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These studies suggest fluoride intoxication symptoms include lethargy, violent movement, severe burns, hypocalcaemia, metabolic poisoning, organ failure, and neurodevelopmental issues, with severity influenced by environmental and genetic factors.
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Acute fluoride intoxication can severely disrupt multiple physiological systems. As a potent acid, fluoride acts corrosively on the skin and mucous membranes, leading to severe burns. It also binds tightly to essential cations, causing profound hypocalcemia, which inhibits normal blood coagulation. Additionally, fluoride acts as a metabolic poison, stimulating some enzymes while severely inhibiting others, such as Na+-K+-ATPase and enzymes involved in carbohydrate metabolism. These disruptions can lead to death, often due to delayed, explosive hyperkalemia .
In fish, acute fluoride intoxication manifests as lethargy, violent and erratic movements, and death due to partial or complete muscle contraction. Excessive mucus production and changes in serum protein patterns are also observed. In rainbow trout embryos, symptoms include lethargy, violent movement, and tetany, with the rupturing of the chorion attributed to violent movements during intoxication onset .
In cases of acute fluoride poisoning, such as the incident in a New Mexico elementary school, symptoms included gastrointestinal distress, with patients experiencing mild and short-duration symptoms. The bitter, salty taste of the water, which contained elevated fluoride levels, deterred large consumption and prevented severe intoxication. Additionally, fluoride inhalation can lead to progressive destruction of bronchial mucosa and lung tissue, and irrespective of the dose, can cause transient renal function restriction or acute renal failure.
Chronic fluoride intoxication primarily affects the skeletal system, inducing differentiation and apoptosis of osteoblasts and osteoclasts, leading to various skeletal injuries. Active osteogenesis and accelerated bone metabolism are key processes in the progression of skeletal fluorosis, resulting in diverse osteogenic lesions.
Fluoride also impacts non-skeletal tissues, inducing free radical oxidation in the cerebral cortex and causing nerve cell damage. In the heart muscle, fluoride exposure leads to oxidative stress, decreased antioxidant enzyme activity, and functional and structural disorders in the myocardium. Additionally, fluoride intoxication can cause degenerative and inflammatory changes in the respiratory system, liver, and kidneys, as well as structural disorders and dysfunction of the thyroid gland. Increased levels of reactive oxygen species and apoptosis in these organs are also noted. In reproductive organs, fluoride exposure results in decreased sperm motility, lack of differentiation and maturation of spermatocytes, and intensified free radical oxidation and cell apoptosis.
High fluoride exposure has been linked to neurodevelopmental delays in children. A systematic review and meta-analysis of 27 studies found that children in high-fluoride areas had significantly lower IQ scores compared to those in low-fluoride areas. This suggests an adverse effect of high fluoride exposure on children's neurodevelopment, warranting further research with detailed individual-level information on prenatal exposure and neurobehavioral performance.
Fluoride intoxication, whether acute or chronic, presents a wide range of symptoms affecting various physiological systems. Acute exposure can lead to severe burns, metabolic disruptions, and neurological symptoms, while chronic exposure primarily impacts the skeletal system and non-skeletal tissues, including the heart, liver, kidneys, and reproductive organs. Additionally, high fluoride exposure is associated with neurodevelopmental delays in children. Understanding these symptoms is crucial for the effective management and prevention of fluoride intoxication.
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