Abstract
The Asembagus irrigation area (East Java, Indonesia) receives a high input of fluoride (F) via surface water that partially originates from the hyperacid crater lake of the Ijen volcano. Endemic dental fluorosis among local residents has been ascribed to F in water wells. In this study, the total F intake by children and adults was estimated, based on concentrations in well waters and foods throughout the area. These values were compared with the Lowest Observed Adverse Effect Level (LOAEL) for dental fluorosis among children and skeletal fluorosis among adults. Fluorosis hazard maps were prepared, identifying the most hazardous locations in the area. It was concluded that there is not only a high risk of dental fluorosis, but also of skeletal fluorosis. Based on the total daily intake, the lowest F concentration in drinking water that poses a risk of developing fluorosis is approximately 0.5 mg/l for dental fluorosis and 1.1 mg/l for skeletal fluorosis. This is below 1.5 mg/l, which is both the guideline value for drinking water from the World Health Organization (WHO) and the Indonesian drinking water standard. This is the first documented case of human health problems that may be directly associated with natural pollutants originating from a volcano-hosted crater lake.
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A Brief and Critical Review of Chronic Fluoride Poisoning (Fluorosis) in Domesticated Water Buff aloes (Bubalus bubalis) in India: Focus on its Impact on Rural Economy.
In the rural areas of India, fl uoridated drinking water, industrial fluoride pollution and fluoride rich feed phosphate supplements are the major sources of fluoride exposure for domesticated water buffaloes (Bubalus bubalis). However, the fluoridated drinking groundwater is the commonest and principal source of fluoride exposure for these ruminants. Chronic
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Fluoride exposure altered metabolomic profile in rat serum
Highlights 58 NEG and 73 POS metabolites were altered in F-treated 3 weeks rat serum. 126 NEG and 70 POS metabolites were altered in F-treated 11 weeks rat serum. Four significantly different metabolites, nicotinamide, adenosine, 1-Oleoyl-sn-glycero-3-phosphocholine, and 1-Stearoyl-sn-glycerol 3-phosphocholine were shared by two models. Urea, N2-Acetyl-l-ornithine, and betaine were
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Health risk in children to fluoride exposure in a typical endemic fluorosis area on Loess Plateau, north China, in the last decade
Highlights Fluoride concentrations were 0.55 mg L-1 in 3427 water consumption points in Shanxi Province. Health risks were assessed for children consumers regarding fluoride exposure. Approximately 10%, 1.3% and 0.06% children are at risk for dental decay, dental and skeletal fluorosis, respectively. The fluoride concentrations were being decreased significantly from
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Downregulation of miR-4755-5p promotes fluoride-induced osteoblast activation via tageting Cyclin D1.
Background Endemic fluorosis remains a major public health issue in many countries. Fluoride can cause abnormalities in osteoblast proliferation and activation, leading to skeletal fluorosis. However, its detailed molecular mechanism remains unclear. Based on a previous study, the aim of this study is to explore the role of miRNA in osteoblast
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Osteo-dental fluorosis in domestic horses and donkeys in Rajasthan, India.
Chronic fluoride (F) intoxication in the form of osteo-dental fluorosis was observed in 23 domestic equus animals, 9 to 23 years old, including 14 horses (Equus caballus), and 9 donkeys (E. asinus) living in F endemic areas of Dungarpur district, Rajasthan, India. The mean F concentration in the drinking water
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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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Tea Intake Is a Risk Factor for Skeletal Fluorosis
A number of recent studies have found that heavy tea drinkers can develop skeletal fluorosis - a bone disease caused by excessive intake of fluoride.
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"Mild" Dental Fluorosis: Perceptions & Psychological Impact
The vast majority of research has found that patients, parents, and the general public alike view mild fluorosis (TF score 3) as a significant blemish of the teeth, one that is likely to embarrass the affected child to a degree that cosmetic treatment would be warranted.
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