Fluoride is the major Cause of Cataract Blindness
Geoff N Pain
Cataract blindness affects tens of millions of people, many of whom will never have access to lens replacement
surgery. Fluoride from various sources including drinking water, tea, salt and drugs, enhances and stabilizes crystal
growth of Hydroxyapatite within the eye. Fluoride is identified as the major risk for cataract and contributes to risk
of other eye diseases including macular degeneration.
Keywords: Alkaline Phosphatase, Anticholinesterase agents, Aphakia, Asteroid Hyalosis, Asthma, Bio-
accumulation, Blindness, Calcification, Cataract, Conjunctivitis, Diabetes, Fluoride, Fluorocarbon, Glaucoma,
Hydroxyapatite, Macular Degeneration, Melatonin, Mortality, Optial Neuritis, Osteosarcoma, Pineal gland, Retina,
In Australia it is estimated that 40% of visual impairment is due to Cataract, with over 1,460,400 sufferers aged 55 or
more (31% of that age group) in 2004. In the same year 429,600 Australians aged 55 or more had undergone
cataract surgery, which represents 9.1% of that age group [AIHW 2005]. The risk of falls and bone fractures,
automobile accidents, premature death and the rates of depression and anxiety are elevated in those visually
impaired by cataract [Smith 2016].
Cataract is the leading cause of visual impairment in Australian Aborigines who suffer earlier onset of cataract in
their generally shorter life spans [Landers 2013].
In underdeveloped countries, the incidence of new cases outstrips the surgical capacity, producing a worsening
human and economic burden [Khanna 2012]. Surgical rate is a measure of wealth of nations and surgical failure is
significant, often resulting in aphakia or eye loss.
There are various types of cataract [Gruebbel 2014], however the focus of this review is the highly mineralized
forms, which have been known since 1843 [Jacob 1851] to be due to deposition of needle-like crystals of “phosphate
of lime”, now known as Hydroxyapatite. Calcified cataract is normally age-dependent but has been reported in
young people [Chiang 2004].
Types of Cataract
There are three main types of Cataracts: nuclear; cortical; and subcapsular.
Nuclear cataracts form deep in the central zone of the lens and are usually associated with aging.
Cortical cataracts occur in the lens cortex, the part of the lens that surrounds the central nucleus and have white,
wedge-like opacities that start in the periphery of the lens and work their way to the centre, resembling spokes.
Subcapsular cataract occurs at the back of the lens. People with diabetes or those taking high doses of steroid
medications have a greater risk of developing subcapsular cataracts.
Synchrotron hard X-ray imaging of whole lenses has allowed identification of Calcium in both cortical and nuclear
cataract crystals [Antunes 2006] while other groups using the technique focused on structural change of protein
Fluoride doped Hydroxyapatite in Cataract
A study of residents in two towns in Texas with different Fluoride levels in drinking water, Bartlett (8 ppm Fluoride)
and Cameron (0.4 ppm Fluoride) found no statistically significant difference due to small sample size and different
age distributions [Leone 1954]. The National Research Council remarked about this study "The greater incidence in
the high fluoride group (Bartlett) of a certain brittleness and blotching of fingernails, of hypertrophic changes in the
spine and the pelvis, and of lenticular opacities of the eyes (Cataracts) requires further investigation.” [NRC 2006].
Correlation between the incidence of senile cataract and concentration of fluoride in drinking water was observed in
a later studies [Kas’ianenko 1984, Shulka 1991].
Down Syndrome (Mongolism) was established to be linked to consumption of fluoride through statistical studies. It
was found that 70% of Down's Syndrome babies were born with cataract [Rapaport 1957; 1957a; 1959].
Early studies of Fluoride content of Cataract found up to 77 ppm Fluoride [Waldbott 1961].
However humans in Balaghat who drank well water at 1.2-2.4 ppm or river water at 2.8 ppm Fluoride, exhibited
remarkably high levels of 20,000 to 50,000 ppm Fluoride in their removed cataracts [Shulka 1991].
These levels exceed those that have been reported in the Pineal gland and indicate that high levels of Calcium,
Phosphate and Fluoride are available to the lens during cataract formation.
Calcium has been shown to induce opacification and proteolysis in the lens of test animals [Truscott 1990]. Proteases
including calpain I, calpain II, and calpastatin are present in the lens [Yoshida 1985].
Effects of industrial Fluoride exposure in humans include opacities of the lens capsule (cataract) and attenuation of
the retinal arteries [Karczewicz 1989].
Fluoride doped Hydroxyapatite in cataracts and other tissues is less easily resorbed, leading to bio-accumulation and
acceleration of Hydroxyapatite Deposition Disease (HADD). Kidney failure with age, part of which is due to the
nephrotoxicty of Fluoride [Pain 2017], produces an exponential retention of Fluoride and risk of cataract growth.
The European Commission adopted a position on Hydroxyapatite in 2016 stating: “The available information
indicates that nano-hydroxyapatite in needle-shaped form is of concern in relation to potential toxicity. Therefore,
needle-shaped nano-hydroxyapatite should not be used in cosmetic products. It is of note that Material 2 of the
submission also includes nanofibres of needle-like structure.” [EC 2016].
Recently in Australia a famous manufacturer of infant formula was forced to withdraw product from the market due
to discovery of nanocrystals of Fluoride doped Hydroxyapatite in its product [Schoepf 2016, Schoepf 2017,Han
2017]. Energy dispersive x-ray analysis of Hydroxyapatite for Fluoride content can be difficult due to other elements
exhibiting peaks in spectra near 7 kEV.
Crystals of Fluoride doped Hydroxyapatite found in infant formula that was withdrawn from the Australian
market [Schoepf 2016, Han 2017].
Crystals of Fluoride doped Hydroxyapatite grown by use of Silver Diamine Fluoride (above left) [Mei 2017] or by
use of acidulated phosphate fluoride (APF) gel to dissolve human teeth (above right) [Kakei 2012].
Global Incidence of Cataract correlates Fluoride in Drinking Water
Comparison of global Fluoride groundwater contamination with severity of cataract prevalence demonstrates good
correlation where data is available.
In addition to the groundwater, many nations are exposed to additional Fluoride hazard from use of rock salt
containing up to 250 ppm Fluoride and high tea consumption.
Much higher incidence of cataracts is found in most tea-consuming countries such as India, Pakistan, Bangladesh,
Myanmar, People’s Republic of China, and other Southeast Asia.
Cataract is the major cause of blindness in Africa [Steinkuller 1983, Rolfe 1997, WHO 2010].
More detailed mapping of Fluoride groundwater contamination shows that the East Africa Rift suffers the effects of
a long history of volcanic venting rich in Hydrogen Fluoride. It is not surprising therefore that the Fred Hollows
Foundation has chosen to perform its cataract surgery programme in Eritrea, Ethiopia, Kenya, Burundi, Rwanda.
Damage to the Cornea and Retina by Fluoride
It has been known since the 1930s that the Retina is easily damaged by Fluoride [Ashton 1957, Akleyev 2014].
Retinal oedema followed by degenerative changes in 17 out of 94 rabbits occurred within five days of giving sodium
fluoride and the effect was enhanced by fasting [Sorsby 1960]. Studies of the action of Sodium Fluoride in destroying
the Retina suggested that it involved inhibition of enzymes involved in glucose metabolism and ion pumps
[Graymore 1959, Sorsby 1966, Vantsek 1969].
The NHMRC specifically excluded a study finding heavy iridocorneal angle hyperpigmentation and glaucoma
associated with fluorosis [Aytuluner 2002]. Likewise NHMRC excluded a study finding that Fluorinated ocular or
periocular corticosteroids have caused death as well as glaucoma in children [Romano 2003].
The World Health Organization recognizes Fluoride as a cause of Conjunctival Hyperaernia [WHO 2014].
Experimental generation of Cataract with Fluoride in Man and Animals
In just six weeks a man given Sodium Fluoride developed optical neuritis [Geall 1964].
Immersing mammalian eyes in Sodium Fluoride solution generates cataracts in a matter of hours [Hamar 1965].
In the experiment with goat eyes, Lipid peroxide level (LPO), and Protein carbonyl content (PC) were significantly
(p<0.001) increased with the fluoride concentration while glutathione level (GSH) and antioxidant enzymes,
superoxide dismutase (SOD) and catalase (CAT) were significantly decreased [Mishra 2014].
Forty percent of rats given commercially available spring water, containing 100 ppm fluoride, for 24 weeks showed
opacifications, epithelial proliferation, and growth changes, including reduced body weight, lengths of body, femur
and tail, compared to controls [Aytuluner 2003].
Above. In 1954 calf eyes were immersed
in Sodium Fluoride solution to produce
cataracts [Nordmann 1954].
Left. A similar experiment using goat eyes
produced the same result [Mishra 2014].
Hydroxyapatite crystals grow in as well as on interocular lenses
A kinetic study showd that Hydroxyapatite crystals in intraocular lenses can be initiated from their interior through
the development of sufficiently high local supersaturation, realized through the diffusion of calcium and phosphate
ions [Drimtzias 2011]. Carbonate inclusion within hydroxyapatite in both intraocular and human senile cataract was
observed by infrared spectroscopy [Lin 2010]. It is significant that fluorine-surface-modified and unmodified lenses
for implantation in pediatric aphakia were investigated in research excluded from consideration by the NHMRC in
2007 [Thouvenin 1996]. The NHMRC also excluded a study of the mineralization of intraocular lens [Lai 2005].
Hydroxyapatite and Age-related macular degeneration (AMD)
Macula retinopathy and degenerative changes in the retina in relation to Fluoridation were reported in early studies
Proof of involvement of Hydroxyapatite in macular degeneration, which involves accumulation of protein and lipid
containing deposits external to the retinal pigment epithelium, was found by examination of cadaver eyes using
electron microscopy and x-ray diffraction [Thompson 2015]. It was observed that the Hydroxyapatite formed
spherules containing amyloid beta (Aβ) peptide or complement factor proteins as well as cholesterol and other
Hydroxyapatite damage to the Eye and Alzheimer’s Disease
The possible link between macular degeneration and Alzheimer’s disease arises from the observation that
Alzheimer’s Aβ-peptide is deposited at sites of complement activation in pathologic deposits associated with aging
and age-related macular degeneration [Johnson 2002]. Fluoride doped Hydroxyapatite is also present in Corpora
Arenacea or “brain sand” [Wilson 2014].
Glaucoma is found five times more frequently in Alzheimer’s disease patients than in aged controls [Bayer 2002].
Calcification of the lens, retina and macular can be assumed, due to reduced light transmission to the
retinohypothalamic tract, to interfere with the Pineal gland melatonin regulating retina suprachiasmatic nucleus axis
which is implicated in aging and Alzheimer’s Disease [Wu 2005].
Accumulation of Fluoride doped Hydroxyapatite is well known in the Pineal gland [Gusek 1983, Alcolado 1986,
Jengelski 1989, Schmid 1993, Luke 1997, Kunz 1998, Kunz 1999, Duffy 2003].
Risk factors for Cataract and related disease involving multiple Fluoride sources
Fluoride in drinking water causes cataract and the effect is dose-dependent. Other risks and associations with
cataract have been identified and are discussed below. The Appendix lists other reported cataract risks.
Table 2. Risk factors and associations with Fluoride for Cataract and related disease
Fluoride Link Reference
Fluoride in drinking water
Waugh 2016; 2017
Heavy Beer drinking
Styburski 2017,Waugh 2017a
Fluoride in Rock Salt
Diabetes > 10 years
Blood Glucose level
Asthma or Chronic Bronchitis
History of Coronary Heart
Chlorpromazine > 90 days
High plasma Homocysteine
Medhi 1990, Weiss 2002
Decreased plasma Folate
Ratan 2008, Susheela 2010
Decreased plasma Vitamin B12
High glycosylated Haemoglobin
Decreased plasma cholesterol
Fed Reg 2003
Fed Reg 1998
Inhaled Corticosteroids > 5
Cumming 1997, Leske
1998, Jick 2001
Hydroxyapatite forms precipitates in the vitreous humor of the eye, sometimes only unilaterally, in the condition
known as Asteroid Hyalosis, previously named Hyalitis [Jervey 1965, March 1975, Winkler 2001, Komatsu 2003,
Based on Fluoride analyses available for lens calcification, we can anticipate future research will identify Fluoride in
the mineral content of these “asteroids”.
Diabetes, metabolic disorders and Cataract
Metabolic cataracts include those associated with Diabetes Mellitus, Galactosaemia, Hypercholesteraemia,
Lipidemia, Endocrinological cataract associated with Hypothyroidism and Hypercalcaemia and cataracts associated
with certain skin diseases such as Atopic Dermatitis [Dawson 1981, Kador 2008].
Elevated Plasma albumin, bilirubin, calcium, cortisol, glucose, sodium and γ- glutamyl transpeptidase levels in
cataract patients were linked to liver disease [Donnelly 1995]. Fluoride is a known hepatotoxin.
Diabetes is associated with severe mitochondrial disorders such as Kearns-Sayre syndrome and Mitochondrial
Encephalomyopathy, Lactic Acidosis, and Strokelike episodes (MELAS). Mitochondrial forms of diabetes mellitus
occur in conjunction with hearing loss, myopathy, seizure disorder, strokelike episodes, retinitis pigmentosa,
external ophthalmoplegia and cataracts. There is evidence of maternal inheritance [van den Ouweland 1992,
Khardori 2017]. Increased glycated haemoglobin level was associated with increased risk of nuclear and cortical
cataracts in those with diabetes [Klein 1998]. Fluoride is known to cause Diabetes [Pain 2015c].
Diabetes is associated with low birth weight and while there is a genetic component to low birth weight [Wang
2016], Fluoride is known to cause low birth weight in exposed populations [Hart, MacArthur 2013].
Prevalence studies on diabetes complications reported up to the early 1990s gave widely variable figures. These
have been reviewed in two studies and include figures ranging from 9 to 16 percent for cataract, 7 to 52 percent for
retinopathy, 6 to 47 percent for neuropathy, 6 to 30 percent for nephropathy, and 1 to 5 percent for
macroangiopathy [Mbanya 2003; Rolfe 1997].
Women diabetics suffer higher rates of cataract and earlier surgery than men. Risk factors from the Framingham
heart study that were significantly associated with cataract formation included: elevated blood sugar, elevated blood
pressure, increased serum phospholipids, decreased pulmonary vital capacity, small stature, and less than seven
years of schooling [Kahn 1977].
A patient suffering diabetes, ischemic heart disease, hypertension and renal dysfunction and taking insulin
developed hydroxyapatite cataracts 4 months after implantation of an intraocular lens. Another patient, diabetic and
taking insulin developed hydroxyapatite cataracts 9 months after implantation. Another patient in good overall
health developed hydroxyapatite cataracts 15 months after implantation. All patients received dexamethasone
sodium phosphate eye drops. [Yu 2001].
Cataract and Smoking
Cataracts associated with smoking have been reported to be dose-dependent [Klein 1993, Solberg 1990, West 1995,
Leske 1998, Krishnaiah 2005, Prokofyeva 2013].
Australian data indicated a population attributable risk for smoking and nuclear cataract of 17%, and a risk of 10%
for UV-B exposure and cortical cataract [McCarty 2000, Robman 2005].
Fluorinated Organic Compounds including Drugs and Propellants cause Cataract
Treatment of glaucoma with potent, long-acting anticholinesterase agents including isoflurophate, diisopropyl
fluorophosphates, for 6 months or longer carries high risk of the development of a specific type of cataract, which
begins as anterior subcapsular vacuoles. The incidence of lenticular opacities was as high as 50% with headache,
brow pain, blurred vision, phacodinesis, pericorneal injection, congestive iritis, various allergic reactions, and rarely,
retinal detachment [Gilman 1985, AMA 1983].
Fluorocarbon anaesthetics are known to be metabolized to yield high concentrations of serum Fluoride ion.
Cataract due to the methoxyflurane anaesthetic metabolite calcium oxalate-monohydrate (Whewellite) has been
observed with the pathway for the biotransformation also yielding ionic fluoride [Bullock 1974]. Calcium Oxalate has
also been reported in the lenses of patients with Morgagnian cataracts [Zimmerman 1958].
Drugs used in treatment of asthma are known to cause cataracts, including Flunisolide, Fluticasone Anon
2007].Fluorocarbon propellants used to deliver drugs to patients via “puffers”, including asthma sufferers, are
known to pose serious health hazards due to their metabolism to free Fluoride ion [Silverglade 1972, Valic 1997,
Cumming 1997, Jick 2001]. The observed higher incidence of cataract in users of inhaled drugs is therefore closely
associated with the propellant, often overlooked in epidemiology studies of the drugs in question.
Tetrafluoroethylene has been demonstrated to cause cataracts [NTP 1997].
Flonicamid, an insecticide, causes atrophy of striated muscle fibers, cataract and retinal atrophy observed in the high
dose female rats [Fed Reg 2003]. Fluazifop-p-butyl causes cataracts in 8 out of 12 dogs [Virgo 1982].
Flufenacet, an herbicide has LOEL of 50 ppm [7.4 mg/kg/day] for males 200 ppm [38.4 mg/kg/day] for females based
on cataract incidence and severity [Fed Reg 1998]. Eye effects also included ocular scleral mineralization.
Fluoroquinolones including ciprofloxacin, gatifloxacin, levofloxacin, moxifloxacin, norfloxacin, and ofloxacin cause
uveitis [Wefers Bettink-Remeijer 2009, Butler 2012, Hinkle 2012, Eadie 2014].
Voriconazole increases serum Fluoride to damaging levels. Among the numerous harms caused by this drug are
colour vision change, persistent or severe blurred vision or sensitivity to light.
Visual hallucinations have been found associated with use of fluoxetine and other selective serotonin reuptake
inhibitors [Bourgeois 1998, Schuld 2000].
Fluorinated corticosteroids cause death as well as glaucoma in children [Romano 2003].
Cataract association with Cancer
As previously reviewed, Fluoride doped Hydroxyapatite has been shown to cause malignant cancer of the Breast and
Thyroid [Pain 2015].
In Taiwan, an increased incidence of breast, liver, and head and neck cancers was observed in patients presenting
with Early Onset Cataract [Chiang 2014].
Breast cancer associated with cataracts has also been observed in India [Faridi 2017].
Reactive oxygen species lead to lens opacification through oxidative damage to lens proteins. Increased incidence of
cataract is found in subjects with the null genotype of Glutathione S-Transferase M1 subtype (GSTM1) (odds ratio-
1.51; p<0.05) [Saadat 2012]. The polymorphisms of GSTM1, GSTT1, GSTP1 and GSTO2 have been shown to be
associated with increased risk of developing breast cancer [Sohail 2013]. Raised serum sialic acid, caused by Fluoride
[Needham 2010], is found associated with both cataract and Osteosarcoma [Sandhu 2011].
Cataract association with increased risk of Death
In non-diabetic women the age adjusted cataract mortality hazard ratios were: nuclear opacity (1.8), cortical opacity
(1.9), and posterior subcapsular opacity (2.1). There was no significant difference in mortality risk for men. Among
diabetics, the mortality was significantly higher in both men and women with cataract with age and sex adjusted
hazard ratio of 2.6 [Reidy 2002].
Other mortality studies have been contradictory. When confined to nuclear cataract, there appears to be a more
consistent trend across studies with 11 out of 15 showing significantly increased risk of death. Unfortunately many
studies do not distinguish the type of cataract and few refer to calcification [Khanna 2013].
Nuclear opacity (RR, 1.40; 95% CI, 1.12–1.75) and cataract surgery (RR, 1.55; 95% CI, 1.18–2.05) were associated with
increased all-cause mortality and with cancer deaths [Clemons 2004].
Higher risks were found for black Barbados residents with cumulative 4-year mortality varied with lens types,
increasing from 3.2% for those without cataract to 6.0% for cortical-only, 8.8% for nuclear-only, and 20.9% for mixed
opacities. Coexisting diabetes further increased mortality: people with mixed opacities and diabetes had a 2.7-fold
increased risk of death [Hennis 2001].
Mechanisms of Fluoride induced Cataract
The toxic effects of fluoride in the eye appear to follow universal mechanisms found in a wide variety of cells
[Barbier 2010, Agalakova 2012].
The mechanisms of fluoride toxicity can be summarized [Pain 2017a] under the following headings:
• Mutation and abnormal embryo development with altered expression
• Endocrine disruption
• Altered enzyme levels and enzyme inhibition
• Oxidative stress with generation of reactive oxygen species and radicals
• Apoptosis via mitochondria mediated and Caspase dependent pathways
• Disruption of ion channels affecting pH, cation and anion balance
• Physical damage from calcification
Fluoride Disrupts Phosphate Pathways
Metabolic disturbance, chronic hypocalcemia and hyperphosphatemia, calcitonin reduction, vitamin D insufficiency
can be responsible for cataract formation [Stein 1980, Ogiso 1990, Brown 2015].
Elevated phosphate levels have been measured in the aqueous humor of cataract patients compared to glaucoma
patients. Variation of various phosphatase levels were also found [Latarya 2012].
Cataract calcification will of course be facilitated by elevated phosphate via enhanced crystal growth of Fluoride
Measurement of Alkaline phosphatase is often used to detect systemic toxic reaction as it is an indicator of abnormal
bone turnover and hepatobiliary diseases [Mallik 2016].
Alkaline phosphatase (10.6%), acid phosphatase (24.09%) increased in brains of mice after administration of sodium
Fluoride [Reddy 2009].
Fluoride inhibits acid phosphatases (protein phosphoseryl and phosphothreonyl phosphatases or PSPs), which are
necessary for the phosphorylation of glucose, adenosine triphosphatase, and enolase, the enzyme responsible for
the formation of phosphopyruvic acid from 2-phosphoglyceric acid [Nordmann 1954]. Sodium Fluoride is sold as a
reagent of choice to irreversibly inhibit Acid Phosphatases [Thermo Fisher Scientific 2017].
Mechanistic studies identify Fluoride attack on the metal ion centres in acid phosphatases, notably Iron and Zinc,
preventing coordination of water molecules essential for their function [Pinske 1999, Srivastava 2015].
Acid phosphatase and lipid peroxidation have been measured in human cataractous lens epithelium. Lipid
peroxidation in mature cataractous lens epithelium was correlated with increased permeability of the plasma
membrane [Vasavada 1993].
Fluoride inhibition of acid phosphatase is also related to male infertility [Nag Das 1984] and prostate disease [Reiner
Congenital Cataracts Facial Dysmorphism Neuropathy Syndrome involves a single-nucleotide substitution producing
a nonfunctional protein in formation of Fcp1 which is the main serine phosphatase for the C-terminal domain of
eukaryotic RNA polymerase II, which regulates transcription by recruiting different factors to nascent mRNA [Varon
Alkaline phosphatase, elevated in cataract patients [Donnelly 1995, Fernandes 2011], is also greatly increased in
osteosarcoma, a neoplastic proliferation of osteoblasts [Krook 1998].
Alkaline Phosphatase is an enzyme which catalyses the hydrolysis of a number of phosphate esters, transferring the
phosphate group to an acceptor molecule. Fluoride has been shown to increase serum alkaline phosphatase that
results in increased deposition of Hydroxyapatite [Farley 1983, Khokher 1990, Shanthakumari 2004, Fernandes
2011]. Chronic industrial airborne Fluoride exposure increased worker serum alkaline phosphatase (ALP) and
superoxide dismutase (SOD).
Raised levels of alkaline phosphatase induce hypocalcemia, which triggers parathyroid hyperactivity [Krook 1998].
Hypoparathyroidism is an uncommon condition characterized by spontaneously lowered synthesis and/or secretion
of parathyroid hormone (PTH), which results in profound hypocalcemia and hyperphosphatemia [Liao 2016]. It is a
result of prevention of calcium reabsorption in renal tubulus and bone matrix, as well as insufficiency of the
synthesis of 1,25- dihydroxyvitamin D3 [1,25(OH)2D3] from its inactive precursor 25- hydroxyvitamin D.
Fluoride induces cell injury in both osteoblasts and osteocytes, initiating a repair response that results in increased
alkaline phosphatase [Krook 1998]. An increase of serum alkaline phosphatase results in enhanced hydroxyapatite
deposition measured as increased bone mass following fluoride dosing. Unfortunately, it seems little attention has
been paid to the more difficult task of measuring the enhanced deposition of hydroxyapatite in soft tissues.
Alkaline phosphatase is inhibited by Fluoride in the gut of the silkworm [Miao 2005].
Rats treated with Fluoride in drinking water for 90 days show high serum alkaline phosphatase accompanied by
hypocalcemia and hyerphosphatemia [Gupta 2016].
Fluoride causes Oxidative Stress leading to Cataracts
Lipid peroxidation is known to cause cataracts from research that was specifically excluded from consideration by
the NHMRC in 2007 [Babizhayev 2004]. Further research by the same group found that oxidative stress in
mitochondria induces generation of reactive oxygen species (ROS) and redox imbalance of the eye lens leading to
human cataract formation with formation of phospholipid hydroperoxides as a common basis for cataract disease
Various oxidative stress markers have been studied in human cataract patients [Sawada 2009, Tomar 2014]. A study
in Jaipur, India, compared randomly selected patients with cataract from a high Fluoride region, ground water F>2.5
ppm, with age- and sex-matched control patients with cataract from a low-fluoride region, ground water F<1.5 ppm
[Tomar 2014]. Oxidative stress markers studied were Lipid peroxide levels (LPO), protein carbonylation (PC),
superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), serum F estimations, and the measurement of
trace metallevels (Cu, Zn, Se, and Fe). Significantly higher LPO and PC were found in the high-F region subjects in
both serum and lenses. Antioxidant enzyme SOD and GSH were found to be markedly decreased in the blood and
lenses of the high-F region subjects [Tomar 2014].
Methylglyoxal is implicated in cataract development by inducing endoplasmic reticulum stress in human lens
epithelial cells, and activating an unfolded protein response leading to overproduction of ROS and altering the
cellular redox balance toward lens oxidation [Palsamy 2014].
Sialic acid, is a marker for inflammation and oxidative stress and is released from the terminal oligosaccharide chain
of some glycoproteins and glycolipids. Cataract is associated with the increase in serum sialic acid level [Mallik 2016].
Fluoride is known to increase sialic acid levels [Susheela 1982].
Gamma glutamyl transpeptidase is another marker for oxidative stress that is elevated in cataract as well as liver and
cardiovascular disease [Emdin 2005, Mallik 2016].
Fluoride Disrupts Ion Transport
As discussed above, Fluoride disrupts the anaerobic metabolic pathways which provide the energy for ion transport.
The lens excretes sodium and concentrates potassium in cataracts [Mallik 2016].
Elevated magnesium was found in the serum of cataract patients [Ringvold 1988].
Light damages cation pump activity via superoxide formation, attenuated by ascorbate in the aqueous humour
Alteration in ion transport can lead to variation in hydration of the lens, leading to myopia and glaucoma.
Attempted amelioration of Cataract
Antioxidant vitamin supplements have been investigated as a means of slowing, if not preventing, eye disease
including cataract and macular degeneration.
Vitamin E showed some promise in one study [Vitale 1993] but proved a risk factor in another [McCarty 2000].
It has been suggested that in Turkey, with the maximum per capita use of tea in the world, supplying up to 376 mg of
caffeine per day, that the antioxidant properties of caffeine might lower incidence of cataract [Varma 2016].
Evidence that is consistent with Fluoride inhibition of metallo-enzymes is the observation that Zinc supplements
provide a protective effect [Clemons 2004].
Salicylates lower plasma levels of tryptophan and prevent binding to the lens, significantly retarding UV cataract
formation in both diabetics and non-diabetics.
Significantly lower incidences of nuclear cataracts 5 years later occurred in those who took thiazide diuretics
(OR=0.79, 95% CI 0.63, 1.00) and aspirin (OR=0.76, 95% CI 0.61, 0.95) at the baseline examination [Klein 2001] with
the aspirin result contradicting increased risk found elsewhere [Christen 2001].
The only safe place for Hydroxyapatite storage is in bone. When deposited in the soft tissues, it resembles asbestos,
causing numerous diseases including those leading to blindness and premature death.
Fluoride doping exacerbates this calcification and every effort must be made to reduce Fluoride exposure in the
diet. The deliberate addition of Fluoride to milk or salt is reckless.
Elimination of deliberate water Fluoridation programmes and defluoridation of contaminated groundwater will
greatly reduce the global burden of preventable eye disease.
Fluoride contribution to incidence of age-related macular degeneration, diabetic retinopathy, glaucoma and a
proportion of “undetermined cause” global blindness should be recognized in epidemiology studies and future plans
to remedy the suffering.
The World Health Organization should update its warnings about Fluoride as a chemical of concern with added
emphasis on loss of vision so that the few remaining countries that have not banned water Fluoridation will have
extra incentive to act [WHO 2010;2014].
Abraham AG, Condon NG, West GE. 2006. The new epidemiology of cataract. Ophthalmol Clin North Am 19:415-425.
Agalakova NI, Gusev GP. 2012. Molecular mechanisms of cytotoxicity and apoptosis induced by inorganic fluoride.
International Scholarly Research Network. Cell Biology. doi:10.5402/2012/403835.
AIHW. Vision problems among older Australians. Bulletin 27 July 2005. 1-36.
Akleyev AV. 2014. Neurological Disorders of Non-Radiation Nature, Fluorosis. In: Chronic Radiation Syndrome.
Springer-Verlag Berlin Heidelberg.
Alcolado JC, Moore IE, Weller RO. 1986. Calcification in the human choroid plexus, meningiomas and pineal gland.
Neuropathol Appl Neurobiol. 12:235-250.
AMA. 1983. American Medical Association, AMA Department of Drugs. AMA Drug Evaluations. 5th ed. Chicago:
American Medical Association, 447.
Anon. 2007. Use of Corticosteroid Inhalers for the Treatment of Asthma and COPD. Allergy and Immunology Blog.
Antunes A, Safatle AMV, Barros PSM, Morelhão SL. 2006. X-ray imaging in advanced studies of ophthalmic diseases.
Med. Phys. 33(7):2338-2343.
Aristei C, Alessandro M, Santucci A, Aversa F, Tabillo A, Carotti A. 2002. Cataracts in patients receiving stem cell
transplantation after conditioning with total body irradiation. Bone Marrow Transplant. 29(6):503-7.
Ashton N, Graymore C, Pedler C. 1957. Studies on Developing Retinal Vessels. V. Mechanism of Vaso-Obliteration (A
Preliminary Report) Brit. J. Ophthal. 41:449-460.
Augusteyn RC. 1981. Protein modification in cataract: possible oxidative mechanisms. In: Duncan G, ed. Mechanisms
of Cataract Formation in the Human Lens. London: Academic Press, 72-111.
Aytuluner E, Mensiz E. 2002.Heavy iridocorneal angle hyperpigmentation and glaucoma associated with fluorosis.
Fluoride 37(1):52-53. *
Aytuluner E, Mensiz E, Candir O, Aydin S. Cataractogenic effect of fluorosis in an animal model. Fluoride 37(1):53-54.
Aytuluner E, Mensiz E, Çandir Ö, Aydin Ş. 2003. Cataractogenic Effect of Fluorosis in an Animal Model. Journal of
Toxicology: Cutaneous and Ocular Toxicology. 22(1-2):23-31.
Babizhayev MA, Deyev AI, Yermakova VN, Brikman IV, Bours J. 2004. Lipid peroxidation and cataracts: N-
Acetylcarnosine as a therapeutic tool to manage age-related cataracts in human and in canine eyes. Drugs in R and D
Babizhayev MA. 2011. Mitochondria induce oxidative stress, generation of reactive oxygen species and redox state
unbalance of the eye lens leading to human cataract formation: disruption of redox lens organization by
phospholipid hydroperoxides as a common basis for cataract disease. Cell Biochem Funct. 29:183-206.
Bahrami M, Hoshino M, Pierscionek B, Yagi N, Regini, J. 2015. Refractive index degeneration in older lenses: A
potential functional correlate to structural changes that underlie cataract formation. Experimental Eye Research
Barbier O, Arreola-Mendoza L, Del Razo LM. 2010. Molecular mechanisms of fluoride toxicity. Chem Biol Interact
Bergman Åke, Heindel JJ, Jobling S, Kidd KA, Zoeller RT. Editors. 2013. State of the Science of Endocrine Disrupting
Chemicals – 2012 An assessment of the state of the science of endocrine disruptors prepared by a group of experts
for the United Nations Environment Programme and World Health Organization.
Bayer AU, Ferrari F. 2002. Severe progression of glaucomatous optic neuropathy in patients with Alzheimer’s
disease. Eye 16:209-212.
Bochow TW et al. 1989. Ultraviolet light exposure and risk of posterior subapsular cataracts. Archives of
Bourgeois JA, Thomas D, Johansen T, Walker DMJ. 1998. Visual hallucinations associated with fluoxetine and
sertraline. Clin Psychopharmacol 18(6):482-3.
Brian G, Taylor H. 2001. Cataract blindness - challenges for the 21st century. Bulletin of the World Health
Organization 79 (3):249-256.
Brown CJ, Akaichi F. 2015. Vitamin D deficiency and posterior subcapsular cataract. Clin ophthalmol 9:1093-1098.
Bullock JD, Albert DM, Skinner HCW, Miller WH, Galla JH. 1974. Calcium oxalate retinopathy associated with
generalized oxalosis: x-ray diffraction and electron microscopic studies of crystal deposits. Investigative
Butler NJ, Suhler EB. 2012. Levofloxacin-associated panuveitis with chorioretinal lesions. Arch Ophthalmol.
Chang JR, Koo E, Agrón E, et al. 2011. Age-Related Eye Disease Study Group. Risk factors associated with incident
cataracts and cataract surgery in the Age-related Eye Disease Study (AREDS): AREDS report number 32.
Charles NC, Rabin S. 1995. Calcific Phacolysis: Salvageable Vision following treatment. Arch Ophthalmol 113:786-788.
Chatterjee A, Milton RC, Thyle S. 1982. Prevalence and aetiology of cataract in Punjab. British Journal of
Chen JS, Yu ZW, Zhu PZ, Wang JF, Gan ZH, Wei J, Zhao YH, Wei SC. 2015. Effects of fluorine on the structure of
fluorohydroxyapatite: a study by XRD, solid-state NMR and Raman spectroscopy. J Mater Chem B. 3(1):34-38.
Christen W. 2001. Aspirin use and risk of cataract in post-trial follow-up of Physicians’ Health Study. Arch Ophthalmol
Chiang S-Y, Horng C-T, Lee W-H, Chang C-J. 2004. Calcified cataractous lens. Journal of Cataract and Refractive
Chiang CC, Lin CL, Peng CL, Sung FC, Tsai YY. 2014. Increased risk of cancer in patients with early-onset cataracts: a
nationwide population-based study. Cancer Sci. 105(4):431-36.
Chitkara D. 1998. Cataract: cataract formation mechanisms, cause of cataract. In: Yanoff M, Duker JS. CD-ROM
Clemons TE, Kurinij N, Sperduto RD, Bressler SB, et al. 2004. Associations of Mortality With Ocular Disorders and an
Intervention of High-Dose Antioxidants and Zinc in the Age- Related Eye Disease Study: AREDS Report No. 13 Arch
Cogan DG, Kuwabara T, Gilbert J, et al. 1958. Calcium oxalate and calcium phosphate crystals in detached retinas.
Arch. Ophthalmol. 60:366.
Cumming RG, Mitchell P, Leeder SR. 1997. Use of inhaled corticosteroids and the risk of cataracts. N Engl J Med
Cumming RG, Mitchell P. Medications and cataract. 1998. The Blue Mountains Eye Study. Ophthalmology 105: 1751-
David LL, Shearer TR. 1984. Calcium-activated proteolysis in the lens nucleus during selenite cataractogenesis. Invest
Ophthalmol Vis Sci. 25(11):1275-83.
Dawson CR, Schwab IR. 1981. Epidemiology of cataract - a major cause of preventable blindness. Bulletin of the
World Health Organization, 59 (4):493-501.
Delcourt C, Cristol JP, Tessier F, Léger CL, Michel F, Papoz L. 2000. Risk factors for cortical, nuclear, and posterior
subcapsular cataracts: the POLA study: Pathologies Oculaires Liées à l’Age. Am J Epidemiol. 151(5):497-504.
Donnelly CA, Seth J, Clayton RM, Phillips CI, Cuthbert J, Prescott RJ. 1995. Some blood plasma constituents correlate
with human cataract. British Journal of Ophthalmology 79:1036-1041.
Drimtzias EG, Rokidi SG, Gartaganis SP, Koutsoukos PG. Experimental Investigation on Mechanism of Hydrophilic
Acrylic Intraocular Lens Calcification. American Journal of Ophthalmology 152(5):824-833.
Eadie B, Etminan M, Mikelberg FS. 2014. Risk for uveitis with oral moxifloxacin: a comparative safety study. JAMA
Eanes ED, Hailer AW. 1998. The effect of fluoride on the size and morphology of apatite crystals grown from
physiologic solutions. Calcif Tissue Int. 63(3):250-257.
EC. 2016. European Commission. Scientific Committee on Consumer Safety (SCCS). Opinion on Hydroxyapatite
(nano). 16 October 2015, SCCS/1566/15, revision of 16 March 2016.
Emdin M, Pompella A, Paolicchi A. 2005. Gamma Glutamyl Transferase, Atherosclerosis and cardiovascular disease
trigerring oxidative stress within the plaque. American Heart Association. 112(4):2078-80.
Fagerholm P, Philipson B, Carlstrom D. 1981. Calcification in the Human Lens. Curr Eye Res 6:629-63.
Fagerholm P, Lundevall E, Trocmé S, Wroblewski R. 1986. Human and experimental lens repair and calcification. Exp
Eye Res. 43:965–972.
Faridi SH, Singh KD, Lodhi M. 2017. Concomitant Presence of Carcinoma of Breast in a Patient with Early-Onset
Cataract: First Case Report of a Potential Association. Journal of Clinical and Diagnostic Research. May, Vol-
Farley JR, Wergedal JE, Baylink DJ. 1983. Fluoride directly stimulates proliferation and alkaline phosphatase activity
of bone-forming cells. Science 222:330-32.
Fed Reg. 1998. Federal Register. June 23, 1998. Pesticide Tolerance Petition.
Fed Reg. 2003. Federal Register: May 23, 2003 (Volume 68, Number 100)] [Notices] [Page 28218-28222]. Flonicamid;
Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food.
Fernandes MS, Iano FG, Rocia V, Yanai MM, Leye AL, Furlani TA, Buzalaf MAR, Oliveira RC. 2011. Alkaline
Phosphatase Activity in Plasma and Liver of Rats Submitted to Chronic Exposure to Fluoride. Braz Arch Biol Technol
Ferrini W, Aubert V, Balmer A, et al. 2013. Anterior uveitis and cataract after rubella vaccination: a case report of a
12-month-old girl. Pediatrics. 132:e1035–e1038
Fledelius H. 1975. Cataracta Ossea and other Intraocular Ossifications. Acta Ophthalmologica 53(5):790-797.
Fluegge K. 2016. Community water fluoridation predicts increase in age adjusted incidence and prevalence of
diabetes in 22 states from 2005 and 2010. J Water Health 14 (5):864-77.
Geall MG, Beilin LJ. 1964. Sodium fluoride and optic neuritis. Brit. Med. J. 8:355-356.
Gilman AG, Goodman LS, Gilman A. (eds.). 1985. Goodman and Gilman's The Pharmacological Basis of Therapeutics.
7th ed. New York: Macmillan Publishing Co., Inc. p124.
Glynn RJ, Rosner B, ChristenWG. 2009. Evaluation of risk factors for cataract types in a competing risks framework.
Ophthalmic Epidemiol. 16(2):98-106.
Graymore C. 1959. In vitro swelling of the kitten retina induced by sodium fluoride inhibition. Br J Ophthalmol 43:40-
Gruebbel MM. 2014. NTP Nonneoplastic Lesion Atlas. Eye, Lens, Cataract.
Gupta AR, Dey S, Saini M, Swarup D. 2016. Toxic effect of sodium fluoride on hydroxyproline level and expression of
collagen-1 gene in rat bone and its amelioration by Tamrindus indica L. fruit pulp extract. Interdiscip Toxicol 9(1):12-
Duffy JF, Zeitzer JM, Rimmer DW et al. 2002. Peak of circadian melatonin rhythm occurs later within the sleep of
older subjects. Am J Physiol Endocrinol Metab 282:E297-E303.
Hammar H. 1965. The formation of amino acids in vitro from glucose in the eye lens of rats and the influence of
sodium fluoride and alloxan diabetes. Acta Ophthalmol 43: 543–556.
Hammond CJ, et al. 2000. Genetic and environmental factors in age-related nuclear cataracts in monozygotic and
dizygotic twins. New England Journal of Medicine, 342:1786-1790.
Hammond CJ, et al. 2000. Genes and environment in cortical cataract: the Twin Eye Study. Investigative
Ophthalmological and Visual Science 41:2901.
Han E. 2017. Study finds potentially toxic nanoparticles in Australian baby formula. Sydney Morning Herald 2 July.
Hart R, et al. Relationship between municipal water fluoridation and preterm birth in Upstate New York. American
Public Health Association 137th Annual Meeting.
Heijl A, Leske MC. 2007. Cataract epidemiology. Ophthalmology 114:201.
Hennis A, Wu SY, Li X, Nemesure B, Leske MC et al. 2001. Lens opacities and mortality : the Barbados Eye Studies.
Hennis A, 2004. Risk factors for incident cortical and posterior subcapsular lens opacities in the Barbados Eye
Studies. Arch Ophthalmol 122:525-530.
Hightower KR, David LL, and Shearer TR. 1987. Regional distribution of free calcium in selenite cataract: Relation to
calpain II. Invest Ophthalmol Vis Sci 28:1702.
Hinkle DM, Dacey MS, Mandelcorn E, et al. 2012. Bilateral uveitis associated with fluoroquinolone therapy. Cutan
Ocul Toxicol. 31:111–116.
Hollows F, Moran D. 1981. Cataract - the ultraviolet risk factor. Lancet 2:1249-1250.
Huxley R, Lee CM, Barzi F, et al. 2009. Coffee, decaffeinated coffee, and tea consumption in relation to incident type
2 diabetes mellitus: a systematic review with meta-analysis. Arch Intern Med. 169(22):2053-2063.
Jacob A. 1851. On cataract, and the operation for its removal by absorption, with the fine needle, through the
cornea. Dublin Medical Press.
Javitt JC, Taylor HR. 1994-1995. Cataract and latitude. Doc Ophthalmol. 88(3-4):307-325.
Jengeleski CA, Powers RE, O’Connor DT et al. 1989. Noradrenergic innervation of human pineal gland: abnormalities
in aging and Alzheimer’s disease. Brain Res 481:378-382.
Jervey ED, Anderson Jr WB. 1965. Asteroid hyalitis: a study of serum calcium levels in affected patients. South Med J
Jick SS, Vasilakis-Scaramozza C, Maier WC. 2001. The risk of cataract among users of inhaled steroids. Epidemiology
Johnson LV, et al. 2002. The Alzheimer’s Aβ-peptide is deposited at sites of complement activation in pathologic
deposits associated with aging and age-related macular degeneration. Proc Natl Acad Sci USA 99(18):11830–11835
Jolly SS, Singh BM, Mather OC. 1969. Endemic fluorosis in Punjab (India). Am J Med 47:553-63.
Judd G F Affidavit of Gerard F. Judd, Ph.D. 1993. In Support of Motion for Summary Judgment Safe Water
Association, Inc. vs City of Fond Du Lac. State Of Wisconsin Circuit Court. Fond Du Lac County.
Judd GP. 1994. Evidence Against Fluoride Continues to Mount. Health Freedom News, November/December p. 29.
Kador PF, Wyman M. 2008. Asteroid hyalosis: pathogenesis and prospects for prevention. Eye 22:1278-85.
Kahn HA et al. 1977. The Framingham Eye Study. II. Association of ophthalmic pathology with single variables
previously measured in the Framingham Heart Study. American Journal of Epidemiology 106:33-41.
Kakei M, Sakei T, Yoshikawa M. 2012. Aspects Regarding Fluoride Treatment for Reinforcement and Remineralization
of Apatite Crystals. J Hard Tissue Biology 21(3):257-266.
Kanthan GL, Wang JJ, Burlutsky G, Rochtchina E, Cumming RG, Mitchell P. 2010. Exogenous oestrogen exposure,
female reproductive factors and the long-term incidence of cataract: the Blue Mountains Eye Study. Acta
Kanthan GL, Mitchell P, Burlutsky G, Wang JJ. 2011. Fasting blood glucose levels and the long term incidence and
progression of cataract – the Blue Mountains Eye Study. Acta Ophthalmol 89:e434–e438.
Karczewicz D, Baranowska-George T, Palacz O, Tokarz-Sawinska E, Stankiewicz W, Krzystolik Z, Lubinski W, Kosmider
K. 1989. Evaluation of the visual system in people having extended contact with fluorine. Klin Oczna 91(1):9-11.
Kas'ianenko AS, Korneva TS, Kovgan NI. 1984. Dissemination of senile cataract among the population of Poltava
Province consuming water with various fluorine levels. Oftalmol Zh 5: 302-304.
Kauh CY, Blachley TS, Lichter PR, Lee PP, Stein JD. 2016.Geographic Variation in the Rate and Timing of Cataract
Surgery Among US Communities. JAMA Ophthalmol. 134(3):267-276.
Khanna RC, Marmamula S, Krishnaiah S, Giridhar P, Chakrabarti S, Rao GN. 2012. Changing trends in the prevalence
of blindness and visual impairment in a rural district of India: systematic observations over a decade. Indian J
Khanna RC, Murthy GVS, Giridhar P, Krishnaiah S. Pant HB, Shantha GPS, Chakrabarti S, Gilbert C, Rao GN. 2013.
Cataract, Visual Impairment and Long-Term Mortality in a Rural Cohort in India: The Andhra Pradesh Eye Disease
Study. PlosOne. 8(10): e78002.
Khardori R, Griffing GT, Bessen HA, Brenner BE, Isley WL, Ligaray KPL, Peters AL, Schade DS, Schalch DS, Schraga ED,
Talavera F, Votey SR. 2017. Type 2 Diabetes Mellitus. Medline. http://emedicine.medscape.com/article/117853
Khokher MA, Dandona P. 1990. Fluoride stimulates [3H]thymidine incorporation and alkaline phosphatase
production by human osteoblasts. Metabolism 39(11):1118-21.
Kleifeld O, Hockwine O, Ayberk N. 1956. The effect of sodium fluoride on the metabolism of the lens. Graefes Arch
Ophthalmol 158: 39-46.
Klein BE. 1993. Cigarette smoking and lens opacities. The Beaver Dam Eye Study. American Journal of Preventive
Klein BE, Klein R, Lee KE. 1998. Diabetes, cardiovascular disease, selected cardiovascular disease risk factors, and the
5-year incidence of age-related cataract and progression of lens opacities: the Beaver Dam Eye Study. Am J
Klein BE, Kelin R, Lee KE. 2002. Incidence of age-related cataract over a 10-year interval: the Beaver Dam Eye Study.
Komatsu H, Kamura Y, Ishi K, Kashima Y. 2003. Fine structure and morphogenesis of asteroid hyalosis. Med Electron
Krishnaiah S, Vilas K, Shamanna BR, Rao GN, Thomas R et al. 2005. Smoking and its association with cataract: results
of the Andhra Pradesh eye disease study from India. Invest Ophthalmol Vis Sci 46:58-65.
Krook L, Minor RR. 1998. Fluoride and alkaline phosphatase. Fluoride 31(4):17-182.
Kunz D, Bes F, Schlattmann P et al. 1998. On pineal calcification and its relation to subjective sleep perception: a
hypothesisdriven pilot study. Psychiatry Res 82:187-191.
Kunz D, Schmitz S, Mahlberg R et al. 1999. A new concept for melatonin deficit: on pineal calcification and melatonin
excretion. Neuropsychopharmacology 21:765-772.
Lai JY, Chen KH, Hsu WM, Lee TH, Lin SY. 2005. Multiple elements in the deposits of opacified hydroview intraocular
lens. American Journal of Ophthalmology 139(6):1123-1125. *
Landers J, Henderson T, Craig JE. 2013. Incidence of visual impairment due to cataract, diabetic retinopathy and
trachoma in indigenous Australians within central Australia: the Central Australian Ocular Health Study. Clinical &
Experimental Ophthalmology, 41:50-55.
Latarya G, Mansour A, Epstein I, Cotlear D, Pikkel J, Levartovsky S, Yulish M, Beit-Yannai E. 2012. Human Aqueous
Humor Phosphatase Activity in Cataract and Glaucoma. Invest Ophthalmol Vis Sci. 53:1679-1684.
Lee do H, Seo Y, Joo CK. 2002. Progressive opacification of hydrophilic acrylic intraocular lenses in diabetic patients
(1) J Cataract Refract Surg 28:1271-1275.
Leone NC, Shimkin MB, Arnold FA, Stevenson CA, Zimmermann ER, Geiser PB, Lieberman JA. 1954. Medical Aspects
of Excessive Fluoride In a Water Supply. Public Health Reports. 69(10):925-936.
Leske MC, Chylack LT Jr, Wu S-Y. 1991. The Lens Opacities Case-Control Study Group: the lens opacities case-control
study: risk factors for cataract. Archives of Ophthalmology 109:244-251.
Leske MC, Chylack LT Jr, He Q, Wu S-Y, Schoenfeld E, Friend J, Wolfe J, Cheung H, Green J, Baker M, Bury L, Jakubicz
G, Karabassi M, Khu P, Libman J, McDonald B, Singer D, . Longitudinal Study of Cataract. 1998. Risk factors for
nuclear opalescence in a longitudinal study. Am J Epidemiol. 147(1):36-41.
Li K, Fu Q, Guam Z. 2003. Impact of fluoride on worker’s skeleton density and serum AKP and SOD. Gongye Weisheng
Yu Zhiyebing 2003 29(5):293-294.
Liao X, Huang X, Lan C, Li J, Tan Q. 2016. Characteristic Cataract Associated with Idiopathic Hypoparathyroidism. J
Clin Exp Ophthalmol 7(4):588.
Lin S-Y, Chen K-H, Lin C-C, Cheng W-T, Li M-J. 2010. Spectral analysis and comparison of mineral deposits forming in
opacified intraocular lens and senile cataractous lens. Spectrochimica Acta Part A: Molecular and Biomolecular
Luke J. 1997. The Effect of Fluoride on the Physiology of the Pineal Gland. Ph.D Dissertation, School of Biological
Sciences, University of Surrey, UK.
Malago J, Makoba E, Muzuka ANN. 2017. Fluoride Levels in surface and ground water in Africa. Amer. J Water Sci Eng
Mallik S, Ray D, Majumdar U, Das P. 2016. A Study of Interrelationship Between Occurrence of Cataract in Patients
Attending Ophthalmology Out Patient Department in Burdwan Medical College & Hospital with Their Liver Function
Profile And Serum Sialic Acid Levels. IOSR Journal of Dental and Medical Sciences 15(12):134-146.
March WF, Shoch D. 1975. Electron diffraction study of asteroid bodies. Invest Ophthalmol 14(5):399-400.
Mansour AM. Cataract Ossea. Journal of Cataract and Refractive Surgery. 31(6):1086.
Mbanya JC, Sobngwi E. 2003. Diabetes Microvascular and Macrovascular Disease in Africa. Journal of Cardiovascular
Risk 10: 97-102.
McCarty CA. 1999. The epidemiology of cataract in Australia. American Journal of Ophthalmology, 128: 446-465.
McCarty CA, Nanjan MB, Taylor HR. 2000. Attributable risk estimates for cataract to prioritize medical and public
health action. Invest Ophthalmol Vis Sci 41: 3720-3725.
Mehdi S, Jarvi ET, Koehl JR, McCarthy JR, Bey P. 1990. The mechanism of inhibition of S-adenosyl-L-homocysteine
hydrolase by fluorine-containing adenosine analogs. J Enzyme Inhib. 4(1):1-13.
Mei ML, Nudelman F, Marzec B, Walker JM, Lo ECM, Walls AW, Chu CH. 2017. Formation of Fluorohydroxyapatite
with Silver Diamine Fluoride. Journal of Dental Research May 1-7.
Miao Y-G, Jiang L-J, Bharathi D. 2005. Effects of Fluoride on the Activities of Alkaline Phosphatase, Adenosine
Triphosphatase, and Phosphorylase in the Midgut of Silkworm, Bombyx Mori L. Fluoride 38(1):32-37.
Minassian DC, Mehra V, Jones BR. 1984. Dehydration crises from severe diarrhoea or heatstroke and risk of cataract.
Mishra S, Tomar S, Sharma A, Chauhan DS, Tripathi S. 2014. Fluoride Induces Morphological and Biochemical
Changes in Goat Eye Lens. J Environ Anal Toxicol 4(5):231.
Mishra S, Sharma A, Choudhary M, Tomar S, Ahmad A, Tripathi S.2013. In vitro effect of Emblica officinalis on sodium
selenite induced cataract in isolated goat eyes. Conference Proceeding, Society of Pharmacovigilance, India, 2013:93.
Mishra S, Sharma A, Tomar S, Choudhary M, Chauhan DS, Singh VP, Tripathi S, Tomar A. 2012. Correlation of Serum
Fluoride Levels and Oxidative Burden in Hypertensive retinopathy Patients in Rajasthan. Indian Journal of Clinical
Mishra S, Sharma A, Choudhary M, Tomar S, Tripathi S. 2012. Association of Increased Oxidative Burden and
Cataractogenesis: In-vitro Study. Journal of Pharmacovigillance and Drug Safety. 9:6.
NagDas SK, Bhattacharyya AK. 1984. The kinetics of inhibition of human seminal plasma acid phosphatase by sodium
fluoride. Biochem Int. 9(5):659-68.
Navarro Esteban JJ, Gutierrez Leiva JA, Valero Caracena N, Buendia Bermejo J, Calle Puron ME, Martinez Vizcaino VJ.
2007. Prevalence and risk factors of lens opacities in the elderly in Cuenca, Spain. Eur J Ophthalmol 17:29-37.
Needham B. 2010. “Killer Smile” Report To Minister For Health And Human Services Water Fluoridation And Ill
Health of at Risk Groups in the Tasmanian Population in 2010.
Nordmann J, Mandel P, Achard M. 1954. Inhibition of Sugar Metabolism in the Lens. Br J Opthal 8:673-679.
NRC. 2006. National Research Council of the National Academy of Sciences. Fluoride in Drinking Water: A scientific
Review of EPAs Standards. National Academies Press, Washington D.C.
NTP. National Toxicology Program. 1997. NTP TR-450. Toxicology and Carcinogenesis Studies of Tetrafluoroethylene
(CAS No. 116-14-3) in F344 Rats and B6C3F1 Mice (Inhalation Studies). NTP, Research Triangle Park, NC. Abstract:
Ogiso M, Saito N, Sudo N, Subo H, Hirano S, Komoto H. 1990. Increase in lens gangliosides due to aging and cataract
progression in human senile cataract. Investigative Ophthalmology and Visual Sciences. 31(10):2171-2179.
Pain GN. 2015a. Fluoride doped Hydroxyapatite and Cancer. A literature review.
Pain GN. 2015b. Fluoride is a bio-accumulative, endocrine disrupting, neurotoxic carcinogen – not a nutrient.
Pain GN. 2015c. Fluoride Causes Diabetes.
Pain GN. 2016. Fluoride causes Heart Disease, Stroke and Sudden Death.
Pain GN. 2017a. Fluoride is a developmental Nephrotoxin – coming to a Kidney near you.
Pain GN. 2017b. Mechanisms of Fluoride Neurotoxicity - a quick guide to the literature.
Pain GN. 2017c. A Quick Guide to Fluoride Harms. Available from ResearchGate.
Palsamy P, Bidasee KR, Ayaki M, Augusteyn RC, Chan JY, Shinohara T. 2014. Methylglyoxal induces endoplasmic
reticulum stress and DNA demethylation in the Keap1 promoter of human lens epithelial cells and age-related
cataracts. Free Radical Bio Med. 72:134-48.
Peckham S, Lowery D, Spencer S. 2015. Are fluoride levels in drinking water associated with hypothyroidism
prevalence in England? A large observational study of GP practice data and fluoride levels in drinking water. J
Epidemiol Community Health 69(7):619-24.
Pinkse MW, Merkx M, Averill BA. 1999. Fluoride inhibition of bovine spleen purple acid phosphatase:
characterization of a ternary enzyme-phosphate-fluoride complex as a model for the active enzyme-substrate-
hydroxide complex. Biochemistry 38(31):9926-36.
Prokofyeva E, Wegener A, Zrenner E. 2013. Cataract prevalence and prevention in Europe: a literature review. Acta
Randall DA, Reinten T, Maher L, Lujic S, Stewart J, Keay L, Leyland AH, Jorm LR. 2014. Disparities in cataract surgery
between Aboriginal and non-Aboriginal people in New South Wales, Australia. Clinical and Experimental
Rao GN. 1991. Light intensity-associated eye lesions of Fischer 344 rats in long-term studies. Toxicol Pathol 19:148-
155. Full-text: http://tpx.sagepub.com/content/19/2/148.full.pdf
Rapaport Y[I]. 1957. Les opacifications du cristallin mongolisme et cataracte senile (Donillees statistiques recentes).
Rev. Anthropol. (Paris), 2(3):133-135.
Rapaport I. 1957a. Contribution a l'etude etiologique du mongolisme. Role des inhibiteurs enzymatiques. Encephale
Rapaport I. 1959. New Research on Mongolism relating to the disease producing role of Fluorine. Bull Acad Natl
Ratan SK, Rattan KN, Pandey RM, Singhal S, Kharab S, Bala M, Singh V, Jhanwar A. 2008. Evaluation of the levels of
folate, vitamin B12, homocysteine and fluoride in the parents and the affected neonates with neural tube defect and
their matched controls. Pediatr Surg Int. 24(7):803-8.
Rautiainen S, Lindblad BE, Morgenstern R, Wolk A. 2010. Vitamin C supplements and the risk of age-related cataract:
a population-based prospective cohort study in women. Am J Clin Nutr 91: 487-493.
Reddy KP, Sailaja G, Krishnaiah C. 2009. Protective effects of selenium on fluoride induced alterations in certain
enzymes in brain of mice. J Environ Biol. 30(5 Suppl):859-64.
Reidy A, Minassian DC, Desai P, Vafidis G, Joseph J, Farrow S, Connolly A. 2002. Increased mortality in women with
cataract: a population based follow up of the North London Eye Study. Br J Ophthalmol 86:424-428.
Reiner JM, Tsuboi KK, Hudson PB. 1955. Acid phosphatase. IV. Fluoride inhibition of prostatic acid phosphatase
Archives of Biochemistry and Biophysics 56(1):165-183.
Ringvold A , Sagen E, Bjerve KS, Følling I. 1988. The calcium and magnesium content of the human lens and aqueous
humour. A study in patients with hypocalcemic and senile cataract. Acta Ophthalmol (Copenh) 66(2):153-156.
Robman L, Taylor H. 2005. External factors in the development of cataract. Eye 19:1074-1082.
Rolfe, M. 1997. Chronic Complications of Diabetes in Africa. In Diabetes in Africa. Gill GV, Mbanya JC, Alberti KGMM
(eds) 43-50. Cambridge: FSG Communications.
Romano PE. 2003. Fluorinated ocular/periocular corticosteroids have caused death as well as glaucoma in children.
Clinical and Experimental Ophthalmology 31(3):279-280. *
Ruigomez A, Garcia Rodriguez LA, Dev VJ, Arellano F, Raniwala J. 2000. Are schizophrenia or antipsychotic drugs a
risk factor for cataracts? Epidemiology 11:620-623.
Saadat I, Ahmadi Z, Farvardin-Jahromi M, Saadat M. 2012. Association between cataract and genetic polymorphisms
of GSTM1, GSTT1, and GSTO2 with respect of work place. Mol Vis. 18:1996-2000.
Salazar-Martinez E, Willett WC, Ascherio A, et al. 2004. Coffee consumption and risk for type 2 diabetes mellitus. Ann
Intern Med. 140(1):1-8.
Sandhu R, Lal H, Kundu ZS, Kharb S. 2011. Serum fluoride and sialic acid levels in osteosarcoma. Biological Trace
Element Research 144(1-3):1-5.
Sasaki H, Jonasson F, Shui YB et al. 2002. High prevalence of nuclear cataract in the population of tropical and
subtropical areas. Dev Ophthalmol 35: 60-69.
Sato M, Hanmoto T, Yachiguchi K, Tabuchi Y, Kondo T, Endo M, Kitani Y, Sekiguchi T, Urata M, Hai TN, Srivastav AK,
Mishima H, Hattori A, Suzuki N. 2016. Sodium Fluoride induces Hypercalcemia resulting from the upregulation of
both osteoblastic and osteoclastic activities in goldfish Carassius auratus. Comparative Biochemistry and Physiology :
Toxicology Pharmacology 189:54-60.
Sawada H, Fukuchi T, Abe H, et al. 2009. Oxidative stress markers in aqueous humor of patients with senile cataracts.
Curr Eye Res. 34:36-41.
Saxena S, Mitchell P, Rochtchina E. 2004. Five-year incidence of cataract in older persons with diabetes and pre-
diabetes. Ophthalmic Epidemiol 11:271-277.
Schmid HA. 1993. Decreased melatonin biosynthesis, calcium flux, pineal gland calcification and aging: a hypothetical
framework. Gerontology 39:189-199.
Schoepf JJ, Westerhoff P. 2016. Detecting Engineered Nanomaterials in Baby Formula. Report prepared for Friends
of the Earth. Arizona State University.
Schoepf JJ, Bi Y, Kidd J, Herckes P, Hristovski K, Westerhoff P. 2017. Detection and Dissolution of needle-like
Hydroxyapatite nanomaterilas in Infant Formula. NanoImpact 5:22-28.
Schuld A, Archelos JJ, Friess E. 2000. Visual hallucinations and psychotic symptoms during treatment with selective
serotonin reuptake inhibitors: is the sigma receptor involved? J Clin Psychopharmacol 20(5):579-80.
Sen SK, Pukazhvanthen P, Abraham R. 2008. Plasma Homocysteine, Folate and Vitamin B12 Levels in Senile Cataract.
Indian Journal of Clinical Biochemistry 23(3):255-257.
Shanthakumari D, et al. 2004. Effect of fluoride intoxication on lipid peroxidation and antioxidant status in
experimental rats. Toxicology 204:219-228.
Sharma A, Tomar S, Aggarwal M, Shukla Y, Mishra S, Tripathi S, Tomar A. 2013. Fluoride affects quality of vision: An
observational study; Conference proceedings, International Society for Fluoride Research; Tehran, Iran.
Shui YB, Holekamp NM, Kramer BC et al. 2009. The gel state of the vitreous and ascorbate dependent oxygen
consumption: relationship to the etiology of nuclear cataracts. Arch Ophthalmol 127:475-482.
Shukla N, Pandey GS. 1991. Fluoride level in cataract lenses in an urban area of India. Fluoride 24(1):40-43.
Silverglade A. 1972. Cardiac Toxicity of Aerosol Propellants JAMA 222(7):827-829.
Smith SD. 2016. Geographic Variation in Cataract Surgery Rates. Searching for Clues to Improve Public Health. JAMA
Sohail A, Kanwal N, Ali M, Sadia S, Masood AI, Ali F, et al. 2013. Effects of glutathione- S-transferase polymorphisms
on the risk of breast cancer: a population-based case-control study in Pakistan. Environ Toxicol Pharmacol. 35:143-
Solberg Y, Rosner M, Belkin M. 1998. The association between cigarette smoking and ocular diseases. In: Seddon J,
Fong D, (eds). Public health and the eye. Survey of Ophthalmology 42:535-547.
Sorsby A, Harding R. 1960. Experimental Degeneration of The Retina V. Fasting and Metabolic Accelerators in
Degeneration Produced by Sodium Fluoride. Brit. J. Ophthal. 44:213.
Sorsby A, Harding R. 1966. Oxidizing agents as potentiators of the retinotoxic action of sodium fluoride, sodium
iodate and sodium iodoacetate. Nature 210(40):997-998.
Srivastava PK, Anand A. 2015. The inhibitory effect of metals and other ions on acid phosphatase activity from Vigna
aconitifolia seeds. Prep Biochem Biotechnol. 45(1):33-41.
Stein R, Godel V. 1980. Hypocalcemic cataract. J Pediatr Ophthalmol Strabismus 17:159-161.
Stein JD, Childers D, Gupta S, et al. 2015.Risk factors for developing thyroid-associated ophthalmopathy among
individuals with Graves disease. JAMA Ophthalmol. 133(3):290-296.
Steinkuller PG. 1983. Cataract: the leading cause of blindness and vision loss in Africa. Social Science and Medicine
Styburski D, Barananowska-Bosiacka I, Goschorska M, Chlubek D, Gutowska I. 2017 Biol Trace Elem Res 177:404-408.
Susheela AK, Sharma YD, Jha M, Rajalakshmi K, Rama NV, Rao M. 1981.Chemical Profile of Human Serum in Fluoride
toxicity and Fluorosis 1. Total Protein, Bound Carbohydrates, Seromucoid and Fluoride Levels. Fluoride 14:150-154.
Susheela AK, Mohan Jha. 1982. On the significance of Sialic Acid and Glycosaminoglycans in the serum of Fluorosed
Human Subjects. Fluoride 15(4): 202-207.
Susheela AK, Mondal NK, Gupta R, Ganesh K, Brahmankar S, Bhasin S, Gupta G. 2010. Effective Interventional
Approach to Control Anemia in Pregnant women. Current Science 28(10):1320-1330.
Sutton PN. 1986. Lung Cancer: Is Fluoride in Cigarette Smoke an Etyological Factor? Medical Hypotheses 20:51.
Tan JS, Wang JJ, Mitchell P. 2008. Influence of diabetes and cardiovascular disease on the long term incidence of
cataract: the Blue Mountains eye study. Ophthalmic Epidemiol. 15:317-27.
Taylor HR. 1999. Epidemiology of age-related cataract. Eye (Lond) 13(Pt 3b): 445-448.
Theodoropoulou S, Theodossiadis P, Samoli E, Vergados I, Lagiou P, Tzonou A. 2011. The epidemiology of cataract: a
study in Greece. Acta Ophthalmol 89: e167-173.
Thermo Fisher Scientific. 2017. Protease and Phosphatase Inhibitors.
Thouvenin D, Arne JL, Lesueur L. 1996. Comparison of fluorine-surface-modified and unmodified lenses for
implantation in pediatric aphakia. Journal of Cataract and Refractive Surgery 22( 9):1226-1231. *
Thompson RB, Reffatto V, Bundy JG, Kortvely E, Flinn JM, Lanzirotti A, Jones EA, McPhail DS, Fearn S, Boldt K, Ueffing
M, Singh Ratu SG, Pauleikhoff L, Bird AC, Lengyel I. 2015. Identification of hydroxyapatite spherules provides new
insight into subretinal pigment epithelial deposit formation in the aging eye. Proc Natl Acad Sci USA 112:1565–1570.
Tomar S. 2014. Fluoride intake increases oxidative burden of cataractognesis in fluoride endemic areas in India. 4th
International Conference on Clinical and Experimental Ophthalmology July 14-16, DoubleTree by Hilton Baltimore-
BWI Airport, USA. J Clin Exp Ophthalmol. DOI: 10.4172/2155-9570.S1.017
Tomar S, Mishra S, Choudhary M, Chauhan DS, Singh PYVP, Joshi DK, Tripathi S, Tomar S, Tomar A. 2012. Increased
oxidative burden in hypertensive retinopathy patients and its association with fluoride exposure in population of
Rajasthan India. Fluoride 45(3Pt1)207-208.
Tomar S, Sharma A Tripathi, SMS, Tomar A. 2013. Fluoride increases oxidative burden in cataractogenesis: An in vitro
and in vivo study; conference proceedings, International Society for Fluoride Research; Tehran, Iran.
Tomar A, Singh VP, Chauhan DS, Mishra S, Joshi DK, Kumar S, Tripathi S, Tomar S, Tomar S. 2012. Excessive
Fluoride exposure delineating the changes of different vitamin concentration and oxidative burden in school children
of eastern region of the Rajasthan India Fluoride 45(3Pt1):207.
Tomar S, Mishra S, Tripathi S, Tomar A. 2014. Potentiated Oxidative Burden and altered Trace Metal Levels from
Excessive Fluoride in Patients with Cataract. Conference abstract. 4th International Conference on Clinical and
Experimental Ophthalmology July 14-16, DoubleTree by Hilton Baltimore-BWI Airport, USA.
Truscott RJW, Marcanfonio JM, Tomlinson J, Duncan G. 1990. Calcium-induced Opacification and Proteolysis in the
Intact Rat Lens. Investigative Ophthalmology and Visual Science 31(11):2405-2411.
Vajpayee RB, Angra SK, Honavar SG et al. 1995. Capsulotomy for phacoemulsification in hypermature cataracts. J
Cataract Refract Surg. 21:612–615.
Valero MP, Fletcher AE, De Stavola BL, Vioque J, Alepuz VC. 2002. Vitamin C is associated with reduced risk of
cataract in a Mediterranean population. J Nutr 132(6):1299-1306.
Valic F, Skuroc Z, Bantic Z, Rudar M, Hecej M. 1977. Effects of fluorocarbon propellants on respiratory flow and ECG.
Vandenberg L N, Colborn T, Hayes T B, Heindel J J, Jacobs D R, Lee D H, Shioda T, Soto A M, von Saal F S, Welshons W
V, Zoeller R T, Myers J P. 2012. Hormones and endocrine-disrupting chemicals: Low dose effects and nonmonotonic
dose responses. Endocrine Reviews 33(3):378-455.
van den Ouweland JM, Lemkes HH, Ruitenbeek W, Sandkuijl LA, de Vijlder MF, Struyvenberg PA, et al. 1992.
Mutation in mitochondrial tRNA(Leu)(UUR) gene in a large pedigree with maternally transmitted type II diabetes
mellitus and deafness. Nat Genet. 1(5):368-71.
Vanysek J, Anton M, Hrachovina V, Moster M. 1969. Some metabolic disturbance of the retina due to the effect of
natrium fluoride. Ophthalmologica 158:684-690.
Varma SD, Chand D, Sharma YR, Kuck JF Jr, Richards RD. 1984. Oxidative stress on lens and cataract formation: role
of light and oxygen. Curr Eye Res 3(1):35-57.
Varma SD. 2016. Effect of coffee (caffeine) against human cataract blindness. Clinical Ophthalmology 10:213-220.
Varon R, Gooding R, Steglich C, Marns L, Tang H, Angelicheva D, Yong KK, Ambrugger P, Reinhold A, Morar B et al.
2003. Partial deficiency of the C-terminal- domain phosphatase of RNA polymerase II is associated with congenital
cataracts facial dysmorphism neuropathy syndrome. Nat Genet 35:185189.
Vasavada AR, Thampi P, Yadav S, Rawal UM. 1993. Acid phosphatase and lipid peroxidation in human cataractous
lens epithelium. Indian J Ophthalmol 41:173-175.
Virgo DM. 1982. Fluazifop-butyl: 55 week oral toxicity study in beagle dogs. Life Science Research, Stock, Essex,
England, 10/15/82. LSR Report No. 81/ILK019/620.
Vitale S, West S, Hallfrisch J, Alston C, Wang F, Moorman C, Muller D, Singh V, Taylor HR. 1993. Plasma antioxidants
and risk of Cortical and Nuclear Cataract. Epidemiology 4(3):195-203.
Vrensen G, Willekens B. 1989. Classification and prevalence of early senile lens opacities in human donor eyes. In:
Hockwin O, Sasaki K, Leske MC. (Eds.) Risk Factors for Cataract Development 17. Krager, Basel. pp. 181-187.
Vrensen GF. 2009. Early cortical lens opacities: a short overview. Acta Ophthalmol 87:602-610.
Waldbott GL. 1955. Chronic fluorine intoxication from drinking water. Int. Arch. Allergy. 7:70-74.
Waldbott GL. 1961. The Physiologic and Hygienic Aspects of the Absorption of Inorganic Fluorides. Arch
Environmental Health 2:155-167.
Waldbott GL. 1962. Fluoride in clinical medicine. Int. Arch. Allergy. 20(Supp):1-60.
Waldbott GL. 1964. Fluoride and Optic Neuritis. British Medical Journal. 945.
Waldbott GL. 1976. Symposium on the Non-Skeletal Phase of Clinical Fluorosis. Fluoride 9:7-10.
Waldbott GL, Burgstahler A, McKinney HL. 1978. Fluoridation: The Great Dilemma. Coronado Press, Lawrence,
Wang T, Huang T, Li Y, Zheng Y, Manson JE, Hu FB, et al. 2016. Low birthweight and risk of type 2 diabetes: a
Mendelian randomisation study. Diabetologia. Jun 23.
Wang T, Zhang Z, Song A, Liu X. 1991. Analysis on serum lipids in patients with Fluorine-associated Aortic Sclerosis.
Endemic Diseases Bulletin. 6(4):51-52.
Warnakulasuriya S, Harris C, Gelbier S, Keating J, Peters T. 2002. Fluoride content of alcoholic beverages. Clinica
Chimica Acta 320(1-2):1–4.
Waugh DT, Potter W, Limeback H, Godfrey M. 2016. Risk assessment of fluoride intake from tea in the republic of
Ireland and its implications for public health and water fluoridation. International Journal of Environmental Research
and Public Health 13(3) article no. 259.
Waugh DT, Godfrey M, Limeback H, Potter W. 2017. Black Tea Source, Production, and Consumption: Assessment of
Health Risks of Fluoride Intake in New Zealand. Journal of Environmental and Public Health
Waugh DT. 2017a. Personal communication.
Wefers Bettink-Remeijer M, Brouwers K, van LL, et al. 2009. Uveitis-like syndrome and iris transillumination after the
use of oral moxifloxacin. Eye (Lond). 23:2260-2262.
Wei M, Evans JH, Bostrom T, Grondahl L. 2003. Synthesis and characterization of hydroxyapatite, fluoride-
substituted hydroxyapatite and fluorapatite. J Mater Sci Mater Med. 14(4):311-320.
Weiss N, Keller C, Hoffman U, Loscalzo J. 2002. Endothelial Dysfunction and Atherothrombosis in mild
Hyperhomocysteinemia. Vasc Med; 7:227-239.
West SK, Valmadrid CT. 1995. Epidemiology of risk factors for age related cataract. Survey of Ophthalmolology, 39:
WHO. 2010. Global Data on Visual Impairments.
WHO 2014. World Health Organization. Chemicals of public health concern in the African Region and their
management: Regional Assessment Report.
Wilson GH III, Gore JC, Yankeelov TE, Barnes S, Peterson TE, True JM, Shokouhi S, McIntyre JO, Sanders M, Abramson
V, Ngyuen T-Q, Mahadevan-Jansen A and Tantawy MN. 2014. An Approach to Breast Cancer Diagnosis via PET
Imaging of Microcalcifications Using 18F-NaF. The Journal Of Nuclear Medicine (7):1138-1143.
Winkler J, Lunsdorf H. 2001. Ultrastructure and composition of asteroid bodies. Invest Ophthalmol Vis Sci 42(5):902-
Wu Y-F, Swaab DF. 2005. The human pineal gland and melatonin in aging and Alzheimer’s disease. J Pineal Research
Yoshida H, Murachi T, Tsukahara I. 1985.: Distribution of calpain I, calpain II and calpastatin in the bovine lens. Invest
Ophthalmol Vis Sci 26:953.
Younan C, Mitchell P, Cumming R, Rochtchina E, Panchapakesan J, Tumuluri K. 2003. Cardiovascular disease, vascular
risk factors and the incidence of cataract and cataract surgery: the Blue Mountains Eye Study. Ophthalmic Epidemiol
Yu AKF, Shek TWH. 2001. Hydroxyapatite Formation on Implanted Hydrogel Intraocular Lenses. Arch Opthalmol 611-
Zimmerman L E, Johnson FB. 1958. Calcium oxalate crystals within ocular tissues, Arch. Ophthalmol. 60: 373.
Appendix: Risk factors for Cataract other than Fluoride
Risk factors for Cataract include physical injury to the eye, exposure to solar radiation (UV-B), intense heat and
dehydration, rare genetic disorders and dietary supplements, not discussed in any detail here.
Below is a brief tabulation of references that discuss identified risk factors for cataract that do not involve Fluoride.
However it is worth noting that some multivitamin preparations do contain deliberately added Fluoride, despite the
USFDA ban on the practice.
Table 1. Cataract Risk Factors not Associated with Fluoride
Family History of Cataract
Multivitamin ⁄ Mineral supplements
David 1984, Hightower
1987, Mishra 2013
Solar, UVB radiation, X-rays
Dexamethasone sodium phosphate
1.1 - 1.5
Latitude (light intensity)
Bone Marrow Transplantation
Measles, Mumps and Rubella
Gout medications, Allopurinol
Oral hypoglycaemic agents
The cataracts associated with bone marrow transplantation are thought to be caused by the radiation [Aristei 2002].
X-rays were noted to induce cataracts in human subjects during the first two decades of the 20th century.
Solar radiation and especially its Ultraviolet component produces significantly more cataracts in people over 65 years
of age living in regions with more hours of sunshine. Comparison of human lenses removed for cataract in Rochester,
New York, Tampa, Florida, and Manila, The Philippines revealed a significant correlation between the prevalence of
black cataracts, proximity to the equator, and outdoor occupation.
Black or brown cataracts are different to mineralized cataracts and exhibit damage to protein and organic structure
and are formed of brown pigments from tryptophan (significantly elevated in UV cataract patients) and free radical
cross-linking of lens proteins in the absence of adequate sulfhydryl groups in glutathione. Tryptophan and its
metabolite, kynurenine, bind to lens protein.
Young children with the inborn error of metabolism, galactosaemia, develop cataract as part of this fatal disorder. It
has been postulated that the excess galactose is metabolized by aldose reductase to dulcitol, which accumulates in
the lens and leads to cataract formation. Similarly, it has been shown that male subjects who lack glucose-6-
phosphate dehydrogenase in their red blood cells have an increased rate of presenile cataract formation in adult life
Calcium-activated proteolysis has been studied in the lens nucleus during selenite cataractogenesis [David 1984,
Hightower 1987, Mishra 2013].