and often traumatic for patients and dentists. The Dean of the Faculty of the Department of Dentistry at The University of Queensland, Professor SF Lumb was naturally interested in water fluoridation (Figure 1). In 1953, Lumb commissioned a young, credentialled, post-graduate research student, Dr Brian Kruger to investigate suitable locations.5 Kruger was Ipswich ‘born and bred’, a Rotary Foundation Fellow who had returned from US study commitments. Kruger was well acquainted with the North American water fluoridation field
2

Professor SF Lumb, Professor of Dentistry & Dean of the Dental Faculty, 1938-1963 (Picture Queensland Collection, State Library of Queensland)

Alan Simmonds, Engineer, Department of Local Government , Queensland’s first strong fluoride advocate. (Reproduced courtesy of John Bristow)

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trials and considered a range of provincial municipalities from their scientific and political perspectives. In consultation with the Department of Local Government, Bundaberg was recommended as one of Queensland’s few locations that satisfied the relevant criteria for a Queensland trial.6 The climate was appropriate in that it was within the extended ranges of the NHMRC’s revised guidelines on climate and fluid intake. The Bundaberg City Council’s engineer, C Brewer, was qualified to supervise the appropriate engineering infrastructure. Moreover, fluoridation equipment could be easily installed at the partly constructed South Bundaberg treatment plant.7 Engineering personnel and infrastructure were often understated but critical factors in water fluoridation proposals.8 Furthermore, the Bundaberg dentists, led by J Wainwright, had expressed strong support and would publicly support the proposal. Other important factors were that the Burnett River divides Bundaberg into two communities with separate sub-artesian water supplies of similar mineral composition. South Bundaberg water could have adjusted fluoride concentrations to achieve the test population while North Bundaberg water remained sub-optimally and naturally fluoridated as the control.9 Another advantage in selecting Bundaberg was the potential for the dental research team to maintain cross-disciplinary scientific collaboration with the Department of Physiology at The University of Queensland

Bundaberg Mayor Fred Buss hosts a public reception for Queen Elizabeth and Prince Philip at the Bundaberg Showgrounds on 11 March 1954. His daughter Bettina welcomes the Queen. (Picture Queensland Collection, State Library of Queensland)

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(in an adjacent building on the St Lucia campus). In 1953, Professor WV MacFarlane, from the Department of Physiology was researching human fluid homeostasis within tropical climates and was a colleague of Kruger. MacFarlane was an appointee on the NHMRC sub-committee that investigated climate and protocols for water fluoridation. Bundaberg cane cutters had a high daily fluid intake due to their long hours of manual labour and exposure to heat from cane fires. Bundaberg’s flat terrain predisposed cane cutters to riding bicycles to and from the cane fields, which further accentuated dehydration. For these reasons, cane cutters, especially Bundaberg’s cane cutters, held a special place in MacFarlane’s research.10 Moreover, in the course of his work, MacFarlane had established a favourable rapport with the powerful Australian Workers’ Union and its Bundaberg secretary, E Barnes, who was supportive of water fluoridation.11 Although the Bundaberg recommendation was primarily based on scientific criteria, political stability was also a consideration. The City Council was stable and its Mayor, Alderman FH Buss (Mayor 1936-58, excluding three years war service) held a secure tenure on the mayoralty. The research team had been informed that Buss was interested in fluoridation. It would also be important to the success of the project to have the support of the major local industry (or at least not have opposition from it). Bundaberg was a “sugar city” and the history of the sugar industry’s attitude towards water fluoridation indicated it would satisfy these requirements and support water fluoridation.12 The 1949-53 era was one of escalating tension between the sugar industry and the dental profession. Dentists’ attempts to restrict dietary sugars as a preventive strategy to reduce dental caries alienated sections of the sugar industry. This antipathy from sections of the sugar industry was particularly strong in Queensland, Australia’s leading sugar producer.13 Tension peaked in 1953 at the Australian Dental Association’s Congress (an international meeting for dentists held that year in Brisbane) with a widely publicised American dental expert’s claim of an association between sugar consumption and caries rates.14 R Muir, General Secretary of the Queensland Sugar Growers’ Council, retaliated with sharp criticism of the dental profession’s management of preventive strategies and its attitude to sugar consumption.15 The Colonial Sugar Refinery Company also responded that ‘fluoridation and general all-round diet’ were better preventive strategies than ‘the elimination of carbohydrates from the diet’.16 Furthermore, former Queensland premier, W Forgan Smith, was the Chairman of the Queensland Sugar Cane Prices Board, and had formally expressed positive sugar industry interest in water

6

Figure 2 Professor SF Lumb to Alderman FH Buss, Mayor of Bundaberg, 12 October 1954. (Reproduced courtesy of The University of Queensland School of Dentistry)

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fluoridation. Though not stated, Lumb and Kruger would have been aware that the sugar industry would either support, or at worst not oppose, the Bundaberg proposal. Hence this proposal to fluoridate Bundaberg’s water supply was carefully planned and historically significant. Under Kruger’s cautious guidance, Bundaberg could have been not only an Australian mainland pilot for water fluoridation research but also an internationally acclaimed field trial like that of Grand Rapids (Michigan, USA).
17

Lumb’s Proposal
In October 1954 Lumb wrote to Buss with a proposal to undertake pilot research into water fluoridation and sought an expression of interest from Bundaberg in participating (Figure 2).18 Lumb forwarded enclosures on American data, costing, engineering assessment and NHMRC protocols to support the proposal. Lumb also stressed the importance of such a pilot, the dental benefits, the need for strict control, Kruger’s availability and the resolution of the NHMRC’s concerns about fluid homeostasis in a climate like Bundaberg’s. In his letter, Lumb indicated that the City Council had to desire water fluoridation. Several aspects of Lumb’s proposal are important in analysing and understanding Bundaberg’s reaction. Lumb disclosed that there had been a discussion with Wainwright leading Lumb to believe that Buss was ‘well acquainted with the literature on fluoridation’ and had ’expressed interest in it as a public health measure.’ The background surrounding this advice is unclear. However, subsequent events revealed that Wainwright, and hence Lumb, misjudged both Buss’s and Bundaberg’s interest in water fluoridation. Secondly, although Lumb and Kruger were commissioned to select a suitable location, Dr A Fryberg, Director General of Health and Medical Services within the Department of Health and Home Affairs (hereafter referred to as the Department of Health), made the final authorisation. Fryberg stressed that financial assistance would be available ‘if the Bundaberg City Council indicated in writing their desire to fluoridate.’19 However, the Department of Health saw its role as advisory and did not engage either the City Council or the community in any form of public debate. Whilst the Bundaberg proposal had administrative and scientific endorsement, this support was provisional because section (vi) part (b) of the 1953 NHMRC protocols stated that: ‘A large proportion of the community should desire that fluorine be added to the water supply, or alternatively, a substantial proportion of the community does not oppose the addition of fluorine to the water.’20 The terms ‘desire’ and ‘oppose’ were not defined and could have implied a range of options from autonomous Council decision to an opinion poll or to a full or partial referendum. In this epoch, the dental profession believed that the emotional, biological

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and financial burden of the caries epidemic would outweigh opposition to this community health measure. However, all parties forwarding the proposal agreed that Bundaberg had to express its interest in water fluoridation before the project could continue. Lumb had provided Buss with the NHMRC protocol and, for reasons that are not clear, Buss quickly announced that a referendum was required in Bundaberg. Another confounding variable emerged when the proposal and the correspondence between Lumb and Buss became public and the subject of media reports.21 Whether Lumb envisaged that the preliminary discussions would be confidential is conjectural, but if Buss had quietly rejected the proposal, it is possible that the research plan may have been quietly withdrawn and submitted to another local authority. However, between Lumb’s proposal of 12 October 1954 and the full City Council meeting of 28 October, there were media releases based on statements by Buss and Wainwright. Both interpreted the approach as a firm proposal for water fluoridation.22 The Bundaberg News-Mail published three articles on water fluoridation in this period. Lumb’s approach elicited an official response in the Council minutes of ‘interest … but would like more details’.23 How that message was conveyed to Lumb involves some conjecture, but anecdotal evidence suggests that media statements and hearsay preceded official communication. The net effect of the publicity was that the researchers were locked into the Bundaberg proposal without the guarantee of final Council approval.

The public reaction
The Bundaberg City Council was an open body, the proposal attracted public interest and councillors’ reservations were published in the Bundaberg News-Mail on the following day of the full Council meeting.24 Buss publicly endorsed a referendum by saying there would be no water fluoridation without one. In essence, the Council neither rejected fluoridation nor endorsed it. The reasons were many: conflicting expert evidence about fluoridation; fear of an experiment; Bundaberg was a ‘guinea pig’; costing; insufficient data; confusion and lack of confidence.25 The Bundaberg News-Mail published more local anti-fluoride views and it was inevitable that community reaction to water fluoridation became an integral part of the campaign for the municipal elections scheduled for April 1955.26 The Bundaberg Ratepayers’ Association capitalised on the timing of the announcement of the proposal and pushed water fluoridation onto the electoral agenda. The Ratepayers’ Association not only opposed water fluoridation but also a referendum, which it perceived as ‘a waste of money’.27 Accordingly, it endorsed two members opposed to fluoridation, J Eriksen and N Spence, as candidates for the imminent elections.

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The “Bundaberg Tragedy” of 1928 – a communal legacy
Although careful planning had gone into the Bundaberg proposal, one local factor had been given scant attention. Significant sections of the Bundaberg community had developed a suspicion of scientific and medical assurances following a vaccination tragedy in 1928. Twelve children died following the vaccination of twenty-one children with a staphylococcalcontaminated multi-dose bottle of diphtheria toxin-antitoxin inoculant. This tragedy and subsequent evidence from the Royal Commission deeply permeated the city’s psyche and divided the community over the need for inoculation.28 In 1992, T Healy, (city council employee 1945-1993 and Health Inspector 1961-1993) reported ‘the memory of 1928 lingered’.29 The Bundaberg-born B Courtice (ALP MHR Hinkler 1987-1993), in commenting on Bundaberg’s fluoridation history endorsed Healy’s view: ‘The 1928 vaccination tragedy had a massive effect on the Bundaberg psyche. It is not obvious now … but previously it was indelible … and it was handed down.’30 This tragedy deeply eroded the perceived veracity of communal health assurances and indirectly reappeared during the Council’s consideration of water fluoridation. These concerns were heightened in October 1954 by an outbreak of poliomyelitis in Bundaberg.31 Polio was an emotive communal health problem with an unknown method of transmission. There was publicity and communal concern over alleged inadequate Council warnings involving large local social gatherings like the ‘Railway Picnic’ and ‘Back to Bundaberg Week’. This concern became political and directed at Buss. The issue was raised at the same Ratepayers’ Association meeting that discussed water fluoridation. In 1954, the parents of the children in the polio scare were the generation directly affected by the vaccination tragedy. Hence this water fluoridation proposal, which some viewed as an experiment, carried unforseen sociological repercussions.

Influence of the 1955 City Council election
Buss partly defused the water fluoridation opposition by restating the need for a referendum. He further distanced himself from fluoride relatedissues with pre-election media statements and assured the electorate that the City Council ‘would move further when it wanted information … and there was no provision in the budget for it [fluoridation]’.32 By midDecember 1954, Buss had conceded ‘that the present City Council had no intention of proceeding with fluoridation’ and, if it was reconsidered, then a referendum would be warranted in spite of the ratepayers’ association policy opposing both water fluoridation and a referendum.33 Over a few weeks, the initial Council response of ‘interest’ had evolved

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into procrastination and thence to an ambiguous refusal.34 This deflected the fluoride focus from the councillors to a media debate between the ratepayers on the one hand and Wainwright and the Australian Dental Association Queensland Branch (hereafter referred to as the ADAQ) on the other.35 Professor Lumb was alienated by the City Council’s failure to personally liaise in detail to the dental faculty initiative; by the politicisation of dental health issues; and by the polarised public reaction and the apparent rejection of a prestigious research proposal in a scientifically desirable locality. Moreover, there were few alternative sites for a similar demonstration in Queensland. In what was a severe blow to the future prospects of promoting water fluoridation in Queensland, Lumb informed the ADAQ that fluoride advocacy was not a Dental Faculty responsibility, but one for the Department of Health or the ADAQ. He played no part in future Queensland proposals.36 Kruger continued by participating in several public functions. However, Queensland’s Social Crediters, some of whom mounted arguments like ‘Fluoridation is Jewish’, targeted Kruger who was not prepared to engage in a political line of debate.37 After 1958 he played no further part in public fluoride politics despite achieving international acclaim for his continuing research into trace elements, including fluoride. In the 1955 municipal elections, Buss was unopposed and all incumbent councillors were returned. Nonetheless, the 1955 return of the status quo did not dampen the enthusiasm of the Bundaberg ADA sub-branch, which was frustrated by the fluoride impasse. The ADAQ Vice-President, Dr FG Christensen, also ‘threw himself into the Bundaberg campaign.’38 Heartened by Christensen’s approach, the Bundaberg ADA Sub-branch members took every opportunity to educate the public at a personal level. As a result, the Bundaberg Junior Chamber of Commerce approached the City Council to reconsider fluoridation.39 The Sub-branch also organised two visits by fluoride advocates. One lecture was given at a public meeting at the Austral Hall in central Bundaberg, at which the motion: ‘that Bundaberg City Council gives such proposals favourable consideration with a view to the fluoridation of the Bundaberg water supply as soon as possible’ was strongly supported (90 for and 10 against).40

Ramifications of the Austral Hall meeting
The public Austral Hall meeting reinstated fluoridation on the public agenda and pressured the City Council to abandon its procrastination. The City Council wrote to the Department of Health and asked questions that had been previously answered by Lumb.41 The Department’s responses reiterated that the City Council had autonomy in any decision regarding the implementation of water fluoridation.42 When departmental advice and

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details of Council minutes were published in the Bundaberg News-Mail it was obvious that water fluoridation did not have Council support.43 Two developments subsequent to the Austral Hall meeting put further pressure on councillors. To begin with, the Ratepayers’ Association continued to reject any fluoridation proposal.44 Furthermore, another civic association, the South Bundaberg Progress Association, called for a referendum on water fluoridation at the next municipal election.45 In July 1956, councillors resolved, ‘That this Council take no action towards fluoridation of the Bundaberg City Water Supply until such time as there is a demand from the people to do so, backed up by a petition signed by at least 3,000 persons eligible to vote at referendum.’46 This resolution absolved the Council’s responsibility by decentralising the decision-making process and placed the initiative on to dentists to support fluoridation. This constraint on future Council response created problems for the ADAQ. It was difficult to promote fluoridation in Bundaberg because of the previously discussed wariness of health assurances. Secondly, antifluoridationists became aware immediately of any petition and had time to organise. Subsequent controversy empowered their cause, created delay and enhanced opposition. Thirdly, the public meeting at Austral Hall triggered the development of a more widespread Queensland anti-fluoride infrastructure and network, as distinct from an isolated local fluoridation opposition in Bundaberg. That evening a leading Queensland antifluoridationist and Social Crediter, J Harding, attended Austral Hall and established the Rockhampton Antifluoridation Group that networked with M Compton, the secretary of the Ratepayers’ Association.47 Queensland’s Social Crediters worked through this Rockhampton group, which would evolve into a dominant force inside the Australian anti-fluoride movement. By 1956, both sides of the fluoridation debate had external advisors as well as local support and the anti-fluoridation group had become stronger and more conspicuous. Bundaberg dentists conducted a domestic campaign and generated favourable, State-wide publicity but could not mobilise sufficient local support. In February 1957, Bundaberg dentists informed the ADAQ that hope of widespread civic support for Bundaberg’s fluoridation was a doubtful proposition, and ADAQ minutes recorded that Bundaberg dentists ‘had reached their limit financially and physically … and were much discouraged.’48 Although the City Council held to the principle of ‘deferral’ not ‘rejection’, opponents of water fluoridation could for all intents and purposes claim success. A number of observations and inferences can be drawn from aspects of the aforementioned experiences and the political responses to them. When viewed in Bundaberg’s socio-political context, a belief that water

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fluoridation was a public health issue and not a political issue was naïve. The activists from both sides of the public debate assumed an adversarial perspective and observers and commentators saw the debate as bipolar. The proposal to use Bundaberg as a pilot study assumed that fluoridation was a legal power vested in a local authority, which allowed the State Government to distance itself from the debate. This assumption was not authoritatively questioned until 1963.49 Moreover, while the Bundaberg proposal was conditional on popular endorsement, no authority established a protocol to define or quantify the NHMRC’s terms of popular ‘desire’ or ‘oppose’. Because the Bundaberg City Council was the first local authority to be offered a realistic prospect of water fluoridation in Queensland, the official response was important. In this sense, the Council’s response was public and political, and established a significant Queensland precedent. In simple terms the City Council won its case against The University of Queensland’s Department of Dentistry, the dental profession and indirectly the State Government. Moreover, Bundaberg’s City Council assumed a pseudo-authoritative status on water fluoridation because other local authorities perceived its response as important. To approach a local authority on water fluoridation immediately prior to a municipal election was poor tactics. Councillors perceived fluoridation as technical, experimental and divisive and were not competent to arbitrate on the scientific merit of this public health measure. Dental health had never been a priority within local authority elections. However, councillors knew their constituents and presumably recognised the paucity of political support from the State Government. The Queensland Treasurer and Member for Bundaberg, E Walsh (ALP) and the Secretary for Health and Home Affairs, W Moore (ALP), were conspicuously silent. Although not obvious within the body of fluoride literature the Bundaberg proposal extended into an era where an entrenched, but divided, state ALP government moved towards the internecine split of 1957. The ensuing coalition years divided political responsibility for water fluoridation between the health (Liberal) and local government (Country Party) portfolios, and this fragmentation permeated Queensland’s fluoride debates for decades.50 Finally, the role and opinion of any local municipal Mayor has subsequently been established as a critical factor within any fluoridation campaign.51 In Bundaberg, Buss was, at best, ambivalent. Elected or bureaucratic advocates (or opponents) to fluoride played a similar role. There was no persistent, public fluoride advocate within the Bundaberg City Council. The converse was true in that some councillors emerged with views opposed to water fluoridation. This evidence suggests that the problems at Bundaberg were political, tactical and sociological. They were not related to the contemporaneous science underwriting water fluoridation.

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This paper integrates a 1952-57 Bundaberg experience into its contemporaneous social context and demonstrates how this interface was projected into the city’s fluoridation politics. The official response to meticulous scientific planning was rejection, framed as a delay to seek information and then to elicit public support. These developments were a significant blow to dental research and damaged prospects for future water fluoridation proposals in Queensland. The methods and outcomes alienated clinicians and researchers within the Faculty of Dentistry at The University of Queensland, demoralised local dentists and demonstrated that political tactics were integral components within community management of fluoride-related controversy. In Bundaberg, water fluoridation passed from a scientific to a political arena. This experience set a Queensland precedent, crystallised formal resistance, generated political concern and exposed problems that still permeate Queensland’s fluoridation debate. The causes were many. Fluoride advocacy was in its infancy and proponents used tactics that ignored the beliefs and attitudes of the Bundaberg community. The Dental Faculty placed too much faith in science over politics. The socio-political circumstances were misread and insufficient attention was paid to the impact of the 1928 vaccination tragedy. However, the contemporaneous NHMRC guidelines, which were reflected in the Department of Health directives, constrained the proponents’ and the City Council’s options. Lumb and Kruger faced additional scientific, geographic and infra-structural restrictions that limited Queensland locations as water fluoridation research sites. The Dental Faculty offered Bundaberg’s municipal leaders an authoritative well-planned pilot scheme and an eminent world-class researcher. However, councillors who were not scientists had to assume responsibility for a scientific decision. They were given discreet administrative support but State parliamentarians failed to publicly endorse water fluoridation. It is not surprising that councillors, who well understood their local community, perceived water fluoridation as a political issue. In response to actions from ratepayer groups, Social Crediters and anti-fluoride groups, councillors forged an innovative referendum policy, requiring 3,000 signatures before a poll would be conducted. This milieu was the partial genesis of an anti-fluoride movement, which in Queensland became self-propagating, institutionalised and still carries consequences for oral health in this state.

Endnotes
1 The authors acknowledge the co-operation of the Bundaberg City Council and Enid Cullen. Commonwealth Department of Health, Fluoridation of water a collection of reports

14 2 and statements, Canberra, Australian Government Publishing Service, 1985, pp. 34-6. HF Akers and SAT Porter, ‘A historical perspective on early progress of water fluoridation in Queensland 1945-54: Sheep, climate and sugar’, Australian Dental Journal, vol. 49, no. 2, 2004, pp. 61-6 and MA Simmonds, ‘The medication of water supplies’, Queensland Dental Journal, vol. 4, no. 11, 1952, pp. 388-93. HF Akers and SAT Porter, ‘The 1945 – 1955 Queensland artesian fluoride experience: a unique phenomenon within the Australian wool industry’, Historical Records of Australian Science, vol. 18, no. 2, 2007, pp. 177-89. National Health and Medical Research Council, National Health and Medical Research Council measures for the partial prevention of dental caries, Canberra, NHMRC, 1954, pp. 1-3. SF Lumb and BJ Kruger, Report on fluoridation, Brisbane, University of Queensland Faculty of Dentistry, 1953, pp. 1-11. SF Lumb to F Buss, 12 October 1954 and SF Lumb to JE Jordan, 31 August 1955, Personal collection in author’s possession. ‘Council to consider water fluoridation’, Bundaberg News-Mail, 20 October 1954, p. 4. HF Akers and SAT Porter, ‘Water fluoridation: the engineers’ perspective’, Water, vol. 31, no. 6, 2004, pp. 44-9. Lumb and Kruger, Report on fluoridation, p. 4. ‘Fluoridation move backed “in interest of dental health”’, Bundaberg News-Mail, 9 May 1956, p. 3. ibid., and J Francis to Bundaberg City Council, 29 May 1956, Personal collection in author’s possession. P Trundle, ‘Is the dentist’s drill on the way out?’, Courier-Mail, 5 June 1953, p. 2 and SF Lumb to W Forgan Smith, 2 March 1953, Personal collection in author’s possession. G Simmonds, ‘Preventive dentistry’, Queensland Dental Journal, vol. 4, no. 5, 1952, pp. 178-80 and J Sagar, ‘Editorial – the role of sugar in dental caries’, Queensland Dental Journal, vol. 4, no. 10, 1952, p. 366. ‘Sugar answers its critics on diet and good health’, Australian Sugar Journal, vol. 46, no. 6, 1954, pp. 361-5. ‘Mr Muir replies to “attack” on sugar’, Bundaberg News-Mail, 9 June 1953, p. 3. P Trundle, ‘Is the dentist’s drill on the way out?’, p.2. Lumb to Forgan Smith, 2 March 1953. Lumb to Buss, 12 October 1954. SF Lumb to Jordan, 31 August 1955. Commonwealth Department of Health, Fluoridation of water a collection of reports and statements, Canberra, Australian Government Publishing Service 1985, p. 35. ‘Council to consider water fluoridation’, Bundaberg News-Mail, 20 October 1954, p. 4. F Martens, ‘Fluorine and caries’, Bundaberg News-Mail, 22 October 1954, p. 3; ‘No danger in water fluoridation’, Bundaberg News-Mail, 26 October 1954, p. 4 and ‘Council to consider water fluoridation’, Bundaberg News-Mail, 20 October 1954, p. 4. Bundaberg City Council Public Utilities Committee, Minutes submitted to Bundaberg City Council on 28 October 1954, pp. 1-2. ‘Decision deferred on water fluoridation’, Bundaberg News-Mail, 29 October 1954, p. 2.

3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22

23 24

15 25 ibid. 26 F Martens, ‘Fluorine and caries’, Bundaberg News-Mail, 22 October 1954, p. 3; L Guth, ‘Water supply’, Bundaberg News-Mail, 30 October 1954; ‘Not “guinea pigs” on fluoridation’, Bundaberg News-Mail, 5 November 1954, p. 2 and ‘Strong attack on mayor over polio’, Bundaberg News-Mail, 4 November 1954, p. 2. 27 ‘Strong attack on mayor over polio’, Bundaberg News-Mail, 4 November 1954, p. 2 and ‘Not “guinea pigs” on fluoridation’, Bundaberg News-Mail, 5 November 1954, p. 2. 28 ‘City in mourning – Bundaberg grief stricken’, Brisbane Courier, 30 January 1928, pp. 13-15. 29 T Healy, ‘The memory lingers’, Queensland Environmental Health, September 1992, pp. 10-13. 30 B Courtice, Interview by H Akers, 25 May 2003 and M Derry, ‘Vaccination tragedy revisited – researching tragic deaths’, Bundaberg News-Mail, 23 November 2002, p. 4. 31 ‘North boy polio victim’, Bundaberg News-Mail, 22 October 1954, p. 2 and ‘Strong attack on mayor over polio’, Bundaberg News-Mail, 4 November 1954, p. 2. 32 ‘Decision deferred on water fluoridation’, Bundaberg News-Mail, 29 October 1954, p. 2; ‘No fluoridation without vote’, Bundaberg News-Mail, 8 December 1954; Bundaberg City Council, Minutes of council meeting, 23 December 1954, p. 2 and ‘Would supply data on fluoridation’, Bundaberg News-Mail, 17 November 1954, p. 5. 33 ‘No fluoridation without vote’, Bundaberg News-Mail, 8 December 1954. 34 Bundaberg City Council, Minute of a council meeting, 23 December 1954. p. 2. 35 ‘Claims argument for water fluoridation “grossly misleading”’, Bundaberg News-Mail, 26 January 1955. 36 Lumb to Jordan, 31 August 1955. 37 DW de Louth, ‘Fluoridation’, Fluoridation and Conspiracy, vol. 5, August, 1956, p. 4 and FT Griffiths, Poison in your water supply, Brisbane, Queensland Anti-Fluoride Association, 1956, p. 2. 38 HG Jones, JA Sagar and W Morrison, A history of the Australian Dental Association (Qld Branch) 1906-1992, Brisbane, ADA (Qld Branch), 1995, p. 123. 39 A Saranin to LJ Lucas, 7 March 1956, Personal collection in author’s possession. 40 ‘Fluoridation move backed “in interest of dental health”’, Bundaberg News-Mail, 9 May 1956, p. 3. 41 L Lucas to A Fryberg, 11 June 1956, Personal collection in author’s possession. 42 A Fryberg to LJ Lucas, 18 June 1956, Personal collection in author’s possession. 43 ‘To seek opinion on water fluoridation’, Bundaberg News-Mail, 8 June 1956, p. 4. 44 ‘Strongly oppose fluoridation in Bundaberg’, Bundaberg News-Mail, 7 June 1956, p. 4. 45 W Smyth to Bundaberg City Council, 25 June 1956, Personal collection in author’s possession. 46 Bundaberg City Council, Minutes of council meeting, 5 July 1956, p. 1. 47 Rockhampton Anti-Fluoridation Association, Minute Book 1956-1968, 4 October 1956 and J Harding, ‘The fluoridation battle in Australia’, 1961, pp. 1-3. Fryer Library, University of Queensland Library, Jack Harding collection, UQFL 265, box 22 and 10. 48 Jones, Sagar and Morrison, A history of the Australian Dental Association (Qld Branch), p. 126. 49 HF Akers, SAT Porter and R Wear, ‘Water fluoridation in Queensland, why not?

16 Timing, circumstance, and the nature of the Fluoridation of Public Water Supplies Act (1963)’, Health and History, vol. 7, no. 2, 2005, pp. 30-55. 50 ibid., and HF Akers and MP Jackman, ‘A paralysis in public health policy: water fluoridation in Queensland (1996-2006)’, ADAQ News, April 2007, pp. 10-14. 51 RL Crain, E Katz and DB Rosenthal, The politics of community conflict the fluoridation decision, Indianapolis, Bobbs-Merrill Company Inc, 1969, pp. 132-3.

IS OUR WATER SAFE TO DRINK?
by J. Gordon Millichap, MD, Pediatric Neurologist, Northwestern University Medical School and the Attention Deficit Disorder Clinic, Division of Neurology, Children’s Memorial Hospital, Chicago, Illinois, and Kathleen Haviland, JD, Managed Care Specialist, On Lok, Inc., San Francisco, California, and former aide to United States Congressman John D. Dingell.

Material for this article was adapted from Dr. Millichap’s new book, IS OUR WATER SAFE TO DRINK? A guide to Drinking Water Hazards and Health Risks, (ISBN 0-9629115-5-0, PNB Publishers, P.O. Box 11391, Chicago, Illinois 60611) The safety of our drinking water is often taken for granted. In recent years, however, environmentalists and the media have drawn attention to the dangers of ground water pollution and the health risks from lead, chlorine, pesticides, organic chemicals, and various microorganisms that have been found to contaminate our public water supplies. Outbreaks of waterborne

diseases are a common occurrence and have involved entire city populations, sometimes leading to serious complications and even fatalities. The potential carcinogenic effects of long-term exposure to certain organic chemicals in our water supplies are of increasing concern in this industrialized society. What is the United States Government doing to safeguard our water? The controlling law governing our drinking water is the Safe Drinking Water Act (SDWA) of 1974, as amended. The SDWA provides the Environmental Protection Agency (EPA) the authority to safeguard public drinking water through regulatory programs that protect groundwater aquifers and to establish standards for the purification, treatment, and testing of municipal water supplies. Both the House of Representatives and the Senate passed their own versions of the reauthorization of the SDWA in the 103rd Congress, but they adjourned before differences could be reconciled and a law passed. In the new 104th Congress, as of press time, contentious issues are delaying debate over the reauthorization of the Act. The Chairman of the Senate Committee on Environment and Public Works, John Chafee (R-R.I.) is favoring the reauthorization vehicle that he co-sponsored in the 103rd Congress, S.2019, which passed the Senate in May of 1994. S.2019 would have given the EPA greater flexibility to consider the relationship between costs and health benefits when setting future drinking water standards. However, the Chairman of the Subcommittee on Drinking Water, Fisheries, and Wildlife, Richard Kempthorne (R-ID), is in conflict with his full committee chairman in that he supports much weaker regulatory language. He favors language that would base standards on what is technologically achievable, as opposed to feasible; he also favors language that would require proposed standards to be subjected to explicit cost-benefit analyses and to be justifiable in terms of the risk reduction produced. The proposals in Congress favor a weakening of Federal standards and controls and the transfer of some responsibility for water quality from the EPA to the States and local governments, which are often ill equipped and under funded. The carcinogenic properties of organic chemicals as well as radionuclides are a main cause for concern. Public health authorities have in the past relied more on filtration and disinfection treatment processes rather than water monitoring to ensure the safety of drinking water, because of the complexity of laboratory analyses. In recent years, more communities are using treatment processes other than disinfection to remove inorganic and organic contaminants. The cost of meeting stricter water quality standards is particularly high for smaller communities.

The proposals in Congress favor a weakening of Federal standards and controls and the transfer of some responsibility for water quality from the EPA to the States and local governments, which are often ill equipped and under funded.

In the State of Illinois, beginning January 1993, all municipal suppliers are required to monitor for 29 synthetic organic chemicals (SOCs), mostly pesticides. All surface water suppliers must test quarterly until no SOCs are detected or the level of each contaminant is below its maximum contaminant level (MCL). Ground water suppliers will test for most of the SOCs before December 31, 1995 unless the present Congress votes to change these regulations and a less restrictive bill is passed into law. Do we need to spend more on improved water purification technologies and a tightening of EPA standards for potential cancer-causing chemicals, or should we cut costs and limit regulation of contaminants to those known to cause the greatest immediate health risks, for instance, lead? The former solution would result in criticism by state and local governments who find the present regulations to be costly and sometimes impractical, particularly for smaller municipalities, while the latter would probably lead to an even greater incidence of cancer (and other diseases) among our citizens and will certainly cause an outcry from environmentalists who are pressing for more stringent controls. Is the consumer sufficiently informed of risks? There is a need for education of consumers regarding the sources and types of water contamination, the recognition of symptoms of waterborne diseases, and home methods for prevention and control of drinking water hazards. Some waterborne health hazards, such as lead, nitrate, arsenic, and mercury, can be avoided by having municipal or well water checked and by taking certain precautions. For example, to avoid lead from old plumbing, flush the faucet until the water is cold before drinking. Bacterial contamination should be suspected at times of flooding or earthquake. The water should be boiled or chlorinated, or bottled water substituted. A sudden change in water appearance from clear to turbid might suggest contamination with the parasite, Cryptosporidium, the organism that caused serious diarrheal illness in one half million of the population of the city of Milwaukee in the spring of 1993, with 100 fatalities. Avoidance of water that loses its clarity or develops an unpleasant odor or

taste could protect the consumer from potential health risks caused by a faulty public water filtration system.

There is a need for education of consumers regarding the sources and types of water contamination, the recognition of symptoms of waterborne diseases, and home methods for prevention and control of drinking water hazards.

While these simple consumer tips and precautions may help in avoidance of acute illness caused by waterborne microorganisms and certain inorganic pollutants, for example, nitrate and arsenic, the far more serious danger of the chronic and lifetime exposure to potentially carcinogenic organic chemicals will persist and remain unanswered. Only our government and a more environmentally responsible corporate industrial society can lower the carcinogenic hazards lurking in our water and food supplies, since only they have the resources to prevent or remove these contaminants. Is the medical profession sufficiently aware of the problem? The massive outbreak of Cryptosporidium parasitic infection in Milwaukee in 1993 was a reflection not only of the inadequate filtration system and inefficient water quality monitoring but also resulted from the slow response of physicians to recognize and diagnose the cause of the waterborne illness in patients who sought medical help. Cases were misdiagnosed as viral gastroenteritis or "intestinal flu" without further investigation, and the special testing procedures required for the detection of Cryptosporidium in stools examined for ova and parasites were not requested. The delay in diagnosis resulted in an outbreak involving nearly one half a million individuals. If the medical community had been more alert to possible contamination of water supplies with parasites, the outbreak would have been contained and the deaths of 100 patients may have been prevented.

. . . a federal lawyer for the AMA stated that "clean water is an environmental and political issue and not strictly a health matter." This apparent disinterest or ignorance of the hazards and health risks of contaminated water by representatives of our medical profession is alarming.

In the treatment and prevention of various cancers, the influence of environmental factors, especially chemical and viral contamination of drinking water and foods, has received little attention in medical oncology research. The American Medical Association is not actively involved in lobbying for cleaner water and the passage of legislation to maintain strict governmental controls of water resources. In answer to a question regarding the role of the AMA in the present overhaul of the Clean Water Act, a federal lawyer for the AMA stated that "clean water is an environmental and political issue and not strictly a health matter." This apparent disinterest or ignorance of the hazards and health risks of contaminated water by representatives of our medical profession is alarming. Contamination of Public Water Supplies and Microbial Disease Outbreaks The safety and quality of drinking water in the United States are dependent on the efficiency and maintenance of the water treatment processes commonly used in most public water systems. The removal of microorganisms by disinfection and filtration has dramatically reduced the incidence of waterborne diseases such as typhoid fever, cholera, and hepatitis, and the banning of lead in pipes and solder has reduced the exposure of millions of Americans to lead and the risks of lead poisoning. The Safe Drinking Water Act of 1974 and the Amendments of 1986 set standards of drinking water quality to protect our health, but deficiencies in filtration technology and regulatory programs enforcing these goads have led to numerous outbreaks of disease. Tests employed to check for certain parasitic organisms and viruses are sometimes inadequate and the disease causing or pathogenic nature of parasites such as Blastocystis hominis, especially in immuno-compromised individuals with cancer or AIDS, is often not recognized.

The Safe Drinking Water Act of 1974 and the Amendments of 1986 set standards of drinking water quality to protect our health, but deficiencies in filtration technology and regulatory programs enforcing these goads have led to numerous outbreaks of disease.

A total of 96 outbreaks of waterborne disease reported to the Center for Disease Control and the Environmental Protection Agency, 1986-1992, accounted for 46,712 confirmed cases of gastrointestinal illness. The

majority of cases were either of unknown cause, presumed viral in origin, or traced to Crybtosporidium. Other common organisms were Salmonella, E. coli, Campylobacter, and hepatitis A. Since the 1993 outbreak in Milwaukee, Cryptosporidium has outnumbered all other organisms in terms of numbers of individuals affected by waterborne illness. Drinking water suspected of bacterial contamination should either be boiled, chlorinated, or bottled water substituted. Chlorination will not remove Cryptosporidium and the water must be boiled or filtered by reverse osmosis. Lead in Our Drinking Water Lead in drinking water contributes between 10 and 20 percent of the total environmental exposure to lead. Young children are particularly susceptible to lead poisoning, and even low dose exposure can cause intellectual deficits and behavior disorders. Water as a source of lead poisoning may increase in relative importance since leaded gas has been abolished and abatement programs have reduced exposure from leadbased paint and urban soil and dust.

Chlorination will not remove Cryptosporidium

The EPA estimated in 1986 that some 40 million Americans were drinking water that contained potentially hazardous levels of lead. Until 1993 the EPA limit for lead levels in drinking water was 50 parts per billion (ppb). The new limit for lead has now been set at 15 ppb. Approximately half a million children with hazardous lead levels in their blood will be benefited, and lead exposure will be minimized for millions of Americans. Simple consumer steps to reduce lead exposure from drinking water These include the following:

Flush the faucet until the water is cold before drinking. Water obtained after flushing will not have been in extended contact with pipes or solder that may contain lead. Never cook with or drink and do not mix the baby formula with water from the hot tap. Hot water dissolves greater quantities of lead more quickly than cold water. Formula preparation with lead contaminated water accounted for 9 of 50 cases of lead poisoning reported in infants in the year 1992.

• •

Have your water tested for lead and purchase bottled water for home and office consumption, if public supplies are suspect. In a newly built home, remove all strainers from faucets and flush the water for at least 15 minutes to remove loose solder or flush debris from the plumbing. Plumbers should use only lead-free materials, but monitoring is sometimes deficient. The newer the plumbing installation, the greater the risk of lead leaching from pipes, especially when the water is soft, acidic and corrosive. Older pipes develop a protective coating of mineral deposits on the inside, insulating the water from the solder and decreasing the danger of leaching lead. Water softeners should be avoided in homes where lead is a problem. They may contribute to corrosiveness of the water and increase the potential for lead contamination. Well water may contain lead from a submersible pump containing brass and bronze alloys. The pump may need to be replaced or a reverse osmosis or cartridge filtering unit installed. The Water Quality Association will advise on water filters for specific purposes (Website: www.wqa.org ).

Contaminants Peculiar to Well Water Coliform bacteria, nitrates, and arsenic contaminate well water more commonly than municipal water supplies. The presence of nitrates suggests that animal or human wastes or fertilizers used in agriculture or on lawns are entering the well from land runoff, seepage, or migration into ground water aquifers. Nitrates are of special concern to the health of young children, and in women of child-bearing age. Nitrates converted to nitrites in the stomach cause methemoglobinemia in infants. The hemoglobin in the blood is oxidized to methemoglobin, a form of hemoglobin that cannot bind and carry oxygen from the lungs to the tissues. The blood turns a chocolate brown color and the patient’s skin becomes gray blue or cyanotic. Water containing nitrate in amounts greater than the permitted maximum contaminant level (MCL, 10 mg/L) should be avoided and bottled water substituted. Nitrate-containing water should not be boiled, since evaporation will result in increased concentrations of nitrate.

Nitrates are of special concern to the health of young children, and in women of child-bearing age.

An outbreak of methemoglobinemia in New Jersey in 1992 involved more than 40 elementary school children in first through fourth grades. They visited the school nurse within a 45-minute interval following the school lunch period. They all suffered from an acute onset of blue lips and hands, vomiting, and headache. Fourteen were hospitalized, and all recovered in 36 hours. The outbreak, due to nitrite poisoning, was traced to soup contaminated by nitrites in a boiler additive. The authors of this reported incident aptly named the soup "Boilerbaisse." Nitrites are also potentially carcinogenic. They act on amines in the diet to form nitrosamines, which have been shown to cause cancer in animals. High levels of nitrate have been found in well waters of regions of China, Columbia, and in two towns in England where the incidence of stomach cancer is unusually high. A link between nitrate in well water and cancer of the stomach needs further investigation. EPA National Survey of well water The EPA has completed a five-year national survey of nitrate and pesticides (NPS) in drinking water wells. Of 10 million rural domestic wells that were studied, nitrate was detected in 57 percent, pesticides in 4 percent, and both in 3 percent. The pesticides detected most frequently in the survey were DCPA (Dacthal) acid metabolites and atrazine. DCPA is a herbicide used primarily as a weedkiller on lawns, turf, and golf courses, and on some fruits and vegetables. Atrazine is used to control annual broadleaf weeds and grasses in corn and soybean farms.

Pesticides had been used at about 80 percent of homes and farm properties where domestic wells were located. These pesticides migrate through soil and some had concentrated in rural domestic wells at levels above their maximum contaminant levels (MCLs) and health advisory levels (HALs).

Pesticides had been used at about 80 percent of homes and farm properties where domestic wells were located. These pesticides migrate through soil and some had concentrated in rural domestic wells at levels above their maximum contaminant levels (MCLs) and health advisory levels (HALs). A variety of potentially carcinogenic chemicals used in industry, business, or households may endanger the safety of drinking water obtained from

wells. The evidence of widespread migration of chemicals into wells demonstrates the need for improved ground water protection. Well owner safety tips include the following:

• •

Avoid sources of contamination, such as use of synthetic fertilizers and herbicides and careless disposal of cleaning fluids and other household wastes; Test well water periodically for nitrate, coliform organisms, and also arsenic in some areas; Consult a health department official if a sudden change in the appearance, taste, or smell of the water is noted and contamination is suspected. Call the EPAs Safe Drinking Water Hotline (800-426-4791) for names and telephone numbers of state certification officers.

Cancer Related Water Pollutants Cancer related hazards in drinking water are man-made and are derived from industrial, domestic, and agricultural wastes, the polluted atmosphere, leaching from soil, land runoff, motorboat engines, and spilled chemicals. There are four main groups of potential carcinogenic chemicals: 1) synthetic organic chemicals (SOCs)—pesticides including lindane, chlordane, 2,4-D, endrin, and toxaphene; 2)volatile organic chemicals (VOCs)—industrial chemicals and solvents, degreasing agents, varnishes, and paint thinners, including carbon tetrachloride, vinyl chloride, and benzene; 3) polychlorinated biphenyls PCBs)—waste products from electrical transformer, capacitor, and plasticizer factories, banned in the 1970s but persisting in the water of rivers and the Great Lakes, where they were dumped years ago; and 4) trihalomethanes (THMs)—by-products of chlorine disinfection of drinking water, especially chloroform. The disinfection of water with chlorine is the source of cancer risk receiving most attention from the EPA. The Food and Drug Administration in 1976 restricted the use of chloroform that previously had been employed in cough syrups, mouthwashes, toothpastes, and other common consumer products. The cancer risk of exposure to chloroform may have decreased over the past 20 years, but chloroform in drinking water is a significant cancer-related hazard.

The disinfection of water with chlorine is the source of cancer risk receiving most attention from the EPA.

The EPA regulates and monitors the maximum contaminant levels (MCLs) of organic pollutants, and the World Health Organization (WHO) issues guideline values, the concentration of a chemical in drinking water associated with an estimated risk of one additional case of cancer per 100,000 population over a lifetime of 70 years exposure. None of these guidelines take into account the additive and synergistic effects of the vast number of chemicals to which we are exposed. Cancer Risk: Incidence and Assessment Cancer may be caused by a combination of factors, both environmental toxins and internal susceptibility. Environmental causes include chemicals, infection with viruses, and ionizing radiation. Internal factors are hormonal, changes in the immune system, and inherited mutations. An interval of ten or more years may pass between exposure to chemicals or radiation and the clinical signs of cancer. A steady rise in cancer mortality rate in the United States has been recorded by American Cancer Society statistics in the last 50 years. One out of every five deaths is from cancer and more than one half million deaths from cancer are expected this year. Although lung cancer is the major reason for this increased incidence, other forms of cancer are also responsible for the increased cancer mortality. For example, breast cancer incidence rates for women have increased about 2 percent a year since 1980, and they now number 110 per 100,000. Breast cancer is the second major cause of cancer death in women and, unlike many other cancers, a five year survival does not necessarily mean a cure of breast cancer. The number of deaths from breast cancer per 200,000 population in 1961 was 24,311 and in 1991, it had risen to 43,583, an increase explained partly by the aging of the population but also by a greater profusion of industrial and agricultural organic chemicals in our environment.

Risk assessments are therefore very rough estimates.

The determination of potential cancer risk from chemicals in water and food is usually based on long-term animal studies. Data are also available on the incidence of cancer in humans, mostly from occupational exposure. Risk assessment is in two stages: 1) identification of the toxic properties of potential carcinogens, and 2) measurement of the degree of human exposure to the chemical. Chemical hazards are tested for oncogenicity in laboratory animals or cell systems and in clinical and epidemiological studies. Levels of exposure through air, water, and food are measured and the degree of contact with the hazard is estimated. Risk assessment is usually based on high-dose exposure for a short time in animals. In setting human safety standards, scientists must extrapolate from animals to humans and from high-dose acute exposures to low-dose long-term conditions. Risk assessments are therefore very rough estimates. The EPA tends to rely on data showing the highest incidence of cancer for setting regulatory controls, but some authorities question the value of present estimates from laboratory animals and call for improved methods more relevant to humans. Water source and risk Epidemiological studies of populations exposed to surface, upland, chlorinated, and reused waters have demonstrated an increased incidence of cancer of the gastrointestinal and urinary tracts. As one example of a population-based approach, United States case-controlled studies in New York counties compared mortality from gastrointestinal and urinary tract cancer with noncancer death controls. There was an excess of male deaths in chlorinated surface water areas from cancer of the esophagus, stomach, large intestine, rectum, liver, kidney, pancreas, and bladder, and an excess of female deaths from cancer of the stomach.

Upland surface water and polluted river sources that have been chlorinated carry the highest risk of cancer. Unchlorinated ground water has the lowest cancer risk.

In England, the relative risks of river Thames reused water and upland water compared to ground water showed a statistically significant increased risk of stomach cancer mortality in persons supplied by upland and river water for drinking purposes. Upland surface water and polluted river sources that have been chlorinated carry the highest risk of cancer. Unchlorinated ground water has the lowest

cancer risk. Studies have shown sufficient evidence of a cancer risk associated with organic micropollutants in certain drinking waters that a causal relationship has been accepted. The high prevalence of polluted and chlorinated waters in public supplies demand the enforcement of EPA regulations to monitor the MCLs of organic pollutants. Consumer risk assessment factor Consumers vary in the way they view these hazards and their respective risks. Some will accept a small risk without concern for health effects whereas others will view any risk as unacceptable and cause for alarm. "Is the Water Safe to Drink?" not "How Safe is Our Drinking Water?" is the question asked by many consumers at a personal level. Unfortunately, a simple "yes" or "no" answer is not possible, given the many variables in water sources, environmental factors, and water treatment processes. Clearly, there is a risk involved by ingesting low levels of organic chemical contaminants every day of our lives. That one additional case of cancer per 100,000 population might be someone close! The following guidelines relate to possible carcinogens in our drinking water:

Use activated carbon filtration in the home to remove chlorine and reduce levels of organic materials, including trihalomethanes, the by-products of chlorination, some volatile organic contaminants, and certain pesticides, including fungicides. The level of contaminant removal will vary with the size and type of filter, the degree of pollution, and the frequency of carbon renewal. All carbon filters require periodic replacement of cartridges to maintain efficiency and to lessen the risk of bacterial overgrowth. Substitute bottled water in areas of landfills where risk of organic chemical pollution is high or where cancer clusters have been observed. Alternate consumption of municipal water with various brands of bottled water, to avoid longterm exposure to one possible source of cancer-related drinking water pollutants.

Bottled Water Usage and Safeguards Public concern with both the quality and safety of drinking water has become so compelling that many consumers now rely almost exclusively on bottled water for drinking purposes. Bottled water is now preferred by millions of Americans and the cost is enormous. To learn that regulations

governing the purity and safety of bottled water are often less stringent than those for municipal water supplies may come as a surprise to some consumers. Bottled water is a luxury to many and a necessity to others. Company advertising has promoted bottled water as "purer," "safer,<!70> "chlorinefree," and an essential component of a healthy lifestyle. It is not generally recognized that one-third of all bottled water in the United States comes from public water supplies and is no safer than the water obtained from the faucet. An Environmental Policy Institute Report (1989) refers to the frequency of contamination of bottled water with low levels of heavy metals, solvents, and bacteria. The carcinogenic chemical migrants (for example, methylene chloride and vinyl chloride) from plastic bottle containers are also a concern. Despite the value of bottled water as an alternative source of drinking water at times of emergency, consumers should not presume that bottled water is invariably preferable to tap water. Buy bottled water
• •

• • •

If your drinking water suddenly becomes turbid, changes in color or taste, or an unpleasant odor develops. If you learn that the public water system has become contaminated and you are instructed to boil the water. Bottled water is a simpler alternative. At times of floods or earthquakes when water contamination is a common hazard. If your home has lead pipes or lead solder. Drink bottled water until your water has been tested. If you have a private well and you suspect contamination with coliform bacteria or nitrates. Drink bottled water until the well water is tested. If your neighborhood has a cluster of cancer patients and water contamination from a landfill is suspected. Bottled water may be safer than community water supplies or private wells. If you need to limit your intake of sodium for medical reasons. Bottled waters of low sodium content or distilled water may be preferred to public supplies. If you are traveling and suspect contamination of local water supplies. Drink only brand named bottled waters from sealed containers. If your water tastes strongly of chlorine. Bottled water is preferable for cooking as well as drinking. Bottled water does not contain chlorine and does not taint food. Buy well known and respected brands of water from approved,

protected sources and bottled at the source. Alternate the brands and check the expiration dates in order to limit the dangers of bacterial growth and the concentration of plastic chemical contaminants after prolonged storage.

Consumer Concerns and Home Water Treatments The most frequent questions asked by consumers are about the level of lead in their drinking water and about taste and odor problems. "Is our water safe to drink?" "Do we need to substitute bottled water?" "Should we install a home water treatment unit and, if so, which type of unit would be most satisfactory for our particular needs?" The EPA provides information in response to inquiries about the necessity for home treatment units. It does not regulate the manufacture, distribution, or use of these units. The EPA stresses that the units should not be relied upon for the removal of organisms and chemicals injurious to our health. Nonetheless, certain filtration units, especially reverse osmosis, will lower the concentration of several contaminants, including lead, copper, nitrates, pesticides, and parasites. No system is warranted for complete elimination of all contaminants.

The government and the medical profession appear to be failing in their duties.

Controversies concerning the sale and use of home treatment units have arisen because of unsubstantiated claims of benefits and scare tactics. Consumers should beware of "free" water testing by a salesperson to determine the drinking water quality. An independent analysis is usually more accurate and meaningful. Conclusion The government and the medical profession appear to be failing in their duties. The former should ensure the safety of our drinking water and the latter should recognize of health risks associated with contaminants. The more we understand about our own local water supplies and the nature of the health risks, the more we as consumers and citizens can do to protect ourselves from these hazardous environmental pollutants and their sources.

_____________ Selected Bibliography American Academy of Pediatrics, 1994 Red Book: Report of the Committee on Infectious Diseases, 23rd edition, Elk Grove Village, Illinois. Askew, G.L. et al., "Boilerbaisse: an outbreak of methemoglobinemia in New Jersey in 1992," Pediatrics 94:381-4, September 1994. Baghurst, P.A., et al, "Environmental exposure to lead and children’s intelligence at the age of seven years," New England Journal of Medicine 327:1279-84, October 29, 1992. Baron, E.J., L.R. Peterson, S.M. Finegold, Bailey and Scott’s Diagnostic Microbiology, 9th edition, Mosby, St. Louis, 1994. Mackenzie, W.R., N.J. Hoxie, M.E. Proctor et al., <169.A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply," New England Journal of Medicine 331:61-7, July 21, 1994. Millichap, J.G., Environmental Poisons in Our Food, PNB Publishers, Chicago, 1993. Millichap, J.G., Is Our Water Safe to Drink? A Guide to Drinking Water Hazards and Health Risks, PNB Publishers, Chicago, 1995. Ram, N.M., E.J. Calabrese, R.F. Christman, Organic Carcinogens in Drinking Water: Detection, Treatment, and Risk Assessment, John Wiley & Sons, New York, 1986. U.S. Center for Disease Control and EPA, "Waterborne disease outbreaks, 1986-1992," Morbidity and Mortality Weekly Reports, 1990, 1991, & 1993. U.S. Congress House Floor Brief, "Safe Drinking Water Act of 1994," October 7, 1994. U.S. Environmental Protection Agency, National Survey of Pesticides in Drinking Water Wells, Phase1 Report, Washington , D.C., Office of Water, Office of Pesticides and Toxic Substances, EPA, November 1990. Idem., "Home water treatment units: Filtering fact from fiction," EPA, Washington, D. C. 1992. Idem., "Drinking Water Protection: A general overview of Safe Drinking Water Act Reauthorization," Office of Water, February 1994.

Article from NOHA NEWS, Vol. XX, No. 4, Fall 1995, pages 3-8.

Isis Announces Award of Up to $8.4 Million in New Government Grants and Contracts to Its Ibis Biosciences Subsidiary for Pathogen Detection and Human Forensics
http://ir.isispharm.com/releasedetail.cfm?ReleaseID=338306

CARLSBAD, Calif., Oct 03, 2008 /PRNewswire-FirstCall via COMTEX News Network/ -- Isis Pharmaceuticals, Inc. (Nasdaq: ISIS) announced today that its majority-owned subsidiary, Ibis Biosciences, Inc. (Ibis), was awarded government grants and contracts from the United States Department of Agriculture (USDA), National Institute of Justice (NIJ) and other government agencies totaling up to $8.4 million. These awards will fund the utilization of several Ibis assays through Ibis' service laboratory to characterize samples provided by the government sponsor and will provide support for further development of assays to support government-sponsored projects. The focus of these projects ranges from human forensics, to detection and identification of influenza viruses and other pathogens, that could have a profound effect on animal and human health. The USDA Animal and Plant Health Inspection Service (APHIS) agency awarded Ibis up to $4.2 million to fund the utilization of Ibis' commercial influenza assay to identify and differentiate avian influenza strains, to distinguish high pathogenicity from low pathogenicity strains, and to aid in the tracking of avian influenza transmissions. The contract also provides funding for the development of assays to detect a broad range of additional agricultural pathogens that are considered important to animal health and that could have a significant impact on the U.S.'s agricultural economy. "We are pleased with the continuing support from our government partners and the opportunity to expand our commercial applications, especially in areas that are vital to our health and economy such as agriculture. As we work closely with the USDA to develop additional products that can aid in the monitoring and surveillance of avian flu, we will expand our detection assays to meet the needs of the agricultural community," said Michael Treble, President of Ibis and Vice President of Isis. The NIJ also awarded Ibis a new two-year project that will fund the development and implementation of next-generation human forensics markers, which are measured on the Ibis T5000(TM) Biosensor System. In addition to the new USDA and NIJ contracts, Ibis also received new contracts from other government agencies that will fund expansion of pathogen detection and identification assays and use Ibis' assay services laboratory. Additionally, with Lovelace Respiratory Research Institute (LRRI), Ibis has successfully completed the first year of a National Institutes of Health grant in which the Ibis influenza assay characterized over 2,000 tissue extracts to

study animal models of influenza transmission. Through LRRI, Ibis has been awarded the next year of funding to continue these efforts. "The utilization of the Ibis platform by our existing partners and the cultivation of new projects with new government agencies is a testament to the broad applicability of our technology. The enthusiasm of our government partners to invest in our technology to meet their objectives in homeland security, animal and human health, and human forensics illustrates the breadth and depth of the Ibis platform," said Steven A. Hofstadler, Ph.D., Vice President of Ibis Research. "To date, we have earned approximately $73 million in revenue to fund development of our biosensor system and our diverse commercial assays in many different areas including biodefense and infectious disease surveillance. We are now in the position to continue to fulfill our government contracts while focusing on clinical applications with Abbott and quickly moving into larger commercial markets," concluded Mr. Treble. ABOUT IBIS T5000 BIOSENSOR SYSTEM AND IBIS BIOSCIENCES, INC. Ibis Biosciences, Inc., a majority-owned subsidiary of Isis Pharmaceuticals, has developed and is commercializing the Ibis T5000(TM) Biosensor System for rapid identification and characterization of infectious agents. The Ibis T5000 is currently intended for research use only and not for use in diagnostic procedures. It is capable of identifying virtually all bacteria, viruses and fungi, and can provide information about drug resistance, virulence and strain type of these pathogens. Commercial applications for the Ibis T5000 Biosensor System include epidemiologic surveillance, monitoring of pandemic diseases, identification of emerging or previously unknown pathogens, forensic characterization of human samples, identification of sources of hospital-associated infections, and, in the future, human infectious disease diagnostics. Ibis develops, manufactures and markets Ibis T5000 instruments and assay kits. Additional information about Ibis can be found by selecting the Ibis link from Isis' homepage at http://www.isispharm.com. ABOUT ISIS PHARMACEUTICALS, INC. Isis is exploiting its expertise in RNA to discover and develop novel drugs for its product pipeline and for its partners. The Company has successfully commercialized the world's first antisense drug and has 19 drugs in development. Isis' drug development programs are focused on treating cardiovascular and metabolic diseases. Isis' partners are developing antisense drugs invented by Isis to treat a wide variety of diseases. Ibis Biosciences, Inc., Isis' majority-owned subsidiary, is developing and commercializing the Ibis T5000(TM) Biosensor System, a revolutionary system to identify infectious organisms. Isis is a joint owner of Regulus Therapeutics LLC, a joint venture focused on the discovery, development and commercialization of microRNA therapeutics. As an innovator in RNA-based

drug discovery and development, Isis is the owner or exclusive licensee of over 1,500 issued patents worldwide. Additional information about Isis is available at http://www.isispharm.com. This press release includes forward-looking statements regarding the development and commercialization of the T5000 Biosensor System, Ibis' technology, and the revenue potential of certain government contracts and grants. Any statement describing Isis' goals, expectations, financial or other projections, intentions or beliefs is a forward-looking statement and should be considered an at-risk statement, including those statements that are described as Isis' goals or projections. Such statements are subject to certain risks and uncertainties, particularly those inherent in the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics, in developing and commercializing systems to identify infectious organisms that are effective and commercially attractive, and in the endeavor of building a business around such products. Isis' forward-looking statements also involve assumptions that, if they never materialize or prove correct, could cause its results to differ materially from those expressed or implied by such forward-looking statements. Although Isis' forward-looking statements reflect the good faith judgment of its management, these statements are based only on facts and factors currently known by Isis. As a result, you are cautioned not to rely on these forwardlooking statements. These and other risks concerning Isis' programs are described in additional detail in Isis' annual report on Form 10-K for the year ended December 31, 2007, and its most recent quarterly report on Form 10Q, which are on file with the SEC. Copies of these and other documents are available from the Company. In this press release, unless the context requires otherwise, "Isis," "Company," "we," "our," and "us" refers to Isis Pharmaceuticals and its subsidiaries. Isis Pharmaceuticals is a registered trademark of Isis Pharmaceuticals, Inc. Ibis Biosciences and Ibis T5000 are trademarks of Ibis Biosciences, Inc. Regulus Therapeutics is a trademark of Regulus Therapeutics LLC. SOURCE Isis Pharmaceuticals, Inc.
http://www.isispharm.com

Copyright (C) 2008 PR Newswire. All rights reserved News Provided by COMTEX

National Pure Water Association

Draft Toxicological Profile for Fluorides
http://www.npwa.org.uk/index.php?option=com_content&view=article&id=103:drafttoxicological-profile-for-fluorides&catid=37:to-be-categorised&Itemid=92

The Draft Toxicological Profile for Fluorides (2001), produced by the US Agency for Toxic Substances and Disease Control (ATSDR), was presented for Public Comment prior to publication. The Toxicological Profile for Fluorides, which is updated from time to time, is supposed, by most toxicologists, to be the quintessential work on fluoride toxicity. However, whilst the Draft Profile deals with some salient aspects of F toxicity, the credibility of the work is compromised throughout by the use of inappropriate dental dogma and the promotion of water fluoridation as a prophylactic for dental caries. After reading the following Comment to the ATSDR, Professor Albert Burgstahler, coauthor of "Fluoride, the Great Dilemma", wrote to George Glasser: "Your letter to the ATSDR is a model of clarity and forensic skill."

Here is that letter February 13, 2002 Agency for Toxic Substances and Disease Registry Division of Toxicology 1600 Clifton Road Atlanta, Georgia 30333 Dear Sirs, "The mission of the Agency for Toxic Substances and Disease Registry (ATSDR), as an agency of the U.S. Department of Health and Human Services, is to serve the public by using the best science, taking responsive public health actions, and providing trusted health information to prevent harmful exposures and disease related to toxic substances." - ASTDR WEBSITE After reviewing the 2001 Draft Toxicological Profile for Fluorides, errors, omissions and misrepresentations of research work were noted in the first and subsequent chapters. Since publication of the 1993 Toxicological Profile on Hydrogen Fluoride, Fluorides, and Fluorine, very substantive findings on the adverse health effects of a variety of fluorides

and fluorinated substances have been published. These have been excluded from the new Draft, while disproportionate attention is given to the prophylactic effects of fluorides on teeth. On page 2, the authors refer to "sodium fluoride" as being "often" used to fluoridate drinking water. On page 15, we read: "One of the principal uses for sodium fluoride is the fluoridation of public water for the prevention of dental caries." There are many similar statements throughout the Draft which mislead readers into believing that this chemical is the most common fluoridating agent. Not until page 60, paragraph 2, do the authors acknowledge (in passing?) ". . . hydrofluosilicic acid, so exposure to this chemical is included in some epidemiological studies". Hydrofluosilicic acid (H2SiF6) is used to fluoridate about 90% of the fluoridation schemes in the US where populations exceed 10,000. The American Water Works Association states very clearly that sodium fluoride (NaF) is used in a very small number of water fluoridation schemes. The only health-related epidemiological studies which directly address H2SiF6 were done by Masters, et al. These were primarily concerned with the effects that silicofluorides in drinking water have on the availability of lead.(1)(2)(3). Why were these references not cited? In his own 1931 review, McClure noted that previous experiments conducted in the 1920s by Taylor, et al showed that calcium fluorosilicate is more toxic to animals than sodium fluoride.(4) Definitive experimental work on fluorosilicates was published by Kick, et al, in 1935(5) (see Table). However, a later paper by McClure, et al in 1950, selectively used Kick's findings to promote the use of fluorosilicates for drinking water fluoridation.(6) None of the early published experimental work on fluorosilicates is discussed or cited in the Draft Profile. Moreover, the McClure review, "Availability of Fluorine in Sodium Fluoride vs, Sodium Fluosilicate"; Public Health Reports Vol 65 No 37; 1175-86; 1950 has been omitted from the Draft. The omission of such a vital body of science provokes the notion that the ASTDR might have sought to avoid addressing the adverse health effects created by exposures to fluorosilicates from any source.

Kick, et al 1935, pg. 61

Fluorine Supplement Time Fluorine Fluorine Fluorine Fluorine Fluorine Fluorine in ingested in feces absorbed in urine balance retained Days Mg. Mg. Mg. Mg. Mg. % Rock Phosphate 10 213.6 131.5 82.1 20.5 +61.6 28.8 Sodium Fluorsilicate 23 269.9 94.3 175.6 93.6 +82.0 30.4 Sodium Fluorsilicate 22 269.9 94.4 175.5 90.2 +85.3 31.6 Sodium Fluoride 18 211.2 116.5 94.7 25.8 +68.9 32.6 Calcium Fluoride 11 229.6 225.5 4.1 4.2 -00.1 0.0 Kick was an eminent early pioneer in animal nutrition. Although McClure referred to the above table in promoting the use of fluorosilicates for drinking water fluoridation, neither he, nor any subsequent scientists took proper account of the data presented. The Table shows significant differences in absorption from ingestion of sodium fluorosilicates than from sodium and calcium fluorides. In their extensive experiments, Kick et al demonstrated the bioavailability of F from the different fluoride salts. They found that:
• • •

The retention of sodium fluoride was similar to that of sodium fluorosilicate. The amount of F absorbed from fluorosilicates was about twice the level as that from sodium fluoride. Urine levels of F in the sodium fluorosilicate groups were three times higher than those found in the sodium fluoride groups.

The initial Kick, et al, experiments were undertaken using pigs as test animals to determine the effects of fluorine in mineral supplements, primarily raw phosphate rock. When the phosphate rock was digested in stomach acid (a process similar to creating phosphoric acid), one of the products was H2SiF6. On autopsy, the scientists found that chronic, parenchymatous nephritis (kidney failure) had occurred in the pigs. They wrote:

They were pale in color, contracted, and firm in texture, and their surfaces roughened by numerous nodules and depressions. The capsules were slightly thickened, and in some instances, firmly adherent to the surface. Occasionally, small cysts containing a clear or amber colored fluid protrudes above the surface, or were more deeply situated in, the kidney. One section of the cortex appeared reduced in width, and frequently the medulla contained a considerable amount of fat.

Microscopically the kidneys showed a nephritis with a varying degree of degeneration of the tubular epithelium and, as a terminal result, the replacement of many tubules and glomeruli with fibrous tissue. None of the animals in the sodium fluoride-fed lot exhibited this condition.(7)

Taylor GE, 1929 noted that calcium fluorosilicate caused more adverse health effects in dairy cows than sodium fluoride.(8) These fundamental experimental findings by Kick, Taylor and their peers, were either missed - or concealed - by McClure. Later scientists, including the authors of the Draft Toxicological Profile for Fluorides, who referenced McClure in their own work also appear to have accepted McClure's own citations on trust alone. These long-standing errors and omissions must be rectified in the new Toxicological Profile for Fluorides. Aluminum fluoride: Speciation of fluoroaluminum complexes in soil and water was briefly discussed in the Draft. However, a large body of science dealing with the effects of fluoroaluminum complexes on G-proteins, neurological effects, etc, (which can be located on Pubmed via the internet), were not addressed. Fluoridation agents added to the drinking water can enhance leaching of aluminum from cookware (Literature review for the NIEHS, 2000).(9) On Page 91, the Draft authors note Varner, et al, 1998. However, extremely important results regarding aluminum fluoride toxicity were omitted by the authors of the Draft Profile, who briefly addressed only the sodium fluoride aspect of the work. (10) The Varner team observed that the animals who drank the aluminum-fluoride-laced water developed sparse hair and abnormal, copper-colored underlying skin which is related to premature aging. Further autopsy results showed serious kidney abnormalities in animals that drank water containing both sodium fluoride and aluminum fluoride. The Varner team wrote: "Striking parallels were seen between aluminum-induced alterations" in cerebral blood vessels that are associated with Alzheimer's disease and other forms of presenile dementia." They concluded that the alterations of the blood vessels may be a primary event, triggering neuro-degenerative diseases. Describing themselves as "astounded," the researchers further stated: "Not only did the rats in the lowest dose groups die more often during the experiment, they looked poorly well before their deaths. Even the rats in the lowest dose group that managed to survive the 45 weeks looked to be in poor health." The Draft authors did not acknowledge that these results were a replication of two earlier Varner, et al experiments addressing aluminum-fluoride toxicity.(11), (12) Following the three Varner, et al, aluminium fluoride studies conducted between 1991 and 1998 80% of the experimental rats died before the end of each of the experiments.

The Draft authors should have mentioned that the NIEHS joined with the EPA to request the National Toxicology Program to commission studies on aluminum complexes - and specifically fluoroaluminum complexes - in drinking water. (Federal Register: December 4, 2000 (Vol. 65, No. 233)] [Notices] [Pages 75727 - 75730].). Other notable omissions 1. The Roholm 1937 data which is cited in all basic fluorine toxicology papers.(13) 2. The toxicology of fluorinated pesticides. While the Draft briefly mentions the use of fluorinated pesticides, no reference is made of the toxicity/neurotoxicity of pesticides and other organic fluorides to which much of the population is daily exposed. The authors failed to provide a list or source of information for fluorinated pesticides, fungicides and herbicides. 3. Fluorinated medicaments Fluorinated medicaments are briefly mentioned, but there is no substantive discussion, nor a comprehensive list. Conclusion The authors of the Draft included some new data, but omitted very troubling findings contained in the early and more recent research. Is the ASTDR prepared to honor its Mission Statement to the American public in the new Toxicological Profile on Fluorides "to serve the public by using the best science, taking responsive public health actions and providing trusted health information to prevent harmful exposures and disease related to toxic substances"? Yours truly, George C. Glasser, Formerly of St Petersburg, Florida.

REFERENCES 1. Masters RD, Coplan MJ, Hone BT, Dykes JE, Association of silicofluoride treated water with elevated blood lead, Neurotoxicology. 2000 Dec;21(6):1091-100.

2. Masters RD, Coplan MJ, Water Treatment with Silicofluorides and Lead Toxicity, Intern. J. Environmental Studies 56, 435-449 (1999). 3. Masters, RD and Coplan, M. Brain Biochemistry and the Violence Epidemic, Nova Science Publishers, Inc, New York (1999). 4. McClure FJ, Mitchell HH (1931) The effect of calcium fluoride and phosphate rock on the calcium retention of young growing pigs, J Agric Res 42: 363-373. 5. Kick CH, et al, Fluorine in Animal Nutrition, Ohio Agricultural Experiment Station, Bulletin 558, Nov. 1935. 6. McClure FJ:, Availability of Fluorine in Sodium Fluoride vs, Sodium Fluosilicate, Public Health Reports, vol 65 No 37; 1175-86; 1950. 7. Kick CH, Bethke RM, Edgington BH, Effect of Fluorine on the Nutrition of Swine, with Special Reference to Bone and Tooth Composition, The Journal of Agricultural Research, Vol. 46 No. 11, January 1- June 15, 1933 8. Taylor GE, Effect of fluorine ration in cattle ration: Experimental evidence indicated fluorine content of raw rock phosphate is the detrimental factor, Mich. Agr. Expt. Station Qrt. Bulletin 11, 101 - 104, 1929. 9. Aluminum Compounds - Review of Toxicological Literature, Abridged Final Report Prepared for Scott Masten, Ph.D., National Institute of Environmental Health Sciences, Contract No. N01-ES-65402, Submitted by Bonnie L. Carson, M.S. Integrated Laboratory Systems, October 2000. 10. Varner JA, Jensen KF, Horvath W, Isaacson RL, Chronic administration of aluminum-fluoride or sodium-fluoride to rats in drinking water: alterations in neuronal and cerebrovascular integrity, Brain Res. 1998 Feb 16;784(1-2):284-98 11. Isaacson RL, Varner JA, Jensen KF, Toxin-induced blood vessel inclusions caused by the chronic administration of aluminum and sodium fluoride and their implications for dementia, Ann N Y Acad Sci. 1997 Oct 15;825:152-66. 12. Varner JA, Horvath WJ, Huie CW, Naslund HR, Isaacson RL, Chronic aluminum fluoride administration, I. Behavioral observations, Behav Neural Biol. 1994 May;61(3):233-41. 13. Roholm K [1937]. Fluorine intoxication: A clinical hygiene study with a review of the literature and some experimental investigations, London, England: H.K. Lewis & Co. Professor of Chemistry, Paul Connett, and Ellen Connett, also wrote a tour de force. It can be read on the FluorideAlert website at http://www.fluoridealert.org/pesticides/Fluorides.Comments.ATSDR.02.htm

National Research Council of Canada NRC Associate Committee on Scientific Criteria for Environmental Quality Environmental Fluoride 1977 by Dyson Rose & John R. Marier National Research Council of Canada NRCC NO. 16081 ISSN 0316-0114
http://www.fluoridealert.org/NRC-Fluoride.htm

The Associate Committee on Scientific Criteria for Environmental Quality was established by the National Research Council of Canada in response to a mandate provided by the Federal Government to develop scientific guidelines for defining the quality of the environment. The concern of the NRC Associate Committee is strictly with scientific criteria. Pollution standards and objectives are the responsibility of the regulatory authorities and are set for the purpose of pollution control. These may be based on scientific criteria starting point but they also take into account the optimal socioeconomic impact of proposed measures as well as the state of existing technology. The Associate Committee's program includes the evaluation of available information on the probability of effects of contaminants on receptors together with the related fundamental principles and scientific knowledge. In this work particular attention is directed to receptors and contaminants (and their interactions) important to Canada. This Canadian approach is necessary because evaluations made in other countries or regions will not always be applicable to the particular circumstances prevailing in Canada. Members of the Associate Committee, its Subcommittees and Expert Panels, serve voluntarily and are selected for their individual competence and relevant experience with due consideration for a balance among all sectors in Canada. Responsibility for the quality of study documents rests with the Associate Committee. Each report is carefully reviewed according to a multi-stage procedure established and monitored by the National Research Council of Canada in order to preserve objectivity in presentation of the scientific knowledge. Publication and distribution of the report are undertaken only after completion of this review process.

Comments on Associate Committee documents are welcome and will be carefully reviewed by the Expert Panels. It is foreseen that these scientific criteria may be revised from time to time, as new knowledge becomes available. All documents published by the Associate Committee are published in both French and English.

FOREWORD This report was requested by the Management Subcommittee of NRC's Associate Committee on Scientific Criteria for Environmental Quality. Dr. Dyson Rose (retired), formerly of the National Research Council's Division of Biological Sciences, undertook the task of preparing this report, with assistance from J.R. Marier of NRC's Environmental Secretariat The report emphasizes Cause/Effect interrelations of environmental fluoride, and also attempts to identify deficiencies in the current scientific knowledge. The compilation covers the scientific literature that came to the authors' attention prior to June 30, 1977. The report has been reviewed by the members of the Management Subcommittee of NRC's ACSCEQ, and by the following individuals: Dr. J. Franke, Orthopedics Clinic, Martin Luther University, Halle, Wittenburg, DDR; Drs. C.C. Gordon and P.C. Tourangeau, Environmental Studies Laboratory, University of Montana, Missoula, U.S.A.; Dr. E. Groth, Environmental Studies Board, National Research Council, Washington, D.C., U.S.A.; Dr. R.J. Hall, Analytical Chemistry Department, U.K. Ministry of Agriculture, Fisheries, and Foods, Newcastle-upon-Tyne, England; Dr. S.S. Sidhu, Newfoundland Forest Research Centre, Canadian Forestry Service, Environment Canada, St. John's, Newfoundland, Canada. The authors wish to express their thanks to the members of the Management Subcommittee, and to the other reviewers, for the valuable comments received. However, we must emphasize that the viewpoints expressed in this report represent our own assessment of the environmental fluoride situation. The authors also wish to express their gratitude to Miss Lynda Boucher and Miss Pat Moss, for their sustained cooperation in typing this report.

Dyson Rose and J.R. Marier October 4, 1977

TABLE OF CONTENTS LIST OF TABLES LIST OF FIGURES INTRODUCTION 1.0 SOURCES AND DISTRIBUTION OF FLUORIDE POLLUTION 1.1 SOURCES 1.1.1 Atmospheric Emissions 1.1.2 Aqueous Discharges 1.1.3 Solid Wastes 1.2 DISTRIBUTION OF FLUORIDE 1.2.1 Airborne Fluoride 1.2.2 Water-borne Fluoride 2.0 EFFECTS OF FLUORIDE POLLUTION ON THE ENVIRONMENT, AND ON AGRICULTURE AND FORESTRY 2.1 EFFECTS ON VEGETATION 2.1.1 Aquatic Vegetation 2.1.2 Terrestrial Vegetation 2.1.2.1 Ecological Effects 2.1.2.2 Fluoride-Induced Effects on Agricultural and Forest Crops 2.1.3 Criteria for Crop Injury 2.2 EFFECTS ON ANIMALS 2.2.1 Aquatic Species 2.2.2 Insects 2.2.3 Wildlife 2.2.4 Livestock 3.0 PHYSIOLOGICAL EFFECTS OF FLUORIDE ON ANIMALS AND MAN 3.1 BLOOD

3.1.1 Fluoride Content of Blood 3.1.2 Effect of Fluoride on Blood Components 3.2 URINE 3.2.1 Fluoride Content of Urine 3.2.2 Effect of Fluoride on Urine Components 3.3 FLUORIDE-INDUCED CHANGES IN ENZYMES AND METABOLITES IN SOFT TISSUES 3.4 BONE 3.4.1 Fluoride Content of Bone 3.4.2 Fluoride Induced Changes in Bone 3.5 MUTAGENIC AND RELATED EFFECTS OF FLUORIDE 4.0 ORGANIC FLUORIINE COMPOUNDS 4.1 METHOXYFLURANE 4.2 OTHER ORGANOHALIDE ANASTHETICS 4.3 MISCELLANEOUS ORGANIC FLUORINE COMPOUNDS 5.0 FLUORIDE AND HUMAN ILLNESS 5.1 FLUORIDE INTAKE BY HUMANS 5.1.1 Intake From Foods and Beverages 5.1.2 Intake From Air 5.2 CARCINOGENIC IMPLICATIONS 5.3 OCCUPATIONAL FLUOROSIS 5.4 NEIGHBORHOOD FLUOROSIS 5.5 ENDEMIC FLUOROSIS (HYDROFLUOROSIS) 5.6 DIETARY-NUTRITIONAL DEFICIENCIES OR IMBALANCES AND FLUOROSIS 5.7 THYROID FUNCTION 5.8 KIDNEY RELATED PROBLEMS 5.9 ATTEMPTS TO ESTIMATE CRITERIA FOR HUMAN INTAKE OF FLUORIDE 5.9.1 Criteria Based on Bone Fluoride and Plasma F5.9.2 Assessment of Fluoride Intake From Air 6.0 OVERVIEW AND RECOMMENDED RESEARCH

REFERENCES

LIST OF TABLES (back to top) 1 - Total Fluoride Emissions to the Atmosphere by Canadian Industrial Sources in 1972 2 - Estimated Soluble Fluoride Emission Rates and Total Emissions for U.S. Industries, 1968 or 1970 Data 3 - Fluoride Emission Rates Collected from Various Reports on the Aluminum Industry 4 - Comparison of Fluoride Emission Rates in the Primary Aluminum Industry in Canada and the U.S. 5 - Fluoride Emissions from Phosphate Fertilizer Plants 6 - Volumes and Fluoride Contents of Some Industrial Waste Waters 7 - Fluoride Content of Water from the East Gallatin River, Montana 8 - Influence of Domestic and Industrial Sewage on the Fluoride Content of Rhine and Ham River Water 9 - Regression Equations Relating Airborne Fluoride Concentration to Plant Response 10 - Fluoride Content of Insects from Polluted and NonPolluted Areas of Montana 11 - Fluoride Content of Bones of Animals Collected in Non-polluted Areas of Montana 12 - Fluoride Levels in the Bones of Wild Birds from Non-polluted Areas 13 - Regression Equations Relating Plasma Ionic Fluoride Levels to Age in Adult Humans 14 - Mean Plasma Ionic Fluoride Levels for Humans Residing in Non-fluoridated and Fluoridated Communities 15 - Effect of Fluoride on the Levels of Various Blood Components in Experimental Animals 16 - Effect of Fluoride on the Levels of Various Blood Components in Humans 17 - Effect of Fluoride on Levels of Metabolites in, and Physiological Activities of, Animal Soft-Tissue Organs 18 - Effect of Fluoride on Some Physical Parameters of Animal Bones 19 - Recent Data Illustrating the Effects of Environmental Factors on the Range of Fluoride in Some Foods 20 - Recent Data on the Daily Intake of Fluoride by Children 21 - Recent Data on the Daily Intake of Fluoride by Adults 22 - The Percentage Contribution of Water and of Various Foods to the Fluoride Ingested by Humans 23 - Health Problems Among Residents Near Fluoride-Emitting Sources 24 - Symptoms Common to Both Fluoride Intoxication and Magnesium Deficiency 25 - Fluorosis in Persons Who Have the Diabetes Insipidus Syndrome

LIST OF FIGURES (back to top)

1 - An illustration of the atmospheric distribution of gaseous fluoride, in relation to elevation and distance from an industrial point source. (see figure) 2 - Influence of airborne gaseous fluoride on the yield of beans, strawberries, and oranges, as plotted from the data of several authors. (see figure) 3 - Influence of dietary fluoride on the weight-gain of young swine. (see figure) 4 - Interrelation between rib bone fluoride content, blood plasma F-, and fluoride intake from three daily meals. Data are for 55-year-old lifetime residents. (see figure)

INTRODUCTION (back to top) "Environmental Fluoride" (Marier and Rose 1971) was largely completed before the National Research Council, Canada, Associate Committee on Scientific Criteria for Environmental Quality had become operational. The document thus differs somewhat in format from later Associate Committees' documents. The relevant Subcommittee therefore requested another document on this topic. Comprehensive reviews on fluoride were published by the World Health Organization (WHO 1970), by the U.S. National Academy of Sciences (NAS 1971), and as "a nonexperimental dissertation on a topic dealing with political aspects of public policymaking on scientific issues" (Groth 1973). These three documents differ from one another in intent, but all agree on the need for further research on the effect of environmental fluoride. Thus the WHO (1970) report states: "Little is known about the in vivo effects of fluoride at the low levels occurring naturally in body-fluids and soft tissues on enzymes and the various facets of general metabolism in the living organism..." "However, the indices of early intoxication are poorly defined and this has resulted in an element of speculation and confusion about the toxic potentialities of the fluoride ion". Similar statements emphasizing the lack of precise knowledge are found elsewhere in the document. Similarily, the National Academy of Sciences document (NAS 1971) states: "The available information is insufficient in depth and scope to allow unequivocal statements to be made about the effects on plants of fluoride at low atmospheric concentrations. One reason for the lack of information is the paucity of experiments designed to relate air quality to effects on plants. A second is the lack of sufficient ambient-air monitoring in connection with field studies and surveys, due in part to the lack of accurate and precise methods for the separation and collection of particulate and gaseous fluorine compounds. A third reason is the inadequacy of present experimental techniques for long-term studies in which field conditions can be simulated".

"Unfortunately, many studies for a better evaluation of the effects of airborne fluoride on human health remain to be done. Not many authors have investigated the incidence and magnitude of effects on the thyroid gland, the hematopoietic system, the cardiovascular system, and the central nervous system. However, these systems respond readily to a number of stresses, not only to fluoride, and a causal relation to airborne fluoride has been established only poorly or not at all. More careful studies are required, with better attention being paid to the nature of the responses, the presence or absence of other medical or physical conditions that might contribute to the occurrence of the responses, and the proper control groups". "The airborne fluorides to which subjects are exposed must be better evaluated with respect to amounts of fluoride-containing material, proportions of gaseous and particulate fractions, chemical and physical properties (including particle size) of the particulate fraction, and meteorologic conditions in the surrounding community when resident populations are being studied". The third document (Groth 1973) presents the need for further research even more emphatically. Thus "...there have been very few studies of potential non-lethal effects of chronic accumulation of fluoride on populations exposed to lifetime ingestion". "Amounts of fluoride ingested by average adults are sufficient to produce chemical and structural changes in the mineral of the bones, and the long-term health significance of these changes is not known". "In short, there are a great many unanswered questions in regard to long-term potential adverse effects of fluoridation, and a number of indications of potential harm which have not been shown yet to be unfounded. In view of the seriousness of some of the possible consequences if fluoridated water is in fact harmful to a fraction of the population, extensive, continuing research would seem imperative. However, there are no ongoing large-scale efforts being made to carry out such research". During the seven year period (1970 to 1977) covered in the present document, there has been a voluminous output of literature related to fluoride pollution and fluoride toxicity to plants, animals and man. This has increased our general knowledge of the multiple effects of chronic exposure to fluoride, and has confirmed and possibly augmented the difficulties attending attempts to relate quantitatively exposure and time factors to effect. Nevertheless, a prime purpose of the present review is to identify criteria (dose-response relations) that may assist in establishing limits of exposure. A second purpose is to identify areas where additional research is urgent. In environmental studies, it is often necessary or convenient to investigate individual sources of fluoride and to focus on the level of fluoride acting through a particular pathway. For example, the pathway involving airborne fluoride, forages, and domestic cattle has been studied extensively. However, it is essential to remember that living

organisms respond to the total fluoride impact from all sources: plants are affected by fluorides in soil, water, and air; animals by fluorides in their forages, feed supplements and water; and man by fluorides in his foods, beverages, drugs and prophylactic agents, cigarettes, and air. Therefore a comprehensive assessment of the cumulative impact of fluorides on man's environment requires consideration of the total fluoride contributed by multiple sources. A serious effort has been made to consider all papers published since 1970 that are relevant to environmental fluoride. Because of the voluminous literature on the dental aspects of fluoride and on the freon-ozone argument, these two areas have been intentionally left for others to summarize and develop criteria. Papers on fluoride therapy in humans have been included only because data on high-dose, short-term effects appear relevant to chronic exposure (low-dose, long-term) situations. Reports on pollution control technology are considered to be outside the scope of this review. Sampling and analytical methodology are discussed only in relation to the interpretation of environmental effects. Undoubtedly we have overlooked valuable research papers particularly among those published in languages other than English and French; for this we apologize to the authors concerned. For conciseness and brevity, we have omitted specific reference to about half the papers we examined. 1.0 SOURCES AND DISTRIBUTION OF FLUORIDE POLLUTION (back to top) 1.1 SOURCES (back to top) The sources of fluoride in man's environment have been discussed by numerous authors (e.g. Marier and Rose 1971; NAS 1971; Bittel and Vaubert 1971; Prival and Fisher 1974; Bojic et al.1975). Sources of fluoride include natural sources such as volcanic gases, and soluble fluorides in the earth's crust. However, the pre- ponderance of pollution problems have been caused by modern-day man-made sources which singly, or in combination, occasionally lead to the presence of harmful levels of fluoride compounds in air, water, food or forage. In this section, we present data on the amounts of fluoride discharged from major man-made sources, and attempt to indicate the extent of the geographical areas affected by the fluoride discharges. Fluoride emission data from industrial sources are often circumscribed by industrial secrecy and by industries' ability to have environmentally-relevant data classified as proprietary to the industry. Also, governments have sometimes been loath to release data gathered at public expense as well as those submitted by industry. The rationale often given for this secrecy is that it allows decisions to be made in the absence of public clamor and emotionalism. Less rationally, it also denies the public's right to take part in decisions involving a balance of economic and environmental objectives. The secrecy situation in Great Britain has been discussed by Tinker (1972). Industrial and governmental secrecy has been detrimental to Canadian efforts to develop

criteria relating the concentration of pollutants to their effects. Thus the studies of LeBlanc and his students (1971, 1972) on the effects of air-borne fluorides on epiphytes and bryophytes could not be related to existing but secret data on fluoride concentrations in the air. Similarly, the author of a report on pollution in the Shawinigan and other areas of Quebec (Pellissier 1973) repeatedly comments on the non-availability of results from related air-monitoring programs. Sidhu and Roberts (1976) encountered a parallel situation in Newfoundland. 1.1.1 Atmospheric Emissions (back to top) In spite of the secrecy discussed above, some information on atmospheric fluoride emissions by industry has become available during recent years. Environment Canada (1976) published data on fluoride emissions to the atmosphere in Canada during 1972. A portion of the data is reproduced in Table 1 and shows that, with the exception of aluminum production, the fluoride emissions are preponderantly in gaseous form. The U.S. Environmental Protection Agency (EPA 1972) reported the corresponding U.S. data in considerable detail, and we present summarized data in Table 2. Unfortunately, the data in Table 1 and 2 are not directly comparable. Fluoride emissions into the atmosphere occur in gaseous and particulate forms, and the particulates vary in solubility. The solubility of the particulate matter has a marked influence on its toxicity to plants and animals (NAS 1971). Thus, the "Total soluble fluoride emissions" as recorded in Table 2 are more directly relevant to environmental-impact criteria than are either the "total" or "percent gaseous" data of Table 1. The primary aluminum reduction industry, which is the largest single-industry source of atmospheric fluoride pollution in Canada (Table 1), and the third largest in U.S., has been the subject of several studies. Data on the rates of fluoride emission (i.e. the amount of fluoride released to the atmosphere per unit of aluminum produced) are presented in Table 3. The low emission rates for recently constructed smelters are indicative of the progress being made in controlling atmospheric emissions by this industry. An interesting comparison can be made between the emissions from U.S. primary smelters in 1970 and those of Canadian smelters in 1972 (Table 4). Effluent fluorides, (i.e. total fluoride at source, before passage through emission control units) per unit of aluminum produced, are similar for Canadian and U.S. reduction lines. However, the average amount of fluoride emitted to the atmosphere, per ton of aluminum produced, is markedly higher for Canadian than for U.S. smelters. The steel industry, which is the major source of atmospheric fluorides in U.S. and third largest in Canada (Tables 1 and 2), does not appear to have been studied as intensively, regarding fluoride emissions, as the aluminum industry. In part, this is probably related to the presence of other pollutants besides fluoride in emissions from steel mills, and to the fact that attention has been primarily focussed on pollution by sulfur dioxide and particulate matter.

In relation to the phosphate industry, which is also a major source of fluoride emissions, Osag et al. (1976) have presented a comparison of "industry wide" and "best controlled" atmospheric emissions (Table 5). It is difficult to relate these data to the rate of emission (3.1 to 4.1 lb/ton of P205 equivalent) in Table 2, but it would appear that the data of Osag et al. refer only to specific steps in the process and not to overall emissions. They probably do not include emissions from the surface of gypsum ponds (King and Ferrell 1975).

Table 1. Total fluoride emissions to the atmosphere by Canadian industrial sources in 1972 (Environment Canada 1976) (back to top) Sector Total fluorides released (US tons) % of Canadian total 56.6% 17.1% 15.5% 3.4% % of gaseous fluoride in effluent 55 >96 80-85 70-75

INDUSTRY Primary aluminum production Phosphate fertilizer and elemental phosphorous plants Primary iron and steel production Miscellaneous sources FUEL COMBUSTION/STATIONARY SOURCES Power generation Industrial and commercial SOLID WASTE INCINERATION TOTAL EMISSIONS 8,852 2,668 2,418 534

1,006 162 4 15,644

6.4% 1.0% <0.1 100.0

>90 >90 >90

Table 2. Estimated soluble fluoride emission rates and totals for United States industries, 1968 or 1970 data (EPA 1972). (back to top) Industry Steel Coal combustion for power Phosphate rock processing Primary aluminum Heavy clay Rate 0.99 lb/ton ore 0.16 lb/ton coal 3.1 to 4.1 lb/ton P205 equiv 8.1 lb/ton prod. 0.81 lb/ton prod Total US tons 64,600 26,600 21,200 16,230 9,700 Reference page or table p. 3-64, Table 3-23 p. 3-131, p. 3132 Table 3-46 p. 3-21, Table 3-6 Table 3-87, p.

products Hydrofluoric acid prod HF alkylation process Expanded clay aggreg. Glass manufacture

4.1 lb/ton HF 0.15 lb/bbl alkylate 1.14 lb/ton aggreg. up to 17 lb/ton glass

8,840 7,000 5,300 3,330

3-249 Table 3-104 Table 3-101 Table 3-93 p. 3-220, calc. from Tables 373 and 3-75 Table 3-81, p. 3-235 Table 3-97 p. 3-307 p. 3-314 p. 3-311 p. 3-321 p. 3-322

Frit smelting Cement manufacture Non-ferrous metals, Copper Zinc Lead Uranium Aluminum anoding

180 lb/ton CaF2 0.008 lb/ton cement

700-840 270 634 246 210 55 + 18 up to 668

Table 3. Fluoride emission rates, in kg/metric ton, collected from various reports on the aluminum industry (back to top) Notes Sweden, newest installations U.S. new control technology Reported emissions rate, kg/metric tons 1.0 total F 0.25 gaseous F 0.64 solid F OECD countries, actual emission OECD, obtainable emissions U.S. U.S. best primary system Best primary & secondary system U.S., weighted average U.S., weighted average 6.1 total F 2.3 total F 4.1 soluble F 1.2-4.7 total F 0.8-2.0 total F 5.1 total F 2.1 gaseous F Singmaster and Breyer 1973, Table 7-1d EPA 1976 OECD 1972 EPA 1972 Rush et al. 1973 Reference Linberg 1971 Rosano and Pilet 1971

U.S. new construction

1.0 total F

Table 4. Comparison of fluoride emission rates in the primary aluminum industry in Canada and the U.S. (back to top) Canada 1972 904,491 (1) 14.1 (3) 6.6 20.7 4.9 (5) 4.0 8.9 United States 1970 3,614,545 (2) 13.1 (4) 8.8 22.5 2.7 (6) 3.2 5.8

Aluminum production, metric tons Effluent fluoride, pre-abatement, kg/metric ton Gaseous Particulate Total Fluoride atmospheric emissions, kg/metric ton Gaseous Particulate Total

(1) Personal communication, Statistic Canada. (2) Singmaster and Breyer 1973, Table 7.3. (3) Environment Canada 1976, p. 4. (4) Singmaster and Breyer 1973, Table 7. 1d, weighted average. (5) Calculated from data of Table 1 (this document), and total production. (6) Calculated from Singmaster and Breyer 1973, p. 7-12 totals.

Table 5. Fluoride emissions from phosphate fertilizer plants (Osag et al. 1976). (back to top) lb.F/U.S. ton of P2O5 Input Industry-wide Best Controlled 0.02-0.60 0.002-0.019 0.12 N/A 0.06-0.5 0.025-0.06 0.20-0.60 0.03-0.31 0.20-0.60 0.04-0.27

Fluoride Source Wet Process Phosphoric Acid Superphosphoric Acid Diammonium Phosphate Triple Superphosphate Granular Triple Superphosphate

In discussing the lesser sources of fluoride emissions shown in Table 1, the Environment Canada (1976) report notes that "It is not possible to rationalize" differences in the fluoride effluent data reported by the Canadian "clay products" industry and by the U.S. Environmental Protection Agency. Environment Canada's estimates of possible fluoride emissions by this source therefore vary from 274 to 2463 tons (249 to 2239 metric tons) in 1972 (Environment Canada 1976, their Table 7). The lower figure was used to calculate the "misc. sources" total shown in Table I .

Glass manufacturing firms in Canada are reported to have "almost totally phased out by 1972" the use of fluorspar as a flux. Fluoride emissions by this industry are therefore thought to be low, i.e. 5 tons (Environment Canada 1976, p. 14, 15). The Environment Canada (1976) report on fluoride emissions by the petroleum industry (hydrofluoric acid alkylation process) indicates an "HF consumption" of 0.3 to 0.8 lb HF/barrel of alkylate. Available information does not enable us to relate "consumption" to emission. However, if we assume that emissions occur at the same rate as in U.S. plants (Table 2), the estimated total 1972 emissions in Canada of "less than one ton" (Environment Canada 1976, D. 19) indicates a Canadian production of alkylate of less than 37 barrels per day. Data published by Energy, Mines and Resources of Canada (EMR 1973) indicate that Canadian HF-alkylation capacity was 13,470 barrels per day in 1972, and had increased to 24,620 barrels per day in 1975 (EMR 1976). Data on fluoride added to the atmosphere by domestic burning of coal in Canada are not available, but the amounts are probably small because of the extensive use of other fuels for domestic heating in Canada. The potential impact of domestic fuel burning on fluoride pollution should be considered if changes in fuel consumption patterns occur. Baum et al. (1972) report that 34 to 72% of the fluoride in coal, which varied from 0.0025 to 0.039% in the coals tested, was contained in the flue gases of an industrial type furnace. We have been unable to locate similar data for domestic-type furnaces. 1.1.2 Aqueous Discharges (back to top) Data on the volumes and concentrations of fluoride wastes being discharged to rivers, lakes and oceans are not plentiful. All wet-scrubbing systems for control of atmospheric emissions probably contribute some fluoride to the aqueous discharge, but economic factors often favor recovery of fluoride from the scrubbers (e.g. as precipitated calcium fluoride) and re-use of the water. Effluents and overflows from limed settling-ponds contribute fluoride to the aqueous environment. General discussions of problems related to pollution of waterways have been published by McCaull (1972) and Cheremisinoff and Habib (1973). Recent data on the volumes and fluoride contents of industrial waste waters (Table 6) make it evident that large quantities of fluoride are being discharged to waterways. For example, it can be calculated that if all North American plants discharge fluoride at the rate (14 kg/metric ton) reported by Teworte (1972), the total discharge by the aluminum industry would exceed 63,000 metric tons, or about 4-fold the amount discharged into the atmosphere. The production of uranium tetra- and hexa-fluorides involves the discharge of significant quantities (625 to 1134 tons per year in U.S.) of hydrofluoric acid by way of aqueous sewage (EPA 1972). Rak (1969) presented data on the discharge of fluoride in waste waters during production

of some inorganic fluoride compounds. The reported discharges ranged from 5.7 kg per metric ton of product for aluminum fluoride, to 55 kg/metric ton of product for cryolite. Pettyjohn (1975) has reported environmental damage caused by an unsuitable aqueous disposal method applied to steel industry "pickling wastes".

Table 6. Volumes and fluoride contents of some industrial waste waters. (back to top) Waste water Industry and location Volume F-content ppm Aluminum, 200,000 litres per metric 70 Germany ton A1 Phosphate fertilizer, 400 gpm (=90,800 1/hr) 35 U.S. Phosphate fertilizer, 13,240 1/hr 14-29 India Stainless steel, U.K. ? 8 Steek, U.S. ? 0.17 kg/metric ton of product

Reference Teworte 1972 Cheremisinoff and Habib 1973 Arora and Chattopadhya 1974 Jenkins 1972 McCaull 1972

1.1.3 Solid Wastes (back to top) Information on the disposal of solid wastes containing fluoride has not been found in any of the papers reviewed in the preparation of this document. Presumably, large quantities are used as landfill or buried (Williams 1975) and, since this practice is considered to be nonpolluting, the quantities involved are rarely reported. However, Stepanek et al. (1972) have reported contamination of surface and groundwaters by fluoride from solid wastes. Williams (1975) has given a brief report on solid wastes from the aluminum industry; individual smelters are reported to produce from 15 to 30 kg of calcium fluoride sludge per metric ton of aluminum produced (30 to 60 lb/ton). The disposal of high-fluoride solid wastes from the reprocessing of nuclear fuels has been studied by Emma et al. (1968) and by Fitzgerald et al. (1969). Combined chemical treatments to reduce fluoride volatility, along with sintering or canning, appear to be prerequisites to safe longterm disposal of these wastes. Polluted soil can also be considered as a form of solid waste. For land-locked factories, all of the air-borne emissions discussed above can be considered as eventual soil pollutants, except for the portion that is carried to rivers and lakes by run-off. This amounts to about 18,000 tons per year in North America (Tables 1 and 2). Soils can also become contaminated with fluoride when fertilizers containing fluoride are

used. The fluoride content of fertilizers varies widely (Ammerman 1974) depending on the method of processing and on the fluoride content of the phosphate raw material used (Forster 1969). Ammerman (1974) reported the following fluoride concentrations: Dicalcium phosphate 0.14% Triple superphosphate 1.87% Diammonium phosphate 2.00% Gordon (1970b) lists fluoride contents ranging from 0.58 to 2.34% for fertilizers sold in Montana. 1.2 DISTRIBUTION OF FLUORIDE (back to top) Reviews on fluoride and fluoride effects (WHO 1970; NAS 1971) usually stress that "fluoride is well-nigh ubiquitous: detectable traces occur in almost all substances" (Hodge and Smith 1977). This can be said about a great number of pollutants; nevertheless, this fact is relevant to a discussion of fluoride for two reasons: (1) it emphasizes the need to consider total fluoride from all sources when investigating fluoride injury to plants, animals and man; and (2) it often makes estimation of the role played by industrial fluoride pollution more difficult. Manmade fluoride pollution nearly always arises from a small geographic area or point-source and is detectable above the natural or background fluoride over a definable area. Assessment of the distribution and extent of these man-made fluoride anomalies is considered in this section. Attention will, of course, be focussed on soluble fluoride as this is the most environmentally-relevant form (cf. p. 10). 1.2.1 Airborne Fluoride (back to top) The presence of fluoride in rainwater collected in areas remote from human settlements (Carpenter 1969) suggests that air which has not been contaminated by human activity does contain some fluoride. However, ambient-air fluoride is usually below the level of detection, which can be roughly defined as less than 0.05 ug F/m3 air (Thompson et al. 1971). Natural phenomena such as dust storms and forest fires can contribute small amounts of soluble fluoride to the atmosphere. Volcanic activity can contribute larger amounts. However, except for unusual circumstances (e.g. volcanic activity), all soluble fluoride found in the atmosphere in excess of 0.05 ug/m3 can be assumed to have originated from man-made sources. From the above discussion, it miqht be concluded that the distribution and extent of abnormal fluoride concentrations arising from point-sources would be relatively easy to monitor. Unfortunately, however, man's activities are so widespread that background levels exceeding 0.05 ug/m3 are not rare, even in rural areas of industrialized countries. The spread of pollution from a major source often must be determined against a somewhat variable background level arising from multiple minor sources (e.g. domestic coal burning) and from distant major sources (Fischer and Brantner 1972). Thompson et al. (1971) reported data on 9,175 air samples collected in various non-industrial urban

sites and 2,164 samples from non-urban sites. The distributions, as percentages found within the limits (ug/m3) shown, were: urban = 88% < 0.05; 12% between 0.05 and 1.0; 0.2% > 1.0; non-urban 98.5% < 0.05; 1.5% between 0.05 and 1.0; 0.14% > 1.0. Davison et al. (1973) reported that only a small percentage of urban air samples from Northumberland contained < 0.05 ug F/m3, and that the average fluoride level was 0.28 pg/m3. On the other hand, "most" air samples from rural sites contained < 0.05 ug F/m3 even though 19% of the samples exceeded the 0.1 ug/m3 level. Data which have become available since 1970 confirm the presence of abnormally high airborne fluoride concentrations in association with many of the industries for which fluoride emissions are shown in Table 2. Peak fluoride concentrations within these highfluoride zones are rarely available, because they occur over company-owned land. In a study of the effectiveness of potroom ventilization, Sutter (1973) recorded mean daily atmospheric concentrations (aluminum industry) of 540 to 3700 ug F/m3. In a study of fluoride emissions from an openhearth (steel smelter) furnace with an electrostatic precipitator, Brown et al. (1971) presented the data shown in Fig. 1. These data are no longer representative of this particular smelter, because the operating procedure has been changed (Schuldt 1977). They do, however, indicate the high concentrations and the atmospheric stratification that can occur within a few hundred feet of a point-source of fluoride emissions. The stratification was still apparent 12,000 feet (3.6 km) from the source (Fig. 1). Data for airborne fluoride concentrations in areas surrounding fluoride-emitting factories have been presented in numerous reports. These include data gathered by static and dynamic air sampling devices (IJC 1971; Linzon 1971; Bourbon et al. 1971) and by analysis of vegetation (Linzon 1971; Gilbert 1971; Carlson 1972; Gordon 1970a, 1976; Keller 1975; Jacobson and Weinstein 1977; Sidhu 1977a). The studies of C.C. Gordon and his co-workers at the University of Montana (Gordon and Tourangeau 1977; Tourangeau et al. 1977) are particularly important because of their contribution to our knowledge of "shielding" effects. These studies clearly demonstrate that vegetation tends to impede or intercept fluoride in air that is moving through the foliage, thus creating an adjacent down-wind area of lower airborne fluoride concentration. (Little or no effect of this sort was observed with sulfur dioxide). The effect is so marked with airborne fluoride that samples of needles taken from the upper, windward side of a pine tree exposed to atmospheric fluoride will consistently contain 2to 4-fold more fluoride than found in equal-age needles from the lower, lee side of the same tree. The effect becomes even more marked when windward and leeward sides of a small grove are compared; also, groundcover vegetation under a stand of pines may contain little fluoride, even in areas that are obviously polluted. Terrain elevations that allow unimpeded impact by airborne fluoride result in an increased amount of fluoride in exposed vegetation (Note also the stratification effect illustrated in Fig. 1). Sidhu (1977b) has similarly observed the effects of terrain elevation and shielding in a fluoride-polluted Canadian coniferous forest. However, to ensure consistency of sampling, he recommends collection of foliage samples from the windward side of the

mid-crown, "because defoliation occurred in the upper crown". In a study of the fluoride content of lichens, Gilbert (1971) observed that even a boulder provided some shielding from fluoride carried by prevailing winds. These observations make the siting of air-sampling devices and the collecting-points for vegetation extremely critical. Gordon and Tourangeau (1977) recommend that the sites for air-sampling devices for Maryland farmlands be "in the middle of open fields, ... one to two feet (0.3 to 0.6 m) above the height of corn crops and away from stands of hard woods which impede or intercept the fluoride-polluted winds". Samples of agricultural crops should be taken from parts of the field that are 50 ft (15 m) or more from hedgerows or other vegetation that is taller than the crops. In non-agricultural areas, sampling should be from near the top of windward slopes, at a height sufficient to be clear of any screening by vegetation. The fluoride content of vegetation varies with the plant species and variety, and with the stage of development (Chang 1975; Weinstein 1977). It is also influenced by the plant tissue sampled (leaf, fruit, etc.), the age of individual leaves or needles (Chang 1975; Gordon 1976), the location of sampled foliage on the plant (Gordon 1976), and the season (Harris 1974). All these factors must be considered when sampling vegetation as a means of monitoring fluoride in air. [See Guderian and Schoenbeck (1971), Teulon (1971), and Sidhu (1977a) for a discussion of other aspects of the methodology.] Uptake from the soil must also be considered (Weinstein 1977). When the above factors are taken into consideration in the planning of a study, reliable data on the extent, concentration and distribution of a man-made atmospheric fluoride anomaly can be determined with reasonable accuracy, even against an urban fluoride background. These factors are influenced by pollution loading, wind velocity and constancy, other meteorological conditions, and geographic factors. Some examples of airborne fluoride discharges are given herein. Preference has been given to Canadian data. Gilbert (1971) studied fluoride levels around a small (20,000 tons per year) aluminum smelter in Scotland. On the basis of an average rate of emission for smelters in O.E.C.D. countries of 6.1 kg F per metric ton of aluminum (OECD 1972), the total discharge would have been only 123 metric tons (135 short tons) per year of total fluoride. The smelter was surrounded by a "bryophyte desert" about 0.5 mile (0.8 km) wide and extending about 1 mile (1.6 km) downwind and 0.7 mile (1.1 km) upwind. This, in turn, was surrounded by a further area of damage, and elevated fluoride levels in vegetation were observed 4.3 miles (6.9 km) downwind. LeBlanc and co-workers (1971, 1972, 1975) studied epiphytes in the proximity of a Canadian aluminum smelter with an unspecified (proprietary company data) amount of atmospheric fluoride discharge. The area of vegetative disturbance, as indicated by an "Index of Atmospheric Purity" based on species frequencies, extended 10 km (6.2 miles) downwind.

Carlson and Dewey (1971), Carlson (1972), and Harris (1974) have reported extensively on the distribution of atmospheric fluoride discharged by an Anaconda aluminum smelter in Flathead County, Montana. In spite of assurances by the company that vegetation damage would not occur (Burk 1972), this smelter had a 10-year history of causing foliage injury in the surrounding territory. Nevertheless, the smelter capacity was greatly expanded between 1965 and 1970. By 1970, foliar material from various species contained fluoride levels in excess of background values (i.e. greater than 10 ppm, dry weight basis) over a 213,760 acre (86,570 hectare) area. Extensive injury, and foliar fluoride concentrations above 30 ppm, were observed over a 69,120 acre (27,994 ha) area. During 1970, this Anaconda plant installed fluoride emission control equipment that reportedly reduced emissions from 7,500 to 2,500 lb (3,410 to 1,136 kg) per day. A subsequent survey showed above-normal (> 10 ppm) fluoride in 1971 foliage over an area of 179,200 acres (72,575 ha) along with serious injury and > 30 ppm fluoride in foliage over 15,200 acres (6,156 ha). Sidhu and Roberts (1976) reported damage and high foliar fluoride concentrations in the vicinity of a Canadian phosphorus plant. The total area affected was 11,434 ha (28,242 acres), but fluoride emission data were "confidential to the industry". However, in a subsequent paper, Sidhu (1977a) reported airborne fluoride concentrations ranging from 0.8 to 20.8 ug/m3 at a 3 0.7 km distance from this factory, and concentrations of 0.06 to 0.34 ug/m at 18.7 km. Preliminary data have also become available concerning fluoride distribution around an aluminum reduction site at Kitimat B.C. (Gordon 1976). At a production rate of 250,000 tons aluminum per year, and a reported emission rate of 5 to 7 lb F/ton Al, total fluoride emissions are estimated at 625 to 875 tons (568 to 795 metric tons) per year or 3,425 to 4,795 lb/day (1,556 to 2,180 kg/day). The data available are insufficient to define the totality of the area affected by these emissions, but "a twenty-plus square mile 'death band' of dead timber trees" (5,180 ha) is reported. Foliage collected from coniferous trees 5, 10, 11, and 20 miles north of the smelter contained higher fluoride levels than Gordon had observed at these distances around other aluminum plants. Fischer and Brantner (1972) studied the fluoride content of beech (Fagus silvatica) leaves in Austrian urban areas of heavy and moderate air pollution, and in open country. Fluoride levels of less than 10 ppm were common in leaves from unpolluted areas. Fluoride levels in leaves from urban areas were up to 47 ppm. Even in wooded areas outside the city limits, fluoride levels well above 10 ppm were encountered at "fronts of collision which were caused by the particular meterological conditions" in the area. 1.2.2 Water-borne Fluoride (back to top) The "average dissolved fluoride content of the major rivers of the world is fairly well defined at 0.01 to 0.02 ppm" (Carpenter 1969). Atmospheric dusts are thought to be the major sources of this "background" fluoride, although the source of a large portion of the fluoride-containing atmospheric dust is a subject of some dispute (Carpenter 1969, Bressan et al. 1974). Leaching of fluoride from rocks increases the fluoride content of

ground waters, but under the conditions observed by Jacks (1973), this source contributed little fluoride to surface waters. The contribution of domestic sewage from cities to the fluoride content of rivers was studied by Masudo (1964). The amount of fluoride found in effluent sewage, in excess of the amounts present in the cities' water supplies, were as follows: Raw sewage ( 4 cities) 1.30 mg/l After primary treatment (23 cities) 1.28 mg/l After secondary treatment (29 cities) 0.39 mg/l Fluoride is considered to be a "difficult to treat" industrial waste (Environment Canada 1975). Soltero (1969) and Bahls (1973) reported fluoride concentrations in the East Gallatin river (Table 7). These data show that elevated fluoride caused by sewage discharge from the city of Bozeman was detectable for a distance of 4 km below the sewage outlet.

Table 7. Fluoride content of water from East Gallatin River, Montana. (back to top) Fluoride content, mg/l Bahls 1973 Average 0.33 0.62 6.1 0.58 4.6 0.37 3.6 0.20-0.55 0.27-2.00

Sampling Location Above sewer outlet Sewage 0.3 km below outlet 1.8 km below outlet 2.2 km below outlet 4.2 km below outlet 5.3 km below outlet 8.2 km below outlet

Soltero 1969 Average 3.8 * 16.5

Bahls 1973 Range 0.14-0.57 0.27-2.00

* Soltero (1969) reported the data in meq/l; it appears probable that his data are too high by a factor of 10.

A study of fluoride input into Narragansett Bay, Rhode Island (reviewed by Groth 1975b) indicated that "36% of the fluoride entering the Bay was due to fluoridation of water supplies in five communities on rivers feeding into the estuary". Data on the fluoride content of the Rhine (Teworte 1972) and Ham (Lee and Whang 1972) rivers (Table 8) also indicate that both domestic and industrial sewage contribute significantly to the total fluoride content. Seepage and leaching from solid and liquid

waste disposal sites can also cause serious pollution of run-off and ground waters (Stepanek et al. 1972; Pettyjohn 1975).

Table 8. Influence of domestic and industrial sewage on the fluoride content of Rhine and Ham River water. (back to top) F-content, mg/l Average Range 0.12 .12 .20 .26 .10-.14 .09-.18 .19-.27 .21-.38 Teworte 1970 0.20 0.22 0.30 to 0.35

Sampling sites HAM RIVER Main Stream City water reservoirs Tributary water, residential areas Tributary water, industrial areas RHINE RIVER at Rheinfeld below Al smelter at Dutch border

Reference Lee and Whang 1972

The distribution of fluoride released into flowing bodies of water such as rivers is usually detectable on the basis of differentials between the fluoride content of samples taken above and below the known or suspected source of pollution. However, lakes, bays, and inlets can present a more difficult problem, although comparative analyses (i.e. in relation to input-sources) can provide meaningful information on the degree and extent of a contaminated zone. Ocean water has a nearly constant fluoride content of 1.35 to 1.4 mg total fluoride/litre, (Carpenter 1969; Bewers 1971), and a fluoride-to-chloride ratio of 6.71 0.07 x 10 5:1 (Warner and Jones 1975). Theoretically, inflow of fluoridecontaminated river water should be detectable as a change in the F:Cl ratio. However, if an ion-specific electrode is used to determine fluoride in brackish or ocean water, it is necessary to correct the observed fluoride ion activities for the complexing effect of magnesium (Thompson 1967; Brewer et al. 1970). Use of the F:Cl ratio has provided considerable information showing fluoride pollution of estuaries and ocean-bays. For example, Kitano and Furukawa (1972) determined the fluoride-to-chloride ratio, to estimate fluoride pollution in Tokyo Bay. Fluoride concentrations in contaminated inflowing waters ranged from 0.15 to 1.07 mg/l, with F:Cl ratios of 1.4 x 10-4 to 3.6 X 10-2:1. Surface samples from the bay contained from 0.63 to 1.28 mg F/kg water, and the F:Cl ratio varied from normal (i.e. 6.71 X 10-5) up to 9.05 x 10-5:1. Values above 7.1 x 10-5 were encountered at 11 sampling points (mostly surface) in the western half of the Bay, but not at sampling points in the eastern half which is influenced by incoming seawater.

The distribution of waterborne fluoride discharged from the aluminum reduction plant at Kitimat, B.C., has led to abnormally-high F:Cl ratios throughout the surface waters of Kitimat Harbour (Harbo e,t al. 1974). Observed F.-Cl ratios ranged from 13 to 1,500 x 10-5 (av. 158 X 10-5) and fluoride concentrations ranged from 0.10 to 11.0 mg/l (av. 1.17). Occasional high F:Cl ratios were also encountered in subsurface waters at depths from 10 to 100 m (av. 7.61 x 10-5; range 6.64 to 15.0 X 10-5). Comparable samples taken from Howe Sound "where input of non-natural fluoride is not known to occur" had F:Cl ratios ranging from 7.8 to 66 X 10-5, av. 14.5 x 10-5 for surface samples; and from 6.55 to 7.42 x 10-5, av. 6.83 x 10-5 for subsurface samples. No investigation of the factors causing high F:Cl ratios in surface waters of Howe Sound was reported. An interesting but incomplete study of water-borne fluoride has been reported for Tampa Bay, Fla. (Taft and Martin 1974). In July 1973, a phosphate plant was discharging an estimated 24,000 lbs (10,900 kg) of fluorine daily, along with quantities of phosphate and nitrate, into Tampa Bay. This resulted in deposition of solid calcium fluoride at the point of discharge and for about 1,000 ft. (300 m) into the bay. The precipitate accounted for only a small portion of the total fluoride in the discharge. Fluoride concentrations in samples of surface water above the fluorite deposit varied between 16.3 and 36.5 ppm. No data were presented for a more extended area of the Bay. Nevertheless, a severe thermal effect was generated at the fluorite:water interface, and this caused a significant increase in the temperature of the surface water. The authors also reported the absence of all living organisms in the afflicted area. The effect of fluoride on aquatic life is discussed in Sections 2.1.1 and 2.2.1. 2.0 EFFECTS OF FLUORIDE POLLUTION ON THE ENVIRONMENT, AND ON AGRICULTURE AND FORESTRY (back to top) The sources of man-made fluoride pollution discussed in Section I result in above-normal concentrations which impinge on terrestrial and aquatic flora and fauna, and on man. The exposure of living organisms to above-normal concentrations of fluoride, which induces fluoride accumulation by the organism, may result in an alteration of the organism's biochemistry and morphology. Directly or indirectly, such changes may restrict the organism's ability to maintain its ecological position. In the plant kingdom, an example of this has been provided by McLaughlin and Barnes (1975) who observed that fluoride accumulation in the foliage of some pines and hardwoods reduced photosynthesis and stimulated dark respiration, thus undoubtedly reducing the amount of carbohydrate available for growth and seed production. In the animal kingdom, Gerdes et al. (1971b) report that exposure of fruit flies to low levels of atmospheric fluoride significantly reduced the fecundity and egg hatchability of the descendants who were not themselves exposed to fluoride. Some published data suggest that exposure to low levels of airborne fluoride can stimulate the growth of some plants (cf. Weinstein 1977). Bennett et al. (1974) suggest that a low level of fluoride and of ozone was the norm under which plants evolved, and

that in tests on the effects of exposure to fluoride the "control" plants should not be grown in fluoride-free air. However, growth that occurs as a result of fluoride stimulation is often abnormal (Weinstein 1977). Even the growth stimulation that resulted in an increased fresh weight in bean plants (Pack 1971a) did not result in an increased yield of beans, and the ripened beans produced by exposed plants developed less vigorous seedlings than did beans from control plants (Pack 1971b). It is thus doubtful that the apparent growth stimulation occasionally observed on exposure of plants to low levels of atmospheric fluoride is of any evolutionary, ecological, or economic advantage. 2.1 EFFECTS ON VEGETATION (back to top) 2.1.1 Aquatic Vegetation (back to top) Available data on the responses of aquatic vegetation to fluoride pollution have been briefly reviewed by Groth (1975a, b). The data are insufficient to allow firm conclusions to be drawn, but do indicate that levels as low as 2 ppm in water can decrease the growth of one species of Chlorella. The data also show that many aquatic plants accumulate fluoride to concentrations that may be many-fold higher than the external concentration. Ishio and Makagawa (1971) report that Potphyxix tenaa, an alga, was killed by a 4-hour laboratory fumigation with fluoride (1.8 ppm in head space of growth chamber) and that the critical concentration appeared to be 0.9 ppm. Kilham and Hecky (1973) have discussed possible ecological effects of relatively high natural fluoride levels in African lakes. The accumulation of fluoride by aquatic plants and plankton is of interest because of its potential impact on animals that consume these organisms. In an unpolluted area of New Zealand, Stewart et al. (1974) observed fluoride levels from 31 to 209 ppm in the shells of species feeding on plankton, and from 1,425 to 1,882 in the skeleton of Blue cod that feed on crabs, shrimp, shell-fish, etc. The data suggest that, for the stages mentioned above, the food-chain concentration factor is at least 10:1. As noted by Groth (1975b), "we have very little knowledge of the sublethal effects of fluoride on behaviour or reproductive processes, or of the potential accumulation of the pollutant in aquatic foodchains. Yet such effects, should they occur, would probably be more important ecologically than the mortality which might result from very high, but short lived, pollution episodes". 2.1.2 Terrestrial Vegetation (back to top) Dochinger (1971) dates the awareness of fluoride-induced damage caused in terrestrial vegetation back to German reports of the 1880's and states that "For the last 30 years, the injury to agriculture by fluorine compounds has intensified because of the expansion of industries ...." Bossavy (1971) has summarized estimates of the damage occurring primarily to forests, in European countries.

Literature on the biochemical and morphological changes caused by exposure of terrestrial vegetation to fluoride has been reviewed by McCune and Weinstein (1971), Chang (1975) and Weinstein (1977). For consideration of some other aspects of the effects of fluoride on plants, such as the uptake of fluoride from soils, the influence of environmental factors on the uptake of airborne fluoride, etc., the reader is referred to Marier and Rose (1971), NAS (1971), Treshow (1971), Miller and McBride (1975) and Weinstein (1977). Terrestrial plants exposed to airborne fluoride frequently display foliar damage, sometimes grow less vigorously, and almost invariably accumulate significant amounts of fluoride in their foliage. These effects are all of aesthetic, economic or environmental significance. The interrelations among, and criteria for, each of these factors will therefore be considered with regard to airborne fluoride concentrations. 2.1.2.1 Ecological Effects (back to top) As noted above, it can be assumed that many of the fluoride-induced changes occurring in vegetation will decrease the plant's ability to maintain its ecological position. However, studies of the actual ecological effects have rarely been undertaken. Coniferous trees seem to be the most seriously affected forest species in many situations (Gordon 1976; Tourangeau et al. 1977; Carlson and Dewey 1971). Moreover, fluoride-induced changes in relative species dominance have been confirmed by Sidhu (1977b), who also commented that: "Preliminary results of a recent long-term study of the effects of fluoride on forest vegetation in Newfoundland showed that the softwood tree canopy (balsam fir, black spruce, larch) was being replaced by undergrowth of hardwoods (white birch, American ash). As the mortality of the original tree cover (softwoods) continued, the shrub layer showed a significant increase in raspberry, skunkcurrant, calamagrostis, and fireweed, underneath the hardwood tree species. Hardwood species (which defoliate every year) tend to accumulate fluorides at higher concentrations and at a faster rate than the softwoods. Therefore, it is suspected that the change from soft- to hardwood tree cover will result in the addition of higher amounts of fluoride to the soil. Also, the wildlife of the area feeding on the hardwoods will experience fluoride toxicity within a shorter period and over larger affected areas." Although epiphytes and bryophytes are considered more tolerant to fluoride than conifer species (Sidhu 1977b), alterations in species frequency among these organisms have been observed (LeBlanc et al. 1971, 1972; Gilbert 1971). LeBlanc et al. (1972) report that a few species such as Frullania ebotrancensis, Lecanora impudens, and Physcia ciliata could not be found within a 12 km (7.5 miles) distance from a fluoride source, although they were prevalent in the surrounding territory. Even the species that were able to maintain themselves close to the source were up to five times more plentiful beyond the pollution zone. Gilbert (1971 also reported complete absence of a Lecanora species in a fluoride-polluted area.

It should also be noted that if fluoride is injurious to pollinating insects (see Section 2.2.2), this could result in an indirect, but potentially extensive, effect on some ecological communities. 2.1.2.2 Fluoride-induced Effects on Agricultural and Forest Crops (back to top) Information on fluoride-induced injury to vegetation, which is often not directly applicable to the development of criteria, has appeared in numerous reports. This information is nevertheless important for an overall concept of fluoride phytotoxicity, and is therefore briefly reviewed. Bennett and Hill (1973) exposed 4- to 8-week-old barley and alfalfa plants to hydrogen fluoride in fumigation chambers for a single 2-hour period, and measured carbon dioxide uptake as an index of photosynthesis. With this short exposure period, 50 ppb HF were required "before clearly measurable inhibition of the net carbon dioxide rates occurred". The percentage inhibition of apparent photosynthesis was linearly related to HF concentration throughout the range from 0 to 250 ppb, with no evidence of a no-effect threshold within the accuracy of the measurements. Poovaiah and Wiebe (1973) noted that fumigation of soybean plants with low (15 to 20 ppb) concentrations of HF for 1 to 4 hours caused stomatal closing, reduced transpiration, and increased leaf temperature. McLaughlin and Barnes (1975) report that trees which had accumulated 10 to 60 ug fluoride per g dry weight of leaf tissue (from sodium fluoride in an aqueous spray) had a reduced rate of photosynthesis and an increased rate of dark respiration. Bale and Hart (1973a, b) exposed seedling roots of barley (Hordeum vulgare) to solutions containing 1 x 10-2, 1 x 10-4 and 1 x 10-6 M (190, 1.9 and 0.019 ppm) fluoride (as NaF or HF) for 12 to 72 hours and examined dividing cells for chromosomal aberrations. They concluded that "it is clear that each of the concentrations of sodium fluoride and hydrofluoric acid used in these experiments is capable of inducing chromosomal abnormalities and of producing mitotic inhibition in the meristematic region of roots". Pack (1971a, b) grew beans from seedling to maturity in the presence of 0.58 to 10.5 ug fluoride/m3 air, then grew a second generation, without exposure to fluoride, from the seeds of these plants. Exposure of the first generation to as little as 2.1 ug F/m3 caused the development of less vigorous second-generation seedlings. Vins and Mrkva (1973) report a decrease of 30 to 70% in the diameter growth of pine trees at pollution levels that caused no otherwise-visible injury. These authors relate the decreased growth primarily to sulfur dioxide pollution, but there is an interesting relation between increasing fluoride emissions between 1960 and 1967 (their Fig. 1) and the rapid decline in annual diameter increments (their Fig. 5) during this same period. (NOTE: See also Carlson, C.E., and Hammar, W.P. 1976. Impact of fluorides and insects on radial growth of lodgepole pine. Proc. Montana Acad. Sci. 35: 39.) Facteau et al. (1973) reported that the growth of pollen tubes in the styles of cherry blossoms was decreased by fumigation with hydrogen fluoride either before or after pollination. Pollen tube length, expressed as a percent of style length 72 hours after

fumigation, decreased linearly as a function of the product of exposure-time and atmospheric fluoride level. A somewhat similar result was obtained in studies with apricot flowers (Facteau and Rowe 1977). Fluoride-induced reduction in pollen germination and tube growth has also been observed in tomato and cucumber plants (Sulzbach and Pack 1972) while inhibited seed production or fruiting has been reported, with soybean, bell-pepper, sweet corn, and cucumber being more susceptible than pea, grain sorghum, or wheat (Pack and Sulzbach 1976). Conover and Poole (1971) found that cuttings of Cordyline terminalis var "Baby Doll", a horticultural foliage plant, suffered serious (approaching 50%) leaf necrosis when set for rooting in water containing 0.5 ppm fluoride. "Soft-suture" of peaches is the "best known example of fluoride injury to fruit" (NAS 1971). Facteau and Rowe (1976) were able to induce this injury in Elberta peaches by spraying the trees at weekly intervals with 0.025% ammonium fluoride solution. Maclean et ae. (1976) conclude that hydrogen fluoride (0, 5.0 and 9.7 ug F/m3 for 7 days) was more phytotoxic to tomato plants grown in magnesium-deficient media than to those grown in complete media. Similarly, Pack and Sulzback (1976) have demonstrated how calcium nutrition can influence the response of plants to airborne gaseous fluoride. Pilet and Bejaoui (1975) report that fluoride added to the culture medium for Rubus hispidus tissues markedly reduced oxygen absorption by the tissues, particularly in media deficient in calcium and magnesium. Increased levels of calcium and magnesium had a protective action, in that they lessened the degree of fluoride inhibition of oxygen absorption. The concept that vegetation may be stressed by pollutants present at levels that induce relatively minor injury, or even at levels that do not induce detectable injury in normal healthy plants, requires further study. The importance of this concept relates to the possible summing of stresses from various sources, with the total stress inducing an injury that cannot be easily related to any one cause. Evidence of such stress-induced injuries resulting from multiple causes is difficult to establish experimentally, but the effect of magnesium deficiency discussed above (MacLean et al. 1976) is probably a dual-stress phenomenon. However, in foliage, there can also be an in situ effect of fluoride on magnesium. In a study of air pollution, Garrec et al. (1977) observed that fluoride accumulation led to a depletion in the magnesium content of pine needles; in addition, there was a similar depletion in foliar manganese content. Probably the most striking example of multi-stress effects is to be found in studies of the relation between atmospheric pollution and insect infestations of forest species. The hostparasite relation is complex, and as noted by Heagle (1973), the presence of an atmospheric pollutant may act to either the advantage or disadvantage of the insect. However, studies of forest species under field conditions have demonstrated that the stress placed on trees by pollutants can increase the degree of infestation by insects. Heagle (1973) states that "A common finding is that trees injured and weakened by pollutants are more likely to be attacked by insects that normally require weakened trees

for successful reproduction". Jensen (1975) notes that "Some evidence has been provided that air-pollution stress can initiate and/or aggravate insect infestation and microbial infection of woody plants". Hay (1975) states that "Insects and mites have been implicated as a stress factor on trees being influenced by pollutant emissions". Most of the above statements have been made relative to pollutants in general, but the work of Carlson et al. (1971, 1974) and of Carlson and Hammer (1974) shows that atmospheric fluoride induces an insect-favouring stress in forest trees. Failure to recognize this stress-factor led prior investigators to incorrectly diagnose a combined fluoride injury and insect attack in the "death-band area" near Kitimat, B.C. (Gordon 1976). When pollutants act in combination, each exerts its own stress, and each can influence a different metabolic function. Thus, the effects of exposure to sulfur dioxide and gaseous fluoride mixtures induced additive effects on citrus species, but may have induced greater-than-additive effects on Zea mays and Hordium vutgare (Reinert et al. 1975). In apricot orchards, trees that were stressed by competition from weeds showed more leaf damage from airborne fluoride than did trees from well-tended plots (Oelschlager and Moser 1969). Fluoride-induced stresses undoubtedly affect vegetation in diverse ways, depending on the species and conditions. One possible mode of action in coniferous trees has been noted by Bligny et al. (1973) who report that exposure to fluoride delayed the formation of epicuticular waxes on the lower surfaces of Abus alba needles. This could increase water loss from the needles, and also increase their susceptibility to invasion by parasitic organisms. Keller and Schwager (1971) have attempted to relate fluoride-induced stress to an increased activity of an enzyme (peroxidase). Yee-Meiler (1974) has shown an increased phenolic content of Norway spruce subjected to "physiologischen Schadigungen" by fluoride (0.257 mg F/dm2 per 30 days). Fluoride concentrations expressed in ug/dm2 per day or month refer to data collected by exposing lime-filter papers to ambient air for the started time. Marier and Rose (1971), using the greenhouse data of Adams (1961), suggested conversion by the equation: Airborne F(ug/m3) = 0.006 x lime-paper (ug F/dm2 per month). Israel (1974a) has compared results based on field trials, and suggested the equation: Airborne F(ug/m3) = 0.003 x lime-paper (ug F/dm2 per month). Israel's estimate of the accuracy of the conversion is + 50%. The difference in conversion factors (0.006 vs 0.003) may relate to differences in air velocity across the lime-paper (Israel 1974a).

More recent, Sidhu (1977a) has also conducted a field-study intercomparison, and has proposed an equation that can be expressed as follows: Airborne F(ug/m3) = 0.0076 x lime-paper (ug F/dm2 per month), which yields values 2 1/2 times higher than Israel's, but only about 25% higher than the Adams equation proposed by Marier and Rose (1971). Furthermore, Sidhu (1977a) concludes that "In the absence of a more reliable and accurate regression equation, Adams' equation can be used to convert the fluoridation plate data to the ug F/m3." 2.1.3 Criteria for Crop Injury (back to top) Regression equations calculated from data presented in recent papers and which indicate mathematical relations between yield and airborne fluoride; or yield and foliar fluoride; or foliar fluoride, airborne fluoride and exposure time, are presented in Table 9. The yield vs airborne fluoride data are also presented in Fig. 2. Because of the small number of data-points available, some of these regressions do not achieve statistical significance. However, taken as a group, they reveal a consistent pattern of increasingly harmful effects with increasing exposure of vegetation to fluoride. Significant correlations between airborne fluoride levels and foliar fluoride concentrations ("C" and 'T' in Table 9) are difficult to attain under field conditions. However, if close attention is paid to the location of sampling sites and to the selection of foliage of uniform age from specific species and varieties, such correlations can be achieved. The correlation coefficient for Linzon's (1971) data (Table 9) is 0.48. In controlled greenhouse studies, the concentration of fluoride and the age of foliage are usually controllable factors; under these conditions, the time of exposure can be included as a component of the regression equation [data of McCune and Hitchcock (1971) and MacLean and Schneider (1973) in Table 9]. The data on the yield of oranqes (Leonard and Graves 1970, 1972) shown in Table 9 and Fig. 2, were for trees exposed for 28 months in field shelters with low ambient levels of fluoride pollution (i.e. 0.1 to 0.4 ug/m3). Data for beans (Pack 1971a) were from a 70-day greenhouse study at high levels of airborne fluoride. Both indicate a severe loss of yield with increasing fluoride levels, i.e. approximately 19% per 0.1 ug/m3 for oranges, and 3% per ug/m 3 (approximately 1.2 ppb) for beans. The data on strawberries (Pack 1972) are from a 5-month greenhouse study, and indicate about a 5% loss in weight of individual fruits per ug/m3 increase in airborne fluoride. This loss in yield (fruit set does not appear to have been affected) was accompanied by a statistically significant decline in fruit quality, as indicated by the "development rating" assigned by the original author. Yield of oranges in field shelters was also related to the fluoride content of the foliage (Leonard and Graves 1972), declining by about 5% for each 100 ppm increase in fluoride in 10-month-old leaves. In field tests, Israel (1974b) observed a highly significant multiple regression between the

fluoride content of forage and of air-plus-soil. This was expressed as: F(foliage) = 11.4 F(air) + 0.0085 F(soil), where fluoride content of foliage and soil is expressed in ppm and of air in ug/dm2 per day absorbed by lime-paper. In a recent survey of a Newfoundland region in Canada, Sidhu (1977a) concluded that "The safe levels of fluoride in air for forest species appear to be between 0.17 to 0.23 ug/m3." This is very close to the lower limit given by the estimates of Marier and Rose (1971), i.e. "The average gaseous fluoride level in ambient air should be below 0.4 ug/m3 and might have to be as low as 0.2 ug/m3."

Table 9. Regression equations relating fluoride concentrations to plant response. (back to top) Plant studied Range of fluoride concentrations Citrus 0.14 - 0.45 ppb Regression equation (1) Y (%) = 99.7 - 176 F Note Reference (2) Leonard and Graves 1970 Leonard and Graves 1972 Hortvedt 1971 Pack 1971a McCune and Hitchcock 1971 Linzon 1971 Pack 1972 MacLean and Schneider 1973

Citrus

Not stated

Y = 381.91 - 1.3132 C Y = 417.25 - 0.8797 C

(3) (4)

Pine Bean Orchard grass Alfalfa Vegetation

Not stated 2.2 - 13.9 ug/m3 up to 11 ug/m3 up to 11 ug/m3

BI = 0.06 + 0.1607 F BI = 0.93 + 0.0027 F C = 14 + 102 F Y (%) = 102.2 - 3.45 F C = 1.13 FT - 1.17 C = 1.89 FT + 0.74

(5) (6) (7) (8) (9) (9)

20 - 128 ug/m3

C = 8.50 + 0.314 F Y (%) = 99.5 - 5.1 F C = 2.555 + 4.120 FT C = 30.288 + 3.820 FT

(10) (11) (12) (13)

Strawberry 0.55 - 10.4 ug/m3 Timothy and 2.3 ug/m3 red clover 5.0 ug/m3 mix

(1) Y = yield, BI = Tip burn index, F = airborne fluoride concentration, C = concentration of fluoride in foliage, T = time; all expressed in units used by the original authors except where (%) indicates our calculations as a percentage of the control value. (2) Data of author's Table 4, average value for 6 varieties, converted to % of control (Pot 6); "F" values from Table 1, "Mean". (3) Author's Figure 1, p. 158, 10-month old leaves.

(4) Author's text, p. 158, "old" leaves. (5) Author's Figure 5, p. 300, 1-year old needles. (6) Author's Figure 5, p. 300, 2-year old needles. (7) Data from author's Table 1, 70-day exposure. We calculated a single average "control" value of "F" for each variety. (8) Data from author's Table 3, yields calculated as a percent of the individual controls. (9) Author's equations from p. 291. (10) Regression equation calculated by us from all complete data, except for three with foliage levels above 200 ppm fluoride, dry weight basis, in author's Tables 1, 3, 5 and 6. (11) Data on "Weight per fruit" from author's Table 3, calculated as a percentage of the weight of fruit from control plants. Calculations based on the author's data suggest that the number of fruit set ranged from 399 to 558 for the control plants and from 348 to 576 for the treated plants and was not significantly affected by fluoride concentration. (12) Author's Table 1, "F" = 2.3 ug/m3. (13) Author's Table 1, "F" = 5.0 ug/m3.

2.2 EFFECTS ON ANIMALS (back to top) 2.2.1 Aquatic Species (back to top) The ecological significance of the exposure of aquatic animals to fluoride has been studied to a limited extent, but much more research is required before broad conclusions can be drawn. The following paragraphs summarize the available recent information. A large number of species have been shown to suffer injury from exposure to fluoride (Groth 1975a). The response of fish to fluoride is influenced by a number of factors such as species and strain, concentration of calcium and chloride in the water, temperature, and the size or age of fish used in the study (Sigler and Neuhold 1972). The response of other species to fluoride is probably influenced by at least some of these factors, but few data are available. Fish and other aquatic species tend to accumulate fluoride from the environment, primarily in the skeleton (including the gills) and exoskeleton. Groth (1975a) has tabulated the accumulation of fluoride by a number of species. Stewart et al. (1974) analyzed specimens from an uncontaminated estuarine-coastal area of New Zealand. They report fluoride levels from 509 to 2885 ppm (ash basis) in the skeleton, and from 31 to 209 ppm in the exoskeletons, of different species. Wright and Davison (1975) also report "background" fluoride levels for a number of species, but give the data only as ug/g fresh weight. These authors also report data from controlled experiments that clearly demonstrate accumulation of fluoride in the exoskeleton of shore crab (Carcinus maenas ). Blue crab (Callinectus sapiduz), exposed to 20 ppm fluoride in water, accumulated fluoride in the exoskeleton and suffered a 4.5% reduction in growth increment per molt (Moore 1971). Moore estimates that this would result in a 52% reduction in the final size of an average crab. Wright (1977) reported a whole-body fluoride concentration of 10 ppm, wet weight basis, in fry of Brown trout exposed to 5 ppm fluoride in tap water for 200 hours. These fry suffered increased mortality, as compared to fry in a control tank, but mortality appeared

to occur only in a susceptible portion of the total population. Hemens and Warwick (1972) and Hemens, et al. (1975) studied the potential environmental effects of the "scrub water" from an aluminum smelter in South Africa. Brown mussels (Perma perma) were the most sensitive of the organisms tested. In this species, mortality occurred at fluoride levels from 1.4 to 7.2 mg/l in sea water after exposure for 15 days, but lack of food during the test-period may have enhanced toxicity. All species tested had accumulated fluoride extensively (wholebody fluoride to waterborne external fluoride ratios varied from 25:1 to 149:1) after exposure for 72 days at 52 ppm fluoride. The authors interpret some of their data as being indicative of a greater fluoride accumulation during deposition of new skeletal material. Lubinski and Sparks (1975) attempted to assess the total toxicity to Bluegills of several pollutants present in the Illinois river by expressing the contribution of each pollutant as "Bluegill toxicity units". They found that fluoride was one of six major contributors to the total toxicity of the river water. Taft and Martin (1974) have reported the absence of all living organisms in a fluoride-polluted zone of Tampa Bay. 2.2.2 Insects (back to top) Data on the effects of exposure of insects to fluoride are limited. Lillie (1970) has reviewed the literature on the toxicity of fluoride to honeybees and concluded that 4 to 5 ug of accumulated fluoride per bee may be the lethal level. Assuming an average dry weight per bee of 30 m , this corresponds to 130 to 170 ppm (dry weight). Trautwein et al. (1972) reported that the average total-body fluoride content of winter-killed bees ranged from 0.63 to 4.81 ug per bee (21 to 160 ppm dry weight basis). The highest levels were found in bees from hives located near sources of fluoride pollution. Carlson and Dewey (1971) report data from the analysis of a number of insect species captured in non-polluted and polluted areas of Montana (Table 10). All insects were presumably collected live, but the honeybees with an average fluoride content of 221 ppm probably would not overwinter successfully. Other insects, such as bumblebees at 406 ppm and sphinx moth at 394 ppm fluoride, must be considered endangered, even in the absence of further evidence. Mohamed (1971) reported evidence that exposure to fluoride caused chromosome damage and mutagenesis in fruit flies (Drosophila metanogaster). In a continuation of these studies, Gerdes et al. (1971a, exposed four strains of fruit flies at airborne gaseous HF levels of 0, 1.3, 2.9, 4.2 and 5.5 ppm for periods of up to 6 weeks. All flies were killed within 3 days at 5.5 ppm. All strains suffered at least 25% mortality in 6 weeks, even at the lowest level (1.3 ppm) of exposure, but the relation between mortality and fluoride concentration was non-linear, especially for the two "wild type" strains. In these two strains, about 65% of the population appeared to be resistant to fluoride, even at the 4.2 ppm level. The offspring of the surviving flies from the 0, 1.3, and 2.9 ppm fluoride levels of the

above experiment were also studied (Gerdes et 1971b). Statistically significant declines in fecundity and egg hatchability with increasing parental exposures were observed. Gerdes et al. concluded that the exposure to fluoride caused genetic damage. The doseresponse plots for vegetation (Section 2.l.3) and swine (see Section 2.2.4) do not appear to indicate the existence of a no-effect threshold for fluoride. If the genetic effects in insects respond to dose in a similar manner, the cumulative genetic, evolutionary, and ecological effects of exposure to low levels of environmental fluoride could become manifest with continued exposure of successive generations.

Table 10. Fluoride content of insects from polluted and non-polluted areas of Montana (Carlsson and Dewey 1971). (back to top) Type of insect Non-polluted area 8 species, all types Polluted area Pollinators Foliage feeders Cambium feeders Predators Range of fluoride contents, ppm, dry weight basis 3.5 - 16.5 58 - 406 21.3 - 48.6 8.5 - 52.5 6.1 - 170

2.2.3 Wildlife (back to top) Considerable data on the accumulation of fluoride in the skeleton of wild animals have become-available recently (Kay 1975; Kay et al. 1975a, b; 1976; Stewart et al. 1974), but data on actual injury to wild species remain sparse. Wild animals accumulate some fluoride from natural sources, and early field studies were handicapped by a lack of data on this "background" level. This lacuna has now been partially filled. The fluoride concentration of femurs from over 30 species collected in non-polluted areas of Montana have been reported (Kay et al. 1975a). Data for species from which bones of 5 or more individuals were analyzed are summarized in Table 11. This tabulation indicates that the bones of carnivorous species contained more fluoride (dry fat-free basis) than did those of herbivorous species, but the data are insufficient to permit firm conclusions regarding food-chain build-up of fluoride. In general, data on the accumulation and distribution of fluoride in the bones of wild species confirm the observations made on laboratory and domestic animals. Fluoride concentrations were lower in "the less metabolically active diaphyseal portion of the long bones" than in the distal portions which are "composed largely of cancellous bone" (Kay 1975). Bone fluoride content appeared to increase linearly with the age of the animal for

6 years or longer (Kay et al. 1976). Geographic variations were observed (e.g. means of 72.5 and 248.4 ppm fluoride in bones from different populations of deer mice), but these were small relative to changes known to result from environmental contaminations (Kay et al. 1975a).

Table 11. Fluoride content of bones of animals collected in non-polluted areas of Montana (Kay et al. 1975a). (back to top) Species HERBIVOROUS Chipmunk Columbian ground squirrel Deer mouse Muskrat Northern flying squirrel Porcupine Red squirrel Redback vole Whitetail jackrabbit CARNIVOROUS Shortail weasel Vagrant shrew * Mean and standard error of mean. No. of animals 19 23 70 11 6 6 9 5 4 5 5 F content of femur ppm, dry fat-free 103.1 + 16.2* 112.5 + 10.2 143.8 + 7.8 266.4 + 59.8 141.8 + 30.7 161.0 + 37.1 151.9 + 29.5 258.0 + 25.3 258.6 + 27.7 363.6 + 97.1 474.8 + 98.1

Stewart et al. (1974) have provided data on the "background" fluoride levels in bones of various species in New Zealand, Tibia or entire skeletons were analyzed; data are reported as ppm in bone ash. (NOTE: Bones contain 50 to 70% ash. Thus a rough conversion of "ppm, ash" to "ppm, dry fat-free" can be made by multiplying the former by 0.6.) The mean value for two opossums was 247 ppm, and that for a single rabbit was 184 ppm fluoride. These values thus agree with those reported for Montana. When compared with these background levels, bone fluoride concentrations ranging up to and above 5000 ppm dry fat-free basis, (Kay et al. 1975b; Newman and Yu 1976; Harris 1974) are clearly indicative of environmental contamination by fluoride and its ingestion by wild animals. Gordon (1970a) recorded extreme values of 12,700 ppm fluoride (ash basis) in the femur of Mus musculus, and of 16,000 ppm in a rabbit femur. A relation between bone fluoride levels in small rodents and the distance from a fluoride source has been demonstrated (Gordon 1970a). The data currently available are not sufficient to indicate the environmental significance of fluoride pollution for wildlife, but there are indications of serious effects. Lameness induced by fluorosis has been observed in wild ungulates by Kay et al. (1975b), who note

that it appeared to be more severe than the lameness observed in cattle at similar bone fluoride levels. In a predator-prey situation, even a minor loss of mobility can lead to rapid elimination of the individual affected. An apparent population age-shift was also observed (Kay et al. 1975b), and this "suggests that fluorosis was so severe that older, most susceptible, deer had been removed from that (the Teakettle mountain) herd". In view of the data discussed above, we feel obligated to disagree with the statement made by Suttie (1977), to the effect that "There seems to be no real basis for assuming that these animals (wildlife) are any more susceptible to the adverse effects of fluoride ingestion than other herbivores, and it is generally felt that if the most sensitive domestic species, cattle, are protected the area will be safe for wildlife". In Section 2.2.4 on "Livestock", we discuss a number of factors that influence the severity of skeletal fluorosis. In a comparison of domestic to wild animals, nearly all of these factors [e.g. nutritional status (particularly in winter), physical exertion, variability of fluoride exposure-level, age when exposure begins, degree of individual variability, etc.] can be unfavorable to the wild animal. Suttie's statement ignores all of these factors, and also ignores the increased vulnerability that even mild fluorosis can create in a predator-prey situation. Kay et al. (1975b) observed that, for a given level of fluoride in the bones, deer appear to suffer more severe lameness than cattle. This confirms that the factors listed above do influence the severity of fluorosis, and also increase the wild animals' susceptibility to fluoride toxicity. Data on wild birds are very limited. Stewart et al. (1974) and Kay et al. (1975a) have reported some background data (Table 12). In general, short-lived, seed-eating birds had lower bone fluoride levels than the longer-lived omnivorous species. The mobility of birds largely precludes sampling of individuals who have remained in a fluoride contaminated area for long periods. However, the high "background" fluoride levels observed in some members of the omnivorous species suggests that there may be some danger of developing skeletal fluorosis. [Note: Fluoride levels exceeding 4,500 to 5,500 ppm, dry fat-free basis in the long bones, are considered indicative of marginal fluorosis in cattle (NAS 1971)]. House martins (Dilichon virbica) may be sensitive to fluoride, as few nests were found in heavily polluted areas (Newman 1977).

Table 12. Fluoride levels in the bones of wild birds from non-polluted areas. (back to top) Reference and bird species Stewart et al. 1974 Carnivorous or omnivorous Red-billed gull White-faced heron Mallard duck 16 3 11 Number of species F content of bones ppm, ash basis Mean Range 4003 2208 1902 1058-8050 1006-3264 430-5440

Black-backed gull Harrier hawk Herbivorous Hedge sparrow Starling Pukeko Kay et al. 1975a Blackbilled magpie Blue grouse Ruffed grouse Sage grouse Sharptail grouse Spruce grouse

16 14 1 14 16

1907 1445 1021

754-3140 379-4775

4 3 5 1 1 2

703 157-1390 489 143-1400 (ppm, dry fat-free) Mean Standard Error 535 155.5 321 40.4 128 16.3 216 97 176 5.5

2.2.4 Livestock Aschbacher (1973) has stated that "Of all airborne pollutants which may affect farm animals, fluorine has caused the most serious and widespread damage". Research on fluorosis in livestock has been extensive and a number of reviews have been published (Shupe 1970; Obel 1971; Shupe et al. 1972; Trautwein et al. 1972; NAS 1974; Fleischer et al 1974; Suttie 1977). In brief, studies on skeletal fluorosis in livestock have led to the following conclusions: (1) Fluorosis results from chronic ingestion of fluoride at levels above those usually arising from natural sources over a prolonged period; thus, it is more commonly observed in older animals. (2) If exposure occurs during the period of tooth formation, tooth damage may occur. This can increase tooth wear and contribute to a decline in the nutritional status and wellbeing of the animal. (3) In severe cases, animals become intermittently or permanently lame, and bone exostoses become radiologically or even visually apparent, especially near the leg joints. (4) The severity of the fluorosis is influenced by a number of factors in addition to total fluoride intake and duration of exposure. Absorption of ingested fluoride is influenced by the chemical form and solubility of the fluoride and by other components of the diet (e.g. calcium, aluminum, etc., NAS 1974). Fluoride toxicity is enhanced by a low nutritional status of the animal (Suttie and Faltin 1973). The schedule of exposure also influences fluoride toxicity, with alternating periods of high and low exposure being more harmful than uniform exposures (Suttie et at. 1972). Physical activity also tends to increase the severity of bone lesions caused by excessive fluoride (Shupe and Olson 1971; Shupe et

at. 1972). The age of the animal when exposure begins also affects the development of fluorosis. This is especially important as regards dental effects caused by exposure during the period of tooth formation, although age also influences the receptivity (i.e. affinity) of bone for fluoride. Evidence for a declining rate of fluoride accumulation with age does not seem to have been presented for large domestic species, but has been shown with rats, rabbits, and dogs (WHO 1970; NAS 1971). Because bone lesions appear to be related to bone fluoride levels (NAS 1971), exposure to fluoride from weaning onward may be more harmful than exposures later in life. (5) There are distinct differences among domestic species in their tolerance to fluoride. Cattle seem to be the most sensitive of the common North American domestic species, whereas swine are less sensitive and poultry are comparatively resistant. Although there is general agreement on the above points throughout the industrialized countries, there is a diversity of opinion as to the levels of fluoride that can be permitted in animal forages and feeds. There are a number of reasons for this diversity, not the least of which has been the emphasis placed on osteosclerosis by many researchers in the field, and the difficulty of quantitatively expressing the degree of osteofluorotic injury. Particular attention should be given to the more insidious forms of osteofluorosis, such as the marked arthritic changes observed in dairy cattle fed fluoride-contaminated phosphate supplements (Griffith-Jones 1977). Three indices of fluoride exposure have been proposed for use with livestock. The most widely accepted index in the U.S. is the fluoride content of fodder (and of feed supplements); however the fluoride content of bone is a more useful diagnostic index, and the fluoride content of urine may also have some diagnostic value. Suttie (1969a) has proposed that standards for the fluoride content of forage should be set at: not over 40 ppm, dry weight basis, as a yearly average; not over 60 ppm, for more than 2 consecutive months; not over 80 ppm, for more than one month. Various U.S. State regulations make it unlawful for an industry to emit fluoride at a level that will cause the fluoride content of locally-grown forage to exceed 30 (Kay 1971) or 40 (Gordon and Tourangeau 1977) ppm, dry weight basis. These levels have been selected largely on the basis of data obtained in controlled animal studies (Suttie 1969a) which are not always relevant to actual farm conditions. In controlled tests, conditions are selected to minimize the effects of many of the factors, discussed on p. 46, that are known to influence the severity of fluorosis. For example, the exposure level is kept constant or varied on a simple controlled schedule; animals of uniform age are selected; adequate nutrition is provided; physical exertion is restricted;

and individual responses are largely eliminated by randomization and averaging. Obviously, the severity of fluorosis observed in such tests will be less than those to be expected in some individual animals in a range herd. In general, it can be concluded that the toxicity of a substance having a crippling effect will be underestimated by studies done on penned animals (i.e., those having restricted mobility) rather than on grazing animals whose nutritional needs cannot be met without mobility. Bourbon et al. (1971) and Gordon and Tourangeau (1977) have suggested a single standard of 20 ppm fluoride, air-dried basis, for all fodder. However, it must be noted that soils and fertilizers also contribute to the fluoride content of fodders. Suttie (1969b) reported that "some rather high fluoride forages (112 ppm) can be found in areas with no known source of industrial fluorides ..." Thus, regulations that attempt to control the level of fluoride in fodders by restricting airborne industrial emissions may prove inadequate. Standards controlling the fluoride content of fodders also fail to provide protection against high fluoride levels in mineral supplements and other types of feed (Suttie 1969b; Marier 1971; Obel 197 Griffith-Jones 1977; Hillman 1977). The fluoride content of bone has also been suggested as a quantitative index of exposure to fluoride (NAS 1971). For monitoring of live animals, this would require an inconvenient biopsy; but, in the case of farm herds, post-mortem samples from slaughtered animals are often available. Results of feeding trials at the University of Wisconsin (summarized in NAS 1971) indicated that bone fluoride levels in "the range of 4,500 to 5,500 ppm (dry fat-free basis in long bones such as metacarpal or metatarsal) might be considered as the marginal zone of toxicosis, and that lower concentrations were not indicative of damage". This conclusion, however, appears to be specific to the experimental conditions used. Another NAS (1974) report has stated: "Cancellous bone such as the frontal ribs, vertebrae, and those of the pelvis, have a higher fluoride content than the more compact metatarsal and metacarpal bones ... There is also a marked variation in the fluoride content of such different anatomical areas (within) bone (such) as the metatarsal or metacarpal; the diaphyseal portion has a lower fluoride content than the metaphyseal portion" Obel and Erne (1971) observed serious fluorosis in calves with 500 to 2,400 ppm, and in cows with 900 to 2,800 ppm fluoride in metacarpal bone ash (assuming 60% ash, these figures correspond to 300, 1,440, 540 and 1,680 ppm, dry fat-free basis, respectively). Obel and Erne suggest that a phosphate deficiency may have contributed to the severity of fluorosis in some of the cattle examined. Zumpt (1975) observed fluorosis in sheep at femur bone fluoride levels of 2,400 to 3,200 ppm dry fat-free basis. The fluoride content of urine has also been suggested (Burns 1970) as an index of fluoride ingestion by cattle. This index might be advantageous because of the ease of sample collection, but the relation between fluoride intake and urinary fluoride is not well established.

Although Burns (1970) reports a reasonably close relation between urinary fluoride and the fluoride concentration in samples from the pasture vegetation, Huber and Schurch (1970) report much less agreement. Israel (1974b) reports a correlation coefficient of 0.87 between annual average urinary fluoride levels from cattle and annual average feed and forage samples. Annual averages of urinary fluoride were based on 3 samples per year from each of 10 to 13 animals per herd. Thus, under practical conditions, it appears that extensive sampling is required for urine analyses to provide a reliable indication of fluoride ingestion. Burns (1970) suggests that 10 ppm would be "a suitable figure to use as a threshold level" for urinary fluoride. Based on the equation given by Israel (1974b), this would correspond to a fluoride content in the fodder of less than 20 ppm. There are continuing difficulties in answering the question of whether or not fluorine is an essential element of diet (NAS 1974). The criteria for essentiality and the difficulties of proving it by animal experimentation have been discussed (Underwood 1962; NAS 1971). One of the greatest difficulties is that practically every natural water supply and foodstuff contains traces of fluoride and it is almost impossible to prepare fluorine-free (e.g. < 0.005 ppm) control diets adequate in other respects (NAS 1974). In view of the conflicting results and conclusions from experiments with mice (Underwood 1977) it is not yet possible to assign an essential role to traces of dietary fluoride. We have found only one set of research data from which a mathematical relation between fluoride intake and the response of a livestock species can be calculated. Forsyth et al. (1972c) fed diets containing 0, 30, 150 and 450 ppm fluoride, as sodium fluoride, to young swine, and recorded average daily weight gains for up to 18 weeks. No data are given on the fluoride content of the basal diet. The data (reproduced in Fig. 3) indicate a linear decline in growth rate with increasing dietary fluoride. In the 18-week experiment, the values at 150 and 450 ppm fluoride are significantly (p < 0.01) different from the control values. The regression equations (our calculations) indicate a loss of about 4% in the average daily weight gain, over the 18-week period, for each 100 ppm increment in dietary fluoride. Said et al. (1974) have reported that "retarded liveweight gain was the first significant sign of fluorosis" in a 25-month study of Wether sheep fed from 53 to 70 ppm fluoride in the total ration. In the absence of additional quantitative criteria, and in view of the fact that the indices of fluorosis discussed above (i.e. bone and urine fluoride concentrations) do not appear to be satisfactory relative to actual farm experience, and do not appear to give adequate protection to wild species, the present authors cannot suggest criteria that would be of use in setting or revising Canadian standards for exposure of animals to fluoride. However, two suggestions can be made. 1. It should be emphasized that total fluoride intake is the only reliable index of chronic exposure for fluoride. The use of maximum "safe-levels" of fluoride in fodders is based on the assumption that intake of fluoride from all other sources, including water, will be low and relatively constant. Reported instances in which fluoride from sources other than fodder detrimentally affected the health of animals (Obel 1971; Griffith-Jones 1972, 1977; Parsonson et al. 1975; Hillman 1977) testify to the need to assess the contribution

from all sources. Oelschlager (1974) has stated that "there appears to be a lack of full appreciation of the extraordinary amounts of fluoride which reach the feed rations through mineral supplement mixtures..." 2. Further research aimed at developing criteria relating fluoride intake, preferably in mg/kg body weight per day, to tissue fluoride contents and injury should be stressed. This research should include studies on animals at less-than-optimum nutritional status. Attention should be paid to the less obvious effects of fluoride, such as the reduced growth of swine (and sheep) discussed above, rather than to osteofluorosis. Blood plasma F- should be assessed, as a possible indicator of fluoride exposure and the likelihood of fluoride intoxication. Nutritional factors are of extreme importance in chronic fluoride intake (see Section 5.6). Chronic dietary deficiencies can aggravate the effects of a given fluoride dosage, and such factors should be considered in the assessment of dose:response interrelations. 3.0 PHYSIOLOGICAL EFFECTS OF FLUORIDE ON ANIMALS AND MAN (back to top) Terrestrial species have evolved in contact with small but variable amounts of fluoride, and can be assumed to have a degree of tolerance for trace amounts of ingested fluoride. Nevertheless, ingestion of even small amounts seems to induce physiological responses, and many of these responses are dose-dependent. At some level of intake and duration of exposure, therefore, the effects will cease to be "tolerable" and will begin to exert a stress on the organism. The level of bioaccumulation of fluoride that will exceed the animal's tolerance is not necessarily constant but may vary with the efficiency of various bodily functions and with the stresses being imposed concurrently by environmental, nutritional, pathological, and other factors. The various physiological responses of animals to fluoride are thus of interest. In the following section, we attempt to review and summarize recent information relative to these responses. 3.1 BLOOD (back to top) 3.1.1 Fluoride Content of Blood (back to top) The presence of fluoride in animal and human blood has been recognized for many years (WHO 1970). About three-fourths of the fluoride in blood is contained in the plasma; the remainder is in the erythrocytes, which make up 40 to 50% of the blood volume. For various reasons, analysis of serum provides the most satisfactory information for the assessment of interrelations between fluoride and other factors (WHO 1970). Cowell (1975) noted that some anticoagulants used in the preparation of serum may contain fluoride as a contaminant; caution is therefore necessary in their use. The forms in which the fluoride in blood exists are still the subject of research. Taves (1968) presented evidence for the existence of two forms of fluoride in human blood, i.e. organically-bound (4.6 umol/1) and free or ionic fluoride (0.7 umol/l; data for people in a non-fluoridated community). The ionic fluoride (F-) moiety was shown to be the one that

responded to changes in fluoride ingestion; total serum fluoride is a less sensitive indicator of such changes (Taves 1968, 1970). Some doubt as to the significance of the organically-bound fluoride fraction was raised when Taves (1971) reported that it was not present in the blood of dogs and rats. Taves had suggested that the bound fluoride was associated with serum albumin, but neither Jardillier and Desmet (1973) nor Ekstrand et al. (1977) could find any evidence for protein-bound fluoride in human blood. Jardillier and Desmet (1973) suggested that the bound fluoride reported by Taves was "en fait du fluor lie par covalence a des petites molecules organiques". This suggestion has now been partially confirmed (Taves et al. 1976) by the isolation of a major component of the bound fluoride, showing "an nmr pattern consistent with a derivative of perfluorinated octanoic acid". Taves et al. suggest that the presence of this compound in plasma is "at least partially the result of contamination from industrial sources". Final identification of the bound fluoride in human plasma, and clarification of its source and physiological significance, must await further research. Its absence from the plasma of dogs and rats (Taves 1971) and from bovine plasma (Taves et al. 1976) may indicate a specificity of human metabolism or a peculiarity of the human environment. As recently as 1970 (WHO 1970), it could be stated that "regulatory mechanisms operate within the body to maintain the plasma fluoride content... within narrow limits". However, improved analytical procedures, greater attention to the ionic fluoride fraction in blood, and more critical studies have now shown that the plasma inorganic fluoride ion concentration responds rapidly and systematically to varying fluoride ingestion and to various physiological factors. Thus, Taves (1970) observed that "serum ion concentrations (of fluoride) were 0.6 and 0.7 umol/l in two individuals after an overnight fasting and increased to nearly twice this level in about 50 minutes after drinking 500 ml of water" containing 52 umoles fluoride per litre (i.e. 1 ppm). Intraperitoneal injection of 0.1 mg F/kg body weight into rats caused a rapid rise in plasma F- values, which reached a peak of about 10 umol/l in less than 10 minutes (Angmar-Manson et al. 1970). Plasma F- levels then declined progressively to levels of less than 2 umol/l 45 minutes after injection. When rats were provided with drinking water containing 50 ppm fluoride, the plasma Flevel increased from 0.17 ± .007 mg/kg to 0.26 ± 0.013 mg/kg in 4 weeks (Singer et al. 1976). After replacement of the fluoridated water with distilled water, plasma F- dropped to the original level in 3 days. Suketa et al. (1976) found that a single oral dose of 50 mg F/kg body weight given to rats raised plasma F- levels to above 2.0 ppm (105 pmol/1) in one hour. This peak was followed by a somewhat irregular decline, and the plasma Fconcentration approached the original level 10 hours after fluoride administration. The plasma F- level of 4- to 5-month-old humans also varied with fluoride intake (Hellstrom 1976). Fourteen infants on breast feeding (low fluoride ingestion) had a mean plasma F- level of 0.027 ppm, while 16 infants on formulae prepared with fluoridated water (1.2 ppm) had a mean plasma F- level of 0.045 ppm (1.42 and 2.37 umol/l, respectively). Kuznetso (1969) reported that total fluoride in the "biological media" of

human fetuses during the 5th to 12th week of pregnancy was 1.56 ppm in unexposed mothers, and 2.72 ppm in mothers working in a superphosphate factory. Posen et al. (1971) reported that plasma F increased with increasing bone fluoride (iliac crest, dry fat-free basis) in human patients undergoing hemodialysis treatment with fluoridated water l ppm. Ericsson et al. (1973) examined humans in a community with 10 ppm fluoride in the drinking water, and reported a positive correlation between bone fluoride (iliac crest biopsy) and plasma F-. Urine fluoride, on the other hand, showed little relation to either bone or plasma fluoride. An interrelation between bone fluoride and plasma F- is also suggested by the data of Parkins et al. (1974), which indicate that both bone fluoride (iliac crest biopsy) and plasma F- increased with increasing age in humans. Equations relating plasma F- level to age in humans have been presented by several authors (Table 13). Some of the researchers found no significant correlation for some of the sub-groups studied [e.g. men under 45 (Husdan et al. 1976)], but the trend towards increasing plasma F- with increasing age is clear. In non-fluoridated communities, young adults tend to have plasma F- levels below 0.7 umol/l, and this increases by about 0.01 to 0.02 pmol/l per year (Table 13). As illustrated by Hanhijarvi's data (Table 13), plasma F levels vary with the amount of fluoride in the drinking water. However, the range of values reported by various workers (Table 14) suggests that interlaboratory standardization of the methodology might be advantageous.

Table 13. Regression equations relating plasma ionic fluoride levels to age in adult humans. (back to top) Community water Fluoridated Non-fluoridated Fluoridated Fluoridated Fluoridated Non-fluoridated Non-fluoridated Subjects Both sexes Both sexes Both sexes Women Men over 45 (2) Men Women Regression equation (1) F = 0.631 + 0.0368A F = 0.761 + 0.00259A F = 0.975 + 0.00929A F = 0.375 + 0.022A F = 0.906 + 0.0101A F = 0.683 + 0.016A No correlation Reference Parkins et al. 1974 Hanhijarvi 1975 Husdan et al. 1976 Kuo and Stamm 1975

(1) F = plasma F-, umol/l; A = age in years. (2) Husdan et al. (1976) report a constant plasma F- level of 0.906 + 0.306 umol/l for men under 45 years of age.

Table 14. Mean plasma ionic fluoride levels for humans residing in non-fluoridated and fluoridated communities. (back to top) No. of individuals Community Plasma F- umol/l Reference

501 1083 14 28 41 41 76

Non-fluoridated Fluoridated Non-fluoridated Fluoridated, 3.8 ppm Non-fluoridated Fluoridated Non-fluoridated 0.15 ppm

0.88 + 0.009 1.3 + 0.0005 3.3 + 0.6 6.7 + 1.2 0.46 + 0.1 0.41 + 0.02 1.1

Hanhijarvi 1975 Jardillier and Desmets 1973 Bierenbaum et al. 1974 Desmet et al. 1975

Administration of 27.15 mg fluoride (as 60 mg NaF) to patients suffering from osteoporosis or Paget's disease gave rise to plasma Flevels of 3.26 to as high as 14.41 umol/l in the individual patients (Cowell 1975). Cowell states that the plasma F- levels "appear to be directly proportional to the dose", but examination of his Figures 8 and 9 suggests that the relation was non-linear. The range of plasma F levels reported by Cowell (1975) for normal adults was 0.31 to 2.21 umol/l. Posen et al. (1971) reported arterial blood plasma F- levels ranging from 8.9 to 23 umol/l in 10 patients receiving hemodialysis treatment with fluoridated (1 ppm) water. The plasma F- tended to increase with increasing time on the hemodialysis program, and the mean F- value increased during dialysis (pre-dialysis mean, 16 ± 4 umol/l; postdialysis mean, 28 ± 3). Cordy et al. (1974) reported a mean plasma F value of 3.35 ± 0.28 umol/l for 34 patients using a non-fluoridated water for hemodialysis, and of 12.30 ± 1.98 umol/l for 7 patients using fluoridated water. Renal insufficiency in humans can result in high plasma F levels. Seidenberg et al. (1976) reported a mean value of 2.40 umol/l in 10 patients suffering from a renal insufficiency in a non-fluoridated area, whereas thirteen "controls" from the same area had a mean plasma F concentration of 0.67 umol/l. Hosking and Chamberlain (1972) observed a slower decline in the plasma F level in anuric than in normal patients following single-dose intravenous injection of 18F; however, in anuric patients with secondary hyperparathyroidism, the uptake of fluoride by bone offset the lack of renal excretion, and plasma F- declined even more rapidly than in control patients. Kuo and Stamm (1975) report that an impaired ability to excrete creatinine was apparently not related to plasma F- levels. Hanhijarvi (1975) has shown that some of the persons with renal insufficiency show no change in plasma F- level, while others have a level 312 to 5 times higher than seen in the similarly-exposed general population. In the same survey, Hanhijarvi has also shown that diabetics have abnormally high plasma F- levels. 3.1.2 Effect of Fluoride on Blood Components (back to top) In addition to increasing the plasma F- levels, ingestion of fluoride influences several blood constituents. Recent reports on such changes are summarized in Table 15 for experimental animals, and in Table 16 for humans. Because of the multiplicity of experimental procedures used and the various blood components studied, comparisons are difficult. The most obvious onsistent observation in animals (Table 15) has been a

decrease in red blood cells; this was observed in both the rabbit and rat, and by various methods of measurement (blood iron, blood hemoglobin, erythrocyte count). This observation is of interest because of the reports of anemia in humans residing near sources of fluoride emissions (see Section 5.4). The relations between some of the changes reported in Table 16 and fluorosis in humans will be discussed in Sections 5.4 to 5.9. For the present, we conclude, in agreement with Manocha et al. (1975), that "More elaborate studies on non-human primates .... are needed to clarify the effects of different doses of fluoride on the biological system". When a single intraperitoneal dose of 20 mg fluoride/kg body weight was given to rats (Baker 1974), total serum fluoride increased by over 100-fold in 5 minutes, serum calcium declined 20% in 30 minutes, and serum phosphorus increased 40% in 1 hour. For all three components, there was a gradual reversal from these peak values, and concentrations were approaching normal 4 hours after injection. For more discussion of this aspect of fluoride interactions, the reader is referred to the reports by Guminska and Sterkowicz (1975) and Manocha et al. (1975), who also discuss various enzymatic processes.

Table 15. Effect of fluoride on the levels of various blood components in experimental animals. (back to top) Species Fluoride source Rat Diet, 450 or 600 ppm Oral, 1 mg/kg Duration of study 3 days 2 weeks 30 days Blood component studied Citrate Citrate Total blood iron Response Increased Returned to normal Decreased Reference Shearer et al. 1971.

Rabbit

Soldatovic and Nadeljkovic-Tomic 1971

"

Oral, 20 mg/kg 30 days body weight daily

Rat Rat

Water, 150 ppm 75 days Air, 0.05, 0.47 and 4.98 mg/m3

Rabbit

Water, 10 ppm

12 weeks

Erythrocytes Leucocytes Hemoglobin Blood iron Red cell count Blood hemoglobin Leucocyte count Erythrocyte count Cholinesterase activity Serum glutamateoxalate transaminase Serum alkaline phosphatase Serum malate dehydrogenase Serum lactate dehydrogenase

Decreased " " " Decreased Decreased " " " Decreased, total period Decreased, 2nd 6-week period Decreased, 1st 6week period Decreased, total period

Kahl et al. 1973 Danilov and Kas'yanova 1975

Ferguson 1976

Rat

Single oral dose, 50 mg/kg body weight

3 hours

12 hours

Serum isocitrate dehydrogenase Erythrocyte fluid potassium " " calcium Plasma acid phosphatase Plasma alkaline phosphatase Mg-activated ATPase Na + K-activated ATPase Mg-activated ATPase Na + K-activated ATPase Whole body hematocrit Erythrocyte volume Plasma volume True blood volume Plasma vol./unit body weight True blood vol./unit body weight Serum triglycerides "" Serum phospholipids ""

Decreased, 2nd 6-week period Increased Decreased Decreased No change Increased Decreased Returning to normal """

Suketa et al. 1976

Rat

Water 57 ppm

70 days

Decreased Slightly decreased Increased " " "

Kahl and Ewy-Dura 1976

Guinea Water; 5, 25 ppm pig High-fat diet Low-fat diet High-fat diet Low-fat diet

20 weeks Decreased Increased Decreased No change

Townsend and Singer 1977

Table 16. Effect of fluoride on the levels of various blood components in humans. (back to top) Fluoride source Industrial exp. Oral, 5 mg/day Water 1 ppm Industrial exp. Duration of study Not stated 6 weeks 3,4 weeks 22 weeks Long-term Blood component studied Manganese Alkaline phosphatase "" "" Manganese Aluminum Cobalt Zinc Iron Erythrocyte pyruvate kinase Serum pyruv. kinase Serum lactate dehydrogenase Response Reference Nikolaev and Kas'Yanova 1971 Ferguson 1971

Industrial exp.

18 years

Decreased Nikolaev and Sidorkin Decreased 1972 Increased Increased Increased Increased Guminska and Increased Sterkowicz 1975 Increased Decreased

Infants on formula, 1.2 ppm 4-5 months in water

Erythrocyte ATP Serum alkaline phosphatase

Increased Hellstrom 1976

3.2 URINE (back to top) 3.2.1 Fluoride Content of Urine (back to top) The fluoride content of urine has been suggested as an index of animal exposure (cf. Section 2), and as a diagnostic test for humans during chronic exposure to fluoride (e.g. Pantucek 1975). A number of reports dealing with the fluoride content of urine under various conditions have been published during the last seven years, and these are reviewed below. Toth and Sugar (1975) reported data from a survey of individuals in an area of Hungary in which the water was low in fluoride and there was no industrial source of fluoride emissions. The average fluoride content of 24-hour urine samples was 0.26 ± 0.01 mg/l; the highest value recorded was 0.57 mg/l. Variations between days, and with time of day, were apparent but rarely exceeded 0.2 mg/l. Mose et a. (1969) reported a relation between average urinary fluoride levels, population density, and degree of industrialization, indicating that urinary fluoride was increased by domestic and industrial pollution. Archer et al. (1975) were unable to detect an increase in urinary fluoride among grade 5 students residing at various distances from an aluminum smelter. However, Archer et al. did not take 24-hour urine samples, and their study was conducted against a background intake from fluoridated (0.8 ppm) water and a mean excretion of 0.97 ± 0.42 mg fluoride per litre urine. This is in contrast with the Mose et al. (1969), study, where the average urinary fluoride level for the "control" rural population was only 0.27 ± 0.03 mg/l (our estimate from authors' bar-gravph). Balazova et al. (1970), and Tsunoda et al. (1973) also report increased urinary excretion of fluoride by individuals residing near sources of airborne fluoride emissions. Mean values from Tsunoda et ai. are (i.e., as mg F excreted in 24 hr):
Men Women Non-polluted area 0.79 + 0.07 0.73 + 0.07 Polluted Area 2.05 + 0.30 1.77 + 0.43

Tsunoda et al. (1973) emphasize the inadequacy of spot-testing of urines as a means of detecting exposure to fluoride. Hodge and Smith (1977) also note that it is "impossible to assess general working conditions from a single spot urine sample from a single individual". The limited usefulness of spot-urine samples is also indicated by the data of Ericsson et al. (1973), who reported that the fluoride concentration of "night urine" from individuals in a community with 10 ppm fluoride in the drinking water was not related to either plasma F- or iliac crest fluoride concentrations. Plasma F- itself was positively

related to iliac crest fluoride. Relative to the absorption and excretion of fluoride by workers and by residents in areas subjected to fluoride emissions. it appears that particulate fluoride is excreted in the urine "as promptly and quantitatively" as gaseous fluoride (Hodge and Smith 1977). Polakoff et ae. (1974) observed small but statistically significant increases in urinary inorganic fluoride by some workers in a polytetrafluoroethylene factory. Pantucek (1975) studied the excretion of fluoride in urine by welders over a one month period. The average urinary fluoride level in groups of unexposed workers was 0.70 ± 0.03 mg1l or less. Exposed workers excreted from 1.4 to 1.8 mg fluoride/l urine before work on Monday, and the level rose progressively to attain 2.0 to 2.3 mg/l on Friday morning. Afternoon samples (between 1300 and 1400 hours) ranged from 2.5 to 3.3 mg/l on Mondays, and from 3.6 to 4.4 mg/l on Fridays. Urinary fluoride excretion in 24-hour samples taken at least 6 days after any period of exposure was markedly higher in long-term aluminum smelter workers (average of 27 years' exposure) than in a control group (Boillat et al. 1976). Values estimated from the authors' graphs are: Controls, av., 0.7 mg/24 hrs; range, 0.2 to 1.1 mg Exposed, av., 2.4 mg/24 hrs; range, 1.2 to 5.3 mg. Dinman et al. (1976a) report a linear relation between 24-hour fluoride excretion in urine and the atmospheric fluoride level to which potline workers in an aluminum smelter were exposed (11 workers over a single 24-hour period). Dinman et al. (1976b) also present curves showing a relation between the concentration of fluoride in post-shift urine and the number of days worked after a 2- or 3-day break, but these curves must be accepted with caution. No probability limits are shown, and the curves are not carried beyond the third working day, because "the variation after the third day was so great between and within job categories, that it was impossible to fit a statistically significant regression line". Calculations from the tabular data (Dinman et a. 1976b, Table 2) give coefficients of variation between 5.8 and 22.9 for days 0 to 3, and between 6.7 and 10.6 for days 4 to 7. Also, the 2.5- to 3.4-fold increases represented by these curves are excessive even in terms of the assumptions made by Dinman et al., that workers in a "non-steady state" excrete 50% of the ingested fluorine, while for workers in a "steady-state" at the end of the week, excretion "approaches 100%" of the dose. Fluoride that has accumulated in the skeleton of humans is not readily excreted in urine, following a reduction in fluoride intake. Thus, when Spencer, Osis and Wiatrowski (1974) administered 10 mg fluoride daily for 32 days to hospitalized patients, a total retention of 114 mg (36%) occurred. Retention was relatively constant throughout the 32day period, with no evidence that the proportion excreted increased with exposure-time. Of the 114 mg retained, only 9.8 mg was excreted in 12 days following cessation of treatment. In a later paper, Spencer et al. (1975) note that a negative fluoride balance

occurred only during the first six-day period following cessation of fluoride administration. The fluoride ingestion subsequent to treatment was 4.36 mg/day from foods and beverages. Jolly (1976) conducted fluoride-balance studies on control and fluorotic patients (10 in each group) having fluoride intakes from dietary sources of 3.74 ± 0.30, and 3.44 ± 0.25 mg/day, respectively, during the test period. Fluoride excretion, over three consecutive 24-hour periods, was 3.34 ± 0:23 mg/day (urine plus feces; feces contributed 8 to 12% of the total) in control patients and was not related to age. In the fluorotic group, excretion averaged 6.55 + 1.52 mg/day, and tended to decline with increasing age. The length of the hospitalization period before the tests is not reported. Presumably, the excess fluoride excretion over intake involves loss of non-lattice bound (i.e. surface) skeleton fluoride from these fluorotic patients (WHO 1970). Hanhijarvi (1975) also reported a variation in renal fluoride excretion with age. Fluoride clearance increased with age "Until about age 50, whereafter a slight decline was found" in communities with either low (0.02 ppm) or high (1 ppm) fluoride in the water. Hanhijarvi interprets the increase before age 50 to "a possible slow saturation of the bones with fluoride", and the subsequent decrease to "diminishing renal function which is characteristic for older people". Urinary excretion of fluoride is affected by a number of factors besides age. Kuo and Stamm (1975) studied groups of men and women classified on the basis of creatinine clearance tests, and recorded the following 24-hour urinary fluoride outputs:
Creatinine clearance: Men Women Normal 0.87 + 0.70 mg 0.70 + 0.58 mg Impaired 0.30 + 0.35 mg 0.24 + 0.12 mg

Hanhijarvi (1975) reported the following renal fluoride clearances for patients with various conditions:
Controls Pregnancy Diabetes mellitus Renal insufficiency (28 patients) (11 patients) (2 patients) (5 patients) 1.10 + 0.10 mg/day 0.84 + 0.08 mg/day 0.59 + 0.19 mg/day 0.59 + 0.12 mg/day

Buttner and Karle (1974) observed greater fluoride retention, which implies lower urinary excretion, in unilaterally nephrectomized rats given 25 to 100 ppm fluoride in drinking water. 3.2.2 Effect of Fluoride on Urine Components (back to top) Fluoride ingestion also influences the concentration of some other urine components. Polyuria occurred in rats following addition of 0.1% sodium fluoride to the diet (Hamuro 1972b). Urinary excretion of calcium and magnesium by rats increased significantly with

increasing fluoride in the diet (Benetato et al. 1970); for the final three months of the test period, the recorded values were:
Fluoride levels: Calcium excretion Magnesium excretion 0 0.16 + 0.010 0.24 + 0.010 2.26 0.19 + 0.003 0.24 + 0.25 4.25 mg/day 0.26 + 0.017 mg/day 0.41 + 0.025 mg/day

Marier (1968) reviewed the importance of dietary magnesium and its interrelations with fluoride. In a more recent study, Hamuro (1972a) observed that, in a strain of mice which are prone to kidney calcification induced by magnesium deficiency, the normallyobserved increase in urinary phosphorus, in response to magnesium deficiency, was largely prevented by increased dietary fluoride. Added dietary fluoride had no effect on urinary phosphorus in normal mice. In a study of kidney calcification, Ophaug and Singer (1976) found that fluoride "exerted an initial protective effect", but that the longer term effect was "to promote calcification of kidneys". They also noted that fluoride significantly retarded the mobilization of skeletal magnesium. Speirs and Adams (1971) reported that ingestion of 2 or 4 mg fluoride per day by healthy men increased the 24-hour urinary excretion of hydroxyproline and of citrate (3-week control period vs 3-week exposure period). These authors conclude that "low doses of fluoride seem to have some (additional) systemic effects, but relatively large daily variations in the urinary composition .... mask the significance of these small effects". Additional observations on the urinary excretion of hydroxyproline (and other metabolites) are referred to in our discussion of fluorosis in humans (see Sections 5.3 to 5.8). 3.3 FLUORIDE-INDUCED CHANGES IN ENZYMES AND METABOLITES IN SOFT TISSUES (back to top) Recent reports in which data on fluoride-induced changes in liver, kidney, bone-marrow, spleen, and some neural tissues of experimental animals have been presented, are summarized in Table 17. Only one corresponding study on humans has been noted: Franke et al. (1973) discussed structural changes in anterior brain cells and muscle cells of fluorotic patients. The involvement of neural and muscle cells in the pathology of fluorosis, as discussed by Franke et al. (1973), accords with observations of Czechowicz et at, (1974) on brain cells, and of Benetato et al. (1970) on neuro-muscular excitability (Table 17). The loss of auditory response in Guinea pigs (Kowalewska 1974) may also be indicative of neural injury. Although a single high dose of fluoride caused an increase in the calcium and magnesium content of rat kidneys, (Suketa et al. 1976), the longer-term response to low doses was a decrease in calcium and magnesium in kidneys (Benetato et al. 1970). Somewhat contrasting changes in enzyme activities have been reported for high (Zhavaronkov and Dubynin 1971) and low (Manocha et al. 1975) doses of fluoride in squirrel monkeys

(Table 17). The changes in liver enzymes related to carbohydrate metabolism observed by Shearer et al. (1970, 1971, 1972) appear to have been transient in normal rats, but observations were not carried beyond 17 days. Related non-transient changes have been reported in guinea pigs (Czechowicz et al. 1974) and squirrel monkeys (Manocha et al. 1975 The changes in iron incorporation by spleen and whole blood (Kahl et al. 1972) are probably related to the erythrocyte changes noted in Table 16.

Table 17. Effect of fluoride on levels of metabolites in, and physiological activities of, animal softtissue organs. (back to top) Species Fluoride Duration Organ or tissue studied source of study Rat Sub-cut. inject. 206 days Liver .3, 1.0 mg/kg " body weight " daily " " Response Reference Zharvoronkov et al. 1969

Rat

Rat

Rat

Rat

Rat

Marked impairment of ATPase act. Decreased ability to absorb 02 and discharge CO2 Decreased respiratory coefficient Decreased alk. phosphatase act. Cytological changes in cell nuclei Oral in milk, 4 months Cerveau, kidney, muscles Decreased calcium Kidney, liver 2.26, 4.52 ,g Decreased magnesium Neuro-muscular F/l Excitability, changes characteristic of latent tetany Inter-perit. 15 min. Liver Apparent inhibition of inject. " pyruvate kinase 2 mg/kg body Possible inhibition of weight enolase Diet, 450, 600 3 day Liver Increased citrate ppm 17 day " Little effect on citric acid Controlled cycle intermediates feed Diet, 450, 600 3 day Liver Citrate increased ppm 14 day " Citrate returned to normal Controlled feed Sub-cut. inject. 12 weeks Kidney Morphological alterations 12 mg/kg body Increased enzyme weight daily activities Decreased alk. and acid phosphatase activity Diet, 600 ppm 3 day Liver, normal animal Citrate decreased 14 day """ Citrate returned to normal

Benetato et al. 1970

Shearer and Suttie 1970

Shearer et al. 1971

Zhavoronkov and Dubynin 1971

Shearer 1972

Rat

Water, 150 ppm

3 day 14 day 75 day

Liver, parathyroidect. rat """ Liver Bone marrow Spleen Whole blood

Citrate increased Citrate remained high Increased incorporation of iron """ Decreased " " " Decreased " " " Microphonic potential decreased Nerve potential decreased Intensified reaction for succinic dehydrogenase, glucose-6-phosphatase, ATPase, alk. phosphatase, and nonspecific esterase. Cytological changes, increased acid phosphatase activity Increased activity of enzymes of citric acid pentose shunt Increased calcium, increased magnesium Increased calcium, increased magnesium, increased Ca++-ATPase

Kahl et al. 1973

Guinea pig Guinea pig

Sub-cut. inject. 90 day 4 mg/kg Inter. musc. inject. 4 mg/kg b.w. daily

Corte organ Auditory nerve

Kowalewska 1974 Czechowicz et al. 1974

3 months Purkinje's cells, (Cerebral cortex)

Squirrel Water, 1, 5 monkey ppm

18 months

Kidneys

Manocha et al. 1975

Rat

Int. perit. 6 to 96 16 mg/kg b.w. hours

Kidney medulla Kidney cortex

Suketa et al. 1977

3.4 BONE (back to top) 3.4.1 Fluoride Content of Bone (back to top) We have already discussed some aspects of bone fluoride in Section 2.2.4. In the following paragraphs, we attempt to summarize recent studies dealing with the physicochemical effects of fluoride on bones. The health aspects of this subject, and the hormonal etc. interrelations, will be considered in Sections 5.1 to 5.8. For additional information on the skeletal effects of fluoride, the reader is referred to recent discussion papers (Spencer et al. 1971; FCT 1973; Franke et al. 1975; Rao and Friedman 1975), as well as to the WHO (1970) monograph, Marier and Rose (1971), Groth (1973), and Section 5 of the present review. Accumulation of fluoride in the mammalian skeleton begins during gestation. Female mice given water containing 50 ppm fluoride gave birth to offspring with a skeletal fluoride content of 900 ppm, as compared to 4300 ppm in the dam's skeleton (Messer et at 1974 . The fluoride level in the newborn mice decreased slightly during breastfeeding, because the fluoride content of milk is low. In swine (Forsyth et al. 1972b), the fluoride content of the bones of newborn piglets appeared to be a linear function of the fluoride fed to the dams, which were given fluoride supplements ranging from 0 to 450 ppm in the

diet. Increasing the calcium and phosphorus content of the dam's diet decreased the fluoride concentration in the piglets' bones. Inorganic fluoride that has been metabolically released from methoxyflurane (a fluorinated anesthetic also used as an analgesic during human childbirth) is "preferentially deposited in the fetal skeleton" in rats after 15 days of gestation (Fiserova-Bergerova 1976). Shen and Taves (1974) showed that, in humans, blood from the fetal cord contained about 75% as much fluoride ion as found in the mothers' blood, indicating that the fetal bones are exposed to fluoride during development. Hanhijarvi (1975) reported a decrease in plasma F- concentration in the mothers' blood during human pregnancy; this decrease presumably resulted from a rapid transfer of fluoride to the developing fetal skeleton. Hellstrom (1976) observed that the fluoride content of the bones of newborn humans were higher, by 50% or more, when the mothers drank water containing 1.1 ppm F, than when the mothers drank low-fluoride (about 0.25 ppm) water. Although a number of ancillary factors have been identified, the accumulation of fluoride in the skeleton of animals during growth and maturity is primarily controlled by three factors: the amount of fluoride absorbed via the digestive system and lungs; the reactivity or receptivity of the skeletal surfaces; and the efficiency of fluoride excretion by the kidneys. Receptivity of the skeletal surfaces is a function of bone age and type, with young bone and cancellous bone being more receptive than old bone or cortical bone (WHO 1970). The efficiency of renal excretion is a function of kidney health, and may decline with increasing age (cf. discussion by Husdan et al. 1976). If no large variations in fluoride ingestion have occurred, analyses of a selected bone sample such as the iliac crest (cf. Franke and Auermann 1972) usually show a progressive increase in bone fluoride with age in humans. Theoretically, fluoride accumulation in bone might occur less rapidly as the fluoride content of bone increases, and a "plateau" effect after about age 50 has been discussed (cf. Jackson and Weidmann 1958; WHO 1970). However, this effect, if it occurs, may be offset by declining kidney efficiency with age, and the net effect in humans seems to approximate a linear relation between bone fluoride content and age. For a population (100 individuals) using a lowfluoride water (0.2 ppm), the regression equation for bone fluoride (iliac crest) and age found by Schellmann and Zober (1975) was: Bone F(ug/g ash) = 136.5 + 6.1 x Age (years) or, Bone F(ug/g fresh weight) = 37.5 + 1.38 x Age (years). For 20 individuals currently using fluoridated water (1 ppm, residence time not reported), Parkins et al. (1974) also analyzed iliac crest bone, and found the equation to be: Bone F(ug/g fresh weight) = 441.9 + 48.3 x Age (years). Comparison of this equation with that of Schellman and Zober (1975) clearly demonstrates the cumulative effect of even 1 ppm fluoride in water on skeletal fluoride of the aging human. Persons with renal failure can have a skeletal fluoride content 4-fold greater than that of similarly exposed persons who have healthy kidneys (Mernagh et al.

1977; Marier 1977; see also Section 5.8). 3.4.2 Fluoride-Induced Changes in Bone (back to top) The changes induced in bone as a result of fluoride accumulation can include both direct and indirect (e.g. hormonal, as discussed in Section 5) effects. Most studies on the direct effects of fluoride on bone, such as those on bone density, attempt to relate the bone properties directly to dietary or drinking-water fluoride (cf. Section 2.2 . 4). However, it appears probable that analysis of blood plasma F- concentrations in exposed individuals and populations would provide a more meaningful index of the chronic exposed and saturation-status of bones to fluoride (cf. Section 3.1.1). Recent reports on some effects of fluoride on physical properties of animal bone are summarized in Table 18. The data in this Table adequately present the complexity of the interrelations involving fluoride, calcium, age, and species. They clearly show, however, that exposure to fluoride, at dose-levels and durations that induce no recognizable symptoms of bone-fluorosis, is nevertheless a potent cumulative agent affecting structure of bone and its response to other stress factors. For more extensive discussion, see Spencer et al. (1971), Cohn et al. (1971), Franke et al. (1976), and Inkovaara et al. (1975). Recent papers have also confirmed that ingested fluoride influences the chemical composition of bones. Wolinsky et al. (1972) analyzed pooled samples of femurs and tibias from control rats and rats given 200 ppm fluoride in drinking water for 2 weeks. Fluoride ingestion decreased the concentration of citrate and of lipids in the bone, and decreased the in vitro formation of lipid from 14C-acetate or citrate. Chan et al. (1973) reported that, in quail, fluoride (750 ppm in diet for 35 days) increased bone ash and the magnesium content of the ash. Rosenquist (1974) observed a higher magnesium level in fluorotic bone from rabbits given 10 mg fluoride/kg body weight per day for 14 weeks. Fluoride ingestion also increased the magnesium content of bone ash of rats, roosters, and quail which had been made osteopenic by control of the calcium and phosphorus content of the diets (Riggins et al. 1976). Miller et al. (1977) report a higher calcium and somewhat lower phosphorus content in bones of cows suffering from osteoporosis as a result of environmental exposure to fluoride. They also observed an increased bone alkaline phosphatase activity, but no change in the citrate content of these bones. Henrikson et al. (1970) found that, in osteoporotic bones of dogs, fluoride caused a slight decrease in calcium content, and an increase in phosphorus content of bone ash. The mineral mass also increased with increasing dietary fluoride, but there was no fluoriderelated improvement (i.e. radiographic etc.) in the degree of osteoporosis. The effects of fluoride on human bone are discussed in Sections 5.3 to 5.6.

Table 18. Effects of fluoride on some physical properties of animal bones. (back to top) Species Rat Fluoride source and Observations duration Diet, 3.4, 10, 45 With adequate calcium, increase in ppm, flexability, no decrease in strength 15 weeks With deficient calcium, increase in flexibility, decrease in strength Diet, 1, 3, 9, 27 With low calcium - high ppm, 287 days phosphorous, no radiologic effects, decreased mineral mass in mandibles, no effect on bending and tension tests Water, 10 ppm Slight reduction in age-related from birth decline in breaking strength 45, then 135 ppm in Increased radiographic density if water during growth calcium adequate Decreased radiographic density if calcium deficient Slightly increased radiographic density Increased radiographic density if calcium deficient Reference Beary 1969

Dog

Henrikson et al. 1970

Mice Rat, young

Rao et al. 1972 Reddy et al. 1972c

Rat, adult Quail

Same as above Diet, 750 ppm, 35 days

Chan et al. 1973

Rat Rat

Reduced breaking strength of femurs Increased radiographic density Erickson and Ekberg 1975 Water, 50, 150 ppm Reduced breaking strength Reduced cross-sectional area Reduced modulus of elasticity Calcium, phosphorous deficiency aggravated these effects Reduced breaking strength in osteogenic bone Reduced breaking strength in osteogenic bone Reduced breaking strength in osteogenic bone Guggenheim et al. 1976

Rat Rooster Quail

Water, 100 ppm, 3 months Diet, 600 ppm, 4 months Diet, 750 ppm, 35 days

Riggins et al. 1976

3.5 MUTAGENIC AND RELATED EFFECTS OF FLUORIDE (back to top) During the past seven years, a number of research papers presented evidence that some inorganic fluorides are mutagenic to plant and animal cells. These papers, exclusive of those dealing with humans, are discussed in the following paragraphs.

Reference has been made in Section 2 to the studies of Bale and Hart (1973a, b) on fluoride mutagenicity in Hordium vulgare (barley), and to the studies of Gerdes et al. (1971b) on mutagenicity in Drosophila melanogaster (fruit fly). As little as 10-6 M sodium fluoride (0.019 ppm F) caused chromosomal-bridges, fragments, and gaps to develop during mitosis of cells in the root tips of barley seedlings (Bale and Hart 1973a). In fruit flies (Gerdes et al. 1971b), 1.3 and 2.6 ppm of airborne fluoride, as hydrofluoric acid, caused genetic damage during a six-week exposure. Mohamed and Kemner (1970) and Mohamed (1971) have also demonstrated chromosomal damage in D. melanogaster after exposing males of a specific genotype to an unspecified concentration of hydrogen fluoride. The degree of chromosomal damage increased with increasing exposure times from 6 to 12 hours. Mitchell and Gerdes (1973) exposed adult D. melatogaster flies to fluoride by allowing them to feed on filter paper strips saturated with a 7% sucrose solution containing up to 6% sodium fluoride. Gene changes in chromosome X were then detected by a cross-breeding technique. The percentage of sex-linked recessive lethals observed was linearly related to the concentration of fluoride in the food (our plot), and was significantly different from the control value at the two highest fluoride concentrations (original authors' calculations). Tests with stannous fluoride gave similar results, except that the stannous salt was about one-third as mutagenic (on a fluoride-equivalent basis) in comparison to the sodium salt. Jagiello and Lin (1974) examined meiotic division stages in mammalian oocytes that were exposed to fluoride, as NaF, in vitro. Chromosomal aberrations were observed at the following concentrations of fluoride in the medium: Mouse oocytes: 91 and 181 ppm Ewe oocytes: 11, 23 and 91 ppm Cow oocytes: 4.5, 11, 23 and 9 1ppm The percentage of ewe oocytes undergoing division was sharply reduced by fluoride concentrations above 23 ppm, and the percentage divisions of cow oocytes was reduced at 4.5 ppm fluoride and above. Mohamed and Chandler (1976) examined cells from the bone marrow and testes of mice after exposure of the animals to fluoride in drinking water at levels of 0, 1, 5, 50, 100, and 200 ppm for up to six weeks. The number of chromosomal breaks and abnormalities increased with the fluoride content of the drinking water and with duration of exposure. The authors concluded that, with mice, even 1 ppm fluoride in the drinking water (the diet contained 0.263 ppm) caused genetic damage. Russian researchers (Voroshilin et al. 1973, 1975; Gileva e,t al. 1972, 1975) have presented data on the mutagenic effects of inorganic fluoride on bone marrow cells of white rats. Inhalation of cryolite or of a cryolite + HF mixture (e.g. 271, 543 and 1628 ug F/m3 as cryolite, 6 hours/day, 6 days/week for up to 5 months) induced chromosomal aberrations and hyperploidy. The extent of damage increased with increasing fluoride concentration. Damage was greater in 17-months old than in one- to two-months-old rats.

Voroshilin et al. (1975) observed no increase in dominant lethals (total embryonic deaths) when male mice were exposed to 1.0 mg HF/m3 for 2 or 4 weeks before mating. On the other hand, Danilov and Kasyanova (1975) reported increases in embryonic deaths resulting from exposure of female rats to 0.05, 0.5 and 5.0 mg HF/m3 (conditions of exposure are poorly specified). 4.0 ORGANIC FLUORINE COMPOUNDS (back to top) The WHO monograph (1970) on "Fluorides and Human Health" repeatedly states that the fluorine-carbon bond is not cleaved by biological processes. However, evidence for biological cleavage of the C-F bond had been presented in 1956 and confirmed in 1961 (cf. Ward and Huskisson 1972). Between 1965 and 1968, Goldman and his colleagues presented a series of papers on the bacterial cleavage of C-F bonds, including that in 2fluorobenzoic acid (cf. Harper and Blakley 1971). During recent years, a considerable volume of additional data on the biological cleavage of C-F bonds has accumulated. It is now apparent that few, if any, organo-fluorine compounds are biologically stable. Much of the recent interest in the biological breakdown of organic fluorine compounds has arisen because there has been widespread use of some organohalides as anesthetics. Under operating-room conditions, anesthetics must be considered as atmospheric environmental pollutants. It has been shown that operating-room pollution with fluorinecontaining organohalides can give rise to an increased urinary output of inorganic fluoride by operating-room personnel (Spierdijk 1972). Spierdijk (1972) also reviewed data indicating an increased "incidence of abortion occurring amongst the wives of male anaesthetists, female anaesthetists and nurse-anaesthetists" during employment. Exacerbation of subclinical myasthenia gravis has been attributed to occupational exposure to methoxyflurane (Elder et al. 1971). 4.1 METHOXYFLURANE (back to top) Methoxyflurane (Penthrane), CH3-0-CF2-CC12H, appears to be one of the most biologically unstable of the organohalide anesthetics. Research on methoxyflurane and related anesthetics has been reviewed by Holaday (1972), Schuh (1974), Conn (1974), and Gottlieb and Tray (1974). Biochemical pathways for the breakdown of several of the organofluoride anesthetics have been reviewed by Loew et al. (1974). Kidney damage can appear within a few days following methoxyflurane anesthesia. This phenomenon was studied by Cousins and Mazze (1973), who reported that peak (i.e. transient) post-anesthesia plasma F- levels in afflicted humans exceeded 90 umol/l. The nephrotoxicity was accompanied by an increased urine volume of low osmolarity, and increased thirst, with the syndrome tending to obey a short-term dose-response pattern in man. Mazze et al. (1972) and Cousins et al. (1974) have shown that kidney damage in rats exposed to methoxyflurane was caused by high inorganic fluoride concentrations and not by oxalic acid, which is also a metabolic breakdown product of methoxyflurane. Taves et al. (1972) also related the nephrotoxicity and polyuria to the

metabolicallyreleased inorganic fluoride. Mazze et al. (1972) showed that the degree of kidney damage was related to methoxyflurane dose in rats. Mazze and Cousins (1974) state that "The predominant factor in the production of nephrotoxicity following methoxyflurane administration appears to be the dosage; however, additional important factors are the rate of metabolism of the drug, renal sensitivity to inorganic fluoride, presence of enzyme induction, and interaction with other nephrotoxins. A high rate of methoxyflurane biotransformation to inorganic fluoride in a patient overly susceptible to fluoride's renal toxic effects could result in the occurrence of marked nephrotoxicity from a relatively low dose of methoxyflurane". A high degree of individual variability has also been noted, relative to other organofluorine anesthetics (see later) such as halothane (Cascorbi et al. 1970). Also, Eichhorn et al. (1976) have postulated that "the threshold for fluoride-induced nephrotoxicity (following enflurane anesthesia) may be lower in diseased kidney". Hagood et al. (1973) reported that nephrotoxicity induced by methoxyflurane anesthesia in clinical practice gave a calculated mortality rate of 50%. The fluoride-mediated toxicity of methoxyflurane is influenced by the presence of other drugs (Churchill et al. 1976; Cousins et al. 1974). Also, metabolic breakdown of methoxyflurane is enhanced in obese patients (Young et al. 1975; Samuelson et al. 1976) and is probably related to the retention of organofluorine compounds in fatty tissue, as noted in studies with halothane (Bhoopathi et al. 1974) as well as methoxyflurane (Bell et al. 1975). In rats, low dose levels of methoxyflurane over long periods were more injurious than were equivalent high-dose short-term treatments (Arthaud and Loomis 1975). In rats treated with either methoxyflurane or inorganic fluoride, nephrotoxicity was associated with plasma F levels of 20 umol/l (Roman et at,1977). Creaser et al. (1974) and Clark et al. (1976) determined the plasma F- levels of mothers and their newborn children when methoxyflurane was used as an analgesic during labor. Measured values in the mother's blood were somewhat higher than in the neonate's blood at birth (e.g. 23.1 ± 1.6 and 16.3 ± 1.4 umol/l, respectively (Clark et al. 1976)). The plasma F level of the mothers' blood declined progressively after delivery, but was still markedly above normal 48 hours postpartum. The infants' blood lost fluoride less rapidly than the mothers' blood, and the plasma F level in infants was not significantly different from that of the mother's blood either 24 or 48 hours postpartum. Fiserova-Bergerova (1976) observed deposition of fluoride in the bones of fetal rats after exposure of pregnant female rats to enflurane or methoxyflurane. 4.2 OTHER ORGANOHALIDE ANESTHETICS (back to top)

Enflurane (Ethrane), CFzH-0-CF2-CFCIH, and sevoflurane, CFH2-0-CH(CH3)-CF3, are also metabolized with consequent release of inorganic fluoride in the human, but the extent of fluoride release is less than with methoxyflurane (Schuh 1974; Loew et al. 1974; Cook et al. 1975; Carter et al. 1976). However, nephrotoxicity was observed within 5 days following administration of enflurane in humans (Mazze et al. 1.977). In these patients, the average (24 hr) plasma F- level was 15 umol/l, and there was no evidence of a no-effect threshold. Other organohalides used to induce anesthesia,'such as fluoroxene (CF3-CH2-0CH=CH2), isoflurane (CF3-0-CClH-CF3) and halothane (CF3-CBrClH), release little inorganic fluoride during oxidative metabolism (Loew et al. 1974; Gion et al. 1974.) (NOTE: Metabolites other than inorganic fluoride compounds may, however, be toxic, e.g. trifluoroethanol (Gion et al. 1974; Tucker et al. 1973; Fiserova-Bergerova 1977).) It appears that this relatively greater stability is attributable to the bonding position of fluorine in these compounds (i.e. entirely on CF3 groups). However, Hitt et al. (1974) noted that isoflurane is approximately one-tenth as soluble as methoxyflurane, and suggested that the substrate concentration in vivo may limit its metabolic degradation to inorganic fluoride. Hitt et al. (1974) observed a release of inorganic fluoride from isoflurane by preparations of rat-liver mitochondria in vitro, especially if the live rats had been preconditioned (enzyme induction) by exposure to phenobarbital. The fluoride of the CF3 groups in these compounds is released during metabolism under hypoxic conditions in vitro (van Dyke and Gandolfi 1976) and in vivo in rats (Widger et al.1976). 4.3 MISCELLANEOUS ORGANIC FLUORINE COMPOUNDS (back to top) As mentioned above, inorganic fluoride is released from 2-fluorobenzoic acid by bacterial metabolism. Inorganic fluoride is also released by bacteria from p-fluorobenzoic acid (Harper and Blakley 1971). However, release of inorganic fluoride from fenfluramine, which has a CF group in the ortho-position on the benzene ring, has not been detected (Arvela et al. 1973; Macrae 1975). Gerhards et al. (1971) reported that fluorine in the 6a-position of fluocortolone (a corticoid drug) is released during metabolism of this compound in the human body. Schellman and Zober (1975) observed an "abnormally-high" iliac crest bone fluoride level (2,640 pg/g ash) in a patient following prolonged treatment with fluorine-containing corticosteroids (see Sections 3.4.1 and 5.3). Excretion of inorganic fluoride by rats after inhalation of various fluorinated ethylene compounds has also been reported (Dilley et al. 1973). Another class of organo-fluorine compounds that has aroused considerable environmental interest involves conversion of inorganic to organic fluoride (i.e. formation of C-F bonds). This conversion leads to the formation of monofluoro-organic acids (e.g. fluroacetate) in some species of vegetation (NAS 1971; Ward and Huskisson 1972).

Studies published since our previous review (Marier and Rose 1971) have shown that both fluoroacetate and fluorocitrate are formed by cultured soybean (Glycine max) cells (Peters and Shorthouse 1972b), and fluorocitrate by cultured tea (Thea sinensis) cells (Peters and Shorthouse 1972a) when 10-3 M sodium fluoride is added to the medium. No correlation between soil fluoride and organic fluoride in plant leaves has been observed (Hall and Cain 1972); however, studies on vegetation subjected to airborne fluoride still appear to be lacking for follow-up assessment of biotransformation phenomena (cf. Marier and Rose 1971). Analysis for organo-fluoride compounds should include plant tissues other than foliage, because Hall (1972) detected high levels of organic fluorides in the seeds of some plant species. Also, Vickery and Vickery (1972, 1975) studied the locale of synthesis and translocation of fluoroacetate in Dichapetalum species. Conversion to long-chain fluoro-fatty acids appeared to occur in the developing seeds. It has been reported that the toxicity of fluorocitrate to rats is much lower when it is administered orally than when injected intraperitoneally (Peters et al. 1972). When 14Clabelled fluorocitrate was administered orally to rats, most of the citrate moiety (73% of the 14C-label) was excreted in the urine within 24 hours, along with considerable quantities of inorganic fluoride. The toxicity of fluoroacetate, which is subject to in situ conversion to fluorocitrate, was essentially unchanged whether it was administered orally or by interperitoneal injection (Peters and Shorthouse 1971). One of the features of this poisoning is the inhibition of aconitase, which results in an elevated blood citrate level (Peters 1957). In recent toxicological studies on the industrial use of BF3 catalysis, Bedford et al. (1977) have isolated "two fluoroacetate precursors" (i.e. 2-fluoroethanol and 2-fluoroethoxyethanol) which are apparently found as by-products, subsequent to fluoride-ion release during catalysis. 5.0 FLUORIDE AND HUMAN ILLNESS (back to top) There has been an increasing utilization of fluorine compounds by our technologicallyoriented society (EST 1972; Farkas and Parsons 1974). There has also been evidence of an increased fluoride content in the human food-chain of several North American localities (Prival and Fisher 1974; Kramer et al. 1974). Studies of the interrelation between human illness and fluoride exposure are largely dependent on uncontrolled exposure of industrial workers to variable concentrations of fluoride, or on epidemiological studies in polluted neighborhoods. Total fluoride exposure from all sources is usually not known. Accurate definition of the dose-response relation is thus rarely possible, even under the specific conditions of a particular study. Because factors that influence the nutritional and health status of some individuals also affect their response to fluoride, meaningful dose-response criteria having broad applicability to all humans are presently unattainable.

Nevertheless, in the following discussion, we attempt to assemble and review recent reports relating to fluoride-induced illness in humans. This includes data on total exposure from all identifiable sources, and information on the clinical and subclinical aspects of fluoride-induced injuries and on their detection. Also, where possible, emphasis is put on the identification and fluoride-response of segments of the total population who, for one reason or another, may be more "at risk" than other segments of the population. In the absence of criteria from which "safe levels" having a defined margin of safety can be determined, observed injuries in such "at risk" groups may provide an indication that exposure levels are approaching those that might adversely affect an "average" individual exposed to various co-existing sources of fluoride in man's everyday environment. 5.1 FLUORIDE INTAKE BY HUMANS (back to top) 5.1.1 Intake From Foods and Beverages (back to top) The amount of fluoride ingested daily from foods and beverages by humans has been a subject of controversy during the period under review. The history of one widely-quoted Table, which appears in the National Academy of Sciences (NAS 1971) and WHO (1970) monographs, has been reviewed by Farkas (1975a). Farkas concludes that composite tables on fluoride intakes published prior to and during the early 1970s were based on insufficient data and included misquoted data. Having examined the original sources, we conclude that these Tables require major revision. Recent reviews on the intake of fluoride by humans include those by Jerard and Patrick (1973), Prival and Fisher (1974), and Marier (1977). Two quotations from these reviews illustrate the concern being caused by increased human exposure to fluoride: "Considering the paucity of recent data available on total fluoride intake, there is a clear need for more accurate, detailed information concerning the distribution of fluoride intake levels in the population" (Prival and Fisher 1974). "Careful study is needed of the upward shift in environmental fluoride and an effort should be made to appraise total exposure from all sources in order to protect the environment and people of varying vulnerability" (Jerard and Patrick 1973). One of the major factors thought to be contributing to the increase in human exposure to fluoride is the increasing fluoride content of foods. Such an increase can arise from three main sources, namely, the use of fluoridated water in food and beverage processing, the exposure of crops to airborne fluoride [and to water-borne fluoride in areas irrigated with fluoridated water (Auermann 1973)], and the use of fluoride-containing fertilizers. Literature on the contributions of fluoride from air, irrigation waters, and fertilizers, to man's total intake has been reviewed by Jerard and Patrick (1973). Bittel and Vaubert (1971) state that: "Il faut noter qu'en general la teneur en fluor des aliments vegetaux de l'homme ne cesse de croitre: il y a a ce fait plusieurs raisons, d'abord l'utilisation, de plus en plus grande,

d'engrais et amendements calciques ou phosphocalciques de moins en moins purifies en vue de contenir suffisamment d'oligoelements (bore en particulier) et, d'autre part, l'influence de plus en plus etendue de la pollution industrielle". Not enough work has been done on food-chain infiltration of fluoride, to assess the extent to which this contributes to total intake from all sources. The data in Table 19 are presented to illustrate the influence of the various environmental factors discussed above. The data are restricted to those that have appeared since 1970, and are representative of the effects of these environmental factors. The effect of fluoridated water used for food processing is apparent from the data on Gouda cheese (Elgersma and Klomp 1975) and beer (Tamacas et al. 1974) and is probably also a factor in the data on baby formula (Farkas and Farkas 1974). The influence of airborne fluoride is obvious in the high values for leafy vegetables reported by Gordon (1970a), Jones et ciL (1971) and Vouilloz. The influence of fertilizer-borne fluoride is less obvious, but the high values for "control" lettuce samples reported by Gordon (1970b) are thought to have resulted from this source. The high fluoride content of wheat, spinach, cabbage, carrots, and other Indian foods (Lakdawala and Puneka1973) presumably results from uptake of soil- or fertilizerborne fluoride. The high value for Cola soft-drink in Bombay was not caused by a high fluoride level in the city's own water (Lakdawala and Punekar 1973).

Table 19. Recent data illustrating the effects of environmental factors on the range of fluoride content in some foods. (back to top) Food Explanation Fluoride content * (ppm, or mg/kg, or mg/l) Normal 0.27 Fluoridated, 1 ppm in processing up to 2.16 water Fluoridated areas up to 1.0 "" up to 0.7 Ready to use 4 to 12 """ 0.9 to 1.0 """ 0.9 Exposed, washed (1) 2.8 to 3.24 (2) "" 12.0 to 19.6 (2) Exposed up to 100 Control samples Exposed As used "" "" "" "" "" Normal Exposed pastures 24 to 80 39 to 226 2.6 to 3.3 4.8 to 6.4 0.8 to 4.1 1.3 to 2.3 1.9 to 4.9 1.3 to 1.4 (4) 0.087 to 0.132 0.287 Reference

Gouda cheese "" Beers Wines Pablum Baby formula Orange juice Cabbage Lettuce Fruits and vegetables Lettuce " Whole wheat Wheat flour Spinach Cabbage Carrots Cola drinks Cow's milk ""

Elgersma and Klomp 1975

Tamacas et al. 1974 Farkas and Farkas 1974

Jones et al. 1971 Vouilloz 1975 Gordon 1970b Lakdawala and Punekar 1973 (3)

Dirks et al. 1974

Pork Cow beef Choice beef Beef Pork

Mechanically deboned "" "" Mechanically deboned ""

8.8 to 13.5 (5) 30.4 to 41.7 (5) 13.6 to 23.3 (5) 9.8 to 16.2 7.6

Field et al. 1976

Kruggel and Field 1977

* As reported by the various authors. Notes: (1) "Exposed" signifies exposed to airborne fluoride pollution. (2) Mean values for various locations and times. (3) Selected items from an extensive table of foods from Bombay, India. (4) Bombay city water contained only 0.08 ppm fluoride. (5) Values for hand deboned products; pork - 1.7 to 3.2; cow beef - 3.1 to 3.5; choice beef - 1.6 to 3.2 ADDENDUM: For a comprehensive review, see Kumpulainen, J., and Koivistoinen, P. 1977. Fluorine in foods. Residue Rev. 68: 37-57.

The data on mechanically-deboned meat (Table 19) indicate how a change in processing procedure can alter the trace element composition of a food. The high fluoride content of the mechanically-deboned meats results from the inclusion of bone chips, and hence is related to the fluoride intake of the animals (Kruggel and Field 1977). Contamination of forages by fluoride increased the fluoride content of milk by 0.15 to 0.19 ppm (Dirks et al. 1974); however, it must be remembered that reconstitution of powdered milk with fluoridated water will cause a much larger increase in the fluoride content of the milk beverage. The same applies to reconstitution of frozen concentrated fruit juice and other such products. A survey conducted by Farkas and Parsons (1974) indicated that the use of fluoridated water for food and beverage processing in Canada is extensive. Specific production data are not available, but 50% of the cities in which breweries were located, and 43% of the cities where carbonated beverages were processed in cans, had fluoridated water. Similarly, 51% of the factories processing vegetables, and of those processing pasta products and soups, were located in cities with fluoridated water. Thus, it is probable that about 50% of the beverages, pasta products, and canned foods consumed by Canadians, contain about 0.5 ppm more fluoride (Marier and Rose 1966; SanFillipo and Battistone 1971) than the same products contained before the cities' waters were fluoridated. Cigarettes may be another significant source of fluoride intake by humans. Okamura and Matsuhisa (1965) reported the following results for fluoride content of cigarettes:
Type of Cigarette Japanese American No. of Brands Analyzed 16 19 ppm F in Cigarettes Range 42 to 640 35 to 420 Average 163 236 ug F per Cigarette (Average) 157 244

This is the only published report we have seen on the fluoride content of cigarettes. Although Cecilioni (1974) mentions cigarettes as a source of fluoride, we are not aware of any published North American study in which the contribution of cigarette smoking has been seriously considered relative to total fluoride intake. A study by Full and Parkins (1975) raises the possibility that Teflon-lined cookware may contribute to the fluoride ingested by humans. Full and Parkins boiled fluoridated (1 ppm) water at a moderate rate until a one-third or one-half reduction in volume was attained, then determined the fluoride content of the residual water by ion specific electrode. In aluminum ware, waterborne fluoride concentration was decreased. In stainless steel and Pyrex ware, fluoride ion concentration increased, but to a lesser degree than expected on the basis of volume reduction. In Teflon-coated ware, the concentration of fluoride ion increased to nearly 3 ppm. This result requires confirmation; but, if it is correct, then the release of fluoride into foods during cooking in plastic-coated wares requires investigation. In their study of English teenagers, Hardwick and Ramsey (1976) estimated that the mean daily intake of fluoride from dentrifice was 0.32 mg, with an extreme high of 5.0 mg. Three children out of 274 "usually swallowed all of the dentifrice used". Fluoride tablets (1 mgF/ tablet) are also available in the U.K., and Hamilton (1974) notes that, in spite of a cautionary statement on the package, "the sale of fluoride tablets does not appear to be related to the fluorine content of the drinking water". Recent data on the amount of fluoride ingested by children and adults are summarized in Tables 20 and 21, respectively. However, few, if any, of these data are all-inclusive estimates of total fluoride intake. None of the data include fluoride intake from dentifrice, or from cigarettes. Kramer et al. (1974) state that their data are "exclusive of drinking water". The "market basket" approach would appear to underestimate the effect of fluoridated water used for domestic and commercial food preparation. In describing this approach, Cummings (1966) listed only five canned foods (fish, corn, pork-and-beans, tomatoes, and peaches). SanFillipo and Battistone (1971) list only one canned food (porkand-beans). Neither author lists any canned soups. This does not appear to be realistic; Kramer et al. (1974) state that, in their survey the hospital diets studied "in great part consist of processed, canned foods ..." Cummings (1966) indicates a "market basket" allowance of only 1800 g (about 63 oz) of soft drinks for a two-week period, which probably does not allow for between-meal consumption of such beverages. Lakdawala and Punekar (1973) discuss the fluoride content of carbonated beverages, but it is not clear whether between-meal beverages were included in their calculated fluoride intakes, as quoted in Table 20. The intakes for adults reported by Jenkins (1973) may be somewhat atypical, because they are estimated on the basis of urinary excretions of 4 to 5 mg/day by people who drink large amounts of tea. Probably the most all-inclusive data in Table 21 are those of Spencer et al. (1970), which

were obtained under hospital conditions. There is no reason to assume that the hospitals diets were selectively high in fluoride. In Table 22, data on the percentage contribution of low-fluoride water and various foods to the fluoride intake are compared for India and North America. The marked differences shown by these data reflect the low estimates of fluoride intake from food that were commonly accepted in North America during the 1960s, especially relating to "baseline" estimates in unfluoridated areas. Until further data become available we recommend that statements relating to fluoride intakes by adults in North America should assume a "from foods" fluoride intake of 1.5 to 2.75 mg/day, and an intake from "foods and beverages" (in areas with water fluoridated at 1 ppm) of 3.5 to 5.5 mg/day. Such estimates should include the caution that these intakes may be exceeded by persons exposed to hot environments, by copious tea drinkers, and by individuals with polydipsia (excessive thirst).

Table 20. Recent data on the daily intake of fluoride by children. Fluoride intake, mg/day Age Locality with Locality with 1 ppm F in water low F in water School 1.0 to 2.15 (1) Infants 1.48 to 1.90 0-1 year 0.37 to 1.29 0.11 to 0.45 9-11 year 1.60 0.89 15-18 year 2.25 1.07 2-8 year 2.7 1.6 under 12 0.74 to 2.0 over 12 1.21 to 2.71 5-6 year 0.85 to 1.1 14 year 1.06 to 2.10 1-4 week 0.32 6-8 week 0.57 3-4 month 1.02 4-6 month 1.23

(back to top) Reference Balazova et al. 1970 Ericsson et al. 1972 Auermann 1973

Jenkins 1973 Lakdawala and Punekar 1973 Lee 1975 Wiatrowski et al. 1975

(1) The high value refers to children living in an area exposed to airborne fluoride. "Food" contributed 1.4 mg in this area as compared to 0.8 mg in a "control" area.

Table 21. Recent data on the daily intake of fluoride by adults. (back to top) Fluoride intake, mg/day 1 ppm F in water 3.57 to 5.37 Low F in water 1.45 to 2.74 Reference Spencer et al. 1970

2.1 to 2.4 1.34 2.45 4.75 7 to 10 (heavy tea drinkers) 1.73 to 3.44 1.23 to 2.41

0.8 to 0.9 ("food stuff" only) 0.81 (without exercise) 1.20 (moderate exercise) 1.98 (strenuous excercise) 0.78 to 1.03 (exclusive of beverages) 0.73 to 0.94 (three meals only)

San-Fillippo and Battistone 1971 (1) Auermann 1973 Jenkins 1973 Kramer et al. 1974 Osis et al. 1974.

(1) A second report by San-Fillippo et alo. (1972) has been omitted from this table as it refers exclusively to military meals.

Table 22. The percentage contribution of water and various foods to the fluoride ingested by humans. (back to top) % contribution of F Source Range Average India (Lakdawala and Punekar 1973) Water (0.083 ppm) Tea Cereals Vegetables Pulses Other U.S. (NAS 1971, Table 9-4) Water (< 0.1 ppm) All foods 2.0 - 10.8 0.7 - 21.0 16.0 - 52.0 9.0 - 45.0 6.0 - 22.0 0.3 - 15.0 5.0 5.3 33 21 11 60 40

5.1.2 Intake From Air (back to top) It is generally assumed that an "average" man doing moderately strenuous work inhales approximately 20 m3 of air in a 24-hour period (NAS 1971). In view of the known relations between fluoride ingestion and urinary excretion (NAS 1971), the rapid response of urinary fluoride to inhaled gaseous or particulate fluoride (Hodge and Smith 1977) is indicative of efficient and probably essentially-complete absorption of inhaled fluoride into the body. Inhalation of air containing 0.1 ug fluoride/m3 [a level that is rarely encountered in non-industrial urban areas (Thompson et al. 1971)] would thus result in an intake of only 2.0 ug fluoride per day. The contribution of airborne fluoride to the daily intake is therefore considered to be negligible (however, see below) by most authorities (e.g. NAS 1971). However, at the other end of the scale, Hodge and Smith (1977) appear to consider it acceptable to expose workmen, during an 8-hour shift, to a fluoride concentration of 2.5

Mg/m3. Assuming the respiration of 10 m3 of air during a working shift (Dinman et al. 1976a), fluoride absorption from the air by workers exposed to this concentration could approach 25 mg. In summer, potroom workers perspire an average of 6 kg sweat per day and may thus excrete 25 to 50% of the ingested fluoride in sweat (Dinman et al. 1976a). Nevertheless, post-shift urinary fluoride concentrations of 7.01 ± 0.47 to 8.65 ± 0.69 mg/l (daily averages for 25 "anode-men" exposed to an average airborne fluoride concentration of 2.19 ± 0.16 Mg/M3) have been reported (Dinman et al. 1976b). These data clearly indicate that, under some circumstances, humans can receive a considerable amount of fluoride from airborne sources (see Section 5.9.2). 5.2 CARCINOGENIC IMPLICATIONS (back to top) Fluorides are known to cause chromosome damage and mutations in plant and animal cells (Section 3.5) and might therefore be considered as possible carcinogens. The majority of studies on correlations between fluoride exposure and deaths from various causes, including cancer, have focussed on fluoride exposure via drinking water. Studies of differences in the "crude cancer death-rate" between cities with nonfluoridated and fluoridated water supplies have led to conflicting results (Nixon and Carpenter 1974; Bierenbaum et al. 1974; Kinlen 1974, 1975; Burk 1975; Yiamouyiannis and Burk 1976, 1977; Hoover et al. 1976). An excess of respiratory-tract cancers was reported in fluorspar miners in Newfoundland and attributed to airborne radon and radon daughters (deVilliers and Windish 1964; deVilliers et al. 1971). Since the rate of incidence in these miners was five times greater (per-unit of radiation exposure) than in Colorado uranium miners, Little et al, (1965) postulated a co-carcinogenic role for fluorspar. Cecilioni (1972a, b) has drawn attention to a three-fold increase in the death rate from respiratory cancer in the steel city of Hamilton, Ontario, in comparison with the Canadian average. Studies of steelworkers (Lloyd et al. 1970) and aluminum workers (Discher et al. 1976; Discher and Breitenstein 1976; Milham 1976) have led to inconclusive results concerning the effect of the work environment on respiratory health. In all the studies involving industrial exposures, no distinction can be discerned among various toxic and possibly carcinogenic factors in the work environment. Such factors can act independently or synergistically. Until definitive studies involving specific exposures to fluorides have been made, we can draw no conclusions about the carcinogenic or co-carcinogenic activity of fluoride. 5.3 OCCUPATIONAL FLUOROSIS (back to top) Hodge and Smith (1977) have recently reviewed occupational exposure to fluoride, as it relates to aluminum or phosphate fertilizer production, with emphasis on clinical osteosclerosis. Other metabolic irregularities (e.g. those affecting respiratory function, arthritis, kidney, blood, etc.) are considered, but Hodge and Smith (1971) state that, in

general, "their relation to fluoride exposure is doubtful, unless the exposure conditions exceed those typical of U.S. operations" However, it is important to recognize that there is usually a preemployment selection of workmen on a health basis. Thus Franke et al. (1975) have reported that "At the examination for employment, persons with the following diseases are considered totally unsuitable: liver and kidney changes, blood and thyroid gland diseases, posttraumatic or congenital skeletal damage, infections and para-infectious diseases of the apparatus of locomotion (rheumatism; Bechterev's disease); also, workers with distinct degenerative changes of the spine and of the large joints are unsuitable". In all probability, there is also a continuing selection for health among exposed workers (cf. Lloyd et al. 1970). Thus, at least some smelters exercise a "selection of the fittest" policy, thereby ensuring that the workmen are in good health and, as such, more likely to tolerate exposure to fluoride. In spite of this, Guminska and Sterkowicz (1975) and Schellmann and Zober (1975) have recently emphasized that fluoride intoxication is a problem of increasing importance in technological countries. Although emphasis in North America has been on the osteosclerotic manifestations of occupational fluorosis, earlier stages of fluoride-induced changes in bone are now being utilized as diagnostic aids by some researchers. Franke and Auermann (1972) have described this procedure, and Horn and Franke (1976) have demonstrated how microscopic scanning techniques can be used to recognize graduated bone changes associated with mild to severe fluorosis. Franke and Auermann (1972), and Schlegel (1974) emphasized that muscular-skeletal complaints can be related to the histological bone changes of mild fluorosis. Moreover, Popov et cit. (1974) observed neurological symptoms in 63 of 80 workmen examined, and noted that the incidence of neurological symptoms was not related to the skeletal stage (whether pre-osteal or definite osteal) of fluorosis. Hiszek et al. (1971) emphasized that the high incidence of locomotor ailments caused by fluoride occur in the absence of obvious radiological evidence of fluorosis. Other recent observations indicate that fluoride-induced bone changes are not necessarily symmetrical or bilateral. Thus, Herbert and Francon (1971) describe the case of a Potroom worker who had left-hip sciatica and nephritis, with diffuse lumbar arthralgias. The fluoride content of the iliac crest bone was between 5,100 and 5,800 ppm, ash basis. Harbo (1973) describes the case of a workman with sensory loss in the upper left extremity, with muscular wasting and pain. The highest fluoride content found in vertebral bone samples was 2,700 ppm, ash basis. In a discussion of bone fluoride levels, Riggins et al. (1974) report that some researchers feel that 2,000 ppm fluoride in dry fat-free bone "should be considered toxic" and that "skeletal fluorosis in humans can be seen when the concentration of fluoride in bone ash exceeds 3,000 ppm". These two values for bone fluoride are compatible with each other, assuming that bone contains about 60% ash. Franke and Auermann (1972) have concluded that "In cases of genuine violent complaints, clear histological changes, and fluorine values above 4,000 ppm in the bone ash of the iliac crest cylinder, the disease should be classified as an occupational one, even with few clinical or radiological

findings". Boillat et al. (1976) advocated bone-biopsy fluoride analysis as a diagnostic aid in the case of workmen with "articular pain and limitation of motion"; these cases had concomitant hypocalcaemia, hypocalciuria, and hyper-hydroxyprolinuria, and Boillat et al. concluded that nutritional factors play an important role in such afflictions. These various observations indicate that the diagnosis of fluoride-related ailments is in a state of evolution, and is approaching a hitherto unknown degree of thoroughness and sensitivity. Respiratory ailments may also be related to occupational exposure to fluoride. Mangold and Beckett (1971) observed an "immediate upper respiratory irritation" by fluorides, as contrasted to a "delayed pulmonary response to cadmium oxide fumes and nitrogen dioxide" among silver brazers exposed to the mixed fumes. This suggests that respiratory ailments may not reflect the total body-burden of fluoride, but might accrue from repeated localized contacts of fluoride (especially HF) with respiratory tissues. It is interesting to note that, after intravenous infusion of Na 18F into rats, the "lungs contained the greatest amount of fluoride" of any of the soft tissues (Knaus et al. 1976). Golusinski et al. (1973) reported that, of 130 potroom workers in an aluminum smelter, 30% had the characteristic changes of rhinitis, with hypertrophic and atrophic lesions. Similarly, Fesenko et al. (1972) found that, of 1,141 workmen examined, 36% had skeletal fluorosis, and 10% of these also had rhinopharyngolarynqltis. The rhinopharyngolaryngitis topic is one that Hodge and Smith (1977) consider worthy of consideration for future research on fluoride effects. As for atrophic rhinitis, Brown et al. (1966) have studied its etiology, pathogenesis, and prophylaxis in swine; among their conclusions, the authors emphasized that an inadequate calcium ingestion (or a low dietary Ca/P ratio) leads to nutritionally-induced secondary hyperparathyroidism and consequent generalized osteitis fibrosa. Thus, we again note the contribution of nutritional inadequacies (or imbalances) in such syndromes. The diagnostic value of plasma inorganic fluoride determinations has been discussed elsewhere in this report (Section 3) and by Marier and Rose (1971), Ericsson and Ekberg (1975), and Inkovaara et al. (1975). Guminska and Sterkowicz (1975) have reported a significant decrease in blood erythrocyte ATP in workmen exposed to fluorides. Nikolaev et al. (1971, 1973) have drawn attention to a 16-to-30% reduction in blood manganese among workers exposed to fluorides. Although Furlanetto et al. (1973) concluded that "manganese seemed not to affect the proportional fixation of fluoride" in bones and teeth, researchers must not lose sight of the fact that a dietary lack of manganese can induce skeletal abnormalities, including generalized rarefaction of bone (Tal and Guggenheim 1965), thickened leg joints with stunted growth, and impaired reproductive function (NAS 1973). Rao and Friedman (1975) have reported that "A further toxic effect of fluoride on bone formation may relate to the fluoride bonding with manganese, a cation necessary for glycosylation, an intermediary step in the formation of collagen". The foregoing examples, along with the blood and tissue changes noted in Tables 15, 16, and 17, attest to the need for consideration of a multiplicity of factors in the assessment

of injuries accruing from long-term exposure to fluorides. The metabolic changes discussed cannot be assumed to be of no biological significance, as regards chronic fluoride intoxication. Hodge and Smith (1977) concluded that a workplace airborne fluoride concentration below 2.5 mg/m3 "will be tolerated without injuring human health during a working lifetime". In contrast, Vishnevski (1969) questioned the U.S.S.R. airborne limit of 0.5 mg/m3 because workmen were found to exhibit increased sensitivity to light, increased toxic symptoms and increased skeletal incorporation of fluoride. Vishnevski concluded that the occupational fluoride level in ambient air should not exceed 0.1 mg/m3. Guminska and Sterkowicz (1975) expressed concern that occupational airborne fluoride concentrations of 0.22 mg/M3 would be deleterious to workers' health (see Section 5.9.2). 5.4 NEIGHBORHOOD FLUOROSIS (back to top) As discussed in Section 5.3 on occupational fluorosis, screening of workmen to assure a reasonable health status (Franke et al. 1975) undoubtedly reduces the incidence of overt fluoride-related complaints. No such protection is provided for people residing in areas adjacent to fluoride-emitting industries. Hodge and Smith (1977) considered this aspect of fluoride pollution, but additional discussion is warranted. It is indisputable that persons exposed to fluorides in the workplace constitute an "at risk" group because of the high concentrations of fluoride to which they are exposed during their working shift. It is less widely recognized that persons residing in polluted areas also constitute an "at risk" segment of the population because of their more continuous exposure to moderate concentrations (cf. Hunter 1969). It must not be forgotten that children, the elderly, and the chronically ill and infirm, all form part of populations residing adjacent to sources of fluoride emissions. Table 23 summarizes some of the metabolic abnormalities that have been observed in such persons. In Table 23, note that the "joint pains" alluded to by Murray and Wilson (1946) and the "neuromuscular arthritis" described by Waldbott and Cecilioni (1969) are similar to symptoms that were discussed in our preceding comments about occupational fluorosis (Hiszek et az. 1971; Franke and Auermann 1972; Harbo 1973; Popov et al. 1974; Schlegel 1974; Boillat et al. 1976). Riggs and Jowsey (1972), in their studies of fluoride therapy for osteoporosis in humans, observed that some patients developed "transient arthralgias and stiffness of the joints. These symptoms are dose-dependent and promptly disappear on discontinuation of the drug (i.e. fluoride)". The occurrence of anemia in "neighborhood fluorosis" accords with earlier observations (cf. Marier and Rose 1971) and with the related data in Table 16, as discussed in Section 3.1.2. In a preceding Section of this report, Tables 15, 16 and 17 presented summaries of biochemical changes induced by fluoride in blood and in soft tissues. It remains to be determined whether some of these changes are consistent features of subclinical or mild forms of neighborhood fluorosis in humans.

Table 23. Health problems among residents near fluoride-emitting sources. (back to top) Place England Source Iron Population 5 adults 4 children 78 children surveyed 31 adults 1 adult 227 children surveyed 27 adults 16 adults Symptoms Reference Murray and Wilson 1946. Rippel et al. 1967 Balazova et al. 1970 Waldbott and Cecilioni 1969. """ Leloczky 1971 Schmidt 1976a Schmidt 1976b

Czechoslovakia Aluminum Canada-U.S. U.S. Hungary E. Germany E. Germany Phosphate Fert. Iron Aluminum HF plant Aluminum

Low hemoglobin with high erythrocyte Neuromuscular arthritis etc. Neuromuscular arthritis etc. Low hemoglobin Early skeletal fluorosis Bone changes

5.5 ENDEMIC FLUOROSIS (HYDROFLUOROSIS) (back to top) This form of fluorosis has been linked to chronic ingestion of naturally-fluoridated waters (WHO 1970). In a recent Algerian study of hydrofluorosis, Poey et al. (1976) have reported that the early stages of chronic fluoride intoxication are associated with changes in blood and urine components, and that these precede radiologically-detectable bone abnormalities. In the early phase, there was an increase in blood urea and acid phosphatase, with a concomitant increase in urinary output of phosphorus and urea. As the fluoride intoxication progressed, there was a gradual impairment of urinary creatinine clearance, leading to renal insufficiency (see Sections 3.2.1, 3.2.2, and 5.8). Much of the information relating to endemic fluorosis has originated from India, where skeletal fluorosis has been associated with water-borne fluoride concentrations of 2 to 3 ppm or lower (Jolly et al. 1968; Krishnamachari 1976). Although osteosclerosis seems to be the only fluoride-related bone abnormality recognized in North America (see Hodge and Smith 1977), the skeletal abnormalities observed in India are not confined to the osteosclerotic form (Teotia et al. 1976). Even at comparable degrees of fluoride exposure, the epidemiological studies in India have provided some striking contrasts. In the Punjab area, Jolly et al, (1968, 1974) have invariably observed the osteosclerotic type of bone disease in fluorotic patients. In contrast, Teotia et al. (1974, 1976) have encountered osteoporosis, rachitis, and the osteomalacia type of bone disease associated with a fluoride-induced compensating secondary hyperparathyroidism. The bone rarefaction phenomena observed by Teotia et al. were not confined to adults, but were common in children 11 to 14 years of age (Teotia et a. 1971). Faccini and Teotia (1974) described the histopathological features of the osteomalacia-like fluorotic bone. This abnormality can resemble the osteitis fibrosa cystica of the "wine fluorosis" described by Soriano (1966). It also resembles the condition reported in fluoridated hemodialysis patients by several researchers (Posen et

al. 1971; Jowsey et al. 1972a; Johnson and Taves 1974; Riggs et al. 1976). In Teotia's surveys, the serum immuno-reactive parathyroid hormone levels correlated positively with serum alkaline phosphatase and with urinary excretion of total hydroxyproline (Teotia et al. 1974; Faccini and Teotia 1974). In studies of hydrofluorosis in Italy, Frada et al. (1974) observed increases in bone alkaline phosphatase and urinary hydroxyproline in fluorotic patients. These observations are in accord with those of Boillat et al. (1976) who reported hydroxyprolinuria in patients with occupational fluorosis. Boillat et al. concluded that nutritional factors play an important role relative to fluorosis-related hydroxyprolinuria. Jolly et al. (1974) discussed nutritional factors relative to the different clinical patterns seen in different regions of India. They state that "In Punjab, where the (daily) dietary intake of calcium averages 1 gram, osteomalacia and rickets are not encountered in cases of fluorosis. However, in Andhra Pradesh and Rajasthan, a low calcium intake coupled with intake of fluoride produces changes of rickets and osteomalacia". This conclusion is supported by other reports. Thus, in the Rai Bareli district, where osteomalacia is the commonly-seen form of bone fluorosis, Teotia et al. (1974) reported a daily calcium intake averaging 645 mg, and a phosphorus intake averaging 1738 mg/day (Ca/P ratio = 0.37). Krishnamachari and Krishnaswamy (1974) reported that the adult male in the Nalgonda district, where Genu VaIgum (see next paragraph) is the prevalent form of fluorosis, has an average daily intake of 297 mg calcium and 2096 mg phosphorus (Ca/P ratio = 0.14). An extremely severe form of fluorosis observed in India is termed "genu valgum", and is characterized by a crippling "knock knees" syndrome with osteosclerosis of the spine and concomitant osteoporosis of the limb bones, and by very high serum parathyroid hormone levels suggestive of hyperparathyroidism (Krishnamachari and Krishnaswamy 1973). Dietary studies indicated no vitamin D deficiency, but low dietary calcium, a low Ca/P ratio, and a high molybdenum content in some locally-grown foods; a high urinary excretion of copper was also noted (Krishnamachari and Krishnaswamy 1974; Agarwal,1975; Krishnamachari 1976). The crucial role of copper was recognized by Krishnamachari (1976) who states that "None of the villagers whose water contained more than 0.1 ppm of copper had Genu Valqum, although their water contained high levels of fluoride". These studies on Genu Valqum indicate that water-borne elements other than fluoride can influence the skeletal abnormalities encountered in endemic fluorosis. Several reports have shown a relation between the development of fluorosis and the calcium and magnesium content of the drinking water. Jolly et al. (1968) reported on the situation in two villages whose water contained an average of 3.3 ppm fluoride, but where the two populations had a markedly different (10% as compared to 45.6%) incidence of skeletal fluorosis. The lower incidence of fluorosis was associated with a higher total hardness of the water. Because the nutritional status, climate, duration of fluoride exposure etc., did not differ between the two villages, Jolly et al. (1968) concluded that the calcium and magnesium components of hard water had a "protective influence". Such a protective

effect has been discussed by Marier, Rose and Boulet (1963). Similar results have been reported from the Rajasthan area of southern India, where Thergaonkar and Bhargava (1974) compared fluoride intoxication in 16 villages with waters of different degrees of hardness and fluoride contents ranging from 0.3 to 2.7 ppm. They concluded that "incidence of fluorosis is probably reduced by (waterborne) calcium ... ard the severity ... is (directly) related to bicarbonates in the water, apart from the fluoride concentration". These conclusions are supported by the data of Kathuria et al. (1974). Teotia and Teotia (1975), in a study in the Uttar Pradesh area of India, did not find a reduced incidence of fluoride intoxication in hard-water areas, and suggested that "the simultaneous intake of excessive amounts of (waterborne) magnesium ... interferes with calcium's (protective) action". No clear relation between waterborne magnesium and fluorosis was observed in the studies conducted by Thergaonkar and Bhargava (1974) or by Kathuria et al. (1974), but the assessment may have been complicated by "low nutritional levels and lack of a balanced diet" (Thergaonkar and Bhargava 1974). A similar survey of human population groups in Czechoslovakia (Vejrosta et al. 1975) attributed a beneficial effect to waterborne magnesium, in terms of ensuring the integrity of mineralized tissues. In Rumania, Benetato et al. (1970) studied calcium and magnesium metabolism in hospitalized patients who had neurological symptoms of early (i.e. pre-skeletal) chronic fluorosis, associated with ingestion of drinking-waters containing 2.85 to 3.6 ppm fluoride. The study included parallel observations in rats, and led the authors to conclude that chronic fluoride intake can induce latent calcium and magnesium deficiency in which the electrolyte changes (especially of magnesium) contribute to the serious metabolic derangements. A report of the Royal College of Physicians of London (1976) concluded that "There is no evidence that the consumption of water containing approximately 1 mg/litre of fluoride in a temperate climate is associated with any harmful effect irrespective of the hardness of the water." The role of drinking water components should not be underestimated. Hankin et al. (1970) found that hard waters can contribute significantly to the total dietary intake, i.e. from 3.5 to 15.9% of the daily intake of calcium, and from 8.9 to 27.3%0 of the daily magnesium. During recent years, the World Health Organization has been emphasizing this area of research (Masironi 1975). Sundstrom (1972) observed bone-resorption cavities indicative of "mild fluorosis" in some rats given 1 ppm fluoride in distilled drinking-water during a 2-year period, and therefore recommend "A special long-term study, in which the effects of (fluoride in) distilled and artificially-fluoridated waters are compared with those of naturally fluoride-containing waters". 5.6 DIETARY-NUTRITIONAL DEFICIENCIES OR IMBALANCES AND FLUOROSIS (back to top) In the preceding discussion, we have considered the influence of waterborne calcium and magnesium, and how this factor may help to protect against the onset and severity of fluorosis.

The beneficial effects of calcium and magnesium in alleviating fluorosis has been confirmed in animal studies. Low-calcium diets increased bone fluoride in rats (Guggenheim et al. 1976), increased the severity of bone fluorosis, with "exostosis" lumps, in rabbits (Reddy and Rao 1972b), and increased bone fluoride and the severity of its effects in monkeys (Reddy and Srikantia 1971). Conversely, high dietary calcium and phosphorus lowered bone fluoride in swine (Forsyth et al. 1972), and calcium supplementation decreased the lesions of fluorosis in cows, horses, and swine (Spencer, Cohen and Garner 1974). Marier (1968) reviewed the metabolic interrelation of magnesium and fluoride; Table 24 represents his summary comparison. Marier notes that, in magnesium-deficient dogs, fluoride supplements prevented soft-tissue calcification, but not the muscle weakness or convulsions; in magnesium-deficient rats, fluoride aggravated the hypomagnesaemia, thereby intensifying the convulsive seizures. Rapidly growing chicks appear to present a particular problem, because they develop a "leg weakness" syndrome when fed diets that contain high levels of both magnesium and fluoride (cf. Marier 1968). Also, Rogler and Parker (1972) have observed that a diet high in calcium could partially prevent the onset of toxicity with the high-magnesium high fluoride diet. An underlying imbalance among the various mineral nutrients is thereby suggested. Hakansson and Svensson (1977) have reported that rapidly growing chicks, especially when given highly concentrated feed, seem to have difficulties in utilizing dietary magnesium, and retaining it in their leg bones. It appears probable that this magnesium-related problem is aggravated by concomitant high-fluoride supplementation, even though the toxic symptoms can be partially alleviated by prior increases in dietary calcium. Hamuro (1972a, b) studied the effects of fluoride on magnesium-deficient mice and concluded, on the basis of 6-day studies, that fluoride supplements prevented renal calcinosis. However, a longer-term study with magnesium-deficient rats indicated (Ophaug and Singer 1976) that fluoride exerted only an initial protective effect on kidney calcinosis, and that the long-term effect was to promote kidney calcification. Suketa et al. (1977) observed that, in rats, a single large dose of fluoride increased kidney calcium 10 times more than it increased kidney magnesium; this would favor in situ calcification (Marier 1968). Pita et al. (1972) have shown that fluoride supplements increased the magnesium content of mineralized tissues in rats. Ophaug and Singer (1976) reported that fluoride exerted a significant effect in retarding the mobilization of skeletal magnesium in rats. O'Dell et al. (1973) observed that fluoride had a "magnesium-sparing" effect in Guinea pigs, but found that high fluoride supplements were toxic when magnesium was severely limiting. O'Dell et al. concluded that "a high intake of magnesium should be highly beneficial in areas where fluorosis prevails". Thus, there is evidence that fluoride intake can increase the long-term metabolic

requirement for magnesium. The same may be true for manganese. Note that we have previously discussed depletion of manganese in fluoride-polluted pine needles (Garrec et al. 1977), and the reduction in blood manganese among workers exposed to fluorides (Mikolaev et al. 1971, 1973). These nutritional interrelations have not yet been adequately quantified. The same considerations apply to vitamin C. Unlike most species, primates cannot synthesize their own vitamin C, and are entirely dependent on their food-chain to supply an adequate intake. In a study of fluoride supplementation in monkeys, Reddy and Srikanti (1971) showed that a diet low in vitamin C enhanced the onset of skeletal fluorosis, and that a low protein intake accelerated rarefaction of bones. Earlier, Gabovich and Maistruk (1963) had shown that vitamin C supplementation reduced the toxic effects of fluoride in industrial workers and in Guinea pigs. Marier and Rose (1971) discussed Russian studies in which fluorosis was found to be most severe in children who had a vitamin C deficiency. Marier and Rose also discussed Australian work, which showed that vitamin C supplementation alleviated fluorosis in Guinea pigs. It appears possible that chronic exposure to fluoride increases the metabolic requirement for vitamin C; but again, such nutritional interrelations have not yet been quantified. There is, however, definite evidence that fluoride supplementation creates a greater metabolic requirement for calcium in humans. Much of this evidence has accrued from attempts to treat human osteoporosis by means of high doses of fluoride. Some researchers (e.g. Franke et al. 1974) have reported success in the treatment of human osteoporosis, using 20 to 60 mg NaF per day (i.e. 9 to 27 mg F/day). However, experiments with several species of animals have shown that administration of fluoride alone does not reverse or improve osteoporosis (Henrikson et al. 1970; Spencer et al. 1971; Reddy and Rao 1972a; Kuo and Wuthier 1975; Griffiths et al. 1975, 1976). Similarly, several researchers have concluded that administration of fluoride alone does not improve human bone rarefaction (Albright and Grunt 1971; Cohn et al. 1971; Inkovaara et al. 1975). Jowsey et al.(1972b) have emphasized that administration of less than 20.5 mg F/day did not consistently increase bone formation, whereas 27 or more mg F/day produced abnormal bone. This form of high-fluoride therapy has been termed "an experimental drug for osteoporosis" (Gordan 1976). Using 25 and 20.5 mg F/day, respectively, Inkovaara et al. (1975) and Zanzi et al. (1975) observed spontaneous bone fractures during the course of treatment. Merz et al. (1970), using dosages usually ranging between 22 and 34 mg F/day, discontinued fluoride administration to their patients, to avoid the eventual development of osteomalacia. (Note: Osteomalacia and spontaneous bone fractures have also been encountered in patients on hemodialysis with fluoridated water; see Section 5.8). Studies with rats, swine, dogs, and monkeys, have shown that, in the absence of fluoride supplementations, a calcium deficiency (or too low a dietary Ca/P ratio) is likely to lead to "nutritional osteoporosis" (Henrikson 1968; Reddy and Rao 1972a; Rantanen et al.

1972; Kuo and Wuthier 1975; Griffiths et al.. 1975 and 1976). The osteoporotic condition will not be reversed or improved by supplementation with fluoride alone (Henrikson et al. 1970; Reddy and Rao 1972a; Spencer et al. 1971 and 1974; Kuo and Wuthier 1975). If the calcium insufficiency is not corrected, fluoride supplementation can induce osteomalacia (Rantanen et al. 1972; Kuo and Wuthier 1975; Griffiths et al. 1975 and 1976). The most positive results in the treatment of human osteoporosis with fluoride have been obtained by use of concomitant calcium supplements. In the studies by Cohn et al. (1971), high calcium supplements reduced bone pain in osteoporotic patients, whereas fluoride administration did not achieve this effect. Jowsey et al. (1972b) have stated that "osteomalacia and secondary hyperparathyroidism observed in previous studies were caused by fluoride and a calcium intake insufficient to mineralize the new bone ... Fluoride might be expected to aggravate any tendency toward increased parathyroid hormone secretion in osteoporosis". Kyle et al. (1975) commented that "in the absence of additional calcium, the bone is incompletely mineralized. If fluoride administration continues ... the net result will be osteomalacia and increased bone resorption". To prevent osteomalacia, the calcium supplement must be "administered concurrently" with fluoride (Riggs and Jowsey 1972). Jowsey et al. (1972b) and Kyle et al. (1975) recommend that, in high-fluoride therapy, the calcium supplements, given concomitantly, should be 35 to 40 times the fluoride supplement, by weight. Marier (1977) noted that the calcium supplement is given in addition to the "adequate" calcium levels ingested in a normal diet, and this is thus indicative of a fluoride-induced increase in the metabolic requirement for calcium. If this same fluoride-to-calcium proportionality applies to chronic daily intake of fluoride, then the ingestion of 5 mg of fluoride per day would require a supplemental intake of 200 mg calcium per day. This extrapolation may not be justified, but it serves to emphasize the need for an adequate intake of dietary calcium during long-term exposure to fluoride. A vitamin D supplement of 50,000 units twice weekly has been recommended during high-fluoride treatment of osteoporosis (Jowsey et ae. 1972b; Riggs and Jowsey 1972; Kyle et al. 1975). However, Takizawa et al. (1975) did not obtain improvement in geriatric patients with this high vitamin D dosage. Riggs et al. (1976) recently compared two dosages of vitamin D (50,000 units, twice weekly, vs 400 units daily) given in conjunction with the calcium and fluoride. They concluded that "we do not recommend the large doses of vitamin D". (The vitamin D topic is also discussed in connection with fluoridated hemodialysis; see Section 5.8). In relating the significance of the various nutrient-versus fluoride interrelations discussed above to low-dose long-term daily exposure of humans to fluoride, it is pertinent to note that ingestion of fluoride has increased over the past few decades and is probably still escalating (Marier 1977; also Section 5.1). When one considers that nutritional surveys have shown that sizeable proportions of the North American population have an

inadequate dietary intake of calcium and of vitamin C (see "U.S. 1969"; "Canada 1973"), the need for vigilance is apparent.

Table 24. Symptoms common to both fluoride intoxication and magnesium deficiency (Marier 1968). (back to top) Symptom Leg cramps, or "pins and needles" Muscular twitching Fluoride intoxication Sauerbrunn et al. 1965 (human) Kretchner et al. 1963; Taves et al. 1965 (human) Ibid. Ibid. Geall and Beilin 1964 (human) Weatherall and Weidmann 1959 (rabbits, cats, and rats) Magnesium deficiency Fourman and Morgan 1962 (human) Hanna et al. 1960; Suter and Klingmann 1955 (human) Fourman and Morgan 1962 (human) Martindale and Heaton 1964 (rats) Fourman and Morgan 1962 (human) O-Dell et al. 1960 (rats)

Tetaniform convulsions (with normal serum Ca) 2 to 3-fold increase in serum P (at time of convulsion) Cataracts (optical neuritis) Bone exostoses and/or soft tissue calcification

5.7 THYROID FUNCTION (back to top) Day and Powell-Jackson (1972) reported that water-borne fluoride appeared to increase the prevalence of goitre in an area where goitre was already endemic. Teotia and Teotia (1975) observed a high incidence of goitre (up to 18% in the total population) in areas of endemic hydrofluorosis. Crawford (1972) has commented on such interactions as follows: "A Medical Research Council (U.K.) memorandum reported that, in some areas, even moderate concentrations of fluoride in drinking-waters could block iodine absorption. It is known that the iodine concentrations are lower in soft than in hard waters .... If fluoride is added to soft waters .... a proportion of the population may come to have suboptimal iodine intake. The effects might be subtle and slow to develop, and would certainly not be picked up by the crude screening used at present". In studies with rats, Back (1970) found that the thyroid preferentially retained increased amounts of fluoride for two weeks following fluoride administration. Zucas and Lajolo (1975) reported that removal of the pituitary gland caused increased deposition of skeletal fluoride, an effect that seemed to be "related to thyroid hypofunction". Bobek et al. (1976) observed that fluoride supplementation for a two-month period caused a slight decrease in blood thyroxine, a phenomenon thought to be caused by a fluoride-mediated alteration in the functioning of thyroxine-binding proteins. Day and Powell-Jackson (1972) recommended further research on the amino-acid precursors of thyroxine, particularly tyrosine and its metabolites, because increased

urinary loss of tyrosine has been reported in fluorosis; also, because tyrosine deficiency is a known cause of thyroid hypofunction. 5.8 KIDNEY-RELATED PROBLEMS (back to top) In the human body, the kidneys are probably the most crucial organ during the course of low-dose lonq-term exposure to fluoride. Healthy kidneys excrete 50 to 60% of the ingested dose (Marier and Rose 1971). Kidney malfunction can impede this excretion, thereby causing an increased deposition of fluoride into bone. Marier (1977) has reviewed data showing that, in persons with advanced bilateral pyelonephritis, the skeletal fluoride content can be 4-fold that of similarly-exposed persons with normal kidneys. Similarly, Mernagh et al. (1977) have reported a 4-fold higher skeletal fluoride content in persons with the renal failure of osteodystrophy. It has also been shown (Seidenberg et al. 1976; Hanhijarvi 1975) that plasma F- levels can be 3 1/2 to 5 times higher than normal in persons with renal insufficiency. It is thus apparent that persons afflicted with some types of kidney malfunction constitute another group that is more "at risk" than is the general population. (Note: Some kidney-related problems have already been discussed in Sections 4.1 and 4.2). Understandably, people who have little, or no, kidney function constitute a particular "at risk" group. This includes persons exposed to long-term hemodialysis with fluoridated (1 ppm) water, which aggravates the bone lesions of uremic renal osteodystrophy, by increasing the severity of bone osteomalacia and the incidence of spontaneous bone fractures (Posen et al. 1971; Johnson and Taves 1974). These effects parallel those observed in high-dose fluoride therapy of osteoporotic patients, i.e. osteomalacia (Merz et al. 1970; Jowsey et al. 1972b; Kyle et al. 1975) and spontaneous fractures (Inkovaara et al. 1975; Zanzi et al. 1975). Inkovaara et al. (1975) recommended that the plasma inorganic fluoride ion (plasma F-) concentration should not exceed 3 umol/l if spontaneous fractures are to be avoided. As a basis for comparison, Nielsen et al. (1973) report predialysis plasma F- levels of 9 umol/l, and Posen et al. (1971) extrapolate their observations to an initial (i.e. before the first dialysis treatment) level of 7 umol/l. Still higher plasma F- levels have been observed during the course of fluoridated dialysis (Posen et al. 1971; Jowsey et al. 1972a; Nielsen et al. 1973; Cordy et al. 1974). The plasma F- can attain a concentration of 36 pmol/l during long-term fluoridated hemodialysis treatment (Fournier et a. 1971), and this level is about 50 times higher than normally found in residents of unfluoridated communities (Taves 1968; Hanhijarvi 1975). During maintenance of patients on fluoridated hemodialysis, the increased body-burden of fluoride is reflected by high levels of fluoride in bone (Posen et al. 1971), and a high molar F/Ca ratio in bone (Jowsey et al. 1972a; Cordy et al. 1974). Posen et al. (1971) administered high doses (as high as 200,000 units per day) of vitamin D concurrently, and it was felt that this contributed to the severity of the bone changes. The patients studied by Cordy et al. (1974) had a daily vitamin D intake of only 460 units (Note: Riggs et al. (1976) now recommend 400 units daily during high fluoride therapy). Cordy

et al. (1974) observed lower plasma F- levels and less severe bone disease than previously reportedly Posen et al. (1971). In a study of fluoridated-hemodialysis patients, Nielsen et al. (1973) observed that 86% of their patients showed evidence of secondary hyperparathyroidism, along with a significant increase in serum alkaline phosphatase. These manifestations have also been seen in endemic fluorosis patients (Krishnamachari and Krishnaswami 1973; Teotia et al. 1974; Faccini and Teotia 1974; Sivakumar and Krishnamachari 1976). As discussed by Rao and Friedman (1973), some dialysis clinics have not encountered problems with fluoridated hemodialysis. Nevertheless, several researchers consider it prudent to use non-fluoridated water, so as to reduce the risk of osteomalacia (Stewart 1969; Posen et al. 1971; Jowsey et al. 1972a; Cordy et al. 1974; Lough et al. 1975; Rao and Friedman 1975). Persons suffering from nephropathic Diabetes Insinidus make up another subgroup that is more "at risk" than the general Population. Table 25 summarizes the observations on 10 such cases about whom we have found reports. A striking feature of this tabulation is the young age at which skeletal fluorosis has become evident in some of these patients. Thus, Juncos and Donadio (1972) diagnosed skeletal fluorosis in an 18-year-old boy and a 17year-old girl. The only other report of skeletal fluorosis in children appears to be that of Teotia et al. (1971), which dealt with endemic hydrofluorosis in India.

Table 25. Fluorosis in persons who have the Diabetes Insipidus syndrome. (back to top) Patient Drinking-water F intake Diagnosis from Age Sex F, Intake, Drinkingmg/l l/day water mg/day 64 M 2.56 4 to 10 10.24 to Skeletal 25.6 fluorosis polydipsia polyuria pyelonephritis Diabetes Insipidus 18 M 2.6 "about 2 approx. 20 Skeletal gal." fluorosis 17 F 1.7 ? polydipsia "large polyuria amounts" renal insufficiency 10 M 1.0 1.25 to 1.25 to 3.0 Dental 3.0 fluorosis 11 M 1.0 1.25 to 3.0 polydipsia 1.25 to polyuria 3.0 nephropathy Diabetes Authors' Comments Reference

"Drinking-water seems to have been his only source of fluoride intake...Prolonged polydipsia may be hazardous to persons who live in areas where the levels of fluoride in drinkingwater are not those usually associated with significant fluorosis." "It is postulated that the renal insufficiency, which resulted in the large intake of fluoride-containing water and reduced excretion of fluoride, combinedto produce systemic fluorosis." "We are reporting two children with nephrogenic diabetes insipidus and fluorosis, and suggest looking for evidence of fluoride toxicity in individuals with polydipsia. Substituting non-fluoridated water as

Sauerbrunn et al. 1965

Juncos and Donadio 1972

Greenberg et al. 1974

Insipidus 35 14 13 10 8 F F F F M 0.5 0.5 0.5 0.5 0.5 10 to 15 10 to 15 10 to 15 4 to 5 4 to 5 5 to 7.5 5 to 7.5 5 to 7.5 2 to 2.5 2 to 2.5 Dental fluorosis polydipsia polyuria Diabetes Insipidus

part of the fluid intake is recommended." "Drinking of large amounts of water, Klein 1975 even with lower-than accepted fluoride content, can produce fluorosis of the teeth."

Comparison of the "Diagnosis", "F intake", and "Age" columns in Table 25 suggests that there is a progression from nephropathy, to renal insufficiency, to pyelonephritis,with increasing age and/or sustained fluoride intake. This is corroborated in the Algerian studies of various stages of human hydrofluorosis, as conducted by Poey et al. (1976). Gradual impairment of urinary creatinine clearance was indicative of progressive inhibition of kidney glomerular filtration, affecting tubular reabsorption of water. In the final stage, urinary excretion of fluoride accounted for only 10 to 20% of the intake (i.e. about 1/6 to 1/3 of normal), and was thus indicative of high fluoride retention. Based on histologically-detectable glomerular degeneration, Poey et al. concluded that fluoride can complicate, or can actually induce, nephropathy. The WHO (1970) report had recognized that "the remote possibility that fluoride may aggravate renal disease has not been conclusively ruled out". In all the cases tabulated in Table 25, the patients had the excessive thirst of polydipsia. As noted by Klein (1975), even if the beverages consumed to satisfy this thirst have a "lower-than-accepted" fluoride content, this can result in an excessive intake of fluoride. Experinmental confirmation of fluoride-induced polydipsia is found in the 18-month study by Manocha et al. (1975), who observed-that fluoride caused a considerable increase in the water intake of monkeys. Another aspect of the Diabetes Insipidus syndrome is the abnormally-high output of urine (polyuria). In a report of a study with rats, Hamuro (1972b) has stated: "The Polyuria induced by fluoride was accompanied by an enhanced sodium excretion and a decrease in osmolality. These results were consistent with previous findings that the administration of fluoride caused polyuria in laboratory animals". In a study with humans, Taves et al. (1972) remarked that "The data .... is consistent with the hypothesis that F (i.e. fluoride) is the cause of the polyuria" Singer and Forrest (1976), writing about drug-induced states of nephrogenic Diabetes Insipidus in humans, state that "these studies (with sodium fluoride) have been interpreted to suggest that sodium fluoride does not grossly impair (kidney) ascending-limb sodium chloride transport, but may cause nephrogenic Diabetes Insipidus, either by washing-out the medullary solute

(since fluoride is a vasodilator in many vascular beds), or by reducing the collecting-duct permeability". Manocha et ai. (1975) reported "significant cytochemical changes" in the kidneys of monkeys which had consumed water containing 1 or 5 ppm fluoride for an 18-month period. Thus, there is suggestive evidence that fluoride may cause nephrogenic Diabetes Insipidus. Corroborative evidence for the above statementsis found in the results of studies on the effect of the metabolically-unstable anesthetic, methoxyflurane, which releases inorganic fluoride to body fluids. Thus, Gottlieb and Trey (1974) have stated: "This (methoxyflurane) syndrome is .... similar to that of nephrogenic Diabetes Insipidus .... these patients were unable to concentrate urine, despite fluid deprivation or administration of vasopressin .... the (kidney) changes indicated that the lesion was of the distal nephron .... None of the control patients developed nephrogenic Diabetes Insipidus, while methoxyflurane patients developed this syndrome. (There was) a relationship among the dose of methoxyflurane .... serum peak inorganic fluoride levels, and renal effects". Cousins and Mazze (1973) also commented on the methoxyflurane syndrome as follows: "Serum hyperosmolality occurring simultaneously with polyuria, and decreased urine osmolality is evidence of water-losing nephropathy, although primary antidiuretic hormone deficiency (Diabetes Insipidus) could produce similar abnormalities. However, unlike Diabetes Insipidus, polyuria following methoxyflurane administration was vasopressin-resistant, indicating a renal lesion .... (Also, excessive) thirst and polyuria added difficulty to post-operative management". With reference to the foregoing quotation, it is pertinent to note (see Table 25) that the patient treated by Sauerbrunn et al. (1965), and the two treated by Greenberg et at, (1974) were vasopressin-resistant; this suggests that they were suffering from fluoride-mediated renal lesions. Conversely, the two youngest patients in Klein's (1975) study responded to vasopressin treatment, i.e. indicative of hereditary Diabetes Insipidus (Cousins and Mazze 1973; Klein 1975). Thus, as noted by Marier (1977), there are identifiable individuals among the general population who are more "at risk" relative to fluoride intoxication, because they are afflicted with the polyuria-polydipsia syndrome of Diabetes Insipidus. Such people ingest abnormal amounts of fluoride in beverages, and retain an abnormally high proportion of the total ingested fluoride, as reflected in Hanhijarvi's (1975) observation that they have a low urinary fluoride clearance and a high plasma F- level. It is therefore appropriate to note that, recently (see JAMA 1976), diabetes (including cases with nephropathy) has been ranked third as a cause-of-death factor, accounting for an estimated 300,000 deaths per year; also, the incidence of diabetes increased by 6% per year during the period 19651975. If an escalation in the incidence of nephropathic diabetes has occurred, it should be carefully considered in relation to the evidence discussed in the present report.

5.9 ATTEMPTS TO ESTIMATE CRITERIA FOR HUMAN INTAKE OF FLUORIDE (back to top) Precise data on the total daily intake of fluoride by humans are scarce. Most studies of fluoride as a possible hazard to human health have reported only the fluoride exposure from a single source (e.g. water, or polluted air in the workplace). This preoccupation with fluoride from one source, coupled with the difficulty of quantifying or even identifying, with certainty, the early stages of a fluoride-induced injury, has inhibited attempts to establish criteria that would define an acceptable level of intake. However, the need for such criteria is apparent, and two recent publications have reported attempts to set a value for an acceptable daily intake. Farkas (1975) attempted to estimate a "safe" level of fluoride intake by means of a questionnaire directed to "authorities" in the fields of dentistry, medicine, nutrition, and biological research. The questionnaire requested a definite estimate in absolute terms (mg/kg body weight per day), but no consensus developed. Many respondents merely indicated that various levels of ingested fluoride, expressed in parts-per-million (ppm), were acceptable or recommended. However, five of the respondents agreed that 0.05 to 0.07 mg/kg body weight per day was a reasonable estimate of the acceptable daily intake of fluoride. Toth (1975) contended that the amount of fluoride "which is ingested with drinkingwater" should be considered optimal. Toth estimated that this amount is 0.045 mg/kg body weight per day for infants, and declines to 0.023 mg/kg for adults. By considering various factors, Toth also estimated a "tolerable dose" (which presumably approximates an acceptable daily intake) of 0.073 mg/kg body weight per day for infants, and 0.033 mg/kg for adults. Reference Man has a body mass of 70 kg (ICRP 1975). Man's total water intake has been estimated to be 2400 ml/day (Spencer et al. 1970). Therefore, ingestion of 2400 ml of water with a fluoride concentration of 1 mg/l would provide a daily fluoride intake of 0.034 mq/kg from water. A more direct, criteria-based, approach to the estimation of an acceptable daily intake is urgently required, and the present authors therefore reluctantly present the following calculations, in spite of the obvious limits to their accuracy. 5.9.1 Criteria Based on Bone Fluoride and Plasma F- (back to top) Kramer et al. (1974) presented data on the fluoride content of drinking water, in relation to the total fluoride intake from three daily meals by adults residing in 16 locations in the U.S. The regression equation calculated (by us) from these data is: Daily fluoride intake, mg = (0.98 ± 0.41) + (ppm waterborne F x 1.63 ± 0.50) This equation (hereafter referred to as "Equation A") has an r2 value of 0.44. Although the error factors are large, this equation enables us to convert waterborne fluoride levels

to daily dietary intakes. It must be emphasized that the Kramer et al. (1974) data do not include between-meal ingestion of drinking-water or other fluoridated beverages, and therefore underestimate the total daily fluoride intake. Hodge (1952) and Jackson and Weidmann (1958) reported the fluoride content of drinking-water as it relates to the fluoride content of dry fat-free rib bone of lifetime residents in four communities whose drinking-waters differ in fluoride content (i.e. 0.06, 0.5, 0.8, and 1.9 ppm). In Fig. 4, we have plotted dietary fluoride intake (calculated from waterborne fluoride by Equation A, above) in relation to the fluoride content of rib bone from 55-year-old individuals, as reported by Hodge (1952) and by Jackson and Weidmann (1958). If a fluoride content of 2500 to 4000 ppm in dry fat-free rib (a cancellous-type bone) can be taken as an upper range of tolerable limits (cf Section 5.3; also Jackson and Weidmann 1958), this would reflect an intake of 2.5 to 4.1 mg fluoride from the three daily meals. For a 70 kg adult, this calculation leads to an estimated acceptable intake, from the three daily meals, of 0.036 to 0.059 mg/kg body weight. Another approach to criteria is based on blood plasma ionic fluoride. Hanhijarvi (1975) has determined the equations relating blood plasma F- levels to age of humans residing in areas with non-fluoridated (0.2 ppm) or fluoridated (1.0 ppm) water. The conversion of waterborne fluoride content to dietary fluoride intake was again calculated (by us) from Equation A, above. Blood plasma F- levels for 55-year-old humans were calculated by using Hanhijarvi's equations. The results are plotted in Fig. 4, where they are extrapolated linearly to allow an interpretive assessment. Inkovaara et al. (1975) have provided the best available estimate of a tolerable maximum level for plasma F-; during a 10-month study of geriatric patients, they observed spontaneous bone fractures at blood plasma F- levels as low as 2.1 umol/l, and recommended that it should not rise in excess of 3.0 pmol/l. In terms of Fig. 4, these levels reflect a range of fluoride intakes of 3.7 to 5.3 mg fluoride from the three daily meals, i.e. equivalent to a range of 0.053 to 0.076 mg/kg for a 70 kg human. In summary (and including the estimates by Farkas and by Toth, cited in Section 5.9), the available estimates of an acceptable daily intake of fluoride for humans are: 0.05 to 0.07 mg/kg (Farkas; questionnaire) 0.033 to 0.073 mg/kg (Toth; "tolerable" level) 0.036 to 0.059 mg/kg (our calculation based on rib bone) 0.053 to 0.076 mg/kg (our calculation based on plasma F-) The agreement among these values is sufficiently close to suggest that the various approaches are meaningful. Serious attempts to increase the data-base for such calculations should be encouraged. However, it must not be overlooked that the acceptable intake derived from such calculations applies only to an "average" individual, and that some "safety factor" must be applied to ensure protection of the less resistant individuals in the general population.

In Sections 3.1.1 and 5.8, we discussed the fact that, in persons with renal insufficiency, the bone and plasma F levels can be 4 times higher than in similarly-exposed persons with normal kidneys. Until there is evidence to the contrary, we must therefore conclude that some persons with renal insufficiency have only one-quarter the fluoride tolerance reported in the above tabulation. In Section 5.1.1, we stated that the current total fluoride intake from foods and beverages, in areas with fluoridated (1 ppm) water, probably ranges from 3.5 to 5.5 mg/day, i.e. equivalent to 0.05 to 0.08 mg/kg/day for a 70 kg "average" human. This range is almost within the ranges for long-term "acceptable daily intake" tabulated above. 5.9.2 Assessment of Fluoride Intake From Air (back to top) The information discussed in Sections 5.9 and 5.9.1 allows an evaluation of human intake of fluoride from air, especially in the workplace where there has been disagreement about what constitutes an acceptable concentration of airborne fluoride. Inhaled fluorides, whether in gaseous or in particulate form, are almost completely absorbed into the bloodstream (WHO 1970; Hodge and Smith 1977). Therefore, assuming an inhalation of 10 m3 of air during an 8-hour working shift (Dinman et al. 1976a), the various airborne fluoride levels discussed for workplace exposure can be converted into daily uptakes of fluoride by a 70 kg human. Because workplace exposure is on a 5 day/week basis, a correction factor of 5/7 was used to express intake on an equalized "per day" basis. [In summary, the airborne fluoride concentration is multiplied by 10 (M3), divided by 70 (kq), then multiplied by 5/7; the overall conversion factor is thus 0.102]. This calculation leads to the following tabulation:
Airborne Fluoride mg/m3 2.5 0.5 0.22 0.1 Fluoride Uptake From Workplace Air mg/kg/day 0.255 0.051 0.022 0.010

Discussed by Hodge and Smith (1977) Vishnevski (1969) Guminska and Sterkowicz (1975) Vishnevski (1969)

These calculated intakes are from air only and must be considered additional to those discussed in Section 5.9.1. it is apparent that the long-term implications of the occupational exposures require careful study, taking into consideration both the nonoccupational exposures to fluoride and the period (i.e. portion of lifetime) of additional exposure to workplace airborne fluorides. 6.0 OVERVIEW AND RECOMMENDED RESEARCH (back to top) 1. Despite improvements in, and more extensive use of, emission control equipment, large quantities of fluoride continue to be discharged into the atmosphere from industrial

sources. In 1972, at least 14,236 metric tons of fluoride (calculated as fluorine) were discharged into the air in Canada, and some 150,000 metric tons were discharged in all of North America. 2. Large quantities of fluoride are also discharged into streams, rivers, lakes and oceans, as a component of industrial waste-waters. It appears probable that the amounts thus discharged are several-fold larger than the amounts discharged into the atmosphere. Many systems utilized for airborne emission-control contribute extensively to the amount of fluoride discharged in wastewaters. 3. Much of the fluoride discharged into the atmosphere arises from "point sources" such as smelters. Dispersion of the pollutant in the surrounding area is not uniform; therefore, the siting of monitoring devices, and the selection of sites for sampling of vegetation, must consider: a) Stratification of the pollutant, with the higher levels of atmospheric fluoride found at the greater heights. This has significance to ecological damage to vegetation on exposed hilltops or mountainsides, even at considerable distances from the emitting source; b) The "shielding" effects of vegetation and other obstacles, which results in lower fluoride exposure (and uptake by) vegetation growing on the downwind side of such obstacles. 4. The ecological impact of airborne fluoride emissions is known to be serious with regard to coniferous forests and to epiphytes and bryophytes. However, lichens and mosses are less susceptible to fluoride injury than coniferous trees. Relatively little is known about the effects of fluoride on aquatic life, even though large amounts of fluoride are known to be released into some waterways. More attention should be paid to fluoride effects on pollinating insects and on plankton. 5. Airborne fluoride has had a serious impact on agricultural and silvicultural species. With airborne gaseous fluoride there is no evidence for a no-effect threshold level below which no reduction in crop yield occurs, especially over the long term. For exposure of Canadian forest species, the average (30-day) airborne gaseous fluoride concentration should not exceed 0.2 ug/M3. There is an urgent need for long-term Cause/Effect studies of species known to be sensitive to fluoride injury. 6. There have been episodes where the impact of fluoride pollution on livestock and on wild ungulates has been severe. To date, regulations limiting the fluoride content of fodders have provided neither adequate protection against economic loss to the farmer nor adequate control of airborne fluoride. For young growing swine, an 18-week exposure to dietary fluoride (whether in forages, feeds, or mineral supplements) can be expected to decrease daily weight-gain by about 4% for each 100 ppm increment of dietary fluoride. The need for further data on which Cause/Effect equations can be based is apparent. Loss of weight-gain may be a suitable measure of sub-clinical (pre-skeletal) intoxication.

7. There is clear evidence that wildlife species are more vulnerable to fluoride toxicosis than are livestock species. The impact seems to be most severe on predator species, because they must capture their prey and because they are more susceptible to the bioaccumulation of fluoride through their food chain. Cause/Effect studies of these species should include consideration of the multiple stresses imposed by the ecosystem (e.g. malnutrition). 8. Researchers in various regions of the world have reported that human hydrofluorosis is less severe when the waterborne fluoride is ingested from hard waters, than from soft waters. There is evidence that chronic intake of fluoride increases the long-term metabolic requirement for both calcium and magnesium. Other studies have indicated that fluoride may increase the metabolic requirement for vitamin C and manganese. The Cause/Effect aspects of these dietary/nutritional factors require urgent attention, with regard to chronic intake of fluoride. There is no doubt that inadequate nutrition increases the severity of fluoride toxicosis. 9. Fluoride has displayed mutagenic activity in studies of vegetation, insects, and mammalian oocytes. There is a high correlation between carcinogenicity and mutagenicity of pollutants, and fluoride has been one of the major pollutants in several situations where a high incidence of respiratory cancer has been observed. For these reasons, the relation between airborne fluoride and incidence of lung cancer needs to be investigated. 10. Long-term ingestion, with accumulation of fluoride in animals and man, induces metabolic and biochemical changes, the significance of which has not yet been fully assessed. It cannot be assumed that such changes are of no significance to human health. There is evidence that neurological complaints are related to the early histological changes that precede overt skeletal fluorosis. There is also evidence that the early bone changes can reflect an entire gamut of abnormalities, depending on factors such as nutritional and metabolic status. Further studies on the early subtle changes of fluoride toxicosis in humans, in terms of both diagnostic aids and Cause/Effect interrelations, should have a high priority. 11. Fluoride is a persistent bioaccumulator, and is entering into human food-andbeverage chains in increasing amounts. Careful consideration of all available data indicates that the amount of fluoride ingested daily in foods and beverages by adult humans living in fluoridated communities currently ranges between 3.5 and 5.5 mg. For a 70 kg human adult, this range is close to the 0.03 to 0.07 mg/kg/day estimated for "an acceptable daily intake". In addition to the food-chain, dentifrices and pharmaceuticals can contribute siqnificantly to the fluoride intake of some individuals. 12. Inhalation of airborne fluoride may contribute several milligrams to the total daily intake of industrial workers, and may be significant for persons residing near sources of fluoride emissions. However, the effect of airborne fluoride on human respiratory tissue is not necessarily related to total bodyburden, but may relate to the direct impact of

fluoride on respiratory tissues. The contribution of cigarette-smoking to fluoride intake also requires study. 13. In the assessment of the impact of fluoride on animals and man, more attention should be focussed on the concentration of inorganic fluoride in blood plasma. Available evidence indicates that accurate assessment of the plasma F concentration can provide valuable information about the body-burden during chronic fluoride intake. 14. In addition to industrial workers, there are several sub-groups of the population who may be more affected by environmental fluoride than the population at large. These are persons who: a) Have a sub-optimal nutritional status, especially with regard to calcium, magnesium, vitamin C, manganese, or a low dietary Ca/P ratio (Note: This also applies to animals); b) Live in the proximity of fluoride-emitting industries; c) Live in regions where goitre is endemic, because there is suggestive evidence that fluoride may increase the incidence of goitre in such regions; d) Have kidney impairments, particularly those with bilateral pyelonephritis or nephropathic Diabetes Insipidus; e) Have the excessive-thirst polydipsia associated with diabetes, because they consume large quantities of fluids. These may be called "critical groups" (ICRP 1977) either because they accumulate more fluoride or suffer toxic effects more readily. 15. Standards limiting emissions or environmental concentrations of fluoride should be based on criteria which include those derived from studies of these "critical groups". 16. In addition to the research recommendations we have made, we would like to acknowledge those presented in a recent U.S. National Academy of Sciences report (see Fleischer et al. 1974): a) Additional detailed studies are needed of the health of human and animal populations exposed to high concentrations of airborne fluorides; b) The gross effects of fluoride on plants and animals have been studied, but much needs to be done on the basic biochemical lesions induced by fluoride, and on dietary factors affecting fluoride uptake by man; c) The very large emission of fluorocarbons (freons), and their rapidly increasing use, require study of their distribution, rate of degradation, and possible effects on plants, animals and humans; d) Waste waters of high fluoride content have been released from phosphate processing and from the aluminum industry, with detrimental effects to such marine organisms as oysters and crabs. Possible chronic effects from exposure of such organisms to lower levels of fluoride need study;

e) In view of the high fluoride content reported to exist in some fish-protein concentrates used as food supplements, the possible impact of this added source of fluoride in the diet should be further investigated; f) Methods of sampling and separating gaseous and particulate forms of airborne fluoride need study and standardization; g) Further work is needed on the relation of the uptake of fluorine by plants to its concentration in the air; h) Study of the form of fluorine in plants is highly desirable, especially the nature of fluorine bonding in plant tissue and its solubility in aqueous solutions; i) More data are needed on the relation of the fluoride content of groundwaters to the mineralogical and chemical composition of the source rocks. These NAS recommendations are fully compatible with the information that we have presented in this report or in our previous review (Marier and Rose 1971).

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U.S. 1969. White House Conference on food and nutrition, Dec. 1969. Summarized in National Dairy Council of Canada, Bulletin Service No. 198, Dec. 1, 1969. Van Dyke, R.A. and Gandolfi, A.J. 1976. Anaerobic release of fluoride from halothane. Drug Metabolism and Disposition 4: 40-44. Vejrosta, Z., Sindelka, M., Feller, M. and Vilser, M. 1975. Study of dental caries in children drinking water with a high content of magnesium. Ceskoslovenska Stomatologie 75: 346-354. Vickery, B. and Vickery, M.L. 1972. Fluoride metabolism in Dichapetalum toxicarium. Phytochem. 11: 1905-1909. Vickery, B. and Vickery, M.L. 1975. The synthesis and defluorination of monofluoroacetate in some Dichapetalum species. Phytochem. 14: 423-427. Vins, B. and Mrkva, R. 1973. The diameter increment losses of pine stands as a result of injurious immissions. Acta. Universitatis Agriculturae (Brno) Series C 42: 25-46. Vishnevski, V.L. 196.9. Materials for setting standards of hydrogen fluoride in the air of industrial areas. Gig. Tr. Prof. Zabol. 13: 60-62. Voroshilin, S.I., Plotko, E.G., Gatiyatullina, E.A. and Gileva, E.A. 1973. Cytogenetic effect of inorganic fluorine compounds on human and animal cells in vivo and in vitro. Soviet Genet. (English translation of Genetika) 9: 492-496. Voroshilin, S.I., Plotko, E.G. and Nikiforova, V.Y. 1975. Mutagenic effect of hydrogen fluoride on animals. Cytol. Genet. (English translation of Tsitol. Genet.) 9: 40-42. Vouilloz, R. 1975. Pollutions fluordes en Valais. Rapport de l'Assoc. de d6fense contre les 6manations nocives en Valais. De'cembre. Martigny, Suisse. (16 pp.). Waldbott, G.L. and Cecilioni, V.A. 1969. Neighborhood fluorosis. Clin. Toxicol. 2: 387396. Ward, P.F.V. and Huskisson, N.S. 1972. The metabolism of fluoroacetate in lettuce. Biochem. J. 130: 575-587. Warner, T.B., Jones, M.M., Miller, G.R. and Kester, D.R. 1975. Fluoride in sea water: Intercalibration study based on electrometric and spectrophotometric methods. Anal. Chim. Acta 77: 223-228. Weatherall, J.A. and Weidmann, S.M. 1959. The skeletal changes of chronic experimental fluorosis. J. Pathol. Bact. 78: 233-241.

Weinstein, L.H. 1977. Fluoride and plant life. J. Occup. Med. 19: 49-78. WHO 1970. World Health Organization. "Fluorides and human health" Monograph Series. No. 59. (364 pp.). Wiatrowski, E., Kramer, L., Osis, D. and Spencer, H. 1975. Dietary fluoride intake of infants. Pediatrics 55: 517-522. Widger, L.A., Gandolfi, A.J. and van Dyke, R.A. 1976. Hypoxia and halothane metabolism in vivo. Anesthesiology 44: 197-201. Williams, R.E. 10,75. Landfills, the 1977 fate of air and waterborne wastes. Ground Water J. Jul.-Aug. pp. 367-371. Wolinsky, I., Simkin, A. and Guggenheim, K. 1972. Effect of fluoride on metabolism and mechanical properties of rat bones. Amer. J. Physiol. 9-23: 46-50. Wright, D.A. and Davison, A.W. 1975. The accumulation of fluoride by marine and intertidal animals. Environ. Pollut. 8: 1-13. Wright, D.A. 1977. Toxicity of fluoride to brown trout fry (Salmo trutta). Environ. Pollut. 12: 57-62. Yee-Meiler, D. 1974. Uber den Einflusz fluorhaltiger Fabrikabgase auf den Phenolgehalt von Fichtennadeln. Europ. J. Forest Path. 4: 214-221. Yiamouyiannis, J.A. and Burk, D. 1976. Fluoridation of public water systems and cancer death rates in humans. Fed. Proc. 35: 1707. Yiamouyiannis, J.A. and Burk, D. 1977. Fluoridation and cancer -- Age dependence of cancer mortality related to artificial fluoridation. Fluoride 10:102-123. Young, S.R., Stoelting, R.K., Peterson, C. and Madura, J.A. 1975. Anesthetic biotransformation and renal function in obese patients during and after methoxyflurane or halothane anesthesia. Anesthesiology 42: 451-457. Zanzi, I., Aloia, J.F., Ellis, K.J., Vaswani, A., Wallach, S. and Cohn, S.H. 1975. Treatment of osteoporosis with salmon calcitonin, sodium fluoride and calcium. Results of in vivo neutron activation analyses. Clin. Res. 23: 335A Zhavoronkov, S.A., Khovanskaya, M.G. and Korolenko, V.P. 1969. Condition of the liver in fluorine poisoning. Vestnik Akademii Meditsinkikh Nauk SSSR 24(9): 39-42. Zhavoronkov, A.A. and Dubynin, T.L. 1971. Changes in the kidneys in chronic fluorine poisoning. Bull. Exp. Biol. Med. 72: 1094-1096. (Trans. Consultants Bureau, N.Y.).

Zucas, S.M. and Lajolo, F.M. 1975. Influencia da hypofise sobre a fixacao de fluor em ossos de ratos. Rev. Farm. Bioquim. Univ. Sao Paulo 13: 103-116. Zumpt, 1. 1975. Chronic fluoride poisoning in sheep. J. South African Vet. Assoc. 46: 161-163.

National Research Council of Canada - 1977 (back to top)

Part I Overview Information

Department of Health and Human Services Issuing Organization
National Institute of Dental and Craniofacial Research (NIDCR), (http://www.nidcr.nih.gov/)

Participating Organizations
National Institutes of Health (NIH), (http://www.nih.gov/)

Components of Participating Organizations
National Institute of Dental and Craniofacial Research (NIDCR), (http://www.nidcr.nih.gov/)

Title: Pharmacogenetics Announcement Type
New

of Fluoride (R01)

Update: The following update relating to this announcement has been issued:

December 8, 2006 - The R01 portion of this funding opportunity has been replaced by PAR07-131, which now uses the electronic SF424 (R&R) application for February 5, 2007 submission dates and beyond.

Looking ahead: As part of the Department of Health and Human Services' implementation of eGovernment, during FY 2006 the NIH will gradually transition each research grant mechanism to electronic submission through Grants.gov and the use of the SF 424 Research and Related (R&R) forms. Therefore, once the transition is made for a specific grant mechanism, investigators and institutions will be required to submit applications electronically using Grants.gov.. For more information and an initial timeline, see http://era.nih.gov/ElectronicReceipt/. NIH will announce each grant mechanism change in the NIH Guide to Grants and Contracts (http://grants.nih.gov/grants/guide/index.html). Specific funding opportunity announcements will also clearly indicate if Grants.gov submission and the use of the SF424 (R&R) is required. Investigators should consult the NIH Forms and Applications Web site (http://grants.nih.gov/grants/forms.htm) for the most current information when preparing a grant application.

Program Announcement (PA) Number:

PAR-06-214

Catalog of Federal Domestic Assistance Number(s)
93.121

Key Dates
Release Date: March 3, 2006 Letters of Intent Receipt Dates: April 17, 2006, 2007, 2008; August 17, 2006, 2007, 2008; December 17, 2006, 2007, 2008 Application Receipt Dates: May 15, 2006, 2007, 2008; September 15, 2006, 2007, 2008; January 15, 2007, 2008, 2009 Peer Review Dates: October-November 2006, 2007, 2008; February-March 2007, 2008, 2009; JuneJuly 2007, 2008, 2009 Council Review Dates: January 2007, 2008, 2009; May 2007, 2008, 2009; September 2007, 2008, 2009 Earliest Anticipated Start Dates: April 2007, 2008, 2009; July 2007, 2008, 2009; December 2007, 2008, 2009 Additional Information To Be Available Date (Url Activation Date): Not applicable Expiration Date for R01 Non-AIDS Applications: November 2, 2006 Expiration Date for R01 AIDS and AIDS-Related Applications: January 3, 2007

Due Dates for E.O. 12372
Not Applicable

Additional Overview Content
Executive Summary
The National Institute of Dental and Craniofacial Research (NIDCR) invites applications for research projects focusing on the genetic basis underlying individual responses to ingested fluoride in tooth mineralized tissues and other physiological processes. Projects should aim to identify and characterize fluoride-responsive genetic variations in humans or animal models. Applicants should specifically address how pharmacogenetics data will be interpreted and translated into risk assessment for public health.

This funding opportunity will utilize the Individual Research Project Grant (R01) mechanism, but runs in parallel with a funding opportunity announcement (FOA) of identical scientific scope PAR-06-215 that will utilize the Exploratory/Developmental Research Grant (R21) mechanism.

Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary. The total amount awarded and the number of awards will depend upon the mechanism numbers, quality, duration, and costs of the applications received.

• •

This FOA will use the Individual Research Project Grant (R01) mechanism. Eligible organizations include for-profit and non-profit organizations, public or private institutions such as universities, colleges, hospitals and laboratories, units of State and local governments including tribal governments, eligible agencies of the Federal government, domestic or foreign institutions/organizations, or faith-based or communitybased organizations.

Eligible principal investigators include any individual with the skills, knowledge, and resources necessary to carry out the proposed research. Individuals from underrepresented racial and ethnic groups as well as individuals with disabilities are always encouraged to apply for NIH programs.

• • •

Applicants may submit more than one application, provided they are scientifically distinct. See Section IV.1 for application materials. Telecommunications for the hearing impaired is available at: TTY 301-451-0088

Table of Contents

Part I Overview Information

Part II Full Text of Announcement

Section I. Funding Opportunity Description 1. Research Objectives

Section II. Award Information 1. Mechanism(s) of Support 2. Funds Available

Section III. Eligibility Information 1. Eligible Applicants A. Eligible Institutions B. Eligible Individuals 2.Cost Sharing or Matching

3. Other - Special Eligibility Criteria

Section IV. Application and Submission Information 1. Address to Request Application Information 2. Content and Form of Application Submission 3. Submission Dates and Times A. Receipt and Review and Anticipated Start Dates 1. Letter of Intent B. Sending an Application to the NIH C. Application Processing 4. Intergovernmental Review 5. Funding Restrictions 6. Other Submission Requirements

Section V. Application Review Information 1. Criteria 2. Review and Selection Process A. Additional Review Criteria B. Additional Review Considerations C. Sharing Research Data D. Sharing Research Resources 3. Anticipated Announcement and Award Dates

Section VI. Award Administration Information 1. Award Notices 2. Administrative and National Policy Requirements 3. Reporting

Section VII. Agency Contact(s) 1. Scientific/Research Contact(s) 2. Peer Review Contact(s) 3. Financial/ Grants Management Contact(s)

Section VIII. Other Information - Required Federal Citations

Part II - Full Text of Announcement

Section I. Funding Opportunity Description

1. Research Objectives
Purpose

The purpose of this Funding Opportunity Announcement (FOA) is to stimulate research on the genetic basis underlying individual responses to ingested fluoride. Although there is a volume of literature describing the effects of fluoride on both mineralized and non-mineralized tissues, the genetic determinants of our physiological responses to fluoride is an unexplored research area. Recent advances in genetic and genomic sciences provide unique opportunities to apply pharmacogenetic approaches to fluoride research; how genetic variations determine heterogeneous physiological responses to fluoride.

Projects should aim to identify and characterize fluoride-responsive genetic variations, e.g. polymorphisms, in humans and animal models. Functional analyses of these variants will be necessary in determining their contribution to differential phenotypes in tooth mineralized tissues or other physiological processes in response to fluoride. Projects may test candidate genetic variants, or search for genetic variants that are accountable for well characterized fluoride-responsive phenotypes. Projects should explicitly state whether a causal relationship between fluorideresponsive genotype and phenotype will be studied, and how this relationship will be established with appropriate controls. Applicants should specifically address how pharmacogenetics data will be interpreted and translated into public health risk assessment. The predicted relevance to human conditions of data generated through animal studies should be addressed. Study design should include fluoride exposure levels that are relevant and typical of human exposures. Gene expression profiling studies are not responsive to this FOA unless there are data to suggest that changes in gene expression level in response to fluoride are due to polymorphisms or epigenetic modifications in the gene of interest. Background

Since the introduction of fluoride in community drinking water in 1945, there has been a steady decline in the prevalence and severity of dental caries among Americans living in fluoridated communities. In fact, water fluoridation was touted by the Center for Disease Control and Prevention as one of the top ten public health achievements of the twentieth century. However, with this decline in caries prevalence, there has been an increase in dental fluorosis among children living in fluoridated communities. It has been estimated that between 20-80% of these children have

mild fluorosis and 4% have moderate to severe fluorosis. A recent analysis of the NHANES datasets indicated that the prevalence of fluorosis among 6-19 year old children increased by 9% since 1987. This increase is thought to be due, in part, to the increase in fluoride intake from sources other than drinking water including fluoridated beverages, supplements and topical fluoride-containing dental products that may be ingested. Factors such as nutrition have been implicated in an increase in an individual’s susceptibility to fluorosis but probably do not fully account for the prevalence observed in the population. On the other hand, although the proper use of fluoride generally reduces dental caries, the extent of its effectiveness varies among different communities.

Ingested fluoride is rapidly and efficiently absorbed through the gastrointestinal system and approximately 35-70% is eventually cleared by the renal system. Most of the fluoride retained in the body is incorporated into bones and teeth. The majority of fluoride related research efforts have focused on tooth enamel. Enamel development begins with the secretion of a set of enamel matrix proteins by ameloblasts that nucleates minerals. Matrix proteins continue to interact with minerals and guide crystal growth. Crystals are aligned in parallel arrays, which further orient themselves to form an interwoven superstructure of hydroxyapatite. Matrix proteins are degraded by proteolytic enzymes and removed leaving enamel that contains 98% minerals. Fluoride is anticariogenic at low concentration. Studies have shown that, during enamel mineralization, fluoride can be intercalated into the enamel crystal structure as fluoroapatite which is more resistant to dissolution than hydroxyapatite. However, excess fluoride results in dental fluorosis characterized by changes in enamel that vary from barely discernible fine white striations to pitted brown lesions. Some studies suggest that fluoride interferes with the activities of enamel matrix protein processing enzymes resulting in a delay in the clearance of matrix proteins during the maturation phase of amelogenesis and incomplete mineralization. Fluoride may also interfere with the maturation and differentiation of ameloblasts. In regard to its effects on bone, fluoride is considered anabolic in that it stimulates osteoblast proliferation and mineral deposition. However, excessive fluoride can result in an increase in bone density which can compromise bone quality and strength such that fluorotic bones have increased fracture rates and delayed fracture repair.

Fluoride might also affect the physiological processes of non-mineralized tissues. Human and animal studies of acute lethal or toxic levels of fluoride show that it affects the gastrointestinal, cardiovascular, renal, reproductive, and neuroendocrine systems. It has also been proposed that fluoride might increase the incidence of osteosarcomas in young males. Most of these studies have been inconclusive and inconsistent. Animal experiments have used relatively high levels of fluoride, whereas well controlled studies using relevant ranges that reflect more typical levels of human exposure are lacking.

The involvement of genetic determinants in fluoride responsiveness has been implicated in several studies. A number of ecological studies of populations around the world living in areas with naturally high levels of fluoride in the water suggest that there is considerable variation in fluorosis among and within these populations. Responsiveness to fluoride cannot be correlated with the total bioburden of fluoride as assayed in urine samples. Heterogeneous responses to fluoride have also been observed in different mouse strains with certain strains exhibiting fluorosis while other strains are unaffected. Several fluoride-responsive genes have been identified but how these genes and their gene products determine physiological responses to fluoride has not been clarified. Nevertheless, these studies strongly suggest that there is a genetic basis underlying the effects of fluoride.

With the completion of the Human Genome Project and rapid advancement of the International HapMap Project, genomic science can begin to be translated into genomic medicine. On the forefront of this progress is the emerging field of pharmacogenetics; an interdisciplinary study of genetic variations that determine heterogeneous responses to drugs and other chemical compounds. Global and high throughput map-based or sequence-based approaches, gene expression profiling and proteomic studies can be utilized to ascertain functionally significant genetic variations in drug responses and to identify polygenic interactions that determine complex drug responses. Genetically engineered animals such as recombinant congenic strains of mice are available to accelerate genetic dissection of complex traits. It is timely to apply these state-of-the-art approaches to fluoride research and to attract new investigators and investigators with diverse expertise to this area. Scope and Objectives

This FOA encourages human and animal studies on: 1) whole genome approaches such as linkage and mapping studies to identify fluoride-responsive genetic variations; 2) candidate gene strategies based on existing knowledge of the mechanisms of fluoride action to identify and characterize functional genetic variants; 3) the development of animal models with clearly defined differential physiological responses to ingested fluoride at levels relevant to normal human exposures and the association of these phenotypes with genotypes; 4) the development and validation of relevant fluoride-responsive genetic variants into predictive genetic standards for an individual’s physiological responses to fluoride; and 5) gene-gene and gene-environment interactions that modify the function of fluoride-responsive genetic variants. Applicants are also encouraged to consider the Nutritional Data System for Research with Fluoride (http://www.ncc.umn.edu/), a software program designed to assess total fluoride exposure, to augment their research design when applicable.

This FOA focuses on capturing emerging scientific opportunities and technologies to provide the genetic and molecular basis for the physiological outcome of ingested fluoride. These studies will pave the way for the identification of specific populations or individuals that will benefit from fluoride supplement and/or exhibit other physiological consequences due to the action of fluoride. The knowledge gained from these studies will serve as the basis for individualized recommendations for total fluoride intake. This information will also elucidate fundamental mechanisms by which fluoride influences biomineralization.

See Section VIII, Other Information - Required Federal Citations, for policies related to this announcement.

Section II. Award Information

1. Mechanism(s) of Support
This funding opportunity will use the NIH Individual Research Project Grant (R01) award mechanism.

As an applicant, you will be solely responsible for planning, directing, and executing the proposed project.

This funding opportunity uses just-in-time concepts. It also uses the modular as well as the nonmodular budget formats (see http://grants.nih.gov/grants/funding/modular/modular.htm). Specifically, if you are submitting an application with direct costs in each year of $250,000 or less, use the modular budget format described in the PHS 398 application instructions. Otherwise follow the instructions for non-modular research grant applications.

2. Funds Available
The NIDCR has not set aside funds for this FOA. The number of awards will be dependent on their scientific merit. Applicants may request up to five years of support. There is no cost limit for the R01 mechanism. Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary. Although the financial plans of the IC(s) provide support for this program, awards pursuant to this funding opportunity are contingent upon the availability of funds and the receipt of a sufficient number of meritorious applications.

Facilities and administrative costs requested by consortium participants are not included in the direct cost limitation, see NOT-OD-05-004.

Section III. Eligibility Information

1. Eligible Applicants 1.A. Eligible Institutions
You may submit (an) application(s) if your organization has any of the following characteristics:

• • • • • • • • • • •

For-profit organizations Non-profit organizations Public or private institutions, such as universities, colleges, hospitals, and laboratories Units of State government Units of local government Eligible agencies of the Federal government Foreign Institutions Domestic Institutions Faith-based or community-based organizations Units of State Tribal government Units of Local Tribal government

1.B. Eligible Individuals
Any individual with the skills, knowledge, and resources necessary to carry out the proposed research is invited to work with their institution to develop an application for support. Individuals from underrepresented racial and ethnic groups as well as individuals with disabilities are always encouraged to apply for NIH programs.

2. Cost Sharing or Matching
Cost sharing is not required.

The most current Grants Policy Statement can be found at: http://grants.nih.gov/grants/policy/nihgps_2003/nihgps_Part2.htm#matching_or_cost_sharing

3. Other-Special Eligibility Criteria
Not applicable

Section IV. Application and Submission Information

1. Address to Request Application Information
The PHS 398 application instructions are available at http://grants.nih.gov/grants/funding/phs398/phs398.html in an interactive format. Applicants must use the currently approved version of the PHS 398. For further assistance contact GrantsInfo, Telephone (301) 435-0714, Email: GrantsInfo@nih.gov.

Telecommunications for the hearing impaired: TTY 301-451-0088.

2. Content and Form of Application Submission
Applications must be prepared using the most current PHS 398 research grant application instructions and forms. Applications must have a D&B Data Universal Numbering System (DUNS) number as the universal identifier when applying for Federal grants or cooperative agreements. The D&B number can be obtained by calling (866) 705-5711 or through the web site at http://www.dnb.com/us/. The D&B number should be entered on line 11 of the face page of the PHS 398 form.

The title and number of this funding opportunity must be typed on line 2 of the face page of the application form and the YES box must be checked.

Foreign Organizations

Several special provisions apply to applications submitted by foreign organizations:

• •

Charge back of customs and import fees is not allowed. Format: every effort should be made to comply with the format specifications, which are based upon a standard US paper size of 8.5" x 11."

• • •

Funds for up to 8% administrative costs (excluding equipment) can now be requested (http://grants.nih.gov/grants/guide/notice-files/NOT-OD-01-028.html) Organizations must comply with federal/NIH policies on human subjects, animals, and biohazards. Organizations must comply with federal/NIH biosafety and biosecurity regulations. See Section VI. 2. Administrative Requirements, "Cooperative Agreement Terms and Conditions of Award".

Proposed research should provide a unique research opportunity not available in the U.S.

3. Submission Dates and Times
See Section IV.3.A for details.

3.A. Receipt, Review and Anticipated Start Dates
Letter of Intent Receipt Dates: April 17, 2006, 2007, 2008; August 17, 2006, 2007, 2008; December 17, 2006, 2007, 2008 Application Receipt Dates: May 15, 2006, 2007, 2008; September 15, 2006, 2007, 2008; January 15, 2007, 2008, 2009 Peer Review Dates: October-November 2006, 2007, 2008; February-March 2007, 2008, 2009; JuneJuly 2007, 2008, 2009 Council Review Dates: January 2007, 2008, 2009; May 2007, 2008, 2009; September 2007, 2008, 2009 Earliest Anticipated Start Dates: April 2007, 2008, 2009; July 2007, 2008, 2009; December 2007, 2008, 2009

3.A.1. Letter of Intent
Prospective applicants are asked to submit a letter of intent that includes the following information:

• • • • •

Descriptive title of proposed research Name, address, and telephone number of the Principal Investigator Names of other key personnel Participating institutions Number and title of this funding opportunity

Although a letter of intent is not required, is not binding, and does not enter into the review of a subsequent application, the information that it contains allows IC staff to estimate the potential review workload and plan the review.

The letter of intent is to be sent by the date listed at the beginning of this document.

The letter of intent should be sent to:

Lillian Shum, PhD Director, Mineralized Tissue and Salivary Gland Physiology Program Center for Integrative Biology and Infectious Diseases National Institute of Dental and Craniofacial Research 45 Center Drive Building 45, Room 4AN-18B Bethesda, MD 20892-6402 Telephone: (301) 594-0618 Fax: (301) 480-8319 Email: ShumL@nidcr.nih.gov

3.B. Sending an Application to the NIH
Applications must be prepared using the research grant application forms found in the PHS 398 instructions for preparing a research grant application. Submit a signed, typewritten original of the application, including the checklist, and five signed photocopies in one package to:

Center for Scientific Review National Institutes of Health 6701 Rockledge Drive, Room 1040, MSC 7710 Bethesda, MD 20892-7710 (U.S. Postal Service Express or regular mail) Bethesda, MD 20817 (for express/courier service; non-USPS service)

Personal deliveries of applications are no longer permitted (see http://grants.nih.gov/grants/guide/notice-files/NOT-OD-03-040.html).

3.C. Application Processing
Applications must be received on or before the application receipt/submission date(s) described above (Section IV.3.A.). If an application is received after that date, it will be returned to the applicant without review .

Upon receipt applications will be evaluated for completeness by CSR. Incomplete applications will

not be reviewed.

The NIH will not accept any application in response to this funding opportunity that is essentially the same as one currently pending initial merit review unless the applicant withdraws the pending application. The NIH will not accept any application that is essentially the same as one already reviewed. This does not preclude the submission of a substantial revision of an application already reviewed, but such application must include an Introduction addressing the previous critique.

Although there is no immediate acknowledgement of the receipt of an application, applicants are generally notified of the review and funding assignment within eight (8) weeks.

4. Intergovernmental Review
This initiative is not subject to intergovernmental review.

5. Funding Restrictions
All NIH awards are subject to the terms and conditions, cost principles, and other considerations described in the NIH Grants Policy Statement. The Grants Policy Statement can be found at http://grants.nih.gov/grants/policy/policy.htm.

Pre-Award Costs are allowable. A grantee may, at its own risk and without NIH prior approval, incur obligations and expenditures to cover costs up to 90 days before the beginning date of the initial budget period of a new or competing continuation award if such costs: are necessary to conduct the project, and would be allowable under the grant, if awarded, without NIH prior approval. If specific expenditures would otherwise require prior approval, the grantee must obtain NIH approval before incurring the cost. NIH prior approval is required for any costs to be incurred more than 90 days before the beginning date of the initial budget period of a new or competing continuation award.

The incurrence of pre-award costs in anticipation of a competing or non-competing award imposes no obligation on NIH either to make the award or to increase the amount of the approved budget if an award is made for less than the amount anticipated and is inadequate to cover the pre-award costs incurred. NIH expects the grantee to be fully aware that pre-award costs result in borrowing against future support and that such borrowing must not impair the grantee's ability to accomplish the project objectives in the approved time frame or in any way adversely affect the conduct of the project. See NIH Grants Policy Statement http://grants.nih.gov/grants/policy/nihgps_2003/NIHGPS_Part6.htm.

6. Other Submission Requirements
Specific Instructions for Modular Grant applications.

Applications requesting up to $250,000 per year in direct costs must be submitted in a modular budget format. The modular budget format simplifies the preparation of the budget in these applications by limiting the level of budgetary detail. Applicants request direct costs in $25,000 modules. Section C of the research grant application instructions for the PHS 398 at http://grants.nih.gov/grants/funding/phs398/phs398.html includes step-by-step guidance for preparing modular budgets. Applicants must use the currently approved version of the PHS 398. Additional information on modular budgets is available at http://grants.nih.gov/grants/funding/modular/modular.htm.

Specific Instructions for Applications Requesting $500,000 (direct costs) or More per Year.

Applicants requesting $500,000 or more in direct costs for any year must carry out the following steps:

1) Contact the IC program staff at least 6 weeks before submitting the application, i.e., as you are developing plans for the study;

2) Obtain agreement from the IC staff that the IC will accept your application for consideration for award; and,

3) Include a cover letter with the application that identifies the staff member and IC who agreed to accept assignment of the application.

This policy applies to all investigator-initiated new (type 1), competing continuation (type 2), competing supplement, or any amended or revised version of these grant application types. Additional information on this policy is available in the NIH Guide for Grants and Contracts, October 19, 2001 at http://grants.nih.gov/grants/guide/notice-files/NOT-OD-02-004.html.

Plan for Sharing Research Data
The precise content of the data-sharing plan will vary, depending on the data being collected and how the investigator is planning to share the data. Applicants who are planning to share data may wish to describe briefly the expected schedule for data sharing, the format of the final dataset, the documentation to be provided, whether or not any analytic tools also will be provided, whether or not a data-sharing agreement will be required and, if so, a brief description of such an agreement

(including the criteria for deciding who can receive the data and whether or not any conditions will be placed on their use), and the mode of data sharing (e.g., under their own auspices by mailing a disk or posting data on their institutional or personal website, through a data archive or enclave). Investigators choosing to share under their own auspices may wish to enter into a data-sharing agreement. References to data sharing may also be appropriate in other sections of the application.

All applicants must include a plan for sharing research data in their application. The data sharing policy is available at http://grants.nih.gov/grants/policy/data_sharing. All investigators responding to this funding opportunity should include a description of how final research data will be shared, or explain why data sharing is not possible.

The reasonableness of the data sharing plan or the rationale for not sharing research data will be assessed by the reviewers. However, reviewers will not factor the proposed data sharing plan into the determination of scientific merit or the priority score.

Sharing Research Resources
NIH policy requires that grant awardee recipients make unique research resources readily available for research purposes to qualified individuals within the scientific community after publication (NIH Grants Policy Statement http://grants.nih.gov/grants/policy/nihgps_2003/index.htm and http://grants.nih.gov/grants/policy/nihgps_2003/NIHGPS_Part7.htm#_Toc54600131). Investigators responding to this funding opportunity should include a plan for sharing research resources addressing how unique research resources will be shared or explain why sharing is not possible.

The adequacy of the resources sharing plan and any related data sharing plans will be considered by Program staff of the funding organization when making recommendations about funding applications. The effectiveness of the resource sharing will be evaluated as part of the administrative review of each non-competing Grant Progress Report (PHS 2590, http://grants.nih.gov/grants/funding/2590/2590.htm). See Section VI.3. Reporting.

Section V. Application Review Information

1. Criteria
Only the review criteria described below will be considered in the review process.

2. Review and Selection Process
Applications submitted for this funding opportunity will be assigned to the ICs on the basis of established PHS referral guidelines.

Appropriate scientific review groups convened in accordance with the standard NIH peer review procedures (http://www.csr.nih.gov/refrev.htm) will evaluate applications for scientific and technical merit.

As part of the initial merit review, all applications will:

Undergo a selection process in which only those applications deemed to have the highest scientific merit, generally the top half of applications under review, will be discussed and assigned a priority score.

• •

Receive a written critique Receive a second level of review by the National Advisory Dental and Craniofacial Research Council.

The following will be considered in making funding decisions:

• • •

Scientific merit of the proposed project as determined by peer review Availability of funds Relevance of program priorities

The goals of NIH supported research are to advance our understanding of biological systems, to improve the control of disease, and to enhance health. In their written critiques, reviewers will be asked to comment on each of the following criteria in order to judge the likelihood that the proposed research will have a substantial impact on the pursuit of these goals. Each of these criteria will be addressed and considered in assigning the overall score, weighting them as appropriate for each application. Note that an application does not need to be strong in all categories to be judged likely to have major scientific impact and thus deserve a high priority score. For example, an investigator may propose to carry out important work that by its nature is not innovative but is essential to move a field forward.

Significance: Does this study address an important problem? If the aims of the application are achieved, how will scientific knowledge or clinical practice be advanced? What will be the effect of these studies on the concepts, methods, technologies, treatments, services, or preventative interventions that drive this field?

Approach: Are the conceptual or clinical framework, design, methods, and analyses adequately developed, well integrated, well reasoned, and appropriate to the aims of the project? Does the applicant acknowledge potential problem areas and consider alternative tactics? Are fluoride exposure levels in the study design relevant and typical of human exposures? Will the study inform a causal or associative relationship between fluoride-responsive genotype and phenotype? Are there appropriate controls in the study design to demonstrate the specificity of the fluoride response?

Innovation: Is the project original and innovative? For example: Does the project challenge existing paradigms or clinical practice; address an innovative hypothesis or critical barrier to progress in the field? Does the project develop or employ novel concepts, approaches, methodologies, tools, or technologies for this area?

Investigators: Are the investigators appropriately trained and well suited to carry out this work? Is the work proposed appropriate to the experience level of the principal investigator and other researchers? Does the investigative team bring complementary and integrated expertise to the project (if applicable)?

Environment: Does the scientific environment in which the work will be done contribute to the probability of success? Do the proposed studies benefit from unique features of the scientific environment, or subject populations, or employ useful collaborative arrangements? Is there evidence of institutional support?

Relevance to Public Health: Does the project have a clearly defined and acceptable standard on how pharmacogenetics data will be interpreted and translated into public health risk assessment? If animal studies were proposed, does the project discuss the predictive relevance to human conditions of the data generated? Will the study generate interpretable and useful information relevant to public health?

2.A. Additional Review Criteria:
In addition to the above criteria, the following items will continue to be considered in the determination of scientific merit and the priority score:

Protection of Human Subjects from Research Risk: The involvement of human subjects and protections from research risk relating to their participation in the proposed research will be assessed (see the Research Plan, Section E on Human Subjects in the PHS Form 398).

Inclusion of Women, Minorities and Children in Research: The adequacy of plans to include subjects from both genders, all racial and ethnic groups (and subgroups), and children as appropriate for the scientific goals of the research will be assessed. Plans for the recruitment and retention of subjects will also be evaluated (see the Research Plan, Section E on Human Subjects in the PHS Form 398).

Care and Use of Vertebrate Animals in Research: If vertebrate animals are to be used in the project, the five items described under Section F of the PHS Form 398 research grant application instructions will be assessed.

Biohazards: If materials or procedures are proposed that are potentially hazardous to research personnel and/or the environment, determine if the proposed protection is adequate.

2.B. Additional Review Considerations
Budget: The reasonableness of the proposed budget and the requested period of support in relation to the proposed research. The priority score should not be affected by the evaluation of the budget.

2.C. Sharing Research Data
Data Sharing Plan: The reasonableness of the data sharing plan or the rationale for not sharing research data will be assessed by the reviewers. However, reviewers will not factor the proposed data sharing plan into the determination of scientific merit or the priority score. The presence of a data sharing plan will be part of the terms and conditions of the award. The funding organization will be responsible for monitoring the data sharing policy.

2.D. Sharing Research Resources
NIH policy requires that grant awardee recipients make unique research resources readily available for research purposes to qualified individuals within the scientific community after publication (See the NIH Grants Policy Statement http://grants.nih.gov/grants/policy/nihgps/part_ii_5.htm#availofrr and http://www.ott.nih.gov/policy/rt_guide_final.html). Investigators responding to this funding opportunity should include a sharing research resources plan addressing how unique research resources will be shared or explain why sharing is not possible.

Program staff will be responsible for the administrative review of the plan for sharing research resources.

The adequacy of the resources sharing plan will be considered by Program staff of the funding

organization when making recommendations about funding applications. Program staff may negotiate modifications of the data and resource sharing plans with the awardee before recommending funding of an application. The final version of the data and resource sharing plans negotiated by both will become a condition of the award of the grant. The effectiveness of the resource sharing will be evaluated as part of the administrative review of each non-competing Grant Progress Report (PHS 2590). See Section VI.3. Reporting.

3. Anticipated Announcement and Award Dates
Not applicable

Section VI. Award Administration Information

1. Award Notices
After the peer review of the application is completed, the PI will be able to access his or her Summary Statement (written critique) via the eRA Commons.

If the application is under consideration for funding, NIH will request "just-in-time" information from the applicant. For details, applicants may refer to the NIH Grants Policy Statement Part II: Terms and Conditions of NIH Grant Awards, Subpart A: General (http://grants.nih.gov/grants/policy/nihgps_2003/NIHGPS_part4.htm).

A formal notification in the form of a Notice of Award (NoA) will be provided to the applicant organization. The NoA signed by the grants management officer is the authorizing document. Once all administrative and programmatic issues have been resolved, the NoA will be generated via email notification from the awarding component to the grantee business official (designated in item 12 on the Application Face Page). If a grantee is not email enabled, a hard copy of the NoA will be mailed to the business official.

Selection of an application for award is not an authorization to begin performance. Any costs incurred before receipt of the NoA are at the recipient's risk. These costs may be reimbursed only to the extent considered allowable pre-award costs. See Also Section IV.5. Funding Restrictions.

2. Administrative and National Policy Requirements
All NIH grant and cooperative agreement awards include the NIH Grants Policy Statement as part of

the NoA. For these terms of award, see the NIH Grants Policy Statement Part II: Terms and Conditions of NIH Grant Awards, Subpart A: General (http://grants.nih.gov/grants/policy/nihgps_2003/NIHGPS_Part4.htm) and Part II Terms and Conditions of NIH Grant Awards, Subpart B: Terms and Conditions for Specific Types of Grants, Grantees, and Activities (http://grants.nih.gov/grants/policy/nihgps_2003/NIHGPS_part9.htm).

3. Reporting
Awardees will be required to submit the PHS Non-Competing Grant Progress Report, Form 2590 annually (http://grants.nih.gov/grants/funding/2590/2590.htm) and financial statements as required in the NIH Grants Policy Statement.

Section VII. Agency Contacts

We encourage your inquiries concerning this funding opportunity and welcome the opportunity to answer questions from potential applicants. Inquiries may fall into three areas: scientific/research, peer review, and financial or grants management issues:

1. Scientific/Research Contacts:
Lillian Shum, PhD Director, Mineralized Tissue and Salivary Gland Physiology Program Center for Integrative Biology and Infectious Diseases National Institute of Dental and Craniofacial Research 45 Center Drive Building 45, Room 4AN-18B Bethesda, MD 20892-6402 Telephone: (301) 594-0618 Fax: (301) 480-8319 Email: ShumL@nidcr.nih.gov

2. Peer Review Contacts:
Not applicable

3. Financial or Grants Management Contacts:

Mary Daley, Chief Grants Management Officer Division of Extramural Activities National Institute of Dental and Craniofacial Research Building 45, Room 4AN 44B 45 Center Drive Bethesda, MD 20892-6402 Telephone: (301) 594-4808 FAX: (301) 480-3562 Email: daleym@mail.nih.gov

Section VIII. Other Information

Required Federal Citations
Use of Animals in Research: Recipients of PHS support for activities involving live, vertebrate animals must comply with PHS Policy on Humane Care and Use of Laboratory Animals (http://grants.nih.gov/grants/olaw/references/PHSPolicyLabAnimals.pdf) as mandated by the Health Research Extension Act of 1985 (http://grants.nih.gov/grants/olaw/references/hrea1985.htm), and the USDA Animal Welfare Regulations (http://www.nal.usda.gov/awic/legislat/usdaleg1.htm) as applicable.

Human Subjects Protection: Federal regulations (45CFR46) require that applications and proposals involving human subjects must be evaluated with reference to the risks to the subjects, the adequacy of protection against these risks, the potential benefits of the research to the subjects and others, and the importance of the knowledge gained or to be gained (http://www.hhs.gov/ohrp/humansubjects/guidance/45cfr46.htm).

Data and Safety Monitoring Plan: Data and safety monitoring is required for all types of clinical trials, including physiologic toxicity and dose-finding studies (phase I); efficacy studies (Phase II); efficacy, effectiveness and comparative trials (Phase III). Monitoring should be commensurate with risk. The establishment of data and safety monitoring boards (DSMBs) is required for multi-site clinical trials involving interventions that entail potential risks to the participants (NIH Policy for Data and Safety Monitoring, NIH Guide for Grants and Contracts, http://grants.nih.gov/grants/guide/notice-files/not98-084.html).

Sharing Research Data: Investigators submitting an NIH application seeking $500,000 or more in direct costs in any single year are expected to include a plan for data sharing or state why this is not possible (http://grants.nih.gov/grants/policy/data_sharing).

Investigators should seek guidance from their institutions, on issues related to institutional policies and local IRB rules, as well as local, State and Federal laws and regulations, including the Privacy Rule. Reviewers will consider the data sharing plan but will not factor the plan into the determination of the scientific merit or the priority score.

Access to Research Data through the Freedom of Information Act: The Office of Management and Budget (OMB) Circular A-110 has been revised to provide access to research data through the Freedom of Information Act (FOIA) under some circumstances. Data that are (1) first produced in a project that is supported in whole or in part with Federal funds and (2) cited publicly and officially by a Federal agency in support of an action that has the force and effect of law (i.e., a regulation) may be accessed through FOIA. It is important for applicants to understand the basic scope of this amendment. NIH has provided guidance at http://grants.nih.gov/grants/policy/a110/a110_guidance_dec1999.htm. Applicants may wish to place data collected under this funding opportunity in a public archive, which can provide protections for the data and manage the distribution for an indefinite period of time. If so, the application should include a description of the archiving plan in the study design and include information about this in the budget justification section of the application. In addition, applicants should think about how to structure informed consent statements and other human subjects procedures given the potential for wider use of data collected under this award.

Sharing of Model Organisms: NIH is committed to support efforts that encourage sharing of important research resources including the sharing of model organisms for biomedical research (see http://grants.nih.gov/grants/policy/model_organism/index.htm). At the same time the NIH recognizes the rights of grantees and contractors to elect and retain title to subject inventions developed with Federal funding pursuant to the Bayh Dole Act (see the NIH Grants Policy Statement http://grants.nih.gov/grants/policy/nihgps_2003/index.htm). All investigators submitting an NIH application or contract proposal, beginning with the October 1, 2004 receipt date, are expected to include in the application/proposal a description of a specific plan for sharing and distributing unique model organism research resources generated using NIH funding or state why such sharing is restricted or not possible. This will permit other researchers to benefit from the resources developed with public funding. The inclusion of a model organism sharing plan is not subject to a

cost threshold in any year and is expected to be included in all applications where the development of model organisms is anticipated.

Inclusion of Women And Minorities in Clinical Research: It is the policy of the NIH that women and members of minority groups and their sub-populations must be included in all NIH-supported clinical research projects unless a clear and compelling justification is provided indicating that inclusion is inappropriate with respect to the health of the subjects or the purpose of the research. This policy results from the NIH Revitalization Act of 1993 (Section 492B of Public Law 103-43). All investigators proposing clinical research should read the "NIH Guidelines for Inclusion of Women and Minorities as Subjects in Clinical Research (http://grants.nih.gov/grants/guide/notice-files/NOT-OD-02-001.html); a complete copy of the updated Guidelines is available at http://grants.nih.gov/grants/funding/women_min/guidelines_amended_10_2001.htm. The amended policy incorporates: the use of an NIH definition of clinical research; updated racial and ethnic categories in compliance with the new OMB standards; clarification of language governing NIHdefined Phase III clinical trials consistent with the new PHS Form 398; and updated roles and responsibilities of NIH staff and the extramural community. The policy continues to require for all NIH-defined Phase III clinical trials that: a) all applications or proposals and/or protocols must provide a description of plans to conduct analyses, as appropriate, to address differences by sex/gender and/or racial/ethnic groups, including subgroups if applicable; and b) investigators must report annual accrual and progress in conducting analyses, as appropriate, by sex/gender and/or racial/ethnic group differences.

Inclusion of Children as Participants in Clinical Research: The NIH maintains a policy that children (i.e., individuals under the age of 21) must be included in all clinical research, conducted or supported by the NIH, unless there are scientific and ethical reasons not to include them.

All investigators proposing research involving human subjects should read the "NIH Policy and Guidelines" on the inclusion of children as participants in research involving human subjects (http://grants.nih.gov/grants/funding/children/children.htm).

Required Education on the Protection of Human Subject Participants: NIH policy requires education on the protection of human subject participants for all investigators submitting NIH applications for research involving human subjects and individuals designated as key personnel. The policy is available at http://grants.nih.gov/grants/guide/notice-files/NOT-OD-00039.html.

Human Embryonic Stem Cells (hESC): Criteria for federal funding of research on hESCs can be found at http://stemcells.nih.gov/index.asp and at http://grants.nih.gov/grants/guide/notice-files/NOT-OD-02-005.html. Only research using hESC lines that are registered in the NIH Human Embryonic Stem Cell Registry will be eligible for Federal funding (http://escr.nih.gov/). It is the responsibility of the applicant to provide in the project description and elsewhere in the application as appropriate, the official NIH identifier(s) for the hESC line(s)to be used in the proposed research. Applications that do not provide this information will be returned without review.

NIH Public Access Policy: NIH-funded investigators are requested to submit to the NIH manuscript submission (NIHMS) system (http://www.nihms.nih.gov/) at PubMed Central (PMC) an electronic version of the author's final manuscript upon acceptance for publication, resulting from research supported in whole or in part with direct costs from NIH. The author's final manuscript is defined as the final version accepted for journal publication, and includes all modifications from the publishing peer review process.

NIH is requesting that authors submit manuscripts resulting from 1) currently funded NIH research projects or 2) previously supported NIH research projects if they are accepted for publication on or after May 2, 2005. The NIH Public Access Policy applies to all research grant and career development award mechanisms, cooperative agreements, contracts, Institutional and Individual Ruth L. Kirschstein National Research Service Awards, as well as NIH intramural research studies. The Policy applies to peer-reviewed, original research publications that have been supported in whole or in part with direct costs from NIH, but it does not apply to book chapters, editorials, reviews, or conference proceedings. Publications resulting from non-NIH-supported research projects should not be submitted.

For more information about the Policy or the submission process please visit the NIH Public Access Policy Web site at http://publicaccess.nih.gov/ and view the Policy or other Resources and Tools including the Authors' Manual (http://publicaccess.nih.gov/publicaccess_Manual.htm).

Standards for Privacy of Individually Identifiable Health Information: The Department of Health and Human Services (DHHS) issued final modification to the "Standards for Privacy of Individually Identifiable Health Information", the "Privacy Rule", on August 14, 2002 . The Privacy Rule is a federal regulation under the Health Insurance Portability and Accountability Act (HIPAA) of 1996 that governs the protection of individually identifiable health information, and is administered and enforced by the DHHS Office for Civil Rights (OCR).

Decisions about applicability and implementation of the Privacy Rule reside with the researcher and

his/her institution. The OCR website (http://www.hhs.gov/ocr/) provides information on the Privacy Rule, including a complete Regulation Text and a set of decision tools on "Am I a covered entity?" Information on the impact of the HIPAA Privacy Rule on NIH processes involving the review, funding, and progress monitoring of grants, cooperative agreements, and research contracts can be found at http://grants.nih.gov/grants/guide/notice-files/NOT-OD-03-025.html.

URLs in NIH Grant Applications or Appendices: All applications and proposals for NIH funding must be self-contained within specified page limitations. Unless otherwise specified in an NIH solicitation, Internet addresses (URLs) should not be used to provide information necessary to the review because reviewers are under no obligation to view the Internet sites. Furthermore, we caution reviewers that their anonymity may be compromised when they directly access an Internet site.

Healthy People 2010: The Public Health Service (PHS) is committed to achieving the health promotion and disease prevention objectives of "Healthy People 2010," a PHS-led national activity for setting priority areas. This PA is related to one or more of the priority areas. Potential applicants may obtain a copy of "Healthy People 2010" at http://www.health.gov/healthypeople.

Authority and Regulations: This program is described in the Catalog of Federal Domestic Assistance (CFDA# 93.121) at http://www.cfda.gov/ and is not subject to the intergovernmental review requirements of Executive Order 12372 or Health Systems Agency review. Awards are made under the authorization of Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and under Federal Regulations 42 CFR 52 and 45 CFR Parts 74 and 92. All awards are subject to the terms and conditions, cost principles, and other considerations described in the NIH Grants Policy Statement. The NIH Grants Policy Statement can be found at http://grants.nih.gov/grants/policy/policy.htm.

The PHS strongly encourages all grant recipients to provide a smoke-free workplace and discourage the use of all tobacco products. In addition, Public Law 103-227, the Pro-Children Act of 1994, prohibits smoking in certain facilities (or in some cases, any portion of a facility) in which regular or routine education, library, day care, health care, or early childhood development services are provided to children. This is consistent with the PHS mission to protect and advance the physical and mental health of the American people.

Loan Repayment Programs: NIH encourages applications for educational loan repayment from qualified health professionals who have made a commitment to pursue a research career involving clinical, pediatric,

contraception, infertility, and health disparities related areas. The LRP is an important component of NIH's efforts to recruit and retain the next generation of researchers by providing the means for developing a research career unfettered by the burden of student loan debt. Note that an NIH grant is not required for eligibility and concurrent career award and LRP applications are encouraged. The periods of career award and LRP award may overlap providing the LRP recipient with the required commitment of time and effort, as LRP awardees must commit at least 50% of their time (at least 20 hours per week based on a 40 hour week) for two years to the research. For further information, please see: http://www.lrp.nih.gov/.

FOR IMMEDIATE RELEASE: April 29, 1994

Roger Rensberger (301) 975-2762 TN-5976

U.S./CANADA/MEXICO TO COOPERATE ON MEASUREMENT AND CALIBRATION LAB PROGRAMS http://www.nist.gov/public_affairs/releases/tn5976.htm

The U.S. Department of Commerce's National Institute of Standards and Technology (NIST), the National Research Council of Canada (NRC) and the Standards Council of Canada (SCC), the National Center for Metrology (Centro Nacional de Metrologia-CENAM) and the Director General for Standards (Direccion General de Normas--DGN) of Mexico have signed memorandums of understanding to establish two organizations: NORAMET and the North American Calibration Cooperation (NACC). The two organizations will serve as a framework to promote closer North American cooperation between the three countries in areas of metrology and calibration laboratory accreditation as part of an overall effort to reduce non-tariff barriers to trade. The inaugural meeting of representatives from the three countries will take place April 30, 1994, at Quer‚taro, Mexico, following the April 29 dedication of the new Mexican metrology laboratory. A U.S. delegation will be led by George A. Sinnott, director of the NIST Office of International and Academic Affairs. Sinnott points out that by signing the MOUs, the countries declared their intention to cooperate in areas leading to mutual recognition arrangements between the three nations concerning metrological development and services and the development of mutual confidence in national calibration laboratory accreditation programs. NORAMET will be a North American regional collaboration in national measurement standards and services. It will be made up of representatives of the primary reference laboratories of the member countries, NIST, NRC and CENAM. The goals of NORAMET are: o to develop closer collaboration between the members in projects connected to measurement and metrological services while respecting their obligations within their own countries; to optimize the utilization of resources and services of the members and to encourage the development of these toward perceived metrological needs; to encourage the sharing of major facilities in order to achieve efficiency and avoid duplication when feasible; and

o

o

o

to improve measurement services and make them accessible to all members within limits agreed upon by the members.

The North American Calibration Cooperation effort will be directed to the development of mutual confidence in national calibration laboratory accreditation programs. NACC also will provide the regional structure to negotiate calibration agreements with similar organizations in other regions of the world such as EUROMET, and the European Cooperation for Accreditation of Laboratories (EAL). Under NACC, the signatories NIST, NRC, SCC, DGN and CENAM, recognize each other as having primary responsibility in their respective countries for the maintenance of accreditation programs for calibration laboratories. The NACC members intend to promote close collaboration between the calibration laboratory accreditation and assessment programs they have implemented, or intend to implement, such as the Calibration Laboratory Assessment Service (CLAS) and the Program for Accreditation of Laboratories in Canada (PALCAN), the calibration program and National Voluntary Laboratory Accreditation Program (NVLAP) in the United States, and the Servicio de Certificacion de Laboratorios de Calibracion (SECLAC) and the Sistema Nacional de Calibracion (SNC) in Mexico. A non-regulatory agency of the Commerce Department's Technology Administration, NIST promotes economic growth by working with industry to develop and apply technology, measurements and standards. -30NOTE TO EDITORS: For information on NORAMET and NACC, contact the Office of International and Academic Affairs, A505 Administration Building, NIST, Gaithersburg, Md. 20899-0001, (301) 975-3089, fax: (301) 975-3530, e-mail: OIAA@micf.nist.gov (via Internet).

(C) Peter Meiers - http://www.fluoride-history.de http://www.fluoride-history.de/p-dentpr.htm

Patents on ingestable dental preparations

see also: - Early European fluoride research: http://www.fluoride-history.de/fteeth1.htm

1874 Alvaro Francisco Carlos REYNOSO, of Paris, France: "Improvement in medical compounds", US Patent 146,781; filed Jan. 16, 1874, patented Jan. 27, 1874; ("Elixir" and "Sirup" containing fluorides of either potassium, sodium or ammonium; "elixir" is "invigorating, nutritious, and complemental to food", "fluorated sirup" is "...for infants at the period when the bones and teeth are in process of formation"; also contains "sugar in sufficient quantity"). Reynoso was a Cuban scientist who lived for many years in France.

1909 Johann A. WÜLFING Company, of Berlin, Germany: "Verfahren zur Herstellung leicht resorbierbarer Fluorpräparate", German Patent (DE) 222,716; filed June 29, 1909, patented June 2, 1910; (Patent is based upon early European work, especially experiments carried out by the chemist Deninger (1896). It is claimed that there´s generally not enough fluoride in a normal diet. To produce an easily absorbable fluoride preparation the company precipitates calcium fluoride (using sodium fluoride plus a calcium salt) together with a protein like egg-white, albumin, casein, to which it becomes adsorbed on co-precipitation.)

1911 Emil LANGER, of Wien, Austria: "Verfahren zur Herstellung leicht löslicher, haltbarer Desinfektionsmittel zur Bereitung von Mund- und Spülwasser unter Verwendung von Natriumfluorid und Natriumsiliciumfluorid", German Patent (DE) 281,148; filed Nov. 28, 1911, patented Dec. 14, 1914; (a mouthwash and disinfectant made of sodium fluoride or sodium fluosilicate; tablets of 0.6 g each, containing 30 parts soda, 15 parts sodium fluoride or sodium fluosilicate, 15 parts tartaric acid, and essential oils to give them some taste: "... simply let the tablets slowly dissolve in the mouth as sodium fluoride and sodium fluosilicate are not toxic to humans ...", the patent says.)

1919 Lecinwerk Dr. E. LAVES, Hannover, Germany: "Verfahren zur Herstellung kolloidallöslicher Fluorcalcium-Amylodrextrinpräparate", German Patent DE 325,561; filed March 12, 1919; patented Sept. 13, 1920 (calcium fluoride preparation made by precipitation from a mixture of sodium fluoride, calcium chloride and amylodextrin; for therapeutic and bakery technical use)

1927 Philip Adolph KOBER, Evanston, Illinois, assignor to G. D. Searle & Company, of Chicago, Illinois, a corporation of Illinois: "Mineral Food Composition and Process of Making Same", US Patent (US) 1,813,936; filed May 19, 1927, patented July 14, 1931 (a calcium, magnesium and phosphate preparation as a food supplement, also containing 350 mg NaF per 1,624 g of the product).

1935 Reinhol GRUETER, Berlin-Charlottenburg, Germany: "Herstellung von Zubereitungen, die Calciumfluorid in leichter resorbierbarer Form enthalten", German Patent DE 695,874; filed October 22, 1935; patented August 8, 1940 (a preparation containing calcium fluoride made from sodium fluoride and a calcium phosphate)

1944 Lyon P. STREAN, Montreal, Quebec, Canada, assignor, by mesne assignments, to

Ayerst, McKenna and Harrison Limited, New York, N.Y.: "Oral fluoride-vitamin preparation", US Patent 2,449,184; filed March 8, 1944; patented Sept. 14, 1948 (calcium fluoride - containing preparation for the formation of fluor-apatite in bones and teeth; author refers to Deaf Smith County where a low prevalence of caries has been reported, and claims "the same is generally true with regard to the prevalence of rickets.")

1954 Charles H. ELBREDER and Edward J. ROSS, St. Louis, Mo., assignors to Charles J. Nemanick, St. Louis, Mo., "Therapeutic Composition", US Patent 2,967,131; filed Feb. 8, 1954, patented Jan. 3, 1961 (water-treating fluoride tablets)

1962 Riyad R. IRANI, assignor to Monsanto Company: "Fluoridation", US Patent 3,279,992; filed May 18, 1962; pat. Oct. 18, 1966 (fluoridated table salt)

1981 Gert-Ulfert HEESE, of München, Gerhard Ferdinand SCHNEIDER, of Haar, Fritz STANISLAUS, of München, Dietrich HENSCHLER, of Würzburg, Germany: "Orale Arzneimittel für die Kariesprophylaxe", German Patent DE 3,127,984, filed July 15, 1981, patented Febr. 3, 1982

1996 Gunnar ABERG, Thomas Patrick JERUSSI, John R. McCULLOUGH, assignors to Sepracor Inc., Marlborough, Mass.: "NSAID / Fluoride periodontal compositions and methods", US Patent 5,807,541; filed Apr. 22, 1996; pat. Sept. 15, 1998 ("It is also known that under certain circumstances sodium fluoride and fluoroaluminates can activate G proteins and thereby induce prostaglandin production in endothelial cells and leukotriene production in platelets, granulocytes and monocytes. The metabolites of arachidonic acid have been implicated as important biochemical mediators of tissue destruction in various inflammatory diseases. ... We have found that fluoride, in the concentration range in which it is emplyed for the prevention of dental caries, stimulates the production of prostaglandins and thereby exacerbates the inflammatory response in gingivitis and periodontitis. The present invention is a method for

preventing dental caries by administering a fluoride salt into the oral cavity while at the same time controlling periodontal bone loss by administering, in addition to the fluoride salt, an amount of an NSAID sufficient to inhibit the production of prostaglandins induced by the fluoride." NSAID = Non-steroidal aniti-inflammatory drug)

HOME

Potability

of Water from the

Standpoint of

Fluorine

Content*

H. V. SMITH

University of Arizona, Tucson, Ariz.
MOTTLED enamel was first described in the United States by Black and McKay' although it had been described in 1901 by Eager,2 who found it in Italian immigrants. Their findings seemed to point to local water supplies as responsible. It was not, however, until 1931 that it was found to be due to fluorine in the water. The proof 3 consisted of giving water which was known to cause human mottled enamel to rats, and also feeding to other rats small amounts of sodium fluoride. In both cases mottled enamel was produced. Added proof in the way of chemical analysis showed low concentrations of fluorine in waters not associated with enamel and high concentrations in waters which had produced the defect. Churchill 4 added further evidence by analyzing waters from several parts of the United States. High fluorine contents were found in certain endemic regions.
has impeded progress in determining the toxic level. At the time the original investigation was made in 1930 the most promising method available was that of Ross, Reynolds, and Jacob,5 in which dry silicon tetrafluoride was distilled into water and the resulting hydrofluosilicic acid determined by titration with a standard base. Using this method in a limited number of analyses, it appeared that waters containing 2 p.p.m. or more of fluorine were associated with mottled enamel as its cause. A year later an extensive investigation 6 was carried out in Arizona for the twofold purpose of -disclosing endemic areas in the state and obtaining evidence from analyses of water supplies from both endemic and non-endemic areas by which it would be possible to determine definitely the concentrations of fluorides in drinking water which interfere with normal enamel development. Since the volatilization method did METHODS OF FLUORINE ANALYSIS not lend itself well to routine deterSince our proof of the causal rela- minations, another method of analysis tionship of fluorine to mottled enamel, was sought, and the Fairchild method the question of potability of water from was selected. In this method ferric iron the standpoint of its fluorine content has in excess is added to the fluorine conbecome of prime importance. Lack of taining water. The iron combines with accurate methods of fluorine analysis the fluorine, probably forming a complex ion. The uncombined iron is then determined iodimetrically and the Read at a Joint Session of the Laboratory and amount of fluorine present calculated. Public Health Engineering Sections of the American The survey disclosed about 45 towns Public Health Association at the Sixty-third Annual or rural districts in Arizona in which Meeting in Pasadena, Calif., September 4, 1934. [434]
*

POTABILITY OF WATER
mottled enamel is endemic. Analyses of 110 public and 75 private water supplies show a fluoride content ranging from 0.0 to 12.6 p.p.m. Concentrations above 2.7 p.p.m. were found to be definitely toxic, that is, always associated with mottled enamel in its consumers. Because of the great interest in this problem, several more sensitive methods for fluorine determination have been developed recently, and the Fairchild method has been shown to give results which are far too high. The methods of Foster8 and of Armstrong9 both depend upon the removal of fluorine by the addition of an excess of ferric chloride as in the Fairchild method. The uncombined iron is determined colorometrically, Foster using ammonium sulphocyanate and Armstrong acetylacetone. Foster has also found that sulphates, chlorides, and other ions act similarly to fluorine and withdraw a certain amount of iron from solution. The effect of these ions is therefore nullified by adding slight additional amounts of ferric chloride. The Steiger method,10 one of the older methods for fluorine, has been modified by both Wichmann 11 and Boissevain.'2 In this a peroxidized titanium chloride solution is bleached by fluorine, the amount of fading being proportional to the amount of fluorine present. It is somewhat difficult to detect differences in the fading produced by samples varying by 0.1 p.p.m. fluorine in ordinary Nessler tubes. Undoubtedly the photo-electric colorimeter of Wilcox 13 used to compare the ferric acetylacetone colors of Armstrong's method would be more sensitive than comparisons in Nessler tubes. Sulphates in excess are known to interfere with this method, and correction is made if the concentration is too high. Willard and Winters,14 Thompson and Taylor,'5 and Sanchis 16 use

435

alizarine red-zirconium nitrate as an indicator in their determination of fluorine. The Willard and Winters method depends upon removing interfering elements by a preliminary distillation. The fluorine in the distillate is titrated with thorium nitrate, using the above mentioned indicator. The Sanchis method has been modified from the Thompson and Taylor method for fluorine in sea water and is adaptable to the analysis of fresh waters. Chloride and sulphate effects up to 500 p.p.M.. are nullified by the addition of hydrochloric and sulphuric acids.
COMPARISON OF ANALYTICAL RESULTS

Analyses of many waters for fluorine using the Fairchild. Foster, Willard and Winters, and Sanchis methods have been made by the writer and the results compared. These data are presented in Table I. Further evidence is here given that the results of the analysis of waters by the Fairchild method are abnormally. high. On the other hand, results by the Foster, Willard, and Sanchis methods compare very closely with each other, the results obtained by any one of these 3 methods being practically the same. The results of the analysis of 54 waters by these 4 methods are grouped into 2 classes: (1) waters which are known to be associated with mottled enamel, and (2) those which have been found not to cause mottled enamel. This division is based on tooth examinations made by M. C. Smith. It may be seen by inspection of Table I that the 33 waters associated with mottled enamel, as analyzed by the Foster, Willard, and Sanchis methods, have a fluorine content varying from 0.7 p.p.m. to 13.2 p.p.m. Twenty-one waters which did not cause mottled enamel had fluorine contents ranging from 0.1 to 0.8 p.p.m.

436

AMERICAN JOURNAL OF PUBLIC HEALTH
TABLE I
WATERS ASSOCIATED
WITH

MOTTLED ENAMEL

Method
Lab. No.
20487 20670 20853 20106 20693 20104 20663 20689 F296 20708 20482 F73 20662 20483 20121

Location

19761 20486
20487

20690 19762 20664

F82 20772 20673 F176 20694
20480 20489

Ajo Aztec Buckeye Cochise Concha Douglas Florence Gila Bend Gila Riv. Joseph Cy. Hayden Wilson, Idaho Laveen Mammoth Mesa (R) N. Gila Sch. Oracle Pinal Co. Hwy. Dept. Hayden Roll Roll Sch. Roosevelt Sch. Dist. # 66 San Xavier Sentinel Sentinel (R. R.) St. David, Merril Sr. Topock Tucson Brickyard Winkleman

Fairchild p.p.m. 5.8
12.0 2.4 2.0

Foster

p.p.m.
2.2 7.2 1.5 0.9 3.9 2.4 0.8 6.8 0.9 1.0 1.3 13.2 1.2

Willard p.p.m.
6.8
1.2 0.9 4.7 2.4 0.8

Sanchis p.p.m.
8.0 1.3

7.5 5.2
2.8 10.6 3.0 2.8 3.0 16.8

2.5

6.7
1.0 1.0 1.4
11.1 1.3 3.9 1.1 2.4

2.5 6.0
3.1 9.1 3.0

3.7
1.0 1.9 1.1

1.7 4.0

1.5
*S. 5.0
-

7.5 8.7
3.3

3.0

4.7
1.3

3.5
3.0 9.3

1.5
0.9 6.0

1.9 1.0

1.7
1.0

7.7 4.6 4.7 2.7 2.8

5.9
1.1 1.0 1.0 1.1

5.5 4.5 1.8 1.1
1.1 1.1

1.0

WATERS NOT ASSOCIATED WITH MOTTLED ENAMEL

20683 20656 20122 20491 20696 21718 20699 20490 19769

Avondale Benson Chandler

1.8
0.9

Clarkdale
Concha
Fairbanks

2.1 1.2
0.9 0.3 1.1 1.1 1.4 0.9 1.1

0.4 0.7 0.3 0.4
0.1

-.

19770
20661 20100 20665 20475 20697 20859

Flagstaff Jerome Pomerene Pomerene Sch.
Prescott

0.5

0.2
0.5 0.5 -0.2
0.1 0.1 0.3

0.4 0.3 0.8 0.5 0.3 0.4 0.3 0.3 0.3
0.6 0.6 0.3 0.4 0.4 0.2

0.8 0.3
...

0.3 0.2 0.1
... ...

Tombstone

Wickenburg Willcox, Stewart Sch.
Winslow Yuma

0.2 1.5
1.2

0.1 0.0 0.2 0.25

0.7
2 .0

0.2 0.4

0.4

*

POTABILITY
Severe mottled enamel of the deeply stained and pitted type appear to be associated with waters containing well over 2.0 p.p.m. of fluorine. Waters containing from 1 to 2 p.p.m. were always found associated with a mild to moderate type of this dental defect. That the lower limit of fluorine content in water which causes mottled enamel probably is slightly less than 1 p.p.m. is shown in Eagar, Tucson Brickyard, Florence (private well), San Xavier, Cochise, and Springerville. These waters were found to produce a very mild type of mottled enamel. In Eagar the effect was variable. About 50 per cent of the children in the community had chalky white patches on the teeth, characteristic of mild mottling. Again it may be noted that other waters with a fluorine content of 0. 7 to 0.8 p.p.m. did not have a toxic effect upon the teeth, as, for example, the city of Chandler. This community, however, is surrounded bv areas in which mottled enamel does occur and in all probability has a fluorine content which is just below the toxic concentration. It is difficult to establish the exact fluorine concentration in a water supply which will damage the teeth of its users. The evidence indicates strongly that any water with a fluorine content of 0.9 p.p.m. (when analyzed by the Foster, Willard, or Sanchis methods) or over is dangerous from the standpoint of probable damage to the teeth. No Arizona water has yet been found containing more than 1 p.p.m. of fluorine which has not been shown to cause mottled enamel. Dahle,'7 Associate Referee for the A.O.A.C. has compared the Foster, Willard, and Steiger methods by means of analysis of synthetic waters made by 8 chemists in different parts of the country. His synthetic water "A " made up to contain 2.08 p.p.m. of fluorine was found to contain 2.08 p.p.m. by Foster method, 2.27 by the

OF

WATER

437

Willard method, and 1.9 p.p.m. by th-e modified Steiger method. Little difference in results obtained by these 3 methods was apparent. Therefore it is safe to conclude that the toxic concentration of fluorine is similar when determined by the Foster, Willard, Sanchis, or Steiger methods, and has as its lower limit 1 p.p.m. or slightly less.
REMOVAL OF FLUORINE FROM WATER SUPPLIES

Because certain communities find it impossible to secure waters containing too little fluorine to cause mottled enamel, a practical method of treating the water to remove fluorine must be developed. Many years ago Carnot 18 reported that it was possible to remove fluorine from water by the use of bone. This removal is probably due to the fact that the CO3 in bone Ca1oCO3(PO4)6 can be replaced with fluorine. A single trial in our laboratory has been made of this method. When 67.5 mg. of bone was used per liter of water, the original fluorine concentration of 2.5 p.p.m. was reduced to 1.7 p.p.m. The possibilities of this method are under further investigation. Willis of the Colorado Springs High School 19 has studied the waters in the mountains above Colorado Springs in an attempt to determine the source of fluorine in Colorado Springs water supply. Analyses of water from the same source showed lower concentrations of fluorine during winter than summer, hence the possibility of " freezing out " the fluorine suggested itself. Through the courtesy of the Arizona Ice and -Cold Storage Company in Tucson it was possible to conduct a freezing experiment under commercial conditions. Water originally containing 0. 7 p.p.m. fluorine was fortified with a sodium fluoride solution. A concentration of 3.4 p.p.m. resulted. The tank containing the mixture was placed in the.

438

AMERICAN JOURNAL OF PUBLIC HEALTH
mained in the solution. Under these conditions fluorine results by the Foster method were lower than by the Willard and Winters method, and it is assumed that aluminum sulphate was responsible for this. Further studies are being conducted to discover the cause. McKee and Johnson 21 have recently suggested the removal of fluorine by the use of activated carbon after the pH of the water has been reduced below 3.0. Cost of carbon, acid, and lime will not permit the use of this method by a municipality. The practicability of any of the heretofore proposed methods for the removal of fluorine from municipal supplies seems doubtful. When it is realized that only 1 p.p.m. of fluorine in water is necessary to cause mottled enamel, it is not surprising that attempts to remove these small amounts have not met with greater success.
SUMMARY

brine to freeze. Agitation was obtained with compressed air. Two cores were removed. The cake of ice was sampled and analyzed for fluorine by the Sanchis method. Results are shown in Table II.
TABLE II REMOVAL OF FLUORINE BY FREEZING Fluorine in p.p.m. 0. 7 Original Water . . ......... . Water and added NaF 3.4
......

First Core Removed ......... Second Core Removed Sample No. 1 Outer Portion.. Sample No. 2 Outer Portion..
......

6.0
4.0 0.7 0.4

It is a well known fact that ice freezes almost pure. In this case the impurities were concentrated in the ccre. It is doubtful whether this method of fluorine removal would be any more practical than distillation. A verbal report of Dr. Frary of the Aluminum Company of America, at the meeting of the American Chemical Society in Chicago in 1933-that activated aluminum would remove all traces of fluorine from solution-apparently has not yet been published. Boruff20 has reported the removal of fluorine from water by the use of aluminum sulphate. Water containing 2 to 3 p.p.m. of fluorine required 85 p.p.m. of the anhydrous salt, or 165 of the crystalline, to lower the fluorine concentration to the safe level of 0.5 p.p.m. At $4.42 per 100 lb. for aluminum sulphate, the cost of treating 1,000,000 gallons of water would be $60.77. This cost is prohibitive for municipal supplies. If only drinking water were treated, the cost of 6.07 cents per 1,000 gallons for chemicals would be very economical. No reports of the use of this method have been noted. The writer has attempted to corroborate Boruff's results and especially to modify his procedure to render it more practical by securing more complete removal with less aluminum. In some cases residual aluminum re-

1. A concentration of 0.8 to 0.9 p.p.m. of fluorine in water has been found to cause mottled enamel if this water is consumed while the children are of a susceptible age. 2. A comparison has been made of 4 methods for the determination of fluorine in water. 3. Experimental work has shown the Foster method to be unsatisfactory when used for the fluorine determination on waters which have been treated with A12 (SO4) 3 for fluorine removal if considerable aluminum remains in solution.
ACKNOWLEDGMENT-The writer is indebted to Jane Rider in planning and executing part of the experimental work presented here as well as for a criticism of the manuscript, and to W. T. McGeorge and T. F. Buehrer for suggestions and help in designing equipment used.
REFERENCES
teeth heretofore unknown in the literature of dentistry. Dental Cosmos, 58:132-156, 1916. 2. Eager. Pub. Health Rep., 16:2576, 1901. 3. Smith, M. C., Lantz, E. L., and Smith, H. V.
1. Black, G. V., and McKay, F. S. Mottled teeth an endemic developmental imperfection of the

POTABILITY OF WATER
The cause of mottled enamel, a defect of human teeth. Univ. of Arizona Agri. Exper. Sta. Tech. Bull. 32, 1931. 4. Churchill, H. V. Occurrence of fluorides in some waters of the United States. J. Indust. & Eng. Chem., 23, 9:996-998, 1931. S. Reynolds, P. S., Ross, W. H., and Jacob, L. D. Volatilization method for the determination of fluorine with special reference to the analysis of rock phosphate. J. Assn. Agri. Chem., 11:225, 1928. 6. Smith, H. V., and Smith, M. C. Mottled enamel in Arizona and its correlation with the concentration of fluorides in water supplies. Univ. of Arizona Agri. Exper. Sta. Tech. Bull 43, 1932. 7. Fairchild, John G. The volumetric determination. 8. Foster, Margaret D. Colorimetric determination of fluorides in water using ferric chloride. Indust. & Eng. Chem., 5:234-236, 1933. 9. Armstrong, W. D. Colorimetric Determination of Fluorine. Indust. & Eng. Chem. Anal. Ed. 5:300-302, 1933. 10. Steiger, G. Colorimetric determination of fluorine. J. Am. Chem. Soc., 30:219, 1908. 11. Wichmann, H. G., and Dable, Dan. Determinations of small quantities of fluorine. J.A.O.A.C., Nov., 1933, p. 612. 12. Boissevain, D. H. The presence of fluorine in

439

the water supply of Colorado and its relation to the occurrence of mottled enamel. Colorado Med., Apr., 1933. 13. Wilcox, L. V. A photronic colorimeter and its application to the determination of fluorine. Indust. & Eng. Chem., 6:167-169, 1934. 14. Willard, H. H., and Winters, 0. B. Volumetric method for determination of fluorine. Indust. & Eng. Chem. Anal. Ed.., 5:7-10, 1933. 15. Thompson, T. G., and Taylor, H. J. Determination and occurrence of fluorides in sea water. Indust. & Eng. Chem., 5:87-89, 1933. 16. Sanchis, J. M. Determination of fluorides in natural waters. Indust. & Eng. Chem., 6:134-135, 1934. 17. Dable, Dan. Private correspondence. 18. Carnot, A. Recherches sur la composition generale et la teneur en fluor des os modernes et des os fossiles des differents ages. Ann. Mines, 9, 3:155195, 1893. 19. Willis, Willet. The source of the fluorine in some water supplies. Bull. Colorado State Dental Assn., 1934, pp. 39-44. 20. Boruff, C. S. Removal of fluorides from drinking water. J. Indust. & Eng. Chem., 26, 1:69, 1934. 21. McKee, R. H., and Johnston, W. S. Removal of fluorides from drinking water. Indust. & Eng. Chem., 26:849-851, 1934.

DISCUSSION
J. M. SANCHIS Chemist, Bureau of Water Works and Supply, Los Angeles, Calif. MR. SMITH has summarized effec- with zirconium in a hydrochloric acid tively the extent of our present solution. knowledge in regard to the various The Foster method is the best known aspects of the problem presented by the of the procedures in which use is made occurrence of fluorides in potable of the ferric ion reaction. This came waters. at a time when the inconsistency of the His timely remarks on the im- results obtained by the then available portance of the part played by methods had thrown laboratory findings analytical procedures in any attempt to into a hopeless state of confusion. Its ascertain the toxic level of fluoride in relative superiority over the other water, based on field observations, can- methods caused its ready acceptance by not be overemphasized. Without a those confronted with the need of reproducible unit of measure, little making fluoride determinations. Howprogress can be made in the evaluation ever, the results obtained by it were of data obtained from widely scattered not always reliable nor easily duplilocalities. cated. Boruff and Abbott I pointed out As pointed out the methods which a number of theoretical considerations have been used most generally in recent by which they proved the fundamental years can be grouped into two main weakness of the method even in the abclasses. Those in one class make use sence of interfering substances. When of the fact that fluorides interfere with to this is added the effect that reducing the quantitative estimation of ferric agents such as hydrogen sulphide have ions, while those in the other class de- upon ferric ions, the difficulty in which pend on the effect of fluorides upon the the thiocyanate colors can be matched color produced when alizarin reacts when using Nessler tubes or the

RULES OF TENNESSEE DEPARTMENT OF ENVIRONMENT AND CONSERVATION BUREAU OF ENVIRONMENT DIVISION OF WATER SUPPLY CHAPTER 1200-5-1 PUBLIC WATER SYSTEMS TABLE OF CONTENTS
1200-5-1-.01 1200-5-1-.02 1200-5-1-.03 1200-5-1-.04 1200-5-1-.05 1200-5-1-.06 1200-5-1-.07 1200-5-1-.08 1200-5-1-.09 1200-5-1-.10 1200-5-1-.11 1200-5-1-.12 1200-5-1-.13 1200-5-1-.14 1200-5-1-.15 1200-5-1-.16 1200-5-1-.17 1200-5-1-.18 1200-5-1-.19 1200-5-1-.20 1200-5-1-.21 1200-5-1-.22 Authority Purpose Scope Definitions Supervision of Design and Construction Maximum Contaminant Levels Monitoring and Analytical Requirements Turbidity Sampling and Analytical Requirements Inorganic Chemical Sampling and Analytical Requirements Organic Chemical Sampling and Analytical Requirements Radionuclide Sampling Secondary Drinking Water Regulations Alternative Analytical Techniques Laboratory Certification Monitoring of Consecutive Public Water Systems Siting Requirements Operation and Maintenance Requirements Reporting Requirements Notification of Customers Record Maintenance Monitoring For Corrosivity Chacteristics Reserved 1200-5-1-.23 1200-5-1-.24 1200-5-1-.25 1200-5-1-.26 1200-5-1-.27 1200-5-1-.28 1200-5-1-.29 1200-5-1-.30 1200-5-1-.31 1200-5-1-.32 1200-5-1-.33 1200-5-1-.34 1200-5-1-.35 1200-5-1-.36 1200-5-1-.37 1200-5-1-.38 1200-5-1-.39 1200-5-1-.40 Reserved Sodium Monitoring Volatile Organic Chemicals Volatile Organic Chemical Sampling Analytical and Other Requirements Reserved Reserved Use of Non-Centralized Treatment Devices Reserved Filtration and Disinfection Fees for Public Water Systems Control of Lead and Copper Drinking Water Source Protection Consumer Confidence Reports Disinfectant Residuals, Disinfection Byproducts, and Disinfection Byproduct Precursors Stage 2 Initial Distribution System Evaluation For Disinfection Byproducts Stage 2 Disinfection Byproducts Requirements (LRAA) Enhanced Treatment For Cryptosporidium Ground Water Rule

1200-5-1-.01 AUTHORITY. (1) (2) These Rules and Regulations are issued under the authority of Public Acts of 1983, Chapter 324. The Division of Water Supply is responsible for the supervision of public water systems.

Authority: T.C.A. §§ 4-5-201 et seq. and 68-221-701 et seq. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. 1200-5-1-.02 PURPOSE. (1) The purpose of these Rules and Regulations is to provide guidelines for the interpretation of §68-221-701 et seq. of the Tennessee Code Annotated and to set out the procedures to be followed by the Department in carrying out the State’s primary enforcement responsibility under the Federal Safe Drinking Water Act. These Rules and Regulations set out the requirements which agents, employees or representatives of public water systems must meet in the following areas: in the preparation and submission of plan documents for public water systems; in the supervision of all phases of construction; in supplying safe drinking water meeting all applicable maximum contaminant levels or treatment technique requirements; in providing adequate operation and maintenance of the system; and in complying with procedural requirements for appealing orders issued by the Commissioner of the Tennessee Department of Health and Environment against a public water system.

August, 2008 (Revised)

1

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.02, continued) (2)

CHAPTER 1200-5-1

Where the terms shall and must are used, practice and usage is sufficiently standardized to indicate a mandatory requirement, insofar as any complaint action by the Department is concerned. Other items, such as should, recommend, preferred, and the like, indicate desirable procedures or methods.

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, and 68-221-701 et seq. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. 1200-5-1-.03 SCOPE. These rules will apply to all public water supply systems that provide water for human consumption through pipes or other constructed conveyances, if such system has at least fifteen (15) service connections or regularly serves an average of at least twenty–five (25) individuals daily at least sixty (60) days out of the year. A public water supply system is either a community water system or a non– community water system. A community water system is a public water supply system which serves at least fifteen (15) service connections used by year-round residents or regularly serves at least twenty–five (25) year–round residents. A non–community water system is a public water supply system that is not a community water system and which generally serves a transient population such as hotels, motels, restaurants, camps, service stations churches, industry, etc. A Non-Transient Non–Community Water System is a non–community water system that regularly serves at least 25 of the same persons over six (6) months per year. These rules do not apply to public water systems which meet all of the following criteria: (1) (2) (3) (4) consists only of distribution and storage facilities (and does not have any collection and treatment facilities); obtains all of its water from, but is not owned or operated by, a public water system to which such regulations apply; does not sell water to any person; and is not a carrier which conveys passengers in interstate commerce.

Authority: T.C.A. §§4-5-202, 68-221-701 et seq., and 68-221-704. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. Repeal and new rule filed August 15, 2005; effective October 29, 2005. 1200-5-1-.04 DEFINITIONS. (1) (2) "Action level" is the concentration of lead or copper in water which may determine the treatment requirements that a water system is required to complete. “Bag Filters” are pressure-driven separation devices that remove particulate matter larger than 1 micrometer using an engineered porous filtration media. They are typically constructed on a non-rigid fabric filtration media housed in a pressure vessel in which the direction of flow is from the inside of the bag to outside. “Bank Filtration” is a water treatment process that uses a well to recover surface water that has naturally infiltrated into ground water through a river bed or bank(s). Infiltration is typically enhanced by the hydraulic gradient imposed by nearby pumping water supply or other wells. “Benchmark” A disinfection benchmark is the lowest monthly average value of the monthly logs of Garidia Lamblia inactivation.

(3)

(4)

August, 2008 (Revised)

2

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.04, continued) (5)

CHAPTER 1200-5-1

“Business Plan” means a document which identifies source(s) of income or revenue sufficient to meet expenses over a three (3) year period. The business plan will identify costs related to retaining a certified operator, estimated annual infrastructure repair costs, depreciation, facility maintenance fees, estimated annual monitoring costs, estimated costs of providing public notices, estimated administrative costs, and any and all other operational, treatment, and related costs (e.g. chemicals and other supplies used to treat water, etc.). The business plan must include the re-payment of borrowed and amortized funds. “Capacity Development Plan” means a document(s) identifying what actions a public water system is taking or shall take to become a “viable water system.” Such plan shall include information concerning retention of a Certified Operator in direct charge; system ownership and accountability; staffing and organizational structure; fiscal management and controls, source water assessment and protection plan; “business plan;” and any and all other information identifying any further action that shall be taken. “Cartridge filters” are pressure-driven separation devices that remove particulate matter larger than 1 micrometer using an engineered porous filtration media. They are typically constructed a rigid or semi-rigid self-supporting filter elements housed in pressure vessels in which flow is from the outside of the cartridge to the inside. "Coagulation" means a process using coagulant chemicals and mixing by which colloidal and suspended materials are destabilized and agglomerated into flocs. “Combined distribution system” is the interconnected distribution system consisting of the distribution systems of wholesale systems and of the consecutive systems that receive finished water. "Community Water System" means a public water system which serves at least fifteen (15) service connections used by year-round residents or regularly serves at least twenty-five (25) year-round residents. "Compliance cycle" means the nine-year calendar year cycle during which public water systems must monitor for certain contaminants. Each compliance cycle consists of three three-year compliance periods. The first calendar year cycle begins January 1, 1993 and ends December 31, 2001; the second begins January 1, 2002 and ends December 31, 2010; the third begins January 1, 2011 and ends December 31, 2019. "Compliance period" means a three year calendar year period within a compliance cycle. Each compliance cycle has three three-year compliance periods. Within the first compliance cycle, the first compliance period runs from January 1, 1993 to December 31, 1995; the second from January 1, 1996 to December 31, 1998; the third from January 1, 1999 to December 31, 2001. “Comprehensive performance evaluation (CPE)” is a thorough review and analysis of a treatment plant’s performance-based capabilities and associated administrative, operation and maintenance practices. It is conducted to identify factors that may be adversely impacting a plant’s capability to achieve compliance and emphasizes approaches that can be implemented without significant capital improvements. For purposes of compliance, the comprehensive performance evaluation must consist of at least the following components: assessment of plant performance; evaluation of major unit processes; identification and prioritization of performance limiting factors; assessment of the applicability of comprehensive technical assistance; and preparation of a CPE report.

(6)

(7)

(8) (9)

(10)

(11)

(12)

(13)

August, 2008 (Revised)

3

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.04, continued) (14) "Confluent growth" means a continuous bacterial growth covering the entire filtration area of a membrane filter, or a portion thereof, in which bacterial colonies are not discrete. (15) (16) "Connection" means the point at which there is a meter or service tap if no meter is present. “Consecutive system is a public water system that receives some or all of its finished water from one or more wholesale systems. Delivery may be through a direct connection or through the distribution system of one or more consecutive systems. "Contaminant" means any physical, chemical, biological, or radiological substance or matter in water. "Conventional filtration treatment" means a series of processes including coagulation, flocculation, sedimentation, and filtration resulting in substantial particulate removal. "Corrosion inhibitor" means a substance capable of reducing the corrosivity of water toward metal plumbing materials, especially lead and copper, by forming a protective film on the interior surface of those materials. "CT" or "CTcalc" is the product of "residual disinfectant concentration" (C) in mg/1 determined before or at the first customer, and the corresponding "disinfectant contact time" (T) in minutes, i.e., "C" x "T". If a public water system applies disinfectants at more than one point prior to the first customer, it must determine the CT of each disinfectant sequence before or at the first customer to determine the total percent inactivation or "total inactivation ratio". In determining the total inactivation ratio, the public water system must determine the residual disinfectant concentration of each disinfection sequence and corresponding contact time before any subsequent disinfection application point(s). "CT99.9" is the CT value required for 99.9 percent (3-log) inactivation of Giardia lamblia cysts. CT99.9 for a variety of disinfectants and conditions appear in Tables 1.1-1.6, 2.1, and 3.1 of 1200-5-1-.31(5)(b)3. CTcalc CT99.9 is the inactivation ratio. The sum of the inactivation ratios, or total inactivation ratio shown as

(17) (18) (19)

(20)

Σ

(CTcalc) (CT99.9)

is calculated by adding together the inactivation ratio for each disinfection sequence. A total inactivation ratio equal to or greater than 1.0 is assumed to provide a 3-log inactivation of Giardia lamblia cyst. Disinfectant concentrations must be determined by tracer studies or an equivalent demonstration approved by the Department. (21) "Department" when used in these regulations shall mean the Division of Water Supply, Tennessee Department of Environment and Conservation, or one of the Division's Field Offices. The terms "State," "Department," and "Division" are often used interchangeably in these Rules and Regulations. "Diatomaceous earth filtration" means a process resulting in substantial particulate removal in which (1) a precoat cake of diatomaceous earth filter media is deposited on a support membrane (septum), and (2) while the water is filtered by passing through the cake on the septum, additional filter media known as body feed is continuously added to the feed water to maintain the permeability of the filter cake.

(22)

August, 2008 (Revised)

4

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.04, continued) (23) "Direct filtration" means a series of processes including coagulation and filtration but excluding sedimentation resulting in substantial particulate removal. (24) "Disinfectant" means any oxidant, including but not limited to chlorine, chlorine dioxide, chloramines, and ozone added to water in any part of the treatment or distribution process, that is intended to kill or inactivate pathogenic microorganisms. "Disinfectant contact time" ("T" in CT calculations) means the time in minutes that it takes for water to move from the point of disinfectant application or the previous point of disinfectant residual measurement to a point before or at the point where residual disinfectant concentration ("C") is measured. Where only one "C" is measured, "T" is the time in minutes that it takes for water to move from the point of disinfectant application to a point before or at where residual disinfectant concentration ("C") is measured. Where more than one "C" is measured, "T" is (a) for the first measurement of "C", the time in minutes that it takes for water to move from the first or only point of disinfectant application to a point before or at the point where the first "C" is measured and (b) for subsequent measurements of "C", the time in minutes that it takes for water to move from the previous "C" measurement point to the "C" measurement point for which the particular "T" is being calculated. Disinfectant contact time in pipelines must be calculated based on "plug flow" by dividing the internal volume of the pipe by the maximum hourly flow rate through that pipe. Disinfectant contact time within mixing basins and storage reservoirs must be determined by tracer studies or an equivalent demonstration. "Disinfection" means a process which inactivates pathogenic organisms in water by chemical oxidants or equivalent agents. “Disinfection profile” is a summary of daily Giardia lamblia inactivation through the treatment plant. The procedure for developing a disinfection profile is contained in 40CFR141.172. "Distribution System" means all water lines up to the point of a meter. For unmetered systems distribution system includes all lines up to the customer's service tap. "Domestic or other non-distribution system plumbing problem" means a coliform contamination problem in a public water system with more than one service connection that is limited to the specific service connection from which the coliform-positive sample was taken. "Dose Equivalent" means the product of the absorbed dose from ionizing radiation and such factors as account for differences in biological effectiveness due to the type of radiation and its distribution in the body as specified by the International Commission on Radiological Units and Measurements (ICRU). “Dual sample set” is a set of two samples collected at the same time and same location, with one sample analyzed for TTHM and the other sample analyzed for HAA5. Dual sample sets are collected for the purposes of conducting an IDSE under the provisions of 1200-5-1.37 and determining compliance with the TTHM and HAA5 MCLs under the provisions of 1200-5-1-.38. "Effective corrosion inhibitor residual" for the purpose of the lead and copper rules only, means a concentration sufficient to form a passivating film on the interior walls of a pipe. "Engineer" means the person or firm who designed the public water system and conceived, developed, executed or supervised the preparation of the plan documents. “Enhanced coagulation” means the addition of sufficient coagulant for improved removal of disinfection byproduct precursors by conventional filtration treatment

(25)

(26) (27) (28) (29)

(30)

(31)

(32) (33) (34)

August, 2008 (Revised)

5

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.04, continued) (35) (36)

CHAPTER 1200-5-1

“Enhanced softening” means the improved removal of disinfection byproduct precursors by precipitative softening. “Filter profile” is a graphical representation of individual filter performance, based on continuous turbidity measurements or total particle counts versus time for an entire filter run, from startup to backwash inclusively, that includes an assessment of filter performance while another filter is being backwashed. "Filtration" means a process for removing particulate matter from water by passage through porous media. “Finished water” is water that is introduced into the distribution system of a public water system and is intended for distribution and consumption without further treatment, except as treatment necessary to maintain water quality in the distribution system (e.g., booster disinfection, addition of corrosion control chemicals). "First draw sample" means a one-liter sample of tap water, for the purposes of the lead and copper rules, that has been standing in plumbing pipes at least 6 hours and is collected without flushing the tap. “Flocculation" means a process to enhance agglomeration or collection of smaller floc particles into larger, more easily settleable particles through gentle stirring by hydraulic or mechanical means. “Flowing stream” is a course of running water flowing in a definite channel. “GAC10” means granular activated carbon filter beds with an empty-bed contact time of 10 minutes based on average daily flow and a carbon reactivation frequency of every 180 days, except that the reactivation frequency for GAC10 used as best available technology for compliance with disinfection byproducts shall be 120 days. “GAC20” means granular activated carbon filter beds with an empty-bed contact time of 20 minutes based on average daily flow and a carbon reactivation frequency of every 240 days. "Gross Alpha Particle Activity" means the total radioactivity due to alpha particle emission as inferred from measurements on a dry sample. "Gross Beta Particle Activity" means the total radioactivity due to beta particle emission as inferred from measurements on a dry sample. “Ground water under the direct influence of surface water” means any water beneath the surface of the ground with significant occurrence of insects or other macroorganisms, algae, or large-diameter pathogens such as Giardia lamblia or Cryptosporidium, or significant and relatively rapid shifts in water characteristics such as turbidity, temperature, conductivity, or pH which closely correlate to climatological or surface water conditions. Direct influence must be determined for individual sources in accordance with criteria established by the State. The State determination of direct influence may be based on site-specific measurements of water quality and/or documentation of well construction characteristics and geology with field evaluation. “Haloacetic acids (five) (HAA5)” mean the sum of the concentrations in milligrams per liter of the haloacetic acid compounds (monochloroacetic acid, dichloroacetic acid, trichloroacetic acid, monobromoacetic acid, and dibromoacetic acid), rounded to two significant figures after addition.

(37) (38)

(39)

(40)

(41) (42)

(43)

(44) (45) (46)

(47)

August, 2008 (Revised)

6

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.04, continued) (48) (49)

CHAPTER 1200-5-1

"Halogen" means one of the chemical elements chlorine, bromine or iodine. “Human Consumption” - means the use of water that involves any drinking or ingestion of the water by humans, any human skin contact or food preparation where the food is not brought to boiling temperatures after contact with the water.. "Initial compliance period" means the first full three-year compliance period which begins January 1, 1993. For public water systems having fewer than 150 service connections initial compliance period shall be January 2, 1996, for the following contaminants: (a) (b) (c) (d) (e) (f) (g) (h) (i) (j) (k) (l) Antimony Beryllium Cyanide Nickel Thallium dichloromethane 1,2,4-trichlorobenzene 1,1,2-trichloroethane dalapon dinoseb diquat endothall (m) (n) (o) (p) (q) (r) (s) (t) (u) (v) (w) endrin glyphosate oxamyl picloram simazine benzo(a)pyrene di(2ethylhexyl)adipate di(2ethylhexyl)phthalate hexachlorobenzene hexachlorocyclopentadiene 2,3,7,8 TCDD

(50)

(51)

“Lake/reservoir” refers to a natural or man made basin or hollow on the earth’s surface in which water collects or is stored that may or may not have a current or single direction of flow. "Large water system" for the purpose of lead and copper rule, means a water system that serves more than 50,000 persons. "Lead service line" means a service line made of lead which connects the water main to the building inlet and any lead pigtail, gooseneck or other fitting which is connected to such lead line. "Legionella" means a genus of bacteria, some species of which have caused a type of pneumonia called Legionnaires Disease. “Locational running annual average (LRAA)” is the average of sample analytical results for samples taken at a particular monitoring location during the previous four calendar quarters. "Man-Made Beta Particle and Photon Emitter" means all radionuclides emitting beta particles and/or photons listed in "Maximum Permissible Body Burdens and Maximum Permissible Concentration of Radionuclides in Air or Water for Occupational Exposure, NBS Handbook 69", except the daughter products of thorium-232, uranium-235 and uranium-238. "Maximum Contaminant Level" means the maximum permissible level of a contaminant in water which is delivered at the free flowing outlet of the ultimate user of a public water system, except in the case of turbidity where the maximum permissible level is measured at the point of entry to the distribution system. Contaminants added to the water under circumstances controlled by the user, except those resulting from corrosion of piping and plumbing caused by water quality, are excluded from this definition. “Maximum residual disinfectant level (MRDL)” means a level of a disinfectant added for water treatment that may not be exceeded at the consumer’s tap without an unacceptable

(52) (53)

(54) (55) (56)

(57)

(58)

August, 2008 (Revised)

7

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.04, continued) possibility of adverse health effects. For chlorine and chloramines, a PWS is in compliance with the MRDL when the running annual average of monthly averages of samples taken in the distribution system, computed quarterly, is less than or equal to the MRDL. For chlorine dioxide, a PWS is in compliance with the MRDL when daily samples are taken at the entrance to the distribution system and no two consecutive daily samples exceed the MRDL. MRDLs are enforceable in the same manner as maximum contaminant levels under Section 1412 of the Safe Drinking Water Act. There is convincing evidence that addition of a disinfectant is necessary for control of waterborne microbial contaminants. Notwithstanding the MRDLs, operators may increase residual disinfectant levels of chlorine or chloramines (but not chlorine dioxide) in the distribution system to a level and for a time necessary to protect public health to address specific microbiological contamination problems caused by circumstances such as distribution line breaks, storm runoff events, source water contamination, or cross-connections. (59) "Maximum Total Trihalomethane Potential (MTP)" means the maximum concentration of total trihalomethanes produced in a given water containing a disinfectant residual after 7 days at a temperature of 25°C or above. "Medium-size water system" for the purpose of the lead and copper rule means a water system that serves greater than 3,300 and less than or equal to 50,000 persons. “Membrane filtration” is a pressure or vacuum driven separation process in which particulate matter larger than 1 micrometer is rejected by an engineered barrier, primarily through a size exclusion mechanism, and which has a measurable removal efficiency of a target organism that can be verified through the application of a direct integrity test. This definition includes the common membrane technologies of microfiltration, ultrafiltration, nanofiltration, and reverse osmosis. "Near the first service connection" means at one of the twenty percent of all service connections in the entire system that are nearest the water supply treatment facility, as measured by the water transport time within the distribution system. "Non-Community Water System" means a public water system that is not a community water system. "Non-Transient Non-Community Water System" or NTNCWS" means a non-community water system that regularly serves at least twenty-five (25) of the same persons over six (6) months per year. "Optimal corrosion control treatment" for the purpose of lead and copper rule only means the corrosion control treatment that minimizes the lead and copper concentrations at user's taps while insuring that the treatment does not cause the water system to violate any primary drinking water regulation. "Person" means any individual, corporation, company, association, partnership, State, municipality, utility district, water cooperative, or Federal agency. "Picocurie" (pCi) means that quantity of radioactive material producing 2.22 nuclear transformations per minute. "Plan Documents" mean reports, proposals, preliminary plans, survey and basis of design data, general and detailed construction plans, profiles, specifications and all other information pertaining to public water system planning. “Plant intake” refers to the works or structures at the head of a conduit through which water is diverted from a source (e.g., river or lake) into the treatment plant.

(60) (61)

(62)

(63) (64)

(65)

(66) (67) (68)

(69)

August, 2008 (Revised)

8

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.04, continued) (70) (71)

CHAPTER 1200-5-1

"Point of disinfectant application" is the point where the disinfectant is applied and water downstream of that point is not subject to recontamination by surface water runoff. "Point-of-Entry Treatment Device" (POE) means a device applied to the drinking water entering a house or building for the purpose of reducing contaminants in the drinking water distributed throughout the house or building. "Point-of-Use Treatment Device" (POU) means a treatment device applied to a single tap used for the purpose of reducing contaminants in drinking water at that one tap. ‘Presedimentation” is a preliminary treatment process used to remove gravel, sand and other particulate material from the source water through settling before the water enters the primary clarification and filtration processes in a treatment plant. "Primary Drinking Water Regulation" means a regulation promulgated by the Department which: (a) (b) (c) applies to public water systems; specifies contaminants which, in the judgment of the Department, may have any adverse effect on the health of persons; specified for each such contaminant either; 1. a maximum contaminant level, if, in the judgment of the Department, it is economically and technologically feasible to ascertain the level of such contaminant in water in public water systems, or if, in the judgment of the Department, it is not economically or technologically feasible to so ascertain the level of such contaminant, each treatment technique known to the Department which leads to a reduction in the level of such contaminant sufficient to satisfy the requirements of Regulations 1200-5-1-.06; and

(72) (73)

(74)

2.

(d)

contains criteria and procedures to assure a supply of drinking water which dependably complies with such maximum contaminant levels; or treatment techniques including quality control and testing procedures to insure compliance with such levels and to insure proper operation and maintenance of the system, and requirements to (i) the minimum quality of water which may be taken into the system and (ii) siting for new facilities for public water systems.

(75) “Public Water System” means a system for the provision of piped water for human consumption if such serves 15 or more connections or which regularly serves 25 or more individuals daily at least 60 days out of the year and includes: (a) any collection, treatment, storage or distribution facility under control of the operator of such system and used primarily in connection with such system; and any collection or pre-treatment storage facility not under such control which is used primarily in connection with such system,

(b)

The population of a water system shall be determined by actual count or by multiplying the household factor by the number of connections in the system. The household factor shall be taken from the latest federal census for that county or city. Water systems serving multi-

August, 2008 (Revised)

9

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.04, continued) family residences such as apartment complexes and mobile home parks shall include each individual residence unit as a connection in determining the population for the system. (76) (77) (78) (79) (80) "Rem" means the unit of dose equivalent from ionizing radiation to the total body or any internal organ or organ system. A "millerem (mrem)" is 1/1000 of a rem. "Repeat compliance period" means any subsequent compliance period after the initial compliance period. "Residual disinfectant concentration" ("C" in CT calculations) means the concentration of disinfectant measured in mg/l in a representative sample of water. "Safe Drinking Water Act" means the Federal law codified in 42 United States Code 300f et. seq., Public Law 93-523, dated December 16, 1974 and subsequent amendments.. "Sanitary Survey" means an on-site review of the water source, facilities, equipment, operation and maintenance of a public water system for the purpose of evaluating the adequacy of such sources, facilities, equipment, operation and maintenance for producing and distributing safe drinking water. "Secondary Drinking Water Regulation" mean a regulation promulgated by the Department which applies to public water systems and which specifies the maximum contaminant levels which, in the judgment of the Department are requisite to protect the public welfare. Such regulations may apply to any contaminant in drinking water (a) which may adversely affect the odor or appearance of such water and consequently may cause the persons served by the public water system providing such water to discontinue its use, or which may otherwise adversely affect the public welfare. Such regulations may vary according to geographic and other circumstances.

(81)

(b) (82) (83) (84)

"Sedimentation" means a process for removal of solids before filtration by gravity or separation. "Service line sample" means a one-liter sample of water collected in accordance with 1200-5-1-.33(7)(b)3., that has been standing for at least 6 hours in a service line. "Single family structure" for the purpose of lead and copper rules means a building constructed as a single-family residence that is currently used as either a residence or a place of business. "Slow sand filtration" means a process involving passage of a raw water through a bed of sand at low velocity (generally less than 0.4 m/h) resulting in substantial particulate removal by physical and biological mechanisms. "Small water system" for the purpose of the lead and copper rules only, means a water system that serves 3,300 or fewer persons. “Subpart H systems” means public water systems using surface water or ground water under the direct influence of surface water as a source that are subject to the requirements 1200-5-1-.31, .39 and 1200-5-1-.17. "Supplier of Water" means any person who owns or operates a public water system.

(85)

(86) (87)

(88)

August, 2008 (Revised)

10

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.04, continued) (89) "Surface water" means all water which is open to the atmosphere and subject to surface runoff. (90) “SUVA” means Specific Ultraviolet Absorption at 254 nanometers (nm), an indicator of the humic content of water. It is a calculated parameter obtained by dividing a sample’s ultraviolet absorption at a wavelength of 254 nm (UV 254/ (in m) by its concentration of dissolved organic carbon (DOC) (in mg/L). "System with a single service connection" means a system which supplies drinking water to consumers via a single service line. "Too numerous to count" means that the total number of bacterial colonies exceeds 200 on a 47 millimeter diameter membrane filter used for coliform detection. “Total Organic Carbon (TOC)” means total organic carbon in mg/L measured using heat, oxygen, ultraviolet irradiation, chemical oxidants, or combinations of these oxidants that convert organic carbon to carbon dioxide, rounded to two significant figures. "Total trihalomethane" (TTHM) means the sum of concentration in milligrams per liter of the trihalomethane compounds-trihalomethane (chloroform), dibromochloromethane, bromodichloro-methane and tribomomethane (bromoform), rounded to two significant figures. “Transient Non-Community Water System” or “TNCWS” means a non-community water system that regularly serves at least twenty-five (25) individuals daily at least sixty (60) days out of the year. A transient non-community water system is a public water supply system that generally serves a transient population such as hotels, motels, restaurants, camps, service stations churches, industry, and rest stops. "Trihalomethane" (THM) means one of the family of organic compounds, named as derivatives of methane, wherein three of the four hydrogen atoms in methane are each substituted by a halogen atom in the molecular structure. “Two-stage lime softening” is a process in which chemical addition and hardness precipitation occur in each of two distinct unit clarification processes. “Uncovered finished water storage facility” is a tank, reservoir, or other facility used to store water that will undergo no further treatment except residual disinfection and is open to the atmosphere. “Viable Water System” means a public water system which has the commitment and the financial, managerial and technical capacity to consistently comply with the Tennessee Safe Drinking Water Act and these regulations.

(91) (92) (93)

(94)

(95)

(96)

(97) (98)

(99)

(100) "Virus" means a virus of fecal origin which is infectious to humans by waterborne transmission. (101) “Waterborne disease outbreak" means a significant occurrence of acute infectious illness, epidemiologically associated with the ingestion of water from a public water system which is deficient in treatment, as determined by the appropriate local or State agency. (102) “Wholesale system” is a public water system that treats source water as necessary to produce finished water and then delivers some or all of that finished water to another public water system. Delivery may be through a direct connection or through the distribution system of one or more consecutive systems.

August, 2008 (Revised)

11

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.04, continued) Authority: T.C.A. § 68-221-704 and 4-5-202. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. Amendment filed November 26, 1990; effective January 10, 1991. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed October 22, 1993, effective January 5, 1994. Amendment filed April 12, 1996; effective June 26, 1996. Amendment filed February 17, 1999; effective May 3, 1999. Amendment filed October 31, 2000; effective January 14, 2001. Amendment filed July 15, 2002; effective September 28, 2002. Amendment filed December 30, 2002; effective March 15, 2003. Amendment filed July 31, 2006; effective October 14, 2006. Amendment filed June 12, 2008; effective August 26, 2008. 1200-5-1-.05 SUPERVISION OF DESIGN AND CONSTRUCTION. (1) (2) Engineering - Plan documents for public water systems shall be submitted to the Department at least thirty (30) days prior to the date on which action by the Department is desired. Expiration of Approval - Approval of engineering reports, proposals, preliminary plans, survey and basis of design data shall be null and void after a period of one year from the date stamped on the documents, unless the general and detailed plan documents have been submitted to the Department. Approval of all other plan documents by the Department shall be null and void after a period of one year from the date stamped on the plan documents, unless the construction is either underway or completed. General Practice - All plan documents for public water system design and construction shall present all information in conformance with accepted engineering practices and the “Design Criteria for community Public Water Systems” as published by the Department. Revisions to Plan Documents - Any deviations from plan documents approved by the Department, which affect location, sanitary and/or mineral quality, capacity, hydraulic conditions, operating units, or the function of unit processes or distribution and storage, must be approved in writing before such changes are made. Any revisions must be made on the master work, i.e., the original tracings. Revised plan documents must be submitted in time to permit the review and approval of such revisions before any construction which will be affected by such revisions is begun. Copies of Plan Documents - Generally, only two copies of the engineering report and two sets of the preliminary plans shall be required by the Department for review and/or approval. At least four complete sets of the detailed plan documents shall be required for final review. Upon the granting by the Department of its approval for construction the documents shall be so stamped and two sets returned to the engineer’s office, one set forwarded to the appropriate Field Office for filing or use in field inspection of construction, and one set retained for the Department files. Upon completion of the project, one set of “As Built” plans and one copy of the executed contract documents shall be submitted to the Department and one set each to the owner. In addition, shop drawings, instruction manuals, etc., on all equipment furnished by the project shall be compiled into one or more documents and given to the owner. Supervision of Construction - One set of the plan document stamped “APPROVED FOR CONSTRUCTION” shall be available at the job sites at all times during construction. The engineer or a person qualified other than the contractor or his representative, and approved by the public water system shall provide continuous adequate inspection during construction to assure that all work is done in accordance with approved plan documents. The Department’s representative shall have access to the project at any time during construction. If the Department’s representative observes work being done in a manner that does not conform to the approved plan documents, he shall have the authority, through the engineer’s representative, the water system’s agent or directly to the contractor, to order the cessation of all work affected by the nonconformity until such discrepancies are rectified.

(3)

(4)

(5)

(6)

August, 2008 (Revised)

12

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.05, continued) (7)

CHAPTER 1200-5-1

Engineer’s Seal - Plan documents for non-transient non-community and community public water systems shall be prepared by a person qualified under Section 62-2-101 et seq., Tennessee Code Annotated, and shall have the necessary professional seal affixed as required by Section 62-2-306 of the Code. (a) Ownership and Operational Organization – No person shall operate a public water system without notifying the Division of Water Supply prior to placing the new system in operation. Any person operating a public water system other than an individual, a municipality, any agency or instrumentality of the United States, any facility owned and operated by the State of Tennessee, or any organization otherwise exempt by law must have a charter or appropriate authorization lawfully issued as set forth in one or more of the following: Utility District – T.C.A. 7-82-101 et seq. General Corporation Act – T.C.A. 48 -1-101 et seq. Tennessee Regulatory Authority – T.C.A. 65-4-101 et seq. Urban Type Public Facilities – T.C.A. 5-16-101 et seq. (b) All public water systems shall comply with all laws, rules and regulations, and policies of the Department. Construction modification and treatment processes must be approved in accordance with all federally designated best available technologies and Tennessee Laws. Every public water system shall, within thirty (30) days following any change in ownership or operation of the system, file a written report of such change in ownership or operation with the Department. Such report shall, at a minimum, contain the name, home address, business address, and home and business phone numbers of the person assuming ownership or operation of the system, and the date such change of ownership or operation became effective. All persons owning or operating a public water system shall keep the Department advised of their current address and must readily accept all mail sent to them by the Department. For purposes of this Rule, registered or certified mail sent with proper postage to the registered owner or operator’s last known address shall be considered adequate notification regardless of whether is accepted or returned unclaimed. Because of the Department’s statutory duty to supervise the construction, operation, and maintenance of public water systems, and because written communication is a necessary aspect of such supervision, an owner or operator’s refusal to accept mail or failure to claim registered or certified mail is a violation of this Chapter and may result in enforcement action.

(8)

(c)

(d)

(9)

Interconnection of Systems - Insofar as feasible, public water systems shall be connected with a municipal, county, regional or other existing approved water system capable of supplying the demand. Where such connection is not feasible, other approved sources may be considered. Each public water system shall be designed in such a manner as will facilitate the connection of the system at an appropriate time to an expanding municipal, county or regional system. Each public water system shall be designed to provide service to all service areas anticipated or projected by the owner.

(10) System Capacity - Whenever a public water system reaches eighty (80) per cent of the design capacity based on average day usage, the supplier of water shall immediately obtain the services of a competent engineer to prepare plan documents for expansion of said system. (11) Turbidimeters – All community water systems using ground water formations under the direct influence of surface water, and serving more than 50 connections or 150 individuals, shall be

August, 2008 (Revised)

13

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.05, continued) required to install turbidity monitoring equipment with power cutoff ability and recording unit. Those systems not included in the above may be required to install turbidity monitoring devices if the Department finds that the system cannot meet the microbiological standard, the turbidity can be seen without an instrument, or there is an outbreak of illness that may be water related. All filter plants serving community water systems shall be required to have continuous recording turbidimeters on the filter effluent line(s). Such instrumentation may be pen and ink, digital, computerized or other record keeping or recording devices approved by the Division. If pen and ink recorders are used they shall be limited to two pens and two filters and shall use a scale of 0 to 2.0 NTU unless specific alternatives are approved in writing by the Division. (12) Monitoring of new sources - All new surface or ground water sources added to an existing water system or proposed for use by a new water system shall have the required biological and chemical water quality monitoring completed prior to being placed in service. The parameters to be monitored shall be those required for drinking water for the specific type of system involved. (13) Delegation of Plans Review Authority – Under Section 68–221–706 of the Tennessee Code Annotated, any unit of local government may petition the Commissioner for certification to review and approve plans for water distribution facilities within its jurisdiction. The unit of local government must have adequate experience and expertise in water distribution and must adopt standards and impose requirements which are at least as stringent as the Department’s. The request for certification must be in writing and contain at least the following: (a) The names of the individual(s) responsible for the review and approval together with his/her experience and education. This person(s) must be employed by the unit of local government and be a registered professional engineer in Tennessee. A copy of the standards, requirements and design criteria legally adopted and enforceable by the unit of local government. The type of projects the unit of local government wishes to receive certification to review. This may include but is not limited to water lines, distribution pumping stations and distribution storage tanks. Procedures for maintaining records of all projects reviewed and approved by the unit of local government. The wording to be used on the approval stamp. Plans review authority fee.

(b) (c)

(d) (e) (f)

The Division of Water Supply will be responsible for reviewing the application for certification and shall have up to 60 days from the receipt of the complete application to make a written response. Units of local government will not be certified to review projects involving state or federal funds, raw water pump stations, new water sources, treatment facilities, sludge handling facilities, or any project designed by the staff of the local government. Any unit of local government which receives certification for plans review shall submit one copy of any plan documents it has approved to the Division of Water Supply. This shall be done within 10 days of the local government’s approval. The commissioner may periodically review the unit of local government’s plans review program and prescribe changes as deemed appropriate. The Division of Water Supply may execute a written agreement with a unit of local government which has received plans review certification. Failure to comply with the terms of the agreement may result in revocation of the plans review certification.

August, 2008 (Revised)

14

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.05, continued) Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 68-221-701 et seq., and 68-221-704. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed April 12, 1996; effective June 26, 1996. Amendment filed October 31, 2000; effective January 14, 2001. Amendments filed August 15, 2005; effective October 29, 2005. 1200-5-1-.06 MAXIMUM CONTAMINANT LEVELS. (1) Inorganic Chemicals (a) The maximum contaminant level for fluoride applies to community water systems. The maximum contaminant levels for nitrate, nitrite and total nitrate and nitrite are applicable to both community water systems and non-community water systems. The maximum contaminant levels for the remaining inorganic chemicals apply only to community water systems and non-transient non-community systems. The effective date for antimony, beryllium, cyanide, nickel and thallium shall be January 1, 1993, or the effective date of this rule whichever is later. The arsenic maximum contaminant level listed in subparagraph (b)2 is effective for the purpose of compliance January 23, 2006. Until January 23, 2006, the arsenic MCL is 0.05 mg/L. The following are the maximum contaminant levels for inorganic chemicals: CONTAMINANT 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. (2) Antimony Arsenic Asbestos Beryllium Barium Cadmium Chromium Cyanide (as free cyanide) Fluoride Mercury Nickel Nitrate Nitrite Total nitrate and nitrate Selenium Thallium LEVEL, MILLIGRAMS PER LITER 0.006 0.010 7 million fibers/liter (longer than 10 microns) 0.004 2.0 0.005 0.1 0.2 4.0 0.002 0.1 10.0 (as Nitrogen) 1.0 (as Nitrogen) 10.0 (as Nitrogen) 0.05 0.002

(b)

Organic Chemicals - The following are the maximum contaminant levels for organic chemicals. (a) The following maximum contaminant levels for organic contaminants apply to community water systems and non-transient non-community water systems. The effective date of these MCLs shall be the effective date of this regulation. CONTAMINANT LEVEL, MILLIGRAMS PER LITER 1. 2. 3. 4. 5. Alachlor Atrazine Carbofuran Chlordane Dibromo chloropropane (DBCP) 0.002 0.003 0.04 0.002 0.0002

August, 2008 (Revised)

15

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.06, continued) 6. 2,4 Dichlorophenoxyacetic acid 7. Ethylene dibromide 8. Heptachlor 9. Heptachlor epoxide 10. Lindane 11. Methoxychlor 12. Polychlorinated biphenyls 13. Toxaphene 14. 2,4,5 Trichlorophenoxyproprionic acid 15. Pentachlorophenol 16. Benzo(a)pyrene 17. Dalapon 18. Di(2-ethylhexyl) adipate 19. Di(2-ethylhexyl)phthalate 20. Dinoseb 21. Diquat 22. Endothall 23. Glyphosate 24. Hexachlorobenzene 25. Hexachlorocyclopentadiene 26. Oxamyl (Vydate) 27. Picloram 28. Simazine 29. 2,3,7,8-TCDD (Dioxin) 30. Endrin (3) 0.07 0.00005 0.0004 0.0002 0.0002 0.04 0.0005 0.003 0.05 0.001 0.0002 0.2 0.4 0.006 0.007 0.02 0.1 0.7 0.001 0.05 0.2 0.5 0.004 0.00000003 0.002

CHAPTER 1200-5-1

Turbidity - The requirements of 1200-5-1-.06(3) apply to filtered surface systems until June 29, 1993. The requirements in this section apply to unfiltered systems that the State has determined, in writing, must install filtration until June 29, 1993, or until filtration is installed, whichever is later. The maximum contaminant level for turbidity is applicable to public water systems using surface water source(s) in whole or in part. Furthermore, the maximum contaminant level for turbidity is applicable to those systems using ground water which are required to install turbidimeters pursuant to Regulation 1200-5-1-.05(11). The maximum contaminant levels for turbidity in drinking water, measured at a representative entry point(s) to the distribution system are: (a) (b) One (1.0) turbidity unit, as determined by monthly average pursuant to Regulation 1200-5-1-.08. Two (2.0) turbidity units based on an average for two consecutive days pursuant to Regulation 1200-5-1-.08.

To meet the maximum contaminant level for turbidity, a public water system must meet both (a) and (b). (4) Microbiological - The maximum contaminant levels for microbiologicals are applicable to both community water systems and non-community water systems. (a) The maximum contaminant level (MCL) is based on the presence or absence of total coliforms in a sample, rather than coliform density. The number of total coliform positive samples shall not exceed any of the following:

August, 2008 (Revised)

16

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.06, continued) 1. For a system which collects at least 40 samples per month, if no more than 5.0 percent of the samples collected during a month are total coliform-positive, the system is in compliance with the MCL for total coliforms. 2. For a system which collects fewer than 40 samples/month, if no more than one sample collected during a month is total coliform-positive, the system is in compliance with the MCL for total coliforms. A public water system which has exceeded the MCL for total coliforms must report the violation to the State no later than the end of the next business day after it learns of the violation and notify the public in accordance with the schedule of 1200-5-1-.19 using the language specified in 1200-5-1-.19. A public water system which has failed to comply with the coliform monitoring requirements, including a sanitary survey requirement must report the monitoring violation to the State within ten (10) days after the system discovers the violation and notify the public in accordance with 1200-5-1-.19.

3.

4.

(b)

Any fecal coliform-positive repeat sample or E-coli-positive repeat sample, or any total coliform-positive repeat sample following a fecal coliform positive or E-coli positive routine sample constitutes a violation of the MCL for total coliforms. For purposes of the public notification requirements in 1200-5-1-.19 this is a tier 1 violation that may pose an acute risk to health. Fecal coliforms/Escherichia coli (E. coli) testing 1. If any routine or repeat sample is total coliform-positive, the system must analyze that total coliform-positive culture medium to determine if fecal coliforms are present, except that the system may test for E. coli in lieu of fecal coliforms. If fecal coliforms or E. coli are present, the system must notify the State by the end of the day when the system is notified of the test result, unless the system is notified of the result after the Department office is closed, in which case the system must notify the State before the end of the next business day. The State has the discretion to allow a public water system, on a case-by-case basis, to forgo fecal coliform or E. coli testing on a total coliform-positive sample if that system assumes that the total coliform-positive sample is fecal coliformpositive or E. coli-positive. Accordingly, the system must notify the State as specified in paragraph (c)(1) of this section and the provisions of 1200-5-1.06(4)(b) apply.

(c)

2.

(d)

A public water system must determine compliance with the MCL for total coliforms in (a) and (b) of this section for each month in which it is required to monitor for total coliforms. No variance or exemptions from the maximum contaminant level for total coliforms are permitted.

(e) (5)

Radionuclides(a) The following maximum contaminant levels for radium-226, radium-228, and gross alpha particle radioactivity are applicable to all community water systems: 1. Combined radium-226 and radium-228: The maximum contaminant level for combined radium-226 and radium-228 is 5 pCi/L. The combined radium-226 and

August, 2008 (Revised)

17

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.06, continued) radium-228 value is determined by the addition of the results of the analysis for radium-226 and the analysis for radium-228. 2. Gross alpha particle activity (including radium-226 but excluding radon and uranium): The maximum contaminant level for gross alpha particle activity (including radium-226 but excluding radon and uranium) is 15 pCi/L.

(b)

Maximum contaminant levels for beta particle and photon radioactivity from man-made radionuclides in community water systems shall be as follows: 1. The average annual concentration of beta particle and photon radioactivity from man-made radionuclides in drinking water shall not produce an annual dose equivalent to the total body or any internal organ greater than four (4) millirem/year. Except for the radionuclides listed in Table A, the concentration of man-made radionuclides causing four (4) mrem total body or organ dose equivalents shall be calculated on the basis of a two (2) liter per day drinking water intake using the 168 hour data listed in “Maximum Permissible Body Burdens and Maximum Permissible Concentration of Radionuclides in Air or Water for Occupational Exposure,” NBS Handbook 69 as amended August, 1963, U.S. Department of Commerce. If two or more radionuclides are present, the sum of their annual dose equivalent to the total body or to any organ shall not exceed four (4) millirem/year. Table A Average Annual Concentrations Assumed to Produce a Total Body or Organ Dose of a 4 mrem/yr. Radionuclide Tritium Strontium-90 Critical Organ Total Body Bone Marrow pCi per Liter 20,000 8

2.

(c) (d)

MCL for uranium. The maximum contaminant level for uranium is 30 micrograms per liter. Compliance dates. 1. Compliance dates for combined radium-226 and -228, gross alpha particle activity, gross beta particle and photon radioactivity, and uranium: Community water systems must comply with the MCLs listed in subparagraphs (a), (b), and (c), beginning December 8, 2003 and compliance shall be determined in accordance with the requirements of 1200-5-1-.11. Compliance with reporting requirements for the radionuclides under appendix A to Consumer Confidence Reports (1200-5-1-.35) and Appendices A and B to Public Notification (1200-5-1.19) is required on December 8, 2003.

(e)

Best Available Technologies The Department hereby identifies as indicated in the following table the best technology available for achieving compliance with the maximum contaminant levels for combined radium-226 and -228, uranium, gross alpha particle activity, and beta particle and photon radioactivity.

August, 2008 (Revised)

18

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.06, continued)

CHAPTER 1200-5-1

Table B.-BAT for Combined Radium-226 and Radium-228, Uranium, Gross Alpha Particle Activity, and Beta Particle and Photon Radioactivity Contaminant 1. Combined radium-226 and radium228 2. Uranium 3. Gross alpha particle activity( excluding Radon and Uranium) 4. Beta particle and photon radioactivity (f) (g) BAT Ion exchange, reverse osmosis, lime softening. Ion exchange, reverse osmosis, lime softening, coagulation/filtration Reverse osmosis Ion exchange and reverse osmosis

No variance or exemption for compliance with the MCLs listed in 1200-5-1-.06(5) are allowed. Small systems compliance technologies list for radionuclides. Table C.-List of Small Systems Compliance Technologies for Radionuclides and Limitations to Use

Unit Technologies 1. Ion Exchange (IE) 2. Point of use (POU2) IE 3. Reverse osmosis (RO) 4. POU2 RO 5. Lime softening 6. Green sand filtration 7. Co-precipitation with Barium Sulfate 8. Electrodialysis/electrodialys is reversal 9. Pre-formed hydrous Manganese oxide filtration 10. Activated alumia

Limitations (see footnotes) (a) (b) (c) (b) (d) (e) (f)

Operator skill level required 1 Intermediate Basic Advanced Basic Advanced Basic Intermediate to Advanced Basic to imtermediate Intermediate Advanced

Raw water quality range and considerations.1 All ground waters. All ground waters. Surface waters usually require pre-filtration. Surface waters usually require pre-filtration. All waters. Ground waters with suitable water quality. All ground waters. All ground waters. All ground waters; competing anion concentrations may affect regeneration frequency. Can treat a wide range of water qualities

(g) (a)(h)

11. Enhanced coagulation/filtration
1

(i)

Advanced

National Research Council (NRC). Safe Water from Every Tap: Improving Water Service to Small Communities. National Academy Press. Washington, D.C. 1997. 2 A POU, or “point-of-use” technology is a treatment device installed at a single tap used for the purpose of reducing contaminants in drinking water at that one tap. POU devices are typically installed at the kitchen tap. See the April 21, 2000 NODA for more details. Limitations Footnotes: Technologies for Radionuclides:

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.06, continued) a The regeneration solution contains high concentrations of the contaminant ions. Disposal options should be carefully considered before choosing this technology. b When POU devices are used for compliance, programs for long-term operation, maintenance, and monitoring must be provided by water utility to ensure proper performance. c Reject water disposal options should be carefully considered before choosing this technology. See other RO limitations described in the SWTR Compliance Technologies Table. d The combination of variable source water quality and the complexity of the water chemistry involved may make this technology too complex for small surface water systems. e Removal efficiencies can vary depending on water quality. f This technology may be very limited in application to small systems. Since the process requires static mixing, detention basins, and filtration, it is most applicable to systems with sufficiently high sulfate levels that already have a suitable filtration treatment train in place. g This technology is most applicable to small systems that already have filtration in place. h Handling of chemicals required during regeneration and pH adjustment may be too difficult for small systems without an adequately trained operator. i Assumes modification to a coagulation/filtration process already in place. Table D.-Compliance Technologies by System Size Category for Radionuclide NPDWR's Contaminant 1. Combined radium226 and radium-228 2. Gross alpha particle activity 3. Beta particle activity and photon acivity 4. Uranium Compliance Technologies 1 for system size categories (population served) 25-500 501-3,300 3301-10,000 1,2,3,4,5,6,7,8,9 1,2,3,4,5,6,7,8,9 1,2,3,4,5,6,7,8,9 3.4 1,2,3,4 1,2,4,10,11 3.4 1,2,3,4 1,2,3,4,5,10,11 3,4 1,2,3,4 1,2,3,4,5,10,11

Note:1 Numbers correspond to those technologies found listed in table C. (6) Disinfectant Residuals and Disinfectant Byproducts (a) Bromate and chlorite. The maximum contaminant levels (MCLs) for bromate and chlorite are as follows: MCL (mg/L) 0 .010 1 .0

Disinfection by-product Bromate Chlorite 1.

Compliance dates for CWSs and NTNCWSs. Subpart H systems serving 10,000 or more persons must comply with this paragraph (a) beginning January 1, 2002. Subpart H systems serving fewer than 10,000 persons and systems using only ground water not under the direct influence of surface water must comply with this paragraph (a) beginning January 1, 2004. The Administrator, pursuant to section 1412 of the Act, hereby identifies the following as the best technology, treatment techniques, or other means available for achieving compliance with the maximum contaminant levels for bromate and chlorite identified in this paragraph (a): Best available technology

2.

Disinfection

August, 2008 (Revised)

20

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.06, continued) by-product Bromate Control of ozone treatment process to reduce production of bromate Chlorite Control of treatment processes to reduce disinfectant demand and control of disinfection treatment processes to reduce disinfectant levels (b) TTHM and HAA5. 1. Subpart L— Running Annual Average compliance (1200-5-1-.36) (i) Compliance dates. Subpart H systems serving 10,000 or more persons must comply with subparagraph (b)1 beginning January 1, 2002. Subpart H systems serving fewer than 10,000 persons and systems using only ground water not under the direct influence of surface water must comply with this subparagraph (b)1 beginning January 1, 2004. All systems must comply with these MCLs until the date specified for Locational Running Annual Average (subpart V) compliance in 1200-5-1-.38. MCL (mg/L) 0.080 0.060

Disinfection by-product Total trihalomethanes (TTHM) Haloacetic acids (five) (HAA5) (ii)

The Administrator, pursuant to section 1412 of the Act, hereby identifies the following as the best technology, treatment techniques, or other means available for achieving compliance with the maximum contaminant levels for TTHM and HAA5 identified in this subparagraph (b)1. Best available technology Enhanced coagulation or enhanced softening or GAC10, with chlorine as the primary and residual disinfectant

Disinfection by-product Total trihalomethanes (TTHM) and Haloacetic acids (five) (HAA5) 2. . (i)

Subpart V—LRAA compliance (1200-5-1-.38) Compliance dates. The subpart V MCLs for TTHM and HAA5 must be complied with as a locational running annual average (LRAA) at each monitoring location beginning the date specified for subpart V compliance in 1200-5-1-.38(1)(c). MCL (mg/L) 0.080 0.060

Disinfection by-product Total trihalomethanes (TTHM) Haloacetic acids (five) (HAA5) (ii)

The Administrator, pursuant to section 1412 of the Act, hereby identifies the following as the best technology, treatment techniques, or other means available for achieving compliance with the maximum contaminant levels for TTHM and HAA5 identified in subparagraph (b)2 for all systems that disinfect their source water: Best available technology Enhanced coagulation or enhanced softening or GAC10; nanofiltration and with a molecular weight cutoff of equal to or less than 1000

Disinfection by-product Total trihalomethanes (TTHM) and Haloacetic acids (five) (HAA5)

August, 2008 (Revised)

21

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.06, continued) Daltons; or GAC20 (iii)

CHAPTER 1200-5-1

The Administrator, pursuant to section 1412 of the Act, hereby identifies the following as the best technology, treatment techniques, or other means available for achieving compliance with the maximum contaminant levels for TTHM and HAA5 identified in subparagraph (b)2 for consecutive systems and applies only to the disinfected water that consecutive systems buy or otherwise receive: Best available technology Systems serving 10,000 or more: Improved distribution system and storage tank management to reduce residence time, plus the use of chloramines for disinfectant residual maintenance Systems serving <10,000: Improved distribution system and storage tank management to reduce residence time

Disinfection by-product Total trihalomethanes (TTHM) and Haloacetic acids (five) -(HAA5).

(c)

Maximum residual disinfectant levels. 1. Maximum residual disinfectant levels (MRDLs) are as follows: Disinfectant residual Chlorine........................………..…….. Chloramines........................……..….... Chlorine dioxide.....................……..…. MRDL (mg/L) 4.0 (as Cl2). 4.0 (as Cl2). 0.8 (as ClO2).

(d)

Compliance dates. 1. CWSs and NTNCWSs. Subpart H systems serving 10,000 or more persons must comply with MRDLs beginning January 1, 2002. Subpart H systems serving fewer than 10,000 persons and systems using only ground water not under the direct influence of surface water must comply with MRDLs beginning January 1, 2004. Transient NCWSs. Subpart H systems serving 10,000 or more persons and using chlorine dioxide as a disinfectant or oxidant must comply with the chlorine dioxide MRDL beginning January 1, 2002. Subpart H systems serving fewer than 10,000 persons and using chlorine dioxide as a disinfectant or oxidant and systems using only ground water not under the direct influence of surface water and using chlorine dioxide as a disinfectant or oxidant must comply with the chlorine dioxide MRDL beginning January 1, 2004.

2.

(e)

Best Available Control Technology 1. The following are identified as the best technology, treatment technology or other means available for achieving compliance with the maximum residual disinfectant level: (i) Control of the treatment processes to reduce disinfectant demand and control of disinfection treatment processes to reduce disinfectant levels.

August, 2008 (Revised)

22

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.06, continued) Authority: T.C.A. §68-221-704. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. Amendment filed November 26, 1990; effective January 10, 1991. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed October 22, 1993; effective January 5, 1994. Amendment filed October 31, 2000; effective January 14, 2001. Amendment filed November 21, 2001; effective February 4, 2002. Amendment filed April 12, 2002; effective June 26, 2002. Amendment filed July 15, 2002; effective September 28, 2002. Amendment filed April 19, 2004; effective July 3, 2004. Amendment filed July 31, 2006; effective October 14, 2006. 1200-5-1-.07 MONITORING AND ANALYTICAL REQUIREMENTS. (1) Microbiological Contaminant Sampling (a) (b) (c) Reserved Reserved The supplier of water for a community water system shall take coliform samples at regular time intervals and in number proportional to the population served by the system during the reporting period as set forth below: TOTAL COLIFORM MONITORING FREQUENCY FOR COMMUNITY WATER SYSTEMS Population Served Minimum Number of Samples Per Month

25 to 1,0001 ..................................................................................................1 1,001 to 2,500 ...............................................................................................2 2,501 to 3,300 ...............................................................................................3 3,301 to 4,100 ...............................................................................................4 4,101 to 4,900 ...............................................................................................5 4,901 to 5,800 ...............................................................................................6 Population Served Minimum Number of Samples Per Month

5,801 to 6,700 ...............................................................................................7 6,701 to 7,600 ...............................................................................................8 7,601 to 8,500 ...............................................................................................9 8,501 to 12,900 ...........................................................................................10 12,901 to 17,200.........................................................................................15 17,201 to 21,500.........................................................................................20 21,501 to 25,000.........................................................................................25 25,001 to 33,000.........................................................................................30 33,001 to 41,000.........................................................................................40 41,001 to 50,000.........................................................................................50 50,001 to 59,000.........................................................................................60 59,001 to 70,000.........................................................................................70 70,001 to 83,000.........................................................................................80 83,001 to 96,000.........................................................................................90
96,001 to 130,000 ................................................................................................ 100 130,001 to 220,000 .............................................................................................. 120 220,001 to 320,000 .............................................................................................. 150 320,001 to 450,000 .............................................................................................. 180

August, 2008 (Revised)

23

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.07, continued)

CHAPTER 1200-5-1

450,001 to 600,000 .............................................................................................. 210 600,001 to 780,000 .............................................................................................. 240 780,001 to 970,000 .............................................................................................. 270 970,001 to 1,230,000 ........................................................................................... 300 1,230,001 to 1,520,000 ........................................................................................ 330 1,520,001 to 1,850,000 ........................................................................................ 360 1,850,001 to 2,270,000 ........................................................................................ 390 2,270,001 to 3,020,000 ........................................................................................ 420 3,020,001 to 3,960,000 ........................................................................................ 450 3,960,001 or more................................................................................................ 480

Includes public water systems which have at least 15 service connections, but serve fewer than 25 persons. 1. 2. Coliform samples shall be collected at sites which are representative of water throughout the distribution system according to a written sample siting plan. Sample siting plans shall be made available to the Department on request. Plans determined to be deficient by the Department shall be revised by the system on the basis of the Department’s findings. Microbiological sampling shall be conducted in accordance with the approved sampling plan.

1

3. (d)

The monitoring frequency for total coliforms for non-community water systems is as follows: 1. A non-community water system using only ground water (except ground water under the direct influence of surface water) and serving 1,000 persons or fewer must monitor each calendar quarter that the system provides water to the public. A non-community water system using only ground water (except ground water under the direct influence of surface water) and serving more than 1,000 persons during any month must monitor at the same frequency as a like-sized community water system, as specified in Rule 1200-5-1-.07(1)(c). For systems using ground water under the direct influence of surface water, rule 1200-5-1-.07(1)(d)4. applies. A non-community water system using surface water, in total or in part, must monitor at the same frequency as a like-sized community water system, as specified in 1200-5-1-.07(1)(c), regardless of the number of persons it serves. A non-community water system using ground water under the direct influence of surface water must monitor at the same frequency as a like-sized community water system, as specified in 1200-5-1-.07(1)(c). The system must begin monitoring at this frequency beginning six months after the determination that the ground water is under the direct influence of surface water. A non-community water system must collect total coliform samples at sites which are representative of water throughout the distribution system according to a written sample site plan. These plans are subject to state review and revision.

2.

3.

4.

5.

(e)

Public water systems must collect samples at regular time intervals throughout the monitoring period. Those public water systems that use only ground water (except ground water under the direct influence of surface water) and serve 4,900 or fewer persons may collect all required samples on a single day if they are taken from different sites.

August, 2008 (Revised)

24

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.07, continued) (f)

CHAPTER 1200-5-1

A public water system that uses surface water or ground water under the direct influence of surface water, and does not practice filtration in compliance with Rule 1200-5-1-.31 must collect at least one sample near the first service connection each day the turbidity level of the source water exceeds 1 NTU. This sample must be analyzed for the presence of total coliforms. When one or more turbidity measurements in any day exceed 1 NTU, the system must collect this coliform sample within 24 hours of the first exceedance, unless the Department determines that the system, for reasons outside the system’s control cannot have the sample analyzed within 30 hours of collection. Sample results from this coliform monitoring must be included in determining compliance with the MCL for total coliforms in 1200-5-1-.06(4). Special purpose samples, such as those taken to determine whether disinfection practices are sufficient following pipe placement, replacement, or repair, shall not be used to determine compliance with the MCL for total coliforms in Rule 1200-5-1-.06(4) provided the water is not served to customers before negative analytical results are obtained. Samples representing water served to customers prior to obtaining analytical results shall not be special purpose samples and shall count toward compliance with the MCL for total coliforms in Rule 1200-5-1-.06(4). Repeat samples taken pursuant to paragraph (2) of this Rule are not considered special purpose samples, and must be used to determine compliance with the MCL for total coliforms in Rule 1200-5-1-.06(4).

(g)

(2)

Repeat Monitoring (a) If a routine sample is total coliform-positive, the public water system must collect a set of repeat samples within 24 hours of being notified of the positive result. A system which collects more than one routine sample per month must collect no fewer than three repeat samples for each total coliform-positive sample found. A system which collects one routine sample per month or fewer must collect no fewer than four repeat samples for each total coliform-positive sample found. The Department may extend the 24-hour limit on a case-by-case basis if the system has a problem in collecting the repeat samples within 24 hours that is beyond its control. In the case of an extension, the Department must specify how much time the system has to collect the repeat samples. The system must collect at least one repeat sample from the sampling tap where the original total coliform-positive sample was taken, and at least one repeat sample at a tap within five service connections upstream and at least one repeat sample at a tap within five service connections downstream of the original sampling site. If a total coliform-positive sample is at the end of the distribution system, or one away from the end of the distribution system, the State may waive the requirement to collect at least one repeat sample upstream or downstream of the original sampling site. The system must collect all repeat samples on the same day and within 24 hours of being notified of a positive result, except that the State may allow a system with a single service connection to collect the required set of repeat samples over a four consecutive day period or to collect a larger volume repeat sample(s) in one or more sample containers of any size, as long as the total volume collected is at least 400 ml (300 ml for systems which collect more than one routine sample per month.) If one or more repeat samples in the set is total coliform-positive, the public water system must collect an additional set of repeat samples in the manner specified in paragraphs 1200-5-1-.07(2)(a), (b), and (c) of this section. The additional samples must be collected within 24 hours of being notified of the positive result, unless the State extends the limit as provided in 1200-5-1-.07(2)(a). The system must repeat this

(b)

(c)

(d)

August, 2008 (Revised)

25

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.07, continued) process until either total coliforms are not detected in one complete set of repeat samples or the system determines that the MCL for total coliforms in 1200-5-1-.06(4) has been exceeded and notifies the State. (e) If a system normally collecting fewer than five routine samples per monitoring period has one or more total coliform-positive samples and the Department does not invalidate the sample(s) under 1200-5-1-.07(3), it must collect at least five routine samples during the next month the system serves water to the public. After a system collects a routine sample and before it learns the results of the analysis of that sample, if it collects another routine sample(s) from within five adjacent service connections of the initial sample, and the initial sample, after analysis, is found to contain total coliforms, then the system may count the subsequent sample(s) as a repeat sample instead of as a routine sample. Results of all routine and repeat samples not invalidated by the State must be included in determining compliance with the MCL for total coliforms in 1200-5-1-.06(4).

(f)

(g) (3)

Invalidation of Total Coliform Samples. A total coliform-positive sample invalidated under 1200-5-1-.07(3) does not count towards meeting the minimum monitoring requirement for microbiological contaminants. (a) The state may invalidate a total coliform-positive sample only if the conditions of 12005-1-.07(3)(a) 1., 2., or 3. are met. 1. 2. The laboratory establishes that improper sample analysis caused the total coliform-positive result; The Department, on the basis of the results of repeat samples collected as required by 1200-5-1-.07(2)(a), (b), (c), and (d), determines that the total coliform-positive sample resulted from a domestic or other non-distribution system plumbing problem. The Department cannot invalidate a sample on the basis of repeat sample results unless all repeat sample(s) collected at the same tap as the original total coliform-positive are also total coliform-positive, and all repeat samples collected within five service connections of the original tap are total coliform-negative (e.g., the Department cannot invalidate a total coliformpositive sample on the basis of repeat samples if all the repeat samples are total coliform-negative, or if the public water system has only one service connection). The State has substantial grounds to believe that a total coliform-positive result is due to a circumstance or condition which does not reflect water quality in the distribution system. In this case, the system must still collect all repeat samples required under 1200-5-1-.07(2)(a), (b), (c), and (d) and use them to determine compliance with the MCL for total coliforms in 1200-5-1-.06(4). To invalidate a total coliform-positive sample under this paragraph, the decision with the rationale for the decision must be documented in writing, and approved and signed by the supervisor of the Departmental official who recommended the decision. The Department must make this document available to EPA and the public. The written documentation must state the specific cause of the total coliform-positive sample, and what action the system has taken, or will take, to correct this problem. The Department may not invalidate a total coliform-positive sample solely on the grounds that all repeat samples are total coliform-negative.

3.

(b)

A laboratory must invalidate a total coliform sample (unless total coliforms are detected) if the sample produces a turbid culture in the absence of gas production using an analytical method where gas formation is examined (e.g., the Multiple-Tube

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CHAPTER 1200-5-1

(Rule 1200-5-1-.07, continued) Fermentation Technique), produces a turbid culture in the absence of an acid reaction in the Presence-Absence (P-A) Coliform Test, or exhibits confluent growth or produces colonies too numerous to count with an analytical method using a membrane filter (e.g., Membrane Filter Technique). If a laboratory invalidates a sample because of such interference, the system must collect another sample from the same location as the original sample within 24 hours of being notified of the interference problem, and have it analyzed for the presence of total coliforms. The system must continue to resample within 24 hours and have the samples analyzed until it obtains a valid result. The Department may waive the 24-hour time limit on a case-by-case basis. (4) Sanitary Surveys (a) Public water systems which do not collect five or more routine samples per month must undergo an initial sanitary survey by June 29, 1994 for community public water systems and June 29, 1999 for non-community water systems. Thereafter, systems must undergo another sanitary survey every five years, except that non-community water systems using only protected and disinfected ground water, as defined by the Department, must undergo subsequent sanitary surveys at least every ten years after the initial sanitary survey. The Department must review the results of each sanitary survey to determine whether the existing monitoring frequency is adequate and what additional measures, if any, the system needs to undertake to improve drinking water quality. In conducting a sanitary survey of a system using ground water having an EPAapproved wellhead protection program under section 1428 of the Federal Safe Drinking Water Act, information on sources of contamination within the delineated wellhead protection area that was collected in the course of developing and implementing the program should be considered instead of collecting new information, if the information was collected since the last time the system was subject to a sanitary survey. Public water systems which do not collect five or more routine samples per month must undergo a sanitary survey performed by the state at least once every five years. The system is responsible for ensuring the survey takes place by informing the state within 30 days of the expiration of the 5-year period. Sanitary surveys conducted by the Department pursuant to Rule 1200-5-1-.40 may be used to meet the sanitary survey requirements of Rule 1200-5-1-.07(4). A public water system may request a sanitary survey re-inspection of its water system provided the public water system requests the re-inspection within sixty (60) days of the receipt of the results of the initial sanitary survey. The public water system requesting the sanitary survey re-inspection shall pay the costs of the re-inspection incurred by the Department.

(b)

(c)

(d)

(e)

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 68-221-701 et seq., and 68-221-704 et seq. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed November 26, 1990; effective January 10, 1991. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed October 22, 1993, effective January 5, 1994. Amendment filed April 12, 1996, effective June 26, 1996. Amendment filed October 31, 2000; effective January 14, 2001. Amendments filed August 15, 2005; effective October 29, 2005. Amendments filed June 12, 2008; effective August 26, 2008.

August, 2008 (Revised)

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CHAPTER 1200-5-1

1200-5-1-.08 TURBIDITY SAMPLING AND ANALTICAL REQUIREMENTS. (1) Ground water sampling – Samples shall be taken by suppliers of water that serve more than 50 connections or that have been directed to conduct monitoring under Rule 1200-5-1.05(11) for both community water systems and non–community water system at a representative entry point(s) to the water distribution system at least once per day for the purpose of making turbidity measurements to determine compliance with Regulation 1200– 5–1–.06(3). Public water systems using water from a source not under the direct influence of surface water are not required to monitor turbidity unless directed to do so under the provisions of 1200-5-1-.05(11). Turbidity measurements of surface water and ground water under the direct influence that employs filtration - The minimum sampling requirements for systems using filtration treatment shall be as follows: (a) Turbidity measurements must be performed on representative samples of the system’s filtered water every four hours, (or more frequently, as authorized by the rules) that the system serves water to the public. A public water system may substitute continuous turbidity monitoring for grab samples if approved in writing by the Department. For systems serving 500 or fewer persons per day, the Department may allow the sampling frequency to be reduced to once per day if it determines that less frequent monitoring is sufficient to indicate effective filtration performance. Systems filtering surface water and ground water under the direct influence of surface water shall comply with the treatment technique standards found in 1200-5-1-.31(4).

(2)

(3)

Ground water systems under the direct influence of surface water and do not filter and have qualified to avoid filtration - The minimum sampling requirements for ground water systems under the direct influence of surface water and not employing filtration shall be as follows: (a) Turbidity measurements must be performed on representative grab samples of source water immediately prior to the first or only point of disinfectant application every four hours (or more frequently, as authorized by the rules) that the system serves water to the public. A public water system may substitute continuous turbidity monitoring for grab sample monitoring if it validates the continuous measurement for accuracy on a regular basis using a protocol approved by the State. Turbidity must comply with the limits specified in 1200-5-1-.31(2)(a)2.

(4)

Reporting (a) Ground water systems - All community water systems using a ground water source with turbidity removal facilities and not designated as ground water under the direct influence of surface water shall be required, if the results of a turbidity analysis indicate that the maximum allowable limit has been exceeded, to confirm by resampling as soon as practicable and preferably within one (1) hour. If the repeat sample confirms that the maximum allowable limit has been exceeded, the supplier of water shall report to the Department within forty-eight (48) hours. The repeat sample shall be the sample used for the purpose of calculating the monthly average. If the monthly average of the daily samples exceeds the maximum allowable limit, or if the average of two samples taken on consecutive days exceeds two (2) NTU, the supplier of water shall report to the Department and notify the public as directed in Regulation 1200-5-1-.18 and 12005-1-.19. All non-community water systems using ground water formations, other than approved sand and gravel formations, may be required to monitor turbidity if the Department finds a system cannot meet the microbiological standard, the turbidity limit is exceeded, or if other health related problems exist.

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(Rule 1200-5-1-.08, continued) (b) Surface water systems and ground water systems under the direct influence of surface water -Turbidity measurements must be reported within 10 days after the end of each month the system serves water to the public. Information that must be reported includes but is not limited to: 1. 2. The total number of filtered water turbidity measurements taken during the month. The number and percentage of filtered water turbidity measurements taken during the month which are less than or equal to the applicable limits specified in 1200-5-1-.31(4). The date and value of any turbidity measurements taken during the month which exceed 5 NTU.

3. (c)

Ground water systems under the direct influence of surface water that have qualified to avoid filtration - Information that must be reported includes but is not limited to : 1. The maximum turbidity level measured during the month, the date(s) of occurrence for any measurement(s) which exceeded 5 NTU, and the date(s) the occurrence(s) was reported to the State. For the first 12 months of recordkeeping, the dates and cumulative number of events during which the turbidity exceeded 5 NTU, and after one year of recordkeeping for turbidity measurements, the dates and cumulative number of events during which the turbidity exceeded 5 NTU in the previous 12 months the system served water to the public. For the first 120 months of recordkeeping, the dates and cumulative number of events during which the turbidity exceeded 5 NTU, and after 10 years of recordkeeping for turbidity measurements, the dates and cumulative number of events during which the turbidity exceeded 5 NTU in the previous 120 months the system served water to the public.

2.

3.

(d)

Ground water systems under the direct influence of surface water that has been directed to install filtration but has not yet done so shall monitor as specified in Rule 1200-5-1-.08(4)(a).

Authority: T.C.A. §§68-221-701 et seq. and 4-5-202. Administrative History: Original rule certified June 7, 1974. Repeal and new rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed November 26, 1990; effective January 10, 1991. Amendment filed April 12, 1996; effective June 26, 1996. Amendment filed August 15, 2005; effective October 29, 2005. Amendment filed June 12, 2008; effective August 26, 2008. 1200-5-1-.09 INORGANIC CHEMICAL SAMPLING AND ANALYTICAL REQUIREMENTS. (1) Monitoring and analysis for the purpose of determining compliance with the maximum contaminant level for antimony, arsenic, asbestos, barium, beryllium, cadmium, chromium, cyanide, fluoride, mercury, nickel, nitrate, nitrite, total nitrate and nitrite, thallium, and selenium shall be conducted as follows: (a) Groundwater systems shall take a minimum of one sample at every entry point to the distribution system which is representative of each well after treatment (hereafter called a sampling point) beginning in the compliance period starting January 1, 1993. The system shall take such sample at the same sampling point unless conditions make another sampling point more representative of each source or treatment plant.

August, 2008 (Revised)

29

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.09, continued) (b)

CHAPTER 1200-5-1

Surface water systems shall take a minimum of one sample at every entry point to the distribution system after any application of treatment, or in the distribution system at a point which is representative of each source after treatment (hereafter called a sampling point), beginning in the compliance period starting January 1, 1993. The systems shall take each sample at the same sampling point unless conditions make another sampling point more representative of each source or treatment plant. Surface water systems include systems with a combination of surface and ground sources. If the system draws water from more than one source and the sources are combined before distribution, the system must sample at an entry point to the distribution system during periods when water representative of all sources is being used. The State may reduce the total number of analyses by allowing the use of composite sampling. Composite samples from a maximum of five sampling points are allowed, provided that the detection limit of the method used for analysis is less than one-fifth of the MCL. Compositing of sample must be done in the laboratory. 1. If the concentration in the composite sample is greater than or equal to one-fifth of the MCL of an inorganic chemical, then a follow-up sample must be taken within 14 days at each sampling point included in the composite. These samples must be analyzed for the contaminants which were detected in the composite sample. If duplicates of the original samples taken from each sampling point used in the composite are available, the system may use these instead of resampling. The duplicates must be analyzed and the results reported to the State within 14 days of collection. If the population served by the system is greater than 3,300 persons, then compositing may only be permitted by the State at sampling points within a single system. In systems serving 3,300 or less persons, the state may permit compositing among different systems provided the 5-sample limit is maintained.

(c)

(d)

2.

3.

(e)

All new systems or systems that use a new source of water that begin operation after the effective date of this rule must demonstrate compliance with the MCL within a period of time specified by the State. The system must also comply with the initial sampling frequencies specified by the state to ensure a system can demonstrate compliance with the MCL. Routine and increased monitoring frequencies shall be conducted in accordance with the requirements of this rule.

(2)

Compliance with the maximum contaminant level for inorganics shall be determined as specified in paragraph (7) of this rule. The frequency of monitoring for asbestos shall be in accordance with paragraph (3) of this rule. The frequency of monitoring antimony, arsenic, barium, beryllium, cadmium, cyanide, chromium, fluoride, mercury, nickel, selenium and thallium shall be in accordance with paragraph (4) of this rule. The frequency of monitoring for nitrate shall be in accordance with paragraph (5) of this rule. The frequency of monitoring for nitrite shall be in accordance with paragraph (6) of this rule. The frequency of monitoring required to determine compliance with the maximum contaminant level for asbestos shall be as follows: (a) Each community and non-transient, non-community water system is required to monitor for asbestos during the first three-year compliance period of each nine-year compliance cycle beginning in the compliance period starting January 1, 1993.

(3)

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.09, continued) 1.

CHAPTER 1200-5-1

All community water systems and non-transient non-community water systems serving more than 10,000 people shall complete initial sampling by December 31, 1993. All community water systems and non-transient noncommunity water systems serving from 3,300 to 10,000 people shall complete initial sampling by December 31, 1994. All other community water systems and non-transient non-community water systems shall complete monitoring by December 31, 1995. Repeat samples shall be collected thereafter on a nine year cycle.

(b)

If the system believes it is not vulnerable to either asbestos contamination in its source water or due to corrosion of asbestos-cement pipe, or both, it may apply to the Division to be excluded from the monitoring requirement in paragraph (3)(a). If the Division agrees to exclude the system, the system is not required to monitor. The Division may exclude a system from asbestos monitoring provided the public water system provides the state with a sworn statement by the superintendent, manager or chief operator of the system that no asbestos materials have been used in its treatment plant and distribution system and that no asbestos containing materials will be used in the system after the date of the system requests to be excluded. An asbestos monitoring waiver if issued by the state remains in effect for three years or until the system installs asbestos containing materials in the system. Systems shall notify the state within 48 hours of using any asbestos containing materials. Systems not receiving a waiver shall monitor in accordance with subparagraph (a) of this paragraph. A system vulnerable to asbestos contamination due solely to corrosion of asbestoscement pipe shall take one sample at a tap served by asbestos-cement pipe and under conditions where asbestos contamination is most likely to occur. A system vulnerable to asbestos contamination due solely to source water shall monitor in accordance with the provision of paragraph (2) of this rule. A system vulnerable to asbestos contamination due both to its source water supply and corrosion of asbestos-cement pipe shall take one sample at a tap served by asbestos– cement pipe and one sample at the entry point to the distribution system under conditions where asbestos contamination is most likely to occur. A system which exceeds the maximum contaminant level at any sampling point shall monitor quarterly beginning in the next quarter after the violation occurred. The State may decrease the quarterly monitoring requirement to the frequency specified in paragraph (3)(a) of this rule provided the State has determined a ground water system has collected two consecutive quarterly samples and a surface (or combined surface/ground water system) has four consecutive samples below the MCL. If monitoring data collected after January 1, 1990 comply with the requirements of 1200-5-1-.09(3), then the State may allow systems to use that data to satisfy the monitoring requirement for the initial compliance period beginning January 1, 1993.

(c)

(d)

(e)

(f) (g)

(h) (i)

(j)

(4)

The frequency of monitoring conducted to determine compliance with the maximum contaminant levels for antimony, arsenic, barium, beryllium, cadmium, chromium, cyanide, fluoride, mercury, nickel, selenium and thallium shall be as follows:

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CHAPTER 1200-5-1

(Rule 1200-5-1-.09, continued) (a) Groundwater systems shall take one sample at each sampling point during each three year compliance period starting January 1, 1993. Surface water systems and combined surface/ground systems shall take one sample annually at each sampling point beginning January 1, 1993. (b) (c) Systems which exceed the maximum contaminant levels shall monitor quarterly beginning in the next quarter after the violation occurred. The State may decrease the quarterly monitoring requirement to the frequencies specified in paragraph (4)(a) of this section provided a ground water system has collected two consecutive quarterly samples and a surface water system has a minimum of four consecutive quarterly samples below the MCL. The system may apply to the State for a waiver from the monitoring frequencies specified in subparagraph (4)(a). States may grant a public water system a waiver for monitoring cyanide, provided that the state determines that the system is not vulnerable due to the lack of any industrial source of cyanide. A condition of the waiver shall require that a system shall take a minimum of one sample while the waiver is effective. The term during which the waiver is effective shall not exceed one compliance cycle (i.e., nine years). The State may grant a waiver provided surface water systems have monitored annually for at least three years and groundwater systems have conducted a minimum of three rounds of monitoring. (At least one sample shall have been taken since January 1, 1990). Both surface and groundwater systems shall demonstrate that all previous analytical results were less than the maximum contaminant level. Systems that use a new water source are not eligible for a waiver until three rounds of monitoring from the new source have been completed. In determining the appropriate reduced monitoring frequency, the State shall consider: 1. 2. 3. Reported concentrations from all previous monitoring; The degree of variation in reported concentrations; and Other factors which may affect contaminant concentrations such as changes in groundwater pumping rates, changes in the system's configuration, changes in the system's operating procedures, or changes in stream flows or characteristics.

(d)

(e)

(f)

(g)

(h)

A decision by the State to grant a waiver shall be made in writing and shall set forth the basis for the determination. The determination may be initiated by the State or upon an application by the public water system. The public water system shall specify the basis for its request. The State shall review and, where appropriate, revise its determination of the appropriate monitoring frequency when the system submits new monitoring data or when other data relevant to the system's appropriate monitoring frequency become available.

(5)

All public water systems (community, non-transient non-community, and transient noncommunity systems) shall monitor to determine compliance with the maximum contaminant level for nitrate. (a) Community and non–transient non–community water systems served by ground water system shall monitor annually beginning January 1, 1993. Community and non– transient systems served by surface water shall monitor quarterly beginning January 1, 1993.

August, 2008 (Revised)

32

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.09, continued) (b)

CHAPTER 1200-5-1

For community and non–transient non–community water systems, the repeat monitoring frequency for ground water systems shall be quarterly for at least one year following any one sample in which the concentration is greater than or equal to 50 percent of the MCL. The State may allow a groundwater system to reduce the sampling frequency to annually after the results of four consecutive quarterly samples are below the MCL. For community and non-transient non-community water systems, the State may allow a surface water system to reduce the sampling frequency to annually if all analytical results from four consecutive quarters are less than 50 percent of the MCL. A surface water system shall return to quarterly monitoring if any one sample is greater than or equal to 50 percent of the MCL. Each transient non-community water system shall monitor annually beginning January 1, 1993. After the initial round of quarterly sampling is completed, each community and nontransient non-community system which has been allowed to reduce its monitoring to annually shall take subsequent samples during the quarter(s) which previously resulted in the highest analytical result.

(c)

(d) (e)

(6)

All public water systems (community, non-transient non-community, and transient noncommunity systems) shall monitor to determine compliance with the maximum contaminant level for nitrite. (a) (b) All public water systems shall take one sample at each sampling point during the compliance period beginning January 1, 1993, and ending December 31, 1995. After the initial sample, systems where an analytical result for nitrite is less than 50 percent of the MCL shall monitor at the frequency determined by the State in accordance with the criteria in subparagraph (4)(g). For community, non-transient non-community, and transient non-community water systems, the repeat monitoring frequency for any water system shall be quarterly for at least one year following any one sample in which the concentration is greater than or equal to 50 percent of the MCL. The State may allow a system to reduce the sampling frequency to annually after determining the system has four consecutive quarters of data less than the MCL. Systems which are monitoring annually shall take each subsequent sample during the quarter(s) which previously resulted in the highest analytical result.

(c)

(d) (7)

Confirmation samples: (a) Where the results of sampling for asbestos, antimony, arsenic, barium, beryllium, cadmium, chromium, cyanide, fluoride mercury, nickel, selenium or thallium indicate an exceedance of the maximum contaminant level, the state may require that one additional sample be collected as soon as possible after the initial sample was taken (but not to exceed two weeks after the date of the initial sample analysis) at the same sampling point. Where nitrate or nitrite sampling results indicate an exceedance of the maximum contaminant level, the system shall take a confirmation sample within 24 hours of the system's receipt of notification of the analytical results of the first sample. Systems unable to comply with the 24-hour sampling requirement must immediately notify the

(b)

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.09, continued) consumers served by the public water system in accordance with 1200-5-1-.19. Systems that give public notice rather than collect a confirmation sample within 24hours must take and analyze a confirmation sample within two weeks of notification of the analytical results of the first sample. (c) If confirmation samples are taken for any contaminant, then the results of the initial and confirmation sample shall be averaged. The resulting average shall be used to determine the system's compliance in accordance with paragraph (10). Results of documented sampling errors may be deleted if approved by the State.

(8) (9)

The State may require more frequent monitoring than specified in paragraphs (3), (4), (5), and (6) of this rule or may require confirmation samples for positive and negative results. Systems may conduct more frequent monitoring than the minimum monitoring frequencies specified in this section.

(10) Compliance with the MCLs for inorganic chemicals listed in 1200-5-1-.06 shall be determined based on the analytical result(s) obtained at each sampling point. (a) For systems which are conducting monitoring at a frequency greater than annual, compliance with the maximum contaminant levels for antimony, arsenic, asbestos, barium, beryllium, cadmium, chromium, cyanide, fluoride, mercury, nickel, selenium and thallium is determined by a running annual average at each sampling point. If the average at any sampling point is greater than the MCL, then the system is out of compliance. If any one sample would cause the annual average to be exceeded, then the system is out of compliance immediately. Any sample below the detection limit shall be calculated at zero for the purpose of determining the annual average. If a system fails to collect the required number of samples, compliance (average concentration) will be based on the total number of samples collected. For systems which are monitoring annually, or less frequently, the system is out of compliance with the maximum contaminant levels for antimony, arsenic, asbestos, barium, beryllium, cadmium, chromium, cyanide, fluoride, mercury nickel, selenium and thallium if the level of a contaminant at any sampling point is greater than the MCL. If confirmation samples are required by the State, the determination of compliance will be based on the annual average of the initial MCL exceedance and any state required confirmation samples. If a system fails to collect the required number of samples, compliance (average concentration) will be based on the total number of samples collected. Compliance with the maximum contaminant levels for nitrate and nitrite is determined based on one sample if the levels of these contaminants are below the MCLs. If the levels of nitrate and/or nitrite exceed the MCLs in the initial sample, a confirmation sample is required in accordance with paragraph (7)(b) of this rule, and compliance shall be determined based on the average of the initial and confirmation samples. If a public water system has a distribution system separate and distinct from other parts of the distribution system with no interconnections, the State may allow the system to give public notice to only the area served by that portion of the system which is out of compliance. Arsenic sampling results will be reported to the nearest 0.001 mg/L

(b)

(c)

(d)

(e)

(11) The state may establish specific times during each compliance periods for public water systems to complete its monitoring.

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CHAPTER 1200-5-1

(Rule 1200-5-1-.09, continued) Authority: T.C.A. §§4-5-202, 68-221-701 et seq., and 68-221-704. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed October 22, 1993; effective January 5, 1994. Amendment filed April 12, 1996; effective June 26, 1996. Amendment filed February 17, 1999; effective May 3, 1999. Amendment filed July 15, 2002; effective September 28, 2002. Amendment filed August 15, 2005; effective October 29, 2005. Amendments filed June 12, 2008; effective August 26, 2008. 1200-5-1-.10 ORGANIC CHEMICAL SAMPLING AND ANALYTICAL REQUIREMENTS. (1) Beginning January 1, 1993, or the effective date of these regulations whichever is later, analysis of the contaminants listed in 1200-5-1-.06(2)(a) for the purposes of determining compliance with the maximum contaminant level shall be conducted as follows: (a) Groundwater systems shall take a minimum of one sample at every entry point to the distribution system which is representative of each well after treatment (hereafter called a sampling point). Each sample must be taken at the same sampling point unless conditions make another sampling point more representative of each source, treatment plant, or within the distribution system. Surface water systems shall take a minimum of one sample at points in the distribution system that are representative of each source or at each entry point to the distribution system after treatment (hereafter called a sampling point). Each sample must be taken at the same sampling point unless conditions make another sampling point more representative of each source, treatment plant or within the distribution system. Surface water systems include systems with a combination of surface and ground sources. If the system draws water from more than one source and the sources are combined before distribution, the system must sample at an entry point to the distribution system during periods when water representative of all sources is being used. Monitoring frequency: 1. Each community and non-transient non-community water system shall take four consecutive quarterly samples for each contaminant listed in 1200-5-1-.06(2) during each compliance period beginning with the initial compliance period. Systems serving more than 3,300 persons which do not detect a contaminant in the initial compliance period, may reduce the sampling frequency to a minimum of two quarterly samples in one year during each repeat compliance period. Systems serving 3,300 or less persons which do not detect a contaminant in the initial compliance period may reduce the sampling frequency to a minimum of one sample during each repeat compliance period. All new systems or systems that use a new source of water that begin operation after the effective date of this rule must demonstrate compliance with the MCL within a period of time specified by the State. The system must also comply with the initial sampling frequencies specified by the state to ensure a system can demonstrate compliance with the MCL. Routine and increased monitoring frequencies shall be conducted in accordance with the requirements of this rule.

(b)

(c)

(d)

2.

3.

4.

(e)

Each community and non-transient water system may apply to the State for a waiver from the requirement of subparagraph (1)(d) of this rule. A system must reapply for a waiver for each compliance period.

August, 2008 (Revised)

35

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.10, continued) (f)

CHAPTER 1200-5-1

A State may grant a waiver after evaluating the following: Knowledge of previous use (including transport, storage, or disposal) of the contaminant within the watershed or zone of influence of the system. If a determination by the State reveals no previous use of the contaminant within the watershed or zone of influence, a waiver may be granted. If previous use of the contaminant is unknown or it has been used previously, then the following factors shall be used to determine whether a waiver is granted. 1. 2. Previous analytical results. The proximity of the system to a potential point or non-point source of contamination. Point sources include spills and leaks of chemicals at or near a water treatment facility or at manufacturing, distribution, or storage facilities, or from hazardous and municipal waste landfills and other waste handling or treatment facilities. Non-point sources include the use of pesticides to control insect and weed pests on agricultural areas, forest lands, home and gardens, and other land application uses. The environmental persistence and transport of the pesticide or PCBs. How well the water source is protected against contamination due to such factors as depth of the well and the type of soil and the integrity of the well casing. Elevated nitrate levels at the water supply source. Use of PCBs in equipment used in the production, storage, or distribution of water (i.e., PCBs used in pumps transformers, etc.). Any other information required by the Department.

3. 4. 5. 6. 7. (g)

If an organic contaminant listed in 1200-5-1-.06(2) is detected (as defined by subparagraph (1)(r) of this rule) in any sample, then: 1. 2. Each system must monitor quarterly at each sampling point which resulted in a detection. The State may decrease the quarterly monitoring requirement specified in paragraph (1)(g)1. of this section provided it has determined that the system is below the maximum contaminant level. In no case shall the State make this determination unless a groundwater system takes a minimum of two quarterly samples and a surface water system takes a minimum of four quarterly samples. After the State determines the system is below the maximum contaminant level the State may allow the system to monitor annually. Systems which monitor annually must monitor during the quarter that previously yielded the highest analytical result. If monitoring results in detection of one or more of certain related contaminants (aldicarb, aldicarb sulfone, aldicarb sulfoxide and heptachlor, heptachlor epoxide), then subsequent monitoring shall analyze for all related contaminants.

3.

4.

(h)

Systems which violate the maximum contaminant levels for organics must monitor quarterly. After a minimum of four quarterly samples show the system is in compliance and the State determines the system is below the MCL, the system shall monitor at the frequency specified in paragraph (1)(g)3. of this rule.

August, 2008 (Revised)

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CHAPTER 1200-5-1

(Rule 1200-5-1-.10, continued) (i) The State may require a confirmation sample for positive or negative results. If a confirmation sample is required by the State, the result must be averaged with the first sampling result and the average used for the compliance determination. The State has discretion to delete results of documented sampling errors from this calculation. (j) The State may reduce the total number of analyses a system must conduct by allowing the use of composite sampling. Composite samples from a maximum of five sampling points are allowed, provided that the detection limit of the method used for analysis is less than one-fifth of the MCL. Compositing of samples must be done in the laboratory and analyzed within 14 days of sample collection. Compliance with 1200-5-1-.06(2) shall be determined based on the analytical results obtained at each sampling point. If one sampling point is in violation of the MCL, the system is in violation of the MCL. 1. For systems which are conducting monitoring at a frequency greater than annual, compliance is determined by a running annual average of all samples taken at each sampling point. If the annual average of any sampling point is greater than the MCL, then the system is out of compliance. If the initial sample or a subsequent sample would cause the annual average to be exceeded, then the system is out of compliance immediately. Systems monitoring annually or less frequently whose sample result exceeds the regulatory detection level must begin quarterly sampling. The system will not be considered in violation of the MCL until it has completed one year of quarterly sampling. If any sample result will cause the running annual average to exceed the MCL, at any sampling point, the system is out of compliance with the MCL immediately. If a system fails to collect the required number of samples, compliance will be based on the total number of samples collected. If a sample result is less than the detection limit, zero will be used to calculate the annual average.

(k)

2.

3. 4. 5. (l) (m) (n)

Reserved Reserved If monitoring data collected after January 1, 1990, are generally consistent with the requirements of 1200-5-1-.10(1), then the State will allow systems to use that data to satisfy the monitoring requirement for the initial compliance period beginning January 1, 1993. The State may increase the required monitoring frequency, where necessary, to detect variations within the system (e.g., fluctuations in concentration due to seasonal use, changes in water source), as determined by the criteria described in 1200-5-1.09(3)(a). The State has the authority to determine compliance or initiate enforcement action based upon analytical results and other information compiled by their representatives and agencies. The state may pursuant to these rules establish specific times during each compliance period for public water systems to complete its monitoring.

(o)

(p)

(q)

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Detection as used in this paragraph shall be defined as greater than or equal to the following concentrations for each contaminant. TABLE 1200-5-1-.10(1)(r) CONTAMINANT Alachlor Aldicarb Aldicarb sulfoxide Aldicarb sulfone Atrazine Benzo(a)pyrene Carbofuran Chlordane Dalapon Dibromochloropropane (DBCP) Di(2-ethyl hexyl) adipate Di(2-ethyl hexyl) phthalate Dinoseb Diquat 2,4-D Endothall Endrin CONTAMINANT Ethylene dibromide (EDB) Glyphosate Heptachlor Heptachlor epoxide Hexachlorobenzene Hexachlorocyclopentadiene Lindane Methoxychlor Oxamyl Picloram Polychlorinated biphenyls (PCBs) (as decachlorobiphenyl) Pentachlorophenol Simazine Toxaphene 2,3,7,8 TCDD (Dioxin) 2,4,5-TP (Silvex) DETECTION LIMIT (mg/L) 0.0002 0.0005 0.0005 0.0008 0.0001 0.00002 0.0009 0.0002 0.001 0.00002 0.0006 0.0006 0.0002 0.0004 0.0001 0.009 0.00001 DETECTION LIMIT (mg/L) 0.00001 0.006 0.00004 0.00002 0.0001 0.0001 0.00002 0.0001 0.002 0.0001 0.0001 0.00004 0.00007 0.001 0.000000005 0.0002

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 68-221-701 et seq., and 68-221-704. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed October 22, 1993; effective January 5, 1994. Amendment filed April 12, 1996; effective June 26, 1996. Amendment filed February 17, 1999; effective May 3, 1999. Amendment filed November 21, 2001; effective February 4, 2002. Amendment filed July 15, 2002; effective September 28, 2002. Amendment filed August 15, 2005; effective October 29, 2005. Amendments filed June 12, 2008; effective August 26, 2008.

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1200-5-1-.11 RADIONUCLIDE SAMPLING. (1) For the purpose of monitoring radioactivity concentrations in drinking water, the required sensitivity of the radioanalysis is defined in terms of a detection limit. The detection limit shall be that concentration which can be counted with a precision of plus or minus 100 percent at the 95 percent confidence level (1.96 sigma where sigma is the standard deviation of the net counting rate of the sample.) (a) To determine compliance with gross alpha particle activity, radium-226, radium-228 and uranium the detection limit shall not exceed the concentration in the Table to this subparagraph. Detection Limits for Gross Alpha Particle Activity, Radium-226, Radium-228, and Uranium Contaminant Gross alpha particle activity Radium-226 Radium-228 Uranium (b) Detection Limit 3pCi/L 1pCi/L 1pCi/L 1/10 the MCL

To determine compliance with beta particle and photon activity the detection limit shall not exceed the concentrations listed in the following table. Detection Limits for Man-made Beta Particle and Photon Emitters Radionuclide Detection Limit Tritium 1000pCi/L Strontium-89 10pCi/L Strontium-90 2pCi/L Iodine-131 1pCi/L Cesium-134 10pCi/L Gross beta 4pCi/L Other radionuclides 1/10 of the applicable limit

(2)

To judge compliance with the maximum contaminant levels listed in Rule 1200-5-1-.06(5) averages of data shall be used and shall be rounded to the same number of significant figures as the maximum contaminant level for the substance in question. The state has the authority to determine compliance or initiate enforcement action based upon analytical results or other information compiled by their sanctioned representatives and agencies. Monitoring and compliance requirements for gross alpha particle activity, radium -226, radium 228, and uranium. (a) Community water systems (CWSs) must conduct initial monitoring to determine compliance with radium-226 and 228, gross alpha particle activity and uranium activity by December 31, 2007. For the purposes of monitoring for gross alpha particle activity, radium-226, radium-228, and uranium and beta particle activity and photon activity in drinking water “detection limit” is defined as in Rule 1200-5-1-.11(3).

(3)

(4)

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(Rule 1200-5-1-.11, continued) 1. Applicability and sampling location for existing community water systems or sources. All existing CWSs using ground water, surface water or systems using both ground and surface water (hereafter referred to as systems) must sample at every entry point to the distribution system that is representative of all sources being used (hereafter called a sampling point) under normal operating conditions. The system must take each sample at the same sampling point unless conditions make another sampling point more representative of each source or the State has designated a distribution system location, in accordance with Rule 1200-5-1-.11(4)(a)2(ii)(III). (i) Applicability and sampling location for new community water systems or sources. All new CWSs or CWSs that use a new source of water must begin to conduct initial monitoring for the new source within the first quarter after initiating use of the source. CWSs must conduct more frequent monitoring when ordered by the State in the event of possible contamination or when changes in the distribution system or treatment processes occur which may increase the concentration of radioactivity in finished water.

2.

Initial monitoring: Systems must conduct initial monitoring for gross alpha particle activity, radium-226, radium-228, and uranium as follows: (i) Systems without acceptable historical data, as defined below, must collect four consecutive quarterly samples at all sampling points before December 31, 2007. Grandfathering of data: The Department may allow historical monitoring data collected at a sampling point to satisfy the initial monitoring requirements for that sampling point, for the following situations. (I) To satisfy initial monitoring requirements, a community water system having only one entry point to the distribution system may use the monitoring data from the last compliance monitoring period that began between June 2000 and December 8, 2003. To satisfy initial monitoring requirements, a community water system with multiple entry points and having appropriate historical monitoring data for each entry point to the distribution system may use the monitoring data from the last compliance monitoring period that began between June 2000 and December 8, 2003. To satisfy initial monitoring requirements, a community water system with appropriate historical data for a representative point in the distribution system may use the monitoring data from the last compliance monitoring period that began between June 2000 and December 8, 2003, provided that the Department finds that the historical data satisfactorily demonstrates that each entry point to the distribution system is expected to be in compliance based upon the historical data and reasonable assumptions about the variability of contaminant levels between entry points. The Department must make a written finding indicating how the data conforms to these requirements.

(ii)

(II)

(III)

(iii)

For gross alpha particle activity, uranium, radium-226, and radium-228 monitoring, the Department may waive the final two quarters of initial

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(Rule 1200-5-1-.11, continued) monitoring for a sampling point if the results of the samples from the previous two quarters are below the detection limit. (iv) If the average of the initial monitoring results for a sampling point is above the MCL, the system must collect and analyze quarterly samples at that sampling point until the system has results from four consecutive quarters that are at or below the MCL, unless the system enters into another schedule as part of a formal compliance agreement with the Department.

3.

Reduced monitoring: The Department may allow community water systems to reduce the future frequency of monitoring from once every three years to once every six or nine years at each sampling point, based on the following criteria: (i) If the average of the initial monitoring results for each contaminant (i.e., gross alpha particle activity, uranium, radium-226, or radium-228) is below the detection limit specified in Rule 1200-5-1-.11, the system must collect and analyze for that contaminant using at least one sample at that sampling point every nine years. For gross alpha particle activity and uranium, if the average of the initial monitoring results for each contaminant is at or above the detection limit but at or below 1/2 the MCL, the system must collect and analyze for that contaminant using at least one sample at that sampling point every six years. For combined radium-226 and radium-228, the analytical results must be combined. If the average of the combined initial monitoring results for radium-226 and radium-228 is at or above the detection limit but at or below 1/2 the MCL, the system must collect and analyze for that contaminant using at least one sample at that sampling point every six years. For gross alpha particle activity and uranium, if the average of the initial monitoring results for each contaminant is above 1/2 the MCL but at or below the MCL, the system must collect and analyze at least one sample at that sampling point every three years. For combined radium-226 and radium-228, the analytical results must be combined. If the average of the combined initial monitoring results for radium-226 and radium-228 is above 1/2 the MCL but at or below the MCL, the system must collect and analyze at least one sample at that sampling point every three years. Systems must use the samples collected during the reduced period to determine the monitoring frequency for subsequent periods (e.g., if a system's sampling point is on a nine year period, and the sample result is above 1/2 MCL, then the next period for that sampling point is three years). monitoring monitoring monitoring monitoring

(ii)

(iii)

(iv)

(v)

If a system has a monitoring result that exceeds the MCL while on reduced monitoring, the system must collect and analyze quarterly samples at that sampling point until the system has results from four consecutive quarters that are below the MCL, unless the system enters into another schedule as part of a formal compliance agreement with the Department.

4.

Compositing: To fulfill quarterly monitoring requirements for gross alpha particle activity, radium-226, radium-228, or uranium, a system may composite up to four consecutive quarterly samples from a single entry point if analysis is done within a year of the first sample. The Department will treat analytical results from the composite as the average analytical result to determine compliance with the

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(Rule 1200-5-1-.11, continued) MCLs and the future monitoring frequency. If the analytical result from the composited sample is greater than 1/2 MCL, the Department may direct the system to take additional quarterly samples before allowing the system to sample under a reduced monitoring schedule. 5. A gross alpha particle activity measurement may be substituted for the required radium-226 measurement provided that the measured gross alpha particle activity does not exceed 5 pCi/L. A gross alpha particle activity measurement may be substituted for the required uranium measurement provided that the measured gross alpha particle activity does not exceed 15 pCi/L. The gross alpha measurement shall have a confidence interval of 95% (1.65 sigma, where sigma is the standard deviation of the net counting rate of the sample) for radium-226 and uranium. When a system uses a gross alpha particle activity measurement in lieu of a radium- 226 and/or uranium measurement, the gross alpha particle activity analytical result will be used to determine the future monitoring frequency for radium-226 and/or uranium. If the gross alpha particle activity result is less than detection, 1/2 the detection limit will be used to determine compliance and the future monitoring frequency.

(b)

Monitoring and compliance requirements for beta particle and photon radioactivity. To determine compliance with the maximum contaminant levels for beta particle and photon radioactivity, a system must monitor at a frequency as follows: 1. Community water systems (both surface and ground water) designated by the Department as vulnerable must sample for beta particle and photon radioactivity. Systems must collect quarterly samples for beta emitters and annual samples for tritium and strontium-90 at each entry point to the distribution system (hereafter called a sampling point), beginning within one quarter after being notified by the Department. Systems already designated by the Department must continue to sample until the Department reviews and either reaffirms or removes the designation. (i) If the gross beta particle activity minus the naturally occurring potassium40 beta particle activity at a sampling point has a running annual average (computed quarterly) less than or equal to 50 pCi/L (screening level), the Department may reduce the frequency of monitoring at that sampling point to once every 3 years. Systems must collect all samples required in Rule 1200-5-1-.11(4)(b)1 during the reduced monitoring period. For systems in the vicinity of a nuclear facility, the Department may allow the CWS to utilize environmental surveillance data collected by the nuclear facility in lieu of monitoring at the system's entry point(s), where the Department determines if such data is applicable to a particular water system. In the event that there is a release from a nuclear facility, systems which are using surveillance data must begin monitoring at the community water system's entry point(s) in accordance with Rule 1200-5-1-.11(4)(b)1.

(ii)

2.

Community water systems (both surface and ground water) designated by the Department as utilizing waters contaminated by effluents from nuclear facilities must sample for beta particle and photon radioactivity. Systems must collect quarterly samples for beta emitters and iodine-131 and annual samples for tritium and strontium-90 at each entry point to the distribution system (hereafter called a sampling point), beginning within one quarter after being notified by the Department. Systems already designated by the Department as systems using waters contaminated by effluents from nuclear facilities must continue to sample until the Department reviews and either reaffirms or removes the designation.

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Quarterly monitoring for gross beta particle activity shall be based on the analysis of monthly samples or the analysis of a composite of three monthly samples. The former is recommended. For iodine-131, a composite of five consecutive daily samples shall be analyzed once each quarter. As ordered by the Department, more frequent monitoring shall be conducted when iodine-131 is identified in the finished water. Annual monitoring for strontium-90 and tritium shall be conducted by means of the analysis of a composite of four consecutive quarterly samples or analysis of four quarterly samples. The latter procedure is recommended. If the gross beta particle activity beta minus the naturally occurring potassium-40 beta particle activity at a sampling point has a running annual average (computed quarterly) less than or equal to 15 pCi/L, the Department may reduce the frequency of monitoring at that sampling point to every 3 years. Systems must collect all samples required in Rule 12005-1-.11(4)(b)2 during the reduced monitoring period. For systems in the vicinity of a nuclear facility, the Department may allow the CWS to utilize environmental surveillance data collected by the nuclear facility in lieu of monitoring at the system's entry point(s), where the Department determines if such data is applicable to a particular water system. In the event that there is a release from a nuclear facility, systems which are using surveillance data must begin monitoring at the community water system's entry point(s) in accordance with Rule 1200-5-1-.11(4)(b)2.

(ii)

(iii)

(iv)

(v)

3.

Community water systems designated by the Department to monitor for beta particle and photon radioactivity can not apply to the Department for a waiver from the monitoring frequencies specified in Rule 1200-5-1-.11(4)(b)1 or 2. Community water systems may analyze for naturally occurring potassium-40 beta particle activity from the same or equivalent sample used for the gross beta particle activity analysis. Systems are allowed to subtract the potassium-40 beta particle activity value from the total gross beta particle activity value to determine if the screening level is exceeded. The potassium-40 beta particle activity must be calculated by multiplying elemental potassium concentrations (in mg/L) by a factor of 0.82. For community water systems, if the gross beta particle activity minus the naturally occurring potassium-40 beta particle activity exceeds the screening level, an analysis of the sample must be performed to identify the major radioactive constituents present in the sample and the appropriate doses must be calculated and summed to determine compliance with Rule 1200-5-1.06(5)(b)1, using the formula in Rule 1200-5-1-.06(5)(b)2. Doses must also be calculated and combined for measured levels of tritium and strontium to determine compliance. Community water systems must monitor monthly at the sampling point(s) which exceed the maximum contaminant level in Rule 1200-5-1-.06(5)(c) beginning the month after the exceedance occurs. Systems must continue monthly monitoring until the system has established, by a rolling average of 3 monthly samples, that the MCL is being met. Community water systems who establish that the MCL is

4.

5.

6.

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(Rule 1200-5-1-.11, continued) being met must return to quarterly monitoring until they meet the requirements set forth in Rule 1200-5-1-.11(4)(b)1(ii) or 2(i). (c) General monitoring and compliance requirements for radionuclides. 1. The Department may require more frequent monitoring than specified in subparagraphs (a) and (b) of this paragraph, or may require confirmation samples at its discretion. The results of the initial and confirmation samples will be averaged for use in compliance determinations. Each public water systems shall monitor at the time designated by the Department during each compliance period. Compliance: Compliance the radionuclide MCLs will be determined based on the analytical result(s) obtained at each sampling point. If one sampling point is in violation of an MCL, the system is in violation of the MCL. (i) For systems monitoring more than once per year, compliance with the MCL is determined by a running annual average at each sampling point. If the average of any sampling point is greater than the MCL, then the system is out of compliance with the MCL. For systems monitoring more than once per year, if any sample result will cause the running average to exceed the MCL at any sample point, the system is out of compliance with the MCL immediately. Systems must include all samples taken and analyzed under the provisions of this Rule in determining compliance, even if that number is greater than the minimum required. If a system does not collect all required samples when compliance is based on a running annual average of quarterly samples, compliance will be based on the running average of the samples collected. If a sample result is less than the detection limit, zero will be used to calculate the annual average, unless a gross alpha particle activity is being used in lieu of radium-226 and/or uranium. If the gross alpha particle activity result is less than detection, 1/2 the detection limit will be used to calculate the annual average.

2. 3.

(ii)

(iii)

(iv)

(v)

4. 5.

The Department has the discretion to delete results of obvious sampling or analytic errors. If the MCL for radioactivity set forth in Rule 1200-5-1-.06(5) is exceeded, the operator of a community water system must give notice to the Department pursuant to Rule 1200-5-1-.20 and to the public as required by Rule 1200-5-1.19.

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 53-2002, 53-2003; 68-221-701 et seq., 68-221-704, and Public Acts of 1983, Chapter 324. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed November 21, 2001; effective February 4, 2002. Amendment filed April 12, 2002; effective June 26, 2002. Amendment filed August 15, 2005; effective October 29, 2005. Amendments filed June 12, 2008; effective August 26, 2008.

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1200-5-1-.12 SECONDARY DRINKING WATER REGULATIONS. (1) The following maximum contaminant levels are established to provide a water that is aesthetically pleasing to the consumer. These standards will apply to all community water systems and to those non-community water systems as may be deemed necessary by the Department. Monitoring for these contaminants will be set in the Monitoring Program for each system, but in no event less than once every year for a surface and surface/ground supply and once every three years for a ground water supply. Maximum Contaminant Level Contaminant (a) Chloride (b) Color (c) Copper (d) MBAS (Methyl Blue Active Substance) (e) Iron (f) Manganese (g) Odor (h) pH (i) Sulfate (j) TDS (Total Dissolved Solids) (k) Zinc (l) Fluoride (m) Aluminum (n) Silver (2) Milligrams per Liter (unless otherwise indicated) 250 15 (Color Units) 1 0.5 0.3 0.05 3 (Threshold Odor Number) 6.5-8.5 250 500 5 2.0 0.2 0.1

The system may apply for monitoring waivers from the monitoring frequency specified in paragraph (1). The Department may issue monitoring waivers after considering: historical data, whether or not there have been customer complaints concerning the contaminant to be waived, any corrective action taken by the water supplier to correct the secondary contaminant problem, and whether or not the system routinely monitors for the contaminant as part of its treatment process monitoring program. The Department shall determine the frequency, if any, a system must monitor after considering the historical data available, the number and nature of customer complaints and other factors that may affect the contaminant concentration, and specify the decision in writing to the system.

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 68-221-701 et seq, and 68-221-704. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed April 12, 1996; effective June 26, 1996. Amendment filed February 17, 1999; effective May 3, 1999. Amendment filed June 12, 2008; effective August 26, 2008. 1200-5-1-.13 ALTERNATIVE ANALYTICAL TECHNIQUES. If an alternative analytical technique is acceptable to the Administrator of the U.S. Environmental Protection Agency as being substantially equivalent to the prescribed test in both precision and accuracy as it relates to the determination of compliance with any maximum contaminant level, they shall become a part of these Rules and Regulations by inference. Authority: T.C.A. §§4-5-201 et seq., 4-5-202, and 68-221-701 et seq. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977.

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1200-5-1-.14 LABORATORY CERTIFICATION. (1) General (a) For the purpose of determining compliance with physical, chemical, biological and radiological constituents and maximum contaminant levels set forth in this rule chapter, analyses of samples may be considered only if they have been analyzed by a laboratory certified by the Department. Laboratories which are certified by the Department are designated "state-certified laboratories." Analysis for turbidity, free chlorine residual, temperature, pH, alkalinity, calcium, conductivity, orthophosphate, daily chlorite, and silica may be performed by persons approved by the Department. Approved methodology must be used. The Tennessee Laboratory Certification Program is established for the purpose of evaluating laboratories to determine technical capability to analyze for one or more groups of the contaminants, disinfectant residuals, disinfection byproducts and disinfectant precursors listed in Rules 1200-5-1-.06 through 1200-5-1-.10, 1200-5-1-.12, 1200-5-1-.21, 1200-5-1-.24 through 1200-5-1-.26, and 1200-5-1-.36 through .40 of this rule chapter. Designation of Department laboratory certification officer(s) shall be from those experienced professional staff members assigned to the Department of Environment and Conservation, Division of Water Supply and certified by the U.S. Environmental Protection Agency. Certification Officer(s) shall supervise the certification program. A laboratory desiring certification in microbiological and/or chemical analysis shall make written application to the Department of Environment and Conservation, Division of Water Supply. The applicant shall indicate those group(s) of contaminants for which it seeks certification: Chemistry 1. 2. 3. 4. 5. 6. 7. General (wet) Inorganic Organic Chemicals Disinfection Byproducts Polychlorinated Biphenyls (PCBs) Radiochemistry Microbiology (i) (ii) (iii) (iv) (d) Enzyme Substrate Coliforms Membrane Filter Coliforms Heterotrophic Plate Count Enterococci

(b)

(c)

The laboratory shall upon request supply to the Department all information requested concerning its equipment, facilities, data, and the qualifications of its laboratory staff. Certified laboratories must have an on-site audit conducted every three years by the certification officer or his/her designee. A laboratory desiring certification will arrange for an American Association for Laboratory Accreditation (A2LA) approved vendor to send performance evaluation samples to the laboratory for testing pursuant to its proficiency testing program. A2LA approved Performance Evaluation venders can be viewed at: http://www.a2la.org/dirsearchnew/nelacptproviders.cfm. The laboratory's performance

(e)

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(Rule 1200-5-1-.14, continued) in correctly evaluating such sample(s) will be sent to both the laboratory and to the certification officer. All direct costs for the performance evaluation samples will be borne by the laboratory requesting certification. (f) The certification officer shall review the written report of the laboratory performance evaluation and together with his review of requirements set forth in this Rule shall determine the certification ranking. Certified laboratories must maintain all records and correspondence used to determine compliance with the requirements of these Rules for a period of not less than six (6) years. Adequate information must be available to reconstruct results for compliance and performance evaluation (PE) samples. This includes all raw data, calculations, and quality control data. Electronic data must be backed up by protected tape, hard disk, or other method approved by the Department. Water system clients should be notified before disposing of any records so that they may request copies if needed. Performance evaluation samples shall be analyzed annually. Certified Laboratories shall comply with all requirements set forth in the latest edition of EPA Manual for the Certification of Laboratories Analyzing Drinking Water except where those requirements differ from the requirements set forth in this rule chapter.

(g)

(h)

(2)

In order for a laboratory to be certified by the Department: (a) It must have a written quality assurance (QA) plan which addresses the following parts: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Laboratory organization and responsibility. Process used to identify clients' Data Quality Objectives. Standard Operating Procedures with dates of last revision. Field sampling procedures. Laboratory sample receipt and handling procedures. Instrument calibration procedures Analytical procedures. Data reduction, validation, reporting and verification. Type of quality control (QC) checks and the frequency of their use. List schedules of internal and external system and data quality audits and inter laboratory comparisons. Preventive maintenance procedures and schedules. Corrective action contingencies. Record keeping procedures. (i) (ii) If a particular part is not relevant, the QA plan should state this and provide a brief explanation. All laboratories analyzing drinking water compliance samples must adhere to any required QC procedures specified in the approved method. Documentation for many of the listed QA plan parts may be made by reference to appropriate sections of the latest edition of EPA Manual for the Certification of Laboratories Analyzing Drinking Water, the laboratory's standard operating procedures (SOPs), or other literature (e.g., promulgated methods, Standard Methods for the Examination of Water and Wastewater, etc.). The QA Plan should be updated at least annually.

(b)

It must complete the performance evaluation samples as described in Rule 1200-5-1.14(9).

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(Rule 1200-5-1-.14, continued) (c) On an annual basis and with each application for certification or recertification, all laboratories except Tennessee Public Water Systems shall convey to the Department, Division of Water Supply, payment for the activities necessary for each group of contaminants it desires certification or recertification. All laboratories except Tennessee Public Water Systems shall pay annually an administrative certification fee as listed in the fee schedule. The fee schedule is as follows: Fee Type 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. Administrative In-State Administrative Out of State General Chemistry-Turbidity, Corrosivity, pH Inorganics- Trace Metals, Sodium, Nitrite, Nitrate, Fluoride, Sulfate, Cyanide, Asbestos, Chlorite, and Bromate Organics Disinfection Byproducts-Trihalomethanes and Haloacetic acids Polychlorinated Biphenyls (PCB) Radiochemistry Enzyme Substrate-Total Coliform and E.-Coli Membrane Filter- Total Coliform, Fecal Coliform, E.-Coli Heterotrophic Plate Count Enterococci (i) (ii) (iii) Fee in Dollars $1000.00 $750.00 $500.00 $500.00 $500.00 $500.00 $500.00 $500.00 $500.00 $500.00 $500.00 $500.00

Certification fees shall be retained by the state even if the laboratory applying for certification does not qualify for certification. If the certification fee is not paid within 30 days after the receipt of the invoice, certification of the laboratory is automatically revoked. The reinstatement fee for a laboratory that fails to pay its certification fee by the invoice due date shall be $500.00 in addition to the fees specified in this subparagraph.

(3)

Ranking Scheme of Laboratories - Based upon a review of the written application, the facts determined from any inspection, and the results of a laboratory performance evaluation, a certification officer may classify a laboratory as follows for the particular group(s) of contaminants for which it seeks certification: (a) (b) (c) Certified - A laboratory that meets the minimum requirements as set forth in these Rules. Provisionally Certified - A laboratory which has deficiencies but can still produce valid analytical data. Not Certified - A laboratory which possesses major deficiencies such that it cannot consistently produce valid analytical data in order to determine compliance with the maximum contaminant level. Analytical data will not be accepted from a laboratory with this ranking. Interim Certification - Interim certification may be granted in certain circumstances when it is impossible or unnecessary to perform an on-site audit. Interim certification status may be granted if, for example, the Certification Officer determines that the laboratory has the appropriate instrumentation, is using the approved methods, has

(d)

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(Rule 1200-5-1-.14, continued) adequately trained personnel to perform the analyses, and has satisfactorily analyzed PE samples, if available, for the contaminants in question. The Certification Officer should perform an on-site audit as soon as possible but no later than three years. An example of a situation where this type of certification is warranted would be a laboratory that has requested certification for the analysis of additional analytes that involve a method for which it already has certification. (4) Downgrading Certification Status - A laboratory certified to perform analyses may be downgraded to a Provisionally Certified status for a particular parameter, or for one or more groups of contaminants for which it has been certified for any one of the following reasons: (a) Failure to analyze a set of performance evaluation samples within established acceptance limits described in paragraph (9) of this rule. If more than one concentration of a particular contaminant was provided for analysis, the laboratory must analyze all concentrations provided except where otherwise stated. Failure to notify the Department within 30 days of any changes either in personnel, equipment, or laboratory location which may impair analytical capability. Failure to maintain the minimum required standard of quality as contained in the most recent version of the EPA Manual for the Certification of Laboratory Analyzing Drinking Water as determined by an on-site evaluation by a Department representative. During a provisional status period, which may last for up to one year plus any extension period pending proceedings for revocation of its certification, the laboratory may continue to analyze samples for compliance purposes, but it must notify its clients of its downgraded status in writing on all reports. Failure to report compliance data to the public water system or the state in a timely manner. Data that may cause the system to exceed a MCL shall be reported as soon as possible to the system and to the state.

(b) (c)

(d)

(e)

(5)

Revoking Certification Status - A laboratory certified to perform analyses may be downgraded from a Certified or a Provisionally Certified status to a Not Certified status for a particular parameter, or for one or more groups of contaminants for which it has been certified, including but not limited to any of the reasons listed in subparagraphs below. Commercial laboratories must notify their public water system customers of the change in certification status by mail within 45 days of a downgrade in status by the Department and retain copies of such notice for six years. (a) (b) (c) (d) (e) Failure to analyze an initial and a follow-up or cross check performance evaluation sample within established acceptance limits. Failure to correct identified deviations (including continued use of unapproved methods and equipment) within the time specified by the Department. Reporting as data derived from its own laboratory analysis, that data obtained from analyses of the sample(s) performed by another laboratory. Falsification or inaccurate reporting of analytical data. Failure to report to the Department on Departmental forms analytical results as specified by Rule 1200-5-1-.18. Forms may be obtained from the Division of Water Supply. A certified laboratory shall submit results of its analyses to both the appropriate Department's field office and the Department's central office on forms furnished by the Department.

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Failure to perform the analysis within the time period prescribed by the analytical procedure. However, the time period shall not be more than thirty (30) days from the sample collection date, except for lead and copper tap samples collected pursuant to Rule 1200-5-1-.33. Failure to notify its drinking water customers of any downgrade or revocation of its certification status and to keep records of the notice to customers. Failure of the laboratory to reject any sample taken for compliance purposes that does not meet acceptable criteria for the type container and preservative, maximum holding time, chain of custody, proper sample collection and transport, and sample report form that contains the location, date, time of collection, collector's name, preservative added, and other special remarks concerning the sample. Indelible ink shall be used for completing the sample report form. Failure of the Laboratory Director to give timely notice to the party responsible for collecting the sample that improper sampling technique, container, transport, holding time, method preservative or documentation was used. Failure to provide written sampling procedures with sample containers sent to customers for collecting drinking water samples. Failure to meet the method detection limits. Failure to maintain all data necessary to reconstruct analytical results reported for compliance samples. Failure to pay certification fees as listed in subparagraph (2)(c) of this rule.

(g) (h)

(i)

(j) (k) (l) (m) (6)

Procedure for Revocation (a) (b) The State, Department, Division of Water Supply or the certification officer shall notify the laboratory by certified mail of its intent to revoke certification. If the local laboratory objects to the determination to revoke certification, the laboratory shall submit a written notice of appeal to the Department within thirty (30) days after issuance of the notice of intent to revoke certification. The notice of appeal will be referred to the Tennessee Water Quality Control Board. The Board will set a hearing date and conduct proceedings in accordance with the Uniform Administrative Procedures Act, Chapter 5 of Title 4. If no notice of appeal is so filed, certification will be revoked. The notice of appeal shall set forth the grounds and reasons for objection and shall ask for a hearing before the Tennessee Water Quality Control Board. It shall be signed by a duly authorized representative of the laboratory such as the president/owner of a commercial laboratory, or the mayor, utility manager, president, or laboratory supervisor in the case of a municipal or utility district laboratory. If the Water Quality Control Board modifies or sets aside the determination of the Department, the Department will reevaluate the local laboratory within sixty (60) days of issuance of the decision by the Board.

(c)

(d)

(7)

Reinstatement of Certification - Certification of a laboratory will be reinstated when it demonstrates to the Department that the deficiencies which resulted in provisional certification or revocation have been corrected. Such demonstration may result from an

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(Rule 1200-5-1-.14, continued) on-site evaluation and/or a successful analysis of samples on the next regularly scheduled performance evaluation. (8) Reciprocity of Certified Laboratories - The Department may authorize acceptance of analyses from laboratories certified by other states or by the U. S. Environmental Protection Agency. Authorization will be granted on a reciprocal basis for laboratories from those states which accept Tennessee laboratory certification. Laboratories desiring Department approval of their certification from the U.S. E.P.A. or from another state must submit to the Department copies of all correspondence pertaining to the grant of certification, including the results of any performance evaluation sample analyses. Proficiency Evaluation (PE) Samples or Performance Test (PT) Samples (a) In order to receive and maintain full certification for an analyte, the following are required for each analyte for which a laboratory is certified: (i) The laboratory must analyze PE samples (if available) acceptable to the Department at least once a year for each analyte and by each method used to analyze compliance samples. PE samples are also referred to as Performance Test (PT) samples. Results from analysis of the PE samples must be within the acceptable limits set forth in this chapter. The laboratory must document the corrective actions taken when a PE sample is analyzed unsuccessfully. A copy of this documentation must be available for review by the certification officer. A make up PE sample must be successfully analyzed within three months of being notified that a PE sample was not acceptable.

(9)

(ii) (iii)

(iv) (b)

Excluding vinyl chloride, the laboratory may be certified for all VOCs if they successfully analyze at least 80% of the regulated VOCs. The 80% Rule does not apply to the regulated trihalomethanes (THM) or haloacetic acids (HAAs). Laboratories are certified for total THMs and HAA5 but each regulated THM and HAA concentration must be reported, evaluated and passed individually to pass the PE sample. If a laboratory fails one of the regulated THMs or HAAs, it cannot be certified for total THMs or HAA5, but must analyze another PE sample and pass all of the regulated THMs or HAAs in a PE sample to be certified to analyze compliance monitoring samples for total trihalomethanes or total haloacetic acids. The following table summarizes the 80% Rule. Analyte(s) PE Success Requirement Vinyl Chloride 100% 20 VOCs 80% * 4 Regulated THMs 100% 5 Regulated HAA5s 100%

*A lab will not maintain certification for analyte(s) which it repeatedly fails. (c) Acceptable PE studies for the determination of total coliforms and E. coli shall be part of a drinking water study. Each study shall contain a set of ten samples in various combinations of total coliforms, E. coli, non-coliforms, and at least one blank. To be certified, laboratories must successfully analyze nine of the ten samples with no false negatives.

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued) (10) Analytical Requirements (a) Microbiology 1.

CHAPTER 1200-5-1

Suppliers of water for community water systems and non-community water systems shall analyze for coliform bacteria for the purpose of determining compliance with Rule 1200-5-1-.06(4). The standard sample volume required for total coliform analysis, regardless of the analytical method used is 100 milliliters. Analyses shall be conducted in accordance with one of the analytical methods in following table:
Table 1200-5-1-.14(10)(a)1.

Organism 2 Total Coliforms

Methodology 3,4,5 Total Coliform Fermentation Technique 6 Total Coliform Membrane Filter Technique 5,7 Presence-Absence (P-A) Coliform Test 8 ONPG-MUG Test 9 Colisure Test ® 10 E*Colite Test ® 11 m-ColiBlue24 Test ® 12 Readycult Coliforms 100 Presence/Absence Test ® 13 Membrane Filter Technique using Chromocult Coliform Agar ® 14 Colitag Test

Citation 9221A, B 9222 A, B, C 9221 9223

1

Footnotes 1 Methods 9221 A, B; 9222 A, B, C; 9221 D and 9223 are contained in Standard Methods for the Examination of Water and Wastewater, 18th edition (1992) and 19th edition (1995) American Public Health Association, 1015 Fifteenth Street NW, Washington, D.C. 20005; either edition may be used. In addition, the following online versions may also be used: 9221 A, B, D-99, 9222 A, B, C-97 and 9223 B-97. Standard Methods Online are available at http://www.standardmethods.org. The year in which each method was approved by the Standard Methods Committee is designated by the last two digits in the method number. The methods listed are the only online versions that may be used. 2 The time from sample collection to initiation of analysis may not exceed 30 hours. Systems are encouraged but not required to hold samples below 10 °C during transit. 3 Lactose broth, as commercially available, may be used in lieu of lauryl tryptose broth, if the system conducts at least 25 parallel tests between this medium and lauryl tryptose broth using the water normally tested, and this comparison demonstrates that the false-positive rate and false-negative rate for total coliform, using lactose broth, is less than 10 percent. 4 If inverted tubes are used to detect gas production, the media should cover these tubes at least one-half to two-thirds after the sample is added. 5 No requirement exists to run the completed phase on 10 percent of all total coliform-positive confirmed tubes. 6 MI agar also may be used. Preparation and use of MI agar is set forth in the article, ‘‘New medium for the simultaneous detection of total coliform and Escherichia coli in water’’ by Brenner, K.P., et al., 1993, Appl. Environ. Microbiol. 59:3534–3544. Also available from the Office of Water Resource Center (RC–4100), 401 M. Street SW, Washington, DC 20460, EPA/600/J–99/225. 7 Six-times formulation strength may be used if the medium is filter-sterilized rather than autoclaved. 8 The ONPG-MUG Test is also known as the Autoanalysis Colilert System. 9 A description of the Colisure Test, Feb 28, 1994, may be obtained from IDEXX Laboratories, Inc., One IDEXX Drive, Westbrook, Maine 04092. The Colisure Test may be read after an incubation time of 24 hours. ® 10 A description of the E*Colite Test, ‘‘Presence/Absence for Coliforms and E. Coli in Water,’’ Dec 21, 1997, is available from Charm Sciences, Inc., 36 Franklin Street, Malden, MA 02148–4120. ® 11 A description of the m-ColiBlue24 Test, Aug 17, 1999, is available from the Hach Company, 100 Dayton Avenue, Ames, IA 50010. ® ® 12 The Readycult Coliforms 100 Presence/Absence Test is described in the document, “Readycult Coliforms 100 Presence/Absence Test for the Detection and Identification of Coliform Bacteria and Escherichla coli in finished water”, November 2000, Version 1.0, available from EM Science (an affiliate of Merck KggA, Darmstadt Germany), 480 S. Democrat Road, Gibbstown, NJ 08027-1297. Telephone number is (800) 222-0342, e-mail address is: adellenbusch@emscience.com. ® ® 13 Membrane Filter Technique using Chromocult Coliform Agar is described in the document, “Chromocult Coliform Presence/Absence Membrane Filter Test Method for Detection and Identification of Coliform Bacteria and Escherichla coli in finished water”, November 2000, Version 1.0, available from EM Science (an affiliate of Merck KggA, Darmstadt Germany), 480 S. Democrat Road, Gibbstown, NJ 08027-1297. Telephone number is (800) 222-0342, e-mail address is: adellenbusch@emscience.com. ® ® 14 Colitag product for the determination of the presence/absence of total coliforms and E. coli is described in “Colitag Product as a Test for Detection and Identification of Coliforms and E. coli Bacteria in Drinking Water and Source Water

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CHAPTER 1200-5-1

as required in National Primary Drinking Water Regulations,” August 2001, available from CPI International, Inc., 5580 Skylane Blvd., Santa Rosa, CA, 95403 telephone (800) 878-7654, Fax (707) 545-7901, Internet address http://www.cpiinternational.com.

2.

Where a determination of fecal coliform density is not required, public water systems must conduct fecal coliform analysis in accordance with the following procedure: (i) When the MTF Technique or Presence-Absence (P-A) Coliform Test is used to test for total coliforms, shake the lactose-positive presumptive tube or P-A bottle vigorously and transfer the growth with a sterile 3-mm loop or sterile applicator stick into brilliant green lactose bile broth and EC medium to determine the presence of total and fecal coliforms, respectively. For EPA-approved analytical methods which use a membrane filter, remove the membrane containing the total coliform colonies from the substrate with a sterile forceps and carefully curl and insert the membrane into a tube of EC medium (The laboratory may first remove a small portion of selected colonies for verification), swab the entire surface with a sterile cotton swab and transfer the inoculum to EC medium (do not leave the cotton swab in the EC medium), or inoculate individual total coliformpositive colonies into EC Medium. Gently shake the inoculated EC tubes to insure adequate mixing and incubate in a waterbath at 44.5 + 0.2°C for 24 + 2 hours. Gas production of any amount in the inner fermentation tube of the EC medium indicates a positive fecal coliform test. The preparation of EC medium is described in Method 9221E in Standard Methods for the Examination of Water and Wastewater, 18th Edition (1992), 19th Edition (1995), and 20th Edition (1998); the cited method in any one of these three editions may be used.

(ii)

3.

Public Water Systems choosing to test for E. coli in lieu of fecal coliform must use the following methods: (i) EC medium supplemented with 50 ug/ml of 4-methylumbelliferyl-beta-D-glucuronide (MUG) (final concentration), as described in Method 9222 G in Standard Methods for the Examination of Water and Wastewater, 19th edition (1995) and 20th edition (1998). Either edition may be used. Alternatively, the 18th edition (1992) may be used if at least 10 ml of EC medium, as described in part 2 of this subparagraph, is supplemented with 50 ug/ml of MUG before autoclaving. The inner inverted fermentation tube may be omitted. If the 18th edition is used, apply the procedure in part 2 of this subparagraph for transferring a total coliform-positive culture to EC medium supplemented with MUG, incubate the tube at 44.5 + 0.2 oC for 24 + 2 hours, and then observe fluorescence with an ultraviolet light (366nm) in the dark. If fluorescence is visible, E. coli are present. Nutrient agar supplemented with 100 μg/ml of 4methylumbelliferyl-beta-Dglucuronide (MUG) (final concentration), as described in Method 9222G in Standard Methods for the Examination of Water and Wastewater, 19th edition (1995) and 20th edition (1998). Either edition may be used for determining if a total coliform-positive sample, as determined by a membrane filter technique, contains E. coli Alternatively, the 18th edition (1992) may be used if the membrane filter containing a total coliformpositive colony(ies) is transferred to nutrient agar, as described in Method

(ii)

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(Rule 1200-5-1-.14, continued) 9221B (paragraph 3) of Standard Methods (18th edition), supplemented with 100 ug/ml of MUG. If the 18th edition is used, incubate the agar plate at 35 °C for 4 hours and then observe the colony(ies) under ultraviolet light (366 nm) in the dark for fluorescence. If fluorescence is visible, E. coli are present. (iii) Minimal Medium ONPG-MUG (MMO-MUG) Test, as set forth in the article "National Field Evaluation of Defined Substrate Method for the Simultaneous Detection of Total Coliforms and Escherichia coli from Drinking Water; Comparison with Presence-Absence Techniques" (Edberg et al.), Applied and Environmental Microbiology, Volume 55, pp. 1003-1008, April 1989. (Note: The Autoanalysis Colilert System is an MMO-MUG test). If the MMO-MUG test is total coliform-positive after a 24-hour incubation, test the medium for fluorescence with a 366-nm ultraviolet light (preferably with a 6-watt lamp) in the dark. If fluorescence is observed, the sample is E. coli-positive. If fluorescence is questionable (cannot be definitively read) after 24 hours incubation, incubate the culture for an additional four hours (but not to exceed 28 hours total) and again test the medium for fluorescence. The MMO-MUG Test with hepes buffer in lieu of phosphate buffer is the only approved formulation for the detection of E. coli. The Colisure Test. A description of the Colisure Test may be obtained from the Millipore Corporation, Technical Services Department, 80 Ashby Road, Bedford, MA 01730. The membrane filter method with MI agar, a description of which is cited in footnote 6 to Table 1200-5-1-.14(10)(a)1. E*Colite® Test, a description of which is cited in footnote 10 to Table 12005-1-.14(10)(a)1. m-ColiBlue24® Test, a description of which is cited in footnote 11 to Table 1200-5-1-.14(10)(a)1.

(iv)

(v) (vi) (vii)

(viii) Readycult® Coliforms 100 Presence/Absence Test, a description of which is cited in footnote 12 to the Table 1200-5-1-.14(10)(a)1. (ix) (x) (xi) Membrane Filter Technique using Chromocult® Coliform Agar, a description of which is cited in footnote 13 to Table 1200-5-1-.14(10)(a)1. Colitag®, a description of which is cited in footnote 14 to Table 1200-5-1.14(10)(a)1. As an option to subpart (iii) of this part, a system with a total coliform-positive, MUG-negative, MMO-MUG test may further analyze the culture for the presence of E. coli by transferring a 0.1 ml. 28-hour MMO-MUG culture to EC Medium + MUG with a pipet. The formulation and incubation conditions of EC Medium + MUG, and observation of the results are described in subpart (i) of this part.

4.

Public Water systems required to monitor under Rule 1200-5-1-.31(2)(a)1 and 1200-5-1-.31(5)(b)2 for total coliforms, fecal coliforms, or heterotrophic bacteria must use one of the methods listed in the following table.
Table 1200-5-1-.14(10)(a)4.

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Organism Total Coliform
2

CHAPTER 1200-5-1

Methodology Total Coliform Fermentation Technique
3,4,5 6

Citation

1

9221 A, B, C 9222 A, B, C 9223

Total Coliform Membrane Filter Technique ONPG-MUG Test Fecal Coliforms
2 7 8

Fecal Coliform Procedure

9221 E 9222 D 9215 B

Fecal Coliform Filter Procedure Heterotrophic bacteria
2

Pour Plate Method SimPlate
9

Footnotes 1. Except where noted, all methods refer to Standard Methods for the Examination of Water and Wastewater, 18th edition (1992), 19th edition (1995), or 20th edition (1998), American Public Health Association, 1015 Fifteenth Street, NW., Washington, DC 20005. The cited methods published in any of these three editions may be used. In addition, the following online versions may also be used: 2130 B–01, 9215 B–00, 9221 A, B, C, E–99, 9222 A, B, C, D–97, and 9223 B–97. Standard Methods Online are available http://www.standardmethods.org. The year in which each method was approved by the Standard Methods Committee is designated by the last two digits in the method number. The methods listed are the only Online versions that may be used. 2. The time from sample collection to initiation of analysis may not exceed 8 hours. Systems must hold samples below 10 deg. C during transit. {8 hour holding time only applies to Rule 1200-5-1-.31(2)(a)1 and (5)(b)2} 3. Lactose broth, as commercially available, may be used in lieu of lauryl tryptose broth, if the system conducts at least 25 parallel tests between this medium and lauryl tryptose broth using the water normally tested, and this comparison demonstrates that the false-positive rate and false-negative rate for total coliform, using lactose broth, is less than 10 percent. 4. Media should cover inverted tubes at least one-half to two-thirds after the sample is added. 5. No requirement exists to run the completed phase on 10 percent of all total coliform-positive confirmed tubes. 6. MI agar also may be used. Preparation and use of MI agar is set forth in the article, ‘‘New medium for the simultaneous detection of total coliform and Escherichia coli in water’’ by Brenner, K.P., et. al., 1993, Appl. Environ. Microbiol. 59:3534-3544. Also available from the Office of Water Resource Center (RC-4100T), 1200 Pennsylvania Avenue, NW., Washington DC 20460, EPA/600/J-99/225. Verification of colonies is not required. 7. The ONPG-MUG Test is also known as the Autoanalysis Colilert System. A-1 Broth may be held up to seven days in a tightly closed screw cap tube at 4 deg. C. 8. 9. A description of the SimPlate method, ‘‘IDEXX SimPlate TM HPC Test Method for Heterotrophs in Water’’, November 2000, can be obtained from IDEXX Laboratories, Inc., One IDEXX Drive, Westbrook, Maine 04092, telephone (800) 321-0207.

5.

Public water systems required to enumerate E. coli in source water as required by Rule 1200-5-1-.39 must use one of the approved methods in the following table:
Table 1200-5-1-.14(10)(a)5.

Parameter and units E. coli, number per 16 100 ml

Method

1

EPA

Standard methods 18th,19th, 20th Standard methods Ed. online

AOAC, ASTM, USGS

Other

MPN

2,3,4

multiple tube,

9221B / 9221F

6,8

9221B-99 / 9221F

6,8

multiple tube/multiple well
13

9223B

7

9223B–97
12

7

991.155

Colilert ®7,9,10 Colilert-18

®7,10

MF two step

1103.1

9222B/9222G , 12 4 9213D 9222B–97 / 9222G D5392–93

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MF single step 1603 , 1604
14 15

CHAPTER 1200-5-1

mColiBlue-24

®11

Footnotes 1 The method must be specified when results are reported. 2 Tests must be conducted to provide organism enumeration (density). Select the appropriate configuration of tubes/filtrations and dilutions/volumes to account for the quality, character, consistency, and anticipated organism density of the water sample. 3 To assess the comparability of results obtained with individual methods, it is suggested that side-by-side tests be conducted across seasons of the year with the water samples routinely tested in accordance with the most current Standard Methods for the Examination of Water and Wastewater or EPA alternate test procedure (ATP) guidelines. 4 ASTM. 2000, 1999, 1996. Annual Book of ASTM Standards—Water and Environmental Technology. Section 11.02. ASTM International. 100 Barr Harbor Drive, West Conshohocken, PA 19428. 5 AOAC. 1995. Official Methods of Analysis of AOAC International, 16th Edition, Volume I, Chapter 17. Association of Official Analytical Chemists International. 481 North Frederick Avenue, Suite 500, Gaithersburg, MD 20877–2417. 6 The multiple-tube fermentation test is used in 9221B.1. Lactose broth may be used in lieu of lauryl tryptose broth (LTB), if at least 25 parallel tests are conducted between this broth and LTB using the water samples normally tested, and this comparison demonstrates that the false-positive rate and false-negative rate for total coliform using lactose broth is less than 10 percent. No requirement exists to run the completed phase on 10 percent of all total coliform-positive tubes on a seasonal basis. 7 These tests are collectively known as defined enzyme substrate tests, where, for example, a substrate is used to detect the enzyme b-glucuronidase produced by E. coli. 8 After prior enrichment in a presumptive medium for total coliform using 9221B.1, all presumptive tubes or bottles showing any amount of gas, growth or acidity within 48 h ± 3 h of incubation shall be submitted to 9221F. Commercially available EC–MUG media or EC media supplemented in the laboratory with 50 μg/mL of MUG may be used. ® ® ® ® 9 Descriptions of the Colilert , Colilert-18 , Quanti-Tray , and Quanti-Tray /2000 may be obtained from IDEXX Laboratories, Inc., 1 IDEXX Drive, Westbrook, ME 04092. ® ® ® 10 Descriptions of the Colilert , Colilert-18 , Quanti-Tray , and Quanti-Tray /2000 may be obtained from IDEXX Laboratories, Inc., 1 IDEXX Drive, Westbrook, ME 04092. ® 11 A description of the mColiBlue24 test, Total Coliforms and E. coli, is available from Hach Company, 100 Dayton Ave., Ames, IA 50010. 12 Subject total coliform positive samples determined by 9222B or other membrane filter procedure to 9222G using NA MUG media. 13 USEPA. 2002. Method 1103.1: Escherichia coli (E. coli) In Water By Membrane Filtration Using membraneThermotolerant Escherichia coli Agar (mTEC). U.S. Environmental Protection Agency, Office of Water, Washington, DC, EPA–821–R–02–020. 14 USEPA. 2002. Method 1603: Escherichia coli (E. coli) In Water By Membrane Filtration Using Modified membraneThermotolerant Escherichia coli Agar ( modified mTEC). U.S. Environmental Protection Agency, Office of Water, Washington, DC, EPA–821–R–02–023. 15 Preparation and use of MI agar with a standard membrane filter procedure is set forth in the article, Brenner et al. 1993. ‘‘New Medium for the Simultaneous Detection of Total Coliform and Escherichia coli in Water.’’ Appl. Environ. Microbiol. 59:3534–3544 and in USEPA. 2002. Method 1604: Total Coliforms and Escherichia coli (E. coli) in Water by Membrane Filtration by Using a Simultaneous Detection Technique (MI Medium).U.S. Environmental Protection Agency, Office of Water, Washington, DC, EPA 821–R–02–024. 16 Recommended for enumeration of target organism in ambient water only.

(i) (ii)

The time from sample collection to initiation of analysis may not exceed 30 hours unless the system meets the condition of subpart (ii) of this part. The Department may approve on a case-by-case basis the holding of an E. coli sample for up to 48 hours between sample collection and initiation of analysis if the Department determines that analyzing an E. coli sample within 30 hours is not feasible. E. coli samples held between 30 to 48 hours must be analyzed by the Colilert reagent version of Standard Method 9223B as listed in Table 1200-5-1-.14(10) (a)5. Systems must maintain samples between 0°C and 10°C during storage and transit to the laboratory.

(iii) 6.

Ground water systems must analyze all ground water source samples collected under Rule 1200-5-1-.40(3) using one of the analytical methods listed in the following table for the presence of E. coli or enterococci.
Analytical Methods for Source Water

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Fecal Indicator E. coli
1

CHAPTER 1200-5-1

Monitoring Methodology 3 Colilert 3 Colisure Membrane Filter Method with MI Agar 5 m-ColiBlue24 Test 6 E*Colite Test 7 EC-MUG 7 NA-MUG Multiple-Tube Technique Membrane Filter Technique Membrane Filter Technique 9 Enterolert

Method citation 2 9223 B. 2 9223 B. 4 EPA Method 1604.

Enterococci

9221 F. 2 9222 G. 2 9230B. 2 9230C. 8 EPA Method 1600.

2

Analyses must be conducted in accordance with the documents listed below. The Director of the Federal Register approves the incorporation by reference of the documents listed in footnotes 2-11 in accordance with 5 U.S.C. 552(a) and 1 CFR part 51. Copies of the documents may be obtained from the sources listed below. Copies may be inspected at EPA’s Drinking Water Docket, EPA West, 1301 Constitution Avenue, NW., EPA West, Room B102, Washington DC 20460 (Telephone: 202-566-2426); or at the National Archives and Records Administration (NARA). For information on the availability of this material at NARA, call 202-741-6030, or go to: http://www.archives.gov/federal_register/code_of_federal_regulations/ibr_locations.html. Footnotes 1 The time from sample collection to initiation of analysis may not exceed 30 hours. The ground water system is o encouraged but not required to hold samples below 10 C during transit. th 2 Methods are described in Standard Methods for the Examination of Water and Wastewater 20 edition (1998) and copies may be obtained from the American Public Health Association, 1015 Fifteenth Street, NW., Washington DC 20005-2605. 3 Medium is available through IDEXX Laboratories, Inc., One IDEXX Drive, West Brook, Maine 04092. 4 EPA Method 1604: Total Coliforms and Escherichia coli in Water by Membrane Filtration Using a Simultaneous Detection Technique (MI Medium); September 2002, EPA 821-R-02-024. Method is available at http://www.epa.gov/nerlccwww/1604sp02.pdf or from EPA’s Water Resource Center (RC-4100T), 1200 Pennsylvania Avenue, NW., Washington DC 20460. 5 A description of the m-ColiBlue24 Test, “Total Coliforms and E. coli Membrane Filtration Method with mColiBlue24 Broth,” Method No. 10029 Revision 2, August 17, 1999, is available from Hach Company, 100 Dayton Ave., Ames IA 50010 or from EPA’s Water Resource Center (RC-4100T), 1200 Pennsylvania Avenue, NW., Washington DC 20460. 6 A description of the E*Colite Test, “Charm E*Colite Presence/Absence Test for Detection and Identification of Coliform Bacteria and Escherichia coli in Drinking Water, January 9, 1998, is available from Charm Sciences, Inc., 659 Andover St., Lawrence, MA 01843-1032 or from EPA’s Water Resource Center (RC-4100T), 1200 Pennsylvania Avenue, NW., Washington DC 20460. 7 EC-MUG (Method 9221F) or NA-MUG (Method 9222G) can be used for E. coli testing step as described in 141.21(f)(6)(i) or (ii) after use of Standard Methods 9221 B, 9221 D, 9222 B, or 9222 C. 8 EPA Method 1600: Enterococci in Water by Membrane Filtration Using membrane-Enterococcus Indoxyl-b-DGlucoside Agar (mEI) EPA 821-R-02-022 (September 2002) is an approved variation of Standard Method 9230C. The method is available at http://www.epa.gov/nerlcwww/1600sp02.pdf or EPA’s Water Resource Center (RC-4100T), 1200 Pennsylvania Avenue, NW., Washington DC 20460. The holding time and temperature for ground water samples are specified in footnote 1 above, rather than as specified in Section 8 of EPA Method 1600. 9 Medium is available through IDEXX Laboratories, Inc., One IDEXX Drive, Westbrook, Maine 04092. Preparation and use of the medium is set forth in the article “Evaluation of Enterolert for Enumeration of Enterococci in Recreational Waters,” by Budnick, G.E., Howard, R.T, and Mayo, D.R., 1996, Applied and Environmental Microbiology, 62:3881-3884.

(b)

Public Water system required to monitor for turbidity by this Rule Chapter must use one of the methods listed in the following table:
Table 1200-5-1-.14(10)(b) Turbidity
4

Nephelometric Method NephelometricMethod Great Lakes Instruments Hach FilterTrak

2130 B 180.1
1 2

Method 2 10133
3

Footnotes

August, 2008 (Revised)

57

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
1 2 3 4

CHAPTER 1200-5-1

‘‘Methods for the Determination of Inorganic Substances in Environmental Samples’’, EPA/600/R-93/100, August 1993. Available at NTIS, PB94-121811. th GLI Method 2, ‘‘Turbidity’’, November 2, 1992, Great Lakes Instruments, Inc., 8855 North 55 Street, Milwaukee, Wisconsin 53223. A description of the Hach FilterTrak Method 10133, ‘‘Determination of Turbidity by Laser Nephelometry,’’ January 2000, Revision 2.0, can be obtained from; Hach Co., P.O. Box 389, Loveland, CO 80539–0389, telephone: 800–227–4224. Styrene divinyl benzene beads (e.g. AMCO-AEPA–1 or equivalent) and stabilized formazin (e.g. Hach StablCal TM or equivalent) are acceptable substitutes for formazin.

(c)

Public water systems required to monitor by this Rule Chapter for any Inorganic contaminants listed in the following table must utilize one of the approved methods for that contaminant listed in the following table:
Inorganic Contaminants Analytical Methods Table 1200-5-1-.14(10)(c)

Contaminant 1. Alkalinity

Methodology Titrimetric

13

EPA

ASTM

3

SM (18th, 19th ed.) 2320 B

4

SM (20th 22 SM Online ed.) 2320 B 2320 B-97 I-1030-85
5

4

Other

D1067-92, 02 B

2. Antimony

Electrometric titration Inductively Coupled Plasma (ICP)—Mass Spectrometry Hydride-Atomic Absorption Atomic Absorption;Platform Atomic Absorption; Furnace ICP-Mass Spectrometry Atomic Absorption;Platform Atomic Absorption; Furnace Hydride Atomic Absorption Transmission Electron Microscopy Transmission Electron Microscopy Inductively Coupled Plasma ICP-Mass Spectrometry Atomic Absorption; Direct Atomic Absorption; Furnace Inductively Coupled Plasma ICP-Mass Spectrometry Atomic Absorption;Platform Atomic Absorption; Furnace Inductively Coupled Plasma ICP-Mass Spectrometry Atomic

200.8

2

D3697-92, 02 200.9
2

3113 B 200.8 200.9
2

3113 B-99

3. Arsenic

2

D2972-97, 03 C D2972-97, 03 B 100.1 100.2
9

3113 B 3114 B

3113 B-99 3114 B-97

4. Asbestos

10

5. Barium

200.7

2 2

3120 B 3111D 3113 B

3120 B

3120 B-99 3111 D-99 3113 B-99

200.8

6. Beryllium

200.7

2 2

3120 B

3120 B

3120 B-99

200.8 200.9

2

D3645-97, 03 B 200.7 200.9
2 2 2

3113 B

3113 B-99

7. Cadmium

200.8

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
Absorption;Platform Atomic Absorption; Furnace 8. Calcium EDTA titrimetric Atomic Absorption; Direct Aspiration. Inductively Coupled Plasma Ion Chromatography Inductively Coupled Plasma ICP-Mass Spectrometry Atomic Absorption;Platform Atomic Absorption; Furnace Atomic Absorption; Furnace Atomic Absorption; Direct Aspiration. Inductively Coupled Plasma ICP-Mass spectrometry Atomic Absorption;Platform 11.Conductivit y Conductance D511-93, 03 A D511-93, 03 B 3113 B 3500-Ca D 3111 B

CHAPTER 1200-5-1

3113 B-99 3500-Ca B3500-Ca B 97 3111 B-99

200.7

2

3120 B D6919-03

3120 B

3120 B-99

9. Chromium

200.7

2 2

3120 B

3120 B

3120 B-99

200.8 200.9

2

3113 B D1688-95, 02 C D1688-95, 02 A 3113 B 3111 B

3113 B-99 3113 B-99 3111 B-99

10. Copper

200.7

2 2

3120 B

3120 B

3120 B-99

200.8 200.9

2

D1125-95 (Reapproved 1999) A D2036-98 A

2510 B

2510 B 4500-CN⎯ C 4500CN⎯G

2510 B-97

12. Cyanide

Manual Distillation followed by Spectrophotometric, Amenable. Spectro-photometric Manual. Spectro-photometric Semi-automated. Selective Electrode 335.4
6

4500-CN⎯ C

D2036-98 B

4500-CN⎯ G

4500-CN⎯ G-

D2036-98 A

4500-CN⎯E

99 4500-CN⎯ 5 E 4500-CN⎯ E- I-3300-85 99

4500-CN⎯ F

4500-CN⎯ F 4500-CN⎯ F99 Kelada-01

UV, Distillation, Spectrophotometric. Micro Distillation, Flow Injection, Spectrophotometric. Ligand Exchange and Amperometry 13. Fluoride
19

16

QuikChem 10204-00-117 X D6888-04 300.0 , 300.1
18 6

OIA-1677, DW
19

Ion Chromatography

D4327-97, 03

4110 B

4110 B

4110 B-00 4500-F⎯ B, D-

Manual Distill; Color.

4500-F⎯ B, D 4500-F⎯ B,

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
SPADNS. Manual Electrode Automated Electrode Automated Alizarin Capillary Ion Electrophoresis Atomic Absorption; Furnace ICP-Mass spectrometry Atomic Absorption;Platform Differential Pulse Anodic Stripping Voltametry 15. Magnesium Atomic Absorption ICP Complexation Titrimetric Methods Ion Chromatography 16. Mercury Manual, Cold Vapor Automated, Cold Vapor ICP-Mass Spectrometry Inductively Coupled Plasma ICP-Mass Spectrometry Atomic Absorption;Platform Atomic Absorption; Direct Atomic Absorption; Furnace 18. Nitrate Ion Chromatography 300.0
6 2

CHAPTER 1200-5-1

D D1179-93, 99 B 4500-F⎯ C

97

4500-F⎯ C 4500-F⎯ C-97 380-75WE
11

4500-F⎯ E

4500-F⎯ E 4500-F⎯ E-97 129-71W D6508, 22 Rev. 2

11

14. Lead

D3559-96, 03 D 200.8 200.9
2

3113 B

3113 B-99

2

Method 15 1001 D511-93, 03 B 200.7
2

3111 B 3120 B 3120 B

3111 B-99 3120 B-99 3500-Mg B3500-Mg B 97

D511-93, 03 A D6919-03 245.1
2 1 2

3500-Mg E

D3223-97, 02

3112 B

3112 B-99

245.2 200.8 200.7

17. Nickel

2 2

3120 B

3120 B

3120 B-99

200.8 200.9

2

3111 B 3113 B D4327-97, 03 4110 B 4110 B 4500NO3⎯F 4500NO3⎯D 4500NO3⎯E 300.1

3111 B-99 3113 B-99 4110 B-00 4500-NO3⎯ F00 4500-NO3⎯ D -00 4500-NO3⎯ E-00 D6508, Rev 22 2 B-1011
8

Automated Cadmium Reduction Ion Selective Electrode

353.2

6

D3867-90 A

4500-NO3⎯ F

4500-NO3⎯ D

601

7

Manual Cadmium Reduction Capillary Ion Electrophoresis 19. Nitrite Ion Chromatography 300.0
6 2

D3867-90 B

4500-NO3⎯ E

D4327-97, 03

4110 B

4110 B 4500NO3⎯F

4110 B-00 4500-NO3⎯ F -00

B-1011

8

300.1 Automated Cadmium Reduction Manual Cadmium Reduction 353.2

6

D3867-90 A

4500-NO3⎯ F

D3867-90 B

4500-NO3⎯E

4500NO3⎯E

4500-N O3⎯ E-00

August, 2008 (Revised)

60

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
Spectrophotometric Capillary Ion Electrophoresis 20. Orthophosphate
12

CHAPTER 1200-5-1

4500-NO2 ⎯B

4500NO2⎯B

4500-NO2⎯B00 D6508, Rev. 22 2

Colorimetric, Automated, Ascorbic Acid. Colorimetric, ascorbic acid, single reagent. Colorimetric Phosphomolybdate; Automated-segmented flow; Automated Discrete Ion Chromatography

365.1

6

4500-P F D515-88 A 4500-P E

4500-P F 4500-P E I-1601-85 I-2601-90 I-2598-85
5

5

5

300.0 300.1

6

D4327-97, 03

4110 B

4110 B

4110 B-00 D6508, Rev. 2
22

18

Capillary Ion Electrophoresis. 21. pH Electrometric Hydride-Atomic Absorption ICP-Mass Spectrometry Atomic Absorption;Platform Atomic Absorption; Furnace 23. Silica Colorimetric, Molybdate Blue AutomatedsegmentedFlow Colorimetric D859-94, 00. 4500-SiO2 C97 4500-SiO2 4500-SiO2 DD 97 4500-SiO2 4500-SiO2 E E4500-SiO2 C 97 200.7 200.7
2

150.1, 150.2
1

D1293-95, 99 D3859-98, 03 A

4500-H B

+

4500-H B

+

4500-H B 00

+

22. Selenium

3114 B

3114 B-97

200.8 200.9

2

2

D3859-98, 03 B

3113 B

3113 B-99 I-1700-85
5

I-2700-85

5

Molybdosilicate . Heteropoly blue

4500-Si D 4500-Si E

Automated for Molybdate-reactive Silica. Inductively Coupled Plasma Inductively Coupled Plasma Atomic Absorption; Direct Aspiration. Ion Chromatography 25. Temperature Thermometric D6919-03

4500-Si F

3120 B

3120 B

3120 B-99

24. Sodium

2

3111 B

3111 B-99

2550

2550

2550-00

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
26. Thallium ICP-Mass Spectrometry Atomic Absorption;Platform 200.8 200.9
2 2

CHAPTER 1200-5-1

Footnotes 1. ‘‘Methods for Chemical Analysis of Water and Wastes,’’ EPA/600/4-79/020, March 1983. Available at NTIS, PB84128677. 2. ‘‘Methods for the Determination of Metals in Environmental Samples—Supplement I,’’ EPA/600/R-94/111, May 1994. Available at NTIS, PB95-125472. 3. Annual Book of ASTM Standards, 1994, 1996, 1999, or 2003, Vols. 11.01 and 11.02, ASTM International; any year containing the cited version of the method may be used. The previous versions of D1688-95A, D1688-95C (copper), D3559-95D (lead), D1293-95 (pH), D1125-91A (conductivity) and D859-94 (silica) are also approved. These previous versions D1688-90A, C; D3559-90D, D1293-84, D1125-91A and D859-88, respectively are located in the Annual Book of ASTM Standards, 1994, Vol. 11.01. Copies may be obtained from ASTM International, 100 Barr Harbor Drive, West Conshohocken, PA 19428. 4. Standard Methods for the Examination of Water and Wastewater, 18th edition (1992), 19th edition (1995), or 20th edition (1998). American Public Health Association, 1015 Fifteenth Street, NW., Washington, DC 20005. The cited methods published in any of these three editions may be used, except that the versions of 3111 B, 3111 D, 3113 B and 3114 B in the 20th edition may not be used. 5. Method I-2601-90, Methods for Analysis by the U.S. Geological Survey National Water Quality Laboratory—Determination of Inorganic and Organic Constituents in Water and Fluvial Sediment, Open File Report 93-125, 1993; For Methods I1030-85; I-1601-85; I-1700-85; I-2598-85; I-2700-85; and I-3300-85 See Techniques of Water Resources Investigation of the U.S. Geological Survey, Book 5, Chapter A-1, 3rd edition., 1989; Available from Information Services, U.S. Geological Survey, Federal Center, Box 25286, Denver, CO 80225-0425. 6. ‘‘Methods for the Determination of Inorganic Substances in Environmental Samples,’’ EPA/600/R-93/100, August 1993. Available at NTIS, PB94-120821. 7. The procedure shall be done in accordance with the Technical Bulletin 601 ’’ Standard Method of Test for Nitrate in Drinking Water,’’ July 1994, PN 221890-001, Analytical Technology, Inc. Copies may be obtained from ATI Orion, 529 Main Street, Boston, MA 02129. 8. Method B-1011, ‘‘Waters Test Method for Determination of Nitrite/Nitrate in Water Using Single Column Ion Chromatography,’’ August 1987. Copies may be obtained from Waters Corporation, Technical Services Division, 34 Maple Street, Milford, MA 01757, Telephone: 508/482-2131, Fax: 508/482-3625. 9. Method 100.1, ‘‘Analytical Method For Determination of Asbestos Fibers in Water,’’ EPA/600/4-83/043, EPA, September 1983. Available at NTIS, PB83-260471. 10. Method 100.2, ‘‘Determination of Asbestos Structure Over 10-µm In Length In Drinking Water,’’ EPA/600/R-94/134, June 1994. Available at NTIS, PB94-201902. 11. Industrial Method No. 129-71W, ‘‘Fluoride in Water and Wastewater,’’ December 1972, and Method No. 380-75WE, ‘‘Fluoride in Water and Wastewater,’’ February 1976, Technicon Industrial Systems. Copies may be obtained from Bran & Luebbe, 1025 Busch Parkway, Buffalo Grove, IL 60089. 12. Unfiltered, no digestion or hydrolysis. 13. Because MDLs reported in EPA Methods 200.7 and 200.9 were determined using a 2x preconcentration step during sample digestion, MDLs determined when samples are analyzed by direct analysis (i.e., no sample digestion) will be higher. For direct analysis of cadmium and arsenic by Method 200.7, and arsenic by Method 3120 B, sample preconcentration using pneumatic nebulization may be required to achieve lower detection limits. Preconcentration may also be required for direct analysis of antimony, lead, and thallium by Method 200.9; antimony and lead by Method 3113 B; and lead by Method D3559-90D, unless multiple in-furnace depositions are made. 14. If ultrasonic nebulization is used in the determination of arsenic by Methods 200.7, 200.8, or SM 3120 B, the arsenic must be in the pentavalent state to provide uniform signal response. For Methods 200.7 and 3120 B, both samples and standards must be diluted in the same mixed acid matrix concentration of nitric and hydrochloric acid with the addition of 100 µL of 30% hydrogen peroxide per 100 mL of solution. For direct analysis of arsenic with Method 200.8 using ultrasonic nebulization, samples and standards must contain 1 mg/L of sodium hypochlorite. 15. The description for Method Number 1001 for lead is available from Palintest, LTD, 21 Kenton Lands Road, P.O. Box 18395, Erlanger, KY 41018. Or from the Hach Company, P.O. Box 389, Loveland, CO 80539. 16. The description for the Kelada-01 Method, ‘‘Kelada Automated Test Methods for Total Cyanide, Acid Dissociable Cyanide, And Thiocyanate,’’ Revision 1.2, August 2001, EPA # 821-B01-009 for cyanide is available from the National Technical Information Service (NTIS), PB 2001-108275, 5285 Port Royal Road, Springfield, VA 22161. The toll free telephone number is 800-553-6847. Note: A 450-W UV lamp may be used in this method instead of the 550-W lamp specified if it provides performance within the quality control (QC) acceptance criteria of the method in a given instrument. Similarly, modified flow cell configurations and flow conditions may be used in the method, provided that the QC acceptance criteria are met. 17. The description for the QuikChem Method 10-204-00-1-X, ‘‘Digestion and distillation of total cyanide in drinking and wastewaters using MICRO DIST and determination of cyanide by flow injection analysis,’’ Revision 2.1, November 30, 2000, for cyanide is available from Lachat Instruments, 6645 W. Mill Rd., Milwaukee, WI 53218. Telephone: 414-3584200. 18. ‘‘Methods for the Determination of Organic and Inorganic Compounds in Drinking Water,’’ Vol. 1, EPA 815-R-00-014, August 2000. Available at NTIS, PB2000-106981. 19. Method OIA-1677, DW ‘‘Available Cyanide by Flow Injection, Ligand Exchange, and Amperometry,’’ January 2004. EPA821-R-04-001, Available from ALPKEM, A Division of OI Analytical, P.O. Box 9010, College Station, TX 77842-9010. 20. Sulfide levels below those detected using lead acetate paper may produce positive method interferences. Test samples

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)

CHAPTER 1200-5-1

using a more sensitive sulfide method to determine if a sulfide in-terference is present, and treat samples accordingly. 21. Standard Methods Online are available at http://www.standardmethods.org. The year in which each method was approved by the Standard Methods Committee is designated by the last two digits in the method number. The methods listed are the only online versions that may be used. 22. Method D6508, Rev. 2, ‘‘Test Method for Determination of Dissolved Inorganic Anions in Aqueous Matrices Using Capillary Ion Electrophoresis and Chromate Electrolyte,’’ available from Waters Corp, 34 Maple St, Milford, MA, 01757, Telephone: 508/482-2131, Fax: 508/482-3625.

(d)

Detection Limits for Inorganic methodology specified below must be equal to or less than the requirements in the following:
Table 1200-5-1-.14(10)(d) Detection Limits for Inorganic Contaminants MCL Detection Methodology Atomic Absorption Furnace Atomic Absorption: Platform ICP-Mass Spectrometry Hydride-Atomic Absorption limit (mg/1) 0.003 0.00085 0.0004 0.001 0.001
7

Contaminant Antimony

(mg/l) 0.006

Arsenic

0.01

6

Atomic Absorption Furnace Atomic Absorption: Platform Stabilized Temperature Atomic Absorption: Gaseous Hydride ICP-Mass Spectrometry

0.0005 0.0014

0.001
8

Asbestos Barium

7 MFL1 2

Transmission Electron Microscopy Atomic Absorption; furnace technique Atomic Absorption; Direct Aspiration Inductively Coupled Plasma

0.01 MFL 0.002 0.1 0.002(0.001) 0.0002 0.000025 0.0003 0.0003 0.0001 0.001 0.001 0.007(0.001) 0.02 0.005 0.05 0.02 0.0002 0.0002 0.001 0.00065 0.005 0.0005 0.01 0.01 0.05 1 0.01 0.01 0.05 0.01

Beryllium

0.004

Atomic Absorption; Furnace Atomic Absorption; Platform Inductively Coupled Plasma2 ICP-Mass Spectrometry

Cadmium Chromium Cyanide

0.005 0.1 0.2

Atomic Absorption; furnace technique Inductively Coupled Plasma Atomic Absorption; furnace technique Inductively Coupled Plasma Distillation, Spectrophotometric3 Distillation, Automated Spectrophotometric3 Distillation, Selective Electrode3 Distillation, Amenable, Spectrophotometric4

Mercury Nickel

0.002 0.1

Manual Cold Vapor Technique Automated Cold Vapor Technique Atomic Absorption; Furnace Atomic Absorption; Platform Inductively Coupled Plasma2 ICP-Mass Spectrometry

Nitrate

10 (as N)

Manual Cadmium Reduction Automated Hydrazine Reduction Automated Cadmium Reduction Ion Selective Electrode Ion Chromatography

Nitrite

1 (as N)

Spectrophotometric Automated Cadmium Reduction Manual Cadmium Reduction

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
Ion Chromatography Selenium Thallium 0.05 0.002 Atomic Absorption; furnace Atomic Absorption; gaseous hydride Atomic Absorption; Furnace Atomic Absorption; Platform ICP-Mass Spectrometry Footnotes 1 2 3 4 5 6 7. MFL = million fibers per liter > 10 microns.

CHAPTER 1200-5-1

0.004 0.002 0.002 0.001 0.00075 0.0003

___________________________________________________________________________________________

Using a 2X preconcentration step as noted in Method 200.7 Lower method detection limits (MDLs) may be achieved using a 4X preconcentration. Screening method for total cyanides. Measures "free" cyanides. Lower MDLs are reported using stabilized temperature graphite furnace atomic absorption. The value for arsenic is effective January 23, 2006. Until then the MCL is 0.05 mg/L. The MDL reported for EPA method 200.9 (Atomic Absorption; Platform-Stabilized Temperature) was determined using a 2X concentration step during sample digestion. The MCL determined for samples analyzed using direct analyses (i.e, no sample digestion) will be higher. Using multiple depositions, EPA 200.9 is capable of obtaining MDL of 0.0001 mg/L.

8

Using selective ion monitoring, EPA Method 200.8 (ICP-MS) is capable of obtaining a MDL of 0.0001 mg/L.

1.

Laboratories must achieve the method detection limit for lead of 0.001 mg/l according to the procedures in appendix B of part 136 of 40 CFR. This need only be accomplished if the laboratory will be processing source water composite samples under Rule 1200-5-1-.33(9)(a)1(iii). (i) (ii) Lead: 0.001 mg/l (only if source water compositing is done under Rule 1200-5-1-.09); and Copper: 0.001 mg/l or 0.020 mg/l when atomic absorption direct aspiration is used (only if source water compositing is done under Rule 1200-5-1-.09).

2.

The Department has the authority to allow the use of previously collected monitoring data, if the data were collected and analyzed in accordance with the requirements of this rule. All lead levels measured between the PQL and the MDL must be either reported as measured or they can be reported as one-half the PQL (0.0025 mg/l). All levels below the lead MDL must be reported as zero; and All copper levels measured between PQL and the MDL must be either reported as measured or they can be reported as one-half the PQL (0.025 mg/l). All levels below the copper MDL must be reported as zero.

3.

4.

(e)

Laboratories must analyze PE samples within the following acceptance criteria:
Contaminant Acceptance limit Antimony Arsenic Asbestos ±30 at ≥0.006 mg/1 ±30 at ≥0.003 mg/l 2 standard deviations based on study statistics ±15% at ≥0.15 mg/1

Barium

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
Beryllium Cadmium Chromium Cyanide Fluoride Mercury Nickel Nitrate Nitrite Selenium Thallium ±15% at ≥0.001 mg/1 ±20% at ≥0.002 mg/1 ±15% at ≥0.01 mg/1 ±25% at ≥0.1 mg/1 ±10% at ≥1 to 10 mg/1 ±30% at ≥0.0005 mg/1 ±15% at ≥0.01 mg/1 ±10% at ≥0.4 mg/1 ±15% at ≥0.4 mg/1 ±20% at ≥0.01 mg/1 ±30% at ≥0.002 mg/1

CHAPTER 1200-5-1

(f)

Sample collection for antimony, arsenic, asbestos, barium, beryllium, cadmium, chromium, cyanide, fluoride, mercury, nickel, nitrate, nitrite, selenium, and thallium under this Rule shall be conducted using the sample preservation, container, and maximum holding time procedures specified in the table below:
Table 1200-5-1-.14(10)(f) Contaminant Antimony Arsenic Asbestos Barium Beryllium Cadmium Chromium Cyanide Fluoride Mercury Nickel Nitrate Nitrate-Nitrite 6 Nitrite Selenium Thallium Preservative HNO3 Conc HNO3 to pH <2 4°C HNO3 HNO3 HNO3 HNO3 4°C, NaOH None HNO3 HNO3 4°C H2SO4 4°C HNO3 HNO3
1

Container P or G P or G P or G P or G P or G P or G P or G P or G P or G P or G P or G P or G P or G P or G P or G P or G

2

Time

3

6 months 6 months 48 hours 6 months 6 months 6 months 6 months 14 days 1 month 28 days 6 months 48 hours 28 days 48 hours 6 months 6 months
5 4

Footnotes 1 For cyanide determinations samples must be adjusted with sodium hydroxide to pH 12 at the time off collection. When chilling is indicated the sample must be shipped and stored at 4 °C or less. Acidification of nitrate or metals samples may be with a concentrated acid or a dilute (50% by volume) solution of the applicable concentrated acid. Acidification of samples for metals analysis is encouraged and allowed at the laboratory rather than at the time of sampling provided the shipping time and other instructions in Section 8.3 of EPA Methods 200.7 or 200.8 or 200.9 are followed. 2 P=plastic, hard or soft; G=glass, hard or soft. 3 In all cases samples should be analyzed as soon after collection as possible. Follow additional (if any) information on preservation, containers or holding times that is specified in method. 4 Instructions for containers, preservation procedures and holding times as specified in Method 100.2 must be adhered to for all compliance analyses including those conducted with Method 100.1. 5 If the sample is chlorinated, the holding time for an unacidified sample kept at 4 °C is extended to 14 days.

August, 2008 (Revised)

65

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued)
6 Nitrate-Nitrite refers to a measurement of total nitrate.

CHAPTER 1200-5-1

(g)

Certified Laboratories performing analyses for Public Water Systems as required by this rule chapter must utilize an approved method for Organic contaminants listed in the following table:
Table 1200-5-1-.14(10)(g)

Contaminant 1. Benzene 2. Carbon tetrachloride 3. Chlorobenzene 4. 1,2-Dichlorobenzene 5. 1,4-Dichlorobenzene 6. 1,2-Dichloroethane 7. cis-Dichloroethylene 8. trans-Dichloroethylene 9. Dichloromethane 10. 1,2-Dichloropropane 11. Ethylbenzene 12. Styrene 13. Tetrachloroethylene 14. 1,1,1-Trichloroethane 15. Trichloroethylene 16. Toluene 17. 1,2,4-Trichlorobenzene 18. 1,1-Dichloroethylene 19. 1,1,2-Trichloroethane 20. Xylenes (total) 21. Vinyl chloride 22. 2,3,7,8-TCDD (dioxin) 23. 2,4-D (as acid, salts and esters)
4

EPA method

1

Standard Methods

ASTM

Other

502.2, 524.2 502.2, 524.2, 551.1 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2, 551.1 502.2, 524.2, 551.1 502.2, 524.2, 551.1 502.2, 524.2 502.2, 524.2 502.2, 524.2 502.2, 524.2, 551.1 502.2, 524.2 502.2, 524.2 1613 515.2, 555, 515.1, 515.3, 515.4 D5317–93,98 (Reapproved 2003) D5317–93,98 (Reapproved 2003)

24. 2,4,5-TP (Silvex)

4

515.2, 555, 515.1, 515.3, 515.4

25. Alachlor 26. Atrazine

2 2

507, 525.2, 508.1, 505, 551.1 507, 525.2, 508.1, 505, 551.1 Syngenta AG– 625
5

27. Benzo(a)pyrene 28. Carbofuran 29. Chlordane 30. Dalapon 31. Di(2-ethylhexyl)adipate 32. Di(2-ethylhexyl)phthalate

525.2, 550, 550.1 531.1, 531.2 508, 525.2, 508.1, 505 552.1, 515.1, 552.2, 515.3, 515.4, 552.3 506, 525.2 506, 525.2 6610

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33. Dibromochloropropane (DBCP) 34. Dinoseb 35. Diquat 36. Endothall 37. Endrin 38. Ethylene dibromide (EDB) 39. Glyphosate 40. Heptachlor 41. Heptachlor Epoxide 42. Hexachlorobenzene 43. Hexachlorocyclopentadiene 44. Lindane 45. Methoxychlor 46. Oxamyl 47. PCBs (as decachlorobiphenyl)
3 3 4

CHAPTER 1200-5-1

504.1, 551.1 515.2, 555, 515.1, 515.3, 515.4 549.2 548.1 508, 525.2, 508.1, 505, 551.1 504.1, 551.1 547 508, 525.2, 508.1, 505, 551.1 508, 525.2, 508.1, 505, 551.1 508, 525.2, 508.1, 505, 551.1 508, 525.2, 508.1, 505, 551.1 508, 525.2, 508.1, 505, 551.1 508, 525.2, 508.1, 505, 551.1 531.1, 531.2 508A 6610 6651

48. PCBs (as Aroclors) 49. Pentachlorophenol

508.1, 508, 525.2, 505 515.2, 525.2, 555, 515.1, 515.3, 515.4 D5317–93,98 (Reapproved 2003) D5317–93,98 (Reapproved 2003)

50. Picloram

4

515.2, 555, 515.1, 515.3, 515.4

51. Simazine

2

507, 525.2, 508.1, 505, 551.1 508, 508.1, 525.2, 505

52. Toxaphene

Footnotes 1. Previously approved EPA methods remain available for compliance monitoring until June 1, 2001. EPA methods 502.2 Rev. 2.0, 505 Rev. 2.0, 507 Rev. 2.0, 508 Rev. 3.0, 531.1 Rev. 3.0 are in ``Methods for the Determination of Organic Compounds in Drinking Water'', December 1988, revised July 1991; methods 506 and 551 are in ``Methods for the Determination of Organic Compounds in Drinking Water--Supplement I'', July 1990; methods 515.2 Rev. 1.0 and 524.2 Rev. 4.0 are in ``Methods for the Determination of Organic Compounds in Drinking Water--Supplement II,'' August 1992; and methods 504.1 Rev. 1.0, 508.1 Rev. 1.0, 525.2 Rev.1.0 are available from US EPA NERL, Cincinnati, OH 45268 2. Substitution of the detector specified in Method 505, 507, 508, or 508.1 for the purpose of achieving lower detection limits is allowed as follows: Either an electron capture or nitrogen phosphorus detector may be used provided all regulatory requirements and quality control criteria are met. 3. PCBs are qualitatively identified as Aroclors and measured for compliance purposes as decachlorobiphenyl. Users of Method 505 may have more difficulty in achieving the required detection limits than users of Methods 508.1, 525.2 or 508. 4. Accurate determination of the chlorinated esters requires hydrolysis of the sample as described in EPA Methods 515.1, 515.2, 515.3, 515.4, and 555 and ASTM Method D 5317–93, 98 (Reapproved 2003). 5. This method may not be used for the analysis of atrazine in any system where chlorine dioxide is used for drinking water treatment. In samples from all other systems, any result for atrazine generated by Method AG–625 that is greater than one-half the maximum contaminant level (MCL) (in other words, greater than 0.0015mg/L or 1.5 μg/L) must be confirmed using another approved method for this contaminant and should use additional volume of the original sample collected for compliance monitoring. In instances where a result from Method AG–625 triggers such confirmatory testing, the confirmatory result is to be used to determine compliance.

1.

To obtain certification for contaminants 1 through 20 listed in Table 1200-5-1.14(10)(g) laboratories must:

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CHAPTER 1200-5-1

(Rule 1200-5-1-.14, continued) (i) Successfully analyze 80% of the contaminants included in the PE sample. To successfully analyze a contaminant a laboratory must achieve quantitative results which are: within ±40% of the actual amount in the PE sample when the actual amount is less than 0.010 mg/l, within ±20% of the actual amount in the PE sample when the actual amount is greater than or equal to 0.010 mg/l. (ii) 2. Achieve a method detection limit of 0.0005 mg/l, according to the procedures in 40 CFR part 136 Appendix B.

To obtain certification for vinyl chloride a laboratory must: (i) (ii) (iii) Achieve quantitative results on PE samples which are within ±40% of the actual amount of vinyl chloride in the PE sample. Achieve a method detection limit of 0.0005 mg/l, according to the procedures in 40 CFR part 136 Appendix B. Achieve certification for contaminants 1 through 20 listed in Table 1200-51-.14(10)(g).

3.

To obtain certification for contaminants 22 through 52 listed in Table 1200-5-1.14(10)(g) certified laboratories must achieve quantitative results on PE samples within the following acceptance limits:
Table 1200-5-1-.14(10)(g)3.

_________________________________________________________________________________________ Contaminant Acceptance limits (percent) _________________________________________________________________________________________ DBCP EDB Alachlor Atrazine Benzo[a]pyrene Carbofuran Chlordane Dalapon Di(2-ethylhexyl)adipate Di(2-ethylhexyl)phthalate Dinoseb Diquat Endothall Endrin Glyphosate Heptachlor Heptachlor Epoxide Hexachlorobenzene Hexachlorocyclopentadiene Lindane Methoxychlor Oxamyl PCBs (as Decachlorobiphenyl) Picloram + 40 + 40 + 45 + 45 2 standard deviations + 45 + 45 2 standard deviations 2 standard deviations 2 standard deviations 2 standard deviations 2 standard deviations 2 standard deviations + 30 2 standard deviations + 45 + 45 2 standard deviations. 2 standard deviations + 45 + 45 2 standard deviations 0 - 200 2 standard deviations

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Simazine Toxaphene Aldicarb Aldicarb sulfoxide Aldicarb sulfone Pentachlorophenol 2,3,7,8-TCDD (Dioxin) 2,4-D 2,4,5-TP (Silvex)

CHAPTER 1200-5-1

2 standard deviations + 45 2 standard deviations 2 standard deviations 2 standard deviations. + 50 2 standard deviations + 50 + 50

4.

Analysis for PCBs shall be conducted as follows: (i) Each system which monitors for PCBs shall analyze each sample using either Methods 508.1, 525.2, 508, or 505. Users of Method 505 may have more difficulty in achieving the required Aroclor detection limits than users of Methods 508.1, 525.2 or 508. If PCBs (as one of seven Aroclors) are detected (as designated by Table 1200-5-1-.14(10)(e)4.(ii) in any sample analyzed using Methods 505 or 508, the system shall reanalyze the sample using Method 508A to quantitate PCBs (as decachlorobiphenyl).
Table 1200-5-1-.14 (10)(g)4.(ii) Aroclor 1016 1221 1232 1242 1248 1254 1260 Detection Limit (mg/l) 0.00008 0.02 0.0005 0.0003 0.0001 0.0001 0.0002

(ii)

(iii) (h)

Compliance with the PCB MCL shall be determined based upon the quantitative results of analyses using Method 508A.

Analytical methods used to determine compliance with Rule 1200-5-1-.06(5) shall be in accordance with Table 1200-5-1-.14(10)(h).

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CHAPTER 1200-5-1
Table 1200-5-1-.14(10)(h)

Reference (method or page number)
Contaminant Naturally occurring: 11 Gross alpha and beta. 11 Gross alpha Radium 226 Methodology EPA
1

EPA

2

EPA

3

EPA

4

SM

5

ASTM

6

USGS

7

DOE

8

Other

Evaporation Co-precipitation Radon emanation Radio chemical

900.0 903.1 903.0 904.0 908.0 908.1 200.8
3 1

p1 p 16 p 13 p 24

Radium 228 Uranium
12

Radio chemical Radio chemical Fluorometric ICP-MS Alpha spectrometry Laser Phosophorimetry Radio chemical Gamma ray spectrometry. Radio chemistry Gamma ray spectrometry. Radio chemical Liquid scintillation Gamma ray Spectrometry

00-01 00-02 Ra04 Ra03 Ra05

p1 p 19

302, 7110 B 7110 C 7500-Ra C 304, 305, 7500-Ra B

R-1120-76 D 3454-91 D 2460-91 R-1141-76 R-1140-76 R-1142-76 Ra-05 N.Y. GA
9

14

p 19

304, 7500-Ra D 7500-U B th 7500-U C (17 Ed.) 3125

N. Y. 10 N. J. U-04

9

D 2907-91 D 5673-03

R-1180-76 R-118176

00-07

P 33

7500-U C (18 or 19 Ed.) 7500-Cs B

th

th

D 3972-90 D 5174-91 D 2459-72 D 3649-91 D 3649-91 D 4785-88

R-1182-76

U-02

Man-made Radioactive cesium.

901.0 901.1 902.0 901.1 905.0

p4 p 92 p6 p9 p 92 p 29 Sr-04 p 65

R-1111-76 R-1110-76 4.5.2.3

7120 (19 Ed.) 7500-I B 7500-I C 7500-I D th 7120 (19 Ed.) 303, 7500-Sr B

th

Radioactive iodine

4.5.2.3 R-1160-76 Sr-01 Sr-02

906.0 p 34 H-02 p 87 306, 7500-3H B D 4107-91 R-1171-76 th 901.1 p 92 7120 (19 Ed.) D 3649-91 R-1110-76 4.5.2.3 902.0 7500-Cs B D 4785-88 901.0 7500-I B The procedures shall be done in accordance with the documents listed below. The incorporation by reference of documents 1 through 10 was approved by the Director of the Federal Register in accordance with 5 U.S.C. 552(a) and 1 CFR part 51. Copies of the documents may be obtained from the sources listed below. Information reguarding obtaining these documents can be obtained from the Safe Drinking Water Hotline at 800-426-4691. Documents may be inspected at EPA’s Drinking Water Docket, 401 M Street, SW., Washington, DC 20460 (Telephone: 202-260-3027); or at the Office of Federal Register, 800 North Capitol Street, NW., Suite 700, Washington, DC. Footnotes 1 “Prescribed Procedures for Measurement of Radioactivity in Drinking Water”, EPA 600/4-80-032, August 1980. Available at U. S. Department of Commerce, National Technical Information Service (NTIS), 5285 Port Royal Road, Springfield, VA 22161 (Telephone 800-553-6847), PB 80-224744. 2 “Interim Radiochemical Methodology for Drinking Water”, EPA 600/4-75-008(revised), March 1976. Available at NTIS, ibid. PB 253258. 3 “Radiochemistry Procedures Manual”, EPA 520/5-84-006, December 1987. Available at NTIS, ibid. PB 84-215581. 4 “Radiochemical Analytical Procedures for Analysis of Environmental Samples”, March 1979. Available at NTIS, ibid. EMSL LV 053917.

Radioactive Strontium 89, 90. Tritium Gamma emitters

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5 6 7 8 9 10 11 12 13 14
th th th th

CHAPTER 1200-5-1

“Standard Methods for the Examination of Water and Wastewater”, 13 , 17 , 18 , 19 Editions, 1971, 1989, 1992, 1995. Available at American Public Health Association, th th th 1015 Fifteenth Street N. W., Washington, D. C. 20005. All methods are in the 17 , 18 , and 19 editions except 7500-U C Fluorometric Uranium was discontinued after the th th th 17 Edition, 7120 Gamma Emitters is only in the 19 Edition, and 302, 303, 304, 305 and 306 are only in the 13 Edition. Annual Book of ASTM Standards, Vol. 11.02, 1994. Available at American Society for Testing and Materials, 100 Barr Harbor Drive, West Conshohocken, PA 19428. “Methods for Determination of Radioactive Substances in Water and Fluvial Sediments”, Chapter A5 in Book 5 of Techniques of Water-Resources Investigations of the United States Geological Survey, 1977. Available at U. S. Geological Survey (USGS) Information Services, Box 25286, Federal Center, Denver, CO 80225-0425. th “EML Procedures Manual”, 27 Edition, Volume 1, 1990. Available at the Environmental Measurements Laboratory, U. S. Department of Energy (DOE), 376 Hudson Street, New York, NY 10014-3621. “Determination of Ra-226 and Ra-228 (Ra-02)”, January 1980, Revised June 1982. Available at Radiological Sciences Institute Center for Laboratories and Research, New York State Department of Health, Empire State Plaza, Albany, NY 12201. “Determination of Radium 228 in Drinking Water”, August 1980. Available at State of New Jersey, Department of Environmental Protection, Division of Environmental Quality, Bureau of Radiation and Inorganic Analysis Services, 9 Ewing Street, Trenton, NJ 08625. Natural uranium and thorium-230 are approved as gross alpha calibration standards for gross alpha with co-precipitation and evaporation methods; americium-241 is approved with co-precipitation methods. If uranium (U) is determined by mass, a 0.67 pCi/ug of uranium conversion factor must be used. This conservative factor is based on the 1:1 activity ratio of U-234 to U-238 that is characteristic of naturally occurring uranium. ‘‘Determination of Trace Elements in Waters and Wastes by Inductively Coupled Plasma-Mass Spectrometry,’’ Revision 5.4, which is published in ‘‘Methods for the Determination of Metals in Environmental Samples—Supplement I,’’ ’ EPA 600–R–94–111, May 1994. Available at NTIS, PB 95–125472. ‘‘The Determination of Radium-226 and Radium-228 in Drinking Water by Gamma-ray Spectrometry Using HPGE or Ge(Li) Detectors,’’ Revision 1.2, December 2004. Available from the Environmental Resources Center, Georgia Institute of Technology, 620 Cherry Street, Atlanta, GA 30332–0335, USA, Telephone: 404–894–3776. This method may be used to analyze for radium-226 and radium-228 in samples collected after January 1, 2005 to satisfy the radium-226 and radium-228 monitoring requirements specified at 40 CFR 141.26.

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CHAPTER 1200-5-1

When the identification and measurement of radionuclides other than those listed in Table 1200-5-1-.11(1), the following references are to be used, except in cases where alternative methods have been approved by the Department. (i) Procedures for Radiochemical Analysis of Nuclear Reactor Aqueous Solutions, H. L. Krieger and S. Gold, EPA-RA-73-014, USEPA, Cincinnati, Ohio, May, 1973. HASL Procedure Manual, Edited by John H. Harley, HASL 300, ERDA Health and Safety Laboratory, New York, NY., 1973.

(ii) (i)

Public Water Systems required to monitor disinfectant residuals by this Rule Chapter must utilize one of the methods in the following table. In addition Water Systems may use of the ITS free chlorine test strip for the determination of free chlorine. Use of the test strips is described in Method D99–003, ‘‘Free Chlorine Species (HOCl- and OCl-) by Test Strip,’’ Revision 3.0, November 21, 2003, available from Industrial Test Systems, Inc., 1875 Langston St., Rock Hill, SC 29730. Free and total chlorine residuals may be measured continuously by adapting a specified chlorine residual method for use with a continuous monitoring instrument provided the chemistry, accuracy, and precision remain the same. Instruments used for continuous monitoring must be calibrated with a grab sample measurement at least every five days, or with a protocol approved by the Department.
Table 1200-5-1-.14(10)(i)

Methodology

SM (19th or 20th ed)

SM 2 Online

Other O3 Free Cl2 X

Residual measured Combined Cl2 X

1

Total Cl2 X X

ClO
2

Amperometric Titration Low Level Amperometric Titration DPD Ferrous Titrimetric DPD Colorimetric Syringaldazine (FACTS) Iodometric Electrode DPD Amperometric Method II Spectrophotometr ic Indigo Method

4500-Cl D 4500-Cl E 4500-Cl F 4500-Cl G 4500-Cl H 4500-Cl I 4500-ClO2 D 4500-ClO2 E

4500-ClD-00 4500-Cl-E00 4500-Cl-F00 4500-ClG-00 4500-ClH-00 4500-Cl-I00

D 1253-03

3

X X X

X X

X X

X X

4500 ClO2 E-00 327.0 Rev 4 1.1

X X X

4500-O3 B

4500-O3 B-97

Footnotes 1 X indicates method is approved for measuring specified disinfectant residual. Free chlorine or total chlorine may be measured for demonstrating compliance with the chlorine MRDL and combined chlorine, or total chlorine may be measured for demonstrating compliance with the chloramine MRDL. 2 The Standard Methods Online version that is approved is indicated by the last two digits in the method number which is the year of approval by the Standard Method Committee. Standard Methods Online are available at http://www.standardmethods.org.

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3 4

CHAPTER 1200-5-1

Annual Book of ASTM Standards, Vol. 11.01, 2004 ; ASTM International; any year containing the cited version of the method may be used. Copies of this method may be obtained from ASTM International, 100 Barr Harbor Drive, P.O. Box C700 West Conshohocken, PA 19428–2959. EPA Method 327.0, Revision 1.1, ‘‘Determination of Chlorine Dioxide and Chlorite Ion in Drinking Water Using Lissamine Green B and Horseradish Peroxidase with Detection by Visible Spectrophotometry,’’ USEPA, May 2005, EPA 815–R–05– 008. Available online at http://www.epa.gov/safewater/methods/sourcalt.html.

(j)

Analysis conducted to determine compliance with Rule 1200-5-1-.12 shall be made in accordance with the methods described in the following table:
Table 1200-5-1-.14(10)(j) SM 18th and 19th ed. 3120 B 3113 B 3111 D D4327–97, 03 D512–89 Reapproved 1999) B 4110 B 4110 B
4

Contaminant 1. Aluminum

EPA 200.7 200.8
2 2 2 1

ASTM

3

SM 20th ed. 3120 B

4

SM Online 3120 B-99 3113 B-99 3111 D-99 4110 B-00

7

Other

200.9 2. Chloride 300.0

300.1

6

4500–Cl D 4500–Cl B

4500–Cl D 4500–Cl B

4500–Cl D-97 4500–Cl B-97

D6508, Rev. 8 2 3. Color 4. Foaming Agents 5. Iron 200.7 200.9 6. Manganese 200.7 200.8 7. Odor 8. Silver 200.7 200.8 9. Sulfate 300.0
2 2 2 1 6 1 2 2

2120 B 5540 C 3120 B 3111 B 3113 B
2 2 2

2120 B 5540 C 3120 B

2120 B-01 5540 C-00 3120 B-99 3111 B-99 3113 B-99

3120 B 3111 B 3113 B 2150 B 3120 B 3111 B 3113 B D4327–97, 03 4110 B
2–

3120 B

3120 B-99 3111 B-99 3113 B-99

200.9

2150 B 3120 B

2150 B-97 3120 B-99 3111 B-99 3113 B-99 I-3720-85
5

200.9 300.1 375.2

4110 B
2–

4110 B-00

D516–90, 02

4500–SO4 F 4500–SO4 C,D 4500–SO4 E
2– 2–

4500–SO4 F 4500–SO4 C,D 4500–SO4 E D6508, Rev. 8 2
2– 2–

10. Total Dissolved Solids 11. Zinc

200.7 200.8

2 2

2540 C 3120 B 3111 B

2540 C 3120 B

2540 C-97 3120 B-99 3111 B-99

Footnotes 1 ‘‘Methods for the Determination of Inorganic Substances in Environmental Samples,’’ EPA/600/R–93–100, August 1993. Available at NTIS, PB94–120821.

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2 3 4

CHAPTER 1200-5-1

5 6 7 8

‘‘Methods for the Determination of Metals in Environmental Samples—Supplement I,’’ EPA/600/R–94–111, May 1994. Available at NTIS, PB 95–125472. Annual Book of ASTM Standards, 1994, 1996, 1999, or 2004, Vols. 11.01 and 11.02, ASTM International; any year containing the cited version of the method may be used. Copies may be obtained from the ASTM International, 100 Barr Harbor Drive, West Conshohocken, PA 19428. Standard Methods for the Examination of Water and Wastewater, 18th edition (1992), 19th edition (1995), or 20th edition (1998). American Public Health Association, 1015 Fifteenth Street, NW., Washington, DC 20005. The cited methods published in any of these three editions may be used, except that the versions of 3111 B, 3111 D, and 3113 B in the 20th edition may not be used. Method I–3720–85, Techniques of Water Resources Investigation of the U.S. Geological Survey, Book 5, Chapter A–1, 3rd ed., 1989. Available from Information Services, U.S. Geological Survey, Federal Center, Box 25286, Denver, CO 80225–0425. ‘‘Methods for the Determination of Organic and Inorganic Compounds in Drinking Water,’’ Vol. 1, EPA 815-R–00–014, August 2000. Available at NTIS, PB2000–106981. Standard Methods Online are available at http://www.standardmethods.org. The year in which each method was approved by the Standard Methods Committee is designated by the last two digits in the method number. The methods listed are the only online versions that may be used. Method D6508, Rev. 2, ‘‘Test Method for Determination of Dissolved Inorganic Anions in Aqueous Matrices Using Capillary Ion Electrophoresis and Chromate Electrolyte,’’ available from Waters Corp, 34 Maple St., Milford, MA, 01757, Telephone: 508/482–2131, Fax: 508/482–3625.

(k)

Disinfection byproducts 1. Systems required to monitor by this Rule Chapter for disinfection byproducts must utilize the approved methods in the following table:

Table 1200-5-1-.14(10)(k)1. Approved Methods for Disinfection Byproduct Compliance Monitoring 1 2 9 EPA method Standard method SM online Contaminant and methodology TTHM 4 P&T/GC/ElCD & PID 502.2 P&T/GC/MS 524.2 LLE/GC/ECD 551.1 HAA5 LLE (diazomethane)/GC/ECD SPE (acidic methanol)/GC/ECD LLE (acidic methanol)/GC/ECD Bromate Ion chromatography Ion chromatography column reaction IC/ICP–MS Chlorite Amperometric titration Spectrophotometry Ion chromatography
5

ASTM method

3

552.1 552.2, 552.3

5

6251 B

6251 B–94

&

post

300.1 317.0 Rev 2.0 6 326.0 6,7 321.8

6

D 6581–00

,

327.0 Rev 1.1 300.0, 300.1, 317.0 Rev 2.0, 326.0.

8

4500–ClO2 E

8

4500–ClO2 E–00

8

D 6581–00

P&T = purge and trap; GC = gas chromatography; ElCD = electrolytic conductivity detector; PID = photoionization detector; MS = mass spectrometer; LLE = liquid/liquid extraction; ECD = electron capture detector; SPE = solid phase extraction; IC = ion chromatography; ICP–MS = inductively coupled plasma/mass spectrometer. 2 19th and 20th editions of Standard Methods for the Examination of Water and Wastewater, 1995 and 1998, respectively, American Public Health Association; either of these editions may be used. 3 Annual Book of ASTM Standards, 2001 or any year containing the cited version of the method, Vol 11.01. 4 If TTHMs are the only analytes being measured in the sample, then a PID is not required. 5 The samples must be extracted within 14 days of sample collection. 6 Ion chromatography & post column reaction or IC/ICP-MS must be used for monitoring of bromate for purposes of demonstrating eligibility of reduced monitoring, as prescribed in Rule 1200-5-1-.36(6)(b)3(ii). 7 Samples must be preserved at the time of sampling with 50 mg ethylenediamine (EDA)/L of sample and must be analyzed within 28 days.

1

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8

CHAPTER 1200-5-1

Amperometric titration or spectrophotometry may be used for routine daily monitoring of chlorite at the entrance to the distribution system, as prescribed in Rule 1200-5-1-.36(6)(b)2(i)(I). Ion chromatography must be used for routine monthly monitoring of chlorite and additional monitoring of chlorite in the distribution system, as prescribed in Rules 1200-5-1-.36(6)(b)2(i)(II) and (b)2(ii). 9 The Standard Methods Online version that is approved is indicated by the last two digits in the method number which is the year of approval by the Standard Method Committee. Standard Methods Online are available at http://www.standardmethods.org.

2.
DBP TTHM Chloroform Bromodichloromethane Dibromochloromethane Bromoform HAA5 Monochloroacetic Acid Dichloroacetic Acid Trichloroacetic Acid Monobromoacetic Acid Dibromoacetic Acid Chlorite Bromate

Laboratories must achieve quantitative results on the PE sample analyses that are within the following acceptance limits:
Acceptance limits (percent of true value) ±20 ±20 ±20 ±20 Comments

Laboratory must meet all 4 individual THM acceptance limits in order to successfully pass a PE sample for TTHM

±40 ±40 ±40 ±40 ±40 ±30 ±30

Laboratory must meet the acceptance limits for all 5 of the HAA5 compounds in order to successfully pass a PE sample for HAA5

3.

Laboratories must report quantitative data for concentrations at least as low as the ones listed in the following table for all DBP samples analyzed for compliance with Rules 1200-5-1-.06, .36, .37, and .38:
Minimum reporting 1 level (mg/L) 0.0010 0.0010 0.0010 0.0010 Comments

DBP TTHM Chloroform Bromodichloromethane Dibromochloromethane Bromoform HAA5 Monochloroacetic Acid Dichloroacetic Acid Trichloroacetic Acid Monobromoacetic Acid Dibromoacetic Acid Chlorite
2 2

0.0020 0.0010 0.0010 0.0010 0.0010 0.020 Applicable to monitoring as prescribed in Rules 1200-51-.36(6)(b)2(i)(II) and (b)2(ii). Laboratories that use EPA Methods 317.0 Revision 2.0, 326.0 or 321.8 must meet a 0.0010 mg/L MRL for bromate.

Bromate

0.0050 or 0.00010

1

The calibration curve must encompass the regulatory minimum reporting level (MRL) concentration. Data may be reported for concentrations lower than the regulatory MRL as long as the precision and accuracy criteria are met by analyzing an MRL check standard at the lowest reporting limit chosen by the laboratory. The laboratory must verify the accuracy of the calibration curve at the MRL concentration by analyzing an MRL check standard with a concentration less than or equal to 110% of the MRL with each

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CHAPTER 1200-5-1

batch of samples. The measured concentration for the MRL check standard must be ±50% of the expected value, if any field sample in the batch has a concentration less than 5 times the regulatory MRL. Method requirements to analyze higher concentration check standards and meet tighter acceptance criteria for them must be met in addition to the MRL check standard requirement. When adding the individual trihalomethane or haloacetic acid concentrations to calculate the TTHM or HAA5 concentrations, respectively, a zero is used for any analytical result that is less than the MRL concentration for that DBP, unless otherwise specified by the State.
2

4.

Additional analytical methods. Systems required to analyze parameters not included in subparagraph (i) and part (k)1 of this paragraph must use the following methods. A party approved by the EPA or the Department must measure these parameters. (i) (ii) (iii) Alkalinity. All methods allowed in subparagraph (c) of this paragraph for measuring alkalinity. Bromide. EPA Methods 300.0, 300.1, 317.0 Revision 2.0, 326.0, or ASTM D 6581–00. Total Organic Carbon (TOC). Standard Method 5310 B or 5310 B–00 (High-Temperature Combustion Standard Method) or Standard Method 5310 C or 5310 C–00 (Persulfate-Ultraviolet or Heated-Persulfate Oxidation Method) or Standard Method 5310 D or 5310 D–00 (WetOxidation Method) or EPA Method 415.3 Revision 1.1. Inorganic carbon must be removed from the samples prior to analysis. TOC samples may not be filtered prior to analysis. TOC samples must be acidified at the time of sample collection to achieve pH less than or equal to 2 with minimal addition of the acid specified in the method or by the instrument manufacturer. Acidified TOC samples must be analyzed within 28 days. Specific Ultraviolet Absorbance (SUVA). SUVA is equal to the UV absorption at 254 nm (UV254) (measured in m-1 divided by the dissolved organic carbon (DOC) concentration) (measured as mg/L). In order to determine SUVA, it is necessary to separately measure UV254 and DOC. When determining SUVA, systems must use the methods stipulated in Rule 1200-5-1-.14(10)(k)4(iv)(I) to measure DOC and the method stipulated in Rule 1200-5-1-.14(10)(k)4(iv)(II) to measure UV254. SUVA must be determined on water prior to the addition of disinfectants/oxidants by the system. DOC and UV254 samples used to determine a SUVA value must be taken at the same time and at the same location. (I) Dissolved Organic Carbon (DOC). Standard Method 5310 B or 5310 B–00 (High-Temperature Combustion Method) or Standard Method 5310 C or 5310 C–00 (Persulfate-Ultraviolet or Heated-Persulfate Oxidation Method) or Standard Method 5310 D or 5310 D–00 (WetOxidation Method) or EPA Method 415.3 Revision 1.1. DOC samples must be filtered through the 0.45 μm pore-diameter filter as soon as practical after sampling, not to exceed 48 hours. After filtration, DOC samples must be acidified to achieve pH less than or equal to 2 with minimal addition of the acid specified in the method or by the instrument manufacturer. Acidified DOC samples must be analyzed within 28 days of sample collection. Inorganic carbon must be removed from the samples prior to analysis. Water passed through the filter prior to filtration of the sample must serve as the filtered blank. This filtered blank must be analyzed using procedures identical to those used for analysis of the samples and must meet the following criteria: DOC < 0.5 mg/L.

(iv)

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.14, continued) (II)

CHAPTER 1200-5-1 Ultraviolet Absorption at 254 nm (UV254). Standard Method 5910 B or 5910 B–00 (Ultraviolet Absorption Method) or EPA Method 415.3 Revision 1.1. UV absorption must be measured at 253.7 nm (may be rounded off to 254 nm). Prior to analysis, UV254 samples must be filtered through a 0.45 μm pore-diameter filter. The pH of UV254 samples may not be adjusted. Samples must be analyzed as soon as practical after sampling, not to exceed 48 hours.

(v) (vi) (l)

pH. All methods allowed in Table 1200-5-1-.14(10)(c) for measuring pH. Magnesium. All methods allowed in Table 1200-5-1-.14(10)(c) for measuring magnesium.

Cryptosporidium. Systems must analyze for Cryptosporidium using Method 1623: Cryptosporidium and Giardia in Water by Filtration/IMS/FA, 2005, United States Environmental Protection Agency, EPA–815-R–05–002 or Method 1622: Cryptosporidium in Water by Filtration/IMS/FA, 2005, United States Environmental Protection Agency, EPA–815–R–05–001, which are incorporated by reference. The Director of the Federal Register approves this incorporation by reference in accordance with 5 U.S.C. 552(a) and 1 CFR part 51. You may obtain a copy of these methods online from http:// www.epa.gov/safewater/disinfection/lt2 or from the United States Environmental Protection Agency, Office of Ground Water and Drinking Water, 1201 Constitution Ave., NW, Washington, DC 20460 (Telephone: 800–426–4791). You may inspect a copy at the Water Docket in the EPA Docket Center, 1301 Constitution Ave., NW, Washington, DC, (Telephone: 202–566–2426) or at the National Archives and Records Administration (NARA). For information on the availability of this material at NARA, call 202–741–6030, or go to: http://www.archives.gov/federal_register/code_of_federal_regulations/ibr_locations.html 1. Systems must analyze at least a 10 L sample or a packed pellet volume of at least 2 ml as generated by the methods listed in Rule 1200-5-1-.14(10)(l). Systems unable to process a 10 L sample must analyze as much sample volume as can be filtered by two filters approved by EPA for the methods listed in Rule 1200-5-1-.14(10)(l), up to a packed pellet volume of at least 2 ml. (i) Matrix spike (MS) samples, as required by the methods in Rule 1200-5-1.14(10)(l), must be spiked and filtered by a laboratory approved for Cryptosporidium analysis under Rule 1200-5-1-.14(10)(l)4. If the volume of the MS sample is greater than 10 L, the system may filter all but 10 L of the MS sample in the field, and ship the filtered sample and the remaining 10 L of source water to the laboratory. In this case, the laboratory must spike the remaining 10 L of water and filter it through the filter used to collect the balance of the sample in the field.

2.

(ii)

3. 4.

Flow cytometer-counted spiking suspensions must be used for MS samples and ongoing precision and recovery (OPR) samples. Systems must have Cryptosporidium samples analyzed by a laboratory that is approved under EPA’s Laboratory Quality Assurance Evaluation Program for Analysis of Cryptosporidium in Water or a laboratory that has been certified for Cryptosporidium analysis by an equivalent State laboratory certification program.

Authority: T.C.A. §§68-13-704 and 4-5-202. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. Amendment filed November 26, 1990; effective January 10, 1991. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed August, 2008 (Revised) 77

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CHAPTER 1200-5-1

(Rule 1200-5-1-.14, continued) November 21, 2001; effective February 4, 2002. Amendment filed July 31, 2006; effective October 14, 2006. Repeal of and new rule filed June 12, 2008; effective August 26, 2008. 1200-5-1-.15 MONITORING OF CONSECUTIVE PUBLIC WATER SYSTEMS. (1) Each public water system is required to provide monitoring data to the Department as required by Rules 1200-5-1-.07 through 1200-5-1-.12, 1200-5-1-.21, 1200-5-1-.24, 1200-5-1.26 and unregulated contaminant monitoring and reporting as required by the Environmental Protection Agency. Those public water systems which do not practice disinfection and which purchase all of their water from one or more public water systems that treats water may utilize the monitoring results obtained under Rules 1200-5-1-.08 through 1200-5-1-.12, 12005-1-.24, 1200-5-1-.26 and unregulated contaminant monitoring and reporting as required by the Environmental Protection Agency to demonstrate compliance if the public water system that treats water is subject to the referenced monitoring requirements. Consecutive systems that do not disinfect will be required to collect and analyze all samples that must be collected at the tap including asbestos. Those systems purchasing water and which practice disinfection shall not use the monitoring results obtained by another system for contaminants to be monitored in unregulated contaminant monitoring and reporting as required by the Environmental Protection Agency. Those public water systems which purchase all of their water and elect to perform the monitoring required by Rules 1200-5-1-.08 through 1200-5-1-.12, 1200-5-1-.21, 1200-5-1-.24, 1200-5-1-.26 and unregulated contaminant monitoring and reporting as required by the Environmental Protection Agency will have compliance with the MCL determined on the analytical results of its sampling. Those public water systems which purchase all their water and elect to use the analytical results of the system from which it purchases water shall be deemed to be in compliance with the monitoring and MCL requirements provided the seller of water is in compliance. Any violation of an MCL or monitoring requirement by the seller of water will constitute a violation for all systems which purchase water unless samples are taken as described in Paragraph (2) of this section. All public notification requirements as contained in Section 1200-5-1-.19 are the responsibility of the individual public water system regardless of which public water system conducts the analysis. All public water systems must maintain records as required by Section 1200-5-1-.20 of all analytical results which pertain to the system regardless of which system actually did the analysis.

(2)

(3)

(4)

(5)

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 68-13-704, and 68-221-701 et seq. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed September 26, 1988; effective November 10, 1988. Amendment filed August 24, 1992; effective October 8, 1992. Amendments filed June 12, 2008; effective August 26, 2008. 1200-5-1-.16 SITING REQUIREMENTS. (1) Before a person may enter into a financial commitment for or initiate construction of a new public water system or increase capacity of an existing public water system, he shall notify the Department and, to the extent practicable, avoid locating part or all of the new or expanded facility at a site which: (a) (b) Is subject to a significant risk from earthquakes, floods, fires, or other disasters which could cause a breakdown of the public water system or a portion thereof; or Except for intake structures, is within the flood plain of a 100-years flood. 78

August, 2008 (Revised)

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.16, continued) (2)

CHAPTER 1200-5-1

All other siting requirements shall be in accordance with those set forth in “Design Criteria for Public Water Systems” as published by the Department.

Authority: T.C.A. §§4-5-201 et seq. and 68-221-701 et seq. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed April 12, 1996; effective June 26, 1996. 1200-5-1-.17 OPERATION AND MAINTENANCE REQUIREMENTS. (1) All community water systems which are designated as a surface supply and classified as a filtration system and all iron removal plants which use gravity filters must have an operator in attendance and responsible for the treatment process when the plant is in operation. Gravity iron removal plants which have installed continuous monitoring equipment including equipment for turbidity and chlorine residual with alarms and/or shutdown ability may seek approval from the Department to operate the treatment plant in an automated mode without an operator in attendance. All iron removal plants with pressure filters and using a ground water source from an approved sand and gravel formation will not be required to have an operator in attendance during all periods of operation provided suitable protection, acceptable to the Department, is provided. Non–community water systems which are classified as a surface supply will be required to have a full time operator in attendance unless certain continuous monitoring equipment is installed. Pursuant to Tennessee Code Annotated 68–221–904, all operators in direct responsible charge of a water supply system, including the treatment plant and/or distribution system, must be certified by the Department as competent to operate same. Because the proper operation and maintenance of water systems is critical to a system’s ability to provide safe water to the public and to comply with these rules, all water supply systems must comply with the provisions of Rule 1200-5-3. A violation of those rules is a violation of this rule as well. (2) All community water systems and those non-community water systems classified as a surface source shall compile and maintain accurate daily operating records of the water works system on forms prepared and furnished by the Department. The daily operating records shall be submitted in a timely manner so they are received by the Department no later than ten days after the end of the reporting month. Any special reports, deemed necessary by the Department to assure continuous satisfactory operation of the water system, shall be submitted to the Department. Water systems which desire to use their own forms to report the daily operating results to the Department must have prior approval of the form from the Department. (3) All water quality tests, other than those listed in Regulation 1200-5-1-.06 shall be made in accordance with the latest edition of “Standard Methods for the Examination of Water and Wastewater” or alternate methods acceptable to the Department. The schedule of laboratory tests followed in controlling the operation of a waterworks system will vary with the character of the water; therefore, all waterworks systems must have the equipment necessary to perform all laboratory tests pertinent to the control of the plant or system operation, and the equipment shall be maintained in good working order at all times. Laboratory tests pertinent to proper operation shall be prescribed by the Department for each community water system. Chlorine is the recommended disinfection agent. Other agents will be considered by the Department provided they are effective and testing procedures for their effectiveness are recognized in the latest edition of “Standard Methods for the Examination of Water and Wastewater”. All community water systems, using ground water as a raw water source and 79

(4)

August, 2008 (Revised)

PUBLIC WATER SYSTEMS

CHAPTER 1200-5-1

(Rule 1200-5-1-.17, continued) serving more than 50 connections or 150 persons shall continuously chlorinate (unless other disinfection methods are approved) and shall maintain a free chlorine residual in all parts of the distribution system in the amount of not less than 0.2 mg/l. Public Water Systems using surface water shall continuously chlorinate and maintain a free chlorine residual of 0.2 mg/l in all parts of the distribution system. The residual disinfectant concentration specified by this rule shall not be less than 0.2 mg/l in more than 5 percent of the samples each month, for any two consecutive months the system serves water to the public. All public water systems serving 50 or fewer connections that do not disinfect shall install continuous disinfection if the system fails to comply with the maximum contaminant level for coliform, experiences a disease outbreak or is directed to install disinfection by the department. All public water systems serving 50 or fewer connections that do not disinfect shall install continuous disinfection if the system fails to comply with the maximum contaminant level for coliform, experiences a disease outbreak or is directed to install disinfection by the department. (5) All systems submitting samples for microbiological examination to the State laboratory must submit said sample in the bottle(s) provided by the State and return the samples to the proper State laboratory in the shipping carton provided by the State. The cost of postage for shipping the sample to the proper State laboratory shall be paid by the supplier of water. All samples submitted for microbiological examination must be collected and mailed to arrive at the proper State laboratory not later than Thursday noon of any week. Thirty hours is the limit allowed from the time of collection to the time of examination at the proper State laboratory. Pursuant to Section 68–221–711(6) the installation, allowing the installation, or maintenance of any cross–connection, auxiliary intake, or bypass is prohibited unless the source and quality of water from the auxiliary supply, the method of connection, and the use and operation of such cross–connection, auxiliary intake, or bypass has been approved by the Department. The arrangement of sewer, soil, or other drain lines or conduits carrying sewage or other wastes in such a manner that the sewage or waste may find its way into any part of the public water system is prohibited. All community water systems must adopt an ordinance or policy prohibiting all of the above and submit a copy of the executed ordinance or policy to the Department for approval. All community water systems shall develop a written plan for a cross–connection control program to detect and eliminate or protect the system from cross–connections. The written plan must be approved by the Department. After adoption and approval of the cross–connection ordinance or policy and plan, each community water system must establish an ongoing program for the detection and elimination of hazards associated with cross–connections. Records of the cross–connection control program must be maintained by the water supplier and shall include such items as date of inspection, person contacted, recommendations, follow–up, and testing results. (a) Public water systems must develop and implement an ongoing cross-connection program. Cross-connection plans and policies shall present all information in conformance with the “Design Criteria for Community Public Water Systems” as published by the Department. The public water system shall ensure that cross-connections between the distribution system and a consumer’s plumbing are surveyed and/or inspected and determined not to exist or contain a significant risk or are eliminated or controlled by the installation of an approved backflow preventer commensurate with the degree of hazard.

(6)

(b)

(7)

Within one year after the effective date of these regulations all community water system shall prepare an emergency operations plan in order to safeguard the water supply and to alert the public of unsafe drinking water in the event of natural or man-made disasters. Emergency

August, 2008 (Revised)

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(Rule 1200-5-1-.17, continued) operation plans shall be consistent with guidelines established by the State and shall be reviewed and approved by the Department. (8) (a) General-Public water systems, construction contractors and engineers shall follow and document sanitary practices used in inspecting, constructing or repairing water lines, finished water storage facilities, filters and wells. In lieu of writing their own disinfection standard operating procedures, public water systems, engineers and contractors may chose to follow the latest edition of the AWWA standards C-651, C-652 or equivalent methods provided the method has been approved in writing by the department and is available during the inspection, construction, maintenance or repair activity. The documentation shall include bacteriological sample results, construction logs, standard operating procedures and may include photographs where appropriate. All pipes, tanks, filters, filter media and other materials shall be properly disinfected prior to being placed in service. Any disinfectant used to disinfect shall be NSF approved or plain household bleach and used in a manner that assures sufficient contact time and concentration to inactivate any pathogens present. Bacteriological results including line repair records indicating adequacy of disinfection shall be maintained on file by the water system for five years. All public water systems, contractors, and engineers shall prepare and follow standard disinfection procedures approved by the state when inspecting, maintaining, repairing or constructing lines, tanks, filters and wells. Procedures to ensure that water containing excessive concentrations of disinfectant is not supplied to the customers or discharged in such manner as to harm the environment shall be implemented. All materials used for new or repaired water lines, storage facilities, filters, filter media, and wells will be inspected prior to use for any evidence of gross contamination. Any contamination observed shall be removed and the materials protected during installation. (b) Disinfection of New Facilities-Bacteriological samples will be collected and analyzed to verify the effectiveness of the disinfection practices prior to placing new facilities in service. Bacteriological samples shall be collected to determine the effectiveness of the installation process including protecting the pipe material during storage, installation, and disinfection. This can be demonstrated by collecting two sets of microbiological samples 24 hours apart or collecting a single set of microbiological samples 48 hours or longer after flushing the highly chlorinated water from the lines. In either case microbiological samples in each set will be collected at approximately 2,500-foot intervals with samples near the beginning point and at the end point unless alternate sampling frequency and distance between sampling points approval has been obtained from the state. Where sanitary conditions were not maintained before, during or after construction, an additional bacteriological sample shall be collected from a location representing the water from the contaminated area. Unsanitary conditions include failure to document the sanitary handling of materials, to conduct construction inspections and to maintain records, and to document sanitary practices during construction and other hazards such trench flooding during construction. If the constructed facility yields positive bacterial samples, additional flushing, disinfection and bacteriological sampling shall be repeated until the water is coliform free. Disinfection of Existing Facilities-Drinking water mains, storage facilities and filters that have been partially dewatered during inspection or repair shall, after the repair or inspection is completed, be disinfected, and flushed prior to placing it back in service. Bacteriological samples shall be collected immediately or as soon as possible after the repair is completed and from a location representing the water contained in the repaired line, tank or filter. The repaired facility may be returned to service prior to obtaining bacteriological results. If the repaired facility yields positive bacterial samples, additional flushing, disinfection and bacteriological sampling shall be repeated until the water is coliform free. 81

(c)

August, 2008 (Revised)

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.17, continued) 1.

CHAPTER 1200-5-1

If one-half or more of either the original or repeat bacteriological samples collected from the repaired or renovated facility are total coliform positive, the system shall notify the state within 30 days that it has reviewed its disinfection and sampling practices in an attempt to identify why the positive samples occurred and revise its disinfection and sampling plans accordingly. If any public water system collects a fecal coliform positive repeat sample or ecoli positive repeat sample or a total coliform positive repeat sample following an initial positive fecal coliform or e-coli sample collected from the repaired or renovated facility, the system shall notify the state within 24-hours and issue a tier 1 public notice using the language specified in Appendix B of Rule 1200-5-1.19.

2.

(d)

Inspectors, contractors, operators, public water systems or engineers that fail to document and follow adequate disinfection procedures, and fail to collect bacteriological samples during repairs, inspections or maintenance activities that potentially would compromise the microbial quality of the water shall issue a boil water advisory to the customers served by that portion of the public water system prior to returning the facility to service. The boil water advisory shall remain in effect until satisfactory microbial tests results are obtained.

(9)

All community water systems shall be operated and maintained to provide minimum positive pressure of twenty (20) psi throughout the distribution system. No person shall install or maintain a water service connection to any premises where a booster pump has been installed unless such booster pump is equipped with a low pressure cut-off mechanism designed to cut off the booster pump when the pressure on the suction side of the pump drops to twenty (20) psi gauge.

(10) All community water systems having more than 50 service connections shall establish and maintain an adequate flushing program. The flushing program established shall help ensure that dead end and low usage mains are flushed periodically, drinking water standards are met, sediment and air removal and the free chlorine residual specified under Rule 1200-51.17(4) is maintained. Records of each flushing are to be maintained by the water system. These records shall include date, time, location, persons responsible and length of flushing. In addition to the above information, the free chlorine residual will have to be measured and recorded on the end of dead end mains after being flushed. (11) All community public water systems serving more than 50 connections and which have their own source of water shall be required to install, operate and maintain duplicate disinfection equipment. Duplicate disinfection equipment means at least two chlorine cylinders connected to at least two chlorinators. Each set of chlorine cylinders consists of one or more cylinders which may be connected together by an automatic switchover valve. The two sets of chlorine cylinders may tee in to a common feed line leading to the chlorinators, but may not be connected together by an automatic switchover valve. The two sets of chlorine cylinders must be weighed independently and operated simultaneously. At least two chlorinators must be operated at all times with each feeding a part of the required dosage. The chlorinators may discharge to a common manifold piping network to allow multiple injection points. Facilities may be exempt from simultaneously operating duplicate disinfection equipment if the facility has a reliable chlorine residual analyzer with an alarm notifying a manned control center capable of immediately shutting down the treatment facility. Facilities, which are staffed during the time water is treated, can use one set of chlorine cylinders with the automatic switchover device provided the free chlorine residual is checked at the facility every two hours. A reliable free chlorine residual analyzer with an alarm system to a manned control center may be used for unmanned facilities that desire to use one set of chlorine cylinders with the automatic switchover device.

August, 2008 (Revised)

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CHAPTER 1200-5-1

(Rule 1200-5-1-.17, continued) All public water systems which use a hypochlorinator shall be required to have two solution pumps, two tanks for bleach solution and operate both units at the same time. (12) All public water systems which utilize a filtration system shall use the following bed specifications and not exceed the following rates of filtration. (a) Rapid Sand Filtration - 2.0 gallons per minute per square foot for turbidity removal, 3.0 gallons per minute per square foot for iron removal. There must be 30 inches of sand media with an effective size of 0.35 mm to 0.55 mm and a uniformity coefficient not greater than 1.70 (b) High Rate Filtration - 4.0 gallons per minute per square foot for turbidity removal, 4.0 gallons per minute per square foot for iron removal. There must be 30 inches of dual media with 10 to 12 inches of sand and 18 to 20 inches of anthracite. The sand shall have an effective size of 0.35 mm to 0.55 mm and a uniformity coefficient not greater than 1.70. The anthracite shall have an effective size of 0.8 mm to 1.2 mm with a uniformity coefficient not greater than 1.85. (c) Existing water systems with rapid sand filters and approved for higher rates of filtration by the Department will be allowed to continue at that rate provided the drinking water standards are met. The water supplier must be able to document that the Department approved the system for the higher rate. All mixed media filter beds will be at least 30 inches in depth and approved by the Department. Filtration rates above 4.0 gallons per minute per square foot will be considered on an individual basis. The Department will take into account the raw water characteristics, the treatment units, operational history, and operating personnel.

(d) (e)

(13) All community water systems serving 50 connections or more shall install duplicate pumps for the raw water, finished water, and distribution pumping stations. A water system will not be required to have duplicate pumps in a distribution pumping station under the following conditions: limited number of service connections, availability of replacement pumps, maintaining adequate flows and pressures without the pumping station, and for emergency use only. All community public water systems using ground water supplies and having more than 50 service connections must have duplicate wells and/or duplicate pumps in a spring supply unless fed by gravity flow. (14) All community water systems serving 50 connections or more are required to have 24 hours of distribution storage based on the average daily demand for the past twelve months. Distribution storage must be located so that the instantaneous demand can be met in all areas at any time. (a) Systems which purchase water for resale may utilize the storage of the supplier provided the supplier has adequate distribution storage. Water systems that have large ground storage tanks will be given credit for distribution storage provided auxiliary power is available to pump water to the distribution system. Systems which have more than three (3) treatment facilities, have more than one source of water, and which have special power arrangements so that it is unlikely that all units would be down at the same time are not required to have distribution storage provided the peak demand can be met.

(b)

August, 2008 (Revised)

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CHAPTER 1200-5-1

(Rule 1200-5-1-.17, continued) (c) Water systems which have an average daily demand of 10 million gallons or more are not required to have 24 hours of distribution storage provided the system has adopted a contingency plan for emergencies that has been approved by the Department. The contingency plan must demonstrate the water system is able to provide residential service to all customers for a 24 hour period during any emergency involving the shut down of the treatment facility. (d) Public water systems which utilize wells and provide only disinfection, pH adjustment, corrosion inhibitor and/or fluoridation as treatment, may use the capacity of the wells and the plant as part of the distribution storage under the following conditions: 1. 2. The existing distribution storage tank(s) are adequate to meet the peak demands on the system, The well(s), disinfection equipment and other pumping facilities needed to supply water to the distribution storage tank are equipped with an auxiliary power source with automatic controls, and The well field capacity is determined by removing the largest well from consideration.

3. (e)

Public water systems may take into account private distribution storage facilities in the following manner: 1. Private distribution storage may be counted as water system storage provided the private storage tank floats on the water utility’s system and the water used serves both the private and utility system demand. The water utility may reduce the amount of needed distribution storage by subtracting the average daily volume of any water user that has its own storage tank. This can be done provided the private storage tank is used on a daily basis. Private distribution storage tanks used strictly for fire protection by the private owner cannot be in the water systems distribution storage capacity.

2.

3.

(15) All community water systems serving 50 or more service connections must have and maintain up-to-date maps of the distribution system. These maps must show the locations of the water mains, sizes of mains, valves, blow-offs or flush hydrants, air-release valves, and fire hydrants. One up-to-date copy of the overall system distribution map(s) is to be submitted to the Division of Water Supply every five years. (16) All vents on wells, springs, storage tanks, overflows and clearwells shall be properly screened. All overflows on springs and tanks shall be screened and protected. (17) All buildings and equipment used in and for the production and distribution of water (to include chemical and other storage buildings) must be well maintained and be reliable and fit for the purpose for which they are used. This includes, but is not limited to: (a) (b) When a water treatment plant is not producing water and an operator is not in attendance, plant entrances must be locked. Equipment such as chemical feeders, pumps, turbidimeters, pumpage meters, alarm systems, and air tanks shall be maintained and in good working condition. Pumps, tanks, hoses, and other equipment used by system personnel shall be disinfected and dedicated to its use if it comes into contact with water that may be consumed by humans. 84

August, 2008 (Revised)

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.17, continued) (c)

CHAPTER 1200-5-1

Duplicate or backup equipment shall be available as necessary to maintain the production of water meeting drinking water standards. Backup equipment or alternate treatment means shall be available for feeding all chemicals critical for adequate water treatment.

(18) All community water systems planning to or having installed hydrants must protect the distribution system from contamination. All water mains designed for fire protection must be six inches or larger and be able to provide 500 gallons per minute with 20 pounds per square inch residual pressure. Fire hydrants shall not be installed on water mains less than six inches in diameter or on water mains that cannot produce 500 gpm at 20 psi residual pressure unless -the tops are painted red. Out of service hydrants shall have tops painted black or covered with a black shroud or tape.. Existing Class C hydrants (hydrants unable to deliver a flow of 500 gallons per minute at a residual pressure of 20 pounds per square inch (psi) shall have their tops painted red by January 1, 2008. The water system must provide notification by certified mail at least once every five years beginning January 1, 2008, to each fire department that may have reason to utilize the hydrants, that fire hydrants with tops painted red (Class C hydrants) cannot be connected directly to a pumper fire truck. Fire Departments may be allowed to fill the booster tanks on any fire apparatus from an available hydrant by using the water system’s available pressure only (fire pumps shall not be engaged during refill operations from a Class C hydrant). (19) Before any new or modified community water treatment facility can be placed in service, it must be inspected and approved in writing by the Department. (20) Public water systems which adjust the fluoride content of the water supply shall maintain the concentration of fluoride in the finished water between 0.9 mg/l and 1.3 mg/l based on the monthly average. Each water system adjusting the fluoride content to the finished water must monitor for fluoride as required by the system’s individual monitoring program established by the Department. (21) New or modified turbidity removal facilities may not be placed into operation until the facility and the operator have been approved by the Department for the turbidity analysis. (22) All pipe, solder, or flux which is used in the installation or repair of any public water system shall be lead free. This shall not apply to lead joints necessary for the repair of cast iron pipes. The term “lead free” in this section is defined as follows: (a) (b) When used with respect to solders and flux shall mean solders and flux containing not more than two-tenths of one percent (0.2%) lead and When used with respect to pipes and pipe fittings shall mean pipes and pipe fittings containing not more than eight percent (8.0%) lead.

(23) All dead end water mains and all low points in water mains shall be equipped with a blow-off or other suitable flushing mechanism capable of producing velocities adequate to flush the main. (24) All community water systems must establish and maintain a file for customer complaints. This file shall contain the name of the person with the complaint, date, nature of complaint, date of investigation and results or actions taken to correct any problems.

August, 2008 (Revised)

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CHAPTER 1200-5-1

(Rule 1200-5-1-.17, continued) (25) The Department may, upon written notice, require confirmation of any sampling results and also may require sampling and analysis for any contaminant when deemed necessary by the Department to protect the public health or welfare. (26) Those public water systems required to monitor for turbidity and chlorine residual must have the laboratory approved by the Department before the results of these analyses can be accepted for compliance purposes. (27) By December 30, 1991, or 18 months after the determination that a ground water system is influenced by surface water, all public water systems classified as a ground water system impacted by surface water shall utilize treatment techniques which achieve: (a) At least 99.9 percent (3 log) removal and/or inactivation of Giardia lamblia cysts between a point where the raw water is not subject to recontamination by surface water runoff and a point downstream before or at the first customer. At least 99.99 percent (4 log) removal and/or inactivation of viruses between a point where the raw water is not subject to recontamination by surface water runoff and a point downstream before or at the first customer.

(b)

(28) All public water systems using surface water shall provide disinfection to control the biological quality of the water. Due consideration shall be given to the contact time of the disinfectant in the water with relation to pH, ammonia, taste producing substances, temperature, presence and type of pathogens, and trihalomethane formation potential. All disinfection basins must be designed to prevent water short-circuiting the system. The disinfectant will be applied in the manner needed to provide adequate contact time. (29) All community water systems using ground water as the raw water source serving water to more than 50 connections or 150 people will apply the disinfectant in the manner needed for adequate contact time. Contact time for ground water systems shall not be less than 15 minutes prior to the first customer. (30) Any surface supplied public water system or ground water systems under the direct influence of surface water required to filter shall employ filtration in combination with disinfection that will achieve 99.9% (3 log) and 99.99% (4 log) inactivation of Giardia lamblia and viruses respectively between a point where the raw water is not subject to recontamination by surface water runoff and a point downstream before or at the first customer. For the purposes of determining removal or inactivation efficiencies for Giardia lamblia and viruses Table 1200-5-1-.17(30)1 and 1200-5-1-.17(30)2 shall apply. The free residual disinfectant concentration in the water entering the distribution system cannot be less than 0.2 mg/l for more than four hours. TABLE 1200-5-1-.17(30)1 ASSUMED LOG REMOVALS BY FILTRATION METHOD AND REQUIRED LEVELS OF DISINFECTION ____________________________________________________________________________________ Treatment Assumed Log Removal Required minimum level of disinfection

Conventional filtration Direct filtration Slow Sand filtration Diatomaceous Earth August, 2008 (Revised)

Giardia 2.5 2.0 2.0

Viruses 2.0 1.0 2.0

Giardia 0.5 1.0 1.0

Viruses 2.0 3.0 2.0

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(Rule 1200-5-1-.17, continued) filtration 2.0 1.0 1.0 3.0 ____________________________________________________________________________________ TABLE 1200-5-1-.17(30)2 CT VALUES FOR ACHIEVING 1-LOG INACTIVATION OF GIARDIA CYSTS1 ____________________________________________________________________________________ pH Temperature ______________ 0.5°C 5°C 10°C 15°C________ 2,3 Free Chlorine 6 55 39 29 19 7 79 55 41 26 8 115 81 61 41 9 167 118 88 59 Ozone 0.97 0.63 0.48 0.32 Chlorine dioxide 1270 735 615 500 ____________________________________________________________________________________ 1 2 3 Values to achieve 0.5 log inactivation are one half those shown in the table. CT values are for 2.0 mg/l free chlorine. CT values for other concentrations of free chlorine may be taken from Appendix E of the guidance manual for Compliance with the “Filtration and Disinfection Requirements For Public Water Systems Using Surface Water Sources,” October, 1989, Edition, Science and Technology Branch Criteria and Standards Division, Office of Drinking Water, USEPA, Washington, D.C.

(31) Each public water system must certify annually in writing to the State that when acrylamide and epichlorohydrin are used in drinking water systems, the combination (or product) of dose and monomer level does not exceed the levels specified as follows: Acrylamide = 0.05% dosed at 1 ppm (or equivalent) Epichlorohydrin = 0.01% dosed at 20 ppm (or equivalent) Public water systems can rely on manufacturer’s or third parties certification for complying with this requirement. (32) New service taps on existing mains that must be uncovered to make the tap, shall be flushed and the free chlorine residual measured and recorded prior to connecting the service lines. These records shall be retained until the next sanitary survey or for three years. (33) All public water systems shall properly maintain their distribution system finished water storage tanks. Each community water system shall establish and maintain a maintenance file on each of its finished water and distribution storage tanks. These maintenance files must be available for inspection by Department personnel. These files must include the dates and results of all routine water storage tank inspections by system personnel, any reports of detailed professional inspections of the water storage tanks by contractor personnel, dates and details of routine tank cleanings and surface flushings, and dates and details of all tank maintenance activities. The tank inspection records shall include dates of the inspections; the sanitary, coating and structural conditions of the tank; and all recommendations for needed maintenance activities. Community Water Systems shall have a professional inspection performed and a written report produced on each of their finished water and distribution storage tanks at least once every five years. Non-community water systems shall have a professional inspection and written report performed on each of their August, 2008 (Revised)

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(Rule 1200-5-1-.17, continued) atmospheric pressure finished water and distribution storage tanks no less frequently than every five years. Records of these inspections shall be available to the Department personnel for inspection. Persons conducting underwater inspections of finished water storage tanks shall comply with AWWA standard C652-92 or later versions of the standard. (34) Paints and coatings for the interior of potable water storage facilities must be acceptable to the Department. Paints and coatings accepted by the Environmental Protection Agency (EPA) and/or the National Sanitation Foundation (NSF) for potable water contact are generally acceptable to the Department. Paint systems for steel tanks shall be consistent with AWWA Standard D102-78. Factory coated bolted steel tanks shall be in accordance with AWWA D103-87. Wire-wound circular prestressed concrete tanks shall be in accordance with AWWA D110-86. (35) By January 1, 1996, public water systems using surface water and ground water systems under the direct influence of surface water that filter shall have rewash capability. Such systems shall perform a rewash cycle, or filter to waste each time a filter is backwashed. The rewash cycle shall be conducted in a way and manner necessary to prevent the introduction of contaminants such as pathogens and turbidity trapped in the filter into the clear well or distribution system. Existing filter plants may be approved to operate without rewash (filter-to-waste provisions) if existing operational and backwash practices prevent water of unacceptable quality from entering the clearwell or distribution system. To operate without rewash the water system must demonstrate to the Department that filtered water turbidity after backwashing is reliably and consistently below 0.5 NTU immediately after backwashing each filter. Approval to operate without rewash must be approved in writing and approval must be renewed if any modifications are made to the operation or design of the plant. Each filter that operates without rewash must have a continuous recording turbidimeter and retain the records for a period of five years. (36) By January 1, 1995, all chemicals, additives, coatings or other materials used in the treatment, conditioning and conveyance of drinking water must have been approved by the National Sanitation Foundation (NSF) or American National Standards Institute (ANSI) certified parties as meeting NSF product standard 60 and 61. Until 1995, products used for treatment, conditioning and conveyance of drinking water shall have been listed as approved by the US EPA or NSF. (37) Any new Community Water System or Non-Transient Non-Community Water System commencing operation after September 30, 1999 shall have a “Capacity Development Plan” and be a “viable water system.” (38) Public Water Systems identified as not complying or potentially not complying with the requirements of the Safe Drinking Water Act and in accordance with the priorities established in the State’s Capacity Development Strategy shall prepare a “Capacity Development Plan” and demonstrate viability. (39) Public water systems are not permitted to construct uncovered finished water reservoirs after the effective date of this subparagraph. (40) Benchtop and continuous turbidimeters used to determine compliance with limits set forth in this rule chapter must be calibrated at least every three months with primary standards and documented. Documentation shall be maintained for a period not less than five years. Primary standards are Formazin, AMCO clear, Stablcal, or alternatives approved in writing by the Division. Dilute Formazin solutions are unstable and must be prepared on the day of calibration. Manufacturers’ recommendations on calibration procedure must be followed.

August, 2008 (Revised)

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(Rule 1200-5-1-.17, continued) (41) Verifications for benchtop turbidimeters are comparisons to approved reference materials. Verifications for continuous turbidimeters are comparisons to approved reference materials or comparisons to a properly calibrated benchtop turbidimeter. Secondary reference materials are assigned a value immediately after acceptable primary calibration has been completed. Acceptable verifications for turbidity measurements greater than 0.5 NTU must agree within ±10% from the reading assigned to the reference material after primary calibration. Acceptable verifications for measurements 0.5 NTU or less must be within ±0.05 NTU or less from the reading assigned to the reference material after primary calibration. When comparisons are made from a continuous turbidimeter to a benchtop turbidimeter, the continuous measurement must be within ±10% of the benchtop reading for measurements above 0.5 NTU and ±0.05 NTU for reading 0.5 NTU or less. When acceptable verifications are not achieved the instrument must be re-calibrated with primary standards according to paragraph (40) of this rule. Approved reference materials for benchtop turbidimeters are primary standards and materials suggested by the manufacturer such as sealed sample cells filled with metal oxide particles in a polymer gel. The 0.5 NTU ICE-PICTM from Hach is an approved reference material for secondary turbidity verifications for Hach continuous turbidimeters when utilized as per Manufacturers’ recommendations. All other reference materials for turbidimeter verifications must be approved in writing by the Division. Verifications for turbidimeters must be performed according to the following: (a) Verification of benchtop turbidimeters must be performed daily and documented. Verifications must include a sample in the expected working range of the instrument or as close to the working range as possible. Documentation must include: assigned reference material value after calibration, recorded daily reading for all reference standards, instrument identification, and date. Combined filter effluent turbidimeters as required by Rule 1200-5-1-.31(5)(c)1. must be verified daily and documented. When reference material is utilized documentation must include: instrument identification, date, assigned reference material value after calibration, and daily value for reference material. When comparisons to benchtop turbidimeters are utilized documentation must include: instrument identification, date, continuous turbidimeter value, and benchtop turbidimeter value. Individual filter turbidimeters as required by Rule 1200-5-1-.31(5)(c)4. must be verified weekly.

(b)

(c)

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 68-221-701 et seq., and 68-221-704. Administrative History: Original rule filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. Amendment filed November 26, 1990; effective January 10, 1991. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed October 22, 1993; effective January 5, 1994. Amendment filed April 12, 1996; effective June 26, 1996. Amendment filed February 17, 1999; effective May 3, 1999. Amendment filed October 31, 2000; effective January 14, 2001. Amendment filed November 21, 2001; effective February 4, 2002. Amendment filed December 30, 2002; effective March 15, 2003. Amendments filed August 15, 2005; effective October 29, 2005. Amendments filed June 12, 2008; effective August 26, 2008. 1200-5-1-.18 REPORTING REQUIREMENTS. (1) Except where a shorter period is specified in this Chapter, the supplier of water shall report to the Department the results of any test measurement or analysis required by this part within (A) the first ten days following the month in which the result is received or (B) the first ten days following the end of the required monitoring period as stipulated by the Department, which ever of these is shortest. All systems shall report to the Department within forty-eight (48) hours of the failure to comply with Departmental drinking water regulations or other requirements (including failure to 89

(2)

August, 2008 (Revised)

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CHAPTER 1200-5-1

(Rule 1200-5-1-.18, continued) comply with monitoring, maximum contaminant level or treatment technique requirements) set forth in these Rules and Regulations, and in case of any of the following events shall immediately notify the Department and responsible local officials: (a) (b) (c) (3) (4) any major breakdown or failure of equipment in water treatment process which affects the quality or quantity of the water leaving the treatment plant; any serious loss of water service due to a failure of transmission or distribution facilities; or any situation with the water system which presents or may present an imminent and substantial endangerment to health.

Systems are not required to report analytical results to the Department in cases where a State laboratory performs the analysis and reports the results to the Department. The public water system, within 10 days of completing the public notification requirements under 1200-5-1-.19 for the initial public notice and any repeat notices, must submit to the department a certification that it has fully complied with the public notification regulations. The public water system must include with this certification a representative copy of each type of notice distributed, published, posted and made available to the persons served by the system and to the media. The water supply system shall submit to the Department, within the time stated in the request, copies of any records required to be maintained under Section 1200-5-1-.20 hereof or copies of any documents then in existence which the Department is entitled to inspect pursuant to the authority of Public Acts of 1983, Chapter 324. The owner or operator of a community water system or non-transient non-community water system who is required to monitor under unregulated contaminant monitoring and reporting as required by the Environmental Protection Agency shall send a copy of the results of such monitoring and any public notice issued under 1200-5-1-.19 to the Department within 30 days of receipt of the results or issuance of the notice. The community water system or non-transient non-community water system shall furnish the following information on forms provided by the Department to the Department for each sample analyzed under unregulated contaminant monitoring and reporting as required by the Environmental Protection Agency: (a) (b) (c) (d) (e) (f) Results of all analytical methods, including negatives, Name and address of the system that supplied the sample, Contaminant(s), Analytical method(s) used, Date of sample, Date of analysis.

(5)

(6)

(7)

(8)

It shall be a violation of these regulations for any person, public water system, engineer, operator or certified laboratory to: (a) (b) Record data or information and/or report any inaccurate, misleading, false or information known or that should be known to be false; or Report any data or information that is inaccurate, misleading or false because the person reporting has not used reasonable care, judgment or the application of his knowledge in the preparation of the report. Provide inaccurate or false statements to the State. 90

(c)

August, 2008 (Revised)

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.18, continued)

CHAPTER 1200-5-1

Authority: T.C.A. §§4-5-201 et seq., 4-5-202, 68-13-704, 68-221-701 et seq., and 68-221-704. Administrative History: Original rule. filed June 30, 1977; effective August 1, 1977. Amendment filed February 3, 1984; effective February 12, 1985. Amendment filed September 26, 1988; effective November 10, 1988. Amendment filed August 24, 1992; effective October 8, 1992. Amendment filed November 21, 2001; effective February 4, 2002. Amendments filed June 12, 2008; effective August 26, 2008. 1200-5-1-.19 NOTIFICATION OF CUSTOMERS. (1) Each owner and operator of a public water system including community, non-transient noncommunity, and non-community water systems must comply with this rule. (a) Each owner or operator of a public water system must give public notice for all violations of national primary drinking water regulations and for other situations as listed in Table 1200-5-1-.19(1). The term national primary drinking water regulation is used in this rule to include violations of the maximum contaminant level (MCL), maximum residual disinfectant level (MRDL), treatment technique (TT), monitoring requirements, and testing procedures described in these regulations. Appendix A to this rule identifies the tier assignment for each specific violation or situation requiring a public notice.

Table 1200-5-1-.19(1) Violation Categories and Other Situations Requiring a Public Notice ---------------------------------------------------------------------------------------------------------------------------1. NPDWR violations: (i) (ii) (iii) (iv) 2. Failure to comply with an applicable maximum contaminant level (MCL) or maximum residual disinfectant level (MRDL). Failure to comply with a prescribed treatment technique (TT). Failure to perform water quality monitoring, as required by the drinking water regulations. Failure to comply with testing procedures as prescribed by a drinking water regulation.

Variance and exemptions under sections 1415 and 1416 of SDWA: (i) (ii) Operation under a variance or an exemption. Failure to comply with the requirements of any schedule that has been set under a variance or exemption.

3.

Special public notices: (i) (ii) Occurrence of a waterborne disease outbreak or other waterborne emergency. Exceedance of the alternate MCL for nitrate by non-community water systems (NCWS), where the non-community system has been granted an alternate standard by the department. (iii) Exceedance of the secondary maximum contaminant level (SMCL) for fluoride. (iv) Availability of unregulated contaminant monitoring data. (v) Other violations and situations determined by the department to require a public notice under this rule, not already listed in Appendix A. --------------------------------------------------------------------------------------------------------------------(b) Public notice requirements are divided into three tiers to take into account the seriousness of the violation or situation and any potential adverse health effects that may be involved. The public notice requirements for each violation or situation listed in Table 1 of this section are determined by the tier to which it is assigned. Table 1200-5-

August, 2008 (Revised)

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(Rule 1200-5-1-.19, continued) 1-.19(1)(b)2 of this paragraph provides the definition of each tier. Appendix A of this rule identifies the tier assignment for each specific violation or situation. Table 1200-5-1-.19(1)(b)2 Definition of Public Notice Tiers -------------------------------------------------------------------------------------------------------------------------------1. Tier 1 public notice--required for NPDWR violations and situations with significant potential to have serious adverse effects on human health as a result of short-term exposure. 2. 3. Tier 2 public notice--required for all other NPDWR violations and situations with potential to have serious adverse effects on human health.

Tier 3 public notice--required for all other NPDWR violations and situations not included in Tier 1 and Tier 2. -------------------------------------------------------------------------------------------------------------------------------(c) Who must be notified? 1. Each public water system must provide public notice to persons served by the water system, in accordance with this rule. Public water systems that sell or otherwise provide drinking water to other public water systems (i.e., to consecutive systems) are required to give public notice to the owner or operator of the consecutive system; the consecutive system is responsible for providing public notice to the persons it serves. If a public water system has a violation in a portion of the distribution system that is physically or hydraulically isolated from other parts of the distribution system, the Division may allow the system to limit distribution of the public notice to only persons served by that portion of the system which is out of compliance. Permission by the department for limiting distribution of the notice must be granted in writing. A representative copy of the each type of the notice distributed, published, posted and/or made available to the persons served by the system and/or to the media must also be sent to the Division within ten days of completion of each public notification.

2.

3.

(2)

Tier 1 Public Notice--Form, manner, and frequency of notice. (a) Which violations or situations require a Tier 1 public notice? Table 1200-5-1-.19(2) of this paragraph lists the violation categories and other situations requiring a Tier 1 public notice. Appendix A to this rule identifies the tier assignment for each specific violation or situation.

Table 1200-5-1-.19(2) Violation Categories and Other Situations Requiring a Tier 1 Public Notice ------------------------------------------------------------------------------------------------------------------------------1. Violation of the MCL for total coliforms when fecal coliform or E. coli are present in the water distribution system as specified in 1200-5-1-.06, or when the water system fails to test for fecal coliforms or E. coli when any repeat sample tests positive for coliform as specified in 1200-5-1.07; 2. Violation of the MCL for nitrate, nitrite, or total nitrate and nitrite, as defined in 1200-5-1-.06, or when the water system fails to take a confirmation sample within 24 hours of the system's receipt of the first sample showing an exceedance of the nitrate or nitrite MCL, as specified in 1200-5-1.09;

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(Rule 1200-5-1-.19, continued) 3. Exceedance of the alternate MCL for nitrate by non-community water systems (NCWS), where the non-community system has been granted an alternate standard by the department; 4. Violation of the MRDL for chlorine dioxide, as defined in 1200-5-1-.36, when one or more samples taken in the distribution system the day following an exceedance of the MRDL at the entrance of the distribution system exceed the MRDL, or when the water system does not take the required samples in the distribution system, as specified in 1200-5-1-.36; Violation of the turbidity MCL under 1200-5-1-.06, where the department determines after consultation that a Tier 1 notice is required or where consultation does not take place within 24 hours after the system learns of the violation; Violation of the Surface Water Treatment Rule (SWTR) 1200-5-1-.31, Interim Enhanced Surface Water Treatment Rule (IESWTR) or Long Term 1 Enhanced Surface Water Treatment Rule (LT1ESWTR) treatment technique requirement resulting from a single exceedance of the maximum allowable turbidity limit (as identified in Appendix A) where the department determines after consultation that a tier 1 notice is required or where consultation does not take place within 24 hours after the system learns of the violation; Occurrence of a waterborne disease outbreak, as defined in 1200-5-1-.04, or other waterborne emergency (such as a failure or significant interruption in key water treatment processes, a natural disaster that disrupts the water supply or distribution system, or a chemical spill or unexpected loading of possible pathogens into the source water that significantly increases the potential for drinking water contamination); Other violations or situations with significant potential to have serious adverse effects on human health as a result of short-term exposure, as determined by the Division either in its regulations or on a case-by-case basis.

5.

6.

7.

8.

9. Detection of E. coli or enterococci in source water samples as specified in Rule 1200-5-1-.40(3). -----------------------------------------------------------------------------------------------------------------------------(b) When is the Tier 1 public notice to be provided? What additional steps are required? Public water systems must: 1. 2. Provide a public notice as soon as practical but no later than 24 hours after the system learns of the violation; Initiate consultation with the Division agency as soon as practical, but no later than 24 hours after the public water system learns of the violation or situation, to determine additional public notice requirements; and Comply with any additional public notification requirements (including any repeat notices or direction on the duration of the posted notices) that are established as a result of the consultation with the Division. Such requirements may include the timing, form, manner, frequency, and content of repeat notices (if any) and other actions designed to reach all persons served.

3.

(c)

What is the form and manner of the public notice? Public water systems must provide the notice within 24 hours in a form and manner reasonably calculated to reach all persons served. The form and manner used by the public water system are to fit the specific situation, but must be designed to reach residential, transient, and nontransient users of the water system. In order to reach all persons served, water systems are to use, at a minimum, one or more of the following forms of delivery: 1. Appropriate broadcast media (such as radio and television);

August, 2008 (Revised)

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(Rule 1200-5-1-.19, continued) 2. Posting of the notice in conspicuous locations throughout the area served by the water system; 3. 4. (3) Hand delivery of the notice to persons served by the water system; or Another delivery method approved in writing by the department.

Tier 2 Public Notice--Form, manner, and frequency of notice. (a) Which violations or situations require a Tier 2 public notice? Table 1200-5-1-.19(3) of this paragraph lists the violation categories and other situations requiring a Tier 2 public notice. Appendix A to this rule identifies the tier assignment for each specific violation or situation.

Table 1200-5-1-.19(3) Violation Categories and Other Situations Requiring a Tier 2 Public Notice ------------------------------------------------------------------------------------------------------------------------------1. All violations of the MCL, MRDL, and treatment technique requirements, except where a Tier 1 notice is required under subparagraph (2)(a) or where the department determines that a Tier 1 notice is required; 2. Violations of the monitoring and testing procedure requirements, where the department determines that a Tier 2 rather than a Tier 3 public notice is required, taking into account potential health impacts and persistence of the violation; and Failure to comply with the terms and conditions of any variance or exemption in place.

3. 4.

Failure to take corrective action or failure to maintain at least 4-log treatment of viruses (using inactivation, removal, or a Department-approved combination of 4-log virus inactivation and removal) before or at the first customer under Rule 1200-5-1-.40(4)(a). -----------------------------------------------------------------------------------------------------------------------------(b) When is the Tier 2 public notice to be provided? 1. Public water systems must provide the public notice as soon as practical, but no later than 30 days after the system learns of the violation. If the public notice is posted, the notice must remain in place for as long as the violation or situation persists, but in no case for less than seven days, even if the violation or situation is resolved. The department may, in appropriate circumstances, allow additional time for the initial notice of up to three months from the date the system learns of the violation. The department will not grant an extension to the 30-day deadline for any unresolved violation or to allow across-the-board extensions by rule or policy for other violations or situations requiring a Tier 2 public notice. Extensions granted by the department must be in writing. The public water system must repeat the notice every three months as long as the violation or situation persists, unless the department determines that appropriate circumstances warrant a different repeat notice frequency. In no circumstance may the repeat notice be given less frequently than once per year. The department will not allow less frequent repeat notice for an MCL violation under the Total Coliform Rule or a treatment technique violation under the 120056-1-.31. The department will not through its rules or policies permit across-theboard reductions in the repeat notice frequency for other ongoing violations requiring a Tier 2 repeat notice. Departmental determinations allowing repeat notices to be given less frequently than once every three months must be in writing.

2.

August, 2008 (Revised)

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(Rule 1200-5-1-.19, continued) 3. For the turbidity violations specified in this paragraph, public water systems must consult with the division agency as soon as practical but no later than 24 hours after the public water system learns of the violation, to determine whether a Tier 1 public notice under 1200-5-1-.19(2)(a) is required to protect public health. When consultation does not take place within the 24-hour period, the water system must distribute a Tier 1 notice of the violation within the next 24 hours (i.e., no later than 48 hours after the system learns of the violation), following the requirements under 1200-5-1-.19(2)(b) and (c). Consultation with the department is required for: (i) (ii) Violation of the turbidity MCL under 1200-5-1-.06; or Violation of the SWTR, IESWTR or LT1ESWTR treatment technique requirement (1200-5-1-.31) resulting from a single exceedance of the maximum allowable turbidity limit.

(c)

What is the form and manner of the Tier 2 public notice? Public water systems must provide the initial public notice and any repeat notices in a form and manner that is reasonably calculated to reach persons served in the required time period. The form and manner of the public notice may vary based on the specific situation and type of water system, but it must at a minimum meet the following requirements: 1. Unless directed otherwise by the department in writing, community water systems must provide notice by: (i) Mail or other direct delivery to each customer receiving a bill and to other service connections to which water is delivered by the public water system; and Any other method reasonably calculated to reach other persons regularly served by the system, if they would not normally be reached by the notice required in subparagraph (c)1(i) of this paragraph. Such persons may include those who do not pay water bills or do not have service connection addresses (e.g., house renters, apartment dwellers, university students, nursing home patients, prison inmates, etc.). Other methods may include: publication in a local newspaper; delivery of multiple copies for distribution by customers that provide their drinking water to others (e.g., apartment building owners or large private employers); posting in public places served by the system or on the Internet; or delivery to community organizations.

(ii)

2.

Unless directed otherwise by the department in writing, non-community water systems must provide notice by: (i) Posting the notice in conspicuous locations throughout the distribution system frequented by persons served by the system, or by mail or direct delivery to each customer and service connection (where known); and Any other method reasonably calculated to reach other persons served by the system if they would not normally be reached by the notice required in subparagraph (c)2(i). Such persons may include those served who may not see a posted notice because the posted notice is not in a location they routinely pass by. Other methods may include: publication in a local newspaper or newsletter distributed to customers; use of E-mail to notify employees or students; or, delivery of multiple copies in central locations (e.g., community centers).

(ii)

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.19, continued) (4) Tier 3 Public Notice--Form, manner, and frequency of notice. (a)

CHAPTER 1200-5-1

Which violations or situations require a Tier 3 public notice? Table 1200-5-1-.19(4) of this paragraph lists the violation categories and other situations requiring a Tier 3 public notice. Appendix A to this subpart identifies the tier assignment for each specific violation or situation.

Table 1200-5-1-.19(4) Violation Categories and Other Situations Requiring a Tier 3 Public Notice -------------------------------------------------------------------------------------------------------------------------------1. Monitoring violations for the primary drinking water contaminants, except where a Tier 1 notice is required under 1200-5-1-.19(2)(a) or where the department determines that a Tier 2 notice is required; 2. Failure to comply with an approved departmental or EPA testing procedure, except where a Tier 1 notice is required under 1200-5-1-.19(2)(a) or where the department determines that a Tier 2 notice is required; Operation under a variance granted under Section 1415 or an exemption granted under Section 1416 of the Safe Drinking Water Act; Availability of unregulated contaminant monitoring results, as required under 1200-5-1-.19(7), and

3. 4. 5.

Exceedance of the fluoride secondary maximum contaminant level (SMCL), as required under 1200-5-1-.19(8). -------------------------------------------------------------------------------------------------------------------------------(b) When is the Tier 3 public notice to be provided? 1. Public water systems must provide the public notice not later than one year after the public water system learns of the violation or situation or begins operating under a variance or exemption. Following the initial notice, the public water system must repeat the notice annually for as long as the violation, variance, exemption, or other situation persists. If the public notice is posted, the notice must remain in place for as long as the violation, variance, exemption, or other situation persists, but in no case less than seven days (even if the violation or situation is resolved). Instead of individual Tier 3 public notices, a public water system may use an annual report detailing all violations and situations that occurred during the previous twelve months, as long as the timing requirements of subparagraph (b)1 of this paragraph are met.

2.

(c)

What is the form and manner of the Tier 3 public notice? Public water systems must provide the initial notice and any repeat notices in a form and manner that is reasonably calculated to reach persons served in the required time period. The form and manner of the public notice may vary based on the specific situation and type of water system, but it must at a minimum meet the following requirements: 1. Unless directed otherwise by the division in writing, community water systems must provide notice by: (i) Mail or other direct delivery to each customer receiving a bill and to other service connections to which water is delivered by the public water system; and

August, 2008 (Revised)

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(Rule 1200-5-1-.19, continued) (ii) Any other method reasonably calculated to reach other persons regularly served by the system, if they would not normally be reached by the notice required in subparagraph (c)1(i) of this paragraph. Such persons may include those who do not pay water bills or do not have service connection addresses (e.g., house renters, apartment dwellers, university students, nursing home patients, prison inmates, etc.). Other methods may include: Publication in a local newspaper; delivery of multiple copies for distribution by customers that provide their drinking water to others (e.g., apartment building owners or large private employers); posting in public places or on the Internet; or delivery to community organizations. 2. Unless directed otherwise by the division in writing, non-community water systems must provide notice by: (i) Posting the notice in conspicuous locations throughout the distribution system frequented by persons served by the system, or by mail or direct delivery to each customer and service connection (where known); and Any other method reasonably calculated to reach other persons served by the system, if they would not normally be reached by the notice required in subparagraph (c)2(i) of this paragraph. Such persons may include those who may not see a posted notice because the notice is not in a location they routinely pass by. Other methods may include: Publication in a local newspaper or newsletter distributed to customers; use of E-mail to notify employees or students; or, delivery of multiple copies in central locations (e.g., community centers).

(ii)

(d)

In what situations may the Consumer Confidence Report be used to meet the Tier 3 public notice requirements? For community water systems, the Consumer Confidence Report (CCR) may be used as a vehicle for the initial Tier 3 public notice and all required repeat notices, as long as: 1. 2. 3. The CCR is provided to persons served no later than 12 months after the system learns of the violation or situation as required under 1200-5-1-.19(4)(b); The Tier 3 notice contained in the CCR follows the content requirements under 1200-5-1-.19(5); and The CCR is distributed following the delivery requirements under 1200-5-1.19(4)(c).

(5)

Content of the public notice. (a) What elements must be included in the public notice for violations of National Primary Drinking Water Regulations (NPDWR) or other situations requiring a public notice? When a public water system violates a NPDWR or has a situation requiring public notification, each public notice must include the following elements: 1. 2. 3. A description of the violation or situation, including the contaminant(s) of concern, and (as applicable) the contaminant level(s); When the violation or situation occurred; Any potential adverse health effects from the violation or situation, including the standard language under subparagraph (d)1 or (d)2 of this section, whichever is applicable;

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(Rule 1200-5-1-.19, continued) 4. The population at risk, including subpopulations particularly vulnerable if exposed to the contaminant in their drinking water; 5. 6. 7. 8. 9. Whether alternative water supplies should be used; What actions consumers should take, including when they should seek medical help, if known; What the system is doing to correct the violation or situation; When the water system expects to return to compliance or resolve the situation; The name, business address, and phone number of the water system owner, operator, or designee of the public water system as a source of additional information concerning the notice; and A statement to encourage the notice recipient to distribute the public notice to other persons served, using the standard language under subparagraph (d)3 of this paragraph, where applicable.

10.

(b)

What elements must be included in the public notice for public water systems operating under a variance or exemption? 1. If a public water system has been granted a variance or an exemption, the public notice must contain: (i) (ii) (iii) An explanation of the reasons for the variance or exemption; The date on which the variance or exemption was issued; A brief status report on the steps the system is taking to install treatment, find alternative sources of water, or otherwise comply with the terms and schedules of the variance or exemption; and A notice of any opportunity for public input in the review of the variance or exemption.

(iv) 2.

If a public water system violates the conditions of a variance or exemption, the public notice must contain the ten elements listed in subparagraph (a) of this paragraph.

(c)

How is the public notice to be presented? 1. Each public notice required by this section: (i) (ii) (iii) (iv) 2. Must be displayed in a conspicuous way when printed or posted; Must not contain overly technical language or very small print; Must not be formatted in a way that defeats the purpose of the notice; Must not contain language which nullifies the purpose of the notice.

Each public notice required by this section must comply with multilingual requirements, as follows:

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(Rule 1200-5-1-.19, continued) (i) For public water systems serving a twenty-five percent or more of nonEnglish speaking consumers, the public notice must contain information in the appropriate language(s) regarding the importance of the notice or contain a telephone number or address where persons served may contact the water system to obtain a translated copy of the notice or to request assistance in the appropriate language. (d) What standard language must public water systems include in their public notice? Public water systems are required to include the following standard language in their public notice: 1. Standard health effects language for MCL or MRDL violations, treatment technique violations, and violations of the condition of a variance or exemption. Public water systems must include in each public notice the health effects language specified in Appendix B to this rule corresponding to each MCL, MRDL, and treatment technique violation listed in Appendix A to this rule, and for each violation of a condition of a variance or exemption. Standard language for monitoring and testing procedure violations. Public water systems must include the following language in their notice, including the language necessary to fill in the blanks, for all monitoring and testing procedure violations listed in Appendix A to this rule: We are required to monitor your drinking water for specific contaminants on a regular basis. Results of regular monitoring are an indicator of whether or not your drinking water meets health standards. During [compliance period], we ``did not monitor or test'' or ``did not complete all monitoring or testing'' for [contaminant(s)], and therefore cannot be sure of the quality of your drinking water during that time. 3. Standard language to encourage the distribution of the public notice to all persons served. Public water systems must include in their notice the following language (where applicable): Please share this information with all the other people who drink this water, especially those who may not have received this notice directly (for example, people in apartments, nursing homes, schools, and businesses). You can do this by posting this notice in a public place or distributing copies by hand or mail. (6) Notice to new billing units or new customers. (a) What is the requirement for community water systems? Community water systems must give a copy of the most recent public notice for any continuing violation, the existence of a variance or exemption, or other ongoing situations requiring a public notice to all new billing units or new customers prior to or at the time service begins. What is the requirement for non-community water systems? Non-community water systems must continuously post the public notice in conspicuous locations in order to inform new consumers of any continuing violation, variance or exemption, or other situation requiring a public notice for as long as the violation, variance, exemption, or other situation persists.

2.

(b)

(7)

Special notice of the availability of unregulated contaminant monitoring results. (a) When is the special notice to be given? The owner or operator of a community water system of a non-transient, non-community water system required to monitor for unregulated contaminant monitoring and reporting by the Environmental Protection

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(Rule 1200-5-1-.19, continued) Agency must notify persons served by the system of the availability of the results of such sampling no later than 12 months after the monitoring results are known. (b) What is the form and manner of the special notice? The form and manner of the public notice must follow the requirements for a Tier 3 public notice prescribed in paragraph (4)(c), (d)1, and (d)3. The notice must also identify a person and provide the telephone number to contact for information on the monitoring results.

(8)

Special notice for exceedance of the SMCL for fluoride. (a) When is the special notice to be given? Community water systems that exceed the fluoride secondary maximum contaminant level (SMCL) of 2 mg/l as specified in 12005-1-.12 (determined by the last single sample taken in accordance with 1200-5-1-.09, but do not exceed the maximum contaminant level (MCL) of 4 mg/l for fluoride (as specified in 1200-5-1-.06, must provide the public notice in subparagraph (c) of this paragraph to persons served. Public notice must be provided as soon as practical but no later than 12 months from the day the water system learns of the exceedance. A copy of the notice must also be sent to all new billing units and new customers at the time service begins and to the department and State public health officer. The public water system must repeat the notice at least annually for as long as the SMCL is exceeded. If the public notice is posted, the notice must remain in place for as long as the SMCL is exceeded, but in no case less than seven days (even if the exceedance is eliminated). On a case-by-case basis, the department may require an initial notice sooner than 12 months and repeat notices more frequently than annually. What is the form and manner of the special notice? The form and manner of the public notice (including repeat notices) must follow the requirements for a Tier 3 public notice in paragagh(4)(c) and (d)1 and (d)3. What mandatory language must be contained in the special notice? The notice must contain the following language, including the language necessary to fill in the blanks: This is an alert about your drinking water and a cosmetic dental problem that might affect children under nine years of age. At low levels, fluoride can help prevent cavities, but children drinking water containing more than 2 milligrams per liter (mg/l) of fluoride may develop cosmetic discoloration of their permanent teeth (dental fluorosis). The drinking water provided by your community water system [name] has a fluoride concentration of [insert value] mg/l. Dental fluorosis, in its moderate or severe forms, may result in a brown staining and/or pitting of the permanent teeth. This problem occurs only in developing teeth, before they erupt from the gums. Children under nine should be provided with alternative sources of drinking water or water that has been treated to remove the fluoride to avoid the possibility of staining and pitting of their permanent teeth. You may also want to contact your dentist about proper use by young children of fluoride-containing products. Older children and adults may safely drink the water. Drinking water containing more than 4 mg/L of fluoride (the U.S. Environmental Protection Agency's drinking water standard) can increase your risk of developing bone disease. Your drinking water does not contain more than 4 mg/l of fluoride, but we're required to notify you when we discover that the fluoride levels in your drinking water exceed 2 mg/l because of this cosmetic dental problem. For more information, please call [name of water system contact] of [name of community water system] at [phone number]. Some home water treatment units are also available to remove fluoride from drinking water. To learn more about available home water treatment units, you may call NSF International at 1-877-8-NSF-HELP.'

(b)

(c)

August, 2008 (Revised)

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CHAPTER 1200-5-1

(Rule 1200-5-1-.19, continued) (9) Special notice for nitrate exceedances above MCL by non- community water systems (NCWS), where granted permission by the department under 40CFR141.11(d). (a) When is the special notice to be given? The owner or operator of a non-community water system granted permission by the department under 40CFR141.11(d) to exceed the nitrate MCL must provide notice to persons served according to the requirements for a Tier 1 notice under 1200-5-1-.19(2)(a) and (b). What is the form and manner of the special notice? Non-community water systems granted permission by the department to exceed the nitrate MCL under 40CFR141.11(d) must provide continuous posting of the fact that nitrate levels exceed 10 mg/l and the potential health effects of exposure, according to the requirements for Tier 1 notice delivery under 1200-5-1-.19(2)(c) and the content requirements under 1200-5-1-.19(5).

(b)

(10) Notice by department on behalf of the public water system. (a) May the department give the notice on behalf of the public water system? The department may give the notice required by this rule on behalf of the owner and operator of the public water system if the department complies with the requirements of this rule. What is the responsibility of the public water system when notice is given by the department? The owner or operator of the public water system remains responsible for ensuring that the requirements of this rule are met and civil penalties assessed against the system for failure to give the notice and for damages and expenses incurred by the department.

(b)

(11)

Special notice for repeated failure to conduct monitoring of the source water for Cryptosporidium and for failure to determine bin classification or mean Cryptosporidium level. (a) When is the special notice for repeated failure to monitor to be given? The owner or operator of a community or non-community water system that is required to monitor source water under 1200-5-1-.39(2) must notify persons served by the water system that monitoring has not been completed as specified no later than 30 days after the system has failed to collect any 3 months of monitoring as specified in 1200-5-1.39(2)(c). The notice must be repeated as specified in 1200-5-1-.19(3)(b). When is the special notice for failure to determine bin classification or mean Cryptosporidium level to be given? The owner or operator of a community or noncommunity water system that is required to determine a bin classification under 12005-1-.39(11), or to determine mean Cryptosporidium level under 1200-5-1-.39(13), must notify persons served by the water system that the determination has not been made as required no later than 30 days after the system has failed report the determination as specified in 1200-5-1-.39(11)(e) or 1200-5-1-.39(13)(a), respectively. The notice must be repeated as specified in 1200-5-1-.19(3)(b). The notice is not required if the system is complying with a State-approved schedule to address the violation. What is the form and manner of the special notice? The form and manner of the public notice must follow the requirements for a Tier 2 public notice prescribed in 1200-5-1.19(3)(c). The public notice must be presented as required in 1200-5-1-.19(5)(c). What mandatory language must be contained in the special notice? The notice must contain the following language, including the language necessary to fill in the blanks. 1. The special notice for repeated failure to conduct monitoring must contain the following language:

(b)

(c)

(d)

August, 2008 (Revised)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.19, continued)

CHAPTER 1200-5-1

We are required to monitor the source of your drinking water for Cryptosporidium. Results of the monitoring are to be used to determine whether water treatment at the (treatment plant name) is sufficient to adequately remove Cryptosporidium from your drinking water. We are required to complete this monitoring and make this determination by (required bin determination date). We ‘‘did not monitor or test’’ or ‘‘did not complete all monitoring or testing’’ on schedule and, therefore, we may not be able to determine by the required date what treatment modifications, if any, must be made to ensure adequate Cryptosporidium removal. Missing this deadline may, in turn, jeopardize our ability to have the required treatment modifications, if any, completed by the deadline required, (date). For more information, please call (name of water system contact) of (name of water system) at (phone number). 2. The special notice for failure to determine bin classification or mean Cryptosporidium level must contain the following language: We are required to monitor the source of your drinking water for Cryptosporidium in order to determine by (date) whether water treatment at the (treatment plant name) is sufficient to adequately remove Cryptosporidium from your drinking water. We have not made this determination by the required date. Our failure to do this may jeopardize our ability to have the required treatment modifications, if any, completed by the required deadline of (date). For more information, please call (name of water system contact) of (name of water system) at (phone number). 2. Each special notice must also include a description of what the system is doing to correct the violation and when the system expects to return to compliance or resolve the situation.

APPENDIX A TO 1200-5-1-.19.---NPDWR VIOLATIONS AND OTHER SITUATIONS REQUIRING PUBLIC NOTICE1
MCL/MRDL/TT violations Contaminant Tier of public notice required
2

Citation

Monitoring & testing procedure violations Tier of public Citation notice required

I. Violations of National Primary Drinking Water 3 Regulations (NPDWR): A. Microbiological Contaminants 1. Total coliform 2. Fecal coliform/E.coli 3. Turbidity MCL 4. Turbidity MCL(average of 2 days’ samples > 2 NTU) 5. Turbidity (for TT violations resulting from a Single exceedance of maximum allowable turbidity level)

2 1 2 5 2,1
6

1200-5-1-.06(4)(a) 1200-5-1-.06(4)(b) 1200-5-1-.06(4)(a) 1200-5-1-.06(3)(b) 1200-5-1-.31(2)(a) 1200-5-1-.31(2)(a) 1200-5-1-.31(4)(a)2. 1200-5-1-.31(4)(b)2. 1200-5-1-.31(4)(b)2. 1200-5-1-.31(4)(b)2. 1200-5-1-.31(1)-(4)

3 4 1,3 3 3 3

1200-5-1-.07(1)-(2) 1200-5-1-.07(1)-(2) 1200-5-1-.08 1200.-5-1-.08 1200-5-1-.31 1200-5-1-.31 1200-5-1-.31 1200-5-1-.31 1200-5-1-.31(4)

2,1

6. Surface Water Treatment Rule violations other than violations resulting from single exceedance of max. allowable turbidity level (TT) [1200-5-1-.31(4)] 7. Interim Enhanced Surface Water Treatment Rule violations, other than violations resulting from single exceedance of max turbidity level (TT) [1200-5-1-.31(4) 8. Filter Backwash Recycling Rule Violations

2

3

7

2

1200-5-1-.31(1)-(4)

3

1200-5-1-.31(4)®

2

1200-5-1-.31(9)®

3

1200-5-1-/31(9)(b) and (d)

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PUBLIC WATER SYSTEMS (Rule 1200-5-1-.19, continued)
9.Long term 1 Enhanced Surface Water Treatment Rule Violations 10. LT2ESWTR violation 11. Ground Water Rule violations B. Inorganic Chemicals (IOCs) 1. Antimony 2. Arsenic 3. Asbestos (fibers >10 µm) 4. Barium 5. Beryllium 6. Cadmium 7. Chromium (total) 8. Cyanide 9. Fluoride 10. Mercury (inorganic) 11. Nickel 12. Nitrate 13. Nitrite 14. Total Nitrate and Nitrite 15. Selenium 16. Thallium C. Lead and Copper Rule (Action Level for lead is 0.015 mg/L, for copper is 1.3 mg/L) 1. Lead and Copper Rule (TT) D. Synthetic Organic Chemicals (SOCs) 1. 2,4-D 2. 2,4,5-TP (Silvex) 3. Alachlor 4. Atrazine 5. Benzo(a)pyrene (PAHs) 6. Carbofuran 7. Chlordane 8. Dalapon 9. Di (2-ethylhexyl) adipate 10. Di (2-ethylhexyl) phthalate 11. Dibromochloropropane 12. Dinoseb 13. Dioxin (2,3,7,8-TCDD) 14. Diquat 15. Endothall 16. Endrin 17. Ethylene Dibromide 18.Glyphospate 19. Heptachlor 20. Heptachlor epoxide 21. Hexachlorobenzene 22. Hexachlorocyclo-pentadiene 23. Lindane 24. Methoxchlor 25. Oxamyl (Vydate) 26. Pentachlorophenol 27. Picloram 28. Polychlorinated biphenyls (PCBs) 29. Simazine 30. Toxaphene E. Volatile Organic Chemicals (VOCs) 1. Benzene 2. Carbon tetrachloride 3. Chlorobenzene (monochlorbenzene) 4. o-Dichlorobenzene 5. p-Dichlorobenzene 6. 1,2-Dichloroethane 7. 1,1-Dichloroethylene 8. cis-1,2-Dichloroethylene 9. trans-1,2-Dichloroethylene 10. Dichloromethane 11. 1,2-Dichloropropane 12. Ethylbenzene 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1 1 1 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 1200-5-1-.31(4) 1200-5-1-.39(11)-(21) Rule 1200-5-1-.40(5) 1200-5-1-.06(1)(b)1. 8 1200-5-1-.06(1)(b)2. 1200-5-1-.06(1)(b)3. 1200-5-1-.06(1)(b)5. 1200-5-1-.06(1)(b)4. 1200-5-1-.06(1)(b)6. 1200-5-1-.06(1)(b)7. 1200-5-1-.06(1)(b)8. 1200-5-1-.06(1)(b)9. 1200-5-1-.06(1)(b)10. 1200-5-1-.06(1)(b)11. 1200-5-1-.06(1)(b)12. 1200-5-1-.06(1)(b)13. 1200-5-1-.06(1)(b)14. 1200-5-1-.06(1)(b)15. 1200-5-1-.06(1)(b)16. 1200-5-1-.33(1)-(6) 1200-5-1-.06(2)(a)6. 1200-5-1-.06(2)(a)14. 1200-5-1-.06(2)(a)1. 1200-5-1-.06(2)(a)2. 1200-5-1-.06(2)(a)16. 1200-5-1-.06(2)(a)3. 1200-5-1-.06(2)(a)4. 1200-5-1-.06(2)(a)17. 1200-5-1-.06(2)(a)18. 1200-5-1-.06(2)(a)19. 1200-5-1-.06(2)(a)20. 1200-5-1-.06(2)(a)20. 1200-5-1-.06(2)(a)29. 1200-5-1-.06(2)(a)21. 1200-5-1-.06(2)(a)22. 1200-5-1-.06(2)(a)30. 1200-5-1-.06(2)(a)7. 1200-5-1-.06(2)(a)23. 1200-5-1-.06(2)(a)8. 1200-5-1-.06(2)(a)9. 1200-5-1-.06(2)(a)24. 1200-5-1-.06(2)(a)25. 1200-5-1-.06(2)(a)10. 1200-5-1-.06(2)(a)11. 1200-5-1-.06(2)(a)26. 1200-5-1-.06(2)(a)15. 1200-5-1-.06(2)(a)27. 1200-5-1-.06(2)(a)12. 1200-5-1-.06(2)(a)28. 1200-5-1-.06(2)(a)13. 1200-5-1-.25(2)(e) 1200-5-1-.25(2)(b) 1200-5-1-.25(2)(1) 1200-5-1-.25(2)(m) 1200-5-1-.25(2)(h) 1200-5-1-.25(2)(d) 1200-5-1-.25(2)(f) 1200-5-1-.25(2)(i) 1200-5-1-.25(2)(q) 1200-5-1-.25(2)(s) 1200-5-1-.25(2)(j) 1200-5-1-.25(2)(k) 3
22

CHAPTER 1200-5-1
1200-5-1-.31(6) 2,3 1200-5-1-.39(2)-(6) 1200-5-1-.39(9)-(10) 1200-5-1-.40(3)(m) 1200-5-1-.40(4)(d) 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09 1200-5-1-.09
11

3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3 3

12 12

1,3 1,3

1200-5-1-.33 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.10 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26

August, 2008 (Revised)

103

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.19, continued)
13. Styrene 14. Tetrachloroethylene 15. Toluene 16. 1,2,4-Trichlorobenzene 17. 1,1,1-Trichloroethane 18. 1,1,2-Trichloroethane 19. Trichloroethylene 20. Vinyl chloride 21. Xylenes (total) F. Radioactive Contaminants 1. Beta/photon emitters 2. Alpha emitters 3. Combined radium (226 & 228) 4. Uranium G. Disinfection Byproducts (DBPs), Byproduct Precursors, Disinfectant Residuals. Where Disinfection is used in the treatment of drinking water, disinfectants combine with organic and inorganic matter present in water to form chemicals called disinfection byproducts (DBPs). EPA sets standards for controlling the levels of disinfectants and DBPs in drinking water including trihalomethanes (THMs) and haloacetic 13 acids (HAAs). 1. Total trihalomethanes (TTHMs) 2. Haloacetic Acids (HAA5) 3. Bromate 4. Chlorite 5. Chlorine (MRDL) 6. Chloramine (MRDL) 2 2 2 2 2 2 2 2 2 2 2 2 9 2 1200-5-1-.25(2)(n) 1200-5-1-.25(2)(o) 1200-5-1-.25(2)(p) 1200-5-1-.25(2)(t) 1200-5-1-.25(2)(g) 1200-5-1-.25(2)(w) 1200-5-1-.25(2)(a) 1200-5-1-.25(2)(c) 1200-5-1-.25(2)(r) 1200-5-1-.06(5)(b) 1200-5-1-.06(5)(a) 1200-5-1-.06(5)(a)2. 1200-5-1-.06(5)(c) 3 3 3 3 3 3 3 3 3 3 3 3

CHAPTER 1200-5-1
1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.26 1200-5-1-.11 1200-5-1-.11 1200-5-1-.11 1200-5-1-.11

10-

3

2 2 2 2 2 2

14

1200-5-1-.06(6)(b)

3 3 3 3 3 3
15

1200-5-1-.06(6)(b) 1200-5-1-.06(6)(a) 1200-5-1-.06(6)(a) 1200-5-1-.06(6)(c) 1200-5-1-.06(6)(c)

1200-5-1-36,.37, and 38 1200-5-1-.36,.37 and .38 1200-5-1-.36 1200-5-1-.36 1200-5-1-.36 1200-5-1-.36

7. Chlorine dioxide (MRDL), where any 2 consecutive daily samples at entrance to distribution system only are above MRDL 8. Chlorine dioxide (MRDL), where sample(s) in distribution system the next day are also above MRDL 9. Control of DBP precursors—TOC (TT) 10. Bench marking and disinfection profiling 11. Development of monitoring plan H. Other Treatment Techniques 1. Acrylamide (TT) 2. Epichlorohydrin (TT) 17 II. Unregulated Contaminant Monitoring: A. Unregulated contaminants B. Nickel III. Public Notification for Variances and Exemptions: A. Operation under a variance or exemption B. Violation of conditions of a variance or 19 exemption IV. Other Situations Requiring Public Notification: A. Fluoride secondary maximum contaminant Level (SMCL) exceedance B. Exceedance of nitrate MCL for noncommunity systems, as allowed by department C. Availability of unregulated contaminant monitoring data D. Waterborne disease outbreak 20 E. Other waterborne emergency F. Other situations as determined by the department G. Source Water Sample Positive for GWR Fecal indicators: E. coli or enterococci

2
16

1200-5-1.36(7)(c)2.(ii) 1 1200-5-1-.36(7)(c)2.(i) 1200-5-1-.36-(7)(d) N/A N/A 1200-5-1-.17(31) 1200-5-1-.17(31) N/A 1200-5-1-.06(b)

2 ,3 1 3 3 3 N/A N/A 3 3

1200-5-1-.36 1200-5-1-.36 1200-5-1-.36 1200-5-1-.36 1200-5-1-.36 N/A N/A 1200-5-1-.09

2 N/A N/A 2 2 N/A 2

3 2

1200-5-1-.19(2)(b) 1200-5-1-.19(2)(b)

18

N/A N/A

N/A N/A

3 1 3 1 1 1

1200-5-1-.19(q) 1200-5-1-.19(1)(a)3. 1200-5-1-.19(10) 1200-5-1-.31(2)(c)2. N/A N/A Rule 1200-5-1.40(3)(l)

N/A N/A N/A N/A N/A N/A N/A

N/A N/A N/A N/A N/A N/A N/A

21

1, 2, 3

August, 2008 (Revised)

104

PUBLIC WATER SYSTEMS (Rule 1200-5-1-.19, continued) Appendix A –Endnotes

CHAPTER 1200-5-1

1. Violations and other situations not listed in this table (e.g., failure to prepare Consumer Confidence Reports), do not require notice, unless otherwise determined by the department. The department may, at its option, also require a more stringent public notice tier (e.g., Tier 1 instead of Tier 2 or Tier 2 instead of Tier 3) for specific violations and situations listed in this Appendix, as authorized under 1200-5-1-.19(2)(a) and (3)(a). 2. MCL – Maximum contaminant level, MRDL – Maximum residual disinfectant level, TT-Treatment technique. 3. The term Violations of National Primary Drinking Water Regulations (NPDWR) is used here to include violations of MCL, MRDL, treatment technique, monitoring, and testing procedure requirements. 4. Failure to test for fecal coliform or E.coli is a Tier 1 violation if testing is not done after any repeat sample tests positive for coliform. All other total coliform monitoring and testing procedure violations are Tier 3. 5. Systems that violate the turbidity MCL of 2 NTU based on an average of measurements over two consecutive days must consult with the department within 24 hours after learning of the violation. Based on this consultation, the department may subsequently decide to elevate the violation to Tier 1. If a system is unable to make contact with the department in the 24-hour period, the violation is automatically elevated to Tier 1. 6. Systems with treatment technique violations involving a single exceedance of a maximum turbidity limit under the Surface Water Treatment Rule, Interim Enhanced Surface Water Treatment Rule, or the Long Term 1 Enhanced Surface Water Treatment Rule (1200-5-1-.31) are required to consult with the Department within 24 hours after learning of the violation. Based on this consultation, the department may subsequently decide to elevate the violation to Tier 1. If a system is unable to make contact with the department in the 24-hour period, the violation is automatically elevated to Tier 1. 7. Most of the requirements of the Interim Enhanced Surface Water Treatment Rule 1200-5-1-.31 become effective January 1, 2002 for Subpart H systems (surface water systems and ground water systems under the direct influence of surface water) serving at least 10,000 persons. The Surface Water Treatment Rule remains in effect for systems serving at least 10,000 persons even after 2002; the Interim Enhanced Surface Water Treatment Rule adds additional requirements and does not in many cases supercede the SWTR. 8. The arsenic MCL citations are effective January 23, 2006, or the effective date of this rule whichever comes first. 9. The uranium MCL tier 2 violation citations are effective December 8, 2003 for all community water systems. 10. The uranium tier 3 violations are effective December 8, 2003, for all community water systems 11. The arsenic Tier 3 MCL violations are effective January 23, 2006 or the effective date of this rule whichever comes first. 12. Failure to take a confirmation sample within 24 hours for nitrate or nitrite after an initial sample exceeds the MCL is a Tier 1 violation. Other monitoring violations for nitrate are Tier 3. 13. Subpart H community and non-transient non-community systems serving ≥10,000 must comply with new DBP MCLs, disinfectant MRDLs, and related monitoring requirements beginning January 1, 2002. All other community and non-transient noncommunity systems must meet the MCLs and MRDLs beginning January 1, 2004. Subpart H transient non-community systems serving 10,000 or more persons and using chlorine dioxide as a disinfectant or oxidant must comply with the chlorine dioxide MRDL beginning January 1, 2002. Subpart H transient non-community systems serving fewer than 10,000 persons and using only ground water not under the direct influence of surface water and using chlorine dioxide as a disinfectant or oxidant must comply with the chlorine dioxide MRDL beginning January 1, 2004. 14. 1200-5-1-.06(6), 1200-5-1-36(5(a)-(b) apply until 1200-5-1-.38(1)-(11) take effect under the schedule in 1200-5-1-.38(1)(c) 15. Failure to monitor for chlorine dioxide at the entrance to the distribution system the day after exceeding the MRDL at the entrance to the distribution system is a Tier 2 violation. 16. If any daily sample taken at the entrance to the distribution system exceeds the MRDL for chlorine dioxide and one or more samples taken in the distribution system the next day exceed the MRDL, Tier 1 notification is required. Failure to take the required samples in the distribution system after the MRDL is exceeded at the entry point also triggers Tier 1 notification. 17. Some water systems must monitor for certain unregulated contaminants. 18. This citation refers to §§1415 and 1416 of the Safe Drinking Water Act. §§1415 and 1416 require that “a schedule prescribed… for a public water system granted a variance [or exemption] shall require compliance by the system…” 19. In addition to §§1415 and 1416 of the Safe Drinking Water Act, 40 CFR 142.307 specifies the items and schedule milestones that must be included in a variance for small systems. 20. Other waterborne emergencies require a Tier 1 public notice under 1200-5-1-.19(2)(a) for situations that do not meet the definition of a waterborne disease outbreak given in 1200-5-1-.04 but that still have the potential to have serious adverse effects on health as a result of short-term exposure. These could include outbreaks not related to treatment deficiencies, as well as situations that have the potential to cause outbreaks, such as failures or significant interruption in water treatment processes, natural disasters that disrupt the water supply or distribution system, chemical spills, or unexpected loading of possible pathogens onto the source water. 21. The department may place other situations in any tier it believes appropriate, based on threat to public health. . 22 Failure to collect three or more samples for cryptosporidium analysis is a Tier 2 violation requiring special notice as specified in 1200-5-1-.19(11). All other monitoring and testing procedure violations are Tier 3.

APPENDIX B TO 1200-5-1-.19. –STANDARD HEALTH EFFECTS FOR PUBLIC NOTIFICATION
Contaminant National Primary Drinking Water Regulations (NRDWR): A. Microbiological Contaminants 1a. Total coliform MCLG mg/l
1

MCL mg/l

2

Standard health effects language for public notification

Zero

See 3 note

foot

Coliforms are bacteria that are naturally present in the environment and are used as an indicator that other, potentially-harmful, bacteria may be present. Coliforms

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1b. Fecal coliform/E.coli Zero Zero

CHAPTER 1200-5-1
were found in more samples than allowed and this was a warning of potential problems. Fecal coliforms and E.coli are bacteria whose presence indicates that the water may be contaminated with human or animal wastes. Microbes in these wastes can cause short-term effects, such as diarrhea, cramps, nausea, headaches, or other symptoms. They may pose a special health risk for infants, young children, some of the elderly, and people with severely compromised immune systems. Fecal indicators are microbes whose presence indicates that the water may be contaminated with human or animal wastes. Microbes in these wastes can cause short-term health effects, such as diarrhea, cramps, nausea, headaches, or other symptoms. They may pose a special health risk for infants, young children, some of the elderly, and people with severely compromised immune systems. Inadequately treated or inadequately protected water may contain disease-causing organisms. These organisms can cause symptoms such as diarrhea, nausea, cramps, and associated headaches. Turbidity has no health effects. However, turbidity can interfere with disinfection and provide a medium for microbial growth. Turbidity may indicate the presence of disease-causing organisms. These organisms include bacteria, viruses, and parasites that can cause symptoms such as nausea, cramps, diarrhea and associated headaches. Turbidity has no health effects. However, turbidity can interfere with disinfection and provide a medium for microbial growth. Turbidity may indicate the presence of disease-causing organisms. These organisms include bacteria, viruses, and parasites that can cause symptoms such as nausea, cramps, diarrhea and associated headaches. Turbidity has no health effects. However, turbidity can interfere with disinfection and provide a medium for microbial growth. Turbidity may indicate the presence of disease-causing organisms. These organisms include bacteria, viruses, and parasites that can cause symptoms such as nausea, cramps, diarrhea and associated headaches.

1c. Fecal indicators (GWR) i. E. coli ii. Enterococci

Zero None

TT TT

1d. Ground Water Rule (GWR) TT violations 2a. Turbidity (MCL)
4

None

TT

None

1 NTU NTU

5

/2

2b. Turbidity (SWTR TT) (surface water and ground water under the direct influence)

6

None

TT

7

2c. Turbidity (IESWTR and 8 LT1ESWTR TT) (surface water and ground water under the direct influence of surface water)

None

TT

B. Surface Water Treatment Rule (SWTR) Long Term 1 (LT1ESWTR) and Interim Enhanced Surface Water Treatment Rule (IESWTR) violations: 3. Giardia lamblia (SWTR/ IESWTR/LT1ESWTR) 4. Viruses (SWTR/IESWTR/ LT1ESWTR). 5. Heterotrophic plate count 9 (HPC) bacteria (SWTR/(IESWTR/LT1ESWTR). 6. Legionella (SWTR/IESWTR/LT1ESWTR). 7. Cryptosporidium (IESWTR/LT1ESWTR) C. Inorganic Chemicals 8. Antimony

Zero

TT

10

Inadequately treated water may contain disease-causing organisms. These organisms include bacteria, viruses, and parasites which can cause symptoms such as nausea, cramps, diarrhea, and associated headaches. Same as B.3. Same as B.3. Same as B.3. Same as B.3.

0.006

0.006

9. Arsenic

11

0

0.01

10. Asbestos (10 µm)

7 MFL

12

7 MFL

Some people who drink water containing antimony well in excess of the MCL over many years could experience increases in blood cholesterol and decreases in blood sugar. Some people who drink water containing arsenic in excess of the MCL over many years could experiences skin damage or problems with their circulatory system, and may have an increased risk of getting cancer. Some people who drink water containing asbestos in excess of the MCL over many years may have an increased risk of developing benign intestinal polyps.

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11. Barium 12. Beryllium 13. Cadmium 14. Chromium (total) 15. Cyanide 16. Fluoride 2 0.004 0.005 0.1 0.2 4.0 2 0.004 0.005 0.1 0.2 4.0

CHAPTER 1200-5-1

17. Mercury (inorganic) 18. Nitrate

0.002 10

0.002 10

19. Nitrite

1

1

20. Total Nitrate and Nitrite

10

10

21. Selenium

0.05

0.05

22. Thallium

0.0005

0.002

Some people who drink water containing barium in excess of the MCL over many years could experience an increase in their blood pressure. Some people who drink water containing beryllium well in excess of the MCL over many years could develop intestinal lesions. Some people who drink water containing cadmium in excess of the MCL over many years could experience kidney damage. Some people who drink water containing chromium well in excess of the MCL over many years could experience allergic dermatitis. Some people who drink water containing cyanide well in excess of the MCL over many years could experience nerve damage or problems with their thyroid. Some people who drink water containing fluoride in excess of the MCL over many years could get bone disease, including pain and tenderness of the bones. Fluoride in drinking water at half the MCL or more may cause mottling of children’s teeth, usually in children less than nine years old. Mottling, also known as dental fluorosis, may include brown staining and/or pitting of the teeth, and occurs only in developing teeth before they erupt from the gums. Some people who drink water containing inorganic mercury well in excess of the MCL over many years could experience kidney damage. Infants below the age of six months who drink water containing nitrate in excess of the MCL could become seriously ill and, if untreated, may die. Symptoms include shortness of breath and blue baby symptoms. Infants below the age of six months who drink water containing nitrite in excess of the MCL could become seriously ill and, if untreated, may die. Symptoms include shortness of breath and blue baby symptoms. Infants below the age of six months who drink water containing nitrate and nitrite in excess of the MCL could become seriously ill and, if untreated, may die. Symptoms include shortness of breath and blue baby symptoms. Selenium is an essential nutrient. However, some people who drink water containing selenium in excess of the MCL over many years could experience hair or fingernail losses, numbness in fingers or toes, or problems with their circulation. Some people who drink water containing thallium in excess of the MCL over many years could experience hair loss, changes in their blood, or problems with their kidneys, intestines, or liver. Infants and children who drink water containing lead in excess of the action level could experience delays in their physical or mental development. Children could show slight deficits in attention span and learning abilities. Adults who drink this water over many years could develop kidney problems or high blood pressure. Copper is an essential nutrient, but some people who drink water containing copper in excess of the action level over a relatively short amount of time could experience gastrointestinal distress. Some people who drink water containing copper in excess of the action level over many years could suffer liver or kidney damage. People with Wilson’s disease should consult their personal doctor. Some people who drink water containing the weed killer 2,4-D well in excess of the MCL over many years could experience problems with their kidneys, liver or adrenal

D. Lead and Copper Rule: 23. Lead

Zero

TT

13

24. Copper

1.3

TT

14

E. Synthetic Organic Compounds 25. 2,4-D

0.07

0.07

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26. 2,4,5-TP (Silvex) 27. Alachlor 0.05 Zero 0.05 0.002

CHAPTER 1200-5-1
glands. Some people who drink water containing silvex in excess of the MCL over many years could experience liver problems. Some people who drink water containing alachlor in excess of the MCL over many years could have problems with their eyes, liver kidneys, or spleen, or experience anemia, and may have an increased risk of getting cancer. Some people who drink water containing atrazine well in excess of the MCL over many years could experience problems with their cardiovascular system or reproductive difficulties. Some people who drink water containing benzo(a)pyrene in excess of the MCL over many years may experience reproductive difficulties and may have an increased risk of getting cancer. Some people who drink water containing carbofuran in excess of the MCL over many years could experience problems with their blood, or nervous or reproductive systems. Some people who drink water containing chlordane in excess of the MCL over many years could experience problems with their liver or nervous system, and may have an increased risk of getting cancer. Some people who drink water containing dalapon well in excess of the MCL over many years could experience minor kidney changes. Some people who drink water containing di (2-ethyhexyl) adipate well in excess of the MCL over many years could experience general toxic effects or reproductive difficulties. Some people who drink water containing di (2ethylhexyl) phthalate in excess of the MCL over many years may have problems with their liver, or experience reproductive difficulties, and may have an increased risk of getting cancer. Some people who drink water containing DBCP in excess of the MCL over many years could experience reproductive difficulties and may have an increased risk of getting cancer. Some people who drink water containing dinoseb well in excess of the MCL over many years could experience reproductive difficulties. Some people who drink water containing dioxin in excess of the MCL over many years could experience reproductive difficulties and may have an increased risk of getting cancer. Some people who drink water containing diquat in excess of the MCL over many years could get cataracts. Some people who drink water containing endothall in excess of the MCL over many years could experience problems with their stomach or intestines. Some people who drink water containing endrin in excess of the MCL over many years could experience liver problems. Some people who drink water containing ethylene dibromide in excess of the MCL over many years could experience problems with their liver, stomach, reproductive system, or kidneys, and may have an increased risk of getting cancer. Some people who drink water containing glyphosate in excess of the MCL over many years could experience problems with their kidneys or reproductive difficulties. Some people who drink water containing heptachlor in excess of the MCL over many years could experience liver damage and may have an increased risk of getting cancer. Some people who drink water containing heptachlor epoxide in excess of the MCL over many years could

28. Atrazine

0.003

0.003

29. Benzo(a)pyrene (PAHs)

Zero

0.0002

30. Carbofuran

0.04

0.04

31. Chlordane

Zero

0.002

32. Dalapon 33. Di (2-ethylexyl) adipate

0.2 0.4

0.2 0.4

34. Di (2-ethylhexyl) phthalate

Zero

0.006

35. (DBCP)

Dibromochloropropane

Zero

0.0002

36. Dinoseb 37. Dioxin (2,3,7,8-TCDD)

0.007 Zero

0.007 3x10
-8

38. Diquat 39. Endothall 40. Endrin 41. Ethylene dibromide

0.02 0.1 0.002 Zero

0.02 0.1 0.002 0.00005

42. Glyphosate 43. Heptachlor

0.7 Zero

0.7 0.0004

44. Heptachlor epoxide

Zero

0.0002

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45. Hexachlorobenzene Zero 0.001

CHAPTER 1200-5-1
experience liver damage, and may have an increased risk of getting cancer. Some people who drink water containing hexachlorobenzene in excess of the MCL over many years could experience problems with their liver or kidneys, or adverse reproductive effects, and may have an increased risk of getting cancer. Some people who drink water containing hexachlorocyclopentadiene well in excess of the MCL over many years could experience problems with their kidneys or stomach. Some people who drink water containing lindane in excess of the MCL over many years could experience problems with their kidneys or liver. Some people who drink water containing methoxychlor in excess of the MCL over many years could experience reproductive difficulties. Some people who drink water containing oxamyl in excess of the MCL over many years could experience slight nervous system effects. Some people who drink water containing pentachlorophenol in excess of the MCL over many years could experience problems with their liver or kidneys, and may have an increased risk of getting cancer. Some people who drink water containing picloram in excess of the MCL over many years could experience problems with their liver. Some people who drink water containing PCBs in excess of MCL over many years could experience changes in their skin, problems with their thymus gland, immune deficiencies, or reproductive or nervous system difficulties, and may have an increased risk of getting cancer. Some people who drink water containing simazine in excess of the MCL over many years could experience problems with their blood. Some people who drink water containing toxaphene in excess of the MCL over many years could have problems with their kidneys, liver, or thyroid, and may have an increased risk of getting cancer. Some people who drink water containing benzene in excess of the MCL over many years could experience anemia or a decrease in blood platelets, and may have an increased risk of getting cancer. Some people who drink water containing carbon tetrachloride in excess of the MCL over many years could experience problems with their liver and may have an increased risk of getting cancer. Some people who drink water containing chlorobenzene in excess of the MCL over many years could experience problems with their liver or kidneys. Some people who drink water containing odichlorobenzene in excess of the MCL over many years could experience problems with their liver, kidneys, or circulatory systems. Some people who drink water containing pdichlorobenzene in excess of the MCL over many years could experience anemia, damage to their liver, kidneys, or spleen, or changes in their blood. Some people who drink water containing 1,2dichloroethane in excess of the MCL over many years may have an increased risk of getting cancer. Some people who drink water containing 1,1dichloroethylene in excess of the MCL over many years could experience problems with their liver. Some people who drink water containing cis-1,2dichloroethylene in excess of the MCL over many years

46. Hexachlorocyclopentadiene

0.05

0.05

47. Lindane 48. Methoxychlor 49. Oxamyl (Vydate) 50. Pentachlorophenol

0.0002 0.04 0.2 Zero

0.0002 0.04 0.2 0.001

51. Picloram 52. Polychlorinated biphenyls (PCBs)

0.5 Zero

0.5 0.0005

53. Simazine

0.004

0.004

54. Toxaphene

Zero

0.003

F. Volatile Organic Compounds VOC) 55. Benzene

Zero

0.005

56. Carbon tetrachloride

Zero

0.005

57. Chlorobenzene (monochlorobenzene) 58. o-Dichlorobenzene

0.1 0.6

0.1 0.6

59. p-Dichlorobenzene

0.075

0.075

60. 1,2-Dichloroethane 61. 1,1-Dichloroethylene 62. cis-1,2-Dichloroethylene

Zero 0.007 0.07

0.005 0.007 0.07

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63. trans-1,2-Dichloroethylene 64. Dichloromethane 0.1 Zero 0.1 0.005

CHAPTER 1200-5-1
could experience problems with their liver. Some people who drink water containing trans-1,2dichloroethylene well in excess of the MCL over many years could experience problems with their liver. Some people who drink water containing dichloromethane in excess of the MCl over many years could have liver problems and may have an increased risk of getting cancer. Some people who drink water containing 1,2dichloropropane in excess of the MCL over many years may have an increased risk of getting cancer. Some people who drink water containing ethylbenzene well in excess of the MCL over many years could experience problems with their liver or kidneys. Some people who drink water containing styrene well in excess of the MCL over many years could have problems with their liver, kidneys, or circulatory system. Some people who drink water containing tetrachloroethylene in excess of the MCL over many years could have problems with their livers, and may have an increased risk of getting cancer. Some people who drink water containing toluene well in excess of the MCL over many years could have problems with their nervous system, kidneys, or liver. Some people who drink water containing 1,2,4trichlorobenzene well in excess of the MCL over many years could experience changes in their adrenal glands. Some people who drink water containing 1,1,1trichloroethane in excess of the MCL over many years could experience problems with their liver, nervous system, or circulatory problems. Some people who drink water containing 1,1,2trichloroethane well in excess of the MCL over many years could have problems with their liver, kidneys, or immune systems. Some people who drink water containing trichloroethylene in excess of the MCL over many years could experience problems with their liver and may have an increased risk of getting cancer. Some people who drink water containing vinyl chloride in excess of the MCL over many years may have an increased risk of getting cancer. Some people who drink water containing xylenes in excess of the MCL over many years could experience damage to their nervous system.
15

65. 1,2-Dichloropropane 66. Ethylbenzene 67. Styrene 68. Tetrachloroethylene

Zero 0.7 0.1 Zero

0.005 0.7 0.1 0.005

69. Toluene

1

1

70. 1,2,4-Trichlorobenzene 71. 1,1,1-Trichloroethane

0.07 0.2

0.07 0.2

72. 1,1,2-Trichloroethylene

0.003

0.005

73. Trichloroethylene

Zero

0.005

74. Vinyl chloride 75. Xylenes (total) G. Radioactive Contaminants 76. Beta/photon emitters

Zero 10

0.002 10

Zero

4 mrem/yr

77. Alpha emitters

Zero

15 pCi/L

17

78. Combined radium (226 & 228). 79. Uranium
16

Zero Zero

5 pCi/L 30ug/L

Certain minerals are radioactive and may emit forms of radiation known as photons and beta radiation. Some people who drink water containing beta and photon emitters in excess of the MCL over many years may have an increased risk of getting cancer. Certain minerals are radioactive and may emit a form of radiation known as alpha radiation. Some people who drink water containing alpha emitters in excess of the MCL over many years may have an increased risk of getting cancer. Some people who drink water containing radium 226 or 228 in excess of the MCL over many years may have an increased risk of getting cancer. Some people who drink water containing uranium in excess of the MCL over many years may have an increased risk of getting cancer and kidney toxicity.

H. Disinfection Byproducts (DBPs), Byproducts Precursors, and Disinfectant Residuals: Where disinfection is used in the treatment of drinking water, disinfectants combine with organic and inorganic matter present in water to form chemicals called disinfection by-

August, 2008 (Revised)

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products (DBPs). EPA sets standards for controlling the levels of disinfectants and DBPs in drinking water, including trihalomethanes (THMs) and 18 haloacetic acids (HAAs): 80. Total (TTHMs) trihalomethanes N/A 080
19 20

CHAPTER 1200-5-1

81. Haloacetic Acids (HAA)

N/A

0.060

21

Some people who drink water containing trihalomethanes in excess of the MCL over many years may experience problems with their liver, kidneys, or central nervous system, and may have an increased risk of getting cancer. Some people who drink water containing haloacetic acids in excess of the MCL over many years may have an increased risk of getting cancer. Some people who drink water containing bromate in excess of the MCL over many years may have an increased risk of getting cancer. Some infants and young children who drink water containing chlorite in excess of the MCL could experience nervous system effects. Similar effects may occur in fetuses of pregnant women who drink water containing chlorite in excess of the MCL. Some people may experience anemia. Some people who use water containing chlorine well in excess of the MRDL could experience irritating effects to their eyes and nose. Some people who drink water containing chlorine well in excess of the MRDL could experience stomach discomfort. Some people who use water containing chloramines well in excess of the MRDL could experience irritating effects to their eyes and nose. Some people who drink water containing chloramines well in excess of the MRDL could experience stomach discomfort or anemia. Some infants and young children who drink water containing chlorine dioxide in excess of the MRDL could experience nervous system effects. Similar effects may occur in fetuses of pregnant women who drink water containing chlorine dioxide in excess of the MRDL. Some people may experience anemia. Add for public notification only: The chlorine dioxide violations reported today are the result of exceedances at the treatment facility only, not within the distribution system which delivers water to consumers. Continued compliance with chlorine dioxide levels within the distribution system minimizes the potential risk of these violations to consumers. Some infants and young children who drink water containing chlorine dioxide in excess of the MRDL could experience nervous system effects. Similar effects may occur in fetuses of pregnant women who drink water containing chlorine dioxide in excess of the MRDL. Some people may experience anemia. Add for public notification only: The chlorine dioxide violations reported today include exceedances of the EPA standard within the distribution system which delivers water to consumers. Violations of the chlorine d