Abstract
A clinical study was made on 65 cases with the syndrome of arsenism and fluorosis (SAD) from March 1982 to August 1989. All the cases with this syndrome had drunk a well water containing arsenic 0.6 mg/L and fluorine 3.45 mg/L for a long period. The patients all had the clinical manifestations of both chronic arsenism and fluorosis. It was a kind of syndrome caused by the combined harmful effects of these two trace elements, arsenic and fluorine. Higher incidences of peripheral neuritis and cardiovascular changes were found in these patients than in that with single chronic arsenism or single fluorosis. The chief diagnostic criteria of the SAF were recommended as follows: (1) having drunk high arsenic and high fluorine water for a long period, (2) having the two principal symptoms of chronic arsenism or one of them, arsenic keratosis and/or arsenic dyspigmentation, (3) having the principal symptoms and/or signs of chronic fluorosis, clinical or roentgenographic manifestations of dental fluorosis and/or osteofluorosis. However, no final conclusion has yet been reached on the morbidity of both skin and visceral tumors in this series. The incidence of skin cancer was 7.7 percent and a patient [with] a grade II squamous cell carcinoma of esophagus was found.
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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Buffalo (Bubalus bubalis) epiphyseal proteins give protection from arsenic and fluoride-induced adverse changes in acetylcholinesterase activity in rats
The objective of this study was to determine the effect of fluoride (F) and arsenic (As) on the activity of acetylcholinesterase (AChE), a critically important nervous system enzyme, and to test the protective role of buffalo epiphyseal (pineal) proteins (BEP) in rats. Arsenic (20 mg/kg BW, intraperitoneally) and F (150
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Curcumin supplementation protects from genotoxic effects of arsenic and fluoride
The present study was aimed to evaluate curcumin as a potential natural antioxidant to mitigate the genotoxic effects of arsenic (As) and fluoride (F) in human peripheral blood lymphocytes. The study was divided into nine groups consisting of negative control, positive control treated with ethyl methane sulphonate (EMS; 1.93 mM)
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Co-exposure to inorganic arsenic and fluoride prominently disrupts gut microbiota equilibrium and induces adverse cardiovascular effects in offspring rats.
Highlights Co-exposure to arsenic and fluoride leads to adverse cardiovascular effects. Co-exposure to arsenic and fluoride results in gut microbiota perturbations. Co-exposure causes more prominent effects than arsenic or fluoride alone. Strong correlations are identified between cardiovascular effects and significantly altered genera. Co-exposure to inorganic arsenic (iAs) and fluoride (F-)
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Inflammatory responses induced by fluoride and arsenic at toxic concentration in rabbit aorta.
Epidemiological and experimental studies have demonstrated the atherogenic effects of environmental toxicant arsenic and fluoride. Inflammatory mechanism plays an important role in the pathogenesis of atherosclerosis. The aim of the present study is to determine the effect of chronic exposure to arsenic and fluoride alone or combined on inflammatory response
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Fluoride, Blood Pressure and Hypertension
Individuals with blood pressure readings that exceed 140/90 are considered hypertensive. Hypertension can increase the risk of stroke, heart attack, heart failure, aortic aneurysms, and peripheral arterial disease. An association between increased fluoride in ground water and increased prevalence of hypertension has been observed, especially among adult males (Amini et
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Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
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