Abstract
The present investigation was conducted to evaluate the teratogenic and developmental toxicity of fluoride and endosulfan alone and in combination in pregnant Swiss albino mice exposed during the organogenetic period (5-14 days) of gestation. Fluoride (25.1 mg/kg body weight in water) and endosulfan (1.8 mg/kg bw by oral intubation) when administered alone and in combination (fluoride 25.1 mg/kg bw + endosulfan 1.8 mg/kg bw) to pregnant mice caused significant teratogenic effects in developing fetuses. There was no maternal mortality but significant decreases in maternal weight gain and numbers of live fetuses and significant increases in numbers of fetal resorption were recorded in the treated groups. The fetal body weight and litter size also decreased significantly in all treated groups. No external malformations were observed in any of the fetuses. The percent of visceral and skeletal anomalies increased in the fetuses of all treated groups. The fetal malformations observed were internal hydrocephaly, microphthalmia, anophthalmia, pulmonary edema, subcutaneous edema, reduced ossification of skull bones, widened cranial sutures, rib anomalies (short, wavy, partially ossified, or absent ribs), and reduced ossification of phalanges. The occurrence of visceral and skeletal malformations was more severe in the combination group, suggesting additive interaction of fluoride and endosulfan in inducing developmental toxicity in Swiss albino mice.
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Environmental Fluoride 1977 by Rose & Marier
The Associate Committee on Scientific Criteria for Environmental Quality was established by the National Research Council of Canada in response to a mandate provided by the Federal Government to develop scientific guidelines for defining the quality of the environment. The concern of the NRC Associate Committee is strictly with scientific
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Effect of deltamethrin and fluoride co-exposure on the brain antioxidant status and cholinesterase activity in Wistar rats
The study evaluated the effect of commercial preparation of deltamethrin, Butox®, and fluoride (F-) co-exposure on the brain antioxidant status and cholinesterase activity in rats. Group A was untreated. Group B was gavaged Butox®, providing deltamethrin at the dose rate of 1.28 mg per kg body weight per day. Group
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Fluoride Sources, Toxicity and Fluorosis Management Techniques - A Brief Review.
Highlights Overexposure to fluoride via drinking water causes several health effects including fluorosis Endemic fluorosis is still persisted in several countries even with advancement in research Most of fluorosis management techniques suggested in the past have come with their own drawbacks Defluoridation techniques based on aluminium materials pose serious
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Fluorine and Fluorosis [June 1944].
Excerpt The first account of mottled enamel in human beings was given in 1902 by Eager of the United States Public Health Service who noticed its frequency among Italian emigrants from Naples. Black and McKay (1916) found it occurring in various parts of the U.S.A. and described it more fully in
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Human health risk assessment in aluminium smelting site: Soil fluoride bioaccessibility and relevant mechanism in simulated gastrointestinal tract.
Incidental oral ingestion is considered to be an important exposure route for humans to soil contaminants, such as fluoride (F). For 25 soil samples containing 4000 mg F/kg from aluminium smelting site in southwestern China, this study investigated F bioaccessibility in the human gastrointestinal tract in vitro. Fluoride bioaccessibility (2.4-48.8%)
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Fluoride's Effect on Fetal Brain
The human placenta does not prevent the passage of fluoride from a pregnant mother's bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning. As highlighted by the excerpts
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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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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 & IQ: 76 Studies
Note: See the Updated list of fluoride IQ studies at https://fluoridealert.org/researchers/fluoride-iq-studies/the-fluoride-iq-studies/ • As of July 18, 2022, a total of 85 human studies have investigated the relationship between fluoride and human intelligence. • Of these investigations, 76 studies have reported that elevated fluoride exposure is associated with reduced IQ in humans. • The studies
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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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