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Fluoride Toxicity in Animals

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SpringerBriefs in Animal Sciences
More information about this series at http://www.springer.com/series/10153
Rakesh Ranjan · Amita Ranjan
1 3
Fluoride Toxicity
in Animals
Rakesh Ranjan
National Research Centre on Camel
Bikaner, Rajasthan
India
ISSN 2211-7504 ISSN 2211-7512 (electronic)
SpringerBriefs in Animal Sciences
ISBN 978-3-319-17511-9 ISBN 978-3-319-17512-6 (eBook)
DOI 10.1007/978-3-319-17512-6
Library of Congress Control Number: 2015936363
Springer Cham Heidelberg New York Dordrecht London
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Amita Ranjan
Department of Veterinary Pharmacology
and Toxicology
College of Veterinary and Animal
Sciences, Navania
Rajasthan University of Veterinary
and Animal Sciences
Bikaner, Rajasthan
India
v
Preface
It is our great pleasure to present the book, Fluoride Toxicity in Animals. Animals
living in areas where fluorosis is endemic in the human population invariably suffer
from the toxic effects of excess fluoride intake. Nevertheless, there has been lim-
ited research on fluorosis in animals whereas fluorosis in the human population has
received more attention from biologists, environmental scientists, and management
authorities worldwide.
This book has been written for higher undergraduate and graduate students of
toxicology, veterinary science, animal nutrition, environmental science, public
health workers, animal welfare activists, public health veterinarians, medical pro-
fessionals, and all others interested in the subject. A brief account of physical and
chemical properties of fluorine and different fluoride compounds is given along
with their relative significance in fluoride toxicity. Important natural and anthro-
pogenic sources of fluoride toxicity in animals are described to help identify the
problem. Basic features of fluoride absorption, distribution, metabolism, reten-
tion, excretion, and fluoride tolerance of different animal species are given in brief.
Methods for sample collection, preservation, and fluoride analysis in biological
and environmental samples are described. Important aspects of mitigation and pre-
vention of fluorosis in animals are given in Chap. 7 to help animal health workers
and management authorities.
No book can be claimed to be perfect and complete in all aspects. The scope
of improvement is always left. We sincerely look forward to readers for critical
suggestions.
We express our gratitude to our colleagues, officers, students, scientists, and
teachers for their valuable support. Thanks to Dr. D. Swarup and Dr. R.C. Patra
for providing the opportunity to work in the field of fluoride toxicity under their
guidance.
In addition we want to thank Lars Koener, Ursula Gramm, Amit Cyril Tirkey
and reviewers of the book for their support and suggestions in publishing this book
in a nice shape.
Preface
vi
We also express thanks to our parents, family members, and friends, as without
their whole-hearted support it would have been impossible to complete this
manuscript.
Rakesh Ranjan
Amita Ranjan
vii
Contents
1 Introduction ................................................ 1
1.1 Fluorine Chemistry ....................................... 2
1.1.1 Physical and Chemical Properties .................... 2
1.1.2 Distribution of Fluorides ........................... 2
1.2 Is Fluoride Essential for Health? ............................ 3
1.2.1 Fluoride and Human Health ......................... 3
1.2.2 Fluoride and Animal Health ......................... 4
1.3 Fluoride Toxicity ........................................ 5
1.3.1 Fluorosis in the Human Population ................... 5
1.3.2 Fluorosis in Animals ............................... 7
References .................................................. 8
2 Sources of Fluoride Toxicity ................................... 11
2.1 Natural Sources ......................................... 12
2.1.1 Forage, Grasses, and Grains ......................... 12
2.1.2 Water .......................................... 14
2.1.3 Volcanic Activities ................................ 15
2.2 Anthropogenic Sources ................................... 15
2.2.1 Mineral Mixture and Other Feed Supplements .......... 15
2.2.2 Airborne Fluoride ................................. 16
2.2.3 Industrial Effluents ................................ 17
2.2.4 Agrochemicals and Household Products ............... 17
References .................................................. 18
3 Fluoride Kinetics and Metabolism ............................. 21
3.1 Absorption ............................................. 21
3.1.1 Gastrointestinal Tract .............................. 22
3.1.2 Respiratory Tract ................................. 23
3.1.3 Dermal and Other Routes ........................... 24
Contents
viii
3.2 Distribution and Retention ................................. 25
3.2.1 Transplacental Passage ............................. 26
3.2.2 Cerebrospinal Fluid ............................... 26
3.2.3 Skeleton and Other Calcified Tissues .................. 26
3.2.4 Teeth ........................................... 28
3.2.5 Exoskeleton ..................................... 28
3.2.6 Hair and Fingernails ............................... 28
3.2.7 Soft Tissues ..................................... 29
3.2.8 Egg ............................................ 29
3.3 Elimination and Excretion ................................. 30
3.3.1 Urine ........................................... 30
3.3.2 Feces ........................................... 30
3.3.3 Saliva .......................................... 31
3.3.4 Perspiration ...................................... 31
3.3.5 Milk ........................................... 31
References .................................................. 32
4 Toxic Effects ................................................ 35
4.1 Acute Toxicity .......................................... 35
4.2 Chronic Toxicity ......................................... 36
4.2.1 General Health Effects ............................. 36
4.2.2 Effects on Calcified Tissues ......................... 37
4.2.3 Effects on Soft Tissues (Nonskeletal, Nondental Effects) ... 42
4.3 Molecular Mechanism of Toxicity ........................... 46
References .................................................. 47
5 Fluoride Tolerance .......................................... 53
5.1 Fluoride Tolerance in Different Animal Species ................ 54
5.1.1 Laboratory Animals ............................... 54
5.1.2 Domestic Animals ................................ 54
5.1.3 Wild Animals .................................... 56
5.1.4 Poultry and Other Birds ............................ 58
5.1.5 Insects and Other Invertebrates ...................... 59
5.1.6 Fish and Other Aquatic Animals ..................... 59
5.2 Factors Affecting Fluoride Tolerance ......................... 60
5.2.1 Animal Factors ................................... 61
5.2.2 Dietary and Nutritional Factors ...................... 61
5.2.3 Chemical Form of Fluoride ......................... 63
5.2.4 Dose, Duration, and Continuity of Fluoride Intake ....... 63
5.2.5 Environmental and Other Factors ..................... 64
References .................................................. 64
6 Fluoride Analysis ............................................ 69
6.1 Titrimetry .............................................. 69
6.2 Colorimetric/Spectrophotometric Methods .................... 70
Contents ix
6.3 Gas Chromatography ..................................... 70
6.4 Neutron or Proton Activation Technique ...................... 70
6.5 Potentiometric Analysis/Ion Selective Electrode (ISE) Method .... 71
6.5.1 Working of Ion Selective Electrode ................... 71
6.5.2 Factors Affecting Performance of ISE ................. 72
6.5.3 Sample Collection and Preservation ................... 73
6.5.4 Electrode Preparation .............................. 73
6.5.5 Checking Electrode Operation ....................... 75
6.5.6 Preparation of Standards ........................... 75
6.5.7 Analytical Techniques ............................. 75
6.5.8 Fluoride in Acid Solution ........................... 77
6.5.9 Fluoride in Alkaline Solution ........................ 77
6.5.10 Points to Remember During Fluoride Analysis .......... 78
6.5.11 Total Ionic Strength Adjustment Buffer (TISAB) ........ 78
6.5.12 Electrode Filling Solution .......................... 79
6.5.13 Storage of Ion Selective Electrode .................... 80
6.5.14 Fluoride in Aqueous Samples ........................ 80
6.5.15 Fluoride in Soft and Calcified Tissues ................. 81
6.5.16 Fluoride in Vegetation and Fodder Samples ............. 81
6.5.17 Fluoride in Soil, Feed, and Mineral Mixture ............ 82
References .................................................. 82
7 Mitigation and Prevention of Fluorosis .......................... 85
7.1 Minimizing/Withdrawing Excess Fluoride Intake ............... 86
7.1.1 Search for Safe Groundwater Source .................. 86
7.1.2 Use of Surface Water .............................. 86
7.1.3 Rainwater Harvesting .............................. 86
7.1.4 Water Defluoridation .............................. 87
7.1.5 Precipitation-Based Techniques ...................... 89
7.1.6 Adsorption and Ion-Exchange-Based Techniques ........ 90
7.1.7 Reverse-Osmosis-Based Techniques .................. 91
7.1.8 Distillation-Based Techniques ....................... 91
7.1.9 Electrocoagulation/Electrolysis-Based Techniques ....... 91
7.2 Preventive and Therapeutic Measures ........................ 91
7.2.1 Minerals, Drugs, and Other Chemicals ................ 91
7.2.2 Vitamins and Antioxidants .......................... 93
7.2.3 Plant Products/Herbal Medicines ..................... 93
7.3 Minimizing Industrial Fluoride Emissions ..................... 96
7.4 Generating Public Awareness ............................... 96
References .................................................. 96
Appendix ..................................................... 101
xi
About the Authors
Dr. Rakesh Ranjan Ph.D. is presently working as Senior Scientist with ICAR-Na-
tional Research Centre on Camel, Bikaner, Rajasthan, India. Earlier, he has served
College of Veterinary Sciences, Guru Angad Dev Veterinary and Animal Sciences
University, Ludhiana, India for about 9 years as assistant professor in the depart-
ment of Veterinary Medicine. He is working on animal fluorosis for the past 11 years.
Dr. Ranjan currently serves on the editorial board of Environmental Pollution, published
by Canadian Center for Science and Education, Toronto, Canada and Indian Journal
of Veterinary Medicine, published by Indian Society for Veterinary Medicine. He is
life member of International Society of Fluoride Research (ISFR), New Zealand and
has presented his research highlights on fluoride toxicity in animals in several national
and international conferences including conferences of ISFR, held at Toronto Canada
(2008) and Szczecin, Poland (2012). He was selected for Raman Fellowship, UGC,
Government of India for postdoctoral research in USA. He has published more than 60
research and extension papers and one book chapter. He has been awarded with Intas
best review article award, ISVM appreciation award and best oral and poster presenta-
tion awards in several international and national scientific conferences.
Dr. Amita Ranjan Ph.D. is presently working as assistant professor (Veterinary
Pharmacology and Toxicology), College of Veterinary and Animal Sciences, Navania,
under University of Veterinary and Animal Sciences, Bikaner, Rajasthan, India. Prior
to that, she was research associate in Department of Teaching Veterinary Clinical
Complex, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana,
Punjab, India, where she worked on toxicity testing of synthesized nanoparticles.
Toxicity of agrochemicals and other environmental pollutants in animals are areas
of her research interest. She is a life member of Indian Society for Veterinary
Pharmacology and Toxicology. She is recipient of award of honour from chief minis-
ter, for securing second position in the Bihar state in matriculation examination. She
received Radha Harihar Prasad memorial gold medal during graduation and senior
research fellowship, Indian Council for Agricultural Research, Government of India
during Ph.D. She has published several research papers in different international and
national journals of repute and authored one book on pet care and management.

Chapters (6)

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, after absorption from the gastrointestinal tract, respiratory tract, or skin and mucous membrane reaches different organs and body tissues through blood circulation. Following oral intake, unabsorbed fluoride is excreted through feces, and 50–70 % of absorbed fluoride is excreted through urine, perspiration, saliva, milk, and egg (in birds) and rest is retained in the body. Calcified tissues, mainly bone and teeth, act as a natural sink for fluoride and contain about 99 % of the total body fluoride burden. Fluoride accumulation in soft tissues is very low, with kidneys having the highest concentration. The placenta appears to protect the fetus from the toxic effects of fluoride as evident from low transplacental fluoride passage in many animal species. Normal cerebrospinal fluid contains very low fluoride concentration, but it increases marginally during chronic fluoride toxicity. The exoskeleton in invertebrates, skeletal tissues in fish, and hair and fingernails in vertebrates also accumulate fluoride and may act as bioindicators of the fluoride burden in animals.
Clinical manifestations of acute fluoride toxicity include hypersalivation, restlessness, body stiffness, convulsion, and respiratory and cardiac failure, eventually leading to death. In chronic fluoride toxicity calcified tissues act as a natural sink for fluoride and hence characteristic lesions develop in bone and teeth. Dental lesions appear more frequently than bony lesions and are characterized by discoloration, hypoplastic pits, chalkiness, fast attrition, and early loss. Intermittent lameness, weakness, and the appearance of bony protuberances are common due to lesions developing in bone. Toxic effects on soft tissues become more evident when bones saturate with fluoride and their capacity to accumulate more fluoride is lost. Excess fluoride can alter the cytoarchitecture and physiology of renal, hepatic, gonadal, and neuronal tissues. Many studies suggested genotoxic, carcinogenic, immunotoxic, and cytotoxic potential of fluoride, although the results were highly variable and even contradictory.
Fluoride tolerance varies with species, age, and sex of the animal; individual resistance; dose, duration, and consistency of fluoride uptake; and dietary, nutritional, and environmental factors. The tolerance levels established by experimental studies may be erroneous sometimes, due to poor correlation between fluoride concentration in feed and water and actual bioavailability of the fluoride. Rabbits, guinea pigs, rats, mice, and some wild rodents are highly susceptible to fluoride toxicity. Among domestic animals, ruminants have less fluoride tolerance than simple-stomach animals. Carnivores are even more tolerant than herbivorous simple-stomach animals. Dental and bony lesions similar to those observed in domestic cattle and buffaloes may appear in wild cervids after excess fluoride intake. Poultry are highly tolerant to fluoride. On the other hand, insects, some other invertebrates, and soft water dwelling fish have low fluoride tolerance.
Fluoride analysis in biological and environmental samples is essential for definitive diagnosis of fluoride toxicity and determining the source of excess fluoride exposure. Several analytical techniques based on titrimetry, colorimetric methods, enzymatic analysis, ion chromatography, proton activation analysis, potentiometric analysis, and so on have been developed. However, potentiometric analysis using an ion selective electrode is rapidly becoming a popular and widely accepted method for determination of fluoride concentration in various biological and environmental samples. Fluoride concentrations in aqueous samples may be estimated directly, whereas preanalysis processing by alkali fusion, ashing, acid extraction, and microdiffusion may be required for others to free the fluoride ions from organic matrix/insoluble complexes. Various aspects of sample collection, preservation, processing, and fluoride analysis by potentiometric technique are described in detail in this chapter.
Nonavailability of a specific antidote and the irreversible nature of bony and dental lesions poses a great challenge in management of fluoride toxicity; hence prevention remains the best way to minimize suffering of animals. In hydrofluorosis-endemic areas surface water, rain-harvested water, or defluoridated groundwater should be offered to animals for drinking. Several defluoridation techniques including the Nalgonda technique, use of activated alumina, KRASS technology, reverse osmosis, distillation, and electrolysis are also available, but the requirements of infrastructure, technical expertise, and high running cost are major factors limiting their use in animal husbandry. Supplementation of certain minerals, vitamins, antioxidants, and plant products can alleviate toxic symptoms of fluorosis. Minimizing industrial fluoride emission by adapting advanced technology and imposition of stringent laws can help safeguard animal health from industrial fluorosis. The generation of public awareness, particularly in rural areas, is essential for effective use of various ameliorative and preventive measures available for fluorosis in animals.
... It has many physiological roles for animals [23] but it may lead to toxic effects in critical doses. Among domestic animals, ruminants have less fluoride tolerance than simple-stomach animals [24]. Fluoride enters the ruminants body by several routes, including inhalation, consumption of contaminated water, or plants growing in contaminated soil leading to fluorosis [8]. ...
... Fluoride enters the ruminants body by several routes, including inhalation, consumption of contaminated water, or plants growing in contaminated soil leading to fluorosis [8]. More precisely, its bioaccumulation in teeth and bones may cause several injurious effects in the form of dental and skeletal fluorosis [ 24,25]. Moreover, increasing the duration of exposure to fluoride has been shown to produce adverse effects in other tissues, leading to oxidative stress, DNA damage, apoptosis, and necrosis [26]. ...
... Rabbits, rats, and mice are all very sensitive to fluoride toxicity [27]. For this reason, these species are widely used in experimental studies to analyze the fluoride toxicity [24]. Oral administration of sodium fluoride altered the development of tooth enamel and revealed chalk-like white incisors with broken tips in rats and mice [28,29]. ...
Article
Full-text available
Environmental pollutants are considered a serious health problem for humans and animals mainly in ruminants for several regions of the world. Previously, many studies have investigated the mechanisms of toxicity of these pollutants on laboratory animals. Afterward, other studies have demonstrated that exposure to environmental pollutants may cause several adverse effects on the ruminant organs, influencing their performance and leading to socioeconomic problems for breeders. Fluoride, lead, arsenic, and cadmium are the most common poisonings in ruminants, they can cause several irreversible toxic effects in many organs depending on the mode of action. The adverse effects of fluoride, lead, arsenic, and cadmium toxicities in laboratory animals and ruminants have been clearly summarized in this review. In addition, several results on protective or ameliorative effects by means of natural products against these toxicities have been illustrated.
... But distribution of fl uoride in any region is under control of regional hydrogeological and climatic condition. Besides hydrogeological set up, the climate and physiography are other important factors that the areas of less rainfall have higher fl uoride content as compared to groundwater in high rainfall areas despite having similar hydrogeological formation [55]. Nevertheless, level of fl uoride concentration in groundwater is much more depends on the weathering and leaching process, chemical composition of parental rocks, the presence and accessibility of fl uoride minerals to water, and the time contact between the source of minerals and water [55]. ...
... Besides hydrogeological set up, the climate and physiography are other important factors that the areas of less rainfall have higher fl uoride content as compared to groundwater in high rainfall areas despite having similar hydrogeological formation [55]. Nevertheless, level of fl uoride concentration in groundwater is much more depends on the weathering and leaching process, chemical composition of parental rocks, the presence and accessibility of fl uoride minerals to water, and the time contact between the source of minerals and water [55]. ...
Article
Full-text available
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 does therefore not occur in the elemental state in nature but forms compounds (fluorides) with other elements, mainly in the form of salts containing the fluoride anion (WHO (World Health Organization) 2002; NRC (National Research Council) 2005; Fuge 2019). It has occasionally been claimed that fluorine is an essential element for humans and animals, but this has thus far not been sufficiently substantiated (Ranjan and Ranjan 2015;Fuge 2019). Uptake of fluoride into the mammalian body occurs both orally and via the respiratory tract (WHO (World Health Organization) 2002;NRC (National Research Council) 2005). ...
... About 99% of the body burden of fluoride is present in mineralised tissues, especially in bones, and the growing skeleton of young animals is a particularly effective sink for fluoride (Whitford 1996;NRC (National Research Council) 2005). The bone lesions due to chronic F toxicity are referred to as skeletal fluorosis, the dental lesions as dental fluorosis (WHO (World Health Organization) 2002; Ranjan and Ranjan 2015). ...
... The reactions of fluoride with hydrogen and hydrocarbons are usually explosive. In the nomenclature, two names for fluoride can be used interchangeably (fluorine and fluoride): fluorine is the name of the element and fluoride is its ion [8,9]. ...
Article
Full-text available
The problem of fluoride toxicity to living organisms is the subject of many studies. Its effect, not always toxic, on the human organism has been well documented. However, although the phytotoxicity of the element has been proved, this issue is still being investigated. It seems to be still relevant due to the progressive pollution of the environment and fluoridation of water. Assuming that the source of food for humans is plants, the content of fluoride in fruits and vegetables is important for human health. In the available literature, fluoride has been demonstrated to be phytotoxic at the level of cell transformations, biometric plant parameters, development of resistance, and biochemical processes in plants. However, several studies have provided information on improvement of certain plant parameters, e.g., the length of roots or shoots, caused by low fluoride doses and improvement of respiratory indices. The aim of this study was to analyze changes caused in plants by exposure to fluoride and to determine its beneficial effects based on the latest literature reports. It was based on the latest knowledge from the last 8 years. Attempts were made to compare earlier research results with contemporary items. In conclusion, the analysis has shown that, although some sources provide information on the positive effect of small fluoride doses, the impact of this element requires further investigations, as has not been fully elucidated.
... It has an oxidation number of -1 and exists as either inorganic fluorides or organofluorine compounds [1,2]. Fluoride (F − ) exposure in humans occurs majorly from consuming water contaminated by F − from various natural and anthropogenic sources such as volcanic eruptions, mining residues, industrial effluents, phosphorus fertilizers, and certain domestic activities [3,4]. F − is considered a double-edged sword, having both beneficial and adverse effects on humans as well as other animals. ...
Article
Free radicals and other oxidants have enticed the interest of researchers in the fields of biology and medicine, owing to their role in several pathophysiological conditions, including fluorosis (Fluoride toxicity). Radical species affect cellular biomolecules such as nucleic acids, proteins, and lipids, resulting in oxidative stress. Reactive oxygen species-mediated oxidative stress is a common denominator in fluoride toxicity. Fluorosis is a global health concern caused by excessive fluoride consumption over time. Fluoride alters the cellular redox homeostasis, and its toxicity leads to the activation of cell death mechanisms like apoptosis, autophagy, and necroptosis. Even though a surfeit of signaling pathways is involved in fluorosis, their toxicity mechanisms are not fully understood. Thus, this review aims to understand the role of reactive species in fluoride toxicity with an outlook on the effects of fluoride in vitro and in vivo models. Also, we emphasized the signal transduction pathways and the mechanism of cell death implicated in fluoride-induced oxidative stress.
... Humans, animals and birds are severely affected in fluoride contaminated areas. The fluoride concentration of up to 1.5 ppm in water causes chronic fluorosis in animals (Ranjan & Ranjan, 2015). Several studies have been conducted on fluorosis in birds, cattle, rabbits and sheep while outbreaks of fluorosis in pigs have also been reported in china (Kazi et al., 2018;Park et al., 2021;Tao et al., 2006).Excess fluoride intake in drinking water results decrease in milk production of cows and an increase in calving interval (Shupe et al., 1972). ...
Article
Full-text available
Fluorosis in humans, animals and birds is often caused by drinking of fluoride contaminated groundwater. e study was designed to evaluate nephro-hepatotoxic effects of fluorosis on liver and kidneys in rabbits and broilers. Sixteen rabbits and sixteen broilers of four weeks age were divided into four subgroups each were given 0mg (con­trol),50 mg, 100 mg and 200 mg Sodium Fluoride /liter in water daily for 18 days. e clinical signs and mortality were noted. Blood was collected at days 0, 5, 10, 15 and 18 of experiment, for evaluation of liver and kidney functions. Dose and time dependent significant (p<0.05) increase in serum Alanine aminotransferase (GPT), Alkaline phospha­tase (ALP), Gamma glutamyl transferase (γGT), uric acid and creatinine levels and significant (p<0.05) decrease of serum calcium levels were noted in all treatment groups of both species as compared to control. In rabbits and broilers, necropsy findings included mild inflammation and discoloration of liver along with nephritis. While in broilers, toxic lesions were observed on mucus membranes of duodenum and proventriculus along with nephritis. Histological lesions observed in livers of both rabbits and broilers included dilation of central vein and sinusoids and fatty degeneration of hepatocytes. Kidney tissues of both rabbits and broilers revealed marked shrinkage of glomeruli with widened bowman’s spaces along with inflammatory cellular infiltration. It is concluded that high dose (200mg/l) of Sodium Fluoride causes liver and kidney dysfunction in both species along with lesions in digestive system of broilers
Article
Groundwater has traditionally been recognized as a reliable, safe, and essential source of drinking water. Rapid population growth increases groundwater demand, resulting in overexploitation. The quality of groundwater is deteriorating day by day due to geogenic forces and pollutants. Fluoride is one of the biggest worries about groundwater contamination, which can have serious consequences for human health mainly as fluorosis. WHO has set a global rejection limit of 1.5 mg/l for fluoride; however, it is exceeded in many places of the world. Where no other source of safe drinking water is available, removing fluoride from drinking water is the only option for obtaining safe drinking water. This review discusses various removal options, based on a number of laboratory experiments and recognized literature. The findings show that the majority of removal methods are based on adsorption processes and suit well in bench scale conditions, but hybrid and real-world application-oriented economic strategies are still being developed. The ineffective removal of fluoride from water by a single treatment has led researchers to look for hybrid approaches. Bioremediation, a usually disregarded approach, is also offered for temporarily relieving fluoride levels due to a lack of wastewater treatment facilities that need large construction costs and phytoremediation is gaining popularity owing to its advantages.
Article
Superhydrophobic (SH) concrete with low adhesion, self-cleaning, and corrosion resistance has the potential to significantly meet the challenges of injury and fatality under various external conditions such as irradiation, chemical corrosion, and biological contamination. However, the traditional process to realize the superhydrophobicity normally brings the concern of compressive strength loss. Herein, we introduced a facile approach to fabricate the superhydrophobic concrete with mechanical robustness based on the sacrificial template strategy. The concrete exhibits prominent water-repellency and admirable compressive strength simultaneously. The superhydrophobicity was well maintained after cyclic robustness evaluations, including sandpaper abrasion, knife scratch, water impacting, corrosive solution immersion, and UV radiation. The superhydrophobic concrete also exhibits broad-spectrum self-cleaning capability, such as easy removal of common dust, bacteria detachment, and resistance of ice formations. We believe that the SH concrete can potentially address the mechanical robustness and long-term water repellency towards the real applications in the future.
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Fluoride contamination has created a drinking water crisis globally.
Chapter
Arsenic, lead, fluorine, nitrogen, and carbon are common in the near-surface environment, but their concentrations in water, solids, and biota are highly variable. The distribution of As, Pb, F, N, and C in the environment is dependent on source, mineralogy, speciation, biological interactions, and geochemical controls. The As minerals interact with environment, and this renders either their dissolution or the formation of secondary minerals, or both. The distribution of the environmental arsenic is determined by the biogeochemical transformations with respect to the redox conditions, the pH, the availability of ions, the adsorption–desorption, dissolution, and the biological activity. The biological transformation and cycling of As can lead to oxidation or reduction of species that mobilize As. Besides, a significant proportion of As can also be remobilized from the soils through the process of anion exchange. Large variations can be observed on all spatial scales influenced by a variety of natural processes including nongeological influences such as climate and vegetation. Continental weathering of bedrocks contributes natural Pb to sediments, while mining and refining of Pb-bearing ores, which are subsequently used for industrial Pb applications, supply anthropogenic Pb to the environment. Lead geochemistry of rivers and costal environments plays a significant role in the biogeochemical cycling of Pb and pollutant delivery at the land–sea interface. Fluorine is ubiquitous in the environment with most deriving from natural sources, these being normal weathering processes resulting in F release from rocks and minerals, volcanic activity, and marine aerosol emission, together with biomass burning, being in part natural. However, there are several sources of anthropogenically derived F, which in some areas represent a threat to the biosphere. Together with carbon, oxygen, and hydrogen, nitrogen is one of the four most common elements in living cells and an essential constituent of proteins and nucleic acids, the two groups of substances that can be said to support life. The important nitrogen pools are soil organic matter, rocks (in fact the largest single pool), sediments, coal deposits, organic matter in ocean water, and nitrate in ocean water. The next most common gaseous form of nitrogen in the atmosphere after molecular nitrogen is dinitrogen oxide. The geochemistry of carbon is the transformations involving the element carbon within the systems of the earth. Carbon is important in the formation of organic mineral deposits, such as coal, petroleum, or natural gas. Most carbon is cycled through the atmosphere into living organisms and then respires back into the atmosphere. Carbon can form a huge variety of stable compound. It is an essential component of living matter. Carbon makes up only 0.08% of the combination of the lithosphere, hydrosphere, and atmosphere.
Chapter
Clinical manifestations of acute fluoride toxicity include hypersalivation, restlessness, body stiffness, convulsion, and respiratory and cardiac failure, eventually leading to death. In chronic fluoride toxicity calcified tissues act as a natural sink for fluoride and hence characteristic lesions develop in bone and teeth. Dental lesions appear more frequently than bony lesions and are characterized by discoloration, hypoplastic pits, chalkiness, fast attrition, and early loss. Intermittent lameness, weakness, and the appearance of bony protuberances are common due to lesions developing in bone. Toxic effects on soft tissues become more evident when bones saturate with fluoride and their capacity to accumulate more fluoride is lost. Excess fluoride can alter the cytoarchitecture and physiology of renal, hepatic, gonadal, and neuronal tissues. Many studies suggested genotoxic, carcinogenic, immunotoxic, and cytotoxic potential of fluoride, although the results were highly variable and even contradictory.
Article
We experimentally constructed a personal-computer-based Picture Archiving and Communication System (PACS) for color images of dermatology clinics. This system should especially satisfy such a demand as to be able to retrieve an image within a few seconds from the database residing in a remote server. Our two objectives in the experiment were: To examine how much time was consumed in each part of PACS while it does a series of jobs, from the requesting of an image to its display on the screen of the workstation of the user. The other objective was to see if a personal-computer-based PACS could satisfy our criteria. Total retrieving time, data reading time, data transporting time and image displaying time were measured. Total retrieving time can be divided into three procedures: Data reading time, data transporting time, image displaying time. Data reading time was about 0.6 second for reading an image with the size of 1 mega bytes (MB). Data reading time and the size of data were linearly correlated. Data transporting time was about 11 seconds for transporting an image with the size of 1 MB through EtherTalk, and 66 seconds through LocalTalk. Data transporting time and the size of the data were also linearly correlated. Data reading time and data transporting time was able to be reduced largely by compression technique. However, smaller data give other important effects to the network system besides reducing the time of data reading, data transporting and data displaying. Most Local Area using image Network (LAN) systems, such as EtherTalk, adopt Carrier Sense Multiple Access with Collision Detection (CSMA/CD) for the way of accessing to other computer. In CSMA/CD, transporting performance suddenly declines if the congestion of signal in a network gets beyond a critical level. This situation fatally impairs the performance of a network. We concluded that data compression plays an important role to improve the performances of PACS, especially those of a server and the network system. A personal-computer-based PACS with EtherTalk and an image compression/decompression hardware, e.g., CL550A chip, satisfies our criteria.
36 4.2.1 General Health Effects
  • Chronic Toxicity
Chronic Toxicity......................................... 36 4.2.1 General Health Effects............................. 36 4.2.2 Effects on Calcified Tissues......................... 37 4.2.3 Effects on Soft Tissues (Nonskeletal, Nondental Effects)... 42
53 5.1 Fluoride Tolerance in Different Animal Species
  • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fluoride Tolerance
Fluoride Tolerance.......................................... 53 5.1 Fluoride Tolerance in Different Animal Species................ 54 5.1.1 Laboratory Animals............................... 54 5.1.2 Domestic Animals................................ 54 5.1.3 Wild Animals.................................... 56 5.1.4 Poultry and Other Birds............................ 58 5.1.5 Insects and Other Invertebrates...................... 59 5.1.6 Fish and Other Aquatic Animals..................... 59
60 5.2.1 Animal Factors 61 5.2.2 Dietary and Nutritional Factors
  • Factors Affecting Fluoride Tolerance
Factors Affecting Fluoride Tolerance......................... 60 5.2.1 Animal Factors................................... 61 5.2.2 Dietary and Nutritional Factors...................... 61 5.2.3 Chemical Form of Fluoride......................... 63 5.2.4 Dose, Duration, and Continuity of Fluoride Intake....... 63 5.2.5 Environmental and Other Factors..................... 64
91 7.2.1 Minerals, Drugs, and Other Chemicals
  • . . . . . . . . . . . . . . . . . . . . Measures
2 Preventive and Therapeutic Measures........................ 91 7.2.1 Minerals, Drugs, and Other Chemicals................ 91 7.2.2 Vitamins and Antioxidants.......................... 93 7.2.3 Plant Products/Herbal Medicines..................... 93
  • . . References
References.................................................. 18
  • Fluoride Kinetics
  • . . . . . . . . . . . . . . . . . . . . . . . . Metabolism
Fluoride Kinetics and Metabolism............................. 21 3.1 Absorption............................................. 21 3.1.1 Gastrointestinal Tract.............................. 22 3.1.2 Respiratory Tract................................. 23 3.1.3 Dermal and Other Routes........................... 24
  • Excretion . . . . . . . . . . . . . . . . . . . . . . . . . . . . Elimination
Elimination and Excretion................................. 30 3.3.1 Urine........................................... 30 3.3.2 Feces........................................... 30 3.3.3 Saliva.......................................... 31 3.3.4 Perspiration...................................... 31 3.3.5 Milk........................................... 31
  • . . References
References.................................................. 32