Fluoride exposure may lead to a reduction in kidney and liver function among adolescents


Fluoride exposure may lead to a reduction in kidney and liver function among adolescents, according to a study published by Mount Sinai researchers in Environment International in August.

The study examined the relationship between fluoride levels in drinking water and blood with kidney and liver health among adolescents participating in the National Health and Nutrition Examination Survey, a group of studies that assess health and nutritional well-being in the United States.

The findings showed that exposure to fluoride may contribute to complex changes in kidney and liver function among youth in the United States, where 74 percent of public water systems add fluoride for dental health benefits.

Fluoridated water is the main source of fluoride exposure in the U.S..

The findings also suggest that adolescents with poorer kidney or liver function may absorb more fluoride in their bodies.

While fluoride exposure in animals and adults has been associated with kidney and liver toxicity, this study examined potential effects of chronic low-level exposure among youth.

This is important to study because a child’s body excretes only 45 percent of fluoride in urine via the kidneys, while an adult’s body clears it at a rate of 60 percent, and the kidneys accumulate more fluoride than any other organ in the body.

“While the dental benefits of fluoride are widely established, recent concerns have been raised regarding the appropriateness of its widespread addition to drinking water or salt in North America,” said the study’s first author Ashley J. Malin, Ph.D., postdoctoral fellow in the Department of Environmental Medicine and Public Health at the Icahn School of Medicine at Mount Sinai.

“This study’s findings suggest that there may be potential kidney and liver health concerns to consider when evaluating fluoride use and appropriate levels in public health interventions.

Prospective studies are needed to examine the impact of chronic low-level fluoride exposure on kidney and liver function in the U.S. population.”

The study analyzed fluoride measured in blood samples of 1,983 adolescents and the fluoride content of the tap water in the homes of 1,742 adolescents.

Although the tap water fluoride concentrations were generally low, there are several mechanisms by which even low levels of fluoride exposure may contribute to kidney or liver dysfunction.

This study’s findings, combined with previous studies of childhood exposure to higher fluoride levels, show there is a dose-dependent relationship between fluoride and indicators of kidney and liver function.

The findings, if confirmed in other studies, suggest it may be important to consider children’s kidney and liver function in drafting public health guidelines and recommendations.

Potential health side effects include renal system damage, liver damage, thyroid dysfunction, bone and tooth disease, and impaired protein metabolism.

Age-related macular degeneration (AMD), cataracts and glaucoma are the leading causes of eye diseases and blindness worldwide.

AMD is caused by progressive degeneration of retinal pigment epithelial (RPE) cells and neural retina. AMD is the leading cause for irreversible damage of the vision of people over the age of fifty [1].

The pathogenesis of AMD, which covers a complex interaction of genetic and environmental factors, is strongly associated with chronic oxidative stress that ultimately leads to protein damage and degeneration of RPE [2].

Among the risk factors for AMD are diet, smoking, obesity, hypertension, cardiovascular disease and diabetes [3,4,5,6,7,8,9,10].

Cataracts result from the deposition of aggregated proteins in the eye lens and lens fibre cells plasma membrane damage which causes clouding of the lens, light scattering, and obstruction of vision [11].

Cataract is a multifactorial disease associated with age, diet, smoking, environmental exposure to UVB radiation and inflammatory degenerative diseases such as diabetes, asthma or chronic bronchitis and cardiovascular disease [12,13,14,15].

A recent meta-analysis also found that hypertension increases the risk of cataract [16].

It is important to note that a significantly higher prevalence of cataract is found in individuals with Down syndrome [17,18,19,20], schizophrenia [21] and diabetes [22].

Worldwide, cataract remains the predominant cause of blindness and moderate to severe visual impairment (MSVI) and was the second most common cause of blindness in 2010, after macular degeneration, in five world regions (high income Asia Pacific, Australasia, Western Europe, Southern Latin America, and high-income North America). Overall, one in three blind people was blind due to cataract, and one of six visually impaired people was visually impaired due to cataract in 2010 [23].

Glaucoma can be viewed as neurodegenerative disease involving a progressive loss of retinal ganglion cells (RGC) and characteristic changes in neuroretinal rim tissue in the optic nerve head (ONH) which are accompanied by visual field loss [24].

Hypertension and diabetes are associated with increased risk of glaucoma [25].

From a population health perspective, degenerative eye diseases place a significant burden on society and the public health system.

In the Republic of Ireland (RoI), it has been estimated that there were nearly 224,832 people with vision impairment and blindness in 2010.

The most common causes of blindness were macular degeneration, glaucoma and cataracts. The total economic cost of vision impairment and blindness was estimated to be €2.14 billion in 2010, which is projected to rise to nearly €2.67 billion by 2020 [26].

In 2016, some 218,000 cataract surgeries took place in the RoI [27], however, due to delays performing surgery and patient waiting lists an increasing number of Irish citizens are travelling abroad for cataract operations A recent study found that the prevalence of AMD in adults over 50 years of age in the RoI was 7.2% [28].

Elsewhere, Nolan et al. reported that the prevalence of early AMD was 28% in a randomly selected sample of Irish subjects over 50 years of age [29].

In the EUREYE Study the prevalence of AMD in persons 65 years and older in seven European countries including, Bergen, Norway; Tallinn, Estonia; Belfast, Northern Ireland, U.K.; Paris-Creteil, France; Verona, Italy; Thessaloniki, Greece; and Alicante, Spain was 3.3%, with no significant differences found among the participating countries. The prevalence of AMD in Belfast, Northern Ireland among person over 65 years was 3.77% [30].

More recently, Colijn et al. reported in 2017 that the prevalence of early AMD among participants from 10 countries in Europe including Estonia, France, Germany, Greece, Italy, Northern Ireland, Norway, Netherlands, Spain, Portugal, and the U.K. was 3.5% among persons aged 55–59 years [31].

Previously, Owen et al. reported that the prevalence of AMD in the U.K. among people aged 50 years or over is 2.4% (from a meta-analysis applied to UK 2007–2009 population data). This increases to 4.8% in people aged 65 years or over, and 12.2% in people aged 80 years or over [32]. In Iceland, it has been reported that the prevalence of AMD among subjects 50 years and older is 2.3% [33], which is similar to that reported in Norway among subjects 51 years and older (2.9%) [34].

In the Netherlands, Klein et al. reported a prevalence of 1.2% for AMD among the population under 85 years of age [35]. In the Japanese population, the prevalence of early AMD in the Funagata Study was 3.5% among all participants 35 years and older and 4.3% in those 50 years and over [36].

Similar to the RoI, significantly higher prevalence rates of AMD have been reported in the United States (U.S.). For example, Klein et al. reported that the prevalence of AMD among persons over 40 years was 6.5%. Among non-Hispanic whites the prevalence was 7.3% [37]. Previous US studies reported that the prevalence of early AMD among non-Hispanic whites was 14.7% among adults aged 60 years and over [38].

In addition to AMD, the prevalence of cataracts among individuals over 40 years of age in the US was 17.2% in 2004 [39]. Furthermore, by 2020, over 30.1 million people are projected to have cataracts in the U.S. [39]. In 2015, some 9000 ophthalmic surgeons were performing 3.6 million cataract surgeries in the U.S. [40]. The average cost of cataract surgery in the U.S. has been reported to be US $2525 [41]. This suggests that the costs associated with cataract surgery alone in the USA may be in excess of 9 billion dollars annually. Elsewhere it has recently been reported that the economic cost of treating diabetes is over 176 billion dollars a year in the United States, of which over 20% is spent on the ophthalmic complications [42]. As previously noted, diabetes is associated with significantly increased risk of cataract, AMD and glaucoma.

A higher prevalence rate of AMD has also been reported in Australia.

Recently Keel et al. reported that the weighted prevalence among nonindigenous Australians 50 years and older was 14.8% for early AMD and 10.5% for intermediate AMD. Among indigenous Australians 40 years and older, the weighted prevalence was 13.8% for early AMD and 5.7% for intermediate AMD. Among persons aged 70–79 years the prevalence was 17.4% for early AMD and 14.7% for intermediate AMD [43].

In Australia a 2.6-fold increase in the total number of cataract procedures was also documented between 1985 to 1994 [44]. Moreover, the rate of cataract surgery per thousand persons aged 65 years or older doubled between the mid-1980s and mid-2000s [45]. McCarthy et al. previously reported that the prevalence of cataracts among Australians over 40 years of age was 12.6% [46].

Rochtchina et al. reported that by the year 2021 the number of people affected by cataract in Australia will increase by 63%, due to population aging [47]. In New Zealand, the prevalence of AMD is uncertain due to a lack of appropriate studies, but it was estimated in 2014 that it affected 10% of people aged 45–85 years, and 38% of people aged over 85 years [48].

It was further estimated that AMD accounts for 48% of cases of blindness among adults aged 50 years and older in New Zealand and causes approximately 400–500 new cases of blindness per year [49,50]. Moreover, it is estimated that 370,000 of the population have cataracts and 30,000 cataract surgeries are performed every year in New Zealand, [51].

As elucidated above, evidence tentatively suggests that the overall prevalence of degenerative eye diseases, particularly AMD, is significantly higher in developed countries with water fluoridation; including, the RoI, U.S., Australia and New Zealand, than in other developed countries without fluoridation of drinking water. Within Europe, the 3-fold differences in prevalence rates for AMD between the RoI the U.K. and mainland Europe are intriguing, especially considering the proximity of the RoI to the U.K. and the shared landmass of the island of Ireland, along with similarities in diet and genetic makeup

It is important to highlight that drinking water is artificially fluoridated in the RoI since 1964, with currently over 80% of households provided with fluoridated water compared to <10% in the U.K. In mainland Europe, drinking water is fluoridated in only one small region, principally the Basque country of Spain since 1988.

Evidence in support of the hypothesis that fluoride (F) intake may be a contributory factor to degenerative eye diseases include several studies documenting that F can accumulate to high concentrations in the eye contributing to retinal toxicity [52,53,54,55,56,57].

An association between chronic F exposure and cataracts has also been reported in human [58,59,60,61,62,63] and animal studies [64,65].

Furthermore, early in vitro studies by Nordmann et al. using calf lens confirmed that a blockage of the breakdown of sugars by F is followed by cataracts [66].

Further in vitro studies examining metabolism of the lens and of retina identified that F is an enzyme inhibitor in ocular tissue [67,68,69].

Consistent with this finding, early research by Dickens and Simer observed that F significantly inhibited glycolysis in the retina [70]. Previous human studies have also reported an association between chronic F intake and iridocorneal angle hyperpigmentation and open angle glaucoma [71].

However, there is a paucity of qualitative research in epidemiology in western countries to examine the possible association between F intake, water fluoridation and degenerative eye diseases and no study until now has elucidated the molecular mechanisms by which F intake may increase the likelihood of AMD, cataracts or glaucoma.

Given the high societal and economic costs of eye diseases in developed countries and globally, a review of modifiable risk factors and the molecular mechanisms by which chronic F exposure may contribute to degenerative eye diseases is therefore warranted.

Although much information has become available in recent decades, evidence of a causal relationship requires plausible biological mechanisms by which chronic F exposure may contribute to degenerative eye diseases.

Consequently, the purpose of the present study is therefore to elucidate for the first time the key biological mechanisms underlying how F exposure may contribute to degenerative eye diseases including AMD, cataracts and glaucoma.

This study therefore provides important insights into the molecular mechanisms by which F intake contributes to degenerative eye diseases and complements the findings of previous human and animal studies making it possible to reach definite conclusions.

An understanding of the mechanisms can also elucidate the conditions under which dietary intervention will be most effective and help to identify target populations who may receive optimal benefits.Go to:

The Role of Fluoride in Oral Health and Dietary Sources of Fluoride

Today, community water fluoridation and F toothpaste are considered the most common sources of F exposure in the U.S. [72].

In countries such as the RoI, U.K., Australia and New Zealand, where habitual tea drinking is commonplace, the major dietary source of F is tea consumption [73,74,75].

In addition to tea, fluoridated water, and toothpaste other sources of F exposure include other beverages produced from fluoridated water (beers, coffee, soft drinks, and fruit juices); pesticide residues in foods, foods processed or cooked in fluoridated water; foods grown in soil containing F or irrigated with fluoridated water; consumption of foods with elevated F levels (i.e., seafood and processed chicken); foods cooked in Teflon cookware; tobacco consumption; use of fluoridated mouthwash; use of medical inhalers containing fluoridated gases, and fluoridated medications, in addition to other environmental or occupational exposures to F [75].

F has no known essential function in human growth and development and no signs of F deficiency have been identified [76]. However, F is considered to have played a major role in the reduction of dental caries in the past decades in the industrialized countries.

It is added as an anti-caries agent to a variety of vehicles, particularly drinking water and toothpastes.

Though F is not essential nutrient, current views of its anti-caries action suggest that it is beneficial in the prevention of dental caries when applied topically on the tooth surface and ingestion is not required [77,78]. However, caries is not a F deficiency disease [76].

Journal information: Environment International
Provided by The Mount Sinai Hospital


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