Abstract
In reviewing the effects of the 2 pollutants on vegetation and domestic animals there can be no doubt that airborne F– is far more harmful than sulfur oxides. F– reaches the blood stream both through inhalation and by ingestion with contaminated food. In plants the translocation of F– throughout the plant structure and its damaging effect on leaves, blossoms and fruit is much more pronounced than that of sulfur oxides. Sulfur oxides irritate, primarily, the upper respiratory tract. They rarely enter the distal portions of the lungs and the alveolar system. They never enter the blood stream. F–, a systemic poison, is promptly absorbed into the blood stream from the upper respiratory tract. It affects primarily the calcified tissue but can also induce considerable damage to many other organs, especially the arteries and the heart. Where there is smoke from buringing coal there is also F–. The systemic damage to humans believed to have been induced by sulfur oxides is likely to be primarily brought on by F– in conjunction with toxic agents such as As, Cd and Hg present in coal.
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Chronic fluorosis: the disease and its anaesthetic implications..
Abstract Chronic fluorosis is a widespread disease-related to the ingestion of high levels of fluoride through water and food. Prolonged ingestion of fluoride adversely affects the teeth, bones and other organs and alters their anatomy and physiology. Fluoride excess is a risk factor in cardiovascular disease and other major diseases, including
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ESPEN micronutrient guideline
Background Trace elements and vitamins, named together micronutrients (MNs), are essential for human metabolism. Recent research has shown the importance of MNs in common pathologies, with significant deficiencies impacting the outcome. Objective This guideline aims to provide information for daily clinical nutrition practice regarding assessment of MN status, monitoring, and prescription. It proposes
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Systematic impacts of fluoride exposure on the metabolomics of rats.
Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,
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Electrocardiogram analysis of patients with skeletal fluorosis
To investigate the degree of myocardial damage resulting from endemic fluorosis, electrocardiograms of 136 skeletal fluorosis patients from an endemic fluorosis area were compared with electrocardiograms of a control group of 40 normal patients from a non-endemic fluorosis area. The results show that fluoride in drinking water consumed over time
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Fluorosis in Aden
The cases to be described here occurred in the Aden Protectorate where for the last 12 years mass screening of the chest to exclude pulmonary tuberculosis has been carried out. The patients had all drunk the brackish water from the wells, and the analysis of the water from a well
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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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Fluoride & Myocardial Damage
Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha
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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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Fluoride & Arteriosclerosis
Healthy arteries are flexible and elastic, allowing efficient transfer of blood and nutrients from the heart to the rest of the body. Arteriosclerosis refers to a stiffening of the arteries, including loss of elasticity. This is a slow, progressive disease that may begin early in life from damage to the
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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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