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Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Excessive intake of fluoride gives rise to fluorosis, a disease characterized by excessive bone hardening leading to bones breaking easily. High concentrations of fluoride in drinking water causes corrosion of the enamel of the teeth, a process called mottling (8). Fluorosis is often observed in people living in areas where the soil is too rich in fluoride. Fluorosis has been observed in some region of China such as Tibet in people who have been drinking brick tea for many years. The fluoride concentration of brick tea is 200–300 times higher than ordinary green tea and black tea because brick tea (tea compressed into brick shape) is made from old stems and leaves of the tea tree, but ordinary green tea and black tea are made from tender leaves and buds (29). High intake of fluoride, in excess of one mg/l, results in mottling of the teeth; the enamel is no longer lustrous and becomes rough, an effect particularly marked on the upper incisors. In concentrations well in excess of ten parts per million, fluoride poisoning can occur, causing a loss of appetite and sclerosis of the bones of the spine, pelvis, and limbs (9).
Ultratrace Minerals
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Because most fluoride intake is derived from water intake, local geographic influences and addition of fluoride to municipal supplies of tap water largely determine fluoride intake. As a result, fluoride deficiencies severe enough to affect dental enamel and bone density appear to be isolated and uncommon. However, fluoride toxicity is an increasing concern.1046 Acute lethal doses of fluoride in man are 32 to 64 mg/kg, an extremely high dose. Nevertheless, accidental acute fluoride poisoning has resulted in at least 45 deaths (43 from an accidental poisoning in a single hospital in the early 1940s).1046 Of more practical concern is chronic fluoride toxicity, manifested as dental and skeletal fluorosis.1046 Dental fluorosis (ranging in severity from white spots on teeth to hypomineralization with staining and pitting of enamel) is increasing in frequency in the U.S. but, overall, is usually mild with no aesthetic changes. Skeletal fluorosis results from chronic ingestion of 10 to 25 mg of fluoride per day for years. Skeletal hypermineralization, soft tissue calcification (especially tendons and ligaments), and exostosis formation are apparent and may progress to crippling.1046 Thus, fluoride exhibits a narrow window of safe and adequate intake. Bone defects are manifested during both deficiency and toxicity of fluoride.
Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice
Published in Pharmaceutical Biology, 2019
Haoyue Yang, Ronge Xing, Song Liu, Huahua Yu, Pengcheng Li
Previous studies in various model systems reported that oxidative stress and oxygen-derived free radicals play important roles in the pathogenesis of NaF-induced thyrotoxicity. Oxidative stress involving fluoride toxicity causes DNA damage in various cell types (Altuntas et al. 2002), which leads to abnormal metabolism and structural damage. Fluoride poisoning increases blood MDA and decreases blood GR and APX, which are manifestations of oxidative stress. GABA is a powerful antioxidant that protects the thyroid from oxidative stress-mediated cell damage (Inoue et al. 2003; Cho and Chang 2007). In this study, it was shown that a daily dose of 50 mg/kg of GABA over 14 days relieved oxidative stress, decreased MDA content, increased GR and APX activities and restored the antioxidative effects of the thyroid in mice exposed to fluoride.
The effect of simultaneous exposure of human fibroblasts to fluoride and moderate intensity static magnetic fields
Published in International Journal of Radiation Biology, 2019
Magdalena Kimsa-Dudek, Agnieszka Synowiec-Wojtarowicz, Małgorzata Derewniuk, Monika Paul-Samojedny, Katarzyna Pawłowska-Góral
Fluoride compounds are present in soil, water and in plant and animal source foods. They are also used in dental products and drugs. Aluminum smelters, the iron and steel industry, the phosphate industry and ceramic plants emit the most fluoride compounds. Moreover, occupational exposure fluoride occurs in plants that convert fluorspar, cryolite and apatite (Jakubowski 2008). Hence, fluoride may enter the body with food, through respiration and the skin. According to the New Hampshire Department of Environmental Services (NHDES 2008), inhalation and skin absorption can be significant for some occupational exposure situations. Therefore, the possibility of chronic fluoride poisoning that might have toxic effects in the future should be considered. Moreover, workers in aluminum production are simultaneously exposed to fluorides and static magnetic fields (SMFs) with a low to moderate induction (Katsnelson et al. 2016). Many studies have been conducted on the human response to SMFs because of the widespread exposure to it in the natural environment as well as occupational exposure. In vitro and in vivo studies into the effects of exposure to an SMF on the DNA structure (Potenza et al. 2004; Ghodbane et al. 2013; Romeo et al. 2016), the gene expression profile (Im et al. 2012; Polidori et al. 2012), the proliferative activity of normal and tumor cells (Sullivan et al. 2011; Varshney and Kumar 2013; Romeo et al. 2016; Tian et al. 2018; Yang et al. 2018; Yuan et al. 2018), the proliferation and ability of stem cells to differentiate (Marędziak et al. 2014, 2015, 2017; Kim et al. 2015), redox homeostasis (Ghodbane et al. 2013), the wound-healing process (Zhao et al. 2017; Song et al. 2018) and a number of others (Albuquerque et al. 2016) have produced largely contradictory results. The effects of this influence may depend on many factors such as the experimental parameters, research conditions, exposure system, exposure times and magnetic flux density of the SMF that is used.
Morbidity and mortality resulting from acute inhalation exposures to hydrogen fluoride and carbonyl fluoride in rats
Published in Inhalation Toxicology, 2018
Adolph J. Januszkiewicz, Matthew A. Bazar, Lee C. B. Crouse, Michael A. Chapman, Steven E. Hodges, Steven J. McCormick, Arthur J. O’Neill
The present experiments revealed that COF2 is markedly more lethal than HF. Hydrogen fluoride also was found to be less lethal than previously reported. The mechanisms by HF which HF and COF2 cause morbidity and mortality are not fully understood. Given their common chemistry and metabolism in the body they likely share similar and multiple injury mechanisms. Tissue necrosis, airways nerve and receptor stimulation, activation of inflammatory pathways, and disruption of cell metabolism may be common consequences of exposure to both gases. However, HF and COF2 appear to present different toxicity profiles. For example, the majority of deaths occurred acutely with the COF2 exposures, while the majority of deaths by HF exposure occurred after a few days post-exposure. HF exposures caused pathologic lesions in kidneys and livers, a previously reported HF outcome (Machle & Kitzmiller, 1935; Rosenholtz et al., 1963) while similar effects were not seen with COF2 exposures. In addition, animals surviving the COF2 exposure tended to recover while the general health of HF-exposed rats appeared to worsen over the 6-day observation period; another reported outcome of HF inhalation (Ronzani, 1909; Stokinger, 1949). Finally, mid-level COF2 exposures caused pulmonary edema while none of the HF-exposed rats demonstrated significant lung weight changes. Given the lack of significant lower airway issues, delayed mortality, and much higher fluoride burden than COF2, the deaths caused by HF are considered to be caused by a combination of fluoride poisoning and associated obstructive and restrictive impediments to normal breathing. Conversely, immediate deaths from COF2 are likely attributed to its stronger irritant properties which elicited a profound physiologic response which ultimately led to asphyxia. It also appeared to initiate inflammatory processes which led to the development of pulmonary edema at mid-level exposure levels. Temporally, the COF2 profile is similar to other inhaled irritant gases known to induce acute lung injury (Miller, 2013). Although COF2 and HF may have common injury mechanisms, COF2 potency as an irritant, capacity to reach the lower airways, and exert effects at a lower fluorine burden, compared to HF, may explain the differences seen in toxicity profiles between these two gases.