Download Sources of Fluoride Toxicity

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
Transcript
Chapter 2
Sources of Fluoride Toxicity
Abstract Sources of excess fluoride intake for animals are diverse and include
drinking water, fluoride compounds used for household and agricultural purposes,
forage and grasses contaminated with industrial fluoride emissions or volcanic
ash, and occasionally, poor quality mineral mixture and feed supplements. Soil
rich in soluble fluoride may also be responsible for fluorosis in grazing animals,
particularly when growing vegetation is small and scanty. Toxicity arising due to
airborne fluoride is rare and oral intake remains the major route of excess fluoride
uptake. A water fluoride level as low as 1.5 ppm can cause chronic fluoride toxicity in several species, although the literature suggests higher water fluoride tolerance levels in most domestic animals. Volcanic-ash–contaminated pasture has been
reported to cause mortality outbreaks in grazing animals in several countries.
Fluoride (F) toxicity can arise due to excessive fluoride intake from a variety of
natural or manmade sources. Important F sources for animals include vegetation/
forage contaminated by fluoride-rich industrial effluents or windblown or rainsplashed soil with high fluoride content, water high in fluoride content either
naturally or due to industrial contamination, mineral mixtures and other feed
supplements containing excess fluoride, vegetation grown on soils high in fluoride content, and a combination thereof (Shupe 1980; Swarup and Dwivedi 2002;
Fig. 2.1). Fluoride is well absorbed by several routes, however, ingestion is the
major mode of fluoride uptake for most animals (Shupe 1980). Soluble fluoride is
distributed over the earth’s surface and atmosphere as a result of natural processes
such as erosion, hydraulic leaching, volcanic activity, and to a lesser extent by
mining and manufacturing processes. Animals when grazing over soluble fluoriderich soil can ingest toxic doses of fluoride, especially if the pasture is overgrazed
and animals are grazing small plants close to the soil (Shupe and Olson 1971). In
this chapter, important sources of acute and chronic fluoride toxicity for animals
are described in brief.
© The Author(s) 2015
R. Ranjan and A. Ranjan, Fluoride Toxicity in Animals,
SpringerBriefs in Animal Sciences, DOI 10.1007/978-3-319-17512-6_2
11
2 Sources of Fluoride Toxicity
12
Water
(drinking)
Feed supplements
Vegetation
(grazing)
(Bone & fish meal)
Animals
Volcanic ash and
gases
Mineral mixture
Industrial F
emission (gaseous
and particulates)
Agrochemicals
Containing fluoride
Fig. 2.1 Sources of fluoride toxicity in animals
2.1 Natural Sources
Fluorosis in animals can occur due to high fluoride concentration naturally occurring
in dietary substances including feed, fodder, concentrate ration, and drinking water.
2.1.1 Forage, Grasses, and Grains
Soil fluoride concentration is believed to have little influence over fluoride concentration in vegetation, inasmuch as most of the fluoride in soils cannot be assimilated readily by plants. However, a direct relation is reported to exist between F
concentration in the soil and selected forage. Fluoride in forage increases by 3 ppm
for each 100 ppm increase in soil F up to approximately 2200 ppm (Mascola et al.
1974). Other factors modulating fluoride concentration in fodder plants include
height of the plant and season. Fluoride content increases with decrease in plant
height. The fluoride concentration is higher in plants grown during winter and
spring in comparison to those grown during summer and autumn (Mascola et al.
1974). Fluoride uptake by plant roots from soil occurs by passive diffusion, and
2.1 Natural Sources
13
thereafter F is carried to the shoot by transpiration. Most of the plants do not
accumulate fluoride in toxic concentrations and the level usually remains below
10 mg per kg dry weight. The tea plants (family Theaceae) can exceptionally accumulate high F concentrations. However, tea plants or their by-products are not a
usual ingredient of animal feed. Many plant species, particularly Acacia georginae and Dichapetalum cymosum (a South African shrub known as “Gifblaar”) can
assimilate soil F and convert them into fluoroacetate, which is extremely toxic
for animals (Shupe et al. 1984). Fluoroaceate is converted in vivo in mitochondria into fluorocitrate through condensation of fluoroacetyl-Co-A with oxaloacetate by the enzyme citrate synthetase which normally supplies acetyl-Co-A
into the citric acid cycle. Fluorocitrate is a strong inhibitor of aconitase, which is
an important enzyme of the Krebs cycle. Thus fluorocitrate inhibits the biochemical pathway for energy production in the organism (Patocka and Strunecka 2002).
It is interesting to note that gaseous fluoride compounds can enter leaves
through stomatal pores and in high concentration they may induce toxicity signs in
plants, including chlorosis, peripheral necrosis, leaf distortion and malformation,
and abnormal fruit development. Long-term exposure to F concentrations greater
than 0.2 μg/m3 may cause injury to plants (WHO 1984). It has been observed that
air-contaminated forage loses a portion of its fluorine to the atmosphere after cutting and during storage as hay (NRC 1960).
The mean fluoride concentration of mineral soils is around 0.2–0.3 g/kg, whereas
that of organic soil is usually lower. The fluoride content of topsoil increases by
the addition of fluoride containing phosphate fertilizers, pesticides, and irrigation water or by deposition of gaseous and particulate emissions from industry. In
New Zealand, it was found that long-term use of phosphorus fertilizers resulted in
an increase in total surface soil (0–75 mm depth) fluoride concentration up to 217–
454 mg per kg (Loganathan et al. 2001). Fluoride uptake by grazing animals through
plant consumption is expected to be much lower than F uptake directly by soil
ingestion because most plants do not accumulate F. Therefore, reducing soil ingestion by maintaining good pasture cover can reduce the risk of fluorosis in herbivores
(Loganathan et al. 2008). Forage and grasses grown in industrial areas are often contaminated by fluoride-rich industrial effluents or by windblown or rain-splashed soil
having a high fluoride concentration. Most industrial fluoride emissions are airborne
and fluoride-rich dust, ash, and fumes may contaminate soil, water, and vegetation
not only in the industrial vicinity, but also up to a considerable distance from the
source of emission (Radostits et al. 2000). In such conditions F concentration in
plants depends upon (1) the amount of fluorine released into the atmosphere, (2) the
distance between the F emission source and the pasture area, (3) the type of vegetation, and (4) the distribution pattern as affected by the wind and topography (NRC
1960). Plants grown in areas where F is emitted into the atmosphere may contain
500–1000 ppm fluoride. Hence, animals should not be allowed to graze in pasture
close to industries such as brick-kiln plants, rock phosphate processing plants, aluminum industry, and so on. Fodder plants grown in polluted areas should be harvested, soaked, and washed with water before offering to animals. This practice will
substantially reduce the available F to animals.
14
2 Sources of Fluoride Toxicity
Grains usually do not contain toxic concentrations of fluoride. Corn, wheat, oats,
and barley grown on F-rich soil have very low F concentrations (less than 10 ppm)
and nearly equal those grown on soil low in F (NRC 1960). Nevertheless, sorghum
(Sorghum bicolor) consumption in human beings has been found to increase the risk
and severity of osteo and dental fluorosis (Krishnamachari and Krishnaswamy 1973;
Hari-Kumar et al. 2007). Sorghum grown in fluorotic areas contains a high molybdenum concentration. Molybdenum reduces urinary fluoride excretion and enhances fluoride retention (Stookey and Muhler 1962). A sorghum-based diet therefore increases
F retention in human beings (Lakshmaiah and Srikantia 1977) and rats (Lakshmi and
Lakshmaiah 1999). It is surprising to note that sorghum plants are more susceptible to
hydrogen fluoride gas exposure than wheat plants (Mac-Lean et al. 1984).
2.1.2 Water
The fluoride concentration of natural groundwater depends upon geological factors,
consistency of the soil, porosity of rocks, pH and temperature of the soil, complexing
action of other elements, depth of wells, leakage of shallow groundwater, and chemical and physical characteristics of water (Li et al. 2014). Both surface and groundwater may have high F concentration in a particular locality, but the level is often higher
in groundwater than the surface water. When groundwater percolates through rocks
containing fluoride-rich compounds, fluoride leaches out and concentration may
increase far above the safe level. The mean fluoride content of rocks varies between
0.1 and 1.0 g/kg. Important fluoride-containing minerals are fluorspar, cryolite, and
apatite. However, in most soils, F is associated with micas and other clay minerals
that make them less soluble and hence less toxic. Sodium fluoride and magnesium
fluoride are also found as natural minerals. Fluoride contamination occurs through
a natural process in which fluoride-bearing rocks crumble and break down, but the
process can be speeded up if the chemistry of the aquifer is disturbed. Climatic conditions may also influence rate and degree of fluoride dissolution in water from rocks
and soil. High F concentration in shallow zone groundwater is largely due to the geochemical F deposition in the vicinity of the groundwater extraction structures. The
toxicity potential of fluoride-rich water is also influenced by the ambient temperature; alkalinity; and calcium, copper, and magnesium concentrations in water.
Water having a fluoride concentration up to 1.0 mg/L is safe, levels in between
1.1 and 2.5 mg/L are marginally contaminated, whereas above 2.6 mg/L are considered highly contaminated and dangerous for drinking purposes for human beings
(Susheela 1999). It is estimated that total fluoride intake by a person when potable
water contains 1 ppm fluoride would be from 0.05 to 0.10 mg per kg of body weight
per day (NRC 1960). Most terrestrial animals, particularly domestic herbivores, are
supposed to tolerate F in water higher than these threshold levels. However, many
reports indicate the appearance of toxic symptoms in cattle, buffalo, and other livestock reared in areas where mean water fluoride concentration is equal to or slightly
above 1.5 ppm (Choubisa 1999; Maiti et al. 2003; Ranjan et al. 2009).
2.1 Natural Sources
15
2.1.3 Volcanic Activities
Domestic and wild animals often suffer from severe fluorosis by ingestion of water
and plants contaminated with volcanic ash (Araya et al. 1990; Bellomo et al. 2007).
Volcanic ash usually has a very high soluble fluoride concentration and can be deposited over a large geographical area. In volcanic areas, the fluoride concentrations in
water and pasture grass may remain high for years even after cessation of volcanic
activities (Araya et al. 1993). The fluoride concentration in volcanic ash emitted by
the Hekla volcano, Iceland, was up to 2000 ppm and the forage covered by ash had
fluoride concentrations of 350–4300 µg/g (Thorarinsson 1979). In Chile in 1988, fluoride-bearing ash arising from the Lonquimay volcano affected more than 10,000 farm
animals and resulted in the death of more than 4000 goats, sheep, cattle, and horses
(SEAN 1989). Likewise, the death of thousands of sheep in 1995–1996 was attributed to ashfall from the Ruapehu volcano eruptions in Mexico (Armienta et al. 2011).
In Argentina, the ash (“tephra”) released from the Puyehue–Cordon Caulle volcanic
eruption in June 2011 reached up to a distance of 1400 km. Severe fluorotic dental
lesions were observed in wild red deer who died after the volcanic eruption, which
was attributed to consumption of grasses contaminated with volcanic ash (Flueck and
Smith-Flueck 2013). In Iceland, thousands of sheep, cattle, horses, and other domestic
and wild animals died due to repeated volcanic eruptions over the years (Armienta
et al. 2011). Occasionally, acute toxicity in animals may occur after inhalation of
hydrogen fluoride released from volcanoes (Weinstein and Davison 2004).
2.2 Anthropogenic Sources
Anthropogenic sources are also responsible for fluoride toxicity in animals. Some
of them have been described in this chapter.
2.2.1 Mineral Mixture and Other Feed Supplements
There are several reports documenting mineral supplements as a major source of
fluoride toxicity in livestock (Griffith-Jones 1977; Hillman et al. 1979; Singh and
Swarup 1995). In a cattle herd numbering 120 animals, introduction of a commercial salt lick with fluoride concentration 1400 mg per kg resulted in the development of fluorotic lesions after one year. The fluoride concentrations in water
and pasture samples were within the normal range suggesting the salt lick as the
sole source of excess fluoride intake (Schultheiss and Godley 1995). In northern
Australia, up to 15 % of cattle in a herd revealed signs of lameness due to use of
fertilizer-grade monoammonium and diammonium phosphate as a mineral supplement. The affected animals were given large quantities of the mineral supplement
thinking that the lameness was due to a phosphorus deficiency as it was an endemic
16
2 Sources of Fluoride Toxicity
problem in that area (Jubb et al. 1993). Chronic ingestion of gypsum that was
included in a feed supplement and also ingested from fertilizer dumps in paddocks
resulted in the death of 226 cattle at a farm over a period of 18 months. Here, direct
toxicity of gypsum as well as the effect of excess fluoride was incriminated as the
cause of heavy mortality in the cattle herd (Bourke and Ottaway 1998).
The starting material for almost all chemically processed phosphates in mineral
mixture and animal feed supplements is rock phosphate which contains approximately 13–14 % phosphorus and 3–4 % fluoride. The rock phosphate is first converted into phosphoric acid which is used for chemical synthesis of various types
of feed phosphates. Phosphoric acid is synthesized from rock phosphate either by
heating the rock phosphate in an electric furnace (dry process) or by treating the
rock phosphate with sulphuric acid (wet process). The phosphoric acid produced
by the electric furnace process has a very low F concentration and can be directly
used for chemical synthesis of feed phosphates. In phosphoric acid produced by
the dry heat process, the P:F ratio is usually greater than 2000:1 (Thompson 1980).
However, the energy requirement per unit of phosphorus produced is approximately
eight times greater in the dry process as compared to the wet process. Hence, the
cost of production of phosphoric acid by the dry process is almost double that of the
wet process. Wet process production methods therefore account for approximately
93 % of the total industrial production of phosphoric acid (Thompson 1980). The
phosphoric acid produced by the wet process should always be defluoridated before
use in feed phosphate synthesis. Defluoridation of phosphoric acid is done by addition of silicon dioxide and heat is supplied in the form of steam. The defluoridation process increases the cost of the feed phosphates, hence some manufacturers
skip this step and use the phosphoric acid produced by the wet process directly for
synthesis of feed phosphates. This may lead to high fluoride concentrations in mineral mixtures and animal feed supplements. Livestock, particularly dairy cattle may
suffer from fluorosis after consuming such mineral mixtures or feed supplements
(Singh and Swarup 1995). The phosphoric acid which has a P:F ratio of at least
100:1 is considered safe for production of feed phosphates for livestock.
2.2.2 Airborne Fluoride
The mean F concentration in ambient air in unpolluted or nonindustrial areas is
generally less than 0.1 µg/m3. The levels may be slightly higher in areas near aluminum smelters or other industries, but should not exceed 2–3 µg/m3. The current
“ceiling” value for F (in the form of hydrogen fluoride) in ambient air, as recommended by the National Institute for Occupational Safety and Health (NIOSH),
Washington, DC, is 2.5 mg/m3 (Weinstein and Davison 2004).
Fluoride is released in the atmosphere by natural processes and human activities in
both gaseous and particulate forms. Gaseous forms include hydrogen fluoride, silicon
tetrafluoride, hexafluorosilicic acid, and sulfur hexafluoride. Particulate forms include
sodium aluminum fluoride (cryolite), aluminum fluoride, calcium fluoride, sodium
hexafluorosilicate, lead fluoride, and calcium phosphate fluoride (fluorapatite). Natural
2.2 Anthropogenic Sources
17
dispersal of gaseous and particulate fluoride into the air has been recognized in regions
of volcanic activity (USEPA 1980). Other natural sources include dust from soil and
seawater droplets carried up into the atmosphere by winds (WHO 1984). Coal contains
a substantial amount of arsenic, silicon, and fluorine. Hence, coal-fired power plants are
important sources of anthropogenic hydrogen fluoride emissions. Fluoride concentration in coal may range 4–40 g/kg (McDonald and Berkeley 1969). According to an estimate, total air emissions of hydrogen fluoride by electrical utilities in 1998, 1999, 2000,
and 2001 were 64.1, 58.3, 58.3, and 55.8 million tons, respectively. In many parts of
China, coal burning for household purposes was documented as the cause of endemic
fluorosis in the human population (Guijian et al. 2007). Small kilns used for making
bricks and tiles are another source of airborne fluorosis in China and India. The fluoride
concentration in coal and mud used for making bricks and tiles may exceed 10,000 mg/
kg, hence a high emission of fluoride in the air occurs after firing (WHO 2000).
2.2.3 Industrial Effluents
More than 28 industries release fluoride-rich fumes and effluents into the environment (Swarup and Dwivedi 2002). Important among them are the aluminum industry, steel production plants, superphosphate plants, ceramic factories, coal-burning
power plants, brickworks, glassworks, and oil refineries (WHO 1984). Livestock
including cattle (Swarup et al. 2001), buffaloes (Patra et al. 2000), sheep (Sahoo et al.
2003), goats (Sahoo and Ray 2004), and camels (Karram and Ibrahim 1992) living in
the vicinity of such industries often suffer from chronic fluoride toxicity. Pasture contaminated with rock phosphate dust emitted from a fertilizer factory resulted in the
occurrence of fluorosis in sheep living in adjoining areas (Zumpt 1975). Wild herbivores are also reported to suffer from industrial fluorosis (see Chap. 5).
Hydrofluoric acid is used in the alkylation process for the production of highoctane fuels by refineries of crude petroleum. Waste products generated from such
refineries are mostly disposed of by land treatment, wherein waste products are
applied onto or into the soil for biodegradation of organic wastes, immobilization
of inorganics, and avoidance of bioaccumulation of hazardous compounds (Loehr
and Malina 1986). This practice results in an increase in soil fluoride concentration and may cause fluorosis in animals living on such soil. For example, fluorotic
lesions along with high bone fluoride concentration in cotton rats (Sigmodon hispidus) living in such petroleum-waste–treated areas was reported from some parts of
the United States (Paranjpe et al. 1994; Rafferty et al. 2000).
2.2.4 Agrochemicals and Household Products
Both organic and inorganic fluoride compounds are used for agricultural and
domestic purposes. For example, sodium fluorosilicate can be used as a rodenticide and sodium fluoride as a feed premix for treatment of roundworms in pigs.
18
2 Sources of Fluoride Toxicity
A few decades back, many fluoride compounds including sodium fluoride, cryolite, and sodium fluorosilicates were widely used for pest control in agriculture.
Accidental exposure to these compounds can cause acute toxicity in man and animals. Mass poisoning and death of about 800 dogs occurred after consumption of
poultry meat contaminated with fluoroacetate or fluoroacetamide in Israel (Egyed
1979). But these compounds are now rarely used and hence are of little significance as a source of fluoride toxicity in animals.
References
Araya O, Wittwer F, Villa A (1993) Evolution of fluoride concentration in cattle and grass following a volcanic eruption. Vet Hum Toxicol 35:437–440
Araya O, Wittwer F, Villa A, Ducom C (1990) Bovine fluorosis following volcanic activity in
southern Andes. Vet Rec 126:641–642
Armienta MA, de La Cruz-Reyna S, Cruz O, Ceniceros N, Aguayo A, Marin M (2011) Fluoride
in ash leachates: environmental implications at popocatepetl volcano, central Mexico. Nat
Hazards Earth Syst Sci 11:1949–1956
Bellomo S, Aiuppa A, D’Alessandro W, Parello F (2007) Environmental impact of magmatic fluorine emission in the Mt. Etna area. J Volcanol Geoth Res 165:87–101
Bourke CA, Ottaway SJ (1998) Chronic gypsum fertilizer ingestion as a significant contributor to
a multi factorial cattle mortality. Aust Vet J 76:565–569
Choubisa SL (1999) Some observations on endemic fluorosis in domestic animals in southern
Rajasthan (India). Vet Res Commun 23:457–465
Egyed MN (1979) Mass poisoning in dogs due to meat contaminated by sodium fluoroacetate or
fluoroacetamide (special reference to the differential diagnosis). Fluoride 12:76–84
Flueck WT, Smith-Flueck JA (2013) Severe dental fluorosis in juvenile deer linked to a recent
volcanic eruption in Patagonia. J Wildlife Dis 49:355–366
Griffith-Jones W (1977) Fluorosis in dairy cattle. Vet Rec 100:84–89
Guijian L, Liugen Z, Duzgoren-Aydin NS, Lianfen G, Junhua L, Zicheng P (2007) Health effects
of arsenic, fluorine, and selenium from indoor burning of Chinese coal. Rev Environ Contam
Toxicol 189:89–106
Hari-Kumar R, Khandare AL, Brahmam GNV, Venkiah K, Gal Reddy Ch, Sivakumar B (2007)
Assessment of current status of fluorosis in North-Western districts of Tamil Nadu using
community index for dental fluorosis. J Hum Ecol 21:27–32
Hillman D, Bolenbaugh DL, Convey EM (1979) Hypothyroidism and anaemia related to fluoride
in dairy cattle. J Dairy Sci 62:416–423
Jubb TF, Annand TE, Main DC, Murphy GM (1993) Phosphorus supplements and fluorosis in
cattle-a northern Australian experience. Aust Vet J 70:379–383
Karram MH, Ibrahim ThA (1992) Effect of industrial fluorosis on haemogram of camels.
Fluoride 25:23–36
Krishnamachari KA, Krishnaswamy K (1973) Genu valgum and osteoporosis in an area of
endemic fluorosis. Lancet 2:877–879
Lakshmaiah N, Srikantia SG (1977) Fluoride retention in humans on sorghum and rice based
diets. Indian J Med Res 65:543–548
Lakshmi AV, Lakshmaiah N (1999) Effect of different cereal-based diets on fluoride retention in
rats. In: Proceedings of the national seminar on fluoride contamination, fluoride and defluoridation techniques, Udaipur, India, 25–27 Feb 1999
Li C, Gao X, Wang Y (2014) Hydrogeochemistry of high-fluoride groundwater at Yuncheng
Basin, northern China. Sci Total Environ 508C:155–165
Loehr RC, Malina JF Jr (1986) Land-treatment: a hazardous waste management alternative.
University of Texas Press, Austin, p 369
References
19
Loganathan P, Hedley MJ, Grace ND (2008) Pasture soils contaminated with fertilizer-derived
cadmium and fluorine: livestock effects. Rev Environ Contam Toxicol 192:29–66
Loganathan P, Hedley MJ, Wallace GC, Roberts AH (2001) Fluoride accumulation in pasture
forages and soils following long-term applications of phosphorus fertilizers. Environ Pollut
115:275–282
Mac-Lean DC, McCune DC, Schneider RE (1984) Growth and yield of wheat and sorghum after
sequential exposures to hydrogen fluoride. Environ Pollut A 36:351–365
Maiti SK, Das PK, Ray SK (2003) Dental fluorosis in bovine of Nayagarh district of Orissa. J
Environ Biol 24:465–470
Mascola JJ, Barth KM, McLaren JB (1974) Fluoride intake of cattle grazing fluoride-contaminated forage, as determined by esophageal-fistulated steers. J Anim Sci 38:1298–1303
McDonald HE, Berkeley PD (1969) Fluoride as air pollutant. Fluoride Q Rep 2:4–12
NRC (1960) The Fluorosis problem in livestock production. A report of the NRC committee on
animal nutrition. Publication 824, National Research Council, Washington
Paranjpe MG, Chandra AM, Qualls CW Jr, McMurry ST, Rohrer MD, Whaley MM, Lochmiller
RL, McBee K (1994) Fluorosis in a wild cotton rat (Sigmodon hispidus) population inhabiting a petrochemical waste site. Toxicol Pathol 22:569–578
Patocka J, Strunecka A (2002) Organofluorine compounds in nature (abstract). Fluoride
35:255–256
Patra RC, Dwivedi SK, Bhardwaj B, Swarup D (2000) Industrial fluorosis in cattle and buffalo
around Udaipur, India. Sci Total Environ 253:145–150
Radostits OM, Gay CC, Blood DC, Hinchcliff KW (2000) Veterinary Medicine, a textbook of the
diseases of cattle, sheep, pigs, goats and horses, 9th edn. WB Saunders Company Ltd, London
Rafferty DP, Lochmiller RL, Kim S, Qualls CW, Schroder J, Basta N, McBee K (2000) Fluorosis
risks to resident hispid cotton rats on land-treatment facilities for petrochemical wastes. J
Wildlife Dis 36:636–645
Ranjan R, Swarup D, Bhardwaj B (2009) Distribution of clinical signs and lesions in fluorotic
cattle. Indian J Anim Sci 79:546–549
Sahoo N, Ray SK (2004) Fluorosis in goats near an aluminium smelter plant in Orissa. Indian J
Anim Sci 74:48–50
Sahoo N, Singh PK, Ray SK, Bisoi PC, Mahapatra HK (2003) Fluorosis in sheep around an aluminium factory. Indian Vet J 80:617–621
Schultheiss WA, Godley GA (1995) Chronic fluorosis in cattle due to ingestion of a commercial
lick. J S Afr Vet Assoc 66:83–84
SEAN (1989) Lonquimay, continued tephra emission: cattle sickened by ash. Scientific Event
Alert Network Bull, Smithsonian Institution 14:2–3
Shupe JL (1980) Clinicopathological features of fluoride toxicosis in cattle. J Anim Sci
51:746–758
Shupe JL, Olson AE (1971) Clinical aspects of fluorosis in horses. J Am Vet Med Assoc
15:167–174
Shupe JL, Olson AE, Peterson HB, Low JB (1984) Fluoride toxicosis in wild ungulates. J Am Vet
Med Assoc 185:1295–1300
Singh JL, Swarup D (1995) Clinical observations and diagnosis of fluorosis in dairy cows and
buffaloes: case report. Agri Practice 16:25–30
Stookey GK, Muhler JC (1962) Effect of molybdenum on fluoride retention in the rat. Proc Soc
Exp Biol Med 109:268–271
Susheela AK (1999) Fluorosis management programme in India. Curr Sci India 77:1050–1256
Swarup D, Dwivedi SK (2002) Environmental pollution and effects of lead and fluoride on animal health. Indian Council of Agricultural Research, Pusa, New Delhi
Swarup D, Dey S, Patra RC, Dwivedi SK, Ali SL (2001) Clinico-epidemiological observation of
industrial bovine fluorosis in India. Indian J Anim Sci 71:1111–1115
Thompson DJ (1980) Industrial considerations related to fluoride toxicity. J Anim Sci 51:767–772
Thorarinsson S (1979) On the damage caused by volcanic eruptions with special reference to
tephra and gases. In: Sheets PD, Grayson DK (eds) Volcanic activity and human ecology.
Academic Press, New York, pp 125–159
20
2 Sources of Fluoride Toxicity
USEPA (1980) Reviews of the environmental effects of pollutants: IX Fluoride. US Environmental
Protection Agency, Cincinnati, p 441 (EPA-600/1-78-050)
Weinstein LH, Davison A (2004) Fluorides in the environment: effects on plants and animals.
CABI Publishing, Cambridge
WHO (1984) Fluorine and fluorides. Environmental health criteria 36. World Health Organization,
Geneva
WHO (2000) Fluorides. In: Chapter 6.5 Air quality guidelines, 2nd edn. WHO regional office for
Europe, World Health Organization, Copenhagen
Zumpt I (1975) Chronic fluoride poisoning in sheep. J S Afr Vet Assoc 46:161–163
http://www.springer.com/978-3-319-17511-9