363.7392 B856f cop. 2 FLUORIDE IN ILLINOIS: SOURCES, ENVIRONMENTAL AND HEALTH EFFECTS, AND A PROPOSED AMBIENT STANDARD DOCUMENT NO. 82/01 inois Department of Energy and Natural Resources Printed by Authority of the State of Illinois UNIVERSITY OF ILLINOIS LIBRARY AT I vlPAIGN 1.x, uKS t AC»^S DOC. No. 82/01 January, 1982 FLUORIDE IN ILLINOIS: SOURCES, ENVIRONMENTAL AND HEALTH EFFECTS, AND A PROPOSED AMBIENT STANDARD by Dee M. Buckler Warren U. Brigham Illinois Natural History Survey Natural Resources Building Champaign, Illinois 61820 Project No. 10.086 Michael B. Witte, Director State of 111 inois Department of Energy and Natural Resources Division of Environmental Management 309 West Washington Street Chicago, IL 60606 NOTE This report has been reviewd by The Environmental Management Division of the Department of Energy and Natural Resources and approved for publication. Views expressed are those of the Natural History Survey Division of the Department. Printed by Authority of the State of Illinois Date Printed: January, 1982 Quantity Printed: 250 Illinois Department of Energy and Natural Resources 309 West Washington Street Chicago, IL 60606 (312) 793-3870 n 363.7*' TABLE OF CONTENTS TABLE OF CONTENTS Hi LIST OF TABLES i V LIST OF FIGURES V SUMMARY VI INTRODUCTION 1 BACKGROUND 1 CHEMISTRY OF FLUORINE 4 FLUORIDE IN THE ENVIRONMENT 9 NATURAL SOURCES OF FLUORIDE 9 MAN-MADE SOURCES 10 AMBIENT LEVELS IN THE UNITED STATES 10 MAJOR INDUSTRIAL SOURCES IN ILLINOIS AND CONTROL TECHNOLOGY 14 OTHER SOURCES 20 ENVIRONMENTAL EFFECTS OF FLUORIDE 23 PLANTS 23 WILDLIFE 31 INSECTS 35 DOMESTIC ANIMALS 37 HEALTH EFFECT OF FLUORIDE 42 STANDARD 66 RATIONALE 67 GLOSSARY 70 REFERENCES . . : 71 111 LIST OF TABLES 1 Summary of sources of fluoride to the environment, including annual contribution to atmosphere from Illinois man-made sources and year of determination, where possible 22 2 Fluoride concentrations in vegetation (rag kg~l)(after Kay, &t al., 1975a) 24 3 Fluoride concentration in bones of animals collected in non-polluted areas of Montana (after Kay, et al. 1975a) 32 4 Standards for fluoride in forage (after Smith and Hodge 1959) 39 5 Recent data illustrating the effects of environmental factors on the range of fluoride contents in some foods (after Rose and Marier 1977) 44 6 Recent data on the daily intake of fluoride by children (after Rose and Marier 1977) 46 7 Recent data on the daily intake of fluoride by adults (after Rose and Marier 1977) 47 8 Effects of fluoride on some physical properties of animal bones (after Rose and Marier 1977) 51 9 Effects of various fluoride concentrations in drinking water upon humans (after McKee and Wolf 1963) 53 IV LIST OF FIGIRES Atmospheric distribution of gaseous fluoride in relation to elevation and distance from an industrial point-source (size of circle roughly proportional to gaseous fluoride concentrations, which are shown by numbers denoting ppb of HF) (after Rose and Marier 1977) 12 The relationship of concentration of atmospheric fluoride (vertical axis) and duration of exposure (horizontal axis) to the threshold for folial symptoms for sensitive, intermediate, and tolerant species of plants (after U. S. Environmental Protection Agency 1976) 68 SUMMARY This document represents a state-of-the-knowledge report on fluoride, a review of all potential sources of fluoride in Illinois (including industry), an evaluation of the hazards posed to humans and the environment by air-borne fluoride in Illinois, and a proposed ambient standard. The intended audience of this document includes those individuals and agencies charged with or having an interest in protecting and maintaining public health and welfare and protecting and maintaining environmental quality. It is especially directed toward those agencies having regulatory powers in these areas. Three natural sources (soil, water, and volcanoes and fumeroles) and eight man-made sources (iron and steel manufacturing, phosphate fertilizer production, combustion of coal, cement production, hydrogen fluoride production, glass manufacturing, wet phosphoric acid manufacturing, and fluoridation of water) are identified as sources of fluoride to the atmosphere. The total annual contribution to the atmosphere by Illinois man-made sources (excluding glass and wet phosphoric acid manufacturing and fluoridation of water [no data avaialable]) equals approximately 2.51 x 10^ kg (2,535 tons). The effects of fluorides upon plants, wildlife, insects, and domestic animals are discussed in detail. A separate section on the health effect of fluoride considers pathways by which fluoride enters the body and considers the deleterious effects of these fluorides. Little information exists regarding the biochemical pathways of these fluorides. The strong affinity of the fluoride ion for calcium and phosphorus accounts for its deposition in bones and teeth. A similar affinity to many metals, for example magnesium and manganese, produces interference with some enzyme systems. In lieu of more VI specific data regarding the effects of fluoride upon organs and organ systems, this report discusses gross effects upon bone; teeth; blood, arteries, and heart; kidneys; enzymes, liver, and the gastrointestinal tract; thyroid and parathyroid glands; and, the central nervous system. Total daily intake of fluoride from all sources is estimated by us to be from 3.5 mg to 5.5 mg per person per day. This range agrees with most published studies. A primary air quality standard for fluoride (to protect the public health) cannot be determined given the available information. However, a secondary standard for fluoride (to protect the public welfare) can be established. A standard of 0.4 ug m~3 fluoride (30-day averaging time) is proposed as an ambient secondary air quality standard for fluoride. This standard will limit fluoride intake by man via respiratory pathways to approximately 0.2% of the average individual total daily uptake. In addition to protecting the public welfare, this level appears attainable using available emission control technology. Vll Digitized by the Internet Archive in 2013 http://archive.org/details/fluorideinillino8201buck 1 INTRODUCTION Background Section 111(d) of the Clean Air Act, 42 U.S.C. 1857c-6(d), as amended, requires the U.S. Environmental Protection Agency to estab- lish procedures under which states submit plans to control certain existing sources of certain pollutants. On 17 November 1975 (40 FR 53340) the Agency implemented section 111(d) by promulgating subpart B of 40 CFR part 60, establishing procedures and requirements for adop- tion and submittal of state plans for the control of "designated pol- lutants" from "designated facilities." Designated pollutants are those for which standards of performance for new sources have been established under section 111(b), but are not included on the list published under section 108(a) of the act (National Ambient Air Oual- ity Standards) or section 112(b)(1)(A) of the act (Hazardous Air Pol- lutants). A designated facility emits a designated pollutant and would be subject to a standard of performance for that pollutant if that facility were new. Subpart B requires each state to develop emissions standards for each designated pollutant emitted from a designated facility. Fluor- ide emissions from the phosphate fertilizer industry have been "desig- nated" in the Federal Register (40 FR 33152). This approach, however, appears inadequate for insuring the protection of public health and welfare in that it requires consideration of only designated sources of fluoride rather than all sources. In order to institute the proper regulatory standards, the Illinois Environmental Protection Agency first must consider all significant sources of fluoride emissions in 111 inois . 2 The objectives of this study are to: 1. present a st ate-of-the-knowledge report on fluoride emis- sions, with special emphasis on current developments in the field, based upon a literature review; 2. propose an ambient fluoride standard (or standards) using the available information; 3. review all potential fluoride sources, including industry, in Illinois, and formulate a general estimate of emissions from the relevant sources; and, 4. evaluate the hazards posed to humans and the environment by air-borne fluoride in Illinois and develop recommendations for mini- mizing or eliminating these hazards. The terms "fluoride" and "fluorine" often are used interchange- ably in the literature as generic terms for both elemental and com- bined forms of fluorine. This document uses the term "fluoride" as a general term wherever exact differentiation among forms is uncertain or unnecessary. The term covers all combined forms of the element unless there is a specific reason to stress a special form of the element. The term "fluorine" is used in reference to the gaseous elemental form F2 • Some confusion may exist with regard to units describing concen- trations of fluoride. This document reports the work of many investi- gators who sometimes used the same or similar units in different ways. Concentrations expressing the weight of a chemical substance per unit weight or volume of a suspending medium (i.e. mg kg -1 or mg liter -i , respectively) are not ambiguous. "Parts per million" 3 (ppm), however, may cause some confusion. Concentrations in solids or liquids, expressed as ppm, are weights per million weight units of suspending medium. They may be converted to metric units with 1 ppm equal to 1 mg kg - * . Note that for water this also equals 1 mg liter - . For concentrations in a gas, ppm means volume of a sub- stance per million volumes of the suspending gas. Thus, conversion to metric units must include consideration of temperature and atmospheric pressure. In reporting air concentrations affecting vegetation, the following assumptions are made: pressure, 760 torr; temperature, 15°C (288°K); and volume of a mole of a gas, 23.645 liters. Thus, ppm = mg m J x 23.645 mol . wt . For air concentrations affecting animals, pressure is assumed to re- main at 760 torr, but with a temperature of 25°C (298°K). Thus, the volume of a mole of gas equals 24.45 liters. Conversion from ppm to mg m - -* is as follows: ppm = mg m x 24 .45 mo 1 . wt . An attempt has been made throughout the text to state the mole- cular formula of fluorine compounds the first time each compound is mentioned. Each fluorine compound and its molecular formula also are listed in the glossary. Chemistry of Fluorine Fluorine (F2) is the 13th most abundant element in the earth's crust (Cholak 1959). In the free state, it is a pale yellow gas with a pungent, irritating odor. It is the most electronegative element, hence the strongest oxidizing agent known. It stands at the head of the halogen family in the periodic table with an atomic number of 9. There is a single stable, naturally occurring isotope with a mass of 19, but radioactive isotopes with mass numbers of 17 (half-life 70 sec), 18 (half-life 112 min), and 20 (half-life 10.7 sec) have been prepared. The melting and boiling points of fluorine are -188°C and -223°C, respectively. Its density relative to air is 1.32. Because of its reactivity, fluorine exists in the free state only in trace quantities. It reacts with all metals and most of the non- metals forming a large number of single, double, and complex salts. Elements having variable valences usually show several oxidation states in combination with fluorine (e.g., the sulfur fluorides: S 2 F 2> SF 2' S 2 F 10» SF 4' and SF 6^- rhe flu° ride ion often forms stable complexes with positive ions, for example [SiF 6 ]~ 2 and [AlFg] -3 . Fluorine reacts with hydrocarbons to form f luorocarbons in which all hydrogen is replaced by fluorine. These represent the parent com- pounds from which a large number of organic compounds are derived. Airborne fluorides, which are the primary concern of this report, are emitted to the atmosphere as gases and as particulates. In the air they undergo physical and chemical changes as they hydrolize with water vapor making them more available for uptake by organisms. The following is a brief summary of the changes sustained by the principal gaseous and particulate fluorides (National Academy of Sciences 1971). Silicon tetraf luoride (SiF^) , a major industrial pollutant, reacts with water vapor in air to form hydrated silica and fluoro- silicic acid (H 2 SiFg) by the reaction: 3SiF 4 + 2H 2 Si0 2 + 2H 2 SiF 6 Fluorosilicic acid is highly soluble in water and is absorbed readily by plants. In concentrated form (30% aqueous solution) it is moder- ately corrosive, attacking glass, ceramics, some metals, and metal oxides . Anhydrous hydrogen fluoride (HF) , another common industrial pol- lutant, combines readily with water vapor to produce an aerosol, or gas, of aqueous hydrofluoric acid, which may be characterized as nHF(aq.). Both of these substances etch glass, but yield different end products. Hydrogen fluoride produces silicon tetraf luoride from the reaction: 4HF + Si0 2 SiF 4 + 2H 2 while aqueous hydrofluoric acid produces fluorosilicic acid, as fol- lows : nHF(aq.) + Si0 2 (n-6)HF(aq.) + H 2 SiF 6 (aq.) + 2H 2 <3 Chlorof luorocarbon compounds of low toxicity have found wide use as aerosol propellants and refrigerants. Included here are trichloro- f luoromethane (CFCI3), dichlorodif luoromethane [freon] (CF 2 C1 2 ), and 1 ,2-dichloro-l, 1,2,2-tetraf luoroethane (CC1F 2 CC1F 2 ) . Although these compounds are relatively inert, they may decompose at high temperatures producing toxic products such as hydrogen peroxide, hydrochloric acid, and phosgene. The use of many chlorof luorocarbons as propellants is declining due to the disturbing results of several recent studies. In the late 1960's, scientists first noted that these gases persisted in the troposphere. Molina and Rowland (1973) discovered that once in the stratosphere, chlorof luorocarbon molecules dissociate under intense ultraviolet radiation releasing chlorine atoms. These chlorine atoms catalyzed the destruction of ozone from the ozone layer shielding the earth from harmful solar radiation. Fluorine and halogen fluorides are not common air pollutants, although they are released by some processes, notably rocket-engine test firings. Hydrolysis reactions of these substances are complex and yield a variety of products. Most of the fluorides emitted by industries in the form of parti- culate matter are stable compounds, not hydrolyzing readily. Among the chief particulates are cryolite (Na3AlF^), fluorapatite (CaF2 ' 3Ca3 (PO^^) , calcium fluoride (CaF2), aluminum fluoride (AIF3), sodium fluoride (NaF) , and sodium f luorosilicate (Na2SiF^). In general, the solubility of each compound in water largely determines the availability of its fluoride to plants and animals. Yet, fluorapatite is not very soluble in water, but fre- quently causes fluorosis in grazing animals when it is present as dust on vegetation. In this case, its solubility is increased by the dilute hydrochloric acid found in the animal's gastrointestinal tract . The presence of other elements can both increase and decrease the solubility of fluorides, hence similarly affecting their uptake by organisms. For example, aluminum, calcium, magnesium, phosphorus, and/or the acidity of the soil affect fluoride uptake by plants. Uptake of fertilizer-borne fluoride, usually considered unavailable due to its insolubility, is enhanced by the presence of borate (Bovay 1969; Collet 1969). In contrast, the phytotoxicity of fluorides was reduced by alka- line air pollutants from a metal foundry in the heavily industrialized Ruhr Valley of Germany (Uahlertand and Schneider 1969). Here, metal oxides reduced the solubility of the fluorides. Similar findings of synergism and antagonism have been reported for animals. For example, Schepers (1961) found that beryllium com- bined with fluoride had a much greater carcinogenic potency than either element alone. In the past, the toxicity of fluorides often was determined by whether or not they were organic or inorganic. Organic fluorides result from the formation of covalent (non-ionic) bonds between fluorine atoms and carbon atoms. It was thought that these substances were less toxic due to their insolubility- A considerable volume of data now exists providing evidence that the fluorine-carbon bond can be broken by biological processes. Recent investigations of a fluorinated anesthetic, methyoxyf lurane [penthrane] (CH3OCF2CCI2H) , found that the substance could be metabolized resulting in high blood levels of inorganic fluoride (Taves, Fry, Freeman, and Gillies 1970). 8 Rose and Marier (1977) discuss Che evidence for fluoride meta- bolism dating back to 1956. They concluded that few, if any, organo- fluorine compounds were biologically stable. Thus, it is evident that both organic and inorganic fluorides must be considered, even though inorganic fluorides probably are responsible for most cases of fluor- ide toxicity. FLUORIDE IN THE ENVIRONMENT Natural Sources of Fluoride The atmosphere receives very little fluoride from natural sources. Rose and Marier (1977) estimated that all soluble fluoride in excess of 0.05 ug m originated from man-made sources, except for unusual circumstances such as volcanic activity. Flouride is dis- tributed widely in both igneous and sedimentary rocks. It occurs chiefly as the minerals fluorspar (CaF2), cryolite, and fluorapa- tite, and is estimated to constitute between 0.06% and 0.09% by weight, of the earth's crust (National Academy of Sciences 1971). Soil also may contain fluorine in or associated with different minerals, including f luorapat ite , fluorite, biotite, muscovite, and hornblende. It should be noted that the latter three minerals do not contain fluoride, but do contain aluminum and silicon. As noted above, fluoride ions often form stable complexes with these metals when they are present as positive ions. The National Academy of Sciences (1971) reported fluoride concentrations from U.S. soils rang- ing from 20 to 8,300 mg kg - * (mean 190 mg kg - * for surface samples) and noted that concentrations increased with depth. The fluoride content of natural waters varies widely depending upon the source of the water, geologic formations present, and the amounts of rainfall and evaporation. In the U.S., surface waters usually contain less fluoride than groundwater. In the northeastern states, fluoride concentrations in water supplies range from 0.02 to 0.1 mg liter - *, while in most of the remainder of the country con- centrations more often are above 0.2 mg liter - *. In regions 10 having rich mineral deposits containing fluoride, concentrations as high as 7 mg liter - * have been reported in the U.S., while some regions of Africa have reported 93 mg liter - . In contrast to these inland sources, seawater contains very little fluoride, approximately 1.4 mg liter . Large amounts of gaseous and particulate fluorides are discharged into the atmosphere by active volcanoes and fumaroles. Hydrogen fluoride is one of the principal emissions, but many other fluoride compounds have been identified, including ammonium fluoride (NH^F) , silicon tet raf luor ide , ammonium f luorosi licat e f (NH^^SiF^J , sodium f luorosilicat e, potassium f luorosi licate (l^SiF^), and potassium fluoroborate (KBF^). The amounts of volatile fluorine, chlorine, and sulfur compounds emitted are known to increase greatly in the weeks preceding some eruptions and have been suggested as possible predictive tools. Man-made Sources Ambient Levels in the United States As noted above, Rose and Marier (1977) estimated that all soluble fluoride in the atmosphere in excess of 0.05 ug m originated from man-made sources. A study by the National Air Surveillance Net- work from 1966 through 1968 indicated that the vast majority of their measurements from both urban and non-urban sites were below this level (Thompson, McMullen, and Morgan 1971). A more recent study reported by King, Fordyce, Antoine, Leibecki, Neustadter, and Sidik (1976) was based upon fluoride measurements in and near six U.S. cities. The proporition of samples yielding no detectable fluoride ranged from 11 42% in St. Louis, Missouri, to 84% in Cincinnati, Ohio. Samples taken near some industrial sources ranged as high as 0.23 ug m . Airborne fluoride concentrations near industrial sources often reach much higher levels than those noted in the 1976 study conducted by King, et al. Air sampling devices at various distances from a hydrogen fluoride factory recorded fluoride concentrations in excess of 10 ug m 50% of the time. Near a phosphate fertilizer plant, _ o fluoride levels peaked at 32 mg m about 0.8 km from the plant, but decreased to 3 mg m 1.6 km from the facility (Cross and Rose 1969). Roffman, Kary, and Hudgins (1977) investigated airborne fluor- ide near a 50-unit coal-fired electric power generator. Downwind from this facility fluoride concentrations averaged 2.25 and 4.8 ug m for the 2 weeks sampled. Several factors, in addition to emission rate, affect airborne fluoride levels. Of greatest importance are topographic and climatic conditions of the countryside surrounding a source. In a study of the fluoride content of pasture forage near one source, isolated elevated levels were noted on ridges several kilometers from the source (McClenahen and Weidensaul 1977). Secondary stream valleys between the ridges funnelled up-valley winds carrying fluorides to the ridge- tops . It should also be noted that the level of fluoride may vary markedly over short alt itudinal and geographical distances. Figure 1 represents data from a smelter which indicate atmospheric stratification within a few hundred meters of a point-source and which remains apparent 3.6 km from that source. Another study demonstrated 12 _ f^_ _ (J) o>o (j>0 ooO ^ £° — ^ ro CD° ID §o a; o C co co •3 CO CO T3 C CO bO 3 O i-l •H CO 4-> C! CO O > -H 0) 01 a> o >> •H i-l H- 4-J ,3. ' (0 bO t* ih 3 2C o> o o 3 0) o o o 0) •H r-l o 0> '-i T3 -r-l o £ o •H O I-l O <4-l 3 O 1-t v_ U-l O 1 *4- N CO «H 3 co O o ^ o> CO 0) C CO o bo u o 3 ■♦— U-l O (O o co 1 • ■» c -u Q o 3 o •r-( tH 4J O o 3 a. JO o •H i-l U CO 03 M 0) CO s i-l 01 4J 4-1 CO a- a bO 3 •H •u O 3 0) -3 en M 0) 42 B 3 c "3 CO 3 O -3 •H 3 J-i >H OJ 4= 3 a co CO o e e o 4-1 M •rH I-l CO X -3 3 CO 13 that vegetation may intercept airborne fluoride that is moving through foliage creating an adjacent down-wind area of lower fluoride concentration (Gordon and Tourangeau 1977; Tourangeau, Gordon and Carlson 1977). 14 Major Industrial Sources in Illinois and Control Technology Fluorides are emitted from a variety of industrial processes in Illinois, yet certain processes account for the greater portion of atmospheric fluorides. McFarland (1974) designated the following pro- cesses as the major potential sources of airborne fluoride in Illi- nois : 1. Iron and steel manufacturing 2. Phosphate fertilizer production 3. Combustion of coal 4. Cement production 5. Hydrogen fluoride production 6. Glass manufacturing 7. Wet phosphoric acid manufacturing. The ensuing discussion has been taken largely from McFarland (1974). His data have been supplemented with a general quantitative evaluation of emissions from each source and a brief listing of appli- cable control technologies. Iron and Steel Manufacturing. A wide variety of fluoride-emit- ting processes are associated with the iron and steel industry. The major process sources of atmospheric fluoride are: 1. Iron ore sintering 2. Blast furnace operation 3. Open hearth furnace operation 4. Electric arc furnace operation 5. Basic oxygen furnace operation. 15 The sintering and blast furnace operations emit gaseous hydrogen fluoride and particulate calcium fluoride. The fluoride emitted from the open hearth furnace is nearly all gaseous hydrogen fluoride. The electric arc and basic oxygen processes emit mainly particulate calcium fluoride. In 1976, approximately 1 x 10 u kg of raw steel were pro- duced in Illinois. The U.S. Environmental Protection Agency (1972) estimated that 0.5 kg of fluoride are produced for every 1,000 kg of steel produced. This rate considers all the processes involved in steel production, including iron processing. Caclulations indicate that approximately 4.5 x 10 kg of airborne fluoride were emitted by the Illinois iron and steel industry in 1976. Electrostatic precipitates, cloth filters, and venturi scrubbers have been used to remove airborne fluoride from the exhaust gases of iron and steel plants. Removal efficiencies ranges from 95% to 99% (U.S. Environmental Protection Agency 1972). Phospha te Fertilizer Production. Illinois contains 4 of the 5 major ammonium phosphate plants in the U. S. and 12 large conventional superphosphate fertilizer plants (U.S. Environmental Protection Agency 1972). The chief source of fluoride emissions from the manufacture of diammonium phosphate is the phosphoric acid used in its production. Fluoride is emitted as ammonium fluoride and f luorosilicic acid from this process. In the production of normal superphosphate, phosphate rock is the source of fluoride which is emitted as silicon tet raf luor ide . For both processes phosphate rock is ground and dried, resulting in the release of dust which contains f luorapat it e . Also, fluorides 16 are emitted from gypsum ponds utilized in phosphate fertilizer production at a rate of 0.18 kg ha - * (Cross and Rose 1969). Total production of superphosphates and other phosphate ferti- lizer materials (100% P2°5) in Illinois amounted to 6.5 x 10" k£ (Current Industrial Reports 1979). The U.S. Environmental Protection Agency (1972) reported a rate of 1.55 to 2.05 g fluorine per kg of ?2®5 equivalent in the product. This rate includes emissions from the gypsum pond. Using this information 1978 fluoride emissions from the Illinois fertilizer plants are estimated to be from 10,100 to 13,300 kg. Recovery and control devices utilized by phosphate fertilizer plants include dry cyclone filters, electrostatic precipitators, and wet scrubbers. These devices are approximately 95% to 99% efficient for fluoride removal (U.S. Environmental Protection Agency 1972). Boscak (1979) recommended the cross-flow packed scrubber because it appeared to be the most efficient and could be applied to many of the processes involved in phosphate fertilizer production. Combustion of Coal. Coal combustion releases fluoride as silicon tet raf luoride and particulate matter. During combustion approximately half of the fluoride in the coal is evolved. Illinois coals contain from 0.007 to 0.012% fluoride (Abernathy and Gibson 1967). Samson and Dingwell (1979) found that 3.77 x 10 10 kg of coal were consumed' in Illinois during 1976. In 1969, these plants burned only 2.7 x 10 iU kg of coal (U.S. Environmental Protection Agency 1972). Most coal combustion-associated fluoride emissions occur in coal-burning electric power plants. Assuming that all of the coal is 17 utilized in power production at an emission rate of 0.08 g kg coal with no abatement measures, approximately 3 x 10° kg of airborne fluoride were released from power generating facilities in Illinois during 1976. Assuming that only 80% of the coal was utilized for power production, approximately 2.36 x 10 kg were released. Electrostatic precipitators and scrubbers are utilized by power facilities to remove regulated pollutates. These devices also reduce fluoride emissions. Roffman, Kary, and Hudgins (1977) calculated fluoride emission rates from scrubber-equipped and preciptator-equip- ped power units. Their data indicated that scrubbers could reduce fluorine emissions by approximately 50% by removing the gaseous forms of fluoride. Cement Production. In 1976, approximately 1.68 x 10 kg of portland cement were produced in Illinois (Samson and Dingwell 1979). The raw materials used in the manufacturing of portland cement are the source of the fluoride emissions, primarily in the form of calcium fluoride from the rotary kiln, with only small amounts of hydrogen fluoride. The estimated soluble fluoride emission rate for cement manufac- ture is 0.004 g kg cement (U.S. Environmental Protection Agency 1972). Using the information, approximately 67,200 kg of airborne fluoride were released in 1976 from this industry. Fluoride emission is controlled efficiently in cement production by cyclone and glass-fiber filters (U.S. Environmental Protection Agency 1972). 18 Hydrogen Fluoride Production . Only one major hydrogen fluoride plant is known to exist in Illinois, a Joliet facility which produces approximately 11.8 x 10" kg annually. Emissions from hydrogen fluoride plants contain hydrogen fluoride and silicon tetraf luor ide . The U.S. Environmental Protection Agency (1972) reported an emission rate of 2.05 g kg -1 hydrogen fluoride from aqueous hydrofluoric acid production. This results in a yearly emission rate for the Illi- nois plant of approximately 24,200 kg. Fluoride emissions are controlled in hydrogen fluoride production by using scrubbers (U.S. Environmental Protection Agency 1972). Glass Manufacturing. The major source of fluoride in the glass industry is the fluorspar which is added in the manufacturing of opal glass to create a translucent quality. Stack gases contain primarily gaseous hydrogen fluoride, along with small quantities of sodium fluoride. Some particulate calcium fluoride is effluxed during the transport of material to and from storage. Other fluorine compounds are evolved during the melting of various kinds of glass and during the firing of enamels. Fiberglass manufacturing also produces fluor- ide emissions during the production, melting, and blow-chamber stages (National Academy of Sciences 1971). In Illinois glass and/or fiberglass is manufactured by companies in DuPage, Lake, LaSalle, Logan, McLean, Macon, Madison, Marion, Mont- gomery, St. Clair, and Will counties (Samson and Dingwell 1979). Glass production levels were not available, so it is not possible to quantify fluoride emissions from these sources. 19 Fabric filters have been used to remove particulate matter from glass production emissions (U.S. Environmental Protection Agency 1972). Glass manufacturing firms in Canada, however, have almost phased out the use of fluorspar, the source of the fluoride, in glass production (Environment Canada 1976). A corresponding elimination of fluorspar by Illinois firms would greatly reduce emission rates in the State. Wet Phosphoric Acid Manufacture. Fluoride may enter the atmos- phere from as many as six points in the production of wet phosphoric acid. Emissions are in the form of silicon tet raf luoride and calcium fluoride. Gypsum ponds, a source of fluoride emissions, also are utilized in this process. Four major wet phosphoric acid plants are located in Illinois. Current Industrial Reports (1979) summarized production for the "east north central U.S." as 6.5 x 10 kg. Illinois production would be an unknown fraction of this value [data unavailable]. An emission rate of 1.68 g fluoride per kg phosphate in the product was reported by the U.S. Environmental Protection Agency (1972). This value includes gypsum pond emissions. Using the total production values, approximately 1,100 kg of fluoride were emitted from east north central wet phosphoric acid plants in 1977. Scrubbers are utilized to reduce fluoride emissions for this pro- cess. Gypsum pond emissions could be reduced by using separate ponds for gypsum and for cooling (Boscak 1979). 20 Other Sources Fluoride is available to plants, animals, and man from many other sources in addition to airborne sources. Although freshwater normally has as a low fluoride content 0.01 to 0.02 mg liter -1 (Carpenter 1969), fluoridation of water sup- plies has introduced fluoride into water systems on a large scale. This fluoride can concentrate, especially during low water levels (Brigham, McCormick, and Wetzel 1980). Industrial processes also dis- charge fluoride into waterways. Airborne fluoride is sometimes con- trolled by scrubbing which introduces concentrated fluoride to the plant's effluent, making the fluoride available to organisms, but in water rather than air. In addition to fluoride in soil from rock weathering, fluoride accumulates in soil from precipitation, contaminated water, particu- late fall-out, and fertilizers. Plant life accumulates fluoride from all the mentioned sources. This fluoride is then available to animals and man through ingestion of food plants. Animal life also contains fluoride which can be passed through the food chain. Seafood and fish are among the richest sources of fluoride. Available data indicate that the fluoride intake of man is aug- mented through food processing, the use of fluoridated toothpaste, the use of teflon pans, beverage ingestion (e.g., tea), the use of certain medicines, and smoking (see below under Health Effects of Fluoride). Although the purpose of this document is primarily to review atmospheric fluoride and assess the extent of the hazard posed by 21 Illinois sources, it should be rioted that water, soil, and food all contribute to man's fluoride burden. Any evaluation should integrate information relating to all of these sources. Table 1 summarizes the sources of fluoride to the atmosphere of Illinois. Where possible, the approximate annual contribution has been calculated. 22 Table 1. Summary of sources of fluoride to the environment, including annual contribution to atmosphere from Illinois man-made sources and year of determination, where possible. Natural Sources Atmosphere Soil Water Volcanoes & Fumeroles Man-Made Sources Iron & Steel Manufacturing Phosphate Fertilizer Production Combustion of Coal Cement Production Hydrogen Fluoride Production Glass Manufacturing Wet Phosphoric Acid Manufacturing Fluoridation of Water 4.5 x 10 4 kg (1976) 1.01 to 1.33 x 10 4 kg (1978) 2.36 x 10 6 kg (1976) 6.72 x 10 4 kg (1976) 2.42 x 10 4 kg 23 ENVIRONMENTAL EFFECTS OF FLUORIDE Plants Airborne fluoride enters plants primarily through the leaf stomata. Inside, it dissolves in the aqueous solution of the internal leaf tissue. The amount of fluoride dissolved will depend upon the solubility of the available fluoride. The fluoride is readily trans- ferred to the tops of plants and margins of the leaves in the transpiration stream where fluorides accumulate. As noted above the primary source of fluoride is from the air, yet plants do absorb some fluoride from the soil. The amounts taken from the soil depend largely upon the soil fluoride concentration and the soil types (Garber 1968). The fluoride absorption capacity of Illinois soils is related to the pH, clay, organic carbon, and amor- phous aluminum content (Omuet i and Jones 1977). The greater the ab- sorption capacity, the less fluoride is available to plants. The fluoride content of soil increases, in addition to natural means, from air pollution and from fertilizers. Fertilizers, which often contain 1 to 3% fluoride, may contribute significant amounts of fluoride, especially to tuber plants (Waldbott, Birgstahler, and McKinney 1978). Another source of fluoride contamination from the soil is by rain splash (Shupe, Olsen and Sharma 1979). This can scatter particulate fluorides on the leaf surface which can be absorbed into the plant or ingested by grazing animals. Normally all plants contain some fluoride, but the amounts vary. Kay, Tourangeau, and Gordon (1975a) determined "normal" fluoride levels in 21 plant species (Table 2). Mean background fluoride levels ranged from 1.0 to 8.6 ppm. Suttie (1969b) measured 107 24 Table 2. Fluoride concentrations in vegetation (mg kg l)(after Kay, et al. y 1975a). Species Mean Std. Coef . Std. Error Exp. Error Dev. Var. of Mean of Mean Alfalfa Medioago sativa 5 months 3 4.9 2 months 1 6.4 1.9 39.1 1.1 22.6 Beargrass Xevophyllum tenax 2 2.6 0.5 19.4 0.4 13.7 Bitterbush Purshia tvidentata 2 8.6 0.3 3.3 0.2 2.3 Bluebunch wheatgrass Agvopyron spioatum 23 5.7 2.5 44.2 0.5 9.4 Cherry, domestic Prunus sp Cambium 32 months 20 months 8 months Composite Total Xylem 32 months 20 months 8 months Composite Total Leaves Buds Flowers 3 3.6 0.8 21.8 4 3.3 1.2 35.4 4 3.0 0.8 27.6 3 4.0 1.0 24.6 14 3.4 0.9 27.1 4 2.6 1.1 45.0 4 2.3 1.1 46.0 3 2.3 1.2 53.2 3 2.8 0.7 27.1 14 2.5 1.0 38.8 6 4.2 0.8 18.6 6 3.8 0.8 22.0 1 5.6 - - 0.4 0.6 0.4 0.6 0.2 0.6 0.5 0.7 0.4 0.2 0.3 0.3 12.6 17.7 13.8 14.2 7.2 22.4 23.1 30.7 15.7 10.3 7.6 9.0 Cottonwood Populus tviohooarpa 6.4 1.8 27.6 0.7 10.5 Crested wheatgrass Agropyvon oristatum 17 months 2 5.6 3.4 60.1 5 months 2 5.8 2.0 34.1 1 month 2 5.6 3.1 55.6 Composite 3 5.9 0.4 7.4 2.4 1.4 2.2 0.3 42.9 24.1 39.3 4.3 continued on the next page Table 2. (continued). 25 Species N Mean Std. Coef . Std. Error Exp. Error Dev. Var. of Mean of Mean Douglas fir Pseudotsuga menziesii 41 months 4 29 months 13 17 months 13 5 months 13 Total 43 Grass Various species 38 Hay Various species 4 Juniper Juniperus soopularum 12 3.1 0.5 16.2 0.2 8.1 3.1 1.1 37.1 0.3 10.3 3.2 1.0 31.6 0.3 8.7 3.3 1.4 43.6 0.4 12.1 3.2 1.1 35.7 0.2 5.4 3.8 1.6 42.9 0.3 7.0 4.2 1.4 33.9 0.7 17.0 4.4 2.4 55.1 0.7 15.9 Larch Larix oooidentalis \ 7.8 Lodgepole pine Pinus aontorta 41 months 29 months 17 months 5 months Total 3 2.0 0.2 10.2 17 2.3 0.9 40.2 18 2.7 1.4 53.5 19 2.3 1.4 60.9 57 2.4 1.2 51.1 0.1 0.2 0.3 0.3 0.2 5.9 9.7 12.6 14.0 6.7 Pondersoa pine Pinus ponderosa 53 months 41 months 29 months 17 months 5 months Total Rabbitbrush Chrysothamnus sp. Red osier dogwood Cornus stolonifera Leaves Stems Flowers 5 1.6 0.7 45.7 13 3.0 1.7 57.7 26 3.3 2.1 64.4 27 2.7 1.4 52.7 27 2.4 1.2 46.2 98 2.9 1.7 57.4 7.0 3.0 3.6 2.8 0.3 0.5 0.4 0.3 0.2 0.2 20.4 16.0 12.6 10.1 8.9 5.6 continued on the next page 26 Table 2. (concluded) Std. Coef. Std. Error Exp. Error Species N Mean Dev. Var. of Mean of Mean Rough fescue Festuoa soabrella 1 1.8 - Sagebrush Artemisia tridentata 6 3.5 1.7 49.1 0.7 20.0 Smooth brome grass Bromus inermus 3 3.8 1.3 33.8 0.7 19.5 White pine Pinus montioola 29 months 4 1.8 0.8 45.0 0.4 32.5 17 months 4 1.9 0.9 46.4 0.4 23.1 5 months 5 2.1 1.0 48.0 0.5 21.4 Total 13 2.0 0.8 43.7 0.2 12.1 Yucca Yucca glauca 7 1.0 0.6 62.3 0.2 23.6 Total Grass 75 4.5 2.1 46.1 0.2 5.3 Total Coniferous Trees 214 2.8 1.5 53.0 0.1 3.6 Total Plants 387 3.4 1.9 56.8 0.1 2.9 27 samples of alfalfa from areas free of industrial pollution. The values ranged from 0.8 to 36.5 ppm, with a mean of 3.6 ppm. The National Academy of Sciences (1971) has suggested the natural forage fluoride content ranges from 5 to 10 ppm. Most other plant species also appear to fall within or below this range. Near a source of fluoride, plants can accumulate large concentrations of the ion. Carlson (1973) found fluoride concentrations averaging from 400 to 600 ppm in all vegetation near an aluminum plant. Thiers (1979) analyzed red and green cabbage from gardens near an enamel factory in Belgium. These tissues contained 65 to 95 times more fluoride than normal. Yet, plant species, even varieties of species, show dissimilar responses to accumulated fluoride. Some factors which affect the severity of injury to plants are discussed below. Biological Character of the Plant The stage of development of the plant affects injury in that young plants more often will be injured after a sudden increase in fluoride exposure while older plants accumulate fluoride during low level exposure with injuries developing later in the life cycle. The rapid growth of young plants of some species protects them from chronic assimilation. Rosenberger and Grunder (1968) found their highest fluoride concentrations in grasses during winter dormancy. The genetic character also affects the severity of injury because different varieties of a species have different tolerances to fluor- ide. 28 Environmental Conditions Surrounding the Plant Optimal climatic and soil conditions can reduce injuries caused by fluoride. Oelschlager, Moser, and Feyler (1979) noted that citrus trees which received ample amounts of water had less damage due to fluoride, yet a higher concentration of fluoride in leaves than trees which were under stress due to dryness, lack of nutrition, and little care. The availability of minerals which inactivate fluoride can also affect the injury. Calcium, magnesium, and phosphorus, in order of efficiency, inactivate fluoride (Navora and Holub 1968). The effects of ample calcium in reducing injury to plants has been reported by Pack (1966) and Pack and Sulzbach (1976). MacLean, Schneider, and McCune (1976) noted that decreased magnesium made fluoride more phyto- toxic to tomato plants. The presence of boron can enhance the accumu- lation of fluoride, when the boron is not in complex with fluoride (Collet 1969). Other pollutants can result in synergistic injury to plants. Reinert, Heagle, and Heck (1975) exposed citrus, corn, and barley to sulfur dioxide and fluoride in combination and alone. The effect on the latter two species was greater when the combination was used than when either was used singly. A similar effect was noted by Mandl, Weinstein and Keveny (1975). Location of the Plant Without doubt, the proximity of a plant to a fluoride source will affect its injury. McClenahen and Weidensaul (1977) found that predominant winds could cause fluoride build-up a considerable distance from a source. Also, Gordon and Tourangeau (1977b) and 29 Tourangeau, Gordon and Carlson (1977) noted that vegetation would impede or intercept fluoride in air moving through its foliage. They found that pines exposed to fluoride contained 2 to 4 times more accumulated fluoride on the windward side than on the leeward side. Physical and Chemical Form of Fluoride Gaseous and soluble particulates are the forms of fluoride most readily available to plants. The chemical environment of the leaf surface can affect the solubility of many of these particulates. Dose and Frequency of Exposure Large doses of fluoride can result in the development of an acid- type burn on the sensitive plant tissue (Taylor 1973) in species which, at lower concentrations, might not have been injured. The con- centration of hydrogen fluoride appears to influence the rate of development of soybean plants (Wei and Miller 1972). Plants exposed to airborne fluoride frequently display foliar damage (necrosis and chlorosis), sometimes grow less vigorously, and always accumulate significant amounts of fluoride in the foliage. All of these effects have aesthetic, economic, or environmental significance. The most obvious physical symptom of accumulation is foliar damage. Other injuries are not as easily visible. See Chang (1975) for a detailed summary of the biochemical and morphological changes in plants caused by fluoride. Growth and production is reduced in several species. Dobbs (1979) noted both reduced germination and yield in soybeans with low- level exposure to fluoride. McLaughlin and Barnes (1975) found that 30 fluoride reduced photosynthesis and stimulated dark respiration in some pines and hardwoods. This would reduce the carbohydrate available for growth and seed production. Weinstein (1977) reported that low levels of fluoride stimulated growth in some plants, but that this growth was abnormal. Conflicting results have come from investigations of the muta- genic effects of fluoride. Mohamed, Smith, and Applegate (1966) initially noted that chromosomal abberations occurred after fumigation of tomato plants with fluoride, the number of abberations increasing with increased exposure. Mohamed again noted genetic abnormalities in a study with corn and tomatoes. Here seeds from the exposed plants produced mutant offspring. In contrast, Temple and Weinstein (1978) found no mutations in a similar study with tomatoes. Bale and Hart (1973a, 1973b) found that exposure to fluoride produced chromosomal abberations in barley. The most significant effect of fluoride on native flora is that it alters the plant's ability to survive. Species intolerant to fluoride will not survive if fluoride is abundant. Near a fluoride source, LeBlanc, Rao, and Comeau (1972) found a 12-km area devoid of three otherwise dominant species. Gilbert (1971), in a study of lichens, also noted a complete absence of some species near a fluoride source. Sidhu (1977b) found a change in the dominant species of trees from softwood (predominantly evergreen) to hardwood (deciduous) in a forest surrounding a fluoride source. The hardwoods were able to defoliate every year thereby reducing their fluoride concentration. The high fluoride leaves, however, contributed fluoride to the soil, 31 to the creek running through the forest, and to organisms ingesting them. Rao and Pal (1978) noted that increased fluoride in soil and litter corresponded to an accumulation of the organic content in the soil surface. They suggested that fluoride may decrease the growth and activity of soil microorganisms. Fluoride can have an indirect effect upon plants by injuring pollinating insect species (see below under wildlife for effects upon honey bees). Fluoride also can induce plant injuries which favor investation by insects (Carlson, Bousfield and McGregor 1977). Wildlife The accumulation of fluoride also has been studied in several species of wildlife. Kay, Tourangeau, and Gordon (1975a) reported the fluoride concentration in femurs of 30 species collected in non- polluted areas in Montana. Table 3 depicts the values for species from which five or more individuals were analyzed. Similar values were reported from New Zealand by Stewart, et al . (1974) for a few species . Wildlife, like domestic and laboratory animals and man, concen- trates higher levels of fluoride in cancellous bone (Kay 1975), and accumulates fluoride linearly with age (Kay, Tourangeau and Gordon 1976). Also, wildlife species differ in fluoride concentrations geo- graphically, the highest values occurring near sources of fluoride (Kay, et_ al. 1975a). Near a source, fluoride accumulates in the bone of wildlife spe- cies to very high levels. Gordon (1970a) recorded a concentration of 12,700 ppm ash in the femur of a mouse and 16,000 ppm in a rabbit 32 Table 3. Fluoride concentration in bones of animals collected in non-polluted areas of Montana (after Kay, &t at, 1975a). No. of F content of femur mg kg~l , Species animals dry fat-free* HERBIVOROUS Chipmunk Eutanrias 19 103.1 + 16.2 Columbian ground squirrel Citellus oolumbianus 23 112.5+10.2 Deer mouse Peromysous maniculatus 70 143.8 + 7.8 Muskrat Ondatra zibethious 11 266.4 + 59.8 Northern flying squirrel Glauoomys sabvinus 6 141.8 + 30.7 Porcupine Evethizon dorsatum 6 161.0+37.1 Red squirrel Tamiasoiurus hudsonious 9 151.9+29.5 Redback vole Clethrionomys gapperi 5 258.0 +25.3 Whitetail jackrabbit Lepus townsendi 14 258.6 + 27.7 CARNIVOROUS Shortail weasel Mustela evminea 5 363.6 +97.1 Vagrant shrew Sovex vagrans 5 474.8 +98.1 *Mean and standard error of mean. 33 femur.* The bone fluoride levels in these species were related to the distance from the fluoride source. Rose and Marier (1977), after reviewing the background levels found in species from non-polluted areas, concluded that concentrations near and above 5,000 ppm, dry fat-free basis, were "indicative of environmental contamination by fluoride and its ingestion by wild animals." Symptoms of fluorosis, however, have been reported at levels well below 5,000 ppm. Newman and Murphy (1979) noted dental fluorosis in deer with metatarsal bone concentrations of less than 2,400 ppm, and morphological changes at less than 2,000 ppm. Kay, et al. (1975b) noted fluorotic symptoms in deer at 3,000 ppm fluoride in the mandibular bone (dry ash-free basis). The effects of these concentrations on wild species range from possible genetic damage to lameness. Mohamed , Weizenkamp-Chandler (1976) examined the cells of bone marrow and testes of mice after exposing them to fluoride with drinking water containing 0, 1.5, 50, 100, and 200 ppm fluoride for 6 weeks. Chromosomal abnormalities increased with increasing fluoride concentration and time. They concluded that even at only 1 ppm (in drinking water), fluoride caused genetic damage to mice. Voroshilin, Plotko, and Nikiforova (1975) observed no increase in embryonic deaths when male mice were exposed to 1 . mg hydrogen fluoride m - - 5 for 2 to 4 weeks before mating. Danilov and Kas'yanova (1975) reported an increase in deaths when using female mice. * For a rough conversion of ppm ash to ppm dry fat-free is to multiply ash value by 0.6. 34 Lameness attributed to fluoride in wild ungulates was observed by Kay, et_ al_. (1975b). They noted that the older individuals did not exist in the studied population and suggested that the loss of mobility made them more susceptible to predation. Another factor possibly weakening the older individuals was the effect of dental fluorosis, in that teeth soften and wear easily, making the individual a less efficient herbivore. Other effects of fluoride, osteof luorot ic lesions and osteopor- osis, were observed in deer and small mammals (Shupe and Sharma 1976). Efforts to quantify the relationship of fluoride levels found in these species and the levels in plants and soil were not successful. In contrast, Wright, Davison, and Johnson (1978) reported a significant relationship between vegetation and soil levels and the levels in animal tissue. This study, however, concerned field mice and field voles which have a more defined territory. Some work has been undertaken with fluoride accumulation by birds, however, these studies are often ambiguous due to the mobility of bird species. Rose and Marier (1977) reviewed the background fluoride concentrations found in bird species and concluded that, generally, the seed-eating, short-lived birds had less bone fluoride accumulation than omnivorous, long-lived species. Accumulation of fluoride was 2 to 9 times greater than controls in the bones of sparrows collected near an aluminum plant. However, birds may avoid fluoride sources. Newman (1977) found few house martins in polluted areas. 35 Accumulation in the egg yolks and shells of domestic and wild bird species was reported by van Toledo (1978). The amount of fluoride found in the yolks and shells varied by species and was significantly greater in individuals collected near industrial areas. Fluoride accumulation in wildlife and its effect have not been investigated thoroughly enough to draw conclusions. Yet, the avail- able data suggest that fluoride accumulation could be lethal to some species or cause genetic damage, but primarily appears to weaken an animal's ability to survive. Suttie (1977) stated that there was "no real basis for assuming that wildlife are more susceptible to the adverse effects of fluoride 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." Rose and Marier (1977) strongly disagree with this statement. They point out that factors which affect the severity of fluorosis (e.g., nutritional status, physical exertion, variability of fluoride exposure, age, etc.) can be unfavorable for wild species. Also, even mild fluorosis can make animals more susceptible to predation. This idea has been suggested by Kay, et_ al . (1975a) who found that deer at a given bone fluoride level suffered more severe lameness than cattle. Thus, the fodder standards proposed by Suttie (see domestic animal section) would not protect wildlife. Insects The accumulation of fluoride in insects has been reported from a series of papers from a study on an aluminum plant, a source of air- borne fluoride. Carlson and Dewey (1971) compared the fluoride 36 content of insects from a polluted area (near an aluminum plant) and a non-polluted area. Carlson (1973) reexamined the data from the study comparing the values obtained after fluoride emissions were reduced from 7,500 lbs/day to 2,500 lbs/day to values obtained with the higher emission rate. He found that insects still contained twice as much fluoride as the controls, and that foliage feeder showed an increased. Dewey (1973) suggested that the relatively high levels of fluoride detected in the "pure" predatory species implied that fluorides either are accumulated through respiration or passed on through the food chain. The effects of accumulated fluoride in insects have not received enough research to draw any conclusions. Mohamed (1971) reported evi- dence of chromosomal damage and mutations in fruit flies. Gerdes , Smith, and Applegate (1971a) tried to relate mortality of fruit flies to airborne fluoride concentrations, but found that the relationship was non- linear. Some strains of flies were more resistant. The same authors (1971b) studied the offspring from the first experiment, and noted a decrease in fecundity and hatching ability with increasing parental fluoride exposure. Accumulated fluoride may have a lethal effect upon some insects. Lillie (1970) concluded that 4 ug to 5 ug of accumulated fluoride may be the lethal level in honey bees. A study by Weismann and Svatarakova (1974) indicated that the lethal dose of fluoride to insects may be related to the calcium level in their bodies. Their conclusions were drawn from a study of three caterpillar species. 37 Domestic Animals Domestic animals intake fluoride mainly through air, water, and their diet. Chronic fluorosis can result from the ingestion of fluor- ide at levels above those arising from natural sources. It is usually more common in older animals. If exposure occurs during the early years during tooth formation, tooth damage, in the form of mottling, can occur. This contributes to tooth wear as the animal ages. The other accepted visual sign of fluorosis is bone damage. In severe cases, animals can become inter- mittently or permanently lame due to bone impairments. Many factors influence the severity of fluorosis: the chemical form and solubility of fluoride and other components of the diet (National Academy of Sciences 1974), the nutritional status of the diet (Suttie and Faltin 1973), the schedule of exposure (Suttie, Carlson, and Faltin 1972), the amount of physical activity (Shupe and Olson 1971; Shupe, Olson, and Sharma 1972), and the age of the animal when exposure begins (World Health Organization 1970; National Academy of Sciences 1971) . Domestic animals differ in their tolerance to fluoride. Cattle seem to be the most sensitive, therefore, they have been the subject of considerable research, and even the indirect basis for some ambient air standards for fluoride. Cattle acquire most of their ingested fluoride through their diet and drinking water. Airborne fluoride contributes through the fodder utilized in the diet and also through direct inhalation. Mineral supplements given to augment nutrition also often contain fluoride. Possible indirect sources include fertilizers and soil which could contribute fluoride to the fodder. 38 Fluoride burden in livestock is determined by three methods: fodder fluoride content, bone fluoride content, and urine fluoride content . The fluoride content of fodder is determined by the conventional vegetation analysis methods and related to total amount of fodder ingested over a period of time at a given level which would produce symptoms of fluorosis. This method is often used as a basis for air standards. The standards are set such that a given fluoride level is not achieved in the plants. Suttie (1969b) proposed that the fluoride content of fodder should not exceed 40 ppm on a yearly basis, 60 ppm for more than two consecutive months, and 80 ppm for more than one month. Several states and countries have adopted these standards or have modified them only slightly (Table 4). The measurement of the fluoride content of fodder does not always give an accurate representation of ingested fluoride. Other sources, such as mineral supplements, contribute to the total intake. Type of fodder also could greatly increase or decrease intake. Mascola, Barth, and McLaren (1974) noted a significantly higher amount of fluoride in forage samples from esophageal-f istulated steers than from randomly collected samples. Suttie's standards, however, are based upon studies of controlled animals. Such a study often minimizes many factors which can intensify the severity of fluorosis, primarily poor nutrition, physical activity, a variety of exposure levels, and age 39 Table 4. Standards for fluoride in forage (after Smith and Hodge 1959) Averaging Time Province or state 12-month average 6-month average 2 -month average 1 -month average No aver age spec ified Canada Newfoundland Manitoba Ontario New Zealand (dry basis) U.S. Idaho 40 ppm 40 ppm 60 ppm 40 ug/100 2 40 ug/100 cm ^ 80 ppm 35 ppm by wt indiv- idual sample 35 ppm in dividual sample 35 ppm Kentucky (dry basis) Maryland (dry basis) Montana New York (total F, dry basis) Texas 40 ppm unwashed forage 60 ppm(30 days for 2 consecutive months 80ppm (max) 60 ppm 40 ppm (30 days for 6 consecutive months) 80 ppm (max) 60 ppm 80 ppm un- unwashed washed for- forage age 40 ppm 35 ppm (max in 28 days) 60 ppm 80 ppm 40 ppm Washington (dry basis) 40 ppm Wyoming - 60 ppm 80 ppm 60 ppm (30 days for 3 consecutive months) 80 ppm (for 2 consec- utive months) 40 ppm 25 ppm 40 differences. These factors would be present under actual farm conditions. Therefore, Suttie's values may underestimate the 'fodder fluoride levels necessary to protect livestock from fluorosis. The fluoride content of bone provides a somewhat ambiguous evaluation of fluoride exposure in livestock. Studies at the University of Wisconsin indicate that bone fluoride at concentrations of 4,500 to 5,500 ppm (dry fat-free basis in long bones) might be considered the "marginal zone of toxicosis" with lower concentrations "not indicative of damage" (National Academy of Sciences 1971). Hillman, Bolenbaugh, and Convey (1979) found an average bone ash fluoride concentration of 2,400 ppm (assuming 60% ash, this figure corresponds to 1,440 ppm, dry ash-free basis) in Michigan dairy cattle with obvious signs of fluorosis. Studies with calves and sheep showed similar low values (Obel and Erne 1971; Zumpt 1975). Variation in experimental design may, in part, explain the apparent discrepancies in the data presented above. For example, the fluoride concentration varies with the selection of bone and with the sampling location on the bone (National Academy of Sciences 1974). Also, if this method is utilized for monitoring, it would be very inconvenient to biopsy live animals. The third method of measurement, urine analysis, is limited by the lack of an established relationship between urine concentrations and total fluoride intake. The importance of studying fluorosis in livestock comes from man's dietary utilization of many of their products. Rippel (1971) studied milk and eggs in a fluoride contaminated area. The 41 average fluoride concentration of milk was 0.6 mg/1, while controls averaged 0.2 mg liter - . Egg yolks from both areas contained similar concentrations, but the egg shells from the contaminated area contained 9 times more fluoride than the control. Although muscles (meat) concentrate much less fluoride than bones, the practice of mechanically deboning meat adds chips of bone, thereby greatly elevating fluoride levels (see section on diet as a source of fluoride under Health Effects of Fluoride). Studies concerning genetic mutations in livestock are of great importance if man is to maintain quality herds. Jagiello and Lin (1974) found some evidence of mutation in their in vivo and in vitro experiments with sheep, mouse, and cow oocytes. They suggested further investigation was needed. Some evidence exists of fluoride reducing the growth rate of livestock. Rose and Marier (1977) calculated a loss of about 4% in the average daily weight gain, over a period of 18 weeks, for each 100 ppm increment in dietary fluoride. These calculations were performed on data gathered by Forsyth, Pond, and Krook (1972b) on swine diets supplemented with sodium fluoride. Said, et al. (1977) reported similar reduced weight gain in sheep. 42 HEALTH EFFECT OF FLUORIDE Man In establishing an ambient air quality standard, we are inter- ested primarily in selecting a value which will not contribute fluoride to the total intake in amounts which would cause chronic fluorosis. Chronic fluorosis develops from long-term exposure to low levels of fluoride. In the past, changes in bone (osteosclerosis) and teeth (mottling) were the only criteria for diagnosing chronic fluorosis. At this point, however, irreversible damage had occurred. Recent studies have tried to develop subclinical symptoms of fluorosis so that the syndrome can be identified and treated before damage occurs. This research has concentrated not only upon the identification of the physiological changes, but also upon defining a set of physical symptoms from which physicians can diagnose the disease. It should be noted that in many of the studies which relate human illnesses to fluoride exposure, the total fluoride exposure of the patient was not known. Also, studies rarely considered factors which affect the toxicity of fluoride, such as the health and nutritional status of the individual. The absence of such information limits this evaluation. Sources To evaluate the hazard to humans posed by airborne fluoride, the total intake of fluoride by man must be estimated. The major portion of man's daily intake of fluoride comes from food and water. The amount of fluoride ingested from these sources has been the subject of 43 controversy recently. Much of this controversy seems to be the result of changing techniques for measuring fluoride and the question of what is included in "an average diet". Beverages, which have been processed with fluoridated water, and coffee and tea often are excluded from determinations, yet these can contribute significant amounts of fluoride to the diet. A number of investigators have gathered data indicating an increase in human exposure to fluoride over the past few years, due primarily to the increasing fluoride content of food. Rose and Marier (1977) have summarized many of these data. They indicate three sources which could cause the increases: the use of fluoridated water in food and beverage processing, the exposure of crops to airborne and waterborne fluoride, and the use of fluoride-containing fertlizers. Table 5, taken from Rose and Marier (1977), provides fluoride values for foods (past 1970) which have undergone processing or been exposed to air- or waterborne fluoride or fluoride-containing ferilizer, in comparison to some control values. The effect of fluoridated water used for food processing is apparent from the data on Gouda cheese (Elgeroma and Klomp 1975) . Also, the influence of airborne fluoride is obvious in the high values for leafy vegetables reported by Gordon (1970a); Jones, Harres, and Martin (1971); and Vouilloz (1975). The high fluoride content of wheat, spinach, cabbage, carrots, and other Indian foods (Lakdawala and Punekar 1973) presumably results from the uptake of soil- or fertilizer-borne fluoride. The high fluoride content of the mechanically-deboned meats results from the inclusion of bone chips (Kruggel and Field 1977). 44 Table 5. Recent data illustrating the effects of environmental factors on the range of fluoride contents in some foods (after Rose and Marier 1977). Food Explanation Fluoride content* (ppm, mg kg -1 or mg liter~l) Gouda cheese Beers Wines Pablum Baby formula Orange juice Cabbage Lettuce Fruits and Vegetables Lettuce Whole wheat Wheat flour 3 Spinach Cabbage Carrots Cola drinks Cow's milk >i ft Pork Cow beef Choice beef Beef Pork Normal Fluoridated, 1 ppm in processing water Fluoridated areas Ready to use Exposed, washed (1) Exposed Control samples Exposed As used Normal Exposed pastures Mechanically deboned Mechanically deboned 0.27 up to 2.16 up to 1.0 up to 0.7 4 to 12 0.9 to 1.0 0.9 2.8 to 3.24 (2) 12.0 to 19.6 (2) up to 100 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 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 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. 45 Recent data on the amount of fluoride ingested by children and adults are presented in Tables 6 and 7, as summarized by Marier and Rose (1977). It should be noted that these data are not all-inclusive estimates for total fluoride intake. Some of the studies exclude drinking water (Kramer, et al. 1974). The intake of fluoridated water with processed food varies due to differing estimates of the amount and kinds of canned food utilized in the "average diet" (Cummings 1966; San Fillipo and Battistone 1971; Kramer, _et_ _al . 1974). Also, the studies often do not include beverages in their estimations. Other studies have indicated additional sources of fluoride to man's daily intake. Okamura and Matsuhisa (1965) reported that American cigarettes contain an average of 244 ug of fluoride per cigarette. Full and Parkins (1975) noted an increase in the fluoride content of water boiled in Teflon-lined pans. Hardwick and Ramsey (1976), in a study of English teenagers, estimated that the mean daily intake of fluoride from dentifrice was 0.32 mg, with an extreme of 5.0 mg. Rose and Marier (1977) have drawn the following conclusion concerning total daily fluoride intake in man: "Until further data become available we recommend that statements relating to fluoride intake by adults in North America should assume a 'from foods' fluoride intake of 1.5 to 2.75 mg/day, and an intake from 'food 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 en- vironments, by copious tea drinkers, and by individuals with polydipsia (excessive thirst)." Taves (1979) reviewed some of the recent studies which have indi- cated an increase in fluoride intake. He concluded that the data 46 Table 6. Recent data on the daily intake of fluoride by children (after Rose and Marier 1977). Fluoride intake, mg day 1 Age Locality with 1 ppm F in water Locality with low F in water Infants 1-4 week 6-8 week 3-4 month 4-6 month 5-6 year 0-1 year 2-8 year School 9-11 year under 12 over 12 14 year 15-18 year 0.37 to 1.29 2.7 1.60 2.25 1.48 to 1.90 0.32 0.57 1.02 1.23 0.85 to 1.1 0.11 to 0.45 1.6 1.0 to 2.15* 0.89 0.74 to 2.0 1.21 to 2.71 1.06 to 2.10 1.07 c The high value referes 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. 47 Table 7. Recent data on the daily intake of fluoride by adults (after Rose and Marier 1977). Fluoride intake, mg day 1 1 mg liter ^ F in wat er Low F in water 3.57 to 5.37 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 1.45 to 2.74 0.8 to 0.9 ("food stuff" only) 0.81 (without exercise) 1.20 (moderate exercise) 1.98 (strenuous exercise) 0.78 to 1.03 (exclusive of beverages) 0.73 to 0.94 (three meals only) 48 were not reliable and that there had not been a significant increase in fluoride intake. He criticized the results of Kramer, et al. (1974) and Osis, et_ al_ . (1974) [who worked with Spencer] primarily on the basis of measurement technique. He cited results obtained from a study which utilized the same foods, but a different method of measurement (Taves and Ning, in preparation). Discrepancies were as high as 200-fold. Agreement was found only for one food item. Taves criticized the results of San Filippo and Battistone (1971) because their food proportions were based on 16- to 19-year-old males, i. e., heavy eaters. He also noted that their measurement technique was only slightly better than the one used by Spencer's group. Scientists which support the lower intake values indicate a total fluoride intake ranging from 0.3 mg to 0.8 mg of fluoride per day from food (Hodge and Smith 1970; Forbes, e£ al_. 1973). Yet, if the additional fluoride due to drinking water is included, the lower intake values are increased. In a recent National Research Council report (1977), the average amount of drinking water (in all forms) consumed per healthy adult was given as 2 liters day - - 1 , a value often expressed in other studies. Total fluoride intake would then range from 2.3 mg to 2.8 mg fluoride per day. Therefore, there is a difference of approximately 1 . 2 mg fluoride per day between this value and Rose and Marier's. The contribution of airborne fluoride to the daily intake is often considered negligible (National Academy of Science 1971). The inhalation of air containing 0.1 ug, a level rarely encountered in non-industrial urban areas, would result in an intake of only 2.0 ug 49 of fluoride per day (note that workmen can be exposed to as much as 2.5 mg m~^ fluoride according to Occupational Safety and Health Adminstrat ion standards. Fluoride intake from the air by workers exposed to this concentration would approach 25 mg (Rose and Marier 1977). Bone Accumulation of fluoride in the skeletal system begins with ges- tation (Messer, Armstrong, and Singer 1974; Forsyth, Pond, and Krook 1972a; Shen and Taves 1974; Hanhijarvi 1975; Hellstrom 1976). The accumulation of fluoride in the skeleton during growth appears to be controlled by three factors: the amount of fluoride ingested via the digestive system and lungs, the activity and receptivity of the skeletal surfaces, and the efficiency of fluoride excretion by the kidneys (Rose and Marier 1977). Young and cancellous bones are more receptive to fluoride uptake (World Health Organization 1970). Thus, with age, the skeleton tends to accumulate more and more fluoride. A "plateau effect", a decrease in fluoride uptake with increased amounts of bone fluoride, has been suggested for older individuals (Jackson and Weidman 1958; World Health Organization 1970). Any decline of uptake, however, would be more than offset by the decline in renal efficiency of the elderly (Husdan, et al. 1976). Schellman and Zober (1975) and Parkens, et aL. (1974) developed regression equations relating age to bone fluoride for individuals using low-fluoride water (0.2 ppm) and 1 ppm fluoride. Comparison of these groups clearly indicate the cumulative effect of even 1 ppm fluoride on skeletal fluoride. 50 Recent work with bone fluoride has dealt with the physical and chemical changes induced by chronic fluoride intake. Data clearly indicate that the dose levels of fluoride which induce no recognizable symptoms of fluorosis are, nevertheless, affecting bone structure and, therefore, bone response to stress (Table 8). Also, recent papers have confirmed that ingested fluoride influences the chemical composition of bone. Chan, et al. (1973), Rosenquist (1974), and Riggins, et al. (1976) observed higher magnesium levels in the bones of animals that had ingested fluoride. Miller, Egyped, and Shupe (1977) and Henrikson, et al. (1976) noted altered levels of calcium and phosphorus in cows and dogs. The earlier fluoride-induced changes in the bone are now being used by some researchers to diagnose occupational fluorosis. The techniques are dicussed by Franke and Auerman (1972) and Horn and Franke (1976). Franke and Auerman (1972) and Schlegel (1974) empha- sized that muscular-skeletal symptoms can be related to structural bone changes in mild fluorosis. Yet, studies to date have not related these symptoms to identifiable bone changes (Hiszek, et al. 1971; Popov, Filatova, and Shirshever 1974). Smith and Hodge (1959) and Franke and Auerman (1972) have indi- cated that bone ash concentrations of 4000 ppm fluoride are required before actual skeletal fluorosis can be diagnosed. Riggins, Zeman, and Moon (1974), however, diagnosed symptoms with bone ash concentrations as low as 3000 ppm fluoride. 51 Table 8. Effects of fluoride on some physical properties of animal bones (after Rose and Marier 1977). Species Fluoride source and duration Observations Rooster Diet, 600 ppm, 4 months Reduced breaking strength Quail Mice Diet, 750 ppm, 35 days Water, 10 ppm from birth Rat, young 45, then 135 ppm in water during growth Rat Diet, 3.4, 45 ppm, 15 weeks Water, 50, 150 ppm Water, 100 ppm, 3 months Rat, adult Same as above Dog Diet, 1, 3, 9, 27 ppm 287 days Reduced breaking strength of femurs Increased radiographic density if calcium deficient Slight reduction in age-related decline in breaking strength Increased radiographic density if calcium adequate Decreased radiographic density if calcium deficient With adequate calcium, increase in flexibility, no decrease in strength With deficient calcium, increase in flexibility, decrease in strength Increased radiographic density Reduced breaking strength Reduced cross-sectional area Reduced modulus of elasticity Reduced breaking strength Slightly increased radiographic density With low calcium - high phosphorus, no radiographic effects, decreased mineral mass in mandibles, no effect on bending and tension tests 52 Teeth Mottling of teeth is a symptom of exposure to excess amounts of fluoride. However, this symptom is present only if the exposure occurs during the first 10 years to 12 years of life (in humans), during the formation of permanent teeth. Most studies concerning the threshold concentration of fluoride for mottling of teeth have not evaluated total fluoride intake. Reliance solely upon drinking water concentrations has produced a wide variation in results (Table 9). Blood Within 10 minutes after ingestion, fluoride is detectable in the bloodstream under ordinary conditions (Carlson, Armstrong, and Singer 1960). About 47.5% is absorbed through the upper bowel and 25.7% through the stomach walls by simple diffusion (Stookey, Dellinger, and Muhler 1964). Gaseous fluoride, especially hydrogen fluoride, readily enters the bloodstream, mainly in the upper portions of the respiratory tract. The uptake of particulate fluorides is governed mainly by the size of the particles. Particles with a diameter from 0.5 u to 5 u will be taken into the lungs and absorbed into the bloodstream within minutes, especially if they are water soluble (Collings, et al. 1952). Larger particles are removed from the body with mucus or are swallowed (Bates, et al. 1966). The metabolism of ingested fluoride can be modified by several factors. The presence of aluminum, calcium, magnesium, and phosphates in food and water can slow down the absorption of fluoride (Lawrenz and Mitchell 1941; Weddle and Muler 1954). Although increased uptake 53 Table 9. Effects of various fluoride concentrations in drinking water upon humans (after McKee and Wolf 1963). Concentration of Fluoride Effect (mg liter" 1 ) 0.2 0.6 0.7 0.8 .8 - 0. ,9 .8 - 1. 0.9 0.9 0.9 1.0 1.0 1.0 ,5 1 .0 - 2. 1.2 1.4 1.5 ,0 1 .7 - 1. 2.0 8 2 .0 - 3. ,0 2 .0 - 3. 2.5 2.5 3-4 3-6 3 .5 - 6. 4.0 4.0 2 4, .4 - 12 5.0 6.0 6.0 6.0 8.0 10 11.8 12 13.7 115 180 2000 i Mottled teeth in 1% of children No effects at this concentration or lower Mild dental fluorosis in 8.5% of children No effects at this concentration or lower Mild mottling of teeth Threshold for mottling of teeth Mild mottling of teeth Mottling occurred as a result of high water use Critical concentration for mottling Threshold for mottling of teeth 10% of children had mottled teeth 90% of children had mottled teeth Mild to moderate mottling No effect at this concentration No skeletal schlerosis found Limiting concentration for drinking water 50% of children had mottled teeth Gave mottling and weakening of tooth structure Retained in system Moderate to severe mottling 75% to 80% of children had mottled teeth No evidence of skeletal fluorosis Not likely to cause endemic cumulative toxic fluorosis in adults Gave severe mottling No adverse effect upon carpal bones of children 90% of children had mottled teeth No disorders other than dental mottling Caused chronic fluorosis and affected skeletal system No effect upon height, weight, or bone Threshold for appreciable effect upon bone 100% of children had motled teeth Pitting and chipping of tooth enamel No deleterious bone changes except dental mottling Some cases of skeletal fluorosis Chronic fluorine intoxication in adults Affects deciduous teeth 100% of children had mottled teeth Sub-lethal in drinking water Toxic to man in drinking water Lethal dose in drinking water 54 of calcium and phosphorus has only a limited effect upon the amount absorbed (Spencer, _et_ jil_. 1975). Ingested fat enhances the absorption of fluoride by delaying the emptying of the stomach (McGown and Suttie 1974; McGown, Kolstad, and Suttie 1976). Fluoride is absorbed more rapidly and completely in an acid stomach, as in persons with stomach ulcers, than in a "normal", less acid stomach (Walbott, Birgstahler, and McKinney 1978). Recent research concerning the fluoride content of blood has been directed toward evaluating the forms of fluoride present in blood, the response of blood fluoride concentration to ingested or injected fluoride, the relationship of plasma fluoride to bone fluoride or to age, the effects of fluoride upon ill health, and the effects of fluoride upon other blood components. Taves (1968) presented evidence that two forms of fluoride exist in the human blood, i. e., organically-bound and free (ionic) fluoride. The significance of the organically-bound fluoride fraction was questioned when Taves (1971) reported that it was not present in dogs and rats. However, Taves, Grey, and Brey (1976) later isolated a major component of the bound fluoride, showing properties consistent with a derivative of per f luor inated octanoic acid. These researchers suggested that the presence of this compound may be a result of industrial contamination. Other research has indicated the absence of organically bound fluoride from rat plasma (Taves (1971) and bovine plasma (Taves, £t_ _al_. 1976). Rose and Marier (1977) attributed the presence of organically-bound fluoride in humans to a "specificity of human metabolism or a peculiarity of the human environment." 55 Recent studies have shown that the plasma fluoride ion concentra- tion responds rapidly and systematically to varying fluoride ingestion rates and to various physiological factors. Taves (1970) observed a doubling of serum fluoride ion concentrations 50 min after fasting individuals ingested 500 ml of water containing 1 ppm fluoride. Several other experiments along this line were performed using rats. Singer, Ophaug, and Armstrong (1976), Angmar-Mansson, Ericsson, and Ekberg (1976), and Suketa, et al. (1976) noted increases and decreases in plasma fluoride concentrations in response to ingested or injected fluoride. Response time varied from 10 min to 1 hr after introduction of the fluoride. Original concentrations returned at a maximum of 3 days after introduction. Several studies have indicated a direct relationship between plasma fluoride ion (F~) concentration and bone fluoride concentrations (Posen, Marier, and Jawarski 1971; Ericsson, et al. 1973; Parkins, et_ _al. 1974). Data gathered by Parkins, e£ al_. (1974) suggest that bone fluoride (iliac crest biopsy) and plasma F~ increased with increasing age in humans. This trend was supported by the findings of Hanhijarvi (1975), Husdan, et al. (1976), and Kuo and Stamm (1975). Rose and Marier (1977), after reviewing the equations relating plasma F~ to age presented by these authors, noted that in non-fluoridated communities, young adults tend to have plasma F~ concentrations below 0.7 umol per liter and that this increases by about 0.02 umol per liter per year. Recent fluoride research also has been directed toward an evalua- tion of fluoride intake upon ill health. Sufficient data exists to suggest that people suffering from renal insufficiency, anuresis, and 56 diabetes should be considered a "high risk group" (Seidenberg, Flueler, and Binswanger 1976; Hosking and Chamberlain 1972; Hanhijarvi 1975). The intake of fluoride influences several other blood constituents. Researchers have investigated several components using experimental animals and humans. A consistent observation in the research with rabbits and rats is a decrease in red blood cells, measured as blood iron, blood hemoglobin, or erythrocyte count. This observation is of interest because of reports of anemia in humans residing near fluoride emission sources (Rose and Marier 1977). Urine Fluoride is removed from the system principally by the kidneys as urine, but also may leave the body as feces, sweat, saliva, tears, or milk. The fluoride content of urine has received the most research. Wide variation in the amount of fluoride thus excreted has been detected, but the cause of this variation is unknown. Toth and Sugar (1975) determined the average fluoride content of urine samples from a low fluoride environment to be 0.26 + 0.01 mg 1 . Several recent studies have noted increases in urinary fluoride of individuals residing near a source (Balozova, Rippel, and Hluchan 1970, Tsunoda, et al. 1973) or working in a f louride-related industry (Polakoff, Busch, and Okawa 1974; Pantucek 1975; Boillat, et al. 1976). The fluoride-balance studies undertaken by Spencer, Osis and Wiatrowski (1974), and Spencer, e_t_ al_ . (1975) reaffirm earlier conclusions that fluoride is not readily excreted in urine, following a reduction in fluoride intake. 57 The work performed by Hanhijarvi (1975) and Jolly (1976) relate fluoride elimination via urine to age. Hanhijarva noted an increase in fluoride elimination until the age of 50, then a decline. This suggested an increase in storage of fluoride in the body. The results of work by Hanhijarvi (1975), Kuo and Stamm (1975), and Buttner and Karle (1974) provide a means of identifying those people with reduced ability to eliminate fluoride by excretion. Pregnant women and people with impaired cretinine clearance, diabetes mellitus, or renal insufficiency shold be considered high risk according to those studies. Enzymes Fluoride inhibits some enzyme systems while other are activated. The strong affinity of the fluoride ion for calcium and phosphorus accounts for its deposition in hard tissues (bones and teeth), while its affinity to many metals, magnesium and manganese for example, accounts for its interference with enzyme systems (Waldbott, et al. 1978). Research on the alteration of enzyme systems in relation to fluoride can be examined in hopes of explaining some of the various symptoms exhibited by patients with skeletal or preskeletal fluorosis. For example, Kaul (1976) recently noted a marked inhibition of succi- nate dehydrogenase activity in experimental animals and patients with skeletal fluorosis. This would impair oxidative metabolism in skel- etal muscles and result in muscular weakness and muscle wasting. This is a condition encountered in both skeletal and preskeletal fluorosis (Waldbott, et al. 1978) . 58 Waldbott, et_ ^1_. (1978) present a discussion of research on enzymatic changes which could explain some of the symptoms they have noted in patients and have diagnosed as preskeletal and skeletal fluorosis. The following paragraphs concerning soft tissues represent a summarization of this discussion. Gastrointestinal Tract Fluoride reacts with water in the stomach and upper gastrointes- tinal tract to produce hydrofluoric acid. Gastric pains and hem- morhages have been noted after the intake of fluoride, in air, in water, or as tablets (Feltman and Kosel 1961; Kauzal 1963; Shea, Gillespie, and Waldbott 1977; Waldbott 1977). Also, Czerwinski and Lankosz (1977) found that 12 of 60 retired aluminum workers had gastric ulcers. Kidneys After examining the recent observations of several investigators, Rose and Marier (1977) suggested that sustained fluoride intake may contribute to degeneration of the kidneys in people with diabetes insipidus, and pointed out that fluoride could cause the syndrome. Waldbott, et al. (1977) discussed several clinical cases they have encountered where kidney impairment seemed to be a result of fluoridated water. Parathyrod Glands These glands regulate calcium and phosphorus in the body. Waldbott, et al. (1978) discussed evidence that the disrupting effect of fluoride on calcium and phosphorus levels can result in hyperparathyroidism. 59 Arteries Waldbott, et al. (1978) noted six clinicians who observed calcification of arteries in association with skeletal fluorosis. They concluded that fluoride in the arteries may attract calcium. Geever, et al. (1971) reported fluoride concentrations of 8400 ppm in the aortas of two middle-aged men. This is the highest fluoride value in soft tissue ever recorded (Waldbott, et al. 1978). Heart Data concerning the effect of fluoride on the heart are sparce. Studies showing heart damage from fluoride usually involve large doses of the ion. Other indications of heart damage come from statistical studies of fluoridated and non-fluoridated populations. No conclusions can be drawn from the available data. Thyroid Studies by Day and Powell-Jackson (1972) and Teotia and Teotia (1975) have noted a higher incidence of goiter in areas with fluori- dated water. Benagiano, Colasanti, and De Simone (1959), however, found both increases and decreases in thyroid function in areas with high fluoride water (2.1 ppm). Galletti and Joyet (1958) suggested that fluoride does not impede the normal capacity of the thyroid gland to synthesize hormone if there is abundant iodine in the blood. If iodine levels are low, however, fluoride interferes with the function of the gland. Liver Fluoride can accumulate in the liver under certain conditions. Research in this area has concentrated upon the enzymatic system of 60 the liver. Alkaline phosphatase, which is involved in the growth of bones and the function of the liver, was elevated when large doses of fluoride were administered to patients with osteoporosis (Srikantia and Siddiqui 1965; Merz, Schenck, and Reutter 1970). Yet, Ferguson (1971) noted an 86% decrease after 4 weeks of use of 1 ppm fluoridated water use by students. After 8 weeks of use, values had returned to normal . Esterase was inhibited in the liver of humans after low doses of fluoride, yet not in the pancreas or bowels (Gomori 1955). Other recent research concerning the liver and fluoride utilizing laboratory animals has been summarized by Rose and Marier (1977). These studies indicate various enzymatic changes associated with the liver. Central Nervous System Waldbott, et al. (1978) noted that many of their patients inflicted with fluorosis experienced headaches, vertigo, spasticity in the extremities, visual disturbances, and impaired mental acuity. They summarize work which indicates that these are manifestations of damage to the central nervous system due to fluoride. Soviet physicians also have noted neurological symptoms in 79% of patients with occupational fluorosis (Popov, Filatova, and Shirshever 1974). Franke, et al. (1973) found structural changes in the anterior brain cells and muscle cells of patients with fluorosis. These results correspond to results of work on the brain cells of guinea pigs (Czechowicz, Osada and Slesak 1974) and the muscular response of rats (Benetato, et al. 1970). However, in another investigation 61 where extensive muscle damage was seen in tissue from humans with skeletal fluorosis, no changes were noted in nerve tissue (Kaul and Susheela 1976) . Others Waldbott , et al. (1978) have summarized the available data concerning fluoride and several other tissues in hopes of explaining some common symptoms they have found among their patients. They present data suggesting that excessive thirst and increased urination may be related to a loss of vasopressin, a hormone secreted from the pituitary gland. The pituitary gland regulates water and sugar metabolism and rate of growth. The vision problems present in fluorotic patients may be associ- ated with the nervous system disruption discussed previously. Enzyma- tic changes in the ear may result in vertigo and tinnitus. Waldbott, et al. (1978) describes a skin disorder called "chizzola" maculae as an early sign of chronic fluoride poisoning. They have found this disorder in association with excess fluoride intake from air, water, and food. They also discuss several cases reported by other researchers where the skin of patients exhibited an allergic response to fluoride. Mutagenic and Carcinogenic Implications Several researchers have investigated the possibility of muta- genic effects from fluoride. Gileva, Plotko, and Gat iyatullina (1975) exposed rats to cryolite with a concentration of fluoride similar to the air in the electrolysis areas of aluminum plants and also to cryo- lite and hydrogen fluoride mixtures. They found 3.5 to 4.5 times more 62 chromosomal abberations in the rats exposed to concentrations above 3 mg fluoride m J and to the mixture. Mohamed and Weitzenkamp- Chandler (1976) noted increasing amounts of gene mutations in mice with increased fluoride in their drinking water. Waldbott, et al. (1978) devoted an entire chapter to a discussion of the possibility that fluoride causes genetic damage, birth defects, and cancer. He noted that some of the evidence on mongolism, chromosomal damage, and cancer had not been refuted. Cecilioni (1972) found that lung cancer was more prevalent in the industrial area of Hamilton, Ontario. The vegetation in that area showed obvious fluoride damage. Cecilioni, however, did not discount the possibility of synergism with other pollutants. Rose and Marier (1977) stated that no conclusion could be drawn concerning the carcinogenic effects of fluoride given the available data. They also pointed out that other carcinogens cannot be excluded, and added that research should be directed toward the specific exposure of fluoride, especially concerning lung cancer. Nutrition and Fluorosis The relationship between nutrition and the severity of fluorosis has been discussed in depth by Rose and Marier (1977). They primarily considered the influence of calcium- and magnesium-rich diets in diminshing the severity of fluoride poisoning. Several studies with laboratory animals have resulted in de- creased or increased symptoms of fluorosis by altering the calcium intake (Guggenheim, Simkin, and Wolinski 1976; Reddy and Rao 1972; Reddy and Srikantia 1971; Forsyth, Pond, and Krook 1972a; Spencer, 63 Cohen, and Garner 1974). Rose and Marier (1978) concluded that fluoride supplements administered in treatment of osteoporosis create a greater metabolic requirement for calcium in humans. They noted the symptoms common to magnesium deficiency and fluorosis and concluded that there is evidence that fluoride intake can increase the long-term metabolic requirement for magnesium. The same may be true for manganese. Some evidence exists, however, suggesting that an adequate supply of vitamin C can reduce the toxic effects of fluoride. Risk Groups Rose and Marier (1977) and Waldbott, et_ al_ . (1978) stress the importance of identifying groups of individuals who are more "at risk" than the general population from fluorosis. One group is those individuals having kidney impairments. They have insufficient ability to void their bodies of fluoride, which results in an increased body-burden of fluoride and a faster rate of accumulation. Persons suffering from nephoropathic diabetes insipidus are included in this group. Polydipsia (excessive thirst) associated with diabetes may result in increased fluoride intake due to the consumption of large quantities of fluids. Fluoride may increase the incidence of goiter in people living in a region where goiter is endemic. Persons having a nutritionally insufficient diet, especially with regard to calcium, magnesium, manganese, and vitamin C and a low calcium/phosphorus ratio. Persons living near fluoride-emitting industries. 64 Persons working in fluoride-emitting industries are exposed to high levels of fluoride and require low ambient levels in their community to "recover." Total Daily Intake for Man To establish "safe" standards, criteria must be developed which define the acceptable level of intake. Yet precise data on the total daily intake of fluoride by humans are scarce. Most studies consider only single sources of exposure and rarely evaluate the effects of duration and concentration. However, the need for such criteria is apparent, and Rose and Marier (1977) have attempted to establish criteria based on the work of Farkas (1975), Toth (1975), and their own calculations. Farkas (1975) directed a questionaire to authorities in the fields of dentistry, medicine, nutrition, and biological research. The questionaire requested an estimation of a safe level of fluoride intake. Although no concensus developed, five 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 ingested with drinking water should be considered optimal. He estimated a "toler- able dose" of 0.073 mg kg -1 body weight per day for infants, and 0.033 mg kg -1 for adults. Rose and Marier (1977) estimated intake values based upon bone and plasma fluoride. Their estimates, though showing some variation, showed sufficient agreement with the values expressed by Farkas and Toth to make them meaningful. Their calculation based upon the rib 65 bone was 0.036 mg kg - * to 0.059 mg kg - , and, based upon the plasma F - , 0.053 mg kg - * to 0.76 mg kg - - 1 . It should be noted that these values apply to an "average" individual and allowances should be made for "high risk" individuals. The daily intake of fluoride discussed in the preceeding para- graphs does not include the fluoride intake from air. Inhaled fluor- ides, in both gaseous and particulate form, are almost completely absorbed into the bloodstream (World Health Organization 1970; Hodge and Smith 1977). Workplaces exposed to 2.5 mg m airborne fluoride could result in a daily fluoride uptake of 0.255 mg kg - * body weight (Rose and Marier 1977). While exposure to "high" ambient levels of 1.0 ug m J would result in daily uptake of 0.00029 mg kg - * [the airborne concentration is multiplied by 20 (nH) , the estimated volume of air utilized per day (National Academy of Science 1971) and divided by 70 (kg), the weight of the Reference Man]. Therefore, the contribution for airborne ambient fluoride levels can be considered negligible compared to the volumes ingested from foods and beverages. 66 STANDARD Fluoride is a widely distributed pollutant which is accumulated by many organisms. Chronic accumulation of fluoride by man is known to cause skeletal damage termed skeletal fluorosis. Recent research has indicated that damage may occur before obvious skeletal effects become detectable. The effects of fluoride upon animals, domestic and wild, are elevated with increasing age and stress. Plants accumulate fluoride in their leaves often producing necrosis and chlorosis. The Clean Air Act as amended, August, 1977, pp. 15 -17, National Ambient Air Quality Standards, § 109(b)(1) states, "National primary ambient air quality standards prescribed, under subsection (a) shall be ambient air quality standards, the attainment and maintenance of which, in the judgement of the Administrator, based on such criteria and allowing an adequate margin of safety, are requisite to protect the public health." This standard cannot be determined given the available information. The Clean Air Act, §109(b)(2) states "Any national secondary ambient air quality standard prescribed, under subsection (a) shall specify a level of air quality, the attainment and maintenance of which, in the judgement of the administrator, based on such criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of such air pollutant in the ambient air." Ambient fluoride levels averaging 0.4 ug m~3 fluoride (30-day averaging time) appear to meet this definition and are proposed as an ambient secondary air quality standard for fluoride. In addition to protecting the public welfare, this level appears attainable using available emission control technology. 67 RATIONALE Ambient air quality standards are usually set on two levels for each pollutant. A primary standard is established at a level which, if attained and maintained, is requisite to protect the public health, with the allowance of an adequate margin of safety. Secondary standards are established to protect the public welfare from any known or anticipated adverse effects. A primary air quality standard for fluoride would designate a level at which man would be protected from the deleterious effects, both acute and chronic, which may result from fluoride intake. This standard cannot be determined given the available information. As discussed earlier in this report (pp. 49 through 65), recent research indicates that man experiences preskeletal symptoms of chronic fluorosis and other physiological effects, but the exposure levels causing these symptoms have not been determined. At this time these symptoms have been associated only with major industrial sources of fluoride. The ability to diagnose chronic fluorosis in its preskeletal phase could eliminate the vast majority of the permanent damage evident in the skeletal phase. A secondary standard for fluoride can be established given the available data. This standard should not result in the accumulation of fluoride in plants which would harm domestic or wild animals, and the level should not cause decreased production in the plants themselves. A number of investigators have suggested threshold daily ingestion rates for man which are in fairly close agreement (approximately 0.073 mg kg - * body weight for infants, 0.033 mg kg -1 for adults). The U.S. Environmental Protection Agency (1976) summarized foliar damage information for tolerant, intermediate, and sensitive plants (Figure 2). 68 HOURS 100 "1 I I I I T I I Intermediate * * •■•*.-:•? ,»J-*S 5».; :'• Swiiitiw J I I '''' ' ' i I I I I I DURATION OF EXPOSURE DAYS Figure 2. The relationship of concentration of atmospheric fluoride (vertical axis) and duration of exposure (horizontal axis) to the threshold for folial symptoms for sensitive, intermediate, and tolerant species of plants (after U. S. Environmental Protection Agency 1976). 69 Their data indicate that foliar damage, which can reduce production, will develop in sensitive plants if fluoride levels are over 0.38 ug m~3 for 100 days. It should be noted that an appreciable amount of this information was acquired in "optimal" greenhouse conditions. McCune (1969) suggested 0.5 ug m -3 as a long-term exposure limit for sensitive species such as gladiolus, sorghum, conifers, and citrus. The U.S. Environmental Protection Agency (1979) stated that the available data suggest that a threshold for significant foliar damage, necrosis on sensitive species, or accumulation of fluoride in forage of more than 40 ppm would result from exposure to a 30-day average air concentration of about 0.5 ug m~3. Rose and Marier (1977) estimated that average gaseous fluoride levels in ambient air should be below 0.4 ug m~3 a nd might have to be as low as 0.2 ug m~3. Sidhu (1977a) concluded that safe levels for forest species were between 0.17 ug m~3 to 0.23 ug m~ 3 . Given the available data discussed earlier in this report, a recommendation of 0.4 ug m~3 per 30 days averaging time is given for a ambient air quality standard for fluoride. As stated previously, this level cannot guarantee the protection of the health and welfare of man from subclinical effects of fluorosis and may result in a limited amount of leaf damage to certain sensitive plants, possibly reducing production. It will, however, limit fluoride intake by man via respiratory pathways to approximately 0.2% of the average individual total daily uptake. This value also will limit accumulation in forage and protect plants and animals important to Illinois economy. 70 Glossary Aluminum flouride, AlFo Ammonium fluoride, NH^F Ammonium f luorosilicate , (NH^^SiF^ Aqueous hydrofluoric acid, nHF(aq . ) Calcium fluoride, CaF2 Cryolite, Na3AlF£ Dichlorodif luoromethane , CF2CI2 1 , 2-dichloro-l , 1 , 2 , 2-tetraf luroethane , CClF 2 CClF 2 Fluorapatite, CaF 2 ' 3Ca3(PC>4) 2 or Cajo F 3( p 04^6 Fluorine, F 2 Fluorite, CaF 2 Fluorspar, CaF 2 Fluorosilicic acid, H 2 SiFg Freon, CF 2 C1 2 Hydrofluoric acid (aqueous), nHF(aq . ) Hydrogen fluoride (anhydrous), HF Methoxyfurane, CH 3 OCF 2 CCl 2 H Penthrane, CH 3 OCF 2 CCl 2 H Potassium f luoroborate , KBF^ Potassium f luorosilicate , K 2 SiF^ Silicon tetraf luoride, SiF^ Sodium fluoride, NaF Sodium f luorosilicate , Na 2 SiF^ Trichlorof luoromethane, CFCI3 71 REFERENCES Abernathy, R. F., and F. H. Gibson. 1967. Method for determination of fluorine in coal. U.S. Bureau Mines Rept. 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