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Fluorosis in dromedary camels in Rajasthan, India

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  • NIMS University Rajasthan, Jaipur-303121, Rajasthan, India

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Natural occurrence of fluorosis was observed in a survey of 18 domesticated dromedary camels (Camelus dromedarius) living in fluoride (F) endemic areas of the Dungarpur district, Rajasthan, India. Among these camels, 15 were mature (up to 12 years old), and 3 were immature or calves (below age 3). The mean F concentration in the drinking water of these areas ranged between 1.4 and 3.3 ppm. Eight (44.4%) of these camels were afflicted with mild to severe dental fluorosis. Front (incisors) and upper cheek teeth were light brown to deep yellow in color. Irregular wearing of teeth was found, however, only with severe dental fluorosis. Three (16.7%) of the mature camels also showed periosteal exostoses, moderate intermittent lameness, and hardening of tendons in the legs as pathognomonic signs of skeletal fluorosis. In these camels colic was common, and abortions, irregular estrus cycles, and stillbirths were also noted in female camels (camela). However, the severity of F toxicity in camels was found less in comparison with other domestic animals of same F endemic areas. To the best of my knowledge, endemic chronic F intoxication in camels in the form of dental and skeletal fluorosis has not been reported previously.
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Research report
Fluoride 43(3)194–199
July-September 2010
Fluorosis in dromedary camels in Rajasthan, India
Choubisa 194194
FLUOROSIS IN DROMEDARY CAMELS IN RAJASTHAN, INDIA
SL Choubisaa
Udaipur, India
SUMMARY: Natural occurrence of fluorosis was observed in a survey of 18
domesticated dromedary camels (Camelus dromedarius) living in fluoride (F)
endemic areas of the Dungarpur district, Rajasthan, India. Among these camels, 15
were mature (up to 12 years old), and 3 were immature or calves (below age 3). The
mean F concentration in the drinking water of these areas ranged between 1.4 and
3.3 ppm. Eight (44.4%) of these camels were afflicted with mild to severe dental
fluorosis. Front (incisors) and upper cheek teeth were light brown to deep yellow in
color. Irregular wearing of teeth was found, however, only with severe dental
fluorosis. Three (16.7%) of the mature camels also showed periosteal exostoses,
moderate intermittent lameness, and hardening of tendons in the legs as
pathognomonic signs of skeletal fluorosis. In these camels colic was common, and
abortions, irregular estrus cycles, and stillbirths were also noted in female camels
(camela). However, the severity of F toxicity in camels was found less in comparison
with other domestic animals of same F endemic areas. To the best of my knowledge,
endemic chronic F intoxication in camels in the form of dental and skeletal fluorosis
has not been reported previously.
Keywords: Camelus dromedarius; Chronic fluoride intoxication; Dental and skeletal fluorosis,
Dromedary camels; Rajasthan, India.
INTRODUCTION
Chronic fluoride (F) intoxication or fluorosis, is a world-wide health problem
and is endemic in areas where the F content of the drinking water is relatively
high. Its primary manifestations in humans and mammals are mottling of teeth and
osteosclerosis of the skeleton.1-6 In India, although many states are endemic for
fluorosis, F intoxication in dromedary camels (Camelus dromedarius) does not
appear ever to have been reported. In the state of Rajasthan, these animals are
commonly found in the sandy plain region (Thar Desert) of western Rajasthan and
are also restricted mainly in numbers to the hilly (Arawali) region of the southern
part of Rajasthan.
Since Rajasthan is hyperendemic for fluorosis in cattle, buffaloes, sheep, goats,
horses, and donkeys,7-10 I considered it of interest to investigate F intoxication in
camels, especially those living in southern Rajasthan.
MATERIALS, METHODS, AND BACKGROUND
During a recent cross-sectional survey of osteo-dental fluorosis in various
species of domestic animals in F endemic areas of the Dungarpur district of
southern Rajasthan, India, 15 mature camels (Camelus dromedarius) between 3
and 12 years of age) and three immature camels under 3 years of age were
examined. These animals were found resting in the agriculture fields of the
Ghataudhani village of Dungarpur district. The mean F concentration in the
drinking water sources ranged from 1.4 to 3.3 ppm.11,12
aFor correspondence: Dr SL Choubisa, Associate Professor and Head, Post Graduate
Department of Zoology, Government Meera Girls College, Udaipur–313001, India; E-mail:
choubisasl@yahoo.com
Research report
Fluoride 43(3)194–199
July-September 2010
Fluorosis in dromedary camels in Rajasthan, India
Choubisa 195195
Relevant information about these animals such as age, medical history, and
source of F intake or exposure other than drinking water was also collected.
Simultaneously, three buffalo calves resting together with these camels were also
examined for further confirmation of chronic F intoxication. In the absence of
urinary and blood analyses, identification of dental and skeletal fluorosis in these
animals was based on clinical examination only.
Background: All these mature camels living for the last four to six years in the F
endemic areas of Dungarpur district were purchased from elsewhere, but the
immature camels were born and lived since birth in these areas. Generally, herds
of these camels move from one place to other in F endemic areas, but their
drinking water sources are hand pumps and dug wells and occasionally pond
water. No other source of F exposure was found.
OBSERVATIONS AND DISCUSSION
Dental fluorosis: Of the 15 mature and 3 immature camels, 6 (40.0%) of the
former and 2 (66.7%) of the latter were afflicted with varying degrees of dental
fluorosis. Enamel of mandibular and maxillary teeth was bilaterally and vertically
stained brown to deep yellow in color (Figure 1).
Figure 1. Front mandibular teeth and upper cheek teeth of 11-year-old male dromedary
camel (merea) showing mild and severe dental fluorosis, respectively. Incisors show
homogenous and vertical light yellowish discoloration, hypoplasia, and fine dots/spots on
enamel surface.
Research report
Fluoride 43(3)194–199
July-September 2010
Fluorosis in dromedary camels in Rajasthan, India
Choubisa 196196
In one of the immature camels,
scattered deposition of fine light to
deep yellowish spots on the
enamel surface of the central
incisors was also observed (Figure
2).
Figure 2. Teeth of 6-year-old female
camel (camela) showing severe dental
fluorosis characterised by deep
yellowish discoloration, diffused to well-
marked spots (central incisors), and
irregular wearing. Recession of teeth-
supporting bone with recession and
bulging of gingival tissue is also present.
(Figure is slightly out of focus.)
None of these camels showed
well defined condensed,
horizontal, stratified brown to
yellowish lines on their incisor
teeth as found in buffalo calves
(Figure 3) living in the same F
endemic area or village. Such
dental fluorosis has been observed
and reported mostly in cattle and buffalo as well as in human beings.6-8 However,
the appearance of dental fluorosis in camels is similar to dental fluorosis in horses
and donkeys,10 but not in cattle, mature buffaloes, or humans. The reason for this
difference is not clear.
Figure 3. Mandibular incisor teeth of 6-month-old buffalo calf showing moderately severe
dental fluorosis characterised by bilateral, horizontal, condensed and stratified light to deep
yellowish discoloration. This appearance of staining is different from dental fluorosis in camels
(Figures 1 and 2).
Research report
Fluoride 43(3)194–199
July-September 2010
Fluorosis in dromedary camels in Rajasthan, India
Choubisa 197197
Skeletal fluorosis: Of the 15
mature camels only 3 (20.0%)
revealed evidence of skeletal
fluorosis. On careful palpation
of mandibular, scapular, tarsal,
metatarsal, carpal, and cage
regions of these camels,
diffuse to well marked bony
lesions (periosteal exostoses)
were found (Figure 4).
Figure 4. Hind legs of 11-year-old
male camel showing diffused to well
marked bony lesions (periosteal
exostoses) on the femoral, fibular,
tarsal, and metatarsal regions. This
camel also had dental fluorosis
(Figure 1).
In these animals mild to
moderate intermittent
lameness, especially in hind
legs, stiffness of leg tendons,
and wasting of main mass of
hind quarters were also
observed. Other signs of F
intoxication, as reported in
other animals,13-17 included
colic, intermittent diarrhoea,
and gas formation, together with impaired reproduction, abortions, stillbirths, and
irregular estrus cycles in female camels. In general, these animals were weak
bodied, indolent, and reluctant to stand (Figure 5). Such conditions were also
found in other animals such as buffalo calves (Figure 6) living together with these
camels.
The presence of these pathognomonic signs of chronic F intoxication in these
camels is further supported by the presence of dental and skeletal fluorosis in other
animals living together with them. However, the severity of fluorosis in the camels
appears to be less than in these other animals in the same F endemic areas.
Possibly, differences in sensitivity to toxic effects of F in the frequency of F intake
are involved. Camels are well adapted to desert ecosystems and can survive more
than 30 days without water. Secondly, the basic food of these camels is tree leaves,
pods, and fruits that are likely to be low in F, but may be rich in calcium and
ascorbic acid (not analysed). Both calcium and ascorbic acid have been found to
reduce the F toxicity.1,18-20 Although various factors besides the amount of F
intake are known to affect F intoxication,21,22 it is unlikely there is a major
difference in susceptibility or tolerance to F toxicity between camel species (C.
dromedarius) and other species of domestic animals, e.g., Bos taurus (cattle),
Bubalus bubalis (buffalo), Ovis aries (sheep), Capra hirus (goat), Equus cabalus
(horse), and E. asinus (donkey).
Research report
Fluoride 43(3)194–199
July-September 2010
Fluorosis in dromedary camels in Rajasthan, India
Choubisa 198198
Figure 5. Emaciated 11-year-old male camel with dental fluorosis shown in Figure 1 and
periosteal bone effects shown in Figure 4. Note wasted thigh and shoulder muscles and bulging
lesions on posterior region of the mandible and lacrimal bones.
Figure 6. Emaciated 6-month-old buffalo calf affected with severe dental fluorosis shown in
Figure 3. Note wasted body muscles and evidence of diarrhoea.
Research report
Fluoride 43(3)194–199
July-September 2010
Fluorosis in dromedary camels in Rajasthan, India
Choubisa 199199
The significance of the present study is that it reports, for the first time, in the
scientific literature, evidence of natural chronic F toxicity in dromedary camels.
These findings also add and contribute significantly to the present knowledge of F
toxicosis in animals.
ACKNOWLEDGEMENTS
I thank the University Grants Commission, New Delhi, India for financial aid
(No.F.34-466/2008,SR). The author is grateful to Dr Zulfiya Sheikh, Assistant
Professor of Zoology, and Mr Pushkar Mali, Research Fellow, for their assistance.
The author is also greatly indebted to the reviewers and editor Professor Emeritus
AW Burgstahler for their valuable suggestions.
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Copyright © 2010 The International Society for Fluoride Research Inc.
www.fluorideresearch.org www.fluorideresearch.com www.fluorideresearch.net
Editorial Office: 727 Brighton Road, Ocean View, Dunedin 9035, New Zealand.
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... The most common bone changes are found as periosteal exostosis, osteosclerosis, osteoporosis, and osteophytosis [46][47][48][49]. These changes manifest clinically as vague aches and pains in the body and joints that are associated with stiffness or rigidity and lameness, stunted growth, obvious bone lesions, and a cracking or snapping sound in the legs when walking in animals [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41]. In addition, these progressive and irreversible bone changes become more severe as the amount of fluoride in drinking water increases and the advancement of animals age. ...
... Fluorideinduced diverse changes in different organs or health complaints are referred to as non-skeletal fluorosis. Among various species of animals, the most common and prevalent health complications or complaints such as gastrointestinal discomforts, frequent tendency to urinate (polyuria) / itching in the region, frequently intake of water (polydipsia), muscles/body weakness, allergic reactions, irregular reproductive cycles, abortion, still birth etc. are found due to resultant of chronic hydrofluorosis [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41]. It is not necessary that all these health problems occur in the same animal and they are all reversible after withdrawal of fluoride exposure [42]. ...
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... In Rajasthan and its scheduled area drinking groundwater is also highly contaminated with F ( Figure 2); [1,[6][7][8][9][10]. It is well known that drinking water containing F above the threshold level 1.0 or 1.5ppm [11][12][13] for prolonged period causes dreaded fluorosis (hydrofluorosis) disease not only in humans [11,14] but also in various species of wild [15][16][17] and domestic animals [18][19][20][21][22][23][24][25][26][27][28]. Chronic F exposure through industrial fluoride pollution is also causes fluorosis in man and animals [29][30][31][32][33][34][35]. ...
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... Due to this drinking water, a number of domesticated animals are becoming lean, weak and lame. But villagers or animal owners do not know that the water of these sources is contaminated with F toxicant, which has started development of lameness and causing fluorosis (hydrofluorosis) disease in them by feeding them again and again (Choubisa & Mishra, 2013;Choubisa et al., 2012;Choubisa, 1999bChoubisa, , 2000Choubisa, , 2007Choubisa, , 2010aChoubisa, , 2010bChoubisa, , 2010cChoubisa, , 2013aChoubisa, , 2013bChoubisa, , 2021bChoubisa, , 2022bModasiya et al., 2014b). The symptoms or clinical signs of dental ( Fig. 5a-g) and skeletal fluorosis ( Fig. 6a-d) in these animals are almost similar as found in human population and also appeared at or above the 1.0 or 1.5 ppm F concentration in drinking water. ...
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health and causes serious fluorosis disease in humans and domestic animals. In Rajasthan, around 40 lakh people are affected with fluorosis which is the highest in the country. At the F range of 1.3-6.7 ppm, the maximum prevalence of dental and skeletal fluoro-sis in villagers and bovine animals was found 84.0% and 32.7% and 88.9% and 37.8%, respectively. Using fluoridated groundwater in irrigation is also harmful and reduces crops productivity. In this communication , division-wise F distribution in groundwater of rural Rajasthan, F-induced diverse adverse health consequences in villagers and their domesticated animals and agriculture crops and preventive measures for control of F intoxication are critically reviewed. Findings of this review are useful in implementation of health policy for the mitigation of F poisoning in rural Rajasthan.
... It is well known, an excessive ingestion and/or inhalation of fluoride through water, food, and air causes the dreaded fluorosis disease not only in human beings [1][2][3][4][5][6][7][8][9] but also in diverse species of domestic animals [10][11][12][13][14][15][16][17][18]. This slow progressing disease is more prevalent or common in those areas where fluoride is endemic. ...
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No doubt, industrialization is relatively more important and necessary for the sustainable development and economy for any country or geographical region. That is why many types of factories or industrial activities work day and night for different types of production. But there are many of these factories which continuously emit fluoride in the gaseous and particulate/dust forms into their surrounding environments and contaminate diverse natural resources such as soil, air, reservoirs, herbage, vegetation, ecosystem etc. In the world or in different countries, the major and most common sources of industrial fluoride emissions are coal-fired power plants and industrial activities, such as the production of steel,
... In India, especially in rural areas, drinking groundwater is naturally contaminated with fluoride [2][3][4][5] and is found to exceed the maximum permissible limit of 1.0 or 1.5 ppm [1,6,7]. Hence, due to drinking of fluoridated groundwater hydrofluorosis is endemic in rural areas of several states and union territories of the country and prevalent not only in villagers or livestock farmers [8][9][10][11][12][13][14][15][16][17][18] but also in their domesticated animals, such as cattle (Bos taurus), water buffaloes (Bubalus bubalis), sheep (Ovis aries), goats (Capra hircus), horses (Equus caballus), donkeys (Equus asinus), and dromedary camels (Camelus dromedarius) [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35]. In this disease many deformities or malformations develop in teeth (dental fluorosis), bones (skeletal fluorosis), and soft organs (nonskeletal fluorosis) as well. ...
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An excessive and repeated high fluoride exposure over a long period of time is harmful to the health of humans and domestic animals and causes several toxic effects in the form of fluorosis disease. If fluoride exposure is due to industrial fluoride, the disease is known as industrial fluorosis. In recent years, due to rapid industrialization in India, various health problems are increasing continuously among domesticated bovine animals, cattle (Bos taurus) feed and water buffalo (Bubalus bubalis) living and grazing in industrial areas due to industrial fluoride pollution. In fact, many coal-burning and industrial activities, such as power generating stations and the manufacturing of steel, iron, aluminum, zinc, phosphorus, chemical fertilizers, bricks, cement, hydrofluoric acid, etc are generally discharging fluoride into their surrounding areas which create industrial fluoride pollution. An industrially emitted fluoride not only contaminates the surrounding environment including soil, air and fresh water reservoirs, but also contaminates vegetation, agricultural crops, and many other biological communities on which bovines generally survive. These animals develop a number of toxic effects on their teeth (dental fluorosis), bones (skeletal fluorosis) and soft organs (non-skeletal fluorosis) due to chronic industrial fluoride intoxication. Due to industrial fluorosis, bovine animals become physically weak and lame, and diverse health problems, such as anemia, gastrointestinal discomforts, polyuria, polydipsia, impaired reproduction, etc. are also found in them. In the country, many domesticated bovines are suffering with industrial fluorosis. In these animals, the maximum prevalence, 84.11% of industrial dental fluorosis and 72.0% of skeletal fluorosis has been reported. In the country, the research works done so far on industrial fluorosis in bovines are briefly and critically reviewed in the present communication. Along with this, the focus has also been on the adverse socio-economic impacts of industrial fluorosis on livestock farmers and how to prevent this disease in these animals.
... It is well known, an excess consumption or exposure to fl uoride for prolonged period through drinking groundwater having fl uoride more than 1.0 or 1.5 ppm [8][9][10] then it causes a serious disease known as hydrofl uorosis. Th is disease has been reported in India in both human populations [11][12][13][14][15][16][17][18][19][20] and diverse domesticated animals such as bovines, fl ocks, equines, and dromedary camels [21][22][23][24][25][26][27][28][29]. In the country, fl uoride emitted from various industrial activities is also causing a fl uorosis disease (industrial fl uorosis) in man and animals [30][31][32][33]. ...
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In India, a slow progressing water-borne dreaded hydrofluorosis disease is endemic in rural areas where drinking groundwater contains fluoride >1.0 or 1.5 ppm. In the rural areas, most people feed their domesticated cattle (Bos taurus) water from hand-pumps and bore-wells, which usually contaminated with fluoride toxicant. Because these drinking water sources are easily available and accessible in rural areas. In the country, drinking groundwater of 23, out of 37 states and union territories is found to be contaminated with fluoride with varying amounts. When cattle exposed to fluoride for a long period of time through drinking groundwater of these sources then hydrofluorosis is developed in them. Thousands of cattle and their calves of rural areas of six states namely, Andhra Pradesh, Chhattisgarh, Karnataka, Madhya Pradesh, Odisha (Orissa), and Rajasthan of the country found to be victimised by this disease. Actually, in this disease, many types of incurable and irreversible deformities develop in the teeth and bones of animals. In general, in hydrofluorosis, teeth of cattle become weak and mottled (dental fluorosis) and animals walk with a limp (skeletal fluorosis). In the country, the highest prevalence, 89.6% of dental fluorosis and 42.7% of skeletal fluorosis at 1.3-6.7 ppm and 1.5-4.4 ppm fluoride concentration in drinking waters has been reported, respectively. In present communication, fluoride distribution in drinking groundwater, endemic hydrofluorosis in cattle and its determinants, economic implications, and prevention and control are briefly and critically reviewed. Along with this, research gaps have also been highlighted for researchers for further research work on chronic fluoride toxicosis in animals.
... It was discovered when people started drinking water from these sources and symptoms of chronic fluorosis started showing in them. Not only humans but their pets also started falling prey to this fluorosis disease [14,15].In fact, this disease is the consequence of this highly successful project, due to which thousands of people and domesticated animals of rural areas in the country are becoming victims of lameness [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. ...
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In the eighties, there was a tremendous infestation of dreaded human nematode parasite, Dracunculus worm (Dracunculus medinensis) in the rural areas of many states of India. Commonly, this roundworm is also known as Guinea worm. Thousands of people were suffering from Guinea worm disease (dracunculiasis), a disease caused by this viviparous female worm. In this water-borne disease, this worm is 1-3 feet long, milk-white, thin, cylindrical, and thread-like from any part (arms, legs, neck, breast, chest, abdomen, back, genital organs, etc.) of the person's body, slowly comes out over a period of 2-3 months. But this worm comes out more from those organs which come more in contact with water, because it makes it easier for it to complete its life cycle. During its emergence, the person feels very severe unbearable pain. Sometimes more than one worm has also been seen coming out of a person's body, which is an even more serious condition. India is now completely free from this dangerous worm and it was last seen in 2006. Now this is a historical human nematode roundworm whose description is only available in the pages of medical and parasitological history. But now these can be seen in the museum of zoology departments and medical colleges in the form of preserved specimens as evidence. But the old people of dracunculiasis endemic villages still tremble with fear after hearing its name. It is true that the history of this historical Dracunculus worm was very scary and dangerous. However, in India, the young generation is unfamiliar or unknown of this historical worm. There is no doubt that people have got freedom from this worm, but due to its eradication, another new health problem of chronic fluorosis has come in India, which is even more dangerous and painful than this. Due to this, not only thousands of people of all age groups, but many species of domestic animals became victims of lameness, that is, "fell from the sky and got stuck in the palm". There is no doubt that this worm has ended from India, but the question is also that can it not come back? Because many other beings are its reservoir hosts in which it is hidden. Whatever it is, its fate lies in the womb of the future.
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Chronic fluoride (F) intoxication in the form of osteo-dental fluorosis was observed in 23 domestic equus animals, 9 to 23 years old, including 14 horses (Equus caballus), and 9 donkeys (E. asinus) living in F endemic areas of Dungarpur district, Rajasthan, India. The mean F concentration in the drinking water in these areas ranged from 1.4 to 3.3 ppm. Eleven (78.7%) of these horses and all nine donkeys were afflicted with mild to severe dental fluorosis. Their incisor teeth were brown to black-yellowish in color. Also present as indications of more severe chronic F intoxication were irregular wearing and excessive abrasions of the teeth, deep dark-yellowish discoloration of exposed cementum and/or remaining enamel surface, and pronounced loss of tooth-supporting alveolar bone with recession of gingiva. Excessive hypoplasia and light brown-yellowish pigmentation on the enamel surface of incisors were also observed in 2 foals below the age of 2 months. Among the mature animals, the following manifestations of skeletal fluorosis were present: periosteal exostoses in mandibular regions, ribs, metacarpus, and metatarsus, intermittent lameness, hoof deformities, and hardness of tendons in the legs. Other signs of F intoxication included colic, diarrhoea, retention of urine, repeated abortions, and sterility were noted. This evidaence of osteo-dental fluorosis in domestic horses and donkeys is reported for the first time in India, and this condition in donkeys is reported for the first time anywhere.
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A Survey was made in fifteen villages of Dungarpur district of Rajasthan for the prevalence of dental and skeletal fluorosis in villagers and their domestic animals. Fluoride concentration (mean) in drinking waters of these villages varied between 1.7 to 6.1 mg/L. An overall 73.0 and 82.9 percent prevalence of dental fluorosis was observed in children (below 18 years age) and adults respectively. Cent percent prevalence of dental fluorosis in children and adults was observed at 5.2 and 3.8 mg/L fluoride concentration respectively. The prevalence of skeletal fluorosis in adults was 32.5 percent and the highest prevalence (60.8%) was observed at 6.1 mg/L flouoride concentration. Male subjects relatively showed higher prevalence of skeletal fluorosis. Out of 1521 cattle and 471 buffaloes, 1007 (66.2%) and 318 (67.5%) showed the evedence of dental flourosis. Cent-percent prevalence of dental fluorosis in calves of both animal species was observed at the above 2.8 mg/L fluoride concentration. The highest prevalence of skeletal fluorosis, 61.6 percent in cattle and 66.6 percent in buffaloes has been observed at 6.0 mg/L fluoride concentration. Simultaneously, 1260 goats and 580 sheeps were also examined for the evidence of fluorosis but not a single case was detected.
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A new study has demonstrated that fluoride-treated rats, with a serum fluoride (F) concentration of 0.263±0.024 ppm F after receiving 5 mg F/kg body mass/24 hr for 8 weeks, have significant changes in spermatozoa: reduced motility, reduced superoxide dismutase (SOD) activity, increased generation of the reactive oxygen species O2·-, increased lipid peroxidation, altered plasmatic membrane, decreased capacity to undergo the acrosome reaction, and decreased in vitro oocyte fertilization ability. These observations indicate that subchronic exposure to fluoride causes oxidative stress damage and loss of mitochondrial transmembrane potential in spermatozoa resulting in reduced in vitro fertility, a finding consistent with previous studies. The serum fluoride level of the rats was about 14 times higher than the 0.019 ppm F level found in human populations consuming drinking water with 1 ppm of F. However, other in vivo studies of rats, chinchillas, alligators, caimans, and horses have found reduced fertility with drinking municipal water fluoridated with fluorosilicic acid, H2SiF6. While the serum F level which has no effect on fertility in humans remains difficult to define, the Precautionary Principle should guide the addition of sodium silicofluoride or fluorosilicic acid to municipal water supplies.
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Chronic fluoride intoxication (fluorosis) was observed in villagers and their domestic animals (cattle, buffaloes, sheep and goats) from ten villages of the Udaipur district of Rajasthan where drinking waters contained 0.3 to 7.0 mg/L fluoride. The prevalence of dental fluorosis and skeletal fluorosis in villagers was relatively higher than that observed in the animals. At 5.8 mg/L mean fluoride concentration, 88.7% of children (<18 years) and 100% of adults were found to be affected with dental fluorosis. The highest prevalence (42.2%) of skeletal fluorosis was observed at 5.8 mg F/L (mean). Males showed relatively a higher prevalence of skeletal fluorosis. In general, the prevalence and severeness of skeletal fluorosis increased with increasing of fluoride concentration and with age. None of fluorotic subjects revealed evidence of genu-valgum syndrome and goitre (hyperthyroidism). Among mature animals, buffaloes were found to have a higher prevalence and greater severity of dental and skeletal fluorosis when compared with cattle. The prevalence of dental fluorosis was higher in calves of both type of animals than in adults. Sheep and goats examined at the same time were found to be free of fluorosis. Radiological findings and deformities in fluorotic subjects as well as fluorosis in relation to fluoride concentrations, age and sex have also discussed.
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The therapeutic effects of ascorbic acid and calcium (Ca 2+) supplementation of reproductive functions of fluoride-treated (10 mg/kg body weight) male rats were investigated. Sodium fluoride treatment resulted in a decrease in almost all parameters studied except concentration of testicular cholesterol, which implies that androgen synthesis might not be affected by NaF treatment. Succinate dehydrogenase activity decreased in testis suggesting that its oxidative metabolism was altered by NaF treatment. Adenosine triphosphatase activity, protein, and sialic acid levels in caput and cauda epididymides also showed a decrease. All these changes resulted in a significant decrease in sperm motility and thereby fertility rate. Glycogen concentrations in vas deferens were altered, probably due to impaired metabolic turnover. The fructose levels in vas deferens and seminal vesixle as well as the acid phosphatase activity in ventral prostate were also decreased significantly by NaF treatment. On the other hand, simultaneous treatment of NaF along with ascorbic acid or calcium resulted in recovery in all the affected parameters studied. The recovery was more significant after treatment with ascorbic acid than with calcium. Therefore, ascorbic acid and calcium may be useful for amelioration of fluoride toxicity in endemic areas.
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Two independent experiences with animals in captivity revealed a dramatic onset of severe debilitating symptoms when the nonfluoridated water supplies were changed to municipal water fluoridated with fluorosilicic acid, H 2SiF6. The first group of animals, chinchillas in a small fur farm operation, quickly more than doubled their water consumption with the change to silicofluoridated water and gradually began to have inferior fur quality, stillbirths, and premature mortality. In the second group of animals, when a similar change in the water occurred, caimans and alligators in a noncommercial private animal collection exhibited swelling and ulceration of eye membranes and later bloated bellies, liver silicosis, spinal deformity, tumors, and shortened life spans. The health of the rat colony in this collection rapidly deteriorated and numerous tumors developed. When hatchling caimans were raised in distilled water, they remained healthy until, because of their size, they were transferred to the silicofluoridated water, after which the above symptoms began to appear. Similarly, when the rats were changed to distilled water, tumor formation ceased, and they became healthy with greatly extended life spans.
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Quantitative tetracycline-based analysis of iliac bone biopsy was performed in 17 patients with endemic skeletal fluorosis. All had lived in endemic fluorosis areas since their birth. The mean age was 25.6 years and duration of symptoms 7.6 years. The mean fluoride content of the drinking water was 17.8 ppm and the mean daily intake of fluoride was 26.2 mg. None of the patients had Vitamin D deficiency, intestinal malabsorption or renal dysfunction. Pertinent biochemical findings were: raised plasma levels of fluoride, alkaline phosphatase and iPTH, and increased urinary fluoride excretion. Static and dynamic histomorphometric measurements revealed the profiles of osteomalacia and secondary hyperparathyroidism in varying combinations in all cases. Increases in osteoid volume, osteoid surfaces, osteoid seams width, resorption surfaces and mineralization lag time and decreases in corrected apposition rate, bone formation rates and tetracycline labeled surfaces were the variable features recorded in each case. Dynamic bone histomorphometry has further increased the understanding of the effects of fluoride on intraskeletal mechanisms affecting the structure and metabolism of the bone but it does not allow clear-cut differentiation from metabolic bone disease. Endemic skeletal fluorosis, therefore, may be regarded as a parametabolic bone disease.
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Chronic fluoride intoxication in the form of osteo-dental fluorosis was investigated in 21 villages of Banswara, Dungarpur, and Udaipur districts of southern Rajasthan, where fluoride (F) concentrations in drinking waters range from 1.5 to 4.0 ppm. Interestingly, a variable prevalence of fluorosis was observed in villages having almost the same F concentrations. At 1.5 ppm, 21.3, 25.6, and 38.9% of children and 33.3, 36.9, and 44.8% of adults in differ- ent villages of these districts were found to be affected with dental fluorosis. The maximum prevalence of dental fluorosis (77.1%) was found in the 17-22 year age group. No significant correlation was found between prevalence fig- ures and gender. At this 1.5 ppm F concentration, 6.1, 6.8, and 9.5% of adults in villages of Banswara, Udaipur, and Dungarpur districts, respectively, showed evidence of skeletal fluorosis. Subjects of these districts showed the highest prevalence of skeletal fluorosis, 32.8, 36.6, and 39.2% at maximum F level of 3.7 ppm, 4.0 ppm, and 3.2 ppm, respectively. No children were found affected with skeletal fluorosis or skeletal deformi- ties, the prevalence of which was higher in males and increased with age and higher F level. Deformities such as crippling, kyphosis, and genu varum were observed most frequently in higher age groups (>40 years) at a F concentra- tion of 2.8 ppm or higher. None of the fluorotic subjects showed evidence of goitre (thyroidism) or genu valgum syndrome. Radiological findings of other deformities in fluorotic subjects were also found. Possible factors responsible for a higher prevalence of fluorosis in villages having similar F concentrations are discussed.